text:
Are identical twins exactly the same?
http://www.scientificamerican.com/article.cfm?id=identical-twins-genes-are-not-identical
According to this article some identical twins show differences with respect to their copy number variants. How is this possible? If mitosis of an egg can lead to this difference, why can't mitosis of any cell in our body?
If we assume that identical twins are exactly identical, then if we make a clone of a twin will all three be exactly identical?

Errors in division occur all the time and can show up in any dividing cell; this is, of course, important for cancer biology.  If one of my cells replicates oddly right now it likely won't matter since it's only one out of trillions, but if that happened at a very early age in development it could be present in many if not all of my cells.  Identical twins indeed come from the same egg-sperm fusion event but they develop separately from a very early state.  It's trivial to imagine a minor replication error in DNA at an early cell stage that results in different genotypes between so-called identical twins.  Besides, we've known for years that identical twins can have major epigenetic differences, so this isn't particularly ground-breaking.

If we assume that identical twins are exactly identical, then if we make a clone of a twin, will all three be exactly identical?

Depends on your definition of "clone" but how identical is identical?  If you mean exact, then probably not; at the very least they will have different numbers of cells, for example, not to even mention CNV or epigenetics.  If you want some SciFi cloning thing then, well, join the club.

If I make a plant out of a single cell, will it be more appropriate to say that the new plant and the old plant are exactly identical genetically or to say that they are more like "twins" ?

In theory, they should be more like "twins" but in practice you could say identical.  For all intents and purposes there's no difference.

Identical twins do start out identical, but their DNA will quickly diverge. Not in a dramatic way, but in point mutations, at random locations, in different cells.  Think of how there is a certain error rate associated with DNA replication - so even from that very first cell, when it divides to form a second cell, there is a chance there may be mutations in the DNA copy.  It is highly unlikely that both twins will make the same mistake in copying the DNA in exactly the same location.  Now repeat that idea millions and millions of times, as they develop, forming all the cells they need to form their bodies, and throughout their lives.  Mutations are random, and they accumulate.
I made a video about this topic - Are Identical Twins Really Identical?

@ biogirl: Why clone? There are quite a number of monozygotic  quadruplets. One zygote giving rise to four identical beings.

The clarification that I require is whether the identical twins are exactly similar or are they mirror images? That is if there is hair whorl on the left side in one, whether it will be on the right side in the other. Functionally also if one is right handed will the other be left handed etc.

@khhsocratica Loved the video ! You guys are doing a wonderful job :)

@RamManoharM there is nothing in the biology of twins that would cause such mirroring. The parts of hair whorls or handedness that are determined by genes will be the same.

The video was good. But then references to scientific studies on twins would have been better.


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Gene Circuits; experiments
First, my background - I'm a newcomer to biology.
What is a gene circuit, and how might I simulate one in a laboratory? Thank you.

What kind of laboratory? Are you looking for computer simulations?

No, I was referring to a physical laboratory. What sort of equipment would I need?

You question is likely too broad in its current format. You have, essentially, two questions in one. Why not do some research on what gene circuits are to start with? Explain briefly what you know, and then get at the question of how to model them in the lab. Learning something about gene circuits first might help you better define your question of how to simulate one.

I'm just going to give a broad idea of what a biological circuit is.  There's definitely more than one way to define them, but hopefully this will give you some idea.
Broadly, biological circuits are reminiscent of electrical circuits in that energy or information flows through the cell.  In biological pathways (a more typical terminology), genes in the cell (usually proteins) will use a signal (usually in the form of a chemical compound or a modification of a protein, but sometimes a simple ion or even electrical current (rarely)).  The signal then can be transmuted into a different chemical compound or it can even alter a protein so that it functions differently.
Here are a couple of classic examples.  The first is the Citric acid cycle (also called the Krebs cycle), discovered in the 1930s.  Here you can see that Citrate is chemically transformed into acetate and carbon dioxide and chemical energy in the form of NADH (reduced nicotinic acid dinucleotide).  Each step of the cycle has a different compound which is handled by a different protein enzyme.  While all the proteins and compounds may coexist in the same part of the cell, there is nonetheless an orderly circuit of chemical energy mediated by the genes of the cell and controlled by the cell as it adjusts the amount of enzymes available for each step of the cycle.

Another example of an entirely different sort of gene pathway works differently but has the same set of concepts.  Mitogen Activated Kinases (MAPKs) are proteins which have generally two states an activated state and an inactivated one.  As you can see below, an outside signal like high salt osmolarity or a signalling molecule is sensed by a receptor on the cell surface.  By some method a MAP Kinase is activated, perhaps by the addition of a phosphate to the surface of the protein or by dimerizing the MAPK.  Once activated, the MAPK will then phoshphorylate another kinase, which may activate yet another.  Finally a protein in the nucleus will be activated and cause transcription of some target genes.

In the latter case, a very small change to the protein costs little energy and information is being transmitted, but by biochemical signals where proteins are modified and affect other proteins.  That's a more subtle circuit than in the former case where relatively many individual molecules might be processed by enzymes together.
This hopefully gives you some idea of what a biological circuit looks like.  There are many other examples and subtle variations but that's a quick tour.
Experiments involving these pathways are too numerous to mention - individual proteins may be modified, their concentration within the cell can be altered by say mutations in the chromosome, pathway intermediate compounds like Succinate might be added to see how the citric acid cycle responds, isotopic labeled compounds can be added to see where they go in the cell.  There's nearly 100 years of experiments here.  that's a lot.
Hopefully this will just give you some idea of where to start.  Nearly any biochemistry textbook covers these topics in better detail, but then they are often over 1000 pages long!

A genetic circuit can be likened to electrical circuits, except rather than switches, resistors, wires, etc., you use promoters, ribosomal binding sites, coding sequences, repressors, etc. - This will get you well acquainted with the new jargon around bioengineering: http://parts.igem.org/Main_Page

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Possible Genotypes of 4 Alleles of Adh
There are four alleles of Adh which are Adh-1, Adh-2, Adh-3 and Adh-4.  Their respective frequencies are 0.11, 0.84, 0.01 and 0.04.  What are the Hardy-Weinberg frequencies of the possible 10 genotypes?
My Attempt:  First I thought that there were more than 10 genotypes (4*3*2*1) = 24.  I've never done HWE with 4 genotypes so im not sure how to use $p+q=1$ or $p^2+2pq+q^2=1$.

I may be wrong but to get the number of possible genotypes isnt it 4+3+2+1=10?. You can have A1A1,A1A2,A1A3,A1A4,A2A2,A2A3,A2A4 and so on. When you multiply you are counting some genotypes twice (for example A1A2 and A2A1. They are the same)

Those Hardy-Weinberg equations are the general case, used for only two alleles.  This question is basically answered here, for three alleles; you've got a situation of four alleles.  That means you need to have:
$(p+q+r+s)^2=1$
Where $p$, $q$, $r$, and $s$ are the frequencies of your respective alleles.  This expands out to the rather unwieldy:
$p^2+2pq+2pr+2ps+q^2+2qr+2qs+r^2+2rs+s^2=1$
Now it becomes a plug 'n chug assignment; simply assign the frequencies and calculate.

 Assuming $p$ is Adh-1, $q$ is Adh-2, etc., $p^2=0.0121$, $2pq=0.1848$, and so on.

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Hardy Weinberg Equilibrium after 5 Generations
1
There is a population not at HWE where red eye = $a^+$ (dominant) and white eyes = $a^-$.
If:
$a^+/a^+ = 0.6$
$a^-/a^+ = 0.1$
$a^-/a^- = 0.3$
what are the frequencies of the $a^+$ and $a^-$ alleles?
My attempt: So if it's not at HWE then I should divide the heterozygotes equally to get $a^+ = 0.65$ and $a^- = 0.35$.
2
We are now at HWE.  What are the frequencies in the next generation?
My attempt: so if $a^+ (p) = 0.65$ and $a^- (q) = 0.35$ then $p^2 = 0.42$ and $q^2 = 0.12$.  Then using $p^2 + 2pq + q^2 = 1$, I can figure out that the heterozygotes make up $0.46$.  So the frequency of the $a^+$ allele is $0.42 + 0.46 = 0.88$, and then $a^-$ should be $0.12$ (because they should add to 1)
3
What is the frequency 5 generations later in HWE?
My attempt:  Wouldn't it be the same answer as #2. I'm not sure how more generations in HWE would change the allele frequencies.

You are almost correct, but with a few modifications/comments.

The calculations in Q1 are independent of HWE, and are just calculating the current allele frequencies in the population based on genotype frequencies (i.e. would be the same irrespectively of if the population is in HWE or not).
In Q2 it is unclear if the questions is asking for genotype frequencies or allele frequencies. Your answer of genotype frequencies of $p^2=0.42$ ($a^+a^+$), $q^2 =0.12$ ($a^-a^-$) and $2pq =0.46$ ($a^+a^-$) is correct if you assume the allele frequencies from Q1 and HWE. However, your allele frequencies are incorrect and should be $p = 0.42 + 0.46/2 = 0.65$ and $q = 0.12 + 0.46/2 = 0.35$, i.e. the same as in Q1. Remember that the allele frequencies shouldn't change under HWE.
Yes frequencies should not change in Q3. This is the textbook definition of HWE, i.e. that allele and genotype frequencies remain constant between generations in the absence of evolutionary forces (i.e. under the HWE).

thanks.  for #1 I thought that i calculated the correct allele frequencies (im given genotype frequencies).

@Kirby Yes the numbers in Q1 are correct, and I was only commenting on that you wrote "So if it's not at HWE then I should ...". The calculation of frequencies (as $p = f(a^+a^+)+f(a^+a^-)/2$ and $q = f(a^-a^-)+f(a^+a^-)/2$ ) is valid with or without HWE.

ok.  for #2 you said that p^2 = 0.35, but isn't that just p and p^2 would be 0.42?

