text:
Isotropy of sarcomere bands in skeletal muscle cells
As seen under a polarization microscope, the A-Band in skeletal muscle fibres is so named because it is anisotropic in its refractive index which is a characteristic of orderly crystalline structure. On the other hand, the I-Band is so named because of its isotropic nature, as far as its refractive index is considered, which is characteristic of Amorphous substances or substances which lack long-range order. Both are filamentous (as opposed to globular) in the sarcomere (Actin is present as F-Actin).

But then why this difference in the characteristics of refractive index,
  which is indicative of order (i.e crystalline or amorphous?) in their
  molecular structure?

Moreover, is the H-Band anisotropic?
If not, then the anisotropy of the remaining part of A-Band must be a consequence of the relative arrangement of Actin and Myosin which are independently isotropic, and hence cannot give a possible isotropic arrangement.
If yes, then that indicates that the myosin filaments are anisotropic in themselves and actin filaments are isotropic. But, in the region of their overlapping (A-Band minus H-Band), the overlap is between an anisotropic (myosin) and an isotropic (actin) component which shouldn't be anisotropic because the randomness of actin filaments (i.e. its isotropicity) should make the entire configuration isotropic?
I am sorry if I am wrong in my understanding of isotropic and anisotropic characteristics, or if my question sounds too "physics-related", but this has been bothering me for quite some while now.
Here is a directly related question I asked on physics.se. It partly solves the problem of possible arrangement of isotropic elements to generate anisotropy.

I am not sure if the "biochemistry" tag applies here. Please edit the tags if it doesn't.

refractive index is not just a property of an amorphous material. Crystalline solids also have refractive index but it may vary with different planes. And i dont think the A-band is in crystalline form. The anisotropy refers to polarization effects. You cannot deduce that myosin conributes to anisotropy. It is a property of a material as a whole (even same substances can exhibit different optical properties in different structural forms)

@WYSIWYG I know refractive index is not the property of amorphous substances. I meant isotropic refractive index is a property of amorphous substances. And I was just saying, that normally, crystalline substances have anisotropic refractive index. Therefore, I wanted to know what property of the molecular structure of actin and myosin contributes to such a division of isotropic and anisotropic bands in the sarcomere

I am not sure about this but if you just take different sections and see how the 2D arrangement looks like then the A-Band region will look different in different sections (x-y and x-z planes). This may be the reason for the observed anisotropy.

This is sort of technical answer, but I hope its helpful I hope.
All these bands in the sarcomere are anisotropic.  Isotropy would imply that the structure/properties of something is equally ordered or coherent in all 3 directions.  The sarcomere has definite structure along its longer axis so the H band is anisotropic.
Since the H band is a small structure compared to the actin and myosin components of the sarcomere, much of the signal that one measures via diffraction or polarization experiments is from those two fibers and less information would be discernible from the anchoring portion (H band) of the myosin filament.
In the case of the A and H bands, which are identified by electron microscopy, the structure along the sarcomere axis is not very strong - they are thin sections of the sarcomere and tend to function structurally to connect the actin and myosin axes.
Because of this the information that you might get from A and H band segment studies will be that 'these bands are not very ordered along the axis of the sarcomere'.  That's not a lot of information, and we know this from other experiments.  But it is information nonetheless because they have some spatial organization.


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Aside from Homo Sapiens, do the males of any other species care for the offspring of those unrelated to them?
Elsewhere I heard that male Long-tailed Tits will care the offspring of their brother if they're unable to have their own. However, I'd like to know if there is a case of such behavior where the two are unrelated to one another.

Wolves? How else would the Roman Republic have come into being?

That particular wolf was of the female persuasion, I believe.

Yes most commonly in a reciprocal altruism fashion, when you aid any offspring of your species or any in your herd/pack. Crocodiles are known for this. They respond to any crocodile (of their species) distress call from any baby crocodiles. This tends to be an advantage because proximity usually means relatedness and even when it doesn't crocodiles are high enough on the food chain the risk to the males is low compared to the time and effort that would be needed to identify the offspring first.
likewise in herd animals it can be an advantage because it ends up with everyone protecting everyone else's offspring but usually has to be paired with some ability to punish freeloaders/cheaters (individuals who don't help protect the offspring).
Of course you also have males who are tricked into it, after all a male does not always know what are its offspring.
You also have males that will help with a current brood to court the mother, or even unrelated females. Basically they are showing off how good a parent they can be, some believe this is what humans are doing. This is seen in some social primates. It might happen in some birds too but I am not sure.

Would be great to have a reference for your claims.

What is cheating/freeloading in this context?

@Ludi a cheater in this context is a parent that does not help defend unrelated offspring.

I think most if not all herding species do this.
I watched one video taping a strong adult elephant (who travel alone) helped a baby elephant who was too weak to follow his/her parents and left alone.

Two examples off the top of my head:
Meerkats (Suricata suricatta).
It's well-known that each member of a meerkat group takes turns minding the pups for the whole group, and this includes both males and females.  Quote from the website http://meerkats.net/info.htm which states this specifically:

babysitter - Stays with the pups while the gang is out foraging for food.                           Different gang members take the responsibility different days, this                            is not domiated by males of females. Generally though the least                            hungry Meerkat will do the babysitting. The alpha female never                            baby-sits. This duty is for Meerkats 6 months or older.

I also found this on the same site:

After sixteen weeks [the pups] are on there own to find there food  Each pup will be taken on by a adult Meerkat which will act as a mentor, who will take the responsibility to teach the pup necessary skills for foraging for food as well as responding to danger.  Male Meerkats tend to mentor male pups and female Meerkats tend to mentor the female pups.  Many of skills Meerkats have are taught by the mentors rather then being instinctual.

(Site author says is an enthusiast compiling information from various sources: very detailed and descriptions square with information I've seen elsewhere, so I think this is a reliable source of information despite its dodgy typing.)
Canada geese (Branta canadensis).
Canada geese often have a "creche" system where one pair of geese at a time will babysit the entire group's goslings while the others forage.  Here's a discussion of this in the Guardian newspaper's Notes and Queries pages from 2011.
https://www.theguardian.com/theguardian/2011/oct/11/childminding-habits-of-canada-geese
(The first letter states that this only occurs on water.  From my own observation, I can say that that's not true.  It may be where Mr Dowsett lives, but I've sometimes seen a whole small flock's goslings asleep on a canal bank together with one pair of adults standing guard over them while the rest forage further along.)

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(Bioinformatics) Protein-Protein Software Prediction
I'm trying to figure out Protein-Protein interaction of two proteins without known crystallography structures. Any way software can predict this without the known structure? The problem is most software that does it is just textmining through articles, I was seeing if they can do some sort of prediction based off of just known sequences and other trivial things?

What options have you tried so far? There a lots of options, but it depends on what biological question you're asking, and the resources available to you.

Based on what I know you won't be able to run docking simulations on a sequence. The reason being our technologies for predicting 3D structures from sequences are not accurate enough to determine biological activity. Currently there is a competition every year for protein structure prediction software and I'm almost certain if someone comes up with a 100% accurate one there will be a nobel prize in it for them. Software that could predict structure from sequence accurately would radically accelerate molecular biology research.

This review about protein docking will hopefully get you started.
Xue, L. C., Dobbs, D., Bonvin, A. M., & Honavar, V. (2015). Computational prediction of protein interfaces: A review of data driven methods. FEBS letters, 589(23), 3516-3526.
There is a page where they provide a short description about the different algorithms used, as well as links to the web servers. I also believe that most of these website should have a downloadable source code that you could compile and use on your own computer/cloud.
Here is a brief summary of the main methods highlighted by the paper:
Homology-based methods. In this approach, biological properties of a query protein are inferred from its homologs. The assumption here is that homologs share significant similarity in their sequence, structure and functional sites. Therefore, this approach performs best when close homologs are available.
Template-free machine learning methods. In this approach, machine learning algorithms are used to classify a target residue as either interfacial or non-interfacial, based on properties of both the target residue and the neighbouring residues. This approach is best used if there is limited availability of homologs, or when templates are not available or of poor quality.
Conclusion: If you have the sequence data available, then the 2nd approach seems most appropriate. You could also apply both methods and see the extent of agreement/disagreement between the methods, i.e, you could use the machine learning approach to detect the interfaces, and subsequently validate your docking predictions based on sequence data, if close-enough homologs are available.

Great succinct answer for a pretty vague question!

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When does a chromatid become a chromosome?
When chromosomes lie on the metaphase plate, they have the characteristic X shape. But these are actually two chromatids that are held together at the centromere. If separation fails and both chromatids are pulled in the same direction it leads to trisomy (three homologues chromosomes). So when exactly does a chromatid become a chromosome if it's not after successful separation?

If no centromere split occurs during anaphase and consequently chromatids are pulled to one daughter cell, the possible outcome is during telophase the chromatids uncoils into chromonema which in subsequent divisions become supernumerary chromosomes.

Welcome to Bio. Can you add citations to back up your answer by any chance?

So the two unsuccessfully separated chromatids could become a single B-chromosome?

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How is membrane capacitance related to the increased speed of saltatory conduction?
Here is the original question which inspired my question. As explained by the answers there, the reason saltatory conduction in myelinated neurons is faster than non-myelinated conduction is because the capacitance of the membrane is lowered by reducing the number of channels (Channel density) or equivalently, increasing the spacing between channels. I also did a preliminary study of membrane electrodynamic modelling here and here.
From what I gathered from the linked question, the decreased capacitance overcompensates the effect of absence of channels reinforcing the sodium current, and on the whole, increases the speed of conduction by allowing the depolarizing potential to travel to the adjacent node faster than in case of an unmyelinated fibre. In view of this, I have a question:-

Why does lower capacitance increase "the effectiveness of nearby
  nodes" or allow the depolarizing voltage to "travel not by ion
  diffusion, but as an electric field"? I am comfortable with capacitors
  and related physics, but why would lower capacitance allow propagation
  of the changing voltage as an electric field, is still unclear to me?
  (The links I have placed also help quantify the problem
  mathematically. This allows us to say that $\lambda$, or the rate of spatial
  decay of potential, increases, decreasing the effective
  length of the neuron. Why should its decrease help faster conduction?)
And another question is, how would reduced density of sodium voltage
  gated channels cause a decreased capacitance?

