text:
Decomposition Rate of A Body In A Wet Environment
I have a photo of a decomposing dog which is in a water logged environment. My peers and I are debating how long that body has been decomposing. They are saying it is at least a year old. I however think it's much more recent (1-3 months).
My understanding is that when a body is put into a wet environment either partially submerged or fully it speeds up the decomposition process provided the water is not lacking oxygen such as if it was deep on the ocean floor.
The carcass has its skull fully decomposed, which I think is due to the bacteria rich water having more access to surface area through the various orifices and also the skull having much less flesh than the rest of the body.
The torso looks for the most part intact, and I don't see any bloating from gas buildup (not sure when and how long such a feature would be present), and there appears to be a pink area which could be muscle.
Would these features be typical of a recent death in this type of environment or am I overlooking some other important processes that could be speeding up or slowing down the decomposition?
Photo (image unboxed in case graphic for some viewers)

Bugs, scavengers, microbes, time, the environment... a lot of factors at play in decomposition, for example: Forensic entomological decomposition.

Could you clarify the question a little? Are you trying to find out how long ago this dog died, or are you after a recognised method for estimating the "age" of a corpse in this specific type of wet environment?

I'm suggesting that this question as off-topic because I find it unclear what the user is asking and I'm not sure forensic methods are on topic.

@rg255 How is forensics not related to biology? There is a whole area of forensics that involves biology see: https://en.wikipedia.org/wiki/Forensic_biology

I'm not sure that the photo alone is enough information to give a precise answer. I'm voting to close for "unclear question" reason, but I enjoy the idea of forensic puzzles for biologists to solve!

It depends on the temperature of the environment as well. In the heat of summer and in a watery environment, I can verify through unfortunate personal reference that stuff can decompose very quickly. I honestly didn't look at the image, but judging by your description it can't have been there a year. There would be nothing left. Hungry bacteria and decomposers would have left nothing but bones by then. I would say your guess is more on target.

Can you please add some references to your answer?

Unfortunately in my case it's simple experience living in a rural/wooded area :/ Occasionally we have to do cleanup.


text:
CNS lymphatic vessels around ventricles lat et 4th?
I am searching for precise locations of the lymphatic vessels of the CNS based on the applications of the article here.
However, I did not find any when having a focus on the immediate region around ventricles (lateral and fourth).
I know this 2D visualization of the lymphatic vessels:

and this visualization at perivascular lobes

I am interested in how much the lymphatic vessels cover the lateral sides and ventricles.
I know this Blender application here where I consider Full hemispheres, each as a single mesh most useful.
However, I have a problem in adding those small membranes on top of each hemispheres and there lymphatic vessels because I do not know how evenly I should put those in the model.
I am particularly interested in the ventricles and how lymphatic vessels are around them.
How can you visualize the CNS lymphatic vessels around the immediate neighbourhood of ventricles (lateral and fourth) in 3D?

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
Electrode locations for neuron study in stereo EEG?
I am thinking where to put optimally depth electrodes in stereo EEG outside sulci in studying the functioning of neural transmission of N neurons over one perivascular space in rodents, mice or rat, where I would like to know how small N can be. The theoretical minimum is one neuron but I would like to understand the Physics how small current you can measure by EEG reliably with not too high Signal Noise Ratio (SNR).
I did not find any meta-analysis about EEG electrode locations in DynaMed Plus.
I am not sure about the anatomic therminology of Neurology so I use the terms cerebral cortex, sagittal and coronal planes in describing directions.
Definition of electrode's location somehow in cerebral cortex
The further the electrode is away from the source, the lower SNR.
This proposes me that there has has to be at least 20 neurons to minimize the variance.
What is the average distance between two neurons?
Here my conjunctures about location of electrodes where the picture is from Virginia's university Nature publication here:

where the electrode is surrounding N neurons and one blood vessel such that one electrode is below the neuron and one above.
It is contraindicated to put the electrode too close to the blood vessel.
Definition of electrode's Coronal-Sagital locations
I am interested in

how close perivascular space can the electrode be? Stereoelectroencephalography (SEEG) implantation method has a safety distance minimally 2 mm but practically more than 5 mm of depth electrodes. [TODO cite]
how superficial can the electrode #2 be? 1.0 - 1.5 mm in microelectrode EEG here i.e. mostly in superficial layers.
how deep can the electrode #1 be? I think mostly in superficial layer i.e. 1.0 - 1.5 mm with microelectrodes. SEEG with depth electrodes - minimally 2 mm but practically more than 5 mm.

Stability of electrodes
The stability is affected by many processes discussed here.
The array of electrodes is allowed to float with the motions of the cortex due

heartbeat
respiration
...

Sources

Talairach J, Bancaud J, Szikla G, et al. Approche nouvelle de la neurochirugie de l’epilepsie. Méthodologie stérérotaxique et résultats thérapeutiques. Neurochirurgie (1974) 20 (Suppl. 1): 1-240.
Cossu M, Cardinale F, Castana L, et al. Stereo-EEG in the presurgical evaluation of focal epilepsy: a retrospective analysis of 215 procedures. Neurosurgery (2005) 57: 706-718.

How can you define evidence-based locations of stereo EEG electrodes?

I am not sure why this question received a down vote. It is usually good to give an indication if it isn't plainly obvious what the problem is. That said, I am assuming that you are asking about rodents, mice or rat. Please clarify with an edit to your question.

@AMR - The downvote was probably the result from trying to measure single cells with EEG, that's impossible. This question is on depth electrodes for single-unit recordings. Further,  the answer to this question is opinion based, because there is no strict definition of where an electrode needs to be. The further away from the source, the lower the SNR.  What is acceptable and what not is pob.

@Christiaan Thank you for your comment! I made the body clearer. The one neuron study is just a theoretical model. I want to understand how you can estimate the amount of neurons required to be optimally within the distance in the cerebral cortex in EEG measurement, minimizing the variance.

The question is still unclear. An EEG is performed with noninvasive scalp electrodes in humans, or, perhaps, with transcranial epidural electrodes in special cases. The figure implies depth electrodes which is per definition not an EEG as far as I know.

@Christiaan Depth electordes are done with stereo EEG so EEG.

That's interesting. I didn't know that. +1

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
How can hyperplasia occur in non-fetal hypokinesis?
I have read that the hypoplasia can occur in fetal hypertrophic cardiomyocytes.
However, I am interested if this can be theoretically be possible in non-fetal cardiomyocytes which are hypokinetic. I think there must be some growth factors to allow this to happen. Other proposals

lysozyme, sepsis and cardiac adrenergic neural response / NO / G protein 1
shear-wave, vortex and refolding of proteins [2 Yuan et al.]

Sources

1 Lysozyme, a mediator of sepsis, impairs the cardiac neural adrenergic response by nonendothelial release of NO and inhibitory G protein signaling.
2 Yuan. Shear-Stress-Mediated Refolding of Proteins from Aggregates and Inclusion Bodies.

How can hyperplasia be regulated in non-fetal hypokinesis?


text:
What happens to fecal matter if it's continually re-eaten?
After class today, the topic of eating one's one fecal matter came up. There was a sharp divide as to how people thought the defecations would change. I realize this is a bit of an odd question but understanding it would help me understand how our body handles waste.
One theory was that the body would continually reuse some elements of the fecal matter such that, eventually and with no other input, nothing would be defecated.
Another theory was that there are elements in the fecal matter that the body would never make any use of, so it would continually get excreted (up until the person died, of course).
Could someone please explain the likely outcome of continually and only eating your own poop (assuming you could stay alive long enough)?

In a healthy person, stool weight depends mainly on the quality and quantity of the diet. The mean stool weight of a normal defecation is about 320 g [1].
Dry weight of fecal matter contains [2]:

30 % bacteria
30 % undigested food and fiber
10-20 % fat
2-3% protein

Let's do the math (the only nutrients in feces are fats and proteins):

20% * 320g = 64g of fats which can release 64 * 9.3 = 595 kcal of energy
3% * 320 = 9.6g of proteins which can release 9.6 * 4.1 = 40 kcal of energy

That's about 650 kcal. 2,000 kcal is a rough average of what people eat in a day. But your body might need more or less than 2,000 [3].
As you can see, fecal matter can't supply enough nutrients. Continuously (re)eating feces and only feces will lead to denutrition, less feces and death.
References:

Seyed Mohammad Kazem Hosseini Asl MD, Seyed Davood Hosseini MD. Determination of the Mean Daily Stool Weight, Frequency of Defecation and Bowel Transit Time: Assessment of 1000 Healthy Subjects
shigeta's answer on What is the composition of human feces?
HowStuffWorks.com. How many calories does a person need daily?

The author seems aware that the person would clearly die from lack of nutrition but is more wondering about the theoretical result. I think you should add that after continuous cycles of digestion, the fat and protein components of faeces would at some point be completely eliminated. So would the bacteria, but while passing through the intestinal environment, new bacteria would inevitably get mixed into the mass again. Thus, the result would be a mixture of undigestible fibre and bacteria.

A very thoughtful response. I guess my further question would be that, with only fecal matter as food intake, would the amount of bacteria and undigested stuff eventually (and theoretically of course) dwindle to nothing? Or would that continue to just be processed and excreted?

@AHungerArtist fibers and bacteria are not processed. Fibers will be excreted over and over again as-is. Bacteria may vary because they are multiplying in the intestine.

Want to add a point that some animals like rabits eat their feces because a single round of digestion is not very efficient.


text:
The Uniqueness of DNA Paradox
How can everyone have unique iris and fingerprints? After a certain amount of human beings have lived on earth, wouldn't it be possible to exhaust all possible combinations?
The same principle applies to DNA. Lets say counting all the nucleotides on a strand of DNA we find that there are a total of $N$. We know there are 4 types of nucleotides, thus the total number of possible DNA sequences equals $4^N$. This is exponential, and since $N$ is immensely huge, $4^N$ will be unthinkably huge as well. However, since $4^N$ is a finite number, how can DNA be guaranteed to be unique? Doesn't that contradict the pigeon hole principle?

