text:
How is Calcium regulated in myocardic AP and plateau phase?
The plateau phase is maintained by influx of calcium and outflux of potassium in the second stage:

My conjecture is that calcium transforms between two phases

ionated phase (free calcium from i/c SR and e/c Ca-ATPase)
non-ionated phase (bound to some proteins).

The initial form can be ionated.
The process of deionisation occurs only in all-or-nothing cases - I see no evidence that this process can be continuous in my data.
My another conjecture why this deionisation can occur is because of the vortexes in the diastolic phase of ventricles (T wave; blood bouncing back to the tricuspid valve).
Which sources can correspond to this non-ionated calcium more?
My conjecture is e/c Ca more because longer travelling distance and entry involves accelerative movement.
Actually, this can differ depending on the situation at hand.
The accelerative movement can also contribute more to ionisation process so the situation can be reverse in some cases.
How is Calcium released from Sarcoplasmic reticulum?
Steadily or in accelerative motion or in a vortex.
How are Calcium forms regulated during action potential of myocardial cell plateau phase?
Keywords: Local Ca2+ signaling in health and diseases.

Aren't there models on this already?

@WYSIWYG Thank you for your good comments! This is the question which I leave open or not delete. There are some visualisations about this but not found any good one. I just need to search it with appropriate words probably. One Google search calcium action potential plateau filetype:swf. Probably, muscle contraction action potential better giving http://course.zju.edu.cn/532/study/theory/2/Cell/Action%20potentials%20and%20muscle%20contraction.swf but I have difficulty in playing this. Other SWF's were not from good sources and bad quality. Better search words needed.

I heard many talks on mathematical models for cardiac action potential and the role of calcium waves. You can see this guy's work. I am not sure if there is an animation but he once showed in one of his talks a nice simulation of spatial waves in heart .

@WYSIWYG Thank you very much for the mentioning the name of one relevant researcher here! I just downloaded a bunch of his articles. If you remember anything more, please write an answer or comment. I will write an overview when I understand this topic better.

Other researcher and Eric's coauthor is here https://www.researchgate.net/profile/Long-Sheng_Song?ev=brs_highl

Speaking of non-ionised calcium means that it is available in the form of Ca atoms, which is highly unlikely in an aqueous environment of a cell. I would better write "bound" and "free" calcium.

@Chris can you please make edits directly to body. I do not undestand to whoch part your comment applyes.


text:
Does tea have its effect if you have a sleep after drinking it?
If I drink tea, then go to sleep for a while, when I wake up, will the effect of tea still be on me (the refreshing effect)?
Does it depend on the duration of sleep?

Caffeine is the stimulant in tea. It has different effects on different people, but if you can sleep right after drinking it, it probably isn't strong enough to have long term 'refreshing effects', And yes, the duration of your sleep does matter. If you sleep for 12 hours, much more caffeine will filter out of your blood stream than after a 1 hour nap.
Some info on how caffeine works, from here:

Caffeine, a component of tea, coffee and cola, induces wakefulness. It binds to adenosine A1 and A2A receptors as an antagonist, but the receptor subtype mediating caffeine-induced wakefulness remains unclear. Here we report that caffeine at 5, 10 and 15 mg kg-1 increased wakefulness in both wild-type mice and A1 receptor knockout mice, but not in A2A receptor knockout mice. Thus, caffeine-induced wakefulness depends on adenosine A2A receptors.

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text:
What "emotions" can a snake feel?
Short:
Thinking in particular of a Royal Python (US: Ball Python) such as some people keep as exotic companion animals, what sorts of "emotions" or "feelings" are they capable of?

Long: http://simonsnakesite.tripod.com/snakebasics.html says that

scientific studies show that snakes just don't have the cerebral capacity for [emotions like joy, anger, and affection] but do have "primitive" feelings like aggression, fear, and pleasure

Based on the parts of the human brain where we develop emotions, and on the more primitive brain in a snake, this makes sense, but beyond being able to tell whether it's feeling the primitives such as "fear" or "safety", what "emotions" or "feelings" can we realistically ascribe to a snake?

Interesting thought. I'd recommend diving into google scholar.

You seem to be confusing emotions and feelings. They are not necessarily the same thing. Definitions vary, can you make your question more precise? What do you mean by emotion?

I think the emotionial capacity of an animal is directly related to it's inteligence.By this mean the more intelligent species can be more emotional.

We can only very indirectly and tentatively ascribe emotions/feelings to animals if we understand their brains functionally, and use functional imaging. This is difficult in practice. There is also a crucial difference in science between the subjective world (happy) and objective world (smiling).
In ethology, you can only observe behavior and its consequences. Stimuli can be appetitive and aversive, positive or negative. Insects, reptiles and mammals can similarly differentiate between sweet water (which they seek out) and bitter water (which they normally avoid). Those are easier behaviors to identify. Of course, in reality, an emotional state is made up of a complex multi-dimensional spectrum of multiple measures (satiety vs. hunger, anxiety vs. relaxation, happiness vs. unhappiness, fear vs. safety, sadness vs. unsadness, etc.) simultaneously. There is also a difference between the measurement and the internal reality. Additionally, there's the choice of measurement and the internal reality, too. One could measure happiness by width of your smile at a given time, but that would not be a very valid and reliable measurement. This is the general difficulty with measuring and detecting emotion - behavior is a more objective quantification.
If you were studying a new species of human, which could not talk or report to you using a language about how it 'felt', and had a brain significantly different from ours, we would also be unwise to ascribe specific emotions so callously. Not because the specimen would be incapable of feeling emotions, but because we wouldn't have the tools to check and verify internal emotional states, or probe whether the snake was conscious of an emotion regardless of its behavior.
However, we do believe that emotions require a big central nervous system to exist. Snakes certainly have large enough brains to experience fear and pleasure. It seems that most large vertebrates can, certainly mammals can such as mice. Whether reptiles or even insects have the 'cerebral capacity' for non-primitive (read: non-humanlike) is an open question.

Pleasure and Displeasure certainly if you have a brain you have these.
Pain, Fear, and Anger is also highly likely just based on their general behavior. these are fairly basic and likely exist in all vertebrates.
Since they can be taught food avoidance likely Disgust as well.
Some snakes show familial ties so Affection/Love may be possible, although this is very tentative.
As SPr points out determining exact emotion ins ethology is extremely difficult, we can't even agree on what emotion humans have.This is partially due to not being able to define basic emotions.

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text:
Will ants arriving with travel luggage form a new colony?
I have found a few dozens of ants in my luggage after arriving back from holiday. Am I at the risk that they will form a colony in my home? Are those ants able to form colonies that are normally gathering food? Will any other kinds of ants be present in the luggage? What will happen to these ants after they start exploring my flat (which is distant from their original colony)?

typically only if the queen is in the luggage. ants definitely arrive with cargo and colonize new continents, so its not unheard of however unlikely it will happen

If they're bringing luggage, they're moving in...

An ant colony is started by a queen ant (reference). Worker ants are sterile, and cannot start a new colony (reference). The ants in your luggage are worker ants (unless you have a colony in there :) ). The original queen ant never leaves her colony, but during a nuptial flight, new queen ants will land in (hopefully) good nesting sites.  (reference) These ants can be told by their wings, which are non-existent in worker ants.
The worker ants have an average life span of 45-60 days (reference), so the ants in your luggage won't be around for very long.
Also see:

If a worker ant gets separated from its colony, it's doomed. No other colony will take it in, and it can't start its own colony--only queens can do that. It might be able to live for a while, but generally not that long--a lost worker is generally more concerned with hunting for its colony than with feeding itself, and its energy reserves are fairly small (depending on the ant species--some have workers that are adapted to taking long foraging trips). A few ant species, however, have "supercolonies," where neighboring colonies are established by queens directly related to one another. When queens are close relatives, their workers tend to have similar chemical profiles, meaning they can move from colony to colony without triggering the usual colony defenses against intruders. (Intruders are recognized by their chemical profile--their odor--and not by appearance, ID card, etc.) In such cases, workers routinely transfer between colonies, so a worker may end up working for its grandmother or, forgive me, its aunt. (From this page)


text:
Why the scent of mouth gets dirty after not eating for a long time?
After a long time of hard workout,not eating and nervousness makes your taste and scent of mouth very uncomfortable and bad why this happens and is there any way to prevent it?

This is caused by a build up of ketone bodies in your blood which lowers the pH of your body and can cause bad breath. Ketone bodies are a response of your body breaking down fatty acids for energy instead of glucose when in a low food intake (fasting) state. This is also true for morning breath since your body has been in a fasting state.
The way to prevent this is to eat the proper amount of calories needed for your body to function normally.


text:
Why does Hunger lead to the aggressive behavior?
I have observed that frequently when people are hungry; they tend to get angry more easily on pointless issues. Does this mean that our fight or flight response is more active when a person is hungry? What is a possible reason for this? Is this phenomenon linked with our cell signaling pathways? If it is, then what would be the pathway that leads to the aggressive behavior?

To summarize the question:
When a person is hungry and they get angry, is it due to a cell signaling pathway? If so, what pathway?

As I recall hypoglycaemia leads to a sympathetic response that can promote fight/flight behaviour.

I think a review should be offered to this post http://biology.stackexchange.com/questions/19515/effect-of-testosterone-hormone to answer this enough well. Testosterone in relation of hunger and aggressive behavior is a valid research topic.

Could you please tell me what u r missing in the answer that Cornelius has given for you have put up a bounty on this question?

I would say simply that when we are hungry, we feel a certain degree of pain and diminished emotional security. this puts us on the defensive and makes it harder for us to bear difficulty, so we snap out at those things (or people) which make our lives harder.

