text:
Why does the Vas Deferens detour over the pubic bone?
I was surprised to learn that the vas deferens detours over the pubic bone instead of taking the obviously more direct path.
https://human.biodigital.com/widget?be=u1P&uaid=1ly5V
Because I would assume that the vas deferens is more prone to damage facing the front. Also its damage would put procreation at stake.
Hence my question: Is there a biological reason for this path? Some advantage which outweighs or balances its disadvantages?

What do you consider the "obviously more direct path"? The vas deferens has to pass over the pelvis somehow to get back to the level of the prostatic urethra. Remember that the vas deferens travels with a number of other structures (vessels/nerves) in the "spermatic cord".

okay, probably I am being a bit naive here - I didn't study medicine or biology, after all. But just visualize your own reproductive system and think of direct path between testicles and prostate. That path would be a third or less of the actual - so this is what I wonder about. And the solid pelvic bone in the back increases the risk of damage in case of a hit from the front.

The path of the human vas deferens is a similar example. from Reddit AMA with Richard Dawkins So (at least) according to Dawkins the path which the vas deferens takes is simply an evolutionary "mistake".

You may want to look at where the abdominal muscles are, since they have go around them to get out of the body cavity.

The vas deferens following this seemingly odd path is just a result of the natural course of our evolution.  Millions of generations ago, our ancestors were quadrapedal (walked on all four limbs).  Similar to if you were to crawl on your hands and knees today.  In this position the pelvis is rotated forward by ~90 degrees from its position in humans currently.  The natural position of the testicles in this position would be to hang straight down due to gravity.  Which means the vas deferens would have a straight path up in front of the pubic bone.
Generation after generation, our taller and more upright ancestors were able to survive slightly better than their less upright siblings.  Meaning that many of the more quadrapedal siblings died while their more upright siblings survived and reproduced.  This process has continued for millions of generations, leading to our current homonid upright posture.
The path of the vas deferens was established long before our ancestors ever began this slow transition toward standing vertically.  So the vas deferens still follows the same path that it always has, but now our testicles have moved down because we stand vertically.  Which leaves the vas deferens with its seemingly odd route of going forward over the pubic bone and then down to the testicles.
Evolution is a continuous incremental process over the course of millions of generations.  There has been no point at which the vas deferens could be 'unplugged' and rerouted around the pubic bone.  So it now just loops in front of the pubic bone and then to its destination.
Richard Dawkins used the word "mistake" in his description because there is not necessarily an advantage to that particular route of the vas deferens(there may even be small disadvantages), but there was a LARGE advantage to our ancestors standing upright.  So as we evolved to stand more upright, the testicles moved down appropriately and the vas deferens just ended up where it is, simply because that's where it always has been.  Not really a mistake, just the way it worked out.
Hope this is helpful.

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Why do Phobia exist if they aren't advantageous?
A phobia is usually the irrational fear of something, and the individual experiencing it is often unable to justify whether there is such detestation of something which might not even be threatening.
I am aware that there are:

Agoraphobia
Social Phobia
Specific Phobias such as Arachnophobia (fear of spiders) or Ophidiophobia (fear of snakes)

My question is, why do some people have e.g. Arachnophobia but not something closely related such as Entomophobia (fear of insects)?
And why do phobias even exist at all? To me they don't seem to serve a purpose (protection), and do not seem to be of advantageous existence.
Furthermore, I am curious to why exactly a phobia exists – and in some cases manages to be  passed on from the parent to the offspring.
DISCLAIMER:
I am aware of there being several psychological processes involved in this such as events that occurred in early years, or if there is a relative with anxiety, the risk of you suffering of a phobia is significantly larger. I also heard there is a high incidence of people developing phobias after traumatic brain injuries.
However, I am interested in the biological aspect of a phobia, and that why if it isn't advantageous to us, why does it exist?

Why do you say that there aren't people with a phobia of insects in general? Can you support that claim? Also, not everything that exists has advantages. Lots of non-advantageous things exist. Phobias, for example are maladaptive. Fear, on the other hand, is often adaptive.

I think the fault in your reasoning is the assumption that phobias are not advantageous to us. As an example of a potentially useful phobia, consider the fear of heights. Now consider two different ancestors: one who was afraid of heights and one who was not. Generally speaking, the ancestor who was afraid of heights would likely avoid such environments and thereby reduce the likelihood of, say, falling off a cliff or high precipice. In evolutionary terms, we would say that natural selection confers an advantage to the phobia-possessing individual(s). This website in particular has some interesting reading:

Others believe that phobias exist because of evolutionary development to avoid danger in order to improve survival. There are several stimuli that are shared by the most phobic people (heights, insects, crowds, etc.) These phobias, with a couple of exceptions, relate more closely to pre-technological societies. Thus, some scientists, such as Martin Seligman, believe that people are inherently "prepared" to fear certain objects. ((5))) In other words, our phobias relate closely to the perils of our ancestors, as through natural selection, those who feared the dangerous stimulus survived while those who didn't, died off. Prepared fears appear to be very easily conditioned. Some scientists, such as LeDoux, believe that preparedness and the ease of conditioning are the result of certain preexisting neurological connections that exist evolutionarily. These connections are turned on with relative ease.

I get your point and appreciate the example, however I am still curious as to why someone could be a sufferer from Arachnophobia but not Entomophobia? Both could be seen to have similar features, would you not agree that it is odd, to see someone having a phobia of something, but not of something which is closely related to the other angst. I'd be very grateful, if you could provide me with some resources/informations on that.

I think there is a difference between rational and irrational fear. Irrational fear is not advantageous; rational fear is. A fear of heights is rational; a phobia is not. A phobia is something that actively disrupts someone's life.

@anongoodnurse: Why is a fear of heights (or of anything) advantageous?  As opposed to sensible caution, of course.  From what I've seen, it actually makes injury more likely, as the phobic person either freezes, or runs in panic.

Okay, so I see the distinction now, sorry that I was unable to answer that in my post. @jamesqf Per the definitions we are using, "rational fear" would certainly be advantageous if it leads to avoidance of the risky/dangerous/fear-inducing situation to begin with. So as I pointed out in my fear of heights example (which imo is a rational fear), the person would avoid precarious and elevated scenarios altogether. Granted, this may be a disadvantage if the person needs (for some reason) to be in such a location. For most of the part, though, it would prove advantageous.

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What is the significance to life of the anomalous properties of water?
I have heard that the anomalous properties of water - e.g the fact its solid form is less dense than its liquid form - is extremely important. In fact, some people have gone so far as to tell me it was crucial for the development of life.
What is the significance of the anomalous properties of water to life?

This is a brief treatment of your question, specifically:

the fact its solid form is less dense than its liquid form - is extremely important. ...crucial for the development of life.

I can't speak to the importance of this property in the development of life (as I don't know the exact conditions of the world when life began, and therefore the role expansion of ice played in it) but life would not continue without it.
Water does not conduct heat very well, therefore water temperature fluctuates more near the surface of a body of water (say a lake, an ocean, or even a river) than in the deeper regions. In the winter, surface water freezes.
If water were denser on freezing, it would sink to the bottom, and liquid water would replace it. That liquid water would freeze, sink, be replaced, etc.
When it became warmer, the frozen water at the bottom would be less affected by surface temperature, i.e. it would be less likely to melt.
Even with summers, because of the failure of deep ice to melt, eventually you would be left with a mostly frozen body of water, and life doesn't carry on well in those conditions (freezing of the cells of plants and animals in the water would cause cell lysis, again, because of the expansion of water within), whereas life in a liquid under a frozen surface carries on much better. Life in the water would die.
If there were no life in water, then life on land would be most difficult. (Consider most of our oxygen comes from phytoplankton in the oceans. Even if the phytoplankton didn't happen to die from being trapped in frozen water, their nutrient supply would be cut off, frozen below.)
That's just the tip of the iceberg, really. The anomalous expansion of water also affects ocean currents and weather in ways that enrich life on earth.
Since you didn't ask about the other properties of water, this answer doesn't address surface tension, etc.
Edited to add: Corrected an error about the thermal conductivity (insulating properties) of ice. Ice does conduct heat more than water. It may be advantageous to the temperature of the water below possibly by holding snow (which does insulate well).
Source
Thermal Conductivity
Plankton: Ocean Drifters

Nice. I would say that frozen water "contains more air" though. You probably just mean that there are fewer molecules per volume --- lower concentration.  And is this lower concentration really related to insulation?  Does solid water really conduct less heat than liquid water? A reference for this?

@Roland - You're right in all your points. The thermal conductivity of ice is greater than the thermal conductivity of water. I've edited my answer.

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Can someone help me answer or explain how to answer questions about DNA coding capabilities?
How is it that a DNA coding system with only 4 bases can yield so many possibilities? Also, how many unique coding sequences can there be with a DNA code that is 8 base pairs long? Hint: 4^n combinations. I've gone through this in my textbook, but I don't understand how to get the answer for it.

The title should be an actual, specific question. Also, homework questions are discouraged if you do not include an attempt to solve them (or at least some initial ideas).

I agree, you should think about this, though I gave you an anwser which I hope will get you to the answer to your problem set.

4 bases (A T C G) leads to 4 possible value per bit of information, which then leads to the formula: 4^n (n being the number of base). For the first part of your question regarding how can you have so much information, it has to do with n, as you increase the number of bases the number of different combinations increases exponentially. For a comparison, your computer stores information in a 2 value bit system (1 or 0).
If you plot the number of possibilities, you will see that DNA outpace computers very quickly, as an exponential of base 4 will go faster (2*2 = 4, 4*4 = 16, already at 2 bits you have 4 times as many possibilities)

With that in mind, you can compute the number of possibilities for any given number of bits (or bases in your case).


