Programming Languages for Bioinformatics

The languages currently popular for bioinformatics work are Python, Java, R, Perl, and BASH, though the use of Perl is gradually declining. Note that Python has become the most popular language in a general context, so it's natural that it's the most popular in bioinformatics too. Of course 'most popular' doesn't mean 'best'. Pick a computer language and I'll point you to some publication that uses that language in a bioinformatics context (perhaps excepting COBOL, and RPG).

Some bioinformaticists spend most of their time performing analyses using existing software, perhaps using a scripting language like Python or BASH to 'glue' together existing programs or to control the submission of jobs to a computational cluster. Scripts and packages using the R language are often used in these analysis pipelines to perform sophisticated statistical analysis and visualizations.

Other bioinformaticists are developing new algorthims. In these cases computational speed can be very important, so languages like C, C++, or Java are often used. However, newer languages like Go, Julia, and Rust are also used, according to the taste of the researcher. New machine learning tools are often prototyped using MATLAB.

If your interest is primarily biology (biochemistry, virology, and immunology) then you'll want to focus on learning the biology, and supplement it with Python, BASH, and R. If your interest is primarily in developing new algorithms, then focus on statistics, and computer science. You'll still want to learn Python, BASH, and R, but you'll also want to add something like C++ or Java. The good news is that once you've learned 2 or 3 computer languages, you can pick up additional languages much more easily.


Why is it common to grow microalgae in bottles or canisters?

Really, the credit for this answer goes to another 'Homo sapien' from the Spirulina manual link in his comment.

Why do they use bottles or any type of bottle-like canister?

Likely, because they are clear. From the manual:

Spirulina needs sunlight so it is preferable that the container in which it is grown be transparent.

Plastic bottles are cheap, clear, and easy to come by, so they make the ideal material.

Why do they insert CO2 to the bottle artificially in cases the bottle doesn't have a cork?

I don't think the tubes in your picture are CO2 tubes. Rather, I'd bet they are bubble tubes (like in aquariums). These are necessary to keep the growth medium moving constantly. Again, from the manual:

Spirulina tends to gather at the top of the growing culture, where sunlight exposure is maximal. Due to this, Spirulina that cannot reach the top will not multiply and will ultimately die.
In order to maximize Spirulina exposure to sunlight, the water in which it is grown must be stirred
...
Another option is a pump, the simplest kind used for aquariums.
(emphasis mine)


Why do stem cells injected into muscle become muscle cells?

Looking at the paper itself, we find that they prepared the stem cells to have myogenic (muscle-specific) properties. They first injected stem cells into the irradiated (which kills muscle stem cells) muscles of immune-deficient mice. This resulted in tumor growth (teratoma - a stem cell derived tumor, where different kinds of tissues are spontaneously formed. Growing in a muscle environment increases the chance of muscle tissue formation.). The tumor cells, which expressed muscle-specific markers, were isolated from the other tissues and then used for regeneration of an injured muscle.

In their teratomas they checked for cells expressing α7-integrin and vascular cell adhesion molecule-1 (VCAM-1), which are markers expressed in satellite cells (muscle stem cells). These factors were expressed in about 10% of the fraction that did not show any hematopoietic and endothelial markers (meaning: there were a lot of other tissues formed as well). They also showed expression of Pax3 and Pax7, which are muscle-specific transcription factors, important for differentiation of myogenic progenitors. These cells were therefore already muscle-specific cells before they have been transplanted for regeneration.

The researchers did, in fact, do in vitro and in vivo differentiation experiments. For in vitro differentiation they subjected their muscle-marker expressing cells to a myogenic medium. This mimics the muscle environment and enables cell differentiation signaling. Here is an example protocol how this can be done. Then they transplanted their muscle stem cells into a muscle and they also managed to differentiate in vivo and regenerate the injured muscle.

The entire process of pluripotent stem cell to muscle cell differentiation can be performed in vitro, but seems to be tricky (1,2). Medium factors or genetic activation of transcription factors can activate different steps in the differentiation cascade.


What is the difference between abundance and dominance in an ecosystem?

There is a difference between dominance and abundance in vegetation science, and your citation is about vegetation.

Abundance is the relative representation of a species in a particular ecosystem. It is usually measured as the number of individuals found per sample.

Ecological dominance is the degree to which a taxon is more numerous than its competitors in an ecological community, or makes up more of the biomass.

In vegetation science, abundance is usually measured as the number of individuals or the percentage of coverage of that species in a plot. An abundant species would typically have a lot of individuals in the plot. A dominant species dominates the other species, so typically covers more than 50% (up to 100%) of the plot. Doing this, it also takes away space (and light!) for other plants.
Usually abundant species also cover a lot, but small species (for example grasses) can be abundant without becoming dominant while large species (like trees) can be dominant with relatively few individuals.


What is the lowest intensity threshold of light for photosynthesis in any species?

Disclaimer: photosynthesis is not my field of expertise.

I assume you are asking about the amount of light needed for photosynthesis to take place, not the light intensity needed to sustain the plant? Since photosynthesis is an interaction between chlorophyll and single photons I would assume that photosynthetic reactions could take place with just single photons of suitable wavelength (i.e. at the limit of defining light intensity), but to measure this might be extremely hard in practice. The article Photosynthesis in the Abyss indicates that this might be the case, saying that in deep sea environments "A single molecule of bacteriochlorophyll receives a single photon only about once every 8 hours" (see also this popular science article). The conditions for deep sea photosynthesis is described in Beatty et al. (2005), which report photosynthesis by green sulfur bacteria at hydrothermal vents, where the only source of light is geothermal radiation.

However, as stated earlier, photosynthesis is not my subject field so I do not know how credible this information is.


In order to do this you would need to find a compound that does all of the following:

Crosses the blood-brain barrier. Many pharmaceuticals are not able to do this.
Binds strongly to, or has some metabolic effect on adenosine. The resulting product must also cross the blood-brain barrier, and be excreted.
Not bind or react with other molecules that are similar to adenosine and cause side effects.
Not cause some sort of immune response - along with the blood-brain barrier issue, this rules out any sort of protein, and really limits the potential specificity for items (2) and (3): there simply isn't a lot of chemistry outside of biochemistry that is that specific.
Not cause systemic effects via depletion of adenosine and products of adenosine. There are several problems caused by a failure of the enzyme that metabolizes adenosine but it seems like most of the primary symptoms are due to an accumulation of adenosine rather than an absence of inosine, so I am not certain how much of a problem this would be.

And probably numerous other issues I haven't thought of yet. The point is, adenosine is a useful biological molecule, not just junk to get rid of, and developing something to "clear" just one specific compound is actually really complicated. If the main concern is the sleepiness caused by adenosine build-up, caffeine is widely available and relatively safe compared to some novel way of actually clearing adenosine.

In fact, I can't really think of many pharmaceuticals that work by actually "clearing" something, but feel free to leave any suggestions in the comments. Chelating agents come to mind, but those are only used in some very specific circumstances.


Can cancer cells transmit from one organism to another?

Yes. Devil facial tumour disease is an example:

https://en.wikipedia.org/wiki/Devil_facial_tumour_disease

Look here for other examples of transmissible cancers.

I have not heard of any human transmissible cancer.


Publicly available resources for learning metagenomics

The Coursera Bioinformatic Methods courses include classes on metagenomics and, more importantly, tools to use when applying these methods. I have not taken this particular course, but Coursera is generally very good with getting hands-on experience using computational tools. A course-like setting may also be conducive to group learning.


I believe it is a type of fission-fusion society or even some hybrid with agent based modeling.

  In ethology, a fission–fusion society is one in which the size and composition of the social group change as time passes and animals move throughout the environment; animals merge (fusion)—e.g. sleeping in one place—or split (fission)—e.g. foraging in small groups during the day. For species that live in fission–fusion societies, group composition is a dynamic property [fission-fusion society].

A classical example is the Bonobo or pigmy chimp.

Bonobo - Pigmy Chimpanzee
Sociobiology
The Social Behavior of Chimpanzees and Bonobos


In my experience, reuse of NADPH stock solutions maintained at pH 7.0 or above is perfectly acceptable. Taking an absorbance spectrum every half-hour or so will probably show that definitively.  However, NADPH is VERY unstable in acid, leading to a 'bleaching' of the absorbance at 340nm.  Try measuring a rate at pH  6 or below, 340nm,  with 100 micromolar NADPH and no enzyme or cosubstrate. There will be a very significant decrease in absorbance with time (ie a 'blank' rate) which will make estimation of enzymic reactions at low pH virtually impossible.


Complementation cloning: what, why and how?

I figured it out. You're complementation cloning when you know the function of a mutant sequence but not it's sequence. For example, your organism (human) gets skin cancer from too much UV light exposure.

With complementation, two mutants can restore the wild type phenotype (well functioning UV repair).

We know E. coli has a well studied UV repair gene so you transform the cDNA library from your human into an E. coli which we know has the mutation, then grow them all under intense UV light. The  E. coli with the human mutant allele (the right cDNA fragment) will survive, so you can amplify that colony, sequence it, and then use it as a diagnostic tool in humans.

I'm wondering why that was vague. Is "complementation cloning" not a well used name for that technique? Was the question too broad or elementary? It's the first time I've used Stack and it seems I may be a little too undergrad for this crowd.


Scoring sequence against position weight matrix

The probabilities are correct. You must take the product (in log space this is equivalent to sum). The reason the probability looks small is just that you are perhaps thinking the score should be close to 1. However, this is not the case. To get a score of 1, you need the PWM to have 1/0/0/0 at all positions and get a perfect match.

So what should you compare to? What people usually do is compare this to a background distribution, the easiest being uniform, so the PWM is 0.25 everywhere. For your example, the score in this case will be 0.25^4 = ~0.004 and this is what you should expect by random.

This is why people usually look at the ratio between the score of the PWM relative to the score for the background model (and usually take the log2 of that), which in your case will be 0.18/0.004 = ~46 so the sequence you got is 46 times more than you would expect by random! And for your second example, 0.072/0.004 = ~18 times more than expected, so that is still high.