@TheLastWord from the answer,I got it that hypoglycemic condition leads to the Release of Epinephrine and nor epinephrine and activation of beta adrenergic receptors, but how the activation of this signalling pathway leads to aggressive behavior? Is their release of any hormone or secondary messenger in this pathway that effects behavior..?? wondering about this, can you explain me this point..please..???

Brain's main energy source is glucose. It uses about 20% of total glucose [1]. Brain hypoglycemia causes depressive-like behaviors in mice through adrenergic pathways [2].
When it comes to humans, here is a study that claims low glucose leads to increased aggression in married couples (see this too):

Self-control requires energy, part of which is provided by glucose. For 21 days, glucose levels were measured in 107 married couples. To measure aggressive impulses, each evening participants stuck between 0 and 51 pins into a voodoo doll that represented their spouse, depending how angry they were with their spouse. ... As expected, the lower the level of glucose in the blood, the greater number of pins participants stuck into the voodoo doll, and the higher intensity and longer duration of noise participants set for their spouse [3].

However, the conclusion is disputed:

Bushman et al.'s study does not demonstrate that fluctuations in blood glucose affect individuals' self-control abilities. As an important consequence, there is no reason to assume that giving couples a sugary “boost to their self-control energy” (p. 3) will reduce intimate partner violence. Because the glucose model of self-control lacks empirical foundation, it does not qualify as a framework for scientifically based intervention strategies [4].

What is sure, is that hypoglycemia activates sympathetic nervous system:

... the neurogenic symptoms of hypoglycemia are largely the result of sympathetic neural, rather than adrenomedullary, activation [5].
Hypoglycemia increases plasma levels of both epinephrine and norepinephrine. These catechols are released primarily from the adrenal medulla. However, it is well documented that hypoglycemic increases muscle sympathetic nerve activity, and that both alpha and beta adrenergic activity increase [6].

And this leads to behavioral changes (at least in animals):

Noradrenaline is involved in many different functions, which all are known to affect behaviour profoundly. ... Part of these effects may arise in indirect ways that are by no means specific to aggressive behaviour, however, they are functionally relevant to it. Other effects may affect brain mechanisms specifically involved in aggression. Hormonal catecholamines (adrenaline and noradrenaline) appear to be involved in metabolic preparations for the prospective fight; the sympathetic system ensures appropriate cardiovascular reaction, while the CNS noradrenergic system prepares the animal for the prospective fight. ... It appears that neurons bearing postsynaptic alpha2-adrenoceptors are responsible for the start and maintenance of aggression, while a situation-dependent fine-tuning is realised through neurons equipped with beta-adrenoceptors [7].

References:

Wikipedia contributors, "Human brain," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Human_brain&oldid=615456836 (accessed July 6, 2014).
Park MJ, Yoo SW, Choe BS, Dantzer R, Freund GG. Acute hypoglycemia causes depressive-like behaviors in mice. Metab. Clin. Exp. 2012 Feb;61(2):229-36. doi: 10.1016/j.metabol.2011.06.013. PubMed PMID: 21820138.
Bushman BJ, Dewall CN, Pond RS, Hanus MD. Low glucose relates to greater aggression in married couples. Proc. Natl. Acad. Sci. U.S.A. 2014 Apr 29;111(17):6254-7. doi: 10.1073/pnas.1400619111. PubMed PMID: 24733932.
Lange F and Kurzban R (2014) Sugar levels relate to aggression in couples without supporting the glucose model of self-control. Front. Psychol. 5:572. doi: 10.3389/fpsyg.2014.00572
DeRosa MA, Cryer PE. Hypoglycemia and the sympathoadrenal system: neurogenic symptoms are largely the result of sympathetic neural, rather than adrenomedullary, activation. Am. J. Physiol. Endocrinol. Metab. 2004 Jul;287(1):E32-41. doi: 10.1152/ajpendo.00539.2003. PubMed PMID: 14970007.
Hoffman RP. Sympathetic mechanisms of hypoglycemic counterregulation. Curr Diabetes Rev. 2007 Aug;3(3):185-93. PubMed PMID: 18220670.
Haller J, Makara GB, Kruk MR. Catecholaminergic involvement in the control of aggression: hormones, the peripheral sympathetic, and central noradrenergic systems. Neurosci Biobehav Rev. 1998;22(1):85-97. PubMed PMID: 9491941.

Ok... I got it that hypoglycemic condition leads to the Release of Epinephrine and nor epinephrine and activation of beta adrenergic receptors, but how the activation of this signalling pathway leads to aggressive behavior? Is their release of any hormone in this pathway that effects behavior..?? wondering about this, can you explain me this point please..???

@katherinebridges Those hormones activate sympaticus (fight-flight-response) - increased blood pressure, irritation, uneasiness when prolonged. Different people react to it differently (different genomics). Some become very aggressive, some are just silent and calm. Probably, testosterone and male gender have something to do with this. Men need more energy than female every day so they are exhausted faster. Link between hunger and testosterone can be one thing.

@Masi can you give me any reference for the involvement of testosterone hormone in developing aggressive behavior due to hunger..??

@Masi you have asked me to provide the reference for the link between testosterone hormone in developing aggressive behavior due to hunger..?

@katherinebridges I am working on this now. It will take some time because I have to study again some of the genetics and embryology related to this one. I try to find something until Saturday.

@katherinebridges I posted a short roadmap about the thing. I will update it when understand better this case. I did not manage to study my all notes in Embryology. I will update the post when I either remember my previous discussion about this thing in genetics or found my notes about this.

This is a short review about the issue and not complete.
This and the earlier answer are not proofs of the link between the two proceses.
To investigate this better, I think it would be much easier first to narrow the case to

testosterone and energy homeostasis (Embryology; or better formulated research case)
catabolism and anger
anger and aggressive behaviour.

Then, think about specific cases.
Think genes which are associated with aggressive behaviour and violence in catabolism (criminal studies).
Terms

Satiety
Appetite
Hunger

I was not sure in which specific area you are particularly interested.
At this stage, we cannot provide a proof between hunger and aggressive behaviour.
It depends so much on the individual (life style; genomics) what is the end result.
Here follows little general pieces of information:
Some cases

InsR/FoxO1 Signaling Curtails Hypothalamic POMC Neuron Number [1]: it's possible that the hormonal and nutrient milieu contributes to alterations in POMC neuron development.
Early-Life Exposure to Testosterone Programs the Hypothalamic
Melanocortin System [3].
Study about testosterone and basal metabolic rate [2].

Nuclei

hypothalamus lateral nucleus
hypothalamus tuberal medial perifornical nucleus [4]
hypothalamus arcuate nucleus (appetite and energy expenditure - POMC-CART; upregulative NPY AGRP)

Receptor

androgenic (NR3C4) (adipose tissue; more in visceral) (no link)

where I found no receptor existing directly between those two events - appetite and testosterone secretion by comparing the NCBI gene databases between those two processes.
It is much more easier to show the thing first in the embryologic studies and then by using the gene found in bigger studies.
At the moment, more work is needed in these studies in Embryology.
My initial clause is based on some of my notes in Embryology.
There are researches who are trying to show this link between studies in embryology.
The problem is at the moment in the development of hypothalamus and something else.
I will update this post when I remember about the situation better and when finding the right things from my notes.
Sources

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271107/#!po=14.0625
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402517/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060636/
John E. Hall. Guyton and Hall Textbook of Medical Physiology. 12Th edition.


text:
How does boiling water revive cut flowers?
A classic tip to revive wilted cut flowers is to plunge the stem into boiling water for some period of time, and then back into cold water.
What process is occurring that causes the flower to be "revived"?

@jmusser A cursory google search shows that this is method is commonly described.

A google search also shows, that this is done to "remove air locks". Maybe the hot water is supposed to widen the capillaries and thus water flow can be restored at places where they were blocked by air bubbles.

I do not know about "reviving" but the process you just described is called "hardening". I do not know how or why it works, but the idea is that after this process the plant will take up more water than before.

I could not find any scientific papers that have done research into this phenomenon but the general reason given for wilted flowers to being resuscitated is given as the hot water being absorbed faster and I quote

Florists use warm water only for resuscitating wilted flowers, because
  warm water is absorbed quickly. For restoring wilted stems, hot water
  (110 degrees Fahrenheit) is recommended. For woody or badly wilted
  stems, very hot water (180 to 200 degrees) is better. Florists then
  move them into a refrigerator (reference).

The reason for absorbtion faster is given as
luke warm water in a vase arrangement because warm water is “thinner” (has fewer air
bubbles) and moves up the stem faster than cold water (reference) and Warm water molecules move faster than cold water molecules and so can be absorbed by flowers with greater ease (reference).

as a physicist I can confirm there is no such thing. Warm water is not "thinner", the temperature of the water (if in normal human range) is in no way tied to the amount of air bubbles in it. After reviewing the "ramsey" reference I am sorry to say that person has no idea what he is talking about, because in addition he states that warm water has more oxygen in it. Uh, no, tiny temperature changes do not alter chemical compositions, thank you very much! Finally warm water molecules move slightly faster than cold water molecules, which, in any event, has no effect on water uptake by plants.

@mathgenius Thank you for your valuable information.


text:
How does a stonefish get oxygen out of water?
It is said that the stonefish (Synanceia) is able to stay out of the water for up to 24 hours. I wonder how they get oxygen from the air. Could someone explain this?

Interestingly all people seem to write down this number without reference. I found one reference from 1961 (Endean, R. (1961) A study of the distribution, habitat, behaviour, venom apparatus and venom of the stonefish.
Austr. J. Marine Freshwater Res. 12: 177-190.) which I am currently trying to track down. This paper has been cited a number of times in connection with the survival out of water.

