text:
(Updated question) Problem with Fold-change mean compared to absolute data (in qPCR)
For the problem below I am aware of the statistics involved but just can't get my finger around the following:
In biology we use qPCR to measure gene expression or basically number of mRNA copies. It does this by counting how many cycles of amplification (2^) it needs to reach a threshold. So to simplify everything lets assume that 1024 copies would require 10 cycles (2^10). If there are more copies it would take less cycles to reach the threshold, therefore 2024 copies would take 9 cycles, 512 copies 11 cycles etc.. Now imagine the following scenario:
We have the following samples:
Sample 1. 1024 copies of gene A and 4096 copies of gene B
Sample 2. 1024 copies of gene A and 16384 copies of gene B

Now we want to compare sample 2 to 1, with gene B in relation to gene A:
In absolute numbers this would be:
Sample 1. 4096 / 1024 = 4x more B
Sample 2. 16384 / 1024 = 16x more B
The average amount more B = (16 + 4) / 2 = 10x more B

Now with qPCR the same samples from above would look like the following:
Sample 1. Gene A 10 cycles, Gene B 8 cycles.
Sample 2. Gene A 10 cycles, Gene B 6 cycles.

Now using the methods standard used for qPCR data we first take the difference between Gene B and A. Followed by the mean of the difference and this is taken 2^.
Sample 1. 10 - 8 = 2 cycles
Sample 2. 10 - 6 = 4 cycles
The average amount more B = 2^((2 + 4)/2) = 8x more B

All publications / software tools etc will compute an average of 8x more B. And I am aware this originated from a log2 scale, however why does this statistically correct method differ in outcome from absolute numbers?
Update
I oversimplified my question therefore below some more details of my "problem".
Condition 1 biorep 1. 1024 copies of ref and 1024 copies of gene X
Condition 1 biorep 2. 1024 copies of ref and 1024 copies of gene X
Condition 2 biorep 1. 1024 copies of ref and 4096 copies of gene X
Condition 2 biorep 2. 1024 copies of ref and 16384 copies of gene X

So to compute in absolute numbers the average amount more of gene X in condition 2 versus 1:
We can forget the reference gene here as cDNA amounts are the same, therefore:
Condition 1 biorep 1 & 2: average (1024 + 1024) / 2 = 1024 copies
Condition 2 biorep 1 & 2: average (4096 + 16384) / 2 = 10240 copies
Condition 2 vs 1: average 10240 / 1024 = 10x more gene X in condition 2 vs 1

Now with qPCR CT values based on the numbers above:
Condition 1 biorep 1. Ref_CT 10 and GeneX_CT 10
Condition 1 biorep 2. Ref_CT 10 and GeneX_CT 10
Condition 2 biorep 1. Ref_CT 10 and GeneX_CT 8
Condition 2 biorep 1. Ref_CT 10 and GeneX_CT 6

Now using the official qPCR calculations:
Condition 1, Ref_CT mean (10 + 10) / 2 = 10
Condition 2, Ref_CT mean (10 + 10) / 2 = 10
Condition 1, GeneX_CT mean (10 + 10) / 2 = 10
Condition 2, GeneX_CT mean (8 + 6) / 2 = 7

Ref_deltaCT (10 - 10) = 0
GeneX_deltaCT (10 - 7) = 3

delta_deltaCT (3 - 0) = 3
Difference Condition 2 vs 1 = (2^3) = 8x

This equates to 8x more of Gene X on average in condition 2 compare to condition 1. Here now is the difference of 8x vs 10x. Also any program you will use to fill in these CT values it will result in a ratio of 8 compared to 10.
Is this perhaps as this method equating to 8 should only be used for technical replicates, and bioreps should use a different equation resulting into 10?

Sample 1. 4096 / 1024 = 4x more B
Sample 2. 16384 / 1024 = 16x more B
The average amount more B = (16 + 4) / 2 = 10x more B

That is not the right way to go about. You are calculating average expression of B in both samples. It does not mean there is 10x more B. There is just 4x more B in Sample-2 relative to Sample-1.
Gene-A does not change its expression between samples and can be used as a reference gene.
If you calculate by threshold cycle the fold change $ = 2^{8-6} = 4x$
See this post too.
The average is calculated between replicates, not between different experimental conditions.
Sometimes the average of two experimental samples is calculated — this is typically done in a MA-plot analysis which is done to filter out genes which show very high fold changes just because of their overall low expression (1:4 vs 100:300).
Answer to your Edit
You should not take the average (arithmetic mean) of Ct. They don't scale linearly with expression (and so is the converse).
For any non-linear function $f(x)$:
$$f(x+y) \ne f(x)+f(y)$$
$$f\left(\frac{x+y}{2}\right) \ne \frac{f(x)+f(y)}{2}$$
Furthermore, for a convex function:
$$f(E[x]) \le  E[f(x)] $$
$$ Jensen's\ inequality $$
where $E[x]$ is expected value of $x$
$a^x$ is a convex function with respect to $x$ ($a$ is any real number > 1). So you can apply Jensen's inequality to Ct values and expression.

I totally agree with your answer, I think I over simplified my question, above I edited my original post to clarify a bit more my question.

The answer you give in your edit is also the answer I expected. However all (commercial) tools assume that the Ct values are on a linear scale and therefore you take the arithmetic mean of the Ct, resulting into 8x. And as you take 2^ of Ct the absolute values are not. This means you would have to take the geometric mean of 4096 and 16384, which is 8192 (which is 8x 1024). Apparently all published methods consider the absolute values not to be on a linear scale, and actually the Ct values are. Which biologically speaking is difficult to grasp.

If someone is interested in average Ct then they may very well do it. But we are not interested in that are we. Independently the values are not in any scale. They scale with other value as per some function. So expression scales exponentially with Ct. So $ Expression = f(Ct)$. I should clarify about it. Edited


text:
Can you build muscles from watching point of view videos of people weightlifting?
According to this, "new research has found that viewing other people exercise actually increases your heart rate and other physiological measures, just as if you were working out yourself".
This got me thinking, can muscles be developed to be stronger and bigger from simply watching videos of people weightlifting from the point of view of the weightlifter?

This post might interest you.

You could always post this on Skeptics, although I like anongoodnurse's answer here.

That is highly unlikely.
The article to which you linked specifically states:

While watching other people exercise may increase your heart rate and have other physiological effects, nothing can replace the health benefits of getting off the couch.

With proper nutrition, muscle is built through exercise by

adding sarcomeres [to muscle cells which is] physiologically determined by the degree of force a muscle can generate that is in turn dependent on the degree of overlap of the thick and thin filaments. Thus, the amount of tension would control the number of in-series sarcomeres in a single muscle fiber.[1]

Watching a show about cooking might stimulate hunger, but it won't put food into your stomach. Watching something that evokes a sympathetic response (fear, fighting, an attractive person exercising vigorously, an athlete in a competitive event, etc.) will elevate heart rate, sweat production, and resting muscle tension, but there is not enough tension to produce muscle growth.
In addition, there might be small deleterious effects to watching emotionally charged movies which elicit a sympathetic response: they cause stress. An effective horror film will elicit tension and maybe even a startle response - making you jump in your seat - but it will also elevate your blood pressure, etc.
Exercise is good for you physiologically. Simple stress without exercise is much less so.[2]
[1] Muscle growth and exercise
[2] The Physiology of Stress: Cortisol and the Hypothalamic-Pituitary-Adrenal Axis (simplified but relevant)

I doubt it. Muscle growth comes from literally damaging muscle fibres by putting them under too much load. This is what causes the muscle pain after a workout. This triggers thickening and increase in number. Without the damage in the first place, there's no reason for the fibres to change.

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Examples of genes involved in plastic responses
Adaptive plasticity involves sensing the environment and responding adaptively to it. Intuitively, I would think that this process may ask for a more or less complex genetic machinery of regulation of gene expression.
Can you give me examples of genes and genetic pathways that are famous for their role in adaptive plastic response?

You might want to check out the work of people like Amanda Bretman and Tracey Chapman, they've done some stuff with plasticity and gene expression if I remember correctly

Instead of genes you can ask about pathways.

Yes, indeed, that what I meant by "genetic processes" as you noticed in your question. I edited my post. And I think I'll checked your your answer!

I assume that you mean gene expression regulation when you say genetic processes. The best example for your question would be that of synaptic plasticity in neurons.
The immediate responses are obviously that of protein modifications (cell signaling). These are fast responses that have immediate effects but are also quite short-lived. During the long term potentiation (LTP) some stable changes happen via gene regulatory mechanisms.
It is to be noted that in a polarized cell such as neuron the distance between the nucleus and the point of action i.e. the synapses (at dendritic spines), is huge. Any event leading to transcription regulation would take a long time to act. Therefore there are post-transcriptional regulatory mechanisms in place. The mRNAs are localized at the spines and are kept in a repressed state; poised for translation when the signal is received. Finally, if the signal is sufficient enough, transcriptional regulation (sometimes stable due to epigenetic changes) takes place.
You can look for the genes involved in this pathway which also include ncRNAs (lncRNA and miRNAs).
Other examples:

Acute stress response (such as Unfolded Protein Response [UPR])
Acute inflammation
Chemotaxis

Here is a paper I just read about translational regulation in LTP, if the OP is interested: http://www.cell.com/molecular-cell/abstract/S1097-2765(12)00400-5

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text:
Why is LH level much higher than FSH level at ovulation?
My teacher showed us an elaborate collection of graphs with one of them showing FSH and LH plasma levels during the menstrual cycle. LH level was almost 3 times higher than FSH level. Why?
Does this have anything to do with their synthesis or cellular responses?

It is not the absolute plasma levels that are important, it is about their relative differences during the cycle. The steep rise in FSH during the first days induces follicle stimulation. The LH surge at day 12 induces maturation of the egg and stimulates its release (see wiki page). The fact that LH's absolute plasma levels are higher may theoretically have to do with the fact that more LH is needed to elicit its physiolocal response. However, the differences of their relative levels is way more important from a physiological point of view.

The LH receptors are not less sensitive...instead they are more sensitive, than FSH receptors...so the same amount of GNRH which affects those receptors, LH secretion is increased almost by 3x, than FSH...

Ah, thanks@souvik bhattacharya, I'll adapt my answer. My point still stands though.


