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What happens in the synapse when cocaine administration occurs in the human brain
As far as i know when you accept cocaine in your blood some cocaine molecules reach some synapses in your brain and fill some Reuptake tunnels preventing the cell to simply "do not know that fired neurotransmitters have achieved their task" and doing so the cell fires neurotransmitters again becuase "it" simple do not know that "it" have achieved its task.
In this case cocaine molecules fill Reuptake tunnels in Dopamin Serotonin and Norepinephrine
orientated neurons.But since the firing occurs when an electrical signal occur how the neurotransmitters are fired again when such electrical signal does not exist?
If im mistaken in my physiology knowledge explained above please correct me!

You are correct that cocaine "fills the tunnel" (the pharmacology terminology is that it "blocks the transporter").  But it is not an autoreceptor, so the reuptake transporter does not send a stop signal, it just removed neurotransmitter from the cleft.  But once you've blocked it with cocaine, neurotransmitter is not being removed from the cleft so it has a much longer and stronger signaling effect on the post-synaptic neuron.
But cocaine can also block sodium channels, which assist in action potential propagation and that has more of a local anesthetic effect.
The effect you are thinking of would pertain to auto-receptors, not reuptake transporters.  Autoreceptors tend to be more like the post-synaptic targets of the neurotransmitter.

so you say a single neurotransmitter can bind to a receptor many times and can do its task many times (like neurotransmitters are not  limited) and by blocking the transporter all neurotransmitters in this case perform their task many times and new neurotransmitters are arriving just because this is the normal function of the brain ?

ligan-receptor kinetics have an "off-rate" and an "on-rate" so yes, they can bind more than once, but some receptors can become "desensitized" from being stimulated.  Regardless, having more neurotransmitter in the vicinity of receptors leads to a larger chance per unit time of ligand finding receptor and activating it.

for example if i have a long dopamine flow like being on cocaine for 1 hour will this dopamine "attack" damage your brain?
Because as far as i know cocaine consumption damage your brain or im wrong?

I'm not a medical expert, but I don't know of any damage to brain from cocaine.  Of course, using cocaine, flooding your dopamine receptors, your body will compensate in the long run by reducing the number of receptors on the post-synaptic neuron (and it will require more cocaine next time).  Once you quit doing cocaine, it will take a while to recover normal receptor levels.

Cocaine is cardiotoxic. After chronic exposure to high doses I would assume that primary damage would attack the cardiovascular system before levels of dopamine would be able to cause damage. Cocaine intoxication deaths have mostly been caused by this cardiotoxicity. Primarily, myocardial infarction, arrhythmia, heart failure, and sudden cardiac death are a result of overdose. Cocaine is a vasoconstrictor, which may be a leading cause to myocardial infarctions.
http://www.ncbi.nlm.nih.gov/pubmed/19463023

how does this answer the question?

I am saying that you would most likely overdose and suffer cardiovascular consequences that result in death before it's possible to have brain damage as a result of too much dopamine in the post-synaptic cleft.

That makes sense


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Can frogs see clearly under and above water?
If humans attempt to see underwater, the image is blurred due to refractive differences in air and water that disrupt the normal refractive effect of the lens in the eye. A diving mask overcomes this issue. How then do frogs accommodate their lenses in both air and water? Are their images clear in water and blurry above, or vice versa?
As far as I know, their lenses are made up of epithelial cells and fiber quite similar to the human eye lens, or am I incorrect here?

Short answer
Frogs are nearsighted on land and farsighted under water.
Background
Frogs are reported to be nearsighted on land, but farsighted underwater (source: Chegg Study). Nearsightedness (myopia) is a condition in which near objects are perceived clearly, but objects farther away are blurry. Farsightedness (hyperopia) is the reverse. The human counterparts of these conditions are shown in Fig. 1. Humans focus images on the retina by changing the shape of the lens; to focus on near objects, light is more strongly refracted by making the lens more spherical in shape. For far-away objects the lens is flattened such that light is less refracted.

Fig. 1. Near- and farsightedness. source: Hyperphysics
In humans refractive errors are common and can usually be successfully treated with corrective lenses.
The cornea adds substantial refraction to the optical system of the eye, namely about 43 diopters. As a comparison, normal prescription glasses often have only a few diopters worth. In water the refractive index of the cornea is mitigated, as water and the cornea have about the same refractive index (source: lasikmd). Hence vision is blurred for humans under water, because images are focused far behind the retina, resulting in hyperopia.
Frogs have another way of correcting their retinal image. They focus on objects at different distances by using specialized (lentis) muscles to move the lens closer to or farther from the retina (Fig. 2), like the focusing mechanism of a camera (Douglas et al., 1985). However, the lentis muscles can adjust the focus only for approximately 10 diopters worth, with an accompanying shift in lens position of about 150 μm. Hence, because of the huge effect that water has on the corneal refraction (~40 diopters), a frog's lens cannot sufficiently correct the refractive state of the eye to achieve normal vision (emmetropia) both above and below water. Apparently it settled evolutionary spoken somewhere in the middle, namely myopic on land, and hyperopic under water.

Fig. 2. Cichlid eye. Accommodation results from the movement of the lens in the pupillary plane using the lentis muscles; the musculus retractor lentis, and the antagonistic ligamentum suspensorium. source: Vision in cichlids
Reference
- Douglas et al., J Comparative Physiol (1986); 158(1): 33–143

+1, Nice answer! Did you use a fish eye image (bottom, a cichlid) because of similarities with amphibians?

@Kara - Thanks! And yes indeed - the lentis muscles are not confined to frogs but are found in many amphibian eyes and fishes. You actually read my post didn't you ;-)

Oh of course, else why bother? It's funny, most students I've come across think the human/mammal zonules of Zinn are ancestral. For fun, you might be interested in looking at the Four-eyed Fish, Anableps anableps, solution to air-water vision.

source: Stack Exchange

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Do animals have social status as humans in our society?
As our society and it's functioning is closely related to the ones of animals, one question arises: Do animals in nature have social status as humans? People often display it publicly, by buying nice cars, searching for women and partners and so on, accumulating wealth and so on. Does similar things happens in nature? How our behavior is similar to animals?

Are you asking if animals try to show off social status?

Yes, exactly this.

Animals certainly have social status as evidenced in the idea of 'pecking order' or dominance behaviors in canine packs.
I think the more interesting question (perhaps what you are looking for) is whether non-human animals 'dress up' their social order either to deceive others about their standing or reinforce their position in society.
If this is the question, then natural displays don't really count. More specifically, is there evidence of animals 'affecting' a position in 'pecking order' that is not theirs otherwise? Or perhaps ask, ' why do men buy BMWs?'

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What does the spectrum of Chlorophyll fluorescence look like?
I've just posted the question Which spacecraft can see plants "glow" during photosynthesis during the day, and what wavelength does it use? in a different SE site. I can't remember the details of which spacecraft this was or how exactly it worked.
My question here is simply about light produced by vegetation during photosynthesis. In this question I've shown a hodgepodge of absorption or sensitivity spectra of photosynthesis, but what I'm looking for is an emission spectrum and some details about where in the process this light is produced.
The Wikipedia article Chlorophyll_fluorescence covers the topic in general and mentions 735nm but I'd like to be able to see a fairly accurate spectrum in order to compare it against absorption lines in the Sun's spectrum.
NASA's OCO-3: Watching Plants Grow and Glow: https://youtu.be/_x-VzdEeq0c

Not to be glib, but rather as a way of clarification, a google search for “chlorophyll fluorescence spectrum” returns a lot of results. Is there something else you are looking for?

@canadianer I'm not a biologist and asking well outside of my field. It's likely that someone knowledgable in photosynthesis will have a better sense where to look for something of high scientific quality and likely to be representative of the most common kinds of photosynthesis. Googling may bring lots of results, but some may be from esoteric species with unusual biochemistry, or may represent nonstandard experimental conditions. For qualitative results this googling was sufficient but here I welcome assistance from someone more knowledgable

I think for your purpose you should start, for example, with this link:
https://academic.oup.com/jxb/article/60/11/2987/533160
UPD:
Chlorophyllous tissues emit radiation of wavelengths approximately 680-760 nm. Source: Plant Physiological Ecolgy, Second edition, Hans Lambers, F.Stuart Chapin III and Thijs L. Pons, New York : Springer, c2008, p. 37, Box 2A.4 Chlorophyll Fluorescence

That looks like an extremely helpful reference, thank you! I will read it today. To be an answer to this question, it would be better to also include a reference that contained a spectrum as well. While there may be spectra in some of the references in that paper, they are likely to be paywalled and I won't have access for several days. If you can add a spectrum to your answer, that would be best.

@uhoh I've just updated the answer adding wavelengths diapasone

If you can find a spectrum but are having trouble posting its image here, let me know; I can help you with that. If you know a book and a page number, you might try to find it in google books and take a screen shot or add a link in comments.

@uhoh I have the book. Unfortunately, there is no image for the spectrum.

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How can we usually "trust a fart" not to be liquid or solid?
Jack Nicholson's character Edward Cole in the movie The Bucket List said ...and never trust a fart, and a search for Al Roker leakage White House will clear up any doubts what that's all about.
How is the adult human body usually able to sense the difference between solid, liquid, and gas and enable the brain to consciously decide on the proper course of action? (e.g stay put, walk, or run!)
Per @theforestecologist's request I'll restate the question using my best "science words": How are adult humans able to determine when pressure in the rectum is the result of solid waste, liquid waste, or flatulence?
A search for answers has turned up the following:
Source: https://www.sharecare.com/health/digestive-health/how-can-i-have-normal-bowel-movements

In a rapid "sampling reflex," these nerves inform the brain about whether the rectal contents are intestinal gas or liquid or solid stoo...

However I can't view this link further.
Searching further for "sampling reflex" I've found this

Sensing of the arrival of stool in the rectum with activation of the recto-anal inhibitory and sampling reflexes which allow stool to enter the anal canal and to be distinguished from flatus.

This provides an opportunity for sensation to take place, but does not describe how  stool is distinguished from flatus, and doesn't even mention liquid.
At this point I'm way out of my depth.

