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Why are there no organisms with metal body parts, like weapons, bones, and armour? (Or are there?)
Reading this question, Why are there no wheeled animals?, I wondered why no organisms seem to make use of the tensile and other strengths of metal, as we do in metal tools and constructions. I am obviously not talking about the microscopic uses of metal, as in human blood etc.
Why are there no plants with metal thorns? No trees with "reinforced" wood? No metal-plated sloths? No beetles with metal-tipped drills? Or are there?
I can think of some potential factors why there are none (or few), but I do not know whether they are true:

Is metal too scarce near the surface?
Are there certain chemical properties that make metal hard to extract and accumulate in larger quantities?
Is metal too heavy to carry around, even in a thin layer or mesh or tip?
Can metal of high (tensile etc.) strength only be forged under temperatures too high to sustain inside (or touching) organic tissue, and is crystallised metal too weak?
Are functionally comparable organic materials like horn, bone, wood, etc. in fact better at their tasks than metal, and do we humans only use metal because we are not good enough at using e.g. horn to make armour or chitin to make drills?

As a predator, I would like to eat a lot of vertebrates and save up the metal from their blood to reinforce my fangs...

A bonus question: are there any organisms that use the high electric conductivity of metal? Animals depend upon electric signals for their nervous system, but I do not think nerves contain much metal. The same applies to the few animals that use electricity as a weapon.

one possible answer is that metals have to be molten and forged.. they dont crystallize by deposition..

@WYSIWYG: Never? So things like pyrite either do not exhibit the desirable properties of metals, or they crystallise under high temperatures or pressure?

Homing pigeons?

Oh, and caddisfly larvae, in symbiosis with French artists

On chemistry SE, I've asked a similiar question (or rather a question inspired by this train of thought): http://chemistry.stackexchange.com/questions/4009/is-it-possible-to-crystallize-a-solid-ingot-of-metal-from-an-acidic-aquaous-so

@mart: Ah, cool!

Link to a previous Q on magnetic bacteria

Almost all metals corrode, and non-living parts of the body (as horn), cannot be renewed. That's all I think.

@TomášZato: Hmm corrosion is an interesting factor indeed. But there are plenty of metals that don't corrode very much, like gold, silver, aluminium, stainless steel...
Horn can be renewed, as in our finger nails and hair. Couldn't metal body parts be renewed in a similar way? Even teeth can be renewed in a way, as sharks do.

Gold and silver are rare, aluminium reacts with water upon acidic conditions and stainless steel oxides to produce highly toxic waste.

@TomášZato: You may be onto something; care to post that as an answer?

Steel really isn't something that is going to happen naturally... :p

@theforestecologist: Why not?

Beaver teeth are heavily impregnated with iron, which makes them stronger and tougher. http://www.dentalproductsreport.com/dental/article/new-study-finds-beaver-teeth-could-provide-insight-human-tooth-decay

Some molluscs incorporate iron into their radual https://www.researchgate.net/publication/44120196_Radula_synthesis_by_three_species_of_iron_mineralizing_molluscs_Production_rate_and_elemental_demand

@John: Ah, very interesting; hence their reddish colour! But the article mentions resistance to corrosion, not tensile strength.

In molluscs and beavers it also results in increased hardness, which makes them more wear resistance. Incorporating iron in small quantities will not do much for tensile strength. Bone already has a quite high strength, comparable to magnesium alloys. Metallic iron is not very chemically resistant and would quickly breakdown. If it did evolve I image a defensive enzyme from plants to encourage corrosion would be easy to evolve.

@WYSIWYG At risk of getting really off-topic now: metals don't have to be forged into a shape, they can be cast or machined instead. (Sorry, I couldn't stop myself and yes, I realise I have a problem.)

Your bones are largely made of metal, calcium is a metal as is potassium sodium and a dozen other elements in the body.

@John: All right, but I was looking for ways in which we use the tensile strength of metal, as when metal is present in the form of a grid/roster; I believe that is not the case in bones? See my full Question above.

The hemoglobin in your blood contains four iron atoms per protein, whereas the hemocyanin in a number of invertebrates contains two copper atoms.

Ad "reinforced wood": cellulose fibers have comparable tensile strength to steel "cabels" of equal diameter. Cellulose fibers in wood are just really really thin (1 fiber = 36 molecules) and arranged in a way that allow cell growth.

@BagiM: Hmm but could those be used in the specially useful ways that metal can, in tools and weaponry?

There are some cases of bio-metallic materials, as hinted at by the comments. But these are relatively small amount of metal.
It's not that there is a lack of metal available. Iron in particular is the fourth most common element in the earth's crust. Most soil that has a reddish color has iron in it.  There are several reasons you don't see iron exoskeletons on animals all the time.
Firstly, metallic iron (in chemistry terms, fully reduced, oxidation state 0) has a high energetic cost to create.
Iron is the second most common metal after aluminum on the earth's crust but it's almost entirely present in oxidized states - that's to say: as rust.  Most biological iron functions in the +2/+3 oxidation state, which is more similar to rust than metal.  Cytochromes and haemoglobin are examples of how iron is more valuable as a chemically active biological agent than a structural agent, using oxidized iron ions as they do. Aluminium, the most common metal on Earth, has relatively little biological activity - one might assume because its redox costs are even higher than iron.
As to why reduced biometal doesn't show up very often, inability of biological systems to deposit reduced (metallic) metals is not one of them.  There are cases of admittedly small pieces of reduced metal being produced by biological systems. The Magnetosomes in magnetotactic bacteria are mentioned, but there are also cases of reduced gold being accumulated by microorganisms.
Bone and shell are examples of biomineralization where the proteins depositing the calcium carbonate or other minerals in the material are structured by the proteins to be stronger than they would be as a simple crystal.  most of the examples here have very little or no metal, but rather minerals like the Chrysomallon squamiferum cited by @navyguymarko and @loki'sbane here.  The Iron Sulfide looks metallic but it is a mineral, akin to a bone.
While iron skeletons might seem to be an advantage, they are electrochemically unstable - oxygen and water will tend to oxidize (rust) them quickly and the organism would have to spend a lot of energy keeping it in working form.  Electrical conductivity sounds useful, but the nervous system favors exquisite levels of control over bulk current flow, even in cases like electric eels, whose current is produced by gradients from acetylcholine.
What's more, biological materials actually perform as well as or better than metal when they need to.  Spider silk has a greater tensile strength than steel (along the direction of the thread). Mollusk shells are models for tank armor - they are remarkably resistant to puncture and breakage.  Bone is durable for most purposes and flexible in addition.
The time it would take for metallized structures to evolve biologically are likely too long. By the time the metalized version of an organ or skeleton got started, the bones, shells and fibers we know probably have a big lead and selective advantage.

mineral deposition is different from free metal deposition and thats what i was implying.. deposited metals hhave to form metallic bond else they'll remain colloidal

While minerals tend to include oxides of elements and metals are different a chemical state, I'd just say that the creation of reduced metal structures could be created by similar sorts of genes.  they can structure the lattice into layers and introduce defects of specific amounts.  i would say that they represent a degree of control that genes could exert on the structure of deposited minerals if necessary.  I see no reason that reduced metals could be built with less control over their structure.  If so, then there are probably other reasons you don't find organic metal structures often.

Thanks for your answer! So you are mainly saying the energetic cost of building and maintaining metal constructs is too high for organisms to be a good investment compared to other materials.

yes - I should have just said this :)   I think its the cost relative to other minerals and organic compounds is high for what you get from using metal.  Metal based tissue could have a hard time healing after damage too.

Beavers and molluscs both incorporate iron into their teeth/radula for increased strength and resistance. there is a high metabolic cost however https://www.researchgate.net/publication/44120196_Radula_synthesis_by_three_species_of_iron_mineralizing_molluscs_Production_rate_and_elemental_demand

@John: Very interesting article. One of the other answers also mentions molluscs. But a comment says they use oxides or other compounds, not metal rosters, so I don't think metal's tensile strength is used?

teeth and shells are nanocomposites they exploit a mixture of materials with various properties, and many iron oxides are plenty strong, hematite comes to mind. in these cases they want hardness and chemical resistance, which metallic iron would not give you.

Gold is the ONLY actual example of a material that is metallic in and of itself being formed by biology, and it doesn't seem to be used. All the other examples in biology that I know of are oxidized rust essentially. Even the "copper" bloodworm teeth which are called "metallic" are just atacamite and organic polymers and maybe other minerals.

A few minor points to add to shigeta's excellent answer:
Biological enzymes don't work well on metals.  Some often incorporate metals (see chelation) but elemental atoms aren't easy to process.  For one, a large molecule would be identical everywhere, so cleavage, for example, would be indiscriminate and just leave a bunch of tiny tiny atoms.
More to the point, once an organism incorporates metal there certainly isn't a lot it can do about that.  A lot of shell-based organisms swap out their shells because of the inflexibility of those designs, and metal would be no different.  It's difficult to grow when you're encased in a self-made iron maiden.

Thanks for your additions! I'm not sure I understand all the chemical terminology, but you seem to be saying that there are chemical reasons why metals are hard to work with for organisms, don't you? // As to metal shells, they could be segmented, or the metal could only cover certain vital areas in patches, or the metal could be used in joints, or other body parts...

good point Amory.  I think the metal could be replaced/resurfaced as calcium carbonate is, but it would degrade much more readily because molecular oxygen is everywhere too.

A self-made iron maiden would have organ-puncturing sharp spikes on the inside. A plate mail would be a better approximation, but not even these are form-fitting in the chest area. Another useful comparison would be to look at how the brain can't grow after birth because it's encased in a solid layer of bone from all sides.

There are good reasons why tissues/structures with a very high metal content might cause problems (I defer to the other answers here).
However, I am aware of one other example: some molluscs incorporate high concentrations of iron into the points of the radula (basically a ribbon of teeth, used for grazing). This is especially important for grazing molluscs, as they essentially make a living by scraping a thin layer of microalgae directly off the rock surface.

That is very interesting, a nice counter-example! So these molluscs use iron to make their radula stronger. Now I wonder why not many other animals or plans to this too...those molluscs don't happen to live in an en environment rich in metals?

