This is a very subtle question and I encourage you to read the Wikipedia articles on these different subjects (t-test, chi-squared test, p-value, etc) because the authors worked hard to combat common misconceptions about these commonly used statistical tests. Here is a rather oversimplified rule-of-thumb for these different tests:

t-test: Used when you are looking at the means of different populations. For example, you might want to determine whether the difference in the mean gene expression level between treated and untreated cells is different, or if the gene expression level of cells in a certain environment differs from what you would expect in a null hypothesis. Assumptions: You are assuming that the populations you are looking at are normally distributed. The variance of the populations is not known (that would be a Z-test), but it is assumed that the variance of each population is the same. Finally, for the t-test to work, the samples of the data from the two populations are assumed to be independent.
$\chi^2$ test: Several possibilities for this. The most common in biology is the Pearson $\chi^2$ test, which is used when you are looking at categorical data, like the number of pea plants with white or purple flowers and round or wrinkled seeds, and trying to see whether the number of individuals in each category is consistent with some null hypothesis (such as the number in each category you'd expect if the genes for flower color and seed shape are not linked). Assumptions: The data points were randomly and independently gathered from the population, and you have a reasonably large number of samples.

I'd hate to have made a huge mistake, so please edit my answer and/or contribute your own if you think I am completely misrepresenting these topics!


Clarification on the "orientation" of chromosomal rearrangements

I think the picture will help you. In fact, to determine which kind of rearrangement for the chromosomal, we need to define an "orientation". However, this orientation is not fixed. It is a definition compared with the two chromosomes before and after the rearrangement. As the picture shows, the duplicated sequence after rearrangement should be in the same orientation, if one of them not, it should be described as "inversion after duplication". For deletion, there is no difference in the orientation if the remain parts still in their previous pattern. The key point to understand,  is to check the sequence before and after the rearrangement and find difference(s) between them, then compare to this picture(which is the definition of rearrangement) to find if the chromosome has one or multiple rearrangements.
Hope this could help you.


Description of the paramaters in the packing parameter?

Following image from (Salim et al 2014) will makes thing clear to you,

When they say volume, it is volume of shape of lipid. Shape can be determined by many factors as described here. Following is modified images from (Sprong et al 2001) which will tell you how change differ in general. Here are examples of few common lipids.


Can someone help me identify this spider?

According to museum.wa.gov.au, there are four solifugid species in Malawi. Ceroma johnstonii, Ceroma zomba, Zeria niassa and Zeria paludicola.

Ceroma johnstonii has a grayish-brown tint, not the dark brown, almost black coloration (and red) of your solifugid. Ceroma zomba is only 8 mm in length, much too small even if your estimate of 50-60 mm was referring to the legspan.

Zeria niassa is only 24-28 mm in body length, significantly smaller than what you saw unless you meant legspan. Zeria paludicola is also smaller than your 50-60 mm estimate, so it must have been the legspan, not the length. The only photo I could find of any Zeria species is from eol.org and is of an unspecified species. In the photo, it has a dark brown coloration and a very faint tinge of red on the side of the abdomen.

So your image is either of Zeria niassa or Zeria paludicola.


How would a warm winter affect maple sap production?

This article has a clear explanation (backed up by good links) of the effects of climate change on maple sap production, including the following:

Maple trees produce the best sap on cool days preceded by freezing nights – the cold weather causes the sap in the tree to freeze, creating a low-pressure vacuum that draws more sap up from the roots. When temperatures rise the next day, the sap melts and oozes through the tree, making for easy collection. When temperatures stay abnormally warm, as they have been lately, this process does not occur.
Additionally, the warm weather causes the trees to begin to bud.  The hormones that trigger budding also decrease the sap’s sugar content and spoil its taste. This means that it takes much larger quantities of sap to boil down to a gallon of syrup.


How does DNA still work after recombination?

One must always be careful not to stretch an analogy further than it can withstand, but since you started these analogies, I will follow up on them and explain the small mistake you've done in their representations.

The two books are not as different as you have in mind. You are not pasting the beginning of Uncle Tom's Cabin with the ending of Harry Potter but only the beginning of Harry Potter with the ending of another Harry Potter in which Ravenclaw is renamed Eagleclaw.

Also, unlike in books, there is no beginning-to-end reading frame for the entire chromosome. There are just genes randomly placed along chromosomes. The reality is that the placing is actually not that random but assuming it is can give you a sense of why it can often be fine to recombine two chromosomes and end up with still functional chromosomes.

For the computer program analogy, it would be like swapping files between branches of the same project (thanks @IronSean for his comment).


How can a tongue-biting parasitic arthropod become a fully functional tongue?

Short answer
There is no evidence whatsoever that the parasitic arthropod Cymothoa exigua develops itself into a functional tongue. Instead, it consumes the fish's tongue and occupies the freed buccal space to continue feeding onto the fish's blood or mucus.

Background
The linked wikipedia page that states that Cymothoa exigua arthropods form fully functional tongue-replacements refers to Brusca & Gilligan (1983) to back up that claim. While the journal is credible, the article itself is a theoretical work. The authors base their conclusion that the tongue replacement is functional on the relatively healthy condition of just 2 specimens of fish. They reasoned that, because the parasitic arthropods were relatively large, the fish had to be hosting them for quite a while. In turn, given the relatively healthy condition of the fish, the authors reasoned the arthropodic tongues may actually have had functionality. In the figure below taken from Brusca & Gilligan (1983) the parasite does indeed look much like the normal tongue.

Source: Brusca & Gilligan (1983).

However, there is no mention whatsoever that the parasitic tongue taps into the nervous system and I have not found any literature supporting such a claim. Further, Brusca & Gilligan (1983) specifically say that:

  [...] we propose [that] a fish with an 'isopod tongue' [is] not feeding as efficiently  as a non-parasitized fish, [but] feeds more efficiently than a fish with no tongue at all [...]

The authors' claim is much more nuanced than the blunt conclusion as drawn in the wikipedia page that it is a fully functional tongue; while the effects on its host may be relatively mild, it may not replace all, or even any, physiological functions of the normal tongue.

Reference
- Brusca and Gilligan, Copeia (1983); 3:813-6


Is the protein in teardrops still attached to cells, or is it released and free-flowing?

I am not sure I understand your question.

According to the article you mention the proteins in teardrops kill the bacteria which are invading the eye (e.g. also present in the teardrops):

  "Those jaws chew apart the walls of the bacteria that are trying to
  get into your eyes and infect them,"

EDIT: These proteins are enzymes called lysozymes. Those are free-flowing proteins of the human tears. These proteins are actively produces in the lacrimal glands and actively secreted into the lacrimal liquid.


Stockholm format to dot-brackets format?

If what you want is to find a consensus structure for a group of alignments in stockholm format then you might try with
RNAalifold
 and for single sequence folding check RNAfold. Both have online servers and can also be run offline.

After you get the consensus structure update the stockholm file by adding  a structure consensus line as: #=GC SS_cons followed by the dot bracket notation.

A nice RNA structure editor that will make your life easier is EMACS when complemented with RALEE. It allows you to view and manipulate RNA structures, predict structure folding and color the alignments based on basepairs relationships. It will be worth it to invest time into mastering RALEE.


I'm not sure if why is referring to the biological basis or the reasoning for why it is beneficial but I've briefly summarised both. If you'd like more detail just accept and ask again clarifying your exact interest in this broad question.

Pain is taken up through the spinothalamic pathway but at may opportunities it may be blocked. It may be blocked by other ascending pathways or by descending pathways. There are a number of structures involved in this including endorphins and Interneurones which are part of the gate control theory of pain. Basically ascending sensory information is blocked when other sensory information is more acute or more pertinent. This is important for survival e.g. when feeling a lion it is important not to feel pain. That same endorphin pathway is highjacked by drugs such as morphine.


Mutation rate

A mutation rate is a rate at which mutation occur. It is typically expressed as number of mutations per site (per nucleotide) per reproduction event. In humans, the average mutation rate per site per reproduction is of the order of $10^{-8}$.

When a mutation occurs, it will exist in only one copy in the population. This mutations might, over time, reach a higher frequency and even eventually reach a frequency of 1.0 (we talk about "fixation" then) but most mutations will never reach a high frequency and just disappear in the coming few generations whether or not the selection was deleterious.

Evolutionary rate

The term "evolution rate" has no commonly agreed upon definition. Depending upon your definition the mutation rate will be more or less correlated with the evolutionary rate.

Phenotypic evolutionary rate

Evolution rate might refer to phenotypic evolution. The Darwin (named after Charles Darwin, obviously) is a common unit to measure phenotypic evolution. Other unit of evolutionary rate could consist at measuring how much time it take for the mean phenotypic trait to change by one standard deviation of the original phenotypic distribution.

Genetic evolutionary rate

One can also consider genetic measure of evolutionary rate such as the number of neutral substitutions in a lineage per unit of time. With this definition, the difference between the mutation rate and the evolutionary rate become a little more blurry as the expected substitution rate at neutral site is equal to the mutation rate.

Always cite your source!

You say

  I have read some jobs that describes analysis

Please, always include your source. There is no way to give any information about what they mean by these terms without having a look at the original paper.

Related post

The post Are we “more evolved” than present-day bacteria? is somewhat related.


There are a couple of strategies that salt-tolerant plants can use to survive in high-salt conditions.

Plants can increase the concentration of compatible solutes in their cell to the point where the intracellular concentration of solute approaches the concentration of the water in the environment. By doing this, the plants are able to minimize water loss through osmosis, while ensuring that the cells do not reach harmful levels of salinity.

However, compatible solutes are often not enough to completely combat the effects of salt stress. Salt stress creates higher concentrations of oxygen free radicals, which can cause harm to DNA and other cell components. Mangrove trees have been found to have heightened expression of repair proteins and anti-oxidants when exposed to salt stress.

Additionally, mangroves have been found to be able to excrete salt from their root cells and their leaves. They have ion-transporters which actively pump sodium ions out of their cells into the extracellular space. They have salt-filtering mechanisms that allow them to uptake the water from salt-water without up-taking the salt in the water.