I actually think you've asked a valid scientific question here, but you've wrapped it in so much non-serious, non-scientific baggage that others are almost certainly to judge this question negatively. I don't think it should be closed (fyi it's not "opinion-based" as one close voter has suggested), but if you do not edit the question you'll have a tough time keeping it positive or getting an answer. Please update accordingly.

@theforestecologist thank you for recognizing the validity of the question, but I think the wording is quite positive! Nonetheless I've added a third sentence. fyi informal words like "fart" have been used in this SE site on many occasions without issue. Biologists are generally comfortable with discussing the human body and it's functions without hiding them unnecessarily behind clinical terminology, and I think in this case a clinical view is not necessary.

you've misunderstood me a bit. it's not the topic or even your choice of using the word "fart" -- these are ok in my opinion. Your entire 1st paragraph is unnecessary and distracting and sets the tone that your question is not serious but rather, it comes across as juvenile. I would delete the first paragraph & perhaps provide more biologically-focused background. We do ask that all question askers provide evidence that they researched their own question, so I recommend that you do some research on your own and then update the question by adding a bit more scientifically-relevant info.

@theforestecologist okay that's a more concrete suggestion, thanks. While I won't remove the levity or existing "research", I've "given it a go" so to speak and added some additional research.

"How is the adult human body usually able to sense the difference between solid, liquid, and gas and enable the brain to consciously decide on the proper course of action?" I think the question is incorrect; the nerves send the proper information to the brain, which then transmits the properties of the stimulus (solid/liquid/gas) to another part of our brain which informs our ability to control the tone of our rectal sphincter, if that makes any sense. It's not just semantics. It's neurology.

@anongoodnurse "...(e.g stay put, walk, or run!)" I don't know about yours, but my sphincter does none of the above. ;-)

Your sphincter is smarter and more athletic than you realize! :-)

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What causes the shape of the dense structure in this "giant squid egg" sac?
The YouTube video Swimming Next To Giant Squid Egg shows a giant egg of a squid and/or an egg of a giant squid. Text in the video's description includes the text quoted below, which indicates that the "egg sac containing hundreds of thousands of baby squid."
Question: The egg sac is mostly transparent and contains an optically dense structure with a very striking shape. If I didn't know it had hundreds of thousands of individual organisms, I'd think there was a brain developing at the top and a body forming below it. Is this shape just random? Does it change over time? Does it represent motion of all the little squids swimming around? It looks to me like it could be a slow-motion murmuration for example.

screenshots from the video linked above; click each for a full size view or just watch the video.

MANDATORY ONSCREEN CREDIT - Ronald Raasch
A team of divers filmed a rare glimpse of a huge transparent egg sac containing hundreds of thousands of baby squid.
The stunning underwater video was filmed by Ronald Raasch, 48, as he was diving with two other team-members from the research vessel REV Ocean in the cold waters outside Ørsta, Norway.
On October 5, the team of divers was swimming back to shore after visiting a WWII shipwreck about 200 metres from the coast, when they had a once-in-a-lifetime encounter with a mysterious object.
Floating 17 metres below the surface and 15 metres above the ocean floor, was a giant transparent orb which the divers quickly identified as a 10-armed squid’s egg sac.


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Why is an allele dominant or recessive?
Alleles refer to duplicate genes, where one allele can be dominant over the other. What makes an allele dominant or recessive, given that both code for a single protein?.

I edited your question a bit for clarity. Feel free to roll back if it is not to your liking!

There are several hypotheses about the evolution of dominance. It is important first of all, to note that empirical observations show that beneficial alleles tend to be more dominant than detrimental alleles. Among the two main hypotheses to explain the evolution of dominance, one has been formulated by Ronald Fisher and one by Sewall Wright.
Fisher's hypothesis
According to Fisher's hypothesis, between two equally beneficial alleles, if one is more dominant than the other than it's heterozygote carrier will have higher fitness. In consequence, beneficial alleles evolve to become more dominant while detrimental alleles evolve to be recessive (so that they can hide from selection in heterozygotes).
Wright's hypothesis
According to Wright's hypothesis, beneficial alleles are more dominant because of the kinetic of biochemical reactions. The rate of a biochemical reaction is a function of the concentration in the substrates of interest. The function is called "Michaelis-Menten function" after the name of the authors. The Michaelis-Menten function looks like this:

Think about a knock-out mutation. Such mutation will decrease by half the concentration of protein the gene in question produce in heterozygotes. Imagine, the concentration of proteins in the wildtype homozygote was 3 (see above graph). The rate of reaction of this homozygote is therefore about 3. The heterozygote would have a concentration of 1.5 and the rate of the reaction is therefore about 2.5-2.75. Assuming that the rate of this biochemical reaction is directly related to fitness, then a the locus of interest, benefical alleles are necessarily dominant and detrimental alleles are necessarily recessive. Selection for dominance is not involved in Wirght's model.
Is Fisher's or Wright's hypothesis correct?
Current state of the art is to consider Wright's model to be correct and Fisher's model to be wrong. In reality, the truth probably lies somewhere in between these two extremes. Note also that some other alternative explanations may exist in the literature but Wright and Fisher original hypotheses are by far the most considered hypotheses for the evolution of dominance. During my undergrad, I remember a speaker (but I forgot his name, sorry!) who showed that some alleles actually have some domain that are directly responsible for decreasing the expression of the other allele on the sister chromosome suggesting that Fisher's hypothesis might sometime be a good explanation as well.


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Loss of appetite during fever
It is a well-known phenomenon that sickness like the common flu is often accompanied by reduced appetite. Why do sick people stop eating?

@AliceD answered this eloquently and scientifically. The very simplified version is: if you were still hungry, you'd have to get up and do something about it. Today, that might be doable. But before food became so easy to obtain, the price metabolically of going out to forage/hunt while sick would be far too high.

@anongoodnurse - thanks for adding the reason why! I added a line with a reference of the merits of loss of appetite.

The psychologic and behavioral components of sickness represent a highly organized strategy of the organism to fight infection. Sickness is generally accompanied by fatigue, numbness, coldness, muscle and joint aches, and reduced appetite. These symptoms are not simply an effect caused by the pathogen. Instead, it now believed to be an active defense strategy of the body, referred to as “sickness behavior”. Sickness behavior is thought to be an adaptive response that enhances recovery by conserving energy to combat acute inflammation (Maes et al. 2012). It is triggered by the proinflammatory cytokines produced by activated cells of the innate immune system due to the presence of pathogens. These cytokines include mainly interleukin (IL) 1 (IL-1α and IL-1β), IL-6, and tumor necrosis factor α (TNF-α) (Dantzer, 2009; Plata-Salamán, 1998).
One of the sickness behaviors is a loss of appetite. Among a host of other effects, cytokines are believed to inhibit feeding by their actions in the hypothalamus. The hypothalamus is an important neural center that regulates food intake (Plata-Salamán, 1998; Meister, 2000).
I refer you to Maes et al (2012), Plata-Salamán (1998) and Dantzer (2009) for backgrounds and further reading, as cytokine immunology is highly complex and this answer is anything but complete.
References
- Dantzer, Immunol Allergy Clin North Am (2009); 29(2): 247–64
- Maes et al, BMJ (2012); 10: 66
- Meister, Vitam Horm (2000); 59: 265-304
- Plata-Salamán, Semin Oncol (1998); 25(1 Suppl 1):64-72


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Where does moss come from?
I've been growing plants in pots for several years, and in some of my pots a patch of green moss appears and steadily grows to fill the whole surface area of the soil. But that doesn't happen in other pots. I've used different bags of soil for different types of plants, but moss doesn't seem to appear only in one type of soil from the same bag.
How does moss appear in the first place? Or is it present in all soil and only grows to a visible size under certain conditions?

Moss produces spores that can travel great distances. If these spores land in favourable conditions, then it will grow there.

Almost seems like a question for the Gardening SE, but I've always wondered about it myself. Always just assumed that humidity + soil = moss. Um... 'cuz reasons.

Short answer
Moss plants form spores; minute, invisible, typically one-celled, reproductive units that are carried off by the wind and into your pots.
Background
Mosses belong to the Bryophytes. Bryophytes are embryophytes; i.e., non-vascular land plants. They are spore-producing, rather than seed-producing and they do not bear flowers.
The leafy moss plant you are describing is the sexual phase of the moss life cycle. When mature, most mosses develop sex organs. Under wet conditions, sperm cells are released from male sex organs (antheridia) and swim to the female organs (archegonia), attracted by a chemical released by the female organ. After fertilization, the egg cells that are embedded in the female organ form a spore-producing plant. This consists of a stalk with a spore capsule and stays attached to the parent moss plant. As the spore capsule matures, it releases its spores into the air, and then dies. If moss spores fall in a damp place, they germinate and grow into leafy moss plants, and the cycle is completed (Fig. 1).
Hence, to answer your question - moss appears in your pots when spores land into it and enough water is available for their outgrowth.

Fig. 1. Reproductive cycle of moss. source: Encyclopedia of New Zealand

I fail to see how the leafy plants are  neccessarily the sexual phase, the sex organs of the mosses are the spore capsules shown in your picture. Some moss plants do not even produce these. Otherwise good answer.


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What processes are responsible for focusing on an image only seen by one of the eyes?
When a person is spying from around a corner with only one eye, it's rather easy to ignore the other eye's image, since it's probably much darker, because one usually spies around a corner standing close to a wall.
But if both eyes get equally bright visual input, it takes some effort to try and stay focused on just one of them. What processes in human body allow such action?