Good question. These molluscs (primarily chitons) occur all over the world, so it's not a question of some local abundance of iron, but I guess it's possible that their rock-scraping habits give them quite a high dietary intake of iron (particularly on non-sedimentary rocks). However, I think it's probably more to do with their need for especially durable teeth, which outweighs any physiological/chemical costs associated with iron impregnation. It's just one of many solutions in the animal kingdom for dealing with tooth wear.

Right! It is interesting to note how humans have fairly recently switched away from metal teeth. I think dentists now use ceramic materials.

@Cerberus according the linked article, their teeth are not metallic, but of iron oxide (rust, a ceramic meterial).

@Anixx: Hmm you're right, they use oxides, not pure crystals. Perhaps it is still relevant, if metallic oxides are still harder than most materials?

some beautiful pictures and the slug looks awesome.  the iron in references are Iron Sulfide, which is a mineral form of Iron(II) its not really metal in the sense that the iron in our bodies is iron, nor is the calcium in our bones metallic (Calcium can form a metal, but its a mineral in our bones. )

Well there is the common Bloodworm (Glycera dibranchiata)which people use for fishing bait. The animals are unique in that they contain a lot of copper without being poisoned. Their jaws are unusually strong since they too contain the metal in the form of a copper-based chloride biomineral, known as atacamite.
http://www.sciencemag.org/content/298/5592/389.long
And unlike the clamworm (Nereis limbata), whose jaws contain the metal zinc, the copper in the mineral in the jaws of Glycera is actually present in its crystalline form.
http://www.pnas.org/cgi/pmidlookup?view=long&pmid=12886017
It is theorized that this copper is used as a catalyst for its poisonous bite.
(I got this from Wikipedia)

Evolution is incredible.

Great example! So the copper serves a double purpose: it makes the jaw stronger, and it works as a catalyst. Smart worm.

Looks like some parasitoid wasps have zinc coated barbs on their ovipositors which may function to help them bore through wood and lay their eggs.
Here's the blog entry about it on IFL Science, and the original article:

parasitoid ovipositor specimens had a weight percentage of zinc of 7.19±3.8% (N=42) in the tip regions, which was significantly higher (P<0.05) than that in pollinator and parasitoid remote regions (<1%; N=10).

Kundanati and Gundiah (2014) Biomechanics of substrate boring by fig wasps. J Exp Bio 217: 1946-1954

https://en.m.wikipedia.org/wiki/Scaly-foot_gastropod
Gastropod that incorporates greigite, pyrite, and graphite on it's shell and foot.
Due to the large quantities of these compounds in dissolved form surround the hydrothermal vents.
Speculation for purpose: the shell is extremely resilient, the metal does improve this greatly. Though whether evolution deemed this adaptation necessary because of an abundance of strong predators, or as a means of detoxification of the injested compounds, is unclear.
The three populations of these snails have varied compositions, one which even being magnetic, due to the different compounds produced by the vents.
Appologies, here is non wiki http://www.esa.org/esablog/research/iron-plated-snail/

Very interesting example! It does seem to be a compound, but it's probably still the iron atoms that make the compound strong?

Digging a little deeper into the references there is more speculation than answers.

Out of the three independent populations, the Solitaire Fields population, does not utilize the granular greigite in scerlites at all. Original hypotheses theorized that the granular pyrite(Dodo field) and granular greigite(Kairei fields) was utilized by the Gastropod to improve defense. Further analysis concluded it is not the compound alone, interfacial geometries, layering, and the incorporation of other materials do aid in penetration resistance, energy dissipation, mitigation of fracture and Crack arrests, and other beneficial traits. Predators include, cones nails and seafaring crabs

I belive it is the structure of the greigite molecules that aid more in the scerlites and shell strength. Shell using layering and scerlites arranged in a shingling manner resembling scale mail. Furthermore, Greigite is only a 4-4.5 on Mohs hardness scale, by itself is not all that hard, comparative materials(Flourite, Nickel, Iron, Steel). Arogonite(polymorph of calcium carbonate) makes up the majority of the tertiary layer of the shell(core), hardness 3.5-4. Secondary layer composition periostracum, fleshy material. Primary layer composition pyrite, greigite, or none(solitaire).

Hmm so...the effectiveness of the shell may not be the result of the typical tensile (or other) strength of metal after all? P.S. I'll believe that crabs might crack shells, but I don't imagine a cone snail could penetrate or crack any half-decent shell anyway, don't you agree? Or does it have special, boring radulae that can do so?

The metal does help greatly for the 2 groups that take advantage of it. My comment on how the 2 minerals are not that hard was addressing that a hardness of 4-4.5 is just under average. Steel has the same hardness. Apatite has a hardness of 5, whivh is harder than steel, and hydroxylapatite is the main component of tooth enamel and bone. For the snails though the greigite and pyrite are harder materials than the shell materials alone. So combination of the metals and Arogonite, and the way they are structured, aid in the tensile strength, heat dissipation, and reflective abilities of the shell

But in other animals the bone and tooth are a harder material than either of these 2 iron compounds.

OK that's clear. I wonder whether hardness or tensile strength would be more interesting for shells: against drilling predators, you want hardness, but against crackers (like crabs), you want tensile strength, don't you?

im no biologist, but while not commonly cosidered, calcium IS a metal, so technically skeletons count.
additionally, while not technically a metal, limpet teeth are quite impressive.
http://www.bbc.co.uk/news/science-environment-31500883

Quite interesting, thanks for the link! As to calcium, while bones are strong, do they actually contain calcium in the form of a metal grid/lattice? I think not?

bones are mineral composition of a Calcium Phosphate called hydroxyapatite

Barden et al (2017) have discovered an extinct species of ant (hell ant) that was alive 95 million years ago that had naturally occurring metal mandibles. Mandibles on ants are essentially the same as fangs on spiders or teeth on humans.

Have you ever looked up the scaly foot gastropod? It uses iron as a form of body armor. Literally scale armor on It's foot.

Oops sorry I just realized someone posted this information already. My apologies.

Now just imagine if the snail had weaponised love darts lol. Metal tipped spears to fight back with instead of reproduction. Yes I know about the conch and it's venomous attack. More proof that nature is just as alien as anything we can imagine.

Your answer provided this great picture, and you explain more clearly how it actually uses pieces of (partly) metal as scale armour on its foot; the other answer was mostly about its shell. A bit more of an explanatory text would improve your answer, though! Incidentally, I wonder why it has a greenish hue, while iron is usually reddish?

yeah i like it too!


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What's the difference between naive and memory B cells?
I understand that when naive B cells are exposed to antigens, they become memory B cells, but what is the functional difference between the two? I've looked at the quite a few article on B cells, but none of them stated the difference clearly enough for me to understand.

The main difference is that memory B cells start an immune reaction much more effective and faster than naive B cells. The reaction is also specific towards the antigen.
The memory B cell has a specific membrane receptor for an antigen. It produces specific antibodies only when exposed to the antigen.
References:

Tangye SG, Avery DT, Deenick EK, Hodgkin PD. Intrinsic differences in the proliferation of naive and memory human B cells as a mechanism for enhanced secondary immune responses. J. Immunol. 2003 Jan 15;170(2):686-94. PubMed PMID: 12517929.
Wikipedia contributors, "B cell," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=B_cell&oldid=612990219 (accessed June 26, 2014).

Naive B cells have not yet been trained by the immune system to recognize specific antigens -therefore the term "naive". Prior to antigen exposure, they must be trained in the bone marrow to recognize certain antigens.
Memory B cells, on the other hand, are formed after antigen exposure and clonal selection. As stated above, they have specific receptors for antigens and can produce antibodies.

They are actually not trained in the bone marrow, but in germinal centers in the lymphatic tissues.

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Is kissing a natural human activity?
The word natural here is meant in contrast to it being a sociological construct.

Is kissing in all its forms something natural for humans? Is it instinctively erotic? Or is it just a conventional form to show trust and intimicy, i.e. the association besically just comes via a social means?

Because the only other advantage of this mouth to mouth contact I could see is maybe for the immune system.

It's probably one of the arbitrary reward systems for actions beneficial to reproduction. Social contact is advantageous for reproduction, so rewarding it makes sense. Kissing may just have developed because the lips are full of sensory receptors for food-proofing purposes already; so it's not a big effort to use them for additional purposes.

Wikipedia actually has a note on the evolution of kissing.  They point out that there are grooming behaviors such as licking and social behaviors like dogs touching noses in many species even insects.  They note that it is not decided at all whether kissing is learned or from some sort of instinct.  They also mention that its reminiscent of feeding behavior common in birds (and other animals) where food is pushed down the throats of young.  (try thinking about that next time!)
I seem to remember though that there are some culture which do not kiss. with their lips at least. This would favor kissing as a learned behavior, but these cases are very rare and isolated peoples and it might be simply a taboo to talk about kissing with researchers or at all, which is a hazard of that sort of work.  In addition, bonobos, one our our closest primate cousins, do kiss frequently with the lips, as a social and intimate gesture and the parallels with most human cultures are difficult to ignore.

And here I thought my wife was making up the "Eskimo kiss" thing.

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Reference sequence for defining single nucleotide polymorphisms
Single nucleotide polymorphism (SNP) or genetic variation in general, by definition are relative to a reference sequence. When we talk about databases of SNP as in ("dbSNP—Database for Single Nucleotide Polymorphisms and Other Classes of Minor Genetic Variation", or "A map of human genome sequence variation containing 1.42 million single nucleotide polymorphisms" -- titles of well known research papers), what is the reference genome? Similarly for defining a "SNP Map/Profile" of a person (in medical genomics), what is the reference genome sequence? Is there a de facto reference, or is it context dependent? There is a sentence "Scientists are trying to identify all the different SNPs in the human genome" at http://www.cancer.gov/cancertopics/understandingcancer/geneticvariation/page36 -
what is the reference genome here?

the reference genome used is usually the hg19 (UCSC) or GRCh38(NCBI). For population based studies involving something like an endemic population a context dependent reference can be used.

dbSNP actually indexes itself against several reference genome builds including hg19.  you can see this in the ssID records  - we use the bulk downloads and you can see them there as well.
Any difference with respect to any two genome builds is really a variant.  You can see this in the case of tri- and quad- allelic variants. There are cases where entire sequences lengths are added or removed compared to a reference genome build.  These are called insert/delete variants, which can contain short or single nucleotide variants as well.
will try to fill this out a bit more later... quick response here.

