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Does the necessary Carbon Dioxide need to be in the atmosphere for mammals?
In the answers to this question, we've learnt that carbon dioxide is necessary for mammalian life, but is it necessary in the atmosphere/to breathe it in?
Or does the act of respiration give a human (or other animal) enough carbon dioxide to fulfill all of the functions that carbon dioxide is needed for?
Or, phrased another way, if you put an animal in a carbon-dioxide-free atmosphere, and continually removed the carbon-dioxide that they generate upon respiration/exhalation, would they get enough carbon dioxide to fulfill these requirements:

fatty acid biosynthesis (FAS)
mammalian/bacterial biotin-dependent carboxylation reactions.
blood pH regulation

possible duplicate of Is there any use of CO₂ in human body?

I think the core of the question is very different from the suggested duplicate. The duplicate is on what CO2 is used for, this question is on how much CO2 is sufficient to fulfill it's roles.

No it isn't necessary to breathe in CO2 from the atmosphere. For the buffer system your brain detects the amount of CO2 (H+ which is an indicator of excess or too little CO2) and adjusts your breathing automatically to compensate so that your blood's pH stays normal. No outside CO2 is needed. Your kidneys also play a similar role but the lungs are what provide a rapid response.

I know this seems intuitive, but can you add sources that support this answer? There are plenty of examples of short term non-CO2 breathing (nitrox, heliox, pure oxygen, etc.) but what about long-term?

The body is producing an excess of CO2 at all times. In fact, we need to keep venting it out just to keep alive. Furthermore, there is always expelled CO2 in our lungs, and since they never get fully empty, we always breathe air with some of our CO2. Therefore, although an answer with an experiment would be slightly better, this answer is well funded enough in basic biology.

No, mammals need not take in CO2 from atmosphere. The body's homeostatic function will maintain its composition by checking the amount of CO2 released out by lungs. So certainly animals would survive if put in a CO2 free atmosphere.

So, fatty acid synthesis (for example) occurs using carbon dioxide created within the body?  Also, got a cite?

@Hari:It would be nice if you add some references to substantiate your claim.:)

It is unneccessary for a mammal to breath in CO2, though our bodies are able to expel unneeded gasses easily. However, if there were no CO2 in the atmosphere, animals would all die, as no oxygen could be produced by plants. In other words, we don't need to breath in CO2, but we need it to be plentiful.


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What is called the "area size that an animal usually lives in"?
What is called the "area size that an animal usually lives in" or "needs for a normal life"? Is there any specific term?

To avoid confusion I just want to add to fileunderwater's answer the equivalent words we use to describe the "area size a population/species lives in".
The spatial range a single individual occupies is generally called home range or territory (as fileunderwater said before me).
The spatial range a single species (or population) occupies is called geographic range or species range and we call the boundaries of this range the geographic range limits or sometimes called range limits only.

Are you looking for 'Home range' (see also the definition in Encyclopaedia Britannica)? Generally, 'home range' is defined as the entire area an individual animal uses, while the 'territory' is the subset of the home range that is actually defended from conspecifics (in animals that show territoriality). 'Home range' is often delimited by the types of environments used and movement patterns of individuals.

Perhaps also Habitat.

The term typically refers to the zone in which the organism lives and
  where it can find food, shelter, protection and mates for
  reproduction...

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How is the type of genetic manipulation determined in CRISPR-Cas9?
I've been reading up a bit on the CRISPR-Cas9 system for gene manipulation. From what I read, it introduces double-strand breaks at specific points determined by the choice of sgRNA. But how do you get from double-strand breaks to editing genes in incredibly specific ways? As far as I read you can fix point mutations, insert whole genes or disable genes with CRISPR-Cas9. How do you specify which kind of repair mechanism is invoked?

But how do you get from double-strand breaks to editing genes in
  incredibly specific ways?

You should read the wikipedia page on CRISPR-Cas system. The target specificity is provided by the tracrRNA.

How do you specify which kind of repair mechanism is invoked?

The repair can be done either by Non Homologous End Joining (NHEJ) or Homologous Recombination (HR). If you provide excessive DNA template by transfection then it is likely to increase the chance of HR and this can be used for trangenesis.
When no template is provided then DNA can be repaired by HR with sister chromatin or NHEJ. Depending on the stage of the cell cycle one of these mechanisms is preferred over the other. HR is shown to be the most active in S-phase and starts declining in G2-phase.
So when you want to make transgenics or specific edits then co-transfect CRISPR-Cas with transgene DNA (with flanks homologous to target DNA sequence) or a homologous DNA with point mutation(s), preferably in cells at S-phase. It is possible to synchronize the cells using nocodazole or other molecules that arrest cell cycle.

I assume "sgRNA", "tracrRNA", and "guide RNA" are all the same thing? And I can imagine getting efficient editing would be a problem, since you have to get at least 2 components into the cells, the Cas gene and guide RNA could be produced by 1 plasmid, but the template DNA to direct the repair would be separate, and you'd probably want several copies per cell to improve the odds of a successful repair.

@user137 yes pretty much the same thing.. It is not that difficult; transgenesis rates are much better than in plain HR. All these kind of techniques are followed by screening and selection.

My thinking comes from in vivo work, where you'd either have to package all the parts into 1 particle, or get get multiple molecules into the same cell. Though I've seen a paper where the corrected cells are accidentally selected for in vivo.

@user137 You transfect the ESC and then implant them in the ICM right? There is still scope for artificial selection.

@user137 If you want to learn more about the Cas9 system, I wrote a detailed explanation of the original publication by M. Jinek on my blog: http://www.qmviews.blogspot.ch/2015/09/literature-004-jinek-et-al-elife-2013.html
Would be glad to hear if it helped.

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A good textbook on GMO
I am interested in learning about GMO. The topic is so wrapped in controversy, that it's hard to find a good book that introduces the basic concepts involved. I went through various university websites, but couldn't find any lecture notes on the topic. I don't know, is it too broad a topic? Is there even a book called Introduction to GMO? Maybe that's the problem.
I am interested in a book that tells you about how gene manipulation is done. How do biology students get introduced to this concept? I hope the question is not too general.

To be honest I don't remember being introduced to this at all in the classroom. I remember 1 lab in genetics where we transformed E. coli with GFP. Everything else I had to learn in the lab doing research at the undergraduate and graduate level.

@user137 Hmm, that would be a little troublesome. There must be some book that consolidates all the basic knowledge on the topic. For example, if I want to learn about Quantum Mechanics, I go look for an introductory text. Am I making a wrong analogy?

Welcome to Biology S.E.! If you need additional assistance, please visit The Help Center.

This is something that is being introduced to me in high school biology; although there hasn't been a major emphasis on it.

@PandaBear I think part of the issue is that so much of genetically manipulating an organism is technique based, and the best way to teach a technique is in the lab. The other part may be that GMOs in the wild are so new that we don't have much good research to write textbooks with yet.

@user137 Oh ok. I didn't think about it that way. That exlains why my search for lecture notes was futile.

I too had difficulty finding any textbooks or notes that focused solely on genetic engineering. However, after some rather intense looking, I did come across several textbooks that may be helpful. I wasn't sure how basic of a text you were looking for but I'm hoping college level is okay because that is all I have been able to find.
The first book was An Introduction to Genetic Engineering by Dr. Desmond S.T. Nicholl.
Another was Principals of Gene Manipulation and Genomics by Sandy B. Primrose.
If you need a more basic biology text for reference, I would recommend Miller & Levine Biology by Prentice Hall (Pearson Prentice Hall). Also, you could do a quick-study on genetics on Khan Academy - Crash Course: Biology and Ecology.
I hope this information was helpful for you!

I'll go the library and check these books out, see if I understand them. Yes, I do need to brush up my knowledge of basic biology.

Before going into the trouble of reading a textbook on GMOs, ask yourself if you truly understand what the "controversy" is all about? I'll restrain the following comment to GMO crops (as I strongly feel it is in that area that the hysteria whipped up by a public that is poorly educated in science harms society the most).
The public perception often seems to be fall somewhere in between these two extremes: "crazy scientists insert genes from jellyfish into [crop], making a jelly-[crop]-fish...which is just weird/wrong and must therefore be opposed" or "evil big corporation inserts bad genes into plants, which can then escape into the wild, transmit their bad genes into all other plants, and unleash..."...err...zombie plants?
However, I would suggest that a lot of people are blissfully unaware that MOST of our cash crops have been heavily genetically modified, through millenia of domestication, hybridisation and selection.
For example, durum wheat (commonly used in making semolina and pasta) is an artificial wheat crop, created sometime around 9000 years ago by farmers who crossed two different species of grass crops and selected for a hybrid polyploid plant that had favourable characteristics.
The modern maize plant is another artificial organism created many millenia ago by mesoamericans through hybridization and artifical selection, two of the traditional genetic modification tools available to early farmers.
The apple is a hybrid plant created through crossing of two different species of plants....again done at the dawn of civilization.
I suspect most people who are vehemently opposed to GMO technology are ignorant of the history of farming, let alone the science behind GMO.
===============================
Anyway, to answer your question, the "concepts" behind gene manipulation are very basic molecular biology techniques, applied in this context at improving the biochemistry of the organism. Therefore, a good place to start would be a basic textbook such as "Molecular Biology of the Cell" by Alberts or something akin. But a basic botanical textbook on crops would be just as beneficial, in my humble opinion.

I mentioned controversy, because whenever I type the word GMO in google, I get overwhelmed by the amount of conflicting information on the topic of safety of GMO. I am not interested in that aspect. Nor in the politics involved. I just want to learn the subject because I feel like I am interested in it.

Fair enough, but my point is that there shouldn't be any controversy about a subject matter that we have been engaging in, and benefitting from, for millenia....


