What causes us to see white light? Humans have three cones of color light, red, green and blue. If the region of the green cone is hit by his photons we will see green light. Now we don't really receive green light but our eyes and brains are 'making' it to look green. But if all the different cones are hit by their photons we will see white. Now the question is why is that white? Why isn't our brain just keeping these different colors, is this a kind of black out of our brain or an overwhelming of input making us blind etc?

Our brain doesn't really use cones to detect green light, and detect red light, and detect blue light. Each cone can be excited by many wavelengths; they're just most excited by green, red and blue wavelengths respectively. The brain then uses the different information it receives from all three cones to infer the wavelengths of the light it receives. It doesn't look at the absolute excitation of a cone so much as the relative amounts of excitation different cones get.

So for example, if the brain sees the green cones are very excited and neither the red or blue cones are, the light is green. If the green cones and red cones are equally excited but the blue ones aren't, then the wavelength may correspond to yellow (a wavelength that excites both red and green cones in the same middling way, and blue cones not much at all), or there could be a combination of green and red wavelengths; and in fact both are seen as the same thing by the brain. That's why colors can combine to make other colors.

This is OK insofar as the point isn't to calculate the exact wavelength of incoming light, but to tell the difference between certain wavelength compositions because that provides more information about the world.

So the reason we see white when hit with all wavelengths is the same reason we see any color when hit with any combination of wavelengths.

As for why "color" feels like a single unified perception and not a combination of three numbers, that's a general aspect of perception in general. We don't sense the raw data our brain gathers; we sense how the world is (as guessed at by the brain from the raw data it gathered).

As such, the colors we see aren't even strictly determined by the wavelengths of photons hitting the cones; because colors are a proxy for what the things we see are like, the brain will not only look at the light it receives, but also use its own assumptions about the world (is this thing in shadow, in bright light, mottled light, colored light, near, far...) to guess at what the color "really" is given the wavelengths it has received. This gives us a sense that color is inherent to objects and doesn't depend on lighting conditions, which is generally accurate (an apple's redness is a feature of the chemicals at the surface of its skin, and those don't change with the lighting conditions).

That's where illusions like that of the blue-black or white-gold dress come from: sometimes you get ambiguous stimuli, where the wavelengths hitting the eye could correspond to a black and blue dress in bright light, or they could correspond to a white and gold dress in shadow, and in that case the brain picks one, and you see the dress as the color your brain decided it must be. Except because the stimuli were ambiguous, different brains (or the same brain at different times) will make different guesses, resulting in very different perceptions. But the guessing is actually what happens all the time, it's just that usually the stimuli aren't as ambiguous so all brains agree on their guess, and the guess does correspond to reality, and so the illusion that we perceive the world directly with no filter remains unbroken.


Immune response to foreign protein In the context of COVID-19, why is it possible to inject someone else’s antibody protein into a person without fear of stimulating an immune response. Does this indicate that, somehow, antibody conformation is universal?
Or rather ...
The immune system must differentiate between cellular and fragmentary material? It will attack any cellular material it deems ‘non-self’. But if foreign non-cellular material enters the body, such as dust, pollen etcetera we are in the realm of an allergic response. The allergic response is not absolute: only certain materials will cause a reaction.
So perhaps foreign protein, such as donor plasma products, are treated as potential allergens which, happily, do not cause an immune response; unlike midge spittle?

The complexity of the immune response requires foreign proteins to be bound first by presenting cells which happen to be like macrophages - cells that are like garbage disposals. Why some proteins are simply gobbled up and yet others are preserved and presented to the resident T cell helper population is related to the size and sequence of the protein. In other cases, even small molecules (allergens) can bind to native normal proteins and make them look abnormal.
The use of immunoglobulin (semi purified blood) was used in treating certain diseases in the past. These sera were usually developed from animals purposely infected with the disease. Though these proteins also elicited their own immune response (side effects) the kinetics of that event was days to weeks whereas the binding of the immunoglobulin to its target(the virus protein) is a first order event occurring in minutes. Clearance of that antibody antigen complex over hours to days Avoids the catastrophic exponential growth of the virus by keeping the numbers low. Eventually tho side effects WILL happen if you keep giving the serum


Can you see the coloration of Sinosauropteryx with the naked eye? In 2010 this beautiful fossil of Sinosauropteryx was put under microscopic examination in order to determine the colors of the preserved melanosomes. It was determined that the feathers were reddish brown with white stripes going down the tail and a white underbelly.

Is it just a coincidence that that's exactly what I would have guessed by looking at the color of feathers in the fossil? Am I falling prey to
hindsight bias? Or is it the case that the feathers are so well preserved that their color is visible to the naked eye?

By Sam / Olai Ose / Skjaervoy from Zhangjiagang, China - Dinosaurs!, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=4209411

Is it just a coincidence that that's exactly what I would have guessed by looking at the color of feathers in the fossil? Am I falling prey to hindsight bias?

Hmm.. TBH, I don't think anyone can tell you that! However, after taking a look at it, I myself may have suggested reddish feathers along the neck and back, with some kind of red/purple coloration going down the tail (though I have no significant expertise in this field).

  Or is it the case that the feathers are so well preserved that their color is visible to the naked eye?

Melanosomes are actually fairly large; about 500 nm (source). Relatively speaking, this is somewhere between the size of the flu virus, and of mitochondria; see here for scale. According to this book, written by the Swiss Institute of Bioinformatics, it states:

  ... besides [zebrafish] being vertebrates like us - their epidermis and their eggs are transparent, and embryonic development can be overved and tinkered with at every stage. Likewise, even melanocytes and their melanosomes are visible to the naked eye.

So, it would seem that it's possible to observe melanosomes with the naked eye, given a high enough (melanosome) concentration. It should also be noted though that, although the fossil did preserve the melanosomes (here), I'm not necessarily sure that that means the color observed in the fossil is the same color that would have been observed in the living organism. If anyone can comment/add to this, that would be quite welcomed.

Here's an image that suggests what this dinosaur would look like, given the discovery and analysis of the Sinosauroterpyx's melanosomes, acquired from the fossil you provided a picture of.


Aquatic Snail Identification I can’t for the life of me find an identification of these snails. They’re thriving in brackish water, but may be freshwater naturally. They’re about .8cm long at their largest. I believe they have live birth due to the lack of eggs but presence of baby snails over the year and a half that I’ve had them.

Looks like a Malayan Live Bearing snail , fairly common in the US aquarium trade. I have inadvertently gotten them into all my tanks. Common aquarium fish can't eat them ( unless you crush them on the glass). I did not know they can tolerate brackish water. Yhey will get to 1.5 mm.


Why do soil bacteria produce nitrous oxide as a result of anhydrous ammonia fertilizer application? The NPR article and 4 minute audio news item Can Anyone, Even Walmart, Stem The Heat-Trapping Flood Of Nitrogen On Farms? discusses unexpected contributions of greenhouse gasses from the manufacture of consumer goods. One example is bread, or agricultural products in general, and part of this is the anhydrous ammonia used in fertilizer.
Carbon dioxide seems to be a bi-product of the manufacture, but nitrous oxide a more potent greenhouse gas is produced by bacteria in the soil as a result of application of ammonia.

Manufacturing nitrogen fertilizer is energy-intensive, burning lots of fossil fuels and releasing carbon dioxide. What's just as damaging, and perhaps even more so, is what happens when it's spread on a field. Bacteria feed on it and release a super-powerful greenhouse gas called nitrous oxide.
These bacteria are naturally present in the soil, says Philip Robertson, a researcher at Michigan State University, "but once they get exposed to nitrogen fertilizer, they really light up" and pump out nitrous oxide.

Question: Is it common for most soil bacteria to make significant quantities of nitrous oxide after ammonia is added, or is there only a small subset of bacteria present in soil that might do this? Also, what is the metabolic pathway in this case? Is this a waste product from "eating" ammonia, or something more complicated/subtle?

below: Anhydrous ammonia tanks in a newly planted wheat field. Walmart has promised big cuts in emissions of greenhouse gases. To meet that goal, though, the giant retailer may have to persuade farmers to use less fertilizer. It won't be easy. TheBusman/Getty Images. From here.

Addressing the first part of your question:

  Is it common for most soil bacteria to make significant quantities of
  nitrous oxide after ammonia is added, or is there only a small subset
  of bacteria present in soil that might do this?

No, not all soil bacteria can oxidize ammonia. According to wiki:

  The oxidation of ammonia into nitrite is performed by two groups of
  organisms, ammonia-oxidizing bacteria (AOB) and ammonia-oxidizing
  archaea (AOA).

The role of archaea in the soil nitrogen cycle is not well-known yet, although it could be greater than that of bacteria. On the other hand, the role and metabolism of AOB are more or less studied.

The process of ammonia-oxidizing is also called nitrification and AOB sometimes referred as nitrifying bacteria. The most known bacteria genera from this group are Methylomonas, Nitrosococcus, Nitrosomonas and Nitrosospira. I think the most studied species is Nitrosomonas europaea Winogradsky 1892.

For reference see: Arp DJ, Sayavedra-Soto LA, Hommes NG. Molecular biology and biochemistry of ammonia oxidation by Nitrosomonas europaea. Arch. Microbiol. 178 (2002) 250-5.

The second part of the question:

  What is the metabolic pathway in this case?

Although, the metabolic pathways vary in different genera, let's look at ammonia metabolism in N. europea.

In the simplest case, it is a two-step process.
According to KEGG:

Step 1. The enzyme ammonia monooxygenase converts ammonia to hydroxylamine. The enzyme contains copper, iron and possibly zinc. It requires two electrons, which are derived indirectly from the quinone pool via a membrane-bound donor. The reaction is:

NH3 + a reduced acceptor + O2 = NH2OH + an acceptor + H2O

Step 2. The enzyme hydroxylamine dehydrogenase converts hydroxylamine to nitrite. This reaction requires specialized cytochrome as an acceptor of electrons. The reaction is:

NH2OH + H2O + 4 ferricytochrome c = NO2 + 4 ferrocytochrome c + 5 H+

While nitrite is the main product, the enzyme from N. europaea can produce nitric oxide as well. Therefore Step 2 can produce nitric oxide (NO). In this case, additional mechanisms of converting NO to NO2 are involved.