Short answer
Image blur on the retina is the most important monocular cue for lens accommodation.
Background
Focussing of an image on the retina is mediated by the lens. Re-shaping of the lens to focus the image on the retina is called accommodation. In general , the main cues for focussing are retinal disparity and blur, and to a lesser extent proximal cues such as looming, motion parallax and overlay of contours.
When looking with two eyes (binocularly) at an object, retinal disparity is by far the most important depth cue for accommodation. The two eyes look at an object from slightly different angles, so they get slightly different views of it. This difference is the disparity (imperfect match) between the two views. The visual system normally fuses these two images into a single perception and converts the disparity between the two images into perception of depth (Source: Indiana university).
When only one eye is available (monocular focussing), use of retinal disparity isn't possible, and retinal blur becomes the most important factor for lens accommodation. When an image is out of focus, its representation on the retina is blurry. By adjusting the shape of the lens the visual system adjusts the image projection to bring it into focus such that blur is minimized (Horwood & Riddell, 2008). Looming (incoming object becomes apparently bigger), motion parallax (objects further away move slower across the field of view) and overlay of contours (objects closer by obscure things further away) also provide monocular cues for accommodation.
Reference
Horwood & Riddell, Vis Res (2008); 48:1613–24


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Do blind birds bob their head when they walk?
Birds try to keep their heads still for short periods of time between steps to improve their ability to see. You can find amusing videos of chickens used as small video camera stabilizers. But does this happen to blind birds? Is it something all birds do regardless of their ability to see?

I did not know that birds (mainly pigeon and a few other species) are moving their head the way they do when walking in order to improve their vision. Do you have a reference for that?

@Remi.b I wouldn't be surprised if it was influenced by this question.

Oh indeed thank you. @user1306322 you should relate (and link) to this post (if it is indeed your reference) and make sure to not over interpret what is being said (it does not talk about walking).

My question was inspired mostly by Mumbles, a chicken born without eyes and prior knowledge about the reason why birds bob their heads. No SE questions were used as inspiration for this post. I'd appreciate if users did not assume unnecessary things for everyone's sake here.

The forward thrusting movement so peculiar of pigeons and other fowl (Fig. 1) while walking is thought to be related to shifting the visual field. The less visible backward motion of the head is thought to be related to fixating the field of view (Dunlap & Mowler (1931).
According to the meticulous observational study by Dunlap & Mowler (1931), blindfolded pigeons stop making head movements altogether while walking. They stop their forward thrusting motion, the backward motion as well as more random scanning head movements. Hence, the authors conclude that the forward and backward jerking movements are related to vision, and not to hold their balance or whatsoever.

Fig. 1. Snapshots of a pigeon walking. The head thrusts forward in the middle frame. source: Dunlap & Mowler (1931)
Reference
- Dunlap & Mowler, J Comparative Psychol (1931); 11(1): 99-113

Is there any other, more recent study on the subject? 1931 was long ago, and it would be strange if no one had investigated this ever again.

@RichardHardy not that I know of, no.

That was fast! Thanks! Does it not seem a bit weird that there are no newer studies? I assume we just might not know of them, but I am not a biologist (nowhere near).

@RichardHardy, yes there might be newer studies.  I must say it took me quite some time to find even one study addressing this. And unfortunately,  it's pretty dated indeed. But nonetheless, it was a well controlled study as far as I can see and it addressed the question here quite directly. And in fact,  I seriously doubt there is any newer study on this,  but I can't be sure.

@AliceD by any chance do you know how one could instigate researchers to organize such a study these days? Perhaps by sending some emails to parties interested in making viral study videos (the credible kind)?

Here is a related YouTube video bearing essentially the same message.


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Is Canine teeth enough evidence to prove that one is a Carnivore?
This question does not assume that we are meant to be carnivores in the first place; In fact I have no idea to which category we belong to anyway! There are several posts online indicating that classifying humans as carnivores and pointing to our canine teeth as evidence might be fallacious.
Also, the fact that Hippos, the largest canine teeth of any land mammal, are herbivores indicates there are exceptions to this view. A couple of other animals like the Gorilla are also herbivores with big and sharp canines. I have also read about the lack of cellulace production in humans as a counterargument to the above.
To what category would we fit in to? What evidence is required to support this idea? Do scientists agree upon a common theory?

We are pretty clearly omnivores.  Our teeth, and more importantly, our actual habits, confirm this.  It is possible for us to live an exclusively herbivorous or carnivorous lifestyle, of course.


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Why is it better to drink room temperature water instead of cold water?
My teacher told me that drinking water that is room temperature is better for you then drinking cold water, but she did not tell me why that is. I want to know because I often drink cold water (with ice), because I can't stand water that is room temperature or warm.

Are we even sure this is true? Countervailing attitudes to cold water exist.

Drink warm water, because calves choose the same! ;-) I don't think it has any significant effect on your health. You may get easier sore throat if you drink too cold, but that's all...

I think this would better fit to skeptics.sx.

I don't there is much difference. The only reason I can think of is that cold water lowers your temperature and therefore your body needs more energy.

better fitted for skeptics SE

http://www.jissn.com/content/pdf/1550-2783-9-44.pdf - this link may answer your q....partially, though...


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What's the name of this caterpillar?
It was found in the state of Virginia, on the east coast of the United States.

I think it might be a species of Fritillary. Below is a picture of a Marsh Fritillary.

Marsh fritillary. Source: Butterfly Conservation.org
I do not think it is a woolly bear or giant leopard moth, just because the hairs seems too sparse for a woolly bear and it lacks the distinct red striping of the giant leopard moth caterpillar. It does not seem to be arctiinae to me.

Could you add a picture of you suggested species? Regardless, +1

http://butterfly-conservation.org/files/marsh-fritillary-larva1_peter_eeels_web.jpg Maybe a marsh fritillary.

It's Woolly Bear Caterpillar: http://en.wikipedia.org/wiki/Pyrrharctia_isabella

Can you explain why you think so? This looks quite different then the larvae that show up in a standard Google search.

Its spikes are short so the closest match I can think of was Woolly Bear. But it can be Giant Leopard Moth Caterpillar.


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What species does this moth belong to?
It was found a few days ago in the state of Virginia, on the east coast of the United States.

Hemithea maybe, is as close as I can figure, although since there is so much variation between them it is very hard to tell.


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How can bats hear such high frequencies?
I attended a talk that glossed over some biology as it was talking about a certain protein. The speaker mentioned humans can hear up to, often less than 20kHz frequencies, whereas bats can hear up to 100kHz. Presumably this is to do with differences in cochlear anatomy.
What about the inner ear of bats is different form ours, and how does this allow them to hear such high frequencies?

Short answer
Echolocating bats have relatively large sensory epithelia in their inner ear, that may correlate with their high upper frequency limit of up to 200 kHz. The basilar membrane is thinner and stiffer, possibly allowing it to decode higher frequencies.
Background
In terms of the place theory of hearing, the cochlea acts as a frequency transformer, where high frequencies are encoded basally, and low frequencies apically. The cells responsive to sound, the hair cells, are located along the basilar membrane (BM). Going from base (high frequency) to apex (low frequency), the BM becomes wider and less stiff, making it more susceptible to encode low frequencies apically. Note that sound is encoded as a travelling wave, where the point of resonance of a particular frequency corresponds with the characteristic frequency of the hair cells (Fig. 2).

Fig. 1. Rolled out cochlea. Source: New York University.

Fig. 2. Travelling wave and resonance frequencies along the basilar membrane. Source: University of Minnesota.
A study in Microchiroptera species revealed that the basal part of the basilar membrane was relatively narrow and stiff, which increases the resonance frequency of the basal part of the BM and hence may allow it to encode higher frequencies in these bats (Pye, 1966).
Because the high frequencies are encoded basally, it would be tempting to speculate the basal region would be enlarged in echo locating bats. Although this is true in some species, it may have more to do with frequency sensitivity than the upper limit of hearing, simply because a larger surface of the BM allows for more exquisite resolution of the BM. Although there is a tendency for larger BM lengths in echolocating bats, it is not consistent (Davies et al., 2013).
The human BM is 33.5 mm, while the BM of the bat with the highest frequency limit known (200 kHz, Hipposideros bicolor) is only 9.13 mm. However, compared to that of acoustically unspecialized mammals of a similar body size, e.g. Sorex araneus (BM length 4.4 mm) and Mus musculus (BM 7.0 mm) it is relatively long. However, as said, other bats with lower upper-frequency limits have longer BM lengths, e.g., Pteronotus parnellii (13.2 mm) and Rhinolophus ferrumequinum (16.1 mm). Indeed, the BM length has been correlated both with an extension in frequency range as well as enhanced frequency resolution (Dannhof & Bruns, 1991).
References
- Dannhof & Bruns, Hear Res (1991); 53: 253-68
- Davies et al., Front Zool (2013); 10: 2
- Pye, J Morph (1966), 118: 495-510

i really don't see how this is an answer. Any other differences except length of BM? cellular anatomy? Different properties of fluid in the cochlea? I believe there is more to it than page from Encyclopedia Britannica

@aaaaaa, I have added material. Thanks for the suggestion. But what page of Britannica? I haven't used it here? There are three credible references listed.

What's also important is basilar membrane thickness, since that is part of what dictates the resonance at various frequencies (as I understand it, thicker = stiffer = higher frequencies).

@AliceD If being thicker at the basal end promotes lower-frequency hearing, than why are the higher frequencies transduced at the basal end? I know width matters, too, but it seems thickness results in stiffness, which--per given load?--should resonate with higher frequencies. E.g: "Part of the stiffness change is due to the increasing width of the membrane and part to its decreasing thickness." (link: http://147.162.36.50/cochlea/cochleapages/theory/bm/bm.htm)

@AliceD Right--my comment was intended to suggest that perhaps these bats have thicker basilar membranes than humans do. But yes, there are other structural factors (and active tuning) which would also be at play.

@Chelonian I understand, but the Pye article is reluctant to interpret thickness as causative factor, also because it can have the opposite affect, dependent on the load on the basilar membrane etc. Very detailed studies across species could elucidate this, but to the best of my knowledge only gross-anatomical features like the ones discussed in this answer have been addressed.


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Patch-Clamping Neurons Resources

Are there any lectures available on Patch-Clamping?
Were can I find a mathematical model of Patch-Clamp? (that can be easily implemented in matlab).
I have found some step-by-step protocols on (Springer book site) but nothing to useful--I am setting up a new rig. Where can I find protocols that have worked and have been tested?

"The Axon guide for electrophysiology & biophysics laboratory techniques" is a very good starting point, albeit a bit biased towards Axon instrumentation. The book used to be hosted and freely downloadable on the Axon Instruments website but since they have now been acquired I cannot seem to find an official link anymore. However many other websites still host it (I won't directly link to them, as I am not sure about the licence of the book. Anyway, again, it used to be available for free).

