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Are there any DNA sequences shared by all/most Viruses?
Is there any one DNA sequence shared by all or most viruses?
I highly doubt there is mainly because of how different all of them are, but it's still worth a try.
Thanks

What length of sequence did you have in mind?

Around 4 to 8 nucleotides would be perfect.

Statistically it seems very likely that every organism would share a 4 nucleotide sequence.

Very true. I'm looking specifically for any sort of shared sequence that is necessary for the survival of all viruses. At first I thought (for RNA viruses at least) it would be some sequence in a gene that codes for reverse transcriptase, however I have yet to find such a sequence. Any suggestions for a sequence like this or any other would be very greatly appreciated, so feel free to mention any ideas you might think of.

There are commonalities within certain related viral families. But no, there are no universal viral genes, there are many reasons for this:

Viral genomes in general are much smaller than the average cell genome and the pressure for selection against extraneous genes is high due to the need to be able to replicate as fast as possible within the host cell. This also allows for rapid evolutionary rates due to the sheer mass of  viruses creates and spread through a given host.
There are viruses that infect wildly different hosts and thus require highly divergent entrance mechanisms and strategies. Due to this difference, there would be no need for the bacteriophage for instance to share the same proteins or genes with those of HIV or another human virus.
It is possible that viruses have evolved multiple times throughout the history of life, this is however not confirmed as of this time. If it is true however, then it would preclude the possibility of universal viral genes as they would not share a common homology.(Though viruses may be able to mix their genetic material by sheer chance, if they share a common host.)
Viruses, by definition lack the common replication, translation and generally, transcription machinery that is shared by their cellular hosts. Thus, they do not have this source of common genes, as living organisms do.

No, virus are polyphyletic and there are no genes that are common to all viruses. There may be similarities in capsid structure due to convergent evolution, but these are not universal. See Moreira and López-García (2009) for further detail.


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Do human visual functions degenerate due to genetic factors or by external factors?
Does eyesight primarily deteriorate 'naturally' due to genetics (genomic/epigenomic factors), or due to external factors such as normal wear and tear, or disease?
By normal wear and tear I include things like repetitive straining of the eyes by reading small text in a dim room night after night.
As a background to my question: By dissecting the causes of visual deterioration into genetic factors versus external factors I hope to relate those causes to the age of onset, and rate of decay of visual acuity.

What exactly is the difference between "natural deterioration" and "degradation through wear and tear"? To me, these are the same and the question is quite unclear, as @anongoodnurse also suggests.

Also, the title and question body don't match. Please clarify the question.

@ChrisStronks - I apologize for my ambiguity. By "natural degradation" I mean an aging process predetermined in length and intensity by some biological factor in the human gene/genome similar to the 'lottery' of vision that is 'given out' at birth. The distinction I am attempting to make between this and aging broadly is the specificity of age of onset and rate of decay.

By "wear and tear" and "over-stimulation" I am implying environmental/behavioral factors such as repetitive straining of the eyes by reading small text in a dim room night after night. The reason I didn't ask specifically about reading is because I'd like to know the broader answer about why does vision degradation occur when it does. Does that help?

please adapt your question and specify what you want to know. From the comment on @anongoodnurse it seems you specifically want to know something about accommodation, while from the above comment it seems you want a very broad answer. Please specify.

@ChrisStronks - I've edited the question body. Does the edits clarify the question?

@ChrisStronks - The answer does cover myopia, and can be a valuable answer for other related problems, imho. Myopia has both a genetic and environmental cause.

@anongoodnurse: your answer is fine (although it does not cover the genetic aging element). The question was however  ambiguous and needs clarification. I proposed an edit that awaits review from the poster.

@ChrisStronks - Thank you! That is certainly much clearer than the original.

Vision deteriorates for both reasons, but I'm not quite sure how to separate the effects of aging from wear and tear.
Cataracts are the leading cause of blindness in the world. Ways in which environment (which falls under the category of wear and tear in my book) affects cataract formation:

UV light: people living at high altitudes (e.g. Tibet) have more cataracts 2° to increased UV light than those at lower altitudes (sunglasses with UV protection delays the process)
lead exposure increases cataract formation.
infections in infancy and childhood (rubella, toxoplasmosis, other)

Macular degeneration is another cause of vision loss. Environmental factors include:

smoking: speeds up age related macular degeneration.
diet: diets low in antioxidants, and obesity increase degeneration.

Retinal damage caused by diabetic retinopathy:

Juvenile onset diabetes has long been thought to be associated with viral infections from coxsackievirus B, cytomegalovirus, adenovirus, rubella, and mumps.
Type II diabetes is influences by obesity, lack of exercise, certain medications, (nicotinic acid, some diuretics, anti-epileptics, psychiatric drugs, and drugs to treat HIV (can impair beta cells or disrupt insulin action); Pentamidine (used to treat a type of pneumonia) can cause pancreatitis and diabetes; glucocorticoids/steroid hormones may impair insulin action.

Corneal opacities:

infections: (Chlamydia trachomatis) bacteria that are spread by close contact with an infected person or by flies, especially common in Africa.
recurrent injury (soot and pathogens from indoor smoke, a dusty, windy environment).
vitamin A deficiency

Nearsightedness:
- near-point work: reading, working with a computer all day, etc.
Glaucoma:
- diabetes, obesity, near-point work, other.
Nonenvironmental causes would be genetics and illnesses associated with aging.

genetic predispositions associated with diabetes, nearsightedness and farsightedness
decreased lens plasticity with age
strokes secondary to hypertension, etc.
amblyopia (“lazy eye”), strabismus (when eyes are aligned in different directions), astigmatisms
hereditary causes of glaucoma and age-related macular degeneration
retinitis pigmentosa, (degenerative disease of the retina)
innumerable genetic disorders (Marfan's, Tay-Sachs, Albinism, Cone-rod dystrophy, various autoimune disorders, etc.
retinoblastoma
predisposition to glaucoma

 Focusing on Vision Through an Environmental Lens
 Glossary of Eye Conditions
 Causes of Diabetes
 Inherited Eye Disease

@anongoodnurse - You answered perfectly, especially given that I am new to Stack Exchange and very poorly worded the question. Your answer was incredibly informative about the types of diseases that affect vision and their factors. My initial inquiry (perhaps naively and certainly not communicated correctly) was what causes the deterioration of vision in individuals who's visual health is not affected by any disease, but have only behavioral factors and biological predispositions as possible culprits. I'm a little lost at this point about how to pursue an answer to that question, however.

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How to know the gestation time of pregnant mice?
In lab mice I wish to establish how many weeks my animals are into their pregnancy. Is there some way?

This is generally done by checking for the vaginal plug in the female after you have set up the breeding. If the plug is visible then it means that copulation has happened. However, this is not a foolproof test because the vaginal plug just indicates copulation and not pregnancy. This, nonetheless works in most cases and helps you in timing the pregnancy (Reference: JAX notes).

For most strains, the rate of pregnancy is highest among
  estrus-suppressed females with vaginal plugs found the third day after
  being placed with a male. As examples, whereas the rate of pregnancy
  is ~100% and 44% respectively for C3H/HeJ and BALB/cJ females with
  plugs found on the third day, it is only 62% and 31% respectively for
  those with plugs found on the fifth day. In contrast, whereas the rate
  of pregnancy for C57BL/6J females is only 39% for those with plugs
  found on the third day, it is 69% for those with plugs found on the
  fourth day.
If the plugged female is pregnant, the first day of gestation is
  considered to be the day after the plug is found.

You can also monitor for an increase in weight of the mouse. This is not a foolproof technique but serves as a secondary evaluation method.
If you have not timed your breeding and checked for these markers, then you may have to rely on ultrasound.

Checking for plugs is regulary done and the results are ok. The only drawback is that you need to check your mice at least twice daily (hence the 0.5 in most embryonic dates) which can be a lot of work.

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Why does ALS start in middle age?
Amyotrophic lateral sclerosis (ALS) often starts at middle age, but I didn't find any suggestion why. Something seems to trigger the symptoms in middle age.
If I am not mistaken, the sporadic ALS is not genetic, but there are genetic variants. So these genes are with the person all his life. But why do the disease symptoms often start only in middle age?

Short answer
The causes of ALS are not well known. Some familial types are associated with toxic proteins, susceptibility to toxins and defective protein metabolism. My personal 2-cents is that metabolic and toxicologic defects tend to cause cumulative tissue damage over time, perhaps explaining the delayed onset.
Background
Amyotrophic lateral sclerosis (ALS), is a progressive, fatal disease characterized by the gradual degeneration and death of motor neurons.
In 90 to 95 percent of all ALS cases, the disease is sporadic, meaning that it appears apparently at random. Individuals have no family history of ALS, and their family members are not considered to be at increased risk for developing it.
About 5 to 10 percent of all ALS cases are inherited. About one-third of all familial cases result from a defect in a gene known as “chromosome 9 open reading frame 72,” or C9orf72. The function of this gene is still unknown. Another 20 percent of familial cases result from mutations in the gene that encodes the enzyme copper-zinc superoxide dismutase 1 (SOD1). In case of mutations in the SOD1 gene it is though that mutant SOD1 protein is toxic.
Other inherited forms are believed to change in the processing of RNA, that may lead to ALS-related motor neuron degeneration. Other gene mutations implicate defects in protein recycling. And still others point to possible defects in the structure and shape of motor neurons, as well as increased susceptibility to environmental toxins.
Source: NIH - ALS Facts Sheet

Thank you, Alice. Also for editing my question. I read this source before. If we talk about familial ALS - it's looks more clear. Accumulation of toxic mutant protein, for example. Some sort of accumulating defects. But what about sporadic? ~90% of the ALS. And also - sometimes ALS starts in young people.

@VGranin - no worries, happy to help. The disease etiology of the sporadic cases are, as far as I understand and as stated in my answer, often unknown. Because they, seemingly, don't have a genetic background, it is probably very hard to pinpoint what is at fault in these folks. In other words - I don't know and as far as I can see, no one really does. That is, implicitly, what 'sporadic' means - random occurrence / cause unknown.