So in conclusion, salt-tolerant plants sequester some salt within their cells, but also use ion-pumps and compatible solutes to limit the concentrations of salt within their cells. They can selectively uptake water from salt water, and use repair mechanisms to limit the damage of high salt concentrations in their cells.

Kao, C.H. 2015. Mechanisms of salt tolerance in rice plants: compatible solutes and aquaporins. Crop, Environment & Bioinformatics 12:73-82.

Wang, L., Pan, D., Lv, X., Cheng, C.L., Li, J. Liang, W., Xing, J, and W. Chen. 2016. A multilevel investigation to discover why Kandelia candel thrives in high salinity. Plant, Cell & Environment 39:2486-2497.

Srikanth, S., Kaihekulani, Lum, Y., and Z. Cheng. 2016. Mangrove root: adaptations and ecological importance. Trees 30:451-465


Debug Fresno; why are the released mosquitos said to be sterile?

Males are effective sterilization vectors
You can think of male mosquitos as fertile only in theory. Any mating of these mosquitos will generate no offspring whatsoever, so they are effective sterile and they spread this characteristic to females.
The bacteria makes they sterile in the end, the same way any disease in others cases.


Are intracortical axon branches myelinated?

A great reference for this question is Tomassy et al. 2014. Axons of cells from all layers lack a myelin sheath at their proximal segment, often called the axon initial segment. This stretch of unmyelinated axon is longer for more superficial pyramidal neurons (~150 $\mu m$) and shorter for those located in deeper layers (~25 $\mu m$), something which does not depend on axonal caliber. These authors observed that some of the superficial neurons didn't have any myelin for the length of axon observed (> 200 $\mu m$). They speculated that these are neurons that send their axons through the corpus callosum.

What is interesting is that superficial pyramidal neurons often displayed intermittent myelination away from that initial segment, with long stretches of axons (up to ~55 $\mu m$) being unmyelinated. Note that these myelin gaps are more than an order of magnitude longer than Ranvier's nodes.

What are these gaps in myelin good for? If these axons target other intracortical neurons, it is unlikely that the predicted transmission delay will have an important impact given the short distances in the cortex (~1 mm). For those neurons targeting other brain areas it may be somewhat more important. It is interesting, however, that these patches of unmyelinated axons both made and received synapses, suggesting that they may have a functional role.

The neurons in the OP's images are corticothalamic cells residing in (lower) layer 2/3 of the visual cortex (upper half) and thalamorecipient cells in layer 4 of the motor cortex (bottom half). Thus it is likely that their axon initial segment is unmyelinated. Although not yet conclusive, the results of the cited paper support the view that the axons of those superficial neurons that project to deeper layers or other brain areas are completely unmyelinated.

modified from wikipedia, CC BY-SA 3.0


If evolution is not about increased complexity, why does so much complexity evolve?

I think possibly the problem here is the way you're approaching the issue.

You're considering improvement as anything that increases the abilities or complexity of the organism—that isn't necessarily what an improvement is though. The outcome of natural selection is that the organism best equipped to survive/reproduce in a certain environment is the most successful. So, for example, thermophillic archaea do much better in 60°C-plus pools of water than humans do. Our capacity to process information, use tools, etc. doesn't actually confer much advantage in that situation. And there can be downsides to that kind of complexity as well, requiring more energy and longer developmental periods. So, natural selection in 60°C-plus pools of water gives you archaea, and in (presumably) the plains of East Africa, it gives you humans.

The comment you quote mentions sickle-cell anaemia, which is a different example. While there is little benefit to having the sickle-cell anaemia allele in a temperate region, in those regions where malaria is endemic, heterozygosity can provide a survival advantage, and so the allele is maintained in the population. If you're someone living in a malaria-endemic region, and you don't have access to antimalarials, heterozygosity for the sickle-cell anaemia allele is arguably an improvement. It depends entirely on how you define the word.

The fundamental principal of natural selection is that it favours the organism most suited to a particular environment. But, that isn't always the most complex organism. It's important not to confuse human-like with better. It isn't the universal endpoint of evolution to produce an organism similar to us, just the organism most suited to the environment in question.

Also, to briefly address the previous question you asked—you asserted that we must be missing something from the process of evolution because we were unable to simulate it. You also pointed out that (in your opinion) we have sufficient computing power to simulate the kinds of organisms you're referring to. But natural selection is intrinsically linked to the environment it occurs in, so the simulation wouldn't just have to accurately simulate the biological processes of the organism, but also all of the external pressures the organism faces. I'd imagine that, in simulating evolution, that would be the real obstacle.


Efficiency of plasmid DNA isolation from frozen E. coli cell cultures

I have done that and it works without any problems. We harvested the cultures at the optimal timepoint (density) and then froze them to do maxipreps later on. Therefore we simply thawed the culture, made sure it didn't got too warm (meaning we worked on ice) and then simply followed the maxiprep protocol. No problems with yield or quality of the plasmide.

What I will do next time is to spin down the culture and take it up in max. 50 ml of medium before freezing. This way freezing will be faster as well as thawing. I have also done minipreps from stock cultures (glycerol stocks of plasmids in E.coli) which accidentally stayed out of the freezer for two days. Here the yields where not so great (but the density of the culture was also much lower), but the quality after standard miniprep was good and the plasmids worked both for subsequent cloning as well as for retransformation to make new stocks.


Why are Mendelian mutations considered rare?

I will focus more on the question of rarity, which the comments have not addressed. Recall that natural selection is operating on the human population. Because of this, bad mutations of large effect (disease mutations such as CFTR in your figure) are very rare, because selection is removing them at some rate from the population (people with cystic fibrosis are unfortunately very sick and are not as fertile as healthy people), whereas mutations with very little effect are not subject to much selection. Paper one and paper two are reviews describing the population genetics in more detail.

As suggested by commenters, Mendelian mutations are so named because they are single loci of large effect controlling traits (approximately). Common variants, by this logic, must have very little phenotypic effect, because they are not purged by natural selection (assuming that they are deleterious, or disease-causing).

Rule of thumb: 'Mendelian' alleles can easily be used to predict phenotypes (like disease) and are acted upon by natural selection. 'Common' alleles are individually not informative about phenotype and are thus mostly ignored by natural selection. Not exactly true, but close.


What are the frequency ranges of most marine mammal vocalizations?

Here there are spectrograms from Bottlenose dolphins (Tursiops truncatus), Killer whales (Orcinus orca) and False killer whales (Pseudorca crassidens).

Here there are spectrograms for Humpback whale (Megaptera novaeangliae) and from Sperm whales (Physeter catodon or Physeter marcocephalus)

Here there are spectrograms from Blue whale, Fin whale and Minke whale.

Some other google search for "spectrogram + your preferred cetaceans" should make your list. Enjoy.


Excretion of various wastes and water requirement

Ammonia is more water soluble and also more toxic than either urea or uric acid but it is energetically less expensive. So, in regions where deficiency of water is not a problem, ammonia is an excretory product. Where water is scarce urea or uric acid is the excretory product but it is energetically more expensive to manufacture them. So, you can see an obvious trade off between energy expenditure and water conservation.

You can refer to any introductory biology book like campbell for further reading.

UPDATE :

Ammonia    : Most toxic , Easily Soluble , Less Energy Requirement

Urea       :Moderately toxic , Moderately soluble , More energy requirement(As needed to be processed from ammonia

Uric Acid:Least toxic , Least soluble , Highest energy requirement ( As needed to be processed from ammonia )

It is obvious now what tradeoffs are involved.

The only tradeoff not deducible from above is that of the eggs/youngs. In birds, eggs are not permeable for water so the best option is to excrete waste in form of uric acid so that high concentration of waste does not build up. Uric acid is excreted in form of solid palette which can stay in the egg without any harm.

We can also think of tadpoles which live exclusively in water and so they excrete ammonia but the frogs live both in land and water and so while on land they excrete urea as dessication is the main problem there.


What makes diffculty to make a human bio-tooth compare to a mouse's?

I believe you're referring to this 2013 announcement from King's College, Biological tooth replacement -- a step closer. So called "BioTeeth" are sought after because

  Current implant-based methods of whole tooth replacement fail to reproduce a natural root structure and as a consequence of the friction from eating and other jaw movement, loss of jaw bone can occur around the implant.

However, Professor Sharpe identified the following obstacle:

  What is required is the identification of adult sources of human epithelial and mesenchymal cells that can be obtained in sufficient numbers to make biotooth formation a viable alternative to dental implants.

For some background, consult Biological tooth replacement (2006; Sartaj, Sharpe)

Unfortunately the 2013 article was the last I heard of it - possibly for the aforementioned reason. If you're really interested, you might consider attempting to contact Professor Sharpe yourself.


Can the apparent drop in insect population be explained by local insects evolving to avoid traps?

From your own PlosOne link comes proof that the selection pressure was very weak:
"Most locations (59%, n = 37) were sampled in only one year, 20 locations in two years, five locations in three years, and one in four years, yielding in total 96 unique location-year combinations of measurements of seasonal total flying insect biomass."

"We collected in total 1503 trap samples, with an average of 16 (4–35) successive catches per location-year combination"

"Between 1989 and 2016, a total of 53.54kg of invertebrates have been collected and stored, over a total trap exposure period of 16908 days, within an average of 176 exposure days per location-year combination."

Wikipedia says about houseflies: "12 generations may occur per year"
https://en.wikipedia.org/wiki/Housefly#Life_cycle
27 years gives 444 generations. That is not a lot of time for evolution, especially with such a weak selection pressure.


if Bushmeat practices (eating meat from non-domesticated animals, in this case HIV-infected fruit bats) have been the same for centuries, why has HIV only really spread in THIS century?

We can't really rule out the existence of similar epidemics in the more distant past. In fact, almost certainly they were transmission events from bushmeat (not necessarily of the same virus). The thing that made 20th century different, as the other commenter rightly says, is the mobility. Previously, such transmissions would have lead to local epidemics which would have run their course - leaving super-controllers or individuals with immunity and killing everyone else. And since most of the African cultures haven't left a written record we wouldn't know about such isolated local epidemics. Not to mention that in the unlikely event of such records existing they would hardly be scientific - the disease would be most likely attributed to "evil spirits" or some other supernatural cause.

