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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

@yamad, thank you for wording the question better!

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


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Understanding Membrane / Resting Potential from the perspective of ions?

From wikipedia article RESTING potential: "there is no actual measurable charge excess in either side. That occurs because the effect of charge on electrochemical potential is hugely greater than the effect of concentration so an undetectable change in concentration creates a great change on electric potential."

the effect of charge on electrochemical potential significantly larger then the effect of charge on concentration - is this a general statement or true in all cases?
And if charge is more significant then concentration in influencing electrochemical potential why does a small change in concentration greatly effect electropotential? Or does it mean electrochemical potential? Either way how does it make any sense, is it correct or nonsense and what is the exact meaning behind the message?
other questions I have:
1) What is the reason Na+ stays at its location right across the barrier on the extracellular side of the membrane? Diffusion? Electrochemical potential? Electric Charge.. if so because of Attraction or Repulsion?
2) If the answer is the electrochemical gradient/potential, because it is trying to move to a "less" positive potential.. if its located extracellularlly isn't that the "great unknown" where any molecules/cells/protein etc. are able to float by and possibly influence it? What happens if one of these has a "LESS" positive potential then the membrane that Na+ is currently attracted?
3) Why can't Na+ be used for the entire process to establish the same voltage interactions leading from resting to action potential (as long as thier was less concentration intracellularly... if it is about LESS positivity ..Or vice versa for K+?)?
I am preparing for ACSM certification exam, so any help is appreciated.

Ah, what a classic biophysics problem.
One first needs to understand how a membrane gets a potential. The lipid bilayer is a large sea of hydrophobic interactions that essentially prevents any ion from crossing. As a result, Na+ and K+ concentrations remain constant and different on the cytoplasmic side and the extracellular side. However, ions can pass through ion channels like the K+ channel. It is important to understand that in K+ channels, only K+ can pass and these channels are actually selective against Na+ (answer to question 1).
There are two potentials at work here. First is a chemical potential created by the flux of K+ from high K+ to low K+. The second is a counteracting membrane potential created by a charge imbalance. Note, that the swapping of a few ions will a) result in a negligible change in the concentration ie. the chemical potential, b) result in a large change in the membrane potential. At some point, the flux out due to the chemical potential and the flux in due to the membrane potential will be equilvant and the cell will reach a resting potential otherwise known at the Nernst potential or equilibrium potential (technically a steady state).
When a cell depolarizes by closing these channels, the local charge will quickly go back to an equilibrium or a non-charged state.
So why K+ rather than Na+? For typical cells, the extracellular concentration of Na+ is 145 mM and cytoplasmic is 12 mM. For K+, it is 4 mM and 155 mM respectively. Doing the appropriate calculations of the Nerst potential, for Na+ it is +67 mV and for K+ it is -98 mV. Qualitatively we can see that this would result in vastly different things.
Most of this information can be found from Pollard and Earnshaw's Cell Biology

For anyone else interested I found a voluminous, free, online resource with animations and very detailed explanations which addresses the topic here: http://www.st-andrews.ac.uk/~wjh/neurotut/mempot.html

The resting potential is only validly called an equilibrium potential in a system containing only one ion species. Of course, cell environments are composed of several ions so the resting potential is not described by any equilibrium potential, because (as you say) the system is at steady-state rather than equilibrium. A more general term is "reversal potential" which describes the potential at which net current switches sign (e.g., inward to outward). The concept of reversal potential simplifies to a Nernst/equilibrium potential in single ion cases, but also covers multiple ion cases.

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What is the difference between a fixed substitution and a single nucleotide polymorphism (SNP)?
I recently read a report that stated "We found 430 fixed substitutions […], with an additional 34 single nucleotide polymorphisms (SNPs) fixed within individual patients." What is the difference between both terms?

I'd need more context to be sure but what makes you think that the substitutions were only a single nt? Also, that sentence could be read as having found 464 SNPs, of which 430 were fixed.

It would be important to read the original paper.

If you look into a certain population, you will find mutations (for example SNPs) in some ratio with the wild-type allele. When a mutation reaches fixation, it will be the only allele, reaching 100% penetrance in this population. See here for more information.
In the context given I would interpret it in the way that a total of 464 SNPs were found, 430 of these were in fixation (so can only be discovered when comparing them to another population) and 34 SNPs which haven't reached fixation and thus cannot be found in all members of the population.

Fixation is a process when one of the polymorphic alleles becomes fixed in the population gene pool due to genetic drift or natural selection and ceases to be polymorphic anymore. Therefore fixed substitution and SNP are two absolutely different concepts. So, the term “fixed single nucleotide polymorphism” seems to be oxymoron as it bears a contradiction. To calculate the real number of fixed substitutions at least one individual from another distant population or closely related species is needed.

Welcome to Bio and thanks for your answer. Could you add sources, links or citations to your answer to allow users to read the backgrounds?

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What is the difference between a phosphotransferase, a phosphatase, a phosphorylase and a kinase?
I've looked in several sources, but I'm still confused. This is what I have so far:

A phosphotransferase catalyzes the addition of a phosphate group.
A kinase is a type of phosphotransferase that transfers a phosphate group from ATP to a substrate.
A phosphorylase is a type of phosphotransferase that catalyzes the addition of a phosphate group from an inorganic phosphate (HPO4) to a substrate.
A hydrolase catalyzes the hydrolysis of a chemical bond.
A phosphatase is a type of hydrolase that removes a phosphate group.

Is this right?
EDIT:
Also adding to the confusion is the enzyme Phosphorylase kinase, which is the kinase that phosphorylates the enzyme Glycogen phosphorylase, which hydrolyzes glycogen.

Phosphatase uses water to remove a phosphate group, while Phosphorylase uses phosphate group to remove the phosphate group

Don't get caught in the linguistic trap of attaching too much significance to the precise meaning of any one piece of scientific jargon. Nomenclature, the system of naming things, utterly sucks in biology, and it sucks even harder for protein biology. There is no one universally accepted classification and naming system for proteins, although there have been plenty of attempts.
For example, phosphotransferases are classified as EC number 2.7. However, Glycogen Phosphorylase is classed under 2.4, which might make you think "well, clearly kinases are enzymes that transfer phosphate groups from organic substrates such as ATP and are classed as 2.7, whereas phosphorylases are enzymes that transfer from inorganic substrates and are therefore classed as 2.4". But wait! RNase PH is a phosphorylase that's classed under 2.7 and uses inorganic phosphate, so um... yeah.
In any case, don't get too hung up on the nomenclature. Unless you're working in an enzymology lab just say "kinase" and everyone will know what you're talking about.

I'm certainly not an expert on this but it seems to me that glycogen phoaphorylase could also be classified as a phosphotransferase (2.7). However, since there's already a glycosyltransferase group (2.4) it was classified there. There is no such group for ribonucleotidyltransferases which is why RNase PH was put in 2.7. This is perhaps a drawback of the EC system in that one catalysed reaction could fit two different groups. Even though glycogen phosphorylase is classified as a glycosyltransferase by EC, it is still also a phosphorylase.

@canadianer That's true. My point was more about the futility of trying to define a short nomenclature for the set of all enzymes. Their complexity defies any simple classification. Save the jargon for when you have specifics to talk about, and talk about generalities in general terms.

As @tel said, there is no clear difference available since there is no international authority which manages such things (like IUPAC) when it comes to biological terms. However, these terms can be understood and differentiated a bit more easily, as long as you don't get into deeper details.
Posphotransferase is a kind of transferase that transfers a phosphate group from one compound to another. The type of substrate remains unspecified (dictionary.com).
Kinase is a type of phosphotransferase that transfers a phosphate group from high-energy phosphate donating molecules (usually ATP) to anothrr molecule. Here, one substrate is specified (Wikipedia).
Phosphorylase is an enzyme that adds an inorganic phosphate ($\ce{PO_4^{3-}}$) to a substrate molecule. The inorganic substrate is not transferred, it is directly added to a molecule (Wikipedia).
Hydrolase is an enzyme that hydrolyzes a substrate i.e. breaks a covalent bond in a molecule and adds water to the resulting molecules. Its like $$\ce{A-B + H_2O \rightarrow A-OH + B-H}$$ where A-B is a single substrate molecule (Wikipedia).
Phosphatase is a type of hydrolase that hydrolyzes the bond between a molecule and phosphate group, resulting in the formation of inorganic phosphate and an alcohol. It is like $$\ce{A-PO_4^{2-} + H_2O \rightarrow A-OH + HPO_4^{2-}}$$ where A becomes an alcohol (Wikipedia).
PS: I am not saying that these are the universally accepted definitions of the corresponding enzymes. These are just examples to help you better understand the meaning of these terms. However, you can always find exceptions to these definitions.


