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When infected with malaria, how many parasites are within a human host?
When infected with malaria, how many P. falciparum cells are within a human host? And how does this compare with the average infection parasitemia of A. gambiae? I can't seem to find a reliable source to guide me on this question.

The uninucleate sporozoites are injected by the mosquito into a human host. They mature in the liver parenchymal cells in schizonts. Each schizont releases into the blood flow 2,000 to 40,000 uninucleate merozoites. Each of them can infect a red blood cell. Here, a merozoite can release other 10 to 36 merozoites [1].
The numer of injected sporozites depends on the bite and the number of bites [2]. And it seems that a parasitemia greater than 5000/microliters which is usually achieved by 10 infective bites during a 28-day period triggers the signs and symptoms [3].
I couldn't find any data on the mosquito parasitemia. It has been found that the infected mosquito and the parasite mutually benefit each other and thereby promote transmission of the infection. The Plasmodium-infected mosquitoes have a better survival and show an increased rate of blood-feeding, particularly from an infected host [4].
References:

James M. Crutcher and Stephen L. Hoffman. Medical Microbiology. 4th edition. 1996, The University of Texas Medical Branch at Galveston.
Garrett-Jones C, Shidrawi GR. Malaria vectorial capacity of a population of Anopheles gambiae: an exercise in epidemiological entomology. Bull. World Health Organ. 1969 Apr;40(4):531-45. PubMed PMID: 5306719.
McElroy PD, Beier JC, Oster CN, Beadle C, Sherwood JA, Oloo AJ, Hoffman SL. Predicting outcome in malaria: correlation between rate of exposure to infected mosquitoes and level of Plasmodium falciparum parasitemia. Am. J. Trop. Med. Hyg. 1994 Nov;51(5):523-32. PubMed PMID: 7985743.
Dr. B.S. Kakkilaya's Malaria Web Site. Life Cycle of Malaria.


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In humans what is the last metabolic process to cease after death?
After death which of our body's metabolic processes will continue functioning for the longest?

Slightly related to this question

I will wait for a better answer because I'm curious too. But here is my answer, you may be surprised because I think the last metabolic process to cease after death is not fancy at all, it can simply be cellular respiration. When oxygen is depleted, cellular respiration stop and it can't do any thing. Just like sleeping, your body is basically stop doing a lot of things except cellular respiration. Here is some info you may be interested. http://www.scientificamerican.com/article.cfm?id=experts-cell-metabolism-after-death

My answer isn't researched; it is speculative.
I interpret metabolic processes as anabolic or catabolic processes. I assert that only anaerobic processes can continue for a long time after vegetative death (the epithelia could house a counter-example of a post-mortem process, but I can't think of one), and I speculate that only catabolic processes are likely to have sufficient pools of reactants to continue after death. So we're looking for a catabolic process with a large reactant pool. Therefore I think that the action of digestive proteases will continue for the longest time, because these enzymes are very stable and could have a lot of substrate around (including, at a very slow rate, cleaving each other.) The neutralization of stomach pH would inactivate this process...I don't know how long that takes.
If something like blood clotting is considered a metabolic process, then probably that continues the longest. The binding of CO₂ by hemaglobin is probably faster than blood clotting. Again, I don't really consider those processes to be metabolic.

I can imagine your digestive proteases cleaving their way through the stomach lining ever so slowly after your death, before eventually the pH is neutralized. Not what I would have thought of. Good answer.

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Fibonacci sequence in nature, truth or just wishful thinking?
I'm reading a bit on the Fibonacci sequence in nature, be it the golden ratio or the golden spiral forming over and over again in biological structures, and then I came across this online article by Donald E. Simanek, refuting a lot of these observations as merely optimistic 'flim flam'.
So which is true?
Does the Fibonacci sequence have a place in nature or is it all just a case of vigorously looking for anything that resembles a correlation?

Search for Vi Hart on Youtube. She makes educational and oddly entertaining math videos and she has one about plants displaying both Fibonacci and Lucas numbers as a way to maximize sunlight reception by the leaves.

I mean, I'm curious too, and Vi's video is all I've heard about this correlation. I'm not asserting she's right, just that you might enjoy it. The video is called Doodling in Math: Spirals, Fibonacci, and Being a Plant.

Thanks I'll give them a watch, I remember watching an entertaining one she did on the nature of infinity I think.

Didn't the Fibonacci sequence arise when modeling the dynamics of rabbit populations?

As far as I remember, Fibonacci patterns emerge in plants from hormone gradients. I.e. an apical meristem forms a leaf where the auxin concentration is highest, and already existing leafs lower auxin concentration, leading to some negative feedback.
See e.g.
http://www.sciencedirect.com/science/article/pii/S1360138507000581
or http://en.wikipedia.org/wiki/Phyllotaxis

I'm aware of how these patterns are seemingly formed, what the question is asking is whether these patterns are indeed examples of proper mathematical Fibonacci sequences or if they merely bear resemblance.

The pattern forming processes generate a fibonnachi pattern, but there are other processes that occur as well.

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Is there an evolutionary explanation for the black spots around a pandas eyes?
I couldn't seem to find one elsewhere, at least not with a scientific source.
It would seem as it's quite a striking feature there would be an advantage it would infer.

From Wikipedia: "Although scientists do not know why these unusual bears are black and white, speculation suggests that the bold coloring provides effective camouflage in their shade-dappled snowy and rocky habitat." With a reference to Giant Pandas by Karen Dudley (1997).

One can create a selectionist explanation for any trait, but all such explanations have very little scientific content.

It could be related to stopping light glare too, not entirely sure why a panda would need that but living in snowy areas there is a lot of sun glare... athletes use this trick, particularly in ball sports http://en.wikipedia.org/wiki/Eye_black but remember, not everything has some wonderful evolutionary explanation, some stuff just exists for no real reason.

As your commenters have suggested, no.
In order for an explanation to be a good evolutionary explanation, it needs to have a testable hypothesis and a mechanism to test it.
The most common mechanism for testing the crypsis (camouflage) hypothesis is to take a large number of closely-related species, and see if their coloration differences are correlated to a particular habitat. Since pandas have few black-and-white relatives, there is no statistical power in this analysis.
Another option is to take a large number of pandas, create a treatment and control group and bleach the treatment group (or their eyespots) white, and compare survival or visual acuity. Unsurprisingly, this has not been done.
Here's a nice article to animal coloration for those that have access:
Caro, T. I. M. (2005). The adaptive significance of coloration in mammals. Bioscience, 55(2), 125-136.

I quite like the explanation I found on the website of "Exploring the BioEdge". Robin and Honeybadger explain the black and white colouration as follows: To minimize the risk of being attacked by the tiger, the colouration of the giant panda is aposematic, warning would-be predators of its vice-like hug and bite. This warning signal, visible even in poor light, consists of a black-and-white contrast on the face (ears and eyes) as well as the body as a whole.”
http://explorebioedge.com/bio-bullets/item/43-warning-colouration-in-the-giant-panda.html


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What's a good simple test for cDNA library quality?
How do I assess the quality of a cDNA library?
I want to clone CDS copies of genes from a library, but I don't know what's a typical expectation of getting a full length clone even for a shorter gene (~1000 bp).  I know it doesn't have to be composed of full length cDNA for sequencing, but I'd imagine quality of starting materials is important there too.
Are there some common transcripts I can try to obtain from PCR that will tell me how fragmented the sequences are in there?
What's a typical result from a commercial cDNA library - are there any QC tests that are quick to run in the lab?

From what kind of cells do you have your library? I think the answer heavily depends on that info.

did you try googling? actin seems to be useful probe target: http://www.ncbi.nlm.nih.gov/pubmed/3273856

@poka.nandor interesting - human testis or spleen - does that help?

quite a lot! At least we know what genes should be expressed, however there are housekeeping genes that expressed in most or all cell types like actin as aandreev suggested.

Is this library for sequencing? What is your experimental setup?  Did you perform reverse transcription and you want to check how well it went? I deleted my answer as when I tried to work on it it raised more questions on the post.

You would usually run you library into a Bioanalyzer and check that the fragment distribution looks something like you expect. From there you can look at housekeeping genes to make sure those are present in the library. The expected fragment length distribution largely depends on the kit, the experimental approach and the sample type you are using so it is pretty much impossible to tell you exactly what you should expect with no information on that. Also the library depends on what kind of sequencer you want to use, you don't want the same library for say Sanger sequencing or a MiSeq run.

I was hoping for something more like this @caligari2005.  how can I tell if the cDNA is fragmented or full length.  I'll change the question.


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Is there a term to quantify how spread a character is on a phylogenetic tree?
Is there a term which can quantify how 'spread out' a particular character is on a tree? I want to distinguish between a character which is only restricted to a particular clade vs. a character that occurs all over the tree.
ETA: by 'all over' I meant it may be restricted to a few branches but those branches are spread out over the tree. It need not be ubiquitous. e.g. the character marked in blue on  compared with the case where these three branches are in a small clade.

Probably off topic here, but 'ubiquitous' or 'widespread' should work.

I think that in the general language of trees, 'clustering' might be the word...

I agree with Terdon's terminology in the comment ("ubiquitous" or "widespread").
You can use clade-specific or species-specific for a restricted character.
For the characters that appear in all species of a branch and in a quantitative way you can also provide the estimated age of the last common ancestor to the branch featuring that character. This tool might help you: http://www.timetree.org/

Isn't a character restricted to a clade synapomorphic for that clade? (at least within the groups being considered.)


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Can HIV mutate to become airborne?
HIV has a very high mutation rate due to its inability to correct errors in DNA replication and it is very adaptable to its environment. Hence I wonder whether is it possible for it to mutate such that it becomes an airborne virus and what mutations was needed for it to occur. After all other viruses such as influenza have done so before. Furthermore from the virus point of view, doing so will allow it to be more successful evolutionary speaking since that would allow the virus to infect more people and hence reproduce itself more quickly. And what will be the consequence if it happens?

