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Mathematical Modelling of Natural Selection
I'm a math undergrad looking for some papers on modelling the process of natural selection. The only paper I've been able to find is by the pre-eminent mathematician Herbert Wilf from 2010,
There's Plenty of Time for Evolution
Unfortunately, Wilf's model is extremely simplistic - he calculates the number of 'generations' required to spell out a 'word', if we allow each letter to 'mutate' with certain probability every generation, and we stop mutating a letter once it is correct (this is the 'selective' feature of the model). So to spell the word 'Evolution' by randomly placing scrabble tiles would require 5.4 trillion generations, but if we keep the correctly placed letters each generation and only allow incorrect letters to 'mutate', Wilf calculates we'd only need about 57 generations on average.
Wilf's model is a good first step towards modelling natural selection, but it's clearly only a first step. In particular, the fact that nature seems to know in advance exactly what letters it needs to keep in particular places and what it needs to throw out to construct a complex genetic 'word' is dubious at best.
As a young maths student the idea of the incredible complexity and diversity of life developing by a directed stochastic process gets me shamelessly excited :) I have been very surprised at just how little mathematical literature there seems to be on this topic, as I say, Wilf's one super-simplistic model is all I've been able to find. Can someone direct me to any other theoretical analyses of the power of natural selection?
Thanks

If you have a strong mathematical and theoretical computer science bend then you might be interested in: Ecology and evolution through the algorithmic lens

Mathematical and computational modeling of evolution is a huge field. To start you off with some broad strokes, there are two main approaches to evolutionary modeling with their own communities: frequency-independent and frequency-dependent models. Of course, in a real biological setting, the truth lies somewhere in between, but models are idealizations of key principles, and so the two extremes are good to study.
For frequency-independent selection, they key concept is the fitness landscape -- a way to map each genotype to a fitness. The population then lives in this landscape and agents with higher fitness reproduce better and so the population slowly movers over the lattice. Under reasonable macroevolutionary assumptions such as very rare mutations and asexual populations, the population will tend to be homogenous and can be just modeled as a single point in the fitness landscape with properly chosen selective sweeps to move the point from vertex to vertx (Gillespie, 1983; 1984).
The most popular concrete approach for frequency-independent selection is [Kauffman's NK model of rugged fitness landscapes] (Kauffman & Weinberger, 1989; Kauffman, 1993). Computer simulations tend to favor this sort of model. Wilf's model would be an NK model with K = 0, and fitness of 0 for incorrect letters and 1 for correct letters (to get the shorter walk). Related questions:

Is local equilibrium a reasonable assumption for evolutionary processes?
Structure of fitness landscapes in the NK model

The frequency-dependent selection approach is dominated by evolutionary game theory. A typical question for this field is the evolution of cooperation, and the most basic approach is to use replicator dynamics and look at evolutionary stable strategies. However, the field is in general saturated with all kinds of exciting models (both analytic and computational). A very friendly book-length intro is Nowak's Evolutionary Dynamics. For a genetle intro and connections to evolutionary psychology look at the slides in this post. A brief and sophisticated introduction aimed at mathematicians can be found in Hofbauer & Sigmund (2003). Related questions:

Sources for Algorithmic Evolutionary Game Theory
Why is 'Grudger' an evolutionary stable strategy?
How exactly are game theoretical evolutionary models described during implementation for computer simulations?
When does weak selection produce qualitatively different results from strong selection?

References
Gillespie, J.H. (1983). A simple stochastic gene substitution model. Theor. Pop. Biol. 23, 202.
Gillespie, J.H. (1984). Molecular evolution over the mutational landscape. Evolution 38, 1116.
Hofbauer, J., & Sigmund, K. (2003). Evolutionary game dynamics. Bulletin of the American Mathematical Society, 40(4), 479-519.
Kauffman, S. (1993). The origins of order: Self organization and selection in evolution. Oxford University Press, USA.
Kauffman, S. & Weinberger, E. (1989) The NK Model of rugged fitness landscapes and its application to the maturation of the immune response. Journal of Theoretical Biology, 141(2): 211-245
Nowak, M. A. (2006). Evolutionary dynamics: exploring the equations of life. Harvard University Press.

Modeling evolutionary processes has a long history in evolutionary biology. Initially, these models were only theoretical or back-of-the-envelope quantitative (e.g., Simpson's Tempo and Mode in Evolution), but with the advent of cheap and accessible computing power, interest in stochastic models has greatly expanded.
The primary literature is vast, so I recommend a few books, which will give you a sampling of approaches and, more importantly, pointers to the relevant literature. If you are at a university, there is a good chance that your library will have one or more of these:

Otto SP and T Day. 2007. A biologist's guide to mathematical modeling in ecology and evolution. Princeton University Press.
Bolker BM. 2008. Ecological models and data in R. Princeton University Press.
Roff DA. 2010. Modeling evolution: An introduction to numerical methods. Oxford University Press.

And want to try your own models and you use R, there is an entire page of evolutionary biology packages. Many of these have built-in functions to simulate evolutionary processes:

CRAN Task View: Phylogenetics, Especially Comparative Methods

One thing to keep in mind is that simple models, like the one by Wilf and Ewens, often encapsulate the question at hand very well. Even though relatively simple, they are nonetheless very powerful. Wilf and Ewens wanted to prove a point about mutation, and they do that very well. It's easy to imagine way to extend their model to be more realistic, but as a start this is a very sound approach.
A rule of thumb for modeling is to make the model as simple as possible at first, including only the essential process or processes. Then gradually add complexity.

Nice answer (+1). I've been trying to find good intro's to modelling recently - just downloaded the Roff book and working my way through the introductory chapters, seems clearly written and informative so far!

I knew there must be some literature out there somewhere :) These look great - my library has them all so I'll take a look at them ASAP :D Thanks

thanks for the plug for my book, but I should point out that while it has useful tools for biological modeling, it doesn't explicitly cover evolutionary models

You might also have a look at some theoretical population genetics, which traditionally models selection as a diffusion process. The best introduction I know is chapter 15 of Karlin & Taylor's Second Course in Stochastic Processes (which, despite being only one chapter, makes up about half the book). From this, you can get results on hitting times, fixation times and other related distributions. Similar results are available in Durret's book, but he goes a bit deeper into the biological interpretations of his results.


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Microscopy Book Suggestions
I've learned programming through great book recommendations; many from the Stack Exchange series of sites. I'm hoping to take this approach in order to gain a fundamental understanding of how fluorescence microscopy and sub-diffraction limit imaging tools work.
What books or reviews do you recommend that offer both a conceptual explanation of imaging biological specimens and practical advice? I'd settle for either one if you find the author to be effective.

Would also like to see a good reference!  ejstrong, would you be looking at cells, microorganisms, subcellular processes?  might be useful to you to be particular.  the game gets very different between butterfly wings and organelles.

Recommendation questions normally end up soliciting lists.  You've narrowed down your your focus a little bit, but there are still scores of books on microscopy out there.  Can you narrow it down any further (as shigeta alluded to)?

I am going to leave this as a comment, because I don't think this is exactly what you need, but the Cold Spring Harbor books about imaging are very good if you are going to use the techniques in the lab (they're very much focussed on practical issues). I own Imaging in Neuroscience: a laboratory manual but you can also find a book on imaging in general, one on live cell imaging, and one on developmental biology.

@Shigeta - sorry for not specifying. I would be looking at both cells and organotypic culture.

@jonsca - I would first want to learn about imaging live cells but would appreciate an overview of fluorescence imaging in addition to learning about specific imaging applications.

Apart from/ along with books, one can also learn through this course on [ibiology][ https://www.ibiology.org/online-biology-courses/microscopy-series/]

source: Stack Exchange

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Do SSRIs downregulate or upregulate the 5-HT3 receptor?
What effect do SSRIs have on the expression of the ligand-gated ion channel, the 5-HT3 receptor?

There are five subunits to this receptor (5-HT3), which are encoded by the genes HTR3(A-D) and differentially expressed depending on cell location in the (human) body. In contrast to the information in the previous answer, my first source actually has shown HTR3A to be most highly expressed in the CNS. The others are almost exclusively found in cells of the gut.
My second source reveals that the 5-HT3A receptors are up-regulated (show increased expression) on the cell surface in the presence of agonists and antagonists to the receptor. So, if an agent was increasing the amount of 5-HT (serotonin, an agonist) outside the cell, as would an SSRI, the expression of the receptor subunit-encoding genes would be expected to increase.

Niesler, B., Frank, B., Kapeller, J. & Rappold, G. A. Cloning, physical mapping and expression analysis of the human 5-HT3 serotonin receptor-like genes HTR3C, HTR3D and HTR3E. Gene 310, 101–111 (2003).
Morton, R. A., Baptista-Hon, D. T., Hales, T. G. & Lovinger, D. M. Agonist- and antagonist-induced up-regulation of surface 5-HT3 A receptors. Br. J. Pharmacol. 172, 4066–4077 (2015).

SSRI's theoretically increase Serotonin levels.  Serotonin is an agonist to the 5HT-3 receptors. The 5HT-3a primarily associated with the upper gut and the 5HT-3b with the lower gut.  I would guess that theoretically again, SSRI's would tend to increase nausea, emesis, and diarrhea.  There may be other effects, but these are the ones I have researched.
The anti-emetics Dolasetron, Ondansetron, Granisetron, and Tropisetron are 5HT-3 antagonists.

You didn't answer the question. I asked what effect SSRIs have on the expression of the 5-HT3 receptor, not its signalling. I already knew that SSRIs would serve as an indirect agonist of the 5-HT3 receptors, but my question was would it affect the expression (think gene expression) of the 5-HT3 receptors!

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How does the eugeroic modafinil work?
How does the drug, modafinil (Provigil), exert its eugeroic (wakefulness-promoting) effects? I've read that it works by increasing dopamine and histamine concentrations in the CNS and by serving as a partial agonist at the dopamine D2 receptor. Perhaps by interfering with the function of orexin?

