Death from too little salt? I know that sodium deficiency can be deadly. But why is it deadly? Is it because of your muscles getting so rigid that you can't get something with salt in it? Is it because of your brain not able to send signals? Is it because of excess urination to try to get the sodium levels right? Is it because of anemia leaving red blood cell ghosts(the membranes of rbcs) in your bloodstream? Is it a combination of all these factors?

Part of this depends on the exact nature of "salt depletion" you're referring to. I have never actually heard of a case of hyponatremia being caused by low consumption of salt. We don't need to consume NaCl. It's present in the foods we eat in adequate amounts. We may want to salt our food, but it's not necessary for life.
Hyponatremia is an electrolyte imbalance, be it due to excess intake of H2O, inappropriate H2O retention, excess Na+ loss, hyperglygemia or other osmotic force, or other cause. For ease of explanation, I'll address acute hyponatremia, as it leads to death more rapidly. Hyponatremia kills because of the difference in the concentration of sodium across cell membranes.
Normal serum Sodium (Na+) is ~140mEq/L. Acute severe hyponatremia occurs when serum Na+ falls rapidly below 120 mEq/l (some authors use 125mEq/L) in less than 48 hours.
Water accounts for 60% of total body weight, with approximately two-thirds being intracellular and one-third extracellular; of that extracellular water, ~75% is in the fluid between/surrounding cells, and 25% is in blood vessels. Distribution of water/Na+ throughout the body is very tightly regulated.
When serum sodium falls too low, free water moves from areas of lower concentration to higher (into the cells). Tissue becomes edematous.  While this isn't a great problem for some tissues, it is for the brain.
The brain is enclosed in a rigid compartment (the skull) with a small amount of fluid (cerebrospinal fluid, or CSF) surrounding it. Inferiorly, there is an small opening called the foramen magmun, where the brainstem leads to the spinal cord.

When water moves from the blood into the cells of the brain attempting to establish osmotic equilibrium, the brain compensates for the increase in volume by forcing CSF out. This buys some time, but not enough; there is headache and nausea. As the brain continues to expand, intercellular fluid is forced out into CSF (which is being displaced by the brain.) This causes hyperexcitability which leads to seizures. In the meantime, astrocytes swell. Blood flow to the brain is reduced because of increased intracranial pressure, which further damages the cells, increases cellular edema and coma ensues.
If this isn't bad enough (it is; it's an almost irreparable  cascade of events), the edema can actually "push" the lower part of the brain down through the foramen magnum resulting in brain stem compression and respiratory arrest. At this point, few people make it back intact with even the best help.
You say,

Basically with too little sodium, it goes from bad to worse until the heart and lungs are affected and the person dies.

Not really. In acute hyponatremia, the brain goes before the rest. Once the brain goes, so follows the body.
in layman's terms
not layman's terms but still easily understandable


What physical force attracts the anti-codon on tRNA to the codon on mRNA during translation? What physical force attracts the anti-codon on tRNA to the codon on mRNA during translation? I know that these two bond together, but what actually makes the tRNA move through the cytoplasm to the mRNA on the ribosome?

As with many processes in cellular biology, nothing really moves anywhere, attracted by specific force. What that means, is that any molecule has a chance to interact with any other molecule, say, bind to it. Only force that is acted is electrical force of attraction of negative charges to positive ones.

Due to diffusion and temperature fluctuations, molecules wander around, bumping in each other. Sometimes, two complimentary molecules will bump into each other in a very desirable, energy-efficient orientation. Their atomic-scale interfaces (with tiny charges on it) will find each other as neat as hand finds glove of the right size/orientation neat and comfy. That is the way, for example, tRNA finds slot on ribosome/mRNA complex to plug into. just simple key-and-lock, or hand-and-glove model, that's all there is. And beauty is that you can try computationally calculate probability and energy of different interactions from molecular 3D structures.

Now, there are many tRNAs, but Glycine-tRNA will bind tightest to glycine-codon/ribosome complex. There is a chance that Alanine-tRNA will get in that spot, but that chance is very little compared to chance of proper interaction. Also, because interfaces of Ala-tRNA and Ala-codone don't match exactly, molecular vibration due to heat (temperature) will destroy this complex quickly. This allows specificity.


Is there an ideal evolutionary body? I am a science fiction fan, and when I watch movies with aliens, I get annoyed at the fact that they're all humanoid. I think, "What are the chances that it will look that similar to humans?" But I wondered recently "What if there is an ideal shape for an organism in a specific environment?" An example is that all mammals have 4 limbs, and all fish have gills and fins (except for some, but I will get to that). What if that is because that is the perfect form for an organism in that kind of environment? Along with that, some fish have evolved to do certain, unique things, whether to camouflage, attack, or develop a symbiotic relationship (am I correct on that?), which brings up the question, how much does the mindset and disposition of an organism affect its end body shape, and how much more random does it make the process of evolution? What I mean to say is, say biologists were able to create organisms and watch them evolve quickly. If you took two single celled organisms that had no similarities, and put them in the exact same environment, would they evolve to look similar? Or would they develop their own, unique ways of surviving in their environment?

All mammals have 4 limbs, and all fish have gills and fins (except for some, but I will get to that). What if that is because that is the perfect form for an organism in that kind of environment?

Different mammals species live in very different environments. We all have four limbs (except exceptions), not because it is adaptive to all of us for a specific environment but because there a strong phylogenetic signal. You should have a look at Why don't mammals have more than 4 limbs?.

All fishes have gills and fins (except exceptions). This is definitely because they inhabit a common environment. Gills allows fishes to get oxygen from water. Fins is a general structure that allows swimming. You will note that marine mammals also have fins (we often talk about convergent evolution) Btw, the post Do fish break a water molecule to absorb oxygen? might be of interest to you

  how much does the mindset and disposition of an organism affect its end body shape, and how much more random does it make the process of evolution?

I don't really understand what you mean by "mindset" and "disposition".

Nothing is random except in the consideration of unknowns. One can make sense of a probability only by consideration of a priories. While tossing a coin is often considered as the random event by excellence, a toss of a coin is everything but random if you were to know the exact forces that apply to the coin. So asking is something is random without stating what are the a prioris you consider knowing and not knowing makes no sense (although it may make some sense in quantum physics).

  say biologists were able to create organisms and watch them evolve quickly. If you took two single celled organisms that had no similarities, and put them in the exact same environment, would they evolve to look similar?

We are actually able to witness evolution in a matter of weeks in lab with organisms with short generation time such as yeast or E. coli.

The repeatability of evolution is a vast subject. The issue with such question is that it depends a lot. It depends typically on what evolution you are expecting to see and the size of the population. For example a simple change in allele frequency at a selected locus in a large population is typically very much repeatable. But if you think about larger time scale then, most think it is wise to consider that evolution would take a totally different path. There is a famous quote that says:

"If the tape of evolution were replayed a million times, a species like ours would not necessarily evolve" Stephen Jay Gould

You should have a look at Is evolution a predictive theory?.


Why doesn't our immune system react to infused antibodies produced in a horse? Calmette tried injecting horses with snake venom and then taking out the serum which has produced antibodies against the venom and injecting in the snake-bitten human.

Shouldn't our immune system recognize this exogenous protein and try to eliminate it as it's a non-self protein?

Our immune system does react to horse antibodies, but as with any adaptive immune response it takes some time for the response to develop. In the weeks before our immune response fully responds to the horse antibodies, the infused antibodies can have their effect.

If you then have a second infusion of horse antibodies, the immune response would not only prevent them from having their beneficial effect, but it might case serious adverse effects.  This serum sickness (Wikipedia link) has been known for over a century; here is a paper from 1918 discussing it as a well-known issue:

  The injection of horse serum either in small or in large amounts in human beings is always followed sooner or later by the development of hypersensitiveness of the skin to subsequent injections of horse serum. For the development of this reaction serum disease is not essential.

--THE RELATION OF CIRCULATING ANTIBODIES TO SERUM DISEASE. J. Exp. Med. Published March 1, 1918

Although there aren't many modern situations in which horse (or other non-human species) serum is injected into humans, when it is (as with anti-venom, which is generally produced in non-human animals) serum sickness is still a concern.

  Serum sickness is a delayed immune reaction resulting from the injection of foreign protein or serum. Antivenom is known to cause serum sickness but the incidence and characteristics are poorly defined. ... The primary outcome was the proportion with serum sickness, pre-defined as three or more of: fever, erythematous rash/urticaria, myalgia/arthralgia, headache, malaise, nausea/vomiting 5–20 days post-antivenom.

--Incidence of serum sickness after the administration of Australian snake antivenom (ASP-22). Clinical Toxicology. Published  2016


can you create an offspring from ancient human's DNA? If a DNA from an ancient human, for example the cheddar man, is still intact, can you make an offspring today using that intact DNA?

https://www.theguardian.com/science/2018/feb/07/first-modern-britons-dark-black-skin-cheddar-man-dna-analysis-reveals

A species is generally defined as a group of organisms that can breed and produce fertile offspring. So, if you are extracting DNA from the an ancient human that is indeed the same species as us (homo sapiens), then by definition, you will be able to combine it with modern human DNA and generate offspring.

This is just stating the theory, the actual biology behind extracting that DNA and using it to fertilize offspring will be... messy.


Identification of a mammal in cage This unidentified animal was trapped in northern part of Kerala State India and images circulated through social media. Doea anyone know what species this is?

To me it looks like some kind of feline with mange.

It is unlikely to be a Lemur given the lack of thumbs on said animal. And this is India not Madagascar. Lemurs are only found on Madagascar.


Which C. elegans would be appropriate for general study? Would wild type N2 be best or Dyp-11? I know they're different, but I just want to observe the worms to see life stages, movement, etc. Dyp-11 seems like it would be easy to see but N2 is the wild type so I need help making an appropriate decision.

I suspect that that dpy-11-mutants (that's what you likely meant) are not very representative neither from the morphological nor from the behavioral points of view, because they have anomalies in body shape (dumpy appearance) and male tail morphology (see in WormBase and in Ko and Chow).

For a general purpose the wild-type should be best.