Quick answer: likely not. HIV is extremely vulnerable outside the body, which is why fluid-to-fluid transmission is required. A huge number of mutations, all in the same virion, would be required to give it the resistance to molecular oxygen, sunlight, dehydration, temperature changes, etc. to become airborne. Also, your statement it is very adaptable to its environment is not quite correct. It is adaptable to escaping immune surveillance, but not to other environments. In fact, many (if not most) of HIV's mutations render it incapable of completing its life cycle in one form or another.

"...other viruses such as influenza have done so before." Are you saying that there was a time when the influenza virus was not transmissible through the air? When was that? As far as I know (I'm not a virologist), the virus doesn't fly through the air with the greatest of ease unless someone sneezes or coughs it out on a droplet.

See this post. It is exactly about what MattDMo is saying. I am afraid this question is quite opinion-based.

I think questions like these can offer some value if you approach them as Fermi problems. MattDMo seems to have correctly identified the barriers the virus would have to overcome, and we can roughly gauge the chances of all of those changes occurring in sequence. Which, without putting too much thought into it, I'd say somewhere around "when pigs fly."


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Time needed for transcription of DNA
How much time would it take to complete the transcription of an average-sized human gene?

Welcome to Bio. Answer: 4 'o clock in the morning! What do you mean with time? Time to do what?

Which organism? Did you try searching anything at all?

I'm interested in human cells. I would like to know the order of time taken to complete transcription of a medium-sized gene in particular.

From Bionumbers, the average transcription rate of RNA Polymerase II is about 3.8 kb/min. Other researchers measured it as 6.3 nucleotides/sec, or 378 bp/min, a 10-fold decrease. In the same paper, however, they measured the maximum rate at 71.6 nucleotides/sec, or 4.3 kb/min. To figure out the differences between the measurements, I suggest reading the paper, but since it's from Nature Publishing Group you'll have to pay for it, unless you're at a subscribing university or institution (or someone posts the paper in the comments <hint hint>).
So, the answer to your question, like most simple questions in biology, is it depends. It likely depends on the size of the gene, its structure, what transcription factors are necessary for the assembly of the polymerase complex, and, last but not least, exactly how and when you measure. Transcription likely initiates in fits and starts, then gets going faster. This is similar to (but not exactly like) measuring the speed of your car from Point A to Point B. Are you starting from a dead stop, or passing the starting marker at speed? Do you have to start the car first, or is it already running? How many turns and other slowdowns are on the road? Do you stop measuring as the car passes the finish marker, or when it comes to a complete stop? All of these things figure into the final answer, and the result given is entirely dependent on the scientists' choices of methodology.
If you are interested in a broader discussion, I got started on this page at Bionumbers.


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Normalised gene counts to edgeR/DESeq2?
Both very popular differential expression packages assume a raw gene matrix count. This makes sense because the statistical model models the library depth.
But what if I normalize my counts with say, the ERCC RNA spiked-in standard? Would that affect the statistical power? False-positive? Why exactly is it not recommended to give a normalized count matrix?

This question should have edgeR and deseq2 tag, but I don't have enough reputation (require 300). Would somebody else add the tags for me?

No need for specific tags. There are hardly any DEseq/edgeR specific questions.

The advice is to not generally use ERCC spike-ins at all because of variations introduced by pipetting at the volumes they recommend.
The thread also explains how to use DESeq and EdgeR with spike-in normalisation, with the process being easier significantly with DESeq, where you can use the calcSizeFactors on a count matrix of spike-in reads alone. With edgeR you will have to pass values using the lib.sizes parameter in the apposite functions.
If you want to use fractional counts through limma-voom should work, I think; I've had good results using voom on RSEM counts, which are fractional.


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What do breeders call the effect when a breed resists modification?
It is impossible to breed a blue rose or a cat with a bulldog shape. This is because breeding is limited by gene variations in the population.
What do breeders call this effect?
UPDATE
I guess this term is from medieval and/or handicraft breeders, not modern and hi-tech.
UPDATE 2
I am speaking not about principal impossibility but just about observable or tangible barrier. We can be sure that it is possible to turn dog into cat in billion years, but it is much harder than turn German Shepherd to Yorkshire Terrier, which is possible for hundreds of years.
So, there are are two main types of changes, ones take hundreds of years, others take hundreds of millions of years. Former require genetic recombination while latter require genetic mutation.
This barrier was felt by breeders in practice and caused some versions of anti-evolution beliefs.
I need to know how this barrier is named.

I'm honestly not sure if one exists. They simply lack the gene/allele - the only specific term I can think of when it comes to lacking a gene is referencing Knockout variations where a researcher purposefully removes a gene from a subject in order to observe the effect.
However, "Knockout Mice/etc." imply intent on behalf of the researcher, not a result of breeding or natural lack of an allele. Perhaps "Genetically Incapable" would be a phrase meaning the same thing - but I'm not aware of any 'official' shorthand for 'Cannot because it's not in their genes.'

There must be a point where a desired trait cannot be obtained by selective breeding or by evolution at all!  Why can't there be viruses the size of houses or elephants as small as a flea?
Those may seem like absurd examples, but that's just to point out that not all traits can be obtained in less than infinite number of adaptive steps.  Jerry Fodor pointed this out (among other things) in his essay "Why Pigs Don't Have Wings".
Exactly what you can get and what you can't get is open to effort.  For instance I suppose you could turn a pig into a pigeon if you had a few million generations to do it - something similar to the evolutionary time back to the time they diverged.  That would be difficult, but you could basically run evolution for another billion years to get small hollow boned pigs with bats wings on their forearms.  you probably wouldn't recognize it as a pig, but then again youd be dead of old age several times over too.
Could you breed a human where bullets bounce off and they can fly?  not so sure of that.


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After hysterectomy does FSH secretion stop?
This question came in an exam, and my reference book says yes, it does. But it hasn't explained why.
If the ovaries are also removed, then the menstrual cycle should stop. In absence of hormones oestrogen and progesterone, there would be no inhibitory effect on FSH, so its secretion should continue.
Or if it stops, then why?

Strictly defined, a hysterectomy is removal of only the uterus.  But sometimes the ovaries are also removed, depending on the reason for the surgery and age of the woman.
If the ovaries are also removed, there would no ovarian or uterine cycling, true.  But without the negative feedback effect of ovarian steroids (progesterone and estrogen), levels of both FSH and LH would be persistently, abnormally high.  The same happens in postmenopausal women (ovaries still present but no longer producing steroids) and spayed pets.
If the uterus is removed but the ovaries left in, the ovaries would continue to mature follicles that release estrogen, ovulate, luteinize and produce progesterone, etc, etc. Even though there is no uterus for the steroids to act on (and no menstruation), the steroids would feed back to the anterior pituitary gland and FSH/LH levels would fluctuate in the normal patterns.
Without the obvious sign of menstruation, it would be tricky for the woman still with ovaries to know whether or not she had reached menopause.  The first woman (ovaries removed) would be thrown into a 'surgical menopause', an abrupt (and nasty) withdrawal of all ovarian steroids.

Could you add sources (references to papers, books, websites etc.) to allow users to background read on your answer?

It would be better if you could add some sources. I had searched Google, but did not find satisfactory results.

It's been already shown that women subjected to hysterectomy but retaining ovaries reach menopause earlier than intact women, so hysterectomy may have an effect on the secretion and feedback pattern of FSH and LH. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3223258/
If what Heidi says is true, ie "If the uterus is removed but the ovaries left in, the ovaries would continue to mature follicles that release estrogen, ovulate, luteinize and produce progesterone, etc, etc. Even though there is no uterus for the steroids to act on (and no menstruation), the steroids would feed back to the anterior pituitary gland and FSH/LH levels would fluctuate in the normal patterns.", it would mean that steroids acting on the uterus would do their job and get back to the blood stream and exert the feedback effect on the hypothalamus.
What happens after they have entered the uterine endometrial cells to exert their effect? Are they metabolized within the cells? Are they excreted with the deciduous cells during menstruation? If that's the case, the amount of circulating FSH and LH in the blood stream of hysterectomized women would be higher than the average levels of intact women and maybe that's the reason why they experience ovarian failure earlier than expected. Another possibility is that the uterus is not a passive organ, but that remains to be proved. Damage to the ovaries during surgery has been speculated, but giving the same results (early ovarian failure) after key hole procedures (laparoscopy), it seems that's not the case.


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How does sodium ion increase blood pressure?
So I have been reading about the RAAS system and I was wondering how  natrium (sodium ) ions increase blood pressure.I have been looking up on the internet and have yet to find an answer.Help

Sodium acts on the juxtaglomerular cells of the kidney, which are then activated to produce and secrete renin. Renin hydrolyses angiotensinogen into angiotensin I. Next angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II.
Angiotensin II is the product that causes the increase in blood pressure, because it is a potent vasoconstrictor. With peripheral vasocontriction the heart has more resistance to pump blood against, thus higher blood pressure. Additionally, angiotensin II stimulates secretion of aldosterone from the adrenal glands, which acts on the distal tubules and collecting ducts in the kidney to retain sodium and water, thereby increasing blood volume and thus blood pressure.

Image: RVC 2008
This pathway is one reason why ACE-inhibitors, such as benazepril, enalapril, lisinopril, or perindopril, are used to treat hypertension (high blood pressure). With less activity of ACE, there is less angiotensin II, and blood pressure goes down. Hypertensive patients are told to consume a lower sodium diet because that will lead to less activation of the JG cells in the kidney, which will eventually result in less angiotensin II, and thus lower blood pressure.

