text:
How to get taxonomic tree data
I am looking for taxonomy data of individual species and their classes something like the following format:
{
  "type": "family",
  "parentType": "order",
  "parentScientificName": "hymenoptera",
  "commonName": "ant",
  "scientificName": "formicidae"
}

{
  "type": "species",
  "parentType": "genus",
  "parentScientificName": "...",
  "commonName": "black ant",
  "scientificName": "lasius niger"
}

Basically, from this, you can construct the full taxonomic tree. When looking at the pubmed taxonomy data I don't see how to reconstruct the tree. Please show me how.

I can't leave a comment at the time of writing this (since I don't have enough reputation right now), so I'll leave this as an answer.
Your question is a bit confusing. It's titled "How to get taxonomic data", but at the end of the post, you mention "Basically, from this, you can construct the full taxonomic tree. When looking at the pubmed taxonomy data I don't see how to reconstruct the tree. Please show me how."
I'll try to address both your questions here.
Acquiring the lineage data:
Are you perhaps looking for something like this?
NCBI taxonomy itself is also accessible programmatically via E-Utilities.
Constructing an evolutionary tree:
You could perhaps use something like the data.tree R package to construct your tree using the lineage data.
Your question is a bit too vague, so I apologize if my answer is of no assistance here.


text:
Are all fusion genes somatic in origin or can fusion genes be germline?
Fusion genes should have an origin.These are essentially hybrid genes that are translocated in its entirety. Eg. BCR-ABL, EML4-ALK are known to be implicated in cancer pathogenesis. Do these translocation events occur somatically or is there a possibility for it to be inherited?

What do you mean by fusion genes? Can you please add some context? At the moment it is unclear what you are trying to ask.

Hybrid genes that are translocated in its entirety. Eg. BCR-ABL,  EML4-ALK are known to be implicated in cancer pathogenesis. Do these translocation events occur somatically or is there a possibility for it to be inherited?

Hi and Welcome to Stack exchange. I think your question is not properly phrased. These hybrid genes you mention are indeed related to carcinogenesis, as in they are mutations commonly found in specific cancer types. It is unclear whether you are asking if (any) translocation events can also occur in the germline, or whether cancer-associated translocation mutations (such as the Bcr-Abl, Tpr-Met or Gag-Onc) can occur in the germline, and thus be inherited.

Thank you. Sorrry if it wasn't clear.  I'm asking if  cancer-associated translocation mutations (such as the Bcr-Abl, Tpr-Met or Gag-Onc) can occur in the germline, and thus be inherited. ?If yes, do you have papers supporting this? I haven't been able to find germline origin fusion genes.

There is at least one (possible) description of an inherited (aka germline) fusion gene:  KANSARL.  See the paper "Identification of KANSARL as the first cancer predisposition fusion gene specific to the population of European ancestry origin" by Zhou, Yang, Ning et al., Oncotarget. 2017; 8:50594-50607.

KANSARL fusion gene is familially inherited and may be ubiquitously expressed in KANSARL-bearing individuals
  The presence of KANSARL fusion transcripts in normal and adjacent tissues in CGD and VPD raised the possibility that KANSARL fusion transcripts are derived from a germline-inherited fusion gene. To investigate this possibility, we performed RNA-seq data analysis for the lymphoblastoid cell lines derived from the families in the CEU population (CEPH/Utah Pedigree 1463, Utah residents with ancestry from northern and western Europe), which includes a three-generation family with 17 individuals [47]. Supplementary Table 9 and Supplementary Figure 8 show that KANSARL fusion transcripts were detected in 15 of 17 family members, as indicated by black squares and circles in Supplementary Figure 8, except son (NA12885), which is deviated from the first Mendel law. A reasonable explanation is that the grandfather sample (NA12889) might have been mixed with the son sample (NA12885). To prove this possibility, we performed analyses of the WSG data (PRJEB3381) and RNA-seq from 1000 Genome Project, and shown that both WSG and RNA-seq of grandfather sample (NA12889) are KANSARL-negative while WGS of the son (NA12885) is KANSARL-positive (Supplementary Table 10). Supplementary Table 10 shows the genomic breakpoint 1 and 2 of the KANSARL fusion gene (Supplementary Figure 5 and 9) identified by analysis of WGS data among some members of CEPH/Utah Pedigree 1463. Therefore, Both WGS and RNA-seq data support that the father (NA12877) and the mother (NA12878) have the genotypes of KANSARL-/KANSARL- and KANSARL+/KANSARL+ respectively and all their offsprings are the genotype KANSARL+/KANSARL-

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text:
Is the medium which transmits the electrical impulse through the heart different to a nerve?
According to Nerve

A nerve is an enclosed, cable-like bundle of nerve fibres called axons

Being an Axon

An axon (from Greek ἄξων áxōn, axis), or nerve fiber, is a long, slender projection of a nerve cell, or neuron, in vertebrates, that typically conducts electrical impulses known as action potentials

In the other hand,
Electrical Conduction System of the heart

The electrical conduction system of the heart transmits signals generated usually by the sinoatrial node to cause contraction of the heart muscle.

The conduction system consists of specialised heart muscle cells
Is this conduction system consisted of cells (which I assume also transmits electrical signals through axons) different in nature to nerves?

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


text:
Is there a link between brain's energy consumption and human experience?
I was read the article (in Scientific American Mind)  about energy consumption of brain. There are:

Say you are learning a new skill—how to juggle or speak Spanish.
  Neuroscientists have made the fascinating observation that when we do
  something completely novel, a broad range of brain areas becomes
  active. As we become more skilled at the task, however, our brain
  becomes more focused: we require only the essential brain regions and
  need increasingly less energy to perform that task. Once we have
  mastered a skill—we become fluent in Spanish—only the brain areas
  directly involved remain active. Thus, learning a new skill requires
  more brainpower than a well-practiced activity.

...

Overall, though, on an individual level, our brain adapts and becomes
  more efficient as we gain mastery. We build new connections among
  neurons to keep pace with the greater demand on our neural resources.
  As our skill level grows in a particular area, our brain will
  inevitably require less energy to perform that task.

I tried to check what was written there. I tried to find experienced facts that refute or support this article. I did not find anything.
Question: are there experimental scientific data that show a decrease in energy consumption by the brain, while doing a certain activity, as professionalism grows? Or maybe there are experimental data that show the opposite? Or is there really no correlation between energy consumption and the growth of professionalism?

@user1136 Your comment could (should) be an answer. Answering in comments is discouraged in the SE model because it's not possible to both up and downvote your comment, it can't be accepted as an answer, and because comments are meant to be temporary and can be deleted at any time.


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Can endometriosis be considered a form of cancer?
In endometriosis the lesions form their own vasculature and compromise organs, arteries, and nerves. It can spread and embed throughout the body. It's difficult to treat as the adhesions resulting from repeated surgeries can cause the same symptoms as the lesions. Treatment often leaves patients with the original level of disability after the 2 year mark.
My question is, for these reasons could one treat and research endometriosis as if it were a form of cancer?
Could the immune system be utilized in treatment as the lesions induce high levels of certain cytokines?
Why or why not?

According to Endometriosis: benign, malignant, or something in between? (PubMed, 2017), endometriosis is not considered cancerous because:

Does not appear as an expansille tumor mass
Is not destructive
The cells in the lesions are normal, like in the uteral endometrium
Is not lethal

Immunotherapy of endometriosis is in the experimental phase - you can read more here: Novel Therapies Targeting Endometriosis (PubMed, 2011). Other treatments mentioned are anti-inflammatory drugs, selective estrogen or progesterone modulators, statins and antiangiogenic agents. There is also a study Open Label Immunotherapy of Endometriosis running - it is briefly described on ClinicalTrials.gov.
Chemotherapy, which is effective in some cancers, is based on killing quickly-dividing cells, but cells in endometriosis do not divide so quickly, so you can't treat it by chemotherapy in the same way.

It is important to note that cancer includes loss of the property of contact inhibition in cells. This leads to uncontrolled divisions in cancerous cells. Although endometriosis includes cells dividing at ectopic locations, they still possess the property of contact inhibition. So, endometriosis can't be called a form of cancer.
For information on Contact inhibition, visit the following link:
https://en.m.wikipedia.org/wiki/Contact_inhibition


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Why didn't these scientists restore electrical activity in this pig's brain?
This experiment was published in Nature Magazine: Pig brains kept alive outside body for hours after death. The researchers used a system called BrainEx to revive certain metabolic and physiological functions to a disembodied pig's brain, but they never attempted to restart electrical activity.
Why did they stop short of restarting electrical activity in this pig's brain?

