There are many examples of parasite manipulation in nature, if you want more examples you can look up the paper of Lefevre and Thomas (2008). I think the key is, in order for a parasite to develop such behaviour, that it should be giving them a fitness advantage. So I don't think it would ever happen for no reason. The paper discusses a few examples where the manipulation results in a higher transmission rate by the parasite.

I guess that because parasite manipulation is happening in many other organisms, it's probable that it happens to some extent in humans too. There are for example indications that when we are infected with  malaria, the malaria parasites can change our odour profile to make us more attractive to mosquitoes, thus increasing it's transmission (Batista et al. 2014, De Moraes et al. 2014). There are also indications that our gut microbiota have an influence on our brain and behaviour, regulating anxiety, mood, cognition and pain, by communicating with our CNS (Cryan and Dinan 2012).


Where do the lysines come from during ubiquitination?

The Wikipedia article on Ubiquitin gives a pretty good answer to your questions. Look at the referenced articles if you want to get more detailed answers.

  Are they just always available for the Ub to find to during the ubiquitination process?

Yes, This [Ubiquitination] process most commonly binds the last amino acid of ubiquitin (glycine 76) to a lysine residue on the substrate.

  Is there a free lysine available on each of the additional Ub added to the chain?

Ubiquitin has seven lysines and each one of them can be bound to the N-terminal glycine of the next ubiquitin.

  After the first Ub is added onto the target protein, does the E2/E3 complex still have to bind each time a Ub is added to the chain?

Yes, but this is more complicated than the general mechanism. A poly-ubiquitin chain can be attached just like a single ubiquitin or one more ubiquitins can be conjuated to an exisiting ubiquitin-protein complex. See for example Brown et al and David et al.


This is a tulipwood tree, which belongs to the species Harpullia pendula. As an Australian native, they're commonly used as street trees along the east coast.

More information about this tree can be found here.


Are there birds with knees instead of elbows?

The joint you are thinking of is not a knee, nor is it an elbow, instead it is an ankle which is bending the same way as us humans. You can see from the below diagram that the knee - the joint between the femur and tibia - is just further up the leg normally hidden by feathers.

Birds have a comparatively elongated metatarsus which gives the impression that the knee bends backwards more like an elbow, but it's just the ankle. (Image from here)

I also liked this diagram from a blogpost on a similar theme...

To follow up there appears to be no animals whose ankles bend the "wrong" way.

http://www.answers.com/Q/Which_animal_has_backward_knees

http://qi.com/infocloud/knees

http://www.ehow.com/info_12317202_birds-knees-backwards.html#page=1

Though these are far from conclusive resources. I'd guess the way knee is defined (it means something to humans but not to nature (a bit like the species being a concept which has weak biological bounds)) has something to do with that


Is there a realtime molecular clock within the genome to co-ordinate the developmental sequences in an embryo?

I think that the "molecular clock" that you refer to and the "molecular signaling" that you are skeptical of are one and the same thing.

In the 1960s, nuclear transplant experiments established that molecular signals in the cytoplasm can dedifferentiate terminally differentiated nuclei, "resetting" your molecular clock, or in the more common terminology "rerunning" the "developmental program" to yield viable animals.

This "developmental program" metaphor has been frequently used to describe this process, seeing development as a series of gene regulatory cascades; they called it a program because they were thinking of procedural computer programs. It isn't really a clock so much as a complex process by which different sets of genes are turned on and off in a concerted fashion, where one step depends on what happens in the previous step. An undergrad course discussing some of the mechanisms of this is posted here.

We've known for many decades that interrupting cellular processes such as transcription, translation, and DNA replication tend to arrest development at different points (for one early example see here).

A good example of a step/series of steps in the developmental program is the maternal-to-zygotic transition in metazoans, where embryos transition from using maternally deposited mRNAs as molecular raw material to de novo transcription of their own mRNAs.

From the linked review:

  As development proceeds, two processes are triggered that together form the maternal-to-zygotic transition (MZT): first, a subset of the maternal mRNAs is eliminated; second, the transcription of the zygotic genome begins. Initially, the destruction of maternal mRNAs is accomplished by maternally encoded products. However, zygotic transcription leads to the production of proteins and microRNAs (miRNAs) that provide feedback to enhance the efficiency of maternal mRNA degradation. In addition, among the earliest mRNAs synthesized de novo in the embryo are transcriptional activators that enhance the efficiency of zygotic transcription. The net result is that the control of development is transferred from the maternal to the zygotic genome.

  Figure 1. A comparative overview of the maternal-to-zygotic transition (MZT) in several model organisms. Key embryonic stages for each model organism are depicted schematically above the corresponding cleavage cycle and time after fertilization. The red curves represent the degradation profiles of destabilized maternal transcripts in each species. The light and dark blue curves illustrate the minor and major waves, respectively, of zygotic genome activation. The last embryonic stage presented for each organism is the developmental point at which there is a major requirement for zygotic transcripts.

This transition requires that the developmental steps based on maternally-deposited mRNAs have completed successfully before de novo transcription of embryonic RNAs can begin.


Identification of a segmented black insect in France

I think this is some sort of soldier fly larva (family Stratiomyidae). That would explain lack of legs. There are thousands of species world wide, with both aquatic and terrestrial larvae, so it might be possible to narrow it down a bit more.

Image from bugguide.net for comparison:

Thanks to @bli for reminding me of dipteran larvae!


The existence of the G-spot remains highly debated among researchers.  Two recent publications (Hines 2001, Kilchevsky et al. 2012) review studies of the so-called G-spot and conclude the evidence is too inconsistent to claim its definite existence.  Foldes and Buisson (2009) argue that the G-spot is actually just a clitoris that is richly  innervated. This would be consistent with the reported variability of G-spot presence or absence due to natural variation in innervation among women. (This last statement is my hypothesis offered without citation).

As noted by @Armatus in the comments, a few minutes following some of the Wikipedia links to the scientific journals (not the BBC, CNN, pop news sites, etc.) would give you lots of information about the G-spot. Still, I thought you question was worth typing up a brief answer for the sake of completeness.

Literature Cited

Foldès, P. and O. Buisson. 2009. The clitoral complex: a dynamic sonographic study. The Journal of Sexual Medicine 6: 1223–31.

Hines T. 2001. The G-Spot: A modern gynecologic myth. American Journal of Obstetrics and Gynecology 185: 359–62.

Kilchevsky, A, et al. 2012. Is the Female G-Spot Truly a Distinct Anatomic Entity? Journal of Sexual Medicine. 719-726.


The Allen's swamp monkey (Allenopithecus nigroviridis) is also know to live near water-rich areas and they sometimes dive to avoid danger.

Also, it was recently shown that the chimpanzee (Pan troglodytes) and the orangutan (Pongo) can swim, dive and even retrieve items form the bottom of a swimming pool. (source)


Making sense out of the visual representation of transcription

Gene sequences are annotated in the sense strand. So, these diagrams are correct.


Organ donation compatibility based on DNA

@zeller

The better answers are being sought in a field called Regenerative Medicine.

A number of techniques have been tried, among them 3D printing of organs and dissolving the cells from a donor organ leaving the collagen scaffolding, then reseeding the organ with a patients stem cells in a bioreactor.

Most of these technologies, unfortunately, are in the proverbial 20 years from now category, which means that there are an incredible number of technical and biological challenges to overcome, but the ideal result would be organs with the patient's own cells and therefore no rejection or need for immunosuppressant therapies post transplant.

A nobel prize was awarded a few years back to Shinya Yamanaka for creating Human Induced Pluripotent Stem Cells. A technology like this would be the likely source of the stem cells necessary to seed these organs, however there have been problems with these cell lines including their tendencies to become neoplastic and form cancers.

So for at least the near and medium term the best alternative is to find organs that are as close a match as possible for Major Histocompatibility Complexes, and as Moderator Chris said, the best way to do this matching is to test for the cell surface proteins, as these are what will be the targets of immune cells. Also an organ has a very short life span after the donor dies to be usable. Sequencing is much slower than the protein screening that is in place today. You run into ethical questions regarding keeping someone on life support for the sole purpose of harvesting their organs.

And we still wouldn't be 100 percent sure that even people with the same alleles for these molecules express them in the exact same way as there may be slight differences in the post translational modifications that are made. The human immune system has evolved to detect small variations and as such we would still need to test the proteins, even if we found allelic matches. People get autoimmune diseases all the time, so there is no guarantee that even allelic matches would not be rejected.


Stage I lactation occurs from midpregnancy onward; stage II is the onset of substantial milk secretion associated with having given birth.

  In humans, stage I occurs at approximately midpregnancy... the gland is sufficiently differentiated to secrete milk, but secretion is held in check by high circulating plasma concentrations of progesterone and, possibly ...estrogen.

You ask,

  ...is anything produced then?

Yes. The mature primed breast produces colostrum, containing sodium, chloride, immunoglobulins, lactoferrin and other substances.

  I’ve heard things about milk leaking out of breasts during pregnancy...

Not at all common that I know of. I'm sure one can manipulate the breast to get a small amount of milky discharge, but that's a big leap from leaking. More common (again, that I'm aware of) is galactorrhea associated with early oral contraceptive pills, prolactinomas, and other conditions.

  the breasts seem very heavy and laden with milk during parturition.

The breasts mature during pregnancy in preparation to make milk; that's why they get bigger. They can get even bigger when they are actually full of milk. It may not be as obvious in a human, but in milk animals (goats, cows, etc.), well, a full udder is pretty obvious.

Different researchers divide lactogenesis into a different number of stages; this is a simple two-stage approach.
Lactogenesis: The Transition from Pregnancy to Lactation


Why would stablising selection ever happen?

It occurs when a beneficial characteristic has been developed over time and it would be harmful to stray from it.  In these cases it is not the individuals at the fringe (as you put it the most adapted) who are the best adapted.

I think it may help if I answer with an example that is widely promoted by AQA in their A2 Biology syllabus.