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Hoechst red and blue spectra - what does the red emission tell us?
I understand that the blue spectrum is emitted when Hoechst 33342 binds to nuclear DNA. But what exactly is the red spectrum telling us?
I read that the red spectrum can be indicative of apoptosis, cellular complexity, or a proxy for cytoplasmic content.
What exactly is the red spectrum indicative of in terms of the cellular context?
edit**
Sorry for not getting back to this question sooner. I found the answer in this paper:
http://www.sciencedirect.com/science/article/pii/0022175995002146#
Apparently condensed chromatin during apoptosis causes hoechst to shift to a red spectrum.

There are several Höchst dyes, you might want to clarify which you are talking about.

I am talking about Hoechst 33342 specifically.

could you provide a link or reference about the function of the dye as "indicative of apoptosis, cellular complexity, or a proxy for cytoplasmic content". I'm quite interested! I know that some dyes such as CyTRAK orange that stains both nucleus and cytoplasm with cytoplasm being a lighter orange colour than the nucleus but the described hoechst 33342 property is new to me, so I would be interested in any links/references you could provide supporting your question!

This question lacks evidence for the main claim made!

That's a problem but it doesn't warrant sniping the question down immediately like this. Give the asker some time to edit the question and explain where he made such a claim before putting him through a tedious reopen procedure. If he doesn't respond within the next days, close it down.

Looking at the hoechst red spectrum is a pretty common practice in flow cytometry (examining the side population for example). It's not some random claim I made. Anyways, I found the answer in a paper. I updated the main question.


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Which blood vessel carries the most impure blood?
There is a question in my Biology textbook:

"Which blood vessel in the human body carries most impure blood after
  few hours of meal."

The answer is given as Renal artery.
But I think the answer should be Hepatic Vein, because the liver produces urea and other waste materials and then it pours it all in the right ventricle of the heart for oxygenation. And then the heart distributes the blood to various parts of the body. So the impure blood brought by the Hepatic Vein and other blood vessels gets distributed through the aorta. This will automatically imply that the Renal Artery will contain lesser impure blood than the Hepatic Vein.
Impure blood is the blood with urea, uric acid and other components of urine.
It would be good if you give your opinion and also a reason for it.

The problem with this question is that "impure" is too non-specific a term. What blood components are impurities?

@AlanBoyd Impurities include urea uric acid and other components which are there in urine.

yup toxins from the liver breaking down and concentrating impurities from the blood.  in physiology its not as vague as it sounds...

It's the renal artery because it will contain everything from the liver as you describe plus all waste accumulated on the way from the liver to the kidney. Here it gets filtered, so there cannot be a place after the kidney that is less "pure".

please read the question again and make necessary changes in the answer. I have revised the question in order to include more details.

+1 - "...plus all the waste accumulated on the way from the liver to the kidney." And there's the rub.

@PranitBauva the changes don't really affect the answer as written

But the urea containing blood liver distributed through the body from the heart , as some of the blood goes to the kidney so renal might not contain that much of urea right? As OP has mentioned

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Why can silicone reduce keloid?
I heard people use silicone sheet for reducing raised scars (i.e., keloids). I was wondering what is the rational behind it, and whether it actually works.

Keloid scars are formed when the scar tissue extends beyond the margin of the original wound and is the most extreme type of scarring. When this scar type occurs, a small wound such as an insect bite or piercing can result in the formation of a much larger elevated area of tissue which even after surgical revision can reform. Keloid scars are not to be confused with hypertrophic scars which are raised and often discolored, but do not extend beyond the boundary of the initial wound. This article discusses in great detail all the biological properties and mechanisms of scar formation and how silicone enhances the recovery.
Role of silicone in scar reduction
The epidermis may take around 2 weeks to sufficiently regenerate after a full-thickness wound has occurred due to it penetrating through the epidermis and into the dermis layers. During this time, intervention with scar development will have little to no effect as high collagen levels are required at this early wound healing stage.12
After this period, the new immature stratum corneum allows abnormally high levels of transepidermal water loss. This dehydration of the stratum corneum signals the keratinoctyes to produce cytokines, which signals to fibroblasts to synthesize and release collagen.
The newly formed collagen rushes to the scar site and is the cause of many undesirable physical and aesthetic properties associated with scarring. The application of SGS replicates the stratum corneum's occlusion properties, normalizing hydration of the scar site to that of healthy skin, perhaps inhibiting the instruction sent to the fibroblasts to produce excess collagen cells.

According to several papers (Sawada and Sone, 1992; Wong et al., 1996), increased hydration appears to be the main mechanism by which silicone oil acts on raised scars. Combined with an occlusive dressing, this preparation would increase hydration of the scar site. Sawada and Sone (1992) compared silicone oil treatment to vaseline treatment and found significantly improved healing with silicone oil, concluding that it was the hydrating action of silicone oil that led to improvement.
Sawada Y, Sone K. 1992. Hydration and occlusion treatment for hypertrophic scars and keloids. Br J Plast Surg 45(8):599-603.
Wong TW, Chiu HC, Chang CH, Lin LJ, Liu CC, Chen JS. 1996. Silicone cream occlusive dressing--a novel noninvasive regimen in the treatment of keloid.. Dermatology 192(4):329-33.

Thanks! By hydration, you mean keep the raised scars wet?

That's the idea.

I cannot say the mechanism, but I can confirm it works, and can say that is generally accepted as working, not as some weird dubious treatment. I had surgery to install a rod in my leg after a broken bone. On the advice of my physical therapist, I purchased "Scar Away" brand silicone oil with roller applicator. Placing a thin layer and massaging with the applicator twice a day for four weeks turned my giant cheloids into small sections of skin which were distinguishable only by their smoothness and lack of hair, not color. He said he used to work for some basketball team and it was common practice to be used in professional basketball.

Thanks! What products did you use and/or recommend?


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How does the NAD+/NADH ratio affect lifespan in vertebrates?
Here's the proximate physical implication of the ratio (from the Wikipedia article on NADH).

The balance between the oxidized and reduced forms of nicotinamide
  adenine dinucleotide is called the NAD+/NADH ratio. This ratio is an
  important component of what is called the redox state of a cell, a
  measurement that reflects both the metabolic activities and the health
  of cells. The effects of the NAD+/NADH ratio are complex,
  controlling the activity of several key enzymes, including
  glyceraldehyde 3-phosphate dehydrogenase and pyruvate dehydrogenase.
  In healthy mammalian tissues, estimates of the ratio between free NAD+
  and NADH in the cytoplasm typically lie around 700; the ratio is thus
  favourable for oxidative reactions. The ratio of total
  NAD+/NADH is much lower, with estimates ranging from 0.05 to 4. In
  contrast, the NADP+/NADPH ratio is normally about 0.005, so NADPH is
  the dominant form of this coenzyme. These different ratios are key
  to the different metabolic roles of NADH and NADPH.

So here's my question: how does this manifest in vertebrate aging? Is it something that's simply the resultant of other aging processes, or can the ratio also contribute to aging in a certain way?

What's the source of this quote?

Wikipedia (have added a note for clarification).

This study found a statistically significant decline in NAD+:NADH ratios and in intracellular NAD+ with age in the organs of rats.
They discuss that the activation of  PARP - the  NAD-dependent enzyme Poly(ADP-ribose) polymerase-1 instrumental in DNA repair - increases in aging organs (heart, liver, kidneys). This depletes cellular NAD+ levels via poly(ADP-ribosylation) of proteins. This reduced cellular  NAD+ then reduces the effectiveness of Sirtuins (Sirt1) which can deacetylate tumor-suppressor proteins such as p53.
Here's schematic showing the basic idea from their figure 10:

So, the inference is that oxidative stress in vertebrates increases with age due to lowered cellular NAD+ - i.e.,  consistent with the free-radical theory of aging.  This could mean that lowered cellular NAD+, NAD+/NADH in any given individual may well decrease said individuals lifespan.
The authors of the first study (Braidy et al 2011) suggest that therapies involved in maintaining high NAD+ levels may alleviate age-associated disorders.

