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Specific location where nerves converge
I'm looking for the "earliest" specific site where the 3 following nerves' sensory signals "converge":

Trigeminal nerve
Median nerve
Superficial peroneal nerve

By "earliest", I really mean the first location in the sensory pathway (to the brain) at which these 3 nerves' sensory signals converge.  And by "converge", I mean "feed into each other". My understanding is that, with sensory nerves, all tactile reception roads lead to the somatosensory cortex, and so, I would imagine all the nerve signals converge/merge into one another at some point.
I would imagine the location I'm looking for is the brainstem, probably the pons, but I'm not a biologist and am looking for either correction or confirmation here. This uneducated guesstimate comes from two sources:

Wikipedia - which states that the cranial nerves feed into the pons; and
The fact that the median and peroneal nerves are spinal nerves, which ultimately feed into the medula, which then turns into the pons.

Am I right or way off track?

Please note: this is not homework!

Not all roads lead to the somatosensory cortex. E.g., visual input is funneled to the visual cortex.

Do you mean where the signals from these nerves integrate? Because the "nerves" can anatomically terminate without converging; the first is a cranial nerve whereas the others are spinal nerves. Moreover a "nerve" has both sensory and motor fibres. This question is a little broad.

Thanks @WYSIWYG (+1) - yes, I do mean nerve signals and have updated my question to reflect that. Thanks again!

@smeeb You really don't have to disclaim all of your questions with "This is not homework!" That close reason is mainly to prevent questions with no research effort that are just copy-pastes from assignments (i.e. "List the organelles found in human mast cells.") Your questions are good and show research effort, so even if they were homework, they would still probably not be closed.

By reasoning, we can make the following distinction:

the trigeminal nerve is a cranial nerve.
the 2 others are peripheral
nerves.

Cranial nerves take their origin into their respective nuclei, and bypass the dorsal columns (main spinal tract for sensory information). Peripheral sensory nerves stem from the spinal roots, and from there go up through the dorsal columns. This would bring you to the thalamus, where all sensory information is regrouped. However, somatosensory information from the face and the rest of the body happen to travel through different thalamic nuclei (ventroposterolateral for the body, ventroposteromedian for the face, If my neuroanatomy is not too far behind me...). This leaves us with the internal capsula (fibers that link the thalamus to the cortex), but I do not think much signal integration occurs there.
In conclusion, the first anatomical level of convergence between the 3 above-cited nerves would indeed be the somatosensory cortex.


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Root etiology of non-pituitary low T4 and low TSH
Please note: I'd like to preface this question by stating that this is neither homework nor me seeking medical advice. I am simply trying to understand the biological, physiological root etiology behind various thyroid-related structures.
This question shows research and is not a duplicate.

My undertanding of the pituitary gland is that it will produce TSH when it senses total T4 (not free T4) is low. So if both total T4 and TSH are low, this implies two things:

There is some underlying reason why T4 is low; but moreover...
There is some other (or related) reason as to why TSH is low

In all the literature I can find, the main antagonist in this scenario is a malfunctioning pituitary gland.
So I ask: if the pituitary gland is deemed functional and non-diseased, are there any other root causes for both a low total T4 and a low TSH? Biologicaly/physiologically, how do they work to produce this low level of hormone production?

Are you sure such a condition exists? Can you link to it? Also, are you sure about your total T4 statement?

Thanks @anongoodnurse (+1) - here is an article showing that a low TSH and a low/normal T4 are attributed to pituitary disorder. I can provide other links as well.

Yes, I'm sure it can happen with a pituitary condition, but you stipulated in your scenario that the pituitary was healthy. I'm asking you if you know that condition to exist, and can you link to it?

Thanks again for verifying @anongoodnurse (+1) - if you scroll to the bottom of that link, you'll see a table where it shows that low TSH and low T4 can be caused by two categories of conditions: (1) "rare pituitary (secondary) hypothyroidism" (which like you understand, we're assuming to not be the case here as the pituitary is healthy), and (2) "Non-thyroidal illness".

When you ask a question, it's much easier to summarize the part you have a question about rather than make a user read the whole paper just to understand what you question.  That's why I asked for more information in my first comment.

source: Stack Exchange

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

sort: votes


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Does the genetic expression of specific physical traits ever correlate to behaviour?
Over at skeptics, there were a couple questions asked as to the correlation of specific physical traits in relation to personality/behaviour.  For instance, the simian line as well as red hair.  Now, I did my best to answer these questions, with what I understand as there being a long history of people attempting to correlate external physical characteristics with behaviour (see the disgraced "art" of phrenology for instance).
However, in answering the simian line question, I did come across some weak correlations.  It got me to wondering if this is an area of exploration in terms of perhaps one gene sequence for a physical trait somehow being tied with another gene sequence for behaviour.
So, do any physical characteristics being expressed through genes correlate to behaviour?

cognitivesciences.SE has started, imho this question belongs there as a biologist has no scientific definition of what "personality" is. There are so many methodical flaws to this question that I dont where to start... Surely you can measure any correlations you want with the "right" measurment setup and self-chossen definitions. Instead of pointing ot "possible" correlations I would rather ignore/close such questions, but thats why I left prejudices(skeptics).SE. Best you can do is to ask if behaviour is manifested in genes. Then its is more a interaction of distinct enviromment and subject

@WernerSchmitt does the edit refine the question more to your liking?

no need to edit immediately, just my view. The problem to me is that behaviour originates from social evolution. "Behaviour" like Autism or Asperger are clearly caused by genes. But then the judgement of such behaviour as unnormal by normal people is kind of chicken or the egg problem. You probably know of epigenetics and that this also affects sexual orientation. So the question to me is more where does behaviour start and personality end...I dont have any clue :) But thats imho a psychological question. I know of experiemts with mice with electrode implantation in their brain to trigger fear

is less/more fear already different behaviour? Not sure.

Aldridge et al. (2011) show a correlation between facial phenotypes and autism spectrum disorders (ASD) in a sample of 8-12 year old boys.
They studied two groups of boys, 65 that had been diagnosed with ASD and 41 who had not. They collected 3D images of the faces and looked for similar patterns among the two groups. They found a significant association between some phenotypes and ASD. But, as with most studies, the results are complex; there a distinct sub-groups within the ASD group.
Keep in mind that this is an association study -- no causation is shown.

I don't think there's any serious possibility that different facial phenotypes cause autistic traits or behaviors. In keeping with the OP's question, the authors seem to assume that biological factors leading to autism also affect facial morphology.

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


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What neuro-motor diseases cause the lower esophageal sphincter (LES) to malfunction?
Please note: This question is neither homework nor seeking medical advice. I'm simply asking for a factual, objective, biological explanation of the various neuro-motor diseases/illnesses that can act as the underlying cause to LES malfunction.

The primary function of the lower esophageal sphincter (LES) is to prevent stomach acid from backwashing into the esophagus. This sphincter is an involuntary muscle, and so, for it to malfunction (unable to fully or properly close), it must be the result of an underlying neuro-motor (autonomic) disease or condition.
What such condition attacks this sphincter/valve, thereby causing it to malfunction and not operate properly? How exactly does this condition effect the sphincter biologically/neurologically?

Update
Looks like the Vagus Nerve (10th Cranial) innervates this sphincter, so I guess the question is: What neuro-motor diseases attack the Vagus Nerve or cause it to malfunction?

Try looking up acid reflux disorders. My aunt has this as well as Multiple Sclerosis and it causes this muscle to spasm, she has to drink water slowly in small sips to calm it down.

This is called achalasia. According to UpToDate, the mechanism for this diseases are generally unknown. What is known, however, is that the esophagus has a neural system called the myenteric plexus and if these ganglion cells in the esophagus are damaged in any way (e.g. physically, followed by Wallerian degeneration, or the primary process of degeneration after physical damaging of neurons), it can lead to lower esophageal dysfunction as these neurons regulate the inhibition of the contraction of this sphincter muscle. Dysinhibition leads to a closed sphincter.
Yes, you are right in that the vagus nerve is the primary route of the myenteric plexus to the central nervous system, so damage here might result in dysfunction as well.
Histological studies have reported fewer myenteric neurons in people with achalasia, and inflammatory cells in the region, perhaps suggesting infection or autoimmune etiology 1.
Additionally, from the UpToDate article, Chagas Disease has been associated with this disease. Chagas disease is a parasitic disease caused by the species Tropanosoma Cruzi, and these parasites multiply within cells, causing them to burst.
Check out pathophysiology of achalasia on websites such as UpToDate.
1 "Histopathologic features in esophagomyotomy specimens from patients with achalasia." Goldblum JR, Rice TW, Richter JE. Gastroenterology. 1996;111(3):648.
EDIT:
I answered the opposite, but the principles still apply. Here is a wonderful resource on this topic ("Physiology of esophageal motility," http://www.nature.com/gimo/contents/pt1/full/gimo3.html. It includes a diagram showing the vagal neural pathway and the main neurotransmitters responsible for each action (relaxation and contraction).

Thanks @Biomed_guy (+1) - however it appears that achalasia occurs when the LES closes and cannot reopen. I am interested about the opposite: what would cause the LES to remain largely open and unable to close?

Sorry about that. However, we are close. Just as there are inhibitory neurons on the LES, there are also excitatory neurons with a different set of neurotransmitters.

Thanks again @Biomed_guy (+1) - so let me see if I understand this. You're stating that anytime there is damage to the Vagus Nerve and/or the myoenteric plexus, that LES can malfunction as a result, yes? If so, then to me, it stands to reason that the root problem either lies in this plexus, anywhere along the Vagus nerve, or the place in the brain that the Vagus nerve feeds into (which, correct me if I'm wrong here, but I believe is the medulla oblongata). Can you confirm that the root of the problem has to lie in one of these areas (or any others you can think of)? Thanks again!

I believe I am qualified to guide but not necessarily completely confirm. Indeed, the medulla and vagus has been implicated for LES dysfunction (http://www.ncbi.nlm.nih.gov/m/pubmed/12061915/) Keep in mind that diseases like GERD may not always be caused by neurological dysfunction. But if you're thinking neurological, than this is a valid thought.