The exact mechanism is not known:

Modafinil has wake-promoting actions similar to sympathomimetic agents like amphetamine and methylphenidate, although the pharmacologic profile is not identical to that of sympathomimetic amines. [...] Modafinil-induced wakefulness can be attenuated by the α1-adrenergic receptor antagonist prazosin; however, Modafinil is inactive in other in vitro assay systems known to be responsive to α-adrenergic agonists, such as the rat vas deferens preparation. [...] Modafinil is not a direct- or indirect-acting dopamine receptor agonist. However, in vitro, Modafinil binds to the dopamine transporter and inhibits dopamine reuptake. This activity has been associated in vivo with increased extracellular dopamine levels in some brain regions of animals [1].

A 2010 study has concluded that:

Recent evidence suggests that modafinil may block the dopamine transporter (DAT) and that the dopamine D1 receptor (D1R) may contribute to modafinil effects [2].

Another one confirms modafinil's dopaminergic activity:

These findings indicate that modafinil has a long duration of action, with alerting properties arising predominantly from dopaminergic activity [3].

It seems to be dependent on catecholaminergic signaling:

It binds competitively to the cell-membrane dopamine (DA) transporter and is dependent on catecholaminergic (dopaminergic and adrenergic) signaling for its wake-promoting effects. [...] Modafinil is an exceptionally weak, but apparently very selective, DA transporter inhibitor. [...] The conformational constraints on the interaction of modafinil with the DA transporter - and probably, as a consequence, its effects on trace amine receptor signaling in the catecholaminergic cell - are unique among catecholaminergic agents [4].

References:

Drugs.com. Modafinil. Clinical Pharmacology. Available from http://www.drugs.com/pro/modafinil.html (accessed 29.07.2014)
Young JW, Geyer MA. Action of modafinil--increased motivation via the dopamine transporter inhibition and D1 receptors? Biol. Psychiatry. 2010 Apr 15;67(8):784-7. doi: 10.1016/j.biopsych.2009.12.015. PubMed PMID: 20132929.
Turner C, Belyavin A, Nicholson A. Duration of activity and mode of action of modafinil: Studies on sleep and wakefulness in humans. J. Psychopharmacol. (Oxford). 2013 Dec 3;28(7):643-654. doi: 10.1177/0269881113508173. PubMed PMID: 24306135.
Wisor J. Modafinil as a catecholaminergic agent: empirical evidence and unanswered questions. Front Neurol. 2013 Oct 7;4:139. doi: 10.3389/fneur.2013.00139. PubMed PMID: 24109471.

Thanks for the great Answer and Solving 1 year old question!!!


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Why do some animals have 8 Limbs (e.g. Spiders, Octopuses)?
Octopuses have 8 tentacles, spiders have 8 legs.
Is there something special about 8? It seems like an animal that needs 360° mobility has 8 legs.

Crabs might be another example (10 limbs but only 8 legs with common sideways--but not 360 degree--motion).

@Kevin, "octopuses" is better form although octopi is used under the mistaken assumption that the word is latin. If you want to be pedantic, it should be octopodes or octopoda since it comes from Greek. See here for a nice discussion.

cool topic, it led me to this page: https://www.echemi.com/community/examples-of-animals-with-12-28-legs_mjart2205252409_313.html

No, there is nothing special about eight legs. You have species with two legs (humans), four legs (most mammals), six legs (insects), eight legs (spiders), ten legs (lobsters), and many more legs (millipedes, centipedes).

The question asked about animals with 360 degree motion.

@PaulA.Clayton I am not sure what it means to have 360 deg. motion.  All organisms use 360 degree motion.  One could argue that radially symmetrical organisms lack a preferred "head" direction, but spiders and octopuses are not radially symmetrical.  Why would a spider be more 360 degree motive than a crab, a mouse, or an insect?

@KennyPeanuts, I think both the OP and I, in my previous comment, were laboring under a misapprehension. 180 degree vision and motion would be more correct. A spider has eyes situated all around its head, allowing for 180 degree vision. The lack of a specific "forward" direction in this species would indeed indicate a greater ability for 180 degree movement. Not so octopuses though, I agree.

I suppose that octopodes (and really all animals, but especially those that swim and fly) have 41,253°² motion, not 360° motion, because they exist in a three-dimensional world.

This is just a wild guess, but for movement on a surface in which legs are lifted from the surface, six legs might be sufficient to provide three points of support at all times (think three-legged stool) while allowing relatively rapid movement (legs on both sides can be moved simultaneously), but such might be both less stable and less friendly to variable direction of movement (since legs are in fixed locations and not evenly/radially distributed in animals with bilateral symmetry, having more legs would facilitate balance for different directions of movement).  Having eight legs allows well distributed support and might allow more simplified motor control.
Having more than eight legs would tend to lengthen the body (for animals with bilateral symmetry) which might tend to bias movement direction (as well as possibly being wasteful of resources).
There might also be correlation of highly variable movement direction with requirements for greater stabilization.  E.g., eight legs might provide greater stability on a web (which surface might encourage more variable movement directions) and better support large claws (which might make sideways movement more useful in face-to-face encounters).
Note that the above does not address non-walking animals nor animals with radial symmetry (For an animal with radial symmetry, six legs might be sufficient to provide support with three.).
Hopefully, a better answer will be given, since I have not even paid attention to how spiders (or crabs) move.  (The manner of movement would give insight into how significant support/stability and motor control are.)

First of all, it's wrong to assume that an organism "needed 360 mobility" and therefore ended up with 8 legs, as the question implied. That would be a misunderstanding of evolution.
No, there is nothing special about 8 legs. Might as well be 6, 10 or 12. Take note, it would have to be an even number all organisms you mentioned are bilaterally symmetrical.
However, for these organisms 8 limbs were obviously something special. But independently, as they aren't closely related - octopusses are molluscs and spiders are arthropods. Maybe octopusses have 8 limbs because it gives them the best moving speed and agility while not expending too much energy. It's always a delicate balance.
The difference between an insect (6 legs; 3 segments), a spider (8 legs; 4 segments) and a lobster (10 legs; 7 segments) - all of them athropods - is in the number of leg segments. By the way, molluscs aren't considered segmented so they don't fall into this category.
When it comes to the difference between 8 and 6, You don't know did spiders "get" an extra leg segment or did insects "lose" one in order for the legs to be less of a burden during flight.
Interestingly, evidence suggests insects are the last to appear in the evolutionary family tree. Spiders also seem to have ended up with 8 legs by reduction as opposed to addition.
To answer the question "why do some animals have 8 limbs" - they have an even number of limbs because they're bilaterally symmetrical. The exact number of limbs in molluscs is a balance of energy consumption and fitness, as always, and the number of limbs in arhtropoda is the same thing, and my personal opinion is that spiders didn't go beyond reducing the number of their limbs to 8 for some reason - maybe because with 6 they were less efficient in walking the spiderweb.


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Colloids in digestion
I am looking for examples of colloids involved in digestion for a cross-curricular (bio-chem-physics) lesson plan.  Although I have found references implicating colloids in both lipid and protein digestion, I haven't been able to identify which colloids they are speaking of.  Can someone provide specific examples?

Fat released from food will form macroscopic lipid droplets in the aqueous environment of the gut. In the small intestine, bile synthesised by the liver is secreted into the lumen via the bile duct. Bile contains bile salts which act as detergents to disperse the lipid droplets by forming micelles. I think this dispersion of micelles could be described as a colloid.
I have no idea what the reference to protein digestion could mean, although some hydrophobic proteins might become associated with the micelles that I've already described, and I imagine that bile salts might help to solubilise protein aggregates in the gut lumen by direct interaction - they, or their derivatives, are sometimes used by protein biochemists as detergents for protein solubilisation (e.g sodium deoxycholate.


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How does Serotonergic (5-HT2A mediated) Psychedelia work?
How does serotonergic (5-HT2A specific) psychedelia work? I've read that there are some theories that it might involve the induction of a glutamate release in certain regions of the brain involved in perception.

Brenton, the linked pdf is called "Multiple receptors contribute to the behavioral effects of
indoleamine hallucinogens". It goes into detail on a a few basic behavioral responses.  I don't know what your background is so if you need help understanding parts point them out to me and I'll give it a go.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3110631/pdf/nihms267079.pdf
https://docs.google.com/file/d/0B0JUrCVOms3MdzdlYmh0SnBmOHc/edit (I'm hosting the pdf on my Google Drive if you aren't able to see the link hosted by the NIH).

Thanks, mate, if I find the article in question sufficiently helpful I'll accept your answer and up-vote it. I'm grateful that you quoted a reliable source. Of course you can't just take people's word on these Q&A sites without some proof because you can't be certain of their qualifications regardless of what they claim. I probably won't need too much help in understanding it, I usually understand such articles, but if I need help I'll ask.


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Why do genitals feel frozen when freefalling?
I don't want to add much more about that. Since childhood I noticed a chilling effect, even when doing rollercoaster-type activities.

Is there evidence that what you are describing is a general phenomenon?

Probably because the blood would be forced, physically, that is, by inertia to move upwards during free-fall, thus causing the genital's blood supply to become obstructed thus reducing their temperature and thus leading to the sensation of them being frozen as you described. Plus you might feel cooler all over your body due to the air flow against it and since your genitals wouldn't be as biologically favoured when your body's survival instincts for low-temperature environments kicks in you're body would probably reduce the blood flow to your genitals and other extremities favouring your vital organs such as your heart, lungs, brain, etc. with a greater blood supply to keep them warm and working.

If it were blood flow, wouldn't your feet be cold as well?

Perhaps but perhaps as part of the person in question's biology the genitals are for some reason more prone to decreased blood flow. Different people have slightly different biologies and seeing  how from what I can tell this isn't a super common occurance in people this theory seems quite valid.

If it's not a general phenomenon, then I think the question is too narrow (i.e., applicable to only one person).