More conceptually, what you are doing is comparing two probabilistic models, your PWM and a background PWM, and comparing the probability to get your observed sequence according to each one of them. This is a common approach in general for comparing probabilistic models, even if they are more complicated.


Regarding cancer cells and radio-frequency ablation

I think you're referring to radio frequency or microwave ablation. It works by heating the tissues up with electromagnetic radiation, just like you'd use to microwave food, but it's heating you instead. Healthy cells have better repair mechanisms and survive these treatments better. Cancer cells tend to have poor repair ability and can be killed more easily. I've heard of injecting metal nanoparticles which collect in the tumor due to the enhanced permeability and retention (EPR) effect. The nanoparticles respond to the microwaves much more powerfully than cells do and get hotter, burning the tumor from the inside out.


There is a reasonable speculation. That is to get more areas where ATP synthases are localized in order to produce ATP. But this doesn't tell why the structure has to be the exactly that shape.

As the review Ilan show, the shape seems to be determined by ATP synthase dimerizetion. The shap may be just a consequence of ATP synthase dimerizetion, although it successfully enlarges the area where ATP synthase is localized.


Has any large-scale origin-of-life simulation/experiment been done?

What you are possibly thinking of is large versions of the Miller Urey Experiment where a mixture of reducing gasses carbon dioxide, ammonia, nitrogen and the like are subjected to electrical arcs in a closed flask reaction, resulting in some biological molecules being produced.

Opinions have changed - Miller Urey did get the atmosphere wrong and so their finding of amino acids is not necessarily, but variations of this experiment continue to be done, with different conditions in the reaction vessel which reflect typical or even unusual conditions.  I've found some nice collections and reviews. There continues to be an enthusiastic effort even today.

Looking over several of these overviews, it's clear that many different conditions are being tried - reactions on mineral surfaces, examining chemicals on meteorites, near volcanic vents, different kinds of radiation.  What I don't see is anyone going to a huge tank.

I think that this might not have been tried (perhaps someone else will find a counter example), but if it were not me, I would probably not try longer experiments either.

There's some good reasons for this, if true.

Firstly all the published descendants of the Miller experiment have produced biologically relevant compounds after a few days.  Extending the experiment a few orders of magnitude may not prove anything new.

Secondly, the longer a reaction is run the more likely the sealed containers and heaters and other apparatus has to fail, causing you to restart or include contaminants that would ruin it.

Thirdly, one is not going to run an experiment that will ever come close to reproducing the time spans or volumes over which life emerged on earth - that was perhaps a few hundred million years over the area of the planet.

That's not to say you won't find out something new - an extra week could produce a new set of compounds or even a replicating system - we don't know if we haven't done it, but the nature of science is that you have a little time and money for a project like this and you would like to prove feasibility  - 'it could have happened this way'.  By selecting the conditions and doing a series of modest experiments which allows some to fail so that you can find something new.

I would say the observation of other planets and analysis of meteorites are getting closer to your idea - they are huge systems and been going for billions of years.  Titan is especially promising.  They just aren't the same conditions as Earth.

In brief, nothing is both affordable and perfect in proto-biotic research.


Where can I find an at least Semi-Comprehensive list of what biochemical reactions Acetyl-CoA participates in?

I may be missing some fantastic resource, but my first thought is to send you to KEGG.  Is that crazy?  Maybe, but a simple search for Acetyl-CoA in humans can give you tons of useful information, including GO terms, enzymes, genes, and, yes, biochemical reactions; just use the KEGG Pathways tool and specify humans (hsa).  You can click on each individual pathway for more information, such as the cholinergic synapse.


Why is the Krebs cycle considered a part of aerobic metabolism if molecular oxygen is not involved in any of the reactions in the cycle

Oxygen is actually not needed in the Krebs cycle - it is needed in the electron transport chain that is downstream of the Krebs cycle to regenerate NAD+ from NADH. NAD+ is a co-enzyme and acts as an electron carrier in oxidizing reactions at various positions in the Krebs cycle. However, note that without O2, NADH accumulates and the cycle cannot continue as it needs NAD+ to run.
Krebs cycle - No O2 needed:

Electron transport chain - O2 needed to regenerate NAD+ essential for the Krebs cycle:


Medical term for "holding urine for a long time"

A swollen organ may be described as distended if the swelling is symptomatic of a medical disfunction.
The purpose of most bladders is to collect and retain a fluid; if that fluid needs to be discharged periodically, and is not able to do so, then there is usually pain as a result of the distension.

Inability to urinate is known as ischuria or urinary retention, and could be the result of obstruction to the urethra, could be a failure of the bladder to fully contract during urination, or could many other possible causes.


Why can't we find a broad spectrum antiviral drug to viruses like antibiotics to bacteria?

One of the main issues with nucleotide analogs is that they can also affect the host replication and transcription (though they have a higher affinity to the viral polymerase), and can therefore have adverse side effects. On the other hand, the broad spectrum anti-bacterial antibiotics specifically affect prokaryotic cellular machinery.

(Note that some antibiotics like streptomycin do affect the host mitochondria and thereby cause toxicity. Ototoxicity and nephrotoxicity are known side effects of streptomycin.)

Nucleotide analogs are actually used as broad spectrum anti-virals: For example, Lamivudine is used for both HBV and HIV, which are different types of viruses.


What is this worm or larva I found in my walls

You are correct!, those are definitely mealworms. If you're not already aware, mealworms prefer to live in dark places (so under/in woodwork is expected) and typically eat decaying material, but are also partial to consuming new plant growth.

During the larval stage of a mealworm (of which will eventually grow into a Darkling Beetle), a mealworm will undergo 10-15 molts before pupating. That being said, the collection of carapaces that are shown in your picture is probably the work of just a few beetles.

I cannot attest as to how long it takes for a mealworm carapace to deteriorate, but sure, those remains could very well have been there for decades. If the location in which you found these remains has a dirt floor, you could possibly try identifying trails that were left by the developed beetles. Their trails looks like this:


This is a click beetle (Elateridae), so not a cockroach. This is most easily seen by the long pointed corners/angles at the posterior part of the pronotum, which is part of the “click” mechanism they use to flip themselves when they land of their back, or to startle predators.


Why is peripheral vision not bleached by daylight?

Short answer
In photopic lighting, peripheral vision is mediated by cones.

Background
The rods are indeed saturated at daylight, and even at twilight (source: Nature). However, the cones are active and although their density in the periphery is low, they are still present (Fig. 1). Hence, peripheral vision in photopic lighting conditions is mediated by cones. Because of their low density in the periphery, however, visual acuity is low (Kolb, 2012).

Fig. 1. Rod & cone densities in the retina. (Kolb, 2012)

Reference
- Kolb, Photoreceptors, In: Webvision: The Organization of the Retina and Visual System. Utah University


Did the jackal (wild African dog) evolve independently or with some form of human domestication?

This answer is just for African golden jackal evolution, but this website (sciencemag.org) explains that...
“...researchers compared genomewide DNA samples from jackals, gray wolves, and dogs. They found that African golden jackals diverged from coyotes and gray wolves some 1.3 million years ago...”.
Also, this Wikipedia article about Canis arnensis (the Arno river dog) (I know that Wikipedia is unreliable but it had related helpful information) explains that...
“The Arno River dog has been described as a small jackal-like dog. Its anatomy and morphology relate it more to the modern golden jackal (Canis aureus) than to the larger Etruscan wolf of that time. It is probably the ancestor of modern jackals.”


Identity By Descent vs Identity By State

The issue of IBD and IBS can indeed be confusing.

The identity by state definition refers to the fact that at some point two individuals, even if they are not related to each other, present the same allele at a specific locus. Because of their un-relatedness this similarity probably arose from a similar mutational event.

On the other side, with IBD two individuals happen to share the same allele because of their coancestry.

Alleles that are identical by descent are also identical by state. But the opposite is not true. (see also https://www.biostars.org/p/174048/#174049 and Powell et al 2010, Nature Reviews Genetics 11, 800–805 (1 November 2010) | doi:10.1038/nrg2865).

Now, about the threshold that you were mentioning in your question, I am not entirely sure what you mean. Eventually, all individuals are traceable to a MRCA (most recent common ancestor). So, I think the threshold you talk about refers to the size of the population in analysis. Depending on the size of your population you will have different proportions of alleles that are IBD and IBS.

Hope this help.


Methanol is highly toxic in humans. As little as 10 ml of pure methanol can destroy the optic nerve and cause permanent blindness,  while 30 ml dose is fatal (Vale et al, 2007). However, its toxic effects take hours to come up after ingestion,  and antidotes are often helpful in preventing permanent damage.

Methanol exerts its toxic effects by two main methods:

Much similar to ethanol, methanol is also a CNS depressant since it enhances the activity of inhibitory neurotransmitter GABA and also interferes with excitatory neurotransmitters.
When ingested, methanol is converted in liver first to methanal by alcohol dehydrogenase, and then to methanoic acid (or formic acid) by aldehyde dehydrogenase (Schep et al, 2009). Under cellular pH,  formic acid exists as formate. Formate interferes with the mitochondrial enzyme cytochrome c oxidase, causing cellular hypoxia and metabolic acidosis (Liesivuori et al, 1991).

To prevent methanol toxicity, two kinds of antidotes are used:

Bicarbonate can alter the metabolic acidosis and potentially reverses the visual deficits.
Ethanol and fomepizole are also used as antidotes to methanol. Since the affinity of liver enzymes alcohol dehydrogenase and aldehyde dehydrogenase is about 10-20 times more for ethanol than methanol, ethanol can thus prevent (or at least delay) metabolism of methanol to formate. During this time, methanol can be removed from the body by kidneys or through dialysis. Fomepizole is also metabolized by the same enzymes, but ethanol is generally preferred due to high cost and low availability of fomepizole (Medscape). Thus, intravenous injections of ethanol can (under some circumstances)  serve as a first-aid measure (although consulting a physician is always the best option).

