text:
How was the Huntington's disease gene's location found?
I read in the book "Why we get sick." by Nesse and Williams that:

Steady detective work and fabulous luck have enabled geneticists to
  pinpoint the Huntington's gene on the short arm of chromosome 4.

I want to know what was the "detective" work and the fabulous luck - the whole story of the discovery of the location of the gene.

A Google search for "Huntingtons disease gene discovery" yielded this page at the Nature Education Scitable website. The following citations are provided regarding the molecular basis of HD:

Huntingtin (HTT) was the first disease-associated gene to be
  molecularly mapped to a human chromosome (Gusella et al., 1983)2. Ten
  years later, scientists identified the DNA sequence and determined the
  precise nature of the HD-associated mutation in HTT (MacDonald et al.,
  1993).

Gusella et al. used restriction fragment length polymorphism (RFLP) analysis to locate a RFLP marker linked to Huntington's disease on chromosome 4. From the introduction of their paper:

We have now identified an anonymous DNA fragment from human chromosome
  4 that detects two different RFLPs in a HindIII digest of human
  genomic DNA. This polymorphic DNA marker shows close genetic linkage
  to the Huntington's disease gene in two separate families, although a
  different haplotype of the marker segregates with the Huntington's
  disease gene in each family. We infer that the Huntington's disease
  locus resides on human chromosome 4.

Further details given in the paper might justify the description given in the question. "Fabolous luck" could refer to the discovery or availability of suitable families and pedigrees for the genetic studies. The "steady detective work" would be the genetic mapping and fieldwork required to establish the link. The following quotes describe some of the efforts spent on the project:

The success of any genetic linkage project depends in large part on
  the quality of family material available for study. We initially
  invested considerable effort in identifying a useful family from the
  National Research Roster for Huntington's Disease Patients and
  Families at Indiana University. An American family of reasonable size
  was selected and blood samples were obtained (...). Subsequently, a
  substantially larger Huntington's disease family was located. This
  pedigree stem from a unique community of interrelated Huntington's
  disease gene carriers living along the shores of Lake Maracaibo,
  Venezuela. (...)For the past three years an expedition has spent one
  month annually in Venezuela collecting pedigree information, tissue
  samples, and clinical data. (...) In Venezuela, many family members
  were examined for three consectuvie years. Permanent lymphoblastoid cell lines were
  again established for each individual to act as a permanent source of
  genomic DNA. In both families each individual was examined by at least
  one neurologist experienced and knowledgable about Huntington's
  disease.

The Scitable page also summarizes the approach and results described in the paper. For the RFLP analysis, several DNA probes were tried, of which one, "G8", resulted in a HD-linked pattern:

James F. Gusella and colleagues carried out a study to determine
  whether they could identify a DNA probe that would show an
  HD-associated restriction fragment length polymorphism (RFLP) when
  used in Southern blot analyses of chromosomal DNA digested with the
  restriction enzyme HindIII (palindromic recognition sequence
  5'-AAGCTT-3'). The team identified one probe out of 12 tested, called
  G8, that showed a specific RFLP pattern associated with HD in two
  large families with a history of the disease (Gusella et al., 1983).
  Using the G8 probe, they next identified two HindIII sites (called H1
  and H2) that were palindromic within this chromosomal region. DNA
  fragments at these sites vary in length among different HD lineages.
  Because researchers used two large pedigrees in these experiments,
  they were able to obtain statistical support for their discovery
  (Figure 3).

However, at the time the origin of the G8 probe DNA in the human genome was not known, so human-mouse somatic cell hybrids were made to identify where the G8 probe DNA belonged. This showed that the G8 probe corresponded to chromosome 4, and indicated that the HD gene would be found there:

Researchers found that the G8 DNA probe hybridized only to Southern
  blots using chromosomal DNA from human-mouse somatic cell hybrid lines
  that contained human chromosome 4. Therefore, researchers determined
  that the G8 DNA probe is located on human chromosome 4, and they
  concluded that the HD gene is located on chromosome 4 near the region
  corresponding to the G8 DNA probe (Figure 5; Gusella et al., 1983).

It was fascinating because Huntington himself described what we now call genetics before the field existed. Then to locate the gene scientists used essentially trial and error. They took enzymes that cut different parts of the DNA and looked at which of these were inherited. If it were inherited then there would be cuts made, otherwise not. Then they matched it up to who had the disease. Of course with 46 chromosomes there were thousands and thousands of places to check but they somehow luckily managed to find it on their twelfth try!
The full story can be found here: http://www.dana.org/Cerebrum/Default.aspx?id=39308


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Near point and far point of myopic eye
Suppose a person wears the specs of power -6D, the far point for that person is 16cm.
But the near point of normal eye is 25cm.
So, is the near point of a  person with myopia (having far point less than the near point of normal person) also changed ?

Let us say this myopic patient has amplitude of accommodation of 8D.  The patient accommodates 8D beyond far point, thus his near point is 1/6+8=0.07m (7.1cm).
If we compare the case with emmetropic eye with accommodation amplitude of 8D, the near point is 1/8=0.12m (12cm).
So, yes, near point of myopic person is different from an emmetropic one. But, you are wrong thinking that near point of "normal" eye is 25cm. The near point is age-and-lens dependent, thus near point is individual one and should be calculated considering amplitude of accommodation.
Look at this picture of age-related accommodation changes -

Look at the scheme of far/near points (near point here is just an example)

Hi!Thank u for answering.I could not understand the first calculation. Why did u take 1/14 instead of 1/8 ? Also - would the near point of myopic eye change after correction of far point ?

That is very simple: in nonaccommodative state the eye in example has 6D and to this power the adds its accommodation power of 8D for nearest point,  thus the near point is at 1/6D+8D...

I forget to answer about correction. By correction we convert a myopic eye to "emmetropic", thus with correction the near point is different (more far from the eye).

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text:
phosphorous availability to mycorrhizae and parent plant, timing - paper search
I'm researching phosphorous uptake in monocots to develop planting mixes for riparian planting.
I recently saw a paper suggesting (the author lacked proof) that root zone mycorrhizae may solubilize phosphorous from the soil solution out of phase with the parent plant's ability to take up the phosphate, resulting in P loss from the system. Sadly I didn't save the paper and so it is still out there on the net. If this is the true, and the loss significant, then it would be an argument against using mycorrhizal plants in stream-side planting.
Does this ring a bell with anyone? Failing that, what is known about the relative phasing of mycorrhizal phosphorous release and timing of plant uptake, especially in monocots?

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Propagation of tool use in primates?
There are several famous cases of great apes demonstrating a surprising degree of wherewithal in communication and tool use - even monkeys can learn some tool use from each other observationally, even if "teaching" would be an exaggeration.
The ready availability of this information will preclude me from bothering to cite a palate of examples.
Has anyone ever considered, as an experiment, taking such primates which display exemplary tool use in the lab and (at least partially) reintroducing them into the wild and seeing if (perhaps specially crafted) tool lessons learned form us humans propagates among their fellows?
If not, why not?

Those that exhibit those behaviors are far too valuable to release. Also, biologists never interfere with natural processes if they can help it. E.g. they don't help a severely wounded animal in the wild because that would meddle with the natural order of things.


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In what circumstances does a mammalian egg copy its DNA?
In the 2nd episode of the new Cosmos series, the host Neil deGrasse Tyson shows how the white-furred bear could have evolved (reasonable scientific speculation, of course).
If you haven't seen that episode, here's the link. Great show, by the way.
So, it shows the bears eggs, and then goes on to show how there can happen an error in the DNA copying, that leads to the brown pigment production malfunction. Here's an excerpt from the subtitles text:
- great bears roamed the frozen wastes of Ireland.
- This might look like an ordinary bear,
- but something extraordinary is happening inside her.
- Something that will give rise to a new species.
- In order to see it, we'll need to descend down to a much smaller scale, to     the cellular level, so that we can explore the bear's reproductive system.
..
- Those are some of her eggs.
- To see what's going on in one of them,
- we'll have to get even smaller.
- We'll have to shrink down to the molecular level.
..
- When a living cell divides in two,
- each one takes away with it a complete copy of the DNA.
- A specialized protein proofreads to make sure
- that only the right letters are accepted
- so that the DNA is accurately copied.
- But nobody's perfect.
- Occasionally, a proofreading error slips through,
- making a small, random change in the genetic instructions.
- A mutation has occurred in the bear's egg cell.
- A random event as tiny as this one can have consequences on a far grander scale.
- That mutation altered the gene that controls fur color.
- It will affect the production of dark pigment in the fur
- of the bear's offspring.

From my (not professional but kind of passionate amateur) knowledge of biology, I I was under impression that all of the mammalian eggs are present at birth. But the story depicted in the show involves the (erroneous) DNA copying. I see dissonance there, and I'd like to solve it.

The episode isn't available outside the US, so can you provide some more details? When does the DNA copying happen? When the eggs are produced?

I edited the port to include the text. Perhaps this is the point where I fail to grasp what's happening: "A mutation has occurred in the bear's egg cell" - at which point a mutation could in fact happen in an egg cell? To my understanding, only a fertilized egg cell divides.

The writers of the show may have been somewhat imprecise either by accident or intentionally to avoid excessive details.
There are several different stages of egg cells, with distinct names for each and for the process that leads from one to the next. The whole process of egg cell creation is called [Oogenesis].1 To quote Wikipedia:

Oogenesis starts with the process of developing oogonia, which occurs
  via the transformation of primordial follicles into primary oocytes, a
  process called oocytogenesis.[4] Oocytogenesis is complete either
  before or shortly after birth.