Thanks for the update @Biomed_guy (+1) - last followup (I promise): you are correct in thinking that I am assuming a neurological cause for GERD. I am very interested in your statement that "GERD may not always be caused by neurological dysfunction." Can you elborate on this and perhaps give some examples? To me, it has to be neurological in nature, because the LES is an involuntary muscle. If you know of non-neurological root causes for LES, please fire away! By "root" causes, I don't mean "obesity", because that's just a vague blanket phrase that doesn' explain the physiology...

I'm sure "obesity" does cause GERD, but then the obvious followup is why? Again, I'm looking for root causes of GERD here, all of which I suspect are ultimately neurological. Thanks again!

Acid erosion of the sphincter. Physical rupture. Anatomical dysruption of of the junction. Just read that the diaphragm contributes to the LES pressure. A hiatal hernia can also result in the forcing open of the LES.  I don't think nyone knows for sure why obesity is associated, but there is a suggestion that these people have higher intragastric pressure which would force open the sphincter, as well as higher incidence of hiatal hernia.


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Understanding the configuration of channels in the 10-20 EEG montage
In a typical 10-20 system there are 21 electrodes placed on the scalp. However, this does not mean there are 21 distinct "channels" or voltage sources.
I've heard that some of these electrodes are "reference" electrodes, while others are "active" electrodes. Sometimes electrodes can setup in a "bipolar" or "differential" fashion.

How many actual channels (that is, distinct input sources) will there be?
What's the difference between reference and active channels?
How does this bipolar/differential setup work differently than a "normal" setup?

Update
Here is my updated understanding based on @Christiaan's answer below:
time (t)    F2v    F3v        F2-F3         F3-F2
=================================================
1           2      1            1             -1
2           3      6           -3              3
3           5      3            2             -2

So, if my understanding is correct, then at time t=1, the voltage of the F2 electrode might be, say, 2 (units; volts, microvolts, whatever), and the voltage of the F3 electrode might be 1. If F2 is the arbitrary active electrode, then the potential difference between F2 and F3 is 2 - 1 = 1. But, if F3 was the active electrode (and F2 the reference), then the potential difference would be the inverse (that is, 1 - 2 = -1).

EEG 10-20 system. source: Wikipedia

How many actual channels are there?

21 in the figure, i.e., the number of active electrodes.

What's the difference between reference and active channels?

The active electrode is the electrode under investigation. Basically this is arbitrary. Consider electrode F2 and F3. When you measure the potential difference between them and F2 is the active electrode and F3 the reference, the signal will be exactly identical as in the reverse situation, only the polarity (the sign of the voltage) is reversed. That's all there is to it. The active electrode is typically the electrode linked to the location you wish to record. The reference is elsewhere.

What is the difference between a bipolar and a normal
  (unipolar/monopolar) setup?

In a regular unipolar setup, each of the electrodes is either measured against a distant reference (e.g. the earlobe) or against the aggregate of all the electrodes. Either way, the reference is distant. This means that the signal will be high, but artifacts will be large too, because artifacts from both the electrodes will be merged into the signal. Consider a reference in the neck; neck musculature activity will add artifacts (EMG) to the signal. Likewise, a reference in the chest area will add ECG to your signal.
In a bipolar setup adjacent electrodes are recorded. This means that large artifacts occurring through eye blinks or whatsoever are recorded by both electrodes and as their polarity is opposite, the large artifact responses will be cancelled and the signal is much cleaner. However, the downside of the coin is that commonalities in the signal, which will be larger when the electrodes are closer will also be subtracted and hence your signal will decrease accordingly.
I have used bipolar setups when measuring eERGs and eCAPs, i.e., electrically evoked activity. The electrical stimuli generated large artifacts and actually so large that their amplitudes were approximately similar between active and reference electrodes. The reduction in artifact by far outweighed the loss in signal. It depends on the situation you are at.
An authoritative work in this field is listed below.
Reference
- Pivik et al., Psychophysiol (1993); 30: 547-58

As always, thanks @Christiaan (+1)! And, as always, a few followup questions for you (if you don't mind)! (1) Please see the update to my question. Regarding your explanation of active vs. reference electrodes, can you please confirm that my understanding (based off the table I provided) is correct?

(2) Whereas I now understand the cons of unipolar setups, I am failing to understand the cons of the bipolar setup. Using the table I provided above, are you saying that - under a bipolar setup - the electrodes are close together and hence will have similar voltages? Hence F2 and F3 might both measure very close to one another (say, F2=2.6 and F3=2.5), hence the potential difference between them (+/- 0.1) will be very small? Is this what you're saying?!

ad(1): My pleasure! The table is kind of OK as a simplification scheme, but you should understand a voltage is always a potential difference. On 1 electrode there is no such thing as a voltage of -3. Voltages exist across points. An electrode placed on the positive pole of a battery and the reference in the air yields 0V.

ad(2): The signal may be smaller in bipolar. The noise as well, simply because the electrodes (may) have overlapping areas of interest.

Sorry I forgot the +1 @Christiaan, I added it! Also +1 for both comments above (thanks!). So it sounds like in my #2 followup above that my understanding is correct (that is, that because the electrodes are close, their voltages will be nearly equal and opposite, which makes using their data more difficult). One last followup question here, I promise!

(3) In a 10-20 system where there are 21 active electrodes, it sounds like the technician has the ability to arbitrarily choose the reference electrodes for each active one. It sounds like - for EEG reading #1 - I might choose F2 to be the active and F3 to be its reference. But, perhaps for EEG reading #2, I might choose F2 to be the active and, say, F8 to be its reference. How does the practictioner decide each reference electrode, and then subsequently, configure the EEG device to measure difference between each arbitrary active/reference combo?

The reference above describes exactly these considerations. As you say, they are arbitrary. But there are guidelines that may help: https://www.acns.org/practice/guidelines I suggest to take a look.


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What is it that specifically kills ALS patients?
ALS is a fatal motor neuron disease, and even though there are many different articles out there on the topic "How does ALS actually kill you?", none of them really delve deep enough into biology to adequately answer the question.
For instance, many articles cite "respiratory failure", or "CO2 poisoning". But the last time I checked, ALS doesn't make your lungs explode or cause your body to start producing toxic levels of CO2. So obviously, we need another level of detail here to support these claims. I'd be willing to be that with "respiratory failure", either the neurons innervating the diaphragm break down (hence you become physically unable to draw air in and push CO2 out), or perhaps the tiny/micronic structures inside your alveoli become impaired for some reason. If the former, then why wouldn't a ventilator/respirator help the patient?
Either way, I'm interested in a biological/neurological explanation for why ALS is considered to be (ultimately) fatal.

TL;DR Ventilation assistance does help but there are other factors.
ALS is a degeneration of the motor neurons, replacing them with hard material (i.e. sclerosis). The neurons innervating the muscles involved in respiration deteriorate and so it becomes difficult to breath, swallow, cough, etc. There's a compounding effect: we know that blood O2 and CO2 levels are balanced by respiration, O2 in/CO2 out, and we know that swallowing/coughing clear secretions from the respiratory tract. Basically you end up with trouble oxygenating your blood and riding it of CO2, hence CO2 poisoning. This can result in what is known as type 2 respiratory failure, characterized by low oxygen and high carbon dioxide levels (hypoxemia and hypercapnia). Low secretion clearance in the lungs can also result in aspiration pneumonia in addition to poor gas exchange.
Ventilation methods such as BCV are capable of mechanically assisting breathing, and maintaining ventilation-perfusion state in a way that prevents respiratory failure, but unfortunately doesn't slow the progression of the disease. The problem then is that in, for example, particularly severe cases, the quality of life has to be taken into account because tongue movement, gross movement in general due to motor neuron degeneration just fails. This can lead to what is essentially locked-in syndrome (LIS), and clinical outcomes can widely vary, though in this article they report the more pleasant outcomes of patients experiencing LIS. I think that for these cases due to poor communicaton patient-reported outcomes are fairly underreported, but family and caregivers at this point have to take into serious consideration options such as euthanasia. Cutting off ventilation can result in type 1 or 2 respiratory failure.
Now, I lack actual data for this statement but I should also point out that not all patients receive the same care or opt for assisted ventilation, in which case late-stage ALS would invariably lead to total neurodegeneration to breathing muscle innervation, where assisted ventilation becomes a requirement for survival.

Thanks @Kendall (+1) - however I'm missing a big part of your explanation!! In your 2nd paragraph you state "Basically you end up with trouble oxygenating your blood and riding it of CO2, hence CO2 poisoning."... but why?!? Is it because you can't swallow/cough/etc. to clear your respiratory track of secretions (meaning, if there's mucuous in your throat, you won't be able to suck air in or let CO2 escape)? Or is some other mechanism at play that actually prevents proper O2/CO2 exchange? Thanks again!

Secretions that block the alveolar gas exchange is one reason, not just in the throat but also down in the lung, and shallow/strained breathing is another.

Thanks again @Kendall (+1) - last followup question here, I promise (!): can I assume that eventually all motor neurons will be affected, including those controlling heartbeat and digestive motility (that is, moving food from end to end, so to speak)? Thanks again!

ALS does not affect the innervation of the heart, digestive organs or urinary organs.


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What is the maximum potential sucrose concentration of plant sap? What keeps plants below this potential?
I am interested in identifying the maximum potential dissolved sucrose (%w/w) that plant sap could have, and which (biological, physical, chemical) factors constrain the observed sucrose concentrations.
For example, sugar maple has one of the highest sucrose contents at 6%, and the solution also contains fructose, glucose, organic acids, minerals (K, Ca, Mn, Zn, Na, Cl), amino acids, volatile organic compounds, phenols, enzymes  (according to Wikipedia), and most sap flow occurs when temperatures cross the freezing point each day.
Is there a way that I can calculate this theoretical maximum from "first principles" of organic- or bio-chemistry, or is this a question better suited for empirical study?
this is a biological application of my question at physics.SE

As the concentration of sugars in the sap increases, so does viscosity. At high viscosity, the sap will not flow at a sufficient rate to provide nourishment to the different plant tissues.
In addition, there are limitations to concentrating the solutes in the sap. As the sap becomes more concentrated, the plant would be working against a osmotic gradient to further increase that concentration. That energy cost may be too great.


