Is cancer caused by vitamin B17 deficiency?

Short Answer: No.

Background: First of all, there is no such thing as vitamin B17. The compound, amygdalin or laetrile, which is referred to by this term, is not a vitamin1. Amygdalin is indeed a cyanogenic glycoside (like glucosinolates, see this answer) which is poisonous to organisms including humans, because it forms cyanide which is toxic2. See this image for its structure:

The notion that amygdalin is a vitamin started when Ernest Krebs Jr., inventor of 'laetrile' (a modified form of amygdalin), rebranded it as a vitamin to get around the new FDA drug regulations and get it approved as nutrient supplement instead of pharmaceutical3. Ernest Krebs Sr., in 1920s, formulated a theory that amygdalin could kill cancer cells4 and the notion was carried forward by his son, though Ernest Krebs Sr. himself considered amygdalin as too toxic for human consumption. This view received a huge uplift when, in 1973, a public relations officer at Sloan Kettering Hospital, which was given the task by the NIH of performing a series of laetrile trials, alleged a cover up of, and leaked, data that claimed potential for laetrile as an anti-cancer agent5, though nobody else was able to reproduce the same test results in a series of followups. Yet, perhaps the most prominent force which still keeps this myth alive is the book World Without Cancer: The Story of Vitamin B17 by G. E. Griffith (interestingly, reviewed by 'Dr.' Ernest Krebs Jr.). According to all these reports, laetrile might work in following ways6:

malignant cells have higher levels of $\beta$-glucuronidase and lesser levels of rhodanase, because of which they are more susceptible to effects of laetrile.
malignant cells have higher levels of $\beta$-glucosidase (different from $\beta$-glucuronidase) and lesser levels of rhodanase, because of which they are more susceptible to effects of laetrile.
cancer is due to deficiency of vitamin B17 (laetrile) and vitamin B17 is required by cells to restore health (though there is no evidence for this).
cyanide released by laetrile has a toxic effect beyond its interference with oxygen utilization by cells. According to this theory, cyanide increases the acid content of tumors and leads to the destruction of lysosomes. The injured lysosomes release their contents, thereby killing the cancer cells and arresting tumor growth.

Laetrile is even supposed to raise the red count in blood, be of value in treating sickle cell anemia, treat parasitic diseases, help regulate intestinal flora, cause lowering of blood pressure in cancer victims and provide relief from arthritis3.

However, all clinical tests have concluded that laetrile is poisonous to humans (and other organisms) due to cyanide poisoning and thus, its effect in cancer treatment is unambiguously negative6,7,8. In fact, use of laetrile has even led to a number of deaths9.

In reality, when amygdalin is ingested, the enzymes  $\beta$-glucosidase, emulsin and amygdalase hydrolyze it into gentiobiose and L-mandelonitrile. Gentiobiose is further hydrolyzed to glucose, whereas L-mandelonitrile is converted into benzaldehyde and hydrogen cyanide, which causes cyanide poisoning2. The concerned process looks like10:

If the quantity of cyanide generated is under the acceptable daily intake limit (0.05 mg/kg body weight)11, then it can be handled easily by enzymes, like rhodanase which converts toxic CN- to non-toxic SCN- ion12. But this quantity is often beyond the limit; a single apricot seed contains about 0.5 mg cyanide13. Hence, it results in cyanide poisoning.

Thus, the so-called vitamin B17 cannot cure cancer.

References:

 1. Lerner IJ (1981). "Laetrile: a lesson in cancer quackery". CA Cancer J Clin. 31 (2): 91–5

 2. Wikipedia contributors. "Amygdalin." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 10 Mar. 2017. Web. 11 Apr. 2017.

 3. United States, Food and Drug Administration. “Laetrile, the Commissioner’s decision” 1978

 4. (1991), Unproven methods of cancer management: Laetrile. CA: A Cancer Journal for Clinicians, 41: 187–192. doi:10.3322/canjclin.41.3.187

 5. WADE, NICHOLAS (1977). Laetrile at Sloan-Kettering: A Question of Ambiguity. Science, 198, 1231-1234.

 6. Ellison NM, et al. “Special report on Laetrile: the NCI Laetrile Review. Results of the National Cancer Institute’s retrospective Laetrile analysis.” N Engl J Med. 7 September 1978.

 7. Milazzo S, Horneber M. Laetrile treatment for cancer. Cochrane Database of Systematic Reviews 2015, Issue 4. Art. No.: CD005476. DOI: 10.1002/14651858.CD005476.pub4.

 8. Milazzo S, Ernst E, Lejeune S, Boehm K, Horneber M (2011). "Laetrile treatment for cancer". Cochrane Database Syst Rev (Systematic review) (11): CD005476. doi:10.1002/14651858.CD005476.pub3. PMID 22071824.

 9. Editors of Consumer Reports Books (1980). "Laetrile: the Political Success of a Scientific Failure". Health Quackery. Vernon, New York: Consumers Union. pp. 16–40. ISBN 0-89043-014-4

 10. Amygdalin - TradMPD

 11. FAO Meeting Report No. PL/1965/10/2;
    WHO/Food Add/28.65;
    Evaluation of the hazards to Consumers resulting from the use of
    Fumigants in the protection of foods

 12. Cipollone R, Ascenzi P, Tomao P, Imperi F, Visca P (2008). "Enzymatic detoxification of cyanide: clues from Pseudomonas aeruginosa Rhodanese". J. Mol. Microbiol. Biotechnol. 15 (2-3): 199–211.

 13. S Krashen. Are Apricot Kernels Toxic?. The Internet Journal of Health. 2008 Volume 9 Number 2.


Does the Enzyme Monoamine Oxidase, Isoenzyme A have an allosteric modulatory site?

I think an allosteric modulatory site has already been found, but it's not specific to Isoenzyme A, if that's what you were looking for.

See these papers:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1564771/

http://www.jbc.org/content/270/17/9856.full


What will happen if there is high concentration of both calcitonin and PTH in blood?

Short Answer: quite surprisingly, both will occur.

Long Answer: as is quite well known, calcitonin lowers blood Ca2+ levels. It performs this task by two methods:

it inhibits the activity of osteoclasts in the bones (Custoff, 2008)
it inhibits reabsorption of Ca2+ in renal tubular cells, allowing it to be excreted in urine (Potts et al, 2008)

However, the second mechanism is only minor. On the other hand, parathyroid hormone (PTH) performs just its opposite: it increases Ca2+ levels in the blood.

So, lets come to the main point: since calcitonin and PTH have opposing functions, what would happen if both were acting simultaneously?

It seems, funnily though, that both the functions will occur simultaneously. Wong et al, 1975, in their research, showed that the target cells of calcitonin and PTH are different i.e. calcitonin and PTH act on different osteoclasts. So, to put it simply, while activity of some osteoclasts would be decreased, that of some others would be increased. Overall, Ca2+ levels in the blood would remain pretty much constant.


The binding is reversible typically; part of the potency of a drug is ow well and for how long it binds to its target. There's a natural equilibrium of binding and dissociation. Many drugs, once bound to their cognate receptor, cause a down regulation of their cognate receptor on the target cell. The bound/activated downstream signalling pathways may be inhibited by ubiquitination of the downstream signals themselves or upregulation of antagonists etc. The hormone itself has a half life, which is very important, thus levels naturally decrease and for some hormones this is incredibly rapid. Levels may decrease due to breakdown or excretion. Increase of binding hormones may decrease free hormone thus it's effect also.


Don't the radioactive labeled molecules of dNTPs or DNA harm themselves or their surroundings?

It's worth considering how many high energy electrons are actually released compared to the number of molecules in the tube. For instance, I routinely work with $^{32}P$-labeled DNA, and measure the specific activity of samples by scintillation counting. For me, a very hot stock sample of labeled DNA (~1000x more concentrated than I would use in an experiment) will register on the order of $10^8$ disintegrations per minute (dpm). That means each minute, about $10^8$ beta particles are emitted by decaying phosphorous atoms inside the sample. But the amount of DNA molecules in that same tube is about 50 pmol, or about $3 \times 10^{14}$ molecules.

So if each of those beta particles were absorbed by a DNA molecule in the same sample, thus damaging it, that would be a rate of self-damage of $10^{-6} min^{-1}$. Of course, most of those beta particles actually make it out of the tube, so the actual rate of self-damage is much lower still. Since we're probably interested in measuring processes on much shorter time scales than this self-damage rate, it becomes negligible.


About acetyl-coA in the Krebs Cycle of respiration

Pyruvate transfers an acetyl group to coenzyme A.

The acetyl group from acetyl co-A is the molecule that provides the 2 carbon atoms that get added to oxaloacetate to form citrate, and as you said, citrate starts the cycle over again.

Without coenzyme A, pyruvate cannot transfer the acetyl group to oxaloacetate to form citrate so without coenzyme A/acetyl co-A, the process would stop.

This is a slightly busy version of the diagram, but it does let you see how molecules in the cycle are formed and where carrier molecules interact with the molecules in the cycle.

- By Narayanese, WikiUserPedia, YassineMrabet, TotoBaggins [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons


This is really the most fundamental concept of Cell Biology, so good question. If you look at the size of a any cell from a whale and compare it to the size of any of cells from a mouse, they are in fact quite similar, despite the extreme difference in the overall size of the organisms they are from. There is a reason why cells are small, and it has to do with the fact that they survive based on their ability to absorb enough nutrients from their environment. As a cell gets larger it needs more to survive (because it has a bigger mass). A bigger cell has also has a larger surface area around it (so it can absorb more nutrients).

HOWEVER, there gets to be a point where the mass of the cell is too large for the surface area to compensate for. Mathematically this is shown by what is called the "surface-area-to-volume ratio". Basically, it states that as a a sphere gets larger, the volume increases at a higher RATE than the surface area. So there is a reason cells get only so big, the 60's horror movie The Blob was not scientifically accurate, a single-cell that large (the blob) would not have enough surface area to absorb enough nutrients to sustain itself. Taller (or bigger) people have more cells (not bigger ones) than others.

Effects of osmotic pressure can alter cell size slightly.

When you are talking about taller individuals, you are (I think) really meaning larger people, people with a higher mass. And yes, they have more cells.

