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Narcan nasal spray
A recent podcast of Radiolab (time index 3:05) described a person who had overdosed given the nasal spray form of Narcan.  The report indicated the patient was awake seconds after the spray was administered to both nostrils.  If this is true, how does it work so fast?
The limit of my knowledge of biology and of Narcan is it binds with opioid receptors.  As I understand it opioid receptors which are located in the brain, in the spinal cord, on peripheral neurons.  Which receptors does the Narcan spray bind with that it works so fast?
Could this be answered in layman's terms?

Q: The report indicated the patient was awake seconds after the spray was administered to both nostrils. If this is true, how does it work so fast?
This is possibly an exaggeration, although intranasal Narcan can have a rapid clinical response time:

Tania Mieke Robertson, Gregory W. Hendey, Geoff Stroh & Marc Shalit, Intranasal Naloxone Is a Viable Alternative to Intravenous Naloxone for Prehospital Narcotic Overdose, Prehospital Emergency Care, 2009, 13:4,512-515, doi:10.1080/10903120903144866

We included patients with suspected narcotic overdose treated in the prehospital setting over 17 months, between March 2003 and July 2004. Paramedics documented dose, route of administration, and positive response times using an electronic record. Clinical response was defined as an increase in respiratory rate (breaths/min)...
The mean time between naloxone administration and clinical response was longer for the IN group (12.9 vs. 8.1 min, p = 0.02). However, the mean times from patient contact to clinical response were not significantly different between the IN and IV groups (20.3 vs. 20.7 min, p = 0.9).

Since it takes time to establish IV access, there isn't a difference between IN and IV Narcan administration in terms of "time from patient contact to clinical response." That said, IN takes ~5 minutes longer than IV (~13 vs 8 minutes) from administration to onset of action.

Amanda Robinson, Daniel P. Wermeling, Intranasal naloxone administration for treatment of opioid overdose, American Journal of Health-System Pharmacy, 2014 71:24,2129–2135, doi:10.2146/ajhp130798

Case reports
In the department of emergency medicine of Western Hospital in Melbourne, Australia, six cases of acute heroin overdose were successfully reversed using intranasal administration of naloxone hydrochloride, with all patients exhibiting a return of spontaneous respiration within two minutes. The doses used in these cases ranged from 0.8 to 2 mg at the treating physician’s discretion, and the time to spontaneous respiration ranged from 30 seconds to two minutes. While this study only looked at data from six isolated cases of acute heroin overdose, the results were encouraging and led to a larger prospective clinical trial comparing the safety and efficacy of intranasal versus intramuscular naloxone administration.

So, there are reports of IN Narcan responses in less than one minute. The instant response described in the podcast might be artistic license at work, but it's not impossible that a patient could respond on the order of seconds.
Q: Which receptors does the Narcan spray bind with that it works so fast?

Robinson and Wermeling, 2014 (above)

Naloxone is an opioid-receptor antagonist, with evidence indicating high affinity for μ-opioid receptors; it is used in the treatment of opioid overdose to reverse central nervous system (CNS) depression and restore respiration.
Naloxone is a pure opioid antagonist with no agonist activity. Prepared from thebaine, a natural opiate alkaloid, naloxone is a synthetic congener of oxymorphone. While naloxone’s mechanism of action is not fully understood, evidence suggests that the drug works by out-competing other opioids for the μ-, κ-, and σ-opioid receptor sites in the CNS, with a greater affinity for the μ-opioid receptor.
The nasal mucosa has a rich blood supply that contributes to efficient drug absorption and transport to systemic circulation. Administering drugs via this route generally avoids the first-pass hepatic metabolism seen with oral administration and leads to rapid systemic and CNS effects.


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Are there different species that profoundly changed the earth?
In the narration of the first episode of the new Netflix series Life on Our Planet it says that one species (humans) “would go on to change our planet like nothing before.” My immediate thought was the Great Oxidation Event and how cyanobacteria changed the earth in a way far more extreme than anything humans have done.
Are there any other species that have profoundly changed the earth?

It's ironic that cyanobacteria may have ushered in the first ice age, and humans may have done the opposite.

source: Stack Exchange

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

sort: votes


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Is there any organism that is born with all the nutrients and resources needed for their entire lifetime?
I understand that adult mayflies have no mouth, but they do take in oxygen through openings in their exoskeleton.
Is there any organism that does not need to ingest any type of nutrition and does not need to take in something for cellular respiration?

Assuming you don't mean an immortal organism, do you mean a type of organism (species) that can reproduce an equivalent offspring organism without inputs?  How could that work, since without inputs the offspring would have to be smaller than the parent (and thus not equivalent)?

@mgkrebbs I'm not familiar with an immortal organism in a biological context.  Yes, I mean a species that can reproduce an equivalent offspring organism.  I wouldn't imagine that would work.  It came up in a discussion making a comparison of biological life with the claim there is a non-biological system that is alive.

You may need to clarify your question: As written, this would be the biological equivalent of a perpetual motion machine. No such organism could reproduce without either violating the first and second laws of thermodynamics, or ultimately evaporating into nothingness as it divides.

Well that answers my question.  There are no such organisms.

No, I think this fails even on simply definitional terms.  That is, Life is (sometimes) defined as meeting certain criteria, such exhibiting growth, metabolism, and response to stimuli.  Those will all require intake of some external substance at some point.
To get even more pedantic, all cells have a cell membrane, which is selectively permeable to certain molecules.  Every organism will thus passively let in some substances from the environment, and thereby failing your criteria.

Luna moth , so I expect there are other moths.

Luna moth caterpillars do feed.

The adult moths do not eat , per Wikipedia.

You are correct that adults don't eat, but the question was about organisms being born with all their lifetime nutrients. I would argue that a caterpillar eating means that luna months are not born with all their required nutrients.

I would point that maybe there is an organism that can pass enough nutrients to 1 generation to survive and reproduce, but not continuously generation after generation.
Search in this camp, you may find something.

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


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If Viruses use Host Proteins, why don't Immune Cells attack Host Cells?
The Wikipedia article for Viral Proteins contains the following line:

Thus, viruses do not code for many of their own viral proteins, and instead use the host cell's machinery to produce the viral proteins they require for replication

If the host-derived (i.e. not encoded by the virus) viral proteins are made following the hosts DNA, are those proteins still flagged as "viral" by cytotoxic T cells? If so, why don't they attack host cells that have those proteins when uninfected?
My guesses:

Those host-derived viral proteins are coded for by the host, but aren't usually produced during normal function
The proportion of host-derived viral peptides matters, with a lower proportion indicating normal cell function and a higher proportion indicates infection
The viral proteins are a mix of host proteins that, separately, are not recognized as viral, but when put together by virus instruction can form composite proteins whose peptides fragments are viral
I'm misunderstanding the quote, and what they meant was "Thus, viruses do not code for self-generation of many of their own viral proteins, and instead code to utilize the host cell's machinery to produce the viral proteins they require for replication"

Comments have been moved to chat; please do not continue the discussion here. Before posting a comment below this one, please review the purposes of comments. Comments that do not request clarification or suggest improvements usually belong as an answer, on [meta], or in [chat]. Comments continuing discussion may be removed.

The phrase “viruses do not code for many of their own viral proteins” in this Wikipedia entry is an obvious oxymoron.
I echo what someone else said: “The beauty of Wikipedia is not that it is correct, but that it is correctable”. So I corrected it.
Unless it has been reverted (let battle commence) the first paragraph now reads as follows:

The term viral protein refers to both the products of the genome of a virus and any host proteins incorporated into the viral particle. Viral proteins are grouped according to their functions, and groups of viral proteins include structural proteins, nonstructural proteins, regulatory proteins, and accessory proteins. Viruses are non-living and do not have the means to reproduce on their own, instead depending on their host cell's machinery to do this. Thus, viruses do not code for most of the proteins required for their replication and the translation of their mRNA into viral proteins, but use proteins encoded by the host cell for this purpose.

To expand for this answer:

Many viruses rely on either the host-encoded DNA polymerase, RNA polymerase or both for replicating their genome, depending on their size and complexity
All viruses depend on the host-encoded machinery of protein synthesis (ribosomes, tRNA, aminoacyl-tRNA synthetases etc.) for the translation of the proteins encoded in their mRNAs (which in some RNA viruses are also their genomes)
Some viruses — especially those enclosed by lipid envelopes — may have host-encoded proteins included in their virions, whether by chance or to serve some function.

The immunity ‘problem’
There seems to be no problem to answer regarding the host’s immune response to viral particles, in any case. The immune response recognizes proteins that are ‘foreign’. Virus-encode proteins are foreign. Any host constituents of the virion are not. (This is the essence of the answer from @PrashantBharadwaj.)

I lack the permissions to delete the question, I have flagged it for moderator review. Regardless of whether it is deleted, I appreciate your answer and your Wikipedia correction

@Gumpf Since David's answer was useful to you, it probably makes more sense to let both your question and also David's answer stand, in case it's also helpful to someone else in the future.

@BryanKrause — Sure. Let it stand. I'll delete the PS.

The short answer is that what is attacked is usually what is recognized as foreign (other than exceptions as in autoimmune disorders). As any epitopes that belong to the host are usually protected from attack during immune cell training/selection.
So if viruses use host proteins, there is no reason to attack host proteins because of that.
Immune system only reacts to viral proteins that they have ready access to - such as the outer capsid or coat proteins - and these are not host derived.
I don't have any direct citations, but this article might be insightful -
Immune recognition of self and non-self explored in new study, from ScienceDaily
PS : I like the analogies in the comments below the question!


