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Are some animals, like dogs and cats, color-blind and how do we know that?
I have heard that some animals, including dogs, cats and donkeys, are color-blind. They cannot recognize any color. Is that true? And how can humans verify that animals are color-blind, or not? During evolution, has color-blindness not bothered them at all?

We can look at the composition of Cone and Rod cells in their retinas and compare them to our own. We can also look at the pigments that they are capable of producing, like Rhodopsin, and get an idea of the wavelengths of light that these animals are sensitive to. These days you could probably do fMRI or EEG studies to see what wavelengths of light generate activity in their visual cortexes.... http://www.cals.ncsu.edu/course/ent425/tutorial/colorvision.html

TL;DR: We have a good physiological understanding of how eyes work, so by examination of other species' eyes, we can tell a lot about what colours they are capable of seeing.
First, a little bit about the physics of colour
Light is made of photons, and each photon has a wavelength. The distribution of wavelengths coming from sunlight looks like this (wavelengths on the x axis):

Any perceived 'colour' is some sort of summary of the wavelengths of the photons which get into an animal's eyes.
Now, a little about colour perception
There are cells in the eyes which respond to being hit by photons: these are called rods and cones. Colour vision is principally achieved using the cone cells, which have a peak sensitivity at one particular wavelength, and are less sensitive at other wavelengths.
We (non-colourblind humans) have three different types of cone cell, sensitive to photons with wavelengths of 560, 530, or 420 nm, corresponding to the peak sensitivities of three different types of light-sensitive opsins which are present in cone cells. Other types of opsin exist in rod cells (Rhodopsin) and our circadian-rhythm entrainment (melanopsin), but the three different opsins in our cone cells are responsible for our colour vision. Because we have three different types of cone cell, we are referred to as 'cone trichromats'. The sensitivities of the three cone types overlap a bit, looking like this when plotted over the visible spectrum:

When cone trichromats perceive colour, what we're doing is taking the information on how active each of our different types of cone cell are, and using that to infer how many photons there are of each wavelength in the light that hits our eyes.
Of course, cone trichromats can't possibly summarise the whole diversity of wavelengths that are coming into their eyes using just three different measures of intensity - the line is way too complicated to summarise from three points. Also note that for humans, there is no cone cell that is sensitive above about 700 nm, or below about 400 nm. This means that we simply can't see differences in the infra-red or UV parts of the colour spectrum.
How does this all relate to colour-blindness in animals?
It is fairly simple to test the peak sensitivity of a cone cell: you take an eye from a freshly-dead animal, hook up an electrode to a cone cell, and then provide light of different wavelengths, and measure what wavelength causes the cell to 'fire' the most. If you repeat this with a large number of different cells, you can confidently determine how many different types of cone cell the animal has, and what wavelengths those cone cells are most sensitive to. This experiment (or similar ones) has been done for many different species, so we have a good background knowledge of what colours different species are capable of seeing.
Many species, including most non-primate mammals, have only two types of cone cell (i.e., they are cone di-chromats, as against non-colourblind humans, which are cone tri-chromats). This doesn't mean they see no colour, but it does limit the types of colour they are able to see. Many tools exist to simulate the visual ability of cone dichromats, for instance here, or here for browsers without flash support. These tools simulate human vision with different numbers of cone cell types. When comparing across species, it is important to remember that both the number of types of cone cell, and the peak sensitivity of each type, may be different, so the tools do not capture the full range of possible colour-perception abilities across species.
There are also cone tetrachromatic (four types of cone cell) and pentachromatic (five types) species. The record appears to be held by mantis shrimps, which have sixteen different types of cone cell. These species can in principle see a greater diversity of colours than cone trichromats.
Does colourblindness present an evolutionary problem?
Not necessarily. Compared to cone tetrachromatic species, humans are 'colourblind', and it seems to have very little impact on our day-to-day survival. Similarly, most colourblind humans (i.e., with one or more types of cone cell disabled compared to non-colourblind humans) get along perfectly fine - a special test is needed to detect colourblindness in humans. If trichromatic vision gives no particular survival advantage, there is no reason to think that it will be favoured by evolution.

If you could add a paragraph on the pigment molecules (opsins) expressed by the cone cells, that are sensitive to light at the three wavelengths you reference and how they enable color vision, it would complete the answer, from a biochemical perspective. Otherwise this answer would be just as valid in answering a question as to how a CMOS or CCD sensor uses a Bayer filter to record color information. Definitely a well researched and informative answer, I just think that tying it to the proteins that cause the cones to respond to color would help.

@AMR: Good point. I've added some detail on the diversity of opsins in our visual and circadian systems.

Awesome answer. Too bad the best answers typically raise the smallest amount of rep.

@AliceD... I think one of us should ask the question, "I live near a nuclear power plant and was bitten by a glow-in-the-dark spider. When should I expect my Spidie senses and web-slinging abilities to kick in?..."

@AMR - Now that would be a cracker :)

@AliceD I would do it too if I didn't think some of our more humorless compatriots wouldn't vote me down into oblivion. I could even photoshop a photo of a spider bite to have a slightly neon green glow too it, and say I have this sudden craving for stew of Calliphora vomitoria (Blue-bottle Flies).

The colorblind simulation tool linked in the answer requires Flash; nowadays Flash is pretty much dead, so do you know of one that doesn't?

Cheers for pointing that out. Have added an example that doesn't rely on Flash.

Might also note that most mammals other than primates are dichromats, while most birds (and I think reptiles) are tetrachromats, being able to see ultraviolet.

Good point. The OP's examples were all mammalian, so I have added some more background and another citation to this effect. The source gives some background on the evolutionary origins of the opsins in different mammalian lineages.

Short answer

Dichromats can discriminate colors;
Color vision in animals can be tested behaviorally;
Trichromatic vision is not essential for most animals, but is believed to be beneficial to species relying on fruits (frugivores).

Background
I would like to complement bshane's excellent physiological perspective with a more behaviorally oriented answer.
Firstly, it is quite incorrect to say that dichromats can't see color. "Color blindness" is a deceptive term, since dichromats are not blind to colors, they are "blind" to some. For example, the most common type of color blindness, namely red-green color blindness (deuteranopia), is caused by the lack of green cones. Because of the red-green opponency in color vision, they have difficulties discerning greens and reds. However, they can see yellow and blues perfectly fine. Hence, 2 cone classes are sufficient to recognize colors, but missing a green cone simply results in reduced resolution in the long wavelengths.
Evolutionary, the added cone in trichromats is the medium-wavelength green cone. Trichromatic vision has evolved relatively late in evolution in New World Monkeys and is thought to have been beneficial to them to distinguish between ripe (red/yellow) and unripe (green) fruits, as their diet consists for an important part of fruits (Osorio & Vorobyev, 1996). Noteworthy is that trichromatism is more of an exception than a rule. Nocturnal animals are often monochromats, as rod-mediated vision is beneficial under scotopic conditions. Nocturnal species not only are not negatively impacted by a lack of color vision, they in fact benefit from it, because all of their retinal space is occupied by light-sensitive rods. The photon-hungry color-receptive cones need photopic conditions. Dichromats are the rule, while trichromatic vision is considered exceptional.
We can show trichromatic color vision in animals using behavioral experiments. Animals can be trained to perform color recognition tasks, like Munsell papers, that test the ability of the subject to recognize  red, yellow–red, green–yellow, green, blue–green, blue, purple–blue, purple and red–purple colors. When the subject is able to succesfully recognize these colors, it is safe to say they are trichromats. For example, Munsell papers have been used to show that capuchin monkeys (Cebus apella) are trichromatic (Gomes et al., 2002).
References
- Gomes et al., Behav Brain Res (2002); 129: 153–7
- Osorio & Vorobyev, Proc R Soc Lond B (1996); 263: 593-9

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How does an amoeba move?
Simple question. It forms a pseudopod, and then flows in to it. But how does it move its material to form a pseudopod? And even so, if it is floating in water, what is it pushing against so that part of it holds still and part can move forward? It would be like trying to move while wearing ice skates by pushing your arms forward in the air: no net force is transferred.

History: in 9th grade, I badgered my Biology teacher until she finally said "I don't know!" in exasperation. I liked her, so I never did that again, but 35 years later, I still don't have the answer.

they use ameoba locomotion or ameoba movement with their pseudopods.

It has a cytoskeleton, a network of fibers stretched across the cell which it can shorten and expand (by adding or subtracting actin monomers which build them) in a coordinated manner to more-less arbitrary change shape.
According to this paper, on surfaces they generally can adhere to it using membrane protein structures, thus the locomotion occurs due to friction.
To swim, they generate bumps near the front end of the cell and move them towards the back, similarly to how a swimmer uses hands.

Wow, thanks. Another thing I can tick off from my childhood list, along with writing a maze generation program... How does it know "how" to do those things? Or where to go, or whatever? Oh, well. A billion years of evolution can't be wrong.

@nocomprende They are using chemotaxis. This basically means that they follow a chemical gradient in their environment and move towards the signal. They have transmembrane receptors that are bound by the chemokine and signal into the interior of the cell. This polarizes the cell and  causes the nucleation of the actin filaments towards the "front" of the cell. And if you think that it is cool for Amoeba, then you will find it interesting to know that many of the cells of our immune system move around our bodies in pretty much the same fashion.

@AMR It is amazing how much complex behavior you can get out of systems that are very simple. Put a few hundred billion nerve cells together and, voila!

source: Stack Exchange

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what makes our body warm?
I would think that there would so many chemical reactions going inside our body,friction produced by blood in veins, subcutaneous and visceral fat acting as heat insulators.
I was wondering to what extent different factors play a role in protecting our
body against cold.for example say blood circulation might be responsible for
creating 70% of the body heat and also a person with high blood pressure may produce more heat in his body.
also, perhaps fever or any other disease would be an exception to the normal
heat creating process in our body.just like the gonads or testes which are
cooler than the rest of the body.