References:

Vale A (2007). "Methanol". Medicine. 35 (12): 633–4. doi:10.1016/j.mpmed.2007.09.014.
Schep LJ, Slaughter RJ, Vale JA, Beasley DM (2009). "A seaman with blindness and confusion". BMJ. 339: b3929. doi:10.1136/bmj.b3929.
Liesivuori J, Savolainen H (September 1991). "Methanol and formic acid toxicity: biochemical mechanisms". Pharmacol. Toxicol. 69 (3): 157–63. doi:10.1111/j.1600-0773.1991.tb01290.x
Methanol Toxicity Treatment & Management: Medscape


What's the maximum pressure inside a bombardier beetle?

According to this study, model data shows a maximum pressure of 110 kPa, that's 16 psi and only 1.086 atm:

  The three-phase process involved in the beetles explosive secretory
  discharge (ESD) process. The inlet size is shown as a proportion of
  the inlet radius. During the first phase of refill and heating (blue),
  only the inlet valve is open. During the second phase (red), the
  chamber is closed. Finally, the third phase (marked by an arrow) is
  the exhaust phase, when only the outlet valve is open. This phase is
  significantly shorter than the first two phases. This cycle then
  repeats with phase 1 starting at approximately 5.1 and again at 7.8
  ms.


Evolution of the (phenotypic) facial features of the indigenous people of (west/central) Africa

Note that I had never heard of the expression "broad african type" and could not find much reference to this term when googling. But anyway, I'm happy to use it to refer to a particular set of typical facial features.

  What is the reason behind this seeming resemblance?

Note that the Homo Heidelbergensis image is not a picture (obviously) and much of what is being depicted was open to artistic interpretation. It is possible that some of the feature you are thinking of are not real. Have a look at the post In reconstructions, how are various shapes of facial features determined from skull only?.

You list several phenotypic traits and it would be too broad of a question if you were expecting an explanation about the evolution of each of these traits. I will just pick one classic trait; the nose.

One of the role of the nose is too even up the temperature of the air that we're inhaling. As such, the shape of the nose is under differential selection pressures depending on the environment. So if the nose of Homo Heidelbergensis looked alike (assuming it really looked like on the facial reconstruction) today's "broad African type", it is probably because of shared environment. Note however that nose shape vary a lot among african lineages and also among non-african lineages. You might want to have a look at this popular article.

A big point of ressemblance is the skin color that you don't talk about. Have a look at the posts Why do we assume that the first humans were dark-skinned? and How did some humans evolve to be white? to learn more about skin color

  Is this appearance an illusion and possibly a construct of a prejudiced mind, or does this have a valid scientific answer?

First, see my above point about facial reconstruction.

H. Heidelbergensis lived in Africa and in this resepct shared an environment that is like the environment that modern african are encountering that what modern Han Chinese are encountering. In this respect, we could expect some ressemblance.

  For example, are most Africans closer to our ancestors than the rest of humanity is?

No, they're not and they cannot be. The MRCA of all humans today is more recent than the MRCA between any human and H. Heidelbergensis. You should have a look at this intro to phylogeny to understand a little bit better how different lineages relate evolutionarily speaking.


Why do chickens not try to get up if laid on their backs?

This phenomenon is called tonic immobility. And those speculations you've mentioned are wrong: they do get back on their feet, only remain in that state for a prolonged time, which depends on the distance and eye contact with whoever laid the chicken on its back, as stated here.

From this experiment, it can be concluded, that this behavior in which the animal is immobile is a defense against predation, because most attackers sense motion primary.


Why is urobilinogen reabsorbed from the gut just to be excreted via the kidneys?

I think that it is missing some details. Note that the vast majority of urobilinogen (~80%) is actually eliminated via fecal elimination. I would recommend looking at the article on enterohepatic circulation, which provides more context on this issue. Basically, bile salts can be useful (even or especially after metabolism by bacteria), so a fraction is reabsorbed by the large intestine and then dumped back into the digestive system:

However, just like bile, some of the urobilinogen reabsorbed is resecreted in the bile which is also part of enterohepatic circulation. The rest of the reabsorbed urobilinogen is excreted in the urine where it is converted to an oxidized form, urobilin, which gives urine its characteristic yellow color.

...

The net effect of enterohepatic recirculation is that each bile salt molecule is reused about 20 times, often multiple times during a single digestive phase.

Obviously urobilinogen isn't one of the salts recirculated that much if most of it gets excreted in feces, but apparently it still happens (possibly just because it is chemically similar to the other bile salts, as you suggest).
I think that the mechanism which is emphasized in the urobilinogen wiki page is a secondary mechanism for excretion when urobilinogen is at toxic levels in the bloodstream (e.g. jaundice). These high levels come for example from blood breakdown as pointed out in the article, which may be emphasized because it is a common medical issue (which is of course not a focus of SE Biology).
So, in other words, the wiki article is targeted towards the potential medical problems (toxic levels requiring elimination via kidney) rather than the normal physiology (mostly eliminated in feces, sometimes-useful salt that helps digest stuff), possibly leading to confusion. This flash card resource succinctly notes the functions of bile salts such as bilirubin and its derivatives and may be helpful for other basic info:

Functions:
(1) Digestion and absorption of lipids and fat-soluble vitamins
(2) Cholesterol excretion (body's only means of eliminating cholesterol)
(3) Antimicrobial activity (via membrane disruption)

More about (unfortunately medical focused) physiology of bilirubin etc. can be found here.


Has anyone used Crispr/Cas to induce a knock-in in MEF cells?

From this paper:

  We chose to test for Cas9-driven targeted mutagenesis on the
  endogenous Trp53 gene in mouse embryonic fibroblasts (MEFs), a cell
  line in which the biology of p53 has been thoroughly characterized and
  where the gene is structurally intact.

Furthermore:

  Seventy-two hours post-transduction, cells were cultured in the
  presence or absence of Nutlin-3a, a specific inhibitor of the MDM2–p53
  interaction (Tovar et al. 2006). Cells were scored for the fraction of
  GFP+ cells after 4 d of Nutlin-3a exposure using flow cytometry (Fig.
  2B). Nutlin-3a potently activates a p53-dependent anti-proliferative
  cellular response, which strongly and specifically selects for any
  cells with disrupted Trp53 function (Efeyan et al. 2007). Much like
  MLP-p53.1224 infected cells, the pQCiG-p53 GFP+ cells were rapidly
  enriched for in the presence of Nutlin-3a, suggesting that
  CRISPR-mediated gene disruption had initially occurred in at least a
  proportion of the initial Cas9-expressing cells.


What is the evidence that australopithecines were bipedal?

Mainly because of the characteristics of the pelvic joint with the femur and the foramen magnum (the hole the spinal cord uses to connect with the encephalon). Also, there are more specimens other than Lucy, and there also exist fossil footprints (for instance the Laetoli footprints). All this evidence points to a bipedal walking.

Source: http://www.talkorigins.org/faqs/homs/pelvis.html

As you can see, the Asutralopithecus pelvis resembles human pelvis more than chimpanzee's (wich is adapted to a primarily quadrupedal movement).

Source: https://web.archive.org/web/20160817080843/http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/P/Primates.html

In this image you can see the position of the foramen magnum in a typical pure quadrupedal mammalian, such as a dog. The foramen inserts in the posterior part of the cranium. In the human, the foramen inserts in the base of the skull, due to de erected position. In chimpanzees, which have quadrupedal march, but can also display some bipedal movements, the foramen is slightly displaced towards the basis of the cranium, in an intermediate position between both.

Source: http://www.fcnym.unlp.edu.ar/museo/educativa/serypertenecer/principal/australopitecinos.html (Spanish)

In this image it shows the foramen in chimpanzees, Australopithecus and modern humans, and you can see that the position in the second is at the base of the skull, just like in Homo.

It is assumed that the bipedal locomotion is an adaptation to the savanna environment, where trees were rare. Bipedalism also allows a better visual field and it has more energetic efficiency.


What material fills the synaptic cleft? Is it water?

There are two types of synapses namely Electrical synapse and Chemical synapse. In electrical synapse there is physical contact between two cells through gap junctions. In chemical synapse there is a small gap between two cells which is termed as synaptic cleft.

The presynaptic and postsynaptic membranes at chemical synapses are separated by a synaptic cleft that is 20–50 nm wide, 10 times the width of the separation at gap junctions. The cleft is filled with a matrix of fibrous extracellular protein. One function of this matrix is to serve as a “glue” that binds the pre- and postsynaptic membranes together.(reference 1)

The same reference also states Water is the main ingredient of both the fluid inside the neuron, the intracellular fluid or cytosol, and the outside fluid that bathes the neuron, the extracellular fluid. Electrically charged atoms, ions that are dissolved in this water are responsible for the resting and action potentials.

Reference 2 mentions, The synaptic cleft is not simply an empty space, but is the site of extracellular proteins that influence the diffusion, binding, and degradation of the molecules, including neurotransmitters and other factors, secreted by the presynaptic terminal

If we think in this direction, of course holding together two neurons at synapse position is important. Moreover, the presence of several dissolved ions (in water) are necessary. If you remember, for the release of neurotransmitters into the synaptic cleft, influx of Ca2+ ions through voltage gated ion channels is essential.Thus, from above all points we can conclude that, the extracellular fluid in synaptic cleft is mainly aqueous in its composition with several ions, released neurotransmitters and several proteins that constitute a matrix.

What force makes the neurotransmitters move toward the receptors?

An essential role of astrocytes is regulating the chemical content of this extracellular space. For example, astrocytes envelop synaptic junctions in the brain, thereby restricting the spread of neurotransmitter molecules that have been released.(reference 1).Thus, it helps to confine the neurotransmitters in the small region, thereby increasing the probability of getting in touch with the target receptor.Also, as reference 2 says, there are several proteins present in the synaptic cleft which influence the diffusion.It means movement of neurotransmitter is by diffusion and above mentioned various factors can influence their movement towards receptor efficiently.

References:

Bear et.al, Neuroscience, exploring the brain, 2015
Neuroscience, textbook by Dale Purves.


Albinism inheritance problem: what are the father's alleles if he got an albino kid?

