what are examples of experimental designs on exposing materal for degradation

Have you heard of qPCR? This method quantifies the amount of DNA in the sample. Another quantitative PCR method you might look into is taqman PCR. Traditional PCR + agarose gel electrophoresis is not going to give you a quantitative measurement of the DNA in your sample.
Here are the wikis on taqman and qPCR.
taqman https://en.wikipedia.org/wiki/TaqMan
qPCR https://en.wikipedia.org/wiki/Real-time_polymerase_chain_reaction
Also, if you have the choice between intercalating agents and fluorescent probes, go with fluorescence. Intercalating agents are hazardous.
Hope that helps.
Edit Adapted from comments -
We don't have access to a real time pcr intrusment sadly. All we have is a traditional pcr machine. Can I get your opinion on this quote I found on the quantitative messures of traditional pcr: '"No, though comparing the intensity of the amplified band on a gel to standards of a known concentration can give you 'semi-quantitative' results." From thermofisher.com/us/en/home/life-science/pcr/real-time-pcr/…. Are there ways to work with the intensity of the bands I get to be " more reliable"? – Ro Siv
Yes, quantification from traditional PCR can be done, though the accuracy is questionable. One method I have heard of uses a computer to analyze the intensity of the bands. You could probably pull this off with some Python code (check out the scikit-image python library). The other option is to do what you said, compare to known concentrations.
If you are familiar with HA titers in virology, you might be able to contrive a similar method, in which you carry out 10-fold dilutions of the sample until there is no more detectable DNA left. The point at which there is no DNA left is called the experimental end-point, and the titer of the original sample is simply the inverse of the dilution factor at the end-point. Check out hemagglutination(HA) in the context of virology. I think a method similar to this would be better than simply eyeballing the intensity of bands, because you will have some quantitative evidence.
If you want to eye-ball, you should use control bands at several different concentrations, so that you can say, 'the intensity of the band falls between control bands A and B, and so the concentratin of the sample is between concentrations A and B'
I bet you could pull off the serial dilutions. It will be good practice, too. To make a 10 fold dilution, just add 1ml of sample to 9ml of saline. Then, from that new solution you just made, do it all again. Take 1ml and add to 9ml saline. Repeat. Each time you decrease the concentration by 10^-1. You can scale it down too - 1ul sample to 9ul of saline. Repeat. Here is a SOP on HA. Honestly, I would go with the serial dilution thing. I bet ur professor would help you out with this. It is cheap, easy, and widely used. cfsph.iastate.edu/HPAI/resources/SOPs/HA_HI.pdf
Question: If I were to do both methods, then would ImageJ be a possible substitute for scikit-image? rsb.info.nih.gov/ij I think its GUI interface is alot more workable for me.
Response: From just skimming that link it looks like it might. You would probably be interested in the density analysis part of the software, but I dont think a computer is necessary, and ya you will have to produce that gradient of concentrations any way. If it were me, I'd first try to do the experiment without computer analysis. Produce the gradient of control DNA concentrations, compare your sample to the control gradient and see where your sample falls.
Then repeat the experiment while varying the independent variable, lets say its time. So take a sample at 5 min 10 min 15 min etc. and produce a plot of surviving DNA concentration vs time. It will probably end up looking something like a sigmoid curve. If you decide you need more precision in your measurement of the DNA concentration, then consider using the image software, but I doubt you will need it, though I admit it would be twice as badass.


Studying changes in DNA for causes of cancer

I tried to comment but what I wrote is too long, so here it is as an answer of sorts.

If I understand the question, you are asking: has anyone done a prospective study where they store the DNA of individuals and then later, when some of these individuals get cancer, have a look for mutations that are associated with that cancer. In fact this is done all of the time, but it isn't necessary to store any DNA because the cancer patients will have the normal sequence in all of their non cancerous tissues - only the cancer cells will have the relevant mutations. See here for a recent example of this type of study that made the news.

Your BBC link is to a story in which the genomes of people will be analysed to determine if there are genetic factors which predispose them to cancer (and other diseases), but these won't be the mutations that actually create the cancerous cells.


Difference between the inactivation of neurotransmitters and hormones

Short answer
Hormones act in the order of minutes or hours. Neurotransmitters in the order of milliseconds. Moreover, hormones are blood-born, neurotransmitters are confined to the synaptic cleft or in the extracelular space directy surrounding the neuron. Hence, their mechanisms of inactivation are different.

Background
The distinguishing feature of hormones and neurotransmitters is the fact that the former are generally released into the blood, while the latter are confined to synapses, or the immediate extracelullar neuronal space. Hence, hormones can be readily cleared by the workhorse of blood clearance: the liver. For example, adrenaline is rapidly (half life 5 - 10 minutes) metabolized mainly by the liver, followed by excretion via the kidneys. Diffusion then will draw adrenaline away from the receptors as blood concentration drops. The relatively slow time course is beneficial, as the effects of epinephrine includes metabolic changes, such as the release of glucose to power up the body (Sherwin & Saccà, 1984). This needs time.

In the synapse, there is no blood flow and inactivation has to occur through other means. Further, epinephrine in the above example is a fast acting hormone. Many hormones work on an even slower time frame. For example, a stress-induced cortisol peak can last for as long as an hour (Kirschbaum & Hellhammer, 2000). Neurotransmitter responses may last for a few milliseconds. For example, some pacemaker neurons may fire at rates of 40-50 Hz (Häusser et al., 2004). Hence, neurotransmitters have to be cleared from the synapse at least within 20 ms. To wait for the released neuroransmitter to passively diffuse out of the synapse is simply too time-consuming. Neurotransmitters act at an entirely different time scale.

References
- Häusser et al., J Neurosci (2004); 24(42): 9215-9
- Kirschbaum & Hellhammer, Encyclopedia of Stress, 3 (2000)
- Sherwin & Saccà, Am J Physiol (1984); 247(2-1): E157-65


DIfference between diversification and differentiation

As already said in a comment: I would guess that ecological divergence emphasizes on the process of speciation by niche differentiation while ecological differentiation emphasizes on the process of niche differentiation due to overlapping niche of non-necessarily closely related species.

But looking to some articles, it seems that they use both term without making any difference. As found on this article for example.

Therefore, I would rather advice to no consider too much difference in meaning between ecological divergence and differentiation. But take time to define accurately the words you're using, especially if you talk about cases that fall on the border of two concepts!


Is erythropoietin released when breaking down RBCs

Erythropoietin is a glycoprotein cytokine (v is wrong) secreted by the kidney (iv is wrong); it stimulates erythrocyte production (erythropoiesis, from multipotent hematopoietic stem cells through erythroblasts through reticulocytes to red blood cells; iii is correct; i and ii are wrong) in the bone marrow.


Why haven't modern grass based crops overrun wild grasses?

Modern grass crops (cereals) haven't run out in the wild is because that was the whole purpose of their development. What differs them from their wild counterparts are the domestication traits, like, seed shattering, uniform maturity, day length sensitivity etc.

  Modern grass based crops are significantly superior to wild grasses, they grow faster, are stronger stemmed, have larger leaves and higher seed yields in terms of individual seed size, giving germinating seeds a significant head start vs other wild breeds.

This is only true under well resourced conditions, such as, irrigation, fertilizer, planned planting density etc. They grow faster and stronger because that is how they are bred. They are bred to utilize these resources better and produce better.

  I've heard time and again that GM crops will escape into the wild with potentially devastating consequences, out-competing wild plants for space and destroying biodiversity.

What people generally talk about here is the genetic transfer due to pollen contamination. But this is generally hard because of species differentiation. Even if that happens it will be with very low frequency compared to wild population. As far as I know modern crops do not and probably will not out compete wild plants under natural conditions.

  So why hasn't this happened already? Our crops are already GM (albeit through different methods and over a much longer time)

Explanation above applies here too.

  Edit: I have seen the odd crop plant growing in the wild, amongst other grasses, but rarely more than one or two clumps of wheat or barely grass amongst a sea of wild grasses.

That is generally due to seed contamination due to somebody threw a seed there. Or it is due to remnant seed from previous year's crop, these plants we call volunteer plants.


What's the current conclusion about humans being omnivores vs herbivores?

Humans are omnivores as they can eat and digest meat. Early humans were hunters and gatherers and meat was a part of the menu from time immemorial. I don't know the exact technic term but some of our teeth were designed to handle meat (canines?). Sure, people can willfully limit their diet to plants only but from the biological point of view humans are omnivores.


What are common causes of unexpected ligation products?

Could be insert polymerization.  If you have your stretch of DNA like this:

 (5')-AATTagctagcatcgtgatcgacg-(3')
          ||||||||||||||||||||
     (3')-tcgatcgtagcactagcagcGGCC-(5')

And you take that, flip it around, it will ligate onto itself, like this:

 (5')-AATTagctagcatcgtgatcgacg-(3')(5')-CCGGcgacgatcacgatgctagct-(3')
          ||||||||||||||||||||              ||||||||||||||||||||
     (3')-tcgatcgtagcactagcagcGGCC-(5')(3')-gctgctagtgctacgatcgaTTAA-(5')

This is easy enough to check for.  Just calculate the size fragments you'd expect from a vector with two inserts (there'd be an extra BcII cutsite now, and the extra fragment would probably be the size of the insert).  If this is just out of curiosity, and one of your things is the correct size, I'd ignore the ones that didn't work and go ahead with your ones that did.

If you do have a problem with it, or you are getting all your clones polymerizing, you can treat your insert with an alkaline phosphatase.  This will eat off the (5') phosphate that the ligase needs to stick the on to the (3') hydroxyl.  The result is that an insert cant bind to another insert, but once it finds a vector it will be able to ligate:

 insert to insert:    AATTagctagcatcgtgatcgacg-(3') :( CCGGcgacgatcacgatgctagct-(3')
                         ||||||||||||||||||||              ||||||||||||||||||||
                    (3')-tcgatcgtagcactagcagcGGCC  :( (3')-gctgctagtgctacgatcgaTTAA

 insert to vector:    ....ctagct-(3')     AATTagctagcatcgtgatcgacg-(3')(5')-CCGGcgacg....
                      ||||||||||              ||||||||||||||||||||              |||||||||
                      ....gatcgaTTAA-(5')(3')-tcgatcgtagcactagcagcGGCC     (3')-gctgc....