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Need for two oxygen sensors in E. coli
E. coli has two oxygen sensors: FNR (fumarate-nitrate reductase) and ArcBA (Anoxic Redox Control, two component control systems). FNR directly senses the oxygen, while the interaction of ArcB with oxygen is indirect one via quinone pool. Out of theree quionones in E. coli, which one (oxidized and reduced forms of all three types)  play roles to what extent in what direction (inhibiting/activating) is much debatable. I would like to see some intuitive level arguments for why a cell, even in principle, need to have two sensors for oxygen?

It is not uncommon for cells to have parallel pathways for same outcome. This ensures foolproof response and makes the system robust. E.coli also has another sensor for aerotaxis (Aer and Tsr proteins). See my answer on your previous post and the linked paper.
Also look for coherent feed forward network motifs.


text:
What is the common diet of food-related IBS patients? Besides most patients being lactose intolerant, what other intolerances do they face?
I am currently writing a paper on irritable bowel syndrome, and I was wondering what the common diet of a patient with food-related IBS consists of. I've already begun discussing the pathogenesis of the disorder, but I want to start making a connection between food and IBS. I understand that most patients tend to be lactose intolerant, but I am also interested to see if there are any other common intolerances associated with IBS.

IBS stands for Irritable Bowel Syndrome. The IBS symptoms include belly pain, diarrhea, bloating and constipation. Different persons have an intolerance to different food items. You can know what's causing trouble in you by taking a test at http://intolerancelab.co.uk/intolerance-2.
The most common diets that you can prefer to get rid of IBS symptoms are:

High Fiber Diets can help prevent constipation.
For some people, high fiber diet is intolerant. They should switch to a low fiber diet.
You should prefer a gluten-free diet.
Have a low-fat diet and get rid of a number of health problems.

Some food items that can cause food intolerance are:

Dairy products
Soy products
Fructose
Wheat
Gluten

Fermentable carbohydrates may cause problems in some IBS patients. Recent work suggests that restricting these foods may improve the symptoms in some patients.
http://www.nature.com/nrgastro/journal/v11/n4/abs/nrgastro.2013.259.html
More information can be found by looking for the FODMAP diet.

This is from a recent abstract relating to FODMAPS:  Food intolerance in irritable bowel syndrome (IBS) is increasingly being recognized, with patients convinced that diet plays a role in symptom induction. Evidence is building to implicate fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) in the onset of abdominal pain, bloating, wind and altered bowel habit through their fermentation and osmotic effects. Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3388522/

The question was originally about food tolerance, but was meant to question intolerance to the food, hence the comment. I think the OP essentially worded the question incorrectly, which has now been corrected. Hence I shall remove the comment shortly.

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text:
Imperfect dosage compensation
Dosage compensation is used to make up for different copy numbers of the major sex chromosomes in males and females (One X or Z chromosome in one and two in the other). Two main mechanisms of dosage compensation exist, inactivation and upregulation.
But dosage compensation is not entirely perfect, the amount of gene product from an upregulated X/Z-linked genes in the heterogametic sex is not exactly that of the two in the homogametic sex.

"In Drosophila, the male-specific lethal (MSL) ribonucleoprotein
  complex mediates dosage compensation by upregulating transcription
  from the single male X chromosome approximately twofold."

On average how well is dosage compensation performed? What is the variance like:

within a single chromosome (between genes)?
within species?
between species?

You mean Y chromosome?

@ChrisStronks no. there is one X in males, two in females. To compensate for this males either upregulate their X or females down regulate (or silence) one of theirs.

Note that there are several sources of variation. There may be stochastic, environmental and genetic among individuals, within individual and within chromosomes variations. For example, in the pseudo-autosomal region (PAR) were the genes are present in two copies in both males and females, you may have much lower change in expression as there is nothing to compensate for. It may (or may not) depend on the protein beeing made and how a shift in the concentration of this protein influence the rate of chemical reaction according to a Michealis-Menten dynamic.

I may have too a selectionist view though and I may overlook how complicated is the question. It is a very interesting question +1

@remi.b selectionist views are more exciting that neutralist ;)

@GriffinEvo I understand but it says X and W chromosomes in your question body, I thought the male chromosome is called Y.

@ChrisStronks ah now I see what you mean. It's in reference to zz/zw systems (and should be a z not a w)

Related, and a partial answer on the inactivation of X-chromosomes and genes that escape silencing can be found here: http://biology.stackexchange.com/a/27743/3624


text:
Is there a difference between polarity and hydrophobicity?
From literature the two terms seem to be interchangeable when discussing protein domains and motifs. But biochemically, what are the specific differences between these two terms?
For example what is the difference in these sentences:

Generally globular protein cores have hydrophobic regions whilst the surface contains hydrophilic exterior facing residues.
Generally globular protein cores have non-polar regions whilst the surface contains polar exterior facing residues.

Hydrophobicity means aversion to water which results because of increase in entropy of the system due to the water-"solute" interaction.
As already pointed out in by inf3rno, polarity of a molecule is because of its net dipole moment. It is true that polar molecules can dissolve in water (because they can interact with water via van der Waals' forces especially Keesom and Debye forces).
CO2 is apolar but dissolves in water (it actually reacts with water). Most apolar substances cannot interact with water via van der Waals forces.
To sum up, usually polar substances are not-hydrophobic (i.e they are hydrophilic), however some polar molecules such as nitriles, ketones and esters can be hydro-neutral (midway between hydrophobic and hydrophilic. See here). Even large polar molecules are insoluble in water such as 1,2 dichlorobenzene and nitrobenzenes (For something to be soluble the solute-solvent interactions should be stronger than solute-solute interactions. "Water insoluble" may not be equivalent to "hydrophobic").
Conversely, apolar substances are hydrophobic (unless they are reactive solutes such as Cl2 and CO2).

I fully agree. :-)

Hydrophilic means attracted to water, while polar means the molecule has electric pole(s).

A hydrophilic molecule or portion of a molecule is one that has a
  tendency to interact with or be dissolved by water and other polar
  substances.

wikipedia - hydrophile

A polar molecule has a net dipole as a result of the opposing charges
  (i.e. having partial positive and partial negative charges) from polar
  bonds arranged asymmetrically.
Bonds can fall between one of two extremes — being completely nonpolar
  or completely polar. A completely nonpolar bond occurs when the
  electronegativities are identical and therefore possess a difference
  of zero. A completely polar bond is more correctly called an ionic
  bond and occurs when the difference between electronegativities is
  large enough that one atom actually takes an electron from the other.
  The terms "polar" and "nonpolar" are usually applied to covalent
  bonds, that is, bonds where the polarity is not complete. To determine
  the polarity of a covalent bond using numerical means, the difference
  between the electronegativity of the atoms is taken. On the Pauling
  scale, if the result is less than 0.4, the bond is generally nonpolar
  covalent. If the result is between 0.4 and 1.7, the bond is generally
  polar covalent. If the result is greater than 1.7 the bond is
  generally considered ionic.

wikipedia - chemical polarity

Water is polar. because oxygen (3.5) is more electronegative than hydrogen (2.2) and the difference (1.3) is between 0.4÷1.7. So the oxygen has a slight negative charge, while the hydrogens have slight positive charges in water.
Polar molecules are hydrophile. e.g NH3, EtOH, etc... Apolar (or nonpolar) molecules are usually hydrophobe, but there can be exceptions e.g. Cl2 is apolar, but more water soluble than CO or CO2, because of a chemical reaction (Cl2 + H2O → HOCl + HCl). Alcohols contain the polar -OH group. Short chain alcohols are water soluble and so hydrophile, while long chain alcohols are less water soluble, they are hydrophob, because most of the molecule contains apolar bonds. Molecules with ionic bonds, like NaCl are hydrophilic, but not necessary water soluble (e.g. AgCl is poorly soluble in water). So I think hydrophilicity and polarity are not synonyms. However these are just the exceptions, most of the hydrophilic compounds are polar and most of the hydrophobic compounds are apolar.
Amino acid residues (and ofc. side chains) are no exceptions, so in the case of them these terms are synonyms (at least by the 20 common amino acid certainly).
The HP (hydrophobic-polar) protein folding model comes from the article of Dill. He talks mostly about solvophobic and solvophilic residues. In the context of water use the terms hydrophobic, polar and charged amino acid residues. This kind of amino acid classification might be older, but (I assume) it was not so important before the HP model.

solvent to a medium consisting of pure solvophobic residues. For the
  treatment of water-soluble proteins, -(q - 2)g thus describes the
  transfer of hydrophobic residues from water to a hydrophobic
  environment; for the treatment of membrane proteins,
  -(q - 2)g characterizes the transfer of polar or charged res idues from an apolar medium to a polar environment.

1985 - Theory for the folding and stability of globular proteins

According to Dill's article residues can be

charged (1 times)
polar (2 times)
hydrophilic (0 times)
solvophilic (8 times)
apolar (0 times)
non-polar (0 times)
water-insoluble (1 times)
hydrophobic (3 times)
solvophobic (23 times)

I checked the google either:

google "* amino acid residue" search

ionic 7
charged 104 000
polar 42 000
hydrophilic 917 000
apolar 101 000
nonpolar 326 000
non-polar 44 000
hydrophobic 111 000

google "* residue" protein search

ionic 2 110
charged 120 000
polar 53 000
hydrophilic 33 000
apolar 4 690
nonpolar 15 600
non-polar 284 000
hydrophobic 148 000

So all of the hydrophilic, hydrophobic, nonpolar, polar, charged words are used frequently. I checked some books and articles, some of them use the "hydrophobic-polar-charged +/-" classification (just like Dill) which seems to be elder than the "nonpolar - polar (neutral, acidic, alkaline)" classification in other articles.

wikipedia - amino acid
Basics of Protein Structure - The 20 Amino Acids and Their Role in Protein Structures
condmat - Amino acids
tutorvista - Amino Acids

Now the question still stands.

For example what is the difference in these sentences:

Generally globular protein cores have hydrophobic regions whilst the surface contains hydrophilic exterior facing residues.
Generally globular protein cores have non-polar regions whilst the surface contains polar exterior facing residues.

I don't think there is any difference between the meaning of these two sentences.
I think the more interesting question is which amino acids are in which groups. I checked some hydrophobicity scales.