Braidy N, Guillemin GJ, Mansour H, Chan-Ling T, Poljak A, et al. (2011) Age Related Changes in NAD+ Metabolism Oxidative Stress and Sirt1 Activity in Wistar Rats. PLoS ONE 6(4)
Smith, J., (2002) Human Sir2 and the 'silencing' of p53 activity, Traneds, Cell Biol. 12, 404


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If I put a cup over a spider, and leave it there for a day, will the spider survive?
Will it travel more slowly since it hasn't had food for a day?
What if I left the cup there for longer?

Just solely in terms of not having food (ignoring the importance of O2 that Ramkryp has pointed out), spiders don't necessarily have to feed on a daily basis anyway.  It's not the same species of spider as you ask about in your question, but consider:

The metabolic and water evaporation strategies in spiders may be part of a set of physiological adaptations to tolerate low or unpredictable food availability, buffering spiders against environmental fluctuations such as those of the high mountains of the central Andes. The aim of this study is to analyze experimentally the variations in metabolic rate and the rate of evaporative water with food and/or water restriction in a high mountain mygalomorph spider population (Paraphysa sp.). We found that the low metabolism of this spider was not affected by water restriction, but its metabolism was depressed after 3 weeks of food deprivation.

from Canals M, Figueroa D, et al (2011). Effects of diet and water supply on energy intake and water loss in a mygalomorph spider in a fluctuating environment of the central Andes. J. Insect Physiol, 57(11), 1489-94.
The biochemical makeup of the spider may be radically different than most other animals, and breaking down energy stores must take place over a longer timecourse.

To answer the first part of your question: it is extremely unlikely that the spider will die or be weakened after just one day.
Wolf spiders (Lycosids) are all predators. Due to variations in prey populations, and low efficiency of consumption at higher trophic levels, they are subject to inconsistent and unpredictable food supply (Greenstone and Bennett, 1980). They are very well adapted to this lifestyle and consequently, long periods of starvation often yield no behavioural changes (Persons, 1999). It is highly unlikely that the spider will die after just one day: Anderson, (1974) observed no changes in activity after starving Lycosa lenta (a species of wolf spider) for 30 days; and Tanaka and Itô, (1982) observed Pardosa astrigera (another species of wolf spider) living for up to 54 days of starvation. Age and sex of the spider are more likely to affect its behaviour and performance than food or oxygen availability (Persons, 1999).
As for oxygen consumption, Greenstone and Bennett, (1980) measure an oxygen consumption of 100µL/hr for wolf spiders. Assuming that your cup is of the size of the unit of volume of the same name, the cup (~0.237L), a small calculation (see figure) shows that there will be enough oxygen for the spider to survive for over 98 days. The oxygen concentration within the cup may decrease as it is used by the spider, however this is likely to have a minimal effect as a cup placed on a surface is unlikely to be hermetically sealed.

In short, oxygen availability is unlikely to have an effect on the spider before other limitations (such as food) are reached. However neither of these effects are likely to cause behavioural changes during the first month.
References

Anderson, J.F., 1974. Responses to Starvation in the Spiders Lycosa Lenta Hentz and Filistata Hibernalis (Hentz). Ecology, 55(3), pp.576-585.
Greenstone, M.H. & Bennett, A.F., 1980. Foraging Strategy and Metabolic Rate in Spiders. Ecology, 61(5), pp.1255-1259.
Persons, M.H., 1999. Hunger effects on foraging responses to perceptual cues in immature and adult wolf spiders (Lycosidae). Animal Behaviour, 57(1), pp.81-88.
Tanaka, K. & Itô, Y., 1982. Decrease in respiratory rate in a wolf spider, Pardosa astrigera (L. Koch), under starvation. Researches on Population Ecology, 24(2), pp.360-374.

Your assertion may be true but the cup contains only about 20% oxygen at sea level. You have to throw in a factor of 0.2, right? That's only about 19 days...

different but related: How much energy does a small spider expend per day just waiting for its web to vibrate? in that there may be at least a rough relationship between the rate of conversion of O2 to CO2 and caloric consumption.


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The oldest common ancesstor of all human beings
Do all human beings have a single oldest ancestor (a man and a woman), or were there were many ancestors at the same time at different places on earth?
This article sheds some light. Is there another authoritative report released more recently?

http://biology.stackexchange.com/questions/7184/what-is-a-mitochondrial-eve-and-y-chromosomal-adam covers much of the same material.

Isn't that Adam? ;)

Possible duplicate of What is a Mitochondrial Eve and Y-chromosomal Adam

This is not a duplicate. The MRCA is different from mtEve and YcAdam.

You are talking about the mitochondrial eve and the chromosome Y adam.  At some point there must be just one pair, though historically the evidence can be lost if there is a near complete extinction event.  Current evidence for eve points to SE Africa.


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Is it correct to regard archeaic humans (i.e.n Neanderthals and Denisovans) as distinct species to Homo sapiens?
There is increasing evidence (e.g. here) that Homo sapiens interbred with contemporary homonins such as Homo neanderthalensis and the "Denisovans". Although these homonins do show differences in their mtDNA, since a species is generally defined as a group of organisms capable of interbreeding and producing viable offspring, should we not regard humans, neanderthals and denisovans as the same species and name them as such?

This question highlights the different species concepts.
If you go by the reproductive species concept (a population of actually or potentially interbreeding organisms), then yes. Apparently, the populations were interbreeding.
If you go by the typological species concept (morphologically distinct), then no. Homo neandertalensis and the "Denosovian" are morphologically distinct enough to be recognized as such.


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Do marine deep sea life forms exhibit circadian rhythms? If so, what entrains them?
I've been reading a lot about circadian rhythms, when suddenly this question popped into my head: do circadian rhythms exist for deep sea organisms (3000 ft / 1000 meters+)?
For land mammals, the entrainment of circadian rhythms is done through exposure to light (retina or other photosensitive elements), but in the deep ocean there is no light. How are circadian rhythms maintained there - what acts as an entrainment signal? Is it the moon, currents, etc.?

This, IMHO, is an excellent question.

very interesting question. just a pointer: http://en.wikipedia.org/wiki/Diel_vertical_migration#Importance_with_the_biological_pump plankton migrates between 100 and 1000 meters of depth, so there are regular signals communicated downwards

This study (http://www.sciencedirect.com/science/article/pii/S0967063707002002) shows cyclic activity of a deep-sea fish, with tidal currents as entrainment signals.

A research paper that recently came out suggests that deep-sea life does have a circadian rhythm, but it is regulated much differently than it is by us surface dwellers. We see light, we eat and digest, and the suprachiasmatic nucleus in the brain (our "biological" clock) keeps track of it and eventually establishes a rhythm of the circadian variety.
Most living things at the surface have some sort of circadian rhythm - the mechanisms vary, but they are present and can be readily observed.
In the deep sea, the mechanisms are quite different since they can't see any light, but the rhythm is still established. When these animals (squid in the research) eat a certain type of bacteria containing a light organ, the presence of certain proteins within that organ actually trigger a change in the gene transcription responsible for encoding the protein controlling the circadian rhythm. Thus, when the squid eats, it ultimately determines what the rhythm will be. The entrainment itself actually happens by means of the light organs consumed in the bacteria.
As far as where the bacteria ultimately get there bioluminescence, there is still research to be done, although I would presume there is a mixture of downward bacterial migration and chemical generation contributing to this.
Link to the article: http://mbio.asm.org/content/4/2/e00167-13

Do you remember the name of the article or a link?

not off the top of my head, but I will look for it tomorrow

Heath-Heckman, E.A., Peyer, S.M., Whistler, C.A., Apicella, M.A., Goldman, W.E. and McFall-Ngai, M.J., 2013. Bacterial bioluminescence regulates expression of a host cryptochrome gene in the squid-Vibrio symbiosis. MBio, 4(2).