Two things to add the the answer from @Chris.
We are used to the idea that fish extract oxygen from water using gills. When such a fish is transferred into air we imagine that it can no longer breathe. However fish do in fact obtain a significant proportion of their oxygen through their skin. Furthermore, as long as the gills remain moist it should be possible to obtain some oxygen by direct diffusion from the air into the layer of water surrounding the gills.
According to Rombough PJ (1998) Partitioning of oxygen uptake between the gills and skin in fish larvae: a novel method for estimating cutaneous oxygen uptake. J Expt. Biol. 201: 1763 - 1769

Adults of water-breathing fish typically obtain 10–20 % of their oxygen across the skin, but values as high as 30 % have been reported (Feder and Burggren, 1985).

The cited paper is: Feder, M.E. and Burggren WW (1985) Cutaneous gas exchange in vertebrates: design, patterns, control and implications. Biol. Rev. 60: 1-45. Table 1 of this paper presents measurements for the contribution of cutaneous respiration for a number of species including, for example, the European plaice (Pleuronectes platessa) which apparently can obtain 27 % of its oxygen through its skin.
There are, of course many fish, which are designated as air-breathing e.g. the European eel (Anguilla vulgaris). Table 2 of Feder & Burggren presents data acomparing the contribution of skin and gills for various air-breathing fish in water and in air. In the eel this goes from (skin/gills) 12%/88% in water to 33%/67% in air at 15 °C.
I don't know if stone-fish are designated as 'air-breathing' but it is clear that as long as they are in a moist environment many fish can obtain significant amounts of oxygen from the surrounding air. @Chris suggests that the fish may "turn down their metabolism" under these circumstances. The very fact that the fish is no longer swimming presumably reduces oxygen requirement considerably.

I have been trying to find an answer to this question, but until now, no one seems to have really analyzed why this is possible. The only hint I found comes from this paper:

A study of the distribution, habitat, behaviour, venom apparatus and
venom of the stonefish.

They state:

At periods of low water, stone-fish are often left partially exposed
  by the retreating tide. At such times they may be surrounded only by a
  small quantity of water which fills the depression in which each lies
  and the main mass of water may be a considerable distance away. They
  can survive long periods (at least 24 hours) out of water providing
  their surroundings are kept moist.

Obviously the fish only needs minimal moisture to get enough oxygen. I would further speculate that the fish turns down its metabolism during this time to minimize the need for oxygen. This paper is widely cited as a source for this survival time, but there seems to be no follow up on it. What is widely analyzed is the toxin of the stonefish.


text:
Effect of testosterone hormone on cell signalling and behaviour?
A steroid, testosterone was injected in female body which led to development of secondary sexual characters but these characters were not developed over night (Response was very slow). What could be possible explanation of this phenomenon

a Steroid hormones produce a slow response because they do not have secondary messenger
Slow response is due to lack of cell membrane receptors and amplification enzymes
Movement of this hormone is very slow in blood
None of the above

I think option 3 is correct because steroid hormones are hydrophobic in nature and cant be transported in the blood without the help of any carrier protein so this may be the reason but I am not sure about this..

Read the title - it is completely valid. Answer to it. Then, lastly read the body. This should be reopened because I think we know too little about testosterone hormone and its effects in cell signalling and embryology.

Steroid hormones produce a slow response because they do not have secondary messenger
It's true that steroids don't have secondary messengers because they don't need them - they can go directly into a cells nucleus and affect transcription there.  This wouldn't slow down the response by much, however.
Slow response is due to lack of cell membrane receptors and amplification enzymes
This is just the inverse of the first option, which again isn't really a cause of slowing down the response.  Steroids are amplified in that they act directly on DNA at the very first step of the synthesis pathways so don't need much amplification.
Movement of this hormone is very slow in blood
 Again I don't think there is much to this option, the difference in speed of distribution of steroid and peptide hormones is likely to be minimal

This leaves us with:
 4. None of the above
I would personally have gone with this answer.  Steroids have a long time of action because they require the new transcription of genes that they activate.  This process takes time and consistent doses are needed to maintain the effect.

It may be important to consider the developmental stage of the "female body" as well. For instance, organizational vs. activational hypothesis--injecting testosterone during a critical period during development (it can be pre-natal, or during puberty) could produce permanent changes in secondary sexual characteristics and sex-specific behaviors; however, injecting testosterone after the organized system has "crystallized" (e.g. receptors are expressed in sex-specific regions, external genitalia is fully developed) may only induce temporary changes that may not be sex-specific.
As for a "female body" to develop secondary sex characteristics with testosterone injections--if these characteristics are "female" secondary sex characteristics (e.g. increased subcutaneous fat deposition in breasts in humans), it is likely that the machinery has already been organized (e.g. more "aromatase" converts testosterone to estrogen, or the location/density of androgen receptors affects sensitivity, or there is less androgen-binding protein to transport circulating testosterone), while if the secondary sex characteristics were "male" (e.g. laryngeal prominence) the testosterone injections happened during a critical development stage and/or were chronically administered (e.g. continuous administration, daily injections...).
Phoenix et al (a review cited above) did a cool experiment that might interest you.


text:
Biology Analogy
In my book are given several paired analogies with me being asked to give reason for them. I could solve all of them except this:

liver = thrifty house-keeper

I mean, I do not understand why the liver is being called so. The functions of liver haven't been taught yet (so this is kind of out-of-course), but still, I thought I should ask it as the functions are not given anywhere in the entire book.

The liver does quite a lot of "housekeeping". It is responsible for a lot of energy metabolism: Gluconeogenesis (the synthesis of glucose), Glycogenolysis (the breakdown of glycogen into glucose), Glycogenesis (the synthesis of glycogen from glucose).
It is important for protein degradation as well as for amino acid synthesis, as well as in the lipid metabolism. This includes synthesis of cholesterols, lipoproteins and fatty acids. The liver produces a number of factors important for coagulation including prothrombin and a number of hormones.
It is very important for the breakdown of Bilirubin and insulin, and it detoxifies the body via the cytochrome P450 system. It is storing some substances as vitamin A, B12, D and K as well as iron and important for their regulation. For more details read the corresponding Wikipedia article on the liver.
So easy speaking does the liver a lot of maintenance in the human body which is important for a lot of different processes.


text:
Accuracy of genome size estimation by flow cytometry
I'm working on a genome project and using an in silico k-mer analysis to estimate the size of our genome based on the available Illumina reads. The k-mer based estimate is consistent across a wide range of k values, but is substantially lower than the previous estimate based on flow cytometry (described in Experimental procedures of this paper). How accurate are estimations of genome size based on flow cytometry?

Could you please edit your question and provide information on how exactly the genome size was determined by flow cytometry?

If I understand the paper correctly, they are using fluorescence of nuclear DNA to estimate the genome size, presumably using a standard curve control, which is very clever and I guess if they do not have any saturation problems in signal detection and if their assumption about fluorescence to DNA size linear relationship holds true (presumably having done a standard curve), and if dense chromosomal areas don't make some kind of odd fluorescent effects then I don't see a major flaw in their work but very interesting and at the same time very simple and potentially high-throughput!

I don't think your results conflict. k-mer analysis is a measure of genome length, and flow cytometry is a raw measurement of DNA quantity. If I understand k-mer analysis correctly, a diploid or polyploid organism will give the genome length under k-mer analysis, and the genome length * the ploidy under flow cytometry. Are your results close to an integer multiple of their results?

@JeremyKemball No, it's not near an integer multiple, so it's not a ploidy issue. The reasoning behind the k-mer analysis is to identify a sequence that occurs once in the genome and count how many times it occurs as a proxy for coverage. Since that unique sequence is unknown, we instead examine k-mer distributions and look for the mode in those distributions.

Perhaps highly repetitive regions in the genome? Those should stand out in your k-mer analysis, though. If the reads have been filtered to remove hard-to-assemble repetitive regions, that might explain the discrepancy.

PI and DAPI can be used to approximate genome size. But you would need standards (known cells) and it is not accurate. I guess you can also estimate genome size by enzymatic digestion and capillary electrophoresis (it is just a guess).


text:
border zone of the infarcted heart
I did myocardial infarction experiments on mice and I am a newbie in this area. I need to isolate RNA and protein from the remote and the border zone. Where should I cut the heart so i can separate the infarct zone, border, and the remote zone? Can anybody help me with this?

I'm no expert but does this help? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1888481/


text:
Odds of Fusion of Chromosome #2
There is strong evidence that chromosome 2 in humans is a fusion of two chimp chromosomes (i.e. common ancestor of chimps and humans) as explained at wikipedia here
The question is what are the odds of a similar event occuring at random in newborns?
I have read conflicting reports, some say these things happen in about 1 out of a 1000 live births, while others placed the odds at somewhere around 1 in 7 billion.

Its not the fusion of two chimp chromosomes. To be more precisely - its the fusion of two chromosomes in common ancestor (chimp & human).

Do those "conflicting reports" write about same field: fusion chromosomes in newborns or rearrangements in cancer, or in between species?

@Pgibas they were estimating the odds of the chromosome 2 fusion happening the way it did in newborns today.

Robertsonian translocations occur with a frequency of approximately 1 in 1100..

Would be good to add the references for the conflicting reports.

@Remi.b couple of articles on line by biologists. not creationists. offhand cant remember the sites.


text:
Do skull bones have pain nerves (nociceptors)?
I recently attended an awake brain surgery  for deep brain stimulation and it seemed to me that only the skin surrounding the drilled hole got local anaesthesia. I know that the brain itself does not have nociceptors, but what about the skull? And how does this compare to other bones in the body? Would you feel a hole being drilled in your skull? Would you feel your leg being chopped off if the surrounding tissue was numbed?