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IPTG and lac operator with e coli for foreign gene question
We did an experiment were we have e coli with a plasmid with a gene from another bacteria in it, and we put in IPTG in for induction. Will after looking up more about IPTG online I see it's related to the lac operator, which from what I've found just deals with lactose. Is there some other function that has? How can this be related to or effect the thing we put in and what we're doing? I'm missing the connection here.

The lac operon contains genes which are important for the metabolization of lactose as an energy source - normally glucose is used for this purpose. Usually the operon is tighly regulated and as long as there is another source of energy it is kept in an inhibited state.
The presence of lactose removes the lac repressor from the lac operon and allows the expression of the genes and thus allowing the metabolization of lactose. The mechanism can be turned on and off depending on the presence of lactose.
IPTG is a substance which mimicks the presence of allolactose (a metabolite of lactose) and it can activate transcription from the lac operon. As IPTG (in contrast to allolactose) cannot be hydrolyzed by β-galactosidase, it's concentration in the cell stays the same. Using the lac operon and IPTG enables you to switch on the expression of the gene on your plasmid and to start the overexpression.

So does the lac operon effect other things then lactose to that could have any affect on our protein? Or would there be something in the plasmid to let it be controlled by the lac operator? Is the presence or lack of the repressor having some effect? I mean what we're doing isn't related to lactose so I just don't get how messing with the lac repressor as an effect on what we put in the cell.

@windy401 In your plasmid (an artificial construct), the gene of interest will be under the control of the lac operator. Lac repressor can be expressed constitutively from another gene on the plasmid.

Finally found this, and after reading it and the rest of the pages(http://www.mfa.od.ua/page274.htm), I get it now.
"The essential element involved in lac-mediated protein expression is not the lac genes, but rather the lac regulatory apparatus. Generally, a gene selected for over-expression is cloned into a plasmid vector behind the lac promoter. Expression of this gene is then under lac control, either as an independent gene or fused to a fragment of lacZ or other genes."
I just wasn't seeing how/why our gene was being controlled by something that just controlled lactose stuff.

You only use the promoter of the lac operon, sorry for being unclear here. This allows the control of the expression of your target gene. I will edit the answer later.


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Do Penicillin based antibiotics affect birth control?
I wasn't sure whether to ask this question on Biology or Chemistry Stack Exchange, since it is really biochemisty, but this is something that's been puzzling me.
Most pharmacists (all that I've encountered) tell you that antibiotics decrease the effectiveness of birth control. There are side-effect warnings on all Penicillin based antibiotics that say they decrease the effectiveness of birth control, and advise you to use a back-up method when taking antibiotics.
However, most health organization websites (Planned Parenthood, Mayo Clinic, NHS) explicitly state that ONLY two antibiotics have been shown to sometimes decrease the effectiveness of birth control-- Rifampicin and Rifabutin.

NHS Website: http://www.nhs.uk/conditions/contraception-guide/pages/antibiotics-contraception.aspx

Yet websites of Pharmacies like Walgreens or CVS say that to a lesser extent Penicillin based antibiotics can decrease birth control effectiveness, or in general remain vague about antibiotics affecting birth control :

http://www.walgreens.com/topic/faq/questionandanswer.jsp?questionTierId=600006&faqId=600022

So--do Penicillin based antibiotics affect birth control?

As I recall from pharmacy teaching, this is one of those things where it was theorised that it might happen due to damaging gut flora which reduces reuptake of oestrogen in the gut, therefore physicians took a cautious approach and gave advice to use barrier methods in addition when taking antibiotics and the OCP

Evidence on the association between antibiotic use and combination oral contraceptive (COC) failure remains controversial, with recent studies reporting no evidence to support decreased effectiveness of birth control with the use of antibiotics except rifampin and rifabutin.
The reasoning is antibiotics might interfere with the effectiveness of COCs by decreasing steroid hormone’s plasma concentrations by hepatic microsomal enzyme induction or inhibition, interference with enterohepatic circulation of
COC metabolites, interference with absorption from the GI tract, competition between two drugs for the same metabolizing enzyme, alterations in plasma protein binding, induction of an opposite physiologic effect, or increased urinary or fecal excretion of the contraceptive.
As you stated, the strongest evidence is for rifabutin and rifampin: a significant decrease in the hormonal levels was noted in women taking rifampin even after a single dose.  Dirithromycin slightly decreased plasma ethinyl estradiol levels, with questionable clinical importance. A recent study in the Netherlands did find a relationship between the use of antibiotics and breakthrough pregnancy in a population-based prescription database; also, individual patients do show large decreases in the plasma concentrations of ethinyl estradiol when they take certain antibiotics, notably tetracycline and penicillin derivatives.
Because of earlier studies, anecdotal reports, and the above (it's not possible to identify whose levels will drop with antibiotic use), a cautious approach is advised. Physicians and pharmacists (80-90% of both) still lean towards believing that broad-spectrum antibiotics decrease the effectiveness of COCs, and continue to advise the use of back-up contraception.
The tide is shifting, however, as new studies come out. Here are a few excerpts of recent studies:

Available scientific and pharmacokinetic data do not support the hypothesis that antibiotics (with the exception of rifampin) lower the contraceptive efficacy of oral contraceptives. (J Am Acad Dermatol 2002;46:917-23.)

Since dermatologists treat acne with antibiotics, and a significant percentage of these patients are young women of child-bearing age, they certainly have a vested interest in knowing if this is true.

Rifampicin and griseofulvin induce hepatic enzymes and do appear to have a genuine interaction with the COCP, leading to reduced efficacy. The situation with the broad-spectrum antibiotics is less clear. There are relatively few prospective studies of the pharmacokinetics of concurrent COCP and antibiotic use and few, if any, demonstrate a convincing basis for any reduced contraceptive efficacy.
We did not find an association between concomitant antibiotic use and the risk of breakthrough pregnancy among COC users. However, due to limited power and potential carryover effects, findings from this study cannot rule out an elevated risk of COC failure among antibiotic users. (2011)

So, the answer is (except with your noted exceptions) the penicillin-class antibiotics probably do not interfere with effectiveness of COCs. However, one unwanted pregnancy is one pregnancy too many, and the use of a back-up method is not a huge deal (just ~14 days).
Until more and larger studies demonstrate a lack of interaction between most antibiotics and COCs, this will likely be the advice people continue to receive. When you look at the risk to benefit ratio of back-up, it's probably the wisest course for people prescribed a short course of antibiotics. It is more significantly problematic for people prescribed continuous antibiotic use for acne, Crohn's and other conditions/illnesses.
Oral contraceptive efficacy and antibiotic interaction: A myth debunked
Interaction between broad-spectrum antibiotics and the combined oral contraceptive pill: A literature review
Antibiotics and oral contraceptive failure — a case-crossover study
Are antibiotics related to oral combination contraceptive failures in the Netherlands? A case-crossover study
Drug interactions between oral contraceptives and antibiotics.
Survey of pharmacists and physicians on drug interactions between combined oral contraceptives and broad-spectrum antibiotics.

Great answer. Thank you for taking the time to type up such a thorough response.


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Is the six-layer cortex model of the mammalian cortex still the most accepted model?
I've been reading a bit about the different layers of the cerebral cortex and its clear that certainly not every region of the cortex has the same number of layers. Thus, the idea that every region has six-layers is clearly false.  And I think this fact is definitely well known.
Do neuroscientists still view the six-layer model as an accurate model? If so, what aspects of it have changed over time that now incorporate the fact not every region has six layers?
Aside:
Let me clarify my question. If not every region has 6 layers, why don't we just say there is a layered cortex and not specify a number? But if we decide to do this, what distinguishes the mammalian "6-layered" cortex from non-mammalian species that have a so-called "3-layer" cortex
See The Microcircuit Concept Applied to Cortical Evolution: from Three-Layer to Six-Layer Cortex by Gordon Shepard for more.

One distinction: cerebral cortex is divvied up into isocortex (6-layered) and allocortex (3-4 layers). This (title: The Microcircuit Concept Applied to Cortical Evolution: from Three-Layer to Six-Layer Cortex) looks like a good read for the relation of three-layered and six-layered cortex.

Nice, I will check it out.

Short answer
The layers in the cortex are histologically and functionally defined. Both 3- and 6-layered cortices are found in the human brain. Hence, the different cortical layers are not models, but classifications based on empirical observations.
Background
The different cortical layers have been defined by histological staining and microscopy. The layered organization of the mammalian cortex is typically explained in textbooks by using the neocortex as an example, which has 6 layers (Fig. 1):

Fig. 1. Layered cortex. Source: What-When-How - Neuroscience.
As one can see in this picture, layer VI can be divided histologically into 2 sub-layers, namely VIa, containing mainly pyramidal cells, and VIb with mainly horizontal cells (Prieto & Weiner, 1999). Hence, a 7-layered cortex could be argued for as well - it is all kind of subjective.
The functions of the 6 layers are illustrated in Fig. 2.

Fig. 2. Functions of the 6 layers. Source: Free-Stock-Illustration.
However, the primary olfactory human cortex (the paleocortex) contains only 3 histological layers, as opposed to the 6 identified layers in the neocortex (Fig. 3). The primary olfactory cortex is part of the allocortex in man.

