text:
How copy number variation thresholds are defined in GISTIC
I am having trouble trying to understand how GISTIC discretize copy number variation to values -2, -1, 0, 1, 2. I am using TCGA copy number variation for ColoRectal Adenocarcinoma.
In cBioPortal FAQ it is written that:

For TCGA studies, the table in all_thresholded.by_genes.txt (which is the part of the GISTIC output that is used to determine the copy-number status of each gene in each sample in cBioPortal) is obtained by applying both low- and high-level thresholds to to the gene copy levels of all the samples. The entries with value +/- 2 exceed the high-level thresholds for amps/dels, and those with +/- 1 exceed the low-level thresholds but not the high-level thresholds. The low-level thresholds are just the 'amp_thresh' and 'del_thresh' noise threshold input values to GISTIC (typically 0.1 or 0.3) and are the same for every thresholds.
By contrast, the high-level thresholds are calculated on a sample-by-sample basis and are based on the maximum (or minimum) median arm-level amplification (or deletion) copy number found in the sample. The idea, for deletions anyway, is that this level is a good approximation for hemizygous given the purity and ploidy of the sample.

The low-level thresholds are quite clear, while the high-level threshold not (the ones used to label +/-2 values).
I tried to reverse engineer the discretization function (the cutoffs are not available on firebrowse). The best solution I found is, for each sample, to:

split the copy number values in two groups (amplified - positive values, deleted - negative values)

for each group (amplified - deleted)

compute the median copy number value inside each chromosome arm
take the maximum (minimum for deleted group) median value across arms and use it as higher (lower) threshold

I tested it using the files:

all_data_by_genes.txt
all_thresholded.by_genes.txt

trying to get the correct discretized value (-2, -1, 0, 1, 2) of the second file from the first. However, a small part of the values are not correctly mapped. Am I missing something?

The best solution is to use only the broad alterations, using the file broad_values_by_arm.txt.
In particular, for each sample, the highest threshold is computed as the sum of the noise (low-level) threshold (e.g. 0.1) plus the maximum value of copy number variation for the sample over all the arms. Similarly, the lowest threshold is the minimum value for the sample over all the arms plus the negative noise (low-level) threshold (e.g. -0.1).

if: Total copy number (major + minor allele copy number by SCAT R) for SMAD4 in a sample = 4
Th estimated ploidy by SCAT for this sample = 4.043696
So, the segment mean (required for GISTIC) for SMAD4  = log2(2/4.043696) =  -1.015675
If I put -td threshold in GISTIC as 1.25, do I miss this loss for SMAD4 in GISTIC output because this is > -1.015675?
In the other word, does -td = 1.25 is the same when I ignore any segment mean < -1.25?


text:
Identity by descent among unrelated individuals
I was reading a couple of papers which talk about IBD (Identity by descent) among unrelated individuals (for eg. http://www.pnas.org/content/109/4/1193.long). However they do not seem to clearly define what they mean there. I was wondering how IBD is defined in such a context. I'd appreciate any help (especially suggested references to look this up).

They are not close relatives of each other I suppose. You are right I think, there should be an exact definition.

I formulated an answer on this post that is very relevant. I was however quite confused and I am not sure whether or not several definitions of IBD exist in the literature.

In the context of GWA studies the IBD is usually different than what defined in population genetics. It represents the relatedness across individuals defined simply as the genotypic correlation between them. In other words, you run a linear regression using two individual genotypes to get an r-sq that can be interpreted as the proportion of similarity in their genetic material. r-squares of 0.5, 0.25 and 0.125 represent respectively parent–offspring, full-sibs, first cousins relationship. This is used as a  control as GWAS statistical tools assume a population of unrelated individuals.

The definition of IBD is always the same - an allele or segment of alleles which is shared between two individuals because of descent from a common ancstor.
In the context of this paper, the authors are referring to segments of the genome between individuals which are IBD. In this case, they are looking at recently isolated populations who are likely to share longer stretches of IBD with one another. This is the case because each individual within a relatively isolated population is likely to be, on avergae, more related to another individual than in an outbred population. In general, it it much easier to detect longer segments of IBD than shorter segments, and this is why they choose to study isolated populations. Also, you can be much more sure that longer IBD segments will share a common ancestor with one another.
More specifically, they define a 'large' IBD segment is one which is longer than L centimorgans of length. Additionally, they define 'IBD-sharing' level between two individuals, as the probability that a randomly chosen genomic position on homologous chromosomes from each of the individuals lies in a large IBD segment shared by the two individuals. Thus IBD sharing takes values between 0 and 1.
There are several different methods, such as PLINK, fastIBD and GERMLINE which can identify IBD segments and their corresponding lengths from genotype data.
If you are interested in a relatively accessible guide to understand the principles of both single locus and segmented IBD, then I would recommended checking out Graham Coops's population genetics notes, section 2.2.

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text:
How many smaller muscles compose the interosseus muscle in the human hand?
When looking at Wikipedia, I read that the interosseus muscle is actually composed of 3 muscles, but on the French Wikipedia, they talk about a 4th muscle.
So how many interosseus muscle components are there, 3 or 4?

The number of interosseous muscles is not constant, because of the evolutional process continuing in modern generations.
Some individuals have 4 interosseous muscles, other have three, however there are still debates about the subject:

+

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text:
Queller's 1985 version of Hamilton's rule
Queller 1985 ("Kinship, reciprocity and synergism in the evolution of social behavior") provides a generalization of Hamilton's rule that allows for non-additivity. To accomplish that, Queller writes the fitness of an individual as
\begin{align}
  W = W_{0} - CP + BP' + DPP'
\end{align}
where $W_0$ is the baseline fitness; $P$ is the phenotypic value (1 for altruist or 0 for nonaltruist); $P'$ is the phenotypic value of the interacting individual; $C$ is fitness cost if $P=1$; $B$ is the fitness
benefit if $P'=1$; $D$ is the deviation from additivity of $C$ and $B$ if
both were altruistic (i.e., $PP' = 1$).
Queller then substitutes this equation into Price's equation $\Delta G = Cov (G, W)$, where $G$ is the frequency of altruism allele in the focal individual($0$, $1/2$ or $1$). The resulting equation is:
\begin{equation}
  - \bar c + \bar b \frac{Cov(G,P')}{Cov(G,P)} + \bar d \frac{ Cov(G,PP') }{Cov(G,P)} > 0
\end{equation}
where $\bar c$, $\bar b$, and $\bar d$ are the sample means of $C$, $B$, and $D$.
My question is: how did Queller arrive at the sample means $\bar c$, $\bar b$, and $\bar d$? I understand that $Cov(aX,Y) = a\, Cov(X,Y)$, provided that $a$ is a constant. But what Queller is doing here is different; he seems to be saying that $Cov(AX,Y) = E(A)\, Cov(X,Y)$.

It is just worded a little wierdly in my opinion. The key line in the paper is: 'Fitness components are also defined for all individuals, for example, $C$ is defined, even for a non-altruist, as the cost it would incur if were altruistic.'
Essentially, if it doesn't matter what individual you are you always pay the same cost, then $C$ is a constant. This is pretty much the definition of a constant! The expectation of a constant is just the constant, $E(C) = C$.
The reason it works is that to find whether or not the cost is realised, Queller simply multiplies by the focal individual's phenotype value $P$, which is either 0 or 1. So either the individual pays the cost or it doesn't.

I think Queller's discussion of his 1985 model in his 1992 paper "Quantitative Genetics, Inclusive Fitness, and Group Selection" (p. 552) is better worded. There he writes the C, B, and D as regression coefficients.


text:
Why is it $q^2$ for the individual count in hardy weinberg?
My understanding:
In Hardy-Weinberg problems the frequency of a homozygous recessive genetic occurrence in a population is $q^2$. So if 1 in 100 people in a population have albinism (homozygous recessive disorder) then we say the frequency is $q^2=1/100$.
We then say, to find the frequency of the allele count $q$ that $q=\sqrt{1/100}= 1/10$.
I don't understand why we say this. Why would the allele count be the square root of the population frequency? There's 2 alleles per person. Why isn't it x2 or /2 instead?
I suppose my problem is understand what exactly is p and q.

p and q are allele frequencies. Did you search anything about Hardy-Weinberg equilibrium.

Yes but I'm having problems seeing why why square them.

Squaring is for genotypes.

This seems a very nice site: http://www.nature.com/scitable/definition/hardy-weinberg-equation-299. I'm not answering this because it's too long ago I took this class, but Nature has awesome basic explanations of a lot of stuff. And it's credible. Check it out!

WYSIWYG you're not understanding the depth of my question.
I think this may actually be too mathematically difficult to answer on biology stackexchange upon further examination.

@paze If you think so,you are dramatically overestimating the difficulty of this question.

Could you answer it then please?

Okay . If p is probability of allele-A then what is the probability of A mating with another A; p×p=p²

First of, let me correct your equation: $q = \sqrt{\frac{1}{100}} = \frac{1}{10} = 0.1 ≠ 10 $.
From allele frequency to genotype frequency
Imagine you were to randomly sample an allele from a population of allele where the allele A is present at frequency $q$. What is the probability that you draw allele A? Answer: $P(A) = q$. Now, put this allele back in the pool and imagine you have to draw two alleles. What is the probability that the two alleles are A. Well it is the probability that the first allele is A times the probability that the second allele is A, it is $P(A) \cdot P(A) = q \cdot q = q^2$.
From genotype frequency to allele frequency
Therefore, under Hardy-Weinberg conditions, if the allele A is at frequency $q$, then the homozygote genotype AA is at frequency $q \cdot q = q^2$. Now let's denote the frequency of the genotype AA by $f_{AA}$. You know that $f_{AA} = q^2$ from the above though experiment. If you take the square root of both sides, you get $\sqrt{f_{AA}} = \sqrt{q^2} = q$. In words, the frequency of the allele A is the square root of the frequency of the genotype AA.
Recessivity and dominance
Btw, you'll note that those calculations tell nothing about the patterns of dominance/recessivity of alleles (Hardy-Weinberg principle assumes no selection anyway).

also 1/100 != 1/10

Ha ha oops. I forgot the square root. Thank you!