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Can introns be removed when designing protein expressing episomal plasmids?
If your goal is to cause a specific protein to be expressed transiently via an episomally maintained gene, could you just exclude all introns and the exons not associated with that transcript variant when choosing what DNA to package into your plasmid for that gene? So far as I know, the role of introns is usually in allowing alternative splicing and in modifying gene expression. But if you're only interested in one transcript variant, you wouldn't need alternative splicing to occur on the episome, and gene expression is handled in plasmid design by the selected promoters and enhancers.
For those reasons, could the introns (and exons not used for that transcript variant) be excluded? And would that affect the protein produced?

Why don't you use a mRNA transcript for expression cloning?

@Chris Sorry, could you elaborate a bit more? When you say mRNA transcript, would you just put the DNA complement of that mRNA into the expression vector?

Exactly. I can write you a more complete answer about this tomorrow. Basically you "use" the mRNA which has the exact sequence of the expressed gene. Avoids you doing a ton of edits and possible mistakes.

@Chris I would appreciate that! Your comments give me some threads to pull at with reading on my own too in the meantime, thank you!

@Chris If you pulled the transcript variant's mRNA from NCBI or similar, would you just form the complement from the sequence listed there? Or is it already "complemented" where that sequence is what you'd want going in the same direction as your other plasmid components? And could you just use the CDS with a custom promoter like EF1a? Or would you typically use the wholesale sequence from NCBI?

Use the coding sequence from the mRNA form available on sites such as NCBI
The sequences on NCBI etc are already in the DNA form; note the absence of any Uracils, indicating that this isn't actually mRNA as such, but rather a DNA copy of the RNA.
These sequences often contain 5' and 3' UTRs, so to be usable for you, you need to find the coding sequence in the sequence supplied. To do this manually, you can look for the start site ATG and stop sites to find the coding sequence. However, there is an easier way, and this is often useful if you have more than one coding sequence from the same transcript (these might be listed as separate entries in the database): find the label "CDS" (coding sequence) under the "Features" section and click on it. It should highlight a portion of the sequence corresponding to the ORF for this coding sequence.
You can then copy this sequence directly into a the MCS of a suitable plasmid.


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How to choose a method for upregulating an endogenous protein?
What factors affect the method that should be chosen to engineer a cell line that upregulates an endogenous protein? I am mostly asking permanent or long-term expression of nuclear proteins in mammalian cell lines, but more selection criteria for more applications would be appreciated too.
As I understand it, the possible methods are the following:

Target the regulatory factors already present in (or adjacent to) the gene of interest responsible for the protein, possibly targeting known variants that express a phenotype associated with high protein expression
Introduce new regulatory elements to improve transcription and translation
If the cell line is immortalized, expand and select for higher expression of the target protein
Introduce a non-integrative element that expresses the mRNA transcript variant

Are there any factors regarding the protein, gene, or cell type that make one of these better or worse? And are there any methods I'm not considering?

This is one of those questions that needs to be determined empirically, as it is highly dependent on the protein in question. For any one system, the best method to use needs to be determined by trial and observation. Upregulation and over-expression can be problematic, depending on the system you are targeting. Check the literature to see what others have used.
You are missing a few methods, namely those that use a lower expression cf. the already determined level in your unaltered line:
In many cases it is possible to find a cell-line that has a naturally higher or lower expression of the protein that can be used experimentally to compare to another that has a lower/higher expression, or use/generate a Knock-Out (KO) version of the cell line. Generation of KO is generally easier than introduction of a gene for stable expression if you are aiming for integration into the genome. The exception here is where the gene is used on a mobile element like a plasmid and is continually selected for using selective marker for over-expression.  Investigate CRISPR/Cas systems for these, as well as viral vector methods (lentivirus, adenovirus etc.)
You can also use methods such as siRNA to target mRNA for degradation, but this is not stable, needs to be done individually for each experiment, and may or may not work for your system.


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How do molecular biologists typically get their oligos?
What's the typical route taken to obtain synthetic DNA/RNA samples in practice? Are they pretty much always custom ordered from a place that prints them using sold-phase synthesis, or can you cobble them together from random "common" samples?
Theoretically I could see an arbitrary 120bp oligonucleotide being made of 2-3 strands from random parts of across a genome or two, where you could separate out those parts with restriction enzymes and then anneal the snippets, but A) I don't know how you'd find those snippets reliably or whether my assumption that they'd exist in a random sequenced genome, or B) whether it's even efficient to try to digest, isolate, assemble and purify oligos that way when compared to buying a printed synthetic oligo

Depends on your application. For smaller to medium sized DNA oligos (<~120 bp) or medium sized dsDNA fragments (<3kb), I will always order them. What you're describing sounds a bit like Gibson assembly cloning (https://en.wikipedia.org/wiki/Gibson_assembly), and I would only go that route for fragments upwards of ~3kb, unless I needed to make several of them at once (also assuming I know the full sequence needed). Larger fragments can be purchased, but the price per bp can get high for very long fragments (still might be worth it for a one-off).

I see, is the same true for RNAs or would you just order a template DNA and run in vitro transcription?

@MikeyC i think that your comment is a different (and possibly more useful) answer from mine if you want to post it there

Depends.
For short defined sequences, IDT or a similar oligo synthesis provider is your best bet. It's very fast and straightforward, compared to trying to do something complicated with a genome. Recall that the number of possible e.g. 120mers is $4^{120}$, or $1.7668471*10^{72}$. That's an astronomically large number, and the probability of finding it in some random convenient genome is small.
For e.g. single well-studied genes, you might order a plasmid vector from AddGene or similar, which you can put into E. coli and grow up to make many copies.
If you are trying to isolate something a little less standard, you will usually clone it out of the genome though.


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What is the cause of "imbalanced" linkage disequilibrium?
With perfect linkage disequilibrium ($D' = 1, R^2 = 1$), you might have the following table of counts for the alleles:
    B     b
A  100    0
a    0  100

With "partial" linkage disequilibrium ($D' < 1, R^2 < 1$), you'll see something like this:
    B     b
A  100   25
a   25  100

But I've sometimes seen the following "imbalanced" linkage disequilibrium ($D' = 1, R^2 < 1$):
    B     b
A  100    0
a   50  100

What gives rise to this sort of situation, where aB occurs, but Ab never does? Is there a name for this phenomenon? Which is a better measure of linkage disequilibrium in this case, the normalized LD coefficient $D'$, or the squared-correlation $R^2$?

This can occur if the Ab genotype is lethal, i.e. you won't observe individuals with a Ab genotype.
Allele lethality is a common mechanisms that can explain non-mendelian inheritance of a trait.
For the question of which LD metric to use, this is tricky. Under the assumption that allele lethality is indeed at play, you observed perfect haplotypes, so D'=1 wouldn't be incorrect. Yet the correlation coefficient is also correct in the sense that SNP A is not a perfect proxy for SNP B.


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Could trophy hunting lead to deer evolving to lack antlers?
There was a recent paper in Science which showed that elephants are quickly evolving tusklessness because elephant hunting imposes selective pressure against having tusks:
Shane C. Campbell-Staton et al., Ivory poaching and the rapid evolution of tusklessness in African elephants.Science 374,483-487(2021). DOI:10.1126/science.abe7389
Is it plausible that trophy hunting among deer (particularly bucks) for their antlers could lead to a similar evolutionary process? Or do the differing population sizes and selective pressures make such a thing unlikely? Are bucks' antlers relatively beneficial to their mating success, compared to the increased risk of getting killed by a hunter?

There's a big difference between hunting for a trophy and killing anything that has antlers; as elephants are killed for ivory - the poachers don't care about how much, just in getting some. Trophy deer tend to be much older (i.e. already sired young), so the genes passed on already. I have no scientific backing for this, just a little deer hunting experience.

@bob1 -- thanks, and please feel free to make this an answer!

thanks - i'll decline as I don't have any references to back it up, though I am sure there is literature on this somewhere in the scientific annals.


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Need help to determine % difference between DNA-strand from two different haplotypes. Known nucleotide diversity and more
Backround:
229 DNA sequences
493 bp in length
Haplotype diversity: 0.9956
Average  number  of  nucleotide  differences: 12.50544
Polymorphic sites: 145
Nucleotide diversity: 0.02426
Is it possible to determine how many percent difference there is, on average, between DNA-strands from the different haplotypes?
The answer may be quite obvious, but this is new to me.

No, unless you have the distribution of haplotype frequencies. In that case you could compute the expected difference in nucleotide across haplotypes based on the average number of nucleotide difference conditioned on that H distribution.


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what kind of insect is this
It has what appears to be antennas in both front and back and legs front and back orange coloured dots ob front and rear of a blackish brown body

This isn't one insect, it's a mating pair; I'm pretty sure they're flies, but can't go further than that on the evidence at hand.

Those are two mating "love bugs". Flies (Diptera) in the family Bibionidae. https://en.wikipedia.org/wiki/Lovebug


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Is it possible to Clone a Dinosaur with a full strand of their DNA?
If you have a full strand of Dinosaur DNA would it be possible to make it living and hatch a dinosaur? Or would it be a failure? Could you use a bird or alligator, for replacein

“A full strand”? Spot the mistake.


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conversion of distance matrices to pdb/coordinates
I am currently facing two transformational issues. Suppose I am given a protein's residue sequence and calpha distance matrix; is there a way to generate the 3d coordinates of the protein's residues from this information(I think there theoretically should be since it is a bijection up to rotation/translation).
The second issue I am faced with is generating pdb files. How does one make a pdb file given the coordinates of the protein's residues along with the sequence? Is this enough information?

We have two questions here: the first one is geometrical rather than biological, the second one would be perhaps better to ask on bioinformatics.SE, but shortly, if you have only coordinates of Cα atoms you can only write a PDB file with coordinates of Cα atoms only.