There will be nicks on the top left, and bottom right, but the bug you put it into should clean those up for you.  You can get alkaline phosphatase for fairly cheap from lots of places, NEB is always a safe bet.


Some trophoblast excreting digestive enzymes in implantation

I have no idea what is meant by 'the simplest trophoblast'. I did, however, find this review, pointing to a role of proteases in the implantation process:

  Salamonsen L.A. Salamonsen and Nie, G. (2002) Proteases at the Endometrial–Trophoblast Interface: Their Role in Implantation. Reviews in Endocrine and Metabolic Disorders, 3:133-143

which discusses the roles in implantation of three classes of proteases : matrix metalloproteinases, serine proteinases and cystein proteinases. The reference to 'trypsin-like' presumably relates to the serine proteases. The review reports the results of a number of gene knockout experiments in mice in which genes for individual proteases have been disrupted which indicate that no single enzyme is identified as being essential.

Referring to

  Afonso S et al (1997) The expression and function of cystatin C and cathepsin B and cathepsin L during mouse embryo implantation and placentation. Development 124:3415-3425.

the authors of the review state that:

  [they] demonstrated that cysteine proteases play a critical role in implantation. Cathepsin B mRNA was expressed by mouse trophoblast throughout the invasive period (days 5.5±10.5) while the proteins for cathepsins B and L were localized to the mature invasive trophoblast giant cells; activity of these enzymes was also demonstrated. Cathepsin L was also present within the stroma particularly in the lateral decidualizing zone. Cystatin C, the major inhibitor of cathepsins, was shown to be a major product of the adjacent decidualizing stroma close to the embryo, suggesting a restraining role. After the completion of placental trophoblast invasion (day 11.5) the trophoblast cells express high levels of cystatin C, probably in association with a switch from an invasive cell type to one providing nutrients to the conceptus [35]. In addition, treatment of pregnant mice with E-64, a synthetic cysteine protease inhibitor, resulted in failure of implantation and normal uterine decidualization.


Why is the Trendelenburg position used when placing and removing Central Venous Line catheters in the sub-clavian vein?

There are 2 main reasons for using the Trendelenburg position when placing and removing a central venous line catheter into the subclavian or even internal jugular vein.

Exactly what C Rags mentioned-- to increase the size of the vein. This position utilizes the force of gravity to pool blood towards the head from the lower extremities. This makes the vein of interest easier to visualize compared to surrounding structures, to palpate since this increases pressure within the vein, and to ultimately puncture.
To avoid air embolisms, which are particularly more damaging if they get into the brain causing a stroke than if they travel inferiorly to the leg, for example. Air embolisms can be introduced when inserting or removing a line.

Ref:

http://emedicine.medscape.com/article/422189-overview#showall


We probably won't really know for certain until we have time to gather more data from survivors. However, infection with existing coronaviruses (including SARS-CoV, genetically very similar to the COVID-19 virus SARS-CoV-2; ref. https://www.nature.com/articles/s41564-020-0695-z) suggests that those who are infected and survive may develop temporary immunity (ref. https://www.statnews.com/2020/02/04/two-scenarios-if-new-coronavirus-isnt-contained/):

The toll of a seasonal-flu-like coronavirus also depends on immunity — which is also scientifically uncertain. Exposure to the four endemic coronaviruses produces immunity that lasts longer than that to influenza, Webby said, but not permanent immunity. Like respiratory syncytial virus, which can re-infect adults who had it in childhood, coronavirus immunity wanes.
“Everyone, by the time they reach adulthood, should have some immunity to some coronavirus,” said Tim Sheahan, a coronavirus researcher at University of North Carolina’s Gillings School of Global Public Health. But because it doesn’t last, older people can get reinfected. The elderly also have a higher death rate from coronaviruses such as SARS and MERS, a pattern 2019-nCoV is following.
“There is some evidence that people can be reinfected with the four coronaviruses and that there is no long-lasting immunity,” Dr. Susan Kline, an infectious disease specialist at of the University of Minnesota. “Like rhinoviruses [which cause the common cold], you could be infected multiple times over your life. You can mount an antibody response, but it wanes, so on subsequent exposure you don’t have protection.” Subsequent infections often produce milder illness, however.

It might also be possible that someone was infected with two different strains of SARS-CoV-2 and did not develop immunity from the first infection. But it could have also been a continuation of the first infection, or testing error. Without virus sequence data, it was not possible to determine what happened for certain (ref. https://www.wired.com/story/did-a-woman-get-coronavirus-twice-scientists-are-skeptical/):

What could be worse than getting the pneumonia-like illness now known as Covid-19? Getting it twice.
That’s what Japanese government officials say may have happened to a female tour bus guide in Osaka. The woman was first diagnosed with Covid-19 in late January, according to a statement released by Osaka’s prefectural government Wednesday. She was discharged shortly after, once her symptoms had improved. A subsequent test came back negative for the virus. Three weeks later she returned with a sore throat and chest pain and tested again. For a second time, she tested positive for Covid-19.
News reports detailing the case raised the possibility that people may not be developing immunity to the new coronavirus, even after they’ve recovered. But several infectious disease specialists say there’s not enough data to support that conclusion. Another possibility is that the virus subsided and flared up again. (Some viruses tend to do that.) Or the test was simply wrong.

If someone was infected twice, comparing the genomic sequences of the virus over time would have helped determine that with more certainty.


It is necessary to distinguish between classical and non-classical actions of thyroid hormones.

Classical action involves nuclear THR (or TR) receptors (TR alpha1, TR beta1, TR beta2). They are activated by T3, 3,5-T2, TRIAC and 3,5-DIAC, and blocked by rT3 and rTRIAC. T4 and TETRAC hardly have an effect on nuclear thyroid hormone receptors, but they are converted in the periphery and in target tissues by deiodinases to T3 and 3,5-T2, and TRIAC and 3,5-DIAC, respectively. From the classical perspective, T4 and TETRAC are therefore prohormones and not hormones in the narrower sense.

Non-classical action denotes binding of thyroid hormones to integrin receptors on the cell membrane. The resulting non-genomic actions may be directly mediated by T4 and TETRAC and don't require deiodination. From the non-classical perspective T4 and TETRAC are hormones sensu stricto.

Figure from Hoermann et al. 2015 (CC BY license)

References

Hoermann R, Midgley JE, Larisch R, Dietrich JW. Homeostatic Control of the
Thyroid-Pituitary Axis: Perspectives for Diagnosis and Treatment. Front
Endocrinol (Lausanne). 2015 Nov 20;6:177. doi: 10.3389/fendo.2015.00177.
eCollection 2015. Review. PMID 26635726
Davis PJ, Goglia F, Leonard JL. Nongenomic actions of thyroid hormone. Nat Rev Endocrinol. 2016 Feb;12(2):111-21. doi: 10.1038/nrendo.2015.205. PMID 26668118.


Is there any known reason why 6 leg mammals are only found in mutations?

If stability is the goal, more legs tend to be better. However, having lots of legs also comes with a cost: they take energy to build and use, have extra weight, etc, and they don't really add any speed.

Insects are incredibly successful and likely evolved from many-legged ancestors, losing legs for efficiency but stopping at six. For small creatures with exoskeletons like insects, having fewer than 6 legs means too much loss of stability, because they rely on a tripod of 3 legs while moving the other three.

However, mammals and the vertebrates in general are larger and don't have exoskeletons and can use balancing and moving strategies that insects cannot. Further, they have evolved with four appendages since before they walked on land.

For a 6-legged vertebrate to evolve, there would need to be a selective advantage for having 6 legs versus 4; since vertebrates get along just fine with 4 legs, adding two more isn't likely.

I would also add that just because you can observe mammals with more than 4 legs does not necessarily mean that is a heritable trait. It could instead be caused by environmentally-induced errors in development. I think for the cases you mention this is probably most likely.

Lanham, U. N. (1951). Why do insects have six legs?. Science, 113(2945), 663-663.


Do the antibodies in a patient suffering from Hashimoto's, attack the thyroid hormones or the thyroid gland (or both?)?

Hashimoto's Thyroiditis is an autoimmune disorder where autoreactive attack on the actual thyroid tissue results in hypothyroidism. Pyzik et al., 2015, provides a good review of what we know about HT. The prevailing theory is that nonspecific infection can induce HLA expression on thyroid cells through the action of interferon gamma.

HLA is an antigen-presenting complex in humans that in our case is the major histocompatibility complex II or MHC-II you will see in texts (to avoid confusing names). Processed segments of protein are loaded onto the MHC-II, and displayed to the extracellular space where T cells positive for CD4 can recognize them. CD4+ T cells, upon recognition of MHC-II, are stimulated into T-helper or Th cells that are specific for the protein antigen they found on the MHC-II. The problem with MHC-II expressed by thyrocytes and the like is they can load either foreign or self peptides, so if it loads a part of thyroglobulin (Tg) on there and that's what the T cell recognizes, it's going to produce an immune response specific for Tg in a complex series of downstream events.

Being said, supplementation of thyroid hormone is a good treatment for hypothyroidism but it won't stop the attack on the actual gland. Thyroid hormones aren't often attacked by autoimmunity because they aren't protein antigens, and different subsets of cells respond to non-peptide antigens.


What does "thermodynamic equilibrium" mean for an enzyme-substrate complex?

Thermodynamic equilibrium means that:

Rate of forward reaction = Rate of backward reaction

In this case:

$E + S\xrightleftharpoons[k2]{k1} ES\\ \ \\
 \ \\ \\ at\ equilibrium:\\ \  \ \\ \ k1.[E][S] \tiny{\ (forward\ rate)}\normalsize=  k2.[ES] \tiny\ (backward\ rate)
$

This was the initial assumption in the Michaelis-Menten model.

Later on this was improvised by assuming pseudo-steady state of ES complex. This means that $[ES]$ does not change over time, which is both as a result of its production by the reversible reaction:  $E + S \leftrightharpoons\ ES$ and consumption by the irreversible reaction $\ ES\ \xrightarrow{k3} E+P$

that is:

$k1[E][S]\tiny\ (production)\normalsize=(k2+k3)[ES]\tiny\ (consumption)$


Most guidelines for HeLa (and most cells of human origin) say they should be kept at a BSL2 level. For example, from a 2007 publication in Applied Biosafety:

  Work with cell cultures from human or primate origin should generally be performed under BSL2 conditions. Containment level 1 may be considered if all manipulations occur in a Type II biosafety cabinet ...

