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Has the concept of allostasis been adopted in biology, in place of homeostasis?
Peter Sterling, among others, has been a prominent critic of the concept of homeostasis.  He instead proposes a process called allostasis.
Homeostasis involves having fixed set points for physiological parameters, and when we deviate from those set points, there are mechanisms that restore them.
However, Sterling argues that this process of homeostasis is inefficient and inflexible.  Instead, he posits that the brain is constantly predicting physiological needs based on environmental and bodily demands, such that the "set point" changes depending on the context.  So your mean blood pressure might be X in one context, but Y in another.  And rather than responding after a deviation from the mean, the brain predicts those deviations and adjusts the body accordingly.  This is allostasis.

Allostasis is much more in line with what we know about the brain (e.g., Clark, 2013), but has this idea been adopted much in biology?  Based on my memory from biology class not long ago, it seems like homeostasis is still considered a central feature of living things.
Thanks!

For those that don't have a subscription to that particular journal, can you find or post a copy in some easily and permanently-accessible place? Or, at the very least, highlight his arguments for it and provide links to supporting evidence? Sometimes ideas like this are just too new to have gotten much traction yet, other times they're crackpot hypotheses that don't fit with existing data. Sure, it sounds nice, but where's the evidence?

@MattDMo  Here's a freely available article of his from 2004 and you can download a more recent article from researchgate here.

Thanks. By the way, just to be clear, I have no opinion at all as to whether this is an accepted hypothesis or not, as this isn't my field of study. But I have been involved in other similar questions asking "Why isn't this theory of Professor XYZ more accepted in the community?" and it turns out that XYZ is a crackpot conspiracy theorist who is chief editor and publisher of his own journal and organization that espouses the garbage he writes about, regardless of any possible "merit" or "scientific evidence". I'll try to link you to the question if I can, I don't remember it at the moment.

@MattDMo  I definitely understand the concern.  Although Peter Sterling is a reputable academic, and a prominent physiologist I work with seems to find strong validity in his theory.  But who knows!

Eh, personal views here as a biologist, so I'll keep this in a comment rather than an answer: Everything in biology comes with huge asterisks and exceptions. This is often a point of confusion for novices and non-biologists, but to me it's just a way of thinking when you deal with life. I think it's pretty clear from your diagram that a major component of "allostasis" is indeed homeostasis: it's homeostasis with a little bit of predictive power. Outside of biology, in control theory, this is a pretty basic part of set point regulation: when you want to keep something at a set point, maybe...

...temperature, you don't just think about your current temperature but you look at rate of change, etc, to make some future predictions. So, is homeostasis everything? No of course not. You can maybe get some publicity if you say "Hey everyone! Homeostasis isn't everything!" But of course that's obviously true: organisms grow, they reproduce, they grow old and die. You might start releasing energy stores when you wake up in the morning rather than when you start jogging. Homeostasis is still a pretty powerful descriptor in most cases, a lot like Newtonian physics on Earth.

I don't know Peter Sterling. Maybe he is just trying to get attention. Maybe he just wants to emphasize the exceptions to the rule. From your description it sounds a lot like a physicist who goes around the party telling everyone F=ma is wrong. Everyone knows he is right, but he isn't really convincing them of anything they don't already know, and they think he's annoying anyways.

@BryanKrause  I suppose I'm a bit confused by your last paragraph.  Peter Sterling is a legitimate, well-respected academic.  He's not trying to get attention.  If you read his articles, they're well reasoned and well evidenced.  Did my language somehow paint him as a crackpot?  (Sincere question.)

@BryanKrause  Also, Peter Sterling isn't claiming that "homeostasis isn't everything."  He's saying that such a process isn't functional without prior knowledge and predictions.  This is very, very important in areas like (human and non-human) neuroscience and psychology (where it's routinely ignored and so theory suffers), so I'd imagine it's also very important in biology.

I'm saying that what he calls allostasis doesn't sound any different from what most biologists would understand homeostasis to include. It seems from your description that he is setting up a straw man for homeostasis. The key flags for me in your question were "instead of" and describing him as a "critic" of homeostasis. No experienced biologist would claim that homeostasis means set points can't change - that's silly, hence why it is a straw man argument.

That said there may be nothing wrong with his work, he may just be stressing an issue he feels is overlooked or not treated explicitly by others. Maybe your characterization of his work is a bit exaggerated? Or maybe he exaggerates himself - it's not a bad rhetorical technique, I think you are just taking it to far with the idea that somehow other biologists aren't accepting that set points change or organisms make predictions on future needs.

@BryanKrause   Got it, thanks!   Although, to be fair, if you look at the history of the concept homeostasis, it has a very specific meaning, so I'm not entirely sure it's a straw man.

@mrt I looked at the Wikipedia page for allostasis, a quote: "Allostasis is the process of achieving stability, or homeostasis, through physiological or behavioral change".
I could define a new term myself, "Ezzting: the process of achieving nutritional intake, or eating, by putting food items in your mouth and chewing them." Do you think that term will take the world by storm and replace the clearly inferior verb "to eat"?

I don't think "allostasis" is as much a farce as my example, but it will not replace homeostasis because the definition of "allostasis" is already the definition most biologists would use for "homeostasis" - no one except the people behind "allostasis" seem to be defining homeostasis so narrowly as to need a secondary term. I came to this conclusion independently, but it looks like I am not alone, as the Wikipedia article on allostasis also led me to this paper which seems to share my take.

@BryanKrause  I think if you read the two papers I linked from Sterling, it would clear up a lot of confusion.  Wikipedia isn't really a great source here.  I can't keep defending something if you're not familiar with it.

What exactly is your question?

Allostasis is more than changing set points. The theory of allostasis attempts to unify the theories of stress and homeostasis. And, although Peter Sterling and Joseph Eyer were the first to coin the term "allostasis", the concept is today proposed by a plethora of researchers.
Allostatic responses ensure „stability through change“ in situations of strain and stress. If in allostatic mode a feedback control system is able to change both its set point and its parameters to approach a state vector that is more suitable for survival. An allostatic response involves the activation of actuator variables that is referred to as allostatic state. Although allostasis is basically beneficial for viability it also exposes the organism to some kind of strain, referred to as allostatic load. If ongoing or being excessive, allostatic load may be life-threatening on its own terms. In this situation, it is referred to as allostatic overload.

Figure taken from Chatzitomaris et al. 2017.
The idea of allostasis might have been omitted in your biology class due to didactical reasons. For an introductory course it may be beneficial to begin with the simpler theory of homeostasis.
Today, the concept of allostasis is of increasing importance for psychology and medicine. As of today, a PubMed search for the term "allostasis" results in 730 papers and a search for "allostatic load" delivers 1123 publications (with growing tendency).
The theory of allostasis helped to improve our understanding of a broad range of diseases and non-pathological bio-psycho-social situations. Typical examples include starvation, obesity, exercise, fever, type 2 diabetes, hypertension, thyroid disorders, post-traumatic stress disorder (PTSD) and psychosomatic diseases. Additionally, the recent development of panels for allostatic load facilitates differential diagnosis near the small ridge between health and disease.
References

Sterling P, Eyer J. Biological basis of stress-related mortality. Soc Sci Med E. 1981 Feb;15(1):3-42. PMID 7020084.
Sterling P. Allostasis: a model of predictive regulation. Physiol Behav. 2012 Apr 12;106(1):5-15. doi: 10.1016/j.physbeh.2011.06.004. Epub 2011 Jun 12. PMID 21684297.
Bizik G, Picard M, Nijjar R, Tourjman V, McEwen BS, Lupien SJ, Juster RP. Allostatic load as a tool for monitoring physiological dysregulations and comorbidities in patients with severe mental illnesses. Harv Rev Psychiatry. 2013 Nov-Dec;21(6):296-313. doi: 10.1097/HRP.0000000000000012. PMID 24201821.
Sagner M, McNeil A, Puska P, Auffray C, Price ND, Hood L, Lavie CJ, Han ZG, Chen Z, Brahmachari SK, McEwen BS, Soares MB, Balling R, Epel E, Arena R. The P4 Health Spectrum - A Predictive, Preventive, Personalized and Participatory Continuum for Promoting Healthspan. Prog Cardiovasc Dis. 2017 Mar - Apr;59(5):506-521. doi: 10.1016/j.pcad.2016.08.002. PMID 27546358.
Chatzitomaris A, Hoermann R, Midgley JE, Hering S, Urban A, Dietrich B, Abood A, Klein HH, Dietrich JW. Thyroid Allostasis-Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming. Front Endocrinol (Lausanne). 2017 Jul 20;8:163. doi: 10.3389/fendo.2017.00163. PMID 28775711.


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How long does it take for a genetic trait to dissipate if its no longer selected for?
Have their been any studies or experiments done that provide insight into the persistence of genetic traits if an environmental shift suddenly causes that trait to be neutrally selected for? Does it take 100s of generations to reach equilibrium or only a few?
For example, how long can we expect the effects of birth control to take in decoupling human behavior related to sex from human behavior related to having children?

It depends on whether it is neutrally or negatively selected (and how strongly so), it depends on the population size, it depends on the mutation rate and mutational variance and - most important of all - it depends on the level of genetic variance for this trait to start with. This variance can be calculated at equilibrium (assuming no important demographic change "recently") from the above parameters though. It may take between 1 generation and a biliion generations.

Lets say its neutral, not negative. I added an example case for reference. Of course it depends on those things, but I'm looking for a more quantitative answer.

The answer still varies between almost 1 generation to many generations.

@Remi.b No it doesn't. There is literally no statistically probable way that a trait will be randomly removed in a single generation. Your comments aren't helpful at all.

If the population is 2, yes it is even quite likely. I wrote an answer to give you a hint about how variable it can be depending on the exact scenario of interest.