To our current knowledge all primary Oocytes are present at birth. The next stage in the maturing process is called ootidogenesis, which produces an ootid.

The succeeding phase of ootidogenesis occurs when the primary oocyte
  develops into an ootid. This is achieved by the process of meiosis. In
  fact, a primary oocyte is, by its biological definition, a cell whose
  primary function is to divide by the process of meiosis.[8]
However, although this process begins at prenatal age, it stops at
  prophase I. In late fetal life, all oocytes, still primary oocytes,
  have halted at this stage of development, called the dictyate. After
  menarche, these cells then continue to develop, although only a few do
  so every menstrual cycle.
Meiosis I of ootidogenesis begins during embryonic development, but
  halts in the diplotene stage of prophase I until puberty. The mouse
  oocyte in the dictyate (prolonged diplotene) stage actively repairs
  DNA damage, whereas DNA repair is not detectable in the pre-dictyate
  (leptotene, zygotene and pachytene) stages of meiosis

DNA replication is completed before Meiosis occurs. So oocytes do not replicate DNA after birth, but they do repair DNA to fix mutations that may occour after birth but before conception. If DNA repair fails, then mutations may persist. So the show would appear to be wrong about egg cells copying DNA in an adult bear, but right in that mutations might occur during its lifetime affecting its offspring.

Wow, that's elaborate, thank you. On what authority I could decide that I can mark your answer as "correct"? I am not competent to decide :)  Why would the show writers choose this particular stage for addressing the mutation introduction? Is that the prevailing hypothesis of how the persistent, evolution-driving mutations occur?


text:
How does gene expression work in an adult organism? Is everything encoded everywhere?
The color of a person's eyes are genetically predetermined. If I knew how and in which gene(s) colors are encoded, I could change these genes in the ovary and sperm and thus change the eye color of the new human being. I only had to work on one or two cells.
What would I need to do to change the eye color of an adult human? Manipulate the genes in all body cells? Or would a limited number of cells suffice (e.g. those in the eye)?

Eye color is just an example. Your answer does not have to deal with this trait.

You would only have to manipulate the relevant cells. Not all genes are expressed in all cells, many of them are regulated in a cell type specific (and also development specific) way.

Take a moment and think - why would you need to change genes in all your body cells to change the eye color ?

@biogirl I'm a biological idiot. Last time I heard of genes was 30 years ago in school. I thought that mutations in cells happen often, and that this mutation is held in check by the surrounding cells that have the "correct" gene. So it seems to me that a larger number of cells need to be changed for a change not to appear as malignant mutation to the rest of the body (e.g. blood cells). Also, since cells constantly die and are recreated (at least in some parts of the body), a limited change might simply grow out and the original eye color return.

Its awesome that u ask questions ! Now that we know precisely what u r thinking we can help u in a better way.

It is very difficult indeed to change genes in an adult organism. Try reading about gene therapy. Its a practical application of what you are trying to imagine !

Cells are not intelligent like that.  They can not look at each other, read each other's DNA, compare it, and decide to kill an outlier.  If a DNA mutation causes a cell to go haywire, the immune system might recognize that its behavior is not right, and kill it, or the cell's own suicide genes might kick in, and kill the cell.  But those failsafes don't always work, and if the effect of the mutation was minor, nothing bad would happen to the mutated cell.

With some exceptions (one being red blood cells), all cells in the body contain the complete genome of the individual. The expression of the genes however is, as mentioned in the comments, heavily regulated and different in various tissues. Early efforts at gene therapy have had mixed results, including some fatalities, and the field is still highly experimental.
Depending on the trait you want to change, you might have to manipulate the genes and/or gene expression in just a particular tissue, or in several. The rates of cell death and replenismhent varies between tissues, and will affect the stability of any introduced mutation. Some traits may depend on too many genes to effectively manipulate with current technology, and eye color does depend on several genes. From the Wikipedia page on Eye color:

Eye color is an inherited trait influenced by more than one gene.
  These genes are sought using associations to small changes in the
  genes themselves and in neighboring genes. These changes are known as
  single-nucleotide polymorphisms or SNPs. (...) There is evidence that
  as many as 16 different genes could be responsible for eye color in
  humans; however, the main two genes associated with eye color
  variation are OCA2 and HERC2, and both are localized in Chromosome 15.

So depending on the original and desired color, you may or may not get away with changing a single gene. However, the pigments that determine eye color are produced in two separate tissues in the eye, making matters a bit more complicated:

In humans, the pigmentation of the iris varies from light brown to
  black, depending on the concentration of melanin in the iris pigment
  epithelium (located on the back of the iris), the melanin content
  within the iris stroma (located at the front of the iris), and the
  cellular density of the stroma

Note that cellular density also plays a role, and this presents a much harder property to change with gene therapy, if it is at all possible.
Eye diseases have been a popular field for gene therapy research and trials lately, and there seems too have been quite some progress. However, the possiblity of using gene therapy for changing eye color has understandably not received much attention, and so there are few if any papers to consult. What can be said though, is that eye color is a complex trait, with a partially known genetic basis. It is plausible that gene therapy can be used to change pigment production and thus eye color, but even so there would likely to be many limitations. on the changes that can be made.

Nice, thank you +1. I edited my question and added a note that eye color is just meant as an example. If you have another example that illustrates the invovled principles better, feel free to add it to your answer.


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Why do different humans look different?
Although farmers appear to be able to tell their cows apart, cows look very much alike to me. And this similarity in appearance seems to be a general trait across the animal kingdom: one individual of one animal species looks much like another.
Why do human facial and body shapes vary so much?
I understand that human beings live in many different environments (e.g. hot and cold) and have adapted to these (e.g. through lighter or darker skin color), but there seems to be much variation that has no apparent evolutionary purpose. So does the difference have a purpose in itself? That is, did we evlove to vary in appearance, and what is the purpose of this variation?

There is a substantial variation in some human traits: hair colour, eye colour, height, weight, skin colour, build etc. etc. HOWEVER there is also considerable variation within other species, to suggest otherwise is naive (though quite common). We often feel like there is more variation within our own species because we are more aware of the subtle differences within our own species (we have evolved to be able to recognise those that are more similar to us). Cows for example also have a lot of variation:

But to answer the question of why traits vary so much generally... There are two principle reasons that demographic patterns might evolve in traits (for example, "Why do Scandinavians tend to have blonde hair?" - [this is just an example, I'm not sure if blonde hair is actually more common in Scandinavia, it could just be a stereotype])
Firstly there is the selectionists view. This is the view that traits tend to evolve for some kind of adaptive reason, therefore most traits (and demographic patterns of variation) exist for some kind of purpose. A selectionist would argue that blonde hair offers some kind of advantage in Scandinavia, over other hair colours, that it doesn't in others. It could be a naturally or sexually selected advantage (perhaps blonde hair is more useful when hunting prey in snow, or there is mate preference for blonde individuals etc.)
In the 1960's though a scientist called Motoo Kimura proposed the neutral theory, a theory that most variation and traits have evolved by neutral processes. For example, scandinavians might be blonde because the humans that colonized Scandinavia were, coincidentally, blondes. Neutralists would argue that the demographic variance we see in humans, and within animal species, is due mainly to random genetic drift.
Here is some more on neutralist vs selectionist, and some on genetic drift. And just to show that other animal species also vary:
Here are some dogs (which have come under a lot of artificial selection specific to generating different physical variants)...

And here are some apes...

The last image is great, where did you find it?

Thank you for your answer. As far as I understand your dogs show different species and subspecies of the family of dogs (Canidae), not members of one species. The same goes for all those "cows", which are actually different members of the genus Bos, many of which aren't actually cows at all but only distantly related. As far as I understand, all humans on the other hand belong to the same species, and current theory holds that there even are no different human races. So it seems to me that you are comparing a species (human) with genera (bovines) and families (dogs). --- +1 for drift!

Well, and acutally I accept this answer :-) Your explanation on genetic drift explains the differences – and I'm not sure about the races and families anyway, so this is perfect for me. Thank you!

Also, it has been shown in several studies that sheeps are able to recognize faces.

@what the pictures are to illustrate the variation within a lineage of ancestry more so - I wasn't focussing on species (tired this morning after a heavily delayed flight!) but of course there are still differences within species as well as within families, genera etc. the concepts of species and such try to put clearly distinct steps on to what is a more fuzzy gradual process.

@Chris http://www.jamesmollison.com/project_apes.php

nice find @what - always nice to find the original, it is an excellent image

Thanks. This is a great image, I will see if I can use it in my next talk.

Other species have plenty of ways to distinguish each other, often driven by sexual selection.  This may even form the basis for speciation, e.g. in birds that are reproductively isolated based on songs.

Vampire bats can identify each other well enough to track food sharing favors. http://rspb.royalsocietypublishing.org/content/282/1819/20152524

The answer by rg255 suggests that individual differences are the result of adaptation or genetic drift. That is, humans look different, because they lived in different circumstances.
While this may explain different skin colors (adaptation to different levels of sunlight) or hair color (accidentally more blondes settled in Scandinavia), it does not explain why facial shape differs in the way it does. Looking at skin or hair color, you would not be able to tell most people apart: there are millions of people with the exact same shade of skin or hair color. There is no individual skin or hair color. But there is an individual facial shape. It is very rare that you find two people (who are not twins) whose faces look so identical that you would confuse them. Facial shape distinguished human beings from one another in a way that hair or skin color does not. And while apes may have different faces as well, the distinguishability declines the further down you look at the phylogenetic tree.
According to a study published in Nature (Sheehan & Nachman, 2014; summarized in the Washington Post), distinct facial features did not evolve as adaptation to some environment, but because
identification of individuals was a necessity for our species.
Facial recognition is the prerequisity for human social relationships. And it is our social life that made us the dominant species on this planet. So, in a way different faces are adaptive, but not in the direct way that light or dark skin is. Facial indentification allows us to form a complex society with a wide variety of roles and finely differentiated relationships, and it is this complex society that allows us to create the culture and technology that in turn enables us to survive in all earthly (and a few extratrrestrial) environments and "have dominion over every living thing that moveth upon the earth".

