text:
How do the connections from V1 to V2 form during early development of the human brain?
I am wondering how corticocortical efferents from layer I and II in V1 develop to forward visual information to layer IV in V2. Is there topology preservation in these connections from the beginning on or does it only emerge later?


text:
What does the 'V' stand for in ECG electrode names?
In electrocardiography, electrodes have the typical names of:

RA (Right Arm)
LA (Left Arm)
RL (Right Leg)
LL (Left Leg)
V1, V2, V3, V4, V5 and V6

What does the V stand for? Is it perhaps from vector, ventricular, or maybe from something else entirely?

I would imagine it's "ventral", because they're placed on the ventral portion of the body (the front), but that's just a guess.

Short answer
V stands for voltage.
Background
The various leads in an ECG montage are shown below:

ECG electrodes. Source: American Heart Association
I am not an expert in ECGs, but as far as I can see, RA, LA and LL are return electrodes as they are situated far away from the heart. In other words, they act as reference electrodes. RL is the ground, basically to correct for baseline shifts. This leaves the V electrodes, which are the chest leads, or precordial leads, and are situated right above where the action is, i.e., the heart. The ECG is determined between the V electrodes and a distant reference, with a ground added. The V electrodes are the active electrodes, picking up the signal. The others are references and a ground only.

Thank you - I already had suspected it could be from voltage, but dismissed it, because other electrodes names are anatomy related. The limbs are in fact not all return electrodes, only the RL one is used to actively eliminate common-mode interference. The other three limb electrodes signals are there for differential measurements - they form a "triangle" of signals obtained from LA-RA,LL-RA and LL-LA.

As a paramedic who does EKGs every day, I can tell you it stands for "VECTOR" meaning the direction the electrode monitors electricity from the heart.
RA, LA, RL, and LL electrodes are ALL the principle electrodes for monitoring cardiac activity. These are referred to as the "limb leads" and are bipolar leads. The direction these leads monitor is determined by the polarity of the lead, which CAN change. For example, with Lead I the right shoulder is negative and the left shoulder is positive; but in Lead III the left shoulder is negative while the left leg is positive. Electricity flows from negative to positive. When it flows towards the positive electrode, the deflection on the EKG is upward. When it flows  away from the negative electrode the deflection on the EKG is downward.
The augmented vector leads are so-called because they have one positive electrode and the negative electrode is augmented. These are aVR, aVL and aVF where R, L and F stand for Right, Left, and Foot respectively. The V stands for vector here. In aVR, the left leg lead and left shoulder lead BOTH provide the negative pole for the EKG while the right shoulder is positive. The augmented vector leads require THREE poles to work: two negative and one positive.
The precordial leads, asked about in the original question, are UNIPOLAR leads. The computer inside the EKG uses the position of all the unipolar leads to create a "dummy" negative point at or near the center of the heart. Each Lead then becomes its own positive, and assumes that it is looking to a negative pole at the center of the heart. These are numbered V1 through V6, and the V stands for Vector. Vector 1, Vector 2, Vector 3 and so on.
One could do an 32-Lead EKG with the 3 Limb Leads, 6 Left Anterior Precordial Leads, 6 Left Posterior Leads, 6 Right Posterior Leads and 6 Left Precordial Leads. It is possible to also do a 64-Lead EKG. But the most common arrangements are 3, 4, 12, and 15 Lead EKGs.

Very likely it means Unipolar. Please note only unipolar leads aVL, aVR, aVF, and all precordial leads have the letter V. They are all unipolar. Long time ago, the "U" may have been misspeled as "V".

source: Stack Exchange

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text:
What is a lethal dose of THC?
With the oil form of THC being stronger then ever. What would happen if one was to take a stomach full of THC oil?

According to the abstract from this paper, the intragastric LD50 of $\Delta^9THC$ (tetrahydrocannabinol) in sesame oil using Fischer rats was 1270 mg/kg. Assuming rats and humans are identical (they're not), for an average-sized adult human weighing 70 kg (~155 lb.), the median lethal dose would be 88.9 grams, or about 3.1 oz.
Keep in mind that's 3.1 oz. of pure THC. That's a lot of weed.

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text:
HSC Cycling Rates
I would like to know how often human hematopoietic stem cells go into cycle in the bone marrow niche (with a paper reference). I have heard they cycle 1-2 times per year but has anyone robustly measured this?

Not knowledgeable in this respect myself, is this what I should be looking for? http://www.bloodjournal.org/content/117/17/4460?sso-checked=true

That is helpful but I would like something where the dynamics are directly measured if it has been done.


text:
Are the sympathetic and parasympathetic nervous systems exact opposites?
Suppose mechanism existed that could block function of the PNS. Would this just mean then the sympathetic nervous system would become overly active?
Do the sympathetic and parasympathetic systems act as opposing forces?

The Autonomic Nervous System is composed of the sympathetic and parasympathetic nervous systems. Each are dominant under different conditions - both are always active but one is dominant.
An important way to understand the the autonomic nervous system is in considering the effects of pharmaceutical drugs.
Sympathomimetic drugs enhance adrenergic function.
Sympatholytic drugs interrupt adrenergic function.
Parasympathomimetic drugs enhance cholinergic effects.
Anticholinergic drugs inhibit cholinergic effects.
For example:
Muscarinic antagonists are parasympatholytic (Anticholinergic) drugs - which reduce the effects of parasympathetic system.
But it is not that simple. They also increase sympathetic tone.
But again it is not always that simple. E.g. for sympathomimetic drugs (enhance adrenergic function) - there is no parasympathetic nervous system effect.
To answer your question, the sympathetic and parasympathetic nervous systems oppose each other sometimes. It depends on which receptors are activated and where.
(E.g.Alpha 1 receptors, Alpha 2 receptors, Beta 1 receptors & Beta 2 receptors).
Source & further reading on pharmaceutical interventions
Source & further reading on receptors

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text:
What does "generalisation" mean?
I am trying to understand a paper about ethanol: "Generalisation of ethanol with drug mixtures containing a positive modulator of the GABAA receptor and an NMDA antagonist" (Stolerman & Olufsen, 2000)
In the abstract it says,

"After drug-appropriate responding with the training mixtures reached 85%, generalisation to ethanol was examined in extinction tests."

I can't find a definition for "generalisation" in Google searches. What does it mean? I don't have a background in biology, so simple answers are preferable. Thank you.

Generalisation

Generalisation is the phenomenon of an organism responding to all situations similar to one in which it has been conditioned.

or

Not biologically differentiated or adapted to a specific function or environment

This means that  the the rats responded to ethanol the same way that they responded to the training mixtures.
Sources:

Mangan, G. L. The Biology of Human Conduct: East-West Models of Temperament and Personality. Oxford: Pergamon, 1982. Print.
"Generalized." - Memidex Dictionary/thesaurus. Web. 04 Mar. 2016.
"Generalisation." - Biology-Online Dictionary. Web. 04 Mar. 2016.

Thanks, but I'm still not sure I understand. If a rat is given substance X, which makes it drunk, and the rat becomes conditioned to seek out that substance, but then it also seeks out ethanol, is that generalization to ethanol? Generalization to substance X? Both?

@user22316 I'd assume that it responds to all situations as in responding to all situations similar to the one in which it has been conditioned.

Thanks, I might understand it now. A rat responds to ethanol in a particular way; it responds in a similar way to substance X; therefore, it is generalized to ethanol, i.e. it doesn't need ethanol per se, just whatever the effects of ethanol (and substance X) are. Correct?

@user22316 It means the rats responded to ethanol the same way that they responded to the training mixtures

Got it. Put that in an official answer and I'll give you the check mark.

@user22316 done

Ha, I didn't notice that you were the one who posted the answer. Thanks for your help.

@user22316 You're welcome!


text:
Is it common to have multiple recessive traits in humans?
I just started thinking about my phenotype and realized I got multiple recessive traits. I have attached ear lobes, my blood type is O-, I got green eyes (I think eye color in polygenic but still somewhat recessive), a few years back I was in the control group of a study that was looking for a link between an allelic variant and the development of diabetes mellitus in patiences with another disease I forgot which, I was the only homozygous among all control patients! so you get the point. I am just wondering if anyone has any notion of how often humans present multiple recessive traits, maybe in terms of allelic frequency or something like that, or where can I find information about it. And maybe if there is something health related that may be worth knowing. I mean apart from a minor allergy I'm a really healthy person, but I may have predisposition to something.

Depends on the allele frequency in the population.

sure, but I guess my question is if there is some database where I can look at some actual numbers...

Think of law of independent assortment and gene linkage.

It depends on how long a population in your dominant heritage was genetically isolated, how common certain recessive traits are.
However, you might reconsider about the "green eyes".  Iridologists claim that there are only blue eyes, and light brown eyes.  All other colours are indicative of bioaccumulation of various substances (evidenced by a return to blue or light brown when the body is supported in excreting these substances), and health issues in certain tissues.
While there is argument about how scientific a technique iridology is, all medicine begins as observation of patterns, and development of models based on those patterns.  Models in medicine are constantly undergoing upgrading and replacement, as old models no longer explain new and well-observed patterns.

Please support some evidence for the claim that some eye colours are caused by bioaccumulation of substances and that the body can be supported to get rid of those substances and eye colour changes can be caused by that.


text:
How only one follicle develops into graffian follicle?
I've studied that one out of many follicle develops into mature or graffian follicle. The fact which confuses me is that, since all follicles are in same ovary, close to each other with equal supply of nutrients. What causes the other follicles to give up the race? Why our body cannot develop mature follicle from a single one?

Why our body cannot develop mature follicle from a single one?-What do you mean?  What causes the other follicles to give up the race?-They don not 'give up'. Though not all but eventually many of the follicles of each ovary with the primary oocytes arrested in diplotene in them make it to Metaphae-II.