There is always a chance of identical DNA sequences, and perhaps even identical biometrics between subjects. However, the chance is simply so small that it is of no problem for forensics and the likes.

I guess the assumption is wrong, that only DNA is responsible for the layout of iris and fingerprints. Even people with identical DNA (like twins) shall have different iris and fingerprints? So comparing the number of resulting combinations to the number of people would probably exhaust the lifetime of our universe.

This really does not relate to DNA, specifically. I say this because there are likely not that many allelic differences that account for pigment in the iris or patterning of fingerprints. This is a developmental question. It is the randomness of how cells migrate and the timing of gene expression that dictates. Each cell will either express from both alleles of a gene or there will be gene choice. The choice however does not need to be the same for each and every cell in a tissue. So where a cell ends up in development and whether it is expressing Maternal, Paternal, or both alleles determines

The uniqueness of irises and fingerprints are, as you said, limited to the number of possible permutations of irises and fingerprints.
A similar problem exists in computer science, and is known as a hash collision. Given sufficient samples, there will always be a collision for a hash of finite size. However, the sample space is sufficiently large for iris and fingerprint analysis for this to not be a problem.
A typical iris analysis system produces 2048 bits of entropy, while a typical fingerprint analysis system produces about 82 bits. Even accounting for the birthday problem, the information space is large enough that the chance of a given false positive is sufficiently low to prevent a random person from passing fingerprint/iris authentication.
For comparison, the current world human population is 7.2 billion, or slightly under 33 bits. The risk of a hash collision occurring is small enough to be negligible.
Of course, side-channel attacks against such biometric systems are relatively simple, but that's another issue altogether.

@Gordon That would be somewhere around 108 billion which has a collision probability of approximately 0.1% assuming a fingerprint is used.

@Gordon you should also consider that the same DNA would not make the exact same individual. There is a lot of randomness involved. Consider, for example, identical twins and their differences in character. You also have random mutations occurring during an individuals lifetime or development. In any case, you should not confuse 2 people with identical DNA with reincarnation which implies some sort of continuity or link between these individuals.

@terdon Unrelated to this question, but this is essentially the main plot point of Jupiter Ascending.

To add to what @terdon said, imagine the probability that two people, with the same DNA and chemical makeup, go through all the exact same experiences in their lifetime. The people they meet would all have to be similar enough to provide the same exact experience. Not to mention language, technology, and other things which are part of society. If the universe is really "infinite", there is an infinite number of positions the objects of the universe could be in. If you argue for a finite universe, then maybe eventually it could happen.

@Gordon My point was that much, much, much longer after that, if the Universe has a finite space and amount of matter/energy, and continues indefinitely without "dying", a person with the exact genetic make up and exact same life could exist on a planet exactly like Earth again. Proof: Pigeon hole principle

@DoubleDouble you are assuming the person is male. X-chromosome inactivation in females is stochastic, and as every woman is a mosaic of expression from either the maternal or paternal X-chromesome for each and every cell, then even a female "clone" would not be identical.

@March Ho's answer is an excellent answer based on the assumption that all of the observed phenotypic variance is due to genetic variance.
Environmental variance
The genetic variance is not the only underlying variance that can explain variance in phenotypic traits. There is probably quite a lot of phenotypic variance that is caused by the underlying environmental variance between individuals. To have a better understanding of what are the different kind of variance you may want to have a look at this post for example. The heritability is typically equal to 0.3 (in fact most studies to report measures of heritability that are not significantly different from 0.3). If this was to be the case for the trait of interest, it would mean that 70% of the observed variance in fingerprints would be due to environmental variance.
Developmental Noise
Also, when talking about minor differences in phenotypes (such as fingerprints), developmental noise (inherent stochasticity of biological processes such as the decay rate of proteins or the production rate of mRNA) might be of real importance. (Raser and O'Shea, 2013) uses fingerprints as example of phenotypic trait which variance is in part determined by developmental noise.
Relevance of an answer that cares only about genetic variance
While @March Ho's answer is pleasant and interesting, I think that it is not of great relevance to the problem given the important amount of non-genetic variance that is underlying the phenotypic variance of interest.

+1, good catch! I didn't think about the correlation of the two variables.


text:
Making positive charged polyacrylamide
I am interested in positive charged polyacrylamide to electrophorese molecules I am interested in.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2643323/
http://onlinelibrary.wiley.com/doi/10.1002/bip.360300309/pdf
The articles shown above use allyltriethylammonium bromide (ATAB), but I am not sure which chemical they mention.
Or is there any other chemical to add to acrylamide to get positive charged polyacrylamide copolymer?

I would say that this question is better suited for chemistry.se.

ATAB contains a quaternary amine and a terminal carbon-carbon double bond. The polyacrylamide reaction links acrylamide by their double bonds forming the polymer. The double bond on ATAB can be incorporated into the growing polymer chain, and the quaternary amine holds a positive charge, making a positively charged polymer.
The immobilines mentioned are probably just a weak acid or weak base group with a terminal double bond like ATAB or acrlyamide. They get trapped into the polymer and if you pour the gel with a pH gradient, they pick up charges according to the pH. I haven't found a good concrete immobiline example, I can't access that second article you linked.
I am away from my good computer and cannot make chemical structures right now.

Thank you. I sensed how it works when I read, but I was not able to find the commercial products so I was wondering why. Now I find it.


text:
Conversion and storage of glucose to glycogen
Why is excess glucose, synthesized to glycogen, stored only in limited amounts, as compared with lipids/triglycerides that are stored in our body?
Why is mature glycogen arranged (polymerized) in 12 tiers polymer?

Glycogen storage limitation is due to these additional facts also:

Glycogen is a hydrophilic molecule. This means an increase in glycogen concentration will cause a proportionate increase cell weight due to water accumulation. As cells can contain only limited volume the amount of glycogen stores are limited. Lipids are hydrophobic hence can be accumulated without increasing the volume and weight of cell due to water accumulation.
As a source of energy lipids are approximately 2.5 times more efficient than glucose.

In this presentation from stanford.edu, it's stated that the number of granules is directly dependent on the number of glycogenin molecules available, and the size of the granule is directly dependent on the need for physical association b/t the glycogen synthase, and glycogenin.


text:
How to obtain virus samples?
I'm trying to observe the behavior of simple viruses in different environments. I'm just looking for simple viruses like the common cold and the flu virus nothing major. Is there a way to obtain them?

As @DonJulian stated you will not get access to human or even mammalian viruses as an individual. Even most Academic research facilities that work with viruses will be highly regulated. Viruses are DANGEROUS. They mutate easily and can go from benign to a killer easily. They can also jump species rather easily. There are, howeve,r ongoing projects to find viruses that attack bacteria, known as Bacteriophages, and these can be found by digging up soil. If you can find an academic sponsor in your school this http://www.seaphages.org/ is one of the projects you can participate in.

First of all, cold and flu viruses are not 'simple viruses', and they are not harmless. They kill tens to hundreds of thousands of people every year.
Secondly, this would depend highly on the risk group that the virus falls in. The NIH sets strict guidelines on who can handle infectious agents. Unfortunately, I can almost guarantee you that no one is going to give you even risk group 1 plant viruses, and they are certainly are not going to give you cold or flu viruses. Risk groups range from 1 to 4. To handle risk group 2 viruses, for example, you are expected to do so in a BSL-2 or higher laboratory, and anyone maintaining stocks of virus is going to do a hefty check of you and your 'facilities' before shipping you anything.
Furthermore, even if you did obtain the virus, you would need to store it or maintain stocks of the virus in tissue culture. Its not like you can just get an eppendorf tube of virus in saline and expect it to survive in your refrigerator at home, and its not like companies are shipping virus willy-nilly to anyone.
That being said, and at the expense of sounding self-righteous, there is really no reason for you to obtain virus particles. You should start by getting a book on virology and reading it. There is plenty of learning material both visual and written out there, and all I will say is if you don't already know how to culture virus or where to obtain it, you shouldnt be doing so, and no one is going to give it to you.
CDC Biosafety in Microbiological and Biomedical Laboratories: http://www.cdc.gov/biosafety/publications/bmbl5/BMBL.pdf
WHO Laboratory Biosafety Manual: http://www.who.int/csr/resources/publications/biosafety/en/Biosafety7.pdf
NIH guidelines recombinant nucleic acids: http://osp.od.nih.gov/sites/defaul/files/NIH_Guidelines.html
I think its great that you are interested, and it sounds like you are interested in histopathological changes caused by virus, so I have included some nice histo pictures below

Syncytia (Herpes Simplex Virus type 1)

Clearer example of syncytia

Characteristic owl-eye (Cytomegalovirus)

Distemper virus inclusion body

Coronavirus particles with 'crown' of surface glycoproteins

Budding HIV virus particles from the plasma membrane

Bacteriophage T4 escape by lysis

Papillomavirus

Rous-sarcoma virus

Tobacco mosaic virus


text:
Do intestinal flora have the same DNA as their host?
Please bear with me, this is not my professional field and I might be mixing things up. In an explanation why seeds won't start growing in one's intestines, the explanation given was that foreign bodies are detected by the DNA they carry and get attacked and digested, separating all strands of amino acids so they can be reused by the host and no DNA mixture can occur.
I also heard that the immune system uses the same technique to detect intruders (and subsequently attack donor-organs).
I was wondering, when a baby gets weaned (starts eating regular food), where do these fauna come from? Does the baby produce them, or are they provided in the food and survive the defense system?