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Does pain scale with mammal mass?
Some biological features scale with the animal mass (see previous Q&A).
Assuming the same concentration of nociceptors on the skin surface, I'm wondering how painful a 1 cm wound will be perceived in mouse, human or elephant. Despite the same firing number of nociceptors, will the mouse feel more pain as a bigger percentage of the body has been injured? Is it known whether pain sensing follows allometric rules?

As you cannot really ask a mouse to rank her sense of pain on a scale of 1 to 10, it will not be possible to find a definitive answer for your question.

@skymninge there are at least 40 [animal models of neuropathic] (http://www.ncbi.nlm.nih.gov/pubmed/20030738), but I'm not inside the field and cannot judge if some of them can be used for allometric studies.

The question if the mouse will FEEL bigger pain is still debatable. As pain is a feeling, not even by questioning different humans you could measure how much pain is felt. You can measure reactions, but pain is a subjective feeling. If I have an especially bad day, cutting my finger might (feel to) hurt more, than on a day I feel very euphoric.


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Relationship between our microbiome and personalized nutrition
Recently, it has been asked whether there are 'metabolic types' between humans that can benefit from a sort of personalized nutrition. One answer suggested that one discerning factor could be the human microbiome. It is known that host–microbial symbiotic states might respond differently to diet and drug intake, but whether this can be useful for personalized nutrition is less clear to me. I wonder:
does the microbiome affect food metabolism? (useful for personalized nutrition)
OR
is the food that we eat affecting the microbiome? (less useful for personalized nutrition)
I know the answer is probably both, but there are examples causally demonstrating one branch and excluding the other?

does the microbiome affect food metabolism?

Most definitely (and not surprisingly). The Arumugam paper [1] notes that

The drivers of [enterotype 1] seem to derive energy primarily from carbohydrates and proteins through fermentation, … because genes encoding enzymes involved in the degradation of these substrates (galactosidases, hexosaminidases, proteases) along with glycolysis and pentose phosphate pathways are enriched in this enterotype […]
Enterotype 2 … is enriched in Prevotella … and the co-occurring Desulfovibrio, which can act in synergy to degrade mucin glycoproteins present in the mucosal layer of the gut […]
Enterotype 3 is […] enriched in membrane transporters, mostly of sugars, indicating the efficient binding of mucin and its subsequent hydrolysis as well as uptake of the resulting simple sugars by these genera. […]
The enriched genera indicate that enterotypes use different routes to generate energy from fermentable substrates available in the colon, reminiscent of a potential specialization in ecological niches or guilds. In addition to the conversion of complex carbohydrates into absorbable substrates, the gut microbiota is also beneficial to the human host by producing vitamins. Although all the vitamin metabolism pathways are represented in all samples, enterotypes 1 and 2 were enriched in biosynthesis of different vitamins […]

[All emphasis mine.]

is the food that we eat affecting the microbiome?

Yes, just as certainly. I don’t have a publication handy but it should be obvious that our food influences our gut microbiome – in the extreme case, it can kill it (consider antibiotics side effects).
[1] Manimozhiyan Arumuga, Jeroen Raes & al., Enterotypes of the human gut microbiome, Nature 473, 174–180, May 2011.

Yes, the microbiome affects food metabolism and the diet affects the composition of the microbiome. +1 to Konrad for his response. This is an area of research in which I and colleagues are engaged. Frankly, it is easier to assess the changes to the microbiome based on diet rather than looking at the fecal material to determine (unused) metabolic energy or potential given a certain input (i.e, from a controlled diet).
Recently, we've fed humans a high number of servings of whole grains. The response is highly individualistic with some declines and others increases in Firmicutes, for example. Typically, Bacteroidetes numbers move opposite to Firmicutes, but not in all individuals. These observations are also seen by others in this growing field of research.
The "enterotypes" paper Konrad cites is beginning to see some resistance in the field in that the three enterotypes defined by those authors are not really so cleanly defined when one takes a closer look at more individuals. Time will tell how well one view or the other holds.


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Is there an "Adam and Eve" for each new trait during (not just human) evolution?
Do new beneficial mutation evolve simultaneously and independently with several individuals of the same specie or only with one specimen who then transfers it to all of the specie?
In other words, when we talks about common ancestor we usually mean a specie, so for example, all earth dwelling reptiles, birds and mammals are the descendants of Tiktaalik (to the best of my knowledge), and we know that Tiktaalik was the first (or one of the first) species to come to land, but was there a first individual Tiktaalik who went to the land, like Tim Minchin's Tony the fish.

Imagine being the first dude ever to have feet...
Imagine you're a fish, and you are swimming in the ocean ... and suddenly out of nowhere Tony just goes "I'm getting out, I'm freezing, I'm just gonna pop out for a bit, maybe lie on my towel, I'll bring you an ice cream"
-"Don't bother ,Tony, you are a freak! Tony is a freak, let's go, let's ostracize him for being different"

It seems to me that from the same species of ancestors there are several descending distinct species, so it seems to me that that that there was a species of reptiles that at some point some individual of that group developed Dinosaur features and traits and whose descendants became Dinosaurs and then Birds, and another individual of that specie or a descending specie (not necessarily at the same time) developed mammary glands whose descendants became mammals, and other individuals who didn't mate with those two whose descendants remained reptiles.
Was there ever a first dinosaur with feathers who is the father or mother of all birds, or the first fish with lungs, the first monkey with opposable thumbs from whom all apes descend, or the first mammal that decided to go for a swim and all dolphins, whale and seals are his direct descendant of that first swimming mammal?
And also for traits that don't lead to speciation, was there a first human who was lactose tolerant, and all the lactose tolerant people on the world are his/her descendants, or the first person with no wisdom teeth, the first person with slanted eyes, and the first person with red/blond hair?
*- If there are gross inaccuracies and/or over-simplification in my understanding of the evolutionary process, this is because I'm not a biologist, and I would accept happily any correction.

I think I'm with Michael Kuhn. The concepts between the questions are very close. Ultimately the answer is 'Yes' - there's an "Adam and Eve" or "Parent" to every extant species today, but it's probably not like you'd expect. They were simply able to pass on their trait more successfully than others.

I'm not talking about speciation here, like the question you reference to, but about new mutation/features. I'm aware that the first dinosaur with feathers is still a dinosaur, and the first fish with lungs is still a fish, the question is, was there only 1 first fish with lungs, who's the ancestor of all creatures with lungs, or were there several fish that all developed lungs independently, and then interbred between themselves to produce all lunged creatures, but there is no 1 specific ancestors to all, but several different individual ancestors.

@IlyaMelamed - So you're talking about different ways traits evolve. Convergent, divergent, etc. If you can find a way to make that clear in your question, then I'd take away my Duplicate vote since there doesn't seem to be a good question covering evolution of traits.

@MCM, I hope it's clearer now

If you a new mutation which is recessive, although there is one progenitor, the phenotype might not be realised until many several generations later when the first homozygous offspring is born. In this case you don't really have an Adam and Eve. You could even have the first exhibitions of the phenotype occur simultaneously in different populations.

@IlyaMelamed by the way, my understanding is that many dinosaurs had feathers, including modern birds.

For most traits, there is no clear line where the trait is present or not. Exceptions are traits that occur with a single mutation, like lactose tolerance. So to pick one example, you had a population of fish that had a lung-like organ, and that by genetic drift that organ got more lung-like in a sub-population. So for most traits, you have a combination of mutations that lead to the traits, and these mutations need not occur in a direct line of ancestors. (I.e., a descendant will combine independent mutations from its parents.)
So there is no "Adam and Eve" in the sense that these are the only ancestors of all living individuals of a species. This would be a terrible genetic bottleneck! See this illustration, which comes with the estimate that the population size of the chimp-human ancestor was around 100,000.

You ask for "a first dinosaur with feathers who is the father or mother of all birds". It's possible that feathers arose multiple times from the same feather-like structures, or only once. But it is clear that this first dinosaur is only one of many dinosaurs that lived at the same time, and who are also ancestors of all birds.
Further reading: Lactose tolerance evolved several times independently (see "Convergent adaptation of human lactase persistence in Africa and Europe.").


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Book on yeast reproduction, evolution and on the use of yeast as model organism
I am looking for a good book in:

Yeast reproduction

mating types
Recombination
mating type determination mechanism

Yeast evolution
Yeast as model organism and its use in experimental biology

It should include common technics used to work with yeast. For example: We can add a plasmid in order to fool yeast and let them think they have another mating type than the actually have.

Note: I am mostly interested in Saccharomyces cerevisiae of course.

Here is my list, in no particular order.
Methods in Yeast Genetics
Some other yeast books at CSHL
Fred Sherman's primer, available free at various sites including here.
The Freiburg manual here
The timeless classics (link to volume 3 but see all volumes)
The YeastBook is an attempt to build a current encyclopaedia to replace the previous item on my list.
The Saccharomyces genome database, probably the best organism-specific resource ever.


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How non-invasive blood glucose concentration measurement work?
Diabetes patients need to conduct the “fingerstick” a few times a day. One of the mechanisms of "fingerstick" is to take small amount of blood sample and put it onto a test strip. The enzyme on the test strip reduces the glucose and the electronics of the glucose meter detect the redox species produced. However, this method is painful and increase the risk of infection.
Photonic sensing technology opens up a new method for non-invasive blood glucose concentration. According to an article of medGadget in 2013 (The link follows http://www.medgadget.com/2013/10/non-invasive-measurement-of-blood-glucose-levels-using-glucotrack-interview.html ), the non-invasive kind was invented. By simply clipping the earlobe (without puncturing the skin), the blood glucose concentration could be measured. Does anybody knows the working principle for that? Or, suggest a paper describing that?

