Why don't protons diffuse out of the mitochondria during chemiosmosis?

Diffusion, is by definition (Ficks Law) describing movement along or against some gradient (here its concentration) even if the mechanism of transport differ: active, passive, facilitated. The setup of the electrochemical gradient across membrane, like any thermodynamic process is not perfect, there are always entropy losses. In this case, this manifests as the the diffusion of protons away from the membrane (one source, there are others). Note the connection between entropy of system (Mitochondria) and diffusion (the inefficient process) in this positive feedback process. I think its interesting as someone learning about this stuff to make these connections.

Recalling protons are being delivered freely into the environment (inter membrane space) by Electron Transport Chain. Some protons will diffuse away from membrane surface before they can be pumped back in since these highly charged species cannot passively diffuse back in. The chemiosmosis process, which is sustained by the energy input to drive ATP synthase, depends on maintaining a strong concentration gradient (separation) of H+ on either side of membrane. Since the outer membrane of the mitochondria is porous, it means the protons are free to diffuse out, and will do so because it is entropically favorable. This relationship is best described by $\ce{\Delta G = RTln(K)}$. Where $\ce{K=\cfrac{[B]}{[A]}}$ for a process $\ce{A \rightleftharpoons  B}$

Where A= Protons near membrane, B= protons diffused out. Having established that thermodynamically they (protons) will diffuse out[3]. It begs the question will they actually reach the outer membrane in a reasonable time.

Of course over long enough time they will. But over some meaningful scale like 1 second, the proton pump rate of ATP synthase, 100s-1 [5], how far can a proton get ideally?.
Back at the envelope calculation (ignoring any resistance effects from solvent, path, etc.) and using some approximate values (for yeast proteins and mitochondria):

From Fick's Rate Law, R,
$ \sqrt[3]{R} = \sqrt[3]{ D A \cfrac{[H^+]_c - [H^+]_m}{d}} = 14 \mu m $

So in 1 s an average proton ideally can diffuse 14 micrometers from the inner membrane, driven by difference in pH between membrane and cytosol. I think i maybe be fair to presume that based on this the mitochondria is leaking protons into into its near surroundings constantly. (for scale the mitochondria is about 100nm).

Hope that was helpful

VALUES:

Thickness of mitochondria,$d$, equal 0.014 $\mu m $ [4]

$\ce{[H^+]_m }$ at membrane = $\ce{-log[H+] = 10^(-6.8),  [H+] = 10^(-6.8)}$ [6]

$\ce{[H^+]_c }$ at in cytosol = $\ce{[H+] = 10^(-7.40)}$

Diffusion coefficient of H+ in aqueous media $D$ = 7000 $\mu m^2$ [2]

A (surface area from which diffusion is taking place) I set to 0.025 $\mu m^2$ (guess from average unit cell of crystallized structure of ETC Complex II in yeast).

REFERENCES:

D. Nelson & Cox (2012). Lehninger, Principles of Biochemistry, 6th Ed
https://esc.fnwi.uva.nl/thesis/centraal/files/f1163457446.pdf
http://www.ncbi.nlm.nih.gov/books/NBKhttp://www.atpsynthase.info/FAQ.html
http://www.ncbi.nlm.nih.gov/pubmed/9245766
http://www.atpsynthase.info/FAQ.html
http://jgp.rupress.org/content/139/6/415.full


The first thing that comes to mind for me is that the transfer seems excessive... isn't histone sub-20 kDa? I have often transferred similar-sized proteins at 4C for 30 min, 30V.

In general, presence of SDS will inhibit transfer efficiency, and increasing alcohol in your TG buffer will counteract the effect of SDS present. Perhaps bring down the methanol to 10%? I would be curious to see that reference regarding the SDS/pre-equilibration, though. That certainly runs contrary to how I understand it working. (Note: I flip-flop between equilibrating or not equilibrated my gels without any observable differences.)

If your acrylamide or ACS had gone bad, your gel wouldn't set.

If you don't already, I'd suggest running a Bradford or BCA on your samples to be sure that you're loading the same amount into each well. Having loaded more into each well could give the appearance of uneven transfer.

To be honest, I don't really see what you mean by uneven transfer, based off the Coomassie and Ponceau. If you're seeing a gradient effect across a large portion of the gel, I would suggest you visually inspect to make sure that the gels you cast are even width all the way across. Having a thicker gel in one place than in another could impact the resistance (heat) in that part of the gel and impact transfer. If you're seeing a lane-by-lane transfer efficiency shift, I would suggest localized pH or temperature changes due to uneven loading of salts, protein concentration, or lipid concentration.

Hope this helps!


Why does the proportion of transposable elements vary so much across species?

I can think of two factors that would influence this, but there are probably more.

1) How do transposable elements (TE) get into the genome in the first place?  The answer is both vertically and horizontally.  Vertical transmission needs no explanation.  Horizontal transmission of TE has been documented in several cases.  In some cases, infectious agents can transfer them between species individuals, for instance, viruses can package transposable elements in addition to their own DNA.

http://www.cell.com/trends/ecology-evolution/abstract/S0169-5347(10)00123-0

2) How efficient can the TE replicate?  For example, in the human genome there are a variety of different types of retrotransposons, but only the L1 element can replicate.  Others like Alu and SINEs parasitize their replication machinery and therefore replicate also but at much lower frequencies.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884099/

So, the difference between species has to do with both of these and probably other factors.  I would imagine in the 2nd case, the selective pressures put upon a given species at any point in time, due to infections or inter-species competition, would surely impact the efficiency of TE replication because they are so important to genomic evolution and adaptation.


What is this yellow sticky excretion from a moth? Details in photos

Some moths exude a yellow lymph excretion when they are threatened.
https://www.nature.com/articles/219747a0
The photo is not very clear, It's difficult to see the species of moth. what did the moth do after? did it fly away? If the moth was looking ill, it could be that it had a parasite.
https://www.insidescience.org/news/meet-moth-produces-both-bird-and-ant-repellants


You seem to be asking if single mammalian cells are capable of intelligence. Yet, in your introduction, you mention that within a cell there are these seven characteristics that are fundamental in defining life. Then, you target more of your supporting quotations and interjections toward the definition of life. Of course cells are alive. You are alive, and so are the bacteria on your skin. Your title question is:

  Is there sufficient evidence that human cells are not intelligent?

You have strayed from your question in your line of reasoning. Let's get back to answering the title question.

Is there sufficient evidence that human cells are not intelligent? The definition of "intelligence" is controversial, but let's look at Wikipedia:

  Intelligence has been defined in many different ways including, but not limited to, abstract thought, understanding, self-awareness, communication, reasoning, learning, having emotional knowledge, retaining, planning, and problem solving.

Human (or any mammalian, fungal or bacterial) cells are able to communicate, and solve problems, but most likely lack abstract thought, understanding, self-awareness, reasoning,  and emotion. Retaining and planning are somewhat more difficult.  Cells are able to retain information about a state of "being" and transmit that to progeny, a recent phenomenon known as epigenetics. Does this qualify as retaining and planning? I don't know. Cells also change based on environmental pressures through stochastic processes (a process known as evolution). Does this qualify as learning? Probably not, since the changes are usually pre-existing. The human equivalent would be finding out that you can swim by falling into water and not drowning. Did the person "learn" how to swim, or did they already possess an aptitude for it?


Where do i find microbes like tardigrades in winter

Tardigrades are best found by soaking moss in water. Even in the winter, under the snow, that is the best place to look. Let tap water sit overnight, uncovered before you add it to the moss to let the chlorine come out. And then strain the water with fine-mesh cloth to see what was in the moss. I would not call tardigrades "microbes" though. Even though "microbes" is not a scientific term, I think of microbes as bacteria, while tardigrades are microscopic animals.


Are the proteolytic enzymes in syconiums and nettles identical to those in rennet?

Rennet is not an enzyme, but rennin is.

Any protease enzyme should be capable of causing milk to coagulate, or prevent gelatin from setting. Examples such as papain and bromelain are all cysteine proteases, and all of them will cause milk to coagulate.

The example of fig protease that you mentioned is a cysteine protease (no specific name found, referred to in scientific literature as fig protease). Nettles are a highly polyphyletic group, and the specific enzyme cannot be named without a more specific phylogenetic group being identified.


ID of this flower/plant and origin if possible

Look like a Spider lily (Lycoris radiata):

Source: NC State University


Rabies causes hydrophobia in the encephalitic stage which means when it affects the brain and causes swelling and inflammation of multiple areas of the brain. Hence, it affects the complex areas in the brain needed for swallowing. Initially into the course of the disease, the patient has involuntary contractions of neck muscles when he drinks water.  At later stages of disease, the patient starts contracting his muscles even at the thought of water. Rabies virus is a neurotropic virus which means that it travels through nerves because of its preference to attach to acetylcholine receptors in the neurons.  That is how the virus spreads from the bite site to the brain(via the nerves).


How do seagulls know it is the 9th inning at a baseball game?

Many animals, particularly some birds, are smarter than we give them credit for. Corvids, for example, are known to not only use tools, but are capable of planning and understanding some cause-and-effect scenarios that require patience.

I know practically nothing about baseball, but if it's like any other human gathering, there are probably a lot of clues that the birds learn:

Noise levels. Big events often culminate in some big fanfare with noise (cheering, music, etc.). If the game changes audibly near the end, you can bet the birds have noticed.
Motion/activity: Any large gathering I've ever gone to often has a small percentage of people leaving early because they want to avoid the crowd or traffic. I'd expect a close-scored game has fewer people leaving, but chances are good that as enough people start getting up to leave, it's another signal the birds can use.
Discarded food: Aside from getting up to leave, toward the end of an event many people will start discarding snacks and drinks. Hopefully in the correct bin, but often just on the ground (humans are messy -- which seagulls love). An increased number of people tossing garbage into bins (and missing or they start overflowing) signals a few gulls that there's scraps to be found.
Temporal.  If these events happen regularly, or even irregularly, the birds associate it with food. People filling a stadium or parking lot, playing music, buying food (birds do have a sense of smell, though not as developed as mammals), etc. The birds over time learn: Increased human activity at this location results in more food some hours later.