I would need to see some logic or evidence that even a population of 2 would dissipate a neutral genetic trait in 1 generation unless the entire population dies. Ya, your population dies you won't have the gene, and that's obviously not what my question's about.

if there is a standing genetic variance of 0.5 (one is carrying the allele A and the other one is carrying the allele B), then the guy with the allele A reproduce while the other don't (let's assume hermaphrodism) and it's done. End of the story. Of course, in such a small population it is likely that there is no standing genetic variance but this very much depend on the detailed scenario of interest. Experimental evolution of selection sometimes don't last more than 40 generations and you already see a strong response.

There is no way to answer this question as there are way too many factors influencing this time.
It depends on too many factors
It depends on:

whether it is neutrally or negatively selected (and how strongly so)
the population size
mutation rate
mutational variance
level of genetic variance for this trait to start with.

This variance can be calculated at equilibrium (assuming no important demographic change "recently") from the above parameters though.

It may take between 1 generation and a billion generations.
For example
Consider for example that your trait is neutral. Assume that the trait can only take two binary state A and B and that only a single locus affect this trait, which two states are also named A and B for simplicity. Let's say A is the ancestral state and we want to know how much time it takes to have a population of B. Imagine the haploid population size is $N=10^5$. The mutation rate for the locus of interest is $\mu=10^{-9}$.
Slow Case
If at the start there are no alleles B, then you have to wait for a mutation to occur. The time for such a mutation to occur follows an exponential distribution with parameter $\mu=10^{-9}$. Because we assumed neutrality, the probability of fixation (fixation is the state when the whole population carry the same allele) is $\frac{1}{N}=10^{-5}$. Conditioning on fixation, the expected time for fixation to occur is $-4N \left(\frac{1-p_0}{p_0}\right)\ln(1-p_0)=399998$ generations. In consequence, the expected time to fixation in this case is $10^{5}*10^{9}+399998 ≈ 10^{14}$ generations, that is about 77 times the age of the earth assuming there is one generation per day! So Obviously, the environment has time to change again. Note that variance is about $10^{28}$ generations! Of course this example is just an extreme slow case, but I have been using realistic parameter values.
Fast Case
If you have a population size of $N=50$ and the B allele is already present at frequency 0.1 and that the B allele is beneficial with a selection coefficient of 1.5, then it might take about 100 generations.

Thanks, this is much more informative. FYI, the answers I'm expecting are along the lines of equations, not a constant answer like "10-15 generations".

Happy that it helps. Note that there way too many processes in play and therefore too many equations (if you're looking for equations). I would recommend that you follow an introductory class to population genetics.

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Origin of melatonin: oxidative stress defense OR circadian rhythm?
Question
Which functional role of melatonin came first?

Regulation of the circadian rhythm
Defense against oxidative stress
Other

Background
I was well aware of the important role melatonin plays in Human sleep behavior, and circadian rhythm regulation, quoting the Wiki page:

Melatonin, also known as N-acetyl-5-methoxy tryptamine,1 is a
  hormone that is produced by the pineal gland in animals and regulates
  sleep and wakefulness.2

What I was not so aware of, but now quite fascinated to learn about, is melatonin's role in oxidative stress management. In fact, the quote below is taken from the sentence immediately following the one above, in the same Wiki page:

it functions as a first line of defense against oxidative stress.3

Related Stack Bio Discussion
I also came across this Stack Biology answer to the question "Does melatonin change the appearance of humans?", quoting it:

Melatonin works as an antioxidant and helps in removing free radicals
  from the body ... I would have to conclude that
  melatonin could have a part to play in maintaining the beauty of your
  skin.

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


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Endemic plant families on islands?
Endemism on islands is quite a common phenomenon, at least at the level of species or genera. Old continental fragments like Madagascar or New Caledonia may even harbour endemic families which went extinct on the continents. I also know of the odd example of Lactoridaceae that comprise only one species which is endemic to the Juan Fernandez Islands.
Do you know other instances of endemic families on islands? What about Hawai'i, the Canaries or Galapagos?

This link (http://lntreasures.com/index.html ) might help you...it doesn't mention particularly about islands...but still I think it's a great site ( if you already don't know about it) for ecologists, like you...

That link is awesome (I didn't know it yet)! +1


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Were there any terrestrial species in the ancestry of all crustaceans?
To the exception of woodlice, Crustaceans live in aquatic (marine or freshwater) environments. Crustaceans are arthropods which is an immensely diverse taxon. Many arthropods live in terrestrial environments and many live in aquatic environments.
Pisani et al (2004) report evidence of fossil of terrestrial arthropods as old as ~450 million years ago. According to Wikipedia > Arthropoda citing Lin et al. (2007) (the paper is behind a paywall, I could not read it myself) report evidence of fossil of arthropods as old as ~550 million years ago.
Were there any terrestrial species in the ancestry of all crustaceans?

Are you asking if all extant crustaceans descend from a terrestrial species?

Yes. Whether the MRCA of all crustaceans (or another organism in that lineage before that) was terrestrial.

There is free pdf from researchgate (link).

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


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Regulation of V. cholerae virulence factors
So I know that several different environmental signals, such as pH, bile, and temperature, regulate virulence gene expression in V. cholerae. Specifically, they control expression of the genes encoding the toxin co- regulated pilus (TCP) and cholera toxin (CT).
But what are the two key (main) transcriptional regulatory proteins that control TCP and CT expression, and where is each localized in the bacterial cell? Also, what does each protein do?
I know that the proteins involved are ToxR/S, ToxP/H, and ToxT, but I don't know which are the MAIN ones and why...

Virulence factors of V cholerae is regulated by a hierarchical regulatory system. The proteins you listed in your question are part of this system. In this paper it is said that the actual activation of TCP and CT is done by ToxT- thus this could be your "key" protein. I'd also like to note that just because these are two different genes does not necessarily mean that there has to be two key factors - this assumption of yours if a bit faulty.
Also because the activation of the virulence factors are regulated by a chain of events, each link is can be considered equally important, because if one of them fails the whole chain is dysfunctional.
The short description of the regulatory chain taken from the article linked above:

The ToxR regulon is a hierarchical regulatory system that activates virulence gene expression in response to environmental stimuli (2). Induction of the ToxR regulon starts with activation of tcpPH expression by AphA and AphB (4, 5). AphA and AphB are cytoplasmic regulatory proteins that cooperatively bind to the tcpPH promoter and activate its expression. Once TcpP is produced, it functions in conjunction with ToxR to activate toxT expression. TcpP and ToxR are structurally similar membrane-bound DNA binding proteins that are thought to modulate gene expression in response to external stimuli (6, 7). When stimulated, TcpP and ToxR bind to the toxT promoter and activate its expression. ToxT then directly activates the expression of the genes that encode for CT and TCP production (8).

This paper might also be helpful. Unfortunately I could only access the full text this way (through researchgate):
Regulation of virulence in Vibrio cholerae: the ToxR regulon.
Brandon Childers, Karl E Klose
Future Microbiology (Impact Factor: 4.02). 07/2007; 2(3):335-44.
DOI: 10.2217/17460913.2.3.335
This paper provides details of regulation and mechanism of ToxT.

Taken from the third linked paper. As you can see the final activator of CT (termed CTX in the picture) and TCP is indeed the ToxT, but as I wrote it earlier each link in the chain is important.


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Potential to destroy viruses using prions?
Could a prion be used to sufficiently deform a viral protein in order to make the virus it is a part of incapable of reproducing? For example, take the common cold's VP1 protein and turn it into a prion, then inject that prion into someone with a cold. Would this prion ever come into contact with the virus? Would it actually deform the virus? Can we make prions?

Issues I see with this idea is that finding a protein that misfolds the VP1 protein in a reliable way would be hard, and getting those proteins to specific cell types to fight the virus would be hard.

I think you are making many questions together that are independent (e.g. can we make a prion and whether it would be in contact with a virus). The context is too broad. Why don't you try focusing on some question one at a time?

Prions are misfolded "versions" of proteins already present in the genome. These tend to bind to their properly folded counterparts and catalyze their misfolding into prions. Although unlikely, it is not impossible to imagine that they might interact with other macromolecules. That being said, injecting a human with prionic particles for any reason (especially in a clinical trial for the common cold) is EXTREMELY unlikely. Even if you prove that it works in animal models, injecting a person would be considered too risky. Additionally, the "benefit" of that would be marginal - curing the common cold, from which > 99% of people recover even without any medication. Given that there is great risk and very little benefit, we will most likely never know for sure how feasible this is (at least for the common cold). As a concept, it could work, but would be extremely difficult to get right.

Now I'm confused. What is the difference between binding with a protein in your body and one in a virus? And why would it be risky? Don't prions only affect their protein? This would also work on Ebola, HIV, and any other viral disease.


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Why do we find some things disgusting and others delicious?
For example, why do I love paprika while my girlfriend hates it? Why do I find broccoli disgusting and she adores it? As humans, there are things we'd all agree on being awful, like rotten meat, for obvious evolutionary reasons - those things are damaging to our body and we should not eat those. But when asked about delicious food, everyone would pick something slightly (or completely) different.
I wonder, is it because our tongues are different and the food does indeed taste different, or is it our brains that interpret the same taste differently? Also, what evolutionary purpose does this serve? To me it only makes planning the dinner a pain without really adding anything to our lives.

Afaik. bowels decide about disgust, and not the brain.

Food preferences are largely cultural (including social). Most people find caviar and oysters, to name a couple of foods, revolting the first time they eat them. It's an "acquired taste" for most. Our tongues are not significantly different.

@anongoodnurse Why not move the previous comment of yours to the answers. I think its bang on. Additionally (although perhaps not relevant) There are also cases of disease that dramatically alter taste, and any degree of anosmia (like a blocked nose) can alter a personal pallet too.