So, it is really the mobility, the public policies (mass vaccinations by colonial authorities that used the same syringes repeatedly) and the fact that we can retain information in a much better way which make the HIV epidemic different than the ones that almost certainly have happened in the more distant past.


At any given moment, how much energy is stored in the human body as ATP?

ATP burned per minute is not a useful number because the turnover is so high. 2000 kcal/day is dozens of kilograms of ATP so obviously ATP is turned over more than once a day, but there's probably more than one molecule of ATP being passed around between all the ATP synthases.

This blog claims 250 grams. Taking the estimate of ATP concentrations(1-10 mM) from wikipedia and multiplying by a 60 kg person pops out 150 grams (for 5 mM). The ATP/ADP ratio is about 5 to 1 under physiological conditions, so I'm comfortable leaving out that source of error.

So: Probably a few hundred grams, depending on a lot of things. Which is about .2-.7 moles, for reference. 6-20 kJ is not a lot, in fact even at the upper end of estimates you're looking at maybe 8 dietary calories, and probably more like 3.


How does blood pressure substantially drop in the capillaries and arterioles?

There are two main reasons why the pressure in the capillaries is lower than in the big arteries:

Arteries are elastic - they increase in diameter with every pulse, so the blood pressure is falling as the blood is moving along.
The total cross-sectional area of the capillaries is greater than the one of the big arteries.

Biology-pages.info

  The pressure of arterial blood is largely dissipated when the blood
  enters the capillaries. Capillaries are tiny vessels with a diameter
  just about that of a red blood cell (7.5 µm). Although the diameter of
  a single capillary is quite small, the number of capillaries supplied
  by a single arteriole is so great that the total cross-sectional area
  available for the flow of blood is increased. Therefore, the pressure
  of the blood as it enters the capillaries decreases.


TATA box is a feature of organisms that have dsDNA as a genetic material. Like most dsDNA promoter elements, TATA box is basically a section of dsDNA.

However a question like "On which DNA strand is TATA box present?" depends on what you define TATA-box as.

If you go by this definition:

  In molecular biology, the TATA box (also called the Goldberg-Hogness
  box)[2] is a DNA sequence (cis-regulatory element) found in the
  promoter region of genes in archaea and eukaryotes

then TATA-box is merely a DNA sequence and is just a representation of a ssDNA region. However, TATA-box is also the binding site for TBP (TATA-binding protein; part of the TFIID complex). While the recognition of DNA elements by the TFs is effectuated by the interaction of amino acid residues with DNA bases and backbone on  one or both the strands, the TF binding and its activity has a stereochemistry.

Likewise, TBP also interacts with bases as well as the sugar-phosphate backbone on both the strands (Juo et al., 1996; PDB:1TGH).

  Figure 2. Stereo pair drawings of the human TBP/DNA complex, with TBP at right and the sharply bent C-G-T-A-T-A-T-A-T-A-C-G duplex at left. (a) Molscript skeletal drawing (Kraulis, 1991). TBP residues that interact with the floor of the minor groove are shown in red with one-letter amino acid codes, and residues that interact with the sugar/phosphate backbone are shown in green. The coding strand of DNA is dark blue, and the non-coding strand is light blue. The two yellow-green base-pairs at bottom are the T1-A2 step that is kinked by interstitial phenylalanine residues, while the equivalent kinked step at T7-A8 is marked in orange. (b) Secondary structure diagram, with a-helices as coils and b-sheet strands as flat ribbon arrows pointing along N-to-C chain direction. Color coding as in (a).

Considering this, you can say that TATA-box is essentially a dsDNA region.

However, another twist in the story is that TBP can also activate genes with TATA-less promoters (Kamenova et al., 2014) and this is possibly facilitated by other protein partners of TBP in TFIID complex.

  Our results are consistent with the model that sequence-specific
  TBP-DNA contacts are not important at yeast TATA-less genes and
  suggest that other general transcription factors or coactivator
  subunits are responsible for recognition of TATA-less promoters. Our
  results also explain why yeast TBP derivatives defective for TATA
  binding appear defective in activated transcription.

This, still does not contradict with the fact that TATA-promoters need TBP and the binding is on both the strands.

So, my conclusion is that TATA-box is a dsDNA element but has a polarity in its mode of action.


What is the correlation between hand and neck flexibility?

The vertebral foramen

What is it, and what passes through it?

  A number of structures pass through the foramen. These are the root of each spinal nerve, dorsal root ganglion, the spinal artery of the segmental artery, communicating veins between the internal and external plexuses, recurrent meningeal (sinu-vertebral) nerves, and transforaminal ligaments.

The nerves in the hand

  Starting in the trunk of the body, the nerves of the arm and hand arise from the cervical and thoracic regions of the spinal cord as spinal nerves. These nerves merge to form a network called the brachial plexus before continuing into the arm. Five major nerves extend from the brachial plexus into the arm: the axillary, musculocutaneous, median, radial, and ulnar nerves. Each of these nerves carries information in the form of nerve impulses to and from a particular region of the arm and hand. Some of these impulses are sent from various parts of the brain and spinal cord; some come from sense organs located in the joints, ligaments, and tendons; and some come from nervous tissue in the muscles themselves.

In this paragraph it is specifically stated that impulses received in the hand by receptors, can come from the brain and spinal cord "and some come from nervous tissue in the muscles themselves."

The vertebral foramen is a part of the spinal cord, and forms a vertebral canal, the nerves running through it, and the impulses which are sent could be received by the receptors in the hand. Which could affect flexibility in both neck and extremities.

Sources:

https://www.innerbody.com/anatomy/nervous/arm-hand
http://www.emory.edu/ANATOMY/AnatomyManual/38.jpg
http://medical-dictionary.thefreedictionary.com/vertebral+foramen
https://en.wikipedia.org/wiki/Intervertebral_foramina
https://en.wikipedia.org/wiki/Vertebra
http://www.spinalhub.com.au/what-is-a-spinal-cord-injury/what-happens-to-the-spinal-cord-after-injury/spinal-nerves-up-close


To understand how the X inactivation can occur in, it requires a bit of understanding of how Barr bodies come about.

The main key players to keep in mind are (From 1):

Xist: Xist   Required for initiation of X-inactivation
Tsix: Tsix (It's Xist spelled backwards!) Represses Xist expression by silencing the Xist promoter, also required for X-chromosome pairing, counting the number of XICs (X-inactivated chromosomes)

From 2, Here is a general diagram of how X-inactivation occurs.

X-inactivation requires first, count how many X chromosomes are present (n). Then, the (n-1) number of X chromosomes are inactivated. The choice for which gets inactivated is largely random.

Therefore, if a male has multiple X-chromosomes (as in the case of Klinefelter syndrome) then X-inactivation would occur in males. However, there is also the case that erroneous counting may lead to the inactivation of the only X chromosome in males early in a developing embryo. But this is lethal, and the embryo would die.

More about Kleinfelter Syndrome can be found here: Klinefelter syndrome

Guided by RNAs: X-inactivation as a model for lncRNA function.
Lessons from X-chromosome ina ctivation: long ncRNA as guides and tethers to the epigenome


How are the paranasal sinuses linked with the capillaries in the ear canals?

There is no direct link between the capillaries in the sinuses and the ear.

The Eustachian tubes drain the middle ear (between the eardrum and the inner ear) into the nasopharynx, the part of the throat that is just behind the nose.

The para-nasal sinuses drain into the nasal passages themselves at different points. The sinuses and middle ear constantly produce some fluid, which is either reabsorbed or drained.

Often what happens is that in the case of a common cold or other upper respiratory tract infection, the nasopharynx and nasal mucosa are both infected. The inflammation causes swelling and blocks off the Eustachian tubes and the drainage pathways of the sinuses and the trapped fluid itself causes sinus & ear pain and can get infected causing sinusitis and otitis media. Alternatively a viral infection can also go up into the middle ear and sinuses causing direct infection.

The process that occurs when you go on a plane is slightly different. The Eustachian tubes and sinus openings collapse due to pressure and thus the natural fluid that is produced accumulates as well as there being an inability to neutralise the internal and external pressure (thus why making your ears 'pop' works- you force the Eustachian tubes open via positive pressure)

Regarding blood supply of the paranasal sinuses and the ear:

The ear is supplied by the posterior auricular and superficial temporal arteries of the external carotid artery.

The paranasal sinuses are supplied by various branches of the internal and external carotid artery including the maxillary artery, anterior and posterior ethmoidal arteries, ophthalmic artery, supraorbital and supratrochlear arteries


Short answer
Walnuts are classified both as nuts and drupes ('stone fruits').

background
According to University of Wisconsin - Madison, Department of Botany , hickory and walnut can be classified both as drupes and nuts, but are best classified as nuts.

Nuts fall into the class of indehiscent fruits: dry fruits that do not open when mature to shed their seeds. Many of this group are one-seeded fruits, such as the nuts. In addition, nuts have a thickened and hardened wall. Examples are beech, chestnut, oak, hazel, walnut and hickory. Because of extrafloral bracts, or "husk", the latter two fruits are sometimes called "drupes").

As opposed to indehiscent fruits, the fleshy fruits have a wall that becomes soft and fleshy as it matures. Drupes ('stone fruits') fall into this class. Drupes one-seeded, simple fruits developed from a superior ovary in which the innermost portion of the wall (endocarp) becomes hard and stony, the outermost part (exocarp) becomes a relatively thin skin, and the middle portion between the skin and the stone (mesocarp) becomes either fleshy or fibrous. Examples are cherry, coconut (the endocarp is the thick wood shell that surrounds the fleshy and liquid-filled seed), but also walnut and hickory. The latter two are, however, best called "nuts".

Indeed, according to a popular scientific article in the Guardian, many tree nuts are also drupes, including walnuts and pecans.


