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Fermentation to acetic acid
How much time is needed for the fermentation to acetic acid production cycle, and the conversion of apple vinegar in a sealed container incubated at 37 °C?
Should be in the fully closed?
What is right yeast?
I do it with powder, grated apple in a plastic soda bottle and I add a few peas and a slice of bread. I am waiting for make that.
If you have a better idea on what to do to get a good apple cider vinegar produce in my own house.

A Google search for "homemade apple vinegar" yields lots of information. Perhaps you will get an answer from an expert here, perhaps not.

Ask this on Seasoned Advice, perhaps?

@LittleWhiteLithe Have you a good idea for it?

Ineresting idea. I have once done this in a lab course - and will definitely try the recipe listed below (which is pretty similar to the instructions we used).

There are some recipes available on the web, my answer is based on this webpage and this information:
The process itself is rather easy and you can either use ready bought apple juice, homemade juice or apple cider (basically unfiltered apple juice). You will need some specially cultivated yeast, baker's yeast is generally not recommended since it might produce a lot of unwanted (and probably bad tasting) side products.
For the fermentation itself you need some (very) clean vessels in which the process can take place. These should be from a material which is not corrosive, as the vinegar would otherwise react with the vessel. Food-grade plastic, glass or stainless steel should be ok.
To have the reaction take place, the process need oxygen, otherwise the reaction will stop at the step of ethanol. This is also why acoholic fermentation is always sealed against the air, to avoid the oxidation of the alcohol the acetic acid. A cheese cloth will leave oxygen in, but keep insects and other contaminations out. If you need to filter the vinegar at the end of the process, a standard coffeefilter is good enough.
The following step by step directions come from this website:

Step 1 - Make or buy your apple cider or apple juice
Apple juice or apple cider is the starting point for making apple
cider vinegar. You can make your own, or buy it ready made, fresh,
bottled or frozen.  You can use a mechanical or steam juicer to
produce the juice / cider. To make your own juice (which is the same
as plain unfermented apple cider), see this page. Keep in mind that
you want to select sweet apples, like Fuji, Delicious, Mutsu, Gala,
etc. Green, unripe and unsweet apples (like Granny Smith) do not have
enough sugar to make good cider vinegar. Tips about selecting apples:
Apples used for cider don't have to be flawless. They do, however,
have to be free from spoilage. You can use blemished apples and small
sized apples. You can mix apple varieties together or use all one
variety. The only rule is to cut out any spoilage areas on otherwise
good apples. Spoiled areas will cause the juice to ferment too rapidly
and will ruin the cider. Don't use apples that appear brown, decayed
or moldy. Apples should be firm and ripe. Green, undermature apples
cause a flat flavor when juiced. The best cider comes from a blend of
sweet, tart and aromatic apple varieties. A bushel of apples yields
about 3 gallons of juice.
Step 2 - Make your starter yeast
Adding yeast to activate fermentation is not essential, but will speed
up the process and can produce a higher quality. Special cultivated
yeasts are available for this purpose at wine-making shops and
biological labs but bread yeasts are not recommended. To make a
starter, crumble one cake of yeast into one quart of cider and mix.
This makes enough starter for 5 gallons of cider; double the recipe
proportionately when making more.
Steps 3 - Making Alcohol and Acetic Acid
Pour all of the juice or cider into one or more containers to about
three-quarters capacity; do not close the lids on the containers.
Instead, cover the openings with cheesecloth secured with a rubber
band or string.
Step 4 - Store out of direct light, but some place with constant temperature
Stir the mixtures daily, making sure the cheesecloth is put back in
place. Keep the containers away from direct sunlight and maintain the
temperature at 60 to 80 degrees F.
Step 5 - Keep stirring daily, monitoring and tasting for the next 3 to 4 weeks
Full fermentation will take about 3 to 4 weeks. Near the end of this
period, you should notice a vinegar-like smell. Taste samples daily
until the desired strength is reached.
Step 4 - Filter Mother of vinegar
When the vinegar is fully fermented, filter the liquid through several
layers of fine cheesecloth or filter paper—a coffee filter works well
for this. This removes the mother of vinegar, shown at right,
preventing further fermentation or spoilage of the product. Mother of
vinegar is completely harmless and the surrounding vinegar does not
have to be discarded because of it. It can be filtered out using a
coffee filter, used to start a bottle of vinegar, or simply left in
and ignored.
Step 6 - Done! Storing Your Vinegar
The vinegar is now ready for storage in separate, capped containers.
Stored vinegar will stay in excellent condition almost indefinitely if
it is pasteurized. To pasteurize, heat the vinegar before pouring it
into sterilized bottles, or bottle, then place in a hot water bath. In
both cases, the temperature of the vinegar must reach at least 140
degrees F to pasteurize the product, and should not exceed 160 degrees
F. Use a cooking thermometer to ensure the correct temperature is met.
Cool the containers and store at room temperature out of direct
sunlight.

Thanks Chris. Seems perfectly good answer.I will try this method.

@M007 I missed your initial post, otherwise I would have answered it much earlier.


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An unknown band appearing in my gel electrophoresis
I am having trouble understanding what is the source of band "2" in the following gel-electrophoresis:

In this experiment, we took an E.coli transformant colony and ran its nucleic acids in the gel, after adding a restriction enzyme which cuts the recombinant plasmid molecule into two corresponding bands ("3" and "5" ["5" is very weak in the scanned version, but is well seen in the "hard copy" )  . I know the first line ("1") corresponds to possible genomic DNA we took from untransformed bacteria, and that the fourth line ("4") corresponds to a plasmid molecule without an insert. 6 is also well understood.
My question is-
What is the source of band "2" which contains more base pairs than any of the parts of the plasmid and its insert , and in particular more base pairs than the insert?
WIll someone please help me understand this ?
Thanks in advance

I think you need some controls. If you can purify the plasmid away from the genomic DNA, run that plasmid alongside this lane. Would also be good to have genomic DNA without plasmid, such as from your untransformed control, in another lane. This should tell you if the mystery band is from the plasmid or the genome. If it's plasmid DNA, are you sure you're getting complete digestion? Uncut plasmids usually produce more than 1 band because supercoiled DNA migrates at a different rate than open circle, which is different from linear. Incomplete digestion could have left supercoiled and circular.

Hi user137, thanks for your answer, as for your suggestions:

I ran four transformed colonies in four different lanes, and this is the only lane when this mysterious line appears, so I guess the problem is not incomplete digestion.
I currently have no possibility of redoing this experiment with other controls. I am sure about the bands I told about, but still have no idea about this one.

As mentioned here:
http://biology.stackexchange.com/questions/19114/why-isolated-recombinant-plasmid-dna-without-any-restriction-is-often-detected
the circular form should run a little bit

less fast than the linear one, so I don't think it is reasonable that this line corresponds to a circular plasmid, since "4" is the line corresponding to a linear plasmid without an insert.
WIll you please help me figure it out ?
Thanks a lot !

So you combined different plasmid digests with genomic DNA from different samples of bacteria and ran it all in 1 lane? Please describe the digestion in more detail. Band 4 is empty vector, but what are bands 3 and 5?

I would also suspect single cut DNA here. Can you give us some details on the digest?

OK. I took a plasmid (containing one restriction target for BamHI) and an insert (containing one more restriction target for BamHI) , and inserted it into E.coli bacteria. I then put the bacteria on a selective bed, and took a colony, homogenize it and then ran the nucleic acid part in electrophoresis. Just notice, that on the bed , around the main colony, I had very small colonies corresponding to non-transformant bacteria that are able to grow only because they feed from the food the main colony is providing them.
As I said before, bands 3 and 5 are the two restrictions products I get

after digesting the plasmid+insert with BamHI.
Got any idea?

The most likely explanation I can think of for band 2 is an incomplete digestion, that the BamHI is missing one of the cut sites and creating a linear plasmid that is longer than band 3 because it also contains band 5. Without further controls I can't really know. And was the selective media using an antibiotic such as ampicillin or kanamycin? Because if so the satellite colonies aren't eating food from the transformed colony, they are surviving in the antibiotic depleted region around the main colony.

Can you put up the plasmid map?

source: Stack Exchange

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

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How to automate this custom gene expression microarray chip?
I have 16 gene sequences that I am interested in their detection in clinical samples. I already measured their RNA levels by using RT-qPCR technique and their benefit has already been proven to help in diagnosis of clinical cases. Now I want to take this gene expression profiling into another level of automation. The first thing came to my mind is the microrray chips. I don't have much experience in micrarrary, I want to have a custom chip containing these 16 genes in question. These are 13 target human genes and 3 reference genes (housekeeping genes) for normalization.
Question
- is it possible to have this custom chip?
- How can I get such a custom microarray chip?
- What is needed to automate this process at a production level?

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


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Why doesn't the cell membrane just...break apart?
Forgive me if this is a silly question. I can't understand the basics. Why doesn't the cell membrane just break apart? What's keeping the layers in the phospholipid bilayer together? I know that the membrane is embedded with proteins and lipids, but I still can't wrap my head around the "why". Are the hydrophobic interactions in the middle "stronger" than the hydrophilic interactions on the outside? What's keeping the individual phosphate heads together instead of, say, one of them just drifting away due to a nearby water molecule?

Related: 1.Why should phospholipid head groups be protected in the bilayer, 2. Why do cell membranes have a bilayer

The membrane bilayer is held together by hydrophobic forces. This is an entropy driven process. When a greasy or hydrophobic molecule is suspended in water, the water molecules form an organized "cage" around the hydrophobic molecule. When two hydrophobic molecules come into contact, they force the water between them out. This increases the entropy because the freed waters don't need to be organized into the cage. Lipid bilayers have many many many hydrophobic lipids that squeeze out a lot of water and greatly increase entropy. The polar phosphates allow the water to interact with the surface of the membrane, without a polar head group the lipids would form a spherical blob instead of a membrane.
Read this section on wikipedia for more.