That is one of the basics of neurophysiology. You will find video lectures on youtube. 2. See GHK (Goldman-Hodgkin-Katz) model

@nico : could you perhaps convert your comment into an answer? This question may not survive. The question is quite broad, but your comment is equally broad and is quite apt. I like it!

@ChrisStronks if nico doesn't respond then we can paste the comment and post it as community wiki

@WYSIWYG I didn't know that was possible?! Interesting! (I'd like to know more about that - something for chat:-) Anyway, I would definitely prefer your suggested option above waiting for the question to be deleted, which will be anytime soon

@ChrisStronks well, the question is on hold now...


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Why would lactate be high in diabetics?
Why are lactate level high in diabetes? For example, type II diabetes are resistant to insulin. If those patients are insulin resistant their gluconeogenesis should be working at a high rate and, because of that, lactate uptake by the liver should be removing lactate from the blood.
Alternatively, type I diabetics don't produce insulin, so the ratio insulin/glucagon would always be very low and gluconeogenesis should be stimulated... So I don't understand why lactate levels are high in diabetes... Can someone help me?
PS. This question came up after doing an experiment in school, with diabetic rats and normal rats. Diabetic rats had higher levels of lactate and my professor said that it was because the diabetic rats don't perform gluconeogenesis and so, lactate accumulates in the plasma. But it doesn't make sense for me.

I talked with my teacher and he said that one of the reasons that can contribute to this state of high lactate in diabetes is that diabetes patients are more likely to use aminoacids as gluconeogenic precursors than lactate, so lactate will accumulate in their blood. Hope this helps someone in the future.

This condition is also known as "lactic acidosis" and can be pretty dangerous, since it influences the pH of the blood.
When we metabolize glucose to produce ATP and NADH it is metabolized finally to pyruvate in a process called glyolysis (I am not going into detail here since this is nicely explained in the Wikipedia). Pyruvate can then be used further in the body in the Gluconeogenesis, the Citric acid cycle and other pathways.
If a lot of energy is needed Pyruvate is converted by the pyruvate dehydrogenase into acetyl-CoA.
The problem with diabetes is that the pyruvate dehydrogenase can be inhibited in diabetes. If the body then needs a lot of energy pyruvate will be converted into lactate which is released by the cells into the bloodstream.
Gluconeogenesis cannot be activated since this needs either Pyruvate, Acetyl-CoA or Oxaloacetate as starting material. The other problem with this process is that this happens in the liver and when the glucose is released into the bloodstream, it cannot be taken up by the cells due to the lack of insulin.
The conversion from Pyruvate to Lactate is katalysed by the Lactate dehydrogenase and needs NADH + H+ as a co-factor. The image below is from the Wikipedia article on Lactate dehydrogenase.

This reaction is highly exergonic which means its preferred direction is to the right side. To change this and make Pyruvate from Lactate you need an excess of NAD+ which usually only happens in the liver.
There is also an epidimiologic study available showing a strong correlation between elevated blood lactate levels and diabetes type II: "Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study."

Thanks, It was clear and explicit! But, one thing, can't you use that lactate to form piruvate by lactate desidrogenase and build a source of pyruvate to gluconeogenesis? Because if you think in the glucagon/insulin ratio (in type I) or insulin non-action in type II , the gluconeogenesis would be stimulated.

Yes, and it dependends on the redox state of the cell, right? So if there's NAD+ sufficient, lactate should be converted to pyruvate... But okay, I'm beggining to understand why it can happen, although it's not clear for me the full mechanism. Thanks! :)

Part1- What is not completly clear for me is how the accumulation is so noticeable since, by the way I was thinking, some gluconeogenesis is still ocurring. For example, in a normal person, insulin would bind to receptors and stimulate mTOR--> Akt --> akt would inhibit gluconeogenesis. But in Diabetes Type II, that mechanism would not occur because the receptors wouldn't sense insulin, so gluconeogenesis would actived.

Part2-Now imagine that the rat is in the fasted state, it would be using fatty acids as fuel source, so there will be a lot of acetil-coA in the mitocondhria and NADH. If there's a lot of acetil-coA, piruvato desidrogenase would not be active, some glucose that would have been turned to piruvate would be converted to oxaloacetato by pyruvato carboxilase. So OAA and lactato could begin the gluconeogenic pathway... what am I thinking wrong?

Yes, because Gluceoeogenesis uses energy to make glucose. The body on the other side needs energy badly (otherwise it wouldn't go for lactate. The production of lactate also consumes a lot of NADH (which is needed as you stated yourself in Gluconeogenesis) so it really doesn't make sense to build up (and use and conserve energy) and use it up at the same time.

Hum, ok! In the case of diabetes, if gluconeogenesis is not active in the fasted state, would ketone bodys be the only fuel for the brain?

Under certain circumstances this can happen. This is why diabetic patients can smell after acetone when they have problems with their insulin.

Ok, now it makes sense. Because of the high NADH/NAD+ ratio, oxaloacetato would be shifted to malate and would not react with the acetil-coA released by oxidation and fatty acids. acetil-coA would go to ketone body synthesis, and with no oxaloacetato, there will only be one precursor left which is lactate. NADH could drift lactate to piruvato, but since it is being exported means that there's a lot of energy expanding going on, so It's not acceptable to use energy to make glucose! Thanks a lot :)


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If tinnitus is, in many cases, caused by damaged ear hair cells, couldn't it be solved by a mini cochlear implant that sends a constant signal?
If my understanding is correct, tinnitus is in most cases caused by damage to the inner ear hair cells, especially on the basal parts of the cochlea, which correspond to high frequencies. So, for example, you lose a few hair cells on the high frequency range (such as 14,000 Hz). This causes your brain to over-compensate the lost signal by essentially down-regulating the activation threshold of that range so much that it ends up assuming the cell is always on, rather than always off.
If that is correct, wouldn't a simple cochlear implant that replaced the lost cells by a dummy electrode that sent a "silent" signal 24/7 solve tinnitus? That electrode would emulate the signal that the lost hair cell would send when silent. That way, as soon as the brain receives that "silent" signal, it would up-regulate the activation threshold, and the ringing would stop.
There are ongoing trials that involve injecting stem cells, or small molecules such as FX-322, in order to re-grow lost ear hair cells, and these trials have shown some success against tinnitus, so, there is some evidence that restoring the absent signals lets the brain renormalize. The catch is, we shouldn't need fully functional hair cells to cure tinnitus. Replacing these cells with a dummy "always silent" cell would do the same job. Of course, the patient wouldn't be able to hear on these ranges, but I don't think most tinnitus sufferers want the ability to hear snapping shrimps, they just want to shut up the ringing.
Is my logic or understanding flawed?

How would you attach the electrodes without occluding the opening of the cochlea or otherwise interfering with the rest of the hearing range? It's  also highly invasive and expensive as the demands of asepsis and precision required are enormous. Apart from those concerns, do you have evidence that an approach like "sending a silent signal" might work? (Perhaps tested on other less-invasive parts).

@JiminyCricket. aren't cochlear implants a common procedure? Except these need to cover the entire hearing spectrum, and be connected to an outside device that sends precise signals, and decode these into the right impulses to emulate cells. So, we have these relatively complex devices as a common procedure already! A dummy electrode that just sends a 24/7 "silent" signal looks trivial in comparison. I could be (and probably am) wrong, but I'd love to learn why/how!

Short answer
You are right, with a few caveats.
Background
Most tinnitus cases are caused by sensorineural hearing loss, as you rightfully indicate, namely due to a loss of hair cells in the cochlea. The deafferentation of the auditory cortex and subsequent chronic inactivity of this region in the brain ultimately leads to the generation of intrinsic brain activity in the auditory cortex, which is perceived as a 'ringing in the ears' (PloS Med, 2005).
Cochlear implantation has been shown in a multitude of studies to ameliorate the symptoms of tinnitus; for a review see Linhares de Freitas Borges et al., (2021). CIs basically mask the tinnitus sounds by swamping it with electrically evoked activity in the auditory system.
A CI is a medical device for treating severe-to-profound hearing loss. It bypasses the damaged hair cells in the cochlea, and restores activity in the auditory nerve by direct electrical stimulation of auditory nerve fibers (Fig. 1). CI is, however, not a first-line treatment for tinnitus and remains in the experimental phase for that purpose, at least as far as I know. Tinnitus has been mainly addressed as a secondary outcome to hearing performance after CI for treating deafness, although prospective randomized controlled trials with tinnitus relief being the primary outcome are underway (Assouly et al., 2021).
However, your idea of a single-electrode 'dummy implant' isn't very feasible, because it is difficult to insert a cochlear implant such that one or more electrodes are in direct electrical contact with the cochlear region corresponding to the frequency (or frequencies) of the tinnitus (Fu & Shannon, 2002). The cochlear regions with hair cell damage differs between patients and depends on the type of hearing loss. Therefore, a regular CI with a multi-electrode array is inserted that covers the better part of the cochlea (barred the low frequencies).
Furthermore, a 'silent' (i.e., below threshold) electrical stimulus would make not much sense, as you wouldn't know when sufficient electrical activity was generated. Rather, these folks are treated with a CI and fitted with a with a clinical program to restore hearing function in that ear.
Another note of importance is the fact that CI results in substantial loss of the residual hearing in the implanted ear due to insertion trauma, and scarring later on. That's why treating an ear with tinnitus due to localized trauma (e.g., noise-induced hearing loss, for instance due to occupation or in professional musicians) may not be a good idea, because a CI doesn't restore acoustic hearing, it allows for the restoration of some hearing function, but it will never be anything like a normal ear. That's why, in general, only ears with severe-to-profound hearing loss should be treated with a CI, including for tinnitus patients (Punte et al., 2011. In the end, it will be a cost-benefit consideration between physician and patient to determine whether the loss of residual hearing weighs up against the chance and extent of treating the tinnitus.