Welcome to Biology.SE. Is your question "How come our gut endosymbionts don't get killed by our immune system?" or is it "Are gut endosymbionts inherited from the mother or are they acquired by the baby through food?"

I think he's asking "Where does the gut microbiotia start from?"

@swbarnes2 Could you suggest a good source for beginners. The wikipedia link that m1clee provided was helpful, but I guess a more ordered source that starts at basics and builds up would be more appropriate. Unfortunately I don't have the time or money to go back to high school (there are many additional subjects I'd love to study if I could :-).

I saw this link tonight. It is related to an exhibit at the American Museum of Natural History about the microbiome. http://www.amnh.org/exhibitions/the-secret-world-inside-you?utm_source=online&utm_medium=banner&utm_content=paid-placement&utm_campaign=SWIYcampaign2015 There are a few movies and it is likely curated for the general public, so you may want to start there before you delve into some of the links in my answer below.

Could you suggest a good source for beginners. - Louis Somers

The interactions between the human body and its microbiome are quite complex. I am going to provide you with an answer that will be based on your comment that you would like an answer from a beginners perspective.
For simplicity sake I will keep the answer to humans as the host organism, though pretty much any multicellular organism can act as a host for microscopic organisms.
Note: A number or the references I use come from Janeway's Immunobiology. The links provided are to the 2001 edition that is on the NCBI bookshelf. The issue, however, is that over the past decade we have learned a great deal more about the immune system since then, and some of the things I refer to were not represented in that edition of the text.

Do intestinal fauna have the same DNA as their host?

The short answer to this question is no. Also, we generally identify microbes of this nature as flora instead of fauna, so you would say intestinal flora.
The human microbiome (microbiota), as it is often referred to, is made up of hundreds of trillions of microorganisms that live in the niche of our digestive tract, airways, urogenital tract, and skin. In fact, the estimate is that there are 10 times as many microbial cells that live on the human body than there are human cells that make up the body itself (1). The difference is that human cells are immense when compared to most of the microbial cells that colonize us (2).
The vast majority of the microorganisms that populate us are single-celled organisms, such as bacteria or fungi (yeasts). Each of these cells is its own entity, in other words is an independent living organism, and they have their own genome (the complete genetic material of an organism) that encodes for their own proteins.
There is a good reference tool, though maybe a little advanced from The University of Utah, The Human Microbiome. This interactive presentation gives a layman's overview. The American Museum of Natural History has also curated an exhibit called The Secret World Inside You.
To add a point for clarification, while the genetic codes of these microbes are different in different species and are different from that of the human host, the molecules that hold the information, namely DNA, are all made of the same nucleic acid building blocks (5). To use an analogy, it is like using the same letters but writing in two different languages. We may use mostly the same characters, but the way we arrange those letters to form words in Spanish or words in English create different meaning.
When these single-celled organisms reproduce, they copy their own DNA and they divide into two new cells, each receiving one copy of that DNA (6).
Since yeast and other fungi are evolutionarily closer ancestors to humans than are bacteria, some of their genes, the sections of DNA that are functional and encode for proteins and RNAs, have a very similar sequence to our own (referred to as having homology) and often perform similar or the same function (7). When this is the case, we say that the genes are evolutionarily conserved, but for the most part evolutionarily conserved genes will vary in sequence from organism to organism, and the variation will usually increase the farther back you go in order to find a common ancestor between the organisms.
The human body is made up of about 37.2 trillion cells, on average (8). Almost all of these cells, with the exception of Red Blood Cells, have a copy of the hosts genome (9). All of these cells arose from a single egg produced by the mother and fertilized by the father's sperm (10). The egg and the sperm contained half the genome necessary for the embryo to develop. The DNA from the mother and the DNA from the father come together when the nuclei fuse. So we have our own genome that came from our mother and father, and the microbes have their own genome which they inherited from the ancestral cells that gave rise to them.
That is a slightly simplified answer as there can be different ways that the DNA can be passed between the organisms, but for the most part, we have our own DNA and, even though they live on us and in us, the microbes have their own DNA.

Your first paragraph.

I cannot tell you necessarily why seed that we swallow and digest do not germinate inside of us. It is likely that the seeds are not receiving the proper signals from the environment of our digestive track to initiate the genetic program to begin germination and development into a plant.

I also heard that the immune system uses the same technique to detect intruders (and subsequently attack donor-organs).

The vertebrate immune system is a diverse, highly-tuned system of surveillance that monitors for pathogens or foreign bodies that are introduced into the body that may be dangerous to the survival of the organism (11).
For humans, the first set of defense are barrier defenses (12). The surface of our skin consists of several layers of dead, keratinized cells that form an impermeable barrier. As long as this layer is not breached, it does an excellent job of keeping yeast and bacteria outside, away from tissue that they could damage.
On the interior surfaces, our airways, gastrointestinal tract, and genitourinary tracts contain specialized cells that produce large amounts of mucus that will coat the surfaces of these tissue. Mucus serves multiple roles. First it keeps the tissue moist, so that it does not dehydrate. Next it keeps the microbes at a distance from our cells, so that they do not come in direct contact with our epithelial cells (The cells that make up the linings of our digestive tract, genitourinary tract, and airways). Third, it can trap microbes in it. The epithelium is able to "sweep" the mucus along and as a result it is able to clear bacteria out of the body (13).
Included in the barrier defenses are actually the microbial organisms themselves. The interaction between the host and an organism which is neither detrimental or actively beneficial is known as commensalism (13). Basically, all of these trillions of microorganisms that life on us do not hurt us. In return, they get an environment in which they can live. As a result of this, commensal organisms will grow on these surfaces, will take up all of the space, and will use up the nutrients that could be used by pathogenic organisms (organisms that are actively able to cause an infection) to establish an infection.
The next level of defense comes from the cells of the innate immune system (14). In innate immunity, specialized cells monitor the area they are in for Pathogen-Associated Molecular Patterns (PAMPs). PAMPs can be sugars that make up the cell walls of the microbe or proteins that get expressed on the surface of the organism, such as Flagellin, a protein only found in the flagella of certain pathogen. The innate immune cells have pattern recognition receptors (PRR) that have a general specificity for recognizing and responding to the PAMPs. Our cells even have PRRs for DNA and Double Stranded RNA's, however those are usually found in vesicles on the inside of the cell. These interactions are very general, however once PRRs bind to the PAMP, they are able to signal into the cytoplasm, which can lead to the production of proteins, among other possible responses.
Here you can think of PRRs like a motion detector in a security system; the dog, or your two year old, or an intruder are going to set off the alarm just the same. It is not specific. The motion sensor "knows" that something that it is supposed to recognize, i.e. a moving object larger than a mouse passed by and it triggered the response, but it cannot tell you which moving object triggered it, only that it was triggered.
The innate immune cells are also able to respond by "eating" the pathogen in a process called phagocytosis. Here, they break up the bacteria, yeast, or the remnants of other dead host cells or large pathogens, things like worms, and put the broken up pieces on protein molecules on their surface.
When innate immune cells do this, they are presenting molecules to specialized immune cells (adaptive immune cells (14)), B-Cells and T-Cells, that are highly specific as to what they will react to. These cells can also cause a lot of damage to the host, so they are tightly regulated. Think of the interactions as keys and locks. A protein from a bacteria should turn a few of these cells on, but a protein from the host should not fit the lock.
All of these immune cells also respond to diffused chemical signals called cytokines. These molecules are secreted by some cells and are received by receptors on the host cells. Sometimes the secretion is by another immune cell, sometimes it is from a non-immune system host cell, and sometimes these molecules can be secreted by the bacteria, fungi, or worms themselves.
Depending on the chemical signals that are secreted, and how the cells are interacting at the time of the message, and which cells are receiving the message, will determine the response to the message. It is contextual. Think of the phrase "You're killing me." If someone says it, while laughing, to a good friend who is telling jokes, it means one thing. If it is screamed as someone is being choked by an attacker, it means something very different.
To summarize, the immune cells are surveilling the environment and trying to pick up what is friend and what is foe and they try to respond accordingly.
Over time and coevolution, our microbiomes have developed ways of communicating with our immune system to let it know that these microbes do not mean any harm. They are able to "train" the immune cells using chemical signaling to temper the immune systems response to them (15), and this is how they are able to coexist within our body and with an immune system that is constantly on seek an destroy missions. Also because of the mucus, our microbiome usually isn't in direct contact with our cells, so it is a different kind of interaction than if an infecting pathogen were to breech the barriers and gain access to sterile areas where no bacteria or fungi should be found, and as a result, the immune system reacts differently.
As for organ and tissue rejections (16), the issue here is that each of our cells, except for Red Blood Cells, present molecules on their surface that identify it as being a cell that was made by the body itself. You can almost think of it as a sport's teams jersey. The immune cells can survey the proteins displayed on the surface of our cells and tell that they are ours instead of from a pathogen. The problem is that each person makes a different array of these proteins, so if I were to give you a kidney, the proteins that the cells from my kidney make and put on their surface for immune cells to look at will be different from yours. In this case, because the keys do not fit the locks, the immune system reacts to the donated organ as an intruder and begins to attack it. Immune cells are extremely lethal and will kill the donated organ if they are not suppressed. That is why transplant recipients need to have their immune systems suppressed in order to survive with the donated organ. You might ask "well what if we just took all these proteins off of the surface so that they don't get recognized?" Well, the problem is that we have another class of immune cells known as Natural Killer Cells that patrol the body looking for cells that are not presenting these proteins, so the immune system is pretty adept and finding and killing things that it does not recognize specifically as self.

I was wondering, when a baby gets weaned (starts eating regular food), where do these fauna come from? Does the baby produce them, or are they provided in the food and survive the defense system?