Another topic of Cell Biology you may want to explore is apoptosis. Let's say you have two individuals both 180 lbs. one of them is 5' tall and the other 7'. Both these individuals have the same number of cells, but the taller one has a higher percentage of them in the superior and inferior regions of the body. It is the process of apoptosis that sculps an organisms shape.


What is open complex in E.coli DNA replication?

The sentence itself is actually the definition of open complex: It is the structure that is created once the DNA double helix is unwinded due to the DnaA proteins.

  This binding promotes destabilization of nearby AT-rich sequences,
  resulting in unwinding of the DNA double helix and the formation of an
  open complex.

I have also found a papera co-authored by Arthur Kornberg himself where the authors self-define "open complex" as well:

  Three tandem repeats of a 13-mer in the AT-rich region are essential
  to the unique replication origin of E. coli and of remotely related
  Enterobacteriaceae. These iterated sequences are identified by
  deletion analysis and sensitivities to endonucleases as the site for
  initial duplex opening by the initiator dnaA protein. This “open
  complex” requires ATP and 38% for optimum formation and stability.

There are several papersb,c that use "open complex" in the same way.

References:

a David Bramhill, Arthur Kornberg, Duplex opening by dnaA protein at novel sequences in initiation of replication at the origin of the E. coli chromosome, Cell, Volume 52, Issue 5, 1988, Pages 743-755, ISSN 0092-8674, http://dx.doi.org/10.1016/0092-8674(88)90412-6.
(http://www.sciencedirect.com/science/article/pii/0092867488904126)

b Ozaki, Shogo, et al. "A common mechanism for the ATP-DnaA-dependent formation of open complexes at the replication origin." Journal of Biological Chemistry 283.13 (2008): 8351-8362. (http://www.jbc.org/content/283/13/8351.full)

c Mukhopadhyay, Gauranga, et al. "Open-complex formation by the host initiator, DnaA, at the origin of P1 plasmid replication." The EMBO journal 12.12 (1993): 4547. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC413885/)


Umbrella term for agonist, antagonist, inverse antagonist, etc.

activity

  "addition of a methyl group to the phenyl ring changed its activity from agonist to antagonist"


The basic process would be (in pseudocode, I don't know python well enough, I'm a Perl geek):

$seq1=ATGCCAGGCTGA
$seq2=ATGGGACCATAA;
for ($i=0;$i<length($seq1);$i++){
   codons1[$i]=amino_acid
}
for ($i=0;$i<length($seq2);$i++){
       codons2[$i]=amino_acid
}

At this point you will have two arrays or hashes or tuples or dicts or whatever holding the amino acid that corresponds to each codon position of the input seqs. You go and do your translation and dS/dN thing and you can then use these lists to map back to the original nucleotides:

for ($i=0;$i<length($ProteinSseq1);$i++){
  print codons1[$i]
}

You will need to adapt this to deal with codons correctly (i++ will only increment by one, you need to extract the triplets) and then to read the gaps but these are all programming issues that have nothing to do with the biological side of things.


Do's and Don't's of Undergraduate Research?

Ask plenty of questions and write everything down. If you do not write notes when someone is explaining something to you, it will be embarrassing to go back and ask them a second time to explain it again. Before you get to the lab I would locate/Ask for review articles related to the project. Realize that you will likely shadowing a senior person while you are there, adapt to their schedule. Don't spend your incubation times face booking. Use this time to build relationships with others in the lab and on your floor and try to absorb as much information about the way the world of science works. Speaking from personal experience the small things you learn there may be insignificant but may come to be important to you in the future. If you have your own project, realize that it will probably be a small one attached to a bigger project another lab member is working on. Thats a good thing, because your time there is not long enough to get into something complicated. A simple, clear, and focused question will be key to your success.

What you should take away from the experience is not necessarily something that will amount to publication, but the actually experience in the actual process of designing experiments, performing them, and analyzing data. Assuming you are doing this to help prepare you to go on to work on a graduate degree in your favorite area of biology then remember that this is here to help you get to the next level. Programs like this allow you to demonstrate that you understand what it takes to perform graduate-level work, and potentially become a successful scientist one day.


How did evolution support sports, fun, entertainment etc

This answer can be from many different perspectives! I'll try to blend them all together as much as possible.

First of all evolution did not choose to make us love sports. Evolution made us social animals. And sports is just one of the tools we use for that purpose. Think about it, because if evolution gave us sports, then you will play sports, your kids will inherit that bit of experience from you and they would be that much better than you. But no, we all start from level 0 when we try to play any games or sports. This is because, sports is primarily a motor memory

So why are we social?

This study back in 2014 was one of the first to suggest that memory can be heritable. It generated a lot of attention and the authors themselves suggested that their findings were standing on a very capricious footing and required further validation.

This point is valid because evolutionary forces require mechanisms by which features/mechanism which bestow advantages towards the survival of the species are positively reinforced. In this case social behaviour is the function.

Do not go googling the word Social behaviour, for some reason the wiki article looks only at dogs and cats. That is unpragmatic, because we also have the same function.

I will broadly breakdown social behaviour into

Accommodation of non-aggressive behaviour from individuals in neutral territory.
A means to communicate

But, you may ask how does social behaviour benefit you? Well the answer is simple, increased survival capacity, and better chances of propagation.

Such studies exist in crows, which have studied social behaviour. Indeed, if you start to consider studies in behavioural biology, you would find that there are instances where female mosquitoes do not just mate with any male mosquitoes, even in this case you can call it a very rudimentary form of socialising.

So in your case sports is a tool which allows us to accommodate and communicate with others in neutral territory.

You can take a look at this which better explains the social aspects of sports


Why do the calicheamicins bind to DNA at the minor, rather than the major, groove?

Accommodation in the major or minor groove

I am not in a position to generalize about all drugs that bind to the major groove of DNA, but at least one well-known example, actinomycin D, does so because it intercalates between the base-pairs in the double helix. Although other weak chemical interactions stabilize this binding, much of it is through base stacking with base-pairs. Hence binding requires it be inserted into the major groove in which the base pairs lie (see e.g. PDB 101 Molecule of the Month article).

Binding of calicheamicins, in contrast, involves interaction with two parts of the molecule. The ‘head’ of the molecule makes specific interactions with a TCCT sequence in the DNA (in the case of calicheamicin γ1), which is achieved from the minor groove (intercalation is not necessary) allowing the saccharide ‘tail’ to fit into the minor groove. (Ikemoto et al. 1995).

(Constructed from 3D Structure images on the Protein Data Bank website)

Sequence specificity

A concern of the poster is the fact that the interaction of calicheamicin is sequence specific (there is apparently a preference for d(T-C-C-T).d(A-G-G-A)) whereas access to the bases is restricted in the minor groove. This is addressed in the paper by Ikemoto et al., but without illustration, assuming you are able to visualize the chemical interactions in your mind. I have used Jmol to view the structure 2PIK, have prepared a couple of screen shots to help illustrate the details I shall quote from the text of the paper.

Cleavage of the DNA is performed by the enediyne aglycone (R), which does not make contact with the bases. Two of the regions that do interact with bases are the thio-sugar ring (B) and the aromatic ring (C). These are shown below in the complex of  calicheamicin (coloured yellow) with a deoxy-oligonucleotide duplex, together with a close-up of the interactions of these rings.

In the left-hand frame the DNA has standard cpk colouring, and the phosphates (orange–red) lining the minor groove are evident. The base-pairs are perpendicular to the plane of the image. In the second frame I have tilted the image slightly to allow the rings of the bases to be seen, and coloured the bases (actually the whole nucleoside) red/white/green/blue for A/T/G/C. Quoting from the Ikemoto paper:

  The thio sugar B is positioned edgewise in the minor groove and contacts the A20 residue through van der Waals and hydrogen bonding (B ring hydroxyl to N3 of the base) interactions. The aromatic ring C is positioned between the walls of the minor groove with its iodine and CH3 groups directed toward the floor of the minor groove.… The S-carbonyl linker, which adopts an orthogonal alignment relative to the plane of ring C (favored by the steric demands of the ortho aromatic ring substituents), bridges the minor groove and makes van der Waals contacts with the opposing walls of the groove.

This may not have the clarity of, say, Watson and Crick base-pairing, but neither does the interaction of proteins with particular DNA sequences — one needs to examine the multiple interactions that occur. What I think it does show is that this drug can make specific contact to bases, even though it binds in the minor groove.


Where can I find large datasets of protein-interaction networks?

There is a bunch of decent protein-protein interaction databases: Biocarta, BioGrid, DIP, InnateDB, IntAct, MINT, PPID.
Some of them aren't available now, but you can download datasets from the Expression2Kinases download page because they are integrated into X2K pipeline as part of Genes2Networks analysis. If you need more proteins, you can submit your list of proteins to X2K and use G2N analysis to connect enriched transcription factors through known protein-protein interactions.

Also, the new dataset called hu.MAP was published recently. It is a dataset of human protein-protein interactions determined by over 9,000 mass spectrometry experiments performed by the Marcotte Lab from UT Austin. A paper that describes the hu.MAP project is available on Biorxiv.

BioPlex (biophysical interactions of ORFeome-based complexes) is another database with experimental verification. Authors describe it as a network that is

  the result of creating thousands of cell lines with each expressing a
  tagged version of a protein from the ORFeome collection.
  Immunopurification of the tagged protein and detection of associated
  proteins by mass spectrometry are the building blocks of the network.
  The overarching project goal is to determine protein interactions for
  every member of the collection.


What is the reason behind that sometimes when I see new thing I feel that I have already seen them?

What you are talking about is a déjà vu, the feeling of familiarity even though the situation is not familiar at all. It is, in fact, a very common phenomenon. A high percentage of people report having had déjà vus. It is nevertheless hard to put a number to it, because the experiences and déjà vu definitions might be different. I have found numbers between 60 and 90% of the population.

The claim that this is a sign of a good memory is related to the view, that a déjà vu is not a false memory, because you actually realize that the situation should be unfamiliar to you (also mentioned here).

But how do déjà vus happen? There are several theories...

It seems clear that déjà vus are associated with activity in the temporal lobe (on the side of the brain). That's where memory is processed, especially episodic memory (things that happen - in contrast to learning a skill). People with epilepsy often report déjà vus right before a seizure that starts in the temporal lobe.