It doesn't mean only one follicle maturates within a lifetime of a woman. For every ovulation only one follicle maturates from the batch of primary oocytes stored within the ovary. Before a female is born, all the primary follicles are arrested in the diplotene stage of prophase I. Still, we do not know exactly the mechanisms that let only one follicle to release a mature egg cell, but studies have shown why it possibly happens.

Granulosa cells surrounding the oocyte have receptors for FSH (follicle-stimulating hormone), FSH activates the production of aromatase, which transforms testosterone produced under the influence of LH (luteinizing hormone) in cells of theca interna into estrogens. Estrogens activate expression of LH receptors on the surface of granulosa cells and further stimulate the production of LH. The more LH activates thecal cells, the more estrogens are produced in granulosa cells and that at the same time increases production of LH receptors on granulosa cells.
FSH also stimulates granulosa cells to proliferate, providing the whole follicle with a large number of FSH receptors and increased production of aromatase and at the same time stimulates the follicle to finish meiosis I. Eventually one of the growing follicles will have enough FSH and LH receptors on the granulosa cells to become able to respond to large surge of LH, which results in ovulation. The rest of the follicles that started to develop degenerate due to insufficient number of FSH and LH receptors. The fact that FSH and LH concentrations drop rapidly after ovulation also halts the development of remaining follicles.
The follicles that did not receive enough FSH, won't grow to the point, where granulosa cells start expressing LH receptors and they won't pass through the 1st meiotic block, therefore they still may be activated in the next month. Those that did pass the 1st meiotic block but couldn't be ovulated, will degenerate.
It is still unclear whether there are some additional mechanisms that help the atrophy of underdeveloped oocytes.
Sources:

Larsen's Human Embryology
https://kjcscientific.wordpress.com/project-excalibur/


text:
What is an extinction test?
In Stolerman & Olufsen (2001) I read the sentence:

After drug-appropriate responding with the training mixtures reached
85%, generalisation to ethanol was examined in extinction tests.

Here is the entire section from the article on the subject of extinction testing:

Extinction test procedure
Effects of test drugs were determined in brief extinction tests of 3 > min duration that took place twice weekly, with normal training sessions continuing on the interven- ing days. Initially, rats were tested once with vehicle and once with the training mixture; they all reached a cri- terion of at least 80% correct responding and they were all used in subsequent experiments. The effects of saline, the single drugs used for training and the training drug mixture were determined in 3-min extinction tests. The different drug treatments were given in random order. Prior to each test, two injections were always given (via the appropriate routes) to equate handling.

What is an extinction test?

wow. I did quite a thorough search and couldn't find the answer. Problem is that the linked article is superbly vague and incomplete in their description of methodology. Extinction is a term used where folks neglect one stimulus out of a pair of stimuli and is used to diagnose hemineglect, e.g. in subjects that have experienced a unilateral stroke. Good luck with this excellent question. +1

By the way - if my lead to temporal neglect is right, you may consider re-posting on CogSci. If you do, let us know so the mods here can take appropriate measures. Up to you.

In the case of this particualr paper, I don't think it has anything to do with hemineglect. It has something to do with pharmacology. I've added the entire section from the article on it. The secontion is called "Extinction Test Procedure."

It's a behavioral thing.
The abstract of the paper says: "...mixtures of two drugs from vehicle in two-lever procedures with food reinforcers..."
In operant behavior, rats (in this case) are trained to associate a stimulus (a tone, an odor, a light, etc.) with an action that leads to a reward, the association is trained by delivering a reward only when the 'correct' action is performed, e.g.:
stim A -> press left lever -> get a reward
stim A -> press right lever -> get nothing (or a punishment, but that is a whole different question)
One can quantify the performance of the animal by looking at the probability of responding left (in this case) when stim A is presented.
Now, we think of the association between stim A and left pressing as being reinforced whenever a reward is present, we call it extinction whenever the reward is not present, basically because the reinforced behavior will eventually extinguish, and we say its extinguished when the probability of response to the left and right is 50%.
"...generali[z]ation to ethanol was examined in extinction tests..."
basically means that they substituted stim A for ethanol (I imagine its all olfactory, just read the abstract sorry) and characterize the response to ethanol without ever reinforcing it, hence the extinction.

Do you have any references you can add to this?

Any 1st year psychology text book will talk about classical and operant conditioning, extinction should be right there, it goes all the way back to B.F. Skinner (https://en.wikipedia.org/wiki/B._F.Skinner), speaking of wikipedia: https://en.wikipedia.org/wiki/Extinction(psychology) The reference section should be a good place to start.


text:
What is the name of the category of viruses that affect only one side of the body?
The Varicella zoster virus causes chickenpox in children and shingles in adults.
When the virus attacks as shingles, one of its distinguishing characteristics is that it only affects one side of the body. (As shown in the link and verbally identified by a doctor I spoke to). This happens because the nerve cells themselves are infected - and are partitioned on different sides of the body.

At first the rash appears similar to the first appearance of hives;
however, unlike hives, shingles causes skin changes limited to a
dermatome, normally resulting in a stripe or belt-like pattern that is
limited to one side of the body and does not cross the midline.[13]
Zoster sine herpete ("zoster without herpes") describes a person who
has all of the symptoms of shingles except this characteristic
rash.[16]
 From Wikipedia

My question is: What is the name of the category of viruses that affect only one side of the body?

I don't think there is a name for the "category", or that it really is a category unto itself.

"unilateral" would make for a convenient shorthand.

Short answer: Viruses that affect only one side of the body are not categorized by this information.
Long Answer: For people who likes details
Several types of virus classification exists:

Baltimore: Classified by the type of DNA or RNA that is carried by the virus
Holmes: Classified by the target organisms of the viruses (plants, bacteria, animals)
LHT: Classified using several physical differences (More specific and complex)

For example, Shingles would be classified as:
Baltimore: Group I (double DNA stranded viruses)
Holmes: Group III Zoophaginae (animals)
LHT:

Order: Herpesvirales
Family: Herpesviridae
Subfamily: Alphaherpesvirinae
Genus: Varicellovirus
Specie: Human herpesvirus 3 (HHV-3)


text:
Why are vegetations in Infective endocarditis common on the atrial side?
Robbin's Pathology says that vegetations of IE are more common on the atrial side in AV valves. In Liebmann Sack's Endocarditis, which is a sterile (non bacterial) type of endocarditis, the underside of the valve also has vegetations. Why is it so? If its just colonization of bacteria in IE, how does it matter where?
Does gravity matter in colonisation of bacteria!! ?

Infective endocarditis generally develops when there is a pre-existing valvular lesion. The location where the vegetation in infective endocarditis develops is based on the pressure of the surroundings. Bacteria tend to colonise places where the pressure is low.
'Where the pressure is low', depends upon what kind of a valve deformity is already present.
In mitral regurgitation, blood when pumped from the left ventricle enters the atria due to the patent bicuspid valve. Naturally, the pressure is more on the ventricular side than the atrial side. Hence, the bacteria settle on the top of the leaf. Moreover, the do so at the edges of the leaves. This is because, since the blood has to squeeze through, according to to bernoulli's theorem (Venturi effect). Hence they form on the edges of the atrial side of the valves

In case of an aortic regurgitation, since there is a backflow of blood from the aorta to the ventricles, the vegetations are found on the underside of the aortic valves.
Liebmann Sacks (which is non infective and happens in lupus) is common in the mitral valve though it can happen anywhere. I assume, since bacteria are living cells, the pressure constraint applies to them but not to sterile vegetations like the one in lupus.
I implore you to have a look at this wonderful video which explains it all.
Picture credits and reference : Endocarditis by osmosis.org

With the bacterial IE, it would look like the vegetations tend to colonize the lower pressure sides of the valve structure (REF1). Something that was made clear that distinguishes the IE vegetations frm the Libman-Sacks vegetations was overall motility. Specifically, Libman-Sacks vegetations exhibit no independent motion and are largely sessile, whereas IE vegetations can be motile (REF2). In terms of where they attach I think this makes sense, the more motile vegetations colonize the less turbulent area, and the sessile vegetations seem to hold up in either scenario. Reference 1 also rather usefully points out that IE vegetations may be located anywhere on the valve structure as well, they just tend to be on the low-pressure side.
So being said i would argue that the motility of the organisms is a deciding factor.

Robbins classifies IE as acute or subacute. Subacute IE is the one where flowing viridans bacteria stick to already damaged valves. Arrhythmia isn't mentioned as a risk factor or a predisposing factor. Rather valve damage/ prosthetics are. Could you suggest a further read regarding the Afib leading to endocarditis thing?

I'll be honest, I don't like that answer that I initially posted, so i'm going to rehaul it here

Thanks for the answer. Could you pls explain what 'motility' means in this context? The vegetations don't move themselves right? Like move with the valve??

Motility meaning "are they capable of moving on their own or are they for the most part adhered to the structure?", in essence.

The Cleveland Cardiology review mentions Mural thrombi as a risk factor for bacterial endocarditis :)


text:
What are the differences among food poisoning, gastroenetritis and diarrhoea?
I have now studied a major chunk of my microbiology course without understanding the basic difference between the three. The terminologies seem to be confusing. Is it a necessity for food poisoning to be cause by bacterial toxins? My texts include Shigella, which causes dysentery under food poisoning. What are the operational definitions for them? Is food poisoning more of an epidemiological term? I understand that they aren't clear cut identities and there is significant overlap. But could someone please help out?