Have a look to the wiki page for Taste Preference

Explaining phenotypic variance
You may want to make sure you have a good understanding of the concepts of the underlying variance of phenotypic variance (discussion linked to the concept of heritability) before reading this answer. In this post, I linked several sources of information on the subject.
Culture (environmental variance)
Variance in food preference is in part (in majority eventually) explained by cultural differences.
Genetic variance
I guess that very few people like the smell of rotten eggs. There is selection on taste and smell preferences. Those who don't like the smell of rotten food increase their chance to suffer from bacterial intoxication and mycotoxins. I remember from my Bachelor degree (can't find the study right now) Nestlé (among others probably) performed a genome-wide association study that showed genetic variance for food preferences.
Adaptation
There are probably many loci that are now fixed (not polymorphic anymore) that were at some point under selection as explaining variance for food preference. In other words, at a given locus there might have no more genetic variance as the current allele is well adapted.
By-products
Also I suppose that a part of the underlying genetic and environmental variance for the variance for food preference might be qualified as by-products. For example, it might be beneficial to appreciate a given smell because the smell when present in the sweat of a partner is associated with greater health. If this odour (or similar odour) happen to be present in food, then we may be indirectly selected to appreciate this food item as a by-product of the selection for recognizing healthy partners.


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Is a Ginkgo tree a conifer?
I know Ginkgo is a gymnosperm, but I was wondering whether Ginkgo is also technically a conifer. I did a Google search, and found several confident authoritative-sounding answers. Unfortunately, those answers were divided between "is" and "is not". So which is it? Is a Ginkgo a conifer?

The scientific answers are pretty clear: Gingkos are not closely related to the conifers, they are closer related to the cycads. See this phylogenetic tree based on the 18S RNA from paper 2:

It shows that conifers and Ginkgos are relative close related, but not on the same sub-branch of the tree. The last common ancestor between Ginkgos and Conifers is older than the one between Ginkgo and Cycadales. This classification has been made on the basis of genome comparisions and also based on an analysis of the chloroplasts.
References:

Chloroplast Phylogenomics Indicates that Ginkgo biloba Is Sister to
Cycads
Molecular Phylogeny of Ginkgo biloba: Close Relationship Between
Ginkgo biloba and Cycads
Advances in Ginkgo biloba research: Genomics and metabolomics pe
rspectives

I see. Now I understand that Ginkgo, cycads, conifers, and gnetophytes constitute (extant) Gymnosperms. Gymnosperms and Angiosperms constitute seeded plants. Filicopsida is a category of fern, used as a convenient outgroup, outside of seeded plants, for this phylogenetic analysis.


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Effect of arteriole dilation on vein
If  an arteriole leading to a capillary bed is dilated will the pressure in the vein coming out from the bed decrease ? Will the velocity of blood in the vein change ?

Do we assume that the dilation of the arteriole was under independent regulation and not a consequence of systemic release of a vasodilator, i.e. all other conditions are assumed to be constant?

@SatwikPasani It was under independent regulation.

All else being constant, velocity of the Venous blood will be reduced.
The Flow-Rate Equation: Q=AV

Q = Flow Rate
A = Area (of the "pipe")
V = Velocity of the Fluid

If we assume that the body will try to maintain a constant Q, then an increase in the A of the Arteriole means a reduced V to compensate and a corresponding drop in Venous fluid velocity.
If we start to assume that things are not constant, then the story becomes more complicated. Since Venous pressure is largely maintained by musculature and other actions, not heart contractions (though the system is essentially closed-loop), an increase in Arteriole flow-rate doesn't always correspond to an increase in Venous flow-rate. When there is an imbalance - either due to mechanical interference or something else - conditions like subcutaneous edemas can occur where the interstitial (between-tissues) fluid builds up enough to cause discomfort or damage.
*Normal Disclaimer: I am not a medical professional. The above us based upon an Undergraduate level of knowledge.


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Mitotic crossover happens in G1?
I was reading this article in wikipedia and came across this :

It has been suggested that recombination takes place during G1, when
  the DNA is in its 2-strand phase, and replicated during DNA synthesis.

If For example - allele A is present on 1 and a is present on 1' and recombination happens such that a is present on 1 and A on 1' and then both get duplicated during S phase.
So how are the daughter cells going to be different from one another and from the mother cell in terms of phenotype? (obviously the alleles around these alleles are going to change)
How can this result in twin spotting in drosophila or any other trait occurring due to coming together of homozygous alleles by mitotic crossovers ?

First off this is called genetic mosaicism and indeed mitotic recombination is a contribution factor.
Mitotic crossover events involve the exchange, by homologous recombination, of regions of chromosomes. 60% of homologous recombination events might occur during G1 and 40% of those event occurs after chromosomes are replicated (see this paper). For twin spotting to occur, you need the homologous recombination to happen on replicated chromosomes (i.e. you need 4 chromatids).
For you question on twin spotting. The following picture illustrates well what are the outcomes of homologous recombination involving two alleles and replicated chromosomes (each line being a chromatid).

If the cell is heterozygous (normal phenotype) for the two recessive alleles, here called y and sn (respectively the "yellow" and "singed bristles" alleles), then two recombination scenarios are possible and differs based on where the recombination occurred. Note that y+ and sn+ are the wild-type alleles and carrying those alleles do not provoke a particular phenotype. The phenotype of the resulting daughter cells are:

Twin spots: Yellow but not singed spots (y/sn+) and singed but not yellow spots (y+/sn) for recombination after the y/sn locus
Single yellow spots: Yellow but not singed spots (y/sn+) and no spots (y+/sn+) for recombination between y and sn

Here the actual picture of what happens:

Therefore this should make clear why daughter cells can show phenotypes that differ from the original parent cell, i.e. the combination of alleles (especially for recessive ones) changes after mitotic crossover events. The twin spot phenotype in Drosophila melanogaster is an excellent example for illustrating that.

Hi! In the answer, you mention that "mitotic recombination occurs after chromosomes are replicated" and it definitely makes much more sense that way. But in the article I have linked, recombination has been said to occur during G1. So is the article inaccurate ?

@biogirl Thanks for pointing that out. I actually incorrectly remembered Lee at al. paper where they concluded that 40% of the mitotic recombination events occur after chromosome are replicated (and not all). This therefore means that indeed 60% of the events might happen during G1. The wiki is correct and lists both possibilities. I updated my answer accordingly.

@biogirl Did the rest of the answer helped you in understanding twin spotting? I am not sure this is really clear.


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Fusion of neuron with a S phase cell
There was some experiment in which a S phase cell was fused with other cell and the other cell also began to replicate DNA. Would the same happen if fused with nerve cell ? Why or why not?

fusing cells is not feasible in all cases (it also causes polyploidy).. cells are immortalized by using oncogenes..

you can also look at this post

Just an addition to the WYSIWYG's answer: phenomenon of neuronal de-differentiation under the influence of oncogenes was shown.

This specific experiment has not been done. Fusing cells is difficult and it also leads to polyploidy. Cells are immortalized by overexpressing oncogenes (or viral replication genes); for example HEK293 cell line was established by transforming embryonic kidney cells with adenovirus.
Now transforming a neuron would immortalize it but would also make it lose its function; for a cell like neuron, replication would compromise its activity for e.g. loss of established synapses. As mentioned in the comments by har-wradim, it was shown that transforming neurons with oncogenes leads to their de-differentiation. Another experiment of transforming neurons gave a contrasting result. Feddersen et al transformed purkinje cells in mice by expressing SV40 viral t-antigen from a purkinje-cell specific promoter and surprisingly it lead to degeneration of cerebellar tissue. Also have a look at this article.


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Change of phase from juvenile to adult in plants
I tried googling this but couldn't get much information on this. Most of the articles were about induction of flowering.
I am more interested in knowing what factors influence the conversion of juvenile phase to adult phase in plants and not the induction of flowering.
Can a plant survive if it is artificially kept in a juvenile phase ?

there are no distinct developmental stages in most plants.. a plant which will grow up to become a big tree may still bear flowers when it is smaller.
there is no juvenile phase in many animals too.. just that they are sexually immature.. only arthropods and some amphibians have a distinct larval stage which is very different from an adult.. they undergo metamorphosis whereas other organisms just grow and develop. you can stop the growth and also inhibit the sexual development but that would be just called as growth retardation

@WYSIWYG There ares some plants like Acacia koa which produce distinct types of leaves in juvenile and adult phase.

After a cursory reading on Acacia koa i gather that even the smaller plant bears the phyllodes along with the compound leaves. So i guess there is still no distinct compound leaf only stage. Just that perhaps the development of the compound leaf ceases after a stage. I am no expert in this topic so cant comment more. But if we go back the the original question - if an organism can be retained in a developmental stage: i guess it is possible to retain an animal in its larval stage by inhibiting metamorphosis.

I know a genetics professor that found the reason for the juvenile leaf into a adult, a gene (151) in the RNA. He is presently working on what factor that promotes this to happen.


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Cytoplasmic determinants in amphibians
If cytoplasmic determinants are distributed before fertilisation then how can an amphibian's embryo, whose dorsal side is determined after fertilisation develop ?


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Need of X or Y chromosome protein after meiosis
After meiosis each spermatid get either the X chromosome or the Y chromosome. I know that the 4 spermatids formed from 1 spermatogonia are connected by cytoplasm and so the proteins made by X or Y chromosome can be shared by all the 4 cells.
I want to know what proteins made by X or Y chromosome are exclusive to the X or Y chromosome and are needed to convert spermatids to sperms.

Are you asking what proteins are exclusive to X and Y from all other chromosomes or are you asking which proteins are on the X but not the Y (and vice versa)? These are two very different questions.

@Armatus I am asking for genes present exclusively on X or exclusively on Y which are needed to convert spermatids to sperms.

@Armatus In simpler words the gene should be present strictly on either X or Y not on both. It should also not be present on autosomes.

I can't think of a particular reason why there would be a need for genes involved in spermatogenesis to be located on the X or Y, all genes involved could simply be on autosomes. I don't know whether any are though (or aren't).

@Armatus It is actually written in tortora and derrickson that the cells are joined by their cytoplasm because of some genes are exclusive to X or Y but I can't find any proteins meeting this criteria. Even I don't know why they couldn't simply be on any autosome.