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What's the mixture of carbon and haemoglobin called
I know of oxyhaemogloblin , the mixture of oxygen and haemoglobin  , but carbon and haemoglobin combination is what's confusing

Carbon and hemoglobin??? Hemoglobin is made of carbon and other elements; it doesn't transport it. Do you mean CO or CO2 perhaps?

Is there a name for it other than Deoxyhemoglobine?

I'm going to agree with the comment left by @anongoodnurse and assume you are looking for the terms that define CO2 + hemoglobin and CO + hemoglobin.
CO2 + hemoglobin = Carbaminohemoglobin
CO + hemoglobin = Carboxyhemoglobin


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Best methodology to compare computed phylogeny tree with taxonomy?
I have computed a phylogenetic tree using an alignement of sequences, and I would like to :

Compare it to the "known" taxonomy (uniprot/ncbi which I know is not
the most up to date one) and extract a metric of how "divergent" it
is.
[Optional] Visualize the differences (I can probably come up with a
solution for that one, but if someone knows of a nice tool to do so
?)

What are the best metrics / tools / methodologies to do such a comparison ?
Thanks !

Take a look at the ape package in R. It has a function called cophyloplot which allows you to visualize two trees like so:

Which is well described in this question (also the source of the image).
There is also the dist.topo function which produces a metric which describes the topological distance between two phylogenetic trees. I don't know if this is what you mean by "divergent" but I hope it helps.


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What's the mixture of plasma and haemoglobin called
I know of oxyhaemoglobin but the mixture of plasma and haemoglobin in the blood gives what?

You and Dr. James must be friends ;)
There is no specific name for the mixture of plasma and haemoglobin, however, when hemoglobin is found in the plasma (i.e. not in blood cells) it is usually referred to as "free hemoglobin." This is a term you are most likely to encounter when dealing with plasma/ serum hemoglobin testing.
Additionally, when haemoglobin is broken down, it forms bilirubin, which contributes to the color of plasma (there is no specific name for the mixture of bilirubin and plasma either, except perhaps "plasma bilirubin").

Hahaha, I noticed that too ;) (first line)


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How long can an octopus survive out of the water?
I saw videos of octopuses crawling on the ground and I was wondering how long an octopus can survive when out of the water? Does it depend on either its size (i.e., does a big octopus from deep sea survive longer than a tiny octopus) or the species?

The Pacific Northwest Tree Octopus only needs water during the early parts of its lifecycle; the rest of the time, it can get what it needs from rain or atmospheric moisture.

Umm.. the Tree Octopus bit is a hoax.. If you read a little of the linked page, above, it mentions its natural predators being the Bald Eagle ..and  sasquatch.

Short answer
Under ideal conditions, an octopus may survive several minutes on land.
Background
Octopuses have gills and hence are dependent on water for the exchange of oxygen and carbon dioxide. Gills collapse on land because of the lack of buoyancy (source: UC Santa Barbara). Octopuses have three hearts. Two of these are dedicated to move blood to the animal’s gills, emphasizing the animal's dependence on its gills for oxygen supply. The third heart keeps circulation flowing to the organs. This organ heart actually stops beating when the octopus swims, explaining the species’ tendency to crawl rather than swim (source: Smithsonian).
According to the Scientific American, crawling out of the water is not uncommon for species of octopus that live in intertidal waters or near the shore (Fig. 1). Because most species of octopus are nocturnal, we humans just don't see it often. Their boneless bodies are seemingly unfit for moving out of water, but it is thought to be food-motivated, e.g. shellfish and snails that can be found in tidal pools.
Octopuses depend on water to breathe, so in addition to being a cumbersome mode of transportation, the land crawl is also a gamble. When their skin stays moist, a limited amount of gas exchange can occur through passive diffusion. This allows the octopus to survive on land for short periods of time, because oxygen is absorbed through the skin, instead of the gills. In moist, coastal areas it is believed they can crawl on land for at least several minutes. Mostly they go from pool to pool, never staying out of the water for extended periods. If faced with a dry surface in the sun, they will not survive for long (source: Scientific American).

Fig. 1. Octopus on land. Source: BBC
Your sub questions; I think small octopuses may survive longer, since passive gas exchange is the mode of survival on land. In general, an increase in diameter causes the volume to increase with a third power, while surface increases with a power of two. Therefore, an increase in body size reduces the surface-to-volume ratio and leads to reduced gas exchange. Because passive gas exchange needs large surface-to-volume ratios, I am inclined to believe small octopuses may cope better with terrestrial environments. However, in hot, arid conditions it is likely a bigger one will have an advantage, because it can store more oxygen in its blood.
In terms of species, I have to say I couldn't find any sources going in so much detail on this. Likely, as said, smaller species may do better in cool, moist conditions, while larger specimens may be better off in dry environments.
Reference
- Harmon Courage, Sci Am; (November 2011)

You do realize fish gills are different than octopus gills, your source for their gills not working is talking about fish not cephalopods.

@John thanks for that. The similarities or dissimilarities between gills across species doesn't change the fact that octopuses need water for oxygen.

Found an octopus today which had attached itself to a rock covered in algae during high tide and had failed to swim back out with the receding tide. We found it at low tide, this means it must have been exposed for a long period of time, definately not only minutes. December in North Wales means it was wet, cold, no direct sun (but no rain). The octopus was moist. It was alive and well, just seemed to need to rest: Once we sat it back into the water, it stayed in one spot for a long time, after vigorously swimming there. Size: Body about palm-sized (12cm lenghth)


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Is complete genetic linkage possible?
Linkage is the tendency of genes on the same chromosome to remain together during the process of inheritance. Is it possible that two genes will remain linked generation after generation without any crossing over between them? Can anyone give an example?

Complete genetic linkage does occur in some cases.
Most of the Y chromosome (present as a single copy in males of many species) does not recombine with the X chromosome. Any genes in this non-recombining region, the "male specific Y" (which is 95% of the Y), will be "completely linked", in other words, they cannot be broken apart by recombination and are inherited as a single unit.

Non-recombining region of the Y marked as NRY from this paper.
The closer two genes are, the higher the general tendency for them to be co-inherited. When co-inheritance is non-random the genes are in linkage disequilibrium. The genetic linkage between genes is measured in centimorgans.
I'm not aware of any completely linked genes in recombining parts of the genome. By definition there is some distance between two linked genes (otherwise it's one pleiotropic gene). Therefore, if recombination is possible, then it is possible for them to become unlinked at some frequency, even if that frequency is extremely small (I could be wrong though, but scholar searches have given me nothing). There are, however, cases of very tight linkage between genes (1, 2, 3).
Note that factors other than genetic linkage can affect linkage disequilibrium.


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What causes the range of severity of neurological deficits in Down's syndrome?
It's known that the severity of symptoms caused by a trisomy 21 varies from individual to individual. Part of the explanation for this range of severity is the finding that 94% of Down's syndrome sufferers have a full trisomy, ie., all of the cells in their body have an extra copy of chromosome 21, while others have an underlying translocation (mostly a chunck of chromosome 21 being attached to 14). The last group has mosaic Down syndrome, where just a portion of cells is affected due to errors later in development.
However, this cannot be the only cause of the variation, as it would basically mean that 94% of all Down's syndrome patients should have similar complaints. Indeed, symptom variability is greater, as far as I am aware. I am specifically interested in the range of mental deficits caused by Down's syndrome:

The majority of children with Down syndrome function in the mild to moderate range of mental retardation. However, some children are not mentally retarded at all; they may function in the borderline to low average range; others may be severely mentally retarded.

What is the source of the variability in the neurological deficits? For the sake of answerability it may be best to narrow the scope down to the larger chunk of Down's syndrome sufferers with a full trisomy. Does any, or all of the variability in neurological deficits has to do with the stochastic process of X-inactivation?

Some useful sources I've read over, section 3 on pg 125 goes over some pathways implicated in intellectual impairment for DS, and more on the 21q22 region. Nothing conclusive yet.

As far as I know, a substantial proportion of the variance within neurological diseases are related to epigenetic marks on the genome. I wouldn't be surprised if this explains some (or perhaps most) of the variability in syndrome severities observed.

The symptoms of Down syndrome occur due to overexpression of genes present on the duplicated chromosome.
If possessing an extra chromosome meant an equivalent change in gene expression, one would expect to observe 50% more protein production for having 3 rather than 2 copies of a chromosome. However, due to complexities in regulation at the level of transcription, translation, and protein degradation, the actual expression levels vary substantially. These complexities can arise from alleles present on chromosome 21 or elsewhere on the genome. I will present some examples from three categories of variation that are known to contribute to the spectrum of symptoms in Down syndrome.
1. Complexity of chromosome duplication
Down syndrome is sometimes caused not by a complete, but rather a partial trisomy 21 (Antonarakis et al., 2004). These variations can also partly explain the severity of symptoms because some individuals do not possess a full duplication. You mention this in your question, but as you note, this is a fairly rare occurrence relative to full trisomy, so let us consider other contributions...
2. Variation of expression levels in normal individuals and those with trisomy 21
It turns out that among the genes expressed on chromosome 21, mRNA levels vary between normal individuals by as much as 40-fold! (Deutch, et al. 2005; Stranger, et al. 2005) This expression variability can explain the susceptibility of different individuals to trisomy 21, depending on the expression levels of the alleles they possess.
Among the different genes present on chromosome 21, some expression levels are consistently elevated in Down syndrome across individuals, some have overlapping but significantly different distributions (suggesting some Down syndrome patients have expression levels in the normal range and others do not), and others are indistinguishable between patients and controls (Prandini et al., 2007).
Presumably, genes in the first category contribute most to the shared phenotype of Down syndrome, and genes in the second category contribute most to the variation. Perhaps alleles that produce mRNA transcripts at the low end of normal for those genes are less susceptible to the effects of chromosome duplication.
A case study: Amyloid precursor protein
One protein of interest in particular is the amyloid precursor protein, APP, which is also associated with Alzheimer's disease (which shares some phenotypic characteristics with Down syndrome). APP expression varies widely among tissue types and individuals. Therefore, although APP mRNA levels are significantly elevated in Down syndrome individuals, the distributions between controls and Down syndrome are very overlapping; for example, see Figure 2B from the Antonarakis 2016 review.
3. Interactions with genes on other chromosomes
The third contributor to the variation of symptoms is the interaction of duplicated chromosome 21 genes with alleles located on other chromosomes. Just for an example where some of the genetic basis is understood, Down syndrome individuals are susceptible to certain leukemias, which are also associated with specific alleles on other chromosomes (Antonarakis, 2016). It seems that trisomy 21 affects histone modification in the areas of those alleles (Lane et al., 2014) and promotes proliferation of B-cells. Therefore, Down syndrome interacts with those other oncogenes to produce a greater combined risk. Individual with Down syndrome but not possessing the other alleles are less susceptible to the increased risk of leukemia
Similar interactions are likely with other systems that are influenced by Down syndrome, though the full molecular basis of all of those interactions are not fully understood. The Down Syndrome Genomes Project aims to, among other things, discover these other alleles outside of chromosome 21 that contribute to Down syndrome symptoms, which may also help understanding of the contribution of those alleles to other disorders (Antonarakis, 2016).