Yeh I know that I will not get some proved reason. But maybe there is some studies that have some good suggestions based on some evidence ...  Also about the genetics -  I think that in all cases there must be some genetic background. The environment could trigger it - but must be something wrong in the genes from the beginning. And in middle ages the body gets weaker - so thinks go wrong more easily. It's only my suggestion.


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What insect is this case from?
I found this insect case in my garden in the south of Melbourne (Australia), on concrete under some dried leaves of a tree that I'd cut down.

It is 8 cm long, which is pretty big for an insect! The photo is of the underside. I don't recognise it. What species is it?

This appears to be the exuvia (i.e., molted) pupa of some sort of moth.
One Australian species with a similar-looking and sized pupa is the bardee or rain moth (Trictena atripalpis; or Abantiades atripalpis):

 Credit: Dianne Clark ; Source: Coffs Harbour Butterfly House
See another similar looking (and coincidentally 8cm long) specimen here:

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Is a Ribonuclease Inhibitor protein the only mechanism employed by the human cell to protect cellular RNA from degradation by endoribonuclease?
Are there any other methods of protection for cellular RNA from degradation by endonuclease (specifically the Pancreatic Ribonuclease RNase II (Eosinophil-derived neurotoxin) and RNase III (Eosinophil cationic protein)) besides Ribonuclease Inhibitor Proteins? Perhaps a method that interacts with the RNA itself rather than compromising the RNase?
Would 5' end capping or 3' end polyadenylation which are normally used to protect from exoribonuclease also protect from endoribonuclease? Could a Ribonucleoprotein Particle (RNP) type strategy protect from degradation?
Thank you,
CDB

Endoribonuclease is not that high in the cytoplasm AFAIK. Yes binding with proteins does confer some protection. Secondary structures can also offer protection from certain RNAses, but not others.


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What attracts cells to: pathogens, professional antigen-presenting cells, and cells with an antigen on its MHC-1 protein?
I have a few questions in regards to attraction/stimulation in the immune system.

What attracts leukocytes and antibodies to pathogens in the first place?
What attracts CD4+ cells to professional antigen-presenting cells (APC)?
What attracts CD8+ cells to cells with an antigen on a MHC-1 protein?
What attracts macrophages to pathogens that have been tagged with antibodies?

Is it just a case of everything bumping into each other and if cells (and antibodies??) bump into chemokines and/or cytokines they will be stimulated (and not attracted) to stay around that area moving to an area of a greater concentration of chemokines and/or cytokines?
That said point 1 can occur without chemokines and/or cytokines (in the case of antibodies, they could be taken/administered by the person).  While in case of point 3, (I may be wrong here) but chemokines and/or cytokines may not be present in the case of MHC-1?

What attracts leukocytes and antibodies to pathogens in the first
  place?

They just bump into them. If secreted antibody is already present in the blood then complement system can be activated.

What attracts CD4+ cells to professional antigen-presenting cells
  (APC)?

APC release chemokines. All that is known is that this is a CC-type chemokine and signals via CCR4/CCR8 receptors. See this list of articles (from Google Scholar). This study reports a peptide called Chemrin that promotes chemotaxis via ChemR23 receptor.

What attracts CD8+ cells to cells with an antigen on a MHC-1 protein?

CD8+/NK cells are activated by CD4+ cells before they kill their target. The MHC-1+antigenic peptide is just a mark for the cells that are to be attacked, as far as I understand.

What attracts macrophages to pathogens that have been tagged with
  antibodies?

Complement factors.
NOTE: Many of these concepts are old but still relevant. You should check out recent articles in this area for novel/atypical mechanisms.

Regarding the answer to the first question: yes, if we are talking about circulating pathogens. But if the pathogen has cytotoxic effects on a tissue, the release of damaged cell components may attract immune system cells by chemotaxis.

yeah forgot to add that.. Cells can release type-1 interferons.

Brilliant, thank-you! I've been reading up on the self non-self theory & the danger theory..So was trying to arduously identify some of the danger signals that were already present.  And thank-you @Cornelius


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Is there a known minimal stretch of DNA that can distinguish any two people in the world?
I imagine this could be used as a universal Identifier.

I guess it depends on the particular stretch of DNA. Some sections of DNA are conserved and under heavy selection pressure (such as p53) whereas others can vary.

Here is what the data says. UK government must have had some scientific evidence when it settled on a 10 variable-length sections of genome for their database, SGM+. In one such variable sections, some people have 10 repeats of CTTT, others have 11, others have 12 etc. The largest of those fragments, at its maximum length, are about 350 base pairs. The US government uses 13 such variable-length sequences for its CIA database, called CODIS. On both sides of the Atlantic, roughly 3-4 thousand base pairs were judged to be enough, with some safety margin, by the most advanced geneticists in the world, working on public money.
The catch is that these variable length sequences are disjoint, so you end up requiring far more than 4,000 bp. If you need these markers on the same DNA strand (chromosome), you should space them by 50 centimorgans, at which distance they recombine independently. But according to http://www.sciencemag.org/site/feature/data/genomes/265-5181-2094.pdf , the longest chromosome only has 350-400 centimorgan. It means you cannot get 10 independent DNA sequences on a human chromosome, be it the longest.
I predict there is no such continuous DNA stretch, that would tell apart any two non-twins. Since it is much better to use multiple chromosomes in DNA fingerprinting, I doubt you will find more relevant experimental data.

When designing PCR primers we typically use a minimum length of 20 bases, because the probability of a sequence of N bases appearing by random is $\frac{1}{4^N}$, and $\frac{1}{4^{20}}$ is about 9x$10^{-13}$, or about 1 in a trillion. Since the human genome is a little over 3 billion bases long, a 20 base sequence should appear only once. However, most of an individual's DNA isn't random, it's inherited from their parents, and they got their's from their parents, etc. Long story short, there isn't a lot of unique DNA in any given person. The uniqueness is only visible on the large scale, you have half of your DNA from your father, and half from your mother. So would any of your siblings, but the specific DNA they got from each parent would be different from yours.
I think we can calculate the odds of getting a specific set of chromosomes from a parent. If there are 23 pairs of chromosomes, then the probability of getting any given set should be $\frac{1}{2^{23}}$, since we have 2 parents, the odds of getting your specific set of DNA is $(\frac{1}{2^{23}})^2$, which is about 1 in 70 trillion. So the odds of you having a non-identical twin that has the same DNA as you is very low. But any given 20 base sequence should have a 50% probability of appearing in you and the sibling.
But if we look at 2 20 base sequences of DNA in you and your sibling, and each had a 50% chance of appearing, then the probability of both sequences appearing in the both of you is 25%. If we add a third, it goes to 12.5%, and so on. If there are 7 billion humans on earth, we need a probability of less than 1 in 7 billion, and $2^{33}$ is about 8.6 billion, so if you looked at 33 different sites on the genome it should be able to differentiate you from every human on the planet
By the way, did I do the math right? I'm not a mathmagician and I could have made a mistake in my probability calculations. I have also assumed that the spontaneous mutation rate and crossing over rates are low enough to ignore, but both would serve to make your DNA a little more unique.


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Can you please identify this mosquito-like insect?
I've seen these insects before (here in Cambridge, UK) and thought that they were probably mosquitoes, but they don't make the annoying noise that mosquitoes do (they fly similarly, but silently):

I also noticed that they are perhaps slightly larger than mosquitoes (maybe 12mm long) and don't have the long mouth which mosquitoes use to sting you.
Sorry for the poor photos, I don't have a camera with a macro lens anymore, and it's night-time. It's casting a strong shadow as you can see in the second photo.

It is most certainly a fly from Chironomidae, which belongs to the same suborder (Nematocera) as Mosquitoes (Culicidae). They have an overall resemblance to mosquitoes, but lack the large sucking mouthparts, and often have the large feathery antenna that are seen in your pictures. Some species are found in large swarms in early spring (but also later in the summer). Larvae can be found in most freshwater, and are called bloodworms due to red colour (high in hemoglobin, adapted to live in oxygen-poor sediment environments)
I doubt that the exact species can be determined from these pictures though.

Agreed as to family, and also to the doubt that further identification is possible: these midges are among the "some disassembly required" insects; the book "Chironomidae of the Holarctic region. — Keys and diagnoses. Vol. 3. Male imagines.(Diptera)" (Entomologica Scandinavica Supplement 34) summarizes a procedure that ends with FIVE cover slips on one slide, each holding part of the specimen!  (The number goes up to seven if you have the last larval and pupal skins of the same specimen.)

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Can you identify these tiny black insects please?
I'm afraid I don't know anything about them except that there are suddenly thousands of them invading my house since about a week ago, and I'd like to repel them. Found in Cambridge, UK.
They are really tiny, about 3 mm long and smaller than a dry grain of rice. I've never seen them fly, just crawl around slowly. They get into everything, including the screen of my monitor!

I tried searching Google for tiny insects but none of the pictures or descriptions that I found seem to match these (I'm pretty sure they are not ants, lice, bed bugs, termites or silverfish).
If you have any idea how to repel or kill them humanely and without dangerous chemicals, I'd really appreciate that too.

Can you provide a clearer picture ?

I would ask did anything happen just before they appeared like a warehouse delivery or 2nd hand book purchase etc. Book lice or dust lice is a possibility. The photo is not clear enough to tell

They have wings so it looks like a flying insect, so not book lice or any of the others suggested so far. Can you describe how they invade (or at least how you find them) and what the conditions are in Cambridge at the moment (heat, humidity) and anything unusual you have noticed around (smells, fungi, plants blooming or fruiting etc.).

As a gardener, whenever I hear the words “tiny black insects”, my first thought is thrips, whether it’s thrips or not, and in spite of the fact that there are many tiny black insects to choose from!