First of all, diarrhea is a symptom, generally defined as passing large amount of loose stool. Diarrhea has countless causes, which include gastroenteritis and food poisoning (although not all types of gastroenteritis or food poisoning cause diarrhea).
Now the other two terms. Strictly speaking gastroenteritis refers to the inflammation of stomach/intestines, but clinically, it is most often used to refer to infection of stomach/intestines. Gastroenteritis is most often caused by viral infections e.g. rotavirus, noravirus, enterovirus, adenovirus... but can also be bacterial in origin.
As for food poisoning, is usually defined as illness (usually gastrointestinal symtoms, including nausea, vomiting and diarrhea) caused by "poisoned food". Food poisoning can be caused by the presence of a microbial toxin (which can sometimes be heat-stable ie not inactivated by boiling/cooking). Examples include S. aureus enterotoxin, B. cereus enterotoxin, shigatoxin... There can be an overlap, when ingestion of food causes an infection of the gastrointestinal system, but gastroenteritis is not necessarily foodborne.
Hope that clarifies things.
References for further info:
Food poisoning
Basics of acute viral gastroenteritis

Thanks a lot! Another important thing I gathered is that food poisoning need not lead only to GI symptoms. Like, the botulinum toxin has its effect on NMJs. Just felt like adding it up here. Anyway, thanks! and could you give examples of non foodborne gastroenteritis (infectious)?

You're welcome. An example for gastroenteritis not caused by food, could be something like an acute rotavirus infection. Although the virus does need to get the GI, it doesn't have to be through food, it could be contact with someone infected.

Could you add source information to facilitate users to do more reading on the topic?


text:
What is the rationale behind reverse cholesterol transport?
Reverse cholesterol transport is transport of cholesterol from the tissues back to liver/VLDL. My question is why do the tissues have this extra cholesterol in the first place?
Why would you synthesise extra cholesterol when excellent feedback mechanisms exist - eg. SREBP SCAP INSIG path??
Does this happen only in the case of an atheromatous plaque? Nowhere else?

This is a great question, I have also wondered this many times but found no clear motivation or data in the literature. My guess is that there is some continuous loss of structural (membrane) lipids in all tissues that proliferate or renew themselves. Possibly the cholesterol in membranes of dead cells cannot be completely recycled (perhaps it gets irreversibly modified somehow). Pretty much all tissues have some rate of cholesterol synthesis, and proliferative tissues have high rates, which suggests continuous turnover. But I don't know for sure, just some food for thought ...

The problem is that we are taught all the cycles, and we learn them blindly. The big picture gets lost in the process. :(

Just remembered that I asked this related question some time ago.  No responses yet ...  http://biology.stackexchange.com/questions/41886/is-there-a-way-to-quantify-in-vivo-cholesterol-transport-rates

this source might be helpful: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2390860/


text:
What is the function of CETP?
I read up that CETP transfers cholesterol from HDL, which collected it from tissues, to VLDL. This VLDL is then sent back to the tissues, ultimately forming LDL internalised by cells.
What is the whole point in taking cholesterol from the tissues only to give it back? I read up that reverse cholesterol transport is for sending the excess cholesterol to the liver for excretion as bile. But LDL receptors are everywhere and not just the liver.
There also happens to be a SRB1 pathway specific to the liver but apparently not significant in humans :(
So pls help me make sense.


text:
Enzymes and Digestion
If biological enzymes (protease,amylase,lipase etc.) just speed up the reaction (in the digestion process), then what actually digests the food?? (I'm a secondary student)

Welcome to Bio. The enzymes do, what else?

@Christiaan What do you mean, enzymes actually digest the good?? Like, the definition of a biological enzyme is that its a catalyst made of protein that speeds up the reaction in digestion. That suggests that another substance actually breaks down the food. Am I right, or am I not getting it correct??

Compounds like proteins and nucleic acid have a natural half-life in an aqueous environment, for example in Belle et al: for ~3,700 proteins in a budding yeast proteome, median half-life of proteins was about 43 minutes. Of course they differ and some proteins can last hours.

The enzymes break down the food.

@Christiaan So why it is said that it "speeds up the reaction" rather than "digesting it" ?  (Sorry if i'm not getting it)

In general, catalysts, and hence enzymes, only speed up the process of reaching equilibrium. Proteins inherently have the tendency to degrade through hydrolysis. The only thing an enzyme does is promote the establishment of that equilibrium. No more, no less. Hence, enzymes speed up a reaction that would occur anyway. Admittedly, it's not the whole story, e.g., ATP-powered enzymes can actually shift the equilibrium.

Reminds me of school days when I was fascinated about the exact same thing. My school bio teacher parried away by saying the stomach does it mechanically!! But the actual answer which is given below, I learnt after high school chemistry and thermodynamics. If the free energy change is negative for a reaction, it is spontaneous but not necessarily instantaneous. You need to get the difference. The reaction is possible but just doesn't happen because of the very high activation energy. Such high amount of activation energy can't be delivered in the body by heat, so enzymes do the work.

I suspect that the question reveals an incomplete understanding of enzymic catalysis and could more generally be rephrased as "If enzymes just speed up biological reactions, what makes the reactions proceed in the first place." The simple answer to this is the fact that the thermodynamics of the reaction are favourable, i.e. the reaction involves a negative change in (Gibbs) free energy.
So what is stopping the reaction proceeding at a reasonable rate without catalysis? The fact that the thermodynamic path of reactions involves an activated state with a higher free energy. In most cases this is sufficiently large that it acts as a barrier to spontaneous reaction. You can get over the activation barrier by e.g. supplying heat (i.e. supplying activation energy) but this is not possible in living organisms. Enzymes act by lowering the activation energy (energy barrier) or raising the ground state (which in effect decreases the activation energy).
One should realize that "just speeding up the reaction" is generally increasing the reaction rate from being negligible to biologically sufficient. So what makes the reaction go is a combination of the reactants being there with a favourable chemistry and the enzyme being there in the right place to deal with them.
If you are unfamiliar with this basic reaction chemistry see:
http://www.ncbi.nlm.nih.gov/books/NBK22384/#A1100
and the image below from Wikipedia.


text:
Why do animals have more heavy nitrogen and carbon than plants?

There are two stable Isotopes of nitrogen N14 and N15. The ratio of
  15N/14N tends to increase with trophic level, such that herbivores
  have higher nitrogen isotope values than plants, and carnivores have
  higher nitrogen isotope values than herbivores. Depending on the
  tissue being examined, there tends to be an increase of 3-4‰ at each
  trophic level.
The tissues and hair of vegans therefore contain significantly lower
  percentage of 15N than the bodies of people who eat mostly meat.
  Isotopic analysis of hair is an important source of information for
  archaeologists, providing clues about the ancient diets.

https://en.wikipedia.org/wiki/Isotopic_signature#Nitrogen_isotopes
But how does N14 'disappear' from plant to animal?

Your last line does not seem to match the rest of the question as you did not say anything about N-14 'disappearing' anywhere else in the question. Yet, herbivores have more N-15 than plants and carnivores have more N-15 than herbivores because of bioaccumulation (https://en.wikipedia.org/wiki/Bioaccumulation). This claim is also supported by @Roland's answer.

Organisms accumulate certain isotopes because their metabolic enzymes have a slight preference for molecules containing that isotope. A well-known example is ribulose-1,5-bisphosphate carboxylase (Rubisco) which is responsible for CO$_2$ fixation in photosynthetic plants: this enzyme is somewhat more efficient with $^{12}$CO$_2$ than with $^{13}$CO$_2$, causing plants to accumulate $^{12}$C.
In animals, there is an enrichment for $^{15}$N because the deaminases and transaminases that transfer nitrogen from amino acids to urea (for excretion) tend to favor $^{14}$N. So in this case, $^{14}$N tends to be removed from the body faster than $^{15}$N when breaking down dietary protein. The differences are very small though: the relative enrichment of about 0.4% per trophic level corresponds to 0.367% $^{15}$N in a herbivore, compared to 0.366% $^{15}$N in a plant.
Source: this article.


text:
constitution of read and gene region (IGV)
I work with fastq files containing NGS reads for some human DNA regions. The reference genome is hg19. I had two fastq files (pair-ended). I generated alignment BAM files. I used "bwa" and samtools to find a possible target gene region (chr7:55,242,376-55,242,574,). This corresponds to a region of the EGFR gene.
Here is a screenshot of the gene region

And here is a screenshot of the primer region

I also have a list of primers and reverse primers:
FORWARD
1. TTGCCAGTTAACGTCTTCCTTCTCTCTCTG
2. CCCTTGTCTCTGTGTTCTTGTCCCCCCCA
3. TGATCTGTCCCTCACAGCAGGGTCTTCTCT
4. CACACTGACGTGCCTCTCCCTCCCTCCA

REVERSE
1. GAGAAAAGGTGGGCCTGAGGTTCAGAGCCA
2. CCCCACCAGACCATGAGAGGCCCTGCGGCC
3. TGACCTAAAGCCACCTCCTTA
4. CCGTATCTCCCTTCCCTGATTA

And I have some adaptors
ADAPTORS 1
AAGACTCGGCAGCATCTCCA

ADAPTORS 2
GCGATCGTCACTGTTCTCCA

I have to answer to the following questions:
1) What is the constitution of each read (adaptor+primer+amplified region)?
The forward primer is obvious and corresponds to the first primer of the list
TTGCCAGTTAACGTCTTCCTTCTCTCTCTG

So why do we have the three other forward primers? I don't understand. And what about the correct reverse primer?
It seems to be the complementary sequence of the end region
GAGAAAAGGTGGGCCTGAGGTTCAGAGCCA

Finally which adaptor is used?
Is [ADAPTOR1 - PRIMER1 - AMPLIFIED REGION] the correct answer? Are there other possibilities?
2) % of reads that map the human genome? what about the unmapped?
Can you please give me some clues about how to answer this question.
I just need some clues I want to do it by myself.
Thank you very much for your help.

You have asked quite a few questions here. I will try to answer a subset of them.
To answer your question, I started by going to the UCSC genome browser, and selected the BLAT from the tools dropdown menu. Then passing your primer sequences as queries, we can clearly see where they map to the reference genome.