References:
Antonarakis, S. E. (2016). Down syndrome and the complexity of genome dosage imbalance. Nature Reviews Genetics.
Antonarakis, S. E., Lyle, R., Dermitzakis, E. T., Reymond, A., & Deutsch, S. (2004). Chromosome 21 and down syndrome: from genomics to pathophysiology. Nature reviews genetics, 5(10), 725-738.
Deutsch, S., Lyle, R., Dermitzakis, E. T., Attar, H., Subrahmanyan, L., Gehrig, C., ... & Antonarakis, S. E. (2005). Gene expression variation and expression quantitative trait mapping of human chromosome 21 genes. Human molecular genetics, 14(23), 3741-3749.
Lane, A. A., Chapuy, B., Lin, C. Y., Tivey, T., Li, H., Townsend, E. C., ... & Yoda, A. (2014). Triplication of a 21q22 region contributes to B cell transformation through HMGN1 overexpression and loss of histone H3 Lys27 trimethylation. Nature genetics, 46(6), 618-623.
Prandini, P., Deutsch, S., Lyle, R., Gagnebin, M., Vivier, C. D., Delorenzi, M., ... & Baldo, C. (2007). Natural gene-expression variation in Down syndrome modulates the outcome of gene-dosage imbalance. The American Journal of Human Genetics, 81(2), 252-263.
Stranger, B. E., Forrest, M. S., Clark, A. G., Minichiello, M. J., Deutsch, S., Lyle, R., ... & Deloukas, P. (2005). Genome-wide associations of gene expression variation in humans. PLoS Genet, 1(6), e78.
(note: the two references I have linked here: Antonarakis 2016 and Prandini et al 2007, are, respectively, a nearly direct answer to the posed question that establishes the current state of knowledge about symptom variability, and an original research paper that provides much more detailed genetic analysis of the variability of expression of many relevant genes than would be appropriate for an answer here; I highly recommend them both for further reading on the subject)

This is really a magnificent and exemplar-styled answer. I'll refrain from either accepting and giving you a well earned bounty until the bounty expires, because I think there may be more to it. This is more of a nature approach and I think the nurture approach may also be an important lead, just as with other mental disorders like schizophrenia and depression. Who knows? Apart from all that, many thanks for this interesting answer. +1

@AliceD Styled after your own answers, no doubt. I believe that "early intervention" strategies can improve the functioning and quality of life of affected individuals, but I am more familiar with similar strategies in ASD so I will have to do some reading. I also expect that all of the factors that influence cognition broadly would have an influence on Down syndrome individuals: things like socioeconomic status, and connected with that nutrition and parental care. I'm not sure what empirical research exists but I will check and may update my answer.

@AliceD (...continued:) I think Parkinsons and Alzheimers might be better analogies than schizophrenia and depression (though all have relevance): both Parkinsons and Alzheimers give some evidence that there can be a fair amount of resilience in the brain, such that symptoms arise not when damage begins, but after damage has accumulated to a sufficient degree. Therefore, I would expect symptoms of Down syndrome to be worse whenever there are other accompanying factors that negatively impact cognitive ability (and vice-versa) and influence the cognitive "ceiling" for that individual.

please do not feel pushed into doing more reading. This answer is great. I was more of hoping another user may step in and give another answer. But then, of course you're more than welcome to add info but that was not the intention of that comment (-: I really haven't the faintest clue whether nurture is involved

@AliceD I don't feel pushed at all, I am quite curious myself. :) I am confident that there is a role for nuture to play, though for the types of "nurture" I have in mind there could certainly be a semantic argument about whether it really reflects the severity of the neurological deficits or rather helps compensate for some of the symptoms to improve quality of life (i.e., does "improved vocabulary" mean the severity is lessened, or just mean a DS patient can communicate better despite the challenge they face?).

The extra genetic material present in DS results in overexpression of a portion of the 310 genes located on chromosome 21. This over expression has been estimated at around 50%. Some research has suggested the Down syndrome critical region is located at bands 21q22.1–q22.3, with this area including genes for amyloid, superoxide dismutase, and likely the ETS2 proto oncogene. Other research, however, has not confirmed these findings. microRNAs is also proposed to be involved.
The dementia which occurs in Down syndrome is due to an excess of amyloid beta peptide produced in the brain and is similar to Alzheimer's disease.This peptide is processed from amyloid precursor protein, the gene for which is located on chromosome 21. Senile plaques andneurofibrillary tangles are present in nearly all by 35 years of age, though dementia may not be present.
Epigenetics
Down syndrome is associated with an increased risk of many chronic diseases that are typically associated with older age such as Alzheimer's disease. The accelerated aging suggest that trisomy 21 increases the biological age of tissues, but molecular evidence for this hypothesis is sparse. According to a biomarker of tissue age known asepigenetic clock, trisomy 21 increases the age of blood and brain tissue (on average by 6.6 years).
Ref-wikipedia.

An interesting read, thanks for that. But it doesn't really target the question - why the range in severity of symptoms?


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Why was the cackling goose split off as a distinct species from the Canada goose in 2004?
According to Wikipedia, in 2004 the American Ornithologists' Union made the cackling goose a new species, splitting it away from the Canada goose.  The British followed suit in 2005.
What was the basis for this split?  Why was a new species required here?  Were offspring of these two found to be consistently infertile, or was the change based on something else?

The accepted answer doesn't point out that you can get the answer straight from the AOU if you have access to a science library: they publish explanations of changes to the AOU Checklist in The Auk! The one involving Branta hutchinsii is from Banks et al. 2004; the exact text they use are:

pp. 59–60. Several genetic studies of geese, including recent work with mitochondrial DNA (van Wagner and Baker 1986, Shields and Wilson 1987, Quinn et al. 1991, Paxinos et al. 2002, Scribner et al. 2003) have verified previous suggestions based on differences in voice, nesting habits, habitat, and timing of migration, as well as in color and size (e.g. Brooks 1914, Aldrich 1946, Hellmayr and Conover 1948), that the forms treated as the single species Branta canadensis by all previous AOU Check-lists and most other works actually constitute at least two species, and further that each of the two species may be more closely related to another member of the genus than to each other. Thus, we divide B. canadensis by recognizing a set of smaller-bodied forms as the species B. hutchinsii, and rearrange our representatives of the genus in the sequence bernicla, leucopsis, hutchinsii, canadensis, sandvicensis. Additional analysis may result in further splitting.

So, yes, this is mainly because of mtDNA analysis and because of several studies between 1987 and 2003, as described in the other answer.

The "white-cheeked" geese have long been subject to taxonomic controversy. From the 1920s to the 1950s, authorities have classified them into between one and four species. Although Aldrich in 1946 asserted there was near-unanimous agreement among Arctic biologists that there were two species, from the 1950s Delacour's taxonomy was most often followed, which had one species (Branta canadensis) and twelve subspecies.(1)
What changed the consensus were DNA studies.  Mitochondrial DNA (mtDNA), which is passed on without recombination, showed distinct sequences supporting two species. One RFLP analysis of mtDNA suggested the split between these two species happened about one million years ago.(1)
The species divide mainly along size and breeding location lines.  The Cackling Goose (Branta hutchinsii) is smaller and breeds on the Arctic tundra. The (present) Canada Goose species (Branta canadensis) mostly takes a larger form and breeds mostly in non-tundra areas.(1)
(1) - Mlodinow, S. G., et al. "Distribution and identification of Cackling Goose (Branta hutchinsii) subspecies." North American Birds 62.3 (2008): 344-360.


text:
What is the lower temperature limit for ion channels function?
What is the cold-block temperature of ion channels? (not of nerves or axons)

The lower temperature limit of ion channels likely is dependent on various factors, including the type of channel and the recording conditions (tissue type, medium etc.). Reports on the suppression of voltage spikes (i.e., the inhibition of action potential firing) range from 1 to -20oC in squid axons, dependent on the species (Leuchtag, 2008). I couldn't find information on specific channels.
Reference
- Leuchtag, Voltage-Sensitive Ion Channels: Biophysics of Molecular Excitability (2008)

thanks, "suppression of voltage spikes " you mean stopping of action potentials right? The fact that an action potential cannot propagate doesn't mean that the channels are blocked but that the threshold cannot be reached right?