Super oober short answer: The father is Cc, the mother is cc, there is a 50% chance the children will be albino (as you predicted).

An explination on Mendelian genetics:

First let's look at (what a lot of people consider) the normal Mendel table from here:

Since the dad is normal, that means he has at least one Normal Gene. Which makes him C ? . We also see that mom is normal, so that means she also carries the gene C ? . In this case, they wind up with one child that is affected which means the child has the trait cc. That means both parents had to give the child one little c so that makes both of the parents Cc.

Your answer:

Now, in your problem the mother is albino, which you correctly put as cc.

The dad is normal, which means his C ?. He could eaither be CC (homozygous dominant - an uneffected non-carrier of the affected gene) or he could be Cc (heterozygous - an uneffected carrier of the affected gene). So at this point all we know about the father is that he is C ? . Which means you were on the right path.

Now we look at their first son. We are told he is albino. That makes him cc. That means that the father HAS to have at least one affected gene making him Cc.

So you were correct in thinking that it was Cc. You tripped yourself up by saying that it would make albanism the dominant. As you were told Albanism is a recessive gene. The big C is the normal gene which would hide the albanism trait.

To draw your table, just change all of your ? to big C.


Why is sheep erythrocyte lysis considered as classical complement activation pathway, and rabbit as alternative one?

The complement system is an innate immune response which has three pathways - as shown in the image below.
The breakdown of red blood cells assesses the functional capacity of the complement system. This experiment is titled: "Total complement activity", "CH50" or "CH100". Is this what you're referencing?
Hemolysis of sheep red blood cells occurs via the classical complement pathway.

More information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4360204/


I cannot obviously speak for the specific case you mention (and, anyway, I am not a medical doctor so I would not make a diagnosis in any case), but one thing that comes to mind is that eyes are part of the immunologically privileged sites of the body. This means that an inflammatory response is not elicited in case of the introduction of an antigen.

I quote from Immunobiology by Charles Janeway

  Some body sites are immunologically privileged. Tissue grafts placed in these sites often last indefinitely, and antigens placed in these sites do not elicit destructive immune responses.
  Paradoxically, the antigens sequestered in immunologically privileged sites are often the targets of autoimmune attack; for example, brain autoantigens such as myelin basic protein are targeted in multiple sclerosis. It is therefore clear that this antigen does not induce tolerance due to clonal deletion of the self-reactive T cells. Mice only become diseased when they are deliberately immunized with myelin basic protein, in which case they become acutely sick, show severe infiltration of the brain with specific TH1 cells, and often die.
  Thus, at least some antigens expressed in immunologically privileged sites induce neither tolerance nor activation, but if activation is induced elsewhere they can become targets for autoimmune attack (see Section 13-25). It seems plausible that T cells specific for antigens sequestered in immunologically privileged sites are more likely to remain in a state of immunological ignorance. Further evidence for this comes from the eye disease sympathetic ophthalmia (Fig. 13.36). If one eye is ruptured by a blow or other trauma, an autoimmune response to eye proteins can occur, although this happens only rarely. Once the response is induced, it often attacks both eyes. Immuno-suppression and removal of the damaged eye, the source of antigen, is frequently required to preserve vision in the undamaged eye.


What if we blend hydras to form a soup. will they still regenerate to form new individuals?

Based on this article, the answer is probably no. Quote (emphasis mine):

Small tissue pieces were excised from wild-type polyps of Hydra magnipapillata, allowed to regenerate, and the size-dependent characteristics of head regeneration were examined. The excised tissue piece was initially a square flat sheet. This piece gradually rounded up and, within 24 hr after excision, turned into a "spherical shell" which had a continuous ectodermal layer outside, a continuous endodermal layer inside, and an empty cavity at the center.
The smallest spherical shell that could be produced had a diameter of 0.2 mm and contained 270-300 epithelial cells. A tissue piece too small to form a spherical shell always disintegrated, presumably due to lack of an osmotic harrier between the tissue and the environment.

In short: any piece of hydra tissue with a diameter less than 0.2mm or that contains less than 270-300 whole epithelial (skin) cells is incapable of surviving and regenerating. It is highly unlikely that any hydras would survive being blended because the pieces would probably be too small or too damaged to be viable. Of course, if you had a chopping machine that cut hydras into large enough pieces without causing any significant cell damage, you could probably manage to create a large number of hydras in a very short time span. (I'm not sure why you would want to, though.)


Can viruses that normally infect eukaryotic cells also infect bacteria?

I'm not so sure about my answer. But I think "bacteriophage" is a polyphyletic name of which was defined by the ability of infecting bacteria, but not defined by the genetic, evolutionary, or morphological relationships.

It seems that if a species (or a taxon in a higher taxonomic level) of virus is infectious to bacteria, it will be classified as a member of the bacteriophage.

Here is a review article about the phage classification.


What's the difference between a plant and an animal?

Yeast are neither plants nor animals; they are fungi. The old classification where things were lumped into only two buckets - plants or animals - has long since broken down. In fact, even things you might think of as plants, like algae or most seaweed are no longer classified as plants. Under the old system, plants and animals were considered kingdoms, and the latest classifications now divide the Eukaryotes into six kingdoms, but even this is poorly evidenced and facing challenge.

The best method of classification is probably cladistics which is based on the evolutionary history of organisms - but even it has problems when you start considering what to do with horizontal gene transfer and endosymbiosis. Because under a cladistic view, plants and animals are defined not by their features but by their ancestors your question becomes moot, I think.


How conscious are mammals that mating leads to pregnancy and offspring?

I have trouble citing the exact source now as it's in one of my books at home, has 'sex' in the title (Sex in History), and I'm at work and can't Google that. But needless to say, the book made mention of studies of isolated, modern human tribes where it was evident that the people of the tribe had not made the connection between pro-creation and child-birth. Rather, intercourse was often tied to specific rituals that had a side effect of birth.

So there are a few things that one can extrapolate from this:

Pre-historic humans may have often not been aware that sex led to procreation
From that one can extrapolate further that no animals have this awareness either, as we are the most intellectual species on the planet

Further, the evolutionary development of sex points to this too. The ultimate cause of child-bearing is propagation, but the proximate cause of child-bearing is pleasure. Before life could be aware of the connection, there needed to be a reason to have sex, and so we would have developed in a way that encouraged pro-creation for no other reason than we liked doing it. Eventually we were bound to connect the dots, but we're oriented for this behavior regardless.


The question is little bit unclear: is in vitro or in vivo introduction in question?

In vivo:

  As the nematode feeds on the plant during its parasitic phase, it
  consequently assures the introduction of dsRNA and/or siRNA molecules
  into the nematode’s digestive system.

in vitro introduction etc  ->

The status of RNAi-based transgenic research in plant nematology


Why don't raisins lose water when in air?

That means that the cells are permeable to water, right?

Correct.

  Then why don't they lose water when kept in air?

They do, but it occurs very, very slowly. It might take a few months (or years in some areas), but if you leave raisins exposed to air they will eventually become harder until the water reaches equilibrium with the surrounding air.

This slow process is why there are tips on how to reconstitute raisins that are too hard to make them more moist and plump after getting a bad batch or finding old ones in your kitchen.


Is it true that viruses cannot be seen with phase-contrast microscopy?

It is true for most viruses. They have a size of roughly 1/100 of bacteria (or smaller), so they are too small to be seen in light microscopy. According to Wikipedia the maximum limit with light microscopy is around 1500x magnification (or making structures, which are at least around 200nm in size visible).

A lot of viruses are smaller, for example the influenza A virus is around 80-120nm, the HIV virus around 120nm and the rhinovirus which causes the common cold around 30nm. They would only be visible in electon microscopy. The measles virus on the other hand has between 350 and 400nm and should be visible in light microscopy. However, since you are very close to the region where you reach the diffraction limit for visible light, it is usually not used very much.


Is there a biological basis to physical attraction?

Yes, there is a biological basis. Your examples seem a little social/cultural to me, though. In any case, here are some examples I came across. One study that showed that women's hormones rose in response to smelling male sweat.  There's also a large psychological component that, for example, shows people find symmetry important in beauty.

A review discusses various aspects of facial beauty, and mentions that several studies have shown certain physical attractiveness standards are common across ethnic groups. It also mentions another study that shows how women are more attracted to a "masculine" face during the high-risk phase of their menstrual cycle.


Are cells guaranteed to get at least one mitochondrion when they divide?

Isn't there a possibility that cell division will result in a daughter
  cell with no mitochondria?

Yes, there is always the possibility. However, there must be a strong negative selection pressure against eukaryotic life that cannot achieve the proper partitioning of mitochondria, so you can imagine that there are mechanisms in place to prevent this case.

Mitochondria are both passively and actively partitioned to daughter cells. This is understood to occur through the cytoskeleton and with the control of mitochondrial fusion and fission at key stages of the cell cycle, prior to mitosis and cytokinesis!

Here is a great review from several years ago that addresses your question well.


First of all, it is corrosive. People which are bulimic often get problems with their teeth getting damaged by the permanent exposure to the acidic stomach fluids. See the paper for more information:

Bulimia and tooth erosion

Then it is a matter of concentration. According to Wikipedia, the concentration of the acid in the stomach is around 0.5% which is a pretty low concentration. Additionally the acid gets diluted when you eat or drink things. And last but not least not all things are very susceptible to a fast degradation by acids. Thing tend also not to disappear suddenly, if they come in contact with acids.


Inbreeding depression can be overcome by the following ways :
1. Out breeding- the breeding of animals which are unrelated to each other and do not have come ancestors for 4-6 generations
2. Out crossing- mating done with the animals osf same breed but after 4-6 generations
3. Cross breeding- superior male mated with superior female of another breed
4. Interspecific hybridisations- male and female  animal  of two different related species


What is the term for awareness of or inclusion of real sounds within a dream?

I think I found a good expression : "sensory incorporation in dreams"

https://www.psychologytoday.com/blog/dream-factory/201409/sensory-incorporation-in-dreams

It doesn't seem reflected in a Google Scholar search however, and I don't find a consistent terminology in the papers that do seem to be about the subject. That article can be a good starting point though.