One theory, put forward in this paper, says that the memory and feeling of familiarity are processed in different areas and there is a false activation of the familiarity area during a déjà vu. The brain is not always working proberly, e.g. false sensations can happen, like hallucinations. So, the false activation of that familiarity center could give us the sense of familiarity in an unfamiliar situation.

Similar to this is the idea, that there might be a mismatch between perception and memory formation. When something we are experiencing right now is "leaking" into our memory due to false activation, we think that this has happened in the past. There is a problem with this explanation: despite having a strong feeling of familiarity during a déjà vu, people fail to give any context to when this previous event happened or which other events have preceded it. So, it doesn't seem to be perceived as a memory.

Another explanation could be a false combination of the experience with something that is loosely connected to it (like planning the trip, watching a movie with a similar scene, etc.). Our brain always tries to connect experiences. It might falsely identify something you've seen in pictures or read in a book as a real experience.

As you see, we still struggle to explain the phenomenon. It is caused by some error in the way our brain perceives a situation, writes or retrieves memory or processes familiarity. This error might be a wrong activation or wrong timing or the like.


Does rainwater contain many fewer micro-organisms than river water?

According to a number of citations listed on Kenyon College's MicrobeWiki, rain can contain microorganisms via a process called "bioprecipitation."

Essentially, microorganisms, dust and other small particles get swept up into the atmosphere, and cold temperatures cause atmospheric water vapor to freeze around the organism/particle. Once the ice-covered particle picks up enough mass, it falls from the sky and reaches earth as precipitation (likely rain if temperature is warm enough).

Here is a schematic from Wright et al. (2104) of how an increase in relative humidity, due to a cold-frontal passage, can trigger biological ice nuclei release followed by seeding of the frontal cloud band with the lofted ice nuclei:

 So How Many (and Which) Bacteria Are in Rain?

Which Bacteria?

According to Wikipedia:

  The ice-nucleating bacteria currently known are mostly plant pathogens

According to MicrobeWiki, these include:

  Exserohilum turcicum, Pseudomonas viridiflava, Pseudomonas fluorescens, Pantoea agglomerans and Xanthomonas campestris.

  The most well described organism that demonstrates ice nucleation is Pseudomonas syringae, which was determined to specifically supply a source of ice nucleators by Leroy Maki in the 1970’s.

According to work by Natasha DeLeon-Rodriguez, Athanasios Nenes, et al. (full paper here and NPR story here), 100s of species of bacteria exist in the clouds and it's not uncommon to find almost 20 species in any given sample (60% of which on average were still living).

Here's a graph showing the relative amounts of various taxa found in their samples:

How Many Bacteria?

DeLeon-Rodriguez et al's (2013) results revealed an average bacterial concentration of somewhere between $5.1 × 10^3 cells /  m^3$ to $1.5 × 10^5 cells /  m^3$ of cloud (depending on method of counting).

Quickly doing some math (1 m$^3$ = 1000000 mL), their results suggest that, on average across a cubic meter of cloud, there is <1 bacteria / mL of moisture.

According to research by Joly et al (2014) that specifically examined ice nuclei (or "IN"):

  there were 0 to ~220 biological IN/mL of cloud water (i.e. 0-22 per m$^3$ of cloudy air based on cloud liquid water content estimates) and these represented 65% to 100% of the total IN.

Comparatively, river water (and drinking water) can contain a lot more bacteria (i.e., 80,000 bacteria / mL) and other microorganisms.

However, this disparity is not always so great, especially if we focus at comparing counts of only one or a few species (and not total bacterial counts).

Based on research of a tropical reservoir by Kaushik et al (2014):

  Levels of E. coli were found to be in the range of 0 CFU/100 mL – 75 CFU/100 mL for the rainwater, and were 10–94 CFU/100 mL for the reservoir water.

Note: CFU = colony forming units. (estimation of microbial numbers by CFU will, in most cases, undercount the number of living cells. [wikipedia]).

Citations

 DeLeon-Rodriguez, N., Lathem, T. L., Rodriguez-R, L. M., Barazesh, J. M., Anderson, B. E., Beyersdorf, A. J., ... & Konstantinidis, K. T. (2013). Microbiome of the upper troposphere: species composition and prevalence, effects of tropical storms, and atmospheric implications. Proceedings of the National Academy of Sciences 110(7), 2575-2580.
 Joly, M., Amato, P., Deguillaume, L., Monier, M., Hoose, C., and Delort, A. (2014). Direct Quantification of Total and Biological Ice Nuclei in Cloud Water. Atmos. Chem. Phys. Discuss 14(3):3707–3731.
 Kaushik R, Balasubramanian R, Dunstan H (2014) Microbial Quality and Phylogenetic Diversity of Fresh Rainwater and Tropical Freshwater Reservoir. PLoS ONE 9(6): e100737. doi:10.1371/journal.pone.0100737
 Wright, T. P., Hader, J. D., McMeeking, G. R., & Petters, M. D. (2014). High relative humidity as a trigger for widespread release of ice nuclei. Aerosol Science and Technology 48(11), i-v.
For further reading, also see the associated citations from MicrobeWiki.
I think you would also benefit by perusing the works of Pierre Amato.


RGB color is a more direct representation of the "raw input" received by the (human) eye, since the three types of cone cell have responsivity spectra that roughly correspond to red, green, and blue light:

Opponent color decomposes color into three "dimensions" of opposing properties: dark or light, yellow or blue, and red or green.  This provides some brightness invariance, since changing the intensity of light will change the brightness but not the yellow/blue or red/green balance of the color, even though the stimulation level of all three types of cone cell will change.

One could speculate that opponent color perception is more "meaningful" in real-world environments.  The dark/light axis represents the overall amount of light, the yellow/blue axis indicates which end of the visible spectrum is predominant, and the red/green axis provides a finer distinction for low-frequency light.


How does the brain avoid feedback loops?

Normally, after an excitatory neuron fires, it becomes more resistant to firing again for a period of time (refractory period). This is due to electrical changes within the excitatory neuron.

After depolarazing and reaching an action potential(firing), the neuron enters the refractory period, in which its charge will go back to normal (resting potential). This refractory period can be divided in two phases: Absolute and relative. During the Absolute refractory period, the neuron cannot be discharged again, since the sodium channels are inactive.

It's the relative refractory phase, however, that is more relevant to your question. During this period, the neuron enters a hyperpolarization states, meaning that it's resistant to firing again, unless it receives a greater stimulus.

So, basically, after firing and for a while, a neuron requires greater stimulus to be fired again. This works as a Feedback control, since even if you overstimulate a neuron it can fire only so often.

Inhibitory and excitatory neurons (and inhibitory and excitatory neurotransmitters) also play a role in the feedback control. Inhibitory neurons reduce the likelihood of a postsynaptic neuron to fire while excitatory neurons do the opposite.

However, sometimes these mechanism fail.

For instance, in Epilepsy, the resistance of excitatory neurons to fire during the refractory period is decreased. A group of neurons begin firing in an abnormal, excessive, and synchronized manner, resulting in a wave of depolarization known as a paroxysmal depolarizing shift, causing seizures.

In Parkinson disease, decreased dopamine causes increased inhibitory output (excess negative feedback) of the motor circuit, which leads to hypokinesia.

In contrast, excess dopamine and dopaminergic neuron activity seem to be related with Schizophrenia.


Why is glucose our primary source of energy?

I thought this was a great question.  In particular because it hints at two questions.  The first is 'why carbohydrates are used to store energy' in general. The second being 'why glucose rather than other carbohydrates?' in particular.

Glucose metabolism (and glycogen storage) is a core gene pathway - its found in bacteria archaea and eukaryotes.  So probably the most that we can readily say about question one is that as @rwst points out this pathway has proven to be useful at a critical juncture of the formulation of living things on earth.  If you look at glucose metabolism pathways, you can see that glycerate compounds and pyruvate are the actual intermediates that are used to create energy.  The first thing about these molecule worth noting is that they have a good mix of carbon and oxygen, which would make it easier to extract energy - creating CO2 from these compounds may even predates the existence of atmospheric oxygen.  So glucose and fructose (which is actually derived from glucose in the metabolic pathway) are actually storage molecules themselves, easily broken down to smaller molecules.

As to the second question: there are quite a few ways to arrange oxygen around the carbohydrate ring.  why glucose?  The advantages of glucose is probably a subtle one.  The structural properties of glycogen might be a reason that the use of glucose monomer is so important for glycogen. There is no evidence that I can find for this, so its always possible that glucose was just the first hexose carbohydrate to be biologically used.  Its sort of hard to imagine that the structure of glucose does not play some sort of role in cell structure though.


How to compare models of evolution to make assumptions about selection?

The answer to this question depends strongly on how you are formulating the different models. Are you for example computing this from dN/dS from a sequence alignment? Or based on explicit phylogenetic models? Those can have quite different formulations. The model names you are using out sound like they might come from PAML, but it's not clear. There are some exercises for this specific case elsewhere.

I am assuming that what you are really asking is how many degrees of freedom to use when e.g. computing a p value.

For this question, you have to think about the LRT a little. What it is really asking is "do I explain the data better by adding parameters to a model (while accounting for the fact that likelihood will by definition increase with more parameters)?"

So what you need to first establish is what the parameters of your models are. Assuming that the models are "nested", you can just use the difference in the number of parameters as the degrees of freedom. "nested" in this context means that the base model (e.g. H0, probably M0 for you) doesn't have parameters that are missing for the alternative model (which is assumed to have more parameters).

More flexible than the LRT are things like the AIC, which gets rid of Chi square and just computes a value from likelihood and model parameter number. This works well in practice and is nice because it's more flexible and a little less convoluted model comparison technique than the LRT. You can additionally use the AIC to compare non-nested models, which doesn't really work for the LRT.

I hope that this helps.


Short-term Lamarckism in asexual single cell organisms

This phenomenon is well known and can be observed in several species. In fact, if you look at the time it takes for E. coli to change its transcription program in order to react to the environment (signal->transcription->translation), you will find it can be longer than its ~20 minute doubling time. You can indeed think of it as a form of Lamarckism. However, it is part of a field that has been booming in the last ~10 years, known as epigenetics.