Read the paper, and presumably they will say. This site is about biological problems, not about mind reading.

I'm not asking for anyone to read the researchers' minds. I was simply hoping that someone could provide a science-backed reason why restarting electrical activity in this brain would be inadvisable. I was expecting that some aspect of the brain's physiology made it too challenging and that someone with the appropriate expertise could explain this physiology to me.

Restarting electrical activity would mean that at least parts of the brain become active again and possibly restoration of almost all cognitive functions. While this would be a tremendous scientific and medical break-through, it would also mean that effectively locked-in syndrome would have been induced for these pig brains. Therefore just attempting to restore electric activity in isolated brains has huge ethical problems and was for this reason probably not allowed (or ever attempted).
Whether or not it should be allowed to test this in pig brains (in order to learn how to adapt the procedure to humans) is a different question (and not one for this SE) - the best way to go about would probably be to restore electric activity not in isolated brains, but with the brains still in animals.

Is this your hypothesis or are there any references in the field that say that's why it's not done?

@Cell The authors of the original paper refer to ethical concerns directly as the motivation for their limited approach.

@Cell This article explains the ethical implications more extensively: https://www.nature.com/articles/d41586-019-01168-9


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Why can't a genetically sound human stay alive for an indefinite amount of time given all the ideal conditions?
I have read that even if we can control our food and lifestyle and keep things as ideal as possible, there are other factors beyond our control like effects from neutrinos passing through our body that would accumulate over time, and may cause harm. More over, Earth's natural radiation, and the Cosmic background radiation may as well play a part.
I wonder what if we somehow removed these as well, will one be able to live forever?!
I have heard people say that this is an impossibility, but I wonder why?!
Thanks.

Your telomeres will kill you long before neutrinos do.

What exactly are telomers @AlexReynolds?...are they the chains at the end of a polymer or something like that?

Related questions: Why does evolution not make our life longer? and Is it possible for a human to live forever if he/she didn't catch any diseases?


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Could Wobble Base Pairing ultimately yield an amino acid that was originally uncalled for or not expected?
How does the cell choose which amino acid to attach to tRNA when there is wobble base pairing involved (not the other way around)? Consider the example below.
For the purpose of this question I'm picking UGC, UGA and UGG codons (Cys, Stop and Trp aa's) so that the 3rd position of the codon really makes a difference (if it does).
I know there are other pairings out there but to keep it really simple for myself I derived the following tRNA anticodons to match the codons using these rules:
G pairs with C or U,
C pairs with G,
U pairs with A or G,
A pairs with U,
I pairs with A, U or C.
UGC: ACG or ACI anticodons
UGA: ACU or ACI anticodons
UGG: ACU or ACC anticodons
My question is (assuming I did my work correctly) if there are multiple possibilities for anticodons to match with each codon how would we know which amino acid will attach to which anticodon? Take for example the ACU anticodon that could potentially match with UGA or UGG codons which codes for STOP or Trp. Wouldn't there be a discrepancy/confusion on which to code for by the cell? Ultimately wouldn't this affect the peptide/protein synthesized?
NB I have edited the original question to clarify my problem, which I do not think is answered elsewhere.

Possible duplicate of Redundancy of the genetic code

Welcome to SE Biology. As you will see, your question has been answered before (by me, among others). You may also be interested in the situation in mitochondria where the wobble rules are different because of the different tRNA structures. See may answer here.

It may be irksome to post a detailed question and be told that it is answered elsewhere. However if you feel that it has not been answered, the solution is not to complain in the title, nor is it any way relevant to cast aspersions on answers to other questions. The latter course of action is likely to lead to the moderators deleting your question. People are trying to help without unnecessary duplication. What you should do is reply to the comment, in a comment, and expand your question as necessary. I have edited your question and will address your clarification in a second comment.

You ask “How does the cell choose which amino acid to attach to tRNA?” It sounds as if you are unfamiliar with the family of amino acyl tRNA-synthetase enzymes and their specificity for cognate tRNAs? If so, please read the section in Berg et al. on line. If this does not answer your problem, please explain why not.


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Genes of the electron transport chain
Where are the genes of proteins that make the electron transport chain of mitochondria?(are they in in the nucleus or they are in the dna of the mitochondria itself?) Thanks for this answering system by the way

Welcome to SE Biology. Please take the Tour and learn about this site. You are expected to do some research before posting, especially for Homework questions. You can easily find the answer to this question by an internet search.  Do this, and then come back if there are particular problems that remain unresolved.

Dear David thanks for your welcoming so much.Honestly I am a student as you guessed but this one was not a school project.It's really nice of you pushing the student's to find the answer themself , instead of just asking them .but I did a search on the web and couldn't find what i wanted since I am not studying in english-there was also nothing on the web in my native language Persian.So if you can help me with the keywords that I have to search to find my answer,I will be really thankful.Have a nice time.

@ArmanJalali Hi, the question can be easily resolved if you try to find articles speaking about each of the four subunits of the transport chain individually. For instance, for the first subunit (NADH oxidoreductase) you can find your answer in the abstract of this paper   Good luck with the rest!

The Wikipedia page on Mitochondrial DNA is an easy first stop. Comes up on the first page of a Google search. You need to search in English, I'm afraid. Your browser should allow you to switch search languages. Firefox does, for sure.

Actually the article is available in Farsi: https://fa.wikipedia.org/wiki/دی%E2%80%8Cان%E2%80%8Cای_میتوکندریایی


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If some humans inherited 3% of Neanderthal DNA, why are we 99.9% same genome?
Many sources say that humans are 99.5 to 99.9 percent the same.
Also some sources state that some humans have 3.4% Neanderthal DNA and some don't share those genes.
Why is that?

Please search past questions on the list (neanderthal, african, denisovian etc). I am sure this has been asked before, but have not time at the moment to find it for you.

3% and 99.9% are from different calculation method.
20% (a rough estimation, might be wrong) of neanderthal DNA survived in the modern human genome, but it is 'diluted' by the human population,  which lead to 2 percent of neanderthal DNA in each human genome. This is the number 3%.
But how can we know it's neanderthal DNA?
If DNA fragment contains several neanderthal special SNP (single-nucleotide polymorphism), we will treat it as neanderthal DNA. (Based on linkage disequilibrium, the inference is reasonable.) The fragment might of tens of thousands nucleotides, but the difference are just one or two base.
But when we compare two human, we calculate the difference at nucleotides level, rather than DNA fragment. This is the number 99.9% come from.
If we have the complete genome of neanderthal and human, by comparing them at base level, the similarity might be great than 99%, I suppose.


text:
Do nerves work as I think they work and what does that mean for our senses?
Let me start off with a couple of metaphors.
In the third Lord of the Rings film, a signal for help is sent from Minas Tirith to Gondor, using a chain of beacons. When the keepers of one of these beacons sees that the one next to his lit, his orders are to light his own thus passing on the chain reaction. When the last one within sight of Gondor is lit, the message that Minas Tirith wants help is received.
There is nothing conveyed in the fire itself, no information within the flames, the beacons are either on or off. The only reason the beacons convey a message is that the citizens of Gondor know why that beacon would be lit.
Imagine a simple pressure sensor inside a building that is connected by a wire to an electric light on a control panel in a security room. When someone steps on the sensor it completes the circuit which sends electricity straight to the light turning it on. A label on the light says what it's connected to and where it is. So that when the light comes on, the person at the control panel knows someone is in that sector of the building.
But to be more precise, he knows someone has activated that particular pressure sensor, if it wasn't labelled he would have no idea what the message meant.
My understanding of the human nervous system is that it works in the same way. Based on information I learned from children's educational programs as a child and a few bits I picked up since.
Our ears have sensors designed to respond to sound. Each and every one has a direct connection to the brain via a chain of nerve cells. When one of the sensors is sufficiently stimulated, it zaps the neuron it's connected to, this in turn causes the neuron to zap the next one and so on all the way up to the brain.
The impulses/spikes themselves contain no actual information, they are just pure electricity, every spike contains the same amount of voltage. The only reason the brain is able to interpret them is because it knows exactly where each and every chain is connected to. When the impulse reaches the brain it knows it comes from a sensor in the ear that is responsible for a particular level of sound, the brain takes these signals and translates them into the sounds we hear. Nerve cells work something like binary, they are either on or off with nothing in between. The frequency of the spikes going along the chain indicates how intense the sound is. If the brain didn't know where that chain was connected to then the signal could mean absolutely anything.
This is supported by the condition known as synaesthesia where, because "wires are corssed" in the brain there are people who hear colour or taste music.
My questions are, is my reasoning correct? Is this exactly how nerves and perception work? Has this been scientifically proven beyond a doubt? Is there something within the impulses that contains additional information? Are the workings of the nervous system debated in scientific circles? I've been told we've never been able to plug an eyeball or any other kind of human sensory device into a computer so we've never been able to examine it as it's working, is this true?
But most of all, does this mean there are things our senses cannot detect?
I already know there are things beyond our range of vision and hearing and the brain blurrs then together. What I mean is this...
I know that we have different senses in our ears that are designed to respond to higher or lower sounds. Say we have a sensor that responds to a level 1 sound (I don't know the unit of measurement for sound) and next to it is a sensor that responds to a level 2 sound. What happens if we try to hear a 1.5 sound? Is it not detected by the ear because we don't have sensors in that range?
Can we only sense something if we have a sensor for it and are those sensors only built to sense one ultra specific thing?

