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How are at home fermentations without starter cultures controlled?
When making fermented food at home, particularly those that are made without the addition of a starter culture, how does one ensure that the correct types of bacteria are carrying out the fermentation? Is this generally due to the properties of the food that is fermented?

can you give an example?

@MattDMo I think a traditional kimchi preparation is a good example. You've added no bacteria of your own except for what you obtain preparing the dish from its ingredients, and then you seal it and let it ferment at room temperature. I think in this case the acidity is what keeps the food pathogens from growing.

A "starter culture" is just a culture of preferred organisms. They probably differ little from local wild organisms. For example, a mixture of flour and water left to stand will (with luck) be colonized by yeast in the air that result in a serviceable yeast culture. Control of this process entails nothing more than observation over time. The environment and nature of the medium suffice to control the bugs that colonize it.
Both the Korean and Chinese versions of kimchee depend on moisture and acidity (and perhaps salinity) to inhibit unwanted molds/bacteria. The process is evidently self-controlled, but I recall seeing a film in which it was said that failure to add salt to the mixture could result in spoilage. Note that in the linked article, the author says cavalierly that one can scrape any mold that forms off the cabbage and continue with the fermentation because mold will not grow in liquid--patently false but probably "true enough" not to affect results.
Aspergillus oryzae colonizes rice, and rice with Aspergillus growth can be subjected to a secondary yeast fermentation that yields sake. The commercial production uses highly-prized starter cultures for both the mold and yeast, but it is possible to substitute other varieties of Aspergillus. For example, one can induce A. niger to grow on a citrus peel, and transfer the colony to rice. The sake that results is fine. But in this case one would want to rule out species of Aspergillus that are associated with toxins. For similar reasons some care is taken in sterilizing containers used to make wine.
In any of these processes there is a possibility of colonization by the wrong flora. The cultures are controlled by the content of the nutrients and climate and observed carefully. Over centuries there have probably been many unfortunate accidents involving unwanted organisms. There is nothing like violent illness to bring the integrity of a process into focus.
In short, the control of home fermentations lies in (1) statistical likelihood that the right organism is present in the environment; (2) the nature of the nutrient and climate; (3) the experience of the person(s) monitoring the process; and (4) luck.

I see. So essentially, conditions are created that likely favour the desired fermanting organisms, and spoilage, if it occurs, might be detected via smelling/looking off, etc.

That seems to generally be true, yes. It's a broad question but I think people acquire a lot of experience and can tell by smelling, tasting, looking. It's probably not infallible.


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What is the difference between a bacterial artificial chromosome (BAC) and a plasmid?
Is it just that a BAC is generally larger and artificially constructed? Or are there any other differences?

https://en.wikipedia.org/wiki/Bacterial_artificial_chromosome, https://en.wikipedia.org/wiki/Plasmid

BACs are a special kind of plasmid, based on E. coli's F-plasmid:

The BAC is based on a plasmid in Escherichia coli that is termed the F (for fertility) plasmid. The F plasmid (or F factor) contains information that makes possible the process called conjugation . In conjugation, two Escherichia coli bacteria can physically connect and an exchange of DNA can occur.
A BAC contains the conjugation promoting genetic information as well as stretch of DNA that is destined for incorporation into the bacterium.

Source
It isn't necessarily larger than a plasmid.

source: Stack Exchange

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

sort: votes


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Acrosomal enzymes and the female reproductive tract
My textbook wrote that the reason why acrosomal enzymes are so securely contained within the sperm (thus needing capacitation to facilitate their release) is to prevent any premature release in the male reproductive tract. If they were released, they would start digesting the male organs. However, wouldn’t this apply in the female reproductive tract too, once capacitation has occurred? Does the female reproductive tract have some sort of protection against this? (I’m assuming that the sperm has been capacitated but has not fertilized the egg yet.)

The acrosome reaction does not take place till the sperm reaches the zone pellucida of the ovum, which causes the acrosome to rupture. Thus the female reproductive tract does not get exposed to the enzymes.
Links:
https://en.wikipedia.org/wiki/Acrosome_reaction

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


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Photoperiodism: Short-Day Plants
My Campbell's Biology textbook discusses photoperiodism of plants and introduces us to short-day and long-day plants. What I don't understand is why short day plants will not flower if they are exposed to a very brief flash of light during the night, even if that brief period + the actual day's length is still less than their critical day length? Or, put more concisely:
Length of Flash + Length of Day < Critical Period    <-- Why does the short-day plant not flower?
The following diagram is from Campbell's and makes no sense to me, because it also seems like a long-day plant which is exposed to a brief period of light during the dark will flower even if that period of brief light + its actual day's length is not greater than its critical period (i.e. it never fulfilled the pre-requisite for flowering).

I think you are looking at other the wrong way around. There is no critical light period, there is a critical dark period. That long-day flower is also a short-night flower. As long as there is never any period of darkness that exceeds the critical dark period, it will flower.
In that second picture at the bottom, exactly that is the case. The dark period is not long enough to prevent the flowering.
And in the bottom example of the first picture, there is no uninterrupted dark period longer than the critical dark period, so the plant never flowers.

What doesn't make sense for me is this: "As long as there is never any period of darkness that exceeds the critical dark period, it will flower." Take a look at part (b) of the diagram and the very bottom scenario. The period of darkness is longer than the critical night period, but the plant is a short-night flower and thus requires a night period that is shorter--not longer--than its critical period. Even with the added flash of light, the yellow bar does not exceed the black bar. Could you please explain that part? That's mostly what confuses me.

The thing to remember is to not add them up. It only counts if it's in one "piece". For those flowers it's not like our sleep, where being awake for 5 minutes between two 4 hour periods still feels like a good night's sleep. For the long day plants, it's only important that no continuous dark period is longer than x hours. Does that help?


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Does modern theory of evolution include modification of physical environment?
Does any branch of modern evolution theories include aspects of evolving organisms modifying the physical environment?
An example from the evolution of life could be early stage introduction of oxygen and carbon dioxide to the atmosphere from single cell bacterial growth, thereby establishing a basis for growth of more complex organisms.
See also somewhat related question: https://physics.stackexchange.com/questions/22771/does-the-universe-follow-a-general-physical-and-computational-principle-of-evolu

Yes, such processes are considered but there is still a lot of work to be done in this field.
Because the question is open-ended I will just define two concepts of interest and let you go through papers if you want to understand how such processes are modelled.
Niche Construction
Niche construction is the process in which an organism alters its own environment. Sometimes, niche construction takes a broad definition and it then refers more globally to any environment change that is induced by an organism regardless of whether the individual/lineage experiencing the environment is the same one than the one causing the modification. Under this broad definition, niche construction has the meaning as ecological engineering to my understanding.
Some obvious examples are bird nests, beaver's dam and humans's houses. The process of niche construction gets really interesting when the niche is inherited by future generations.
Ecosystem engineering
Ecosystem engineering is the process in which an organism alters the its environment and the environment of other lineages/species. Ecological facilitation is one class of examples.
Ecosystem engineering vs Niche Construction
To my understanding, the term niche construction is more often used in the evolutionary ecology literature, while the term ecosystem engineering is more often used in the ecology literature. Note again that (in my understanding) niche construction in its broad sense takes the same definition as ecosystem engineering but not in its narrow sense.
Models of niche construction in evolutionary biology
There are a number of models of niche construction in evolutionary biology. I am not expert in this field and am not able to make a good summary (would take a while even for an expert anyway). Here are a few papers (that I haven't fully read) that you may want to consider

Niche construction - Odling-Smee et al. 1996
The evolutionary consequences of niche construction: a theoretical investigation using two-locus theory - Laland et al. 1996
Evolutionary consequences of niche construction and their implications for ecology - Laland et al. 1998
Macroevolution of ecosystem engineering, niche construction and diversity - Erwin 2008

Note that depending on your level of understanding of evolutionary biology, these papers may be a bit complicated to fully understand.


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What is the actual function of HDLs and CETP?
I know that HDLs collect cholesterol from peripheral tissues and transport it back to the liver using SRB1 - Reverse cholesterol transport and dumping it in bile. So the tissue is producing some extra cholesterol (why would it? apart from some atherosclerotic condition) and our HDL gets it back to the liver.
This is a bit fine. But then there is CETP which is giving back the cholesterol to VLDLs.
So is it not confusing that our HDL took the excess cholesterol from the tissues only to give it back via VLDL?
So my questions -
Q1 - Why would a tissue have extra cholesterol?(when excellent feedback mechanisms exist - eg. SREBP SCAP INSIG path). Does the HDL pathway make sense only when there is some atherosclerosis?
Q2. Reverse Cholesterol transport refers to the SRB1 part only or SRB1 + CETP combined?
Q3. What is the rationale behind handing over the cholesterol back to VLDLs by CETPs? I know that considerable LDLs get back to the liver too but isnt just SRB1 pathway just fine? Why is it so important to equilibriate your lipid content across lipoproteins? I understand this is the mechanism how torectrapib works but presence of CETP in the body signifies that it must have some ulterior motive, right?
please help :)

this question has a VERY large focus - you probably could have posted each of the 3 subquestions as individual posts... might be hard to get someone to tackle the whole thing - but I bet eventually someone will

Split it into 3 questions :) Do you know of any other forum which caters to medical students' doubts? Just asking.. What to do of questions which don't find an answer!


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HIV and open reading frames
In Wilk et al. 2001 I saw that HIV has 3 open reading frames. In the Watts et al. 2009, I noticed they mentioned HIV has 9 open reading frames. I don't understand this very well.
e.g.

[ATG] GAT GTA AGT
A[TG G]AT GTA AGT
AT[G GA]T GTA AGT

Could anyone explain this to me?

Can you please link to the two articles you mention?

An open reading frame in this sense can, and in this case indeed it does, refer to transcribed regions.