SNPs are discovered not only in whole genome sequencing projects. It's just a type of molecular markers.

certainly this is so.

I don't see your point. If we take e.g. the definition from Wikipedia:
SNP "is a DNA sequence variation occurring when a Single Nucleotide ... in the genome ... differs between members of a biological species or paired chromosomes",
there is no place for reference genome. SNP is just a variable position with (commonly) two alternatives in individuals of the same species. In whole-genome sequencing projects some SNPs can be discovered (namely those which are in heterozygous state), but definitely not all.
One can investigate SNPs and/or use them as genetic markers irrespective of the availability of the reference genome. That's the way one does it for non-model organisms - e.g. utilizing RAD Seq: you discover SNPs simultaneously with genotyping.

How is the location/position of genome where we look for variability/alternative defined?

If you are talking about coordinates, than they are defined either by location on the reference genome, by the location on the genetic map or not defined at all.


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Can children restore brain cells?
By "children" I mean young people at the age of 10 or lower.
I know that the adult brain cannot restore brain cells, but what about children? I mean, the brain must develop from a few cells to a 90 billion cells somehow, when do we lose this ability?
I'm also interested in cases when a child gets hit into the head (concussion). Can the damage  be fixed over time?

There is a misconception in your question about the absence of neurogenesis in adults. It is definitely present in adults as has been shown by a host of recent studies. If you want some technical details on neurogenesis or a question about what exactly changes in children at the end of critical period.

@Artem Kaznatcheev: true, however neurogenesis and regeneration are not necessarily the same thing (i.e.: neurogenesis does not imply regeneration, although the opposite is obviously true).

@nico I didn't mean to suggest that they were, otherwise I'd submit my comment as an answer. I was just going off a vibe I got from the question. I don't know anything about regeneration and so did not got beyond a comment.

@Artem Kaznatcheev: surely I was merely pointing that out in case it was not completely clear especially for the OP :)

Just a note, the definition of the word 'children' is 'pre-pubescent'. It is frequently misused to refer to adolescents and even post-adolescent young adults colloquially, but in scientific settings you should be safe using it properly.

I am not an expert in neurobiology, but this is what I have been able to find:
In general, the PNS (peripheral nervous system) does have remarkable neuroregeneration capabilities. However, the CNS (central nervous system), which includes the brain, has extremely limited neuroregeneration abilities. However, there are some interesting examples of CNS recovery:

Children under six who undergo, unfortunately, a hemiectomy, whereby one half of their brain is taken out, are able to regain almost normal function because of the brain’s ability to rewire and literally take over the functions of the missing other half of the brain.

I am guessing one thing that can explain this is that in children, the CNS is still developing, and so if there is damage, the CNS can just entirely replace damaged parts (this might be different than "fixing" which is required in adults).
Again, I am not an expert on this and would be glad to hear a neurobiologist's opinion.

Would be nice to find a proper source for the hemiectomy quote

@nico here is one relevant reference I found: http://brain.oxfordjournals.org/content/126/3/556.long

Hemispherectomy is prognosed with good outcome results in kids, but not because they re-generate all the lost neurons. The example is an interesting one, but not so relevant in the light of the question.

Speaking to Artem Kaznatcheev's comment, it is not true that the adult brain is post-mitotic.
Dr Bernard Rabin has shown is his scientific research, often in collaboration with and funded by NASA, that the adult brain is not post-mitotic, meaning that cell growth and division does occur. The primary focus of his work is to examine the relationship between high-energy irradiation of the brain (such as on a long-term space mission, say to Mars) and normal aging, and how diet can affect that age-mimicking decline. A list of papers he has published in the field of the aging brain is here.

As to your first question: Also adults can regenerate brain cells, albeit in a few restricted, specific regions of the brain. A continuous level of neural regeneration occurs throughout adult life in at least two locations. The first is the subgranular zone of the dentate gyrus of the hippocampus, the region of the brain involved in learning and memory. The other is located in and near the anterior lateral ventricular wall of the cerebral cortex. While neurogenesis in the adult hippocampus is relatively limited, the subventricular zone is thought to continuously replace interneurons in the olfactory bulb (Clarke, 2003).
As to your second question: a single blow to the head is generally considered not much of an issue. It is repeated injuries to the brain that kills neurons. For example, a knockout in boxing seems impressive and damaging to the brain, but it is in fact the repeated hits to the head, e.g. during the course of numerous bouts of boxing (or American football), that irreversibly injure the brain. A single blow will likely be dealt with by healing processes of the neural damage. Multiple blows will eventually kill neurons. As to whether those killed cells are regenerated; perhaps a few, as it is known that brain damage can result in the attraction of new cells, but it is the plasticity of the brain that will play the biggest role in the healing process, i.e., lost functions are redirected to other parts of the brain, but not regenerated.
Reference
- Clarke, Bone Marrow Transplantation (2003); 32: S13–S17

This isn't quite the same; however, children can have parts of their brains removed and then the remaining parts of the brain can take over for that removed part. There are not also lasting effects of this even.

There is a neurosurgeon by the name of Benjamin Carson who has done a procedure called a hemispherectomy. A hemispherectomy is the act of removing one side of the person's brain. This procedure can only be done in children under the age of either 10 or 12 (I am so sorry, I can't remember right now).

The reason this can only be done in children is because the side of the brain not removed is able to take over for the removed side, this cannot occur in adults.

As far as I recall, the age cut off for the procedure you're describing is closer to 1-2 than 10-12

@RoryM sorry about that. I guess I definitely didn't remember the age:)

This answer can be ascribed to neuroplasticity alone (existing cells take over other functions).


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Is eating salt dangerous for the brain?
I read somewhere that eating a lot of salt will raise blood pressure, which will in turn damage brain tissue. This is because water molecules gather around salt ions, thus making it harder for the body to remove the excess water from the blood.
Is this true? How much salt is actually dangerous?

This thread may be helpful.

Eating salt raises blood pressure that is true.  Increased blood pressure is a risk factor in a variety of diseases.  Sodium however is also essential in the diet, as sodium and potassium are the key elements involved in generating action potentials in neurons.

I have recently read about a murder by force feeding salt to a kid. Tragically, the kid went crazy and then died...See also http://en.wikipedia.org/wiki/Hypernatremia and http://www.hawaii.edu/medicine/pediatrics/pemxray/v3c14.html

Good question. The answer really depends. There is a normal range of plasma sodium concentration that ranges from about 135 to 145 mM. You body has multiple endocrinologic and neurological mechanisms to closely regulate this concentration. So even if you went out and ate a ton of salty snacks, your body would still keep your plasma sodium concentration within this range. A salt concentration much lower or greater than this can start to cause problems depending on how fast it happens and how far from the normal value. Brain surgery patient are often given lots of extra salt to keep their brains "salty" as this protects from cerebral edema and counteracts salt wasting that often occurs with brain injury. However, the opposite or very high sodium concentrations are also not good. As you said, a diet high in salt can lead to high blood pressure and chronic high blood pressure can cause damage the small blood vessels in the brain and cause small strokes over time or very high blood pressure can cause larger bleeds. Usually we see this in patients with very high uncontrolled blood pressures in the 170-200s systolic range. I'm kind of pulling those numbers out of my memory and you would have to check the literature to verify.

Thanks for the answer. I have a very frequent and apparently strong pulse, but low blood pressure. Does low blood pressure mean that I'm 'safer' when eating salt than other people? Also how do I detect small strokes?


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Is every part of a virus important for replication?
Is every component of a virus absolutely essential for its infection and replication in a host cell? Or can you just have parts of it to cause infection?

If you are a fan of Richard Dawkins (or at least like his reasoning), every gene in every organism supports replication.  Infection and replication are hard to separate in the case of HIV.  There are genes for which we have little or no clear understanding of how they might help the replication.  http://en.wikipedia.org/wiki/The_Selfish_Gene#Genes_and_selection

HIV has nine genes. According to the paper cited below, three of these genes (vpu, vpr and nef) are not required for replication in cultured cells.

Gibbs JS et al. (1994) Construction and in vitro properties of HIV-1 mutants with deletions in "nonessential" genes. AIDS Res Hum Retroviruses 10: 343 - 50
Abstract
  Auxiliary genes that are not essential for viral replication in cell culture are found in all known lentiviruses. The "nonessential" auxiliary genes of HIV-1 are vif, vpr, vpu, and nef. Sequences within the upstream region of U3 in the LTR are also not required for virus replication in cell culture. We constructed a panel of 23 mutants with single and combination deletions in these regions in the wild-type HIV-1 infectious molecular clone NL4-3. Deletion of the vpu, vpr, and nef genes and the U3 upstream sequence (US), individually or in combinations, did not appreciably alter virus replication in either chimpanzee PBMCs, human PBMCs, or in the B/T cell hybrid line CEMx174. In contrast, deletion of the vif gene dramatically delayed virus replication in all three cell types. This collection of HIV-1 deletion mutants will be useful for elucidating the functions of these genes and for investigating antiviral immunity in animal models.

(PBMC = peripheral blood mononuclear cell)
As might be expected, none of these genes encodes a component of the virus - they are regulatory genes involved in co-ordinating the infective cycle of the virus. They are however implicated in HIV-associated disease symptoms. According to the Los Alamos National Laboratory HIV Sequence Compendium 2008:
vpu is an integral membrane protein which promotes extracellular release of viral particles and degrades CD4 in the ER.
vpr promotes nuclear localization of the preintegration complex, inhibits cell division, and arrests infected cells at G2/M
nef downregulates CD4 and class I MHC


text:
What is the lifetime of the vasopressin receptor V2?
I was looking at the production of vasopressin receptor 2, also known as V2R or ADH-R. What I found is that it is coded by the AVPR2 gene and degraded by the Alix protein (source).
But I did not get a sense of the timescale. After a receptor protein has been produced and embedded itself in the cell membrane, how long does it live? Is it days, weeks, months? Does it live until the cell dies or is it degraded before that?
Does the lifetime differ between each receptor, or on the cell type, or is it roughly the same for all G coupled receptors?