--Animal Cell Cultures: Risk Assessment and Biosafety Recommendations

ATCC general guidelines recommend BSL2 containment for the broad category covering HeLa:

  Biosafety Level 2

  Cell lines that harbor mycoplasma or any other BSL 2 agent (See: NOTE)
  Cell lines exposed to or transformed by a primate oncogenic virus
  Primate cell lines that contain viruses
  Cell lines carrying a part of certain viral genomes, even if whole virus is not released from the cell

--ATCC® ANIMAL CELL CULTURE GUIDE: tips and techniques for continuous cell lines

Their specific page for HeLa also recommends BSL2, with the note "[Cells contain human papilloma virus]".

That said, HeLa cells have been very widely used, including for decades before modern lab safety practices were agreed on, and I'm not aware of any actual problem ever arising (including such amazing practices as injecting live HeLa cells into convict "volunteers" to see if cancers would appear - They did not).

So the answer to the question is that it is safe to work with HeLa cells, but that proper BSL2 lab practices should be followed.


This looks like Horse Chestnut Leaf Miner (https://www.rhs.org.uk/advice/profile?pid=533).  It is very common, and infects most of the horse chestnut trees around here.  Some years are worse than others. It has been spreading for the past few years.  It doesn't seem to seriously harm the tree, but there is no cure I have heard of.  The link I posted from the RHS offers some ideas about collecting the leaves and composting them in sealed bags, until the moth larvae have died. Occasionally, trees have been found that are genetically resistant to the disease.

Don't worry about the grass, the tree needs the light and water from that bit of soil, but you could try some bark mulch around the trunk to cover the soil, and keep the moisture in.


Is Einstein's mass energy equivalence ($E=mc^2$) relevant to biological systems?

Short answer

Any law of physics will of course be applicable to living beings. However, in the absence of mass gain and mass loss, the input = output equation for matter holds true and does not require any spontaneous creation and destruction of matter to equate. In other words, the effects of Einstein's discovery has no measurable/practical consequence on biological system (it is here but it is negligible) and the law of conservation of mass applies nicely.

Input and outputs of matter

There are two main sources of matter input:

Eating and drinking
inhaling (gas through the trachea and the lungs)

There are three main sources of matter output

excretion (urine and feces)
exhaling
sweating

The importance of inhaling and exhaling

Just to get an intuition about the importance of inhaling and exhaling matter in this input = output balance, note that when one make sport to lose weight, she/he principally lose weight through exhaling (see this popular video from SciHow). Similarly, trees mass mainly comes from  what they inhale (see this popular video form Veritasium)

Possible duplicate on Physics.SE

You might also want to read the How does mass leave the body when you lose weight? on Physics.SE.


How is HIV evolutionarily viable despite its extreme virulence?

Human Immunodeficiency Virus is a mutated form of Simian Immunodeficiency Virus. In simians (Apes and Monkeys, not including humans), SIV is not pathogenic, in most cases, however, when the mutated form made the jump to humans, it became highly contagious and virulent. You can find a basic description in the wikipedia article here: Simian Immunodeficiency virus.

As for your second question, I would likely say that influenza has killed more humans in total than HIV, so you would have to provide a reference for your claim.

However, because HIV is a retrovirus that incorporates into the genome of the immune cells of its host, it can survive in the body for long periods of time in a dormant state. A person may not know they are infected for months or years, and they can pass the virus on to other people. Slow killing viruses such as HIV are very dangerous, as they can be transmitted to large swaths of the population before people are aware they are sick.

Update:

Based on comments, there may be a misunderstanding of the term virulence. From The Karolinska Instetutet medical subject heading (MeSH) definition:

  The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. The pathogenic capacity of an organism is determined by its VIRULENCE FACTORS.
  -The Karolinska Institutet; Virulence

The emphasis is mine, but virulence also refers to the ability of the virus to infect its host, and does not necessary lead to the hosts death. The virus that causes the common cold is highly virulent, but for almost the entire human population it causes nothing more than discomfort.

A virus like Ebola on the other hand is highly virulent in both senses of the term. The reason that there are far fewer cases of Ebola is that it kills the human host so quickly, that an afflicted person will on average only go on to infect about two other individuals, mainly because victims 1) die quickly, 2) are only contagious after symptoms manifest themselves, and 3) requires direct contact with the infected person's bodily fluids.

Contrast that with Influenza which a single person can infect tens to hundreds of people and is contagious before they are displaying symptoms and spreads it with casual contact, or as stated above, with HIV, where a person can be contagious for weeks, months, or even years before they are aware that they are infected, and you see why HIV is very sustainable in the Human population.

HIV also has the added weapon in its arsenal that it can lay dormant in cells for long periods of time so as to escape the detection of the host immune system, and as the disease attacks and kills immune cells, when the dormant virus activates again there are far fewer specialized cells to address the active infection.

Another thing is it is the comorbidity with other diseases that often results in the death of a patient with an HIV infection. AIDS results from other diseases having the opportunity to go unchecked after HIV has decimated the host immune system.


Can Western Blots be used to quantify the activity of a protein?

I see 3 parts to a complete answer:

If you define the phosphorylated protein as active, and non-phosphorylated protein as inactive, and you have a total protein blot (as you say, via pan-specific antibodies) as you describe, then you have done everything correctly.

It's simple math from there on based on radioactivity or fluorescence or mass or whatever you use to quantify your band intensity. The 3 components should match up with the inactive protein amount (active + inactive = total). If this is consistent, you have additional evidence that you have done it correctly.

However, here come the hidden assumptions: this is all assuming that (i) you are not experiencing significant protein loss during your preparation steps, that (ii) your antibodies are good (specific and yield the complete protein extract), that (iii) the blotting procedure is performed correctly, and most importantly, that (iv) your initial definition is valid, that the phosphorylated protein is truly the active form of the protein, and that the unphosphorylated counterpart is the inactive form. You see, this is not always the case, though with some (most?) kinases, it is. If it has not previously been demonstrated, one may raise the reasonable objection that your assumption is wrong. However, I take it that in your specific case, the kinase activation by phosphorylation is well understood.


There are a few answers here, it is a little unclear which is closest to what you want.

[edited to be more complete and direct]

1) Nei's distance is mostly for comparing populations of the same species, so it should be fine if that is what you are doing. I am guessing that based on your post, you are more interested in cross-species comparisons. Of course, the logic is the same, it's just the math is different. For among-population divergence, Fst (fixation index) is also commonly used. But if you are using a sequence alignment or some such data to compute genetic distances, there are lots and lots of metrics. Some of them are very simple- for instance you could use Hamming distance and just count the number of residue differences between each sequence.

As for computing these metrics, there is a webserver called GenePop online that will compute Fst for you if you plug in a dataset. I don't know of R packages that compute these things, I would guess just by looking at wikipedia that coding functions to do this would be relatively trivial (if you are comfortable with r).

2) If you are truly looking among species, a somewhat more appropriate approach might be to model your species in a phylogeny, rather than to use distance methods (though the two are attempting to solve sort of the same problem). There are lots of easy-to-use online programs for this, for instance: FastML. You can just copy-and-paste a seq alignment in there. After you have the tree in for instance newick format, there are good tools for visualizing trees both online at iTOL, and through R with APE.

APE also has good utilities for modeling phylogenetic processes, so you could in principle directly model changes in protein folds through evolutionary time (assuming you have a meaningful summary of protein folding, either continuous or discrete).

I don't have enough reputation to link to more of the resources I mentioned, sorry.


What is a good list of unsolved protein structures?

There are some funded projects and analyses available just for this purpose.

Structural genomics or high throughput structure projects take all available peptide sequences group them into families and make sure sequence families pointing to most likely novel folds were available.

Here are the status and target list for the joint center for structural genomics. This list is filtered by species as well as by project status.

Their analysis is availble for us to browse through.  http://www1.jcsg.org/prod/newscripts/psca/help/document.cgi

Sorry this isn't so thorough.  Nature also hosts Target Track, which allows several high throughput structure centers to coordinate their efforts.  Each might have resources which could do your work for you.


FRET only works for interactions between 1nm to 20nm.

To get an elaborate answer on this one, I guess you should ask at physics. Very basically, FRET works by that an excited chromophore transfers energy to a nearby chromophore, through dipole-dipole coupling, which in turn emits energy (light) which can be detected. This is a quantum mechanic effect, i.e. these are very small energies. The emission energy between from the donor to the acceptor chromophore is inversely proportional to the distance between to the power of six according to the equation:

Where r is the distance and R0 the Förster distance between the donor/acceptor-pair (distance which the energy transfer efficiency is 50 %).This means that the energy to be detected very rapidly decreases. The Förster distance is in the range 2-10 nm for different chromophore pairs, which leads to the upper limit of FRET use.

The lower limit I don't know if it's due to steric effects or some quantum mechanical effect I do not know about. But since proteins are in the size range of the lower limit they must be in really close vicinity in order for their interaction to be detected using FRET.


Why do we encode information in DNA in binary and not in base 4?

In the research article on the effort, they give the following explanation for doubling up nucleotides, rather than have each nucleotide stand for two bits:

  This allows us to encode messages many ways in order to avoid sequences that are difficult to read or write such as extreme GC

In practice, they chose which base of the pair it was randomly (so a 50% GC content), while disallowing homopolymer runs greater than three.

Their scheme also uses barcodes and addresses as the "table of contents"/"index"/"page numbers". (The data wasn't stored on a single long piece of DNA, but on a large number of shorter fragments.) By having a slightly flexible coding scheme, this allows them to potentially avoid inserting those annotation elements within the contents.

Furthermore, a slightly flexible coding scheme would allow them to avoid accidentally encoding a text with part of a select agent's genome. (That is, you wouldn't want to synthesize part of the smallpox genome when you're storing your novel. If you can change the nucleotides used, you can avoid that.)