To be honest, the majority of the microbiome is laid down during vaginal birth and breast feeding. Passing through the birth canal, microbes from the mother's vagina and feces are ingested by the newborn and this is their first real dose of microbiome, though some research is suggesting that the microbiome begins to form in the fetus before birth and is transferred through the placenta from the mother to the fetus.
Assuming we do not kill these bacteria with antibiotics, have other pathogenic bacteria take over the territory (yes, bacteria and fungi, like gangs, have turf wars; that is why we often find our antibiotics as compounds secreted by these organisms), or have a disease that wipes out the microbiome, and provide it with a health diet, then the microbiome pretty much is maintained by the microbial cells reproducing by cell division.
Also we will pick up these bacteria from the environment. We are constantly shedding enormous amounts of these cells into our environment. Babies touch things and put their hands in their mouths. This transfers good microbes as well as bad ones, and it is really just a natural part of the process. That is why the overuse of antibiotics and antibacterial soaps can cause unintended consequences. We are killing the good as well as the bad.
This reference, Your Changing Microbiome, again from The University of Utah is a good resource.
So to summarize, babies get the microbiome at birth through vaginal flora and maternal feces. They are also getting daily doses from the microbes that colonize the mother's skin when she nurses the child. Then these bacteria are also in the environment, so babies touch things, then they put their hands (or feet, the little contortionists) in their mouths and they get doses this way. Raw fruits and vegetables will also have microbes on them that will be taken in. As for the microbes, they have cell walls that allow them to live in environments that would be hostile if they did not have the cell walls. They also communicate with our immune system and "train" it not to kill them, and as long as nothing that we do, such as take antibiotics or get a disease, the microbiome will pretty much maintain itself through replication.

Wow, Thanks for all the effort you put into this! It is allot more complicated than I thought. I have yet to follow the provided links, but the text has been an enjoyable read! Thanks again!

@LouisSomers Always willing to put in effort to help someone who expresses a sincere and honest interest to learn. I could see from the comment on your question that it was worth the time to put together as complete a response as possible. As you work through the references, don't hesitate to raise questions about things that might be confusing. I, or one of the other contributors here will be happy to clarify. Best of luck on your journey. Biological knowledge can be truly mind-blowing when you start to see its complexities and its interconnectedness.

3k! Congratulations :D Close voting is all open up now :-)

@Christiaan Thank you. I'm in it for the knowledge... I figure the blood, sweat, and tears I put in to acquiring it should benefit someone other than me.


text:
Can an argument be made that humans are 90% bacterial?
On the blog, All about Scientist in Microword: Microbiology, I read the post We are 90% bacteria, actually, which says that humans are 90% bacterial cells.
If this is the case, then why don't we behave like them and why isn't the bacteria genetic material more dominant?
As bacteria helps us in making many enzymes for us, can we say that we are symbiotic creatures?

Can you please cite the source you are talking about? Your point is not completely wrong, since we harbour indeed a lot of bacteria in our gut and on our skin and their numbers (depending on the source) outnumber the number of our cells by about one magnitude. Still, they are not part of us.

The bacteria within and on our bodies do engage in a symbiotic relationship – defined as an interaction between two different organisms living in close physical association. It can even be said that the relationship between certain bacteria and humans is mutualistic. For example, the bacteria residing on our skins and within our intestines benefit nutritionally, while we benefit from the bacterial "barrier effect".

One could consider energy: If you count human somatic cells as zero percent bacterial (you cheater!) then you ask what fraction of heat comes from those as opposed to bacteria. I think it is ~8% bacterial, almost all form the gut, but am not sure.

I am not sure what you read as you have not supplied any references, but humans are not 90% bacterial cells. (OP subsequently provided; see Edit 2)
Humans are 100% human cells, however for every one human cell, approximately 10 single celled organisms (Bacteria or Fungi) live in (colloquially) or on the human body. This is referred to as the microbiome. You can find more information in the link I provided or in the answers to the following questions on Biology SE.

Do intestinal flora have the same DNA as their host?
How many diseases can be linked to disruption in the microbiome of a human?
What is the function of E-coli bacteria in our stomach?
How heavy are all foreign microorganisms in and on the human body?

Think of it this way; just because the human body provides these organisms with a home does not mean that it is composed of them, that would be like saying an apartment building is made up of x percent of humans or pets or mice or insects just because that is where they live.
You may also find some interesting information at The Secret World Inside You from the American Museum of Natural History.
Edit

As bacteria helps us in making many enzymes for us, can we say that we are symbiotic creatures?

The definition of symbiosis is:

The interaction between two different organisms living in close physical association, typically to the advantage of both.

Given that definition, and given the fact that there are some bacteria in our microbiome that are able to produce metabolites that our cells cannot, and we provide them with a "home" with the necessary nutrients for their propagation, then you can say that this is in fact a symbiotic relationship.
The more technical description that is often used for the microbiome is that these organisms that populate the human body are commensal.
Commensalism is defined as:

An association between two organisms in which one benefits and the other derives neither benefit nor harm.

In this respect, the majority of our microbiome are commensals, they live on us, but give us nothing in return, and for the most part do us no harm.
Some of the organisms can be opportunistic pathogens in the sense that if they are able to gain access to normally sterile areas of our body, such as in peritonitis arising when the intestines are perforated, then they can be harmful, but in their general niche, they are just there.
As we learn more about the microbiome, we are beginning to see that there is a far more complex relationship between host and microbe than we anticipated, so over time, the views on the microbiome are likely to change from the understanding that we have today.
Edit 2
To address the source that you added All about Scientist in Microword: Microbiology, I would say that the blogger is guilty of hyperbole. While Steven Gill, the molecular biologist that the blogger quoted, may not have chosen his words carefully, he was not implying that humans are 90% bacteria, as the blogger then posits.
Gill makes the mistake of using the word "in" when he states "There are some estimates that say 90% of the cells in our body are actually bacteria...." The microbiome exists on the surfaces of our body not in it.
We forget that the gastrointestinal tract, urogenital tract, and respiratory tract are lined with epithelial cells and are thus external surfaces, just as our skin is an external surface. So the microbiome lives on our body, and not in it or as a part of it.
No place in our body do we have organs or tissue that is a homogenate of human cells and bacterial cells functioning together normally. And while there are bacteria that are able to infiltrate cells and live within vesicles or the cytoplasm, this is a pathogenic condition and not what we would normally expect to see in a healthy human.
We know that this is the case, because developmentally all of our body cells and germ cells arise for the fertilized egg. It isn't until much later in development or at the moment of birth (there are some reports that microbiome begins to cross the placenta prior to birth) that we acquire our microbiome. If it were the case that humans, or any eukaryotic organism for that matter, were 90% bacteria, then we would not develop in the sterile environment of the amniotic sac. The lack of bacteria during development would be fatal.

http://microbioresearch.blogspot.in/2008/06/we-are-90-bacteria-actually.html

this is the link where you will find about the fact I discussed.

@user101184 Please edit your question to include the reference. Also, you should quote what in the site brought you to your conclusion.

But we can say that 90% of human weight is actually bacterial. "and for the most part do us no harm." - we weigh more, so we are less enduring. We run slower and jump lower. Isn't it so? Then don't they cause us a disadvantage?

I just wanted to tackle the interesting numbers here.  So there are roughly 10^13 human cells in our body, and 10^14 bacterial.  That is where your 90% bacteria number comes from.
But remember that bacterial cells are much, much smaller than human cells.  E. coli ranges from 0.5um to 2um.  Human cells are ~100X larger at 0.1mm or 100um.  That translates to:
Surface area - E. coli is ~3.14um^2, human cells are ~32,000um^2.
Volume - E.coli is ~0.52 um^3, human cells are ~524,000um^3.
From an information content point, each of your cells contains 3 billion base pairs of genetic information, an e. Coli cell is ~4 million base pairs (bp).  So your cells contain 3^23 bp, while the total bacterial content is closer to 4^21 bp.  There is almost 100 times as much of your information as bacterial information.  Also yours is all the same, vs the different types, colonies, and progeny of bacteria in your body.  To put in similar terms as your question, while bacterial numbers account for 90% of your total cell numbers, their genetic information accounts for ~1% of the total.

Nice analysis and good insight.

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


text:
How body loses more fat in CO2 form than in sweating form?
Yesterday, I saw TV Game Show.
There is question like this: Body loses more fat in which form?
It gave 4 options:
1) CO2
2) sweating
3) xxx
4) xyz
sorry i didn't remember 3 & 4 options.
so right answer is CO2. anchor explaining the reason behind it, suddenly my brother switch the channel. all gone.....
Everybody thinks sweating is right answer, i have reason for it, if we work out our body whole fat comes out in sweating form.

Sweat is the release of water that evaporates, allowing the body to cool itself under exertion. When fats are converted to energy, they are used as an input into the Citric acid cycle. The molecules are eventually broken up and the byproduct is CO2.

