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RNAs arising from intergenic regions
Which type of RNA molecule is coded for in intergenic regions? I think it must be a non-coding RNA but I'm unsure which type.

The term intergenic is more or less obsolete now. In fact it is ironical to say that a gene, which can give rise to a functional protein or an RNA, is expressed from an intergenic region. However the usage continues for both lncRNAs and miRNAs (other major type of ncRNA in metazoans1 - piRNAs have different classification). lncRNAs are vaguely classified as sense-overlapping (expressed in the same direction as a known gene but not completely overlapping), antisense (expressed from the antisense strand of a known gene) or intergenic; similarly miRNAs are classified as intronic or intergenic.
It is not necessary that the intergenic RNA has to be strictly non-coding, it can be coding as well; a novel protein.
In all these cases the term intergenic means - not overlapping with a known gene. Better nomenclature is necessary as the field of genomics makes more progress.
See this article.
1 Most metazoans.


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What's the composition of Actinobacteria's hyphae?
I'd like to know which chemical compounds form hyphae in Actinobacteria. Is it the same structure of the cell wall?
Thank you

Can you specify this a bit more? You want to know the single building blocks of the hyphae?

I understood that cells grow in tubular structures that form the hyphae, but i'd like to know how cells build this structure. Which are the chemical compounds that cells secrete to bulid the hyphae?
Is it clear?

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Can different strains of Rhizobium share an infection thread or symbiosome?
Rhizobium infection can be triggered at root hairs of legumes, creating infection threads.
Can these infections threads be colonized by more than one type of Rhizobium (e.g. Fixing and non-fixing)?
What about when the infection is inside the plant cells? Can symbiosomes be co-inhabited by different bacteria?

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Salbutamol's Pathways of Interaction and Classification
Salbutamol is a very commonly used direct-acting β2-agonist.
This suggests me that it is sympatholytic.
However, it has sympathomimetic pathways, see PubChem for Sympathomimetic.
I am trying to think the group of Salbutamol.
Sympathomimetic or sympatholytic.
How can you classify Salbutamol into a group?

An agonist works with the receptor: a substance that initiates a physiological response when combined with a receptor; in the case of salbutamol (or albutarol in the US) they activate the beta-2 receptor on the muscles surrounding the airways. They are also known as sympathomimetics, as they imitate β2 adrenergics.
A blocker (or antagonist) is one that that blocks the action of endogenous catecholamines; for that reason, they are also called sympatholytic: antagonistic to or inhibiting the transmission of nerve impulses in the sympathetic nervous system.
It appears you have experienced a simple confusion in terms. Salbutamol/albuterol is definitely a sympathomimetic, used extensively on asthma and COPD.
Pharmacology and Therapeutics of Bronchodilators

You seem to be right. I read this A short-acting beta-2 adrenergic agonist as beta-adrenergic antagonist which is false. Thank you for excellent answer!


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Phenotype choice for one of a MZ twin pair in a genetic association study
I was having a discussion with a colleague and this question came up...
It is commonplace in molecular genetics studies to only genotype one of a pair of monozygotic twins (and then implicitly impute the other's genotype by assuming the pair is genetically identical).
My question is this: assuming a quantitative trait study, what should the phenotype be? Should it be the phenotype of the genotyped twin OR should it be an average of the two twins' phenotypes?
Example:

I genotype Twin A
Twin A has a phenotype score of 4
Twin B has a phenotype score of 6
Should Twin A's phenotype for the genotype-phenotype test be 4 (the individual's phenotype) or 5 (the average phenotype of the genome)?

Answers from experience and from theory welcome!
Thanks!

I think it's quite unclear what you are asking

Can you suggest what further information you need? Have added an example, if that helps?

Interesting, perhaps it depends what analysis you plan to do later. If the study aims to estimate the heritability of the trait, wouldn't you want to record a separate datum for both twins, so that you can compare the variation present with different degrees of relatedness or genetic similarity.
Can you explain what sort of quantitative trait study you mean and how it is done? Thanks!

Hi Teige, what I meant by quantitative trait was that the phenotype was continuous rather than dichotomous, and so doing an average would make sense (if the test is YES/NO, then it makes little sense to be half a YES!)
I'm assuming there is no genetic variance between identical twins, so there's no new information gained by having both twins' genotypes. I'm talking about an analysis where you're not using the fact they're twins per se, but rather just using one of them as an individual - do you randomly select one twin, or do you combine their phenotypes into one?


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PCR processes number of amplicons produced
Beginning with 600 template DNA molecules after 25 cycles of PCR how many amplicons will be produced?

This is a homework question, right? These are off-topic unless you show some effort solving them yourself.

yes it is . I thought the answer should be 2^26 based on the equation 2^N where N is number of cycles

This is a theoretical consideration, as PCR depends on a number of factors as optimal priming, salt concentration, enzyme activity, available dNTPs and so on. Ideally the number of DNA molecules is doubled with every cycle. So the general formula to calculate the number is:
$ n \times 2^{cycles} = $ number of DNA molecules at the end of the PCR
n is the number of molecules set into the reaction
So for our 600 DNA molecules with 25 cycles this would give:
$600 \times 2^{25} = 20.132.659.200$ or roughly 20.1 billion molecules of DNA.


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Bigger animals needs bigger amount of oxygen?
Bigger animals, like Elephants, or Dinosaurs for example, are in need for more oxygen than the amount of oxygen that small animals need? (humans, dogs, cats, etc)
Thanks in advance.

If all animals need the same concentration of oxygen throughout their tissues, larger animals need more O2 because they more tissue, but metabolism is probably more important than size alone. One thing to consider isn't so much the amount of oxygen but the diffusion of oxygen. Large animals have trouble getting oxygen to all of their tissues, so they have lungs, hemoglobin, and efficient circulatory systems to move the oxygen in and CO2 out. Small animals have less tissue to diffuse through, so they can rely more on simple diffusion of atmospheric oxygen through their bodies.

I'm not an expert but I think it's pretty obvious.. Bigger animals do require more energy and thus more oxygen for cellular respiration. They also have bigger lungs, although the rythm of the breathing is slower.

Animals with the same metabolic rates need the same amount of oxygen per unit body mass, larger animals have slower metabolisms than smaller ones (that's also why they need less food per unit body mass).  1 ton of rats use more oxygen than 1 ton of elephant. bigger animals need better ways to distribute the oxygen, that is better ways to absorb and transport it. One of the reason Sauropods got so big was they have a much better breathing mechanism than mammals.


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What is the difference between tonic and phasic firing?
I am reading about dopamine, and I have realized that dopaminergic neurons can fire phasically or tonically. What is the difference between these two modes of firing?

Tonic firing typically occurs without presynaptic input and can be viewed at as background activity. Tonic activity is often characterized by a steady action potential firing at a constant frequency. Note that not all neurons may have tonic activity at rest. It may serve as keeping a steady background level of a certain neurotransmitter or it can serve as a mechanism where both an inhibition or increase in presynaptic input can be transmitted. When a neuron is silent at rest, only an increase in presynaptic activity can be transmitted postsynaptically.
In contrast, phasic firing occurs after a neuron is activated due to presynaptic activity and it incurs activity on top of any background activity a neuron may have. It is typically restricted to one, a few, or a short burst of action potentials, whereafter the activity quickly returns to the resting state.
Reference
Tsai et al., Science (2017); 324: 1080-4

Could you please explain what causes tonic firing? I.e. how can a neuron depolarize itself?

@VivekSubramanian: cyclic changes in restig membrane potential or inputs from other neurons

@AliceD , from the paper you reference, both tonic and phasic activity seem evoked, instead of tonic activity being passive background activity. The definition I would extract from that paper is instead that phasic activity consists of faster firing, maybe only bursting, and tonic firing is lower-frequency firing:   Caption figure 2: "(D) Whole-cell recording of DA neurons showing spontaneous activity and tonic and
phasic firing evoked by 1-Hz and 50-Hz light flash trains, respectively". Or: "low-frequency tonic activity and phasic bursts of action potentials" (first page)

Maybe tonic = constant for a longer duration (like muscle tone), whereas phasic = in phases ?


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Does transplanted heart have full sympaticus without medication?
I am reading this and this where I am considering this sentence

[N]o baseline parasympathetic innervation [in transplanted heart].

Does this sentence imply that the heart work then in full sympaticus all the time?
Probably, through altered systems, but still.
At least the regulation of blood pressure strongly supports this, here for the generic medication plan.
Does transplanted heart have full sympaticus without medication?
Notification of terminology. I tend to use overloading in writing.
For instance, I can say that there is sympathetic and parasympathetic supply to the heart i.e. innervations of S and PS through endocrine system to the heart.
I am not yet completely sure how the recipient's body can target the alpha and beta receptors of donors in heart. Are there any variations of these receptors? If yes, then the effect of sympathetic stimulation would also differ from the original stimulation.
So full sympaticus (or original) may not be present.
The new stimulation may lead to greater or smaller activation of sympaticus.

Downvoter! Leave, a feedback.

The parasympathetic supply to the heart is by nerves and that is truncated during surgery as pointed out.
The sympathetic supply to the heart is by two means:

Through sympathetic nerves from the sympathetic trunk
From the adrenal medulla which secretes both adrenaline and nor-adrenaline directly into the blood stream

The heart contains the beta receptors for the sympathetic system, especially the ventricles and nodes (SA) and conducting fibers. These receptors respond to the presence of adrenaline and nor-adrenaline in blood. Thus the sympathetic response is preserved while the parasympathetic responce is lost.
There is a minimal level of nor-epinephrine in blood at all times which thus influences the heart.
Receptors in Heart:
The heart contains adrenergic (sympathetic) and cholinergic (Parasympathetic) receptors. When the heart is transplanted, the donor heart also contains the same receptors. The only thing missing are the nerves.
The sympathetic system does not suffer as much as the parasympathetic system, because of the adrenal medulla which secretes the nor-epinephrine (same as nor-adrenaline) into the blood, which upon reaching the heart can stimulate the beta receptors on the heart.
There is no organ which releases acetyl-choline into blood, (fortunately, as such a release would be disastrous leading to shock and rigor, possibly death). So the parasympathetic receptors in the heart do not receive any stimuli.
Edit 1:
In response to your edit, yes there are polymorphisms in all receptors. But the structure of adrenaline and nor-adrenaline are pretty much constant. This means that the donor heart will be at a similar level of sympaticus as it was in the donor when (s)he was alive. Although this will not be the same as the recipients pre-surgery sympaticus state of the now removed heart.