What culture medium should we use for tap/drinking water bacteria?

Usually when culture-based methods are used to test drinking water a range of selective culture media are used (media that favor the growth of a specific category of bacteria, e.g. the MacConkey Agar mentioned in the article you linked to). This is because the aim is to test for the presence of known harmful bacteria.

I would suggest that any of your suggestions (LB agar, Nutrient Agar or Tryptic Soy Agar) would work just fine.

On another note: How are you inoculating the agar? The concentration of bacterial cells in tap water is very low, to test for bacteria usually a large volume (~ 1 liter) is passed through sterile filter paper which is then pressed onto an agar plate to transfer the bacteria.


Is it possible to merge the genomes of photosynthesizing and electron-transporting bacteria to make an electric cell?

What you're describing is a phototrophic biofilm microbial fuel cell! They're pretty neat.

Essentially the sun powers the bacteria and the bacteria in the anaerobic side passes electrons through the graphite electrode to use oxygen at the cathode. There's another explanation here. You could also "unfold" cyanobacteria and layer them and you'd probably get an efficiency increase but the system would be pretty fragile. Compared to other MFCs, though, everything is fragile. Dirt even works(not very well, but it's dirt).


I believe this is an Arboreal Salamander (Aneides lugubris).
http://www.californiaherps.com/identification/bayareaherps.html#Lizards
http://www.californiaherps.com/salamanders/images/alugubrisbr1108.jpg


Why is Thermus aquaticus and Taq Pol stable?

Here is an article from Razvi and Scholtz that help you understand the thermostability found in thermophilic proteins. They compared protein stability of thermophilic proteins and their homologous versions in mesophilic bacteria (i.e., bacteria that grow in more normal temperature ranges), and compiled these proteins into a database. Their method was to make estimates of protein stability curves for each of these proteins through a model of free energy based on the known physical parameters of these proteins. From the article:

  [...] the most common way to attain a higher [melting temperature] in proteins from thermophiles is to raise the stability curve to higher values of ΔG (higher intrinsic stability) at all temperatures."

This is achieved through mutation of just the linear sequence of the protein. Fundamentally,

  "...each of the methods of stabilization are results of features like an increased number of hydrogen bonds, salt bridges, improved core packing, shorter and/or tighter surface loops, enhanced secondary structure propensities, or oligomerization."

Also, everything I have seen about the genus thermus places them as Gram negative bacteria.

Razvi and Scholtz. Lessons in stability from thermophilic proteins. Protein Science, 15(7) 2006.


It depends on how accurate you want the description to be. Ideal bond lengths are normally assumed, so the structure can be described using φ, ψ, ω (for the backbone) and χ1-χ5 (for the sidechain) angles. This is what is used in most cases. However, the positions of the hydrogens in the sidechains are not uniquely defined by this description. This also does not describe hydrogen bonds and disulfide bridges, but those could be deduced from the relative positions.

You can get more information here: http://kinemage.biochem.duke.edu/teaching/anatax/html/anatax.1b.html

This description should be enough for most applications, though.


What are good resources for self-learning modern molecular biology concepts?

Sure it's feasible! Of course, there are lots of papers that I can't read even with a recent education, but you should be able to make a good dent by:

Getting a good modern textbook like Molecular Biology of the Cell by Alberts et al. This is becoming a standard text and gives pretty good coverage of the field. I find that it doesn't always get as detailed as I would like, but such is the nature of textbooks I think. Another textbook that some people like is Molecular Cell Biology by Lodish et al, although I don't have experience with it myself.
Watch online lectures. MIT OpenCourseWare has a pretty good molecular biology course. It may get basic for you at times, but the lecturers are well-respected molecular biologists and geneticists.
Read reviews in things like Nature Reviews to get a 30,000-foot view. Review authors often touch on concepts that primary literature assume you know. Armed with a good text, you should be able to get a good idea of what people are talking about. On a similar note, the "News and Views" commentary articles that accompany "high-impact" papers are great for giving people unfamiliar with the field a taste of why a certain paper deserves attention.
Come back here and ask!


Is there some research paper which focus on the influence of using cancer cell as experimental materials on experimental result?

There are several articles on this. You may look at these for a start:

Masters, John RW. "Human cancer cell lines: fact and fantasy." Nature reviews Molecular cell biology 1.3 (2000): 233-236.
Masters, John R. “False Cell Lines: The Problem and a Solution.” Cytotechnology 39.2 (2002): 69–74.
Masters, John R. "HeLa cells 50 years on: the good, the bad and the ugly." Nature Reviews Cancer 2.4 (2002): 315-319.
Holliday, Deborah L., and Valerie Speirs. "Choosing the right cell line for breast cancer research." Breast Cancer Res 13.4 (2011): 215.
Lacroix, Marc. "Persistent use of “false” cell lines." International journal of cancer 122.1 (2008): 1-4.


Do housekeeping genes vary between tissues

My experience is: Yes they can vary quite a lot (according to differences in the genetic profile of the cells) and you have to test this. As a primer I can recommend reading the articles listed below. These are mostly looking into this in the context of realtime PCR, but this should be valid for RNAseq as well. For some applications it is also a good idea to use more than one gene for normalization.

References:

Accurate normalization of real-time quantitative RT-PCR data by
geometric averaging of multiple internal control genes.
Selection of housekeeping genes for gene expression studies in human
reticulocytes using real-time PCR
Reference Genes / Housekeeping Genes
Gene Ontology Based Housekeeping Gene Selection for RNA-seq
Normalization


How stable is in vivo whole cell patch clamping?

After talking to a few electrophysiologists, I found out that they have very diverse opinions.

It seems that a common way of stabilizing the movement of the brain with respect to heart beat is to press the brain with some softish-rigid material like agar. Also, draining the CSF could help but then this cannot be done without sacrificing the animal.

The quality of the patch degrades over time, and it could be held for an hour or more (anecdotal).


How to calculate the percent of mitochondrial heteroplasmy

I emailed the authors of the paper "Age-Related Accumulation of Somatic Mitochondrial DNA Mutations in Adult-Derived Human iPSCs" and they confirmed that they calculated the % of mtDNA heteroplasmy by the following:
Aligned all mtDNA genomes against the reference sequence. Any deviance at a specific position from the reference was a "mutation". The % heteroplasmy was calculated by dividing the total number of mutations at a certain nucleotide position by the total number of genomes represented at the position multiplied 100.
So in other words, to go back to my original question- if there were 10,000 genomes aligned and there were 700 mutations at the same position, that mutation would have 7% heteroplasmy.


Why are spiders afraid of flies caught in their web?

from https://www.researchgate.net/figure/234696071_fig5_Figure-1-Differences-in-attack-strategies-upon-safe-and-dangerous-prey-in-orb-web

The linked article is pretty cool.  Bottom line: predators need to be careful.  If they get hurt they cant hunt and they starve.  Spiders have different strategies depending on perceived dangerousness of a prey item.  The linked article, for example, categorizes dipterans (flies) as nondangerous to spiders but orthopterans (crickets) as dangerous.  How are crickets dangerous?

For your spider I can think of 1 of 3 things.

1: Fly is dangerous to spider in a way not obvious to you.  Maybe it is poisonous, or can bite, or has sharp spines on the leg.

2:  Fly is perceived by spider as similar to dangerous prey.  I have watched spiders address wasps in their webs and the spiders are careful.   If there are flies that mimic the appearance of wasps / bees to get respect, why not one that behaves in the web like a wasp to get respect?  A cool idea and testable too.

3:  What you see is the danger.  A big fly thrashing around might be enough to damage the spider.  A spider not desperate for food might not want to risk getting hit.  Spiders are not that durable.  That makes sense to me.


Your question could be phrased more specifically to avoid ambiguity, but rephrasing it the way that I suspect you mean it, ("Is there any evidence showing that [the rate of] copy number variation changes over time?"), then yes, there is indeed.

The rate depends on many factors including which mechanism and which organism and which region of the organism's genome and as @Michael wrote, also what scale (et. al.) is under consideration too.

So your assumption that the rate is static should probably be stated explicitly.

Nature Reviews Genetics 10, 551-564 (August 2009) | doi:10.1038/nrg2593


How specific is the adaptive immune response?

The adaptive immune response is highly specific and is made to fit a specific antigen. The antigen binding sites are located on the ends of the two short arms of the Y-shaped molecule, as seen in the figure below:

The recognition site is made of the ends of one short immunoglobulin chain and one long chain. The ends (shown in yellow in the figure) are also called variable regions and are the key to the big variety of different antibodies.

When B cells develop, there B cell receptor (which is basically a membrane bound antibody) is tested if it reacts to components from the own organism. If not, they are released into the periphery (blood stream). These B cells are then called naive, since they haven't come in contact with an antigen. They express a B cell receptor which usually only has a weak affinity to an antigen - but the body produces quite a wide variety of these cells. (see the second figure).

When the body comes in contact with an antigen (like a virus), it is taken up by the so called professional antigen presenting cells (dendritic cells, macrophages, B cells) of the immune system, broken down into small pieces and these are presented to the immune system. This activates the affinity maturation of the B cell receptor, somatic hypermutation and finally the clonal selection of the cells, which produce the antibodies with the highest affinity (the strongest binding) to the antigen.

There are estimates that the human immune system can produce around 10 billion different antibodies. This variability is achieved by the genetic variability of the mutation of the variable region of the antibody (the whole process is nicely explained here).

For further information on this topic I can recommend reading the following articles:

Development of the immunoglobulin repertoire.
Immune receptor editing: revise and select.

The reaction of the body afterwards is always the same, as you state yourself. The specificity of the adaptive immune response is "only" mediated by the specificity of the antibodies. This also makes the system very strong against new pathogens, since only one part of the system needs to be adapted, while the cascades behind it (like apoptosis) are always the same and can be activated fastly if needed.

This can cause some problems, too. Think about self-antibodies, which occur in autoimmune diseases. Here the body can not distinguish between a legitimate immune response against a foreign antigen and those, which are from the own body.