In lieu of any better thoughts: Thrips (Thysanoptera). A large diverse group of tiny insects generally approximately 1 mm long. Well known for being invasive pests of many plant species, and being capable of transmitting a number of plant viruses. Which of the many species this would be, I don't know, but likely a common one like the Onion Thrips (Thrips tabaci).
According to Wikipedia:

In addition to damaging plants, thrips may invade houses and infest household objects such as furniture, bedding and computer monitors - in the latter case by forcing their way in between the LCD and its glass covering.

They all have a fairly well defined body shape, with an elongated abdomen and wings that are often shorter than the abdomen. They are known to rapidly reproduce, outstripping predator control, so you can get clouds of them around if the conditions are right.
If you have crops or gardens near you, thrips might be the insect you are seeing.

Thank you, someone here told me they were thrips too, so I'll go with that!


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What causes a polypeptide to fold into an Alpha helix over a Beta pleated sheet
I know how they fold, but what causes some polypeptide chains to preferably fold into Alpha-helix rather than Beta-sheets (or vice-versa). What force makes it fold into one conformation over the other?

look into the primary sequence and the energy minimization if you are into the computational side of things. This (http://en.wikipedia.org/wiki/Protein_folding) should help.

I don't think this is homework. This is about relative preference of structures (this is usually not explained in detail in textbooks)

I'll answer this question in a while. Meanwhile you can have a look at Ramachandran Plot

All the residues in a polypeptide chain tends to configure into their lowest potential energy state. except the peptide bond all the other bonds are free to rotate, alpha helix makes optimal use of internal H bonds. The overall structure is stabilized by H bond between the hydrogen atom attached to the electronegative nitrogen atom of peptide linkage and the electronegative carbonyl oxygen atom. The arrangement of amino acids in the peptide plays a very important role in forming alpha helix. Different combination of amino acids results in different combination of dihedral angels, hence it determines alpha helix conformation.


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Can a human acquire a memory of an animal?
I would like to know if it's possible for a human to acquire an animal memory.
I mean, animals store their memories in their brain, right? And so do we, humans, store our memory.
So, is it possible to cut off an inch (or something like that) of an animal brain,
also to cut off an inch of a human brain, and to replace that animal brain-piece in the missing part of the human's brain?

No, it can't be done for a lot of reasons. Here are just a few.
1) Memories are stored in electrical pathways, not the the cells themselves. You don't have 1000 memories in a chunk of brain that contains 1000 neurons. If you don't get the entire pathway, you won't get the memory.
2) Once a nerve is cut, it won't fuse with another cut nerve. All you'll have is a chunk of dying animal brain in your head. Even if a skilled neurosurgeon united the blood vessels of your brain to those of the chunk to keep it alive, the nerves themselves wouldn't become a working part of your brain. All you'd have (at best) is a useless chunk of another animal's brain sitting where your now-missing chunk was.
3) Animals are different from us. Your body would recognize the different-animal brain matter as foreign, and would make antibodies to it and reduce it to mush (if one didn't die of infection before then).

@ShadowRealm if this answered your question, please indicate as such by clicking the check mark next to it (it will turn green). Please see What should I do when someone answers my question? for more details.

Do we even comprehend memory that well? Cause from what I know we don't.

The other answer has been deleted but I think raised an important point specific to the original question : "is it possible to transfer animal memories into a human's mind." This answer answers the more broad question : "is it possible to physically transplant one brain's memory into another person's brain."  If we assume that memories are in no way transferable, then there is no need to distinguish between human-to-human vs animal-to-human. But if we accept a science-fictional possibility (think Dollhouse) for human-to-human, are other animals still too foreign to transfer?

@Anthony - I'm not aware of how memories were transferred in dollhouse. Can you explain?

It's pretty silly. "Dolls" undergo a procedure where their brain is "wiped" and special hardware is installed, making their memory "storage" like a blank floppy disk. Meanwhile, a source mind can have their minds mapped to get their mind's "image" mapped and copied into some storable format. This image can then be loaded to the doll's brain. Think of it as "copy as image" and then printed to reformatted disk.

It's interesting that through the ages, our brains have been compared to the latest technologies. Descartes compared the brain to a hydraulic machine. Freud likened emotions to pressure building up in a steam engine. The brain later resembled a telephone switchboard and then an electrical circuit before evolving into a computer; lately it’s turning into a Web browser or the Internet. But the brain isn't like a computer. If it's wiped, truly wiped of higher functions, we would not be able to reprogram it, or reboot it, or replace it. What was there before would be gone forever.

Is there a citation for the memory stored in electrical pathways? I didn't know human memory was figured out.

@vajra78 - just out of curiosity, where/how do you think memories are obtained/kept? Here's one small example. Intracellular Correlates of Acquisition and Long-Term Memory of Classical Conditioning in Purkinje Cell Dendrites in Slices of Rabbit Cerebellar Lobule HVI

I don't know. But electrical pathways run across the cells. It is clear that networks of neurons store memories. I can't find one nice study done using a new type of optical technique to turn memories on and off in a mouse model. Even so with all the research no one would bet their life on understanding how a memory is stored. There could very well be molecular structures associated with those networks allowing for differentiation. Something must make one network standout from another.

Also instead of transplanting nerves, what if the signals were routed via a wire. The thing is you would need the references from the animal mind. I'm jumping here but I would wager that a complete memory references memories from the sense and emotional regions in the brain. Very much like a relational database. But I wouldn't bet to much money.

@vajra78 - I would wager with you.


text:
Can an electrocardiogram be recorded with a single electrode?
Is it possible to do an electrocardiogram with one electrode? Or is it neccesary to have multiple electrodes? I do not understand much about EKG, so I am sorry if this question sounds naive.

Short answer
Any electrophysiological recording of potentials, including the electrocardiogram (ECG or EKG), measures a potential difference. Hence, two or more electrodes are necessary.
Background
The ECG measures the rhythmic voltages changes generated by the heart muscle. Voltage is defined as a potential difference between two points. Therefore, a voltage is always measured across two or more points. For example, when
you measure voltage when holding one out of two recording electrodes to one of the two poles of a battery, nothing will be recorded. This, because no current will flow through the potentiometer by connecting just one pole of the battery. Likewise, electrophysiology needs at least two recording channels to determine the voltage differential between the two. One channel is typically called the active electrode, the other the reference. The configuration of active and reference determines the polarity of the recorded voltage. Often a ground electrode is added to remove background noise.

This might sound odd but I was wondering, is it possible to make something like voltage clamp with ECG?

@Dexter - Theoretically yes, by adding stimulation capabilities to the electrodes. However, ECG records muscle activity typically by surface electrodes, and to voltage clamp the heart large currents would need to be injected. That would be akin to a defibrillator :)

Actually, yes you can. But you will not be able to make use of what you're seeing. There are six leads which are unipolar: V1, V2, V3, V4, V5 and V6. Any of these can monitor electrical activity in the heart without a second lead being present. In this instance, V1 or V6 would probably be the best for rhythm identification and monitoring.


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The meaning of RNA-seq data
many papers I read mentioned "RNA-seq data". While searching for the meaning of this word, I could not find any layman's definition.
As far as I understand, RNA-seq data is the complete RNA information in a cell (or all of the cells) of a species that is extracted at a certain time.
Am I correct with this definition? If yes, does this mean that by extracting all the RNA information ones knows all the RNA sequences in that species (like AUGGUCAUCAG....)? Or does it mean I have the RNA, but not the sequence?

@terdon could you explain it if it is possible ?

RNA-seq data usually provides a snapshot in time of the transcriptome of that which is being sequenced. Single-cell sequencing is possible, but less common than RNA-seq on a sample (containing many cells).
You are correct that RNA-seq provides one with knowledge of RNA sequences, like AUGGUCAUCAG and so on. However, one will not necessarily have information about all possible RNA sequences from a particular species. Performing RNA-seq on the same cell type of a species at two different time points, or two different cell types at the same time point, may result in different profiles for the RNA sequences you get back. It depends on which parts of the genome are being expressed by the cells in a sample at the time of RNA extraction.
The data one gets back from RNA sequencing depends on the technology and company used. Typically, RNA-seq involves using a reverse transcription step so that the sequence data you get back is actually reported as the cDNA version of your original mRNA transcripts. Usually one gets a (very large) file of sequencing 'reads'. One can either then 'assemble' these directly to form a snapshot of the transcriptome or one can map them to a known reference genome. One of the main benefits of RNA-seq is that we learn not just what the sequences of the RNA molecules are, but also their relative abundances within the sample. Knowledge of this can be particularly useful in testing or developing a large range of biological hypotheses.

+1, being able to know relative RNA abundances is an important feature

RNA sequencing occurs when you perform an RNA extraction and then sequence them, which usually involves fragmenting them.
You do in fact know all of the sequences for all of the RNA molecules that are being sequenced. I can't see an interpretation that does not result in you having the sequences of the molecules, what with it being called "sequencing" and all.

we start to know sequence of the RNA after sequencing right ?

Yes, you will only know the sequence of the RNA after sequencing. Prior to sequencing, you will only know they are fragments of RNA.


text:
Can a single axon propagate multiple simultaneous action potentials?
I have not been able to locate any research that indicates whether a single axon of a neuron or nerve cell can conduct multiple simultaneous (i.e. spatially separate) action potentials. I am aware that in many neurons refractory periods would preclude this possibility, however in some cases delays along axons are large enough.
Is this the case? Can you point me to any citations supporting your answer?

Yes, but there is an upper bound to the maximum amount of energy per axon. There is no empirical evidence of this about what is the exact energy spectrum which each axon can hold. This would also show you which action potentials an axon can propagate or hold. There is no sufficient imaging technology there openly which could be used to do some of the research.