Excellent answer! So the type of sympathetic stimuli is from adrenal medulla in transplanted heart. In normal heart, two types - from the former and from sympathetic trunk.

Yes, adrenal medulla is kind of a sympathetic endocrine system, stimulating the whole body at times of need

Assume adreniline/stimulates tissue. There are alpha and beta receptors. How is the sympathetic action potential generated? From receptor to periphery and to heart? Can you see this action potential generated by adrenaline and noradrenaline clearly in some channel of ECG? Probably, II or MLII. I would like to find the channel and situation where action potential from sympathetic trunk is not visible.

I think I gave you the wrong idea. I will explain further in the answer

I don't understand your comment. There are no nerves to heart and thus no action potential in generated in any nerves. The receptors are in the heart muscle cells and conducting fibers. The effects are as described above

There is vagus nerve to the heart so I think action potential is generated through the release of acetylcholine in heart. There is sympathetic trunk to the heart similarly neuronal. What do you mean that there are no nerves "to" the heart? I mean by this that there is the neuronal component combined with the endocrine system + receptors i.e. something to heart.

In that case you are correct, there is no parasympathetic supply to heart.

In your definitions, is there sympathetic supply to heart? I tend to overload terms and say that there is both S and PS supply to heart through endocrine system.

Yes, maybe that's why I was confused. I also confused myself with the term 'action potential' I forgot about the muscle action potential. Did that answer your question?

I am not yet completely sure how the recipient's body can target the alpha and beta receptors of donors. Are there any variations of these receptors? If yes, then the effect of sympathetic stimulation would also differ.


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Why do Sorghum Bicolor leaves roll up?
In A level Bio today we talked about abcesic acid as a stress hormone, and its ability to reduce osmotic potential around guard cells to close stomata.
My question is, is abscesic acid in sorghum bicolor leaves responsible for its ability to roll up in lack of water?


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Why are Merkel cells innervated by an axon, and not a dendrite?
Here are two images from Google. Afferent neurons receive input and send it to the central nervous system. Input is received by the neuron's dendritic end and send away centrally via axon terminals that are sheathed with Schwann cells. Axon terminals synapse to motor neurons (muscles and glands).
How is it possible that Merkel cells, which supposed to be a sensory cell, synapse with an axon, and not with a dendritic end?

I edited the question to improve clarity. Feel free to roll back when it doesn't reflect your original question.

There is nothing out of the ordinary with the Merkel cell, as it functions in the same way as photoreceptors and hair cells (see Further Reading #1).

Fig. 1. Merkel cell. Source: Gallery for Share.
The Merkel cell depicted in Fig. 1 is a specialized receptor neuron. It has no axon. It relies on a secondary sensory neuron (a somatosensory afferent) onto which it synapses to direct the touch signal to the brain.
Note that neural information flow goes from dendrite to axon. An axon terminates into a synapse. The Merkel cell, which does not have an axon, features a synapse directly onto the dendrite of the secondary neuron (See Further Reading #2).
Further Readings
1. Can axons act as receptors?
2. What are the functions and differences between axons and dendrites?.

I don't understand your last paragraph: there is no dendrite depicted in the figure, only the body (and some dendrite-like processes) of a Merkel cell, the meniscus tactus (supposed to be a dendrite?), and the axon of the secondary sensory neuron. But the meniscus tactus looks more like a part of the postsynaptic axon - why then "features a synapse directly onto the dendrite"?


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About artificially induced processes that would normally cause a cell to self-destruct
Are there certain biochemical processes that would normally cause a cell to self-destruct but if the cell being tested has apoptosis mechanisms that have malfunctioned or been 'turned off' the cell will not 'malfunction' because of the induced process ? Are there such biochemical processes that could indirectly indicate which cells have no functioning apoptosis mechanisms? If so would this be a possible test for cancerous cells?

In some cases yes — when there is a mutation in apoptotic regulators such as Bcl2 family of proteins. In other cases it is difficult to identify and only identification is that those cells are growing rapidly; in other words failure to undergo apoptosis is not the cause but the effect of the cancerous transformation (as in case of p53, Ras, Myc mutations etc).


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Regarding the apoptosis mechanisms in cells and cancer
If all the cells in a cancerous tumour had their apoptosis mechanisms 'turned back on' or reactivated or repaired by some 'yet to be discovered' process would this cause the tumour to 'self destruct' or be destroyed? Are there known processes that can repair or reactivate the apoptosis mechanisms in a cell?

Theoretically yes (but since nobody did that, we don't know). Yes there are therapies which aim to reactivate apoptosis. "Inhibiting the anti-apoptotic Bcl-2 and Bcl-XL proteins may allow cells to restore their ability to undergo apoptosis" Btw. there are many more programmed cell death mechanisms, not just apoptosis (e.g. necroptosis).

The processes of apoptosis is not so simple, there is a lot of genes and proteins that participate in it. In cancer cells some of them mutate and not working properly.
Lack of apoptosis is the main problem in cancer. If cell not working properly, it dies. But not in cancer.
So theoretically, yes. If we will fix the apoptosis, the cell probably will die.
It's gene engineering direction. You need to target the cancer cell, and to change problem genes. It's really difficult processes. And every type of cancer has different mutations ...
Read this for example http://www.jeccr.com/content/30/1/87
(Journal of Experimental & Clinical Cancer Research )

Welcome to biology SE - it would be great if you could add some references to your answer(s)

Is there a process or set of biochemical events that can repair or re-initialize the apoptosis mechanisms in any cells whether they're normal, pre-cancerous or cancerous. If there is some such process one wouldn't have to specifically target cancer cells.

No such processes as far as I know, and to "target cancer cells" is the main problem in curing cancer. If we could "target" them, to kill them is pretty easy task.

Read this for example http://www.jeccr.com/content/30/1/87 (Journal of Experimental & Clinical Cancer Research )


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Are there any similarities in the DNA of a humans and animals?
As the title says, i've been wondering if there are any similarities between the DNA of humans and the DNA of animals?
Like, maybe monkeys are more similiar in their DNA to humans, than dogs are (to humans)?
Thanks in advance, sorry if there are any english mistakes.

see: http://biology.stackexchange.com/questions/20038/same-dna-vs-genes

Genome-wide variation from one human being to another can be up to 0.5% (99.5% similarity)

Chimpanzees are 96% to 98% similar to humans, depending on how it is calculated. (http://genome.wellcome.ac.uk/doc_WTD020730.html)

Cats have 90% of homologous genes with humans, 82% with dogs, 80% with cows, 79% with chimpanzees, 69% with rats and 67% with mice. (http://genome.cshlp.org/content/17/11/1675.full)

Cows (Bos taurus) are 80% genetically similar to humans (http://www.sciencemag.org/cgi/content/full/324/5926/522)

75% of mouse genes have equivalents in humans (http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.1000112), 90% of the mouse genome could be lined up with a region on the human genome (http://www.genome.gov/page.cfm?pageID=10005831) 99% of mouse genes turn out to have analogues in humans (http://www.nature.com/nature/journal/v420/n6915/full/420509a.html)

The fruit fly (Drosophila) shares about 60% of its DNA with humans (http://www.genome.gov/10005835).

About 60% of chicken genes correspond to a similar human gene. (http://www.sciencedaily.com/releases/2004/12/041208230523.htm)


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How is incomplete dominance different from codominance?
Ok let me start with the definitions of incomplete dominance and codominance.
incomplete dominance - The situation in which the phenotype of heterozygotes is intermediate between the phenotypes of individuals homozygous for either allele.
codominance - The situation in which the phenotypes of both alleles are exhibited in the heterozygote because both alleles affect the phenotype in separate, distinguishable ways.
It is the standard textbook example of incomplete dominance to show a cross of red and white Snapdragons of pure bread. Which yields the phenotypic ratio of 1 red : 2 pink : 1 white. The standard text example of codominance is AB blood type where the A glycoprotein and B glycoprotein together produce a distinguishable phenotype apart from AA or BB.
I really don't understand the distinction between intermediate phenotypes and distinguished phenotypes. How is pink not distinguished from white and red. Consider a hypothetical example of some insect that interprets red, white and pink as distinguishable signals where perhaps red is a safe flower, white is ignored, and pink is dangerous. Say these signal recognitions have evolved based on the insects contrast against the flower pigment and the probability of being eaten by a predator because of increased exposure while getting nectar from the flower. I suppose I have a misunderstanding but wouldn't the red, white, and pink phenotypes be distinguishable rather than intermediates in that case?
So I'm probably just being an idiot but how is incomplete dominance different from codominance?

"Co-dominance, where allelic products co-exist in the phenotype, is different from incomplete or semi-dominance, where the quantitative interaction of allele products produces an intermediate phenotype. For example in Co-dominance, a red homozygous flower and a white homozygous flower will produce offspring that have red and white spots." - from the wiki on dominance

But aren't pink flowers just red and white spots at a molecular level?

I think you may find the answer you are looking for in this post

I ran across this reference for a break down of dominance in "Human Molecular Genetics 3" by Strachan & Read.
http://www.ncbi.nlm.nih.gov/pubmed?cmd=historysearch&querykey=2

Certainly if you are talking about signals, red, white, and pink phenotypes are distinguishable rather than intermediates...
But inheriting a character is far away from the concept of distinguishing signals. As genotype of an organism decides its phenotype, you should know that in a hybrid both the paternal and maternal traits would exist. If one is dominant then it is expressed and the recessive is not.
However if the dominant gene is unable to express itself independently in presence of the recessive and if the recessive is partially expressed, then both the dominant and recessive give rise to an intermediate phenotype which "only one of them cannot produce"
This is what we call blending. In case of Snapdragons, pink is a phenotype that allele responsible for red or white alone could not have produced.
In case of co dominance you can notice multiple dominance. i.e., no recessive character is there. All alleles are expressed "independently of one another" in an organism.
Eg:- AB blood group.
Also consider cross between black coat coloured cat and white cat. The offspring produced has black and white patched coat colour. i.e., Black and white didnt blend to give rise to grey. I mean, alleles responsible for these traits are independently expressed.
Hope that clears your doubt. :-)

incomplete dominance are more likely mean blend, like you make juice contain apple and pear by blender, you can not distinguish them.
codominance can be think as mix, like you a salad that contain apple and pear.
like the example of incomplete dominance: pink flower, pink is differ from white and red, but it related to the two color,
as the example of codominance ABO blood type, blood type AB means it contain A antigen and B antigen, we can distinguish them

AB blood group is the best example one can give about co dominance. What matters is both A and B are dominant and are expressed independently of one another. The quantity they are produced is not important here as our genetic make up cannot do relatively very large difference between synthesis of the two.