Epigenetics is a field of research that deals with hereditary information that is passed by non-genetic mechanisms, i.e. not in the DNA sequence. This includes several mechanisms including passing of proteins/RNA, chemical modifications of DNA (methylation) and chromatin (histone modification). It turns out that epigenetic effects can be observed in virtually all species (including human) and affected phenotypes can be significant (leading to disease, for example).

This is a very interesting field of research and is very wide, so I would recommend reading a bit. Specifically regarding protein/RNA passing, I believe this is somewhat less deeply studied, perhaps due to the fact that the effect decreases exponentially (due to dilution), can be limited by protein/RNA stability and some measurement difficulties. However, I think I recall mathematical treatment of this in Prof. Uri Alon's book. You can also catch his systems biology course online on youtube, which I think touches on some of this material.


Is there such thing as "biological cycles" of activity/performance/etc in mammals?

With regard to episodes of increased activity/performance over a mammal's lifetime, I can add migration to breeding/mating and hibernation or torpor. Birds of course are better known for migration, but some mammals, notably in Africa migrate over an extended time.


What difference does it make in the organism's physiology/metabolism whether oxygen binds reversibly or not?

I think I see where you are coming from.  There is a misunderstanding here.

Ice-fish have relatively lost their hemoglobin gene over time because they have adapted such a slow metabolism in the cold water where the oxygen is richer (oxygen content in cold water is higher).  The don't need any binding of oxygen to a carrier protein like hemoglobin because enough oxygen diffuses in from the water for the needs of their tissue.

There is no binding - reversible or irreversible in their blood - that would imply that the oxygen is binding to a protein like hemoglobin or hemocyanin, which the fish does not have.   The oxygen is just diffusing into the fish from the water around it.  The circulatory system is helping by flushing the system out and keeping everything fresh as well.


Is DEET (as in the mosquito repellent), a substituted phenethylamine?

While I feel like this might be a better question for the chemistry SE, lets take a look at the molecular structures:

The basic structure of a phenethylamine (left, modified from here) versus DEET (right, modified from here):

The important chemical differences are:

DEET only has a C-alpha between the nitrogen and the ring, whereas phenethylamines have a C-alpha and a C-beta (see red annotation)
DEET has a carboxylic functional group (an amide bond), whereas phenethylamines have an amino group (see green boxes)

Taken together these differences mean that DEET is not a phenethylamine.


How far can free radicals from UV radiation diffuse through the skin?

The life of the radicals decides how far they move.

This paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4310837/#!po=6.92308 has a table of half lives of radicals, the longest lasting ones (the radical of nitrous oxide and nitrogen dioxide) have half lives of seconds.

Diffusion theough the skin would be slow

Technically the problem is "reactive oxygen species" (ROS) and "reactive nitrogen species" (RNS) that are the damaging chemicals that includes free radicals. The reactive species that are not radicals have a longer half-life or are even fairly stable and so could diffuse further before making mischief.

The wikipedia article has problems - that is mentioned on the talk page.


Proteins are actually pretty calorific but indeed much less than fat. From wiki > food Energy

However, we crave for proteins for other reasons. We digest proteins to get their building blocks, the amino acids. With these amino acids we can rebuilt our own proteins. Proteins are at the very center of our metabolic activity. From wikipedia > protein

  Proteins perform a vast array of functions within organisms, including catalysing metabolic reactions, DNA replication, responding to stimuli, and transporting molecules from one location to another.

Many of our DNA sequence are called protein-coding-sequence (often just called gene although definition of what a gene is vary quite a bit). Those sequences are transcribed into mRNA and then translated into protein in order to have some effect on our body. A protein could be an enzyme for example.

For more information on the role of proteins in living organisms, have a look at an intro course to Biology such as for example those of Khan Academy. Khan Academy > macromolecules > protein and Khan Academy > Central Dogma.


Sloths have long, thick, sticky tongues covered in a carpet of tiny, rear-ward pointing spikes that they can pull leaves in with.

So the tongues are quite different from human tongues and likely much less "soft" to touch and more "rough".

According to scanning electron microscopy studies on the topography of a sloth's tongue, the following results were found:

  The results revealed that the rostral part of the tongue presents a
  round apex and covered by filiform and fungiform lingual papillae and
  a ventral smooth surface.


Why can't intermediate filaments be used as tracks by motor proteins?

Polarity essentially means a plus end (growing/polymerising) and a minus end (depolymerising). Look at microtubule (MT) (http://en.wikipedia.org/wiki/Microtubule). So molecules such as Kinesin-1 (http://en.wikipedia.org/wiki/Kinesin) use the hetero-dimeric nature of MT (alpha and beta subunits) and its polarity to orient themselves and move directionally along MT in an energy dependent manner.


Can a postsynaptic neuron 'shut itself off?

An example would be the neurons that switch off/switch on based on our sleep cycle. Nerve-signaling chemicals called neurotransmitters control whether we are asleep or awake by acting on different groups of nerve cells, or neurons, in the brain. Neurons in the brainstem, which connects the brain with the spinal cord, produce neurotransmitters such as serotonin and norepinephrine that keep some parts of the brain active while we are awake. Other neurons at the base of the brain begin signaling when we fall asleep. These neurons appear to "switch off" the signals that keep us awake. Research also suggests that a chemical called adenosine builds up in our blood while we are awake and causes drowsiness. This chemical gradually breaks down while we sleep (reference and reference). Here is a study based on switch on/switch off of fear i mice (reference).

There are also artificial ways in which to shut down receptors like our sweet receptors (reference). There have also been studies done on other organisms where one particular study showed the switch on/switch off of olfactory receptors in cockroach antenna (reference).


Biosphere that simulates sun and moon shifts

Sun and moon-faking devices exist. Not sure about 'biosphere'. I have personally observed one for honeybees, but that one was fairly crude(bees are dumb). It was just a big room with a hive stand in the middle and a series of fluorescent lights on the ceiling that turned on one after the other. The goal was to mess with bee circadian rhythms and see which genes became more or less expressed in their brains.

There's a slightly more sophisticated thing called a 'grow cabinet'. It has expensive lights to produce sun-spectrum light at direct sunlight intensity and humidity and temperature controls. Scientists use them for crop research when the weather is too random and unpredictable and absolute control is required.

I believe advanced versions simulate moonlight and angle of insolation, but that sort of thing is expensive.

I don't know of any full-sized biodomes with fake celestial objects. The cost of such a biodome would be prohibitive, and the experiments it enabled might be easier(certainly cheaper) to do in a smaller container.


in order to align genome multi-fasta files, do you ignore the chromosome sections?

If the fasta really are chromosomes, there will be one per chomosome. Check this in case the multi-fasta you have is an incomplete sequencing of an organism. If incomplete there will be many more fasta. There is a bioinformatics site on Stackexchange now at https://bioinformatics.stackexchange.com .You would get better answers there.


Why can't the immune system start at the mating time?

These questions are not completely easy to answer, since the immune reaction in this area is not completely understood. There are two different mechanisms  which play a role here:

Semen is immunogenic and can cause the generation of specific antibodies against it in men and women. The main question here is if the presence of semen in the females reproductive tract is the consequence of a suppressed immune reaction or because it is not recognized. There are indications for both possibilities but I think the first is a bit stronger. The mucus from the vagina is immunosuppressive as well as the seminal fluid, which contains prostaglandins which have the same effect. Have a look at this article for some more background:

Sperm survival in the female reproductive tract: presence of
immunosuppression or absence of recognition?

For the situation in the uterus between mother and fetus the situation is better understood. This is the so called immune privilege of some tissues (among them are the uterus, testes and the eye) where immune reactions are suppressed.

The placenta forms an immunologic barrier which seperates mother and fetus. This is done by secreting immunomodulary substances and also by the subpression of some T cell subpopulations. For more details see here. This is a highly developed system to protect the developing fetus (which is foreign) from the mothers immune system.


Can Escherichia coli survive on glucose and water alone?

The minimum requirement for E. coli and other bacteria to grow and survive is called minimal medium.  It's even defined at Merriam-Webster:

  a medium that contains only inorganic salts, a simple carbon source (as carbon dioxide or glucose), and water

Water and glucose are pretty easy, but the source of salts may often change; regardless, you really need some potassium, phosphate, and nitrogen for amino acid synthesis.  This page has a bunch of information on bacterial growth, including some "recipes" for a few bacterial strains.  For E. coli, the classic media is M9, which over at Sigma is made of:

  33.9g Na₂HPO₄.7H₂O
  15g KH₂PO₄
  5g NH₄Cl
  2.5g NaCl

  per litre of solution.

Here are some other recipes.


Non-disjunction and trisomy 13.

Why can't this be 1st meiotic division non-disjunction as well?

It absolutely can be 1st meiotic division non-disjunction as well. Patau syndrome can occur as a result of either meiotic non-disjunction event, and furthermore a mosaic form of the disorder can occur after mitotic non-disjunction.
Non-disjunction generally.
Non-disjunction can occur in meiosis I, but it's not necessarily the same result as non-disjunction event in meiosis II. This image helps describe the formation of the gametes from non-disjunction events.

(source: bioninja.com.au)
The most obvious point is that there are more aneuploidy cells born from a meiosis I non-disjunction event than a meiosis II non-disjunction event.
Furthermore non-disjunction occurs between homologous chromosomes in meiosis I or between sister chromatids in meiosis II. Was this subtlety perhaps what your lecturers/teachers were trying to describe?
Confusion somewhere in the question perhaps.
I think the problem comes from your first diagram, which appears to be an inaccurate sketch of what trisomy 13 looks like in a karyotype. This is what trisomy 13 actually looks like:

(source: iupui.edu)
How non-disjunction leads to a disease karyotype.
Lets pretend that the 'long' chromosomes in the first diagram of this answer are chromatids of chromosome 13. Thinking about the fusion event between gametes - the aneuploidy (n+1) gamete formed from either meiotic non-disjunction event and a normal (n) gamete could fuse to make the trisomy 13 result shown in the karyotype above; there would be three 'long' chromatids rather than two.


How do I find a protein from this DNA sequence?

You might want to try searching against NR/NT database using BLAST. This way you will get to know what this sequence might be similar too. The length of the sequence is too short to code for any meaningful protein.


How big should the human population be, as predicted by body mass?