Fig. 3. Neocortex versus paleocortex. Source: Slideshare.
The primary olfactory cortex receives direct sensory input from mitral cells in the olfactory bulb in the outermost layer Ia. layers Ib, II, and III receive input via local and long-range intracortical connections. Sensory and intracortical inputs converge in layers II and III. The three-layered palaeocortex is different from the six-layered neocortex in sensory areas. In the neocortex, sensory and intracortical microcircuits are distributed to two different layers. Sensory inputs from the thalamus target layer 4. Layer 4 subsequently projects onto layer II/III, which distributes and receives intracortical associative fibers. Note that the olfactory system is exceptional in that it does not relay its information via the thalamus, explaining the absence of layer IV (Wiegand et al., 2011).
Reptilians and birds typically have a 3-layered cortex (Nauman et al., 2015).
References
- Nauman et al., Current Biology; 25(8): R317–R21
- Prieto & Weiner, J Comparative Neurology (1999); 404:332–58
- Wiegand et al., J Neurosci (2011); 31(34):12149 –58


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how to extract promoter regions given a TF binding site
I have constructed a PWM and want to test its accuracy. Scanning an entire chromosome (chr3, hg18) yields very high false positives (magnitudes higher than the true positives). Scanning the entire genome is much worse.
From some literature and biostars posts, its recommended that I only scan sections of the genome to get an understanding of the accuracy of my PWM. Some posts talked about just scanning the promoter regions with my PWM (or say, a 1000bp neighbourhood around the promoter region).
So, is there a database or some sort of annotation that tells me where the promoter regions are?
I have a feeling that this question may not be well formed because to get "promoter" regions, I need to be talking about genes. Since I am only working with the MEF2 family of transcription factors, is there a way to retrieve promoter regions in which these transcription factors bind?
My idea: Since the TF binds upstream of the gene, usually in a promoter region, AND I know the true binding sites, would it be sufficient to just extract a 2000bp neighbourhood around the binding site?
Here is what my data (only the first couple of lines) looks like:
>chr1:6585537-6585547(-)
------ctatttatag-------
>chr1:228916512-228916522(+)
------ctatttatag-------
>chr12:50731227-50731237(+)
------ctatttatag-------
>chr13:49597702-49597712(+)
------ctatttatag-------
>chr14:103058980-103058990(+)
------ctatttatag-------

So again, is it sufficient to take chr1:6585537-6585547(-), extract a 2000bp neighbourhood around it, and scan this neighbourhood with my PWM. Clearly, I know there is one true binding site and I'll compare it with the number of false postives it gives me.
edit: Background
I have information (coordinates) for a total of 1875 binding sites. From these, only about 140 coordinates to binding sites on chromosome 3. These are my "true binding sites". If I scan chromosome 3 with my PWM, it gets around 85,000 hits.. ie, 85000 sequences that have scored very high that could be potential binding sites. They are, for all intents and purposes, false positives unless they fall (or overlap) the true binding site. Out of 85000 hits, only a very overlap the true binding region.
Now, literature recommends that instead of scanning an entire chromosome (or the entire genome), its better just to scan promoter regions. I guess there is confusion here, because the question can be "promoter regions for what gene?"
But I guess we have bonafide promoter regions if we take say 1000bp neighbourhoods about our true binding sites.

From your question it is unclear what you mean by "scanning an entire chromosome" with PWM and arriving at "false positives" and "true positives". How do you define your PWM matches to the genome and what are you comparing them against?

Is defining promoter regions as a 500bp or so upstream of transcription start sight is no good for you? You could get transcripts (for example RefSeq annotation) from UCSC Table browser. then parse out transcription start sites from the table and slop them, e.g. using bedtools utilities

@Sergei that sounds like a good idea. I've added a edit to my post, but if I can get all the TSS and grab a 200-500 bp upstream, that would solve my problems.


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Pros/cons: linear vs. circular DNA
Why did Eukaryotes evolve to have linear DNA and not circular like Prokaryotes? What are the pros and/or cons?

Some prokaryotes have linear DNA too..

This question has been asked before: Is there an advantage to linear chromosomes?
Firstly, I should state that the generalisation that ALL prokaryotes have circular genomes is incorrect. A growing number of prokaryotes have been discovered which have linear chromosomes, such as Borrelia burgdorferi ,which causes Lyme disease, members of the Streptomyces family and Agrobacterium tumafaciens, which has both a circular and a linear chromosome.
Anyway, on to the question being asked:
Generally, my feeling is that large circular chromosomes would have much greater supercoiling and related torsional problems, making it difficult to unwind them for transcription, replication or repair. This limitation on physical size limits the amount of genetic information that can be carried in a single chromosome, thereby limiting complexity of the organism.
You could increase the number of circular chromosomes to compensate for their lack of size, but again, you end up having a physical limitation (size of the nucleus or size of the cell for anuclear organisms) on how many chromosomes you can pack into the cell.
Linear chromosomes are just a more efficient shape when it comes to larger sizes.
=====================
Here are a few good references to dig further, if you're interested:

A new beginning with new ends: linearisation of circular chromosomes during bacterial evolution. Pubmed: http://www.ncbi.nlm.nih.gov/pubmed/10802162
Why do we have linear chromosomes? A matter of Adam and Eve. Pubmed: http://www.ncbi.nlm.nih.gov/pubmed/10422538 -- Proposes that meiosis was the driver for linear chromosomes.

I concur with your argument but it would be great if you can add some references.

Added, as requested.
Here's a really interesting experiment where they linearised the normally circular E. coli genome and studied the cells: http://www.ncbi.nlm.nih.gov/pubmed/?term=PMC1796773


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DNA replacement: new species
This is a hypothetical question
What would happen if the DNA of a prokaryote was replaced with the one of a prokaryote of another species, would the cell structures change and adapt to the new DNA and would the cell survive?
(Would the result be similar if we did the same with two eukaryotic zygotes of different species?)

Such genome transplantation was performed between two Mycoplasma species in Craig Venter institute Genome transplantation in bacteria: changing one species to another. They found that the donor genome completely changes the recipient cell to accept the identity of the original donor cell.
Note of caution: the above experiment was conducted between two highly similar species, and as of yet it is unclear what is going to happen if the exchange is performed between two distantly related bacteria species.
As for eukaryotes -- the transplants may be not viable at all, because naked DNA is going to lack epigenetic information (histone modifications, DNA methylation) that is preset during gametogenesis.


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How does the size of insert affects the rate of Homologous Recombination in yeast?
When performing genetic knockouts in yeast using homologous recombination to replace a target gene sequence via a vector DNA, does the region between the flanking regions in the vector have to be the same length as the site of recombination in the host cell's gene?

If I understand correctly, I think what Adelina's asking is if the DNA between the flanking regions (i.e. the insert being integrated) needs to be the same length as the gene being knocked out. The answer is NO.

As pointed out by aandreev, the greater the size of the insert relative to the flanks lower will be the recombination rate. This is because the donor DNA essentially becomes non-homologous. See the figures below:

Figure1: Effect of insert size on recombination efficiency. Kung et al. (2013) Appl Environ Microbiol. Mar;79(5):1712-7

Figure2: Effect of flank size on recombination efficiency. Kung et al. (2013) Appl Environ Microbiol. Mar;79(5):1712-7

However, you mentioned that you want to make gene knockouts. In this case you just need to make a small mutation (for example introducing a premature stop codon).
Use of genome editing tools such as Crispr-Cas, ZFN and TALEN increase the rate of transgenesis by introducing DNA double strand break.
These can also be used for making knockouts when NHEJ dominates over HR as the DNA repair mechanism. NHEJ is error-prone and can cause indels that can disrupt gene function.

Impressive. Nicely researched work. +1

first figure is very nice. Also, I will use all of them to argue in the lab later.

In my view there is direct link between probability of recombination and size of the insert. Smaller inserts with larger flanks get incorporated easier. That I understand from reviewing studies based on Cas9/CRISPRs system. Same should stand for HR-mutagenesis in yeast.
So, short answer will be: shorter inserts are more efficient. However, I couldn't find any studies of relation between recombination efficiency and using smaller than target inserts, or relation between sizes of target and insert. Cas9/CRISPR system was used to insert loxP site (34nt) instead of ~10 bp in mice ES cells. People usually try to insert GFP or something similar in size instead of shorter genomic sequences.


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What is the purpose of narwals' tusks?
I've heard that narwals can grow their tusks up to 16 ft long. What do they need the tusk for? Hunting?  Comunication?

Probably for male mate competition, but nobody knows really.

The evidence shows that the tusk is innervated, and acts as a sensory organ to the outside environment, as well as a mating tool.
Sensory ability in the narwhal tooth organ system

Nice finding, this paper will help a lot I guess! If it is an sensor organ, I'd be curious to hear more about why it is present only in males. Would be great if someone could make a short summary of the different hypotheses of how this organ evolved. In the abstract of the paper you linked, they also say New findings of sexual foraging divergence [..] add to the discussion of the functional significance of the narwhal tusk. So, it seems that this organ may also eventually be involved in foraging behaviour.


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How can we know or measure pain in animals?
Is there any standard way to know how much pain an animal feels when it gets hurt like when a bird loses it's wing or hen when killed etc. All pain sensation points?
Hey I'm new to biology. :)

Pain is subjective
Pain is a subjective experience; you cannot even tell with certainty how much pain your fellow human is experiencing, which is why we ask people; they then can tell us. Pain relief (both physical and emotional) is a significant part of medicine, yet we still have "pain scales" for self-reported pain, one of the more common ones being the Wong-Baker Faces Pain Rating Scale:

Now, note well that even this scale must be interpreted for the patients. For instance, a patient might look like a 6, but be reporting a 10, in which case, a nurse must try to ascertain their actual level of pain.
My point is evaluating pain is contentious even in humans who can express themselves.
Definition of pain
The International Association for the Study of Pain (IASP; www.iasp-pain.org) defines pain in humans as

an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

Pain usually involves a noxious stimulus that activates nociceptors in the body that carry signals to the CNS where these signals are processed (and generate responses) including the “unpleasant sensory and emotional experience.”
The following are examples of common types of noxious stimuli for different tissues:

Skin: thermal (hot or cold), mechanical (cutting, pinching, crushing), and chemical (inflammatory and other mediators released from or synthesized by damaged skin, and exogenous chemical stimuli such as formalin, carrageenan, bee venom, capsaicin)
Joints: mechanical (rotation/torque beyond the joint’s normal range of motion) and chemical (inflammatory and other mediators released into or injected into the joint capsule)
Muscle: mechanical (blunt force, stretching, crushing, overuse) and chemical (inflammatory and other mediators released from or injected into muscle)
Viscera: mechanical (distension, traction on the mesentery) and chemical (inflammatory and other mediators released from inflamed or ischemic organs, inhaled irritants).

