Simple interpretation of effective population size?

Like, would it be overly simplistic to say that the sampled individual could be expected to contain ~1/1000 of the population's standing variation?

It is a little unclear what you mean by "variation" here. If you mean "genetic diversity" aka "expected heterozygosity", then it would not just be simplistic, it would be wrong to say that!

  Or to say that a given (observed) nucleotide state has a 0.001 probability of being fixed?

Ah that one is pretty good. If the effective population size $N_e = 1000$, then the probability of fixation a a new neutral mutation is $1/2N_e$ (assuming diploidy). The probability you indicate would be correct in a haploid population if you are talking about a new neutral mutation.

Another simple statistic you might want to consider is that, in absence of mutations, the genetic diversity would decrease by a factor $\frac{2N_e - 1}{2N_e}$ at every generation (assuming diploidy again).

You can derive a whole bunch of statistics of interests. For example, the expected genetic diversity in the total population at a locus at which the mutation rate is $\mu$ is $\frac{4N_e\mu + 1 }{4N_e\mu}$. You can derive many other statistics you might be interested in such as the expected number of segregating sites in a sample of size $k$ or the expected coalescent times for examples.

For more information just have a look at an intro course to population genetics. You'll find book recommendation in this post.


What Ultimately Controls DNA Transcription?

Transcription of DNA is ultimately controlled by "various transcription factors, small nuclear RNAs and so on" in the cell.

The molecules which make up the "various transcription factors", etc. are already present in the cell when a new transcription begins.  As you note, most all of these molecules are themselves dependent on the transcription of DNA, but also of the availability of component molecules (e.g. nucleotides, amino acids) and of processing mechanisms such as ribosomes.

So, a new instance of transcription requires a working cellular environment, and that environment was created and maintained as directed by DNA molecules at an earlier time.  Usually those DNA molecules were exactly the same as the ones from which the transcription is proceeding. Occasionally, those DNA molecules would have been physically different, but adequately compatible, such as the source chromosomes which were copied during mitosis to create the current DNA molecule.


Difference between protein channels, protein carriers and protein pumps?

No, carriers are not the same as pumps. Carriers may or may not carry out active transport and pumps always use energy. Carriers, for example, can make use of the concentration gradient of a certain ion built up by pumps to transport other molecules actively against their gradient. For example, the glucose transporter uses the sodium gradient to transport glucose against the concentration gradient into the cell, while getting the energy by co-transporting sodium into the cell along the gradient. The sodium import yields energy. That in turn is caused by the Na+ K+-ATPase, which builds up the sodium gradient using ATP. The glucose transporter is called a symporter, because it co-transports sodium into the cell. An antiporter transports another particle in the opposite direction.
Yes, true. The glucose transporter as explained above is an example of active carrier-mediated transport. Other carriers just mediate passive diffusion of, for example, large molecules that don't fit through channels and won't readily cross the cell membrane.
Yes, pumps always use energy under physiological conditions. The energy source is always ATP.

Will add references shortly.


Is it possible to make humans extinct artificially?

Trick question. By driving humans to extinction, you almost certainly will be driving all human-specific parasites and pathogens to extinction as well.


Null cells are a "slang term" for cells of the lymphocyte progeny that are not APC (antigen presenting cells) and lack T and B cell receptors - therefore they are the natural killer (NK) cells.


Why does muscle tissue have relatively constant AMP + ADP + AMP?

Adenosine triphosphate (ATP) is often thought of as the energy currency of cells. It is not "used up" per se, but energy is released from the conversion of ATP to ADP (adenosine diphosphate), and yet more can be obtained by removing another phosphate to make AMP (adenosine monophosphate).

Here's a chemical schematic of ATP, you can see the three phosphates to the left.

Your slides state that the amount of (ATP + ADP + AMP) remains constant in the muscle, which makes sense because ATP is not used up, but converted to ADP. So as cells use energy, they do not actually reduce the total concentration of (ATP + ADP + AMP). Energy is required to add the phosphates back onto an ADP or AMP molecule - the process is called oxidative phosphorylation in cellular respiration (although this is not the only way).

I hope I didn't misunderstand your question.


How do bees help flowering trees survive?

One of the goals of every living organism (including plants), thus it seems, is to create offspring for the next generation. This is the way plants (angiosperms) have sex.

That said; I personally define pollination as:

  The act of transferring pollen grains from the male anther of a flower
  to the female stigma.

It should be noted that not only Bees play a very important role in pollination, but also other insects like wasps, beetles, mosquitoes etc.

When a bee sits on the flowers to collect nectar, its feet pick up pollen grains ( the powdery stuff) from the anthers and transfer it to the female stigma (which is sticky to hold the pollens).

Michigan State University:

  When a bee lands on a flower, the hairs all over the bees' body attract pollen grains through electrostatic forces. Stiff hairs on their legs enable them to groom the pollen into specialized brushes or pockets on their legs or body, and then carry it back to their nest. Individual bees tend to focus on one kind of flower at a time, which means it is more likely that pollen from one flower will be transferred to another flower of the same species by a particular bee.

Then the pollen grain makes its way into the ovary of the flower through the long stalk (style) and fertilizes the egg. Then the flower matures to for a fruit and the ovules become it's seeds.
It's a symbiotic relationship where the plant provides food and the bees pollinate them in turn.
Also, certain bright colouration of flowers and their sweet smell attract more insects.

A declining population of pollinating insects signal the decline of the whole ecosystem including plants and trees.
Entomologists keep a check on various insect populations. They have found a decline in the population of bees world wide! This is an alarming situation. This will cause huge damage to fruit industries including kiwifruit, watermelon, squash and many others. It's time we take the environmental issues seriously.The reports aren't vague!

Penn State College of Agricultural Science:

  Historically, managed honey bee populations in the US and Europe have been monitored due to their vital role in providing pollination services in agricultural systems.  Several studies indicate that American and European beekeepers are suffering large annual losses.  In the US, beekeepers have lost ~30% of their colonies every year since 2006, with total annual losses sometimes reaching as high as 42%

Edit

Citations:

https://en.m.wikipedia.org/wiki/Pollinator#Honey_bees

https://en.m.wikipedia.org/wiki/List_of_crop_plants_pollinated_by_bees

A brochure from FAO on importance of bees as pollinators :
http://www.fao.org/3/I9527EN/i9527en.PDF

Penn State College of Agricultural Science on declining population of pollinators :
https://ento.psu.edu/pollinators/resources-and-outreach/globally-pollinators-are-in-decline

Wikipedia on the same issue:
https://en.m.wikipedia.org/wiki/Pollinator_decline


Why is the body cooled during cardiac surgery?

As you mention, hypothermia is routinely induced during cardiac surgery. There is a blog post including a photo of a heart being cooled with ice chips here: https://www.heart-valve-surgery.com/heart-surgery-blog/2010/10/17/ice-cardioplegia-open-heart-surgery/

The primary therapeutic benefit of deliberate hypothermia was long thought to be, as you say, the slowing-down metabolic processes, which reduces the amount of oxygen needed by the brain and other vital organs (source). Cooling the blood during open heart surgery therefore allows the operation to be performed more slowly (2-4 hours).

However, according to this open-access article on the benefits of therapeutic hypothermia for cardiac surgery:

  the widely held notion that hypothermia protects because lower
  temperatures slow metabolism is not completely accurate. Recent
  research has shown that hypothermia can alter a plethora of cell death
  and cell survival pathways including gene regulation resulting in the
  inhibition of apoptosis and inflammation and the up-regulation of
  anti-apoptotic or trophic factors.

So basically it does slow down the metabolic processes but it also reduces inflammation and cell death.

After surgery, rewarming needs to be done slowly to maximise the chances of recovery (source).


What's the aim of genetically modifying of foods/organisms?

GMO foods have a huge potential to make food cheaper to produce and more nutritious.

The most common GMO foods have at least one gene added to them - an enzyme that makes the plant resistant to RoundUp - an herbicide made by the same company (Monsanto).  this makes the farmers able to grow their crops with much less intensive labor to keep the plants healthy. It does cost some money and people wonder whether using so much roundUp is good.  I won't come down on the benefits of this, but you can see how it might be more economical way to grow crops.  roundUp is biodegradable and does break down in about 3 weeks, just FYI.

Other GMO foods can make the crops more resistant to drought, disease or insects. This might enable crops to be grown in areas and or with longer growing seasons - a big advantage for thirsy crops like tomatos or rice. Other GMO project may allow us to make the crops more nutritious.  A famous example of this is golden rice, which has been enhanced to produce pro-vitaminA, which will help malnutrition in millions of children who can die annually because of a lack of vitamins in their diet.

There is also an effort in nutriceuticals, where vaccines and common drugs maybe produced by edible plants for easily processing or even direct distribution of pharmaceuticals.

For people who can afford organic food and free range beef, I think its great that its available, but at for a hungry world, GMO foods can help solve some vital problems.


Are the seeds in a single capsicum fruit genetically identical?

No, the seeds are not genetically identical.  Each seed come from the fertilization of an ovum with a sperm from a separate pollen grain.  Since each pollen grain can come from a different plant, the seeds will generally differ from one another.
Additionally, even ova from a single plant will not usually be genetically identical to one another.  This is because the process that creates the ova (meiosis) shuffles the genes of the parent plant on then places only half into the ovum.  The same kind of shuffling goes on in the creation of pollen grains.
In the chili pepper genus (Capsicum), plants are predominantly self-pollinating. This means the majority of the pollen for the seeds in a fruit will come from the very same plant.  This generally reduces the amount of variation seen in the offspring compared to complete cross-plant pollination. Some cross-pollination can nevertheless occur if there are other varieties in the neighborhood.  The fruit will not show the effects of the new genetic combinations present in its seed, but only a plant grown from the seed will make the differences evident.


We die of old age because the biological cost of making us live forever does not improve our chances of passing on our genes. In nature something else would kill us eventually so there was never a reason to evolve the ability to live indefinitely. There are multicellular organism  that are biologically immortal(all unicellular are), they live slow low activity lives. A lot of the evolution of more "advanced" life is trading regeneration or longevity for higher activity. Literally live fast die young, leave more offspring.


Is it possible for a sex chromosome to be homologous?

How can a male fly be pure-breeding?