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Is there a superterm combining "animal line" and "cell line" in disease models?
Biologists researching diseases will frequently use animal models. The way I understand it, there are species of animals, such as "mouse", and lines of mice, such as Black six, NMRI or also genetically engineered lines like B6.Cg-Tg(CAG-cre/Esr1*)5Amc/J. But they also sometimes take cell lines such as HeLa and transplant them into animals, or treat them in vitro.
Is there a word which covers both "animal line" and "cell line" and is in widespread use? I thought that "model organism" would be a good way to express it, but a biologist working in disease models told me that when she hears that, she only thinks of animals, never of cell lines. She wasn't able to come up with a term which covers both. Her best try was "experimental system", but she conceded that, if used out of context, no biologist would recognize that it is about animal and cell lines.

'disease models' sounds pretty good actually.  maybe 'model system'

Is there any relevance in discerning or not discerning cell line and animal line apart from terminology? If you combine a transplant with a host - and there is no rejection - this might still not be an "animal line", as there are - in spite of non rejection of transplant  - are different, allogenic MHC cells, in that animal line. It is not a "cell line" either. You are not asking about combining allogenic cells  i.e. you are not asking for a term that denotes transplanting cell line into animal line?

There is no super-term that I can think of but you could say genetically modified (mouse) samples/specimens?

No, because not all mice or cells are genetically modified. The Black Six and NMRI I listed above are examples of wildtype mice, and they are still lab lines.


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Do mammals develop tolerance to anticholinergics?
I know that first generation H1 antagonists, commonly known as antihistamines have anticholinergic effects. Their sedative side effects go away due to tolerance, but as for their anticholinergic side effects well that's something that is unknown to me at least. You might say use second generation H1 antagonists, but for this application the antiemetic effects that are unique to H1 antagonists that cross the BBB (i.e., first generation H1 antagonists) are desired.

The tolerance to antihistamines is an ongoing debate in the community. Although there were early studies citing that tolerance to therapeutic effects of antihistamines could occur, more recent data, especially studies involving nonsedating antihistamines, indicate that tolerance to the therapeutic effects of these drugs does not occur.
Overall, it seems like the mechanism driving the sedation vs. the therapeutic effects are two separate down stream effects of regulating the inflammatory response. Neuronal tolerance and synaptic transformation is a fairly fluid and ongoing process, whereas the inflammatory response is much more robust. Meaning, the neuronal response is, theoretically, more able to adapt to chronic use of the anihistmaine while still giving the therapeutic effect. This hypothesis is supported by data, but yet to be confirmed, thus creating polarization on the topic.
Also see, Goodman and Gillman Pharmacological Principles of Therapeutics


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What does "Activation" refer to in the context of the symptoms of Schizophrenia and Schizoaffective Disorder?
In this journal article certain symptoms are called "activation" in nature. I have never come across this term prior to coming across this article, so I would like to know quite simply what does it mean.

This question might be better placed over on [cogsci.SE] , and they could really do with some more questions

The authors use the Positive and Negative Syndrome Scale (PANSS) to assess symptoms.  One of its cluster scores is activation factor.
Summary:
http://en.wikipedia.org/wiki/Positive_and_Negative_Syndrome_Scale
Original publication of the article, which doesn't list activation factors:
http://schizophreniabulletin.oxfordjournals.org/content/13/2/261.long
Marketed currently here:
http://www.mhs.com/product.aspx?gr=cli&id=overview&prod=panss
None of the sources I saw specified what is meant by activation factor, and many didn't even mention it. It's possible that it's the hyperactivity mentioned in the original publication.  Also, it's possible that it's a modified category in the version sold at the last link. Hopefully this is enough information to get you started, if you want to hunt down the details.


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What type of distribution should binding affinities fit?
I've been averaging Ki values from the PDSP Ki Database, and I can't help but to wonder: how I can determine p values for the binding affinities, so I can exclude anomalies in the data if need be?

What does your distribution of Ki look like? If it's reasonably normal, then convert to Z scores and pick an unacceptably low probability to discard (e.g., +/-3).

@kmm Ki values have to always be >0, yet normal distributions normally give a high probability for Ki values <0 and hence the normal distribution is something I'm wondering whether I should discard. It depends on the drug and receptor target too so I would like a nice and general answer if possible. I find that the kstest usually comes up for a p<0.1 that it fits a normal distribution so it might, but the negative values do concern me.

Can you add a histogram of your Ki values? Not all normal distributions have a mean of 0.

P-values reflect how well the data fits some background model. This background model should reflect some assumptions you make about the data. What assumptions do you think would be reasonable in this case? For example, do you assume high values are more likely to be incorrect?
Throwing away outliers like kmm suggested is probably not a good idea, because it means you will remove $K_i$ values which are very high or very low. It is not clear there is much biological justification for that, since we know some $K_i$s can be low and some can be high, but it doesn't tell us they are wrong.
The bottom line is that without making some assumption about what the values should look like, you can't identify what incorrect values look like.


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What is the chemical composition of an egg shell?
It ought to be some combination of C, O, and H, I presume. But really why should I care if eggshell gets in my eggs while I'm cooking?

Could you specify which animal's egg shell ?

Sure eggs from hens

Just google eggshell :) By the way, it is mostly calcium carbonate stabilized by a protein matrix. I have heard that excess calcium carbonate may cause some side effects but I don't have any good source.

@biogirl I don't want to google things; I would like to ask questions here to build a larger index of Q&A. Sure, I could always google things, but, asking questions here in the fashion that I have, is a catalyst for participation. If everyone feels that I should seek to answer my own questions through google, (which I am perfectly capable of doing), why have biology stack exchange? I would rather get the unique, human, and academic perspective from biologists and biology enthusiasts alike.

@RustynYazdanpour you should do a google search.
From the help pages http://biology.stackexchange.com/questions/how-to-ask: "Search, and research. Have you thoroughly searched for an answer before asking your question? Sharing your research helps everyone. Tell us what you found (on this site or elsewhere) and why it didn’t meet your needs. This demonstrates that you’ve taken the time to try to help yourself, it saves us from reiterating obvious answers, and above all, it helps you get a more specific and relevant answer!"

I took time to ask my question here, (help myself). My asking of a question spurred participation. SE is optimized for Q&A, so please do not tell me to google things. Perhaps they should make a biology overflow for serious research questions.

If you feel the question is obvious-- ignore it

@RustynYazdanpour I am sorry if you felt hurt by my comment. The first part of your question is easily searchable so I like the second part more because it is something I never thought before and got to learn something new ! On SE asking thought provoking questions will be appreciated. Do keep on asking good questions !!

It's the same stuff that makes up most sea shells, calcium carbonate, $CaCO_3$.
Incidentally, this explains why egg shells dissolve in vinegar (acetic acid which, since it is an acid, provides the Hydrogen ions in the reaction below):
$CaCO_3+ 2H^+ -> Ca^{2+} + H_2O +CO_2$
This simple reaction (which is what would happen in your stomach as well) produces water, calcium ions and carbon dioxide, none of which are particularly harmful.
The specific reaction with acetic acid is
$CaCO_3 + 2CH_3COOH → Ca(CH_3COO)_2 + H_2O + CO_2$
which also produces calcium acetate.
Anyway, there is nothing particularly toxic about $CaCO_3$, it's basically chalk. I wouldn't recommend eating a lot of it but you shouldn't freak out if some falls into your omelet either.
However, don't forget that an egg has exited a chicken's anus (well, cloaca) so their shells are likely to have come into contact with feces and they are porous so they are not necessarily the cleanest thing around. This is just not because of any chemical toxicity.

I thought that the calcium carbonate dissolves in olive oil, and calcium acetate forms. Should I have anything to worry about as far as calcium acetate goes?

@RustynYazdanpour calcium acetate is harmless. As you can see in that link even at very high concentrations (like those you will get if you buy it from a chemical company) it is an 'irritant'. In the concentrations you might find in your kitchen you can safely ignore it.

@Rustyn Yazdanpour: I doubt you'll get acetate from olive oil... it would rather come from the reaction terdon wrote (where he omitted acetate ions). In any case no worry about that either, although there are definitely much better uses for eggshell (composting for instance).

@terdon Ok, this is a full comprehensive answer. I really hope that the kinds of questions I'm asking are appropriate for this forum. Otherwise, if the community would prefer, I can ask some of these questions on chemistry stack exchange.

@terdon Sorry for my derisive tone that I may or may not have taken with you yesterday and thank you for your answer.