Fig. 1. Cochlear implant system. Source: Mayo Clinic
References
- Assouly et al., BMJ Open (2021); 11: e043288
- Fu Shannon, Ear Hear (2002); 23(4): 339-48
- Linhares de Freitas Borges et al., Brazilian J Otorhinolaryngol (2021); 87(3): 353-65
- PLoS Med (2005); 2(6): e194
- Punte et al., Cochlear Implants Int. (2011); S1: S26-9

Thanks for taking your time to provide this extremely information-rich, well-researched answer. Just a small clarification, if I may: as we know, cochlear implants are designed to restore hearing, not to treat tinnitus. If treating tinnitus requires a simpler mechanism (i.e., constant stimulus, and covering just the outer part of the cochlea), it is still possible that there are simpler interventions that don't require drilling the cochlea, right? Or would anything in that space absolutely need to be internal?

@MaiaVictor thanks, happy to write about this stuff! I happen to work in the field :) I have clarified the answer (CIs are indeed designed to treat hearing loss, no more, no less). I however am afraid I don't understand what you mean with 'the outer part of the cochlea'. The cochlea is a bony structure and the auditory nerve cannot be accessed electrically easily through this bony capsule because of resistance issues. The reason that it is inserted in the cochlea is to maintain tonotopic (frequency specific) stimulation...

...this way functional hearing can be more easily restored. Because often tinnitus is caused in deafened ears, treating deafness and collaterally tinnitus is an interesting option. In case tinnitus is caused by causes other than profound hearing loss, a simpler solution may work, yet you have to mask the tinnitus by providing perceivable sounds. Therefore you could generate electrical white noise, but that would impair normal hearing, effectively making you hard of hearing. Inserting a CI at least provides you with meaningful stimuli. I have added the 'masking' effect in the answer, thanks!

I was thinking of stimulating the auditory nerve as it comes out from the cochlea, but now I see why that would be impossible. Thanks again for your answer. This disease is debilitating, and the fact it doesn't have a non-psychological treatment is depressing. I hope this will change soon.


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How do cold conditions help organ transplants?
Body organs are kept cold in-between explanting them from the donor and implanting them in the new host. How do these cold conditions help organs to stay viable while they haven't fresh blood, energy and oxygen supply?

I edited the wording slightly. If you aren't happy with these changes feel free to roll back.

No worries, +1, nice question

By lowering down the metabolism of these organs. Since metabolism is lowered the requirement for oxygen and energy goes down.

Thanks, its true but I am looking for a more informative answer like SolarLinux's answer.

This paper actually goes into the whole history of organ transplants.
In short it seems to have the following effects:

preservation - usually with a specific solution to help.
slows down extracorporeal ischaemic damage
slows down hypoxic damage
slows down the metabolism (energy consumption) and thus the need for oxygen that blood provides.

Remember that the cooling doesn't allow the organ to live indefinitely, and may only work for a few short hours depending on the organ.
I highly recommend reading the paper if you'd like to know more about organ transplant. They went into great detail about the past and present and the abstract also says they discuss new techniques about to be don't in clinical trials.

This site is so useful and its participants are great. Thank You

Of course, glad I could help. I was quite impressed by the paper myself @MySky


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What is the impact of sertraline on white blood cells?
This simplified video and RT.com article discusses how the mechanics of the death of a white blood cell can be useful as an "alert mechanism" to other white blood cells of an incoming infection.
Also in the article it describes how this same notification mechanism might enable the transmission of certain types of pathogens and it has the following quote:

"We found that a commonly used antidepressant can block this whole process and an antibiotic can promote this event,” said Ms Atkin-Smith.

The full report is available here.
Can anyone explain, (with a summary in layman terms) the impact of Sertraline on white blood cells?
Does taking Sertraline increase the risk of susceptibility to illness, or decrease it?

Short answer
While sertraline may theoretically affect the immune system, there is no evidence, as far as I know, that it negatively impacts immune status.
Background
In the article (Atkin-Smith et al., 2015) sertraline (a.k.a. Zoloft, an antidepressant) is shown to block the formation of ‘beads-on-a-string’ protrusions and apoptotic bodies after from dying white blood cells.
Generally, when cells die physiologically, they do not just disintegrate, they undergo programmed cell death called apoptosis.

Beads-on-a-string from a apoptotic monocyte. Source: (Atkin-Smith et al., 2015).
The authors hypothesize that these beads-on-a-string and apoptotic bodies may boost immune responses by containing antigenic material, or that they may contain a warning signal for other immune cells that a pathogen is on the loose.
These claims, however, are hypotheses.
There are many reported side effects of sertaline, but immune suppressant effects are not evident. The only side effects reported touching on it are, e.g., a fever and a sore throat. However, such general symptoms can be caused by a variety of causes and were not reported frequently.
Indeed, in a small study in HIV patients, sertraline showed no adverse effects on the immune system (Rabkin et al., 1994).
References
- Atkin-Smith et a. Nat Comm (2015); 6: 7439
- Rabkin et al. J Clin Psychiatry (1994); 55(10):433-9


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Possible to remove accumulated haze on fluorescence interference filters?
I have a few different fluorescent microscopes, the two that use Mercury  lamps are older than 7 years. I notice on those that the thin film filters in the filter cubes (green, red, blue) have accumulated this haziness. Both the excitation and barrier filters seem to have this, more so on the ex filter and it's not present on the dichroic.
I've always referred to this as the filter being "burned" and my rational is that it's from the heat & intensity & low wavelengths from the Mercury lamp.  But in all honesty I don't know what it is or if it's removable and if so how? I would like to see if removing it improves my image clarity.
I know a picture would help here and I'm having trouble showing it but will keep attempting and add it to an edit for this question. However I have seen this on many microscopes if you have one with a merc arc lamp and it's getting up there in age take a look at the filters on it. Let me know if you see this too.

In fact, filters can be damaged by heat. However, newer filter coatings are less prone to heat damage [details].
For the barrier filter, it's less likely to be heat damage. The older/less expensive filter coatings do degrade slowly over time and have to be replaced.
So I would guess that the haze represents permanent, non-removable damage to the coating. You should replace the filters with hard-coated filters, which are more durable if you do ever need to clean them for some reason.
Just to be safe, you may want to get a heat filter between the lamp and the excitation filter. One caveat with the heat filter: if you are using near-IR dyes (Cy5/AlexaFluor 647) check the transmittance of the heat filter to make sure it doesn't interfere with the ~640 nm excitation.

Its probably not from heat.  Filters are basically a glass substrate with some ionic compound deposited in thin layers.  These won't oxidize at reasonable temperatures, and furthermore since you have it on the emission filter as well, its even less likely to be from the source.
More likely its just accumulated organic material from the environment.  7 years is a long time, and microscopes are exposed to a lot of chemicals and other substances which can gradually build up on optical surfaces.
Most vendors have a recommended way of cleaning their optics, but usually it involves lens paper or lint free swabs and methanol (or sometimes acetone for more durable stains).  You must be very careful though, as you do not want to scratch the filter.
Semrock for instance has a detailed guide here:
https://www.idex-hs.com/resources/resources-detail/how-to-clean-optical-filters

Thank you for this I haven't considered that strongly. However other glass on console is fine however. The excitation filters are considerably more burned than the barrier ones on the cubes. Your right about the time however. I have tried solvents but they don't remove it. I need/will get a pic up for this.

Thats interesting.  I haven't seen something like that, but if even acetone won't clear it, then I think you'll have to replace it.  Possibly its just a poorly made filter that degraded over time.


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Real-time PCR result interpretation
I performed real-time PCR and I was looking for expression fold changes for 2 genes and I had two sample pools, one treated and the other not treated (for each gene). The problem is that my housekeeping gene (UBQ 30) got a fold change on the treatment. Therefore, what is the correct interpretation and data treatment?
I mean, is it correct to use each control and treatment I got for UBQ CT values to normalize the other two genes corresponding CT, as housekeeping genes are "by definition" expected not to change? (and that is why indeed they are used to normalize)
or should I rather make a mean of my whole UBQ CT-s and normalize all other genes CT values with that mean?

In principle the housekeeping genes should be constant. But: Changes, that happen to the whole cell, can happen. So it is advisible to have more than one housekeeping gene if possible.

You should try another housekeeping gene like GAPDH since the very definition of these genes is that they shouldn't change with your treatment

good advice - this is a list of even better ones...http://www.ncbi.nlm.nih.gov/pubmed/17394773

There is quite a list of genes that can be used - sometimes even GAPDH or Actin change. This needs to be verified for each experiment.

and how could i objetively discrimine if a given change for CT values is significable as to consider to change my housekeeping gene?

As Chris says you will have to verify that your housekeeping gene doesn't change between experiments.

As pointed out by others a reference gene should not change its expression between the control and test samples. Reference gene need not be a housekeeping gene; housekeeping genes are generally used because they are present in all cells are are not subject to any specific regulation. However, global changes in the cell, such as stress or development, can affect housekeeping genes.
When you are not sure about which gene to choose as a reference then you can use a spike in control.
The change in your experiment could be a result of human error. You should replicate the experiment to see if the trend remains the same. If your gene shows consistent trend in all replicates then the change is not likely because of human error.
In general you should choose the reference gene based on your prior knowledge about the condition that you are testing. For example if I am studying cell migration then I would not use Actin as a control. If you are studying processes that may affect metabolic rate then you should perhaps not use GAPDH as a control.
Another good reference gene(s) that is also constitutive would be that for a ribosomal protein.
Also have a look at this post for statistical analysis of RTPCR data.

I'm gonna throw a curve ball here. :) I think the "housekeeping" or "reference gene" concept is fundamentally flawed, because it rests on circular logic. In order to verify that a "housekeeping" gene X is constant across your samples, you must assume that the $C_t$ values themselves are actually a valid measure, so that you can assess the expression level of X directly. But if $C_t$ values are assumed valid, then you don't need a housekeeping gene in the first place! This procedure assumes what it intends to prove; therefore it is circular.
The normalization problem is just not solvable without additional assumptions. A spike-in control works if you are worried about technical variation, but it does not address biological variation. A reasonable assumption I think is that the total mRNA pool is constant; this underlies most normalization methods used in microarray or RNA-seq analysis. For RT-PCR, this assumption can be tested using cDNA dyes, as in this paper. (cDNA is advantagous rather than isolated RNA, because the reverse transcription step is notoriously noisy and should be controlled for.)
In my mind, housekeeping genes are only useful it you really know in advance that they must be constant, and do not need to check this assumption; then the logic is not circular. In this case, if you observe changing $C_t$ values for the housekeeping gene, then you must conclude that the experiment went wrong somehow, and the data should be discarded. But I think this is rarely the case in practise.
This is not the most common opinion on this often-debated matter, but I think it is the right one. :)

1. Regarding the vicious cycle of reference gene selection:  Ideally there should not be a change in Ct value if there is no change in expression. There may be no need to have a reference gene if situation was always ideal. Here, reference gene simply does the job of a loading control. The perfectly done experiment may not need one but getting that perfection is hard; but once you have established a right reference you can forget about perfection.