Looking at the figure above, I can guess that your data comes from a targeted sequencing experiment (exome, or gene panel, etc); where you have primers around each exon of EGFR on two strands, on 5' end of exon sequence on each strand (think about DNA polymerase acting in PCR to amplify the number of DNA molecules before sequencing).
Regarding the adapter, I am not sure which read you are referring to. Can you clarify please?
About percentage of mapped vs unmapped reads, you can use bamtools.
Example Usage:
/user/me/src/bamtools/bin/bamtools-2.3.0 stats -insert -in my-sequence-file.bam
Example output:
Total reads:       103277668
Mapped reads:      90088436     (87.2293%)
Forward strand:    58136735     (56.2917%)
Reverse strand:    45140933     (43.7083%)
Failed QC:         6529806      (6.32257%)
Duplicates:        0    (0%)
Paired-end reads:  103277668    (100%)
'Proper-pairs':    87439672     (84.6646%)
Both pairs mapped: 87910438     (85.1205%)
Read 1:            51638834
Read 2:            51638834
Singletons:        2177998      (2.10888%)
Average insert size (absolute value): 6317.39
Median insert size (absolute value): 301

Thank you very much. They all use the same 2 adaptors. Is that possible? It's seems weird for me.

just one last question How do you pass your primer sequences as queries in BLAT? And obtain such a nice figure

Glad I was able to help. I generated a fasta format input with your eight sequences. Then after performing BLAT, selected the browser link for one one your sequences, zoomed out by a factor of 10 a few times so that all the query sequences are in the range. By default, one gets a crowded display in genome browser. You can press 'hide all' button below the genome view figure, and follow by setting BLAT and refGene/refSeq options to full.


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Are there bacteria that respire anaerobically in aerobic conditions?
There are facultative anaerobic bacteria that switch to anaerobic respiration in an anaerobic state, but are there any organisms that would still perform anaerobic respiration even when shifted to aerobic conditions? Obligate anaerobes would die when introduced to an aerobic condition right? Are there any which can survive?
This doubt came into my mind while reading the Hugh-Leifson Oxidative Fermentative test. Such a bacterium would be read false positive for oxidisers in such a case because it would ferment glucose even in aerobic conditions.

There are aerotolerant anaerobes.

Are there any organisms that would still perform anaerobic respiration even when shifted to aerobic conditions?

Yes, there are. They are called aerotolerant anaerobes as shown in this figure on tube 5. In the thioglycollate broth, growth is seen throughout the length of the tube
Legend

Obligate aerobe
Obligate anaerobe
Facultative anaerobe
Microaerophilic
Aerotolerant anaerobes

Are there any which can survive?

Obligate anaerobes wouldn't survive in aerobic conditions. Hence they are named so.

Such a bacterium would be read false positive for oxidizers in such a case because it would ferment glucose even in aerobic conditions.

The thioglycollate broth shown here is used to differentiate bacteria into the above said criteria. The Hugh-Liefson test does'nt do that. You can not conclude that a bacteria is aerobic or anaerobic using that test. The H-L test, is interpreted in two ways.

Fermentative - When both the closed tube and open tube show a colour change
Oxidative - Colour change only in the open tube

In short, the words aerobic/anaerobic are not used to interpret the H-L test. But we can draw parallels.

Obligate aerobe - Open tube (+), Closed tube (-) - Oxidative
Obligate anaerobe- Open tube (+ at bottom), Closed tube (+) - Fermentative
Facultative anaerobe- Open tube (+), Closed tube (+) - Fermentative
Microaerophilic- Open tube (+), Closed tube (-) - Oxidative
Aerotolerant anaerobes- Open tube (+), Closed tube (+) - Fermentative

Yes, for example bacteria that perform lactic acid fermentation are anaerobic but aerotolerant.

Welcome to BiologySE! do you think you could put some references into your answer? we always appreciate cited references - and it will increase the value of your answer (by allowing others to read more if interested).

Sorry, I'm new here. Which kind of reference would you prefer? you can find infos about lactic acid bacteria and their fermentation in Brock "biology of microorganisms"'s book.


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Can bacteria metabolize fatty acids for fuel?
I'm not a microbiologist, but rather a physiologist  curious about microbial metabolism. Much like humans bacteria can utilize glucose, but when it comes to long chain, medium chain, or short chain fatty acids, what are the pathways that microbes use to break these compounds down for fuel?
It seems plausible that bacteria can take up short chain fatty acids, but with longer chain species are there impediments to uptake? Are the oxidative enzymes similar between bacteria and humans?

Beta-oxidation happens in mitochondria. So there is a good reason to assume that bacteria can metabolize fatty acids.

I don't see the connection between bacteria and mitochondria. Bacteria don't have mitochondria. If you are referring to the endosymbiosis theory, mitochondria are likely descendants of archaea, not bacteria.

I found this review about bacterial lipid metabolism. There it says:

Exogenous long chain fatty acids are utilized by E. coli in two ways. Firstly, they can
  be incorporated into the membrane phospholipids by the acyltransferase system (PlsB
  and PlsC; Section 4). Secondly, they can be used as the sole carbon source for growth,
  and are in fact an important source of energy for E. coli in their normal habitat, the
  intestine [16]. The CoA thioester of the fatty acid is the substrate for both of these
  pathways. Fatty acids greater than 10 carbons in length require the fadL gene product
  to be taken up from the growth medium in sufficient quantities to support growth.

So yes, bacteria can grow on fatty acids alone and they can utilize long fatty acids as an energy source. However the uptake of the long fatty acids requires the protein produced by the fadL gene.

+1 that's a great review included in your answer. I was mostly interested in whether or not bacteria could use triglyceride as fuel because I was unsure if they expressed a lipase to break down the triglyceride to individual fatty acids (like pancreatic lipase produced by humans for lipid digestion). I wanted to start by trying to understanding if there were limitations to fatty acid metabolism. However, in that review it states that some bacteria do express an outwardly directed, membrane-bound lipase for that purpose. Very cool!

Glad I could help :-)

I wanted to start by trying to understanding if there were limitations
  to fatty acid metabolism.

There are aerobic bacteria that can reduce fatty acids. However, there are no bacteria that reduce fatty acids without any oxygen equivalent to, say, fermantation (sugar->alcohol).
You can try this in the lab or even at home. Put tomato purée or sugar in a bottle. Put a layer of oil above it. Keep one bottle open and the other one closed (air-tight). You'll see that the bottle that is open will get molded while the closed bottle will not. This is because there are no bacteria that can penetrate the layer of oil because there are no enzymes strong enough to work anaerobically.
Also, good tip to preserve your food at home.
Source: I'm a biotech engineer.
Carlson, Karin; Linder, Claes et al.


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How is the side-polarity of the myosin filament in myofibril maintained?
If myosin molecules are the properly oriented relative to their position in the myosin filaments, the sarcomere is not functional. But how is the orientation of the myosin molecules determined? Why is there a symmetry in the arrangement of myosin molecules in the myosin filament? And are there any diseases associated with the improper arrangement of myosin molecules?

There are a lot of other proteins like titin and dystrophin to name few which maintain the sarcomeric structure. But got no clue of anything specific. Its important to know that it's not just the actin and myosin floating in the muscles as textbook diagrams show.

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


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Current scientific theories for evolution of Cucurbita
I'm attempting to find research on scientific theories surrounding the evolution of certain plants, and am unable to find any footing with respect to a certain genus.
In this case, I am researching Cucurbita (ie: squash, pumpkins, etc), and can't find any basis for how it survives inherently without outside manual intervention. Unlike hot peppers (eg: Capsicum annuum), it is not easily ingested by birds, who do not suffer from the painful effects of capsaicin, and effectively transport the seeds, undigested, to new areas to spread the plant.
Also, unlike fruit growing on a tree, such as apples, it doesn't (seem) to provide a means to transport seeds any meaningful distance.
Finally, it seems most animals; ruminants, scavengers, and insects alike, would consume and digest the seeds.
Are there any generally-accepted (or at this point, plausible) theories with research to back it with respect to how such plants could survive long term without being manually grown and harvested by a species which eats them? While I understand (and acknowledge) the scientific theory of evolution, I'm not sure how the survival of such plants seems to be a special case.
Thanks!

I don't remember much, had studied botany a long time ago. But isn't cucurbitaceae that genus where the fruit blasts to disperse the seeds?? Then you dont need animals to eat taht stuff..

Many plants that we use for have gone through thousands of generations of intensive artificial selection

Sorry, should be family cucurbitaceae

@DavidBlomstrom Very interesting read. It does coincide with this question, but it seems the information on the mechanics and history of the subject elude me.

@DavidBlomstrom I just found some articles by adding "extinction" to my searches that indicate the same case with avocados (lack of mega mammals to transport the seeds via their dung). My mistake was assuming the seeds would be destroyed via digestion. It seems humans did indeed help it survive after large mammals started to die out, like the avocado. If you'd care to re-create your comment as an answer, I will mark it as accepted. Cheers!

@rg255 I'll agree 100% with you on that. Please don't mistake me for a theist trying to find a smoking gun or counter-example to evolution (ie: "checkmate atheists!"). I'm genuinely interested in how these species survived.

I would maybe change the title to something like "Seed dispersal in Cucurbitaceae"

Don't worry @Dogbert I was only giving a hint as to why it may be hard to see an adaptive point to many features of crop plants (and domestic animals for that matter; dogs and cats are very different from wolves and lions!)

You're right that modern species would have a hard time spreading group seeds, though you're not quite right about the reasons.  Cucurbita rinds are extremely bitter, so that modern mammals are reluctant to (or unable to) process the rinds to access the seeds.
According to a recent article (Gourds and squashes (Cucurbita spp.) adapted to megafaunal extinction and ecological anachronism through domestication), the explanation is that wild Cucurbita first co-evolved with North American megafauna, like mammoths and mastodons, who could tolerate the toxic/bitter rind. (The authors also suggest that megafauna also produced suitable habitats for their growth.)
Following the extinction of these megafauna, humans picked up the slack, with most wild Cucurbita going extinct and only domesticated versions remaining.

Collectively, these results point to wild-type declines coinciding with widespread domestication. ...megafauna consumed Cucurbita fruits and dispersed their seeds; wild Cucurbita were likely left without mutualistic dispersal partners in the Holocene because they are unpalatable to smaller surviving mammals with more bitter taste receptor genes. ... Thus, anthropogenic landscapes provided favorable growth habitats and willing dispersal partners in the wake of ecological upheaval.