If you don't get any more chemical than this, you're fine. If you are asking about specific reactions chemistry might be better. If it is about their effect in a living system, they belong here. And no worries, you're very welcome :)

Indeed, you're more likely to find salmonella on the egg shells than in the yolk or whites themselves.


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What is the function of nodes of Ranvier in axons?
In a neuroscience class I'm taking, it was explained that myelin covers axons in sections, the uncovered sections are called nodes of Ranvier, and signals propagate much faster in the covered sections.
But if it is faster for signals to propagate along myelinated regions of the axon, why doesn't the entire axon get covered by myelin? Wouldn't that make it faster?

Every signal rapidly fades out with distance if it is not amplified. So if the whole axon were covered with myelin, action potentials wouldn't reach their target. Each Ranvier node can be seen as an active signal repeater.

Can you reference any original research paper about this "distance" that every myelinated portion should have?
In another question I just posted ( https://biology.stackexchange.com/questions/67879/why-myelin-sheat-does-not-cover-the-whole-axon/67882#67882) @Kesley R. told me that the optimal myelin sheat lenght is about 1 μm.
But wouldn't it depend also on diameter of the actual axon and other physical properties?

Action potentials arise and propagate by membrane depolarization.
A myelin sheath is present in most neurons and is responsible for insulating the membrane against ions. The function of the myelin sheath is to prevent leakage of charge, by effectively restricting ion channels only at certain regions called Nodes of Ranvier. This ensures that depolarization at one node is effectively equivalent to depolarization at another node, which initiates an action potential at the later node and as a result the action potential effectively "jumps" from node to node - this is called saltatory conduction and it speeds up the signals.
In axons without a myelin sheath, the signal does (passively) travel the full length of the axon.


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How is Hypertonic Urine Produced in a Mammalian Kidney?
I know that the ascending loop of Henle is impermeable to water and ions, and, by end of the ascending limb, the osmolarity of the tubular fluid is very low due to the active transport of ions out (e.g, sodium, potassium, chloride).
However, what if the person had to produce hypertonic urine due to dehydration or some other circumstance? Would the increase in osmolarity be done through a decrease in removal of ions in the descending limb, or has the distal tubule and collecting ducts got something to do with it?

aquaporins in the distal tubule absorb water. they are controlled by vasopressin (anti-diuretic hormone)

The process of urine concentration in mammals occurs due to the interaction of the loop of Henle and its nearby collecting tubule. When someone is dehydrated, the kidney will aim to a maximal water reabsorption.
To concentrate urine, a maximal amount of ions will be reabsorbed. This is to maximalize the concentration gradient for water. However, the main driving force for water reabsorption is the urea concentration gradient (created by the loop of Henle). Then aquaporins will allow water to flow from the collecting tubule to the nearby medulla because of the presence of the neighboring loop of Henle. It is this proximity between the loop of Henle and the collecting tubule that allows such a high efficiency for water reabsorption.
Concentrating urine is not about leaving more ions in the water, it is about reabsorbing a maximal amount of water.


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EGFR, sialylation, and cancer progression
EGFR (epidermal growth factor receptor) has been intensively studied in cancer and treatments have been developed to inhibit EGFR signaling.  Sialylation of EGFR is known to block dimerization  and down regulate signaling.  I just read this paper:
Liu et al. 2011. Sialylation and fucosylation of epidermal growth factor receptor suppress its dimerization and activation in lung cancer cells. PNAS 108: 11332–11337. (basically just read conclusion if you don't have time).
What I don't understand is that the authors seem to say that increasing sialylation might be a good thing to prevent cancer progression since it inhibits EGFR dimerization.  However, wouldn't this go against almost 50 or 60 years of research that suggest that increased levels of sialic acid are one of the well known hallmarks of cancer that aid in its progression and metastasis?  What could explain this apparent discrepancy?

Wikipedia claims (without reference) that

Metastatic cancer cells often express a high density of sialic
  acid-rich glycoproteins. This overexpression of sialic acid on
  surfaces creates a negative charge on cell membranes. This creates
  repulsion between cells (cell opposition)[5] and helps these
  late-stage cancer cells enter the blood stream.

so I assume this is a summary of the "50 or 60 years of cancer research" that you mentioned. I don't doubt you, I've just never read up on this particular aspect of cancer. Be that as it may, there is a difference between a cell's expressing high levels of sialoglycoproteins overall, and inducing high sialylation of one protein in particular, in this case EGFR.
As you may be aware, EGFR dimerization induced by multiple methods, including EGF binding, overexpression, mutation, chemical or antibody crosslinking, etc. activates tyrosine kinase domains in its intracellular region to auto-phosphorylate specific Tyr residues in its tail, which then recruit adapter and scaffolding proteins which support downstream signal transduction.
The paper you read shows how increasing sialylation of EGFR reduces its trans-affinity for itself and inhibits dimerization, and hence the downstream signaling cascade. This is a good thing in certain types of cancer which are driven by aberrant EGFR signaling, whether through overexpression of EGF and/or EGFR, mutations in the kinase domains, mutations in the dimerization domains, or otherwise.
This paper is also a great example of an apparent bad thing turning out to be good, when properly targeted and controlled. Excess sialylation of a cell may be bad, but specific over-sialylation of EGFR could turn out to be very useful, if we can learn how to modulate and target it. Another common example of this phenomenon is radiation therapy. Normally, high levels of radiation are bad for your body, and can actually cause cancer, among a range of other illnesses. But, there are many different ways of specifically targeting radiation to a tumor to kill it while sparing (to varying degrees) the surrounding tissue and the rest of the body.

Thanks for the response Matt. I guess I just don't see how it is possible to target siaylation of a specific glycoprotein in a cancer cell. Not only would that likely require cancer cell specificity, it would require activation of some metabolic pathway that would only sialylate EGFR--in otherwords subcellular accuracy. I don't think I've ever read of a way to specifically control glycosylation of a targeted single protein. I guess I simply don't agree with the authors' conclusions where they state that shutting down transferases might be a "bad" thing because it would promote EGFR dimers.

I know many people have long been trying to create glyco-transferase inhibitors to try to inhibit things like sialyation of cancer cell surfaces to prevent metastasis.  This paper alludes to the idea that this might be bad because it would promote EGFR activation.  I can't see why the authors would reach such a conclusion based solely off the study of just 1 glycoprotein when there are many others on the surface that may have negative influences if excess sialylated.

@GPI - that's why I put "specific over-sialylation of EGFR could turn out to be very useful, if we can learn how to modulate and target it" in there. It's a pretty big if.


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Does the Urea Cycle exist in invertebrates?
Do invertebrates (like Drosophila and C.elegans) have a urea cycle?

Questions that ask about "invertebrates" as if they were one group always make me uncomfortable. "Vertebrates" are a well-defined group, but "invertebrates" are just animals that aren't vertebrates. They are diverse, and it is nearly certain that the answer to your question is "some do, some don't".

C. elegans is missing all of the urea cycle enzymes. Drosophila is missing just one enzyme, but there's a shortcut which may enable it to nonetheless complete the cycle. (For comparison, here's the pathway map for human with the complete cycle.)

Perhaps worth adding that the role of the urea cycle in terrestrial vertebrates is the disposal of excess N derived from protein metabolism. Such animals are ureotelic. Arthropods, in contrast, are uricotelic, using uric acid for N disposal, so it would make no sense for them to have a functional urea cycle. (Nematodes - I don't know.)
The importance of avoiding having a urea cycle when it is not needed is illustrated by the situation in yeast (Saccharomyces cerevisiae). In yeast some of the enzymes that would be part of the urea cycle are used in degrading arginine, while others are used in the biosynthesis of arginine. Yeast cells will carry out one or the other of these processes depending upon their metabolic status. If both processes were to be active at the same time this would result in a urea cycle that would waste ATP. This is avoided by having a multienzyme complex consisting of arginase and ornithine transcarbamoylase (in the degradative and biosynthetic pathways respectively), allowing reciprocal regulation so that only one of these is active at any time.


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How the concentration of an antibiotic is chosen for YPD medium?
I need to prepare YPD plates containing hygromycin, but I don't know which concentration I can use. I'll select transformants of Hansenula polymorpha.

Presumably this will depend upon the promoter that is driving expression of the marker, and the copy number of the plasmid. Do you know anything about either of these parameters?