Stabilising Selection in human birth weight

It is harmful for an infant to be born with a very low birth weight. They are much more vulnerable to heat loss due to their high surface area to volume ratio and consequently their respiratory demands are very high.  Pre-term babies (which account for 67% of low-birthweight infants(1)) are particularly susceptible to respiratory problems (lack of surfactant in the lungs), cardiac problems (Patent ductus arteriosus - the lungs are still bypassed when the umbilical cord has been cut) and dangerous intestinal problems (Necrotizing enterocolitis) amongst many other conditions can all be fatal (further information on mentioned conditions) and are reflected in high mortality rates at these low birth rates.  It is therefore not beneficial to be on the extremes of birth weight.

Similarly, delivering a child of too high birth weight can cause complications with delivery if the head and shoulders are too wide to pass through the mother's hips.  Therefore the other extreme of high birth rate is also not beneficial and will not be selected towards.

This leads to selective pressures in both directions, stabilising towards a mean birth weight as shown below:

This is an example of evolution not pushing a species forward but ensuring that individuals have the best chance of getting to reproductive age themselves.

(1) Martin, J.A., et al. (2007). Births: Final Data for 2005. National Vital Statistics Reports, 56(6).


Mathematical models of lineage selection

The writings by Samir Okasha (philosopher of biology/science) could be a good starting point. In his book Evolution and the Levels of Selection, he explicitly uses the Price equation to discuss selection at multiple levels (e.g. chapter 2.3: Price's equation in a hierarchical setting), and also derives a multi-level version of the Price equation:

$$\bar{w}\Delta\bar{z} = Cov(W,Z) + E(Cov_k(w,z))$$

where the first part on the right hand side represents collective-level selection and the second part particle-level selection. This is mostly aimed at aspects of group-level selection though. There is also a chapter on "Species Selection, Clade Selection, and Macroecolution" (ch. 7), but this is not directly tied to the Price equation. A note though; I own the book and have read parts of it casually, but I haven't worked with the Price equation myself, and I haven't checked exactly how the extended version of the Price equation is developed and used in the book.

A couple of references that might be useful are Frank (1998) (and other papers by him) and papers by Vrba. The work presented in this recent conference abstract by Rankin, Fox et al (2014), "Using the Extended Price Equation to Analyze Species Selection in Mammalian Body Size Evolution Across the Paleocene/eocene Thermal Maximum", seems to describe exactly the type of theoretical developments that you are looking for (I didn't attend the conference, and haven't heard the talk though).


I don't know if we can calculate the exact values. The only thing I can say is that the potential of the soil will be less negative than -3 while that of the leaf will be more negative.

You know that water travels from higher potential to lower potential. So, it will travel from a region of less negative water potential to a region of more negative water potential.


Are descriptive statistics sometimes more useful than tests of significance?

I'm not a statistician, but I think the comments have got it right.  There is never a reason to omit P values, statistical power or some other measure that you have done something that is not a random outcome.

For the sake of reference lets define the terms you reference:
Eta squared is a ratio of the variances of two sets of measurements
Cohen's d is a measure of the difference between two means.
R value or Pearson Correlation describes the linearity of two numbers, usually one of them being a measurement and the second being an experimental variable.

These numbers as you say are descriptive, but they could be created by throwing coins and writing them up.  With small numbers of measurements, and a large enough range of possibilities, its possible to get terribly large numbers here.

Biology, medicine, social science and economics are really susceptible to this.  You go into the field and measure butterfly wings or do surveys of people's opinions, or try to guess who is going to win the election and its quite expensive to do more measurements.

If you are measuring something hard to determine because accuracy is important such as a close election race or that is really complicated such as which genes convey a susceptibility to type 2 diabetes (a problem which remains unsolved because so many genes play a role) you need large numbers of responses.  Yet each study that comes out gets some answer, but if you want to believe it these numbers should convince no one in most cases.

Microarray data and RNASeq data analysis for instance often suffer from this problem.  The measurements are all statistically significant but each one costs hundreds or even thousands of dollars.  Most experiments do a minimal three measurements to understand the variance in each measurement and then do 2 to 8 actual measurements.  That's not going to so revealing when working with a system with thousands of genes in it. one bad sample with slightly different culture conditions can ruin the experiment.

Our butterfly biologist may measure 100 butterflies and stop when the P values are 0.05 or 0.001 - its a lot of work camping out and setting nets.  The truth is that 5% is a number that can happen at random a lot.  Even a 0.1% error will happen in one in ten such experiments.  In thousands of experiments published that means that 10% of them have a mistake.  Not so great.

It gets worse though - not only significance, but bias needs consideration.  Because biologists and most other scientists don't understand statistics, the assumptions that we use when we calculate a P value are often inappropriate and don't give honest estimates of the chance that this is a random phenomenon.

If good looking result is chosen specifically to show to prove the point or some data are thrown out because they simply don't look good, or if a hypothesis is chosen in a biased way simply to fit an unreliable set of data.

Or the statistical assumptions of the calculation might simply be so inappropriate that to really cite them is an out and out lie. An everyday example of this is to do a BLAST search.  The E-value calculations, if read as a P value would be wrong, even though they are mathematically correct - two strings that show a 10% identity will have a small E value - 10^-8 for instance, but this is only the chance two strings of these lengths will have so many letters in common.  Anyone who plays with BLAST will quickly throw out anything that has less than 30% identity unless they are desperate, even though the E-values are infinitesimal.

John Ioannidis has made this subject his focus and has published widely on this topic.  A good place to start is his commentary "Why Most Published Research Findings Are False".

  There is increasing concern that most current published research findings are false. The probability that a research claim is true may depend on study power and bias, the number of other studies on the same question, and, importantly, the ratio of true to no relationships among the relationships probed in each scientific field. In this framework, a research finding is less likely to be true when the studies conducted in a field are smaller; when effect sizes are smaller; when there is a greater number and lesser preselection of tested relationships; where there is greater flexibility in designs, definitions, outcomes, and analytical modes; when there is greater financial and other interest and prejudice; and when more teams are involved in a scientific field in chase of statistical significance. Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true. Moreover, for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias. In this essay, I discuss the implications of these problems for the conduct and interpretation of research.


Where does the fate map of a human embryo end?

In the developing embryo you have the three germ layers: Endoderm, mesoderm and ectoderm. From these layers all cell lineages of the body develop and can be traced back through their differentiation and migration to this three layers.
Have a look on the image below, which illustrates this pretty nicely:

The figure is part of this PhD thesis, which also seems worth reading when you are interested in this topic.


Tight junctions are very specifically a structure found in epithelial cells, so your teacher is incorrect. Tight junctions are what allow epithelial cells to form a selective barrier between compartments. Fibroblasts can be induced to form tight junctions under certain experimental conditions, but I'm not aware of any case where a skeletal muscle cell expresses a tight junction. Regardless, it would not be normal physiology.

You can read more about tight junctions here, in the online Albert's Molecular Biology of the Cell. This figure from that Chapter illustrates the barrier function.

If you want to get into more of the details re: what we know about the various proteins involved in creating and regulating tight junctions, this is a good review.

One small correction to your reasoning, though, I wouldn't say the primary purpose of tight junctions is cell-to-cell adhesion, per se, it's selective permeability. These junctions may help the cells to hold together, but the tissues can resist shear stress in knock-out models. A knockout model without a necessary tight junction protein, however, will not maintain selective permeability.


Do human cells contain only one copy of the genome?

As a quick answer, yes, most human cells carry 2 copies of the genome and are known as diploid cells. One copy comes from each of your parents, so they aren't identical, but usually pretty close. Sperm and egg cells only carry one copy of the genome and are known as haploid. During fertilization the 2 cells merge their copies and make a diploid zygote. At the chromosomal level, humans have 23 chromosomes, so a diploid cell has 2 copies of each so a total of 46.

As far as repairing damaged DNA, using one chromosome to repair its damaged counterpart is known as Homologous Recombination.


Hamilton's derivation of direct fitness from his 1970 paper

Actually the derivation is pretty straightforward. It's easier to use the fact that $Cov(X,Y) = E(XY) - E(X)E(Y)$ to derive this result. Suppose
$x_{j} = \sum_{i} s_{ij}$.
\begin{align*}
  Cov (x_j, q_{j}) &= E (x_{j}q_{j}) - E (x_{j}) E (q_{j}) \\
                    &= \frac{1}{n}\sum x_{j} q_{j} - \frac{1}{n}\sum
                      x_{j} q \\
                    &= \frac{1}{n} \sum x_{j} (q_{j} - q)
\end{align*}


Which animal species are known not to murder (a targeted attack leading to death) members of their own species?

Here are a few suggestions:

Any coral
Any sponge
Blue mussels
Sheep
Dugong
brown-headed cowbird
Blue whale
Common earwigs
Plasmodium falciparum (causing malaria)

If by the use of the term "evidence", you are expecting a peer-review paper that discuss the matter, I am afraid you wont find any as it is not really a question of interest to researchers. If you can prove wrong any of the above suggestions I will be happy to remove it (and eventually add some others).


Generalisation

  Generalisation is the phenomenon of an organism responding to all situations similar to one in which it has been conditioned.

or

  Not biologically differentiated or adapted to a specific function or environment

This means that  the the rats responded to ethanol the same way that they responded to the training mixtures.

Sources:

Mangan, G. L. The Biology of Human Conduct: East-West Models of Temperament and Personality. Oxford: Pergamon, 1982. Print.
"Generalized." - Memidex Dictionary/thesaurus. Web. 04 Mar. 2016.
"Generalisation." - Biology-Online Dictionary. Web. 04 Mar. 2016.


What factors make a sequence evolve non-randomly?

Fay and Wu test is a test that compare expected sequences under a standard coalescent theory model, that is a single panmictic population with non-overlapping generation of constant size $N$ and effective population $Ne=N$, that is the variance in allele frequency at any following generation is $\frac{p(1-p)}{2N}$, where $p$ is the frequency of a given allele. As such Fay and Wu (as well as Tajima's D and other tests) are not only test of selective neutrality but also tests of demographic neutrality as underlined in Nielsen 2001.