A fly or any organism can only be pure-breeding for a certain trait, not all traits at once. If the trait-determinant allele is found on an autosomal chromosome, this is not a problem. If it's on a sex-chromosome (chr1 in flies), it is sex-linked, and therefore cannot be pure-breeding because it may depend on the sex of the offspring whether the trait is expressed. For instance, you may have a male carrying an allele on its X chromosome; its female offspring will inherit the X, but male offspring will not (those inherit the Y chromosome), i.e. it is not pure-breeding. Male flies cannot be pure-breeding for traits determined by loci on their sex chromosomes. Similarly, you may have a heterozygous female carrying an allele on one of its X chromosomes (A/a); its female offspring will only inherit one allele, either A or a, so it is not pure-breeding either. A female fly must be homozygous for an allele on its sex chromosomes to be pure-breeding for that trait.

Male flies can be pure-breeds for traits determined by alleles on autosomes.

Also, cool and useful funfact, Drosophila sp. male flies do not experience homologous recombination during meiosis. This is called achiasmy! This is useful to know when designing complicated crosses when there is a difficulty in balancing a genotype.

  Does it make sense to speak of homologous sex chromosomes?

The X chromosomes in females (X + X) are homologous, but the male Y chromosome is not homologous to the X. They are vastly different, just like the X and Y sex chromosomes in humans.

  Pure-breeding implies a homozygote gene

Correct. Pure-breeds are allele homozygous so that all offspring, regardless of recombination, inherit the allele.


Plating 96-well bacterial transformations

I think your approach very much depends on how essential it is that you get discrete single colonies, and if this is a one off or a regular process. To preface, similar to what Maximilian Press said, using a single welled plate like a nunc omnitray would be your best bet.
The main consideration you need to take into account for high-throughput transformations is the transformation efficiency (TrE). Naturally in a big petri dish, 100 µL of a single 1:10 or 1:100 dilution of your recovery culture can bring out nice discrete colonies. When you start reducing surface area and volumes, the chance of discrete colonies obviously diminish.
The best way I've found is to do a test transformation using the backbone of your choice and gauge the average TrE over a few runs to hone in on a 'one size fits all' dilution/volume, then apply that to your full high-throughput run. Assuming your inserts are of similar size, you should see a relatively similar TrE between them (bar edge cases). Another option would be set up three 96-well plates and do three separate dilutions, 1:10, 1:100 and 1:200 at 100 µL a pop so you at least get some fudge factor.
In terms of the chemical transformation itself, doing them in a 96 well plate format will guarantee lower TrE simply due to the characteristics of the plate itself. Thicker plastic and sub-optimal heating (if you aren't using a thermocycler and PCR plate) requires a slightly longer heat shock, and recovery in media requires much more vigorous shaking due to the mixing characteristics within the wells.
If you don't care about plating out in 96 well plates, like Maximillian Press said, use a single welled plate and format it in a 96/48 well fashion. Will save a massive headache when pouring. Just make sure you leave it to dry to prevent any running culture.
In terms of actually growing the colonies in a 96 well plate, if you're making the agar yourself I'd recommend adding an extra 0.5% agarose to thicken it up (I doubt you'll be using one, but make sure your plate is non-tissue culture treated). Wait for it to cool just above its solidifying temperature (around 45 °C in my experience) and then transfer out using a pipette or low volume serological pipette to reduce the meniscus formation. If the agar forms a high angled meniscus, your colonies may form smears and will not be discrete. Leave the plate out to dry as well, colonies may also smear from the agar being moist.


Standard notation for dominant and recessive allele

[H]ow exactly we mark out genotype in science? Do we use D's and r's?

General rule

The general rule is to indicate the dominant allele with a upper-case letter and the recessive allele with a lower-case letter.

The most commonly used letter is the first letter of the alphabet. The two possible alleles are a and A and the four possible genotypes here are therefore aa, aA, Aa and AA. Only aa has blue eyes in your example. Note that it is very common to merge together Aa and aA (that is to not consider whether the A allele was inherited from the father or from the mother) and just call it Aa.

More than 2 alleles OR no clear dominance relationship

It is quite common to use A1 and A2 as well but when doing so, we don't implicitly indicate a relationship of dominance. This notation also has the advantage to be able to deal with cases where there are more than two alleles segregating in the population (A1,A2,A3). Note that in reality perfect dominance is quite rare.

More than 1 locus

When dealing with more than one locus, we generally use A/a for the first locus, B/b for the second locus, C/c for the third etc... However, in general when dealing with several loci, authors don't have identical loci ad therefore they directly name them and use appropriate letters. For example, in models of recombination under control of a modifier locus, the modifier locus can often take the values M and m, while a random linked locus under purifying selection would take the letters A and a.


Generally the codon optimization is the most frequent tRNA found in your species of interest. However, your codon must not result in something that disrupts standard molecular biology practices. For instance, if your codon places a restriction site in a unique cloning vector, then the algorithm will just look for the next best codon which does not cause unwanted addition or elimination of a cloning site. Places like IDT will also weigh the cost of the codon vs. the ease of manufacturing in their algorithm (see here.)

What you describe as translational pausing that is 'needed' by the organism to optimize proper gene expression is a consequence and not a necessity of infrequent codons (to my full understanding). See here. That means you don't want to add this translational pausing in optimized gene expression. It is a simply an evolutionary byproduct.

Edit -

To answer your question more bluntly, I can tell you with some experience to trust the codon optimization algorithms from biotech companies like IDT. I find they work very well. Rice is a common enough organism :)


Help me identify this insect from Bangladesh

This is actually the flying adult of a scale insect (superfamily Coccoidea). Specifically, this appears to be some species of the genus Drosicha.

Here is a picture resembling your specimen:

 Source: John Horstman

And another from Vietnam that looks very similar:

 Source: Dan Doucette

I can only find info on a closely related species, Drosicha corpulenta, and here's a tree of related species.

Scalenet provides numerous keys and references that could be useful for positively IDing this specimen.

I will keep searching for more details, but this might be the best you get without asking a scale insect expert.


What would happen if Carbon-14 was in a glucose molecule and decayed into Nitrogen?

I am not experienced in the topic, and could not find any article related to these kind of reactions, but my guess is the following. During the nuclear transmutation the radiocarbon will lose an electron (beta particle), so the nitrogen product will have positive charge. After that there are 2 possible scenarios.

a.) less plausible scenario

The beta particle carries away the energy of the decay, so the molecule will have low energy and it will be able to rearrange.

The electron shells will collapse a little bit, since the nitrogen has smaller nuclear radius. The part after that depends on which carbon we are talking about in the glucose molecule. I would guess the following rearrangements:

${-CH2OH} \rightarrow {-NHOH} + H^+ $
${=CHOH} \rightarrow {=NH} + H^+ $
${-CHO} \rightarrow {-NO} + H^+ $

It is not easier to break an N-H bond compared to the N-C and N-O bonds according to this table, but I think what really matters here is the stability of the final product, and $H^+$ is way more stable than any $^+O*$, $^+C*$, etc. ion.

b.) what really happens

The beta particle carries away the energy of the decay only partially. So the nitrogen will have a lot of energy, which is more than enough to break all of the bonds. According to wikipedia the decay energy is 0.156476 MeV. Let's compare it with the bond energies:

$ 0.156476 MeV = 2.50702189 \cdot 10^{-17} kJ $

${2.51 \cdot 10^{-17} kJ} \cdot {6 \cdot 10^{23} \cdot 1/mol} = 1.51 \cdot 10^7 kJ/mol$

According to our table the covalent bonds have about a few hundred kJ/mol energy, e.g. a C-N bond has 305 kJ/mol energy. So it is very likely that the chemical bonds will break immediately after the decay and the molecule will fall apart.


What is the identity of this spider from India?

Anyone identify this little guy?

That is a Siler semiglaucus, which is a type of jumping spider. It has the nickname of "metallic jumper", and can be found all throughout India, Indonesia, Philippines, and Thailand.

  He has 8 legs, but the two on the front is raised above his head, just like a crab does.

Here is a wonderful collection of more images, which also includes locations of discovery.


Is flowers nectar secreation influenced by bees/pollinators?

In short, yes, it seems many flower species have mechanisms to replenish nectar after removal. For example, in Luo et al. 2014 Journal of Pollination Ecology,  9 of 11 species of plants they studied in the Colorado Rockies showed significant additional nectar production after some nectar was experimentally removed. Furthermore, the magnitude of this behavior was greater for flowers known to be heavily visited by bees:

https://www.researchgate.net/publication/268523373_Stimulation_of_flower_nectar_replenishment_by_removal_A_survey_of_eleven_animal-pollinated_plant_species


What is the definition of a stringent/relaxed plasmid?

In short, yes, the definitions are still correct:

The number of copies of a plasmid in the cell is determined by the mechanism of its replication: whether it is synchronized with the replication of the bacterial chromosome or is independent of it.

In the first case, the initiation of replication is performed by the same mechanisms of replication of the bacterial chromosome. This means that the origins of replication, as well as all proteins involved in the initiation of replication, are shared between the plasmid and the bacterial chromosome. For plasmids, which replication is synchronized with the replication of the bacterial chromosome are under stringent control of replication. The stringent control of replication is characteristics of plasmids with low copy number. These plasmids contain DNA regions called par-locuses (from partition) that control the correct division of the plasmids in the two daughter cells.

Plasmids with high copy number are under relaxed control of replication. These plasmids are replicated independently of the replication of the bacterial chromosome. They have individual mechanisms for initiation of replication. The plasmids themselves encode the initiation factors for replication, which are mainly RNA molecules. Once the plasmid replication is initiated, it continues with the same machinery used by the bacterial chromosome.

Reference (Textbook): Bacterial Genetics, Margarita Pesheva (2000)


Free software for measuring parts of an image?

ImageJ is all you need. Particularly see the documentation sections on setting the image scale and measuring.


Standard Free energy of hydrolysis of phosphoenolpyruvate (PEP)

An answer to this is given in the online version of Berg et al.

  Why does phosphoenolpyruvate have such a high phosphoryl-transfer potential? The phosphoryl group traps the molecule in its unstable enol form. When the phosphoryl group has been donated to ATP, the enol undergoes a conversion into the more stable ketone—namely, pyruvate.