Figure 1 - hydrophobicity scale summary

Amino Acid Hydrophobicity for the Kyte - Doolittle (kd), Wimley - White (ww), Hessa  - Heijne (hh)
Hydrophobicity Index for Common Amino Acids for the two indexes
tutorvista - Amino Acids for the pI values (pI can be used to filter the charged ones)

It seems to be far from obvious. As you already mentioned it is a continuous spectrum and hard to create groups. It was interesting that Trp (which is strongly apolar) had negative numbers on two scales (maybe the data was not reliable). What you can tell, which amino acids are certainly polar (hydrophilic) and which are certainly apolar (hydrophobic). Based on this information you can tell which residues will be in the apolar core (hydrophobic residues) and which will be on the polar exterior (hydrophobic residues) and which will create the backbone hydrogen bonds (polar residues) and probably salt bridges (polar, charged residues). Ofc. all of these can more or less depend on the pH...

There is ambiguity in the way we talk about hydrophobicity. For example; polarity is a spectrum between non-polar and polar. However hydrophocitiy is a spectrum between hydrophlic and hydrophobic. I also suppose I want to know about domain hydrophobicity and polarity rather than the entire protein. Will edit to clarify.

@GoodGravy I think the two sentences mean the same. I'll try to find evidence, but I think it will be hard.

@inf3rno I had an inkling they might be (for all intents and purposes!). I'll dig around more too and see if there is something we are missing.


text:
Insects or Birds covering least distance but most wing moves
I was in search in of list or detail about Insects and Birds which move their wings most but cover least distance.
I know that in insects house fly moves its wings about 200/sec and covers 5mph (about 7.3 feet) distance and in birds Hummingbird moves its wings about 80/sec and covers 60mph (about 88 feet) distance, but I am in search of about 10 in each insects and birds. And also about their heart beats.
If you have combine list, it will be much appreciated. If you know any book or website about same topic it will much helpful.

When hummingbirds are hovering, they go 0 distance at ~80 Hz flapping frequency and ~1200 bpm heartrate. http://www.hummingbirds.net/about.html#wingbeat


text:
How do insects survive the winter?
I had an interesting discussion today in which the question arose how insects survive in the winter. Since they need a high enough external temperature to be active, this seems a bit difficult in the winter. With frost they should completely freeze and I don't think they will survive this. Do they rely on eggs laid in the fall (which have to survive freezing temperatures as well) or do they employ other techniques for that?

As there are many insects, there are also a number of different strategies. As you already said, insects depend on the temperature of the environment and cannot produce enough heat with their metabolism. The major strategies are:

Migration,
Communal living
Cold tolerance (by means of antifreeze proteins)

Only some of the insects can opt for " Migration" , those which are big enough to travel long distances. A good examples for this migration of insects is the monarch butterfly which migrates from summer habitat in the north-eastern US and southern Canada to Mexico in the fall. Using this strategy, the insects avoid life-threatening temperatures.
"Communal living" helps insects to get over the winter, as the colony produces enough heat to survive. A prominent example are bees, which maintain relatively high temperatures in their hives; another would be ants.
"Antifreeze proteins" are also employed by a few. Some insects contain special proteins or glycerol in their hemolymph (the equivalent to blood) which either prevents it from freezing and/or prevents the formation of ice crystals which destroy the cells. An example for such an animal would be the New Zealand Mountain Stone Weta which can stay frozen for months until the temperature gets high enough for living again. Some insects go into some kind of winter sleep, in which they survive the cold temperatures. Their living cycle is synchronized with the seasons of the year.
The answer is based on this and this article, have a look for further information and references.

The above answer is perfectly correct...except it deals with mainly ectothermic insects...now there are some endothermic insects as well..& many of them adopt this following curious technique to elevate their body temperature....
Here the hawkmoth's capacity to elevate their body temperature depends on their powerful flight muscles which generate large amount of heat during when operating. The insects use shivering to warm off before they take flight..they contract their flight muscles in synchrony before flight, so that only slight wing movements occur but considerable heat is produced. Chemical reactions , & hence cellular respiration speed up their warmed-up flight motors enabling them to fly during cold days & even during night....

Also some endothermic moths take help of 'time-trusted' countercurrent heat exchanger, that helps to maintain a high temperature in thorax...where majority of flight muscles are located...thus maintaining a constant temp. of about 30 degree celcius at the body core when the outside temperature is,sometimes ,even near subzero...

Also...this particular mechanism is applied by insects & animals...ectotherms & endotherms alike...
Introduction of cholesterol in the cell membrane thus hindering solidification at low temperture by disrupting the regular packing of phospholipids...

please don't just copy and paste from a source, especially if you are not crediting them (http://insects.about.com/od/adaptations/p/wintersurvival.htm) see the help pages on how to write a good answer

Sorry...I'm changing my answer...& this time it's not a copy-paste...

Well, these are some nice pictures, but your answer has nothing to do with the actual question. Do insects use this mechanism survive the winter? As far as I know, they don't. If you want to correct minor issues in an answer, please use the comment function.

@Hav0k , just look up the highlighted points...


text:
Why is the threshold between human embryo and human fetus defined as 8 weeks after fertilization?
Why is the threshold between human embryo and human fetus defined as 8 weeks after fertilization? What's happening on the 8th week?

Note: definition of embryo based on Wikipedia's current definition.

Are you seeking for a science article that define the words "baby" and "embryo"?! This is going to be hard to find as these words are so easy and common. Similarly there are probably no science article who define the word "increase" as everybody know what it means. But I don't know maybe someone will find what you're looking for. But you should probably not expect a different definition from the wikipedia ones!

So the question might be "Why did we use the threshold between the definitions of human embryo and human fetus at 8 weeks after fertilization and not at 7 weeks or 9? What's happening at the 8th week?". Is that right?

@Remi.b does my question now appear more clear? Are there any further specifications that I might make?

I would recommend you to just reduce your whole question to what you copy-pasted from my comment (and modify your title accordingly).

@Remi.b done. I'll remove my comments, you might do so as well.

I delete my answer as it does no longer address your question. I don't have enough knowledge in developmental biology in order to answer your question, so I'll let someone else working on your question. You may still receive some comments on your introduction but I think the question will be accepted from now on. You should cite wikipedia for the definition you are using of embryo.

@Remi.b will you vote to re-open? I don't see where any opinion is involved...

An embryo is called a fetus at a more advanced stage of development
  and up until birth or hatching. In humans, this is from the eighth
  week of gestation. However, animals which develop in eggs outside the
  mother's body are usually referred to as embryos throughout
  development; e.g. one would refer to a chick embryo, not a "chick
  fetus" even at late stages.

wikipedia - embryo

I can answer what "more advanced" means with the following 2 pictures. I think you can see the difference. (Real photos were too disgusting for me.)

Figure 1 - 7th week embryo - source

Figure 2 - 8th week fetus - source

For the sake of blind people and google, the 8th week fetus has a face and a human form, while the 7th week embryo doesn't.

From the 10th week of gestation (8th week of development), the
  developing organism is called a fetus.
All major structures are already formed in the fetus, but they
  continue to grow and develop.
Since the precursors of all the major organs are created by this time,
  the fetal period is described both by organ and by a list of changes
  by weeks of gestational age.
Because the precursors of the organs are now formed, the fetus is not
  as sensitive to damage from environmental exposure as the embryo was.
  Instead, toxic exposure often causes physiological abnormalities or
  minor congenital malformation.

wikipedia - prenatal development

So the scientific explanation of the threshold is that the precursors of all the major organs are created by that time.

I don't think this answers the question. That the embryo/fetus becomes more advanced over time is a given, but it does not answer the question of why the 8/9 week divide was chosen as a threshold. A 12 week embryo/fetus also has a more "advanced form" and is more "human-like" than a 11 week embryo/fetus.

@fileunderwater Edited my post.


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How to evolutionary explain menstrural cycles synchronization?
Sorry, I can not indicate the source, but I read that menstrual cycles of women who live in the same house over time sync. Is it true? How does it work?

It is a myth which most likely came from methological flaws in the original study. It could never be reproduced. Read here for details.

@Chris that's really interesting, I am aware of much anectodal evidence that suggests this is true. The wikipedia link you gave cites PMID:23480070 but I don't have access to it. Do you? Does it indeed confirm that it is a myth (the abstract suggests so but I don't know for sure)?

@terdon You can find the paper here, the part regarding the mentrual synchronisation starts on page 30 in the document. If you want to summarize the criticism in an answer, go for it.

This question appears to be off-topic because the claimed fact is not supported by any reference. Suitable for Skeptics SE.

@ChrisStronks I guess you meant to ask Chris not me. There is nothing in my comment

Ok, made the comment into an answer.

This is a myth which most likely came from methological flaws in the original study. It could never be reproduced. This paper ("Darwin’s Legacy: An Evolutionary View of Women’s Reproductive and Sexual Functioning") deals with it. The interesting part starts from page 30 and says (the references can be ressolved in the article):

Critiques of MSH Studies
Wilson (1992) and Yang and Schank (2006),
  among others, have criticized the study design, methods, and
  statistics used by McClintock (1971) and others who have claimed
  evidence of MS. For example, McClintock
  incorrectly used the Page test for ordered hypotheses with multiple
  treatments (she used the same groups of women repeatedly instead of
  independent treatments), making it impossible to evaluate the true
  level of significance of her reported findings. Likewise, reports of
  greater estrous synchrony in chimpanzees caged together than in those
  caged apart (Wallis, 1985) and synchronization of estrogen peaks in a
  sample of five golden lion tamarins (French & Stribley, 1987) are
  rendered moot by the use of unsuitable statistical tests (Schank,
  2001). Furthermore, computer simulations suggested that the null
  hypothesis of no synchronization could not be rejected in either the
  chimpanzee or tamarin samples (Schank, 2001).

Thanks for this enlightening answer Chris. It has been a long-standing myth that I believed for true.


text:
Where does crop biomass come from?
Each year, large volumes of crop are harvested from fields.

Where does this biomass get replenished from?

@user137 - It is easy to write a specific answer when you edit the question to your answer...

That's why my answer seems a bit off now :)

Since this is now the second thread where editing the question is not liked by the original author, I will open a thread on meta on this.

@Chris let me know when you do - I don't see anything yet.

There is already an old question about it. I think this can be used as well, it is here.