When you say multiple simultaneous action potentials I assume that the stimuli for all of them are temporally overlapping. In such case a neuron can integrate the different stimuli and launch an action potential. Of the multiple stimuli some can be excitatory while others can be inhibitory. The net response would be an integration of all the signals [ref].
However, if there is a gap in the stimuli then the cell may not react as it would be in its refractory period (which results until the ions levels are back to their original state and the membrane potential is restored).
There can be long delays, which depends on various factors such as ion deficiency, ATP deficiency (ATP is needed by Na+/K+ ATPase) or neuropathological conditions. In case of nervous signaling over many neurons then synapses can suffer from synaptic fatigue, which results because of depletion of neurotransmitters.
EDIT:
Maximum AP propagation speed/Nerve conduction velocity = ~120m/s (Can't find original source. From wikipedia)
Longest myelinated axon (sciatic nerve in humans) = ~ 1m
Time required to reach synapse = ~8ms
Time required for repolarization = ~5µs
So multiple action potentials (~160), are possible (lets call it situation-X).
The squid giant axon is ~500µm. I believe it is also non-myelinated. In this case if NCV is less than 100m/s then situation-X can happen. NCV can go as low as 0.5m/s (again the reference is wikipedia as I cannot find the original source).
Having said that, situation-X can also cause synaptic fatigue if the firing rate (AP frequency) goes beyond a certain value. This value would depend on how much neurotransmitter is released per AP, how much is in storage and the uptake rate.

"stimuli for all of them are temporally overlapping" ... this is not the right idea. the question is not about summation of stimuli but production of APs in short succession which are simultaneously propagated in the same cell (obviously with some spatial distance). Also refractory periods are discussed in the question.

@watsonic Ahh. You mean what if in a long axon the first AP has not reached the synapse but the soma/dendritic region is already repolarized?

yes, for example. or one AP on the axon proximal to the soma and one distal.

@watsonic see the edit. I hope it answers your question.

Let us continue this discussion in chat.

I don't see why not, once the sodium and potassium channels along the axon have returned to their resting state. But I am not aware of a hard citation. I would suggest looking in the recent optogenetic literature, where researchers are exciting axons and axonal terminals using channelrhodopsin. People have most likely quantified action potentials for varying illumination durations and intensities, and you might be able to judge by the maximum firing rate how feasible multiple simultaneous spikes would be.
Also, it's most likely possible to trigger an antidromic spike while the neuron is firing an orthodromic spike. Not quite what you asked, but close.

Antidromic electrically evoked potentials plus normal  physiological responses :) - Good thinking !


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How do parrots stabilize their field of view without moving their necks while walking?
Based on my search online, I have found some theories which try to validate the activity of some birds (like pigeons) which involves moving their heads and neck while walking. These theories include - Assistance with balance, Providing depth perception, Sharpening their vision. Also, most of the studies state that similar to our eye movement, they need to move their heads along with their eyes to stabilize their surroundings visually.
If the above mentioned hypothesis is true, then how do some birds which do not move their heads while walking, manage to visually stabilize their surroundings and balance themselves?

why can't you just Google your question ?

I googled it, and found some possible reasons as to why the birds have to bob their heads while walking, but I did not find any theories about why some don't do so. Also, I think that finding interesting answers and rational discussions here on Stack Exchange from real knowledgeable people here on Stack Exchange can be quite enlightening for some people  with much less effort online. So repeating the same answer (which is found online),maybe in more detail, if the question wants something more, which is not found easily, it should be answered. Even if you say so, I will modify the question.

You can include your research results or any details you want to share in order to get a clarified answer, but a question with only two sentences and without even mentioning what you know about this so far, can make everyone believe that it is a home work type. Re framing the question may help. In future please feel free to use our Helpcentre

Edited. Is it OK?

@a.aniq This question is still so broad. Tell me do you have an answer for why the gaits of different animals are different or why dogs wag their tails but monkeys do not?


text:
Is our color vision calibrated to sky, vegetation, and blood?
Our color vision is based on three types of receptors (cones) which are sensitive to three distinct locations on the spectrum:  420–440 nm, 534–555 nm, and 564–580 nm.  We label them "red", "green", and "blue", but these names are arbitrary.  However, their locations on the spectrum may not be arbitrary.
I notice that they correspond to the colors of the three most important things in our natural habitat:  sky (the above), vegetation (the below), and blood (the sign of potential food or alarm, depending upon whether you are the hunter or the prey).
Am I on to something here, or am I just dreaming in technicolor?

It is proposed by various groups that color vision developed due to its evolutionary benefits in enhancing the recognition of (ripe) fruits. I think it's all highly speculative but I can dig up some articles if needed. The evolutionary benefits of recognizing sky seems remote, especially for terrestrials. Recognizing the color of blood makes no sense as prey is most often not yet bleeding and wounds are recognized through pain. Rather, the 3 cone types and with color opponency enable the visual system to see many colors in the visible spectrum, that reportedly help to recognize fruit.

Fruit!  I hadn't thought of that.  I guess that does make a lot more sense than sky.  Thanks, Chris.

And most mammals don't have the receptors to see blue light. But flowering plants are relatively recent, do non-flowering plants make colored fruits?

Also, I think dogs and some other predator animals lack red cone cells in their eye due to never having the pressure to need to easily detect berries (often red). [Citation needed] I have never heard anything about needing to see blood as a sign of alarm/food. Emphasising what @ChrisStronks said, if an animal is bleeding so heavily that it can be seen at distance, odds are as a predator that your job is done. As for tracking/alarm, smell would and does serve much better for animals +doesn't require staring at the ground as much.

Short answer
Color vision is not based on a calibration to the sky, vegetation and blood. The current leading theory of the development of trichromatic vision in humans is based on the foraging of fruit in our primate ancestors.
Background
The places of red, green and blue wavelengths in the spectrum are physically defined and, therefore, not arbitrary; see this question on Biology SE.
Before continuing, it is good to mention that trichromacy (the presence of red, green and blue cones in the retina) is typical for primates. For example, dichromacy (<500 and >500 nm cones) is the most common configuration in mammals. The split in red and green photopigment in primates developed relatively late in evolution (30-40 mln years ago), inferring trichromacy in primates from a dichromatic ancestor. Note that many avian and aquatic species may be tetrachromats or up (4 or more photopigments) (Nathans et al. 1999), with the mantis shrimp featuring no less than 10(!) different photopigments (Cronin & Marshall, 1989).
It is believed that the red-green-blue system in primates has evolved due to its benefits for identifying fruit on a background of foliage, and to assess the ripeness of fruits. The food of monkeys typically consists of fruit, and young leaves. Young leaves are light-green, while ripe fruits are often yellow (e.g., bananas) and orange (e.g. oranges, mangos) (Osorio & Vorobyev, 1996). Unripe fruits typically contain chlorophyll and resemble the color of foliage (green). Hence, to discern ripe, nutritious fruits (yellow-orange or 570-620 nm) from foliage (green or 495-570 nm - frequencies mentioned were copied from wikipedia), it makes sense to have good resolution in the red-green area. The red opsin has its maximum at 530, and the green at 560 nm. The blue has its peak a lot lower at 425 nm (Nathans et al. 1999). Hence, the red and green opsins, which evolved late in evolution, are both right in the "ripe fruit area" and have absorption spectra very close together. Hence, there is a lot of color sensitivity (high color resolution) in the red-green area, which covers reds, oranges, yellows and greenish colors. This gives primates a very high sensitivity to recognize fruits, and especially ripe fruits in a green background. The resolution in the green-blue range is smaller (blues, purples).
As a background: color vision in trichromats works by color opponency, and specifically a yellow-blue and red-green color opponency. This means there exists no yellowish blue hue, or a reddish green (De Valois & De Valois, 1993). The red-green opponency means that we have exquisite sensitivity in the red-green pathway, as red cones suppress green cone output and vice versa. In other words, there is a high color acuity in the red-green area that helps to recognize fruits.
As a side note: The trichromat color vision scenario in primates supports the notion that cats (for example), being predators with dichromatic vision, do not benefit from being able to identify ripe and unripe fruits, as mentioned by @GoodGravy. In contrast, cats need excellent night vision and motion sensitivity, being nocturnal hunters. Indeed, color vision versus night vision, and color vision versus high motion sensitivity are both trade-offs that do not go hand in hand (Kelber et al, 2002).
References
- Cronin & Marshall, Nature (1989); 137-40
- De Valois & De Valois, Vis Res (1993); 33(8): 1053-65
- Kelber et al., Biol Rev (2003); 78: 81–118
- Nathans et al., Neuron (1999); 24(2): 299–312

Thank you, @ChrisStronks.  This is a wonderful answer.  I have heard about the mantis shrimp and its numerous color receptors.  Amazing!  It makes you wonder what their experience of the world is like.  I've seen multispectral and hyperspectral imagery.  It's an overwhelming amount of information.  Anyway, thanks again.  I'm now in the mood for some fruit...

Is our color vision calibrated to sky, vegetation, and blood? TL;DR; No
Normal person has 3 types of detectors in his eyes called cones that are responsible for color vision. Cones can be: red (only name), green, or blue. They do not respond to single color but rather to range of frequencies. Under few layers of specific cells they connect to optic nerve and nerve transmits signals to the brain. (This is simplified version as same nerves are responsible also for intensity) Based on intensity (how much nerve fires) of signals from different color nerves brain is capable of figuring out what color it really is. Every type of cone has it's responsive frequency range.

If you would look at the samples below of peak ranges, it makes it pretty visible that Red cones peak at what normal person perceives as yellow (it could be 👽 blood though :) ) and not red, while blue cones peak at very intense blue-violet that sky isn't, green is on the right track though.
So I must regretfully say that a very 'romantic' theory on vision calibrated to sky, vegetation, and blood cannot be right since 'red' cones in fact respond to yellow light.
Blue cones peaks

Green cones peaks

Red cones peaks

Here, you can find the tool that I have used to get RGB/Hex values from wavelengths.


text:
Rescue cell lines function
I'm reading in a paper in which the authors have made three cell lines to study the function of a gene of interest (Mbd3):
The one is knocked out for the gene of interest [Mbd3 -/-], the other is floxed for the one allele [Mbd3 fl/-], and the third is rescued knock out cell line [Mbd3 -/- (rescued)], that means that in the cell line of knocked out cells they have stably transfected a plasmid expressing the gene of interest. I am then wondering, why they use this rescue cell line, instead of using the wild type cells with the wildtype alleles of Mdb3?