Further destiny of released nitrite can be different. In one process it could be oxidized by different microorganisms (bacteria, archaea) to nitrate (NO3) which could be consumed by plants or washed out to deeper horizons with water. In another case, nitrite, nitric oxide and nitrate could be involved in process of denitrification. During this process, a group of denitrifying organisms (bacteria, archaea and fungi) consume nitrogenous compounds and reduce them to nitrogen (N2), which can escape to the atmosphere. This process can occur through different metabolic pathways mainly with aid of reductases like nitric oxide reductase. One of the possible intermediate product of such pathways is a nitrous oxide (NO2). If N2O escapes from cells we can observe a resale of nitrous oxide from soil.

Let's return to your first question, and particularly to the part where you ask about significant amounts of nitrous oxide.

First of all, nitrification is a natural process and is a part of the nitrogen cycle. Some organisms fixate nitrogen and convert it to ammonia, some oxidize ammonia to nitrous compounds and some of them reduce it back to nitrogen. It occurs everywhere virtually in all terrestrial and water biocenoses. In a healthy ecosystem, the inflow of nitrogen is theoretically equal to the outflow (with temporal deposition in trophic chains). In such natural conditions, the release of nitrous oxide should be neglectable.

The situation changes significantly when we add an ammonia to soil artificially as a fertilizer. The main problem is that we break an equilibrium between nitrogen fixation, nitrification and denitrification. The second big problem is that an ammonia is toxic for most organisms, so we can alter microbiome. In such case, we can expect an excess of products of nitrification and improper denitrification with exaggerated levels of released nitrous oxide. The actual proportions vary significantly depending on both biotic and abiotic conditions, therefore it is difficult to predict real levels of nitrous oxide released without in situ examination.

P.S. sorry for possible bad writing.


Why is wound contraction very slow? I am working on mathematical model for healing of dermal wounds. For anyone who's a bit familiar with Physics and Math, for the model I use the Cauchy Momentum Equation as a basis, and from there I use already established literature to expand to a so-called morphoelastic model.

From a physical perspective, if a force is exerted, you would expect a material to start moving, upon which stresses arise, until a new balance is found. This all usually happens on a timescale of second. Now when wound healing is regarded, the contraction force is exerted by fibroblasts. I have read that wound contraction happens at a speed of up to 0.75/mm per day. On the one hand this is impressive, yet on the other hand it is very slow when viewed from the mechanical perspective.

So my question is: Is there a biological effect or phenomenon that slows down? Could it be that the migration speed of fibroblasts is the bottle neck? Or maybe skin is in some way tethered to underlying tissue? I know very little about biology, so any help would be appreciated!

Thanks in advance

Short Answer : You can not pinpoint any single step for this delay. It is a combination of multiple processes.

Long Answer : I think there are multiple factors that can contribute to this. Dermal Wound healing is a multi-step and complex process typically includes inflammation, new tissue formation and remodeling (Gurtner et al 2008). Each of these stages involved very complex signaling pathways of various components. In addition, there are multiple types of fibroblast cells involved in this process. You are most likely talking about Myofibroblasts who bring the edges of a wound together. However, this itself is a very complex process involving interaction with the proliferation and migration of both mesenchymal and epithelial cells. This is further tightly controlled by Keratinocyte-fibroblast interactions (Werner et al 2007).

So what can you do? : The the physical analogy, which you are trying to implement here, has to apply within some assumptions. You can declare some fitting parameter(s) which can contribute to all the process and validate it according to good experimental data, probably with some kind of mutant data where the wound healing process is slowed down or accelerated. While deciding your assumptions, use as fewer assumptions as possible else you will end up creating Spherical Cow.


Classify chemotherapy drugs? I'm studying a TCGA dataset trying to find correlations between gene expression and clinical data which might shed light on some pathways. One column of the clinical data provides a list of chemotherapy drugs the patient received and I'm pretty sure there's a wealth of possibility in this column but I don't know anything about how chemotherapy drugs work or what kinds of things it makes sense to classify about them.

I'm making a spread sheet that will have the following columns:

Drug_Name
Number_of_Patients_Received
Mechanism
Associated_Drugs

But I don't know what else is important to know about these drugs. What would you think is important to know to help understand how these drugs might have played an interactive role with the pathways. Also, if you have any recommendations of online resources, I'll appreciate you mentioning them with a short explanation of what I might find there.
But my primary question is else should I look up about these drugs to help me understand their role/impact.

There's this database of genetic/drug interactions, which I think is pretty much exactly what you're looking for.

Probably your best approach is to classify your drugs into a couple different categories of action. Some drugs will have to be in several categories at once(I'm lookin at you anthracyclines) Dose-dependent mutagens(cisplatin), growth-dependent mutagens(fluorouracil), topoisomerase inhibitors, tyrosine kinase inhibitors, microtubule inhibitors, retinoid signaling, immune adjuvants, and then 'misc'.

Alkylating agents and platinum-containing drugs like cisplatin directly damage DNA, while there are other drugs(methotrexate,fluorouracil) destroy or damage DNA by pretending to be nucleotides and breaking things that way.

Anthracyclines bind into DNA strands damaging it, directly create free radicals, disable topoisomerase II, and displace histones.

There are the topoisomerase inhibitors which prevent cell growth by preventing DNA from being unwound for replication.

There is a fairly diverse(chemically) class of 'mitotic inhibitors' that screw up microtubule formation or proper microtubule dissolution, any of which prevents mitosis.

Sunitinib blocks tyrosine kinases, which are involved in blood vessel formation(and nerve formation and some other things). Other tyrosine kinase inhibitors are more specific to vascular endothelial growth factor(VEGF) receptors, but most tyrosine kinases target more or less specifically VEGFR and related receptors. Some are antibodies, some are just small molecules that bind TKRs.

There are a few retinoid-related drugs most of which influence the vitamin A pathways, like tretinoin, bexarotene, etc. Dual use in skin creams.

Immunoadjuvants are designed to activate the immune system to aid in tumor cell destruction. Interferon-alpha, imidazoquinoline, et cetera.

In the miscellaneous category:  Bortezomib, a short peptide that interferes with proper protein degradation. L-asparaginase slows all protein production by destroying asparagine, an amino acid. Some blood cancers respond to corticosteroids, and some ovarian/testicular cancers are treated with sex hormone inhibitors. Nearly any blood-borne poison works as a chemotherapy agent due to the EPR effect, so heavy metals or radioactive isotopes also are sometimes used. Arsenic trioxide, for instance, is just arsenic.

It's also worth looking at the steroids that are given along with cancer treatment(dexamethasone) to mitigate side effects. As regulatory hormones, there's going to be a hefty impact on genetic regulation from regular steroid injections. If nothing else it's a confounding effect you'll need to control for.

The preparations/solvents of chemotherapy agents can also be significant. Cremophor was used to suspend some anticancer drugs, but recent developments imply that might be on its way out.


DIY storing family DNAs' samples for future uses (eg medical) I have a question I could not get an understandable reply from Google and I am no expert in the matter, so my plead to you is if you could give me practical and relatively easy to follow advice.

With the view of the breakthroughs in DNA research and all the anticipated applications to medicine in the near-future, I am willing to build a storage of the DNAs in my family (eg 20-30 people, some at a very old age). The use may not be for cloning :) but rather, for eg to map and trace specific hereditary genes when such services become more available to the wide public; and thus, probably help with a personalized medicine for someone, or find genome problems, and probably be able to 'turn them off' at some point.

Is there a way I can extract cells (ie from inside the cheek, or hairs), and store them for a few decades while preserving the DNA (eg put them in a freezer at -18C or in some solution)?
I have only common knowledge in this area so apologies if the examples are silly, but I assume you can understand my point.

I would be grateful if you provide practical instructions as: "you buy 500ml of the chemical xx"; or "mix 150ml of xx and 200ml of zz", so me and anyone who finds the idea appealing, can follow.
Ps-the lower the costs of the procedures, the better (I found some personal "dna vaults" costing several '000$).

Thank you for your consideration!

If you have access to a laboratory (or at the very least a centrifuge and pipettes) and some laboratory experience you can extract the DNA from the cells which would be much easier to store. There are a number of commercial DNA extraction kits available that are easy to find on google and order online. I don't want to promote any particular brand but I've mostly used DNEasy made by Qiagen (really just because that's what I'm used to). All the step-by-step instructions are in the kit and all the reagents are also in the kit with the exception of 100% ethanol which should be easy to obtain.

If you have significant molecular biology experience and access to a full lab with a fumehood and appropriate safety installations you can try a manual extraction using trizol or phenol-chloroform. This would be slightly cheaper however given the toxicity of these agents I wouldn't recommend this for you. It really doesn't sound like you have these resources available to you.

Once you have the DNA extracted you can dilute it in Tris-EDTA or the elution buffer that comes in the kit. You can store extracted DNA in a regular fridge (4C) for several years. If you're looking to store for decades you may want to rent space in a -80C freezer but this would be more expensive. A fridge may be just right to suit your needs. You should be careful that this fridge has a backup power supply.

I should be clear that although extracting DNA is the easiest way to do this for somebody with experience, you should not try if you don't know what you're doing. Some of these reagents are dangerous and you are likely to ruin the samples you've taken from your family members and end up with no DNA at all. Good luck!


Why does gaining a hydrogen in biology considered reducing a molecule? I've learnt in chemistry that gaining electrons means reduction, while losing electrons means oxidation. But why is it in Biology textbooks I sometimes come across the term gaining hydrogen??

Hydrogen can accept electrons or donate them, so it can get a bit confusing. For instance, hydrogen donates electrons from a reducing agent. For example, in biology, consider cellular respiration. A co-factor will carry electrons often by reducing an atom with a nitrogen.

Consider NADP+ to NADPH.

The nitrogen atom on the Pyridine group has an oxidation state of +1. When it picks up a hydrogen, to become NADPH, the oxidation state will go to 0 by gaining electrons brought by the hydrogen. Although the hydrogen doesn't bond to the nitrogen directly, it breaks the double bond on the para carbon (The carbon on which the new hydrogen is attached) at the top of the ring, and thus distributes the electrons to the nitrogen.