I kind of think you shouldn't be discussing that with me but rather with the asker under the question itself seeing how its more applicable to him/her. Put it to him/her that if they cannot find someone who experiences this too under those circumstances the question will be closed.

i think its all the ennervation in the region - they are quite sensitive compared to other ... regions


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Which Receptors are Involved in the antidepressant effects of SSRIs?
From what I've read the major receptor subtypes involved in the antidepressant effects of SSRIs are:

5-HT1A
5-HT2C
5-HT3
5-HT6

Please cite journal articles to back up your claims, I don't want any piece of information to be unverifiable.

I noticed you've asked a few questions about antidepressants recently--did you know that there's a cogsci stack that you can try too? I'm not saying these questions should be there instead of here, just saying you could ask in both places and see if it's helpful.

No, I didn't know that. Thanks for this suggestion, Alexandria.

You're right, those are all important! There are several good reviews on the mechanism of action antidepressants. I like Molecular Pharmacology, by Nestler, or even Principles of Neural Science, by Kandel. I think a textbook is going to be your best bet, in terms of getting up to speed here, as this is largely an already-researched issue, but here are some good review articles as well:

Bonhomme et al., 1988
Charney et al., 1981
Norbert & Esposito, 1998
Spencer, 2012

If you have a more specific question, let me know!

The question was which receptors are involved in the antidepressant actions of SSRIs, bupropion isn't a SSRI. I was going to say you're a little right up until I saw that you were talking about NDRIs -- by blocking the 5-HT2C receptors or downregulating them they manage to increase the dopamine and norepinephrine concentrations in various regions of the brain thus increase the activity of their respective receptors.

@BrentonHorne: Ah, sorry about that. I started talking about antidepressants and got carried away, I think!

@BrentonHorne: If you're really interested in SSRIs, I highly recommend the Nestler text--it talks about all classes of drugs, but it is one of the best bits of scientific writing I have encountered.

Which one's the Nestler text?

@BrentonHorne: The Molecular Pharmacology one. It's a text book, but totally worth the money, I think! I think it's most recent edition is 2008, but it's definitely a good overview of everything up until that point!

@BrentonHorne: I removed the Bupropion part to my answer, as it didn't pertain to your actual question.


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How can a three-base codon evolve from a two-base codon?
Inspired by this question among others.
It's widely suggested that the current 3-base codon system of encoding protein sequences in DNA evolved from an earlier 2-base codon system. This makes sense if you look at the coding sequences themselves but I fail to understand how it can evolve? Wouldn't any shift wreck the coding of all existing proteins?
Perhaps they could overlap, but wouldn't even that produce nonsense and how would it shift to non-overlapping codons? Perhaps both systems could run in parallel, but how would anything useful come from that in the short term? What selective of advantage of 3-base coding could be strong enough to overcome any disruption?
Has anyone developed a coherent model of what intermediate stages might look like?

It is not suggesting a 2-base->3-base code in the way you are thinking, but of a non-coding, two-coding triplet pattern occurring first.
This means you would have 16 different coding sequences with 4 possible spacing bases in between.
Later, the spacing bases could become used as part of the code.
Does that make more sense?
Instead of AA,CG becoming AAT,CGT; AAX,CGX becomes AAT,CGT etc.
Its also likely that between 2 and 3 base codes a 2 base pyrimidine/purine system was used. Today the third base can often be switched for its pyrimidine/purine pair without changing the resulting amino acid.

Yes, that does make more sense. Thanks, Nick. Do you have a source for this, though?

Erives' paper is interesting:
A model of proto-anti-codon RNA enzymes requiring L-amino acid homochirality.

Why is it interesting?  Try to include a summary of anything you're linking to in your own words.


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Why am I getting low transformation efficiency with DB3.1 E.coli cells?
I am making competent cells using DB3.1 E. coli cells. Even after following the exact protocol (Inoue method for ultracompetent cells) given in 'Sambrook and Russel', I am not getting transformation efficiency of more than 104. I am using a 5.1kb plasmid for checking transformation efficiency.
I will be thankful if any of you can share your experience in this experiment.

How are you storing the cells?  Competent cells can be very finicky.  In my lab, we usually flash-freeze them with ethanol/dry-ice and store at -81 degrees (long-term use) or we store them surrounded by ice at 4 degrees (short-term use).


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Why do antidepressants have a delayed onset of action?
Why do antidepressants take so long to reach efficacy? I've read of theories about it perhaps being due to the strength of negative feedback via serotonergic and adrenergic autoreceptors during the first few weeks of treatment. What I'm looking for in an answer is the following:

The current theories regarding why currently-in-practise antidepressant regimens have a delayed onset of action.
The evidence for these theories.
How these theories fit in with the monoamine hypothesis or whether it is inconsistent with the monoamine hypothesis and how.
Possible solutions to this problem of delayed responses to antidepressant therapy.

All of this is strictly theoretical, there are no actual people involved here, this is simply a scientific inquiry.

Short answer
The mechanism of action of serotonin-specific reuptake inhibitors, a commonly-prescribed class of antidepressants, is a downregulation of 5HT1A receptors through negative feedback. This downregulation of receptors takes time.
Background
Serotonin-specific reuptake inhibitors (SSRIs) are a class of antidepressants commonly prescribed to treat depression. Their therapeuric effects may need weeks of treatment (Celada, 2004), which can be explained by their action on 5HT1A receptors in the dendritic region of the serotoninergic neurons in the raphe nucleus. By blocking serotonin (5HT) reuptake, negative feedback mechanisms cause the 5HT1A receptors to downregulate. This downregulation of the presynaptic modulatory 5HT1A receptors changes the firing pattern of the serotonergic neuron into a more fluttering mode, so that it releases more 5HT (Duman, 2007). More 5HT makes you feel better. That is how it fits into the monoaminergic hypothesis. To have the 5HT1A receptors respond this way takes time, as it is an adaptive response that downregulates of 5HT1A receptors, i.e., less receptors are present on the cell's membrane.
This is only an expanation of delayed action of SSRIs, a specific subclass of antidepressants. For example, there are newer classes of antidepressants that seem to work faster (5HT4 action) (Duman, 2007).
References
- Celada et al., J Psychiatry Neurosci (2004); 29(4): 252–65
- Duman, Neuron (2007); 55(5): 712-25

All regulatory administration (any reg. admin, FDA, TGA, EMA, MHRA, etc.)-approved antidepressants have a delayed onset of action, although mirtazapine may act slightly faster. So it isn't just the SSRIs. Even antidepressants with no appreciable serotonergic effects (e.g., bupropion) have a delayed onset of action.

Intetesting! I wasn't aware of that. I have made some changes in my answer, as it applies to SSRIs only. Thanks!

Did I start a trend?!? @AliceD

+1 thanks bunches Alice! Interesting that there are delayed and non delayed classes. I was not aware of this. Very cool

@StanShunpike - thanks for your appreciation. I improved the answer too. It's one of my first answers and it needed some additional referencing. Thanks!

@AliceD I have realized how much effort some contributors put in and appreciate it. I also know the feeling of writing an answer and having no one say anything and no acceptance! I'm sure u understand that feeling. I have gotten in the habit of thanking more as a result, where appropriate. :D

There's some clinical evidence for the relevance of 5HT1A autoreceptors, namely that pindolol augmentation accelerates the effects of SSRIs, but it doesn't do much more than that, i.e. ultimately if someone is unresponsive to SSRIs, pindolol augmentation apparently does nothing.

And @BH2017 is correct that even for drugs like bupropion, there's no difference in scores over time from SSRIs... at least in one study which is pretty damn odd, although perhaps there's not enough data.


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Are all Autoreceptors Downregulated by their Respective Endogenous Ligands?
I know that the 5-HT1A and $\alpha$2 adrenoreceptors receptors serve as autoreceptors for serotonin (5-HT) and norepinephrine respectively and are down-regulated by repeat exposure to their respective ligands, it's believed that this is likely the cause for the therapeutic delay in the actions of antidepressants that target the serotonergic and noradrenergic systems.  My question is this: "Is this the case for all autoreceptors? Are all autoreceptors down-regulated by the actions of their respective ligands?"

Autoreceptors - are receptors of the presynaptic terminal.
α2 adrenoreceptors receptors are down-regulated due to repeated exposure.

Pharmacodynamic tolerance begins when the cellular response to a substance is reduced with repeated use. A common cause of pharmacodynamic tolerance is high concentrations of a substance constantly binding with the receptor, desensitizing it through constant interaction

This is a common occurrence - not just for autoreceptors but receptors in general.
But for your interest here is one for dopamine autoreceptors (Pay-wall).

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Resource for model organism anatomy/physiology for biological experiments
I'm looking for a resource that best surveys the anatomy and physiology of common genetic model organisms, and how their characteristics are particularly useful for biological experiments.
For example, I'm studying the eyeless Drosophila gene, but it would help to know that species' specific compound eye anatomy and normal development, so that I can weigh the pros and cons of using that particular model organism over another.

I don't think you will find a global DB like that. You will probably need to use flybase, mousebase, dictybase, wormbase etc etc.

In the Bgee database, you can look at gene expression and anatomy of various model species, e.g. Drosophila. This doesn't give you the full anatomy, but at least an ontology of tissues and cell types.


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Do serotonergic (5-HT2A-mediated) psychedelics elicit stimulant effects?
I know that 5-HT2A partial agonism is the key mechanism of action of serotonergic psychedelics but I also know that some research (e.g. the selective (no activity on any other known receptor sites) 5-HT2A inverse agonist/antagonist eplivanserin was being investigated as a sedative) says that central blockade of the 5-HT2A receptors induces sedation which is in opposition to the effect of 5-HT2A partial agonists.
I have a partial answer to my question. I heard from LSD users that they find it regularly causes sleeplessness for the duration of its effects, which is likely due to stimulant/wakefulness-promoting (eurogenic) effects. Albeit just because it is true for one serotonergic psychedelic doesn't necessarily mean it is true for all serotonergic psychedelics. Especially since LSD affects a wide range of serotonin and other receptor subtypes.

You have some great questions that I wish I knew the answers to.  Just a suggestion, you might want to see if your library can get Goodman and Gilman's for you.  I don't know if the answer to this would be in there, but it is definitely the "go-to" reference book for pharmacology.