Very nice question! I'll go through your three questions sequentially.
Q1: Why does lower capacitance increase "the effectiveness of nearby nodes" or allow the depolarizing voltage to "travel not by ion diffusion, but as an electric field"?
A: Capacitance basically results in sequestering of charge of opposite polarities along the cell membrane, which basically results in a neutralization of charge differences. The effect of this is explained on the website of Amrita and I quote:

[...] a higher capacitance results in a lower potential difference. In a cellular sense, increased capacitance requires a greater ion concentration difference across the membrane.

What myelin does is insulating the neuron, thereby decreasing its capacitance. You could say that by increasing the thickness of the membrane, the negative insides of the cell do not attract positive charge outside the cell. It's a bit simplified, yet it effectively describes what myelin does (see cambridge web page on capacitance).
So in a myelinated axon, when Na+ enters the cell in a node of Ranvier, the positive charge entering the cell is not counterbalanced by outside negative charge and hence, the charge is not or at least less counterbalanced. This allows for the depolarizing potential to be transmitted by electric charge. If there were no myelin, the depolarizing potential would fade out pretty quickly along the axon by neutralizing charges outside the cell. Without myelin the opening of more sodium channels in the direct vicinity are necessary not only to transmit the action potential across the axon, but it is also necessary to amplify the signal to prevent it from dying out. In a myelinated axon, hence, the depolarizing potential reaches much farther and in answer to your next question:
Q2:This allows us to say that λ, or the rate of spatial decay of potential, increases, decreasing the effective length of the neuron. Why should its decrease help faster conduction?)
One could say that myelination effectively decreases the length of the axon (the lamba parameter) as the depolaring potential reaches further along the axon.
The fact that the depolarizing potential reaches further means that voltage-operated sodium channels can be activated at larger distances from a certain depolaring potential. Hence, adjacent nodes of Ranvier can be spaced by as much as 1.5 mm. Due to the fact that the next node is activated by passive spread of an electric field, which is pretty much instant, it skips the intervening distance with about light speed, greatly enhancing conduction velocity.
Q3: And another question is, how would reduced density of sodium voltage gated channels cause a decreased capacitance?
Basically there are no ion channels below a myelin sheath as they are totally useless there. It is the myelin that decreases capacitance and there happen to be no channels underneath.

Wonderful answer. One follow-up question, though. Is the decrease in capacitance due to myelination a consequence of only the increase in separation of the charges or is there some contribution by the actual material of the myelin?

@SatwikPasani - sorry for this slow response. Capacitance can only be mediated by insulators because charges have to be separated. Conductors will allow charge passage. So yes, myelin should be insulating and therefore a fatty substance like myelin is best. Salinic watery substances should be avoided.

The Hodgkin-Huxley model:
$$I=C_m\frac{dV}{dt} + g_k(V_m - V_k) + g_{Na}(V_m - V_{Na}) + g_l(V_m- V_l)$$
Where $C_m$ is membrane capacitance per unit area and $g_i$ are membrane conductances.
Reducing the number of channels does not affect capacitance; it basically reduces membrane conductance.
Myelination causes reduction of number of channels (concentrating them only at the nodes of Ranivier) and also increases the effective membrane thickness.
Capacitance decreases as an inverse function of "inter-plate distance" (of parallel plates) which is the membrane thickness. This reduces the capacitative current.It also prevents the build up charge and thereby allowing it to propagate forward (Longitudinal current). IMO, the effect of myelination of capacitance would be much less than that of its effect on conductance.

Hi, do you know how myelination causes reduction of number of channels? See my question here.


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How does optogenetics work?
I am aware of the post here 'Optogenetics - How do microbial opsins work?'
however it is a bit too technical for me. I am struggling to understand how the neurons can be genetically engineered to produce these light-sensitive molecules in optogenetics, and how genetically engineering the neurones is even a usable method considering it seems you would have to genetically engineer the neurons one by one. So I suppose my question is: in the trials run of optogenetics so far (with mice), how where the neurons made to respond to the light stimulus?
Also, I was wondering whether the principle behind optogenetics- controlling calls with light- could be used for other treatments e.g. to kill cancer cells?
My biology knowledge is limited to A-Level (final year of high school), however I really want to understand this topic thoroughly, so detailed but not too technical answers would be much appreciated! Thank you!
EDIT: I just wanted to add two more quick questions...

Are the light-sensitive molecules (which I now have read are channelrhodopsins) present all along the axolemma, or just the membrane of the soma of the neuron? (I hope I used those terms correctly!)
Wikipedia says that these channelrhodopsins are non-specific (with some exceptions: The L132C mutation (CatCh) increases the permeability for calcium and generates very large currents.[17] Mutating E90 to the positively charged amino acid arginine turns channelrhodopsin from an unspecific cation channel into an anion channel. This chloride-conducting channelrhodopsin (ChloC) inhibits neuronal spiking when illuminated with blue light.[18]). How then can these channels work, if any cation can diffuse any way through the channel?

I'm not too familiar with optogenetics in neurons, but I've seen part of a talk about it, and I think they had to run fiber optics through the brain to get the light to specific areas. I assume getting light to other sites in the body would also need fiber optics, if it wasn't close to the skin.

Fiber optics are not needed :) will try writing up an answer later. So to grasp your level of knowledge, do you know the following terms: viral vector, transformation, photoreceptor, neuron, retina, optic nerve. You can just call out which you don't know.

@ChrisStronks Unfortnately I am unfamiliar with several of those terms! Viral vector (although I am guessing it is just the inactive virus that injects the DNA strand into the cell), transformation, photoreceptor (but guessing that these are just light-sensitive cells like rods and cones. I don't really know how these work though...).

Expecting your answer @ChrisStronks. Please talk a little about it's uses too

@ChrisStronks so if you have the right wavelength of light at high enough intensity you can just beam it through the body? Maybe the fiber optics were used to get specific areas of the brain.

Short answer

Optogenetics can be used to make cells responsive to light. One striking use of this technology is to restore vision in the blind by making the surviving neurons in the retina light-sensitive. This can be done by transfecting the retina with genetically engineered viruses that induce the expression of bacterial channelrhodopsin proteins in retinal neurons.

Background
I will explain optogenetics by focusing on one of the most striking applications: to make the blind see. In humans light is sensed by photoreceptors in the retina (see further reading #2). Rods infer grey-scale vision (i.e., night vision), while cones provide color vision when there is enough light available. Rods and cones contain light-sensitive proteins: the photopigments. The pigment in rod photoreceptors is called rhodopsin, in cones they are referred to as cone pigments, which are used for color vision. When light hits the rods and cones, the photopigments catch the light and activate a cascade of second messenger reactions, eventually causing hyperpolarization of the membrane. This hyperpolarization in turn activates secondary neurons in the retina, which eventually carry the receptor signal to the brain, where it is processed and used to generate a visual percept.
Light sensing across single-celled and multicellelar animals is mediated by two large families of proteins: the opsins. Opsin genes are divided into two distinct superfamilies: microbial opsins (type I) and animal opsins (type II). The rohodpsin and cone pigments found in humans belong to type II. Among other differences, type I opsins are bound to ion channels, while type II is not. Type II opsins therefore need a battery of intracellular second messenger molecules to operate. In contrast, the type I opsins, being channel proteins, directly cause intracellular changes by changing the membrane potential upon activation due to ion flow. Type I opsins, being channel proteins are referred to as channelrhodopsins.
In retinal degenerative diseases such as retinitis pigmentosa (RP) the photoreceptors degenerate and patients eventually loose their vision. The secondary neurons in the retina, however, partly survive. As explained above, these secondary neurons are responsible for processing the photoreceptor signal and sending it to the optic nerve. Hence, although RP patients miss the photoreceptors, the rest of the visual pathway is ready to rock! Hence, somehow these neurons should be activated. There are a battery of approaches to do just this. Retinal implants activate the neurons directly by electrical activation (see further reading #3).
Optogenetics (Fenno et al., 2013) is another approach where the secondary surviving neurons are made photosensitive, thereby bypassing the photoreceptors by turning the secondary neurons into photoreceptors. The neurons are made photosensitive by making them express channelrhodospins. This is done by injecting a viral vector into the eye such that the virus infects the retinal cells. Instead of a viable virus, however, it is tinkered aound with and the only thing the virus does is incorporate the channelrhodopsin into the genome of the neurons, which start to express it.
Channelrhodopsins are cation channels, and therefore, upon light activation, they allow positively charged ions (notably Na+, but also Ca+) into the cell. This depolarizes the neuron and can induce action potential firing (see further reading #1). Action potentials is the neuron way of transmitting signals to the brain. Hence, by activating the secondary neurons through channelrhodopsin transformation, they start sending light-induced neural activity to the brain. The brain will handle this input as if evoked by photoreceptors and hence will interpret it as light-evoked visual stimuli.
With regard to cancer: It has been shown that expression of channelrhodopsin and illumination of whole-mice resulted in diminished subcutaneous cancer cell counts (yang et al., 2013).
With regard to your first added question: dependent on the exact peptide regulatory sequences added to the protein, or by using viral vectors specifically targeting axons, expression of channelrhodopsins can occur wherever one likes.
Your second added question: Cation channels activate neurons, anion channels inhibit them. This means you can play around with different variants to control neurons at will.