Please don't cross-post your questions.

I am sorry! I just don't know the two sites are connected somehow.

I'm not exactly sure how it is done non-invasively in the manner you describe but suspect that it has to do with IR absorption spectroscopy. Glucose has distinct bands in the near-IR frequency range. So by illuminating the ear lobe and the capillaries in the surface, picking off the refracted light, and spectrally analyzing you should be able to determine the amount of glucose relative to some reference calibration.
I worked for a start-up company that did this semi-invasively for glucose measurements in the ICU. We drew a small blood sample and optically analyzed it in a glass cell using a scanning interferometer - then returned the blood to the patient.
The optical method that draws blood probably is the best approach with regards to accuracy - where you would like to get within 10 mg/dL - but it also has its problems including response to 'interferents' in the blood that can pose as glucose not to mention high cost for the interferometer and fouling of the blood access system.

see http://inlightsolutions.com/

Thanks for your sharing, docscience! What are the possible "interferents" in human blood if I am targeting glucose?

Other types of sugars, sugar alcohols, some more than others. I don't recall the list but remember mannitol was one of the interferents. Our experts were working on ways to eliminate interferents, I believe by utilizing multiple peak responses of glucose.


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Insect identification by example
Upstate NY USA here.
I am trying to identify the type of insect that this is:
Top-side:

Bottom-side:

Is this a cockroach? If so what type/sub-species might it be? If not, what other type of bug have I stumbled across here?

Size approximations would be helpful. It's not a cockroach by the looks of it; just a harmless beetle of some sort.

This is some species of Ground Beetle (family Carabidae); the trochanter of the hind leg (just before and somewhat overlapping the femur) and the threadlike antennae helps point to that group.  The book The beetles of northeastern North America by N. M. Downie and Ross H. Arnett (Sandhill Crane Press 1996; now out of print but in at least some libraries) may help with a species identification (fair warning: the keys are not profusely illustrated).


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Are the Chromosomes organized in any meaningful way?
So my major is in pharmacy but both my master and my (currently in progress) doctoral degree are both in theoretical chemistry. My thesis is about quantum chemistry and proteins, but it has a certain amount of phylogeny and evolutionary biology such that I've had to learn some phylogenic analysis methodology and have had my share of experience using sequence databases and analysis tools around the web. Although I do not focus particularly in the human genome, or even human proteins for that matter, I got myself thinking about a rather curious question.
I am by no means a specialist in molecular and evolutionary biology, but I do understand that chromosomes and genes come up in the population by several mechanisms. Now, it is interesting to me that all the information regarding biological sex in humans is contained within a single chromosomal switch, the Y chromosome. Given that fact, I asked myself
"Do we have some order in the arrangement of our genes in their chromosomes?"
So now I turn that question to you people, who seem to be more well-equipped to tackle theses questions than I certainly am. Forgive my ignorance and indulge my curiosity!
[EDIT FOR CLARIFICATION]
Okay, clarifying some points that were raised in the comments:
The question is about whether there is a pattern in the organization of genes into chromosomes. For example, the Y chromosome clearly contains a lot of genes associated with sexual dimorphism in humans. I was wondering if chromosomes in general follow that general pattern. If, for example, Chromosome 1 contains such and such kinds of genes, as if it had hints of an overarching "theme" to it.
Is that clearer?

Welcome to Biology.SE! From wiki: "In classical genetics, synteny describes the physical co-localization of genetic loci on the same chromosome within an individual or species"

Welcome! What exactly is your question? The title indicates that your question concerns (1) the organization in the ordering of the various chromosomes, the question in the body hints that (2) you are interested in the Y chromosome, while the quoted question asks about (3) gene placement/localization on chromosomes in general. It is unclear as of know what exactly you need to know.

You should narrow down your question a bit..

I don't think this is too broad or unclear. It's a simple yes or no question: are genes arranged in a specific way? The answer happens to be yes for some and no for others.

This can be narrowed down. The point that is a bit unclear is this: are you interested to know if the order is conserved — homologous syntenic blocks or if the order itself has a significance. If you clarify this then at least the first question is answerable. The second question can be answered at least with respect to E.Coli with some precision. For eukaryotes there are many factors to be considered. I haven't voted for closure yet because the question is interesting.

@WYSIWYG Ah, I see your point now.

@OP.. this is still not clear.


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Mass spectrometry versus western blotting for validation
I have mass spectrometry data (LC-MS/MS) from rat cortices under either drug or control treatments. The results were performed in triplicate (three pairs of rats, drug or control per pair). In addition to some of the bioinformatics analysis I am doing, I will have to validate some of the fold-changes from the mass spectrometry by Western blot in order to have my results published.
Some of the proteins I have chosen to to validate work very nicely by Western blot which captures the same trend as the mass spectrometry. However, other proteins that I have attempted to validate go in the exact opposite direction.
My questions:

In general, how accurate is mass spectrometry compared to Western blotting?
Is it unusual to have a lot of variability between the results of the two methods? I am worried that I might have to try multiple proteins before I see the results replicated and this seems problematic to me. That leads me to the third question.
Which result should I trust?

Other information - Some of the proteins I have chosen for validation come from lower in the list where not as many peptide fragments were detected. In some cases, fragments were detected in only 2 of the 3 biological replicates. I did not chose to validate proteins where the 2 or 3 replicates varied widely in normalized spectral count values so I would expect these readings to be accurate. Additionally, the mass spectrometry part of the experiment was performed by a reputable lab that has filtered erroneous data using FDR cutoffs. There is a high correlation overall between all three replicates for a particular treatment and low standard error between samples across the population so, statistically, I trust the mass spec results.
If you need more information please ask - I don't know what exactly will be useful to answer my questions.
EDIT :
This article discusses the justification for using western blotting to validate mass spec results. It suggests using selected reaction monitoring assays as an alternative. Some of the points made by commenters in this thread are reiterated in this article.

Trying to answer any question other than "is this protein actually present in my sample" with a Western seems like a fool's errand. I think that it's completely reasonable to expect a large variability between your two methods.

@tel This is my thinking as well. However, the reviewers did not agree. In their comments they have asked us to follow up with biological validation, including Western blots that support the trends. I have looked at other mass spectrometry papers from this journal and they all follow their data up with Western blots that replicate the trend.

Ohhh, reviewers and their blots. I think that I have heard similar stories several dozen times now. Have you done replicates of the blots?

Yup, I've heard the same too. Each protein is 4 biological replicates (ie. from 4 homogenized rat brains) and each has 3 technical replicates. I'd like to do more but all these rats and antibodies are starting to add up...

My impression is that Western is the gold standard that MS is measured against, but not rightly so. As you have witnessed, it's perfectly possible for Western to fail because of eg. poor antibodies when MS will perform fine. It is not necessarily better than MS. Generally, if MS and Western disagree, I don't think you should really just trust one (whether you would get away with it is a different matter). Either one could be an artifacts. Without additional experiments, it's very hard to say.

Make sure you're running your Westerns with the exact same samples that you're using for mass spec. You mentioned in your question that the MS samples were cortices, but you're using homogenized (total?) brains for the Westerns - there definitely could be differences in protein expression and regulation, as you're essentially looking at two different samples.

@ MattDMo I was not clear in my comment. The fractions of brain homogenized are identical between the Western blotting and mass spec (I am comparing the post-synaptic density in the two methods, not the total lysates). I have been running the same rats for the Western blots but from the other hemisphere. Unfortunately, the entire sample had to be submitted for the mass spec so I don't think there would be a way to run the exact same samples, but at least it's from the same rat.

It is a common practice to prove a result using an orthogonal technique. Like RNAseq followed by qRT-PCR etc.
Western blotting is not a robust technique and cross comparisons are difficult because of difference in the avidities/affinities of different antibodies. So comparisons can be made only with one protein-control pair in different conditions.
LC-MS is more sensitive and less biased(IMO). So the general trick is- don't do westerns for all proteins just report the ones that behave well (say that you "chose" these because they are important). I know this is a wrong practice and I should not be advocating it. For your own scientific validation try it with another MS technique; if you used ESI-Quadrupole/ion-Trap etc then try with MALDI-TOF or iTRAQ. Some luddites will continue to cling to westerns.
I think it is better to not test the proteins that have low peptide counts. See what is known as MA plot. This is frequently used for microarrays. Here M denotes fold change and A denotes total expression in both samples. Don't pick proteins that are low in expression in both samples; they might not be meaningful. For example if you have 2 molecules of X and 100 molecules of Y in control condition and 5 molecules of X and 200 molecules of Y in test; then the fold change in X would seem important; however this change may not be relevant and can be a result of stochastic fluctuation/measurement error. If you have many samples you can see if something is stochastic or not but the limitation is the number of samples.
Note: I am not saying that 2→5 molecule increment should be meaningless. But to know if they have a meaning or not you would require more complex models; better avoid them at this moment.

I mentioned in my original post that we sent our samples to another lab for processing and mass spec. They returned "normalized spectral count" data back to us. From what I have been able to gather, the MA plot would be utilized in obtaining these normalized spectral counts (though I am not sure what method(s) they used for normalization). If I understand correctly, I would need the raw data - not the normalized data - in order to generate the MA plot, is this correct? Lastly, I have read about volcano plots; would it be more appropriate than an MA plot?

@syntonicC Perhaps you can ask them what normalization they have done. It is certainly possible that the overall expression was low in a certain sample and this can be normalized so that the two samples are comparable (as in quantile normalization). Even then the low expressing ones will remain so. And you can remove them. You don't actually need to plot. You can use a general low expression protein (from knowledge) for comparison. I hope you have the entire normalized data including the non-differentially expressed ones.

@ WYSIWYG I have emailed the lab for the information on the normalization method. And yes, I have the full data set. Thank you for your information on the comparison, this will be helpful for me moving forward. Additionally, I found an article discussing some of the things mentioned in this thread and I've added it to my original post.