It may be hard to make good predictions about the extend and direction at which a given selective or demographic event will affect a given statistic such as Fay and Wu's H. Therefore, in answering the following questions, I am not specific to Fay and Wu's H. Also, answering the questions fully would require making an introduction to coalescent theory which is subject to a whole book rather than a simple post. To fully understand such test, you will need to follow an introduction to coalescent theory. You can have a look at the books recommended in the paragraph General Entry Books to Population Genetics of this answer.

  Does negative selection differ from a selective sweep because a sweep is a form of positive selection?

Let's first clarify the terms just in case. Reduction in polymorphism at linked loci due to positive selection is called "selective sweep" while when due to negative selection it is called "background selection".

Generally speaking, selective sweep is much stronger than background selection. Also, selective sweep has a higher impact on Tajima's D, then background selection.

To my knowledge, methods trying to disentangle the two processes of selective sweep and background selection mainly use inter-species comparisons to infer what types of sequences are concerned. If The loss of polymorphism is adjacent to a highly conserved sequences and is found in related species, then it is probably background selection at play. If there is a fixed mutation that isn't found in related species and loss of polymorphism isn't found in these related species, then it is probably selective sweep.

  After a selective sweep, any rare mutations you see must have come after the selective sweep. Is it because they can't have come during it else they'd 'be diluted' by the positively selected alleles?

A selective sweep indeed modifies the Site Frequency Spectrum (SFS, distribution of allele frequencies) to create an excess of high frequency variants (or a relative lack of low frequency variants). See wikipedia > Tajima's D

  Population contraction can create a bottleneck, which makes all individuals come from a common ancestor. But how does population expansion make a sequence evolve non-randomly?

Population expansion yield to longer coalescent times and therefore lack of rare alleles. See the introduction of Excoffier et al. 2009 for nice explanation and figure.


Butterfly identification: Dorset England, July.

The silver-studded blue is frequently found feeding on this plant, cross-leaved heath. There are good numbers of this species to be found on the heaths of Dorset in July and I would suggest that this is certainly silver-studded blue.


how do they identify different protein chains?

Chains are individual polypeptides that make up a multimeric protein complex.

  I'm curious as to how they are first found and what causes them?

SDS-PAGE will resolve all the different chains (if they are different in molecular weight). Chains are products of translation (and some modifications such as clipping and/or other PTMs etc) and they assemble to form final protein complex.

  As far as I understand, the protein backbone could be in any of
  several conformations and each conformation has a label? Is that
  correct?

Yes. The labels are assigned as per the reported conformation.

  Is one chain more common than the other? What causes translation to
  produce different chains in this case? And finally, during the x-ray
  crystallography, how do they identify them when they grow the crystal?

There can be different kinds of multimers. There can be homomultimer or a heteromultimer or a multimer of this configuration $(XX)_2$-$(YY)_2$ (a heterodimer of homodimers- just one arbitrary case) etc.
Each chain is a polypeptide and is encoded by a distinct gene. It is possible that in a multimer there are more number of a certain chain than the other for e.g. $X_3$$Y$. This is not because $X$ is produced more then $Y$ but rather because of the way the multimer is assembled.
In X-ray crystallography you basically get the arrangement of atoms. You can also understand which atom is what and similarly the termini can be found out. In any case people don't just proceed to crystallography without understanding the subunits and other biochemical properties.


You seem to have many misconceptions about how we see and how that relates to light. I'll address them one sentence at a time:

  Why are we able to differentiate between colored objects without the presence of light?

Answer: the premise of the question is wrong: we aren't able to differentiate between colors without the presence of light, because we aren't able to see without the presence of light. Light is what allows us to see. "Seeing" is the act of detecting the light coming from the environment and using it to derive what the environment is like.

  Rods help us to see during the dark.

It sounds a bit like you think rods help us to see during the dark... without light ? This is not the case: BOTH rods and cones absorb light and thus allow us to see. Rods help us see in low light because they are more sensitive (to light !) than cones. Nothing can help us see with no light.

  We can see colour of the object when it reflects light.

It depends on how much light it reflects ! The correct form of that sentence is "We can see the object when it reflects light". (even more correct would be "when it reflects enough light to trigger the light receptors in our eyes, i.e. rods and cones). Whether we can see its colour depends on whether it reflects enough light to trigger the cones specifically.

  But in a dark room(room of any color but the light is switched off and it is night),we still can differentiate between colored objects if we open our eyes for sometime.(although not very much clearly)

Indeed; this is because no room is completely dark. Even more so in our artificially lit world, but even in a moonless cloudy night you may have a few errant photons coming from the stars and Sun (via diffusion in the atmosphere), fireflies, what have you; to be fair in our artificially lit world I haven't experienced it. As far as I know you can get true pitch darkness in things like underground caves (once you're far enough from an exit of course).

Basically, if you can see anything then there is some light. (well, short of your optical cortex confabulating stuff, which in fairness it will do).

  How the colors are seen when there is no light?

As I hope you understand now, they aren't.

  Do we see as the brain remembers their colour?

I think that may actually be one reason we perceive colour in low-light environments. I'm sure some of it is that there's enough light to trigger the cones a little bit, but I wouldn't underestimate our brain's ability to show us the world as it knows it is as opposed to as whatever information it's receiving right this second says it looks like.

EDIT

Some references :

The state of seeing things in such low light that we only use the rods is called "scotopic vision" :
https://en.wikipedia.org/wiki/Scotopic_vision

Some sources for how "dark" environments still contain low amounts of light (one word for "amount of light" being "illuminance", measured in Lux) :
http://www.engineeringtoolbox.com/light-level-rooms-d_708.html
https://en.wikipedia.org/wiki/Aphotic_zone (thank you to @Johnny for that one)

HOPEFULLY LAST EDIT

On reflection I thought I'd say some more about scotopic vision since it's very relevant to the question. It turns out "scotopic" vision is opposed to "photopic" vision (the vision we have in full lighting, where the cones do the work because the rods are saturated), and in between there is an intermediate range called "mesopic" vision, which is likely the kind of vision we experience when it's dark but we still see color (this is ignoring our brain filling in colors, which could also be a factor and in that case could also happen with scotopic vision - but I didn't find any sources on that).

Mesopic vision is used under lighting conditions that seem to range from low indoor lighting or streetlights to starlight; scotopic vision is used with luminances darker than that. This page is all about it and includes a very nice drawing, sadly it's a pdf so I can't show it in the answer:

http://www.visual-3d.com/Education/LightingLessons/Documents/PhotopicScotopiclumens_4%20_2_.pdf


It looks a lot like Queen Anne's Lace, but yellow and with more slender leaves. I believe it's Sweet Fennel (Foeniculum vulgare). It's in the Apiaceae family, which has a lot of edibles: carrots, parsley, fennel, anise, caraway, celery, chervil, cicely, cilantro, cumin, dill, parsnips and more. Black swallowtail butterflies lay their eggs on this, so often you can find a really fine caterpillar on them; bees like the flowers as well.

Apiaceae has 3,700 species spread across 434 genera; it is the 16th-largest family of flowering plants. It has a few poisonous plants, like water hemlock (white flower) and poison hemlock (also white). Wild parsnip has a very similar yellow flower but it's sap is wildly irritating in the medical sense (it will cause pain and blisters); its leaves are very different.

If you crush some of the slender leaves between your fingers, it should smell like fennel (a common spice, e.g. in Italian sausage), or if you aren't familiar with that, a bit licorice-like.

Sweet fennel (left, up to 6 feet tall)        Wild Parsnip (right, 3-5 feet tall)


Does DHA increase the effects of clarithromycin?

You've misread the paper. Clarithromycin is metabolized in part by CYP3A, but to an active metabolite. A significant proportion of clarithromycin and its active metabolites are excreted unchanged in the kidney. Clarithromycin, and other macrolide antibiotics do inhibit CYP3A enzymes, as you noted in your answer. You can read about this in chapter 55 of Goodman & Gilman's the Pharmacological Basis of Therapeutics.

We certainly worry about clarithromycin and other macrolides increasing the half-life of drugs that are primarily metabolized by CYP3A4 (again, see Goodman and Gilman). Midazolam is an example, and is what the paper you cite was about. If you give clarithromycin together with midazolam, expect the effects of midazolam to last longer. The important relationship between CYP3A induction and clarithromycin discussed in the paper is not that it reduces the effectiveness of clarithromycin, but that CYP3A induction does not overcome clarithromycin mediated CYP3A inhibition.


Is organ transplantation race dependent?

No, race is not a factor taken into account. However, due to higher genetic similarities between people of the same race, it is usually easier to find a match within a race.

Source 1

Source 2


What keeps the resting potential of neurons constant at -70 mV?

The neuronal cell membrane is quite permeable to K+. Because the Na+,K+-ATPase pumps K+ inside of the cell, K+ tends to diffuse outward again, thereby taking positive charge outside the cell and making it negative inside (see Further Reading 1). This outward flow of K+ stops at a certain point, because the driving force of K+ diffusion out of the cell along with its concentration gradient, equals the charge gradient, which becomes more and more negative inside the cell as more K+ diffuses out (see Further Reading 2). Hence an equilibrium is reached which is close to the resting membrane potential of -70 mV. Other ions such as Cl- are also relatively permeable and affect the resting membrane potential (see Further Reading 1). Ions such as Na+ and Ca2+ are typically highly impermeable and do not substantially affect the resting potential.

As to your second sub-question:voltage-gated channels are gated through voltage differences (Purves et al., 2001), not ion concentration differences.

Further Readings
1. If the average resting potential of a neuron is -70 mV, why is there such a high ratio of K+ ions inside relative to out?
2. Why do negative ions flow into a cell in an inhibitory synapse, even though a neuron has a negative resting potential?

Reference
-  Purves et al., Neuroscience (2001). 2nd ed. Sunderland (MA): Sinauer Associates


How does better sperm result in more viable offspring?