What recovers normal polarisation after hyperpolarisation? I have been taught that a $\ce{Na+/~K+}$  pump helps to recover normal polarisation after-hyperpolarisation in neurones. I could not find out how it does that, since I've also been taught that such a pump moves $\ce{3Na+}$  out of the cell and $\ce{2K+}$  into the cell. That implies that the potential can only get more negative. How does this work?

My hypothesis was that the potential 'leaks' out and recovers the 70 mV that way. I couldn't verify that, however.

Remember that the action potential gets more positive in the first place, so increasing positivity is achievable. Net Na+ movement into the cell makes the potential more positive. This occurs as the Na+ gate (right on the image below) are open. The key message is that the membrane can move charge to cause an increase in either positive and negative potential.

Imagine one side becomes more negative. The Na+ diffusion will correct this to reach an equilibrium around 3 to 4 milliseconds (ms) after the stimulus to reach the resting potential
 (as alluded to my @MCM in the comments).

There are some great animations demonstrating this principle on the University of Bristol's website. They clearly show how positive charge can be conferred over the membrane.

A (now deleted) comment linked to the below image that shows the potential and when the gates are opened and closed. I would still go to the bristol website too to see it in action, but this figure is a quick go to once you get your head around the timing of ion flux.

As with most biology, it is a little more complicated than that overly simple model. There are entire books on how neurones control their charges.

Note: The key terminology is somewhat muddled and there doesn't seem to be a standard term. I have seen this "recovery" phase called undershoot, overshoot (and overshoot rather unhelpfully also refers to another part of the action potential), the refractory period, and discussed as part of hyperpolarization. The go to term is afterpolarisation if you want to research this more thoroughly.


How does the body detect irreversible binding to receptors? I have read an article on Wikipedia about irreversible agonists and antagonists. These permanently bind to a target receptor on a cell. However, the receptor protein is then internalized and recycled by the body after the binding occurs. How does the body detect when a protein has been irreversibly bound in such a way? Is there some pathway involved in that or are proteins simply regularly recycled by the body?

Article: https://en.wikipedia.org/wiki/Irreversible_antagonist

The process of downregulating a receptor by internalizing and degrading it in response to (sometimes prolonged) activation or (sometimes prolonged) failure to activate is what pharmacologists call desensitization (in either context). You can read about this generally in Goodman and Gilman's Pharmacological Basis of Therapeutics, Chapter 3, under the subsection "Receptor Desensitization and Regulation of Receptors". There are a number of mechanisms, not all well understood, but the basic idea is that when a signal is constant (either always on or always off), it no longer has any value as a way of providing information. Receptor regulation, or desensitization, is a mechanism for, effectively, resetting the cell or tissue. Removal of the receptor can be followed by recycling, or protein synthesis and return of new receptor to the site.

One well studied mechanism for desensitization is seen in G protein coupled receptors (GPCRs), such as some Dopamine receptors. It is well reviewed here.

To answer your specific question, binding that leads to desensitization is detected the same way any other binding is detected. A receptor produces a signal on binding (or stops producing a signal). The downstream effect of that signal includes a process that involves internalization of the receptor from a location where it can receive signal.

Here that process is mediated by phosphorylation by GRKs (GPCR kinases), which allows for binding of arrestin, and so on...


Empirical evidence for Group Selection? A controversial concept in Biology "Group Selection", has caused confusion and conflict amongst scientists since the since the mid 1990s. The more general realm of study is termed the "unit of selection" discussion.

Definition

A simple working definition for "group selection" (edit/discuss this!) is:

  "Selection for traits that would be beneficial to a population of units at the
  expense of an individual unit possessing the trait" (here)

Question

  "What examples of group-selection are there?"

To add more structure, perhaps answers would consider the following details:

Organism/Species in question
Unit that experiences cost in fitness
Group that experiences benefit in fitness
Group-selected trait
Explanation

Forward Example (trait whose presence benefits the group)

Organism: Homo sapiens, Humans
Unit: Cells and their genes
Group: Collection of all cells in one individual Human body
Group-selected trait: anti-cancer traits, e.g. apoptosis (programmed cell death) via p53 ("guardian angel" gene that "kills" cancerous cells)
Explanation: Apoptosis is costly to the perspective of a cell, since it kills the cell and its genes. This enables the individual as a whole to live for long enough to mate and yeild offspring. Fitness of cells relative to other cells in the body is reduced, but fitness of the genome as a whole of that individual is increased relative to other individuals of that population -as a result of cancer-directed apoptosis.

Reverse Example (trait whose absence benefits the group)

Organism: Cervus elaphus, Red Deer
Unit: Individual red deer and their genomes
Group: Isolated population of red deer and the population gene pool
Group-selected trait: Lethal potential of antlers (e.g. sharp single antler instead of two blunt antlers).
Explanation: Consider a one-antlered stag, whose single antler is imbued with a jagged edge and is the product of a point mutation in his genome. During a rut he is able to win against other males as his antler inflicts potentially fatal injuries. This allows him to mate many females and have many offspring - however this leaves the population at risk of becoming extinct since the mating season would either have too few males to form a rut, or due to deleterious inbreeding defects in the next generation.

Links

Wiki: http://en.wikipedia.org/wiki/Group_selection
History: http://ib.berkeley.edu/courses/ib160/past_papers/beroukhim.html
Published Review: http://arxiv.org/abs/1204.6491

Of course do not feel restrained in your answers by the above suggestions - the point is to discuss the topic and learn!

Let's start with your definition.

"Selection for traits that would be beneficial to a population of units at the expense of an individual unit possessing the trait"

This is not a good definition of group selection. In reality, selection can act on groups regardless of the direction of selection at the individual level. This definition sounds to me (your link is directing me to somewhere unpleasant) like one that has been set up in order to study whether group selection can act as an explanatory principle for the evolution of individual-level altruism, which is an altogether different question than the title of your post (the two questions are often conflated for historical reasons).

To expand the debate, I will introduce two formal definitions of group selection both of which are defined by alternative forms of Price's equation (See Okasha's book Evolution and the levels of selection for a thorough analysis).

Interdemic group selection

Interdemic selection occurs when selection acts on both groups and individuals within groups separately. That is, both groups and individuals within those groups must be units of selection in their own right. We must be able to assign fitness to both levels of selection some way, and track the offspring produced at each level. In this form of group selection, group fitness corresponds to the ability of a group to survive and produce more groups of a similar kind, and individual fitness corresponds to the ability of an individual within a group to survive and produce more individuals of a similar kind within that group. A good example  is selection on multicelullar organisms and selection on cells within those organisms. If there are greater than two levels of selection, interdemic selection is commonly referred to as multi-level selection 2 (MLS2) (see Okasha).

'The extinction of some groups and the ``reproduction'' of others are essential features of evolution by group selection. If groups are the units of selection, then they must have the properties of variation, multiplication, and heredity required if natural selection is to operate on them.' Maynard Smith

Intrademic group selection

Intrademic selection occurs strictly among individuals within a meta-population. That is, individuals are the only units of selection we study. The groups in which individuals reside are seen as part of the structure of the environment in which individuals live. In this form of group selection, individual fitness corresponds to the ability of an individual to survive and produce more individuals of a similar kind, given that they reside in a particular group. A good example of this perspective on group selection is selection cells of the quasi-multicellular organism Dictyostelium. Cells of this species are units of selection in their own right that occasionally group together into bodies that may also act as units of selection. If there are greater than two levels of selection, intrademic selection is commonly referred to as multi-level selection 1 (MLS1) (see Okasha).

'A way of looking at this is that the [intrademic] group selection approach looks at the evolution of individual characters in a group structured population, whereas the [interademic] group selection approach looks at the evolution of group characters.' West et al

Equivalence

It is worth pointing out that there is currently equivocation in the field about whether these two selective processes are different perspectives on the same underlying biology or distinct causal processes.

Another important point to note is that it is the intrademic form of group selection that leads to the conclusion that kin selection and group selection are really just different perspectives on the same selective process. This has been shown mathematically by Queller.

There is not yet a conclusive proof either way showing that interdemic group selection and kin selection are equivalent or not. Some evolutionary theorists feel that they are, while many feel that they are not.

Group selection versus group adaptation

It is also important to point out the distinction between the process of selection acting on groups (which most evolutionary theorists accept - I mean, it definitely does happen!), and whether or not this selection gives rise to group adaptations (which evolutionary theorists are equivocal about). Some argue that all adaptation can be explained from selection acting on lower-level units (right down to the gene, remember Dawkins?), whereas others think there may be nested levels of causality that cannot be reduced in this way.

Empirical research

There are many examples of laboratory and field based studies of group selection. Too many to list here. In a response to a theoretical paper by Gardner, a history of empirical research on group selection was given by Goodnight. The original paper, its response, and its counter response are worth a read to understand some of the different perspectives on the debates. In particular, two different perspectives on the evolutionary dynamics of cancer are presented that nicely illustrate the differences between MLS1 and MLS2 thinking.


What happens to eyeball when you push your eye muscles harder? I have myopia and I read that the rays of light intersect before the retina.
When I can not see clearly I can push somehow my eye muscles and can see a bit clearly. The object gets clear but moves some distance ahead (getting smaller).
My question is: What is in fact happening to the eyeball? Do the eye muscles contract it and make it more round than ellipsoid thus bringing the retina forward  so the light intersects on it?
In fact I have the feeling that the eye ball gets longer (ellipsoid).

Do you mean squinting? Any sort of tension on the eyes would result in changing of the shape of the eye. A change in shape will bend light differently. The perceived effects you're describing are most likely from you changing the shape of your eyeball to take in more light.
In terms of squinting, eye strain like that won't lead to blindness or worse vision. There's more danger with UV from the sunlight (cataracts) or getting wrinkles from squinting too much in the long-run.


What is the mechanism of regulation of PER /CRY genes? I've read multiple descriptions of biological/circadian clocks and they all mention PER, CRY and CLOCK genes. While I kinda get how they are connected, what interests me is how these actually regulate each other. Do these genes encode proteins that once created bind to the DNA and cover the transcription sites for other genes(like PER protein covering the binding site of CRY)?