It is certainly possible to use general relationships to predict human population density or abundance. The relationship between population density/abundance and body size is an old topic in ecology that falls within the field of allometrics (how different features of organisms scale with body size). A closely related allometric relationship is Kleiber's law, which deals with the relationship between body size and metabolic rate.

Your assumption of a generally negative relationship between body size and abundance is correct, and the relationship is approximately linear on a log-log scale. As mentioned in the comments, the exact shape of the regression will depend on what organism groups are included, since the scaling relationship is known to differ between taxa. However, to get a reasonable ballpark figure we can look at a the classic paper by Damuth (1981), which include 307 mammal herbivores. The scaling relationship found there is:

$$D = 10^{4.23}*W^{-0.75}$$

where density (D) is in individuals per km2 and body weight is adult body mass in grams. Using your example of 70kg for humans would result in a predicted density of 3.9 individuals/km2. The scaling coefficient -0.75 (or -3/4) is often labelled "Damuth's rule", and is usually also found when pooling both ectotherms and endotherms.

However, remember that this regression was based on primary consumers, i.e. mainly herbivore grazers. Alternative data for groups of mammals can be found in Peters & Raelson (1984). That paper presents regressions for both carnivores+omnivores as well as for all groups of mammals (herbivores, carnivores, omnivores). The relationship for carnivores + omnivores (CO) is:

$$D = 15.7*W^{-1.15}$$

and the regression with all groups is (HCO):

$$D = 40.7*W^{-0.859}$$

In both of these regressions body weight is expressed in kg. Using the CO regression results in a predicted human density of 0.1 individuals/km2, and the HCO regression gives a human density of 1.1 individuals/km2.

Looking at these values, it is reasonable to assume that the predicted "natural" population density of humans lies in the range 0.1 - 4 individuals/km2, but certainly biased towards the lower part of the range. I suspect that a regression looking only at primates would predict an even lower value, so I would not rule out values below 0.1 individuals/km2.

To get a grasp of what this means in actual population numbers, we can extrapolate the densities to the entire earth. If we use the predicted density from the carnivore+omnivore model in Peters & Raelson (1984) and the entire land area of the earth, which is ~150 million km2 (Wikipedia: Earth), the predicted human population would be about 18 million. Using the high estimate from Damuth (1981) would correspond to about 600 million people. However, remember that this is using the entire land area, including deserts, mountain ranges and arctic areas.

Another point of reference is the estimated historical human population density during the Paleolithic, when we lived as hunter-gatherers. I have often seen population densities in the area of 1 per mile2, i.e. 2.6 individuals per km2. These estimates are naturally very uncertain, but shows that the allometric scaling relationships seem to provide at least reasonable order-of-magnitude estimates of "natural" human population density.

It is also somewhat enlightening to consider that our current human population size of 7 billion corresponds to the predicted population size of a 380 gram carnivorous mammal (using the CO relationship from Peters & Raelson (1984)), making the unrealistic assumption that this mammal has managed to colonize all land areas on earth. This shows pretty clearly what an outlier modern humans represent.

The generality of these types of relationships for predicting densities of individual species can however be questioned. For instance, the regression relationships also differ between climatic regions (see Peters & Raelson (1984) for more), and, as indicated in the comment by @remi.b, it is also unclear what population states that should be included. For instance, should only population densities in "ideal" habitats be used, when we know that population densities of the same species can differ by orders of magnitude in different habitats? It is also unclear if/how to consider the effects of modern humans. Silva & Downing (1995) also argue that the scaling relationship is nonlinear on the log scale, with a more shallow slope for larger species, and also find essentially no relationship between body size and density within some groups of species. More recent papers have also highlighted that studies on global relationships between density and body size often mix-up several different processes and relationships, see White et al (2007) for an overview on this.


Older papers initially presumed that it was part of a mechanism called "catch" in invertebrates like molluscs which is a "sustained contraction."  However, paramyosin was also found in insects.  There is a very detailed review on invertebrate muscle from 2008 that you should read through (or, you know, search through) points out that recent evidence has shown that paramyosin is not involved in catch; that review also has this to say on the subject (emphasis added):

  Furthermore, paramyosin’s presence in almost every invertebrate muscle (including those with relatively small thick filaments) suggests that paramyosin should not be considered a ‘special’ molecule whose presence needs explanation. Paramyosin is instead an everyday constituent of invertebrate muscles, similar, for instance, to the giant sarcomere associated proteins (see Hooper and Thuma, 2005). Indeed, a more salient question might be why vertebrates do not have paramyosin.


DNA is a bit more complicated than some molecules due to it's length and composition variability.
In water.
According to Integrated DNA technologies:

DNA oligos can be resuspended to a near maximum concentration of 10mMolar; to achieve such a high concentration will require a lot of vortexing and it may take up to a day for the oligo to go into the solution.

DNA is a polar molecule and as far as I have experienced dissolves in water very readily. However there doesn't seem to be an exact quantifiable number for DNA solubility in water. If I correctly understand it, this paper claims that a 200,000Da-8,000,000Da oligonucleotide is soluble in water, however they never quantify this. An answer on a related question pointed out that high molecular weight DNA oligomers, like genomic DNA, is enhanced in solutions with dilute monovalent cations.
Cleaver & Boyer (1971) have some data on this, however it is somewhat outdated, and they were only using this solubility to demonstrate dialysis in water was capable of desalting the oligonucleotides.

Oligonucleotides larger than 5 bases in length remained within the dialysis
bag (Fig. 2) and losses of 10% and 40% occurred for tetra- and trinucleotides,
respectively.

There is a lot of work done on optimal temperature and pH for solubility of DNA so perhaps a more specific query might throw up some results.
In ethanol.
Ethanol precipitates at least 10–20 % of all classes of oligonucleotides. Oligonucleotides longer than 15–16 nucleotides are precipitated to about 65%.


What does ensemble-based model of enzyme mean?

An 'ensemble' is a set of related models of a structure.

For example, conformational ensembles describe the structure of flexible proteins. There is a database of such structures here : http://pedb.vib.be/.

When NMR is used to determine a structure, the result is an ensemble of structures (see this paper for a comparison with crystallography). However, it is possible to see multiple structures for crystallography as well. This paper on "Accessing protein conformational ensembles using room-temperature X-ray crystallography" describes limitations to the idea of crystal structures having one unique structure.


What does this sentence about angina mean?

Ambulatory means there is no emergency and refers to where the patient is and not to the disease itself (here the patient is out of hospital): for example there is no need to perform urgent PTCA or other procedures related to unstable CAD (coronary artery disease).

Another option is - to hospitalize the patient to perform urgent or planned procedures if the patient is unstable and there is deterioration in his/her status which may worsen and threaten the life.

The key word in this sentence "stable".


Are there any animals that are unable to hear the human voice?

Are there (apart from those with no sense of hearing at all) any
  animals that are unable to hear human voices at all?

I don't know of any examples off the top of my head, but let's think about this systematically.

The voiced speech of a typical adult male will have a fundamental frequency from 85 to 180 Hz, and that of a typical adult female from 165 to 255 Hz.

These are fundamental tones, and DO NOT include overtones (harmonics) of higher frequencies, that are actually responsible for the timbre of the voice, i.e. its characteristic sound and full content sonic content.

Here is a Fourier transformation of an audio clip of a female voice (a plot of frequency vs. amplitude, whereby the original recording was broken down into its constituent sine waves).

As you can see, the vocal cords produce overtones up to - and beyond - 7.5kHz. These overtones theoretically go to infinity in frequency, but are very negligibly quiet past around 10kHz in our case. Certainly very low in terms of decibels (though do not confuse real decibels with the -70dB sensitivity on the graph; with audio processing gear, 0dB is at which the signal is maximally saturated, or 'clips'). Let's assume 10kHz is the upper limit for normal female speech.

Keep in mind this does NOT mean that one could not perhaps sing a high note, and produce overtones past 10kHz - this is in fact doable. But let's stick with regular speech in our case.

Below you'll find the hearing ranges of some animals (source).

You'll find that all animals listed (save one) can hear some significant range of a regular (female) human voice. The little brown bat would not be able to hear the upper harmonics of a typical female speaker, given that they speak in a monotone.

Lastly, please keep in mind the difference between decibels ('loudness') and frequency (ability to sense a pitch). Some of the extreme high overtones are very quiet, so even if an animal would be able to sense them, they may not have a sensitive enough ear to pick up how quiet these sounds would be.

And really lastly, remember that sound produces vibrations and resonates through objects that sound waves hit. These resonate at different frequencies, so your voice can be sensed indirectly too through these resonating frequencies.


Technical term for a mutation that only occurs after a preceding one

The description of the second mutation depends on the nature of its relationship to the first mutation.

If the first mutation reduces fitness of the organism, and the second mutation tempers the fitness reduction, then the second mutation would be compensatory.

Compensatory mutations are common in bacteria that acquire antibiotic resistance.  Consider a strain of E. coli that acquires resistance to streptomycin by mutating the rpsL gene, which encodes a 30S ribosomal protein targeted by streptomycin.  In the presence of streptomycin, the rpsL mutant is obviously more fit than wild type E. coli.  In the absence of streptomycin, however, ribosomal mutations lead to inefficient translation.  Compensatory mutations may then arise elsewhere in rpsL or within another gene involved in the ribosomal complex, partially alleviating the fitness defect caused by the initial mutation to rpsL.

If, instead, the mutations are synonymous and otherwise unrelated in their functional potential, I would simply call those mutations coincident in the genome, though this isn't really a "technical" term. If you wish to describe the relevance of these synonymous mutations in context of the three distinct genotypes given in the question, you could say that the first T to G transversion differentiates strain X from ancestral Wild Type, and the second A to T transversion differentiates strain Y from ancestral strain X.  This assumes that both of these mutations occurred once in the genetic history of this population.


What bug is this? I found several in my flat and I have no idea

That is the larva of a carpet or skin beetle, family Dermestidae.https://en.wikipedia.org/wiki/Dermestidae
These eat dried flesh, skin, and other dried organic matter. They are the bane of entomologists because they eat insect collections. They are used by bone-collectors to clean skeletons, and are the last insects to arrive at a corpse.