Rescue experiments are the gold-standard for confirming that an effect is due to the gene of interest.
Removing a gene may have off-target effects but if you can return function to 'normal' by supplementing the gene back into the cell-line/animal then this is strong evidence that the gene and its product are the cause of effects that are seen in the experiment.
Wild-type cells would normally be included to show what 'normal' response  is.


text:
Has the acronym DNA ever been widely understood to stand for deoxyribose nucleic acid?
I have a friend familiar with evolutionary biology who was recently bragging about how much he knows.  I asked him what DNA stood for, and he answered it stood for 'deoxyribose nucleic acid'.  When I claimed it stood for deoxyribonucleic acid, he said it depends on the source you go by.  I was curious and decided to look into it, but the only source I could find using his answer was the paper "Molecular Structure of Nucleic Acids: A Structure for Deoxyribose Nucleic Acid" published in the 1950s, and no explanation regarding if and when the term was officially changed.  Can anyone shed light on the history of the term and explain if deoxyribose nucleic acid is still acceptable?

DNA is not an acronym. It is an initialism.

First off, that paper is the seminal discovery and publication of the structure of DNA, and is absolutely worth the read.  It's one of the most important pieces of scientific literature.

The short answer is no.  DNA stands for Deoxyribonucleic Acid.
The long answer is... this is really just picking at nits.1  DNA, deoxyribonucleic acid, is a type of nucleic acid, specifically a deoxyribose nucleic acid.  So, if your or your friend wants to be pedantic, you can call DNA a type of deoxyribose nucleic acid that stands for deoxyribonucleic acid.
You probably shouldn't, though, since if you really want to be pedantic, saying "deoxyribose" implies it's a sugar, which once it has formed the DNA backbone, it no longer technically is.  Watson and Crick clearly used the phrase your friend has, but suffice to say that British papers from the 1950s used language differently than most folks today.
As a side note, there are nucleic acid analogues, such as PNA and LNA, which generally use the "Whatever Nucleic Acid" construct for naming, but I suspect that's mostly because "peptide" is a broad category, and "locked" isn't actually a biological word.
Also, "it depends on the source you go by" is just a way of getting out of being wrong.
ETA: WYSIWYG correctly notes in the comments that it used to be called desoxyribonucleic acid, such as in this extremely important paper by Avery, MacLeod, and McCarty.

1: See what I did there?  Most people would say "nitpicking" but "picking at nits" is basically the same thing, even if almost nobody says it.

In the old days, they used to call it desoxyribonucleic acid.

Technically, it's not even an acid: http://chemistry.stackexchange.com/q/61457/7399


text:
Complementation cloning: what, why and how?
I get that you're cloning a whole cDNA library, but why does E. coli need a complementary gene to allow the gene expression?
Why is that complementary gene considered to be a mutant?
AND how does one detect the gene of interest after cloning?
What is this kind of cloning used for?

Your question is unclear, which is why there are four votes to close it. I have constructed cloned cDNA libraries and I have no idea what your question means. Please clarify it if you want an answer.

I thought your question was clear enough, but it may be closed as too broad since there are multiple questions on what is a rather large subject. Given that you apparently now understand the basics, perhaps you could    narrow your question to the specifics of what is still confusing you. Or start a new question.

PS You're not "too undergrad" (ha!) for the site. Most questions asked here are at an undergrad or popular science level.

@canadianer great that makes me feel much better because I really love this site! I will take you up on the advice to narrow the questions, thanks!

I figured it out. You're complementation cloning when you know the function of a mutant sequence but not it's sequence. For example, your organism (human) gets skin cancer from too much UV light exposure.
With complementation, two mutants can restore the wild type phenotype (well functioning UV repair).
We know E. coli has a well studied UV repair gene so you transform the cDNA library from your human into an E. coli which we know has the mutation, then grow them all under intense UV light. The  E. coli with the human mutant allele (the right cDNA fragment) will survive, so you can amplify that colony, sequence it, and then use it as a diagnostic tool in humans.
I'm wondering why that was vague. Is "complementation cloning" not a well used name for that technique? Was the question too broad or elementary? It's the first time I've used Stack and it seems I may be a little too undergrad for this crowd.

If my answer clarifies, please feel free to fill in gaps I left out because I'm still trying to understand some of the reasons this technique works and why we'd use it.


text:
What is the biological limit on hearing resolution?
I sometimes wonder how many different individual musical scales could be perceived by human ears. I define a musical scale as a collection of notes that relate to some fundamental frequency by specific ratios. For instance

do $2^{0}f$
re $2^{\frac{1}{6}}f$
mi $2^{\frac{1}{3}}f$
fa $2^{\frac{5}{12}}f$
sol $2^{\frac{7}{12}}f$
la $2^{\frac{9}{12}}f$
ti $2^{\frac{11}{12}}f$
do $2^{1}f$

I once did an experiment where I took various sine waves at different frequencies and multiplied them by the appropriate ratios. I found for the ones I tried that I did indeed heard the major scale. But a mathematician will look at the positive real numbers $\Bbb{R}^+$ and say there are an infinite, uncountable number of possible frequencies. However, Biologically I cannot imagine the human ear is capable of distinguishing between an infinite number of frequencies.
What is the biological limit on hearing resolution? Is there a way to estimate how many different major scales one can hear? In other words, how many different frequencies can be heard?

Short answer
The main limitation to frequency discrimination is loudness.
Background
The cochlea is tonotopically organized - it basically acts as a Fourier transformer, where different frequencies are analyzed on a place map  (Fig. 1). Frequency tuning of cochlear hair cells is mainly limited by sound intensity. The louder a pure-tone sound stimulus gets, the larger the area on the basilar membrane that is activated and hence the wider the range of cochlear hair cells that is activated, and hence the worse the frequency resolution becomes (Fig. 2).

Fig. 1. Cochlear tonotopy. Source: Cochlear Implant Help

Auditory nerve fiber tuning. The louder the stimulus, the worse the tuning to frequency. Source: - Fettiplace & Hackney, 2006
As to the quantitative aspect of this question, namely what the frequency difference limen is, and an indication how many frequency bands can be distinguished I refer you to below linked question. Both depend highly on the method used to determine the just-noticeable-difference, and as said also on the sound intensity applied. Moreover, it is dependent on the frequency under consideration. The higher the frequency, the larger the frequency band becomes expressed in Hz. This is an example of Weber-Fechner's law (Hecht, 1924). The cochlea is organized in octaves, meaning that higher frequencies have less cochlear space devoted to them and hence less hair cells to code a particular frequency range.
Further Readings
- What's the frequency resolution of the human ear?
Reference
- Hecht, J General Physiol (1924): 235-67
- Fettiplace & Hackney, Nature Rev Neurosci (2006); 7: 19-29


text:
How does a change in the potential across a neuron's membrane get turned into a signal that is sent down the axon?
I understand

How a signal is propagated down the axon.
How the membrane potential of a neuron changes during the course of it's "firing".

But I don't understand how physically the change in the membrane potential actual starts the signal down the axon.
A stimulus causes the voltage gated sodium channels to open and sodium ions rush in. This creates a positive charge density inside the cell and negative charge density outside. This difference is by definition a potential difference.  Potassium gates sensitive to this difference then open, the potassium ions to rush out, which again flips the polarity of the inside and outside such that positive charge density outside the cell and negative charge density inside.
But how does that actually lead to the signal that is propagated down the axon? Can someone explain?

As you pointed out sodium as sodium enters the cell depolarizes (becomes more positive). Recall the sodium gates open the more positive the voltage is, which in turn opens more sodium gates. If a patch of neural membrane is depolarized, the charge  diffuses into the nearby patches of neural membrane. This will open the sodium channels of the nearby membrane patch. Now once enough sodium channels open, the neuron will fire a action potential, at this point potassium channels open and potassium rushes out of the cell repolarizing it(making it more negative). Furthermore the sodium gates close at positive voltages which further repolarizes the neuron and prevents back propagation.
So the key is the influx of the sodium ions diffusing down the axon and causing a downstream depolarization of the axon.
I find this website instructive, as well as this picture:

Update:
As the voltage builds up in the soma the charge spills over into the Axon Hillock (an area of high concentration of sodium and potassium gates) If enough sodium ions diffuse into the axon hillock and passes a (somewhat ill defined) voltage threshold then the sodium gates will open and start the action potential. Then the action potential proceeds down the axon as described above
A useful metaphor is the soma, and by extension the Axon Hillock, sums up the synaptic input from the dendrites, and again, if its over the threshold then the sodium gates open, if not, they slowly return to rest.
The synaptic input can be excitatory (cause depolarization) or inhibitory(hyper polarization) depending on the type of receptors and channels in the dendrites, but in general these voltage changes in the dendrite diffuse down into the soma and are eventually reach the axon hillock.


text:
Are there nerves in the umbilical cord?
I have always imagined that cutting the umbilical cord after birth might be painful. But I have always been confused about who would feel the pain and why. It occurred to me that the mother or the infant could only feel pain if they had nerves connected to the umbilical cord.

Do either mother or infant have nerves running into the umbilical cord that carry nociceptive information?
If not, is there a reason why no pain receptors are present?