Perhaps worth adding that the formation of the bilayer increases the entropy of the water, but the entropy associated with the phospholipids will decrease. The net change in entropy is favourable.

Also the bilayer maximises van der Waals interactions between the closely-packed hydrocarbon chains, again contributing to the stability of the bilayer.

also surface tension.. which is basically because of the interactive forces..

Artificial vesicles can be produced using the same principle. They are quite stable, but the larger ones (giant unilamellar vesicles) are fragile to any strain: cell-sized vesicles would not resist in a tissue or blood flow, and the cell actomyosin cortex or RBC spectrin network are necessary for this.

without a polar head group the lipids would form a spherical blob instead of a membrane I am not so sure about this sentence. Even with the polar head-group, spherical blobs do form as micelles.

@James Micelles and membranes are possible. It's related to the shape of lipid. A phospholipid with two lipid tails prefers a membrane structure due to the more rectangular shape of the hydrophobic portion, while a detergent like molecule with 1 tail prefers a micelle due to the more conical shape of the hydrophobic portion.


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Question about mutation of multiple nuclei?
If an organism with multiple nuclei, such as the slime mold Physarum polycephalum, was to be exposed to a mutagen, such as 5-bromouracil, what would be the effect (besides death)? Especially if multiple nuclei were effected differently by the exposure.


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Is there a metabolic pathway that generates methanol?
I've been looking for help topics about methanol in metabolism. Specifically, I wish to know what is a common dietary component that generates methanol following metabolism and comment on its toxicity?  I cannot seem to find any relevant data and i'm seeking to know if anyone here has any experience and knowledge of this.

This source may be a good place to start.

This is an old question by now, but I found it interesting, so here's my two cents :)
Methanol has long been known to normally occur in humans; one study from 1963 demonstrates its presence in breath.
One major source for methanol in humans is breakdown of pectin by bacteria in the gut. Pectin is a complex carbohydrate found in many fruits and other non-woody parts of plants. Pectin is not well metabolized by humans, and so has low nutritional value and counts as dietary fiber. Still, some species of bacteria in the gut are able to degrade pectin, and this process produces methanol.
This article reports measurements of methanol levels in the breath of subjects consuming pectin. Here, 10--15 grams of pectin (equivalent to ~1 kg of apples) was estimate to yield about 0.4--1.4 grams of methanol. The authors also state that there is a basal production of methanol in humans as well, of about 0.3 grams per day; the origin of this methanol seems unclear.
There are also pathways in human cells capable of forming methanol. This study demonstrates this fact by showing that infusion of ethanol (bypassing the gut) leads to a rise in methanol levels.
A recent review of metanol metabolism in humans can be found here.

So this is a really recent and IMO good review of methanol metabolism in humans: Metabolic Methanol: Molecular Pathways and Physiological Roles, there's a paywall though. Humans also encode their own PPME that generates methanol in regulating PP2A (same protein that generates methanol from pectin in plants I think).

@CMosychuk  Fantastic! I will add it to the answer, many thanks!

I can't comment on dietary components or toxicity, but the Kegg database has an entry for methanol with links to the pathways in which it is an intermediate. You might find it useful to check that if you haven't already done so.
http://www.genome.jp/dbget-bin/www_bget?C00132


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aspartame in relation to generating methanol
So I posted another question with respects to methanol and aspartame in metabolism with respects to toxicity.  So another question I have is "Why is aspartame used as a dietary component to generate methanol following metabolism?"  This is a topic of discussion in my thermonuclear pharmaceuticals class at my institution, and more or less it's also part of an active assignment that we're expected to cover for a weekly discussion which is no graded; otherwise I wouldn't seek free advice on this.  As much as I read in my book it does not go into detail and I am curious if anyone out there has any advice on this or perhaps you could point me towards relevant articles?

Aspartame is the methyl ester of the aspartic acid phenylalanine dipeptide. Esters are very easily hydrolyzed by esterase enzymes in the body. This will create an acid and an alcohol. In this case the alcohol is methanol, because it was generated from the methyl group. I'm not familiar with why thermonuclear pharmaceuticals would be concerned with aspartame, generally thermoncuclear refers to nuclear fusion, and even radioactive drugs don't undergo fusion.
Anyway, some people are afraid that aspartame is toxic because the methanol it generates is toxic. This fear is unrealistic because the amount of methanol it takes to cause blindness is about 10mL, and the smallest amount needed to kill someone is about 30mL 2. To generate this much pure methanol from aspartame would require you to eat an impossible amount of aspartame.


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Effect of alcohol on parasites
I recently came across an article saying that fruit flies use alcohol to deter parasites. The researcher was quoted as saying there have not been any studies on the effect of human alcohol consumption on parasites. Is there any research being done on this? Another related question I have is whether the fruit flies can tolerate higher alcohol concentrations than mammals/humans.

Drosophila is seen as a highly alcohol tolerant species which is mainly dependent on the environment it lives in. So are flies, which are captured in the cellar of a wine yard more tolerant to alcohol than flies which are captured outside (see first reference).
The environment in which the flies grow up and live does not influence the activity of the alcohol dehydrogenase enzyme but seems to influence the expression (amount) of it. The more alcohol is present, the higher the expression is (see reference 2).
I haven't seen explicit data on the comparison between humans/mammals and drosophila, but since drosophila is seen as a good model organism to study alcoholism, I would think it is not too different. (see reference 3).

Micro-differentiation in a Natural Population of DROSOPHILA
MELANOGASTER to Alcohol in the Environment
Alcohol tolerance, ADH activity, and ecological niche of Drosophila
species
Functional Ethanol Tolerance in Drosophila


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How does Temperature influences the rate of protein turnover?
Question
How (quantitatively speaking) does temperature influences rate of turnover of transcription factors?
Which protein?
As I am not looking for any accurate number I am talking about an "average" transcription factor. I leave to you the choice of answering this question with some very accurate example (Transcription factor GTF II A for example) or with some broad observation on how temperature influences protein turnover.
The organism I'd like to model is a typical unicellular eukaryote such as a yeast for example that lives at "standard" range of temperature (between 5°C and 35°C roughly speaking).
Of course, I am not interested in considering a transcription factor that is directly involved in some response to a change in environmental temperature. I am interested in transcription factors which are involved in developmental pathways that have nothing to do with reaction of the body to temperature.
I am looking for a referenced answer $\ddot \smile$

See this answer

Would you want to close this question as you can find the answer in the other post?

That makes you the first person to close their own post :P


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Do biological facts determine when a human fetus is considered alive and human?
I often hear or read this statement:

"It's not a human, it's a fetus."

In other words, some think a fetus is non-human until a certain point.
And another similar statement:

"The fetus isn't alive until 26 weeks of gestation."

So some think the fetus is not actually "alive" until a certain point.
What does biology have to say about these two statements?
I encounter these statements often in discussions about abortion, but that issue, and other similar philosophical issues, are outside this question. I'm wondering strictly from a scientific/biological standpoint: are these statements true?
Is the fetus in a human mother non-human until a certain point?
Does the fetus not classify as "alive" until a certain point?
The people I encountered truly believed these statements (3 of the 4 in mind also claimed science was on their side), so it's not as if the question has no merit. I assumed that in the realm of science and biology, there must be a convincing and sure answer.

Define "alive". Because a fetus almost definitely is alive. Perhaps they meant it isn't sentient until that point?

@JanDvorak, I have no idea what the person meant by "alive." I copied and pasted these statements from actual quotes as representations of general ideas I often encounter, but I don't know in what way they were using the terms.

Do you have any specific sources for these claims? To me it sounds like someone is trying to justify something they shouldn't.

I have never received sources from anyone claiming either of these things. I personally do not agree with the statements, but I would rather those with expertise in biology speak clearly to the statements. Again, I have run into these statements so many times, I thought it wise to gain more understanding from those more versed in this area.

MAYBE one possible 'indicater' of something being 'alive' is the ability for 'it' to move or 'change' itself in some 'way' that does not involve any 'help' or 'resources' from an 'outside' source. Note a fetus can move it's arm or 'kick' independently of it's Mother. However many philosophers have tried to argue 'within' adults there is no mind; we are just neuro-mechanical 'robots', so by this definition we adults are not 'alive' (just like robots are not alive)!

You need to clarify what you are asking here: 1) The human foetus is of course human, it's not a bird, sunflower, donkey or other. 2) The foetus, by definitions of life that I've seen, is probably classed as "living" but that could be debated. 3) It may appear that you are interested in whether or not the foetus is concious, aware, intelligent, able to process independent thoughts feelings and emotions, or sentient (judging by the quotes you've put in) - I don't think that belongs here so you should clarify that a little so people answer the first two points but not the third.

I feel like you are trying to get confirmation by biologists of your side of a moral, ethical, philosophical or political question. To do so, you have paraphrased your opponents' point of view in a way that might caricature or 'straw-man' them. The fact that you can't point to any place these specific statements have been made reinforces this suspicion. If you think that an answer based on a narrow biological reading of these statements will prove something about the wider question you are wrong. As questions about biology they are pointless and uninteresting.

Might you have mistaken "... alive until 26 weeks of gestation" for "... a life until 26 weeks of gestation". The latter does at least have a meaningful interpretation; the former does not - a growing foetus can't be anything other than alive, but whether or not you consider it a life is an arbitrary distinction, and one subject to much philosophical pondering, all of which is off-topic here.

It depends. My little finger is certainly "alive" and "human". But I wouldn't expect it to last long on its own, and I'm pretty sure no one would interact with it as a "human" if they found it on a sidewalk.

@JohnWasham I don't see where you previously said that these statements are from a discussion you had last night. Rather you said that you 'often hear or read' these statements.

@jwg, as I mentioned in my previous comment, these are exact quotations of a discussion I had last night (comments from Joji-chan at 8:37pm and from AKAMrWobbels at 9:07pm on https://plus.google.com/b/118125465432602950506/113663424599392189408/posts/6XTbtDrdY3v ). It is quite frustrating to me that in spite of my intentional avoidance of personal opinion in the question, you have read opinion into the question against my wishes. Sigh.