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What's the term for energy that is/isn't usable by an organism?
Every healthy organism stores some of its biochemical energy in reserves (e.g. adipose tissue, glycogen), but much of an organism's biochemical energy is bound in ways that aren't normally accessible to it (e.g. protein in muscles or vital organs).
The latter quantity has some thermodynamic implications. For example, the inaccessible energy can be transferred to a predator if the organism is eaten, and a fetus's inaccessible energy must be obtained from its mother.
To research these concepts, I'm looking for a term for energy that's accessible by the organism and a term for energy that's not accessible by the organism.
I've searched the web (and StackExchange specifically) for a variety of terms, (e.g. "expendable", "reserved", "essential", "innate", etc.) but none of them produced relevant results.

The body will only use the energy in protein (muscle mass) under severe malnourishment so it isn't really considered an energy store to my knowledge. You should look on PubMed for the literature.

Are you looking for a word/phrase other than short term and long term? Take a look at the Wikipedia article on glycogen, that lays it out from Creatine TP all the way to protein breakdown. Could you then edit to clarify what's missing.

I'm looking for a term for energy that's usable by the organism and a term for energy that's not usable by the organism. The former includes both short-term and long-term energy stores. The latter includes energy that isn't in any energy store but could, e.g., be obtained by a predator eating the organism. Does that clarify the question? If so, then I'll update it.

Do please update your question with this clarification. Also remove the reference to "essential structures" as this was quite confusing to me. I would focus on what you appear to want (not what is usually considered by biochemists) which seem to me the potential of the cadaver of a prey to supply energy to the predator. Is this so? There may be terms in use by social nutritionalists, but certainly not by biochemists. I would try to replace the bald term "energy" in any phrase you may have to devise as a solution.

I have been working on nonequilibrium thermodynamics related to life and its implications for Hegelian philosophy and this concept you describe is quite interesting. Imagining that there is a being, an agent, that takes advantage of a certain mass for its survival, the simplest term would be "metabolize", from the Greek μεταβολή (change, transformation) with the suffix indicating transformation.
While metabolizable is a generic term for using something, I have distinguished between two varieties of metabolization. On the one hand, simple catabolization, decomposition into smaller parts for structural reuse, from the Greek καταβολή. Literally, καταβολή means to throw down. This "throw" is somewhat strange, but as it is an established term, it is better to use it.
On the other hand, the use as a mere energy resource, we should use "trophic", from τροφή (trophē): "feeding" or "nutrition," derived from the verb "τρέφω" (trépho), which means "to feed" or "to nourish.", giving metatrophism to the mere feeding without integrating into the body structure.
Finally, let's see how to adapt this nomenclature to describe the concepts of your research, of things that are beyond the reach of use as energy:

Parathrophic (parathrophizable) - unsuited to use as food (such as sand).
Parametabolic (parametabolizable) - unsuited to decompose to use as structural elements (such as meat for vegetarians).
Paracatabolic (paracatabolizable) - unsuited to decompose (such as cellulose for humans).

Hope this helps with the nomenclature in your research!

Thanks. Even though that nomenclature isn't standard, it sounds consistent and useful, so I've upvoted.

I assume that, as suggested by the original form of this question and the comments requesting clarification, that the interest is in the energy a carnivorous animal predator can obtain from its killed prey. In this case, the most appropriate terms to describe this would seem to be those employed by nutritionalists. From a perusal of this topic in various Wikipedia articles I find no internationally recognized phrase, but would suggest the following as consistent with the terminology in this field:

Dietary Energy Equivalent

The use of the word “dietary” (or something similar) is important as it makes it clear that one is not concerned with the energy reserves that the living animal deposits for its own use, although these obviously contribute to the ‘dietary energy equivalent’.
(One of the Wikipedia articles that prompted this suggestion was: https://en.wikipedia.org/wiki/List_of_countries_by_food_energy_intake — a table heading therein.).

Thanks. Although that terminology doesn't capture the distinction that I'm looking for (which is between the parts of an organism's DEE that it can or can't use for itself), it's helpful for further research.

@MatthewMilone — As I keep telling you, the distinction is unnecessary because you are talking about chalk and cheese, not cheddar and brie. As far as the organism is concerned, energy reserves are by definition fuels it can use for itself and the only thing a biochemist or physiologist or the organism itself would consider with respect to that organism.

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


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Identifying eggs on my window
I live at the western tip of Britanny, France, near the town of Brest.
I noticed a strange spot on my window, inside the house, which I hypothetised was eggs of some unknown organism. Sadly, I have no better photo equipment than my phone, no tripod, nothing, so that is the best photograph I was able to make, as it was very hard to be steady and focus both.

The maximum length is around 12mm. The legs are laid flat in one layer.
A publishing amateur entomologist told me it was probably not an insect. Though it is not his domain, he is somewhat dubious about arthropods in general.
That's the extant of my research, apart from googling "ponte + keyword", "ponte" being the scientific french word both for the act of laying eggs, and for the resulting total items (i.e. the picture represents some 50 eggs and one "ponte"). I tried insects, arthropods, snails, ...
As for googling it in english, I am not aware of an english language word equivalent to the french word.
That's gonna me my first question, what keywords would lead me in the right direction.
My second question is obvious : does someone have any idea about this ? :D
The eggs matured into something looking like fish larva : a big black spot and a larval tail. Then died.
I managed to take a better picture of the "larval stage" :

Finally, thanks to a binocular, but still a phone, sadly, a picture of the "larva" :

Thanks for your interest, best regards :)

I agree they look like eggs, I would assume eggs of an insect, surprised by your friend rejecting that possibility. I think it's going to be difficult to narrow it down since so many different species might lay eggs in a similar fashion, I'd assume your best bet would be if you spot any adults indoors. Sometimes people on this site surprise me, though :)

Not an answer for you, but moths in the dark are known for laying eggs on a nice cool and flat surface.

He is the world specialist of family Tessaratomidae, so I tend to trust him, but indeed you are right that trust and science often don't mix well.

@pouzzler An amateur and also world specialist? Seems contradictory.

A professional is paid. An amateur is not. Amateurism is a different sense of the same word.

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


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Can anyone identify the worm in this video clip?
My wife came across this youtube clip of a spider and a worm. Can anyone identify at least the phylum?

I think it's a Gordian worm or more accurately known as Spinochordodes tellinii . Good music for a parasitic event like that by the way. Nematomorpha is the phylum.

If your a molecular guy, check out Spinochordodes tellinii and the WNT pathway, pretty cool stuff.


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What is the most effective way to eliminate silverfish (g. Thysanura) from walls and floorboards?
I've had our home fumigated, but the silverfish seem to return unaffected.
Are their eggs unaffected?
What's the best way to eliminate them from your home?

This question does not appear off-topic to me. I just want to say that the question might also be a good fit on lifehacks.SE.

If you say "return", haven't they just re-populated your house?

Yes, return = re-populate.

They feed on fungi, which grow wherever there's high humidity levels. So the best way to get rid of them would be to lower the air humidity. For example, by increasing the temperature in your (presumably) bathroom.


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Are there any theories why such an imbalance in chirality of molluscs?
Most gastropods exhibit sinistral  (right hand) winding of their shells. But very few species are anti sinistral. Have there been any theories as to why such a great difference?

"Sinistral" means left-handed. I believe most gastropod species have a dextral coil  (which works out to be your intended meaning).

@BenKovitz If I accept an answer,  it doesn't lock out other answers , does it? I don't believe so. If you have a good answer,  please go for it. Thanks.

It doesn't lock out other answers, but it does discourage them. It says "The OP is satisfied with this answer," suggesting that the conversation—and competition—are basically finished, unless someone persuades you to reconsider. On most SE sites, answerers tend to focus on questions that don't have an accepted answer. Here's a nice message about this on a different SE. I don't have another answer for this question, but I'm very skeptical that "non-independent trials means that no explanation is possible".

@BenKovitz Thanks for the advice. I'm about a year working with SE posts, but still learning the ropes.

Why so many molluscs exhibit sinistral winding?
The estimates of the number of molluscs vary quite greatly between 50,000 and 200,000 species. Of those molluscs species, about 70'000 are Gasteropoda. Gasteropa is most diverse Mollusca phylum.
The winding you describe is present in all Gasteropoda and is often called the torsion. So the answer to why there are so many molluscs that make a torsion is simply, because of phylogenetic independence. The torsion evolved only once in the gastropods. The answer to the more specific question, why is the torsion right handed rather than left handed in all gastropods is 1) phylogenetic independence again. The torsion evolved only once and was therefore either sinistral or anti-sinistral. There is no need for an explanation of why they are all sinistral because the observations are not independent.
Why has the torsion evolved at first place?
One may ask but why did the torsion evolved at first place?. I think the reasons are still to be discovered. The following is a summary of what I read on wikipedia (torsion#evolution)
"Why torsion is bad"
As a result of this torsion, the anus is found next to the mouth which is an obvious hygiene issue and therefore seems rather deleterious. Moreover, there are a whole bunch of issues about organs spinning around and entwining. Also, ventilation seems to be reduced by the torsion which is pretty deleterious.
"Why torsion is good"
However, because there's no "hole" left in the posterior position, the torsion may help preventing sediments. Some have suggested that the torsion may allow to move sensory organs closer to the head. The most likely explanation is that the torsion might have evolved as a defense mechanisms against predation as torsion allow an organism to hide its head behind its shell. Finally, citing from wikipedia:

The evolution of an asymmetrical conispiral shell allowed gastropods to grow larger but resulted in an unbalanced shell. Torsion allows repositioning of the shell, bringing the centre of gravity back to the middle of the gastropod’s body, and thus helps prevent the animal or the shell from falling over.

Note also that

Whatever original advantage resulted in the initial evolutionary success of torsion, subsequent adaptations linked to torsion have provided modern gastropods with further advantages.