I'll attempt an answer, but please know you don't have a clear nor defining question to address. This is more suited for conversation or open discussion, and I recommend starting a chat on the topic. Please be wary the question may be put on hold. I'll give it a go and respond from the top down. I absolutely don't think this is going to be fruitful for other people. Here goes:

Our ears have sensors designed to respond to sound. Each and every one
  has a direct connection to the brain via a chain of nerve cells. When
  one of the sensors is sufficiently stimulated, it zaps the neuron it's
  connected to, this in turn causes the neuron to zap the next one and
  so on all the way up to the brain.

Take the example of the eye; the retina is composed of photosensitive neurons, a type of sensory neuron. The inner nose is innervated with olfactory sensory neurons. The cochlea is similarly innervated by neurons. Firstly, you haven't made it clear that the neurons are the sensors. But indeed, the sensory neuron is the first order neuron. The processing of sensory information proceeds through first, second, third and higher order neurons until the information is integrated functionally somewhere in the brain. There exist neurons that modulate the signal along the way (e.g. lateral inhibitory interneurons) that are not on the information highway but rather beside it, regulating the input and output of neurons. It's quite complex, but you have the general gist of the hierarchy of neurons from sensory input (e.g. odor) to output (behavior, response, perception).

The impulses/spikes themselves contain no actual information [...]
  Nerve cells work something like binary, they are either on or off with
  nothing in between.

The exact temporal dynamics of this communication highway between neurons is very important. At some level, auditory volume may be coded by frequency, but this is restricted only to some level. Information is very quickly encoded and the 'raw' information sensory neurons provides becomes processed and transformed quite early in the chain. For instance, you may trigger circuits responsible for reflexes, which are (so-to-speak) dormant until a kind of neural activity activates them. Vision is well described in terms of encoding; at the first processing area of the brain for vision, things are simple, and are progressively more high-levels of encoding as the information is processed; there are regions responsible for motion, color, object recognition, even specialized regions for the recognition of faces, for instance.

If the brain didn't know where that chain was connected to then the
  signal could mean absolutely anything.

Correct. Remember though that the brain is very plastic, and can learn. There are many curious cases in neuroscience where this is apparent. One well-known widely described example: you can wear glasses that invert the world, and this would feel strange. After some time though, your perception would switch the world the "right way up". The retina has been largely unaffected, but the perception and the integration of the information can drastically vary quite independently.

Is there something within the impulses that contains additional
  information?

Remember that there are two kinds of connections between two neurons. Electrical and chemical synapses. A wave of depolarization does indeed travel through a neuronal axis, but in most cases, this does not occur across neurons. Instead, neurons (and related cells such as glia) release chemical messengers (neurotransmitters and neuromodulators) that act as inter-cell signals. These can inhibit or excite the post-synaptic neuron. Simply put, it's not a string of wires; it's a line of wires that interface with each other chemically; at each interface, chemicals must diffuse across the gaps and interact with the membrane-bound sensors found on the receiving neuron. This is not at all binary. And please know we are simplifying the system in order to describe it.

Is this exactly how nerves and perception work?

This is a simplification of how neural circuits work. How perception works is a completely different thing you have not even begun to address. This is a completely different topic of discussion. Bonus link!

But most of all, does this mean there are things our senses cannot detect?

A sensory system can only detect what it can detect. Your skin cannot detect radio waves. Your eyes cannot detect infra-red light. Your mobile phone, similarly equipped with sensors, cannot detect neutrinos.

I don't know the unit of measurement for sound

Decibel (volume) or hertz (pitch or frequency).

What happens if we try to hear a 1.5 sound? Is it not detected by the
  ear because we don't have sensors in that range?

You are describing the spectrum of volume as a graded, discontinuous thing. It's not! And more generally, yes. If your sensors cannot detect something, the organism is oblivious to it. Obvious.

Can we only sense something if we have a sensor for it [...]?

Yes. But you underestimate the power of a sensor such as a photosensitive cell. It can transmit information about the amplitude of the light, and responds to a range of light. Moreover, each photosensor has a response spectrum and does not respond equally to different (although similar) wavelengths of light. More so, if you have a patch of photosensitive cells, you can infer motion, direction, speed, size, distance, and all the merry things we associate with vision. The wealth of information is easy to underestimate.

... are those sensors only built to sense one ultra specific thing?

It depends on how you define specific. The equipment of a neuron in the retina is usually specific (e.g. expression of proteins responsible for light sensitivity) but it's possible to have a neuron that is responsive to several things. Have you ever tried to rub your eyes, and you see phosphenes? Your retina is responding to the increased pressure. You could say these cells are sensitive to light and pressure. That's not ultra specific. You can similarly activate these neurons at short range electrically, or magnetically. That's starting to sound like a pretty unspecific sensor, depending on how you define it for yourself.
I absolutely don't mean to aggravate, I very much suggest you do some readings on the topic. It's one thing to have a pub-level confidence in vaguely worded funfacts about sensory circuits, and another to understand and appreciate the nuances and complexity and the many knowns and unknowns of neuroscience. It's not too difficult to grasp. I would instead ask you to ask about fundamentals before you ask to correct your outlook on biological sensory systems. Books are cheap and the internet comes in handy sometimes, and you may even spare someone else's time!


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What do lower case nucleotides mean in this gene sequence?
The following table (image linked below) shows promoter sequences recognized by different sigma factors. The sequence given for, e.g. sigma B is "GTTTaa"; why are the "a"s lowercase?

(from "A sigma factor toolbox for orthogonal gene expression in Escherichia coli", Bervoets et. al. 2018)

How would we know, without reading the paper, which you can do yourself? It is in no way a standard convention, as some databases have all nucleotides in lowercase.

The case refers to the degree of conservation of a particular nucleotide in the consensus sequence. Highly conserved nucleotides are written in uppercase. At positions where the sequence varies, the most common nucleotide is given in lower case. That said, I'm not sure what the cut-off would be between "highly conserved" and "most common" and, in my opinion, is something that should be explained in the paper (though, in this case, it does not appear to be). There may be some convention I am unaware of.

@canadianer Can you make that an answer rather than a comment?

@BryanKrause Okay, though I don't particularly like ending an answer with "I am unaware".

Here's a link to the paper, for those interested: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5829568/ No mention of what the frequency cutoffs are for conserved-bases/less-conserved-but-higher-than-background-bases, but contacting the authors may help with getting specific percentages. (That's what the contact info is for!)

The case refers to the degree of conservation of a particular nucleotide in the consensus sequence. Highly conserved nucleotides are written in uppercase. At positions where the sequence varies, the most common nucleotide is given in lower case. That said, I'm not sure what the cut-off would be between "highly conserved" and "most common" and, in my opinion, is something that should be explained in the paper (though, in this case, it does not appear to be). This paper, for example, uses uppercase where a base is conserved in four of the five sequenced promoters. There may be some convention I am unaware of.


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In touchdown PCR, should the extension temperature match the annealing temperature in phase 1?
For TD PCR, it's recommended that the annealing temperature (T_a) be 10°C higher than the normal cycling T_a for the first 10 cycles or so, dropping 0.5 to 1.0°C/cycle. Should the extension temperature (T_ext) match this pattern to prevent miss-annealing? It seems that if the initial T_a was 75°C, then T_ext was set to 72°C (or whatever is optimal for the polymerase), the purpose of the high T_a would be lost.
Instead, should T_ext match T_a with an increased extension time until the optimal T_ext is reached?