To understand population genetics and the Hardy-Weinberg equilibrium you first need to clearly separate genotype frequencies (the frequency of individuals in a population having a genotype) and allele frequencies (the frequency of an allele in the population gene pool). In your question p and q represents allele frequencies, while p2, q2 and 2pq represents genotype frequencies (if $p=P(A)$, $p^2$ is $P(AA)$). Genotype frequencies can be thought of as the probability that two particular alleles are located in the same individual, and the calculation of these probabilities is a simple application of the multiplication rule of probabilites for independent events.
Therefore, if the allele frequency p is 0.2 the probability of having two copies of this allele is $p \times p = p^2 = 0.2^2 = 0.04$. If there are only two alleles in the population, q has to be 0.8, which means that the other two genotype frequencies are $ 2pq = 2\times0.2\times0.8 = 0.32$ and $ q^2 = 0.8^2 = 0.64$. As you can see, these genotype frequencies also sum to 1, since they represent the genotypes of all individuals in the population,

In Hardy-Weinberg problems the frequency of a homozygous recessive
  genetic occurrence in a population is q2.

Sort of but not quite. If the locus has two possible alleles, $A$ and $a$, the frequency of each allele in the population is $p$ and $q$ respectively. If the population size ($N$) is 500 diploid individuals, there are 1000  loci ($2*N$, because of diploidy) which each could have either $A$ or $a$, and each of the 500 individuals could have the genotypes $AA$, $Aa$, or $aa$. If we know that the population of loci has 100 copies of $A$ then $p = 100/1000 = 0.1$, and $q$, the frequency of $a$, must then be $1-p = q = 0.9$.
The value of $q^2$ tells us how many individuals in the population, under the assumptions of HWE, will be of the genotype $aa$ - it says nothing about the recessivity (or dominance) of the allele, nor the phenotype. In the example above, $q^2 = 0.9^2 = 0.81$ - under assumptions of HWE 81% of the population will be genotype $aa$.
In terms of math it is simple probability theory. If we have a bag of coloured marbles, 5 red and 5 blue, the frequency of red ($p$) is 0.5, and blue ($q$) is 0.5. If we draw one marble from the bag, the probability of the marble being blue, $P(blue)$, is equal to the frequency of blue, $q$, which is 0.5. If we then return the marble to the bag and make a second draw, the probability of drawing a blue marble is again $b$, 0.5. The probability of both of the drawn marbles being blue $P(blue) * P(blue) = 0.5 * 0.5$, or $q^2$. The probability of drawing one red and one blue is $2 * p * q$, and probability of two red marbles is $p^2$.


text:
Are amantadine and rimantadine MOAs unknown to evolution?
Are any natural (human or otherwise) antiviral mechanisms similar to the antiviral mechanisms of amantadine and rimantadine, or are these mechanisms undiscovered by evolution? Are drug researchers discovering completely new mechanisms to attack viruses?
http://www.rapidreferenceinfluenza.com/chapter/B978-0-7234-3433-7.50014-1/aim/mechanisms-of-action-of-antivirals
The mechanism by which antiviral drugs (amantadine and rimantadine) interrupt the replicative cycle of influenza is illustrated. M2 inhibitors prevent the M2-mediated acidification of the interior of the virus while it resides in endosomes and the subsequent uncoating of the viral genome, thus inhibiting viral replication. Neuraminidase inhibitors (NAIs) prevent cleavage of sialic acid residues and thus newly formed virus cannot be released from the cell surface to infect adjacent cells; also, virus particles remain associated to one another.

Welcome to Biology SE. It is an interesting question, but I don't know if there are any experts on animal virus life-cycles in this group. In terms of evolution and discovery, there are definitely pharmaceutical companies (the ones I've heard of were based in Japan) who maintain cultures of purified soil microbes, and then assay the microbes' used culture media for "natural" compounds that affect a lucrative biological process.


text:
What is Meriva Phytosome Curcumin?
What is Meriva Phytosome Curcumin other than being a food supplement?
Is it a plant? A type of plant extract?
I googled it but still couldn't figure out exactly what it is.
The reason I'm asking is because I came across the following list in a site selling vitamins and other food supplements:
Meriva Phytosome Curcumin
Turmeric (Curcumin)
Turmeric Formulas

It wasn't clear to me if Meriva Phytosome Curcumin is a specific kind of curcumin since it seems to be sold under a few different brands.

Well, http://meriva.org states that

Meriva® is a patented formulation of curcumin, a dietary phenolic, with soy lecithin (non-GMO)(1). The two compounds form a non-covalent adduct in a 1:2 weight ratio, and two parts of microcrystalline cellulose are then added to improve formulation, with an overall contents of curcumin of 20%

A phytosome is

[...]  a complex of a natural active ingredient and a phospholipid.
It is claimed that phytosome increases absorption of "conventional herbal extracts" or isolated active principles both topically as well as orally.
The complexation with phospholipid has been applied to many popular herbal extract or active molecules including [...] curcumin isolated from turmeric [...].

And Curcumin is

[...] is a diarylheptanoid. It is the principal curcuminoid of turmeric, which is a member of the ginger family (Zingiberaceae). Turmeric's other two curcuminoids are desmethoxycurcumin and bis-desmethoxycurcumin. The curcuminoids are natural phenols that are responsible for the yellow color of turmeric. Curcumin can exist in several tautomeric forms, including a 1,3-diketo form and two equivalent enol forms. The enol form is more energetically stable in the solid phase and in solution.

So, Meriva Phytosome Curcumin is a phytosome of curcumin developed by Meriva.

When I googled it I didn't reach any of those (except curcumin), perhaps because Google results are personalized...

@traveh It's not that it's personalised, it's that you have to know how to look for the answer. Adding things like "NCBI" or "PLOS ONE" to the end will help you find scholarly articles (same with using google scholar). Also, it might help to break things down into different parts, like searching for Miriva, phytosome and curcumin sepeartely. If you add quotations around a part of the search, that part is prioritised by google.

To summarize terdon's excellent answer:
curcumin is a chemical found in the plant turmeric (Curcuma longa)

I know what curcumin is, I was wonder what is "Meriva Phytosome Curcumin" specifically. :)


text:
Why do these earthworms stay between the road lines?
This article shows pictures of earthworms during floods in Texas. The worms ball up, supposedly in order to survive the floods.

Photo Credit: Texas Parks And Wildlife Department
Can anyone explain the phenomenon a little? I can't seem to find anything about this online. I know that earthworms surface when it rains for oxygen, but it seems weird that they meet in the middle of the street.

Interesting...It is almost as if earthworm herds perform gradient descent (or ascent in this case) like an intelligent robot to find the driest place in the surrounding area and moves to that location - but I wonder if the earthworms were moved in between the yellow lines intentionally to induce some journalistic shock value

Agree, we know they've been poked with a stick.
Perhaps the reason is not biological but hydrological. Roads are crowned to improve drainage, so in a flood the center is most likely to be exposed as the water recedes.  There's also something dark in the mass that  I can't make out but it doesn't look like worm; maybe it's important.

The first question: what the worms do on the ground during the flood? One of the answers to this question is -
"It gives them an opportunity to move greater distances across the soil surface than they could do through soil," said Dr. Lowe. "They cannot do this when it is dry because of their moisture requirements."
The second question: why they form ball after moving to the ground. There are two answers to this question:
First, as a part of surviving mechanism to prevent drying. As you can see, they cannot come back to the soil across the asphalt, thus they form balls and wait the weather to improve.
Second reason to form the balls - communication:
"The earthworms use touch to communicate and influence each other's behaviour, according to research published in the journal Ethology.
By doing so the worms collectively decide to travel in the same direction as part of a single herd."

I think another aspect to this has actually nothing to do with worm biology and instead relates to the roads and cars:

Roads are typically graded so that water runoff moves off the roads -- this usually means that the center line(s) are a high point in the road.

See here for example
As a result, the worms would experience the least amount of water and runoff force if they congregated in the middle.

Two "forces" could prevent formation of balls in the middle of either lane.

Water runoff might be stronger there preventing a stable "footing" for the worms to remain.
Even if balls formed in the lanes, car traffic would almost certainly destroy them leaving little evidence of them behind (especially if rain was washing them away).

I'm sure the other answers play a part in this phenomenon aswell, but I was taught that worms do this because the worms dont have eyes, yet they still can sense light from dark, because staying out in the sun too long would dry them out,
So they are between 2 yellow lines (to them they think that must be light) and the middle line is dark (the asphalt itself) so ultimately the worms are very confused and think they are somewhere safe and dark (like underground)
They pass the first line trying to get through the light in search of darkness, and get stuck in the middle because they think the next line is more light. They sadly believe they have found a safe haven.

Thank you for your answer but it would be great if you could cite some authoritative references. References are important so that one can verify the information and can learn the details of the topic. Good references include peer-reviewed articles, books and websites of reputed academic/scientific organizations. Wikipedia is also good if it in turn is properly referenced.

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text:
How are smell and taste in fish differentiated?
The senses of taste and smell in different fish classes are described as two distinct senses; smell is mediated by the nasal openings, and taste by epithelial taste buds.
They are both forms of chemoreception and therefore it is not clear to me what intrinsically defines them as two distinct senses. The more so because reception of chemical substances is mediated by water.
What defines them as different senses? Is it only the difference of receptors that defines them as two distinct senses, or are there other reasons to differentiate them?

One difference is that they are controlled by different parts of the brain. But both are GPCRs and perhaps have common evolutionary origins. I am in a hurry now so cant look up the answer but I can point you to this article that talks about functional difference between olfactory and gustatory response towards the same chemical.