Greater choice and variety of mates increases a female's chance to produce more viable offspring.

The claim is a little hard to address because it is vague. However, one can give a simple example to give you a feeling of why this could be the case.

This example is based on Zaahavi handicap principle. Spermatozoids aren't free to produce. A male that can produce more and stronger spermatozoids can do so because he is a healthy males. As many of the traits that determine health, in a general sense are heritable, healthier males tend to have healthier offspring.

  On the other hand, what helps a particular entity to survive is determined by many parameters. Some of them are: speed, endurance, strength, agility, stealthiness and savvy.

You are mainly listing traits that are very specific to human's sport ability. In reality, there are loads of other traits that are much more fundamental such as the efficiency of the potassium pump or of the mechanism to produce ATP.

  [..] it helps in natural selection [..]

I don't understand what you mean by this sentence.


This is known as a "long-headed grasshopper", and belongs to the species Acrida sp. Of the species I've been able to find images of so far, I think is most closely resembles

Acrida conica

and

Acrida bicolor

A full list of species for this genus can be found here.


Reliability of SARS-CoV-2 tests - false negatives

Also, is there any possibility of the virus mutating in such a way that what makes it COVID-19 from a public health point of view remains the same but its genetic identity changes enough to no longer be recognized by the existing tests?

That's unlikely. These assays look for several specific regions of the viral genome under high selection pressure (i.e., highly conserved) to make a clinical diagnosis (such as orf1ab, N, and S genes, ref. https://www.thermofisher.com/us/en/home/clinical/clinical-genomics/pathogen-detection-solutions/coronavirus-2019-ncov/genetic-analysis/taqpath-rt-pcr-covid-19-kit.html and https://www.fda.gov/media/136286/download for examples), with the aim to minimize test error from off-target effects (varieties of genomic mutations, ref. https://en.m.wikipedia.org/wiki/Off-target_genome_editing) and misidentification with other respiratory viruses.
I can't speak to the other questions in your question with numerical error rates of tests, except to say that controls, procedures, and better PCR primers can be used to increase sensitivity, to get a true positive (ref. https://en.m.wikipedia.org/wiki/Sensitivity_and_specificity). Sensitivity is a real issue for test kits in Russia, where one must have high viral counts (and likely be very ill) in order for a test to give a positive diagnosis (ref. https://abcnews.go.com/International/russia-reporting-covid-19-cases-cover/story?id=69717763)

According to PCR News, the Russian test is based on the same method used by other countries.
But the Russian test, PCR News wrote, only detects the virus when there are over 100,000 copies of it per milliliter in a sample. That is far more than in other countries’ tests. A test in use in the U.S., for example, will pick up the virus with just 6,250 copies.
“That would mean it’s about 10-16 times less sensitive than what’s available in the U.S.,” Carmen Wiley, president of the American Association of Clinical Chemistry, told ABC News by a phone. At such a level, she said there was a risk the Russians were missing cases, in particular where people were asymptomatic.

From a public health standpoint, I suspect diagnosis of sick people is less useful than diagnosis of asymptomatic carriers who feel fine but are shedding virus everywhere. You want a test to let you quickly tell positive people to self-quarantine, before spreading it around.


Do the light and dark reactions happen at the thylakoid?

The light dependent reactions involve an electron transport chain with enzymes embedded in the thylakoid membrane. NADPH and ATP are generated in the stroma and water is oxidized in the thylakoid lumen.

I'm not sure if it's correct to say that the light independent reactions occur "at the thylakoid" since, in plants, they could really occur anywhere in the stroma (not necessarily "at" the thylakoid, and certainly not within it). It's possible that the enzymes involved in the light independent reactions are somehow localised at the the stromal side of the thylakoid membrane for efficient use of substrates, but I have no idea if that is actually the case and I don't have time to review any literature.

In plants, all of these processes occur in the chloroplast. However, photosynthetic bacteria don't have chloroplasts so you can't categorically say that the photosynthetic reactions occur only within chloroplasts. Cyanobacteria do have thylakoids where the light dependent reactions occur.


Are there any examples of predators that ambush scavengers?

Saltwater crocodiles in Australia are reputed to do this; storing meat under water and later eating the fish and crustaceans that are attracted.
Having trouble finding a good source for this.
Article from national news service below.
https://www.abc.net.au/science/articles/2004/01/15/2045125.htm
Feel free to add references if you can find them.


Is there software or a website where I can browse extinct species?

You can search for species that are "Extinct" or "Extinct in the wild" at the IUCN red list website (International Union for Conservation of Nature and Natural Resources). That list currently includes 903 species, but some of the assessments might be obsolete (see annotations). From that list, you can click and get some basic information about each species.

Also note that many countries have regional Red Lists, where you can find information about regionally extinct species (i.e. species that have gone extinct in a particular country). For instance, 209 species are labelled "reginally extinct" in Sweden (http://artfakta.artdatabanken.se/, site only in Swedish), most of them insects, while still being present in other parts of the world.


What are the types of interactions in biological network (protein networks)?

Most of them are pretty self-explanatory. KEGG pathways are often vague, as a lot of the specific biology for some proteins has yet to be properly investigated - sometimes you only know that two proteins associate, not what they actually do.

The relationship between the two is easier to predict when you know the function of one, e.g. a protein interacting with a kinase is likely phosphorylated by said kinase. A lot of those relationships correlate to post-translational modifications (glycosylation, phosphorylation, ubiquitination, acetylation, methylation, etc) made to one protein by another. Wikipedia actually has a decent overview of these with lots of examples.

Several of the other relationships have to do with regulating protein activity or expression. This goes somewhat hand in hand with what I stated above. Some proteins are only activated once phosphorylated or demethylated, etc. Other enzymes may remove phospho groups, leading to repression. Others still may interact directly with a protein, inhibiting it from binding its substrate or target. Maybe the binding induces a conformational change in one protein that allows it to bind its substrate when it can't normally. Some proteins function as transcription factors that activate or repress the expression of certain genes, indirectly affecting protein levels.

There are all sorts of possibilities - the KGML files try to represent them in a way that at least gives some indication of how the interactions between two proteins may affect each. I hope that provides some insight.


How does aminoacyl-tRNA synthetase recognize different tRNAs?

You give the answer in your question:

  binding areas that recognize a particular tRNA through unique identity sites at the acceptor stem and/or anticodon loop of the tRNA.

The point is that aminoacyl-tRNA synthetases that recognize tRNAs with different anticodons have to supplement any partial codon recognition with recognition of common features elsewhere, in particular the anticodon loop. Unfortunately this has evolved on a case-by-case basis and there is no simple ‘code’ one can refer to.

Thus, Berg et al. (Chapter 29), in discussing  threonyl-tRNA synthetase, write (my emphasis):

  As expected, the CCA arm extends into the zinc-containing activation
  site, where it is well positioned to accept threonine from threonyl
  adenylate. The enzyme interacts extensively not only with the acceptor
  stem of the tRNA, but also with the anticodon loop. The interactions
  with the anticodon loop are particularly revealing. The bases within
  the sequence CGU of the anticodon each participate in hydrogen bonds
  with the enzyme; those in which G and U take part appear to be more
  important because the C can be replaced by G or U with no loss of
  acylation efficiency.

The four codons for Thr are ACN, so in this case recognition of two bases of the anticodon will identify all tRNAs.

A diagram from Berg et al. showing the multiple interactions in threonine tRNA-synthatase is shown below.


Blood become denser when you are dying of deshidration?

Yes blood becomes denser on dehydration (water dilutes the blood, if there's no water in blood it becomes dense). No, body does not draw water from the blood. When you are dehydrated, blood is the first source to be depleted. Then blood pulls water from cells (there are various hormones acting on kidneys and blood vessels trying to preserve the remaining amount of water by increased reabsorption, decreased excretion and vasoconstriction to comparitively useless parts of the body) and on continued dehydration, heart is not getting enough blood to pump as liver is sacrificing all its blood to the brain and cells are being depleted of water and are dried up. So blood is dense and there is not enough amount to reach the brain and brain cells don't get enough glucose (ischemia) and build up of urea and BUN in blood on the other side. Brain Cells switch the metabolism as they try to keep the cells alive only to produce radical oxygen species as by-products which in turn destroys the cells. And hence. Death. Eventually.


No, you cannot. Although we don't know how sleep works, we know that lack of sleep is very devastating to the body, and nothing (including laying in bed relaxed but awake) can replace it. If a rat experiences 100% lack of sleep (somebody keeps it awake all the time), this will kill it sooner than 100% lack of food would. There are no wake-until-you-die studies in humans, but even reduced sleep has very bad effects, both cognitive (it impairs you similarly as if you were drunk) and physiological (metabolic changes: you need more energy for the same actions, and food intake increases disproportionally).

If you have insomnia (and yours sounds severe), you need to get it treated. There are different options depending on whether an underlying cause is found, and whether behavioral therapies turn out to work for you. There are no alternatives which replace sleep.

The above is just a summary. For a dry but very reliable source on sleep, see Principles of neural science (ed. Kandel et al), Chapter 51 written by David McCormick and Gary Westbrook. For a very good popular science book on the subject, see Sleep thieves by Stanley Coren, I can recommend it for anybody with insomnia.


Autotrophic and heterotrophic organisms in anaerobic condition

It is not necessary that all heterotrophs are aerobic. Many are anaerobes (yeast etc.)
Anaerobic Heterotrophs

These anaerobes live on glycolysis and fermentation (as far as I know). These two processes don't require Oxygen for release of energy.

Glycolysis

Alcohol Fermentation

Lactic Acid Fermentation

Alcohol Fermentation takes place in yeast (just an example) and Lactic Acid Fermentation in Muscle Cells.

The autotrophs will take care of themselves as photosynthesis require no Oxygen. If place in correct conditions (light and water are available), then they will thrive.