Short answer
There are no functional nociceptors present in the umbilical cord.
Background
Having had the opportunity to cut the umbilical cord of one of my kids, I can anecdotally confirm neither newborn nor mother gave any sign of pain during the procedure. That is, when cutting the umbilical after the birth of a full-term baby. The only person clenching his teeth was dad :)
In fetuses at gestational age of 18-36 weeks no stress response was noted after puncturing the umbilical (Teixeira et al., 1996), indicative of the absence of pain receptors connected to the baby's brain.
I couldn't find information about pain in the mother, but I cannot imagine that the maternal central pain centers are being connected to the umbilical, which would be pretty extraordinary. This, because long-distance neural connections are rarely, if ever, established in adult humans. Also, I haven't heard any reference to the mother feeling pain because of injury to the umbilical cord. For example, knots in the umbilical cord, or cords wrapped around the fetus' neck due to excessive movements of the fetus are never noticed by the mother, and are only revealed during ultrasounds.
Note, however, that the umbilical cord is innervated by cholinergic neurons that are thought to be involved in the control of blood transfusion to the fetus, but presumably do not carry sensory information to either fetus or mother (Ellison, 1971).
References
- Ellison, Am J Anat (1971); 132: 53-60
- Teixeira et al., The Lancet (1996), 347: 624

Yes there are
THE placenta and foetal membranes are usually described as being devoid of neural elements1,2. In other descriptions, the possibility of an innervation is not considered3,4. Nevertheless, reports of the presence of nerve elements in these foetal tissues continue to appear in the European literature5–7.
https://www.nature.com/articles/214103a0
They are especially small

a reference from within the last 50 years would be prefered.


text:
How does a microelectrode work?
On Wikipedia, the entire microelectrode page states only the following:

A microelectrode is an electrode of very small size, used in electrophysiology for either recording of neural signals or electrical stimulation of nervous tissue. Initially, pulled glass pipette microelectrode was used with later introduction of insulated metal wires. These microelectrodes are made from inert metals with high Young modulus such as tungsten, stainless steel, platinum and iridium oxide and coated with glass or polymer insulator with exposed conductive tips. More recent advances in lithography yielded to silicon based microelectrodes.

Can someone provide a more elaborate explanation of how it works?
Like ideally, I would like something as specific as the usual descriptions you see in introductory chemistry books for how emf works in a battery. In other words, I know how electric potential works, but I am not understanding the exact mechanism of the microelectrode works.
If there are many types of microelectrodes, just give me the properties of one involving small shafts of hollow glass filled with a conductive salt solution.
Pictures would be great.

A microelectrode is quite literally a small electrode and they come in a variety of shapes.
The glass pipette electrode you are specifically referring to is mostly used for patch clamp experiments. Patch clamp experiments are performed using various configurations:

Source: Leica
So basically there is the cell-attached configuration, where a patch of cell membrane is sucked slightly into the pipette. Upon stronger suction the membrane is ruptured and the whole-cell patch clamp configuration is obtained. Here, access is gained to the cell, but a high-impedance seal is maintained between pipette and cell membrane. Lastly, there is a configuration where the patch is broken off the cell to exclude effects of the entire cell. This patch configuration is often used to obtain single-channel recordings. Dependent on the exact technique an inside-out or outside-out patch configuration is reached (see the picture above).
Hence, the glass pipette is basically only there to obtain a proper seal (cell-attached), to gain access to the cell (whole-cell), or to break off a piece of membrane. Notably, in whole-cell mode the pipette provides a means to administer compounds into the cell (think ions or drugs).
The recording electrode is situated inside the pipette and is a simple metal wire (platinum or platinum/iridium) and nothing different from any microelectrode as you rightfully state in your question. The electrode wire simply picks up a voltage difference (or current flow) between the interior of the cell (in whole-cell mode) and the exterior. The exterior is measured using a reference electrode outside the cell.
Furthermore, current can be injected to stimulate the cell, or to current-clamp the cell at a specific current. Likewise, voltage can be applied to voltage-clamp the cell. Therefore, an inert material is often chosen such as platinum or platinum/iridium to maintain integrity and prevent electrolytic breakdown. Electrodes are made out of metal to provide a low-resistance means to pick up currents or voltage-differences.
Voltage differences or currents can be amplified with an amplifier, registered and analyzed. See the following picture for the basic recording setup:

Source: Robinson et al. (2013)
Reference
 - Robinson et al. Front Neur Circuits 2013; 7: 1-7


text:
Is the human collarbone supposed to break?
I've read it in a book and have heard people mention it, but I can't find any documentation about it. But the point being made is this:

The human collarbone acts as a shock absorber for impact on the shoulder or stretched arm. If too much force is put on the shoulder (EG: during a fall), the collarbone is designed to break to prevent injury to the neck and/or head.

Is this actually true and if so, can anybody point me to some documentation about it?

This looks like a misinterpretation. Because collarbone is the only horizontal long bone of the human body [1], it is the first to fracture when falling on the shoulder.
Its fracture can affect many structures:

The muscles involved in clavicle fractures include the deltoid, trapezius, subclavius, sternocleidomastoid, sternohyoid and pectoralis major muscles. The ligaments involved include the Conoid ligament and Trapezoid ligament [1].

It is indeed a shock absorber, but for the upper torso (some way or another any bone can be considered a shock absorber):

The clavicle also serves as something of a "shock-absorber" for the upper torso. Physical contact from the side will be partially absorbed by the clavicle. Because of this function, the clavicle is a very commonly broken bone [2].

The fracture can lead to severe injuries:

Displaced or comminuted clavicle fractures are associated with complications such as subclavian vessels injury, hemopneumothorax, brachial plexus paresis [...] [3]

References:

Wikipedia contributors, "Clavicle fracture," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Clavicle_fracture&oldid=615723256 (accessed July 30, 2014).
Erich Rosenberger M.D. Anatomy And Physiology (2009). Available from http://www.sciences360.com/index.php/anatomy-physiology-299-12859/ (accessed 30.07.2014)
George Mouzopoulos, Emmanuil Morakis, Michalis Stamatakos, Mathaios Tzurbakis. Complications Associated With Clavicular Fracture. Orthopaedic Nursing, October 2009, Volume 28, Number 5, Pages 217 - 224 - See more at: http://www.nursingcenter.com/lnc/cearticle?tid=938803#sthash.F09wonvJ.dpuf

It's hard to accept a "nevagtive answer" as the accepted one. I had found all the links you have and read them. So maybe it is a "Misinterpretation", but it sure seems like a plausible one. Even doctors/physicians seems to mention it. And googling for Crumple zone collarbone gives a ton of people mentioning it. So I'll upvote for the effort, but i'm not ready to accept it yet.

Forgot to come back and accept. Sorry for the long wait.


text:
Is numbness the absence of one or all touch sensations?
I am studying the effects of tetrodotoxin and its symptoms when consumed. Numbness is one of the first sensations reported.
But I googled numbness and I couldn't find information about whether this means all touch sensations (e.g. thermal, mechano, etc) have to be absent for numbness or just one specific kind.
My Question:
Can someone

Define numbness
Explain whether numbness is the absence of one or more than one or all touch sensations.

1. This may be of your interest.

I think this is borderline off-topic, since the definition of numbness is basically a semantic issue. However, I assume that numbness can have a technical meaning in the medical field, and that this is what you're after(?).

Yeah, it came up in a homework assignment in my bio class. I just wasn't sure what it meant and brought it here.

The definition of numbness has been answered by yourself, and I will focus on the second part of the question.
In terms of the underlying physiological mechanism behind numbness I think it's good to narrow the question down and focus on local anesthetics, which numb a local area of the body for minor surgical procedures. Cocaine and related compounds have been shown to block not only pain, but also warmth, cold and touch perception, as well as blocking motor function. Cocain and related compounds are basically voltage-gated Na+ channel blockers, but also block K+ channels to some extent. Their affinity to various different channels differs, explaining the differential effects. E.g., pain is blocked more effectively than motor functions (Scholz, 2002).
We all know the feeling of numbness when our limbs are asleep due to restriction of blood flow. Likely all neural activity is blocked here too, as the cutting off of oxygen affects all neurons.
Given the broad range of effects of local anesthetics and restriction of blood flow, I would tentatively conclude that numbness can be interpreted as a reduction of sensitivity of all the senses.
Reference
- Scholz, Br J Anaesth (2002); 89; 52-61

This is much more what I had in mind. To be honest, I thought this was what numbness was before getting into the use of the term.

An Initial clarification of what "loss of sensation" means:

The history in the patient with “numbness” is extremely important. First of all, as with most neurologic complaints, you must determine what the patient means by “numbness.” Some patients are describing loss of sensitivity (anesthesia or hypesthesia) or distorted sensations (paresthesia), which is often described as tingling. Actual loss of sensitivity is more likely to represent true damage to sensory pathways in the nervous system, while paresthesia has a much broader differential. Dysesthesia, that is the perception of an unpleasant (often burning) sensation or allodynia (the perception of innocuous stimuli as being painful) may result from damage to the nervous system or, more commonly, be the manifestation of an underlying painful condition.

Some properties of numbness

The pattern of numbness may help define its origin. Numbness confined to a specific nerve or nerve root distribution (see the maps of dermatomes and peripheral nerve sensory innervation) lead to consideration of peripheral nerve or nerve root damage. Loss of sensation on one side of the body is more likely to result from central nervous system damage and if the sensory loss also involves the same side of the face, you can be sure that the cause is located above the level of the pons.
When there is a clear sensory level (a line on the body, below which sensations are lost), a spinal cord lesion must be suspected. Loss of sensation over the upper limbs or upper part of the trunk bilaterally, with preservation over the lower limbs and buttocks, suggests an expanding intraspinal mass. This so-called “sacral sparing” is seen with intraspinal tumors or syrinxes. Numbness over one side of the face, while being a relatively common presentation of psychiatric disease, can also be caused by damage to the lateral part of the brain stem, or upper spinal cord (spinal tract of the trigeminal). Lateral brain stem damage can also produce a picture of sensory decrease on one side of the head and on the opposite side of the body.

But the article concludes

In summary, the evaluation of numbness can be quite frustrating due to its subjective nature.

So it is in essence a term that can have specific meanings uncertain contexts, but one must be careful to clarify exactly how the term is being used since there isn't one single meaning.
This is all from this link here
https://www.dartmouth.edu/~dons/part_2/chapter_13.html

Does this answer (both of your) your question(s)?

Do you have anything to add? The sum of this seems to be it is subjective. If that is correct, then yes I am satisfied.

I wrote this mainly so that, in case the link breaks, the info is available.