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What is the name of the property of viruses can activate a second time, with different symptoms?
The Varicella zoster virus causes chickenpox in children and shingles in adults.
It appears after the initial infection, it can go dormant in the nerve, and reactivate itself decades later.
In chickenpox - the symptoms are:

characteristic skin rash that forms small, itchy blisters, which eventually scab over. It usually starts on the chest, back, and face then spreads to the rest of the body

In shingles - the symptoms are:

a painful skin rash with blisters involving a limited area. Typically the rash occurs on either the left or right of the body or face in a single stripe.

My question is: What is the name of the property of viruses can activate a second time, with different symptoms?

Viral latency is the best term to use for viruses that can lie dormant.
I have not come across a specific term for latent viruses that recur with different symptoms. This is probably because "different" is very subjective. Many pathogens can cause several different forms of disease depending on factors such as the route of exposure (i.e. where and how the pathogen got to its destination). Obviously the latent infection has a different pathophysiology to chickenpox. Due to its latency in dorsal root ganglia, shingles typically results in a localised rash, but there are less common disseminated forms of shingles that can look very similar to chickenpox.


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Does TSH and Growth hormone have any role in menstruation?
Actually, I came across this on a mcq (multiple choice question) exam:
Name the hormone which has no role in menstruation:
A. LH
B. FSH
C. GH
D. TSH
(only 1 correct option)
Both FSH and LH have direct roles in the menstrual cycle, they're responsible for the follicular phase and ovulation, respectively. Menstruation takes place due to the decreased levels of progesterone. Does GH and TSH have any role in the process? If so what is that role?

I don't think they have a direct role but can affect menstruation indirectly by influencing metabolism.

TSH has an effect slightly similar to that of FSH and LH. This is found to be problematic in thyroid diorders. For example, in hypothyroidism the TSH overflow causes children to become fertile at an earlier stage, compared to the norm [1].
[1] Ann N Y Acad Sci. 1997 Jun 17;816:280-4. PMID: 9238278. http://www.ncbi.nlm.nih.gov/pubmed/9238278

If hypothyroidism or hyperthyroidism resulted in menstrual disorders, then can't we say that thyroxine(secreted by thyroid) has a role in the proper functioning of the menstrual cycle, rather than TSH?

Not necessarily, correlation doesn't equal causation. While Thyroxine is the main hormone secreted by the thyroid, it doesn't directly mimic FSH and LH like TSH.


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What is the difference between Founder effect and Bottleneck effect?
Both are examples of genetic drift in which there is a change in the allele frequency when the population size becomes small.
What is the difference between the two?

Genetic drift is an EVOLUTIONARY PROCESS
Source: Wikipedia > Genetic Drift

Genetic drift (also known as allelic drift or the Sewall Wright effect2 after biologist Sewall Wright) is the change in the frequency of a gene variant (allele) in a population due to random sampling of organisms.

I think that these terms are used without a perfect semantic. An obvious case
A population bottleneck is a DEMOGRAPHIC EVENT
Source: Wikipedia > Population Bottleneck

A population bottleneck [..] is a sharp reduction in the size of a population due to environmental events (such as earthquakes, floods, fires, disease, or droughts) or human activities (such as genocide)

A founder effect is an EVOLUTIONARY PROCESS THAT RESULTS FROM A FOUNDING EVENT
Source: Provine 2004

The “founder” principle, as introduced by Mayr in 1942, was an auxiliary mechanism (less important than random drift) for producing reduced variability in an isolated population started by a few individuals or even by a single fertilized female. Mayr saw a distinction between the “founder” effect and random drift. The founders were not a random sampling of the main population, but, once isolated as a small population, would undergo random drift

In other words, a founder effect does NOT refer to the ppulation bottleneck causing by a founding event. A founder effect refers to the increase in genetic drift (loss of genetic diversity is expected) caused by a founding event. A founding event is the event by which few individuals (eventually only one) quit a large population to settle down a new small populations. As such, a founder event is a type of population bottleneck. I think that one could further extrapolate the term "founder effect" to any increase in genetic drift caused by a population bottleneck.
Do all authors use the same definitions?
I have not done a good literature review to answer this question but I would not be surprised if different authors, use slightly different definitions.
For example, some authors (e.g. Peery at al 2012, Raymond and O'Brien 1993, Duarte et al. 1992) have used the term "genetic bottleneck" instead of "population bottleneck". Wikipedia indicates that these two terms are synonyms. However I could not find any paper that formally define the term genetic bottleneck but all the papers using this term seem to be specifically interested into the genetic signature of population bottleneck. As such, the semantic relationship between population bottleneck and genetic bottleneck could be the same as between founding event and founder effect. Genetic bottleneck could be defined as the increase of genetic drift that is caused by population bottleneck.

Founder effect and population bottleneck are not necessarily examples of genetic drift. The common thing in all three is a resulting reduction in genetic diversity.
Genetic drift is a change in allele frequencies due to process of random sampling to form a finite offspring population from parent population. Ultimately some alleles gets fixed and genetic diversity decreases. However decreasing population size or small population size is not a necessity for drift to happen.
Population bottleneck and founder effect are similar population genetic events that are happening in different ecological context. Both results in decreased population size (for the population of interest) and decreased genetic diversity. But the exact ecological context determines how much of the decrease in diversity is due to drift and how much of that is due to selection.
Population bottleneck refers to an event, where a population is intact but only small portion of the individuals are able to pass their alleles to future generations. This may be associated with strong natural selection, if possessors of a trait are more fit under the condition that causes the bottleneck (if the condition is a draught, better water preserving traits would be favoured for example). Or the process may be associated with drift if individuals don't have traits that would provide them an advantage (if the condition is a volcano eruption, survivors would be random with respect to their alleles).
Founder effect refers to an event when a small subpopulation migrates to an isolated region. Isolation may be due to distance or some geographic agent.
Here, again the individuals to form the subpopulation may be random with respect to their alleles, or there may be a selection towards traits that provide some advantage in migration for example.
I think that a population bottleneck is more likely to be associated with strong negative selection and a founder effect is more likely to be associated with genetic drift.
However these concepts are not about relative importance of drift and selection. (I emphasized my answer on drift/selection because the question considers them as examples of drift.) These both concepts are about the loss of genetic diversity due to decreased population size, and for that matter, I would say they are the same thing in different ecological context.
Edit:
You can refer population genetics text books by Hamilton (Hamilton, 2009) or Gillespie (Gillespie, 2004) for example. You can find related discussion on sections about effective population size.
There you can see that neither population (or genetic) bottleneck nor founder effect are treated as “examples” of genetic drift or defined as events caused by genetic drift.
Let me explicitly state my point.
Population (or genetic) bottleneck and founder effect are events (driven by some ecological factor) of sharp but temporarily decrease in population size. Due to this decrease, genetic diversity is decreased and stays low even after population size increase again. This is an example of the case, where effective population size and census population size are very different.
Now comes the part creating the confusion:
Both of these effects enhance genetic drift. But they are not caused by genetic drift. Genetic drift can be effective also when population size does not decrease.
Also they are not necessarily examples of genetic drift, meaning that, there may cases where the ecological factor causing the mentioned effects does not affect individuals within population randomly with respect to some of their traits. In that case some loci will lose its allelic diversity due to selection. But here again it is not selection that causes the mentioned effect, the cause is some ecological factor. The ecological factor causing the bottleneck may or may not cause selection. Population expansion/shrinkage is a dimension, selection/drift is another dimension.
Gillespie, J. H. (2004). Population Genetics: A Concise Guide (2nd ed.). Johns Hopkins University Press.
Hamilton, M. (2009). Population Genetics (1st ed.). Wiley-Blackwell.

So the bottleneck effect can happen due to a strong selection pressure too?? Interesting! Could you add in a reference?

Even though the reference I mention is not the most scientific one, it clearly differentiated selection and drift

You mentioned that the two effects are not examples of drift.Is it because natural selection has a role in bottleneck effect? My Text says they are.. So can you give a reference?

Ha! school mein thats how they taught.. Maybe this is correct. Lets wait for the reference :)

To emphasize again, genetic bottleneck or founder effect are caused by (are due to) neither genetic drift nor natural selection.

The Founder and Bottleneck effect are both examples of Genetic drift as you mention. The end result is pretty much the same, i.e., a reduction in the genetic diversity of the population. The main difference is the cause underlying the drift.
Say there's a very colorful ethnically rich and all population. As in, having whites, blacks, Chinese, Indians and all.. Suddenly two blacks are for some reason disappointed and migrate to an uninhabited island. The future generations would definitely be black. So the initial population which had all these Indians Chinese and all was definitely genetically more diverse than this population of only blacks. So this Founder effect lead to a reduction in genetic diversity (compared to the original population) - due to the fact that only the blacks chose to colonise.
On the other hand, the Bottleneck effect happens when there's a natural calamity. Say, there's an earthquake in the area where our rainbow population resides. All houses have collapsed and people have died except for the house in which the blacks lived. This happened just as a matter of chance. This is very important since it should be differentiated from natural selection. If the blacks survived because they were too smart to run out of the house during the quake unlike the others or if they were too strong to hold the roof even as it was collapsing, a component of selection would be introduced since they (or their progeny) would be genetically predisposed to do a similar thing if the earth shakes sometime later.
But here in genetic drift which is another explanation for evolution, different from natural selection, its just a matter of chance.
So all in all, Founder and Bottleneck effects are different in their cause not the effect which happens to be the same.
There are some real examples which I would urge you to refer online.
Here's a reference similar, simple and crisp
http://science.opposingviews.com/comparison-bottleneck-effect-founder-effect-5188.html

Do you have any citations/sources to support your answer?

Yup. Just adding them in :)

I wouldn't write my answer if I saw yours before I post. But I am not sure if these effects are defined such that they refer only to cases where selection is not taking place.