X chromosome has many important genes required for general housekeeping. So we need not really talk about X-chromosome genes. Here is a list of genes present on the X-chromosome.
@Armatus, if all those genes were on autosomes then presence of Y wont be mandatory for male development. There are autosomal genes that are involved in sexual development for e.g. Anti-Mullerian Hormone gene is present on chromosome 19. However, there must be a master regulator that is male specific and since sex determination is chromosomal in mammals, the Y-chromosome must encode that master regulator.
Sry, encoded in Y-chromosome, is one such protein that is absolutely essential for male sexual development. Having said that, it could be very well possible that the basic genes required in the process of spermatogenesis are autosomally encoded. In fact it is so. I just took the list of genes that were associated with sepermatogenesis in KEGG and checked their chromosomal locations. They are all autosomal.
Gene --- position
SPATA1  ---  1p22.3
SPATA25  ---  20q13.12
SPATA32  ---  17q21.31
SPATA9  ---  5q15
SPATA19  ---  11q25
SOHLH1  ---  9q34.3
SPATC1L  ---  21q22.3
SPATA18  ---  4q12
SPATA2  ---  20q13.13
SPATA21  ---  1p36.13
SPATA2L  ---  16q24.3
GMCL1  ---  2p13.3
SPATA7  ---  14q31.3
SPATA5  ---  4q28.1
SPATA6L  ---  9p24.2
SPATA4  ---  4q34.2
SPATA24  ---  5q31.2
SPATS2L  ---  2q33.1
SPATA16  ---  3q26.31
SPATA6  ---  1p33
SPATA12  ---  3p14.3
SPATS1  ---  6p21.1
SPATC1  ---  8q24.3
SPATA22  ---  17p13.3
SOHLH2  ---  13q13.3
SPATA13  ---  13q12.12
SPATS2  ---  12q13.12
SPATA20  ---  17q21.33
ASUN  ---  12p11.23
SPATA8  ---  15q26.2
SPATA17  ---  1q41
SPATA3  ---  2q37.1
SPATA5L1  ---  15q21.1
GMCL1P1  ---  5q35.3
SPATA41  ---  15q26.3
SPATA42  ---  1p13.3
SPATA33  ---  16q24.3

If the genes involved in spermatogenesis are all autosomal, then what is the point of having a connected cytoplasm ? Is it because of X chromosome's proteins which are involved in spermatogenesis ? How can I search for those proteins ?

i dont understand what you are trying to ask here : "then what is the point of having a connected cytoplasm" ?
How to find X chromosomal proteins: find all the genes involved in spermatogenesis and find their locations. So the list that i posted is what i obtained in KEGG when i searched for spermatogenesis; no gene from this list is on the X chromosome. But this this may not be exhaustive.

I will quote a paragraph from Bruce Alberts : " Unlike oocytes sperm undergo most of their differentiation after nuclei have completed meiosis to become haploid.The presence of cytoplasmic bridges between them means that each haploid sperm shares a common cytoplasm with its neighbor.In this way,it can be supplied with all the proteins of a complete diploid genome. Developing chromosome that carry Y chromosome ,for example, can be supplied with essential proteins encoded by genes on the X chromososme.Thus, the diploid genome directs sperm differentiation just as it directs the eggs's."

This is given on pg 1149 chp 20 fourth edition.

you are confusing different things here... the products of the diploid genome is used to nourish the sperms.. Some X-chromosomal genes are involved in basic housekeeping functions and their products are involved in this nourishment process... This doesn't mean that X-chromosome genes are involved in spermatogenesis.. Analogous situation: Neurons require glucose to thrive. That doesn't mean that hexokinase is involved in neurogenesis.

I think I used the wrong term but my basic question remains the same. What are the genes on X which are required to nourish that process ?


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When do kinetochores attach?
I am really confused as to when kinetochores are attached to centromeres. Are they attached soon after replication or after condensation ?

after condensation..

@WYSIWYG Would you like to elaborate and write an answer to this question ?

i will if i find time.. have stuff to do today.. if you found the answer then answer it yourself..

Kinetochore (KT) is a multilayer protein complex. It's main function is to link chromosomes to the positive ends of the spindle microtubules. Also it plays role in the formation of heterogenic region at and around the centromer. The attachment of the KT is not uniform among living species. According to this paper on KT assembly in yeast:

.  ...  KTs  remain attached to the MTs throughout the cell cycle in this organism. However, a temporary detachment of chromosomes  from  MTs  occurs  (for  1–2 min)  at  the  time of CEN DNA replication in S phase in S.cerevisiae (Kitamura et al. , 2007). After completion of CEN replication, a KT reassembles and reestablishes its attachment with  MTs.

source:http://femsle.oxfordjournals.org/content/femsle/338/2/107.full.pdf
(CEN - centromere, MT- (spindle)microtubules)
Thus the exact time of kinetochore attachment depends on the organism, though I must note that S. cerevisiae has somewhat different mitosis than us.


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Development of vitreous humor
I have tried reading about development of vitreous humor but it is all very confusing. When does it first developed ? Does it renew itself ? Please provide reliable sources..

Look at this scheme -

As I stated before, vitreous is 99% water and is not an organ itself, thus the "replacement of vitreous" is actually = 99% water re-production and the only organ inside the eye which can perform this - ciliary body.
Consequently, if the vitreous was removed and replaced by gas or saline it will be replaced by aqueous which produced by ciliary body - this process takes 8 weeks to completely replace foreign substance as a gas by aqueous.


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Identifying structures from anterior end of dissected prawn
Note: This image might be disturbing.
I want to know what the red and the black structures (directly posterior to the red structure) are. I guess it's the heart.

are you sure about the antero-posterior axis in this picture ?
BTW, The image is not that disturbing but i think it is not a very good dissection :P

I guess you got your antero-posterior axis wrong. If I am correct then anterior is right and posterior is left in your image. In that case the black structure should be the cerebral ganglion and the red should be the heart. See the image below.

Aren't eyes of a prawn located at the anterior end ? If so, the red is towards the anterior end and the black towards the posterior. (I am not talking about the two black structures ie eyes. I am taking about the "black" to the left of the heart in the picture which would be posterior to the heart in prawns.

eyes are in the anterior but i cant see the eyes in your picture

see this picture. this is another species of shrimp but you can clearly see eyes anterior to the cerebral ganglion. also it seems that you have dissected on the ventral surface; eyes are present on the dorsal surface.

I have dissected the dorsal surface and the 2 black structures are definitely eyes.

No.. The two dark things in the right of this pictures are the eyes/

Sorry for the bad dissection + bad orientation of the photo.

let us continue this discussion in chat


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C. elegans are either male or hermaphrodites, but why aren't there any females?
From my understanding C. elegans are mainly hermaphrodites but are occasionally males to increase genetic variation. Why is it that random females aren't born instead to achieve he same goal (genetic diversity)?

The evolution of self-fertile hermaphrodites is thought to be a specialization that occurred several times in the nematoda. For example, most of small, free-living soil nematode species related to C. elegans are male/female. C. briggsae, which last shared a common ancestor 80 myr ago is also male/hermaphrodite, but I believe their ancestor is thought to have been male/female.
At the developmental level, the first germ cells to mature in the somatic gonad develop as sperm and then the Germline switches over to make oocytes.

Re: the origin of spontaneous males in a culture. This occurs due to non-disjunction during meiosis of the XX Germline. About 1/700 times a nullo-X germ cell is randomly generated. Fertilization then results in an X0 embryo, which develops as a male. To get an actual female C. elegans you would need a genetic mutant that interrupts spermatogenesis.

C.elegans makes use of an X0 sex determination system, so there is only one sex chromosome (X), which only allows for two sexes (XX and X0) as 00 is not viable.


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Why are killer whales found in the Gulf of Mexico smaller than ones found in the Pacific?
I recently found out that there are killer whales that live in the Gulf of Mexico, but they are smaller than killer whales that are commonly found in the Pacific Ocean. Why is it they are smaller in size?

Animals living in colder climate / environment are larger because this way they have better body surface / volume (mass) ration thus they're more resistant to cold. Animals living in warmer areas are smaller thus they have larger body surface compared to their volume(mass) to dissipate heat easier.
Check this wiki page for more details.

Has Bergmann's rule been suggested for the size disparity in Orca?

It's a general rule, but as written on the page I inked there may be exceptions, yet I do not see reason why would it not apply for Orcas.


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What is the surface area to volume (SA:V) ratio of a red blood cell?
According to this author, red blood cells (RBCs) are biconcave to allow easier bending. The standard explanation in biology for higher surface area to volume ratios is that it improves reaction rates. When a RBC squeezes through narrow veins I imagine that it gets deformed. Considering that a RBC's function is to exchange oxygen in narrow capillaries, I was wondering whether it is appropriate to reason that the biconcave shape promotes gas exchange. So what is the SA:V of a biconcave RBC and by how much does the SA:V change depending on where in the body the RBC is traveling?

I googled "surface area of a red blood cell" and this paper was the first result.  It should answer your first question. Though it was unclear to me what the surface area unit of measure was, which may require a bit further reading.  There's also this article, which goes a lot more into the math of calculating these two things.
As for your second question about how much it changes, intuitively I would guess very little and it probably does not significantly change exchange rates.  I couldn't find any research on the topic.  The hard part is defining all the shapes they may get squeezed into, then either calculating or measuring SA:V. Possible?  Surely, a well written computer model could do it at some point.  But worth the time/money?  Probably not.

The first article is interesting. SA:V ratio is mentioned a few times but without specific numbers. Table 1 in the article shows RBC volumes and Table 2 shows RBC surface areas. However, there is no approximation of the ratio. Dividing the entries in the tables with each other gives lower than expected results. The SA:V of a sphere, for example, is 4.836 One would expect the SA:V ratio of a RBC to be higher than that. Googling "surface area to volume ratio of a red blood cell" doesn't return the results I'm looking for either. Plenty of references to the SA:V being high, but no approximations.

Can you run me through the calculation you're using to get 4.836?  When I run it for a sphere of 6um diameter I get 1,000,000.

See this link.

I see the number, but I'm still unclear on how it's derived.

I don't know either.