Sources

Sheehan, M. J., & Nachman, M. W. (2014). Morphological and population genomic evidence that human faces have evolved to signal individual identity. Nature communications, 5:4800. doi:10.1038/ncomms5800 Available online at http://www.nature.com/ncomms/2014/140916/ncomms5800/full/ncomms5800.html


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Why does pH have an effect on enzymes?
I am currently studying biology and would like to know why enzymes work best in a particular narrow range of pH (the so-called pH optimum).
Unlike temperature change, I do not think this has much to do with energy. Do pH-related changes in enzymatic activity have anything to do with the active site?

What do you mean by increasing? Coming from pH 1 and increasing it until the optimum is reached?

@Chris Yes that is what i mean

"When the pH gets closer to the enzyme's pH optimum, the enzyme activity also increases." Why? Because of the way the English Language works. It would be absurd if an enzyme's activity was not highest at its optimum. I have reworded the question so it makes sense.

Enzymes have a more or less narrow optimal pH at which they work, depending on the conditions of their environment. Pepsin for example is active in the stomach which is pretty acidic and has an optimal pH of 2.0, while Trypsin, which is active in the small intestine has an optimal pH around 8.5.
Changes in the pH first affect the form of the protein, hydrogen bonds between the amino acids of the molecule and so on and also the form of the active center of the enzyme. Small changes in pH do little or nothing, then reversible changes occur and finally the enzyme gets irreversibly denaturated.
The relationship between enzyme activity and pH always looks like this (the curve can be steeper, if the optimal range is small and broader if the range is wider):

It is taken from this website, which is a nice introduction to enzymes. Another one is here.
At the optimal pH for the enzyme the conformation of the protein is as it should be (in the ideal state) while this changes when the pH is not optimal. This can lead to improper substrate binding, changes in the active center and so on.

Proteins are polymers of amino acids. Each amino acid has a side chain. Many of these side chains contain ionisable groups. The ionization state of these groups is dependent on the pH. A group that is protonated at pH=2 and neutral, for example, may become deprotonated at pH=8 and become negative. See the Henderson-Hasselbalch equation.
Protein structure is held together by many intermolecular interactions: dipole-dipole, hydrophobic, electrostatic, etc. The correct protein structure is necessary for function. At different pH levels, the protonation and deprotonation of ionisable amino acids affects the intermolecular interactions within the protein and its conformation will change. At a certain pH, the conformation of the protein will be optimal for its function and this is where it will have maximum activity. As pH deviates to either side of the optimum, the conformation changes and the structure will no longer be correct for proper function.
The ionization state of amino acids is also important in the active site but not only because of conformational changes. Catalytic residues must have certain properties to catalyze their specific reactions. As an example, two Asp residues (which have carboxylates on their side chains) in the active site of DNA polymerase are responsible for coordinating two magnesium ions that promote polymerization. If the pH were to decrease to a point where the Asp residues were protonated, they could no longer bind the Mg2+ ions and the enzyme would not function.

Don't know why this question has suddenly come up after 4 years, but this is the best answer. The ionization state of the groups involved in catalysis is the key factor, not just for interacting with magnesium ions or the substrate, but for the actual catalytic mechanism in many cases. See the chapter on mechanism of catalysis in any textbook of biochemistry.

@David Thanks. Some one posted a question as an answer which is now deleted but bumped this post up. You’re absolutely right and, if I had the time, I could write something about general acid/base catalysis.

Enzyme function is largely determined by its 3-D shape. Enzyme shape is affected by pH among a couple other things. The enzyme only retains its optimal shape at the optimal pH, as you creep outside of it the enzymes shape changes and hence so does its function.

The statement "The enzyme only retains its optimal shape at the optimal pH" convey no scientific information whatever.


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How do nutrients get to the cells they need to get to?
I understand the basics of digestion. I know that nutrients get absorbed by the microvilli, enter the bloodstream and travel to the liver but after all that, what is the biological mechanism that guides these nutrients to the proper receiving location?

Just dropping this link here for reference - it contains some info on membrane transporters which is of relevance to your question: http://themedicalbiochemistrypage.org/membranes.php

Broadly speaking, nutrients that enter the blood from the gut, and those that are released into the blood by the liver, are available to any cells that require them. So there is no "guiding to the correct location" in the sense that you suggest.
Lipids for example are present in the various lipoproteins and can be acquired from these by all cells. Iron is bound to transferrin, and any cell with transferrin receptors can internalise the transferrin and take the iron. Glucose is available in solution in the plasma, and free fatty acids are bound to serum albumin in the blood. During starvation the liver produces ketones ("ketone bodies") which are taken up by many different tissues/cell types.

Are you saying that myriad nutrients just float along through the blood stream just bumping into myriad receptors at random and when there is a connection, the nutrient will be absorbed?

@max Basically, yes.

Pharmacokinetics must be a fun field! How different a concentration of iron, e.g., do different organs see? Clearly depends on rate of flow vs binding rate...


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Why is the human body hair not uniformly colored?
Most of my body hair is black however my lip hair is light brown/blonde the rest of my beard region is black. Since hair color is genetic what causes this?

The hairs you mention are also called "androgenic hairs", meaning their growth and pigmentation is influenced by androgens. These include pubic hair, the hairs on the breast and shoulders (almost exclusively for men) and the beard.
It seems, that these hair bulbs have different sensibilities (number and expression of androgen receptors) so they react differently to androgen levels. This includes balding, pigmentation, growth and so on.
These articles should be a good starting point, if you want to dive deeper into the topic:

Androgen actions on the human hair follicle: perspectives.
Mechanism of action of androgen in human hair follicle.

I've heard it mentioned that gene dosage is implicated in this. Gene dosage is the number of the alleles present in the cell.

Could you give some references for this ?


text:
What is this abbreviation CT in female reproductive system
I have this sentence in my notes

Ovary is surrounded by tunica albuginea and the cortex keeps the primordial follicles. The medulla containing CT and blood vessels develop from mesonephros.

I have these words in my mind about CT

tunica
cyto- (maybe cytotrophoblast)
corona (no other than corona radiata so not)

What can CT be here?

Homework question and too easy. Please, close.

I think CT is an abbreviation for connective tissue. Some examples of its use in that fashion:
http://en.wikipedia.org/wiki/Connective_tissue
https://web.archive.org/web/20151024041339/http://www.vetmed.vt.edu/education/curriculum/vm8054/Labs/Lab5/Lab5.htm
http://www.pitt.edu/~sshostak/biosci1450/hislec03.html

I found this as well, and it is a fact about the ovaries.

Thank you for your fast answer! Yes, it makes sense.

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text:
Do tall people have more cells?
Within a single species, how does the relative number of cells in the body relate to the relative size of the organism?
Let's say we take two humans, one of them is 6 feet tall and the other one is 5 feet tall.  They have similar BMI, age, physical condition, genetic background (aside from height) and are the same sex.
Does the tall one have more cells? Or does he have bigger cells?
PS: Ideally, answers should be backed up by appropriate sources.
PPS: While I'm grateful to everyone for the very nice answers I got, I should point out that I'm waiting for an answer which includes references to accept it.

In retrospect, I have presented a false dichotomy. As jarlemag has pointed out, a tall person may have neither more cells nor bigger cells - their height (or size, see discussion in buzrw's answer) may be due to more non-cellular mass (eg. more ECM).

This is really the most fundamental concept of Cell Biology, so good question. If you look at the size of a any cell from a whale and compare it to the size of any of cells from a mouse, they are in fact quite similar, despite the extreme difference in the overall size of the organisms they are from. There is a reason why cells are small, and it has to do with the fact that they survive based on their ability to absorb enough nutrients from their environment. As a cell gets larger it needs more to survive (because it has a bigger mass). A bigger cell has also has a larger surface area around it (so it can absorb more nutrients).
HOWEVER, there gets to be a point where the mass of the cell is too large for the surface area to compensate for. Mathematically this is shown by what is called the "surface-area-to-volume ratio". Basically, it states that as a a sphere gets larger, the volume increases at a higher RATE than the surface area. So there is a reason cells get only so big, the 60's horror movie The Blob was not scientifically accurate, a single-cell that large (the blob) would not have enough surface area to absorb enough nutrients to sustain itself. Taller (or bigger) people have more cells (not bigger ones) than others.
Effects of osmotic pressure can alter cell size slightly.
When you are talking about taller individuals, you are (I think) really meaning larger people, people with a higher mass. And yes, they have more cells.
Another topic of Cell Biology you may want to explore is apoptosis. Let's say you have two individuals both 180 lbs. one of them is 5' tall and the other 7'. Both these individuals have the same number of cells, but the taller one has a higher percentage of them in the superior and inferior regions of the body. It is the process of apoptosis that sculps an organisms shape.

You are correct that I, in effect, meant "larger people", because I specified that their BMI is similar.

+1 sounds like a good answer for the cell biologist that I am NOT. You may add some elements about how (and why) cell size varies from one species to another. This article also might be of interest.