EDIT -
Hydrogen comes from some reducing agent, not a free hydride I'm sure.


Extracting DNA from a kiwi I have two questions regarding this experiment.

Online instructions say to use 5g washing up liquid, 2g salt and 100ml tap water mixed together with a mashed up kiwi. Do I use a full kiwi ?

Instructions say to use coffee filter paper or a fine sieve. Would laboratory filter paper work or would it be too fine ?

Also, how can I improve on this method to get maximum yield etc ? All advice and suggestions welcome.

Yes, a full kiwi. The method is rather crude and the yield you get is not so high, because you will not break up all cells and also loose some of the DNA which is bound to the cell debris.

Lab filter paper of course works as well, as would a fine cloth (cheese cloth for example). The receipe is designed to work with stuff that people have usually in their kitchen, which is true for coffee filters, but usually not for laboratory filter paper ;-)


Is receptor antagonism just long-term binding? By my understanding, a substance that binds to a receptor and activates it is called an agonist, while a substance that binds to a receptor without activating it is called an antagonist. (Wiki) What is the fundamental difference between binding to a receptor and activating it?

EDIT: I guess the receptor is a complex enough beast that fitting into it and staying there can be accomplished by some sections of the interface being completed, without necessarily completing the "usual" interfacing process between the receptor and its agonist -- thereby blocking the receptor geometrically without imparting the proper energy to it chemically.

The details of activation vary by receptor of course, but talking in the popular key-lock picture:

An agonist is a key, that fits the lock and opens ("activates") it.
An antagonist is a key that you can put into the keyhole, but it does not open the lock. What this means is: while the "wrong" key is in the keyhole, you won't be able to open the door, even if you have the correct key, as long as the wrong key is in the keyhole.

As far as Wikipedia goes, the articles for Agonist (and the links contained therein) might be more informative than the one you quoted.

https://en.wikipedia.org/wiki/Agonist


Why did translation develop a specific codon for initiation? The translation of mRNA is initiated by a specific methionine-accepting tRNA at a specific initiation codon, usually AUG (complementary to the tRNA anticodon). However translation at suitable (albeit unphysiological) conditions in vitro does not require a specific initiation codon or a specific amino acid, so it is not difficult to envisage an earlier stage in the evolution of the translation apparatus in which this specific initiation system was absent. Instead there might have been random initiation or initiation from the 5′ end of the mRNA.

A specific initiation codon puts constraints on the sequence of the mRNA and adds an unnecessary amino acid to the N-terminus — one that is sometimes unwanted and needs to be removed.

  What advantages can one envisage for initiation at a specific internal
  site, rather than at, say, the 5′ end of the mRNA?

I appreciate it is impossible to prove which factor was actually responsible during evolution, but by soliciting concrete explanations I trust that this question is as valid as the original from which it is derived (see Footnote).

FOOTNOTE

This question has been expanded from one part of a three-part question posted some time ago on “Why is AUG the Initiation Codon?”. This recently resurfaced, and as nobody had answered this particular part, and as it is site policy to ask one question at a time, I decided to remove it from the original and repost it here so it could be considered on its own merits, without the distraction of other questions such as the choice of codon or of methionine over other amino acids. I shall contribute an answer with some thoughts of my own, but, of course, anyone can join in.

It is not clear to me where initiation took place in the translation of artificial polynucleotides such as (UC)n which Khorana used in experiments that, following up the work of Nirenberg and Matthaii, helped decipher the genetic code. It may well have occurred at random positions rather than the 5′ end. Such a mode of translation would obviously have been wasteful if it occurred during early evolution as a mixture of products would be formed, many of which would be inactive and might even compete with the active species. If this were the original situation,  it is easy to see how a change to initiation at a specific point would be advantageous.

But why not start at the 5′ end? Contemporary eukaryotic initiation complexes recognize the 5′ end of the mRNA, even though they then scan further to find a specific initiation codon that will respond to the initiator tRNA. As there is no physical separation of  genes on a chromosome, it is obvious why transcription needs to start at a specific point within the DNA, but the need not be true for the translation of individual mRNA transcripts.

I can see two ways of approaching this question.

The first is from the standpoint of the contemporary ‘DNA World’. The arguments one can make  include:

In a general sense 5′-end initiation may be regarded as restrictive
in that it would not allow the 5’ end of mRNA to provide other
functions such as forming a secondary structure to regulate the ease
of translation.
5′-end initiation would preclude the polycistronic mRNAs we see in
contemporary bacteria.
In 5′-end initiation it might have been difficult to distinguish the
ends of mRNAs from other RNAs before the modification of bases that
we see in contemporary eukaryotic mRNAs had developed.
Likewise, as suggested by @John in a comment on the question, 5′-end initiation might have caused translation of fragments of RNA as they degraded.
The selection of a specific codon was secondary to the need for a
single initiator tRNA, which has been discussed in relation to
another SE question, although the arguments there relate to more recent stages in evolution.

However there is another approach which considers the situation in a putative ‘RNA World’.

The difference here is that — like some contemporary RNA viruses and bacteriophages — the genome might also have been the mRNA but without a system to produce many copies of the ‘plus’ strand for translation. Translation may have been on the genomic RNA.

To translate several proteins it would have been advantageous to have
several initiation sites on what would have been a polycistronic
messenger (rather synthesize a polyprotein like poliovirus).
The 5′-end of the RNA may not, in any case, have been available for
encoding protein as it might have another (e.g. replicative)
function, and it is also possible that part of what in contemporary
systems is a separate part of the translation apparatus was
physically incorporated into the genome.


A little help understanding DNA supercoiling I am studying molecular biology from Lewin's Genes XII and got confused in the supercoiling topic. Since then I read from several other sources and so far understood the following. However, I can't seem to connect the dots. A bit of help in connecting the dots would be greatly appreciated.

So these are the stuff that I understand so far

Supercoiling is coiling of already coiled double helix
Positive supercoiling overwound the DNA (increase the number of turns thus decreasing the number of base pair per turn making it more twisted)
Negative supercoiling underwounds the DNA
Linking number is the sum of twist and writhe, twist is basically number of turns and writhe refers to the number of supercoil. It remains constant as long as phosphodiester bonds are not broken
unwinding DNA at replication fork results in positive supercoil downstream

Now coming to the confusion

In the diagram we can see that negative supercoiling has taken place. Twist value has gone up and to compensate that (to keep the linking number constant as no phosphodiester bond has broken in this case of cccDNA) six negative supercoils have been introduced.

All the books clearly mention that negative supercoil is something that underwounds the DNA resulting in less turns with more base pair per turn. But in this case it is clearly seen that the number of turns have increased (from 36 to 42) and to compensate that -6 supercoil is introduced. So here negative supercoil has resulted in over wounding instead of underwounding

similarly, from the linking number equation > Lk = Tw + Wr, If there is positive supercoiling (i.e., Wr is positive) the Tw (twist value) will go down to keep linking number constant. So, the statement saying positive supercoil wound overwound the DNA is not matching at all. shouldn't positive supercoil increase the Tw as well (I understand mathematically it is not possible because then linking number would change, but all I'm saying is that I fail to connect the concept that says positive supercoil overwounds the DNA (more twisted) with what I see in the equation i.e., twist number drops and only writhe goes up.

After studying this topic a bit more I came to the conclusion that supercoiling itself does not overwound/underwound the DNA any further that it already is. Supercoiling just relieves the stress introduced after DNA gets further twisted in the first place, it relaxes the DNA by decreasing the twist back to normal (10.4bp per turn just like normal relaxed B-DNA) (in case of positive sueprcoiling and vice versa for negative) and the extra tension that made the DNA twisted in the first place now increases/decreases the writhe for positive and negative supercoiling respectively. The authors might have considered a DNA molecule with higher writhe value also a more wounded form of DNA that's why they used the term 'overwound'

Please correct me if I am wrong


Amount of carbon captured in photosynthesis by a plant Is it more proportional to the mass or the volume of the plant? I thought it might be helpful to think on the cellular level here. Even a reference to an external explanation would be useful.

Welcome to Biology.SE! I am not entirely sure what your are asking but here are some places you might want to start:
Photosynthesis Molecular Biology
If you want to know about the number of sugar molecules created 'per photon' by photosynthesis you can explore the light-dependent and light-independent reactions used in photosynthesis. In particular you might want to look at the Calvin Cycle and how NADPH is used there and how NADP is reduced to NADPH in the light-dependent reactions.
Carbon Capture Efficiency
You might be interested in the variation between plants in carbon capture efficiency, i.e. not all plants are equally 'good' at photosynthesis. To think about this you might want to look at different photosynthesis mechanisms (C3 vs C4 and CAM; different forms or amounts of Rubisco enzyme) or you might want to look at sunlight 'capture' mechanisms (photosystem I and II and the accessory pigments like chlorophyll and carotenoids) or even at adaptations to different light environments (trichomes, leaf shape, etc).


What is the justification of Chargaff's second parity rule? First parity rule
The first rule holds that a double-stranded DNA molecule globally has percentage base pair equality: %A = %T and %G = %C. The rigorous validation of the rule constitutes the basis of Watson-Crick pairs in the DNA double helix model.
Second parity rule
The second rule holds that both %A ~ %T and %G ~ %C are valid for each of the two DNA strands. This describes only a global feature of the base composition in a single DNA strand.

[source]
It makes sense that in the context of dsDNA, that A = T and C = G, but I don't see an obvious reason why in a single strand of DNA, A ~ T and C ~ G.