2. Regarding spike-in: In cases where there is biological variation of the gene pool, spike-in would be particularly useful. For example, during growth/development a lot of proteins accumulate, including housekeeping genes. They may even be subject to regulation. Spike in would let you know the absolute change in the RNA expression. In these cases the housekeeping gene can also be used to understand correlation and differentiate general regulation from specific regulation. In certain cases you can transfect the spike into the cells prior to RNA isolation.

I however concur that the choice of reference is dependent on prior knowledge about the condition. +1 for the alternate opinion :)

@WYSIWYG, regarding (1), my point is that in order for a  gene X to be a control for suspected variation in Ct, we must assume that gene X is constant, and we cannot verify this by measuring Ct; that becomes circular. For (2), yes spike-ins allows quantitation, but doesn't solve the normalization issue, you still need to relate the measurement to something --- tissue weight, cell number, total protein, or RNA (which I suggested).


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The arrangement of retinal cells?
The section of retina shows a layered arrangement of the various retinal cells. Starting from the inside (where the light strikes first) is the nerve fibre layer, ganglionic layer, amacrine cell layer, bipolar cell layer, horizontal cell layer and finally rods and cones (and that too in inverted position, i.e. the actual receptor portions are farther inwards).

Why is this stratification inverted? If the receptors would have been the innermost cells, they could have received the maximum
  quantity of unaltered light. Does this "inverted" arrangement, i.e.
  arrangement with the receptor cell behind a screen of several other
  layers not hinder the process of photoreception by blocking a lot of
  incident light and hence the formed image? What is, if any,
  advantage of this reverse arrangement?

I don't have an other explanation than pointing to evolution. It was obviously not a problem to evolve the way it did. One article I found (see "The Inverted Retina: Maladaptation or Pre-adaptation?") called it a sign of pre-adaptation, where forms exist before they get their final function.
Another pretty comprehensive review can be found here: "Evolution of Phototransduction, Vertebrate Photoreceptors and Retina."

Thank you. And great references, as usual.


text:
TSS of a gene vs TSS of a transcript
I have an annotation from gencode.vM1.annotation of a mouse. Exons, genes, transcripts and UTR are listed there. For each feature a start and end positions are present.
I need to find a TSS for each gene. Will it be wrong to define one TSS for all transcripts belonging to one gene? So, I want to define a TSS for each gene as a minimum start UTR from all transcripts.
Example:
gene id, transcript id, feature, start, end

gene A, transcript A1, UTR, 102, 205
gene A, transcript A1, UTR, 506, 520
gene A, transcript A2, UTR, 78, 205
gene A, transcript A2, UTR, 502, 512

So, for gene A I would define a TSS on position 78 (minimum start UTR). And the gene body end on the position 520 (maximum end UTR).

There is no TSS of a gene. Geneic region will be a union of all the transcripts arising from that locus (including introns).
Sometimes two variants of a gene can have different TSS. You can define a 5' boundary of the geneic region which would be the most 5' TSS amongst all variants. You can also give scores to the TSS based on the expression of the different transcripts.
Nevertheless, I am not sure why you want this.


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Is consuming proteins different vs. consuming amino-acids and how?
Yesterday I had a discussion with a friend. He said that consuming proteins and amino-acids is different. He said that those who grow muscles would agree on that. I wanted to argue against that statement, but I lacked arguments... As far as I know, amino-acids are part of proteins. So, when proteins go to our body with food, we digest it and make amino-acids. Then they can form any kind of proteins we need. The same would happen when consuming amino-acids directly, not in protein form. Maybe then the process would be faster. But from my point of view, there is no much of a difference. Could anyone please give me a more sound opinion on why is consuming proteins and amino-acids different, if it is?

I am not an anabolic expert, but I bet that for growing muscle specific aminoacids are needed more than others. Hence, consuming aminoacids may give the body builder the opportunity to provide targeted supplements?

Essential amino acids are important for muscle synthesis. The only benefit I could draw from consuming amino acids is that there's some time-dependent benefit vs digestion time of whole protein. On the flip side, however, you find that amino acid supplements can require half the bottle to get the same output as, for example, a whey powder. Some of these pills are sometimes simply whole protein anyways. Consuming essential amino acids should be the goal, and how to time this for best performance could be a legitimate literature search.

What bodybuilders usually consume are not pure amino acids (which would usually be too expensive) but protein powders prepared from various sources - wheat, soy bean and so on. It helps building up muscle mass when training accodingly.

To put it shortly:

Proteins have properties that individual amino acids that make up the protein does not have.
Similarly the individual amino acids have properties that the protein does not have.

This is analogous to elements vs compounds.
The site referenced below quotes 3 experiments done to examine this phenomena.
All experiments compared effectiveness of whey protein with that of essential amino acid (EAA) supplements. Experiments 1 and 2 involved old people while experiment 3 involved young people.
Conclusion of experiments is as follows:

Both EAA and whey protein (15 g of EAA and 15 g whey was taken by the respective groups) induced muscle growth, however EAA had better anabolic effect as compared to whey.
In this 3 groups were compared. 15 g of whey vs 6.72 g of EAA vs. 7.57 g of non-essential amino acids. Whey had higher anabolic effect as compared to EAA while the third group showed no improvement. This additional anabolic effect is attributed to unknown mechanisms. The anabolic effect was measured using a different method add compared to the first experiment. So results may not be comparable.
In this 3 groups of young men were compared. The first group was given carbohydrate (30 g) and EAA (15 g) drink, the second group liquid meal containing same quantity of EAA and total 850 calories while the third group was given both. The conclusion:

The third group, as expected had the highest anabolic rate
The first group (protein and carbohydrate drink) had better anabolic rate when compared with the liquid meal group though they both took the same amount of EAA. The difference was in carbohydrate content. The liquid meal had higher carbohydrates content when compared with the first group.

Whey has insulinogenic effect invitro. Whey also has the same effect whether taken before or after exercise while the protein drink has better effect when taken before exercise.
Among amino acids leucine, when taken alone has anabolic effect comparable to a mixture of EAA.
In conclusion:

However, whey contains various bioactive peptides that act to enhance recovery and potentially in other ways that positively effect the adaptive process to exercise (12). These bioactive peptides are not found in EAA, BCAA, or Leucine, and appear to be a unique quality to dairy proteins. So what we can't say is that these aminos are the deciding factor in whey's effects...or that we can use one in place of the other (interchangeably) in all cases.

http://www.vpxsports.com/article-detail/supplements/whey-protein-versus-amino-acids-whats-the-difference
Please read the article which has more details and graphs and references for further study.

I have only quickly skimmed this article, but I would be very cautious about  relying on it. It is full of claims without supporting references, and it's written by the company that sells these supplements. The studies cited are small, short-term and measure wildly different things.


text:
What stimulates a nociceptor?
For instance, when pressure is applied to the skin, what determines how much pressure results in nociceptor stimulation. And when a sharp object pierces the skin, why is pain, rather than simply touch, perceived? Also, what causes nociceptors to sometimes be stimulated when there is no painful stimulus present, such as during a migraine when the skin feels painful to touch and in chronic pain?
Thank you in advance :)

All of these are affected by specific characteristics of the nociceptors.

Nociceptors are only sensitive to high pressure. The low pressure stimulus would only stimulate mechanoresceptors which would not cause a perception of pain. Receptors like $TRPA1$ sense mechanical stimulus of a higher degree. $P2X/P2Y$ sense ATP which is released due to mechanical tissue injury, as mediated by high pressure or a sharp object injury. Further more, several cells die as a result of nociceptive mechanical stimuli releasing mediators the receptors to which also act as nociceptors.
Exaggerated response to a noxious stimuli is called Hyperalgesia. A sensation of pain in response to a normal stimulus is called Allodynia. Both of these are mediated by specific sensitizing receptors on the nerve endings sensitive to Bradykinin, %HT, Serotonin, Substance P etc. All these are commonly found in conditions where these two are observed, as in the case of burning on touching following sunburns, or increased pain adjacent to an inflammatory foci.

Source:- Ganong's Review of Medical Physiology


text:
Why do you die if you cannot breathe?
I was wondering what the actual reason for death by suffocation is. Obviously it is related to oxygen deprivation. But what is the underlying cause of death?

Is it due to insufficient oxygen for aerobic respiration, and the resulting lack of ATP (as anaerobic respiration forms less ATP)?
Or is it because of the build-up of lactic acid, causing enzymes to denature?
Or is it the lowering of the pH of the blood because of a build-up of carbon dioxide which forms carbonic acid and subsequent denaturation of enzymes?

Your brain, being the most oxygen-hungry part of your body, goes to sleep-mode and eventually dies due to insufficient ATP levels. Glycolysis (carried our by glial cells, not the neurons themselves) doesn't produce enough energy. You may want to read this.

@Chris I'm afraid I lack enough expertise in the field (and enough free time to overcome this) to expand my short comment into something worth a full-blown answer. Moreover, Christiaan has it covered pretty well. If you want to elaborate on my comment, I would really appreciate the effort and the information.

