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Minimal viable EEG equipment for dissertation research on BCI / BMI
I am planning out a dissertation study of Brain-computer Interface (a.k.a. Brain-machine Interface, BCI, BMI, etc) applications.
One of the 3 papers in that dissertation will involve collecting original data, analyzing it, and writing a biofeedback application based upon this data.
I'm in a Computer Science department at a university which does not have a med school, so as far as I know I'll have to purchase the equipment myself out of a very modest research budget.
Thus, my question is "what's the lowest-end (i.e. cheapest) kind of EEG machine which would still be considered modern and sophisticated enough to be publication worthy in journals?".
Of course, I've done a good bit of research on this by reading recently publications on Google Scholar and will continue to do more research, but there's a lot of information overload and I have no prior background with EEG equipment, so any insight would be greatly appreciated.
From what I can tell the main thing driving price is the number of leads or sensors. They seem to range from 1 lead in consumer EEG toys to 100 leads, with a lot of products being advertised that have 16 or 24 leads. There are of course a lot of other features, so feel free to answer using either specific products or in terms of whatever features you've found important.

I have been working with BCI since some time and would recommend you to try these ones. They all have been widely used in MS/PhD research and their results are more or less accepted everywhere:

Emotiv
NeuroSky  (Starts from 99$)
g.tec (Most accurate/Expensive one - not recommended for startups)

P.S: Last, but not least, feel free to have a look at BCI Competition datasets. I remember I used them in my semester project. Plus, if you are interested in getting the dataset of invasive BCI, I can provide you the email of respective research as well. Best of luck in your Research!!

That's highly useful! Neurosky only has 1 sensor though, right? Is that enough for most purposes?

@Hack-R I would recommend you Emotiv (hence first in list). Emotiv has been used by MS Thesis students regularly here, so its quality would do for you!


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Urgent: Bird hatchling identification
Yesterday evening I found this baby bird in one corner of my house's verandah on the floor. I picked it up and placed it safely in a tray hoping that tomorrow morning its parents will find it (actually I initially suspected it to be a sparrow hatchling). When I saw it today morning I found that it is probably a bird of prey. As you can notice the large long beak and claws.
I'm really confused now what to do with it. Please suggest something.

EDIT

I live in Uttar Pradesh, India.
Its relatively plain where I live. (No mountains or lake nearby)
Temperature: 35-20 degrees Celsius
Added a photo for size estimation

RSPCA would be a good start.

Identification may or may not be possible, but more information is needed, e.g. your location, bird size indication, and whether near seacoast, lake or mountains..

@GrahamChiu What's that?

Royal Society for Prevention to Cruelty to Animals.

https://www.peta.org/action/how-to-save-baby-birds/

Actually I found a nest of "Laughing Dove" in my yard. I've placed the baby back into the nest.

https://en.m.wikipedia.org/wiki/Laughing_dove

Yes, it is a most probably a laughing dove

@Serotonin I guess, you already know that you can write (and accept) your own question and describe, why/how you identified the hatchling?

As you've pictured this is a fledgling that you found which has a mixture of adult feathers and immature feathers.  This indicates that it flew to your location, and a nest is nearby.  You should either attempt to find the nest, or just leave the fledgling alone and let it make its own way home as indicated in this online resource.

Fledglings are juvenile birds who have a mix of fuzzy down and adult feathers and are learning to fly. You may come across them hopping along on the ground, perching on low-hanging branches, or hiding under bushes, but as long as they’re healthy, just let them be.
Note: Fledglings are often “rescued” from their natural environment when they don’t need to be.

source: Stack Exchange

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sort: votes


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Why do type 1 diabetics experience hypoglycemia?
I know that type 1 diabetics do not produce enough (possibly none) insulin since beta cells of pancreas are damaged and as far as I know glucagon is produced by alpha cells (which are healthy in diabetic body, I suppose). So, my question is that since glucagon is released when the blood glucose is low, why do the diabetics experience hypoglycemia? Shouldn't the glucagon be released and increase the blood sugar?

Note that in Role of Alpha Cells in Diabetes1, the following is stated:

Glucagon responses to hypoglycemia have been known to be blunted in
  type 1 diabetes of long duration, and this may be a result of a loss
  of alpha- and beta-cell communication secondary to insulin deficiency.

Rudy W Bilous. Role of Alpha Cells in Diabetes - Medscape - Apr 11, 2003.

Have you attempted to solve this on your own? Can you show us what you found?

@anongoodnurse What I found is that it may be a result of a loss of alpha- and beta-cell communication secondary to insulin deficiency.

Key to this question is that untreated, type 1 diabetics would never have hypoglycemia.  It is insulin treatment that causes the hypoglycemia.  Insulin brings sugar down and without insulin (as the case with type 1 diabetics) sugar just goes up.    Exogenous insulin will bring sugar down in anyone, diabetic or no.  Since Type 1 diabetics use insulin all the time, there is more chance for an accident (hypoglycemia).
Also, some Type 1 diabetics might not compensate against hypoglycemia or correctly perceive that they are hypoglycemic.  Reasons for this are laid out in the following article:
From Hypoglycemia in Type 1 Diabetes

Three major defects in this homeostatic response contribute to the
  high frequency of hypoglycemia in type 1 diabetes.

The article summarizes what those are - basically a blunting of normal reactions to hypoglycemia stemming from the disease itself.  It then summarizes:

Thus, the glucose counterregulatory defense against hypoglycemia in
  individuals with diabetes becomes impaired at almost every level and
  rendered even more defective through intensive insulin therapy

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ID for red millipede swarm near my place
Location:Hyderabad,South India.
These worms usually come out when it rains,these worms are the most common ones any help in figuring out them,they come in groups too.

Certainly a swarm of some Diplopoda species. Couldn't identify them any better, though. Video, other photos, news report.

Based on the body structure and double pair of legs per body segment, this is a millipede.
Based on the small size and spacing between body segments, it could possibly be in the Paradoxosomatidae family. You could check by examining the specimen more closely:

Most species possess a groove or furrow ("sulcus") on the dorsal surface between the keels (paranota) on each segment.

National Geographic ran a story/video on swarming Paradoxosomatidae in Senegal in 2017:

Some species swarm together during mating season or to hunt for food, and some studies have theorized juveniles swarm together for protection from predators.

Bellairs et al. (1983)1 studied a similar swarming species of millipede in India:

The adults of Streptogonopus phipsoni (Pocock), an Indian polydesmoid millipede, emerge from the soil at the onset of the monsoon and mate. Eggs are laid in the soil and the adults die. The larvae leave the soil at stadium III and, apart from moulting periods, remain on the surface until the end of the monsoon. The larvae are aggregated in swarms, usually consisting of several hundred individuals. They are active on open ground, including metalled roads, during daylight, but usually spend the night in an inactive state under cover of stones or vegetation. If a swarm is disturbed, the individuals scatter but later reaggregate.

 Source: Bellairs et al. (1983)
I couldn't find any additional reputable (or really much of any) detail about S. phipsoni in English sources online. So I think I'll leave you with this information for you to explore in your native language more closely.

Though, Bellairs et al. cite Hoffman (1980) 2 and Attens (1937) 3 as their identification sources.
Also, Golovatch & Wesener (2016)4 provide a relatively up-to-date species checklist of the millipedes of India, so I'm certain that reference would be a good place to continue learning more.

 Citations:
1  Bellairs, V., Bellairs, R. and Goel, S., 1983. Studies on an Indian polydesmoid millipede Streptogonopus phipsoni Life cycle and swarming behaviour of the larvae. Journal of Zoology, 199(1):31-50.
2  Hoffman, R. L. (1980). Classification of the Diplopoda. Geneve:  Musee d’Histoire  Naturelle
3  Attems, C. (1937). Myriapoda 3. Polydesmoidea 1 Fam. Strongylosomidae. Tierreich 12:1-300.
4  Golovatch, S.I. and Wesener, T., 2016. A species checklist of the millipedes (Myriapoda, Diplopoda) of India. Zootaxa, 4129(1):1-75.

@SonicSplasher please consider accepting ("checking") my answer if it adequately answers your question. If it does not, please let me know what lingering question/doubt you have and I'll try to address it if appropriate or possible.

I am really sorry for responding this late, I had life stuff to do and totally forgot about stack.exchange. I'll review this and let you know fast

As soon as I spot these badboys, I'll take a few and probably try to identify them from a checklist of characters.

Streptogonopus phipsoni, probably IV or V stadium.
For reference, see: Bhakat, S. (1987) and other

for a reference, it is very helpful to include a web link. Lacking a web link, a full reference (e.g. journal, publisher, title) would help the asker to evaluate this answer.

you are bhakat.s

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PCR primer in highly repetitive region
Is there any way to design a PCR primer if region of interest is highly repetitive (tens of kilobases only SINE's & LINE's)?


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How does natural selection favour large body mass and size (or so it seems)
I was walking through a park this afternoon and observed a few birds having fun flying around and it got me thinking why would natural selection favour birds with flesh at all if it hinders their flight.
We started first with single-cell and micro-organisms flourishing the ponds and then they evolved into massive dinosaurs. It therefore seems, there are some unique reasons for growing to such a large size.
However, I thought it's counter intuitive because the large body slows down locomotion, requires lots of food and energy upkeep, is a big flesh target for predators, makes hiding ineffective.
Although it is obvious that the flesh protects the internal organs, but it seems like a chicken and egg problem because without a massive body, perhaps then there is no need for the internal organs.
On a different perspective, perhaps those animals that evolved without flesh are called plants.
That sums up my naive train of thoughts.
So, any expert can shed some light?

Situations where large body could help (some are estimations, some are known): birds in winter - large birds can go without food for longer, larger shelled turtles are harder for sharks to attack - they don't fit in to the sharks mouth so easily so less likely to be crushed, blue whales are large - the sea is cold and large animals radiate heat less rapidly.