Your initial annealing temperature 75°C would mean nomal cycling annealing temperature 65°C. That is really high. Is there a reason why you did not design your primers with Tm ~60°C (normal annealing ~55°C)?

I do not if I understand correct the question. But I write you an example. For example for the amplification of the gene nirS, I used a touchdown PCR. The Tm of the primer is 60°C. I created a touchdown from 65°C and each cycle decrease of one degree (total cycle of the touchdown is 5). The thermoprofile is the following:
94°C for 3 min; 5 cycles of 94°C for 15 sec, 65°C (touchdown -1°C) for 30 sec, 72°C for 30 sec; 34 cycles of 94°C for 15 sec, 60°C for 30 sec, 72°C for 30 sec; followed for 72°C for 10 min.
Is better that in total your PCR do not make more than 40 cycles.
I hope that this help you
Jo


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What species of thermophilic prokaryote is present in hot compost that creates white mould like threads?
A method known as the "hot composting" method aims to create the right ratio of carbon rich and nitrogen rich materials in the pile in order to encourage thermophilic organisms to thrive in order to accelerate the process of making compost.
The following source 1 explains:

Need optimum temperature of 55-65 degrees Celsius. At temperatures over 65 degrees Celsius a white “mould” spreads through the compost, which is actually some kind of anaerobic thermophilic composting bacteria, often incorrectly referred to as”fire blight”. (It appears when the compost gets too hot – over 65 degrees Celsius and short of oxygen. It disappears when the temperature drops and aerobic composting bacteria take over).

What specific species is this organism?
I say prokaryote in the question title as I'm aware it may be a bacteria or archaea. Many sources incorrectly refer to archaea as bacteria.
Hot Compost – Composting in 18 Days

sorry i don't have enough time to answer this completely but here's a reference incluing a list of common bacteria they found. It really sounds like you are talking about a fungus, but cross referencing this list could make a complete post.


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What is this black insect?
  I found it in my computer but I don't know what it is

Please provide your location and the approximate size of the bug you found. Thanks.

It appears to be a Boxelder bug, which are common in areas of North America with maples, ash, or other host trees:
 (photo by Katja Schulz via Wikimedia Commons)

A hemipteran, yes, but the OP's specimen has quite different color patterns than the species you suggest. Can you explain the difference in colors or provide stronger support for why Boisea trivittata is the correct answer despite these morphological differences?


text:
What species is this little white bird?

This bird was found in my backyard in the north east of Italy. It's about 5cm long and can fly as high as 1.5m (so far).

It's probably a white zebra finch:

Such as... do you need instructions for an ophtalmologist.


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Meaning of letter "c" in description of mutation: "Homozygous c.195C>G; (p.Cys65Trp)"
In a table in a paper titled Cerebral folate deficiency: Analytical tests and differential diagnosis, there's the following description of a mutation in a patient:

Homozygous c.195C>G; (p.Cys65Trp)

I wonder what the letter c means here.

Well, if it is not in the paper, I’d try emailing the authors. They should know.

@David - thank you! I just imagined this might me a super-easy question, that's why I asked here.

It’s not. There will be people in the field who will know, but it would be good if the authors were made aware of the narrowness of their writing (if this is, indeed, the case).

I typed "c dna mutation" in Google and this article was the first hit:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1867422/
The "c" denotes coding DNA, which given the context of the amino acid mutation having the letter "p", this makes sense.

It means coding DNA reference sequence. Please refer the following link for more information. https://varnomen.hgvs.org/bg-material/simple/ . This should help.


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How does the human body extract energy from ethanol?
I was talking about alcohol and obesity with a colleague. I always thought the only cause of that is the sugar that is found in most alcoholic beverages. But my colleague pointed out that ethanol itself provides calories to human body.
I checked that and it seems to be the case. What I don’t understand is how is it possible. On wikipedia I found following statement:

If catabolism of alcohol goes all the way to completion, then, we have a very exothermic event yielding some 1325 kJ/mol of energy. If the reaction stops part way through the metabolic pathways, which happens because acetic acid is excreted in the urine after drinking, then not nearly as much energy can be derived from alcohol, indeed, only 215.1 kJ/mol.

The statement relates to these reactions:
$$C_2H_6O (ethanol) → C_2H_4O (acetaldehyde) → C_2H_4O_2(acetic acid) → acetyl-CoA → 3H_2O + 2CO_2$$
Now note that the wikipedia calls the pathway "exothermic". However, I don’t think that human body can derive energy from heat. Or can it?
Since most articles claim that ethanol alone has positive caloric value, how exactly is this energy extracted and used or stored as fat?

Exothermic means that a reaction yields heat, not that the body uses it. Alcohol has 7 kilocalories per gram, which is almost twice as much as carbohydrates (4 kcal/g).

To quote from the editorial on the Wikipedia page: "This article has multiple issues. Please help improve it or discuss these issues on the talk page". Wikipedia is a product of people like you and me. Be aware of that.

Preamble
The question suggests unfamiliarity with the nature of biochemical oxidations and their relation to energy transfer in biology. The naïve reader is recommended to consult a text for a coverage of this subject: all I feel is appropriate here is a general summary followed by a brief indication of the key reactions.
General principles of energetic value of and biological oxidation of foodstuffs

The energy available from the oxidation of foodstuffs such as starch, fat and alcohol may be represented as the thermodynamic Gibbs Free Energy change (ΔG) in their complete oxidation.
This value can be determined chemically by bomb calorimetry in which the oxidation is done directly by oxygen and the energy produced is in the form of heat.
In biological oxidations the immediate oxidant is a molecule (an enzyme cofactor) such as NAD+ (or NADP+ or FAD), and part of the Gibbs Free Energy change is translated into chemical energy in formation of the reduced compound — NADH etc. Only some is lost as heat; but enough to give an overall negative ΔG, that causes the reaction to proceed.
The reduced coenzymes can be used to produce ATP by oxidative phosphorylation (involving oxidation by oxygen) or in reductive processes such as the synthesis of fatty acids, depending on the organism’s energy requirements.
Likewise, the molecular intermediates produced in the course of the biological oxidation (e.g. acetate) can be oxidized completely by oxygen (the terminal electron acceptor of the electron transport chain) to carbon dioxide and water (with production of more NADH in the tricarboxylic acid cycle, and hence more ATP), or can be converted to other metabolic intermediates or used as the precursors of other molecules, including storage molecules.
If the organism has a sufficient supply of energy (ATP) already, surplus intake of foodstuffs will lead to the deposition of energy reserves.

The case of ethanol
The question rightly states that ethanol is converted to acetaldehyde and then to acetic acid, but fails to include the oxidant, NAD+, which is an essential participant in the biological reactions:

[ADH: alcohol dehydrogenase; ALDH: aldehyde dehydrogenase ]
Thus, two molecules of NADH are produced, providing either ATP or reducing power.
The question assumes that after conversion of the acetate to acetyl-CoA it will be oxidized in the tricarboxylic acid cycle*. However in a fed subject with sufficient energy the cycle is suppressed and the acetyl-CoA will be converted to malonyl-CoA, the precursor of fatty acid synthesis. These processes require both reducing power (NADPH, which can be obtained from NADH) and ATP (ditto):

*The quotation states that “acetic acid is excreted in the urine…”. I have no knowledge of what proportion of ethanol is disposed of in this way, but I would imagine it is small — certainly not enough to prevent beer belly. However this is not the main reason why “catabolism of alcohol” does not “go(es) all the way to completion”.
Postscript
The biochemistry above is covered in Section 30.5 of Berg et al., entitled “Ethanol alters energy metabolism in the liver”. This was formerly freely available to read online, but unfortunately this is no longer the case. However copies of this edition can be picked up very cheaply on eBay, for example, and the student can rely on its coverage of basic biochemistry.


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What happens to eyelids when we feel sleepy?
Why is that whenever we feel sleepy, our eyelids start to feel heavier.

It is not like we can any time close our eyes and will immediately fall asleep. But, when we feel sleepy our eyelids automatically become heavy.

What causes heaviness of eyelids? Is it because of sleep hormone or something?


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Protein misfolding
Protein misfolding is usually prevented by molecular chaperons. Rarely, the chaperons are not able to prevent the misfolding as a result of which the infectous molecules called prions will form.
My question is, why does the misfolding occur like what are the reasons of misfolding and what kind of mechanism occurs? I somehow find limited information on this issue.

Prions only occur with specific proteins. Again please do some research before posting.

Your question is very broad. You can find entire review articles (or even books) dedicated to this topic. Please check out pubmed or Google scholar.