I think you'll like this article. It's on monoamine release / reuptake inhibition for a host of different psychedelic and empathogenic drugs.
This wakefulness inducing effect you describe for LSD is widely reported for all common 5-HT2 mediated psychedelics.


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are female bonobos "always" pregnant?
Given that bonobo chimps are more sexually active then humans, are the females almost always pregnant? if not how not?
also are they so sexually active in the wild as well or is it just in captivity?

In most species, females are pregnant as often as they can be. Since the availability of sex is rarely a limiting factor, it seems likely that female bonobos are as "always" pregnant as other chimps and socially living primates. The actual rate of pregnancy will be hormonally limited by things such as reduced fertility during lactation and so on.

I think this is normally true for humans - we only need to have sex once a month to make this true - not nearly as often as bonobos.


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What software is there available for quantitative structure–activity relationship (QSAR) pharmacological studies?
QSAR modelling in pharmacology basically hangs on using mathematical modelling to approximate the effects different molecules will have on various pharmacological targets. I would like to know what software is available to assist me in doing these studies.

On the G6G Directory of OMICS and Intelligent software, I searched for "QSAR Analysis, and received two product abstracts:
1) SYBYL®-X Suite which contained:

3D QSAR: use the power of industry leading CoMFA in a new way to
generate novel ideas for R-groups - predict the level of biological
activity or potency based on structure-activity data, Not just yes/No
activity predictions;
Cheminformatics: produce highly focused queries that avoid false
positives using a rich set of 3D queries; on-the-fly conformational
searching means you only store a single conformation of your
molecules, keeping database size small and very transportable; and...
Link to this abstract:
http://g6g-softwaredirectory.com/bio/proteomics/structure-modeling/20710-Tripos-SYBYL-X-Suite.php

2) Fujitsu GhostMiner
GhostMiner can be employed in a number of business intelligence areas and the following areas:

Bioinformatics - genetics, proteomics, Quantitative Structure
Activity Relationship (QSAR) modeling...
Link to this abstract:
http://g6g-softwaredirectory.com/ai/neural-networks/20154-FQS-Poland-Fujitsu-GhostMiner.php

Perhaps the above will help.

Click2drug is a good ressource for in silico studies.
See this link.


text:
What accounts for size variation in breeds of dogs?
My assumption is that dogs vary so much in size because of artificial selection pressures coming from human breeders, but are there genetic loci that roughly determine approximate size?  Do other feral species of animals exhibit such a wide range in sizes or is this something that only occurs when breeders intervene?

Shigeta did a great job summarizing what we know about genotypes and dog size variations, does anyone know whether there are wild species that also very so dramatically in size?

This is a fascinating bit of genetics.
Dogs are especially variable in size and many appearance, behavioral and temperamental phenotypes.  It was long expected that variations in developmental genes were the reason that dog breeds were responsible for the amazing flexibility of dog sizes.  One early locus found was IGF1 (insulin like Growth Factor 1).
This 2011 PLOS paper actually review the specific genotypes of dog breeds and identifying loci that are strongly associated with breed phenotype supports this idea.

... (we scanned) the genome for signatures of selective sweeps in single breeds, characterized by long regions of reduced heterozygosity and fixation of extended haplotypes. These scans identify hundreds of regions, including 22 blocks of homozygosity longer than one megabase in certain breeds. Candidate selection loci are strongly enriched for developmental genes. We chose one highly differentiated region, associated with body size and ear morphology, and characterized it using high-throughput sequencing to provide a list of variants that may directly affect these traits.

Emphasis added.
This theory has an intuitive appeal as well - no dog breeds (I think) are larger than the wolf, the stock from which all dog breeds are descended.  All such breeds being derived from earlier developmental stages of the wolf makes an intuitive, if imprecise description of the effect here.
Regardless, dogs remain an important model organism for so many traits because relatively few genomic regions can cause so many important phenotypes, including size, but also behavioral and morphological variations.
In the below figure you can see how few genomic regions are responsible for the 46 breeds Vaysee et al. examined.


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What is the point of being selection-free?
I'm reading "Highly efficient endogenous human gene correction using designed zinc finger nucleases" by Urnov et al. They propose a way to use zinc finger proteins for gene therapy. They repeatedly claim their method is "selection free" and it seems they are claiming that as an advantage to their method.
Why would selection free be an advantage? Wouldn't you have to select for the transformed cells anyway to be relevant in a clinical setting?

Urnov et al. are trying to effect gene therapy - where a mutation causing a genetic form of severe combined immunideficiency (SCID) (also known as the bubble boy syndrome). Affected SCID patients can have little to no immunity to infection what so ever.  SCID in this case is caused by a single site mutation in the IL2R-gamma gene.
Their method is to use a DNA binding protein (containing zinc finger domains that bind the DNA) which attracts a DNA repair enzyme.
The result is that 18% of the cells have the SCID gene repaired.  This would have been a trivial result if they had applied selection, which generally refers to any method which eliminates cells which were not affected (in this case having their DNA repaired) by a transformation like their treatment.  They claim that 18% of all the cells were repaired (I assume this is in a cell culture).  This implies that if their treatment were applied to living tissue, 18% of the cells would be repaired in situ, which should be enough to restore immune function.
While its possible to apply a selection method to gene therapy, it would be far better if you did not.  Cancer chemotherapy for instance is a selection based treatment for instance, relying on toxins which kill fast dividing or growing cells preferentially, leaving the slower growing tissues relatively viable.   Still its quite toxic and disruptive to the patient.

-1. "This implies that if their treatment were applied to living tissue, 18% of the cells would be repaired in situ." Not at all. If only it were true that findings in a dish could draw such a straight line to results in the body!

i used the word 'implies' for this reason. I think this is a Nature article because they have suggested this very thing.  They are trying to demonstrate potential for in vivo gene therapy without selection as far as I can see.

I agree that they are trying to demonstrate a method that will be applicable for in vivo gene therapy. The results are suggestive of some rate of efficacy for in vivo repair. However, an 18% fraction of repaired cells in a dish does not point to, or even imply, an 18% fraction of repaired cells in a body.

I'm sure most would agree with that. Gene therapy has been an extremely difficult idea to realize in practice.  So much so that what is a preliminary result like this is published in a top tier journal.  This is promising, but far from a resolved problem.  It would be a strong contender for a Nobel Prize in Medicine if it did turn out to be a real treatment for SCID.

Thanks shigeta - this makes it very clear. I understand yamad's point, but I also get that this points to a possibility that some non-trivial amount of cells could in theory get transformed if this treatment were developed in situ.
So this does mean, right, that this treatment could only be applied to cases where cells are deficient in some manner or have some loss of function. If the cell were to gain some active malfunction - repairing a small proportion of the cells may not actually have a great impact. Would you agree?

The idea is to make an in situ edit in the DNA - it could be a repair of function or, less likely, a disruption of function that corrects a disease.  in many cases of repair of function a proportion of 20% of the cells probably would be a cure in many cases.  This condition was perhaps chosed because the repair in question would be helpful; in this case it would confer immune activity and most cells are not active all the time in any case.  The better the yield the more diseases would be ameliorated, but there are many where 1 in 5 would be a major lifestyle change for patients.


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Why do cells have an average 'life span'
I've heard of Henrietta Lacks. As a result of a genetic mutation, her cells never died. I've heard/read that overtime, our cells stop multiplying as much, (as an effect of aging). Why? Why do we age? Why do cells eventually die? What causes our bodies to degenerate? It is encoded for in our genes? If we treated our bodies in the highest regard, accounted for accurate diet and sleep, with the introduction of genetic engineering, could everlasting life be possible?

Henrietta Lacks had cervical cancer, and her cancerous cells somehow survived in culture (I don't know if this was due to proper handling by the lab staff or otherwise).

@Rustyn Yes, the possibility of immortality in the sense of everlasting of the body is a more and more accurate hypothesis

We refer to the number of times the cells of an organism can possibly divide as the Hayflick limit for that organism. The Hayflick limit serves as a theoretical life span, because telomeres (on the ends of chromosomes) get slightly shorter with each round of division, until they are gone completely. Telomeres are put on the ends of chromosomes by the enzyme telomerase, which is abundant in infants (who are growing and undergoing rapid mitotic divisions) but bodily abundance of the enzyme quickly diminishes with age. Without telomeres, our actual chromosomes would shorten in length during each round of division -- essentially, this is what happens after the telomeres are eroded away at in the later years of life. The Hayflick limit for humans is given to be 120 years -- with perfect self-care, 120 years of life is possible.

Nice answer. Do you have a reference for the 120 years claim?


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The fundamental importance of R.E.M. Sleep. (Rapid Eye Movement)
Question:
I know that experiments have been conducted to determine the importance of R.E.M. sleep in our sleep cycle. It is particularly important for learning, information synthesis, and recovery from distress. Why else is R.E.M. sleep important? What experiments have been done/observations been made to determine the neurological mechanisms underlying R.E.M. sleep? I know that we exhibit high frequency $\alpha$ waves, similar to the waves we experience during wakefulness.
Wiki:
During REM sleep, high levels of acetylcholine in the hippocampus suppress feedback from hippocampus to the neocortex, and lower levels of acetylcholine and norepinephrine in the neocortex encourage the spread of associational activity within neocortical areas without control from the hippocampus. This is in contrast to waking consciousness, where higher levels of norepinephrine and acetylcholine inhibit recurrent connections in the neocortex. REM sleep through this process adds creativity by allowing "neocortical structures to reorganise associative hierarchies, in which information from the hippocampus would be reinterpreted in relation to previous semantic representations or nodes.
Do these reorganized neocortical hierarchies remain this way?
Just HOW integral is R.E.M. sleep to our brain development?