Concerning the second issue, an easy way is described here. By the way, it is a quite common manipulation under Python, but finding a library can present few difficulties. Concerning the first issue, some advanced features library (such as PyRosetta) shall help you.

@ElieKerArno - Welcome. A link-only answer is not considered an answer. An answer should be self-containing and self-explanatory. Mentioning a source however is great practice. I'm converting this to a comment, but feel free to expand on your comment and post a new improved answer. Check out the help center on answering questions.


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A question on cell division rates
It seems that in the adult human body the rate of cell division should be approximately equal to the rate of cell death, but how is this reconciled from the developmental phase where a single germ cell becomes the many trillions of cells in the human body. Is there some change in the rate of cell division throughout lifespan?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

"Is there some change in the rate of cell division throughout lifespan?" Yes, there is. Is there something specific about this you want to know?


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Do human genes get affected by irregular sleep and other factors
I'm new here so please go easy on me.
Do our genes-the ones that carry our appearance, intelligence and other traits get destroyed or lost due to irregular sleep, excessive body heat, smoking, drinking and other factors?
Asking cause, I have some relatives of mine with really good genes that are worth passing down but afraid that their children wouldn't get it because of the abovementioned habits.

Personal medical questions and health advice are off-topic on Biology. We cannot safely answer questions for your specific situation and you should always consult a doctor for medical advice. In this site, we just answer academic queries about biological principles. You should reformat the question to remove all the references of health advice if you don't want your question to be put on hold. Moreover, try to put in some research effort from your side. We would really appreciate it.

This is a good opportunity to correct some major misconceptions. I'll be brief and avoid being technical because this is introductory biology.
First, genes are present on DNA, and "store instructions" on building proteins, among other things. Poor diet, lifestyle and sleeplessness do not primarily affect the DNA itself, but rather the reading of it and the production of the proteins. Genes seldom get lost or damaged in a way that affects the next generation, at least in modern humans. Analogy: genes are the recipe in the cookbook, not the prepared dish. Lifestyle choices affect the dish.
This is because the aforementioned "bad habits" must affect cells responsible for the next generation (sex cells) - which is unlikely - unless the effects of the "bad habits" are strong enough to influence the entire system and cause damage to the production or maintenance of sex cells or their DNA. Sex cells are well isolated from the rest of the body. The other foreseeable way these habits can affect the next generation is to affect pregnancy itself. Poor sleep or smoking during pregnancy is obviously not advised. Gestation is a critical period in development.
In short, the expression and action of genes is certainly affected by sleep, diet, and so on, but the genes themselves are much less affected. Mutations may build in the body and contribute to the formation of cancer and other disease, but the sex cells specifically are very likely to remain mostly unaffected; it is these cells' DNA that is passed down to children.
As for the I have some relatives of mine with really good genes that are worth passing down* statement... That's a matter of eugenics and short-sighted opinion, which is strictly not scientific. Let's not address that!

There can be epigenetic effects on the gametes; see this. Moreover, lifestyle can affect the mutation rates and germ cell differentiation all of which can affect the quality of the gametes.

At least age is shown to be correlated with increased de novo mutations in the sperm.

@S Pr sorry, I never meant to come out as a racist person. Apologies, but I really didn't mean it. Although I do understand why it can be misinterpreted.


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How to interpret a phenotypic frequency density plot

I just read a paper that ran an evolutionary agent-based simulations aimed to test how genetic preparedness and social learning affect survival in various environmental conditions (changing environment, danger level, etc.). The full paper is here.
I'm a psychology student, and quite new to this area of literature.
About the graph, I get that density refers to the population density of different strategies at the end point of the simulation, but what does x-axis stand for?
I cannot find any specific mention about the x-axis in the paper, so I presume the graph is a standard one that does not need elaboration.
Could someone explain to me how to interpret the graph?

Judging from the first section of the Results part of the paper, it looks like the x-axis represents a continuum between two divergent phenotypes.  At one end is parental learning, and at the other end is social learning.  The density (y axis) represents the proportion of the population that displays a given balance between the two extremes.
Generally, density plots are a normalised way of presenting observations, such that the overall area underneath each density plot is equal, regardless of the number of actual observations making up any given plot.

The paper (and the graph) shows 4 strategies - just observational learning, horizontal learning, vertical learning, and hori + vertical learning. Then do you think x-axis stands for the proportion of each strategy used by agents? So for hori + vertical learning ("advanced learning"; orange graph), 1 would mean an agent who has exclusively used advanced learning strategy?

It could be that, sorry I only read some of the paper quickly and missed that point.


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What are the bare minimum nutrients required to survive as a human?
I am trying to determine the bare minimum nutritional requirements to survive as a human, ignoring energy (caloric) requirements. Another way to ask this question is: What elements can humans not live without? I am not inquiring solely about what nutrients are needed, but also their approximate amounts.
Imagine pills that a person can take that covers all their base nutritional needs and that after taking this pill the person can eat whatever they want to meet their caloric requirements. Hypothetically, this pill could have some amount (how much?) fat, carbohydrates, protein, fiber, minerals, and vitamins, and the person could subsequently eat any other food to meet their caloric requirements knowing their nutritional needs would already be otherwise met. Lets ignore the possibility of the person suffering from health issues due to eating too much of any specific food to meet their caloric requirements (e.g., taking the magic pills and then eating only butter).
A person in this situation could think "Ok I've got most of my bases covered, now I just need to ingest another 1000 calories of (almost) anything I want).
What nutrients are absolutely necessary for humans to survive indefinitely, and how much of these nutrients are required?
I am hoping for a complete list with approximate amounts (e.g., 20g fat, 20g carbohydrates, 1mg Vitamin X, .05mg Vitamin Y, 10mg mineral X).

This is not very answerable because each person is different, significantly enough that most recommendations are on the safe side of (mal)nutrition. Every human being requires essential micronutrients and macronutrients which are well known and established by now, but the amounts depend extremely on what you consider doing with the body. The bare minimum calorie intake will not allow you to thermoregulate in the cold or move. Similarly, people have quite varied uptake of nutrients; e.g. people with malabsorption of iron can have anemia, and their minimum iron intake may be relatively higher.

My whole point is to ignore calories and to focus on the rest. Are you telling me that a hard working farmer needs orders of magnitude more of minerals and vitamins than an average person? Calories yes, but the rest?

I’ll also add that approximations and ranges are acceptable answers. The fact that the answers are hard to pin down does not make it unanswerable.

These sorts of "numbers demands" questions are not typically well-received here: that's not how biology (or medicine) works. The way you are responding to comments giving you good information with demands for what is an 'acceptable' answer is (probably unintentionally) rude. I'd normally recommend closing this question as too broad, but I think you've gotten a good frame-challenge answer that rescues the question a bit.

I get what you're saying, but of course this is how medicine and biology work. There is a number that makes approximate sense for how many of each nutrients the average human needs. It varies yes, but we know 1mg of Vitamin C isn't enough in a day, and 5000 is too much. Nutritional labels are universal and focus on this question, so certainly there is a rough answer. Maybe the answer simply involves tabulating all of recommendations and perhaps justifications for some of them.

what have you done to answer this question?

Not sure how that is relevant, but I have looked at guidelines. Unfortunately they're all mostly recommendations based on caloric intake and how to spread the calories around. I'm primarily interested in the nutritional needs OUTSIDE of calories.

If you are interested in the "bare minimum" amounts, I suggest you search for minimal requirement for proteins, fats and iron. Carbohydrates are theoretically not needed for survival, so there is no minimal requirements for them. If you need this for practical purposes, I can tell you that searching for minimal requirements of other nutrients (vitamins and minerals) is probably waste of time - I can't imagine how this could help you. If you insist, you can search for "RDA" or "DRI" of "vitamins and elements." For macronutrients, you can search for "AMDR."

@Jan the fact that carbohydrates are not needed for survival means that any typical recommended nutrition list (e.g., from the FDA)  will not be a good answer to my question since they all recommend carbohydrates. Thanks for bringing that up.

Incinerate a minimum daily meal and the ashes are about the result.

Essential nutrients include (NutrientsReview):

Water
9 amino acids: histidine, isoleucine, leucine, lysine, methionine,
phenylalanine, tryptophan, threonine, valine
2 fatty acids (alpha linolenic and linoleic acid)
Vitamins: A, B1, B2, B3, B5, B6, folic acid, biotin, B12, C,
D, E and K (and choline, which is considered a vitamin-like substance)
Minerals: calcium, chromium, chloride, copper, iodine, iron,
manganese, molybdenum, phosphorus, potassium, selenium, sodium, zinc

The "bare minimum" intakes of most nutrients needed for survival are not known, because they could be determined only by studies in which participants would be given various low amounts of nutrients and observed for how long they can survive. The following are estimations of the lowest intakes of some nutrients needed to remain healthy.. Note, that this are not "recommended" or "optimal" intakes.
Protein = 35 grams per day (Metabolic Basis of Obesity)
Fat = 20% of total calorie intake, that is 44 g per day in a 2,000 Calorie diet (PubMed, 2017)
Carbohydrates = zero (National Academic Press)
Only 2 fatty acids and 9 amino acids are essential, so theoretically, you could consume only those and would be fine. In foods, these acids usually do not appear individually but as part of fats and proteins, so the recommendation is given for fats and proteins - if you meet that, you will likely consume enough of the essential acids. Theoretically, you can survive without consuming any carbohydrates, because all of them you need can be synthesized in your body. People have survived and remained healthy without consuming carbohydrates for a year or more (National Academic Press).
Sodium = 200 mg per day (Recommended Dietary Allowances: 10th Edition)
Water = 1 liter per day (only in ideal circumstances with minimal sweating; in the table, water requirement = "net water loss") (National Academic Press)

Here's a table with dietary reference intakes for vitamins, minerals, carbohydrates, fats (and separately for the 2 essential fatty acids), proteins and water (Nationalacademics.org), which should be sufficient for most individuals in a given sex/age group to remain healthy long-term. These amounts can be considerably greater than what is needed just for survival.
In Recommended Dietary Allowances: 10th Edition, in the Table 6-1, there are "estimates of amino acid requirements" for all 9 essential amino acids.
There was a man who was fasting for more than a year, drinking only water and getting potassium supplements, and the concentrations of most nutrients in his blood remained normal and he had no health issues (Postgraduate Medical Journal, 1973). This shows how difficult is to find "bare minimal" amounts of nutrients.
Yes, it is possible to make a "pill" with only essential nutrients in required amounts included. Such products already exist, but I don't want to promote them, because there is no evidence of their long-term health benefits and safety.