But where did you read about this particular example? Certainly we can find some additional information from that source. But in any case, the turnover of different GPCRs shouldn't be the same.. There is no strong reason to assume so.

@WYSIWYG This is the one study I found about V2R degradation, it is the one which concentrates on Alix.http://ajprenal.physiology.org/content/292/5/F1303 I don't remember where I got the info about the encoding gene, it was simply a table listing hypophyse hormones I found somewhere, and it had a column listing the gene.

Okay.. can you cite that article in the question?


text:
How many cells does the smallest animal have?
Note: question rewritten to prevent misunderstanding and make it more answerable
I know that some small animals like C. elegans display surprising sophistication with a very small number of cells. But I wonder, among the animals with known/estimated cell count, which has the fewest cells?
To make the question answerable, please note these constraints:

I'm only asking about members of the kingdom Animalia, so single cell organisms and colonials like Vovox are excluded. If there are single cell organisms which are classified under Animalia (I think there aren't, but not 100% sure), I still want to know about the smallest multicellular animal.
I'm only asking about species where we can distinguish individuals. If some kind of polyp or sponge is just a bunch of cells which can merge with or separate from other cells and remain a viable organism, it's not interesting.
Please only consider species where the adult form reaches some size and stops growing. (Macroscopic) examples like the tapeworm, which continues building more proglottides throughout life, or fish which continue getting larger as they age, are excluded.
If the species consists of distinctive, stable "subgroups" of different sizes, the smallest size subgroup counts. For dogs, the size of the average chihuahua counts. For C. elegans, the size of the hermaphrodite (959 cells vs 1031 in the male) counts.
What counts is the number of cells in a healthy adult of the species or the relevant subgroup. For non-eutelic animals, make that the average healthy adult. Not the smallest ever observed exemplar, and also not amputated or stunted exemplars.
I am aware that we haven't discovered all microscopic animals yet, and haven't counted the cells of all discovered ones. Still, I'd like info on the current level of knowledge, including current known cell count, evidence that something has less than the current lowest known-for-sure count, and other relevant information.

What is an "actual animal"? This will be hard to define. Take a worm like C.elegans which has around 1000 cells (there are different numbers available here).

@Chris one officially classified in Animalia, the taxonomic kingdom. I know of C. Elegans, but I wonder if there are smaller ones.

I doubt that the number of cells has been estimated for many organisms, especially since most small animals are also usually poorly known (with C. elegans as a model organism being the exception). I therefore think you will have a better chance of getting accurate answers if "smallest animal" is framed in terms of actual body size (which is better known) instead of number of cells.

@fileunderwater but that would be boring :) and also an example of a tend which personally bugs me, as in "X, which interests us, is hard to measure, let's take the related Y and pretend we are talking about the same thing." I'm really interested in cell count, so I'd prefer to frame it as the smallest known, estimated or suspected cell count. I assumed that this is implicit, as we are unlikely to have discovered all microscopic animals anyway.

@rumtscho I'm not saying that its hard to measure, I'm saying that it is unknown for most animals. Therefore, any answer you get on cell count is most likely not the animal with the smallest cell count (just the smallest known cell count).

Also, I think that your last secondary question (cell count of small organisms fixed or not) should be posed as a separate quesion, since it's interesting on its own.

@fileunderwater thank you for the discussion. I realized that the original wording of the question wasn't so clear, so I rewrote it, including constraints on some of the factors you spoke of.

Rotifers are microscopic protostomes with around 1000 cells apiece.  This website claims the smallest rotifers have less than 100 cells, but I couldn't confirm this.  Most rotifers are eutelic — within a given species, each adult individual has the same number of cells (Encyclopeia of Life: Rotifers).

(Source)
Edit: Myxozoans might be even smaller.  These are microcsopic parasites that have been classified as cnidarians based on molecular studies.  They have complicated life cycles including a single-celled stage.

(Source)

About the edit: the single cell stage is probably not relevant. The Q is asking to adult stages. You've also had a single-celled stage - just after fertilization.

@fileunderwater Good point.  But it's hard to point to a single "adult" stage for myxozoans, they have two different hosts so they alternate between spores and infectious forms.

I don't know about all known animals, or actual cell count. However, males of the wasp Dicopomorpha echmepterygis are considered the smallest known insects with a body size of 139 μm. This should at least be a contender for smallest animal. As a reference point, C. elegans are usually about 1mm long.
However, given that we know only about 10% of the estimated number of species, and the ones we know are biased towards larger animal species, the smallest animal is most likely undescribed. In the case of parasitic wasps (or other insect parasites) these are extremely poorly known and new species are often described. Our knowledge of soil communities are also poorly known and includes many extremely small animals.
For the record, answers to a question like this depends alot on exactly what you include and how size is calculated. Could it be either sex or the average between sexes?

comments to downvotes are always appreciated...

Some of the smallest animals have only one cell. Paramecium Aurelia

Can you please indicate the species name and its position in the eukaryote phylogeny?

As far as I know, there are no single cellular animals. All single cellular organisms belong to other kingdoms. I admit that my taxonomy knowledge is not very good, so I may be mistaken. If there are single cellular animals please expand the answer, I'd like to learn more about them.

I just saw you have added the species name. I'm afraid a Paramecium is a member of the Chromalveolata kingdom, not of Animalia. Even in the early, not-so-clear worded version of the question, I specified "animal kingdom", and clarified in a comment that I mean the formal definition of an animal belonging to the taxonomic kingdom Animalia. So this doesn't give me the information I was asking about, even though it's related.

@rumtscho Agreed. Previously, many Protozoa (now obsolete) were considered animals, but they are not part of Animalia.

@fileunderwater the way I learned it, Protozoa were always considered separate from animals taxonomically, even though some of them were considered "animal like" and others "plant like" on an informal level.

@rumtscho Agreed, but in a loose/colloquial sense many labelled them animals.

@fileunderwater Chromaveolata is closer to plantae than to animalia; Chromaveolata and Plants fall under bikonta.

The classification of protozoa as animals (note "protozoa" means "first animals") dates back to a very old taxonomic system in which all living things were classified as plants or animals. I learned in high school that bacteria were plants. Really, this is just wrong and should be contradicted at every opportunity.


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HIV Rapid Tests
The hiv antigens that are used in the oral rapid tests, are they infectious? The tests do not contain any actual virus but I am curious if the antigens themselves could somehow create the virus on their own if they get into the bloodstream? Like do they contain all of the parts needed for replication inside them? (Not the actual virus but the antigen).

nope - the test contains antibodies to HIV proteins, but nothing from HIV itself.  The 'antigen test' tests for antigens, it doesn't itself contain any antigens.
Antibodies are proteins that animals (like humans) produce to fight of viral and bacterial infections, they don't come from viruses.
Even if the test did contain HIV proteins, it could not infect anyone.  You really have to have the HIV RNA, and almost certainly the rest of the virus too,  to cause any infection.

Okay. but the proteins don't contain that RNA do they? Sorry I am not very good at this stuff and get easily confused.

@Sarah: no, RNA and proteins are two completely different things. Anyway, there is nothing from HIV in the tests.

@Nico: Oh okay. Yeah I was just curious because of what I read about the hiv antigen. It kind of scared me because I wasn't sure if those were infectious or not. So just for clarification: proteins and rna are two separate things. The proteins do not have the RNA inside them and without the RNA there can be no infection?

@Sarah: Exactly. The test contains something (an antibody) that -if present in the sample- binds to HIV proteins.

No, the protein components of viruses may be able to initiate the infectious process, i.e. injection, but if there is no RNA or DNA, there is no virus to inject into the target cell. Hence none of the viral genome's action such as replication or transcription will occur and the cell itself will remain unchanged.
However, some effects of viral infection are actually part of an immune response of some kind, and these are often triggered by viral proteins themselves.

By taking proteins produced by bacteria and virii and then introducing them with a Carrier the body will mount an immune response and react when the real danger is presented. This is called the Hapten-Carrier effect, and is how we make many vaccines. The Innate Immune response is first, and the Adaptive Immune response creates the "memory" of the encounter so it can effectively fight the actual bacteria/virii/etc.


text:
Can a tumor produce something not currently found in our own bodies?
While speaking with my co-workers, the topic of tumors growing things came up.  The examples were (and backed by images) of tumors growing a tooth, hair, and sometimes even more complex objects such as an eye.
My question is, could a tumor reproduce something that isn't typically found in the human body?  Could it grow something that maybe a very distant ancestor would have had?

I doubt it - tumours usually originate from differentiated cells where a few growth-restricting genes are turned off by mutations - I'd consider it extremely unlikely for them by chance to mutate and turn on the whole patterns of genes that work in alternation and conjunction to cause correct differentiation and produce tissues other than lumps. But I can't refer to any papers so I might be wrong and hence this is only a comment :)

@Armatus but we do see tumors in one place in a body grow something from a completely different place in the body.  I know that isn't as drastic as something not currently found in the body, but it's still mutating far from what the cell was supposed to be.

can you post links to your examples?  just mentioning them is not as clear...

Isn't a tumour by nature something not inherently found in our body?

@shigeta http://en.wikipedia.org/wiki/Teratoma

@Armatus Take a look at teratomas for examples of crazy "whole things" growing in/from a tumor. That first paragraph (with the references) will surely pique your interest.

Would a mutated protein be a good example of something produced by a tumour that is not normally in our body?

If you look at a cancer textbook (eg. Robert A. Weinberg's The Biology of Cancer), you'll find that by definition, a tumor arises from tissues normally found in the patient's body. There's a great deal more to it than just that simple statement, but given the context of the question, I think that answer should suffice.
In writing, "...tumors growing a tooth, hair...", I think you're talking about teratomas. These contain "normal derivatives of all three germ layers". These arise naturally from cells "...typically found in the human body..."
Cancer is a process where mutations in a single cell transform that cell into something that is by definition not "typically found in the human body." But a human cell transformed by mutation into a tumor (benign or malignant) is never (to the best of my knowledge) going to magically become a cell from another species or a very distant ancestor (ie. something that is not "typically found in the human body.").