@Remi.b I'm not sure if that paper applies to my question per se, but it was a fascinating read! Thank you.

Well written, but I have 2 issues. 1. I can't imagine that 2 individuals of the same mass always have the same number of cells! Intracellular "stuff" (e.g. proteins & other macromolecules) varies b/w cell types -- think about adipose with a "full" vacuole vs RBCs. 2. Your post does not address extracellular "stuff" -- either space or non-cellular material (e.g. H2O) -- which could account for greater body size (both space and mass) . I know it's an old post, but please add some citations; otherwise I have to downvote as a "sounds good but probably isn't true" post. Thanks

Not sure it is proven, but this paper makes use of the assumption: West et al, PNAS 99:2473, http://www.pnas.org/content/99/suppl_1/2473.full
Btw, this paper may be relevant for you as it focuses on the metabolic activity, which is not quite propotional to body mass (power 3/4: it's growing slower)

With respect to the relationship between body mass and metabolic rate: https://biology.stackexchange.com/questions/25912/statistical-method-for-characterizing-the-relationship-between-body-mass-and-met/66659#66659

The taller person has more cells. Most cells can only lengthen up to a certain point. Whilst the neuronal cells will be longer and likely some others, the rest of the cells will just be of larger number.

Just to play the devil's advocate, are there actually any sources that confirm this? Couldn't it also be that tall people have the same number of cells, but with more extracellular matrix and larger spacing between the cells?

@jarlemag That's a very good point (which I originally missed); I added a comment to my question to clarify.


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What is an irreversible reaction?
There are reactions with large Delta G negative values. Why these reactions are irreversible? As in: out of 10 steps of Glycolysis, 3 are irreversible steps. I need an explanation for why they are irreversible.

About which reactions do you think?

A short answer is that they are irreversible because in the conditions of the cell they happen far from equilibrium (which is actually what having a "large \Delta G" means).

The term "irreversible" means that the reverse reaction occurs so rarely that it is considered negligible. This means that you do not have to consider equilibrium, as you have to for reversible reactions. Instead, you can assume that all of the reactants will eventually become product.
As you stated, this is true for reactions that have a very negative Gibbs free energy.  Remember the formulation of the Gibbs free energy in terms of the equilibrium constant:
$$
\Delta G^o =  -RTln(K)
$$
This can be rewritten as follows:
$$
K = e^{-\Delta G^o/RT}
$$
As $\Delta G^o$ gets very negative, you can see that $K$ gets very positive.
The equlibrium constant has two definitions that are both useful. First, it is the ratio of the products to the reactants. Therefore as $K$ gets very positive, the equilibrium ratio of products to reactants approaches infinity, implying that all of the reactants will be consumed.
More useful is the definition of the equilibrium constant as the ratio of the rates of the forward and reverse reaction. From this definition we can see that as $K$ gets very large, the ratio of the rates of the forward and reverse reaction approaches infinity. This means that the rate of the reverse reaction becomes negligible compared to the rate of the forward reaction. This is exactly what it means to be irreversible.
Note that it is possible to make (what I think is) a more convincing argument using the concept of activation energy, using Hammond's Postulate to describe the character of the transition state. If you'd like, I can write this out. However, I think the argument given above is more easily understood with a basic chemistry background.

yes! all chemical reactions are reversible.  its not said enough in frosh chem.

I understood it properly, its very helpful but if you are comfortable to explain by using the concept of activation energy then, Then i want to understand that concept too.. :)

@katherinebridges Have a look into the Wikipedia on activation energy. It contains an image which explains the concept pretty nicely. Basically most chemical reactions (even those which set free energy) doesn't start on its own. To do so, they need an initial amount of energy to start. Think of a sparkler. It contains chemicals which are capable of setting free a lot of energy when reacting, but under normal conditionss nothing happens. If you add the activation energy through a match, the reaction will go off and set off a lot of energy.

@Chris Ok, I will consult wikipedia to understand that concept,Thanx for the help..

"[...] you can assume that all of the reactants will eventually become product" this characterises a total reaction. A total reaction is irreversible by definition, but the opposite is not necessarily true.

The confusion between irreversible and total is also here when you write that "as $K$ gets very positive, the equilibrium ratio of products to reactants approaches infinity, implying that all of the reactants will be consumed". A reaction can be irreversible whatever the value of its equilibrium constant or of its standard Gibbs free energy of reaction. Again, total implies irreversible, but not the contrary.

I'm not familiar with this concept of a "total reaction" that you propose, and I don't see it referenced in a quick search in google or google scholar. Maybe this is terminology of your specific field? Could you give a reference?

Whether a reaction is reversible or irreversible, in the presence or absence of an enzyme, is not related to activation energy. An enzyme lowers activation energy in both directions.
A reaction is reversible or irreversible depending on the conditions in which this reaction occurs. If there's a sustained high concentration of substrates, most of the reaction flux goes from substrates to products, and the reaction is practically irreversible. The same happens the other way. Note that whether the concentrations are high enough or not depends on the kinetic constants involved.


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Possible Genotypes -- Linked Genes
Please consider the following question:
Genes A and B are located on the same chromosome. If two individuals with the genotype shown below are crossed, which genotype could be formed?

Let / represent the line in the image above.
a.)AB/ab
b.)Ab/Ab
c.)aB/aB
d.)AB/Ab
Why can't the answer to this question be all of the choices? I thought that recombination was completely randomized through the process of crossing over. Why is only one of the choices correct and how would I go about doing this on my own?

The answer is for Genes A and B on the same chromosome is
a.
AB/ab

One of the alleles for each gene must come from the parent on the right hand side. That parent only has a and b alleles (is homozygous) - meiotic crossing over will not change this. So the offspring must inherit at least one a and one b. That should point you to the answer.


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Do people with gout live longer?
Antioxidants reduce damage to tissue (by scavenging the free radicals) and thus may reduce ageing.It is known that Uric acid is a very good antioxidant.
People with gout have excess accumulation of uric acid.
Considering the above information the authors of the book  "Why we get sick?" put up an interesting question : Do people with gout live longer ?
I would like to know if there are any studies done to answer the question.

As far as I'm aware, the suggestion that anti-oxidants increase lifespan doesn't have any real scientific evidence. Even if ageing is largely due to oxidative damage, antioxidants often do not get access to the mitochondria where the majority of oxidative damage is likely to occur. Moreover, there is some evidence that anti-oxidants disrupt oxidative signalling in the cell, and so may actually cause more problems.

It is actually disputed if antioxidants do good, or if they prevent cells from dying which then can develop into cancer cells. There are a few publications out now, which support this hypothesis.

@chris I remember reading about some of the myths of antioxidants in a Scientific American article but the evidence was not conclusive.

I can look up the references later today.

@biogirl Some more popular written text (which has some references in it can be found here, two original papers are here and here.

In men, gout is associated with a higher risk of death from all causes. This would imply that their life expectancy is shorter. From a review by Kim et al. (1):

Among men who did not have pre-existing coronary heart disease, the
  increased mortality risk is due primarily to an elevated risk of
  cardiovascular death, particularly from coronary heart disease. Also,
  an extension study of a large clinical trial among men with
  above-average risk for coronary heart disease found that a diagnosis
  of gout accompanied by an elevated uric acid level is associated with
  increased long-term (approximately 17 years) risk of all-cause
  mortality that arises largely from an increased risk of cardiovascular
  disease (CVD) mortality.

This does not rule out that some subset of people with gout (patients with less severe symptoms?) might benefit in some way from an antioxidant effect, but in general gout is obviously not good for life expectancy.

The reason some gout patients live longer is beacuse they often get treated with xanthine oxidase inhibitors like allopurinol which have beneficial effects regarding vascular oxidative stress:
https://www.youtube.com/watch?v=v7DL24uca_I
Allopurinol has beneficial effects in several regards:
http://pharmrev.aspetjournals.org/content/58/1/87.long
The high level of uric acid in humans in general is due to the defunct gene for urate oxidase. That mutation appears to be a disadvantage for humans.

David, could you add an article citation instead of the youtube video. Even if the video is scientific, there is no guarantee that it is scientifically correct. You may look at  Dr. Rutledge's (one who posted the video) website or mail him to ask for a reference.

I wrote him without any reply. I also did some searching without any precise hit.


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Protein Conformation Modeling
I'm interested in learning about computational modeling in biophysics. I have heard some amount about people modeling proteins as a network of ideal springs to examine things like conformation switching. I was thinking it would be cool to try to make a very simple model of a small motif undergoing denaturation at certain temperatures while being stable at others.
Does anyone know of a good reference about protein modeling that would be understandable to someone who is decent with math/physics/programming but is in no way a mathematician/physicist/computer scientist?
Also, if you have a better idea of a simple project for me to practice computational modeling in biophysics (or even just any biology) I would appreciate hearing it.
Thanks

Well I sometimes use PDB files from proteins whose structure has been identified and study them. I use swiss PDB viewer software to do this and its pretty neat! I haven't looked at the biophysical data associated with a PDB file but I'm pretty sure they are there since you wouldn't be able to make the calculations and resolve the protein structure and confirmation without that kind of data. All you need is to download the software, go to Uniprot database and use the accession number of a protein you are interested in, see if its structure is resolved and either download the PDB file or use the accession number to download the file inside the software.


text:
Manifestations of open foramen ovale in adults
I read that foramen ovale opens in 30% of adults.
I do not know how much of these openings can then close again.
Probably, none.
It is not pathogenic if no symptoms.
It allows blood to enter from right atrium to left atrium (fetal), but from left atrium to right atrium in adults.
Assume that 50% of blood is doing so in adults.
This means that 50% of blood is not oxygenated.
Heart has to pump stronger to get some level of oxygenated blood as before.
Some thoughts about manifestations of open foramen ovale

hypertension
ischemic hypoxia
Clubbing
possible organ failures
higher risk for infections, SIRS and sepsis

Therefore, I think open foramen ovale can be a risk factor for myocardial infarction.
What are the manifestations of an open foramen ovale in adults?