  Thus, the high phosphoryl-transfer potential of phosphoenolpyruvate arises primarily from the large driving force of the subsequent enol-ketone conversion

Note that Berg et al. use the term “high phosphoryl-transfer potential” or “high phosphoryl group-transfer potential”, as explained in sections 14.1.4 and 14.1.5. These sections are worth reading, and this terminology is worth following.


Mathematical representation of "gene signatures"

There are mathematical definitions of "gene signature". Please have a look at the supplemental material of Subramanian et al. PNAS 2005, one of the first papers on "gene signatures", and a method and tool which is still commonly used in basic research.

Note that Subramanian et al. have multiple definitions and that copying them here would exceed the scope of this page.


This is incredibly oversimplified, but the short answer is that both T and B cells can have degenerate recognition, though the molecular mechanisms are somewhat different.

T cells recognize linear sequences of amino acids that have been excised from their parent proteins, from 8 to 16 or so amino acids long, and that are associated with MHC proteins.  The association with MHC proteins depends on the specific sequence of amino acids, and you can think of this association as depending on a number of amino acids (let's say 4 or 5) that point "down" into the MHC.  That leaves maybe 4-10 amino acids pointing "up" that can interact with the T cell receptor.  If you search for a random set of 4 amino acids with a given spacing, it's quite likely that it will turn up several times in a large protein database; even more often if you allow some degeneracy (similar amino acids can substitute sometimes).  Therefore, yes, T cells tend to have a moderate amount of degeneracy in their epitope recognition.  However, while search a whole database may find duplicates, the degeneracy is not terrible, and the MHC binding requirement also reduces it quite a bit. Also, of course, during T cell development, TcRs that have broad and degenerate recognition of many structures are selected against.  So T cells are definitely cross-reactive, and sometimes extensively so, but in single individuals it's probably not a common thing.  (Ray Welsh and Liisa Selin have looked at cross-recognition between viruses and find quite a bit of cross-reactivity, though, so this may be understated.)

Antibodies, unlike T cells, recognize conformational epitopes rather than linear sequences.  However, just as with linear epitopes, it's not impossible for two unrelated proteins to end up with similar conformations, even with rather different amino acids.  As well, antibodies can be more or less "forgiving" in their recognition; some are extremely specific, but others can interact with a wider range of shapes.  You can imagine a "flat" antibody binding surface that is rather generic, that could interact with many different shapes. Again, B cells with broad cross-recognition are selected against during development, though not as rigorously as are T cells.


In the world of physics, you can distinguish between random motion (e.g. thermal Brownian walk) and directed motion (called ballistic: think of a cannon ball) by studying the mean square displacement of the object: you'll be able to fit this displacement as a function of time by a linear law if it is random, and by a quadratic one if it is directed. Exponents in between will give you an indication of the degree of randomness. The advantage of this (even if it is not specialized for your case) is that there's a large body of work using this, including for living organisms.

Note also that if your motion is as in the first case above, you'll have ballistic motion for times smaller than the travel time from left to right, and diffusive (random) for times larger than that. This has been used e.g. to analyse the run-and-tumble motion of bacteria who have a short-time ballistic motion and then after some time tumble to explore another randomly-chosen direction.

Example of this type of coexistence of two regimes:

In the field of biophysics, much of this was initiated by Howard Berg and coworkers

In your first case, you'll have an initial ballistic regime and then something that plateaus (because you stay between A and B). The transition time-lag will be the travel time between A and B.

In your second case, you'll be able to characterize the random walk: if the animal is aiming at going from A to B but randomly errs for short times, you'll have a short-time diffusive behaviour, and an intermediate time ballistic one. (And then again a plateau, as in the first case and for the same reasons). If the animal reaches B by mere chance, on the contrary, you'll have a diffusive regime only before this plateau.


It's only a partial answer, but a Nile crocodile can eat up to half its body weight at a sitting, according to National Geographic. Since few freshwater fish weigh half as much as a crocodile, we can probably assume these croc feasts occur when they're able to ambush ungulates (e.g. zebras and antelope).

So one guess is that a crocodile feasts on ungulates about fifty times a year, though its normal diet is fish. Of course, I could be wrong - perhaps five fish caught in the space of an hour are considered a full meal as well.

I never knew crocodilians ate fruit. (The link you provided doesn't mention fruit, by the way.) But this article says they can eat "large quantities" of fruit, suggesting they're looking for more than supplemental vitamins. But who knows? It sounds like scientists don't yet know much about fruit-eating crocodilians.


Why does sequencing virus proteins take time?

Sequencing a viral genome requires isolation of the virus, propagation in cell culture, extraction of nucleic acids, and preparation of a sequencing library.  Once sequences are obtained, a genome can be assembled de novo using (untargeted) shotgun reads, and gaps in the genome can be spanned with (targeted) Sanger sequencing.  This process can take weeks to months depending on the availability of resources and the growth characteristics of the virus.
For details on how the 2019-nCoV genome was sequenced, see Zhu et al., published January 2020:
A Novel Coronavirus from Patients with Pneumonia in China, 2019


What is the name of this tree with compound leaves?

It is Cussonia spicata,  It is one of the favorite foods of wild elephants.

The attractive leafs grow from the end of thick branches to form rounded heads.

Source

Wikipedia


Short answer
All of your sources are correct as they are not mutually exclusive. PCR is used to isolate and amplify DNA to yield small quantities of pure target product. Gene cloning can subsequently be applied to scale the production of the fragment up. PCR thus can be part of the DNA cloning process.

Background
Cloning in general simply means duplicating. Cloning in Biology refers to

  [Making] an exact copy of an animal or plant created in a laboratory from the
  animal’s or plant’s DNA

source: McMillan Dictionary

Gene cloning, as far as I understand refers specifically to the isolation of one single gene and inserting it into cells to amplify it:

  The production of a lineage of cells all of which contain one kind of DNA fragment of interest derived from a population of many kinds of DNA fragments.

source: Northwestern University

PCR is a technique to amplify a specific strand of DNA that can be used to subsequently clone DNA into host cells (source: New England Biolabs). The cloning is done to upscale the quantity of DNA. PCR uses primers and can be used to isolate and amplify the DNA up to the scale it is easily clonable.


Thermodynamics of spontaneous protein folding: role of enthalpy changes

Summary

The first explanation is commonly encountered.
The second explanation cannot be correct, as it stands, as it ignores the free energy change in the protein.
A modification of the second explanation (perhaps what was intended) is that it is necessary to consider the protein folding and change in the water as being coupled, in which case the overall free energy change — the sum of the two considered separately — is the determinant of protein folding. The assertion would then be that a negative free-energy change in the water system is the deciding factor. This view has been persuasively advocated on the basis of experimental measurements.

Free energy change in individual transformations

It is standard practice in biochemistry to consider the Gibbs Free Energy of transformation of the sort A → B in isolation in determining whether it will proceed spontaneously. A chemical reaction for which ΔG is negative may generate heat (i.e. have a negative enthalpy change (ΔH) ) which affects its aqueous surroundings, but it seems justified to consider the reaction in isolation as there is no sense that the change in the vibration of the water molecules is driving or coupled to the reaction.

This approach has been applied to the structural change of protein folding with the conclusion (consistent with the first explanation) that the change in enthalpy (ΔH) is sufficient to produce a negative ΔG and hence drive protein folding (Citation 1, below).

Free energy change in coupled transformations
Many biochemical changes involve transformations which individually have a positive free energy change, but are made possible by coupling to another reaction with negative free energy change, of greater magnitude:

  A → B , ΔG1 = +x

  C → D , ΔG2 = –y

If y>x and these two reactions are coupled (generally through a complex reaction path on an enzyme) , then we have:

  A + C → B + D , ΔGoverall = –ve

See also Berg et al.

Although one can reject the second explanation in the question as it stands because it ignores the free energy change in the protein folding, perhaps it was intended to mean that the folding of the protein (A → B) should be considered as coupled to the change in the environment of the water (C → D), and that the negative ΔG for the aqueous environment made a greater contribution to the overall ΔG than that for the protein folding.

Is it valid to consider these two systems as coupled? In the original version of my answer I argued against this point of view, but am no longer convinced by my own arguments. The water environment is clearly essential for the hydrophobic effect — the burying of the hydrophobic residues in the centre of the protein away from the water. This is evident if one considers the same protein in a hydrophobic environment such as a cell membrane — it would not fold. In membrane proteins it is hydrophobic residues that are exposed to the lipid bilayer and it is their interiors that sometimes have hydrophilic channels.

So in this coupled system, what is the determinant of the negative free energy change? Minikel (Citation 2, below) asserts that there is no net enthalpy change for the protein folding, and it is the entropy effect on the ΔG for the aqueous environment that drives the folding. He indicates that this view is supported by differential scanning colorimetry and, although he doesn’t cite references, there is a recent (if rather complex) review of this topic by Christopher M. Johnson.

Citation 1: Assertion of role of ΔH of protein

The following explanation, taken from Essential Biochemistry, treats the protein folding in isolation and asserts that change in enthalpy is sufficient to produce a negative free energy change:

  The folding of a protein also provides an example of the "ΔH" and "–TΔS" terms competing with one another to determine the ΔG of the folding process. As described above, the change in entropy of the protein as it folds is negative, so the "–TΔS" term is positive. However, in addition to entropic effects there are enthalpic contributions to protein folding. These include hydrogen bonding, ionic salt bridges, and Van der Waals forces. An input of thermal (heat) energy is required to disrupt these forces, and conversely when these interactions form during protein folding they release heat (the ΔH is negative). When all of these entropic and enthalpic contributions are weighed, the enthalpy term wins out over the entropy term. Therefore the free energy of protein folding is negative, and protein folding is a spontaneous process.

Citation 2: Rebuttal of role of ΔH of protein and assertion of role of water

The following explanation, taken from on-line lecture notes of  of Eric V. Minikel of Harvard University, rebutting the point of view above:

  An incorrect and simplistic view of protein folding is as follows. An unfolded protein has high configurational entropy but also high enthalpy because it has few stabilizing interactions. A folded protein has far less entropy, but also far less enthalpy. There is a tradeoff between H and S here. Note that because ΔG = ΔH - TΔS, increased temperature weights the S term more heavily, meaning that higher temperature favors unfolding.