The astonishing thing is not that proteins misfold, but given the astronomical number of possible ways of folding they manage not to misfold. So you are coming at the problem with the wrong mindset. If you can access to it through a university library, try this review.


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SDS-PAGE compared to western blotting
SDS-PAGE and western blotting are both used to separate and isolate proteins. My question is, which technique should be used when? Does one of them has advantages over the other one?

Blotting sits on top of SDS-PAGE, so it really depends on the question of your research which one you do...

Please do some research before asking questions. Your premise is incorrect.


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What kind of ribes is this?
I have a plant in my USDA zone 5 garden that appears to be in the ribes genus.

Details:

The location is east of Toronto (Ontario, Canada).
The plant is currently flowering (today is May 18th, 2019).
It is approx 4 feet tall.
The plant flowers every year, but does not set fruit (not self-fruitful).

More photos here:

https://i.stack.imgur.com/coEp5.jpg
https://i.stack.imgur.com/wv0TA.jpg
https://i.stack.imgur.com/pFmtk.jpg
https://i.stack.imgur.com/KvjGe.jpg

What species is it?

I think this is Ribes americanum or wild black currant.
I'm basing this on page 306 of Newcomb's Wildflower Guide, an excellent source for the Eastern US and some of Canada.  On that page we have two main choices:

Base of flowers prickly or bristly... or

Base of flowers not prickly or bristly...

Your excellent pictures suggest that your specimen is in category 2.
From there, we have:

a. Flowers solitary or 2-3 in a cluster; branches bearing a few thorns. or
b. Flowers 5 or more in racemes.

Your specimen looks to have quite a few flowers, so in category 2b we have a choice of Ribes americanum:

Whitish or yellowish flowers, longer than wide (and fruit black, you can check later I guess),

or Ribes sativum:

Greenish flowers, wider than long (and fruit red).

Color in the white/green/yellow range is a bit subjective, but your flowers look longer than wide, hence Ribes americanum.
Of course, with this in mind you might re-inspect the plant and refine this a bit.

I'm glad the photos worked out. I was just using an old phone camera. The key seemed to be to take lots of photos; one of them was bound to be in focus. :)


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Help me ID snake
Could someone please tell me if this is a cotton mouth?  Found 2 on my back porch, one got away.
Location: Fayetteville, AR (USA) [Note: there are several ponds nearby]

Hi, for a better identification, please read the recommendation in the species-identification tag wiki here

The head does not look triangular or big enough to be a cottonmouth. The few times I have encountered cottonmouths in my yard they have been very calm , do not scurry off quickly. ID depends on where you are : here in E Tex it could be a green water snake or a yellow-belly water snake. Is there water nearby ? If not , maybe a rat snake. I did kill a cotton mouth once by mistake ; It looked like a green water snake that eats fish in my ponds. The greens disappear fast so I hit it before I could look at it closely. Too late I saw it was a cotton mouth ( which do not like small ponds so rarely come here).

I live in Fayetteville, AR. Yes there are several ponds nearby, which is where we usually see cotton mouths.  Rarely do they venture into our back yard.

This is not a cottonmouth, it's Nerodia rhombifer, a diamondback water snake. It's nonvenomous and important for the ecosystem. Given that the water snakes compete with cottonmouths, it's important to not kill them to keep their populations high and not make room for cottonmouth populations to grow.

I had a diamond back water snake in my pond; He was much lighter in color , tan with brown "diamonds" .

Not certain why this post was downvoted given that it is the correct answer. Perhaps the downvoter doesn't believe in mutually-respectful dialogue. That's a shame.

Hi @ChrisMoore. Posts with citation notices generally attract downvotes (sometimes regardless of their correctness). I would advise providing a link or citation to a source that supports your answer. We're not looking for anecdotal comments, expert opinion, or short answers without explanations. We're looking for long answers that provide some explanation and context of why your answer is correct with citations/links to supporting evidence. [tag:species-identification] posts likewise benefit from providing images from reputable sources to further support your answer. Please revise. Thanks!


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Can something cause both breaks and cross-links in DNA?
A double strand break in DNA is exactly that: the strands of DNA are severed. A cross-linkage occurs when something forms a covalent bond between two nucleotides in DNA. However, is it possible for something to form both a cross-linkage and a double-strand (or single-strand) break? For instance, could one part of a molecule cause a break while another reacts to form a cross-linkage?
For the purposes of this question, enzymes or proteins which do this (If there are any) also count.

Cisplatin forms DNA-protein crosslinks (so DNA-protein-DNA by extension) in vitro [1] and a review [2] says that cisplatin leads to DSBs (although I can't access the primary source at the moment). But you know, with the exception of ionizing radiation, mutagens usually don't directly cause DSBs. It's caused by repair processes or things like stalling at replication forks because of the mutagen.
[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1874601/
[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4047912/#!po=11.9919

Ultraviolet radiation can induce both DNA crosslinking and double strand breaks.
Here is a paper reporting sequnce determinants of UV-induced intra-strand crosslinks:
https://www.ncbi.nlm.nih.gov/pubmed/11342214
Here is a paper where the authors propose that UV-induced double-strand breaks are a consequence of repair of oxidative lesions, rather than a primary result of UV photochemistry.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3488256/


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Why can dogs hyperventilate without consequences like humans?
During the heat of summer, dogs usually breathes very fast, like 100 times per minute or more. If humans do so, we will experience an array of negative effects like dizziness, finger tingling or losing consciousness, by the results of blood alkalosis and reduced oxygen level. The question is, why don't our canine buddies seem to experience the same consequences?


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Is it possible to change the DNA of all the cells of an adult human
The process of making and transferring changes is pretty straightforward relatively speaking in an embroyo. You change the DNA of one cell and all the cells now inherit this change.
But let's say that after x amount of years from now on we are capable of creating perfect changes to the DNA of a person.
What could the process of transferring this change be for an adult human being? Given that there are about approx. One trillion cells in our body, is it even possible to change it?
I think that using a designed virus could be one way, T4 bacteriophages do a pretty good job of taking over the nuclear material of the bacteria. But I don't think it can be too effective given that most of the viral activity is restricted to the blood. Also I don't think the blood brain barrier let's the viruses across.
Highly speculative topic but I would appreciate any insights on this.

What has your research told you?

@BryanKrause He's given a decent rundown of his research.  I think it's reasonable that he's posing the question to the community now.  It's a speculative topic (as he said) but I think interesting to some people here.

I agree with @sterid. That being said, I would consider the question "Is it possible to change the DNA of all the cells of an adult human" to be on-topic but the question "Assuming it will be possible to change the DNA of all the cells of an adult human in the future, what are the possible ways for this to happen" to be border line off-topic and should maybe rather be asked on worldbuilding.SE. I am not sure which question the OP is asking.

I apologize for the confusion. The latter isn't my question, it's an assumption necessary to make to pave way for the question that whether or not is it possible to implement the change made in the DNA of one cell to be implemented in now a trillion cells. By "what are the possible ways for this to happen?" I am not referring to the ways of changing the DNA but to implement the change presumably made.

@sterid OP is speculating that maybe a virus could be used, and the question doesn't mention anything to suggest they have considered existing approaches to use viruses to change adult human DNA.

Is it possible to change the DNA of all the cells of an adult human?

In development? Yes.
Changes in the DNA prior to S-phase in the zygote will result in all the cells inheriting the changed DNA. Before or during the 1-cell stage in embryology, any changes will be ubiquitous in the developing adult and all their cells.
In the adult? No.
No technologies for this exist. None are on the horizon either, to my knowledge. The closest concepts are in targeted gene therapy. There are plenty of workable ideas, but they are all restricted to specific targets.
In the future? Most probably not.
In all cells, in all tissues, in a controlled manner? I very much doubt it, it's an extremely complex undertaking, and (all) the laws of statistics and chemistry are against you. We can speculate all we want but all in all, it's smarter to make the changes in specified locations (see answer two), or at the right time (see answer one).

As an addendum: think of it this way... You can achieve interior design in many ways. You can move your couch around to achieve an aesthetic, or you can draw a plan before you furnish a room to save the trouble of experimenting. Similarly, here too we can speculate about whether it's possible to detonate dynamite in your living room as a way to rearrange your furniture in a pleasing manner. It's probably not going to be a method of approach in the future, simply because the alternatives are a hell of a lot easier, and likelier to bring more tangible results.

But the question wasn't "is it possible now?" but "could we in the future". And your answer is the subjective "probably not". The question is off-topic and best ignored until there are enough votes for close. You certainly haven't answered it.