@JohnWasham  I understand that you are pretending to ask a neutral question about objective facts. My point is that you actually aren't. You are trying to move a Facebook debate onto a site which isn't the right place for it.

@jwg, is there a right answer here or not? I figure there is, which is why I asked the question. Did I ask for someone to come and back me up on something? How is this not clear? I asked the question and left it for someone smarter than me to answer. Your jumping to conclusions is quite frustrating.

@GriffinEvo, here is the man's full quote: "Well the fetus isn't alive, based on elementary principles of organismal biology (i.e. Bio 100), until 26 weeks of gestation, so what else is it if not non-living human tissue that develops into a living organism, known as a human, at 26 weeks of gestation?" That was his claim, so I simply asked the question to figure out if his claim was valid. I think you would agree he did not seem to be claiming your 3). He legitimately thought the fetus wasn't alive. What he meant by "alive," I'm not sure.

Although I don't necessarily like the question, I don't see anything wrong with it.  Fetal stage is generally accepted as beginning at the eleventh week in gestational age, which is the ninth week after fertilization.

@yamad, thank you for wording the question better!

@JohnWasham I understand your frustration, but feel that a couple of clarifications/definitions are needed in the question to make it answerable. However, the answer might then be rather self-evident. First, I would like to see a definition of "human" (as used here). I assume that you are going for "human" as in "belonging to the human species". Also, the term "alive" probably means "cannot live independently". I understand that this vagueness is caused by the person making these statements, probably to use a highly charged term ("alive") to drive home a point and win an argument.

The vagueness of the terms is also shown in how you have worded the question. In the title you write "..a human fetus is considered...", but in the first statement the terms "human" and "fetus" are used as incompatible opposites (""It's not a human, it's a fetus.""). Your title is also basically a tautology (if not, the use of human is vague): "Do biological facts determine when a human fetus is considered ... human?".

Life, human, and human life are being used interchangeably, but they're not interchangeable terms. The empirical terms "Alive" (has measurable ribosomal activity for example), and "human" (DNA testable) cannot be compared to "human-life" (philosophical subjective definition). If we are talking about "is a fetus a human-life?" then the question is off topic. If the question is "is a fetus human and alive?" then we can answer it (and @Susan's answer is a good answer at that!)

Life is generally distinguished from non-life by metabolism and growth. As such, a fetus is alive. The reference to "not...until 26 weeks gestation" that you've heard likely refers to viability.* With the most aggressive medical care, this is the approximate age when a fetus may be able to survive outside the womb.
The term human from a biologic perspective is a species label.** Given that a fetus is genetically indistinguishable (in broad strokes) from a post-natal human, I think it would be hard to argue that it is anything other than human.
Summary: Yes, a human fetus is both alive and human.

*Note that this use of the word viable is standard but deviates somewhat from the etymology of the word.
**I'm ignoring here other ancient species (homo-) which may be considered human but are irrelevant to the question.

on the other side of things, there are many things that are alive which have different levels of priority.  our feces is also alive.  a sneeze is full of life.  So you want to also think about that.  Life is amazing, but also very common in the everyday.

@shigeta - I'm missing your point. Bacteria in feces are alive, no doubt. Bacteria in the nasopharynx that may be expelled with sneezing are alive, no doubt, as is the creature doing the sneezing. How is that related to this question/answer?

Note that the question is not whether the foetus is human (adjective), but whether it is a human (noun). It's an important difference, and takes us out of biology and into philosophy and ethics.

@EnergyNumbers - mmm, not sure I agree with that distinction, but I do agree that it's not a great question for this site, not because it's un-answerable but because the answer is extremely simple (when limited to biology). I don't have enough rep to VTC, so instead I answered it as best I could within the scope of the site.

I think the point is that the question almost certainly comes from the context of the abortion debate, i.e. whether killing a fetus should be a right or a crime. In that regard, whether a fetus is alive does not matter much, since we necessarily kill many things that are alive without giving it a thought.

@MichaelBorgwardt, you are correct. The statements in the question were copied and pasted from two commenters last night in a discussion about abortion, but I intentionally left all opinion out of the question and no mention of abortion. The man who claimed "the fetus isn't alive" said that statement was "Biology 101." So while you and others may view this question as too simplistic, it obviously isn't to some people. I decided to let those who really know biology speak to the truth of these statements.

@Susan, thank you for the simple and concise answer and for the sources.

When I read this question, I immediately knew it was a consequence of a debate on abortion. A biologist who supports the right to choose abortion would carefully make a distinction between the definition of something that is alive and human (like a zygote, or even the sperm and egg) and a human being (in other words, a person).

The fetus is certainly "alive" from the very beginning, since conception. The second comment hence does not make sense.
Regarding whether it is "human" or not, that would depend on the definition of "human". It seems to be more a philosophical than biological question. From the biology point of view it all goes down to this, a fetus in a human womb is a "human fetus", certainly not a "mouse fetus". Fetus only indicates a time period in the development of a mammal (before being born). Another question is whether the fetus has attributes of grown up humans, like the ability to talk. But then, a newborn does not have many of those attributes yet it is considered a human.

To think of it, fetus leads a parasitic life till it is born.

@WYSIWYG But note that a newborn human is also unable to survive without an adult caretaker.

Any definition of "human" someone tries to use besides this one (that it is human regardless of how far through gestation it is) will almost certainly end up excluding some "obviously human" segment of the population.  This answer is very well-worded.

@WYSIWYG But a parasite does so without the host consent and is recognized by the immune system as a threat. A female mammal sacrifices herself in order to provide the environment for the proper development of the new organism, until it is able to survive outside.

@ddiez a female can get pregnant without her consent. Parasite need not be detected by immune system- immune system is just a hurdle to its parasitic lifeform. Plus, fetuses can also invoke immune responses. Parasitism is a way of life in which one individual thrives at the cost of other.

@ddiez IIRC, mother's immune  system only recognises the fetus after it settles down in the womb wall and starts producing a hormone (essentially an immunosuppressor, IIRC) into the mother's bloodstream. Until then it's just a foreign body.

@Susan. well yes but that's strongly true for human babies. My statement was general. Moreover a newborn is not a parasitic anymore. The adult has a choice to abandon the baby (though it sounds harsh).

@WYSIWYG no sane person would ever do that, though (Yes, I'm well aware this is a statement about the sanity of mankind)

@JanDvorak.. yeah.. and some pathogens also elicit responses that allow them to escape the immune system.

A parasite escapes the immune system. The mother enables the fetus to grow in a immune tolerant environment. Organisms reproduce to perpetuate the species. This is one of the defining characteristics of life. Note that parasite has a harmful connotation and typically (if not always) involves different species. I do not think it correct to consider the fetus a parasite.

@ddiez You can see this post. Some discussion about the definition of parasitism. Whatever be the initial turn of events, the fetus is actually eating the nutrients from the mother depriving her of those. Mother chooses to eat more and let the fetus grow for lets say some greater good; that doesn't change the nature of this interaction. The terms escapes or enables are just literary; mechanistically there is no difference.

And I didn't actually state that fetus is a parasite. I just raised an opinion. You see, pregnancy is always a burden for the females. My point was- if you consider a fetus "alive" then it is a parasite. Otherwise you can call it some congregation of cells that is catalyzing the process of reproduction. Cell cycle in a bigger scale!! So imagine a unicellular organism- you won't call the cyclins and newly replicated DNA as life, right? We can continue this discussion on chat because this can go very very long as it is just exchange of opinions

In fact, by pretty much any sensible definition, the unfertilized ova and sperm are also just as alive as the fertilized embryo is. Just because these haploid gametes make up a relatively small part of the human life cycle doesn't change the fact that they move, they metabolize, and, crucially, they're capable of reproducing (by first fusing into a diploid zygote, which then grows and produces more gametes). Or, as somebody once quipped, "a chicken is an egg's way of producing more eggs."

@IlmariKaronen, don't unfertilized ova and sperm carry the same DNA of their host? And aren't fertilized embryos wholly separate and distinct life forms from his or her mother?  I was of the understanding they have their own set of DNA and are, at the point of conception, a completely separate human life form. That seems much more of a distinction than your comment describes.

@JohnDubya: Each ovum or sperm cell carries half the DNA of the parent that produced them; when an ovum is fertilized, the resulting embryo inherits half its DNA from the ovum, and half from the sperm. An ovum or a sperm is thus equally related to the parent that produced it, as to the child produced from it. If you consider the child "wholly separate and distinct" from the ovum, then, by the same argument, you should also consider the ovum "wholly separate and distinct" from the parent. (Well, almost. Relatedness gets a little tricky when ploidy changes, as notably seen in social insects.)

@JohnDubya: ... In any case, my point wasn't about whether, or to what extent, sperm and ova are distinct from the diploid life stages preceding and succeeding them, but about whether they count as "alive". It's very hard to come up with an objective definition of "a distinct living organism" that would exclude a human sperm cell without also excluding, say, a drone bee.


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Why can't the immune system start at the mating time?
The immune system has a great role in our body. When foreign particles
enter our body, the immune system can recognize and start
defense mechanisms such as the complement system and others. But when sperm enters
into the female organism, why does her immune system not recognize this?
In that time which kind of mechanism is active in the woman's body?

The obvious, if simplistic, answer seems to be one of evolutionary exclusion.  If the female did develop an immune reaction to sperm, the individuals with this quality would not be able to reproduce, and the trait would die out.

"But when sperm enters into the female organism"... sperm never enters the female organism. The lumina of vagina, uterus and fallopian tubes is external to the body. Fecundation, by the way, happens outside the female body. Only 1 week after that the embryo actually "enters" the female body (implantation).