Three: http://jvi.asm.org/content/75/2/759.full

Nine: http://www.nature.com/nature/journal/v460/n7256/full/nature08237.html


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Enzymes and plasmids
A high school class has analyzed plasmids by the help of restriction enzymes and electrophoresis.
The class got delivered two different plasmids, pBR 322 and pC 508. These two plasmids were going to be clipped by EcoR I and Hind III.
Figure 1 shows the two plasmids with specification of the two cutting points for EcoR I and Hind III.
Furthermore, the cutting points are also shown for the enzyme Pst I.
In figure 2 you can see the result of the restriction analysis.

Questions:
1) Analyze and explain the results in figure 2
2)  What DNA-pieces would be formed if you had clipped with Pst I ?
1) You can see that the figure is showing the result of the restriction-analyzis. As for the plasmid pBR 322, you see that the result of the cutting of Hind III and EcoR I, is that both enzymes have the same size. Figure one shows that Hind III cuts over 0 bases and EcoR I cuts at 0 bases.
In pC508 you see that both enzymes have cut two times. EcoR I have cut at 1200 and 5800 bases, which you can see on figure 1. You can see the result of this in figure 2 (the gel electrophoresis). Hind III cuts at 6400 and 1200 bases, which again is an explanation as why the DNA-molecyles (figure 2) have different size.
2) If Pst I was used instead on the plasmid pBR 322, you would get the same size as Eco and Hind, because they all cut one place. If you had cut in pC508 you would get the bases 4800 and 6700 (as figure 1 shows)
Are these questions correctly answered?

Your estimation of the sizes of the fragments for pC508 are incorrect.
Look at the size of the plasmid at the center of the circle.The size of your fragments has to add up to that number. So if you were sure that one fragment was 1000bp, then the other fragment would need to be 6300bp.
You should also notice that fragment sizes for EcoR1 and HindIII digests should not be the same size.
You also need to say something about the type of DNA you have in the pBR322 lanes. Is it linear, circular, supercoiled?
For question 2, your explanation for pBR322 is okay, you should still mention the type of DNA you have in those lanes.
You need to explain not only where PSTI cut but also the size of the fragments that it produces.
A place where a restriction enzyme cuts is called the restrictions site, so instead of saying cuts in one place, or two places, you should say at a single restriction site, etc.

Thank you, but what do you mean by:
"You should also notice that fragment sizes for EcoR1 and HindIII digests should not be the same size.
"You also need to say something about the type of DNA you have in the pBR322 lanes. Is it linear, circular, supercoiled?"
As for 2) its obviously circular? but, maybe i dont understand what you mean?

Do the math to figure out the length of each fragment. Also look carefully at your Gel for pC508 digestions. Are those fragments the same number of basepairs? As for '2)', really? What have you done to the pBR322 plasmid before loading it onto the Gel, and what does that do to DNA?


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Degree of complementarity
Apologies in advance for asking bit naive question. I have looked up for this concept a lot but didn't find anything.
The wikipedia (I know its not authentic all the time, but I think works well for definitions atleast) page on Complementarity says:

The degree of complementarity between two nucleic acid strands may vary, from complete complementarity (each nucleotide is across from its opposite) to no complementary (each nucleotide is not across from its opposite) and determines the stability of the sequences to be together

This is quite new concept for me and how come we can have basepairing between opposite nucleotides if there isn't 100% complementarity? Any evidences behind it?

This can happen when DNA separates after melting and then reanneals.
You likely will not see this in chromosomal DNA in the cell, but I would assume it can happen to RNA molecules sometimes as they are single stranded and can self-anneal.
Mostly though, we think about this issue when performing PCR or DNA/RNA hybridization assays. Shorter pieces of DNA will be more likely to bind and anneal incorrectly, especially if the DNA is rapidly cooled after it has been melted.
Rapid cooling does not give the DNA time to "test" the different combinations of complementarity and sometimes can get stuck in a place where there is very little complementarity.
You also need to remember that while A-T G-C hydrogen bonding is favored, bases are able hydrogen bond to other bases, it just makes the double stranded molecule less stable.


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Red fox with blue legs
On the Wikipedia I found this photo of a red fox, labeled as being taken at Quesnel Lake, British Columbia:

Why would the fox have blue legs? Is that normal for a Red Fox?

It is black skin and fur. The blue is just a problem with the White Balance of the photograph. Remember the Blue Dress thing on Facebook earlier this year?

I suppose one could expand on @AMR to make an answer.

I find it kind of hard to believe the legs appear blue because of "white balance". The nose and upper part of the legs are black, so it is not like all the black in the photo is appearing blue.

If you look at the top of the nose, it also appears blue. The black parts that are in full light appear blue: it's just a matter of lighting

Original vs. Adjusted

Adobe Camera Raw Temperature Adjustment +30 / Tint Adjustment +3
The fox has black skin and fur. The blue is just a problem with the White Balance of the photograph. See Adjustments made above.
This is similar to the Blue Dress / White Dress Meme this year.

I find it kind of hard to believe the legs appear blue because of "white balance". The nose and upper part of the legs are black, so it is not like all the black in the photo is appearing blue. – Imprisoned Rhesus

The reason the legs look Bluer than the Nose is that the nose is mostly black with no white and the front part is in shadow. The top part, which is reflecting some of the sky appears blue in the original.
The reason the legs look more blue is

They are not in shadow
There is a good amount of white fur mixed in with the black

The white fur will look far bluer when the white balance is off and will trick your eyes into seeing the black as blue.

Anyone know how to edit to place the photos side-by-side?

How to put images side by side. Nice answer btw +1


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Which organs need to have fluid compartments in order to develop properly?
I am a student, slightly struggling with the new concept of fluid compartments. I know that there are two main types of fluid compartment, extra and intracellular fluid. I also read that most organs need to have these fluid compartments (established by cell-cell adhesions within tissues) in order to function and develop properly.
My question is what type of organs require these fluid compartments? Would it be the kidneys and the intestines for example?
thanks

Organs consist of different tissues and cells. To function properly each cell needs intracellular fluid. All cellular processes (energy metabolism, signal transduction) occur in aqueous environment, otherwise the required chemical reactions could not take place. Extracellular fluids provide nutrients to the cells and also information from other cells or organs. It can be divided in three categories:

Interstitial compartment: between tissue cells; provides nutrients and helps the cells to communicate within a tissue or organ.
Intravascular compartment: content of blood vessels; transports nutrients, information and immune cells within the body e.g. from one organ to another.
Transcellular compartment: all spaces in the body where only a small amount of fluid is present, normally between organs.

So all organs need these fluid compartments to function properly. The only organ where this is different is the skeleton. But the bone building cells (Osteoblasts) also need extra and intracellular fluid to build a scaffold of collagen. Only after that, they can fill up the interstitial space with hydroxylapatite.
The kidneys clean up the blood and excrete the waste via the urine which occurs in aqueous environment. The intestinal tract absorbs nutrients which are solved in water. Hence, saliva and gastric juice are produced when you ate something.
So every organ needs fluid compartment to do its job. So does the whole organism to make sure all organs are working together (via blood circulation and nervous system).


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Cellulose - why is it fibrous and not granular?

I was reading a book where it said that the 1 - 4 Glycosidic bond of the Beta Glucose meant that cellulose is fibrous and not granular.
First, what does it mean to be granular and why is not granular unlike Amylose?
Thanks, Dave.

Ive been wrong several times before so take my word with a a heavy "grain" of salt. (pun get it? :D )    But Cellulose is a linear polymer and therefore makes a fiber. I guess the linear in this case implies fiber.   Amylose has a helical structure to it i think. Here is an image i found that shows the difference. http://3.bp.blogspot.com/-WpoQllkgT3M/Ug51lW5oEPI/AAAAAAAACCI/vuJmfjHCk0Q/s1600/3starchcellulose.gif

@RoSiv Thanks a million! Please respond with your answer so I can mark you up and tick you! Good pun too!

Cool I got something right :D
Cellulose is a linear polymer and therefore makes a fiber. I guess the linear in this case implies fiber. Amylose has a helical structure to it i think. Here is an image I found that shows the difference.


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Why would the citrulline content of the watermelon be so high?
Citrulline is a non-proteinogenic amino acid (that is, citrulline is an amino acid that is not coded for in mRNA), and it is an important metabolic intermediate in the Urea Cycle. The Urea Cycle is critical for nitrogen (e.g. ammonia) excretion in humans as well as other mammals.
Citrulline is an interesting amino acid, given its vital function in the Urea Cycle, but also because it has such a high concentration in the watermelon. The name citrulline is actually derived from citrullus vulgaris, which is the Latin word for watermelon.
A notable fact about the watermelon is that the watermelon is the only food known to have such high content of citrulline. There are NO other foods that have such high endogenous levels of this amino acid.
As a physiologist citrulline is very interesting metabolically, but I wonder why the watermelon would have such a high concentration? Why would that occur? Would high citrulline content offer some type of competitive advantage to the watermelon in terms of out-competing other plants? As biologists, we usually think about things from a teleologic perspective in order to make sense of the world around us. With that perspective, is there a logical reason that citrulline would be so enriched in the watermelon? It seems very odd that it would be the only plant with notable quantities.

I am just a novice undergrad in biology and am a poor student and probably way off base. My chemistry is also really bad. But I read via the wikipedia page that citrulline is a " precursor to producing nitric oxide". I feel like i am using "ad hoc" logic but i also read Nitric Oxide can be responsible for retaining water (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC116475/) and for disease prevention via cell death (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1810256/). Sorry if im way off base, but I always try and make an effort to answer questions, even if I am lost myself.

@RoSiv, you may not have been that far off, though I think it is likely related to seed development and germination. Google Scholar for Seed Development and Citrulline and Seed Development and Nitric Oxide. I would check Cantaloupe and Cucumbers, things that maintain their seeds in the pulp of the fruit.