Teratomas are thought to be a particular type of cancer, present from early development.  As cells which are essentially developmental cells, they seem to have a fairly unique ability to develop hair follicles, teeth and even structures like organs. Indeed malignant teratomas often require chemotherapy or radiation therapy.
I think this bizzarre quality of producing organs or hair etc, is the result of the fact that the origin cells are programmed to develop into these organs before they become tumorous.  Later in life, we have no developmental stem cells in the body which will differentiate into organs and so other sorts of teratomas would seem to be unique.
Cancer cells are still cells programmed to perform the roles they started with, but they are usually not capable of generating whole functional tissue or organs. If they do they would normally be found amongst the tissue they would grow (e.g. liver cancer might produce tissue that looks like liver) so it would not have the unusual quality of teratomas of producing differentiated and specific tissues in isolation.

Sometimes cancer arises when you have crossing over between non-homologous chromosomes. In the process, a chimeric protein arises. A chimeric protein is a protein that consists of parts of two separate proteins spliced together. In this way, cancer cells end up producing a substance (in this case a protein) that is absent in a healthy person. A good example is the fusion gene bcr-abl whose product leads to chronic myelogenous leukemia.
See http://en.wikipedia.org/wiki/Philadelphia_chromosome for more details on bcr-abl.

Definitely NOT for cancer.
What you are speaking about are teratomas - results of incorrect development of stem cells. Stem cells are the type of cell that can become any other cell type. That way the growth of stem cell tissue may result in production of any organs.


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Does this patient have HHV6 or HCMV after transplant surgery?
I have been given mock results from a PCR test on blood samples taken from kidney recipient patients and their donors. The PCR reaction can detect single copies of viral DNA. I have been asked to determine whether 5 patients have been infected with either human herpesvirus 6 (HHV6) or human cytomegalovirus (HCMV) following kidney transplants. I have results for patients pre-transplantation and 1/3 weeks post-transplantation.
The results are as follows:
Donors:

Donor for patient A = HCMV+
Donor for patient B = HCMV+ & HHV6+
Donor for patient C = Neg for both viruses
Donor for patient D = HHV6+
Donor for patient E = HCMV+ & HHV6+

Recipients:

Patient A = HCMV+ before and 1 & 3 weeks post-transplant
Patient B = Neg for both viruses before, then HHV6+ at week 1 & HCMV+ at week 3 following transplantation but negative for HHV6.
Patient C = HHV6+ before and 1 & 3 weeks post-transplant.
Patient D = HCMV+ before and HCMV+ & HHV6+ 1 & 3 weeks  post-transplant
Patient E = HHV6+ before and HCMV+ & HHV6+ 1 & 3 weeks  post-transplant

Answers: I am guessing that Patient A was re-infected by donor A. Patient B was neg for both viruses, developed HHV6  week 1 but this test was neg week 3 & instead positive for HCMV – these viruses do not disappear, you either have it or don’t so assuming there is no contamination error then what virus did he develop post-transplant?? Patient C was HHV6+ prior to transplant but donor is neg for both, so what virus did he develop following transplant? I can see that Patient D was infected with HHV6 from donor post-transplant. Patient E was infected with HCMV from donor post-transplant.
I am struggling to determine what virus Patient A, B and C was infected with following transplant. Can anyone help? I know almost 100% of us are infected with both viruses but do not cause disease in healthy people, that both latent and active viruses show positive when in blood and that both viruses can re-activate under certain conditions such as via infected organ transplants and immunosuppression.

I get the feeling that there's something we should probably know from your textbook or notes that you have not included. As-is, here's my best shot:

It is impossible to determine if Patient A was infected by the transplant since the virus they had before the transplant is the same virus carried by the transplant itself. Without running further tests to separate the two lineages you can't tell. It's likely, though.
While HHV6 has been known to precede HCMV in certain cases the conditions don't seem to apply here. My best guess, which is something I'm pretty loathe to say, is that if you're positive the tests are accurate then it's possible that Patient B's immune system alternately suppressed each virus below detectable levels. Since Patient B is receiving donor tissue with both viruses, and transplant patients are put on immunosuppressants following surgery, it could simply be that at first the immune system was capable of dealing with HCMV for the first week, but not HHV6. Then as it adapted to HHV6, HCMV evolved to evade so it showed up on the assays. That is entirely speculative, though. Another explanation might be that the viral titers of HCMV were too low to detect at Week 1, but it had reproduced enough to show up at Week 3 while the immune system dealt with HHV6. There's a lot of information that's missing on how the virii behave, the characteristics of the immunosuppressants given to the patient, and so on.
Patient C was clearly infected with nothing. They already had HHV6, and that's what showed up post-op.
Patient D was infected with HHV6. They had HCMV before, and both after.
Patient E was infected with HCMV, although like Patient A they could have been infected with a different strain of HHV6 as well, but the tests probably aren't specific enough to determine viral lineages for the before and after strains.


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Can the RNA in the HIV virus make viral enzymes without entering the nucleus?
If the provirus was not formed yet, can the virus make viral enzymes?
(I know that it already has some, but supposing it doesn't)

"...but supposing it doesn't.."
What you mean is: it would be feasible for the virus only  to translate (in cytosol) the reverse transkriptase, then transcribe "all" from the DNA ("provirus").  And if so, would "making (any other) enzymes" from RNA, not DNA,  be contradictory to such rule? This seems a "hidden" no win question...

I am afraid your question is really not clear. You are asking one thing in the title of your question, another in the question body and a third in your comments. If you are asking (as you did in your comment above) what would happen if a virus with no enzymes were to infect a cell, see below.
In the case of HIV (and other retroviruses) some of the most important enzymes contained in a normal viral particle are:

A reverse transcriptase (RT): this enzyme reverse-transcribes the viral RNA genome to cDNA,
An integrase: incorporates the cDNA produced by the RT into the host cell's DNA.
A ribonuclease : an enzyme that can degrade (cut up) RNA. In the case of HIV this is the same protein as the RT.
A protease: an enzyme that can degrade other proteins.

Viruses work by copying their genetic material (their DNA or RNA) into the host cell's genome and then hijacking the cell's replication machinery to make more copies of the virus. So, what would happen if these enzymes were absent?

Without an integrase, the virus would not be able to insert its reverse transcribed DNA into the cell's genome.
Without an RT, the virus would not be able to copy its RNA into DNA.
The ribonuclease activity is also needed for successful reverse transcription to double stranded DNA (see [1] for a review and explanation of why.)
The protease is necessary for the formation of new viral particles. Mutations in this enzyme result in aberrantly assembled virus particles with low infectivity [2].

What you really must remember is that viruses are extremely streamlined. Everything they contain is essential. In some ways, you could say that viruses are the most highly evolved species (assuming they are living species), they are the most highly specialized "life forms" we know of and they have managed to get rid of all non-essential functions. The flip side of this is that everything that is left is essential, the virus cannot function without it.
So, to answer your question, a virus without any enzymes is, essentially, not a virus. It would not work, would not successfully infect cells.

References:

Greg L. Beilhartz and Matthias Götte, HIV-1 Ribonuclease H: Structure, Catalytic Mechanism and Inhibitors, Viruses 2010, 2:900-926
Bukrinskaya A. HIV-1 matrix protein: a mysterious regulator of the viral life cycle. Virus Res. 2007 124(1-2):1-11.

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


text:
Are all body atoms really recycled several times during a life?
I heard a point, that all (human) body atoms are recycled withing short period like few years. Recycled means "old" atoms are replaced by "new" ones during metabolism, leaving only structure unchanged.
But this looks contradicting with knowledge about DNA. DNA molecule looks unchanged and the fate of all it's atoms looks known.
Yes I know there are some spontaneous damages which are repaired, but most of DNA atoms remain in place. Even during cell division, 50% of atoms goes to one of the descendant cells. I.e. they don't go outisde body.
So, if the point is wrong concerning DNA atoms, then may it is wrong at all?

Rudolf Shoenheimer and David Rittenberg were key figures in introducing the isotopic tracer technique to biology.
This technique, which may be dated to the discovery of deuterium by Urey in 1933, produced a revolution in biological thought.
Much of the early work was done at the Department of Biological Chemistry at Columbia University under the chairmanship of H. T. Clark.
Up to this time it was thought that the components of tissues were relatively stable, and that ingested food was metabolized immediately to provide a source of energy.
The first experiments showed that when deuterated fatty acids were fed to mice, most of the label was initially deposited in adipose tissue.
It was concluded that adipose tissue acts a 'fuel depot' that is in a state of metabolic flux and is the direct source of fatty acids burned as a fuel (see here for refs). Fats present in food are not primarily used an an immediate energy source.
When a stable isotope of nitrogen became available (N15), it was found that proteins were also 'in a state of dynamic flux' and were being continuously regenerated and broken down.
The first experiments were done with N15-labeled tyrosine and it it worth quoting from the paper (Studies in Protein Metabolism. VII The metabolism of tyrosine by D Rittenberg Rudolf Schoenheimer &  S. Ratner)

The results indicate that in our rat the nitrogen of at least one
amino acid, tyrosine, was only partly excreted in the urine, while
almost half of it was retained in the body proteins.
Of this deposited nitrogen only a fraction was found attached to the original
carbon chain, namely to tyrosine, while the bulk was distributed over other
nitrogenous groups of the proteins

Shortly after giving a series of lectures at Harvard University in 1941, Shoenheimer took his own life.  The lectures were published posthumously as a classic book called The Dynamic State of Body Constituents.
Further information about the early  work on isotopes, their role in changing completely the way we think about metabolism, and the role of Columbia University in shepherding in this great era, may be found in the following open-access article by Eugene. P. Kennedy:
Hitler’s Gift and the Era of Biosynthesis
Another good reference on the work of Schoenheimer may be found here

So are all proteins broken down and regenerated?  I know of any one exception and that is the lens crystallins where there is virtually no turnover
throughout the life of an individual.
The crystallins in our lens are synthesized at birth and remain with us virtually unchanged for life.
There is a very nice open-access paper on this published in PLOS One:
Radiocarbon Dating of the Human Eye Lens Crystallines Reveal Proteins without Carbon Turnover throughout Life
(Lynnerup et al. 2007)

In the original answer I said that the original isotope experiments were done with radioactive fatty acids.  This, of course, is rubbish. They were done with deuterated fatty acids.