REM sleep stimulates the brain regions used in learning. This may be
  important for normal brain development during infancy, which would
  explain why infants spend much more time in REM sleep than adults (see
  Sleep: A Dynamic Activity ). Like deep sleep, REM sleep is associated
  with increased production of proteins. One study found that REM sleep
  affects learning of certain mental skills. People taught a skill and
  then deprived of non-REM sleep could recall what they had learned
  after sleeping, while people deprived of REM sleep could not.
Some scientists believe dreams are the cortex's attempt to find
  meaning in the random signals that it receives during REM sleep. The
  cortex is the part of the brain that interprets and organizes
  information from the environment during consciousness. It may be that,
  given random signals from the pons during REM sleep, the cortex tries
  to interpret these signals as well, creating a "story" out of
  fragmented brain activity.

Source: link

Relevant quotes should support your answer rather than form it in it's entirety

@RoryM While I do agree, I think this quote was helpful and answered my question well. By the way, it's: its.


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Why don't we form immunity to some infections?
I read another question, and its answers, about how vaccines work, but I don't see there, and and don't understand, why some infections can, seemingly, not be immunized against at all. For example, someone who gets the flu (or the flu vaccine) is immunized against that particular strain of flu for life (which was relevant, IIRC, when H1N1 came back a few years ago: many people above a certain age had immunity), whereas one person can get group-Α strep throat over and over again. Why is this?

The answer is sort of hidden behind the very first paragraph of your linked question:

Vaccines work by introducing an attenuated strain of the pathogen (or alternatively the antigens that are normally present on the pathogens surface) into the body, whereupon the body mounts an immune response.

The body mounts an immune response based upon a particular epitope (molecule/protein chain) derived from the infection itself.
If the bacteria/virus/parasite evolves so that the molecules/proteins on its surface change significantly, then the version stored in Memory Cells will no longer apply. There's some wiggle room depending on epitope length and specificity of the Immune Response (highly specific MHC proteins will invoke a very strong, very efficient response - while less specific [usually B-cell or early T-cell responses] will invoke a weaker, less effective response), but because pathogens can mutate so quickly it's not uncommon that you'll encounter a descendant of a virus you already encountered that has dramatically different characteristics.
Some pathogens are also just very "clever" at avoiding the immune system. Sometimes they can produce shells which can't be broken down to derive epitopes from, sometimes they live within host cells and simply hide (the most well known example being HIV), other times they can present the same "I'm part of the body!" MHC proteins that tells the immune system not to attack them, and they can even hide in parts of the body where the immune system rarely visits (eyes, brain, other very specialized tissues).
And at times the pathogen can be both very adaptive and very "clever", as in the case for Staphylococcus aureas - which can inactivate antibodies through surface proteins and has the ability to adapt to new antibodies very quickly.
You can think of it like a game of chess. If you play against the same person all the time you're going to learn their moves, their strategy, and be able to beat them very quickly. If you switch partners, or your regular partner learns new moves, you'll spend some time adapting to the new play style you've encountered before being able to win consistently again. Bacteria and virii are simply very, very good at coming up with new play styles.

MCM's answer is quite correct. There are quite a few specific ways various pathogens escape "immunity" (long term, often not truly life-long, protection).
To quickly restate what he has said:
First the pathogen can mutate to be different enough that your body won't recognize it (ie different strains of flu or HIV), it can hide in cells or immunoprivileged areas of the body, it can actually shut your immune system down, actively combat your immune system, or prevent an immune response from being mounted.
And just a few more thoughts:
There are certain pathogens we are still trying to figure out how they avoid the immune system (the technical quality is immunogenicity).  A good example human respiratory syncytial virus (RSV).  Again this is actually an active field of study for a great many pathogens.  When we test many of these "tricky" pathogens in animal models, we find that they often can gain immunity.
+1 @MCM, I was trying to cram this into a comment, but I didn't think I could.
Some interesting areas to read up on if you are interested in the subject are immune avoidance/evasion and forward genetics.  You will more often hear about reverse genetics, but forward genetic experiments can allow us to see how the "chess game" will be played out by the pathogens in new situations.


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How to find Exons in mRNA Computationally
I'm having trouble finding a method to find exons in the original DNA sequence used to create the mRNA, even given the sequence of the mRNA, as I cannot find a way to reliably identify the beginning and end of introns and exons. Is there an algorithm or method that I can use to do this? What information am I missing to be able to find the beginning and end of exons and introns?
Thanks in advance for answers.

The only information you are missing is a way to identify the splice sites. There are many ways of doing what you need. The simplest, assuming you are sure of the origins of the mRNA, is to use a BLAST flavor, either plain BLASTn or, even better, BLAT, to compare your mRNA sequence to the genome of interest. BLAT really should be all you need if the mRNA comes from the genome you are aligning it to.
BLAT however, has no knowledge of splice sites and will simply cut your mRNA so as to maximize local alignment scores. If you need something more sophisticated than BLAT, use a specialized aligner as @SteveLianoglou suggested. These programs include a model of splice sites (both canonical and non) and will align exons correctly. My personal favorite is exonerate.
Assuming you are using Linux (which you should be if you are planning on doing a lot of this type of analyses), you can install it on a Debian based distribution (such as Ubuntu and its variants) with this command:
sudo apt-get install exonerate

Then, to align the mRNA to its gene do:
exonerate -m est2genome -n 1 mrna.txt dna.txt > out.txt

-m is the model that exonerate will use to align your two sequences. Since the important thing in your case is to correctly model splice sites, you should use either est2genome or, if you are comparing different species, coding2genome, or if you have a full length cDNA including UTRs, cdna2genome.
-n 1 means find the best match only. Assuming you are aligning an mRNA to its coding gene, this is all you are interested in.

I realise that this is not a very biological answer. I did mention splice sites though, four times!

You should ask this question over at biostars.org -- and could use a bit more clarity.
Do you actually have RNA-seq data that you want to use to find the exon/splicing structure of an mRNA?
First step would be to use a splicing-aware aligner. A few free ones are:

STAR
TopHat
GSNAP

Let us know why that wouldn't do what you want when you re-ask this question over at biostar.


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Is there any kind of immortality in plants?
I asked a question about immortality of hydra and learned good things about senescence. Now I would like to know about immortality in plants, if there is some kind of immortality in plants and how this occurs - how does it protect itself from senescence?

Hi there. There is a somewhat similar question here (http://biology.stackexchange.com/questions/2055/do-trees-age-on-a-microscopic-level/) that I have posted an answer to.

Just found this amazing example of a really old tree - >4000 years old! http://www.ncbi.nlm.nih.gov/pubmed/11295507

I can find no examples of immortal plants, but then again immortality is rather hard to prove, it's rather like trying to prove that space will never turn in to a pony - as long as time exists it could still occur, only if you go beyond the end of all time would you be able to say that it has or has not happened but then time would no longer exist and nor would space/the pony.
However, for examples of long lived plants it is perhaps best to look at trees - there are some species that live a long time and they can easily be aged. Here is a list of oldest known trees. It is difficult to tell how old these trees can become, and thus whether they are "immortal", because anything that lives that long is likely to encounter sources of extrinsic mortality during it's lifetime - predation, deforestation, extreme weather, erosion, natural disasters, contaminants, humans, disease, parasites etc. (rather than intrinsic dying of old age).
A lot of plants go through some kind of apoptosis, where cells are programmed to die. Plants such as annuals, biennials etc. die after a few months or years in a programmed way. It is difficult to say whether long lived species of trees would do the same after a few thousand years of life, because we just don't get to see many reach that stage of life, or if the mechanisms causing it have been suppressed (which could explain their long life).
Luke has posted a very thorough answer on the cellular and genetic aging of plants here. And to quote him:

"...it seems to me likely that plants may also have enhanced maintenance
  against other cellular stresses than DNA damage, such as build-ups of
  aberrant proteins. It therefore appears that in a protected
  environment some plants could live indefinitely"

Wikipedia has some very good pages on the evolution of senescence & aging. This article has also a good section on plant aging and I hope you can access it.
and finally, if you want to have a laugh, take a look at this entry on plant immortality and aging from creationwiki.org...

"Plants are actually or potentially immortal organisms that will live
  indefinitely provided their environmental requirements are met. In
  striking contrast to plants, humans and animals have a maximum life
  expectancy regardless of whether their needs are fulfilled. Although
  it is true that some plants grow as annuals, all plants are actually
  perennials by nature, and have adapted to a programmed life cycle in
  some instances to match growing seasons. Otherwise, plants only die
  because of biochemical starvation or disease. If their physical
  requirements are met, plants will grow indefinitely."

Some great clear science there, well done creationists... but it's just plain wrong.

Since meristems (the parts of plants from which growth happens) are constantly creating new stem cells, plants have a theoretical capacity for immortality. Of course, in practice, the vast majority of plants still senesce and die. But there are some notable exceptions such as bristlecone pines and quaking aspens which live for thousands of years. If you consider new individuals produced through clonal reproduction to be extensions of the original individual, then even more plants could be seen as immortal.

In addition to the above answers, the answer to your question also depends on your definition of immortality. There are a number of clonal organisms (the most famous of which is probably Pando, a quaking aspen https://en.wikipedia.org/wiki/Pando_%28tree%29 ) where there is a large area, sometimes multiple square miles, where individual shoots are sent above ground, giving anyone in the area the impression of a forest, but all of the trees are connected underground in one single large root system.
Such an organism could certainly be considered immortal, as its stems will constantly die off and be replaced by new organic material, enabling the network as a whole to live for tens of thousands of years (so far).


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Why do we yawn?
I've read a new study which suggests that yawning may help you keep a cool head. Also, the findings might hold some hope for sufferers of insomnia, migraines, and even epilepsy.
Is there any conclusion about what the function of yawning is and why do we yawn?

In an abstract, Brainerd at al. (2004) report the presence of yawn-like behaviors in "cartilaginous and ray-finned fishes, a lungfish, salamanders, caecilians, mammals, turtles, lizards, an alligator and birds".
So clearly the motor patterns necessary for this behavior evolved before air breathing and apparently have been conserved for ~400 million years. They reject the increased oxygen delivery hypothesis and associate yawning with stretching:

Yawning also has been thought to serve a similar physiological
  function to stretching. We measured the stretching movements of fins
  and limbs in association with yawns, and found that they follow the
  same movement pattern as jaw opening and closing. This lends support
  to the existing hypothesis that yawning and stretching serve a similar
  function, but the detailed nature of this function remains unclear.