You can edit your original answer, you know. . .

But aren't pink flowers just red and white spots on a flower petal cell at a molecular level, just like A and B proteins on a blood cell? I don't know the mechanism, I suppose if the red and white proteins on a flower petal interacted to form another protein then that would be blending. Otherwise, wouldn't the pink just be a pointalistic illusion.

I'm pretty sure the mechanism is that the pink flowers don't make as much functional pigment as the red ones, because that "white" allele for that gene in the pigment process is just broken.

incomplete dominance is when one allele is partially dominant over the other allele of the same trait.both these alleles are dominant but one is more powerful than the other .for examples a mating between a white female and black male in humans and have a colored child.
co-dominance is when two alleles are equally expressed.

I doubt your example is correct. Human skin color is polygenic inheritance.

Remember, the vast majority of traits don't conform to the Mendelian paradigm, even when its stretched a bit like this.  So this really is a very academic question, and neither term is applicable to a huge number of real-life situations.
To use the examples of snapdragons and blood types, an AA, AO or AB blood type all show no reaction at all to the A antigen.  If AA was protective towards A blood, but AO and AB showed weak reactivity, we'd likely call them incompletely dominant.
For the snapdragons, it really doesn't make any sense to call either allele dominant.  What's really going on there is that the "white" allele is a broken gene in the process that makes red pigment, and flowers with only one working allele don't make as much red pigment as flowers with two working copies.  Whereas one working copy of the ABO gene (that is, the A or B alleles) is enough to teach the immune system not to react.
So I'd say that incomplete dominance is usually a results of haploinsuffieicny; one allele is broken, and the other by itself doesn't do as good a job as two working copies, and co-dominance is usually two working alleles both doing different things.


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Henrietta Lacks and HeLa cells
Why did Henrietta Lacks die when her cells didn't die? As I understand it only the cells from her cervix were immortal so perhaps the cervical cancer took her life and the cells never died.

It's the feature of cancers. The normal cells die via apoptosis or stop to replicate, cancerous cells lose their specialization, travel in the body, and grow tumor by anarchic replication.

@Quidam This is very interesting because I have the same understanding: "cancer cells are "immortal" in the sense of permanent division". So HeLa cells are not very specific. But sometimes, Henrietta Lacks is presented as a unique discovery. Why is that? Is it because her cells were the first to be cultivated?

The cells never died in the sense that they kept replicating, individual cells still died. They were safely cultured in petri dishes before Henrietta Lacks died. The cells came from a tumor that developed from her cervix. The cervical cancer cells had developed high telomerase activity. Telomerase builds telomeres on the ends of DNA, protecting the chromosomes. In normal cells, telomeres tend to get shorter as the cells divide, eventually the DNA is damaged and the cells die. HeLa cells are protected because their telomeres are well maintained.
There was nothing special about Henrietta lacks that made her tissues immortal, so digging her up wouldn't be worth it. Her family would probably get mad too.

Yeah that makes perfect sense! I guess I took the word 'immortal' literally. Now I don't have to commit a crime. XD Thank you so very much!!! I really really appreciate it!!! Wising you a happy Thanksgiving! ;D

There has also already been some controversy over using HeLa cells. Permission to use HeLa genome was never explicitly granted by the family until the relatively recent HeLa agreement. nature.com/news/deal-done-over-hela-cell-line-1.13511 - Nature 500, 132–133 (08 August 2013) –


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How Circumcision could reduce the chance for a HIV infection?
Circumcision removes the foreskin of the penis which mainly acts as a cover to the penis. Normally removing the foreskin makes more vulnerable to any STD, so how could circumcision reduce the risk of a HIV infection?

Who says that circumcision can do so?

@Chris - The CDC, at least, has evidence that circumcision decreases the incidence and transmission of HIV. This is why it is recommending the adoption of the procedure in African countries. If you're asking the OP for a source, please ignore this.

@anongoodnurse I was curious about it, since I didn't know it. Thanks for the answer.

This is an interesting question, which has not been answered yet. It is also questionable, if this protective effect is present at all. There are around 40 studies on the topic available which have subsequently undergone meta-analysis. In a meta-analysis all data from recent studies which meet certain quality criteria are analysed together. This gives a much bigger dataset and stronger statistical data. It also helps eliminating the effects of too small test groups.
One of these meta-analysis identified circumcision to have a positive effect on the prevention of HIV infections (reference 1). The authors recommended considering it as a preventive measure.
Two other meta-analysis were more cautious on the topic and either found only a weak link (reference 2) or that only "randomized control studies" (reference 3) would provide clear data. The problem with all these studies is, that they are observational studies, where unknown other effects can play a bigger role than the supposed main effect. It is ethically very difficult to make controlled trials on the transmission of deadly diseases in humans. This is also the reason why all trials on this have been stopped.
There is a hypothesis on how circumcision may help preventing the infection with HIV (when you not get infected in the operation itself due to improper hygienic standards). The skin in the penis contains a large number of immune cells (dendritic cells, CD4/CD8-T-cells) which are the target cells of the HIV virus. It is thought that the virus can more easily penetrate the relatively thin skin of the foreskin. It is also possible, that the surface size is important here, as there are reports which show that men with a larger foreskin also have a larger risk of getting infected. See reference 4.
Another hypothesis has to do with the with the bacteria which live under the foreskin. The number of different strains present is much lower in circumcised men, which led to the conclusion that the dendritic cells, which present these to the immune system have an easier job in the circumcised men and are more likely to prevent the infection with HIV.
See reference 5 and 6 for more information.
References:

Male circumcision and risk of HIV infection in sub-Saharan Africa: a
systematic review and meta-analysis
Male circumcision for prevention of heterosexual acquisition of HIV
in men
HIV and male circumcision--a systematic review with assessment of
the quality of studies.
Male circumcision for HIV prevention: current research and
programmatic issues.
Why Circumcision Lowers Risk of HIV
Male Circumcision Significantly Reduces Prevalence and Load of
Genital Anaerobic Bacteria

Unfortunately overlaying all of this is a social aspect that is difficult to eliminate. Virtually any male researcher into this topic has a vested interest in vindicating his own penile condition. Men feel strongly about the perfection of their own penises, however they find them.
It is very clear from the discussion and tone of many of these studies that the researchers are themselves circumcised, and want circumcision to be treated as the norm. The same effect is possible in the other direction, but seems to occur to a lesser extent because intactness is the biological norm and requires no action to make it so.
For that reason, studies out of the USA (including those led by American researchers in Africa) disproportionately favour circumcision, while those out of Europe do not. One reason this bias can creep in is that it is difficult to do double-blinded and/or placebo-controlled trials of circumcision. Thus experimenter and experimentee effects can creep in at every stage.
Circumcision is an intervention with deep social, religious, historical and cultural roots, and once it has become customary, rationality about it is difficult to achieve. Especially considering the operation on healthy infants, the fact that the foreskin is an integral part of an adult sexual organ gets lost from sight.
It is very common for the circumcised penis to be treated as the norm (with terms like "uncircumcised" common, where "normal" "whole" or "intact" would apply to any other body part that had not been surgically reduced). After that, circumcision may be treated as equal and opposite to the alternative of doing nothing, when it is no such thing. Thus the yawning gap between "circumcision [somewhat] reduces the incidence of X disease" and "all male babies should be circumcised" can be leapt in a single bound.

One of the first proponents that circumcision could be helpful is indeed a strong advocate of circumcision.

This doesn't seem to me to really answer the question (which is about a hypothetical biologic mechanism), although it's relevant and interesting. Do you have any sources comparing the American vs European sourced research findings? If not, at least citing a major consensus statement from a European group that conflicts with a similar statement from a US group or some such thing would strengthen this "answer."

I'm also with @Susan here, you should provide at least two samples of a EU and US groups saying contradicted statements on the issue

@Susan In case Hugh Young doesn't respond, here is the American Academy of Pediatrics statement in 2012 in which they state "Evaluation of current evidence indicates that the health benefits of newborn male circumcision outweigh the risks and that the procedure’s benefits justify access to this procedure for families who choose it."

@Qchmqs Here is a response from a large group of European doctors in which they state that most of the benefits cited by the AAP "are questionable, weak, and likely to have little public health relevance in a Western context, and they do not represent compelling reasons for surgery before boys are old enough to decide for themselves."

Here's another link (updated in Oct 2014) that Hugh Young might want to include in his answer - the UK's National Health Service says that "most healthcare professionals now agree that the risks associated with routine circumcision, such as infection and excessive bleeding, outweigh any potential benefits."


text:
Why do human ears have a lower boundary for the lowest energy perceivable signal than eyes?
I am currently hearing a lecture about human machine interaction. The lecturer is not a biologist (neither am I, we are both computer scientists), but he makes some statements about biology which I think are questionable.
One statement was that the energy of the lowest perceivable signal for eyes is  and the energy of the lowest perceivable signal for ears is . He cites those values from the following (German) source:

Schmidtke, H. et al. Handbuch der Ergonomie mit ergonomischen
  Konstruktionsrichtlinien und Methoden. Koblenz: Bundesamt für
  Wehrtechnik und Beschaffung (BWB)
HdE (2002): 2.4.1, Abb. 2
[KIT-Bibliothek: 2007 E 1808-1(2) (Präsenzexemplar)]

It is clear that those values vary from person to person. Assuming they don't vary too much, it is interesting to know why the human ear can detect signals with lower energy than the human eye.
According to my lecturer, the reason is because we can hear in all directions, but see only in one direction. He argues that hearing is much more important for this reason to detect predators, even if they are silent.
However, this argumentation seems very weak to me. I would rather think that there is a range in which "interesting" signals occur. If the interesting signals have lower energy for sound than for visual signals the ear adapted to this range.
I guess if the hypothesis of my lecturer is correct, then animals which can see in all directions would (always / very often) have much worse ears. If my hypothesis is correct, then there would be no significant difference in animals with "panorama-vision" and animals without in terms of lowest perceivable energy for ears and eyes (assuming fair comparisions; unfair would be comparing fish with land animals as the medium might play a big role).
Is there any source (written by somebody from biology, not form computer science) which makes a claim about this question?