Also, it's worth mentioning that the immune system will attack the sperm cells if they enter the organism of the very male that produced them. Sperm cells in a male, from the rete testis to the urethra, are always outside the body.

These questions are not completely easy to answer, since the immune reaction in this area is not completely understood. There are two different mechanisms  which play a role here:
Semen is immunogenic and can cause the generation of specific antibodies against it in men and women. The main question here is if the presence of semen in the females reproductive tract is the consequence of a suppressed immune reaction or because it is not recognized. There are indications for both possibilities but I think the first is a bit stronger. The mucus from the vagina is immunosuppressive as well as the seminal fluid, which contains prostaglandins which have the same effect. Have a look at this article for some more background:

Sperm survival in the female reproductive tract: presence of
immunosuppression or absence of recognition?

For the situation in the uterus between mother and fetus the situation is better understood. This is the so called immune privilege of some tissues (among them are the uterus, testes and the eye) where immune reactions are suppressed.
The placenta forms an immunologic barrier which seperates mother and fetus. This is done by secreting immunomodulary substances and also by the subpression of some T cell subpopulations. For more details see here. This is a highly developed system to protect the developing fetus (which is foreign) from the mothers immune system.


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Can we influence evolution by teaching primates to control fire? Should we?
Most people with a strong interest in biology will have heard of Kanzi the Bonobo, the ape that has the wherewithal to collect fuel for a campfire and play pac-man.
But is it conceivable to influence the course of their evolution so that it becomes more likely they gain the intelligence to support a civilization in the distant future?
Let's face it: it's easy to imagine that Bonobos are looking superficially like early human ancestors.  They have been forced to become more peaceable and social because they are polyamourous (which is why the human phallus is shaped the way it is).
If we are willing to genetically modify them, we would have to do so so heavily the depend on the genetic modifications, or they might just get bred out again - intelligence may be delicate.
In conclusion, is it conceivable to "enlighten" some groups of primates and send them into the wild, in the hopes they (much) later evolve intelligence?  Their existence would serve as an "insurance policy" on intelligent life in the not unlikely event we destroy ourselves.

are you ready for the ethical issues that come with it?

The ethical issue isn't really one for this Q&A site, and as a side note I think most likely circumstances (global warming etc) in which we destroy ourselves are also likely to wipe out a large portion of complex life, particularly terrestrial due to flooding.

This question appears to be off-topic because it is about ethics

Is it conceivable to influence the course of their evolution so that it becomes more likely they gain the intelligence to support a civilization in the distant future?

No, I don't think so, based on what is known about evolution.
Your idea is in keeping with the opening of Kubrick's 2001: A Space Odessey, where the monolith inspires one of the primates to see a femur as a weapon. He picks it up, hits an opponent with it, and the idea catches on within his group; the implication is that this inspired male's (female's?) group goes on to domination and are the progenitors of the human race.
In real life, that's not how intelligence is passed on. You can teach a gifted bonobo how to build a fire, but if he's not into roasted meat, or really cold, or trying to scare away predators (or if he doesn't realize that's what fire is good for), all you have is one bonobo who can start fires. It doesn't influence his genes.
To actually influence evolution of bonobos, I imagine it would look like this: You capture 4/5ths of all the bonobos in the world (leave the 1/5 for genetic pool variation). You test them for basics of quick-wittedness. Kill all the bonobos that fall below a certain threshold, and release. Repeat several generations later. Keep doing so for 50 cycles. What you will have are a race of quick-witted bonobos - maybe. Because if the quick-wittedness you selected for doesn't provide them with a survival advantage, it (and they) will die out. What if the smarter bonobos all want to be alphas, and all that fun cuddling and sex-as-peacekeeping were to disappear? They might not survive the bonobo-chimpanzee wars, because they won't live in large, peaceful, cooperative groups any more. Maybe you can teach the bonobos to plant crops, assuring a food source. Will they irrigate, too? What would this decrease in roaming mean for pygmies who hunt bonobos for food?
My point is, we can't control evolution very much unless we also control the total environment they live in. That's one way we have been able to have such an impact on a rather extraordinary species: dogs. But in the end, a dog, whether it's a sheep-herding or rat-catching or boar-hunting or bull-baiting or duck-fetching breed, is still only a dog. Invaluable helpers, but after all that selective breeding, they're just dogs. The smartest dog in the world still likes to play fetch more than anything in the world. Even eating, if she's anything like my two Border Collies.


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Regarding cellular self-destruction
I heard and read telomere 'health' or 'length' ( if that's right ) has alot to do with cell 'health'. If telomere 'abilities' are 'restored' to a 'healthier' status then the cell it is in functions as though it were 'younger'.  I was wondering since cancer cells grow without limit and 'older' cells or unstable cells grow with less ferver do cancer cells have functioning telomeres within them and would they somehow be alot more 'robust' then telomeres in normal cells? If this is true could telomeres from cancer cells somehow revitalize the telomeres in normal cells?

Do cancer cells have telomeres? Since cancer cells grow unceasingly would their telomeres be 'extra' robust?

You can edit your question when you want to change it. There is no need to do this in the comments.

Telomeres are at the end of the chromosomes and get shorter with every cell division, since the lagging strand is missing a start point for the DNA polymerase. This limits the number of cell divisions to 40 to 60 before the cells go into senescence and stop dividing (they are not dying at this point). This phenomenon is called the "Hayflick limit".
Cell populations which need to divide more often or cells which need to maintain a long telomer status (stem cells) because they give rise to other cell populations, have an enzyme called telomerase which has it's own (RNA) template and can enlarge the length of the telomere. See the figure how this works (from the Wikipedia article on Telomerase):

To answer your question: Younger cells have longer telomeres (compared to older cells). Usually cells stop dividing, when their telomeres get too short to avoid chromosomal damage, due to the progressive shortening of the chromosomes. In cancer cells the pathways controlling this (for example p53 and the retinoblastoma pathway) are often mutated, so that the cells divide forever. This leads to chromosomal instability, further mutations and chromosomal disarrangements, which can cause real havoc.
It also happens for some cancers that they manage to reactivate their telomerase, thus keeping their telomers at a healthy length and preventing chromosomal damage. By this activation they get around reaching the Hayflick limit for the maximum number of cell divisions and are truly capable of living forever. The famous HeLA cell line for example is telomerase positive.
The activity of the telomerase in one cell has no effect on the neighboring cells.

In some types of cancer cells, an enzyme called telomerase can actually rebuild the telomeres, making a cell appear "younger" than it actually is and preventing it from senescing (reaches a point where it stops dividing).

Telomerase, a eukaryotic ribonucleoprotein (RNP) complex, helps to stabilize telomere length in human stem cells, reproductive cells and cancer cellsby adding TTAGGG repeats onto the telomeres using its intrinsic RNA as a template for reverse transcription.

Shay et al. 2001
This Myerson review from 2000, Role of Telomerase in Normal and Cancer Cells,
 provides a good overview of telomeres in normal and cancerous cells.
It's not that telomeres (shown in image below) are more robust in cancer cells, they are actually rebuilt by the telomerase enzyme.

(Socratic)

Is senescence related to apoptosis in some way?

Do stem cells have a special type of telomere?


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epitope prediction/ mapping
B-CELL EPITOPE PREDICTION
Regarding this article:

"Such a molecule can be synthesized or, in case of a protein, its
gene can be cloned into an expression vector."----- is a particular
line in this article. What does expression vector mean here??
"antipeptide antibodies"---- what are these?
"immunogenic peptides"----these are basically epitopes, am I right??

An expression vector is a (usually circular) piece of DNA which is able to replicate inside a (bacterial) cell independently of the genome. Vectors can be transferred between bacteria and can express proteins from their own DNA sequence. They are used to express proteins inside of bacterial cells which can subsequently be purified. In this case the sequence for an immunogenic peptide is cloned into a vector and expressed in bacteria.
These are antibodies which are directed against a certain peptide. This is one technique of generating these antibodies. Making a (synthetic) peptide and then immunize animals against it. Then you can purify the antibodies from the serum of the animal.
Yes. You make short peptides of 8-12 amino acids (which is the length that the antibodies binds to) and use them for immunization.

"independently of the genome" -did not understand this term.
"Vectors can be transferred between bacteria and can express proteins from their own DNA sequence"-This line means that one bacteria can carry the gene of another bacteria and hence express the proteins of its main parent bacteria in the new parent bacteria??
"ïmmunize animals against it." - meaning the newly created antibodies are injected into the body of victim so that they can fight that particular peptide??

Can you please ask this in a new question? It is easier to answer (since pictures can be added) and it is also considered more appropriate.

I could but if i ask, it will be closed down... so whats the point?

It is basically a piece of DNA which is independent from the cells genomic DNA. Have a look at the Wikipedia page, which also contains an image.


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Where do lost membrane proteins go after exocytosis?
Exocytotic vesicles take away membrane proteins and glycocalyx on the cell's plasma membrane surface. When those vesicles are released into the interstitial fluid and wherever else, where do they go?
Do they stick to the vesicle everywhere? Or do they get removed from the vesicle? If the vesicle fuses into another cell, do those proteins and carbohydrate attachments stick to the new cell?

In the process of exocytosis materials which are about to be released are transported in small vesicles to the plasma membrane. The plasma membrane fuses with these vesicles and this sets the substances free on the outside of the cell. See the figure (from here):
The other possibility for transport vesicles is that they arrive at their target cell and either fuse with the membrane and release the transported substance into the cell or that they are taken up in another vesicle which is then targeted towards the endosome/lysosome. See the figure (from here):

It doesn't matter which way is chosen, the membrane of the vesicle is recycled either by integration into another membrane of by going through the lysosome.

I see. I must have confused the 2nd way with exocytosis


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How fast do cancer cells divide (compared to normal cells)?
This question suggests that we have, on average, 50-70 billion cell divisions per day. I just read that cancer cells divide more often and are therefore more prone to radiation.
I am wondering, for a specific type of cancer, how fast cancer do cells divide (approximately) compared to normal cells. Does the ratio of cancer mitosis rate to the normal cell mitosis rate varies a lot?
I checked bio-numbers but there's not much data there.