Similar to http://biology.stackexchange.com/questions/111/do-large-animals-often-evolve-into-smaller-animals/114

Well first of all I don't know if natural selection favors larger animals - most of the living things in the world are single celled.
Still there are advantages to being larger.  I don't know if I can list them all!  In no particular order:
1) Living things that are large are more metabolically efficient. The amount of food required goes as a 3/4 power of the size of the animal.  Thus a cat 100 times the mass of a mouse requires only 31 times more food.  I don't believe that it is not known how this works.
2) r vs K selection: larger animals have greater individual "value".  Smaller animals tend to live by r-selection - they are cheap and reproduce in large amounts, then lead short and highly competitive lives where most offspring die without reproducing.  Larger animal tend to live longer and reproduce offspring with a greater chance of life. In the extreme case you can compare a cockaroach to an elephant here.  This is not a hard and fas rule, but cheap offspring do tend to be small.
I seem to remember that there are lots of other surveys done and body size correlates to life span and any number of other attributes, which I will try to add after I get some sleep unless someone slips in and lists them all.
3) Cope's rule - an observation as much as a rule that size must convey some advantge because most animals become larger the longer they are around.  Not always true, but there is a trend that the longer evolution works, the more likely a large animal will show up.  This might be because as niches for smaller animals are filled, niches for larger animals become more accessible?

also a lot of direct benefits to survival and mating https://pubmed.ncbi.nlm.nih.gov/16701331/

i'm a personal fan of both of those things @John :)

Another reason could be that bigger animals can better fight for resources like food or sex. Ususally it's the stronger (and often bigger) male that gets a chance to mate or defend their prey.
Bigger animals are also harder to kill and therefore have to fear less predators.

Unless you're living on an island! If you're reasonably large but got stuck on an island for a long time, you will get smaller. This phenomenon (which also goes the other way - if you're small you tend to get bigger if stuck on an island) is called insular dwarfism: http://en.wikipedia.org/wiki/Island_dwarfism

yes - lots of reasons to be small too.  insects rarely get large (or smart) for instance.

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Modeling inclusive fitness
Consider a population of two altruist with coefficient of relatedness
$r$. The average inclusive fitness of this population will be
$w_{0} + br -c$. Like in this example, assignment of inclusive fitness
I've seen in books and articles follow the rule that you should
not count changes in inclusive fitness that result from the
action of your neighbor. For instance, in our example, the calculation
of average inclusive fitness include the increase in indirect fitness
to the actor (i.e., $br$), the costs (i.e., $c$), but do not include
the effects of the altruist behavior of the neighbor (i.e., $b$). That
is, the average inclusive fitness is not $(w_{0} + br -c) + b$.
My question is: why is it that, in inclusive fitness models, you do
not count changes in inclusive fitness that result from the
action of your neighbor? Wouldn't it make the model more accurate to
take into account the effects of your neighbor's behavior? In other
words, in our example, why isn't $(w_{0} + br -c) + b$ a better value
for the average inclusive fitness than simply $(w_{0} + br -c)$?

Note:
As @Corvus pointed out, if we include changes in inclusive fitness that result from the action of your neighbor, we will double-count benefits. Consider the example mentioned above once again of a population of two altruists with a coefficient of relatedness $r$:

If we write $w_1 = w_2= (w_{0} + br -c) + b$, the help of 1 on 2 appears as $rb$ in $w_1$ and as $b$ in $w_2$. If we write the fitness in the right way, $w_1 = w_2= (w_{0} + br -c)$, the help of 1 on 2 is only counted once (i.e., $br$ in $w_1$). However, I cannot help but ask "Why not count the help of 1 on 2 twice?" We are counting the help of 1 on 2 twice, but each time we are assigning it to different individuals, 1 and 2.

This is a very good question and in short the answer is that inclusive fitness is only an approximation or what natural selection maximizes. That said, the quantity you propose is not a better explanation; it ends up double-counting benefits.  I'll try to write up a more detailed description soon.

It is good to have questions about social evolution. It is a superficially easy field that very quickly gets quite complicated when you dig into it. +1

@Remi.b Initially I thought that it wouldn't take me long to have a good grasp of the basic models of social evolution. I was sooo wrong.

Generalities
There are plenty of ways at looking at phenotypes that affect the fitness of the carrier and of other individuals. One of them is group selection and another one is kin selection. Those two concepts are just two different ways of looking at the same processes. Now let's consider only the kin selection way of looking at these processes.
You can either consider the impact of the phenotype of a focus individual to neighbour individuals or the impact of neighbour individuals to the focus individual. Looking at it both ways, would yield to count the effect of your phenotype on twice. It doesn't make much sense to talk about the mean inclusive fitness of a population. You can only talk about the mean fitness of a population.
The confusion
The reason for all these confusion boils down to what $B$ and $C$ really mean. One of the issue is that you confuse $B$ and $b$, $C$ and $c$. The formulation $rB>C$ is a oversimplification of the reality. Hamilton did not use this formulation at first and interpreting $b$ as the benefit for the carrier might be misleading. It is important to understand Hamilton's rule in its original formulation and it is important to understand the evolutionary game theory that underlies the evolution of social traits.
What is Hamilton's rule
One cannot study the evolution of social traits under the kin selection framework if (s)he doesn't understand the underlying game theory. $rB>C$ assumes that the game we're playing is the Prisoner's dilemna. You can learn more about game theory. You can learn more about evolutionary game theory on wiki or in this book. Here is a Khan academy video on Prisoner's dilemna
Let's assume we are playing prisoner's dilemna. The fitness of an individual which cooperate is by definition $w_o + b - c$ (note the letters are not capitalized). If you cooperate and the other don't, your fitness is $w_o - c$. If you don't cooperate and the other does cooperate, you fitness is $w_o + b$. If nobody cooperates, your fitness if $w_o$. And by definition , $b>c$. Knowing the frequency of people that cooperate in the population $y$ and knowing and your probability of cooperating is $x$. Then, the level of altruism (frequency of cooperations) increases in the population if and only if
$$R\cdot\frac{dw(x,y)}{dx}>\frac{dw(x,y)}{dy}$$, where $R$ is the coefficient of relatedness which can itself be expressed as a correlation between the variables $x$ and $y$. $w(x,y)$ is the fitness of the the individual being altruistic with probability $x$ in a population where individuals cooperate with probability $y$ and $\frac{dw(x,y)}{dx}$ is the partial derivative of the fitness function with respect to $x$. By definition, $\frac{dw(x,y)}{dx} = B$ and $\frac{dw(x,y)}{dy}=C$ (capital letters).
The mean fitness of the population therefore depends on the frequency of cooperation $y$. Let's assume for simplicity that $y=1$ (equilibrium), then the mean fitness of the population is $w_o + b - c$ (note that the letters, $b$ and $c$ are not capital letter), and the variance in fitness is null. All individuals has a fitness of $w_o + b -c$ as all individuals are altruistic and perform action that has a negative impact on the fitness $-c$ and a positive impact on their fitness $b$.
In short
$b$ and $c$ in your question, correspond to $b$ and $c$ in my answer and not to $B$ and $C$. If you're playing prisoner's dilemna, then by definition, if everybody cooperate (no variance in the population), then everybody has a fitness of $w_o + b - c$ and the mean fitness is $w_0 + b - c$ (as there is no variance). Now the question of whether everybody ends up cooperating depends on $B$, $C$ and $R$.
In your edit, you write $rb$ and $c$ but you get confused about the meaning of $b$ and $c$. If you are playing prisoner's dilemna, when you cooperate with someone that is also cooperating, you inclusive fitness is $b-c + r(b-c)$ and if you cooperate with someone that is not cooperating, your inclusive fitness is $b-c + r(b)$.

What is the quantity $w(x,y)$?

Sorry, it was unclear. See edit. $w(x,y)$ is the fitness of an individual cooperating with probability $x$ in a population that cooperate with probability $y$

You correct me if I am wrong, but your point seems to be that if we formulate Hamilton's rule using PD, my question doesn't arise. The reason seems to be that the derivation of Hamilton's rule via PD only deals with direct fitness. That is, instead of measuring the degree of genetic relatedness, $R$ measures positive assortment (i.e., how likely an altruist will interact with another altruist).

See the "in short" paragraph that I added. I am not sure I am answering your question. You will let me know.

I think I get what you're saying. This is an interesting way of deriving Hamliton's rule. If I understood it correctly, it looks for the conditions in which $dw/dx > 0$. Once we use the chain rule, we get the version of Hamilton's rule you wrote where $R = \beta_{yx} = dy/dx$.


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What jellyfish is this?

I saw this jellyfish at Brighton Beach, Victoria, Australia. I have searched jellyfish images but there is nothing similar. It is round with a diameter of approximately 80cm and the blue part looks like hundreds of thin tassels.

Please copy the picture to your post directly using the edit button and then pasting the link into the photo uploader. Thanks

diameter of 80 cm! are you sure you haven't done a typo

https://jellywatch.org/

Looks like Pseudorhiza haeckeli. Based on cross motif, and long tail. Grows over a metre across. There is a photo at https://www.abc.net.au/science/photos/2012/01/11/3406019.htm?xml=3406019.mediarss.xml#bigpicturepos
but dont copy it here - copyright.


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What purpose do the opening(s) serve in diapsid and synapsid skulls?
Did synapsid skulls evolve from diapsid skulls or vice versa?
Aditionally, do birds have diapsid skulls? The research I have done has yielded some mixed results.

It is believed that originally the holes evolved to give the jaw muscles a place to expand into as they contract. They evolved as the the  otherwise larger jaw muscles are trapped between the bones and cannot contract properly. I say "believe" because the original function is still debated, and it is not something that can be easily tested.
Diapsids likely evolved from early synapsids, however the evidence is tentative at best and it is just as likely that they both evolved independently from anapsids.
Birds are diapsids. However many modern birds have lost the bony partition between the two holes, separating them by cartilage and soft tissue only. Just as some mammals have lost the bony partition between the jaw muscles and the orbit. Additionally in many mammals and birds the expansion of the braincase makes it harder to identify the holes for the laymen as they are pushed down and to the side.

thanks for the helpful answer! One more thing for clarification...so birds, dinosaurs, and most reptiles (except for turtles) are diapsids, but are amphibians, and fish diapsids as well?

turtle are sort a diapsids, they closed the holes after they had them you can see this is the early fossil turtles, they actually end up closer to crocodiles and dinosaurs than other lizards. euryapsids (extinct) did something similar . the ___apsids are all amniotes and are defined as such, so  amphibians and fish which do not have the holes and are not diapsids but are not anapsids either becasue they are not amniotes.


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Pros and cons of amino acid structure vs DNA sequences for evolutionary comparison
This is an analysis question for a lab on the amino acid differences in beta globin amongst different primates, and using such differences to construct a cladogram and infer evolutionary relationships from it. Any input is greatly appreciated!
Question:
What do you see as the strengths and weaknesses of using amino acid structure of proteins for evolutionary analysis? In your opinion, would it be more useful to use DNA sequences for this type of evolutionary comparison between living and extant species? Why or why not?

Since this is homework/coursework, youre usually expected to show your own effort first. But to give you a hint, the real key is in the redundancy of the amino acid sequence.