Pretty much Mitochondria.

I cannot vouch for this source, but it has a basic overview of mitochondrial heating. http://education.seattlepi.com/heat-human-body-generated-mitochondria-6094.html

Specifically, we are burning the carbon-carbon bonds in the sugar molecules we ingest. You could call this oxidation; oxygen is the terminal electron acceptor in the electron transfer chain (as in loss of electrons is oxidation, and gain of electrons is reduction). The process is not 100 % efficient, so while some of the energy is captured as ATP, or reducing power, the portion that is not captured is given off as heat. Phillip Morrison has a great video of cyclists in the Tour de France where he burns a pile of donuts on a barbecue to show how much energy they burn every day.

In summary, cellular respiration and thermogenin.
Most of the energy in our body comes from cellular respiration. Cellular respiration is how ATP, the major source of cellular energy, is made from glucose. Cellular respiration generates heat mo matter what because not all of the energy from glucose is converted to ATP.
In certain cells, a protein known as thermogenin allows the protons in the cellular respiration to flow from the inner membrane to the matrix (the protons are in the inner membrane of the mitochondria as the electrons from glucose were used to pump them). This generates heat. In regular cellular respiration, the proton gradient is used to make ATP, but now, it juet generates heat.
Also, ATP can be hydrolyzed directly in brown fat cells and muscle cells to produce heat along with inorganic phosphate and ADP.

Not only respiration generates heat; pretty much all cellular processes generate heat, including the usage of ATP to drive various things. Muscle contraction is a large contribution.

@Roland yes, but isn't cellular respiration the process in which most of the heat is generated?

Respiration is certainly a large component, but I'm not sure it's the largest. Basically it amounts to how large the free energy of a reaction is and what fraction of that energy is released as heat. I don't have the numbers, but certainly muscle contraction is a large component too.

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What is the term for being younger than the body age?
I remember that I once attended a seminar in which the speaker talked about the heart rate of different kinds of butterflies. Normally, the heart rate of the adult butterfly will be more complex than the heart rate when it is in the larvae form. However, there are some species that have complex heart rates even when they are in the larvae form, and there are others that have simple heart rates even when they are in butterfly form.
So if we are talking about the butterflies' heart, we can say that some species' heart are younger than their real age, while others are older than their real age. What is the name of this phenomenon?

I'm very confused about what you are asking.  Your title is about "being younger than usual" and your question seems to be about either the rate of heartbeat or the complexity of heartbeat.  I would suggest posing a clearer question.

I'm not sure about a general biological context, but an old word for looking younger than one's years is neanimorphic.  A search on pubmed found zero results for this, so it is probably not the term you are looking for.

Well looking younger or having features of a youngling is called neoteny but I don't think you are referring to that.

@WYSIWYG yes, that's the word I'm looking for. May I ask why you don't think I'm referring to it?

Neoteny

Neoteny (/niˈɒtəni/), also called juvenilization, is the delaying or slowing of the physiological (or somatic) development of an organism, typically an animal. Neoteny is found in modern humans. In progenesis (also called paedogenesis), sexual development is accelerated.
Both neoteny and progenesis result in paedomorphism (or paedomorphosis), a type of heterochrony. Some authors define paedomorphism as the retention of larval traits, as seen in salamanders.
Both neoteny and progenesis cause the retention in adults of traits previously seen only in the young. Such retention is important in evolutionary biology, domestication and evolutionary developmental biology.


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What causes the pain when a bone fracture is healing?
Why does a fracture still hurts when it is healing? I understand the pain at the beginning - the bone is not in its place, there is a pressure against the nerves, also the swelling pushes the nerves etc. But why does it still hurt after several weeks, when the swelling is gone, the bone is more or less fixed? Is the cause of the pain mechanical, or chemical?

At the initial phases of the healing the broken ends are mobile (and this is time when it can be set and put into a cast).
At later stages soft callus than hard callus forms and now any movement will pull on the broken ends and stimulate the nerve endings: it hurts.
This also has the effect that the nearby muscles will spasm in an attempt to immobilize the bone. Another source of the pain can be that these muscles become tired and start to hurt as well.
The pain will continue until the two broken ends are completely welded together so there is no longer any movement that would stimulate those nerves.

Well, but aren't the two broken ends more or less welded together after 3-4 weeks? Why does it hurt longer?

@HonzaZidek It's not fully welded together until the cast is removed, which takes 6-8 weeks usually. Even after that there is a remodeling phase which can cause disconfort as your body restores the bone's original shape. Also the changes in posture during the 2-3 months injury needs to be corrected, unused muscles need to regain their strength, overused ones need rest, which can cause pain (even elsewhere).


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Can general soap kill bacteria?
I have read that general soap can kill bacteria by opening holes in the bacterial membrane.
http://questions.sci-toys.com/node/90
However, I found some articles as well saying that it cannot.
http://goaskalice.columbia.edu/answered-questions/does-soap-kill-germs
There seems split answers among experts,
so I would like to know which one is correct.
Could anyone advise me?
Thanks.

If you look all the way down at to bottom of that ask Alice post, you will see that it was originally posted in 2001. Many major health organizations have done efficacy studies since then and have weighed heavily in favor of the use of regular soap over antibacterial. However if the choice is antibacterial or not washing your hands, then go with the antibacterial.

Soap kills nearly all the bacteria it comes into contact with by dissolving the bacterial membrane.  Some viruses with protein coats can resist soap, but many viruses have similar membranous coats (like HIV) and are usually disrupted by soap.  I'm sure it washes some away too, but to say they don't kill bacteria is misleading. In the end, though, they are gone.
Antibacterial soap with triclosan does not kill bacteria on contact and are no more effective than if they had no triclosan at all.  That's actually a good thing since really using an antibiotic would probably accelerate antibiotic resistant bacteria which is a serious - probably catastrophic public health failure. A recent study showed that killing bacteria by soaking with triclosan took 9 hours to start showing an effect.
To achieve full sterility, surgeons bathe their gloves in iodine (see details in the comments below) and their instruments will be sterilized by heating them beyond the boiling point in an autoclave under pressure.   That's useful when you are breaching the skin in surgery, but the skin needs some bacteria to be healthy long term and works well to fend off bacterial infections.
Your confusion seems to come from finding a page full of errors. Alice didn't really do her homework.

In a surgical setting, isn't the iodine use in the form of Betadine (povidone-iodine)? Also, Chlorhexidine is use a lot as a patient preoperative prep and also a wound cleanser.

@AMR  you clearly know more than I - happy to accept these amendments!

"Soap kills nearly all the bacteria ... by dissolving the bacterial membrane."
I thought soap only worked to dissolve lipids. Aren't bacterial cell walls are made of peptidoglycan (non-lipids)?

Soap is a detergent. It actively emulsifies the bacterial membrane, thus killing them by breaking this membrane. So yes, soap kills bacteria. Some bacteria are more or less resistant to this depending on the constituents of their lipid-bilayer membrane.
The reason why soap doesn't hurt your own cells is that for the most part, your outer skin layer is comprised of dead cells that have numerous cross-linked keratin filaments mixed with oils from your sebaceous glands that provide a nice nearly airtight, watertight barrier.
Excessive hand-washing or washing hands with stronger detergents can actually get rid of this protection and break down the barrier mentioned in the prior paragraph, leading to dry and cracked skin.

How does the soap get passed the bacteria capsule and cell wall to the bacteria's cell membrane to emulsify the membrane? The capsule and wall are not made of lipids.

Are you confusing a viral capsid coating made of proteins with bacterial cell membranes?  Some bacteria, under stressful environmental conditions can also encapsulate, but most of the bacterial we pick up from the environment and food are not encapsulated.

I'm looking at the gram-positive bacterial cell here. https://en.wikipedia.org/wiki/Bacteria#Cellular_structure It seems like at least that bacteria has a capsule and also a cell wall, then a cell membrane. Ah, but maybe where I'm confused is that not all bacteria are structured like that?

No, you aren't confused. Gram negative bacterial have two "lipid bylayer membranes (inner and outer)", but also a peptidoglycan layer between.  That layer between is much harder to disrupt with detergents, and thus they present more of a problem!

Generally, the goal for using non-antimicrobial soap is simply to pick up and remove organisms and dirt from our skin. This is achieved first by the soap chemically bonding to certain molecules (i.e. oil or lipids). Second, friction from rubbing mechanically and rinsing with water pick up and removes the soap and chemically bonded particles. Thus, the more soap and the longer the hands are rubbed together, the less oil and microbes left on your hands.
For a more scientific answer:
Soap is a detergent, meaning one side of the molecule is hydrophilic (likes water), and the other is hydrophobic (likes oil). Cellular membranes are also made out of a dual sided hydrophobic and hydrophilic molecule called a lipid. The soap solvates the hydrophobic parts of the lipid cell membrane, and you're left with a mixture of lipids & oils suspended in the soap. These are washed away when you rinse with water (imagine how cooking oil floats on top of water).
For another (longer) response to this question see here.

Comments on website credibility:
I'll also comment that at any point that you do an online search, you REALLY need to pay attention to the source of the information you're looking at. The internet is crawling with misinformation and inaccuracies -- often represented as fact or even presented by a so-called 'expert'! Typically, .edu websites (from academic institutions) are MUCH MUCH more trustworthy than .com, .org, etc. because they typically originate from some kind of peer-review or life-long study of a topic.
Be cautious, however, that you don't end up on a .edu page that contains a student's (or other non expert's) thoughts/opinions/or (possibly wrong) response to a question. Further, unfortunately it's not always this simple, as .org or .com info isn't necessarily wrong.
If you want to increase your odds of finding the most accurate information,  go straight to the peer-reviewed literature (start a search here). If this is too daunting a task or if you can't find what you're looking for, then I'd suggest focusing on .edu websites for info. You can use the "site:" operator in a Google search to specify a domain -- specifically, if you’re looking for high-quality references, you could use site:.edu to only pull up results from .edu domains.
That being said, I think it's clear that your first link is not nearly as trustworthy as your second, and in this case can be dismissed as internet misinformation.
Hope this helps!