Animals need us to interpret their pain into language. For political and emotional reasons, humans are ill-disposed to do so (how could we then justify eating, exploiting, experimenting on animals, etc.). Even into the late '80's, veterinarians were taught that animals didn't perceive pain per se.
How we know animals understand pain
To determine whether animals can experience actual pain (not simply nociception), it is necessary to show that they

can discriminate painful from nonpainful states; make decisions based on this discrimination in a way that cannot arise from evolved nonconscious nociceptive responses; demonstrate motivations to avoid pain; and display affective states of fear or anxiety if threatened with noxious stimuli. In addition, animals experiencing pain might be expected to exhibit spontaneous behavioral changes including sustained signals of distress and impairments in normal behaviors such as sleep.

Animals show all these behaviors. Additionally, there is ample evidence that emotional pain in animals is real. The mere threat of foot shock (electric) induces signs of stress in rats and mice that can be alleviated with anxiolytics (drugs that reduce anxiety).
Even fish show responses to a painful event: guarding behaviors, unresponsiveness to external stimuli and increased respiration, all of which improve with morphine. This is called analogous evidence: evidence that they are, mechanistically at least, directly analogous to pain responses in more complex animals.
Humans are animals
The nervous system of mammals is fairly identical to our own (we are animals). A chimpanzee who is afraid of a pin after being stuck with one 20 times in a row clearly feels physical pain and fear. That a chimp can mourn the death of a parent by not eating and not moving for days clearly indicates that they can experience emotional pain.
In summary:
Pain is subjective. I cannot really tell exactly what you feel if your arm is ripped off (your bird-wing example) or (don't read if queasy type)

 if you are given an electric shock, your throat is slit and, while still bleeding, you are dipped in boiling water to remove your body hair in a whole body hair plucker (which is how most poultry - usually males, not hens, btw - meet their makers).

By definition, only you can tell us.
But common sense and experience tells us it would be painful. And, yes, animals feel pain pretty much exactly like we do. Because we are exceedingly "more alike" than we are "slightly different".
Can animals feel pain?
Pain in Research Animals: General Principles and Considerations
Which Responses Indicate Pain and Which Nonhuman Vertebrates Display Them?<- read this if you really want to know
Evolution of pain

so what about those waveforms which you guys were discussing in this question... http://biology.stackexchange.com/questions/25986/what-does-pain-look-like-in-wave-form

@Wiser - Since it's unethical to experiment on humans, most of the information you read about action potentials and waveforms and such were derived from animal studies and applied to the understanding of human physiology. More proof that we are alike.

@anongoodnurse and since each species is a bit different and extrapolating from mice isn't particularly accurate, most practical data and measurements on human pain (and other) thresholds comes from the (thankfully) few times/places where we did experiment on humans some 70 years ago.

@Peteris - I'm sorry that you believe what you do, but very little of real science came from that period. Probably the most (hideously) useful information is about limits of endurance, not anything more scientific. Also, I would challenge you to refute me with science, not philosophy. We are exceedingly more similar than we are slightly different.

This answer is really solid and well-worked out. +1. I totally agree with @anongoodnurse that, in the end, the only way to guess how another animal species experiences pain, is to assess ones own experiences with a similar noxious stimulus and assume it is experienced similarly by an(y) other animal. I also agree with the similarity between species, as analgesics work pretty much the same for all mammals, at least as far as I know.

We work a bit with pain and memory. My understanding is that you can measure what in behavioral field is called "pain" by detecting aversive response of an animal. That is there is always something unpleasant and attractive in nature. Only difference is that pungent smell will not kill subject. Evolution taught animals that bad smells and loud sounds might bring danger and thus pain, so they try to escape. But pain per se is something that is definitely tissue-damage inducing at some point of intensity. Pain is only signal that tissue damaging influence has approached.
ADD: I re-read your question. There is no way to tell whether or not bird feels pain when wings are cut without anesthesia. Nice experiment would be to rip off human's arms and bird's wings while both are in fMRI scanners or other functional brain imager. If same areas of brain light up, it means that feeling might be similar.


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Why is oxaloacetate made in the mitochondria?
I'm looking at the gluconeogenic pathway:
Pyruvate is shuttled into the mitochondria from the cytosol, converted to oxaloacetate by pyruvate carboxylase, converted to malate which is then shuttled out of the mitochondria, and then converted back to oxaloacetate in the cytosol.  Why is the mitochondrial step necessary?  Why can't pyruvate just be made into oxaloacetate in the cytosol?

http://www.chembio.uoguelph.ca/educmat/chm452/lecture6.htm

Got it.  The ratio of [NADH]/[NAD+] is about 100000 lower in the cytosol than it is in the mitochondria.  The conversion of malate to OAA reduces a molecule of NAD+ to NADH, and that NADH can be used for the later step in gluconeogenesis: the conversion of 1,3-bisphosphoglycerate to glyceraldehyde 3-phosphate requires a molecule of NADH.

It's a way to transport reduction equivalents across membranes, you are absolutely right.


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How to increase contrast with only a top entry specimen holder
My question is: If my microscope had a top entry specimen holder, instead of a side entry holder, what additional option(s) should I have to increase the contrast with the same constraint that I only have a single objective aperture? Why would this option work?
Any ideas are welcome. Thanks in advance!

What is a top entry specimen holder? What kind microscope is it?

If your doing EM you can ignore, out of my area of know how :-(


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Demultiplexing symmetric PacBio reads
I have PacBio CCS.h5 and the corresponding fasta and fastq files and I would like to demultiplex them. Does anyone know of how this can be done in the absence of bas.h5 files.
Thanks for your help!
Mandy

It is more likely that you will get an answer over at biostars.org. Not that it is wrong here, but this place is dedicated to bioinformatics.

I'm voting to close this question as off-topic because it's about a specific problem in a specialized software environment.

@Chris Stronks, Which software are you referring to? I am not sure how familiar you are with PacBio and demultiplexing but in my opinion, the question fits within the topic of sequence-analysis.

Do you mean demuxing the FASTQ into the FASTA and QUAL streams? The FASTA format only contains one data stream, so I don't see what you want to demux out of it.


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Is any known plant magnetic?
Is there a plant (not a microscopic type but one that is visible to the naked eye) that has so much iron (or magnetite), cobalt, or nickel in its body that it can attract a magnet?
In this case "attract" would mean that a person holding a small magnet next to the plant can feel a small attraction between the magnet and the plant.

Fun answer: Tesla trees should be somehow magnetic: http://www.odditycentral.com/wp-content/uploads/2009/12/Tesla-Christmas-tree2.jpg as well as http://en.wikipedia.org/wiki/Tesla_trees

There was a 2011 study where they used a sensitive atomic magnetometer to try to detect a plant's magnetic field. They stated that:

To our knowledge, no one has yet detected the magnetic
  field from a plant. Biochemical processes, in the form of ionic
  flows and time varying ionic distributions, generate electrical
  currents and time-varying electric fields, both of which produce
  a magnetic field. However, contrasted to muscle contraction
  and brain processes, which have a characteristic time
  scale shorter than one second, plant bioprocesses span several
  minutes to several days and the expected magnetic field from
  such processes is correspondingly smaller.
Measurements with a sensitive atomic magnetometer were performed on the Titan arum
  (Amorphophallus titanum) inflorescence, known for its fast biochemical processes while blooming.
  We find that the magnetic field from these processes, projected along the Earth’s magnetic field,
  and measured at the surface of the plant, is <
   0.6 lG.

So according to this, no, you wouldn't be able to sense the magnetic field from a plant with a magnet.

I would like to add from my random-seminar experience that there are magnetic bacteria, that orient along magnetic field due to magnetosomes, e.g. Magnetospirillum magnetotacticum. Please look into Wiki article. So one can imagine symbiotic association between plant and such bacteria.
More to OP's question, remember that any electric current (aka moving charges) creates magnetic field around it. If net charge of plant's xylem sap is non-zero than there will be magnetic field created when current flows. But it will be minuscule.

The first paragraph should be a comment, since it has almost nothing to do with the actual question. The second paragraph contains nothing at all that isn't in the already accepted answer.


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Effects of lactic acid ingestion
What would happen if I drink lactic acid?
I use lactic acid to clean an espresso coffee machine and I wonder what injuries could occour drinking it.

Welcome to Biology S.E.! If you need additional assistance or have questions regarding policies, please visit The Help Center.

You should not ask personal health questions on this site; however, I do not believe this is a personal health question. I am going to try and find you some authoritative information on the subject and get back with you.

I voted to close this as a personal medical question, although it could be easily changed so that it's not. The question is also kind of hard to answer without knowing the specific parameters. It is an acid, so drinking a concentrated sample probably wouldn't be too pleasant. However, it is produced naturally by the body and is often present in milk, hence the name. You could drink rat poison if sufficiently dilute.

I'm OBVIOUSLY not asking for personal medial advice and I OBVIOUSLY not going to drink lactic acid. If I were into it, I would, at least, be nice enough to auto-answer my question :P This is hypothetical of course, since LA is endogenous I wonder if it can be drunk up to some amount and what effects this will have. After all Caffeine is a poison but we drink it anyway.

@knm241 We do ingest some - every time we ingest some type of milk product.

@L.B. I didn't realize that milk contains LA thought it sounds obvious. My question however is more on the line of: What if I drink a small glass of LA? What about a glass? a cup? a bottle?

@knm241 I had a really difficult time finding information on that subject. I thought at least I could cover the basics of what happens.