  That entire explanation only considers the energy of the protein and
  not that of the solvent. In fact, hydrophobic domains of a protein
  constrain the possible configurations of surrounding water (see
  explanation above), and so their burial upon folding increases the
  water’s entropy. Moreover, it turns out that the hydrogen bonding of
  polar residues and the backbone is satisfied both in an unfolded state
  (by water) and in a folded state (by each other). Therefore enthalpy
  is “zero sum,” and protein folding is driven almost entirely by
  entropy.


Databases for gene regulatory network graphs?

For a free resource, try GenMAPP. Commercial products like Ingenuity Pathway Analysis do the same thing with prettier graphics and a curated approach to network-building, but access can be expensive if you're not affiliated with an institution that will foot the bill.


More proteins from diet when common cold and flu?

Your body needs more energy when you are ill to facilitate the recovery process which includes the production of white blood cells to help fight the infection. This shouldn't be limited to proteins though, carbs are also very important as they are provide high amounts of energy. Basically just making sure you eat a varied and balanced diet is more important when you are ill to make sure your body receives the nutrients it needs to fight infection and heal itself. As it is having to work harder when you are ill it makes sense to eat more high energy foods. Micronutrients are also very important!

  Minerals such as selenium and zinc work to keep the immune system strong. These minerals are found in protein rich foods such as beans, nuts, meat, and poultry. — Source

Although if your diet is varied you should be getting plenty of these anyway, without needing to take supplements.


Do we have evidence of heritable personality traits in chimpanzees?

There has been some research in order to explore this direction, for instance, see this reference:

A. Weiss et al. - "The Heritability of Personality Factors in Chimpanzees", Behavior Genetics, Vol. 30, No. 3, 2000.,

in which the authors study five human-like factors - Surgency,
Dependability, Emotional Stability, Agreeableness, and Openness.

Quoting verbatim their findings:

  Only Dominance ... was significantly heritable. Dependability showed evidence that it might be heritable, but the parameter estimates were not statistically significant ... Two other personality traits, Agreeableness and Emotional Stability, showed positive heritability estimates but the parameter
  estimates were nonsignificant and small. Openness and Surgency showed no evidence of heritability.

In fact, the statistical correlation between dominance and heritability makes a strong sense.  Here's what I make out of this - this was a correlation based study, or kind of an experiment, hence the stress on statistical significance. But the question it raises is - is there a causal relationship between the two, i.e. does there exist any proper mechanism for the inheritance of "dominance". Finding such a mechanism was clearly beyond the scope of this study, but I believe the requisite answer for your question is if one stumbles on to such mechanisms, and not statistical correlations, which are mere pointers.

But on the basis of the study at least, all that one can safely conclude is - statistical correlations suggest that inheritance of "dominance" appears plausible, but the exact mechanism of how this implements out in practice, is beyond the scope of this study.


Did Darwin explain why he believed that domestic dogs descend from several distinct species of ancestor?

"Does (Darwin) explain elsewhere his detailed reasons for his conclusion?"

Yes. After Origin of the Species, he wrote a whole book, The Variation of Animals and Plants under Domestication (1868), which begins with Chapter 1.I on "Domestic Dogs and Cats".

He writes that "we shall probably never be able to ascertain their origin with certainty" and then gives detailed sources for both sides of the argument. It's Pallas against De Blainville.

  Firstly, the great difference between the several breeds; but this
  will appear of comparatively little weight, after we shall have seen
  how great are the differences between the several races of various
  domesticated animals which certainly have descended from a single
  parent-form. Secondly, the more important fact, that, at the most
  anciently known historical periods, several breeds of the dog existed,
  very unlike each other, and closely resembling or identical with
  breeds still alive (...)

  (A)t a period between four and five thousand years
  ago, various breeds, viz. pariah dogs, greyhounds, common hounds,
  mastiffs, house-dogs, lapdogs, and turnspits, existed, more or less
  closely resembling our present breeds (...)

  As long as man was believed to have existed on this earth only about
  6000 years, this fact of the great diversity of the breeds at so early
  a period was an argument of much weight that they had proceeded from
  several wild sources, for there would not have been sufficient time
  for their divergence and modification. But now that we know, from the
  discovery of flint tools embedded with the remains of extinct animals
  in districts which have since undergone great geographical changes,
  that man has existed for an incomparably longer period, and bearing in
  mind that the most barbarous nations possess domestic dogs, the
  argument from insufficient time falls away greatly in value (...)

  The existence of a single race, remarkably constant in form during the
  whole Neolithic period, is an interesting fact in contrast with what
  we see of the changes which the races underwent during the period of
  the successive Egyptian monuments, and in contrast with our existing
  dogs. The character of this animal during the Neolithic period, as
  given by Rutimeyer, supports De Blainville's view that our varieties
  have descended from an unknown and extinct form.

At this point it's not looking good for Pallas. But Darwin continues:

  (W)e should not forget that we know nothing with respect to the
  antiquity of man in the warmer parts of the world. The succession of
  the different kinds of dogs in Switzerland and Denmark is thought to
  be due to the immigration of conquering tribes bringing with them
  their dogs; and this view accords with the belief that different wild
  canine animals were domesticated in different regions (...)

  The main argument in favour of the several breeds of the dog being the
  descendants of distinct wild stocks, is their resemblance in various
  countries to distinct species still existing there.

Moreover,

  (s)everal canine species evince no strong repugnance or
  inability to breed under confinement; and the incapacity to breed
  under confinement is one of the commonest bars to domestication.
  Lastly, savages set the highest value (...) on dogs: even half-tamed
  animals are highly useful to
  them: the Indians of North America cross their half-wild dogs with
  wolves, and thus render them even wilder than before, but bolder: the
  savages of Guiana catch and partially tame and use the whelps of two
  wild species of Canis, as do the savages of Australia those of the
  wild Dingo. Mr. Philip King informs me that he once trained a wild
  Dingo puppy to drive cattle, and found it very useful. From these
  several considerations we see that there is no difficulty in believing
  that man might have domesticated various canine species in different
  countries. It would indeed have been a strange fact if one species
  alone had been domesticated throughout the world (...)

  If any wild canine species had distinctly exhibited the tan-coloured
  spots over the eyes, it might have been argued that this was the
  parent-form of nearly all our domestic races. But after looking at
  many coloured plates, and through the whole collection of skins in the
  British Museum, I can find no species thus marked. It is no doubt
  possible that some extinct species was thus coloured (...)

  The belief that our dogs are descended from wolves, jackals, South
  American Canidae, and other species, suggests a far more important
  difficulty. These animals in their undomesticated state, judging from
  a widely-spread analogy, would have been in some degree sterile if
  intercrossed; and such sterility will be admitted as almost certain by
  all those who believe that the lessened fertility of crossed forms is
  an infallible criterion of specific distinctness. Anyhow these animals
  keep distinct in the countries which they inhabit in common. On the
  other hand, all domestic dogs, which are here supposed to be descended
  from several distinct species, are, as far as is known, mutually
  fertile together (...)

  Pallas assumes (...) that a long course of domestication eliminates that
  sterility which the parent-species would have exhibited if only lately
  captured; no distinct facts are recorded in support of this
  hypothesis; but the evidence seems to me so strong (independently of
  the evidence derived from other domesticated animals) in favour of our
  domestic dogs having descended from several wild stocks, that I am
  inclined to admit the truth of this hypothesis.

  There is another and closely allied difficulty consequent on the
  doctrine of the descent of our domestic dogs from several wild
  species, namely, that they do not seem to be perfectly fertile with
  their supposed parents. But the experiment has not been quite fairly
  tried; the Hungarian dog, for instance, which in external appearance
  so closely resembles the European wolf, ought to be crossed with this
  wolf: and the pariah dogs of India with Indian wolves and jackals; and
  so in other cases. That the sterility is very slight between certain
  dogs and wolves and other Canidae is shown by savages taking the
  trouble to cross them.

Concluding:

  Notwithstanding the difficulties in regard to fertility given in the
  last two paragraphs, when we reflect on the inherent improbability of
  man having domesticated throughout the world one single species alone
  of so widely distributed, so easily tamed, and so useful a group as
  the Canidae; when we reflect on the extreme antiquity of the different
  breeds; and especially when we reflect on the close similarity, both
  in external structure and habits, between the domestic dogs of various
  countries and the wild species still inhabiting these same countries,
  the balance of evidence is strongly in favour of the multiple origin
  of our dogs.

In short the main support for multispecific origin is that different breeds of the domestic dog, differing from each other in many physical respects, are very ancient and they are similar to wild species in the same geographical areas.


NCBI-geo differences between platforms,series and samples

The platform at NCBI-GEO means the particular microarray that was used (because originally most of GEO was just microarrays), OR, more recently, it could mean the type of NGS machine that was used.  For example, every microarray manufacturer creates an ADF (array data file) that maps the DNA sequence at every position on the Chip to an accession ID. And this ADF mapping file gets registered at GEO as a GPLxxxxxx. This was presumably to facilitate direct comparisons between different experiments from various labs using identical Chips (e.g. Affymetrix, or Nimblegen).

With the advent of NGS the Platform has to be a name from an approved list of companies and devices: ILLUMINA, HiSeq, etc.

A series is constructed by the data providers and allows them to cluster the results from related samples. So, for example, in the modENCODE consortium, I believe all of the C. elegans RNA-Seq from Bob Waterston's lab/Project are clustered together under one overarching GSExxxxxxx. More details at www.modencode.org and links therein.


Self-fertile PRUNUS: Approximately how much of the genome gets rearranged by meiosis?

It makes little sense to give a percentage of the genome impacted by recombination and segregation. I think you should read about segregation and recombination and that would be clear to you why giving a percentage makes little sense.

Segregation

Segregation causes that the two haplogroups of the parent can be rearrange at the among chromosome level. So, for example if, in this lineage, each individual has 3 pairs of chromosomes. Let's denote each haplogroup by a capitalize vs non-capitalize letter, we can represent the genome as

a|A b|B c|C

Without segregation (and recombination), a parent could only transmit either

a b c

or

A B C

in a given gamete. This results in the three possible zygotes

a|A b|B c|C
a|a b|b c|c
A|A B|B C|C

segregation allows the creation of gametes like for example

A b C

resulting in possible zygotes such as for example

A|a B|B c|C

Recombination

Recombination typically occurs at a rate of one recombination event per chromosome (that is 100 centiMorgan per chromosome as a rule of thumb; see here to understand what a centiMorgan is). Further rearrange creating new haplogroup from the two existing haplogroups. So for example, from the pair of chromosome

A|a

an individual could create a new haplogroup from recombining the end of A with the beginning of a (or vice-versa).