Why sinistral rather than anti-sinistral
To repeat myself, we only have one single observation of torsion (as it evolved only once) and this observation is either sinistral or anti-sinistral. It sounds therefore quite likely that stochastic processes have driven the evolution of sinistral (rather than anti-sinistral) torsion. In other words, the first mutation allowing for some degree of torsion was probably causing a sinistral torsion and this is it.
But there might eventually be a more functional reason for why torsion evolved to be sinistral. The reasons would then be related to the already existing asymmetry of organs. For example, anti-sinistral torsion may yield to more entwining between the gut and the respiratory system, or to not squeeze too much the one lung, who'd be smaller than the other one due to the presence of circulatory organs. I don't have enough knowledge in the anatomy of the molluscs ancestors to have a good intuition of whether I'd expect sinistral or anti-sinistral torsion to be more beneficial.

all of what you posted is very interesting and all makes sense, my main interest was in why so many gastropods have right hand coiling, and so few left hand. What evolutionary factor might have selective favor of right hand over left?

I developed the second paragraph and the added a section to try to better address this point.

Good hypotheses. Perhaps worth a rudimentary analysis, study.

Stimulating answer! Here are some reasons for doubt, which could be addressed in an edit or by other answers. 1) How do we know that only one torsion mutation ever happened? 2) Most gastropods actually have dextral coils. 3) A few gastropod species and genera are sinistral. 4) Amphidromus perversus has both. 5) A few sinistral snails appear in populations of mostly dextral snails. (Info mostly from Wikipedia. I am not an expert on molluscs.)


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Does long term use of antibiotics in humans actually lead to a greater risk of infection?
I've read about the overuse of antibiotics leading to antibiotic resistant strains of bacteria, so generally does long term use of antibiotics breed these strains in the bodies of antibiotic users and increase the risk of various bodily infections?

Not usually in the individual, but in a population, improper antibiotic use can lead to resistant strains and more infections. Improper use usually means stopping therapy short and not using all the pills, using antibiotics for diseases they cannot help with, or very-long-term use in a healthy individual. Antibiotic resistance is basic a probability function, with the increase exposure to the antibiotics increasing the probability resistance will develop. Regimes are designed so that bacterial populations stay isolated/small and the chance for resistance remains small.

Not really your question but another problem of an overuse of antibiotics, is that there are many bacteria in your body especially in your digestive system which are important to stay healthy but are also killed by antibiotics. To get these bacteria back into your body there is a discussion about "poo pills"

does long term use of antibiotics breed these strains in the bodies of antibiotic users[,] and increase the risk of various bodily infections?

Yes to the first question (although I would use the words select for). No, not usually for the second question in the individual(*), yes in the population.
This should be looked at as a problem in populations of both people/animals and bacterial populations in general. Given time, any living organism will be favored if a mutation involving a selective pressure (like an antibiotic) is introduced, not only in those towards which the antibiotic is directed but also among the normal microbiota. The longer the selective pressure (antibiotic treatment), the greater the probability that a resistant strain of one bacteria or another will develop.
That's why there's a push (in studies) to limit the number of days of antibiotic use necessary to the least number needed which still proves efficient in eradicating an infection. (The trend is towards kill 'em quick and kill 'em all - higher doses for shorter periods, or make it strong and only long enough to cause the extinction of the illness-causing bacteria and not long enough for selection of resistance mutations.)
It is quite normal to have potentially pathogenic bacteria as part of one's microbiome. Usually other beneficial bacteria and conditions keep these in check. But antibiotic resistance, once selected for, can persist for longer periods of time than previously recognized (up to four years in one study). This gives even a small population of resistant bacteria to genetically transfer resistance to others.
Short-term use is less likely to select for resistance in one individual, but, in terms of populations of people, antibiotics are used so ubiquitously that resistant strains will be selected for in shorter treatment intervals by sheer numbers of people being treated.

When resistant and susceptible organisms compete to colonize or infect hosts, and use of an antibiotic has a greater impact on the transmission of susceptible bacteria than resistant ones, then increasing use of the antibiotic will result in an increase in frequency of organisms resistant to that drug in the population, even if the risk for treated patients is modest. Antimicrobial use and patient-to-patient transmission are not independent pathways for promoting of antimicrobial resistance, rather they are inextricably linked.

"Long term use" in one individual is relatively uncommon and unnecessary, but if necessary, usually does more good than harm to that individual. Almost all (if not all) of the population of the bacteria you're trying to eliminate from one site will be susceptible to the antibiotic and will die, leaving, in a few cases, a few resistant ones that your body can handle naturally, or that can repopulate to "normal" levels without causing illness. But they are then there, the resistant ones, to spread within a population of the individual's microbiome, and the population of people. The next person with a problem, who might have picked up that resistant strain, will not respond well to the same antibiotic. Nor will the patient who was initially treated, if the problem recurs with an antibiotic resistant strain. So, as I said, yes and no.
That's why people (doctors, vets, and - with help - patients) should consider a risk-to-benefit-ratio whenever using an antibiotic. From that standpoint, it is always unethical to use an antibiotic for what is probably a virus, because the benefit to a patient is very small, but the risk - to that patient, who might suffer complications from its use, and to the population if a resistant strain is selected for - is relatively high. Better to wait it out to see if it is bacterial (if one can't test for it directly), and treat it if it does turn out to be. Of course, the risk of not treating in certain populations must also be considered: the elderly, the immunosuppressed, infants, and people with other illnesses or predispositions to infection.
It's not just use of antibiotics in patients/humans that causes problems; its use in any situation can lead to selection for resistance. This is well documented to occur in the meat industry, where a grower often tries to minimize the effect of cost-efficient but insalubrious growing conditions by giving antibiotics to the entire population of meat-animals (beef or poultry) to cut the monetary losses associated with potential illnesses.
It's a multifactorial, and often monetarily driven, problem. Doctors share the blame, but so do patients who demand antibiotics thinking they know better than the doctor, and who will doctor-shop until they find one who will do their bidding, or make a stink for the doctor who refuses. Some doctors still refuse, but they pay a heavy (non-monetary and sometimes monetary) price for doing so.
In the meat industry, it's always a monetarily driven process.

This review focuses on agricultural antimicrobial drug use as a major driver of antimicrobial resistance worldwide for four reasons: It is the largest use of antimicrobials worldwide; much of the use of antimicrobials in agriculture results in subtherapeutic exposures of bacteria; drugs of every important clinical class are utilized in agriculture; and human populations are exposed to antimicrobial-resistant pathogens via consumption of animal products as well as through widespread release into the environment.

What YOU can do:
Do not take an antibiotic for a viral infection like a cold or the flu.
Do not save some of your antibiotic for the next time you get sick.
Take an antibiotic exactly as the healthcare provider tells you. Complete the prescribed course of treatment even if you are feeling better. If treatment stops too soon, some bacteria may survive and re-infect.
Do not take antibiotics prescribed for someone else.
If your healthcare provider determines that you do not have a bacterial infection, ask about ways to help relieve your symptoms. Do not pressure your provider to prescribe an antibiotic.
Antibiotic resistance: delaying the inevitable
Get Smart: Know When Antibiotics Work
Short-Term Antibiotic Treatment Has Differing Long-Term Impacts on the Human Throat and Gut Microbiome
Antimicrobial Use and Antimicrobial Resistance: A Population Perspective
Comparison of 8 vs 15 Days of Antibiotic Therapy for Ventilator-Associated Pneumonia in AdultsA Randomized Trial
Plasmid encoded antibiotic resistance: acquisition and transfer of antibiotic resistance genes in bacteria
Industrial Food Animal Production, Antimicrobial Resistance, and Human Health


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Why do some cells like myofibrils have multiple nuclei?
I see that myofibrils (muscle cells) contain not one, but multiple nuclei.

Why is this so?
Do all the nuclei participate in cell division?

Is your question about "how it happens" or "what is the importance of such a phenomenon"

@WYSIWYG The first question particularly - more towards a reason why this came about in evolution. Could an equally efficient mechanism as the myofibril come about that didn't require multiple nuclei. Benjamin Markus did answer my second question.

First Myofibrils are not muscle cells. Many myofibrils (essentially long strips of the muscle cell) make one muscle cell, which is known as a muscle fibre. And it's the muscle fibres that have multiple nuclei. And they have multiple nuclei because they were formed from the fusion of multiple myocytes. Why? Probably because the muscle cell is quite a large cell(because it is long) so multiple copies of DNA are required to produce the proteins required to maintain the muscle cell. Also muscle fibres do not divide, so no the nuclei do not participate in cell division. About other cells I am not sure. I am only aware that some cardiac muscle cells also have multiple nuclei, for similar reasons.

Osteoclasts can also have multiple nuclei, usually around 5.

In the case of myofibrils this is the case because of the syncytial nature of that given structure. It means that in developing muscle tissue after a certain stage the cell divisions become somewhat different in that the final step, being separation of the daughter cells via invagination of cell membranes, does not happen. The nuclei though keep dividing after that. In the end what we have is a big membrane coated structure (basically a cell), with lots of nuclei in it.

What you are describing is a coenocyte (nuclear division without cytokinesis).


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Metabolic control theory: proof of the summation theorem?
I'm looking for a rigorous proof of the summation theorem of metabolic control theory. The only sources I find are the original papers by Kacser and Burns 1973 and Heinrich and Rapoport 1974, both of which are unclear to me.
The summation theorem is the following. Consider a linear metabolic pathway
$X_0 \xrightarrow{E_1} X_1 \xrightarrow{E_2} X_2  \cdots \xrightarrow{E_n} X_n$
Let $J$ be the steady-state flux through the pathway, and let $e_i$ be the concentrations of the enzyme $E_i$. The flux control coefficients $C_i$ is defined as the partial derivatives
$C_i = {\partial (\ln J)} / {\partial (\ln e_i)}$
The summation theorem states that for any such system, it holds that $\sum_{i=1}^n C_i = 1$. Intuitively this means that if the concentration of some enzyme has a large impact on flux, then the other must have a relatively smaller impact. It seems reasonable, but is far from obvious I think. So a proof is needed.
The proof (sketch) given by Kacser and Burns seem to rest on the assumption that $\partial (\ln J) = \sum_{i=1}^n \partial (\ln e_i)$, and given this, the proof is trivial; but this assumption is never explained further. Heinrich and Rapaport states the summation theorem in passing (p.94, "it is worth mentioning that the following relation holds"), but I don't see a proof. (But their paper is rather dense so I may have missed it.)
Anyone know of a proof of the general case?