EDIT: other good one: "influence of external stimuli on dreams".

https://journals.ub.uni-heidelberg.de/index.php/IJoDR/article/view/15754


Can something like McDonalds be considered a life form?

No. First of all, an "organism" is not automatically a "life form". And it is easy to see that McDonald's does not have an information repository in the form of a genome-like structure, where mutations are quantum-acausal, but still have causal consequences on the bearing reproductive units and they trace an evolutionary path all the way down to the ancestor. In your food stores there is no such a thing. Everything is just engineered and organized by us humans. This is "intelligent design" (although fast food is not really an intelligent thing to do) and has nothing to do with evolution in the biological sense.


Are sensory mechanoreceptors and mechanical nociceptors the same type of neurons or are they different?

Short answer
Nociceptors are different from mechanoreceptors.
Background
Mechanoreceptors in the skin have specialized dendritic regions that facilitate their specific role in sensing different types of mechanical force, e.g., pressure receptors (Merkel’s disks) versus vibration receptors (Pacinian corpuscles and Meissner's corpuscles). See Fig. 1 for schematic representations of these types of receptors (Iheanacho et al). By contrast, pain receptors (or nociceptors) do not have specialized dendritic regions and consist of free nerve endings that respond to harmful mechanical forces (Purves et al., 2001).

Fig. 1. Skin receptors. source: Teach Me Phsyiology
References
- Iheanacho et al., Mechanoreceptors. In: StatPearls. Treasure Island (FL): StatPearls Publishing (2020)
- Purves et al., eds. In: Neuroscience 2nd ed. Sunderland (MA): Sinauer Associates; 2001. Nociceptors


What biological specimen is this? Seed? Excrement? Fungal form?

All right, I'll say it if nobody else will.  Insect feces.  The "wood chips" you saw are bits of your oak (or some other over-hanging tree) that have graduated from the arthropod digestive tract, so to speak.  The pellets soak up water because the bugs are on a tight water budget and extract all the water before making a deposit.  Never heard of a gall infestation that produced feces like this, but who knows?  Look for dieing, deformed, or discolored leaves.  Look for bugs on the tree and on fallen leaves.  On the 2nd page of the document linked below is a larger specimen of what you are getting.  http://collier.ifas.ufl.edu/CommHort/CommHortPubs/Stained_sidewalks_under_Oaks.pdf


How many genes does D. melanogaster have?

EDIT

Personal correspondence to representative at FlyBase.org

  In FlyBase we have been gathering information about genes and phenotypes for over 20 years including information from papers and resources older than that.  We annotate gene models on the Drosophila melanogaster genome assembly and when possible associate those annotations with other information (eg. phenotype, function etc) that is known about the gene.  However, in some cases, especially for genes and phenotypes that were described in the older literature before the genome was sequenced we still have some information about those genes but have been unable to associate that information with a genome annotation.   Those are what we call unlocalized genes (i.e. those without a annotation on the genome).


Are SNPs always in linkage disequilibrium with other SNPs

There can be a number of reasons for Linkage Disequilibriunm (LD). Here is a non-exhaustive (non-referenced also) list.

Random LD happens
Epistasis
A recent selective sweep
Hybridization
Population structure
Genetic drift can also create negative LD (see Barton and Otto, 2005)

Of course, in all cases, reduced recombination rate will help to create an LD and to retain it for a longer period of time.


It appears like a pellucid hawkmoth (Cephonodes hylas; also called coffee bee hawkmoth). This belongs to the same family as the hummingbird hawk moths.

  From wikipedia

Many photographers have misidentified this one as the hummingbird hawkmoth (See the picture and the link below. So if you google hummingbird moth india, you'll get pictures of the pellucid hawkmoth too).

  Courtesy: Nitin Prabhudesai


Relatively interesting evolution question --- hypothesis regarding reasons for certain evolutionary traits can be debated (this particular question, scientists seem to have many theories). However, here is one possible explanation:

Pubic hair near the sexual organs is likely for hygiene function; especially for women infections from parasites were common in those areas. The hair would act as a protection barrier, and hence the different texture of that hair being a little thicker.
Pubic hair in arm pit regions may keep pheromones, or chemicals your body produces that send subconscious messages to other humans. Often, these chemicals are released from sweat, and hence it would make sense to have hair in those regions to trap them there. The texture of the hair in those regions probably evolved to be more effective in keeping oder.

https://www.self.com/story/why-you-have-pubic-hair
https://blogs.scientificamerican.com/bering-in-mind/a-bushel-of-facts-about-the-uniqueness-of-human-pubic-hair/


How can the Ames test detect a human carcinogen?

The Ames test aims to find out if a chemical (not yet known to be mutagen) is indeed a mutagen, either directly, or following treatment with liver enzymes (which may metabolise a chemical to mutagenic derivatives during "detoxification"). As you explain, the test involves looking for reversion of various histidine auxotrophic strains of Salmonella.

If the chemical is found to mutagenic in the Ames test then there is a good chance that it will be a carcinogen because of the link between mutagenesis and cancer. In practice further unrelated tests are needed to eliminate false positives.

In this review of the method

  Mortelmans & Zeiger (2000) The Ames Salmonella/microsome mutagenicity assay. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis. 455: 29-60

the authors state that:

  ...there is a high predictivity of a positive mutagenic response in the Ames test for rodent carcinogenicity...ranging from 90% to 77%...


Short answer; It depends. Darkling beetles is a very large family of beetles (Tenebrionidae) where some species can fly and some do not. Looking more narrowly at the genus Tribolium (i.e. mealworms), which many people refer to when they talk about darkling beetles, it also differs. The common Tribolium castaneum (red flour beetle) as well as T. molitor are good fliers, while T. destructor does not fly. The same goes for the confused flour beetle (T. confusum), which is not know to fly from what I know.


Methanol and brain damage -- special affinity for optic nerve or just really toxic?

Methanol toxicity is relatively rare and comparatively little is known about its etiology. I found a correspondence published in the journal Nature in 2004, it seems to a good review of the literature, given that I could not find a recent review on the topic. Please take a look, especially at the sources that the following paragraph cites:

Methanol is particularly toxic to the optic nerve, leading to acute
blindness. Based on a histopathological study, the retrolaminar optic
nerve myelin sheath seems to be selectively vulnerable to methanol
poisoning due to its anatomical structure. In the acute phase, the
hyperaemia and swelling of the optic disc has a papilloedema-like
appearance. The axoplasmic flow stasis at the nerve head and
alteration of the myelin sheath in the retrolaminar nerve segment were
demonstrated in experiments using rhesus monkeys. The pathogenesis is
presumed to be histotoxic anoxia in a vascular watershed area, which
is the result of direct inhibition of cytochrome oxidase by formic
acid. Additionally, the increasing pressure following oedema in the
visual pathway might further aggravate the deterioration due to
ischaemic changes. Therefore, effective methods to treat the oedema
might be important, such as the use of intravenous steroids and
diuretics. The mechanism of subsequent optic atrophy in patients with
methanol poisoning is still unknown, it was suggested to be due to
progressive demyelination. The distinct glaucomatous-like cupping of
the optic disc suggests extensive loss of retina ganglion cells, which
has been thought to result from retrograde degeneration of optic nerve
axons.

It seems that in our best understanding, the optic-specificity of the action of methanol seems to be due to the nature of the myelin sheath that insulates the optic nerve.


How do anticholinesterase pesticides kill nematodes?

Cholinesterase inhibitors and plant-pathogenic nematodes
While it is true that cholinesterase inhibition does not affect gas exchange in nematodes, it does produce other effects by paralysing motor activity:

Inhibition of larval hatching

Reduced movement to new roots

Impairment of root invasion and feeding

Impairment of copulation

Acetylcholine also has a role in sensory neurotransmission in nematodes, which could further contribute to the toxic effects.
Thus cholinesterase inhibitors do not directly kill nematodes, but only slow down their growth and reproduction. This is why some prefer to use the term 'nematostatic' over 'nematicidal' for these compounds.
Effects on vertebrate pathogens
Pyrantel is a cholinesterase inhibitor used to treat intestinal nematode infections in man and other mammals. Little is known about how exactly it works, except that it causes spastic paralysis of the worms. Possibly, it impairs feeding and reproduction (like its counterparts in plant pathogenic nematodes).

References and further reading:

Wright DJ. Nematicides: modes of action and new approaches to chemical control. In Zuckerman BM, Rohde RA, editors. Plant parasitic nematodes. Vol. 3. New York: Academic Press; 1981. p. 421-449. Link to publisher site.
Martin RJ, Robertson AP. Mode of action of levamisole and pyrantel, anthelmintic resistance, E153 and Q57. Parasitology. 2007 Aug 1;134(8):1093–1104. https://doi.org/10.1017/S0031182007000029


Trying to identify a beetle seen in Ontario, Canada...and its babies, or parasites?

Thanks to pascal's answer, I looked at the genus Nicrophorus and agree that this is some member of that genus. (The spelling Necrophorus has been used in the past but is now deprecated.)  The 60+ members of this genus are commonly known as burying beetles or sexton beetles from their behavior of burying dead small animals to serve as nourishment for their offspring.
However, instead of N. vespillo, I think the species might be N. tomentosus:
(Photo: Judy Gallagher via Wikimedia Commons)
The most distinguishing feature seems to be the green or gold hairs on the thorax as seen clearly in the large version of OP's photo. These hairs or setae Wikpedia mentions as separating N. tomentosus from other members of the genus.  A common name for the species is "gold-necked carrion beetle". Two other photos of this species are here and here.


Are there any small peptides with protease activity?

60 residues is the smallest I could find, ref below.

https://jbiomedsci.biomedcentral.com/articles/10.1186/1423-0127-19-54


Why African species are larger in size compared to other parts of world?