As I recall the 30% of patients are only probe patent and therefore of little significance in terms of blood mixing under normal conditions where right sided pressure is lower than left sided (therefore RA will NOT flow into LA).  They are at higher risk of stroke from paradoxical embolism (which does cross through the PFO).  I'm not convinced by any of those bullet points as your original premise is off - a PFO will not cause a 50% shunt right to left.

I think what you may be thinking of is Eisenmenger's Syndrome though you should also read through the Cyanotic Heart Defects section.  Can you also clarify what you mean by "COPD-hypoxic-nails"?

@RoryM COPD-hypoxic-nail like curved nails caused due to hypoxia in peripheral system.

Clubbing?

A fully patent foramen ovale (pfo) is rare however a partial or small pfo is present in about 30% of the population.
Now the manifestations you described are partially correct. A pfo causes a left to right shunt in the adult whilst a right to left shunt in the fetus. In the fetus this is normal. In the adult, it is left to right because the left atrium is at higher pressure than the right. Due to this some of your manifestations are the wrong way round but still correct.
For example you mentioned hypertension, but presumably you meant systemic hypertension. It is more common at least in the early stages to get pulmonary hypertension. The pressures in the left atrium cause the pressures in the right atrium to increase when there is shunting. This is frequently seen when pressures in the left are increased due to factors like systemic hypertension. Coronary artery disease can also worsen the shunt and increase pressures in the right atrium and pulmonary pressures because the left ventricle can be stiffer.
Despite all this the more common presentation of a clinically significant pfo is right heart failure. Volume overloaded,the right heart dilates and fails. This will cause the usual presentation of right heart failure i.e. peripheral oedema, ascites and hepatomegaly.
Of course increased pulmonary pressures also causes strain to the right heart and can also cause right heart failure.
They then may go on to develop congestive cardiac failure and the exertional dyspnoea that comes with it. The inadequacy of the right heart can lead to excess strain to the left heart through a number of mechanisms that leads to it also failing. Dilation of the right heart can also lead to atrial fibrillation which in turn leads to stroke all being other possible presentations.
Cyanosis usually doesn't occur at least early in the disease as there isn't a shift from right to left (unoxygenated to oxygenated) but the other way round.
The severity of the pfo will lead to the severity of the clinical manifestation and how early it is picked up. Most people have routine checks of their heart (the murmur is usually pretty loud) so it is frequently corrected before any clinical disease manifests. In patients with small pfos they may never notice unless they become hypertensive or put strain on their heart during pregnancy. Yes they have a slight disadvantage as they lose some oxygenated blood but not anything noticeable.
If anything is unclear or you have more questions, please ask.

Thank you very much for your clear answer! I corrected the mistake in my question body. I am digesting your answer and will ask when I get new thoughts which I cannot solve myself.


text:
Appropriate statistical test for a student lab?
I am a HS Bio teacher and doing a microevolution lab involving candy. Essentially students use four candy types and push them together until one cracks (Nat Sel). They also do simulations of migration, mutation and genetic drift. They then calculate the "allele frequency" of each type per generation and look for changes. I want to have my students do a simple statistical test to see whether the change was significant or not from each evolutionary factor. I was going to do a chi square test, but someone told me that is not appropriate to this type of experiment.
So, can anyone confirm, is chi square inappropriate, and if it is..
Can anyone point me to a more appropriate test. These are high school kids with no stats background (and I have forgotten virtually all the stats I learned 20 years ago)...

It seems that you're looking for one test that would fit all situations encountered in evolutionary biology. This obviously does not exist. You should provide more information about what you want to test and describe the kind of data you have. And then, I am afraid the question might be off-topic as it is about statistics and not about biology. You may want to try to ask your question on crossvalidated.SE

You may have a point on the off topic bit, though I've already started, so.... :)   To clarify the lab a bit: Students press candies together over three rounds of "natural selection" (starting with 12 candies of each type- m&ms, skittles, etc- 4 types total). Survivors go on to the next round and replicate when the population gets below a certain number. We do another round where kids pour the candy on desks pushed together and some bounce in to the neighbors areas to represent migration, and another simulation for a bottleneck. Students then look at how much each factor affected the #s.

To choose the right statistical method (it is more than just saying "use the t-test") you need to think about your experiment. A good starting point is this figure from Bitesizebio:

There are two relevant articles on that website:

Let’s Talk About Stats: Comparing Two Sets of Data
Let’s Talk About Stats: Comparing Multiple Datasets

Probably also interesting is the definition of statistical terms:

Let’s Talk About Stats: Understanding the Lingo


text:
Can protein precipitate out in alcohol during DNA extraction?
In common lab sessions to extract DNA from strawberry or cheek cells, will there be protein contaminating the DNA extract in alcohol? If so, how can we prevent protein from precipitating out of the solution?

Yes, Ethanol can precipitate proteins during a DNA precipitation as well, although Acetone will be more efficient. Usually you do a proteinase K digest or a proteinase K digest followed by a Phenol/Chloroform extraction to avoid this problem. I was usually doing the later, I can post my protocol if you are interested.

A proteinase eg.proteinase K is usually added when extracting dna.


text:
coverage calculations approach for clipped reads
Experiment: deep sequencing for mutants in 700nt fragment.
the fragment of dna was preamplified by primers flanking the fragment followed by hiseq.
per base coverage was calculated by coverageBed -d -abam in.bam -b ref.bed > out.cov
Observation: two distinct peaks in coverage at the ends as below plot.. coverage vs positions

the peaks are made from reads having part of primers..thus also show soft clipping at ends..
there is a huge difference in the calculations if i include such reads And if I exclude them.
Question: is there anyone who knows how to handle such a situation?

It's absolutely not clear, how you prepared your library for sequencing, where the boundaries of your primers are and what exactly bothers you in this context.


text:
Why isn't the phosphoglycerate kinase reaction of the glycolysis pathway irreversible?
Step 7 of the glycolysis pathway is the conversion of 1,3-bisphosphoglycerate into 3-phosphoglycerate by the action of the enzyme phosphoglycerate kinase, resulting in the production of 2 ATP molecules (per glucose).
This reaction has a large negative value of ΔG (-18.5 kJ/mol). If reactions having large negative value of ΔG are classed as being irreversible, then why is Step 7 of Glycolysis reversible?

I like to think of it as saying "there's enough 3-PG around and so little 1,3-BPG around that we do actually have to consider the reverse reaction." As @AlanBoyd points out, in erythrocytes this reaction is actually pretty close to equilibrium. So we can't call this "irreversible" because the simplifying assumption applied to "irreversible" reactions is that there is no equilibrium (K is infinitely large).

The free energy change that you quote for the phosphoglycerate kinase (PGK) forward reaction is, of course, the standard free energy change (ΔG0') for the overall reaction. The standard free energy change is defined for all reactants at a concentration of 1M. Note that this value includes the formation of ATP -  the free energy of hydrolysis of 1,3-BPG would be much larger, and some of that energy is 'captured' in the ATP product.
The actual free energy change for the PGK reaction, ΔG,  will differ from this value because of the fact that the actual reactant concentrations are very far from the idealised 1M. You can find a Table here which compares, for each step in glycolysis, the standard free energy change with a true free energy change, calculated on the basis of cellular conditions in erythrocytes (also shown). You will see that for the PGK step the actual free energy change is 0.09 kJ mol-1 rather than the -18.9 kJ mol-1 that you quote in your question.
You can also see from the Table that there are only two reactions in the glycolytic pathway with large negative values for ΔG: those catalysed by phosphofructokinase and by pyruvate kinase. These are of course the two steps that are bypassed in gluconeogenesis because they are essentially irreversible.
So - your reasoning was correct, but it was based on the wrong ΔG values.
added much later
As pointed out in the comments, the 1st step in glycolysis also has a large negative value for ΔG and is also bypassed. Not sure how I forgot to include that!

"You can also see from the table that there are only two reactions...." Isn't 1st step of glycolysis having very large -ve ∆G? So there are 3 irreversible steps, not 2.

You have to look at the complete reaction including the cofactors. In general, you can drive a chemical reaction into directions which are not favorable by:

removing products from the environment (if they are gaseous for
example or react further)
having a huge excess of substrates (and thus making the back reaction
less likely to happen)
and by coupling the main reaction to a second, which provides the
necessary energy for the main reaction to happen

If you look at the reaction of 1,3-BPG to 3-PG this looks like the following (picture from Wikipedia):

The back reaction to 1,3-BPG needs ATP as a co-factor, so that the enzyme has the necessary phosphate group to add. The lysis of  the phosphor diester bond from ATP to ADP delivers the energy to make the reaction possible.
This reaction is the control point in either generating ATP (glycolysis), when there is little ATP and much ADP present or generating glucose (gluconeogenesis) when there is much ATP and little ADP. This makes sense when you consider that ATP is a rather instable molecule with its high energy diester bonds, while ADP is more stable.