No, don't drink it... And here's why.
Ingesting lactic acid or for some reason having too much of it in your body can cause a variety of health problems ranging from mild to deadly. There are two types of lactic acidosis; the first is called metabolic acidosis and the second is known as respiratory.
Metabolic acidosis - which is what would be caused by ingestion - occurs when the fluids in your body build up too much of the acid and your kidneys can no longer keep up with the demand placed on them. Or they over respond and remove too much base from your body, leaving you acidic.
Respiratory acidosis is caused when your lungs cannot effectively remove CO2 from the blood. A buildup of CO2 leads to a more acidic body chemistry.
Regardless of what the cause of the acidosis was, you can expect some of the following.
Symptoms of metabolic acidosis:
~Rapid and shallow breathing
~Confusion
~Fatigue
~Headache
~Sleeplessness
~Lack of appetite
~Severe acidosis can cause shock, organ failure and even death
Diagnosis of acidosis:
A series of blood tests will check calcium, sugar and electrolyte concentrations in your blood.
My sources for this information:
Healthline
WikiPedia on Lactic Acidosis

Whoever did the down vote, please do tell me why. I would be very happy to edit my question if necessary.

Pardon moi, I'm not an expert in biology: So LA will pass intact in the stomach and adsorbed by intestine and make to the bloodstream. Since then it is analogous to the naturally produced LA and I will experience the same symptoms? Assuming the concentration is not high enough to sore my throat

@L.B. I did not downvote but whoever did probably did so because your answer sounds rather facetious -- i.e, practically speaking, normal/healthy humans would probably have no more trouble tolerating an acid load from some lactic acid solution than they would by simply eating a lemon, for example. So, your answer is simply quite the exaggeration for normal/healthy folks, to say the least!


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Is there a fundamental reason that plants cannot fix their own nitrogen?
Plants must have nitrogen to grow. According to the answer to this question, there are no plants that can fix their own nitrogen (without the help of bacteria).
Plants get their nitrogen in the form of nitrates (NO3-) or ammonia (NH4+). Nitrates and ammonia get into the soil through

lightning (causing N2 and O2 to combine to form NO which then reacts with atmospheric water and is brought to earth by rain)
nitrogen-fixing bacteria associated with leguminous plants
fixed nitrogen from dead plants/animals (ammonification), urine, etc.
ammonifying and other bacteria

The answer also states that it seems to be possible to engineer plants to be able to fix nitrogen.
So one could think plants could have evolved to be able to fix nitrogen, but did not.  Maybe it just did not happen based on it's probability to happen.
Is there any other explanation?
Maybe the ability to fix nitrogen would have a harmful effect on plants? Or fixation requires a complex set of related mutations? Are there enough areas with soil depleted of nitrates to exert a selection pressure for nitrogen-fixing plants?

Edited your question a bit. Please feel free to roll back if you feel the edit detracts from your intent. :-)

That is an interesting question. But rises some line of thought by analogy, e.g. why people won't evolve to produce their own ATP without mitochondria? (I mean of course Eukaryotas in general). I don't see any reason why multicellular organism cannot incorporate bacterial functionality either as happened with mitochondria, or as just separate cell type, that will provide desirable enzymatic reactions.
The answer, no matter how unsatisfactory, might be simple: because it so happened. We definitely can create experimental conditions lacking N-fixing bacteria as well as varying amounts of nitrates, nitrites etc. And then produce and screen line of mutants for ability to fix nitrogen without symbiotic partners.

I don't think it would be an unsatisfactory answer to conclude it could have happened either way, with some probability, and the random outcome was it did not - without any known mechanisms influencing the probability.

i feel that in biology there are many thing that are just are. but such an answer is always insufficient to my taste. for example, why DNA is winded that way and not opposite, or others. in case of nitrogen, maybe, it was easier for two different specialized organisms to live together rather than to one of them acquire some special traits.

DNA is winded in the Type B double helix because it is usually the lowest energy conformation available. There is almost always a good reason why something happens, it may not be known for nitrogen fixation, but the reason probably exists. See http://en.wikipedia.org/wiki/Nucleic_acid_double_helix#Helix_geometries

I meant right- versus -left-handedness of the helix, or chirality of glucose (bacteria eats only D-Glu)

The most obvious answer to your question is that the enzyme responsible for nitrogen fixation is inactivated by oxygen. So photosynthesis, which produces oxygen, rules out nitrogen fixation, and, as you know, plants photosynthesise.
However, they could have evolved specialized cells for nitrogen fixation, which do not photosynthesise. In fact, some colonial cyanobacteria, which photosynthesise, form such specialized cells called heterocysts.
So why haven't plants evolved such specialized cells? I think a fundamental answer to this question would invoke the evolutionary theory of specialization which says that specialization in one thing at the cost of the ability to do something else is selected for when the trade-off is convex, i.e. when you can be really good at only one thing, and being able to do both implies you are actually quite bad at both.
I hope this sets you off to find the fundamental reason you are looking for.

Interesting answer. Can you please add some references to it?

Nitrogen fixation occurs in some species of Cyanobacteria, which would be impossible if your hypothesis is correct.

@MarchHo, doesn't the second sentence of the second paragraph of my answer give an reason why it is possible? I.e they create anaerobic circumstances in specialized cells that do not photosynthesize, where N2 fixation takes place, thus separating the two processes?

@Chris, I was taught at uni about heterocysts and the inhibition of N fixation by O2. I don't have references ready for it. You can read about it at Wikipedia, but I wouldn't refer to Wikipedia to substantiate claims. The evolutionary theory I got from Adaptive Dynamics, see e.g. fig 2.2 of this book. If I have time I will add refs.

I believe that evolution is driven by the needs of the organism to adapt not by the need to adapt for human beings consumption. meaning that some nitrogen gets back to the soil through the effect of nature e.g. fixation of nitrogen during storms  and when fecal matter decomposes in soil and these I assume provide enough nitrogen for normal plant growth and so the plant is not "forced" to adapt to say a deficiency in nitrogen but for humans I assume because of agriculture the land gets "exhausted" and so we need fertilisers but plants have not evolved becuase I assume there was no pressing need for it. That is my own thinking assuming I understood your question


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Can I use yogurt to prevent the growth of black mold?
I have a mold problem in my bathroom.  There is a narrow groove between the top of my tub and the wall it is attached to where a black gunk repeatedly grows.  I can shoot the material out with a spray bottle but it grows back.
I've been taught many times that a bacterial film can prevent the growth of other bacteria, because the film created by one prevents another from colonizing that spot.  I have the inclination to think yogurt has bacteria.  If I were to clear the groove of the material, then spray the groove with a mixture of yogurt and water, would the bacteria in the yogurt colonize the freshly cleared groove and prevent the growth of what I assume to be mold?

I assume this is on topic as I am looking for a sort of corroboration/rejection of this scenario rooted in the biological workings of bacteria.

You need to replace the caulk, use a caulk with a mildew inhibitor.  The applications for what you are talking about would be more for treating vegetables and such like in a garden. Putting yogurt in your bathroom is strange and kinda gross.

@rhill45 - people put yogurt in their mouths and in their bodies? Why would you think a dab of yogurt around the tub is gross?

Because it smells worse than vomit

If it were possible, how would you get around the problem of water often washing away the yogurt?

@rhill45 - Speak for yourself! I would prefer yogurt to vomit any time.

Maybe we should put yogurt in tile, caulk and other hardware products. Sorry I get weary when people think yogurt, vinegar and incense will clean everything in their house. Just a personal pref!

@anongoodnurse I assume if the bacteria in the yogurt could colonize the groove, then it won't matter if the yogurt is eventually washed off, since the little ones will just cling to the surface.

Nice thought, but the bacteria need an appropriate growth medium, which would not exist in that crack area. But, as I said, nice thought. :)

ohhh, so the moist environment wouldn't be enough huh?  Post thy answer, @anongoodnurse

@rhill45 - not to extend discussions in comments, but I would be a happier camper if people cleaned their houses with a lot of water, a little vinegar or baking soda, and elbow grease, leaving all these other silly cleaning products (aerosolized and other noxious, polluting forms) in the warehouses of the money-grubbing, panic creating manufacturers where they belong.

@anongoodnurse good point re safety but if it's a toxic black mold, maybe time to pull out the big guns :/)

You should consider treating the cause instead of the symptoms. Opening the windows can do a huge part in inhibiting mold growth by reducing the humidity. Also, IMO this fits better on Life Hacks or DIY SE.


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How does HIV mutate into other strains while keeping their virulent phenotype?
How does a virus like HIV mutate into so many strains, and yet all of them are  harmful to our immune system? What gives this virus the ability to mutate so efficiently?

Others have already touched the important points. Consider this as a summary.

What gives HIV the ability to mutate?

All organisms mutate by two mechanisms:

Replication errors
Mutagenesis by physical/chemical agents that cause a chemical change
(lesion) on DNA

The main enzyme responsible for HIV replication is reverse transcriptase which makes a DNA copy of its RNA genome. All RNA and DNA polymerases make some amount of error but the error rate of reverse transcriptase is much higher than usual DNA-dependent DNA polymerases because it does not have a proofreading mechanism.

How does a virus like HIV mutate into so many strains, and yet all of
  them are harmful to our immune system?

As indicated in previous answers, the mutations will produce a virions with a spectrum of infectivity/pathogenicity (some can even be non-infective).
However, the immune system acts as a selective barrier which selects only those mutants that can survive (similar to what happens in evolutionary process of natural selection). The selected strains expand their population and that is how these strains get established.