I've read that healthy hepatocytes divide about once per year. However, this rate can vary quite a bit since the liver can regenerate, and regenerating liver will have a much higher rate of mitosis. Hepatocellular carcinoma will have a much faster rate of mitosis than healthy tissue but I haven't found a rate yet. There has to be a wide range in division rates from tissue to tissue, because healthy skin cells probably divide a lot more than once per year, skin cancer cells may divide faster yet.

Some literature quantifies cell growth esp. in tumors in doubling time. An article I'm having trouble recalling quoted 60 days for aggressive cancers, and 100 days for slower cancers.. sorry about having little detail. As for actual growth rate as in individual cells, that's a little harder to find, since the growth rate is dependent on the cell type, as well as the developmental characteristics of the forming tumor, which may not be symptomatic or identified early enough. Most importantly, though, cancer cell are normal cells that have lost replicative restraint, and times may not vary.

I think your question is not accurate enough. There is no such thing as "normal cell". We could use average division rate or something like that as base of comparison, but I think the exact numbers would be much better.

Tumors can be benign (they don't bother you at all eg: a mole which does not change) and malignant (also called cancer).
The difference is based on:-

Degree of differentiation - How much the tumor cells resemble the normal cells
Rate of growth - In general (over generalised) benign tumors are slow growing while malignant tumors are fast growing
Spread to nearby tissues - Benign growth don't cross tissue planes as defined by basement membranes/fascias, while malignant tumors invade across tissue planes
Metastasis - Spread to a remote location in the body through blood, lymph vessels, transcoelomic (peritoneal, pleural, pericardial spaces) routes - This is ONLY seen in malignant tumors.

Coming specifically to rate of growth, these factors must be considered:

What is stated above in 2 is the general case:

Malignant tumors a.k.a cancers grow fast
Benign tumors are slow growing
That being said some benign tumors grow faster that malignant tumors. Eg: Fibroid - grows very rapid under the influence of estrogen as in pregnancy

The rate of growth of malignant cancers depend on their degree of differentiation (look point 1 above).

Well differentiated cancers grow slow - Cancers that are very similar to normal cells are considered to be well differentiated
Poorly differentiated cancers grow faster based on the "poorness" of differentiation,i.e. the worse the degree of differentiation, the faster the growth. Totally undifferentiated (unidentifiable as any tissue type) are called anaplastic cancers and these grow the fastest

The rate of growth of cancers may vary over time

Due to excessive division probability of mutation is high and a sub-clone may emerge with faster rate of division thus a previously slow growing cancer could suddenly start growing fast
Due to the same process some cancers may suddenly decrease in their growth rate and may eventually even vanish! (become necrotic and get cleared away)

This is taken from Robbin's Text book of Pathology,Ed.8, chapter 6
Edit 1:
To know the numbers you need, you have to find out the rate of increase in volume (by measuring size at two points in time) and divide it by the approximate volume of one cell. This will give you the number of cells that has newly divided within the two measured points (growth in interval). Which can then be converted to cell divisions per second.
As pointed out, the rate is going to vary extremely, based on the cancer type.

That said I don't know if the rate of cancer growth has been measured by the rate of cell division or if the data you require exists.

I am also wondering how to measure it. Numbers like that are only estimates.

Different cancers divide at different rates. One way to qualitatively visualize this is observe hair loss in patients who are undergoing chemotherapy. Commonly, a drug like cisplatin will be administered which will cross-link DNA, inhibiting cell division by activating apoptosis. Tissues which are killed most readily by cisplatin are those which are dividing most rapidly: intestines, head hair, red and white blood cells, tumors.
Despite the loss of hair on the head, many patients do not lose slower growing hair on their arms, eyebrows, eyelashes, etc. Likewise, though cell death in the intestinal lining may be dramatic on cisplatin, the skin may not show lesions as it is a more slowly dividing population of cells.
The rate of cell division correlates with the rate of cell death while taking the chemotheraputic drug cisplatin.
You may make a rough visual survey of the cells in the body which divide so rapidly that they die, and divide so slowly that they largely survive chemotherapy.
The rate of cell division of head hair and other body hair spans the rate of cell division over which cisplatin effectively acts on tumor cells.

Hair cells are not dividing. What happens here is that you kill the cells in the hair bulb which produce the hair which leads to hair loss.

What kills the cells in the hair bulb is the process of cell division with cross-linked DNA. It's the rate of the division that determines how cytotoxic cisplatin is. What do you mean hair bulb cells aren't hair cells?

I mean mostly keratinocytes and melanocytes. These cells are usually not dividing but making proteins at a relatively high rate (otherwise the hair cannot grow and will not be pigmented) so this probably makes them vulnerable. I will check for more details here, but it might take a day.

or two...... :D

@12345678910111213 Are you saying that cisplatin damages DNA indiscriminately, and apoptosis is activated in a cell with damaged DNA only when the cell tries to divide? (Because https://en.wikipedia.org/wiki/Cisplatin#Pharmacology says "The damaged DNA elicits DNA repair mechanisms, which in turn activate apoptosis when repair proves impossible.", so I am confused.)

I think you should start with immortalized cell lines and so in vitro division rates by perfect conditions. This is easier to measure than in vivo division rates. E.g. HeLa has a division time of 23 hours. MDA-MB-231 and A549 division times are around 28 hours.

Growth of HeLa Cells
Comparative Analysis of Dynamic Cell Viability, Migration and Invasion Assessments by Novel Real-Time Technology and Classic Endpoint Assays

So I assume there is a physical barrier somewhere around one division per day or so, and it simply cannot grow faster. While bacterial division times are much lower (down to 20min), they also depend on special mechanisms (see this question/answer) and are orders of magnitude smaller than mammalian cells, so they don't count as a counter argument to this.
If you check zygote division times (10-12h, 14-16h, 22-24h, ...), you can see that they highly depend on the cell size. After some divisions the zygote depleted the reserves necessary to divide at higher rates, so after that it is limited by the ~24h barrier too.

Time-Lapse Cleavage Rating Pr
edicts Human Embryo Viability

Same 24h data here by rapidly proliferating cells.

The Cell: A Molecular Approach. 2nd edition.

So we can assume that 1/24h is the maximum rate of cell division by cancer. Let's read more about cancer in vivo, because it behaves completely different than immortalized cell lines in in vitro tests.

Originally tumours were thought to grow because they consisted of
  cells that multiplied more rapidly than cells in the surrounding
  tissue. In fact the average cell cycle of 48 hours for human tumour
  cells is slightly longer than the cycle of non-malignant cells. ...
When a normal cell divides, it does os only to replace a cell that has
  been lost and in this way a constant cell population is maintained. In
  tumour cells the control mechanism appears to have been lost: as the
  cell divides it adds to existing numbers of cells and increases the
  total population. ...
A measure of the rate of tumour growth is the time taken for a given
  population of malignant cells to double in size (doubling time). If
  the cell cycle takes between 15 and 120 hours, the doubling time can
  be between 96 hours and 500 days, depending on the histological type
  of the tumour, its age and whether it is a primary or metastatic
  growth. A shorter doubling time (less than 30 days) can be between is
  seen with teratomas, non-Hodgkin's lymphomas, and acute leukaemias;
  common solid tumours such as squamous cell carcinoma of the bronchus
  and adenocarcinoma of the breast and bowel have doubling times in
  excess of 70 days. In the patient the growth of a cacncer is only
  detectable and observable during the last 10-14 of its 35-40 doubling
  times.

Cancer Nursing: Care in Context (page 270)

So according to this book the division rate of cancer cells are similar to healthy cells.
According to another book this statement is from Dougherty & Bailey 2001, but I wasn't able to find the scientific article. :S

Tumour cells appear to have lost control mechanisms which prevent cells from growing until replacement is required. Human tumour cells are thought to have an average cycle time of 48 hours. This is not more rapid than the cycle of most normal cells. The reason tumours become larger is because their cell division creates additional cells rather than replacements (Dougherty & Bailey 2001).

Stoma Care and Rehabilitation

While ~24h is a reasonable maximum estimate for eukaryotic cells, this is very wrong for bacteria. Laboratory strains of e.coli can double the cell number in ~20 minutes (see this question)

@Nicolai Feel free to correct the answer.

The fastest carcinoma cell I have seen is the HCT-116 line, its doubling time  is about 17h. They are quite small cells.

@Roland My guess would be that it depends on the cell surface / volume ratio, but reality use to be much more complex. :-)

Please notice that cancer cells do not grow or divide faster than
  normal cells, although many people believe that, and most forms of
  chemotherapy were designed on the assumption that they grow faster.
  Actually, what makes cells cancerous is the lack of control of cell
  growth, so that they keep on growing without limit, even if slowly. On
  the other hand, some kinds of cancer cells do grow quite rapidly, even
  if not faster than certain normal cell types, such as those in the
  bone marrow that constantly replace blood cells, and those in the
  intestinal lining and skin (including hair follicles) that constantly
  renew those structures. In one form of lymphoma, the abnormality has
  nothing to do with growth or division at all, but instead is a lack of
  apoptosis (programmed cell death), so that the cells accumulate
  without limit.

Cancer in One Easy Lesson by Biology 166 Unsolved Problems in Cell Biology Albert Harris

Your answer is correct and the citation is relevant. However, it would be better if the citation is from a scientific article or a book instead of course notes.

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


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Meiosis I or II
Suppose an organism has 8 chromosomes.  When the female and male organisms mate,  how many chromosomes will the mother contribute to the offspring? Why?

Same issue as this question. We're not going to do your homework for you.

@MikeTaylor This likely IS a homework question. However, this person DOES NOT SPECIFICALLY SAY IT IS A HOMEWORK QUESTION!