Thank you for this helpful answer. I'm a bit confused about the fat comment, since the "essential nutrients" list you shared actually does not include fat beyond the two essential fatty acids recommended. The man who fasted for a year is a wonderful example that gets to the point of my question. This guy seemed to be straggling the line of the bare minimum!

Can you elaborate on how fats proteins and carbohydrates are not essential? Are you suggesting that a person could live a long healthy life without consuming any fat beyond a reasonable amount of those two fatty acids? Most importantly to my question is how many grams of fat and protein are needed to reach the recommended amount of fatty and amino acids? Assuming you could consume those nutrients in pure form.

Yes, theoretically it is enough if you consume only essential fatty and amino acids. Check my updated answer.

thank you. For curiosity's sake I tabulated the total mass required to address the essential nutrients you mentioned based on FDA guidelines and such. It seems to add up to about 20g for an average young man, and taking into account the fat and amino acids (ignoring protein because that is taken into account with the amino acids?) it seems like the energy value for these nutrients is only about 75 calories. Does this mean the average young man can have his nutritional needs met by ingesting 20 grams and 75 calories (ignoring energy requirements) +water?

I didn't calculate it myself, but your reasoning seems to be right. I added a link to an article that shows requirements for 9 essential amino acids.

'it seems like the energy value for these nutrients is only about 75 calories' @Behacad these nutritional requirements have nothing to do with energy content. These are substances your body requires to sustain life regardless of your caloric intake. Think of it this way: your car may have a full tank of gas, but if your engine doesn't have any oil, you engine will seize up in a matter of minutes. The engine doesn't get energy from the oil, but it need's it to function. Similarly, you may be getting plenty of calories, but if you don't have the right nutrients you'll die of malnutrition.

@Charles E. Grant Thanks for contributing. I was just pointing out an observation that those nutrients seem to include a surprisingly small amount of calories!

You are not going to get an exact number because of variation in body mass, age, sex, and metabolism. life style also has a huge effect,what someone doing hard labor needs is vastly different that what a comatose person needs.  Minimums are harder because of the ethical problems with studying the bare minimum humans can survive on long term.
The best you will get is averages for a healthy intake of different age/sex brackets. which can be found here. These reflect the minimum below which it starts having a noticeable negative impact on health.
Essential Macronutrients are materials you need in bulk and generally fall in to the categories of water, amino acids, nucleic acids, carbohydrates, and lipids. Some of these are also major caloric sources, but there still is a daily requirement even if another source is supplying calories.
Essential Micronutrients are materials you need trace amounts of, basically essential vitamins and minerals.

I don't need an exact number, but approximate numbers are good enough. Certainly these don't vary by such a great deal. I doubt a very large man needs 10x more Vitamin C and an average woman. If I am wrong here, let me know, but still approximate values are good enough. Second, you mention doing labor and metabolisms, but these require calories, not nutrients, which is what my question is getting at. I'm not interested in calories, I'm interested in the rest! A hardworking farmer needs many more calories yes, but does not need much more iron.

Behacad,  the requirements for non-caloric nutrients (micronutrients = minerals and vitamins) actually do increase with calories someone spends, as John said. Someone who burns a lot of calories and then consumes 2,000 Calories worth of carbohydrates, will likely need twice as much vitamin B1 than someone who consumes 1,000 Calories of carbohydrates, because vitamin B1 is involved in carbohydrate metabolism.

The US FDA has published many of these, conveniently summarized here: Reference Daily Intake, but the original sources are here. I know that the link only answers are discouraged, but there is really too much information to be summarized here.
This information may be somewhat misleading, since the form of food is important too. Famously a certain amount of inert dietary fiber needs to be consumed to keep the digestive tract healthy.

Do these values represent a suggested amount (e.g., if you need 2000 calories, then you can eat X grams of fat), or biological requirements? For example, would some people get in trouble for eating less than 65g of fat?

@Behacad, not to be cranky, but I'm not going to read the articles for you. I'd suggest you read the original papers from the National Academy fo Sciences, Medicine that I link to. They go into great detail defining what it means to be "required".

No worries, I get you. Just thought I would ask in case you happened to know!


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Gene density percentage
What do we mean when we say that: Haemophilus influenza genome is 85% genic.
How do we measure gene density in percentage, especially for the above-mentioned case?

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


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Dark and bright sides in fluorescence microscopy images?
I have used Phalloidin to label F-actin in ethanol fixed cells ( I know formaldehyde might have been a better choice for fixation). I am new to new to this and I am experiencing that one part of image is bright while other portion is dark (please see attached image). I have already checked that its not due to the lever which we use to shift from bino mode to image mode (eye to camera mode). i have captured images previously and they looked perfect.I dont know what's wrong? Does anyone know what might be the problem?
As I said, I am new to this so it might be a very stupid question but I preferred to ask.
Thanks in advance!
Best,
Ankur

My fluorescence microscopy is rather rusty, but it looks like you have a light gradient from left to right (as opposed to a fixed line).  Is it possible that you have a light focusing adjustment that's out of wack?

Also, the background (at least on my screen) appears to follow that gradient, suggesting to me that it's not an issue with the staining, but rather with a light source direction.

@rotaredom explanation is the most likely, i.e. that the light source is not properly aligned. You can test that by, for example, imaging another specimen that you know has worked before. Alternatively, you may want to double-check that the slide is truly parallel to the objective, although everything looks reasonably in focus to me.

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


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What is this spider spinning a bright green web?
Here is the picture of it I took with my phone while I was out working:

Here is a close up:

Location: Texas (winter).

Welcome. Do you have a close up image of the critter?

Here are close ups on the so called critter (https://i.sstatic.net/9pUjL.jpg)(https://i.sstatic.net/0tWee.jpg)

As beautiful as they are one both dont spin weds at all and he is so hard to get a close up picture of because he is smaller then a fingernail + it's a phone camera so don't expect great quality as long as I lives never have I seen a spider spin a Wed other then the color white

Check out the Green Lynx Spider (Peucetia viridans) here.  The spots on the body look similar.  If the legs are similar this is a good candidate.  It's hard to tell by the photos if this is it or not, but it may help.

Source: http://www.spiders.us/species/peucetia-viridans/

I'll go with the jumping spider, for two reasons - first, the Lynx Spiders make a normal brown egg sac, and second, there is a strikingly similar jumping spider in Australia, called Mopsus mormon, that also makes a green egg sac (although, to be fair, it's the eggs that look green rather than the silk..)
http://malcolmtattersall.com.au/wp/2015/10/mopsus-mormon-mummy/


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What is this fruit
What is this fruit? Is it edible?
Found it in my backyard, in the Lehigh valley, eastern PA.
Here's the photo:

Is a better photo possible? Maybe a photo of the entire plant with leaves?

What is the size of the fruit? Did you find any more? What habitat did you find it in? Can you describe or provide a photo of the plant it came from? Did you cut the fruit open - if so, please describe or provide a photo. Species ID questions need to be detailed and complete to avoid getting wrong answers (especially those that are unfortunately upvoted due partially to question vagueness). Please [edit] your post with more details to ensure you get an accurate answer. Thanks.

Considering how many of them I’ve seen growing on the ground where I live in PA, it’s likely a mock strawberry. The plants grow on runners on the ground and have yellow flowers with five petals that become the fruit. The seeds come off easily when you rub it.
They’re safe to eat (wash them and make sure your lawn isn’t treated with chemicals though) but lack the flavor of real strawberries. I’ve eaten them before.
The fruit doesn't get much bigger than the one you're holding either. Here is a zoomed-in picture from Wikipedia:

Please provide a direct citation regarding the safety of eating the species you list. You must realize you're encouraging someone to eat a specimen you've ID'd from a poor-quality photo and without documenting that you've done your own homework on the safety of doing so. Personal experience is valuable but not good enough to suggest that someone else try it. (this is especially true for a fruit that's historically been regarded as dangerous to eat). Please [edit] your post to provide stronger evidence for the safety of consuming this fruit or please remove the statement about its consumption.

A reputable citation such as this would be preferable.

@theforestecologist Technically I cited Wikipedia which cited that page, but now I’ve linked to it directly.

thanks for the edit. Suggesting that something is safe to eat to complete strangers likely should be supported more directly than a footnote in a link. (FYI I've seen someone try to eat an Amanita mushroom before based on incomplete/faulty (and not at all cited) information.) In this false-strawberry case it doesn't appear to be all that big a deal, but it's just good practice when sharing information online. More generally, we prefer that all major claims made in posts on Biology.SE be supported directly. Thanks :).

It looks quite similar to the fruit of arbutus unedo (a.k.a. strawberry tree), which is edible:

But your image is too low definition to be certain.