So, the answer to your question would be that both can survive. It varies from species to species. If you select the correct one then, both would survive or only one of them.


why can a queen wasp sting many times but a worker bee can only sting once?

It's not true that all stingers have barbs. Wasps, and many other species, don't have barbed stingers, and therefore they can afford to sting you repeatedly without being killed. Worker bees, on the contrary, have a barbed stinger that gets stuck in your skin.

Although wasps have a more powerful venom than bees, with bees usually the venom sack remains attached to the stinger and will keep pumping venom even after the bee itself has run away and died, causing the sting to be more painful. However, because bees died after stinging, they are less likely to sting you compared to wasps, hornets, yellow jackets and bumblebees.


Why Do Ruminants Require A Multi-Compartment Stomach To Digest Food?

There is more difference than just the parts of plants that are eaten.

Two of their stomachs - rumen and reticulum are not used for digesting food at all. Multiple rounds of chewing and mixing with saliva, wich result in very small particles of undigested food help the bacteria in those stomachs reach, digest and use that cellulose-rich plant material. Cows "eat" the bacteria from their stomachs and the grass is just food for these bacteria. You could say that cows are not herbivores but secondary consumers.

Look at this picture (from Wikipedia article on ruminants, a good place to check all this in more detail but still simpler than most professional books):

See that the ruminants have the same second and third part of their digestive system (though the bacteria use up most of carbohydrates, so some difference in absorbed material), but have an additional part in the front - where the microbes digest and ferment the food, that the ruminant has provived them. The reticulorumen needs to be large in order to provide space for all that plant material and bacteria.


Are all fusion genes somatic in origin or can fusion genes be germline?

There is at least one (possible) description of an inherited (aka germline) fusion gene:  KANSARL.  See the paper "Identification of KANSARL as the first cancer predisposition fusion gene specific to the population of European ancestry origin" by Zhou, Yang, Ning et al., Oncotarget. 2017; 8:50594-50607.

  KANSARL fusion gene is familially inherited and may be ubiquitously expressed in KANSARL-bearing individuals
  The presence of KANSARL fusion transcripts in normal and adjacent tissues in CGD and VPD raised the possibility that KANSARL fusion transcripts are derived from a germline-inherited fusion gene. To investigate this possibility, we performed RNA-seq data analysis for the lymphoblastoid cell lines derived from the families in the CEU population (CEPH/Utah Pedigree 1463, Utah residents with ancestry from northern and western Europe), which includes a three-generation family with 17 individuals [47]. Supplementary Table 9 and Supplementary Figure 8 show that KANSARL fusion transcripts were detected in 15 of 17 family members, as indicated by black squares and circles in Supplementary Figure 8, except son (NA12885), which is deviated from the first Mendel law. A reasonable explanation is that the grandfather sample (NA12889) might have been mixed with the son sample (NA12885). To prove this possibility, we performed analyses of the WSG data (PRJEB3381) and RNA-seq from 1000 Genome Project, and shown that both WSG and RNA-seq of grandfather sample (NA12889) are KANSARL-negative while WGS of the son (NA12885) is KANSARL-positive (Supplementary Table 10). Supplementary Table 10 shows the genomic breakpoint 1 and 2 of the KANSARL fusion gene (Supplementary Figure 5 and 9) identified by analysis of WGS data among some members of CEPH/Utah Pedigree 1463. Therefore, Both WGS and RNA-seq data support that the father (NA12877) and the mother (NA12878) have the genotypes of KANSARL-/KANSARL- and KANSARL+/KANSARL+ respectively and all their offsprings are the genotype KANSARL+/KANSARL-


Is it true that ethanol can have some positive effects?

Alcohol has caloric value.

First worlders today have a wealth of high calorie food choices which make the caloric value of alcoholic drinks either irrelevant or detrimental.  But it was not always this way. In circumstances where other caloric sources were limited or unpalatable, alcohol supplied calories needed to supply the energy demand of workers.  Persons working energy-intensive jobs (such as field labor or factory work) have historically supplemented calories from food with calories from ethanol.  The below excerpt discusses the dietary habits of metalworkers in the late 1800s.

Drink, Temperance and the Working Class in Nineteenth Century Germany

  Despite the overall improvement in dietary standards of the previous
  two or three decades, the situation of these Manheim workers suggests
  that alcohol remained an essential part of the working-class diet. If
  provided necessary calories in palatable form. The sharp flavor of
  alcoholic beverages could add spice to otherwise monotonous fare,
  providing a sense of warmth and fullness even when meals were cold and
  unsatisfying. Perhaps most important, alcohol provided energy in
  concentrated form. Alcohol, whether in the form of beer or spirits,
  enabled workers to reduce the sheer quantity of food that had to be
  gotten down each day. The distinguished physiologist Max Gruber
  calculated that a worker who consumed even a 10th of a liter of
  schnapps with the meal could come up with no energy loss, reduces
  potato and rye bread consumption but some 288 and 122 g
  respectively.”Try eating a kilo of black bread or two or more kilos of
  potatoes day after day”, Gruber told his well fed middle-class readers
  in 1888, “and you’ll discover what a relief it can be to substitute a
  pungent and stimulating beverage for a 10th of this mass”.

The health benefit of alcohol consumption here would be that of not starving in situations of high caloric expenditure.   calories are concentrated as compared to carbohydrates and distilled spirits also have an indefinite shelf life - not true of grains and potatoes.


Why is a heritability coefficient not an index of how "genetic" something is?

Rather than discussing what heritability is not through wordy sentences, let's just talk about what heritability is. There are two "types of heritability":

Heritability in the broad sense
Heritability in the narrow sense.

I will discuss a few concepts and slowly introduce the concept of heritability in both senses.

Phenotypic trait

The phenotype is the consequence of the genotype on the world. In brief, a phenotypic trait is any trait that an individual is made of!

Quantitative trait

A quantitative trait is any trait that you can measure and ordinate, that is any trait that you can measure with numbers. For example, height is a quantitative trait as you can say that individual A is taller than individual B which is itself taller that individual C.

Variance of a quantitative trait

In a population, different individuals can have different values for a given phenotypic trait $x$. Because we are talking about quantitative traits we can calculate the variance of the trait in the population. Let's call this variance $V_P$ such as

$$V_P=\frac{1}{N}\sum_i (x_i - \bar x)^2$$

In the above equation, $x_i$ is the value of the phenotypic trait $x$ of individual $i$. $N$ is the population size (there are $N$ individuals in the population) and $\bar x$ is the average phenotypic trait $x$ in the population.

$$\bar x = \frac{1}{N}\sum_i x_i$$

What is causing phenotypic variance

Why would a population display any phenotypic variance? Why wouldn't we just look exactly the same? What explains these differences?

For some traits, we see very little variance. To consider the example the OP gave in the post, the number of arms in the human population shows very little variance. However, there is quite a bit of variance in terms of the number of IQ, in terms of height or of weight.

There are two (main) sources of variance that are underlying this phenotypic variance. The first one is the genetic variance and the second one is the environmental variance. We will call the genetic variance $V_G$ and the environment variance $V_E$.

If in a population, people vary a lot in terms of how many hamburgers they eat, then there is a non-negligible $V_E$ underlying the phenotypic variance $V_P$ for weight. If in a population, there is a lot of variation of genes affecting weight, then there is a non-negligible $V_G$ underlying the phenotypic variance $V_P$ for weight.

By the way, a gene (or another non-coding sequence) that is polymorphic (i.e. has more than 1 allele in the population) and which explains some of the variance in the phenotypic quantitative trait is called a Quantitative Trait Locus (QTL). A locus is a sequence (of any length) on the genome.

Math reminder

Variances of uncorrelated variables can simply be added! For simplicity, we will assume for the moment that we are considering uncorrelated variables. As a consequence, we can express the phenotypic variance $V_P$ as a sum of the phenotypic variance that is due to environmental variance $V_E$ and the phenotypic variance that is due to genetic variance $V_G$

$$V_P=V_E+V_G$$

This equation is slightly simplified and this will affect the below calculations. See the section Other sources of phenotypic variance for more info.

We can now talk about heritability!

Heritability in the broad sense

Heritability in the broad sense $h_B$ is defined as the fraction of phenotypic variance $V_P$ that is explained by genetic variance $V_G$. In the equation, it gives:

$$h_B=\frac{V_G}{V_P} = \frac{V_G}{V_E+V_G}$$

Heritability in the narrow sense

Heritability in the narrow sense $h_N$ makes one further trick. We have to consider that the genetic variance $V_G$ that is underlying the phenotypic variance can itself be decomposed into a sum of variances. The variances that we like to consider the additive genetic variance $V_{G,A}$ and the dominance genetic variance $V_{G,D}$.

The additive genetic variance is the genetic variance that is due to additive interaction between alleles. The dominance of genetic variance is due to non-additive interactions between allele.

We can now define the heritability in the narrow sense $h_N$ as the is defined as the fraction of phenotypic variance $V_P$ that is explained by the additive genetic variance $V_{G,A}$. In the equation, it gives:

$$h_N=\frac{V_{G,A}}{V_P} = \frac{V_{G,A}}{V_E+V_G} = \frac{V_{G,A}}{V_E+V_{G,A}+V_{G,D}}$$

In the special case, when all the genetic variance $V_G$ is exclusively done through additive interactions, then $V_{G,D} = 0$ and $V_{G,A}=V_G$ and therefore $h_N=h_B$

Interpretation of the heritability

If all of the phenotypic variance is due to genetic causes (and regardless of whether there is a lot or a little variance), then $h_B=1$. If all of the phenotypic variance is due to environmental variance, then $h_B=0$.

So what does a $h_B=0.3$ means?

It means that 30% of the phenotypic variance is explained by genetic variance and that 70% of the phenotypic variance is due to environmental variance.

So, what if there is no phenotypic variance in the population? if $V_P=0$, then the heritability is undefined (as dividing by zero is undefined). However, in general, we tend to think that there is always a tiny bit of environmental variance and most people would just go on saying that heritability is 0 when $V_P=0$.