I can add something to question two, which seems unanswered. Let me know if you are interested.

Yes, that will be great. I am going to accept your other answers too by the way. I just have had to mull them over a bit. Thanks for your efforts :)


text:
If a blocker prevents repolarization, will the neuron be stuck in a depolarized state forever?
Potassium channels help to repolarize the cell after depolarization. But if the potassium channels are blocked, potassium ions cannot flow out of the cell to increase the membrane potential. Thus, one would expect that, at least for some period of time, the cell would be "stuck" in a depolarized state.
How long can this state last? Can a neuron go on indefinitely in a depolarized state if potassium ion channels are blocked? Will it find some other way to depolarize the cell? Will the cell die?

The voltage-gated potassium channels are there only to swiftly repolarize the membrane potential. Ultimately it is the Na,K-ATPase that has to pump the various ions back where they belong (Na out, K in), also when potassium channels are active. So when the potassium channels are blocked, the Na,K-ATPase will restore the membrane potential, albeit in the order of seconds instead of milliseconds.

That was my intuition, but I couldn't find anyone who would confirm that the pumps have enough power to actually do that sufficiently to  return the membrane potential to its resting voltage. excellent!


text:
If the average resting potential of a neuron is -70 mV, why is there such a high ratio of potassium ions inside relative to out?
My bio teacher was discussing the ratios of different ions inside versus outside the cell.
$$\text{OUT:IN}$$
$$\text{K}^+ (1:20)$$
$$\text{Cl}^- (11.5:1)$$
$$\text{Ca}^{2+} (10000:1)$$
$$\text{Na}^+ (10:1)$$
Can someone provide specific details as to the relative quantities of these different ions relative to each other? In other words, given these ion ratios, provide me with how much of each type of ion there are and show why this adds to to -70 mV. I just want to make sure I have a realistic picture of the concentrations.
I think I am mixing up concentration with the ratio between inside and out. Although for every potassium ion outside there are 20 inside, the charge from the total number of potassium ions must be less than that of chloride or it would not be negative inside, right?

you need to add up all kinds of ions (K and Na mainly)

Representative ion concentrations are shown in Fig. 1:

The membrane is mainly permeable to K+. Because the Na+,K+-ATPase pumps K+ inside of the cell, it tends to diffuse outward again, thereby taking positive charge outside the cell and making it negative inside (extracellular space is pretty much devoid of charge due to its vastness). Because the membrane is mainly permeable to K+, the membrane potential can be estimated using the Nernst equation by taking into account only [K+]:

This delivers about -90 mV, using the values in Fig. 1, which is quite close to the cell membrane resting potential.
However, other ions have some limited permeability too and especially Cl- also has quite a large leak current. To add the permeability p of the various ions (for K+ p=1, for Na+ p=0.04 and Cl- p=0.45) into the equation and take multiple ions into account, the Goldman equation is needed:

This equation yields closer estimates of the membrane potential than the Nernst equation taking only K+ into consideration. However, other factors such as buffer effects (Cl- is often buffered) as well as active transport mechanisms may alter the outcome of the Goldman equation slightly.

Awesome! I couldn't figure out how that equation worked. Thanks as usual AliceD :D


text:
What determines whether an action potential is inhibitory or excitatory?
What determines whether an action potential is inhibitory or excitatory? Is it determined by the receptors, the neurotransmitters, or some other mechanism?

Short answer
The physiological state of the postsynaptic cell ultimately determines the effect of an incoming action potential.
Background
An action potential occurring in a chemical synapse is neither inhibitory or excitatory. An action potential is a binary '1', an-all-or-nothing signal without any information, i.e., there is not a -1 or +1 action potential. Similarly, there are no excitatory or inhibitory neurotransmitters.
Notably, the principal excitatory neurotransmitter in the nervous system, glutamate, can have inhibitory effects dependent on the receptor activated. While most metabotropic glutamate receptors (mGluRs) and ionotropic AMPA and NMDA receptors are indeed all excitatory, the inhibitory glutamate receptors (iGluRs) are not (Cleland, 1996).
Conversely, GABA, the principal inhibitory neurotransmitter in the nervous system, can have excitatory postsynaptic effects. For example, hyperpolarized neurons may actually depolarize upon GABAA receptor activation, simply because the resting membrane potential is more negative than the reversal potential of Cl- (i.e., Cl- flows out of the cell due to the negative membrane potential) (Marty & Liano, 2005).
The existence of both excitatory and inhibitory glutamate receptors shows that it is the postsynaptic receptor that determines whether an action potential will inhibit or excite the postsynaptic neuron. The excitatory effect of GABAA activation shows that on top of that, even principal inhibitory neurotransmitters (GABA) with principal inhibitory receptors (GABAA) can excite a neuron dependent on its physiological state.
Besides chemical synapses there are electrical synapses. In these synapses action potentials are transmitted directly electrically through gap junctions. In this case, any action potential is excitatory as the signal will be carried forward if it is strong enough (Purves et al., 2001).
References
- Cleland, Mol Neurobiol (1996); 13(2): 97-136
- Marty & Liano, Trends Neurosci (2005); 28(6): 284-9
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates; 2001.

After reading your answer, my impression is my question is a bit nonsensical. Does it seem that way to you? I can't tell if I asked a meaningless question or the answer is "it depends and without further info that can't be specified." Thanks for replying btw.

I think your question makes a lot of sense, because too many people talk about excitatory neurotransmitters and the likes. There are no inhibitory or excitatory neurotransmitters. +1 for the question.

@AliceD, I'd vote for peppering in a few judicious "strictly speaking"s to your answer, since I'd bet most working neuroscientists would give a minor eye roll to your italicized comment point.

@Chelonian - I'm a working neuroscientist. Which comment are you addressing?

@Chelonian - and given the nature of the question I don't think any eye roll would be rather misplaced.

@AliceD I was addressing "There are no inhibitory or excitatory neurotransmitters." in your comment to Stan Shunpike, but it also applies to "Similarly, there are no excitatory or inhibitory neurotransmitters." in the answer you gave. I wasn't quite sure what you meant by the 2nd comment to me; do you mean you do think they would be misplaced? I think you're right, just that maybe putting "strictly speaking," in these sentences (or something like that) may be helpful, since there are thousands of pieces of legitimate text that refer to "excitatory neurotransmitters", etc.

The state of the postsynaptic cell does NOT always determine the outcome of an action potential. You seem to be neglecting the whole presynaptic and autoreceptor literature in your answer. The neurotransmitter released doesn't even have to reach the postsynaptic side, it can lower or increase the probability of release in the presynaptic cell for example so your answer needs to be toned down.                                                                                c.f Tzingounis, A. V. & Nicoll, R. A. Nat Neurosci 7, 419–420 (2004).

@V_ix in the light of the question, the answer is valid. Further,  autoreceptors by no means change the effect of an action potential, only subsequent ones. The fact whether neurotransmitter reaches the postsynaptic neuron, in the light of the basic nature of the question that's a bit of an overkill detail. I'd rather not tone down anything and I think you are overinterpreting the question.

@AliceD I have a related question: You say that NTs are not per se inhibitory or excitatory, but neurons themselves are typically classified as one of the two. How is this possible, given that say the NT released by an inhibitory neuron can also have excitatory effects (depending on the receptor it binds to)?


text:
What does to "evolve" exactly mean?
In this article, the author says:

Evolution isn’t “leading up” to anything, it just drunkenly limps along using the same set of tricks in slightly different orders.

On other occasions, however, the term "evolution" is often deployed as a process that develops gradually, typically from a simple to a more complex form, or from not adapted to more specialized and "fit".
These contrasting interpretations of evolution make me wonder how I should interpret "to evolve" and "evolution" in the context of processes involved in speciation?

Do you mean that the word is misused in biology, in the dictionary defintion, or in public/general use? To me, this is unclear from the question. 'Evolve' is certainly used in different ways with different meanings.

@Ooker - I slightly edited your question to improve wording. Feel free to roll back. it's just a suggestion.

In biology. I know that language is sometimes, erm, evolve and a word can adapt a new definition. But since the original definition of the word (develope from simple to complex) had had a long time before the biological definition appeared, and because of that, the former meaning dominates the latter in our mind. I suspect that even biologists are still using it wrong.

@Ooker I think you are misrepresenting and simplifying 'evolve' when you say that it originally (only) meant "...developed from simple to complex". The previous use wasn't this clearcut.

@fileunderwater that's the definition you will find in Oxford

@Ooker that is one particular modern definition, which doesn't take etymology or historical use into account. Look at http://www.merriam-webster.com/dictionary/evolve, http://www.oxforddictionaries.com/definition/english/evolve and http://www.collinsdictionary.com/dictionary/english/evolve?showCookiePolicy=true for other definitions, more in line with the biological use of the term.

@fileunderwater I don't get your point. All the dictionaries you give define evolve as I define, which means that I don't misrepresent or simplify it. Do you mean that evolve has adapted a new meaning and all we need is careful not to use the wrong definition?

@Ooker My point is that those other modern defintions are more inclusive and often explicitely refer to "biological evolution". Languages and the meaning of words always change (...evolve), and under current use the biological meaning is rather unproblematic. I think the most interesting part of your question is whether the biological adoption of the word (late 19th century) deviated strongly from the previous use.

I think this may be off-topic because it is about semantics, not biology.

In any case, as has already been pointed out to you, you cite just one definition and even that one only states that it is "especially from a simple to a more complex form." That does not mean exclusively. Other definitions include the specific meaning used in biology. Also, dictionaries do not define words. Usage defines words and those definitions are then included in dictionaries. Finally, there are many examples of evolution leading from a simple to a more complex organism, just like your definition suggests. I don't see an issue here.

@terdon I know that this question is somewhat off-topic, but as I say, I ask it here so that it can reach to more biologists. If it has to be closed, which site should it be moved to?

@Ooker The premise of your question is based on a misunderstanding. Biology uses the word "evolution" to mean something. Dictionaries that fail to record that definition are deficient. It's not the biologists who are deficient. You can trace the etymology of the word and muse about whether or not the initial usage in biological contexts was appropriate, but for a word that's as established as this one is now, there's really little point in disputing it.