-1. Thanks for the answer but this is almost certainly WRONG. This shrub is found in the  Mediterranean region of Europe, not Eastern Pennsylvania (USA). According to your Wiki article, the plant is found in the US, but it has been planted in the mediterranean climate of Western USA -- again, quite a different climate than Pennsylvania. Also note that the fruit of your tree grows to be larger than the specimen in the OP's picture.


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Do pyrocalciferol and isopyrocalciferol form in vertebrate skin?
I heard that pyrocalciferol and isopyrocalciferol can only be formed above 100°C/212°F, yet some images in the web depict them as forming in vertebrate skin. So, I wonder if pyrocalciferol and isopyrocalciferol do form in vertebrate skin. If they do, is there something catalyzing the thermal transformation of previtamin D or is it also a result of UV irradiation?

Could you add links to references of both claims?

An example of the former is ScienceDirect, which claims that "By increasing the temperature to 100-200°C, a new electrocyclization takes place, resulting in formation of pyrocalciferol (7) and isopyrocalciferol (8).". Example for the latter is the second image in the chemistry section of the "About Vitamin D" web site, which shows both pyrocalciferol and isopyrocalciferol (albeit with the names and compounds reversed) forming in skin.

ScienceDirect is a website which hosts over 900000 articles. Adding a link to specific article would be much better. You can read here on how edit your question to add links. I am not versed in skin chemistry, but people here could help you better if thay can read and evaluate your sources directly. When I write "About Vitamin D" in search engine I get numerous result sites without any way of knowing which is the one you have. Again adding a specific link would be much better.

For first, 'https://www.sciencedirect.com/topics/chemistry/provitamin', then use search in page tool, with pyrocalciferol inputted. For second, 'https://vitamind.ucr.edu/about/', then go to chemistry section.


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Is fever a disease or not?
I have seen this question where the author is asking why people take drugs for fever. So my question is: Is fever is a disease or not?

Fever is due to increase in the levels of some cytokines (IL 1 - being most common cause) in the body. These cytokines generally (speaking broadly) are secreted by either immune cells or injured cells. So when there is a large scale immune response or injury, the response is Fever. So Fever is a symptom showing what is happening inside the body

I know pretty much nothing in medicine!
Fever is an abnormally high body temperature. Fever is a symptom and not a disease per se. Different medical conditions (incl. various infectious diseases) causes a patient to have fever.
Note that fever might be in some/most situations an adaptive response to a disease. In other words, for infectious disease causing fever, fever might be good for the host and not for the parasite. However this issue remains controversial (see the post linked in the OP's question for more info).
As GoodGravy said in the comments, many people get confused and consider fever as a disease instead of what it really is; a symptom. One likely reason for this confusion is that when one has fever, (s)he very often treat fever directly (taking drugs like Aspirin for example) rather than treating the underlying cause (the virus for example) of the fever.

I agree, but furthermore to end the confusion: Fever is the symptom of an underlying disease/infection, but it is very treatable and often is treated rather than the underlying cause of the fever. I think the fact that the fever is treated rather than the infection is what causes confusion. Although if you were to be pedantic I suppose you are not in an eased state due to the fever so I guess semantically you are in "dis-ease" directly because of the fever... Let me think a while...

Any malfunctioning in the body is the result of either external pathogens, environmental changes or it can be manifested by the body itself. Based on which we can call it a disease or a disorder.
Some can be viewed with the help of its underlying symptoms. Fever is a natural response of the human body to any kind of imbalance, for example, temperature fluctuations, infections, etc., and that is why we can get fever by any number of reasons. What is important is that it shows us of some other underlying reason of change. Therefore I think it's more of a symptom than a disease.


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Is this adaption of the Gillespie algorithm using Michaelis constants justifiable?
I would like to run a discrete simulation of a biological system as it can be done, e.g., using the Gillespie algorithm. However, the Gillespie algorithm requires you to know the reaction rate constants of each involved reaction whereas I only know the Michaelis constant $K_M$ and the maximum rate $V_{max}$ of each reaction.
Since the Gillespie algorithm only uses the reaction rate constants to calculate the reaction rate $v$ (which, again, is used to determine the probability of a given reaction), I wonder wheter it is justifiable to simply replace this calculation of $v = k * [S]$ by $v = \frac{V_{max}\cdot[S]}{K_M + [S]}$ for each reaction $S \rightarrow P$ and, apart from that, use the Gillespie algorithm as is? If not, is there any better way to run a discrete simulation of the system with the given parameters?
Note: I've already asked in a different question whether it is possible to get (an estimation of) the reaction rates knowing only the parameters $K_M$ and $V_{max}$. I hope my both questions are sufficiently distinct to justify two different posts.

The answer of @WYSIWYG is wrong in parts. (I can not comment because I have not enough reputation.) Gillespie does not make the assumption that "the reaction propensity (probability) in an infinitesimally small interval of time is same as the macroscopic reaction rate." He rather derives this statement from physical considerations about collisions of molecules. The derivation is given in Gillespies 1977 paper "Exact Stochastic Simulations of Coupled Chemical Reactions".
The derivation holds for elementary reactions only. Michaelis-Menten rate obviously does not describe an elementary reaction.

The stochastic simulation algorithm by Gillespie makes the assumption that reaction propensity (probability) in an infinitesimally small interval of time is same as the macroscopic reaction rate. (For details, you can see my answer in Chemistry.SE).
You can model and simulate every step of enzyme catalysis or you can also use the Michaelis-Menten model. In any case, you can extend the same approximations to the stochastic model.
This is also applicable to other Michaelis-Menten like (or Hill) functions of the form $$\frac{x^n}{k^n+x^n} \qquad \text{or}\qquad \frac{k^n}{k^n+x^n}$$.
There are many papers that have done this. Note that the non-linear nature of these functions results in deviation of the stochastic behaviour from the deterministic behaviour. Read about stochastic focussing. Modelling each step exactly (binding, unbinding and catalysis) may result in different behaviour depending on your parameters. Whether you should use Michaelis-Menten function to describe reaction rate totally depends on how reasonable your approximation is.

Very interesting question. People use Gillespie's algorithm for several sort of kinetic functions such as Michaelis-Menten (MM), Hill etc., no matter what the original assumptions of Gillespie's algorithm are.
Concerning MM, There was a 2011 paper by Gillespie himself that shows that the approximation is applicable in discrete stochastic models and that the validity conditions are the same as in the deterministic regime.
https://www.ncbi.nlm.nih.gov/pubmed/21261403
Remember that, because MM is derived under a QSSA, you can break down the S->P transformation as its single-step components. See for instance a comparison here
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578938/


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Questions about ChIP-seq reads and MACS
I had a few questions raised by the below diagram in relation to how ChIP-seq reads look like (source). I would be very grateful for your insight on them!
From the below diagram, it seems that, in a ChIP-seq experiment, we get information about the binding site in relation to both the Watson and Crick strands. That is, from our experiment, we get reads complimentary to both strands.
(Q1) I suppose this is because proteins bind to both strands of DNA, so that in our ChIP-seq experiment, we ultimately sequence reads from both the Watson and the Crick strands? Is that true?
Also, my impression from the MACS paper was that "ChIP-Seq tags represent only the ends of the ChIP fragments, instead of precise protein-DNA binding site" (Background).
(Q2) Therefore, shouldn't it be that we get reads mapping to either side of the binding site on BOTH strands? That is, we get reads more towards the 3' end of the Watson strand, and reads more towards the 5' end of the Watson strand, and similarly for the Crick strand.
(Q3) The diagram below shows we only get reads more towards the 5' end of the strands. Why is that?
(Q4) Finally, I know that MACs shifts reads by some bases towards the 3' end for each strand, in order to interpret the precise binding site location. It seems to assume what I am asking about in (Q3). However, if the answer to my (Q2) is "yes, we do get 4 such clusters of reads", then why doesn't MACs account for that?

Some transcription factors bind to a DNA promoter sequence near the transcription start site and help form the transcription initiation complex.  Do you mean transcription factors (TFs) in your Q1?

"ChIP-Seq tags represent only the ends of the ChIP fragments, instead of precise protein-DNA binding site" (Background).

(Q2) Therefore, shouldn't it be that we get reads mapping to either side of the binding site on BOTH strands? That is, we get reads more towards the 3' end of the Watson strand, and reads more towards the 5' end of the Watson strand, and similarly for the Crick strand.

Sequencing-by-synthesis (the approach used by Illumina which is the most common tech for ChIP-seq) always proceeds 5'->3' because of the way DNA is synthesized. So you read off only the 5' ends of the fragment, but not the 3' ends.
(More precisely: the 3' ends are the template, so the 5' is what you see in the read.)
Thus you only expect (start positions of) the reads to be at the 5' of each strand, as shown in the figure. So we only get 2 "clusters of reads", as implied by the figure and the MACS workflow, which only shifts 3' as you say.


text:
How can combusted methane from landfill samples be quantified?
Background:
For my studies I'm wanting and attempting to make a landfill greenhouse gas emissions (GHG) model that predicts the amount of greenhouse gas equivalent emissions ($GHG_{eq}$ [tonnes/year]) by analysing a series of landfill core drill samples and extrapolating the data to predict how much GHGs would be produced if the samples can be representative of the landfill as a whole and allowed to naturally degrade. Note that this comes with the assumption of minimal heterogeneity which I know is not the best assumption for most landfills but I'm hoping to get a LOT of data (it's better than nothing).
As the most notorious GHG from landfill is methane, I'm going to simplify this question to just predicting the amount of methane which would be produced from the (combustible) material in landfill assuming it would just sit there forever.
Note that I have cross-posted my question from the chemistry stack exchange.
The Data:
I have this data which is the average of 3 landfill drill core samples and shows the type of waste which has been calculated from sorting and weighing different types of material found in landfill (Table 1) and the chemical composition and high heating value (HHV)/calorific value of the material (Table 2) which I've had tested in an independent lab. For Table 1, an assumed "type" of plastic, rubber, wood (etc.) is made with a constant chemical composition to simplify the model (although I do recognise that there are many different types of plastics and woods etc.).