Short answer
This is a difficult question to answer. As far as I am aware, asphyxiation results in excitotoxicity, which causes unconsciousness, brain damage and eventually, death.
Background
Asphyxia is a condition of the body that occurs from severely inadequate oxygen supply, or because of excessive carbon dioxide in the body (First Aid and CPR courses). The brain is the organ most sensitive to hypoxia (Medscape). Nerve cells in the brain can survive only up to four minutes without oxygen (First Aid and CPR courses). Consciousness is lost after approximately three minutes (Forensic Pathology). Permanent brain damage begins after approximately 4 minutes without oxygen, and death can occur as soon as 4 to 6 minutes later (Medline). Asphyxial deaths typically involve respiratory arrest with bradycardia / asystole (low heart rate / cardiac arrest) because of the hypoxia-induced dysfunction of the respiratory centers in the brainstem (Forensic Pathology).
Despite the small size of the brain (2% of body weight), it is, however, the largest consumer of total body oxygen (20%) and glucose (25%), which are delivered by 15% of the total cardiac output (Schur & Rigor, 1998).
A lack of oxygen may result in so called hypoxic-ischemic encephalopathy (HIE), i.e., neuronal cell death due to hypoxia. Its pathophysiology is related to the lack of energy because cellular respiration diminishes. This initially causes neurons to stop firing, and eventually in an arrest of cellular functions and cell death. Even sublethal HIE can set in motion a series of toxic reactions that kills injured neurons and even neurons that have not been damaged during the initial insult. Thus, following global brain ischemia, neurons do not die suddenly or all at once. In some of them, damage develops hours or days after the insult. Most neurons undergo necrosis. In some neurons, HIE triggers apoptosis (Neuropathology).
Specifically, energy depletion is believed to result in a failure of the Na+,K+ ATPase, leading to depolarization of the neuronal membrane (Fig. 1). Synaptic function and conductivity cease at this point. Depolarization causes neurons to release glutamate (Glu) into the synaptic cleft. Glu is the most common excitatory neurotransmitter. In small amounts, it is indispensable for neuronal function. In excessive amounts, however, it is neurotoxic. Some Glu receptors, such as the NMDA and AMPA receptors, are non-selective cation-permeable ion channels. Initially, over-activation of these channels causes a passive influx of  Cl- (and Na+) into cells causing osmotic (cytotoxic) edema and rapid death (Neuropathology).
Additional structural damage develops hours or even days later as a result of Ca2+ influx into neurons through NMDA and AMPA receptors (Fig. 1). This delayed cell death is caused by an over-activation of NMDA and AMPA receptors by the excessive release of glutamate, which causes massive influx of Ca2+ into neurons. Ca2+ activates catabolic enzymes (proteases, phospholipases, endonucleases), and also NO synthase. NO is a free radical and other free radicals are generated due to the impairment of oxidative phosphorylation. Free radicals and activated catabolic enzymes destroy structural proteins, membrane lipids, nucleic acids, and other cellular contents, causing neuronal necrosis. DNA damage from endonucleases and mitochondrial injury from free radicals trigger apoptosis (Neuropathology). Collectively, these effects are referred to as excitotoxicity (Choi, 1992). When enough brain cells die, the person perishes with them.

Fig. 1. Schematic showing the excititoxic effects of excess glutamate in the brain. Source: Neuropathology.
References
- Choi, J Neurobiol (1992); 23(9): 1261-76
- Schur & Rigor, Dev Neurosci (1998); 20: 348-357

Really nice answer +1. One thing that isn't really addressed is that the depletion of oxygen does bring oxidative phosphorylation to a grinding halt. Oxygen is the final electron acceptor and without it ATP Synthase can no longer generate ATP. Without ATP most cellular signaling and a lot of enzymatic function stop systemically. DNA repair fails and cells die. I also think that mitochondria begin to release calcium and cytochrome c into the cytoplasm, which is pretty bad.

@AMR - Thanks for the appreciation. I did quite some research into this one, and the tricky part is whether your proposed mechanism is what causes neuronal death. Your mechanism is definitely true in general, but in the brain it is shown that anaerobic respiration can keep stuff going quite well (see the cited Schur & Rigor paper). Instead, the lethal consequences to the brain, afaik, is more directly related to excitotoxicity.

True. The question itself is a bit more general than just neuronal death. The reason I didn't attempt an answer was I really am not sure what will kill you. Obviously damage to the brain stem will short-circuit everything, but I didn't know the rates of damage, whether other vital organs could survive the lack of oxygen longer. I guess if we keep the brain alive these days, we can artificially get most of the other systems to function. Changes the calculus. I was also wondering how cryotherapy helps to protect the brain, as it seems to extend time to damage, but that is a different question.


text:
Are there histones present in the cytoplasm?
In this paper the authors depleted core histone heterodimers H3-H4 at 90 % from the cytoplasm of Xenopus oocytes. They state that their concentration is in the order of 6 uM.
My question is, are histones found in cytoplasm besides the nucleus location? (ignoring the newly sythesized ones), and if so, is there any known function?

I can't access that paper, how did they deplete the histones? Did they use siRNA?

@user137 The experiment was done with cell extracts. Histones were depleted with anti-histone antibodies and Protein A coated beads.

This is quoted from the paper: The cytoplasm of Xenopus eggs contains a large stockpile of core histones in complex with specific chaperone proteins. Histones H3 and H4 are stored as soluble heterodimers… This paper may also interest you: http://www.nrcresearchpress.com/doi/abs/10.1139/o06-082#/doi/abs/10.1139/o06-082

In early embryogenesis, cell division called cleavage occurs every 30 min and there is no transcriptional activity. Oocytes have accumulated important gene transcripts and synthesize the proteins at right times. However, histone is one of the most abundant proteins and it would be difficult to supply enough histone proteins during early embryogenesis while oocytes translate other gene transcripts regulating differentiation.
This is my speculation, but the article calls cytosolic histones "stockpile". Just in case, I don't mean that I deny some other roles of histones in cytosol if there are any.


text:
What is the fate of micronucleus DNA?
Micronuclei are cellular structures that are formed as a by-product of, usually, defective mitosis. The piece of chromosome in a micronucleus may, or may not contain a centromere and the DNA is wrapped in a double lipid membrane.
I have tried to find information, but I failed to find out what the fate of these structures is within the cell once formed? And is the DNA within it lost for the cell?

Emergence of Micronuclei and Their Effects on the Fate of Cells under Replication Stress (2010) explores how micronuclei behave and determine cell fate. It found that micronuclei is pretty closely related to apoptosis. If the cells with micronuclei didn't go through apoptosis, there were instances where the micronuclei would literally just disappear. They were unable to determine if it was expelled by the cell or reabsorbed into the main nucleus. However, there were also cases where there would be an increase in the number of micronuclei.
They concluded that there is a number of ways for the cell to get rid of the micronuclei and they were unable to determine which is the most likely.
I was unable to find any more recent in-depth studies (that I could understand).

So, according to this paper there are several answers...

Case 1: It is reabsorbed into the nucleus and most likely the information within is saved.
Case 2: It is expelled from the cell and the information within is lost.
Case 3: The cell undergoes apoptosis and all information is lost.


text:
How to find conserved residues across species?
I want to identify if certain phosphorylation sites are conserved for protein X across humans and yeast. I know from MS data that there are 4 phosphorylation sites in Human protein X. In order to identify if these residues, and therefore potentially the phosphorylation sites, are conserved, is it correct to align both sequences using pairwise comparisons by using software like Needle? Or should I rather perform a bigger alignment and use clustal omega? Are there better approaches?

I'd perform a bigger alignment using clustal or mafft or something. Pairwise alignments will give you a lot of noise from random chance and the set of pairwise alignments will be really large. Multiple sequence alignment will detect smaller conservation signals.
Compare against several species of yeast and maybe other mammals for context. When the alignment is done, perhaps draw it? I like logos for vertically large alignments.


text:
What is the difference between rheobase and threshold?
Neuronal tissues can be excited by electrical stimulation. Two commonly encountered characteristics for electrically stimulating nerve cells is the threshold and the rheobase. My question is what the difference is between rheobase and threshold? In the definitions I've read it's described as almost the same thing. The threshold, or minimal stimulus, is defined as "the electrical stimulus whose strength (or voltage) is sufficient to excite the tissue. Rheobase is defined as "the minimum strength (voltage) of stimulus which  can  excite  the  tissue". What is the difference?

You need to clarify your question with a short background. 'Threshold' is a general term, not only dealing with membrane potential (which I assume is what you're after).

by threshold i mean that strength (voltage) that can cause action potential

Add this to your question, along with the confusing/unclear definitions that you've read.

Excellent question! The difference is the fact that the rheobase is an example of a threshold measure. The threshold, as you correctly suggest, is the minimal energy (typically current level and not voltage as you suggest) to excite neural tissue. The threshold applies only under the specific experimental parameter settings used. These parameters include the type of electric stimulus (for example, a biphasic current pulse), the electrode configuration (for example, bipolar stimulation) and the stimulus duration (for example 200 microseconds).
The rheobase is the minimal current level needed to excite a tissue when an infinitely long stimulus would be applied. The rheobase is typically found by plotting the threshold level (as defined above) as a function of stimulus duration. The reason for developing this measure is the fact that excitable membranes integrate the injected current, so charge builds up in the tissue. In other words, increasing the pulse duration decreases the threshold current level needed. Hence, the rheobase is a convenient threshold measure because it incorporates the duration parameter of the stimulus. It will still depend on things like electrode configuration and stimulus shape.
The function of the strength-duration relationship can be fitted with a decaying exponential:
I = Ith / ( 1-e(-t/Tsd) )
where I= Threshold current level;
Irh = rheobase
t = stimulus duration
Tsd = Tau = exponential
Here is a picture of a theoretical strength-duration curve copied from the wiki page on rheobase. [NB: I find the wiki page needlessly complicated].

The rheobase is the horizontal asymptote. An often used parameter to characterize the function is chronaxie, which is the pulse duration equivalent to two times the rheobase.
The explanation given here was adapted from the book "Cochlear Implants", chapter 5 "Biophysics and Physiology" by Abbas and Miller, two veterans in cochlear implant electrophysiology. Unfortunately I cannot give you a link to the pdf as I own the work in hard copy.

PS: If you want access to the chapter your library will be able to get a hold on a copy of Cochlear Implants (Zeng & Popper, Eds.) I'm sure.


text:
Unwanted E. coli product in plasmid product
Using a TOPO XL Cloning kit, our lab took some amplified human DNA, inserted it into the vector, and attempted to clone it in E. coli. However, upon sequencing the purified plasmid product, the sequence we got back was E. coli rather the human we had amplified. The primers sat down in the plasmid as intended, just the sequence between the primers appears to be from E. coli (as implied by BLASTing it against a human, getting no results, and then blasting it against E. coli and getting a hit).