Amino acid (protein) structure has its advantages over raw DNA.
Protein structure already has introns (noncoding regions) trimmed out which aren't obvious from a plain DNA string.
A protein can have different shapes (such as unbound/bound) or even folded/misfolded (as in the case of prions). DNA doesn't have a way of encoding these changes as they are dependent on substrates, environmental factors and available energy.
Visualizing the 3D structure of a protein can give insight into its functionality that you can't read off a DNA string.

But in the context of this question, we want to use either the DNA or amino acid sequence to build something like a phylogenetic tree. I'm not an expert in phylogenetics, but I assume that important information would be in those introns, because they usually have more freedom to mutate than exons. So two species could have a protein with the same amino acid sequence, but different DNA sequences in their introns. You could use those differences to help identify how they are related.


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What is an interaction motif with respect to protein sumoylation?
While am reading about protein sumoylation this morning I got stuck on sumo interaction motifs and consensus motif line. I heard the the word motifs for the first time. What does motifs mean in this context and What does canonical Sumo consensus motif ΨKx(D/E) mean also? Would you please elaborate the formula and thanks in advance.

A motif means a pattern. Since nucleotides and proteins have a sequence, they can have some patterns of sub-sequence that may serve some kind of function. For example TATA box in DNA serves as a promoter element. Similarly proteins can have some sequence motifs that can serve as recognition sites for binding partners (amongst other functions). Similarly there can be structural motifs in proteins, network motifs in big networks etc.
In this case the motif is a sequence motif.
From Gareau and Lima (2010):

Many SUMO-modified proteins identified contain an acceptor Lys within a ψKX(D/E) consensus motif, where ψ is a large hydrophobic residue

This motif serves as a recognition site for the SUMO-Ligase.
Here,
K=Lysine
X=Any amino acid
D=Aspartic acid
E=Glutamic acid
From the below figures (Rodriguez et al., 2000), you can observe that ψ can be leucine (L) (original residue in Ran GAP1), isoleucine (I), phenylalanine (F) or valine (V).
I am not sure about the effect of double hydrophobic residues on rate of SUMO conjugation.

@Meti If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered.

@WYSIWYG I did not understand what the plus signs mean in the figure. So could you please explain the figures more in detail. Thanks

@Meti It is just an arbitrary symbol to denote affinity; more plus signs means higher affinity. You can have a look at the paper for more details.


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Mutating a protein without mutating the gene?
Is it possible to mutate a region of a protein (says about 300 amino acids long) without actually mutating the gene?
One possible way that I can think of is to use RNAi and specifically block that region of the mRNA which codes for the 300 amino acids in the protein?
But then wouldn't it cause a problem in the translation of the remaining region of the protein?
Are there any methods out there to mutate a region of a protein without mutating the DNA?

"One possible way that I can think of is to use RNAi and specifically block that region of the mRna which codes for the 300 amino acids in the protein?".... Not possible. RNAi doesn't work that way.

Maybe there is a chemical to make error during translation by ribosoms.

I assume that you mean changing the amino acid sequence in a single protein in an organism to one that no longer reflects the sequence predicted from the DNA sequence.  In that case, I would suggest using ADAR (Double-stranded RNA-specific adenosine deaminase) or similar enzymes.  ADAR deaminates adenosine to inosine, which is read by the ribosome as a guanine.  I know that it's activity is regulated, but I'm not sure how you could redirect it (perhaps with an antisense RNA that yields a double-stranded binding stretch in the target RNA.

To a certain extent, maybe. However RNAi would not work as you describe because it causes the whold mRNA to be degraded not just a portion of it.
If the gene in question is spliced, you could probably influence the splicing pattern by triggering certain signalling pathways. But this is limited to producing different splicing variants of your gene and is likely equally or more difficult than mutating the actual gene.
Another alternative would be to produce mutated mRNA and inject/transform/transfec that into the cell in question but again this is likely as difficult or more difficult than mutating the gene.


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Energy transformations in chemiosmosis and ATP synthase
In terms of energy, how does chemiosmosis drive ATP synthase? How does electrical energy turn into mechanical energy and then into chemical energy? Would the movement of $H^+$ be considered passive diffusion or secondary active transport?

Why close this question? It is a complex topic and the question is clearly formulated. Vote for leave open here.

@AliceD because it is a problem statement question, aka, here is problem community do my work to produce answer.

Do you want to know the exact mechanism of the binding change mechanism, i.e. which subparts of the synthase are altered and how their binding with other units ultimately bring about ATP synthesis, or just how, intuitively speaking, would a concentration gradient drive something apparently unrelated, ATP synthesis?

ATP synthase is basically a pump operating in reverse: while transporters such as the Na/K ATPase uses ATP to push ions against a chemical gradient (resulting in potential energy), ATP synthase uses the H+ gradient across the mitochondrial membrane to make new ATP.
A pump uses ATP (chemical energy) to achieve one-way transport by inducing conformation changes in the protein (mechanical energy), which either opens the channel only when ions come in contact with the low-concentration side, or closes the channel when ions come in contact with the high-concentraton side. In either case, the result is that ions can pass only in one direction, and a concentration gradient will build up (potenial energy).
In the case of ATP synthase, the process is simply reversed: an H+ ion entering the channel from the high-concentration side (the intermembrane space) causes a conformation change that opens the channel, and is coupled to the synthesis of ATP. Precisely how the ATP synthase accomplishes this on the molecular level is a complicated topic, and still an active area of research. See this article for an overview.
Note that ATP synthase is clearly reversible: if the mitochondrial H+ gradient collapses, for example if respiration is blocked, then ATP synthase can run in reverse, consuming ATP to pump H+ out of the matrix. There is even an ATPase inhibiting protein dedicated to blocking the ATP synthase in this situation, to prevent the depletion of ATP. Also, the lysosomal ATPase is structurally similar, but operates in the reverse direction to create low pH in lysosomes.

ATP synthase is a wonderful protein. I'll try to answer to your question without going into too much detail.
The protein complexes of the respiratory chain actively pump H+ to form a proton gradient between the two side of the membrane. ATP synthase uses the movement of the protons down their electrochemical gradient to synthesizes ATP molecules.
The transmembrane domain of the ATP synthase (FO) is a passive proton channel. Flow of protons causes the rotation of FO. Rotation of FO causes the rotation of the gamma subunit that connects FO with the catalytic domain of the ATP synthase (F1). Rotation of the gamma subunit causes the rotation of F1 that causes the synthesize of ATP. So the mechanical energy is transferred from FO to F1 via the gamma subunit. In F1 the mechanical energy is transformed into chemical energy via the synthesize of ATP.


text:
What would be the effect of excess taq polymerase on the PCR?
I just had one question regarding the possible effect of putting to much Taq polymerase in my PCR tube?
Instead of 5µl I put 50µl (10x more).
Do you think it will have a bad effect on the reaction??
Thank for your help.

I'm voting to close this question as off-topic because it is a question of no general interest to the Biology community, which is what this site is trying to accumulate.

@David, I think it is valid question for newcomers.

Costly error.
And yes, it will affect your reaction, since the concentration of Magnesium ions, which are needed as a co-factor by the enzyme, is too low. If you need so much PCR product, you can now adjust the rest of the reagents or you could start over and put this on your personal list of errors. Always check the amount of volume, if it is suspiciously high, check again.
If you decide to proceed and work with a 10x larger volume, make sure that the single PCR reaction is not bigger than 50µl, because the bigger volume also affects how fast the reaction heats up and cools down. If your reaction is too slow to reach 72°C for example, the elongation time might not be long enough to get the full product. If denaturating is too short, your efficiency will drop.

Thank you very much for all these explanations.


text:
Help me identify this insect from Bangladesh
I have seen this insect flying literally everywhere in Dhaka city (Bangladesh) over the last two months. It's small -- around 1-1.5 inches long. It's not an agile flyer and can be easily grabbed by hand during flight.

This is actually the flying adult of a scale insect (superfamily Coccoidea). Specifically, this appears to be some species of the genus Drosicha.
Here is a picture resembling your specimen:

 Source: John Horstman
And another from Vietnam that looks very similar:

 Source: Dan Doucette
I can only find info on a closely related species, Drosicha corpulenta, and here's a tree of related species.
Scalenet provides numerous keys and references that could be useful for positively IDing this specimen.
I will keep searching for more details, but this might be the best you get without asking a scale insect expert.

Female looks very different. https://flic.kr/p/cysZ9S


text:
Are there any examples of viruses that have powered motion or do they all rely on passive diffusion?
Swimming, or any locomotion will presumably require energy which will in turn require metabolism which viruses lack supposedly.
Are they general able to direct their movement in any manner (e.g like sailing) or are they strictly limited to Brownian-like motion? If not, are there any exceptional examples that indeed can control their motion?

Click bait title ("can viruses swim") won't attract the people that know an answer IMO (feel free to roll back). I came here to close the question, but it's actually a reasonable and interesting question! Unfortunately, there is already a well answered duplicate.


text:
Will plants accumulate toxins from soil contaminated by toxic substances like paint thinner/lead paint?
After my grandfather died, demolition crews dumped garbage from the house onto his huge vegetable garden, including lead-painted windows, aluminum, asbestos tiles and more.  Much of it got burned in a few bonfires, which I assume released the toxins into the soil.
I've cleaned out every object I can see from that pile, but I'm wondering if the vegetables grown in that soil will be toxic?  It's been about three years since the demolition.
Also, to avoid the possible toxins from that area, we created a raised container garden using soil from a different location.  Yesterday, 3 Tablespoons of paint thinner mixed with water was dumped accidentally on one of the plants. We hosed it down, and it's still alive, but I'm thinking that the squash it will eventually produce is now toxic too, right?
Thanks in advance. We're new to gardening and really want to understand how this works.

Was the paint thinner still clean (i.e. not mixed with actual paint)? Paint thinner itself is pretty volatile and will evaporate soon.

You could use other plants to extract harmful substances from the soil. There are plants which are called hyperaccumulators which absorb high amounts of contaminants from the soil.
Have a look at at Phytoremediation where the process of phytoextraction is described in detail.
Normally phyotextraction needs several generations of plants to be grown in order to be effective. Consequently you could just plant your vegetables as usual but take samples and test them for heavy metals or other contaminants of concern.


text:
Identification: Creepy 'nope'
While walking back from our routine evening stroll through the hills, we stumbled upon some insect(?). It was the size of an index finger, and it appeared to have some sort of wings. While I tried to take pictures of it, it started turning towards me with it 'claws'.
Additional info:

Origin: Romania, in the hills
Date/time: 17 August 2017, 19:15, sunset
Warm sunny day, just started to cool down, 19 degrees celcius

My wife doesn't want to go outside anymore unless she knows what it is, and she won't allow me to go and pet it.