What will affect the heritability?

A measure of heritability is true for one population, in one environment.

If you change the population, add a few mutations for example, you might well create a polymorphic locus that is causing some phenotypic variance. If you put the same population in another environment, you could suddenly have more or less phenotypic variation due to environmental variance. Typically, if you measure heritability in the lab in a controlled and constant environment, then you will likely overestimate the heritability (as you underestimate $V_e$) compared to the same population that is living in a very heterogeneous environment.

What heritability is not!

If a trait has low heritability, it does NOT mean that it is (or is not) an adaptation. It only means that there is no genetic variance that explains the phenotypic variance.

Why do we care about heritability?

If there is no genetic variance for a trait, it means that the only way this trait can change through time is by changing the environment (or by creating a non-zero genetic variance through mutations). If there is a non-zero genetic variance and if there is a difference in fitness between individuals having different trait value then, the trait is under natural selection.

The most commonly used index of heritability in the heritability in the narrow sense $h_N. $Why do we care about $h_N$?

Let $\bar x_t$ be the mean phenotypic value of the trait $x$ at time $t$. One generation later, that is at time $t+1$, the mean phenotypic value is $\bar x_{t+1}$. Let's define the response of selection $R$ as the expected difference between these two quantities, that $R=E[\bar x_{t+1} - \bar x_t]$. Let's define the strength of selection $S$ and the heritability in the narrow sense $h_N$, then

$$R=h_N \cdot S$$

As a consequence knowing $h_N$ allows us to predict the effect of selection on a given trait.

This equation is called the breeder's equation (see this post about its interpretation).

Other sources of phenotypic variance

Saying $V_P=V_G+V_E$ is a little too simplistic. In reality, there are other sources of phenotypic variation such as variance due to epigenetic changes $V_I$ and variance due to developmental noise $V_{DN}$ for example. It is also sometimes very important to consider the covariance between any pair of such variance. So, the equation would more correct if stated as

$$V_P = V_G + V_E + V_I + V_{DN} + COV(V_G, V_E) + COV(V_G, V_I) + COV(V_G, V_{DN}) + COV(V_E, V_I) + COV(V_E, V_{DN}) + COV(V_I, V_{DN})$$

Note that everyone is free to further decompose any of the above variance into a sum of variances as we did above for the genetic variance. For example, the environmental variance $V_E$ could be decomposed into the sum of the phenotypic variance due to variance in temperature $V_T$ and the phenotypic variance due to variance in precipitation $V_{\text{precipitation}}$ assuming the other types of environmental variances are negligible.


Evolution of sexual reproduction from asexual

Sexual reproduction is a process where two cells fuse to form a diploid cell. Unicellular organisms (or even multicellular lower organisms like alga, fungi and protists) prefers to reproduce by asexual means under favourable conditions. But when the conditions become unfavourable, they opt to follow sexual reproduction. This suggests, sexual reproduction evolved to increase the chances of survival under unfavourable condition.

So how does sexual reproduction helps in increasing survival rate? By fusion of cells i.e., sexual reproduction a cell now becomes diploid and hence have two copies of its genome. This increased copy of genome is beneficial in repairing any breaks or alteration in genome, as the other copy will act as a template for repair (via homologous recombination).

To get a better hold of this, let us take an example. Let there be a population of haploid cells. This population was exposed to conditions which would cause damage to genome, specifically would cause breaks in DNA. There were two cells "Fella A" and "Fella B". They both knew that their genome has suffered damages, but neither was successful in repairing the DNA as they required an intact DNA template for repair. Suddenly "Fella B" came up with this great idea to fuse with "Fella A". This would work, reasoned "Fella B", as the position of damage in the DNA in his genome is different from the position in "Fella A". Fusion of cells was the first step towards evolution of sexual reproduction.

Later on the biological system realised importance of variation generated by sexual reproduction and hence this mode of reproduction caught on with various lineages.


Can a person be infected with Polio even after vaccination in childhood?

Short answer: Yes.

Slightly longer answer:
Recall how a vaccine works - it introduces an antigen to the body, which provokes the body to produce antibodies towards that antigen.

Antibodies, simply explained, call upon the remainder of the immune system to fight off a potential infection of foreign body. If there is no immune system to mobilize, the infection would most likely run its course. However, the immune system would have to be sufficiently weakened in order to not be able to fight the infection.


Identification: Stinging walking/flying skin cells

That is a Lace bug (Hemiptera). Family Tingidae. https://en.wikipedia.org/wiki/Tingidae.
From Wikipedia: "Lace bugs sometimes fall out of trees, land on people, and bite, which, although painful, is a minor nuisance. No medical treatment is necessary."


Turgor pressure is the force within the cell that pushes the plasma membrane against the cell wall.

It is also called hydrostatic pressure, the pressure measured by in fluid when at equilibrium.

It's term taught in biology class in school for plants that sag.

I saw a mushroom that had come through a new pavement once. it was cool.

pascal is the atmosphere at sea level:


How are isovolumetric contraction and afterload related in the cardiac cycle?

The important thing to remember is that the "afterload" on the heart is the diastolic blood pressure in the aorta. In other words, the pressure in the aorta that the heart must overcome to open the aortic valve and create a pressure gradient to force blood into the aorta and generate flow. The isovolumetric part of the contraction is the generation of pressure up to the afterload 'pressure'. Once the pressure in the heart is higher than the pressure in the aorta a pressure gradient is generated and the aortic valves open and blood flows out of the heart into the aorta. During this movement of blood the heart is contracting again and changing volume (i.e. not isovolumetric anymore).

If the afterload is higher (i.e. higher blood pressure or hypertension) it increases the work on the heart because it has to generate an even higher pressure within the heart to open the aortic valve to generate the pressure gradient and flow.

If the afterload is lower (i.e. low blood pressure or hypotension) the work on the heart (with all other factors remaining constant) would decrease because the pressure to open the aortic valves and create flow is lower. The diagram below is available online at this link. This is a very common picture/diagram that can be found in any cardiovascular physiology textbook.

Note: In the picture below the isovolumetric contraction is only the time between the two vertical lines as indicated. During that isovolumetric contraction you can see that the volume (i.e. the red line) stays the SAME, but the pressure in the ventricle significantly increases up to the point of aortic pressure.


Why do live crabs in a bucket prevent each other from escaping?

There should be a dictum somewhere that states, "Never ascribe to psychology what is caused by instinct."

By that I mean, the captured crab has a survival instinct. It's not going anywhere on the bottom of the bucket; it needs (I don't even know if I would say, "It wants") to get out. Out means "up", since "sideways" doesn't get them out, which doesn't prevent them from trying that as well (as shown by scuttling around the bottom repeatedly.)

The sides of the bucket are slick; there's nothing to grab onto. So if one crab climbs atop another, suddenly there's something "above" (a shadow? An outcropping? Another crab?) to grab onto to hoist itself up the side. So the crab instinctually grabs onto something above it. Unfortunately for the higher crab, there's nothing for it to hold onto above it, so he falls back into the bucket.

If only they would work together, a few of them might make it out. If they were chivalrous, the females and the young ("women and children") would go first.

I don't really know crab psychology, nor do I know any crustacean psychologists. All kidding aside, however, there have been some attempts to study stress in crustaceans. Science Daily published an article about stress in declawed crabs. What you and I think of as "stress" may be different than how the author thinks of it, but from the article, it's pretty clear that Dr. Elwood means psychological stress. However, there is no evidence to support that; the increased mortality of declawed crabs is more likely to be due to physiological stress (as in the second cited paper.) He has been called out on this by fellow biologists.

Crabs are invertebrates. If you want to learn about invertebrate psychology, the octopus is your animal.

Declawing Crabs May Lead To Their Death
Assessing Stress and Predicting Mortality in Economically Significant Crustaceans


Why do human ears have a lower boundary for the lowest energy perceivable signal than eyes?

Preamble. There is a lot of misunderstood science here and you are more than right for questioning the lecturers interpretation of these energy values; something the other answers do not discuss. The problem arises from a dodgy reference and a lot of conjecture.
In summary.

Light and sound cannot be compared energetically in a biological context.
Our ears probably don't hear lower energies than our eyes see to avoid prey.

Let us ignore the reference...
The reference is from BWB which is as far as I can tell a non peer reviewed federal technical publisher and that this is a textbook about ergonomics. But given its obscurity, it having never undergone peer review, it being not biologically scientific, it is safe to ignore from the context of a scientific biological topic. The fact it is in German doesn't help either.
If anyone can provide an open link to this reference or correct me on this I would be grateful. Google scholar turned up no hits other than a citation.
Let us give your lecturer the benefit of the doubt. This answer assumes that there are derived energy values for sight and sound as your lecturer suggested and that eyes sense higher energy than ears.
Is hearing omnidirectional to detect predation?
I'm going to use the term sensory setup to describe that our senses use fixed ears that hear omnidirectionally and forward facing directional eyes.

... hearing is much more important for this reason [omnidirectional] to detect predators, even if they are silent.

Let's flesh out this hypothesis so that it makes sense in practical terms.

A small movement is made by the predator. This generates some sound and some change in light. In the case of forward sighted animals, the sound is much more difficult to detect than the light would be as it contains less energy. The ears must compensate by detecting lower energy signals than the eyes would need to in order to detect the predator.

Before we question the physics, this biological hypothesis is very tough to swallow. Without citation I would say it is unreasonable conjecture.
Examples that contradict this hypothesis:

Gorillas have no natural predators or prey but have a very similar sensory setup to ours that helps social bonds.

Meerkats on the other hand rely on sentries that broadcast a series of bleats after spotting prey by sight. Other meerkats immediately hide when hearing this signal (interestingly, this call is mimicked by Drongos who steal the meerkat food that is abandoned in the panic) before checking if a predator is present. Meerkats have a similar sensory setup to ours.

There are other megafauna like deer that are prey for the big predators; predators that would have put ancestral humans on the menu. Deer-like prey animals rely heavily on near-omnidirectional eyesight and can angle their ears to focus on an area to hear stealthy predators. This is the "opposite" sensory setup that has the same conclusion of predator evasion.