This is an excellent question, which was the cause of some confusion in the field over the years:

"The validity of the second Chargaff rule was unexpected. Obviously it should be regarded as a global rule, i.e. applicable to large sections of chromosomes. Nonetheless, not being derived from a compelling principle, such as the one underlying the first rule, it remains a mystery. This is even more so, when one studies extended versions of Chargaff’s second rule." (paper)

There are a few things to note here:

Chargaff's rules were purely observational; they pre-existed the double helix (see your same Wikipedia ref), and thus pre-existed the double helix model (which was in fact famously a rendering of the first rule in a 3-D model, as Watson wrote about in his book "The Double Helix"). There is thus no logical or mechanistic justification for the rules; they were simply what Chargaff et al. observed for dsDNA and ssDNA. Perhaps I have misinterpreted, but I felt the question implied a belief that there must be some logical requirement for this.
Note that the first rule uses "=" and the second rule uses "~" ("approximately"). That is, if we believe that all bases in a genome are paired, then it follows as a mechanistic/logical requirement that Watson strand and Crick strand must match up compositionally. This is obviously not the case with ssDNA, as I think you indicate in the Q. However, it is nonetheless true that genomes have overall compositional biases; they tend to have consistent (G+C)/(A+T) ratios across the molecule (on average). More recently, it has become clear that this is true not only for single nucleotides, but also for $k$-mers, or short DNA sequences of length $k$ (paper). Indeed, these patterns have been used to match up different pieces from the same genomes (paper). These biases exist on both strands, therefore each strand of a genome is subject to these biases. (The reasons why these biases exist are often argued over, but may have something to do with mutational biases). Therefore, both ssDNA strands of a dsDNA genome have the same compositional biases, and they must complement each other's similar biases, so even within a strand the statistical expectation is Chargaff's second rule. Chargaff, again, probably didn't know many of these things when he came up with the rules. This explanation for Chargaff's second rule has been explicitly discussed in the literature, in the first paper cited.

Notably, the second rule only holds reliably for long sequences, because in short sequences sampling error may lead to a failure to match the biases of forward and reverse strands. This is more or less what everyone means when they call it a "global" rule.


How can someone share 50% of their DNA with their parents yet all humans share 99.9%? I have heard that humans share 99.9% of their DNA with other humans. I have also heard that a child shares 50% of their DNA with their parents. How do I resolve this apparent contradiction? It has been really bothering me.

It will be clear with a simple analogy.

You are 50% related to any one of your parent

Let's say you don't have any biology books. You have two friends, Alice and Bob. They each give you a copy of the book Campbell Biology. You now have two Campbell Biology. You have received 50% of your Campbell biology books from Alice and 50% from Bob.

Similarly, you inherit 50% of your DNA from your mother and 50% from your father. You are related at 50% to any one of them.

Two randomly sampled individual are 99.9% identical

Now consider the list of all the copies of Campbell Biology in the world. As there exist different editions, all Campbell Biology won't exactly be the same.
Let's say you randomly sample two Campbell Biology from around the world and you align them letter by letter. What is the expected fraction of the letters that will be identical? If, for example you find the two sentences

  Selection is a fitness variance associated to a genetic variance among individuals in a population.

and

  Zelection is a fitnezz varianze azzociated to a genetic varianze among individualz in a populazion.

There are exactly 9 mismatches out of 99 characters, that is a 90% similitude.

Similarly, if you randomly sample two humans, align their DNA (a DNA sequence look like ATTTCGCTGTCGAATCGATCGGTA), you'll find that the fraction of mismatch is lower than 0.1%. Therefore, we all share 99.9% of our DNA.

Of course, alining DNA sequences (or normal sentences) is not quite that easy as some sequences (or sentence) can have more nucleotides (or letters) than others but I won't go into the details here.

How do these two measures relate?

Let's say that instead of giving you a book, Alice actually produced a copy of its book and gave it to you. The book you have received from Alice (that is 50% of all your Campbell Biology books) is 100% identical to Alice's book in term of mismatch.

Similarly, the 50% of your DNA that you inherit from your father (or mother) is 100% identical to the copy of the genome found in your mother.

Note however that

Your mother probably made between 10 and 100 mutations when copying her DNA so that the DNA you received from your mother is not exactly 100% identical to your mother's DNA

Similarly Alice could have miscopied her Campbell Biology book that she passes to you

Your mother actually recombined her two haplotypes

Similarly Alice actually had two different editions of Campbell Biology and she mixed them up a little bit before copying the resulting book!


Why shouldn't dogs eat chocolate? I was wondering why dogs shouldn't eat chocolate. Can't dogs just excrete the indigestible component in their droppings?

It's common knowledge that dogs shouldn't eat chocolate. What I don't know is why chocolate would kill them, from a specifically biological perspective.

The reason is simple: Chocolate contains cocoa which contains Theobromine. The darker the chocolate is (meaning the more cocoa it contains) the more theobromine it contains. This is a bitter alkaloid which is toxic to dogs (and also cats), but can be tolerated by humans.

The reason for this is the much slower metabolization of theobromine in the animals (there are reports for poisonings of dogs, cats, birds, rabbits and even bear cubs) so that the toxic effect can happen. Depending on the size of the dog, something between 50 and 400g of milk chocolate can be fatal. As mentioned by @anongoodnurse the cocoa content in milk chocolate is the lowest and much higher the darker the chocolate gets.

The poisoning comes from the Theobromine itself, which has different mechanisms of action:

First it is an unselective antagonist of the adenosine receptor, which is a subclass of G-protein coupled receptors on the cell surface which usually bind adenosine as a ligand. This influences cellular signalling.

Then it is a competitive nonselective phosphodiesterase inhibitor, which prevents the breakdown of cyclic AMP in the cell. cAMP is an important second messenger in the cell playing an important role in the mediation of signals from the outside of the cells via receptors to a reaction of a cell to changing conditions. The levels of cAMP are tightly controlled and the half-life of the molecule is generally short. Elevated levels lead to an activation of the protein kinase A , an inhibition TNF-alpha and leukotriene synthesis and reduces inflammation and innate immunity. For references see here.

The LD50 for theobromine is very different among species (table from here), with LD50 as the lethal dose killing 50% of the individuals and TDlo the lowest published toxic dose:

The LD50 also differs between different breeds of dogs, so there are online calculators available to make an estimation, if there is a problem or not. You can find them for example here and here. The selective toxicity makes it even an interesting poison for pest control of coyotes, see reference 4 for some details.

References:

Chocolate - Veterinary Manual
Chocolate intoxication
The Poisonous Chemistry of Chocolate
Evaluation of cocoa- and coffee-derived methylxanthines as toxicants
for the control of pest coyotes.


Intrinsically disordered proteins as potential drug targets Intrinsically disordered proteins (IDPs) are a class of proteins that do not adopt a stable secondary or tertiary structure under physiological conditions in vitro, but still have biological functions. Many IDPs are implicated in cancer, neurodegenerative diseases, and diabetes, which makes them attractive drug targets. Are there any successful examples of that? Are there any drugs which disrupt protein-protein interactions (as one of the protein being IDP)?

IDPs are indeed attractive drug targets and there are ongoing efforts to develop drug molecules that block interactions between a disordered and a structured protein. According to this relatively recent paper, however, these efforts have not brought a drug on the market, yet.

A few promising studies have shown drug-like molecules that inhibit protein-protein interactions based on intrinsic disorder of one of the partners and target:

oncogenic fusion protein EWS-FLI1 and RNA helicase A. A small molecule has been found that targets the disordered region of EWS-FLI1, blocks the interaction with the helicase and inhibits growth of Ewing's sarcoma.
p53 tumor supressor and its interactor Mdm2. Mdm2, by binding to an intrinsically disordered region of p53, targets p53 for ubiquitination and also causes it to be transported out of the nucleus. Promising small molecules  have been found that associate with Mdm2 and thereby block its interaction with p53.
c-Myc oncoprotein and the interaction with its partner Max protein. This study demonstrates two small molecules that bind to c-Myc and stabilize its disordered conformation, which inhibits its interaction with the Max protein.

The challenge in targeting protein-protein interactions for therapies stems largely from the fact, that the protein-protein contact surfaces are much larger than those involved in protein–small-molecule interactions (1,500–3,000 Å2 and (300–1,000 Å2, respectively) [2]. They are often flat and have no defined binding pocket. Also, IDPs often don't bind natural small ligands, that could act as starting points in developing drugs.

You may find this paper helpful:

Metallo SJ, Intrinsically disordered proteins are potential drug targets, Curr Opin Chem Biol. 2010 14(4): 481–488.

BTW: for a comprehensive, manually curated list of disordered proteins and regions, please check the Database of Protein Disorder.


Why do I always close my eyes when someone takes a photo of me using a flash? Everytime some tries to take a photo of me with a flash I manage to close my eyes (blink).

It's not intentional and it's quite annoying.

Why am I doing it?

What you are describing is called a "corneal reflex" and it is a measure to protect the eye from too bright light or foreign bodies.

It is a involuntary movement (i.e. not intentional, as you say), mediated by the cranial nerves, specifically the ophtalmic branch of the trigeminal and the temporal and zygomatic branches of the facial nerve.

I have to admit that I had a very hard time finding an exact complete explanation of the phenomenon, which makes me think (but I may be wrong) that it has not been widely researched. Although it is not difficult to imagine how the trigeminal nerve could be stimulated by a foreign body touching the cornea, it seems that several theories exist on how light can stimulate it.

The great part of the information that I could find at this regard are about a similar reflex, called the  the photic sneeze reflex or or ACHOO (Autosomal Cholinergic Helio-Ophtalmologic Outburst) syndrome. This occurs in ~1/4 of the population, and consists of sneezing when looking at the Sun.

In this case, several theories have been proposed, that essentially boil down to the fact that some other nerve (e.g. the optic nerve) stimulates the trigeminal after having being itself stimulated by bright light.

From: "General anaesthesia and the photosternutatory reflex" - Yarrow - Anaesthesia. 2003

  The physiology underlying the photosternutatory reflex remains unclear and several mechanisms have been proposed. The theory of optic-trigeminal summation holds that the optic and trigeminal nerves are intimately linked in the midbrain. Bright light stimulates the optic nerve, causing photophobia and pain via the ophthalmic branch of the trigeminal nerve. Conversely, nasal irritation can lead to blinking and lacrimation. It is suggested that intense stimulation of the optic nerve could cause sneezing if the maxillary branch of the trigeminal nerve was stimulated as well as the ophthalmic branch. The theory of parasympathetic generalisation invokes co-activation by one stimulus of neighbouring parasympathetic branches. Light falling on the retina stimulates pupillary constriction (via the third cranial nerve) and lacrimation
  (via the seventh). A stimulus of sufficient intensity could generate
  enough parasympathetic activity to cause nasal congestion and secretions, and
  stimulate sneezing by an effect on the maxillary branch of the trigeminal nerve.
  The theory of parasympathetic hypersensitivity suggests that individuals
  with photic sneezing may have a more active or sensitive parasympathetic system,
  leading to hypersensitive nasal mucosa.