What gives HIV the ability to mutate?
HIV is a single standed RNA virus. DNA is much more stable than RNA as it has a stronger backbone and it is typically double stranded. But HIV mutates at a rate far higher than just being a RNA virus. That's because it uses an enzyme called reverse transcriptase (RT) to build it's RNA genome from RNA bases.
RT is meant to copy the old HIV and make a new one but it does a rubbish job. Most the time it copies it well but every now and then (3 x 10−5 per nucleotide base) it puts in a random base. That might seem like a small rate but that's HUGE if that was coding our genome we would die (if we ever even lived). And since HIV's replication rate is enormously high, there's always going to be a range of good and junk HIV (but it's mostly just junk - next answer for why that's not a bad thing).
But that's not all, RT doesn't just use one old HIV to make a new one. It can use several different old HIVs to make a new one that's not only a combination of all the other ones but then add in the mutations from above, completely different.
So I get that there's lots of mutated strains all over the place. Surely that'd make them useless because the mutations are random?
Yeah they are random and yes that does mean some virus particles are useless. But it's very variable. There's ones which are greatly infectious, partly infectious, slightly infectious and basically junk. The body doesn't really know which ones are which and that's the beauty of it all. The body tries to fight all of them and has no clue which one to get. If it happens to target the greatly infectious one, the numbers of this go down but then the partly infectious one will become the most infectious one and the cycle continues. The junk HIV is basically just a sticky pool of most of the HIV particles that just gets the immune system going crazy and diverts it from the real threat.

Viral recombination produces genetic variation that contributes mostly to the evolution of the HIV-1 virus.
HIV being an RNA Virus utilizes  an enzyme called reverse transcriptase, which produces DNA from RNA. HIV also has two RNA genomes. After infection and then replication, which is catalyzed by reverse transcriptase, recombination between the two genomes can occur. specifically the single-strand (+)RNA genomes are reverse transcribed to form DNA. Then during this reverse transcription the nascent DNA can switch multiple times between the two copies of the viral RNA and multiple recombination occur throughout the genome. Furthermore, multiple events per genome may occur during each replication cycle, thus compounding the mutation.

Simple answer is that those mutations that create inactive virus, will never show up on screen, since it  will be asymptomatic. In same fashion if virus loses its ability to infect new target (via sexual contact or blood directly) it will show up only in first victim, so that effectively be a non-problem for society.
Addendum: I think I answered portion, starting with "and yet...", which seems to be most important in the question. I think that exact mechanism of mutagenesis must be covered in literature, if known. Also, it seems that since there are no vaccine for HIV, it's mutagenesis cannot be really "efficient", since it is not actively fighting anything.

First, you have to keep in mind that patients are not infected with a single strain. Because HIV is a chronic disease, and given its rapid mutation rate, it has enough time to evolve into a pool of enormous strains called "quasi species". So the virulence manifested is not virulence of individual strain, but the overall virulence of the quasi species.
Actually, because of its high mutation rate, HIV produces many failure strains. These strains are even unable to replicate and account for around half of its progenies! So they're certainly avirulent. But these progenies will die out very soon. However, HIV makes billions of copies per day. So there will always be fully replication competent and fully virulent strains. That's how its virulence sustains. So patients will always develop AIDS if left untreated.
Also, HIV may produce progenies with varying virulence. But the overall virulence is not determined by a single strain. And our immune system may serve as a natural selection. Only strains with good replication efficiency and immune evasion ability can survive. This may also explain how the virulence sustains.
Actually, there're a few people infected with Nef deficient HIV mutants. Nef is an accessory gene. HIV without it can still replicate but cause much milder disease. However, Nef is crucial to the immune evasion mechanism of HIV. So HIV strains without it are more likely be out competed by fully virulent ones.
I think influenza is another example. Influenza is also rapidly mutating, but its virulence varies greatly. From highly pathogenic avian flu to mild seasonal flu. I think the reason is that influenza don't cause chronic infection, so they don't generate quasi species, and there's no natural selection process. That's why the virulence of influenza fluctuates greater. Warning, this is just my guess.


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About modern dating techniques
In a comment to this question, it was said that

Radiocarbon dating won't work. For a start the tree needs to be dead, which since you're not using the rings I'm assuming it isn't. Also the atomic testing in the 20th century completely messed up the level of C14 in the atmosphere, so radiocarbon dating can't be used for anything that didn't die 70 years ago or more.

I did not know this. So, what kind of dating techniques biologists use today? :-)

The question involved dating a live tree. Radiocarbon dating does not work on live organisms, as they are assumed to be still in equilibrium with the environment. It measures the time after death of the organism.

In order to date the age of a tree, you have three solutions :
If you can cut the tree then you can simply count the number of rings. Note that for very old trees the central rings will have rotted and you will only have a lower bound on its age.
If some parts of the tree are dead, you can use radiocarbon dating to estimate the time of death with a relatively bad precision (the error is about 100 years which can be a lot for a tree)
You can estimate its growth rate (either using the width of the rings, or by doing multiple measurements for several years), and deduce the age from its size.


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What's keeping living species from rotting?
Why do only corpses of species rot and be eaten by bacteria? What is keeping us from rotting?
Just like fruits, and foods we eat; meat and vegetables rot when left uneaten. Like food, corpses rot and get eaten by maggots. Why?
Why don't these apply to living species?

One can calculate that there are more non-human cells (mainly bacteria) inside human body than there are actual human cells. Why those bacteria don't eat us from within? Epithelium is pretty good barrier between outer world and internal systems. It is essentially one-cell thick layer that protects internal organs and infrastructure. In cases when epithelium breaks, bacteria can get into blood stream and start very bad infection, which can cause necrosis (effectively, rotting, tissue decay). Natural cell death is fought by natural cell proliferation so that there are no gaps in defense layers.
Also one should not forget about immune system that is looking for invaders or anything that should be where it is. In healthy person immune response will close gaps in epithelium and kill bacterial infections pretty quick.
Dead people, as well as dead plants, have their skin and epithelium, immune system destroyed by cell death or infection. Then bugs start to eat vessels, tasty nerve tissues, muscle and cartilages, blood cells filled with proteins and everything eatable.

What's rotting mean?
The stages of rotting or decomposition are Fresh, Bloat, Active decay, Advanced decay and Dry/remains.
Fresh decomposition is first and is typically required before the other stages. It is caused by failure to remove carbon dioxide (which makes things acidic) and provide oxygen to tissues (because the hearts stopped for example). There's lots of bacteria in us but they're kept in check by our immune system and also the presence of oxygen (a lot of them are anaerobes which dislike too much oxygen). They start eating are carbohydrates, fats, protein and making chemicals such as acids, gases like methane and ammonia. Multiplication of these bacteria and continued production is called putrefaction and leads to the next stages.
So in summary it's the cell barriers, the oxygen and the immune system stopping this first stage from happening (which let's the next insect stages occur).
Rotting in living organisms
Sometimes this can happen in living organisms such as in gangrene where parts of the body (typically the toes or fingers) aren't getting oxygen and then rotting can occur in a living organism. It's a great idea to then chop off the affected part before these bacteria eat into a blood vessel and spread throughout the body.


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Why is blood removed from meat?
Blood is removed from meat before it is consumed. Below is, for example, how chickens are processed from Wikipedia.

Removed from transport cages
Hung by the legs on a shackle, mounted on a conveyor chain.
Stunned using an electrically charged water bath
Killed by cutting the blood vessels in the neck
Bled so that most blood has left the carcass
Scalded to soften the attachment of the feathers
Plucked to remove the feathers
Head removed
Hock cutting to remove the feet
Rehung in the evisceration room
Gutted or eviscerated to remove the internal organs
Washed to remove blood and soiling from the carcass
Chilled to prevent bacterial spoiling

Why is the blood removed? Does it just simply taste bad? This might be a stupid question but being vegetarian, I may not know.

we find in the Bible a command not to eat blood and to drain it before eating flesh. This practice may have its roots there.

Just a guess: blood may contain active immunological modulators and endocrine molecules. But this may be just a general practice because blood is consumed as food.

I'm voting to close this question as off-topic because it is about processing of food. Changing the pitch of the question may help.

Blood finds use in many different dishes as well as biotechnological applications. Research-grade BSA (bovine serum albumin) is derived from cow's blood, there are not special facilities, same cows go for steaks and car seats. So part answer is economical: blood can be processed further. Also it is just easier not trying to preserve liquid inside vessel already opened by slitting the throat. It also seems that blood can rot faster than other tissues, maybe, because in dead animal immune responses are deteriorated and every infection in blood will activate.

Can you add some references, especially for your last sentence?

I will try to add some reference, but my guess is that bacteria can travel faster in liquid, rather then in tissue through extracellular matrix.

Right, it's your guess, which is why I asked for references.

I wouldn't have thought it was to do with rotting, but clotting.

I found a forensic article that states the following:

Because the protective agencies of the body are absent, the bacteria spread through the blood vessels using the proteins and carbohydrates of the blood as culture media.

I was unable to find anything more on this with my limited searching skill, though I plied it to the best.
There was an interesting study on the relation between decompostion of animal meat and the bacterial load though. It was a good read!

Please cite the reason for downvote, so that I can improve the answer.


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Can your immune system's cells destroy you? (Critical thinking and Fictional sense)
In an imaginary sense, If you alone were replicated into 2 so that there should now be 2 of "you" (meaning you both have the same DNA). Then let's say one of you shrunk to the size of a bacteria, and was placed inside the other you (normal human size. Let's call this the actual you).
The question is how would your immune system affect the bacterial sized you in your own body?
Would white blood/T cells try to get rid of the smaller you?
If so, how? And could the smaller you die from this?

I'm voting to close this question as off-topic because this is not a biology question but something that belongs on World Building.

Placed where inside the body? The question basically canbe reduced if surface antigens can be auto-immunogenic when implanted. @NocTurn - if this last sentence still matches your intention, it will have a much better chance of being answered. The question has a fair bit of Sci-Fi content as of now. Good luck.

was this question answered?