Thanks for your answer Alexandria,
As you didn't seem entirely confident about the innervation in the skull bone, I ended up asking the neurosurgeon, and she indeed only anaesthetises the skin surrounding the drill hole and the subcutaneous tissue as the bone does not have nociceptive innervation in that area.
So you are right for the leg: if chopped off, you would still feel the pain from the nerves in the bone. In the case of deep brain stimulation however, the skull does not have nociceptive innervation in the area where the holes are drilled.
This leaves the question of why there are some exceptions to bone innervation, but that's a problem for another day.

Yes, bones can be innervated. I say "can be" because although I'm not certain that ALL are, I know that most are. "Innervation" is your key word to learning more about the presence or absence of nerves reaching to any body part. Googling "are bones innervated" yields plentiful results, but the short answer is yes.
If you were to chop your leg off with surrounding tissue numbed, you would still feel it for this same reason.

Can you put in some references please

Sure thing: http://www.mananatomy.com/basic-anatomy/nerve-supply-bones and http://www.ncbi.nlm.nih.gov/m/pubmed/12123694/as well as http://www.ncbi.nlm.nih.gov/m/pubmed/19425099/

Sharp acute pain in response to acute physical breach comes mainly from the superficial periosteal innervation, and not much from internal bone innervation.
I am an orthopedic surgery internee. It's in our routine to drill ~3-5mm dia rods (steinmann pins) through bones of lower limb including femur, tibia and calcaneum. We too only inject anesthetic deeply into the skin, but that probably covers the perisoteal innervation too. At the end, when we doo the drilling, despite the great width of these aforementioned bones in comparision with the skull, patient seems calm while we transit through bone, and is only uneasy when the two skin ends are breached.


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regarding genetic disorders related to protein production
I am not completely familiar with biology, but i had a genetics course in college along with practicals. Forgive me if there is something wrong with my question.
Is there a genetic disease which results in partially functioning or complete non functioning of genes resulting in little or no production of protein for eg Muscular dystrophy.
so why can't we supply these protein from outside the way we do in the case of diabetes(insulin)?

There are many protein deficiency issues caused by genetic mutation for eg: Protein C whose deficiency causes abnormal blood clots. This protein is controlled by the PROC gene whose mutation causes Type I Protein C deficiency (reference).
There are treatments of replacing proteins like in the case of Protein C deficiency, protein C concentrates are used (reference). In the case of Alpha-1-antitrypsin (AAT) deficiency, augmentation is done with weekly intravenous infusion of the AAT protein (reference).
So in many cases protein is actually supplied from outside the body and also many protein deficiency conditions can actually be controlled with balanced diets (reference) which unfortunately is not a solution for insulin deficiency.

thanks but what is the problem in case of say muscular dystrophy where patient is almost rendered with no cure or improvement at all?

You can fairly easily substitute peptides (short proteins) from the outside of the body, but you have to supply them by injection. They don't survive the low pH of the stomach unless you encapsulate them into an acid-resistant matrix. Short peptides are often very local and short acting, present only during specific times of the embryonic development (for example, morphokines). However, assuming that you have a peptide hormone like insulin, you can administer it systemically and it will work. There is however over 350 peptides/short protein that are extracellular and many of them are locally restricted. So, you should not just inject them. The problem with larger proteins is, that they do not cross the cell barrier like these small peptides (which have a receptor for crossing/uptake). Many of the broken genes carriers (patients) of genetic diseases have in their genome, are coding for large intracellular proteins, often even tissue-specifically expressed. You cannot get them easily to the right destination, nor can you get them easily into the cell. You have to use a virus that encodes them and infects the cell. Read some Cell / Molecular Biology textbook if you want to learn more details.


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Assembling DNA fragments with ~10kb overlap in vitro
Let's say I have two fragments of bacterial DNA (~50kb in length each) that overlap on the ends by roughly ~10kb; the overlap sequences are unknown. I would like to assemble these into longer fragments (in vitro) in some way, but the methods I've found so far rely on 24-40bp known overlaps (e.g., the isothermal assembly process in DG Gibson et al., Nature Communications 2009).
Anyone have any idea? I'm kind of new to this molecular biology stuff, so if this is an open problem, I apologize. I'm mainly just making sure I'm not overlooking something obvious. For all I know, there could be a standard protocol for this. Thanks in advance!

As far as I can see, typical overlaps are between 20 and 100 bases. These extreme long overlaps may generate some "funny" results which may result in a DNA that you don't want. What do you know about the bacterial DNA you are working with? Can you sequence the ends to find out how big the overlap is?

Thanks for your comment! My problem is essentially that I need fairly long DNA fragments from cells, but the extraction process tends to break them apart more than I would like. I'm just wondering if there exists some method to re-assemble them after extraction without sequencing. The overlap may be anywhere from nothing to several kilo-bases.

Can you use a different extraction method? Look into methods to prepare BACs from bacteria, they are several hundret kB in size and need to be prepared intact in order to use it further.

Good point. I currently get the DNA already-fragmented from a collaborator and could request a different method for future purposes. I thought if there were some way to easily assemble the ones I already have then it would be worth a shot, and if there wasn't a method already, then it would at least be interesting to think about :)


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If two definitive ovums are fused will they form an organism?
Pretend that somehow in a laboratory two definitive ovums (finished 2nd miotic divisions) are
are fused together. Will they form a new species?

Are you thinking about fusing ovums from different species?

no the same species (humans)

No, it is not possible. The reason is the genetic imprinting, which takes place on the parental DNA in the egg and the sperm. Here small modifications are added to the DNA which marks them as silenced. So some genes are expressed from the mother (while the fathers copy is not expressed) and vice versa.
There are even genetic diseases which are caused by imprinting. One example is the loss of a gene region on chromosome 15. Depending in which copy its lost, either the Prader-Willi Syndrome or the Angelman Syndrome occur. PWS is inherited via the father, Angelman via the mother. Another interesting article on imprinting can be found here.
If you combine two eggs, some genes, which are not imprinted in the father, will not be expressed in the developing embryo which will finally lead to death of it. However, researcher deleted the maternal imprinting in mice and mimicked the from the father and made off-springs from two mothers possible. This is something which is ethically very problematic in humans. The article can be found here:

Birth of parthenogenetic mice that can develop to adulthood


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Master Catalog of all Fossils / Literal Fossil Record?
Is there a website or other resource that catalogs all fossils ever found? Basically, is there a literal "Fossil Record"?
Where do scientists gather their results from excavations? Are they just scattered in various peer-reviewed papers in science journals?
I'm imagining something like manuscripts and master texts. You have some researchers who analyze manuscripts to produce the text of that manuscript in electronic form, for instance. Then, other researchers take these various readings and assemble a master text, taking into account the variations and attempting to recover the original work.
By analogy, this would be like when a paleontologist at a dig site submits a paper about his/her findings to a science journal. Is there another group of scientists who look at all of these papers and compile a "master text" of the fossil record?

No main website because it is expensive to make one and involves risks. Those found in internet are mostly useless for research purposes. Those fossil collections are located mostly in their owners. It is a research advantage to have such collections. Similar situation is with iPS cell collections and embryo samples. Iran has the biggest iPS collection, while Japan biggest embryo collection. It depends how you define fossils and in what context to say where are the most significant collections.

Honestly, I think what you would do is contact a institution that you know has an excellent collection of what you want, and ask them for their catalog of their samples.

what kind of fossil records are you looking for? I don't think all of them would be segregated in the same database but there could be separate lists for dinosaurs maybe.

@TheLastWord I thought there would be some kind of master catalog, per species listing the find and the estimated date attached to it... Like a Messier catalog for fossils. I'm just surprised it doesn't seem to exist.

@John Can you go through http://fossilworks.org/ and http://paleobiodb.org/ . Let me know if they suffice. Paleobiodb has a map based view which I found quite interesting.

@TheLastWord Wow... this is really cool. Submit this as an answer and I'll accept it for the bounty.

fossilworks.org and paleobiodb.org are reasonably good databases for fossil records. Paleobiodb has even got a map based view which is really convenient. Thank you.


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What does the term 'modified residue position' in phosphorylation mean?
Does it mean the position of the amino acid in the protein sequence, or something else?
For example, I came across the phrase "S 368 phosphoryation" where S is the modified residue and 368 is the modified residue position. What does it all mean?

You are correct, the 368 stands for the position of the amino acid in the protein's sequence - this particular serine is the 368th residue in the protein counting from the amino-terminal end.


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Efficiency of plasmid DNA isolation from frozen E. coli cell cultures
Has anyone isolated plasmid DNA from frozen (at -20degrees) E. coli cell cultures (not pellets)? Has that worked and if so, with what yields? What would be the quality of the isolated plasmid DNA if run on a gel? Would most of it be degraded or intact?

I have done that and it works without any problems. We harvested the cultures at the optimal timepoint (density) and then froze them to do maxipreps later on. Therefore we simply thawed the culture, made sure it didn't got too warm (meaning we worked on ice) and then simply followed the maxiprep protocol. No problems with yield or quality of the plasmide.
What I will do next time is to spin down the culture and take it up in max. 50 ml of medium before freezing. This way freezing will be faster as well as thawing. I have also done minipreps from stock cultures (glycerol stocks of plasmids in E.coli) which accidentally stayed out of the freezer for two days. Here the yields where not so great (but the density of the culture was also much lower), but the quality after standard miniprep was good and the plasmids worked both for subsequent cloning as well as for retransformation to make new stocks.

Thanks Chris. I tried it with 25ml cultures and I got great yields! I did not run them on a gel to check the quality of the DNA, but the sequencing results looked good!

Great to hear. In my experience plasmids are incredible stable given how complex this macromolecule is.


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What is the name of this type of inflorescence?
I was having a look at a rhizophora plant (from the mangrove family), and I got curious about its inflorescence. I can't make out what kind of inflorescence it is.
Here is a photo of the inflorescence.

Does anyone know which kind of inflorescence it is?