Fatty Acid Metabolism and The Citric Acid Cycle. And for perspiration

This is a curious case of a rather poorly stated question that actually has something pretty interesting underneath --- where does the atoms from fatty acid oxidation go? CO2? Water? Now I don't know how to vote :)

If you exercise heavily, you can sweat enough where you have to drink to replace it. But on a normal day, you don't sweat all that much.
On the other hand, when you metabolize food, you essentially burn it. According to the Merck Manual,

Carbohydrates, proteins, and fats supply 90% of the dry weight of the diet and 100% of its energy. All three provide energy (measured in calories), but the amount of energy in 1 gram (1/28 ounce) differs:
4 calories in a gram of carbohydrate or protein

9 calories in a gram of fat

A typical diet is 2000 calories per day. If you get 50% of your calories from fat (shame on you!), that is 1000 calories of carbohydrate or protein, or 250 grams. It is 1000 calories of fat, or 111 grams. 361 grams total.
We will simplify. CH bonds contain little energy compared to CC bonds. H weighs little compared to C. We don't change much by ignoring H. There is some O and other stuff, but we will ignore that too. It will still be roughly right. So you burn about 361 grams of C.
For every C atoms you metabolize, you must breathe in 2 O atoms, and breathe out all 3 atoms as CO2. C atoms have an atomic weight of 12. O is 16. So CO2 is 44. Every 12 grams of C becomes 44 grams of CO2. So to burn 261 g of C, you breathe out 1324 g of CO2.
1324 g of water would be 1.324 liters. It is easily possible to sweat that much in a day, but you typically don't. You typically breathe out more CO2 than you sweat water.

I think this is rather misleading. The CO2 produced in fatty acid oxidation is not derived from O2 but from water, via hydration reactions. O2 is the terminal electron acceptor in the respiratory chain. You must take this into account when estimating water production. Also, C-H bonds are as important as C-C; many high energy electrons are extracted in fatty acid oxidation by replacing C-H with C-O bonds.

@Roland - I am sorry. I did not see this until today when someone upvoted. I thought I was supposed to be notified. You clearly know more than I about this. How should I improve the energy estimate of CO2 production? The O in CO2 can originate from water in a hydration reaction, but C cannot. Also this was about sweating, not the total water produced by metabolism. Some water is breathed out, some goes in urine.

Yeah the questions was pretty vague to being with. I would just ignore the effect of oxygen since it doesn't originate from fat anyway, and say that since fat is mostly (CH2) units with mass ~14, then by mass 12/14 = 85% of fat is exhaled as CO2 and 2/14 = 15% leaves as water.  Of course we're tallying up parts of molecules here but it's the way the question was posed I think. The energy yield is not relevant I think.


text:
Unable to identify a muscle of the anterior thorax
I was watching an YouTube Anatomy Video which goes over the major muscles of the anterior superficial thorax. There is a structure present throughout the video which goes unmentioned, and I can't seem to identify.

It is shown as a pair of structures, each running from the manubrium to the xiphisternal junction along the lateral margin of the anterior sternum, perhaps with a second head attaching to the costal cartilage.
I'm probably missing something obvious, but for the life of me I can't think of what that could be.

This appears to be the sternalis muscle. The reason it is not mentioned may because it is not present in all individuals, and is therefore relatively poorly characterised.
The image is from An Atlas of anatomy by regions by John Charles Boileau Grant.

Another image of the muscle can be found in Pocket Atlas of Human Anatomy by Thieme:


text:
On which amino-acids residue is the SDS acting on?
I would like to know exactly what is the mechanisme of the SDS, and I would like to know on which amino-acids residue the SDS is acting on.
Can you help me please ?
Thank you in advance !

If your talking about Sodium Dodecyl Sulfate(a detergent) it has a two main functions:
(1) It disrupts all non-covalents bonds in proteins i.e hydrogen bonds from the main chain, or hydrogen bonds between residues which are dependent on protein shape.
(2) It coats the proteins with a negative charge which is useful for laboratory techniques such as gel electrophoresis.
Your question states "what amino acid residues does it act on?". You can be safe to assume that the SDS will coat the entire protein. About 0.1% SDS solution is enough to sature the polypetide chains of protein molcules with about one SDS molecule per two amino acid residues.


text:
Calculating pairwise Fst from allele frequencies
I am trying to refresh my memory on population genetics for a project, and I'm having some trouble.
Assume I have genetic data on 3 populations with 5 individuals in each of a given species, with the following number of genotypes:
      0101 0102 0202 0103 0203 0303 0204
Pop1   2    3    0    0    0    0    0
Pop2   1    1    1    1    0    1    0
Pop3   1    0    3    0    0    0    1

I have named alleles 01-03. So 0101 is a homozygote individual for allele 01, 0102 is a hetorozygote individual etc.
Is it possible to do this, from the following formulae:

If I input the information above into Genepop to calculate pairwise Fst using the following dataset:
Test Genepop
TestLocus
pop
Pop1, 0101
Pop1, 0101
Pop1, 0102
Pop1, 0102
Pop1, 0102
pop
Pop2, 0102
Pop2, 0103
Pop2, 0303
Pop2, 0101
Pop2, 0202
pop
Pop3, 0101
Pop3, 0202
Pop3, 0202
Pop3, 0202
Pop3, 0204

it produces the following result:
Pop    1       2
2    0.0278
3    0.2308   0.0669

However, how can this result be reproduced and calculated by hand?

The original Wright's formulation
$$Fst=\frac{var(p)}{\bar p}$$
, where $\bar p = \frac{1}{J} \sum_{j=1}^J p_{j}$ and $var(p) = \frac{1}{J}\sum_{j=0}^J (p-\bar p)^2$ is the variance in frequencies among populations.
This original formulation is valid only for a bi-allelic locus. Nei (1973) generalizes this definition to loci that have more than two alleles.
Nei (1973) general formulation
I recommend to have a look a the paper (Nei 1973), it is a really nice paper.
Nei shows that defining that within Subpopulation gene diversity (a.k.a. expected heterozygosity) $H_S$ and the Total gene diversity (a.k.a. expected heterozygosity) $H_T$ as
$$H_S = \frac{1}{J}\sum_{j=1}^J \frac{1}{I}\sum_{i=1}^I p_{ij}^2$$
$$H_T = \frac{1}{I}\sum_{i=1}^I \left(\frac{1}{J} \sum_{j=1}^J p_{ij}\right)^2$$
, where $I$ is the number of alleles and $J$ is the number of populations. Then Wright's definition of $F_{ST}$
$$F_{ST} = \frac{var(p)}{p(1-p)}$$
generalizes (for cases with more than one allele) into
$$Fst = \frac{H_T-H_S}{H_T}$$
Have a look at Nei 1973 to understand why they are equivalent.
Weir and Cockerham (1984) formulation for several loci
Averaging $Fst$ over several loci is more complicated than one would expect at first place. The solution is given in Weir and Cockerham 1984.
The formulation is a little cumbersome so I just invite you to have a look at the paper.

Thank you for your reply, Remi.b. I am aware of both papers, but I will read through them again.
In this case, I was mostly interested in the practical approach of solving a calculation as the one above.
Would you say, that it is not possible from the formulars I have listed?

I am not sure I understand what you mean. You have two formulas, one defining $H$ and one defining $Fst$ from $H_T$ and $H_S$ (but not $H$). How would it be possible to calculate $Fst$ from the frequencies in each population $j$ ($p_j$)?


text:
Question about proto-oncogenes and oncogenes?
My textbook says:

Growth-promoting genes are called proto-oncogenes. Some can be changed into oncogenes by a point mutation that alters the ability of the proto-oncogene to be switched off. They remain permanently switched on. Oncogenes promote unregulated cell division. Such cell division leads to a tumour.

Does this mean that the change from proto-oncogene to oncogene is not a mutation in the exon, but rather in the intron?
I hope I used these terms correctly. Thank you for any help :)

I think that this is a good example of how a question should be asked. You provided the passage that was causing you some confusion and you posed your question based on how you were thinking through the situation. Good job. :-)

I am going to add to @MattDMo 's answer a bit.
Proto-oncogenes Function, Developmental Program, and Regulation
Proto-oncogenes are normally functioning genes that are more often than not in the pathways that lead to mitosis and cellular replication. They have important roles in the development, growth, and maintenance of the organism. Proto-oncogene is an accurate description of the genes, but I unfortunately think that sometimes people think that the genes themselves are bad and that isn't the case.
Growth and development in multicellular organisms are highly regulated processes with many checks and balances. Certain cells need to grow in certain places at certain times, and then they need to go into and remain in interphase. If they don't, or they do things at the incorrect times, the multicellular organism will not develop properly or will develop conditions such as cancer.
It is often these points of regulation that become dysregulated when a proto-oncogene becomes oncogenic. If there are regions of allostery that are affected by a mutation in the coding sequence (exon) and a control molecule that represses the activity of the enzyme through conformation change can no longer bind, then that enzyme can remain active, always turned on.
You can also have a situation where you have transcriptional regulators of proto-oncogenes that can be effected making the gene product oncogenic. If there is a mutation in an enhancer (intronic) of the gene that affects the binding kinetics of enhancers leading to a great increase in transcription, this concentrational difference can lead to uncontrolled grown and tumor formation.

You could also have a situation like MattDMo talked about where you generate frameshifts and premature stop codons, though I would think this is more relevant in tumor suppressor gene mutations, as these types of mutations tend to kill the protein rather quickly, but it is possible that it can cause a problem.

RAS
There are however other types of mutations that can effect proto-oncogenes, making them oncogenic. One classic example is RAS. RAS is a G-protein that associates with G-Protein Coupled Receptors at the cell surface and transduce signals into the cell leading to the initiation of the cell cycle. In its inactive form, RAS is bound to GDP. When a signaling molecule binds to the plasma membrane receptor it is associated with the RAS molecule, a Guanosine-Exchange Factor removes the bound GDP, and because of concentration, GTP enters the binding pocket and activates RAS, which activates a phosphorylation cascade, leading to transcription of growth factors.
Normally RAS has GTPase activity and will quickly cleave the gamma phosphate of the GTP in its binding pocket, leading to GDP and inactivating itself. However if the mutation were to knock out this GTPase activity from RAS, then it would have no way to cleave the Gamma phosphate, and therefore it would remain activated and continue the signal transduction, even when it should not.
However, the problem does not need to be with RAS to drive RAS to oncogenesis. If RAS GEF becomes hyperactive and starts to exchange GDP for GTP constitutively, whether or not there is a signal, then RAS will constantly be activated, even if it is still able to cleave the Gamma phosphate and inactivate itself. So there can be Cis-acting drivers of oncogenesis and Trans-acting drivers as well.