I wouldn't use a number you don't understand as a start.  I believe it's supposed to be the SA:V of a unit sphere but the numbers don't come back right to me.  The important thing is you can ignore that entirely as it doesn't really matter.  The SA and V you're looking at can be calculated easily, at least for a sphere.  From the first paper you can just compare SA:V ratios.  A sphere comes up at 0.833 and the biconcave at 1.49.  So it's almost twice as high.  I imagine when units are factored in properly its 833,000 and 1,490,000 for the true ratio.

https://arxiv.org/ftp/arxiv/papers/1403/1403.7660.pdf
human erythrocyte avg dia: 7.2, vol 91.31 cubic microns, surface area 136.55 square microns

The biconcave shape or desk of the RBC enables gas exchange because the biconcave desk enables it to bend in other words travel through narrow blood vessels or capillaries for exchange of gases e.g oxygen, remember one of the functions of RBC is to exchange gases, now gases like oxygen for example is found in the blood vessels because it is transported in the blood. Now for exchange of gases to happen in the blood vessels by the RBC the biconcave desk enables it to be able to squeeze or bend into the blood vessels for exchange to take place. This means that if RBC didn't have a biconcave desk there'd be problem with exchange of gases because RBC won't be able to enter the blood vessels for exchange of gases. Hope this helps

You seem to have stated the same thing three times, and none of the times is it an answer to the question. You would also be expected to support an answer with references and citations. Please take our [tour] and refer to the [help] for guidance to our ways. Enjoy the site.

This does not provide an answer to the question. Once you have sufficient reputation you will be able to comment on any post; instead, provide answers that don't require clarification from the asker. - From Review

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VMD set molecule as top using script
I have 10 molecules in VMD main screen and I was wondering if there is a script command to change what molecule is the top.
For example, molecule ID 9 is the top. But I want to change the top to 1, without using mouse.
Thanks!

Welcome to Biology.SE, Daniel. VMD has a mailing list, which may also be able to provide an answer.

Great! Thank you very much for you help. I'm gonna ask there :)

VMD -> atomselect top ID


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Does the Peptide bond produce water in our organism?
According to Wikipedia http://en.wikipedia.org/wiki/Peptide_bond , when a peptide bond is made a water molecule is released as a secondary product.
So, my question is simple (perhaps silly). Considering that proteins are being made every time in our organisms and this water molecule is being released in every peptide bond, why our bodies are not flooded of water?
Thanks!

The simple answer is that there are literally thousands of chemical reactions (mediated by enzymes) going on in the cell. Some produce H2O, others consume it. For example, when proteins are broken down into their individual amino acids as part of normal turnover in the cell, a water molecule is necessary to break the peptide bond. Therefore, the overall balance of water produced vs. water consumed is fairly equal, especially when you take into consideration the consumption of water and its excretion via urine and sweat.

I was thinking about this recently and I'd be curious if there was ever any study into the net water usage or production in a cell.

@canadianer I suppose it would depend on the cell type and what it's doing. An active muscle cell hydrolyzing ATP at a rapid clip would probably be different than an inactive neuron, for example.


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brain activity responsible for imagination
Which part of brain is responsible for advance or unseen imagination
For example:ones brain can make a situation in mind which is impossible to happen ...which part of brain is hyper active?

Edit: Added two studies to better show how different types of imagination tasks use different parts of the brain.
Imagination is a complex process that can use many regions of the brain. Insights into how our brain imagines have been gained through a number of studies. There is not an "imagination" area of the brain. Instead, different areas, and often several at a time, may be used depending on the type of imagination. I'll highlight a few examples here.
Ogino et al. (2007) asked 10 male participants to imagine feeling pain while watching pictures suggesting either pain or fear. Both pain and fear tended to activate an area of the brain called the anterior cingulate cortex (ACC), which helps to regulate blood pressure and heart rate among other basic nervous functions. Imagining pain activated not only the ACC but also another four areas of the brain were especially active. In comparison, fear tended to activate the ACC and the hypothalamus, which regulates the "flight or fight" response. Both sides of the brain were activated at the same time.
Boly et al. (2007) studied 12 brain-injured patients who where not capable of communicating. They were not in a coma. They were asked to imaging tasks involving spatial skills or motor skills. The two most common areas of the brain that were activated were the supplementary motor area, which helps to control movement, and the dorsal premotor cortex, which may contribute to movement and spatial coordination. (Wikipedia information so interpret cautiously.)
A detailed study was recently provided in a study by Schlegel et al. 2013. (An alternate version is here; both versions are open access.) Summaries of their work written for the general public can be found in Popular Science and Science Daily.
The scientists identified what they called the "mental workspace" which is not a particular region of the brain but instead is several different regions of the brain (from both sides of the brain) interacting together.
The researchers asked the study participants (9 males and 6 females) to select from a set of abstract shapes to assemble a particular target shape.  The target shape (the one the participants had to create) was a 2x2 grid. Each abstract shape that to be selected would fit one of the grids. So, four abstract shapes had to be selected to assemble the target shape. They also tested the reverse: Given a target shape, could the participants identify the four abstract shapes needed to make the target shape.
During the task, the researchers used functional magnetic resonance imaging (fMRI) to monitor brain activity. After the analysis of the fMRI results, they identified 11 distinct regions of the brain were active during the task.  In nearly all cases, the regions were active in both sides of the brain. However, I noticed that one region, the medial frontal cortex, only appeared to be active in the left side of the brain. This region was identified as one important component of the mental workspace for certain tasks.
The researchers concluded that four of the 11 regions were most important. You can see the regions of the brain in any four of the links above (and the abstract shapes in all but the Science Daily article). They argue that the interaction among the four major and seven minor regions contribute to our process of imagination.
Each of the three studies I highlighted requires the participants to perform different types of imgination tasks. Each type of task showed that different regions of the brain were used. Each type of task also required that several areas of the brain were used simultaneously during the imagination process. Together, these results show that no single part of the brain is used for imagination. Instead, many different areas are used, depending on what the person is imagining.
Citations
Boly, M. et al. 2007. When thoughts become action: An fMRI paradigm to study volitional brain activity in non-communicative brain injured patients. NeuroImage 36: 979-992.
Ogino, Y. et al. 207. Inner experience of pain: Imagination of pain while viewing images showing painful events forms subjective pain representation in human brain. Cerebral Cortex 17: 1139-1146.
Schlegel et al. 2013.  Network structure and dynamics of the mental workspace.  Proceedings of the National Academy of Sciences USA 110: 16277-16282.


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How do macromolecules (large drugs) in the eye reach the bloodstream and what are the relative significances of these pathways?
I am considering the elimination pathways for antibodies (50-150 kDa) from the vitreous humour to the blood stream. My overarching question is what is the most significant route such antibodies could take to get there?
Elimination from the vitreous humour to the aqueous humour is known to be quite a substantial route of clearance, but does drug eliminated through passage into the aqueous humour travel to the blood stream? Notably there are two routes of exit from the aqueous humour, one is directly into the bloodstream and the other is through Schlemm's canal, but where does that lead?
Also for example is the choroid directly in contact with the hyaloid membrane of the vitreous play a significant role in elimination? We also also such drugs penetrate into (and through) the retina, at that point they reach vasculature, however they have to work quite hard to get there.

Antibodies are a unique case.  I recommend reading PubMedID: 26726925 regarding the pharmacokinetics of ranibizumab (Lucentis), a Fab fragment, after intravitreal administration.
"We assume that the principal pathway for the ocular clearance of large molecules is by a first-order transfer process from the vitreous to the aqueous chambers, from which the molecule is absorbed into the circulation via Schlemm’s canal by the physiological process of aqueous humor turnover."
A comprehensive analysis of the pharmacokinetic processes are included in the mechanistic model that they have developed.  I will not copy and paste them here.


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How much smaller is the diffusivity of a molecule in the retina as opposed to the vitreous of the eye?
I'm interested in the diffusivity of macromolecules inside the mammalian retina, relative to the vitreous.
For example is the diffusion coefficient for a macromolecule (protein, 50-150 kDa for example) 10 or 100 times smaller in the retina than the vitreous?
The diffusion coefficient for such a macromolecule is about 10^(-6) cm^2/sec in the vitreous - roughly that of a protein in water. I can't seem to find any information on how much smaller it would be in the retina, a tightly packed tissue.

Unfortunately, I don't have a good, simple answer for you. The reason is that the answer may depend significantly on details of the macromolecule more than its size - like how strongly it binds to the environment.
In addition, within an environment that is more elastic than viscous, and with a very complex shape, you might expect to get various sorts of anomalous diffusion, rather than a single diffusion coefficient.
Transport in tightly confined biological spaces is complex, and still pretty controversial. A paper I found useful as a simple introduction to some of this:
Morphogen Transport - http://dev.biologists.org/content/140/8/1621

Thank you! This is useful information. It's interesting that this is a controversial topic! I'm building a diffusion based model you see, so for my purposes I require some numerical estimate to compare between the two areas.
The macromolecules I'm interested are antibodies and fragment antibodies, which bind to VEGF, all these molecules are in the range of 50-150 kDa, and do not bind (at least for my purposes within the model) to any structures within the vitreous or retina.

It's an interesting issue! I recommend seeing what experimental data you can find for any sort of transport properties, but be prepared for there to be a significant spread (don't stop after getting the first estimate).


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What is the radius of the Ora Serrata and lens in rabbits?
I'm interesting in estimating the surface area of the hyaloid membrane connecting the vitreous and aqueous chambers. This is a crude estimate however i'm struggling to find parameter values for rabbits.
I have estimated in humans the radius of the Ora Serrata, measured from the
centre of the lens, to be 1 cm. The radius of the lens to be 0.5 cm, giving the surface area of the region between the two to be roughly 2.36cm^2.


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Is the Hypothalamus part of the Central Nervous System or Endocrine System
Sorry for a certainly naive question.
Some references (for example https://faculty.washington.edu/chudler/nsdivide.html) seem to to indicate that the hypothalamus is part of the Central Nervous System. Others (for example http://kidshealth.org/teen/your_body/body_basics/endocrine.html) place it in the Endrocrine System. I would have said it is part of both, but then I read the two systems are distinct. Could anyone explain me to which one it belongs and why?
Thanks,
Gilles

CNS refers to the brain and spinal cord. Its a very general term. Hypothalamus is part of the CNS but its unique in a sense that it secretes many chemicals into the bloodstream like glands! so they are both correct!