How much does the Hayflick limit/telomere length vary across taxa and within humans?

Many studies, including those of Hayflick himself, have found a strong correlation between a species' Hayflick limit and its maximum lifespan. For example, Galapagos tortoises, which can live over a century, have a Hayflick limit of 90-125, and mice, which live only a few years, have a Hayflick limit of 14-28.

However, the mechanism connecting the maximum number of cell divisions and maximum lifespan is not entirely clear. Cell division is associated much more with growth and development than with the maintenance of mature tissues. Cells that have stopped dividing can be perfectly functional for decades. Cells that don't stop dividing are called "cancer". So, while the correlation is strong, the reason for the correlation remains something of a mystery.

Rose, Michael R. 2005. The Long Tomorrow: How Advances in Evolutionary Biology Can Help us Postpone Aging. Oxford University Press, New York. pp 20-23


I know this response is coming a bit late but in case you're still curious I have a response!

I'm a M.Sc. student working in Agricultural entomology in Northern Canada (between 55 and 59 degrees North). You are correct, up at more Northern latitudes our short growing season mainly limits what crops we can grow, but less so our yield. We are also restricted in where we can farm by soil conditions as the further north you go the more you are on the Canadian Shield - so less fertile. If you look at growing regions in Northern Alberta, North West territories, etc. you'll see that they tend to stick fairly close to rivers. Further south in Canada, moisture conditions play a much bigger role in determining yield. Mainly we stick to crop species and cultivars that can produce a good yield in a short time - canola, wheat, barley, peas (although corn and soybeans have some large acreages in the Eastern prairies and Ontario).

Climate wise, the comment about light intensity is not really accurate in the summer. The longer daylength definitely compensates for any differences in light intensity. Even at 59 degrees latitude it can get well into the 30's (Celcius) in the summer.

Canada already produces a large amount of wheat and canola, we are the 6th largest exporter of wheat according to a quick google search. So I would argue that while Canada may not be the bread basket of the world it is pretty close already.

It's tough to say how climate change will affect agriculture, because it's really tough to determine how climate change will affect local climate. The changes to weather patterns (changes in amount and timing of rain and moisture, changes in spring or fall frost timing) will have a large impact on agricultural outputs.


I eventually figured it out. It is the one-seed juniper, Juniperus monosperma.


Why is there low hepcidin levels in hemochromatosis?

From what I remember it all depends on which type of hemochromatosis we are talking about. There are several types depending on the cause and some of those like the hemojuvelin gene mutation-related have low levels of hepcidin as the CAUSE of the hemochromatosis (since like you mentioned, seeing it as a consequence wouldn't make much sense)
The first 4 pages of this paper should clear things up a little bit https://www.aasld.org/sites/default/files/guideline_documents/Hemochromatosis2011.pdf


Found an unknown species, whom should I contact?

Natural History Museum; UK, is a good resource.

http://www.nhm.ac.uk/take-part/identify-nature.html

  According to their webpage;

  Have you found a strange bug or a new plant in your garden, or stumbled across an intriguing animal bone or fossil while out on a country walk? Let us help you find out about it.

  Four ways to identify your specimens and sightings

  Check our selection of ID guides and apps below to see if one is relevant.
  Upload your photos and descriptions to our online identification forums for help from our scientists and other naturalists. Please tell us as much about your specimen as possible, including a detailed description, where and when you saw it, and its approximate size.
  Post your specimen or photographs to:
  Identification and Advisory Service
  Natural History Museum
  Cromwell Road
  London SW7 5BD
  Visit the Centre for UK Biodiversity at the Museum and show your wildlife or geology specimen to a member of our ID team. Drop in between 10.00-12.00 and 14.00-16.00:
  Monday to Friday (except bank holidays)
  the first Saturday of the month (or the second Saturday after a bank holiday weekend)
  If you need to discuss the best way for us to help with your enquiry, call our Identification and Advisory Service team on +44 (0)20 7942 5045 or email us.

  See more at: http://www.nhm.ac.uk/take-part/identify-nature.html#sthash.UGsoIYvE.dpuf

They also have provided some downloadable apps and pdf document resources in their webpage.


Case study and speculations on the brain of Edward Mordake

Mordake was a conjoined twin fused at the head (Fig. 1). Twins conjoined at the heads are rare, occurring only once in every 2.5 million live births. Moreover, in Mordake's case it was a parasitic twin head with an undeveloped body that was fused with his own head. This condition is referred to as craniopagus parasiticus, or épicome / epicomus. Craniopagus parasiticus is an extremely rare teratology, of which only six cases have been recorded in the medical literature (Bondeson et al, 1989).

Fig. 1. Wax reproduction from Edward Mordakes face. Source: Bosmia et al., (2014).

The story of Edward Mordake is, however, obscure and met with skepticism. Moreover, no medical details are known as far as I know. However, he was reported to be intelligent and healthy, just depressed by the second parasitic head (Bosmia et al, 2014). To me it appears a story of a person with a normal brain and a parasitic face attached to his head. However, there are rumors that the parasitic head could talk independently, leaving open the possibility that the parasitic head may have contained a separate brain, or shared Mordake's own brain.

More is known about the double-headed Bengal of Everard Home (Fig. 2).

Fig. 2. Skull of the double-headed Bengal (museum exhibit, left) and an artist's impression of the case (right). Source: Bondeson et al, (1989)

The natural head and body were perfectly normally developed, but a number of anomalies were noted on an examination of the parasitic head, such as excessive tearing and the absence of pupil reflexes. Upon dissection the parasitic head was shown to show various anomalies, such as missing anatomical elements (e.g. auditory canal) or underdeveloped structures (e.g., small lower jaw bones).  Importantly, the brains were separate from each other and covered in individual and proper coverings. The dura mater of each brain adhered firmly and contained
many large vessels. Bondeson et al. (1989) describe the remainder of the six cases as well, which were still-borns or lived just very shortly. They had completely separated brains too.

References
- Bondeson et al, Surg Neurol (1989); 31:426-34
- Bosmia et al, Childs Nerv Syst (2014)


Sugar in high concentrations acts osmotic. This means that the water available in the cells is drawn towards the high concentration of a solutant (sugar), like in the image below (this is demonstrated with a plant cell, but the principle is the same for bacteria and other microorganisms):

Since microorganisms can not survive without water, they are not able to grow or reproduce. This effectively safes food. The same mechanism works when salt is used to conserve meat or fish.


Apoptosis can occur without cell cycle already being arrested.  For instance, in the case of extrinsic apoptosis, which could be induced by T lymphocytes, for example, a trimeric receptor such as TNF-R or TRAIL-R's containing a DD can be bound at any time by the death ligand secreted by (TNF, TRAIL) or bound to the immune cell membrane (FasL, TRAIL).
The DD (death domain), independent of where cell cycle is, recruits adaptor proteins with DED domains (ie., FADD), which in turn recruit procaspase 8.  Procaspase 8 is cross-activated (becoming caspase 8) when two of them are recruited, then released.  It then begins activating procaspases 3, which begins the actual work of killing the cell (cutting cytoskeleton => blebbing, etc.), activating CAD.
It bears mentioning, however, that once it's kicked in, cell cycle will inevitably stop, since CAD will start fragmenting the DNA...  It also bears mentioning that caspase 8 also activates the intrinsic pathway via Bid => tBid => Bax => Bak => mitochondrial leakage, cytochrome C activating caspase 9...

Sources:

Sayers, Thomas J. 2011. Targeting the extrinsic apoptosis signaling pathway for cancer therapy. Cancer Immunology, Immunotherapy 60 (8): 1173-80.

Eimon, P. M., E. Kratz, E. Varfolomeev, S. G. Hymowitz, H. Stern, J. Zha, and A. Ashkenazi. 2006. Delineation of the cell-extrinsic apoptosis pathway in the zebrafish. Cell Death and Differentiation 13 (10): 1619-30.


How does fluorouracil inhibit pyrimidine synthesis?

Your cells produce thymidine by converting uridine using an enzyme called Thymidylate Synthase. 5-Fluorouracil irreversibly inhibits this enzyme.

Here is the structure of 5-Fluorouracil:

Here is the mechanism the enzyme uses to make thymidine:

It looks like the enzyme forms a bond to the uridine ring through a sulfur. 5-Fluorouracil probably inhibits the reaction at the next step because fluorine is much more electronegative than the proton it replaced. This makes it harder for the electrons on the double bond in step 2 to attack the folate. Might also inhibit step 3 because the fluorine won't want to give up its electrons to reform the double bond. Because 5-fluorouracil is stuck to the enzyme's active site, the enzyme can't perform its given duty of converting uridine to thymidine. Because you can't use uridine in your DNA, your cells don't have enough thymidine to copy the DNA and replication is slowed. If thymidine supplies are low enough, cells might die.


Abbreviations for molecules: What are CheW, CheA, CheY?

Here is the paper that first defined them:

Armstrong JB, Adler J. 1969. Complementation of nonchemotactic mutants of Escherichia coli. Genetics 61:61-66.

Che is an abbreviation of chemotaxis. In this paper, complementation studies revealed three different loci that, when mutated, result in defective chemotaxis. These were termed CheA, CheB and CheC. Originally they were thought to be genes, but the following paper refined the definitions when the CheA locus was found to contain CheA and CheW genes while the CheB locus contains CheB, CheX, CheY and CheZ genes:

Silverman M, Simon M. 1977. Identification of polypeptides necessary for chemotaxis in Escherichia coli. J Bacteriol 130:1317-1325.

I'm not going to search for the discovery of every Che gene, but hopefully you have an idea of where the letters come from.


Are drugs made bitter artificially to prevent being mistaken for candy?