There are biogeochemical cycles for the building stones of the biomass (e.g. hydrogen, carbon, nitrogen, oxygen, etc...), so all of these atoms are recycled. To recycle them the organisms need energy, which they get from sunlight, from chemical materials, etc... (check microbial metabolism for further details).
Plants use sunlight as energy source, CO2 from air as carbon source, water and O2 from air as oxygen source, and so on... You can find more info about plant metabolism on wikipedia.

The matter in plants is mostly carbon, hydrogen, oxygen, and nitrogen, with various metal ions and some sulfur and phosphorus. The carbon, hydrogen, and oxygen are taken from carbon dioxide in the air and water from the soil through photosynthesis. Nitrogen is taken up from the soil as ammonia or nitrates, or fixed from nitrogen gas, but this only happens in legumes. Phosphorus is also part of a nutrient cycle. Metal ions such as sodium, potassium, magnesium, and calcium are taken up through the roots with water.
If you're asking about how this material is replenished, fertilizer is an important answer. For centuries, nitrogen was a limiting nutrient in farms because it would get removed faster than it was replaced, especially if crop rotation was not used or legumes weren't grown. Thanks to the Haber Process we can produce humongous amounts of ammonia from nitrogen gas, this has greatly increased the amount of nitrogen available for plants, but has also resulted in nitrate pollution in waterways and algal blooms and eutrophication. Phosphate and potassium are also used in fertilizer and are usually mined, however phosphorus reserves are limited.

The biomass of crops is definitely mostly carbon (from the air in the form of CO2) and water. However, in terms of how it affects the environment: Crops use up trace elements that make up a tiny fraction of the biomass, but it is these trace elements that are not ubiquitously available. Most notably phosphorus and to a lesser extent nitrogen. The impact on the environment is that farming, and especially monocultures, deplete the environment of these essential trace elements. It is often these elements that restrict growth due to competition. Therefore, it may inhibit growth of native species. However, a far more devastating effect is that farmers will re-supply these trace elements in excessive amounts through artificial fertilizers, leading to surplus and run-off phosphates (phosphates are the main form in which phosphorus is applied in fertilizers) (Hart et al, 2004). This in turn dramatically shifts the natural competition for this normally restricting element, in turn promoting growth of non-native plants and promoting the growth of P and N-tolerant plants while suppressing the growth of plants that are intolerant. As most plants are actually intolerant it will eventually lead to species loss and imbalance in the ecosystem (popular link).


text:
What could live inside a pillow?
I have a phobia of bugs (or other small creatures) living inside my pillow and crawling into my ear in the night. It might seem silly, but bare with me.
Recently I got wondering, what organisms could actually live inside a casual foam pillow?
I machine-wash it every now and then to keep it clean.

Millions of organisms can live in your pillow if you include single-celled organisms (e.g.bacteria) etc. I think this is a bit too broad.

@anongoodnurse I think it's a better wording to say I'm asking about things that can actually crawl into an ear, question updated. I'm not a bacteriophobe.

do you want an honest answer ;)

@ChrisStronks It affects the way I sleep already anyway so I can't really see any further damage being done.

Bed bugs (wiki)! However, you will definitely be able to notice when they are around by bite marks and blood residues.

@anongoodnurse - I am afraid I am not following you :-) Language barrier perhaps - 1. Elections kick the stuffing out of one - you think this is a bad answer? In fact it is haha. Or do you mean Mad Scientist is leaving us? 2. I lost one as well - did you loose a mod ship? 3. I am running for mod :-)


text:
What does it mean for the signals for transcription and translation to be "conserved"?
I was reading this article: "Overview of vector design for mammalian gene expression."  for an explanation of why mammalian cell lines are used for expressing cloned genes, and one of the reasons given is that "DNA cloned from higher eukaryotic cells is readily expressed since the signals for transcription, mRNA processing, and translation are conserved in higher eukaryotic systems." What does it mean for the signals to be "conserved," and why does this make mammalian cells a better host than other types of cells?
Follow-up question, in case the answer to that question doesn't make it clear: the article also says the machinery for protein folding and assembly are "conserved" - what does that mean (if not the same thing as in the first question) - and again, why does this make mammalian cells a superior choice of host for expressing cloned genes?

It means the signalling pathways or the mechanisms used for a particular process is the same across a number of species. The reason an eukaryotic cell was used for the expression of a gene is that the particular gene in question required a certain machinery and processes which are found in eukaryotes so for example expressing that gene in an E. coli might not have been suitable/worked. In research its always the best idea to express a gene from the species it came from to ensure its expression.

I concur with @Bez but wish to elaborate on the meaning of 'conserved'. It is generally used in the context of evolution. A conserved characteristic or gene or protein means that it has 'survived' a long time without being altered. As @Bez mentions, certain parts of the protein machinery in eukaryotes is very different from prokaryotes, the latter being considered to have arisen much earlier in evolution. For example, some post-transcriptional processes (e.g. splicing and many more differences) only occur in eukaryotes. But there are many similarities as well, such as the basic use of mRNA etc (see book section). The latter are examples of conserved mechanisms.  In the context of your question, it means that when you take eukaryotic DNA to express eukaryotic proteins it doesn't really matter which cell or host organism you take as it will be transcribed and folded correctly. For example, yeast is often used to express DNA from higher organisms as its protein synthesis is much the same across various eukaryotic species. However, expressing eukaryotic DNA in prokaryotes likely ends up in misfolded proteins without proper post-transcriptional modification and should be avoided.
As to your follow-up question: Folding of proteins happens in the endoplasmatic reticulum (ER) in eukaryotes (wiki), a cell organelle absent in prokaryotes as they lack a nucleus and associated organelles. Again, expression of eukaryotic genes in a prokaryotic expression system will end up in mis-folded proteins.
To get back to your overall question - the 'signals': DNA transcription, splicing, protein synthesis, post translational modification and folding are all regulated by signals, such as specific DNA codons to start and stop transcription, RNA codes for splicing and start translation and protein tags that are placed on specific amino acid combinations. These signals are well conserved across eukaryotic species.

I only made an edit to the post - nothing more.

auch - it's Bez thanks @Chris. Must be your name ;)

I think you agree that it's a special name :-)


text:
Is the poison from Stink Bugs dangerous?
I just went to kill what I thought was a moth on the wall, and instead it fell on the floor and it sounded like dropping a coffee bean (because of the hard shell)
I live in the UK and have never seen one of these things before, I thought maybe it was a variant of a woodlouse, so I just crushed it in some kitchen roll I had over my hand and saw a little stain on the paper, but I assumed it was just blood.
When I looked on the internet and discovered what it was, I smelled my hand and it stank (I'd literally washed my hands like a minute or two before killing this thing). Since I've touched my laptop keyboard and stuff, is that a problem? If I use my laptop and now eat something will it poison me or leave an awful taste in my mouth?
P.S. If this seems OTT I do have slight OCD when it comes to hygiene and bugs.

Apparently there are no poisonous species (see this website), and some species are even eaten (website). No worries.


text:
What are some places where biofilms could develop?
I'm trying to think of places where a biofilm could develop other than on medical equipment or food processing equipment such as stainless steel mechanized blades or knives. I'm thinking more along the lines of biofilms on typical house hold things such as the bottoms of shower curtains

Biofilm is sort of an organized bacterial colony. It can develop anywhere and depends on the kind of bacteria involved.

Try thinking about places that are not very often cleaned and disinfected such as the toilet. Not only that, but the bottoms of shower curtains and in drains. Plaque on teeth is a biofilm, catheters, in/on wounds.

They can certainly develop in the toilet. Just try not to disinfect for a week...
Another place is the surface of living organisms, e.g. dental plaque or the leaves of a plant, etc...

They will develop if you disinfect or not. Most disinfection processes are not done by qualified people and are too short, use the wrong disinfectants or have other failures. And it is usually not necessary to disinfect your toilet - clean it, yes, disinfect it, no.

@Chris Disinfectants and/or cleaning reduce the number of microorganisms in the biofilm (by killing or washing out them). Without the systematic usage of these methods the biofilm will grow and will be much more obvious that it is there...

The problem with biofilms is that they withstand a lot of disinfectants. It is really much less of a problem than commonly thought.

@Chris In toilet maybe, by diseases biofilms are a serious problem e.g. by Staphylococcus + Streptococcus biofilms.

I know. They are a serious problem in tubings in patients for example. And since it's a biofilm they are more resistant.

biofilms also form in almost all systems with water flow (e.g. water tap, central heating), which also include environments outside of the household such as rivers and the famous yellowstone park hot springs.


text:
Ripening bananas artificially: What is the biological theory behind?
I am a resident of the tropical island of Sri Lanka, and we have a strange traditional method to ripen our banana harvest quickly.
What we do is this: We dig a pit in earth that is enough to put the whole banana cluster in. Then, after safely laying the bananas in the pit, we cover up the pit with a sheet such that only a small hole from a side remains: visualize a small 3-4 inch door to the pit.
After that, we light a fire with semi-dry leaves just outside the pit's door. (Semi-dry leaves are used to get as much smoke as possible. Dry leaves do not give that much smoke, because they completely oxidize quickly). And the smoke is sent through the door by blowing it with the aid of a bamboo.

This sends a good amount of smoke and warms the inside of the pit considerably. And by experience I can tell you that this makes the bananas to ripen really quickly. I have done a controlled experiment where half of the cluster was not put into the pit. Bananas in the pit ripen overnight and the control sample took days to ripen.
Can anybody explain what are the bio-mechanisms that are working here?

Nice illustration :P

Smoke emanates Acetylene and not Ethylene, it still triggers the ripening activity in Climacteric fruits

Ripening of bananas (and other fruits) is induced by acetylene and ethylene (Ethyne and Ethene) (see reference 1), which acts as a hormone and induces the ripening process. The incomplete combustion of the leaves produces ethylene, additionally the warmth of the process will help the enzymes as well. There is even a paper about this technique (although it is unfortunately not accessible), see reference 2 for more information. Smoking Chambers are routinely used in this process, see reference 3 and 4.
References:

Role of Ethylene in Fruit Ripening
Effects of smoking on some physiological changes in bananas.
Fruit Ripening
Technology for ripening fruits as important as marketing them

This is also why you can ripen bananas (or other fruits) by placing apples (or pears) next to them - apples emit ethylene as they ripen, thereby speeding up the ripening process in the banas.

Yup, that would be a natural way to do this at home.