Gulls are very gregarious, and notice when just one bird has found a morsel. As soon as a few birds get the first discards, the rest of the flock notices and starts to mobilize; circling and calling.

I would argue that the birds don't really know when a game or event is about to end, but they are adept at reading their environment, even if it's an urban one.

Per @theforestecologist's comment, references are requested. While I do not have a reference for each specific behavior described above, the following list covers avian intelligence generally, learning and problem-solving, and physiological adaptations. Many of the described behaviors are products of associative learning and elaborate communication, traits that gulls exhibit in other activities such as dropping clams from heights.

References:

Ravens parallel great apes in flexible planning for tool-use and bartering
Can Kabadayi, Mathias Osvath
Science; 14 July 2017, Vol. 357, Issue 6347
Ecology and Conservation of Birds in Urban Environments
edited by Enrique Murgui, Marcus Hedblom
Springer Nature; 10 February 2017
Cognitive ornithology: the evolution of avian intelligence
Nathan J. Emery
Philosophical Transactions of the Royal Society of London; 7 Dec 2005, Vol. 361
Bird Sense
Tim Birkhead
Bloomsbury Publishing; 2 Feb 2012
Auditory and visual mechanisms in food-finding behavior of the Herring Gull
Hubert Frings, Mable Frings, Beverly Cox, and Lorraine Peissner
Wilson Bulletin 67; January 1955


What is going on with these buccal epithelial cells?

The cell you've marked "B" is dead, as is common in cells in a saliva sample. The particular path to cell death is very hard to say with an unstained light micrograph, but the fact that you have a dead blebby cell in a saliva sample is not diagnostic or indicative of anything.


Why is sexual reproduction so much more common than asexual (in macroscopic organisms)? Fundamentally, what makes it better?

Genetic diversity is needed to prevent everyone from dying of the same disease. This is the problem with monocultures. Higher organisms are more susceptible to disease and thus reproduce sexually.

Furthermore, basically all organisms exchange DNA so they are effectively sexual.


Why "broad" instead of "large" cross-immunoreactivity?

Broad means wide as in a wide range. Normally, antibodies have one epitope they recognize, i.e., one specific target; they are said to have a narrow range of targets.

Some antibodies, however, recognize multiple targets, i.e. the number of targets they recognize is larger and their target range is widened. They are said to have a broad cross-immunoreactivity.

A 'large' cross-immunoreactivity, however, is ambiguous, as 'large' can also imply 'large reactivity', and then 'large' becomes synonymous to 'strong'. Wide is unambiguous as it always implies a large range.


Can anybody identify this kind of plant?

I think this is some kind of Hypericum.  In Costa Rica and the Andes there is a high altitude ecosystem called the paramo in which shrubby Hypericum are characteristic species.  The area in your photo looks to be covered with shrubby species, and you are at decent altittude.  Looking at your picture (at full size) the leaves look approximately decussate which is typical of the genus, and also, the stems are ridged which is also pretty characteristic.

There is a good paper here on Hypericum of the Mediterranean region.  It mentions some groups that are shrubby or dwarf but thus far I have not been able to find a species that looks just like your picture.

Update: Possibly it is Hypericum aegypticum which looks about right relative to your picture, esp, the leaf color and size.  Also known to grow at that altitude. Decent picture here plus the one at Wikipedia both look similar to yours.

Update 2: On fresh look, the bases of the leaves for Hypericum aegypticum don't compare well to your picture, but I still think it is a Hypericum.


Enzyme Assay, absorbance change to concentration change

see here.

y-intercept = $\frac{1}{V_{max}}$

To convert absorbance to concentration, plot the standard curve and get the linear relationship between the two quantities. Make sure that the line that you fit (for standard curve) passes through origin.


How can I label cryotubes in a way that eliminates the problem of legible hand-writing?

This is indeed a problematic point. I have been using machine printed labels for a while now (sometimes with some extra scotch tape around it to prevent it from falling) off, which worked pretty nicely.

However, there is a printer available on the market (though I haven't tested it yet) which claims that they can print on any tube. This printer is called Tubewriter, which is probably also worth a look. The backside is the price, Fisher Scientific lists them around 40.000$, which will make them unavailable for most labs, except for cell banks etc.


When someone gets infected with influenza, and gains some immunity, is that immunity just as good as getting it from a vaccine?

Natural infections almost always yield a better immunity than that acquired through vaccination. However, vaccines yield a better immune-response than getting infected with influenza. That is so to say the side effects.
I want to backtrack to part of your questions where you say I'm sure the immune system will "remember" that particular strain just as well as getting a vaccine. and add a little bit of interesting information regarding influenza.
Some Influenza (A) stereotypes that infect humans are: H1N1, H2N2, H5N1, etc...
The H stands for Hemagglutinin and N is Neuraminidase. These are important in vaccine development. The H and N are proteins located on the surface of the virus and allow for entry into a cell for infection.
Strains are classified according to their hemagluttinins and neuraminidases. Every year when the vaccine for the seasonal flu is developed we don't know with 100% certainty which strain might be the most prevalent. Rather, surveillance data is used in deciding which flu might be the most prevalent. More info on the CDC Website.
So back to the question:

Does the immune system remember that particular strain just as well as
getting a vaccine?

Yes it does and there's a paper in PNAS that looked at something similar. This is related to something called “Immunological Honeymoon”. A theory that the first infection during childhood provides stronger immunological memory than a later infection.

The paper found that people who were 28 year old were more susceptible to the Spanish Flu (H1N1) in 1918 because they had been exposed to the wrong virus as children.
The elderly, however, had been exposed to H1N1 as children and were well protected. People who were middle aged or in their teens in 1918 had been exposed to H1N8 as children and were partially protected.
This I recon is just as good as vaccine, but more to show that the immunity acquired through infection is, in fact, remembered. For how long? That's a totally different question that varies from infection to infection. Some are life-long (such as measles), other are short lived requiring re-infection, or booster shoots in case of vaccination.


Colonial Cells Demonstrating Cell Specialization

Probably not what you are looking for but the protozoan slime mold Dictyostelium discoideum lives as free amoebae which can coalesce into a multicellular migratory slug that eventually forms a fruiting body in which some cells form the stalk while others form spores.

Slug formation is by chemotactic signalling with cyclic AMP as the signal. I seem to remember that there is a predatory species of slime mold which uses cAMP to attract D. discoideum as prey, but I can't bring the name to mind and have failed to find it online.


How to write a palindrome sequence as-wish (create, theoretically) ? (self-answered)

I once developed a method, but it is so-basic and simple that I'm pretty sure it is already discovered. Here I "shared my knowledge, Q&A-style"

Step-1

Write a small sequence randomly.

    5'... A T G C C

Step 2

Write the sequence in opposite-direction, on the next line. It will end at just at the next-place of last place of previous sequence, i.e.

         -------->

   5'... A T G C C

                        C C G T A ...5' .

                    <-------------

Step-3

Fill-in-the blanks following base-pair rule, and the sequence is now ready.

5'... A T G$\:$ C C$\:$ | G G C A T ...3'

3'... T A C G G | C C G T$\:$ A ...5'

Addendum (courtesy: user@Another'HomoSapien')

The previous method was similar way we usually read a verbal palindrome (though unlike a verbal palindrome, any reflection-symmetry was Not present ). But  there is a rotational-symmetry (2-fold), (rotational symmetry means it contains parts which are superposable on rotation).

So we could create a palindromic sequence using rotation also.

Or could rotate pre-filled up sequence (if exactly follow the user's instructions)

The brown dot indicates the axis of rotational-symmetry of the written-sequence, vertical to the plane of paper.


I just saw this bird outside my apartment. Anyone know what it is? (Texas, US)

It is American Woodcock, Scolopax minor.

  Superbly camouflaged against the leaf litter, the brown-mottled American Woodcock walks slowly along the forest floor, probing the soil with its long bill in search of earthworms. Unlike its coastal relatives, this plump little shorebird lives in young forests and shrubby old fields across eastern North America. Its cryptic plumage and low-profile behavior make it hard to find except in the springtime at dawn or dusk, when the males show off for females by giving loud, nasal peent calls and performing dazzling aerial displays.

The newborns are even more camouflaged in downs.

References:

Audubon
All about birds


Lab technique to distinguish between single stranded and double stranded DNA?

Single and double stranded DNA have different electrophoretic mobilities, ssDNA will move faster on an agarose gel, so if you know the length of your DNA and it moves further than you expect
 relative to a dsDNA ladder it's probably ssDNA. The hyperchromic effect means that ssDNA also absorbs more strongly than dsDNA, so you can heat up your DNA and if the absorbance changes it was dsDNA and if it doesnt then its ssDNA (you should take an aliquot for this so that you have the rest of your sample in tact). You could also take an aliquot and add a single stranded exonuclease and run the products on a gel together with the DNA before the digestion, if nothing is present after in the digested well then you had ssDNA if there is still a band after then you had dsDNA (i don't think this method is really used as you could just run it on a gel which is simpler and you lose less sample, but it should still work).


Why is the Tm defined as the temperature at which 50% of dsDNA has changed into ssDNA?

If you search for DNA melting temperature plots you will see they have a sigmoid shape. It's common for those kinds of plots to be described by the 50% value for example the therapeutic index and the 50% lethal dose of a substance (LD50). This is because at really low and really high temperatures all DNA molecules become dsDNA or ssDNA respectively so that information is not really useful. You could maybe talk about the first temperature at which DNA becomes 100% denatured but the curves are highly nonlinear at that region so it's difficult to quantify. The 50% is an easy way to compare different molecules since that region is usually linear and easy to compare in a meaningful way (basically all molecules have the same ends of the sigmoid shape, but it's the middle part that changes the most).


How does axon guidance system precisely targets specific axons?

In a nutshell, I would say neurons do have "specific instructions."  However, it isn't so much "ignore netrin X amount then stop."  It's more like "express receptors 1, 30, 48, and 62" which as a unique combination gets the growth cone where its going and prevents it from forming an erroneous connection along the way.  I've provided more context below that might help this make more sense.