Short answer
A bittering agent may be applied to therapeuticals to prevent pediatric poisonings, but many drugs inherently taste bitter by themselves.
Background
Bitter taste is thought to have evolved as a way to decrease the risk of ingesting toxic substances, which may explain why many drugs taste bitter. In other words, classes of compounds that may harm the body often taste bitter (Menella et al., 2014). These include the often dangerous compounds like alkaloids and glycosides (source: University of Delhi). These include the familiar psychotropic compounds found in hallucinogenic plants, and the potentially deadly heart glycosides found in Digitalis species, respectively, among other classes of substances.
Paracetamol can be regarded as an alkaloid (Fig. 1), but not aspirin, as it lacks a nitrogen atom (Fig. 2). An alkaloid is defined as

any of a class of naturally occurring organic nitrogen-containing bases. Alkaloids have diverse and important physiological effects on humans and other animals. Well-known alkaloids include morphine, strychnine, quinine, ephedrine, and nicotine...

All of which are quite toxic. As cleverly noted in the comments, aspirin is not an alkaloid in its strictest sense, as it is not naturally occurring. However, it is chemically obtained by acetylation of salicylic acid (Mund et al., 2016), as shown in Fig. 2. Both of the reactants in themselves are naturally occurring; salicylic acid can  be sourced from willow bark, and acetylation is a widely occurring biochemical reaction (Gibbs, 2017).
I myself have never had the chance to taste aspirin, unfortunately (although I performed the acetylation shown in Fig. 2 for my Organic Chemistry class :-). Originally, aspirin was developed from salicylic acid (Fig. 3) just because the taste of salicylic acid was so bitter. Acetylation diminished the bitterness, yet the anti-inflammatory action remained (Wu, 2000)). Besides reducing bitterness by chemical modification, masking the bitterness of drugs with, e.g.., sweeteners, can help to overcome the aversion to the bitter taste. This can aid in helping patients, especially pediatric ones, to take their medicine and adhere to their treatment regime (Chauhan, 2017).
Reversely, coming back to your question, adding bitter-tasting additives to drugs indeed seem to be an effective way to reduce pediatric poisonings (Menella et al., 2014)
References
- Chauhan, J stem cell Bio transplant (2014); 1(2): 12
- Gibbs, Trends Plant Sci (2015); 20(10): 599–601
- Menella et al., Clin Ther. 2013 Aug; 35(8): 1225–1246
- Mund et al., J Occup Med Toxicol (2016); 11: 32
- Wu, Circulation (2000); 102: 2022–3

Fig. 1. Paracetamol, or acetaminophen. source: Wikimedia Commons

Fig. 2. Synthesis of Aspirin, or acetylsalycilic acid, from salicylic acid. source: Imperial College, UK


A free book/resource for learning genetics?

As you said, the question is pretty broad. Genetics is a big gigantic field and it is quite hard to know what you are exactly looking for. If you could refine into one of the subfields (molecular genetics, population genetics, phylogenetics, etc..) it would be much easier to give you better advice. As you talk about both biology and bioinformatics, it might be worth to specify whether you are looking for learning more in fundamental genetics or learning more in the methodologies to analyse genetic data.

Principles of Genetics

You may want in an introductory class in genetics. Here is a course on MIT Open CourseWare, but it may be too easy for you.

Bioinformatics

You may want to take a bioinformatics course. There are so many bioinformatics course online that there is a wikipedia page to list them (there).

Side skills

Programming

You may just want to learn to code in R, Python, Perl or Shell script (to cite few examples). You'll find tons of beginner tutorial online.

Statistics

Or you might want to learn more about statistics. KhanAcademy has a very good (but very introductory) statistics class.


Could there be any effects from low powered infrared being used to track eye movements long term?

I would have said that IR is safe, but some studies have suggested otherwise.

This is a vague study on rabbit eyes:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116568/

https://academic.oup.com/annweh/article-abstract/35/1/1/170395

So there may be a dosimetric exposure limit of some kind that you have to aim for. LED's are very controllable. I'm amazed that they talk about cataracts with a chemically soft, non -ionizing wavelength like IR, because we get IR all day from the sun. If you control the levels to be less than a sunny day, you may find that you can use equivalent of 1hr of sun exposure to run many hours of eye tracking. the figures are a matter of research.


Techniques to look at whole cells are: Light microscopy (cells, large organelles), electron microscopy (detailed analysis of subcellular structures and even proteins) and confocal fluorescence miscroscopy (look at particular cellular planes, reconstruct 3D images).

And of course you can analyze the insides by Biochemistry by breaking the cell membranes and look at individual proteins and DNA/RNA by extraction and electrophoresis followed by Western / Northern / Southern blotting, or isolate organelles by centrifugation.

It is a broad question, and I just gave the most obvious examples of techniques (not anywhere near exhaustive). By googling the bold-out terms you may provide some details to your sis.


What is this insect? Possible assassin bug? or kissing bug?

Yes, it does seem to be a Western Conifer Seed Bug (Leptoglossus occidentalis). Not a hazard to people.
Photos from Italian language wikipedia.

This ref below suggests it may be looking for somewhere indoors to wait out the winter. It lays eggs on conifer leaves.
http://www.zin.ru/animalia/coleoptera/pdf/steyrer_perny_2008_new_insect_species_in_austria.pdf
"Two New Insect Species in Austria: One Established, the Other One Not (Yet)" by
Gottfried Steyrer and Berhard Perny,
Forstschutz Aktuell, num 44, 2008


Why don't housekeeping genes have TATA Box regions in their promoter sequences?

Two possible answers:

First, TATA boxes has been found to cause increased "noise" in gene expression, such that the expression of genes that have a TATA box is highly variable. See this review for example.

A different set of results suggests (here) that TATA acts only as an amplifier of expression.

Regardless of whether TATA amplifies expression or also increases expression variance, this is not suited for housekeeping genes, which generally have low and constant expression.


The ruby-throated hummingbird flies 500 miles nonstop across the Gulf of Mexico during both its spring and fall migrations

The Bering Strait is about 82 kilometres (51 mi) wide at its narrowest point, between Cape Dezhnev, Chukchi Peninsula, Russia

Based on the two facts above, it appears possible for a humming bird species to cross the Bering Straits if the weather becomes suitable to survival. Who would have thought?

That said, I am not sure how a humming bird who know which direction to fly in to make a successful crossing.


How easy is it to carry out de novo sequence assembly?

You can try looking around biostars.org, which is like stackexchange, but for bioinformatics.

Velvet is one example of a de novo assembler.

But 30 bp is really short, and animals have big genomes (not as tough as lots of plants and fungi, but still tough)

What you would get is a bazillion short contigs.  It would not be pretty.


How do you increase eumelanin but not pheomelanin?

I doubt that this will be really successful, since the synthesis is rather complex and can be influenced (positively and negatively) in many ways. First, the synthesis pathways looks roughly like this:

The first step is identical for both melanin forms, it is the conversion of the amino acid tyrosine into dopaquinone by the enzyme tyrosinase. The next steps are different for each process and only one of the possibilities can happen at any given time. The decision is done by the availibility of the necessary components. When the cysteine concentration in the cell is high, the pathway goes exclusively into the direction of pheomelanin, only when the cyteine concentration is lower than 0,76µM eumelanin is made (see here and here for details).

But this is not the only influence on the reaction. The availibility of dopaquinone is critical, and the activity of the tyrosinase can be influenced by the pH of the melanosome (the compartiment in which the pigment production takes place). The tyrosinase activity for people with dark skin is about 10 times higher than for people with pale skin (see here and here for details). The difference here is mainly the pH, which is neutral for dark skinned people and acidic for pale.

Then there is of course the availibity of tyrosine (which is less of a problem, as this amino acid is not essential) and also the availibity and activity of downstream enzymes for the eumelanin production as tyrosinase-related protein 1 and dopachrome tautomerase.


Why doesn't G-actin concentration fall once microfilament polymerization begins?

The critical concentration is better defined as the "equilibrium concentration of the pool of unassembled subunits"1.

An analogy that might be helpful is thinking about a NaCl (table salt) solution — once you add enough salt some will start to precipitate, but the amount in solution will remain the same.

You can think of the solution as having the capacity to support a certain concentration of molecules (or ions) — below that concentration subunits will separate from the polymerized form faster than it can accumulate new subunits, above that concentration the subunits will stick together faster than they "fall off" the polymer.

For more a detailed molecular understanding of why this is so, you probably need to read up on chemical equilibria — for example Chemistry or even Khan Academy might be helpful.

Reference:

1: Lodish, H., Berk, A., Zipursky, S. L., Matsudaira, P., Baltimore, D., & Darnell, J. (2000). Section 18.2 — The dynamics of actin assembly. Molecular Cell Biology.


Remember than Pvu1 cuts in the middle of AmpR, and when you insert your gene you'll be disrupting its function, meaning that any transformed colonies will no longer be able to grow on Amp-containing media. This is why you want to cut with BamH1 - the disruption to the TetR gene is irrelevant, and it leaves Amp resistance in place.

The point of growing on antibiotic-containing media is to select for cells that have taken up your plasmid - cells that haven't can't grow.


Can exhaustive algorithms produce MSAs that are suitable for 3D structure modelling?

No.

Methods for multiple sequence alignment (MSA) like T-coffee, which you mention, and Clustal (http://www.clustal.org), which is also widely used, employ heuristics for the alignment for the very good reason that exhaustive algorithms to do this are NP-complete.

You mention the dynamic programing algorithm as exhaustive in your comment. Alignment of two sequences by dynamic programming has an order of time complexity (big O) of $n^2$ and may take a few minutes depending on sequence length etc. Alignment of three has a big O of $n^3$ and can be done if you have lots of time on your hands, but it should be obvious that that's the limit to the number of sequences that can be aligned using dynamic programming.

There's no shame in heuristics. Perhaps the most widely used bioinformatics program in the world, BLAST, employs a heuristic. (And your brain makes decisions that your life depends on every day using heuristics.)

The methods that use heuristics for MSA have been successively modified to deal with known factors that can cause problems, so often they perform very well. How can you tell? What you need to do in using MSA programs is to perform a "sanity check" on any alignment that the programs produce — does it look reasonable, has it matched up similar regions well or are there vast gaps introduced or obvious regions of homology missed. And if you are doing 3D modeling and you don't get an alignment that looks good, then your modelling isn't likely to work.