The Method (?):
I've seen the generic methanogenesis combustion reaction as:
$$CO_2 + 4H_2 \longrightarrow CH_4 + 2H_2O$$
I've also seen an elemental formula for hydrocarbon combustions along the lines of:
$$C_xH_y + (x + \frac{y}{4})O_2 \longrightarrow xCO_2 = \frac{y}{2}H_2O + Heat + Light$$
I know how to calculate the conversion rate going from any GHG such as $CO_2$ or $CH_4$ to $GHG_{eq}$ but it's this first step - the predicting of the GHGs themselves with what formula - which I'm lost at.
The Questions:

How can I calculate $CH_4$ from landfill samples with the attached data and which reaction should be used?
(Bonus) What other considerations should be accounted for with any of the other data? (e.g. the Sulfur going into $SO_2$ emissions (etc.)).

If this doesn't work on biology, try [sustainability.se] or [earthscience.se], though it's unclear to me where this question fits best. Please take the tour, read the help centre before posting etc..

Sounds like an interesting project. Is your aim simply to utilize existing models to predict methane production from this landfill, or to test different models with empirical experimentation? After a quick web search, I found several reports on methane production from landfills or municipal solid waste. Several of them cited the IPCC First Order Decay (FOD) method, which should be accessible online. Also saw at least one cite the LandGEM model, accessible on the US EPA website.

Hmmm, I suspect this will be much much harder than you think. You would need to know the decomposition rates of each of the different carbon sources, and the biological utilization under the different conditions. You might be able to get some sorts of models for some plant-based waste from industrial composting studies. You should also note that paper ~= wood, as it's almost entirely made from cellulose derived from wood, and how do these differ from "organic"? To a chemist organic means carbon-based - including plastics! It has no special meaning in biology other than in farming/production.

@MikeyC I saw the LandGEM model and some other (licenced) ones online but I'm really looking to make a model from the ground up to be honest, that way I can fully understand what's going on. If it indeed becomes too challenging then I'll try and look for another model.

@bob1 Yes I'll need to make some assumptions certainly, great points. But rather than focusing on the scope of the whole landfill site as it's certainly too broad, what about the specific landfill drill core samples themselves on a case-by-case basis? Then I can process multiple samples and plot the heterogeneity.

Why would you reinvent the wheel? Real people doing real work with landfills in the real world are using existing models. It seems your first step should be not to build from the ground up but to understand the existing models, and only propose changes if you can find an improvement.

I’m voting to close this question because it is cross-posted across the network here ansd here with an upvoted answer at Chemistry.SE.

Good point Bryan. @AliceD I have not declared any answer as correct yet, this question is not solved. I also upvoted the answer here? Im still processing answers. There have been brilliant other insights I've had from posting on other stack exchanges which you are limiting by closing this thread for unsubstantial reasoning. You are preventing dialogue and thus critical thinking capability.

Cross-posting across the SE network is discouraged network wide. FWIW: I flagged the other cross-post as well for mod attention. In the future, please post a question only on the most suitable site. The community will then decide whether it's appropriate. If not, it can be migrated.

Why then did the mods from chemistry stack exchange request me to post to other stack exchange websites? Logic doesn't add up.

Methane production in landfills is a biological process that is carried out in 4 steps: hydrolysis, acidogenesis, acetogenesis and methanogenesis. In the first step, organic matter (for the sake of the this argument, let's consider carbohydrates, fat and proteins) is hydrolysed into less complex compounds (monosaccharides, fatty acids and aminoacids). In the second step, these compounds are fermented into fermentation products (FP) such as acetate, propionate, butyrate among many others; in the third step, the FP are converted by acetogens into acetate, which is converted into methane by methanogenic bacteria in the last step.
Each of the 4 steps mentioned are carried out by different bacteria and they also release other gases such as H2 and CO2 that can be used to produce methane, or are simply released to the atmosphere. Because protein contains nitrogen and sulphur, other gases can be produced (e.g. NH3, NO2, NO3, H2S, SO2, etc..). The process as while increases in complexity when others less prevalent organic compounds are considered, or simply by taking into account other materials that you mention in Table 1.
To answer your questions, I don't think you have enough information to build your model. Considering that more than 50% of your waste is organic, I would find a way to fractionate it into the 3 major components. From there, in the literature, you can find plenty of data regarding the conversion of waste into methane and what you could expect in a landfill with similar composition. Of course, ideally, you would even get actual data from similar landfills to feed your model. A similar process could be done to the other materials that are dumped into the landfills you are studying. The more you fractionate and the more you can estimate how much methane comes from each fraction, the less error your model with have in the end.
As for the sulphur, as far as I know, most of it will come from the metabolism of protein, so if you can measure the amount of protein that is dumped to the landfills, then you will be able to know how much SO2 is expected to be generated (again, there should be literature available regarding how much it is expected).
Good luck with you project.


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Does the given pedigree show a Y-linked dominant trait?

I think that since every generation has males affected only, the trait must be Y-linked. Also, since every generation expresses the trait, I think it should be dominant. However, the answer key says that the answer is autosomal dominant. Could someone please clarify this and give a tip on how to recognise the difference?

Unfair question. With that short pedigree, it's hard to distinguish Y-linked from autosomal. And given that none of the females is affected I would have also opted for Y-linked dominant.

You're right that this could just as well be Y-linked dominant (althought that is pretty rare due to the small size of the chromosome).
The only reason pointing more towards autosomal dominant is the mention of "extra fingers and toes". Most cases of polydactyly are inherited in an autosomal dominant way.
Does seem like an unfair question, though, since (at least in theory) there's more than one possible answer.

(more likely to be X-linked recessive than Y-linked dominant, though)
Why is that? What about the fact that none of the females are affected?

Y-linked is very rare in general, just because there are so few genes on the Y chromosome. - X-linked recessive, on the other hand, is fairly common (hemophilia, anyone?) and also only affects males (because females have two X chromosomes, therefore one mutant copy doesn't affect them)

ooops, yes, you're right - thanks for pointing it out; I'll edit my answer.

Ok so this is how I solve a pedigree:

This clearly shows that the disease is autosomal dominant. But there is one problem.
An autosomal dominant pedigree has the following features:
1. Appears in both sexes with equal frequency.
2. Both sexes transmit the trait to the offspring.
3. Doesn’t skip generations.
4. When one parent (heterozygous) is affected, and the other parent is unaffected, there is a 50% chance of the offspring getting affected. (You can refer to the cross I’ve drawn below your picture)
The pedigree in the question satisfies all 3 points except the last one. If there are 6 offsprings, at least 2 of them should be affected (if not 3), but there is only one, and that too a male.
Since only the male is affected in all generations, you’re right in thinking it’s Y linked. In my opinion, it can be Y linked dominant, since that’s very rare. And your question specifies that the trait is rare. It could DEFINITELY be autosomal dominant, had there been more affected offsprings in the third generation.


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The nitrogen cycle
As I understand it, bacteria absorb nitrogen from the air, and deposit nitrates in the soil. These are absorbed by plants which use them to build complex molecules such as proteins. This enters the food chain. Eventually an organism dies and decays, and nitrogen is released into the atmosphere again.  This is called the nitrogen cycle.
Am I correct so far?
My question: what percentage of atmospheric nitrogen is involved in the cycle per year?
Background to the question: On another forum I was involved in discussing the old statement that every breath we take contains a molecule of Caesar's dying breath. We raised the point about molecules being ripped apart, and created by biological processes. One person said that the nitrogen cycle is so slow that virtually all the nitrogen molecules from Caesar's time still exist unchanged. That statement is one I found surprising.  Is it correct?

Welcome to SE Biology. This is a question and answer site, not a personal  proof-reading site as you will see if you finish reading the [Tour]. Please do so. We work on the basis of one question per post. What is your question? Initially it appears to be about the percentage of atmospheric nitrogen fixed each year — a consideration that is hardly at the forefront of modern biology, but must be of interest to somebody. However then it seems to morph into astrophysics, in relation to the conservation of nitrogen on earth, together with the speed of the cycle — whatever that may mean.

I thought my question is perfectly clear: "what percentage of atmospheric nitrogen is involved in the cycle per year?"  The rest is merely stating the reason why I'm asking the question.   I don't see what proofreading has to do with it, nor astrophysics.

Proof-reading: "Am I correct so far". Astrophysics: "all the nitrogen molecules from Caesar's time still exist unchanged" suggested loss from the earth's atmosphere.

Not proofreading. It's just establishing if I've understood the basic premise correctly.  You can ignore that line if you wish. As for astrophysics, it's not about losing from Earth's atmosphere,  it's about chemical reactions destroying molecules, and creating different molecules.  I thought I made that clear.

OK, OK. You could have found the answer yourself — simple queries, first page of answers — but I've done it for you.

Mass of Nitrogen in Atmosphere
ca. 4 x 1018kg (Wikipedia page on “Atmosphere of Earth”)
Nitrogen fixed by natural, nonagricultural organisms per annum
ca. 2 x 1011kg (“Global Nitrogen: Cycling out of Control”)
Atmospheric nitrogen fixed per annum
ca. 0.5 x 10–5 %
Conclusion
If we are still breathing molecules of Caesar’s dying breath, they will be quite diluted.

I wasn't expecting us to "run out" of nitrogen, since any nitrogen fixed by bacteria will eventually be released back. Aside from that, thanks for the answer.