@Mr.ShinyandNew安宇 thank you so much. Make it an answer and I will accept yours

Ooker, [elu.se] would be the best fit but you'd just receive the same answer as posted by @Mr.ShinyandNew安宇 above. Almost certainly by Mr Shiny himself. Feel free to post there or flag it and ask for migration. Just be warned: the ELU folks don't believe in the kind of prescriptivist ideas that prompted your question :). They're a firmly descriptivist bunch. You might also want to discuss it in the ELU chat room

I edited the question and hope for re-opening. I think it touches on such a fundamental principle in Biology that it deserves a round of evolution (and evaluation) itself.

@Ooker - my pleasure, but feel free to roll back. it's just a suggested edit and it may be totally off from your original intentions.

To put in my view on this issue, I disagree this is a semantics question. This question specifically identifies itself as requesting the biological definition of evolution, which is significantly different from a classical, non-biological definition.

A couple of comments, but maybe not an answer; I think misuse is the wrong word - alternative meaning is better. 'Evolve' as a word is much older than the theory of evolution, and has its origin in the Latin evolvere:

evolve (v.)
      1640s, "to unfold, open out, expand," from Latin evolvere "to unroll, roll out, roll forth, unfold," especially of books; figuratively "to make clear, disclose; to produce, develop,"
  from assimilated form of ex- "out" (see ex-) + volvere "to roll" (see volvox). Meaning "to develop by natural processes to a higher state" is from 1832. Related: Evolved; evolving.

from Online Etymology Dictionary. Implicit in that definition is the laying out of something predetermined, which can relate to going from simpler to more complex.
Also note that Darwin only used the word 'evolve' once in On the Origin of Species (1859), in the final sentence:

There is grandeur in this view of life, with its several
  powers, having been originally breathed into a few forms or into one;
  and that, whilst this planet has gone cycling on according to the fixed
  law of gravity, from so simple a beginning endless forms most beautiful
  and most wonderful have been, and are being, evolved.

The implication of progress was one reason why Darwin disliked the word 'evolve' and preferred "descent with modification".
The same root was then used as a name to the theory of Evolution, but then in a much more specific sense than the older, general meaning.
If you look back at the etymology above, it is quite clear that biological evolution (The Modern synthesis version) emphazise the connotations 'expand', 'produce' and 'develop', but not the 'unroll' and 'unfold' parts (which both to some extent imply something predetermined).

As far as I remember, Darwin also wanted to avoid the hard confrontation with the church by not using evolving.

@Chris Quite possible, but I don't know if this was a stated motivation. Do you know of an account from Darwin that express this concern?

@fileunderwater - it was most definitely the reason for his vagueness, and perhaps the only reason. As far as I know, people were hanged for questioning the 7-day Creation back in the days.

@ChrisStronks Sure, but his book was just as inflammatory by stating "descent with modification". Did the church use the word 'evolve' themselves in any way, or is there any account that they reacted particularly strongly to this word? I'm not saying that this wasn't the reason, I'm only wondering if there is any proof/account that this was the reason. The older implication of progress is a good enought reason for Darwin to dislike the term.

As far as I know he was concealing the true meanings by talking around it. Just as Sir Wallace did before him (Darwin stood on the shoulders of giants himself). If you are interested I can look up references?

I think it's alike with relativity. I remember that Einstein also hate using this word to say everything is relativity

Great question
I think evolution and its derivatives are among the most misconceived and abused terms in Biology. Evolution is often seen as the driving force that pushes life to perfection. For example, what I often encounter are things along the line: "Organism A has trait X, A has been evolving for Y years, thus X is evolved into a useful and optimal token for survival, so we have been exploring X... bladibla". No - the trait X is there because it may be useful at present, or it has been useful in the past, or perhaps it is simply there because it occurred by chance and hasn't proved detrimental in Y years. Evolution is not only survival of the fittest (X is optimized), it is, and probably even more so, the extermination of the unfit (X is not detrimental). The "termination of the unfit" may, in fact, be more apt than "survival of the fittest", as survival depends on out-competing (and hence terminating) others. The interpretation of evolution as "survival of the fittest" is, however, the most encountered interpretation, perhaps unfortunately.

do all biologists aware of this when they use the word evolve?

@Ooker - no, otherwise they would be more careful using the term :)

@Ooker actually, biologists are quite careful when using the term. It is just horribly abused by the popular press. Things like "more evolved" for example will not be used by people working in the field.

@terdon I have seen in many biological contexts, evolve means "optimizing", as Christ Stronks says.

I don't agree with your interpretation. Survival of the fittest implies death of the non-fittest by modus tollens.

@MarchHo - please elaborate - I love this topic. We could go on chat actually. But not now :)


text:
Are resonances the reason receptors work?
From Visual phototransduction - Wikipedia:

When struck by a photon, 11-cis retinal undergoes photoisomerization to all-trans retinal which changes the conformation of the opsin GPCR leading to signal transduction cascades which causes closure of cyclic GMP-gated cation channel, and hyperpolarization of the photoreceptor cell.

From the physics point of view, does this mean the proteins in the eye are combinations of oscillators, each of them in charge for a specific wavelength, so that if one oscillator resonates with the photon, the signal is produced? In general, does all receptors work this way? Note that physical oscillators should have exponential or sinusoid functions. See this Photography question: How to capture a swinging pendulum?

Photoreceptors themselves dont act as oscilators, a single receptor is either 'on' or 'off' - it does not respond differently to different wavelenghts. Humans have Trichromatic vision, which means that we have 3 different kinds of photo-receptors that respond differently to light of a given wavelength at a given intensity. By combining multiple signals from these 3 different receptor types the brain can translate this to different colors (its actually kind of similar to how RGB color works).
Therefore I would say that even photo-receptors don't work like oscilators, only their specific ligands switch between the 11-cis & trans state, but this is more of a statistical and physico-chemical process (which does involve resonance between the energy of the photons and the electrons in the cis bond)

In general, how is a sensory receptor stimulated? I suppose that by the peak of intensity of the signal, right?

Receptors accept a huge variety of molecules as ligands.
In the example that you outline the receptors are called photoreceptors. The ligands for photoreceptors are generally contain alkene backbones which switch cis and trans forms on exposure to a certain wavelength. The oscillator analogy holds true to a certain extent.
However, not all receptors function similar to photoreceptors. Photoreceptors are designed in a way to sense a wide signal spectrum (the visual spectrum). On the other hand receptors which work on a much local scale e.g. delta receptor for the notch ligand are not similar to oscillators at all i.e. there is no factor of resonance with external stimuli.

Do you mean the ligands of photoreceptors switch cis and trans back and forth, which has two and only two configurations? That's not what I mean by oscillators. Physical oscillators should have exponential or sinusoid functions. See this Photography question: How to capture a swinging pendulum

The function will definitely be not exponential as the receptor will be recycled i.e. it will come back to ground state as negative regulation of receptors exists to maintain homeostasis. I think the process can be modeled sinusoidally. However, there will be lag periods between two peaks as the receptor has to be primed to be able to respond to the next stimulus.


text:
Books for biology,popular but rigorous?
There are very goods in physics and mathematics (like Feynman lectures for exemple) that give an elementry but but broad view of their,therefore I'd like for help to find help to find a biology book that:
-Covers a variety of subject in an elementary fashion.
-Is written for the non-specialist.

Wikipedia is fairly decent :P

Where I studied, every undergrad read Campbell Biology. You can start it as a non-specialist but you will not be one at the end..

Such a good book.

The Campbell Biology is a good very introductory book to biology. It is popular book but a very standard text book. I am not aware of any popular and introductory book that are broad enough to encompass all of biology.
I would suggest that you get the campbell and in parallel you can follow free online courseware. There are lots of them. Starting with KhanAcademy is maybe a good solution. It gives some introductory courses to a bunch of disciplines. ItunesU is also a good solution to search for further introductory courses given by the best universities such as Berkeley and the MIT typically.

I would suggest something like "The Selfish Gene" by Richard Dawkins. It covers many examples or organisms and how their behaviour at a molecular level is ultimately selfish in order to ensure survival by passing their genes, which is perhaps the most important biological function of any living organism. However, as pointed in comments below, this book primarily concentrates on evolutionary biology and little else (at least in any noticeable depth) and puts forward many philosophical arguments regarding survival and passing your genes but doesn't talk about proteins or mRNA. "The Extended Phenotype" by Richard Dawkins again is an evolutionary biology book but it does talk about protein synthesis and the idea of phenotype and how genotype effects this and how the genotype of an organism can affect the environment!
Books by Richard Dawkins tends to give examples of whole organisms and in a sense the bigger picture to make his points about elementary concepts which allow life and its propagation and how it shapes the environment but doesn't go too much into details in order to keep the attention of the reader and keep it interesting to the lay audience. [for the lay audience] It is much easier to imagine a bird and its mating habits and how genes control this than knowing the molecular mechanism behind the signalling pathway responsible! However since the question is slightly subjective, my response tends to reflect a subjective response.

The Selfish Gene is indeed a very popular book but it talk exclusively about evolutionary biology and about nothing else. One that reads the selfish gene will probably not have any clue about how mitosis works, about the chemistry of life (proteins, mRNA,..) or about cytology! Also the Selfish Gene gets into some philosophical and epistemiological issues in biology. I don't this is what the OP is looking for.

indeed. I agree! I shall edit my response to clarify this point. thanks.

I am a Richard Dawkins fan too !

Alongwith campbell ,look up some "advanced" books - like  Bruce Alberts molecular biology of The Cell , Lehninger, etc. It is not necessary to read everything in those books. Read whichever topics interest you the most.
There is also a very good site : ibiomagazine.org which has videos of some of the big shots of biology.
And remember, most important is to keep all your senses open always. There is so much biology going around. Observing and thinking about it can teach you things which 100 textbooks can't !