Although what you describe does not involve sneezing I think we can assume the same, or a similar afferent pathway is activated also in that case.

Recent works also found an activation of visual regions of the cortex in response to this stimulus.

From the conclusions of:

When the Sun Prickles Your Nose: An EEG Study Identifying Neural Bases of Photic Sneezing - Langer et al. - PLoS One, 2010

  We propose that the photic sneeze phenomenon might be the consequence of higher sensitivity to visual stimuli in the visual cortex and of co-activation of somatosensory areas. The ‘photic sneeze reflex’ is therefore not a classical reflex that occurs only at a brainstem or spinal cord level but, in stark contrast to many theories, involves also specific cortical areas.


Assumptions of Hardy-Weinberg rule The post Solving Hardy Weinberg problems offers an easy explanation of Hardy-Weinberg rule. The current top answer explicitly does not talk about the assumptions of Hardy-Weinberg. A model makes sense only if one is able to tell its domain of definition and therefore it is critical to understand the assumptions underlying Hardy-Weinberg assumptions.

What are the assumptions of Hardy-Weinberg rule?

Here are the assumptions to the standard Hardy-Weinberg rule (HWr) formulation
$$p^2 + 2p(1-p) + (1-p)^2 = 1$$
See Solving Hardy Weinberg problems for more info about this formulation.
Assumptions
The locus of interest is bi-allelic
This is an obvious assumptions, however it is very easy to extrapole HWr to any number of loci.
Organisms are diploid
This is another obvious assumption that is very easy overcome. This also means that HWr does not hold for loci present on sexual chromosomes as those chromosomes do not display a simple diploid behaviour.
Only sexual reproduction occurs
If some individuals are able to undergo non-sexual reproduction, then the rule does not hold anymore. See also Panmixia as these two assumptions are related.
Panmixia
Panmixia is often called "random mating". Panmixia is the state where each individual is equally to mate with any other individual in the population (including itself). There is therefore no population structure and no mate choice.
Let $N$ be the number of individuals in the population, in absence of selection (see If selection, it must be on fecundity alone), the probability to mate with any given individual (including itself) is $\frac{1}{N}$. You will note that it requires that individuals are able to self (but not clone as reproduction must still be sexual).
If selection, it must be on fecundity alone
If selection occurs, then it must on fecundity (right before reproduction). If selection occurs on survival during the lifetime, then the selected genotypes will be in excess in comparison to Hardy-Weinberg expectations.
If migration, it must be right before reproduction only
For the same reason as above, if there is migration, then it must be right before fecundity. If migration occur during the lifetime, then it will have a very similar effect than selection. Selection would increase the frequency of selected genotypes above HR expectations. Migration would increase the frequency of incoming genotypes above HR expectations.
Non-overlapping generations
This means that everyone reproduce in the exact same time and die right afterward. Very few species would qualify for such assumptions.
Population of infinite size
If previous assumptions already seemed hard to meet in the real world, the assumption of infinite population is absolutely impossible to meet.
Deviation from this assumption will cause deviations from expectations. Such deviations are often tested via a Chi squared goodness-of-fit test.
Note by the way that if the population is of infini size, there is no mutation, no migration and no selection, then there is no evolution.
Other assumptions
Biology is a science of complex systems. There are always other assumption one might want to consider. For example I did not talk about sex-specific selection or sex-specific mutation rate. But I am hoping that with the above I went over the most important assumptions.
So what's the point of HWr?
All models are wrong but some are useful. There exist no real life example of a population that perfectly fit into HWr assumptions but it does not mean the model isn't useful. Actually most population approximate HW expectations quite well. You will note also that it is by understanding how a scenario lead to a specific observation that we can interpret how derivation from the expectations can be achieved.
So yes, HWr is one of the most basic and most important rule in population genetics. It is so basic, that I would hardly name it in any fancy way as it is just the simple application of basic probability theory. See Solving Hardy Weinberg problems for more info.


In plant species' description, does the leaf length include the lamina and petiole, or only the lamina? The description (partially pasted below) of Ramosmania rodriguesii in Verdcourt (1996) states that the leaves are up to 30 cm long. Does this length include both the lamina and petiole, or only the lamina?

Reference (source of above paragraph):
Verdcourt, B. (1996). Ramosmania rodriguesii Rubiaceae. Curtis's Botanical Magazine, 13(4), 204-209.

According to "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001) [my emphases added]:

A leaf is "an expanded, usually photosynthetic organ of a plant"

A lamina is the "expanded portion" of a leaf

A petiole is a "leaf stalk" and a stalk is "the supporting structure of an organ, usually narrower in diameter than the organ."

I know you know the definitions here, but I'm using this as evidence that the petiole is often considered separate from the leaf itself.
I do not know of a flora, key, or guide that uses the petiole as part of the measurement.
Since Kew's Plants of the World Online lists this species as having 30 cm long leaves (and assuming they do not include the petiole as is common practice), I would assume your source likewise is not including the petiole.
Disclaimer: I have never seen Ramosmania rodriguesii, so I can't comment from personal experience/knowledge of this specific species. However, if typical measurement practices have been employed, I assume the petiole is excluded in leaf length measurements.


Density of Receptors of a mammal I know it's a very open question. It's for a paper.
So as a reference I'm looking maybe for the average density of insulin receptors per cell of a human tissue. I want to compare it to the density of MC1R (around 1000 per cell) and it says that's a low amount.

It would depend on the type of tissue. But if you are interested in any tissue, then have a look at this BioNumbers entry. It says that there are 100000 insulin receptors per cell in rat adipose tissue. Divide it by the surface area of the cell and you'll get the density. Cell dimensions can also be found in BioNumbers


Is the protein in teardrops still attached to cells, or is it released and free-flowing? A ScienceDaily article says that the protein in teardrops can kill bacteria.

But how does it reach the bacteria?

I am not sure I understand your question.

According to the article you mention the proteins in teardrops kill the bacteria which are invading the eye (e.g. also present in the teardrops):

  "Those jaws chew apart the walls of the bacteria that are trying to
  get into your eyes and infect them,"

EDIT: These proteins are enzymes called lysozymes. Those are free-flowing proteins of the human tears. These proteins are actively produces in the lacrimal glands and actively secreted into the lacrimal liquid.


Does precipitation influence the UV spec reading? I have been checking my sample for Hydroxyl radical scavenging activity. I have dissolved Hydrogen peroxide in Phosphate buffer. My sample is clear and reagent is also clear but when I have mixed my sample extract with Hydrogen peroxide reagent a precipitant is formed. Control is very less than solution that is kept for reaction to proceed. So I am getting an answer in negatives (230 nm). Is that formation of precipitate affect the absorbance of the solution? Does precipitation increase the OD value compare to clear solution?
 Mine is mushroom powder. It is extracted with Ethanol. Extract is dried and finally it is dissolved with solvent above said. That has been used for Hydroxyl radical scavenging activity. Hydrogen peroxide 0.01 milli molar reagent is prepared with Phosphate buffer. First i have taken reading for H2O2 and added extract kept for ten mins and took reading. in 230 nm..

The answer to the question as asked is that yes, any precipitate will affect the value that you are reading in your spectrophotometer. The basis of spectrophotometry is that light passes through a sample, and less light emerges than the amount which entered. The amount of light that has "disappeared" is used to deduce something about the solution in the cuvette. Light can be absorbed by chemical groups (this is the basis for e.g. DNA having an absorbance value) or it can be scattered by particulate material (this is the basis for measuring the cell density of a bacterial culture). If you are trying to make a measurement of the first type (absorbance) and you get a precipitate your reading will be distorted by the light scattering effect.

Precipitates are incompatible with spectrophotometry.

As the comments have noted: if you give more details of your protocol someone may be able to help. Phosphates are, of course, notorious for generating unwanted precipitates.


Is heat released during work due to ATP breakdown or a increased blood flow? Is heating up of a body during work or exercise an effect of increased speed of blood or is it because of the extra energy released while harvesting energy from the ATP

Is heating of a body the result of increased blood flow or extra energy from ATP?

It is mainly because of the breakdown of ATP (Adenosine Triphosphate, a type of nucleic acid with an Adenosine base, a Ribose sugar, and 3 Phosphate groups), alternatively and more formally known as ATP Hydrolysis. During hydrolysis by water, ATP splits into Adenosine Diphosphate (ADP) and an inorganic Phosphate (Pi), releasing some energy. I'll explain more below how exactly this works.

How or why does ATP Hydrolysis release energy?

If you take a look at a diagram of an ATP molecule, you'll notice that it has 3 phosphate groups, each with a Hydroxyl group (-OH) that has a net negative charge due to Oxygen being highly electronegative and hogging electrons from the Hydrogen bonded to it. Consequently, you have 3 molecules with slightly negative charges attached to each other. If you've ever played with magnets, you'll know that like charges repel. So overall, the ATP is highly unstable because of these repulsive forces that are situated so close to each other. When the bond between the 2 inorganic phosphates is broken, a large amount of energy is released. Here's a diagram from Campbell's Biology 9th ed (note that the Hydrogens in the phosphates are not shown for simplicity):

When the last phosphate is broken off, you are left with one molecule of Adenosine Diphosphate (ADP) and an inorganic phosphate group (Pi). Energy has been released. However, this is not the entire story. Generally speaking, ATP Hydrolysis does not occur without another component: an endergonic process. An endergonic metabolic process is any which requires energy input in order to proceed. Think of it with the following analogy: imagine a ball trying to roll uphill by itself. At the bottom of the ramp, the ball is very stable and has low potential for performing work. But uphill, the ball would have a higher potential energy. It is impossible for the ball to roll uphill from a state of low energy to a state of high energy. Thus, we first need an input of energy--say the mechanical energy of our hand pushing the ball--in order for it to move up.