A lot of diagrams and descriptions of the process are very complex, and I would appreciate a simple answer (if it exists).

Wikipedia gives a very good explanation of this, on the page for the suprachiasmatic nucleus.

  For example, in the fruitfly Drosophila, the cellular circadian rhythm
  in neurons is controlled by two interlocked feedback loops.

  In the first loop, the bHLH transcription factors clock (CLK) and
  cycle (CYC) drive the transcription of their own repressors period
  (PER) and timeless (TIM). PER and TIM proteins then accumulate in the
  cytoplasm, translocate into the nucleus at night, and turn off their
  own transcription, thereby setting up a 24-hour oscillation of
  transcription and translation. In the second loop, the transcription
  factors vrille (VRI) and Pdp1 are initiated by CLK/CYC. PDP1 acts
  positively on CLK transcription and negatively on VRI. These genes
  encode various transcription factors that trigger expression of other
  proteins. The products of clock and cycle, called CLK and CYC, belong
  to the PAS-containing subfamily of the basic helix-loop-helix (bHLH)
  family of transcription factors, and form a heterodimer. This
  heterodimer (CLK-CYC) initiates the transcription of PER and TIM,
  whose protein products dimerize and then inhibit their own expression
  by disrupting CLK-CYC-mediated transcription. This negative feedback
  mechanism gives a 24-hour rhythm in the expression of the clock genes.
  Many genes are suspected to be linked to circadian control by "E-box
  elements" in their promoters, as CLK-CYC and its homologs bind to
  these elements.

  The 24-hr rhythm could be reset by light via the protein cryptochrome
  (CRY), which is involved in the circadian photoreception in
  Drosophila. CRY associates with TIM in a light-dependent manner that
  leads to the destruction of TIM. Without the presence of TIM for
  stabilization, PER is eventually destroyed during the day. As a
  result, the repression of CLK-CYC is reduced and the whole cycle
  reinitiates again. (http://en.wikipedia.org/wiki/Suprachiasmatic_nucleus#Fruitfly)

The suprachiasmatic nucleus (SCN) is a tiny part of our brain residing in the center. It maintains a biological clock through a gene expression cycle in the individual neurons. The mechanism for humans is very similar to the mechanism for fruit flies, as explained above, but to rehash a bit...

In the fruit fly model there are five players: CLK, CYC, PER, TIM, CRY.

CLK and CYC are transcription factors for PER and TIM, and bind to their promoters in order to activate the expression of PER and TIM.

When the expression level of PER and TIM gets very high, the PER and TIM proteins return to the nucleus, and inhibit their own transcription factors (CLK and CYC) through molecular interactions.

The CRY protein is light-sensitive, and so daylight (or artificial light) will cause CRY to destroy the TIM proteins. Without TIM, we no longer get the PER-TIM dimers that inhibit the CLK-CYC transcription factors.

In humans and other mammals it's the same concept, but with slightly different players (e.g., homologous genes).

What's important here is that we have a biological clock on the cellular level. We haven't gone into how this clock is used yet... But, it's my understanding that the SCN uses the information to tell the pineal gland when to produce melatonin.

The melatonin causes us to be drowsy, lowers our body temperatures, and causes us to fall asleep.

You can see another cycle at work here - our body temperature, which rises with wakefulness, and declines with sleep.

This gives a more general answer to how circadian rhythms are used to influence our sleep cycle. Your question was how the genes involved in circadian rhythms regulate each other. The answer is the transcription-translation negative feedback loop described above.

Hope this helps...


How does the choice of blood draw site influence the possible specificity of a serological test? The news has reported that a new serological test for the presence of anti-SARS-CoV-2 antibodies has received an emergency use authorization from the FDA, and notably has a higher specificity than other tests (99.8%).

The new test requires blood to be drawn from a vein, rather than a finger prick, and a quote from the test's manufacturer reads, "If you take blood from a finger prick, you will never be able to achieve the same level of specificity that you will achieve … when you take blood from the vein" (non-scientific news outlet source). Although the question is prompted by news related to COVID-19, I'm interested in the general case as well.

It is unclear to me why this would be the case, since antibodies should be present in capillary blood taken from the fingertip. I would suspect one of two reasons, but I don't have enough of a biology background to verify whether they make sense:

1) The volume of blood which can be drawn from a vein is much larger. This would make sense if it improved the sensitivity to a low-concentration antibody of interest, since there may not be enough antibodies in a fingertip sample to bind to antigens in the test. However, it's not clear why having a larger sample would help with specificity.

2) Fingertip blood samples are contaminated with lymph, matter from the skin surface, and so on. I'm not sure how it would affect the specificity of the test. In my naive understanding of serology tests, the reagent would consist of a synthetic antigen of interest, plus either anti-human-Ig or a second moonoclonal antibody for the antigen that would be used to detect any bound antibodies from the sample. It's not clear to me how these sorts of contamination could cause false positives for this sort of binding.

This ref, https://academic.oup.com/ajcp/article/144/6/885/1761216
show that drops of finger prick blood vary more than venous blood.

The main reason for using venous blood is licensing. A test is licensed only for an exact procedure and materials. If you vary any conditions the license is invalid.

However, I would not expect a test for antibodies (present vs. absent) to show much variation except for detecting the lowest levels of antibodies. (Sorry I cannot find a ref for this).


Identification of black growth on onion skin I have encountered this black-colored growth on onion skins a lot. It seems to develop over the course of weeks and I have rarely, if ever, encountered the material on fresh ones. If I peel the onion and it streaks the onion flesh, it appears, dark blue-ish. It looks like a fungus, perhaps a bacterium, but I am unsure. It is often found 'hiding' under the outer layer of skin on the deeper skin layers. In the photo the outer layer of skin was peeled off. It never seems to invade the edible parts below, though.

The pictures below are standard white onions from the local supermarket in Canberra, Australia (Canberra [Australia's capitol yes!] lies between Sydney and Melbourne). I must admit, I don't know if they are imported. The pictures below were taken mid-winter. Temperatures in our kitchen plummet during the day because of bad insulation. In the evenings and weekends it's room temp with heating. The onions are stored in the dark, in a kitchen cabinet. Humidity is low and mostly the days are dry and sunny. However, we cook in the kitchen so at times there is plenty of moist.

Also, I wonder, would it be harmful? No self-help medical issues here, I always wash and fry/cook my stuff and no issues whatsoever, just curious.

I understand there is little to go with. However, a general genus or group of fungi would already be cool. I googled and sought for images to no avail.

I think it is Aspergillus niger:

On the second place I'd suggest  Black Mold disease caused by Alternaria species.


DNA barcoding and real-time PCR I recently read an article on how DNA barcoding was used to identify species present in health products.

I also read an article about how Real-Time PCR was used to identify meat species in meat products.

I'm curious as to why one method is used over another. I know that DNA barcoding uses mitochondrial DNA to detect species, and Real-Time PCR uses species-specific primers to detect species.

Am I correct in thinking that real-time PCR cannot identify unknown species, but can tell you if the DNA matches a specific species you're looking for? For example, if I test for E. zebra but find something else, I cannot identify that unknown species and more testing is required?

Whereas in DNA barcoding, all I do is match the results against a huge list of known species in a database, which means I can identify unknown species without providing any prior knowledge?

You've done a pretty decent job of answering your own question, but there are a few things that can be elaborated on.

The general convention is to use the mitochondrial Cytochrome C Oxidase 1 (COI) gene for barcoding animals and chloroplast genes (rbcL, matK, and trnH-psbA) for plants. The three biggest reasons for selecting these genes are 1) their ubiquity; 2) the presence of many copies per cell, so it's easier to PCR amplify the sequences; and 3) mitochondrial and plastid DNA has a much higher mutation rate than nuclear DNA, making it possible to uniquely barcode very closely related organisms. This method is incredibly sensitive, reliable, and easy. The original DNA barcoding publication can be found at doi: 10.1098/rspb.2002.2218

Thanks to the efforts of consortia like CBOL, BOLD and iBOL, there are now many millions of reference sequences databased, covering pretty much any multicellular organism you are ever likely to encounter (assuming you don't work on a deep-seq sub or something).

As you say in your post, there are significant limitations to using qPCR to identify species. You have to know beforehand what it is you are looking for, and you are left with a simple yes-no. This is not to say there is no place at all for qPCR in the species identification game, however. The method is very fast, and in cases where you are only interested in detecting a single species or small number of species, it's much more convenient than getting the DNA sequenced (for example, during quality control in a meat processing plant, doi: 10.1080/02652030701584041).


Which brain regions are D1 dopamine receptors expressed, and which brain regions are D2 dopamine receptors expressed? This is a follow-up question to If D1 receptors stimulate adenylate cyclase (through GPCRs) and D2 receptors inhibit it, then why do mutations in both have similar effects?.

As a further question - I'd like to ask: do D1 dopamine receptors have the same (excitatory) effect everywhere in the brain? And do D2 dopamine receptors have the same (inhibitory) effect everywhere in the brain?

As to your main question, I imagine the Paul Allan Brain Atlas has what you're looking for. In 3D even.

Human Brain Map
D1 Receptor
D2 Receptor
Also comes in mouse flavored.

Offhand, I cannot be of assistance for the second question.


Identification of Insect found on beach in Maharashtra Six legs, two antennas, Neon green colour pattern with black. Had no wings.

This appears to be a Lychee Shield Bug, Commonly found in India, formerly considered a beetle, but now classified as a True Bug.


Is evolution always unidirectional? Is it possible, at least in theory, for a species to evolve into another species and then evolve back into the first species?

It's possible, but very unlikely.  Usually it takes a substantial number of genetic differences to qualify two organisms as different species.  One might think that reversing the direction of selection pressure could reverse a genetic change, but genetic change begins with random mutations which are not determined by selection pressure.  It's very unlikely for one random process to undo another random process (imagine mixing black and white sand in a jar by shaking it, then trying to unmix by unshaking!).