@David I don't think anyone can actually answer this question cause apparently we just don't know enough about epigenetics and gene expression yet.

@SPr I don't agree with this not being a preferred method of approach in the future. Let's say a human is born on earth but it turns out that he will have to spend a significant portion of his life in space for whatever reasons. He probably won't want to be stuck with a body that isn't adapted to space. The window of changing the DNA before birth is very small and it does not contain the consent of the actual person. So given that everyone wants their DNA changed when they are adults, won't the next question be that how to sync the DNA of all the cells with this newer version.

@Arkilo Do you think research in the future will aim to change DNA in every single cell in the adult body? I will pay you the compliment of assuming you understand how stupefyingly unlikely that is to work. Restricting to small areas or subtypes of cells (e.g. progenitors) is already in development though. I'm also sure we can agree it's easier to make a spaceship hospitable and build spacesuits to protect from radiation, rather than mutating DNA comprehensively, precisely and confidently enough to make us radiation or lack-of-oxygen tolerant. Even our pedant David would probably agree!


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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?

It would be easier to read if a key was provided, rahter than a description of the colours

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.

The strategies change depending on the scenario


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Are cells guaranteed to get at least one mitochondrion when they divide?
If mitochondria exist at random within a cell, isn't there a possibility that cell division will result in a daughter cell with no mitochondria?  If not, what is the process for guaranteeing at least one is present in each daughter cell?  If so, what happens to that cell?

Isn't there a possibility that cell division will result in a daughter
  cell with no mitochondria?

Yes, there is always the possibility. However, there must be a strong negative selection pressure against eukaryotic life that cannot achieve the proper partitioning of mitochondria, so you can imagine that there are mechanisms in place to prevent this case.
Mitochondria are both passively and actively partitioned to daughter cells. This is understood to occur through the cytoskeleton and with the control of mitochondrial fusion and fission at key stages of the cell cycle, prior to mitosis and cytokinesis!
Here is a great review from several years ago that addresses your question well.

The review is just 5 years old. If it's "several years old" then what would you say about the waiting time to be eligible for an academic job?

I’m not sure there needs to be any strong selective pressure for this whatsoever. Stochastically, it’s quite likely (actually, virtually assured) that both daughter cells end up with at least a few mitochondria and if not, well, then one of the daughter cells dies and the other one simply divides again. Little harm done, except in gametes. And gametes mis-segregate all the time. One more error in a centillion isn’t going to make a difference.

I thought about this too. But mitochondria are no ideal gas and do not follow such rules. Also, not all mitochondria-hosting life is multi-cellular and tolerant to such errors. I would agree with your randomness point, given the following suppositions: 1. mitochondria are randomly distributed in their host cells (untrue); 2. the number of mitochondria in the daughter cell is always unimportant (untrue); 3. cytokinesis is symmetrical (very often untrue); 4. cells without mitochondria are not selected against (which cannot be universally true in all ecological scenarios).

In addition to S Pr's excellent example, I wanted to point out that some very recent research describes some special behavior in oocyte development specifically related to mitochondria selection.
Here's a easy-to-read version:
https://www.sciencedaily.com/releases/2019/05/190515131741.htm
Here's the original version in Nature:
https://www.nature.com/articles/s41586-019-1213-4
Specifically, during meiosis, the oocyte specifically "puts the mitochondria to the test" by separating all of them (fragmentation) and having each of them operate independently.  (Typically mitochondria act in concert, each one potentially making up for deficiencies in their peers).  Any that do not "make the cut" are eliminated, and the result is an egg cell that has the best mitochondria to pass along to the next generation.

This is really interesting! I'd like to understand more about what "mitochondria act in concert" means. Perhaps one is better at one function while its "peer" is better at a different function? Or do you just mean that stronger ones make up for weaker ones that aren't "pulling their own weight"?

@uhoh Probably both. Mitochondria have many different functions, and they're very susceptible to genetic damage (since they store their genome in an oxygen-rich environment). Over the lifetime of an organism, many mitochondria fail to perform all or some of their functions, and one typical thing that happens with cancerous cells is that mitochondria replicate far more than usual. In the end, these rarely cause significant issues (beyond the effects of aging etc.) - with one major exception, which is the production of ova. There a single broken mitochondrion can "doom" the offspring.

Can you also cite the original research?

@WYSIWYG I added a link to the Nature article... Is that acceptable?  (I'm not sure how to find the link to the original research.)

A typical animal cell has 1000-2000 mitochondria.  From a statistical point of view, assuming a random distribution of the mitochondria and that the cell splits in half, the probability of having 0 mitochondria is (1/2)^1000 or 9e-302.  This makes it an impossibility for all practical purposes.
With enough mitochondria, a process to ensure the cell splits roughly in half and a somewhat random distribution of mitochondria would be sufficient to get at least one mitochondria in each daughter cell.
To address the assumptions:

Random distribution of mitochondria - assumed in the question
Cells split roughly in half - source on dividing assymetries "In somatic divisions, however, cell size asymmetry is mild and, only rarely, one daughter cell is more than double the size of the other."

I think both of your assumptions are highly suspect, unless you can cite research to back them up.

@Mike While I agree that some citation would increase the quality of this answer, I really like the perspective of it. Other answers regard the high evolutionary pressure on cells without mitochondria and refer to mechanisms to actively prevent that case by distributing mitochondria to the daughter cells. This one brings perspective to the importance of these mechanisms: It certainly is beneficial to actively control the mitochondria distribution, but is this a necessity or just a "nice to have" feature? The actual numbers certainly are not very representative, but I like the idea of it.

@NiklasMertsch Exactly.  I'm simply trying to demonstrate that in a certain class of cells, there are enough mitochondria that a random process will sufficiently guarantee distribution to the daughter cells; no active process necessary.


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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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How to map the N6-dimethyladenosine by primer extension?
I am trying to map N6-dimethyladenosine on rRNA using primer extension (low dNTPs assay) method. But i am not able to detect map my position. I went through some articles they mentioned like they hydrolysed the RNA but they did not mention exactly by which hydrolysis method (enzyme, alkaline). can you please help me?
Great. I used (10 g) of Total RNA for primer extension reaction with 100,000 cpm [- 32P]ATP-labeled oligonucleotide. After annealing at 55–60 °C for 15 min and chilling on ice for 2 min, 1 unit of reverse transcriptase (Expand RT, Roche) and 1 unit of RNase inhibitor were added and an extension reaction was performed at 42 °C for 90 min. The extension products were ethanol precipitated and analyzed on 6% polyacrylamide, 7 M urea gel. (DOI 10.1074/jbc.M308997200)
This method specialized for 2’o methylation on rRNA, my interest is N6-dimethyladenosine (M26-A). In the literature M26-A blocks the RT I did not get the extension. In this publication, they have mentioned the RNA was hydrolyzed but hydrolysis has many different types (alkaline, enzyme) (https://doi.org/10.1091/mbc.E15-02-0073)

It would be helpful if you could give more details of the method and your experimental strategy, together with the reference(s) to the method. Your question is quite specialized.


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Can radiation exposure cause cancer later in life even if no traces of radioactive material are present in the body anymore?
I had a long-lasting debate with a friend of mine about the Fukushima incident.
The question that we tried to solve was if radiation or toxin exposure can cause cancer later in life even if no traces of radioactive material or toxins are present in the body anymore.

Yes it can, because exposure alone can cause mutations in your genes which is usually the main cause of cancer.
For example, when we get exposed to UV light for longer periods of time, we can get skin cancer/melanoma. Here , of course no traces of these rays are present in our body, its just all due to prolonged exposure.
Now to the fact that why does it even happen , according to wikipedia is

Cancer is a stochastic effect of radiation, meaning that the probability of occurrence increases with effective radiation dose, but the severity of the cancer is independent of dose. The speed at which cancer advances, the prognosis, the degree of pain, and every other feature of the disease are not functions of the radiation dose to which the person is exposed.

So since once induced, it just keeps on increasing even though you are not exposed to that particular rays anymore, you most probably are going to have it. This is the reason why cancer is so dangerous, because once it is there you can't stop and even can't make any precise stats about it until a certain stage.
For more details , visit https://en.wikipedia.org/wiki/Radiation-induced_cancer#Mechanism
I hope this answer helps you :)


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Do all restriction enzymes have palindromic recognition sites?
I am trying to find out the requirements for a segment of DNA to be the recognition site of a restriction enzyme.
Acording to the article on Restriction Enzymes in Wikipedia, "many of them" (referring to recognition sites) are ‘palindromic’ (in the sense that the sequence of nucleotides on one strand should read the same as the that on the other strand, from the opposite direction).
Is this true for all recognition sites?