This is a thorough answer, and I like the graphic. However it's a DROP in sodium that is detected by the macula densa that ticks up RAAS. That's the whole point of the system: since water follows salt the two parameters usually have a high degree of correlation and a drop in sodium suggests a drop in blood volume. Thus the need to kick up AT2 to keep the blood pressure up when volume is low.

The increasing of the concentration of sodium ions in blood would attract water from the surrounding tissues, because of the osmotic pressure.
The increasing of the total volume of blood(it has adsorbed water) makes the blood pressure higher.
That is why in summer the blood [pressure decreases]. In  fact, sweating makes us lose body salts, so the volume of blood decrease and so the pressure.
http://www.bloodpressureuk.org/BloodPressureandyou/Yourlifestyle/Eatingwell/Salt
http://www.medscape.com/viewarticle/489515

"I guess" is not an acceptable supporting citation for an answer. Please support your claims with links to the relevant primary literature, or at the very least from secondary sources that cite primary ones, such as Wikipedia. I'm very interested in particular to see supporting evidence for your claim that blood pressure decreases in summer.

Please add a reference that can be accessed (ideally through PubMed). The one from Medscape cannot be accessed.

Your body removes unwanted fluid by filtering your blood throught your kidneys, the extra fluid is eliminated in urine. Basically the kidneys uses osmosis to draw the extra water out of your blood, using a delicate balance process of sodium and potassium. When you eat too much salt it increases the sodium in your bloodstream than wrecks the delicate balance, reducing the ability of your kidneys to remove the water. So the blood preassure gets higher due to the extra fluid and extra strain on the delicate blood vessels leading to the kidneys.
Here´s a link to help more : http://www.bloodpressureuk.org/microsites/salt/Home/Whysaltisbad/Saltseffects


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Why must DNA be packed into chromosomes during mitotic phase?
Why does DNA have to be packed into chromosomes? Why can't DNA just divide itself evenly?

They don't pack into chromosomes. Chromosomes are made of DNA and during the metaphase, the chromosomes packed and look like the standard x-shaped(-ish) representation of chromosomes that we are all used to.

You have some misconception here: Chromosomes are an organisation unit for the DNA.

So is my concept of what chromosomes are is that they are basically DNA but condensed into the x-shaped representation correct ?(correct me if my concept is wrong)

A chromosome is simply a length or segment of DNA. Bacteria have few structural proteins on their DNA, and they have one circular chromosome. In humans, before DNA replication, the nucleus contains 46 strands of DNA, i.e. chromosomes (22 chromosomes in two copies and usually two X or one X and one Y for males and females, respectively). All chromosomes are DNA that is bound by histone proteins that are organised in nucleosomes, approximately every 147 base pairs.
What you are referring to is a condensed chromosome in metaphase, which confusingly in humans is actually an X shape consisting of 2 identical chromatids, structurally condensed and joined at the centromere to form a duplicated chromosome.
The duplicated chromosomes must condense and join before the cell can divide because a tangle of 96 chromosomes as chromatin would be almost impossible to organise and separate properly. The joining of identical chromosomes and compacting process allows all the 46 compacted and duplicated chromosomes (i.e. 96 chromatids) to simply align along the spindle apparatus that forms in centre of the cell during mitosis, and have separation of the chromatids during anaphase so that each of the new cells has a full set of 46 chromosomes.

If you mean to say why DNA is in the form of chromosomes, then obviously answer is simple: For Compression and Packaging - Around 2metre long DNA must be compressed (at an unbelievably high ratio) to let it fit in the tiny nucleus (order of micrometers)


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What is the actual storage form of energy in muscles? ATP or Glycogen?
I was asked this question in my latest exam. I think the answer is Glycogen because ATP doesn't store energy for a long time so it isn't the ACTUAL storage of energy. Some classmates argue that in muscles there are other substances, not only glycogen, that are used to produce ATP. In the process of contraction ATP is required so, they say, the question needs the answer to be ATP. Could someone please clarify this discrepancy?

This is a typical MCQ which in order to answer you have to have been at somebody’s lectures or be able to read his mind. The antithesis of education! Cells don’t store energy like car batteries.
Glycogen in muscle is a store of carbohydrate. It can be used to generate ATP if it is broken down to glucose and the glucose glycolysed. I wouldn’t have chosen this as an answer.
The concentration of free ATP in the muscle cell is not sufficient for it to act as store of a high group-transfer potential compound (which is presumably what the question means by energy). This is definitely not the right answer.
However if creatine phosphate (a.k.a. phosphocreatine) was a choice on your MCQ, that was probably the answer expected as it is used in muscle as a storage molecule which can be rapidly converted by creatine kinase creatine and ATP.
PS
As you say in your comment that the only choices were ATP or glycogen, then glycogen is what is expected.

OK, David, but I didn't have creatine phosphate as a choice I had ( Glucose - Glycogen - ATP) , and you have jus told me that the latters are wrong and I don't think that glucose is the correct answer, but the question really confuses me. You said that Glycogen is broken down to generate ATP, why wouldn't you chose it as an answer then?

Because It's a two-step process to get ATP from glycogen. However if there's no creatine phosphate choice I imagine that's the expected answer. My point is you should be able to understand and describe a process. For example, if I asked you to describe what happens when muscle glycogen is exhausted (no MCQ), would you be able to?

I would be able to describe what happens, but the MCQ confused me, so anyway thank you, David.

You're welcome Asmaa, and don't mind me. I detest MCQs, but fortunately don't have either to answer MCQs or (any more) to set them. However you have no choice but to play the system. Just try to see the big picture as well.

If you are only given glycogen and ATP as choices, then glycogen is the correct answer. The reason for this is, that muscle cells need ATP also for other very important processes (such as keeping the membrane potential stable and preventing cramps). Thus, while ATP is the actual fuel that powers myosin to create the muscle force, the cell needs to keep the ATP concentration constant in order to avoid negative impacts on other metabolic processes. Therefore glycogen is the actual energy storage.
However glycogen is not the only energy storage used in muscles. The muscle actually uses a quite clever energy management system:
During the first 2-7 seconds it uses phosphocreatine (or creatine phosphate) to quickly replace used ATP (as mentioned in the answer by David). This means a 100m Sprint can be almost completely performed using this energy storage system.
For the next ~30 min (but can be up to several hours for well trained endurance athletes), the muscle relies mainly on energy stored as glycogen. The glycogen is broken down into glucose and the glucose is then converted into glucose-6-phosphate and then ATP during glycolysis. Glycolysis creates ATP much faster than oxygen respiration. However, a side-effect of this is that glycolysis generates lactic acid which is further broken down by oxygen respiration, and in the liver. Overtraining can cause lactic acid accumulation whcih can acidify the muscle and cause lactic acidose
There is much more energy stored in glycogen than in phosphocreatine which also makes this the more likely answer to your question.
Finally, after glycogen stores are depleted, the muscle needs to reduce its energy output and rely on external energy provided by the liver and by fat reserves of the body. This is the reason why some trainers claim that you need to exercise for more than 30 min to start burning fat and thus to reduce weight but this is wrong because the glycogen stores in the muscles are also restored using energy from body fat (which means that the best and only way to loose weight is to burn more energy than you consume either by increasing exercise or reducing food intake or both).

ATP is the end result of breaking apart glycogen. This isn't a trick question, it's in every textbook that glycogen is a primary store of "will soon become ATP" materials, like glucose.
The keyword here is "primary," as there are other ways of getting and storing ATP... that is, putting oxygen and glucose into the cells, and then there is always glycolysis, which doesn't use oxygen (makes lactic acid which is why muscles burn during weight training, because there was no more oxygen for cellular respiration).
But glycogen breaks down fast, and holds thousands of calories, hundreds in the muscles alone, so it is the primary store of ATP.

What is the storage form of ATP?
Answer: Creatinine phosphate


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why a testosterone pill can't be effective?
Why estrogen, progesterone etc. in the contraceptive pills survive the acid environment of the stomach and all the digestive enzymes, while testosterone needs to be injected or spread with a gel on skin?
I have no idea of why this difference in assumption, because I know testosterone and "feminine" hormones have the same steroid based structure...so I can't pick up why testosterone differently from "feminine" hormones can't resist the digestion.

Testosterone can be administered orally as undecanoate ester (brand name Andriol). The big challenge of oral steroid hormones is not the acid degradation, but liver first pass metabolism. (Which is mitigated by adding alkyl group at the alpha-17 position, or use of fatty acid ester; see for instance ethinylestradiol, levonorgestrel, or estradiol valerate)

so why the testosterone pill is very rarely prescribed? It is proved that the female pill with the chemically modified hormones is effective. So why the testosterone pill is not considered enough effective in the oral form so that It is rarely prescribed.

Probably depends on where you live, it isn't rarely described here in the Netherlands, although transdermal gels are winning terrain. I think an argument from a pharmacological point of view would be the varying bioavailability of oral testosterone undecanoate.

As stated in the comments by Eliane B., testosterone can actually be administered orally when an undecanoate ester is attached. The reason regular testosterone cannot be adminstered orally is because it undergoes extensive first pass metabolism (oxidation of the 17b-hydroxyl group to a 17-keto group, catalyzed by 17b-hydroxysteroid dehydrogenase enzymes, which are active in the liver). The undecanoate ester makes the substance lipophilic enough to be transported by the lymphatic system to the circulation after absorption by the intestines. Without the ester it will first reach the liver via the portal vein, thus exposing it to first pass metabolism. Nevertheless, bioavailability of oral testosterone undecanoate is estimated to be less than 10% [1].
Besides that, there are also derivates of testosterone which have a high oral bioavailability. These derivates have an alpha-oriented alkyl group, usually methyl, at position C-17, which retards hepatic metabolism. However, this can lead to hepatotoxicity [2].

https://www.ncbi.nlm.nih.gov/pubmed/3770015 (note, the subjects were women, but in the literature it is assumed that similiar bioavailability is obtained in men)
https://www.ncbi.nlm.nih.gov/pubmed/27372877


text:
The most reliable way of identifying deer antler measurements?
I am creating a (theoretical) study on how males use antlers to assess fellow males' abilities. I thus would need to have accurate measurements of antlers, including length, width, number of tines etc.
The papers I am reading are either really vague, using data already available, or they are relying on antlers which are cast each year to obtain the measurements. In a real life study, the last would be least intrusive and the most ethical, but would it be the most reliable?
I am equally unsure of the efficacy of waiting for deer to cast their antlers to then obtain measurements, as well as having the issue of changes / potential misidentification. I could take the DNA from the antler and use that to identify the deer that they came from.
Does anyone have any experience of this / any input as to what would be the most ethical, reliable method of doing this?
I understand there are confounding factors in this study, with other traits likely affecting deer fights. They seem to be largely un-dealt with in the literature, and I am giving them thought also.
With thanks.