I think you're right. DNA contradicts the notion of "total mass turnover." So the point is not generally correct. Of course, how incorrect the statement is reflected by the mass ratio of DNA to non-DNA components -- most all of those other components do turn over multiple times in a lifespan (including things that seem frozen-out like bone calcium).
Turns out the order of magnitude estimate for the mass of DNA in a human is (http://ask.metafilter.com/67006/What-is-the-mass-of-my-DNA) something like a pound. So the statement is on the order of 1% error for a typical adult human.

But how do we know that other atoms are turned over? May be ribosome or cytoskeleton proteins are also persist?

Are you asking, what experimental techniques monitor the turnover of biochemicals? Whole-animal metabolic studies are the main historic source of these kinds of statements. Let's say you give a mouse 14C-labeled food for its first six months of life, then switch it to unlabeled food. Monitoring the whole-mouse 14C content over time lets you quantify turnover.

or even 13C - 14C is a radioactive isotope :)  expensive!

still with cell turnover and early growth, we're talking about just a few percent of the cells whose DNA is not new every few years.

Y'all are neglecting the fact that cells die and are continually replaced, which would include replicating the DNA with new atoms.  The most interesting study I've seen on this is summarized in this New York Times article. Above ground nuclear testing up until 1963 released a great deal of Carbon-14 into the atmosphere.  This ultimately became incorporated into the DNA of anyone living at the time, and was used as a marker for how quickly specific tissues turned over in the body.


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What is the mechanism of oxygen uptake in E. coli?
How does E. coli uptake oxygen? Most of the literature I found is concerned with response to oxygen level supplied in the medium, as opposed to how much is actually transported inside. Can they shut down the oxygen uptake if required? For example, to avoid damaging effects of reactive oxygen species.
There exist bacteria which die in presence of oxygen (strict anaerobe), while some use oxygen when available but also can survive in absence of it (facultative anaerobes, like E. coli). Are there bacteria which cannot consume oxygen for metabolism, but when exposed to oxygen they don't die, rather simply discard the oxygen and carry out fermentation? In a sense, they are strict anaerobe (their mode of metabolism is anaerobic), but they can still survive in presence of oxygen in environment.

Have a look at this related post too

This question got me thinking about what are the metabolic enzymes that take oxygen up in E.coli. I searched the metacyc database for reactions that consume molecular oxygen and there are only 3 that take in oxygen and one that produces oxygen.
All three consumers of oxygen in E.coli are the oxidation of ubiquinone by at two sites in cytochrome-bcl or by cytochrome-bo.  All of these export protons to create the gradient that drives ATP formation by F₀F₁ ATPase in the periplasm (the region between E.coli 's inner and outer membrane).

On the production side, superoxide dismutase reduces superoxide to oxygen to control oxidation damage.  Apparently the innards of E.coli are somewhat oxygen tolerant.

Thank you, is diffusion alone the mechanism of uptake?

yes, as @canadianer describes. I'd only wanted to add a description of how oxygen is taken into the system and consumed, which seemed like part of your question as well :)

I would be grateful if you could provide me some  references on how oxygen uptake capacity ( diffusion capacity) changes over growth rate or other variables, if any.

The plasma membrane is quite permeable to oxygen and thus oxygen enters the cell simply by diffusion. Reactive oxygen species can be reduced enzymatically in aerobic organisms. Obligate anaerobes lack or don't produce sufficient quantities of these enzymes. An organism that doesn't use oxygen for metabolism but is also not relatively harmed by it can be classified as aerotolerant.

Image from: http://en.m.wikipedia.org/wiki/Anaerobic_organism
Original Caption: Aerobic and anaerobic bacteria can be identified by growing them in test tubes of thioglycollate broth:
1: Obligate aerobes need oxygen because they cannot ferment or respire anaerobically. They gather at the top of the tube where the oxygen concentration is highest.
2: Obligate anaerobes are poisoned by oxygen, so they gather at the bottom of the tube where the oxygen concentration is lowest.
3: Facultative anaerobes can grow with or without oxygen because they can metabolise energy aerobically or anaerobically. They gather mostly at the top because aerobic respiration generates more ATP than either fermentation or anaerobic respiration.
4: Microaerophiles need oxygen because they cannot ferment or respire anaerobically. However, they are poisoned by high concentrations of oxygen. They gather in the upper part of the test tube but not the very top.
5: Aerotolerant organisms do not require oxygen as they metabolise energy anaerobically. Unlike obligate anaerobes however, they are not poisoned by oxygen. They can be found evenly spread throughout the test tube.

Can you please give me an example of aerotolerant bacteria?

I think some Streptococcus and Lactobacillus spp.

Clostridium intestinale has been described as aerotolerant.

E. coli is a facultative anaerobe…

I would like to get example of aerotolerant but strictly anaerobic bacteria.

I am adding a supplement/concluding remarks to the existing answers.
Some points to be considered:

Electron transport chain can work without oxygen and can use other chemical species as electron acceptors.
E.coli is capable of aerobic respiration, anaerobic (anoxic) respiration and fermentation (substrate level phosphorylation).

How does E. coli uptake oxygen?

Short answer as already mentioned by canadianer: Passive diffusion

Can they shut down the oxygen uptake if required?

Oxygen is the primary electron acceptor and E.coli would prefer oxygen to other electron acceptors. Only in the absence of oxygen is the FNR regulon switched on. Other bacteria can show negative aerotaxis i.e. running away from oxygen (they obviously have to be motile) [ref]. This paper also comments that positive and negative aerotaxis happens via a common mechanism- sensitivity of proton motive force to O₂. However, ROS has no role to play in it. It is most likely that at high oxygen levels E.coli will try to jack up anti-oxidant response. To conclude- they cannot regulate oxygen uptake.
Aerotolerant anaerobes: Clostridium perfringens, Clostridium intestinale.


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Gene distance and Recombination Frequency: Mechanism
Why is the recombination frequency higher if the genes are farther apart?

Alan, thanks for your excellent analogy. We're talking about the probability of a random event happening at some place on the string.To me the key in the analogy is the probability of this random event happening. Whether that's "cutting", or "tied-up", or even "melted together", the random event, in my mind, is affected by how many marks there are on the string, and how far apart they are relative to each other. This probability calculation is the recombination frequency.

The genetic phenomenon referred to as recombination reflects the process of crossing over which occurs during meiosis. Crossing over creates an exchange of genetic information between homologous chromosomes. To a first approximation cossing over events take place at random positions along the aligned chromosomes. Consequently the further two loci are apart, the more likely that there will be a crossing over event between them. Thus the recombination frequency can be used to measure the distance between two genetic loci (or genes).
Supplement added in response to comment from OP

An analogy
Imagine a piece of string. It has 6 marks on it (1-6 on the diagram) which divide it into 7 intervals (A-G). We are going to cut the string at one of the marks. We throw a die to decide which position to cut.
What is the probability that our cut will separate A and G? It's 100% since all single cuts will do this.
What is the probability that our cut will separate A and D? It's 50% since single cuts at 1,2 or 3 will do this.
What is the probability that our cut will separate A and B? It's 16.7% (1/6) since only a cut at position 1 will do this and the probability of throwing a 1 on our die is 1/6.
Think of the intervals (A-G) as genes and the cut sites (1-6) as possible crossing over events. If two homologous chromosomes are going to undergo a single crossover somewhere at random, then the closer together are the genes (intervals), the less likely is it that the crossover (cut) will take place between them. This assumes of course that the site of crossing over is chosen at random.
In the model presented here, if the order of the letters was scrambled and didn't know what it was but we were told the frequencies of occurrence of the separation of the intervals with random cutting we could deduce the order of the letters.

To me the statement "Consequently the further two loci are apart, the more likely that there will be a crossing over event between them" is still not obvious. It is the core of my question. Please elaborate further.

Thank you very much for the effort. However, I am not yet clear, sorry for this. Crossing-over involves genes physically being 'tied up' temporarily. I fail to see how is cutting analogous to it? Why should chances of such 'tying up' increased if the genes are farther apart?

I don't know what you mean by being 'tied up'. Crossing over involves a physical interaction between two aligned chromosomes at a randomly chosen point. The further that two genetic loci are apart then the more likely it is that the randomly chosen point of crossing over will lie between those loci. I really can't think of any other way to explain this, so I hope someone else comes along and gives you the explanation you are looking for.

@DurgaDatta, i absolutely got it why you're not understanding. You simply don't understand how the crossing over happens on a visual level. https://www.youtube.com/watch?v=jd3H0pgVCr8. Minute 1:06 . If you pay atention to this frame, you'll see that, had the cut been a little over the loci on the top, the meiosis would yield the "same" old gametes - at least in terms of these loci. But, since the cut was between the two loci, we're having recombined gametes, like Ab and aB. Thats why one would say that if two loci are very further apart, crossing over between them is very likely.


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Does fat on our heart come from the fat that we eat?
If we eat fat:
Does the fat go into heart, arteries and fat cells.
OR
Is the fat digested, following which our body creates fat that goes into heart, arteries and fat cells.
Which one is right?

Fat is, in molecular terms, triacylglcerol. In order to be absorbed in the small intestine triacylglycerol molecules are broken down by lipases into fatty acids and monoacylglycerols. Once these have got across the enterocyte membrane they are reassembled into triacylglycerols and packed up into a special class of lipoprotein particle, a chylomicron, which enters the bloodstream via the lymphatic system.
The triacylglycerols in the chylomicrons are then able to be passed around through the system of lipoproteins (LDL, VLDL etc.) and pretty much can end up anywhere, including fat cells (adipocytes) or they can be metabolised as fuel molecules
So, because of that initial digestive step I would say that a single intact dietary fat molecule cannot end up as a body component directly, but complete metabolism of the components of the fat molecule is not necessary for these to contribute to body fat.