@AMR I like your thinking along with Ro Siv, but unlike watermelon - cantaloupe and cucumbers have very little citrulline... I'm trying to understand why watermelon in particular would have such high concentrations of citrulline compared to all the other known fruits/veggies - seems strange but there must be some type of reason

One of the things I saw was that it was concentrated in the rind. Look to see if watermelon has homologs to PADI4... Maybe it has Multiple gene duplications that are all active... or check its overall arginine distribution in its genome... Maybe its reading frames code for an inordinate amount of arginine when compared to other plants.

Asking why things happen evolutionary is a bit misleading. One can guess pretty well (for example, skunk cabbage being thermogenic gives it a distinct advantage as it flowers when few other plants can compete for pollinating insects) but the answer, ultimately, is that for some reason, this is how it came to be. May be as simple as an accidental duplication of a particular gene, whatever. But "why" is in this case probably only a guess in an evolutionary perspective.

@anongoodnurse I agree with what you are saying - I come from a medical/mammalian background and citrulline is very interesting from a scientific perspective... I posted the question and tagged it with "botany" to see if anyone with plant expertise might be able to rationalize an explanation for what all that citrulline might be doing - it seems odd that only watermelon has that high of a citrulline content. It might just be one of those biological mysteries - but I wanted to see if anyone might have some good ideas. I think this is a great forum for asking and can't find an explanation for it

Good question. I don't know the answer, but there are several examples of specific amino acids accumulating in certain tissues also in animals. One hypothesis is that is it advantageous for specific cells to specialize in storing one amino acid (as opposed to all cells storing all of them) because a high intracellular amino acid concentration can shift equilibria of related reactions and thus interfere with metabolism. For example, it might be advantageous to store citrulline in a tissue that does not have urea cycle activity.

Also, keep in mind that present-day watermelons are not evolved in nature, but bred by humans.  So observed traits might not be advantageous to the melon, but to us.  Maybe high citrulline makes for tasty melons  ;-)

I can see a pretty outlined role for citrulline in nitrogen metabolism. A couple articles that caught my eye may point toward a role for citrulline in the rind that pulls toxins out of the flesh: l-Citrulline: An active corrosion inhibitor component of watermelon rind extract for mild steel in HCl medium, and A fixed bed column study for the removal of Pb2+ ions by watermelon rind.

@Roland I happened to run across the answer to this question according to some molecular botanists  (and will post). Just happened to run across it by chance while doing some other work for a book chapter - you were exactly correct! The reason for high citrulline is an "evolutionary hold-over" from wild watermelons that isn't really needed in our agricultural society nowadays.

According to molecular botanists and plant physiologists, watermelon is the only plant that is known to contain significant amounts of citrulline. Interestingly, it appears that the reason for this tremendous enrichment in citrulline stems from the environment in which wild watermelons naturally thrived hundreds of years ago prior to the development of agriculture.
According to botanists, drought is one of the most severe stresses to which a plant can be exposed. Drought generates a high level of free radicals and oxidative stress, in part because plants maintain their photosynthetic machinery even in the face of severe drought. A number of investigators have shown that different plants have unique molecular mechanisms/systems to allow them to tolerate such harsh conditions and oxidative stress.
Wild watermelon plants inhabit the Kalahari Desert in Botswana, where the annual rainfall is less than 2 cm. Despite the minimal rainfall, the watermelon (a xerophyte) can tolerate the extreme conditions well with an exceedingly high drought tolerance. Surprisingly, this tolerance to intense drought conditions by watermelon plants even persists despite a sub-optimally developed root system. In the case of the watermelon, citrulline is overproduced in the leaves (and apparently the rest of the plant) and citrulline acts as the major hydroxy radical scavenger that allows wild watermelon to tolerate the drought-induced oxidative stress. From this same source (Annals of Botany - link below), there are also other proteins that may also be involved in these mechanisms as well. Even though the citrulline content is predominately used in the leaves to buffer oxidative stress, it appears that it secondarily accumulates in the melon itself.
Note: The image below is from Annals of Botany paper in the links below - it is OPEN ACCESS, which is why I posted the picture and included the reference link. You can clearly see the before and after pictures of drought and how the watermelon leaves appear minimally changed, unlike the radish and cucumber leaves.

See below for some interesting Papers about citrulline, watermelon, and mechanisms of drought-resistance:
Ann Bot. 2002 Jun;89 Spec No:825-32.
Citrulline and DRIP-1 protein (ArgE homologue) in drought tolerance of wild watermelon.
FEBS Lett. 2001 Nov 23;508(3):438-42.
Citrulline, a novel compatible solute in drought-tolerant wild watermelon leaves, is an efficient hydroxyl radical scavenger.

It seems to me that this is a teleological explanation for "why" ("because it suited it's growth in certain regions") as opposed to an objective reason ("because it contains multiple copies of a certain gene for the [etc.] found in plants originating in x region."). I dunno, maybe not. Maybe just me.

@anongoodnurse agreed, teleologic indeed - not my area of expertise but i happened to run across it working on a book chapter (go figure) - I would love someone with a plant background to answer who might have more insight

http://www.watermelon.org/Contact Maybe they will be able to give you the contact of a botanist that studies the plant in detail... One interesting fact I didn't know is that the rind is edible as well, and that is where most all of the citrulline is found.

Also it also appears that the citruilline pathway uses Ornithine instead of Arginine as the human pathway does. But there only appeared to be a single Ornithine cyclodeaminase gene. http://www.icugi.org/cgi-bin/ICuGI/genome/search.cgi

@AMR heard back from watermelon.org... actually send me some scientific studies about the benefits of citrulline, but no idea about why it is enriched in watermelon - FYI


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How can hyperthyroidism induce osteoporosis?
It says in my physiology notes that hyperthyroidism can cause osteoporosis.
I've been trying to figure out how this could be possible for a little more than an hour now. Every article that I look at seem to agree with the fact, but I can't find the explanation as to why it is that way.
In MarieB, it says T3 and T4 favor bone growth. Calcitonine also favors bone formation.
How can.... too much of an hormone that favors bone growth, cause bone resorption?

T3 stimulates osteoclast formation. Osteoclasts are cells that break down bone tissue. They are essential for bone growth in children, because they allow bone remodelling. However, elevated stimulation of osteoclast formation leads to osteoporosis in adults, where bone remodelling is not necessary.
In hyperthyrodism, T3 levels positively correlate with levels of calcium ions in blood, which confirms the break down of bone tissue. Calcium ions are then excreted in urine, because they cannot be efficiently reabsorbed. This constant loss of bone tissue cannot be reduced with high calcium diet, only by drug treatments that affect T3 levels.
Definitely can recommend further reading, especially regarding different types of thyrodism:
DOI: 10.1002/jcp.20041


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Why does it take many sperm for one sperm to fertilize an egg?

Hundreds of acrosomes must undergo exocytosis to digest holes in the zona pellucida. This is one case that does not bear out the adage, “The early bird catches the worm.” A sperm that comes along later, after hundreds of sperm have undergone acrosomal reactions to expose the oocyte membrane, is in the best position to be the fertilizing sperm.

—Human Anatomy and Physiology, 9th edition (Marieb)
I’m having trouble understanding why this would be the case—the last sentence, that is. Perhaps it does take a lot of sperm to break through the zona pellucida, but why would any sperm that comes after have an advantage? Do the sperm cells die after the acrosomal reaction? If not, can’t the first few sperm cells be the ones in best position to attach to the oocyte’s receptors once the zona pellucida has been penetrated with the help of other acrosomes from other sperm?
Moreover, are the acrosomal enzymes degraded? Why would there be a need to have so many acrosomes if the enzymes can continue working through the zona pellucida? All you would need is time and soon the zona pellucida would be broken down, even just by a low number of enzymes, would it not?


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Corpus luteum during the luteal phase and gonadotropins
Does the corpus luteum operate independently of the hypothalamic-hypophyseal-ovarian axis? I know that hCG sustains the corpus luteum in the absence of FSH and LH, but in an ovarian cycle where there is no pregnancy, do FSH and LH affect the corpus luteum? It seems to produce a lot of estrogens and progesterone even when FSH and LH levels are low.
(Online I saw that the corpus luteum degenerates because of low FSH and LH levels. Is this true? Why doesn’t the corpus luteum degenerate immediately after the LH surge, then, whereafter FSH and LH levels are so low? If not, then why does the corpus luteum degenerate?)

http://biology.stackexchange.com/questions/43937/how-only-one-follicle-develops-into-graffian-follicle

Lots of questions, so I'll break them down one at a time:

Does the corpus luteum operate independently of the hypothalamic-hypophyseal-ovarian axis?

The corpus luteum does depend on intact pituitary signalling.  Hypophysectomy at the beginning of lutenization will result in cessation of corpus luteal growth and subsequent drop in progesterone; in essence, the corpus luteum won't grow and function properly in the absence of pituitary hormones.  In some species, estradiol is needed, so intact gonadal steroidogenesis is also required.

In an ovarian cycle where there is no pregnancy, do FSH and LH affect the corpus luteum?

Elaborating on the above, yes pulsatile secretion of LH is required to fully develop and maintain the corpus luteum (not so much for FSH).  Other pituitary hormones, such as growth hormone are also involved.  In pregnancy (or pharmacologically), a large dose of hCG can sustain the corpus luteum.  hCG and LH are homologous.  Depending on the species, prolactin and estradiol are also required.

Is it true that the corpus luteum degenerates because of low FSH and LH levels?

The corpus luteum degenerates (luteolysis) because of prostaglandin produced by the uterus.  In the absence of a uterus (and therefore prostaglandin), luteolysis is delayed.  It is reported that estradiol from the next batch of follicles triggers oxytocin release by the posterior pituitary and subsequent release of prostaglandin and thus is the penultimate cause of luteolysis.

Why doesn’t the corpus luteum degenerate immediately after the LH surge, then, whereafter FSH and LH levels are so low?

As described above, it is not low FSH and LH that cause luteolysis.

If not, then why does the corpus luteum degenerate?

Described above.