As the ethylene acts as chemical messager between different organisms (different banana trees) the word pheromone would be better than hormone (though hormone is also valid as the plant emitting the ethylene is also affected by its own ethylene). Other than that, a perfect answer.

+1, I often have to explain to folks who bought their potted plant at the grocery store why it is seeming to die for no reason. They are often on a stand near fruit, and ethylene is toxic to many growing plants.


text:
What is meant by "genes involved in the stress response"?
I would like to know about the term stress response. For example "some genes of a species under study is involved in stress response". What does that mean? I got this as a part of my assignment question.

In which context did you find this phrase?

Sounds like genes that are activated during stress, e.g. during the pathway of cortisol synthesis.

heat shock proteins are the first thing that came to my mind! could you elaborate on the type or the context of stress?

@Chris : Please see the edit.

The comment by @fileunderwater is apt: stress-response-related genes are genes that are activated during stress, such as exposure to heat. In bacteria, for example, there are heat-shock proteins that are involved in keeping the tertiary structure of proteins (folding/3D shape) intact during periods of heat exposure. Genes encoding these heat shock proteins are then called to be upregulated, and you would find them back in a typical micro array experiment. Hope this helps.


text:
Mechanisms of genotype*sex interactions
I'm looking for suggestions of the mechanistic level at which genotype*sex interactions can occur. These give different phenotypes from the same genotype dependent on the sex they are expressed in. For example, cis-acting sex-specific modifiers can affect gene expression.
What other mechanisms can create a gene*sex interaction?

I am a little unclear about what you mean by gene*sex interaction

genotype*sex interaction in determining the phenotype, so a single allele could produce different phenotypes depending on which sex it is in, I am trying to find some known examples of how these sorts of things occur (e.g. known sex-specific gene expression regulation pathways) @WYSIWYG

Something like this and this ?

Are you talking about genomic imprinting?

So you want to know about the specific molecular mechanisms (e.g. interactions between gene products), and not just examples of gene*sex interactions?

Yes @fileunderwater


text:
Converting fmri data to association matrix
I am currently working on a new tool for the analysis of (large) weighted networks. Association matrices (correlation matrices) as obtained from fMRI data are perfect examples of the kind of data I am looking for. Unfortunately I am only able to locate raw fMRI data and the task of converting them is way outside my expertise.
Can anyone point me to a place where such converted data can be found, or where I can download software which automatically converts the data? Preferably a dataset divided into control/disease.
Thanks!

Are you looking for something like this (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0040709)? GAT is a matlab package that allows for a GUI. If this is correct then please let me know and I can post it as an answer.

@Bez: I will have to take a closer look. Do you know if the software is freely available?

It says its open source so it should be! also perhaps try this (http://rfmri.org/GraphVar)

You can get raw FMRI data from https://openfmri.org/ on that website you'll also download your conditions files for the experimental design (you'll need this in creating your matrix). This is a link to an experiment(it's data) with "healthy" participants and participants diagnosed with schizophrenia: https://openfmri.org/dataset/ds000115
Raw image files from a scanner will be in .dcm format. You can use http://www.mccauslandcenter.sc.edu/mricro/mricron/dcm2nii.html to convert the multiple ".dcm" images of a scan into a 3 single 4D images for anatomicals, also known as T1 images. That converter will also convert the BOLD images into a single 4D image.
After conversion, the images you will want and need to load into whichever fmri data analysis software you're using will be in ".nii.gz".
Your question suggest that you don't need data analysis software but if you do,  I'm only familiar with FSL, you can find information on FSL from here http://fsl.fmrib.ox.ac.uk/fsl/fslwiki/
Hope this helps.

I would suggest you to learn the basics of fMRI data analysis. It is not easy to understand everything in depth, that is for sure. Anyway, luckily, you can start with some good software (e.g. http://fsl.fmrib.ox.ac.uk/fsl/fslwiki/) that does many things for you. Knowing just the basics can get you far then.
For the data, try to have a look at http://www.humanconnectome.org/data/. I think they have even preprocessed datasets.


text:
A website for identifying birds
I am not sure if this is the right place to ask this question, but I guess that ornithology enthusiasts (or ornithologists) will have the best knowledge about it.
I am wondering if there is a website which would identify birds by their looks. For example, I would specify that the bird is similar to a sparrow in size (just a little bigger), it has a gray back and yellow-ish-orange-ish belly and it would tell me the exact species.
Does such a website exist?

There are actually a few, the problem with these websites is that they usually cover only a part of all birds on this planet. I use:

Bird identifier: Usefull website for a lot of European birds.
Backyard Bird Identifier: Useful for some European birds but
mostly for North American and Canadian birds.
All about Birds: Useful, but needs more knowledge for the identification

What I also do is using Google with a description of the bird, which sometimes works surprisingly well.

I've ran into problems today while trying to identify a bird provided as an example in the question on google. Turns out it was a nuthatch - the first website you provided gave me that answer. Thanks!

If you're looking at birds in Britain the RSPB's bird identification web pages have worked well for me and it works in a way described in the question.

If you are on the go, the Merlin app for your smart phone is great. Especially if you are in North America!
Merlin is a smartphone app that you can download via your preferred app provider (apple, google, etc.). It is maintained by the Cornell Lab of Ornithology, and is related to the All About Birds online archive.
The app does exactly what you are looking for, where you specify the approximate size, up to three colors, where the bird was seen (in water, at a feeder, in trees or bushes, etc) and where and when you saw it and it can provide a list of suggested birds. The suggestions have information on identifying the bird species, maps of the species distribution, and example sounds that each species makes.
If you are an avid birder that records your sightings in eBird (also created and maintained by the Cornell Lab of Ornithology) there is an option to add the bird to your "Life List" from within the Merlin app.

Please add a bit more context to your answer. If your link dies, then we are left with basically no information here. A summary, screengrab, highlights, etc all could be useful. (FYI: don't use the 7 year old other answer as a guide -- our standards have increased since the very early years of the site)

I didn't think that was necessary because it a smartphone app, but more background has been provided.

There is a proposed edit from "selene" — are you posting using more than one account? If so, you may find this information on merging accounts to be of interest ...

I don't think so? I think it is just one one account. I only see one, and keep track of points in one.

So, is the currently pending edit on your answer something you wrote or not? If it is yours, then you are definitely posting using two different accounts (possibly from different devices) and you should merge those accounts. If it isn't, then you should either approve, edit, or reject the pending edit.

I added the edit with more info about how Merlin works.

I see now. Great edit, @selene!


text:
Do human visual functions degenerate due to genetic factors or by external factors?
Does eyesight primarily deteriorate 'naturally' due to genetics (genomic/epigenomic factors), or due to external factors such as normal wear and tear, or disease?
By normal wear and tear I include things like repetitive straining of the eyes by reading small text in a dim room night after night.
As a background to my question: By dissecting the causes of visual deterioration into genetic factors versus external factors I hope to relate those causes to the age of onset, and rate of decay of visual acuity.

What exactly is the difference between "natural deterioration" and "degradation through wear and tear"? To me, these are the same and the question is quite unclear, as @anongoodnurse also suggests.

Also, the title and question body don't match. Please clarify the question.

@ChrisStronks - I apologize for my ambiguity. By "natural degradation" I mean an aging process predetermined in length and intensity by some biological factor in the human gene/genome similar to the 'lottery' of vision that is 'given out' at birth. The distinction I am attempting to make between this and aging broadly is the specificity of age of onset and rate of decay.

By "wear and tear" and "over-stimulation" I am implying environmental/behavioral factors such as repetitive straining of the eyes by reading small text in a dim room night after night. The reason I didn't ask specifically about reading is because I'd like to know the broader answer about why does vision degradation occur when it does. Does that help?

please adapt your question and specify what you want to know. From the comment on @anongoodnurse it seems you specifically want to know something about accommodation, while from the above comment it seems you want a very broad answer. Please specify.

@ChrisStronks - I've edited the question body. Does the edits clarify the question?

@ChrisStronks - The answer does cover myopia, and can be a valuable answer for other related problems, imho. Myopia has both a genetic and environmental cause.

@anongoodnurse: your answer is fine (although it does not cover the genetic aging element). The question was however  ambiguous and needs clarification. I proposed an edit that awaits review from the poster.

@ChrisStronks - Thank you! That is certainly much clearer than the original.

Vision deteriorates for both reasons, but I'm not quite sure how to separate the effects of aging from wear and tear.
Cataracts are the leading cause of blindness in the world. Ways in which environment (which falls under the category of wear and tear in my book) affects cataract formation:

UV light: people living at high altitudes (e.g. Tibet) have more cataracts 2° to increased UV light than those at lower altitudes (sunglasses with UV protection delays the process)
lead exposure increases cataract formation.
infections in infancy and childhood (rubella, toxoplasmosis, other)

Macular degeneration is another cause of vision loss. Environmental factors include:

smoking: speeds up age related macular degeneration.
diet: diets low in antioxidants, and obesity increase degeneration.

Retinal damage caused by diabetic retinopathy:

Juvenile onset diabetes has long been thought to be associated with viral infections from coxsackievirus B, cytomegalovirus, adenovirus, rubella, and mumps.
Type II diabetes is influences by obesity, lack of exercise, certain medications, (nicotinic acid, some diuretics, anti-epileptics, psychiatric drugs, and drugs to treat HIV (can impair beta cells or disrupt insulin action); Pentamidine (used to treat a type of pneumonia) can cause pancreatitis and diabetes; glucocorticoids/steroid hormones may impair insulin action.