@george. Yes, correct on the AP firing, I edited the answer to make that more clear. Isn't threshold increase a consequence of inhibition? I.e., I don't follow your dichotomy posed. As a rule, if you find the answer useful, we upvote the question to let others know it's a useful answer. If you think it is the answer you can accept it too. You can also downvote it when it's a poor answer.


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What is the correlation between hand and neck flexibility?
I am trying to understand this statement in the book, Mudras, Yoga in your Hands by Gertrud Hirschi:

There is a direct relationship between the hands and the neck since the nerve paths run through the vertebral foramina in the arms, hands, and fingers.

Furthermore it is stating that neck flexibility is correlated to hand flexibility.
Where is the vertebral foramina and what is it?

The vertebral foramen
What is it, and what passes through it?

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

The nerves in the hand

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

In this paragraph it is specifically stated that impulses received in the hand by receptors, can come from the brain and spinal cord "and some come from nervous tissue in the muscles themselves."
The vertebral foramen is a part of the spinal cord, and forms a vertebral canal, the nerves running through it, and the impulses which are sent could be received by the receptors in the hand. Which could affect flexibility in both neck and extremities.
Sources:

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


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Are alpha-ketoglutarate and glutamate involved in all transamination reactions?
Is it true that for all biochemical transamination reactions, that alpha-ketoglutarate and glutamate serve as the amino group acceptor and donor, respectively?
If this is true, then is it safe to assume that alpha-ketoglutarate is necessary for every transamination reaction?

The major transaminases such as the aspartate transaminase and alanine transaminase involve the glutamate α-ketoglutarate interconversion. Even the GABA aminotransferase employs glutamate/α-ketoglutarate. It seems that all transaminases use glutamate/α-ketoglutarate; in fact most of them do.
These are a few that don't:

Beta-alanine--pyruvate transaminase.
Tryptophan--phenylpyruvate transaminase.
Pyridoxamine--pyruvate transaminase.
Aminolevulinate aminotransferase.
Serine--pyruvate transaminase.
Aspartate--prephenate aminotransferase.

And a few more (see here). Most of these are present in plants.


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How is the brain kickstarted during development
The brain is a complicated beast, that operates (generally) by electrical activity. During development, all cells originate from the a single "cell": the zygote.
At some point during development, the cells will begin to form into the specialised cells of the brain. But how does the brain activity start?
Is there some process that gets things going, akin to jump starting a car? Specifically, I'm referring to the mammalian (and more specifically human) brain.

Given the right set of molecular machinery, neurons can start firing spontaneously. No kickstart needed.

If nothing else, touch, temperature and other sensory neurons will start firing in response to stimuli detected by the embryo, which will start firing impulses into the brain.


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Electrocardiogram: Missed beats in presence of Ectopic beats or Premature Atrial/Ventricular Contraction beats
I have been working on analyzing Electrocardiogram data.
So far, i have identified Ectopic beats and Premature Atrial/Ventricular Contraction beats.
I am working on identifying Missed Beat in the Electrocardiogram.
The definition of Missed Beat is:
"The characteristic of a missing beat in ECG is the unexpected absence, together, of P-, QRS-, and T-waves."
My question is, do we have to consider missed beats in presence of Ectopic or Premature beats also ??
For example, if an ECG contains premature/ectopic beats, then should the R-R interval between these beats should be compared to R-R interval between normal beats to search a missed beat ??

After developing and checking the algorithm with simulated ECG data, i found out that premature beats (as the name suggests) itself arrive prematurely i.e. their R-R peak interval is less then the R-R peak interval between normal beats.
In that case, i am considering the averaged interval between normal beats and compare it to the interval between next arriving beats. If that interval is more than twice the averaged normal interval, then i classify it as a missed beat.


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What is the process of degradation of proteins into amino acids inside living cells?
Just like beta oxidation does our cells have a distinct mechanism for degradation of proteins? There are processes for degradation of amino acids but where does these amino acids come from, is it all from dietary proteins? Are they not obtained from the proteins(enzymes) that are being continuously made inside the cells?

Proteolysis (the breakdown of proteins into amino acids by the action of enzymes)

There are two major pathways through which proteins are degraded in your generic cell: In a lysosome or in a proteasome.
The Lysosome
It's considered an organelle. It has a lipid bilayer that encloses a potent cocktail of acid hydrolases working at a low pH. The pH is maintained by a Cl-/H+ antiporter(Ref). Acid hydrolases that are being processed in the golgi are targeted to the lysosome through mannose-6-phosphate residues which are recognized by the trans golgi M6P receptors, packaged into clathrin vesicles, and targeted to acidic late endosomes which fuse, forming the lysososome (Ref).
So through endocytosis or phagocytosis, vesicles full of extracellular proteins are uptaken and may fuse with a lysosome. The hydrolases thus digest whatever they can. In a cell stress response cells may also digest their own contents with the aid of lysosomes in a process called autophagy. We can take a look here at some established lysosomal enzymes current to 2009, and if you spot a protease you can generally take a look at it's specific mechanism to see how it works. So I'll pick one out of the bunch (a lysosome has many different hydrolases remember), Dipeptidyl-peptidase I aka Cathepsin C. The mechanism of proteolysis is that of a cysteine protease which follows a bit of a generic mechanism like so:

... and so forth, you can look at a given given protease, and roughly determine how it cleaves peptides.
The proteasome
This one is a a much more directed form of protein degradation. Proteins must be tagged on lysine residues by molecules of ubiquitin, at least 4, referring to the term polyubiquitination. These are added sequentially by proteins denoted E1, E2 and E3 (see proteasome wiki). Proteins that get degraded in this manner are often damaged or come from within the cell, unlike the lysosome where the proteins probably came from outside the cell.
The catalytic domain of the proteasome is a threonine protease which follows the generic mechanism of the catalytic triad, one of the most well-studied protease mechanisms. We can view this generally through the mechanism of a serine protease, like so:

If you read through the whole thing, two notes: (1) the generic term for protein degradation is proteolysis, and (2) The mechanism depends on the protein performing the proteolysis, namely a protease.

Good answer. I would add that lysosomes also can degrade the cells own proteins (not only extracellular proteins obtained from endocytosis) during autophagy. https://en.wikipedia.org/wiki/Autophagy

@Roland Duly noted, added a tidbit on autophagy! Thank you.

@CMosychuk What are the main sources of these proteins that are being proteolysed?

@SanjuktaGhosh So there's a number of places it can possibly come from, and it depends on some conditions. Largely: When you eat, digestive proteolysis breaks whole protein into small peptides that are capable of passing into the bloodstream. Thus the bloodstream becomes the main source. Otherwise cells are capable of scavenging from extracellular fluid/matrix, or nearby cells that die or undergo apoptosis (specialized cells called phagocytes normally take care of dead cells, though).

In addition to proteasome and lysosome, soluble (non-organelle) proteases may become important, depending on circumstances.


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Do desulfhydrase-catalysed reactions take place in animal cells?
It isn't a homework question. I'm just stuck with desulfhydrase reactions and am unable to find enough information in the usual places.
Any external source on this topic would be helpful.

A desulfhydrase catalyzes the removal of hydrogen sulfide from a compound. So the answer is yes, but it's not the most-commonly annotated reaction for the enzyme cystathionine gamma-lyase.
I didn't know off-hand. Here's how I answered the question:
I searched Entrez Protein (or NCBI...whatever the thing's called) with the following terms:
(desulfhydrase) AND "Homo sapiens"[porgn:__txid9606]

And got three hits for isoforms of cystathionine gamma-lyase. I clicked on one of them and started reading. Key things I noted:

EC_number="4.4.1.1"
...
Cystathionine gamma-synthase is a PLP dependent enzyme and catalyzes
  the committed step of methionine biosynthesis. This pathway is
  unique to microorganisms and plants, rendering the enzyme an
  attractive target for the development of antimicrobials and
  herbicides.

So it's a good question because, if people normally characterize this enzyme in terms of Met biosynthesis, then we don't have a desulfhydrase. But I trusted the thing was annotated properly and that the comment above was just too medicine-oriented (as much biochemical literature is).
So to really understand the enzyme itself I searched MetaCyc for the Enzyme Commission identifier 4.4.1.1.
This let's me easily visualize the catalyzed reaction. And the annotation spells it out clearly:

Enzyme Commission Summary: A multifunctional pyridoxal-phosphate
  protein. The enzyme cleaves a carbon-sulfur bond, releasing L-cysteine
  and an unstable enamine product that tautomerizes to an imine form,
  which undergoes a hydrolytic deamination to form 2-oxobutanoate and
  ammonia. The latter reaction, which can occur spontaneously, can also
  be catalysed by EC 3.5.99.10, 2-iminobutanoate/2-iminopropanoate
  deaminase.
Also catalyses elimination reactions of L-homoserine to 2-oxobutanoate and ammonia, of L-cystine, producing thiocysteine,
  pyruvate and ammonia, and of L-cysteine, producing pyruvate,
  hydrogen sulfide and ammonia.

I removed my comment, my mistake on the EC number.

In addition to the reaction described in Ryan's answer, cystathionine beta-synthase (CBS) also catalyses a reaction that yields hydrogen sulfide. These two reactions are thought to be the major sources of hydrogen sulfide in mammals.


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Are humans evolving since their first appearance?
Is the evolution a very prolonged progress, or are we going to witness further evolution of the human species?
If so, in which direction? Are there any widely predicted changes for humans?

Sorry - posted the answer link (found it by searching for my answer to it!) http://biology.stackexchange.com/questions/5007/how-is-evolution-possible-in-contemporary-humans

also this one http://biology.stackexchange.com/questions/9739/are-there-any-scientifically-based-predictions-or-theories-of-future-human-evolu

Humans are still evolving.
If you have a proper understanding of evolution you will not doubt this....
What is evolution?