That is a woody compound umbel. A compound umbel is one with more than one set of pedicels between the peduncle and the flower. Hydrangeas also exhibit this type of inflorescence, although not necessarily woody.
In the picture below, I've marked all the levels where the pedicels branch.

End of peduncle, beginning of primary pedicels
Beginning of secondary pedicels
Beginning of tertiary pedicels
Beginning of quaternary pedicels, which bear flowers


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does order of genes in a chromosome matter?
does the order of genes within a chromosome matter? or is the main thing that the genes are there.
so for example, our DNA is very similar to that of apes not only by the genes themselves but also by the arrangement of those genes in the chromosomes.
is the order of this arrangement significant? Or if it were shuffled around, then the functional impact would be more or less the same?
Another example, an international study in the mouse genome has revealed that virtually all mouse genes have direct counterparts in humans, i.e. humans and mice contain virtually the same set of genes. is the difference between humans and mice due primarily to the different order of the genes or to the slight differences in the genes themselves?
This question was raised from a claim here which seems to imply it does not matter.

The chances are infinitesimal that human chr 2 were to resemble those
  of other primates at random. This is what you say in science when you
  mean 'impossible'. One simply doesn't see a segment of DNA the size of
  Chr 2A and 2B being so similar for such a length when we look at rats,
  dogs, worms or any more distantly related living thing.

is the difference between humans and mice due primarily to the
  different order of the genes or to the slight differences in the genes
  themselves?

The latter.

This question was raised from a claim here which seems to imply it
  does not matter.

You are talking about two different things.  Gene expression is often controlled by nearby DNA sequences that don't code for protein.  Moving a gene away from the DNA that controls it can change its expression a lot, and have huge consequences on the organism.  But in many cases, you can move a whole gene, including its controlling sequences, to another place, and nothing much will happen.
People were bringing up synteny as evidence of evolutionary relatedness, not as the cause for all primates looking similar.

Ye, the order matters. This can be seen in chromosomal translocations which can cause cancer.
A example for that would be the translocation of IRF4 which happens in a subtype of multiple myeloma. The translocation is permanently activating the transcription factor. See here for details:

Translocations activating IRF4 identify a subtype of germinal
center-derived B-cell lymphoma affecting predominantly children and
young adults.

The main reason for this is the regulation of the genes - when the order is changed, the regulatory elements which are important for regulating the expression are missing. A lot of these regulatory elements are located many kB away from the gene and are still important for its activation or silencing.
This can look like the image below (image from here):

Regarding the mouse question: On which chromosome a gene is located is not really important if you compare different species. The gene I worked on for a while is functionally equivalent between mouse and human (the human version works perfectly in mouse), but they are located on different chromosomes. It again comes down to different regulation and in some cases also a different amino acid sequence. Also mice (as other animals as well) have quite a number of genes which are unique for them and which make a difference between the two species. There are a few interesting papers on that topic:

Lineage-Specific Biology Revealed by a Finished Genome Assembly of
the Mouse
Comparison of the genomes of human and mouse lays the foundation of
genome zoology

That's kind of cheating though. Most cancer-causing translocations are either because their insertion causes frameshifts that disable other genes or because, as in your example, regulatory elements are left out. The modern definition of a gene tends to include its regulatory elements so here, you're not changing the order of the genes but breaking them up which is a whole different thing. I can't think of any cases where the order of the genes itself is important (in eukaryotes anyway, barring operons and the like) and would be quite interested to know of any.

authors: Юрий Евсюков


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What is the difference between drought resistant non-succulent plants and plants that cannot be allowed to dry out?
What features make one plant able to withstand dry spells better than another with relatively similar structure? For instance, one of my Rudbeckias is wilting from drought at the moment, and an Oenothera next to it is not yet showing signs of dryness.
Or like jewelweed (Impatiens capensis), which wilts even while the soil is damp, in full sun, and ragweed (Ambrosia artemisiifolia), which will grow in very dry locations without being phased.
Is it caused by a faster transpiration rate in some plants than in others?

The difference may be related to how the plants fix carbon. While all plants convert CO₂ and H₂O to glucose and oxygen, there are at least three pathways that are used to do it. The C3 pathway is older and less efficient than the CAM and C4 pathways. Many drought tolerant plants use the CAM or C4 pathways because less water is needed. The C4 pathway is better than C3 in drier climates, hotter climates, and when CO₂ or nitrogen are limited. The hard part about this answer is that I'm not a botanist. Wikipedia lists some plants that use C4, CAM, and C3, but there is no comprehensive list, so I can't match up all the plants you mentioned in your question. In general, a higher percentage of monocots, especially grasses, use C4, but a wider diversity of dicots use C4. But you still can't draw conclusions about families of plants, because while corn and sorghum use C4, rice and barley use C3. Ragweed, a plant you say grows well in dry conditions, is a member of Asteraceae, which includes many plants that use C4. However, rudbeckias are also members of Asteraceae, but don't do as well in dry conditions. The C4 pathway has appeared and disappeared in several different plants, making any general claim hard to make. Here are some links that might help:

http://www.en.wikipedia.org/wiki/C4_carbon_fixation
http://www.en.wikipedia.org/wiki/C3_carbon_fixation
http://www.en.wikipedia.org/wiki/Crassulacean_acid_metabolism
http://www.brown.edu/Research/Edwards_Lab/reprints/sage_etal_2011jexb.pdf

If you know more about plants than me, that last link might be helpful, it's about the evolution of C4 pathway in plants and includes lists, but uses the formal species names I just don't recognize.

Plants in drier conditions usually have reduced surface area, thick waxy cuticle covering the epidermis, reduced number of stomata, and water storage tissues that presides in its roots and leaves.
This means that even if the plants are similar, one of them might express more of one of the features shown above.

But ragweed (one of my examples) has a large, thin leaf, barely any storage area, and no waxy cuticle, and withstands quite a bit of drought. Jewelweed, although it has a much reduced leaf area, and thick, watery stems, needs constant moisture.

i think this is a good answer inside, which is that there are lots of adaptations that cause drought tolerance.  i would avoid citing any particular adaptations as universal, though many are common.


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How can I determine the sex of a tree seedling?
I would like to plant some home grown female mulberry trees in a circle, with a male plant in the center for pollination. How do I determine the gender of a tree seedling? I know it's possible, because I've seen mulberry trees labeled as 'male or 'female' at nurseries. Do I need special equipment?
I've seen the related question: Can you tell the sex of a white willow when it's not flowering?

There is absolutely no way to tell to be honest because mulberry trees have the capability of changing sex (reference). From a paper titled "Diversification of mulberry (Morus indica var. S36), a vegetatively propagated tree species", I quote

The sex expression of plants appears to be a function of hormonal
  control; there seems to be evidence that dioeciously plants (male and
  female reproductive organs on separate plants) are potentially
  bisexual and that a delicate internal hormonal balance results in one
  sex "over-riding" the other. A traumatic incident might, therefore,
  act by temporarily upsetting this balance, which is later restored in
  a way that leads to the opposite sexual character being manifested.
  Another pointer in this direction is the fact that a variety of
  artificially applied chemical substances has been shown to affect the
  sexual expression of a significant number of different plants. It is
  also reported that some chemicals known as the steroid hormones might
  be a major key to the sex expression lock. Thus, it is
  possible that to "create" a new sex in a plant by either a physical
  shock or a controlled chemical process

They could also have male and female flowers (monoecious) on one plant with most of them being self pollinating (references).
So, in effect, nurseries that are advertising these trees by sex are ignorant or quite plainly taking people for a ride. I would suggest that you plant your seeds and don't worry about it too much since they have the ability to self pollinate. If by bad luck, you find them all male/female or are not pollinating to your liking, go for a tree sex change after consulting an expert on the topic. Here is a basic guide to identifying between male and female trees/branches (reference)

White mulberry male flowers (reference)

red mulberry female flowers (reference)

Funny... I ran across both of those photos while researching.

@jmusser well u know I did my research as well then..


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Do species which have a closer common ancestor to humans tend to be more intelligent?

Q: Do species which have a closer common ancestor to humans tend to be more intelligent?

Our closest living relative, the chimpanzee, seems to be regarded as intelligent:

Chimpanzees make tools and use them to acquire foods and for social displays; they have sophisticated hunting strategies requiring cooperation, influence and rank; they are status conscious, manipulative and capable of deception; they can learn to use symbols and understand aspects of human language including some relational syntax, concepts of number and numerical sequence; and they are capable of spontaneous planning for a future state or event.

Does this hold in general?  And, if so, how strong is the correlation?

humans being more intelligent than other animals is a hotly debated topic :-D http://www.huffingtonpost.com/2013/12/11/human-intelligence-animals_n_4400395.html

I agree with point 1 in Remi.b's answer; what do you mean by intelligence?
Generally though, no it doesn't. Crows have tools, octopuses and goldfish solve puzzles, dogs respond to human voices, whales have language. There are too many exceptions to say that 'generally' the closer to humans the more "intelligent" the species.
And who said we're top of the "clever test"? Could you do this? http://www.independent.co.uk/news/science/video-chimpanzees-have-faster-working-memory-than-humans-according-to-study-8496034.html

Probably not. Ravens can solve multistep problems, showing some level of premeditation. Border Collies have been shown to associate over 1000 human words with specific objects. Dogs are one of the only animals able to interpret pointing by humans, and their brain responses in fMRIs to photographs of strangers to owners (Loved ones), shows pretty much the same patterns as humans exhibit. Pigs are believed to be one of the only animals other than humans that have self recognition when looking at their reflections in a mirror. Dolphins and whales probable have language. Gorillas do sign language.

Several issues here that make your question unanswerable:

Intelligence is not defined. How would you define it?
What kind of relationship are you exactly looking for? Comparing average intelligence between groups or trying to fit a regression with intelligence on the Y-axis and relatedness to human on the X-axis?
The general issue hidden behind methods of species comparison is "How do you define a species?"