I know it's only an anecdote, but as a kid I thought it would be a good idea to learn to yawn while keeping my lips together. (No need to put my hand in front of my face! Yay!)
Today I get a cramp every time I open my mouth too far. Great for eating burgers, visiting the dentist and yes, yawning. (May contain sarcasm.)


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Birds placing sticks on train tracks?
I live in a semi-rural area in Germany, close to a park which trains go through every 20 minutes.
Today, I saw something that left me perplexed.
There is a large population of birds that look like crows or ravens, yet fatter. They seem to be quite social and move around in large groups. Today, I spotted one carefully laying sticks from a nearby tree on the train track while the others seemed to spectate.
What exactly was that bird doing? Is this common? Did it have a purpose, or was it just coincidental?

Some corvids do use tools, and are fast learners. Could these be using the train and tracks as tools to cut sticks up smaller?

There is a book, In the Company of Crows and Ravens that details human-corvid interactions. That might provide insights for you. The link is: http://yalepress.yale.edu/yupbooks/book.asp?isbn=0300100760

@EnergyNumbers - I want to believe :)

If the birds are doing in this in a place where you can watch them repeatedly, why not set up camera to watch them?  I recommend a pocket camcorder with a big SD card (which is nice to have in general).  I don't think anyone will be able to tell you for sure without footage of what they do after putting them on the tracks. They could have just chosen a really bad place for a nest, or it could even be courtship behavior.

If the sticks were somewhat large, they may have been putting them on the tracks so that the trains would break the sticks into smaller pieces (which would probably be easier to build nests with).

There is a large population of birds that look like crows or ravens,
  yet fatter. They seem to be quite social and move around in large
  groups.

First of all, this seems like a crow. Crows are very social birds, they live in flocks or murder.

Theory: It may be a Mating Ritual?

No! The have a very spectacular mating ritual!.

Theory: It's Making a nest

Obviously No! Crows nests are always way hidden at 18-60 feet above ground(mostly) in the tree trunk.
My Theory
Crows are very curious birds. What you saw, might be a new play the young crows found. It's common that crows will do unusual thing when spectated by the elders and siblings.

Crows have been known to use human actions in order to accomplish their own purposes: read this story about them using cars and waiting for the lights to change at a crossroads. Then of course, the question is whether they have a specific purpose in your case with these sticks, or whether it's just... for the fun of it?


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Does Sansevieria trifasciata really absorb Carbon Dioxide at night?
There's a claim that Sansevieria trifasciata (Mother-in-law’s Tongue) generates oxygen from carbon dioxide during the night.
This seems surprising to me: that process requires energy; plants generate O₂ from CO₂ through photosynthesis, requiring light. So not photosynthesis, and no CO₂ absorption, at night.
Am I missing something, or is this claim false?

This is an interesting topic!
Crassulacean acid metabolism is a second CO₂ fixation pathway where CO₂ is absorbed at night.  The CO₂ is fixed into maleic acid HOOC-CH₂CH(OH)-COOH which stores some of the CO₂ in the form of carboxyl groups.  During the day carboxylases release the CO₂ for fixation during the day.
This is an adaptation where the stomata open at night to take in the CO₂ and are closed during the day - the plants sort of 'hold their breath'.  The energy for this process is derived for glycolysis which were stored during the day (nice detailed review here).
The paper says that about 6% of plants (including Mother-in-Laws Tongue) do this and you can imagine with night breathing how closing the stomata during the day would really help with dehydration.  Its interesting to note that this is found in a wide variety of plants "CAM is found in five taxonomic classes, comprising monocots and dicots, encompassing 33 families and 328 genera".  That says that CAM is a pretty old development in plant evolution and not so expensive that it is easily lost.

What does "fixation" mean in this context?

So, at night it takes in CO_2. When does it emit O_2? Also at night? ("during the day - the plants sort of hold their breath" sounds like gas exchange only happens at night)

'fixation' refers to carbon fixation - taking CO2 and putting it into a 'reduced' form or in this case a vitamin the plant uses to make food and cells - the anti GHG profile of plants :)

I think all plants emit oxygen during the day - the photons from the light are directly used to turn water into Oxygen gas at the photosynthetic reaction center - one of our most important proteins!  https://en.wikipedia.org/wiki/Photosynthetic_reaction_centre

Shigeta submitted his answer as I was writing this!
Sanseveria is one of a wide group of plants (mainly succulents) that adopt a photosynthetic strategy referred to as crassulacean acid metabolism (CAM).
Recall the basics of photosynthesis. The light-dependent reactions use energy from captured photons to generate ATP and NADPH, with the generation of O2. In the light-independent reactions (the Calvin cycle) this ATP and NADPH is used to fix CO2 to form three carbon sugars, which can then enter standard metabolic pathways to produce other metabolites.
In order to obtain CO2 for the fixation reactions plants have pores in their leaves called stomata to promote gas exchange (via diffusion). This presents a challenge for plants that grow in arid conditions: if they open their stomata during the day they lose water as water vapour. Many such plants use CAM to solve this problem. Basically what these plants do is to only open their stomata at night, capturing CO2 in the form of organic acids (oxaloacetate, malate, maleate) which are stored in vacuoles. Then, during the day, these acids can be metabolised to release the CO2 again for use in the photosynthetic reactions.
Notice that in this scheme the O2 will still be generated during the day. So when does it leave? Does it have to wait until the stomata open at night, or is it able to diffuse out through cells (recall that O2 readily diffuses through biological membranes)? I have been unable to find a definitive answer to this question so far (this is old literature), but my guess is that it is lost throughout the day.

bread and butter!

I think it's important to note that from a health point of view, baring any serious lung issues; Oxygen levels are not important. CO2 levels will reach fatal levels long before you begin to feel the effects of O2 deprivation; assuming the only process involved is mammalian respiratory in a closed environment.


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What is the average volume of the hippocampus?
I'm trying to find any information on sizes of the hippocampus?
Ideally in the average adult male & female brain

The average values of right hippocampus were recorded as follows weight 4.11572 gm, length 6.996 cm, width 1.998,volume 13.978 and surface area11.839 cubic centimetre while left hippocampus mean values were weight 3.96458gms,length 6.995, width 1.998,volume 13.976 and surface area 11.713cc. B. Narasinga Rao, K.R.S. Prasad Rao, R. Ramana Rao. 2012. Morphometric study of hippocampus in adult human brains. Int J Basic Appl Med Sci 2: 139-143.
Men and women had identical volumes of amygdala and hippocampus, as well as dorsal prefrontal cortex Ruben C. Gur, Faith Gunning-Dixon, Warren B. Bilker, Raquel E. Gur. 2002. Sex Differences in Temporo-limbic and Frontal Brain Volumes of Healthy Adults. Cerebral Cortex 12: 998-1003
Hippocampal volume change with age: Hippocampal volume diminished by 20% from 3,584 ± 136 mm3 at age 36 to 2,870 ± 220 mm3 at age of 85, corresponding to a volume loss of about 14.6 mm3/year (Schuff N., et al. 1999. Age-related metabolite changes and volume loss in the hippocampus by magnetic resonance spectroscopy and imaging. Neurobiol Aging 20: 279–285).


text:
What nutrients can humans absorb in the mouth?
For instance, I realise being able to absorb simple sugars in the mouth is pivotal in the rapid action of oral glucose gel. Thus I was wondering what nutrients in general can be absorbed directly within the mouth, and at what speed?

This could be a fairly long list, though off the top of my head Vitamin C and Glucose would be good places to start for nutrients and drugs GTN and Aspirin.  This Question is also related.

Quite a bit can be absorbed through the mouth. Most commonly, starches are broken down to maltose (two glucose molecules formed by a condensation reaction) and are easily absorbed by the bloodstream.
A lot of other factors balance into this, ie pH, lipid solubility, and molecular weight. Generally, if a substance is easily dissolved in saliva, it can be administered buccally or sublingually because the only remaining step is the diffusion into the subepithelial capillaries. In regards to speed, anything properly absorbed via buccal or sublingual administration goes to work much faster than a standard oral medication, and with a higher availability in the bloodstream. You are taking first pass metabolism and enzyme breakdown in the stomach out of the equation by diffusing the drug directly into the bloodstream.
There is quite a laundry list of medications that can be administered transbucally or sublingually, just a few of these:
Nitroglycerin
Acetylsalicylic acid (aspirin)
Glucose gel (as you mentioned)
Fentanyl (a narcotic painkiller)
buprenorphine (for opioid dependency)
Benzodiazepines (alprazolam, clonazepam)

so you said pH and lipid solubility... if the salivary secretions are alkaline would that mean that alkaline compounds would be deprotonated and more lipophilic, hence better absorbed?

This answer could be improved by including references.

The mouth or the oral cavity is lined by oral mucous membrane. The oral mucous membrane has two parts the epithelium and its supporting connective tissue known as lamina propriya. The charecter of the epithelium and lamina propriya varies to a great extent from the gingiva and hard palate to the floor of the mouth based on functional requirements. However basically the mucous membrane lining the oral cavity is not designed for absorbing nutrients, which was the primary question.
As for the oral glucose gel - read the American Red Cross, Scientific Advisory Council recommendation that the buccal absorption of glucose is limited and not recommended. ARC SAC Advisory

Actually, absorption does take place through the mouth.There is a ptyalin enzyme in the saliva which hydrolyzes carbohydrates of the food.  These contents are then absorbed in the blood through the facial vein.The facial vein opens into subclavian vein,and it opens into the superior vena cava.

I think the main question of the asker is "which" nutrients are absorbed through the mouth, the fact that absorption takes place in mouth is taken as a given fact.

Many vitamins are absorbed in mouth. Even spraying vitamins will help you overcome vitamin deficiency.
Even some drugs can be absorbed directly into mouth.