Breeding mosquitoes at lower temperature It is well known fact that, to slow down the growth of drosophila, they are grown at 18-19 degree Celsius. It helps in maintaining stocks for longer time without frequent change of food. Is it applicable to mosquitoes? especially Aedes aegypti?  can we slow down its growth by growing them at lower temperature?

Check "breeding temperature" and similar obscure phrases for the search.

There's a study on physical aspect of mosquitos bred in cold, they perhaps didn't note any significant metabolism change, you can read the articles, they mostly cover wing length scales and follicles.

There's a study on lave development speed which passes over breeding temps, it may however cover "egg temperature".


Can I use PCR buffer instead of cDNA synthesis buffer? I am using Fermentase First strand cDNA synthesis kit but its buffer is over. I need to work today but I have not access to any sorce currently. I have PCR buffer in the lab. Can I use PCR buffer instead of cDNA synthesis buffer? What are your other suggestions? Thank you

This page has the recipe for 10X M-MuLV RT buffer:

500 mM Tris-HCl
750 mM KCl
30 mM MgCl2
100 mM DTT
pH 8.3

If you have the basic reagents, I suggest making that.


Why are human eye colours limited? Related to the question What causes the colors we see in eyes?, I am wondering why human eyes are restricted in colour. Most common eye colours are blue, green and brown. Why not yellow, orange, purple, red and so on?

I am guessing this is related to the function of the iris and that other colours do not have the same effect on light absorbing or something like that.

There is only one main "coloring" agent, or pigment, in the eyes.  That pigment is melanin.  To a much lesser extent, at least in health individuals, you can have lipofuscin produced which gives a golden-amber color to the eyes.  It should be noted that lipofuscin is most likely produced because of oxidation damage/stress in your eye, and not something to be hoping for (Beatty et al has a good review of the subject (1)).
Indeed, lipofuscin in the eyes can be seen as a symptom to physicians, so for the rest of the answer I will only consider melanin, eumelanin and pheomelanin in particular, as the normative pigment in the iris.
To make additional colors, we would need to develop an additional pigment, and or modify eumelanin so that it produces different scattering properties.  So why do we have melanocytes in the eye producing melanin in the first place?
As much as we might consider it as a factor now, sexual selection was probably not the main pressure for having pigment in the eyes.  Instead UV protection almost assuredly is (2, 3).  Thus for another pigment to be selected for, it would probably need to do a better job protecting us vs. UV (also, further selection in humans is hampered by all kinds of things like behavior, medicine, and life span).
Eumelanin does a good job protecting us from UV (2, 3) and in fact does a better job than phenomelanin (4).  It seems incredibly unlikely that we would develop the necessary evolutionary pressure to have our pigment epithelium to produce a totally foreign pigment.
And that is what prevents us from naturally having a whole rainbow of colors in our iris.  One could conceivably engineer a better pigment, and have the genetic information needed to produce it delivered in gene therapy (I hate to think of people purposefully infecting their pigment epithelia).  I, for one, wouldn’t sign up for that.
(1) Beatty S. et al. The role of oxidative stress in the pathogenesis of age-related macular degeneration. Surv Ophthalmol. 2000 Sep-Oct;45(2):115-34.
(2) Hu DN. et al. Role of ocular melanin in ophthalmic physiology and pathology. Photochem Photobiol. 2008 May-Jun;84(3):639-44. doi: 10.1111/j.1751-1097.2008.00316.x. Epub 2008 Mar 8.
(3) Simon JD, Peles DN. The red and the black.  Acc Chem Res. 2010 Nov 16;43(11):1452-60. doi: 10.1021/ar100079y. Epub 2010 Aug 24.
(4) Hu DN et al. Uveal melanocytes, ocular pigment epithelium, and Müller cells in culture: in vitro toxicology. Int J Toxicol. 2002 Nov-Dec;21(6):465-72.


The best free and most up to date phylogenetic tree on the internet? I found phylogenetic tree in wikipedia is lacks of accuracy. It actually confusing with versions. Some terms was not scientifically accurate with dna analysis anymore

So are there anyone know where is the most updated datasource on the internet?

Available ressources

I would recommend oneZoom.org is probably the best ressource. oneZoom.org is based on openTreeOfLife.org (for phylogenetic relationships) and eol.org (Encyclopedia Of Life) (mainly for the pictures I think). If you do not fancy to much the display and links of oneZoom/org, then I would just recommend openTreeOfLife.org.

There is also tolweb.org but it is not as nicely updated as openTreeOfLife.org (and therefore openTreeOfLife.org) and the dates are harder to find.

Particularities of oneZoom.org

I particularly like that for each node oneZoom.org offers links to

wikipedia
encyclopedia of life
the red list
NCBI

, which makes it a very appreciable tool. oneZoom.org has the advantage of a nice display (although a bit slow to load IMO) and is easy to navigate and get time to the Most Recent Common Ancestor of a lineage.

I also like that you can just add the species name after "#" in the URL and it will jump to its node. Here is the Kagu for example.

Potential issues in oneZoom.org

Of course, oneZoom.org contain a few mistakes! Some of them are unintentional (wrong picture, misrepresentation of what is known from the literature, fail to update information), some of them are caused by lack of knowledge of true phylogenetic relationships. oneZoom.org does not say how certain we are that a given speciation event is correct or correctly dated, it just display the best estimates we have. If a specific node is of interest to you, you will need to go to the scientific literature which will give you much more information about what we know and what we roughly guess.


What does it mean to "write an image and GIF into the DNA of bacteria"? BBC News recently published an article saying that:

  An image and short film has been encoded in DNA, using the units of inheritance as a medium for storing information ...
  The team sequenced the bacterial DNA to retrieve the gif and the image, verifying that the microbes had indeed incorporated the data as intended.

The news article shows an image of a hand (shown above) and a short film (not shown here) of a horse rider that was encoded into the DNA "using a genome editing tool known as Crispr [sic]".

My question is, what does this mean? Did the scientists break down an image into 0's and 1's and (install?) it into bacteria?  How does a scientist (download?) an image into bacteria and then (redownload?) the image later?  How does DNA hold information of a picture that can be (downloaded)?

The image was not in the DNA as such, only as an abstract representation that could be converted into an image from knowledge of the code.  Briefly, they encoded the image into DNA, using a couple of different strategies in which DNA represented pixels -- either with a single DNA base representing a pixel, or with a triplet representing a pixel.  Knowing the code they used, they could then extract the information and turn it back into an image.

Quoting from the original article, CRISPR–Cas encoding of a digital movie into the genomes of a population of living bacteria:

  We began with an image and stored pixel values in a nucleotide code ... We first encoded images of a human hand using two different pixel-value-encoding strategies: a rigid strategy, in which 4 pixel colours were each specified by a different base; and a flexible strategy, in which 21 possible pixel colours were specified by a degenerate nucleotide triplet table ...  To distribute the information across multiple protospacers, we gave each protospacer a barcode that defined which pixel set (denoted as ‘pixet’) was encoded by the nucleotides in that spacer. Four nucleotides define each pixet, and the pixels of a given pixet are distributed across the image ...

Their 21-color strategy is outlined in this figure:

Note: The paper isn't open-access. If you want a full-access version, Church often puts freely accessible versions of his papers on his web site; this paper, #441 on his list, is still shown as "in press" there, but check back at intervals and maybe it will be available there


Natural enemies boost deep evolutionary fitness? "Two species that reduce one another's fitness on microevolutionary
  (short-term) timescales can increase each other's macroevolutionary
  (long-term) fitness"

Opinions?

Intuitive Examples:

Body Size - Predator-prey relationships or interference relationships
(fighting, e.g. for territory) are often documented to put seletion
pressures to grow in body size, often a positive feedback loop. In
the short term the presence of the natural enemy in this case often
leads to decreased population fitness (probability of being
eaten/probability of fatal conflict over territory). But in the long
term such large body sizes acts as an advantage over potential future
enemies of the same kind. This is particularly relevant to marine
ecosystems - where the size of fish often determine where in the food
chain that fish is.
Speed/agility - Predators and prey that rely on speed/agility to
capture (predator) or escape (prey) undergo an evolutionary arms race
leading to positive feedback of speed/agility boosting morphologies.
In the short-term the natural enemy of the prey acts as a burden to
population fitness (probability of being eaten) but in deep time the
prey has acquired morphological advantages over potential future
natural enemies such as competitors for resources.
Venomousness -Why do venomous animals live in warm climates?

The question is interesting.

I am afraid about the use of the word "fitness" in you question. The fitness is usually defined as the number of offsprings an individual can sire in its lifetime. Most often we talk about relative fitness which is the relative number of offspring in an individual can sire in its lifetime compare to the individual in the population that sire the greatest number of offsprings.

How would you compare fitness of individuals between different species? Just by counting the number of offspring they left behind? Or did you mean that most fit species are actually those species that can outcompete others? If yes, then I would say that saying

  Two species that reduce one another's fitness on microevolutionary (short-term) timescales can increase each other's macroevolutionary (long-term) fitness

can be restated

  Two species that reduce one another's fitness on microevolutionary (short-term) timescales can increase each other's macroevolutionary (long-term) species competition ability

and it is actually just a special case of

  One species that evolve under many strong selection pressure ends up being a very competing species.

The explanation is the following:

One species that undergoes one selective pressure, will see its genetic variance decreases. The weak individuals will disappear letting places to the strong individuals. Then newly arisen variance (mutation) will come up only in the strong individuals (as the other ones disapeared). This is what J.Gould meant by saying "Natural selection creates the fit". As a consequence a species that undergo many successive selection pressure will end up with purified and very strong genotypes while, in a species that were free to evolve without selection they would have evolved many different genomes with some good mutations nested in very poor genetic background.

You could as well use the concept of lineage selection and states that lineage that succeeds to outcompete others will thrive while species that suffer from competition with other species will get extinct. As a result, if you compare all species that were in competition with another species in the past with all species that were not in competition, you will find out that those that were in competition are more resistant to competition. But I guess this is not exactly what you meant when saying: "Two species that reduce one another's fitness on microevolutionary (short-term) timescales can increase each other's macroevolutionary (long-term) fitness"

Finally you might think of the ability of species to evolve better. This ability is called "evolvability" (see this book for example). You might say that species that undergo many selection pressures were selected to resist to newly arisen selection pressure. As a result, species that are under competition might end up with a greater evolvability than those that were not under selection. Resulting that species that were under competition will tend to increase to always increase their fitness in the long term.