Corneal opacities:

infections: (Chlamydia trachomatis) bacteria that are spread by close contact with an infected person or by flies, especially common in Africa.
recurrent injury (soot and pathogens from indoor smoke, a dusty, windy environment).
vitamin A deficiency

Nearsightedness:
- near-point work: reading, working with a computer all day, etc.
Glaucoma:
- diabetes, obesity, near-point work, other.
Nonenvironmental causes would be genetics and illnesses associated with aging.

genetic predispositions associated with diabetes, nearsightedness and farsightedness
decreased lens plasticity with age
strokes secondary to hypertension, etc.
amblyopia (“lazy eye”), strabismus (when eyes are aligned in different directions), astigmatisms
hereditary causes of glaucoma and age-related macular degeneration
retinitis pigmentosa, (degenerative disease of the retina)
innumerable genetic disorders (Marfan's, Tay-Sachs, Albinism, Cone-rod dystrophy, various autoimune disorders, etc.
retinoblastoma
predisposition to glaucoma

 Focusing on Vision Through an Environmental Lens
 Glossary of Eye Conditions
 Causes of Diabetes
 Inherited Eye Disease

@anongoodnurse - You answered perfectly, especially given that I am new to Stack Exchange and very poorly worded the question. Your answer was incredibly informative about the types of diseases that affect vision and their factors. My initial inquiry (perhaps naively and certainly not communicated correctly) was what causes the deterioration of vision in individuals who's visual health is not affected by any disease, but have only behavioral factors and biological predispositions as possible culprits. I'm a little lost at this point about how to pursue an answer to that question, however.


text:
Do metastatic cells still have their parent's identity?
If a liver cancer, for example, gives metastases. Will metastatic cells still have liver identity? I mean, if we mark liver cells, will we see the cancer cells too?
Thanks a lot!

Welcome to biology stack exchange. This is an interesting question and could be important in certain cancer research. I suspect the answer is highly dependent on what you're using to label the liver cells and how the cancer cells have mutated as they migrated throughout the body, but don't know of any specific examples. You might want to consider some edits to grammar and wording to make this a little more readable.

My English grammar is really bad, sorry. I tried to edit a little. Thank you for the answer!

I made an attempt to improve the grammar.

Welcome to stack. This is a good question.
To answer your question: Generally, yes.
Howeve like @user137 stated below it can depend on many factors most notably how many division cycles they go through, and also where they metastasize to. The immediate environment of a cell is very effective at altering gene expression.
I use Hepg2 cells regularly. These are hepatocellular carcinoma cells that can be cultured. These cells are known to express 3-hydroxy-3-methylglutaryl-CoA reductase and hepatic triglyceride lipase, two enzymes characteristically highly expressed in liver cells. If we want to do a quick quality control typing we will perform rtPCR for those enzymes. I have seen the expression drop off after about 4 months (~35 passages).
Looking at gene expression (ideally through microarray) is a very valid way to identify/type a cells tissue of origin.

I used to use HepG2 cells a lot too, but we never looked at gene expression and would pass them for months until they died, usually when we forgot to pass them. How do you get "new" HepG2 cells? We'd just ask the university cell repository, but I never bothered to ask where they got them.

ATCC has the lowest passage number, for most every cell line. Your looking at about $400 a line though- reficulous if you ask me but I believe they take qc pretty seriously. Hepg2 cells are pretty stable so your probably ok. If your validating a cell line (not submitters question) it's better to type it by polymorphism. http://www.promega.com/products/str-analysis/cell-line-authentication/cell-line-authentication-service/


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Can human brain memory be removed by EMP?
The human brain is the most complicated human organ so it is hard to examine it completely but based on what we know do you think (or do you know from some source) if a human memory can be removed by emp(electromagnetic pulse) ? (If so do you think it would be pernament or temporary?)

Given the large number of people who were exposed to atomic bombs in Hiroshima and Nagasaki and subsequent atomic testing in the 50s and 60s and did not lose memory, I doubt EMP could erase memory ( unless you count total brain obliteration ). However, I am not aware of actual studies exposing brains to high EM fields to test memory.

This is perhaps best suited for http://skeptics.stackexchange.com

http://www.reddit.com/r/askscience/comments/z3lkd/if_you_were_hit_by_an_emp_pulse_would_you_notice/ it won't have any effect on neurons

I think humans are a less interesting case than electric fish, platypuses, and other such animals. To them, the EMP is probably like a flashbang. I believe there have also been reports of birds being confused by strong electromagnetic fields.

This isn't a ridiculous idea; Transcranial Magnetic Stimulation is used in research and even has some use as treatment for depression (http://www.mayoclinic.org/tests-procedures/transcranial-magnetic-stimulation/basics/definition/prc-20020555)

http://en.wikipedia.org/wiki/Electromagnetic_pulse mentions the following natural sources of EMP, which I have ordered by frequency / period, from the shortest to the longest:

Electrostatic discharge from objects coming into contact (normally too small to be of any concern)
Lightning (milliseconds)
Solar flares (hours.) Such flares cause geomagnetic storms (more on this later.)

Several artificial sources of EMP are mentioned, of which the only ones of interest are military:

Non-nuclear weapons. The page links to a general article on directed-energy weapons, which mentions microwave devices for causing pain and for targeted damaging of electronic equipment.
Nuclear weapons. http://fas.org/nuke/intro/nuke/emp.htm gives more information on this, listing three phases.

The EMP produced by the Compton electrons typically lasts for about 1 microsecond, and this signal is called HEMP. In addition to the prompt EMP, scattered gammas and inelastic gammas produced by weapon neutrons produce an “intermediate time” signal from about 1 microsecond to 1 second. The energetic debris entering the ionosphere produces ionization and heating of the E-region. In turn, this causes the geomagnetic field to “heave,” producing a “late-time” magnetohydrodynamic (MHD) EMP generally called a heave signal.

The same reference also indicates:

...the region where the greatest damage can be produced is from about 3 to 8 km from ground zero. In this same region structures housing electrical equipment are also likely to be severely damaged by blast and shock.

As far as I am aware, memory loss was not a major recorded symptom among the survivors of Hiroshima and Nagasaki. The only recent data for sufferers of EMP would be from victims of lightning stikes. While the frequency spectrum is admittedly different from nuclear weapons, victims of lightning strikes are surely subjected to greater magnitudes of EMP than those who managed to survive nuclear bombings (who suffered many other traumas, such as blast waves and radiation.) Those who survive the immediate physical (burns) and neurological (cardiac arrest) effects of lightning strikes must surely be knocked unconscious and be disorientated when they regain consciousness. But again, I am not aware of medium or long term memory loss being a particular symptom.
It is worth comparing the structure of the brain (a fairly homogenous mass of tissue of high water content, relatively conductive) with the structure of electronic equipment (components of ever smaller size and greater resistance in order to save power, surrounded by a nonconductive medium such as air, and interconnected by wires, which serve to channel voltage.) It is unsurprising that the brain is less subsceptible to electrostatic damage than electronic components (electronics workers have to take precautions in order to avoid damaging sensitive components with static discharges from their bodies and clothing.)
The most widespread damage to equipment caused by EMP is from the long-period pulses, which are channeled by electric cables. These act over distances much larger than the size of the human body.
From the last reference:

...distortion of the geomagnetic field was observed worldwide in the case of the STARFISH test. ... the signal from this process is not large, but systems connected to long lines (e.g., power lines, telephone wires, and tracking wire antennas) are at risk

and

The first recorded EMP incident ... nuclear test over the South Pacific ... resulted in power system failures as far away as Hawaii.

http://en.wikipedia.org/wiki/Geomagnetic_storm mentions cases of damage caused by long period EMP, including electric shocks suffered by telegraph operators during solar flare events.
So in conclusion, any amnesia caused by EMP is likely to be caused by normal biological shock mechanisms to individuals unfortunate enough to be electrocuted, and not by any direct electrical effect on the brain itself.

Perhaps it is worth mentioning also people who work on high-voltage electrical transmission lines - they also experience dramatic EM changes (though perhaps less rapidly). While they have many involved procedures to avoid electrocution, I haven't heard of anything beyond some anecdotes of slight headaches or dizziness in terms of impairing brain function.

@Superbest I think long term exposure to mains and higher frequencies is a separate question. There are a lot of people who campaign against mobile phone masts while hypocritically carrying a mobile phone around in their pocket. I would be cautious about concluding mobile phone masts have ZERO health effects, but the phone you are carrying right next to your body will affect you more than the mast. Years ago I used to get a slight headache after talking for half an hour (my phone was a big brick and it got hot) but I phones have improved since then.

@steverrill Agreed, but I was referring to alleged headaches experienced by electrical workers when they come near (as in, within a meter or so) high voltage lines.

The brain is not an electronic device.
An EMP is basically a large amount of electrons flying by all at once. They are negatively charged, and as they pass by they distort your local EM-field (hence the name). This distortion induces current in the wires (a phenomenon known since Faraday) - since most wires aren't made with a large tolerance, the sudden current spike overheats the wire and burns components. In the brain, there are no wires to induce current on.
It is true that electromagnetism plays a role in neuron function, and action potentials can be measured or manipulated with electrodes. However, this is just a consequence of the ion concentration being used for signaling - there is not a flow of electrons across a conducting wire that is driving the process.
Memory is not stored electrically. The two major mechanisms of memory are strengthening of the synapses and the chemical state of the neurons (metabolites and proteins such as cAMP or CaMK, RNA levels, DNA methylation). These aren't very sensitive to electrons moving past - you're essentially trying to catalyze a chemical reaction by applying a strong EM field outside of the beaker.
Also, I suspect the skull and tissue surrounding it may act as a Faraday cage to shield the brain itself from the EM field.
I'm sure it is possible to create an electron flux so heavy that it manages to induce enough current in cells to kill them (or current in your bloodstream to cause cardiac arrest). However, the nuclear explosion that produces this would probably be much deadlier due to other effects, like blast shockwave or gamma rays. So to answer your question, a nuclear EMP would either kill you or not affect your memories, although if you had some exotic, very powerful, very precise pure EMP generator perhaps you could get some sort of stunning effect or give people a headache. I don't think it could erase memories without killing large parts of the brain.

This isn't a ridiculous idea; Transcranial Magnetic Stimulation is used in research and even has some use as treatment for depression (http://www.mayoclinic.org/tests-procedures/transcranial-magnetic-stimulation/basics/definition/prc-20020555)
In TMS a strong, localized magnetic field can disrupt normal functioning of regions of the brain. For instance it can be used on the visual cortex to cause temporary blindness (actually, can cause a condition called blindsight: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2234142/)
As for memory though, TMS does not seem to be able to cause permanent memory loss (in fact, there is research indicating that it may be able to boost memory). Plus, the magnetic pulse would have to be either extremely strong, or very close, for it to have an appreciable effect.


text:
Basic question about multiplex PCR
Let's say I have a DNA sequence with the following structure:
$$ 5' - N_n - S_1 - N_{1000} - S_2 - N_{1000} - S_3 - N_n - 3' $$
Here, the $N$s represent stretches of arbitrary sequence of the indicated length. $S_1$, $S_2$ and $S_3$ are all unique sequences 20 bp in length.
I design a forward primer PF that anneals to the positive strand at $S_1$. I design two reverse primers PR1 and PR2 that anneal to the negative strand at $S_2$ and $S_3$ respectively. Their annealing temperatures are reasonably close.
Clearly, PF and PR1 together will produce a 1040 bp PCR product, and PF with PR2 will produce a 2060 bp product.
Now let's say I add 0.2 μM PF (standard concentration), 0.1 μM PR1 and 0.1 μM PR2 all in the same reaction. I then run a PCR, with extension time sufficient for the 2 kb product.
I can see the following possible outcomes:

I get a 50/50 mix of 1 kb and 2 kb products.
PR1 competes aggressively and I get hardly any 2 kb product and a lot of 1 kb product.
After a few cycles, the 1 kb product that has accumulated serves as an efficient forward primer for PR2, and I end up getting mostly 2 kb product and little 1 kb product.