Isn't this comparing apples and pears? Electromagnetic stimuli and vibrational stimuli are not in anyway comparable. The first are, arguably,  considered to be energy packets (photons) while the latter are transient air pressure differences.

@ChrisStronks That was another concern I had. I will ask him next week.

@ChrisStronks You could calculate the energy required to make a minimum audible air pressure difference and minimum visible number of photons. Maybe that's what going on here, even though it doesn't make sense to compare them.

@user137- of course both visual and acoustic stimuli at threshold contain a certain amount of energy that can be calculated. But it is comparing apples and pears as they are totally different physical stimuli.

The hypothesis about seeing in all directions is not correct.  Horses, for instance, have a nearly 350 degree field of view, with as good or better visual acuity than humans (though limited depth perception), and much better hearing than humans.  They can also rotate their ears for directional hearing: http://www.extension.umn.edu/agriculture/horse/care/horse-hearing/

Does the citation provide the confidence interval? It may well be the case that even though the average threshold energy for hearing is lower, the mode is higher.

Preamble. There is a lot of misunderstood science here and you are more than right for questioning the lecturers interpretation of these energy values; something the other answers do not discuss. The problem arises from a dodgy reference and a lot of conjecture.
In summary.

Light and sound cannot be compared energetically in a biological context.
Our ears probably don't hear lower energies than our eyes see to avoid prey.

Let us ignore the reference...
The reference is from BWB which is as far as I can tell a non peer reviewed federal technical publisher and that this is a textbook about ergonomics. But given its obscurity, it having never undergone peer review, it being not biologically scientific, it is safe to ignore from the context of a scientific biological topic. The fact it is in German doesn't help either.
If anyone can provide an open link to this reference or correct me on this I would be grateful. Google scholar turned up no hits other than a citation.
Let us give your lecturer the benefit of the doubt. This answer assumes that there are derived energy values for sight and sound as your lecturer suggested and that eyes sense higher energy than ears.
Is hearing omnidirectional to detect predation?
I'm going to use the term sensory setup to describe that our senses use fixed ears that hear omnidirectionally and forward facing directional eyes.

... hearing is much more important for this reason [omnidirectional] to detect predators, even if they are silent.

Let's flesh out this hypothesis so that it makes sense in practical terms.

A small movement is made by the predator. This generates some sound and some change in light. In the case of forward sighted animals, the sound is much more difficult to detect than the light would be as it contains less energy. The ears must compensate by detecting lower energy signals than the eyes would need to in order to detect the predator.

Before we question the physics, this biological hypothesis is very tough to swallow. Without citation I would say it is unreasonable conjecture.
Examples that contradict this hypothesis:

Gorillas have no natural predators or prey but have a very similar sensory setup to ours that helps social bonds.

Meerkats on the other hand rely on sentries that broadcast a series of bleats after spotting prey by sight. Other meerkats immediately hide when hearing this signal (interestingly, this call is mimicked by Drongos who steal the meerkat food that is abandoned in the panic) before checking if a predator is present. Meerkats have a similar sensory setup to ours.

There are other megafauna like deer that are prey for the big predators; predators that would have put ancestral humans on the menu. Deer-like prey animals rely heavily on near-omnidirectional eyesight and can angle their ears to focus on an area to hear stealthy predators. This is the "opposite" sensory setup that has the same conclusion of predator evasion.

Even those non-exhaustive examples makes the hypothesis questionable at best.

...there is a range in which "interesting" signals occur. If the interesting signals have lower energy for sound than for visual signals the ear adapted to this range.

This answer too is based on pure conjecture it seems, however it more aligns with how biology might work.
It is sensible to say evolution selected for animals that could detect noises and lights that, if reacted to, saved the organisms life to continue propagating. This hypothesis bypasses the idea that sound and light are comparable energetic signals too, which is good (discussed below).
This hypothesis also allows for various morphologies to have evolved depending on what an "interesting signal" is to that species.
Light vs Sound.
These aren't the same thing.
The elephant in the room of this question is that light and sound are non-comparable energies. This is due to source, speed, distance, medium, mechanisms for receiving the energy (eyes and ears) and most significantly in a biological context neural interpretation. These values are so abstract that even if an energy value is calculated, it is not in anyway quantitatively comparable in biological organisms. For example a really loud subsonic whale call is not the same as a small change of grass parted by a wolf as it sneaks up on you. One is absolutely essential for survival, the other is undetectable. Both could theoretically have the same "energy".
Note Frequencies are the biologically important part of the "energy" but must be considered as two different methods of acquiring sensory information. The difference between a chimp mating call and a territorial threat are very similar but for their frequency, and eating the delicious red berries compared to the toxic blue berries is also down to the frequency reflected from them!
There is little to no biological literature that uses energy values as sensory input. This would just obscure the actual important physical aspects of the sensory input values.

I hope that helped clear things up and accurately discussed your dis-satisfaction with your lecturers' hypothesis despite being months too late!

I can't check the sources, but I think they must estimate the relative energy of a threshold-sensitivity signal. I don't think the energy of a sound wave can be assigned an arbitrary value the way a photon can...certainly only a photon can propagate in a vacuum...
Both light and sound waves scatter less, as they propagate, if they're higher frequency/energy. So all things being equal blue light scatters less than red light, and ultrasound scatters less than infrasound. So audible sound is less directional than visible light, and any sound receptor provides information that is less directional compared to any light receptor. So of course sound's a good thing to pick up for alert signals, that doesn't really mean it's been prioritized over vision through evolutionary processes.
Since most of vertebrate evolution occurs in the ocean, where sound and light propagation are quite different than in the terrestrial milieu, the lecturer's conjecture is likely irrelevant. Our sense organs are far more influenced by their evolutionary history than considerations of "best possible" (globally optimal) function.

Audible sound is less directional than visible light? This does not make sense. The scattering you mention may add some noise, but sound is highly directional and the auditory system is remarkably well equipped to localize sounds horizontally and vertically. Furthermore, if you refer to hair cells with 'sound receptors' than they not only have little directional sensitivity, they have none. Photoreceptors, due to their retinotopical organization, are directional, but only in the field of view. In contrast, we can localize sounds from behind. Your arguments don't make sense.

Yes, sound is less directional than light, comparing audible sound and visible light. Sorry this doesn't make sense to you. Maybe another commenter can suggest a better way to explain this.

It is my understanding that the dark-adapted eye can perceive single photons. Those have a well-defined range of energies in the visible spectrum. Also, as others have pointed out, light is very directional and localized: if you are not looking at the source, it will not be perceived. Sound comes to the ears from all directions at all times. The waves are so large that low frequencies cannot even "fit" inside a typical room, so direction is meaningless. Trying to define a particular energy for them when they can vary in both frequency and intensity (unlike photons, which only vary in frequency and number of them impinging) is not likely to be exact.
If I was told that two completely unlike forces differed by a factor of 4, I would say, "could be that one is actually more or less than the other, too close to tell." In electronics, component values can vary over a range of half to twice as much and be in specification.
Generally speaking, the senses evolved to the point where any further sensitivity would result in perceiving noise. Then, quite reasonably, they stopped. If you could hear the air molecules banging on your eardrums (if ears were 10 dB more sensitive) you would go mad. Light does not have this noise characteristic, so we can see the lowest possible value: one photon.

Are you saying that at ambient temperatures a 10 dB sensitivity increase would allow you to hear air molecules without any external air pressure differences acting upon them? Could you provide the math or a reference? As our frequency optimum is 20 Hz - 20 kHz (http://biology.stackexchange.com/questions/27898/can-humans-perceive-sounds-above-20-khz/27901#27901) air molecules should be vibrating within these limits. I don't believe this to be true.

I disagree that you will go mad even if you could hear noise from air molecules. Sensory adaptation is a well documented phenomenon.


text:
Restriction Mapping - Homework question
I have trouble in solving this exercise.
Exercise

A circular plasmid of 10,000 base pairs (bp) is digested with two restriction enzymes,A and B, to produce a 3000 bp and a 2000 bp bands when visualised on an agarose gel. when digested with one enzyme at a time, only one band is visible at 5000 bp. If the first site for enzyme A(A1) is present at the 100th base, the order in which the remaining sites (A2,B1 and B2) are present is?

Why I struggle with this exercise
How can a 10,000bp plasmid produce 3000bp and 2000bp only on agarose gel. I mean where are the remaining 5000bp? I dont know if my concept is right.
Linearised bands on an agarose gel may be doublet. That can clear the doubts in problem. But still I dont know how to do a reasonable restriction mapping and find out sites of different enzymes.

I edited your question so that it is shorter, easier to read and understand and sounds a bit less dramatic!

This is not as hard, as it first seems. Lets have a look at the single enzyme digests first: The digest with enzyme A and B only leads to products which are 5kB (5000 bp) away from each other. Since they are of the same size, both equally sized restriction fragments appear as one band. So each enzyme cuts the plasmid exactly in half.
The double digest is a bit more tricky, but not much. You get two products from it, with 2kb and 3kB. This means that enzyme B cuts between the restriction sites for enzyme A, resulting in these two fragments. Have a look at the sketch I made below (only a quick one and not to scale):

A1 and A2 are the cutting sites for enzyme A, B1 and B2 the sits for enzyme B. The numbers on the outside are the positions on the DNA sequence. You can see that a single digest leads to two fragments of 5kB (doesn't matter which) and that both A and both B sites are located 5kB from each other.
A1 is at position 100, A2 has to be at position 5100, B1 is located 2kB behind A1 (and therefore at position 2100), and B2 2kB behind position A2 (and therefore at position 7100). To get the same restriction pattern it is also possible that B1 and B2 are located 3kB behind their respective enzyme A position (so at 3100 and 8100) and you still get the same pattern of 2kB and 3kB on the gel.


text:
B-cell and T-cell activation by parasites
Parasitic infections lead to the production of parasite-specific IgE, but they also lead to the activation of nonspecific, polyclonal B-cells and T-cells. How do parasites trigger non-specific activation?