Nature of Dengue Fever Genetic Material Once the genetic material for Dengue Fever is inserted into the human DNA, would the Dengue Fever molecular material be in the form of its own isolated DNA fragment or will it be inserted directly into some existing piece of our DNA?

In a 2011 Nature review they provide a figure for the life cycle of the Dengue virus,

Source: Immunity to dengue virus: a tale of original antigenic sin and tropical cytokine storms

The Dengue virus is a positive-sense ssRNA virus. This means the ssRNA that enters the host may immediately be translated. The viral ssRNA does not integrate with the host genome!


How do fishes "breathe" while eating? First of all, a fish opens its mouth and water enters which passes through its gills. This helps in oxygenating its blood. So, if any food particle is in its mouth, how can it "breathe" i.e. how does exchange of gases occur? Shouldn't the pathway where water flows from mouth to gills be clogged like a drain full of sludge?

They can pump water over their gills with their opercular flaps (i.e., the structure that covers and protects the gills). This is assisted by the branchiostegal rays. Food would generally not interfere with this process. Additionally, gill rakers assist in keeping food in the mouth.

Some great references for questions like this:

Barton, M., & Bond, C. E. (2007). Bond's biology of fishes. Thomson.

Moyle, P. B., & Cech, J. J. (2004). Fishes: an introduction to ichthyology (Vol. 726). Upper Saddle River, NJ: Pearson Prentice Hall.


Why gout attacks mostly big toe? A gout attack typically causes pain, swelling, redness, and warmth (inflammation) in a single joint, most often the big toe.

What makes big toe more susceptible for gout?

Also I was said that it mostly occurs in right big toe, if this is correct then what could be the reason for its right sidedness?

Source : http://www.webmd.com/arthritis/gouty-big-toe

The question has been explored in great depth in the cited paper. Have a look.

Roddy E. Revisiting the pathogenesis of podagra: why does gout target the foot?. Journal of foot and ankle research. 2011 May 13;4(1):13.

Summary:

Nucleation factors: The site of Gout depends on where the Monosodium Urate (MSU) crystals are likely to form. This process of nucleation depends on a variety of factors. One is temperature, its solubility decreases with temperature and hence the fingers and the toes are more likely sites of MSU precipitation. Further, trauma and pH also affect the nucleation. Repeatedly stubbing a toe makes the first metatarsophalangeal joint (MTPJ) specifically vulnerable.
Cartilage damage and Osteoarthritis(OA).OA sites are correlated with those of higher MSU deposition and cartilage damage (for reasons and evidence, refer to the cited paper). Hence, factors which make MTPJ more susceptible to OA can increase the predilection for MSU deposition. These include "increased concentrations of chondroitin sulfate, degradation of protein-polysaccharide complexes, and epitaxial MSU crystal nucleation and growth on cartilage fragments"

The right sided predilection might be because most people are right-handed, and they might be more likely to injure or stub their right toe.


What is the "Spandrels" debate about? In a former question, as a side question, I asked a clarification about the "Spandrels" paper. Being not a biologist, it was the first time I encoutered it.

Subsequently I tried to collect some information, because I read that the paper is debated and deemed "wrong" by at least a part of the community.

Despite my efforts I have not fully grasped what the issue is:

is the incorrect reference to the architectural element? (i.e., the paper is wrong because it uses a not fully agreeable comparison)
are some (or all) the claims in it wrong? if yes, are there any suggested reading to understand why?

I ask specifically because the first reference I encountered points to Dawkins, and I would like to understand if this paper is a mere pawn in the big "gradualists versus punctuationists" debate or if it has merits on his own.

Short version

The paper has nothing to do with punctuated equilibrum vs. gradualism (see also here), which was published a few years earlier. This debate is much different (but equally important, I think).

The authors of the Spandrels paper criticized evolutionary biologists of taking a very narrow view of the evolutionary process. They claiming (wrongly) that evolutionary biologists believed that every single trait on an organism was an adaptation that resulted from natural selection. The trait would not be present unless it was an adaptation. The authors claimed (rightly) that traits could not be considered independently. Instead, the traits had to be considered in light of the evolutionary history and developmental biology of the organism. To your specific questions:

The architectural metaphor was wrong. Does it make their entire argument wrong? No. They did not understand architecture. That does not mean they did not understand evolutionary biology.
Are some of their claims wrong? I think yes and no, but the full answer requires more nuance than can really be given here so read the long answer below if interested. I don't know of a single reference that supports/rebuts the Spandrels paper but consider Why Evolution is True by Jerry Coyne, The Greatest Show in Earth by Richard Dawkins, and Endless Forms Most Beautiful by Sean Carroll. None of these address directly the charges lodged by the Spandrels paper but they do show how evolutionary biology is integrative of many ideas instead of isolating each trait without considering the biology of the entire organism. (I have no commerical interest in any of these books. I simply support the ideas presented.)

Long version from my perspective.

In 1979, Stephen J. Gould and Richard C. Lewontin (hereafter, G&L) published a paper, "The Spandrels of San Marco and the Panglossian Paradigm: A Critique of the Adaptationist Programme", in the Proceedings of the Royal Society of London, Series B.  The title of the paper mixes two metaphors. The first is the character Dr. Pangloss from Voltaire's "Candide." Dr. Pangloss is a bit of an optimist, who says,

  It is demonstrable ... that things cannot be otherwise than as they are; for as all things have been created for some end, they must necessarily be created for the best end. Observe, for instance, the nose is formed for spectacles, therefore we wear spectacles. The legs are visibly designed for stockings, accordingly we wear stockings. ... [A]nd they, who assert that everything is right, do not express themselves correctly; they should say that everything is best." - Dr. Pangloss

Dr. Pangloss is saying that everything has a purpose, and each thing is designed specifically for that purpose. G&L extend this metaphor to evolutionary biologists.  G&L claim that evolutionary biologists (at least to the time of their publication) tended to make claims similar to Dr. Pangloss: every trait that could be found on an organism results from natural selection and adaptation.  G&L write,

  An adaptationist programme has dominated evolutionary thought in England and the United States during the past forty years. It is based on faith in the power of natural selection as an optimizing agent. It proceeds by breaking an organism into unitary "traits" and proposing an adaptive story for each considered separately. - G&L

Hence, the Panglossian paradigm. Every trait has an adaptive purpose and is necessarily the "best" that it can be. G&L then argue that evolutionary biologists of the time failed to consider the entire organism when assigning adaptive value to each trait separately.

  We criticize this approach and attempt to reassert a competing notion ... that organisms must be analyzed as integrated wholes, with bauplane so constrained by phyletic heritage, pathways of development, and general architecture that the constraints themselves become more interesting and more important in delimiting pathways of change than the selective force that may mediate change when it occurs. - G&L

G&L are saying that the many organismal traits are functions of evolutionary history, developmental pathways, and other structural contraints.  G&L argue that most evolutionary biologists of the time did not consider the entire organism when ascribing adaptive value to any one trait. In G&L Panglossian metaphoric terms, evolutionary biologists had decided that the adaptive value of the nose was to support glasses, but they had failed to consider that the nose may have evolved for other reasons (e.g., smell) and that the supportive value of the nose was an evolutionar by-product instead of an evolutionary cause.

This brings us to the second metaphor, the architectural spandrels. Spandrels are triangular spaces that form when two arches meet, or when an arch meets a rectangle.  According to G&L, spandrels are a necessary by-product of the architectural joining of the two shapes. The spandrel itself serves no purpose. In evolutionary terms, spandrels have no adaptive significance that resulted from natural selection. Instead, they are an evolutionary by-product that resulted from selection on other traits (arches and rectangles).

While the architectural metaphor apparently fails, their primary argument does not change.  Traits cannot be considered individually. Traits of an organisms must be evaluated as one part of the entire organism, together with it's developmental biology and its evolutionary history.

Here are two examples to represent their argument, written for a general audience. The first example is based on the human hand.  Our hand has five fingers. Each finger except the thumb has three bones (called phalanges), which you can see easily when you curl your finger. The thumb has only two phalanges. What is the adaptive value of having four fingers with three bones each, and a thumb with two bones? You might say that such a structure imparts excellent manual dexterity, from grasping to manipulating objects. But, would we not have that same dexterity if we had four fingers, or six? Why does the thumb have only two bones and not three? How could that be adaptive? These specific traits may not be the direct result of natural selection.

The structure of our hand is explained by our evolutionary history. Our primate ancestors had five fingers. So did our earliest mammalian ancestors, as did our earliest reptilian ancestors. However, some of the earliest amphibian ancestors, such as Acanthostega, had more than five digits (toes, fingers). Somewhere in early amphibian evolutionary history, our ancestral lineage converged on five digits, and most descendant vertebrates retain that five digit pattern. Even those vertebrates today without five digits usually display five digits during development, such as the ostrich (scroll down to image of blue-stained bones). If we assigned an adaptive purpose to the  human hand independently of its evolutionary history, we might very well be wrong.  Science doesn't like wrong.

Think about the five toes of your foot. Each toe has three bones except for the big toe, which has two bones. Manual dexterity? No. Evolutionary history? Yes.

The second example is the groove in your upper lip below your nose. This groove is called the philtrum. Can you think of an adaptive function for the philtrum? You might think that it helps to direct odors towards our nostrils, or hypothesize some other adaptive purpose. However, it appears that the philtrum is a by-product of the development of our embryonic face (YouTube video). The trait of our philtrum may not have adaptive significance. It is a by-product our face formation when the two sides meet in the middle.

G&L's publication produced quite an uproar. It's easy to find criticisms of the paper. Some have criticized the architectural metaphor. A bad metaphor does not necessarily make a bad scientific argument. Others have criticized the scientific rigor of their arugments. This blog entry, associated with the respected ecology journal Oikos, dislikes the paper and identifies several problems. The Oikos blog also links to several other sites that either support or dislike the G&L article. Most evolutionary biologists disliked the claim that they did not see the "whole organism."