@WYSIWYG - I hve waited a month before answering, but I am assuming you have other priorities now as a mod. I hope you don't mind me taking this opportunity to answer this interesting question  :)

@AliceD No problem at all. You can add my comment in your answer if you want. That article was not accessible to me then.

one thing is not clear to me... are you asking about taste-and-smell of fishes  to us when we eat them? or you are asking about fishes's perceptions about their underwater environment?

Short answer
One way to distinguish between the olfactory and gustatory system in fish is by their  anatomical differences. For example, olfactory receptors are clustered in the nasal region, while gustatory receptors are scattered in the head region and beyond. In turn, olfactory information is sent via a single cranial nerve to the brain, while the gustatory system includes three cranial nerves.

Background
The olfactory and gustatory system both receive their inputs through chemoreceptor cells. The chemoreceptor proteins in both systems are G-protein coupled receptor systems. However, the olfactory and gustatory systems are anatomically separated.
The olfactory end organ is in fish comparable to that in humans, namely sensory epithelia situated in nostrils. The olfactory receptor cells form axons that are grouped into the olfactory nerve (cranial nerve I). The nerve innervates the olfactory bulb, where its axons synapse onto mitral cells. Mitral cell axons group into the olfactory tract that projects to the telencephalon in the brain.

Schematic of olfactory system of a fish (not all structures shown). Source: Global Warming Australia.
The gustatory end organs are less well anatomically localized. The taste buds can be found in various structures including gills, barbels, fins, oral cavity and pharynx, dependent on the species. Unlike the olfactory system, gustatory information is transmitted to the brain via three separate cranial nerves: facial (cranial nerve VII), glossopharyngeal (cranial nerve IX) and vagal nerve (cranial nerve x). Normally, the facial nerve innervates taste buds on the extraoral surface, the glossopharyngeal on the anterior part of the oral cavity, and the vagal nerve on the pharynx. The facial and vagal nerves respectively terminate in the facial and vagal lobes in the medulla. The glossopharyngeal nerve terminates in a dorsal medullary region between the facial and vagal lobes.

Reference
- Hara, Rev Fish Biol Fisheries (1994); 4: 1-35


text:
How does ecology differ from biology?
What precisely is ecology? How does it differ from biology? Because I never studied biology after high school, please explain as if I were 10 years old. I only know that ecology is a subset of biology
I tried some dictionaries but they  didn't  adequately discriminate. I tried to find an explanation from a scientist: the following appears to claim that only ecology concerns some organism's external interactions with other entities? But how? Biology must also? For example, suppose that someone studies prions' interactions with humans, and not just prions. Then this is biology, not ecology?
Source: by  Matthew Fraser, PhD Candidate (Marine Ecology) at University of Western Australia

So what makes us fully fledged marine ecologist different from our biologist counterparts?  Well, I think that marine ecology is even cooler than marine biology because as marine ecologists we link what we know about the biology of a given species with other plants/animals and the environment as well. [...]
If we were splitting hairs, ecology is technically a form of biology, but I felt the need to write this post given how passionately I see some researchers stating that they are in one camp or another. [...]  But as an ecologist (albeit a biased one!) what gets me excited isn’t just finding out how the amazing plants and animals we find in the ocean work, but how they interact with each other and their environment, explaining why we see certain species in some places and not others!

Does the Wikipedia article not adequately define ecology for you? "Biology is a natural science concerned with the study of life and living organisms, including their structure, function, growth, evolution, distribution, and taxonomy" whereas ecology "is the scientific analysis and study of interactions among organisms and their environment." What other information are you looking for?

@MattDMo Sadly, no. The definition there for ecology also applies to biology; biology also concerns interactions among organisms and their environment.

Ecology is a subset of biology, and also includes some elements of other disciplines as well, including earth science. "Biology" is an extremely broad term encompassing a huge number of sub-specialties. I urge you to read the entire article I linked, it explains the field of ecology quite well.

The definition of ecology fits within the definition of biology because it is a field of biology. There is no clear cut between ecology and biology, it's like trying to find a clear separation between physics and astrophysics, sharks and fish, humans and mammals, our sun and stars - they are just definitions, ecology satisfies the criteria to be defined as biology but not all biology is ecology.

Some might argue that, given its interdisciplinary nature, ecology does not fit  entirely within biology.  Think human cyborgs and mammals.

Ecology has two meanings. The popular and the scientific meaning.
Ecology: the popular definition: Here the term ecology is probably quite poorly defined. To my gut feeling, the concept relates to the concept of global change. It encompass many fields such as biology (ecology (in the scientific sense), evolutionary biology and conservation biology especially), ethics and moral, politics, meteorology, public policy, ...
Ecology: the scientific definition: Ecology is a subfield of biology and earth sciences that studies interactions among organisms and their environment. interaction is an important word here.
Biology has a much broader meaning. Biology is the science that studies life. Biology studies the structure, the ecology (impact on their surrounding), the evolution, development biochemical processes, etc.. of living things. Biology is a very big field of science. A researcher in biology will probably not really consider him/herself as a biologist but rather as a molecular geneticist, a neurologist, a epidemiologist, a plant physiologist, a biochemist, a bioinformatician, a system biologist, etc.. For example, I would appreciate to consider myself as a population geneticist rather than as a biologist as there are many fields of biology I know nothing about. For example, I am a pretty bad naturalist.
In short, ecology is to biology what optics is to mechanics is to physics. Some people may not like this comparison as mechanics might take a larger part of physics that what ecology does to biology. Earth scientists may not like this comparison as well, as they are part of ecology without necessarily feeling like being part of biology. But anyway.
From the text you cite

[..] as an ecologist [..] what gets me excited isn’t just finding out how the amazing plants and animals we find in the ocean work, but how they interact with each other and their environment [..]

It shows that indeed ecologist are interested in the interaction between organisms and between organisms and their abiotic environment. Matthew Fraser says "he's not only interested in how they work". 'How they work' is obviously an extremely inaccurate sentence. A less misleading reformulation would be: I am not interested in everything about the biology of marine animals, "I am especially interested in how animals interact with each other and how they interact with the environment", but obviously that is less exciting for the reader. The goal of Matthew I guess was to create the interest and the excitation of the reader (or audience) on ecology and for this purpose he kinda implied as ecology being more than biology, while ecology is only a subfield of biology.
For more information, wikipedia is your friend!

Yes, there is overlap and the line is rather fuzzy.  As a distinct discipline within biology, ecology is a fairly young science.  The word itself did not exist until 1866.
Biology is focused on living things usually at the organismal level or smaller (organs, cells, proteins, biochemistry, etc.)   Generally when biologists consider abiotic factors, it is how those factors affect an organism (water, light, air needed to live).
Ecology usually looks at the organismal level and higher (species, population, community, etc.).  Ecologists also study the two-way interaction between biotic and abiotic factors, how organisms change their habitat, and how the habitat changes the population.
Modern biology is such a large subject that most scientists will specialize in a sub-field such as botany, zoology, genetics, etc.  One of those sub-fields is ecology, but ecology is also interdisciplinary and draws from fields beyond biology  like chemistry, geology, climatology, etc.
A biologist might study one or two species of fish in a lake and the plants they feed on.  An ecologist might study the lake itself, how the water got there, how an invasive species is changing the lake's biodiversity.


text:
What makes heavy metals toxic?
I'm not sure all heavy metals are toxic, but most are.
Some may be present as insoluble compounds, or otherwhise hard to get into an organism, but that's a side aspect.
For example, I would count copper as toxic, even if some salts are triggering to vomit just too quickly to swallow poisonous doses.
So, in this sense, are they all toxic?
Is the toxicity based on the same mechanism?

http://en.wikipedia.org/wiki/Metal_toxicity

Heavy metal toxicity is actually due to the inhibition of the body's natural enzymes as well as the denaturing of proteins that it causes.
Here, Tchounwou et. al go into detail about the mechanics of different heavy metals and how they interact with the human body specifically. It even suggests ways that the heavy metals could be introduced.
A short summary on the damage caused by what was studied:

Arsenic inhibits DNA repair.
Cadmium toxicity isn't well known, but they think it causes single
strand DNA damage.
Chromium causes chromosomal abnormalities thought to be caused by
oxidative damage.
Lead prevents the body from interacting with Calcium which is a key
element in many biological processes. It also competes with other
metals for the active sites in different enzymes.
Mercury depletes the body's antioxidants.

So to answer your question, no, the heavy metals are not all working on the same mechanism. It all depends on what dose, how it was introduced, and the particular metal. Also, anything can be toxic in the right amount (people have died from water toxicity in drinking contests).

Water is not toxic. Excess water causes hypervolemia.

Fatal water intoxication is what I learned it was called in school.

Yeah.. Actually it is not an intoxication by water, you see. Excess water just dilutes up the electrolytes. Water is not inherently toxic.

Huh, wow I didn't know that, thanks @WYSIWYG I never actually looked into the mechanics of it.


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DNA extraction methods for hair?
TLDR: Can anyone state a extraction and isolation method(s) for genomic DNA for hair that will be used for PCR, in detail is preferable since I am a novice.
I tried googling for DNA extraction methods for hair(follicles and/or root) and found various sources, the one that had the most detail involved the use or organic compounds we do not have access to. Is their preferred method of extracting DNA from hair, given that the genomic DNA would be in low amounts, I figure that might have something to do with the extraction process.

Can you please give us some background? It would make answering the question easier.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0069588

@Chris          That was pretty much all the background there is, I am a undergrad novice who needs to extract DNA from hair for a proffesor's research. He sent me on this task as a way of self learning i believe, but I guess I am not "up to snuff", given my asking here.

@MattDMo        I saw that source, but i lack the powder(s) to do it.

@RoSiv When you write that you have no access to certain organic compounds without specifying what you can do, it is hard to give recommendations.

@Chris          This speaks to my ineptitude i suppose, I have no access to the phenol or chloroform and cant do the organic extraction method. I do not really want to either, given i have never worked with it before. I was hoping there would be a "simple" solution with alot of "common" lab ingredients.