@Pete — Seemed a bit bald without a comment. Perhaps I’ll try a different tack. The actual turnover time is a more difficult question. It may have been 50 years or for the average Roman emperor to return to the earth, but much less for the rats in the streets.

+1 Nice article (second link). I did not know that, like, no clue whatsoever. So Thanks for that.

Suggestion: The best practice is to write numbers in scientific notation in terms of the base unit kg, not the unprefixed unit g. This helps when doing calculations, e.g. kg × m/s^2 = N (newton). So, 4×10^21 g = 4×10^18 kg.

@Nayuki — You may well be right, but I am unaware of that practice. Can you provide a link documenting it? If you are correct I will change it.

The dying breath part needs fleshing.  Tidal volume = 500 mL /(15 mol/L at 37C) = 1/30 mol air = 38 mmol N2 = 2.9E+22 molecules with negligible fixation in 2000 years (0.01%).  Atmosphere has (4E21g/28 g/mol)*6E23/mol = 8.6E43.  New breath gets (2.9E+22/8.6E+43)*2.9E+22 = 10 molecules.  (Unless the old tyrant was poked so full of holes that the last breath was more like a faint gurgle, that is...  more pleasant to run this math for the Sermon on the Mount, no?)

@David I looked through the SI Brochure and it has surprisingly little to say about style. As far as I can tell, all examples in the document use kg, such as on page 150, "m_n = 1.674 927 471 (21) × 10^−27 kg".

@David Using g instead of kg is factually and numerically correct, but it makes advanced usages harder. Look at the Wikipedia page for Earth or proton, and you'll see their masses stated in scientific notation kilograms. Secondly, other units are "coherently derived" from base units, meaning that you multiply base units together with a trivial scale factor of 1. For example, 1 newton = 1 kilogram × metre / second^2 = 1000 g × m/s^2. When doing calculations, it's tremendously helpful when all quantities are stated in base units - and that means using the kilogram.

@David It's true that the other 6 base units have no prefix (metre, second, etc.) and behave nicely. But for historical reasons, the community reneged on the gram and then decided to base everything else on the kilogram - the newton, pascal, joule, volt, etc. So now we're stuck with a coherent system having a base unit that has a prefix, but does not take double prefixes (e.g. μkg → mg) and thus also behaves as though gram is the base unit for the purpose of prefixing.

@Nayuki — OK. Thanks. We biochemists tend to think small, so that the question seldom arises. Will fix when I have a mo.


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immune system - how does adaptive work without innate?
The way I understood immune system is that:

phagocytes detect viruses and present it on their surface and become antigen presenting cells.
Then, T-helper cells try to bind to these phagocytes that have antigen on their surface and found, T-helper cells become effector T-helper cells which then cause the activation of B-cell.

Question 1: If phagocytes can't detect virus, that means T-helper cells wouldn't be activated(there would be no process of cytokines) and if no cytokines, B-cell activation wouldn't happen. and if no B-cell activation, no antibodies releasing. So This means unless phagocytes detect the virus, B-cell activation doesn't happen, but this would be too bad, because if B-cell activation depend on the phagocytes finding the virus, this means if innate immune response fails, adaptive also fails. I'm wondering when would still B-cell be activated even without phagocytes finding the virus in the first place ?
otherwise, B-cell always depending on phagocytes would be too bad...
Question 2: Am I right that B-cells can detect/identify the virus that couldn't have been identified by the phagocytes ? I think so, because phagocytes have general PRR which sometimes might be unable to detect, but B-cells have more combinations of variable portion proteins that could detect more stuff ?

B cells can be phagocytic, and can present antigen to T cells both via MHC-I and MHC-II pathways. Different PRRs can be found in many cell types so they can detect infection and signal that to the immune system. You might be interested in the topic of immune evasion.

Thanks for the answer. But am I right about my 2nd question ?


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immunotherapy - how would the inhibitor detect
It's a known fact that if PD-L1 happens to be on cancer cells, it will signall off to the T-cell's receptor(PD-1) to turn off its activation, resulting in a fact that cancer cell won't be destroyed.
Question 1: Even if with immunotherapy, we stop the blockage (PD-1 vs PD-L1), (Let's say PD-L1 was expressed high with NGS), why does this mean that T-cell now will kill the cancer cell ? Yes, we removed the blockage, but it could still happen that binding between the proteins of T-cell and proteins of cancer cells might still result in NO T-activation, hence no cancer cells being killed. So If I'm right, having PD-L1 expression high on NGS still doesn't give you anything and you gotta risk it and see !
Question 2: It turns out some healthy cells also have PD-L1 expression on them, but much less amount than on cancer cells. For simplicity and example, let's take our body's own cell (cell-Y - I just named it up). This cell-Y has PD-L1 as well. If we give the Atezolizumab(tecentrik) to the body, which will stop the blockage between PD-1 vs PD-L1, would the T-cell now destroy this cell-Y ? I'm asking this because it's said that using PD-L1 inhibitors also cause good cells to destroy. But I don't get why. Even after stopping the blockage, T-cell shouldn't kill cell-Y, because this cell-Y is body's own cell, the other proteins it has on the surface, binding it to the T-cell, still shouldn't cause destruction. What do you think ? or this is random and nobody knows ! the only protection our immune system had for cell-Y was PD-L1 on it, but if we block it, then we get to the random scenario and got no idea whether T-cell now can destroy it or not(depending on their receptors binding). Question is, do we actually get to the random scenario or we know for sure that without PD-L1 on cell-Y, T-cell will always kill it ?
Question 3: How is it possible that with tecentrik immunotherapy, T-cells don't kill good cells, but kill cancer cells ? I've read somewhere that it's about the dosage and frequency, but how would that work ? how does the process differ between giving high dose of tecentrik and low dose in a sense that it's possible that T-cell won't kill good cell even after blocking PD-1 vs PD-L1 ?

These are technically complex questions. Can you please restrict yourself to one question per question?

Can you link or cite sources for your statements? It would be nice to look at the basis for your question to evaluate how best to answer it. (Also, Chris is right)


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What are the enzymes with the lowest concentrations in a cell?
Or are there any enzymes which are only translated one time per cell?

Please include your question in the body of the question. A title is not part of the question. You can't start a question with "or". You mention a cell. Clarify. Eukaryotic or porkaryotic. If eukaryotic, multicellular or unicellular? There are often low concentrations of enzymes in non-specialised cells, when these are hugely expressed in other differentiated cells. Really only enzymes or any proteins?


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Why can Anaphylaxis lead to death?
Why can the immune system kill its host?
It is always better to just take up the insect poison, or peanut protein etc. instead to kill the host by preventing the breathing.
Is it just a modern symptom or did humans always have to fear death from anaphylaxis after an insect sting?


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Bottleneck effect
Is it true that animals that faced a severe bottleneck will have genetic deficiency for a long time? Does it mean they will all look the same for a long time?

A population bottleneck (see also founder effect), by definition is an event of sudden reduction of genetic diversity due to a sudden reduction in population size. Of course, such reduction of genetic diversity is not restricted to animals (unlike you seem to suggest) but to any population of living creatures.
Given that part of the phenotypic variance is caused by genetic variance, it means that after a bottleneck, phenotypic variance will be lower after the bottleneck than before the bottleneck indeed. However, a bottleneck might be coupled with a environmental change which could change the genetic variance in itself and the above might not be true anymore (see this post for an introduction to quantitative genetics).
Because, deleterious alleles tend to be recessive, a reduction in genetic diversity often causes a reduction in mean fitness. In humans, cases of founder effects have been shown to be associated with an increase in recessive genetic disease such as observed in Quebecois or in Amish.
The time needed to restore the genetic diversity very much depend upon the exact demography at play, as well as the mutation rate and selection coefficients. As a rule of thumb that many population geneticists use in numerical simulations; if $N$ is the population size at equilibrium (after bottleneck), then $10 \cdot N$ generations is enough to restore a good genetic diversity.


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Overexpression by integration of an additional copy vs promoter exchange
In Becker et al (2011), the authors increase the expression of several genes through different methods. For some genes (e.g., lysA, ddh), they achieve overexpression by integrating an additional copy of the gene and its flanking regions. On the other hand, for other genes (e.g., lysC, dapB, fbp, and the tkt operon) they take another approach and instead replace the native promoter with a strong constitutive promoter (Psod or Petfu).
Is there an advantage of one technique over the other? Why was one technique preferred over the other one for certain genes?

Modifying promoters can give finer, more targeted control of expression than changing copy numbers. In the paper you referenced, for the ddh gene, it sounds like they just wanted to boost production of that protein, so making a second copy made sense. But with some of the other genes, they wanted to alter metabolite fluxes through a more complex pathway. Copying a whole operon would not achieve this, because then you would just get two pathways doing the exact same thing. But even copying the one or two genes in the operon that you want to investigate might change their relation to the other genes in the operon. Bacterial operons are generally organized such that the genes for the transcriptional regulators are located adjacent to the genes they regulate. This proximity is necessary for the proper functioning of the operon, and if you copy a gene, depending on where you put the copy, it may not function as it usually does. In these cases, it's better to mess with the promoters because you can leave the organization of the operon largely intact.