Related: What species of insect is this?

That's some kind of mole cricket (Gryllotalpidae).
According to this website there's only three species found so far in Romania:

Gryllotalpa gryllotalpa
Gryllotalpa stepposa
Gryllotalpa unispina

It's most likely you've encountered a specimen of the first species as it's the most common and widespread one in Europe, Gryllotalpa gryllotalpa:

Due to the context of the question it might be helpful to add whether they are aggressive, dangerous, poisonous etc. or mostly harmless

Thank you very much. Even though they are common here in Romania, apparently actually meeting one is not an everyday occurrence.

See also: https://en.wikipedia.org/wiki/Mole_cricket, the one shown here seems to stem from Australia, though (see https://en.wikipedia.org/wiki/Gryllotalpa_brachyptera), the one from the question looks more like Gryllotalpa orientalis

@TobiasKienzler It indeed looks like the orientalis, but what's it doing in Romania?

@PierreDuc Good question, it probably hitch-hiked

@TobiasKienzler Stop it. Next thing you will start writing cricket as krikkit.

@MrLister Oh no, I wouldn't do that. Not again.


text:
What causes this eggplant scar?
This eggplant fruit is featuring a big scar. What causes such a scratch? Is it a disease or maybe the fruit was hit and then it healed the crack? Is it correct to call it "Eggplant scab"?

do you know if that is where it lay on the ground? if not, it's probably due to the fruit being bred to grow very big compared to it's wild version.

@comprehensible - no idea. I got them from the fruit shop

perhaps someone threw a grenade near it when it was in the trenches, or it fell off it's motorbike when it was doing 30. even more likely is that it was in contact with planks/rods/a stem/the ground/some stones. perhaps try brushing it with a toothbrush.

return it and get a new eggplant

I like com.prehensibe's comment.Melons get cracks like this on the places where they sit on the ground. Melons are cucurbits too,this looks like it happened where the eggplant sat on the ground. Wash it off,it's still good.


text:
Is this sentence about RER correct on Wikipedia?
While studying about Endoplasmic Reticulum on Wikipedia, I came across this sentence

A ribosome only binds to the RER once a specific protein-nucleic acid complex forms in the cytosol. This special complex forms when a free ribosome begins translating the mRNA of a protein destined for the secretory pathway.

To my knowledge, most proteins are synthesized and modified post-translation in association with RER. Then why is protein destined for secretory pathway mentioned?

Your knowledge is defective. Read the article and search for associated articles. You may even find something in the archive here.

As stated in a comment, your understanding of protein translation in eukaryotes is not accurate. In order to provide a concrete reference that isn't wikipedia, I'll quote here from Biochemistry (2nd ed) by Voet and Voet (1995 / John Wiley & Sons) pg. 307:

Cytologists have long noted two classes of eukaryotic ribosomes, those free in the cytosol, and those bound to the ER so as to form the rough endoplasmic reticulum (RER ...) Both classes of ribosomes are nonetheless structurally identical; they differ only in the nature of the polypeptide they are synthesizing. Free ribosomes synthesize mostly soluble and mitochondrial proteins, wheras membrane-bound ribosomes manufacture transmembrane proteins and proteins destined for secretion, operation within the ER, or incorporation into lysosomes ... These latter proteins initially appear in the RER

Pretty succinct and thorough description.
The wikipedia text you quoted is a bit shallow (on its own) and somewhat incomplete, but essentially correct. The RER isn't solely associated with synthesis of proteins destined for secretion, but this is one of the classes of proteins synthesized in association with the RER. It would be more accurate to say that proteins destined for transmembrane insertion, secretion, or certain other kind of 'special handling' are synthesized in association with the RER rather than free in the cytosol.
The details of how, for example, these different classes are targeted to the RER are fascinating but somewhat beyond the scope of the question. Well explained in the referenced text, though, if you're interested.


text:
Why does drinking milk lead to increased fractures?
Milk has always been associated with strong bones due to the high amount of protein and calcium in it. Yet reading it up on wikipedia,

A study published in The BMJ that followed more than 45,000 men and 61,000 women in Sweden age 39 and older had similar results. Milk consumption in adults was associated with no protection for men, and an increased risk of fractures in women. The risk of any bone fracture increased 16 percent in women who drank three or more glasses daily, and the risk of a broken hip increased 60 percent. It was also associated with an increased risk of death in both sexes.

My question is:
Why did this happen? Can someone explain the biological reason of this observation?
Even though milk really does provide large amount of calcium and proteins yet isn't is contradictory that the fracture rates increase?
This is the aforementioned study.
Michaëlsson, K.; et al. (2014). "Milk intake and risk of mortality and fractures in women and men: cohort studies". The BMJ. 349: g6015. doi:10.1136/bmj.g6015.

The authors suggest a reason in their abstract:

Given the observational study designs with the inherent possibility of residual confounding and reverse causation phenomena, a cautious interpretation of the results is recommended.

There are variables they haven't measured that lead to the observed patterns. A simple one is that the respondees to the initial survey are self-selected (they return the survey). What if milk-drinkers are more likely to respond? Even if the base rate of fractures remains the same, then there will be an apparent association of fracture with milk consumption.
They also discuss physiological reasons, which is the subject of a different answer.

And: As far as I see, this is only one obeservational study which shows this results. I would be very careful to draw conclusions from this study unless this has been replicated, to say the least.

This paper should be in the BMJ christmas issue instead of in October issue.


text:
A grey water bird with brown head

A greyish bird, with brown head and relatively long, pointy beak.
Size comparable to mallard.
Spotted in central Poland, on small, artificial pond, populated by mallards and Eurasian coots.
Photo has been taken today (late September).

I'd be grateful for any information that could be used to identify this bird.

It is a goosander

Based on the location and picture I believe this a Goosander (Mergus merganser) which is the European name, the North American name is the Common Merganser.
You can find more information about them here.

They undergo two main molts, breeding plumage in December and eclipse plumage in May. Here is a description of the eclipse molt by Bent, 1923:

In May the adult male goosander begins to assume its eclipse plumage.
  The adult male in August has the crown reddish brown, with a gray
  tinge; chin white, and the rest of the head and upper neck rich red
  brown.

By the looks of your photo, you either have 2 females during the breeding plumage phase (January - May) or either sex during the eclipse phase (June - December). It will depend on when the photo was taken.
Here is an image with a breeding plumage male (left) alongside some females:

References:
Bent, Arthur Cleveland. 1923. Smithsonian Institution United States National Museum Bulletin 126 (Part 1): 1-13. United States Government Printing Office

Thank you so much for the answer. It looks like a good match, and I've already heard about goosanders in the area - just haven't seen one. This year somone introduced fish, to keep the pond clean -  I guess it become a nice dinner plate.


text:
What is the difference between average sperm epimutations and intersection sperm epimutations, in the context of the attached article?
The paper of interest is Manikkam et al. (2014).
In research for a school Year 10 Science project, I came upon this article and the following two graphics. I don’t quite understand the difference between the two graphics in the context of the article: what is the difference between average and insertion epimutations? Also, what do the Mb’s along the x-axis mean? Is it in a reference to genetic information size, like megabytes? And how does it refer to the loci of the epigenetic changes? I want to be able to interpret and explain this graph, so could someone provide an analysis and explanation of these graphics.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0102091

Welcome to Biology.SE. I added the link in the post. It has no good reason to be in a comment. Maybe you did not know how to add a link in a post.

Yeah, it wouldn’t let me add more than 2 links to a page, and I think the images counted as links.

Oh indeed users with less than 10 points of reputations are limited to two links apparently. I'm not sure why this restriction though!


text:
Is there a publically available database of microbes that details what their wastes and food sources are
Is there a publically available database of microbes that contains what their wastes and chemical food sources are in addition to other traits.
So that I could do like a sorted search for microbes that eat Ammonia or excrete sulfuric acid?
Cant seem to Google this one.

You could try to look into the kegg database. It's main purpose is to describe biochemical pathways, but it also has information on which species actually have these pathways (not sure how well this annotation is for bacteria though).
You should be able to pinpoint a few key pathways that start on free ammonia or have sulphuric acid as a sink/endpoint and then check for all annotated species. I wouldnt expect such lists to be comprehensive, but it should give you at least a starting point.
As an example the Nitrification and Anammox sub-pathways of the Nitrogen-metabolism page show direct usage/incorporation of free ammonia. If you click on some of the enzymes/genes (the boxes with numbers) and follow through to the 'taxonomy' box under genes, you'll get a list of some bacteria species each.


text:
Why do living organisms replicate itself or procreate
Why do living organisms spontaneously replicate itself or "procreate" (my understanding is that it does).
From a uni-cellular and micro-organism point of view. Is there some sort of stimulant in the environment? A chemical reaction that causes it? Is is there a physical or emotional motivation? Is it by choice?
Note: I may have some terms used wrongly as I am not a biologist. In this question, I am interested at living organism nearer the forms of single smallest unit of life form.

Its unclear what you're asking. Do you want to know about the biochemistry of the cell cycle or how evolution drove organisms to replicate? "Is there some sort of stimulant in the environment?" Nutrition is required and some molecules can encourage rapid division. "A chemical reaction that causes it?" A complex biochemical one yes. "Is is there a physical or emotional motivation?" No. "Is it by choice?" No.

If there are enough nutrients, a unicellular organism will "eat" and grow until it reaches a certain size. Through different mechanisms, it can sense that it is large enough and has enough metabolites to divide. Then, the organism will duplicates its DNA, separate the duplicated DNA and divide. (This is called fission for prokaryotes.)
So why does it happen? One of the characteristics of life is replication. In favorable conditions, the organism replicating the fastest will out-compete all other organisms. So there is no motivation or stimulus of some sort needed (or possible), by their very nature cells are made to divide as soon as feasible.

"One of the characteristics of life is replication" is that part of the definition of life? i.e. if a thing has all characteristic of living organism except "desire" to replication, then it is NOT a living organism?

@Jake yes, well perhaps not "desire" but a thing must replicate itself/reproduce to be classified as alive.

Yes, reproduction is part of the definition of life. However, this doesn't mean that a sterile animal doesn't live.