A number of factors come into play with proper axon pathfinding and guidance, but I think the two below are sufficient for this:

There are different receptors present or absent on the cell surface depending on what cell type it is, which allows different cell types to respond only to specific cues. However, most developing axons express multiple types of receptors, so they can respond to multiple guidance cues (or respond to a cocktail of different cues).
There are non-diffusible signals present along the path in which the axon is growing.  You can read about one type here: https://www.nature.com/articles/nn.2231.  The main point about non-diffusible cues is that they can either stabilize the growth cone (which might promote growth or initiate the formation of a synapse) or they can repel the growth cone.  Therefore, they play an important role in informing the growth cone what is and is not the proper target.

There are now two things from your question should bring it all together.  First, you state that the precise path comes from a "specific combination of AGMs."  Exactly! The key word here is "combination."  Because there are so many AGMs that can affect the growth cone in so many ways, the combination of receptors (and intracellular secondary messengers) expressed on the growth cone and how they work in concert is what's critical.  Second, you state that growth cones will "ignore" potential targets as they pass them by.  That might sort of be the case (i.e., if a growth cone doesn't have a receptor for something the target is expressing, it won't "grab onto" or respond much to its presence).  However, it may also be that these potential targets express some non-diffusible cue that repels the growth cone, and it doesn't recognize that spot as a its final destination.

This article can also help provide more insight on the nuances of axon guidance:  https://dev.biologists.org/content/145/10/dev151415.long


A missing endogenous retrovirus in humans, but present in gorillas and chimpanzees?

I think your question boils down to:

Why do modern chimpanzees contain endogenous PtERV1 whereas humans do not?

This is discussed in the original research article:

Kaiser SM, Malik HS, Emerman M. 2007. Restriction of an Extinct Retrovirus by the Human TRIM5α Antiviral Protein. Science 316(5832):1756-1758.

PtERV1 was active after the phylogenetic split of humans and chimpanzees, so any infection would be from separate events. In other words, the endogenous virus was not inherited from a common ancestor:

  Comparison of individual PtERV1 proviruses in gorilla and chimpanzee genomes suggest that this virus was active 3 to 4 million years ago, after the separation of chimpanzee and human lineages.

They hypothesize that modern humans evolved from ancestors that were protected from PtERV1 by TRIM5α:

  Although we cannot rule out the possibility that PtERV1 never infected human ancestors for other reasons, our data do suggest the possibility that TRIM5α was fixed in human populations because of its ability to confer protection against PtERV1 and that modern humans have descended from ancestors who resisted infection.

This does raise the question of why humans were not infected whereas chimpanzees were, despite both containing PtERV1 restricting TRIM5α. This seems to be out of the scope of your question, but they do talk about it in the article if you're interested.


How are lipid-coated mRNA-based vaccines transported into cells for expression?

I can't give an authoritative answer on this because my PhD work was based on mRNA delivery using peptides instead of lipids, but many of the concepts are the same. I also don't have time to provide proper citations, but this is probably too much for a comment.

Anyway, mRNA is a very fragile molecule, it can be broken down extremely quickly in the blood by serum nucleases. Therefore we must protect the mRNA by mixing it with some other chemical, in this case a mixture of positively charged lipids. The positively charged lipids are attracted to the negatively charged phosphate backbone of the mRNA, and form a nanoparticle trapping the mRNA inside and hiding it from the nucleases. The lipids are often, but not always, PEGylated, which means that a molecule of polyethylene glycol (PEG) is attached to the lipid. The PEG groups form a layer on the outer surface of the nanoparticle that helps prevent protein binding.

These mRNA lipid nanoparticles are then injected into a patient. This will probably be an intramuscular injection so that the particles are most likely to be taken up by muscle cells. The exact mechanism explaining why lipid nanoparticles are attracted to cells isn't entirely clear, but it's likely a combination of electrostatic attraction between the positively charged nanoparticle and the negatively charged cell membrane and proteins that bind to the nanoparticle and are then recognized by receptors on the cell surface.

After the particle is taken up by a cell it is usually trapped inside a membrane-bound structure called an endosome. As the endosome matures it is acidified, and as the pH drops from about 7 to about 5.5 the nanoparticle is disrupted. The lipids that made up the nanoparticle can merge with the lipids that make up the endosomal membrane, disrupting that membrane and breaking open the endosome, allowing the mRNA to escape into the cytoplasm.

Once in the cytoplasm the mRNA will find a ribosome and produce protein. Just like you said, the protein in this case will be membrane bound and expressed on the outer surface of the cells for eventual immune recognition.


I presume you are talking about Peperomia pellucida. It is called  Mashithandu in Malayalam.

Reference: Wikipedia

You might like to go through this.

  Description

  Delicate, glabrous annual herbs; stems erect, 5-30 cm tall, pellucid,
  branched when well developed.

  Global Distribution

  Native of Tropical America; now Pantropical

  Indian distribution

  State - Kerala in all Districts


Question regarding when it's a homoplasy in a phylogenetic tree

Phylogenetic tree vs first generation offspring

Please note that on a phylogenetic tree, the time scale is big enough so that the generation time is completely undistinguishable. Hence, questions of first generation offspring won't rise. Also, in practice when reconstructing a phylogenetic tree, our level of accuracy does not allow us to distinguish exactly at what generation did specific mutation occur.

Rephrasing your question

The term homoplasy is typically used in the context of phylogenetics. Also, most of the time the term homoplasy refer to phenotypic trait and not to genetic sequence but I will not go into these specific complications here. The term is also mainly used in intro textbook and not so much in the peer-reviewed literature. In all cases, one can define the concept of homoplasy as a shared trait that is caused by a mutation that is not identical by descent. In other words, if in two lineages/individuals that share the same trait, the trait is caused by the same mutation(s) (same, not only by its state but by descent), then the shared trait does not represent a homoplasy.

With this, I can rephrase your question as

  If two siblings share a (heritable) trait that the direct parent does not have, are the traits identical by descent?

If two siblings share a (heritable) trait that the direct parent does not have, are the traits identical by descent?

Well.. it depends as to whether the mutations happened happened twice independently in the two different gametes or if the mutation happened once in the (germ line) lineage that gave rise to these gametes in the parent body.

The second is much more likely. Because, it is very unlikely for the same mutation to happen twice independently in two different gametes for the same individual and much more likely that the mutation happened once in a cell that gave rise to the two gametes, it is very much more likely that the shared trait among the two offsprings is caused by a mutation that is identical by descent. Hence, not a homoplasy.


Mutation Rate in Multicellular Eukaryotes

The real mutation rate of any organism depends by too many factors both external, like the environment, and internal, like the error rate of the DNA polymerases and DNA-repair enzymes and even from different region in the same genome (the mutation rate of non-coding DNA tend to be higher than the one of actively used DNA).

In general however it is possible to determine an average mutation rate for a given organism and usually it is expressed in mutation per base pair (or single nucleotide) per generation.
If you want to know roughly the mutation rate per gene or per genome you just need to multiply the mutation rate by the number of bases of the gene or genome.

Good papers on the topic are:

  Drake JW, Charlesworth B, Charlesworth D, Crow JF (April 1998). "Rates
  of spontaneous mutation". Genetics 148 (4): 1667–86.

  Ossowski S, Schneeberger K, Lucas-Lledó JI, et al. (January 2010).
  "The rate and molecular spectrum of spontaneous mutations in
  Arabidopsis thaliana". Science 327 (5961): 92–4.

  Nachman MW, Crowell SL (September 2000). "Estimate of the mutation
  rate per nucleotide in humans". Genetics 156 (1): 297–304.

If you want to know about some specific organism you have to dig into the literature...


How do individual plants adapt to changes in temperature?

As far as I know, the main challenges the plants have to face in cold environment are metabolism reduction and membrane fluidity. If the temperature is even lower, they may face freezing.

Increasing the metabolism is quite hard, because plants usually are unable to increase their temperature by its own. Plant may produce more pigments in order to absorb more sunlight; grow trichomes and other structures that may generate an air layer which acts as an insulator or simply reduce its metabolism by, for instance, hibernation. The amount of stomata is also related to temperature, and a plant growing in low temperature needs less stomata.

In bacteria sometimes there exist isoforms of many enzymes that are expressed during different conditions, and since plants usually have large genomes with tons of duplications, it's reasonable that some plants may express different genes for the same processes in high and in low temperature. One group of genes that are certainly expressed in cold exposition are membrane desaturases, which introduce unsaturation in the lipids, increasing the fluidity of the membranes. Some plants also protect themselves of freezing by accumulation of some substances, such as glycerol or proline, avoiding the formation of ice inside the cells.


Most well studied termite species or a species that I could use to compare termite genes for functional annotation

Apparently, the most closely related insect to termites is cockroaches. Interesting article I found on the subject. However, that still didn't help because cockroach genes are not included in the STRING database.


I suspect this question is a lot easier than it makes itself out to be, though I may not be thinking straight. It doesn't matter how many cells you start with or how many doublings there are. Nor, for that matter, does it matter how many genes each cell has. There's a 2% chance that a random mutation will affect "crucial genetic information"; I must assume that that refers to genes. So $0.02*4000=80$ mutations would be expected to affect genes.


Is the theory of evolution being disproved by bats?

Take a look at this little fellow:

It's a flying squirrel — a shy little nocturnal rodent which lives in trees and, despite its name, does not actually fly.  It does, however, have a skin membrane called a patagium between its fore and hind limbs which allows it to glide from tree to tree and thus evade ground predators.

It's not hard to see how the flying squirrel's patagium may have evolved: after all, ordinary squirrels, to which the flying squirrel is indeed related, also spend most of their time in trees and avoid the ground, often performing quite impressive leaps to cross from one tree to another.  With sufficient pressure to minimize time spent on the ground, any little morphological changes that allowed longer leaps would be favored by natural selection.