@Kirby Yes correct. That was a typo on my part. Allele freq $p = 0.65$ and genotype freq $p^2 = 0.42$ ($f(a^+a^+)$).

@Kirby Feel free to mark an answer as 'answered' if you find it satisfying.

At generation 1, the frequencies of $a^-$ is $p=0.35$ and the frequency of $a^+$ if $q=0.65$.
Assuming random mating (and no change in allele frequency) after any number of generation is given by $p^2$ (=0.1225), $2pq$ (=0.455) and $q^2$ (=0.4225).


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Survivorship Curves: Type II curve mortality rate is not constant?
In graphs of survivorship curves, I'm seeing that the Type II curves are straight lines, and the supplementary text says that the mortality rate is constant (i.e. the slope of the line is constant). However, it's also clearly stated that the y-axis is a logarithmic scale, which means that the original Type II curve is exponential:
$$\ln y=-rx+b$$
$$y=Ae^{-rx}$$
This implies that the real mortality rate is not constant, but changes as $$y'=-Ar(e^{-rx})$$
How are we defining the word rate, anyway?

Presumably $r$ (or $-r$) is the rate, which would appear to stay constant.

$r$ is the individual mortality rate per time step. Survivorship curves (plotted on a log scale) show the proportion of individuals surviving with time, and with a Type II curve a constant proportion is dying at each time step (constant mortality with age, $r$). When the model is expressed as $y$ you are looking at the number of individuals surviving to a time step, which is an negative exponential for Type II, since a smaller and smaller proportion of the population remains at each time step. Therefore $y'$ is the change (slope) in the number of individuals surviving over time. This can be seen as a rate, but it is not the mortality rate of individuals, and it is not accurate to describe it as the "..real mortality rate..".
For an introduction to survivorship curves you can also look at "Survivorship Curves" from Nature Education

For Discrete Time
There are two quantities you should be careful not to mix up.

One is the number of individuals who will die during a given interval: $d_x = N_x - N_{x+1}$.
One is the fraction, out of those alive at the beginning of a given interval, who will die during the interval: $q_x = \frac{d_x}{N_x}$

($N_x$ being the number of survivors at age $x$.)
On a regular plot, if $d_x$ is constant then survivorship will decrease linearly; if $q_x$ is constant then survivorship will decrease geometrically. On a semilog plot, when $q_x$ is constant then this geometric decrease will look like a straight line. This is, as far as I know, the main reason to even use semilog plots in the first place; it makes geometric decrease easy to recognize. $d_x$ is sometimes called the death rate and $q_x$ is sometimes called the mortality rate.
(In my opinion this usage is careless; they aren't rates, but just numbers. Compare: there is a distinction between travelling 10 miles in an hour, and travelling at 10 miles per hour.)
$q_x$ can also be thought of as estimating the probability that someone who is age $x$ will die before age $(x+1)$. It is therefore sometimes also called the "Age-Specific Probability of Death". Notice that it is bounded between 0 and 1.
(Probabilities can't be lower than 0 or higher than 1; and the fraction dying has to be somewhere in between "none of them" and "all of them"!)
Here's an example survivorship curve, on a regular plot, I made for constant $q_x = 0.1$.

This much should be enough to answer your question. But, for completeness...
For Continuous Time
I complained about calling $d_x$ the death rate. That's because rates have a unit of $time^{-1}$ ("...per second", "...per hour" etc.) Of course, dividing $d_x$ by the length of the interval, does give you the average death rate over the interval. And,

The slope of the survivorship curve (multiplied by -1; we want a positive rate of decrease, instead of a negative rate of increase) gives you the instantaneous death rate at age $x$: $-N^{'}_{x}$.

(For instantaneous rates to be useful, we have to "smooth-out" the survivorship curve instead of letting it be a stepped curve. If it was stepped, then the slope would just always be horizontal or vertical.)
This brings us to another quantity: the "Force of Mortality":

The instantaneous, age-specific, per-capita death rate; or, the death rate at age $x$, divided by the cohort size at age $x$: $\mu_x = -\frac{N^{'}_{x}}{N_x}$

To illustrate, if the death rate at age $x$ is "60 deaths per minute", and if at that instant there are 60 people, then the per-capita death rate is "1 death per person per minute". Because choice of time unit is arbitrary, this is the same as saying "60 deaths per person per hour" or "525600 deaths per person per year".
The Force of Mortality is unintuitive ("per-capita" death rate? - but everybody only dies once!) but the formula is coherent. The point of having a "per-capita rate" is to enable comparison between cohorts of different sizes, or the same cohort at different ages when it was bigger vs. smaller, and so on; in general the idea is that death rate has something to do with the number of members, but also something to do with the condition of each member, and $\mu_x$ is trying to get at the latter. It can be visualized as the slope of the survivorship curve (multiplied by -1 to make it positive), divided by the height of the survivorship curve.

There is a similarity between these two quantities, and the two which were defined for discrete time. If $-N^{'}_{x}$ is constant, then so is $d_x$; and if $\mu_x$ is constant, then so is $q_x$. And, again: on a regular plot, if $-N^{'}_{x}$ is constant then survivorship will decrease linearly; and if $\mu_x$ is constant then survivorship will decrease exponentially.
But they are distinct. It is the $time^{-1}$ dimension, and the fact that time units are interchangeable, which makes the difference.
If there are only 60 people, then it's obviously not possible for more than 60 people to die in the next year $(0 \le d_x \le 60)$; and it's not possible for the fraction dying to be higher than "all of them" $(0 \le q_x \le 1)$.
But suppose the rate of death at this instant is "60 deaths per hour". That's the same thing as saying it's "1 death per minute" or "525600 deaths per year". There's no implication that that many people will in fact die, because there's no implication that the rate will be kept up for the whole year. If this particular death rate were held constant as long as possible, then the cohort would all be dead in exactly an hour and then the rate would then hit 0. The instantaneous death rate can be as high as you like; it just can't stay high forever.
(If a death rate of "60 deaths per hour" is measured at an instant when there are 60 people, then the per-capita death rate is "1 death per person per hour" - or, equivalently, "$\frac{1}{60}^{th}$ of a death per person per hour", or "8760 deaths per person per year".)
Although the absolute death rate can't stay high forever, the per-capita death rate ($\mu_x$) can. That's what happens during constant $\mu_x$ (exponentially decreasing $N_x$), for example. The reason why this is not paradoxical is that the slope ($-N^{'}_{x}$; the numerator) is constantly decreasing; it's just that so is the height ($N_x$; the denominator).
The Force of Mortality $\mu_x$ has also sometimes been referred to as the "mortality rate". The equivocal use of language is unfortunate. It is also, especially in reliability engineering, known as the "hazard rate".
By the way
$q_x$ and $\mu_x$ have often been conflated, at least in gerontology (with which I am most familiar). But they are not the same. The first estimates a probability, and is bounded between 0 and 1. The second is not a probability, and has no upper bound.
One way they have been conflated is with the "Gompertz equation".
A Type II Survivorship Curve is one which is decreasing exponentially. When this is the case, both $q_x$ and $\mu_x$ are constant. We would call such a species "non-aging" or "non-senescing": your age makes no difference to your vulnerability.
But many species do age.
Benjamin Gompertz proposed that for many species including humans $\mu_x$ grows exponentially throughout adulthood:

Gompertz' Law of Mortality: $\mu_x = \mu_0 \cdot e^{Gx}$
Or, in its logarithmic form: $ln(\mu_x) = ln(\mu_0) + Gx$

(Where $\mu_0$ is the "initial mortality" and $G$ is the exponential "Gompertz parameter". In the logarithmic form, $ln(\mu_0)$ is the intercept, and $G$ is the slope.)
Whether or not $\mu_x$ follows such a law indefinitely is an empirical matter. (It's actually debated whether it decelerates in late life, and if so why.) But notice that $q_x$ couldn't possibly grow exponentially forever, since $q_x$ couldn't possibly ever exceed 1. And yet, due to the conflation, in recent times it has often been in terms of $q_x$ that the Gompertz equation has been presented and discussed.
Further Reading
Unfortunately, as far as I know the literature (both professional and pedagogical) is sorely lacking in treatments which are both intuitive and accurate!
Peter Medawar's "The Definition and Measurement of Senescence" (Chapter 1 in The CIBA Foundation Colloquia on Ageing, Vol. 1) is probably still the best introduction to the rationale behind why we care about survivorship curves and mortality, from the perspective of biogerontology. Medawar gives the correct definition and formula for $\mu_x$ (though he doesn't stress its distinction from $q_x$; indeed, he doesn't mention $q_x$ at all).
The distinction between $q_x$ and $\mu_x$ is discussed in Gavrilov and Gavrilova's The Biology of Life Span: A Quantitative Approach, as well as in some of their papers. They present the correct forumula for $\mu_x$, but do not really try to explain it.

This is a statistical property of the curve - in time to event analysis (which is what a survivorship curve is), a constant hazard (the instantaneous probability of an event occurring in time t given it has not occurred already) will yield an exponentially distributed survival function. When graphed on a log axis, this function looks like a straight line.


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Are there any online resources one can use to access raw clinical trial data without having to contact those involved in the study?
I want to do some statistical analysis and I have a preference for real data so I was wondering if there's somewhere I can get such data for free without a heap of bother in phoning those involved in the studies in question.

Have you seen this question on stats SE: http://stats.stackexchange.com/questions/18833/where-to-find-raw-data-about-clinical-trials ?

More options in a similar question on Open Data SE: http://opendata.stackexchange.com/questions/11/de-identified-patient-data

See these three sites:

ClinicalTrials.gov
NIDA
ClinicalStudyDataRequest

For clinical trials conducted by other agencies (in different countries), you may have to contact those authorities.


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What are the effects of muscle and fat mass on survivability?
If we have humans A, B and C who are different:

A is thin (skinny) without significant muscle or fat mass.
B is muscular
C is fat

Which one of them has the best body for survival in accidents like car crash, aircraft crash, fall from the ladder, fall down the stairs, being hit by a car, slip in the bathroom, etc?
What are the effects of muscle and fat mass on survivability?