This is a very interesting question. As others have alluded to, the body generally recognises self and non-self. However, as with any biology it's not that simple. Even leaving aside autoimmune disorders, the body doesn't always attack non-self and doesn't always leave self alone. Think of a pregnancy - the foetus is non-self, and yet the body doesn't reject it. The same can be said for a whole host of molecules that enter the body, such as food or things breathed in (e.g. pollen).  For this reason, Charles Janeway put forward the infectious non-self theory. This postulated that the body had a degree of leniency towards non-self, and would only attack if the macrophages became activated. This is done through recognition of Pathogen Associated Molecular Patterns, or PAMPs, binding to Pattern Recognition Receptors, PRRs. These PRRs are receptors present on immune cell surfaces, though most relevantly on macrophage surfaces, and when they bind to PAMPs it sends a message to the cell that it's likely in contact with a pathogen (or at least there is likely a pathogen in the area somewhere). This causes activation, and starts an immune response.
However, it's also too simplistic to suggest that the immune system always leaves self alone, and in fact one of the key jobs of macrophages is to clean up self cells that are damaged, and undergoing apoptosis - programmed cell death. (You can read more on macrophages here and more on apoptosis/other methods of cell death here). Therefore Polly Matzinger put forward what is known as the "Danger Model". This basically speculates that in order for an immune response to occur, the body has to recognise certian molecules that are evolutionarily associated with danger. PAMPs would indeed count, but there could also be endogenous molecules such as HSPs - proteins produced when a cell is under duress through heat, pH, cold, irradiation, viral infection etc. This tells the immune cell that detects it that the body is in danger, and allows activation and mobilisation of an immune response.
So the question here is, would the body respond to a miniature version of yourself? That would depend on a number of factors:
Where in the body would you go? If you were to stay in the digestive tract, so get swallowed and 'passed through' the body, I would say it's very unlikely you would be attacked. The body has a high tolerance for places such as the gut, because it's constantly exposed to external and non-self molecules. If it were in the blood stream, it's more likely because you're more likely to come across immune cells.
How is this 'shrinkage' achieved? Growth comes in two ways, through increase in cell size and increase in cell number. Which of these are you reducing? Are the cells the same size, but there are many fewer of them (unlikely, especially given that the opening question specifies to bacterium size, which are many times smaller than human cells already) or do you have the same number of cells but each cell is shrunk to a much smaller size (given that the entire body is the size of a bacterium, each cell would have to be many times smaller than a bacterium). If the cells were the same size, or even a bacterium-sized each, then an immune response is much more likely. If the whole organism is the size of a bacterium, the cells are going to be far too small to elicit an immune response.
Are you causing danger signals? As mentioned above, if no danger signals are present then it's unlikely an immune response will be launched regardless of anything else. Provided you're not killing or injuring cells, the body will pretty much ignore you.
I would say you wouldn't be attacked if you shrunk down as far as you've suggested. Everything would be too small for the body to recognise. However, if you didn't shrink down nearly as far, so your cells remained a size the body could recognise, and then started blundering about causing all manner of danger signals around you, the body may pick up some of your antigen and launch a response against you. On the other hand, the body is likely to have become tolerant to your antigens so even if this was the case, a full immune response is unlikely.

The immune system recognizes patterns - incase of innate immunity and shapes - incase of active immunity.
I am making a few assumptions:

The Shrinking would result in a smaller version of "the person" - meaning he/she is a bacteria sized person capable of executing all actions that a human can do.
The shrunk person is placed inside the blood vessel or some place where the immune cells will have easy access.

Now, the answer would basically depend on two factors:

The pattern recognition: It is higly unlikely that the innate immunity would recognize anything that is so small - As the person himself is the size of bacteria, the pattern recognition would be unable to find the patterns.
The Shape recognition  - This might be able to identify a specific structure. The structure in question may be a whole cell or a cluster of cells or a hair follicle, etc... The epitopes on foreign organisms which are recognized by the active immunity are much smaller than the organism itself. Infact a single bacteria may have thousands of epitopes. The epitopes are usually proteins and what is recognized may be as small as 3 to 4 amino acid cluster. Thus this system has the potential to identify and eliminate the shrunk person.

The shrunk person will not be considered as "self" because on shrinking, the "self-shapes" don't apply anymore. Think of it as a glove specifically made for the hand of an adult. A child's hand will not fit into it. Likewise any change in size of proteins will eliminate all question of self and everything in that "new size" is considered foreign.

When your body develops, immune system learns which tissues are foreign and which are innate. So usually immune system does not attack host's cells. Opposite case is autoimmune diseases. Immune system does that by addressing surface proteins of cells. Only foreign cells, never presented before, cause response.
If you think that large-you immune system will not attack large-you cells, then you should agree that large-you immune system will not attack small-you. Except, maybe, for bacteria that are on the skin on small-you and now sitting in blood stream of large-you.
The question boils down to: why my cells are not attacked by my immune system? Answer: because in healthy animals it discriminates host vs invaders due to memory of immune system.

How does the body know you is you?
There's two forms of immunity: innate and adaptive.
Innate
The innate immune system is the first line of defence that basically works on pattern recognition. "If I see these chemicals, they're usually bacteria/fungi/viruses, so I'm going to kill anything with these chemicals." Little you wouldn't have any of these chemicals unless of course the fact is our body is covered in bacteria which might be recognised (were the chemicals big enough to be recognised). Then they also try to kill things when they're worried somethings causing damage. So if they see that the area is inflamed because little you accidentally broke something, they might come and gobble you up because they're extra activated by the inflammation.
Adaptive
As for the adaptive immune system, this looks for certain markers and can identify specific bacteria and things that aren't us. There's these proteins on cells called MHC (a.k.a HLA). Our body cells are covered in OUR ones and everyone has different ones (unless you're an identical twin). So in little you's case as long as those proteins were there, the body would think you're okay.

Its impossible to happend, why worried about it? Maybe you`re writing a fiction book. I cant answered using biological arguments because this is fiction.

This is actually the best answer so far.


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What is the relationship between protein-protein interaction networks and metabolic networks?
I am trying to find out how these networks can be linked together. I know that Protein-protein interaction networks and metabolic networks both fall under the Intra-cellular type of biological networks that describe the cellular functioning. But what is the relationship between them?
Thank you very much.

Metabolic processes are carried out by enzymes and regulated by hormones. Both enzymes and many hormones are proteins. You may have to specify your question further.

Did you find answer helpful?

Proteins interact with each other often for regulation purposes and for localization of several enzymatic reactions for increased efficiency. For example, some proteins inhibit their binding partners. Or DNA replication complex is made of bunch of proteins, many of which do different jobs, but they are in physical complex (e.g. helicase with DNA polymerase).
Metabolic networks are sets of chemical reactions, they might even happen in different compartments inside the cell. While you can try to investigate protein interaction network by cross-linking proteins and then analyzing complexes you extract, metabolic networks are constructed by deciphering sequences of chemical reactions (e.g. metabolic cycles) and finding appropriate enzymes for each reaction.
Metabolic process (e.g. DNA replication) can be run by interacting proteins, but also might include proteins that don't directly interact with each other. For example, DNA polymerase complex does not produce nucleotides, but they are necessary for it's function.

In short, proteins in Protein-protein interaction networks perform a function by directly interacting with one another.  They may for instance bind to one another forming permanent or momentary complexes (e.g. insulin binding to insulin receptor or the pieces of F0-F1 ATPase combining), or they may chemically modify one another (e.g. protein kinases adding a phosphate to the residue of another protein).

Proteins in a Metabolic network might never be in physical contact one another. They effect one another by producing chemical compounds which are utilized by other enzymes, forming a network of chemical transformations.
Of course an enzyme in a metabolic network might also have its activity modulated through interacting with other proteins in a protein-protein network.  The two terms are of course not mutually exclusive, but describe different sorts of relationships between proteins.

I think you should try to connect the figure more clearly to your answer.

The basic struture of the metabolic networks  (MN) is like this:
molecule1 -> molecule2, where the edges are enzymes.
And the basic structure of the PPIN is like this:
Protein1 - Protein2, where the edges are van der Waals forces between proteins.
There are some diferences, PPIN isnt directional and  MN is directional in the way of the spontaneous reaction. PPIN has two modes of interaction date interactions (1-1) and party interactions (many-many).
One easy way to combine both is to invert the MN so the enzymes are now the nodes and the metabolites are now the edges, like this: enzyme1 -> enzyme2, and then add the proteins in the PPIN, like this: enzyme1(protein1) -> enzyme(protein2). But in this way you need to demostrate that some properties of the network are conserved.


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Arm at Heart Level when Measuring Blood Pressure
How come that one's arm has to be at heart level so that the blood pressure can be measured accurately. I've tried researching this question, but most answers to it were just "if the arm is above the heart level the blood pressure is too high and vise versa," but I want to know why this is so.

This page (and many others) explain the idea rather well. This is more of a physics than a biology question, but the fundamental concepts are the same.
In fact, contrary to what you wrote in the question, the measured blood pressure should be lower than expected if the arm is elevated above heart level.

When you reduce the pressure on the bent pipe, the water level on the side where the pressure is reduced rises.
Similarly, When the arm is elevated, it is equivalent to the right hand side of the image, where the right hand tube's water level is higher than the left hand side. Raising the arm above heart level, with the pressure of blood at the heart level remaining constant, will result in a lower pressure being measured, due to the heart effectively having to pump the blood up the distance.
For the same reason, giraffes have very high blood pressures (double that of humans) due to their long necks. If their blood pressure was at the level of humans, they would faint when raising their necks, due to the blood pressure falling to zero at their brains.


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Help needed in fish identification
Please help me identify these fish. I looked around but wasn't able to determine its species.

No sure id, but the shape woudl hint at some kind of archerfish, I'd say. On a seperate note, I would think the bowl is way too small for them...

We would actually count these as off topic for fish identification. I will see what people say. The images are also blurry.

would you need to have it be identified? There are plenty of stores that handle fish that could tell you.

It's look like platy to me.

Hi guys, I have relinked the pictures. No need to close now I guess?

It looks like southern platyfish (Xiphophorus maculatus) to me.

Courtesy: http://aquaticszone.blogspot.in/2011_04_01_archive.html

My first thought as well, and a very common aquarium fish. Might be similar closely related species though.