I've found a great article that says:

Mitogens   and   superantigens   have   been   described   to
  explain the strategy used by microorganisms to avoid the
  host specifc immune responses and to ensure persistence.
  These  moieties  are  responsible  for  the  initiation  of  non-
  specifc  (polyclonal)  immune  responses.

Mitogens are chemicals (usually proteins) that promote mitosis. Superantigens (sAg) form a subclass of antigens and are capable of inducing massive polyclonal T-cell activation and cytokine release (Cytokines crucial role in immune system mediation). Their ability to inflict massive T-cell activation comes from the fact that they bind directly to MHC-II without any pre-processing, and stimulate T-cell activation.
Source: https://escholarship.org/uc/item/47g8w51m
Also there are B-cell sAgs that stimulate B-cells, and their activation.
These altogether (mitogens cytokines, sAgs) result in rapid expansion of B-cells and T-cells.
Also this paper might help to understand why parasites trigger polyclonal T and B-cell activation. Namely to avoid host specific immune system, dilute the pathogen specific anti-bodies. It is important to note that chronic infections could lead to several auto-immune diseases.

Maybe we should attack the superantigens if they are so strong virulence factors, instead of developing antibiotics, which don't work.

Yepp, there is some research in the topic: http://www.mdpi.com/2072-6651/6/6/1724/htm http://informahealthcare.com/doi/abs/10.1517/14728222.2012.682573
Btw. afaik. superantigens are a subgroup of mitogens.

@inf3rno -  Well mitogen is a broad term, so I guess you can view it as such.


text:
What is different between the pigment of giraffes and the pigment of flowers?
I saw this video created by Derek Muller and he says there that it is very unusual to evolutionary develop the colour of the skin without the pigment. That sounds reasonable but if so, what nutrients have to get animals with pigment to get colored? Is it an active job of the cells or skin cells are just full of colorful minerals?
In case of giraffes: How does skin correct the shape of the spots? (For instance in cause of zebras it is clear according to this video)
And what about purposely colorful flowers? What nutrients do they need?
Thank you very much.

Pigmentation in most animals which is between black, brown, red, yellow and which is made up by the mixture of two pigments: Eumelanin (yellow to red) and Pheomelanin (black to brown). The ratio between these two makes a color. These are pigmental colors which are made by a special kind of cells in the skin, in mammals they are called melanocytes (and I will only look into mammals here, as this is already complicated enough). Additionally there are other colors, especially in fish and insects iridescent color play an important role.
This pigmentation is made by a cascade of enzymes from the oxidation and polymerization of the amino acid tyrosinase. So there are no minerals involved in the process. See here for more details.
For the pattern: As far as I know the literature, these pattern by x-inactivation are only present in cats. Here one of the enyzmes which is important for the generation of the dark pigment is encoded on the x-chromosome of the animals. Gene defects on this chromosome then lead to pigmentory defects.
Pigmentation patterns can be explained by a model which was formulated by Alan Turing and which is called "Reaction Diffusion Model". You can find an interesting article about this in reference 1.
Basically two different morphogens (different pigment cells) influence each other with positive and negative signals. If these signals would occur independently, than only relative incomplex two-dimensional colorations would be possible. See the figure from reference 2:

References:

How the zebra got its stripes, with Alan Turing
Reaction-Diffusion Model as a Framework for Understanding Biological
Pattern Formation

Ok,thank you but how do flowers create their pigment without their partner´s chromozome?

I'll add a section on it later.


text:
Why does hair thicken and become more rough after a razor shave but not after one using a trimmer?
If a razor cuts only the hair, then how does hair thicken and become more rough with a razor shave and not after one using a trimmer? If both are used for hair removal, why is there a difference in hair growth?
I have been using a trimmer for 1 year, but the growth of hair remained unchanged.  When I started shaving with a razor, the hair growth thickened.

http://lifehacker.com/5873922/10-stubborn-body-myths-that-just-wont-die-debunked-by-science, and under skin and hair in this page http://en.wikipedia.org/wiki/List_of_common_misconceptions

This is a myth and your evidence is purely anecdotal - voting to close as not on topic. Might suit skeptics.se

This question appears to be off-topic because it belongs on skeptics

May I ask how this belongs in Skeptics? It is a question seemingly based in biology that has a biological answer...

@SamuelBarnett Because the question is based on a flawed premise. It's a myth, a wives tale, that hair does this. Before it is possible to answer a question of why something happens we should first have reason to believe it happens. We know that it doesn't so there is no question of why it does happen.

@GriffinEvo Are you saying that the removal of the tapered end is a misconception? and that the "truth" behind the misconception is a misconception itself? If so can you provide some evidence for it?
Also if (the previous is not the case) people ask a question with a flawed logic or understanding behind it surely we should reply with a scientific answer not direct their question to the sceptics site even if we know the answer.

Hair does not grow back thicker when it is cut. This is somewhat of an optical illusion because when you shave with a razor it leaves the top of the hair flat rather than pointed so it appears thicker. For instance see this picture:

As you can see the hair is tapered at the top and when cut loses this taper to leave a large cross-sectional area. I would say that for your question with with the trimmer that it is probably cutting the hair further up the taper where the hair is 'thinner' to begin with. A razor cuts closer to the base and thus gives a thicker appearance.
Evidence: http://www.scientificamerican.com/article/fact-or-fiction-if-you-shave-or-wax-your-hair-will-come-back-thicker/
http://www.sciencedirect.com/science/article/pii/S0190962299701817

could you provide a source for A) a hair being tapered as in the diagram, and B) cutting it flat makes it appear thicker then when tapered.

could you summarise the important findings of the paper - its behind a paywall

@GriffinEvo I am sorry my institution automatically passes me through paywalls so I didn't realise. I will sum it up in the morning as it is getting quite late here.


text:
What is the exact chemical composition of human body?
I've just watched Breaking Bad Season 01 Episode 03. In that Walter gives the chemical composition of human body. The conversation is as follows

Walter White: Let's break it down. Hydrogen. What does that give us?
Gretchen Schwartz: We're looking at 63%.
Walter White: Sixty-three, that is a big bite. My next step's gotta be
  oxygen.
Gretchen Schwartz: Oxygen, 26%.
Walter White: Twenty-six. There you have your water.
Gretchen Schwartz: Carbon, 9%.
Walter White: Carbon, 9.
Gretchen Schwartz: For a total of 98%.
Walter White: Right.
Gretchen Schwartz: Nitrogen, 1.25%.
Walter White: One-point-two-five.
Gretchen Schwartz: That brings you to 99 and a quarter. Which only
  leaves you with the trace elements down where the magic happens.
Walter White: Oh, wait a minute. What about calcium? Calcium's not a
  trace. Got a whole skeleton to account for.
Gretchen Schwartz: You would think, right? Calcium's only 0.25%.
Walter White: What? That low? Seriously? Damn, I never would've
  thought that. Okay, so where does iron fit in.
Gretchen Schwartz: Iron. 0.00004%
Walter White: What? You can't have hemoglobin without iron.
Gretchen Schwartz: Apparently, it don't take take much. No doubt. Go
  figure.
Walter White: Sodium.
Gretchen Schwartz: Sodium, 0.04%. Phosphorus, 0.19%.
Walter White: Point-one-nine. There we go. So the whole thing adds up
  to... 99.888042%. We are 0.111958%. Shy.
Gretchen Schwartz: Supposedly that's everything.
Walter White: Yeah? I don't know, it just... it seems like something's
  missing, doesn't it? There's got to be more to a human being than
  that.
Gretchen Schwartz: What about the soul?
Walter White: The soul? There's nothing but chemistry here.

When I searched for it, Wikipedia has something different.
Which one is correct?

Not quite a dupe.

Neither are correct if you are looking for the "chemical" composition. Water, proteins, and fats are chemicals that make up most of the composition. Oxygen, hydrogen, carbon, and nitrogen are elements that make up those chemicals.

That conversation is strange. While different tables exist, the very first elements seem messed up. If the body is 60 (some sources say 70)% water, then oxygen has to be the most abundant element by weight (water - H2O - has a molecular weight of ~18 g/mol, with hydrogen contributing only 2g/mol of that weight).
The usual figures are roughly Oxygen (65%), Carbon (18%), Hydrogen (10%), Nitrogen: (3%), Calcium (1.5%), etc.
However, the writers of Breaking Bad weren't stupid. So, they weren't discussing percentages of the mass of each element, but rather the frequency of that atom in the body. The number of hydrogen atoms does indeed exceed the number of oxygen atoms.
So, by atomic percent, Oxygen is 25.6%, Carbon: 9.5%, Hydrogen: 63%, Nitrogen: 1.3%, Calcium: 0.24%, etc. So yes, the numbers are approximately correct for a normal, average, youthful (more water) 70 kg male.
So here is a table incorporating both percent by weight and percent by abundance. The writers were pretty well informed.


text:
Is there any stem cell or biogel method that exist for muscle and tendon lengthening?
Is there any stem cell or biogel method that exist for muscle and tendon lengthening?
It is known that height surgery is limit to six inches with two surgeries and three inches each, it is also true that there is limit because the muscle and tendons could stretch no more. Is there some research about this?