@RoryM Thinking out loud: Due to pre-perception of a living thing, defining it with "ability to reproduce" seems to suggest that when the thing reproduce, it does so under its controlled will. However if i am asked WHY a kitchen sponge absorbs water with its ability to do so, I am unlikely to suggest that the sponge has a will. In a way, the sponge MUST absorb water. So to answer the "why", either living thing MUST reproduce, or the more approperiate question becomes, "does living thing desire to reproduce" or "can living thing inherently stop (temporarily) reproduction?" Hope I make sense...

In your words, living things "must" reproduce - they have the ability to do so, and if the environment allows it, reproduction will spontaneously (i.e. without "will", "intention" or "motivation") happen. Compared to the original first molecule that had this ability, even the simplest cell is an incredibly complex organism with highly sophisticated control mechanisms which integrate all the necessary requirements for favourable reproduction and scan the environment (both internal and external) for these conditions.

This is a very interesting question but the answer (or as much of the answer as is known) can fill a few books. There are many many signals that control cell division.
As a horrible simplification, the cell can be compared to a car parked on a slope with a driver's foot on the brake. If she lifts her foot, the car will roll downhill. In the cell, there are various proteins (P53 is the most famous) that have their metaphorical foot on the brake. Various external and internal stimuli can cause these proteins to stop suppressing replication and the cell will then continue its cycle and replicate.
So, a cell's "natural state" is to replicate, there is a complex network of interacting factors (primarily proteins) that actively block replication in resting cells. When the conditions are "right" (what that means depends on the cell in question) the block is removed and the cell replicates.

So in your metaphor, rolling down slope is the process of replication?

@Jake, yes, the point I am trying to make is that replication is the natural state of cells and needs to be actively prevented for the cells to not proliferate.


text:
How much food can an average person eat, and which animal is that equivalent to?
When the average person overeats, how much food can he eat in a day? Which animal's average meal would that be equivalent to?
When documentaries are talking about animals feed, they usually say something like "The fish can eat 500kg of prawns in a day!" But when it comes to humans, they calculate in calories. Which animals are we closest to in terms of capacity?
Note: I think I can be slightly loose on the definition of overeating here. It can mean eating beyond the point of feeling full, or the human maximum stomach capacity.


text:
Herbal vs Chemical Insecticides
Well, insecticides are used to kill insects.
I have always wondered why are herbal / natural insecticides more effective in killing insects than chemical ones. I have read this at many places but havent found a reason for it.
Also why don't insects develop resistance to herbal insecticides while they do for chemical ones?

All insecticides are chemicals by the definition of a chemical.

References for the latter two points would be helpful

@Ben point accepted, but still they are way different in terms of effectiveness.. also my main pointt was to differentiate between insecticides available from natural sources and those made by man

You can't really compare these two groups (herbal vs. man-made).  If a certain herb and a certain commercial insecticide contain the same active ingredient, they may very well have the same level of effectiveness.  There's many commercial insecticides which are ineffective - they just don't make it to market.  There's also billions of "herbal insecticides" which are completely ineffective - we call them "herbs".

I think you probably mean insect and pest control from plant extracts.
I have seen posters where extracts from herbs were pretty effective in killing insects.  Really common herbs - rosemary, basi.   It makes sense that plants (and animals) would evolve chemical defenses against insects.
For instance, a quick search under google scholar talks gives you an idea of the research going on (mostly not in the US) here.  Pestoban, an Indian herbal preparation is quite effective against some pests while less effective (~50% effective) in removing fleas from treated livestock.
It also stands to reason that the compounds found in edible herbs and plants would tend to be selectively effective against insects found in the environment local to the plants.
Another related topic is the search for antibiotics in herbs and spices.  Tumeric is a common topic of research, which explains one of the possible reasons its used in cooking. Garlic components show interesting medical properties too.
While this may seem suspect to some, the research is done in the West too, but it is usually spun a different way. In general if you are looking for bioactive compounds that are not completely toxic (like heavy metals or cyanide for instance), you would want to look at compounds which are made by living things.  Nearly all pharmaceutical designs come from or are derived from plant or microbial / fungal extracts.   This is in fact the field of Natural Products Chemistry which is still a big thing in chemistry and biochemistry.  Few if any of the hot targets of organic synthesis are not some fancy compound found in a plant, fungus or sponge extract.  E.g. the surreally complex Palytoxin, the miracle breast cancer drug Taxol, and the venerable cholesterol control drugs, the Statins.


text:
Definition of nucleotide-associated proteins and RNA-polymerase associated proteins
Nucleotide-associated proteins and RNA-polymerase associated proteins, I found those two terms in an article but I didn't understand what they mean exactly, is there any relation between those terms and DNA-binding proteins ?
The article : DNA supercoiling-a global transcriptional regulator for enterobacterial growth?

Could you post the article for context?

@canadianer I added the link to the article.

In short:
Nucleotide-associated proteins are DNA-binding proteins that bind DNA. RNA-polymerase associated proteins bind RNA-polymerases and are required for its functionality.
In more detail:
DNA-binding protein is a higher level term that comprises all proteins that bind to DNA. These can be seen as nucleotide-associated proteins as they interact with the nucleotides in the DNA strand, even though I did not hear people use that term very often. There are two types of binding:

Non-specific DNA-binding proteins that do not bind to specific sequences DNA sequences, e.g. structural proteins.
Specific DNA-binding proteins that bind to specific DNA sequences, e.g. transcription factors. These proteins mostly have specific DNA binding motifs like zinc fingers or helix-turn-helix motifs.

RNA-polymerase (RNAP) associated proteins are different from that. RNAP itself is a DNA-binding protein, but proteins binding to RNAP are necessary for it to be fully functional. The fully functional RNAP then is a holoenzyme. For example RNAP II requires an initiation factor called sigma in bacteria and several general transcription factors and regulatory proteins in eukaryots.

"Nucleotide-associated proteins are DNA-binding proteins that bind DNA." Written in a hurry perhaps? Is DNA the only nucleotide then? And are there a class of  DNA-binding proteins that do not bind DNA? Accepted or not, your answer needs serious revision. And although you give a host of links, none are to the two terms the poster enquires about. In the absence of such I am not prepared to accept your short definition of RNA-polymerase associated protein either.

Neither of the terms “Nucleotide-associated protein” or “RNA-polymerase associated protein” are standard in molecular biology in so far as they are not defined in the reference Gene Ontology. (In contrast, “DNA-binding” is.)
An internet search does not bring up many examples of the former usage (at least) and in those it brings up it is not defined. One can only conclude that it means exactly what it says and no more, presumably because the author has limited information about the function of the protein.(Without the original reference I cannot be sure.)
A “Nucleotide-associated protein” is therefore “a protein that in some way interacts with a nucleotide”. On may imagine that it might bind the nucleotide, but the nature of this binding is unspecified and could be reflect the fact that the protein is a kinase of some sort and ATP (or GTP etc) is a substrate. It therefore need not be a DNA-binding protein, in contrast to the statement in the accepted answer from @AlexDeLarge. In fact the term would most likely imply a mononucleotide-binding protein, i.e. a protein that bound ATP or cyclicAMP or GDP or dUDP etc. If it bound a polynucleotide, this could equally well be RNA as DNA.
Likewise, an “RNA-polymerase associated protein” is “a protein that in some way interacts with RNA-polymerase”. It is more likely that this is a protein that forms a complex with — i.e. binds to — RNA-polymerase, but the fact that the author does not use the term “binding” suggests that he is being cautious because he has no evidence for this. Perhaps both proteins are found in the same immunoprecipitate.


text:
What is a topological domain?
I found this definition on Wikipedia, but I didn't quit undestand it :

Topologically associating domains (TADs) are genomic regions ("chromosome neighborhoods") used to summarize the three-dimensional nuclear organization of mammalian genomes.

Can anyone explain it more, and give examples if it's possible ?

TADs were initially discovered by computing contact probabilities between regions of the genome using HiC (a chromosome conformation capture method, that try to provide an idea on how the genome is organized inside the nucleus by computing the probability of each contact to be located nearby another locus). People have found that instead of being random, some loci were in contact with some regions of the genome rather than the others, implying some form of functional significance.
In short: a TAD is a genomic region of increased contact probability. They are of functional relevance (for instance, Enhance-Promoter gene expression regulation occurs primarily within one TAD rather than between two (adjacent TADs).
You might be interested in the following papers:

A 3D Map of the Human Genome at Kilobase Resolution Reveals Principles of Chromatin Looping (might be behind paywall)
Topological Domains in Mammalian Genomes Identified by Analysis of Chromatin Interactions

Finally, the following picture (extracted from the latter publication) provides an example of two TADS:

The bottom panel shows the contact probability: two regions of the genome appear to be isolated whereas they are nearby. They show significant self-interaction. One interpretation for that (top panel) is to imagine that the genome exhibit some reproducible condensation, explaining the increased contacts.

Topological aspects of DNA structure arise primarily from the fact that the two DNA strands are repeatedly intertwined. Untangling these two strands, which occurs in all major genetic processes may prove rather difficult. In the simplest case of a linear DNA in solution, untangling is possible due to the free rotation of the ends of the DNA. However, for all natural DNAs, free end rotation is either restricted or forbidden altogether. Consequently, untangling the two DNA strands becomes topologically impossible (Figure 1 illustrates this for the imaginary case of a circular DNA molecule where the two strands are tangled only once).

A DNA segment constrained so that the free rotation of its ends is impossible is called a topological domain (Figure 2). A canonical example of a topological domain is circular DNA, which is typical of bacteria, mitochondria, chloroplasts, many viruses, etc. In this case, there are obviously no DNA ends at all, since both DNA strands are covalently closed. Although eukaryotic chromosomes are linear overall, they consist of large DNA loops firmly attached to the nuclear matrix. These loops represent topological domains, i.e. they are equivalent to circular DNA topologically. The ends of linear DNA can also be affixed to the membrane, as has been shown for some viruses, making this DNA topologically closed. Finally, a stretch of DNA situated between the two massive protein bodies can also be considered a topological domain.

Source : DNA Topology Fundamentals


text:
Is the transcription starting site located before or after the promoter?
It's maybe a stupid question, but I really want to know the answer.
The definition of Promoter (From Wikipedia):

In genetics, a promoter is a region of DNA that initiates transcription of a particular gene. Promoters are located near the transcription start sites of genes

And the definition of the transcription start site (From Wikiversity):

The transcription start site "is the location where transcription starts at the 5'-end of a gene sequence.