It's more of somewhere between then. So they are broken and then reassembled into the same molecul?

Yes, but the pieces that are reassembled are unlikely to have been derived from the same original molecule. It must happen occasionally I guess, just by chance.

Fat is digested just like any other food you consume, and eventually the energy you do not expend ends up as an energy reserve in shape of fat cells.
So, the second statement is right.


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Sources for common laboratory Saccharomyces strains?
I'm used to working with bacteria - some of the more common laboratory strains sometimes come with an order from some vendors.  What's the most convenient source to order common straings of Saccharomyces for lab work?

The Saccharomyces Genome Database has a list of sources here. One of them is the Japanese Yeast Genetic Stock Center: I checked their site out and found that they charge ¥390 per strain which is around USD4. There is also a USD5 fee on all orders. I searched for a couple of standard strains, and these were in the catalogue, so it looks like a good possibility.
(Incidentally I have used USD here rather than $ because there seems to be a bug when typing that symbol  twice in a post - try it and you'll see what I mean.)

thanks this looks good @AlanBoyd.  that's close enough to free for me!

One very important resource is EUROSCARF. http://web.uni-frankfurt.de/fb15/mikro/euroscarf/
It is one of the very famous and dedicated strain repository for yeast (S. cerevisiae) strains. You can even find some very useful yeast plasmids here.
Another resource I would recommend will be the original labs, which made the mutant strains/plasmids. Yeast researchers as a community are very nice, I have almost always obtained the strains and plasmids that requested from the original labs.
Hope it helps,
Cheers!!


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What is the difference between "dikaryotic" and "heterokaryotic" states in the sexual lifecyles of fungi?
Many fungi undergo a reproductive phase in which more than one genetically distinct nuclei (from 2 separate mating types) is present within the same cytoplasm. In the Ascomycota and Basidiomycota, this phase is termed "dikaryotic", whereas in other fungal phyla the phase is "heterokaryotic." What is the difference here? Is it purely number of nuclei per cell, or does the difference depend on how many genetically distinct nuclei are present (2 or >2)?

A heterokaryon is a fungal cell which has two or more genetically-distinct but allelically-compatible nuclei, as suggested by this resource, as well as this Wikipedia article.
A dikaryon is a fungal cell which has precisely two genetically-distinct but allelically-compatible nuclei, as shown here and here.
In this sense,  a heterokaryon is a general term, whereas a dikaryon is a specific term. A dikaryon and a trikaryon (although not often seen in literature) are both heterokaryons.

So heterokaryon is the general case, and dikaryon is a specific case?

Good answer, thanks - one other thing I found is that a dikaryon may then divide, with each nucleus being replicated once per division, to form  dikaryotic hyphae. In Basidiomycota, the entire basidiocarp (mushroom) is formed from these dikaryotic hyphae.

dikaryotic does - by definition - mean that there are exactly two nuclei in the cells, it does not say that the two nuclei are genetically distinct!
heterokaryotic does also mean only one thing: the nuclei (the number is not important) are genetically distinct.
that's the reason why, for example webster, writes "heterokaryotic dikaryon".
in fact the nuclei are distinct in almost all cases, that's why some only write "dikaryon"

Heterokaryotic = contains two or more nuclei
Dikaryotic = one cell contains two separate nuclei that are not fused; usually indicated as n+n

Welcome to Biology.SE! It isn't clear that this is adding anything to the already existing answers.  In addition, answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). ——— You may also wish to take the [tour] and then consult the help pages on the standards for additional advice on [Answer] effectively. Thanks!

A dikaryotic fungi contains only 2 genetically different nuclei but a heterokaryotic fungi may contains more than 2 nuclei

can you add some references to back up your answer?


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Does a woman's G-spot actually exist?
Does a woman's G-spot actually exist? Are there any research studies?
Links:

G-spot (Gräfenberg spot) at Wikipedia
U.S. gynaecologist says he has found the G-spot

The links you provide contain all the material you could likely get in an answer here. There's hence not really any use in asking here as you could just as well read the Wikipedia article and its linked resources.

The existence of the G-spot remains highly debated among researchers.  Two recent publications (Hines 2001, Kilchevsky et al. 2012) review studies of the so-called G-spot and conclude the evidence is too inconsistent to claim its definite existence.  Foldes and Buisson (2009) argue that the G-spot is actually just a clitoris that is richly  innervated. This would be consistent with the reported variability of G-spot presence or absence due to natural variation in innervation among women. (This last statement is my hypothesis offered without citation).
As noted by @Armatus in the comments, a few minutes following some of the Wikipedia links to the scientific journals (not the BBC, CNN, pop news sites, etc.) would give you lots of information about the G-spot. Still, I thought you question was worth typing up a brief answer for the sake of completeness.
Literature Cited
Foldès, P. and O. Buisson. 2009. The clitoral complex: a dynamic sonographic study. The Journal of Sexual Medicine 6: 1223–31.
Hines T. 2001. The G-Spot: A modern gynecologic myth. American Journal of Obstetrics and Gynecology 185: 359–62.
Kilchevsky, A, et al. 2012. Is the Female G-Spot Truly a Distinct Anatomic Entity? Journal of Sexual Medicine. 719-726.


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It is possible for person with AIDS be negative for HIV antibodies?
I'm just curious as there was a bit controversy around this topic. It is possible for person with AIDS be negative for HIV antibodies?
As of 1989, the CDC reported that 5% of all U.S. AIDS patients who had been tested for HIV to that time were HIV-negative. No figures have been reported by the CDC since 1989.
If so, how it's possible?
See:

Unexplained CD4+ T-Lymphocyte Depletion in Persons Without Evident HIV Infection -- United States at Centers for Disease Control and Prevention

You need to decide what you want to know. The paper you link talks about patients wihich have a low CD4+ count, but are not positive for HIV. So you want to know how this happens? Or do you want to know if it is possible for someone who is HIV positive (and has developed AIDS, which is the latest stage of the infection) to not develop antibodies against HIV?

Yes, how it's possible that they were HIV-negative or in general if there are any other more recent studies. More information, then better.

Ur question is still pretty confusing to me. Could you please edit it. Your question speaks about something and the comment you posted talks about something else.

There is no need to downvote this question. I can still be clarified but nothing further.

The main question is as in the title, if it's possible for person to be HIV-free. Based on CDC report it seems it is possible, but somehow this is not considered as a fact. So I just wonder why is that.

If you're looking for support for your "HIV doesn't cause AIDS" conspiracy theory, you're in the wrong place. This paper doesn't mean what you think it means, it isn't evidence for your conspiracy theory like you think it is.

I don't see anything bad in asking the question. If the paper doesn't mean what I think, then you can elaborate/explain further. I'm not biologist, therefore I ask.

@Mad Scientist: If you'll keep down-voting by not explaining the questions/inaccuracies, then I assume you don't know, then you should ignore the question and leave it for the people who know the answers. By not answering the question and closing them, you just keeping the people in the dark, therefore promoting the conspiracy theories, and not people who just ask. BTW. I'm not looking for "HIV doesn't cause AIDS" theories, just answers.

Depends on the sensitivity of the antibody detection kit

@WYSIWYG: Did they use bad antibody detection kits in the past?

perhaps they were not very sensitive.. There is always a scope for improvement

Usually an antibody test against HIV is positive three month after the infection. Before this time a test can only be done with molecular biology methods as PCR. However, it is possible, that patients which have definitely been tested in an early phase using molecular biology methods and which afterwards receive a antiretroviral therapy (ART) that these patients do not develop high serum levels of antibodies, as the virus titer in the blood is not high enough for a sufficient reaction and thus stay undetected by the tests. This has been improved, so that the kits are supposed to have a higher sensitivity now. See these papers for more details:

Seroreversion in subjects receiving antiretroviral therapy during
acute/early HIV infection.
The effects of early antiretroviral therapy and its discontinuation
on the HIV-specific antibody response.

I haven't found any papers on the decline of HIV-antibodies in AIDS (which is the late stage of the disease), but if they do, this is probably due to the effects of the infection on the immune system.
Low counts in CD4 positive T cells (which are usually associated with an HIV infection) can also occur with other diseases. See these papers (especially the first, as this is a review which contains a lot of further references):

Idiopathic CD4 Lymphocytopenia: Spectrum of opportunistic infections,
malignancies, and autoimmune diseases.
Decreased CD4 and increased CD8 counts with T cell activation is
associated with chronic helminth infection.
Acquired immunodeficiency without evidence of HIV infection: national
retrospective survey.

Sure, it is possible in the late stages of AIDS. Once the immune system is pretty much wiped out, the person has AIDS and is unable to produce HIV antibodies. There is nothing left of the immune system to produce antibodies of any sort.
https://www.ncbi.nlm.nih.gov/pubmed/18649337
This is why DNA based HIV detection system using quantitative PCR is better. It is not dependent on an immune response that is being destroyed by HIV.


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How can we calculate the minimum sustainable number of the panda population?
I have a degree in Biology so I'm a little embarrassed that I never learned this, but...
How do we know 1600 Pandas isn't enough?
I know that we have historical numbers (although I couldn't find them) which show the population has declined, but we also know the usable habitat has declined and it would be foolish to not consider that when trying to replenish the wild population. It seems to me that if there's only 1600 Pandas in the wild, that's probably the right number. How do we know it's not?
I will accept answers about other endangered animals, if they show how we can calculate the approximate "appropriate" number for a species.

Relevant question: http://biology.stackexchange.com/questions/305/smallest-viable-reproducing-population

That would be part of a good answer - "we think 1600 is below the smallest viable population"

Minimum viable population (MVP) can be predicted in two ways.

Computer simulations.
Population viability analyses (PVA)

PVA is considered generally more common practice by ecologists and without a reference to the 1600 panda population you mention, my guess would be that this is what they did. PVAs work well for endangered species prediction.
A typical example of PVA was carried out on an endangered species Fender's blue butterfly an endangered species (Schultz et al., 2003). However there is currently no scientific standard on how a PVA should be done.