I'm sorry, you don't have access to laundry powder? I find that very difficult to believe.

@RoSiv These are important informations that belong into your question. I am used to  work with hazardous chemicals (with the right protective equipment) as  this is part of my training. Nothing special about it.

@Chris               If I were to do the organic, phenol/chloroform extraction, would you have any advice or suggestions, sources/methods even?

I've been trying to figure out something that works for some time.  I have recently tried 3 cheap protocols using commonly available lab reagents.  I was using buccal samples (0.2 ml of spit).
1) Boil the sample in Tris EDTA Buffer
2) NaOH Extraction
3) Direct N Lyse
I compared them to a genomic DNA extraction kit (FAST DNA Prep - MP Biomedicals).
I have heard lots of people use NaOH extraction to get DNA from tissue and cell preps, but none of the first three worked for me after 2-3 tries.  One of the people in my lab said that I could replace the bead beater with vortexing with glass beads.
I tried vortexing with beads with all four methods, including the kit and only the kit worked.  I got a PCR result from control primers.
When you look at the costs of getting all the ingredients for the buffers kits are not so expensive - $1-$2 per sample.
A lot of these kits can handle solid animal tissues, though the one I have doesn't specifically cite hair.  I would try it out.
I guess the point of my post was that there are lots of simple sounding published methods, but they don't always produce results without a bunch of debugging.  I know alkaline lysis has worked for several people I know and is the basis of the kits.  Its pretty simple.
That's my experience anyway.

Awesome to see you active (you are one of two with 20k+ and full privileges after graduation :-) ! However, I was wondering if the buccal cavity contains hair, given OPs question?

Great, interesting, +1!


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A request for an overview of the cranial nerves
Is there any resource that contains motor and sensory innervations, or pathways of all the twelve cranial nerves (i.e., cranial nerve I to XII)?
I have found this book chapter on the cranial nerves, but it is too broad for me -  I'm still at high school.

A lot of the information that you are looking for is in the book chapter, but I can understand how it might be overwhelming.  Unfortunately, anything "easier" is probably going to be too cursory and sugar-coated, so you may just have to slog through it and cherry pick what you need.  Also, you're in the perfect spot to ask specific questions about the material already! :)

"Too broad"?  to me that means something lacks detail, isn't specific enough.  It sounds like you find that chapter too dense or too deep.  Can you clarify?
What is the context, what do you already know, and what do you need to know?  (and what do you not need to know)

I am not entirely sure what you are after, but I (as have others that commented on this question) interpret your question as "The linked chapter contains too much technical information". Quite frankly, after scanning the book chapter, I have to agree with you. Therefore I have sought for a quick overview image of all the cranial nerves including their sensory and motor targets.

Encyclopedia Britannica has published all the cranial nerves and their sensory and motor innervations in a single comprehensive figure:

Cranial Nerves and their targets. Source: Encyclopedia Britannica
I can highly recommend this online encyclopedia. Their articles are more concise and better accessible than similar topics on wikipedia. Moreover, this encyclopedia is not freely editable by everyone on the planet, and everything I have seen so far on their website is credible.

This is exactly what I need! Thank you for helping me!

@Ridho - my pleasure! :)

Very nice find!

If you're still learning the names and functions of all 12 cranial nerves, something like this page may help you get ready for more in depth material like the chapter you found.
https://faculty.washington.edu/chudler/cranial.html
I like the fact that they include activities for each nerve to help give you one more way to remember their functions.


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Why do athletes see a dip in performance in their thirties?
I have noticed a lot of athletes hit their prime when they are in their 20s and that by the time they reach their 30s they are past it and start to decline. Great athletes tend to prolong their careers by adjusting their game strategy, but even so they can't do the things they used to do when they were younger. Examples of this are abundant in the NBA, NFL, MLB, NHL, football, etc.
Why do athletes suddenly have such a drop off in performance? What happens to their bodies,  muscles, etc that prevents them from doing what they once did? Can someone explain the biological/physiological reason for this?

A lot of sports cause damage to the body, compare the average retirement age of gymnasts and footballers to that of golfers and cyclists

That is a great point. I never thought of it like that.

The decline in athletic performance is a result of senescence; the question then becomes "why do we senescence?"
A number of questions on this site have addressed this. These include Why does evolution not make our life longer?, Why do we age?, and any number of others that one can pull up with a search for senescence. It is key to distinguish between proximate (how, physiologically ) and ultimate (why, evolutionarily) explanations. It's not entirely clear to me from your question which of the two you are asking.

I am asking about the physiological mechanisms. And I don't think simply saying they are getting old is succifient. By any normal person's standards, they can still compete at an exceptional level.

@StanShunpike Yeah, but normal people also drop off the same way.  By your mid- to late-twenties, your body is basically finished getting better simply through development and now only gets worse.

But why physically as opposed to mentally? Why doesn't the mind drop off the sane way?

Who says it doesn't?  We can keep learning of course but there's solid evidence that brain development has largely wrapped up by our mid- or late-twenties.


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If red blood cells have no mitochondria how are they able to metabolize glucose?
I have read that red blood cells (RBCs) metabolize glucose. However they don't have any mitochondria because there is just so much hemoglobin that there is no room for mitochondria without expanding the cell.
So how is it possible for them to metabolize glucose if it is mainly O2, CO2, H2O, fatty acids (in cell membrane), and hemoglobin?

What exactly do you mean by "metabolize glucose"? Glucose is mostly converted to lactate in red blood cells, but some is oxidized to CO2 by the pentose phosphate pathway. Are you askiing about metabolism to CO2?

I mean metabolism to atp and co2.

In humans (and all mammals), red blood cells lack mitochondria and therefore has no functional TCA cycle. They metabolize glucose mainly via glycolysis, forming lactate which is released from the cells; this yields 2 ATP for each glucose molecule, much less than complete oxidation (ca 30 ATP), but enough to support the red blood cells' energy needs.
There is some oxidation of glucose to CO2 in red blood cells though. This occurs mainly in the pentose phosphate pathway or "shunt", where 1 carbon of glucose is released as CO2, and the energy extracted is used to reduce NADP to NADPH, which functions as an antioxidant. The resulting 5-carbon sugars (pentoses) are then rearranged to a 3-carbon sugar (glyceraldehyde phosphate) which enter glycolysis again. Hence the term "shunt": 5/6 of the glucose carbon that enter actually comes back to glycolysis again.
By varying flux through the PPP, cells can balance the use of glucose for ATP (energy) or NADPH (antioxidant). Studies estimate that in human red blood cells, 10--30% of hexokinase flux is diverted through the PPP, and the remainder through upper glycolysis (see this and this article). This corresponds to 2--5% of glucose carbon released as CO2, and the remainder metabolized to lactate.
Note that the above apply to mammalian red blood cells. Red cells of other vertebrates, including birds and fish, retain both their nucleus and mitochondria, and their metabolism is different.

While hemoglobin makes up about 90% of the protein in an RBC, there are many other proteins present as well, including enzymes in the anaerobic pentose phosphate pathway, which is responsible for metabolizing about 90% of the glucose entering the cell (the aerobic pathway takes care of the other 10%). There are also proteins responsible for maintaining the oxidation state of the hemoglobin-bound iron atoms. The iron in oxidized hemoglobin, or methemoglobin is in the $Fe^{3+}$ (ferric) state, which is unable to bind oxygen. The NADH-dependent enzyme methemoglobin reductase converts the iron to the $Fe^{2+}$ ferrous state, which binds $O_2$. NADH just happens to be one of the most important products of the pentose phosphate pathway, along with ATP and 2,3–BPG, which helps regulate $O_2$ release from hemoglobin. NADPH is also produced by the anaerobic pathway, and is a cofactor in the reduction of oxidized glutathione, acting as one of the major reducing agents in the cell to protect against oxidative stress. Other enzymes such as superoxide dismutase, glutathione peroxidase, and catalase also help prevent or reverse oxidation. All of the oxygen moving to and fro results in the formation of reactive oxygen species such as superoxide and hydroperoxyl radicals ($\cdot{O_2^-}$ and $HO_2\unicode{x22c5}$) and peroxides like hydrogen peroxide ($H_2O_2$), necessitating the presence of these defensive proteins.

where do you get your numbers from? I've never seen any cell metabolize 90% of its glucose through the penthose phophate pathway. Typical numbers are more like 10--30% of hexokinase flux diverted through the PPP, and the remainder through upper glycolysis (see for example http://www.sciencedirect.com/science/article/pii/S0165022X99000056). In terms of carbon, this corresponds to 2--5% evolved as CO2, and the remainder metabolized to lactate.

I thought most of the anaerobic metabolism comes from glycolysis and lactic acid fermentation(which unless you are talking about fructose eventually turning into glucose or DNA or RNA does not involve the pentose phosphate pathway).

@MattDMo, also NADH and ATP is not produced by the pentose phosphate pathway, but NADPH is. On the other the "anaerobic pathway" (I assume you mean glycolysis?) does not produce NADPH, but does produce NADH and ATP. It seems like you have mixed up the names of the pathways?

@Caters, glycolysis and the PPP are interconnected, but yes, most glucose carbon in red cells is processed "straight" through glycolysis and converted to lactate. The PPP can operate to yield NADPH without producing ribose for RNA/DNA though. I posted an answer to clarify the details.

@Roland I apologize for not including all my sources - while a lot was found in the links I gave, I also based some of the answer on this page from the Children’s Hospital & Research Center Oakland.

@MattDMo I see, it really looks like you have mixed up glycolysis and the PPP as your description is pretty much exactly the opposite of that given on the page you're citing. I would suggest you edit your response for correctness.