"Evolution means change, change in the form and behaviour of organisms
  between generations. ... When members of a population breed and
  produce the next generation we can imagine a lineage of populations,
  made up of a series of populations through time. Each population is
  ancestral to the descendant population in the next generation: a
  lineage is an ancestor-descendent series of populations. Evolution is
  then change between generations within a population lineage."

Evolution is simply a process of change, which Darwin called descent with modification. It is a change in trait values of populations over time. It results from four mechanisms: mutation, migration, drift, and selection. The first three lead to random change from one generation to the next, which may increase or decrease fitness, while selection will generally lead to adaptation.
How do we know evolution still occurs in modern humans?
Well human traits (characteristics like hair colour, height, eye colour ...) are often determined, to varying degrees, by genetic information. That information is passed from parent to offspring (inheritance) and that information can accumulate new variation (e.g. by mutation), while some variation can be lost from the population (by drift, migration, selection). These are the conditions required for evolution. Therefore, from one generation to the next, population trait values can change.
How will humans evolve in the future?
Difficult to say, evolution is a quite random process and difficult to predict. However, the process of adaptation (the result of genetic variation and selection) is a little more predictable. Following from the above, if there is genetic variation in a trait then there is a good opportunity for it to evolve by selection (Fisher's Fundamental Theorem). For example, we now see more women choosing to have children later in life, this means selection will be stronger against genes which cause early-life mortality in women and selection will favour genes that slow reproductive ageing in women.  Conversely, modern medicine is reducing selection against genetic diseases as we are better able to combat them, so we will probably evolve to show genetic diseases more frequently - selection against genetic diseases is weaker, therefore disease causing mutations can persist more easily in the population, see mutation-selection balance.
If you are able to prove that a trait is subject to selection and that there is genetic variation then you should be able to say that, in the short term at least, evolution in that trait will proceed in a predictable manner. Here are some posts (1, 2) about evolution in modern humans, open ended evolution, and why selection might not produce the predicted response.

Are humans evolving since their first appearance?

The idea of first appearance suggest an important misunderstanding. There is no such as a first appearance of humans (or any other species) that would not be arbitrary. The Homo lineage evolves and keep evolving but don't think of humans as being created at some point and then eventually evolving. Life came to existence 4.6 billions years ago and it is evolving and diversifying ever since but no species has ever been created anew.

Is the evolution a very prolonged progress

The only, non-arbitrary definition of evolution is a change of allele (=gene variant) frequency in a population over time. Such change occurs several times every second in humans. So evolution is constantly occurring. It really does not take much time. However, I realize that when layman ask "How much time does it take for evolution to occur" they mean something of the kind "How much time does it take for a previously absent phenotypic trait to come to existence in a population?". The problem is that the answer very much depend on what phenotypic trait and what are the selection pressures on this trait.

are we going to witness further evolution of the human spieces?

Yes, we had, we are and we will. Humans are still evolving and you might want to have a look at the post Human Evolution in Modern Times.

If so, in which direction?

In plenty of directions in the same time. Each phenotypic trait will evolve (not completely independent of each other though). There is no single direction for a whole species. You should therefore specify the trait of interest for the question to make sense. Again I think that the post Human Evolution in Modern Times will help you.
Want to have a basic understanding of what evolution is?
Understanding Evolution (UC Berkeley) is a free online very introductory course to evolutionary biology. It will help you to very quickly raise you level of knowledge of evolutionary processes.


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Would a colony with only one male and female collapse?
This is a thought experiment:
If we form a population with only a single founder pair, can this population survive? What would happen? Would this inbreeding cause the population to go extinct? Could such a population continue to exist indefinitely?

There is only a probabilistic answer to this question. However, if you exclude external factors such as environmental stochasticity, predation pressure etc., and only care about the genetic component, there should be formulae to estimate this probability. You would still have to make some assumptions, e.g. the degree of heterozygosity of the initial pair...

If we're talking about lab mice, this is routinely done, since pure strains of lab mice are all genetically identical (barring the low level of spontaneous mutation).  If we're speaking more generally, inbreeding is generally bad and may well lead to extinction, but it's not inevitable; the presence of introduced species on e.g. islands originally populated with only a handful of individuals shows that it can be overcome.

Populations founded by a single pair are quite common in the lab
The Drosophila Genetic Reference Panel, one such example of high artificial inbreeding, is a series of inbred lines where the researchers mated brother and sister flies for 20 generations to form the lines, which means they will be highly inbred. When you do these though you often lose many of the initial lines because of inbreeding depression. Inbreeding depression is reduced fitness as a result of increased homozygosity in the lines - deleterious mutations are more frequently expressed. I have tried to find the number of initial pairs they used to make the ~200 DGRP lines but come up unsuccessful, but I've heard it was around 1500 pairs, although that may be well off the mark*.
What would happen to your mice?
Just like the DGRP lines, there is a high risk that the population would collapse. However, if they do get through a few generations of inbreeding, and are kept in steady conditions (i.e. selection doesn't change once the lines are formed), then they have an ok chance of persisting. If you started with multiple founder pairs then there's a better chance you will still have some (very inbred) mice in a few generations. The success rate will depend on the frequency of deleterious mutations and strength of their effects.
What is inbreeding?
Inbreeding is increased homozygosity in the population than would be expected under random mating. For example, if the frequency of two alleles ($A_1$ and $A_2$) at a gene are $p = 0.1$ and $q = 0.9$ respectively, the expected frequency of $A_1A_1$ homozygotes is
$p^2 = 0.1^2 = 0.01$
the expected frequency of $A_2A_2$ homozygotes is
$q^2 = 0.9^2 = 0.81$
and the expected frequency of heterozygotes is
$A_1A_2$ is $2pq = 2 \times 0.1 \times 0.9 = 0.18$
If the true frequency of heterozygotes ($A_1A_2$) is less than 0.18, then there is inbreeding.
Is there a benefit to inbreeding?
Well inbreeding can be a good thing. Imagine all of those lines that did not collapse. It is possible that a population formed out of those would have higher fitness than the original population, because deleterious mutations may have been purged (lines carrying deleterious mutations are more likely to collapse). So a highly inbred population can prosper. However, that population would also have lower genetic variance. Genetic variance places limits on the potential for adaptation, low genetic variance means low potential to respond to selection. So, if selection is not constant, then inbred populations are more likely to go extinct as they are unable to adapt to novel scenarios.
Inbreeding in nature
One classical example of high inbreeding in nature is in cheetahs, where it is beleived they went through a strong genetic bottleneck ~10,000 years ago. The problems faced by cheetahs today really highlights the problems of high inbreeding because they are struggling to adapt. Genetic bottlenecking is a  serious long-term problem for many species including the Javan rhino, the Kakapo, Mountain Gorillas, and others; even if we can stop poaching and habitat loss wiping out these species in the short-term, they will struggle to adapt to changes in the climate etc..

"As a species, cheetahs have famously low levels of genetic
  variation. This can probably be attributed to a population bottleneck
  they experienced around 10,000 years ago, barely avoiding extinction
  at the end of the last ice age. However, the situation has worsened in
  modern times. Habitat encroachment and poaching have further reduce
  cheetah numbers, consequently snuffing out even more genetic variation
  and leaving cheetahs even more vulnerable to extinction."

* Supporting material from the DGRP paper would suggest that it was indeed formed from 1500 isofemale lines.

There have been several studies with similar structure and background as your experiment, such as  "Inbreeding Effects on Reproductive Outcome: A Study Based on a Large Sample from the Endogamous Vadde of Kolleru Lake, Andhra Pradesh, India" from 1992.
It was an experiment to investigate this hypothesis:

Sanghvi's hypothesis on long term effects of inbreeding was tested in Kotas. Kota is a numerically small tribal population in the Nilgiri district, Tamil Nadu State, India. Consanguineous marriages are common in this tribe. A total of 95 couples were taken for this study and necessary data were collected on a set proforma. Of the 95 couples, 28 (29.5%) were consanguineously related. The inbreeding coefficient for autosomal genes is 0.022 and for sex-linked genes is 0.03. Inbreeding effects on reproductive losses were examined through an exponential regression model. Although the regression coefficient B values are positive, they are insignificant, suggesting no consistent relationship between degree of consanguinity and the reproductive losses. The estimates of genetic load is 1.8 lethal equivalents per gamete and the average B/A ratio is 5. These findings empirically support the Sanghvi's contention.

The abstract of the experiment from 1992:

Inbreeding effects on reproductive outcome vis-à-vis fertility, prenatal loss and prereproductive mortality, and secondary sex ratio of live and dead children were examined in a large sample of 2078 women of the Vadde fishing population of Kolleru Lake in Andhra Pradesh, India. Demographically, this population is a single endogamous unit. By using an exponential regression model with the proportion of offspring survival as a dependent variable and the inbreeding coefficient as an independent variable, I further examined the inbreeding effects. The results were compared with results from other fishing groups and other southern Indian and non-Indian populations. The results among the Vadde were consistent with those found for other groups of Telugu-speaking fishermen and several other southern Indian populations in that the effects were neither perceptible nor significant. The average B value and the number of lethal equivalents found for the highly inbred southern Indian populations in general and for the Vadde in particular were much smaller than those from other parts of the world, providing empirical support to Sanghvi's hypothesis on long-term effects of inbreeding.

The hypothesis was also supported by another investigation, looking at The effect of inbreeding on mortality and morbidity among Telugu-speaking populations of Kharagpur, West Bengal, India.