References
Fenno et al. Annu Rev Neurosci 2011;34:389–412
Yang et al. Cell death and disease 2013;4:e893

Further reading
 1. Action potentials and neurons: how-do-the-brain-and-nerves-create-electrical-pulses
 2. Photoreceptors: parallels-between-pixelized-image-and-the-human-retina
 3. Retina and retinal implants: does-the-retina-encode-visual-information-like-a-bitmap-or-an-svg

Too good! Real nice answer.

@OneFace - Thanks! Your appreciation is welcomed - as you indicated elsewhere - the answers that take most of your time get the least upvotes, at least so it seems lol

Nice answer. But you would still need fibre optics to activate the specific neurons. In the comments you said it is not necessary. Can you clarify that point?

@WYSIWYG If you use this technology for retinal repair, then light that enters the eye will activate the transgenic cells that express channelrhodopsin

@OneFace only in the retina. Optogenetics is usually (till now) used to study neurons in the brain; to stimulate those neuron optical fibres are required. However optogenetics can be used in other cells too by using opsin-GPCRs. Mitochondia expressing rhodopsin has been shown to produce ATP in the presence of light. See this post.

Addition to the previous answer.

How to express channelrhodopsins in neurons?

Other than the method involving direct viral injection, as described in the previous answer, these proteins can be expressed in specific cells by making transgenics (by using promoters that will express the downstream gene in only specific cells).

How does it work?

When a neuron is made light sensitive by ectopic expression of channel-rhodopsins, then they can be made to "fire" (generate action potential) by simple illumination. Fibre optics are used to illuminate specific neurons in the brain. See the image below:

Are the light-sensitive molecules (which I now have read are
  channelrhodopsins) present all along the axolemma…

They would be expressed everywhere but their expression on the axons can be limited because of myelination. It is possible to make certain proteins express in the dendritic region. This requires localization signals called zipcodes (this process is still not understood very well).

How then can these channels work, if any cation can diffuse any way through the channel?

Chr2 can conduct Na+, Ca2+ and K+. Its conductivity for sodium is higher than that for potassium. When the channels open the higher inward flow of sodium would trigger action potential (AP). Moreover Calcium also helps in strengthening the AP. Though the channel can conduct Li+, the ion is not present in the extracellular fluid. Usually the nonspecific channels are not used.

Also, I was wondering whether the principle behind optogenetics-
  controlling calls with light- could be used for other treatments e.g.
  to kill cancer cells?

Light (as lasers) is used for killing cancer cells but it does not involve optogenetic techniques. You would need to genetically modify the cancer cell first.


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Wet weight measurements: Setting up cultures for measuring growth rate via wet weight
I have some isolates which I am trying to grow in some toxic leachate in order to measure their growth rate I also want to measure the growth rates of certain combinations of these bacteria.
I've tried a few ways to measure their growth rate in leachate (mostly turbidity), all of which have been unsuccessful. My supervisor has therefore recommended I try wet weight measurements.
I am a chemical engineering undergraduate, and I have never done wet weight measurements before, so please forgive my naivety!
My set up is as follows:

I have overnight cultures of the isolates which are being grown up
in leachate (themselves inoculated from agar plates) in falcon tubes
as an inoculum for my wet weight cultures.
I plan on having several (~20) 250ml conical flasks with leachate in them. I will innoculate these from my overnight cultures, so that different flasks contain different isolates
I want to take daily kinetic measurements in order to get the wet weight of the bacteria growing in leachate. This will be done over a period of 5 days.
I will take an aliquot each day for 5 days from the conical flasks, centrifuge in order to pellet the cells, then remove the supernatant and weigh the biomass.

So what I don't know are the specifics of how I might set this up.
I know that my isolates grow slowly in leachate, and therefore I will need a relatively large volume of liquid (around 5-10ml) in order to get a meaningful change in biomass.
So my queries are;

How many replicates is sensible for this sort of wet weight measurement? I know that they can be quite varied from replicate to replicate, but I have limited room in my incubator. I think 4 replicates might be too many, but I don't know the extent of the variability when it comes to wet weight measurements.
In 250ml conical flasks, what is the maximum volume of liquid I can put in them before there is not enough head-space remaining?
What volume of an inoculum would be sensible for this experiment? And if I am wanting to get a growth rate, then does it even matter? As I am only concerned with the rate of change of biomass over time and not the final amount.
I want to take large enough aliquots to demonstrate an increase in biomass, but obviously not too much that it begins to affect the culture growth. As this is destructive sampling, what volume of my culture can I afford to lose?
I have demonstrated that in a volume of 5ml of leachate, and given 72 hours, my isolates' biomass increases by approximately 8,000 μg - 10,000 μg. So by this logic, is it right to say for the daily measurements, aliquots might should be 15ml so that I can get meaninful readings?

I already know it is not feasible for me to do dry-weight measurements simply because of time and the system I'm working with.


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How do adult differentiated somatic cells divide?
My textbook (which is Biotechnology by David P. Clark) states, when talking about fate-mapping potential stem-cells:

"If the marked cell is not a stem cell, the marker will not be passed
  onto descendants since normal differentiated somatic cells do not
  divide by mitosis."

He then goes on to say:

"Most adult differentiated cells do not divide at all and are
  considered postmitotic."

So there are some differentiated somatic cells which divide, but apparently not by mitosis? So what is the technical term for their division?
Here is a screenshot of the passage:

There is no known alternative mechanism of proper cell division apart from mitosis and meiosis in animals. I think this is an unfortunate phrasing where the author is trying to introduce the term "postmitotic". The reason for saying "most  adult differentiated cells" is because some cells in adults are considered differentiated but they still proliferate under certain conditions, like for example the cells of the adaptive immune system.
It could also be that the author is trying to be overly cautious because there are cells that split parts of themselves off and release them. These mechanisms could be considered cell division in some sense but are neither mitosis nor meiosis. Examples of this are the release of platelets by megakaryocytes and the release of extracellular vesicles by cells undergoing apoptosis.

Mammalian cells can do either mitosis or meiosis. Depending on the context, meiosis might be an option but usually this is not the case, and many articles don't explicitly state it when they refer to mitosis.
I do understand your confusion. All I can think of is that perhaps the passage was referring to the fact meiotic cells are not as pluripotent as some other stem cells.

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text:
Do animals follow tactics?
Are animals able to plan hunts, give tasks if they do it in groups and fulfil it adapted to the current situation? Do they use unique tactics for special circumstances (e.g. based on experiences)  or they just act from instincts?

the size of the animal's brain is a factor here I think.  ants vs wolves and dolphins are a spectrum of scenarios in the ability to plan I'm sure.

Do some research on wolves hunting. They certainly have tactics that change depending on the prey that they're hunting, the terrain, danger posed by other members of the prey's herd or family (if any), etc. They're very capable of learning, and use fairly complex communications. They run in packs, live with their mother for a number of years, and have a rather involved family structure that allows for the passing on of behaviors learned from previous generations. It would be difficult to tease out exactly which behaviors are instinctual, and which are learned, but you could say the same of humans as well.


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Do mitochondria digest fats?
I am a student and I'm currently using the IB biology Oxford textbook. A few weeks ago I had a test on biochemistry. I studied on my textbook and it stated the following: "Mitochondrion: (…) fat is digested here if it is being used as an energy resource in the cell" (page 22) "The energy store from them (Triglycerides) can be released by aerobic cell respiration" (page 78). My teacher told me that I was wrong to write these statements in my test. Is there something wrong? Is the term 'fat' too generic? Do different kinds of fats undergo either aerobic or anaerobic respiration? I am currently confused as I do not know who is right and who is wrong… Can someone answer my questions?
Thank you

You are not far off the mark I would say. Strictly speaking it's not correct to say that mitochondria oxidize fat. By "fat" we usually mean triacylglycerides, and these must first be hydrolyzed into free fatty acids (by enzymes known as lipases) that can be oxidized in the mitochondria. But many researchers and textbook authors are not always careful with this distinction.
Most fatty acids are indeed oxidized ("digested" sounds strange to me) in the mitochondria into acetyl-CoA units, in a process known as beta-oxidation. The acetyl-CoA units produced are then further oxidized into CO$_2$ by the TCA cycle. These processes generate NADH and FADH$_2$ which is converted into ATP by the respiratory chain.
There are exceptions though. Very long-chain or branched fatty acids are instead oxidized in peroxisomes, which contain enzymes specialized for this purpose.
There is no such thing as "anaerobic respiration": in animals, respiration always uses oxygen as the terminal electron acceptor. Mitochondrial beta-oxidation is coupled to the respiratory chain, and therefore requires oxygen. Peroxisomal oxidation is not directly coupled to respiration, but the process still requires oxygen, which in this case is reduced directly by the fatty acid oxidases. So there is no truly anaerobic form of fatty acid oxidation.


text:
What is the aqueous solution for DNA immobilization?
This paper
Electric-field assisted immobilization and hybridization of DNA oligomers on thin-film microchips
Which is talking about how the electric field improve the DNA immobilization process.
Unfortunately, I have no biology background, I could only understand about 50%  contents.
In the section 2.3.1, its says "the chip was exposed to a aqueous solution of the DNA probe".
What is the aqueous solution of the DNA probe?
Is it DD water (DI water) + DNA? or it is some kind of buffer solution + DNA?

The methods mention a BSA buffer with reference 14 and a borate buffer with reference 30 for immobilizing on their 2 different types of chip. They also mention an SSC buffer, which is a saline sodium citrate buffer commonly used in DNA or RNA hybridization experiments.

But where they mention about BSA buffer if at DNA hybridization step. The solution is the same with DNA immobilization?