Since antler size is important for hunting regulations, I imagine hunters and related organizations (such as rangers or game wardens) might compile such data. Hunted animals could also provide a source of data that does not require antlers to be shed.


text:
What is the distance between the 3' 18s rRNA (the Kozak consensus sequence) and the A-site of eukaryotic ribosomes during protein translation?
Reposted from Quora
The Kozak sequence is shown to be important in translation initiation, and the A-site is the anti-codon recognition site. If the distance is not known, how could I find out what it is? Is the crystal structure of the whole mRNA-rRNA-tRNA complex determined? If so, what modeling program would be best for establishing intermolecular distances?

Kozak consensus sequence (KCS) is present near or overlapping with the start codon. I am not sure what you mean by distance between that and A-site. Start codon is localaized at P-site at the time of translation initiation. Distance between start codon/KCS and A-site at initiation is same as distance between P- and A- sites (I guess ~20Å). A-site keeps moving during translation and hence the distance keeps increasing. Crystal study is available; See here.
See this figure from the abovementioned study for the relative positions of start-codon, P-site (exit) and A-site (entry).


text:
When should endocytosis inhibitors be used in cell binding assays?
I'm beginning to do some cell-binding assays and I would like for my proteins to not be endocytosed by my mammalian cells. Typical suggestions are for the cells to be kept on ice and that the binding experiment also occurs when the cells are chilled.
However, to be sure it has been suggested that I use endocytosis inhbitors. So my questions are, when are the endocytosis inhibitors necessary? How would I know that endocytosis inhibitors are necessary? Which ones would I actually use?
I recognize that there are both clathrin and non-clathrin mechanisms of internalization. Which mechanism would be more useful to study for an antibody-receptor interaction?

As with so many things, it depends. Also, I'm a bit unclear when you say antibody-receptor interaction, do you mean that you have an antibody that's specific for a receptor, or that you're studying Fc receptors binding to antibodies? (for the following, I assume the former)
For most cell types and most cell surface molecules, simple antibody binding isn't going to induce endocytosis, and keeping the cells on ice is sufficient to prevent most background endocytosis (i'd do the assays in a cold room as well so that even when you take tubes out of the ice bucket they stay cold).
On the other hand, if you're using highly phagocytic cells (like macrophages), and/or you're triggering a receptor through cross-linking or some other mechanism, you might get some endocytosis that affects your results.
The mechanism (clathrin vs non) can also vary, again depending on what's being bound.
You should do some optimization - ie: do the same assay on a set of samples, with or without  inhibition and see if your antibody binding is affected. But be aware that a lot of drugs for inhibiting endocytosis can do other stuff too, so watch out for artifacts. Maybe read this: http://www.ncbi.nlm.nih.gov/pubmed/18369934


text:
What is the extent of the effect of Tris on E. coli?
I was a fool and dissolved my antibiotic (Kanamycin) into Tris Buffer rather than H₂O. The Kanamycin still seems to be active but a fellow labmate mentioned that Tris messes around with the membrane permeability of cells. I was curious to what extent this actually influences experiments.
Tris(hydroxymethyl)aminomethane buffer modification of Escherichia coli outer membrane permeability.

The cited article describes effects of Tris on the outer membrane of E. coli. Like all Gram negatives E. coli has an inner (or cytoplasmic) membrane which is a typical phospholipid bilayer membrane containing many membrane proteins including transporters and, of course, an electron transport chain. Surrounding this there is a layer of peptidoglycan, and then the outer layer of the cell envelope is the outer membrane, which is a special (highly atypical) bilayer structure containing phospholipid and lipopolysaccharide as well as a number of proteins including the porins. The space between the two membranes is the periplasm, or periplasmic space which contains a number of small secreted proteins.
The outer membrane is susceptible to disruption by a number of treatments including EDTA treatment. For example, many cell lysis procedures for E. coli use EDTA to disrupt the outer membrane sufficiently to allow lysozyme to gain access to the peptidoglycan.
Cells with destabilised outer membranes could display increased fragility, but in general I would imagine that this would not normally cause any specific problems: obviously this would depend upon exactly what your experiments are.
Finally it is worth noting that the concentration of Tris that you will be adding with your kanamycin must be pretty low. Even if you have used 0.1 M Tris you are presumably using a 1000x stock, so the final concentration of Tris will only be 0.1 mM. The work in the cited paper looked at cells resuspended directly in 0.1 M Tris. I don't think that you need to worry about this at all.

Thanks! I had the same conclusions in regard to the dilution factor so I wasn't too worried. However, it's always better to have a good idea of the mechanism.


text:
Hardy-Weinberg Equilibrium: To compute probability of finding two siblings (random mating)
I've been working a little with M. G. Bulmer's Principles of Statistics (Dover, 1979) and cannot see how to properly compute half of one question. This should be a basic probability computation, but I am not getting the same answer as the book's suggestion.
Here is the question (Chapter 2, Problem 2.4): If the three genotypes (i.e., AA, Aa, aa) are all distinguishable, find the probabilities that a) a pair of siblings and b) a pair of unrelated individuals will appear the same when p=q=.5.
The book offers .59 for a) and .38 for b). I can get b correctly, but I don't understand how to properly compute part a).
This does not seem like a complicated exercise!

I got .59. In response to WYSIWYG:
(Note: I'm using A and a for the two alleles. My copy of Bulmer uses B for the second, which makes a little more sense if the alleles are codominant.)
a.) The AA x aa cross should be twice as common as the AA x AA and aa x aa crosses, just as HT is more common than HH or TT when we toss a pair of identical coins. In particular, this cross should occur with frequency 2*(.25*.25)= .125. Same goes for AA x Aa, AA x aa, and Aa x aa.
b.) In an Aa x Aa cross, there is a 3/8 probability that two offspring will have the same genotype. I reasoned as follows:

There is a 0.5 probability that the first offspring will be heterozygous (Aa). In that case, there is a 0.5 probability that the second offspring will also be heterozygous.
There is a 0.25 probability that the first offspring will be homozygous AA: In that case there is a 0.25 probability that the second offspring will also be AA. Likewise for aa.
Summing these: (1/2)^2 + (1/4)^2 +(1/4)^2 = 1/4 + 2/16 = 3/8.

I believe that resolves the issue. Apologies if I've missed something.

this seems to be right. Thanks for correcting.

Are you sure it is 0.59 because I am getting 0.5625 for part (a) and this is how I computed.
To check genetic similarity of siblings we first have to pick up mating pairs. Six mating pairs possible with following offspring probabilities (choice of first mate x choice of second mate x same offspring genotype freq).

AA x AA : will always give same type of offspring: prob = 0.25x0.25x1
aa x aa : will always give same type of offspring: prob = 0.25x0.25x1
AA x aa : will always give same type of offspring: prob = 0.25x0.25x1
Aa x Aa : will give Aa in half the number of times: prob = 0.5x0.5x0.5
Aa x AA : will give two types of similar offsprings, half the number of times - AA and Aa: prob = 0.5x0.25x0.5x2
Aa x aa : will give two types of similar offsprings, half the number of times - aa and Aa: prob = 0.5x0.25x0.5x2

Total probability = 3x(0.5x0.5x0.5) + 3x(0.25x0.25) = 0.375+0.1875 = 0.5625
Assumptions:

Population is infinite
Population in equilibrium

For what it's worth, I repeated this calculation in my own peculiar way and also got 0.5625

@AlanBoyd: can you tell me how you approached it ?

By peculiar I meant I did it in a spreadsheet - probably it is exactly the same logic as your calculation. See https://www.dropbox.com/s/k46xhff3x0p1oc7/HW2png.png

Thanks to you both for your comments. .5625 is what I got as when I did this, too. It may simply be an error on the solutions page, but I couldn't rule out that I was making an error.


text:
Why is China experiencing such a surge in acute cases of COVID?
The majority of western nations have lifted most if not all COVID restrictions, however we are not seeing a massive rise in serious cases of COVID-19.
Why is it different in China? Do they have a different strain?

The claim that "we are not seeing a massive rise in serious cases of COVID-19" requires reputable sources.  From all the publicly available data I have analyzed, there appears to be no data to support any such claim.  Of course, I suppose, one could define "massive" to mean whatever they want, which is why it is best to use scientific terminology and methodology and refrain from using such ambiguous terms.

There are a number of different reasons, all adding up to the current situation.

The strain: There is not a special strain going on in China, according to different references it is mostly the Omicron BF.7 substrain. This strain is highly transmissible (with reported $R_0$ over 10, meaning each infected person infects on average another 10; the Delta strain (which was also already seen as highly infectious) "only" came to an $R_0$ of 5-6). Additionally this strain has accumulated mutations which allow immune escape, a shorter incubation time.

Covid politics: China went from a very strict zero Covid politics to no restrictions at all in the matter of days. Additionally, testing almost completely stopped. This happened with the rise of the highly contagious variant. People started getting together and spread the virus very fast, leading to the current problems.