When it comes to mammals this cannot really be evaluated without taking the Megafaunal mass extinction into account. This mainly refers to the extinction of large mammals from the Pleistocene Megafauna, which affected different parts of the world differently. More species were extinct in the Americas, Australia and northern Eurasia, and fewer species in Africa and southern Asia. One of the reasons for the differential extinction is thought to be the shorter evolutionary history together with humans in the areas that were more affected (since over-hunting is though to be one of the main explanations, see e.g Sandom er al. 2014).

If you only look at currently extant animals, you ignore the Wooly mammoth, the Woolly rhinoceros, Ground sloths and many other large species inhabiting higher latitudes, and this will give a very biased picture when searching for evolutionary reasons for the differences in body size between continents.


What does characterization mean in a genomics context?

There's no technical definition for "genetic characterization". It is simply a phrase used by authors based on the normal meaning of the words: (1) having to do with genes and heredity, and (2) describing the essential character.  Of course the bounds of the genetics and the essence of their nature are entirely in the eye of the author and reader, so no particular definition applies across all papers in genomics (or in other fields).


Will a dog develop similar feelings with a robot as like human?

Assuming you mean a robot "designed to be human" (that means human-like behavior patterns, human-comparable intelligence, being self-aware and able to learn), then from the dog's perspective, the only significant difference is the differing smell.

There is no scientific evidence for mystical or metaphysical "connections to the world".

From the dog's perspective, the defining factors are:

Owner's behavior (petting, feeding, walking, training, rewards for good behavior or learning tricks). In this case, the robot is no different from the human.

Owner's speech (voiceprint). There's evidence that dogs understand human speech to some extent (https://www.independent.co.uk/news/science/dogs-can-understand-human-speech-scientists-say-a7216481.html). Given how adaptable organic brains are, I assume a dog would be able to adapt to even a synthetic (digitally altered) voiceprint over time or one that spoke in a conspicuously robotic manner (for example: "Temperature alert. Please fetch an external cooling fan./Your assistance above your designated specifications continues to be noted." instead of "It's getting hot in here. Grab a soda from the fridge over there?/Good dog!"

Owner's scent. The only real difference from a dog's perspective. A robot would lack the distinctive scent cues from a human, except if the robot was designed to produce those as well. Even if those aren't present, a dog should be able to adapt to a robotic owner's distinctive smell (plastic with motor oil and a hint of ozone).


What is a catalytic domain of an enzyme?

Both parts overlap. Proteins are a chain of linked amino acids. This chain can be grouped into functional units which are called protein domains. Usually all parts of a domain are closely located in the protein and they form functional domains in the 3D structure of the protein. Proteins usually contain more than one domain (these are manifold but for example can be dimerization, activation or binding domains).

The catalytic domain is the part of the protein chain which contains the region where the catalyzed chemical reaction takes place. The 3D structure of the catalytic domain forms the active site, so the enzyme requires proper folding to be active. If you denature the enzyme, the catalytic domain will still be present (as this is a function of the protein sequence) but the active site will be gone.

As there are really many enzymes for all kinds of reactions it is hard to define a general form for the active site. A motif which is present in a lot of enzymes is the the form of a catalytic pocket or groove to which only the correct substrate of the enzyme has access. Additionally the binding of the substrate to the enzyme often induces a conformational change in the protein which closes this pocket. When the reaction is finished and the substrate is not bound anymore by the enzyme, the conformation changes again and releases the products of the reaction. See the image for a schematically drawing of this principle (image from here):


Why do small organisms make faster movements than big organisms?

It's a general phenomenon that the time scale correlates with the size scale of complex systems.
Energy consumption is the main concern dealing with the speed for biological organizations.
In the absolute sense, a turtle has a higher speed than a small bug. But based on their sizes, the bug seems much quicker and faster. So we need to normalize the speed with the size scale which we can temporarily call 'fastness".

Here is the relationship between the fastness and the mass:

Where u is speed of the organism, M is mass, alpha is a constant which we assume that the metabolic energy is related to the body mass of the organism with a power law.

The final equation says that if alpha > 1.67 then the larger would be faster. But our observation tells us that the smaller the faster. Therefore, we know alpha < 1.67.
In fact Kleiber's law tells us that the alpha is about 0.75.

You can check some numbers related to some animals here


What is meant by 'proteolytic activation' of a virus?

Viruses all have some mechanism to enter cells' lipid membranes, and these need to be prevented from activating prematurely. Often this means the virus is in an inert state while it is assembled and trafficked out of the host cell, then activated by some chemical signal such as the low pH of inner endosomes. So "activation" is usually going to refer to a chemical change that removes the barriers to cell entry.
For example; in flaviviruses such as Zika or Dengue, the E glycoprotein that handles most of the host entry functions is assembled while bound to prM protein. Once virions are assembled with E in an inert arrangement, prM is proteolytically cleaved. When the new host cell absorbs the virion into an endosome and lowers the pH to digest it, the E glycoproteins rearrange into spikes that can penetrate the endosomal membrane and induce fusion with the viral membrane. If prM isn't cleaved, the virus can't infect cells. Here's a recent paper that discusses this process, with high resolution structures. For these viruses there are two rounds of activation, and only the first one is proteolytic.


If inhibiting S6 kinase decreases protein translation, then could inhibiting S6 kinase could possibly slow down long-term potentiation in neurons?

I can't rule it out, but it sounds a lot like trying to tune a piano with sledgehammer.

Neuronal LTP depends on protein translation, but so does absolutely everything else in the cell. Inhibiting protein synthesis at the ribosome will block the formation of all proteins, not just the ones responsible for LTP. Unless there's a link I don't know about between LTP and total levels of protein translation, you're really going to want to look into inhibiting the production of proteins specifically responsible for LTP and not protein synthesis in general.


Phenotypes caused by mutations in mitochondrial DNA?

Assuming that I have understood (and reworded) the question correctly, I find the logic strange. It is the disruption of or change in process that produces phenotypic changes following a mutation in the gene, so if the process is critical for life — like those occurring in the mitochondrion are — what difference does it make where it is encoded?

Perhaps the problem is the endosymbiotic theory of mitochondrial origin. Yes, most of us believe that, but, whatever it was millions of years ago, the mitochondrion is an integral part of modern eukaryotes. Extensive changes have occurred, the most relevant to clearing up this way of thinking is the fact that most human mitochondrial genes are now encoded in the nucleus. Would you these genes would be any more or less likely to produce phenotypes on mutation? Hardly.

Now to the facts. There are certainly mutations in mitochondrial genes that are associated with disease in man and hence produce phenotypes. Some are listed in the table below, taken from a review by Taylor and Turnbull in 2004.

An account of Mitochondrial DNA and Mitochondrial Diseases written for less advanced audiences is this Scitable article.


Typical neuronal firing rates across the human cerebral cortex

Here's a good reference to start you off where you can access an atlas of different properties of neurons.
Cell types from the Allen Brain Institute

Remember that when you say typical firing rates you have to specify what kind of cells you are talking about because interneurons can fire faster for example than pyramidal cells. Also there are differences in basal vs active firing rates.


Answer below is copy-pasted from the section Do we have documented cases of outbreeding depression? of my answer here.

Many cases of inbreeding depression have been documented in humans (McQuillan et al. 2012, Strauss et al. 2013, Lettic et al. 2008, Gellera et al. 1990) but cases of outbreeding depression seem much rarer if any!

I spent some time screening through the literature searching for potential evidence of outbreeding depression. The only paper I found is Udry et al. 2003.

Udry et al. 2003:

First, note that they do not place their results in the context of our present discussion and do not talk about outbreeding depression.
They report that children of "mixed-race" in US colleges report having more behavioural troubles. One would obviously note that there could well be true that "mixed-race" children experience a different environment (incl. social environment) than "non-mixed-race" children. Such results therefore does not suggest the existence of any outbreeding depression.
They also reports more skin problem in mixed-race children. Unfortunately, 1) their p.value is only slightly significant and 2) they track tens of variables without correcting for multiple comparisons and only one came out significant suggesting it is likely to be a false positive.

So, in short: No, there is little to no evidence of outbreeding depression in humans

It is not impossible that there is a publication bias in which researchers looked for inbreeding depression more than for outbreeding depression but I doubt it would be the case. Such bias seems possible only if the outbreeding depression, should it exist, would be very slight and hard to detect outside a rigorous scientific study. In essence, such potential publication are impossible to detect.


What is the most genetically complex organism?

Edit: I would define genetic complexity as either genome size or number of genes. Either answer or information would work.

Largest genome: Paris japonica, a rare plant. Its genome is 149,000,000,000 base pairs large. Approximately 50 times larger than the human genome, by base pair count.

Higher number of genes in an organism: Daphnia pulex, a very common species of water flea. 31,000 protein-coding genes.

As already pointed out, the most genetically complex organism is an unclear question. Complexity can be interpreted in different ways, and I don't think we could agree on a satisfying measure (or definition, for that matter) of genetic complexity.


Do human women smell different before they enter labour?

It is not a definite myth but is a subject of much debate. However, it may well be that it is from smell (olfaction). We certainly know that cats have a significantly larger number of scent receptors, being approximately 200 million, compared to the 5 million receptors humans have. Cats also have an organ called the Jacobson's organ found in many animals that helps to pick up scents even more, especially chemicals - hormones.

As an example, the primary hormone released to progress labour is oxytocin, which causes the body to perform homeostatic positive feedback (initial stimulus is increased until an end result). This begins when the baby's head puts pressure on the cervix, which triggers contractions. This in turn starts oxytocin release which speeds up both the frequency and intensity of the contractions.

This increased concentration of oxytocin could well be what the cat is smelling as animals are well known to detect human hormones such as adrenaline in situations of fear. Although oxytocin is usually present in the body even apart from childbirth, in the moments leading up to labour and just afterwards, the oxytocin concentration is at its highest concentration. The cat probably sensed the 'abnormally' strong smell and began to behave accordingly as it recognised it from instinct (cats release oxytocin in labour too).

It's still all very hypothetical though so I don't know of any authoritative investigations for you to have a look at – it’s one of those anecdotal subjects which has yet to have any concrete evidence.


What does the Gini index mean in a biochemical context?