And in the 2nd type chip with E-assist experiment (section 2.4), They said "a solution of FITC-labelled ssDNA probes with a volume of 2 cm3 is added" which is different from "a 0.5 µM ssDNA probe solution in borate buffer" (section 2.3.2). The previous one did mention about in borate buffer but later one no. Should they be the same?

You're right to point out the BSA, the SiO2 crosslinking relies on either a thiol or amine reaction, and BSA could interfere with those reactions. They may have used the borate buffer for immobilization on both chips, or they may have just added water to their oligos directly from the manufacturer, in which case the buffer would be whatever salt the manufacturer provided. This seems unlikely, as most DNA storage solutions are typically a Tris buffered EDTA. I have only looked at the methods section, I don't have time to read the whole thing. Sorry.

Thank you very much for the detail explanation, it is very helpful.  :)


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Do river sharks (genus Glyphis) have reduced rectal glands for salt removal?
Do river sharks of the genus Glyphis have reduced or absent rectal glands for salt removal?
The rectal gland of marine sharks removes excess salts to maintain osmotic balance (Oguri 1964).  In freshwater stingrays (Potamotrygon spp.), the rectal glands are greatly reduced in size  (Thorson et al. 1978) but are apparently functionless (Goldstein and Forster 1971). This is not surprising because freshwater rays do not experience the regular influx of salt water.
I have been unable to determine whether such degeneracy or loss has been observed for the river sharks of Australia (genus Glyphis). Pillans et al. (2009) suggest that osmoregulation is probably similar to bull shark, which would not be surprising because they are in the same family. However, bull sharks that live in salt water but regularly enter fresh water have rectal glands that are normal size (Oguri 1964). River sharks are obligate freshwater species and thus have no need to maintain a large rectal gland for the same reason as the freshwater rays.  From an evolutionary perspective, I would predict reduction or loss of the rectal gland.

I contacted Richard Pillans, the primary author of the article linked to in the question. He told me that he did not know whether the rectal gland was reduced. Researchers are hesitant to capture and dissect the freshwater sharks because of their endangered status.
He did tell me that they have gathered much more data on the movement of the sharks since the 2009 paper was published.  Apparently, river shark is a bit misleading (my words, not Dr. Pillans). Glyphis does occur in freshwater (no salt) but tends to be found in the middle range of brackish water. Brackish water is considered to be anything that is not purely freshwater nor purely salt water, with typical values between 0.5 and 30 parts per thousand (ppt). Freshwater is 0 ppt and open ocean salt water is 35 ppt, the equivalent of 35 grams of salt in one liter of water.
If Glyphis is found primarily in the mid-range of brackish water, then I would expect the rectal gland not show signs of reduction. Pillans and Franklin (2004) showed that rectal gland mass of brackish water bullsharks (Carcharhinus leucas) in Australia did not differ significantly from either freshwater or saltwater individuals.  So, pending further evidence, I would conclude that Glyphis, which in the same family as bull sharks, probably does not show rectal gland reduction.

Pillans, R.D. and C.E. Franklin, 2004.  Plasma osmolyte concentrations and rectal gland mass of bull sharks Carcharhinus leucas, captured along a salinity gradient.  Comparative Biochemistry and Physiology, Part A 138: 363-371.

Your answers are always impressive and supported by several references! Even better when you make both the question and the answer! It is good to have you on this website $\ddot \smile$.

@Remi.b Thanks, I am happy to be here. I keep trying to get to some of your questions but I keep getting diverted with the other questions that to me have an interesting bit of biological trivia (like the one nostril thing). Besides, your questions take more thought and research! :)


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What do the haploinsufficiency scores in the clinVar database represent?
I understand that haploinsufficiency occurs when one of the two copies of a gene is mutated to the point of being unusable, and the single copy remaining is unable to cope with the cell's demands for a given peptide, resulting in a phenotypic deficiency.
In the clinVar database, there is a "haploinsufficiency score" (example here) which seems to range from 0 to 3 (though that is anecdotal only; based on the genes that I've looked at).  I assume it refers to how phenotypic or how deficient the cell is.  However, I fail to find a place where this is clearly outlined...
Am I correct in this assumption, and if so, what does a score of 3 (for example) represent?

Okay, I finally found an official source outlining what the dosage sensitivity scores represent.
0 represents no evidence of dosage sensitivity: clinical interpretation is that dosage differences is "likely benign."
1 represents little evidence of dosage sensitivity: This can be marked if only secondary evidence shows dosage sensitivity; clinical interpretation is that dosage sensitivity is "uncertain."
2 represents "Emerging evidence," meaning that the evidence suggests fairly strongly that the gene is dosage sensitive, but that there is insufficient evidence to prove it.  The clinical interpretation is that dosage sensitivity is "Uncertain, likely pathogenic."
3 represents "Sufficient evidence," meaning that the evidence is sufficient to prove that the gene is dosage sensitive.  Clinical interpretation is "Pathogenic."

Source:

Riggs ER et al., Towards an evidence-based process for the clinical interpretation of copy number variation. Clin Genet. 81(5): 403–412.


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Why do mints make your mouth feel cold?
Why do mints make your mouth feel cold?  And specifically, why does your mouth feel so cold if you eat a few mints and then drink a glass of cold water afterwards?

Hmm.. duplicate of http://chemistry.stackexchange.com/q/558/170, but different stack!

Duplicate of http://biology.stackexchange.com/q/31648/3340

Personally, I think @Daniel's dupe marking is more accurate.  I would have been hard pressed to find the post on biology as it refers specifically to oil on the outside of the skin.  Granted, they have the same answer, but how was I to know?

The feeling of cold from mints is caused by menthol. Menthol affects the TRPM8 receptor on skin and also in the mouth. TRPM8 is also a general cold receptor: so if you are in contact with menthol the receptor reacts just like when you are exposed to cold (Bautista et al., 2007).
The receptor is strongly activated at temperatures below 26 degrees Celsius (Bautista et al., 2007). Drinking water is usually colder than that. So if you ate mints and drink cold water afterwards, the receptor response is even stronger.

And it's very refreshing!

So if I eat mints and drink water that's warmer than 26C, nothing much should happen?

Do menthal and Capsaicin cancel out?

@David Richerby: Menthol would still trigger the receptor which creates a cold sensation independent from other influences.

@JDiugosz: I would not except cancelling out as only the mechanism is comparable: Capsaicin activates a different receptor (TRPV1). I do not really know what effect the combination actually has in terms of cold/heat sensation  - I will try this out later and report. ;)

@AlexDeLarge That would probably be a very weird sensation.

@AlexDeLarge "Today, I am going to eat a breath mint dipped in hot sauce... FOR SCIENCE!"

I can only say one thing: Yuck.

@JDiugosz: It does not seem to cancel out - you actually keep both the hot/pungent sensation and have a cooling effect (I ate a tomato curry spiced with Bhut jolokia and had a Fisherman's Friend afterwards). In fact, e.g. Turkish cuisine uses both spicing with mint and pul biber, probably exploiting these sensory antagonistic effects..

@DavidRicherby, he said it was strongly activated at temperatures below 26 degrees Celsius.  That probably means that it is activated, just less strongly, above that temperature.


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At what total rate is water used in metabolic processes over the entire biosphere?
A recent column on "The Straight Dope" website discussed the idea that water molecules are largely cycled around through the water cycle, and that therefore the water molecules that come out of your tap could have been drunk (and excreted) by the dinosaurs.  Cecil Adams (the author) points out a few flaws with this argument, namely that we've been burning fossil fuels for a couple of centuries and releasing water into the atmosphere, and that liquid water is constantly dissociating and reforming;  so it's not strictly true to say that every water molecule on Earth has been around since the time of the dinosaurs.
One thing that occurred to me in reading this article is that biological processes have also been consuming and producing water for many millions of years now;  this would be another mechanism by which water molecules can be "reshuffled".  Is is possible to estimate how much water participates in these processes (per annum)?  I know that there are estimates out there about how much carbon dioxide is produced/consumed by the biosphere, for example, but I'm not sure whether one can straightforwardly extrapolate from "carbon consumed" to "water consumed," and I don't know if there are other significant metabolic processes that consume/produce water molecules.

The lifetime of a water molecule is less than 1 millisecond, in the sense that two particular protons will not remain bonded to same oxygen ion for longer than that order of time.  Also, the protons of water are constantly exchanging with protons of other molecules and ions, such as alcohols, amines, carboxylic acids, bicarbonate, and countless acids.   So it would only make sense to discuss the rate at which the oxygen atoms of water become atoms of another substance (beyond just hydroxide or hydronium) such as dioxygen or sugar.
For photosynthesis, one molecule of water is consumed for each molecule of carbon dioxide.  The link says that about 110 billion tons of carbon undergoes photosynthesis per year and since a water molecule is 1.5 times the mass of a carbon atom, this means 160 billion tons of water consumed in photosynthesis.
So at a minimum, biological processes destroy and create 160 billion tons of water per year (on the basis of whether an oxygen atom is or isn't part of a water molecule).


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How to tell if/how allele frequencies change (USABO question)
This is question number 34 from the 2014 USABO Open Exam:

Black and white mice live on an island and have allele frequencies of B=0.20, b=0.80. On the continent, there is a much large population of mice with allele frequencies B=0.80,b=0.20. Ships begin moving back and forth between the island and the continent. Occasionally, a mouse finds its way onto the ship and leaves the ship and breeds with
the mice of the other population. Equal numbers of mice ride in each direction. If the ships move continuously between the island and the continent, will the allele frequencies
ultimately stabilize? (Assume that no other forces are affecting allele frequencies.)