Great comments on the credibility of that website.  It was horrid.

Please upvote the response then, so that more people are drawn to it. Thanks!


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What is the attacking mechanism of RF on IgG?
Rheumatoid Factor (RF) attacks Fc portion of Immunoglobulin G (IgG), I want to know the underlying mechanism at molecular level. Also, what type of bond or attachment is made by RF and Fc portion of IgG?
// I'm a student of mathematical physics and have no detailed knowledge in biology, this question comes in my mind because my sister is suffering from Rheumatoid arthritis. All I want is to understand this disease from physical aspects//

RF factors comprise antibodies that your body makes that exhibit auto-immunity (recognition of self as an antigen). They often recognize and bind to IgG antibodies as illustrated in this picture:

So the answer to your first question is that the underlying mechanism is inappropriate recognition of self from your immune system.
For your second question, I am not an expert in the type of chemical bonds employed by antibody-antigen interactions, so I looked it up briefly. This article was quite informative for that: Antibody/Antigen Complexes.  The majority of binding seems to be hydrogen and ionic binding.
Hope that gets you going in your own searches.

Thanks sir, the link helped me a lot. I was searching something special in bonding of RF & IgG so that we can separate them via external forces. Here uniqueness and speciality is important in the RF-IgG bond because in breaking the bonds from external forces can destroy the bonding between another antigen and antibodies.

Great.  Mark my answer if it answered your question. That is how it works.

But I didn't get unique property of RF-IgG bond, the bonding between antigen and antibodies are generalized in that link.

Antibodies have variable regions that are just that.  Through VDJ recombination, this could be a multitude of ways. I don't know of a way to characterize a unique binding pocket for this process.  You might be able to do so if you could crystallize a monoclonal AB/IgG protein complex.  But my understanding in humans would be you would have many different auto antibodies coming from different B cells.  Anyone else that can chime in, please do.


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Difference between protozoa, protists, protoctista?
Are protozoa, protists, protoctista different classes of organisms or simply different names for the same?

These terms are all somewhat obsolete as taxonomic terms, but they may still be used to describe certain groups of organisms.
The term "protist" is used informally in two different ways.  One usage refers to the paraphyletic group consisting of all eukaryotes other than the animals, plants, and fungi.  The other usage is to refer to those eukaryotes that exist as independent cells or, if colonial, do not form colonies with differentiated tissues.
The term "protozoa" is used informally to refer to the "animal-like" protists, i.e. those that are non-photosynthetic and motile.
Wikipedia gives a good summary of how these terms were used historically.

Protozoa as of 2017 is how Microbiologists define one of the six categories of microorganisms.
Microbiologists classify microorganisms into:
Bacteria, archaea, fungi, PROTOZOA, algae, and small muticellular animals
Then you have how Biologists categorize things, and they classify not into 6 groups but into three groups --> Bacteria, Archaea, and Eukaryote
Then you have the further refining that Biologists use which is Kingdom-  which is Bacteria, Archaea, Fungi, Protista (old name for this kindom USED TO BE protozoa), Plantae and Animalia
SO in 2017 , if someone says protozoa, they are no longer talking a kingdom they are talking about a microbiological category for a microbe. If they do say protista, this is the correct kingdom terminology for the protists... which make up the category !
Reference
Bauman, Microbiology with Diseases by Taxonomy, 4th ed. (2014)

Welcome to Biology. Thanks for your interesting answer. Could you possibly add sources to allow other users to background read on your answer?

microbiology with diseases by taxonomy fourth edition by robert bauman

Thanks. I edited your answer and I will delete this comment string shortly. +1

According to Wikipedia Protist and Protoctista are equivalent. "The term protozoa is used to refer to heterotrophic species of protists that do not form filaments." - from the same wiki.


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Trisomy 21 and Down syndrome
Can Down syndrome occur without trisomy 21 in the karyotype of an individual? Or vice versa can a person have trisomy 21 while unaffected by Down syndrome?

First question: No, all Down Syndrome patients have a inappropriate duplication of part or all of chromosome 21.
Second Question: More complicated.  The phenotype can vary in severity depending how much much of chromosome is duplicated, whether it is duplicated and stuck onto the end of chromosome 14 (translocation vs. non-disjunction).  Lastly, a rare form of this event is defined by incomplete penetrance or mosaicism of cells that contain duplication.  Short Answer: No, In rare cases, a carrier can pass on trisomy 21 without being affected themselves but they themselves are a "balanced carrier" and don't have extra chromosome 21 material. See last paragraph below from the NIH and this quote from the Mayo Clinic:

When translocations are inherited, the mother or father has some rearranged genetic material, but no extra genetic material — this means he or she is a balanced carrier. A balanced carrier has no signs or symptoms of Down syndrome, but he or she can pass the translocation on to children, causing extra genetic material from chromosome 21

Types of Down Syndrome details from: NIH Down Syndrome Information Page

Research shows that three types of chromosomal changes can lead to Down syndrome.
Complete trisomy 21. In this case, an error during the formation of the egg or the sperm results in either one having an extra chromosome. So after the egg and sperm unite, the resulting cells will also have three copies of chromosome 21. The complete extra copy of chromosome 21 is in all of the person's cells—or a complete trisomy. Complete trisomy 21 is the cause of about 95% of Down syndrome cases.1,2,3
Mosaic trisomy 21. Not every cell in the body is exactly the same. In about 1% of Down syndrome cases, most of the cells in the body have the extra chromosome, but some of them don't. This is called "mosaicism." Mosaic trisomy 21 can occur when the error in cell division takes place early in development but after a normal egg and sperm unite. It can also occur early in development when some cells lose an extra chromosome 21 that was present at conception. The symptoms of someone with mosaic trisomy 21 may vary from those of someone with complete trisomy 21 or translocation trisomy 21, depending on how many cells have the extra chromosome.1,2
Translocation trisomy 21. In this type of chromosomal change, only part of an extra copy of chromosome 21 is in the cells. The extra part of the chromosome gets "stuck" to another chromosome and gets transmitted into other cells as the cells divide. This type of change causes about 4% of Down syndrome cases. There are no distinct cognitive or medical differences between people with translocation trisomy 21 and those with complete trisomy 21.
Sometimes, a parent who does not have Down syndrome may carry a translocation in chromosome 21 that can be passed on to children and cause Down syndrome. Studying the parents’ chromosomes can reveal whether this is the cause of the syndrome. A genetic counsellor can assist families affected by translocation trisomy 21 in understanding the risk of Down syndrome in future pregnancies.1,2,3

Added EDIT:

Also important to note that people can have trisomy 21 develop in somatic cells spontaneously, later in life without having most of the effects of DS. But this can significantly predispose to leukemias shown here, which is an interesting area of study.  Thanks to @The Nightman.

@user5034361 Great!  Welcome to Biology!

What is xsome? I don't think it is a standard term for chromosome. I edited all instances. (When I google "xsome" I get hits about threesomes and foursomes :D)

Thanks WYSIWYG, its holdover shorthand notation from a professor of cell biology I had 25 years ago!  Some habits are hard to break. Sorry for the confusion.  Good catch on the British spelling of counsellor.  Odd that the NIH info page didn't catch that, but since it is a direct quote, probably not good to change.

Also important to note that people can have trisomy 21 develop in somatic cells spontaneously, later in life, and this can predispose to leukemias. 'http://download.springer.com/static/pdf/94/art%253A10.1007%252Fs00431-014-2430-3.pdf?originUrl=http%3A%2F%2Flink.springer.com%2Farticle%2F10.1007%2Fs00431-014-2430-3&token2=exp=1445874867~acl=%2Fstatic%2Fpdf%2F94%2Fart%25253A10.1007%25252Fs00431-014-2430-3.pdf%3ForiginUrl%3Dhttp%253A%252F%252Flink.springer.com%252Farticle%252F10.1007%252Fs00431-014-2430-3*~hmac=170badd7df784094a3e026e183dbda9936a844a8add14ad5640fd6b7bb690032'


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How do you interpret this microbiology/ bacteriology research figure?

This is a figure from a research article that I am to do a senior presentation for. It is showing  bacterial replication of an enteric bacteria population. The researchers hypothesize that the number of regions near the replication origin will be the highest point (peak) on the graph and the terminus region will be the lowest point because there are least copies of this region in a dividing species. The determine that the ratio of the peak to the trough will reflect the growth rate of the species. That all being said, I don't understand their use of color. The peak has several different colors that do not seem to match any of the examples on the right. Wondering if anyone can help me decipher this? Thanks!

The short answer is that it looks like the colors are meant to represent different, partial copies of the bacterial genome in the process of being synthesized.
When bacteria replicate, they initiate replication at the origins of their chromosomes.  In fact, these origins can be replicated multiple times before it gets to the "end" of the bacterial chromosome (terminus). Looks like the stacking on the right figure shows this, with the colors just aiding in differentiating the partially replicated chromosomes. The coverage plot on the left shows how this might look based on read coverage from deep sequencing (again the colors just show different, partially replicated, chromosomes).

I think the figure has the answer. "High copy number near the origin". This is depicted in the graph by the spike at x = 4Mbp. The graph also shows that the number of reads is lowest at a point opposite the ori (2Mbp).
Mbp stands for Mega-base pairs, or 1 million nucleotides. Mbp in the graph refers to a point on the chromosome, with 4Mbp being at '12 oclock', the origin of replication(ori), and 2Mbp being at '6 oclock' opposite the ori. The researchers are measuring the number of DNA fragments(y-axis) that map to a certain position on the chromosome (x-axis). I am slightly color blind, but it seems to me that the colors generally match up. Also note that the reads that fall within the lower-most bracket on the right side of the x-axis span the entire x-axis. This is because these fragments map completely to the chromosome, and indeed they are labelled 'original genome'.
Hope that helps.