Vaccinations: In China only the relatively inefficient Sinovac vaccine has been used, as far as I know only two vaccinations are common, with no preference for the older part of the society. How this vaccination (which happened some time ago mostly) will be able to prevent severe disease and death remains to be seen. However, the vaccination status could be better.

Immune status: Curiously, this point is connected to the zero Covid policy. This lead to many people in the Chinese society having never had contact to SARS-COV2. Without this contact, immunity cannot be built (besides vaccinating), this may be an advantage for other societies which had more contact with the virus, although immunity wanes over time.

Population: All the areas where Covid surges now are urban centers with a really high population density. Additionally public transport leads to a lot of potential contacts.

Every of this point attributes a bit to the current problem, but only the combination made it so severe.
References

WHO concerned over increasing reports of severe COVID-19 cases in China
COVID spreading faster than ever in China. 800 million could be
infected this winter
China’s COVID Wave Is Coming
Omicron BF.7, major strain causing latest outbreak in Beijing, has
strong infectious ability: medical expert

All of them, plus a very dense population and a highly interactive urban dynamic.
In each of the biggest cities, subway networks transport more than 10 million passengers per day, and more than 108 billion domestic postal packages last year, etc.

@XZhang Right, I forgot to mention the high population density and dynamics. Thanks, I added this point.

I think 4. is especially relevant. In Most western countries, a vast majority of the population had Covid.  A lot of people even multiple times. Often enough more or less harmless (being out of order for a week) but still built immunity far beyond any vaccine (and most often on top of it). This constant natural re-innoculation keeps numbers low

with reported 0 over 10, meaning each infected person infects on average another 10; the Delta strain (which was also already seen as highly infectious) "only" came to an 0 of 5-6 => these estimates are likely to be overblown. See this article.

Indeed. Important questions when doing such comparisons: What is the vaccination coverage in China vs the countries you compare it with? What's the effectiveness of their vaccine vs the one used in the countries you compare it with? Don't forget to account for boosters and population density. The closer people are together, the more vaccines for such viruses matter.

Allegedly, the Sinovac vaccine is on par after the third dose. The source is somewhat controversial, but there is a reference to the primary source in it.

@Hobbamok wrote: built immunity far beyond any vaccine - I'm interested in reading about your claim.  What are your reputable peer reviewed sources?

@RockPaperLz-MaskitorCasket mate. Calm down. All curent Covid vaccines effectiveness decays. You'll find a source for that easily enough. Any further interaction with the virus (be it live or another shot) increases the immune systems effectiveness. Since anything beyond a 4th shot is not recommended for most people, the constant lowkey reinfections with covid (or successfully defended intrusions of the virus) keeps antibody count high. It's not rocket science.

Another important point is that a good bunch of the western world went, and stayed, remote. It's harder to get the virus if you're not stuck inside an office with someone sick.

Great answer to a challenging question! (potentially interesting/helpful in the NYTimes: How Bad Is China’s Covid Outbreak? It’s a Scientific Guessing Game. (In the absence of credible information from the Chinese government, researchers around the world are looking for any clues to determine the size and severity of the surge.)

@Hobbamok Please do not tell anyone to "calm down" when they politely ask you to cite sources for your unsubstantiated claim.  You want us to simply believe you and your claims and that immunology is not "rocket science" but you literally have earned zero reputation on this site.  Sorry, but you need to back up your claims with references or provide documentation of your expertise.  You are correct on one matter, however.  Immunology is not rocket science.  It's much more complicated and not as well understood.

however we are not seeing a massive rise in serious cases of COVID-19.

Because we've already had a huge Omicron wave in December 2021/January 2022 while China is only reopening today. This means that their population is highly vulnerable to becoming infected with the Omicron variant and they need to go through a massive COVID wave to acquire proper immunity. See the Boston Wastewater data tracking the presence of COVID in the city:

That giant spike in late 2021 is precisely what's going on in China right now. Note that they're in an even worse shape than the US because <1% of their population was infected prior to December 2022 and their vaccine efficacy is lower compared to Pfizer/Moderna's product. They'll go back to having the same baseline of cases as the US once the initial wave subsides and the herd immunity threshold is reached.

Did Boston reopen in dec 2021? or did something else caused this sudden rise?

@moshevi compared to China Boston was never locked down in earnest and the worst restrictions were dropped by spring 2021. The only thing that happened is Omicron.

1/ China hasn't built up natural herd immunity, only 0.1% has had it.
2/ Restrictions are lifting in winter, the worst time to lift them for a low immunity nation.
3/ Some Chinese populations are frustrated by extreme and unreasonable covid rules, they may not quarantine voluntarily after watching the world cup.
4/ China has administered 3,5 billion doses of a fairly effective vaccine, it reduces mortality by 90+ percent, however they may have administered the second dose too long ago in 2020 and 2021 to be very effective today.
5/ Everyone knows that the government gives false information, they don't know what is true and what isn't.

ad 1) As far as we know, there is no herd immunity to be obtained as the virus can mutate.
ad 3) Unfortunately, not following the orders can result in pretty hard restrictions in China, so I doubt this is a major factor.
ad 4) The vaccine is far less effictive than other available ones.

1/ that's a fair argument, however the global infection figures with unrestricted contact and without recent injections are 5-10 times lower on new year 2022 than they were exactly one year ago, when there was major vaccination and contact restriction... Even though herd immunity is less than i.e. smallpox, immunity is causing 10x less infections in previously infected populations one year on. 3/ Home quarantine apartment blocks are difficult to police and the restrictions are reducing 4/ the vaccine has 95% reduction in mortality according to current medical sources.

also consider the financial benefits to labs that announce "natural immunity may be insufficiant", because that plays exactly into the hands of pharma bosses that say "boost your immunity with our product (at 10x prices now)" ... Industries love false science that promots their product, i.e. cellulose insulation was banned for 40 years at the profit of fiberglass/rockwool because of a single false study promoted by the rockwool stating a fire risk, which was reverse when they found cellulose has mininal fire risk.

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


text:
Do mutations in a fundamental structure of a virus [Omicron Variant] make it more transmissible?
I am not a microbiologist, nor a virologist so I had a question - in the new Omicron virus variant, a large number of mutations were reported for the protein spike.
From my naïve understanding, the spike is an integral part of how the virus replicates inside a host - thus, does it mean that changes in protein spike structure would lead to a more transmissible - therefore deadly variant?
And if so, won't the effect of vaccines reduce drastically since there's a fundamental change in the virus' structure which the immune system might not anticipate? Or the antibodies be able to handle?

Omicron as an escape variant might be a good example for  questioning  a rule that says "... more transmissible - therefore deadly variant". Any changes the success of which depend on immune escape  bear a chance that pathogenic factors are reduced and relinquished for the sake of transmissibility.

(Converted from a comment.)
We have no idea at this point. Mutations are worrisome because they could indicate changes in transmissibility or virulence or capability for immune evasion, but it's almost impossible to predict.
efficacy of vaccine/natural immunity
The easiest aspect to measure (approximately) will be immune evasion, by measuring the affinity of antibodies raised by existing vaccine to virus of the new strain in vitro ... transmission and virulence are much harder to quantify (or quantify proxies for) in the lab.
Antibody trials to evaluate efficacy are what a lot of immunologists will be spending their time doing over the next week or two: for example, from this article

[Prof Penny Moore at the University of the Witwatersrand will engineer] “pseudoviruses” – harmless, non-replicating viruses used to model coronavirus variants ... to carry Omicron’s mutations. These will then be exposed to antibody-carrying blood plasma from vaccinated people and those who have recovered from Covid infection to see if they neutralise the virus.

[Prof Alex Sigal from the African Health Research Institute in Durban] is growing batches of live Omicron from people who became infected in the recent surge in Gauteng in South Africa. Once he has enough to work with, the variant will be tested against blood plasma from vaccinated people and those with some natural immunity after a Covid infection.

transmissibility
Again, it's hard to predict what will happen to transmissibility simply from knowing the genetic sequence. It is possible to do in vitro studies with cell lines to try to estimate changes in transmissibility, although these do not perfectly predict how much a real live infected person will transmit (for example, these tests are done without any involvement of the immune system). e.g.: Hou et al 2020, Plante et al. 2021.
virulence
Virulence describes the severity of illness in a person infected with a given strain. This is probably the hardest of the three characteristics to measure in the lab; we may just have to wait until the omicron strain has spread and observe the fraction of cases that need to be hospitalized or sent to the ICU (although this still won't tell us what fraction of people who are infected have very mild or asymptomatic cases and are never even recorded as COVID cases ...)

Hou, Yixuan J., Shiho Chiba, Peter Halfmann, Camille Ehre, Makoto Kuroda, Kenneth H. Dinnon, Sarah R. Leist, et al. “SARS-CoV-2 D614G Variant Exhibits Efficient Replication Ex Vivo and Transmission in Vivo.” Science 370, no. 6523 (December 18, 2020): 1464–68. https://doi.org/10.1126/science.abe8499.
Plante, Jessica A., Yang Liu, Jianying Liu, Hongjie Xia, Bryan A. Johnson, Kumari G. Lokugamage, Xianwen Zhang, et al. “Spike Mutation D614G Alters SARS-CoV-2 Fitness.” Nature 592, no. 7852 (April 2021): 116–21. https://doi.org/10.1038/s41586-020-2895-3.


text:
Giving a sign to Pressure Potential, Osmotic Potential And Other Similar Quantities
When these quantities are mentioned with what reference do we give signs to them?
Why is Osmotic Pressure positive, but Osmotic Potential, negative?
What about Turgor Pressure (Pressure exerted by the protoplasmic fluid on the cell wall) and the Wall Pressure (Pressure exerted by the Wall as a reaction to the Turgor Pressure), what signs do we assign to them?
What I understand is that it's based on the tendency of water to enter or exit the system being studied, but I lack clarity on how signs are being assigned to these different quantities. When we talk about soil having a low, does low mean more negative or does it mean a lower magnitude osmotic potential, for example?