Increased mortality and morbidity including congenital malformations among the offspring of consanguineous marriages have been widely reported in human populations from different parts of the world. However, there are few studies on the effect of the intensity of inbreeding and different degrees of inbreeding on mortality and morbidity. The present study is an attempt to examine the effects of inbreeding on mortality and morbidity including congenital disorders in different levels of inbreeding among Telugu-speaking populations of Kharagpur, West Bengal, India, based on data collected through extensive pedigrees. The study reveals that the frequency of spontaneous abortions and stillbirths is higher in the offspring of consanguineous marriages than in that of non-consanguineous marriages. A similar effect is also observed in the infant mortality rate, which is known to have a genetic component, but is not seen in the mortality rate of children and juveniles. The rate of morbidity is consistently higher in the offspring of consanguineous marriages with a sex bias in favour of inbred females. The increased morbidity rates in inbred individuals tend to be inversely correlated with the increase in average autosomal inbreeding coefficient. This appears to strengthen Sanghvi's hypothesis of a decline in the frequency of deleterious genes with intensification of inbreeding through generations. The present study also confirms an increase in genetic disorders with an increase in inbreeding in almost all populations.

Sources & Further Reading:

http://www.jstor.org/stable/41465109?seq=1#page_scan_tab_contents
http://www.popline.org/node/184635
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2080450/
http://www.ncbi.nlm.nih.gov/pubmed/1398609
http://www.newworldencyclopedia.org/entry/Exogamy_and_endogamy

It's generally best to write up an answer in your own words. By quickly scanning the pasted excerpts, I can't find an answer to the question.

What is "Sanghvi's hypothesis on long term effects of inbreeding"? This post doesn't answer the question at all well and simply pasting text from a paper is generally not a good approach


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Can an emulsion enter a cell?
I've been tempted on cooking.stackexchange to answer a question, and I did, out of my mind.
(In retrospect, I shouldn't have done so, based on my lack of citable resources.)
I've heard that a water in oil emulsion can penetrate cell walls.
Is it true, and how does it work?

Under the right conditions, emulsions of lipids (fatty compounds) and water can cross cell membranes. If the emulsion is prepared correctly, a structure known as a liposome forms, which is essentially a "bubble" with a layer of fatty molecules on the outside and water at the center. This has been studied intensely in biotechnology, because such liposomes can be used to carry DNA inside (DNA is water-soluble) and then be used to deliver DNA to cells, as in gene therapy.
Typically, oil, which contains triglycerides, is not used for this though, but another compound known as a phospholipid. This is also a "fatty" substance, but unlike triglycerides, one end of the molecule is polar, which helps it interface with water. Phospholipids are the main ingredient in cell membranes, and therefore liposomes made of this stuff can interact with cell membranes. Essentially, the liposome can "merge" with the cell membrane in such a way that the water inside it (and any other contents) ends up inside the cell. For an example of how this technique is used, see this article.
As for the cooking-related question, I would say oil-water emulsions found in foodstuffs are unlikely to cross cell membranes. They contain mostly triglycerides which are not so effective at this, and they are probably not prepared in the right conditions (oil/water concentrations, etc) for liposomes to form.
Also, even if there would be liposomes in some foods that could cross cell membranes, foodstuffs do not actually get into contact with cell membranes in the digestive system, until they are broken down into smaller (harmless) molecules. In the mouth, esophagus, stomach, etc, tissues that come into contact with foods are heavily protected by layers of mucus to prevent cells getting "attacked" by all the weird biomolecules (and organisms) that we eat.
Finally, various molecules from food don't actually enter the cells of taste buds; instead, they are sensed by taste receptors present on the outside of the cells. (Well, the sour taste sensor involves transport of small ions, but not larger molecules.) So you should probably revise you answer on Cooking SE.

Aren't phospholipids usually negatively charged?

Hmm, good point ...  I was thinking of the positively charged amine group in phosphatidylcholine, -ethanolamine, -serine.  But you are right there is an esterified phophate too, carrying a negative charge. I think they are actually zwitterions at pH 7, so overall uncharged, but polar.  Will revise the answer.


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What is the meaning of "within-season variation"?
I am reading a paper about phenology and climate change for my assignment and I found this concept "within-season variation", can someone explain it to me? and how it is related to changes over time?

Could you link to the paper please

"Within-season variation" may be referring to one of two things (depending on the context):

More commonly: the variation of a variable within a given season (i.e., between months or days within that season).

Öst (1999) demonstrates an example of this use (in the context of breeding season).

Less commonly: the variation of a variable between the same season of different (often consecutive) years. Though this would more often be termed "between years". This is as opposed to "between seasons" which would be be between two different seasons of the same year.


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Does DNA polymerase I require a $3^\prime$ end?
DNA polymerase III adds nucleotides in the $5^\prime \rightarrow 3^\prime$ direction because it can only add nucleotides to the $3^\prime$ end of the previous nucleotide. This is why it requires a primer. However, does DNA polymerase I operate by the same criterion? Does it require a $3^\prime$ end of a previous nucleotide in order to bind successive DNA nucleotides?
If it does, then how can it do so for Okazaki fragments when each Okazaki fragment is unbonded to each other? It is the DNA ligase that finally catalyzes the phosphodiester linkage between the $3^\prime$ end $5^\prime$ beginning of two Okazaki fragments, isn’t it?
If it does not, then what’s the deal with telomeres? After each DNA replication event, the DNA gets shorter and shorter at the very ends because that final primer can be removed but not replaced by DNA via DNA polymerase I, correct? This suggests to me that DNA polymerase I requires a previous nucleotide's $3^\prime$ end to work with, and it has confused me regarding its action on Okazaki fragments in conjunction with DNA ligase.

DNA Pol I does require the 3' end of a previous nucleotide to initiate elongation.
Regarding Okazaki fragments, this is accomplished by the annealing of small RNA primers to the lagging strand part of a replication fork. DNA Pol I extends the lagging strand off of the 3' end of those primers, generating the Okazaki fragments. The RNA primers are later removed, leaving gaps between Okazaki fragments, which are later filled in through the combined actions of DNA PolI and DNA ligase.

In the case of telomeres, the final RNA primer can't be filled by DNA Pol I because polymerase requires a free 3' hydroxyl for the attachment of the first DNA nucleotide. After removing out the RNA primer, the first DNA nucleotide would need to be attached to the DNA nucleotide preceding it, which is not found in the case of the final primer on a telomere, since it's all the way at the end of the linear strand.
In this case then, DNA Pol I removes the RNA primer is removed by DNA pol I but cannot replace it with DNA, leaving a gap (step 6 in the following image).

DNA Pol III is involved, but the current understanding, as far as I can tell, is that Pol I fills in the gaps between RNA primers on the lagging strand, thereby generating the Okazaki fragments, while Pol III is more involved in the continuous extension of the leading strand. From this review (http://www.ncbi.nlm.nih.gov/pubmed/21622658), it looks like Pol I and Pol III interact during DNA extension in ways that still aren't fully characterized, so there may be some crossover.

@MarchHo - anytime! :-)


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Hydrogen bonding and the blocking thereof in nucleic acids during nuclear processes
In transcription, RNA polymerase unwinds the DNA double helix and begins attaching RNA nucleotides to the template strand. In its wake, the DNA double helix closes back—this is only natural, seeing as the DNA bases have the tendency to hydrogen bond. In DNA replication, this closing is prevented by single-strand binding proteins.
I have three questions regarding this:

In transcription, the pre-mRNA strand peels off the template strand in the wake of RNA polymerase. Why? There are just as well hydrogen bonds between the pre-mRNA strand and the DNA template strand as there are between the two DNA strands.
Why doesn’t the pre-mRNA stick onto the DNA indefinitely and block the non-template DNA strand from reattaching to the template DNA strand?
In DNA replication, why is it imperative that the separated DNA be stabilized by single-strand binding proteins? Won’t the replicated strand block the template strands from closing together?


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Basic Genotyping
As a disclaimer, I'm from a computer science / statistics background, working on some bioinformatics problems. I've got some genotyping data (VCF from Exome Sequencing), and I'm struggling to get my head around the Genotyping notation.
As far as I understand, at a single base in the human genome, there can be two possible alleles, which would make sense given the standard notation for a lot of software is AA, AB, BB. So that means there are three possibilities homozygous, heterozygous, or homozygous respectively.
The A or B alleles are derived from the paternal and maternal copies of the same base in a person's genome. The major allele is the one that occurs most frequently, and the minor occurs the least.
When it comes to guessing which base is A and which is B, is there a general consensus as to which is which? i.e. is A the major allele?
I'm just not sure my assumptions are right, it's been a while since I've studied any biology, and I've found that online resources are either too vague or are so complex, that they overlook these basics.
Any tips would be really appreciated!
Thanks,

Refer to the following image. What you want to note is that this is a mitotic chromosome. Your cells are generally diploid, meaning for humans where n=23 your somatic cells have 46 chromosomes that form 23 homologous chromosome pairs.
For each chromosome in a pair, they have what amounts to the same genetic information with variations. At the locus for hair color, it will always code for the color of your hair but since you got half your genetic information from each parent, on one homolog the hair color locus might amount to red hair, while the other one might amount to brown hair. Scroll past the image:

In summary, the gene locus is for hair color, but there are red and brown alleles, or variations in a given gene locus for a given trait (see gene mapping). Thinking about traits and how they translate to features is complex in humans however due to features of our genomes such as epigenetics, epistasis, pleiotropy, etc. So when we describe in genetics traits such as color and how those related to AA, Aa or aa and so forth, it's nice to look at a much more simple organism like the pea plant that Mendel studied.
As for which allele is dominant? The actual wikipedia page for genetic dominance provides a good section:

By definition, the terms dominant and recessive refer to the genotypic interaction of alleles in producing the phenotype of the heterozygote. The key concept is genetic: Which of the two alleles present in the heterozygote is expressed, such that the organism is phenotypically identical to one of the two homozygotes. It is sometimes convenient to talk about the trait corresponding to the dominant allele as the dominant trait, and the trait corresponding to the hidden allele as the recessive trait. However, this can easily lead to confusion in understanding the concept as phenotypic. For example, to say that "green peas" dominate "yellow peas" confuses inherited genotypes and expressed phenotypes, and will subsequently confuse discussion of the molecular basis of the phenotypic difference.