I also Found this image (The source):

I'm asking this question because as far as I know, the RNA Polymerase binds to the TSS, and a friend of mine told me that's it binds to the Promoter.
PS : I'm interested in bacteria.

You might be interested in this.

From what I remember the promoter is not necessarily transcribed and not necessarily close to the Gene being transcribed, but somehow brings RNA pol to the right place, i.e. the TSS... I'm not sure it's a hard and fast rule though.

Note that that image is wrong: the gene includes both of the untranslated regions. You can also consider the regulatory regions as part of the gene, some do, but I have never heard of a definition of "gene" that limited itself to only the coding parts of a transcript.

You will find the answer to this question in any standard text book of Biochemistry, Molecular Biology or Molecular Genetics. There are several on-line at NCBI bookshelf, and these are generally far better than Wikipedia. I quote from section 28.1 of Berg et. al., dealing with transcription:

Transcription starts at promoters on the DNA template. Promoters are sequences of DNA that direct the RNA polymerase to the proper initiation site for transcription.

This is then followed by a description of prokaryotic promotor sequences and the consensus TATA box.

A striking pattern is evident when the sequences of many prokaryotic promoters are compared. Two common motifs are present on the 5′ (upstream) side of the start site. They are known as the -10 sequence and the -35 sequence because they are centered at about 10 and 35 nucleotides upstream of the start site.

The methodology by which this was established is described, from which it becomes evident that another way of regarding the promotor is the site on the DNA at which the RNA polymerase binds.
From the embolded part of the quotation above (my emphasis), the promotor is clearly before (5′) of the start site. This is summarized in another small graphic:

Sorry if this is an east question to answer but, what designates a specific part of the DNA to be the “transcription start site”?

Just in addition to David's answer, there are examples of internal promoters (those which have elements 3' of the transcription start site). As an example, internal promoter elements of tRNA genes direct binding of and transcription by eukaryotic RNAP III:
White RJ. 2011. Transcription by RNA polymerase III: more complex than we thought. Nature Rev Genet 12:459-463.

Many class I retrotransposons also contain internal promoters which allows them to be transposed along with the other elements:

LINE - internal RNAP II promoter
SINE - internal RNAP III promoter


text:
Proof of the equivalence between two ways of defining ESS
Background
Two common ways of defining what an Evolutionary Stable Strategy (ESS) are:
First definition:
Consider a population composed of populations playing two strategies, $\mathbf{p}$ and $\mathbf{q}$.
Let us denote $W(\mathbf{p})$ the average fitness of the
strategy $\mathbf{p}$. A population consisting of individuals playing $\mathbf{p}$ will be an ESS if, whenever a small amount of deviant individuals playing $\mathbf{q}$, the old type $\mathbf{p}$ fares batter than the newcomers $\mathbf{q}$. This means that for all
$\mathbf{p}\neq \mathbf{q}$,
\begin{equation}
  W(\mathbf{p}) > W (\mathbf{q})
\end{equation}
Second definition: $E(\mathbf{p},\mathbf{q})$ is the payoff for $\mathbf{p}$-strategist against a $\mathbf{q}$-strategist. The strategy $\mathbf{p}$ is an ESS if and only if the following conditions are satisfied:

$E(\mathbf{p},\mathbf{p})\geq E(\mathbf{q},\mathbf{p}) \quad \forall
  \mathbf{q}$
If $\mathbf{q}\neq \mathbf{p}$ and $E(\mathbf{p},\mathbf{p}) = E(\mathbf{q},\mathbf{p})$, then
$E(\mathbf{p},\mathbf{q})> E(\mathbf{q},\mathbf{q})$

Question (shorter version)
The above two ways of defining what an ESS should be equivalent. How can I prove such an equivalence? Alternatively, do you know of a book (or a paper) that has this proof?
Question (longer version)
I understand that the first definition implies the second. According to the first definition:
\begin{align*}
   W(\mathbf{p}) - W (\mathbf{q}) &>0\\
   (1-\epsilon) [E(\mathbf{p},\mathbf{p}) - E(\mathbf{q},\mathbf{p})]
   + \epsilon [E(\mathbf{p},\mathbf{q}) - E(\mathbf{q},\mathbf{q})] &>0
 \end{align*}
where $\epsilon$ is frequency of individuals playing $\mathbf{q}$. Since $0<\epsilon<1$, if the above inequality is true, the conditions 1 and 2 in the second definition must be true. The part that I find less clear is how the second definition implies the first definition. More specifically, that if $\mathbf{p}$ is a strict Nash equilibrium (i.e., $E(\mathbf{p},\mathbf{p})> E(\mathbf{q},\mathbf{p})$), then $W(\mathbf{p}) > W (\mathbf{q})$.

Aren't these definitions applicable to different models of evolution?  It seems like the first is applicable in a case where each strategy has, regardless of the other strategies, a known distribution of payoffs.  The second seems to have a payoff which is dependent not only on the strategy but also on the other players' strategy.  If they are different models, I am not sure what it means to be equivalent.

@Hans The equivalence between these defs is mentioned in a few textbooks, such as p.232 of Gintis Game Theory Evolving and on p. 63 of Hofbauer & Sigmund's Evolutionary Games and Population Dynamics.

We need to show that if $\mathbf{p}$ is a strict Nash equilibrium, $E(\mathbf{p},\mathbf{p})> E(\mathbf{q},\mathbf{p})$, then $W(\mathbf{p}) > W (\mathbf{q})$ for some sufficiently small $\epsilon$. When $E(\mathbf{p},\mathbf{q}) \geq E(\mathbf{q},\mathbf{q})$, $\mathbf{p}$ clearly dominates $\mathbf{q}$.The less obvious case is when $E(\mathbf{p},\mathbf{q}) < E(\mathbf{q},\mathbf{q})$.
Since $E(\mathbf{p},\mathbf{p}) - E(\mathbf{q},\mathbf{p})>0$, there should be a strictly positive number $k$ such that
$$k[E(\mathbf{p},\mathbf{p}) - E(\mathbf{q},\mathbf{p})]+ E(\mathbf{p},\mathbf{q}) - E(\mathbf{q},\mathbf{q})>0$$
is true. Whatever this number is, we can write $k$ as $(1-\epsilon)/\epsilon$ for $0<\epsilon<1$. Substituting this into the equation above gives us the desired result.


text:
The replicator equation vs the Lotka-Volterra equation
Background
The replicator equation with $n$ strategies is given by the differential equation:
\begin{equation}
  \dot x_{i} = x_{i} \left( \sum_{j=1}^{n} a_{ij}x_{j} - \phi \right)
  \qquad i = 1, \ldots, n
\end{equation}
where $x_i$ is the frequency of the strategy $i$, $A=[a_{ij}]$ is the payoff matrix, and $\phi$ is the average fitness of the population. Basically, what the replicator equation is saying is that the rate of increase of the strategy $i$ (i.e., $\dot x_i/ x_i$) is the difference between the fitness of $i$ (i.e., $\sum_{j=1}^{n} a_{ij}x_{j}$) and the average fitness $\phi$ of the whole population.
The Lotka-Volterra equation with $n-1$ species is:
\begin{equation}
  \dot y_{i} = y_{i} \left(r_{i} + \sum_{j=1}^{n-1} b_{ij}y_{j}\right) \qquad
  i=1, \ldots , n-1
\end{equation}
where $y_i$ is the abundance of species $i$, $r_i$ the intrinsic growth rate, and $b_{ij}$ describes how the species $i$ and $j$ interact (wiki entry on the Lotka-Volterra eqn).
According to Nowak's book Evolutionary Dynamics, these two equations are equivalent to each other (the same result appears in Hofbauer and Sigmund's Evolutionary Games and Population Dynamics). This is a neat result because it shows that results in ecology based on the Lotka-Volterra equation has a game theoretic interpretation and vice-versa.
Question
This would mean that the replicator equation for two strategies (e.g., the Hawk-Dove game) is equivalent to a single species interacting with itself under the Lotka-Volterra equation. How could that be? The replicator equation would describe the frequency of two strategies in the population, but the equivalent Lotka-Volterra equation would describe the evolution of a single and undifferentiated population. My problem is not so much with the proof of the equivalence between these two equations (Hofbauer and Sigmund give a proof of this equivalence in their book), but with the interpretation of the equivalence between the two eqns.

Can you please define all the parameters in both equations?

Sorry. I've just added a description of the parameters.

It'd be great if one could already prove this equaltiy between the two models. Did M. Nowak referenced his claim? Do you have references also for the replicator and the Lotka-Volterra equations? The L-V equation seems a little weird to me. It doesn't quite match with what I found on wiki. Also, it feels weird to talk about $n-1$ species, rather than replacing all the $n-1$, by $n$ in the equation and make it valid for $n$ species. +1

Nowak refers to this result in his "Evolutionary Dynamics" but the proof appears in Hofbauer & Sigmund's "Evolutionary Games and Population Dynamics." Regarding the L-V equation, my understanding is that Nowak is referring to the generalized version of this eqn rather than the one used to study competition between species. I could follow the proof but, like you, I still find it very weird that we are mapping a game theoretic model with $n$ strategies to a L-V equation with $n-1$ species. It's one of those cases in which you understand the math but you cannot quite understand what is going on.

The key point is that the first equation is describing frequencies, i.e., $\sum_{i=1}^n x_i = 1$, so there are only $n-1$ degrees of freedom. For instance, if $n=2$ (as in Hawk-Dove), you can totally describe the state of the system with just $x_1$, because $x_2$ is just $x_2=1-x_1$. This constraint is enforced by adjusting $\phi$.
To convert the Lotka-Volterra model to the first equation, define $x_i\equiv y_i/\sum_j y_j$.


text:
Using viruses to treat altered or misconfigured DNA
Consider how a Retrovirus can modify existing cell DNA to 'execute instructions' on its behalf.
I wondered: Why can we not utilize lab-generated viruses to infect sick patients with a 'healthy' virus that would rewrite bad segments of DNA with something either correct or non-malus? This of course is assuming that we have a solid understanding of the relationship between genomes and precise viral functions, additionally that we had some sort of gene replacement functionality.

Consider how a Retrovirus can modify existing cell DNA to 'execute instructions' on its behalf.

Not only retroviruses do that. Actually, pretty much all viruses use the machinery of the host cell on its behalf.

Why can we not utilize lab-generated viruses to infect sick patients with a 'healthy' virus that would rewrite bad segments of DNA with something either correct or non-malus?

We actually do that. We use viruses (incl. retrovirus but not only) to insert DNA segments into eukaryote genome. See vectors in gene therapy > viruses

Retrovirus to reverse another retrovirus

Note that I don't really understand your title so, I ignored it a bit focusing on the content of the post.