Indeed, there are plenty of other groups of mammals which have independently evolved very similar adaptations to gliding.  Given how many small arboreal mammals there are, this is perhaps not surprising.  What's special about bats is not the fact that they possess flight membranes — it's that they're the only group of mammals, so far, to have taken the next step to actual powered flight.


What is this plant, and should the lowermost leaves be curling up?

I may be wrong, but I believe these are two Foxtail Agaves (Agave attenuata). These resources may help you take care of them.
Foxtail Agave Care Information
And for the wilted leaves:
How to Save a Dying Agave Plant
Also, the Gardening SE may be able to help more.
Hopefully this helps!


The front end of the plastron (the flat 'ventral' part of the shell) is hinged, so that the turtle can enclose itself almost completely, a characteristic of box turtles.

  Box turtles are turtles of the genus Terrapene native to North America (United States and Mexico). They are also known as box tortoises, although box turtles are terrestrial members of the American pond turtle family (Emydidae), and not members of the tortoise family (Testudinidae). The twelve taxa which are distinguished in the genus are distributed over four species. They are largely characterized by having a domed shell, which is hinged at the bottom, allowing the animal to close its shell tightly to escape predators.

Your turtle certainly has a domed shell. There is a lot of wear and tear on the shell, but not so much on the plastron. Box turtles can live 100 years.

From the lack of coloration on the top part of the shell and the paucity of markings on the plastron, I think it is either a Three-toed Box Turtle (Terrapene carolina triunguis), or a Mexican Box Turtle. The Mexican box turtle can grow slightly larger than the Three-toed box turtle. I can't really tell them apart. Boxturtles.com might help.

  Their appearance is similar to that of the Three-toed Box Turtle.

The three-toes refers to the hind feet (which can also have four toes, to make matters worse.)

  Three-toed box turtles have a domed shell which grows to an average 4.5 to 5 inches in length. The record shell length for this subspecies is 7 inches. The highest part of its carapace or upper shell is more posteriorly positioned than in the other subspecies. The dorsal and limb coloration is commonly completely absent, although some dark blotches are common in adult turtles. These areas more often being a uniform olive green or tan color.

From another site:

  Shy and quiet are the traits of a Three-toed Box Turtle, both in its personality and in its coloring. Unlike the bold patterning and color seen on other eastern box turtles, the color of this species is quite subdued. Occasionally there will be a Three-toed that is more brightly colored, but for the most part they are a fairly uniform olive-brown to brown or horn color.

See also Reptiles & Amphibians


Exercise causes number of cell divisions to approach Hayflick limit faster? And hence shorten life expectancy?

Following damage to muscle (e.g., as a result of strenuous activity) the injured fibers are removed (by immune cells) and then replaced by new myofibers (individual muscle cells that join to create new muscle tissue). This is why for a few days after exercise your muscles can be sore - it is the tissues being initially cleared of damaged cells and repaired.

Muscles, like other tissues, have resident stem cell populations ("satellite cells") that are used to replace damaged cells.

Stem cells have potentially indefinite replicative potential, as they express telomerase and thus do not have a traditional Hayflick limit.

Volonte D, Liu Y, Galbiati F. The modulation of caveolin-1 expression controls satellite cell activation during muscle repair. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2005 Feb;19(2):237–9.


Issue in your introduction

I thought that massive changes among organisms are over long periods of time.

Actually, some evolutionary events can happen on a very short time scale. A single mutation can have a massive impact on the phenotype of an individual (see for example Doebley 2004). If this new phenotype has much higher fitness, then the mutation might spread over the whole population in a matter of weeks (typically if the population is not too large, without barriers to gene flow and more importantly if the generation time is short).

This is caused by, to my knowledge:

Evolutionary pressure

Natural/artificial selection

Non-detrimental mutations

The term evolutionary pressure typically encompass natural and artificial selection, mutations (regardless of their mutational effect, that is regardless of whether they are beneficial or detrimental) and other processes that you don't mention (such as genetic drift for example; you have now edited your post to include drift).
Answer to your questions

Will mutations be the only factor in human change?

By "human change", I will assume you mean "human evolution". The answer is: no, mutations are not the only process that leads to human evolution. All standard evolutionary processes are at play in humans as they are in other species. You might want to have a look at the posts Human Evolution in Modern Times and How is evolution possible in contemporary humans?.

Will humans change at all over a long time?

Yes, humans are currently (and will continue to do so in the future) evolving. Again, you might want to have a look at the linked posts.
Want to know more?
Your questions are quite introductory and show a number of misunderstanding you have about evolution. I would recommend having a quick look at Understanding Evolution by UC Berkeley which is a very introductory course to evolutionary biology that is fast and easy to follow.


This article claims that ants do sense approaching rain and modify their activities in preparation. The claim is not sourced. This weather site also speaks of ant mound-building before a rain but frankly places it in the "some folks say" category. The AntBlog is associated with AntWeb, a large multi-university-affiliated database. The author of the linked blog states that ants can sense humidity with their antennae, which strikes me as a plausible means of anticipating rain.

That ants might sense changes in barometric pressure is an intriguing idea but has not to my knowledge been demonstrated.

A 2010 article in Journal of Neurophysiology reports an almost unbelievable sensitivity to temperature in ant antennae, allowing them in principle to sense minute temperature changes ($0.005^o$C) over a wide range of temperatures and over 0.2 second time intervals (5Hz). This is said to assist them in orientation in their microenvironment but I think it goes a long way to accounting for an ability to detect looming weather fronts. Humans can sometimes 'smell' rain and we can detect gross temperature changes that almost always accompany rain, but to be able to detect humidity and micro-scale temperature changes would give the ants a real advantage in forecasting. After all, not all rainstorms are preceded by a dramatic drop in temperature but probably the majority are preceded by minute step-wise drops in temperature that evidently the ants can sense.

So while I think the building activity may be anecdotal (and probably true for some species) the ability to sense humidity changes and micro-scale temperature changes accounts for their ability to sense rain ahead of time.

Ants are very well-studied and it's hard to rule out that one has missed something. There are a few "ask the expert" questions on this topic online and no one seemed sure.


Once food has been properly cooked is it absolutely safe?

No, no food is ever 100% safe, Prions for instance can survive anything short of incineration, spores can land on food in the transition from oven to wherever, some bacterial spore can survive high temprature, ect.


Cloning DNA fragment - at least trying to

The fragment size itself shouldn't be a problem in principle.

Cloning has many steps, so anything you didn't specifically test could be causing problems. If different vectors are also not the problem, you should probably look at your experimental steps:

One problem can often be residual EtOH from cleanup steps, which will make your ligation and transformation very inefficient.
You should also test your competent cells with another plasmid to be sure, that they are still viable
Have you checked that all fragments run at the correct size on a gel? You might have star-digestion or bound enzymes that cause problems. Additionally you could also check the ligation product on a gel (though you won't be able to use that for transformation), to see if the reaction works correctly


Does too much Genetical Modification leads to formation of new species?

yes it possible, in one article show a study for Mycoplasma genitalium which have 525 gene, however only 382 genes are essential for biological functions, they take out the nature gene and place the ' artifical gene' which synthsis in vitro, to test if the M. genitalium will survival when the No. of gene lower than 382. If it survival it will be a new species.


Is the male bee's penis homologous to the female bee's stinger?

After a little bit of digging I was able to find a couple of facts that seem to verify that the drone bee's penis is in fact homologous to the worker bee's stinger:

This Wikipedia article about the stinger that says a honey bee's stinger is "a modified ovipositor as in other stinging Hymenoptera".

This book (actually about soil arthropods) states very specifically that, "The ovipositor, with which the female lays her eggs, is homologous to the male's penis.".


How can I determine the sex of a tree seedling?

There is absolutely no way to tell to be honest because mulberry trees have the capability of changing sex (reference). From a paper titled "Diversification of mulberry (Morus indica var. S36), a vegetatively propagated tree species", I quote

  The sex expression of plants appears to be a function of hormonal
  control; there seems to be evidence that dioeciously plants (male and
  female reproductive organs on separate plants) are potentially
  bisexual and that a delicate internal hormonal balance results in one
  sex "over-riding" the other. A traumatic incident might, therefore,
  act by temporarily upsetting this balance, which is later restored in
  a way that leads to the opposite sexual character being manifested.
  Another pointer in this direction is the fact that a variety of
  artificially applied chemical substances has been shown to affect the
  sexual expression of a significant number of different plants. It is
  also reported that some chemicals known as the steroid hormones might
  be a major key to the sex expression lock. Thus, it is
  possible that to "create" a new sex in a plant by either a physical
  shock or a controlled chemical process

They could also have male and female flowers (monoecious) on one plant with most of them being self pollinating (references).

So, in effect, nurseries that are advertising these trees by sex are ignorant or quite plainly taking people for a ride. I would suggest that you plant your seeds and don't worry about it too much since they have the ability to self pollinate. If by bad luck, you find them all male/female or are not pollinating to your liking, go for a tree sex change after consulting an expert on the topic. Here is a basic guide to identifying between male and female trees/branches (reference)

White mulberry male flowers (reference)

red mulberry female flowers (reference)


Do non-human animals suffer from insomnia?

Insomnia most certainly occurs in other animals. One interesting example is the case of insomnia in Drosophila melanogaster. In this study 3 day old male and female flies that demonstrated reduced sleep time were crossed together over 60 generations to create flies insomnia-like (ins-l) that sleep less than 60 minutes a day compared to 800 min a day in their control flies, which are generation 0 (Fig 1B). These (ins-l) flies exhibited difficulty initiating sleep, maintaining sleep and showed cognitive impairment. They also had difficulty maintaining balance with elevated levels of triglycerides, cholesterol and fatty acids and although their core molecular clock remained intact, ins-l flies lost their ability to sleep in constant dark. Using whole-genome transcriptome profiling using Affymetrix high density nucleotide microarrays, these flies are compared against the control flies and many genes were over-represented (changed in expression compared to control flies) which are involved in metabolism, neuronal activity, behaviour and sensory perception with changes in lipid metabolism and synaptic transmission being consistent with increased adiposity and learning defects in flies. In addition, these ins-l flies were hyperactive and hyper responsive to environmental simulations and the over-representation of genes associated with sensory perception suggests that hyperarousal in insomnia may be attributed to increased activity in the sensory system and that these processes are under genetic control. Two genes in particular Filamin-A (Cheerio) and Malic enzyme (Men), which were found to be differentially regulated (changed in expression) in files are also modulated (changed) by sleep loss in humans, showing that the same processes are involved/get effected in humans and flies during insomnia.