Good place to start: Wikipedia
What you should also note is that dominance isn't intrinsic to the allele. Just because it's dominant to another allele doesn't mean it can't be co-dominant with another, and so forth. It also has no bearing on the population distribution of alleles, as certain dominant or recessive alleles can be either exceedingly rare or excessively common.

The A or B alleles are derived from the paternal and maternal copies
  of the same base in a person's genome. The major allele is the one
  that occurs most frequently, and the minor occurs the least.

That's likely going to depend on the population you are talking about.  An allele might be more common the general population, but rare in an ethnic sub-group.

When it comes to guessing which base is A and which is B, is there a
  general consensus as to which is which? i.e. is A the major allele?

If you have the vcf, you can probably go with the ref allele being the "major" allele.  Are you sure that it really matters for your analysis which allele is more common in the population?


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What are wave frequencies in the EEG?
Here is a typical EEG reading:

(source: frontalcortex.com)
I understand that each row corresponds to the signal read between two sensors on a standard 10-20 (or 10-5) distribution setup (e.g. C3-P3).
What I'm missing here is: what waves are we actually seeing here - alpha, beta, etc.? Or do EEGs not really contain wave types, and instead just show voltage differentials between sensors?

Actually I believe you may be seeing all the bands and will need to do a fast Fourier transform to get the actual frequency, however, I could be wrong as I am studying the MEG currently, not the EEG.

Thanks @SolarLunix (+1) - so I assume there's a way to use FFT to decompose V(t) (voltage as a function of time) back out into constituent waves?

EEGs are often analyzed in the frequency domain, where signals are subjected
to spectral analysis, typically by Fast Fourier Transformation, or FFT.
What an FFT basically does is decomposing a signal in the time domain into one in the frequency domain. It does this by decomposing the input signal (any signal, including EEG) into a series of sinusoids. These sinusoids are not present in the original signal; it is a mathematical trick. If you would add all the sinusoids back together, the approximate original signal is restored.
Typically not a single frequency is analyzed, but a band of frequencies, because the frequencies within these bands are associated with similar brain states. The frequency bands that are typically reported on are shown in Table 1, including the brain state they associate with as well as sample EEGs:

Table 1. Typical analyzed EEG frequency bands. Source: Conorrus Somanno
Reference
- Nelson Garcia et al. Device and method for cognitive enhancement of a user (2014). Patent EP 2681729 A1

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Do repetitive movements on EEGs show up as discernible patterns?
Here is a typical EEG reading:

(source: frontalcortex.com)
If I am connected to an EEG, and am sitting perfectly still, and then begin doing some repetitive motion, say, 10,000 times, will we see discernible patterns emerge in the output?
In other words, would it be possible to categorize a particular pattern in the output and say "Waves with this signature correspond to the subject wiggling his left pinky"?
I would imagine that, over time (and many trials) wave patterns converge to predictable signatures for a given movement.

Specific events, e.g. finger flexions, generate synchronized neuronal responses in the brain that can be measured on the scalp with EEG. However, a voltage response to a single event typically generates a low-amplitude response relative to the background EEG. One way to enhance the signal-to-noise ratio is to repeatedly record the EEG in response to the same event. By time-locking the event with the EEG and averaging the individual event-related EEGs, the random background noise will be reduced (stochastic noise) and the event-related potential (or ERP) can be extracted from the EEG (Woodman, 2010). An example of an ERP to repeated index finger flexions is shown in Fig. 1. Such a wave doesn't need 10,000 repeats. 25 may be sufficient.
If you characterize this ERP and determine specific features of it (duration, amplitude, latency after event etc.) you can generate algorithms that detect these features in the raw EEG, without the need to do repeated measures. In fact, thinking of a motor movement (e.g. grasp that coffee mug) generates very similar EEG activity as the factual act of grasping that mug. By recording the ERPs using events like think of grasping that coffee mug from a person missing a hand, and subsequently designing the necessary algorithms to detect that waveform near-realtime in the person's EEG, one can design brain-computer interfaces to control prosthetic limbs (Guger & Pfurtscheller, 2016).

Fig. 1. ERP to voluntary index finger flexions. Motor activity was recorded from the motor area. Source: Ball et al. (1999)
References
- Ball et al. NeuroImage (1999); 10: 682–94
- Guger & Pfurtscheller, AAATE 5th European Conference Advancement of Assistive Technology (2016)
- Woodman, Atten Percept Psychophys (2010); 72(8): 10.3758

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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What does pseudo-irreversible mean?
In this publication (PDF) I encountered the following word:

Binding of rupatadine to histamine H1 receptors isolated from the
  guinea-pig cerebellum and lung was demonstrated by inhibition of
  3H-mepyramine binding; equilibrium inhibition constant (affinity) [Ki]
  values were 26–256 nM in the various experiments. Binding was
  time-dependent and pseudo-irreversible. Rupatadine was ~7.5 and
  10-times more potent than the structurally-related anti-histamines
  loratadine and fexofenadine. H1 receptor occupation by rupatadine in
  guinea-pig cerebellum and lung after oral (PO) dosing was relatively
  rapid (with maximum binding evident at 2–4 hours post-dose) and
  dose-dependent; low or no binding was seen at 48 hours post-dose.

In this context, what does pseudo-irreversible mean? Since it goes on to say the binding had dissipated within 48 hours, it seems to mean persistent or long-lived. Is that correct or does it have a more specific meaning in biology?

it seems to mean persistent or long-lived. Is that correct...?

Yes, it's correct, but how persistent the effect is is related to the rate of dissociation or rate of turnover of the receptor. It is relative, so to speak; relative to the effect of non-irreversible receptor binding.
Irreversible inhibition of, say, a cell surface receptor means that a drug (agonist/antagonist) binds permanently to the target receptor, usually by binding covalently; the chemical reaction is not reversible. This isn't synonymous with a permanent effect on a cell or organism; that depends on turnover of the receptor. A "faulty" receptor may be replaced quite quickly or not; it depends of the cell and the receptor.
Pseudo-irreversible means that the drug acts in a manner similar to  irreversibly bound agonists/antagonists, but there is no covalent bond formed; if a drug/molecule which has a sufficiently high affinity for the receptor is introduced (in a sufficiently high quantity), the new molecule will replace that which was strongly bound before (the pseudo-irreversibly bound drug.)
Some of these types of reactions have been studied more than others. One  example of this can be seen with h5-HT7 receptors, which are subject to pseudo-irreversible inactivation by risperidone and 9-OH-risperidone.
Clozapine and other competitive antagonists reactivate risperidone-inactivated h5-HT7 receptors: radioligand binding and functional evidence for GPCR homodimer protomer interactions

Sigh... why didn't you just answer the question in Health?

@CareyGregory - That wasn't asked on Health, at least not to my understanding.


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Why is the species-diversity of deadly parasites greatest in the tropics?
There are so many parasites living in tropical regions of Africa, South America, or Asia, but very few in Europe or North America.
Is this due to climate, or are there other reasons?
Many of the tropical diseases and parasites are transmitted by insects, such as flies and mosquitoes. Well there are flies and mosquitoes in Europe as well.
There might be malaria-transmitting mosquitoes in the very south of Europe, and there is encephalitis transmitted by ticks. But that's it. Why don't the hundreds of different parasitic species from Africa spread to Europe ?

Parasites aren't the only group to show this pattern. Many clades and ecological groups are more diverse in the tropics. This pattern is known as the Latitiudinal Diversity Gradient

Related Q/A: http://biology.stackexchange.com/q/14472/3624

The diversity of parasites shows a gradient with increasing diversity from the poles to the equator. Several reasons have been brought forth to explain the latitude-dependency of parasite diversity:

An increased diversity overall around the equator; species diversity in general is greater in the rain forests and hence more hosts are available and thus more parasitic species can develop that target specific hosts;
Larger amounts of precipitation and higher temperatures around the equator may favor the development and transmission of parasites (Nunn et al., 2005);
Increased available energy overall around the equator (Guernier et al., 2004).

References
- Guernier et al., PLOSone (2004): 0020141
- Nunn et al., Diversity and Distrib (2005); 11: 249–56

Nice answer +1 (and good post +1)! I have two questions: 1) Does "increased available energy" affect parasite diversity other than by increasing overall diversity (in which case the third bullet point would be the same as the first)? 2) I have a good intuition for what higher precipitation would favour parasite transmission but I fail to have a good intuition for high temperature. Can you explain? Thanks

@Remi.b - Thanks! 1) I think total energy has more to do with the gross number of animals present. Higher numbers of vectors and hosts will promote development of parasites overall. It's more of a general factor. 2) Most processes, including growth in general, goes faster at higher temperatures. Again, it's more of a general factor. The first bullet point has the strongest association, the 2nd and 3rd less so afaik.


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On vs. off-plant ripening: which one yields a more nutritious fruit?
Many fruits may ripen either when attached to the plant, or once it is detached from the plant. Which option yields a more nutritious fruit? In other words, if one picks a fruit when it is still unripe, then wait for it to get ripe, will the fruit has similar nutritional properties as if one wait for the fruit to ripe before picking it?