Our endergonic process (such as in protein synthesis by a ribosome or the phosphorylation of glucose in glycolysis, the first step of cellular respiration) requires some energy input from ATP in order to proceed in an exergonic manner--that is, in order to release energy without any help. With our analogy, this is like pushing the ball to the top of the ramp and then letting go, allowing the ball to roll back down from a state of very high potential energy (and therefore instability) to a state of low energy. The energy that we had to input from ATP is known as "activation energy", because it's literally energy that we need in order to unlock or "activate" an endergonic pathway.

Example of ATP Hydrolysis releasing heat:

When you have an infection in your body, your hypothalamus will raise the body's set temperature point to induce shivering. Shivering consists of many muscle contractions, all of which require hydrolysis of ATP. The result is a release of a large amount of heat that increases body temperature to a point at which pathogens cannot survive.

What about blood flow?

Blood flow does not actually produce heat by itself, but it can direct heat to the surface of the skin, such as when the body needs to cool down. The main source of heat in the body remains the ATP.

EDIT: much of the information here can be reviewed in this wonderful YouTube video by Andrew Douch


Confusion about Photosystem 2 with regards to lysis of water I am slightly confused about the role of $\ce{H2O}$ lysis in PII. I know that this releases $\ce{H+}$ ions, which I think are important because they drive the production of $\ce{ATP}$ through F-Atpase across the thylakoid membrane. But I don't understand how else this is important? With my current understanding, I would think that it is perfectly sufficient for PII to receive photons to excite an electron in the primary pigment reaction centre, which goes along the electron transport chain to PI. Is the water lysis there to replace electrons lost by photosystem 2? If so, how is it controlled that the correct number of $\ce{H2O}$ molecules are lysed so that excess electrons aren't generated?

Generation of ATP via photons is the primary aim of the photosynthesis pathway, which is accomplished by the generation of a chemiosmotic gradient of $\ce{H+}$, which then drives the ATPase pump. All the other enzymatic setups are designed to just let this process run in the most efficient way.

  I would think that it is perfectly sufficient for PII to receive photons to excite an electron in the primary pigment reaction centre

While you are partially correct in assuming this, since the ETC also participates in creation of a chemiosmotic gradient (Plastoquinone), such a mecahinsm would not be able to run repeatedly. Without the replenishment of the electrons of the PSII, it will not be able to initiate another round of electron transport. Hence, the oxidation of water is crucial in providing PSII the electrons it passed onto plastoquinone, so as to allow another round of photon-absorption and continuation of the photosynthetic process.

  how is it controlled that the correct number of H2O molecules are lysed so that excess electrons aren't generated?

This is achieved by a complicated interplay of the enzymatic components within the PSII. In summary, utilizing the four stable oxidation states of manganese core in the redox center ($\ce{Mn}^{(2-5)+}$, four separate states of the center ($S1\rightarrow 4$) are formed. These states cyclically shunt one electron during each step, until a water molecule is bound to $S4$ which is then directly converted to $\ce{O2}$ by $P680+$, formed in PSII due to photon absorption, which is a strong reducing agent. Since the final step occurs only with water molecule bound to $S4$, which in turn is formed only by the cyclical transition between the various states of the redox center with systematic sequential loss of electrons, the overall process is very tightly constrained to extract only the limited number of electrons preventing any troublesome redox intermediates.

See here for some basic treatment of photosynthesis.


Snake Identification - St. Louis, MO We found this tiny snake in the finished part of our basement today. We live in the St. Louis, Missouri area.

The snake is dark greenish-grayish and has very faint lines running the length of its body.  Any idea if it is dangerous/what we should do with it?

It might be a juvenile lined snake (Tropidoclonion lineatum). The What Snake Is That page for Missouri says they are native. In your photo, I see very faint black stripes with a central tan line, which matches a lined snake. Photos of juveniles seem to be rare though.

Lined snakes grow to about 2 feet long and are non-venomous. According to this natural history page, the only venomous snakes in Missouri are pit vipers (of which 5 are native).


If number of children born were spread more evenly among all parents, would our species' genetics have more variability? Instead of some parents having lots of kids, if the number of kids were spread more evenly to parents having few kids and people who have no children, would it introduce more genetic variability in our species in general?

Well the obvious answer is of course yes of course it would. That is the essence of natural selection. Variability leads to different phenotypes and selection for and the amplification of beneficial traits. Evolution. Except if there is no selection (everyone has the same amount of kids) no traits are amplified so everything in a large population is static. Until you introduce mutations and that increases variability. Eventually each individual would have such a large degree of variation from the next that I would assume speciation would be a very imminent result of any form of seperation or selection, which is against your original premise.


Pregnancy from two parents with incompatible blood types, can it lead to complications? Let's take Alice and Bob, both healthy adult human specimens. Alice is (A-). Bob is (B+).

If they decide to have a child, would Alice's pregnancy involve any additional risk or complications compared with, say, Abraham and Abigail's pregnancy (both AB+)?

Background

I overheard claims that pregnancies from parents with different blood groups can lead to complications in pregnancy due to interactions between the mother and the child's blood. (These claims were not officially backed, otherwise I would have brought them up on Skeptics.SE). The explanations and my Google browsing went beyond my biology knowledge. I know these pregnancies must be viable, since the AB group exists, but I do not know if there are edge cases that lead to complications that would not happen with same blood type parents.

Related question

Can the mating of a couple with Rhesus positive and negative blood types result in miscarriage? This question only asks about Rh+ and only if it leads to miscarriage.

The rhesus factor (the + / - part of the blood group) can cause complications with pregnancy under certain conditions and lead to the so called Rh disease:

If the mother is rhesus negative and the father, rhesus positive; then the birth of a child with Rh+ blood group (inherited from the father) can cause the mother to build antibodies against this blood group. Therefore, a second pregnancy with a child that also has Rh+ blood group can have complications if no precautions are taken at any other point.

If these specific conditions are not all met, then no complications should arise from the blood groups.


How fallible are DNA paternity tests? Is it possible to get either a false positive or a false negative from a DNA paternity test and what would be the likely mechanisms behind this?  For example, is it possible that a father's DNA could have changed during his lifetime enough to be unrecognisable to that of his children?

Discounting lab error and other kinds of human incompetence, there aren't very many things that can confound a paternity test. Normal DNA damage cannot, but there are kinds of genetic chimeras that get strange results.

Normal human DNA damage can't add up fast enough to change the results without killing you several times over, but there are a surprisingly large number of people who are chimeras.

The relevant particular flavor of chimerism is tetragametic chimerism, where essentially parts of your body are sibling-related to the rest. This occasionally is discovered during paternity testing, in one vivid instance when a woman was provably not the mother of the newborn that she had just given birth to. Technically I suppose the baby was her skin's niece.

The incidence of this was thought to be very low, but it's almost impossible to detect without DNA testing. We know the incidence is much higher than we thought, but we don't know how high.


What does the phrase 'background level' mean? I was reading BIOS Biochemistry and stumbled upon a phrase 'background level' in the following excerpt $-$

  The lac operon contain lacZ,lacY and lacA genes encoding $beta$-galactosidase, galactoside permease and thiogalactoside transacetylase, respectively, preceded by an operator site and a promoter. The operon is transcribed by RNA polymerase to produce a single polycistronic mRNA that is translated to produce all three enzymes. When lactose is present the background level of $beta$-galactosidase converts some lactose to allolactose, which induces transcription of the lac operon.

What is meant by background level? Does it refer to the basal level of transcription, the constitutive transcription of facultative genes?

The phrase “background level” is generally used in an experimental context where you are measuring the effect on a variable of some agent or stimulus. You might expect that your control condition(s) — without the stimulus — would give you a measurement of zero, but often that is not the case, and one needs to subtract this control value — often referred to as ‘background’ — from the experimental value.

Such background values can be real — e.g. background radiation — or artefacts caused by fundamental limitations in the measuring system used. Generally the implication is that their origin is unknown or is not specific. That is why I think that the use of the term ‘background’ in the context of the lac operon is somewhat unfortunate. I would have used (and encourage you to use) the term ‘basal level’ instead*. As the text states, there is a low — but specific and necessary — expression of β-galactosidase in the non-induced situation, so that when lactose is added some of it can be converted to the inducer, allolactose, which will then result in the synthesis of the greater amount of β-galactosidase needed to deal with the rest of the lactose.

*Footnote

In fact I hate the term ‘level’ except for water in the bath tub, and I would have used ‘amount’ or ‘activity’, but that’s not the point at issue here.


DNA preparation for sequencing In shotgun sequencing method or some related method that DNA is break up into random fragment. The fragment that have about 3kb in size is inserted into plasmid by enzyme ligase and then plasmid transform to E.coli using electroporator. As i understand, the goal is amplify the fragment to be sequencing.

At this time, i have a question :

After the e.coli growth up, we have too many different type of miscellaneous DNA strand with same size in a colony. How to purify a type of fragment to be sequencing ?

For example, i have 20.000 different DNA strand with the same 3kb in size after break up into random fragment :

-- AAAAAAAAAAAAAAAAAAAA...AAAAAAAAAAAAAAAAATTTTTTT -- (3kb fragment of chromosome 1)

-- GGGGXXXXXAAAAAAAAAAA...AAAAAAAAAAAAAAAAAAAAAAAA -- (3kb fragment of chromosome 2)

-- 19998 DNA fragment left ............................. -- (3kb fragment of random chromosome)

So after amplify them i have :

1000000x of -- AAAAAAAAAAAAAAAAAAAA...AAAAAAAAAAAAAAAAATTTTTTT --

1000000x of -- GGGGXXXXXAAAAAAAAAAA...AAAAAAAAAAAAAAAAAAAAAAAA --

1000000x of -- 19998 DNA fragment left........................ --

These DNA strand is mixed together in a colony. We cannot run sequencing them together as mixed, so how to have the only one for sequencing :

1000000x of -- AAAAAAAAAAAAAAAAAAAA...AAAAAAAAAAAAAAAAATTTTTTT --

I hope I understood your question correctly.