I am providing you a link to Scitable's page on Proto-oncogenes to Oncogenes to Cancer. It gives the following summary which is a helpful summary:

Point mutations, deletions, or insertions that lead to a hyperactive
  gene product
Point mutations, deletions, or insertions in the promoter region of a proto-oncogene that lead to increased transcription
Gene amplification events leading to extra chromosomal copies of a proto-oncogene
Chromosomal translocation events that relocate a proto-oncogene to a new chromosomal site that leads to higher expression
Chromosomal translocations that lead to a fusion between a proto-oncogene and a second gene, which produces a fusion protein with oncogenic activity

thanks for expanding, I didn't have time to write this much :)

The mutation(s) can be anywhere, but frequently they are in the coding region of the gene - the exons. These oncogenic mutations can result in a reading frame shift, a premature stop codon, or a codon change that results in a different amino acid being incorporated into the protein.


text:
Why are the Galápagos islands so special?
Why did Darwin formulate his theory of evolution just after his visit to the Galápagos islands? Why were they so special from an evolutionary point of view?

Charles Darwin formulated his theory after travelling the world aboard the Beagle, here's the route. He found the Galapagos Islands particularly inspiring,

'The natural history of this archipelago is very remarkable: it seems
  to be a little world within itself.'

This is a more detailed account of his relationship with the Galapagos islands, and there is also a book called "Voyage of The Beagle" (I think it is available as a free kindle download) which is basically his diary.
A big part of the reason it is so famous is because of "Darwin's Finches," which are 12 species of finch on the island that have all evolved to specific niches. This is one of the classic examples of evolution. Darwin noted the differences between the birds, thinking they were of different families, but it was later discovered they were all finches and the differences had evolved because of factors like the food they eat (seed eaters had fatter beaks.. etc).
The Galapagos islands offer opportunities to study evolution and adaptation because the islands are distant from the mainland, have differences between the islands, and migration between the islands is difficult. Studies like this one (which I happened to be reading at the time of the question being asked whilst writing a manuscript) are an example of how cool a place it is!

I want to point out that Darwin did not notice about the finches as everybody thinks until the captain of the Beagle (Robert Fitz Roy) pointed that to him. Also it was after a lifetime of collecting evidences not only from his voyages but from experiments in his own house and contributions from colleagues that he developed his theories, many years after his voyages. Which doesn't diminish his contributions at all. He made one of the greatest contributions to biology and human knowledge in general ever.

upvote for that last paragraph.  Among his other accomplishments Darwin also established the use of Islands to study evolution. Other islands do have these properties, but the Galapagos are nicely isolated from the mainland.

absolutely, he was very lucky to find such a place!

You suggest it, but it actually took Darwin many years of intensive study after the voyage to fully formulate his ideas on evolution and natural selection. The question suggests more that the Galapagos Islands provided a Eureka moment, and it was more that it provided him evidence that gave him insight many years after his visit.

Galápagos islands are one of few islands with a unique fauna and flora. This can only happen when the distance to other land is great enough, and when the island exists long enough that flora and fauna could grow (volcano islands are sterile for a long time).
Now Galápagos is even more unique because it is comprised of several islands that are distant enough that some animals cannot cross the distance like small birds. That leads to a unique fauna and flora that also differs between islands, so you can see differences just by visiting the next island. This made it practically a museum of evolution.


text:
What errors can occur during DNA replication?
When there is an error in copying DNA (a mutation), what exactly goes wrong?
If G goes with C and A goes with T, I don't see how that part can mess up.
Is the idea that when the double helix is split, an A gets ruined and replaced with a G by mistake, which then pairs with a C in one of the copies? So something that was supposed to be AT is now GC.

The Wikipedia entry for DNA repair might be helpful to understand the types of damage and errors that can occur. http://en.wikipedia.org/wiki/DNA_repair

There are many way in which DNA can be damaged. As already pointed out in the comment by @skymninge, the Wikipedia page on DNA repair, as well as the mutation page detail some of the things that can go wrong.
You say:

If G goes with C and A goes with T, I don't see how that part can mess up.

This, however, would imply that the four bases are completely different so that mispairing cannot exist. This is (may I add luckily?) not true.
Indeed the chemical structure of the bases is very similar, and changes between one base and another (transversions and transitions) are common.

These can result for instance from exposure to external agents such as ionizing radiation and alkylating agents, or from exposure to endogenous products such as reactive oxygen species.
Furthermore, the enzyme synthetizing DNA, called DNA polymerase, can insert the wrong base, although most of these errors can be corrected by its "proof-reading mechanisms". However, it is estimated that

the frequency at which human DNA undergoes lasting, uncorrected errors range from $1 * 10^{-4}$ to $1 * 10^{-6}$ mutations per gamete for a given gene.

Source: Nature Scitable
So, in summary, the system is not perfect, and mutation can be introduced even endogenously. This may seem bad, but, at least for relatively small rates of mutation, is not, as it allows change in the population, which is the basis for evolution.

just to clarify, youre saying a C can transition into a T sometimes? or, are you saying a C can pair with a T sometimes? or both? btw, thanks!

Transitions are transformations between purines or between pyrimidines (that is C becoming a T or viceversa and A becoming a G or viceversa). Transversions are between a purine and a pirimidine (the red arrows in the picture). You can also have so called "wobble pairings" or "non Watson-Crick pairings" such as C-C, T-G, A-C.

Pyrimidine dimers are another example that cause errors is replication. Though this generally results in premature attenuation of replication, and not mispairing. Still a messup, and the primary cause of the skin cancer melanoma. Another is the incorporation of 8-oxo-Guanine residues. This paper is a good review of DNA mutations http://www.ncbi.nlm.nih.gov/books/NBK22525/
8-oxo-Guanine wiki https://en.wikipedia.org/wiki/8-Oxoguanine


text:
Are the byproducts of mammalian digestion simply depleted versions of the food or liquid consumed?
When mammals consume food and digest it or drink fluids that are then filtered by their kidneys, are the waste products generated simply depleted versions of what they consumed?
Are there other byproducts of metabolism and filtration contained in that waste that are generated by the body and are not directly a part of the food or liquid that was consumed that are excreted?

If you are saying if it has modified any food, of course it has. Eg. Urea but if you are saying something totally not derived from food in any way, I think that is impossible. (Except from some microbes in urine/faeces)

The answer really depends on what aspect of the urine and feces one is considering.
On the atomic level, no, urine and feces are composed entirely of atoms taken from our environment. As one would expect, as there is no "Humanium" on the periodic table. In fact, all the atoms in urine and feces were originally created by stars.
On the molecular level, yes. The body produces molecules that we do not ingest, or that we ingest in minute quantities, such as urea and bile.
On the cellular level, yes. The body produces, for instance, red blood cells even if the person eats a vegan diet with no blood intake. The proteins that make up the cells are created by breaking down ingested proteins into their constituent amino acids, which are then used to construct new proteins.
Also at the cellular level are the huge amount of bacterial cells that we support. Estimates of the number of bacterial cells in our body range from ten to 100 times the number of our own cells. The bacterial component in feces is massive - up to 1/3 of feces by weight are bacteria. Urine, being produced from the blood by the kidneys, is relatively sterile.

I totally forgot about the bacteria... of course!


text:
Why is menstruation in wild animals not a disadvantage to organismal survival?
When I watch wilderness specials for more than a few minutes, I notice a familiar pattern: predators are depicted as being alerted by the scent of blood. Wounded animals seem to make the best prey and predators seem to have a heightened awareness for the smell of blood.
It would seem that it would then be a disadvantage to evolutionary survival for female organisms to menstruate. How do females of a species not attract predators to the signal of menstrual blood?
Do female organisms in the wild actually menstruate? If so, is there a difference in the composition of menses that does not alert predators? How would this not at the very least give predators an idea of the general vicinity of the female?
If wild animals excrete their menses, do they have ways in which they are able to mask the evidence of its release or are they somehow internalizing the tissue so that they are not released?
If female organisms in the wild do menstruate, then why is this not a survival disadvantage?

Most mammals reabsorb the endometrium (estrous). I believe only primates actually menstruate.

In addition to the rarity of menstruation in animals, it's worth noting that menses are only about 50% actual blood, the remainder being tissue and mucus. The smell is probably distinct and unlikely to be confused with wound blood. A menstruating female is also neither pregnant nor nursing very small offspring, and is therefore more resistant to predators. Why follow a scent signal to a prey species that's both healthy and adult? That's the opposite of what you want to do as a predator.

Thanks to the other answer for pointing me in the right direction with some references. It seems that two biologists in the early 1990s had a back-and-forth over this topic in The Quarterly Review of Biology.1,2
A statement of the problem:

The function of menstruation is a central enigma of mammalian, and especially primate, reproductive physiology. Each cycle the uterus builds a glandular epithelium with a high secretory capacity and an elaborate microvasculature, only to reabsorb or void it with the menses if implantation does not oc-cur. Why does the endometrium not maintain a steady state of readiness for implantation by the blastocyst? What is the selective advantage of cyclical regeneration and regression?1

One hypothesis2
In  1993, Margie Profet hypothesized that menstruation is primarily advantageous as a defense against pathogens transported by sperm. During mammalian insemination, she stated, bacteria from the male and female genitalia cling to sperm tails and are transported to the uterus. Menstruation, triggered by the abrupt constriction (causing necrosis of endometrial lining) followed by dilation (causing shedding of said necrotic tissue), forces loose not only the endometrial lining but sperm-borne pathogens contained therein. In addition to shedding the uterine tissue harboring these bacteria, menstruation delivers immune cells to the uterine cavity, triggered by the mechanical pressure exerted via the shedding of endometrial lining.
In this 50 page (!) article, Profet also points out that other mammals with covert menstruation take advantage of some of these same benefits, as the immunological stimulation includes phagocytosis of pathogens by cells that may be expelled in cervical/vaginal mucous. Further, proestrous  bleeding (i.e. that preceding ovulation, 180 degrees off from the human cycle), which occurs in some mammals (domestic dog, coyote, etc), seems to serve a similar function.