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Why don't most animals have "heads" in the middle of their bodies?
For example, humans. It would seem like, to me, if our brains and eyes, ears, etc. were situated in our stomach area they would be more protected from harm and more central than up at the top in and on a fragile skull. The same goes for other organisms. For example, horses have eyes on the sides of their heads; why wouldn't the eyes be near their stomach area? To me, it would seem like it would make it more safe and the horse could still see alot. I looked at this question, but it didn't fully answer my question.

We generally define a "head" as something that comes at the top/front of the body. I think that, we're likely to ignore examples of animals with nervous systems / sensory systems not at the top/front of their body as "animals without heads" rather than "animals whose heads are not at the top/front". For example, sponges and jellyfish.
Some animals who do, arguably, have heads, have their heads in the center of their bodies:

Image by james_michael_hill (CC BY-NC-ND 2.0)

The evolutionary - developmental roots of head position (or having a "head" at all) go very deep (although despite this, some organisms, like the starfish above, shifted evolutionarily and shift developmentally from bilateral to radial symmetry).

Regarding your concluding line: evolutionary, radial symmetry came first?

@AliceD  Developmentally, starfish and other echinoderms start out with a bilateral body plan as larvae and only become radial as adults.  So they actually evolved from a bilateral animal and developed radial symmetry secondarily.  However, some other early-branching animal lineages like cnidarians (jellyfish, sea anemones, coral) and ctenophores (comb jellies) are more or less radially symmetric.

Point 2 is a little misleading, since the oral opening of a starfish is not really homologous to the head of a human or horse.

@augurar - Thanks for explaining; I was talking evolutionary, you were talking developmentally. Glad that is sorted out:) However, removing "evolutionary" in point 2 may help to clarify. Overall, nice perspective on this question. And yes, I agree. To define the oral cavity in star fish as the head is tricky.

Animals with a "front" and a "back" are known as Bilaterians.  There is ongoing scientific debate about what the most recent common ancestor of the bilaterians, or "urbilaterian", was like.  One proposed form is a simple wormlike animal with some form of eyelike structures, a segmented body with internal organs, and a centralized nervous system.  This is contrast to animals like jellyfish which have radial symmetry with a central mouth and a network of nervous system structures distributed throughout the body.
Bilateral animals often exhibit directional motion with a defined "front" and "back" end.  Eyes and other sensory structures are positioned at the front end so the animal can sense where it is going and what it encounters.  The brain is located near the eyes because these structures require fast, intensive information processing.  This process may also have been constrained by development, since evolution occurs by gradual modifications to the existing features of an organism.  The Wikipedia article on cephalization has some more discussion of this topic.

Here is an example of two possible urbilaterians, taken from (Hejnol & Martindale 2008):

Image (a) shows a "traditional" model with segmentation, an anteriorly-located mouth (light blue), and a central nervous system (yellow).  Image (b) shows an alternate model proposed by the authors of the paper with a mouth in the middle of the body and a decentralized network of neural tissue.
Hejnol, Andreas; Martindale, Mark Q (27 April 2008). "Acoel development supports a simple planula-like urbilaterian". Phil. Trans. R. Soc. B 363: 1493–1501. doi:10.1098/rstb.2007.2239.

The brain is located near the eyes because these structures require fast, intensive information processing. The visual system is among the slowest in the body. The argument may hold for the ears though.

@AliceD It's the slowest because the information being processed is so complex.  If the brain were farther away it would be even slower.  But of course this too is speculative.

Eyes and other sensory structures are positioned at the front end so the animal can sense where it is going: In the case of insects they often have 360-degree vision. So the eyes are rostral, yes, but not because they need to see where they are going.

Small correction: bilaterian doesn't actually mean an organism with an anteroposterior/dorsiventral axis. It primarily means that these organisms exhibit bilateral symmetry i.e. symmetry across left-right axis.

@WYSIWYG True, I was being somewhat general.  Having a front/back is not at all a synapomorphy of Bilateria, just a common feature within the clade.

Here too is a speculative answer, but evolutionary why questions are many times speculation, as it cannot be directly scientifically tested (there are no animals with a head in their tummies), only inferred in retrospect. I will sum up a few reasons to build the eyes and ears into a solid, rotational structure and not in the torso:

The eyes are hardwired to see depth. The most important depth cue is retinal disparity, which is defined by a slight difference in the positioning of the field of view on both the retinas. This retinal disparity varies between people because it is dependent on the exact distance between the eyes. Hence, babies must learn to judge depth, as it is subjective perception deducted from a flat retinal surface. Hence, you want the two eyes to be contained in a solid, unmoldable structure and not in a bodily structure that is subject to change due to adipose tissue (belly) or breathing (rib cage).
The ears are hardwired to sense direction. The auditory nervous system does this by measuring microsecond-delays between the sound arriving in both ears to sense the azimuth. Again, along the same reasoning as for the eyes,  the ears must be contained in a solid structure.
Directional hearing is less well-developed in the vertical plane, and when a sound comes from behind it may be hard to figure out exactly where it comes from. Also, pure-tone sounds are hard to distinguish in terms of elevation. Simply turning your head helps to re-locate the source to the side, or simply being able to see it. If you have to move the whole body, you lose time and effort. In case of a T. rex running in attack modus from behind, it means the difference of life and death.
Eating needs a mouth. Consider a bat using echolocation. If the bat targets a fly using echolocation, it wants to devour it. If the ears are in the belly, it still couldn't catch its prey. The same goes for vision (birds of prey) etc.

In horses and many other prey species, the eyes are on the sides of the head and have a largely non-overlapping field of view with reduced depth perception.

@augurar, yes but the hearing arguments still count. They are examples, not fixed arguments.

Many animals do not have external ears and sense vibration in a variety of ways.  In mammals, the ear bones evolved from former jaw bones, which evolved from the gill arches in fish.  So the positioning of ears on the head is more happenstance than an inevitable outcome of the demands of hearing.

@augurar - evolution is happenstance, but a fixed position is what counts here. And hearing is sensing vibration.

Right, but in this case mammalian ears are probably positioned on the head simply because that's where the structures they came from were positioned, not necessarily because that was the best place for them.

@augurar yes but it is about them being fixated not where they are. That's my only point. On the rib cage they move about and directionality is lost in the brain due to added degrees of freedom

Let us continue this discussion in chat.

I think part of the reason is that our distant ancestors were aquatic - fish, for us vertebrates*.  Living in the water, fish need to be streamlined, so a long, narrow body plan works well.  Given this, and adding in the often limited visibility underwater, it makes sense to put the mouth towards the front, and sense organs near them, since they get to the food first.
This body plan got inherited by the descendants of that first fish to crawl out on land.  It would require a major re-organization of the genes to get a radically different plan, and there was no great evolutionary pressure towards some different one.  In many cases the mouth & eyes in the front works best - for predators, of course, but also think of a giraffe trying to browse on trees if its eyes were near its stomach.  For most land vertebrates, food goes directly to the mouth.  Only a few types - humans, elephants, and so on - have anything like hands to get food at a distance.  (And if you look at an elephant, they do seem partway to a mouth near the stomach plan.)
If you think about creatures like the starfish, that have a central mouth, "brain", and sense organs, their food tends to be sessile.  The starfish commonly crawls on top of its prey, and everts its stomach to digest it, so their the radially symmetric body plan works well.
*I don't know that much about arthropod evolution, but am guessing similar logic applies.


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What do ants do with human finger nails?
There is place in my house where I cut my nails. Here, there is an ant hole where an ant colony is seen.
Whenever I cut my nails from here, they take my nails inside their hole. I was wondering what they do with them.
Do they protect their houses with them or feed them to their young ones?

How fast are your nails growing that you cut them daily? (I cut my finger nails about weekly, the toe nails even less often.)

Me too cut weekly. I was just kidding in comment to MattDMo's answer. :)

If nothing else, they can probably make  a throne for their queen out of this flexible material!

That is gross....

Based on the confliction of the two answers, can you take a photo of the ant closely so we can identify which ant it is?

Can't see the image..!

But please leave out the nails on the macro. If you do close-up those nails I will close-vote and bribe the moderators ;-)

@AliceD Gross for you, food for them. :D

My pet ant found this page by googling what can we ants do with all these fingernails we've collected.

@Imprisoned It's not gross. It's called curiosity to know science behind. :)

There are a number of papers studying the ability of fungi to metabolize keratin, the primary structural component of nails (as well as skin and hair). Ants are also known to cultivate fungi for nutrients, so this may simply be a case where the ants are bringing food for their "farm animals."

Nice explanation. Thanks :) Now, I will feed the hungry ants daily :D

It's true that some fungi can break down keratin, and that some ants cultivate fungi, but these two facts do not imply that this is what is going on here.

Do you have any evidence at all to support this? I agree that it makes sense as a possibility but that's not enough for accepting it as fact.

@terdon I never claimed to represent it as fact. The OP didn't state what part of the world s/he was in, and it's impossible to identify the ants in the picture. I stated "this may simply be a case ...", not "this is exactly what's going on, and no other explanation is possible." The other answer is just as much of a guess as this one. One couldn't know for certain unless they were on location, excavated the anthole, and studied the whole situation in situ.

Fair enough, I only posted that comment because your answer has been accepted. It is a very intriguing suggestion if true but it's not really all that likely. I was just hoping you might have a reference to support it is all.

I believe that MattDMo's hypothesis is incorrect.  Only one group of ants, the Attini tribe, cultivates fungus as a food source.  This group is exclusively a New World group, thought to have originated in the Amazon rainforest and spread out from there.  I see from your profile that you are located in India, which is outside the range of the fungus-cultivating ants.
So if the ants aren't using your fingernails for fungus cultivation, what are they doing with them?  Fingernails are primarily composed of keratin, a very tough protein which ants cannot digest.  However, it is likely that the clippings also contain materials like dead skin, nail fungus, or other organic substances that the ants can eat, making them worthwhile for the ants to collect.
References:

U.G. Mueller, T.R. Schultz, C.R. Currie, R.M.M. Adams, & D. Malloch (2001). "The origin of the attine ant-fungus mutualism". Quarterly Review of Biology 76 (2): 169–197. doi:10.1086/393867

Maybe fungi are on the nail digesting keratin partially on the ground so that ants can eat partially digested nail.