A. Both populations will end up at approximately B=0.80, b=0.20.
B. The island and continent populations will stabilize with an allele frequency of B=0.50, b=0.50.
C. Black mice will move to fixation in both populations, because the B allele is dominant.
D. Both populations will end up at B=0.20, b=0.80.
E. The continent's allele frequencies will not change; the island will settle at an equilibrium that is somewhere between the continent's and the island's original states.
The correct answer is A.
I guessed E, because I thought the difference in allele frequencies on the continent meant that the B allele was selected for there, and since the population was so big, I thought that the immigration and emigration wouldn't affect the allele frequency there so much, while the island's allele frequencies would change a little because of the smaller population.
Why is the answer A, why is E wrong (besides that A is right), and is there a math way or some sort of rule to solve this problem (or are you just supposed to reason it out)?
Thanks! :)

Just think about it logically.


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Are there animals which produce sound through direct muscular oscillation?
Obviously, muscles are involved in producing sound, but usually not directly. I.e., the muscles that control human vocal cords do not actually vibrate the vocal cords--a different set of muscles forces air past them, and the moving air makes them vibrate. Rattlesnakes use muscles to oscillate their tails, but the sound comes from rattle sections hitting each other, with frequency components much higher than the tail oscillation. Some insects have muscles directly attached to a tympal, but the sound comes from individual ribs deformity, again unrelated to the frequency of muscle contraction.
So, are there any animals that produce sound like a speaker, by directly causing something to oscillate at the intended frequency by contracting and relaxing muscles to move it with no intermediate steps?

Would hares stamping on the ground count, or must the sound be directly coupled with the air and continuous?

As I understand it, crocodilians may be a candidate, but from what I can find, there's little known directly about how their vocalizations are produced; particularly the low growl (circa 8-10 Hz) might fit.

@JiminyCricket. Stomping on the ground feels like same category as snake rattles. The sound comes from percussion, not the frequency of muscle motion. Now, if they kept their foot in contact with the ground and jiggled it to induce seismic waves at the muscle frequency, that would count.  But even elephants don't do that; they still use air as an intermediary to generate sound waves that couple to the ground.

Bees.
Research has been done into their waggle dance. Bearing in mind that inside the hive there are very low light levels, and that only  a certain number of bees can be in direct physical contact with a bee at any given time.
The "waggle" of the abdomen occurs at between 12-15 Hertz and is modulated as part of the communication. The peculiar thing is, the sound is quite directional, and at the head, the pressure changes are at a minimum - indicating to nearby bees the direction at that point in the dance, and the direction and amplitude of maneuvers expressed.
The wing beats are pulsed at 20 ms duration at frequencies ranging between 200-300 Hz. These generate near-field sound which is heard by others, detected by the second segment of their antennae, and the sensilla (hairs found all over their bodies, though I'm not sure if it's known which are frequency-sensitive).
There is also my personal testimony:
My dad was an apiarist. When a bee gets angry and decides you're a threat, it releases pheromones which smell a bit like bananas.
When it gets really angry just before it stings, it buzzes a loud high-pitched whine with it's wings, while hovering near or just attached to it's target (me, often enough to not discount it as a one-off). I hypothesize that this gives a signal to nearby bees - more directional that pheromones which can swirl around objects with the breeze. Or maybe to scare the threat away. I'm darned if I can find reference to this phenomenon on-line.


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Can viruses replicate in a cell that's already dead?
Suppose a virus randomly lands on a cell that's just lying around. This cell may have just recently died, or died a while ago. This cell may also be part of tissue of a dead organism.* Does the virus know that cell is dead? Would it attempt to inject its DNA into the cell?
*If it's a single cell, not part of a tissue, I imagine a "dead" cell would be lysed, so a virus landing on a "single dead cell" wouldn't happen - pleae correct me if I am wrong. So I'm asking how it would be for a dead organism because we can still see those dead tissues ..

Which virus, which cell?

Sorry, I don't know much about different types of viruses and their specific hosts so I can't give a specific example.. If anyone could recommend some examples that could help. @James

A lysed cell may be defined as a leaky one, which doesn't have to be dead yet. I think the question hinges on 'What is a dead cell?' and what is 'a lysed cell?'

I agree with @Christiaan; without an operational definition of 'death' at the cellular stage for multicellular organisms, this is too vague to answer.


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How do (marine) cells not lose potassium?
Eukaryotic cells keep a sodium-potassium gradient across their external membrane. The concentration of potassium ions is about 5mM outside the cell. Although the potential gradient keeps most of these ions close to the membrane, won't some of these ions diffuse away from the cell/organism? Over long periods of time, wouldn't cells 'dry' out of potassium? I guess the same sort of question can be asked about phosphate.

Might help to focus your question: which organism (unicellular, multi-celluarl) and water kind of water (sea water vs. fresh water)?

If I understand correctly, all organisms in water would be continuously losing potassium by diffusion. Unicellulars in fresh water more so than thick-skinned multicellulars in sea water.

If cells are in a condition where there is low potassium outside, and some of the inside potassium leaches out via diffusion, then they use mechanisms like the Na-K pump to restore the cellular levels.

I think that answers the question. It follows that cells require a certain minimum concentration of potassium in the surrounding water to survive, or at least must replenish it via roots or food.


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Is alternative splicing possible in the same cell?
I know alternative splicing is possible in different cell types of an organism, or within the same cell at different developmental stages. There are several examples like this. But are there any instances of alternative splicing within the same cell at the same time? Perhaps some melanin variants producing shades of different color for example. Normal cells, not cancerous.

In complex eukaryotes like humans, alternative splicing is the rule, rather than the exception.
Eukaryotic splicing is managed by a complex regulatory system, including more than 100 different elements, some of which are enhancers and regulators.
Thus, while one form will often be dominant, one should generally expect at least some alternatives to be present in a cell.
While the amount of work on population-level heterogeneity is still much larger than that on variation within single cells, studies of splicing heterogeneity have identified that multiple forms are often present simultaneously within a single cell. For example, in this recent study, Figure 2 shows that although the distribution between two splicing alternatives is bimodal, single cells exist with the full range of fractional mixes between the two forms.

Provirus of HIV makes a 9kb pre-mRNA which can go under alternative splicing to produce a variety of different mRNAs. Therefore alternative splicing in this infected cell can happen at the same time.

I do not recall any cases of such behaviour for normal cells, off the top of my head but it must exist. Probably, alternative splicing in the same normal cell can happen in early embryo differentiation or in the case of protein localization of a specific peptide in different compartments of a cell.

What you write is correct, but the question clearly relates to cellular, not viral transcripts.


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Is there a word for the assumption that a sufficiently complex and refined organ must be the result of natural selection on a large time scale?
Is there a term for the valid assumption that a sufficiently complex and refined organ must be the result of natural selection on a large time scale?
Example:
A biologist exists in a world where nothing has eyes.  They find a creature with an eye as developed as a modern mammal's in our reality.  Assuming this biologist understood what the eye was able to do as far as limiting and focusing incoming light and sending visual information to the brain, etc - it would go without saying that this was a gradually evolved system.
It would be impossible for a parent from a completely eyeless ancestry to spawn a child that had the equivalent of a fully developed modern mammalian eye, both because of the statistically improbability of that happening, and possibly even because of limitations in the way dna works.
Is there a word for this assumption? e.g. "As per the Axiom of Reliable Intuitive Ancestry Determination for Sufficiently Complex and Refined Traits, we will start our genetic research confident that the eye must be the result of iterative natural selection on a large scale of time."
Preferably a term that acknowledges the validity or reliability of this assumption when it comes to very complex and refined organs or systems, such as the eye, the brain, or the circulatory system.

It's clear to me what you are asking. How can a biologist that exists in a world without eyes know what an eye is? That biologist must not also have eyes.

This is a clunky question. As for as I'm aware, whilst it fluctuates, phenotype changes via natural selection are necessarily gradual (unless this has a technical meaning I'm unaware of). Are you looking for a word to describe the difference between "Eyes were selected for via natural selection" and "Eyes were selected for via laboratory/agricultural intervention"?

@James - it's more like:     "how do you know those bumps on the face weren't a recent addition to this creatures genome?  Did you do any testing?"
"No, I didn't have to.  These bumps actually are actually very complex beneath the surface of the skin and perform a vital and well adapted function.   The complexity and refinement alone are enough to know these must be the result of long gradual selection, even in the absence of other evidence."

I think I've almost grasped the question. Could you say "What is the word for assuming that the phenotype has a genetic underpinning?"

Unless I misunderstand, wouldn't all phenotypes have a genetic underpinning?  From my previous comment, one might say "We can conclude that the bump in the forehead is not just an oddball family trait that neutrally came into play a couple of generations ago." -   "Do you have genetic or fossil evidence?" - "No, but we were able to determine some complex and well developed functions that this bump provides." -  A way to shorten this to "do you know this through genetic evidence, fossil evidence, or [blank]?"  [Blank] being a word or phrase that means the complexity itself is evidence enough.

The 'term' you are looking for is actually gradual change or gradual evolution. If you want to make clear that this is an assumption or a theoretical consideration, you could say assumption of gradual change or theory of gradual change, replacing change with evolution if you like.
The idea comes from Darwin directly and was challenged in the 1970's by biologists like Stephen Jay Gould that suggested that evolution is not driven by gradual accumulation of changes but rather by morphological equilibria disturbed by many rapid adaptations forming new species, a concept called punctuated equilibrium.
It speaks for itself that these concepts are opposing but not mutually exclusive. They are rather two extreme states in a continuum.
Edit: As pointed out in a comment by Daniel Weissmann gradual changes also occur in neutral evolution; this is what we call accumulation of mutations - in fact, it also applies to (at least slightly) deleterious variants, especially in populations with small effective population sizes. This means, that the concept of gradual evolution can be generalised to neutral evolutionary processes. However, it does not mean, that the process involving natural selection cannot also be described by gradual evolution. You just have to specify what you are actually talking about. When talking about obviously complex adaptations, you would assume that they have not evolved neutrally.