If you want to compare average intelligence between groups, meaning that you want to compare average intelligence of a group of closely related species of human to the average intelligence of all animals? Then the answer to your question will probably be "Yes" as primates seem in average to be more intelligent than the average animal and mammals tend to be in average more intelligent than the average animal. I'd expect too that vertebrates are probably on average more intelligent than the average animal. Let's not forget that some animals have no brain (e.g. Sponge).
But now if you want to fit a regression between intelligence and relatedness to human for all animals, you will probably have some trend (a regression with a significant slope (positive correlation)), but you will have many group of points that will not fit on your line. Many birds for example may be considered as much more intelligent than humans depending on your definition. Many invertebrates such as octopuses are very intelligent, too. If you allow for a broad definition of intelligence, then you may also consider the intelligence of social insects which may be surprising. Some aquatic mammals are very intelligent although other, more seemingly stupid mammals, are closer to humans than aquatic mammals.
In short, keep in mind that intelligence is not easy to define, and depending on the definition, the answer will be different. Typically, if you use a very human-like definition of intelligence, you will probably find that intelligent species are more closely related to human. There is a correlation between intelligence and phylogeny (=tree of life), therefore yes, closely related species to humans may have some tendency to be fairly intelligent, but there are many other clades (groups of species on a phylogeny) that show some impressive intelligence, especially in insects, in mollusca, in  birds, the carnivora and the cetacea.


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Does myopia tend to decrease the risk for later hyperopia?
It seems like being nearsighted for much of your life due to elongated eyes would make it easier in general to focus on near objects rather than far since the lens would not have to change much. Since in old age we lose the ability to focus close images due to a hardening of the lens over time, wouldn't having eyes shaped more for near images be helpful in maintaining the ability to see close up, and thus nearsighted, or myopic people, would be less likely to develop farsightedness, or hyperopia, with age? It seems then that nearsightedness is more of an adaptation that occurs at a young age, so that these people can work up close for longer periods of time both in the the short term(studying) and long term(age). I'd love to hear if any research has been done on this subject, and any other input you have.

It is generally understood that we tend to become hyperopic as we age (reference). As to whether this aids in decreasing myopia is stated as marginal in papers. One paper titled "Is there a hyperopic shift in myopic eyes during the presbyopic years?" states that

it was found that almost all hyperopic and emmetropic eyes showed an
  age-related hyperopic shift; but only a small proportion of myopic
  eyes shifted toward hyperopia, with others remaining relatively stable
  and still others increasing in myopia.

In a second study titled "Age-Related Decreases in the Prevalence of Myopia: Longitudinal Change or Cohort Effect?", it was found that there is a decline in the prevalence of myopia in older adults.
Some people in personal experiences have stated that their myopia has decreased (reference) while others found themselves wearing bifocals (reference). In closing, I would say that this is something that your Ophthalmologist may be able to predict better but it is not a given that your myopia would decrease. It may or may not be so with many factors like your eye shape coming into play.

Let me see whether I can explain this quickly. The eye size is tightly regulated genetically. Babies don't have big eyes, they have exactly the same sized eyes like adults, only their head is smaller. Myopic eyes are larger than normal and hyperopic eyes are smaller than normal, even though the difference is only 1 to a few millimeters. When you focus to the far point, the light focusses to the nearest point possible in the back of your eye. When you come closer to an object, the focus point inside the eye moves further out. Thus, the farsighted person with the small eye can only see when the object is away. Moving closer moves the focal point inside the eye to behind the retina. The opposite is true for myopic people with too large eyes. When a person gets old, the lens gets stiff and cannot adjust the focal point inside the eye to the distance of the retina. Thus, the lens remains stiff in the most relaxed state (extended), or - in other words - at the most distant focal point the person had when it was young. A normal-sighted person has his old-age focal point at the horizon and since his lens is stiff, can only see sharp from the horizon to a few meters in front of him (depending on the intensity and wavelength of the light - blue light better than red). A short-sighted person is of disadvantage when old, since his far point remains to be at short distance. He gains a little sharpness over the normal sighted person in the short distance, but loses it in the distance like he always did. You can calculate this nicely, actually. All physics.


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cerebral edema and blood pressure, pulse
What happens to blood pressure in cerebral edema; does systolic and diastolic rise equally? So the pulse actually slows down? Can't find anything about that, please help

Can you rephrase your question please? Is your question on whether blood pressure decreases when you have cerebral edema?

In cerebral oedema the observations (blood pressure, pulse, respiratory rate etc.) can be all over the place. They can depend on the cause e.g. infectious more likely to have raised pulse (tachycardia) with lower blood pressure (shock) but with the anxiety there might be raised blood pressure. Then with the vomiting, a symptom of cerebral oedema, this could lead to dehydration which leads to lower blood pressure or movement of fluid from the blood to the brain because it is oedematous could also drop the blood pressure. With the cerebral oedema affecting different structures, particularly the brain stem in coning (brain swells, pushes brain out through the big hole at the bottom where all the nerves come out particularly affecting respiratory rate) the respiratory rate could be low. It could also be high due to structures getting less oxygen causing the body to push the sympathetic nervous system to increase heart rate and respiratory rate.
In conclusion, things can be completely over the place but usually blood pressure is low and there's reflex tachycardia for the reasons explained above. For these reasons, to diagnose cerebral oedema we usually use the characteristic symptoms of nausea, vomiting, faintness and other features in a patient we know is at risk because of the signs and symptoms of the original disease or cause of the cerebral oedema e.g. the cancer, trauma or infection.


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How did the Chromosome #2 Fusion propagate?
There is strong evidence that chromosome 2 in humans is a fusion of two chromosomes of a common ancestor of chimps and humans as explained at wikipedia here
Was it necessary for the common ancestor with fused chromosome 2 to mate with another creature whose 2 chromosomes fused in a similar manner?
If yes, what would their offspring look like? would they also need to mate within themselves or could they mate with the chimp population?
if possible, also, how in the world could a genetic disadvantage take over the population? doesn't this contradict natural selection?

Was it necessary for the common ancestor with fused chromosome 2 to
  mate with another creature whose 2 chromosomes fused in a similar
  manner?

Of course not.  People with balanced translocations have kids with people with the wild-type chromosome arrangement all the time.  Such people have some fertility problems, due to problematic meiosis leading to more inviable gametes, but they can still reproduce.
Someone already mentioned Robertsonian translocations to you in your previous question.  Didn't you look it up?

would they also need to mate within themselves or could they mate with
  the chimp population?

What chimp population?  There were no modern chimps when the fusion happened.
Look, you could ask a million questions here, and still learn nothing.  This board is helpful for people who have a good, accurate framework of the facts of biology, but who want specific holes in their knowledge base filled.  I don't think that's you.  I think you think you know the right answers to your questions, based not on science, but on other things, have imbibed or made up a whole slew of very wrong stuff about biology, and are asking questions here expecting people to confirm your wrong beliefs, trying to trick people in to confessing that mainstream biology is wrong, and you are right.
Picking at one bit or another of evolutionary biology is not going to help you.  You need to start by assuming that a lot of what you think you know about the scientific facts is wrong, and learn the real stuff.  It is not at all easy to get wrong information out of our brains, but until you do, this exercise isn't going to educate you much at all.

you wrote "What chimp population? There were no modern chimps when the fusion happened.". correct - my mistake. I  meant "common ancestor". frankly, I am surprised by your reaction. in all honesty, if I thought I knew the answer to my question, I wouldn't be asking it here. I fully realize there is much I don't know and that is why I am asking, hoping to get an honest answer.


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How long does it take for a cell to synthesize an enzyme?
Where can I find data regarding the times distinct cells take to synthesize distinct enzymes?

on an average it takes ~10 hours to reach steady state.. this is called the response time- not synthesis time.

In human cells it takes about 20 s to make a 20,000 dalton enzyme.
Assuming that the cells concerned are already making mRNA for the enzyme, there will be two main factors:
(1) The time taken to synthesize the polypeptide
(2) Any time taken to fold the protein
(If the enzyme is secreted from the cell there will also be the time taken for the protein to traverse the secretory pathway - perhaps you want to include this time - if so it could be 10's of minutes.)
Here I will focus on (1). What is the rate of polypeptide elongation?
For bacteria:

Young & Bremer (1976) Polypeptide-chain-elongation rate in Escherichia coli B/r as a function of growth rate Biochem. J. 160: 185-194

They quote values of:
17 s-1 for fast-growing cells
and 12 s-1 for slower-growing cells.
For yeast:

Bonven & Gullov (1979) Peptide chain elongation rate and ribosomal activity in Saccharomyces cerevisiae as a function of the growth rate. Mol. Gen. Genet. 170: 225-230

minimal glucose 9.3 s-1
minimal acetate 5.5 s-1
In human cells:

Ramabhadran & Thach (1981) Translational elongation rate changes in encephalomyocarditis virus-infected and interferon-treated cells. J. Virol. 39: 573-583

They measure a control value of 9.4 s-1 and quote (with citations) values of 9-10 s-1 in reticulocytes and CHO cells.
Let's use 9 s-1, and assume 110 daltons per amino acid
Then e.g. a 20.000 dalton enzyme (= 182 amino acids) requires 20 seconds.


text:
What is the outcome of a human population starting with only 2 individuals?

Starting with a human population N = 2, is there any way the genetic variability seen today could have come about? I don't know that much about meiosis, but isn't there a very limited number of alleles that could be passed on by the parents? Without a population to start with, wouldn't the lineage eventually turn into clones of each other like the cheetahs are now?
Are there any known mechanisms besides mutation that replenish the variability in alleles?

Once again a first-time poster with a "Please help me respond to a creationist" question.