First, it would help if you could provide any more information on the figure (how it was made, is it data based or representative of a model?)
Given that there is little to go on, I can offer my two bits - and I hope it will help you get thinking about it - but ...
It appears to me that these data are a snapshot of the replicating bacterial genomes isolated from many cells at a given timepoint. The right side of the figure shows a model of the (circular) genome in black with a number of smaller fragments of the genome caught partway through the replication process. The left side shows the same fragments stretched out in a linear representation.
The green fragment is the largest as it is nearly finished copying. Other colors show different sized fragments at different points in the copying process. It sounds like the graph is meant to relate the number of different sized fragments to growth rate (assuming you measure fragments from the same number of cells).
So, what does this tell you? (I think it would be helpful for you to think this out yourself form here and determine if you believe this is a good measure or not.)

Would you agree that "genomic location" (x axis title) shows that they are splitting the circular chromosome into 4 regions?

Bryant, I don't think they mean to break it into regions. The X - axis is a measurement (in mega-base pairs = millions of bases) according to an arbitrary start point. Replication begins at the origin and extends in both directions. Note the point of symmetry for each of the fragments around the origin.


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Can electricity be harvested from the soil around plants?
This is a rehash of a question I originally wrote on Skeptics which got moved to Physics, but I'm really after an answer from a biological perspective.
A device called the E-Kaia is making news by claiming to harvest enough electricity from the soil of a pot plant to charge a phone. They claim they can draw 600mA from the soil, which actually wouldn't charge most smartphones in the 1.5 hours they claim in the article (thanks Physics.SE!).
Is there really electricity in the soil around a plant? I can't imagine there being 600mA there for the taking in the soil of a huge tree let alone a pot plant. Maybe it isn't electricity in the soil but some other kind of energy or chemical that can be extracted to generate electricity - it sounds like the lemon battery experiment, which relies on a chemical reaction.
And surely, even if there was electricity there, extracting all of it would damage the plant?

Actually this is a chemistry question. If you put an anode and a cathode in an electrolyte and a salt bridge, you should get a current. If I remember anything about plant biology (which I really don't) nitrogen fixers should be able to pump Nitrogen to bacteria at their roots that convert it to ammonium, which is a cation and nitrite which is an anion. Add some water and you probably have enough of an electrolyte to generate a current of electrons, though how much and if it is efficient enough to charge anything, I don't know.

The question in its entirety sounds like off-topic. I suggest that you can break down the question into subquestions which can individually be on-topic in either physics, chemistry or biology. For biology, your question should be on the lines of whether soil bacteria can create electrochemical potentials of the order of 100mV. Note that even this is a broad question because this all depends on soil type, temperature, mineral/water content and the microbiota.

Electricity may be indirectly generated from plants through the use of a microbial fuel cell, in which biologically-catalyzed chemical reactions are used to drive an electrochemical cell.
A non-technical description of the technology can be found here.  The basic idea is that plants produce organic compounds, which are broken down by soil microorganisms to produce carbon dioxide, electrons, and hydrogen ions.  Ordinarily the hydrogen ions and electrons combine with oxygen to form water, but there are various ways to divert the electrons to travel through an electrical circuit before the oxidation reaction takes place.  This flow of electrons (electricity) can be used as a power source.
This technology is still in its early stages but the process has been demonstrated in some laboratory proof-of-concepts:

Strik, David P. B. T. B.; Hamelers (Bert), H. V. M.; Snel, Jan F. H.; Buisman, Cees J. N. (2008). "Green electricity production with living plants and bacteria in a fuel cell". International Journal of Energy Research 32: 870–876. doi:10.1002/er.1397.
De Schamphelaire, Liesje; Van den Bossche, Leen; Dang, Hai Son; Höfte, Monica; Boon, Nico; Rabaey, Korneel; Verstraete, Willy (2008). "Microbial fuel cells generating electricity from rhizodeposits of rice plants". Environmental Science and Technology 42 (8): 3053–3058. doi:10.1021/es071938w.

The E-Kaia company has not released enough information to say whether their product is in fact a plant microbial fuel cell, a simple earth battery, or a mere scam.

Can you cite the claim that the product is in fact a microbial fuel cell?

@MarchHo  Based on the company's Facebook page, the product uses a "biocircuit" to "capture the residual energy of plants" (in other words, it runs on "woo").  The Daily Mail article implies that the technology is similar to the plant-e technology, which is definitely a microbial fuel cell.  The other possibility is that the E-Kaia product is a simple Earth battery and the plant plays no actual role in power generation.

@MarchHo I have revised my question to primarily address the larger question "Can electricity be harvested from the soil around plants?"


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Is Roundup toxic?
Roundup, as we all know, is a herbicide that kills weeds. It does this by preventing the production of amino acids in plants. One of these amino acids is tyrosine. Tyrosine is a nonessential amino acid so it is produced in the human body. So is Roundup toxic because it could also affect the human tyrosine synthesis pathways? Or are the pathways for tyrosine synthesis different for humans and plants?

"Glyphosate specifically inhibits an enzyme that is essential to plant growth; this enzyme is not found in humans or other animals, contributing to the low risk to human health from the use of glyphosate according to label directions." http://www.monsanto.com/products/pages/roundup-safety-background-materials.aspx

Glyphosate works by inhibiting 5-enolpyruvylshikimate-3-phosphate (EPSP) synthase. Plants and microbes have this gene, and humans do not.
So, Roundup is toxic to plants because because it inhibits the production of critical amino acids as you surmised (EPSPS makes 5-enolpyruvyl-shikimate-3-phosphate (ESP) which is used as precursor to not only amino acids but also other plant hormones and aromatic chemicals).  It does not do this in humans.
It is a very controversial compound though, and weight of evidence for human toxicity has not clearly overwhelmingly swung one way or the other yet. There are some very impassioned believers on both sides of the fence, and I suggest reading pubmed epidemiology studies to make up your own mind.

The pathways are different. Humans synthesize tyrosine by hydroxylating phenylalanine. Plants use the shikimate pathway to produce all of the aromatic amino acids. Roundup inhibits an enzyme in the shikimate pathway but does not affect the human enzyme involved in producing phenylalanine. None of this is to say, however, that it is or isn't toxic.

The MSDS shows it to be pretty much non-toxic. LD50 is greater than 5g/kg in rats... California wants to list it as a carcinogen but that may be more political than fact based.

@AMR Thank you for the info. It seems most things are "known to the state of California" to cause cancer.


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Why to use transgenic mice in ALS models?
In ALS mice model with mutant SOD1 - there are use of transgenic mice, with insert of human mutant SOD1.
Why is that? Why not to mutate directly mice SOD1 ?
In transgenic mice, after few generations these human gene thrown out and not present any more.. Why thrown out? Is the second question.
Looking for an answer for a while. Thanks a lot.

Have you done any research what-so-ever on humanized mice and transgenics? You are manipulating the gene one way or the other. Starting with a null background then adding the human gene of interest through homologous recombination is how you produce an animal that can actually give you data for the question you are investigating. Your third paragraph is completely wrong. Doing speed transgenics it will take you about 4 generations to breed the humanized allele into a homozygous state in the animal. Once it is homozygous, you can then start to analyze the data you are producing.

The use of a mouse with the replacement of one of its genes with a human version is to better mimic the human disease phenotype, or to prove something about the biology of the human phenotype with research that can't be conducted in humans.
Genes and their corresponding proteins or RNA usually differ somewhat between mouse and humans. If you wanted to study whether a certain SNP in a gene (found in humans) was the reason for part of your phenotype, you may want to use transgenic mice to test hypotheses with different exacerbations (treatments).  One way to do this is to create a mouse with the human gene replacing the mouse gene, and another mouse with the human gene containing the trait-linked SNP.
If you tried to do this with the mouse gene, you couldn't be sure that the same SNP would have the same functional consequences.  If you didn't remove the endogenous gene from the mouse before replacing it with the human version, you would never be sure if observed experimental phenotypes weren't confounded by both copies of the gene and their corresponding gene products being active in the same animal.
In your example, with SOD1 and ALS, creating a humanized mouse with human SOD1 allows researchers to more fully study the same protein product made in humans, while giving the mouse treatments that would be unethical in humans.
Your understanding in your last part is incorrect. Mice don't lose genes after a few generations.

Thank you. You wrote about replacement. Is there some reference for this, in ALS SOD mice? Thanks again.

http://www.informatics.jax.org/reference/J:76718 contains the reference for the original humanized mice with WT human SOD1 and mutant human SOD1 containing a SNP.  Pubmed reference to that paper is here : http://www.ncbi.nlm.nih.gov/pubmed/8610185?dopt=Abstract .  Manuscript is here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC39778/pdf/pnas01514-0539.pdf  From a cursory reading, it doesn't appear that the endogenous mouse gene was removed first.  Making the results even more interesting, and very convincing that a G93A mutation in human SOD1 contributes to ALS phenotypes. Hope that helps.


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Difference between the P4 and P5 subtypes of P-type ATPases in plants
In plants there are various kinds of P-type ATPases. What is difference between P4-ATPase and P5-ATPase?

There are numerous differences between the various subtypes of P-type ATPases, simply because they have different amino acid sequences. Three important differences between P4 and P5 subtypes of P-type ATPases are the following:

Structurally, P4 ATPases have their supporting structural domain (S) in the C-terminus, while P5 ATPases have the S domain divided over the N and C termini. Figure 1 shows the basic structure of P-type ATPases.
Structurally, P4-ATPAses require a beta-subunit for proper function (Poulsen et al., 2008). As the substrate for P5-ATPases is unknown, it could not yet be tested if they also require a beta-subunit.
Functionally, P4-ATPases are putative lipid flippases, while P5-ATPase pumps have so far (per the 2011 report cited) no assigned substrate specificity.