Which steps occur in each phase of Meiosis and Mitosis

Mitosis:
1. Yes, the spindle fibers attach to centromeres at the prometaphase

http://www.biology.arizona.edu/cell_bio/tutorials/cell_cycle/cells3.html

Meiosis:
1. The nuclear membrane breaks down in Metaphase 1 and reforms during Telophase. It breaks down again in Prophase 2, reforming after that in Telophase 2 in the daughter cells.

The spindles attach to the centromere is Metaphase 1
Yes the spindles attach to the sister chromatids in Metaphase 2

Check out this animation, it might be pretty useful


How many recombination events are there per generation in humans?

Back-of-the-envelope calculation

The definition of the centimorgan is that it is the length of DNA in a chromosome corresponding to a 1% chance of crossover occurring.

In human chromosomes 1 cM  = approx. 1Mbp.

Your value for the length of DNA in the genome = 3.3 Gbp = 3300 MBp

Ignoring complications like the Poisson distribution:

1 cM corresponds to a probability of 1% chance of a detectable crossover. Detectable, because only an odd number of crossing over events between 2 genetic markers can be observed as a recombination, but even numbers instead go unrecognised. Therefore the actual chance of crossing over is doubled relative to the cM value.
If 1 cM = 2% actual chance of crossover, there will be on average 1 crossover per 50 cM or per 50Mbp

Therefore crossovers per human genome = 3300/50 = 66  or approx 2-4 per chromosome

This guess comes near empiric data:

Actual data

This Table, taken from here shows the number of chiasmata by chromosome for 8 human cells. (Note that it believed that there has to be at least one chiasma per chromatid pair since they have a structural role.)

The average chiasmata per chromosome for each chromosome can be estimated by dividing the number in the final column by 8. These vary from (rounding aggressively) 3.5 for Chr 1 and Chr 2, to 1 for Chr 20. So my back-of-the-envelope calculation seems to have produced a reasonable answer.

What is the amount of DNA exchanged? I'm not sure this question matches well with the picture that emerges from these numbers.


How does hibernation reduce risk of radiation-induced mutation?

This is still an area of active research, and there doesn't appear to be a single definitive answer for the mechanisms behind the reduction in radiation-damage during hibernation.
A recent review by Cerri et al. (2016) covers a lot of the known biology behind hibernation and resistance to radiation damage.
A few select quotes from this review:

At the cellular level, it is well known that cells irradiated in
resting state, and left undisturbed for 24 h after irradiation, are
more resistant than cells re-plated immediately after exposure. This
effect is known as delayed plating, and is generally attributed to the
potentially lethal damage repair (PLDR) in resting phase.
...
The oxygen level during hibernation may contribute to the enhanced
radioresistance. Hypoxia is a well know protective mechanism, and is
arguably the main reason of local control failure in radiotherapy.

Rockwell et al. (2009) discuss the underlying reason behind reduced radiation sensitivity in a hypoxic environment:

Molecular oxygen (O2) is a potent chemical radiosensitizer. This
radiosensitization does not result from any of the metabolic or
physiological effects of oxygen, but instead reflects the fact that O2
is an extremely electron-affinic molecule that participates in the
chemical reactions that lead to the production of DNA damage after the
absorption of energy from ionizing radiation [21,22].

My personal take would be that the reduced risk of radiation-induced damage is probably not due to the structural arrangement of DNA, but rather the overall cellular environment. This is perhaps linked to an enhanced ability to repair damaged DNA, but is also likely to be highly dependent on cellular oxygen levels.


Correct term for initially neutral mutations that subsequently cannot be reversed

Mutation A is a suppressor of Mutation B. The Wikipedia article on the topic (https://en.wikipedia.org/wiki/Suppressor_mutation) mostly describes situations where Mutation A occurs after B and reverses B's deleterious effects, but the principle is the same.


How do fish tolerate pH changes in water?

Often, in terms of a water body becoming acidified, it depends on the rate of acidification.  Fish and other aquatic species, such as invertebrates, are fairly resilient to miniscule changes, but they also have a threshold at which not a lot of them, adapted or no, can survive.

From the U.S. Environmental Protection Agency (http://www.epa.gov/acidrain/effects/surface_water.html):

  Acid rain causes a cascade of effects that harm or kill individual fish, reduce fish population numbers, completely eliminate fish species from a waterbody, and decrease biodiversity.  Low pH [...] is directly toxic to fish. In addition, low pH and increased aluminum levels cause chronic stress that may not kill individual fish, but leads to lower body weight and smaller size and makes fish less able to compete for food and habitat.

  Some types of plants and animals are able to tolerate acidic waters. Others, however, are acid-sensitive and will be lost as the pH declines.

Commonly, benthic invertebrates (including insects, crustacean and molluscs) are used as indicators for ecosystem health.  Invertebrates that need a high amount of calcium, such as crayfish (for their exoskeleton), are typically not found even in slightly acidified lakes.  Other invertebrates can be used as indicator species because they respond to changes in water conditions, such as pH.

A good example of this is the acid rain that occurred in Sudbury, Ontario, Canada as a result of sulfur dioxide emissions from mining activities, which were especially high in the 1970s.  This affected the lakes in the area not only from acid rain, but the runoff as well as there were no trees left.  The pH was so low that it effectively made all lakes in the area sterile. Since then, a lot of effort has been put into bringing back the native aquatic species, such as liming the lakes and restocking them with species such as Brook Trout (Salvelinus fontinalis).  More information can be found here:

http://link.springer.com/article/10.1007%2FBF00160348

Therefore, I do not know that aquatic animals necessarily behave a certain way as a natural indicator of acidity, however it is more of their presence or absence that biologists use to determine acidity and the overall ecosystem health in lakes and rivers.


Is there any evidence of blue jays preying on other birds?

Yes! This article gives an account of a Blue Jay killing and consuming a Cedar Waxwing, and further it clearly states that at times Blue Jays do predate on fledgling and adult birds, and gives a hefty amount of sources to back that up, if you're in the mood for further reading.


You have to remove the salts, remove the dye, digest the protein, extract the digested peptides from the gel etc.

For details, see this protocol.


Because mammary glands define us (mammals), the genetics of the ability to make milk has been of interest.[1] Because we consume milk, we have a dairy industry. Because the industry places a monetary value to certain milk constituents, the genetics of milk component production has been a viable area of study[2]. Since you are talking of cream production, we'll stick to that.

The effect of nutrition and the environment (e.g. temperature) on milk fat production has long been known, and the ability to selectively breed for higher fat content has been exercised for decades if not longer[3][4], But the molecular genetics of milk fat production is only recently starting to be understood.

Mammals with the highest fat content are those in cold environments where an insulating layer of fat is required, such as gray seal milk (53.2% fat), whale milk (34.8%), and polar bear (31%). Humans and cows have approximately the same milk fat percentage (~4.5% fat).[5]  The gene most studied to date is the DTAG1 allele[6] on chromosome 14.[7]

It is very clear that genetically milkfat production is under the governance of part of chromosome 14.[7][8] Since this chromosome is identical in both breasts, genetically one breast cannot make milk with a higher fat content than the other. Environmental and nutritional factors affect both breasts equally, so those can be ruled out as a source of fat percentage differences. The only factors left that can be variables are 1) fat content of one breast over the other, and 2) demand from one breast over the other.

In cows, more frequent milking increased milk production but decreased fat percentage; in the end, the effect on fat in milk was the least influenced by frequency of milking (significance questionable).[9]

Triglycerides in milk are synthesized in the smooth endoplasmic reticulum of the mammary alveolar cell from precursor fatty acids and glycerol (obtained from blood nutrients), and while other cell types are involved in milk let down, etc., there is no known function of interstitial adipocytes (fat cells).[10]

That was the long answer. The short answer is: no[11].

[1] The origin and evolution of lactation
[2] Milk Components: Understanding the Causes and Importance of Milk Fat and Protein Variation in Your Dairy Herd
[3] A review of nutritional and physiological factors affecting goat milk lipid synthesis and lipolysis
[4] Factors affecting milk composition
[5] The Highest Percentage of Fat in the Milk of an Animal
[6] Evidence for multiple alleles at the DGAT1 locus better explains a quantitative trait locus with major effect on milk fat content in cattle.
[7] Identification of novel single nucleotide polymorphisms in the DGAT1 gene of buffaloes by PCR-SSCP
[8] Scientists pinpoint gene linked to fat in cow’s milk
[9] Covariance among milking frequency, milk yield, and milk
composition from automatically milked cows
[10] MILK SECRETION: AN OVERVIEW
[11] Does a bigger breast give creamier milk?


I've had some experience with Karen Strier's 'Primate Behavioural Ecology', and it's solid. It's a nice overview with (obviously) a strong ecology/ethology bent. I don't think it comes in ebook though.

Here's the Amazon link.


This is a species in the Peristediidae family, commonly called armored searobins or armored gurnards.

  found in deep waters around the world, with most species in tropical regions. They are related to the searobins in the family Triglidae, and some authorities classify them in that family,2[3] but they are encased in heavy scales with prominent spines. They have prominent and often elaborate barbels on their chins.

Characteristics of Peristediidae [Source]:

  The scorpaeniform family Peristediidae (armored sea robins) is characterized by (1) a body entirely enclosed by four rows of spinous bony plates (scutes) on each side; (2) a large bony head with spines and ridges; (3) each first infraorbital (lachrymal) anteriorly extending in distinct rostral projections; (4) barbels on the lower jaw, and (5)pectoral fins with the two ventral most fin rays free and enlarged (Miller 1974; Miller & Richards 2002; Richards 1984, 1999; Kawai 2008, 2013)

Specifically, this looks similar to other species in the genus Satyrichthys.

 Satyrichthys welchi (Source: Taiwan Biodiversity Informaiton Facility)

According to Pogoreutz et al. 2013:

  The genus Satyrichthys is diagnosed as follows: (1) no teeth in upper and lower jaws; (2) lateral margin of the head smooth; (3) the ventral row of bony plates on caudal peduncle extending posteriorly, separating the posterior bony plates of the lower lateral series; (4) only the posterior lip and chin barbels branched, and (5) fewer than 20 soft rays in dorsal and anal fin (Kawai 2008, 2013).