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Are animals that can make facial expressions more visually communicative?
This is more like a shower thought but I was really interested in finding an answer. If this is the case, I would like sources that support this and gives reasons to why this may be the case. In the meantime, I'll try to find some evidence or a counterexample that disproves this and will post it on here. Thanks in advance.
Sources:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2826104/ -Emotional communication in primates: implications for neurobiology
Lisa A Parr,1 Bridget M Waller,2 and Jennifer Fugate3
https://www.researchgate.net/publication/337975455_Differences_in_facial_expressions_during_positive_anticipation_and_frustration_in_dogs_awaiting_a_reward
"Therefore, this session was stopped and we only analysed positive and negative trials of the
Testing session (Step 4) for every subject." This line in the second article I mentioned may hinder the credibility of the experiment, reffering to not having a control case.

How do you measure whether an animal can make facial expressions? How do you measure the extent to which an animal is "visually communicative"? If making a facial expression is being visually communicative, isn't this a tautology?

Yeah, plenty of animals that communicate visually (though not necessarily by facial expression) including insects, fish, mammals, birds and reptiles. If the signal gets the point across, that's sufficient, so you can't make it more communicative...

@BryanKrause I apologize for leaving my question a bit vague. by "visually communicative" I meant animals that primarily uses visual clues(such as facial expressions and pointing) rather than using other forms such as smell or auditory clues. By facial expressions I meant shoving teeth for anger, "smiling"(though I've not seen it very much) when amused.

what attempt to answer this on your own have you done, you are expected to show some background research.

@John I have added sources I've researched to the "Sources:" part of my question.


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Bivalve Respiration
Minor question:  Is it "Mollusk" or "Mollusc"?  I've encountered both spellings, and am unsure which is correct.  For now, I'll use the "-k" spelling, but if anyone can correct me, that'd also be helpful.
EDIT:  This part has been addressed and revisions to the question have been made.  Thank you!
Howdy!  I'm doing some spec-evo stuff, and came upon this particular question about Mollusks - particularly bivalves like clams and oysters.  I understand that, like many mollusks, bivalves pass water across their gills with siphons.  Water flows into their bodies, across the gills, then flows back out, in a manner like this:

I am also led to believe that, like many other mollusks, they also use this technique as a means to remove bodily waste and gametes/larvae from within their body cavities.  The anus and gonopores reside within the body on the exhalant/outcurrent side, and any waste or reproductive cells are expelled along with water flowing out, like this:

My question is this: how do bivalves prevent this waste material from getting stuck in their gills?  I would assume that waste material interacting with the gill would lead to infection or damage, and it doesn't seem as though any mollusk encounters the problem of accidentally breathing their own waste.  If these diagrams are accurate, then it likely has something to do with how water flows within their bodies that prevents "backdrafts", so to speak.  But I don't understand how exactly this works, and my own research has turned something of a dead end.  Any advice would be immensely appreciated.
Image source:
https://youtu.be/IWzOGB7bBuA?si=LT6s_pzayu6P2Gaq

Both "Mollusk" and "Mollusc" have existed since the 1830s; "Mollusk" used to be more common, then in the late XIX century "Mollusc" surpassed it in UK and Dominions, while the former remained predominant in the USA. The proponents of Mollusc abide by the rule that the vernacular name should be the Latin word "Mollusca" minus the last letter (or something like that); the proponents of Mollusk mantain that the preferred way to write the sound /sk/ at the end of an English word should be "sk" (or something like that).

Mollusk (and history) guy ->  https://web.archive.org/web/20120303002304/http://www.conchologistsofamerica.org/articles/y1996/9609_rosenberg.asp
$$$$
Mollusc guy -> Brusca & Brusca. Invertebrates (2nd ed.), chapter 20, footnote.


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Does each ovary release an egg with multiple uterus?
If I understand correctly, uterus didelphys is when the uterus is split in two, creating two uterus connected to only one ovary.
Usually only one ovary release an egg for a given cycle, but since everything is separated in this case, this would mean that only one is fertile at any given time.
I tried asking a gynecologist but was told that it doesn't matter, without any details.
So, in case of uterus didelphys, does each ovary release an egg each cycle? If not, how does it work?

Welcome Telrunya. Please remember to show your own attempts to answer the question, what you searched and found. Showing prior research is a requirement here.  For reference, see our [ask] section of the [help].

Remember to link to your sources when you edit.

In your first sentence, are you meaning that the uteri are each connected to one ovary, or that both are connected to the same ovary?

@anongoodnurse I'm aware of that, but I was hinting that the wording is unclear.


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Relation between a compound's toxicity and it's concentration level
I know that ammonia is toxic for the body since it disturbs enzymes of mitochondria.
I want to know that why the ammonotelic animals don't get affected by it?
I mean that even if there is plenty of water to remove ammonia from their body, does ammonia not cause any damage till it's inside body?
Does toxicity depends on concentration level?
Can anyone tell me its evolutionary significance?
Sorry for the previous question. .
Actually it was a easy one and I got the answer.
Sorry for the unclarity.;)

I read it .   It was like this-"uric acid being less toxic,can be removed with a minimum loss of water".       Another one-"Terrestrial adaptations necessitated the production of lesser toxic nitrogenous wastes like urea and uric acid for conservation of water".   Am I interpreting it wrong or is there some relation between them?

I read it in our high school book.    I want to know that' is  there a evolutionary significance of it.'... I mean isn't it a coincident  at the same time, a less toxic and less soluble substance is formed?   I want to know how are they toxic to our body and can this TOXICITY be related to LESS NEED OF WATER FOR EXCRETION? Can there be any  structural significance of these compounds in their toxicity?

Toxicity does depend on concentration levels. If you want to know the evolutionary significance, add it to your question. And add the evolution tag to the question so that it gets attention

The article at linked at the bottom says that the marine organisms keep the concentration of Ammonia under very strict control.

pH of the ECF (Extra Cellular Fluid) is said to play a very important role.
The concentration of ammonia in the environment (ambient ammonia levels) also plays an important role.
Less importantly temperature also plays a role.
Ionic strength of water also is involved.

The NH3:NH4+ ratio seems to be more important than the abosolute value of ammonia.

Ammonia is more toxic than ammonium ion. The lipophilic (ammonia is amphiphilic - soluble in both water and lipid) nature of ammonia allows it to easily cross the cell membrane and the blood brain barrier (in organisms where BBB exist) and affect the physiologic functions. The ammonium ion on the other hand can't enter the cell as easily, as it is not as soluble in lipid as ammonia.

For ammonia and marine organisms see http://www.sciencedirect.com/science/article/pii/S1546509801200053
For more on ammonium toxicity see: http://www.ucl.ac.uk/~ucbcdab/urea/amtox.htm


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Alcohol consumption and central nervous system
After alcohol intake, the cerebrum related functions like vision and speech is affected first and later on there's problem with the cerebellar functions like balancing and hand-eye coordination.
My question is- why is it so? Why do they appear in that order?
Like does it have anything to do with differential rate of absorption in cells, or anything else like related to anatomy rather than physiology.

Can you give a source for your statement? There is a big difference between being affected and feeling something. I would say your oral/esophagal and gastric mucosas would be the first body part affected (hence oral cancers in drinkers who smoke.) The liver is next. Alcohol affects a lot of body parts, so this question is fairly unclear to me. Could you possibly edit to make your question clearer? Thanks.

@anongoodnurse - i didn't exactly read that in a book or anything. It's just a question which was asked in some competitive exam. Cerebrum was preferred over cerebellum as the answer. Plus, here, I'm talking about not the long term effects of alcohol drinking. I'm asking which body part is affected first just after intake of alcohol.

@anongoodnurse -I think i have made my question a little bit clearer.

The first body part(s) affected after drinking alcohol are the oral/esophagal and gastric mucosas. Have you ever swallowed whisky and felt it burn? As to cerebellum vs. cerebrum, read about which does what, and think about which is affected first when you drink. You'll figure it out.

@anongoodnurse - i do get your logic. That's true that the mucosal lining will be the first affected part, then liver since the absorbed alcohol will go through hepatic portal vein to it. Then any cerebral effects should be seen. But my question isn't about what symptoms are seen and in what order. It's rather about why cerebral related things are affected first (like vision and speech) and then later on cerebellar symtoms appear like problems in balancing and hand eye coordination? PS: i can't do the practical you said since I'm 18 and 21 is an average drinking age in india!! Hehe =)

I'll try to edit my question accordingly

After alcohol intake, the cerebrum related functions like vision and speech is affected first and later on there's problem with the cerebellar functions like balancing and hand-eye coordination. My question is- why is it so? Why do they appear in that order?

It is and it isn't complicated. When you include what each does, it's an interesting question.
We know from experience (and even research, though the ethics of carrying out such research is questionable) that of the noticeable effects on the brain, the first part of the brain (that we can see the effects of) are on the cerebrum. At relatively low doses, the drinker feels more relaxed, more talkative, less inhibited. (there is also a measurable decrease in information processing and reaction time, as well as other less obvious effects.) All these are under the control of the cerebrum.
At this stage, the cerebellum is affected as well, but not grossly (in a manner that we can observe as change in behavior.) The cerebrum is critical to functioning; the cerebellum is critical to survival. Although it's presented as a teleological argument, the simple fact is that effects of alcohol and other sedatives on various parts of the brain are dose-dependent.

First, dose-dependent functional magnetic resonance imaging (fMRI) changes were revealed in orbitofrontal (OF) and motor (but not cerebellar) regions; visual and medial frontal regions were unaffected. Second, cerebellar regions were significantly associated with driving behavior in a dose-dependent manner. Finally, a global disruptive effect of alcohol on the ICA time courses was observed with highly significant differences in OF and motor regions. Alcohol thus demonstrated some behavioral effects and unique, disruptive, dose-dependent effects on fMRI signal within several brain circuits. The fMRI data also suggest that the deficits observed in alcohol intoxication may be modulated primarily through OF/anterior cingulate, motor and cerebellar regions as opposed to attentional areas in frontoparietal cortex.