Thanks for the reference, but the confusion arises: does selection have any 'role' on bottleneck effect or is it just a matter of chance? That is where the difference is in the two answers.


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how to make plasma cells adhere to the bottom of a microplate?
I am isolating single plasma cells by FACS sorting into 384-well plates, with the intent to assay the supernatant and clone H/L chains from positive wells. The efficiency of the PCR is however low, because the medium must be removed, yet many plasma cells get sucked up during medium removal. Is there any way to make plasma cells adhere to the bottom, and therefore withstand sucking? I am thinking of poly-L-lysine, gelatine, or similar things - but I do not know whether these would be effective, or even tolerated by the plasma cells.

Have you tried spinning the plate down (say, 400xg for 5 minutes) just before removing the sup, then using a robot to slowly aspirate 1/2 or 2/3 of the well?

We use a PE Janus to suck the medium, and may be moving to a Biotek robot. The problem is that >95% of the medium must be sucked off, or else the PCR won't work. Spinning will not help since microscopy shows that the cells are already at the bottom of the plate. I still wonder whether some kind of gluing may help.

Oh, I didn't realize the PCR wouldn't work with excess liquid. How long are you culturing the cells before assaying for Ig (I assume) in the sup and deciding to PCR? If it's a relatively short amount of time (maybe 24-36 hours or less?), I can't see great harm in trying poly-D-lysine or gelatin or something. Have you tried Corning's Cell-Bind plates? I've had mixed results with them increasing adherence of suspension cells. Unfortunately, I haven't every tried adhering plasma cells, as I've always had microfluidics devices available should I need to do single-cell cloning.


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What makes worms' eggs float or sink?
In parasitology, while examining the stool sample, one important thing you do is test whether the eggs float on water or sink. We never did that since our coursework limits itself to microscopic examination, but we still are expected to remember examples of eggs under each
category.
So my question is, what makes flotation such an important criterion? And how is it done? How do you know if the eggs are floating or not? Does it depend on from where you take the sample (as in, add the stool sample to water and then either take from top or bottom)?
Another interesting thing we are expected to remember is that the fertilized eggs of Ascaris float while unfertilized ones sink. What's the basic funda behind all this? What's in fertilization that changes the buoyancy?

Are you sure you've got the test right? From a quick search online it sounds like the test for fertilised Ascaris eggs is done with zinc sulphide solution rather than water, so the density is different. Furthermore, it sounds like with zinc sulphide it's the unfertilised eggs which sink, not the fertilised ones (http://www.med-chem.com/para-site.php?url=org/ascalumb).

@arboviral sorry! Ya, its the other way round. Edited :)

Okay, I found the last part of your question the most interesting and can't give a full answer to that, but I just noticed I can answer the rest so here goes.
How it works (the simple version)
It works on the principles of buoyancy. The eggs and oocysts are less dense (lighter) than the fecal flotation solution and, consequently, they float on the very surface of it. The feces themselves are more dense (heavier) than the fecal float solution and, as a result, they sink to the bottom of the solution, out of the way. Commonly used flotation solutions include sodium nitrate, Sheather's sugar solution, zinc sulfate solution, sodium chloride solution and potassium iodide solution.
The eggs of some important parasites (for example. Schistosoma species and Fasciola hepatica) are more readily diagnosed by fecal sedimentation (sediment) tests because their eggs tend to sink in flotation media.
What makes it so important?
Some parasite eggs float and some don't. Faecal flotation is a simple, rapid and helpful diagnostic that narrows down the agent causing the clinical signs in the animal.
How it's done
Use a "Fecalyser", a commonly used test kit for faecal floats. The best stool samples to get are those that are fresh - straight out of the animal within the last 30 minutes where possible. Detailed walkthrough of the protocol here and video tutorial here.
Why is there a difference in the buoyancy of fertilised versus unfertilised eggs?
No idea, sorry.  Similar effects are seen in some insect eggs - Stomoxys eggs which sink mostly hatch, while floaters don't hatch. The fact that Anopheles eggs have floats and Culex lay egg rafts implies to me that their viable eggs would otherwise tend to sink too (this could be to do with oxygenation levels being higher at the surface, but I'm speculating here). During embryonation, a serosal cuticle forms which makes the eggs highly desiccation-resistant; non-viable eggs dry out. However, according to some sources online it sounds like for parasite eggs it's the unfertilised eggs which sink, not the fertilised ones.

Thanks! Now I get it! This method can be used only for eggs that float, eggs that don't, simply sink along with the debris and are not picked up on the slide/cover slip, so we just can't see them! (At least using this method) I had thought that a sample is taken from both the meniscus and the sunken part, but I guess only the meniscus is used. Thanks :)

Glad to help! There is something called a sedimentation test or sediment test for eggs that sink; I've added a couple of lines to the answer mentioning them.

@Polisetty Any chance you could accept this if you're happy with it? :)

Waiting for the why part..

I'm at a meeting of (mostly) parasitologists this week, so I'm trying to get an answer to this for you...

Whoa! That'd be great!! :D

Nobody knew. Although someone did point out that potentially a more interesting question is why Ascaris would lay any unfertilized eggs...

Whoa! That's an altogether new and amazing question! Sometimes it amazes me on how we fail to question such stuff, which is right in front of our eyes!

Agreed! This has turned out to be a particularly interesting question, by the way - thanks for asking it.


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Is there a way to determine how many times a given cell divided?
Do cells divide into exact duplicates? If not, is there a way to determine how many times a given cell divided?

I suppose you implicitly talk about multicellular organisms and implicitely mean "since last fertilization" and not "since the origin of life" or anything else. Is that right?

Do you ask this question by curiosity or because you are trying to achieve something specific?

@Remi.b yes, multi cellular, since last fertilization. Curiosity, and maybe a way to determine "objective" age of an organism

There is no such thing as objective age except eventually the time separating fertilization to the current time. You are trying to find an estimate of this age, not a new definition of the age of an organism.

Telomere length is probably something that you want to consider.

Can you provide some clarification on what kind of cell you are interested in? While come cells do lose their telomeres, others do not. We are not even considering prokaryotes here, are we?

Yes, its called the HayFlick limit. A cell will divide until their telomeres reach a critical length,which is usually around 40 to 60 cell divisions. The cells then enter cellular senescence and cease to divide. However, cells may also stop dividing due to (ROS) or reactive oxygen species, cell to cell fusions, or activation of oncogenes, the latter of which is a gene that has the potential to cause cancer.


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When you have your gallbladder removed, how does it affect bile flow into your small intestine?
Cholecystectomy, or surgical removal of the gallbladder, is an extremely common operation around the world. The gallbladder is typically viewed as a storage organ for bile produced by the liver, but is not necessary for life.
The classical teaching from digestive physiology is that bile is stored in the gallbladder and then released in a pulsatile fashion from the gallbladder in response to nutrients/hormones in the intestine during a meal. The major function of bile for digestion is to solubilize dietary fat so it can be digested by digestive enzymes in the small bowel.
When you don't have a gallbladder and there is no storage of bile, how does that affect bile flow into the intestines? Has anyone ever examined the effects of gallbladder removal on the release of bile from the liver? Is bile continuously released by the liver or is there still pulsatile release in response to intestinal nutrients?

Bile is stored, concentrated, and acidified in the gall bladder. Schwartz Principles of Surgery ch. 32 has a good section on this. After recovery from an uncomplicated surgery, the loss of the gall bladder does surprisingly little (other than, usually, resolve the symptoms of gallstones). This was a bit of a surprise to the medical community when the first cholecystectomy was performed in 1882, and it remained a controversial procedure for some time.
There are a number of studies on the effects on bile flow and the overall cyclic release, reabsorption, and return to the liver of bile via the portal vein called enterohepatic circulation.  Animal and human studies demonstrate compensation by the liver, bile duct, and the sphincter of Odie. Overall bile flow is reduced, there appears to be greater release into the intestine during fasting states, and there do appear to be changes in the composition of bile, but, most importantly, enterohepatic circulation is still pulsatile, in response to a meal, as you can see in the figure below.

Both solid lines are subsets of bile acids, measured in the serum of cholecystectomized patients in a classic 1978 study. The shaded areas represent control (not cholecystectomized) patients. These measurements suggest that enterohepatic circulation still follows a pulsatile pattern after cholecystectomy.


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Is the amount of blood same in the pulmonary and systemic foetal circulation?
We learn that the stroke volume is the same for the right and left side of the heart. So the amount of blood in either circulations should also be the same. (is it? I myself doubt this statement. As in, does it need to?)There's also a list of adaptations in the pulmonary vasculature that accommodates the huge volume of blood. But that's the adult. What about the foetus?
My doubt is that, in the presence of a patent ductus arteriosus in the foetal circulation, doesn't this distribution change? This shunting of blood into the systemic circulation would result in a low pulmonary venous return and hence, a low left ventricular stroke volume. So in the foetus, both blood distribution (in the two circulations) and also the stroke volumes (of either side of the foetal heart) should be differrent. Is this so?
This actually concerns me because the DA joins after the initial three branches (left brachiocephalic and the carotids). So, wouldn't such a shunting drastically reduce blood flow/perfusion to the brain? As in there would be decreased flow to the carotids when compared to the adults.
Finally, what are the consequences of the differential blood volumes in the two circulations and differential stroke volumes of the two ventricles due to a patent ductus arteriosus in a foetus? (If happens)


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What is the oxygen carrying capacity of reticulocytes?
What is the oxygen carrying capacity of immature red blood cells, or reticulocytes? Is there any difference between oxygen carrying capacity of mature and immature red blood cells?

This was studied by Steve Fishbone et al and concluded that the Hb content of a Reticulocyte is slightly higher than that of a mature RBC. The CHr, which is the Hb content of a reticulocyte in CRF patients receiving Erythropoetin is around 27.5 +/- 2.5 pg
Ref: Fishbone S, et al. Reticulocyte Hemoglobin Content in the Evaluation of Iron Status of Hemodialysis Patients. Kid. Int., 1997; 52: 217-222

Interesting.  Is this the Hb content per cell?  Is it considered a normal value?