Rightfully so, I think. I do not know of one evolutionary biologist (myself included) that has ever considered a particular trait without considering the broader evolutionary history of an organism. Indeed, considerable effort is spent by evolutionary biologists to determine how the evolutionary history of an organism influences its trait. The same applies for evolutionary developmental biology and other biological processes. For example, Martin et al. (1993) related evolutionary rate to body size, metabolic rate, and generation time of various animals, a very integrative (not isolating) approach.

To be fair, I think the G&L paper needs to be considered in the context of its time. Remember that i was published in 1979. Reread the first G&L quote above. They say, "during the past forty years."  The G&L paper was published in 1979. Forty years before this paper was published was during the "modern evolutionary synthesis." Without going into details (ask another question on Biology.SE!) the modern evolutionary synthesis provided the genetic mechanism (and so much more) that explaiend how Darwin's concept of natural selection could actually work. Once the relationship between Mendelian genetic inheritance and natural selection was proposed, many evolutionary biologists tested this connection. It is not surprising to me that G&L perceived this strong "bias" towards a selectionist (Panglossian) paradigm because many biologists of the time were trying to understand how Mendelian genetics contributed to natural selection.

At the time of the modern synthesis, the structure of DNA was not yet known.  The structure was finally realized by Watson and Crick (and Franklin!) in 1953, only 26 years before G&L's paper. Today we think nothing about the DNA structure but molecular genetics has advanced so much since G&L's publication that we have a much greater understanding of evolution and natural selection at the genetic level. Today, you can't study the evolution of a trait without considering its underlying genetic architecture.

In my opinion, one of the most, and perhaps the most, important development in the field of evolutionary biology is the field of evolutionary developmental biology (evo-devo). This field did not really mature as a discipline until about 2000, when the Proceedings of the National Academy of Sciences in the US devoted an entire issue to the topic. Developmental biology was a discpline that G&L had argued was important to consider. I'd bet that even they had no idea how important the evo-devo discipline would become to understanding evolutionary change. Still, recognition of the relationship between evolution and development was recognized as long ago as the mid-1800s by Ernst Haeckel. Evolutionary biologists were not necessarily considering traits in isolation from evolutionary history or developmental biology.

In the end, G&L used broad brush strokes to paint evolutionary biologists into a small canvas, claiming that biologists had a narrow evolutionary viewpoint. The evolutionary biologists responded (then and now) that their perspective was wide, even when focused on a particular trait.

The G&L paper continues to prompt considerable debate, which I think is the value of their paper. Every young graduate student should be required to read the paper. Even jaded scientists need a refreshing jolt to an established way of thinking. Our thought processes will alway benefit when we are reminded that evolutionary biology is a broad discipline that must embrace many other disciplines to arrive at a full understanding of the history of life on Earth.


How do anaerobic bacteria produce ATP for their own cellular activities? Anaerobic bacteria utilise glycolysis:

Glucose + 2 P + 2 NAD+ => 2 ATP + 2 H + 2 NADH + 2 H2O + 2 Pyruvate

followed by fermentation:

Pyruvate + NADH => Lactate + NAD+

The resultant NAD+ formed can then be used again to break down more glucose molecules in glycolysis to produce ATP.

However, besides NAD+, glycolysis also requires an input of 2 ATP at the beginning (for the phosphorylation of glucose to glucose 6P, and fructose 6P to fructose 1,6 BP)

Since only 2 ATP is produced from glycolysis initially, would these 2 ATP be reused in another round of glycolysis?

If so, how do anaerobic bacteria produce a net amount of ATP for cell activities and growth?

The product is 4 ATP not 2, 2 is the net product because two are used to start the reaction.

Looking at the complete glycolysis reaction helps.

ATP can be used to start another round of glycolysis which yields 4 ATP which can then start 2 rounds of glycolysis which yields 8 ATP, rinse, repeat. It is an exponential process, ATP can be taken from this for other processes since as long as you still have 2ATP around to can restart the exponential cascade. For example from the yielded 8 if you take half for other uses, you still get 8 ATP from the next round of glycolysis reactions.


Answer the questions in one word with help of clues and images given Name the things associated with Antonie Van Leeuwenhoek - (6 pictures are given for help and four of them are associated with these clues)

a)Leeuwenhoek was the first to describe these and hence called the "Father of Microbiology"

b)He found many of these (rotifers) in the rainwater collected in ditches and canals

c)Leeuwenhoek was the first to describe plant vessels in this cross section of an ash tree

d)Leeuwenhoek used this to observe microorganisms.

Since you have apparently tried to answer the question here is my interpretation. I list the six pictures (numbered from top to bottom) and link four of them to an answer.

1 - yeast cells?

2 -  ash tree section (c)

3 - rotifer (b)

4 - muscle fibre??

5 - bacteria? (a)

6 - Leeuwenhoek's microscope (d)

According to the WP page on van Leeuwenhoek he did describe the banded pattern in muscle, but there is no mention of yeast (although he would have had no trouble seeing these cells if he could see bacteria).

It's a very odd question.


Why doesn't life produce diamond, graphene, nanotubes, etc? Could it? It seems that life is really good at assembling carbon into extremely complicated molecules (e.g. DNA). Graphene is stronger than any materials currently used by biology. Diamond is harder than any biological materials. Do we know about some inherent difficulty that prevents this? Is there any reason to think that humans will never be able to genetically engineer say, bacteria/fungi/ourselves, to produce diamond, graphene, carbon nanotubes, etc?

I'm looking for specific metabolic hurdles that would make this difficult or impossible. (For example, enzymes/proteins can't do that for this reason, or ATP metabolisms don't have enough energy to form the needed bond.)

Biology does not have too many uses for super hard but brittle materials like a diamond. The hardest biological materials are also very tough as well since they need to form complex shapes for maximum utility. Limpet teeth are the hardest biological material known but are also incredibly strong, stronger than steel, not super brittle like diamond1.

As for graphene, the big problem there is reactivity; graphene is a great substance except it is pure carbon and has a huge surface area. If you put it in a solution full of carbon reactive chemicals, it starts doing weird things, and it has particularly weird interactions with cell membranes. Structurally, it is far more trouble than it is worth in something made of cells2.

You also have to remember that, in evolution, it is generally about "good enough", not perfection. Making a pure carbon structure would be an incredibly costly process in a biological (and thus aqueous) environment.

References:

Extreme strength observed in limpet teeth
Exploring the Interface of Graphene and Biology


How do people wake up just before their alarm goes off? I can wake up less than 2 minutes before my alarm goes off regularly.
I read the common wisdom on the subject which says "circadian rhythm; PER proteins; internal clock". I am skeptical of this for two reasons:

I go to sleep at night at different times ranging from 11:00 to 2:00 and rarely check the time, so if I don't even know the sleep start time, how can my body measure out the duration of sleep and get the end time right?
People's chemical levels vary from day to day depending on a ton of variables (food intake, physical activity, stress, etc). It appears that we are not deterministic machines that are constant from day to day to that level of precision

I have a few hypotheses that I haven't heard before:

Maybe the subconscious is queuing off the light level in the room? (this a unique property of the specific minute of wakeup, as there would be less light a minute sooner and more light a minute later)
Maybe while sleeping, the eyes periodically open, view the clock, process the numbers, and wake up accordingly (just like people  can sleepwalk and use their eyes to process where the walls and doors are)

Any thoughts?

The biological answer is presumably cryptochromes.  The foregoing applies to humans who have CRY2 blue light receptors in the inner retina (the neural layer, not the photoreceptors).  I've seen claims these respond particularly well to the light before dawn, though I didn't track those down just now.
That said, a proper skeptic would dismiss this as confirmation bias, at least until proven otherwise.


Non-harmful bacterial invasion of cells There are bacteria that can enter body cells as parasites.

Could it be that some of these are benign, such that the guest will not kill the host cell it lives in (especially in human)?

Survival of the host cell is in many cases dependent on the egress strategy of the pathogen. There are many examples documented in various species. The only case I found that's somewhat relevant to human cells was were mutant Legionella pneumophila, defective in the lytic pore complex, did not produce necrosis of the host cell. However, the cells did release the bacteria after a while, probably apoptosis due to accumulation.

EDIT: I found an article documenting Cryptococcus neoformans infection.

  Cryptococcus neoformans causes disease in people with immune deficiencies such as AIDS. Upon infection, C. neoformans cells are ingested by macrophage immune cells, which provide a niche for survival and replication. After ingestion, macrophages can expel the fungi without causing harm to either cell type, a process named nonlytic exocytosis.


Why do fetuses have membranes between fingers and toes? Are the membranes present between the fetal fingers and toes a remainder of the phylogenetic evolution, or just a way organs do grow most easily?

Short answer
The transient membranes between the fingers and toes in embryos are a myth.

Background
The presence of transient membranes in developing embryos supposedly points to our fishy evolutionary origins. However, I couldn't find any credible sources to support this myth. In fact, I couldn't find any source mentioning the presence of webbing between the fingers and toes at any stage during development.

To support this lack of evidence, I have posted several photos of embryos and fetuses in various developmental stages. None show any signs of the "swimming webs". Note that the age mentioned is the developmental age, counted from the moment of conception (add 2 weeks to have gestational age):

Fig. 1. Five-week embryo. source: Palm Reading Perspectives

Fig. 2. Seven-week embryo. source: Wikipedia

Fig. 3. Eight-week embryo. source: WemMD

Fig. 4. Fourteen-week foetus. source: WemMD

Fig. 5. Eighteen-week foetus. source: WemMD

Fig. 2 may seem to show some webbing, but if we look at some close-ups of the hand and feet at week 7 in Fig. 6 below, we can see that there is no real webbing; fingers and toes are simply budding from the primordial hand and foot structures.

Fig. 6. Developmental stages of the hand and feet around week 7. source: I am Pregnant

Note that an embryo is called a fetus only after the first trimester, i.e. after some 12 weeks. There is certainly not any sign of webbings in healthy fetuses.