The paper by Graczyk (2007) is probably relevant for you. It says that the Gini index is a measure of reactive selectivity of kinases, with values close to zero indicating no selectivity and values close to one indicating high selectivity, and it is created in direct parallel to the Gini index in economics, which is used to describe economic inequality. In its basic form, the Gini coefficient is a measure of statistical disperson. Also see Anastassiadis et al. (2011) for a more recent example where the index is used.

  Abstract
  A novel application of the Gini coefficient for expressing selectivity of kinase inhibitors against a panel of kinases is proposed. This has been illustrated using single-point inhibition data for 40 commercially available kinase inhibitors screened against 85 kinases. Nonselective inhibitors are characterized by Gini values close to zero (Staurosporine, Gini 0.150). Highly selective compounds exhibit Gini values close to 1 (PD184352 Gini 0.905). The relative selectivity of inhibitors does not depend on the ATP concentration.

References:

Graczyk. 2007. Gini coefficient: a new way to express selectivity of kinase inhibitors against a family of kinases. J Med Chem. 50(23)

Anastassiadis et al. 2011. Comprehensive assay of kinase catalytic activity reveals features of kinase inhibitor selectivity. Nature Biotechnology 29: 1039–1045


Is sugar absorbed into the bloodstream through the walls of the mouth?

Simple sugars such as glucose, fructose and galactose will be absorbed.

They are most probably transported by a common carrier, which is why if you present both glucose and galactose, the presence of one will inhibit the absorption rate of the other.
Uptake rate also seems to partly depend on the concentration of sodium ions in the buccal cavity. This was identified and explored subsequently.
It seems that at the cellular level, absorption is not the quickest but there is a lot of vascularization which allows it to enter the bloodstream quickly, regardless.

Here's a back-of-the-envelope calculation: about 10mg is absorbed in 5 minutes when you hold a solution of 3.6g/l in your mouth. A normal gulp volume is around 10ml. That's 36mg of sugar in a mouthful. Result: you can absorb 10mg of sugar from a theoretical maximum of 36mg. In other words, within 5 minutes, you absorb ~30% of all available sugar. That's pretty good, given that a sugar solution is not a more concentrated, solid sugary food!

Worthy to note that most complex sugars will not be absorbed. Note that many complex sugars actually won't be uptaken even in rest of the GI tract, like cellulose.

See other posts already here on the topic.


How do dopamine agonists like amphetamine/methylphenidate affect acetylcholine signalling?

Amphetamine and methylphenidate are not (direct) dopamine agonists.

Dopamine agonists are the substances that would specifically bind to dopamine receptors and activate them, thereby mimicking the effects of dopamine release.

Amphetamine/methylphenidate are so-called indirect sympatomimetics. This means that they stimulate the simpatyc nervous systems (with neurotransmitters noradrenaline and dopamine in CNS), but in indirect way: they don't bind to the receptors. Rather, they promote the massive neurotransmitter release from the presynaptic part. The released transmitter (DA, NA) then just diffuses to the postsynaptic membrane and binds to its own receptors.

There are some works done on investigating the effect of these substances on parasympatic system with acetylcholine as neurotransmitter.

Sympatomimetics like amphetamine generally lead to increase of acetylcholine release throurout the nervous system: in hippocampus and caudate nucleus, nucleus accumbens and generally in forebrain and cortex.

This effect of amphetamine is indeed in many cases mediated through dopamine receptors. Same time some direct dopamine receptor agonists were found to supress ACh release in some brain regions.


In developed countries we usually consume enough salt (sodium to be exact) without actually adding table salt to food. Everything can become toxic when consumed in excess - even water - and when we frequently add more salt to foods, we tend to consume sodium in potentially harmful excess. That's what your friends are referring to.

However, salt (sodium) is one of the most essential substances your body needs to stay alive, for several reasons. One of the main purposes of sodium is the upkeep of blood's osmolarity (i.e. concentrations of osmotically active compounds. Higher salt concentration on one side of a permeable membrane attracts water to that side - I'm sure you've heard that before). There are numerous systems in your body to make sure the osmolarity of blood is correct. If they fail and blood becomes hypo or hypertonic, your cells will be sucked dry or pumped full of water and in either case, burst and die.

Look up the renin-angiotensin-aldosterone system for example: when the kidney filters blood, it reabsorbs or lets through water depending on the current blood osmolarity; leading to higher or lower amount of higher or lower concentrated urine. You drink lots, your blood is diluted, it becomes less tonic, kidney registers that and lets water through more, you urinate more. There are many more elements involved there, including blood pressure, nerve signals stimulating thirst or hunger of different kinds, some hormones etc.

As you can see, there's a reason why the basic infusion given in hospitals to replace lost blood quickly isn't just water but normal saline.

Delayed update to pick up some side aspects of your description: 1) There are of course things that humans do which have absolutely no value to them whatsoever. Anything that plays into the feel-good-reward-circuit in our brain can become such an unhelpful habit. Take smoking and drug consumption as examples. 2) About evolutionary relevance: Being a key player in maintaining body function, evolution selected for instictively liking salt. Simultaneously, most people will not like food that is extremely salty - a protective mechanism against excess.


Does the human abdominal cavity use pressure to maintain posture?

I found this review which can help to clarify this notion of intra-abdominal pressure : Intensive Care Med. 2009 Jun;35(6):969-76.
What is normal intra-abdominal pressure and how is it affected by positioning, body mass and positive end-expiratory pressure?
De Keulenaer BL1, De Waele JJ, Powell B, Malbrain ML.
The authors mention that there is indeed a positive pressure in the normal subject. This IAP is contributed by gravity, uniform compression (abdominal contraction, diaphragmatic contraction, mechanical ventilation, rib cage excursions) and shear deformation, this last one depending on the intrinsic stabilty of the tissue.
The authors conclude that "the abdomen behaves as a hydraulic system with normal IAP of about 5–7 mmHg..". Kind of a can of soda, without the bubbles...
Pathologies affecting this pressure are named "abdominal compartment syndrome) and result from multiple etiologies (obesity, trauma...,).


Yes; there are byproducts of metabolism and maintaining the body that must be excreted, which has nothing to do with taking in unneeded nutrients. For just a few examples, urea is produced normally as part of the constant building and break down of proteins, but must be excreted, the brown color of feces comes from the breakdown of red blood cells, and a substantial weight of the feces is gut bacteria, some of which are necessary for proper digestion of some of the nutrients you take in.


Can oncogenesis happen without apoptosis pathway being affected?

Usually the cell death mechanisms are overridden and therefore oncogenesis. The pathway components themselves are not mutated. One classical case I can cite is that of Ras-oncogene. See this article for details. Usually the survival/growth signals (MAP-kinase) are activated with simultaneous inactivation of apoptotic regulators (Akt-pathway). A mutation of MAP-kinase component ERK can also cause cancer but apoptosis is nonetheless supressed because of the interconnections of these tow pathways in the gene regulatory network.

Whereas in the case of tumor suppressors, the cause of cancer is genomic instability and failure to initiate apoptosis.


Do other animals suffer from myopia or hypermetropia?

do they have such eye defects?

Yes, eye defect is not specific to humans of course. Cases of eye defect are very common in animals. It is most often witnessed in domestic animals and they are the ones we observe the most (see The physiology of domestic animals)

Eye defects have typically been observed in tree shrews, monkeys (incl. macaques), cats, dogs, horses, rats, elephant and a Cape buffalo.

You should have a look at the wikipedia article Myopia in animals

  howw do they overcome it?

They don't wear glasses obviously!

Humans uses the sense of vision a lot. Many animals uses smell (and taste), hearing or touch much more than humans do. For such non-visual animal, having a slight eye defect is not too big of a deal.

  Do they feel selection pressure against them in such cases?

That is a bit of an awkward question. Nobody can feel a selection pressure on themselves. A selection pressure is a fitness differential associated with genotypes. A selection pressure is therefore defined at the population level. There is no such thing as a fitness pressure against a single individual.

Let me rephrase this last question to something that makes more sense. I am not sure I will address the specific question that was of interest to you though.

  Are non-humans animals that have an eye defect aware that they have an eye defect?

It is unlikely that any animal would have the cognitive abilities to notice that they see more poorly than another animal of the same species. Doing so, would at least require having the ToM and only few species do.


Welcome to Biology.SE.

About your post

It is a very standard question and a common source of misunderstanding from the general public. If you just google do we descend from monkeys you will get tons of hits that will answer your question.

Because this question is introductory and has already received a lot of answers online, there is therefore no point for me to make a long and extensive answer here. I will just state the essentials and let you investigate it further through the multiple online sources that exists.

Note by the way, that if you want to get some introductory knowledge in evolutionary biology, you might want to have a look at a few course on Understanding Evolution by UC Berkley

The actual answer

In short, It makes no sense to say of any species that it descends from any other extant species. Two extant species share a common ancestor though. The Most Recent Common Ancestor (MRCA) is of particular interest. Following this logic, humans do NOT descend from modern days chimpanzee, but humans and chimpanzee have a common ancestor. Their MRCA was another ape, but not an ape that exists today (even though it may look like one).


Why can't we call dog breeds different species?

I don't enjoy the idea of comparing people to dogs, but this is a bit akin (please note the bit) to asking if people who are genetically short (or "little people", both proportionate and disproportionate dwarfism), pygmies, short people, normal sized people, tall people, very tall people, and people with acromegaly (gigantism) can be called different species. I compare because it's fairly clear to most individuals that we are all the same species: homo sapiens. About breeding, it is very likely that a reproductive specialist would be quite concerned (I certainly would be) about a woman with drarfism carrying the child of a very tall person (who had very tall parents), but not the opposite pairing.

Below is a photograph of the wedding of Tom Thumb and Lavinia Warren. That union produced no children. Her bridesmaid Minnie, (her sister), who was only 27 inches tall, also married a little person (Edward Newell). She became pregnant with a normal-sized child, but died during the birthing of a 6 pound baby (her baby died as well).