Even those non-exhaustive examples makes the hypothesis questionable at best.

...there is a range in which "interesting" signals occur. If the interesting signals have lower energy for sound than for visual signals the ear adapted to this range.

This answer too is based on pure conjecture it seems, however it more aligns with how biology might work.
It is sensible to say evolution selected for animals that could detect noises and lights that, if reacted to, saved the organisms life to continue propagating. This hypothesis bypasses the idea that sound and light are comparable energetic signals too, which is good (discussed below).
This hypothesis also allows for various morphologies to have evolved depending on what an "interesting signal" is to that species.
Light vs Sound.
These aren't the same thing.
The elephant in the room of this question is that light and sound are non-comparable energies. This is due to source, speed, distance, medium, mechanisms for receiving the energy (eyes and ears) and most significantly in a biological context neural interpretation. These values are so abstract that even if an energy value is calculated, it is not in anyway quantitatively comparable in biological organisms. For example a really loud subsonic whale call is not the same as a small change of grass parted by a wolf as it sneaks up on you. One is absolutely essential for survival, the other is undetectable. Both could theoretically have the same "energy".
Note Frequencies are the biologically important part of the "energy" but must be considered as two different methods of acquiring sensory information. The difference between a chimp mating call and a territorial threat are very similar but for their frequency, and eating the delicious red berries compared to the toxic blue berries is also down to the frequency reflected from them!
There is little to no biological literature that uses energy values as sensory input. This would just obscure the actual important physical aspects of the sensory input values.

I hope that helped clear things up and accurately discussed your dis-satisfaction with your lecturers' hypothesis despite being months too late!


Check on 23andme what type of CYP2D6 substrate metabolizer I am

Unless your polymorphisms have been tested against a particular drug, you can't extrapolate a starting dosage for it based only on your genotype.  It's better to actually take the drug, and change dosage based on observations.

See this paper

https://www.ncbi.nlm.nih.gov/pubmed/24935087

  CONCLUSIONS AND RELEVANCE: In this meta-analysis of randomized
  clinical trials, a genotype-guided dosing strategy did not result in a
  greater percentage of time that the INR was within the therapeutic
  range, fewer patients with an INR greater than 4, or a reduction in
  major bleeding or thromboembolic events compared with clinical dosing
  algorithms.

.

  why isn't this information more readily accessible to 23andme users,
  given the relatively large risks incurred by not knowing one's
  reaction to a large number of drugs?

Because no-way no-how does 23andMe want to be in the business of giving medical advice.  Nor should they be, because for most things, we have no idea how to convert genotype knowledge anything medically actionable.


Has anyone modelled calcium oscillations using Matlab software?

I wish to share an open-source modelling study on Ca2+ oscillations in astrocytes which contains a detailed description of the underlying math and even better, it has supplementary Matlab code published alongside (Zeng et al., 2009). This may be of help to check your formulae and script.

Unfortunately I do not feel inclined to start troubleshooting and bug-fixing your formulae and Matlab code, because, as mentioned in the comments, the issue can be anywhere in the chain of events.

Reference
Zeng et al., Biophys J (2009); 97(9): 2429–37


Formula for Oxygen Consumption for Atlantic Salmon (Mathematical) - insecurities regarding variable

Yeah, it's hours.
Further down in the paper, you can read,

The mass exponent was estimated to be −0.33 (b in Eq. (4)) for the specific metabolic rate \begin{equation} V_{O_{2}} (mg\space {O_{2}} \cdot kg^{-1} \cdot h^{-1}) \end{equation}

Rate by very definition implies an extent of time; since mg refers to oxygen and kg refers to water, the only variable left is h, which evidently refers to hours. Hours also jives well with the experimental design.

Source:

Grøttum JA, Sigholt T. 1998. A model for oxygen consumption of atlantic salmon (salmo salar) based on measurements of individual fish in a tunnel respirometer. Aquacultural Engineering 17(4): 241-251.


Our eyelids close when we sleep probably for the obvious reason that it prevents the sclera and cornea from drying out, becoming accidentally scratched (such as blowing dust) and allowing oxygen diffusion from the inside of the eyelid (to the sclera and cornea). Fragile corneas are a requirement for our vision. Thick corneas are much less fragile but then attenuates more light.

From terdon:

1) blinking requires muscle movement which sort of defeats the purpose of resting

2) closed eyelids offer much better protection than periodic blinking

3) if you can blink, you have eyelids.


How are different types of cells created from zygote?

I'm not sure about the first developmental stages but, given you already have hundreds of cells with slightly different physiology, the next developmental stages like dev. of neural tube happen through excretion of translation factors and growth factors in several cells. Each of those cells that are in a region where more than one excretion overlaps get a higher dose than the others. This is the signal for the cell to differentiate into another type, by changing its physiology. Such factor excretions are important events, and the genes encoding for the factors are evolutionally highly conserved (so called homeobox proteins).

However, this has nothing to do with mitosis. The newly divided cell does not decide on its own but reacts to a stimulus, like skin cells develop into skin cells because they are on the outside of the cell ball. Excreted factors do the fine tuning.


Why does it matter to predict protein structure?

How do you want to predict function and binding partners without knowing how your protein looks like? The sequence itself contains only limited information. Similar sequences might fold into similar structures with similar functions. These motifs can be used to transfer your knowledge from one protein to another, which might have similar e.g. binding abilities. But the motif might be nonfunctional in the second protein, because it is hidden in an inaccessible part of the protein due to its folding structure.

Interactions between proteins are weak compared to intramolecular bonds and dynamic. Different amino acid side chains have different characteristics (like polarity, hydrophobia etc.) which make specific interactions possible. Specific amino acids have to be accessible and while they might be far apart in the sequence, the folding of the protein brings them close together in its final shape.

Even small modifications like phosphorylation can alter the structural conformation significantly and e.g. change the enzymatic activity. Therefore, for analyzing protein function, finding binding partners or designing binding compounds (drug development), we need to know its three-dimensional structure. With the structure you can simulate binding affinity/dynamics. Scientists also try to resolve the protein structure in its different states to clearly see the differences.

Keep in mind that complex diseases can be caused by a single mutation, which exchanges only a single amino acid in the sequence but can have severe implications for protein function. Knowing the structure, the position of the amino acid and how the change affects the characteristics of the protein domain (e.g. charge), we can fully understand what's happening on the molecular level.

Since it is far from trivial to analyze the structure of a protein, predictions bridge the gap for functional predictions until the molecular structure of the protein has been reconstructed. But only with atomic resolution you will be able to properly identify interactions.

The question of how to do structural prediction might be beyond the scope of this answer. Pubmed lists around 400 papers each year on this topic. Depending on the amount of information you have about the protein or its family members (proteins with very similar sequences), you can use other known structures to predict an unknown structure:

https://medium.com/@HeleneOMICtools/a-guide-for-protein-structure-prediction-methods-and-software-916a2f718cfe


Hamming distance between two DNA strings

Your logic on the problem seems correct. The wikipedia article about the Hamming distance describes both a python and a C implementations. The python version assumes two strings of equal length:

def hamming_distance(s1, s2):
    #Return the Hamming distance between equal-length sequences
    if len(s1) != len(s2):
        raise ValueError("Undefined for sequences of unequal length")
    return sum(ch1 != ch2 for ch1, ch2 in zip(s1, s2))


Why does something taste less sweet after eating something else that is sweet?

It's a general flaw (IMO bad design) in organic/neural sensor frameworks where inputs tend to be measured relative to previous experience rather than absolute quantitative.

This happens with weights as well. There have been plenty of experiments where people are asked to pick up a heavy weight and then a light weight, then record/estimate the perceived light weight. The next day, they pick up a medium weight and then the same light weight and record the perceived light weight.

The 2nd recording turns out "heavier" because of relative perception.

Suggestion: Computer-mediated nerves designed to measure in absolutes.


What is the function of epidermal ridges on human fingers (that produce fingerprints)?

I found many plausible claims that fingerprints increase friction. However, the following article claims, at least under their experimental conditions, that fingerprints actually decrease friction with smooth surfaces by reducing contact area.
Fingerprints are unlikely to increase the friction of primate fingerpads.

It is generally assumed that fingerprints improve the grip of primates, but the efficiency of their ridging will depend on the type of frictional behaviour the skin exhibits. Ridges would be effective at increasing friction for hard materials, but in a rubbery material they would reduce friction because they would reduce contact area. In this study we investigated the frictional performance of human fingertips on dry acrylic glass using a modified universal mechanical testing machine, measuring friction at a range of normal loads while also measuring the contact area. Tests were carried out on different fingers, fingers at different angles and against different widths of acrylic sheet to separate the effects of normal force and contact area. The results showed that fingertips behaved more like rubbers than hard solids; their coefficients of friction fell at higher normal forces and friction was higher when fingers were held flatter against wider sheets and hence when contact area was greater. The shear stress was greater at higher pressures, suggesting the presence of a biofilm between the skin and the surface. Fingerprints reduced contact area by a factor of one-third compared with flat skin, however, which would have reduced the friction; this casts severe doubt on their supposed frictional function.

That said, the author does later discuss their potential role in gripping of rough or wet surfaces:

So why do we have fingerprints? One possibility is that they increase friction on rougher surfaces compared with flat skin, because the ridges project into the depressions of such surfaces and provide a higher contact area. Experiments on materials of contrasting known roughness are needed to test this possibility.
A second possibility is that they facilitate runoff of water like the tread of a car tyre or grooves in the feet of tree frogs (Federle et al., 2006), so that they improve grip on wet surfaces. Though there is evidence that friction falls on fingers coated with high levels of moisture (Andre et al., 2008) it is possible that it falls less quickly on fingertips than on flatter skin. Once more, suitable experiments could test this idea.