ATP is not hydrolyzed in the reverse reaction. Instead, a phosphate carboxylic anhydride is formed. If you're trying to do a Hess' law type analysis then you need to consider the hydrolysis of 1,3-BPG, which is much more favorable than -18.5 kJ/mol (in fact 30.5 kJ/mol more favorable).

I just looked it up like this. Where does the phosphate group come from then?

ATP transfers a phosphate to the 3-PG to form ADP and 1,3-BPG. Hydrolysis is when water cleaves the phosphodiester, forming ADP and inorganic phosphate.

Ahh, got your point.

Not sure why you are calling it "phosphodiester" bond (which I think is what you mean by 'phosphor diester')...there is no ester here! Its just a bond between two phosphates, not a carbon-linked phosphate and a carbon-linked hydroxide :/


text:
Can oil be used instead of water in preparing wet mounts for microscopy?
Is there a reason that oil (e.g., vegetable or clear mineral) is not used to make wet mounts in microscopy? I am not referring to oil immersion technique but substituting oil for water in wet mounts in bright field microscopy.
The question is mostly about moss or mold, things that appear plantlike on a slide. The optical properties may be good and the viscosity, as with glycerine, gives a little depth to the slide. Maybe it causes some sort of distortion? I don't see this listed as a suggestion on microscopy sites.
Thanks.

One thing is that the slide must be viewed quickly, otherwise spores tend to bunch up adhere to other structures. FWIW.

Typically wet mounts are used to observe the mobility and behavior of microorganisms. A classical use for a wet mount would be to study something like pond water were you could see all the different organisms swimming around like they would in their natural environment. Oils are more viscus and would impede mobility and might impact behavior or even be toxic to the microorganisms.
If you were an olive oil manufacturer, and you thought you had some odd microbial contamination of your olive oil you might look at a drop of your olive oil between a slide and cover slip thus using an oil based wet mount like you are describing. You might also do this if you were studying the microbiology of an oil spill in water.
There is nothing saying you could not suspend a sample in oil. There may even be a unknown benefit of using this method in certain circumstances, that is waiting to be discovered.

Have you looked at a mold under the microscope using vegetable or mineral oil?

Can't say that I have. I may not be understanding your question. You mention depth of the slide... If you are trying to view them in more of a 3-D environment then a wet mount might be helpful. Try it with oil and see.


text:
Why doesn't the sperm die if there is citric acid and acid phosphatases in the semen?
While studying I read that sperm needs alkaline medium for its survival.But when I studied the composition of semen it revealed that semen contains citric acid which acts as a sperm nutrient along with fructose.It also contain acid phosphatases.So in such sitution how can the sperm survive?

Can you provide some sources?

From TextBook of Medical Physiology By Guyton and Hall.

Citric acid is a weak acid so in the context of a buffered physiological medium (semen pH 7.7) it will not cause any significant acidification. Acid phosphatases are enzymes with a pH optimum below 7 (as distinct from alkaline pho sphatases). Their presence has no implications for the pH of semen, although it is interesting to speculate why an alkaline fluid would contain an acid phosphatase.

Vaginal pH is ~4. The acid phosphatases likely have some function in this environment.


text:
What makes teeth feel sticky after drinking Coca-Cola?
I asked some of my friends and we all agree that teeth feel funny after drinking Coca-Cola. Other similar soft drinks also cause this effect, but this one most noticeably. It's like teeth become sticky and moving them against each other (by moving jaw) creates rubbery feeling.
What ingredient in this soft drink makes teeth like that?

I'm not sure where this question belongs, but as I'm interested in whatever ingredient causes this effect, I posted here. Not sure about tags, too.

Or chemistry - I'm not sure whether I'm unterstanding questioner right: Coke makes teeth soft - due it's phosphoric acid. After consuming Coke teeth may feel ... rough? sticky? (Note: Never ever brush your teeth right after drinking soft drinks/acidic fruit juice! You will brush your teeth away.)

sugar? :-) [saying that because I don't feel this way with coke zero, but I do with regular coke]

we don't have zero in our region, so I can't compare

I see the question as wildly off topic. We are not a site for everything about food; we only focus on how to cook food, and all effects of the food on the body are off topic. The last rule mostly saves us from healthiness crackpots, but even if your question is not so likely to attract them, we still don't have the expertise to answer it.

I could imagine that happens due the calcium in the saliva. This reacts with the phosphoric acid from the coke to calcium phosphate, which is more or less insoluble. I am not sure though, if this thread fits here.

Glucose and other ingested sugars have a natural affinity to bind to surface proteins on teeth (as well as many other proteins in tissues). This process is called glycosylation, and is expedited both by acidic environments (such as provided by the acidic soft drinks as indicated by The Last Word) or metabolism of adherent bacteria on the tooth surface (see one example). A discussion of oral cavity lubrication and how this influences tooth surfance glycosylation and biofilm formation has also been reported. The fuzzy feeling is a result of plaque formation. Plaques form as a byproduct of metabolism of bacteria on the tooth surfaces, that ingest and break down dietary sugars, and also secrete acids as a byproduct of this metabolism. The result, if left long enough, is plaque formation and eventually tooth decay. You can also notice this fuzzy feeling after a day or so of not brushing your teeth, as the bacteria have had a long time to metabolize the sugars ingested over that period to produce a plaque.

The sticky feeling comes from the sugars present in soft drinks. The sugar sticking to the surface of the teeth is then broken down into acids by bacteria and this affects the teeth. A list of the amount of sugars in different soft drinks can be found here. Also reading the dental decay section of Wikipedia gives the info that many carbohydrates are present including glucose, fructose and sucrose. On a dentistry forum (reference), it says that even artificial sugars can stick to teeth and get metabolized except xylitol.


text:
Can a tree survive if someone cuts all buds?
My thought was to cut all buds of a deciduous tree at spring and see if it can survive a year and develop new buds and leaves next spring. Assuming the tree is already grown and not a sapling.
If the loss of all buds would be to fatal, how many would a tree need to recover?


text:
Why did women historically have such a high mortality rate during birth?
Historically women had a relatively high chance of dying while giving birth.
At first thought it seems to me that this would be a disadvantage for the species for the obvious reason that a dead person can no longer give birth (and can't care for her offspring).
Is this outweighed by some advantages? I can imagine that there would be some evolutionary advantage to have the "weaker" women die during child birth and let the "stronger" ones live to produce more children with "stronger" genes.
Or is the high mortality rate in humans during child birth a result of civilization (pre-moderne civilization of course, with the general lack of hygiene/medical knowledge)?
What is it like for the relatively un-civilized tribes around the world?
How is it compared to other closely related mammals?

Dying during or shortly after birth has two main reasons: First is bleeding to death when the big blood vessels which support the developing embryo are not closed correctly or if the placenta gets stuck. The other are infections to wounds that occur during birth as tetanus infections. While the second is mostly a problem in less developed countries, the first still happens and can be very dangerous. The death rate went down pretty much, when doctors and midwifes started taking basic hygienic measures.

That's an interesting question. And it is also a common misunderstanding of evolutionary processes.
Thanks to @Chris comment, we know/can assume that high mortality rate is not a consequence of industrialization but has ever been before the era of modern medicine.
Women don't let themselves die in order to improve the species. Those women that carry a gene forcing them to commit suicide in order to improve the species won't pass on their genes, and in consequence no women will ever suicide in order to improve the species. In other words, altruistic behavior cannot appear and spread over time. This is the standard view of selection (and probably the good explanation in our case).
Now, I have to say that I lied in the previous paragraph! There is a field of study called social evolution which aims to study social traits. Social traits are those traits which influence not only the fitness of the individual carrying the trait but also the fitness of other individuals in the population. Theoretically all traits are somehow social traits! Typically altruistic behavior is among those social traits that cause a decrease (a cost) in the carrier fitness for an advantage (a benefit) for one or several other individuals in the population. There are several models (which are still debated in particular concerning the assumptions of these models) to explain the evolution of such traits. The most famous, most commonly used and most theoretically studied one is Kin selection/Hamilton's rule. You'll find some explanations about this rule on this post. The concept of population structure is key in the understanding of Hamilton's rule. Also important are the concept of levels of selection, which gives a possible explanation for the evolution of altruism, the concept of lineage selection, and finally the concept of reciprocity (but that doesn't make much sense in the current context!). Some people would not classify these models as I did, some would add other models, some would melt two models into one…
For one of these models to be correct we would need high lineage split and extinctions in human history which I don't think is really the case. Or we'd need that the death of a woman is particularly benefit to her family. I don't think first human were cannibals. Women were probably very often pregnant and males had to fight to be the father. So dying would probably not free much opportunities for the sisters and brothers…. One would need to write some equations and gather more information than what I have but intuitively I don't think that high mortality rate in women while giving birth is an altruistic behavior.

Human females have one of the worst  chidbirth experiences. This is because of our extremely high cranial capacity compared to the apes. This had an obvious evolutionary advantage and made us what we are today. However this creates problems as the braincase has to pass the pelvic cavity during childbirth. The wider hips in women compensate for this but still it is much harder than in case of other apes. Shorter women are in greater danger. Much easier for our closest cousins the chimps or gorillas. Compared to tribal women the civilised lineages have survived with more assistance...


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Are cell lines potentially dangerous?
More specifically, if a human subject was exposed to, say, a human cancerous cell line (via intravenous injection or through an open wound, for example), is it possible that they would develop any conditions associated with the cell line?

This post will probably interest you.