Which one will happen? If it depends, what are the major factors on which it depends? Primer concentrations, extension time, annealing temperature, dNTP amount, number of cycles?
This question is basically a very simplified multiplex PCR. While much has been written about practical applications of multiplex PCR, I am hoping that answers will help me understand the considerations that go into deducing optimal multiplex PCR conditions without doing any empirical calibration. This isn't to circumvent the calibration, but to understand the process conceptually.

I haven't done this exact experiment. I am just deducing from the known facts about PCR.
The product of PF and PR2 will serve as a template for both 1kb product (P1) and 2kb product (P2).
Lets assume that after 2nd cycle there is 1 copy each of P1 and P2 (Delay of 1 cycle to make a smaller length product. See here).
Lets assume that the primer binding affinity is equal (and for just preliminaries consider that only one primer can bind a template — such as in overlapping binding sites). So half of P2 will bind to PR2 and half to PR1.
Number of copies at nth cycle is:
P2(n) = 1.5 × P2(n-1)

P1(n) = 2 × P1(n-1) + 0.5 × P2(n-2)
However this is not really the scenario; the primers are not competing for the template.
Which means that both primers can bind to the substrate simultaneously.

DNA polymerases (except Klenow) will remove any DNA strand bound to the template, ahead of it. In that case P1 will not form. But when PR2 runs out, the unused PR1 can produce P1.
Now there are additional factors, such as the distance between PR1 and PR2 binding sites. If the distance between the primer binding sites is less than the smaller product then the abovementioned case occurs. If the inter-primer distance is larger than smaller product then both products will form (and just like the competing primers case, P2 will serve as a template for both products). In this case the copy numbers will be:
P2(n) = 2 × P2(n-1)

P1(n) = 2 × P1(n-1) + 1 × P2(n-2)
This means that P1 will dominate.
Other assumptions:

No limiting concentrations of dNTP, primers etc
PCR efficiencies are equal for both primers and is equal to 2 (in non-competing cases)
Primer annealing temperatures are same i.e binding affinities are same.

you say DNA polymerases (except Klenow) will remove any DNA strand bound to the template do you mean DNA Polymerases have 5'-3' exonuclease activity? or helicase activity? if it'S the second, then both products should be preserved, right?


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Can Omega 3 Fatty Acids prevent chest pain in periodic Atrial Fibrillation?
It is debated if omega-3 polyunsaturated fatty acids (N3PUFa) may be effective in preventing AF (atrial fibrillation), meta-analysis here.
However, much less has been considered this: Do N3-PUFAs prevent acute symptoms of periodic Atrial fibrillation?
The meta-analysis concentrate only in the long-term effects of prevention.
My proposal focuses on the short-term i.e. the fact that the user can recognise AF first and then uses N3-PUFAs.
Please, assume that there is a validation method by which the user can easily detect that he has AF - he does this if he suspect it, i.e. feels special discomfort and special wave-like-pain the chest.
He takes each time in this case 20 ml of Müller omega-3 oil which has also vitamin D.
The effect of recovering is immediate in prophylaxis.
Assume the user has less than < 20 ng/ml vitamin D in blood each case, most of the time, 9 ng/ml so avitaminosis.
My conjecture is that N3-PUFAs can prevent the acute symptoms of periodic AF.
How can N3-PUFAs prevent the acute symptoms of periodic AF?
What is the role of vitamin D here?

Does it matter what the cause is of said atrial fibrillation? IHSS, CHF, valvular disease, DM, HTN, MI, other?

@anongoodnurse Thank you for your good comment! It does not matter what is the cause. I will specify this when I understand what could be most practical to study and detect.

Omega 3 Fatty Acids cannot prevent the the acute symptoms of periodic A Fib, nor is there a role for vitamin D in the treatment of acute symptoms of periodic AF.
Atrial Fibrillation with the symptom of chest pain is very worrisome and requires urgent or emergent treatment. The most common treatments are heart rate control via IV antiarrhythmics, or cardioversion, either electrical or chemical, usually done in the emergency room.
There has never been a study wherein AFib accompanied by symptoms of chest pain was treated by Omega 3 Polyunsaturated Fatty Acids and there never will be, because N3PUFA does not cardiovert arrhythmias nor does it effect heart rate in AFib.
No medical body of any kind would support such a study.
Finally, there is no convincing evidence that N3PUFAs decrease the incidence of AFib, and this has been studied often, because eating 4-5 servings of fish per week has been shown to have a beneficial effect on A Fib. That gives reason to hope that N3PUFA supplements might be similarly beneficial. However:

The role of omega-3 polyunsaturated fatty acids in the setting of AF is controversial. Although some studies demonstrate a lower incidence of AF recurrence with omega-3 polyunsaturated fatty acids use, others have shown an increased risk. Further studies are needed to assess the role of N3-PUFAs in the prevention of AF.[1]

If N3PUFAs have not been proven to help AFib long term, there is no hope whatsoever that studies will be undertaken to shown their effect in the acute treatment of symptomatic AFib, which is the scenario you have described.
Atrial Fibrillation becomes symptomatic when the arrhythmia results in decreased perfusion of various organs. If there is decreased perfusion to the heart, the presenting symptoms may be of ischemia (usually chest pain or pressure) or shortness of breath due to decreased cardiac output and decreased oxygenation in the lungs. If it is severe enough, fainting may occur from decreased blood pressure, and decreased perfusion of the brain. If it is not severe, it may result in a sensation of flip-flopping in the chest, or palpitations (irregular, thumping, or pounding heartbeats). There are other symptoms of A Fib but since you mentioned chest pain, I won't elaborate.
[1] Atrial Fibrillation in the 21st Century: A Current Understanding of Risk Factors and Primary Prevention Strategies

Actually, I read somewhere that high doses in the case when the patient feels flip or flop in the chest can actually worsen atrial fibrillation. So the admission of this in high amount should be avoided in such cases. No positive effect shown. The elevation of the sleeping position is the way to go until the patient feels go unless no other approach made for the particular patient.


text:
Word denoting genetic state
Is there a single word, or brief phrase, that denotes the state of the total genetic machinery (genome + transcriptome + proteome + ...) of a cell or organ or organism at a particular point in time?

If you are including things like the proteome you are sort of tacitly including everything. In that case I would go with 'state'? I guess?

how about "Global profile" or "global expression profile" or the "omics state" or "omics profile"

@Bez I've heard people say "omics" at conferences, so that might be acceptable vernacular.

I think as long as you define what you mean initially, you could just say state.


text:
Tumour resistance: single-cell or population effect?
Drug resistance can arise through a number of mechanisms. For instance, EGFR mutation when treating with EGFR inhibitors, or compensatory activation of alternative survival pathways. But does it occur at the level of a single cell, or would it be a population effect? In other words, would cells exposed to e.g. targeted kinase inhibitors slowly compensate with other pathways (and that would happen in every such cell) or would there be a sub-population of cells that is sensitive to inhibitors and another subpopulation inherently resistant and predisposed towards amplifying other pathways.

I don't know if this can help. There's something called the Allee effect. http://www.nature.com/nrc/journal/v14/n5/full/nrc3712.html

Both can happen.

And much more: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3488437/

http://www.rjme.ro/RJME/resources/files/510210259264.pdf

There certainly can be co-operation or competition among cancer cells within a tumor that can provide some types of population-based influences on cancer-cell survival. Present evidence, however, suggests that resistance to therapy is almost always due to resistant sub-populations of cancer cells within the tumor. In many cases, such as after treatment with EGFR inhibitors, the resistance mutations have been identified. Sometimes these mutations are in such a small fraction of the cancer cells that they can't be detected in the original tumor before treatment, but in most cases they probably were already present before therapy, caused by the mutations that are inevitable during tumor growth. This review on intra-tumor heterogeneity is a good place to start learning about this topic.


text:
How are amino acids neutral at physiological pH?
Amino acids with non‐ionizable side chains are zwitterions when they are at physiological pH, pH 7.4. This is what my book says. But I do not understand why. The Pka for a carboxyl group is around 3 and the pKa for an amino group is around 9. So the isoelectric point should be around ( 9+3) /2 = 6 for an amino acid with no ionizable side chain. At pH 7.4 it would be slightly negative, would it not?
Also what exactly is a basic amino acid? Is that an amino acid that has a PI value of more than 7?
Thank you.

You are right, most of the amino acids have pI around 6, so they are slightly negative at pH 7.

Calculating approximate isoelectric points for amino acids and peptides

The isoelectric point depends on the amino and carboxylic-acid groups and the groups of the side chain. E.g. lysine has an amino group on the side chain, so it has a pI of 9.74.

If an amino acid has two amino groups and only one carboxyl group (like arginine and lysine), then they are positively charged (++ vs. -) at neutral pH. On the other hand, if amino acids have two carboxyl groups and only one amino group (like glutamic acid and aspartic acid), they are negatively charged at pH7 (-- vs. +). You are not correct that the groups are truly neutral. The carboxyl group is negatively charged in a solution much higher than the pKa of the carboxyl group (which is pH 2.48 for arginine). Same is true for the amino groups (pKb is at pH 11.5 for arginine). So, at pH 9.5, the ratio of the positively charged amino group to a neutral amino group is 100:1 (at the pKb it would be 50:50). At a pH of 4.48, the carboxyl group of arginine would be 1:100 negatively charged, versus neutral. So, at pH7, all of the carboxyl group is negatively charged (COO-) and all of the amino groups (2 of them) are fully positively charged (NH3+). Net charge is plus 1, in the case of arginine at pH7.