I think you already know the sign convention in calculating the water potential: the addition of solutes lowers the potential (negative vector), while an increase in pressure increases the potential (positive vector).(Another way of saying the same would be more solute = more negative.) {1} This is the same everywhere.

Pressure potential: The pressure potential in a plant cell is usually positive. In plasmolysed cells, pressure potential is almost zero. Negative pressure potentials occur when water is pulled through an open system such as a plant xylem vessel.{1} This means that it is negative during a "suction" action, otherwise, it is positive.

Osmotic potential (solute potential): The relationship of solute concentration (in molarity) to solute potential is given by the Van't Hoff equation:
Ψπ=−MiRTΨπ=−MiRT

(The formula, note, has a -ve sign.)
For example, when a solute is dissolved in water, water molecules are less likely to diffuse away via osmosis than when there is no solute. A solution will have a lower and hence more negative water potential than that of pure water. Furthermore, the more solute molecules present, the more negative the solute potential is.

Turgor pressure and wall pressure: I recommend reading this for a clearer understanding.

...This actual pressure which develops within such a cell is called turgor
pressure. This term can be applied with equal appropriateness to the actual
pressures developing in purely physical osmotic systems such, for example, as a
sucrose solution enclosed within a collodion or cellophane membrane and immersed
in water. As will become clear in the following discussion, TPs in osmotic systems
can sometimes be negative in value.

When the TP
is negative, that is, when the cell sap is under tension (see later), the WP is
likewise negative, the wall being subjected to a centripetal pull because of its
adhesion to the protoplasmic layer and cell sap mass within the cell.

On the basis of fundamental physical principles it is generally considered
that the WP and TP of a cell are equal in magnitude and oppositely directed.
This situation is not difficult to visualize for a cell in an equilibrium condition.
For dynamic states in which water is being gained or lost by a cell, however,
the validity of this assumption has been questioned.

{1}-https://en.wikipedia.org/wiki/Water_potential


text:
What is this thing? It is hairy mostly a cocoon, and i saw a white worm pop out of it. It is spreading rapidly
I suspect it is originating from the mud. This has some plastic bits with it. They are spreading all over my walls. I think it is some  kind of cocoon for worm. Should it's rapid growth in terms of number be a matter of concern? found in Bangalore, India,

Bagworms?
https://en.wikipedia.org/wiki/Bagworm_moth
I don't know how destructive individual species are. They probably aren't more than an aesthetic concern.

Example: https://www.youtube.com/watch?v=H3o3lIVXANg

No, it doesn't seem like a bagworm.


text:
What is "KK1 enzyme"?
In the book "The Kaizen Way" by Robert Maurer, I've read the following:

When we’re sitting, our muscles go into a form of hibernation, causing
our bodies to shut down the enzyme (called KK1) that breaks down some
of the fat in the blood.

However, when I tried to google "KK1 enzyme", I got nothing about any enzyme. I mean, I got this website and this article, but they don't contain the name "KK1" at all.
What was meant by that? Is it scientifically accurate?

KK1 is a putative potassium channel blocker in the venom of the Manchurian scorpion, but I couldn't find any evidence for a mammalian KK1 protein of any function, let alone fat metabolism.

Sounds as if he has no idea what he is talking about. I'd trash the book immediately.


text:
How might one determine if bacteria are nitrogen fixing or not?
If you had an isolate bacteria sample how would you determine if they were nitrogen fixing?

Would stable isotope probing be useful?

@zenbomb more of a comment than an answer :)

Never mind found the answer myself you can use the acetylene reduction assay.

as a quick screen, often nitrogen fixing bacteria die or stop fixing nitrogen when exposed to oxygen.

This is true, nitrogenase has a very low half life in the presence of oxygen- around 30 seconds. Never thought of that could be useful for further lab testing... Thanks.

I'd suggest doing a bioinformatic search of the bacterial genomes first before doing the experiments. You should be able to find homologues of the "nif" (nitrogen fixation) genes there.

Not ideal if you have no idea what the colony is at all though.


text:
How does sequence independent single primer amplification work?
I'm having difficulty finding an explanation of how single primer amplification of DNA works in the literature available to me, can anyone explain the methodology and what it accomplishes?

This process is called sequence-independent single primer amplification (or in short SISPA). Its used to amplify unknown sequences for amplification, for example in unknown viruses.
The primers used for this process contain random sequences which should bind to the DNA to be amplified and also known sequences, which can be used a adapters. In the first rounds of PCR only the random primers give rise to specific products, which are amplified exponentially in the later rounds of PCR since the primers fit perfectly then. This is described in detail in this publication:"Random priming PCR strategy to amplify and clone trace amounts of DNA"
Another interesting paper describing the method is:"Sequence-independent, single-primer amplification (SISPA) of complex DNA populations."

single primer amplification is used to find unknown regions of DNA if you have no idea what to use as a primer further upstream. It works on the idea that any primer given a certain temperature will misprime. That it, it will anneal to a non specific location. So it is PCR, but at this temperature, the five prime region primer will bind specifically to it's known location. On the three prime end up to 3500 bases away, the low annealing temperature will allow this specific primer to bind to something resembling its complementary sequence but not exactly. This way you will still get a successful PCR reaction. Then as the cycles continue, the 3' end binds specifically to your one primer and you can raise the temperature to make it more specific. The primer design and temperatures have to be considered very carefully.
Sources
Roth Lab


text:
When designing primers how important is the GC clamp?
I'm designing a set of primers and reading about the principles of primer design one of which is:

GC Clamp: The presence of G or C bases within the last five bases from
  the 3' end of primers (GC clamp) helps promote specific binding at the
  3' end due to the stronger bonding of G and C bases. More than 3 G's
  or C's should be avoided in the last 5 bases at the 3' end of the
  primer.

From here.
My question is how essential is it to have a GC clamp?

If it is important to have G or C why more than 3 G or C should be avoided ?

@biogirl more G/C should be avoided because in an event of pairing between the primers you don't want the pairing to be too strong. Otherwise you'll get a lot of primer dimers.
Ben, GC clamping is important as it will allow strong bonding at the 3' which is good for elongation but this is not the primary parameter to be tweaked. There are other important parameters to handle (for e.g self complementarity, low-complexity etc).

GC clamping at 3', that is having a single G or C at the 3' end or a couple of G/C within the last 6bp at 3' end of primer, can help retain the primer on the template during elongation, because of stronger bonding compared to A=T. This is not mandatory; it's one of the characters of the primer which might improve your PCR reaction.
At the same time, avoid a sequential combination of GC in the last 6bp which might lead to self-dimers.
Example: 5'-.....GCGC-3' has higher chance of dimer formation than 5'-.........GCCG-3'; in such cases you can still use the latter primer sequence.

Unless you are PCRing something you know to be challenging, just use primer3 and don't worry about it.
http://bioinfo.ut.ee/primer3-0.4.0/


text:
How was the heritability of IQ tested?
I have read that IQ is highly heritable.
How could this be tested?
For honest testing, it seems to me that only children who were abandoned should have been tested, to exclude education effect. Was it really done?
UPDATE
Intelligence is one of the traits, that can be inherited both by genes and by education. You can't educate your children to have blue eyes, but you can educate them to count or to read.
So, to study heritability of intelligence, educational inheritance should be excluded.
I know that usual way to study heritability is to compare variability for monozygotic and dizigotic twins. Being sufficient for other traits, this method is highly insufficient for intelligence (which is obvious). Having identical perception system, monozygotic twins will respond identically to an education, so they will be more closely educated, even if IQ is completely independent of genes.
So, to study IQ heritability, subjects should be studied under different education conditions. I.e. they should be abandoned by parents and/or adopted separately.
My question is: was this done or not?
If not, then the question is, how education effects were eliminated?
Also I would like to know, if my reasoning about why just studying twins is insufficient is wrong.

I don't really know what you mean by "abandoned children".  Adopted children?  Children in the wild?  Have you read the Wikipedia article on the subject?  If you want to know how it was studied, just take a look at the references, it's pretty straightforward.
Heritability simply means how much variation in a trait is due to genetics, which is usually easiest to test in monozygotic twins.  Here's a good example where they did just that - they compared identical (monozygotic) and fraternal (dizygotic) twins raised apart or separately, finding:

General cognitive ability yielded a heritability estimate of about .80 in two assessments 3 years apart as part of the Swedish Adoption/Twin Study of Aging. This is one of the highest heritabilities reported for a behavioral trait. Across the two ages, average heritabilities are about .60 for verbal tests, .50 for spatial and speed-of-processing tests, and .40 for memory tests. For general cognitive ability, the phenotypic stability across the 3 years is .92 and stable genetic factors account for nearly 90% this stability.

Here's another example doing basically the same thing.  The rest of the enWiki article gives a good breakdown of all the various factors involved in making this such a complex issue, as well as what was studied.

My question is how verbal (educational) inheritance was excluded. Your answer is it wasn't at all? Comparing monozygotic and dizigotic twins does not help to exclude education. Monozygotic twins can show lower variation just because they respond to education similarly.

P.S. Explanation about what is child abandonment http://en.wikipedia.org/wiki/Child_abandonment

I know what child abandonment is but I don't see how it's useful to your question.  By studying children raised in the same environment, you remove the educational/verbal barrier.  As stated above, they looked at twins raised together (same education) and twins raised  separately (different education).