Is this question specifically about resilience to falls/impacts? Or does this question also include disease risk? A major factor would be the age of the people in question... for instance, a high BMI is predictive of increased cardiovascular risk when younger, but in aged individuals (>65) a high BMI is actually protective, which may be due to an inverse correlation with frailty, or other complicating factor. Also, if you down-vote, provide a constructive comment for the poster.

The question is about resilience to falls/impacts. For example, can stronger neck muscles prevent my neck from breaking if I fall?

Depends, if C falls on their but, they'll be better off, if they fall on their heads the fat will make no difference. This is really way too broad, the details of how the fall occurs will always decide the outcome, voting to close.

I'll be happy with a broad answer. There is no need to go into extreme details nor close the question, that would just be a cop-out.

For car crashes, it's a mixed bag:

Better
Better
Worse
Worse

Basically, it looks like, if wearing a seat belt, slightly overweight is more likely to survive a car crash, but if no seat belts are worn they are at a disadvantage; the very obese are always more likely to die, however.  Also, some of this was found only for males, not females.

Interesting. What about muscles? Do they have the same effect as fat?

That's harder to test, as you can't measure "muscles" from old data but you can estimate BMI from height and weight.  That being said, muscles might help a bit, but only because people are muscular tend to be "harder," that is, they have stronger bones and joints and have stronger muscular walls protecting their organs.  Conjecture, of course.

@Amory, the studies you referred to look at BMI, but it doesn't specify whether the BMI increase was due to muscle or due to fat.  After all, muscle is heavier than fat.

Correct, but most people aren't Arnold Schwarzenegger.


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Does a large effective population size result in faster decay of linkage disequilibrium (LD)?
I am thinking about an invasive species that was introduced into North America just a few (<20) generations ago. Using microsatellite genotypes (105 loci), I have identified almost no significant linkage across the genome. I'm tempted to speculate that this has something to do with rapid population expansion that has caused LD to decay that quickly, but I'm not sure whether this is a reasonable train of thought. Can anybody think of why this might or might not be the case?

It is certainly possible as yes, rapid population growth will reduce LD.  From Slatkin, 1994:

In a rapidly growing population, however, there will be little chance of finding significant nonrandom associations even between completely linked loci if the growth has been sufficiently rapid.

Or Nature Reviews, 2002

Przeworski... showed that population growth tends to decrease the extent of LD, especially for longer periods of growth. By contrast, population subdivision tends to increase the extent of LD, especially when a sample contains individuals from several strongly differentiated subpopulations.

See also box 1:

Rapid population growth decreases LD by reducing genetic drift.


text:
How do I measure bacterial growth in agar dishes (either by cell mass or by cell count)?
I am doing an experiment in which I am growing S. mutans in agar dishes, and I am not sure how I would measure the growth of the S. mutans. I am also not sure if I would do this by measuring cell mass or by cell count. Any ideas?

please specify what exactly you starting with and what exactly you want to achieve

@aaaaaa he hasn't been here for over 2 years.

The most simple way is seeding the plates with a suspension of bacteria ensuring that you spread the solution properly. Then you can count the number of colonies, wich would be equal to the number of single cells.
If you want to mesure the growth speed, usually it's simpler to just measure the diameter of the colonies, always ensuring you inoculate the plates with the same amount of inoculum.
Lastly, it's even easier to estimate the growth if your culture is un liquid media and you measure the optic density with an spectophotometer.

I don't understand the effect of not "always ensuring you inoculate the plates with the same amount of inoculum."

If you inoculate a plate with 100bacteria/ml and a second plate with 1000bacteria/ml, the second one will have more colonies, even if the effect of the experiment would have the opposite effect.

Thank you so much. And thank you for clarifying that statement. I was about to ask the same question. Also, I understand the second part, but I am still confused on what you mean by "seeding the plates with a suspension of bacteria ensuring that you spread the solution properly. Then you can count the number of colonies, which would be equal to the number of single cells." I'm sorry if this is a silly question, it's just that I'm in 8th grade and pretty new to this. I am doing this for science fair, actually.

Imagine you have a liquid media with a concentration of 100 bacteria/ml and you inoculate a plate with 1 ml. In theory, every single cell will grow to form a colony, so you must have around 100 colonies. If you don't spread it properly, all 100 colonies will appear clustered, and you won't be able to identify single colonies. That's why you must spread the inoculum yo form an homogenous layer over the agar, normally using an inoculation loop.

"Then you can count the number of colonies, wich would be equal to the number of single cells." - it won't. It will be equal to the number of CFUs, not cells.

you will almost certainly want to perform serial dilutions of your suspension, and plate the serial dilutions using the spread plate method (or pour plate method). The dilutions will make it much easier to count the number of bacteria.
Generally, it is not recommended to count more than 250 colonies on a plate for reasons of accuracy (but I never count more than like 50, because that is the whole reason for doing serial dilutions). Here is a nice picture of what I am talking about. It includes a description of how to calculate the number of organisms in the original solution. They have chosen to count the number of bacteria on the fourth plate (1:10,000 dilution) in order to estimate the number of bacteria in the original inoculum. Hope this helps]1

By the way, the prototypical selective media for S.mutans is mitis-salivarius agar. You should check out this paper about growing S. mutans http://jcm.asm.org/content/4/1/95.full.pdf

Your answer makes me happy, because it provides a real microbiological technique used in labs. You would make it even better by clarifying the difference between CFU counts and cell counts. And it would be nice to add that the process must be replicated to estimate error.

Ehhh alright, well CFU stands for colony forming unit. Each one of those dots on the plate is a colony, and we are assuming that each colony is the result of a single cell from the original solution. So by counting the number of colonies on the plate we are also counting the number of single cells in the original solution that started the colonies on the plate, aka colony forming units(CFU). And sure, you could do this in dup or triplicate if you want and report the average of the counts, but this method is understood to be just an estimation, so choose the methodology that fits best for you.


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Why Do Healing Wounds Feel Warmer To The Touch?
I fell over on my bicycle trying to avoid running over a rattlesnake, and ended up badly skinning my knee. It immediately began to bleed, but soon clotted.
It has been 2 days now and it has formed a thin scab and is healing well as far as I can tell. I was chilly from the air conditioning, and I noticed the wounded knee was much warmer than the healthy knee. It was very warm, while the other was rather cold to the touch.
I read here about skin healing, and thought, maybe it is because the blood rushed there to clot the wound. But, the wound is already clotted and sealed and the worst is over. So my question is:

Why is my wound and the area around it so much warmer days after the injury?

This is personal medical question territory.  Your knee is not yet fulled healed so it is reasonable to expect the ongoing healing process would produce heat.  Heat can also be a sign of infection.

The wound is warm because of increased blood flow to the area.  This may be part of the natural inflammatory process, or you may have infection.  Wait and see what happens.

@Amory: Cryptic didn't ask what to do about it or if it is unhealthy. I think it is perfectly fine to ask about the biological reason for this, even if a personal example is used.

@Amory: I'm not asking for medical advice. I want to know why wounds are warmer than normal, please don't misread the question.

This is a normal part of the inflammatory process. Inflammation is your body's localised defensive response to tissue injury of any kind, and it is characterised by four cardinal signs- redness, swelling, heat and pain (severe inflammation involves a fifth, loss of function).
Your body is performing three main processes here:

Mobilisation of the body's defences.
Involves release of vasoactive chemicals, which cause the blood vessels to dilate and increase blood flow to the area. This causes the pain and heat, The blood vessels also produce cell-adhesion molecules which make immune cells (leukocytes) stick to the walls of the your blood vessels.
Containment and destruction of pathogens.
The immune system then goes to work clearing up any bacteria which have got into the wound. The leukocytes release chemicals called cytokines to attract more immune cells, to contain and destroy bacteria.
Tissue cleanup and repair.
Dead cells, cell fluid and other debris (pus) is then absorbed by the lymphatic system. Platelets and endothelial cells then secrete growth factors which stimulate cells called fibroblasts to multiply and produce collagen. The heat also increases metabolic rate and increases the rate of tissue repair.

Do you think you could provide times to your answer as well (e.g. after 3 hours this happens).  I'm curious as to the timeline of normal inflammation compared to the questioner's timeline of heat after 2 days.

there is increased blood flow during healing as well. also there is some secretion (perhaps histamine) which makes wounds itchy.. the reason for which i dont know myself.. and some involuntary rubbing can again trigger blood flow..

The increase in temperature is due to dilatation of the capillaries in an area of inflammation, here brought about by trauma and is one of the five cardinal signs of inflammation'. This is a natural process which helps to bring in more blood supply for repair and removal of damaged tissue components.

Skin wound healing is a dynamic and regulated process of cellular and molecular mechanisms and starts directly after skin injury.

The first stage of physiological or acute wound healing
is about the hemostasis and the formation of a provisional wound matrix. It occurs immediately after injury. When skin injury breaks up the epidermal layer, blood and lymphatic vessels are traumatized, flushing the wound to remove microorganisms and antigens. The different clotting cascades are then initiated by clotting factors from the injured skin (extrinsic system), and thrombocytes get activated for aggregation by exposed collagen (intrinsic system).
At the same time the injured vessels follow a 5- to 10-min vasoconstriction, triggered by the platelets, to reduce blood loss and fill the tissue gap with a blood clot comprised of cytokines and growth factors.
This blood clot contains fibrin molecules, fibronectin, vitronectin and thrombospondins, forming the provisional matrix as a scaffold structure for the migration of leukocytes, keratinocytes, fibroblasts and endothelial cells and as a reservoir of growth factors.
The vasoconstriction is then followed by vasodilation in which thrombocytes invade the provisional wound matrix as discussed in this article. In addition, platelets influence the infiltration of leukocytes by the release of chemotactic factors. Both platelets and leukocytes release cytokines and growth factors to activate the inflammatory process which results in local warmth (hyperemia) and edema (swelling) of the wound.