In doing search into muscle stem cells, I found some articles which discuss roles of satellite stem cells and non satellite cells  involved in muscle regeneration: (Yin, Price and Rudnicki, 2013,Seale and Rudnicki, 2000, and Mitchell et al, 2010).
Other articles, that I found discussed the splicing of insulin-like growth factors (IGF-1) into the satellite stem cells rodent muscles and the subsequent expression of the gene were studied to understand how is plays a role in muscle repair (Hill and Goldspink, 2003, Musaro et al, 2004). Another study looked at how transforming growth factor-β (TGF-β) and its interaction in the Notch signaling pathway play a role in smooth muscle repair (Kurpiinski et al, 2010)( Review Articles by Péault et al, 2007  and Seagers and Lee, 2008 )
As for current methods on the application of stem cells to myogeneration or myoregeneration, there are a few papers that I found but, it seems like we are still too far away from anything that is medically feasible (Zhu et al, 2014, Milner and Cameron, 2013)
Hopefully that answered your question or at least put you on the right track in your research.
EDIT: I found some papers on tendon repair and growth, but the conclusions are the same, in that there is much more research and technology improvements to be done (Awad et al, 2007 and Breidenbach et al, 2014)

Limb lengthening surgery is usually used to treat sequelae caused by bone disease, trauma, pygmyism or inflammation. I personally do not recommend to use surgical methods to increase height. Typically Limb Lengthening requires Achilles pre-lengthening surgery and a lot of postoperative rehabilitation. Moreover, Limb lengthening surgery may cause pain, infection, muscle atrophy, joint stiffness and delayed bone healing. There's a lot of related research cause this study is timely for some patients.
ALDEGHERI, R., RENZI-BRIVIO, L., & AGOSTINI, S. (1989). The callotasis method of limb lengthening. Clinical Orthopaedics and Related Research, 241, 137-145.
De Bastiani, G., Aldegheri, R., Renzi-Brivio, L., & Trivella, G. (1987). Limb lengthening by callus distraction (callotasis). Journal of Pediatric Orthopaedics, 7(2), 129-134.
Paley, D. (1988). Current techniques of limb lengthening. Journal of Pediatric Orthopaedics, 8(1), 73-92.
Paley, D. (1990). Problems, obstacles, and complications of limb lengthening by the ilizarov technique. Clinical Orthopaedics and Related Research, 250, 81-104.
Szoke, G., Lee, S. H., Simpson, A. H., & Prescott, J. (2005). Response of the tendon during limb lengthening. The Journal of Bone and Joint Surgery.British Volume, 87(4), 583-587.

It seems that just a Russian researcher named Dr Alexander Teplyashin has made any progress into using stem cells for LL (Limb lengthening). Conventional way to go about it would always be surgeries which are detailed in Wikipedia (reference). This is a relatively new development, so I could not find any relative publications to support the claim of this particular researcher. There is however a website detailing the news in English, most others being in Russian (reference) Here are a few publications of his (reference). There are already lengthening methods available which is a combination of both surgery and stem cells (reference). As far as there is some credible proof, I would take the claims of that Russian researcher with a pinch of salt.

I upvoted it, however it is bone lengthening, not the muscle and tendon lengthening i asked

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


text:
Why do humans have only two nipples?
If other animals have more than 2 nipples, then why do humans have only 2 nipples?
Even my pet dog has more than 2 nipples.

There is a condition called supernumerary nipples where people have extra nipples. This is an evolutionary holdover from when we needed a lot of nipples.

Well, for one things we don't often need them. There are times where humans have more than twins... But these aren't terribly common.

The post Why don't mammals have more than 4 limbs? is related, not by its subject but by the nature of the question.The top answer very much makes a similar point as @Ryan's answer but give some more information.

Questions of the type, "why does organism X have feature A?" invite teleological (just so) explanations which are difficult to substantiate. For example, the number of teats on a cow are difficult to explain in terms of providing milk to humans!
We should look to evolutionary history to explain human traits, not "just so" stories. The simple answer is that humans are primates, and primates have similar bodies and lifestyles. If there's a single pressure that lead to the number of teats in primates, it's likely the arboreal niche, not the mean litter size. Indeed, litter size is usually a plastic trait, even in primates, and is certainly not an accurate predictor of the number of teats.
There are no strict restrictions on nipple numbers in humans; they can occur anywhere on the milk line. So humans tend to have two nipples because that's what primates tend to have, because of our evolutionary history.
A better answer than this one would locate a candidate common ancestor to the primate and non-primate lineages and make reference to the embryonic development of the mammary tissue.

An example of a mammal with large litter sizes but only two teats would be quite convincing that this merely represents an ad hoc fallacy; I would welcome such an example. Indeed, in your own example of plasticity of litter size, the lemurs in question have 6 nipples. With such explanations, one should try not to throw out hypotheses that make sense on 'principle'. As for cows having four teats, I did not say that was for humans, but that it was exploited by humans. Which it has been, for thousands of years.

The 6 nippled lemurs certainly temper your claim that "[a]ll primates have two nipples." I would think you'd clean up your answer before challenging mine.

May I restate that: all arthropoids have 2 nipples; lemurs are a subgroup of primates called prosimians. I see you are remaining in character for comments to me.  Shame, really. My challange still stands, without all the attempts at casting aspersians that you revel in.

@anongoodnurse, if you'd like me (or the remainder of the StackExchange community) to research an answer regarding a hypothetical correlation between nipple numbers and brood sizes, free free to ask a question.  I think you're probably correct in asserting a positive correlation. I'm happy with my response to OP's question as-is, and you don't seem interested in improving your own answer (as you refine "anthropoids" here but leave "primates" in your actual answer.)

@anongoodnurse Evolution does not think sense. I agree with Ryan's answer but some explanation can be provided for the loss or gain of teats. For this, one has to make a comparison between primates, other mammals and the common ancestor of all mammals, as already pointed out by Ryan.

@WYSIWYG - I agree with you that evolution doesn't think or plan. However, "because it didn't confer a survival advantage" is usually acceptable. A dog with two teats and 9 puppies does not seem advantageous to me. Pigs and cows had a many-nippled ancestor. Cows clearly lost them for a reason. I'm comfortable that my answer has truth involved somewhere.

@anongoodnurse it looks like you are assuming number of nipples are the primary factor of milk production

@Macond - heck no! http://biology.stackexchange.com/questions/21789/does-a-bigger-breast-give-creamier-milk/21796#21796

@anongoodnurse - or should we assume that every baby should be fed simultaneously? like nipples are some kind of oxygen masks? I simply don't understand that haste to associate every feature to reproductive success. Just because it seems convenient, doesn't mean that it is a product of an optimization process.

Your pet dog needs more than two nipples because she can have up to 11 or more puppies. If she had two nipples, most of them sound starve.
Twins are rare enough in humans. Two nipples are fine, and fit with bilateral symmetry. All primates have two nipples. So do many animals with one, two, and rarely three offspring at a time. Elephants: 2 teats, 1 calf (usually). Goats: 2 teats, 2 kids.
Why a cow has four teats, I'm sure I don't know, but I'm sure that's what made them valuable as a milk source to man.

someone mentioned to me that not all primates have two nipples. Is that right? And is there some evidence that the number of teats is correlated with the litter size? That makes sense, I'm just wondering if there is evidence to this end.

There is in rodents at least https://www.ncbi.nlm.nih.gov/pmc/articles/PMC323835/


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Viral Mutation Mechanism
I think I have a wrong concept about viral mutation process. First of all what is mutation actually? I mean, I know it's a sudden change in DNA, happening when subjected to mutagenic agents.
But can it occur due to internal urge of an organism, say virus? If not then how can virus like Ebola undergo rapid mutations so that no vaccination can be given as specificity for antigen is lost?
What accounts for such a viral behaviour?
In evolution, internal urge for survival causes development of  some beneficial characters. What is meant by this at molecular level. like gradual mutation!!

A mutation is a change in the genomic sequence - this can either be in the DNA or for viruses also in the RNA which carries their genetic information. This can either happen due to external influences (chemicals, radiation) or internal (mistakes while copying the information) reasons. See the figure below which shows the principle:

DNA based lifeforms usually have pretty good proof reading functions which eliminate most mutations, as they are often causing problems. RNA based viruses (as the flu virus or the ebola virus) do not have a proof reading function which raises their mutation rate drastically. See the figure below, which shows the mutation rates of several organism groups (image from this paper):

These higher mutation rates indeed produce high number of mutated viruses which are different from the original form. This leads to a high number of viruses which are non-functional due to this mutations, but also to a few which are better adapted or look different due to this mutation. This can help in evading the immune system (when surface proteins of the virus change) or to adapt better to a host.
Since the number of viruses in an infected individual is very high (billions of viruses) it doesn't matter and the the mutations which are beneficial for the virus are positively selected for.
This can lead to difficulties in the production of vaccines when the proteins used in the vaccine mutate. Usually this is accounted for by using proteins for immunization which only mutate slowly or not (because their function is important and mutations disrupt it). For more information have a look at the following review:

RNA virus mutations and fitness for survival.

The key to rapid evolution of viruses is high mutation rate, as pointed by @Chris, and high population size.

But can it occur due to internal urge of an organism, say virus?

If your question is whether in the case of Ebola the vaccination caused the mutations the answer is no. The vaccination lead to the fixation of some mutations that would have happened anyway (but the would not have fixed without the vaccination).
There are however a few exceptions, for example stress-induced mutagenesis.


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Optimization of E. coli growth in D₂O (heavy water)
I would like to find a method of increasing the biomass of my D2O cultures because my current method is not yielding enough protein. I would like to also minimize the amount of H2O in my culture.
My current methodology is a small scale growth of 3mL with 75% D2O and LB grown for approximately 9hrs. This culture is then used to seed a 20mL 100% D2O and M9 culture overnight and this entire culture is used to seed a 1L D2O and M9 culture.
Thanks for your time.

It looks like you're very stringently avoiding $^1\mathrm{H}$. You may want to consider replica plating your transformations onto $\mathrm{D}_2\mathrm{O}$ plates (selecting for $\mathrm{D}_2\mathrm{O}$ tolerance earlier.)
I assume you're doing protein NMR and want "triple labeling." Depending on how specific your carbon labelling is, you may want to grow your starter cultures on triple labeled agal hydrolyzate (something like "Bioexpress.") You can buy some unlabeled stuff for fairly cheap (\$55 USD at CIL for 10 mL of 10X stock) and if your starters grow well you can spring for the same quantity of $^2\mathrm{H}$,$^{13}\mathrm{C}$,$^{15}\mathrm{N}$ for around \$405.

A guy I talked to who was doing triple labeling said he had to give his bacteria several generations to adjust to increasing amounts of non-normal isotopes. I can't remember any other details, but you might not just be able dump the bacteria in a labeled media and make it work well.