This is highly unlikely because the immune system would detect these cells and atack them as foreign. There is at least one case described in the literature in which a woman died of lung cancer after receiving a donor organ from a smoker. This is due to the fact that after transplantations people have to take drugs to suppress their immune system to avoid an immune reaction against the transplanted organ. This allows tumor cells to survive.
The same problem is true in research animals. For the transplantation of tumor cells you need mice with a severely deficient immune system (so called "SCID" (Severe Combined Immunodeficiency) mice) to allow tumor cells to grow. This is different when you work with viruses (like the human papilloma virus) which can cause cancer. Here you have to take appropriate safety measures.

This is largely correct, but there much more known cases, including one case of transmission from a patient to surgeon

Thanks for the addition. The case of the Tasmanian devil is also interesting, but these animals are genetically so closely related that the immune system is not detecting the foreign cells as not own.

@har-wradim.  Your reference includes specific examples of needlestick transmission in humans-would be useful if you expand your comment into an answer.

No, I don't mean the contagious cancers of devils and dogs. I mean the section, which starts with "Direct transmissions of cancers are not entirely restricted to animals..."

I read this as well. And it says that this is very rare and from the cases cited only one (the one of the surgeon) is from a person without an affected immune system. As I said: It is highly unlikely...

@Chris. (The needlestick with the cell line was also not immune compromised).  I'm not sure these reports  can say much about likelihood of growth after a puncture, other than the frequency of suitable puncture incidents is probably very low.  Imho, if anything, these reports remind us that there's probably plenty of room for improvement in our understanding of the immune response.


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Why are there ecosystems?
Why would things self-organize in such a manner? I'm a mathematician and I have no baggage in ecology or biology. If the question is too broad maybe someone can point me to formal sources where this type of issues are tackled.

The question is interesting. But maybe a bit broad indeed. Below are some examples of question that might be underlying yours. 1."why are there interdependencies between live forms?" 2."Why are ecosystems of this size (how much information)? There could have just one big ecosystem. Why is there such a spatial interdependence?" 3."Why is the relationship between organisms so (apparently) stable through time?" 4. "How is it possible that a species becomes adapted to its relation to another species (co-evolution)?" Let us which of these questions (or another I haven't listed) pick your interest.

The mathematical answer is "feedback loops, and a very long time for the initially chaotic system to settle into something vaugely resembling local stabiliity"

Basically, they don't. Ecosystems are pretty much either de facto, delimited by geographical boundaries, or defined by us. For example, an underground lake would be an ecosystem and it is organized in such a way for the simple reason that there is no communication between it and any other system.
Most ecosystems however, do communicate. For example, we call a desert an ecosystem but what of creatures living in the borders? That can survive both the harsh desert and the milder outskirts. Do they belong to the desert ecosystem? To the surrounding one? To both?
Basically, we divide nature into ecosystems because we can study them better that way. Species that form part of the same ecosystem tend to interact in one way or another and species from completely separate ecosystems tend not to. This is not some kind of rule however, it is simply the way we categorize things.
To take a different example, how would you define a city? Where does a city end and the countryside begin? Ecosystems are similar, there are seldom very clear cut lines separating them, they sort of bleed into one another.
In other words, your question is moot, ecosystems don't really self organize as such. The organization that does exist is between the different species and is an emergent quality of the complex system that is the ecosystem. Thinking of ecosystems, however, as distinct and well defined entities is generally wrong.

standard example of communicating ecosystem are the mangrove and the coral reefs. If one disappear, the other disappear too.

The definition of ecosystem here is missing, but if you mean "an inter-dependency of different organisms that all live in the same geographic region" then I think that competition and cooperation are big drivers of the establishment of these roles.
Some animals and plants are so interdependent that they evolve together despite being different species.  The hawk moths have terribly long probiscus which are co-evolved with flowers with deep cup shapes.

The flowers and the moths create more exclusive relationships - the flowers are more reliable food sources for the adult moths when other pollinators can't get to them and the flowers are more likely to succeed in pollination with the moth feeding of fewer kinds of flowers.  Cooperation of this nature tends to be show up spontaneously in the ecological milieu because of the utility and stability it can bring.
Competition is the other side to this side of ecosystem evolution.  Because living things reproduce to the point where nutrition and security are scarce (meaning that there isn't enough for every plant/animal) cooperation becomes an important advantage.

This may be an answer to why are there communities (although the data don't really support it) but an ecosystem is defined as the interrelated system of living and non-living components of the environment.  Thus, coevolution can only afford a partial solution.

actually cooperation is the answer, co-evolution is an example.

Fair enough but since you are only considering species interactions and not the impact of the abiotic environment you are describing community-level organization and not ecosystem level organization.

What non-artificial environments do not have ecosystems and interdependencies?  at some level the laws that biology works with are a reasonable explanation.

An ecosystem is a community of living things that exist in conjunction with and rely on nonliving things like a rock, a sandy beach, air, or water. Each organism has an ideal environment, and they may not be able to survive outside that environment. Thus you see a pond with fish living it in next to a forest with squirrels. The division and self organization is natural: the fish do not do so well on land and the squirrels have trouble surviving underwater so they stay in their own ecosystems.
If your question is more along the lines of "why is there a desert here next to a mountain with a forest on the other side of the mountain." This organization occurs due to chance mitigated by the physical laws of the universe based on things like planetary geography / climate, tectonics, and astrophysics.


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How does GC-content evolve?
Background
GC-content refers to the frequency of base pairs that are either C or G in the genome, or in other words the number of GC base pairs divided by the addition of the number of GC base pairs plus the number of AT base pairs.
$$GCcontent = \frac{N_{GC}}{N_{AT}+N_{GC}}$$
Question
How does the GC-content evolve and why does the GC-content differ between populations/species/lineages? Does it evolve under Genetic drift only? Under selection? Intuitively, I'd say that the ratio of the probabilities of mutating from A or T to G or C should be an important factor driving the evolution of the GC-content. Does it? Does the overall mutation rate influence the GC-content? What other traits/forces influence the evolution of the GC-content?

GC base pairs are more stable than AU/AT base pairs. I could imagine situations in which this plays a role, though I don't know if this is actually a relevant effect.

Yes it is probably an important factor. Note that if this difference in stability is the only thing that explain the evolution of GC-content, then I'd expect that very little variation would exist between species and the equilibrium point should be given by $$\frac{P_{CG \space |\space AT}}{P_{CG\space |\space AT}+P_{AT\space |\space CG}}$$, where $P_{CG\space |\space AT}$ is the mutation rate from $A$ or $T$ to $C$ or $G$.

I think the key work here is 'evolve'.  Overall GC/AT ratios change by mutations, whose rate is constant.  The probability that given a mutation event that one base will be substituted by another one has been modeled in several ways where the probabilities of different mutations may or may not be the same.
Overall the GC content will tend to close to 50%.  What causes GC rich genomes to become GC rich (60-70%) are that mutations to GC base pairs have selective advantages either in regions or in the genome overall that cause them to be retained. The mutation rate may be no different (or even lower) in GC rich organism (many of them are deep underground or deep underwater.  GC rich genomes occur because AT->GC mutations convey an advantage and they stick around.
The reasons that the GC content migrates away from 50% fall into two categories I will call entropic and selective.
By entropic I mean specifically that coding sequences for genes and other features such as binding sites on the DNA or other features such as centromeres, which will cause the overall ratio to vary from 1 because the sequence is constrained by the information it contains.  While coding regions have a ratio higher than 1, GC content tends to hover around 54%.  Eukaryotes have GC islands and etc, but this also does not overall change the GC content
So gene rich genomes and typical functional features of the genome do not really explain some of the spectacularly high GC contents found; up to the 70% range.  While the link above looks at GC bias in coding regions, its a given that any part of the genome that is merely a spacer between elements with specific functions will freely vary to GC if it is useful.
Selective factors for high GC content include high pressure and temperature environments for instance, which usually strongly bias to high GC content by this mechanism.  You can imagine how this works: high GC content genomes are thermodynamically more stable and can survive the extra molecular collisions of higher energy of those environments more readily.
GC rich genomes are not simple adaptations to live with.  All the genes for DNA oriented processes such as transcription, chromosome packing, DNA polymerase have to adjust a lot. As the organism adapts to hotter temperatures or higher pressures, each individual protein produced will have to also change to be stable and function in the new conditions.  As such, these changes happen only over long evolutionary times.  This is probably a good part of the reason why the archaea niches have not been superseded by eubacteria in all 1+ billion years since life has been on Earth.

Thanks for your answer. I am not sure I understand though. Let me try to rephrase differently and you'll correct me.Temperature or any factor that modifies the state_to_state specific mutation rate will modify the GC-content influence the GC-content and those factors are likely to vary from species to species explaining the differences observed.

Also the kind of sequence we consider (and the amount of DNA sequence that are of this type in a given genome) influence the GC-content. Coding sequences for example are not free to vary their information too much (usually it is only the third base pair that is free to vary). Did you say anything else? Did I understand?

I tweaked my answer. in short though, the mutation rate may be no different for these organisms, coding sequences can migrate to 70% GC.  its all selection in certain environments.  lmk if i'm making a good case here.

Everything is clear now! I got what I missunderstood ;) Thanks a lot.

Glad to hear it!  There is now a lot of research going on to identify processes which mediated and accelerate adaptation and therefore evolution.  On this level there isn't so much controversy I think...