Schematic outline of P-type ATPases. Source: Palmgren & Poul Nissen (2011)
References
- Palmgren & Poul Nissen, Annu Rev Biophys (2011); 40: 243–66
- Poulsen et al., Plant Cell (2008); 20: 658–76


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Why is 70% ethanol preferred for aseptic techniques?
Are other concentrations (say 80%) less effective,or is this just for convenient manufacturing? Is the concentration chosen only because it is less volatile than 100 percent ethanol and hence safer?

70% ethanol is the minimum concentration when used in a lab setting for aseptic technique. You don't want to go lower, because it will not kill the microorganisms you are trying to kill.
However the solution requires water to be effective at doing its job. The 30% water is necessary to provide sufficient polarity to the solution.
EDIT

A rough indication of a solvent's polarity is a quantity called the dielectric constant. The dielectric constant is a measure of the solvent's ability to insulate opposite charges (or separate ions) from each other...
Water is the most effective solvent for promoting ionization, but most organic compounds do not dissolve appreciably in water. They usually dissolve, however, in alcohols, and quite often mixed solvents are used. Methanol - water and ethanol - water are common mixed solvents for nucleophilic substitution reactions.

Dielectric Constants

Water - 80
Methanol - 33
Ethanol - 24

-Organic Chemistry 11E T.W. Graham Solomons et.al.

Note
Dexter's answer provides experimental evidence for why 70% ethanol is used. My answer is based on my experience and understanding and the concentration that I have used in the lab. I would add that 70% was likely chosen as a balance between cost and effectiveness. If you are a little off on mixing the solution from 95% Ethanol stock, then you are still at a bactericidal level, where as if you err at 60% concentration, you could start to let a few bacteria survive.

70% ethanol is still flammable and should be handled with care. The issue with ethanol greater than 98% pure is that the only way to distill the last 2% of water out is to add benzene, and benzene is a known carcinogen. There will always be trace amounts of benzene in 100% reagent grade ethanol.

I thought ethanol to be pretty polar? More importantly,  I thought higher percentages EtOH caused microorganisms to dehydrate, killing the cells, but conserving the viable spores of spore-bearing bugs?

DAMN IT @AliceD... you actually went there and you made me drag out the Organic Chemistry text book... I am hating you right now! ;-)

I disagree about cost and effectiveness point. That is not correct. Main reason to add water is to denature protein faster. You can still kill bacteria with crude ethanol but with different amount of exposure time.

@Dexter That comment refers to the choice between using 60%, 70% all the way up to 95%, as the data you provided showed that 60% to 95% by volume had the same efficacy at killing all of the S. pyogenes. You don't go for 60% because mixing errors can make it less effective. 70% has the same bactericidal activity as 95%, but by cutting with water, you get equal efficacy at lower cost.

Yes, that data is for one species. But point of showing that table was not to comment on percentage dilution but to show that other dilutions can also be used with different exposure time. Cost effective point make sense if below 70% ethanol is very less effective. In that case, we could have used 60% or 50% instead.

It is not very clear to me how dielectric constant has a role in the potency of the disinfectant.

I read recently that absolute ethanol might just cause severe dehydration, and that would preserve the bacterial cells in a bacteriostatic condition, not letting the alcohol enter.

@WYSIWYG the dielectric edit was to address AliceD's comment about the polarity of ethanol and why adding water increases polarity.

@AMR How does polarity contribute to the disinfectant efficacy?

@WYSIWYG That is probably worth its own separate question.

General disinfectants
You need two things for good aseptic agent or disinfectant,

It should be able to kill most of microbes (Spectrum)
It should do it in short time (Speed)

Many chemical disinfectants including ethanol are non-specific antimicrobial. Their predominant mode of action is by protein coagulation or by denaturation. This results in disruption of cytoplasmic integrity, cell lysis etc. Protein coagulation occures at optimum alcohol concentration. In presence of water proteins are denatured fast compare to without water. Alcohol induced coagulation occurs at cell wall involving various plasma proteins.
Ethanol
Ethanol is highly efficient in killing non-sporulating bacteria and mycobacteria but inefficient against bacterial spores. Ethanol is effective bacteriostatic at 10% (Vol/Vol). It is bacteriocidal at concentration above 30% depending on species, exposure time and water content. Following images taken from (Seymour 2001) shows how it is effective within given parameters for one specific species. ("+" sign indicates growth of test organism, "-" sign indicates no growth of test organism )

In 1950, people have standardized set of parameters which are most efficient for killing wide spectrum of microbes with very short duration. Hence ethanol can be used in different concentration but you have to fine tune exposure time accordingly (You can see in above figure, that 50% and 100% can still act as a bactericide, they are less efficient than 60%-95% and require longer to kill all of the S. pyogenes.). 70% ethanol helps in killing wide spectrum of microbes with very less time.

I think that you need to explain how to interpret the figure you added. What do the pluses and minuses indicate. Does in mean that S. pyogenes survives in 50% for 20s but all are dead by 30s? Do the minuses mean that all bacterium were dead at that time point?

Original paper says "+" sign indicates growth of test organism, "-" sign indicates no growth of test organism while "+/-" sign indicates growth in some test and failed in another

Okay, so then I am not sure how you draw the conclusion that you make in the italicized parentheses. 50% and 100% show some growth given a certain time course (Must have used the concentration, then significantly diluted to stop, spun down the bacteria and plated), where there was no growth seen at any of the time points for 60% to 95%. I think the correct interpretation is that at 50%, the concentration is low enough that S. pyogenes can survive about 20s and still grow while they are actually able to survive better in 100% ethanol (60s), due to it being a lower polarity solution.

I concluded in parentheses for reason it is effective with very small exposure time. And I doubt you can comment on it's polarity. Reason you add water is to make protein denature faster. Again the concentration and exposure time you have to standardize accordingly.

You are saying 50% and 100% are more efficient that 70%, but that is not what the figure shows. Plus in this instance is bad because it means that they when they plate bacteria exposed to 50% for 20 seconds, colonies formed, and at 100% they were getting bacterial colonies even when the bacteria was exposed for 1 minute. From 60 to 95% you see no growth, even when the bacteria were only exposed for 10 seconds, therefore those concentrations are the most effective. You are interpreting that chart incorrectly, assuming that what you said about + and - is correct.

1- How would adding water denature proteins faster? You would need detergents to do that. If anything water would maintain the protein conformation as the hydrophobic regions on the inside would  stay on the inside. 2- Solvency is based almost entirely on polarity. That is why salts don't melt in oil, though some ionic compounds won't even dissolve in water, and you need nonpolar solvents such as hexane to dissolve nonpolar organic compounds. Lipopolysaccharides are amphipathic molecules, you need the water to solvate the polar parts and the alcohol to dissolve the less polar parts.

The water helps alcohol enter the cell.If all the water is removed( as would be the case if absolute ethanol was used),the cell is completely dehydrated- making it hard for the ethanol to permeate and denature plasma proteins.


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Why does black and yellow indicate danger?
It is a well-known fact that combination of black and yellow indicates danger or poisonousness.

In western society it seems obvious this comes from bees and wasps, but it seems like many tropical frogs use yellow and black. Black and yellow also indicates toxicity in some fish species and the order of the colors seems to communicate whether we see a harmless milk snake or a venomous coral snake.

So which came first: the fear of black and yellow or the color of bees? Are there any studies about the color combinations effect on human brain? Is it learned or congenital?

I think it is more to do with contrast between Black and Yellow which is important that color itself. This contrast creates optic flow. Most of these organisms use change in optic flow for either navigation or predator detection. We use black and white gratings to scare zebra fish :P I am pretty sure they will invoke same response for Back and Yellow gratings.

@Dexter Wow, that's a good point. You're right, gepards, panters or tigers also use this pattern. Yet I think I will stay with the claim, that it is just a product of sexual selection as it is evolutionary so disadvantageous.

Not only yellow and black, white and red is common as well...

@Probably Could you explain why you think it might be sexual selection??

@rg255 Yes! Since Tabmath has suggested the camuflage I am not sure about it, but in priciple, runaway selection often stands behind the evolution of this coloring.

I think you are perhaps misguided @probably - sexual selection often leads to extreme traits, but it is not the only cause of extreme traits. Fpr example: colour might act as a warning to predators which learn what is poisonous - predators will then not eat the brightly colored animals because they won't get benefit from doing so. For the same reason we see mimicry, non-poisonous species using the same conspicuous colours to make predators hesitate.

First of all, great question! What you describe here is known as aposematism. Aposematism is the adapation of warning signals against the predator. This word is used for any sound, coloring, and odor used as a warning signal. Of course, for this question the focus is color.
Honest indications
Animal coloration is usually an honest indication of their noxiousness. The brighter they are, the more noxious and toxic they are (http://rspb.royalsocietypublishing.org/content/276/1658/871). In the linked article, there are many references one this positive correlation of toxicity of prey to predator and the brightness of the coloration. In the article they use mathematical models to support the mathemstical evidence. But one thing is for sure: bright colors do mean the prey is armed with defenses, whether the correlation is positive or not.
Why then is it black and yellow?
The conspicuousness of the coloration is very important because it is important to see from a far away distance. The reason colors like yellow and black are used is because (http://rspb.royalsocietypublishing.org/content/279/1728/417):

— They provide high contrast against the background (e.g. red/yellow against green foliage), which promotes detection.
— They are resistant to shadows (which are rich in blue-UV), and to changes in illumination (e.g. black should not change during day, whereas white could become ‘pink’ at sunset and sunrise). Therefore, they provide a reliable signal under varied habitats and light conditions.
— Yellow/red and black has both high chromatic and luminance contrast.
— Such colours may allow distance-dependent camouflage if yellow/red and black ‘blend’ to an average colour that matches the background at a distance when predator vision is no longer sufficient to discriminate individual marking components.
— Such colours are distinctive from profitable species.