Schultz, Cheryl B.; Hammond, Paul C. (October 2003). "Using Population Viability Analysis to Develop Recovery Criteria for Endangered Insects: Case Study of the Fender's Blue Butterfly". Conservation Biology 17 (5): 1372–1385.


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Questions regarding ELISA
I have recently peformed an ELISA (Enzyme-linked immunosorbent assay), but I still have some questions, let me first outline what I did:

We had a number (20) of tubes containing fake 'bodily fluids' , namely saliva. One of these tubes contained the Epstein-Barr virus, which on its turn causes Pfeiffer's disease, aka the 'kissing disease' (so we basically conducted an experiment to see how fast the virus would spread within a class if everybody started kissing each other, if you don't mind the crudity).
Everybody mixed their saliva with the saliva of 3 other people, so at the end everybody had a tube with the saliva of 4 different people in it.
Since we worked in pairs of 2, every duo got a microtiter plate with 12 wells in it: 3 wells for a positive control, 3 wells for a negative control, 3 wells for the fluids of 1 of the duo and 3 wells for the fluids of the other one. You pippete in (is that correct?) the fluids accordingly.
After a while you rinse and clean the wells with wash buffer.
Then you pippete in the primary antibody in each well.
After a while you rinse and clean the wells with wash buffer.
Following this you pippete in the secondary antibody (conjugated with the enzyme HRP).
After a while you rinse and clean the wells with wash buffer.
Finally, you add the enzyme substrate (TMB) to each well. This causes a blue color if when in contact with HRP. The positive controls must come out blue, the negative must come out colorless, and the other wells can go either way, depending if you have the virus.

I hope this is not to crudely explained, again. These are my questions concerning the experiment:

What do the components of the acronym 'ELISA' actually stand for? Does immunosorbent refer to the binding of the antigens to the wells? My English isn't too good, and these acronyms and abbreviations often seem foreign to me (nevermind that they are foreign since I'm not English, you get the point I hope).
When you pippete in the saliva in the wells, what actually sticks to the wells? All of the antigens in your saliva? Because it's hard to believe that they make special microtiter plates for every single antigen seperately. I assume it is only the antigens, since the primary antibodies attach to the antigens only, so there is no need for the microtiter plate itself to bind to antibodies.
How would we get the primary and secondary antibody? This is my assumption: The primary antibody we get is by injecting some antigens of the Epstein-Barr Virus into a human and then taking a serum. The secondary antibody could be gotten by injecting a random human primary antibody into ANY animal, irrelevant which anyimal, and then taking a serum. After that you conjugate an enzyme to the secondary antibody. Is this correct?

ELISA is Enzyme-Linked ImmunoSorbent Assay (capitalisation to point out source of acronym).
You can read about the various ways to do an ELISA here.
In your case this was probably an indirect ELISA. All ELISA techniques make use of the fact that proteins stick to plastic. In your case the protein components of the saliva, including the virus (the viral coat is proteinaceous) will stick to the wells. After rinsing out the sample the wells are treated with another protein (usually bovine serum albumin (BSA)) to completely block all available protein binding sites. At this stage these wells will no longer bind protein non-specifically, but will bind anti-EBV Ig because of the presence of the EBV particles bound to the plastic. This bound anti-EBV can then be detected with a secondary antibody. The protein complexes will build as follows:
plastic/EBV/rabbit anti-EBV/goat anti-rabbit IgG-HRP conjugate
It would also be possible to do this experiment as a sandwich ELISA. In this format the wells would have been pretreated with anti-EBV serum (or purified anti-EBV IgG) then blocked with BSA. At this stage these wells will no longer bind protein non-specifically, but will bind EBV because of the presence of the EBV-specific antibody. Once samples have been incubated in these wells (so that any EBV can bind to the antibody coating the wells) another antibody (raised in a different animal) is added, and this will bind to the EBV that has been captured by the original antibody that coats the wells. This latter antibody is then detected with a conjugate. The protein complexes will build as follows:
plastic/mouse anti-EBV/EBV/rabbit anti-EBV/goat anti-rabbit IgG-HRP conjugate
Your description of how to get the antibodies is basically correct, except that the primary antibody will probably have been raised in rabbits or mice, and certainly not in humans.
Added later: I didn't read the first question carefully enough. An ELISA is an assay because it measures something. It is based on a binding reaction mediated by an antibody-antigen interaction (immunosorbent). It is enzyme-linked because the secondary antibody is present as an antibody-enzyme conjugate. It is the amount of this conjugate that remains bound at the final step which is what is measured - the assay is set up so that the amount of this enzyme is a measure of the amount of the original molecule that is being assayed.

So, if I understand correctly, the primary antibody of mice and rabbits will also respond the same way as human antibodies to the Epstein-Barr virus?

Yes, any animal will generate an antibody to any antigen, as long as it isn't recognised as "self". So for example you could not raise an anti-rabbit-IgG in a rabbit. The coat protein of EBV is just another antigen as far as a mammalian immune system is concerned - if it is foreign, there will be an immune response.


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What are possible health risks to women having large numbers of children?
What is the possible health issue the women would face in this record?

The record for most children born to a single couple belongs to the
  first wife of Feodor Vassilyev of Russia. In 27 pregnancies between
  1725 and 1765 she gave birth to 16 pairs of twins, 7 sets of triplets,
  and 4 sets of quadruplets for a grand total of 69 children.

Just as a hint so you can go look yourself, the medical term for having more than 6 children is "grand multiparity", or a "grand multiparous" woman, or a "grand multipara".

A common problem for any woman who has experienced pregnancy and childbirth is damage to the levator ani muscle, which comprises a portion of the "pelvic floor."

 from here
This can cause a number of symptoms, including urinary incontinence (due to an increase in pressure on the bladder from less effective muscular support), and possible prolapse of the bladder, uterus, or rectum into the vagina, again due to the weakening of the pelvic floor.

One health risk from going through multiple pregnancies is the risk of a uterine prolapse, also called a prolapsed uterus. The weakening of ligaments basically leads to the cervix and uterus "sagging". In the most severe cases, the uterus ends up in the vagina.

Parity and obesity were strongly associated with increased risk for uterine prolapse, cystocele, and rectocele.

Pelvic organ prolapse in the women's health initiative: Gravity and gravidity
Parity in this context is the number of pregnancies that led to a viable gestational age (pregnancies excluding miscarriages)
Uterine prolapse makes subsequent pregnancies high-risk and can lead to fetal and maternal problems.
The general risk of anything happening increases due to going through multiple pregnancies in a short time span, though. Without sufficient recovery between pregnancies, women are at a higher risk of placental abruptions and placenta previa. For the baby, this leads to a higher risk of premature birth with the associated issues of low birth weight and small size.


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Do plant-plant interactions inhibit growth?
Plants produce lots of compounds that inhibit (kill or irritate) microorganisms and insects.  They have defenses against plant viruses and infections.
What kinds of compounds or hormones to plants use to regulate the growth of other nearby plants?  I have hear of ethylene, but I would like to hear about more specific compounds that might be known that work against specific species or kinds of plants?

The phenomenon you are asking about is allelopathy.
Remarkably, it has its own journal - Allelopathy Journal (ISSN:
0971-4693) published since 2009 and currently at volume 30, issue 1.
Here are the titles of the papers from the most recent issue:

In-vitro assessment of allelopathic effects of wheat on potato.
Allelopathic effects of sunflower on seed germination and seedling growth of Trianthema portulacastrum.
Effects of simulated acid rain on the allelopathic potential of invasive weed Wedelia trilobata.
Allelopathic effects of Brachiaria ruziziensis and aconitic acid on Ipomoea triloba weed.
Effects of Butia capitata pyrenes extracts on the germination of lettuce seeds.
Effects of root exudates from crop plants on the growth of Fusarium oxysporum f.sp. niveum.

So, if you have specific questions, this might be the place to look.

thanks - this helps quite a bit - i know nothing about plants!


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Is there any complex organism that is both autotroph and heterotroph?
Possibility also include "adaptation mode" if such exist. I don't discern whether autotrophic/heterotrophic part play only minor role either.

Does "complex" mean multicellular here? Or something more? Plants are usually autotrophs - do they count as complex?

yes multicellular at least

For example sundews are plants (so autotrophic), but they "hunt" for insects to get additional nutrients, e.g. nitrogen. As far as I remember the nitrogen is the main reason for eating other organisms but they also use other substances, including carbohydrates, from their prey.

To add to this: Those which are both are called photoheterotrophs or chemoheterotrophs. They get their energy from the sun/chemicals (via oxidation of electron donors) respectively but do not get all of their carbon from carbon dioxide, it is subsidised by the consumption of other matter.

@jkadlubowska: OK, but it make sundews ambiguous to fungi or other parasitic plants. I'm expecting more extreme case, maybe invertebrate?

@dhubris could you make what you actually want clearer? in the question it says "complex organism" then in the comments you define that as "multicellular at least" and now here you set the bar higher and want invertebrates, clarity will get the best answers. There are some cases of symbiosis between chemoautotrophs and invertebrates almost exclusively in deep sea environments (http://www.geology.wisc.edu/~wiscsims/pdfs/Dattagupta_ISME2009.pdf). However, in the definition of the animal kingdom it states that all animals are heterotrophs (http://www.windows2universe.org/earth/Life/animalia.html)

I think the concept of autotrophy and heterotrophy is narrower than the one you are using here. They refer to the source of carbon and not just source of matter. If we accept that sundews are auto- and hetero- troph, then we'll have to accept that we (human) are also hetero- and auto- trophs as we are mining for salt.

Just look up kleptoplasty
http://en.wikipedia.org/wiki/Kleptoplasty
The slugs who most frequently employ it would fit your more restrictive definition. Now, if we're getting technical, they aren't born that way. They steal the chloroplasts, but you didn't say, so I guess you need to revise your expectations again. ;)

now that is a cool symbiosis!

Do these slugs use inorganic carbon? Do they have a Calvin cycle of carbon fixation? If not, they only get energy from light, meaning that they are photoheterotroph and not autotroph.