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How important is getting enough glucose for maximal brain performance / cognition?
I know from many studies that have been done, that resting versus active use of the brain has relatively similar overall energy expenditure levels.
On the other hand, however, we know that the brain along with our eyes require glucose in order to function properly. Ketone bodies, lactate, etcetera may act as glucose sparing agents, but certain parts can definitively only use glucose as an energy source.
Anecdotally, I’ve noticed that when performing low intensity mental tasks like jogging or hiking for example, if I haven’t eaten for a while and am in a fasted state, I might get hungry for a bit, but if I just keep on going, after a while I feel fine and can pretty much go on forever after that. With high intensity mental tasks like programming though, the feeling of hunger doesn’t really seem to go away, and if I try to push through it, it just results in consistent brain fog and an inability to perform at any meaningful level.
My theory is that in cases where high mental performance is not required, alternative sources of metabolism provide the needed energy to function, and where intensive cognition is required, the rate of glucose production is unable to keep up with demand from the parts of the brain that depend on it which effectively creates a bottleneck in the cognition process causing the aforementioned brain fog and low performance.
Is this what is actually happening though? I’d like to think that it makes sense, but I’d prefer to have a biologically accurate understanding first and foremost.

In short: skipping a meal lowers blood glucose levels, which can reduce cognitive performance, for example, memory.
Let's say that between meals you are in fasting state for 8 hours during which you do some desk work and some moderate exercise for 1.5 hours. With such level of physical activity, your last meal and your glycogen stores should provide enough glucose for all your body needs, including the brain. So, during this time, you do not need any ketones or lactate as additional source of energy. According to Medical Hypotheses, 2014:

Estimated amount of glycogen in the human organism is about 200–500 g,
  and in certain specific conditions could reach up to 1.0 kg, which
  seems to be optimal for human organism. This amount is definitely
  sufficient for keeping optimal concentration of glucose in the blood
  during usual fasting periods not exceeding 24 h (between meals, during
  sleep, in case of exercise, etc.)

Skipping a meal can lower your blood glucose levels. According to WebMD:

Normal blood sugar levels are less than 100 mg/dL after not eating
  (fasting) for at least eight hours. And they're less than 140 mg/dL
  two hours after eating.
During the day, levels tend to be at their lowest just before meals.
  For most people without diabetes, blood sugar levels before meals
  hover around 70 to 80 mg/dL. For some people, 60 is normal; for
  others, 90 is the norm.

Blood glucose fluctuations related to meals:

Image source: Wikipedia, Creative Commons License
In some studies (AJCN, 1998), skipping breakfast was associated with lower blood glucose levels and worse memory test but not intelligence test results:

This article compares the findings of three studies that explored the
  role of increased blood glucose in improving memory function for
  subjects who ate breakfast. An initial improvement in memory function
  for these subjects was found to correlate with blood glucose
  concentrations. In subsequent studies, morning fasting was found to
  adversely affect the ability to recall a word list and a story read
  aloud, as well as recall items while counting backwards. Failure to
  eat breakfast did not affect performance on an intelligence test.


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Are hybrid-species individuals considered to be of the same species as their parents?
This question arises given the definition of father and mother as seen in the Spanish dictionary composed by the Royal Spanish Academy. Basically it says that a father/mother is a man/woman or a male/female animal that has engendered/given birth to an individual of the same species (Spanish: "especie").
The Spanish word "especie" could also be translated here as "kind", but let's assume it refers to its zoological definition. That definition would be mostly true, but what about mules or ligers?
In the case of mules, they are the offspring of a male donkey and a female horse. A male donkey is considered to be of the species Equus asinus, while a female horse is an Equus caballus. The mule is an individual of the species Equus asinus♂ × Equus caballus♀, but what is exactly that? It is the set resulting from the addition of the two parent species, or is it a complete, new species? In other words, are mules considered to be of the same species of a donkey or a horse? Or what they all have in common is just the genus?

Mules are not a species because they can't reproduce.  The problem seems to be that the dictionary definition doesn't correspond to the real world.

TL/DR We usually don't give specific names to those hybrids.
This is a fairly complicated question, actually, without an easy answer. Hybridization can have different outcomes, depending on how different the hybridizing species are. The cases you mention (liger, mules) actually do not deserve a specific names, because, first, they don't occur in nature, and, second, they are sterile, so there's no reproduction, hence no progeny. This lack of descendants goes against any defenition of species that we have in biology. There are cases where hybrids might become their own species, for example the butterfly Heliconius heurippa appears to be a species that evolved through hybridization between two closely related Heliconius species. There are also many examples in plants and more are being discovered in animals. These cases do receive a species name, because they occur in nature and populations can be predictably found.
Another case, similar to the cases you mention, involve hybridizations that occur in nature, but are rare and the individual rarely has any significance effect on the population. Sometimes those individuals are fertile, but look so different that might not be able to reproduce. Other times they can only reproduce with one of the parental species and if this happens successfully, new alleles can be introgressed into the parental genome. But for what we know, reproductive barriers between species tend to be successful in nature, tend to be broken down with human intervention (captivity, movement of species, among others) and, in most cases, don't have a significant evolutionary impact, except the cases when they do.


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Why are there no fresh water osmoconformers?
I'm just having trouble understanding this. I know that often marine fish are osmoconformers, and freshwater (like bony fish) are often osmoregulators, but why?

There are virtually no freshwater osmoconformers but there are some exceptions like being both an osmoconformer and an osmoregulator based on the salinity of the environment.
Osmoconformers keep their internal fluids isotonic to their environment and they maintain an internal salinity similar to the surrounding water. The concentration of solutes in freshwater is very low and if any organism were to have that low concentration of solutes in its body, it would not have enough proteins, ions, etc. to effectively conduct the biochemistry of living.
Here is a rare example of a freshwater species Daphnia which can be both an osmoconformer and an osmoregulator:

For freshwater osmoconformer species, most of the time there is a gradient between their internal
  osmotic concentration and that of the external environment; consequently, osmoconformers will
  vary in their cellular osmotic volume contents and as a result, some FW species (e.g. Daphnia),
  osmoregulate at low salinity levels but are osmoconformers at raised salinities. Some physiological
  processes, including reproduction and metabolic rate however, can be affected negatively by these
  changes (this group regulate their osmotic pressure actively) (Chen and Stillman, 2012).
https://eprints.qut.edu.au/107457/1/Azam_Moshtaghi_Thesis.pdf

Additionally, there is the term euryhaline used for the aquatic organisms who are able to tolerate a wide range of salinity. There are fish species that can live in salt water, fresh water and brackish water. You can see a list in the Wikipedia/Euryhaline Article.


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How does heredity work with Endogenous retrovirus?
Q1: If someone in a species gets infected with an endogenous retrovirus, does that mean that absolutely all of their children will have that endogenous retrovirus? Or is it based on chance?
Q2: is there such a thing as an allele for the virus being there, and for it not being there? How does it work?
Q3: how can an endogenous retrovirus disappear from a species? And when it cannot disappear?

For a provirus to be heritable, the infection must occur in the germ line. The initial integration would occur at one site in the genome and thus the locus could be described as hemizygous. Inheritance would indeed be probabilistic, depending on whether an offspring inherits the provirus-containing chromosome or its uninfected homolog.
Eventually, the endogenous retrovirus (ERV) can become fixed or lost in a population by genetic drift and natural selection. Additionally, retrotransposition and, more importantly, reinfection can greatly increase copy number and allow ERV persistence despite a lack of fixation at specific loci. It should also be noted that more recently acquired ERVs exist that have not reached fixation in humans.

References and Further Reading:
Boeke JD, Stoye JP. Retrotransposons, Endogenous Retroviruses, and the Evolution of Retroelements. In: Coffin JM, Hughes SH, Varmus HE, editors. Retroviruses. Cold Spring Harbor (NY): Cold Spring Harbor Laboratory Press; 1997.
Belshaw R, Pereira V, Katzourakis A, Talbot G, Pačes J, Burt A, Tristem M. 2004. Long-term reinfection of the human genome by endogenous retroviruses. Proc Nat Acad Sci 101(14):4894–4899.


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[IAL Biology]: Struggling to understand how pH and temperature affect haemoglobins affinity for oxygen

As seen in the graph above, why do we say that increasing pH increases haemoglobins affinity for O2, but decreasing pH reduces its affinity? If the pH increases above or decreases below haemoglobins optimum pH level, wont haemoglobins affinity for oxygen decrease either way? Same goes for temperature. Why do we say that decreasing the temperature increases haemoglobins affinity for oxygen and vice versa? If the temperature goes above or below the optimum temperature of haemoglobin, wont its affinity for oxygen decrease anyway? So how does this make sense?

I think you have the wrong idea about what "optimum" means - what's hemoglobin's job? What would happen if it bound oxygen strongly and never let go?

Does this answer your question? If during exercise the affinity of oxygen for haemoglobin is decreased, what are the general consequences for tissues?

Further to the comment from @BryanKrause, the idea that haemoglobin (Hb) has a pH optimum is nonsense. There is a normal tissue pH, which can act as a signal for lack of oxygen, to which Hb responds. I'd forget about temperature. Body temperature is normally maintained in a narrow range, but pH change is of the essence. The molecular nature of this response is dealt with in my answer to another question: https://biology.stackexchange.com/questions/55683/effect-of-2-3-bisphophoglycerate-2-3-bpg-on-haemoglobin.

I think you might be misunderstanding the term affinity, which is a measure of how strongly the two molecules (for example, haemoglobin and oxygen) bind to each other. High affinity means there is a strong bonding, and low affinity means the bonding is weak. Affinity can also be more formally defined via affinity (or binding) constant, $K_{\mathrm{a}}$.
Now take a look at you graph and choose some partial pressure of oxygen, say $P_\ce{O_2} = 30 \; \mathrm{mmHg}$. In the intermediate regime under physiological conditions (solid line), approximately $60\;\%$ of haemoglobin molecules have oxygen bound. However, when pH is increased (upper dotted line), the percentage of haemoglobin with oxygen raises to approximately $75\;\%$ – this is an indication of a stronger bonding (higher affinity). Conversely, when pH is decreased (lower dotted line), the percentage drops to only $35\;\%$ because the bonding is weaker (and we say the affinity is lower).