Say this new species not only has a complex organ like the eye, but also a large lump on it's forehead. We think the forehead lump may be there to keep dirt off of it's nose.  However, without a close examination to other factors, like parents, environment, dna, etc, we cannot assume gradual change.
It may be very well be an anomalous mutation in this individual or incidental to adaptations elsewhere, or DNA evidence might show it in fact has been gradually evolved.
With the eye we can make this determination with no evidence aside from how well adapted and complex it is.

I don't think this is what OP is looking for. The assumption of gradual change doesn't really say anything about natural selection -- it's generally taken to apply equally to neutral evolution.

@DanielWeissman: Thanks for your comment. I edited my answer to account for your argument.


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Why do Proteins store energy when the body already contains Carbohydrates and Lipids?
We already know that lipids are a source of long term energy and carbohydrates are much faster energy releasing sources. So why do we need specific proteins within the body to store energy?
Are proteins some sort of much quicker sources of energy?
I really can't understand.
Thanks for answering.

Which protein energy-stores are you referring to? Could you add sources to your claim?

Well I was referring to plant seeds and eggs which have proteins which act as energy sources.

Proteins aren't used to store energy but to build structures. They can be burnt if needed though.


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Why is Artemisinin Compound Therapy preferrable over Artemisinin therapy with regards to drug resistance?
How does adding other anti-malarial drugs to artemisinin, to obtain a "combined" therapy result in reducing the frequency of emergence of resistance?

And it is given in the form of artemisinin combination therapy,
  combined with another anti-malarial drug, with the goal of reducing
  the frequency of emergence of resistance. (Cf source).

The idea is rather simple. When an antibiotic is used, it becomes a driver to select for a mutant that has resistance towards the antibiotic. Let say the probability for that happening is P1 (Lets say 1 in 10, 0.1).
When you use two antibiotics with different modes of attack, the probability of acquiring resistance to both is P1 x P2. (Let say P1 =0.1 and P2 = 0.15). So P1 x P2 = 0.1 x 0.15 = 0.015
Hence the probability of becoming resistant to both antibiotics at the same time is very much lower. And as the antibiotics are always used together, the time a bug needs to develop resistance to the therapy becomes longer. The duration which you can use the drug is increased.

When was this discovered?

From Google, the concept has been around since the 1960s. I found an article in New England Journal of Medicine, 1960. However, it appears we only start to start considering antibiotic-antibiotic combination in the 1990s when MR started appearing at high frequency.


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How would a herbivore's digestive tract differ from a human's?
How would a herbivore's digestive tract differ from a human's? What are parts (organs, tissues, etc.) or enzymes that can't be found in one but is in the other? Also, is it correct to say that a herbivore's digestive tract would be more complex than a human's because herbivore diets tend to  contain a lot of complex carbohydrates to digest?

it's a bit of simple quesiton... you would have such a more studied answer if you just look at cow digestion online. For one, vegetarianism requires a longer digestive tract, i.e. 5 stomachs and bigger intestines. and they have different intestinal flora than specialized animals of all other kinds. https://en.wikipedia.org/wiki/Ruminant#Ruminant_physiology

Herbivorous animals certainly tend to have very different digestive tracts to humans, or other carni-/omnivores.  In general, mammals cannot produce enzymes that will digest cellulose, so if an animal is to use cellulose as an energy source there must be another way of extracting its energy.  Principally, this is fermentation.
Fermentation is the process of bacterial breakdown of a sugar-like compound to other molecules, such as gases, acids or alcohol.  Herbivores provide an internal environment that is hospitable to cellulose-fermenting bacteria, and provide them with cellulose (by eating plants!).  They then use the breakdown products of fermentation as an energy source - often the relevant compounds are volatile fatty acids.
Different species have solved the problem of having an internal fermentation chamber in different ways.  Cattle, as many people are aware, have a complex and expanded foregut, and regurgitate their stomach contents to allow further mechanical digestion.  Horses have a vastly expanded hindgut (caecum and large intestine).  Rabbits have an expanded hindgut, and also eat (certain types of) their droppings to allow further mechanical digestion.
One other difference that we can observe in herbivores is in the structure of their teeth.  A carnivore such as a lion will have sharp, pointed teeth and a wide opening jaw to allow catching and killing prey, and tearing of flesh.  Herbivores have broad, flat teeth with rough occlusal surfaces to allow efficient crushing of prehended food.  They may also have adaptations for dental longevity - the horse, for example, has hypsodont or long rooted teeth, that erupt through its lifetime to combat the wear of extended chewing of rough material.

Welcome to SE Biology. This answer would be improved with some links that confirm your main points. Irrespective, +1 from me.

The information contained in this post requires additional references. Please [edit] to add citations to reliable sources that support the assertions made here. Unsourced material may be disputed or deleted.

It depends on the method of digestion the herbivore utilizes and what they eat, grasses, leaves, fruit, or nuts . Ruminants are only one form of herbivore. A wonderful introduction to the various methods can be foundd here. http://vetsci.co.uk/2010/05/14/comparative-digestion/#
For comparison gorilla which are far more herbivorous than human have a much longer small intestines which is one reason they need a much wider trunk. They also of course need larger teeth with thicker enamel and much larger jaw muscles to chew the tough plant fibers. Not so much more complex digestive systems just bigger/longer.

Cutting/pasting an entire answer is not a good way to answer a question on any SE site. Please look at the answers section of the help section.

Good point let me fix it.

Happily removed my DV and replaced with an UV.

The digestive tracts of ruminants (cud chewers) such as
cattle, goats, and sheep are specialized to maximize the benefits
of their endosymbiotic microorganisms. In place of the
usual mammalian stomach, ruminants have a large, four chambered
organ.
The first two chambers, the
rumen and the reticulum, are packed with anaerobic microorganisms
that break down cellulose by fermentation.
The ruminant
periodically regurgitates the contents of the rumen
(the cud) into the mouth for rechewing. When the more thoroughly
ground-up vegetable fibers are swallowed again, they
present more surface area to the microorganisms for their digestive
actions.
The microorganisms in the rumen and reticulum metabolize
cellulose and other nutrients to simple fatty acids, which
become nutrients for their host.
The food leaving the rumen carries with it enormous numbers
of cellulose-fermenting microorganisms. This mixture
passes through the omasum, where it is concentrated by water
absorption.
It then enters the true stomach, the abomasum,
which secretes hydrochloric acid and proteases. The microorganisms
are killed by the acid, digested by the proteases, and
passed on to the small intestine for further digestion and absorption.
The rate of multiplication of microorganisms in the
rumen is great enough to offset their loss, so a well-balanced,
mutually beneficial relationship is maintained.
It would be more correct to say that Herbivores have special adaptations for digesting cellulose rather than complex as humans also have a complex digesting system.
Hope that helps you.

"The rate of multiplication of microorganisms in the rumen is great enough to offset their loss, so a well-balanced, mutually beneficial relationship is maintained." -- well that's how it should work - in modern farming feeding practices often result in derogation of the rumenal bacterial population.


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Plants with no chlorophyll
If chlorophyll or chloroplast is needed for the process of photosynthesis then how do non green plants with no chlorophyll get food

Welcome to Biolgy.Se. Most, if not all, plants without chlorophyll are parasitic plants.

You tagged this question [mushroom]. Mushrooms are not plants, they are fungi, and heterotrophs - they feed on decaying matter.

As @AlexDeLarge mentioned, all non-photosynthesizing plans are holoparasites because they lack the mechanisms for autotrophy. Although it is worth mentioning that it is not always chlorophyll that is doing the photosynthesis in all plants, and that even "non-green" plants can still photosynthesize (see note below).
There are generally two classifications of holoparasitic plants: those that require fungal mycorrhizal hosts called myco-heterotrophs and those that require other plants as hosts. Some examples of non-photosynthesizing myco-heterotrophic plants include those in the genus Monotropa. Examples of plant-specific holoparasitic plants include those in the genus Boschniakia.
In both cases, the parasite is partitioning nutrients directly from its host plant through a specialized root called the haustorium that penetrates the host's roots or hyphae, essentially bypassing the need for its own photosynthetic production. Technically, those parasites that attack other plants are still relying on photosynthesis (of the host), although indirectly.
This is a good review paper on some of these species:
Leake JR. 1994. The biology of myco-heterotrophic ('saprophytic') plants. New Phytologist 127(2): 171-216.

Note: For instance, when deciduous trees turn yellow and red in the fall, they are relying on the carotenoids, xanthophyll and carotene. So, while the plant is not utilizing chlorophyll to absorb light, the carotenoid compounds are incapable of transferring light energy directly to the photosynthesis pathway themselves, and thus still require chlorophyll as a pass-thorough.


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Do E. coli produce both cellulose and curli?
I read a paper that describes a specific stain for cellulose and curli (simultaneously) in Salmonella. I think this should work for E. coli but I'm not sure if all strains produce it. If they do, are the tertiary structures similar to those from salmonella?
Real-time optotracing of curli and cellulose in live Salmonella biofilms using luminescent oligothiophenes


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Insect identification (SP/Brazil)
Found this insect in São Paulo/Brazil. Its length is ~2cm
Any help to identify this insect would be appreciated.

Also see my video

Well, it's a type of firefly, belongs to the order of 'Coleoptera' (beetles), suborder of 'Polyphaga', family of 'Lampyridae' (firefly beetles). It's quite similar to the 'Photinus obscurellus' species (and probably the same species too), however it doesn't always have a black head like yours, however, articles have suggested that  firefly species in Brazil (Sao Paulo State) have 'adapted to mesophyl tropical forests, secondary growths, marshy areas, and open fields' (source = https://www.researchgate.net/publication/233574632_Fireflies_Coleoptera_Lampyridae_from_Southeastern_Brazil_Habitats_Life_History_and_Bioluminescence).
This adaption may have led to species having black heads as oppose the more colourful head of the Photinus obscurellus. However the bodies and the dimensions match yours very closely.
This image is from Google Images (more specifically : http://bugguide.net/node/view/194980/bgimage)

Why don't you add a picture of Photinus obscurellus as reference? It will be easier for OP and other readers to comprehend your answer.