Source of this info?

Alcohol, a very important source of nutrition in undergrad students, can also be absorbed through the mouth.

www.crohns.net/Miva/education/aboutsprays.shtm

@biogirl that's not really a credible source


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How common is bacterial mediated transformation? In plants? In animal cells?
The most common method to transform plants is by soaking plant tissue in cultures of agrobacteria (this is not their current classification) which transfer DNA into the plants.
Is lateral gene transfer ability like this found a lot in nature?  Is agrobacterium tumificans especially good at this or is its use in plant genetics only because this strain is well studied?
Is a method like this used for animal cells at all?

An early report of conjugative transfer into mammalian cells (CHO cells) is:

Waters, VL (2001) Conjugation between bacterial and mammalian cells, Nat. Genet. 29: 375–376.

This work used the broad host range plasmid RK2 to mobilise shuttle vectors carrying selectable markers. To rule out transfection DNAse I was added (and in controls this was shown to block transfection by a large amount of vector DNA). In any case, the fact that the transfer of the vector required the presence of the mobilising plasmid is pretty strong evidence for a conjugative mechanism.
There is also more recent evidence for transfer into human cells via Type IV secretion systems: here is a recent example:

Fernandez-Gonzalez et al. (2011),Transfer of R388 Derivatives by a Pathogenesis-Associated Type IV Secretion System into both Bacteria and Human Cells. J Bacteriol 193: 6257-6265

And here is a recent review of the topic:

Llosa et al. (2012) New perspectives into bacterial DNA transfer to human cells Trends in Microbiology 20: 355-359.

In animal cells the process is called transfection, to differentiate from transformation which is the process by which cells become immortalized (cancerous). I'm mainly familiar with mammalian cells, and in these systems some reaction is required to open pores of some sort in the cell membrane to allow the genetic material to enter. Viruses can mediate cellular entry on their own, but I am unaware of any method that uses live bacteria (although this doesn't mean that some specialized method doesn't exist).


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Do Fatty Acid Synthase Inhibitors Selectively induce Apoptosis in Cancer cells without inducing the same in healthy human cells?
Do Fatty Acid Synthase (FAS) Inhibitors (e.g. cerulenin) selectively induce apoptosis in cancer cells without inducing the same in healthy human cells?

"Inhibition of fatty acid synthase (FAS) suppresses HER2/neu (erbB-2) oncogene overexpression in cancer cells" http://www.ncbi.nlm.nih.gov/pmc/articles/PMC490000/

I found this reference: "Inhibition of fatty acid synthase (FAS) suppresses HER2/neu (erbB-2) oncogene overexpression in cancer cells".   Cerulenin is not a magic bullet, but in some cases it may help.


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What does effect would Sulforaphane have on Kennedy's Disease?
Sulforaphane is a isothiocyanate found in cruciferous vegetables including broccoli and cauliflower. Its 2D structure is as follows:

It's been found to serve as a histone deacetylase 6 (HDAC6) inhibitor and to inhibit androgen receptor expression in prostate cancer cells.1 This caused me to become curious as to whether it would do the same in lower motor neuron cells and thus manage to prevent their polyglutamine-induced death and thus halt the progression of spinobulbar muscular atrophy (SBMA; Kennedy's disease).


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Why Do Most Humans & Cats Have Blue/Bluish Eyes At Birth?
I've read that the eye color at birth for most humans and for cats may not always be the the true genetic color at first. This is due to the lack of melanin in the iris. This makes sense as there is no light in the womb to stimulate the production of melanin.
My question(s) though is:

Why does the lack of said melanin produce a blue/bluish colored iris?
Why is it not say green, red, clear, etc?

The blue colour is an example of structural colour, caused by light interacting physically with something. Some examples of structural colour are the iridescence of insect wings and body surfaces (usually caused by repeating chitinous structures), and of certain birds feathers, as well as the non-iridescent colours of the blue and yellow macaw.
In the case of the eye it is the stroma of the iris that is responsible. This is a network of fibrous tissue which scatters light. When light is scattered in this way (Rayleigh scattering) it is the short wavelengths which are most scattered. So when you look at the sky (away from the sun) you are seeing diffuse blue light created by this scattering in the atmosphere. In the case of the iris what you are seeing is light reflected from the eye being scattered within the iris, creating the diffuse blue colour. As you say in the question, everything else is down to melanin.

The generation of iris color is quite complex and the exact color of the eyes depends upon many different factors, not just melanin. In fact, blue coloration does not depend on a specific chemical, but on the structure of the eye itself.
This very nice review (free) summarizes our current understanding:
Genetics of human iris colour and patterns - Sturm and Larsson, 2009
From the Introduction (bold is mine)

In the brown iris there is an abundance of melanocytes and melanin in the  anterior border layer and stroma whereas in the blue iris these layers contain very little melanin. As light traverses these relatively melanin-free layers, collagen fibrils of the iris scatter the short blue wavelengths to the surface, thus a blue iris is a consequence of structure not of major differences in chemical composition. Different shades of blue, and in irises with a limited amount of melanin, different shades of grey, green and hazel, are determined
  by the thickness and density of the iris itself and the extent of accumulation of white collagen fibres, as well as patches of tissue loss in the anterior border layer and stroma.
  However, a careful examination of people’s irises makes it clear that there are characteristics other than eye colour that present in the human iris. The iris has been analysed to show that it can display a degree of complexity encompassing over 240 degrees of freedom (Daugman, 2003).

Thanks for the edit @Alan... too early in the morning to speak proper English :P

Mammals are born with blue eyes because the melanin level has not yet been established to give brown/yellow. Blue is the absence of melanin, so that eyes reflect outside light which is seen as blue. Melanocyte cells respond to light and will start to make melanin in the first few weeks after birth. Melanocyte cells have a range of activity and will produce roughly the same amount of melanin that the parents had.

Welcome to Biology.SE! Your answer sounds reasonable and, if correct, it better addresses the original question than the existing answers. However, it is much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support non-specialists will have difficulty in evaluating your claims. ——— You may also want to take the [tour] and consult the help pages for additional advice on [Answer] effectively on this site. Thanks!


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How does formaldehyde cause protein-DNA crosslinking?
How does formaldehyde cause protein-DNA crosslinking?  I would guess it's because the strongly polar water molecule interacts strongly with polar residues on a protein-DNA complex, and adding a less polar solvent causes the DNA and protein to pull more tightly on each other than their pull on the solvent, but I haven't been able to find an answer online.

aldehydes actually react with amines in protein and DNA to covalently attach the protein to the DNA in such experiments.  check out slides 3+ http://synapses.clm.utexas.edu/lab/howto/cross-linking%20fixatives.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866014/
In this work they find that formaldehyde crosslinking happens by formation of a methylol adduct (due to nucleophilic attack by N or S in case of proteins) in protein which then attacks the DNA or vice-versa.
The final crosslink is by a methylene bridge
Formaldehyde can react to amino groups in nucleotides and proteins and form a schiff's base, but i dont have a clue how this is involved in crosslinking


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Which sex has higher variance of reproductive rate in modern societies - male or females?
Who has a more varied reproduction rate in modern western societies - men or women? The average rate is the same of course, but I wonder which sex have higher variance - higher variance means that reproduction is more concentrated in some subgroup of given sex so this subgroup transfer their genes at higher rates then average rate in whole population. The next question would be 'is that subgroup somehow homogeneous' ?

Good question.  I wouldn't be surprised if the distributions of fecundity (offspring reduced) were multi-modal (have more than one peak).  When you just look at sex, the answer is lopsided in more than one way.  http://www.telegraph.co.uk/news/newstopics/howaboutthat/3685314/Young-women-have-more-sexual-partners-than-men.html  http://www.nytimes.com/2007/08/12/weekinreview/12kolata.html

The problem with Bateman is that he was only looking at zygote production. There are many more factors influencing reproductive variance aside from number of sperm vs. number of eggs. If I were you, I'd read the book titled "Dr. Tatiana's Sex Advice to All Creation: The Definitive Guide to the Evolutionary Biology of Sex." The author is Olivia Judson (by the way, it's a very fun read and it is hysterical :)). In her book, she gives numerous examples of species wherein the females have a much higher rate of reproductive variance than traditionally thought. I hope I've helped!

Sperm are cheaper than eggs
According to Bateman's Principle the males of a species are (typically) more able to produce a greater variance in the number of offspring. This is because generally the males can produce many gametes and achieve many matings whereas females are limited by the number of eggs, resources, and time lost to pregnancy. Therefore, just by simple logic, it would appear likely that males have greater variance in mating success (strong/attractive males would be able to mate with many females while weak/unattractive males would have little to no offspring). See Wikipedia for an introduction to Bateman's Principle. Also see this paper about sexual selection and mating success variance.
An Example
An extreme example of higher variance in male mating success is that seen in lekking species. These species form groups of males called leks where females enter and choose mates. Often one/few males will sire the majority of offspring in the next generation. Fallow deer are one lekking species where males have higher mating success variation than expected by chance.
In Humans
Here is a blog post discussing a paper which showed that males have greater reproductive success variance than females in humans. In the paper see table 1 (Vm:Vf column) which indicates the majority, particularly those close to ancestral type lifestyles, have much greater variance in male reproductive success. Only one measured (Finland) is the reverse pattern.

nice reference.  polygamous cultures are a good illustration (see blog post table 1) of how 'some guys get all the luck'.


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Can you consider a human as alive, or is it the cells on the body that are alive?
Sorry if this question seems strange, but in the recent time I have been interested in the question of what life is and how you can define life.
My question:
How long can individual cells live on a human body from the point the human dies? When a human dies, legally he is dead, but how is the medical explaination? Can a human be partly dead, that the heart and brain has stopped, but the cells on the body are still alive?
When you talk about a human life, is it one life or could you consider each cell on the body as a living piece and the whole human body itself including the consciousness is just a container for the cells?

Or: "Is Henrietta Lacks still alive?"