Related posts

There are probably a lot of related posts. Here are a few of them:

Do only one or both pairs of homologous chromatids exchange genetic material during the process of crossing over?
Gene distance and Recombination Frequency: Mechanism
Is the discovery of dominant and recessive genes the only reason Mendel matters?
What is Mendelian Segregation and how is it related to the Hardy-Weinberg equilibrium?
Genetic linkage greater than 50 centimorgans
What are the exceptions of Mendel's laws?


True or False: Vaccines are designed to protect against invaders that are encountered rarely, not all the time

Not true. Vaccines were initially made for the highly contagious diseases that used to cause epidemics (which obviously means they were not rare).

The efficacy of a vaccine depends on multiple factors which includes adaptability of the pathogen.

The all-the-time encountered pathogen that the article is talking about is HIV; the reason for why no effective vaccine exists for it is because it has high mutation rate.


How long can Vibrio cholerae live in its ambiental optimal context?

I Found It!!!!    SURVIVAL OUTSIDE HOST: Cholera can survive in well water for 7.5 ± 1.9 days and the El Tor biotype can survive 19.3 ± 5.1 days(Footnote 21). The bacterium can survive in a wide variety of foods and drinks for 1-14 days at room temperature and 1-35 days in an ice box(Footnote 21). It has also been found on fomites at room temperature for 1-7 days(Footnote 21).

Source>>http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/vibrio-cholerae-eng.php


It looks like an Imperial Moth (Eacles imperialis):

Source: https://www.butterfliesandmoths.org/species/Eacles-imperialis

As shown on the distribution map at this link, they can be found in central Illinois.


Walk me through microsatellite markers and PCR

It's actually very simple. You misunderstood the term polymorph in this situation.

A microsatellite is a sequence composed of a short repeated DNA motif. A polymorph satellite is then simply a microsatellite varying in length between individuals, i.e. composed of more or less repeats of the motif.

The flanks of the microsatellite are the DNA sequences targeted by the primers.

In essence, using two primers flanking the microsatellite you will amplify this specific DNA region and because it varies in length between individuals you can detect that by simple gel electrophoresis.

Note: Microsatellites can also change in sequence (also called polymorphic regions) as they are prone to a high-mutation rate but in this case you would need to sequence it to know how the sequence differs between individuals.


Location of nucleotide synthesis and transport

Correct, all but one step in pyrimidine synthesis occurs in the cytosol, and purine synthesis occurs in the cytosol only.

Nucleotides freely diffuse through nuclear pores but are actively transported through mitochondrial membranes via embedded membrane transport proteins (i.e. ATP-ADP translocators, GTP transporters, and pyrimidine nucleotide transporters).

http://themedicalbiochemistrypage.org/nucleotide-metabolism.php


Are lymphocyte sizes clustered in two groups?

Unlike erythrocytes that have a very rigid shape and almost cannot change their size (hence the size distribution is indicative and can be used for diagnostic purposes in medicine), lymphocytes can change their size in a wider range, this is why you see the numbers 6-9 and 10-15 μm.

And they indeed cluster into several different groups: so-called "large granular lymphocytes", also known as NK-cells or "natural killers" (usually >10μm) and "small granular lymphocytes", constituted by a large family of T- and B-lymphocites(usually <10μm). But this clustering is not really distinct, for as I said above, both NK and T/B-cells can shrink (if the osmolarity of the external medium grows due to acidosis, inflammation etc.) and swell (on binding many IgE/IgG complexes, on certain cell factor released etc.). Besides, there are also some intermediate size cells, called NKT-cells, that also flatten the distribution.

So, what you can definitely say is that the typical size distribution of lymphocytes has two peaks: around 8 and 12 μm respectively.


maximum # of generations possible in a population of cannibalistic rats

Here's a back of the envelope answer: one generation if you have a LOT of rats.

Numbers according to the Great State if Indiana.
Assuming also that we start with adult breeding rats.  50% females / 50% males.
The gestation period is 21 days.
The adult rat can eat 1/3 of its body weight each day. Assuming that the rat is eating about 80% of the 'victim' rat body weight, the colony reduces in size about 40% each day.

Lets say the rats are going to be a bit hungry and the colony loses 30% of its size each day. And they don't eat their own feces, which I think they can do, but also assuming that the malnutrition from eating only rat for food will not cause problems.

Over the period of gestation, 21 days the colony will have a final size of 0.3^21 = 0.000559 times its original size.  So in order to have a surviving gestating female you'd have to start with 1791 rats.  Also assuming that the last rat is a very pregnant female who can compete with the male cannibals who are not pregnant.

Then the average litter is not 1790. So you'd need something like 1790^N rats for N generations.  and they'd have to be pretty lucky rats to boot.

BTW similar numbers would be true for any animal including human beings. This is one reason that cannibalism is usually only a social ritual, not a means of acquiring nutrition except in extreme cases.


Yes, GMO are safe to consume! See Is Genetically Modified food safe to consume?. Now, there are other (potential or real) issues related to the use of GMOs such as for example a loss of genetic diversity if every farmer plant the exact same strain. Talking about such issues will require talking about ethics, economy and sociology and it can therefore not be answered in a science website only.

Your teacher's argument does not make much sense (although a direct quote would have been helpful). GM plants also have to develop. They are organisms too!

  [W]hat are disadvantages of selective breeding to compare with genetic modification?

Keep in mind that it is practically impossible to define GMO. Many of the things that we would call GMO actually don't result from much more than just selective breeding. Following this logic corn, wheat, sunflower oil, lettuce, broccoli, cauliflower, peanuts and pretty much everything else you eat is a GMO.

Attempting to let aside the semantic issue a comme argument is a lack of lack of familiarity and this is why extra precautions and testing must be done. See What risks exist with GMO, but not with selective breeding?

  can I use the mutagenesis as the example of selective breeding [..]?

Mutagenesis and selective breeding are two different processes (although often used together). One is not an example of the other.


Alternative Heart Morphologies

Amphibians and some reptiles have a three-chambered heart, with 2 atria and a single ventricle. There are still separate circulatory pathways for the lungs and the rest of the body, but the oxygenated and oxygen-depleted blood mix in the ventricle, and are pushed at the same time to the lungs and body.

The disadvantage of this system is that it is less efficient at providing oxygen to the body than a four-chambered system, because the blood pumped to the body is a mixture of blood that has recently been to the lungs and blood that has not.

You seem to be suggesting another system, where there is just one serial pathway from heart to lungs to body, or from lungs to heart to body. This is more like the two-chambered heart of a fish: blood is pumped from the heart through the gills, and then to the body.

Lungs and body in series, and fluid dynamics

So why wouldn't this work for a mammal? It could, but gills and lungs are very different. The vasculature of the lungs requires a lot of pressure to get through, which is generated by the right ventricle.

Pressure is required to push fluids through a constriction (note that even a straight pipe is a constriction). After a fluid passes a constriction, there is always a pressure drop. That pressure drop is a function of the rate of flow and size of the constriction. If you give less pressure at the start, there is less pressure to "drop", and so you get a lower flow rate (note that this is nearly a perfect analogy with electricity, where flow is current, pressure is voltage, and the size of the tube is the conductance).

If you want to pass through a second constriction, you have to use pressure that is "left over" after the first drop: you can't use the pressure you started with because that was lost getting you through the first constriction. In reality, in a closed system, the total flow rate will be determined by the summed series resistance, so adding a second constriction slows the flow rate for the whole system, and you get a partial pressure drop after each.

If you put the lungs and body in series with each other, no matter which comes first, you need to have enough pressure left over when you pass one to get you through the next one, otherwise the flow will slow down. Blood in a human aorta has a mean pressure around 100mmHg, whereas back in the vena cava it is close to 10mmHg. That suggests you need about 90mmHg to get enough flow through the body's circulation. The lungs use a little less, but you still have a pressure drop of around 50-60mmHg. Therefore, you would have to increase the blood pressure by 50%-75% to get circulation through both lungs and body.

Higher pressures lead to more turbulent flow and take more effort to achieve. The four-chambered heart, with 2 ventricles, is simply more efficient.


What is the depression between bridge of nose and brow called?

Nasion [New Latin nāsion : nas(o)- + Greek -ion, diminutive suff.] is the region below glabella , also known as the bridge of the nose.

  The nasion is the midline bony depression between eyes where the frontal and two nasal bones meet, just below the glabella.It is one of the skull landmarks, craniometric points for radiological or anthropological skull measurement.

Source:https://radiopaedia.org/articles/nasion


Neandertal DNA has been completely sequenced multiple times now, using DNA from bone and tooth samples found in cool or cold environments.  The first Neanderthal genome sequence was described in 2010:

A Draft Sequence of the Neandertal Genome

Since then, as well as higher-quality sequence, more genomes have been completed; at least 6 individuals have been sequenced (perhaps more; I've lost track a little).  As well, complete genome sequences from several Denisovans -- a Homo species that were approximately contemporary with Neandertals, but a distinct species -- have been recovered.

The science of recovering ancient DNA has advanced very rapidly in the last decade, and while it isn't routine to sequence 50,000-year-old DNA it isn't as magical as it used to be.  The current record for sequencing ancient DNA is 700,000 years, which is earlier than the sapiens/neandertalis split.


Is covid vaccine helpful for a covid patient?