A classic study of IQ heritability is Skodak & Skeels (1949). They studied heritability of IQ in children who were adopted at a very young age, with IQ data of the children, of their biological mothers, and of their adoptive mothers. It is important to keep in mind that heritability is a measure of the proportion of variance that is attributable to genetic inheritance in the population; it is formally the ratio between genetic variance in a population to the phenotypic variance in a population. The above mentioned study found a high heritability between biological mothers and their children (0.88), but no heritability between adoptive mothers and their children. Yet the mean IQ of children were similar to adoptive mothers, and much higher than their biological mothers.
This is not a contradiction. High heritability does not mean that environmental factors are not important. Indeed, environmental factors (such as upbringing, education, socioeconomic status) may have a large effect on mean values, hence why the children had IQs similar to their adoptive mothers. However, heritability explains variance not mean; in the above study, there is a high correlation between where children fell on the normal distribution of IQ scores among the children and where their biological mothers fell on the distribution of biological mothers, but no correlation with where their adoptive mothers fell on the distribution of adoptive mothers.


text:
What is doubling of genetic material invented in flowering plants?
David Attenborough in his Kingdom of Plants 3D said, that flowering plants made two inventions: (1) doubling of genetic material and (2) symbiosis with animals.
What was meant by "doubling of genetic material"? Appearing of diploidy or something else?
UPDATE
Let me explain my doubts. Inventing of ploidy I regard as inventing of sex and syngenesis. This was done ~500 million y.a. in Ediacarian, if I am not mistake. Hence, this can't be done 140 m.y.a when flowering appears. I.e. both plats and insects had sex 140 mya.

Yes, D. Attenborough probably refers to ploidy number
Ploidy number
Humans for example are 2N (except during the spermatozoid and ovule phase of human existence) meaning that they carry two copies of each autosome (=non-sexual chromosomes). Some species are 1N (haploid), some are 3N (triploid), etc… It would actually be more correct to talk about the time a species spend in each of its phase or talk about the number of cells in each of its phase because many species undergo change in chromosome number during their existence as it is the case for humans. Humans are 2N most of the time but they are 1N when they are ovules or spermatozoid. The correct word to describe the human lifecycle is diplontic. Some species are diplontic, some are haplodiplontic and some have phases when they have a greater number of chromosomes. Those species are said to be polyploid.
Ploidy number, chromosomes and chromatids
To make sure one don't mix up things... One chromosome is made of one or two chromatids (depending on the cellular phase). The chromatids of the same chromosome (called sister chromatids) are (almost completely) identical. A given "chromosome type" is either alone (1N) or accompagnied by one very similar chromosome (2N) or two other very similar chromsomes (3N), etc.. Considering the case of a 2N individual: If at a given locus (position in the chromosome) the two alleles (gene variant) are different than the individual is said to be heterozygote for this locus. The ploidy number describe "this number of chromosomes"! Now there may have different number of different "types of chromosomes". Humans for example have 23 different types of chromosomes and in its haploid phase has therefore 23 chromosomes (23 or 46 chromatids depending on the cellular phase) and has 46 chromosomes (46 or 92 chromatids depending on the cellular phase) in its diploid phase
Ploidy number in angiosperms and other plants and non-plants organisms
Yes, D. Attenborough (who I don't know and I haven't read anything of his work) probably means doubling, tripling, quadrupling, .. the number of N of chromosomes. And, yes indeed polyploidy (3N, 4N, 6N, 8N) is relatively often observed in flowering plants. There are many crop species that are polyploid. According to this article an important part of the speciation that occurred in plants is accompanied by a change in ploidy number but this is not only true for angiosperms.
Polyploidy is also found in many fungi species and some animal species as well. There are lots of terminologies linked with the discussion of chromosome number and reproductive system and many articles discuss these mechanisms and also the evolution of polyploidy. I found the work of Sally Otto to be of the greatest interest for example.
Notes
The words inventions are not really used in evolutionary biology but rather in popular books. Also, there are many non-angiosperm plants that have symbiotic relationship with animals. For examples: some angiosperms and the squirrels or birds. But it is true that angiosperm have particularly important symbiotic relationship with animals, in particular insects and this probably allowed an important diversification in both angiosperms and insects. As already said angiosperms are not the taxon of plants to include polyploid species. There are other characteristics that allow to tell an angiosperm apart from other plants. The number of aperture on pollen grain or the positions of the meristems (tissue where mitotic division of unspecialized cells occur allowing the growth of the plant) for examples.
You may be interested in reading this post on the effect on fitness of ploidy number

I haven't seen this particular film, but other documentaries by Dr. Attenborough are very accurate and well done.
In contrast to Remi.b, I'm pretty sure Attenborough referred to the ancient whole genome duplication event in land plants recently discovered in angiosperm genomes by the presence of multiple paralogous genes. The scenario is that at a certain moment either a hexaploidization or a genome fusion event occurred and was followed by gene losses, chromosomal reorganizations and gene diversification. In Selaginella, a spikemoss, no traces of this event were found.
A similar event, a tetraploidization, is hypothesized for vertebrates.


text:
Why cancer mutations do accumulate sequentially?
According to Knudson hypothesis, cancer mutations accumulate in order. Statistics says, that cancer probability increases as sixth order of age, which may mean six consequential steps to cancer.
But, mutations are random in nature. There is no apparent cause, why mutations ABCDEF can't occur in reverse order, i.e. FEDCBA and any other possible orders.
If unordered, any number of required mutations should cause flat age dependency.
Hence, something is ordering these mutations, i.e. making mutation B impossible until A occurs and so on.
What is it?
UPDATE
Cancer incidence dependency on age:

The graph is not linear, which means that mutations are not independent.
UPDATE 2
Let's regard some cancer, which requires 6 mutations. It's incidence distribution should be like shown above.
Now suppose we knew the distribution of all precancer stages, i.e. the distribution of people with 1, 2, 3 and so on mutations. These distributions should look similar to final distribution

Now let's regard only one (first) mutation.
Why is it's incidence age dependent?
Mutations are random. They should not depend on age. If they do depend on age, then they are not random. If "they" are not random, then "they" are not mutations.
Or, in other words, the cause of progression is not a mutation itself.
Isn't it true?

if this is true - and it might not be - i'd say its possible that mutations out of order are simply not viable and disappear from the cell population. cancer is a fault in cell division so it could be the case that most oncogene mutations are selectively removed.

I can't imagine how malignant mutations can be viable by one but not viable in sequence (and, finally, fatal if 6).

there are cellular mechanisms to kill badly behaving cells.  i tend to agree with you - i doubt the sequence is a rigorous set that must be followed exactly in some order.

This is a very broad topic that deserves an entire book. I would like to add to the given answers that not all the mutations occur sequentially.
This is the case of chromothripsis and similar massive reshuffling events that occur in around 2-5% of all cancers.

The sequence of mutations is important. Some mutations may allow other mutations to be not deleterious to the cell. For example, p53 loss will help oncogenic RAS mutations. The latter mutations will otherwise cause senescence response. Also, epigenetic changes, like p16 inactivation, can be a precursor that may allow oncogenic mutations to be selected. Thus the order of mutations is highly important, and non-genetic events preceding this order is also important. Wonder if there is literature on rate of mutations as a cell ages. Because if mutation rate increases, then that could also explain t

TL;DR:

A sixth order probability curve of cancer does not mean six steps. The order of the curve has nothing to do with the number or sequence of mutations.
Causes why ABCD could be more likely than DABC exist and have been extensively studied
Repair and control ("defence") mechanisms are what does the 'ordering' of steps by selecting for mutations which can circumvent them

The sigmoidal shape of the curve thus reflects the slow accumulation of "defence"-damaging mutations, which increase their own probability and thus the slope of the curve. I don't know if the slight decrease in slope towards the end reflects a real limit to the incidence of cancers, or if it's an issue related to the data, its availability or the way it is gathered (but has no basis in substance i.e. there isn't actually a limit).
To elaborate:
There are many biological factors which play into helping you understand the problem you are wondering about, and the fact that different cancers work differently does not make it easier. I would highly recommend that you check out Hallmarks of Cancer, the Wikipedia article also cites the interesting original publication. Basically, certain principles underly all cancers, but different cancers have different tendencies to develop certain hallmarks in a particular order.
Randomness of mutations:
Mutations are not random. The nature of DNA sequences affects their susceptibility to DNA lesions, i.e. damage caused by chemical processes such as a nucleotide losing its base, dimerisation of thymidine, single or double strand breaks and so on. Lesions occur all the time, so there are mechanisms in place to fix all types of DNA lesions. Occasionally however, the circumstances will permit e.g. two lesions to coincide or the repair process itself to make an error, which then leads to a permanent change of the DNA sequence that cannot be fixed anymore because the original sequence has been lost. This is a mutation, and mutations are also not random because the nature of DNA sequences affects the chancefor them to incur lesions that cannot be repaired.
Hence, one reason why certain mutations occur more frequently than others is because they are actually more likely to occur. But this isn't the main reason.
Cell self-control
There are higher levels of control than DNA repair. Various mechanisms in the cell exist to detect malfunctioning proteins (due to mutations in their gene) and degrade them - though sometimes malfunctioning proteins can still escape these mechanisms. Even in this case, there is an additional safety layer created by various mechanisms which lead a cell to kill itself (apoptosis). These are triggered for example if excessive DNA damage is detected, or if the cell-internal signals for and against proliferation are conflicting.
Sequential accumulation of mutations
The result of repair and control mechanisms (which I will now call "defence mechanisms") is on the one hand that we are far more resistant to mutations than we would be without them. On the other hand however, they create selection for mutations which are not affected by them.
This is where multi-hit models of cancer come from. A "first hit", "enabling mutation" or whatever you want to call it would be a mutation which itself is not affected by defence mechanisms - and simultaneously impairs the defence against other mutation(s). The "second hit", "initiating mutation",... would be a mutation which causes cancerous cell behaviour, but would be eliminated by a defence mechanism without the first hit.
This means that mutations do not always occur in the same sequence but rather, they occur in all sequences and sequences other than those that we find in cancer cells are eliminated.
Note that not all cancers have several mutations or a sequence. For example, chronic myeloid leukaemia (CML, a blood cancer) in the vast majority of cases is caused by a translocation from chromosome 19 to chromosome 22 which results in the famous Philadelphia chromosome and produces the BCR-ABL fusion gene. This single mutation is sufficient to cause CML.
Age-dependency of mutations:
Mutations can affect all parts of a cell's machinery, including the lesion repair mechanisms. This means that throughout its life time, a cell can (and will) accumulate mutations which increase the likelihood of further mutations. Mature cells usually have short life spans and mutations to their DNA repair machinery die with them relatively soon (days or weeks). However, pluripotent stem cells (PSC) in the tissues are just as likely to develop these mutations as mature cells - and PSCs are the ones which renew the tissue throughout life by differentiating into mature cells.
Thus, a mutation in a PSC remains for life, and the longer you live, the higher the chance that one mutation will affect the chance for gaining further mutations. This is why for all cancer types, the risk to develop them increases with age (though there are a few which are most likely at young age!)