Source: http://physrev.physiology.org/content/80/1/1.long


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Why does a fetus drink and urinate into the amniotic fluid?
I was reading this website saying that fetuses urinate into the amniotic fluid. It also mentioned that, because we drink the amniotic fluid, we’ve been drinking our urine for months.
However, why do we produce urine as fetuses? I always believed the placenta was our source of waste removal; then why have fetuses the need for filtering their blood through their own kidneys?
In addition, why would fetuses drink the amniotic fluid? Is there a benefit for doing that?

In utero, the growing little human is getting ready to be an independently functioning individual. While it is everything but that, it must be able to obtain fluids and nutrients through its mother's milk, and that from pretty much the first hour of its life.
To develop proper kidney function, the growing fetus needs to ingest fluids just as it will do post partum. Because a mini bar isn't available, it has to drink whatever is available, i.e., amniotic fluid and indeed, its own urine. Shortly after the kidneys start to produce urine, the fetal swallowing commences.
Amniotic fluid is 98% water and 2% salts and cells from the baby. Until the fetal kidneys start working during month four, amniotic fluid is made by the mother’s body. But after month 4, the fetus starts to make his contribution to the amniotic fluid by urinating into it (Penn Medicine). Production of amniotic fluid is then predominately accomplished by excretion of fetal urine (300 ml/kg fetal weight/day or 600 to 1200 ml/day near term) and the secretion of oral, nasal, tracheal, and pulmonary fluids (60 to 100 ml/kg fetal weight/day). Fetal breathing movements also contribute by efflux of lung fluid into the amniotic fluid. Removal of AF is predominately accomplished by fetal swallowing (200 to 250 ml/kg fetal weight/day) (Underwood et al., 2005).
The water in amniotic fluid originally comes from maternal plasma and passes through the fetal membranes. As the placenta develops, water and solutes from maternal plasma pass across the placenta to the fetus and then to the amniotic fluid (Underwood et al., 2005), see Fig. 1.
Swallowing its own urine is not only not dangerous, it is essential to proper development. A decrease in fetal urine production or excretion can result in a reduced amount of amniotic fluid (oligohydramnios). Oligohydramnios can result in fetal lung deformations (pulmonary hypoplasia) and increased risk of infection.  Fetal mortality rates as high as 80-90% have been reported with oligohydramnios diagnosed in the second trimester (Source: Patient Info).
If the fetus would have to prevent the production of urine in utero, the kidneys would have to remain nonfunctional during development, which would be disastrous once it is born. Renal failure is in fact pretty common in newborns, but can be fatal without proper treatment (Andreoli, 2004).

Fig. 1. After month 4, amniotic fluid is derived from maternal plasma that passes via the placenta, to the fetus and then to the amnionic fluid. Source: Underwood et al., (2005).
References
- Andreoli, Semin Perinatol (2004); 28(2): 112-23)
- Underwood et al., J Perinatol (2005); 25: 341–48

The fetal swallowing exercises the swallowing mechanisms and the fluid absorption paths of the digestive tract, which may be helpful. Note that since the kidneys need to function in utero, if the fluid used by them came only from the placenta, the volume of amniotic fluid would need to continually increase.

@lightweaver Why argue with almost a billion years of evolution; it seems to have gotten us this far.

@Christiaan I am fairly certain that Brian Griffin had a Minibar in utero.... :-)

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Is it possible to isolate cells harboring a specific DNA sequence?
Suppose on cell subpopulation harbours within its genome a specific DNA sequence that do not exist in other cell subpopulations. Is it technically possible to isolate such subpopulation ? and if yes, how ?
Some additional information about the cells. All different subpopulations are B-cells. But only one of these subpopulation harbors a specific DNA sequence. We do not think that this sequence is transcribed, and if so in a very lowly expressed manner. We also know that this sequence is only present in one of the two alleles. The main idea of this experiment is to follow this subpopulation at different time points. As the relative abundance of this subpopulation compared to the whole B-cell population is low, we wanted to isolate them in order to study them (DNA mutation, RNA expresion, etc...)
Thanks

If you can distinguish these cells from other cells somehow, yes, there are possibilities.

The sequence you're trying to find, is it something you're inserting in the organism, and you want to find which have accepted the sequence, or is this an arbitrary sequence?

All the cell subpopulations (say subpop A, B and C) are part of the same cell type (in my case T-cells). And subpop A harbos the specific DNA sequence (~50-100nt long).And the sequence is not something that I insert into the cell.

@NicoBxl Is the sequence in population A transcribed? In my mind, staining for a specific mRNA sequence would be a lot easier than looking for a DNA sequence, especially because of signal amplification. For DNA, there are at most 2 sequences per cell (assuming the cell is homozygous), while there could theoretically be tens to hundreds to thousands of mRNA copies per cell. Please [edit] your question and include as much detail as possible about your cells and the sequence you're trying to detect (obviously, you can anonymize specific genes or whatever if necessary).

I can't think of any such technique off hand. Would it be more convenient in your case to genetically engineer the cells to include that specific DNA sequence instead?

@MarchHo No it's not possible as we have mutliple in-vivo samples (differents time points). We do not want to have an artifical scenario (even if might be a interesting idea to dig into)

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0113549 here's an interesting technique

The only technique I can think of off the top of my head is FISH.


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Values of Miu_max and Ks from parameter estimation?
Background
I have this simple biomass growth model:
$$
\mu = \mu_{max}\cdot \left(\frac{S}{K_S+S}\right) \cdot \left(\frac{1}{1+S/K_{iS}}\right) \cdot \left(\frac{K_{iP}}{K_{iP}+P}\right) \\
\frac{dX}{dt} = \mu \cdot X \\
\frac{dS}{dt} = -1 \cdot ( \frac{\mu}{Y_{XS}} \cdot X + mS \cdot X) \\
\frac{dP}{dt} = a \cdot \frac{dX}{dt} + b \cdot X$$
Problem
I can fit the model on experimental data (see the Figure), but the values of $\mu_{max}$ or $K_S$ are often quite unrealistic. In this plot the $\mu_{max}$ is 3.9 and $K_S$ is 10.

Question
Since $\mu_{max}$ and $K_S$ are bounded in Monod-based $\mu$ expressions, is it possible to get real values of both of these particular parameters through parameter estimation techniques? Or one of these parameters should be obtained by other methods?

If you are getting unrealistic values in your model fitting then something is missing or wrong in your model or assumptions. That's the beauty of mathematical models, when they fail, they tell you something is missing :) Plus I don't know why do you think those are unrealistic ?

Can you give some more details on how you fit the model?  A nls fit tends to create strong correlation between the fit parameters. A fit using heuristic rules of thumb can be sensitive to a few points.

@Dexter : the biology professor I'm working for tells that $\mu_{max}$ can be no higher than 0.7 or 0.8. According to that, Ks=10 might be ok, but $\mu_{max}$ so high can never be ok.

@Hans : I use summed RMSE from multiple experiments with different initial substrate concentration. The values are estimated for 8 parameters (miu_max, Yxs, mS, Ks, Kis, Kip, a, b), so they fit fairly well with all experiments. The parameter estimation is done by a global optimization algorithm Differential Evolution from SciPy. I have also set bounds for the parameter values according to the literature. The problem is only with values of $\mu_{max}$ and Ks. When I increase boundaries for them, they both tend to increase until one of them has reached the defined ceiling.

@MartinsM My experience fitting time series tends to yield highly correlated parameters.  You might look at the joint distribution of the $K_S$ and $\mu_{max}$ fits (that is a plot of the objective function for z, and the two parameters for x and y).  It is possible they fit for a realistic pair, but the best fit is when both are way off.


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Microbiology- Pseudomonas aeruginosa, BSAC data
I tested Pseudomonas aeruginosaagainst various antibiotics, using Stokes and Kirby-Bauer. When I compared my results with BSAC data it was completely different (understandable) but why for a lot of the antibiotics did BSAC state 'no information available'?


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Why Isn't mineral transport in xylem multi-directional?
According to our textbook, Xylem transport is only unidirectional while transport through phloem is multi-directional.
But minerals are taken up by xylem from the surrounding tissues actively, and even though they flow along with the water column, they are actively unloaded near 'sink' sites. Sometimes, minerals are also taken up from aging parts and transported to growing areas of the plant. Then shouldn't mineral transport through xylem be multi directional?
Please Explain

Physics: movement from high concentration (soil/roots) to low concentration (air/stomata) + surface tension properties of water and capillary action...

Movement through the xylem is powered by transpiration of water through stomata in leaves and a sustained tension in the xylem itself due to water's cohesive properties.  See: https://en.wikipedia.org/wiki/Xylem#Cohesion-tension_theory
The "multi-directional" transport you are talking about does not actually occur in the xylem.  Minerals have to be transported OUT of the xylem before they can move other ways.  Transport THROUGH the xylem is uni-directional; transport OUTSIDE of the xylem can be multi-directional.

Movement of water through the xylem is caused by root pressure, capillary action and mainly via transpirational pull. All these factors results in a net upward movement of water molecules through the xylem vessel.
In the phloem, movement is multidirectional because of the presence of companion cells. These companion cells have many mitochondria that can carry out aerobic respiration to provide sufficient energy for active transport of substances in the desired direction.
The xylem vessel has no protoplasm, hence water cannot move due to active transport — hence it can only go upwards.

the movement is not multi-directional because the minerals that are transported in the xylem vessel do not need to go anywhere else apart from going up the plant for the leaves to use them this includes the water carried by them.All the leaves are in one direction (which is up the plant)therefore there is no need for the vessels to have a lot of directions which would slow down the plants processes are rather avoided.

Welcome to the site!  Would you ind adding some references for this, please?