What about the combination of black and yellow?
In the same article, they mention that:

Many warningly coloured prey have markings comprising repeated pattern elements. Such arrangements in signal structure may increase redundancy in the signal but improve the likelihood that the strategic component will be detected by the receiver. In addition, repeated elements may be rare in many natural environments, thus increasing conspicuousness of the prey animal. Simple pattern components (such as stripes and spots) may facilitate detection and also speed up avoidance learning if they are easier to memorize.

The research seem to show that the patterns, such as the stripes, lead to increased avoidance, but it is not sure whether or not it is due to the stripes itself or due to the constrast of the black and yellow.
I hope I have answered your question and if you have any questions, feel free to ask in the comments.

@TannMath Thanks! Do you think that the fact leopards, tigers and cheetahs use also black and yellow is a coincidence caused by sexual selection?

@Probably well this research was done mainly for prey animals... the main hypothesis for leopards and tigers is that it allows them to hid in their environment better, allowing them to pounce on their prey

Sorry for the late response....  I think the short answer is Game Theory.  Obviously any colour scheme could in principle be used to signal toxicity.  However, if a scheme was chosen that did not stand out it would not be an Evolutionary Stable Strategy (ESS).
Let's take an example.  Suppose a poisonous insect was coloured with green and brown markings.  This is good camouflage since green is the colour of chlorophyll and brown the colour of mud.  Therefore there would be zero downside to a non-poisonous species to mimic the markings of the poisonous species.  Eventually individuals from the non-poisonous species with the markings would massively outnumber individuals from the poisonous species, and brave predators would start eating insects with those markings.  If, on the other hand, the poisonous species chose a colour scheme that made it stick out, there would be a cost associated with mimicry, and in the Nash equilibrium the proportion of species that mimic the markings would be smaller.
In game theory any signalling without an associated cost is known as "cheap talk".  An example is where you go to an auction and before the bidding starts you go around telling everyone "I have a lot of money and I really want this item".  No one will believe you because, well, you would have said that wouldn't you!  However, if before the bidding starts you pull out a Havana cigar and light it with a $100 note, that's not cheap talk, and will probably cause a number of your competitors to quietly back off.

PS: I highly recommend the book "Game Theory: A Very Short Introduction".  Although the example I've given isn't in the book, the book does contain lots of other successful applications of game theory to biology.  In fact GT is probably more successful in  biology than in economics.

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


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On which amino-acids residue is the SDS acting on?
I would like to know exactly what is the mechanisme of the SDS, and I would like to know on which amino-acids residue the SDS is acting on.
Can you help me please ?
Thank you in advance !

If your talking about Sodium Dodecyl Sulfate(a detergent) it has a two main functions:
(1) It disrupts all non-covalents bonds in proteins i.e hydrogen bonds from the main chain, or hydrogen bonds between residues which are dependent on protein shape.
(2) It coats the proteins with a negative charge which is useful for laboratory techniques such as gel electrophoresis.
Your question states "what amino acid residues does it act on?". You can be safe to assume that the SDS will coat the entire protein. About 0.1% SDS solution is enough to sature the polypetide chains of protein molcules with about one SDS molecule per two amino acid residues.


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How to predict a mRNA secondary structure with a large sequence?
When I use some web servers to predict a mRNA secondary structure, I find they always required in a small size sequence. If I use a long sequence and cut it into small parts, do these small parts change the energy or thermodynamic data from the origin sequence when predicting? Is there any effective way to find the right sites when cutting the long sequence?

I would think that it would matter.  Can you list the tools you have used and their constraints?  Have you tried http://rna.urmc.rochester.edu/RNAstructureWeb/Servers/Predict1/Predict1.html ?

Yes, the structure predicted by splitting up the sequence may not represent the actual structure of the full-length RNA. A simple hypothetical case would be that of an RNA whose 3' and 5' UTR interact to cause circularization.
I am afraid there is not clear rule for choosing the subsequences such that the assembly of the individual secondary structures is closest the the actual structure.
We may expect that, with better computational power, the limitation on the size of the sequence for secondary structure prediction, can be overcome.
However, there are experimental techniques using RNA-sequencing that can determine the actual secondary structure — SHAPE-seq (ver 2.0; Loughrey et al. 2014) and structure-seq (Ding et al. 2014). Structure-seq in-fact, tries to determine the RNA secondary structures in-vivo and hence may be a more powerful tool.
However, you said you are working with mRNAs. I guess for mRNAs you can predict the structures of UTRs and the CDS separately. Actually depends on what you are interested in. CDS usually does not harbour any structural motif and any secondary structure in the CDS is usually resolved by the helicase activity of eIF4A. However, secondary structures can slow down the translation elongation rate (Mao et al. 2010, Gorochowski et al. 2015).

Loughrey, D., Watters, K. E., Settle, A. H., & Lucks, J. B. (2014). SHAPE-Seq 2.0: systematic optimization and extension of high-throughput chemical probing of RNA secondary structure with next generation sequencing. Nucleic acids research, 42(21) e165.
Ding, Y., Tang, Y., Kwok, C. K., Zhang, Y., Bevilacqua, P. C., & Assmann, S. M. (2014). In vivo genome-wide profiling of RNA secondary structure reveals novel regulatory features. Nature, 505(7485), 696-700.
Mao, Y., Liu, H., Liu, Y., & Tao, S. (2014). Deciphering the rules by which dynamics of mRNA secondary structure affect translation efficiency in Saccharomyces cerevisiae. Nucleic acids research, 42(8), 4813-4822.
Gorochowski, T. E., Ignatova, Z., Bovenberg, R. A., & Roubos, J. A. (2015). Trade-offs between tRNA abundance and mRNA secondary structure support smoothing of translation elongation rate. Nucleic acids research, gkv199.


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How does mass spectrometry detect histone methylation?
In this research paper they talk about the methylation of histone.  They use mass spectrometry to identify which peptide position is methylated. Does the number yielded by the spectrometer calculate the mass of the amino acid with and without the mass of methyl group? I wonder because I saw some introduction saying the number present the molecular mass of the molecular. I also would like to ask the mechanism of it and how you interpret this data? Thank you!

Can you provide link to that paper ?

The link is http://www.sciencedirect.com/science/article/pii/S1931312813001145 Thanks

It is not simple MS, it is tandem MS. They send the sample through multiple MS and they fragment it between them. So they can get info about the molecular structure as well, not just the mass/charge of the molecule.
A quote from your article:

MS/MS spectra of the methylated H3 protein (top down) and fragments
  upon electron transfer dissociation fragmentation. Fragments of the
  methylated H3 have a mass shift of 42 starting at C14, indicating a
  modification site at the K14 at the N terminus of the peptide.
  Normalized collision energy = 35%, activation Q = 0.250, activation
  time = 100 ms, accumulation time = 5 min.

A reference from your article:

Frese et al., 2011 C.K. Frese, A.F. Altelaar, M.L. Hennrich, D.
  Nolting, M. Zeller, J. Griep-Raming, A.J. Heck, S. Mohammed
Improved peptide identification by targeted fragmentation using CID,
  HCD and ETD on an LTQ-Orbitrap Velos
J. Proteome Res., 10 (2011), pp. 2377–2388

The numbers yielded by any mass spectrometer are always the mass divided by charge (m/z).
Figure 2B in the paper shows the peaks from a peptide that was isolated and then fragmented inside the mass spectrometer. The ideal scenario is that each peak has an m/z that corresponds to a potential fragment of the peptide (or whatever is being analysed).
The fragment ions that indicate the methylation include the monoisotopic mass of three methyl groups (~42). These ions (C14 - C21) also carried two electrons. The machine provides m/z so add the monoisotopic mass of peptide + monoisotopic mass of three methyl groups + mass of two electrons and then divide by the charge (2).
The effect of the charge state can be seen when you look at C13(+;1360.79 m/z) and C14(++;766 m/z).
I didn't know how to address the "mechanism of it".


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Which class of animals constitute the largest biomass?
I found here that species-wise it is cow. But, collectively, insects may exceed even mammals. So, which class of animals constitutes the largest biomass?

Prokaryotes still rule the world. Bacterial and Archaeal biomass far exceeds any other class of living organism.

But prokaryotes are no animals.

according ot this, arthropods. https://www.weforum.org/agenda/2021/08/total-biomass-weight-species-earth the big kicker is krill, there is a LOT of rill in the ocean.

Following from MarchHo's comment, I have not been able to find class-specific (in the formal sense) estimates, but if you meant 'class' in an informal sense, the following may be useful.
A nice infographic covering the relative biomass of all land mammals is here, and a full table for species groups (at the level of domesticated vertebrates, invertebrates, etc) is here (reproduced below).

Short answer: amongst animals, invertebrates are where the mass is.

Don't invertebrates make up multiple phyla and not a single class though?

@MarchHo Good point. I read the question as 'group' in the informal sense, but that was based on the comments mentioning Kingdom-level groups, rather than the question itself.


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Why are female not competitive for reproduction like males?
I have wondered if competition for mate among males and the race among sperm cells would result in healthy offspring,
why no such mechanisms exist among females and egg cells?
(Even females are genetically responsible for the offspring.)

And generate an oocyte arms race... how? How to outrun a sperm cell as fast as possible?

You are asking two very different things. One is a social, group dynamics construct and one is regarding developmental biology. Decide which of the two you want answered and formulate that single question.

I think the question has been poorly executed, please think carefully about your question(s) and edit to make it clearer

are you talking about humans or sexual species in general? and are you asking about sperm/egg competition or organism competition becasue there are very diffrent?