Also note that webbings may be the result of birth defects, such as syndactyly and pseudosyndactyly (Fig. 7):

Fig. 7. Infants with Syndactyly (left) and Pseudosyndactyly (right). sources: Wikipedia & University of Columbia

Original photographic image source (Figs 1 & 5)*
- Nilsson, Ett Barn Blir Till

* Credits go to rg255


Why are female clones more often produced As a student of biology when ever I come by artificial cloning, I always find examples of females being cloned - Dolly the sheep, CopyCat, Daisy, etc. The only male I could see was Fibro mouse and a few more. What is the reason behind this? Is the male genome more difficult to be cloned? I am specifically looking for genetic reasons or other complications.

They aren't, anymore.  It was a fair guess at the time, but first I think we should define what cloning in this context mean.

Our own cloning tag says:

  The process in nature or in the lab by which a new organism is created that is genetically identical to its predecessor.

For animals - I'm going to use Dolly as an example since you do as well - when we say "cloning" we usually mean somatic cell nuclear transfer.   This image from Wikipedia sums up the process:

Basically, you take the nucleus of your to-be-cloned animal and put it inside the egg cell from another animal.  Dolly was not produced by one animal but by two - a donor and and a surrogate.  She was made using mammary tissue (another good image here) from the donor, which is important to note.

Dolly was the only one out of 277 egg cells that made it.  This is a hard technique, and we still don't understand a lot of it.  With even less information at the time, some prevailing ideas were:

Maybe there's something special about reproductive-based tissue
Maybe there's something special about female tissues

Even when using a different technique (e.g. Cumulina), early cloning attempts hedged their bets with those same tissues. That's why Fibro, the first male cloned (from tail), was a big deal - he showed that any tissue could be used, and that reproductive or female tissue wasn't inherently special.  You still need an egg and a surrogate, but if you can get the nucleus right it's just as doable.


Statistician confused about exact SNP data type I'm from a statistical (not biological) background, and I'm very confused about what exactly is the "data" associated with a SNP. Below, I'll explain things as best I can--please correct me if any point is wrong or otherwise unclear. Assume we're working with humans, since the following will change depending on the species. (Assume all cases of interest are biallelic.)

When a locus has an allele on least one chromosome, the measurement AA, Aa, or aa is called a SNP (pronounced "snip"). Therefore, using statistical language, SNPs are three level factors--this is the data associated with a SNP. As said earlier, if the factor has 1 level (ie it's only aa or only AA) then it's not a SNP.
Sometimes for humans it seems like people say a SNP is actually just one allele (so a two level factor, a or A). How is this possible? Do people sometimes only measure one allele instead of both to get the genotype?

SNP is not a specific data type but rather a biological phenomenon. The abbreviation "Single Nucleotide Polymorphism"  only means there is a variability (between individuals) in a single letter in a specific position in DNA sequence. It depends on the speaker how they decide to describe the variability; wether they choose to focus on the possible sequences and say for example "There is only A or T in this position" or they focus on possible human genotypes and spells out all combinations (AA, AT, TT).
What constitutes as SNP data depends entirely on research question, used organism (diploid/haploid/polyploid) and experimental design.
Article you link in your comment uses oat lines and not individuals from outbreeding population. Oat like arabidopsis is naturaly highly self polinating so creating highly homozygous inbred lines is relatively easy. In this case it is reasonable for the researches to expect only AA or aa genotypes in each line.
Edit: Since you asked for more examples where the researcher chooses to focus on alleles instead of genotypes. Many SNP genotypes distribution fit Hardy-Weinberg equations. If that is the case, the frequency of genotypes can be calculated from an allele frequency in population. The researcher might ask: "Is the frequency of allele a different in population/group 1 from population/group 2?" They collect data from indivuduals in group 1 (AA, AA, Aa, Aa, aa) and group 2 (Aa, Aa, aa, aa, aa). They decide to treat each allele as independent measurement (not dependent on individual it comes from) and poll the data: group 1 (AAAAAAaaaa), group 2 (AAaaaaaaaa) and then they do simple binomial test to answer their question.
Note: Even if Hardy-Weinberg equilibrium is not met, the questions about of allele frequency are is still valid biological questions (with slightly different use/interpretation down the line).


What triggers meiosis in gonadal cells? What specific biochemical processes are involved in inducing meiosis rather than mitosis? Why are gonadal cells the only cells in the human body which do undergo meiosis?

Ultimately, it seems that follicle-stimulating hormone (FSH), released from the pituitary gland, may be the direct signal for spermatocytes to enter meiosis [1]. It's worth noting, though, that these results come from in vitro studies, where spermatocytes were co-cultured with all cell types of seminiferous tubules in an artificial medium, which makes it a rather crude approximation of in vivo conditions: mimicking the complete spermatogenic cycle in vitro remains to be done [2].

It's a little bit more complicated with oocytes. They start meiosis during prenatal development, are arrested in diplotene stage of the first meiotic division, and then a surge of luteinizing hormone (LH), just before ovulation, makes them resume. But they are arrested again in the last phase, and only after conception do they finish meiosis. The pause occuring in prenatal development is thought to be induced by some kind of an "arrester" secreted by cells in the oocyte environment (specifically, mural granulosa cells) and sustained by high cAMP levels, that are produced in response to both intrinsic and extrinsic stimuli. [3]

Another matter, and quite interesting, is the issue of timing: meiosis starts in a distinct moment of a male mammal develompent, and then goes on continuously, but mammal oogenesis is a series of starts and stops. More on this can be found in [3] and [4].

[1] Tesarik, J., Guido, M., Mendoza, C. & Greco, E. Human spermatogenesis in vitro: respective effects of follicle-stimulating hormone and testosterone on meiosis, spermiogenesis, and Sertoli cell apoptosis. J. Clin. Endocrinol. Metab. 83, 4467–4473 (1998). PMID: 9851795. Free access.

[2] Sousa, M., Cremades, N., Alves, C., Silva, J. & Barros, A. Developmental potential of human spermatogenic cells co-cultured with Sertoli cells. Hum. Reprod. 17, 161–172 (2002). PMID: 11756382. Free access.

[3] Zhang, M. & Xia, G. Hormonal control of mammalian oocyte meiosis at diplotene stage. Cell. Mol. Life Sci. Epub ahead of print. (2011). PMID: 22045555.

[4] Albertini, D.F. & Carabatsos, M.J. Comparative aspects of meiotic cell cycle control in mammals. J. Mol. Med. 76, 795–799 (1998). PMID: 9846949.


What's the name of this bird? This morning I saw a bird that I have never seen before. Since it was quite big, I'm very interested in knowing its name.

The bird was quite big, at least 2-3 times of a common blackbird. The wings were completely black but the whole back strip was quite yellow. Also the tail was yellow. The tail widens towards the end.

The bird flew very strange... it trundled towards the ground and then flew back up some meters before trundling down again. I observed the bird in Zurich, Switzerland at the outer border of the city. A big forest is quite near and there are some huge trees very close to the bird.

Then one last thing to add: I'm not really sure about that, but it could be that the bird had a nest on top of a big tree.

Any ideas which bird that could be?

Hmmmm... the only one I can think of fitting at least in part your description would be the golden oriole (Oriolus oriolus).

I say partly because it definitely is not 2-3 times a blackbird, could be slightly bigger, but on average it is the same size. Also it sounds extremely unlikely that you have spotted it in early March in Zurich, as they should be in Southern Africa right now.

Image, from Wikipedia:

I could not find anything else fitting your description in my field guide (Mullarney & Svensson - Birds of Europe)


How to use a published phylogenetic tree? I would like to know how should I use a phylogenetic tree from an already published article, to put it on my own article so I can analyze the evolution of a trait. Is there any software I can use, or do I only have to "edit" the tree with a traditional image editing software?

I've seen that using trees from other authors is a common practice. Many times they summarize the trees. But no paper seems to tell you how they did it.

Thank you!!

I don't know how generalized this is, but some journals require the authors to deposit the trees in a database, like treebase. In this case, papers should indicate the accession numbers of their trees.

You then need the appropriate software to load the tree, manipulate it and print it, for instance ete.


Does the composition of a meal play a big, or small, role in food's thermogenic effect on the body? Reading in: "Diet and Health: Implications for Reducing Chronic Disease Risk /  Calories: Total Macronutrient Intake, Energy Expenditure, and Net Energy Stores" [NCBI Resources]:

  "The thermogenic effect of a meal usually amounts to approximately 10% of the caloric value of the ingested food, and is higher for carbohydrates and protein than for fats".

Does that mean that the thermogenic effect of a meal fluctuates between 9% and 11%, depending on it's composition? If so, the thermogenic impact on the body by a meal's composition would be quite small in comparison with the impact of a meal's calorie content. Or, does food's composition play a bigger role than that? Looking for information from reputable sources.

Calories: Total Macronutrient Intake, Energy Expenditure, and Net Energy Stores

According to Diet Induced Thermogenesis (Nutrition & Metabolism, 2004), the percent of calories converted to heat depends on a nutrient:

Proteins: 15-30%
Alcohol: 10-30%
Carbohydrates: 5-10%
Fats: 1-3%
A mixed meal: ~10% (this is an estimated average)

The thermic effect of nutrients is not a fixed value and can vary greatly within a person and from person to person:

  Reported intra-individual variability in DIT, determined with
  ventilated-hood systems, is 6 to 30% [7,8]. Reported within-subject
  variability in DIT, determined with a respiration chamber, is 43 to
  48%.


Where should I start looking for an online gene library? Is there an online library that includes all known genes in stored in their nucleotide form of all living organisms?

I'm presuming that such a database doesn't exist. So to kick of my search, how can I find a gene amongst all the other databases? Where is a good place to start looking for information about my gene given that it is a well studied sequence? The issue is that I have been provided with the sequence, but I just don't know what organism the sequence belongs to or what it codes for.