If the above comment has answered your question, please let me know so I can post it as an answer so that the question does not remain unanswered.

Hi Bez, I was just waiting a little to see if anyone else would argue with what you said. Please post it as an answer as it is exactly what I was after.

CNS refers to the brain and spinal cord. Its a very general term. Hypothalamus is part of the CNS structure but its unique in a sense that it secretes many chemicals into the bloodstream like glands hence part of the endocrine system! so they are both correct!

Can you add some references to your answer? Actually it is more a comment.

@Chris Apologies for failing to reference. Hope the response references are satisfactory.

It is part of the CNS and does not secrete hormones into the bloodstream. Instead, it delivers input to the pituitary gland, which is an endocrine organ and secretes hormones into the bloodstream. Please refer to http://en.m.wikipedia.org/wiki/Hypothalamus and specifically the section "Neural Connections". Otherwise, any basic neuroscience or endocrinology textbook covers this under hypothalamic-pituitary axis or the likes. Hope this helps.

Can you add some references to your answer? Actually it is more a comment.

I have added some suggestions Gilles. Hope that helps.

Ps. Questions like these are not naive and opportunity for interesting discussions!


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mRNA Transcription from Nuclear DNA
How does a cell "know" the coding strand vs. the non-coding strand of DNA during transcription of mRNA?

This is determined by the promoter -- the DNA sequence to which RNA polymerase binds. It's assymetric, and the polymerase binds in a specific orientation, that determines the strand and the direction it will go once elongation begins.

Strands in DNA double helix (and other nucleic acids) are anti-parallel: one strand in the helix is in 5'->3' direction while another is in 3'->5' direction. RNA polymerase can only synthesize RNA in 5'->3' direction, and so it uses the 3'->5' strand as the template (the second DNA strand is, I think, completely ignored by the polymerase during synthesis).
From one promoter transcription of both forward and reverse genomic strands can theoretically happen. However, the two possible nascent RNA strands are synthesized outward from the promoter and away from each other (i.e. they are not overlapping).
During evolution position of some promoters (but definitely not all of the promoters in the genome) have evolved to be in the place were at least one of the two theoretically possible RNA products can be translated. Transcription in the opposite direction (i.e. away from the gene) actually frequently happens in eukaryotes. These RNAs belong to a class of promoter associated RNA, but but they were not shown to be translated (their function is largely unknown).
UPDATE (2015/02/19): New publication in Molecular Cell by Duttke et al. is demonstrating that genic promoters are "intrinsically directional" and, just as @Leon Avery commented here before, the divergent (i.e. bidirectional) promoters are actually two unidirectional promoters side-by-side, in reverse orientation relative to each other. So my above statement "From one promoter transcription of both forward and reverse genomic strand can theoretically happen" is incorrect. However, the authors also say that approximately half of gene promoter regions in HeLa possess this bidirectional initiation property, so it is still an important feature to keep in mind when thinking of transcription of eukaryotic genes.

In short for me: You say that transcription runs into both directions and both strands are produced as mRNA? If not, please edit your question, at the moment this can be read into it.

Sorry for not emphasizing this importnat point: a gene promoter typically leads to syntesis of mRNA transcripts in one direction from one strand only. However, other RNA transcripts, generally referred to as promoter associated RNA, were show to be syntesized at promoters in both directions. Promoter associated RNA was shown to be up to a few hunderd bases long, most frequently just about 18 bases long (I think the 2008 Science paper from Lis lab was one of the first papers on this phenomenon, but there was other important research into it since).


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How does HPV start?
Not "infect" others. That's common knowledge - sexual activity.
But how does it start? Literally from non-HPV carrier to HPV carrier?

Through sexual activity. Someone has sex with someone who is a carrier and contracts the virus.

Are you trolling me? Because that is not what I'm asking, and I specifically stated that in the first 2 sentences.

I would like to better understand what you're asking; please clarify. As it stands now, though, the comment is correct. How do you think it might happen?

I would like to know how HPV can start in a person. Not infect. I guess one can say that I'm asking about the origin.

There is no such think as spontaneous generation; it can't just "start" in a person. The virus exists, and it comes from someone else. It is spread person to person, penetrative, skin to skin, orally, or, in an infinisimally small number, perhaps from a contaminated instrument. From another carrier is the only known way to acquire it. If you are looking for the origin of the virus, that is a different question altogether, and should be asked as a different question.

I believe what you are asking is the origin of the HPV virus, however currently, there is no real answer to that question. Nor is there an answer to how any virus came to be.
Right now, there are 3 theories as to how viruses originated, all of which can be found in this article from the Nature Journal. The theories are as follows:

The Progressive Hypothesis

This theory suggests a parallel between components of eukaryotic genomes called retrotransposons and viruses. More information can be found in the article enclosed, but basically, retrotransposons, which can be can be "transcribed into RNA, reverse-transcribed into DNA, and then integrated into a new location within the genome" -- just like retroviruses, are hypothesized to be the foundations for the evolution of viruses.
Here is a link to a depiction of a retrotransposons' replication process, with a description. (if you're interested)

The Regressive Hypothesis

The next theory is considered a bit less plausible than the Progressive Hypothesis, but again... no one knows. This hypothesis recognizes that there are some bacteria that have evolved from complex creatures into the parasitic organisms there are currently. This is known as regression. Summarized by this website is a description of this observation as it applies to viruses:

The Regressive Hypothesis: Viruses evolved from more complex free-living organisms that lost genetic material as they adapted to a parasitic approach to reproduction.

The Virus-First Hypothesis

And finally, this theory assumes a world where viruses (or the primitive versions of them) existed even before cells did. This theory states that viruses were once just self-replicating units that, over time, (like many things in our world) got more complicated. This is similar to the Progressive Hypothesis in that it suggests evolution forward and not backward (regression), but it differs in that it suggests that before viruses are/were merely just units even simpler than cells that became more intricate.
Now back to your question, HPV is like any other virus in that there is no known origin for it. However, since the virus has been conceived (no pun intended), it has lived through sexual transmissions and is kept alive like so.


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How many Amperes to kill fruit flies and mosquitoes?
As above. Making a homemade trap to kill them all.

If you were to presume that the resistance of the arthropod is about 1000 ohms, then it'd require about 2 amperes.

I have this bug-zapper in the form of a tennisracket. It takes only two AA batteries of 1,5 Volt. It is succesfull in killing mosquitoes but often fails at big flies.

It's not the Amps that matter, it's the voltage. humans are safe up to about 80V DC. 4V is like moving energy in a slow train, 1000v is like moving energy in a bullet. Therefore, 1000V also can arc more easily through the air. If you use 240V at 0.1 amps, that's 24W it's probably quite enough to kill a mosquito. A 200W source in 4V will not hurt a human, but in 3000V it will kill him easily. I can't confirm that 20W at 300V is not dangerous to a human. You will probably find yourself using an CC Constant Current supplying about 10W at a low voltage and upping the voltage a bit to zap the moz.

Current kills. Voltage is potential difference.

there's an electronics topic for that, it states: Most flyswatters conform to electrical safety standards for humans: a limit on the charge stored in the capacitor. A discharge of less than 45 µC is considered safe, even in the unlikely scenario that the current from a flyswatter would be flowing from one arm to the other arm, partly through the heart.1 This means that the capacitor of a 1000 V flyswatter should be less than 45 nF. Due to this precaution for humans the initial shock is usually inadequate to kill flies. a limit on the current after the initial discharge. The maximal continuous current of most flyswatters is less than 5 mA. This current is safe, even when flowing from one arm to the other arm
here: https://electronics.stackexchange.com/questions/19367/can-i-test-bug-zappers-voltage-with-multimeter
there is a slow mo zapper here. https://www.youtube.com/watch?v=oUJLgKkmllA

I am not an electrician and may not be the right person to answer this. But I recently read this paper (Keller et al., 2016) and maybe this helps ... Keller et al. (2016) have a look at laser induced mortality in mosquitoes. It might not be fully adaptable to your needs (there is not much context in your question, though; I have no idea what kind of trap you are trying to build ... if it's going to be a fancy laser trap, the cited paper will be your perfect guide through the building process - however, you have to figure out the automatic camera detection (they are planning that, too) for yourself as they have not published that, yet).
Now, giving a concrete answer: Keller et al., (2016) found that lasers with 0.5W to 4W are sufficient for efficient mosquito inactivation. If you are planning to use a plug bucket (230V) this would be (0.5W/230V=) 0.002A to (4W/230V=) 0.017A. You could also set this up with a 9V battery. With a 4W laser this would be (4W/9V=) 0.44A. Using a lithium-based battery this would last for about (1000mAh/(4W/9V=0.44A)=1Ah/0.44A=) 2.27h total laser time.
I do not know if this easily translates to electric current, though ...

What did Keller et. al. use as the ohms of the insects in their investigation?

They did not assume any. They tried this with a variety of powers and pulse lengths and then measured mortality rates.

Sorry, laser's not applicable. The trap's made up of loads of exposed wires alternating between live and ground over a food source, waiting for a fly/mosquito to close the circuit to (hopefully) fry them. Not going to plug it into the mains, though. Too dangerous. Thanks for the power details.

@user3635998: Ah, ok. Maybe you should have a look at how these  electric fly flaps work, I think they are powered with two AA batteries and get up to 1000V with a voltage converter.


text:
Which biosynthetic pathways take place in the plastid and were are they located?
I know that the isoprenoid, jasmonate, glucosinolate, fatty acids, chlorophyll, starch, and aromatic amino acid syntheses are located in the plastid. But I don't know if they are located in the thylakoidlumen or in the stroma.


text:
Why is the upper respiratory tract so vulnerable to infections?
Wikipedia has the following statement on its Upper respiratory tract infection page:

In United States URIs are the most common infectious illness in the
  general population.

What is it about the upper respiratory tract that makes it so vulnerable to infections?