Finally you always have to consider the possibility that there aren't any proteins of known structure that are similar to the one you want to model so you'll never get a good MSA.


ID Sunbird in Oman - White, Dark Grey, Yellow

There are 4 species of Sunbirds in Oman.
https://en.wikipedia.org/wiki/List_of_birds_of_Oman

Based on your description and how common are the different species I think they were most likely mainly Purple Sunbird (Cinnyris asiaticus) https://en.wikipedia.org/wiki/Purple_sunbird
At the moment, in fact, they are not purple at all. They are moulting their feathers and also the male have extensive yellow on breast and belly. Among the species of Oman's Sunbirds it is the only one that shows black wings (in males) contrasting with the brownish/grey upper parts precisely as you observed.

MOULTING MALE

FEMALE (left)


In the diffraction pattern of a protein crystal what exactly determines the intensities of the spots?

Two questions here:

1) What does the symmetry of the crystal mean?

The symmetry of the unit cell is the symmetry of the crystal.  Its really useful thing to know about the crystal in practice.  You can always pretend that any crystal is space group P1 - with no internal symmetry.  This implies half of the diffraction data is needed to get a complete set.  Why half? The Laue symmetry of typical X-ray diffraction shows that the diffraction should be centrosymmetric  I(hkl) = I(-h,-k,-l).

If you do this and the crystal has more symmetry than that you are collecting too many data.  Here I take the example of a 2-fold axis.  Along that axis the space group shows that the symmetry of the crystal should be 4 fold along the x axis (x axis is chosen by convention):

I(hkl) = I(-h,-k,-l) (as above) and I(hkl) = I(h,-k,-l)

This fact means we actually can collect less data and know the crystal diffraction pattern easily.  In practice we collect from more than just the unique data, but the more diffraction data we take it also means that we can assume equivalence and have taken more  measurements, giving us better experimental accuracy for the same effort. It also means that when we build a molecular model for structure in the crystal we have a simpler model - one only creates a model for the unique assymmetric unit of the crystal unit cell. Fewer atoms in the structure, fewer degrees of freedom and less error in our resulting model.

There's more... screw axes 2(1), 3(1) and non primitive lattices create systematic absences which helps us collect more accurate data and do refinement more easily in the same vein...  but maybe this gives you an idea...

2) how does the unit cell contents reflect the diffraction intensities

X-ray scattering from crystals is the result of the photon causing an elastic scatter from atomic, inner shell electrons - Bragg scattering.  By considering the crystal as a series of slits in 3 dimensions, it can be shown that the average positions of atoms in the crystal reinforce each other to give the reciprocal lattice that is diffraction data in 3D.

In the picture above from Wikipedia you can see a beautiful protein crystal diffraction pattern.  The rings of spots are a spherical section from a 3D orthorhombic lattice of spots.

Rather than digress into the reason the diffraction appears this way, back to your question: what causes the intensities to vary from spot to spot and crystal to crystal.  The crystal lattice contains atoms which are in the same position in every unit cell which are creating the diffraction by Bragg scattering.  As such, it is the positions, relative electrons in orbit that dictate the diffraction intensities measured.

The models built to model diffraction typically translate a set of atomic positions to the structure factors (square roots of the diffraction intensities), but this is an approximation that works pretty well - the full model is not atomic positions, but an electron density function in space.

There are other sorts of scattering methods, more that could be said about all these subjects, but I hope that gives you some help with your specific questions. If you want clarifications in this, I can edit the answer from comments...


Do fat people have more chances of developing nitrogen bends?

Well, you're right! First of all,

  Nitrogen Bends or Decompression sickness (DCS) is a disease that arises as a consequence
  of bubbles forming within tissues. Inert gases, such as nitrogen
  and helium, enter the body through the lungs during inspiration.

  Increased BMI (Body Mass Index) implies an increased fat content of the body. This
  increased body fat leads to increased nitrogen storage and hence
  possible excessive nitrogen bubble formation and thus increased the
  risk of development of DCS.

Learn more about the relation between Fat and Nitrogen Bends by reading Diving and Hyperbaric Medicine  Volume 36 No. 3 September 2006


Why are bees attracted to Stag Hides in Lime bath

Short answer: They are probably looking for minerals from the lime

Explanation:
Insects from time to time need minerals (salt) they can't get from there floral diet. Because they can't chew these directly of rocks, they suck these up from puddles or occasionally from human sweat. This behaviour is well known from butterflies, but also from honeybees

Notice BTW that there are indeed several bee species (Probably Apis mellifera, Bombus terrestris agg. and Bombus lapidarius), but also several flies including Eristalis cf. tenax, a hoverfly.

Why not from the sheep hides? I'm not sure, but the water around the sheep hides looks awfully brown, suggesting there are a lot of humic acids un the water. That might be less attractive to the insects.


Interesting question!

There has been at least one study that bypassed a spinal lesion site with autografted neuronal tissue (Tadie et al., 2004 - doi:10.1089/089771502320317069). The study participant regained voluntary motor skills 8 months after bypass surgery. The surgery involved the implantation of nerve autografts between the rostral spinal ventral horn and the caudal ventral roots. Regain of motor function was observed after the patient had been paralyzed for 3 years.


How can I determine the mRNA sequence from a given template DNA strand?

I'm assuming you are working with a small sequence, but for larger sequences, or if you want to double check your answer, you can use tools like this one: http://www.attotron.com/cybertory/analysis/trans.htm


Does polyploidy always isolate the polyploids from the diploid source population?

Ploidy and reproductive isolation in plants

Speaking generally, there is simply no question that for flowering plants there can be a sexual pathway between diploid and polyploidy levels. The question is how wide is the bridge and how much flow is there in either direction. In other words the questions become "How much flow?", "How meaningful the flow?", "How much flow back to the original diploid and polyploid populations?", and "How often over the last 200 million years has such interaction been an important factor in the evolution of flowering plants?".

Examples from Rhododendron

In the following, I will give a number of examples from the plant genus Rhododendron to show how ploidy level can function in relation to sexual isolation. In this taxa, diploid X tetraploid normally produces triploids although occasionally a tetraploid or even a diploid offspring is produced. The triploid offspring of diploid deciduous azalea species X tetraploid deciduous azalea species often look very similar to the tetraploid pollen parent.  'Margaret Abbott', which is a seed fertile tetraploid deciduous azalea, has a fragrant white flower produced by crossing a fragrant pink flowered diploid seed parent with a non-fragrant yellow flowered pollen parent.

Our research on hybrid elepidote Rhododendron indicates that triploids, although reluctant to reproduce sexually, can produce diploid, triploid, tetraploid, and pentaploid offspring when crossed with pollen from diploids, triploids, and tetraploids. 'Phyllis Korn' is an example of a fourth generation triploid. 'Graf Zeppelin', which exhibits polyploid characteristics, is an example of a diploid offspring of a triploid. 'Countess of Derby' is an example of a tetraploid offspring where both parents are triploids. 'White Ginger' is a an example of a pentaploid offspring of a triploid. 'Pink Pearl' is an example of a triploid that has produced diploid, triploid, and tetraploid offspring from interaction with diploids.

In deciduous azaleas triploid X tetraploid crosses often produce aneuploids between triploid and tetraploid. Such crosses can on occasion produce pentaploids.

Our limited experience working with triploids and pentaploids as seed parents indicates that in general pentaploids are better seed producers than triploids.

An interesting finding is neotetraploids can produce diploid offspring in the first generation. In general tetraploids can produce diploids, triploids, tetraploids, and pentaploids when crossed with pollen from diploids, triploids, and tetraploids.

Triploids are common in natural contact zones where diploid deciduous azalea populations overlap with tetraploid deciduous azalea populations. There is strong evidence indicating there is gene flow from the diploid population to the tetraploid population in these contact zones. There is some evidence of gene flow from the tetraploid population to the diploid population. There is some evidence to suggest multi-generational triploids exists in these contact zones.

Worth noting is that the meiosis for triploid deciduous azaleas that do set seed is distributed around 1.5x gametes ranging from 1x to 2x with an occasional 3x gamete. This uneven distributed splitting of triploids is what produces aneuploid offspring between 3x and 4x when semifertile triploids are crossed with pollen from stable tetraploids. Cyril Dean Darlington in the late 1920's and early 1930's documented this uneven distributed splitting of triploids during meiosis. Evidence suggests that neotetraploids can also undergo uneven distributed splitting during meiosis.

Darlington's history of the garden hyacinths showing a triploid pathway from diploid species to tetraploid hybrids parallels the history of the hybridization of the tetraploid elepidote Rhododendron 'Countess of Derby'.

We have some evidence for deciduous azaleas that 3x X 4x can produce aneuploids close to 5x indicating that some of the "3x gametes" are coming from first an uneven splitting of the triploid followed by a failure to reduce in a later phase of meiosis. However this result of aneuploidy near pentaploid has not occurred often enough to be certain that is what is happening.

In general for deciduous azalea species;

diploid X diploid normally produce seedpods and high percentage of
viable seed.
tetraploid X tetraploid normally produce seedpods and high percentage
of viable seed.
diploid X tetraploid normally produce seedpods but a highly variable
percentage of viable seed.
tetraploid X diploid almost never set seedpods.
triploid X tetraploid sometimes produce seedpods and a low percentage
of viable seed.

For hybrid elepidote Rhododendron, 2x X 2x, 2x X 3x, 2x X 4x, 3x X 2x, 3x X 3x, 3x X 4x, 4x X 2x, 4x X 3x, and 4x X 4x are all documented to have occurred.

For deciduous azaleas, we have produced viable seed from 2x X 2x, 2x X 4x, 3x X 4x, 4x X 4x, 4x X 6x, 4x X 8x, 5x X 4x, 6x X 4x, and 6x X 6x.

The flow cytometry for this research on the genus Rhododendon was performed by Dr. João Loureiro, Dr. Silvia Castro, José Cerca, and Mariana Castro
Plant Ecology and Evolution Group,
Centre for Functional Ecology,
Department of Life Sciences,
Faculty of Science and Technology,
University of Coimbra, Portugal.