If you want to know why different parts of the brain require higher doses to become impaired, that is easy in theory but very complicated in reality. In theory, the brain is no different than any other complex organ in the body: it's made up of different cells. Sure, they're all neurons (excluding glial/etc cells), but not every neuron is the same, just like not every cardiac myocyte is the same. In reality, the answer is unknown.

Neuronal mechanisms underlying alcohol intoxication are unclear. We find that alcohol impairs motor coordination by enhancing tonic inhibition mediated by a specific subtype of extrasynaptic GABAA receptor (GABAR), α6β3δ, expressed exclusively in cerebellar granule cells. In recombinant studies, we characterize a naturally occurring single-nucleotide polymorphism that causes a single amino acid change (R100Q) in α6 (encoded in rats by the Gabra6 gene). We show that this change selectively increases alcohol sensitivity of α6β3δ GABARs. Behavioral and electrophysiological comparisons of Gabra6100R/100R and Gabra6100Q/100Q rats strongly suggest that alcohol impairs motor coordination by enhancing granule cell tonic inhibition. These findings identify extrasynaptic GABARs as critical targets underlying low-dose alcohol intoxication and demonstrate that subtle changes in tonic inhibition in one class of neurons can alter behavior.

The above sounds like a reason, but it is debated still. I think it's safe to say that like so many cellular reactions, the answer will come down to receptors and their activation or inhibition, be it for GABA/NMDA, combinations or others.
Alcohol impairment of behavior in men and women
Differential effects of ethanol on motor coordination in adolescent and adult rats
Alcohol Intoxication Effects on Simulated Driving: Exploring Alcohol-Dose Effects on Brain Activation Using Functional MRI
Modulation of GABA A receptors in cerebellar granule neurons by ethanol: a review of genetic and electrophysiological studies
Ethanol affects NMDA receptor signaling at climbing fiber-Purkinje cell synapses in mice and impairs cerebellar LTD

In the fMRI part; visual and medial frontal regions were unaffected. It means that they are affected but not in dose dependent manner. Am i interpreting it correctly?

It means (sorry to be a stickler) that no activity was seen at that dose on fMRI. I can't really say more. :)

Okay, got it! Thanks! It really helped a lot  .No need to be sorry. =)


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CD4+ as Monocytes cell surface receptors
Today in class,  our teacher was discussing about the pathogenecity of the HIV virus.
He said that the binding between HIV virus and macrophages is done by the interaction between the GP120 of the virus and CD4 receptors,chemokine receptors(CCR-5 and CXCR-4) and fusin receptor present on Macrophages.
My doubt is
I think CD4 receptors are present on T-helper cells only. Are they present on Macrophages too? Do i have a wrong notion about CD4 receptors?
If not, then are there some other receptors responsible for the transfer of viral particles inside monocytes and dendritic cells?
Any extra information is appreciated.

Macrophages and monocytic cells can express CD4, CD8 or even co-express them.

@CMosychuk - what's the function of these receptors on monocytes? As in I know their function in T helper and T cytotoxic, but What are they doing on monocytes?

Macrophages and monocytic cells can express CD4, CD8 or even co-express them. The CD4 and CD8 molecules interact with MHC complexes on neighboring cells, and as you can imagine elicit varying effect in a cell type-dependent manner.
Plainly enough, Zhen et al. demonstrated that monocytic CD4 ligation to MHC-II molecules on other cells, such as activated endothelium, induced an expression pattern conducive to macrophage differentiation (1). Gibbings et al. also demonstrated that CD8 associates with FcyR on the monocyte's surface similar to CD8/TCR associations, and stimulates the secretion of cytokines (2).
I'll try to find a model source, but CD8a on dendritic cells can associate with MHC-II molecules on T cells like HLA-DR and aid in cross-priming the T cells.
Now what CD4 does on functional, differentiated macrophages is less clear to me, and I need to review the literature on that a bit more. It could just be expression imprinted because they're monocyte-derived cells, or it could also elicit an effect like CD8/FcryR above. I do not know.
There are more cases, so these serve as selected examples.

Thank you! It was helpful. But if you get any extra information related to this, please post it up too!  =)


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ATP generation during respiration
How many ATP molecules are generated from oxidation of FADH2 formed during complete oxidation of 10 molecules of maltose?

40
60
80
20

My method-

As maltose is a disaccharide ( made up of two glucose molecules )and for one glucose molecule , 2 FADH2 are formed after complete oxidation.
Then for one maltose molecule 4 FADH2 will be formed (since maltose has 2 glucose molecules).
Such 10 molecules of maltose will give 40-FADH2.
1-FADH2 produces 2ATP during oxidative phosphorylation ,so total ATP formed =80

Try not to ask homework questions(direct option based questions) on this site. You'll get downvoted everytime. First, try to solve the question by yourself. If you encounter any problem in any step or can't understand something, then put forward your methods and ask the question(how should we do it and all). You can ask any conceptual problems related to particular topics but remember : NEVER post direct questions.

its not homework one it was asked in exam

look how i solved in  EXAM

as maltose is disaccharide made up of two glucose molecules and for one glucose molecule 2-FADH2are formed after complete oxidation then for one maltose molecules 4-FADH2 will be formed (22[2 in glucose{fadh2}]and [maltose=glucose+glucose])and such 10 molecules of maltose so40 FADH2(410).And each FADH2 produces 2ATP during oxidative phosphorylation so TOTAL ATP formed-80(40*2)

i know it's not a homework question (if u take the meaning literally). What I'm saying is try to make your question look much more presentable (like add your methods,thinking,reasoning,sources you use,etc.). If you don't show your efforts in finding out the answer, people will be less interested in answering it. And it'll also get downvoted since it'll seem like you didn't even take the effort to do it. You just posted it to get the answer. You're new to this site, so it'll take sometime to get used to it. So, don't worry if you're getting downvoted. just better luck next time!  =)

As far as i can see, you have done nothing wrong. Maybe the answer given is wrong?

@Bhavya-No problem =)


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Can human perception differentiate between monochromatic and polychromatic light?
Maybe monochromatic is not the right word, what I mean is light consisting of a single wavelength (i.e. a spectral color) versus light composed of photons of multiple wavelengths (intermediate color).
For example, suppose we had a single, violet "laser" and a set of "lasers" combining into a purple color.*
Is it possible to combine the latter light sources such that their composite would perfectly match the violet one such that both look the same to a human eye (assuming perfect alignment)?
And would they look the same to all human eyes?
My guess is a no, because people might have different susceptibility to red and blue hues, and their aggregation functions may differ as well.
* Apparently, there are alternative definitions to distinguish the two colors (purple is reddish, violet bluish), but I am referring to the ones found in Wikipedia: Purple being an intermediate color and violet being a pure spectral color.
Interesting article on color perception in the animal kingdom:
https://arstechnica.com/science/2020/06/experiments-show-hummingbirds-see-colors-youve-never-dreamed-of/

The short answer is no. Because of metamerism, the human vision system cannot distinguish monochromatic light from the infinitely many metameric equivalents that elicit an identical tristimulus response as that of the monochromic light.

There might be nonlinearities in the photoreceptor, and chromatic aberrations of the lens (optics) that might allow a well trained eye to discriminate using tricks...(just a guess, hence not an answer)

Err... You're presumably reading this on a computer display, no?  Which produces colors by combining essentially monochromatic red, green, and blue pixels.  So can you see differences?

@jamesqf well, people can perceive flickering on computer displays, even on LCDs with temporal dithering, as I do, and there may be reasons why people distinguish between purple and violet, even leading to different names for the "same" perceived color. And if you look closely at an RGB display, you can see red, green and blue dots. Also, some people are tetrachromats and can see differences in skin tones where trichromats cannot. Some can even see polarization. Certain purple and violet hues might look the same to some people but different to other people, unless proven otherwise.

@jamesqf also, I don't have proper, comparable monochrome light sources to compare them in any scientifically significant manner, much less people to experiment on.

@Archimedix:  Those red, blue, and green dots are monochromatic, or nearly so, yet combining them produces a multitude of perceived colors.  What I'm suggesting is that you experiment on yourself, and see whether those computer-generated colors look different than "natural" ones.  As for the flicker that some people can see (I'm one, at least on older displays), that's a function of scan lines & refresh rates, nothing to do with color.

@jamesqf I have no polychromatic light sources I could compare to those RGB dots, and I have no monochromatic light that is comparable to a mic of those RGB dots. Regarding flicker, temporal dithering uses different colors one after another to create an "average" color, so yes, in theory, most people should have similar perception (maybe along a Gaussian distribution). However, a prism would be able to make a monochromatic ray of light distinguishable from a ray of polychromatic light, and lenses do have prismatic effects.

@Archimedix: Why not create an image that is say all red - RGB = (255,0,0)?  That should be a pretty good approximation to a monochromatic source, no?  (You could test it with a prism.)  Then compare it to something that is naturally red,

@jamesqf say I compare a red patch on the screen with a piece of red paper of the same size: Both look different to me, of course, but this is because of their different surfaces/textures/hues/brightness/reflection/viewing angle and one consists of pixels where maybe one third is black while the paper is all red. Using a red LED will yield different properties, but the verdict is the same. Too many factors. Does something that looks the same to me look the same to everyone else? Is it because my two test objects are not equal enough, or do different eyes/brains render them differently?


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The skin color of bonobos
Why is that bonobos skin color on the areas not covered by hair are dark throughout life unlike the chimpanzee?

"disprove the idea that skin color evolved".. How is this related to evolution?

I removed it. If it wasn't related then excuse me.

Most likely they're different because ... they're different. Chimps and bonobos are separate species, and have evolved many different traits from each other over time. The difference in skin color may have evolved as an evolutionary advantage of some sort (maybe bonobos spend more time in direct sunlight than chimps), or it may just be an artifact, or side effect of some other mutation.