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How does the Pectoralis Major work when doing a bench press?
Disclaimer, I'm not a biology undergrad and I only know the basics about muscle movement.
I know that doing a bench press works the chest, and specifically the Pectoralis Major because, well, I feel muscle soreness. However, it is not obvious to me what the Pectoralis Major has to do with extending the arm.
Thinking about muscle contraction, I see clearly how, for example, the Bicep flexes the elbow when it contracts. In a similar way, when the Pectoralis Major contracts you get horizontal shoulder adduction.
But what about the bench press? The majority of the movement consists of raising the arms upwards from a tucked position, and the is little shoulder adduction.
Thanks!

The bench press is almost entirely shoulder adduction....

The pectoralis muscle attaches to the top to the inner half of the clavicle, just underneath the biceps on the inner part of your arm and the breastbone (a.k.a the sternum) which is found in the middle of your ribs. See below:
So taking that in account the pectoralis muscle helps bring your arm closer to your body (adducts your arm), pulling it forward in front of you (flexes the humerus) to push up like you would when you bench press. This action can be seen below.

Oh okay, pretty stupid on my part. There is a lot of adduction in a bench press. The only difference is that the triceps also extend the arm. Thanks!

Not a stupid question :) It also assists in forward flexion which is part of a bench press.


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How far can we go in engineering our own evolution?
After recently seeing Christopher Nolan's Interstellar and reading Kip Thorne's The Science of Interstellar, I've seriously been reflecting on the challenges mankind faces in becoming space pioneers, which in my belief will be a necessity to survive as a species. Not just the technological challenges, but the biological ones as well.
Technology can only go so far to aid and protect an organism against the brutal environment of space travel. And so the day may come where we have to make a choice on engineering our own evolution to become a hardier species that can better cope with that environment. The two immediate attributes that come to mind are resistance to radiation and extended life spans.
And this brings me to my question. Putting aside for the time being the question Should we make this choice ?, my question is How far could we go towards engineering a space-durable human species?

How far could we go towards engineering a space-durable human species?

I think this question is likely to get closed as off-topic. It is extremely hypothetical and would be a better fit on WorldBuilding.SE. But here is my messy attempt to answer this question.
Assumptions
So, I guess in your question, you assume that we know everything about how our genotype (≈the genes of an individual) make up the phenotype (≈how we look basically). So, I will try to give a short answer to this question by assuming that we were to know exactly what would happen if we were to add the sequence ATTTAG in the somewhere in the alpha-globulin gene or the sequence CCTATA somewhere in the regulatory sequence of the lactase gene. It is important to understand that today we are very far from having such knowledge. I also assume that we are able to recreate the environments we need to develop the new thing (human2.0 if you want) that we would have engineered. For example if we make up humans that need to grow in a different environment than the womb. By the end of the answer, I will pretty much assume that we know everything that can be known about organic chemistry and how chemicals process genetic information. Note that to the point we're doing the drastic modifications I will be talking about, it will be a philosophical issue to decide whether the new species we created is a human or not (it may even come to the discussion whether the new thing we created is a living thing or not).
Resistant to evolution as a species or only resistance as an individual?
Are talking about a species that would definitely be resistant to survive in these extreme environments or are you talking about a bunch of individuals surviving in this extreme environments. The difference is "evolution". Species evolve and not necessarily in the right way. High radiation may yield to high mutation rate and therefore to mutational meltdown (decrease in mean fecundity of the population through time yielding to extinction of the species).
General Limitation
With these very extreme assumptions, then we are only limited by physics. We could not add wings of the size of the wings of a warbler to a big animal like human and hope that it is going to fly.
Resistance to radiation
I know little about this subject but will try to say some things that may eventually help you. We cannot really make our DNA insensitive to radiation (although we may eventually make our DNA slightly more stable) because radiation will alter matter. It is a physical process that cannot be altered. We may create a lot more of tumour suppressor genes to protect ourselves from developing cancer. Eventually we could create a species that would be able to synthesize (and carry) a concrete shield around its body to protect itself from radiation. But it might eventually be easier to code genetic information with something else than DNA! Eventually made up of quartz because quartz is relatively insensitive to radiation. We could indeed create a whole new form of life.
High radiation yield to high mutation rate and high mutation rate may likely lead a species to extinction (mutational meltdown) but not necessary directly kill the first generations of this made-up species.
Extending lifespan
This sounds "easier". We may "just" target the alleles (=variant of a gene) that are known to diminish the human lifespan, to slightly (but probably considerably) increase human lifespan. Again, I assume that we can know these alleles and can replace them with better variants. However, evolutionary processes will just recreate those genes, just because there always has an equilibrium between the rate at which new deleterious mutations appear and selection purging the genome from these mutations. Moreover, at an age where reproduction has already occurred selection is less important and it allows for deleterious allele that are expressed late in the age of the individual to eventually spread in the population.

"What are you talking about?" - modifying our genetics to become less influenced by the space environment. To have  control over our genetics in getting into the space environment, and maintaining control once we are there. "Resistance to radiation" I guess something like emulating insect physiology. I once read something regarding how cockroaches have a high resistance to radiation.

I am not sure what you mean with your comment. I renamed the "What are you talking part?". Hope that makes more sense to you.

Well it is definitely not worth trying to answer bad questions if we receive downvotes for that!


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Should hydrogen peroxide be applied on a bloody nose?
When I was a kid, my parents taught me to apply hydrogen peroxide on my nose whenever it bled. It's a rare event, but my nose bleeds from time to time, and when it does, I always go through the same procedure of dipping a cotton bud in hydrogen peroxide, and applying it to the inside of the bleeding nostril. It always stops the bleeding immediately and I get on with my day.
It happened right now, and since I always just go through the motions without thinking about it, today I was curious about the principles at stake here. In looking for an answer about why it does what it does, I found only references to the effects of drinking hydrogen peroxide, which looks like a controversial subject whose benefits may be non-existent; but I didn't find a single mention about the application of hydrogen peroxide directly on a bleeding nose, which made me worried if what I'm doing is even recommended or if I'm doing something potentially dangerous.
So my question is: is this practice beneficial, and why?

Update: This question mentioned oxygenated water, which is the literal translation of "água oxigenada" (PT), but apparently that's only the commercial name for "peróxido de hidrogénio" where I live, which translates to hydrogen peroxide (H2O2); and since that returns many more hits on google, I've renamed all instances of oxygenated water to hydrogen peroxide in this question.

I'll doubt it. Oxygen is taken up via the lungs, water is not supporting the coagulation process of the blood, it prolongs the time as it dissolves the first (and pretty fragile) aggregates.

What is oxygenated water?

oxygenated water is water that has more oxygen diluted, with process, I believe, similar to that of carbonated water production

After some digging, I realized that a more accurate name would be hydrogen peroxide. I added an update at the end of the question with more details.

The main reason to use hydrogen peroxide is simply to "decoagulate" the exposed blood across the nasal cavities.
Human blood naturally coagulates to protect exposed areas and inhibit further blood loss -- kind of like a bandage. It can be a problem, however, when this coagulated bandage gets in the way of the tissue underneath from fully healing and completely restoring itself (as it was previously).
Hence we can use hydrogen peroxide to take off these bandages whenever needed.

Otherwise, keeping these coagulations in the nose for too long is just a ticking time bomb for an even bigger nosebleed --- that is, when we decide to blow our noses (or pick them) some time afterwards, for whatever reason, and these coagulations simply...pop out!

No, I don't think oxygenated water does anything to stop bloody noses. But holding a wet cotton swab with pressure to the inside of the nose might.
The vast majority of bloody noses in healthy individuals arise from one specific area in the nose (on either side):

In the mucosa of the nasal septum (the cartilagenous structure separating the nose into two sides), there is an area where several arteries "meet", giving it an exceptionally rich vascular supply, called Kiesselbach's plexus. It is on the anterior surface, and exposed to dry air and trauma (even such as might be sustained by a bad cold). Bleeding typically occurs when the mucosa erodes for any reason, and the capillaries and venules (and sometimes arterioles) become exposed and subsequently break. The result is the familiar bloody dripping of a nosebleed.
The most common treatment is direct pressure (squeezing the sides of the nose together) for 5-10 minutes. This works because putting direct pressure on any bleed stops the blood flow long enough for a clot to form and the arteriole to close down.
If needed, more aggressive control can be achieved by a professional.
If you happen to apply pressure with the wet cotton swab to a large enough part of the plexus (or somewhere near the spot from which your nose is bleeding), your nosebleed will stop. But it really doesn't matter what you use to wet the cotton swab (plain water, oxygenated water, carbonated water (ouch!), or other. (Noted: OP added that the liquid is hydrogen peroxide. This is not a good idea as it is an irritant and actually can cause mucosal damage.) Sufficient pressure and clot formation (and subsequent tenderness with the nose) is all that is needed.*
What doesn't work:

icepacks to the neck
leaning your head forward (increases blood flow) or back (may cause the blood to flow into your throat)
lying down (increases blood flow)
frequent 'peeking' to see if bleeding has stopped
a dry object placed against the area of bleeding (it will break up the clot when pulled away from the septum)

Aftercare and prevention is another subject.
Note: The safest way to end a common nosebleed is by squeezing as much of the 'rubbery' portion of the nose together for up to 30 minutes if necessary. Putting something into your nose poses the risk of infection.
*more serious or recurrent bleeding needs medical attention

IMO You should refrain from giving medical advice. For the same reasons as asking for one. This is not really an advice per se but it encourages these kind of posts.

Hydrogen peroxide, very potent oxidant, is used in case of skin cutting, small wounds etc. I think, firstly, It helps by killing bacteria that might otherwise cause infection. I couldn't find evidence of hydrogen peroxide promoting clot formation.
However, being an oxidative agent, H2O2 might be very harmful to gentle epithelium of nose. Theoretically, it can destroy it by chemical burns. Imagine pouring acid into your throat or intestines, it will definitely not be good.
You don't find information on applicating of H2O2 to bleeding noses because it is very harmful in first place.