In short, no. It's not harmful but it won't do anything to prevent or mitigate the current infection.
How vaccines work in general is that they train the immune system to respond to an infection so that they are prepared for it. Generally protein component of the virus or an inactivated form of the pathogen is used as a vaccine. The immune system recognises the proteins as 'foreign' and develops anti-bodies to fight them. Then you are immunised to the virus without having to suffer the symptoms of infection. Vaccines work before you are infected as a preventative measure. Then when you are infected, the immune system is prepared and can fight of the virus with the antibodies already developed since the virus has the same "antigen" proteins as you immune cells have already been exposed to from the vaccine.
So what happens when you are vaccinated when you are already infected? Basically nothing.
The benefit of a vaccine is a head-start to train your immune system how to fight it to prepare for the early stages of infection. If you are vaccinated, your immune system will destroy the virus before the it multiplies or gives you symptoms. If you've already been infected then the active virus has already infected many of your cells and multiplied into many copies. Adding inactivated viral particles or spike protein antigen won't help your immune system, it's already been exposed to them by the ongoing infection. Your immune cells are just playing catch up to the infection that's already taken hold. The virus has already stormed the beaches and the immune cells were not prepared. Vaccination now is arguably pointless. They will eventually produce antibodies against the virus already in your system even if you weren't vaccinated.
Lasting immunity after recovering from infection is not guaranteed and a vaccine could give immunity to other strains. For these reasons, it could still be recommended by medical professionals if you've already been infected. However, you need to be vaccinated before exposure to the virus for it to be effective. A vaccine is not a treatment.
Note: the currently available AstraZeneca, Pfizer, Moderna, and Johnson & Johnson vaccines for SARS-CoV-2 do not contain live or inactivated coronavirus. They trick the host system into producing the spike protein from instructions carried by the vaccine.
Citation for clinical application: Jenner, E (1798) An Inquiry into the Causes and Effects of the Variolae Vaccinae.


Since b/w screening is a means to  selection, you want maximum selection pressure. This will be obtained by incorporating all optimal conditions. The many enzymes of the lac operon are going to function best at their optimal temp.

Why would you do this? If it is because you can't go in the next day it's better to do it when you're available. You're only going to doubt your results when you get them.


How do firing patterns arise from the activity of many ion channels?

Typically the activities of the ion channels are not called firing patterns as in neuroscience we refer to "firing" when we mean the elicitation of action potentials (spikes) but yes: Whenever an AP was fired a sufficient amount of sodium channels had to be open and therefore I thing your reasoning is correct. In other terms what you are saying is that the effective channel conductances change during an action potential.

On your conclusion: In the regime of natural parameters the time scale of firing pattern 1 mostly depends on the time constants of the voltage gated ion channels and not so much on the absolute number of channels (especially if all the conductances would scale equally).
In the world of Hodgin-Huxley like coupled- and nonlinear-dynamical systems the voltage does not scale strictly linear with increasing the participating max. conductances. The interplay of max. conductance and temporal gating dynamics resulting in the effective conductance itself depends on the voltage and there are nonlinearities. So the correlation between the number of channels and the AP rise time is not expected to be strictly linear.

See the figure for a little example: I tested my reasoning by increasing the max. conductance for the sodium channel of a simple HH model and checked the max. steepness of the voltage (normalized by peak voltage).

Hope that answers your question(s).


Can anyone identify this spider for me, please?

The spider on your ceiling looks like a sac spider, more a Cheiracanthiid (like a yellow sac spider) than a clubionid (a leafcurling sac spider).
But the colour contrast of the dark red thorax to yellow abdomen suggests it may be broad-faced sac spider, which a is actually classified closer to a wolf spider than to the above two sac spiders. It is considered non-aggressive and non-harmful to humans.
It is hard to tell from the photo whether the cephalothorax is actually red or just dark. So you are probably the best judge from here.
Compare what you saw to:

trachelas tranquillus (broad-faced sac spiders) https://bugguide.net/node/view/26291/bgimage?from=72
cheiracanthium (yellow sac spider) https://bugguide.net/node/view/3383/bgimage?from=0


Which is the most extreme thermophilic bacteria known?

Geogemma barossii, initially designated Strain 121, can survive and reproduce at 121°C, with an optimal growth temperature of 103°C. It's not a bacterium though, but a member of the Archaea domain.


Why do our epiphyseal plates close up in our late teens or early twenties?

During Endochondral ossification  chondrocytes in the plate are rapidly dividing, newer daughter cells stack facing the epiphysis while the older cells are pushed towards the diaphysis. As the older chondrocytes degenerate, osteoblasts ossify the remains to form new bone.

In puberty increasing levels of estrogen, in both females and males, leads to increased apoptosis of chondrocytes in the epiphyseal plate. Depletion of chondrocytes due to apoptosis leads to less ossification and growth slows down and later stops when the entire cartilage have become replaced by bone, leaving only a thin epiphyseal scar which later disappears. Once the adult stage is reached, maximum height is reached.

Your question addresses the genetics of this process however it is more so regulated by the endocrine system. There has not been a single gene assigned to growth plates, or its regulation, and I find it unlikely that there ever will be.

Rather, endochondrial ossification takes place because of hundreds of genes interacting with each other. If you start to look at genes involved in apoptosis and the estrogen receptor pathway, you will begin to appreciate more the complexity behind the physiology.

I have a hunch you were looking for a gene, that with age just shuts off, or turns on. Recent evidence has show this does in fact happen as methylation may be a candidate mechanism of mediating not only environmental, but also genetic effects on age-related phenotypes.

http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1002629


Does estrogen increase muscular growth in females?

The article named "Estrogen replacement and skeletal muscle: mechanisms and population health supports this hypothesis, when applied to postmenopausal women:

  Evidence suggests that HT will also help maintain or increase muscle mass, improve postatrophy muscle recovery, and enhance muscle strength in aged females.

This particular passage suggests it might not be exclusive to postmenopausal women:

  One of the reasons for the relatively new interest in estrogenic effects on skeletal muscle was the identification of estrogen receptors (ER) in this tissue.

Passage containing more specific information:

  Although research findings over the past 20 yr have reported conflicting results of HT on muscle mass in postmenopausal women, the preponderance of more recent evidence has “tipped the balance toward a positive and measurable impact of HT” and have highlighted the “proanabolic” effects of HT on skeletal muscle. Several recent studies examining postmenopausal women showed significantly greater muscle mass in women taking HT relative to nonusers.


Proof of the equivalence between two ways of defining ESS

We need to show that if $\mathbf{p}$ is a strict Nash equilibrium, $E(\mathbf{p},\mathbf{p})> E(\mathbf{q},\mathbf{p})$, then $W(\mathbf{p}) > W (\mathbf{q})$ for some sufficiently small $\epsilon$. When $E(\mathbf{p},\mathbf{q}) \geq E(\mathbf{q},\mathbf{q})$, $\mathbf{p}$ clearly dominates $\mathbf{q}$.The less obvious case is when $E(\mathbf{p},\mathbf{q}) < E(\mathbf{q},\mathbf{q})$.

Since $E(\mathbf{p},\mathbf{p}) - E(\mathbf{q},\mathbf{p})>0$, there should be a strictly positive number $k$ such that
$$k[E(\mathbf{p},\mathbf{p}) - E(\mathbf{q},\mathbf{p})]+ E(\mathbf{p},\mathbf{q}) - E(\mathbf{q},\mathbf{q})>0$$
is true. Whatever this number is, we can write $k$ as $(1-\epsilon)/\epsilon$ for $0<\epsilon<1$. Substituting this into the equation above gives us the desired result.


It's more an issue of the extent of reflux than anything else. If you look at the data on scarring, you'll see that grade III and IV VUR present with lateral scarring as well. So, any pyelonephritis that is associated with gross dilation of the ureter and collecting system will give diffuse scarring. Mild dilation, you'll get scarring where the reverse flow goes first. I can't answer the question about why the reverse flow goes to the poles first. The authors of the paper I linked have their own speculation. Robbins has another. Neither have evidence on the mechanism.


From Study.com >>

On the off chance that nondisjunction happens amid anaphase II of meiosis II, it implies that no less than one set of sister chromatids did not isolate.

In this situation, two cells will have the typical haploid number of chromosomes. Additionally, one cell will have an additional chromosome (n + 1) and one will miss a chromosome (n - 1) due to the nondisjunction of the chromosomes.

Here is a picture reference taken from Google.ca >>

In the image provided in the question, the chromosomes are not indicated clear and concisely, so it is very hard to follow through the logic of segregation of the daughter cells to (n + 1) and (n - 1) chromosomes.

As you can see from the updated image reference in the answer, we can notice that the cell that underwent nondisjunction in anaphase 2 gives rise to 2 daughter cells, in which, one cell receives the non-segregated chromosome plus one copy of a sister chromatid which makes it (n + 1) and the other daughter cell receives one segregated sister chromatid ONLY which makes it (n - 1).

On an additional note, from Biology Exams 4 U >>

  Fusion of n+1 gamete with normal gamete (n) = 2n + 1 or Trisomic.

  Fusion of n-1 gamete with normal gamete (n) = 2n - 1 or Monosomic.

  In short, Nondisjuntion in meiosis II leads to trisomy (2n+1) or
  Monosomy (2n-1).


Males of the carnivorous Jackson's chameleon (Trioceros jacksonii) have three hornlike structures on their heads (also found in a couple of related species). From what I know, these are true horns, which means that they are pointed keratin-covered protrusions that have a core of living bone, see e.g. this website from Toronto Zoo (this page also claims that their horns show annual growth rings). However, there are many definitions of horns (some only consider the horns in Artiodactyla to be "true" horns), so you need to be specific in what you are asking for. Used casually, the antlers of Cervids or other similar structures, are often considered as horns.

As for birds, the closest thing to a horned bird I can think of are species of the Australian Cassowary (Casuarius). They have a bony crest on the top of their heads, which is covered by keratinous skin. However, the bony crest is supposed to be relatively soft and spongy, and can hardly be counted as a horn is the strict sense of the word.

(Southern cassowary, Casuarius casuarius, from Wikipedia)


What is the maximum number of babies a human woman can have?

How do you define the biological limit?

It very much depends on how you define a biological limit. If you prefer, it very much depends on how you define a human! Some women are completely sterile while others are highly fertile and there is genetic predisposition to that.  How much "perfect" should the genotype of an individual be so that it is still considered as a human? There is genetic variance underlying fecundity that is important to consider. For example, in your calculation you took lifespan as a constant but it obviously is not a constant. Fecundity is reduced by all these small mutations segregating in the human populations that reduce the fecundity of any single human. There exist no human that is free from all deleterious alleles. Imagine a giant woman with 10 independent reproductive system! Would she still be a human? That was probably kind of a too extreme thought experiment. Imagine a woman that can have a reproductive lifespan of 100 years. Would it still be a human? The issue behind this question reminds me an old post (now closed, I can't find it anymore) that asked whether a leopard would run faster if it had more legs. Well... one can imagine something running faster than a leopard, but it would not be a leopard anymore. So how many changes from a leopard are we allowed to make to answer the question. So I had to chose a definition of what a "perfect woman" is. Or a definition of a woman that would set this so called biological limit.