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


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What is the full name of E. G. Gray?
E. G. Gray is Neuro scientist who found and described first the two major morphologically defined synapse types (Gray Type I (asymmetric) and II (symmetric)) in his work
E G Gray (Oct. 1959). “Axo-somatic and axo-dendritic synapses of the cerebral cortex: an electron microscope study”. In: Journal of Anatomy 93.4, pp. 420–433
However I am unable to find his full name nor further information about his life.

Is this really a biology question?

@Amory I think questions on the history of the science are pertinent to its future study, but others may not share that opinion

See http://meta.biology.stackexchange.com/questions/51/should-questions-about-the-history-of-biology-be-considered-on-topic

I couldn't agree more, but I don't know that this is history so much as a question involving an historical biologist.  "Initials" aren't exactly history, but I admit I'm not sure there's a better place.

It's about his bio, isn't? * ironic smile *
I shared your doubts, but I think this question will be useful especially for people using this SE site. Though I have to admit that main reason I asked it here instead of a more general site like Yahoo answers, is that I knew the people here were most likely to answer this question correctly. And Indeed it was correctly and comprehensively answered within minutes by @jonsca. Thank You very much therefor!

Edward George Gray went by the first name of George, which isn't evident from his initials (he was born Edward George), but I happened to stumble upon the Wikipedia article below.  From there, I found his obituary.
From his obituary:

GEORGE GRAY was a pioneer in the study of brain ultrastructure. He was Professor of Cytology in the anatomy department at University College London from 1967 to 1977 and then headed the Laboratory of Biological Ultrastructure at the National Institute for Medical Research.

From the Wikipedia article for synaptosome:

In a collaborative study with the electron microscopist George Gray from University College London, Victor P. Whittaker eventually showed that the acetylcholine-rich particles derived from guinea-pig cerebral cortex were synaptic vesicle-rich pinched-off nerve terminals.  Whittaker coined the term synaptosome to describe these fractionation-derived particles and shortly thereafter synaptic vesicles could be isolated from lysed synaptosomes

Might be worth putting in his full name in there, Edward George Gray

@Amory Good idea

@Amory made the edit.


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Can a chicken's lard become liquid depending on its diet?
On Cooking.se, somebody asked a question about the fat in chicken stock sometimes being liquid and sometimes solid once the stock has cooled. The only answer until now suggests that the difference is due to the percentage of saturated fat in the chicken lard, which will vary depending on the chicken's food.
I am not entirely happy with this explanation. I am aware that the proportion of saturated to unsaturated fat in an organism's cell walls will vary with diet, and could imagine that the fat stored within its adipose tissue will be different too. The person who provided the answer also posted references which confirm that part. But I doubt that the effect will be strong enough that, if an animal on low-saturated-fat diet is processed to lard, the resulting lard will be a viscous liquid, as opposed to the usual soft solid. If my memory doesn't fail me, my grandma used to keep her animals on a mostly starch-based diet, and still was able to process them for (solid) lard.
Can somebody confirm or disprove this theory?

What is your reason for thinking that "cell walls" (I assume that you mean cell membranes) composition will vary with diet? My recollection is that the fluidity of the phospholipid bilayer is tightly regulated, and since organisms can saturate or desaturate acyl chains this would be easy to achieve. As far as stored lipid is concerned my feeling is that fluidity might be somewhat less critical so could vary.

@AlanBoyd I have read it as the explanation to why saturated fats are unhealthy: the cell walls membranes of the eater become stiffer and less flexible by incorporating molecules made with saturated instead of unsaturated fatty acids. I don't remember my sources, they were some kind of popular science, not peer-reviewed literature, so it is possible that they were wrong, or that they were oversimplified enough to give me a wrong understanding of what is actually happening.

Without going into the biochemical details of fatty acid digestion, mobilization, and synthesis, the brief answer is that the animal regulates its own fatty acid composition to within a specified range regardless of its food. Lipid metabolism does not differ from the metabolism of other compounds, in that it is a highly regulated, enzyme-mediated process, which ultimately is genetically determined.
It must be stressed that a heterotroph assimilates its food, not as complete macromolecules, but as their base components. For example, the starch-fed chickens you described would digest the starch down completely to glucose, which would then be converted in the liver to fatty acids. These fatty acids would be, of course, those that the chicken had the enzymes to synthesize, which are consequently mostly saturated fatty acids of a certain length that happen to solidify when cooled.


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Why are urban birds still scared of humans?
I understand that animals are naturally scared of humans because we basically slaughtered every living thing we found in our way for millennia. How long does it take for them to genetically 'forget' we are a threat?

What's your evidence that an individual animal who has never encountered humans before is "scared" of humans more than other species?

@MCM I am not really sure I understand? I was referring to animals that have encountered humans before. I am mostly curious about the recent phenomenon of urban birds who have co-existed alongside with humans for a few decades now, and that for the most part these humans presented no threat to them. It seems to me that even after years of co-existence they still prefer keeping a safe distance from us humans.

@IsopycnalOscillation, if they have seen humans before then their natural fear response is justified.  In the city I live, I've noticed that some children are particularly cruel to birds constantly chasing them away.

I don't follow the premise of the question. Urban birds are a lot less scared of humans than wild birds.

a) Plenty of birds in the city will get very close to humans, relative to countryside birds (if you've ever been to Trafalgar square in London you will know how close birds are willing to get, try getting that close to a pheasant in a field!). b) It may be that "scaredness" (let's go with timidness) is not a genetic trait - or has a very large environmental component (i.e. largely determined by previous experience of human).

Perhaps counter-intuitively, fear of humans is often a learned behaviour. There are accounts, such as one made by Charles Darwin following his visit to the Galapagos islands;

In Charles Island, which had then been colonized about six years, I saw a boy sitting by a well with a switch in his hand, with which he killed the doves and finches as they came to drink. He had already procured a little heap of them for his dinner, and he said that he had constantly been in the habit of waiting by this well for the same purpose. It would appear that the birds of this archipelago, not having as yet learnt that man is a more dangerous animal than the tortoise or the Amblyrhynchus, disregard him, in the same manner as in England shy birds, such as magpies, disregard the cows and horses grazing in our fields.
From "The Voyage of the Beagle" - http://www.ling.upenn.edu/courses/hum100/Beagle17.html

Birds born and bred in proximity to humans will have learned that we are actually to be avoided.
Ducks and swans, for instance, (and this is quite anecdotal) live in very close proximity to a lot of humans in cities, and feel confident walking picking up food. However if you try to get close to one they are very quick to get out of the way. The only exceptions to this are learned behaviours, such as when someone stands and feeds them.
In the wild animals may be cautious of humans if we are much bigger than them, but if they have no experience at all of human contact they  may just ignore them. This quite often happens with film crews in Antarctica, as in the below image from the BBC's Frozen Planet series.

I guess I am biased because I would never hurt an animal. There may as well be other people out there doing just that - therefore perpetuating their fear of us. It's just so sad, when I go to the local creek, I would love to see more birds, I know they are there because I can hear them...

@IsopycnalOscillation I would guess that this is much beyond animal cruelty and probably goes as deep as innate behaviour. We hunted ducks and swans for food, ones that were innately fearful of humans survived and propagated and the next generation were predisposed to fear humans a bit more. Rinse and repeat for thousands of years. This would only be compounded by learned behaviour.

@GoodGravy Great point.


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Would Bubling Oxygen Through "Dead Zones" Like A Fish-Tank Make Much Difference?
I am a dilettante when it comes to dead zones. I realize that they vary from fleeting algal blooms to continuous dead zones. For the continuous dead zones it would seem to me that adding a "bubbler" like for fish tanks might help restore the depleted oxygen content, which would increase microbial activity and thereby increase the quantity of nitrogen removed from the water (hopefully) before it reaches the open ocean where the fleeting algal blooms occur. Has this been investigated or could it at least be assessed from a scientific perspective?

algal blooms consume all the oxygen in the water to make it anoxic.  You'd have to bubble a lot of oxygen into the water.  It probably depends on the nutrient mix in the water.  If the algae can continue to grow and consume the oxygen as you bubble it in, then it won't help.

@shigeta If the algae continue to grow and consume oxygen, they they are also consuming nutrients that would otherwise contribute to algal blooms and/or dead zones. The idea is essentially to exhaust the runoff nitrogen through speeding algae growth - not necessarily to instantaneously solve the problem of dead zones. This should reduce the extent of dead zones.

i see.  it would take some work to figure this out - it might end faster but in any case i'd be surprised if all the other living things aren't dead by then.  is the goal just to end up with a little nitrogen in the water?

@shigeta The goal is to remove nitrogen from the river water, since in the open ocean nitrogen is the limiting  reagent for algal growth.

Actually, if you could get the oxygen in there, you would probably turn the dead zone into a "feast zone," because all that algae would be food.  But I think it would be prohibitively expensive.  Fish tanks aren't deep, so it doesn't take much pressure to force air bubbles into the bottom.  And they're not large in volume, so you don't need huge amounts of air bubbling.  Oceans, or even rivers or harbors, would be another matter.
Also, some of the algal blooms are poisonous "red tides."

Going from our comment train I thought I'd put this into an answer.
This is similar to the proposal to dump iron into the sea as that's also supposed to be a limiting reagent for growth.  There the goal was to sequester carbon from carbon dioxide as dead plankton which would sink into the depths of the ocean.  I'm assuming they did their home work and the cost of producing iron metal, which uses a lot of oxygen is actually worth it.
Its interesting to observe here that oxygen depletion was not a concern here.  Assuming they have done enough work to show that iron is the only reagent needed to induce the algal blooms, that's a different angle on the problem than you propose.
In any case the critiques are many because of the scale proposed are likely to create other unanticipated side effects, not the least of which is the massive release of the powerful greenhouse gas nitrous oxide.
The iron dumping experiment was mostly rejected because it was too simplistic.  So, this proposal would require a model - there's no simple back of the envelope calculation that would give a thumbs up/down on this proposal.  The question is - what's the next limiting factor after oxygen/nitrogen?  I'd be surprised if that was not dependent upon location climate and local water chemistry.
A lot of red tides are caused by fertilizer and sewage dumps so you may be on to something here. If the goal is to remove nitrogen from the water, not only would it work, but would the cost be reasonable for what you're hoping to get?
Unless someone has already built the model I'd guess it would be up to you.