At pH 7.4 a carboxyl group is mostly present as COO-, while an amino group is present as NH3+. So when a molecule has both groups, such as an amino acid, the molecule as a whole is neutral. As it is a Zwitterion (equal + and - charges) the hydrogen can also flip flop between amino and carboxyl group. Making the molecule 'truly' neutral as both groups are not charged.
A basic amino acid has a basic group such as an amino group (Arginine) on its side chain.

The truly neutral (no positive charge on the amino group and no negative charge on the carboxyl group) does not really exist, since pH7 is far away from the pK of the individual groups (amino and carboxyl). Probability is much less than 1:100.

Technically yes, most amino acids will be slightly negatively charged at physiological pH. But we need to understand what that means. Let's take alanine as an example. Any individual alanine molecule can either be uncharged or have an integer net charge- it's either protonated or it's not. You will never find a "partially charged" alanine molecule. However, if you have a bunch of alanine molecules in solution physiological pH, they won't all behave in exactly the same way at exactly the same time. One molecule may have a protonated N-terminus while another has a deprotonated N-terminus. At physiological pH, the C-terminus is pretty much completely deprotonated, so we just have to pay attention to the N-terminus. We can use the Henderson-Hasselbach equation to figure out what percentage of alanine molecules will have a protonated (positively charged) N-terminus and what percentage is deprotonated. pH = pKa + log(deprotonated/protonated).  If we substitute in our known numbers, we get 7.4 = 9.5 + log(deprotonated/protonated)
Therefore -2.1 = log(deprot/prot) and 10^-2.1 = deprot/prot = 0.008. That means that out of 1000 alanine molecules, about 8 of them are deprotonated and therefore negatively charged. The other 992 are zwitterions. So for all intents and purposes alanine is neutral at physiological pH.

Please add some references to your answer.


text:
Can cracking fingers cause Arthritis?
I have been cracking my fingers for 2-3 years and on the first year I was told that I'm going to get arthritis because of it.
I've been researching this since the first year and I've never gotten an answer. Most people say either Yes, No or I don't know.
Arthritis is mainly cause by bones rubbing together and cracking fingers is just air sockets poping.
I've asked my biology teacher and he said that he's not sure. He then explained to me that the cracking sound from people cracking their fingers is just air sockets poping.
So can finger cracking cause arthritus?

I believe this has been answered on skeptics

Thanx @RoryM I think your link answers my question. So in conclusion, Cracking your fingers causes some harm but it's so negligible it's not worth worrying about.

Similar: http://biology.stackexchange.com/q/19850/6422

@Cornelius It is similar but it doesn't answer my question. Sorry for the reeeaaallly late answer. Although I did get the answer that I was looking for from http://skeptics.stackexchange.com/questions/1325/is-popping-your-knuckles-bad-for-you


text:
Searching for comprehensive textbook
I am extremely interested in science in general and in particular biology. Due to a different choice of career-path I probably will not be learning any more biology anytime soon.
So I would love to get my hands on a comprehensive textbook biology which hopefully will enable a goal in lifelong learning of biology.
What are some good recommendations? I looked up biology textbooks on Google and found candidates such as Campbell Biology by Reece and Biology by Brooker. But as there are so many of them, I have no clue which one to get.
So, biologists of stackexchange, can you help me out?

Hello and welcome to SE Biology! A simple search in the SE would have revealed many similar questions! Please look at this link (http://biology.stackexchange.com/search?q=biology+textbook)

Is the there a specific area of biology you're interested in, or just general?

Try Campbell biology.....it covers almost all the topics under biology in a lucid way...also the book has packed quite a volume of info in it ranging from a beginner level to a fairly advanced level....excellent book also in matters of presentation & writing style so that one won't feel bored....

Pros:

Genetics ( both classical and modern)
Ecology (including ethology)
Evolutionary biology
Animal classification
Immunology

Cons:

Biochemistry ( it somewhat feels short)
Plant anatomy ( not adequately covered)
Plant classification ( same as above)

& the rest of the chapters are like animal physiology etc. they are mixed...like some
principles they have gone thoroughly...some others not...but it's acceptable as they have to cover everything in one book...
But of course it's my personal opinion...so before considering it I would rather recommend downloading the book in pdf format & have a look at it yourself...but I feel you won't be disappointed....


text:
What are the rules for plasmid names?
What are best practices for naming newly created plasmids?
For example, a common format is pABC123. What is the exact specification? Must there be 3 letters?
What databases of plasmid names exist? How much care is taken to avoid name collisions?

So there are no rules per say (although I wish there were). But there are commonalities among plasmid names and they can help people identify them:
Include the empty backbone name in your plasmid name. This simple piece of information can often convey many important details. Once you know the backbone a plasmid is based on, you can usually derive: a) the bacterial antibiotic resistance, b) the promoter that drives the insert, and c) any other selection markers (for use in other cell types, e.g. eukaryotic cells).
Include information about the insert in your plasmid name. This is often a 3-6 letter representation of the gene (or DNA sequence).
Often researchers will add a lower case letter to the beginning of their insert abbreviation to specify what species it is. Example: ‘h’ is for Human (homo sapiens), ‘m’ is for mouse (mus musculus), ‘r’ is for rat (rattus rattus or rattus norvegicus), etc.
Add any tags or fusions that are on your insert. Typically you would list any tag or fusion protein in the order they appear in the plasmid and their relative position to the insert. Example, if you have a Flag tag on the N-terminal of your insert, you would list it first.
e.g.   pBACKBONE-Flag-hGene
If there was also an EGFP fused to the C-terminal of your insert you would list it after the insert.
pBACKBONE-Flag-hGene-EGFP
If your insert contains a mutation or modifcation, this should be included in the plasmid name.  Mutations are generally listed as the amino acid change and not a nucleotide change. The proper way to denote an amino acid mutation is to list the one letter abbreviation of the wild type amino acid immediately followed by its position (number) relative to the start Methionine (Met) followed by the one letter abbreviation of the mutated amino acid currently at that position.
Check for more information at Addgene.com they are the largest plasmid repository in the world.
By collisions I'm guessing you mean naming your plasmid something that is already "taken." This is a benefit of submitting to a repository, they will ensure this doesn't happen.if your planning on filing a patent, your parent attorney will do it.

One of the most common methods (described by AddGene) is p (for plasmid), followed by the name of the backbone, a dash, and inserts delimited by more dashes. From this we get things like: pBluescript-CMV-mACT1-GFP.
Another method which I prefer is to name all your plasmids in the format given in the question: pABC123. Here ABC is a 3 letter designation that the researcher should consistently use for every plasmid they create (often their initials), and the numbers are sequential (padded with zeros for better sorting by programs).
AddGene is one of the largest plasmid repositories out there. Unfortunately, collisions are a common problem - you should always search the name of a plasmid before assuming things based on the name. While the above two strategies help reduce the odds of collision, there are very few 3 letter combinations that haven't been taken.


text:
What's the meaning of this notation?
In Wang et al., the authors state on page 663 at the top that

Furthermore, Bax-/- Bak-/- cells were completely
  resistant to paclitaxel-induced apoptosis.

What's the meaning of the -/- notation? Bax and Bak are proteins involved in apoptosis.

-/- means both copies of the gene (both alleles) are knocked out

I guess I need to brush up on my molecular biology, but by "both copies" you mean, both copies present during mitosis?

As chromosomes come in pairs (bar the X chromosome in males), each gene is also present twice. -/- means both are knocked out.


text:
Why does a cockroach not die even after decapitation?
Why does a cockroach not die after its head is cut off?

Could you give a citation referring to this fact?

Based on an article here, unlike humans, cockroaches have an open circulatory system. They don't have a huge network of blood vessels like that of humans, or tiny capillaries that you need a lot of pressure to flow blood through. Hence after you cut their heads off, very often their necks would seal off just by clotting.
According to the article cockroaches breathe through spiracles, or little holes in each body segment. Plus, the roach brain does not control this breathing and blood does not carry oxygen throughout the body. Rather, the spiracles pipe air directly to tissues through a set of tubes called tracheae. In addition cockroaches are poikilotherms, or cold-blooded, meaning they need much less food than humans do. Hence cockroaches can survive decapitation.

Although the answers to date are all factual and sufficient to answer the question why cockroaches would live without its head, some answers don't seem to be necessary as explanations.
Summarizing the given answers so far.

Roaches' simple  circulation would still function without its head.
Roaches' decentralized respiratory system can still function without its head.
Roaches are cold-blooded and demand less energy.

However, chickens can live without its head as long as the injury does not significantly damage its brain stem, which controls the animal's vital reflexes such as respirations.

Chickens do have complex network of blood vessels and capillaries.
Chickens don't breathe via spiracles and do have centralized respiration system like us.
Chickens are warm-blooded.

Thus, an animal (such as a cockroach) can live headless if its remaining organs can still control its "vital functions".

"Thus, an animal (such as cockroaches) can live headless if the remaining organs can still control its "vital functions".- until & unless it's internal food resources are depleted...

@souvik bhattacharya However, Mike the Headless Chicken from SYK's link finally died by suffocation. It could eat if fed.

Cockroaches are insects which means their brain is distributed.

The predominant characteristics of the cockroach central nervous
  system (CNS) are its segmented nature and decentralization of control
  processes (Ganihar et al., 1994; Pipa & Delcomyn, 1981)

.
 There is a pair of ganglion on each segment- head, thorax and abdomen. The ganglion on head is controlling the antennae inputs,proboscis,mandibles,eyes etc. When we cut off its head the ability to control all the above described organs fails(although, that doesn't matter because these organs are also decapitated) & it can't eat.. but the ganglion on the thorax is actually responsible for the breathing and digestion of food(with the help of ganglion on the abdomen). So if there is any food in the gut it will be normally digested and cockroach can live days consuming this energy. Also when head is gone there is no need to provide resources for the organs in head. So it can live more days by saving these resources.Plus, it can copulate if it is placed properly and this copulation is controlled by the ganglion on the abdomen.

Hello and welcome to SE Biology! It would be great if you added some references to support your response!

It's part of writing a good answer @souvikbhattacharya, Bez is perfectly right to request this - consult the help pages

@GriffinEvo , I get your point...but what if I already know that the answer provided is correct???

ok..I get it..it's for greater good...

@griffinEvo: :)