How do we know if the folding@home project results are right?

in silico modelling of anything in biology is an active field of research. It's very useful for making predictions and developing hypotheses, but any findings need to be confirmed experimentally.
From the Folding@Home website:

Folding@home has been a success. In 2000-2001, we folded several small and fast folding proteins with experimental validation of our method. We are now working to further develop our method, and to apply it to more complex and interesting proteins and protein folding and misfolding questions. Since then (2002-2006), Folding@home has studied more complex proteins, reporting on the folding of many proteins on the microsecond timescale, including BBA5, the villin headpiece, Trp Cage, among others. In 2007, we crossed the millisecond milestone by simulating a protein called NTL9, and the 10 millisecond barrier in 2010 with ACBP.
More recently (2006-present), we have been putting a great deal of effort into studying proteins relevant for diseases, such as Alzheimer’s and Hunntington’s Disease. You can learn more about our results and peer-reviewed scientific achievements on our Papers Page.

As they say, you should check out their research contributions for how it's being practically applied.
You may also be interest in this article for the science behind and prospects of protein folding prediction: Bowman GR, Voelz VA, Pande VS. 2011. Taming the complexity of protein folding. Curr Opin Struct Biol 21(1):4-11. At least try reading the conclusion for a less technical overview.


What happens to deep sea creatures if they reach the surface?

It varies depending which creature is considered. The faster they are made to lower the pressure and raise the temperature, the worse the effects are. Some animals have a liver, which can help to counteract toxic effects at lower pressures, and some fish at 2000m have an air bladder, so they explode if they are hauled up.

Deep sea fish sometimes arrive at the surface with their inner organs popped out of their mouth.

They have different lipid types than us, because lipids are packed together differently at high pressures, and lowering the pressure on their lipids can make them malfunction.

Chemicals can act differently at high and low pressures, so a chemical that can be inert at a low pressure, can produce a different reaction at high pressure, producing gas, precipitating into component chemistries. Urea can be toxic at high pressures and fine at low pressures.

Proteins fold and change shape under pressure, so deep sea animals can use different proteins that may chainge their shape and function at lower pressure.

Dolphins can get the bends if they are scared back to the surface by deep sea exploration industries, too fast for their bodies to adapt.

here are some info sources:
http://www.deepseanews.com/2016/03/under-pressure/
https://www.quora.com/Do-deep-sea-animals-experience-decompression-sickness-if-brought-to-the-surface


What would happen if there were no SOX9 in an XY human?

Quoting the abstract of this paper verbatim:

  Sox9 is an Sry-box-containing gene that encodes a transcriptional
  activator. During mouse gonadogenesis, Sox9 is detected in the male
  gonad at 11.5 days postcoitus (dpc). At 12.5 dpc, testicular cords
  form, morphologically distinguishing the male gonad from the ovary.
  From this stage onwards, Sox9 expression is restricted to the Sertoli
  cell lineage and persists in the adult. Humans with heterozygous
  mutations in SOX9 develop a skeletal syndrome known as campomelic
  dysplasia. Furthermore, most XY SOX9 heterozygotes show variable
  male-to-female sex reversal, implicating SOX9 in testis development.
  Sox9 heterozygous knockout mice die at birth with a syndrome similar
  to that of human campomelic dysplasia. In contrast to humans, XY
  Sox9+/- mice form normal appearing testes. Germ-line knockout of Sox9
  using a conditional null allele provides a tool for generating Sox9-/-
  mice by simple genetic crosses. However, Sox9-/- mice die soon after
  11.5 dpc because of cardiovascular defects. In vitro culture of the urogenital ridges of XY Sox9-/- results in gonads lacking testicular
  cords and Sertoli cell marker expression, but with the expression of
  ovarian-specific markers. Therefore, Sox9 is essential for diverting
  an intrinsically ovarian program of organogenesis toward testis
  formation.

From MGI page on Sox9:

  Null mutant heterozygotes and conditional knockout mutants display
  perinatal lethality with cleft palate, hypoplasia and distortion of
  numerous cartilage-derived skeletal structures, and premature
  mineralization in many bones. Specific conditional knockout mutations
  are sex-reversed.


Can inhibition of lymphocytes migration be a direct cause of chronic inflammation?

The mechanism is likely very straightforward. Activated macrophages already in the area are releasing pro-inflammatory cytokines like TNFα, IL-1β, IL-6, IL-12, MIP-2, etc. These are not only important for granuloma formation, but they also recruit other immune cells to the area. However, since cord factor has this anti-migratory effect, once the cells get there they can't leave. This is important because activated macrophages are key antigen-presenting cells (once they kill and break down the antigen, in this case Mycobacteria), and they need to move to the spleen to assist in the upregulation of the adaptive immune response. By preventing this, mycobacteria can evade part of the immune system - part of the reason why TB is so hard to clear once acquired.


Relationship between turgor pressure and osmotic pressure?

Turgor Pressure(T.P) is defined as the amount of pressure inside a cell solely due to its water content, whereas Osmotic Pressure(Pi) is defined as the pressure required to stop osmotic flow between the cell and a pure solvent when the pressure exerted by water is zero.

Osmotic Pressure is often given as the negative of the Osmotic Potential(or Solute Potential) of the Cell.(Because more the solute, more pressure will be required to stop the osmosis, but against the gradient). (1)

Therefore, it can be easily seen that Osmotic Pressure is solely dependent on the solute concentration of the cell.

The Total Suction Pressure(S.P) of a Cell is the pressure required outside of a cell to stop the water flow in a pure solvent.

The T.P in such a situation would try to reduce the S.P (More the T.P, less would be the pressure on the outside). Whereas, the O.P in such a situation would try to increase the S.P (More the solute inside a cell, more would the water on the outside try to get on the inside)

Hence, Mathematically (considering no other pressures to be responsible for Total Suction Pressure)

S.P = Pi - T.P

This can Also be proved in the following way:

Water Potential(Psi W): Total Pressure inside a Cell.

Solute Potential/Osmotic Potential(Psi S): Reduction in Water Potential Magnitude due to addition of a Solute(solute reduces kinetic energy of water due to bonding)

Pressure Potential(Psi P): Hydrostatic Pressure, i.e, pressure exerted by the water present inside a cell if there were no solute particles.

By definition

Psi W = Psi S + Psi P

(We know, Psi S = -Pi) As written above in (1)

Psi W = -Pi + Psi P

(We know, Turgor Pressure is the same thing as Psi P)

Psi W = -Pi + T.P

Suction Pressure is the negative of Total Pressure inside a Cell

(S.P = -Psi W)

(Water flows from high water potential to low potential, but from low Suction Pressure to an area of High Suction Pressure)

Therefore

-S.P = -Pi + T.P

multiplying by -1

S.P = Pi - T.P


Does there exist a reagent that can only be precipitated by Haemoglobin and nothing else?

This very point is well addressed by Laura J Snyder in Sherlock Homes: Scientific Detective (a great read) where the author challenges the view that Conan Doyle is the 'father of scientific crime detection' and argues that the new science of forensics actually influenced Conan Doyles' writing, rather than his novels being the inspiration for the new emerging discipline.

Furthermore, not all his claims were scientifically valid, and the 'infallible test for bloodstains' is a good example.

The relevant passage is as follows:

  Let us examine, for example, the ‘infallible’ test for bloodstains Holmes is presented as having ‘invented’. By1887, when A  Study  in  Scarlet was published, many researchers already shared the desire for such a test; this desire was not satisfied until the turn of the 20th century,when the spectroscopic method was developed.

  A modern chemist has noted that the method Holmes describes – one which would precipitate a brownish dust and change the color of blood in water to mahogany – would need an acid to increase the oxidation rate, as well as a material to be oxidized. By examining the possibilities for the ‘few white crystals’ and the ‘drop of transparent fluid’ that Holmes uses, this chemist suggests that the ‘Sherlock Holmes test’ would probably have had a sensitivity similar to the guaiacum test that Holmes derides as being ‘clumsy and uncertain’[15].

  Moreover, Holmes’ test does not distinguish between human blood and the blood of animals– a problem that, by 1887, was considered an even larger concern than the sensitivity of the blood tests currently in use. A solution to this problem did not arise until the work of Paul Uhlenhuth in 1901 [16].

The two references quoted in the above passage are:

[15] Gerber, S.M. (1983) A study in scarlet: blood identification in 1875. In Chemistry and Crime: From Sherlock Holmes to Today’s Courtroom (Gerber, S.M. ed.), pp. 31–35, American Chemical Society (Columbus,OH, USA)

[16] Thorwald, J. (1965) The  Century  of  the  Detective (Winston, R. and Winston, C. trans.), Harcourt, Brace and World


Why does allele linkage cause disproportionate phenotypic ratios?

I found the explanation at this site helpful:
http://www.ndsu.edu/pubweb/~mcclean/plsc431/linkage/linkage1.htm

I don't have a clear sense of what you mean when you ask about assorted phenotypes occurring before recombination ("crossover"). All of your examples deal with diploid organisms. If they are multicellular then the cells that can undergo meiosis are highly specialized, and eventually become haploid. As the chromosomes are prepared they tend to become compact, and are often not expressed. So it is difficult to assess the phenotype of those haploid cells. The rest of the cells in the organism are diploid  and at least some of them can express the alleles that give rise to the phenotypes that you are scoring.

At the moment of fertilization there is no further recombination, as the zygotic cells undergo mitosis.  There is no segregation, no independent assortment, no linkage (that you can measure--the genes are still arrayed along their chromosomes). Each mother cell divides to give two perfect copies of itself. Then the daughters divide, etc. Even in the cells that are going to become germ cells, they divide by carbon copy mitosis right up until they enter meiosis.

So there is no mechanism that would lead to genotypes different from the genotype of the zygote (until meiosis).


Birds learn new tricks very often, using roads to crack nuts, opening foil milk bottles (tits), and Hawks are known to catch Koi.

These pages say that Cooper Hawks specifically do catch fish: http://forums.gardenweb.com/discussions/1997093/hawks-taking-koi
http://www.outdooralabama.com/coopers-hawk

Here is a cooper hawk catching a duck and swimming around with it: https://www.youtube.com/watch?v=A08jxYinAG8

if you put cooper hawk pond into youtube, you will find 10+ videos of them bathing in ponds, and 2 videos of them scouting at a pond.