The iron dumping was shown to be quickly removed from the seawater through its incorporation into some component of the algae that then sank: much like nitrogen. I think the iron might have been incorporated into a shell of some sort as part of the algae--possibly mixed in with CaCO3 or something. That was the reason Iron dumping was abandoned: it was hoped the iron would remain in the ocean ecosystem for longer.

My point is just that your proposal is probably deserving of more thought - similar sorts of questions would have to be answered before the proposition would be considered valid.  I myself couldn't find any preliminary work on this. and it does seem to be the case that they might have already considered oxygen. best of luck.

Bubbles have actually been tried as described on Wikipedia. Usually the issue is layer stratification where the top layer has oxygen but the bottom layer where the decomposition of algae takes place lacks oxygen. Therefore mixers have been employed to bring the de-oxygenated water to the surface where it naturally re-oxygenates. It is interesting to note that one proposed and highly experimental idea is to use mixers to bring cold water from below to reduce the surface temperature to prevent or weaken hurricanes.

During heavy rain, London's sewage storm pipes overflow into the River Thames, sending dissolved oxygen levels plummeting and threatening the species it supports.[14] Two dedicated McTay Marine vessels, oxygenation barges Thames Bubbler and Thames Vitality are used to replenish oxygen levels, as part of an ongoing battle to clean up the river, which now supports 115 species of fish and hundreds more invertebrates, plants and birds.[14]
The dissolved oxygen concentration within Cardiff Bay are maintained at or above 5 mg/L. Compressed air is pumped, from five sites around the Bay, through a series of steel reinforced rubber pipelines, laid on the beds of the Bay and Rivers Taff and Ely. These are connected to approximately 800 diffusers. At times this is insufficient and the Harbour Authority is using a mobile oxygenation barge built by McTay Marine with liquid oxygen stored in a tank. Liquid oxygen is passed through an electrically heated vapouriser and the gas is injected into a stream of water which is pumped from, and returned to, the bay. The barge is capable of dissolving up to 5 tonnes of oxygen in 24 hours.[15]

Water Aeration


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What is the cause of the spots on this leaf?
On a hiking trip to the Alps I found trees whose leaves showed those spots you see on the picture. I am curious about what the cause is.
Higher resolution pictures of front and back side.

This site is not for specific medical or botany advice.  Please consult your local botanist for a specific diagnosis.

I was just kidding

This is a "Tar Spot" disease usually found in Europe and North America. It mostly affects the Maple tree leaves. Tar spot is caused by 'Rhytisma acerinum' a plant pathogen fungus. This pathogen does not seem harm to tree but disturbs the leaves as it finds a suitable condition in summer with bit of wetness. It enters the leaves through stoma and then creates yellow lesions of various sizes over the leaf area which later gradually turns into brown-black tar colored spot. It reduces the photosynthesis process of leaves and thus creating more wide dark spots on the leaves. After sometime the leaves will fall.
Entire detail is available in the Wikipedia link with the detail of the pathogen. (Add some more info if you find this detail not enough)


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Aerobe or facultative anaerobe organism that metabolizes acetate?
I'm assuming bacteria, but will take any suggestions.  Organism must survive primarily on the acetate (plus trace elements), but I can give/take electrons, if necessary.  Not interested in strict anaerobes.  I've tried Shewanella oneidensis, but have not succeeded in getting it to eat any acetate (just lactate).  Feel free to give journal refs.  Self-promotion won't be frowned upon if it's helpful.  :-)  Opportunity for joint pub, if successful.

You could try Paracoccus denitrificans.
Here is a study where acetate is used as the growth-limiting substrate: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.320.1692&rep=rep1&type=pdf
Here's the details of its version of acetate kinase: http://www.uniprot.org/uniprot/A1B9S8
I'd be happy to collaborate with you further on this.

Thanks for the info.  In this paper, the acetate is only 0.34% (v/v).  Do you know if P. denitrificans can handle higher concentration, say 1% to 3%?  (Many organisms are killed by acetate, hence pickling to preserve food.)  Or is 0.3% its limit?

This study: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC182557/?page=1 has P. denitrificans at 1% v/v sodium acetate. I don't know how much higher it can go though.


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Which is the tissue damaging agent in krokodil (street desomorphine)
I've just read about krokodil and saw some quite hideous pictures about what it does to the human body. I guess just desomorphine alone wouldn't have this effect.
Which ingredient(s) causes the damage to the tissue?

Desomorphine is made from Codeine back in USA in 1932. But Codeine is made from caffeine, paracetamol, or diphenhydramine in Russia. Finally Krokodil as it is called in Russia is made from crude method by mixing codeine-based headache pills with iodine, gasoline, paint thinner or alcohol. I do not know what else they mix as it is done by purely amateurs. So these toxic substances might produce some byproducts which might cause those damages.

Note: Don't click on the links, or even search for information, if you don't have a strong stomach
From what I've read, it's not necessarily 100% known, most likely because it's not easy to study (small, reclusive users who die quickly of a complex concoction) but the line everyone has quoted is:

"They extract [the drug] and even though they believe that most of the oil and gasoline is gone, there is still remnants of it. You can imagine just injecting a little bit of it into your veins can cause a lot of damage… it eats you from the inside out".

That's from Dr. Frank LoVecchio in Phoenix, Arizona, who saw two cases within a week.  It's not hugely scientific, but it's not wrong.  Krokodil is never pure and highly toxic chemicals are thus injected into the veins.  If you want specifics, then gasoline, hydrochloric acid, phosphorous scraped off matchboxes, paint thinner, iodine, and cleaning oils.  Injecting any one of those should be enough to kill a repeated user.  Those substances rupture blood vessels, and the subsequent leakage creates gangrenous wounds like you see in the pictures.


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RNA-seq Data on domestic animal with different environment
I want to find the RNAseq data available on domestic animals in different environments. If microarray data is available, it would be more useful. If you know I would appreciate to inform me.

There is something called GEO, which is maintained by the NIH and is a massive collection of data obtained from RNA seq, microarray, etc. experiments. One thing you can do is search for a paper that has done what you are looking for. The paper may have a GEO accession number, and you can use that number at the GEO website to find the data you want. You may also search GEO directly but Im not too familiar with it. It may just be easier to find a paper with a GEO accession number.

There's also the ArrayExpress database maintained by the EBI.


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Hydrophilicity and polarity
If any given molecule is polar, and is capable of hydrogen bonding, I can be sure that it's hydrophilic.
However, are those two the only conditions that make a molecule hydrophilic?

Is this a biology/biochemistry question?

its a common term used in biochemistry

As phrased right now it's a chemistry question.  Maybe if it asked about specific biological molecules instead?

I think the answer is no.
The definition of polarity is basically that a molecule has a dipole, and as water has a very large dipole, if a molecule will mix with water readily, its usually pretty polar.
Water also can share its hydrogens in hydrogen bonding, which is an actual shared covalent bond where a hydrogen atom is shared between two acceptors.  The hydrogen bond is fairly weak (~ 0.5 kcal/mol) but water does a lot of hydrogen bonding.
So hydrogen bonding and polarity are often a shared characteristic of an molecule, but are not the same thing.
Ions are quite hydrophilic but do not need to be hydrogen bond donors or acceptors.   Chloride  (Cl - ) is not a hydrogen bonding atom - its so acidic that it exists nearly entirely in the Cl- form in water solution. But its definitely electro negative and really soluable in water. Are Ions polar though?  Chloride is symmetrical and so its not really polar.
Still is there a polar molecule which is neither a hydrogen bond donor or acceptor?  Acetone and the cyanide ion (CN-) are a polar molecules which have no hydrogen bond donor, but can accept them.
I think sulfate is an example of a polar molecule which does not form hydrogen bonds.
Sulfate (SO4 -- )  has four S-O bonds arranged in a tetrahedron but each of them is highly polar - with 90% of the negative charge on the oxygen.  But like the Chloride ion its so acidic that it much prefers its free ionic state.  It would have very little hydrogen bonding character even when its in water.  Sulfate can form hydrogen bonds, but I think they will only be stable when there are several of them at once.  Sulfate binding protein has seven hydrogen bonds when it binds sulfate, using the chelation effect to make the binding strong enough to be stable.


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Osmoregulatory Acclimatization in amphibians
If a frog is gradually exposed to increasing concentration of salts can they acclimatise or will they die of exosmosis ?

Can you be more specific? e.g., What kind of frog? How much of an osmotic challenge? What length of time?

@kmm A frog with no special adaptation. This is those kinds of homework question with limited information :)

It will depend on how quickly the salinity is raised and to what level.  Two studies (Karraker 2007, Karraker et al. 2008) looked at the effects of road salt (used to reduce icing on roads in winter) in the spotted salamander, the wood frog (a small frog), and the green frog (a big frog). Their studies showed that survival decreased, especially for larval individuals, as salt concentration increased. Deformities in embryos and larvae increased with salt concentrations$^1$.
Another study (Shpun et al. 1992) showed that a few species of frogs and toads that could tolerate high levels of blood plasma urea concentrations could also tolerate elevated levels of NaCl in their environment (but not all species that had high urea tolerance could tolerate high environmental salt concentrations.)
There would naturally be an upper limit of salt tolerance in amphibians, especially if they are not able to retain or regain water at a rate they are losing it to the high salinity environment.  The studies suggest that higher salinities do decrease survivorship and increase deformities. While they may acclimate to the short term, I would question long term adaptation unless the rate of salinity increase is very gradual.
Footnote

They made their salt solutions based on conductivity, measured as microsiemens. For lab experiments, they made salt solutions that varied from 5 µS (control) to 3000 µS. These translate to 1 mg/L to 945 mg/L Cl$^-$.  In the field, they measured salt concentrations that were more than 3000 µS.