Updated the title. That makes sense, thank you for giving me a direction to continue research!


text:
Are cytotoxic (killer) T-cells always present or are they only produced during a cell mediated immune response?
The book I'm studying says the following
"During a cell mediated immune response, the release of IL-2 by helper T-cells is resposible for stimulating the production of Cytotoxic T-cells, which have receptors that match the anti-gen of the infecting pathogen."
I'm not exactly sure if this is impliying that cytotoxic T-cells are only produced and present during an immune response or not, since I also have an older version of the book that simply says "the IL-2 released by helper T-cells activates cytotoxic T-cells" which seems to indicate that they are normally always present, but just inactive

Naive T cells are regularly matured in the thymus where they're released into the blood. A majority are CD4+, but many are also CD8+. As a caveat, many are TCRαß+, and few are TCRyδ+ (outside the scope here but fun to look up and read).  From there, they home to the lymph node where they hang in the T cell zone until blood trafficking signals coax them into the blood. T cells regularly navigate the body in response to signals from different cells such as blood vessel endothelium, lymphaptic vessel endothelium, epithelial cells, and so forth (1).
The basic process behind an adaptive immune response is that antigen-presenting cells get ahold of foreign antigens and head back to the lymphoid organs like lymph nodes. By the time they get there, they've matured into "licensed" professional antigen-presenting cells. They interact with both CD4+ or helper T cells, and CD8+ or cytotoxic T cells. It's more complex than that, but the point of the helper T cell is to produce "help" signals. These include IL-2, and other cytokines which not only assist the CD8+ T cells in their activation, but also determine a lineage they'll take based on other factors.
So they're both there, in the lymph node at the time the antigen-presenting cell, such as a dendritic cell, arrives to activate the lymphocytes in that region. Take home point: the naive lymphocytes are there until they are activated, in which you would be correct in your last line. But they do actually do things other than sit there, other take home point. They aren't simply anergic and waiting.

By other things, do you mean seeking and killing cancer cells and foriegn tissues and parasites (though these two I think could be the same thing as just an immune response, since they're foriegn) ? That's also breifly mentioned but just that, it isn't talked about much.

Well to be certain, cancer cells are subject to immunoediting, which is another complex term you can look into. There are also things handled by innate immunity and B cells. The naive T cells, however, can extravasate into tissues secreting chemokines in response to say, a pathogen. There are intra-epithelial lymphocytes and dendritic cells and macrophages that hang out in tissues like the gut mucosa and have the potential to active lymphocytes in situ. So "other things" can mean a great deal of things.


text:
Why is prothrombin time used to monitor warfarin and not activated partial thromboplastin time?
Warfarin is said to change prothrombin time (PT) but not activated partial thromboplastin time (aPTT) (for practical purposes at least anyways, not really sure). But looking at the mechanism of action of warfarin, I dont see why that is.
Warfarin works by inhibiting vitamin K, or more specifically, vitamin K-mediated post-transnational modifications of certain clotting factors (X, IX, VII and II) which are important for the activity of said clotting factors. Warfarin affects factors in both the extrinsic and intrinsic pathway (and maybe a bit silly and irrelevant, but the same number of factors in each too; 3 by 3!). So, why is it that PT is affected by warfarin but aPPT isnt? I looked alot and couldnt really find any satisfactory answer (there werent many answers to begin with either). What I've found and have gotten from my professor are the following points:

Warfarin's effect is more pronounced on PT because factor VII (the first factor in the extrinsic pathway) has the shortest half-life and is therefore the quickest to get depleted. But in that case, warfarin usually takes a few days to be considered effective enough to stop administering patients heparin with it; wouldnt all the affected factors be depleted enough by that time to also affect aPTT?
Warfarin affects factor VII, which is the initiating factor (tissue factor aside) for the extrinsic pathway, which is why it affects PT more? Honestly I don't know how these tests work exactly so I'm not sure if this would matter. This was what my professor answered with when a student asked (or at least it's what I recall).

This article tells that warfarin can prolong aPTT too.
Now look at the image below

It is almost 5 days and some extra hours when anticoagulant effects start, during which we give heparin, also called as heparin bridge.

But in that case, warfarin usually takes a few days to be considered effective enough to stop administering patients heparin with it; wouldnt all the affected factors be depleted enough by that time to also affect aPTT?

PT is used as a standard measure not just for initiating but also for monitoring  warfarin therapy using the INR(international normalised ratio) because it gives the earliest result(as half life of factor VII is shortest) to start another treatment according to guidelines, when INR is altered beyond normal range

Warfarin affects factor VII, which is the initiating factor (tissue factor aside) for the extrinsic pathway, which is why it affects PT more?

Well I might not have any sources to answer that, but I can try to deduce answer by some logical arguments. In intrinsic pathway there is multiplication of factors, for eg. Factor XII activate factor XI and factor XI activate factor IX but by this time more and more factor XI are getting activated thus causing more interaction with whatever factor IX is left in blood(factor IX is less here due to warfarin) so no relative profound anticoagulant effect of warfarin is present. But in case of extrinsic pathway factor VII is the intiating factor and is already less due to warfarin, and there is no such factors multiplying before that to cause their maximum interaction and therefore activation of factor VII so relatively more profound anticoagulant effect is present.


text:
Can bats echolocation discern what insects they are preying on?
Insectivorous bats feed on many different types of insects such as mosquitoes, moths, beetles, and bees.  According to the Bat Conservation Trust, bats can discern insects from other objects but I'm having trouble finding any research saying whether bats can discern between the insects they are chasing?

Why don't they just use their ears? I can tell a mosquito just from hearing it.

Yes, some bat species can distinguish the species of insects by echolocation. One of the better studied species is the greater horseshoe bat (Rhinolophus ferrumequinum).

Echolocating greater horseshoe bats (Rhinolophus ferrumequinum) detect insects by concentrating on the characteristic amplitude- and frequency modulation pattern fluttering insects impose on the returning echoes. This study shows that horseshoe bats can also further analyse insect echoes and thus recognize and categorize the kind of insect they are echolocating.
von der Emde, G. & Schnitzler, HU. J Comp Physiol A (1990) 167: 423. https://doi.org/10.1007/BF00192577

Further reading:

Hans-Ulrich Schnitzler, Elisabeth K. V. Kalko; Echolocation by Insect-Eating Bats: We define four distinct functional groups of bats and find differences in signal structure that correlate with the typical echolocation tasks faced by each group, BioScience, Volume 51, Issue 7, 1 July 2001, Pages 557–569, https://doi.org/10.1641/0006-3568(2001)051[0557:EBIEB]2.0.CO;2

Ulanovsky, N., & Moss, C. F. (2008). What the bat’s voice tells the bat’s brain. Proceedings of the National Academy of Sciences of the United States of America, 105(25), 8491–8498. http://doi.org/10.1073/pnas.0703550105

Roverud, R.C., Nitsche, V. & Neuweiler, G. J Comp Physiol A (1991) 168: 259. Discrimination of wingbeat motion by bats, correlated with echolocation sound pattern https://doi.org/10.1007/BF00218418

Hearing by Bats (edited by Richard R. Fay)


text:
Hamilton's inclusive fitness approach
The underlying intuition of Hamilton's model of inclusive fitness is that we should study social behaviors from the point of view of actors -- rather than the recipients. To build his model, Hamilton expresses the genotype of the actor $j$ in terms of the genotype of the recipient of
the behavior, $i$. The genotype of $j$ is decomposed in two parts,
``genes which are copies by direct replication of genes in $i$; the
other part consists of non-replica genes'' (Hamilton 1970, p. 1219).
Hamilton (1970) further defines $q_{i}$ as the gene frequency of the
replica part, $b_{ij}$ represents the replica fraction, and $q$ is the average gene frequency in the population. From these definitions Hamilton (1970) jumps to the equality:
\begin{equation}
      E (q_{j}) = \frac{1}{1-b_{i}}\left\{ (b_{ij} - b_{i})q_{i} + (1-b_{ij})q\right\}
\end{equation}
where
\begin{align*}
  b_{i} = \frac{1}{n}\sum_{j}b_{ij}
\end{align*}
How did Hamilton derive the above equation?

Here is what I think Hamilton is doing. My impression is that the above equation expresses $E(q_j | q_i)$ as a linear regression on $q_i$. In other words, I think the above equation is equivalent to:
$E(q_j | q_i) = E(q_j) + \beta (q_i - E(q_i))$
$E(q_j | q_i) = q + \beta (q_i - q)$
In fact, this equation is equivalent to Hamilton's equation if the regression coefficient is:
$\beta = (b_{ij} - b_i) / (1 - b_i)$
However, I haven't been able to derive this regression coefficient. Given that $\beta = Cov (q_j, q_i)/Var (q_i)$, I suspect that the way to go is to rewrite $q_j$ and $q_i$ in terms of $b_{ij}$ and $b_i$ and calculate the regression coefficient.

Reference:
Hamilton 1970 "Selfish and Spiteful Behaviour in an Evolutionary Model"
http://www.nature.com/nature/journal/v228/n5277/abs/2281218a0.html

Hamilton's papers are always sooo complicated!

Agreed! I think his 1964 papers are even worse. I suppose the above equation is a linear regression of $q_j$ on $q_i$. But I still don't see how Hamilton arrived at the equation above.

Sad to see that research-level question often don't receive as much attention as basic questions. I hope you'll get some more upvotes and will get someone less lazy than me that will be ready to dive into Hamilton's article.

I can't access the paper so can you provide more detail about the model. Also, $E(q_j|q_i)$ conditional expected value?

@dustin: Hamilton does not use conditional probabilities. I'm the one that wrote that way when I was explaining my question. I changed this now.