Xylem is just an array of emptied dead cells with no inherent directional structure. It will/would pass fluid equally well in either direction. Likewise, phloem is also just a series of tubes, but live ones that are sustained by an adjacent cell. It can and does pass fluids in either direction.
Functionally, flow in xylem is only in one direction primarily because roots are at one end of the tree and evaporation/transpiration is at the other. Water also gets unloaded throughout the tree by osmosis. Tracking the detailed osmotic flow might show water and minerals moving downward locally, there is no significance to this (largely academic) exception.
Functionally, the phloem is actively loaded with the products of photosynthesis. Consequent osmosis generates pressure in the phloem that affects transport away from the source leaf. Importantly, it is via this pressure that nutrients and signalling molecules are supplied to the apical meristem. This is how a new shoot is nourished to grow from buds. This is how flowers are produced. After a new shoot has extended, new foliage will load the associated phloem and 'stuff' will flow the opposite direction. Hence, the phloem is emphasized to be multi-directional.


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How does paracetamol work?
Hinz et al. 2008 found that COX-2 may be inhibited by paracetamol, and this is attributed to it's analgesic and antipyretic properties. However, there are other more recent claims from Andersson et al., 2011 that a toxic intermediate metabolite, NAPQI, may be acting on TRPA1-receptors in the spinal cord. Whilst I'm vaguely aware that the end goal is to affect prostaglandins, to me at least it remains unclear how that translates to painkilling.
There are also other theories I would imagine.
This exceedingly common drug seems shrouded in mystery. I know very little about pharmacology (evidently!), so some expert insight into the popular theories, and why they're popular, would be greatly appreciated.

What are the most popular theories in a nutshell?

Why are they a popular theory?
Which protein is targeted?
How does that inhibition introduce the analgesic and antipyretic properties?

Is it possible multiple theories are correct?
Why is so little known about paracetamol? Is it exceptionally difficult, or the norm in pharmaceutical research of relatively old effective drugs? If it ain't broken, why fix it!

The modern pharmacology of paracetamol: therapeutic actions,
mechanism of action, metabolism, toxicity and recent
pharmacological findings.--
Supra-spinal FAAH is required for the analgesic action of paracetamol in an inflammatory context.--
TRPA1 mediates the hypothermic action of acetaminophen..--
I think these are some good articles, but they may have paywalls.

@Kendall , not to forget placebo effect of paracetamol like this.

@Dexter Fascinating! I imagined there would be placebo to an extent with the pain. I wonder if there are any inflammation placebo affects from paracetamol.

That's possible. Need to search a bit.

Maybe this is why you can't get a satisfactory answer. "Paracetamol (acetaminophen) works through known mechanisms...Although it is widely used, there are only hints as to how it and other common drugs actually work." -The science myths that will not die: Nature News & Comments

What are the most popular theories in a nutshell?

To date, the mechanism of action of paracetamol is not fully understood. There are some experimental evidences, but it is difficult to put things togheter. It is now clear that  paracetamol acts contemporaneously via at least three pathways:

The inhibition of cyclo-oxigenase (COX)

The main mechanism proposed is the inhibition of COX, it's highly selective for COX-2.
COX are molecules involved in the metabolism of arachidonic acid (aa). It catalyzes the reaction to form prostaglandin H2, a pro-inflammatory compound, from aa.
Paracetamol, as other NSAIDs,  block this step , thus reduce the amount of prostaglandin H2. The reduced amount of prostaglandin H2 in the CNS, lowers the hypothalamic set-point in the thermoregulatory centre.
The exact mechanisms by which COX is inhibited in various circumstances are still a subject of discussion.
Some authors state that paracetamol works by inhibiting the COX-3 isoform—a COX-1 splice variant—of the COX family of enzymes.
This variant is expressed mostly in brain, so it is the one supposed to be involved in the antalgic effect of this compound.
There is another physiopathologic possibility to explain its action, that is: paracetamol would block COX, but in an inflammatory environment where the concentration of peroxides is high, paracetamol itself is oxydated and thus inactive. When it founds a non inflammatory environment, such as CNS, it become reduced and thus active (it reduces temperature, it has anti-dolorific action, etc).

The modulation of the endogenous cannabinoid system, through its metabolite AM404, a compound that inhibits the reuptake of the endogenous cannabinoid/vanilloid anandamide by neurons.

The COX model can explain quite well the action of paracetamol, altought it has been demonstrated an important role of the endocannabinoid system aside of COX. When cannabinoid receptors are blocked with synthetic antagonists, paracetamol's analgesic effects are prevented.  This is tought to be due by an active metabolite of paracetamol, that is called AM404 and inhibits the reuptake of anandamide.
Anandamide reuptake lowers synaptic levels of anandamide. This results in a more activated pain receptor (at least the main one, called TRPV1, or according to an old nomenclature: vanilloid receptor). The high levels of anandamine, due to inhibition of its reuptake, desensitise this receptor in a way similar to the capsaicine.
Furthermore, this active metabolite (AM404) inhibits sodium channels, this chemical behaviour is shared with lidocaine and procaine, two common anesthetic drugs.
These two actions by themselves have been shown to reduce pain, and are a possible explanation of paracetamol's mechanism of action; but one other specific activity of this compound remains unexplained by these two models.

Serotonin receptor agonism.

It has been observed that this compound can reduce the social rejection in humans. This can't be explained with COX or type I endocannabinoid system modulation.
Increase of social behavior in mice dosed with paracetamol, wich models a reduction of social rejection response in humansdoes not appear to be due to cannabinoid receptor type 1 activity. .
In the animal model, it seems a result from  serotonin receptor agonism.

Aside of this main features, some other evidences are in bibliography.

In 2011 a debate started on scientific journals. Some has found  a hint to the analgesic mechanism of paracetamol, being that the metabolites of paracetamol e.g. NAPQI, act on TRPA1-receptors in the spinal cord to suppress the signal transduction from the superficial layers of the dorsal horn, to alleviate pain.
This findings has been contested in a  new hypothesis paper  on how paracetamol might act.
This second study concedes that NAPQI is the active metabolite but that this reactive compound should react not only with the thiol in TRPA1 but also with any other suitably available nucleophile that it happens to encounter. This broad interaction with thiol groups in cysteine proteases, like the ones that process  procytokines, might be the targets giving rise to overall analgesic effects, changing the global cytokyne environment.
Even if there are evidences of drug-body interaction with formation of active metabolites and there are some models of drug action, many things are not fully cleared and the debate is still open.

Why are they a popular theory?

Are popular because are based on experimental and clinical evidence. Also, this theories can model lot of the biological effects of this compound.

Which protein is targeted?

Not any time it can be possible to reduce a pharmacological interaction at this level. For instance, in one theory it inhibits an enzyme, the cyclooxygenase (COX); in one other model entire classes of molecules, the sodium channels, are modulated...
Unfortunately many times, dealing with living organisms, it is not possible  to offer an hard, mechanicistic explanation of things.

How does that inhibition introduce the analgesic and antipyretic properties?

In the COX inhibition model, the analgesic properties can be explained trough an affinity for COX3; and the antipyretic activity can be due to the reduced amount of prostaglandin E2 in the CNS, in the thermoregulatory centre it lowers the hypothalamic set-point. The endocannabinoid model can explain preety well the anti dolorific actions, as well as the serotonin receptor interaction the behavioral one.

Is it possible multiple theories are correct?

Yes, there is a substantial overlap between different regulatory systems, so that is straight to think that the same chemical (or some of its different active metabolites) can modulate different systems.

Why is so little known about paracetamol? Is it exceptionally difficult, or the norm in pharmaceutical research of relatively old effective drugs? If it ain't broken, why fix it!

Is it not that difficult topic! One can say that is as tricky as any clinical pharmacology topic. The problem is that many compound are clinically used as drugs even if their molecular functionig is unknown if they are safe and of proved usefullness. This is true for paracetamol as well as many other drugs, like a lot of anaesthetic agents as Propofol.

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By what mechanism is NADP+ converted to NADPH in Photosystem I?
Here is my current understanding:
$\mathrm{NADP^{+}}$ takes 2 electrons from Ferredoxin at the end of the electron transport chain to generate $\mathrm{NADP^{-}}$.  An $\mathrm{H^{+}}$ ion in the stroma binds through the extra electron, generating $\mathrm{NADPH}$.  All of this is facilitated by Ferredoxin-$\mathrm{NADP^{+}}$ reductase.
Sources: https://en.wikipedia.org/wiki/Ferredoxin%E2%80%94NADP(%2B)_reductase
http://www.bio.davidson.edu/Courses/Bio111/NADPH.html

Exactly what is your question?

This came off to me as a mechanistic question, I edited the title. I'm unsure why this was closed, though, since some good papers exist to elucidate the FNP mechanism in photosystem I.

OVERVIEW (verbatim from the article)

Plastidic ferredoxin−NADP+ reductases (FNRs) accept electrons
  by two sequential one-electron transfer steps from two
  molecules of the one-electron donor ferredoxin to generate
  their fully reduced hydroquinone state, FNRrd, through the
  formation of an intermediate neutral semiquinone form, FNRsq.
  FNRrd then transfers both electrons as a hydride to the
  nicotinamide adenine dinucleotide phosphate (NADP+
  )
  coenzyme in a single step (Figure 1A).1,2

Theoretical Study of the Mechanism of the Hydride Transfer between Ferredoxin–NADP+ Reductase and NADP+: The Role of Tyr303 (Institutional access will be required!)
Basically, FNR is a flavoprotein with a stabilized FAD prosthetic group that can alternate 3 oxidation states with 0, 1 or 2 electrons. NADP+ binds in the FNR active site, and recognition of the AMP group causes a conformational change that brings the nicotinamide portion in proximity with the isoalloxazine group of the FAD. Ferredoxin is a single-electron carrier where two molecules of ferredoxin sequentially donate electrons to the FAD group that produces a hydroquinone FADH2. The actual architecture of the charge transfer complex formed in the active site mediates the formal hydride transfer that produces NADPH*. As far as I can tell, the hydride transfer occurs while the ferredoxin is still bound due to the effect electron transfer to FAD has on the pKa and protonation of a Glu312 that stabilizes NADP+ too much in the absence of ferredoxin (source).
NADPH ends up getting released after the catalytic cycle.
*I'm still trying to find some more detailed information on the catalytic mechanism.