My aunt saw a buzzard, Buteo Buteo 50cm tall, catching a yellow Koi right out of the water while I was out for the day. The Koi was 30cm long, 12", it dived on the water and flew away with a fish on the wing. The Koi had indeed vanished as my aunt had said.


I've worked on a couple of these for biofuel production. The answer varies widely according to plant P and how well studied plant P is. In terms of what data is used, it includes but is not limited to: temperature, insolation, length of the day, cloud cover, rain, soil composition, soil type, soil density, other local effects like wind or pests, altitude, humidity, and pH. For corn(food) and miscanthus(experimental biofuel crop) the models are quite good if the year is pretty normal and you're in a well-studied parameter space, mostly because corn and grass grows straight up. For trees, non-crops, non-corn crops, etc the models are almost completely useless. It's a question of testing nearly every possible combination of parameters for each plant P, and how much people care about how tall it gets.

Given how much data goes in, it surprises me that even under ideal conditions(well-studied) some of the parameters the model spits out are impossible/wrong. There's a measure of leaf overlap(just as an example) that's especially poorly defined but a rough proxy might be "number of leaves that shade a specific point, on average" and it's regularly measured at <10 and regularly predicted at well north of 50.


What kind of fruit is this? It is the size of a small avocado or a plum

After doing a bit more research and asking a few friends, I found out that it was a feijoa, or pineapple guava. I think the ones in the picture aren't fully ripe yet, though.


Spectrophotometric Values of Individual Nucleotides

If it's so important to you that you need a quotable source for this, I'd measure it myself with the equipment I use for the real experiment.

Otherwise I'd suggest you look at a chemical database such as NIST:
http://webbook.nist.gov/cgi/cbook.cgi?ID=C58617&Mask=400 and use the spectra that can be found there.


Does a reduction in stem cells mean possible earlier death?

Stem cells persist because they have the capacity to self-renew.  At birth you will have a finite number of each stem cell type (e.g. hematopoietic stem cells that make blood, gut epithelium stem cells that make gut lining etc).  The general picture is that as tissues require replenishment, a stem cell divides. One daughter cell starts to differentiate (and divide) into mature cells required by the tissue, whereas the other daughter cell retains stem cell function.

So a stem cell is typically defined as a cell with the capacity to: (i) self-renew and  (ii) to give rise to one or more cell types in a tissue. A hematopoietic stem cell can give rise to T-cells, B-cells, neutrophils, red blood cells, platelets etc.  The ability to self-renew means that, in general, stem cells don't 'run out' during a lifetime.

[ Its important to note that to define a cell as a stem cell, scientists use strange hybrid of: in vitro or animal assays + cell surface markers + location in the tissue + measures of 'having the capacity to make continued contribution to new cells'.  So lets just say that stem cells are only ever as well defined as our choice of assays combined with the interpretation of those results. ]

I mention the challenge of defining stem cells because, in recent years as assays and technologies improved, cells such a oocytes (eggs) or adult neurons, which were once thought to be finite, have been shown to have be replaced/renewed, presumably by some 'stem cell like' cell(s).

As noted above, stem cells are usually involved in the replenishment of a particular tissue type.  So liposuction, which will remove fat cells, should not affect the numbers of hematopoietic or neural stem cells and so on.

Any claim of clinical benefit of a 'stem cell treatment' using liposuction should be backed by clear data.

A longer answer would get into:
(i) the concept of 'plasticity' where the classical view - a fixed pathway between a stem cell giving rise to one daughter cell that  gives rise to mature cells and the other returns to a stem cell state - is open for debate, and
(ii) the idea that since stem cell definitions are only as good as our assays, there may be potential plasticity even among stem cells that we cannot 'detect' yet.


How was the Huntington's disease gene's location found?

A Google search for "Huntingtons disease gene discovery" yielded this page at the Nature Education Scitable website. The following citations are provided regarding the molecular basis of HD:

  Huntingtin (HTT) was the first disease-associated gene to be
  molecularly mapped to a human chromosome (Gusella et al., 1983)2. Ten
  years later, scientists identified the DNA sequence and determined the
  precise nature of the HD-associated mutation in HTT (MacDonald et al.,
  1993).

Gusella et al. used restriction fragment length polymorphism (RFLP) analysis to locate a RFLP marker linked to Huntington's disease on chromosome 4. From the introduction of their paper:

  We have now identified an anonymous DNA fragment from human chromosome
  4 that detects two different RFLPs in a HindIII digest of human
  genomic DNA. This polymorphic DNA marker shows close genetic linkage
  to the Huntington's disease gene in two separate families, although a
  different haplotype of the marker segregates with the Huntington's
  disease gene in each family. We infer that the Huntington's disease
  locus resides on human chromosome 4.

Further details given in the paper might justify the description given in the question. "Fabolous luck" could refer to the discovery or availability of suitable families and pedigrees for the genetic studies. The "steady detective work" would be the genetic mapping and fieldwork required to establish the link. The following quotes describe some of the efforts spent on the project:

  The success of any genetic linkage project depends in large part on
  the quality of family material available for study. We initially
  invested considerable effort in identifying a useful family from the
  National Research Roster for Huntington's Disease Patients and
  Families at Indiana University. An American family of reasonable size
  was selected and blood samples were obtained (...). Subsequently, a
  substantially larger Huntington's disease family was located. This
  pedigree stem from a unique community of interrelated Huntington's
  disease gene carriers living along the shores of Lake Maracaibo,
  Venezuela. (...)For the past three years an expedition has spent one
  month annually in Venezuela collecting pedigree information, tissue
  samples, and clinical data. (...) In Venezuela, many family members
  were examined for three consectuvie years. Permanent lymphoblastoid cell lines were
  again established for each individual to act as a permanent source of
  genomic DNA. In both families each individual was examined by at least
  one neurologist experienced and knowledgable about Huntington's
  disease.

The Scitable page also summarizes the approach and results described in the paper. For the RFLP analysis, several DNA probes were tried, of which one, "G8", resulted in a HD-linked pattern:

  James F. Gusella and colleagues carried out a study to determine
  whether they could identify a DNA probe that would show an
  HD-associated restriction fragment length polymorphism (RFLP) when
  used in Southern blot analyses of chromosomal DNA digested with the
  restriction enzyme HindIII (palindromic recognition sequence
  5'-AAGCTT-3'). The team identified one probe out of 12 tested, called
  G8, that showed a specific RFLP pattern associated with HD in two
  large families with a history of the disease (Gusella et al., 1983).
  Using the G8 probe, they next identified two HindIII sites (called H1
  and H2) that were palindromic within this chromosomal region. DNA
  fragments at these sites vary in length among different HD lineages.
  Because researchers used two large pedigrees in these experiments,
  they were able to obtain statistical support for their discovery
  (Figure 3).

However, at the time the origin of the G8 probe DNA in the human genome was not known, so human-mouse somatic cell hybrids were made to identify where the G8 probe DNA belonged. This showed that the G8 probe corresponded to chromosome 4, and indicated that the HD gene would be found there:

  Researchers found that the G8 DNA probe hybridized only to Southern
  blots using chromosomal DNA from human-mouse somatic cell hybrid lines
  that contained human chromosome 4. Therefore, researchers determined
  that the G8 DNA probe is located on human chromosome 4, and they
  concluded that the HD gene is located on chromosome 4 near the region
  corresponding to the G8 DNA probe (Figure 5; Gusella et al., 1983).


Can an Ichthyologist identify this Canadian freshwater fish?

Judging from the curved caudal (tail) fin, which is more square in brown trout, this appears to be a chinook salmon. The mouth also appears to be black whereas in brown trout the mouth is white.

Sources: Michigan Department of Natural Resources


Why is coconut oil healthier when it has so much saturated fat?

coconut oil is composed mainly of medium-chain triglycerides, 1)it is smaller than other long-chain triglycerides so that it can be digested easily, 2)the digestion of coconut oil does not involve in the Pancreatic digestive enzyme system, 3) liver prefer use medium-chain triglycerides as the fuel sources 4) medium-chain triglycerides will convert to monoglyceride and medium-chain fatty acid which have strong antibacterial


NaCl role in CTAB - DNA complex in DNA extraction

CTAB forms insoluble complexes with nucleic acids and can be used to selectively precipitate them from solutions, see this reference:

The isolation of bacterial nucleic acids using cetyltrimethylammonium
bromide (Cetavlon)

When you add NaCl in a concentration between 0.4 - 0.7M, the nucleic acids stay in solution, while polysaccharides and other substances, which may interfere with the DNA preparation do not. See this paper: "Rapid isolation of high molecular weight plant DNA."


Rigorous definition of the kinship coefficient and proof of a recursion thereof

The definition as set by Kenneth Lange's book is indeed quite vague and thus unrigorous. It is a probability not conditioned on observing an allele $a$ at a locus of $i$ but conditioned on the following where we focus on one particular locus. It is rigorously defined as follows. Then we will give the correct formulation of the correct recursive equation akin to Equation $(1)$ which is in general wrong.

A graph of lineage contains nodes, which we call persons, of a particular locus. Each node, or person, contains exactly two genes. We draw one and only one directed edge (parental relationship) from a gene of a parent person to the gene of a child person if the latter is inherited from the former.  This is a directed acyclic graph (DAG). Each gene can be connected by no more than $1$ edge directed to (as opposed to away from) it. The two genes in one person cannot be connected by edges. Two persons are said to be connected if there is an edge pointing from a gene of one node to a gene of the other node. Two persons cannot be connected by more than one edge. For a pair of connected persons and their directed edge between them, the edge is equally probable to connect to one gene as the other gene of a person, i.e. the probability is $\frac12$. A pair of genes (persons) are said to be connected if there exists a undirected (simple) path from one gene (person) to the other. Two connected genes are called identical by descent.
In this setting, the DAG with respect to the persons is given and deterministic whilst any directed edge in the DAG assigned to two persons are random with independent probability $\frac12$ with respect to the genes within each person.
For a pair of persons on a lineage DAG that is connected, the probability of one gene equally probably chosen amongst the two genes of one person being connected, or identical by descent, to one gene equally probably chosen amongst the two genes of the other person is the coefficient of kinship.
As an additional assumption, the genes that are connected have to be the same and thus assume the same allele.
Definition: Suppose a lineage DAG is given. Let the kinship coefficient between person labeled $1$ and person labeled $2$ be $\Phi(1,2)$.  Denote the set of parents and children of person $1$ each of which is on an undirected (simple) path between $1$ and $2$ as $S_2(1)$.
Lamma: Denote the set of paths through an ordered persons $p$ in that order as $P(p)$. $\{P((1,i,2))|i\in S_2(1)\}$ partitions $P((1,2))$.
Proposition: $$\Phi(1,2)=\frac12\sum_{i\in S_2(1)}\Phi(i,2).$$
Note: The summation in the Proposition is over $S_2(1)$ rather than the set of all parents and children of person $1$. That fixes the condition under which Equation $(1)$ is valid.
Corollary: $$\Phi(1,2)=\sum_{p\in P((1,2))} \frac1{2^{n(p)}}$$
where $n(p)$ is the number of persons on path $p$. $n(p)=|p|+1$.