  An important character in separating species of the genus
  Satyrichthys is the number of lip and chin barbels (Miller 1964, Kawai 2008, 2013)

One similar looking species is Satyrichthys welchi (the Robust armoured-gurnard) [pictured above] found in the South China sea:

 Source: AquaMaps

According to FishBase, here are some characteristics of Satyrichthys welchi:

Dorsal spines (total): 7
Dorsal soft rays (total): 17
Anal spines: 0
Anal soft rays: 18


How can CI repressor both activate and repress $P_{RM}$ promoter found in $\lambda$ phage?

There's no rule that says a transcription factor must be either a repressor or an activator. The lambda repressor (CI) is in fact a repressor and activator of transcription, depending on where it is bound and to what promoter you are referring to. I know your question isn't directly about lambda phage, but I think this mechanism may be best explained in the context of where it was first invented: nature. So, I will try to briefly explain how the lambda repressor's dual role allows regulation of its own expression and controls lysogenic induction.

The cI gene is under the control of the PRM promoter. The PRM promoter is weak because the sigma factor of RNA polymerase (RNAP) holoenzyme has low affinity for it. Binding of RNAP to PRM, and thus transcription from there, at a reasonable level requires an activator. There is another protein involved in this process as well, called Cro, that can also bind the OR operators. The cro gene is under the control of the PR promoter. PRM is not a constitutive promoter because it requires an activator. I have heard PR called constitutive because it is a strong promoter and can bind RNAP without an activator. But, at the same time, it is under the control of the lambda repressor. I suppose it depends on which definition of 'constitutive promoter' you use.

The OR operators are not identical and thus CI and Cro bind them with different affinities: CI has the highest affinity for OR1, followed distantly by OR2 and OR3, while Cro binds OR3 with highest affinity. Binding (of any two molecules) is dependent on both their affinity to each other as well as their effective concentration. At lower concentrations, CI can only bind OR1 and OR2 cooperatively. That is, each lambda repressor dimer binds to another, forming a tetramer, with one half binding OR1 and the other binding OR2. Binding both operators as tetramer allows for a stronger interaction. At higher concentrations, CI can bind OR3. Furthermore, OR1 and OR2 are located in the PR promoter, while OR3 is located in the PRM promoter.*

Most lambda genes are under the control, directly or indirectly, of the PR and PL promoters (PL is similar to PR, but the promoter itself is not directly involved in cI regulation). When lambda exists as a prophage, its DNA is integrated into the host genome and most of its gene expression is repressed. This requires CI repression of PL and PR. When the viral DNA is first integrated, there is no CI in the cell (because it is a phage gene). Expression of cI is initially dependent on a different promoter (PRE), but I won't get into this here. Once CI concentration is high enough, it can bind to OR1 and OR2 as a tetramer. Binding here physically blocks the PR promoter and prevents expression of cro (CI acts as a repressor of PR here). It also interacts with RNAP (actually the sigma factor) and facilitates is binding to the PRM promoter, which leads to further cI expression. This process is commonly called recruitment: since CI is bound tightly to the DNA and has some affinity for RNAP, it can create a stronger interaction between the DNA and the RNAP-CI complex. Simply put, it induces the PRM promoter and is thus functioning as an activator of cI transcription. As CI concentration increases, it will bind OR3 more (which is located in the PRM promoter) and repress the PRM promoter by physically blocking RNAP from binding. In these ways, cI can autoregulate its expression level, both positively and negatively.

When the lysogen is in some kind of stressful condition, normal host processes will result in proteolysis of CI and its DNA/sigma binding domain is cleaved from the dimer- and tetramerization domains. This means that CI can no longer oligomerize and is no longer able to bind cooperatively to OR1 and OR2. The result is loss of PRM activation (leading to vastly reduced cI expression) and also a loss of PR repression (leading to cro expression). Cro can then bind OR3 and represses PRM. Lack of PR repression also allows expression of early phage genes (which are under the control of PR).

Note that a similar situation occurs at the PL promoter region, and binding of CI to both OR and OL as well as CI octomerization is important in prophage regulation, but that seems even further out of the scope of your question. Hopefully you can see how he lambda "repressor" actually functions as both a repressor and activator of transcription. If this kind of stuff interests you, I highly recommend a textbook called Molecular Biology of the Gene by Watson et al.

*See comments. Upon further research, the PRM and PR promoters both overlap OR2 (Autoregulation and Function of a Repressor in Bacteriophage Lambda, Ptashne et al.), as the diagram in the OP shows. It appears that the -35 region of both PRM and PR overlap OR2 by 2 and 3 base pairs, respectively. That led me to wonder that if CI binds to OR2, which is in PRM, wouldn't it physically inhibit RNAP binding and thus repress transcription? Well it appears that CI interacts with the same region of sigma that is responsible for binding the -35 region of PRM (Amino acid substitutions in the -35 recognition motif of sigma 70 that result in defects in phage lambda repressor-stimulated transcription, Kuldell and Hochschild). So instead of blocking sigma binding here, it enhances it.


How will rising carbon dioxide levels in the troposphere affect photosynthetic producers?

There are several key ways in which rising atmospheric CO₂ concentrations will affect photosynthesis, and these are related to the different types of photosynthesis. In order to properly answer your question, I'll provide some background about photosynthesis itself.

Photosynthesis evolved in a high-CO₂ atmosphere, before the oxygen-enrichment of the atmosphere (which actually happened as a result of photosynthesis). Most plant species operate C3 photosynthesis. In these plants, carbon dioxide diffuses into the cell where it is fixed by Ribulose-1,5-bisphosphate carboxylase oxygenase (RuBisCO) into a 3-carbon molecule (hence C3), which is then polymerised to make sugars. A crucial fact about RuBisCO is that it has both carboxylase (carbon-fixing) activity and oxygenase (oxygen-fixing) activity. This means that oxygen and carbon dioxide compete for the active site on the enzyme complex, leading to RuBisCO being quite inefficient and slow at fixing carbon in higher oxygen concentrations. That didn't matter in the high-CO₂ atmosphere of the early Earth, but in todays atmosphere O₂ concentrations are high enough that they severely limit the productivity of C3 plants.

However, plants haven't just been growing slowly all that time - several mechanisms for increasing photosynthetic efficiency have evolved. The most influential systems involve concentrating carbon dioxide in a particular area, excluding oxygen, and concentrating RuBisCO in that same area. This avoids the oxygen competition for the active site and allows RuBisCO to operate more efficiently. The key adaptation here is C4 photosynthesis - the system which is present in most grasses and many of the most productive plants on Earth (e.g. maize, sugarcane, Miscanthus). It has evolved at least 62 times independently. It works by having RuBisCO concentrated within 'bundle sheath' cells which are surrounded by a layer of suberin wax. This layer prevents CO₂ escaping and O₂ from getting in. CO₂ from the atmosphere is then fixed in different cells - 'mesophyll cells' - by another enzyme - Phosphoenolpyruvate carboxylase (PEPC), resulting in a four-carbon molecule (hence C4). This 4-carbon acid, (malate or oxaloacetate depending on the system) is then shuttled into the bundle sheath cells. There, the CO₂ is released again by a variety of enzymes depending on the system, creating a high CO₂ concentration in the cell where RuBisCO can then work efficiently.

In general, C4 plants are much (about 50%) more efficient than their C3 counterparts, and they are particularly well adapted to high temperatures and moist environments. So, to answer your first question: as atmospheric CO2 levels continue to rise, C3 plants will gradually be able to photosynthesise more efficiently. Interestingly though, C4 plants are predicted to also benefit from increased atmospheric CO₂. If global temperatures rise as predicted, both C3 and C4 plants will be able to operate more efficiently than they currently do, up to a maximum temperature beyond which enzymes will begin to denature faster and efficiency will drop. One consideration is that the difference in efficiency between C3 and C4 systems will decrease, which may significantly alter the makeup of plant communities around the world.

This is a vast oversimplification, but it is accurate for the predicted overall effects. Localised effects (i.e. productivity changes in a particular region or for a particular crop) will depend on habitat, physiology, etc.

Some key papers to launch you into the literature:

Leakey, A.D.B., Bernacchi, C.J., Dohleman, F.G., Ort, D.R. & Long, S.P. (2004) Will photosynthesis of maize (Zea mays) in the US Corn Belt increase in future [CO2] rich atmospheres? An analysis of diurnal courses of CO2 uptake under free‐air concentration enrichment (FACE). Global Change Biology. [Online] 10 (6), 951–962. Available from: doi:10.1111/j.1529-8817.2003.00767.x [Accessed: 31 January 2012].
Morgan, J.A., LeCain, D.R., Pendall, E., Blumenthal, D.M., Kimball, B.A., Carrillo, Y., Williams, D.G., Heisler-White, J., Dijkstra, F.A. & West, M. (2011) C4 grasses prosper as carbon dioxide eliminates desiccation in warmed semi-arid grassland. Nature. [Online] 476 (7359), 202–205. Available from: doi:10.1038/nature10274 [Accessed: 31 January 2012].


What is this species of green frog found in store-bought flowers in France?

This looks very much like a tree frog of which there are many similar looking species. Without knowing where your flowers came from or more characteristics about the specimen, it'll be difficult to provide an accurate answer*.

One possibility may be the European tree frog (Hyla arborea).

According to Wikipedia:

  Members of the H. arborea species complex are the only representatives of the widespread tree frog family (Hylidae) indigenous to mainland Europe.

which is supported by genetic work by Stöck et al. 20081

Description [source]:

Small (3.2-5 cm in length)
Slender body shape with long legs and smooth dorsal skin+
Usually green (but variable) with dark brown lateral stripe across eye caudally to groin and whitish ventral skin surface.
Gripping discs on toes

The range of this species also includes much of France:

 Image Source

+ Although the description states this species has smooth dorsal skin (possibly like the OP's specimen -- I can't tell for sure), many of the pictures I've seen seem to suggest that the dorsal skin of this species is actually rather granular. For example, see here.

*Feel free to update your post with additional info and perhaps a better response will be added.

 Citations:

 1 Stöck, M., Dubey, S., Klütsch, C., Litvinchuk, S.N., Scheidt, U. and Perrin, N., 2008. Mitochondrial and nuclear phylogeny of circum-Mediterranean tree frogs from the Hyla arborea group. Molecular Phylogenetics and Evolution, 49(3), p.1019.