Is it from the E. coli genome, or from the plasmid itself?

Genome. So it's like (M13F Primer)(E. coli)(M13R Primer)

So you need to troubleshoot.  Is the "amplified human DNA" what you think it is? Are you confident in the insertion before the amplification in E. coli? Are you certain you're actually sequencing plasmid? Is there any chance your primers are incorrectly designed, mixed up, or produced wrong by the synthesis company?

The root cause turned out to be a lying spec. Using a different one, it was revealed that there was next to no template DNA in the initial amplification. No DNA, no good plasmids.


text:
Help with STRING database data
I'm working with data downloaded from STRING database (string-db.org) for protein-protein interactions.
My idea is to compare the topology of connections of the same protein on different organisms.
However, I noticed that the same protein can receive different ID on each organism.
So I would like to know if there is any way to convert all ID's into just one pattern.
Thanks.

Proteins evolve and have different sequences between species, so you would have to define what you mean with "same protein". One option would be to use an orthology database like eggNOG. (eggNOG has the same protein identifiers as STRING.) Then you could figure out 1:1 correspondences between proteins.
You probably also want to read up on Roded Sharan's work, e.g. Global alignment of protein-protein interaction networks.

Hello @Michael this was exactly what I was searching for. Thanks for your help and for the reading suggestion.

If I understand it correctly you have downloaded for example 1000 protein sequences with 1000 IDs, but there are duplicates in sequences so in reality it is like having 600 unique sequences with 1000 ID's? If so it should be fairly easy to write a script which would create a set of unique sequences with all corresponding IDs so you could choose which one to use.
In python it could be done using the sequence as dictionary key with the ID as a value. While looping over each sequence check if the sequence is already in dictionary. If yes, append the new ID as a value.
Finally you would get
seqs = {
'DFABIODFAFDIOAF....':['ID001', 'ID007'],
'ANOTHERUNIQUESEQUENCE':['ID50'],
...
}

from which it should be easy to choose
TBH not sure about efficiency of this but this depends on the size of dataset? How large is it? Just give me a sample dataset and I can write it.

Hello @Pocin thanks for your help and for your answer, but my problem was how to convert the protein ID used on STRING to a different database ID (e. g. Uniprot). Using solution provided by Michael I 'll be able to make this correspondence.


text:
What role does the eardrum and ossicles play in hearing, versus cilia?
Modern electronic sound recording equipment employs a physical membrane that triggers the piezoelectric effect in a metallic element, to transform sound waves into electric signals.
I had always thought that the eardrum (or tympanic membrane) was the main instrument of hearing in vertebrates, that it physically transduces sound waves into nerve signals. However, in looking into it, I find that the eardrum transmits sounds to inner ear anatomy, where more structures are encountered before the sound waves become nerve signals.
I also find that small hairs, cilia, are sensitive to sound, and appear to be what actually turns sound waves into nerve signals, perhaps analogously to rod and cone cells in the eye. These cells line the ear canal, and when I read about them, they seem to be the real mechanism of hearing, and not the ear drum or inner ear bones.
At this point I'm confused as to actually how sound waves are transduced into nerve signals in vertebrates. Can someone explain the the roles of the various parts of anatomy in vertebrate hearing, in the overall, big picture? What roles do the large parts play, versus the microscopic cilia?

Sounds are pressure waves in air, but the inner ear is a liquid-filled space. This presents an impedance matching problem where sound is reflected rather than transmitted.
The eardrum and inner ear bones perform this mechanical impedance matching/transduction of air-to-liquid sound. From Purves' Neuroscience:

Sounds impinging on the external ear are airborne; however, the environment within the inner ear, where the sound-induced vibrations are converted to neural impulses, is aqueous. The major function of the middle ear is to match relatively low-impedance airborne sounds to the higher-impedance fluid of the inner ear. The term “impedance” in this context describes a medium's resistance to movement. Normally, when sound travels from a low-impedance medium like air to a much higher-impedance medium like water, almost all (more than 99.9%) of the acoustical energy is reflected. The middle ear (see Figure 13.3) overcomes this problem and ensures transmission of the sound energy across the air-fluid boundary by boosting the pressure measured at the tympanic membrane almost 200-fold by the time it reaches the inner ear.

Some sources will refer to this as "amplification" which is correct in some ways (without it, sound would be too "weak" in the inner ear) but doesn't quite explain the whole problem.
Inner hair cells do the actual sensory transduction, converting vibrations into electrical signals when the "hairs" are stretched apart mechanically, causing a fragile "tip link" to pull on a physical channel, opening it and allowing ions to flow through. The cochlea is a frequency-analyzer, vibrating at different frequencies along its length and allowing different hair cells to respond maximally to different frequencies of sound.

As a side note, although you asked about vertebrates, aquatic vertebrates like fish don't have these middle ear bones, their hearing is quite different from the mammalian ears I am most familiar with. I'm not sure at all about hearing mechanisms in aquatic mammals that evolved from terrestrial ancestors, like whales and dolphins, but that might be a good subject of a later question.

The auditory system (Fig. 1) is basically comprised of 3 main parts - the outer, middle and inner ear (the cochlea).
Generally spoken, the outer ear captures sounds, the middle ear transmits them, the inner ear acts as a transduction system to translate the acoustic pressure waves into electrical signals.

The pinna of the outer ear funnels acoustic waves into the ear canal (meautus) and amplifies it. The pinna changes the transfer function that aids in sound localization in the vertical plane (Fig. 1A).
The middle ear conveys the pressure waves from the ear drum (tympanic membrane) to the ossicle chain, amplifying the sound further (Fig. 1A).
The inner ear is where the action is, see Fig. 1B for a sectional view. The cochlea is a fluid-filled tube. The ossicles transfer the acoustic energy into the fluid of the scala vestibuli. From there it travels through the cochlea as a traveling wave that rides on the basilar membrane (Fig. 1C). The traveling wave in turn sets the hair cells in motion. These hair cells have hairs (cilia) that allow current to pass when deflected. This in turn leads to release of neurotransmitter that in turns activates the auditory nerve to generate action potentials that are transmitted to the brain (Fig. 1D).

Fig. 1. The auditory system. source: Morgan et al. (2020)
Reference
- Morgan et al., Medizinische Genetik (2020); 32: 2


text:
Why are Merkel cells innervated by an axon, and not a dendrite?
Here are two images from Google. Afferent neurons receive input and send it to the central nervous system. Input is received by the neuron's dendritic end and send away centrally via axon terminals that are sheathed with Schwann cells. Axon terminals synapse to motor neurons (muscles and glands).
How is it possible that Merkel cells, which supposed to be a sensory cell, synapse with an axon, and not with a dendritic end?

I edited the question to improve clarity. Feel free to roll back when it doesn't reflect your original question.

There is nothing out of the ordinary with the Merkel cell, as it functions in the same way as photoreceptors and hair cells (see Further Reading #1).

Fig. 1. Merkel cell. Source: Gallery for Share.
The Merkel cell depicted in Fig. 1 is a specialized receptor neuron. It has no axon. It relies on a secondary sensory neuron (a somatosensory afferent) onto which it synapses to direct the touch signal to the brain.
Note that neural information flow goes from dendrite to axon. An axon terminates into a synapse. The Merkel cell, which does not have an axon, features a synapse directly onto the dendrite of the secondary neuron (See Further Reading #2).
Further Readings
1. Can axons act as receptors?
2. What are the functions and differences between axons and dendrites?.

I don't understand your last paragraph: there is no dendrite depicted in the figure, only the body (and some dendrite-like processes) of a Merkel cell, the meniscus tactus (supposed to be a dendrite?), and the axon of the secondary sensory neuron. But the meniscus tactus looks more like a part of the postsynaptic axon - why then "features a synapse directly onto the dendrite"?


text:
What are the floating translucent little objects called in the field of view?
Sometimes we see these small translucent shapes moving by when the eyes are open. When the eyes are moved they seem to follow that movement, but with a certain delay, as if they are floating in a thick viscous liquid. What is this phenomenon called?

First of all microorganisms are not visible to naked eyes. Secondly it is not clear what you mean by 'organism like structure'? The question is very likely to get closed as unclear. Please add some more information.

BTW, floaters as mentioned below are typically more prevalent for the nearsighted. The floaters are sometimes indicators of problems, sometimes not. You should consult an eye doctor.

This was never disclosed to me.  I didn't know this would happen as I grew older.  I want my money or my years back!

"Oh squiggly line in my eye..."

I think you are talking about floaters (a.k.a. eye floaters or flying flies). You may want to have a look at this english.SE post in case you were not talking about floaters.

Floaters are deposits of various size, shape, consistency, refractive index, and motility within the eye's vitreous humour, which is normally transparent.

You can read the wikipedia article to better understand the causes. These floaters are typically not microorganisms unlike you seem to think. Their scientific name is 'Muscae volitantes' and they are mostly caused due to degenerative changes in vitreous humour due to aging.

Are you referring to the "worms or strings/dots swimming on the eye/vision"-phenomenon?
These are also called "eye floaters" and quite common. According to IFLscience: http://www.iflscience.com/health-and-medicine/what-those-strange-things-you-see-floating-your-eye/ they are usually harmless, but may of course cause visual annoyance.
I was unable to quickly find a scientific source, but hope this helps.
If this was not what you were talking about, I misunderstood.
Regards

What you might be referring to are white blood cells in your retina as described here: https://en.wikipedia.org/wiki/Blue_field_entoptic_phenomenon

The blue field entoptic phenomenon [...] is the appearance of tiny bright dots [...] moving quickly along squiggly lines in the visual field, especially when looking into bright blue light such as the sky. The dots are short-lived, visible for a second or less, and traveling short distances along seemingly random, curvy paths.

The rapid, random movement does not match the description in the question.

What you are likely seeing are tiny shadows cast upon the retina from strands of protein (and other debris) in the vitreous humor. They are indeed harmless and do correlate with age.
However, any which obscures your vision should be investigated as blood may have leaked into the eye.
Reference Floaters

Please add some references to your answer.