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Heterozygosity under genetic drift
The wright-Fisher model of genetic drift is:
$$p_{ij} = \binom{2N}{j}\left(\frac{i}{2N}\right)^j \left(1- \frac{i}{2N}\right)^{2N-j} $$
,where $\binom{2N}{j}$ is a binomial coefficient.
From this equation one can infer that the expected heterozygostiy should decrease by $1-\frac{1}{2N}$ at each time step because:
$$E[x_{t+1}(1-x_{t+1}) \space|\space x_t] = (1-\frac{1}{2N})x_t(1-x_t)$$
I don't understand this equality. That might be very simple though! Can you help me making sense of it?
source

To derive it, first use that $E[x(1-x)]= E[x-x^2]=E[x]-E[x^2]$ and that $E[x^2]=\text{Var}[x]+E[x]^2$ to rewrite the left-hand side:
$$E\left[x_{t+1}(1-x_{t+1})\right] = E\left[x_{t+1}\right](1-E\left[x_{t+1}\right])-\text{Var}\left[x_{t+1}\right].$$
The equation for $p_{ij}$ is just saying that $2Nx_{t+1}$ is binomially distributed with $2N$ trials with success probability $x_t$, so $E[x_{t+1}]=x_t$ and $\text{Var}[x_{t+1}]=x_t(1-x_t)/(2N)$. (Note that $\text{Var}[\alpha x]=\alpha^2\text{Var}[x]$.) Plugging these values into the equation above gives the form you're looking for.

I feel close to the understanding! Can you help me understanding why $$E\left[x_{t+1}(1-x_{t+1})\right] = E\leftx_{t+1}\right-\text{Var}\left[x_{t+1}\right].$$

@Remi.b: If Var(x)= E(x(x-1)+E(x)-E(x)^2 = E(x(x-1)) + E(x)(1-E(x)) then -E(x(x-1)) = E(x(1-x))= E(x)(1-E(x)) - Var(x). See, e.g., math.ubc.ca/~feldman/m302/binomial.pdf –  daniel 11 mins ago

@Remi.b It should be: http://www.math.ubc.ca/~feldman/m302/binomial.pdf

You are welcome. Sometimes you don't see a tree in the wood :-)

My bad. It was just a cite for the variance. Sorry.

The notation at this site resembles that in your question but preserves the $\frac{x_t}{2N}$ notation for probability of selecting an allele.
$$E[\frac{x_{t+1}}{2N})(1 - \frac{x_{t+1}}{2N} )|x_t] = (\frac{x_{t}}{2N})(1 - \frac{x_{t}}{2N}) (1 - \frac{1}{2N})  $$
The expression $(\frac{x_{t}}{2N})(1 - \frac{x_{t}}{2N}) $ is the probability of heterozygosity at step $t.$
Your expression says that the expected heterozygosity at step $(t+1)$ is equal to the heterozygosity at step at $t$ multiplied by $(1-\frac{1}{2N}).$
For a population of size $2N,~(1-\frac{1}{2N})^{2N}\approx 1/e,$ so large populations are insulated from this effect and small ones may lose genetic diversity rapidly.
A typical explanation can be found here. The notation at this site condenses the expression $(\frac{x_{t}}{2N})(1 - \frac{x_{t}}{2N}) $ to $H_n$ and explicitly says it is $1 - F_n, $ in which $F_n$ is the probability of homozygous at step $n.$


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Which disorders are fully concordant?
I work in neuroscience, mostly Alzheimer's disease (AD), with some work in autism spectrum disorder (ASD). The work is in gene regulation and epigenomics. I'm familiar with monozygotic twin (MZ) discordance for AD and ASD and the methylome studies done in discordant MZ for those disorders. I began to become curious.
What disorders have never had MZ discordance reported in the literature? Even sickle cell has MZ discordant progression (Amin et al. 1991. Hemoglobin. 15:247-56). Do any disorders lack MZ discordance?

For those that don't know about it, could you expand a little on what MZ discordance is and what it means for a disease?

MZ discordance is when MZ twins do not have the same phenotype. Twin A gets Alzheimer's. Twin B does not. If Alzheimer's were fully genetic, both twins would get it, since their genomes are (very close to) identical. The higher MZ discordance for a disorder, the more effect environment is presumed to play. What is interesting is when a very Mendelian disease, like sickle cell, still shows MZ discordance on symptoms or a disorder with high genetic risk, like ASD, still shows non-patient/patient MZ discordance. My question means "Do any diseases have airtight evidence as being 100% 'genetic'"?

Complete concordance is generally rare because environment will always have some influence on the trait. In general all disorders that are not quite lethal are susceptible to environmental effects and buffering


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What happens when seeds are refrigerated before planting?
My son is doing a science research project at school, and he's chosen to research what happens when seeds are refrigerated before planting.
I cannot provide any information in regards to background research (I couldn't find any), but I want to know if refrigerating seeds before planting them will have any effect at all on the seed (so that my son's experiment can be interesting).
Thanks.

What kind of seeds? Some seeds require cold in order to germinate (search for "cold stratification").

@kmm Sorry - silverbeet seeds, but it would be best if a generalised answer would work.

That might be a good experiment.
I know that before planting bulbs you want to put them in the refrigerator or even the freezer sometimes.
In fact this process of cold treating seeds has a name: Stratification.
To paraphrase: some seeds become inactivated at higher temperatures like lettuce and delphinium.  You can place the seeds in medium and put them in the fridge or freezer for a day or two.
You can see how this makes sense.  The seeds have adapted to start growing when they are freezing because the timing results in the plants breaking ground as early as possible when the temperature is warm enough in the spring.
A quick search doesn't seem to imply that silverbeet needs to be stratified before planting.  The result might be negative, but there is definitely some good expectation that it makes a difference to some plants.

That's the main idea, apparently - that the silverbeet seeds do not need stratification - so my son's testing the results.

i think that's awesome.  nice project really.  Every year I judge science fairs and that one sounds pretty good!


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How the lungs clear themselves?
Looking at my computer's fan I can say that a lot of dust is collected on it not less dust should be collected in the lungs, not to mention some inhaled parts of food.
How the lungs clear themselves from dust, smoke, food particles?

nuhcole is mostly correct.
Airborne particles first pass through the nasal passageways and/or mouth and throat and many are caught, but those that enter the lungs become trapped in mucus.
Your cilia act like a constant escalator, bringing up that mucus from your lungs 24/7.  You reflexively swallow it without even realizing it.  That is why when you are healthy, you might not even notice.
If you are sick (or asthma/allergies), more mucus is produced.  That is when you may notice the increased quantity coming up, and may need to cough to bring more up.
If your cilia are damaged (like in smokers), then mucus does not clear well from the lungs. In this case, people must cough more in order to bring it up.

Our respiratory tract is lined with cilia, which are hair-like structure that extend from the outside of the cells. They wave back and forth and act like brushes to catch dust particles before they enter the lungs.
Some particles do get past these cilia and enter the lungs, however. The lungs will secrete mucus that collects the dust. You then cough up the mucus to get rid of the dust particles.
The mucus your lungs excrete also help against pathogens you inhale. Bacteria and viruses are also collected in the mucus, and then removed via coughing. This is why you may cough up phlegm when you're sick.

I do not cough when I am not ill.

@Anixx of course you do, try going into a dusty room and breathing deeply, you will sneeze or cough.


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Does Science Say That We Should Die?
Excluding situations where you die from accidents, the main reason for death is -generaly- diseases.
And usually it is about an organ which becomes "tired" after many years. These results are all from experience and statistics:

But I've never heard of any study that said: "people can't live longer than x age because the heart can't live longer than that".
From my point of view, I think it's us who control the way we live and consequently someone can live longer than the other. For example, smokers die at an early age.
But even the oldest person in the world, lived for 122 years and 164 days. For me this isn't enough. It seems that someone can't control his age after all.
Basically my question is: Does science provide any limit that a person isn't able to live more than it? For instance can someone live more than 1000 years?

Note: I don't think someone is able to do this because simply even our healthiest habits are not "so" healthy. But imagine someone who doesn't live like any of us as humans, i.e. Can have a very healthy and natural life

Quoting a great biologist Peter Medawar :

It is by no means difficult to imagine a genetic endowment which can
  favor young animals only at the expense of their elders; or rather at
  their own expense when they, themselves, grow old. A gene or
  combination of genes that promotes this state of affairs will, under
  certain numerically definable conditions, spread throughout a
  population simply because the younger animals it favors have, as a
  group, a relatively large contribution to make to the ancestry of the
  future population.

From Why We Get Sick :

Imagine that there is a gene that changes calcium metabolism so that
  bone heals faster, but the same gene also causes slow and steady
  calcium deposition in the arteries. Such a gene might well be selected
  for, because many individuals will benefit from its advantages in
  youth, while few will live long enough to experience the disadvantage
  of arterial disease in old age. Even if the gene caused everyone to
  die by age 100, it would still spread if it offered even minor
  benefits in youth. This argument does not depend on the prior
  existence of senescence. Other causes of death—accidents, pneumonia,
  and all the rest—are sufficient to reduce the population at older
  ages. Nor does the theory depend, like Haldane’s, on cessation of
  reproduction.

The message I am trying to get across is that - As organisms are like vehicles which carry DNA and DNA just "madly" wants to replicate itself and pass itself from generation to generation, Natural Selection will favour those traits that maximise reproductive success. These may be traits that provide maximum benefit in youth but cause gradual damage and lead to senescence and death.
You could also think like this - Every machine has wear and tear and must be thrown away after it is irreparable. Same is with our body, it is the most beautiful machine in the world but it is also subject to the same wear and tear.
Also there is the end replication problem. See telomeres if you dont know what I am talking about. There is a limit to number of times a cell can divide.
So all in all I would say that there is a biological limit - a certain age up to which a person may live.

If you want more examples of such traits see this where the chapter on  ageing from the book Why We Get Sick is available.