I think, you misidentified the unpaired anal fin of coelacanth as an extra pair of limbs.

I personally haven't ever heard of six-legged vertebrates, although the phenomenon of supernumerary legs is well known as an anomaly. Such anomalies can be easily induced in different vertebrates (including mice: Rutledge et al), if you treat their embrya with retinoid acid (which normally defines embryonic polarity) or fibroblast growth factor. In nature, different factors can lead to development of extra legs, and the most well-known and wide-spread cases are limb abnormalities in amphibians, induced by trematodes and pollution (including retinoid acid mimics?) (Blaustein & Johnson).

That said, I would not be surprised by a discovery of a fossil amphibian with extra limbs. But such a find then should be interpreted as an abnormality, if not proved otherwise. It's true that the fore and the hind limbs are serial homologues, but their number seems to have been fixed very early (in contrast to the number of the fingers).


How do you go from virus infection to disease?

In viral infections, the disease (on the cell/tissue level) is mainly due to immune response that results in inflammation, for example, of the throat mucosal lining, which can trigger symptoms, such as dry cough.

Each symptom has its own trigger. For example, in flu:

  The mucous membranes lining the nasal and sinus cavities can become
  inflamed when infected with the flu virus. This results in increased
  pressure around the eyes and face, which may lead to a magnified
  headache (National Headache Foundation).

and

  The immune reaction to the viral infection and the interferon response
  are responsible for the viral syndrome that includes high fever,
  coryza, and body aches (StatPearls).

How viruses cause symptoms is a broad question - it depends on the virus and exact symptom, so just few more examples:

In viral pneumonia, immune response triggers inflammation in the lung alveoli, which can result in shortness of breath (StatPearls).
In AIDS, HIV virus destroys CD4 lymphycites and thus impairs cell-mediated immunity, which makes the infected person vulnerable for infections, so most symptoms are from those infections, for example, oral thrush due to overgrowth of Candida yeasts in the mouth (MerckManual).

Viruses usually do not cause disease or symptoms by merely changing the function of the cells, but by damaging them, so it's more about "injury" than just a changed function. The damage of the cells and the viruses themselves trigger inflammation and most of symptoms usually originate from it.


Do couples having children later in life act as an evolutionary mechanism?

Many factors have to be considered.  First, although more women are delaying pregnancy until after the age of 35, the overall percentage of women doing so remains very small, as shown by this figure from this New York Times article. Only about 9% of pregnancies in the United States (for 2008) were in women over the age of 35. Most pregnancies still occur in younger women. I suspect this is especially true when considered globally.

Getting pregnant later in life is more difficult, is more likely to result in miscarriage, and is more likely to result in some types of birth defects. The issues are discussed by the Mayo Clinic, WebMD, and summarized by Parenting Magazine. On average, individuals with birth defects are themselves less likely to reproduce (Skjaerven 1999).
For natural selection to favor a particular trait (such as later pregnancy), the individuals with the trait must have higher relative fitness, meaning they produce more offspring on average compared to other individuals. However, relatively few women have late-age pregnancies, more of the offspring are likely to have birth defects, and those offspring are themselves less likely to reproduce. In other words, on average, late-age pregnancies would have reduced fitness compared to individuals that get pregnant at earlier ages.
Most importantly, though, the decision to wait until later in life is a conscious choice, not a genetic trait. Natural selection can only work on genetic variation associated with particular traits. If the choice for delayed pregnancy has no genetic basis, then it is invisible to natural selection, and so cannot evolve.

Citation
Skjaerven, R. et al. 1999. A population-based study of survival and childbearing among female subjects with birth defects and the risk of recurrence in their children. The New England Journal of Medicine 340: 1057-1062.


Can endometriosis be considered a form of cancer?

According to Endometriosis: benign, malignant, or something in between? (PubMed, 2017), endometriosis is not considered cancerous because:

Does not appear as an expansille tumor mass
Is not destructive
The cells in the lesions are normal, like in the uteral endometrium
Is not lethal

Immunotherapy of endometriosis is in the experimental phase - you can read more here: Novel Therapies Targeting Endometriosis (PubMed, 2011). Other treatments mentioned are anti-inflammatory drugs, selective estrogen or progesterone modulators, statins and antiangiogenic agents. There is also a study Open Label Immunotherapy of Endometriosis running - it is briefly described on ClinicalTrials.gov.

Chemotherapy, which is effective in some cancers, is based on killing quickly-dividing cells, but cells in endometriosis do not divide so quickly, so you can't treat it by chemotherapy in the same way.


This is a neophyte that has been recorded in Europe since 1979:
Sceliphron curvatum, in German also known as orientalische Mörtelwespe. Unusually large considering what else is buzzing around, but mostly harmless.
The nests, or rather individual larvae cells, are made of mud and while there are about thirty species in the genus, only Sceliphron curvatum is found in Germany - there‘s no other wasp or other insect in Germany that builds similar nest cells, especially the size is a good indicator. Your description of nest location in a window frame is typical, curtain folds or (vertical) nooks in furniture, e.g. shelves are also welcome. Our specimen picked a hiding spot behind a few books a few years ago.
Because of their size, there are usually some articles about them in the low-news summer media lull, describing baffled citizens and their “discovery”. A few less sensational descriptions, photos and further information can be found here (sorry, in German).
Nice find!


I had a look at white-flowered plants flowering in July in a site about the flora of the French Alps, and the best I could find was Parnassia palustris:
http://www.florealpes.com/fiche_parnassie.php

At this developmental stage, it looks quite similar to your photo, with the same kind of structures at the base of the petals.
The site says that there are heart-shaped leaves at the base, plus one on the stem. This last leaf matches your description. The site says it can grow up to 2500m.

The Italian Wikipedia says:

  In Italia è presente solo nelle regioni settentrionali e centrali, nonché in Campania.[2] In montagna si spinge fino a circa 2000 m, ma sulle Alpi è stata segnalata anche a quote superiori (3000 m sul versante svizzero del Monte Rosa).

This means that it can be found in the Italian Alps too, including at 2000m.


Is there variation of AT/CG ratio along species?

That ratio is essentially, as WYSIWYG pointed out, called GC-content.  In actuality, GC-content is reported as $(G+C)/(A+C+G+T)$, converted to percent; i.e., what percent of the genome is G or C.

There is vast variation in GC-content, both amongst species and within a given species' own genome.  For example, in humans the first intron and exon are generally more GC-rich than following introns/exons.1  Genes themselves are often found in higher GC areas,2,11 in particular CpG islands are found near a large number of (mammalian) promoters.3

Across species, there can be a big difference.  Yeast and Arabidopsis are both around 35%4,5 whereas Plasmodium falciparum is around 24%;6 Carsonella are even lower, at around 16.5%.14  On the other hand, the plankton Emiliania huxleyi is around 65%7.  We can use these differences to study genomic history.  Bacteria often have genes from all over the place thanks to horizontal gene transfer, and GC-content can be used to differentiate between their own genes and those from horizontal gene transfer;8 a good example is the CRISPR-Cas system,9 even in a virus!10

Here's a list of a few things genomic GC-content is correlated with:15

genome size
whether the bacterium is free-living or not
the environment
aerobiosis
nitrogen utilization

In the lab, high GC-content often means a harder region to work with, as the presence of three instead of two bonds (between A and T) requires more energy to break;12 anything involving primers can be made more annoying, including (especially, to some) sequencing.  There is a theory that high GC-content would be an adaptation to high temperatures, to avoid DNA damage, but that is controversial.13,16,17,18


The answer is right in the second half of the sentence:

  running from the orbital frontal cortex to the cingulate gyrus, striatum (cuadate nucleus and putamen), globus pallidus, thalamus and back to the frontal cortex

Orbital frontal cortex, cingulate gyrus, striatum, globus pallidus, thalamus, and back to (orbital) frontal cortex: these are all different brain regions. If A connects to B, B connects to C, C connects to D, D connects to E, and E connects back to A, you've made a loop.

The page is saying that there is a hypothesis that there is dysfunction somewhere along this loop in OCD; it doesn't say where exactly, but you can infer that changing something along this path would affect all of the other regions connected in the loop in some way, because they are all causally related to one another.


Do people often blow out the air from their lungs a lot when living in the cold condition to keep their lungs warm?

In a cold climate, do people often blow out the air from their lungs a lot when living in the cold condition to keep their lungs warm?

No, and it wouldn't make any sense: breathing more means inhaling more cold air that needs to be warmed up, so the result is a heat loss. The more so, as cold air (< 0°C) has a low water vapor pressure, while the lung likes to have the air at body temperature and well moistened. Which means that you also loose the vaporization heat of the water.

The function of moistening and heating the cold and dry air as well as recollecting some of the heat and water when breathing out is done by the nose. So the sensible (and done) thing in cold weather is to avoid breathing by mouth and instead keep your mouth shut and breathe by nose.
Nevertheless, neither German nor English, nor any of the Scandinavian Germanic languages is spoken through the nose.

My experience is that cold air (personal minimum: -40 °C) in the mouth is very unpleasant, and makes me cough as it is still cold when it arrives in the throat, but of course breathing out by mouth is less of a problem. But breathing out by mouth and in by nose means that the nose cannot recollect the heat and moisture from the outgoing air.

In any case, the amount of breathing is linked rather to oxygen demand and $CO_2$ to be gotten rid of), and even the fastest speaking people I know do not get close to hyperventilation by speaking, not even speaking German or English.
Which means that speaking Germanic languages needs less breath to produce the sounds than what you need to breathe for physilogical reasons even at not much above base rate metabolism (sitting while talking) anyways. Which would imply that the breathing difference between Germanic and Sino-Tibetan languages would not cause an important driving force in language evolution.

A side point is that I don't agree with your concept of cold climate. Both Germany and England are counted as temperate climate. Actually, Frankfurt has higher minimum temperature all year round than Lhasa (as you mentioned Tibetan in your language family).
Also note that the Indo-Germanic language family covers a range of climates from tropic to polar just as the Sino-Tibetan covers some cold regions as well), so maybe language families that are spoken only in polar regions vs. such that are spoken only in tropic regions would be better to look at (see e.g. the Wikipedia language family map).