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Reason for the source of fetal bovine serum
What is the reason that perhaps the most commonly used serum in labs is fetal bovine derived? Is there something about fetal serum that is particularly useful over say serum just harvested periodically from adult cows, or cows going to slaughter?

As a cattle farmer, I can contribute a little to why FBS is so expensive at least. Slaughterhouses HATE receiving pregnant cattle, so they go out of their way to not buy them. Therefore stockyards avoid buying them as well, and will send a cow back to the rancher if they determine it's pregnant. This means that the number of bovine fetuses that evade detection and make it to the slaughterhouse for processing is small, which keeps the supply of FBS low and prices high.

The reason fetal bovine serum (FBS) is used is because it supports a wide variety of cells and really supports their growth.  It has a high concentration of growth factors, but also a low concentration of antibodies.  So it promotes growth in almost any cell or tissue type without also having antibody reactions with it.
Adult cows blood will have the opposite concentrations, higher levels of antibodies and lower levels of growth factors as they have already grown.
There are currently several research projects looking for a alternative or synthetic FBS, but nothing has worked as a total replacement.  There are a few substitutes for specific purposes, but nothing with the diversity of uses that FBS has.


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In terms of ecology what is optimality?
I am studying animal science and I have been learning about reproductive theories however i cant seem to understand the theory of optimality

Can you give more context to your question?  In biology, most references to optimality mean passing on your genes more successfully than others.  However many proxies for this exist, such as gaining food, or investing energy in offspring.  Usually these proxies are optimal in the context of a model which assumes some connection to the general problem of passing on your genes.

What type of optimality are you referring to, i.e. what is optimalized? Fitness, energy use, foraging, life-history trade-offs etc?

Optimality theory
Optimality theory is a concept of linguistic. See wiki > Optimality theory. This is probably not what you were referring to.
What is optimality
Optimality is the condition under which something is maximized! In behavioural ecology, this something is often fitness and the condition is often measured in terms of magnitude/intensity of a behaviour.
Optimality models
In ecology, we call optimality model any model that separate the benefits and costs (in terms of some measurement, often fitness) of a given phenotype (often behaviour). By weighing benefits and costs one can figure out what is the optimal phenotype. The principle is extremely simple. Such graphs are quite standard:

In the graph, the X-axis represents the magnitude of a phenotype (often a behaviour) and the Y-axis represents the benefit and cost of this behaviour (with the same scale) often in terms of fitness.
By definition, the fitness is maximized when $B-C$ is maximized. In other words, compute B-C and look for the maximum (through derivation) and you found the optimal phenotype (often behaviour). In the above graph, the optimal phenotype is a little bit left to the position of the B label.
Optimal foraging theory
Foraging behaviour has been subject to much investigations using optimality models. We refer to this body of knowledge as Optimal foraging theory.


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Dreaming after passing out
I'll have few questions about passing out and dreaming. English is not my native language, and my biology knowledge is very limited. So bear with me.

What exactly is blackout? (in a really simple way)
Are there different types of blackout? (see below)
Do fainting, passing out, and blacking out mean the same thing?
Can someone have a dream/vision after loosing consciousness? (during blackout?)

I'm asking these because I had a similar experience and I'm trying to make sense of it.
We were goofing around and a friend of mine had me in an arm triangle. I suspect he choked me, because I lost consciousness for a few seconds, max 3. While in that state, I kind of had a dream or vision, whatever it is called. It felt like hours. This was a long time ago and I still remember the dream, but can't make sense of it. What I've seen was really interesting and I couldn't just let it go.
I'm not asking for dream analysis or anything, but the biological/neurological aspect of what happened, so don't get me wrong.

I'm also new in here, though not to stackexchange, so the tags might need a modification.

Fainting, passing out, and blacking out are all common terms for the same thing, a sudden loss of consciousness of short duration.  The medical term for this is syncope. It is caused by a decrease in blood flow to the brain, limiting the the availability of oxygen and nutrients to the brain cells.  Brain cells have high energy requirements, so this causes them to stop functioning, causing loss of consciousness and muscle tone.
There are many causes of syncope.  In the situation mentioned, a likely possibility is a pressure change in the carotid sinus which is located at the side of the neck. When sensed by a nerve, this can cause primitive parts of the nervous system to change the dilation of blood vessels and the beating of the heart in a manner that brings on syncope.
Dreaming during syncope is not uncommon and that fact may be useful in distinguishing syncope from epileptic seizures according to research by Chiesa et al..


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Development and function of spindle neurons
In his book How to Create a Mind author Ray Kurzweil makes some claims about spindle neurons that he provides no source for.
Concretely he states that spindle cells:

Are Involved in handling emotion and moral judgement;
Are believed to first have occurred in the last common ancestor of chimpanzees and humans;
Are non-existing in newborns, but appear around the age of four months, and increase significantly in number from ages one to three.

Is there a scientific consensus backing these claims?

I fell the common origin of these questions justify bundling them. If not, I apologise for the mistake.

The spindle-shaped brain cells you refer to are called von Economo neurons —named after the man who first described them  (source: Smithsonian).

In humans, von Economo neurons reside only in the anterior cingulate cortex (ACC) and the frontal insula (FI) (Allman et al., 2011). These two regions are particularly active when people experience emotion and they are reportedly important for "self-monitoring," such as noticing bodily sensations of pain and hunger, or recognizing that one has made a mistake. The ACC seems broadly involved in nearly every mental or physical effort (Smithsonian). By contrast, the FI may play a more specific role in generating social emotions such as empathy, social awareness, and self-control (Allman et al., 2011), but also trust, guilt, embarrassment, love, and even the sense of humor Smithsonian).
Humans and the great apes (chimps, bonobos, gorillas and orangutans) have von Economo cells. Lesser primates, such as macaques, lemurs and tarsiers, do not. That means the neurons evolved in a common ancestor of all the great apes about 13 million years ago, after they diverged from other primates but well before the human and chimp lineages diverged about six million years ago (Smithsonian). However, elephants and whales have them too, possibly explaining their complex social behavior (Allman et al., 2011).
I couldn't find literature on the development of these cells in children. Note, however, that, as far as I know, the presence of these cells can be only detected using microscopic techniques, i.e., on coupes of post mortem tissue (e.g., Santos et al., 2010)). This will make research in infants and children difficult.

References
- Allman et al., Ann N Y Acad Sci (2011); 1225: 59–71
- Santos et al., Brain Res (2011); 1380: 206 – 17


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What is the name of this snake?
This baby snake just came inside my house in Sri Lanka, and I'm wondering whether it is venomous. Do you know this snake?

I am posting this from my phone so I am unable to format properly. And I have small children in my house, therefore I am worried about their safety.
Size: < 30 cm (I think it was a baby snake).
Location: Sri Lanka (in southern Asia)

We live in an urban area without any rivers near by.

Could it be the rat snake? http://bio.davidson.edu/herpcons/herps_of_NC/snakes/Elaobs/Ela_obs.html

no it's not a rat snake. At least not the black rat snake you linked to.  These are typically very black and live in the Eastern / Mid-Western portions of the United states

This is non venomous wolf snake.

I'm not an expert by any means, and anyone with proper training could probably provide a more informed opinion, but here's my thoughts. The patterning looks similar to Oligodon taeniolatus, an small, nonvenomous snake found throughout the region:

I'm not entirely sure about this identification, mostly because the pattern on the head looks a bit different. Sri Lanka has a large diversity of snakes and finding an definitive identification might be difficult without better images. There seems to be only a handful of snakes considered deadly, and this doesn't appear to be one of them. However, as I said, I'm not an expert, and even if it's not one of the 'deadly' ones, that doesn't mean it couldn't be dangerous to small children or pets. If you intend to capture and release the snake away from the house, I'd still recommend caution when handling it or contacting a professional.

The color seems similar but I don't think this is the snake, as the one in the picture doesn't have any patterns on it. I tried googling for golden/yellow snakes but couldn't come up with a closer match myself.

The one in the question clearly has patterns on it

The back dotted pattern looks similar, but I agree there doens't seem to be the same head design in the OP's picture. Possible juvenile or indication of sexual dimorphism in this species.

Just to add another option:
My guess (though no more confident than @p.s.w.g's answer)   is Balanophis ceylonensis (Sri Lankan Keelback) or related species.
The two features that stand out to me from your photo are

the dotted markings on the back of the snake, and
the dark line running behind the snake's eye.

You'll notice the keelback in this picture copied  from Fernandoa et al. (2015) has an almost identical skin tone and line running behind the eye.

However, this image does not show the dots.
Though a mature snake is very different colored, you'll notice from this picture that the mature keelback has a very similar spotting design as the snake you've photographed.

IF this is the case, and this is in fact your species, then there is at least one source (Fernandoa et al. 2015) that suggests that the snake is venomous.

This seems to be a good guess also. Here's another image of B. ceylonensis that looks similar the one in the question (here called a Sri Lankan Blossom Krait).

According to my mom (she is not a biologist) this is a rat snake (my question). https://biodiversityofsrilanka.blogspot.com/2013/09/garadiyarat-snake-ptyas-mucosa.html

My answer's coming late but thought it's worth checking out the comment made by Anutapa bhattaharya that it was a wolf snake. I realise he only said it with no references or photos but still, since his name strongly suggests he's from Sri Lanka, I thought I'd see.
I believe he's correct and the snake in the photo is an Indian wolf snake (Lycodon aulicus), a common non-venomous snake that's encountered often enough in houses at night that it's earned the name 'house snake' in Sri Lanka.
I enhanced the first photo shown in Isuru's photo to better make out the markings and believe he's correct. Here are a few photos I found through Google of wolf snakes.