Maybe the ants are stupid and don't realise fingernails are useless to them. They could smell delicious to an ant but not be usable.

Maybe the ants are really smart and need the fingernails to complete the human they are building.

Do you have any evidence that the only cultivating ants are in the New World?

@MattDMo, 10 second Google search found this.

@MattDMo Added a source, can be read for free on JSTOR but requires registration.

@JasonC  This hypothesis and several others have been proposed here.


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What's the name of this beetle?
I found him in a kitchen located in Toronto, Ontario, Canada.

This looks very similar to a click beetle. Some of them are pretty popular in south Canada.

Lay the beetle on its back. If it inverts itself using a strong clicking action then you have yourself a click beetle.

@docscience I can't, I already released it a few days ago. But the image on the Wikipedia page looks very similar so I'll assume that's what it was.


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What's the name of this caterpillar?
It was found in the state of Virginia, on the east coast of the United States.

I think it might be a species of Fritillary. Below is a picture of a Marsh Fritillary.

Marsh fritillary. Source: Butterfly Conservation.org
I do not think it is a woolly bear or giant leopard moth, just because the hairs seems too sparse for a woolly bear and it lacks the distinct red striping of the giant leopard moth caterpillar. It does not seem to be arctiinae to me.

Could you add a picture of you suggested species? Regardless, +1

http://butterfly-conservation.org/files/marsh-fritillary-larva1_peter_eeels_web.jpg Maybe a marsh fritillary.

It's Woolly Bear Caterpillar: http://en.wikipedia.org/wiki/Pyrrharctia_isabella

Can you explain why you think so? This looks quite different then the larvae that show up in a standard Google search.

Its spikes are short so the closest match I can think of was Woolly Bear. But it can be Giant Leopard Moth Caterpillar.


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Are corn kernels considered a grain
I have seen corn described as a seed, a grain and a fruit.
What are the kernels or a corncob considered to be? A grain, a seed or a fruit?

The fact that you asked about corn kernels is important, I think.  @March-Ho's answer is good, but the maize plant itself is a cereal grass.

I think the answer has to depend on the context.  To a farmer at harvest, it would be grain; at planting time, it would be seed.  And to a cook it might well be a vegetable most of the time, but a grain when making cornbread or tortillas.

The grain of corn is known as a caryopsis, which Merriam-Webster defines as:

a small one-seeded dry indehiscent fruit (as of corn or wheat) in
  which the fruit and seed fuse in a single grain

This image by Encyclopedia Britannica shows that the corn seed, enclosed by the seed coat (testa) is then further surrounded by the pericarp, which consists of the layers of tissue around the fruit.
Therefore, the corn kernel can be described as any of the terms that you have mentioned.

I like this line here: "Corn, Zea mays, belongs to the Poaceae family, and while eaten sometimes as a vegetable and sometimes as a grain,it is actually classified by botanists as a fruit, as are tomatoes, green peppers, cucumbers, zucchini and other squashes."


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aluminum sulfate vs (NH4)2SO4 in Colloidal Coomassie Staining Sol
I have been interested in Colloidal Coomassie Staining to detect proteins in PAGE gel.
I found 2 different recipes: one of them uses aluminium sulfate, the other, (NH4)2SO4. I am wondering about sensitivities of these recipes, and other advantages/disadvantages compering these two.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3149902/
This article describes a recipe using aluminum sulfate.
http://onlinelibrary.wiley.com/doi/10.1002/elps.200305844/epdf
(NH4)2SO4 is used in this article.


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Book-recommendation: plant biophysics
I'm a physicist by training am looking to learn more about the biophysics of plants.
Can you give me your recommendation of good resources on plant biophysics? Books are preferred.

Seeing that someone voted to close this post, I completely rewrote your post (incl. title and tags). Don't hesitate to switch back if you don't like my edits. Disclaimer: I know nothing about plant biophysics!

Book recommendation questions are considered 'opinion-based' if specific details are not provided. Please edit your question to add details.

Plant physiology by Salisbury and Ross, would give you a very good beginning.

Though some very old (and perhaps forgotten) works; here are 2 volumes of a book by a pioneer of biophysics, J. C. Bose.  Life movements in plants:    1.   http://www.gutenberg.org/files/48280/48280-h/48280-h.htm
2.     http://www.gutenberg.org/files/40050/40050-h/40050-h.htm

@Remi.b This question should be kept open like many-other book-recommendation question.

@WYSIWYG can you please expand on what specific details are missing? To me, the question seems on-topic. 'Plant biophysics' doe snot seem too broad as a subject but I might be mistaken.

IMO it contains insufficient detail on the users background in bio, the level of book required (high school, undergrad, post grad), and what specific topics need to be covered


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What species does this moth belong to?
It was found a few days ago in the state of Virginia, on the east coast of the United States.

Hemithea maybe, is as close as I can figure, although since there is so much variation between them it is very hard to tell.


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Why does flu vaccination only work against specific strains?
I was wondering why the flu vaccination doesn't protect us from all different types of flu. I know there are 3 major groups A, B and C and they mutate really fast. For example Influenza A virus has 2 different proteins on the surface hemagglutinin (H) and the neuraminidase (N). There are 18 different hemagglutinin subtypes and 11 different neuraminidase subtypes. So if they produce a vaccination which covers 187 of the virus (from H1N1 to H18N11) wouldn't it mean that the Influenza Type A could be eradicated from the world ? And wouldn't it work the same way for Type B and C?

I'm going to try and focus on the latter part of your question; if you want to know why the tri- or quadrivalent flu vaccine doesn't provide protection like many other vaccines, that's already been answered.
Anyway, the main reason we can't is because there are simply too many.  You say 187 (not sure why, 18*11=198) but the truth is that not all H1s are the same.  The different subtypes constantly mutate, so one H1N1 may not be the same as another H1N1.  There are hundreds upon hundreds of flu types, constantly changing.  And that's not even accounting for type B viruses.
When you make a vaccine, you need a certain amount of protein.  The major quadrivalent vaccine study used 15µg of protein of each strain.  The more protein you put in, the bigger the vaccine, the more it hurts, and the more likely the body is to have a significant negative reaction.  You'd have to test all of them as well - the FDA doesn't usually work on a "three is safe, four is safe, so hundreds is safe" principle.
Plus, you have to MAKE all that protein.  We're not very good at making enough for the tri- or quadrivalent vaccines now, much less hundreds or thousands of times more.  We simply don't have the capacity for that level of production.  Even if we could, it's not likely that immunity to all strains would take.  Besides, erradication is unlikely because there are large animal flu reservoirs (avian and swine, most famously) that can and will jump over to humans.  That's the piece everyone forgets about smallpox - with no animal reservoir, it was easy to eradicate.
That's not to say the cause is lost.  Intense research has begun on universal flu antibodies, and it looks somewhat promising.

There is a number of different multivalent vaccines available on the market. This is not really a problem.

There are 18 different hemagglutinin subtypes and 11 different neuraminidase subtypes that have been reported! The point is that many more are present in the overall viral population and some variant will escape the effect of the vaccination. In general however, to cover multiple variants with the same vaccination sounds a good idea.


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The Human Menstrual Cycle
1) What happens in the ovary and in the bloodstream that brings about this change in the uterus?
2) Why does the level of FSH decrease and remain at a relatively low level during the luteal phase of the cycle?

For 1 I was thinking: So estrogen levels increase and the follicle matures which first cause menstruation and then the lining reforms??
For 2 I was thinking: the follicle has already ruptured by the luteal phase

I addressed this topic in an answer to a related question. Although it’s a different question, I think both of yours are answered in the background I provided in that answer. (P.S. You need to specify what you’re referring to by “this” change in the first question - probably either a proliferative or secretory endometrium, or maybe menstruation? Or if it corresponds to the title, do you mean the entire cycle - “these changes”?)

Please expand on he abbreviation FSH

This sounds quite a lot like a homework/exam question, so I added the relevant tag.


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Do rare earth metals actually repel sharks?
Stroud claims that sharks are effectively repelled by the use of rare earth metals in the water. There has even been a patent issued by the same author for rare earth-wrapped fish hooks to reduce the shark by-catch.
Apparently these metals work by generating an electric current that repels sharks via the shark's electric sensing organ.
Is the repellent action of rare earth metals scientifically confirmed? And if so would it be effective even on the largest and aggressive white sharks?
Also if effective why haven't dive equipment manufacturers developed shark repellent devices for sport divers?

@AliceD from Canberra - thanks for the edit and go at it. So looks like good science hasn't sifted all the facts through the sieve quite yet. There are demonstrations of the effect on YouTube & the NOVA episode with David Pogue that are impressive. But looks like no one is investing in the design of rare earth diving gear quite yet ; )

@AliceD A small correction. Elements cannot degrade (unless it is a nuclear reaction). You should say that lanthanides react with water.

I'm voting to close this question as off-topic because this question does not ask about the biology of this phenomenon and is therefore much more suited to skeptics SE

I really hate it when science blogs do not cite the original articles and in such cases the authenticity of the information is not only questionable but also unverifiable. However there seems to be a wikipedia and a natgeo article on this. Even these do not cite any scientific research. Overall the claim seems unverifiable.

As pointed out earlier by AliceD, lanthanides react with water to form hydroxides with a concomitant release of hydrogen. A single electrode like that  cannot generate EMF.

@rg255 - this is definitely not for skeptics (way too specific) and I got disciplined by a mod of late for referring people there :)

personally I think it is absolutely perfect for skeptics, and not well suited to here. From skeptics help pages: "Skeptics is about applying skepticism — it is for researching the evidence behind claims you encounter." Specificity cannot be a valid reason for not being suitable to skeptics because the very nature of the posts on their site is the search for specific and solid detail.