However, there are probably some confounding influences that need to be taken into account. In cold weather, you do not sit or stand around chatting with people as much. And in the polar climates, historically farming has hardly been possible. So you have populations where hunting has been very important for survival, and regions with very low population density. Both mean that on average, you'll be silent instead of talking. As for having a chat with someone, you'd ask them in - or the length of the chat is limited by temperature.
Which means that if cold is a driving force for the type of pronouciation that evolves, it would be a rather weak link. And in any case, speaking less will overcompensate all these breathing differences.


Evolutionary reasons why you cannot tickle yourself but masturbate

I think there is a bit of a logical leap here (or at least in the title).

The simple answer is that there are many biological phenomena for which there is no logically satisfactory explanation. For instance: why do people have wisdom teeth? We come up with some hand-wavy explanations about ancestral diets, but at the end of the day we just have wisdom teeth (or at least most of us do) and there isn't a great immediate causal pathway that tells us why this rather inconvenient thing exists in modern humans and hasn't been lost.

Getting back to the question at hand, there are a number of assumptions that seem to come along with this question:

Most importantly, why is it assumed that there must be an evolutionary "reason" for a biological phenomenon? In many/most cases there is no such reason. Most (molecular) evolution is neutral and random.
Why is it assumed that there is an equivalence between tickling and sexual stimulation? (then again, a cursory google search suggests there is a relationship...)

Both tickling and masturbation are phenomena that seem to occur in primates. However, this does not require that there be a link between them even if they appear to be similar superficially. Furthermore, it is not logically required that either of them satisfy any particular purpose, even if we can imagine a possible purpose (as some of the commenters have).

Of course, there are lots of reasons why these things exist if you're willing to drop the evolutionary mumbo-jumbo. For instance: both of these things can be fun and God loves us and wants us to be happy. This is the same as the platitude from Ben Franklin on why booze exists. Substitute your favorite demiurge.

These arguments are not much different from arguing that constant ejaculation leads to better sperm on evolutionary time scales. There is equally good (better?) evidence that having to produce more sperm leads to a higher prevalence of birth defects and other disorders. So maybe masturbation is bad from one reasonable point of view, and is in fact a deleterious vestigium like wisdom teeth. The "scientific" answer depends a bit on which literature you pay attention to.

Evolutionary answers of this type tend to be this kind of just-so stories. They give an air of precision and authority with uncertain logical backing, and they don't even have the folksy philosophy as a consolation.

This may not be an answer in the fashion the OP intended, but hopefully it does at least give a perspective on thinking about these kinds of questions.


Missing 4 $\ce{H_2O}$ (per glucose) in Cellular Respiration... Where can they be?

First thing to make clear is that net $6 \, \ce{H_2O}$ go out of the reaction.($12 \,\ce{H_2O}-6\,\ce{H_2O}$)

Let me tell you my calculation, you should then be able to figure out what went wrong.

For the Left hand Side, $6\,\ce{H_2O}$ are accounted here :

$2\,\ce{H_2O}$ go in conversion of 2-Phosphoglycertae to phosphoenolpyruvate.
$2\,\ce{H_2O}$ in TCA from conversion of Oxoloacetate to Citrat by combining with Acetyl CoA.(One for each Acetyl CoA molecule)
The aconitase -cis-aconitase-isocitrate water molecules cancel out. Equal no go in and out.
$2\,\ce{H_2O}$ in TCA from conversion of fumarate to Malate.

For the right hnd side, if we calculate the no. of NADH formed = 10 and assume that each participates in respiratory chain, we have $10\,\ce{H_2O}$ from there. The other $2$ will be from the $2$ FADH produced.

So we have 6 on the LHS and 12 on the RHS. Hope this makes sense !


According to the book Stomatal function (Zeiger et al, 1987), many aquatic angiosperm plants have stomata (since they have evolved from terrestial plants), while some have reduced or complete loss of stomata.

However, the book also states that:

  ...aquatic plants living underwater are devoid of stomata. Leaves that float in water, which are common in ponds, have stomata on their upper surfaces but lack them on the surfaces in contact with water.


Help me identify this insect found in fishtank

This is a Damselfly, suborder Zygoptera. Together with the Anisoptera (true dragonflies) they belong to the order Odonata, usually also named dragonflies.

Damselflies are smaller and more slender then Dragonflies, both as larva and as adult, although there are exceptions (mostly tropical species).

It can be distinguished from mayflies by it's broad head and the broad, flat lamellae; the 3 'tails' as you call them.

Some beautiful pictures can be found here


Is there an agreed-upon definition as to how many nucleobases constitute a gene?
If not, why not?

There is no such definition. A gene is a region of the DNA that is transcribed. Typically a gene should have a transcription start site dictated by a promoter and a transcription stop site marked by termination signals (like terminators and poly-A signal etc.)
There are some little RNAs (~18nt) that are produced from TSS of usual genes but are probably products of failed elongation. These are not really considered genes as they are heterogeneous in size and are not marked by any boundary.
There may technically be a minimum cutoff on gene length which could be the length of DNA necessary for the RNA-polymerase to sit and also include the termination signals. As indicated in the comments, the smallest gene may be the tRNA. However, the smallest annotated gene from the GENCODE annotations is TRDD1 (just 7nt long!!!). This is not based on gene prediction; it is manually annotated by the HAVANA team.

What is the average length of a gene?

I just did a rough calculation from the GENCODE human genome annotation file (version 23).
The average transcript length seems to be around: 1.5kb
The average gene length seems to be around: 29kbp
The genes would be longer than (or equal to) their corresponding transcripts because the latter gets shortened due to splicing.
I made a histogram plot of these lengths for convenience:

Transcript length distribution

Gene length distribution

Note the sharp peaks at 100bp. Quite interesting!

Remi has user19099 have mentioned that the longest gene in humans is titin. It seems that it is the longest gene in many other diverse animals. See What's the longest transcript known? for more details.

Methodology (so that limitations can be identified)
To calculate gene length distribution: I parsed the GTF file for "genes" (third field i.e. feature) and subtracted the fifth field (stop) from fourth (start).
To calculate transcript length distribution: Got the transcript fasta file from the annotated locations. Calculated their lengths. Plotted the distribution.


Why do SRIs help in serotonergic neurotransmission?

Excellent question.

Different neurotransmitters operate at different temporal scales (and even the same transmitter can operate at different temporal scales). Examples of the fastest-acting neurotransmitters are glutamate, GABA, and acetylcholine (with the caveat that they can also act more slowly). These neurotransmitters (usually) open ion channels in the postsynaptic cell, and are cleared rapidly after release, which allows for a temporally precise code, with each release event individually important.

Other neurotransmitters are also considered neuromodulators, such as dopamine, serotonin, epinephrine/norepinephrine, and others. While the basic machinery for release is the same, these neuromodulators aren't cleared as fast, bind to g-protein coupled receptors, and their concentrations can build in the synaptic space between neurons when the presynaptic cell fires multiple action potentials in sequence. For these neurotransmitters/neuromodulators, the amount of neurotransmitter sitting around outside the cell acts as a time average of release in the recent past.

SRIs/SSRIs/similar drugs slow down the reuptake process, such that the concentration of serotonin reaches higher levels with the same presynaptic activity.

Although reuptake can also be important to "restock" the presynaptic cell with neurotransmitter for release, there is typically enough precursor around that reuptake is not the only limiting step.

Your suggested reasoning that is closest to the truth is both: "...because the neurotransmitter must remain in the synaptic cleft for a certain amount of time? Is it because the reuptake takes place before the neurotransmitter could bind to the receptors of the postsynaptic cell?" but it isn't that the transmitter "must remain" longer or that reuptake takes place "before" it can bind: it is that if the neurotransmitter remains longer it has a larger integrated effect on the postsynaptic cell.

Lastly, "good thing" is relative - of course increasing SERT activity would help with faster transmission, but faster transmission might not be important/necessary/fit the function of the circuit where serotonergic signalling is involved.


What is this whitish jelly-like substance on a branch?

Looks like a Tremella fuciformis, which is actually a sort of yeast that produces jelly-like fruiting bodies. AKA the white jelly mushroom.


What exact characters determine an animal's Genus?

I don't think there is any non-arbitrary concept being used to tell whether two species belong to the same genus or not. The same goes on with any other taxonomic rank. Systematicists build some intuition within each clade about what a genus could mean and use it to argue what is the most strategic grouping but the concept of genus may well vary a lot from clade to clade (from spiders, to mammals or to flowering plants, ...).

Note that even the concept of species is not as nicely defined as you may think. Have a look at How could humans have interbred with Neanderthals if we're a different species? for discussion on the concept of species.


Do they close is a better predictor.

before cooking tap the bivalve if they remain open do not cook or eat them.  Unresponsive bivalves of any kind not safe to eat are dead and there is no way to tell for how long. Whether they open during cooking is meaningless for mussels they can stay locked tight even if healthy and freshly killed.  Smell is also a good predictor never eat shellfish that smell off.

The differences between wild and farmed mussels makes this even less useful, wild mussels may be filled with sand making them heavy even if dead. Of course if a mussel is comes pre-cooked only smell is useful.

float vs sink is not really useful since it relies on how tightly sealed a bivalve is and whether it trapped air when it closed. A air seal is not a guarantee with many bivalves, mussels included, nor is trapped air. It is just not a useful metric.


every advantage has a disadvantage.
self seeding means less genetic diversity, fast growing also means more energy requirements  and even a structurally weaker plant, fast reproducing means tiny sieeds so individual seeds have a very small chance of survival. Biology is all about cost vs benefit, there is no such thing as universal advantage.
regrowing is actually something all plants can do provided they have enough resources, this is one way humans replicate crops. Weeds are often more sensitive to ground conditions, and don't do well in places where humans have not cleared and irrigated the land. weeds are often pioneer species good at taking over open land, one effective way to deal with weeds is to plant a cover crop because weeds can't actually compete well when there is already healthy grass. Many crops on the otherhand are being grown in sub-optimal conditions, in climate/soil other than the the one they evolved for while weeds tend to be native plants already adapted for the local conditions.


Why can't neurons undergo cell division?

Morphological point of view

Neurons cannot divide because they lack centrioles.

  Because centrioles function in cell division, the fact that neurons lack these organelles is consistent with the amitotic nature of the cell [1].