@Ryan Thanks for the reply but it seems like this would not be a financially viable method for our lab. We recycle as much D2O as we possible can and to make agar plates with D2O would be wasteful for us. Additionally, we do use BioExpress and the labeling is not an issue. It just seems like our issue is with the amount of E. coli biomass.

@user137 Do you by any chance know how many generations he grew his cultures?

@gravityassist if you're already using Bioexpress that contradicts your stated use of M9. So I'm confused what you're trying.

@gravityassist I'm sorry, I don't. It was a 5 minute talk at a poster presentation over a year ago, so I don't remember much.

@Ryan No, my statement of using M9 and Bioexpress together is correct. I use both in my D2O labeled and unlabeled cultures. M9 is just my media base, if I need to label my carbons I use the appropriate glucose and Bioexpress.

@Ryan As a clarification, I use the Bioexpress as an additive to the media not as the main media.


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Does THC excretion increase if urine volume increases?
In regards to the body metabolizing and excreting THC: if urination is increased as a result of drinking lots of fluids, does that mean that more THC is leaving the body? To rephrase the question, is metabolism required for urination? Or can you simply urinate as a body process without metabolizing toxins from your body?

It depends on the molecule. Liver makes it water soluble if it can. After that it can be excreted with the urine. If it cannot make it water soluble, than the body can store it in fat or excrete with bile. According to wikipedia, THC is poorly water soluble and more than 55% of THC is excreted in the feces and ~20% in the urine (after processed by the liver ofc.). Since we are talking about a few amount of drug and the main bottleneck of urine type metabolism is the liver, drinking more water won't help.

This question asks about the urinary excretion of THC. Before answering the question I think you're getting at, I'll first note that cannabinoids (of which THC is one) are primarily metabolized by hepatic cytochromes rather than being excreted directly. This article is a classical pharmacokinetic paper on the topic if you’re able to access it; this one is a more recent general review accessible on Pubmed Central.
Cannabinoid metabolites are excreted both renally (via kidneys) and in the feces, so I’ll understand your question to refer to the renally excreted portion. When considering renal excretion of any substance we think in terms of glomerular filtration rate, which refers to the volume of blood filtered through the glomerular capillaries per unit time, often estimated as creatinine clearance. The question then boils down to:

Does excess hydration increase GFR?

And the basic answer is: no. The  kidneys control both volume and osmolality more distally, i.e. after the event of glomerular filtration.1
In the scenario you posit – drinking a lot of dilute fluid – osmoreceptors in the hypothalamus will sense the decreased plasma osmolality and suppress ADH (antidiuretic hormone, a.k.a. arginine vasopressin), the hormone that acts on the distal nephron to control water reabsorption. If ADH is completely suppressed, the kidneys can produce up to 25 L/day of urine with an osmolality as low as 60 mOsm/kg.2,3 This huge volume of urine, however, reflects water homeostasis achieved at the distal tubule rather than increased glomerular filtration. It does not correlate with increased excretion of THC metabolites or anything else at the level of the glomerulus.

Notes and References

1. If this makes no sense to you, you may want to check out this basic introduction to renal physiology that is available online. The referenced textbook in #3 below is more comprehensive but requires a library or purchase for access.

2. "Normal" urine osm ~300-800 mOsm/kg; plasma Osm ~280-290 mOsm/kg.

3. Christopher Lote. (2012). Principles of Renal Physiology. Springer New York.

P.S. If the question you really wanted to ask was, "Will drinking lots of water make my tox screen negative faster?".... I'm not answering that question. For reasons largely unrelated to the discussion here (but see references in paragraph #1), I suggest assuming that THC metabolites will be forever detectable via tox screen. ;-)


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Problem on number of amino acids that an alien can use
A new life form discovered on a distant planet has a genetic code consisting of five unique nucleotides and only one stop codon. If each codon has four bases,what is the maximum number of unique amino acids this life form can use ?
I tried this and got 624 (Using permutation method 5×5×5×5 = 625). But the answer given was 3124. Please help.

when you say you tried, what was your logic. Can you add that in your question.

Using permutation method 555*5 = 625 amino acid codons of which one is stop codon.

Plus. It is not that by increasing information content in DNA you can increase the number of amino acids that are put in use. In fact with the current genetic code 63 amino acids can be encoded but there are only 22. Feel free to give me the address of the person who posed this question to you; a cruise missile would be on its way :P
BTW 624 is right and 3124 is incorrect.

i thought there were only twenty, what are the other two?

@CognisMantis its 23 now. 20 standard and 3 non-standard http://en.wikipedia.org/wiki/Amino_acid

I also got 624. Maybe the answer is incorrect.
My processing is:
Each codon has four bases, the species contain five unique nucleotides, so for the first position in the codon, there are 5 possible results, also, for the second position in the codon, there are 5 possible results, it is same in third and forth position,
so the result should be  5*5*5*5-1=624

Hi, the question I posted above is from a competitive exam I appeared. Answer key says 3124 is the correct answer. Help please. I dont know which is correct. But everytime I end up with 624. I could not clear the exam because of 2 marks that is contributed by this question. I really need to know how to solve it.  Please help.


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What is actually systematics? What is the difference between it & taxonomy?

In the last century, even during the past decades of the present century, students of systematics could not have thought of any fundamental distinctions among Taxonomy & Systematics . These terms appeared to them more or less synonymous and hence often misunderstood until G.S.Simpson(1961) analysed each of the terms separately & gave a comprehensive definition of each term and its workable areas so that their underlying fundamentals became clear.

This is what I found in my book. But what is actually Systematics? And what is the difference between it and taxonomy??

Systematics studies the diversification and relationships of past and present living forms. Taxonomy is only a part of systematics as defined by Michener et al. in 1970:

Systematic biology (hereafter called simply systematics) is the field that (a) provides scientific names for organisms, (b) describes them, (c) preserves collections of them, (d) provides classifications for the organisms, keys for their identification, and data on their distributions, (e) investigates their evolutionary histories, and (f) considers their environmental adaptations. This is a field with a long history that in recent years has experienced a notable renaissance, principally with respect to theoretical content. Part of the theoretical material has to do with evolutionary areas (topics e and f above), the rest relates especially to the problem of classification. Taxonomy is that part of Systematics concerned with topics (a) to (d) above.

Source: Michener, Charles D., John O. Corliss, Richard S. Cowan, Peter H. Raven, Curtis W. Sabrosky, Donald S. Squires, and G. W. Wharton (1970). Systematics In Support of Biological Research. Division of Biology and Agriculture, National Research Council. Washington, D.C. 25 pp.
via Wikipedia contributors, "Systematics," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Systematics&oldid=635316421 (accessed November 30, 2014).

To put it simply, you know that Taxonomy is the branch of biology that deals with the classification of living organisms.
Systematics, on the other hand, is nothing but Taxonomy + Phylogeny (i.e evolutionary relationships b/w organisms)
Hence, we can say that Taxonomy is a part of Systematics. Talk about evolutionary history/relationships between organisms, and you get Systematics.
Hope this helps :)


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How are lysosomes formed?

Lysosomes are irregularly shaped membrane bound organelles containing 50 different types of enzymes.

But how are they formed? How are they produced??

Could you show what you have found on the matter so far?

@Bez: My book wrote:
lysosomes are formed from ER or golgibodies. That's all I know. But how?

http://www.ncbi.nlm.nih.gov/books/NBK9953/

Cells take up external material in the process pf phagocytosis. This involves creating a vesicle from plasma membrane that will contain the external material. The vesicle enters the cytoplasm where it is called (early) endosome. The cellular membrane components of this endosome are recycled and gave back to the plasma membrane. The endosome pH decreases and it is now called late endosome.
Meanwhile, peptides (which will form the future hydrolases) are produced in the ribosomes of the endoplasmic reticulum and mannose 6-phosphate is added to these peptides. They are further transported to the Golgi apparatus which "packs" them into lysosomal vesicles.
The lysosomal vesicles fuse with a late endosome and due to the acidic medium of the endosome, the peptides dissociate from mannose 6-phosphate. This process turns the late endosome into a mature lysosome that is capable to digest material taken up via endocytosis.

My book wrote: lysosomes are formed from ER or golgibodies.

ER and Golgi help supply the enzymes to endosomes, thus turning them into lysosomes.

References:

Wikipedia contributors, "Lysosome," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Lysosome&oldid=635272974 (accessed November 30, 2014).
Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. Lysosomes. Available from: http://www.ncbi.nlm.nih.gov/books/NBK9953/


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What is the mechanism of action of lithium-induced polyuria?
I was reading in my pharmacology textbook on lithium in treating bipolar disorder, and I was curious to know if there was any specific action lithium takes to produce symptoms such as polyuria and polydipsia. Any help would be great. Also, what is the most common way to monitor lithium levels in the body?

Lithium changes the effect of at least three substances that play a role in diuresis:

aldosterone:  lithium partially inhibits its ability to increase the expression of ENaC receptors on apical membrane thus increasing sodium losses [1].
arginine vasopressin (AVP): because lithium can induce hyperparathyroidism, parathyroid hormone can act as partial agonist to AVP, inhibiting its hydroosmotic action [2].
antidiuretic hormone (ADH): lithium blocks its stimulatory effect on adenilate cyclase. The result is a decrease of cAMP levels in the cells from collecting tubules. cAMP promotes formation of water channels, thus improving absorption from collecting tubules. Because lithium decreases cAMP levels, diuresis is stimulated [1].

All these result in polyuria.
Lithium levels can be determined from the blood. Usually the test should be performed 12 hours after last dose of Lithium [3].

References:

Eleanor Lederer, MD; Lithium Nephropathy on http://emedicine.medscape.com/article/242772-overview#a0104
Carney SL, Ray C, Gillies AH. Mechanism of lithium-induced polyuria in the rat. Kidney Int. 1996 Aug;50(2):377-83.
http://labtestsonline.org/understanding/analytes/lithium/tab/sample/


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After vasectomy, where does the sperm go?
After vasectomy, where does the sperm go?
Vasectomy Procedure cuts only vas deferens, But Our Testes still produces sperm, if there is no output for sperm, where does it go?