As @Dexter said, there are examples of species where female compete for the access to the males but most often it is the other way around; males compete for the access to the females.
The reason for this discrepancy is mainly explained by Bateman's principle. Citing wikipedia:

Bateman's principle suggests that in most species, variability in reproductive success, or "reproductive variance," is greater in males than in females. This is ultimately a consequent of anisogamy. Females, especially mammalian females, almost always invest more energy into producing offspring than males invest. Bateman's principle anticipated and is consistent with Robert Trivers's theory of Parental investment—in most species females are a limiting factor over which males will compete. This competition results in some males being more successful than others, leading to greater reproductive variance among males than females

At first, I misread as Batman's Principle and got excited :P

@Dexter It might be the martini, but that made me laugh.

Actually there are lot of examples in which females are competing for mating which also have evolutionary consequences. It is also widely spread in nature. This competition may arise at cellular, molecular, genetic, behavioral level. Quoting from (Stockley and Bro-Jørgensen 2011)

female competition is associated with many diverse adaptations, from overtly aggressive behaviour, weaponry, and conspicuous sexual signals to subtle and often complex social behaviour involving olfactory signalling, alliance formation, altruism and spite, and even cases where individuals appear to inhibit their own reproduction.

Following table taken from (Gwynne 1991) which shows lot of examples in which females are competing

There are many more you can find by just searching on pubmed!

Males in monogamous species don't compete much for females. According to "The selfish gene", monogamy is an evolutionary stable strategy. They tend to only produce the number of kids they can get enough food to rear because those that produce more kids almost certainly can't rear all of them and maybe even 2 of them will starve because of the extra energy of producing the extra kid and of the kids fighting with each other for food. If any of them fight for more than their fair share of food, those who fight back those who fight for more than their fair share will be selected for because there's nothing to lose in fighting back for more than their fair share let alone their fair share. After that, those that start a fight for more than their fair share will be selected against because of the possibility of losing the fight and getting even less food, which is why they don't start a fight for more than their fair share of food in the first. At an evolutionary stable population size, each individual can on average get enough food to rear 2 offspring. It's an evolutionary advantage for a female to pick a male that doesn't already have another mate because if she picks a male who already has another mate, there will be 3 parents so they can get enough food to rear 3 offspring but each one will only have a 50% chance of being her own, making it pretty impossible for a male to get a second mate. Since there are about the same number of males as females, almost all males get one mate with almost no left over males or females. Males who fight against any male who tries to take their mate away from them are selected for which in turn causes males of a monogamous species who fight another male for a second mate to be selected against.
According to https://www.dailymotion.com/video/x1e19qg_bonobo-ape-our-closest-relative-nature-documentary_tech, bonobos are also peaceful. All the members of a group have sex with each other all the time and no male knows which baby is his removing the advantage in males fighting. They're probably also peaceful for a similar reason, that those that fight back to not get less than their fair share of food are selected for which in turn causes those that fight to get more than their fair share to be selected against.


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My eyes were accidentally exposed to high infrared radiation and they hurt, why?
My eyes were exposed to high amounts of infrared radiation. They hurt - why?

I think you should contact doctor rather than asking question here.

@Dexter You should talk to a doctor, yes. However, I think we still need to be willing to answer the question! The person asking isn't asking about how to take care of their eyes, but rather WHY their eyes hurt!

Every kind of electromagnetic radiation can burn if the intensity is strong enough. If you didn't feel burning heat or something like that, then most probably something else causes your eye problems.

Be aware that most of the light sources are not coherent, like lasers, so they emit on different frequencies. Usually we filter the unwanted frequencies, e.g. by solarium we filter the higher frequencies than UVA.

@L.B. I said contact doctor because sometimes people try to self medicate. It is better not to give any medical advice on open online forum.

@Dexter Haha, true, I do it all the time :)


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How does one insert cas9 into animal cells?
How could cas9 be inserted into cells by researchers looking to edit a genome? I imagine for engineering bacterial systems you could just put in the cas9 coding region in an expression vector, but is that how it is also done for eukaryotic cells?

In short, yes. It's just under a mammalian promoter.

Any other notable adjustments that would need to be made?

I should clarify my earlier comment - it's under a promoter appropriate to the organism of interest. I work with mammalian cells, so I have "mammalian" stuck on my brain...

Right, I guess what I mean is, are there any amino acid substitutions or things like that from the bacterial cas9 sequence? Or does it generally fold nicely and work well just using the same ORF?

If you are talking about the nuclease functionality of Cas9, then you aren't adding the Cas9 gene into the genome, you are transfecting it on a plasmid. Usually there is either some form of permeabilization done to the cells, or the construct is inserted into a viral vector in order to transfect the cells in tissue culture. In multicellular animals, you would need to use the viral vector route as would need to be done with any gene therapy technique. Addgene is a nonprofit plasmid repository that has many of the CRISPR/Cas9 constructs that have been developed, and they have an excellent resource on their Website.
You wouldn't really want Cas9 active in the cell after it has done its job, as you increase your likelihood of off-target hits. The target shouldn't be in the genome anyway if the targeting event occurred, because you have either substituted in another piece of DNA or you have cut the DNA and the DNA repair mechanisms have introduced random nucleotides in order to repair the double stranded break.
Eukaryotic cells, for the most part, cannot maintain plasmids. The Cas9 gene will be transcribed along with the guide RNA. The resulting protein/RNA complex targets the sequence of interest and makes a cut. When the cell replicates the plasmid will likely be lost, but the daughter cells will inherit the genomic edit made by the targeting event.
If you are looking to insert a different gene at the target site, say a reporter into the genome, then you co-transfect a linear piece of DNA with homology arms around the cut site so that that donor will be inserted via homologous break repair.
One of the Cas9 constructs that has bene developed has disabled the nuclease activity, so that the Cas9/RNA complex ends up acting as a binding protein to suppress the activity you are looking to study without actually deleting or replacing the gene. In this case you may look to insert the Cas9 cassette, in which case you would use a recombination event as you would with any other type of incorporation into the genome.


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How long can human tissue last without blood?
I've heard it said various times that the body's tissues will begin to necrotize after being cut off from the blood supply for only a few minutes, but that can't be true.
A few years ago, I woke up one morning and apparently I'd been sleeping just right so that the main artery to my left arm was totally pinched closed, because it was completely numb.  Not just "arm's fallen asleep", either; I had no mental control over the entire arm and no feeling in it.  I could lift it up with my right hand, and it would fall back down immediately when I let go of it, and I didn't feel anything when it landed on the mattress.  It kind of freaked me out at first, but in just a few minutes I felt the "pins and needles" feeling of circulation returning, and it was 100% back to normal within less than an hour.
Given that I had presumably been sleeping on it like that for several hours, and yet I somehow didn't end up with a dead, useless arm that needed to be amputated, I know from personal experience that tissue doesn't die within a few minutes.  So how long does it really take?

Your supposition is incorrect. A limb or other body part goes numb because a nerve is blocked, not because the blood supply is cut off. If you had truly completely cut off either the subclavian or brachial artery for that long, your arm would be deep purple.

It depends on the tissue type and on the circumstances. Brain cells start to die after 5 minutes, while heart cells die after 2 hours without oxygen. You can slow down the process by cooling down the body.

In medical school, we called this Saturday Night Palsy (or Honeymoon Palsy) - key emphasis on palsy - a nerve injury, not an arterial blockage.

@anongoodnurse "Saturday Night Palsy (or Honeymoon Palsy)" is that because it is generally alcohol that suppresses your CNS so that you do not move or change position in your sleep? Or does it have to do with someone else sleeping on your body part and it going numb from nerve compression? Serious question.

@AMR - Both, actually. Seriously. The inebriate falls asleep in a bad position and stays that way; the honeymooners snuggle, her head on his arm usually.

It sounds more like your put pressure on your nerves rather than cutting blood supply. Your arm didn't turn purple or black.

@MasonWheeler, Maybe you reduced the blood supply by 90% or even 99% but not 100.0%?

As EMT (Emergency Medical Technician) instructors will tell you now, when wearing a tourniquet, you have about four hours to get the injury to a vascular surgeon and get it cared for appropriately. The rule therefore is four hours. However, the common thread I see in most sources is that about an hour and a half is the longest you want to go without blood flow to a limb.
As far as what happened to you, it sounds more like the limb simply fell asleep. When a limb falls asleep, it is getting the nerve pinched off for a time as well as loosing some blood flow. However, this is not a complete loss and so your arm is able to survive because it is still receiving enough oxygen and other nutrients to sustain its existence (as well as having toxins and CO2 pumped away from it).
I had a very difficult time finding any concrete, scientific information on this subject overall.
So, if you would like more information about this, please visit the following links. The first is a WikiPedia link on Limb Infarctions (or an embolism in a limb). The second is from Mental Floss on Why Limbs Fall Asleep. The third is a somewhat random article on someone's personal experience on Sleeping on their arm.
So, in summary: although I could find no solid evidence on how long a limb can live without its blood supply, it appears to be about 2-4 hours (some sources say 5-8); however, I would like to add that your case appears to be a severe case of an asleep limb, you were/are likely in no danger. Also, if your arm indeed did have circulation completely cut off, it would have turned pale, then blue and later a livid red and purple as the blood began to pool; you then would begin to experience the effects of the limb dying i.e. necrosis, gangrene.

The Mental Floss article says that it involves circulation being cut off as well as the nerve being pinched.

@MasonWheeler Oh dear... Thanks for pointing that out, I shall change that when I get the opportunity.


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How does the drug MBC effect the depolymerization of microtubules in eukaryotic cells?
I have tried to look for the mechanism of how methyl benzimidazol-2-yl-carbamate affects microtubules in eukaryotes, but what I found wasn't very useful:

Quilan et al 1980 assert that it acts by inhibiting polymerization of microtubules rather than by directly depolymerizing them.
In "The Cytoskeleton: A Target for Toxic Agents", it is mentioned that

..strains of Aspergillus that were resistant to the drug had a lower affinity for MBC in a binding assay, whereas super-sensitive strains had a higher affinity for the drug.