Source

Source

Source

+1 Seems like a pretty close match to me, also.


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What is the Genetic Cause of Homosexuality?
So, I'm just wondering about this because I read the following in my Biology textbook about fruit fly genes:

"Normal male and female flies express distinct forms of the fru gene. When females are genetically manipulated to express the male form of fru, they court other females, performing the role normally played by the male..."

Out of curiosity, have any studies been conducted to see what causes homosexuality? Is there a similar gene in humans that, if randomly altered, causes attraction to same-sex individuals?
EDIT: a similar post exists, but nobody provided an answer related to the poster's question.

The phrasing suggest some misunderstanding of what genetic cause could mean. On this answer I linked a number of posts where I explain the concepts of heritability (which is related to this misunderstanding even if it is not necessarily obvious to you right now).


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How can low cholesterol cause mortality?
I am studying processes 1. stroke, 2. heart disease, and 3. cancer, and their mechanisms associated with low cholesterol which is a result of lowering cholesterol especially in elderly, Low cholesterol is associated with mortality from stroke, heart disease, and cancer: the Jichi Medical School Cohort Study.
Stroke's manifestation is primary intracerebral hemorrhage ICH confirmed by many exclusion articles of other factors such as liver disease).
In the heart disease, there CAD and ischemia.
In the cancer, metastasis.
I started to think what could be enough general for all of these.
In the energy sense, one possibility could be glycogen, since it is used as an acute energy storage in all those organs.
Mechanisms could be the macro/microstructures of storage which are mostly unknown, presenting roughly 80/20 proportions.
So I propose that the lack of energy causes those conditions.
I noticed that many authors use the word remnant cholesterol when speaking about the subject. I did not understand its biophysical meaning.
Remnant cholesterol is an independent factor of cardiovascular manifestations apparently through the larger triglyceride-rich lipoproteins' (TRL) remnant kinetics.
Remnant cholesterol does not seem to cover all aspects of low cholesterol.
How can you low cholesterol cause stroke, heart disease and cancer?

can you please clarify your question above? Especially the very last sentence where it says "how can you low cholesterol cause stroke… "– That doesn't even make any sense. Did you mean to say how can lower cholesterol cause stroke? Or, why would lowering cholesterol cost stroke? I'm not sure what you're talking about (?) Would be happy to take a stab at answering this question if I could understand what you're actually asking.

@VanceLAlbaugh I attached the full title of the publication which says that low cholesterol is associated with mortality from stroke, heart disease and cancer. I think it is not only stroke that is associated with low cholesterol especially with elderly. Yes, you are right that the situation is caused by lowering cholesterol.

Cholesterol provides rigidity to plasma membrane and is also essential for certain cell-signalling pathways.

What you have asked for is a causal answer to correlated findings. There is no cause-effect evidence (at least from my searching) showing low cholesterol will indeed cause stroke. Associations like this are dangerous in the sense that we shouldn't think that one causes the other. But, we can speculate on how they are linked, which is always fun.
I'll be going off my understanding of cholesterol transport and will include the reference at the bottom. Essentially, cholesterol is used in the cell membrane to change the permeability of the membrane. The more cholesterol, the less permeable the membrane is to water. However, this also changes the physical properties of the cell membrane, making it more rigid and structured. If I had to guess (which is again PURE SPECULATION) I would think that decreasing the cholesterol to the point of a dangerous level would increase the cell permeability of vital cells, the most sensitive would be neurons who depend on ion based signaling to perform primary functions. Since ions are very small and easily pass through the membrane if the membrane is leaky, they might be the first indicator that the something is wrong and the membrane isn't strong enough. Again, purely speculative with no evidence. An experiment one could do is examine the amount of cholesterol required in a cell to keep ions from crossing the membrane and see if there are any other effects that occur within or around the cell before ion passing. If you aren't in this type of research yourself, maybe you can fund it!
Source= Cassarett and Doul's Essentials of Toxicology. Textbook, 12th edition

Interesting answer! I need to classify first how cholesterol presents in imaging. And also its subtypes. Do you know any 1D signals which has a high focus about cholesterol?

I had an old professor (Bruce Hammock) that used to do mass spec quantification of lipid concentrations. Check out his papers. Here is also a paper for reference and good measure: http://onlinelibrary.wiley.com/doi/10.1111/j.1742-4658.2009.06869.x/pdf

Is there any raw data about these mass spectrometry results? Some 1D data. I want to characterize it my way.

I'm not sure if there is any out there. Most mass spec data is priority classified due to the specific methodology each person uses. Aka. often most people don't post mass spec stuff because they don't want other people analyzing their data in a different way, thus generating a different result (one of the faults of mass spec). Your best bet is to look at publications and see if they added supplement info (http://www.ncbi.nlm.nih.gov/pubmed/16458590 another ex). Or check the ncbi bioinformatics database


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Mitosis versus Meiosis I: What's the difference?
At the end of mitosis, one cell has divided into two diploid cells. But at the end of meiosis I, there are two haploid cells. How are the two processes different to produce these two types of cells?

At the start, all the cells are 2n, diploid cells. By far the largest difference between meiosis I and mitosis is that mitosis results in genetically identical, diploid somatic cells. Meiosis, in it's entirety, results in gametes of haploid genetic information, but the genetic information is not identical due to crossing-over events that happened during meiosis I.
What you should also note from the figure: Each chromatid represents 1 DNA molecule. In mitosis, the cell will begin with 4 chromosomes and 8 chromatids. After cytokinesis, the somatic cell will have 4 chromatids and 4 chromosomes. This propagates during the next round of mitosis. In meiosis: The cell starts with 8 chromatids and 4 chromosomes. After meiosis I each cell has 4 chromatids and 2 chromosomes. After meiosis II, each cell has 2 chromatids and 2 chromosomes. You're halving the amount of genetic material each round of meiosis, and this can't be propagated indefinitely.

Source: Tortora, GJ (2008). Principles of Anatomy and Physiology. 12th ED.

Where have you found this figure?

@Ana Wiley library system, source link. It's Tortora "Principles of Anatomy and Physiology," 12th ed.

the difference with easy way that the arrangement of chromosome on equatorial plate in metaphase
1- in mitosis all chromosome arrange on equatorial line randomly and single  so when it separate in anaphase separate to chromatide ( all chromatides), and each cell have 2n
however
2- in meiosis 1 chromosome arrange in duple or couples so when it separate as one chromosome , and each cell have n only
i hope it is useful for u

This doesn't make any sense


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How does heat generated by metabolism differ compared with heat generated through exercise?
I am from a mathematical background so I don't have much knowledge on biology. I'm building a mathematical model to predict heat generation with parameters of metabolic heat generation and exercise heat generation.
Metabolic heat generation as far as I understand is the heat produced through body's chemical processes, digestion of food, and elimination of waste.
In this article here, the value for metabolic heat generation is given as 33800$W/m^3$. But the exercise intensities as given here only has values of around $582 W/m^2$.
I think we produce more heat when we exercise than through metabolic activities alone. Is this correct?
If so, why does this huge difference in values of 33800 and 582? Why would the heat generated via exercise be such a low value? (Of course they are not measured in same units.)
Is there any other unit other than $W/m^2$ that measures the heat generated through exercises so that it gives a resonably at least closer value to metabolic heat generation?

I tried to clarify your question and make the text easier to understand...you can change things back if I have unintentionally changed the meaning of your question.

You did notice that the units you listed are different right?  One is W/volume and other is W/area.

@akaDrHouse Yes the units are different. I am asking if there a way to compare the metabolic heat and energy from exercises? metabolic heat per volume is so higher than the exercise heat per surface. Shoudn't exercise generate more heat?

First, you have to convert your numbers to the same units for any comparison to make sense. Consider that the average human body has a surface area of about 1.8m$^2$ and a volume of about 66L = 0.066m$^3$. Then your numbers are equivalent to 2230W metabolic heat and 1050W exercise heat for an average person.
The value 2230W for basal metabolic rate (from Table 1 of the Bagum et al paper) is nowhere near what's measured in practise. Basal metabolic rate ("metabolic equivalent", 1 MET) would be 105W for an average person according to the wikipedia page you cited, which equals 2150 kcal / day. That's about the recommended daily calorie intake, so it makes sense. I don't know where their value of 33,800 W/m$^3$ for "metabolic heat generation" comes from, perhaps it's meant represent something else (can't say I understand the article) but it's not the metabolic rate for an average human tissue.


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Why are oceans said to have "low productivity" in terms of photosynthesis?
80% of the world's photosynthesis takes place in the ocean. Despite this, oceans are also said to have low productivity - they cover 75% of the earth's surface, but out of the annual 170 billion tonnes of dry weight fixed by photosynthesis, they contribute to only 55 billion tonnes. Are not these two facts, which I have come across separately, contradictory? If oceans fix 80% of the total $\ce{CO2}$ fixed by photosynthesis on earth and release 80% of the total $\ce{O2}$ released by photosynthesis on earth, they should have accounted for 80% of the dry weight produced as well. Is there any way to reconcile these facts? In any case, if 80% photosynthesis occurs in oceans, that hardly seems low productivity - then why are oceans said to have low primary productivity (a host of reasons are also given for this - that light is not available at all depths in oceans, etc.)? A large amount of photosynthesis taking place should mean a large productivity!

It'll help if you can provide where you found those two statistics (80% of the world's productivity takes place in the ocean and 55/170 million tonnes of dry weight is produced by the oceans)

Actually both were my [high school level] textbooks. But here is a reference for the 170 billion tonnes figure.

BioNumbers suggests that the 170 and 50 Gt values are roughly correct, as measured by the papers cited.