First I'll linearize this plasmid. because I want it to be integrated into the genome. (linearized DNA integrates to the genome in H. polymorpha). So there will be no additional copies. And tef1 promoter is present before hygromycin gene.

According to this site,
for yeast (I assume this means Saccharomyces cerevisiae) you should use 50 µg/ml to 200 µg/ml; for fungi (!) use 100 µg/ml to 300 µg/ml. The site also stresses the importance of the pH of the medium.
I think that, unless a Hansenula expert comes along,  you will have to try an initial experiment to measure the sensitivity of untransformed cells across the range indicated. Then you can try selecting resistant cells at a concentration somewhat higher than that which kills untransformed cells. Finally, you can check to see how resistant the transformants are, to enable you to decide on a useful concentration for routine selection of transformants.


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If only dicots have pith, what is the foam in the middle of cornstalks?
I've heard that the only plants that have pith are dicots, because of the shape of their vascular bundle. If that is true, what is the foam inside of the corn plants, which are monocots?

Monocots do have pith in their stems. The link even has an image of a maize stem:


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How did the huge dinosaurs cope with gravity and loads on bones, etc.?
It's very costly to be a huge animal. Your mass grows in cube when you scale up, but you still only have two/four legs to support the same weight. This increases the pressure that your body needs to cope with.(this is easy to see if you compare an ant with an elephant. The elephants legs are much thicker and strudier in comparison to it's body)
Looking at a T-rex for example, speciemns have been found that are believed to weight more than 9 tonnes, compared to an elephants 10 tonnes. T-rex has ofcorse has only two legs. The heaviest dionsaur is believed to have weight 80 tonnes. That is the weight of about 20 cars on each of their feet.
How could they support such massive weights?

I've heard that the greater amount of oxygen in the atmosphere was a factor, at least in the large size of the dinosaurs.

@shigeta Actually atmospheric oxygen was lower then present day throughout the time of the dinosaurs.

A t-rex's leg bones are a lot thicker than an elephants, for larger t-rexes the femur is almost 3 times thicker.

Assuming that gravity was essentially the same (other answers to this question notwithstanding), very large dinosaurs were dealing with the same forces that they would today. There are two clades of dinosaurs in which gigantism evolved, Sauropoda (quadrupdeal sauropods) and Theropoda (including T. rex). Each "solved" the problem of large size in different (but also somewhat similar) ways.
The main reason why large size was not a problem was that, if posture changed to align the forces between the animal and the ground, the bones are compressed. Bone is very strong in compression.
Theropoda
Theropod essential operate as a see-saw, with a large muscular tail balancing a large head. As such, they did not likely use much active muscular force to balance. The analogy is a human standing. Just standing, you don't need much muscle force to balance.
Hutchinson and Garcia (2002) showed that, because of a lack of plausibly large leg musculature, T. rex could not run. For a range of postures, they estimated how much muscle would be required to balance the animal and found that running behavior was unlikely.
Hutchinson, J.R. and M. Garcia. 2002. Tyrannosaurus was not a fast runner. Nature 415:1018-1021.
Sauropoda
Sauropods show many similar adaptations as elephants, the largest extant land mammals. Their limbs were held upright (erect), which requires less energy for balance. Some sauropods had air-filled bones, which would also lighten the skeleton. Wilson and Carrano (1999) document the evolution of posture through sauropod evolution from a biomechanical perspective.
Wilson, J.A. and M.T. Carrano. 1999. Titanosaurs and the origin of “wide-gauge” trackways: a biomechanical and systematic perspective on sauropod locomotion. Paleobiology 25:252–267.

I love your answer! I have been pondering this for year! Do you have any knowledge regarding their ability to survive a fall (I'm mostly thinking of the two-legged giants)

I think this paper (http://www.jstor.org/pss/4523665) deals with falling T. rex.

This is the best day of my life!

Ornithopods got just as large as Theropods, right?

If so why do elephants have trouble with tiny jumps?

@user2617804 mammals are really poorly adapted for being large. Things like having a lumbar spine and having lost a large number of bones( chevrons, gastralia, lumbar ribs, cervical ribs, ect), mammals just lack a lot of support structures dinosaurs have. Pillar style posture also makes for really poor shock absorption, esspecially from falling any distance.


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What does the human body use oxygen for besides the final electron acceptor in the electron transport chain?
My biology teachers never explained why animals need to breathe oxygen, just that we organisms die if we don't get oxygen for too long. Maybe one of them happened to mention that its used to make ATP. Now in my AP Biology class we finally learned the specifics of how oxygen is used in the electron transport chain due to its high electronegativity. But I assume this probably isn't the only reason we need oxygen.
What other purposes does the oxygen we take in through respiration serve? Does oxygen deprivation result in death just due to the halting of ATP production, or is there some other reason as well? What percentage of the oxygen we take in through respiration is expelled later through the breath as carbon dioxide?

Doesn't the body use sunlight and oxygen to create Peroxide in the skin for immune reasons? I heard this once from somewhere

Oxygen is actually highly toxic to cells and organisms – reactive oxygen species cause oxidative stress, essentially cell damage and contributing to cell ageing. A lot of anaerobic organisms have never learned to cope with this and die almost immediately when exposed to oxygen. One classical example of this is C. botulinum.
Oxygen is incorporated in several molecules in the cell (for instance riboses and certain amino acids) but as far as I know, all of this comes into the cell as metabolic products, not in the form of pure oxygen.
The oxygen ($\ce{O2}$) we breathe is completely used up during aerobic respiration. The stoichiometry of this is given by the following simplified equation:
$$\ce{C_6H12O6 + 6 O2 -> 6 CO2 + 6 H2O + heat}$$
WYSIWYG’s answer goes into more detail.

Oxygen is not converted to carbon dioxide!  It's converted to water.

Superoxide, O2− is created by the immune system in phagocytes (including neutrophils, monocytes, macrophages, dendritic cells, and mast cells) which use NADPH oxidase to produce it from O2 for use against invading microorganisms. However, under normal conditions, the mitochondrial electron transport chain is a major source of O2−, converting up to perhaps 5% of O2 to superoxide. [1]
As a side note, there are two sides to this coin.  While this is a useful tool against microorganisms, the formation of the reactive oxygen species has been incriminated in autoimmune reactions and diabetes (type 1). [2]

[1] Packer L, Ed. Methods in Enzymology, Volume 349. San Diego, Calif: Academic Press; 2002
[2] Thayer TC, Delano M, et al. (2011) Superoxide production by macrophages and T cells is critical for the induction of autoreactivity and type 1 diabetes,60(8), 2144-51.

You probably know by now that cytochrome c oxidase, the last complex of the electron transport chain, belongs to a class of enzymes called oxidoreductases, that use oxygen atoms as electron acceptors. One type of oxidoreductases are oxidases, enzymes that (at least in theory [1]) use molecular oxygen--O2, like in air--as their electron acceptor. From what I know, however, sometimes that isn't the case: xanthine oxidase, that converts xanthine to uric acid, gets its oxygen atoms from water [2]. Examples of the "true" oxidases include L-amino-acid oxidase and cytochrome P450 (aka. CYP family).
Despite cytochrome P450 being a numerous and important enzyme family, responsible for most of known drugs metabolism and some essential lipids transformations, it probably consumes only a fraction of oxygen that animals breathe in. I wasn't able to find any estimations, but would be surprised if it was more than perhaps 0,1%.

[1] Introduction to EC1 class
[2] Metz, S. & Thiel, W. A Combined QM/MM Study on the Reductive Half-Reaction of
Xanthine Oxidase: Substrate Orientation and Mechanism. J. Am. Chem. Soc. 2009, 131, 14885–14902, PMID: 20050623.

The overwhelming use of oxygen is to provide us (in combination with food) with energy.  We have a great need for energy in our cells, which is why we have these lungs, diaphragms, red blood cells, etc.; they assure we get the oxygen to obtain the energy (via the electron transport chain).
The overall metabolism of glucose (C6H12O6) is a representative reaction:
 C6H12O6 + 6 O2 --> 6 CO2 + 6 H2O + energy
You can see that just as much oxygen goes out as gaseous CO2 as came in as gaseous oxygen (O2).
The energy is temporarily kept in the form of the phosphate bond in ATP molecules so that it can be shuttled around the cell to the multitude of cellular processes that need energy.
Energy is so essential to the cellular processes that maintain animal cells that lack of that energy, which results quickly when there is oxygen deprivation, soon causes irreversible damage and death.