The research above clearly demonstrated the genetic regulation and effects of insomnia in other animals and shows that its not just a human dysfunction.


Why lab technicians use indirect (antibody reaction) method for diagnosing?

Short answer: Antibiotic treatment is important because the body can't always keep up with the infection even if it has launched a response.

Background:

First, let's look at what the antibody reaction method is actually doing.

Taking a sample of blood or body fluid
Testing the sample with known pathogens - viruses, bacteria, fungi, etc.
Identifying which infection causes a reaction.

This allows us to determine which infection we are dealing with. This can be especially useful when the infection is hidden in a place we are unable to easily swab - the stomach, heart, a small wound that has already healed. Sometimes this test is just used to monitor how well you are fighting the infection, but it also allows them to evaluate what the best course of treatment is for you. (Reference 1)

Just because the body has an immune reaction doesn't mean that the body's immune system can actually finish the battle against a disease. In the example case of Strep A, you may be able to get over the infection yourself but it will take longer than if you are prescribed antibiotics against it.

See this question on the CDC:

  Q: How common is invasive group A streptococcal disease?

  A: Approximately 9,000-11,500 cases of invasive GAS (Group A Streptococcus) disease occur each
  year in the United States, resulting in 1,000-1,800 deaths annually.

Note that invasive Strep A usually infects children, elderly, and  immunocompromised people (anyone with a weaker immune system typically).

Unless you have absolutely no immune system at all, there will be an antibody response put out by your body. The NHS goes into detail about different parts of your immune system.

Recall also that Strep A (our example) could divide faster than the body can keep up with. So we would need antibiotic help to fight the disease. Using the "indirect" method we can find a hidden infection.

According to the NHS the antibiotics put a stop to growth and spread which allows the body to come in and finally finish them all off, or they disrupt a process the bacteria needs to survive and kill the infection for the body. Thereby helping the immune system (the body's best line of defence) finish off the infection when it couldn't do it on its own.


By what mechanism does coeliac disease cause excess fat in the feces?

Coeliac disease is an immune disorder resulting from a reaction to ingested gluten (a protein found in wheat, barley and rye). It is associated with inflammation of the small intestine resulting in a generalised reduction in the capacity for digestion and absorption. According to this paper:

  Celiac disease is associated with pancreatico-biliary disease. Postulated mechanisms include reduced gallbladder emptying due to impaired cholecystokinin release and pancreatitis due to malnutrition.

Cholecystokinin is a peptide hormone that is produced by specialised cells in the small intestine and which stimulates the production and release of pancreatic enzymes and bile. Digestion of fat is critically dependent upon the emulsifying properties of bile salts in bile, together with pancreatic lipase. Any breakdown in this stimulatory pathway would result in reduced capacity for digestion of dietary fat.

Failure to digest fat results in fatty stools (steatorrhoea) which is one of the classic symptoms of the disorder.


Cell-level selection and inheritance of acquired mutations

In any reproductive event, we transmit new mutations to the offspring. In absence of cell-line selection, whether the mutation occurred during a meiosis or a mitosis is of little interest.

In absence of cell-line selection

A big difference between acquired mutations and Lamarck's acquired inheritance is that under Lamarck's view point, characters are being adaptive. Under Lamarck's view point, individual try to perform some action, stretch their muscles and other organs toward what is optimal for their needs and this phenotypic modification is being transmitted. The classical example is the example of giraffes. Giraffes stretch their neck trying to reach for high leaves, their neck is getting longer and their longer neck is being transmitted to their babies.

With acquired mutations, in absence of cell-line selection, there is no reason for adaptive mutations to be transmitted more often than non-adaptive one.

With cell-line selection

Now, if there is cell-line selection, beneficial mutations (beneficial at the cell level) are more often transmitted. The mutational process itself stil remain "random" (see Are mutations random?) but selection will increase the ratio of beneficial to deleterious mutations. Now, mutations that are beneficial at the cell level are not necessarily beneficial at the organism level. A typical example is cancer.


To answer your second question, one of the main reasons primers anneal before your target re-anneals to itself is not because it binds stronger, but because you add primers in large molar excess to their targets.  The primers will find your template faster than your template will find another matching template, and once the primer is annealed the template cant bind onto another template even if that reaction is more energetically favorable.  This molar excess is a requirement for the exponential amplification in PCR, and when you start to lose the excess primer concentration you lose exponential increase due to your targets re-annealing (and you get the production of unwanted PCR artifacts like chimeras).  As for the temperature, it depends on your template, but I guess it has to be somewhere between the primer annealing temp and the temp of your melting step.


How do polygyne Carebara affinis or C. diversus (a.k.a. Pheidologeton affinis and P. diversus) colonies work?

I don't know about their polygyne nature, but carebara diversa queens are between 20-25mm and carebara affinis queens are between 14-16mm and are slightly lighter in colour. Hopefully that should help you identify them.


If what you trying to get is 1kbp of repetitive 150bp sequences, then synthesis as a large chunk might be better idea. It costs ~150-300$ but will potentially save tons of time. (see gBlock from IDT in US)

PCR and ligation with repetitive sequences is pain the butt. It might be true that you save money, but time and frustration could be more expensive.


Does a presence of ants on a plant mean that the plant has been infested by aphids?

Simple answer is no:

$Ants \neq Aphids$

However, they could be used as evidence that aphids are there depending on the reliability of the coexistence. Ants and aphids are independent entities and do not rely on each other so can exist in non-overlapping populations. Applying this idea to the correct species of ant and aphid is, of course, important for it to work as an indicator - it will only be true in those combinations where this "aphid protection" occurs.

I can't find any information on the reliability of the relationship, especially not knowing which species you are looking at. If there was a high positive correlation of ant density and aphid density then one would expect the presence of ants to be a good indicator to the presence of aphids. If the correlation is low there is a higher chance of a false positive (where a false positive = when you see ants, conclude there must be aphids, and there are no aphids).


Answer: You are right that if you had one big pipe that was getting progressively narrower, the pressure in that pipe would increase. In the vascular system, you have one big pipe emptying into exponentially more small pipes. The total lumenal diameter of the small pipes is actually greater than the single big pipe.

Even though each individual capillary has a smaller lumenal diameter than each artery, the sum lumenal diameter of all of the capillaries is much greater. This is because there are way more capillaries than there are arteries.

More detail: The following image plots total cross-sectional area and pressure in the pipe against the level of the circulatory system. The sum cross-sectional area of the vessels is highest in the capillaries, simply because there are so many capillaries. You can see the pressure decreases accordingly.


Can the "Cas9"(involved on the Crispr-cas9 mechanism) be considered as a restriction enzyme?

Cas9 is an endo-deoxyribonuclease (UniProt-Q99ZW2). It also has a 3'-5' exonuclease activity by which it trims the DNA a little bit, from the cut site (but not too much).

Although, Cas9 is an endonuclease and is evolved as a mechanism of immunity against viruses (like restriction enzymes), they are not considered restriction enzymes. One of the most important differences is that the restriction enzymes do not need an RNA or a DNA as a tether to identify the target sites in the DNA; their DNA binding domains can recognize the restriction sites by themselves.

Cas9 cannot just cleave any DNA complementary to the guide RNA. It needs PAM (protospacer adjacent motifs) sequences adjacent to the target site to cleave that latter.

For details check out the wikipedia page on CRISPR or read a review.


What happens if someone with mutations to alcohol dehydrogenase (ADH) drinks alcohol?

People, which have no ADH wouldn't be able to process methanol. Since the specificity of the ADH is higher for ethanol you get quite large amounts of ethanol for days (until the methanol level is under a specific level). Another possibility is to treat patient with the ADH inhibitor Fomepizole.

This also makes problems for the ethanol metabolization, but according to this paper ("The biochemistry of alcohol metabolism - a brief review") there are two other pathways of breakdown. One takes place in the peroxisomes and utilizes catalase and hydrogen peroxide (but is limited by the availability of peroxide), the other take place in the smooth endoplasmatic reticulum and uses the Cytochrome P450 enzyme.

I am not sure, if complete losses of ADH really happen (haven't found any reference) but mutations in this enzyme are quite common leading to a lower enzyme activity.


Why didn't Mendel ever see the recombination?

I'm not sure what you mean by "recombination".  Peas have 7 chromosomes.  Mendel's seven published traits are each on a different chromosome.  Mendel's second law states that all genes assort independently.  This is wrong, but it is correct for genes located on different chromosomes, which Mendel's were.


For emphysema, which of the respiratory volumes is affected?

To learn obstructive/restrictive lung diseases, I find it easiest to think in extremes at first, with vivid descriptions of why.  So in obstructive lung diseases, like COPD/emphysema:

Total volume increases because so many of the walls of the alveoli have been destroyed, they are like giant floppy bags instead of nice firm bubbles.  There's more empty space, and total volume is therefore increased.

Reserve Volume and End Respiration Volume increase because these alveoli are large and stretched and floppy and can't push as much air out, even when you try.  (Decreased elastic recoil.)  They also flop shut often before the air is expelled - trapping air in.

Tidal volume may not change at all, but it takes longer to exhale than with normal lungs.  That is why FEV1 and FVC are lower, for the same reason.

Residual volume


I found this insect in Utah, USA. What is it?

It looks very much like the Indian meal moth, Plodia interpunctella, to me. The size, morphology of the antenna and wing tips, and the pale band of scales are all fairly distinctive. (The proboscis isn't very clear in the photo below but it is in most other images you could find via Google; I just couldn't find a better one with a license allowing me to post it here.)