Literature Cited
Karraker, N.E. 2007. Are embryonic and larval green frogs (Rana clamitans) insensitive to road deicing salt? Herpetological Conservation and Biology 2: 35-41.
Karraker, N.E. et al. (2008). Impacts of road deicing salt on the demography of vernal pool-breeding amphibians. Ecological Applications 18: 724-734.


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Deducing synaptic strength from electron micrographs?
There are several promising techniques for connectomics based on iterative sectioning and imaging of tissue with scanning electron microscopes (e.g. FIB-SEM and ATUM)
By looking at such micrographs, one can identify synapses:

Is there any way to measure synaptic strength using these types of techniques?

i guess you cant determine synaptic strength by just detecting synapses.. perhaps by labeling the receptors you might be able to say something using confocal.. there are some studies like that

Thank you @WYSIWYG. Would you mind pointing me to some of those papers?

I am sorry.. I don't know of papers. I just heard them in some talk.. i shall look up and get back..

@WYSIWYG: I would be extremely wary of using such approach... you should really combine it with some ephys.

@nico: totally agree on that.. i just said that there are some studies which check protein activity at the synapses using labelled proteins. It is not absolute.. Btw i still need to find reference for it.

First of all, definitions. By synaptic strength let's understand ability of post-synapse to elicit current flow/depolarization in response to neurotransmitter appearance in the synapse. How can NT appear? By release from pre-synapse or through uncaging (optical activation of "caged", or inactive NT).
Second, post-synapse contain all sort of stuff, but main sources of current/depolarization are ionotropic receptors of NTs, e.g. NMDA-R or AMPA-R. This molecules are not just floating ion membrane but attached to extensive scaffolding just below of the membrane. Scaffolding includes actin, and more importantly PSD95 (in case of excitatory synapses).
I work in vivo and don't do any EM. But in vivo issue of observing molecules is that you can't label sensitive proteins without disturbing function. Some things are just too delicate to be labeled with fusing GFP.
PSD95 has been used for in vivo labeling with GFP. One paper I will point you to, is this knock-in work in mice: Live Imaging of Endogenous PSD-95 Using ENABLED: A Conditional Strategy to Fluorescently Label Endogenous Proteins, J Neurosc. 2014
This is the figure that shows strong correlation between brightness of synapse (aka number of PSD95 molecules) and current that occurs in cell body when authors uncaged glutamate at different synapses.

Figure description
Now, how does that relates to your image? PSD stands for "post-synaptic density" protein, because in EM synapse is very dark. I don't know links, but I would assume some correlation between brightness of synapse in EM and its strength.


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Is there a website that shows population sizes?
I'm looking for a website that shows the population sizes of a species (doesn't matter which) as a function of time at a geographic coordinate. Is there a government website or other free database with such information?

Will humans do? You can probably get this from the OECD site.

You can access the Imperial College global population dynamics database.  They will have time series data at specific locations.  http://www3.imperial.ac.uk/cpb/databases/gpdd
There is a sister database as well that might be useful. http://lits.bio.ic.ac.uk:8080/litsproject/
These contain several hundred time series, and you can see a paper that used them here:  http://onlinelibrary.wiley.com/doi/10.1111/j.1461-0248.2011.01702.x/abstract

My first idea as well, and definitely the best source around.

Would you happen to know one with more recent data (e.g. 2005 and above)? Thanks.


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How are non-glucose sugars metabolized in the body?
In my biology book's section on disaccharide metabolism and glycolysis, it states that sugars other than glucose must be acted upon to enter glycolysis. Let's take sucrose as an example. Sucrose is hydrolyzed in the small intestine by sucrase. The resulting fructose and glucose are absorbed and transported to the liver via the portal vein. My question concerns the fate of fructose.
To undergo glycolysis, the book states that fructose is converted into either fructose-6-phosphate (F6P) or fructose-1-phosphate (F1P). Let's say it is converted to F1P. Aldolase splits this into dihydroxyacetone phosphate and D-glyceraldehyde. Triose kinase then converts D-glyceraldehyde to glyceraldehyde-3-phosphate, a glycolytic intermediate. Where is this occurring in the body? Are we still in the liver? I can't imagine that all the fructose we consume is undergoing glycolysis in the liver. To leave the liver as a sugar, it would have had to been converted to glucose, right?
In classes I've taken, I've been told that sugars that enter the liver are pretty much all converted to glucose. Once they are converted to glucose, they can be distributed to the rest of the body, stored as glycogen, etc. If we are going straight from fructose to F1P to a glycolytic intermediate, we couldn't have left the liver. How is such a transformation even useful? Anyone care to shed some light on this?

Where is this occurring in the body?

Almost totally in the liver.

To leave the liver as a sugar, it would have had to been converted to glucose, right?

Correct, but it's not a direct conversion.
Fructose is metabolized almost completely in the liver in humans, and is directed toward replenishment of liver glycogen and triglyceride synthesis...
...Increased concentrations of DHAP and glyceraldehyde-3-phosphate in the liver drive the gluconeogenic pathway toward glucose-6-phosphate, glucose-1-phosphate and glycogen formation. It appears that fructose is a better substrate for glycogen synthesis than glucose and that glycogen replenishment takes precedence over triglyceride formation. Once liver glycogen is replenished, the intermediates of fructose metabolism are primarily directed toward triglyceride synthesis.
So, Fructose is almost entirely made into something else first, and then that something (Glycogen or the Glycerol from triglycerides) gets broken down into Glucose or an intermediate.
Fructose stays in the liver because Fructokinase has a pretty low Km (0.5 mM) compared to Glucokinase (12mM) for Fructose, so almost all of the Fructose that enters the liver is phosphorylated into F1P - which cannot leave.


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Which organisms have introns?
From Wikipedia:

For example, introns are extremely common within the nuclear genome of higher vertebrates (e.g. humans and mice), where protein-coding genes almost always contain multiple introns, while introns are rare within the nuclear genes of some eukaryotic microorganisms,[8] for example baker's/brewer's yeast (Saccharomyces cerevisiae). In contrast, the mitochondrial genomes of vertebrates are entirely devoid of introns, while those of eukaryotic microorganisms may contain many introns. Introns are well known in bacterial and archaeal genes, but occur more rarely than in most eukaryotic genomes.

In my biochemistry course we learned that bacteria have no introns and eukaryots nearly always have them. What's correct?
Do viruses have introns as the Wikipedia article claims?

As a general rule, a blanket statement in Biology should always be considered false.
It so happens that bacteria do have 'introns' (or at least the intron genomic sequence has been determined) in the sense of the cis-acting autocatalytic Group I and II introns. These are sequences of RNA that adopt such a conformation to catalyze their own excision from an mRNA transcript, and thus may be considered ribozymes, enzyme made of ribonucleic acid.
Although not generally considered 'introns' segments of RNA are removed during the course of tRNA in both prokaryotes and eukaryotes.
Now introns that are removed by the action of the spliceosome are strictly found in eukaryotes, as bacteria lack the spliceosome.
There seem to be a considerable number of papers regarding the question of intron (particularly spliceosomal) phylogeny that should be relatively easy to find if you are so interested.
One example paper in which viral introns (Group I) are reported:
http://nar.oxfordjournals.org/content/22/13/2532.abstract

As a general rule, a blanket statement in Biology should always be considered false. I could not agree more.


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Is there a human form of estrus?
Now I just learn that estrus is a trait in all mammals except Humans. So does it occur significantly in Humans? Of course I'm aware of the cliched "horny", "aroused" etc., but is it a biological function in Humans too? and if so, when and what is it called?

By 'human estrus', I take it to mean that the female shows some increased desire when they are fertile.
At the height of fertility, which coincides with estrus, female behavior changes a stronger interest in sexual activity is exhibited.  In many primates in general, the female may give of a strong scent or even physically show color or swelling that indicates even to observers of other species that they are fertile, also engendering sexual behavior in the males.
For instance, baboons are well known for reddening of the female's rump and they also emit a strong scent.  Non - primates also show estrus - most of us know how dogs and cats can change their behavior.
Human signs of Estrus is of great interest to primatologists, evolutionary biologists and psychologists as it influences the biology and the social nature of people.  It has been proposed that humans do not exhibit estrus and this is still an influential idea. Certainly its difficult to look at a woman and tell whether she is ovulating and most women themselves cannot tell when that is happening.
Still, examination of behavior and appearance have shown that womens appearance does change over their monthly fertility cycle.  Women's faces may become thinner at higher fertility and this and other cues make them more desirable on the average.  While their sexual desire is not clearly higher, female perception of men's faces changes too.
While this is quite different than the typical definition of estrus, the biochemical cycle of fertility does affect human social behavior and preferences, perceptions.  The evolutionary reasons for these changes are probably adapted to the highly social nature of human existence and the fact that offspring are such a large investment.


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What happens to potassium after an action potential?
If I understand right, after repolarization, much of the potassium is outside the membrane and much of the sodium / calcium is inside. How does it get back to the original concentrations (i.e. potassium inside and sodium/calcium outside)?

During the repolarization, relatively few ions need to cross the membrane for the membrane voltage to change and therefore the change in ions concentration outside and inside the cell is neglible. After repolarization, the concentrations are restored by the continuous action of Na⁺/K⁺-ATPase. The same happens for calcium, but I don't know exactly what kind of pump is used.


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RNA seq and using of Poly(A) or non-Poly(A) based amplification of RNA
I'm studying "Deep sequencing the circadian and diurnal transcriptome of Drosophila brain" Hughes et al., 2012. I've got some problems with the materials and methods.
Before RNAseq, the authors amplify RNA. They use two kits: Poly(A) based and non-poly(A) based. For the samples Poly(A) based amplified they do a sequencing to generate 100 bp paired-end and for the samples Non poly(A) based they do a sequencing to generate 75 bp single-ends.
I read in the strategy:

Total RNA was amplified, and ribosomal RNA was depleted, using a non-poly(A)-based amplification kit, which significantly diminishes the 3' bias in downstream libraries used for RNA-seq (see Methods).