The definition I am using to answer this question

In the below answer, I will assume that by biological limit you mean the expected fitness of a female that would live in the same environment than we live in today but would not carry any single of the deleterious locus that are segregating in the human population. In other words I assume that you accept that the "perfect woman", that is a woman that would not carry any single of the deleterious mutations that segregate in the populations will set this biological limit to woman maximal fecundity.

Mutation load Theory

The decrease in the mean fitness of an idealized population where no deleterious mutations would exist compared to the realized mean fitness of a population is called the mutation load. The mutation (in an infinite population) is a function of the genome-wide mutation rate only. Let the genome-wide mutation rate in human be $U=2.2$, the mutation load $L$ in the human population is equal to $L=1-e^{-2.2}=0.89$. The estimates are taken from this video. You may want to have a look to the video in order to have a better understanding of why $L=1-e^{-U}$ and what are the assumptions of these calculations. The main assumptions are 1) infinite population size, 2) multiplicity of fitness effects at different loci and 3) additivity of fitness effect between alleles at the same locus.

So what does mutation load theory predicts?

The above calculation means that segregating deleterious allele reduce the fitness of the average woman by 89%! If we assume that an average woman can have 10 babies (this number is just a random guess) if she wants to, then the maximum biological limit of a "perfect woman" (in a world where there is no more competition than the one in which we are living) is $\frac{10}{1-0.89}≈91$  babies!

According to wikipedia, the world record is 69 and is owned by Mrs. Vassilyev. It is reasuring to see that the observed world record (69) is lower than the the biological limit we just calculated (91). If we were to know the distribution of maximal number of babies per woman (not to be confused with the realized number of babies), we could calculate the probability to have 69 or more babies and compare this probability to the total number of females that has ever lived (or the total number of females that would have never had the idea to have so many babies). Always according to wikipedia, the world record for men would be 867 and is owned by Ismail Ibn Sharif. However, sounds possible to me (but I really have no idea) that some sperm donor may have overshoot this number today.


Where does the carbon in new spring leaves of a deciduous tree come from?

While I can't provide references to actual studies, simple observation suggests that it must be stored in the roots, at least in part.  That observation is the existence of maple syrup (and other tree syrups, such as birch: https://practicalselfreliance.com/trees-species-tap-syrup/ In the spring, before leaves start to grow, sugar-rich sap rises from the roots, and can be collected by tapping the tree.


Why is succinate dehydrogenase attached to the inner mitochondrial membrane?

The reason behind this lies in the properties of FAD+. Unlike NAD+, FAD+ is not free to diffuse within the mitochondrion, it is an integral part of the inner mitochondrial membrane. Its reduced form FADH2 contributes electrons directly to ETC.


Counting the number of hydrogen bonds of multiple PDB files

The number of hydrogen bonds cannot actually be said from software only inferred. But you could try using STRIDE (http://structure.usc.edu/stride/) which takes the file name with a -h flag to output the number of hydrogen bonds. You could then write a small shell script which would pass in each file and store the data you wanted in whatever format you liked.


Does this patient have HHV6 or HCMV after transplant surgery?

I get the feeling that there's something we should probably know from your textbook or notes that you have not included. As-is, here's my best shot:

It is impossible to determine if Patient A was infected by the transplant since the virus they had before the transplant is the same virus carried by the transplant itself. Without running further tests to separate the two lineages you can't tell. It's likely, though.
While HHV6 has been known to precede HCMV in certain cases the conditions don't seem to apply here. My best guess, which is something I'm pretty loathe to say, is that if you're positive the tests are accurate then it's possible that Patient B's immune system alternately suppressed each virus below detectable levels. Since Patient B is receiving donor tissue with both viruses, and transplant patients are put on immunosuppressants following surgery, it could simply be that at first the immune system was capable of dealing with HCMV for the first week, but not HHV6. Then as it adapted to HHV6, HCMV evolved to evade so it showed up on the assays. That is entirely speculative, though. Another explanation might be that the viral titers of HCMV were too low to detect at Week 1, but it had reproduced enough to show up at Week 3 while the immune system dealt with HHV6. There's a lot of information that's missing on how the virii behave, the characteristics of the immunosuppressants given to the patient, and so on.
Patient C was clearly infected with nothing. They already had HHV6, and that's what showed up post-op.
Patient D was infected with HHV6. They had HCMV before, and both after.
Patient E was infected with HCMV, although like Patient A they could have been infected with a different strain of HHV6 as well, but the tests probably aren't specific enough to determine viral lineages for the before and after strains.


why finger of hands and feet become wrinkled due to to water?

There are a few hypothesis around it, but it is known that its associated with the function of distal nerves of the hands and feet. I suggest reading this short case for a glimpse at this - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2464382/

Also another tip I can give is that professional swimming athletes for example, eventually experiment an adaptation process in which this wrinkling reaction diminishes due to being exposed to the same stimuli repeatedly and for long periods of time.


Great question. It is unfortunate that more people don't understand what "radiation" is and how it affects biology.
Firstly, you must distinguish between ionizing radiation and non-ionizing radiation.
Wikipedia describes the former rather well:

Ionizing (or ionising) radiation is radiation composed of particles that individually carry enough kinetic energy to liberate an electron from an atom or molecule, ionizing it. ...
When ionizing radiation is emitted by or absorbed by an atom, it can liberate an atomic particle (typically an electron, proton, or neutron, but sometimes an entire nucleus) from the atom. Such an event can alter chemical bonds and produce ions, usually in ion-pairs, that are especially chemically reactive.

X-rays, alpha, beta, and gamma radiation are all ionizing forms of radiation. Non-ionizing radiation, as you might guess, is radiation of a sort which lacks enough energy to to strip an electron from an atom. All light is actually "radiation."
The reason why ionizing radiation can be so damaging is because the molecular underpinnings of our cells depend on many very specific chemical bonds. Changing those bonds can damage or even break anything from proteins to strands of DNA itself. Our bodies naturally try to repair damage, but the amount of damage is a crucial factor in how successful our bodies can be. More radiation means more damage; also greater amounts of radiation increases the chances of serious genetic damage to one or more cells. Damaging a cell's rulebook in just the right ways can disable its repair processes and even its fail-safes that keep it from becoming a hazard to the rest of the body (such as growing uncontrollably into a cancerous tumor).
A more in depth explanation of radiation effects can be found at http://www.epa.gov/radiation/understand/health_effects.html#q1

In general, the amount and duration of radiation exposure affects the severity or type of health effect. There are two broad categories of health effects: stochastic and non-stochastic.
Stochastic Health Effects
Stochastic effects are associated with long-term, low-level (chronic) exposure to radiation. ("Stochastic" refers to the likelihood that something will happen.) Increased levels of exposure make these health effects more likely to occur, but do not influence the type or severity of the effect.
Cancer is considered by most people the primary health effect from radiation exposure. Simply put, cancer is the uncontrolled growth of cells. Ordinarily, natural processes control the rate at which cells grow and replace themselves. They also control the body's processes for repairing or replacing damaged tissue. Damage occurring at the cellular or molecular level, can disrupt the control processes, permitting the uncontrolled growth of cells cancer This is why ionizing radiation's ability to break chemical bonds in atoms and molecules makes it such a potent carcinogen.
Other stochastic effects also occur. Radiation can cause changes in DNA, the "blueprints" that ensure cell repair and replacement produces a perfect copy of the original cell. Changes in DNA are called mutations.
Sometimes the body fails to repair these mutations or even creates mutations during repair. The mutations can be teratogenic or genetic. Teratogenic mutations are caused by exposure of the fetus in the uterus and affect only the individual who was exposed. Genetic mutations are passed on to offspring.
Non-Stochastic Health Effects
Non-stochastic effects appear in cases of exposure to high levels of radiation, and become more severe as the exposure increases. Short-term, high-level exposure is referred to as 'acute' exposure.
Many non-cancerous health effects of radiation are non-stochastic. Unlike cancer, health effects from 'acute' exposure to radiation usually appear quickly. Acute health effects include burns and radiation sickness. Radiation sickness is also called 'radiation poisoning.' It can cause premature aging or even death. If the dose is fatal, death usually occurs within two months. The symptoms of radiation sickness include: nausea, weakness, hair loss, skin burns or diminished organ function.

Another thing to understand about why the dose matters is that we are surrounded by ionizing radiation. We always have been. Our bodies have evolved needing to successfully deal with ionizing radiation. You can find a very informative and fun visualization of this fact at https://xkcd.com/radiation/.


Effect of single-gene overexpression in the cell's response

Which are the factors that modify the overall gene differential
  expression by introducing a vector for single-gene overexpression

This is a very relevant question and the field of experimental biology needs to revisit the experimental strategies.

One of the explanations that you gave is correct- that the overexpressed protein might override the cellular processes.

Another problem that this practice gives rise to is incorrect inference. We are mostly interested in knowing what a protein does in a cell at general physiological conditions. If the stoichiometry is altered wrong results will definitely pop up.
For example in the case of a repressor/activator with multiple targets: At its general physiological concentration it may not really activate gene-X because of low affinity but in high concentrations it just may, and we end up concluding that gene-x is a target of repressor-1 by an OVEREXPRESSION experiment.

A synthetic biological approach is very good in studying small signaling/transcriptional modules. The entire module can be cloned and expressed in a cell under an inducible/constitutive promoter. This can be implemented in a heterologous cell also. A mathematical model generally helps in making certain predictions.

Other strategies which can be used instead of overexpression:

using sensor constructs harboring a functional or non-functional
target sites instead of overexpressing the upstream protein
downregulation experiments


Effects of smoking tobacco compared to inhaling other smoke

(at an epidemiological scale)
WHO on tobacco

more than one billion smokers worldwide...
Tobacco kills nearly 6 million people each year.

WHO on indoor air pollution

Around 3 billion people still cook and heat their homes using solid
fuels in open fires and leaky stoves. About 2.7 billion burn biomass
(wood, animal dung, crop waste) and a further 0.4 billion use coal...
Nearly 2 million people a year die prematurely from illness
attributable to indoor air pollution due to solid fuel use.