(Image by Kaldari (Own work) [Public domain], via Wikimedia Commons; URL https://upload.wikimedia.org/wikipedia/commons/5/50/Indianmeal_moth_2009.jpg)


How can Giant squid have $20,000 mm^{-2}$ photoreceptor cells, but no cones?

First squid lack both cones and rods, they evolved their eyes independently, the cells they use most closely resemble rods but they are by no means identical.

In vertebrates there are two types of cells rods and cones both of which can be used to see movement (movement is just detecting changes in the visual field). rods are better at it becasue they are smaller so they can be packed tighter, thus they can detect smaller changes, but that is by no means their primary function. Rods detect luminosity, that is the intensity of light, but react to light from all parts of the visual spectrum.

There is a lot of debate about how much color squid and octopi can see. behaviorally they appear to recognize color, but they don't have differentiated cells or opsins to detect them.

I appears they have stumbled on a completely different way to achieve color vision, they appear to use weird shaped pupils and chromatic aberration.
I suggest reading the linked paper as you have to dive pretty deep into the physics of optics to understand. Basically different colors of light are bend by slightly different amounts by a lens, and they are using the multiple images of their U shaped pupils to gain color information.


Why do we suffer abdominal pain after we get very angry or stress?

Cortisol produced from the zona fasciculata of the adrenal cortex is directly caused by stress.

According to http://en.wikipedia.org/wiki/Cortisol

  Cortisol stimulates gastric-acid secretion. Cortisol's only direct effect on the hydrogen ion excretion of the kidneys is to stimulate the excretion of ammonium ions by deactivating the renal glutaminase enzyme. Net chloride secretion in the intestines is inversely decreased by cortisol in vitro.

This increase in gastric-acid secretion can irritate the lining of the GI tract, especially if there are ulcers or inflammation, resulting in pain. In addition, the fight-or-flight response causes

  inhibition of stomach and upper-intestinal action to the point where digestion slows down or stops.

(see http://en.wikipedia.org/wiki/Fight-or-flight_response)

Those things, paired with increased muscle tension and vasoconstriction cause pressure changes in the GI tract, which can cause pain.


What is the cause of a protuberant belly in kwashiorkor?

The Gastroenterology paper you cite doesn't mention distended bellies at all.  There is no dispute that fatty liver is a symptom of kwashiorkor.  But the Wikipedia article makes it quite clear that the cause of the distended belly is edema.

  The extreme lack of protein causes an osmotic imbalance in the gastro-intestinal system causing swelling of the gut diagnosed as an edema or retention of water.[4]

And:

  Compromised fluid recovery results in the characteristic belly distension observed in highly malnourished children.[14]

Here's another source:

  To understand the reasoning for this, it is important to know that in malnourishment, the rounded abdomen is not due to fat accumulation. Instead, the water retention and fluid buildup in the body cause the abdomen to expand. This results in a bloated, distended stomach or abdominal area.

The rest of the article goes into more detail on the phenomenon and mechanism of action.

This source seems less authoritative, but also suggests that weakened abdominal muscles (due to protein deficiency) also play a role:

  The swollen belly is the result of not only that enlarged liver, but also the loss of muscle mass, which leads to weak abdominal muscles. Together with a weakened lymphatic system that is unable to keep up with the body’s liquid wastes, when those wastes accumulate in the abdomen, the belly becomes distended.

So the author suggests that fatty liver contributes to belly distension, but is not a sole cause.  None of the sources I looked at mentioned fat accumulation as a contributor, but rather eliminated it.


What would kill you first water or cola?

The LD 50 listed on the wikipedia page you link to is 90 mL/kg, which would be about 6 liters for a 68 kg (150 lb) person. This is consistent with at least one report, where someone died from drinking 7 liters of water in 1.5 hours.

The mechanism by which water kills people is by lowering the amount of ions (chiefly sodium) in the blood. A condition called hyponatremia.

Coke contains four relevant looking ingredients: Water, sugar, phosphoric acid, caffeine. Coke also has carbonic acid from the carbonation, but I'll assume we're either talking about uncarbonated Coke, or that the carbonation does not contribute to toxicity (perhaps a bad assumption).

Before worrying about whether the water will kill you, let's verify that the caffeine and sugar won't kill you first.

It seems unlikely that the caffeine in the coke would kill you before the hyponatremia. The concentration of caffeine in coke is about 0.1 mg/mL, and the LD50 is > 150 mg/kg, so for the same 68 kg person, it would take about 100 L of coke to get a lethal dose of caffeine.

The sugar in coke is more deadly, but still not as bad as pure water. There are about 0.11 g sugar per mL of coke. The LD50 of sucrose is apparently around 30 g/kg. So it would take about 2 kg of sucrose to kill our 68 kg person. That is about 18.5 L of Coke.

The concentration of phosphoric acid in Coke is about 5 mM which is about 0.5 mg/mL. The LD50 is about 1530 mg/kg. Which works out to about 212 L of Coke to kill by phosphoric acid.

Now that we've ruled out some other possibilities, lets get back to whether coke will kill you faster or slower via hyponatremia than pure water will.

Take another look at the the nutrition information for Coke. Notice that Coke actually contains some sodium, about 0.13 mg/mL in fact. A drink called "Powerade Isotonic"  which claims to have a proper electrolyte balance contains sodium at 0.28 mg/mL.

So given that (A) what kills you first from drinking too much water is hyponatremia. (B) Coca-cola contains a non-trivial (but still less than many electrolyte drinks) amount of sodium. and (C) other potentially toxic components of Coca-Cola, such as acid and caffeine, require much higher doses to be toxic. It seems reasonable to conclude that Coca-Cola has a lower acute toxicity than distilled water.

Caveats:
I did not consider osmolarity. There could be some effect here that I'm overlooking.
I did not consider the effects of carbonation (soluble carbonic acid).
For people with certain medical conditions, such as diabetes or caffeine sensitivity, Coca-Cola may be toxic at much lower doses than for other people.


Is the bulbourethral (Cowper) gland turned on during puberty or is it on at birth?

Yeah, because the bulbourethral glands are from accessory glands of the male reproductive system as the seminal vesicles and prostate gland. The male reproductive system starts working at puberty.


Searching for the quote you included led me to the original source.

I wouldn't spend too much time worrying about this particular source, and look at some other sources for more information on acquired lactose intolerance. I think there may be some translation/language issues with this section in this particular source. I believe what the author is trying to convey is not that the intolerance is coming from the increased intake, but that the symptoms of intolerance are coming from a sudden increase in lactose intake following a period of low/no lactose intake, where "sudden" essentially means "faster than lactase induction can occur."

That said, I think this is really more an issue of poor wording in a textbook. The whole section is a bit strangely worded, particularly the part on "flatulence" which this author describes as "characterized by increased intestinal motility, cramps, and irritation" - while these issues may certainly accompany flatulence, this definition of these symptoms characterizing flatulence is not correct, as one can certainly have flatulence with normal intestinal function.


BLAST, using Smith-Waterman in the last step and S-score

The BLAST algorithm is a heuristic to find which the path through the matrices formed between a query sequence and a target sequences from the database is ‘best’. Such paths represent an alignment which is has a completely different basis to that of the Smith-Waterman dynamic programming algorithm. Not only is it ungapped, but it based on comparison of tuples with matches scored according to frequency, and then proceeds by trying to join those with certain relative scores.

The speed of the program is partly the result of rapidly discarding unpromising paths, storing and continually refining only the current best candidates. The alignments will not be Smith-Waterman alignments, but there is no point in performing a Smith-Waterman alignment on each high-scoring sequence pair as this is not the basis of inclusion in the pool of best candidates. Performing such an alignment would be a waste of time for those candidates that will ultimately be discarded.

Only when the run is complete is it appropriate to perform the Smith–Waterman alignment on the final top candidates to produce a gapped alignment from which statistics such as the E-value are calculated (using S, the raw score from such Smith–Waterman alignments).


what the best E-value cutoff in the miRNA homology search

If you are using BLAST for short nucleotide searches then you should reduce your word size to <=7. It is better to align with mature sequences.

E-value depends on the database size. If your target database is huge then you should increase the e-value cutoff. If miRBase (for a few organisms) is your database then there is no need to run BLAST, also. You can simply run SSEARCH (Smith-Waterman Local alignment algorithm).

If you are running BLAST against miRbase you can set the e-value cutoff at 10. This is fine because there are many similar looking miRNAs with different function. If you reduce the e-value cutoff then you may lose these.

There are some other criteria for miRNA conservation- e.g there should be very high (almost exact) similarity at the seed region. After the BLAST, make sure that seed region is conserved.

  Can we can use DAVID for miRNA functional analysis.

I don't think DAVID can be directly used (miRNAs have to be annotated in their database). What you can do is that you can predict the targets of your miRNA and then pass them to DAVID. DAVID won't do the predictions but there are other programs (see this post). You can also try BioMart (provided by ENSEMBL) for getting GO details. Even BioMart does not provide functional annotation for miRNAs (I just tried, to verify). So best thing is to check for the targets.


Understanding ancestry testing mathematically

I'll give here a simple, non-technical answer because I'm assuming you don't need to actually perform an analysis of ancestry.

So, detecting ancestry is a non-trivial task. Given your genome sequence, you would need to compare some "informative" regions of the genome with the homologous sequences of some population (say, of a database with other genomes). These informative regions are usually some parts of the genome that vary across individuals (variation is used because differences are informative: some populations vary on particular sites, distinct from other populations). At the core, this is a question on how to compare "character strings" (DNA is composed of 4 characters, namely, A, T, C, and G). But these strings exist in a complicated structure: a human genome is partitioned in 23 pairs of chromosomes, within each individual. However, the question of ancestry is not about individual sequences really, but about population-level changes in DNA composition. So, in fact, you need to consider population-level factors: size of the populations to consider, the rates of recombination (DNA exchange across chromosomic pairs), mutation rates, and even population structure (people move geographically!).