I am not sure we have to be so categorical with creationist question. It is indeed good to close creationist question when the answer has nothing to do with biology but with the philosophy of knowledge or philosophy of logic. This question clearly concerned evolutionary biology (except the first question that had to do with the definition of information).

I agree that creationist motivated questions are a bit too common on this site and often ask for very long answers mixing philosophy and biology. In the meantime research level questions are very uncommon and we ave to accept more introductory questions. Opinions still vary in the Meta site

@Remi.b: Introductory questions are fine I think. But the low-rep creationist questions are IMO not worth the trouble, notwithstanding your good answers. The questions are not motivated by curiosity but by a desire to convert, which in context strikes me as inappropriate for this or any science forum.

@daniel I'm referencing a past discussion that I came across. I never intended to debate anyone (including the creationist in question). If I had left out the reference, you would probably think I was a creationist troll, when in reality I simply wanted to know the biological reasons why the argument was nonsense.

@scubadude22: I don't doubt this and you are probably not the only one. But I think the answers to very general evolution questions are available elsewhere and so on balance the site should avoid them. As Remi.b notes, not everyone agrees with me.

Indeed natural selection decrease variability and therefore decrease information and mutation recreate this information. You can think of a bunch of pens of different colors. If you select
for the red pens you will decrease the variability in pen colors as the other colors will slowly disappear. If you allow for mutation to occur you will recreate blue and black and purple and yellow pens to occur again in your population of pens.
Is it an accurate statement that less variability means less total information?
Yes, less variability means less information. Information is a concept that increases as predictability decreases. If no variability exist, you can predict at 100% what allele a given individual is carrying. You may want to have a look to shannon's theory of information here on Khan academy. Note: this has not much to do with biology but it has to the mathematical definition has to do with mathematics, probability and computer science.
Are there any known mechanisms besides mutation that replenish the variability in alleles?
No, there is nothing else than mutations that creates new alleles. "Mutation" means any kind of structural change of DNA. So by definition any change in the DNA is due to mutations, therefore only mutations creates new alleles. Note: that some people may use the word mutation in a more narrow sense including some kind of DNA change such as indels but excluding chromosome rearrangement for example. I used here the word mutation in the broad sense.
Segregation and Recombination
Two other concepts may interest you though: Segregation (See Mendelian inheritance) and recombination(also called crossing over).
For example if 2 individuals $AB$ (Allele $A$ on one chromosome and allele $B$ on the other chromosome) reproduce they can create the individuals $AA$, $AB$ or $BB$ thanks to segregation.
Two Genes set on chromosomes and if two genes are on the same chromosome, one might think that these two genes cannot segregate independently one from the other, they are linked! For example imagine an individual has the alleles $A_1$ and $B_1$ on two loci of one chromsome and alleles $A_2$ and $B_2$ on the two same loci but of the homologous chromosome. If this individual transmit the allele $A_2$ it must necessarily transmit the allele $B_2$ and can't transmit $B_1$ if recombination does not occur. But recombination does occur and allows for partially independent segregation of these two genes.
You will find more information about these two concepts on wikipedia. I don't want to go too much into details but in short these processes can in some conditions increase the phenotypic variance but in any case these phenomenon do not create new alleles. New alleles are created by mutations only.
Can 2 individuals carry as much genetic information than today's world population?
No! As a very simple argument, two individuals can only have 4 different alleles. But we know several loci (sing: locus, position on a chromosome) where there exist more than 4 different alleles. Therefore, mutations must have happened at some time.
And only to enjoy some further arguments: if these two individuals had together 4 alleles at all loci, it would be extraordinary unlikely that their variation would have remained in today's population. Let's imagine two heterozygote (=who has two different alleles on their two chromosomes for a given locus) individuals are $AB$ and $CD$ that have two offsprings. The probability that their 4 alleles are present in the two offsprings is $1/4$. I don't when Adam and Eve were supposed to exist but it very sound like their variability would have not been maintained through times. This random process which diminish variability is called genetic drift. To be a bit more accurate, in a population that do not change in size, the expected loss of alleles due to genetic drift at each generation $1/2N$, where $N$ is the population size. So the bigger is the population size, the lower is the loss of alleles due to genetic drift. In the above example $N=2$ and therefore the expected loss is $1/4$.
I don't know that much about meiosis, but isn't there a very limited number of alleles that could be passed on by the parents?
Yes, as said above, one individual can only have two alleles at a given loci and can therefore not transmit more than two different alleles.
Without a population to start with, wouldn't the lineage eventually turn into clones of each other[..]?
Yes, because in absence of mutations (and in absence of different special types of selection such as overdominance) the variability is slowly lost due to the randomness of segregation. This process is called genetic drift.

I removed the unrelated part about information theory from my original question. Thanks

authors: Улжан Кошкарова


text:
Will a vasectomy prevent genetic engineering of a child?
Making the assumption:

Within 10 years, an adult will be able to genetically engineer (modify, enhance, clean, etc.) a child from their own DNA (and the DNA of a non-related partner).

then would getting a vasectomy today preclude this?

From the wording of your question the 'genetic engineering' that you are envisaging will involve sperm. So the question is really, does vasectomy affect sperm production?
The answer is that it does, but it doesn't abolish it. For example:

McVicar et al. (2005) Effects of vasectomy on spermatogenesis and fertility outcome after testicular sperm extraction combined with ICSI. Human Reproduction 20: 2795-2800

These authors found that sperm yield fell to about 35% > 5 years post-vasectomy.

Thanks, but I didn't mean to imply that sperm or an egg need to be involved, just DNA.

DNA from which cells?


text:
Stem cell that can pass through blood vessel
I know that blood cells can pass through the smallest of capillaries, but I was wondering is it possible for stem cells to pass through the smallest of capillaries?
In other words, is it possible for a type of stem cell therapy where stem cells are injected into the vein in the arm for example and the stem cell would pass through into the tissue through a type of targeted therapy involving ultrasound or magnetic field.
Thank you very much ,
everyone

What should ultrasound or magnetic fields help here?

yes they can.. unless of course if the stem cell is not very huge..

I am still wondering do the stem cells just simply diffuse through the walls of the capillaries?

I am thinking of some type of encapsulated stem cells where ultrasound, heat or magnetic fields from the MRI would break up the encapsulation releasing the stem cell at the targeted area. Is that plausible?

Yes, stem cells can pass through blood vessels and capillaries (as @WYSIWYG points, these cells should be small enough to fit inside that capillary). The interesting thing is that they posses multiple mechanisms of transmigration. They are attracted by TNF-alpha activated endothelial cells [1] and can pass through by [1]:

leukocyte-like diapedesis
paracellular migration between endothelial cells
transcellular, directly through individual endothelial cells

I am thinking of some type of encapsulated stem cells where ultrasound, heat or magnetic fields from the MRI would break up the encapsulation releasing the stem cell at the targeted area.

Note: I don't know if the following is plausible. It is just something I thought of and I consider it to be more effective than what you suggested.
Then what is the purpose of using stem cells that are capable of chemotactic movements and can go by themselves in targeted areas? The encapsulation you propose could be used to fit inside the cell a drug-containing capsule that would break upon external electromagnetic, ultrasonic (etc.) stimulation. This means that the capsule would also contain a substance capable of inducing cytoplasmic membrane lysis, so the drug could reach the interstitial space. Or the cell could be genetically engineered to secrete that drug, when available in cytoplasm, through exocytosis.
But why not get rid of that capsule? A cell could contain (for example) a cytostatic drug in its cytoplasm and also be fitted with membrane receptors for a specific tumoral marker. When it reaches the tumor, receptor stimulation should trigger exocytosis of drug.

References:

Teo GS, Ankrum JA, Martinelli R, Boetto SE, Simms K, Sciuto TE, Dvorak AM, Karp JM, Carman CV. Mesenchymal stem cells transmigrate between and directly through tumor necrosis factor-α-activated endothelial cells via both leukocyte-like and novel mechanisms. Stem Cells. 2012 Nov;30(11):2472-86. doi: 10.1002/stem.1198. PubMed PMID: 22887987.

A couple of points: there are many kinds of stem cells (hematopoietic, gut epithelium etc etc) and its likely their respective ability to 'home' to a target tissue varies.   Entry into a target tissue occurs when adhesion receptors on the circulating cell bind to ligands on the activated endothelium of the vessel. Another approach is to transduce the cells with an enzyme that acts on a prodrug per this type of approach


text:
Phosphorylation alters structure: Specific Example?
Why does phosphorylation activate an enzyme?
A common answer to this question is that the introduced phosphate group "alters the structure" of the enzyme.
Can somebody point out a specific example of such an alteration? I.e. like a "before/after" illustration?
Or is the whole mechanism of activation still largely uncharacterized?

check the conformational change in $G \alpha$ subunit of GPCR

@WYSIWYG has answered the question neatly. Many mechanisms of activation are mostly uncharacterized. It's easy to see why: You need to do X-ray crystallography or extremely clever FRET experiments to see exactly how the structure changes shape. X-ray crystallography is really hard for proteins, especially big, asymmetric enzymes that bind things and don't like to form crystals. So that's why we don't have data on lots more enzymes.

I have no problem believing that's it's challenging to get the structures. But I am surprised that there is only so little data- many times I find the statement that xyz-pathway is among the most thoroughly characterized cell biology aspects. So I would have thought getting detailed mechanistic insight would have been among the highest priorities.


text:
Classify chemotherapy drugs?
I'm studying a TCGA dataset trying to find correlations between gene expression and clinical data which might shed light on some pathways. One column of the clinical data provides a list of chemotherapy drugs the patient received and I'm pretty sure there's a wealth of possibility in this column but I don't know anything about how chemotherapy drugs work or what kinds of things it makes sense to classify about them.
I'm making a spread sheet that will have the following columns:
Drug_Name
Number_of_Patients_Received
Mechanism
Associated_Drugs

But I don't know what else is important to know about these drugs. What would you think is important to know to help understand how these drugs might have played an interactive role with the pathways. Also, if you have any recommendations of online resources, I'll appreciate you mentioning them with a short explanation of what I might find there.
But my primary question is else should I look up about these drugs to help me understand their role/impact.