Functional point of view

New cells in the nervous system wouldn't do any good. The whole nervous system is based on interneuronal connections, so adding an extra neuron would mess up these connections and alter both the functionality and the "stored" information.

  Each nerve cell has a specific place in our nervous system. Its job is all about taking a signal from one specific place to another one. Adding new nerve cells would mess up these very specific connections in a very complex system [2].

References:

SEER Training. NERVE TISSUE. Available from http://training.seer.cancer.gov/anatomy/nervous/tissue.html
UCSB Science Line. Available from http://scienceline.ucsb.edu/getkey.php?key=1710


Like the comment said this question is very broad but Im going to try and clear some things up for you. A "genetic test" is just simply a test that tells you whether or not you have a certain genotype. Yes, it is often times used to tell if a person has a disease or not, but that doesnt always have to be the case. I may just want to know, for example, if a mouse I have carriers a certain transgene. The reason why genetic tests are good at determining if someone has a disease is because many diseases are simple, or at least have a well-defined genotype. Sure, you can make a genetic test for a complex disease like obesity if you want, but no one does this because as you pointed out in your question there are sometimes more than one gene involved, so a genetic test for that would not be very good.

But for genetic tests of diseases of a known genotype, they are very accurate. Of course you have some false positives and false negatives. Look up the terms selectivity and sensitivity. If you have a sensitive test you will catch a lot of people with the disease but also many false positives. If you have a selective test you will not have many false positives but you may miss people who actually have the disease. Its a trade-off. Testing someone twice will clear things up usually.

And then there are cases where you have a disease with a known genotype but still have an inaccurate genetic test on rare occasions. Heres a paper about a disease known as Spinal Muscular Atrophy. There is a genetic test that works 95% of the time but sometimes it does not match up with the phenotype. In the paper they find a mutation that explains why the genetic test does not match the phenotype. Two things are interesting about the paper. One, the genetic test is not wrong, its just that the phenotype is not what you'd expect. And two, not all people who have a discordant genetic test have this mutation. So whats going on in these patients and why their test doesnt match their phenotype is anyone's guess.

The first point is especially important so I will repeat it. The genetic test was not wrong, the phenotype just did not match it as expected. Genotype and phenotype are not always correlated, and mistakes can happen when you assume they are.


Hypovolemia and orthostatic hypertension

The pathophysiology of orthostatic hypertension has not been elucidated. It is believed it involves activation of the sympathetic nervous system [1], vascular adrenergic hypersensitivity and diabetic neuropathy [2]. High levels of plasma atrial natriuretic peptide and antidiuretic hormone were observed in children [3].

Hypovolemia causes:

baroreflex-mediated increase in muscle sympathetic nerve activity [4]
release of epinephrine and norepinephrine [5]
activation of renin-angiotensin axis [5], thus increasing ADH levels

All these reactions result in vasoconstriction and blood pressure raising. But not up to absolute hypertension.

  Orthostatic hypertension is diagnosed by a rise in systolic blood pressure of 20 mmHg or more when standing [6].

This is possible. A raise of 20 mmHg from hypotension could result due to vasoconstriction.

References:

Fessel J, Robertson D. Orthostatic hypertension: when pressor reflexes overcompensate. Nat Clin Pract Nephrol. 2006 Aug;2(8):424-31. doi: 10.1038/ncpneph0228. PubMed PMID: 16932477.
Chhabra L, Spodick DH. Orthostatic hypertension: recognizing an underappreciated clinical condition. Indian Heart J. 2013 Jul 5;65(4):454-6. doi: 10.1016/j.ihj.2013.06.023. PubMed PMID: 23993009.
Zhao J, Yang J, Du S, Tang C, Du J, Jin H. Changes of atrial natriuretic peptide and antidiuretic hormone in children with postural tachycardia syndrome and orthostatic hypertension: a case control study. Chin. Med. J. 2014 May;127(10):1853-7. PubMed PMID: 24824244.
Ryan KL, Rickards CA, Hinojosa-Laborde C, Cooke WH, Convertino VA. Sympathetic responses to central hypovolemia: new insights from microneurographic recordings. Front Physiol. 2012 Apr 26;3:110. doi: 10.3389/fphys.2012.00110. PubMed PMID: 22557974.
Wikipedia contributors, "Shock (circulatory)," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Shock_(circulatory)&oldid=612494727 (accessed June 26, 2014).
Wikipedia contributors, "Orthostatic hypertension," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Orthostatic_hypertension&oldid=603984647 (accessed June 26, 2014).


How can viruses have an incubation period of only 3 days?

A viral plaque assay is an artificial system which limits the physical dispersion of newly released virions. It is designed to count the number of infectious virions (plaque forming units) in a given sample, not to measure the rate of reproduction or spread. Since each plaque begins with a single infected cell, the number of new cells infected with each cell burst is going to be limited by the physical proximity of cells to the infected cell, not by the number of infectious virions released.

In a living system, a single cell burst from a viral infection can release anywhere from a few hundred to up to several tens of thousands of new virions which will then be carried in all manner of different bodily fluids to infect new cells, dramatically increasing the potential number of new cells infected after each replication cycle, compared to a plaque assay.

Another consideration is that some of the symptoms of the common cold are generally similar to those common in the prodrome phase of most viral infections, so it is probably difficult to distinguish its true incubation period from the onset of any acute viral infection.


Sextuplet corn (Zea mays with branched ear)

This looks a lot like a ramosa mutant (for example see the ears in panels A,G,H - taken from Figure 2 from Gallavotti et. al. 20101).

Ramosa mutations affect the branching pattern of the inflorescence (i.e. the ear and tassel in maize - aka. corn in the US) and are typically highly variable.  These are thought to be partial reversions to the phenotype of teosinte, which is the putative ancestor of maize2,3.
The unusual ear you collected may have resulted from a spontaneous mutation (possibly transposon driven), but also could be due to infection by a fungus (these sometimes secrete hormones that create developmental effects), or even insect damage to the developing ear.
If this phenotype was due to a heritable mutation you may notice an effect on the tassel (more densely branched), but IIRC this can be quite subtle. The best evidence for this being genetic would be seeing this phenotype recurring in subsequent generations. If possible plant kernels from the strange ear in an isolated area. It is also possible to do controlled crossing in maize — if you go this route I would suggest that you try to self pollinate (i.e. take pollen from each plant's tassel and put it on that same plant's ear).
You also might find this short video to be of interest.
If you get plants with similar phenotypes in this or a subsequent generation I can put you in touch with someone working on ramosa genes who might be interested in having some of the seed if you're willing to share ...
References:
1: Gallavotti, A., Long, J. A., Stanfield, S., Yang, X., Jackson, D., Vollbrecht, E., & Schmidt, R. J. (2010). The control of axillary meristem fate in the maize ramosa pathway. Development, 137(17), 2849-2856.
2: Iltis, H. H. (1983). From teosinte to maize: the catastrophic sexual transmutation. Science, 222(4626), 886-894.
3: Bennetzen, J., Buckler, E., Chandler, V., Doebley, J., Dorweiler, J., Gaut, B., ... & Walbot, V. (2001). Genetic evidence and the origin of maize. Latin American Antiquity, 84-86.


Carrot (Daucus carota) is a biannual plant that accumulates massive
  amounts of carotenoid pigments in the storage root.

The root of the carrot was not orange before domestication.

  Although the root of carrot plants was white before domestication,
  intensive breeding generated the currently known carotenoid-rich
  varieties, including the widely popular orange carrots that accumulate
  very high levels of the pro-vitamin A carotenoids b-carotene and, to a
  lower extent, a-carotene.

As stated in the comments people did this to give a better taste to the roots. This is simply economical more beneficial because otherwise only the leaves of the carrot could be used for consumption (and not the roots which are a major part of the carrot), wasting this root would result in a lot of waste (and thus a lot of money waste) and because of an increase in carotene (and other compounds which contribute to the flavour) this would save money and provide more tastefull and appealing roots.

  It is likely that wild carrot plants had uncolored roots of a bitter
  taste and a woody core but were initially cultivated because of their
  aromatic leaves and seeds.

So the only reason (as far as I can find) is that this is ineed because of cultivation by stimulating a flux in the direction of the carotenoid biosynthesis

I think this picture will explain it all:

   (source)

I'm not sure how familiar you are with biology so I described this not in that much detail about the genes and expression of them etc. If you would like to know this I would highly recommend to read these articles:

Biosynthesis of carotenoids in carrot: an underground story comes to light. (which I mainly used to write this)
New insights into domestication of carrot from root transcriptome analyses


What happens to the excess immune cells or WBC in our body?

The process you are asking about is called the termination of the immune response, and for a long time it was not studied very much for some reason, with scientists preferring to analyze initiation instead. However, this has changed in recent years, and while we still don't know a good deal, the picture is much clearer than it had been a decade or three ago.

Here is a special edition of Immunological Reviews focusing on termination of the immune response. While the site says you need to pay to access each article, they're actually available for free in PubMedCentral, so just look it up there for access. For a very brief overview, this section of the Wikipedia article on inflammation lists some of the mechanisms involved.

In regards to your question about immune cells and antibodies, a couple of things happen. First, the vast majority of responding cells are either "turned off" or directed to commit suicide (apoptosis) by a variety of signaling mechanisms, such as anti-inflammatory cytokines like IL-4, IL-10, IL-13, and IL-35, along with other molecules like TGFβ and IL1RA, soluble receptors to pro-inflammatory cytokines like TNFα and IL-6, or through "death receptors" like Fas/CD95 and others. However, some cells are prompted to turn into long-lived memory cells, which are able to be quickly activated upon re-exposure to antigen, in many cases completely clearing it without the need for a full-fledged immune response (such as one generating fever and sickness).

As for antibodies, like most circulating serum proteins, they are metabolized mainly in the liver and can be excreted via the kidneys. Their half-lives vary by isotype, but can be as long as three or more weeks. This is assisted by FcRn, the neonatal Fc receptor, which recycles antibodies back into circulation, protecting them from breakdown:

FcRn: the neonatal Fc receptor comes of age
Derry C. Roopenian & Shreeram Akilesh
Nature Reviews Immunology 7, 715-725 (September 2007)
doi:10.1038/nri2155