Please read our homework policy which requires that you demonstrate that you have done some research to answer the question yourself before posting here. Did you read the Wikipedia article on this topic?

Yes i did, and it tells that "many of them" (referring to recognition sites) are palindromic and that left me in confusion. Does that mean there are recognition sites that aren't palindromic? Unless i didn't see some certain part in that article.

Instead of writing "I suppose" you should have stated that you had read the Wikipedia article, giving a link, and quoted the phrase, as in your comment. You can find the answer by reading further in the article, but so as not to discourage you, I will rephrase your question, and briefly answer it.

thanks and i apologize for the late reply.i get it now

The article cited in the question goes on to discuss the different classes of restriction enzyme, for which the recognition ‘style’ differs. Not all recognize palindromic sequences.
Type II restriction enzymes
These have been divided into a number of subclasses (reviewed by Pingoud and Jeltsch). Those regarded as orthodox — which are the ones generally used in DNA cloning — appear always to require palindromic sequences in their recognition sites, although those in some other classes do not (see list here).
This statement is subject to the proviso that you regard as palindromic 5-base recognition sites, such as AlwXI, GCAGC, and others with a ‘non-conforming’ central region, such as ApaBI, GCAN5TGC. The reasons for including the latter (which provides an alternative way of defining the requirements of the recognition sequence) can be seen by examining the symmetrical manner enzymes of this class bind the site, which can tolerate a non-symmetrical central region. This is described in more detail in an answer I gave to another SE question on restriction enzymes.
Type I restriction enzymes:

…cut at a site that differs, and is a random distance (at least 1000 bp) away, from their recognition site. Cleavage at these random sites follows a process of DNA translocation, which shows that these enzymes are also molecular motors. The recognition site is asymmetrical and is composed of two specific portions—one containing 3–4 nucleotides, and another containing 4–5 nucleotides—separated by a non-specific spacer of about 6–8 nucleotides.

Type III restriction enzymes:

…recognize two separate non-palindromic sequences that are inversely oriented. They cut DNA about 20–30 base pairs after the recognition site.


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Does cat urine really fluoresce? If so, why?
I temporarily got caught in the Sad and Useless website, and found Science is Fun.
Most of the claims seem plausible, but I can't guess why cat urine would fluoresce.
Comments have directed me to Why Does Urine Glow Under a Black Light? which says:

You can use a black light to detect body fluids. It's actually a good way to look for pet urine or make sure a bathroom or hotel room is really clean. Cat urine, in particular, glows very brightly under ultraviolet light. Urine glows under a black light primarily because it contains the element phosphorus. Phosphorus glows yellowish green in the presence of oxygen, with or without black light, but the light imparts additional energy that make the chemiluminescence easier to see. Urine also contains broken down blood proteins that glow under a black light.

Certainly other mammals including humans have both phosphorus and broken down blood proteins in their urine, so is the proposed specificity to cat urine just an issue of concentration perhaps?

I don't find it implausible, but why cat urine specifically, and not of other animals?

I actually think thoughtco simplifies quite a bit. I don't think there is pure P in urine.

Could possibly be because of Urobilin. Also, diet also influences the urine composition. Some of the excreted products can be fluorescent (for e.g. riboflavin)

Cat is a carnivore. Myoglobin is also a heme protein and its breakdown would also produce the "bile pigments" and their downstream excretion metabolites. It is possible that a carnivore might produce more bile pigments because of their diet, compared to a herbivore. However, I am not sure about it.

@John Dvorak: In fact, other sorts of urine, including human, fluoresce under UV light.  Don't happen to have a cat, so I can't check relative intensity :-)


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How do primers anneal to ssDNA?
In a PCR type protocol, the high temperature stage of the cycle will cause dsDNA to denature, as well as any annealed primers. At the lower temperature the denatured dsDNA will remain denatured. As far as I understand, though, the primers are re-annealed.
My question is this: are there any enzymes that catalyses this re-annealing, or does this happen by chance?

No enzyme is involved in base-pairing (annealing).
This does happens by chance, but the chances are governed by stoichiometric considerations.
The main such consideration is that the (low molecular weight) primers are added at a high concentration (greater than that of the DNA) and therefore have a greater chance of encountering the appropriate region of the DNA than its complementary strand does. (Reannealing of the denatured DNA strands can occur, but not over the time period of PCR.)


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Does a cell suspend or exit cell cycle at G0?
In an exam, there was one question which asked whether the cell exits or suspends cell cycle at G0 phase.
I answered that it exits cell cycle but the official answer key says it suspends cell cycle.
I marked exit because a cell in G0  undergoes differentiation and maturation. Is there a difference between the two terms?

The answer is exit. I had given this exam this year and marked the same answer as yours and its correct.

and also if you wanna know the difference between the two words , a similar terminology has already been answered on SE. Visit - https://unix.stackexchange.com/questions/265911/what-are-the-differences-between-kill-suspend-and-terminate-of-a-process

I've always heard of it referred to as exiting and re-entering the cell cycle. Of course some cells do not re-enter. This seems to be a matter of semantics. I don't think it's prudent or even sensible to make an exam question based on what verb to use to refer to the process of delaying or avoiding entry into the G1 phase of the cell cycle. Mandatory reading.

It is actually suspend and yes the words do differ. This is because the cells that enter the G0 stage is not actually exiting the cell cycle because when situation demands it will divide. It is metabolically active and therefore the word suspend suits better

Please add some references so this doesn't get downvoted :)


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What kind bottom feeder is this?

It’s about 2 1/2 inches long and had a little tail on the end. Also has short feelers that almost look like a moles.

By the first look it seems to be a lamprey. But I would suggest to give some more context to the place you took the animal. (see the species-identification tag wiki.

It's a kind of loach. You have to include the location in your query.
i.e. a black khuli loach:

a weather loach:
http://badmanstropicalfish.com/profiles/profile103.html


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What the "due to" means in the definition of heritability?
According to Wray and Visscher,

heritability is formally defined as the proportion of phenotypic variation (VP) that is due to variation in genetic values (VG).

My question is, what does “due to” mean here?
My first thought is that its meaning is causal. By using Pearl’s causality framework, I’d think that we could say something like:
I have a variable T (trait), and a pool of genes (G) as cause. Also, other variables (not genes) also cause T, let’s call them U. Thus, it seems that this is a (simple) causal model behind heritability:

However, let’s say the trait is accent. It is unlikely that genes have a causal effect on this trait, so the arrow from genes to this trait would not exist. However, if we measure it in some way, we will probably be able to compute the heritability of this trait, especially because white Americans, for instance, speak with a different accent than Afro-Americans (thinking about the USA). So, we should conclude from this that the “due to” in the definition above has nothing whatsoever with causality. It is talking about correlation: how much of the variation in the trait we can associate with genes. So, if we have the following causal model (to make things simple), we would still be able to compute the heritability of a trait.

However, the only effect of gene on accent is mediated by an environmental variable (segregation), which has no direct effect whatsoever of genes.
So, my question is: does heritability depend on having a causal model? If so, are estimates done with an explicit causal model like a DAG? Do they try to control for confounding and other things that may cause a biased estimation?

Welcome to SE Biology. I have tidied up your question a little, in particularly decreasing the dead white space in your diagrams to make the whole readable. Please note that it is not correct practice to cite a journal as being responsible for a statement, unless it is an unsigned editorial. The authors bear the responsibility or should receive the cudos, as the case may be.

Thank you. I'll write better questions in the future. Lesson taken.

Related: This basic explanation of the definition of heritability

In your second model, you indicate that genes determine race, when race is not a biological category. Rather, the genes determine skin colour, which is one factor that becomes a part of how people define "race". More to your question, the model of causality is separate from the argument of which genes or environmental factors are causal for a particular trait.


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Can you identify this red insect?
Location: Lansdowne, Uttarakhand, India
Date: 27 May 2017
Time: 5.33 pm
The insect was found walking upwards on a plastic table. It was about 3-4cm long, as far as I remember; its been a long time since I encountered it.
Spotted near a small shack in the Terai forests.

A note as to the animal's size might help (there isn't quite enough here to get that); other than that, I'm certain it's a true bug (Order Hemiptera, Suborder Heteroptera), and believe it to be a stink bug relative (Superfamily Pentatomoidea), but not knowing the Indian fauna I can't go deeper than that.