@L.B. If is not, then I'm sure Camille would be happy to clarify her questions for us. :)

Both the male and the female would give half of the total number of chromosomes for their species (assuming both cells are normal). So if the organism has a total of 8 chromosomes, the mother and father would each give 4.


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Evolutionary support for parenting book "The happiest baby on the block"
The book by Dr Harvey Karp (MD) The Happiest Baby on the Block proposes that the duration of human gestation has evolved as a tradeoff between cranial size and development of the infant.  He hypothesizes that from an overall developmental perspective human babies are all premature and would benefit from additional time in their mother's womb; however, because humans have such big brains, and therefore our babies have big brains, the infant needs to be born earlier than would be developmentally ideal so that it doesn't get stuck in the birth canal.  The result is babies that have big brains but are highly vulnerable and dependent on their parents until their development progresses further.
I discussed this with some students in class as an example of the use of ideas from human evolutionary ecology and life history theory in the popular press, but with the disclaimer that I had no idea if any of Karp's ideas are backed up by any evolutionary or anthropological data.  Could anyone point me towards literature that support or contradicts Karp's claims?  For example, are human infants more dependent than those of other primates?
[The upshot of Karp's theories are that the best way to have a "happy" newborn is to mimic conditions that it would experience in the womb, such as swaddling.  Works for my child!]

How many more weeks in utero does Karp think would be ideal? I don't know Karp at all, but a quick search indicates he's known for soothing babies by swaddling. Great. My mother swaddled all her infants many decades ago.
If he is comparing human neonates to  primate neonates, he's correct. Baby primates are born pretty much knowing how to cling onto the mother with four extremities, necessary because primates are quadripedal, and need their arms to walk as well, meaning baby needs to hold on, aided by opposable toes. (Chimps and gorillas do support the baby with one hand longer, though.
But what evolutionary advantage would it serve for our infants to come out grasping? humans are bipedal, meaning we have arms that can be used to carry an infant. If we need our arms, we have the intelligence to fashion slings or carriers.
The same goes for any ability: sight, motor skills, etc. They don't need to be born with these skills, because they are cared for.
Antelopes drop a newborn which is up in minutes and able to see and run. Cats drop a newborn which can wiggle, crawl some, is blind and as helpless as a human.
Babies, through evolution, are able to live outside the womb (assuming no complications) without extraordinary maternal assistance from about 36 weeks on. A look at growth charts show steep rises in both cranial size and weight gain.

But you can see that a baby's head at the 10%ile takes at least six weeks to catch up to a baby the size of one born at 90%ile. Why doesn't that baby just gestate for 6 more weeks?
There is much more than head size going on here. There is the placental size, the amount of amniotic fluid, the possibility of meconium aspiration, etc.
Stillbirths are twice as common at 42 weeks and 4 times as common at 43 weeks.

Approximately 20% of postterm (41 weeks gestation) fetuses have fetal postmaturity syndrome, with chronic intrauterine growth restriction from uteroplacental insufficiency. These pregnancies are at increased risk of umbilical cord compression from oligohydramnios, [low Apgar scores], intrauterine passage of meconium, and short-term neonatal complications (such as hypoglycemia, seizures, and respiratory insufficiency). ...[T]he 4-fold decrease in the incidence of the meconium aspiration syndrome in the United States from 1990-1998 has been attributed primarily to a reduction in the postterm delivery rate [(induced delivery at 41.5 weeks)]. Postterm pregnancy is also an independent risk factor for neonatal encephalopathy and for death in the first year of life.[17, 18]

Maternal complications and death also increase with post-term deliveries.
Are term babies actually evolutionary preemies? I haven't read Dr. Karp's book or heard his reasoning, but it seems superficial to me. Medically, from an infant and maternal standpoint, a 38 week delivery is ideal. Over hundreds of thousands of years, the female uterus and pelvis, and the fetal placenta and amniotic fluid found the most favorable time for delivery into a human environment.
If we gestated for two years, like elephants, yes, our babies would be more capable at birth, but we aren't elephants, and mothers and babies would die.
Postterm Pregnancy (Medscape)
Elephant birthing and calves (Wikipedia)


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3 end RNA seq library construction
I have tried to make cDNA libraries from FFPE tumor blocks (highly degraded RNA) using the 3' end RNA seq protocol provided by West lab. Here is the link for the same.
http://med.stanford.edu/labs/vanderijn-west/Protocols.html
After PCR enrichment, a gel purification step follows. My trouble was, the fragments always gave rise to a smear rather than a band between 200-300 bp. Can anyone provide any suggestions as to why this may be happening?
Thank You

RNAse contamination?


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Fisher's Geometric Model for Dummies
Fisher's geometric model is still today one of the most important and fundamental model in evolutionary biology but it seems to me that most student in evolutionary biology don't really understand it (and I am one of these students). Such standard models are often found on wikipedia but in this case the wikipedia article (here) offers nothing more than a simple analogy.
According to Orr 2005:

Fisher's geometric model shows that the probability $P_a(x)$ that a random mutation of a given phenotypic size, $r$, is favorable is $1-\Phi(x)$, where $\Phi$ is the cumulative distribution function of a standard normal random variable is a standardized mutational size, $x=r\frac{\sqrt{n}}{2z}$, where $n$ is the number of characters and $z$ the distance to the optimum.

Can you please explain what the Fisher's geometric model and the math behind it (how are these functions calculated)?

If you haven't seen it, you might find this blog post from Dynamic Ecology interesting: The fitness landscape of beer: Fisher’s geometrical model vs. IPA.

Fishers Geometric Model (FGM) is a theoretical prediction about the adaptation process in traits. There are a number of things to establish before attempting comprehend FGM. Firstly, shifts in an adaptive landscape, in natural scenarios, are generally quite small. Because populations have been evolving for such a long time and the small shifts in adaptive peaks it means that most populations should be near or on a local fitness optimum within the relevant landscape. The adaptive landscape comes from S. Wright, discussed in the Orr paper, where he spoke of a field of possible gene combinations" each with a fitness value, some combinations are fitter than others. Adaptive peaks represent the fittest combinations of all traits.
We can picture all of this using a single trait:

Here there is a local optimum (which is also global, Fisher assumed that adaptive landscapes are less rugged than Sewall Wright and had only one optimum) for the trait. The population starts at point A (the red ball), just off the adaptive peak for the initial fitness distribution (blue trace). Then selection alters (red trace), initiating a new bout of adaptation, making the population (green ball) further from the optimum.

From here lets imagine this is two seperate populations, the green population (A) wants to move along the red line to the highest point, the red population (B) along the blue line also for its own optimum.
If a mutation which has a very small effect arises then there is 50% probability in both populations that it will improve fitness (assuming no neutral mutation) because it will either be recessive or deleterious. This value is shown in box 2 figure 1 of the Orr paper.

Now if a large effect mutation was to arise in then there is less chance of it being beneficial for population B than for population A, this is because B is closer to its phenotypic optimum so a large effect mutation is likely to "overshoot" the optimum. (The black line illustrates where either population would end up after a large effect mutation in the direction of the adaptive peak). You can see this mutation would put population A very close to its peak (the red line) and population B would have a reduced fitness. This is summed up nicely in the opening to the Orr paper.

"Precise adaptation is possible only if organisms can come to fit their environments by many minute adjustments"

So, descriptively, this is why we see a reduced probability of large effect beneficial mutations as we approach an optimum; we expect most bouts of adaptation to be due to small shifts in adaptive landscape and populations to start bouts near to the former adaptive peak.
The FGM expands this out beyond one trait (or, as Kauffman and Gillespie did, the sequence - with the latter seemingly being more successful than the former). As shown in figure 1 of the Orr paper,

This is a highly multidimensional space, with one dimension per trait, therefore more complex organisms by definition will have more complex spaces. The centre of this sphere is the phenotypic optimum, and each layer represents and adaptive movement, or substitution of the wild type as in the Maynard-Smith adaptive walks system. The red line shows the movement made by the population through this sphere.
And now for some math. (Refer to box two in the Orr paper). $P_a (\chi)$ is the probability that a mutation (of effect size $r$) is favourable. Thinking about what I discuss above, that is, $P_a (\chi)$ is the probability that a mutation will increase fitness, which must therefore be a product of the landscape complexity (the number of characters affecting the fitness), the distance from the population to the optimum, and the size of the effect. $\chi$ is the standardized mutation size, which accounts for the distance to optima, as $z$, the number of characters affecting fitness as $n$, and the effect size $r$. This means that $\chi$ = $r \sqrt{n} /2z$: therefore an increase in the distance to the phenotypic optimum ($z$) reduces the value of $\chi$ (thus increasing the probability that a mutation has a beneficial effect), whereas increases in $r$ or $n$ will decrease the probability that the mutation is beneficial (i.e. large effect mutations and high complexity). In the context of the above example, both populations have an $n$ of 1, and the values of $z$ vary - this means population A can tolerate a larger value of $r$, or in other words, population A is more able to make adaptive substitutions because it is further from peak fitness, thus more tolerant to large effects, than population B.

Difference between $r$ and $\chi$: $r$ is the raw value of effect size of a mutation, whereas $\chi$ is the standardized effect size. Assuming equal effect sizes the relative effect of mutations will depend on the number of traits affecting fitness (see the diagrams below), thus we have to correct for this.
How does complexity affect the probability of beneficial mutations? Look at the following diagram.

Each point represents a possible combination of traits when we have three traits affecting fitness, each with two possible incarnations (A or a [most fit and least fit respectively]). The outer green ring has one possible occupying combination (aaa) which is the least fit - it's the furthest from the optimal combination, the red point. On the green ring the probability of increasing fitness with a mutation is 3/3 (because there are 3 possible mutations all of which increase fitness). Note, assume all changes are equal effect. If we change one trait to the A version we can have 3 possible outcomes (Aaa, aAa, aaA) which occupy the yellow ring. From the yellow ring a further single mutation has four possible outcomes, of which 3 can increase fitness so the probability of improving fitness with a mutation is reduced (3/4). In the blue ring there is a 1/4 probability of increasing fitness. Jumping to the red point, where all traits are A, every possible mutation will reduce fitness (0/3).