If not eliminated prior to estrus, these tenacious pathogens might otherwise attach to incoming sperm during estrus and ascend the oviducts.

As to why humans and other primates are subject to overt bleeding in contrast to other mammals, she lays out a theoretical argument that selection pressure to menstruate should increase with decreasing per-cycle “fecundability” (the probability of pregnancy) because copulation not followed by bleeding risks infection. In contrast to, e.g., mice (98% fecundability), humans have some of the lowest fecundability rates, primarily due to “concealed” ovulation which de-couples copulation and ovulation. (Contrast this to most mammals whose females have a defined estrous period during which they are receptive to male sexual advances; the data for the existence of such a period in humans are controversial, and sexual behavior is driven primarily by “higher” social, environmental, and cognitive cues.)
A different view1
In response/objection to this paper, Beverly Strassman in the same journal published an article outlining an alternative hypothesis about the potential adaptive value of menstruation. She proposed a hypothesis based on energy conservation:

[T]he uterine endometrium is shed/resorbed whenever implantation fails because cyclical regression and renewal is energetically less costly than maintaining the endometrium in the metabolically active state required for implantation.

Her research determined that, in its regressed state (i.e. s/p endometrial shedding), oxygen consumption in the endometrial tissue is markedly declined, nearly sevenfold. Although this would seem to be a trivial component of whole-body metabolism, she argues otherwise:

Metabolic rate is at least 7% lower, on average, during the follicular phase than during the luteal phase in women, which signifies an estimated energy savings of 53 MJ over four cycles, or nearly six days worth of food.

Her argument shares with Profer’s the implication that mammals with lower fecundability are more likely to menstruate. In those with high probability of pregnancy at every cycle, the energetic benefits of ridding the body of the need to support endometrial lining (relevant only in the absence of pregnancy), are decreased. Her hypothesis also predicts the larger volume of menstrual shedding in humans and chimps in contrast to other mammals related to the increased uterine size relative to the female body (a ratio that is largely determined by the especially large head of the human fetus).
Conclusion
As noted in the comments, only primates have overt menstrual bleeding. The adaptive benefits have been variously explained, and it is probable that there is more than one operative explanatory model. Whatever the small decrement in survivalship incurred by the intermittent and uncontrolled depositing of blood in the wild, it is apparently outweighed in these species by the processes described above.

References and Notes

1. Strassmann, Beverly I.  The Evolution of Endometrial Cycles and Menstruation The Quarterly Review of Biology, June 1996; Vol. 71, No. 2 pp 181-220.

2. Profet, Margie. Menstruation as a Defense Against Pathogens Transported by Sperm. The Quarterly Review of Biology, Sept 1993; Vol. 68, No. 3  pp. 335-386.

Note: Your comparison to urine and feces is an interesting one. Perhaps a vaginal sphincter would be a good idea…..were it not for men and babies….

Another view is that high host of pregnancy (e.g. brain development) is driving menstruation (it is worth to remove substandard zygotes): http://aeon.co/magazine/science/pregnancy-is-a-battleground-between-mother-father-and-baby/ and http://www.quora.com/What-is-the-evolutionary-benefit-or-purpose-of-having-periods. This way it explains why it makes sense for primates, but not - other mammals.

I found a nice write up elaborating what @PiotrMigdal is talking about - reddit

It is a very nice question.
From wikipedia:

Though there is some disagreement in definitions between sources, menstruation is generally considered to be limited to primates. Overt menstruation (where there is bleeding from the uterus through the vagina) is found primarily in humans and close evolutionary relatives such as chimpanzees. It is common in simians including Old World monkeys and apes and New World monkey, but variably expressed in prosimians, being completely lacking in strepsirrhine primates and possibly weakly present in tarsiers. Outside the primates it is known only in bats and the elephant shrew.

This other wiki article says:

Many have questioned the evolution of overt menstruation in humans and related species, speculating on what advantage there could be to losing blood associated with dismantling the endometrium rather than absorbing it, as most mammals do. Humans do, in fact, reabsorb about two-thirds of the endometrium each cycle. Strassmann asserts that overt menstruation occurs not because it is beneficial in itself. Rather, the fetal development of these species requires a more developed endometrium, one which is too thick to reabsorb completely. Strassman correlates species that have overt menstruation to those that have a large uterus relative to the adult female body size

I just cite two wiki articles but it is probably worth going through some more reading in order to give a more complete overview of the selection pressure underlying the evolution of menstruation in mammals and especially in primates. In the first paragraph above, wiki cites 5 articles. From the title of one of those, it seems that menstruation is also a defense against pathogens transported in sperm. I hope someone will give a better answer than mine.


text:
What was Protein G named after?
Protein G (the bacterial antibody binding protein) is often used to pulldown antibodies, for example in chromatin immunoprecipitation (ChIP) experiments.
However, I was unable to find a site describing the history of the said protein, and how the name of Protein G came about, due to the fact that the similarly named (but completely different) G protein came up higher in search results.
What was Protein G named after? For example, Protein A was named after the antibody fraction in which it was found, and G protein was named because it bound GDP and GTP.

This paper seems to suggest that protein G is so named because it was isolated from group G streptococci.

@canadianer is correct. Group G comes from Lancefield serum type G and it was a method that used to be used to classify bacterium and Group G Streptococci could be identified using this method. The protein was isolated from G148 S.aureus. Canadianer should post as an answer. +1

G148 is a Streptococcus strain. I incorrectly used the Genus and Species for Staphylococcus aureus in my prior comment. Protein A was isolated in S.aureus, Protein G in Streptococcus G148.

As @canadianer mentions in his comment, Protein G is more than likely named after the human group G strain of Streptococci, G148.

Protein G, a bacterial cell wall protein with affinity for immunoglobulin G (IgG), has been isolated from a human group G streptococcal strain (G148).

Purification and some properties of streptococcal protein G, a novel IgG-binding reagent. - Björck et.al.
Protein G is a  Streptococcus protein that can bind the the Fc portion of the Immunoglobulin G protein. While it is similar to protein A, it was found to have better binding affinities to the different varieties of heavy chain constant regions of IgG molecules.
The G comes from Lancefield grouping. Lancefield grouping was a method that used to be used to classify bacterium. Group G Streptococci could be identified using Lancefield serum type G and that is how they received their classification.


text:
Layman definition of genetic polymorphism?
I am reading an article about Genetic Polymorphism and there are lines in the article about genetic polymophism that I don't quite understand like.

In this area, there are six different chemotypes that are the expression of a genetically controlled polymorphism in T.vulgaris(24).

Can someone explain genetic polymorphism and morphic distribution in layman terms.
Thanks

Can you link the article.

Read the wiki article on polymorphism (genetic section) and then ask if you don't understand something specific http://en.m.wikipedia.org/wiki/Polymorphism_%28biology%29

Polymorphic sites
Consider the following sequence of DNA
ATTTGC
Now consider that in a population of 5 haploid individuals (in reality populations are larger of course) you have the 5 following sequences

ATTTGC
ATTTGC
ATCTGT
ATTTGC
ATCTGC

Looking at those sequences you can identify two sites (site 3 and site 6) for which the nucleotides vary throughout the population. For example, at site 3, 3 individuals have a T while 2 individuals have a C. Sites 3 and site 6 are said to be polymorphic sites (a.k.a. segregating sites).
Statistics of genetic variance related to polymorphic sites
Note that there are all sorts of ways to describe the genetic diversity in this population. You could calculate the total number of segregating sites or the average number of pairwise difference between any two sequence. Or the average expected (and not observed) heterozygosity (which is sometime refer to as genetic diversity). One could calculate the frequency distribution of the number of individuals carrying a given variant (called the site-frequency spectrum).
Other polymorphism
Note that I emphasized on polymorphic sites for the moment but there are a whole bunch of different reasons that two genomes may differ. Two sequences may differ in their length as well (insertions and deletions of nucleotides). Genomes may differ in the number of copy of a given sequence (copy number variation). Genomes may differ in the number of copy of very very long sequences or in the order of those sequences (synteny). Genomes may differ in their number of chromosomes or in their ploidy level.
About the citation

In this area,there are six different chemotypes that are the expression of a genetically controlled polymorphism inT.vulgaris(24)

It is hard to say anything without the link to the article.
There are six different chemotypes (found in the population). Not all individuals have all chemotypes (eventually each individual has one or two chemotypes). Having one or another chemotype depend on your DNA sequence.
Assuming that the difference is due to polymorphic sites (which is impossible to say for sure without reading the paper), there is therefore one (or several) polymorphic sites that explain the variance in chemotypes in the population.

Did you mean nucleotide instead of amino acid?

Google NINJA!!! http://www.pnas.org/content/110/8/2893.full


text:
Why don't housekeeping genes have TATA Box regions in their promoter sequences?
Housekeeping genes are genes that are continuously transcribed. Like all other genes they have promoter sequences, but they don't have TATA box sequences that are used to specify from where transcription is going to begin.
Why don't housekeeping genes have a TATA Box in their promoter sequences?