Mutations occur indeed randomly. Most of them are either repaired or the cells go either into senescence or apoptosis and will cause no harm. Some mutations are harmless while others are among the ones which can cause cancer.
These genes, which are often mutated in cancers are called oncogenes and they are either mutated (permanently activated or inactivated) or misregulated (up- or downregulated, amplified etc.) in many cancers. These are preferrably genes which are involved in the regulation of cell cycle (which is usually halted if cells acquire mutations, something that the cell has to overcome), growth, division, differentiation and also apoptosis (genes which are regulating apoptosis are very often affected).
These mutation doesn't have to occur in a certain order, they need to overcome some "threshold" to transform the cell. During this whole process the tanforming cell has to escape the checks of the body which eliminates these cells.

Sorry, didn't understand. How threshold makes power dependence on age? If we observe 6th power, then we need 6 thresholds.

I am a bit unsure about six necessary mutations. This is something he analysed for retinoblastoma cells and it may not be true for other cancer types. The idea that you need more than one mutation on the other hand is widely accepted as far as I know.

But any graph of any cancer incidence is not linear. While any number of required random mutations would give flat graph. For example, if we require 3 mutations with probabilities of P1, P2 and P3 respectively, then graph will be P(t) = P1P2P3 = const. I.e. the probability that required 3 mutations occur simultaneously. To have curved plot, we need that mutations be not independent.

The question here is how you see the term dependent. Are they dependent in a way that they need to occur in a certain order? Not to my knowledge. Are they dependent that they happen in a number of oncogenes? This is something I would answer with yes. This and this links should be interesting.

ok I agree, that mutations should not appear in one sequence, but they should appear by one. Why? See my update 2 pls

I think this is a semantic misunderstanding. Her link says that incidence accumulates as the sixth power of age (i.e., a 6th order polynomial describes the relationship). This has nothing to do with the number of mutations, much less the order. It is a misunderstanding of the idea of sixth power.

Maybe your question is essentially semantic.
You have I think misinterpreted the phrase "sixth order." A sixth order* polynomial is one of the form $p = k_6 x^6 + k_5x^5+k_4x^4+k_3x^3+k_2x^2+k_1x +k_0.$ The $k_i$ are constants.
The graph caption in the first link in your post [Nordling] says that cancer mortality increases as the sixth power of age. You refer to this mathematical modeling idea in your question. This has nothing to do with the number of mutations or the order in which they occur. It simply means the trend can be modeled with a sixth degree polynomial.
In the case of your graph something like $y = k\cdot x^6 + 2000$ for an appropriate value of k gives an idea.

Knudson's hypothesis, also known as the "multiple hit hypothesis," says nothing about the order in which mutations occur.
Edit: The word 'random' as applied to mutations (and almost everything else), while still in use, may be incorrect and I removed it from this answer.
*The reference in the linked article uses the term "power." The term "order" in this context is a slight abuse of language. The correct term would be "degree," as in, a "sixth degree polynomial." Order is related to the highest degree of a set of polynomials spanning a vector space, not the topic here.

That's what I think, too. Thanks for pointing it out so clearly.

The ordering is due to how the most dangerous mutations knock out tumor-suppressing genes.
Assuming that mutations are random and uniformly distributed, most random bad mutations will be caught and prompt DNA repair or apoptosis. The best way for a mutation to avoid being caught is to disable DNA repair or tumor-suppressing genes. An obvious no-brainer example would be a nonsense mutation in TP53. After that, further mutations will quickly follow and bad mutations that would have previously been caught are now allowed to slip through.
The 2nd other prominent source of cancerous mutations are malfunctions in cell growth/migration signaling, although the most dangerous forms of these also require tumor-suppressing genes to be disabled first.


text:
What is the length of anaerobic biodigestion stages?
I have built an experimental portable batch biodigester to process organic garbage. A 50L drum filled half with garbage, half with water and with some cow dung added for inoculation, is connected from the top to a truck tire, boxed into another, larger drum.
I consider filling the bin within a week, based on the amount of daily garbage my home is producing. After a week, the bin is filled in with water and inoculated, and connected to the gas-holder.
How long would the biodigestion take in average before I can disconnect the bin and use the remaining slurry?
I have looked at existing information regarding the biodigestion process. The stages of biodigestion are explained in Chapter 4 of the Biogas Handbook sample I have:

Aerobic
  Oxygen will inevitably enter with the raw materials put into the generator, and so aerobic bacteria use this oxygen up,
  meanwhile doing what they can to break the materials down. CO2 is
  released, and some heat is generated.
Extracellular enzymes
  In this stage, anaerobic bacteria release enzymes that attack large molecules which are still outside their own
  bodies (extracellular), so these molecules will be broken down into
  “bite sizes.”
Acid digestion
  The bite size molecules (still fairly large) are absorbed by the bacteria and digested. The main byproducts of this
  third process are simple molecules such as the short chain fatty
  acids, H2 and CO2. (We’ll get into the short chain fatty acids soon.)
  It’s interesting to note that at this stage, hydrogen gas, an
  excellent fuel, is evolved. Hydrogen does not often show up in the
  final biogas apparently because it is used by the anaerobic bacteria
  (in the next stage) in making CH4, methane.
Gas digestion
  Now comes the part we’ve been waiting for. The fatty acids are now gobbled up by the last group of bacteria, who turn them
  into H2O, CO2, and best of all, CH4.

Alas, the length of these stages is not explained. However, Biorealis suggests the length of the Acid Digestion and Gas Digestion in a critique of conventional continuous-feed biodigesters vs. the two-phased biodigester it has developed:

Conventional single-stage digesters are not only unstable, they are
  also relatively inefficient. For example, if the system is operated at
  a hydraulic retention time (HRT) conducive to growth of acidogens (2-3
  days), any methanogens present will be washed out of the system faster
  than they can reproduce, preventing them from ever becoming
  established. On the other hand, if the system is operated at an HRT
  conducive to growth of methanogens (20-25days), the faster growing
  acidogens will be maintained at the low growth rates of the endogenous
  growth phase - essentially at starvation level.

NB: I opted for a batch biodigestion system to avoid the complications mentioned by Biorealis here above and because Biorealis' two-phased biodigester is more expensive and less easy to build.
So far I have a rough biodigestion calendar of:

3 days of acid digestion
20-25 days of gas

But I still lack some information on the stages:

how about the length of the two previous stages mentioned in the Biogas Handbook?
on what do those stages depend and can I accelerate digestion somehow? (I already know about heat at 21°C, how about water ratio or anything else?)
how long does it take to digest a big chunk of food, say a 27cm² bit of carrot? (Important because I hope the garbage is completely processed before I toss the slurry in the garden as fertilizer)
in short after how much time can I confidently unplug the batch, knowing the biodigestion is complete?

Could you help me shed some light on the length of biodigestion stages? Thanks.

I'm sending this over to [biology.se], it fits in their scope much better than ours and probably will get a better answer there :)

To give timescales for the different processes is very difficult because the speed (in g/d product yield) depends greatly on the number of bacteria, so first you'd have to modl the bacteria growth. I assume you don't want to go that road.
Also note that not all of the substrate is in the same state of fermentation at the same time, more so if you have bigger lumps. Like whole carrots.
One industrial batch-style fermneter I know of uses total retention times of 3-4 weeks, and they mix half the digestate into the fermenter again to provide for inocculum.


text:
How can I estimate the CO₂ uptake of a plant?
I would like to make an estimation of the CO2 uptake of plants I cultivate, including, lettuce and aromatic herbs, such as thyme, basil, rosemary. What I want is to end up with a rough indicator for business purpose, not some super-accurate measurement.

Is there already average CO2 uptake data per plant type available?
Will this uptake vary drastically per plant type?
Can I calculate the estimate through a simple measurement (e.g. of plant weight) or does it require tight lab experiments? In the former case, how is that measurement made?

Please bear in mind I'm not a scientist, but and end-user of science. Thank you for helping me this question if needed.

Can I calculate the estimate through a simple measurement (e.g. of plant weight) or does it require tight lab experiments? In the former case, how is that measurement made?

In the textbook Plant Physiological Ecology*, they state that about 40% of the dry weight of plants is carbon, and I believe the vast majority of that is from CO2 from the atmosphere. You can take a fresh weight of an entire plant, and then dry it at the lowest temperature in your kitchen oven for a couple of days to get a reasonably accurate dry weight. That dry weight times 0.4 will give you an estimated total carbon, though I have seen other factors used. Plants can also be analyzed for Total Organic Carbon in some agricultural laboratories. Fast growing plants are going to absorb more carbon than slow growing ones.

* Lambers, H, Thijs L. Pons, and F S. Chapin. Plant physiological ecology. New York: Springer Verlag, 2008. Print. ISBN:978-0-387-78341-3