There seems to be more consensus on the idea that fingerprints are useful for tactile sensation. The following are just some articles which discuss this.
Effect of fingerprints orientation on skin vibrations during tactile exploration of textured surfaces.

In humans, the tactile perception of fine textures is mediated by skin vibrations when scanning the surface with the fingertip. These vibrations are encoded by specific mechanoreceptors, Pacinian corpuscules (PCs), located about 2 mm below the skin surface. In a recent article, we performed experiments using a biomimetic sensor which suggest that fingerprints (epidermal ridges) may play an important role in shaping the subcutaneous stress vibrations in a way which facilitates their processing by the PC channel. Here we further test this hypothesis by directly recording the modulations of the fingerpad/substrate friction force induced by scanning an actual fingertip across a textured surface. When the fingerprints are oriented perpendicular to the scanning direction, the spectrum of these modulations shows a pronounced maximum around the frequency v/λ, where v is the scanning velocity and λ the fingerprints period. This simple biomechanical result confirms the relevance of our previous finding for human touch.

The role of fingerprints in the coding of tactile information probed with a biomimetic sensor.

In humans, the tactile perception of fine textures (spatial scale <200 micrometers) is mediated by skin vibrations generated as the finger scans the surface. To establish the relationship between texture characteristics and subcutaneous vibrations, a biomimetic tactile sensor has been designed whose dimensions match those of the fingertip. When the sensor surface is patterned with parallel ridges mimicking the fingerprints, the spectrum of vibrations elicited by randomly textured substrates is dominated by one frequency set by the ratio of the scanning speed to the interridge distance. For human touch, this frequency falls within the optimal range of sensitivity of Pacinian afferents, which mediate the coding of fine textures. Thus, fingerprints may perform spectral selection and amplification of tactile information that facilitate its processing by specific mechanoreceptors.

This paper also asserts a reason for the elliptical nature of fingerprints:

In humans, fingerprints are organized in elliptical twirls so that each region of the fingertip (and thus each PC) can be ascribed with an optimal scanning orientation.


Trick fruit trees into flowering later in the spring

You are on the right track, but snow is the wrong way.  When the snow is around it insulates the ground.  Soil surface temps stabilize at close to freezing.

Instead, do the reverse.  Remove, or firmly pack the snow.  Do so about 1.5 times the dripline radius.  (If the dripline is 10 feet from the trunk, pack out to 15.)

This allows the ground to freeze deeper.  However see other answers.  I'm not nearly as confident about this now.

Now once melt starts in earnest, cover the ground with a couple of layers of the insulated tarps used by contractors to pour concrete in freezing conditions.  This will keep the ground cold, both by reflection (most tarps of white) and by insulation, and by wind reduction.  This should slowdown bud break by at least a week, and more likely two weeks.

For a single tree, you may be able to do protection with an oscillating sprinkler (for a big tree) or a impact rotary.  Key thing with these is to start them before the temperature gets down to freezing.  The initial few minutes while it's working with dry air you can get supercooled droplets that kill your buds instantly.   Start the sprinkler when the temps are about +6

A third way that may help is to graft onto a different root stock.  The russians work with pear on cotoneaster.  This dwarfs the pear strongly, but also forces it into dormancy earlier.  I haven't read what it does to bud break, but given that pears also tend to be early bloomers, it must help.  These interspecies grafts are working in Siberia in zone 2.

Look at using prunus that tend to go into dormancy early in the fall.

Another way to experiment with would be to keep them a bit thirsty in the fall.  If the roots are slightly dehydrated, then the first moisture they get in spring will be used to rehydrate.  This may delay bud break by a day or two.

Some trees do their budding on reserves in the bud and twig itself.  I see this some years when a winter has killed roots.  The leaves break bud, inflate about to about 1/4 size, then wither.  For these guys it's a matter of enough degree days or the day length on the bud itself.

If it's degree days, you may be able to stretch things out by making the tree lighter coloured.  Many people spray dormant oil in late winter anyway.  By adding some cheap latex paint to the dormant oil mix, you lighten the colour of the twig, and so reduce sun warming.


Mechanics of going from DNA sequence to metabolic network

The question is not too broad, just involves a fair bit of work to both do the research and compose a response. I'll do the latter, but in brief.

The strings of the four nucleotides encode genes. Sometimes these genes are broken into protein-coding portions (exons) and sometimes intervening, non-coding regions (introns). Bacteria, for example do not have introns within genes while most human genes do. The nucleotides in the protein-coding portion of the gene do just that - give instructions on how to synthesize the protein by directing which tRNAs the ribosome uses to translate the genetic code into a protein chain.

A useful phrase is protein sequence dictates protein structure and that structure dictates function. So, the proteins do things and many act as enzymes or modulators of enzyme activity. An enzyme catalyzes a biochemical reaction, lowering the activation energy to go from reactant(s) to product(s). One enzyme can be thought of as one unit within a metabolic network. A modulator might activate or deactivate an existing enzyme. A protein kinase is a good example of a modulator.

Next, string some of those enzymes together to build a pathway. A common example is glycolysis. Think of this as a chain where the output or product of enzyme A serves as input to enzyme B, whose product is the input to enzyme C, and so on. These pathways are two-way, but it is exceedingly difficult to travel from the final product all the way up such a pathway to the initial input within the confines of a biological system. Thus, the pathways in practical terms are thought of as one-way.

However, the pathways do not function in isolation. The final product may serve as input to one, two or more other pathways. Your pathway of choice may begin with the output of another process. Furthermore, pathways can branch: Glycolysis can proceed to glyceraldehyde 3-phosphate and pyruvate, or directly after glucose 6-phosphate formation can be shunted to the pentose phosphate pathway to yield reducing power and 5-carbon sugars (to be used in ATP, CoA, FAD, NAD+, DNA and RNA). Now, pathways leading to other pathways and branches and such make a network.

You and your colleagues might want to know if genes within a metabolic network are over- or under-represented in a test compared to control. Or, genes for a given network are not present in one species compared to several others. Or, one could estimate the flux through such a network given a set of measures.

Peruse examples at both KEGG and Reactome, expecially at KEGG where you can view pathways pertinent to your organism(s) of choice.


It is one of the many species and hybrids of Clematis that is grown in gardens. It looks similar to the common Clematis alpina but might be a closely related species or à hybrid.

(Picture of C. alpina fr.o.m. Wikipedia)


Hepatitis Lab diagnosis based on serology

HBcAg is capsuled by HBsAg and therefore can't be detected, while within the cells it's still free (before assembly of the virus).
The test checks for presence of antibodies (IgM) against HBcAg. It does not try to detect HBsAg anyways.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC154683/


What decides between the synthesis of eumelanin and pheomelanin on a biochemical level?

Let's have a look at the pathway first (this figure is figure 2 from reference 1), which shows the basic pathway of pigment biosynthesis:

The first important step, the oxidation of the amino acid tyrosine to Dopaquinone (DOPA) by the tyrosinase is the same for both pathways (eumelanin and pheomelanin production) and rate limiting.

The important step is the next one: Either the formation of Cyclodopa (for eumelanin) or Cysteinyldopa (for pheomelanin). As long as the concentration of cysteine in the melanocyte is above 13µM (see reference 1) the formation of pheomelanine is favored and biochemically much faster than the cyclisation of DOPA.

If there are high levels of tyrosine and normal to low levels of cysteine, the cysteine will be depleted at some point and only eumelanin is made.

The opposite will happen if either a lot of cysteine or little tyrosine is available. It will also happen, when the available tyrosine cannot be oxidized into DOPA when there is little or reduced Tyrosinase activity.

And this is actually what happens in the case of the MC1R mutation. MC1R is a receptor on the pigment producing cells which regulates the production of pigment upon external signals (as UV radiation to the skin) (see reference 2 for more details). When mutated is is not or much less functional leading to much less (or no) signals to the downstream gene (MITF) which regulate the enzymes for the pigment production.

Low signals lead to low tyrosinase production which then can only produce little DOPA. Since the cysteine stocks of the cells will not be depleted then, only pheomelanin is produced causing people with MC1R mutations to be red haired and having light skin and freckles.

References:

Chemistry of mixed melanogenesis--pivotal roles of dopaquinone.
MC1R, Eumelanin and Pheomelanin: their role in determining the
susceptibility to skin cancer


Which species has the highest proportion of homosexual individuals?

Homosexual behavior have been observed more than 1500 species (according to Museum of Natural History of the University of Oslo). A full comparison between all known species is far beyond the scope of this site, but below I discuss three species of interest. Also, the details of what counts as an homosexual behavior, and also whether you compute incidence or prevalence makes the whole discussion semantically complicated.

According to Simon Levay and Aldo Polani, in domesticated sheep, 10% of the rams (males) prefer mating with other rams than with ewes (females).
About 25% of black swans are homosexuals (Braithwaite, 1981).
In lions, 8% of the mounting is in between two males (Bagemihl 2000)

In humans, around 3%-5% of the surveyed people claim being homosexual or bi-sexual (see wiki > demographics of sexual orientation#Modern_survey_results).


Why Doesn’t Hypercalcemia Cause Muscle Spasms?

Hypercalcemia does indeed cause muscle spasm, but as someone else wrote, hypercalcemia indicates the calcium levels in blood and not in the sarcoplasmic reticuli.

One example where you can observe that increased calcium leads to increased contraction is when you take the cardiac glycoside, digoxin. Digoxin inhibits the Na+/K+ ATPase causing an increased concentration of intracellular sodium ions. Indirectly, the increased levels of sodium will disturb the sodium gradient (because of the accumulation of sodium ions inside the cell) and stop the Na+/Ca2+ exchanger. The consequence of the disturbance of the sodium/calcium exchanger will lead to the increased levels of calcium and the increased storage of calcium in the sarcoplasmic reticulum and thus cause positive inotropy of the myocytes.

You can read more about it here:
Gheorghiade, Mihai, Kirkwood F. Adams, and Wilson S. Colucci. "Digoxin in the management of cardiovascular disorders." Circulation 109.24 (2004): 2959-2964.