Why is not fermentation a possible solution? We need numbers (about the amount of energy) and references.

This representative reaction is not really correct and you know that. The OP has already indicated that they know about the role of oxygen as the terminal electron acceptor.

Another small addition

There is class of oxidoreductases called oxygenases which incorporate molecular oxygen into the substrates and not just use it as an electron acceptor like in oxidases (note that the terminal enzyme in ETC is an oxidase and there are other such oxidases). In other words, oxygen is not a cofactor but a co-substrate. Oxygenases are further classified into dioxygenases and monooxygenases which incorporate two oxygen atoms and one oxygen atom respectively. Examples:

Cytochrome P450 family (monooxygenease): involved in detoxification of xenobiotics
Cyclooxygenase (dioxygenase): involved in production of prostaglandins which are involved in pain and inflammation. Many NSAID painkillers like aspirin, paracetamol and ibuprofen target cyclooxygenase-2 (COX2)
Lipoxygenase (dioxygenase): Involved in production of leukotrienes which are involved in inflammation.
Monoamine oxidase (monooxygenase): Involved in catabolism of neurotransmitters such as epinephrine, norepinephrine and dopamine.

Does oxygen deprivation result in death just due to the halting of ATP
  production, or is there some other reason as well?

Death predominantly occurs because of halt in ATP production. Some cells such as neurons (and also perhaps cardiac muscles) are highly sensitive to loss of oxygen (for energy requirements) and clinical death because of hypoxia usually occurs because of loss basic brain function.

What percentage of the oxygen we take in through respiration is
  expelled later through the breath as carbon dioxide?

As already mentioned, it is said that there is a rough 1:1 ratio of CO2 production and O2 consumption. However, as indicated in a comment by CurtF, O2 does not form CO2; it forms water in the last reaction of ETC. CO2 is produced in other reactions of Krebs cycle.
Glycolysis produces 32 molecules of ATP for 1 molecule of glucose via ETC (see here). There are three complexes in ETC and the third is dependent on oxygen; so you can assume that 1/2 a molecule of O2 consumed for production of 3 ATP molecules. Therefore 32 molecules of ATP would consume 4 molecules of O2. Seems like there is a 1:1 ratio of CO2 production and O2 consumption.
We can see it like this:
FADH2 enters ETC at the second complex whereas NADH enters at the first. We can say that as long as NADH is present FADH2 would not require an extra oxygen.
An NADH or a FADH2 molecule would require 1/2 molecule of O2. There are 8 molecules of NADH and 2 molecules of FADH2 produced during glycolysis+krebs cycle which would require 10/2 = 5 molecules of O2. Glycolysis produces 4 molecules of CO2 during krebs cycle.
However, 2 cytosolic NADH molecules require 2 ATPs (in other words another NADH molecule) to be transported to mitochondria. So the net effect may be actually close to 1:1 O2:CO2.
Another factor to keep in consideration is that the three complexes do not actually produce ATP; they just pump proton to create a chemical potential. The F0F1-ATP synthase would probably work only after a threshold of H+ potential is established. The 1 ATP molecule per complex is most likely the mean value and not exactly what really happens per reaction.


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Is the appendix a vestigial structure in all vertebrates?
In humans the Appendix is a vestigial organ. Does it serve no apparent purpose in all the vertebrates that have one?

I don't think the appendix is vestigial in humans.

Smith et al. (2009) provide a survey of the morphology of the cecal appendix. One current hypothesis is that the appendix provides "safe harbor" for symbiotic gut bacteria. Among mammals, there is a vast array of cecal appendices:

In summary:

A comparative anatomical approach reveals three apparent morphotypes
  of the cecal appendix, as well as appendix-like structures in some
  species that lack a true cecal appendix. Cladistic analyses indicate
  that the appendix has evolved independently at least twice (at least
  once in diprotodont marsupials and at least once in Euarchontoglires),
  shows a highly significant (P < 0.0001) phylogenetic signal in its
  distribution, and has been maintained in mammalian evolution for 80
  million years or longer.

Aside from humans, it is largely rodents and most notably rabbits that have an appendix.  Therefore, using rabbits as my example:
In rabbits, the appendix is thought to have a key role in the development of the immune system.  Specifically it has been shown experimentally that when neonatal rabbits are given an appendectomy levels of Immunoglobulin A and G (IgA/IgG) fall dramatically. Both these polypeptides are prominent antibodies - IgA plays a key role in mucosal immunity whilst IgGs in humoral immunity.  These effects were localised to the small intestine of the rabbits, however were statistically significant. 1
In infants, the rabbit appendix resembles the chicken bursa and sheep ileal Peyer's patch (both performing similar functions as described above).2
This has led to some ongoing research as to whether the human appendix has a similar properties in having function in infants 3:

If the human appendix functions as a primary lymphoid organ, it may occur during the first few months of age when the GC T-cell density is low.

1Neonatal appendectomy impairs mucosal immunity in rabbits. Cell Immunol. 1997 Nov 25;182(1):29-37
2The appendix functions as a mammalian bursal equivalent in the developing rabbit. Adv Exp Med Biol. 1994;355:249-53.
3A morphological and immunohistological study of the human and rabbit appendix for comparison with the avian bursa. Dev Comp Immunol. 2000 Dec;24(8):797-814.


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How is eye color in humans inherited?
In high school we studied the inheritance of eye color, as it was explained to us in the most simple way: blue eye color is a recessive, monogenic, autosomal trait. Now I know that it is a bit more complicated than that; there are several genes which determine the inheritance of eye color. That's as far as I my knowledge goes.
Which are these genes and what do they encode for? How is the eye color trait inherited? Provided that a man with blue eyes and a woman with brown eyes have a child, can the probability of their child to have blue eyes be calculated?

It is mainly determined by the OCA2 gene, but it also likely involves several other genes, including TYR, TYRP1, HERC2, and several others. To complicate things further, it is not a "mutant/wild type" trait, but multiple normal alleles can be found in the population, and it is believed that the sum of these single nucleotide polymorphisms (SNPs) determine the final phenotype.
I took the info from a 2004 review by Sturm and Frudakis and a more recent paper from Liu et al, 2009

This answer is so close to be good... why don't you expand a little on what those genes do and how they influence color? I know you linked the papers but it would be much nicer if the answer were self-sufficient. For instance you could say that OCA2 encodes for the P protein, a (supposed) Tyr transporter that allows Tyr, a precursor of the brown pigment melanin, to get into the cells.

@aleadam Thanks for your answer, it really looks promising, but I was about to ask you the same thing as nico did: can you please expand it and make it more clear and easy to read and understand?

omim might also be helpful: http://www.genome.jp/dbget-bin/www_bget?omim+227220

There is a nice page that tries to explain this:

The known Human Eye color genes are: EYCL1 (also called gey), the Green/blue eye color gene,
  located on chromosome 19 (though there is
  also evidence that another gene with similar activity exists but is
  not on chromosome 19). EYCL2 (also called bey1), the central brown eye
  color gene, possibly located on chromosome 15. EYCL3 (also called
  bey2), the Brown/blue eye color gene located on chromosome 15. EYCL3
  probably involves mutations in the regulatory region just before the
  OCA2 gene (which produces a protein that is expressed in melanocytes).
  A second gene for green has also been postulated. Other eye colors
  including grey and hazel are not yet explained. We do not yet know
  what these genes make, or how they produce eye colors. The two gene
  model (EYCL1 and EYCL3) used above explains only a portion of human
  eye color inheritance. Both additional eye color genes and modifier
  genes are almost certainly involved.

There is even an interactive calculator available.


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What is Peter's rule in neuroscience?
I have heard and read about Peter's rule informally in the past, but never saw a formal definition or description.
Informally I have learned to understand Peter's rule as the assumed correlation between the amount of overlap between axons and dendrites and the post synaptic density in the synapse. Here is a sample of the search results in Google.
Is my interpretation correct? Is there a more rigorous, perhaps quantitative,  definition of Peter's rule?

Your link is not working. Also, it would be nice if you give a short 'informal' description of it yourself.