The ancestry for 'Phyllis Korn' illustrates that triploids can be multi-generational.

The diagram below illustrates how the triploid 'Pink Pearl' has produced diploid, triploid, and tetraploid offspring when interacting with diploids and has produced a tetraploid offspring by interacting with another triploid.

The family tree for the Rhododendron elepidote hybrid 'The Duchess' illustrates that interploidy interaction can be multi-generational.

\

Picture of 'Margaret Abbott' with a quote from Frank Abbott.

Picture showing how much the offspring of a diploid crossed with a tetraploid looks like the tetraploid pollen parent.

Picture showing the successful development of seedpods from crossing a diploid by a tetraploid.

Picture showing the failure in developing seedpods from crossing a diploid by a tetraploid.

Picture showing interploidy hybrid swarm at Audra State Park, WV.

References

Meiosis in Polyploids
by W. C. F. Newton and C. D. Darlington
in Journal of Genetics 1929

The history of the garden hyacinths
by C D Darlington, J B Hair and R Hurcombe
in Heredity 1951

Rules of Engagement: Have Pollen—Will Travel
by John Perkins · Sally Perkins
in Azalean 2010

Frank Abbott's Village of Azaleas
by John Perkins · Sally Perkins
in Journal American Rhododendron Society 2011

Ploidy level estimations in deciduous and elepidote hybrids of Rhododendron
by José Cerca de Oliveira, Mariana Castro, Francisco J. do Nascimento, Sílvia Castro, John Perkins,Sally Perkins, João Loureiro
in Jornadas Portuguesas de Genética, Coimbra, Portugal; 05/2011

Weighing in: Discovering the ploidy of hybrid elepidote rhododendrons
by Sally Perkins, John Perkins, José Monteiro de Oliveira, Mariana Castro, Sílvia Castro,  João Loureiro
in Rhododendrons, Camellias and Magnolias, Royal Horticultural Society, Editors: Simon Maughan, pp.34-48 2012

Untersuchung des Ploidiegrades elepidoter Rhododendron-Hybriden
by Sally Perkins, John Perkins, Mariana Castro, José Cerca De Oliveira, Silvia Castro, João Loureiro
in Rhododendron und Immergrüne , Deutsche Rhododendron-Gesellschaft e.V. , Seite 21: pages 21-42; 11/2013


Bonding in the primary structure of a protein

Peptide bonds (also called amide bonds) are definitely covalent bonds.
This is also mentioned in the first line of wikipedia entry: https://en.wikipedia.org/wiki/Peptide_bond


This is a great quesion! There is lot of work still being done on this. Unfortunately I don't think I know enough about CS or computer engineering to make analogies, so I'll give a quick crash course and some examples instead and hope you find it helpful. Long story short though is that we are just now making really exciting headway into how memory might actually be stored and recalled and its usually a very dynamic, active, and possibly even stochastic process, not really like a search algorithm in a computer at all.

The brain works differently than a computer in that it encodes all of its information in frequency of signal firing and the patterns of firing between circuits with varying stregnths of connections based on experiences. Frequency is dependent on the neuron itself and patterns of firing between circuits are dependent on where the neurons project to, and how strongly they interact with the next neuron. At this very basic level memory is stored and recalled by placing proteins in the membranes of neurons that are strongly activated to make them easier activated in the future. These are sort of the first steps toward memory. This is called long term potentiation and just means that this neuron is primed to fire more readily and stronger in response to similar input in the future.

To build on this,  there is a classic example of this occuring and causing sensitization ( an exaggerated response to the same stimulus) in conditioning experiments in the sea slug Aplysia. Aplysia has a reflex where it will withdraw its gills slightly if you touch its siphon. You can pair a shock to the tail (unconditioned stimulus) which elicits a large withdrawal of the gills, with a conditioned stimulus (touching its syphon to elicit the withdrawal reflex) to get the sea slug to associate the two. The end result is that the sea slug will learn/"remember" to withdraw its gills fully in the presence of the syphon touch. No learning cannot happen without recall of some sort, and in this example the slug was associating and learning from two "circuits" to produce a different behavior.

In something a little more complex than a slug, memory and recall still functions much the same way, its just the circuits that are interacting are entire brain regions. Most people view the hippocampus as acting sort of like a relay center and boot loader for different memories by taking external input and sorting them to the right parts of the brain. A good example of this would be the difference between dorsal and ventral streams of information in the brain. For a really basic breakdown of this phenomenon there are two areas of your brain that I will focus on - the parietal lobe and the temporal lobe. The parietal lobe is known to be involved in spatial processing, and the temporal lobes are known to be involved in semantic and auditory processing. When information enters the brain (eyes, ears, nose etc.) it will be processed by sensory structures, sent to the thalamus and hippocampus to be "relayed" to the right areas of the brain. Relayed in this case is going to be dictated by whatever connections and how strong they are in the brain. In this case from proteins expressed in the cellular membrane that make some neurons in the hippocampus more responsive than others, so they are more likely to fire. Then, it depends on where they are projecting to that determines where they information is sent.

It just so happens the brain is arranged in such a way that neurons projecting dorsally, or to the parietal lobe I mentioned, will tell you "where" the stimulus is, and those projecting ventral to the temporal lobes will tell you "what" it is. This is achieved because these lobes are highly interconnected to even more regions in the brain and send their processed "where" and "what" info as input to other regions. These regions will all fire a certain way in response to this information and that pattern of firing can be considered a recollection or memory. Sorry that this is dense and so crash course-y but I hope it is helpful in clarifying how the brain recalls some information. Of course this is  a developing field and we are learning more about how it functions every day. These are just some classic examples.


$F_{ST}$ when considering a multi-allelic locus

Short answer: yes, people have formulated ways to estimate $F_{ST}$ for multiallelic loci, e.g. microsatellites. For a review, see here.
Specifically, Nei could define $F_{ST}$ for multiple alleles as
$F_{ST} = \frac{(H_t - H_s)}{H_t}$,
which is to say the proportion of total heterozygosity that is across rather than within populations. This is agnostic to the number of alleles, as it just uses heterozygosity. I believe there are other formulations as well.
There exist alternate statistics such as $G_{ST}$ and $R_{ST}$ (links under each) which are devised specifically for the multiallelic problem, see also the review for further discussion. Basically, microsatellites have high mutation rates such that they deflate the statistic; this will likely be the case for most multiallelic loci.
It's not clear though which statistic works best in practice as far as I can tell.


Does darker skin color make it easier to live under sun?

It isn't about heat but ultraviolet light. Melanin is the pigment that makes our skin colour whatever it is and in darker skin there's more melanin. Melanin dissipates UV, which otherwise would cause skin cancer as it introduces mutations into DNA. Melanin production is stimulated by UV so that's why tanning beds work, our body senses the danger and responds by making our skin darker. Yes this makes us hotter but that's a small price to pay, melanin needs to be dark to do its job well.


LC-MS map they refer to is the projection of two separation method (Liquid Chromatography - Mass Spectroscopy) results into an imaginary plane. It's a conceptual map. From this map, peptide signals referred to as "features" (article uses this term) are selected for the next level of fragmentation and then MS again.

Figure 1 of the article you cite simulates a small fraction of this larger map.


What cells would have the CD3 marker on them (other than T-cells)

CD3 is initially expressed in the cytoplasm of pro-thymocytes, the
  stem cells from which T-cells arise in the thymus. The pro-thymocytes
  differentiate into common thymocytes, and then into medullary
  thymocytes, and it is at this latter stage that CD3 antigen begins to
  migrate to the cell membrane. The antigen is found bound to the
  membranes of all mature T cells, and in virtually no other cell type,
  although it does appear to be present in small amounts in Purkinje
  cells. This high specificity, combined with the presence of CD3 at
  all stages of T cell development, makes it a useful
  immunohistochemical marker for T cells in tissue sections. The antigen
  remains present in almost all T-cell lymphomas and leukaemias, and can
  therefore be used to distinguish them from superficially similar
  B-cell and myeloid neoplasms.

Source: http://en.wikipedia.org/wiki/CD3_(immunology)


Values of the blood tests pancreatic amylase and lipase

It is not necessary a fixed value. I think it depends on the doctor that interprets it. For e.g if amylase's normal value is 70, and laboratoy value is 80, i would say it is slightly elevated. A value of 300 is strongly elevated.


Are there parts of DNA that do not have genes?

Most the genome is not coding for proteins. Here is a pie chart of what the human genome is made of

As you can see, only 1.5% of the human genome codes for proteins. The term gene is often a bit vaguely defined but if we assume that a gene is all the exons, all the introns and all the regulatory sequences, then 25.5% of the human genome are genes. So, yes many "parts of the genome" do not contain genes.

Now, it is worth highlighting that there is a very high correlation between the genome size and the number of protein-coding genes among lineages. Consider the below graph based on data from NCBI genome reports and styled after Koonin (2011).

There is a high correlation but there are also important outliers. See for example the eukaryotes (green dots) at the bottom right of the graph (probably mainly polyploid plants) that have very big genomes but relatively few protein-coding genes.

So, even though there is a strong correlation, it was quite obvious to me that the answer your teacher was expecting was no, because most of the genome is not coding and despite an existing correlation between genome size and number of genes among lineages there exists species with a very high density of genes and others with a very low density of genes in their genome.


Growth is neither even nor constant, It can vary quite a bit from month to month as hormone levels change, the growth curves you are seeing are a rough average.

You are having a hard time finding anything because it one of those pieces of knowledge that is so old people only rarely research it directly focusing more on deviations from it and you will likely only find good reference to it in textbooks. For a layman this means searches based on the terms you think you should use never find what you want, something as simple as adding the word "textbook" can make a huge difference. Google scholar will also help.

http://adc.bmj.com/content/51/3/170.short

https://books.google.com/books?id=YA-LdtyHJ9QC&pg=PA226&dq=evolution+of+the+growth+spurt&hl=en&sa=X&ved=0ahUKEwjkl4zCztjRAhVB74MKHRiuB7kQ6AEIHzAA#v=onepage&q&f=false