Alrighty then, done

The insect in the picture doesn't have a colourful head(prothorax)? Also mention the source if the picture isn't taken by you.

Yeah, I just found this photo know on google images, most are slightly different bum ur it is the same species, that's why I edited my answer to 'usually colourful'

Note that the systematics of fireflies is in a bit of a flux. Also, @LucasDyson-Diaz, please cite the source of the "articles" you've read (especially the one that you quote) and provide proper reference to the image if possible. It's always good to see where you got your info since the internet is so full of deviously wrong info


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O-Group names of Salmonella serotypes?
What liposaccharides are represented by the O-group designations of Salmonalla serovars in the Kauffman-White classification scheme?  I mean to ask, how do the numbers in a Sal serovar (1, 9, & 12 for Enteriditis, for example) describe the oligosaccharide(s) present on the cell membrane?  Continuing said example, does 1, 9, 12  indicate three different types of liposaccharides, or one type of oligosaccahride containing three distinct features?


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Rate of growth of an RNA or DNA sequence
Given, e.g., a mixture of the necessary components in optimal conditions, what would be the average rate of attachment of nuceotides to ribose molecules?  This is related to the study of how long it would be expected take for a particular genome to evolve.

Your question is too vague and unclear. What exactly are the "necessary components"? Are there polymerases involved? Is there a template sequence? If you just take some RNA and mix it with ribonucleotides, exactly nothing is going to happen unless you have some sort of catalyst present, like an enzyme or ribozyme. The same is true of DNA. It takes energy to attach both nucleotides to ribose, and to attach (deoxy)ribonucleotides to each other. Please [edit] your question and clarify exactly what you're asking.

Also, this has nothing to do with how genomes evolve.


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How can bobcats feel the mice under the snow?
I've just seen the Planet Earth II's second episode "Mountains" where they shock us with these North American bobcats that can feel mice from the distance of several meters, sneak to them and kill them with a single jump. What is their biggest source of information about them? The smell? Feeling of the quiet rumbling of the earth? Hearing it? Any of it seems almost impossible to me, with regard to the conditions of the polar regions.

You can smell roughly where your pan is cooking, but you can hear it with more precision, in order to pin point something you would tend to use your ears, especially if it is under snow.
Cats use all their senses and experience to hunt. The mice have tunnels under the snow to get around and they mark their territory randomly, so the smell doesn't provide a very precise coordinates for tracking: it propagates via wind, through snow, and takes a lot longer than sound to be sensed by the cat. Smell can travel further amd mouse piss smells strong, and freezes. Freezing temps prevent aromatics from diffusing outwards and from reacting with other chemicals. Snow is a very good thermal and therefore airflow insulator. Wind doesnt go through snow very fast, and aromatics take a while to get through (aromatic molecules can even travel through steel and glass)
Cats can hear higher-pitched sounds than either dogs or humans, detecting frequencies from 55 Hz up to 79 kHz (a range of 10.5 octaves) and dogs hear from 67 Hz to 45 kHz, a range of about 9 octaves.
To compare the hearing of a cat to that of a bat, the most sensitive range of bat hearing is 15 kHz to 90 kHz. A human adult hears up to 16-18khz and a child up to 20-22khz.
Sound arrives at the cat nearly instantaneously and provides a direct triangulated reference to the mouse position... One sound arrives slightly later than the other depending on the position of the sound source, and the entire sound spectrum is used in the brain to construct a clear image of the mouse position... shuffling sounds and percussive grey noise generated by animal movement tends to have peaks of energy distributed over a wide range. If the mouse is out of it's den in the middle of winter, it means that it's mostly searching for food, forageing, actually quite noisy activities.
Snow dampens the propagation of sound, so in winter you may notice that ambient sound is different in snowy conditions. That cats can pin point a mouse under snow is not that suprising, given the ambient silence of mid winter, the foraging of rodents, and the olfactory and auditory faculties of felines. it's a good quesiton because you wonder what cats do near mole hills, they are probably sensing a lot of activity there that we don't think about.
https://upload.wikimedia.org/wikipedia/commons/thumb/5/5d/Animal_hearing_frequency_range.svg/512px-Animal_hearing_frequency_range.svg.png

And from personal experience, even humans can sometimes hear mice/voles/similar critters under the snow in favorable conditions.

The bobcats have a very sensitive nose, and also a keen sense of sight. They use their senses to view the environment around them.

and their keen eyesight and hearing are always on the alert for possible danger. Very capable predators, bobcats hunt by stalking their prey.
  from National Trapers Association

Nice answer but needs to be supported by a reference


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Which life is supported in sterilized 100% pure water?
As sterilized 100% pure water does not contain any mineral and ion, so which type life can survive in sterilized 100% pure water?

Are you asking about what kinds of life can survive in 100% pure water, or what kinds of life can grow in 100% pure water?

If any living form is introduced to the system, that living should be able to survive without any external aid to support energy formation or supply.

If a lunged terrestrial animal is submerged in it, about a few minutes :-) this question needs more background and research to make sense.

Of course many life forms can survive for some time in 100% water. A human for example can survive about 4 minutes in 100% water but I doubt this is what you are interested in! Although there is no commonly accepted definition of life, I think we can say that we all agree that any life form needs to reproduce or somehow grow. So I take your question as

What life forms can reproduce or at least grow "potentially indefinitely" in 100% water?

Any life forms, to grow or reproduce needs matter to make its own constituents. As such, pure water won't provide with such nutrients and no life form can survive in the long run in 100% water.

by going in dormant stage or doing something magical to use the water for energy source. Or device some way to survive till their life expectancy?

Doing something magical :) Energy source is not so much the trouble as the could use solar energy. The main issue are the nutrients to create its own constituents. An organism cannot create a body part from water only. Sure, an organism can be dormant and survive in water for eventually a long time. However, I specifically explained why I would focus on life forms that can reproduce or at least grow in 100% water. Otherwise, pretty much all organisms, incl. humans, are able to survive some time (about 4 minutes for a human I think) in 100% water.

Theoretically, 100% steril
ized means devoid of any kind of microbe, i. e,  bacteria, fungi or virus. But it very difficult to  ensure this. And if we could were able to produce such a pure water then also it's not completely safe. Since other than viruses there are other non cellular pathogens like prions (malicious proteins) which can thrive in a microbe free system.  But it is not to be counted as living.


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Error frequency of DNA replication without proof reading activity of DNA polymerase?
Different domains of DNA polymerase contain different activity, like 5'->3' polymerisation and 3'->5' proof reading activity (a general case), and these domains can be exploited separately to make them perform single activity at a time. For example if we are conducting detection of some sort of mutation on a strand of DNA, we need to suppress the activity of DNA polymerase proof reading, ie, stopping it to correct the error it makes.
Since the proof reading activity increases the fidelity of replication to some 99.9%, I want to know what would be the efficiency if there is no proof reading activity.
To simplify my question-
If DNA repair system commits 1 mistakes out of 10^8 base pairs it added in nucleotide chain, how many errors would occur if we remove it's proof reading mechanism?

What research have you done to find the answer to this question yourself? Have you looked at related questions on this list? Try the right-hand side bar. There were questions recently on this topic and you will find the answer there.

Actually I don't understand the dna sequencing tag

@David do I need to show you my research papers or my notes to be able to ask question here?

@Shred DNA sequencing tag is for those people who mostly use DNA exonucleases for sequencing which is also related to my question.

The objective of this site is "to build a library of detailed answers to every question about biology". So, obviously, the first thing you should do is check that there isn't already an answer to your question here. The Help to this site provides tips on asking good questions, in particular : "Have you thoroughly searched for an answer before asking your question? … This demonstrates that you’ve taken the time to try to help yourself, it saves us from reiterating obvious answers."

Instead of falling in any ambiguity I should stop being here as I thought that I can have discussion beyond what I read through books. As books don't have hypothetical or very current ideas.

Klenow Fragment could be used to have a polymerase which lacks the exonuclease activity: not just the 5' -> 3' but also the 3' -> 5' .
Lacking the exonucleases activity, the only kind of control is given by the biochemical property of the enzyme: remember that the DNA polymerase has an active site similar to a right hand, which make possible to have correct couple between A,G,C,T. Then, according to this study, the error rate is something around 1e-4.


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Spermatogenesis in humans - timing of phases and chromatin modifications
I'm interested in the timing of events during human spermatogenesis, ideally with some references I can build off of. Specifically, I am trying to pin down the number of days for:

Spermatogenesis, beginning to end (I have come across 65, 75, and 100).
Leptotene stage
Zygotene stage
Pachytene stage
Spermatozoa maturation and histone-protamine transition
Time in epididymis (I have come across 12 days)

Again, I want to know the timing of these events in humans, not mice or rats. Specifically, I am trying to pin down the major epigenetic reprogramming stages, with a focus on those occurring in mature males.

Spermatogenesis (Beginning to end):
64 +- 8 days (range 42 to 76)

There is considerable individual variation. This includes time in epididymis.
Amann 2008 argue for 74 days based on early study by Clermont 1972.
Also argue that biopsies are still needed on top of radiolabelling.
Substages:
Calculated from Amann 2008, Figure 1 using percent time in 16 day cycles.
Leptotene:
26.5 days (~70 days total - 26.5 days = ~ 43.5 days pre-ejaculation/conception)

Zygotene:
31.2 days (~70 days total - 31.2 days = ~ 38.8 days pre-ejaculation/conception)

Pachytene:
32 days (~70 days total - 32.0 days = ~ 38 days pre-ejaculation/conception)

Histone-Protamine transfer:
68.8 days (~70 days total - 68.8 = ~2 days pre-ejaculation).