Are they a different species? No. A paleontologist (a good one) would be able to tell that the bones of a little person was actually of the same species based on certain conformations, just as I believe paleontologists today could distinguish prehistoric small cats from very large cats. Size matters, but not nearly as much as the type and distribution of teeth, the shape of the jaw, etc.  In other words, I strongly disagree with the following:

  If somehow the recognized [dog] breeds existed only as fossils, paleontologists would consider them not one species but many—certainly more than the thirty-six species of wild dogs that live in nature today.

That statement is based on a fairly profound error in thinking: a cognitive bias that is mistrustful of science in general due to a lack of familiarity with the rigors involved in the scientific methods of paleontologists in particular. I say this without rancor or animus of any kind; where I settled down (in the deeply religious region), the vast majority of my children's friends' parents are creationists, and the vast majority of our friends are fundamentalists. We argue about science all the time; I know the basic arguments. I'm familiar with their websites. I personally find myself in the camp of Christian thinkers like geneticist Francis Collins, M.D., Ph.D., the director of the Human Genome Project, who understand genetics and find no threat to their faith in evolution or science. (E.g. Creationists reject all science which indicates the age of the Earth is >~6000 years.)

The truth is that the definition of a species is not that easy, even for prokariotes. Difficult as well is a pure definition of life.

Finally, about size. The domestic dog exhibits greater diversity in body size than any other terrestrial vertebrate. This is due to a small number of (or perhaps even a single) alleles: the IGF1 Allele. It's hard to argue difference of species on the basis of a small number of alleles: we allow much more variability for other alleles without wanting to classify as different species: eye color, hair color, hair length, straight vs. curly coat, degree of tail curl, ear morphology, etc.

A Single IGF1 Allele Is a Major Determinant of Small Size in Dogs
Lessons learned from the dog genome
A species definition for the modern synthesis
Single-Nucleotide-Polymorphism-Based Association Mapping of Dog Stereotypes
Canine Genetics Facilitates Understanding of Human Biology
How many species of prokaryotes are there? (PNAS)
Ernst Mayr and the modern concept of species (PNAS)
Hybridization, ecological races and the nature of species: empirical evidence for the ease of speciation
Is it Useful to Have a Clear-cut Definition of Life? On the Use of Fuzzy Logic in Prebiotic Chemistry


Which X-Y chromosomes have the developmental genes for mammals?

First, while half the chromosomes come from each of the two parents, these two sets of chromosomes are not termed X and Y (they would usually be called maternal and paternal).  The terms X and Y refer to potential members of just one pair of the 23 pairs (in humans) of chromosomes, and X chromosomes can come from either the mother or the father.  The presence or absence of a Y chromosome determines sex in mammals.

The Y chromosome contains one gene, SRY, which determines sex, and almost no nother genes.  SRY simply switches on the "make a male" program in the cells.

Essentially all other genes, including any toolbox genes, come from both parents, one copy from each.  (An exception, in males, are those genes on the X chromosome, which in males are present in only one copy and which came from the mother.  Another exception is mitochondrial genes.)


What part of the cactus photosynthesizes?

In wiki there is a good answer for your question http://en.wikipedia.org/wiki/Cactus#Leaves

In plants photosynthesis takes place in chloroplasts. Chloroplasts may be in the cells of fruits, stems, but most of all in leaves. In some succulents (such as cacti), the main photosynthetic activity is associated with a stem.


Do plasma B cells express the BCR or only produce soluble antibodies?

B cells can secrete antibody before they are terminally differentiated into plasma cells, so there is a phase during which both membrane-bound and secretory antibodies can be produced by the same cell:

  When a naïve or memory B cell is activated by antigen (with the aid of a helper T cell), it proliferates and differentiates into an antibody-secreting effector cell. Such cells make and secrete large amounts of soluble (rather than membrane-bound) antibody, which has the same unique antigen-binding site as the cell-surface antibody that served earlier as the antigen receptor (Figure 24-17). Effector B cells can begin secreting antibody while they are still small lymphocytes, but the end stage of their maturation pathway is a large plasma cell

--Molecular Biology of the Cell. 4th edition.

Plasma cells, generally speaking, have little or no surface immunoglobulin, but it's been claimed that some subsets of plasma cells do have surface Ig:

  Surprisingly, although IgG PCs downregulated surface IgG expression, IgA and IgM PCs expressed their respective isotype both intracellularly and on the plasma membrane (Figure 1A, lower panel). Importantly, concordant Ig’s were also detected on the plasma membrane of IgA and IgM, but not IgG, PCs isolated from BM or colon LP indicating that this property is a characteristic of PCs present in their physiological niches

--A functional BCR in human IgA and IgM plasma cells


What is the essential benefit of center-surround organization of retinal ganglion cells?

You are assuming that light comes in perfectly in spots, and that the purpose of vision is to replicate a "bitmap" of the incoming light. This would actually be very inefficient computationally.

In reality, vision relies on detecting salient features. Imagine a simple scene, maybe like this one:

Most of the white space of the wall is pretty uninteresting: you have no need to really process that information besides knowing it's one solid area. What is interesting in the image, if you are trying to understand the space your are occupying, is to see the edge between the floor and the wall. In fact, that's what really tells you this is a wall and a floor: if you only had the upper 1/4 of the image, you would just have a white box: you wouldn't know if this is a floor, a wall, a ceiling, the paint on someones car. The edge between the floor and wall gives you the needed context.

Lets think about how center-surround organization would respond to this image. In the whole blank white space, white light is hitting both the center and the surround: these cancel and there is little response. However, imagine what happens for an on-center off-surround cell right at the edge with the floor. That cell is getting white at its on-center, but only on about half of it's off-surround: the other half of the off-surround instead gets the darker wood floor. This cell would therefore respond to the imbalance in the average surround vs average center!

You can then combine many of this circular receptive fields to detect straight edges, like this:

From https://grey.colorado.edu/CompCogNeuro/index.php/CCNBook/Perception

Note: the LGN (thalamus) receptive fields are very similar to the retinal ganglion cell receptive fields. In V1, primary visual cortex, these receptive fields are added together to make "simple cells" which respond to edges.

I think this picture comes closest to answering your question about how overlapping receptive fields can be useful.

This image from the Wikipedia page on receptive fields shows what you get when you put a scene through a center-surround filter: note how all the edges are emphasized!

Other benefits: this type of detector works well over a range of light levels, for example different steps of gray will appear the same, even though the pixel intensity varies a lot. This way, you get similar responses to edges in both a dark and light room. These detectors also help to sharpen images. Note that computer vision uses some of these same strategies as well!

What if you wanted to detect spots of dark instead of spots of light? We often think of eyes as being "light detectors" but they are just as appropriately described as "dark detectors." Imagine you are a rodent looking up at the sky, for example: an important, salient stimulus for you might be a dark spot where a hawk is blocking light from the sky. Therefore, having an off-center, on-surround type of cell is just as useful as the opposite (and indeed, the retina contains both types of retinal ganglion cells).


Skin (epithelial) stem cells: unipotent or multipotent?

In this article on sciencedirect.com epithelial skin cells are described as the products of epithelial multipotent stem cells and/or unipotent "progenitor" cells (which I presume is a way of describing a stem cell that only produces one type of cell - in this case an epithelialor skin cell). The epithelial multipotent stem cells can produce a variety of cells.

Most epithelial tissues self-renew throughout adult life due to the
presence of multipotent stem cells and/or unipotent progenitor cells [emphases mine].
Epithelial Stem Cells and Their Lineages Epithelial stem cells can generate tissues that display a fascinating array of cellular
architectures, each of which are specifically tailored for distinct
functions. In this review, we will focus on four well-characterized
epithelial stem cells whose tissues possess diverse architectural
designs and physiology: intestine, epidermis, mammary gland, and
cornea.

So it seems the answer to my question is: both.


Clustal Omega - convert from distance into # of substitutions

It uses a gonet matrix to compare each of these two sequences. Since you you could have insertions and extensions as well as substitutions, it becomes a 3 parameter problem. 1*open + 6*penalty + substitution_penalty = X. X can be solved by a linear combination of substitution_penalties, extensions, and insertions. So I think this will be really really hard

with that being said. Clustal outputs the multiple sequence alignment. Why don't you just look at sequence 1 and sequence 2 and see what the insertions and substitutions are!


What is meant by [protein name]+/- (ie "Myod+" and "Myod-")

The Stem Cell Reports paper linked in the question is open-access, so anyone can download it freely. Unfortunately the Nature paper is not.
There are two different abbreviation conventions being used in the open paper – MyoD+/MyoD- and MyoD+/MyoD-. The italicized version indicates the genotype of the cell, tissue, or individual being referenced, so for example MyoD- indicates the MyoD knockout they made. This convention is very widely used to refer to genes or mRNA.
Examples where the gene name is not italicized refer to the protein product of that particular gene and its presence or absence. So, MyoD+ cells express the wild-type protein, while MyoD- cells do not. This convention is also very widely used to refer to the presence or absence of the indicated protein.


How does blue white screening work in selecting E coli that have taken up a plasmid vector?

The traditional blue/white screening is set up so that blue colonies are considered negative for the insert, and white colonies are positive for recombinant DNA. The gene responsible is the lacZ gene, or beta-galactosidase. This enzyme converts a synthetic substrate, X-gal, into an insoluble blue compound.

The pCR2.1 TOPO plasmid is a blue/white selection plasmid in which white colonies are considered positive for the insert. The way this works is by inserting the DNA sequence to clone inside the coding region for lacZ. By having any inserted DNA interrupting the sequences of lacZ, so that the enzyme has lost its function (because it is no longer being translated correctly in the bacteria). On the other hand, no insert present means that lacZ is ligated back together, and the entire enzyme is correctly made, and therefore can metabolize the X-gal substrate to form an insoluble blue dye.


Why don't cells double gene expression after S-Phase?

When the double strand is duplicated, the old strand (or, in other terms, the template) is methylated : this modification is enough to prevent the bind by the RNApol system and, by so, the transcription.
By methylation, DNA-repair systems are able to detect which is the newer strand, to discover and fix replication errors.

Here you can find additional infos