I'd argue it's the exposure to foreign bodies which predisposes the upper respiratory tract to infection. Though, it's not until these invaders begin penetrating the tissue or in some way evading the immune response that we see any sign of infection. All things equal, you could even argue the entirety of the alimentary canal is at risk. However, in most instances, all is not equal, and most foreign bodies are in for some real punishment trying to invade those areas.

That makes sense, but beyond upper respiratory tract and the digestive system, there are many other tissues in constant contact with foreign bodies, like most of our skin, eyes, lips, the ear canal; and even though there is more air flow in our respiratory system, which could help explain its vulnerability, we don't see the same rate of infection along the lower respiratory tract. That's why it seems probable to me that there's something about those tissues that makes them so reliably exploitable by pathogens in well known cyclical patterns.

Well, the lower respiratory areas have whats known as a "ciliary escalator," as well as IgA in the mucus and alveolar macrophages. Which, you find that lower respiratory infections are more relatively severe given the evasion of such a complex of defenses. Other parts of the body, microbes are at competition with your normal flora, immunoglobulins in secretions like saliva and tears, lymphoid tissue, etc.

Mostly because it is in almost constant contact with aerosols from the outside world (with regard, of course, to a thin layer of mucus), therefore any pathogens they might contain.
You also have to remember what separates an airborne pathogen from any other pathogens- infection location. A pathogen is airborne when it infects and irritates the throat or nasal passage enough to make the organism's normal deterrence functions kick in. In most cases this would be coughing or sneezing, which produce contaminated aerosols for other organisms to inhale through their own upper respiratory tract.
I hope this answers your question!

It partly answers the question, but only partly. The external skin is also in almost constant contact with aerosols (and other forms of contamination) from the outside world, but it is not nearly as vulnerable to infectious agents as the upper respiratory tract. A full answer to the question would explain what constraints prevent the upper respiratory tract from being as well defended as the external skin.

The external skin is most definitely not in contact with aerosols (the living part at least). The first layer of skin we have is the epidermis, the first layer of the epidermis is the stratum corneum, which is composed of dead skin cells that form an infection-proof layer over the living skin cells (which is why cuts get infected). I apologize for the confusion, I was under the impression that this was common knowledge.

Sure -- but this just begs the question of why a similar infection-proof layer could not coat the upper respiratory tract as well.

Well, think about it. If there were a layer of dead cells in our lungs, oxygen would not be able to enter the alveoli and diffuse into the blood. However, you must remember that there actually is a layer like this, the mucus layer of course (oxygen can diffuse even while the mucus is present), but it does not protect nearly as well as a layer of skin, as we can see by the infection rates.

This doesn't answer the question either, because the question was asking about the UPPER respiratory tract, not the lower. The upper respiratory plays little if any role in oxygen exchange.

Aha, but that's where you're wrong. The upper respiratory tract plays a vital role with this in that it is designed to purify the air before it even reaches the lungs (lower respiratory tract) by pulling most of the contaminants out using mucus, which, of course, pathogens stick to, thus why it is prone to infection. You see, my comment certainly does answer the question, you just need to think about it a little.

Let us continue this discussion in chat.


text:
How do cell repair mechanism ratios change as they age?
I have seen that embryonic stem cells are shown to use homologous repair for double strand breaks rather then non-homologous end joining (NHEJ). [1]
I am wondering if something also happens to a cell's usage of certain repair mechanisms after diversifying.
For instance, is there any evidence that two cells in the same lineage but of different ages (one from a person who is 20, another from someone who is 80) use different ratios of repair mechanisms? Has there been any research on this or is there any indirect data that could support such an idea?

The mechanism of DNA repair depends on the stage of cell cycle. Different cell types spend different relative times in different stages of cell cycle and so their preference for the DNA repair mechanism varies.

Yes I know this but I am asking about two cells of the same type but in organisms of different ages.
Has there been any comparison between two cells that are the same type, from the same species, but from two organisms that are at different stages of life to see if there is a difference in what repair mechanism type that they prefer?

I haven't come across any such studies but if the cell is self renewing at the same rate at both the ages (and has no other accumulated mutations), the preference ratio should remain the same.

I'm mainly wondering since we know that mutations occur more often as an organism ages and if perhaps there is more at play than telomere shortening, build-up of junk, etc.
The most I can find is this study http://www.nature.com/cr/journal/v18/n1/full/cr2007111a.html
However it really focuses on the decision between choosing NHEJ or HR and pretty much said what you said about there being differences during cycle and between types of cells. It'd be interesting to study but right now I can't find any evidence that would lead me to think it is happening or deserves investigation.

Also this http://www.fasebj.org/content/14/10/1325.full, but other than that I can't really find anything that could lead someone to support this idea.

This choice would probably depend on specific mutations (for e.g. XRCC which is mutated in some cancers) which down/up-regulate the activity of one type of repair pathway.

More of the emphasis of degeneration and aging has been placed on mitochondria these days. Telomere length usually almost never enters the equation as most tissue is replenished from Adult Stem Cells that continue to express telomerase. 2) If the information you are interested in has been researched and published, it will have likely been done in either Yeast, C. elegans, or Drosophila, so your best bet is to look for data on studies from those model organisms.


text:
Which insect is this?
I just found what i think is an insect on floor of my balcony. From what i know, it is a Praying mantis. I want to keep it as a pet but for that i want to its exact species.

If it helps:
 Location: Bangalore, India
Temperature : $23^{\circ}$ C

Could someone help me identify it pleas.

I presume it is an Indian bark Mantis , Humbertiella ceylonica.

This mantis can be kept at between 21 and 28 degrees comfortably and does not need a drop in temperature at night.

References: bugzuk.com and Google


text:
What are the metabolic consequences of negative mechanical work in muscle contractions?
When a muscle contracts while it shortens (concentric), it consumes ATP I believe primarily due to cross-bridge shortening to remove the myosin head from it's attached state.
However, when a muscle contracts while it lengthens (eccentric), it must absorb negative mechanical energy. Is this negative mechanical energy absorbed used to disengage an attached cross bridge and thus doesn't require as much ATP?
If fatigue of concentric muscle contraction results from a shortage of ATP for contraction, is there a similar rule for eccentric contractions. Since it is known that eccentric contractions cost 5x less metabolically then concentric contractions, where do these savings come from?


text:
How are neural networks encoded in the DNA?
The central nervous systems as well as the brain->muscles and sensory cells->brain nervous pathways, need to be precisely wired for life to be possible. Moreover they are wired almost exactly the same way for the individuals of a same species (animal, man, insects, etc.).
This information, must therefore be somehow encoded in the DNA.
I have never heard of any study or theory on how this would be possible - only about how proteins are encoded, and I couldn't find any bit of information on this topic (I am not a biologist though).
I would like to have a broad idea of what is currently know about the construction of such networks, i.e. not detailed explanation but rather takeaways facts and references.

How is information about neural connections encoded in the DNA?

e.g. are there any genes linked with neurons (e.g. coding for neurotransmitters)? Do the DNA code for precise neural connections? Can development of specific parts of the brain be linked to specific parts of the DNA? How does a neuron knows from the DNA to which neurotransmitter be sensitive?

How are connections between specific neurons established?

e.g. how an axon does know where to establish deliver a potential? How can the end of an axon move to the correct place?

A small note on semantics: Science doesn't know anything. Humans know stuff; science is nothing but human knowledge.

Related post: http://biology.stackexchange.com/questions/31459/how-is-instinct-carried-from-one-generation-to-another

This question is broad. The genetic basis of instincts itself is a broad question and is something that is still not elucidated. I would, therefore suggest that you focus your question on a specific instinct or a neural pathway. You should also read about Hox genes and their effect on early embryonic patterning. It would be difficult to explain the level of complexity you are asking without you knowing about the early events in development. In short, as the question is written, one can write an entire book which would still not answer the question fully.

Hi WYSIWYG, I don't have the relevant background to ask specific questions about specific neural pathway as you suggested. However, I believe it is an interesting question and any piece of information is welcome. I am not looking for a book long answer neither precise description of all the mechanisms involved, but rather to have of a rough idea of what is going on and how much is known about this.

@Nicolas The edit is good, but I'm still unsure about what you want to know in a clear succinct answer. Re your bullet points 1.Networks are above a cellular level, the underlying genetics work at a protein level. To describe a genetic instruction for networks would take a monumental effort by an answerer. 2. This is more answerable, but still would take a lot of effort to answer and only for half the question. Consider rethinking this question and resubmitting it as a new question by itself.

HI Good Gravy. I understand the concern. However, it s a bit of limbo: the question is about the encoding of neural connection in the dna, which you say can't be answered. About the second point, I see it linked to the first: how is the information in the dna exploited to build the connection. I refocused the question on point to point connections.

HHMI Biointeractive has a whole series of resources on Developmental Biology.  This subtopic deals specifically with Neuroscience and neuronal development. There are some case studies, but there are also some basic information resources as well.

Here's at least one paper describing some of what is known about development of neural network in Caenorhabditis elegans
http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1001044
It mentions at least one relevant gene
" There is evidence showing that several guidance molecules like Netrin and Nerfin-1 are expressed in the early stages of development. Netrin is a protein involved in axonal guidance in vertebrates as well as in invertebrates [21], [22], [23] and is specifically known to influence early path-finding events [23], [24], [25]. Nerfin-1 belonging to a highly conserved family of Zn-finger proteins, is found transiently expressed in neuron precursors and plays a role in early path finding. Studies involving pioneering neurons in the central nervous system of Drosophila melanogaster have shown that Nerfin-1, whose expression is spatially and temporally regulated [25], is essential in early axonal guidance. "
You can also have a lot at the Wikipedia article called  "Development_of_the_nervous_system_in_humans"
One interesting fact is that C. elegans has 20 000 genes, 302 neurons and about 5000 chemical synapses, 2000 neuromuscular junctions and some 500 gap junctions. In humans there are an estimated 20 000-25 000 genes in humans, about 85 billion neurons and 100 trillion synapses.
This excerpt from http://www.tandfonline.com/doi/full/10.3109/0954898X.2011.638968 explains this seeming paradox though
"studies in a range of species suggest that fundamental similarities, in spatial and topological features as well as in developmental mechanisms for network formation, are retained across evolution. ‘Small-world’ topology and highly connected regions (hubs) are prevalent across the evolutionary scale, ensuring efficient processing and resilience to internal (e.g. lesions) and external (e.g. environment) changes. Furthermore, in most species, even the establishment of hubs, long-range connections linking distant components, and a modular organization, relies on similar mechanisms."