I don't understand why they use both kits. Actually, they say that they want to asses the bias introduced by an alternative amplification methods BUT the following sequencing is not the same in both cases so there is more than one parameter which change between the two protocols so I don't understand how they can compare.

For the poly(A) based I understand that the rRNA are not polyadenylated so they remove rRNA from the amplified sample. However, don't they remove non-coding RNA too (long or short)?

For the non poly(A) based, I don't understand how they remove the rRNA but I understand that since they don't select the RNA according to their poly(A) tails they keep the rest of the RNAs which are not kept in the poly(A) based amplification.

When I look to the RUM statistics, I see that there are fewer total aligned reads in non-poly(A) based: 70-80% (non polyA) and 80-90% (polyA). So it seems like we lose some information with non-poly(A) based.

To sum up, why the authors use Poly(A) and non-poly(A)? Why do they show all the rest of the results from the non-poly(A) amplification since they have less aligned read? How do they compare since the following sequencing is not the same? How the rRNA are removed in both techniques and especially in non-poly(A)?
I didn't find the protocols kit with exactly the same name but here are the links to the protocols which are closer (I think).
http://www.mscience.com.au/upload/pages/nugen/nugen_ov_rna_seq-brochure.pdf
http://excilone.com/client/document/ug-arcturusE%E2%80%9E%C2%A2-riboamp%C3%82-hs-plus-amplification-kit-user-guide_38.pdf

Yes, it was odd that they said that. The second protocol with the polyA based method had another purpose though, which was "examine the reproducibility of period-regulated genes in an independent genetic background". I would suspect this was its main purpose, and not so much to look at fragment bias, which has already been done in other papers. They didnt even publish this data in the main paper, they put it in the supplement.
Yes, this would remove any transcript without a polyA tail.
One way of purifying is by using oligos that are antisense specifically to rRNA. The oligos will be attached to some solid phase, on a column or a bead or something, and the rRNA will stick to it and everything that doesnt is what will remain in your sample
It is not safe to say that you lose information with polyA based kits. The polyA based technique had reads that were single end and only 75bp long. This is compared to the other protocol which was 100bp paired. Reads that are 75bp will align much more easily than 200 bp (100 x 2 since its paired). However, there will not be as much certainty in the alignments, as there is a greater chance it will align to multiple locations in the genome, or align to the wrong location. So yes they have more reads aligned but I would be hesitant to make any conclusions from this. And if you look at total numbers of reads, the non-polyA method aligned more. Again, I dont think the main purpose was to show that one method is better than another.

Basically the method you choose depends on your experiment and your samples. Random hexamers will give you non-coding RNA which is important in some experiments, and that is its main advantage. It will also give more uniform coverage across the gene (no 3' bias). Poly(A) selection will give you only mRNA, however you will miss any transcripts that are degraded or partially degraded. If you have a high quality sample or a large amount of starting material this is less of a concern. As mentioned before you end up missing parts of the 5' end on some transcripts with this method. If you have a low abundance transcript that you are trying to find, polyA selection is probably best, as it is more likely to be captured and you will capture the whole thing, rather than just getting bits and pieces of it with random hexamers. They both have advantages and disadvantages. Hopefully this helps you or someone make a decision.

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


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What's a non-allelic gene?
Non-allelic or non-alletic
I stumbled across the term in my Human Genetics textbook. It didn't explain it there, and a quick google search only showed scientific papers that refer to 'recombinations with non-allelic genes' without explaining what they are.

http://www.newton.dep.anl.gov/askasci/mole00/mole00779.htm

Note that I have never read the term non-allelic genes in a peer-reviewed paper!

It is my understanding that a non-allelic gene is one that affects another's traits, but is not as a typical dominant / recessive manner. If I am correct, this is the same thing as  epistasis - meaning that one gene modifies how another is expressed.
There exists epistatic genes for horse coat color. One gene is the coat color itself (horses may have either brown or red color alleles at this loci), the second gene is for a protein that allows the coat color gene to be expressed.
For example, a horse has two brown alleles at the coat color locus. It also has a wild type gene in the second (modifier) position. This modifier allows the color brown to be expressed and the horse is brown.
B/B, wt/wt --> Brown
If the horse has the two brown alleles, but has a mutant allele at the modifier position, then coat color is not expressed and the horse is white.
B/B, mt/mt --> white
Because the modifier alleles are separate genes from the coat color alleles, the two are non-allelic - yet they both affect the same trait in some way.
I hope this helps.

+1 This is also my understanding of terdon's link. I would argue that the name non-allelic gene is very poorly chosen though. Theoretically speaking there might not have any single gene that does not affect the phenotypic expression of other genes. And of course a non-allelic gene can be a non-allelic gene only if it is polymorphic (and have multiple alleles)!

The context of the term "non-allelic" is non-allelic recombinations which means recombinations between genes that are not exactly alleles but have enough sequence homology to permit recombination.

Is sequence homology needed for recombination?

@CRags For homologous recombination, yes. Even for other kinds of recombination (for e.g. VDJ) there is a stretch of sequence that acts as a homologous block.

Just to expand that recombination is not always needed: there is NJEH (Non-Homologous End Joining), which for example, is how CRISPR works. As it's name suggests in NHEJ, no sequence similarity is required and 2 DNA stretches are simply ligated together at their respective blunt faces.

From "Gene Interactions: Allelic and Non-Allelic" (biologydiscussion.com)
'Non-allelic or inter-allelic interactions … occur where the development of single character is due to two or more genes affecting the expression of each other in various ways.'
'Two non-allelic gene pairs affect the same character. The dominant allele of each of the two factors produces separate phenotypes when they are alone. When both the dominant alleles are present together, they produce a distinct new phenotype. The absence of both the dominant alleles gives rise to yet another phenotype.'
'When a gene or gene pair masks or prevents the expression of other non-allelic gene, called epistasis. The gene which produces the effect called epistatic gene and the gene whose expression is suppressed called hypostatic gene.'
———
From "Genetic Terminology" (ncbi.nlm.nih.gov)
'Whereas Drosophila geneticists used to talk of two loci for a gene, and human geneticists used to talk of two genes at a locus, modern geneticists talk of “two alleles of a gene” or “two alleles at a locus”; this last, which is nowadays so common, is the terminology that will thus be used in this book. It then follows (rather awkwardly) that two alleles at the same locus are allelic to each other, whereas two alleles that are at different loci are non-allelic to each other.'
———
From slides "Interaction of genes" (slide_9) (slideshare.net)
'Non-Allelic gene interaction: In inter allelic genetic interactions, the independent (non homologous) genes located on the same or on different chromosomes interact with one another for the expression of single phenotypic trait of an organism.'


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Is it a limitation of the eyes, or the brain, that we can't see a moving bullet?
Are the photoreceptors in our eyes not fast enough to register the fast moving bullet, or is the brain not powerful enough to make sense of something happening that fast?

It's less a problem of speed and more of raw photon count. Assuming a brightly lit day, the bullet will move so fast that it doesn't reflect enough photons to register against the background. High speed images of bullets usually involve a very bright flash (and other controlled settings) for the camera to pick it up. (Also, a very short flash helps the bullet to appear stationary in the image.
On the other hand, seeing where your bullets are going is pretty useful. Therefore tracer bullets were created, which are essentially a pyrotechnic flare that you substitute in every 5th bullet, typically in machine gun ammunition. Proof that if you make a bullet bright enough, you can register it just fine.
http://en.wikipedia.org/wiki/Tracer_ammunition

It's not even necessary to use tracers if one is in a shooting range where all the illumination is from behind the shooter and the background is dark.


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How do rodenticides with delayed effect work?
Most modern rodenticides are claimed to cause death no earlier than several days after ingestion.
That's quite strange - once a chemical was ingested it will be absorbed in the digestive system and enter the blood stream and rapidly spread around the body (something like within ten hours - that's what most human medications claim in pharmacokinetics sections of their manuals). I'm pretty sure a rodent is very similar to a human in terms of digestive system functioning.
Then how do rodenticides not kill the rodent earlier than in several days after ingestion?

Not sure about the specifics of rodenticides but you should take into consideration that a drug may not be directly bioavailable. It may be given as an inactive form which is metabolized to the active form. It may be retained in adipose tissue and slowly released. Also, the effect which may be fairly rapid, but not immediately fatal. If I remember correctly rodenticides are often anticoaugulants, so the effect may not be immediatly obvious.

These poisons prevent recirculation of vitamin K and thus formation of prothrombin which is essential for coagulation of blood and are required for maintaining the integrity of capillaries. The depletion of vitamin K is slow and in a couple of days internal hemorrhage occurs extensively and the animal dies of shock. Early recognition of poisoning in humans and other animals can easily be treated with administration of vitamin K.
http://en.m.wikipedia.org/wiki/Rodenticide


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Do people of the same height walk at the same speed?
I'm working on a project that concerns movement and the human body. Before I begin to experiment, I need an answer to a question I'm sure has an answer, but doesn't Google well.
What I need to know is firstly whether I can assume that if people have the same height, they will also have the same leg length?
Secondly, if two different people have an identical height, will they take the same amount of time to cover the same distance when running at the same speed, regardless of their unique technique for running?
An Example:
Say I'm with a friend, we're both 6 feet tall exactly, we both get on to treadmills side-by-side and set it to a speed of 7.5km/hour.
Will we be moving exactly the same body parts at the same time - will our feet land on the treadmill at the same time?
Is there a possibility that people of the same height do not have the same leg length? If so, how likely is it on average?

People of the same height can easily have different leg lengths. Think western women models - currently they are typically women with relatively long legs while ordinary people can easily have shorter legs for the same total height. There's even leg-to-body ration section in Body proportions Wikipedia article.
This is why pedometers always require calibration - the procedure in which you have to walk a known distance and count steps and then know how much steps you need per mile. There're no tables that would assist by assuming certain steps-per-mile ration for known height.