Bearing this in mind, let's change n (the number of traits affecting fitness) from 3 to 4. The least fit starts in the red ring (aaaa), from here there is a 4/4 probability of increased fitness via mutation. From the green ring there is a 6/7 probability. From the yellow ring there is a 4/8 probability of increasing fitness, and from the blue a 1/7 chance. Compare this to when n=3, from the blue ring there was a 1/4 chance, when n=4 it is 1/7 - there are more possible combinations and still only one fittest combination
Put another way; if we consider it in terms of single point mutations in a sequence, a mutation which affects 1 trait affecting fitness (n=1) then the probability it will increase fitness is drawn from the distribution of probable fitness effects. If the point mutation affects 5 traits then the effect is drawn from the distribution 5 times, and because we assume most mutations are deleterious and beneficial ones are relatively constrained to being small, there is a greater probability of reducing fitness when n>1.
Fisher's geometric model
Below is some R code to generate the model's prediction that small effect mutations have a 50% chance of being favoured. The probability crashes rapidly as the effect of the mutation increases.
r = .01 # random mutation of phenotypic size r
n = 1 # number of characters
z = 1 # Distance to the optimum
standardized.mutational.size <- function(r, n, z) {
  (r * sqrt(n))/(2 * z)
}

# Get the standardized mutational size of various distances to the optimum
mutation.sizes = standardized.mutational.size(r, n, seq(0, 3 , by = .0001))
plot(x = mutation.sizes, y = 1 - pnorm(mutation.sizes),
     xlim = c(0, 3), ylim = c(0, 1),
     type = "l",
     main = "Fisher's geometric model of adaptation")
abline(h = c(0, .5), lty = 3)

Thanks a lot for your answer! The first part was very clear to me. I would rather think that complexity influences the number of traits $n$, therefore increasing $\chi$, though. Isn't it the way it should work? I still don't fully understand where does the $r\sqrt{n}/2z$ comes from. The formula would have been $2n\sqrt{r}/2z^2$ I would not be able to argue that the formula is wrong. Also I am a bit unsure of my understanding of the differences between $r$ and $\chi$.

edits made for you @Remi.b


text:
Transmembrane Protein Problem
Problem
A transmembrane protein has 1000 aa. The 5th aa is found on the external side of the cell membrane. It interacts with the aqueous environment outside the cell. Amino acid 90 is inside the membrane bilayer. Aa 100-600 are intracellular, and 200-400 make a tight ball with minimal exposure to the aqueous cytoplasm. Amino acid 979 is found on the extracellular side of the protein where it forms a weak ionic bond with Cl-.
a. Can you draw the protein and mark positions of all mentioned aa in it?
b. What are the properties of these amino acids?
￼￼￼￼￼

I dont necessarily want/need the exact answers to these questions, rather i would like some guidance in what principles i would need to understand and conceptualize to attack this problem. Thanks all !

Please read our homework policy. For questions like these, we want to see some effort from you in trying to answer your question(s), and then we can clarify/correct you from there.

@MattDMo Please do note, that he is NOT requesting answers. He needs help figuring out where and how to start :)

Thank you L.B If there is anything more i need to add by all means please let me know. I would just like more knowledgable members to help me on the core "philosophy" to this.

@Macedon93 It would be great if you could share some of your thoughts about this. It is easier to help people when you know where they got stuck.

Ok, I see that this problem is a test to my knowledge of membrane proteins, atleast that is what i am assuming at this point. I can assume that question A.) is referring to the protein connexin, which traverses through lipid bilayers. However not completely sure. What really stumps me is the jargon in the question, such as "1000 aa", and "Aa 100-600".

Not completely sure as to what they signify.

I would start by drawing 2 horizontal lines. The space above the top line is the external side, the space below the bottom line is the cytoplasmic side, and the space in between is the membrane bilayer itself. Now fill in what you're told, placing dots and lines and circles to represent the structures were given in the right spaces. Then connect the dots.

@Macedon93 those are the amino acid residues. 1000aa is 1000 residues long, aa 100-600 means amino acids 100-600.

What is a weak ionic bond?

All ionic bonds are considered relatively weak in comparison to other bonds. Ionic bonds are forces of attraction between ions of opposite charge

Ionic bonds and covalent bonds are stronger than hydrogen bonds which are stronger than weak bonds like van der Waals. The term 'weak' isn't usually used in connection with ionic bonds in my experience, which is why I was puzzled.

I made a quick sketch on the basis of the information you gave (this is not to scale):

Aminoacid 5 (aa5) of the protein is on the outside, aa90 is inside the membrane. What we don't know here where the transmembrane part starts (directly with aa6 or later) and how it is organised (I indicated this as a transmembrane helix, but this can of course be different). Then we know that the border between the transmembrane part and the cytosolic part is somewhere between aa90 and aa100, that aa100 to aa200 seems to be some connecting part. The aa200 to aa400 is a globular domain which shields hydrophobic amino acids from the cytosol, so this part has to contain a high percentage of hydrophobic amino acids.
The part from 400 to 600 is again cytosolic but with no further information about the structure. After aa600 starts a second transmembrane part of the protein, but here we don't know how long it is. The maximum possibility would be until aa977, since we know the aa978 is outside of the membrane.

Thank you for your help. I followed your lead and my professor told me this is what she wanted to see, and with the help of shigeta, I now know how to illustrate this problem. However, what exactly tells you where aa5, aa90, aa200 etc are located ? What information are you basing its locations off of ? Or are you simply drawing a transmembrane protein, and labeling its respective amino acid sequences based off of common knowledge

@Macedon93 No, I am going along the text you provided. As I said, this is a quick sketch, for a more detailed figure you need to have more information (for example where the transmembrane sections begin exactly and so on). I knew that aa5 is outside and aa90 in the membrane. I also knew for example the aa200-400 is globular.

Duh, so stupid i realize these were stated in the question. Thanks again !

Membrane proteins are usually drawn as topological digrams with two parallel horizontal lines representing the membrane.  lines as 'extracellular' and below the lines as 'intracellular' for instance, but that is not what is being asked for here.
Its not clear to me that the number of transmembrane spans are fully described, nor are the boundaries of the transmembane spans.  I think what is being asked for could be a domain diagram of the amino acid chain.
Draw a line on graph paper representing the peptide and use a scale to label each point described. For regions draw a box around the peptide line to describe a domain, and label it.
I think its hard to talk about amino acid properties other than hydrophilic/hydrophobic.  hope this helps?

I think there's enough information given here to map out the protein. It probably starts on the external side, moves inside the cell, has a large cytoplasmic domain, then moves back out. The position and descriptions of the AAs also tell us something about their properties, even if it's subtle, such as "forms a tight ball with minimal surface exposure". The chloride ion interaction should also tell you something about charge.

Possibly, but if you had the full amino acid sequence, you would normally use a transmembrane domain algorithm.  There could be three helices.  Such mps are known.  The problem is a pretty limited set of facts and it doesn't seem like you need to jump to any conclusions imho.

Thank you for the insight. Illustrating this has become much more logical. Still have a decent way to go !


text:
Regarding inherited fertility in animals
If an animal is fertile does it follow that both its parents of the same species (not necessarily the same species of the offspring)? Was it Mayer who said a fertile male and fertile female of two different species, if they 'reproduce' and the offspring survives it won't be fertile. Reproductive isolation I think this is called. So if an animal is fertile then both its parents should be of the same species, right?

No it isn't necessary that the parents should be of the same species. Mules (male donkey X female horse) have been found to be fertile (reference). The wikipedia page on hybrids lists many inter-species hybrids that are fertile including Beefalo (Domestic male cattle X american bison). There are also many canine hybrids which are fertile. Wholphins have been found to be fertile.

A wholphin or wolphin is an extremely rare hybrid born from a mating
  of a female bottlenose dolphin (Tursiops truncatus) with a male false
  killer whale (Pseudorca crassidens).

So in short, for a hybrid offspring to be fertile, it doesn't necessarily need to be of the same species.

I know this is 'heresy' but if two different species are fertile and have a fertile offspring maybe they are not really different species but different subspecies.

@user128932 I wouldn't call them sub-species but atleast closely related species because a donkey and a horse can hardly be called a sub-species of one or the other. You can read this article. http://www.detectingdesign.com/donkeyshorsesmules.html

Do a donkey and a horse have a common ancestor ( with four legs)?

If a fertile female 'individual' , call it 'A' ,and a fertile male 'B' of a 'similar' but distinct species ; both have important differenses in their respective physiologies ; 'A' might have an important physiological process that 'carries out a certain biological tasks yet 'B' might not have something similar to this. So when passing on their important biological info. to their offspring how are possible physiological-process differences resolved. For Example a cat and a dog must have unresolvable physiological differences ; no one has bred a Dat or a Cog.

@user128932 Yes, they do have a common ancestor and your question here about the resolution of physiological processes in species crossbreeds needs to be asked as a separate question.


text:
What is the Baculovirus and how does it help in research?
I was reading up about Biotechnology and the use of insects, and came across an interesting article about Insect Cell culture Techniques that specifically talked about the usage of the Baculovirus. If I understand correctly does this virus help express certain genes when inserted into a cell?
Sorry if I am way off or did not use proper terminology, I am a high school IB Biology student who still has a a lot to learn
Thanks!