What terms or concepts are used to describe the morning metabolic phenomenon involving glucocorticoids, glucose, and blood pressure?

Morning surge, Prewaking surge, Sleep-trough surge, Rising surge.
Example of article using the terms:
"Morning Surge in Blood Pressure and Cardiovascular Risk"
https://www.ahajournals.org/doi/full/10.1161/HYPERTENSIONAHA.110.157149
This one is interesting in that it lists other articles and the term they used for the period you are looking for.


Effect of single nucleotide deletion or insertion on primer annealing

We used this kind of primers to generate out of frame mutations or to add additional bases. In my experience your PCR will work (probably a a lower efficiency) and you will get a product with an additional base. We used primers with bigger differences in PCR based site directed mutagenesis of plasmids, there up to 10 bases didn't match but the primers where also longer. For single nucleotide mismatches (either + or - one base) we used primers around this size.

Regarding the literature, this publications might be useful:

A guide to the design and use of mismatched and degenerate
primers
Effects of primer-template mismatches on the polymerase chain
reaction: Human immunodeficiency virus type 1 model studies
The Effects of Internal Primer-Template Mismatches on RT-PCR: HIV-1
Model Studies
Effect of primer mismatch, annealing temperature and PCR cycle number
on 16S rRNA gene-targetting bacterial community analysis

Especially the first publication contains a lot of other interestings references.


What happens if the Nematode epidermis becomes damaged?

Nematodes have external skeleton in the form of a cuticle. Their muscles are attached to this external skeleton and when a muscle cell contracts it moves a segment of the cuticle relatively to the other segments, which in turn allows the pushing of the environment and thus, motility. This is very similar to how we, humans, move.

Damaging the cuticle in nematodes results in motility impairment. For example, some C. elegans strains have a mutation that results in a non-normal cuticle formation which makes the animals roll instead of moving peristaltically (like a snake).

In addition, some muscles are not skeletal muscles, or body wall muscles in the case of nematodes. These muscles affect movement of an organ like the pharynx in nematodes or the heart in humans.

for further reading regarding the body wall muscles and cuticle interaction you can see wormatlas.org

References:

Labouesse, M. 2006. Epithelial junctions and attachments. WormBook, ed. The C. elegans Research Community, WormBook, doi/10.1895/wormbook.1.56.1


I don't know what else to say as an answer but here is a link to the user manual. If you are looking for more specific usage instructions, I would suggest that you try Biostars though I can't guarantee that you receive an answer.


Can aflotoxin presence be inferred from the mild discolorotion at the middle parts of a hazelnut?

Depends on who you bought them from and how you stored them.
Molds can grow in nuts and nutmeats and produce mycotoxins (from toxin-producing strains such as aflatoxins by Aspergillus flavus). The mold is usually visible and below is picture of Aspergillus flavus growing on a nut product. Source

The amount of aflatoxin produced by the mold is dependent on weather conditions and storage. We can only account for or control the storage conditions. When food substances are not well preserved, fungal growth may occur, leading to the production of mycotoxins.
The pictures presented could also just be an improper storage (with no health risks). There's indication that storage of wet nuts in poorly ventilated silos increases the potential for developing kernel brown centers. Source
If these nuts were stored in improper conditions from farm to store and the farm has been associated with a breakout of Aspergillus flavus then there's chance, but slim. QA/QC and aflatoxin levels are regulated. Codex Standard 193-1995 mentions the maximum levels of aflatoxins and sampling plans.
If the nuts had mold on them and they were washed to get rid of the surface mold, they could have spores from Aspergillus flavus capable of producing alfatoxin. Aspergillus fungi can case discoloration of  certain grains (rice), but that implies that you're able to see them on the product (the mold growth). The nuts in the picture seem quite clear.
In terms of where you bought the product, street vendors are at higher risk of having their products present alfatoxin problems rather than commercial enterprises, because of the location the product is sold at. Source


What exactly is the time constant of an ion channel gating?

Although the membrane time constant is very important in neuroscience, the time constant described in the original question is about ion channel gating rather than the rate of change of membrane voltage.

The "tau" when referring to ion channel gating is indeed referring to how long it takes to open/close.

When the membrane voltage changes, there is a new equilibrium value for the probability of the channel to be open versus closed (note: there can be other states for channels too, but for this explanation I will stick to open/closed). The rate at which this equilibrium is approached from the previous open probability is described by an exponential function, with "tau" as the time constant of that approach. A small value of tau means that the new equilibrium is reached very quickly. This site has a good explanation of the terminology and gating process, as do many others.

Time constants are involved in any system described by an exponential (these are called "linear time invariant" processes), whether decay or increase, and it is equal to the time it takes to progress approximately 63.2% of the way to the equilibrium. The cool thing about time constants (and linear time invariant processes in general) is that it doesn't matter what your starting point is or how far into the process you are, the time constant stays constant and every time "tau" passes you are now 63.2% closer to equilibrium than you were at time t-tau.


Deducing protein sequence length from gene DNA sequence length

If you look at the DNA sequence in the patent, you will see that it does not start with ATG and does not end with a stop codon. The disclosed sequence has some additional bases in it, therefore the discrepancy in protein and DNA length. Those additional bases almost always occur in cDNA, e.g. because of polyadenylation, Kozak sequences, etc.


What is this row of pits along the "upper lip" of theropod skulls?

They are called Nutrient Foramen which are innervation of blood vessels and nerves, you see the same thing in reptile and bird skulls (mammals tent to pack it all into one or two large openings). They feed blood vessels and nerves to the gums, lips, and face.

Dinosaurs do seem to have more of them, but size making them more noticable is also a factor. The increase in dinosaurs may be involved with pressure sensitive scales as seen in crocodiles or alternatively something like lips, or both. Here is a great article on them. Paleontologist are hampered here becasue the related animals are birds (who have beaks) and crocodiles (which are entirely scaly). So it is hard to pin down exactly what a dinosaur oral facial anatomy would look like.


Is the Klein's bottle a good analogy to the relation between T-tubule and sarcolemma?

If we're looking at diagrams for the t-tubule with respect to the sarcolemma, we see the two are actually fused:

The function therein is to allow depolarization to penetrate the interior of the cell quickly. The surface isn't transected anywhere, it simply folds inward. You can visualize this by sort of pushing a hole through some putty with a finger, and making a hole to the other side. Really no need to upvote me here, just easier to paste images in answers.


In the context of experimental evolution, replicate lines are simply separate experimental (or control) lines the are established from the founder population at the beginning of the experiment. In this paper, the authors must have established 10 separate experimental lines that then evolved in different carbon dioxide levels. For example, 10 separate aliquots of algae are drawn from the same source population and then separately subjected to the agent of selection. These replicate lines should remain separate and not be mixed or crossed.

Replicate lines are useful in experimental evolution for a few reasons. Because you are studying a population that is experiencing a selection pressure, you expect that genetic changes are in response to that pressure. However, changes can also occur due to drift. Replicate lines (and a consistent response to selection among them) is important to ensure that changes are a response to selection rather than to some other force (drift, mutation). Some drift is bound to happen when the lines are founded, because you are selecting a subset of the population, which is actually a good thing. Each line gets a random subset of genes which then evolve together. This potentially allows discovery of different genetic pathways to the same adaptive response.

The background and lots of examples are in Garland and Rose, Experimental Evolution (UC Press, 2009).


Tumour resistance: single-cell or population effect?

There certainly can be co-operation or competition among cancer cells within a tumor that can provide some types of population-based influences on cancer-cell survival. Present evidence, however, suggests that resistance to therapy is almost always due to resistant sub-populations of cancer cells within the tumor. In many cases, such as after treatment with EGFR inhibitors, the resistance mutations have been identified. Sometimes these mutations are in such a small fraction of the cancer cells that they can't be detected in the original tumor before treatment, but in most cases they probably were already present before therapy, caused by the mutations that are inevitable during tumor growth. This review on intra-tumor heterogeneity is a good place to start learning about this topic.


Are there genes in humans from the common ancestor of all organisms?

I very much agree with bitwise's answer. I just want to point out that even in terms of nucleotide sequence there are some extremely conserved genes.

The most highly conserved are ribosomal RNA genes. The image below shows the conservation of 16S rRNAs from archaea, bacteria, and eukaryotes (eukaryotes do not have 16S in their cellular genome but the gene is present in the DNA of mitochondria and chloroplasts). Residues in red are conserved across all domains of life (image source):

A very nice study from 2008 [1] identified tRNA genes as the next most conserved and ABC transporter nucleotide binding domains (NBDs) after that. The alignment below (taken from the paper) shows the conservation of NBDs from various species. Note that they include eukaryotes, archaea and bacteria:
[2]

If you look at orthologous genes in general, without specifying a specific level of sequence identity, then you can find various genes (notably those coding for the enzymes of the glycolysis pathway as mentioned in the comments) that are conserved across most, if not all, cellular life.

So, to answer your question probably yes. At least, there are genes in humans today that can be found in all or almost all other life forms. Whether there were present in LUCA we cannot know for sure, it does seem likely however given how widespread they are today.

Reference

Isenbarger T.A. et al, The most conserved genome segments for life detection on Earth and other planets, Orig Life Evol Biosph. 2008 Dec;38(6):517-33.


This looks very similar to a click beetle. Some of them are pretty popular in south Canada.


Strenuous exercise apparently increases urinary and sweat losses that may increase magnesium requirements by 10-20% according to this paper.