@rg255 - OP is asking for scientific evidence; If that is Skeptics and not Bio, then that way every question asking for evidence (Is-This-True? questions) should be deterred to skeptics

@WYSIWYG regarding "one electrode" not necessarily so. You can consider the shark's body serving as the other electrode with seawater as the electrolyte, but also as current paths. Current grows larger as the shark gets closer to the metal. Like biting down on aluminum foil with amalgam fillings. Just a few milliamps - very uncomfortable.

Please don't kill the question. Give it some time and perhaps someone working in this area will come up with an answer. If you throw it over to physics, chemistry or skeptics it certainly won't receive the same attention some ichthyologist may give it. It is a multidisciplinary question but belongs with biology. Also I'm not asking for experimental 'proof' - that doesn't exist. And I'm not asking for help from the mythbusters. Just looking for strong experimental inference and further detail of what's going on.

@docscience Have a look at this article. It suggests that permanent magnets (both iron and rare earth based) affect shark's electroception. But I don't know what they mean by electropositive metals (all metals are electropositive).

@WYSIWYG I believe that's common knowledge - that electromagnetic fields in general affect sharks. More so of what I'm interested in is if any of the lanthanides (cerium, neodymium, samarium, etc.) by themselves - not necessarily in the form of an alloyed magnet accomplish similar reactions.

@docscience See this too. They actually say that nothing of that sort happens.

Can't believe the moderators closed this question. If it doesn't 'fit' in biology, not sure where else would be a more appropriate spot that would receive that many views. It's received over 1000 views, and a good answer.

Short answer
Electropositive metals such as the Lanthanides generate electrical currents when they come in contact with (sea) water. This electrical activity may repel sharks by over-stimulating their lateral line organ. However, the effectiveness of lanthanides as shark repellent depends on many factors. For example, hungry sharks, or sharks engaged in a feeding frenzy may simply ignore the stimulus altogether.
Background
Rare earth metals are Lanthanides - metals with a low electronegativity. Metals with low electronegativity are called electropositive. Electropositive metals (EPMs) react vigorously with water when immersed and generate electrical potentials that are thought to overstimulate the sharks’ highly sensitive electroreceptors, the ampullae of Lorenzini.
Many electropositive metals fall in groups I and II of the periodic table and explosively react with water. Examples include sodium and lithium. The Lanthanides, on the other hand, contain some less reactive elements.
There is in fact a considerable body of primary literature on the use of EPMs to deter sharks, because the by-catch of sharks is a recognized problem of modern fishery. However, much of this literature shows very mixed results of EPMs, and therefore I have based my (second :-) answer attempt on a recent review article by Hart and Collin (2015), which is available on-line and cites some fifteen primary research articles on the topic:
EPMs are primarily intended as a mechanism to reduce shark bycatch and catch depredation in longline fisheries, without affecting the catch of non-electrosensitive target teleost fishes. As you indicate in the question, EPMs can be formed into shapes that are easily attached to a fishing line or hook.
Early tests in the laboratory with captive sharks showed that several EPMs (including magnesium and rare-earth lanthanide elements such as cerium, lanthanum, neodymium and praseodymium) were effective in repelling various shark species. However, more recently, several studies showed no such repellent effects other species of shark, and it was shown that aversive behavior was highly dependent on various factors such as duration of food deprivation prior to testing. Specifically, hungry sharks ignored the EPM, especially when feeding in groups (feeding frenzies).
The results of field trials with EPMs were also mixed, with some studies showing a reduction in the catch rate of various shark species, while other studies showed no such effect. The authors of the review article summarize a range of factors that may influence the efficacy of EPMs in repelling sharks, including the type of EPM used, the relative sensitivity of the electrosensory system, shark density and competition, hunger level, and differences in feeding ecology. Other impediments to large-scale adoption of EPM technology by commercial fisheries include the relatively high cost of the rare-earth metals (although magnesium may represent a cheaper alternative), potential toxicity to other marine animals, and the fact that they dissolve rapidly in seawater and, therefore, must be replaced frequently. The use of EPMs for personal shark deterrent devices is also hampered by the limited effective range (<85 cm) of the electrical field they generate.
Instead, for use in scuba dive gear a rechargeable battery-powered capacitor-discharge unit connected to two or four electrodes is sufficient as shark repellent. Also, electro-magnetic induction using permanent magnets may be a more suitable alternative (Hart and Collin, 2015).
Regarding the great white: this shark has a lateral line featuring ampullae of Lorenzini, so EPMs may repel it, theoretically.
Reference
- Hart & Collin. Integrative Zoology; 10(1): 38–64

"Lanthanides are very rare elements, and that is the reason your article speaks of rare earth elements" - actually 'rare' is a misnomer. The lanthanides are highly abundant in the earth's crust. Reference to rare rather comes from the difficulty in separating them from one another since the chemical properties are very similar.

"However, when a magnet is combined with a rare earth element the repellent action is more vigorous" So then why? Is it something chemical plus the magnetic field of the ferro magnet or just because you can make stronger magnetic fields with rare earth materials?

@docscience - The Lanthanide definition is updated in my secnd attempt, and it's about current, not magnetism for EPM, so your second comment is also answered as such.

Nitpicking: Magnesium does not react explosively with water. From the second group calcium metal would react strongly.

@Chris - I  have deletet the Mg example, thanks! Nit pick away!


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Can suppression of the immune system help cure chronic diseases?
I am not a biologist, but recently while reading an article on Scholarpedia about self-organization I encountered a fascinating biological observation concerning immune response to infections.  To quote the article:

Whether the resulting patterns are stable or oscillating depends on the relation of the time constants. If the antagonistic reaction has a longer time constant than the self-enhancing reaction, oscillations or burst-like activations will occur. An example is the time course of an infection: The infection with few viruses could be sufficient to trigger a sickness since the viruses replicate themselves (self-enhancement). The antagonistic reaction, mediated by the immune system, is much slower. It takes a day to become sick, but a week to become healthy again. (What appears on a first inspection as a disadvantage is in fact a good strategy. If the immune system would be much faster, an equilibrium between virus production and virus removal would be established. After a single infection we would fight for the rest of our life against the virus. However, due to the burst mode, we become sick for a short while but the virus is subsequently completely eliminated).

Since the quote may be hard to parse out of context, I'll recapitulate: The writer is asserting that the immune system's response to infections is slower than might be physically possible because such slowness actually makes the response more effective.  By waiting a few days, the patient is sick for longer than they might be happy about, but when the infection goes away, it's gone for good.  If the immune system responded immediately to an infection, it might result in a low-level infection that persists indefinitely.
This makes me wonder: For chronic diseases, is the reason they are chronic related to the time scale of the infection vs. that of the immune system's response?  Could such diseases possibly be cured by suppressing the immune system for a time so as to get the "burst" effect alluded to in the quote above?

I fail to follow the logic of that quote. Furthermore, components of the immune system are active as soon as an infection is recognized.

@canadianer I'm not an expert, so I can't say with authority, but as I understand it the implication is not that the immune system waits before taking any action, but rather that the time scale for the overall response is "intentionally" longer than the time scale for the infection itself, the idea being that the delay in response can make it more effective in eradicating the infection.

It's entirely possible that I'm missing something, but why would a delayed response be more effective?

@canadianer That's exactly the point, and it's why I found this so surprising! :)  I don't claim to know why it should be true in the case of infections, but I can believe it based on analogies from other systems with multiple competing agents.

@canadianer Here's a basic way of rationalizing it to myself: The immune system will take some minimum time to prepare a counter-offensive against the infection.  If it were to start attacking the infection before it was completely prepared, perhaps the infection would be able to adapt and reach a stand-off.  On the other hand, if the immune system delays, it will be able to wipe out the infection entirely before it can adapt.  I don't claim this explanation is right--I only propose it as a heuristic for why it might be advantageous to delay response.

I can not answer clearly, so I write comment here. Take vaccination for example. Some virus infection causes acute symptoms, but if you are vaccinated, you do not get any symptoms. This means your immune-system is fully functional to eliminate viruses as soon as viruses are invaded. You do not need to wait propagation of virus to eliminate them.

What should be the benefit of this delay? It raises the chances that our body is overwhelmed by the virus and dies. The delay of the adaptive immune system is simply caused by the fact that it needs some time to launch a highly specific immune response. The innate immune system (you could call this our first line of defense if you like) acts very fast and almost immediately. Additionally viruses get used to our immune system and adapt, see HIV for example. I can make this into a full answer later today.

@Chris is right here.  The quote is both wrong and misleading.  The immune system clears an infection after a delay because the adaptive immune response takes a few days to develop.  Chronic diseases almost always are due to an ineffectiveness of the immune system or inability to respond appropriately.

@canadianer and everybody wondering about the logic behind the q: this type of equilibrium is best known to biologists from the Lotka Volterra rule. Start out with a balanced ecosystem, say 100 rabbits and 10 wolves, and you'll have rabbits and wolves forever, in changing ratios. But if you start with 100 rabbits and 50 wolves, you'll run out of rabbits before the wolf number goes down. The assumption behind the q is that waiting for a large virus population elicits an overproportionally "large" immune response which kills all viruses instead of the supposedly "small" response to few viruses.

@rumtscho I understand what the quote is saying, but the immune system does not follow a predator-prey relationship. The quote suggests that a delayed immune response is an adaptive advantage rather than a mechanistic requirement. That is the logic I did not follow, with the implication that it is incorrect.

@canadianer I see. Then I had misunderstood your first comment - it now seems we agree on what the exact problem is with the quote. I thought it important to write it out explicitly, because when somebody presents with a wrong idea, it is frequently best to hunt down the exact place where a wrong assumption is used, else he is unlikely to understand the correct explanation. And sometimes the experts have the hardest time to spot the problem in understanding, because they know the subject so well, they can't imagine that somebody will make an "obviously" wrong assumption.