This is a question of emergence

I'd love to see answers to the specific questions 'how long can individual cells live in a human after death' (in normal circumstances - HeLa excluded :P) I'm thinking alveolar squamous epithelium might do fairly well  in terms of maintaining oxygen supply.

Humans are social animals.  If you entirely isolate a human from all human contact (e.g., solitary confinement in prison, or lone shipwreck survivor on deserted island) for years at a time, usually the person will go insane, to some degree.  So, can you say that an individual human is alive?  Certainly, no individual human can reproduce, thus failing one of the usual criteria for life.

After heart dies, unless oxygen and nutrients can be supplied, cells will die within a short time.

Muscles of patients with motor neuron disease will undergo degeneration. For maintaining muscles even in a living person (meaning not brain dead), nerves are essential.

Life of multicellular organisms consists of life of all important unicellular organisms (which are called cells, and not just organisms because they can't live long when the "big" organism dies). But this question also might boil down to the meaning of the word "life" and then it's not biology.

The definition of life is the main issue here. That is one of the great philosophical questions in Biology (and not only Biology) and is way beyond the simple Q&A format of this site. However, most definitions of life can be boiled down to1:

A self replicating entity that interacts2 with its environment.

Or, even more simply [1]:

Life is self-reproduction with variations

In both cases, the answer to your question depends on which level you are focusing on, your resolution if you like. If you take a human cell and apply either of the definitions above, it is alive. A cell is capable of autonomous reproduction, and metabolizes substances harvested from its environment. The same holds true of you look at the human body. However, the definition will not hold for a part of the human body, for example an arm or kidney.
Consider also that a human cell is capable of making more copies of itself, more individual cells. A human body is also capable of making more copies of itself, more human bodies. They can, therefore, both be taken as alive.
There are even more complex examples like Dictyostelium discoideum an amoeba that can exist (and be alive) either as a single cell or as a colony sporting different cell types and rudimentary organization. However, the organism is alive in both of these stages. In one case, you would consider the cell to be the fundamental unit of D. discoideum life, and in the other you could consider the colony.
So, to answer your question both a human cell (as long as it is alive, actively metabolising and capable of reproducing) and the entire human body can be taken as alive. That my cells are alive does not lessen the fact that I am too. It is just a matter of perspective.
References

Trifonov EN., Vocabulary of definitions of life suggests a definition. J Biomol Struct Dyn. 2011 Oct;29(2):259-66.

1 Yes, I know this is a simplification, I just don't want to be drawn in to a long winded discussion on what the definition of life is. My answer is applicable to any of them really.
2 Metabolism can be seen as a form of interaction.


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Systems identification in small neural network
When analyzing data from cortex, we often try to understand what each neuron does in terms of its inputs from other neurons - a specific kind of a systems identification strategy. Most current approaches use generalized linear models for that purpose (Review article).
For very small systems like the worm c.elegans it must be possible to record from all neurons at the same time, at least optically. How well can we understand the output of each neuron based on its inputs in such simple systems? What are the best databases to ask such questions?
The reason I am asking this question now is because the human brain project that just got roughly a billion dollars in funding basically needs such data for every cell in the whole brain.

Hi Konrad. I'm also very interested in the same question. I do not know of any such data available though.

Hi Memming - Nice to see you here. I posted it here to clarify a question I sent to @OpenWorm - who may know best.

For very small systems like the worm c.elegans it must be possible to record from all neurons at the same time, at least optically.

While it is true that whole organism optical recording is technically possible in C. elegans, I'm not aware of any published work  where all neurons were identified and recorded from simultaneously and then combined with connectivity data in a systematic way.
I should note, that this isn't limited to C. elegans. Florian Engert's lab has published whole-organism recordings from zebrafish as well. At the moment, though, there are still technical challenges to work out before we get the input-output relationships you desire on a whole organism level. First off, the recordings aren't truly simultaneous, in the sense that it still takes time to build up 3D images from z-stacks. Second, the image processing to label neurons is not yet robust.  And finally, the most popular optical indicators  are based on calcium levels and thus provide only a proxy for membrane potential and furthermore they have limitations in time resolution, range and accuracy.
The field, however, is progressing rapidly and I suspect that these challenges will be overcome in the next few years.

What are the best databases to ask such questions?

There are no database yet for C. elegans neural activity,  likely because the number of groups publishing optical recordings in C. elegans is still fairly small. But as more labs pick up the technique, I think the value of a database will become more obvious to the community and the OpenWorm project is providing some well-needed leadership in this area.
Finally, I should point out that in the end we may find that neural activity and connectivity provide only one part of the story. It is likely that in C. elegans neuromodulators and other "unwired" connections between neurons could play very important roles as well.


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What are the mechanisms that cause bananas to ripen? How is or isn't it related to the banana peel ripening?
So recently our commercial kitchen got some bunches of bananas with a curious feature. On the inside they were firm and delicious (no jokes, please), on the outside they looked incredibly sickly. Specifically, they had this grey/green/brownish yellow with lots of black spots, some of them with depth.
Situational details: these are Cavendish bananas, and a weekend of ripening in the open air did nothing for them.
This got us curious about the mechanisms of banana ripening - it's clearly not as closely related to how good the banana is to eat as we previously thought! Can someone explain it more?

Check the situational details I just added.

Ah, not Canarian then. In any case, this question is not really on topic here as it has nothing to do with the underlying biology. I would suggest,however, that you have one half-opened banana, allowing your customers to see that the inside is fine despite the blemishes. If you place the peeled banana next to the others, your customers should see that they should never judge a banana from its peel!

I couldn't find a cooking/culinary/restaurant .SE, so I posted it here as the most relevant field.

Yes, indeed, and you took pains to politely acknowledge the possibility of its not being on topic. My last comment was not a complaint. You could try your luck over at cooking.SE.

If you flag your post, you can ask a mod to migrate it for you.

Actually, I'm going to do it manually, so I can split the topic into the mechanics of it (here) and what other people do to reduce the problem (cooking.SE).

You can get the basic mechanistic details on wikipedia http://en.wikipedia.org/wiki/Ripening - for example fruits are shipped before ripe and then gassed with ethylene. This is a chemical important in apoptosis and ripening processes, it is given off by ripe/damaged fruits. So, what you can do is pick fruit before it is ripe, store it in a cool dark place then when you want to ripen put the desired amount in a paper bag with a few slices of apple.

@rsegal (can I recommend you change this question completely to ask "what are the mechanisms which cause fruit to ripen?" or something along those lines)

I'm closing this as it has been answered on Seasoned Advice


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Why is second pKa value of phosphoric acid different across different sources?
Am I missing something very fundamental here for phosphoric acid's second pKa value?

I check the Wikipedia page and these are the values: (1) 2.148, (2) 7.198, (3) 12.377
Then I check Sigma-Aldrich website and it says: (1) 2.15, (2) 6.82, (3) 12.38

Why is the second pKa value different? Any ideas?
I need to prepare potassium phosphate buffer for my proteins and got stuck with this simple problem.

for the reasons that alan outlines below you usually prepare buffers and then adjust them with a pH meter rather than preparing them from a recipe.

Yes, I did exactly that; I was just curious why there are two different values :). Also, I didn't want to introduce a lot of ions by using excessive acid/base when adjusting pH. It is best to start with the correct recipe to end up with the correct molarities of ions in the solution.

I used to mix 1M stocks of each H2KPO4 and HK2PO4 to avoid unknown NaCl from NaOH and HCl, but this was also wasteful...

Someone will probably come along and move this to "chemistry", but here goes anyway.
The answer is: it depends upon how you measure it.
See:

Jungas, RL (2006) Best literature values for the pK of carbonic and phosphoric acid under physiological conditions. Analytical Biochemistry 349 1-15

The author states that   "..the best value for the true thermodynamic second dissociation constant of phosphoric acid in pure water at 38°C is 7.180, rounded to the nearest 0.005."
He then goes on to re-analyse the data reported in:

Cohn, EJ (1927) The activity coefficients of the ions in certain phosphate solutions: a contribution to the theory of buffer action. J Am Chem. Soc. 49 173-193

and concludes that under physiological conditions of ionic strength and pH the best estimate is 6.795.


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What's the difference between a plant and an animal?
Are there some living things where the distinction between plant and animal is blurry or unclear?  I wouldn't know where to put something like yeast.  I also thought of photosynthesis, but then I heard that some salamanders have photosynthetic cells.  So, what's the difference between a plant and an animal, formally?

Yeast are neither plants nor animals; they are fungi. The old classification where things were lumped into only two buckets - plants or animals - has long since broken down. In fact, even things you might think of as plants, like algae or most seaweed are no longer classified as plants. Under the old system, plants and animals were considered kingdoms, and the latest classifications now divide the Eukaryotes into six kingdoms, but even this is poorly evidenced and facing challenge.
The best method of classification is probably cladistics which is based on the evolutionary history of organisms - but even it has problems when you start considering what to do with horizontal gene transfer and endosymbiosis. Because under a cladistic view, plants and animals are defined not by their features but by their ancestors your question becomes moot, I think.

Just a small addition (with some few examples): According to the new classification by Cavalier-Smith fungi and animals are in the same clade -opisthokonta, whereas plants and some protists like plasmodium, are in another clade called bikonta.
Some unicellular lifeforms have been called algae for a long time but they are close to plasmodium and have obtained their chloroplasts from a secondary endosymbiosis (they actually captured an alga which in turn has a cholorplast). Same is the case with diatoms.

That "photosynthetic" salamander is clearly an animal, with smaller photosynthetic organism living in it symbiotically.
And yeah, cladistis is the way to go.  You build your tree based on DNA, and see if the data lets you group organisms in a useful way. You might find a few organisms whose genome makes them edge cases, but this salamander is not one of them.  Yeast very clearly falls way outside both categories.

Classification is not only based on one or a few features, but you have to consider lots of features in classification of livings. for example plant cells globally have chloroplast, cell wall, and vacuole and have not centrioles. Animals are different in all this features with plants. furtherly plants are autotroph and steady while animals are not. Other organisms are also different in these features or other features with plants and animals.