There's this database of genetic/drug interactions, which I think is pretty much exactly what you're looking for.
Probably your best approach is to classify your drugs into a couple different categories of action. Some drugs will have to be in several categories at once(I'm lookin at you anthracyclines) Dose-dependent mutagens(cisplatin), growth-dependent mutagens(fluorouracil), topoisomerase inhibitors, tyrosine kinase inhibitors, microtubule inhibitors, retinoid signaling, immune adjuvants, and then 'misc'.
Alkylating agents and platinum-containing drugs like cisplatin directly damage DNA, while there are other drugs(methotrexate,fluorouracil) destroy or damage DNA by pretending to be nucleotides and breaking things that way.
Anthracyclines bind into DNA strands damaging it, directly create free radicals, disable topoisomerase II, and displace histones.
There are the topoisomerase inhibitors which prevent cell growth by preventing DNA from being unwound for replication.
There is a fairly diverse(chemically) class of 'mitotic inhibitors' that screw up microtubule formation or proper microtubule dissolution, any of which prevents mitosis.
Sunitinib blocks tyrosine kinases, which are involved in blood vessel formation(and nerve formation and some other things). Other tyrosine kinase inhibitors are more specific to vascular endothelial growth factor(VEGF) receptors, but most tyrosine kinases target more or less specifically VEGFR and related receptors. Some are antibodies, some are just small molecules that bind TKRs.
There are a few retinoid-related drugs most of which influence the vitamin A pathways, like tretinoin, bexarotene, etc. Dual use in skin creams.
Immunoadjuvants are designed to activate the immune system to aid in tumor cell destruction. Interferon-alpha, imidazoquinoline, et cetera.
In the miscellaneous category:  Bortezomib, a short peptide that interferes with proper protein degradation. L-asparaginase slows all protein production by destroying asparagine, an amino acid. Some blood cancers respond to corticosteroids, and some ovarian/testicular cancers are treated with sex hormone inhibitors. Nearly any blood-borne poison works as a chemotherapy agent due to the EPR effect, so heavy metals or radioactive isotopes also are sometimes used. Arsenic trioxide, for instance, is just arsenic.
It's also worth looking at the steroids that are given along with cancer treatment(dexamethasone) to mitigate side effects. As regulatory hormones, there's going to be a hefty impact on genetic regulation from regular steroid injections. If nothing else it's a confounding effect you'll need to control for.
The preparations/solvents of chemotherapy agents can also be significant. Cremophor was used to suspend some anticancer drugs, but recent developments imply that might be on its way out.

Thank you, this looks very useful. I expect I might have more questions once I've had a chance to digest everything you've said; do you think its better to post follow-up questions here or as a new question?

Probably depends on the follow-up question you have. Clarification should probably go here, related but distinct questions should be new questions. I'm not a stack exchange protocol expert, so....

Resonating provided a good general classification scheme that could be implemented for categorizing chemotherapeutic agents. Another resource that could be used is the following: http://www.genome.jp/kegg/drug/. This is a pretty good classification of drugs based on ATC resource (http://en.wikipedia.org/wiki/Anatomical_Therapeutic_Chemical_Classification_System). These two resources are good starting points.


text:
which signalling pathway is involved in cancer?
Columnar epithelial cells from the colonic mucosa are studied to identify abnormalities in cell signaling pathways. Abnormal epithelial cells from colonic adenocarcinoma are shown to have a mutation that blocks hydrolysis of GTP-bound active RAS. Normal columnar cells have active RAS protein that undergoes hydrolysis to the inactive GDP-bound form. Which of the following signaling pathways is most likely abnormally stimulated in the carcinoma cells?
a. Jak-Stat Pathway
  b. MAP kinase pathway
  c. p53
  d. Both a & b
I think its MAP kinase pathway because RAS is part of MAP kinase pathway that ultimately leads to transcription and expression of genes but if GTP is not hydrolyzed then RAS will be constantly activated leading to continued gene expression that may lead to cancer but I am not completely sure about it because p53 is also a tumor suppressor gene.

Is this a homework/test question? It looks a lot like one.

Homework questions are off-topic unless you show some effort of solving them yourself. What are your thoughts about it?

Hi, this very much sounds like a homework question! It will be great if you show some evidence of what you think the likely answer is and why so that any input would be constructive!

I think it is MAP kinase pathway because if GTP is not hydrolyzed then it will lead to constant activation of RAS as RAS is in MAP kinase pathway..so what is your opinion..?

Perhaps also take a look at Jak-stat and see what pathways influences it! and as correctly mentioned p53 is an inhibitor so it can't be the right answer!

The answer is b, as the mutation constantly activates the RAS protein. RAS is part of the MAP-Kinase pathway, constant signaling of it permanently activates this pathway and leads to changes in gene expression. See the image below:

If you are interested in more details, have a look at these papers:

RAS oncogenes: weaving a tumorigenic web
RAS mutations and oncogenesis: not all RAS mutations are created
equally

Whoever downvoted my answer, what is your problem with it? I can (and will) improve it, when you can tell what you think is wrong with it.

yeah you are right that both are involved in cancer but in question a specific condition is mentioned that is "mutation in RAS" and it is constantly activated that leads to cancer so its only MAP kinase pathway...as no RAS in JAK-STAT pathway..by the way I didn't downvote your answer..

@emi Yes, you are right. I missed that point somehow. Adapted the answer.


text:
Is there any research paper state the pros and cons for human to be taller?
Is there any research paper state the physical health pros and physical health cons for humans to be taller?
For example, shorter people seems to more likely to get involved in heart diseases and taller people to be more likely to be involved in cancer

People with Shorter height may outlive Taller ones.
It is a statistically established fact that they are more successful in terms of money,
as the study published Journal of Applied Psychology, (Vol 89(3), Jun 2004, 428-441).
But, still in the health, the counterpart succeed over the former.

The Effect of Physical Height on Workplace Success and Income: Preliminary Test of a Theoretical Model.

Author: Judge, Timothy A.; Cable, Daniel M.

In this article, the authors propose a theoretical model of the
  relationship between physical height and career success. We then test
  several linkages in the model based on a meta-analysis of the
  literature, with results indicating that physical height is
  significantly related to measures of social esteem (p = .41), leader
  emergence (p = .24), and performance (p = .18). Height was somewhat
  more strongly related to success for men (p = .29) than for women (p =
  .21), although this difference was not significant. Finally, given
  that almost no research has examined the relationship between
  individuals' physical height and their incomes, we present four
  large-sample studies (total N = 8,590) showing that height is
  positively related to income (β = .26) after controlling for sex, age,
  and weight. Overall, this article presents the most comprehensive
  analysis of the relationship of height to workplace success to date,
  and the results suggest that tall individuals have advantages in
  several important aspects of their careers and organizational lives.
  (PsycINFO Database Record (c) 2012 APA, all rights reserved)
  Source: http://psycnet.apa.org/journals/apl/89/3/428/

Long back in 1975, the relationship between breast cancer and height had been nearly established.

Breast Cancer Incidence and Nutritional Status with Particular Reference to Body Weight and Height
Author: F. de Waard
Cancer Res 1975;35:3351-3356.
Summary The epidemiological literature on breast cancer is reviewed with particular emphasis on the possible etiological role of
  nutritional status as reflected by weight and height. The results of a
  prospective study and preliminary results of a population-based
  case-control study seem to indicate that body size or body mass rather
  than overweight (obesity) is a risk factor. A considerable proportion
  of the differences in incidence between the Netherlands and Japan can
  be explained by differences in body mass. The biological mechanisms
  mediating nutritional status and breast cancer are believed to be of
  an endocrinological- metabolic nature.

Primarily the investigators started with overweight problem but they have found a better correlation with height. They have concluded:

A further lead to biological mechanisms might be derived
  from the fact that several endocrine and metabolic functions
  (e.g., basal metabolic rate and cortisol production rate)
  seem to correlate better with body surface area than with
  body weight. The rationale for using surface area is often
  lacking except for the fact that it is estimated from both
  weight and height.

Height and cancer risk are fairly clearly linked, with a 16 per cent higher relative risk for every extra 4 inches of height.
The answer may lies in the metabolic rate:

For one, taller people tend to weigh more than shorter people, even if
  their BMI isn’t any higher. For another, poor nutrition and stress can
  stunt height growth, and higher calorie diets have been associated
  with increased height. And that doesn’t even begin to take into
  account the psychosocial variables like increased income, education,
  and socioeconomic status.

Other Diseases
On the contrary, in a study examining cardiovascular disease risk and height in men found that men who were taller than 6′ 1″ (185 cm) had a 35% lower risk of having a heart attack than men who were shorter than 5′ 7″ (170 cm). Every inch a man gained in height resulted in a 2-3% decrease in heart attack risk.
In a study in among, Israeli civil servants, shows height was also associated with lower stroke risk. Taller people are more likely,around 76%,  to suffer from recurrent blood clots.
LINKS:

http://blogs.discovermagazine.com/crux/2013/11/08/is-being-tall-hazardous-to-your-health/#.U79p3vmSzQJ
http://scienceblog.cancerresearchuk.org/2011/07/21/height-and-cancer-risk-%E2%80%93-the-long-and-short-of-it/

Link-only answers can become obsolete if the content changes or the page disappears. Instead, please summarize the information found in the link in the body of your answer, and provide the link for reference. The answer should be able to stand on its own without the external resource.