I think what you are missing is that after you break up the DNA, you dilute the concentration so that each bacteria will incorporate ~1 DNA molecule. Then, you dilute the bacteria on a plate and spread it so that they each single bacteria is far from other bacteria. Finally, after they grow you get one genetically identical colony per DNA fragment.


Can allelopathy succesfully be used against algal blooms? Algal blooms caused by man (harmful algal blooms) are a major ecological problem. An excessive amount of algae causes hypoxia and logically, most marine wildlife can't be sustained in hypoxic conditions.

Can't we use allelopathic plants to reduce the amount of algae significantly?

This has been tried and it sorta works.

Algae in general seems to be inhibited by rotting barley straw in the water.
There is also an observation (not universally accepted) that many plants in the water do not have as much algae.  This post is from April 2011, so it seems pretty current.


How does the cardiac cycle and electrical activity all relate to blood pressure in the heart? I know how the cardiac cycle works and understand the electrical activity in the heart such as the AV nodes, SA nodes and Bundles, but how do they work together in relation to blood pressure?

Blood pressure is determined by cardiac output and the total peripheral resistance, where, from Ohm's Law (Q= P/R):

Mean Arterial Pressure (MAP)= Blood flow (Q) x Total Peripheral Resistance (R)

The cardiac cycle and heart activity will essentially control the cardiac output through the FORCE and the FREQUENCY of contraction.

Cardiac output is determined by the stroke volume, and the heart rate:

CO= Stroke volume x HR

Changes in HR is linked to changes to the SAN and is controlled by sympathetic and parasympathetic inputs. An increase in HR, will cause cardiac output to increase, causing an increasing in blood pressure (simply put, other physiological changes can also influence blood pressure, such as vasoconstriction and vasodilation).

With regards to the AVN, SAN and bundles of His, this allows electrical conductance which causes the contraction of the heart. The contraction of the heart leads to blood being ejected (i.e. blood flow, which is linked to cardia output). This, together with the peripheral resistance of blood vessels will be linked to blood pressure.


DNA sequence from the middle of a gene Someone gives you a short DNA sequence that comes from the middle of a gene.

5'- TCTAACTGATTAGC -3'
3'- AGATTGACTAATCG -5'

From this sequence, determine the following:

Is the promoter located to the left or right as the sequence is written?
Is the sense strand the top or bottom strand?
What amino acids are encoded by this gene fragment?

The only thing I have been able to come up with, is that since this is from the middle of a DNA sequence I need to choose a frame with no stop codons.

TCT AAC TGA TTA GC

T CTA ACT GAT TAG C

TC TAA CTG ATT AGC

AGA TTG ACT AAT CG <<< this is the ORF

A GAT TGA CTA ATC G

AG ATT GAC TAA TCG

If the sequence comes from the middle of a gene we assume it should encode an open reading frame.
For this sequence only 1/6 frames does not include a stop codon (shown above in italics). So in standard format, with promoter to the left we can write the ds sequence as:

5'-AGATTGACTAATCG

3'-TCTAACTGATTAGC

Since this is homework I'll leave the rest to you.


How to determine externally that a whale is a mammal? Mammals have external qualifying characteristics like body hair, ear pinna, etc. But a whale has none of that. So, can it be identified as a mammal just by external observations?

A whale has a horizontal tail fin which is a typical feature of mammalian marine animals see link. Mammalian sea animals typically have a vertical movement of the tail fin for swimming. Fishes like sharks have a vertically oriented tail fin and move it side-ways for locomotion.


Aside from Homo Sapiens, do the males of any other species care for the offspring of those unrelated to them? Elsewhere I heard that male Long-tailed Tits will care the offspring of their brother if they're unable to have their own. However, I'd like to know if there is a case of such behavior where the two are unrelated to one another.

Yes most commonly in a reciprocal altruism fashion, when you aid any offspring of your species or any in your herd/pack. Crocodiles are known for this. They respond to any crocodile (of their species) distress call from any baby crocodiles. This tends to be an advantage because proximity usually means relatedness and even when it doesn't crocodiles are high enough on the food chain the risk to the males is low compared to the time and effort that would be needed to identify the offspring first.

likewise in herd animals it can be an advantage because it ends up with everyone protecting everyone else's offspring but usually has to be paired with some ability to punish freeloaders/cheaters (individuals who don't help protect the offspring).

Of course you also have males who are tricked into it, after all a male does not always know what are its offspring.

You also have males that will help with a current brood to court the mother, or even unrelated females. Basically they are showing off how good a parent they can be, some believe this is what humans are doing. This is seen in some social primates. It might happen in some birds too but I am not sure.


Does loss of dopaminergic neurons totally eliminate voluntary muscular control? Breathing is a function that is not only autonomic, but can also be temporarily overridden and placed under voluntary control. In fact, you are now breathing manually. Now, suppose that someone has completely lost the ability to voluntarily control his/her muscles due to destruction of the brain's dopaminergic neurons in the substania nigra (such as due to Parkinson's Disease or MPTP poisoning). This would normally result in total paralysis of voluntary muscles and inability to move. Would that person be able to breathe manually if he/she so wished, or would he/she only ever breathe autonomically? What about defecation (Which requires one to voluntarily relax the anal sphincter)? What about rolling the eyes?

Suppose that someone has completely lost the ability to voluntarily control his/her muscles due to the destruction of the brain's dopaminergic neurons in the substania nigra

This is not correct. The substantia nigra plays an important role in both reward and movement. The degeneration of dopaminergic neurons in the substantia in Parkinson’s disease leads to loss of fine motor movement (leading to limited movement and tremors) and some loss of non-motor skills (loss of smell).

What locations control breathing?

The autonomous regulation of breathing is controlled by bundles of neurons called the dorsal respiratory groups (DRG) and ventral respiratory group (VRG) that together make up the medullary respiratory center. Source.

Though the exact mechanism of how we control our voluntary breathing is still a debated. We have a general idea:

  Voluntary control of breathing is mediated primarily via the
  corticospinal and corticobulbar tracts and is important in activities
  such as speech, singing, and voluntary breath-holding. Disorders
  involving this mechanism occur mainly in bilateral pontine infarctions
  and lesions involving the pontine tegmentum that interrupt the
  descending motor pathways. - Neurology and Clinical Neuroscience, 2007

Would that person be able to breathe manually if he/she so wished, or would he/she only ever breathe autonomically?

Although the exact mechanism for voluntary breathing is not fully understood, the voluntary process is controlled by a series of nerve bundles. If the nerve bundles were severed, there would be decreased voluntary control over the breathing process. Losing the ability to manually breath could be bad for overall health. One study has found that a lack of the ability to manually breath can lead to poor spinal stabilization and posture.

What if you lost autonomous control?

There is a rare disorder known as central hypoventilation syndrome (CHS) that results in respiratory arrest during sleep (also known as Ondine's Curse). This disorder is caused by a lack of development of the neural tube (aka Medulla and the VRG/DRG) during birth or some type of traumatic brain injury. Treatment for this disorder is a lifetime of mechanical ventilation.


How can tree branches grow upwards against gravity? I saw this tree in front of my room with those branches, and I asked myself why they didn’t grow downward in the direction of gravity since that would be easy for them? And I came to the conclusion that they are seeking sunlight. Is there any research which explain how they can do that?

I found that this mechanism is called Gravitropism (Tree Branches grow against gravity, while roots grow into the soil in the direction of gravity) but I didn’t find a clear explanation.

This review paper might help answer your question: http://www.plantphysiol.org/content/120/2/343.full

It seems that starch-filled organelles called amyloplasts sediment in the cell according to the pull of gravity, and in doing so this gives the cell some form of basic up-down polarisation.  If my memory serves correctly, this can then cause changes to the growth of the cell in the branches, meaning the side of the cell opposite the amyloplasts grows slower and the side closest the amyloplasts grows faster, causing the upwards curvature of the branches seen in your tree.


What cell types comprise the median eminence and the tuber cinereum? I have tried pretty hard to get a detailed description of what exactly the median eminence and the tuber cinereum are but to no avail. I am very familiar with their anatomical relationships (spatially) with the hypothalamus, 3rd ventricle, mammillary bodies, etc; however, I still do not quite understand what they are or what cell types comprise them.

Are they areas of grey matter? Are they some sort of modified ependymal cell layer of the 3rd ventricle floor?

Or are they areas of connective tissue that merely "house" white matter projections from the hypothalamus to the pituitary? So, to repeat the inquiry from above:

What cell types comprise the median eminence and the tuber cinereum?

And, moreover, what's the actual function of the cell types that comprise them?

The tuber cinereum is the "swelling" at the ventral surface of the hypothalamus (Subarachnoid space surface) at the base of the infundibular stalk. The median eminence (a circumventricular organ) is an elevation on the ventricular surface of the infundibular recess of the 3rd ventricle.


How does one calculate the amount of oxygen produced by trees? I'm currently working on a project to measure the impact of tree planting.
Calculating the amount of oxygen seems harder than I imagined.

Of-course there's the type and size of the tree and the environment (soil and air consistency), but there are plenty of other variables in play of which I have no knowledge of (being an engineer, not a biologist).

From a computational standpoint I'm looking for rough and finer methods of calculation for the amount of oxygen the following produce:

A tree
A large forest
Multiple countries with their forest

The one tree can be calculated exact, given enough variables. Oxygen during the day, during the night, tracked over it's age, etc.

A large forest will be calculated more approximate. Extra relevant would be how growth and oxygen production are influenced by tree density (trees per square mile).

Calculating multiple countries would be a whole other problem. It looks like it's very hard to prevent estimations from completely destroying the accuracy of calculations.

Basically I've written down some concerns and now I'm looking for a way of actually calculating these numbers and preferably some real numbers to validate against. The internet is crawling with estimates ((1)(2)(3)(4) and many, many more), but finding decent sources to compare your calculations seems hard.

How does one usually tackle this calculation problem?

With detailed mechanistic models. There are a huge number of variables here, and you'll need to account for nearly all of them. Here is a similar project for crops.