Baculoviruses are a a class of viruses which infect only a pretty small number of insects (or their cells in cell culture). To do so, the virus has to infect a cell, take it over to produce the own proteins and DNA to make new virus particles and finally set these new particles free. This is basically what is shown in the image below (from here):

From the proteins encoded by the viral genome, not all are essential, meaning removing them will not do harm to the virus or its function. And this is used in Biotech to produce proteins of choice. One of the non-essential proteins is replaced by the sequence of the protein you want to have produced by the cells. You then take insect cells in cell culture (these are single insect cells which live in a big vessel full of culture medium), infect these cells with the modified virus and eventually harvest the protein from the culture.
The advantage of Baculoviruses is that they only infect the insect cells on which they are specialized so they are a safe way of producing proteins for pharmaceutic applications. If you want to read some more about this, start here.


text:
Is there any research on how accurately people can follow a beat?
I'm currently helping develop a rhythm game, and as part of the scoring system, I'd like to make scores and ranks based more on accurate pattern recognition rather than hitting notes very exactly on time as is the case for many games of this variety.
In many cases, the margin of error for the best judgment in rhythm games is so small that it seems to be a matter of chance more than skill that a certain judgment is counted between "excellent" and "good" (for example, one game has the margin as small as ±0.011 s).
Of course, some people are better at hitting notes accurately than others either naturally or through practice, but I would like to find some actual research into what the base neurological limitations to rhythmic precision are and to what degree practice can actually improve it.

As a baseline benchmark for the best judgment, I was thinking of looking for some research into how accurately people can follow the tick of a metronome - for example, by measuring the average deviation of somebody tapping a button to a regular beat after about 100 beats or so when they've gotten used to it.
A Google search didn't return anything useful, probably because the search terms draw up so much other, irrelevant content. Is there any prior research on this subject? If so, where can I find it? If not, how could I conduct such an experiment myself?

You might begin your search with the characteristics of Parkinson's disease. This degenerative disorder is precipitated by the death of neurons in the substantia niagra. This brain structure is composed of multiple neurological nuclei. Its function is to connect cortical regions and nuclei together, most significantly with the basal ganglia. The difference between nuclei and cortical brain circuits is important to your question.
The symptoms of Parkinson's are directly correlated with the function of nuclei in central nervous system: the integration of information. It's the integration of conscious thought, muscle memory, sensory-motor pathways that makes voluntary movement possible. Disruption of this network in Parkinson's degrades one's ability to voluntarily execute a movement.
The cerebellum also controls voluntary movement. As a cortical structure, it is involved more with the formation and maintenance of muscle memory than information integration. Damage here results in the loss of fine motor control as opposed to gross motor control in Parkinson's.
This problem has a sensory and motor component. It might be difficult to tackle your problem as a whole. Perhaps breaking it down into smaller pieces would shed some light on what you're looking for.
Here are 2 articles I found relating motor control with the cerebellum and substantia niagra.
Relating cerebellar damage with learning sequence information
Relating the substantia niagra with interval timing

In performing a cursory Google Scholar search using the terms "keeping tempo", I found these articles that seem to cover your topic of interest:
Schulze, Cordes, and Vorberg (2005) Keeping Synchrony While Tempo Changes: Accelerando and Ritardando
Scheirer (1997) Tempo and beat analysis of acoustic musical signals
McKinnet and Moelants (2006) Ambiguity in Tempo Perception: What Draws Listeners to Different Metrical Levels?
Hopefully, these papers are a help to you. It doesn't hurt to conduct experiments that others have conducted. All that really does is add more information and data to what is currently available/known.


text:
Why can't a corn cob have 13 rows of seeds?
Every time before eating a corn, I count its lines. I would always find 12 or 14 rows of seeds, but never 13.
Is there any biological/scientific reason behind this?

Most varieties of corn bred for modern use have between 8-20 rows of kernels (Bommert et al. 2013.. Nearly all varieties have an even number of kernel rows.  This is due to the early development of the ear.  Ears of corn are developed from pistillate flowers on the ear (Bortiri and Hake 2007). Pistillate flowers are the female flowers, so they will bear seeds. The seeds are the individual kernals.
Long before the ear of corn has the kernels, it has several rows of flowers. The flowers develop on the ear in long rows. Early in development of the ear, the individual rows of flowers double, forming rows of double flowers, as shown in the simple diagram from Bortiri and Hake (2007). Both male flowers (left) and female flowers (right) have this two-row structure.

You can see the doubled pattern forming in this scanning electron micrograph of the very early development of the ears, also from Bortiri and Hake (2007). Notice the tip of the ear still has the single rows but the rows begin to double a little farther away from the tip. You can usually see this even on mature ears of corn.

You can see remnants of this arrangement if you look carefully at a cross section of an ear of corn. I've drawn arrows to show the connections where the flowers once connected together. If you look carefully at the ear of corn, you can identify the rows. The doubled rows have the kernels exactly opposite of each other. Each doubled row is staggered slightly from the neighboring rows. I've drawn lines to highlight each doubled row.  These two photos are from the agriculture extension office at Purdue University.

The development of corn flowers and all other flowers follows what is called the ABC model of floral development (Krizek and Fletcher 2005). The model has been greatly expanded since molecular genetics has increased our understanding of flower development. Many genes are involved, and the genes are used in different ways by different species of plants. The pattern of gene usage is similar in most grasses, which explains the double-flower arrangement of corn. Most grasses have the double-flower arrangement, and corn is a type of grass.
Some highly inbred variety of corn can produce odd numbers of kernel rows, as shown in figure below, taken from Bommert et al. (2013). KRN is kernel row number.  RIL is recombinant inbred lines, which means different varieties that have been inbred for particular traits. Thirteen is possible, as are other odd row numbers. An odd number of rows is unusual, however.

Citations
Bomblies, K. et al. 2003. Duplicate FLORICAULA/LEAFY homologs zfl1 and zfl2 control inflorescence architecture and flower patterning in maize. Development 130: 2385-2395.
Bommert, P. et al. 2013. Quantitative variation in maize kernel row number is controlled by the FASCIATED EAR2 locus. Nature Genetics 45: 334-337.
Bortiri, E. and S. Hake. 2007. Flowering and determinacy in maize. Journal of Experimental Botany 58: 909-916.
Krizek, B.A. and J.C. Fletcher. 2005. Molecular mechanisms of flower development: An armchair guide. Nature Reviews Genetics 6: 688-698.

The FFA logo must be at the upper limit of kernals, spent 4 years in FFA and never took the time to count.

@user31782 - Sure, happy to help. If you find the answer satisfactory, feel free to click on the green check mark by the top of the answer. That's the StackExchange way of saying thanks! :)

@MikeTaylor yeah I know that. Actually I have just started to study biology, so I will accept your answer after I understand it completely.

@user31782 Absolutely.  If there is something I can clarify for you, just ask. :)


text:
Did the Britons 100 years ago have different intestinal flora and fauna?
Note: this is not a question about history, but about human digestive system over time :)
I know a lot of colleagues who traveled for business trips to India. All of them caught  terrible diarrhea there, in spite of keeping all the rules related to use of reboiled or canned water only, eating only peeled fruits, not eating the street food etc.
My question is: how did the millions (or hundred thousands, I am not sure with the amount) of Britons survived in India during the time of the British Raj 1858-1947?
Did they have to keep the same safety dietary rules as the contemporary Westerners all the time? (I cannot see this as technically possible...)
Were our intestinal flora and fauna different one hundred years ago?
Was the hygiene level and quality of water much lower in Europe then so coming to India was not such a biological shock? (Well, I would believe this in the 1800s but not in the 1900s...)
Or did just some of them die and the rest got accustomed?
EDIT:
I am aware that there is an initial shock for your body when travelling to a very different area generally. However, the Indians (and other Asians) can easily drink the tap water in most of the EU countries and eat the street food, which is not valid vice-versa. So there must be some difference.

Its true for any place in the world.. When you shift initially, in most cases, your body would need time to get adjusted to the food there. Not only the food but the weather is also a cause for diarrhea in many places. When I was visiting Britain, the initial few days played havoc with my bodily functions too which I attributed to a couple of pork sausages..

Who said they did not have the same problems? I'm sure they did and I'm sure most of them had horrible diarrhea.
A quick google search brought up Man and Microbes: Disease and Plagues in History and Modern Times, by Arno Karlen which states that

In 1817, when the first cholera pandemic began [...]. In Calcutta and Jessore, cholera killed 5,000 British soldiers within weeks

However, those who survived would get used to it eventually. Cholera is much more serious than simple dysentery of course but its main symptom is also diarrhea.
The locals of wherever you happen to be are used to the pathogens that are common in the drinking water. If I am not from a place and drink water with new pathogens, I will be sick. I will also, however, eventually get over it and my body will be used to them. Depending on the details, either because I have developed an immunity or because I have developed the necessary intestinal fauna to deal with it.
So while the intestinal fauna may indeed have changed over time, this has absolutely nothing to do with what you're asking. First because your assumption is wrong (the British were subjected to the same health issues as modern Europeans visiting Asia) and second because people adapt.

terdon, do you have any reference proving your statement "the British were subjected to the same health issues as modern Europeans visiting Asia"? And also - we have had many Indians visiting the company I work for, they have drunk tap water and have eaten everything and they have not caught diarrhea!


text:
What is the physiological difference between cortisone and cortisol?
There is only hydrogen bond different.
Cortisol is synthesized by our body, while cortisone is given to the patient.
Why you cannot give cortisol directly to the patient?
I think the reason is metabolism that cortisol will break (probably in liver) and not be useful.
Or expansive to produce.
Cortisone however can be given.
What is the physiological difference between cortisone and cortisol?

Cortisol is directly given to the patient - it is then called Hydrocortisone. I don't know why this is done but probably to avoid confusion because both names are too similar.
The difference between both forms is one hydrogen atom at the C11 position of the molecule in Cortisol (or Hydrocortison) (image from here):

Otherwise is Cortisol (or Hydrocortisone) the active version, while Cortisone isn't very active in the human body.
Both forms can enzymatically turned into the other form (from active to inactive and vice versa). Since Cortisone needs to be activated in the liver, it can only be used for oral uptake. Most of the uses which are colloquially called Cortisone in fact contain Hydrocortisone.