Thanks for your answer. I understand that neuron migration is an important part of the process, that long distance connections are established early on, and that neural hubs also develop early on. Is it known if the the migration mechanisms using identical signal for each neurons or if they widely differ from neuron to neuron? I unfortunately can't access the second article which is not open access. Would you recommend any paper specifically about the encoding in the DNA?

I don't have a very detailed overview of all migrations mechanisms, but I think there's a handful basically. Here's one paper you might find interesting http://www.med.nyu.edu/dasenlab/assets/publications/Neuron_Review_2013.pdf

Not sure if it's allowed to write here, but I usually use sci-hub.io if there's a paywall article I can't access.


text:
Can genes be expressed sequentially?
As I understand it, any gene on an exposed/unpacked region of a chromosome is continuously being expressed. Regulatory genes may increase or decrease the amount of protein synthesised due to its expression, but its expression is still fairly continuous.
Assuming I am correct, is there any regulatory framework by which genes are sequentially expressed. That is where the expression of one gene causes it to be turned off and another turned on?
For example, say some chromosome has genes A, B, and C. Is there a situation where gene A is expressed for some period, then gene B, and then gene C, but no more than one is ever expressed at once and they only are expressed in that order?
EDIT: I'll clarify that I don't expect genes which are suppressed to somehow still be accessible. Making them inaccessible is (as far as I know) how they are shut down. My point in mentioning how accessible genes are expressed is to highlight the uncontrolled nature of gene expression in relation to sequential gene expression and therefore to ask how the genetic machinery can get around this problem.

Herpesviruses are a good example of this. Upon entry the nucelocapsid, which is surrounded by this proteinaceous tegument, is translocated to the nucleus along with a tegument protein called VP16. VP16 induces transcription of immediate early phase α genes. These α genes tell host machinery to make ß genes that result in viral genome replication (in concert with α genes), after which you get robust transcription of late gamma genes. Described in part here, gamma genes code for structural elements that assemble before budding.

Although I'll add that for each phase, the genes aren't completely shut off, and still maintain some level of transcription.

I would say exposed/unpacked regions are ready to be expressed. https://www.bioscience.org/1998/v3/d/stein/d849-864.htm

Sequential expressions could be explained by expressions of transcriptional factors, which could bind to the enhancer regions of genes ready to be expressed.

@243 Wouldn't depending on the expression of transcriptional factors be pushing the problem back one level? Solving the question of how one set of genes are expressed sequentially by depending on the sequential expression of a different set?

Simple answer: yes, this happens all the time.
A couple of notes:
Firstly, pretty much everything in biology is continuous. If a gene is expressed at a level of 1 protein per million cells, everybody would say it's not expressed, even though I guess you could argue the point. And don't underestimate how much regulation can affect expression -- you can easily have thousand-fold or million-fold differences between tissues and conditions.
Now, regarding the expression cascade: This is exactly what happens during the cell cycle. As the cell grows, there are genes that can sense the availability of nutrients and all the other signals that control initiation of cell division. Those then can turn on the genes first phase of the cell division cycle. Other regulators can sense whether that phase completed, and turn on the next set of genes, and maybe degradation signals for the genes from the first phase. And this then continues through the cell cycle.
Here's a figure from a paper that looked at gene expression in synchronyzed yeast cells (http://www.pnas.org/content/104/43/16892.full):


text:
Why do asparagine and glutamine have two different abbreviations?
I'm looking at amino acid abbreviations and on every site I visit, asparagine and glutamine have two different abbreviations. Is there a reason for this? Do they represent different forms of the amino acid that may have different properties?
I'm looking at the abbreviations on this site as an example:
http://www.hgmd.cf.ac.uk/docs/cd_amino.html
On the page, asparagine has an abbreviation of 'N' and an abbreviation of 'B'. The abbreviation 'B' doesn't correspond to a codon so why is it there?
Glutamine also has two abbreviations ('Q' and 'Z'). The abbreviation 'Z' doesn't correspond to a codon either.

Welcome to Bio. Are you askinh whether Arg and Gln are different amono acids??

Great edit - @Roland has given the right answer - see the official IUPAC website

The abbreviation Asx (B) is used if it is uncertain whether the amino acid at a given position in a peptide sequence is Asparagine or Aspartate. Similarly, Glx (Z) is used when there is uncertainty between Glutamine / Glutamate.
These two pairs of amino acids can be ambiguous in peptide sequences because Asp/Asn and Glu/Gln differs only by a terminal amide (-NH2) group in the side chain, and this amide group can be spontaneously lost from proteins by a deamidation reaction. When this occurs, asparagine is converted to aspartate/isoaspartate, and glutamine to glutamate/glutamate. These cannot be distinguished from "real" aspartate or glutamate by classic peptide sequencing, nor by mass spectrometry, since their mass is identical. Hence, protein sequences obtained directly from protein frequently contains Asx/Glx entries.

Asparagine (Asn) and glutamine (Gln) are derived forms of the amino acids aspartic acid (Asp) and glutamic acid (Glu).
Both amino acid pairs (Asn/Asp, Gln/Glu) consist of the same carbon backbone,
their side chains only differ in their functional group.
Aspartic and glutamic acid include a carboxylic acid (-COOH), whereas asparagine and glutamine are carboxamides (-CO-NH2).
Here you can see asparagine and aspartic acid as example:

Asparagine (Asn)

Aspartic acid (Asp)

The reason is simple: These are two different amino acids with different side chains. They look very similar, but they are not:

This is L-Glutamine, its chemical formula is C5H10N2O3.

This is L-Asparagine, its chemical formula is: C4H5N2O3. This shows that L-Asparagine has one CH2 less than L-Glutamine.

From the reference in the question, the query seems to be asking "Why does an amino acid have two abbreviations, such as Asn and N for asparagine, and Gln and Q for glutamine?"
This is because both abbreviations are commonly used in the scientific literature.  The longer, 3-letter, abbreviation is useful because it is a recognizable shortening of the amino acid's name.  The 1-letter abbreviation tends to be very arbitrary (e.g. Q for glutamine), so it is not very mnemonic. However, the single letter form is much easier to make use of for long sequences of amino acids, as in giving the sequence of a particular protein.


text:
Effect of hemoglobin on colloidal osmotic pressure
If Hemoglobin gets out of RBCs, my book says that colloidal osmotic pressure of plasma increases.
Hence, filtration of fluid across capillaries is prevented.
So the heart increases its work to be able to filter fluid to tissues.
Could someone explain this mechanism for me? simply please!

First:  what is oncotic pressure?

Oncotic pressure, or colloid osmotic pressure, is a form of osmotic
  pressure exerted by proteins, notably albumin, in a blood vessel's
  plasma (blood/liquid) that usually tends to pull water into the
  circulatory system. It is the opposing force to hydrostatic pressure.

"Colloid" can be any macromolecule.  It can be albumin (the normal one).  Immunoglobulins can increase blood oncotic pressure.  Intact red blood cells do too and they can be important in that role.  Blood substitutes using free and modified hemoglobin (loose in the blood not in RBC) also increase blood pressure by reducing fluid filtration across capillaries and keeping fluid in the blood vessels.
Thompson A et al.  Stroma-free hemoglobin increases blood pressure and GFR in the hypotensive rat: role of nitric oxide.  J Appl Physiol (1985). 1994 Nov;77(5):2348-54.
I think of it like rice in a salt shaker.  The rice soaks up humidity because the humidity is attracted to and stays with the macromolecules in the rice.  So too blood full of protein.  The water likes to stay with the big molecules and so stays with the blood.
If you get too much macromolecule in the blood it can increase colloid pressure of blood and raise blood pressure and that can cause trouble.  Maybe a professional bike rider has too high a hematocrit because he is abusing erythropoietin (that would be colloid pressure of whole blood, not just plasma).  Maybe someone has a cancer like Waldenstroms that churns out loads of immunoglobulin (that would be colloid pressure of cell free blood, or plasma).  High blood pressure is what you see in these cases.  I suppose if you infused a rat with too much free hemoglobin blood substitute the same thing would happen.
People with high blood pressure still perfuse their organs.  Filtration of fluid across capillary walls is decreased but the organs do ok.  The converse situation is where people have problems: low colloid pressure allows fluid to freely leak across the capillary walls and people get edematous and puffy.
The situation you propose is a weird one.  A person who has hemoglobin getting out of RBC has hemolysis: the red cells are leaking or blowing up.  Common situations for hemolysis are malaria and sickle cell disease.  Any increase in colloid blood pressure from the free hemoglobin is balanced by a decrease in colloid blood pressure because the red cells are gone.  Congestive heart failure is not a problem with persons who have sickle cell crises or malaria unless they become super anemic which is rare and involves a different mechanism.
Not simple; sorry.  But it would be easier to be simple if this actually happened (the free hemoglobin making heart work harder) and it does not.
No offense but maybe you have it wrong?  Maybe take a photo of the text you reference and edit your question to add it (that little box with the mountains and moon will let you add a picture).  Or type it in as you see it?


text:
Why do Major and Minor grooves exist in dna strands?
I've been trying to find what causes the periodic appearance of major and minor grooves in DNA but have not yet been successful. Geometrical explanations would also be appreciated as I cannot understand any of the geometrical explanations I have come across so far. As far as my knowledge of DNA is concerned I know of all the high school basics (e.g complimentarity, bonding between the individual components of a nucleotide etc.)

Please [edit] your question and explain what you have learned so far, and where exactly you're stuck. As it stands now, this question is too broad.

It is all explained here in Wikipedia. You are referring to Watson-Crick base pairs in the B-DNA structure.