You could try this model for a single tree but I don't envy trying to scale that up to entire countries.

Just to ballpark some figures, you could consider photosynthetic efficiency, average insolation, and shading effects. X amount of light falls on this country on average, and of that light .1% is converted into oxygen, so that's how much oxygen is made.

You could also approach it from the other direction and estimate how much each tree weighs. Tree dry weight is going to be mostly carbon, and necessarily nearly all of those carbon atoms were once carbon dioxide and represent one O2 molecule each. This approach has the advantage of taking into account respiration, unlike the light approach. The light approach measures total oxygen produced, but the carbon approach measures total oxygen released.


How does a nerve cell adjust if O2 diffusion is interrupted? What effects would it have on a nerve if the oxygen supply is cut off? Is there any data on this?

Does the nerve conductance velocity increase? What about the Amplitude and receptor-channels on/in the nerve?

Funnily enough it's insanely hard to come by an answer to this question, or maybe I'm just searching at the wrong places....

If Oxygen diffusion is interrupted, there is a serious problem. Neurons inside of the brain slowly start to die, many other things like change in personality or the inability to process pain impulses occur if the brain is deprived of oxygen.If this is not fixed within 15 minutes it is impossible to survive.

The actual effects on the neurons are as follows:
Like in most cells the first solution to this kind of circumstance is anaerobic metabolism, the same happens in neurons but it does not last long and it is inefficient. As far as i'm concerned nerve conductance decreases in this kind of scenario and the receptors shrivel.

Well if the receptors are shriveling, they shouldn't be able to transfer impulses meaning that nerve conductance should stop.

This link to an article on the effects on the brain from oxygen deprivation.
https://www.livestrong.com/article/106179-effects-lack-oxygen-brain/


Which surfaces contain no epithelial tissues and which epithelial tissues are vascular? Epithelial tissues are found on all the surfaces of the body; including external surfaces and surfaces of organs etc.
Are there any surfaces which do not have epithelial? I have read in my book that almost all the surfaces has epithelial tissues but there are some exceptions. What are the exceptions?

Similarly, almost all the epithelial tissues are avascular. But there are some exceptions which are vascular? Which epithelial tissues are vascuar?

*I'm talking about a human body.

I think you're talking about two different things.  I assume Rafique is referring to vascularized epithelium, but user4693 is referring to vascular epithelium.  Although the terminology is very similar, the difference is important.

vascular epithelium = endothelium of a blood or lymphatic vessel.

vascularized epithelium = epithelium with a blood supply, meaning that small vessels invade the epithelium (pass between epithelial cells) rather than simply occurring in the underlying basement membrane or connective tissue.

Most epithelia are avascular (lack blood vessels).  As far as I know the only vascularized epithelium in humans is found in the inner ear (1).  I've been told that the lips have vascularized epithelium (which is why they appear reddish), but I don't completely trust that source and I cannot find anything online to support it.

Also, some pathological conditions can cause vascularization of certain epithelia, like the cornea (2).


What are these near microscopic white bugs from my comb? I saw a whole bunch of white bugs crawling on my comb in the medicine cabinet, they didn't photograph well but I did manage to get a bunch of them in mineral oil and eventually take some micrographs.

The good news is that a dermatologist says I'm not infested with anything and, after nuking the bathroom with poisons and cleaning products, they haven't come back.

Here's 3 different specimens at 40X and 100X.  The live ones seemed to be in the 0.2 to 0.8 millimeter range.

(Click for larger images)

What are these things?

Those look like they could be dust mites and are certainly some sort of mite. Dust mites are found everywhere in homes and are around 0.2 mm in length.

Dust mites image by Gilles San Martin:

Dermatophagoide pteronyssinus (European house dust mite):

Dermatophagoides farinae (American house dust mite):

You can learn more about dust mites from the BBC and the US NIH.


Which are the best programs to analyze circular RNA? Hello I'm just started with bioinformatics and I would like to know which programs are best for the task of finding circRNA (circular RNA) in sequences of tissues and different cellular types. I have heard about circRNA finder, find circ, CIRCexplorer, CIRI, and MapSplice which all are different programs to find circRNA, but I really don't know which one is the most used and easy to use, and which one is most accurate for finding circRNA.

According to the most recent paper (https://doi.org/10.1093/bib/bbx014), CIRI2 shows a balanced performance on sensitivity and FDR.

"Computational detection methods have been widely used in studies on the biogenesis and the function of circular RNAs (circRNAs). However, all of the existing tools showed disadvantages on certain aspects of circRNA detection. Here, we propose an improved multithreading detection tool, CIRI2, which used an adapted maximum likelihood estimation based on multiple seed matching to identify back-spliced junction reads and to filter false positives derived from repetitive sequences and mapping errors. We established objective assessment criteria based on real data from RNase R-treated samples and systematically compared 10 circular detection tools, which demonstrated that CIRI2 outperformed its previous version CIRI and all other widely used tools, featured with remarkably balanced sensitivity, reliability, duration and RAM usage."


Are the brains of any herbivorous animals capable of utilising ketone bodies as an energy source? I ask this question because earlier today I heard from a lecturer at my university that a sheep's brain cannot utilise ketone bodies as an energy source and hence with insufficient glucose supply for their brains they die.

My answer is limited to sheep.
Background
The metabolites referred to as ketone bodies (which I will refer to as ketones from now on) are acetoacetate and β-hydroxybutyrate. In humans these are produced in the liver when the amount of acetoacetyl CoA being produced exceeds the capacity of the TCA cycle. These acetyl groups are instead used to produce acetoacetate, and this can be reduced to β-hydroxybutyrate.
The production of significant amounts of ketones occurs during fasting (diabetic ketosis will not be considered here). Once glycogen has run out, the bodies requirement for glucose has to be met by gluconeogenesis (mainly in the liver) - glucose is synthesised from various carbon skeletons including glycerol and the products of amino acid catabolism (coming from muscle protein turnover). This means that in the liver the function of the TCA cycle shifts almost entirely to supplying oxaloacetate for gluconeogenesis, via the activity of phosphoenolpyruvate carboxykinase. Thus there is no oxaloacetate available for citrate synthase, so acetyl CoA cannot enter the TCA cycle. However, because fasting also results in fat mobilisation the level of acetyl CoA in liver cells goes up (acetyl CoA is the end product of fatty acid breakdown).
So what is going on here? During fasting the fuel economy of the body has to switch from being heavily glucose-based to one which uses carbon from fat and from protein. The ketones are the manifestation of this, and many tissues become heavy users of ketones during fasting as blood levels rise to 5 mM within a few days. This means that the glucose being produced by the liver can be directed towards tissues which are more dependent upon glucose. The classic example of such a tissue is the brain, but in humans even the brain begins to use ketones heavily during fasting.
In ruminants the situation is entirely different. Ruminants rely upon the bacteria in the rumen to metabolise carbohydrate in their diet and this results in large amounts of alimentary ketones entering the blood directly. For their glucose supply ruminants rely entirely upon gluconeogenesis, and the substrate for this is propionate, another end product of bacterial metabolism in the rumen: a lactating dairy cow will synthesise over 3 kg of glucose per day.
So, when I read this question my reaction was that the statement must be incorrect - surely it would make sense for sheep to use ketones in all tissues. However my intuition was wrong - according to

Pell JM.& Bergmane N(1983) Cerebral metabolism of amino acids and glucose in fed and fasted sheep. Am. J. Physiol. 244: E282-E289

cited in

Heitmann RN et al. (1987) Hepatic ketogenesis and peripheral ketone body utilization in the ruminant. J. Nutrition 117: 1174-1180
"Although there is some oxidation of ketone bodies by the brain tissues of humans and rats during prolonged fasting, Pell and Bergman ,using an elegant in vivo preparation, have shown no significant uptake or oxidation of ketone bodies by sheep brain."

I don't have access to the Pell & Bergmane paper so I cannot explain what they actually did. What is clear from the review by Heitmann et al. however is that fasting ruminants respond in the same way that we do, switching to hepatic ketogenesis, and presumably they also maintain gluconeogenesis, using not propionate, but amino acid carbon skeletons. The context of the statement quoted above suggests that even in the fasted state the sheep brain doesn't use ketones.


Fecundity per woman in early humans The average fecundity per woman varies a lot from country to country. I call average fecundity per woman the average number of born children per woman. In Homo sapiens, what was the average fecundity per woman during the paleolithic age for example? Is it about 2 offspring per woman or about 12 offsprings per woman?

Infant mortality was high during the paleolithic, so the fecundity of females had to be quite a bit higher than 2 to sustain viable populations.

A recent paper by White (2014) that explores how the ratio of young and old individuals in a population relates to demographic rates compiles data on hunter-gatherer societies from previous studies that you will probably find useful. Among other statistics, that paper reports a range in total fertility of 2.6–8.0. One of the source papers (Hewlett, 1991, pdf here) has data for individual hunter-gatherer societies (along with data from other types of pre-industrial societies). Many populations lie in the range 4-7 offspring. Note however that most (all?) of these values are from current or recent hunter-gatherer societies and not paleolithic societies. However, to give a ballpark estimate they are probably useful and fairly accurate. Also note that the child mortality rate of these societies are often between 40-50% (infant mortality ~10-30%)


Why is the spirit bear/Kermode bear a subspecies of the American black bear Ursus americanus? The Kermode bear Ursus americanus kermodei is only found in British Columbia,Canada. The Kermode bear has single nucleotide polymorphism at the melanocortin 1 receptor gene (mc1r) locus which cause the white color. 1 out of 10 indviduals are white and are refer as Kermode bear. However, is the black version of the Kermode bear still a Kermode bear Ursus americanus kermodei? If not, why?

It is because somebody wrote a paper that described it as such, and the paper was published. I don't mean to be flip. Its just that taxonomy is done through publication, not committees (although the peer reviewers could be considered a kind of committee). Subspecies are less stringently regulated than species, and this subspecies does have a particular unique set of gene frequencies that occasionally (as you mentioned) show up in the phenotype. The fact that it has been culturally recognized as special may also have something to do with its subspecies status. A subspecies need not be reproductively isolated from its parent species, and need not have any fixed characters.