Given these (and, many other) factors, people build models of "coalescence": given a sequence of interest, how likely is that it shares some ancestor with another query sequence? So, the models try to relate these two sequences (say, the one you are interested), with a query (say, a "consensus" Scandinavian sequence), and then make a model of a 3rd sequence (the ancestor!). This process is repeated to test many hypothesis, so you end up with many probabilities. On top of this, you can estimate the ancestry for any given part of your genome, and this is what most companies do (say, 23 and me).

In summary, you are correct that a "% Scandinavian" does not mean sequence similarity per se. It implies an estimation of common ancestry. This estimation comes from models of shared ancestry. If you're unsatisfied with this simple answer, and want a more technical answer, I recommend reading this paper. An intermediate-level explanation is found here.


why is DNA antiparallel? Can it be parallel?

Interestingly the answer is yes. The problem with parallel strands is that the DNA is not pairing in the known way it does when it is combined anti-parallel (or Watson-Crick-pairs).
I have found different images illustrating the problems:

Both images are from this blog post (originally from a publication cited there which is not available online). Both pictures show a distorted DNA structure.

This article ("NMR structure of a parallel-stranded DNA duplex at atomic resolution") shows a more schematic solution of this problem by showing the single pairings. C and G cannot build up 3 hydrogen bonds as they do this in the Watson-Crick-pairing.

Subfigure A and C show the Watson-Crick-pairs, the others come from parallel bindings.

This changes in structure disrupts the function of the DNA (which for example depends on the reverse strand for proof reading). Enzymes which replicate, transcribe, repair etc. DNA will not work on this changed structure, as their function depends on the structural features of the DNA.


Usage and mechanism of the Bastien protocol to treat amanitin poisoning

I know nothing about this subject, except that I can recognize edible and poisonous fungi, to the extent that it concerns me in a practical sense. However, as I have access to a range of journals through my university I thought I would see if there was anything ‘out there’ on the topic.

A recent paper entitled Amanita phalloides poisoning: Mechanisms of toxicity and treatment by J. Garcia et al. in Food and Chemical Toxicology 86 (2015) 41–55 contains a table listing the drug therapy used in a range of countries. There is no reference to Bastien in this paper and the most frequently used therapies are benzylpenicillin and silybin.

Abiocine is another name for dihydrostreptomycin and nifuoxazide is nifuroxazide is an oral nitrofuran of questionable efficiacy. So they are not identical to the agents mentioned and Bastien’s protocol does not appear to be in current use.

The impression I get from the article is that the agents used for treatment are not strict antidotes, but rather part of a strategy to treat the general effects of the poison. To eliminate the poison activated charcoal is often used.

If Bastien’s protocol really had an effect I imagine it may have acted in a similar manner to the current agents, although I have no idea what the vitamins might have been doing (if anything). Incidentally it was the subject of a letter (in English) to Lancet in 1981, in response to previous scepticism expressed in a previous editorial.


When a muscle contracts, but not all the muscle fibers are activated, what happens to the remaining muscle fibers?

I don't think the unused sacromeres will contract though because every time you contract, it requires ATP and so it will be really expensive if you contract when you don't need to. I believe the unused muscle fibre will just be compressed or bent, since cells have a certain degree of compliance. I am guessing that is also why you won't feel your muscle as hard if you are not doing MVC


This is an ongoing discussion, and entire textbooks are written in this field, but I will try to clear up some misconceptions and point you toward some further reading that may help.

Is dopamine pleasure?

"Pleasure" is an emotional phenomenon; dopamine is a neurotransmitter. Dopamine can be involved in the perception of pleasure, but there was a now-outdated hypothesis that "dopamine==pleasure".

More recent evidence says that this is not the case, because endogenous dopamine release occurs in some brain regions during the anticipation of a pleasurable event, and really doesn't correlate with pleasure itself at all. Instead, dopamine is currently thought to reflect a "reward prediction error": a signal that tells the brain "hey, we just got something better than we expected!"

Why is a prediction error useful?

This signal can then be used by the brain to upregulate circuits that were recently active, effectively using the heuristic: "I just got something I didn't expect, so whatever I did just before must have been a better thing to do than I previously thought! I should do that more often!"

There are 'degrees' of unexpectedness, however, which is why you get a dopamine signal when a positive event is expected. Let's say a cue, like a bell, signals a coming reward. The reward is now expected, so it won't produce an error signal, but the bell itself produces an error signal: prior to the bell, you didn't know the bell was coming, so you didn't know the reward was coming. Now you update your brain circuits to try to do things to make bells ring!

This is a powerful learning algorithm that is also used, in a form, in artificial neural networks.

Context in drug abuse

If a drug of abuse causes a release of dopamine, that's a signal to the rest of the brain "Hey, something good just happened, let's try to do that again in the future!" Dopamine is the message, not the experience.

Further reading

The two bolded works below are a recent review and a highly relevant original paper, respectively.

Peter Dayan, Wolfram Schultz, and Ray Dolan were recently awarded for their work in this field and you can find lots of popular press that describes their work, as well.

References

Schultz, W. (2013). Updating dopamine reward signals. Current opinion in neurobiology, 23(2), 229-238.

Schultz, W., Dayan, P., & Montague, P. R. (1997). A neural substrate of prediction and reward. Science, 275(5306), 1593-1599.

Fiorillo, C. D., Tobler, P. N., & Schultz, W. (2003). Discrete coding of reward probability and uncertainty by dopamine neurons. Science, 299(5614), 1898-1902.

Glimcher, P. W. (2011). Understanding dopamine and reinforcement learning: the dopamine reward prediction error hypothesis. Proceedings of the National Academy of Sciences, 108(Supplement 3), 15647-15654.

Pessiglione, M., Seymour, B., Flandin, G., Dolan, R. J., & Frith, C. D. (2006). Dopamine-dependent prediction errors underpin reward-seeking behaviour in humans. Nature, 442(7106), 1042-1045.


How to interpret dual luciferase assay result (RLU)?

Relative luminometer units (RLU) have no unit. They are the result of the luciferase reaction and proportional to the expression of the luciferase gene, meaning the higher the numbers are, the higher the expression is.

To analyze these numbers, you usually use a control, to which your samples are then relative to. So expression from your luciferase vector is 10x higher in the treated sample compared to the control for example.

As the RLU has no unit, it is hard to compare measurements directly. To overcome this problem, you can use a second luciferase reaction (the renilla luciferase) to be able to normalize between samples and to correct for transfection efficiency, but still, your values are only relative.

They are influenced but the kit you use for the measurement, the machine you use (so always use the same machine) and so on.

To normalize the values, you divide each firefly luciferase value by the value for the renilla in the same well. Ideally alls renilla measurements are the same (as you transfected the same amount of plasmid in each well, have the same number of cells etc., but if not, this corrects exactly this problem). You cannot calculate the transfection efficiency from this control.

To calculate the relative expression ratios between your sample B and the respective control A, you set the control to 1 by dividing A/A=1 (for example: A=10, 10/10=1) The relative expression of B is then B/A= relative expression (for example: B=5, relative expression: B/A= 5/10=0.5). In the example the relative expression of sample B would be half the one of the control.


Why eyebrow growth stopped after it has specific length?

Activation of the mammalian gene Lhx2 leads to increased hair growth. Lhx2 is a transcription factor which regulates hair formation.

"...length of the hair is determined by the duration of the growth phase; for example, the growth phase for scalp hair can proceed for a number of years, while the growth phase for eyebrows last a few months."

Other genes that have been associated with hair disorders include: FOXN1, ALX4, HOXC13, MBTPS2, VDR, CDH3, HR and ANTXR.


Is Batesian Mimicry a form a parasitism? To what extent is the species with real defenses harmed by the defenceless species?

In my own opinion, I would not classify this as parasitism, as more unpalatable species are eaten with Batesian mimicry (and eating causes death). Parasitic organisms often do not kill the host, whereas in this case, it does. However, you are correct in stating that a unpalatable species with aposematic coloring is detrimented by the presence of a palatable Batesian mimic.

Predators often recognize the aposematic coloring of an unpalatable or dangerous species. They "train" themselves not to eat that particular prey, as it is detrimental. The presence of a Batesian mimic which is palatable or not harmful, in simple terms, "untrains" predators of the harmful nature of that particular aposematic coloring. Predators are "confused", and are thus more likely to eat preys with that aposematic coloring, and results in more death of the species being mimicked, while providing protection to the species that is mimicking.

As far as I'm concerned, within an ecosystem, this phenomenon happens with any Batesian mimicry to some degree. Factors that may influence this degree is the recognizability of the aposematic coloring, as well as the ability of a predator to recognize this coloring.

I hope this clears things up.


Are recessive, deleterious alleles less common on the X chromosome than the autosomes in humans?

"Monosomy for the X chromosome in humans creates a genetic Achilles' heel for nature to deal with."

The article I quoted1 tackles this issue.  It's from the turn of the century, though, so quite old in sequencing/genetic terms, but the science is still sound as far as I can tell.  Here's the money quote:

  Hence, the X chromosome appears to have a lower gene density and should yield fewer deleterious mutations per megabase of DNA.

In short, yes, you're correct.  There appears to be less overall information on the X-chromosome, deleterious or not, and selection is faster; the X chromosome is just flat-out less diverse.  This article goes into quite a bit more but says essentially the same thing: "On one hand, the greater effectiveness of selection on males due to the hemizygous expression of the X, which may be further reinforced by sexual selection, is expected to lower the mutation load for females at shared loci."  Here is a more recent article stating the same: "This finding [X-chromosomes with lower linkage disequalibrium] is consistent with more rapid selection against deleterious mutations when the X is monosomic in males, and to a lesser extent, under random inactivation (Lyonization) in females."

Finally, here is a piece written a few years back by a colleague of mine that goes into depth on the subject.  The second half deals with population differences (also fascinating), but the first part has a lot of good detail on what you want.