Hi Roland! Thats the value in CRF patients! It could be slightly lesser by about 5-10% in normal individuals


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Accessing Expression Levels for Genes of Interest from GEO Experiments
I have a list of 100 lncRNAs (long non-coding RNAs). For each of these RNAs, I would like to query GEO to find any experiments that used a high throughput sequencing platform and detected expression levels of that RNA in FPKM. To filter further, I'd like to have those expression levels found in controls only. The last filter is to find experiments which found the specific RNA's expression in smooth muscle tissue.
Here are some example lncRNAs:

CDC37L1-AS1
LCMT1-AS1
FLJ21408
CDIPT-AS1
LINC00920
TAT-AS1
SUZ12P1

Is there any way to do any of this? Any help would be appreciated.
Thanks.

You cannot query GEO or SRA using the gene names that are present in an expression data. You have to manually do this. Or you can download selected datasets. Otherwise, as Maxim has pointed out, you should refer to papers/databases that have collected information from different datasets.

You could look at supplementary and methods section of "The Landscape of Long Noncoding RNAs in the Human Transcriptome" paper. They've collected RNASeq samples from TCGA, ENCODE and MCTP and processed it with their pipeline (most of it are filtering and GSEA) to detect novel lncRNAs and associate them with cancer pathogenesis. Their statistics, processing and cross-validation look clean and accurate.
To extract signatures from GEO, you could use GEO2Enrichr. Then calculate the differential expression of tissue-specific libraries in Enrichr. Also, you could submit gene list to Enrichr's Crowd libraries and find GEO entries with a reasonable number of mapped genes first.

That paper had some great baseline FPKMs of interest. Using R, I was able to grab their data and work with it nicely. Thanks for the help.


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Why don't rats have a gallbladder, unlike other rodents?
It has long been known that rats do not have a gallbladder, though other species including humans, monkeys, cows, reptiles, dogs and mice, all have a gallbladder.
In this paper from almost 100 years ago, scientists were studying what differences the presence or absence of a gallbladder gives the composition of bile. The authors found (what we now appreciate very well) that bile from mice who have a gallbladder was much more concentrated than rat bile - i.e. one of the functions of the gallbladder is to concentrate bile.
I know this is a very speculative question, but is it known whether having or lacking a gallbladder confers some sort of evolutionary or biologic advantage (or disadvantage)?

It is perhaps worth noting that rats aren't unique in this respect. Although most rodents and lab mice species have a gallbladder, there are other rodents (e.g. species of mice and gophers) that lack a gallbladder. Equines, most camelids, cervids, cetaceans, and many birds also lack a gallbladder.

@HarryVervet completely agree - thanks for including these other species. It seems so random that some species have a gallbladder and some do not.

Just providing a possible thought here: it might also be worth considering that the disadvantage of having a gallbladder includes the potential development of life-threatening diseases in the gallbladder. Infection of the bile duct, duodenum or pancreatitis can occur due to the formation of gallstone, which is formed from bile components. Having a gallbladder allows bile to concentrate, possibly increasing the risk of developing gallstone-induced diseases.

You only need a gallbladder if you have a diet rich in concentrated fats or engage in binge eating (aka most carnivores), otherwise the liver can produce bile on demand just fine. leaf herbivores and other animals that eat low concentrations of fat or forage continuously like rats don't need the gallbladder.

Just a thought: A gallbladder not only has advantages. For example if humans contract Salmonella infections some get chronic infections. And "excrete" (life)long these bacteria with their faeces. And as a matter of fact its the gallbladder where the Salmonellae are nesting. Maybe this could be a reason why it can be advantageous to have none, especially when you have an urban rats diet?!

There are many different theories on this aspect of evolution, some of them are proved and others are just conjectures. Materials and research in this particular aspect is very few. Here I tried to provide an answer in reference to the particular animal you mentioned, i.e. rat.
Rats don't have a gallbladder possibly due to the following reasons -

The concentrating power of bile in rat's liver is high, so the main function of bile concentration by gallbladder is unnecessay in them. This is probably the most supported theory regarding this.
Rats frequently take their food so they require a continuous supply of bile. This eliminates the necessity of bile storage.
Harbivore animals relatively lack fat in their food. This reduces the need of large amount of bile salts in the intestine.

References -

https://theparadigmshiftgroup.com/animals-no-gallbladder/
Zoology textbooks
http://www.sciencedirect.com/science/article/pii/S0375090613000323?np=y

As I understand the main purpose of the gallbladder is to ensure the full digestion fatty or otherwise difficult or complex foods to digest in support of the liver.
Both rats and mice breastfeed for about the same amount of time 4-5 weeks.  but mice don't have gallbladders; it's likely not a simple matter of ingesting less fat in their diets. Most mammals including humans developed gall bladders through evolution to aid in the digestion of fatty diets into adulthood.  Rats instead developed larger cecum for the slow digestion of seeds and grains, which works in them because of their very specific gut microbiome.
http://www.drturumin.com/en/GallAcids_en.html
**http://www.differencebetween.net/science/difference-between-a-human-digestive-system-and-a-rat-digestive-system/

Please give the answer directly and provide references for it rather than giving a reference instead of an answer.

It's probably due to the fact that rats have an usually "harder do digest" diet. A gallbladder means a source of extra bile at the time of digestion. As you said mice have one but smaller, possibly rats used to have one of the same size, but as they adapted to urban live, bigger ones became advantageous.

Any sources you can add to this?


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What causes people to feel sleepy due to recycled air?
I notice this the most in cars, when I set the air con to recycling air (instead of pulling in fresh air). After a while, I start to feel sleepy, and the sleepiness passes almost as soon as I open a window or change the air con setting to bring in fresh air.
I notice it also in shopping centers, or long bus rides, where there is inadequate fresh air. I know a lot of people who get sleepy from this, but also some people who just notice the air smelling 'stuffy' - but there's no particular smell, just 'stuffy'.
What causes recycled 'stuffy' air to smell stuffy? Is the sleepiness to do with increased Co2 / decreased O2 due to people breathing? Then is the 'stuffy' smell just the smell of CO2?
Any ideas how big of a change in concentrations we're talking about? Wikipedia says concentration of O2 in air is 20.95%. So are we talking about a drop by less than 1%, or a drop by a few %, etc.?
Is this 'stuffy air' bad for you? e.g. hypothetically if I have trouble sleeping, could I seal my bedroom (as sealed as an ordinary passenger car is), install an air con, and have it start recycling air when it's bedtime. Would this be bad for me long term?

do you have any reference besides your own experience to confirm that other people are also feeling sleepy with recycled air?

Yeah, just google "recycled air drowsiness". It doesn't seem to be unusual, and there are some articles / forum threads where people talk about CO2 levels. Although nothing about O2 levels (Does higher levels of CO2 necessarily mean lower levels of O2?). I'm more interested about whether it's bad for you, i.e. the sealing my bedroom and using an aircon hypothetical.

Happens with me too!! :D But wouldn't recycled air also have lesser oxygen?

@Polisetty yup that's kind of what I'm wondering about...

It's more of a psychosomatic phenomenon.  Your car isn't air tight, even if you have the internal air switch on.  Hence you can sleep in your car with the windows up and not die.  If it was O2/CO2 content you'd never know the difference and not be able to identify it as stuffy. Neither of those gases have a smell.  Likely it is reminiscence of smells in that air or the warming of the air that is making you sleepy.  If you actually sealed your bedroom, depending on it's size and your height from the floor, you could die from the CO2, so i would say take some Ambien.

Lot of questions in your post. You should try to emphasize one of them

Carbon dioxide is not the only waste product which is exhaled. NASA scientist Wolverton goes into detail in his book, "How to Grow Fresh Air".  We exhale 70% of the body's waste products in gaseous forms.  Breathing these in repeatedly and at ever-higher concentrations causes a whole host of health problems, starting with, you guessed it, an inability to stay alert and sustain full brain function.

Good question. CO2 doesn't smell though, it's one of the many odourless gases. That stuffy feeling is a very mild CO2 toxicity. But there would most likely need to be a change of more than 1% for a significant change in comfortability as we exhale 15.74% of that of that 20.95% unchanged. The sleepiness is caused both by the mild CO2 toxicity and the lack of O2 to your brain and muscles. Installing an air con largely depends on the size of your room (bigger is better), your age (younger is better), and your overall health, specifically how much physical activity your sustain on a day to day basis. Assuming you sleep for 8 hours you would only need 0.2 kg of O2 (0.6kg/24hr is needed for the avg. person at rest). If your room was the size of a twin bed (hypothetically) there would be around 0.15kg of O2. Taking the exact measurements of your room, you can calculate the amount of oxygen available using the molecular masses available on a periodic table. Personally, I feel you should be fine even without an air con but consider the factors listed above.
This is a very useful equation: kg = number of moles over molarity. But, you can always use a site like this: http://www.unit-conversion.info/molar-mass.html.
This is a copyrighted material so I can only give a reference: Organic and Biochemistry for Today, 7th Ed. ISBN 0538734310 Seager, S.L.; Slabaugh, M.R. Thomson/Brooks/Cole

Isn't it 75.13% of the 20.95%?

No 15.74% (approximately, most text books will give a range orbiting around 15.7%)

Which part of your answer is the reference relevant to?

It's semantics.  You've stated it "15.74% of that 20.95%", which sounds like 20.95% times 0.1574 giving you a return of 3.30% from the 20.95%.  75.13% of that 20.95% is 15.74%.


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Pooling for qPCR
I am comparing miRNA expression levels in 3 different groups but I am low on money and time. I have to get some preliminary results to get the actual research going so I decided to pool my samples and get the results for 372 miRNAs and then if any of them shows prominent differential expression, I will investigate the expression levels of those candidate miRNAs in larger groups. But I can't decide how to group my samples for pooling. Should I pick 3 individual samples for each of the 3 groups (9 samples in total) or should I extract the total RNA for each sample for each group, make 3 pools of RNA and then just perform triplicates for each pool? The time and money spent in both situations is going to be the same. I think the second method is more appropriate yet I fear it might produce some deflated p-values, resulting in false discovery.