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How can microarrays be used to quantitatively determine level of gene expression?
This is probably a stupid question because I don't fully understand how microarray experiments work. I'm trying to understand how microarrays work but I'm confused about something which I can't seem to get around without fully understanding how microarrays work, which seems impossible without understanding this.
I understand the principle of how microarrays work. But I don't get how microarrays can tell you how much mRNA is expressed in one kind of tissue vs another kind of tissue. Wouldn't that depend on how much tissue you started with? So if you started with more cells of one kind you will get more mRNA/cDNA and so the intensity of fluorescence at the corresponding spot on the microarray will be greater. So even if the amount of gene expression is lower in one type of tissue the corresponding spot on the microarray might show a greater fluorescence intensity compared to the other type of tissue if more tissue was used.
Also another related question: if you put the mRNA you obtain from cells through PCR will you get the same proportion of mRNA as before PCR? From what I understand PCR can be used to make more mRNA before doing the microarray but because PCR is a random process I'm not sure if it will affect the proportion of mRNA.
Hopefully my questions make sense.

While someone is no doubt putting together an excellent answer, for some good visuals, Google "Microarray presentation" and the first few hits are good powerpoints for microarrays.

Briefly, you can compare different samples, which may have started out as different amounts of tissue, by using control genes. The numbers reported by most standard microarray experiments are not absolutely quantitative (There are 2450 copies of this RNA per cell in this sample), but are rather a proportion as compared to a set of housekeeping genes whose levels are not expected to vary much between the samples you are analyzing.

What about PCRs? do you get the same proportion of mRNA after applying PCR? I would still like an answer to the second question

@MattDMo gave a great answer. For PCR amplification, you are right, this is a random process and while you would expect most RNAs to be similarly amplified, biases can and will occur. Amplification biases are usually assumed to be identical between similar samples and therefore will (mostly) cancel out during the differential analysis.

Housekeeping genes are rarely used in microarray analyses, and there are many issues with finding housekeeping genes by itself  (See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4430495/ ) .
Models that work with microarrays usually work with making distributions between samples comparable based on the notion that most genes will not be differentially expressed between two conditions. This can involve scaling, or loess normalisation, or the very popular quantile normalisation. RNA-seq analyses oft use library size or upper quartile normalisation to ensure comparability.

From the comments:
MattDMo:

You can compare different samples, which may have started out as
  different amounts of tissue, by using control genes. The numbers
  reported by most standard microarray experiments are not absolutely
  quantitative (There are 2450 copies of this RNA per cell in this
  sample), but are rather a proportion as compared to a set of
  housekeeping genes whose levels are not expected to vary much between
  the samples you are analyzing.

cagliari2005:

For PCR amplification, you are right, this is a random process and
  while you would expect most RNAs to be similarly amplified, biases can
  and will occur. Amplification biases are usually assumed to be
  identical between similar samples and therefore will (mostly) cancel
  out during the differential analysis.


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How is recruitment of multiunit smooth muscle cells fine tuned if they are innervated by varicosities?
In my physiology textbook (Silverthorn) and on wikipedia it says that:

Multiunit smooth muscle tissues innervate individual cells; as such,
  they allow for fine control and gradual responses, much like motor
  unit recruitment in skeletal muscle.

However, that does not seem right to me. Although potentially each cell could be innervated, they are innervated by autonomic neurons. These neurons use the rather crude method of varicosity innervation. Such neurons recruit all the cells adjacent to its varicosities, not just a few. Hence, does this not mean that there is no 'fine' control of unit recruitment of smooth muscle cells?  Or is there an other way in which recruitment of smooth muscle cells is fine tuned?

Welcome to Bio and +1 for a good question. Could you link that wiki page?

I removed Moreover Silverthorn states that smooth muscle cells are responding in an all or nothing fashion, as I don't understand its relation to the question. Feel free too roll back any edits if any or all of my edits are not to your liking.


text:
How much energy does a neuron use for information processing as opposed to just surviving?
That is, as part of a neural network in a brain.

Are you interested in theoretical or experimental information? Checking the Bionumbers database for experimental data: glucose consumption averaged per neuron .

There are many, many different types of neurons. Some of them show very high spontaneous firing rates, while others are pretty silent. I think @Mustang's is great, but this question needs clarification.

Mainly interested from a theoretical computer science POV

http://quantum-mind.co.uk/anaesthetics-and-brain-energy/
About 80% of the brain’s energy consumption is devoted to neuronal firing with only 20% involved in maintenance activity.
The energy for firing is mainly supplied by glia and astrocytes, the maintenance of the neuron itself is done mainly by the cellular machinery in the neuron.

The text literally says "neural signalling", which is a lot broader than APs only. Without other references you may want to edit the wording. +1 nonetheless, nice way to tackle such a broad question.


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What were the main discoveries in Biology?
What were the greatest achievements in Biology? Can you please provide a short list of discoveries that you would consider as being the most important discoveries of the history of Biology.

I edited the post to match my answer (as I misread the question to start with). The post is now on-topic I think and I am voting to reopen.

Here are a few things coming to my mind

Discovery of cells by Robert Hook
Discovery of bacteria by Antonie Philips van Leeuwenhoek
Discovery of antibiotics by Alexander Flemming
The basis of heredity by Gregor Mendel
Evolution (On the origin of species by C. Darwin)
Watson and Crick discovery of DNA structure
Vaccination
The concept of ecosystem

yes they were incredible :D but i meant UN discovered things in biology which would be awesome :)

OP says would be, not what were

It always amazes me that a Canadian like you has trouble with these things, being so 'close' to the US. I have to visit Canada some day to pick up the flavor of it. Nonetheless, nice list +1 I would even recommend editing the question in line with your interpretation, because your interpretation is less pob (but still is), while the original question is definitely going to be closed.

@Christiaan I definitely misread the post indeed. I edited the post as you invited me to do. I feel quite proud when you call me "Canadian". In reality I have lived in Canada (Vancouver, BC) for the past 1.5 years but grew up in Switzerland.

That explains everything haha. Both very nice and interesting countries.  I'll vote to reopen. But it may still be pob...

@Christiaan Actually, in this context, the OP's would be is equivalent to what were. If you were to rephrase the "would be" expression, it could be something like "what would you consider to be some of the greatest achievements". People commonly use the two interchangeably in colloquial speech here in the US. Although if you want to to be technical about it, the OP 'should' have said "were", but this is SE Bio, anyway, not ELU :)

@AleksandrH - touche :)

Oh indeed! I like to think that this is why I understood the post the way I did. Thanks @AleksandrH

I don't understand the 2 down votes I received. Comments are welcome.


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Relationship of bases in a gene to amino acids
One of my study questions for a biology test was:
A gene contains 1200 bases. How many codons will be on the mRNA immediately after transcription?
My initial answer was 400 codons, because 1200 bases = 1200 nucleotides and 1200/3 = 400. But since DNA is double helix, and only one of the two strands is used in mRNA creation, would only 600 bases be used instead of the full 1200?

My instinct would be to divide the number of bases by 3 like you did. I've never seen gene length described as twice the number of base pairs.

@user137 Do you mean that the number of bases in a gene are usually counted using one strand (in double helix DNA)?

Yes, if a gene has 1000 base pairs, we refer to the sense strand, the other strand is implied. Of course we typically use the term "base pairs", and maybe your professor is being pedantic about bases vs base pairs. You won't know for sure until you get the test back.

I believe the question should have been "A gene contains 1200 base pairs. ...."

Assuming that all 1200 bases in the gene code for mRNA, then 1200/3 = 400 is the correct calculation.
It's important to understand that a gene will only ever be transcribed from one strand of double-stranded DNA. Think about it mechanistically - first, DNA is transcribed to RNA by a polymerase that can only move in one direction. Second, the strand complementary to a gene's transcription start site is that sequence's complement and therefore not a start site itself. Hope that clears it up. :)


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How fast is the patellar reflex?
I have found a lot of content on the patellar reflex, but I cannot find any studies on how fast the reflex is, from onset of stimulus to innervation of muscles.  Does anyone know of either a study or at least a ballpark number for how fast that reflex is?

Mamizuka et al. (2007) calculated acceleration data of the patellar reflex.
Their study measured the reflex generated in response to the tapping force applied to the patellar tendon with a customized tendon hammer. They measured using a tri-axial accelerometer placed at the ankle joint.
They found:

the time delay (29.6+/-6.0 ms) and the acceleration time (150.8+/-19.5 ms) of the speed response were quite constant for all participants.

Mamizuka, N., Sakane, M., Kaneoka, K., Hori, N. and Ochiai, N., 2007. Kinematic quantitation of the patellar tendon reflex using a tri-axial accelerometer. Journal of Biomechanics, 40(9): 2107-2111


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Electrocardiogram: Difference between Atrial Fibrillation and Atrial Flutter
I have been working on analyzing Electrocardiogram data.
I have read several documents related to conditions of the Atria during fibrillation and flutter, the most lucid being that atria quiver with rapid rate.
This manifests as multiple P-waves (some documentation refers to them as "F-waves" and regards P-waves as absent) in the Electrocardiogram.
However in this condition, we get a completed QRS-complex in the Electrocardiogram.
Now, coming to my question, in both scenarios i.e. Atrial Flutter and Atrial Fibrillation, i get multiple P-waves(or F-waves) with completed QRS.
So how do i differentiate between the two conditions ??

A-Flutter will have discernible waves that can be counted, usually. The R-R interval will be regular or maybe slightly irregular if there's a variable conduction block in the AV Node. A-Fib will ALWAYS be completely irregular without discernible pattern.
You can also modify the position of your limb leads. There is an EKG placement called the S5-Lead that basically makes it where the QRS disappears because it's electrical impulse is perpendicular to the monitoring leads. The Atria however, become super-visible on the EKG.
To do S5:
Place the RA electrode on the patient's manubrium.
Place the LA electrode on the 5th intercostal space, right sternal border.
Place the LL electrode on the right lower costal margin.
Then set the EKG to view Lead I