Molecular simulations without capping n- and c-terminus of polypeptide

Interesting question. I have to admit, that I haven't really come across it, but for the moment it seems to me that this mechanism is used mainly to protect short alpha helices and stabilize them.
See this articles: "Helix stop signals in proteins and peptides: the capping box." and this one: "Helix capping."
A lot of research is done in combination with actin filaments, where the capping plays an important role in stabilizing the filament strands - either prohibiting the addition of new monomers and on the other hand preventing the removal of elements from the polymer strand.
This review gives an overview:"F-actin capping proteins."
This research article might also be interesting when doing simulations:"N- and C-capping preferences for all 20 amino acids in alpha-helical peptides." As always, if you have some problems with access to the articles, let me know.


Identify a small bug, possibly a plant bug?

This is a plant bug (family Miridae); going deeper isn't possible on the basis of a photograph, except for some common economic species (the key to genera in How To Know the True Bugs is almost 200 couplets long!).  Most species of the family are plant feeders (hence the common name); biting humans is unlikely.

Reasoning (from Comments):

The top right photo [from the OP's post] shows that the front wing has a cuneus (a section of the hardened part of the wing on the outer margin set off by a groove), which is characteristic of that family and the broad-sense "Anthocoridae" (which includes three smaller families); none of the photos show simple eyes (the eyes we see are compound), which eliminates "Anthocoridae" and the subfamily Isometopinae of Miridae; the remaining seven Nearctic subfamilies are still possible


Why is HPV vaccines targeted for preteens?

A lot of sexually active adults carry one or another strain of HPV but most do not develop cancer. You can carry HPV — and spread it to others — without showing any symptoms yourself:

  HPV infections are so common that nearly all men and women will get at least one type of HPV at some point in their lives. Most people never know that they have been infected and may give HPV to a sex partner without knowing it. Nearly 80 million Americans are currently infected with some type of HPV. About 14 million people in the United States become newly infected each year.

There is less reason to give a vaccine to someone older, generally, who is almost certain to be infected with some form of HPV. A vaccination is not a broad cure, though it can provide some protection against infection from strains of HPV that someone is not already infected with:

  But the vaccine also offers some protection for HPV-positive women, reducing cervical lesions by 17% and genital warts by 35%. HPV-positive women usually aren't infected with all four of the targeted strains. In clinical trials, those infected with one or more of these strains before vaccination were protected against the remaining ones.

Pre-teens are unlikely to be infected with any forms of HPV, having no or much less sexual contact, and so they are the best candidates for being administered the vaccine.

This cohort will get the most protection from those strains that the vaccine protects against, strains which are most likely to cause relevant cancers.


Enzootic and epizootic are analogous to endemic and epidemic, respectively.

Enzootic means something that affects a population of non-human animals  in a limited spatio-temporal region whereas epizootic is relatively more widespread.

Endemic and epidemic are more general terms and do not, technically, apply to only humans.


Anatomy of nervous system's sensory pathways

The key player you are lacking is the thalamus, which integrates a lot of stimuli, and pre-processes them before sending them to the cortex


What is the meaning of "within-season variation"?

"Within-season variation" may be referring to one of two things (depending on the context):

More commonly: the variation of a variable within a given season (i.e., between months or days within that season).

Öst (1999) demonstrates an example of this use (in the context of breeding season).

Less commonly: the variation of a variable between the same season of different (often consecutive) years. Though this would more often be termed "between years". This is as opposed to "between seasons" which would be be between two different seasons of the same year.


On average how many genes / alleles do people share?

I will attempt to answer the question. Allele is defined, in simple terms, variation of a given gene, e.g. through deletions, SNPs etc. Humans are diploid organisms, meaning we have two sets of chromosomes, one from mother and one from father. Now since we have two sister chromosome, we can only have (share) two alleles of a given gene (one from mother and one from father) unless there are multiple copies of a gene or chromosome, which is mostly observed in disease conditions but that's not what we are talking about. Now since every humans have SNPs at roughly 1 every 1000 base pair, there are genetic variations between sequences of genes between humans, although there are some hot spots, which are more varied and some genes are very highly conserved due to their critical function such as cytochrome C. This just means that parents of the child you are describing (if not related to each other) are not likely to share the exact same, sequence wise, genetic code for a given gene selected at random.

The inheritance of a given allele of a gene on a chromosome happens through independent assortment (a process which happens maternally and paternally), meaning a child (offspring/zygote) would get one copy of a gene/allele (from the possible two that each parent themselves have) from maternal and one copy from paternal side at random. This is one source of genetic variation in a zygote. The other source of genetic variation is gene cross-over (through homologous recombination) meaning bits of the maternal or paternal chromosomes swap at gamete stage before the gametes are fused together to form a zygote, which makes the offspring unique and no offspring alike (except MZ twins but thats another discussion). This overall means that you can inherit a maximum of two alleles of a given gene (assuming again the parents of the child are not closely related) and even then the sequence of the offspring genes are not likely to be exactly the same as their parents, which makes every human unique. But saying that, you have a much higher gene sequence match to your parents than any other non-related human selected at random.

One thing worth noting here is that mitochondrial genes, are inherited exclusively from you mother (through the egg) and males inherit the Y chromosomes paternally so there are circumstances I guess you could say you inherit certain gene/alleles paternally or maternally.

What I speculate you might be thinking about is how many homologues (similar versions) of a given genes humans have and I think the average in the human genome is 3 but do check this! Flies (Drosophila) tends to have one, which is why its such a great model organism to study genetics and genetic interactions with as you do not tend to get redundancies.

I hope this answers your question


Does eating nonsalty food with MSG make you thirsty?

MSG (monosodium glutamate) can trigger thirst simply because it's a spice or because foods with MSG often contain other spices.

Relationships between human thirst, hunger, drinking, and feeding (PubMed, 2008)

  Drinking may occur at meal times to facilitate chewing and swallowing,
  improve sensory stimulation and food palatability, reduce aversive
  sensations evoked by irritants such as spices, or in anticipation of
  physiological deprivation.

Thirst after ingestion large amounts of MSG is described here as part of Chinese restaurant syndrome; the mechanism involved is a transient release of acetylcholine:

  symptoms experienced by individuals following intravenous MSG were
  similar to those experienced by individuals following intravenous
  acetylcholine (ACH).

So, does MSG trigger thirst? It may, but not necessary.


How do people wake up just before their alarm goes off?

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


How can the number of genes increase through evolution?

Mutations can have all sorts of impacts on genetic architecture. A mutation can have a small impact on a genetic architecture such as

Substitution
Insertion
Deletion

or can have a much bigger impact on a genetic architecture such as

Amplification (incl. gene duplication)
Deletions
Chromosomal translocations
Interstitial deletions
Chromosomal inversions
Chromosome duplication
Change in ploidy number

Some of these mutations (gene duplication, Chromosome duplication, change in ploidy number) typically allows duplicating DNA segments. After duplication, the two copies of a gene can diverge through neofunctionalization or subfunctionalization. Have a look at wikipedia > gene duplication to understand what biochemical processes can cause such mutations (e.g. ectopic recombination, retrotransposition event, replication slippage).

  Am I correct in thinking that creatures within the same species who mutate to have an additional gene in their genome would normally be infertile?

You are being mistaken. I understand the naive intuition that a change in copy number of a given gene would be extremely deleterious but in reality, living organisms seem much more resilient to such Copy-Number Variation (CNV) than you would think. Of course, some CNV are associated with diseases but it is not the case of all (McCarroll and Altshuler 2007).

Gene duplications are actually quite common whether in C. elegans (Lipinski et al. 2011) or in humans (Cotton and Page 2005). Chromosomal duplications are also common (Bowers et al. 2002). Even whole-genome duplications (see a classical example in Wolfe 2015) have played major roles in the evolution of many lineages (Whitton and Otto 2010) including vertebrates (Dehal and Boore 2005).

Below is a phylogenetic tree of sequenced green plant genomes highlighting some of the main events of whole-genome duplication.

For the record, some species of strawberries are decaploid (10 copies) (Hummer 2012). Then there are the extremes. In Entamoeba populations, there can be variation in ploidy level among individuals ranging from diploid (2 copies) to tetracontaploid (40 copies) (Mukherjee et al. 2008)!


Short answer
I can be 75% sure that the lights are synchronized within 0.02 - 0.2 seconds of one another.

Background
Interesting question, but hard to answer! Because it has been unanswered for quite a while I will try to formulate an answer that may provide an approximate value for the minimal asynchrony perceivable.

The temporal resolution of the visual system can be quantified in a number of ways. As you are referring to relatively simple stimuli, the critical flicker fusion frequency is probably the most relevant. At a certain critical frequency, a flickering stimulus will appear as a continuous stimulus (Holcomb, 2009). For example, the good old CRT screens can sometimes seem to be flickering. The mains is 50 Hz (US) or 60 Hz (Europe, Australia), and indeed the critical flicker fusion frequency is 5 - 50 Hz, dependent on the lighting conditions (Kalloniatis & Luu). Hence, stimuli separated by 200 ms (low lighting) to 20 ms (high lighting conditions) can be temporally resolved.

I am aware that your question is different, as you ask whether two stimuli on the retina can be perceived as being asycnchronous. Flicker fusion testing is mainly done with flash stimuli, i.e., a single stimulus per image, not two. However, from the various measures of temporal resolution of the visual system that have been used to date, the critical flicker fusion has the most conservative value, in that it provides the top-value of temporal resolution. Higher-level processing is much slower and values of around 4 Hz are obtained. For example, when subjects are tested on a stimulus of dots that are white when moving right and black when moving left, and they change directions/colors at a certain frequency, it becomes hard to tell whether the color change and direction change are synchronized at alteration rates of ~5 Hz and higher (Kalloniatis & Luu).

As to your question what the percentage chance is that stimuli separate by 20 -200 ms are separable, I can say that in general, psychophysical procedures determine the threshold defined as halfway between chance and 100% correct. Assuming a typical yes/no tasK (are the traffic lights synchronous yes/no?), chance would be 50% (guessing), and threshold would thus be defined as halfway between 50% and 100%, i.e., 75% correct.

References
- Holcomb, Trends Cog Sci 2009; 13(5): 216-21
- Kalloniatis & Luu, WebVision, chapter "Temporal Resolution" 2007