First, we have to know which are the most important criteria for photosynthesis to occur; these are: light, CO2, water, nutrients.
docenti.unicam.it/tmp/2619.ppt
Second, the productivity, you are talking about, it should be called "primary productivity" and it is calculated, dividing the amount of carbon converted per area (m2) by the time.
ww2.unime.it/snchimambiente/PrPriFattMag.doc
So, thanks to the fact that oceans occupy the larger area of the world, the marine microorganisms can convert lots of inorganic carbon into organic (principle of photosynthesis).
A big problem in the oceans is availability of nutrients; these tend to deposit or react with water or other chemical compounds, even though the marine photosynthetic organisms are essentially found on the surface, where, of course, light is present. This reduces as a consequence the  photosynthetic productivity potential of oceans.

You should provide some references to support your answer.

If oceans fix 80% of the total CO2CO2 fixed by photosynthesis on earth
  and release 80% of the total O2O2 released by photosynthesis on earth,
  they should have accounted for 80% of the dry weight produced as well.

First, what is meant by "O2 released"? Does it mean "O2 released from the oceans into the atmosphere, where it contributes to a growing surplus"? That can't be the case since the amount of O2 in the atmosphere is pretty constant, and there is evidence that it is significantly lower than in Jurassic times.  Overall the global O2 sinks must balance the O2 sources, or if anything must slightly exceed them, resulting in the current gradually increasing atmospheric CO2 levels at the expense of O2 levels.
So by "released" we have to just mean "released by the process of photosynthesis, at the point of its operation".
Oceans fix 80% of the total CO2 fixed by photosynthesis, yes, but they also unfix it at a similar rate. For every algal cell that's photosynthesising, there's one that's dead or dying and being consumed by bacteria (which consume O2), or that's consuming oxygen itself in order to keep its metabolic processes operating at night. So the NET amount of O2 released by the oceans is something close to zero.
Now we have to ask what we mean by "productivity" in this context. If a molecule of CO2 gets fixed due to algal activity but then almost immediately gets unfixed again, does that count as "productivity"? But, blink and you'd miss it! Even if you don't blink, it's hardly likely to be measurable. The dry weight of the algae at the end of the of the process is the same as at the beginning. so if we define "productivity" as "increase in dry weight of algae" then the productivity is zero.
For algal photosynthesis to have an enduring effect on global CO2 or O2 levels, the fixed CO2 has to become incorporated into something less fleeting than algae. Something like cod or hake, which as a bonus can be harvested and placed on tables. "Productivity" usually refers to the power of the oceans to replenish the stocks of these things post-harvest, and that is indeed low when compared to the ability of the land to produce repeated harvests.
It would be a different story if we were to regard algae as potentially suitable for mass harvesting, so that their ability to grow like wildfire in the presence of fertilizer runoffs from the land was regarded as "productivity" rather than as a profound nuisance. But this is not the case.
In other words, we tend to define "productivity" in terms of what is useful to us as a species, and algae are generally not useful.


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gene transformation from plant to plant - transgenic plant
I want to know if the expression of a transfered gene depends on source of the gene, if e.g.:
1] I isolate a gene from plant and transfered it to the same plant?
2] I isolate a gene that is highly expressed in plant, and transfer it to another plant ?
3] I isolate a gene that is lowly expressed in plant and transfered it to another plant
Is there a difference between the expression of the transferred gene in these three cases? What does the expression of the transfered gene depend on?

There are many factors that could influence in the level of expression of a gene, but the two most important are the promoter and the place where your gene has introduce in the genome of de recevier plant.The first one, the promoter depends of the original expression of the original plant, if the expression was high in the original plant, it will be in the receivier plant (if you include the promoter in the construction of the transferred gene and both plant are close in filogenetically).The second one,the place where your gene has introduce in the genome of de recevier plant is a matter of luck, if you use a Agrobacterium, if you gene was introduce in a heterochromatin region it won´t express.
Sorry for my bad english, hope I was useful


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Normal cells and the immune system
Normal or healthy cells have a natural ability to avoid being attacked by the immune system.
 So if a cancer cell has all inherited 'strategies' for avoiding the immune system (that are from their earlier pre-cancerous states) does this make them hard to detect or be affected by the immune system.

In short, the major histocompatibility complex.

This is an important question ; how can I make it less 'broad'?

The development of cancer has various reasons. For example in more than 50% of tumors, p53 is mutated. p53 among other things regulates mitosis and forces the cell to arrest in a specific growth state if other systems detected a mutation in the DNA.
But in your special case we have to look at major histocompatibility complexes (MHCs) and NLRC5. There are two types of MHC, namely MHC class I and class II. MHC II presents mostly bacterial peptides to CD4+ T cells causing a immune response. However, MHC I presents viral peptides and peptides from your own body. These peptides are detected by CD8+ T cells which are cytotoxic T cells initializing apoptosis. Without these own peptides natural killer (NK) cells are activated because of a missing-self signal causing apoptosis, too.

Watson et al. (figure 1, Watson et al., Int.J.Cancer, 2006) showed that patients with high MHC I expression or an absent MHC I expression have a higher survival than patients with low MHC I expression. If patients express high levels of MHC I, the chance that these proteins present cancer peptides is higher than patients expressing low levels of MHC I and therefore cancerous cells get killed by cytotoxic T cells probably more often. Without MHC class I, NK cells will initiate apoptosis and cancerous cells will die, too. Patients with low MHC class I expression won´t present so much peptides to cytotoxic T cells and therefore less cancer peptides are presented. But as they have MHC I, NK cells keep inactive. So the cancer finds an escape mechanism in tricking the immune system.
NLRC5 is the biggest member of the NOD-like receptors (NLRs). Expression of NLRC5 can be enhanced by IFN-gamma which activates the JAK/STAT signaling pathway. STAT 1 enhances the expression of NLRC5 and NLRC5 itself can build an enhanceosome with RFX. This enhanceosome raises the expression of MHC class I! NLRC5 is often mutated for example in colorectal cancer. Research now has to focus on how to enhance NLRC5 and therefore MHC class I expression in different cancer types and out of these results to develop an efficient cancer treatment.
I hope that I could help you. Further literature especially on NLRC5 you can find in following paper.
Kobayashi et al., Nat. Rev. Immunology, 2012
Meissner et al., PNAS, 2010
Neerincx et al. (different paper, just google it ;) )
Staehli et al., J. of Immunology, 2015
Yao et al., Protein&Cell, 2012
Of course there are even more, but I think, these paper show a nice overview about this field.

It would be really perfect, if you could add the links for the references.

Watson et al. link,
Kobayashi et al. link
Meissner et al. link
Staehli et al link
Yao et al. link

NLRC5 is only a small part of the picture. The whole topic of immune surveillance and tumor escape is quite broad in scope (much broader than your answer would have us believe), but it is also too broad for this site, which is why I voted to close this question. Nothing you said is incorrect, but I think it's a bit misleading. Otherwise, every drug company on earth would be targeting NLRC5 and we'd have cured cancer by now. I know your own research can seem like the most important topic on Earth, but you need to have some broader perspective and a more nuanced view of how cancer works.

I never said, that NLRC5 is the only responsible protein for these escape mechanisms. I know, that this topic is much greater, but I don´t know every aspect of it, so I wanted to show at least one aspect. If we want to discuss this question in total, we would have to write a book. So NLRC5 and MHC I are two proteins, which show some insights into this broad field and now 201044 has some indications for research also on other involved molecules, if he is interested.

Great information ; I'm just an amateur researcher or like an 'armchair philosopher' I'm an armchair theoretical biologist.  I just wonder if these 'escape mechanisms' as mentioned can be inherited by any daughter cells of a pre-cancerous cell?

Do cancer cells inherit 'survival' strategies from their 'parent' cells?

Either from the parental cells or by mutation.

Do you mean a cancer cell can get a immune system avoidance strategy from only a mutation and not its parent cell? Can some type of radiation cause a mutation that can give a cancer cell some immune avoidance ability??


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Why do PCR manufacturers recommend assembling the reaction mix on ice?
Many PCR manufacturers recommend preparing the reaction mix for the reaction on ice. For example, here is NEB's recommendation for their Q5 polymerase. Other manufacturers also include similar steps:

We recommend assembling all reaction components on ice and quickly
  transferring the reactions to a thermocycler preheated to the
  denaturation temperature (98°C).

However, I can't think of a good rationale for this. This ResearchGate thread describes a few reasons, but they don't seem to make much sense.
Primer mispriming onto bacterial gDNA - Highly unlikely, since the initial melting step would melt away these misprimed primers and allow them to prime the correct sites.
Polymerase is proofreading (3'-5' exonuclease) - Proofreading activity should not affect any of the components, since the primer oligos are present in very large quantities, and the template should not be significantly affected by any proofreading, since they already have the correct sequence.
RNA is degraded by the polymerase - An extremely ridiculous answer, since PCR does not use RNA as a template, and RT-qPCR uses reverse-transcribed cDNA as the template. Whether the RNA is stable or not has no bearing on the activity of a DNA-only PCR once the RNA has been reverse-transcribed.
Polymerase is thermolabile - This is probably the most ridiculous answer to the question. The whole point of using polymerases like Taq, Pfu and Q5 is that they are from thermophile organisms, and they are highly thermostable to withstand the high temperatures during PCR.
What, then, is the reason PCR reactions are recommended to be assembled on ice?

As I was told as an undergrad, polymerase is thermostable but it could also activate on room temperature. As you are carefully going to cycle between temperatures, you don't want the reaction to start early on room temperature.

Actually I do not care the temp much. But, primer mispriming could happen, that's why hot start method is developed. Polymerase is proofreading (3'-5' exonuclease) can disturb your PCR. Primers are excess as you mention, but truncated primers may miss-anneal to unexpected regions and once PCR reactions occur in these regions, primers anneal, 3'-5' exonuclease adjust the sequences and PCR reactions occur again. In addition, having various length of primers in a reaction tube is not good in general.

I agree with skymingen but Taq's activity at RT is low. However all this may matter much only for real-time PCR. As with primer mispriming- all misprimed primers would dissociate during the heating annealing step. IMO, keeping in ice is just a long followed lab practice and it is better making mix at RT if you are not fast enough.