@rumtscho Your comment was good, I just wanted to clarify mine to avoid looking like a complete dolt ;)

No, this wouldn't happen. The logic of your proposition assumes that chronic diseases are caused by the strength of the immune response being insufficient to kill off the virus, resulting in a long-term equilibrium between the amount of virus particles produced and the amount of virus particles killed.
In reality, this is not how chronic diseases work. Only a small amount of chronic diseases are caused by viruses. There are many which have other causes, not all of which can be defended against by the immune system - e.g. chronic depression is not curable by immune response.
But even if we focus on chronic virus infections such as herpes simplex, they are not sustained by the mechanism you describe. They happen due to the fact that our immune system simply does not know how to get them out of their new home within our body, they are just that good at hiding during latency. So even if you could cause a strong immune response all at once, it wouldn't kill all viruses at once.
Even if we have viruses whose serum presence depends on a constant growth vs. destruction dynamic (I don't know if these exist at all), an overly strong immune response won't be that good for the human host. Inflammation is a dangerous state, most of the unpleasant feeling you get when you are sick is not due to the virus itself but due to your own immune response, which causes the fever, muscle pains etc. associated with many acute infectious diseases. If we were to ramp this up, you'd probably get a fever high enough to cook you alive, or some other undesirable effects.

On a side note, I also doubt the author's argument which suggests that long-ish convalescence times evolved because shorter ones would leave the system in an undesirable equilibrium. Sure, an alternative reality is thinkable where the innate and adaptive responses described by Chris occur much stronger at the beginning, leading to steeper curves and shorter healing times. But the simpler explanation for that is that 1) our immune system is not perfect, and it evolved to the highest healing speed it could achieve, and 2) an immune system with higher acceleration would have been way too costly in terms of resources available to the body. An evolutionary advantage in having a low-acceleration immune system is a strong assumption for which I see no support, especially considering that the residual immunity provided by the adaptive immune system would prevent the dynamic equilibrium suggested in your quote.

I think the person who wrote the quote does not really understand how an immune response is happening. There is no real "waiting period" until the immune system starts attacking the virus (or bacteria or whatever), this happens instantaneously when the virus is recognized.
To do so, we have two, independent systems, the innate immune system and the adaptive immune system. The innate imune system reacts immediately and launches a unspecific, but still very effective answer to a virus. The adaptive immune system delivers a highly specific (via antibodies) immune response, which takes a while since the generation of specific antibodies takes some time (the body produces antibodies which are then matched against the virus). It works like shown in the figure (from here):

It is also the adaptive immune system which mediates the long-lived immunity against pathogens which have triggered a immune response. Once you get in contact with such a pathogen again, the adaptive immune system can react immediately and protect you. This is also how vaccinations work.
Both immune answers start immediately upon pathogen recognition, there is not benefit in delaying (or suppressing) this immune response. In contrary, this is highly dangerous for the individual, as you can see in persons, which have received a transplant. These need to suppress their immune system in order to prevent a transplant rejection, but at the price that they get sick a lot easier.
However, there are some diseases, where a partly modulation of the immune system is beneficial. These are autoimmune diseases where the immune system is directed against the own body. Examples would be rheumatoid and reactive athritis.


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ATP required for cell processes
I haven't been able to find anything that tells me how much ATP is needed for DNA replication, transcription, and translation in humans, just papers that mention ATP used in those processes.
I need to know how much ATP is needed for these processes because once my cell from scratch is alive I feed each cell 50 nanograms of glucose which yields 5 trillion ATP. If I use these numbers plus the numbers for other metabolic processes I get roughly the amount of ATP needed per cell before mitosis. If I know this then I will know if I need to feed my cells more glucose or if 50 nanograms is enough.
So how much ATP is needed for DNA replication, transcription, and translation? I want it in terms of per nucleotide and per amino acid so that I can multiply that by the amount of DNA total, amount of DNA in any given gene, and amount of amino acids in any given protein.

This is difficult to answer. Do you wish to include the ATP required to synthesize nucleobases, nucleoside triphosphates, amino acids, charged tRNA, etc?

I have given a rough answer and you can go into finer details (like accounting for NAD). You have not done any research towards the question and I am inclined to close the question.

The information you provide is not nearly enough to figure out the energy needs of a cell before mitosis. You need to measure at least glucose uptake, lactate release and oxygen consumption, and do growth curves. Every cell line is different, so you need data on your cells. See http://www.ncbi.nlm.nih.gov/pubmed/14697210 and http://www.ncbi.nlm.nih.gov/pubmed/5817088. But you don't need to know this just to culture cells --- as long as they grow and look healthy, and the medium pH is not to low, they have enough glucose.

Culture media for mammalian cells usually contain 1 to 4 gram/l. For example, when 10^6 cells are seeded on a 10 cm dish, you could grow them to about 10^7 for several days using 10 ml culture medium. For some cells you might have to replace medium with fresh one once before they reach 10^7 cells. You could know how much cells need glucose practically. When you have pyruvate in media, it goes TCA cycle so that glucose is not only the source of ATP.

In addition, ATP is required for sugar modification of proteins, protein phosphorylation, and probably amino acid and lipid synthesis as well as mechanical cell movement, vesicle transport, chromosome segregation and ... what else...

I myself have done research by trying to look up how much ATP is needed for DNA replication, transcription, and translation and finding out that ATP is involved in all of these processes.

Well I am growing totipotent stem cells which I am planning to differentiate into all kinds of cells and then build organs cell by cell at newborn size. Totipotent stem cells I assume would take the average amount of energy of all human cells including trophoblasts and embryonic stem cells.

For DNA replication and transcription you need NTPs. In a dsDNA purine content will be same as pyrimidine content. I am considering that all nucleotides are synthesized de novo which would consume more ATP than getting nucleotides from the salvage pathway.

Fig 1: Pyrimidine synthesis. Taken from Wikipedia.

Fig 2: Purine synthesis. Taken from Wikipedia.

CTP synthesis requires one extra ATP:
UTP + Glutamine + ATP + H2O → CTP + ADP + Pi
UTP synthesis requires 2 (Step 1; Fig 1) + 1 (Step 5; Fig 1: PRPP requires 1 ATP to form) +  2 (UMP → UTP) = 5 ATPs
CTP requires 6 ATPs
GTP requires 8 ATPs (Fig 2) (ATP synthesis would also require 8 ATPs but for simplicity let us assume that ATP is already present).
Conversion of dNTP from NTP requires thioredoxin which in turn requires NADP but let us forget that.
Assuming a 50% GC content one base pair of DNA would require in an average 10 ATPs (assume a stretch of 4nt — ACTG, this would require 1+6+5+8 ATPs; i.e. 5 ATPs per nt; 10 ATP per bp)
For RNA the ATP consumption would be 5 ATPs per nt.
For protein synthesis, for every codon, the elongation factor requires one molecule of GTP and aminoacyl-tRNA synthetase requires 1 molecule of ATP. So the net consumption per amino acid would be 9 ATPs.
I am ignoring the initiation reaction that also requires ATP to phosphorylate the initiation factor. Also, I assume that amino acids are obtained from diet and are not synthesized by the organism.


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Why increasing the vector concentration does not increase the effeciency of bacterial transformation?
I was reading some old description of the protocols used for the transformation of bacterial cells.
In the description I read that the transformation works best with low amount of DNA, and if we increase the amount of DNA used the amount of transformant cells does not increase proportionally.
I just wonder why, since in my eyes the process of entering the cell is mainly related to the diffusion principles, and therefore concentration dependent.

If there are many times more plasmids than cells, increasing their concentration when the cells are already saturated would therefore not increase the transformation ratio.

Thanks, but then it is similar to a enzymatic kinetic. So in theory I will have an increased transformation at higher concentration of plasmid till a saturation point that, I would guess, depends from the strain I use to transform?

According to the Hanahan transformation protocol (one of the highest competencies published), a transformation of 200µl will contain $1×10^8 - 1.7×10^8$ cells.
Assuming that the pBR322 plasmid is used, 1ng of plasmid will convert to 0.36fmol of plasmid, or $6×10^8$ plasmid copies.
As we can clearly see, even at very low quantities of DNA used, there are multiple plasmids per cell. Since transformation is thought to be mediated by DNA channels, massively increasing the quantities of DNA would not equally increase transformation efficiency once all of these channels are saturated.
The example from NEB Turbo DH5α cells seems to show this quite well, that once DNA quantities exceed 1ng, the transformation efficiency drops precipitously.

This being said, if the amount of plasmids available is very large, there is no reason to avoid adding more than 1ng of DNA, as they would not reduce the total number of transformation colonies, but only the efficiency.

Thanks very much for your nice answer. I am thinking though that in the example you do there will be around 6 copy of plasmid available per each cell. For my understanding there could be hundreds of possibilities (e.g.DNA channels, electroporetic generated holes) for the DNA to go in. SO in theory if we create a saturation curve we can see that the number of transformant is increasing with the amount of plasmid we add, at least at the beginning. When saturation is reached he amount of DNA is not influent. It would not make sense to add more DNA from the start to have higher transformant?

@efrem I am not sure if Michaelis-Menten kinetics (in the sense of the saturation curve) apply in this case due to the mix of many different means of plasmid entry, but the general concept of channel saturation should still apply.

thanks! So the efficiency drops, but the number of transformed cells increase exponentially. Therefore, if someone is not limited in terms of plasmid amount, and has cells that do not transform so well, it would be better to increase the amount of plasmid to get a higher number of transformant, even though with less efficiency.

@efrem The increase is most notably NOT exponential. It is in fact worse than linear, considering the X axis is log but the Y axis is linear. However, in most cases of bacterial transformation, you are using high concentration plasmids in any case. I can't think of a way to reduce the number of total transformation colonies by adding too much DNA.

right, sorry. It is indeed linear. Anyway, it seems to me that there is not any major drawback in adding too much DNA (plasmid), in terms of total number of transformed cells.