@dustin: I also added the relevant portion of his paper. What Hamilton does earlier is to express the fitness from the point of view of the recipient. This is described here: http://biology.stackexchange.com/questions/26396/hamiltons-derivation-of-direct-fitness-from-his-1970-paper

It is not a regression (not at this stage of the paper, a regression will be done latter)
The only complicated thing to understand is $b_i$, which is the 'base relatedness', ie how $i$ is related to a random individual (to be compared to how related it is to individuals with whom it interacts).
To simplify let's first consider the situation where $b_i = 0$:
$E(qj) = b_{i,j} q_i + (1-b_{i,j}) q$ is just the translation of 'the gene frequency of the replica part is q_i' and 'the gene frequency of the non replica part is $q$'; because $b_{i,j}$ is the fraction of the replica part, ie the chances that our locus of interest belongs to the replica part of individual $i$ in individual $j$.
Now let's re-introduce $b_i$. The idea is to compare relatedness of the two individuals $i$ and $j$ to the average relatedness of $i$ with a randomly picked individual in the population (this random relatedness is exactly $bi$). This is important because $q$ already accounts for this 'random relatedness'.
So instead of giving probability $b_{i,j}$ to $q_i$, we give it probability $b_{i,j}-b_i$, which is the chance that the allele of interest is present because of the replica fraction being higher than random. And because now the quantity varies between 0 and $1-b_i$ we normalize it by $1-b_i$

The underlying intuition of Hamilton's model of inclusive fitness is that we should study social behaviors from the point of view of actors -- rather than the recipients

Not exactly, it is saying that we should study social behaviors from the point of view of the alleles causing it, that may be shared between the actors and the recipients. But this paper is not the paper that introduces inclusive fitness, quite the opposite it is the paper that tries to reconciliate kin selection with Price equation.

you say that $(b_{i,j}-b_i) \in [0,1-b_i]$. My impression is that  $(b_{i,j}-b_i) \in [-b_i,1-b_i]$.  $(b_{i,j}-b_i)$ will be negative when the individual $j$ is less related to individual $i$ than average.

I suppose the lower bound of $\frac{(b_{ij} - b_{i})}{(1-b_{i})}$ is $- \frac{b_{i}}{(1-b_{i})}$ (since $0\leq b_{ij} \leq 1$). However, this doesn't seem right because, otherwise, $\frac{(b_{ij} - b_{i})}{(1-b_{i})}$ could assume values in the interval $[0, -\infty)$.

From the limited information, I can provide the following but I am not sure if this is what you are looking for. Also, I still don't see the statement where the author concludes we get the Linear regression model $E(q_i) = Aq_i + C$ which is odd notation since it says the expected value is a linear regression. In fact, if it is a linear regression, it should say $q_j = Aq_i + C$.
$$
A = \frac{\text{cov}(q_i,q_j)}{\text{var}(q_i)}\quad\text{and}\quad C = E[q_j] - \frac{\text{cov}(q_i,q_j)}{\text{var}(q_i)}E[q_i].
$$
Now, we can write the variance and covariance as
\begin{align}
\text{var}(q_i) &= E[q_i^2]-E^2[q_i]\\
\text{cov}(q_i,q_j) &= E[q_iq_j]-E[q_i]E[q_j]
\end{align}
where the expected value of a discrete random variable $X$ is calculated as
$$
E[X] = \sum_{i=1}^Nx_ip_X[x_i]
$$
where $p_X[x_i]$ is probability of $x_i$ and $N$ can be countable infinite.

The mean of conditional PDFs comes up in optimal prediction where the minimum mean square error is $E_{Y\mid X}[Y\mid x]$. This optimal prediction covers linear and nonlinear. For the standard Gaussian PDF, the optimal prediction will be linear since $E_{Y\mid X}[Y\mid x]=\rho x$ where $\rho$ is the correlation coefficient. I am going to short hand $E_{Y\mid X}[Y\mid x]$ to $E[Y\mid x]$
$$
E[Y\mid x] = \mu_Y + \frac{\rho\sigma_Y}{\sigma_X}(x-\mu_X)
$$
where $\mu_i$ $i=X,Y$ is the mean and $\sigma_i$ is the standard deviation. If $X$ and $Y$ are not Gaussian, then the model can be nonlinear. Are there examples of non Gaussian be linear probably.

You're right. Hamilton does not say that this equation is a linear regression. This is something that I assumed (I changed my question to reflect that). My guess is that Hamilton's above equation expresses $E(q_j\mid q_i) = E(q_j) + \beta (q_i - E(q_i))$, where $\beta$ is the regression coefficient.

@falsum what do you mean by $E[q_j\mid q_i]$. I know it has a conditional expected value. Is that what you mean?

Yes. This is what I mean. My guess is that Hamilton is providing an equation that is trying to predict the gene frequency of a random actor (i.e., $q_j$) from a given $q_i$.

@falsum If we use that definition, there is a chance it will be a nonlinear predictor not linear.


text:
Hamilton's derivation of direct fitness from his 1970 paper
In his 1970 paper "Selfish and Spiteful Behaviour in an Evolutionary Model", Hamilton uses Price's equation to derive his well-known rule $rb -c >0$. My question is about one of the steps in his derivation.
Hamilton considers a population of $n$ individuals. Let $s_{ij}$ be the effect of individual $i$ on the fitness of $j$. The fitness of an individual $j$ is defined as $w_j = 1 + \sum_i s_{ij}$, $w=1/n \sum_j w_j$ is the mean fitness in the population, and $q=1/n \sum_j q_j$ is the average frequency of a certain allele. Using Price's equation, we get
$w \Delta q = Cov (q_j, \sum_i s_{ij})$.
So far so good. But Hamilton then says that this equation can be rewritten as
$w\Delta q = \sum_i 1/n \sum_j (q_j - q)s_{ij}$
Based on the definition of covariance (i.e., $Cov (X,Y) = E((X-E(X))(Y-E(Y)))$, this seems to only be the case if $E(\sum_i s_{ij}) = 1/n \sum_j \sum_i s_{ij} = 0$. But this would imply that the average fitness wouldn't change over time, which sounds odd for me. In sum, I don't understand this step in Hamilton's paper. What am I missing?

Actually the derivation is pretty straightforward. It's easier to use the fact that $Cov(X,Y) = E(XY) - E(X)E(Y)$ to derive this result. Suppose
$x_{j} = \sum_{i} s_{ij}$.
\begin{align*}
  Cov (x_j, q_{j}) &= E (x_{j}q_{j}) - E (x_{j}) E (q_{j}) \\
                    &= \frac{1}{n}\sum x_{j} q_{j} - \frac{1}{n}\sum
                      x_{j} q \\
                    &= \frac{1}{n} \sum x_{j} (q_{j} - q)
\end{align*}


text:
Multi-modal distribution for gene expression data
Why would some genes have more than two modes in their expression distribution? What external factors would cause this anomaly?
I'm referring to the expression distribution of a gene across different tissue samples. For example, if one was to download a bunch of data from NCBI GEO, and pinpoint one gene and plot the expression level versus the frequency for that gene across all those data sets, some genes would have more than 2 modes (2 expression levels with very high frequency). This is the only case I'm interested in: more than 2 modes - not bimodal. So what would cause more than two modes?

Could you expand please? Expression distribution over what? The same tissue? Same cell over time? Different tissues?

@nico's point is spot on, we can't answer until we know more. Also, should I intepret your question to mean you are not interested in bimodal (i.e exactly 2 modes) distributions? Those are usually easier to explain, have more concrete examples, and should generalize to a multimodal case. But if you are not interested in bimodality please make that clear.

My original question was a bit vague - here are some clarifications. I'm referring to the expression distribution of a gene across different tissue samples. For example, if one were to download a bunch of data from NCBI GEO, and pinpoint one gene and plot the expression level versus the frequency for that gene across all those data sets, some genes would have more than 2 modes (2 expression levels with very high frequency). As I alluded to in my post, this is the only case I'm interested in: more than 2 modes - not bimodal. So what would cause more than two modes?

@newintern Edit your question instead of clarifying in the comments.

One trivial situation in which this can happen is when the tissue used for expression studies is heterogeneous. Different cells express different levels of the gene.
Bimodality can be observed when the system can actually occupy two stable states; i.e. a gene can either have a high expression or a low expression. When you sample the population you would get two peaks. Bistablity (two stable steady states) is a common phenomenon in biological systems and positive feedbacks generally exhibit such behavior. In bistable systems there is also an unstable steady state which lies "between" the two stable states (like a mountain separating two valleys). If the system is in the unstable state, it can fall to either of the two stable states. (See this article for an example). This concept can be extended to multistable systems but they are a little more complex than the simple feedbacks. However they can theoretically exist (I don't know of a biological example yet).
Bimodality/multimodality can be also observed in the absence of a deterministic bistability in the system. This happens because of the expression noise due to stochasticity and is observed in case of transcription bursts (See here).

Sure - different cells can express different levels of the gene, but the frequencies will be relatively smaller, won't they?

@newintern Depends on the parameters. They can be comparable as well.

Just saw your edit. If this raw expression data were clustered or smoothed to eliminate noise would transcription bursts still be significant enough to be considered another major peak?

@newintern This is true biological noise not a technical noise because of the experiment. By removing it you are dismissing a natural phenomenon. And yes the bursts can give rise to significant effects. See the linked paper.

Alright I understand now. This will help me explicate my data. Thanks!


text:
The relationship between the shape of the bacterial DNA and the blocking of replication machinery
I was reading a course about tolemers when I arrived to this phrase :

[...] The ends of a linear DNA molecule cannot be replicated by the cellular replication machinery (which may be one reason why bacterial DNA molecules are circular).

I want to know what is the relationship between the circular shape of the bacterial DNA and the blocking of replication machinery ?

What research have you done to answer this yourself? Please read the Wikipedia articles on telomeres and telomerase to understand what happens with linear chromosomes. You should also read about DNA replication in both prokaryotes and eukaryotes. Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

It’s not a homework question, it’s a question out of curiosity, I’m trying to understand an idea proposed by Liz Parrish to reverse aging by adding some portions of telomers to the human DNA, so I want to know, how the shape of the bacterial DNA makes the bacteria immortal (if I can say so).

Prior research is still required, regardless of whether the question is an academic assignment or not. Additionally, please [edit] your question to add and expand upon what you just put in your comment, as it makes the scope of your question completely different than what you originally asked. Remember, you need to include as much information as possible in order to get the answer you're looking for. Include what research you have done, what you understand so far, and where exactly you're stuck.

This has been covered elsewhere (I highly recommend this page ) but it basically has to do with the priming of the strands and the fact that all polymerases work from the 5' prime to the the 3'. I made a quick schematic to illustrate (the explanation is below):

The priming is done with RNA during DNA replication in the cell, unlike PCR where you use DNA oligo's to prime. This RNA-DNA is called the Ozakazi fragments. After replication RNAse H will remove these primers leaving only DNA's and gaps. In the middle of the sequence the gaps can be filled in by the normal repair machinery but at the ends there is no 3' terminus to fill in the gaps. That is where the telomerase comes in and fill these gaps with a fixed sequence (also based on an RNA template but that is going into details).
If you have a circular chromosome there is always a 3' to complete the gap.