Any references would be appreciated.
In Summary: I would like to know how the drug MBC effects the depolymerization of microtubules in eukaryotic cells. I would also appreciate any scientific references.

Welcome to Biology Stack Exchange! I made a few edits to your post, you are welcomed to change it back to the original if you feel it better describes your question.

Carbendazim inhibits microtubule polymerization by directly binding to tubulin, preventing subunits from interacting. Therefore, mytotic spindle malforms and potentially causes aneuploidy in affected cells. Mechanisms of resistance are often shown to be changes in membrane permeability to the compound.

CARBENDAZIM (addendum)


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How do I read a species description that uses both ≡ (triple bar) and "incl." to denote synonymy?
I'm trying to understand the relationship of plants formerly classified as Dorstenia crispa with distinct individuals continuously classified as Dorstenia foetida. I would assume that the distinctive phenotype would warrant a var. or forma, if not a subspecies, but I haven't seen it written as such anywhere.
I turned to monographs, which in one case stated:

incl. Dorstenia crispa Engler (1898); ... incl. Dorstenia crispa var. lancifolia Rendle (1915) ≡ Dorstenia foetida ssp. lancifolia (Rendle) Friis (1983);

Would this indicate that a specimen identified as D. crispa is properly identified no more specifically than as D. foetida?
Does this indicate that a specimen of D. crispa v. lancifolia is properly D. foetida ssp. lancifolia; or simply recognising that D. crispa v. lancifolia and D. foetida ssp. lancifolia would refer to the same individuals, which are properly still called nothing more than D. foetida?
Since these formerly-recognised infraspecific taxa do exist as separately-kept lines in cultivation, would they be properly recognised as cultivars?

My answer may simply be the closing remark in the above-quoted description, "Since the various forms are connected by intermediates, it is impossible to recognize infraspecific taxa." However, that's deeply-unsatisfying if cataloguing a collection that contains several now-synonymous specimens.

Welcome to Biology Stack Exchange! I think this is a fine question, and I look forward to hearing (or rather seeing) the answers!

Thank you! I appreciate the welcome, and hope this gets some answers myself. :-D

This seems like the type of thing that might vary from publication to publication. If you have access to the full book, maybe there's a key/glossary where you can find what the authors mean by these symbols

According to the Taxon guidelines for authors (pdf, pg 205), a triple-bar (≡) indicates a homotypic synonym:

Homotypic names are cited in chronological order in a single paragraph with
  the identity sign (≡), followed by the type.

So, in your example, Dorstenia foetida was described on the basis of the same type specimen used by Forsskål in 1775 to describe Kosaria foetida -- or possibly a neotype was designated linking these two names, possibly by Schweinfurth in Bull. Herb. Boissier 4(App. 2): 120 in 1896. More information about the relevant type specimens would help sort this out.

That makes sense. How does it play with "incl.", then? I see, then, that D. crispa var. lancifolia shares a type with the superceding name D. foetida ssp. lancifolia. What relationship does that type have to D. foetida, indicated by the incl.? Is it simply that the taxonomist preparing this monograph is indicating his belief that they all should share a type, even though currently they don't?

I'm afraid I have  no idea! If I had to guess, I'd guess that "A: incl. B" means that all individuals associated with the name B are considered by the taxonomist to belong to their circumscription of name A, without the requirement that they share a homonym. In some cases, it looks like B is a subspecies or variety, suggesting that these should be subsumed into A and not considered a separate entity. I'd hoped someone more knowledgeable would chime in but since that hasn't happened yet, here's my somewhat-informed guess!


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Gene silencing in C. elegans
I am trying to silence the tph-1 (tryptophan hydroxylase) gene in C. elegans using the pLT63 plasmid to check if that particular gene has anything to do with the pharyneal pumping or not. Am I using the right plasmid for the purpose?

"pLT63 contains 0.8 kb of the fem-1 gene inserted into the L4440 vector" (1). The gene fem-1 is involved in determining the male sexual trait in C. elegans (you can verify this on uniprot). It may be best, however, to stick to a "normal" plasmid like L4440 that'll just have your tph-1 insert ligated in.

Is there any direct link between tph-1 and pharyngeal pumping in the worms that you know of?

I did read through some literature and while some evidence says tph-1(mg280), a deletion of an allele, alters the ability of the worms to fine-tune the speed of their feeding, i think that was here. But overall, and we see in this study, the worms have relatively normal feeding. I haven't done the experimentation myself, however, so I can't 100% make a claim here.

Check out the WormBase site at www.wormbase.org. Just type tph-1 in the search box on the right hand side at the top of the page.


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How does acupuncture work?
Can anyone actually tell me how acupuncture works?
There are numerous websites with little actual explanation, but assert that it works. For example the below article:
http://www.health.harvard.edu/blog/acupuncture-is-worth-a-try-for-chronic-pain-201304016042
However I have failed to find any article about how acupuncture works, or the mechanism at play. Can anyone tell me how it works?

Welcome to Biology.SE. Do you have any evidence to support that it actually works? If not, your question is off-topic because "primarily-opinion based". If you are looking for evidence f whether it works or not, then you should go on Skeptics.SE. You will find here on skeptics a lit of questions tagged acunpuncture that will probably already give you some answers.

@Remi.b https://scholar.google.hu/scholar?as_ylo=2011&q=acupuncture+placebo+controlled&hl=hu&as_sdt=0,5 There are many placebo controlled articles, it is better than placebo. (Btw. it is interesting, how you do placebo acupuncture. :D)

Dear questioner, let me help: https://scholar.google.hu/scholar?q=acupuncture+mechnism&btnG=&hl=hu&as_sdt=0%2C5&as_ylo=2011

@inf3rno sham needles!

@TanMath I checked the video, but it wasn't about whether acupuncture works. It was about that doctor - patient relationship has placebo effect which I already knew. http://www.dailymotion.com/video/x1moo91_horizon-2013-2014-8-the-power-of-the-placebo_lifestyle

@inf3rno that wasn't my video.. I was just saying sham needles can be used as control

@TanMath Ohh okay. :-)

@TanMath I checked 4-5 article about placebo controlled experiments by different diseases. None of them was better than placebo. It is a bit early to tell, but maybe it is really just placebo. :-)

What is acupuncture
Acupuncture is a form of alternative medicine by which needles are pierced through the skin and helps to treat diseases.
Science behind acupuncture
So far, the research on acupuncture has shown that acupuncture can help to suppress pain but probably will not treat diseases.
Really, it all has to do with connective tissue. Connective tissue is tissue that connects, supports, binds, or separates other tissues or organs. In the connective tissue, there are cells known fibroblasts. According to an article in The Scientist (http://www.the-scientist.com/?articles.view/articleNo/35301/title/The-Science-of-Stretch/):

the cells that are responsible for synthesizing all the proteins that make up the extracellular matrix. These cells reside within the matrix they create, responding to mechanical stimulation by regulating the amount of collagen and other matrix proteins produced, and by secreting matrix-degrading enzymes in response to chronic changes in tissue forces.

Their research also showed that:

the fibroblasts initiated a specific Rho-dependent cytoskeletal reorganization that was required for the tissue to fully relax. Rho is an intracellular signaling molecule known to play a role in cell motility and the remodeling of cell-surface proteins that connect the fibroblast to its surrounding matrix.

They also mentioned that the fibroblasts secrete ATP, which is converted to adenosine which is an analgesic. This leads me to a second article in in Discover Magazine (http://blogs.discovermagazine.com/notrocketscience/2010/05/30/a-biological-basis-for-acupuncture-or-more-evidence-for-a-placebo-effect/#.VjAmFyPn_qD). In this article, they mention about a paper that described the importance of adenosine.
Criticism
The research showed that the A1 receptor for adenosine is important for acupuncture to work. But they mention in the Discover article that there is nothing special about acupuncture. They say:

o answer that, clinical trials have used sophisticated methods, including “sham needles”, where the needle’s point retracts back into the shaft like the blade of a movie knife. It never breaks the skin, but patients can’t tell the difference from a real, penetrating needle. Last year, one such trial (which was widely misreported) found that acupuncture does help to relieve chronic back pain and outperformed “usual care”. However, it didn’t matter whether the needles actually pierce the skin, because sham needles were just as effective. Nor did it matter where the needles were placed, contrary to what acupuncturists would have us believe.

It is hard to also have a control but it seems the best may be the sham needles. However, much of this research is debatrd.
I hope I have answered your question. Please ask anything more in the comments.

It works via the placebo effect which according to recent research, is not the sort of trivial effect as it was thought to be.

What about the research in the articles described in my answer?

@TanMath What has transpired in recent years is that sham acupuncture and real acupuncture work just as well, the best results are obtained when  patients have long discussions with the doctor about the complaints  before undergoing treatment, whether it is a sham or real treatment.

but there is scientific evidence that it is a physical phenomenon...

@TanMath The relevance of such induced phenomena must be established. E.g. if I treat patients suffering from vertigo by letting them be subject to a roller coaster treatment, then obviously I'm subjecting them to nontrivial physical effects that influence balance. However, if I'm not doing any better than alternative treatments where they are not subject to such influences, then I can't say that the roller coaster had any effect on the vertigo. My theory may well be very plausible, there may exist experimentally confirmed mechanisms that support my theory. But it's then all irrelevant.

@inf3rno says that your video wasn't about whether acupuncture works... Maybe another link about placebo and acupuncture is better?

If you watch the entire video, you'll see sham acupuncture with patients discussing complaints compared to real acupuncture.

Every major, large, blinded, well-controlled study shows that it is no better than placebo.
Here's one article with references:  https://sciencebasedmedicine.org/acupuncture-doesnt-work/