Should I pick 3 individual samples for each of the 3 groups (9 samples
  in total) or should I extract the total RNA for each sample for each
  group, make 3 pools of RNA and then just perform triplicates for each
  pool?

Depends on the nature of your samples. In general, pooling would average out the expression of different individuals. Pooling is generally done when you have low RNA yield per individual sample. If that is not the case then you should sample multiple individuals per group (three should be fine; more is better). This will let you know inter-individual/sample variation within a group. You can in turn set up three technical replicates for the qPCR to measure technical variation. So, in total, you would have 27 PCR reactions. This would not be very costly (unless you are using TaqMan like assay. Even then, sometimes working with more number of samples allows you to save the amount of reagent used per sample.


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Why do fruits have to ripen?
It seems like most fruits that we consume undergo some sort of ripening process either before or after they are picked from the vine, tree, etc. I understand that sugars are released during the ripening process and this is why ripe fruits are sweeter and more palatable than non-ripe fruits.
Why, though, do fruits have to undergo this process of ripening?
Wouldn't it be simpler to just grow and already be "ripe"? Does the ripening process confer some sort of advantage to the plant?

@DavidBlomstrom that would make a lot of sense - I don't know much about botany, but if the seeds aren't developed before the fruit is ripe that would be a reason that you wouldn't want to grow a "ripened" fruit. I guess I was thinking about it from a fruit consumer perspective, not a plant development one - thanks for your comment!

Some of the main reasons for delayed fruit ripening are to protect immature seeds, to save energy, and incompatibility between fruit and flower morphologies.
Fruits that are sweet have generally evolved that way in order to attract animals that disperse the seeds. But, this attraction is only useful once the seeds have been fertilized and fully matured. If a plant were to develop a fruit that was immediately sweet this would attract the animals too soon and they would remove or damage the seeds before they were capable of producing a new plant.
Sweet fruits are very energetically costly. Many plants produce many more flowers than actually get successfully pollinated. It would be a great waste of energy to fill the ovaries of those flowers with sugar when the ovules might not ever get fertilized. In fact, one of the main theories for the success of flowering plants is the ability to abort fruit development in unsuccessful flowers.
Finally, in most cases having fully-formed fruits would get in the way of flower pollination. One of the most common arrangements of floral parts is to have the ovary sit between the petals and the stigma (superior ovary, hypogynous). If the ovary were very large that would render the petals useless. For plants with inferior (epigynous) ovaries, large fruits would probably ruin the arrangement of the floral display. A large fruit would also increase the distance between the stigma and the ovules, forcing pollen tubes to grow much longer, possibly reducing or delaying fertilization.

Mature, viable seeds have to form in most fruits, which involves the maturation of embryonic tissue. That can take a little time, from just a few days in some weed species to months and perhaps longer in some fruits like pineapple.


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What is the difference between [Clinical Trials as Topic] category and [Clinical Trial [Publication Type]] category in pubmed?
Dears in biology stackexchange community, I hope that everyone is fine.
I am using pubmed in my current review. My focus is about an application on the scope of Clinical Trial. When I used MeSH for narrowing my research scope on Clinical Trial, I got two different categories which I cannot find any clear difference between them. They are:

Clinical Trials as Topic
Clinical Trial [Publication Type]

However, when I search on the two different categorises, I found very different resulted papers. That means that there are a difference between the two categories where my ignorance is.
Could you please tell me what is the difference?
Possible examples of two queries:
1. ("Clinical Trial" [Publication Type]) AND "Prostatic Neoplasms"[Mesh]
2. ("Clinical Trials as Topic"[Mesh]) AND "Prostatic Neoplasms"[Mesh]
Many thanks to you for your time, in advance.

The actual definitions provided with the MeSH terms look essentially interchangeable:
Clinical Trial as Topic:
Works about pre-planned studies of the safety, efficacy, or optimum dosage schedule (if appropriate) of one or more diagnostic, therapeutic, or prophylactic drugs, devices, or techniques selected according to predetermined criteria of eligibility and observed for predefined evidence of favorable and unfavorable effects. This concept includes clinical trials conducted both in the U.S. and in other countries.
Clinical Trial [Publication Type]:
A work that reports on the results of a clinical study in which participants are assigned to receive one or more interventions so that researchers can evaluate the interventions on biomedical or health-related outcomes. The assignments are determined by the study protocol. Participants may receive diagnostic, therapeutic, or other types of interventions. While most clinical trials concern humans, this publication type may be used for clinical veterinary articles meeting the requisites for humans.
But the difference is simple. CT as Topic refers to publications that talk about Clinical Trials in general, as a subject itself. But CT[Publication Type] refers to an article that is actually reporting the results/analysis of one or many clinical trials.
To show you what I mean, these are first PubMed results using the two MeSH heading, when you specifically tell the search engine to not include other branching MeSH terms:
Clinical Trial as Topic:

Clinical Trial[Publication type]:

Dear Maljam, many thanks for your kind, generous and clear answer. You helped me a lot, bless you.


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How does Ultra-pasteurized milk compare with pasteurized milk?
I am specifically interested in whether all proteins and nutrients lose their structure permanently because of the very high temperature of ultra-pasteurization.
What is the case for pasteurized milk?

Have you done any research on your own? What have you found?

From the basic web research I did, I found that many proteins are permanently destroyed. However, I would prefer someone with references to a study on this.


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Whole gene sequence analysis to determine source infection
Is it possible to use whole gene sequence analysis to distinguish between a common source infection and a person-person disease transmission?

Is this a question out of general curiosity or is it part of a homework or research project?  I ask because while genome sequencing of pathogens can be used to distinguish routes of transmission, it is not usually necessary.  Usually just sequencing specific regions is sufficient.

Thanks for this. A guest lecturer referred to this practice while giving a talk. I cannot understand the process or understand how it would work. Many thanks.

Are you able to comment any further  please?

Sure, the idea is pretty straight forward.  Suppose you have a single source of an infection: each new infection should be fairly similar to that original source.  However if the infection transmits person to person, each new copy should be similar to the original copy, so errors will be more likely to accumulate.


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What happens to the cell during post-hypothermia?
A friend of mine said that the cell membrane somehow changes after rewarming from hypothermia and that the body does not recognize it's own cells, thus leads the immune system to attack it self. Is this true? And do anyone know how/why the cell changes?

interesting question - we use therapeutic hypothermia in critically ill patients following cardiac arrest  commonly in the hospital - I've seen patients wake after 48h of hypothermia and have no long term effects (at least that are detectable) - not sure how things change on a cell membrane level or whether or not this has been studied in  patients

here is a link to a open access paper from the journal Circulation that discusses therapeutic hypothermia and how long/how cold we keep people - as well as a discussion of whether or not we should cool people longer and/or colder... should be useful for this question... http://circ.ahajournals.org/content/131/7/669.long


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Cloning Ice Age Lion Cubs
It was just on the news that scientists discovered "Two cubs in Russia's Sakha Republic last August in a near-perfect state".  And the South Koreans and Russians are attempting to clone these extinct Ice Age lion cubs. (Link to one such news coverage)
According to this answer, we seem to be able to sequence its genome but cloning may be difficult.  However, is this find likely to be the rare large chunk of well-preserved material that makes cloning possible?

The answer that you link to provides a pretty good overview of what it might take to clone an extinct organism from preserved tissue and what some of the challenges are. I won't repeat that answer, but in a nutshell, two big obstacles are incomplete sequences and a host womb.
To get at your question of whether this preserved "chunk" of flesh will lead to the cloning & revival of extinct species...you're a little late to the game. :-)
In 2003, researchers used preserved DNA to revive the Pyrinean Ibex, a goat native to the Iberian Peninsula, that had recently gone extinct. The results were mixed. The experiment worked, in the sense that the scientists were able to successfully bring a recently extinct animal to term, but unfortunately, the revived goat only lived for a few brief minutes, due to developmental abnormalities. It's important to note that this was achieved using DNA that was even better preserved than that of the cave lions in the Mirror article.
So, will the DNA found in the cave lion cells lead to successful cave lion revival? If such a revival occurs, I'm betting that it will be due to advances in how the ancient DNA is integrated with reference DNA and in how fertilization and implantation are carried out, more than on the quality of the found DNA.


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How many calories do gut bacteria burn?
It has become well-accepted that microbiota of the gut (a.k.a. gut bacteria) consume calories that are ingested and can have significant effects on energy metabolism in humans. For example, if you take the feces from mice that have had a gastric bypass and transplant those into the colon/GI tract of obese mice, then the obese mice lose weight (See here for article about this study).
Are there any known estimates on how many calories the typical gut microbiota in an adult human consumes? That is, about how many calories your gut microbiota use per day?
For more information there is a freely available source on Pubmed, "The Human Microbiome, Diet and Health Workshop Summary."

Depends on the diet, right?

@WYSIWYG I don't necessarily think so (but definitely not sure). If someone is eating a diet high in fiber I'm sure that the microbes have increased access to that compared to amino acids, carbohydrates and fatty acids that can be transported across the intestine into the body. The GI bacteria must be in some sort of steady-state because they aren't overtaking anyone's body, thus you could assume the energy utilization by the entire gut microbiome is somewhat constant (I think) - I'm wondering how many "calories" that would be overall that we're eating, but they're actually using.

A recent study by Bahr et al. found that "healthy" gut microbes increased non-aerobic resting metabolism by 16%, compared to gut microbes being treated by risperidone. Risperidone is an antipsychotic drug that causes weight gain and Bahr et al. were trying to determine why. In addition to to the article, their university issued a non-technical press release on the article.
This article doesn't exactly answer your question but does provide a good staring place.