Thanks @Gergana. I have updated my question and fixed the link. Let me know if there is anything else I can do to improve it.

I think that your interpretation is correct, although Principles of Neural Science (Kandel et al.) doesn't mention Peter's rule (which is where I would have hoped to find a simple explanation).
According to Binzegger et al. (2004), the idea behind Peter's rule dates back to Peters and Feldman (1976) and Peters and Payne (1993), though the Rule per se may have been coined by Braitenberg and Schultz (1991; at which point it was still called Peters' rule). Binzegger et al. describe it as:

They assumed that axons simply connect in direct proportion to the
  occurrence of all synaptic targets in the neuropil. The rule can be
  extended to provide more precise estimates by taking into account the
  detailed morphometrics of the dendritic and axonal trees of the
  different neuronal types.

To paraphrase Binzegger et al., in the simplest form of Peter's rule, the number of synapses in a cortical layer are evenly distributed across the potential target neurons. So there would be a direct proportionality between synapses and targets.
The second sentence of the quote above is the meat of the Binzegger paper. They also present a mathematical model of a more complex and realistic variation of Peter's rule which takes into account different types of postsynaptic neurons and the fact that not all cells receive synapses.
Braitenberg V, Schüz A (1991) Peters' Rule and White's Exceptions. In: Anatomy of the Cortex, pp 109–112. Berlin: Springer.
Peters A, Feldman ML (1976) The projection of the lateral geniculate nucleus to area 17 of the rat cerebral cortex. I. General description. J Neurocytol 5:63–84.
Peters A, Payne BR (1993) Numerical relationships between geniculocortical afferents and pyramidal cell modules in cat primary visual cortex. Cereb Cortex 3:69–78.

"taking into account the detailed morphometrics", i.e. looking on an EM image? :P see another exception

So one should cite the papers Braitenberg1991 and Peters1976 at least if one talks about Peters' rule?

Here is a definition taken from a Scholarpedia article on computational neuroanatomy:

The critical underlying question remains: how does the number of synapses between two neurons depend on the overlap between their dendritic and axonal trees? According to "Peters rule", synaptic contacts occur where dendrites and axons happen to be in apposition. These "potential synapses" are required but not sufficient for an actual synapse formation; and the expected number of connections between two neurons is proportional to the product of their dendritic and axonal trees densities (e.g. Peters et al., 91).

This seems to be saying that there are really two pieces to Peter's rule-- first that "synaptic contacts" (potential synapses) actually occur where axons and dendrites share space, and secondly that the proportion of these contacts that are real synapses is proportional to tree density.


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How to decide which is the correct scientific name for a particular species
To start with, I am not a person having sound knowledge in biology. When I started my search for phyto-chemicals in a particular family in the plant kingdom, I got confused. The scientific papers use a particular name, and when I searched in these 2 websites, (just to name it) I got the message that some of the names are  "not resolved"  or "synonyms".
My questions are

Biologists do they accept  the names mentioned in  website 1? If not where can I find authentic names?
Who controls / monitors the name of these plant species?

Out of curiosity, what name are you looking for?

I would go with results from the first site you mention (www.theplantlist.org)

iPlant provides an automated name resolver: http://tnrs.iplantcollaborative.org/TNRSapp.html

When it comes to plants and animals, common names clearly differ from region to region.
A first effort to univocally classify them was done in the 16th century by Carl Linnæus (see my answer to this question for some historical background).
The nomenclature of plants is governed by the International Code of Nomenclature for algae, fungi, and plants (ICN), and for animals from the International Code of Zoological Nomenclature (ICZN).
The fact that there are rules, however, does not imply that names are conserved over time, nor that there is a rule for everything!
As time goes by rules change, certain species may be assimilated by others, or a certain subspecies will separate and become its own, and at times name changing proposals even raise havoc in the scientific community.
In summary, it is important to remember that taxonomy poses rules that are there to facilitate talking about science. Those are not absolute rules, sometimes they are arbitrary, and therefore for certain species there is no univocal name (and surely there is no correct name).

can you just share the "Official" website of ICN. I could not any hits when i googled it.

@Anil: The International Association for Plant Taxonomy hosts the full text of the Vienna code. I could not really find the latest version (Melbourne code), although the IBC2011 website may be of help.

For completeness' sake, the Melbourne code is now up at http://www.iapt-taxon.org/nomen/main.php

Nico provides a nice answer, but implies that the names are more fluid than they actually are.
It is possible to get an current standard nomenclature, and to update it each time the ICN releases a new edition.
The ICN requires that any changes be made by an international botanical congress, and changes are included when a new addition of the ICN is released. Also, note that the ICNCP is used for cultivated plants.

You misunderstood my point. What I am saying is that, well, names are names, and can change. That is why nowadays you would say Chroicocephalus ridibundus, rather than Larus ridibundus when talking about a Mediterranean Gull, although some years ago the opposite was true. That does not mean that anyone can change the names at his own will, but it is important to remember that there is no strict rule for nomenclature [continues...]

[continued...] The case of Drosophila Melanogaster vs Sophophora Melanogaster is a beautiful example of this flexibility: the name ought to be changed, sure, but everyone knows Drosophila by that name, so we will keep it like that, even if there are scientific reasons to opt for a change.

I was mostly pointing out that name changes are tractable through the ICN, and that the keeping up to date with the ICN is sufficient.

I realize this question is very old, but there is an important point missing from the current answers: That is the difference between the nomenclature and the taxonomy.
By "taxonomy" I mean the understanding of how organisms are related to each other. Key questions here would be whether taxa sharing some group name (the same genus, for example) form a clade (i.e., there exists an ancestor whose descendants include all and only members of that genus), and whether particular taxa or specimens are the same species or not.
By "nomenclature" I mean the names applied to each taxon and groups of taxa.
The key point is that nomenclature exists within some accepted taxonomy, and that when name changes occur, it's usually because of a conflicting or updated understanding of taxonomy. The rules of nomenclature are comprehensive and quite rigid, but for taxonomy there are no rules at all. Each researcher is free to adopt a taxonomy based on their own understanding of the evidence, however within the taxonomic framework they choose, they must follow the rules of nomenclature.
A "synonym" refers to a named species that the current author considers to be a part of another, earlier named species. For example, the white-veined wintergreen, Pyrola picta Sm., was described in 1819. Later, the cryptic wintergreen, Pyrola crypta Jolles, was described in 2014 when the authors determined that molecular evidence and subtle morphological features marked some P. picta as distinct.
Botanists can (and do) have good-faith disagreements about whether these represent two species. There is no over-arching authority that makes that determination. Botanists who think they are different will use both P. picta and P. crypta, respectively. Those who think they are best considered a single species must use the name P. picta for all of them, and list P. crypta as a synonym.
The example previously given of Drosophila melanogaster possibly being renamed stems from a different issue. Each genus name is pinned to one particular species (the "type species"). In the case of Drosophila it is D. funebris. This means that if the genus Drosophila is recognized as a genus, then it must contain the species D. funebris, but not necessarily any other species. What probably happened is that a new family tree (phylogeny) of Drosophila and related genera was constructed, and D. melanogaster came out as being more closely related to flies in a different genus, than to D. funebris.
Ideally, all the members of a genus would form a clade, because, for example, it can be confusing to have Drosophila melanogaster be more closely related to some other genus, than to other members of Drosophila. So to remedy this, some fly taxonomists suggested reshuffling these taxa to make more neat clades and less of a jumble (D. funebris though, would have stayed in Drosophila).
Normally this happens and nobody notices except for the few researchers who work on that group. Here, however, scientists from all over the world in a dizzying array of disciplines have studied and published results related to "Drosophila melanogaster". It would have lead to huge headaches and confusion to rename this iconic species. In this case, a formal proposal was made to create an exception to the normal rules by changing the type species of Drosophila from D. funebris to D. melanogaster. That way, as long as Drosophila is recognized, then D. melanogaster would also exist.
One final point is that @nico's statement "surely there is no correct name," is incorrect. In the world of nomenclature "correct" is a term of art. For a particular taxonomy there is exactly one correct name. It's just that the taxonomy is subject to the interpretation of the researcher or author.

Excellent answer. The only way it could be slightly improved would be to provide links to back up your answer - I realize that's pretty difficult for this topic, as I don't think the rules (other than nomenclature) are defined particularly well.