Databases
There are too many databases to list here, but Wikipedia has a decent list of the genome databases. For example, there are databases dedicated to genes of individual species, like Wormbase, SGDB and countless others. Alternatively, as others mention a great place to kick off your search is the NCBI.
Finding your nucleotide sequence in databases
It sounds like you already have your sequence. If you want to see if your sequence has been found elsewhere or if there are any similar sequences, you can use BLAST from NCBI. Although it is not strictly a database in itself, it looks to align your sequence to similar sequences in external NCBI databases and quantifies the sequence similarity. It will reveal the species for you to go to a more appropriate database along with a lot of other information about the gene.
There are plenty of parameters to alter to suit your specific needs, but generally, the default settings are a great place to start analysing your gene. You'll need to run a nucleotide test since you want to find the DNA sequence. The results might be difficult to interpret.


What does differentiation of B-cell mean? Does differentiation of B lymphocytes mean the formation of plasma cells and memory cells by matured B lymphocytes?

Immature B lymphocytes mature into either plasma cells or memory cells. If a B cell is mature, that means it's already a memory or plasma cell.


What is this bird species in India? I spotted this bird in India a day ago in a park located inside a city. There are no nearby water bodies around the park. The bird is slightly larger than the average person's fist. Does anyone know what species of bird is it?

Looks to be either a chestnut-tailed starling (AKA grey-headed myna, Sturnia malabarica) or a Malabar starling (Sturnia blythii) in the Sturnidae (or starling) family.

S. blythii was previously considered a subspecies of S. malabarica.

 S. malabarica, Source: universebirds.com

 S. blythii on the left and S.malabarica on the right.

Description: Adults are approximately 20 cm long. They have grey heads/neck, blackish remiges, and reddish-brown (i.e., "rufous") belly and undertail. Their beaks are yellow with pale bluish bases.

The poor coloration in your photo seems to show the base of the beak being a paler grey color (vs. the yellow of the rest). I'm going to guess that this was really at least slightly bluish in hue and the color did not show up in your low-quality photo.

Range: As you can see in the map below, they are present throughout most of India:

 Source: Natural Earth and Myself

According to here, S. blythii is more constrained to just southwest India.

You can see videos of specimens here.

Further References:

Fina a list of most (all?) species of birds in India on Wikipedia.
Here is a good site with hundreds of photos of Indian bird species.


Does age affect the frequency of flatus? Is there any relation between age and the frequency of flatus? I often have this feeling that older people f*** more often than younger ones. Is this feeling scientifically correct?

I do not have access to journals, but there is this paper claiming in its abstract that age DOES NOT play a role in flatus frequency.

Reference:  Furne JK, Levitt MD. 1996. Factors influencing frequency of flatus emission by healthy subjects. Digestive diseases and sciences 41: 1631–5.


Book Recommendations: GRE Subject Test In Biochemistry, Cell And Molecular Biology There are probably a lot of really good answers that may vary significantly in terms of content.  I'm looking for a set of books that I can read in preparation for the GRE Subject Test In Biochemistry, Cell And Molecular Biology.  I have a Bachelors of Science degree, but never really studied any of the material on this exam (it's in a field which is not really related).  I'm interested in applying for a doctoral program in Biology, and would like to add something to my application so that it doesn't appear to come out of "left-field", as they say.  When I look at the questions from the sample exam in the link above, I can't tell whether they are introductory in scope or would require advanced study in particular areas.  Could somebody recommend a set of textbooks that would cover all of the ground for this test?  If one textbook exists which is sufficient, that would be wonderful, but I'm guessing that multiple texts will be required.  My goal is to learn the material necessary to do well on the exam as thoroughly as possible.

As an aside, I tried looking for study materials in online bookstores, but wasn't able to find anything that consistently got good reviews.  I don't think Princeton Review or Barron's have books on this subject, unless I overlooked something.  At any rate, I'm okay reading through a set of undergraduate university textbooks, but I really have no idea which ones would be good.

Thank you in advance!

Edit:  I just changed the word "efficiently" to "thoroughly".  Sorry about that...  This more accurately reflects the goal.

You can also try Lehninger Principles of Biochemistry...It covers all the topic except the part about cell motility...& possibly, the 1-A-g ( I'm not too sure about it)...but the book is for pretty advanced levels...& I would not recommend it as a last minute reference book..but for thorough study it's great....& of course it's my personal opinion...so before you consider any book, I would rather advice you download a pdf copy of the same, to get a 1st hand experience...hope this helps & good luck for your exam...


Human spine: Is the coccyx really fused? Prologue: This post is about the adult (say, a 20 year old) human skeleton; I'm not particularly interested in infant skeletons.
The human spine has is composed of cervical, thoracic, lumbar, sacral and coccygeal vertebrae

 Image source

My school textbook (which has a history of possessing erroneous/outdated information) states:

The coccyx consists of 4 coccygeal vertebrae that are fused to become a single bone.

However, this Wikipedia article states:

Most anatomy books incorrectly state that the coccyx is normally fused in adults. In fact it has been shown that the coccyx may consist of up to five separate bony segments, the most common configuration being two or three segments.

Is Wikipedia correct?
If so, what is the (most common) number of bones that constitute the spine? Is the number of vertebrae that constitute the spine going to be different?

This other Wiki article appears to be particularly contentious:

A fully grown adult features 30 bones in the spine, whereas a child can have 33.

The cervical vertebrae (7)

The thoracic vertebrae (12)

The lumbar vertebrae (5)

The sacral vertebrae (5 at birth, later fused into one)

The coccygeal vertebrae (5 at birth, some or all of the bones fuse together but there seems to be a disagreement between researchers as to what the most common number should be. Some say the most common is 1, others say 2 or 3, with 4 being the least likely. It is counted as 1 in this article.)

I understand that there is little to no variation in the number of cervical, thoracic and lumbar vertebrae among humans, so they altogether constitute $\mathrm{7+12+5 = 24}$ vertebrae/bones (in this case, I believe "vertebrae" and "bones" are synonymous).
Assuming that the sacrum really is one fused bone (my question's regarding the coccyx, so I'm not going to question the anatomy of the sacrum in this post) consisting of five vertebrae (I think there's a bone-vertebra distinction here, so they aren't the same thing)
In that case, the cervical, thoracic, lumbar and sacral contributions are $\mathrm{ 24 + 1 = 25}$ bones, or  $\mathrm{ 24 + 5 = 29}$ vertebrae. (Right?)
According to the Wikipedia article I cited above (the second one), the adult human spine has 30 bones.
So the coccyx contributes $\mathrm{30 - 29 = 1}$ bone to the spine, or $\mathrm{30 - 25 = 5}$ vertebrae to the spine.
In other words, the second Wiki article implies that the coccyx is a single (fused) bone. However, the first article states that the coccyx is really composed of 3-5 (say, 4 on an average) bones.
This is horribly contradictory.

If the finer points of my question was lost, I'll restate them here:
1) Is the coccyx a single bone or multiple bones?
2) How many bones are there in the adult human spine?
3) How many vertebrae are there in the adult human spine?

The wikipedia article links to two papers. The first article has data for 120 pain-free and 51 affected patients with data on the number of coccygeal segments in each. We can back-calculate a reasonable approximation of segment distributions from their percentages:

1 Segment: 7%
2 Segments: 51%
3 Segments: 38%
4 segments: 4%

So 2 or 3 segments makes up almost 90% of the population. Given that only 7% of the subjects had single element coccyxes, I think it's safe to call the coccyx usually made of multiple elements.

Whether you refer to those multiple elements a single bone if largely a semantic argument. Since there is variation, it seems reasonable to call the collection 5 of variably fused terminal vertebrae the "coccyx".

As a practicing anatomist, I would say that there are 29 vertebrae, as in 29 vertebral elements (but you can't say 29 ossification centers, because each is made of multiple centers). These fuse into 24 free vertebrae, the sacrum (5 fused vertebrae) and one coccyx, which is variably fused.


Is there a difference between visual sensation and imagination in the brain? How substantial is the difference between the neural signal associated with seeing an image and the imagination of that image? Surely, it can not entirely copy the pathway from the sensory organs to the emotional centers, but approximately how large is the common pathway for both processes?

Is there some principal difference in the neural pathway of these two processes, or is the imagined image just more of a slurred version of the visual image?

Short answer
Visual perception and visual imagery draw on much of the same neural machinery.

Background
I have interpreted your question as: What are the common neural circuitries between visual sensation and the imagination of sensation?

In neuroimaging, mental imagery of visual images is a big deal. For example, there is a large body of literature on cross-modal activation of visual areas in the brain in blind people. It is known that visual deprivation results in neural plasticity and the recruitment of visual areas in the brain for other sensory systems. For example, blind Braille readers show activation of the primary visual cortex when reading Braille (reviewed in Stronks et al., 2015). However, interpretation of these findings is difficult in late-blind individuals, because they have experienced visual input earlier in life. Hence, while Braille reading they can be mentally reproducing the visual representation of the Braille cells using visual neural circuitry.

Indeed, it has been shown with fMRI that visual imagery and visual perception draw on most of the same neural machinery (Ganis et al., 2004). However, the spatial overlap of the activated regions is neither complete nor uniform. The overlap in this study was more pronounced in frontal and parietal regions than in temporal and occipital regions, indicating that cognitive control processes function comparably in both imagery and perception, but not identically.

Various studies reveal different results, however. In another imaging study, 'just' two-thirds of brain regions overlapped in visual sensation and imagery (Kosslyn et al., 1997). Indeed, the experimental task used may have important effects on study outcomes.

Most notably in this regard is that approximately half of the studies done have found activation of the primary visual cortex during imagery (Kosslyn et al., 1999). This is interesting, because the primary visual cortex is generally thought to be an early, low-level area in the visual system that depends on thalamic input that relays information from the optic nerve to the brain. I.e., it is generally believed to depend on sensory stimulation. Generally, only the higher-level associative visual areas are associated with higher cognitive processes.

References
- Ganis et al., Cognitive Brain Res (2004); 20: 226–41
- Kosslyn et al., Neuriomage (1997); 6; 320–34
- Kosslyn et al., Science (1999); 284; 167–70
- Stronks et al. Brain Res (2015); 1624: 140–52