Please type your questions without using ">" this makes the text appear as if it is a direct quote. See guide to formatting here: http://biology.stackexchange.com/help/formatting

A vasectomy [...] is a contraceptive procedure in men in which the vas deferens, or sperm duct, is cut and the cut ends are sealed in order to prevent the transportation of sperm. Sperm is still produced, but does not leave the body. Vasectomy is usually done as a means of sterilization and is sometimes reversible.
(from http://urology.med.miami.edu/specialties/male-urologic-health/vasectomy)

When the vasectomy is complete, sperm cannot exit the body through the penis. Sperm are still produced by the testicles, but they are soon broken down and absorbed by the body. Much fluid content is absorbed by membranes in the epididymis, and much solid content is broken down by the responding macrophages and re-absorbed via the blood stream. Sperm is matured in the epididymis for about a month before leaving the testicles. After vasectomy, the membranes must increase in size to absorb and store more fluid; this triggering of the immune system causes more macrophages to be recruited to break down and re-absorb more solid content.
http://en.wikipedia.org/wiki/Vasectomy

A vasectomy only blocks sperm and does not affect your sexual drive, your ability to have an erection, orgasm or ejaculation or your ability to have and enjoy sex. Sperm is only a small fraction of the total liquid in your semen(almost 4-5 %). The amount of fluid, intensity – even color and texture – does not appear to change when sperm is absent.
...
The body absorbs unused sperm cells normally – whether or not you’ve had a vasectomy. After the procedure, the testicles will continue to produce sperm, but they will not leave the body in the semen. They dissolve and are simply and naturally absorbed by the body.
(from http://urology.med.miami.edu/specialties/male-urologic-health/vasectomy)

Sperm are produced in the testicles.  They are stored and reach maturation in the epididymis, a tightly coiled, muscular tube that is 15 to 18 feet long and leads into the vas deferens.   The muscle of the epididymis and the vasdeferens contract to propel the sperm through these structures and into the urethra at the base of the penis so the sperm eventually can fertilize an egg.
http://vasectomyreversalcenterofamerica.com/microsurgical-vasectomy-reversal/faqs/

Sperm are produced in the seminiferous tubules of the testes, and this does not change. A vasectomy does not affect the function of the testes. It is a physical separation of the vas deferens from each testis, so that the sperm cells cannot be ejaculated. However, the rest of the semen, which is made in the seminal vesicles behind the bladder and which is stored in the prostate, is ejaculated so the male reproductive experience will not change. He can still ejaculate, but there will be no sperm cells in the semen, so there can be no fertilization of an egg cell during intercourse.

You need to include references and clearly state when you are copying materials from other sources. The answer also becomes very disjointed when you do not synthesise the knowledge, but only copy different sources.

@fileunderwater I had quoted the text which I copied from the source

The first and third section were included as normal text, without any reference to http://urology.med.miami.edu/specialties/male-urologic-health/vasectomy, even though they are word-by-word quotes.

@fileunderwater: Its omitted by accident.....the question changed so I couldn't find that....Any way thank you !

This help page has useful guidelines: http://biology.stackexchange.com/help/referencing

As a general rule, quotations should be used to support your own answer rather than form it in its entirety


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What initiates primase to add an RNA primer to a DNA strand and what makes it stop?
What initiates primase to add an RNA primer to a DNA strand and what makes it stop adding RNA nucleotides? Is there tags added to the DNA back-bone?

I'm studying "Biology" by Cambell et. al. and nothing is mentioned in the book.

Prokaryotic primases are activated by DNA helicase [1, 2] while the eukaryotic ones are triggered when they form a complex with DNA polymerase alpha and its accessory B subunit [2].
I couldn't find too much information about what exactly triggers activation, but according to De Falco M et al. (2004):

[...] synthetic function (of the prokaryotic primase) is specifically activated by thymine-containing synthetic bubble structures that mimic early replication intermediates. [3]

It stops when it finishes reading a DNA template:

The Sso DNA primase utilizes poly-pyrimidine single-stranded DNA templates with low efficiency for de novo synthesis of RNA primers [3].

References:

Wikipedia contributors, "Primase," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Primase&oldid=593928284 (accessed December 1, 2014).
David N. Frick, and Charles C. Richardson. DNA PRIMASES. Annual Review of Biochemistry. Vol. 70: 39-80 (Volume publication date July 2001). DOI: 10.1146/annurev.biochem.70.1.39
De Falco M, Fusco A, De Felice M, Rossi M, Pisani FM. The DNA primase of Sulfolobus solfataricus is activated by substrates containing a thymine-rich bubble and has a 3'-terminal nucleotidyl-transferase activity. Nucleic Acids Res. 2004 Sep 30;32(17):5223-30. Print 2004.


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Determining break/border of movement
A population given inhabiting an area. I can trace every individual and I've got the hypothesis there is a break in distribution like individuals born in the upper half of the area will rarely move to the lower half and vice versa.
Tracking each individual how can I determine the line/border which divides the population in a upper and lower half. What's the math or algorithm behind to draw this imaginary line?

Make sure to not let your hypothesis cloud your analysis. What if there are three, or five populations with distinct moving patterns?

Even if there are more than two populations the general question is still to determine if there is a break in distribution and how "geographically" locate this.

You should look into ordination techiques, to which you can apply different clustering techniques. Take a look at the R package vegan, which can do but ordination and calculate clustering.

There are a lot of approaches to this kind of problem. Starting with the simplest approach I think you'd benefit from using a K-means classification, with K=2 (or higher numbers to address @Luigi's concerns about model bias.) Once you've defined the geometric center of each population, you can treat them as foci, and use the equidistant points between each focus to define the boundary of interest. That does import another assumption (that the boundary is equidistant to the two points).
A more sophisticated way to divide two clusters is with a support vector machine but because this is a machine learning approach, you'd need to manually annotate a number of training data sets as "group 1" or "group 2." But after training, the SVM will define the optimal boundary (hypersurface) between these groups.
The two types of approaches (clustering versus machine learning) differ in where the manually-imported assumptions lie. One can combine them fruitfully -- using K-means to define the populations and SVM to define the dividing boundary.


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Simple Mendelian Genetics Question
here is my question:
In certain plants, tall is dominant to short. If a heterozygous plant is crossed with a homozygous tall plant, what is the probability that the offspring will be short?
My Solution:
Let T be the allele for the tall phenotype and t be the allele for the short phenotype.
Then the parental cross would be Tt x TT = 100% tall phenotype (1/2 Tt, 1/2 TT).
Hence the probability of having short offspring should be $\fbox{0}$.
However, the answer key for this question says the answer is $\fbox{$\frac{1}{2}$}$. How can this be??? It really bothers me when the answer key is potentially incorrect because it makes me very unsure, and I end up wasting time trying to figure out if the key is wrong or if I am. Can somebody please let me know if what I did was correct/incorrect??
Thanks

What's the source? I'd suggest it is an incorrect answer key... or does the question say anything about dominance (if t is dominant to T then the answer would be 1/2). Edit: re-reading your question T is dominant to t thus the answer should be 0.

Agree with @GriffinEvo. If you have restated the question accurately, the given answer must be wrong.

Assuming you have stated the question correctly, the answer key is incorrect for exactly the reasons you have given and your reasoning and consequent answer are correct.
I would double-check you have read the question correctly and then conclude the answer key is incorrect. It happens.

This is a test cross - a cross with a recessive pair of alleles and either a heterozygous or homozygous pair of dominant alleles( eg- Tt X tt or TT x tt respectively). These crosses are carried out to check the if genes are homozygous or not. In this the ratio is always 1:1.
So don't worry. :)
Be confident about your answer, because it is obvious that the answer cannot be half if you work it out using the Punnett square.


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Change in synthesis rate of a molecule changes equilibrium concentration
I was reading the topic of 'The concentration of the molecule can be adjusted quickly only if the lifetime of a molecule is short' from Molecular Biology of the Cell by Alberts.
At the end of pg-837 (this part can also be found here), the author says -

"In fact, after a molecule's synthesis rate has been either increased
  or decreased abruptly, the time required for the molecule to shift
  halfway from its old to its new equilibrium concentration is equal to
  its normal half-life—that is, equal to the time that would be required
  for its concentration to fall by half if all synthesis were stopped."

What do they exactly mean by 'shift halfway'? I am not able to understand quite clearly what the above sentence means. I hope some of you may be able to help me. Thanks.

Note: The term equilibrium is different from steady-state w.r.t chemical reactions. Steady state is the right term for the above example. Equilibrium is used in the sense of forward and reverse reactions in a single reversible reaction. The above example considers two irreversible reactions — production and degradation.

... ... the time required for the molecule to shift halfway from its old to its new equilibrium concentration is equal to its normal half-life

This is not true if the degradation reaction is zeroth order or if these reactions are nonlinear. But for a linear production degradation set of reactions ($X$ is a biomolecule formed at a constant rate $\alpha$ and degraded at a first order rate  $\beta$ ), the reaction rate can be represented by the following equation.
$$\frac{d[X]}{dt}\bigg|_1=\alpha _1 - \beta [X]$$
At steady state $\frac{d[X]}{dt}=0$, which means $[X_{ss_1}]=\Large\frac{\alpha _1}{\beta}$
Half life as defined, by setting $\alpha$=0 and solving the differential equation = ${\Large \frac{log(2)}{\beta}}$
When the formation rate is changed to a new value:
$$\frac{d[X]}{dt}\bigg|_2=\alpha _2 - \beta [X]$$
and $[X_{ss_2}]=\Large\frac{\alpha _2}{\beta}$
From the above equation following equation can be deduced (by integrating the differential equation):
$$-\frac{1}{\beta}.log(\alpha _2 - \beta [X]){\large|}_{X_{initial}} ^{X_{final}}= t_{\frac{1}{2}} $$
when you substitute $X_{initial}=X_{ss_1}=\frac{\alpha _1}{\beta}$ and $X_{final}=\Large\frac{\frac{\alpha _2}{\beta} - \frac{\alpha _1}{\beta}}{2}$ (halfway between new steady state and old steady state)
you would obtain: $$t_{\frac{1}{2}}= -\frac{1}{\beta}log\left(\frac{\alpha _2 -\beta\frac{\alpha _1}{\beta}}{\alpha _2 - \beta \frac{\frac{\alpha _2}{\beta} - \frac{\alpha _1}{\beta}}{2}}\right) = \frac{log(2)}{\beta} $$