The resolution of the data doesn’t really let us get at Epididymis vs. histone-protamine transfer, though.
Time in the Epidymis:
10-14 days.

References:

Misell LM, Holochwost D, Boban D, Santi N, Shefi S, Hellerstein MK,
  Turek PJ. 2006. A Stable Isotope-Mass Spectrometric Method for
  Measuring Human Spermatogenesis Kinetics In Vivo. The Journal of
  Urology 175:242–246.
Amann RP. 2008. The Cycle of the Seminiferous Epithelium in Humans: A
  Need to Revisit? Journal of Andrology 29:469–487.
Durairajanayagam D, Rengan AK, Sharma RK, Agarwal A. 2015. Sperm
  Biology from Production to Ejaculation. In: Schattman GL, Esteves SC,
  Agarwal A, editors. Unexplained Infertility. New York, NY: Springer
  New York. p. 29–42. Available from:
  http://link.springer.com/10.1007/978-1-4939-2140-9_5

Great effort, thanks for coming back to your question!


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Fst Differences Between Mature Trees and Seeds
For a single co-dominant locus in two populations of blue oak, I am given genotype frequency data (genotypes are AA, AB, BB) for adult trees (at least 150 years old) in both populations (pop 1 and pop 2) and from sampling of seedlings taken in fragmented woodland from the same populations (pop 1 and pop2) very recently. I am asked to detect any difference in Fst among adults and seedlings, and propose a hypothesis explaining how any difference observed could have come about.

To tackle this question, I calculated the Fst value between Pop1 and Pop2 using the adult's genotypic frequencies and then Fst between Pop1 and Pop2 for seedlings using the respective genotypic frequencies given for the seedlings.
The Fst values for the adult's was 0.004 and the seedling' was 0.113.
Clearly there is genetic differentiation between population 1 and 2 in seeds, but not much in adult trees.
I'm mostly stuck on the explanation for why this would happen. My gut response was that there is some selection against certain adult genotypes in population 2 in that they are unable to produce seeds? Or maybe that adults in population 2 are mating non randomly and therefore produce seeds that do not match the genotypes of the adult population?

I will assume the claim Clearly there is genetic differentiation between population 1 and 2 in seeds, but not much in adult trees. is correct and that you have done your stats correctly.
A complete analysis of the situation depends of how you calculated Fst. Did you use Weir-Cockerham Fst or standard Nei's formulation? How did you average (with or without weights) over population and loci? But without going to these details, here is an extreme scenario that explain why you could observe such patterns.
Imagine, the migration rate from any population and to any population is 0.5. In such case, in absence of selection you would not expect any divergence between populations. However, if genotypes AA and AB both have seed survival probability of 0 in pop2 (but not in pop1), then pop2 will be fixed for A2A2 at the adult stage even though when looking at the seeds you cannot see any evidence of divergence.

I'm not quite understanding your answer. In the context of the question and genotypic frequencies given, I just don't understand how the genotypic frequencies of pop1 and pop2 could be very in the adult stage, yet have moderate differentiation in genotypic frequency in the seedling stage. I apologize if I'm being unclear..


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What is the relationship between r/K strategy and filial infanticides?
In other words, is the frequency of killing one's own offspring among species dependent on their location on the r/K strategy spectrum?

infanticide does not mean killing your own offspring, but offspring of your own species, the vast majority of the time animals are killing someone elses offspring. often it is a way of freeing up a mate to have your offspring.

@John You're right. That's what filial infanticide means. Google before critique.

I'm not sure if the short form is doing any favours. From your question, it sounds like you are asking "are species that kill members of their own species more likely to have 'cheap' or 'expensive' offspring?" That's still not very clear. Are you asking if infanticides in populations have been modelled before? Are you asking how to model infanticides in a population? Are you asking if the r/K spectrum is a sensible way of thinking about infanticide?

From what I can tell there isn’t any work done on this specific form of infanticide. Here is a review on the subject Here
My assessment would lead me to believe the more r selected a species is the more likely infanticide (if it happens at all) done by the individual would be toward kin. This would probably be due to a need for resources.
One thing to recall though is that this actually violates a basic inference from natural selection. Fitness is measured by how much of your alleles you contribute to the next generation. If you are eating your own offspring you are effectively reducing your fitness. The individual may however increase their long term fitness by doing this.
A possible way to locate a species that might do this would be one that sexually matures later in life but has a relatively long reproductive life with the higher number of offspring being produced in the later age groups. Finding some life history on some K selected species might help you find what you are looking for.
I’m sorry that I can’t better answer your question. and for the spelling and grammar.
cheers,

I think there is.
We know that each and every organism has sufficient resources provided by Nature for its survival.
Lets do a case study.
Let us say a population of 10 foxes lives in a jungle (whose biodiversity is undisturbed by any Non-Natural factors ).So, this particular jungle is well equipped to ensure the survival of 10 foxes.
Now, if we by any means alter the r-value - what we are actually doing is disturbing the initially stable number of organisms present in the jungle at different tropic levels.
That can occur by altering any little characteristic because all are interdependent by food webs and chains.
For eg, if the number of plants drops due to say fertility problems of the soil, then the number of herbivores would also drop (As herbivores' only source of food are plants).
This would result in competition between the carnivores for food as carnivores feed upon herbivores, whose population are dropping due to lack of sufficient food.

Competition is a type of relationship from which no one benefits.Its kinda like war- There shall be a winner but there shall be no side that doesn't suffer losses.

So, back to the situation, competition among carnivores here let's say the foxes would increase day by day as the number of plants drops. So, foxes would resort to killing their own species so as to decrease the number of organisms vying for the same food i.e here herbivores.
You know what prevails the most in nature is - The Survival of the fittest.
So, who do you think would be killed first ?
The one who has had experiences in fighting for food and such stuff or the one who is an infant i.e has not yet experienced the dynamics of the intraspecific competition

Its also worth mentioning here that of all the types of competition, Intraspecific competition is the most brutal as here organism compete for the same resources.

So, I think lesser the r-value of a location, more shall be the chances of filial infanticide.
PS: Note that I used the word chance because we can't predict 90 % of the natural things with certainty.We can make our best guesses. Say here, we don't take into account the protective nature of animals towards their offsprings.So animals are fiercely protective towards their own offsprings that they shall sacrifice themselves first while some eat their own offsprings first.

The cheetah mom is a hard-working single mother, who raises two and eight cubs at a time. In addition to feeding and teaching them, she protects them from lions, hyenas, and other predators. To keep her litter safe, the mother cheetah moves her cubs to a new location every few days.
Insects, fish, amphibians, reptiles, and birds also have been implicated in killing, and sometimes devouring, the young of their own kind.
The best example that I think I could give to you is Cannibalism. We say that Humans are the most self-conscious beings.So, if they can resort to killing their own species
  for a) food b) money (female infanticide) , then why can't animals who have supposedly lesser consciousness of their actions than humans

Thanks, I too, would incline towards K-strategists as more prone to filial infanticide but I'd say interspecific selection is stronger in r-strategists as with the greater number of individuals, there's a greater potential gain in winning this race over (as r-strategists have a greater chance of dying, fixation in the population is infinitely more valuable). My thinking is, K-strategists invest much more so it is better to end an unsuccessful trial than to continue it for the rest of your life. But I can't evaluate all the other effects.


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Understanding the paper "Why war is a man's game"
I have read this article
https://royalsocietypublishing.org/doi/10.1098/rspb.2018.0975
but I don't understand the mathematics which tries to explain why war is male-exclusive. In which branch of mathematics the mathematical theory outlined here can be seen? Is it Game theory? Which mechanisms this mathematical model predicts?
Is this really a new theory?

One has to follow the references, since the method is not explained: judging by the figures it is non-linear equations analysis, such as appears in common population, competition or epidemiologic models. These are obviously motivated by some game-theoretical analysis and basic population biology/genetics considerations.

I am sorry but questions here have to be comprehensible in themselves. Unless you can include the mathematics that you do not understand then it doesn’t fit the SE model.

Judging from the plots it seems like non-linear dynamics. Steven Strogatz's book on the subject is a good introduction.

you are probably better off changing the title to reflect the need for help with the math. you need very specific help. you should also edit your question to include the math itself, this will help as not everyone will be able to access the full article.

@John the article is open access, so everyone (with an internet connection) should be able to access it. Understanding the math is another issue entirely...

evolutionary game theory is probably the closest rubric.


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Can tissue flow apart instead of being tightly attached?
Every tissue of our human body consists on cells and cells are not like static "LEGO bricks". They are highly dynamic and can actively move around, due to myosin-actin networks inside the cell that are fueled by the hydrolyzation of ATP. However, most of the tissue is attached tightly in place. Clearly there is cell migration e.g. in case of wound healing.
But is it possible that tissue flows apart from the body due to the active nature of cells? Under which circumstances this can happen?

Do you mean like placenta separation?

Yes, similar like this.

Blood is considered a specialized form of connective tissue and it can flow.
https://en.wikipedia.org/wiki/Blood

Early in embryogenesis, there are motions which do not flow apart from the embryo, but flow within it in order to shape it.
See e.g. this movie Drosophila embryogenesis
These collective motion are not migration (they don't rely on propelling cells with respect to a substrate) but rather a flow (since there is a change of neighbourhood relations between cells, which is a characteristic of liquid-like flow compared to solid-like deformation), see that other movie at cell scale
Actomyosin is also a crucial player in those movements. The fact that extra-cellular matrix is not yet existent or only nascent during most of these movements is believed to be a key reason why these movements can be much more liquid-like than most deformations in later development.