Of course, yes you're correct. Thanks for the link. Do you know of any other variable I could use to determine leg lengths? So far I've got trouser length (not a strong option) or establish a baseline via other methods.

@Dominic: When clothes are crafted the typical measure is "inner leg length" measure which more or less maps to how long a leg is. This typically has one inch increment though and so I guess isn't very reliable.


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Need of X or Y chromosome protein after meiosis
After meiosis each spermatid get either the X chromosome or the Y chromosome. I know that the 4 spermatids formed from 1 spermatogonia are connected by cytoplasm and so the proteins made by X or Y chromosome can be shared by all the 4 cells.
I want to know what proteins made by X or Y chromosome are exclusive to the X or Y chromosome and are needed to convert spermatids to sperms.

Are you asking what proteins are exclusive to X and Y from all other chromosomes or are you asking which proteins are on the X but not the Y (and vice versa)? These are two very different questions.

@Armatus I am asking for genes present exclusively on X or exclusively on Y which are needed to convert spermatids to sperms.

@Armatus In simpler words the gene should be present strictly on either X or Y not on both. It should also not be present on autosomes.

I can't think of a particular reason why there would be a need for genes involved in spermatogenesis to be located on the X or Y, all genes involved could simply be on autosomes. I don't know whether any are though (or aren't).

@Armatus It is actually written in tortora and derrickson that the cells are joined by their cytoplasm because of some genes are exclusive to X or Y but I can't find any proteins meeting this criteria. Even I don't know why they couldn't simply be on any autosome.

X chromosome has many important genes required for general housekeeping. So we need not really talk about X-chromosome genes. Here is a list of genes present on the X-chromosome.
@Armatus, if all those genes were on autosomes then presence of Y wont be mandatory for male development. There are autosomal genes that are involved in sexual development for e.g. Anti-Mullerian Hormone gene is present on chromosome 19. However, there must be a master regulator that is male specific and since sex determination is chromosomal in mammals, the Y-chromosome must encode that master regulator.
Sry, encoded in Y-chromosome, is one such protein that is absolutely essential for male sexual development. Having said that, it could be very well possible that the basic genes required in the process of spermatogenesis are autosomally encoded. In fact it is so. I just took the list of genes that were associated with sepermatogenesis in KEGG and checked their chromosomal locations. They are all autosomal.
Gene --- position
SPATA1  ---  1p22.3
SPATA25  ---  20q13.12
SPATA32  ---  17q21.31
SPATA9  ---  5q15
SPATA19  ---  11q25
SOHLH1  ---  9q34.3
SPATC1L  ---  21q22.3
SPATA18  ---  4q12
SPATA2  ---  20q13.13
SPATA21  ---  1p36.13
SPATA2L  ---  16q24.3
GMCL1  ---  2p13.3
SPATA7  ---  14q31.3
SPATA5  ---  4q28.1
SPATA6L  ---  9p24.2
SPATA4  ---  4q34.2
SPATA24  ---  5q31.2
SPATS2L  ---  2q33.1
SPATA16  ---  3q26.31
SPATA6  ---  1p33
SPATA12  ---  3p14.3
SPATS1  ---  6p21.1
SPATC1  ---  8q24.3
SPATA22  ---  17p13.3
SOHLH2  ---  13q13.3
SPATA13  ---  13q12.12
SPATS2  ---  12q13.12
SPATA20  ---  17q21.33
ASUN  ---  12p11.23
SPATA8  ---  15q26.2
SPATA17  ---  1q41
SPATA3  ---  2q37.1
SPATA5L1  ---  15q21.1
GMCL1P1  ---  5q35.3
SPATA41  ---  15q26.3
SPATA42  ---  1p13.3
SPATA33  ---  16q24.3

If the genes involved in spermatogenesis are all autosomal, then what is the point of having a connected cytoplasm ? Is it because of X chromosome's proteins which are involved in spermatogenesis ? How can I search for those proteins ?

i dont understand what you are trying to ask here : "then what is the point of having a connected cytoplasm" ?
How to find X chromosomal proteins: find all the genes involved in spermatogenesis and find their locations. So the list that i posted is what i obtained in KEGG when i searched for spermatogenesis; no gene from this list is on the X chromosome. But this this may not be exhaustive.

I will quote a paragraph from Bruce Alberts : " Unlike oocytes sperm undergo most of their differentiation after nuclei have completed meiosis to become haploid.The presence of cytoplasmic bridges between them means that each haploid sperm shares a common cytoplasm with its neighbor.In this way,it can be supplied with all the proteins of a complete diploid genome. Developing chromosome that carry Y chromosome ,for example, can be supplied with essential proteins encoded by genes on the X chromososme.Thus, the diploid genome directs sperm differentiation just as it directs the eggs's."

This is given on pg 1149 chp 20 fourth edition.

you are confusing different things here... the products of the diploid genome is used to nourish the sperms.. Some X-chromosomal genes are involved in basic housekeeping functions and their products are involved in this nourishment process... This doesn't mean that X-chromosome genes are involved in spermatogenesis.. Analogous situation: Neurons require glucose to thrive. That doesn't mean that hexokinase is involved in neurogenesis.

I think I used the wrong term but my basic question remains the same. What are the genes on X which are required to nourish that process ?


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Division of Polar Body
The first polar body formed after meiosis-I is completed in oocyte, may or may not divide.
Why is the statement that "it may or may not divide"? Is it random ?


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Rate of Evolution of population of long lived individuals
Is it necessary that rate of evolution of longer lived trees will be lesser than that of annuals ? I understand that new individuals will come up faster in annuals  and it may adapt to varying conditions faster but does it necessarily imply that long lived trees will evolve slower ?

That is true to a certain extent in normal environments, where there is not an excess prevalence of mutagenic elements. The "Generation Time Hypothesis" explains why a smaller generation time and hence a higher reproductive rate ( as in annuals) corresponds to a higher rate of mutation (substitutions in DNA) and therefore have a faster evolutionary rate as compared to slow reproducing and longer generation time individuals(for example, long-lived trees).
Since "fitness"-increasing adaptations produced by somatic variations are very less, the formation of new offsprings giving rise to individuals carrying a DNA which has been subjected to processes (Repeated divisions, replications and translations, amphimixis, and different environment) making it more vulnerable to mutation, becomes mandatory, to propel evolution. This process is much faster in annuals than in long lived trees like Sequoia. Moreover Sexual selection (especially in animals) operates at a much slower rate in longer-generation time individuals. Next, smaller individuals, having higher metabolic rates usually have shorter generation time (more pronounced in case of animals). Higher metabolic activity is linked to greater mutation rate (Due to metabolic intermediates acting as mutagens) and hence faster evolutionary rate. Higher metabolic rate also is linked to higher temperature (faster mutation) and these individuals have a geographic distribution favouring the tropics.(Again increases evolutionary rate)
All these, imply faster evolution for short lived individuals(which usually have higher reproductive rate) as compared to long lived trees. But under "normal" environmental conditions (not drastic and fast changes), the evolutionary rate of large individuals is fast enough to preserve their existence (as the Sequoia prevalence indicates). However, in fast changing environment, larger and long-lived individuals are more likely to be wiped out (probably, this applied to Dinosaurs!).


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Organelles present in sieve tubes
I know that sieve tubes do not have ribosomes, nuclei and cytoskeletal elements.
What other organelles does it not have? Does it have a cytoplasm?

A cell without a cytoplasm is not a cell.

The sieve tubes of the phloem in angiosperms consist of sieve tube elements or members. These are cells which lose their nucleus, ribosomes, and vacuoles at maturity.  They of course have cytoplasm, and it is connected by channels to companion cells (which do have these organelles).  The sieve tube elements retain mitochondria and plastids. See the Wikipedia page and this page for more details.


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Effect of arteriole dilation on vein
If  an arteriole leading to a capillary bed is dilated will the pressure in the vein coming out from the bed decrease ? Will the velocity of blood in the vein change ?

Do we assume that the dilation of the arteriole was under independent regulation and not a consequence of systemic release of a vasodilator, i.e. all other conditions are assumed to be constant?

@SatwikPasani It was under independent regulation.

All else being constant, velocity of the Venous blood will be reduced.
The Flow-Rate Equation: Q=AV

Q = Flow Rate
A = Area (of the "pipe")
V = Velocity of the Fluid

If we assume that the body will try to maintain a constant Q, then an increase in the A of the Arteriole means a reduced V to compensate and a corresponding drop in Venous fluid velocity.
If we start to assume that things are not constant, then the story becomes more complicated. Since Venous pressure is largely maintained by musculature and other actions, not heart contractions (though the system is essentially closed-loop), an increase in Arteriole flow-rate doesn't always correspond to an increase in Venous flow-rate. When there is an imbalance - either due to mechanical interference or something else - conditions like subcutaneous edemas can occur where the interstitial (between-tissues) fluid builds up enough to cause discomfort or damage.
*Normal Disclaimer: I am not a medical professional. The above us based upon an Undergraduate level of knowledge.


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What are the methods for infering genetic interactions?
Is there a classification of methods for inferring genetic interactions? I mean some work published, utilizes genetical genomics data.  Is this possible with expression data alone? And how about perturbation screens? I guess they all need information about mutants/genetic variations?

The questions is vague and difficult to answer because there "genetic interactions" is a catch-all bag for anything that isn't a monogenic trait - which is to say, most of them.

BioGRID is an interaction database, and they catalogue interactions by (among other things) the class of experiment that discovered them. See http://wiki.thebiogrid.org/doku.php/experimental_systems#genetic_interactions
Other than that, you should look at recent reviews and publications, but you will easily get lost unless you figure out some important particulars, like:

What species? Yeast, worm, human, cell line?
What sort of interaction? Synthetic lethality? Complicated, fancy epistasis?
How much? Genome-wide? 2-3 genes?