It looks like a nymph of eusthenes femoralis

This is a nymph of a shield bug in the Tessaratomidae family, commonly called tassarotimids (or sometimes "giant shield bugs" due to typically being 1.5 - 4.5 cm long).
According to Wikipedia:

They are mostly found in tropical Africa, Asia, and Oceania though a few species can be found in the Neotropics and Australia. There are about 240 species known

Of the subtaxa, only a few genera are even found in India:
Empysarus, Neosalica, and numerous in the subtribe Eusthenaria (e.g., Asiarcha, Aurungabada, Carpona, and Dalcantha). A key (Leston (1955)+)to this group of insects is available for purchase or institutional subscription on Wiley
Specific Taxa:
Similar to a comment under the OP's post suggests, this page appears to suggest that the nymph of a Eusthenarian called Eurostus validus (shown below) appears quite similar to the OP's specimen. However, I cannot find definitive record of E. validus being in India.

 Source: Vic wicked on Pinterest
the availability of useful information (keys, reputable websites, etc.) for this group of insects (especially for India and in English) are extremely limited, so I will just leave you here with the understanding that your insect is a tassarotimid nymph that is closely closely related to Eurostus validus, Eusthenes femoralis or some other member of the Eusthenaria.

 + Leston, D., 1955, April. A KEY TO THE GENERA OF ONCOMERINI STÅL (HETEROPTERA: PENTATOMIDAE, TESSARATOMINAE), WITH THE DESCRIPTION OF A NEW GENUS AND SPECIES FROM AUSTRALIA AND NEW SYNONYMY. In Proceedings of the Royal Entomological Society of London. Series B, Taxonomy (Vol. 24, No. 3‐4, pp. 62-68). Oxford, UK: Blackwell Publishing Ltd.


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How do NSAID's work and what are the differnces between COX-1 and COX-2?
NSAID's work by slowing down the COX enzym, but how do does enzymes cause pain? because I've read that they're also needed for the body and do "good" things.

NSAIDs work by inhibiting COX-1 and/or COX-2. These are the key enzymes in prostaglandin biosynthesis. Prostaglandins act as messenger molecules in the process of inflammation and therefore can cause pain and other inflammatory symptoms. Source
COX-1 is normally present in different tissues of the human body and is for example important for maintaining the stomach lining. By contrast COX-2 mediated prostaglandin synthesis is only induced by injuries and inflammation. The analgesic effect of NSAIDs is therefore mainly based on the inhibition of COX-2.
There are to different classes of NSAIDs, non-selective (aspirin, naproxen, ibuprofen, ...) and COX-2 selective (celecoxib, parecoxib, ...-coxib). Due to the different roles of COX-1 and COX-2 these different drug classes have different adverse effects and differ in their analgesic effect depending on the dose. E.g. use of aspirin can lead to ulcers of the stomach or duodenum while COX-2 selective drugs do not cause gastric problems (but others).


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what causes epigenetic dysregulation in cancer?
Do mutations in regulatory gene sequences lead to changes in epigenetic alterations   in cancer, and if so which ones? I know abnormal hypermethylation of GCP islands occurs in promoters of tumour supressors, but what drives the abnormal methylation? Thanks

Your question is very broad. There are multiple factors that lead to epigenetic changes. I am not sure if the "first" signal that causes cancer progression has been identified but many histone modification proteins (HDAC, HMT etc) are dysregulated and are even being considered as targets of cancer therapy. So, to answer "what really causes the epigenetic dysregulation" an entire review article would be required.

But ultimately are epigenetic changes due to changes in gene sequence from mutational events? For example, would gene sequence change cause increase activity of DNA methyltransferase to cause increased methylation?


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Does the nature of nervous impulses give us a finite number of things we can perceive?
This is a subject that is very disturbing to me and one that I've been obsessing over for years. I warn you now that this is probably not the sort of thing you get asked on this website and I'm not even sure if I'm explaining it very well but please bear with me.
I have, or at least used to have, a great passion for art and have always been a very creative person. But years ago I began obsessing over the idea there are only a finite number of possible images that we can perceive. And therefore everything I have ever created or will ever create is part of a predetermined, limited set of possibilities.
The amount of knowledge I have about how perception works is that when light hits a photoreceptor in the eye it fires electricity into its connecting nerve cell, this triggers the nerve cell to zap the next one and so on until it reaches the brain. The brain has a memory of where each chain of nerves is connected to and so it identifies that otherwise indistinguishable zap as coming from a particular photoreceptor in the eye. That each chain of nerve cells simply transmits it is on or off and nothing else. I worried that meant our perception works exactly like am LED screen, meaning that when light shines on the grid of photoreceptors, the image that gets sent to the brain is made of dots of exactly one solid colour and the only reason we don't notice it because the brain smooths the edges. This would mean that, if eyesight works like a digital camera there is a finite limit of things that we can possibly see because there is a finite number of images you can possibly create with a digital camera.
I even found an article on the Internet that claim that's exactly how it works, they even have a diagram:

Eventually I found a way around it when it turned out that the eye is constantly making microscopic movements even when holding still.
But what about hearing? I know we have sensors in the form of hairs that trigger a nervous impulse to the brain when they are stimulated. But as I understand it, each one can only send that on/off binary signal when they are triggered by a very specific level of sound. What happens if there is a sound that is in between two hairs? Do you simply not here it? Is the same true for all the sensors we have?
I know that the brain processes a lot of what is sent. I know that there are things outside our range of perception such as ultrasonic and UV light. And I know we all have our personal reactions and even perceptions. But none of that matters to me.
What I want to know is, can our senses cover a continuous spectrum? Or, is everything we perceive a number of discrete and finite possibilities made up of digital, pixelated, quantised information? Can we only perceive image A and image B with nothing in between, or can we perceive image A.012744 and A.064212454 And A.24545157845?

I know we have sensors in the form of hairs that trigger a nervous
  impulse to the brain when they are stimulated. But as I understand it,
  each one can only send that on/off binary signal when they are
  triggered by a very specific level of sound.

Your overall question borders on philosophy and the biology of consciousness which is hardly understood at all. However, your picture of sensory input is a huge oversimplification. That's not really your fault, it's the sort of thing you are likely to pick up from pop science descriptions, which in turn are faulty because this is not a dead field where everything is understood to a T. Even the question of which parts of perception "are" digital and which "are" analog is still under investigation. However it makes your question hard to answer because it's sort of ill-posed since is assumes a purely digital model.
To address one oversimplification, our perceptions of the outside world are not necessarily binary on off bits. It is hypothesized that some neurons signal by changing the rate at which they fire. Is the rate continuously variable? It's not clear, but it certainly provides a much larger range of encodings than 1 and 0.

Can we only perceive image A and image B with nothing in between, or
  can we perceive image A.012744 and A.064212454 And A.24545157845?

I don't know how this meshes with your statement that 'And I know we all have our personal reactions and even perceptions'. If you've ever looked into color blindness then you already know that some of your fellow humans can't distinguish between A.012744 and A.064212454, even if you can. It's not that they can't see them, they just can't tell that they are different.

Correct a digital model is just all wrong for the brain not because a neuron is not digital (it is) but because the signal from one neuron to another is not. Due to how neurotransmitters and inhibition interact. A neuron is on or off but the signal from one neuron to another can have a variety of states. The closest electronic analog is a memristor.

I have already read that the frequency of spikes denotes the intensity of what is being sensed. But frankly this doesn't answer my question.

Here's how I understand eyesight works: imagine a control room inside the brain, one that has a screen made out of light bulbs, each bulb capable of only displaying one solid colour. As I understand it, when light hits the photoreceptors in the eye, the electricity passes along the chain of nerds and makes that lightbulb turn on because that's the one it's connected to. The lighting and colouring of these bulbs generates the image we see in our heads.

What bothers me is that there is a highly quantised nature to this image, there are real-world details that escape the process because they are in between the photoreceptors/light bulbs. Sort of like trying to view the world through a colander or a grill.

Is that how eyesight works? Does it work like in the diagram I posted? Do we not know a great deal about human perception already?

I've spoken at length to someone I knew about this (although he wasn't an expert in this field) he was very insistent that the brain could do all kinds of things with the information received and that made our visual possibilities infinite. I strongly counter argued that I was talking about our ability to perceive the real world and that depended on the information we are capable of receiving in our brains.

Recently I felt a little better about this problem because I read that our eyes are constantly making microscopic movements even when we are staring at a fixed point, that would allow our eyes to fill in the gaps. But then I thought about hearing, the senses in our ears are still discreet and quantised and ears don't constantly move around. Aren't they then bound by the limitations I've already described?