It seems that there are 10 types of eukaryotic promoters, and only 32% are TATA-containing promoters, the rest of the eukaryotic promoters don't have a TATA box: http://bmcgenomics.biomedcentral.com/articles/10.1186/1471-2164-13-512

Two possible answers:
First, TATA boxes has been found to cause increased "noise" in gene expression, such that the expression of genes that have a TATA box is highly variable. See this review for example.
A different set of results suggests (here) that TATA acts only as an amplifier of expression.
Regardless of whether TATA amplifies expression or also increases expression variance, this is not suited for housekeeping genes, which generally have low and constant expression.

The TATA-box element (and notion of house-keeping genes) are classical textbook examples of trying to explain complex biology in a simplified manner.
In fact, most mammalian genes do not have a TATA-box element and most transcription start sites (TSSs) are spread over a larger area in the 5' end of the gene. Each TSSs contributing to differences in gene expression strength and gene product. This phenomenon has been extensively investigated using cap analysis of gene expression (CAGE). For a short summary of the major findings you can refer to Rikens website here.
Sandelin and Carninci et al wrote an excellent review on the findings of the first CAGE experiments here, and how this contradicts classic textbook promoter structures Nature.
In addition, the CAGE technology, has been used to map out cell-type specific enhancers which contribute hugely to the correct gene regulation, Anderson et al. Nature.
I know this answer does not directly address your question, but rather raises a lot of new questions.

Quick googling located online version of Lodish et al Molecular Cell Biology. 4th edition.
From TATA Box, Initiators, and CpG Islands Function as Promoters in Eukaryotic DNA section:

These genes, which generally are transcribed at low rates (e.g., genes encoding the enzymes of intermediary metabolism, often called “housekeeping genes”), do not contain a TATA box or an initiator

Also, from Transcriptional Regulatory Sequences of the Housekeeping Gene for Human Triosephosphate Isomerase (Boyer et al, J Bio Chem 1989):

In contrast to facultative gene promoters, these promoters are
  characterized by [...] and, notably,
  the lack of an appropriately positioned TATA box
  [...]
  Based upon these structural differences,
  the possibility exists that initiation of housekeeping and
  facultative gene transcription proceeds through distinct mechanisms.

I can imagine you can google more information, but it seems to me that reason for lack of TATA is necessity for constant low-level expression (hence no strong promoter) and separate mechanism of regulation (hence some common structure). Last point might arise from redundancy argument: when regulation of TATA-containing genes become faulty, housekeeping genes regulation stays same because it is somewhat independent.
However, you should be aware that your original assumption is at least controversial (from same J Bio Chem paper):

Unlike most housekeeping gene promoters that have been
  described to date, the human TPI promoter harbors a canonical
  TATA element (5’ TATATAA 3’) that spans positions
  -27 to -21. LS mutagenesis demonstrated that this TATA
  box clearly represents a control element, the integrity of which
  is essential for the maintenance of both the fidelity and the
  frequency of TPI gene transcription initiation.


text:
Why do rabbits often have white hindquarters?
There are several species of herbivores that have a very visible white hindquarters: several kinds of deer, rabbits, antelopes, etc.
Does the white fur serve a functional purpose, or is it purely random?  Is it defensive enabling them to escape predators, or is it for intraspecies communication?
Examples photos to clarify:

deer
Notice that otherwise relatively well camouflaged animals have visible white fur.

Pronghorn, I have a 2-link limit for the post: http://www.gpnc.org/images/jpegs/animals/flare.jpg

Apparently the most noticeable research on this subject of a rabbit's white behind has been done by Dr Dirk Semmann of the University of Goettingen. He proposes that

these spots actually confuse predators because of their very
  noticeable nature. By focusing on the bright spot, the would-be
  predator ignores the larger body of the animal. Then, when the rabbit
  executes a sharp turn, the spot disappears and the predator has to
  readjust to focus on the camouflaged coat, losing vital seconds
  (reference 1, reference 2).

It could be the same reason for the white behind of a deer. As to why deer flag their tails, there is a paper on the subject which lists 4 possible reasons for the behaviour.
1) Flash behaviour
2) Alarm Signal
3) Cohesive signal
4) Detection signal
More can be read about it in this paper.


text:
What are the effects of removing CD4 receptors?
If the gene for the CD4 receptor was removed, would the person's immune system work normally?  Could a new artificial receptor be substituted in place of CD4?
Could HIV infection be prevented in this way?

The CD4 receptor is vital for the proper functioning of the immune system. It is found not only on T-Lymphocytes, but also on macrophages and dendritic cells. Its function on T-cells is to stabilize the interaction between the T-Cell receptor and the MHC Class 2 (often known as HLA II in humans) antigen complex on antigen presenting cells and improves the affinity dramatically.
CD4 is also vital for the activation of Helper T-Cells (2). It is needed in the signaling which occurs in the thymus that selects for CD4+ T-Cells. If you were to delete CD4, you are, in effect destroying the adaptive immune system in humans, as there would be no CD4+ produced. In this situation, you would not get activation of B-Cells or Cytotoxic T-Cells, and the immune system would only be left with its innate defenses to protect it. This is found in diseases such as Severe Combined Immunodeficiency and can only be cured with early bone-marrow transplantation.
A better target would be the CCR5 receptor. This receptor acts as a coreceptor for the interaction between GP120, the receptor on the surface of the HIV capsid and the CD4 receptor. People who have a mutation in the CCR5 receptor are resistant to the most prevalent isoform of HIV, as the interaction is necessary for the capsid to fuse with the plasma membrane of the CD4+ cell.
See this article about the CCR5-∆32 mutation. HIV Resistant Mutation

I think it's deathly important to note how critical CD4 is for the activation of T-helper cells, and thus a myriad of downstream immune cells such as B cells:
When an APC presents an antigen through its MHC-II molecules, the TCR-II complex must interact with the Ag-MHC complex to transduce an activating signal. Note that the T-helper TCR is composed of α/ß molecules associated with the CD3 complex and CD4. CD4 is associated with an intracellular tyrosine kinase called Lck. Upon recognition of MHC-II by CD4, Lck phosphorylates the CD3 complex intracellular tails and the ITAMs of the CD3 zeta chains in concert with Fyn. Zap70 binds these phosphorylated sites to transduce the signal further (CD4 function, TCR signal transduction, and ignoring co-stimulation). To that, end there's some risk in knocking down CD4, or inadvertently modifying the receptor into loss-of-function.
Knocking out CD4 in a human would probably result in something similar to SCID (severe-combined immunodeficiency syndrome). If you're unable to develop T helper cells (Thymic selection), you're cutting off much of the ability for your immune system to modulate its defenses. B cells can still activate in a T-independent manner, but the types of antigens and responses are largely different (T-independent activation).
Being said, HIV primarily binds to CD4 through its gp120 membrane protein, and then facilitates membrane fusion through association with a chemokine coreceptor. Because of the above, you can't just delete CD4, it's quite dangerous from an organismal standpoint. Engineering a different receptor is a difficult way to go about it, as we don't know how that'll affect normal functioning, either. You can modify the chemokine, but it's also not guaranteed that the HIV wont shift to a different coreceptor (HIV tropism). Thus the best preventions so far have been to block adsorption, block HIV normal functioning through antiretrovirals, etc.
The take-home message is that modifications to our own cells have a capacity to do a lot of harm, but through good experimental design we can also do a lot of good, see chimeric antigen receptor T cells. We're also at an arms race with the pathogen as well, however, so it's a multi-dimensional problem that goes beyond the viral receptor!

Kudos on a very detailed answer, but you've introduced a lot of jargon and abbreviations in your second paragraph that won't be accessible to people without a decent grounding in immunology—which almost certainly includes anyone looking for an answer to this question. A simplified explanation of how CD4 has a crucial role in cell-mediated immunity would be helpful to people with less immunology training.


text:
Which of these methods is both effective and reliable in elongate muscle and tendon for use in humans: growth factors or stem cell technology
Which method is it the most effective, but also the most reliable for elongating muscle and tendons for clinical trial; using modern growth factor technology or using modern stem cell technology?
Being able to stimulate muscle elongation is a key step towards improving the standard of living for people afflicted with severe Poliomyelitis or people with limb Malformations. There are already techniques to culture living bone implants in the lab from stem cells for human beings. I am looking for an analog for muscle tissue.
Please provide references with your answers.

Modern science might not know the answer to this question, and it might vary by patient. Consider narrowing down the question a little perhaps?


text:
Why would deer continue to cross a river full of crocodiles even though some of them have been killed?
I recently watched a clip on Discovery Channel, where I saw deer crossing a river full of crocodiles, ignoring the fact that some of them would have been killed doing so.
Is there a possible evolutionary reason for this behaviour?

What's with the down-votes? At least give a reason!

I agree, this is a perfectly reasonable question. If you're going to downvote, have the courtesy to leave a comment explaining why.

Have not downvoted nor upvoted the question, but I surely would say that the formulation is quite "rough" as it stands. It could, however, be a good question if better rephrased.

The question would be better if you replace "deer" with "antelopes" or "bovid" such as the hordes of wildebeest crossing the Mara river each year, feeding a lot of crocodiles.

The reason for their behavior is that exactly the fact that even though some of them do indeed get killed, most of them survive -- what you have said.  The deer cross the river because that allows for the better continuation of the species rather than if they had stayed on the original side of the river. You could think of it this way: If there was a crowd of 5000 people crossing a field of grass and aliens were abducting them one by one, the actual chances of them abducting you are rather little.

The deer do not live for the continuation of the species, but otherwise this answer is correct. The genes which control the urge to cross the river proliferate despite a small amount of predation by crocodiles. Presumably this is because there is a great reproductive or food payoff of crossing the river to better breedinbg/feeding grounds.

@Richard Yes, I agree I could've worded that better.

@Chase Yuan: feel free to edit your question to improve it so to include Richard's suggestions!