Nonlinear (Quadratic) selection gradients formula

Coefficient $1/2$ is a matter of definition/convenience. One could have written $\beta x_i + \gamma x_i^2+\bar{w}$, but then a factor of $2$ would surface in the other forumals.
The other two equations are adapted to one-dimensional case (one trait) from the Lande and Arnold's paper The measurement fo selection on correlated characters. In particular, the equation with covariance is their equation (13a), which follows from their more general equation (4) for quadratic selection. The last equation is the restatement of their (14b).
Update
Here I retake the notation of the above-mentioned article by Lande, but adopt it to the case of a single trait. Then the variance matrix $P$ is just a number (variance). Equations (14a) and (13b) define
$$\gamma=\frac{1}{P^2}C, (A)\\
C=Cov\left[w, (z-\bar{z})^2\right],
$$
which is the definition of $\gamma$ in the OP. It is essential here to use the correct expression for the covariance:
$$
Cov\left[f(z), g(z)\right] = \int \left[f(z)-\bar{f}\right]\left[g(z)-\bar{g}\right]p(z)dz=
\int f(z)g(z)p(z)dz -\bar{f}\bar{g}
$$
In our case we thus have:
$$
C = \int w(z)(z-\bar{z})^2p(z)dz - \bar{w}\overline{(z-\bar{z})^2},
$$
where $\bar{w}=1$ by definition, whereas $\overline{(z-\bar{z})^2}=P$ is the variance of the trait. We thus have
$$
C = \int w(z)(z-\bar{z})^2p(z)dz - P, (B)
$$
where
$$
p(z)=\frac{1}{\sqrt{2\pi P}}e^{-\frac{(z-\bar{z})^2}{2P}}.
$$
Let us now consider the integral
$$
\int \frac{\partial^2w(z)}{\partial z^2}p(z)dz=
\frac{\partial w(z)}{\partial z}p(z)|_{-\infty}^{+\infty} - \int \frac{\partial w(z)}{\partial z }\frac{\partial p(z)}{\partial z }dz=\\
\frac{\partial w(z)}{\partial z}p(z)|_{-\infty}^{+\infty} -
w(z)\frac{\partial p(z)}{\partial z }|_{-\infty}^{+\infty}+
\int w(z)\frac{\partial^2 p(z)}{\partial z^2 }dz
$$
The first two terms vanish, since $w(z)$ is bounded, whereas $p(z)\rightarrow 0$ as $z\rightarrow \pm \infty$.
We thus have
$$
\int \frac{\partial^2w(z)}{\partial z^2}p(z)dz=
\int w(z)\frac{\partial^2 p(z)}{\partial z^2 }dz=
\int w(z)\frac{\partial^2 }{\partial z^2 }\frac{1}{\sqrt{2\pi P}}e^{-\frac{(z-\bar{z})^2}{2P}}dz=\\
\int w(z)\left[\frac{(z-\bar{z})^2}{P^2}-\frac{1}{P}\right]\frac{1}{\sqrt{2\pi P}}e^{-\frac{(z-\bar{z})^2}{2P}}dz=
\int w(z)\left[\frac{(z-\bar{z})^2}{P^2}-\frac{1}{P}\right]p(z)dz=\\
\frac{1}{P^2}\int w(z)(z-\bar{z})^2p(z)dz - \frac{\bar{w}}{P}=\\
\frac{1}{P^2}\left[\int w(z)(z-\bar{z})^2p(z)dz - P\right]=\frac{C}{P^2}=\gamma,
$$
where we used $\bar{w}=1$, and equations (A) and (B) above.


How does motor nerve innervation determine type of muscle fibre?

'Slow' and 'fast' motor neurons differ in their firing patterns. This differentially affects intracellular calcium concentrations and energy usage of the innervated muscle fibers over time, and thereby influences their gene expression. The following review extensively covers this: http://www.ncbi.nlm.nih.gov/pubmed/22013216


Plantigrade.

  The penguins are highly specialized for their flightless aquatic
  existence. The feet are located much farther back than those of other
  birds, with the result that the bird carries itself mostly upright;
  its walk can thus be described as plantigrade (i.e., on the soles).
  The sole comprises the whole foot instead of just the toes, as in
  other birds. The most notable characteristic of the group is the
  transformation of the forelimb into a paddle. This is accompanied by a
  body morphology particularly adapted to movement in a liquid medium.
  The thoracic (rib) cage is well developed, and the sternum bears a
  pronounced keel for the attachment of the pectoral muscles, which move
  the flippers. The flipper has the same skeletal base as the wing of
  flying birds but with its elements shortened and flattened, producing
  a relatively rigid limb covered with very short feathers—an ideal
  organ for rapid propulsion. The body plumage likewise consists of very
  short feathers, which minimize friction and turbulence. The density of
  the plumage and the layer of air that it retains provide almost
  complete insulation of the body.

https://www.britannica.com/animal/penguin#ref3467


Complexity in creating transgenic animals (e.g., mice)

One reason is the low likelihood of success. Modifying a gene almost always involves a recombination event of plasmid DNA with a target site in the genome (and I say almost just because there may be some method that I don't know about, but all the ones I'm familiar with do). The likelihood of that decreases exponentially with the number of genes you're trying to modify. If you're trying to make several mutants of individual genes the likelihood of success decreases only linearly.

Another reason is having more knowledge and experimental power. You can learn little from a double mutant if you don't also have the individual mutants to compare. In fact, most reviewers would ask for individual mutant data if you've made a double mutant in your paper. This is especially true with flies and worms, as crosses take less time with them.

Also, the more mutant genes you have, the weaker the animal. Your mutants may not be viable at all with too many mutations.


Within and Between Allelic Class Diversity

The term allelic class is defined in Innan and Tajima (1997)

  Suppose that there are two nucleotides, say A and T, in a particular site.Then, we can divideDNA sequences into two classes: one class includes sequences with A and the other includes sequences with T in this site. We call such a class an allelic class

Two elements that were misleading (for me at least) in the article

Implicitly, in the paper of interest (Charlesworth et al. 1997), they define allelic classes for a site that is known to be under selection (and that can only be bi-allelic). The concept of allelic class is not for a polymorphic neutral site they look at but always for the same site (the one under selection).
The formula has an extra parenthesis. The real formula should be $2 \sum x_t(1-x_t) + y_t(1-y_t)$.

What is $x$ and $y$?

Consider a polymorphic (bi-allelic) locus (that is not under selection) and calculate the frequency of one allele in the first allelic class (defined for the site under selection) (this is $x$) and calculate the frequency of the same allele in the other allelic class this is $y$. In other words, consider the selected has two alleles $A$ and $B$ and the neutral locus has two alleles $a$ and $b$. $x$ is the frequency of sequences containing $A$ that also contain $a$ and $y$ is the frequency of sequences containing $B$ that also contains $a$.

Meaning of the formula

The formula is just the sum of the expected heterozygosity within each allelic class. $$2x(1-x) + 2y(1-y) = 2 (x(1-x)+y(1-y))$$. Then, we just have to sum over all time step during which the neutral locus is polymorphic and we get $$\pi_A = \sum_{i=1}^T 2 (x_t(1-x_t) + y_t(1-y_t)) = 2 \sum x_t(1-x_t) + y_t(1-y_t)$$, where $x$ and $y$ are now function of the instant (time) considered and $T$ is the total number of time steps.

What values can $\pi_A$ take?

This measure takes values between 0 and $T$ as all $x_t$ and $y_t$ take values between $0$ and $1$ (and therefore $x(1-x)$ and $y(1-y)$ take values between 0 and 0.5). Dividing the whole thing by $T$ will result in a measure that is bound between 0 and 1.

I would have not been able to understand without the help of @AMR. Thank you


What happens to IP3 molecules after release from IP3 receptors?

All biomolecules are eventually broken down. This process is called turnover. Since inositol is a signalling molecule it is necessary to remove in order to terminate the signal, despite adaptive mechanism in the ER calcium channels.

IP3 is generally dephosphorylated by a family of phosphatase enzymes called inositol polyphosphate phosphatases. After dephosphorylation, the inositol can be recycled into the membrane by phosphatidyl-inositol synthase.

Reference:

The IUPHAR/BPS Guide to PHARMACOLOGY 1

1 I'm citing this website instead of a research article because apart from citing the original research articles, it also has other informative links about the enzymes and the substrate molecules. It is also from a very reliable source.


How many cell membranes are oxygen and carbon dioxide diffuse through in the lungs?

Oxigen goes from the alveolar's lumen to the cytoplasm of the erythrocyte, and that's 5 membranes:

the "top" of the alveolar epithelial cell
the "bottom" of such cell
the "top" of the endothelial cell (capillary)
the "bottom" of such cell
the erythrocyte membrane

You got all the cells right, but your only problem was this: oxygen diffuses through the cell membrane entering the cell, moves through the cytoplasm, and diffuses through the membrane again exiting the cell. So, for each cell, you have to count 2 membranes. For the last one, the erythrocyte, you have only 1 membrane (because it is $\ce{O2}$ final destination).

For the $\ce{CO2}$ the situation is a little bit more tricky. We have the same 4 membranes (2x epithelial cell and 2x capillary), but $\ce{CO2}$ can come from 2 locations:

from the erythrocyte, where it is formed from $\ce{H2CO3}$ (by the reaction $\ce{H2CO3 -> H2O + CO2}$) or released from the N-terminal group of proteins, like haemoglobin (where it has previously bound)
from the plasma (around 9% of the $\ce{CO2}$).

In the first case we have 5 membranes, and in the second case just 4.

So, the correct answer is D.


Yes. Moreover, even if they were not urinating at the time of death, they likely would at death, assuming adequate filling of the urinary bladder. There are two sphincters that close off the urethra. One is under control of the autonomic nervous system and the other is voluntarily controlled (somatic). At death, both sphincters will relax, releasing the bladders contents.


Sigma gives a solubility of 200 microMole in water containing 2% ethanol.
They state:

  Forskolin is soluble in water (with 2% ethanol) up to 0.2 mM by first
  dissolving in ethanol at 5 mg/mL and doing subsequent dilutions with
  water.

The datasheet can be found here.