Do we use 100% of our cerebral capacity?

The idea that we only use 10% of our brain capacity is a myth.  There is a great article at wired.com that discusses the myth and it's history.

There is really no reason to evolve an entire brain of which only 10% is used.  One great point that they make is that minor brain damage can cause devastating effects, not what you would expect if you had 90% spare capacity waiting around.

The entire brain is rarely firing all at once, and it is hard to average how much is being used because it changes with activity.


Colorful Large Wasp (?) on Milkweed Arizona USA

Possibly a tarantula hawk (because of its red wings and metallic blue body), and because they inhabit the Southwest US. It being on the flower in the picture makes sense as “...adult tarantula hawks are nectavores and feed on flowers”. They have very painful stings, but as with most insects, if nobody bothers them, they won’t bother you.
The females hunt down and paralyze tarantulas and lay their eggs in them, hence the name. Freaky, isn’t it?

Reference


why does the score matrix influence the E value (BLAST)

Perhaps this BLAST tutorial by Steve Altschul will be helpful:  The Statistics of Sequence Similarity Scores

There is also the BLAST book by Mark Yandell and Ian Korf.


DNA modifications other than 5-mC/5-hmC/5-fC/5-caC in vertebrate genomes?

There can be other modifications resulting from DNA damage (oxidising agents etc). Those may include Xanthine and Hypoxanthine (caused by chemical deamination of guanine and adenine).
There are no other known modifications resulting because of a physiological process.


Do the BLAST scores have any relation between them?

Yes there is a relationship between them but you may not be able to observe correlation between some of them.

Number of matches and score are definitely proportional, however higher similarity would translate to higher score only if the lengths of the scoring pairs are the same. Gap would have a negative effect on the score but it totally depends on what your scores/penalties are (see BLAST help and documentation).

E-value is basically the likelihood of two random sequences having a certain match score from a given database. So whether or not it is low for a hit depends on the score distribution of the database. Lower E-value does not mean higher similarity. It means that a hit of this score has a low likelihood to be found by random chance. The score distribution is generally skewed towards low scores and so high scores usually have low E-value but what a "high" score is totally dependent on your queries and therefore this statement cannot be generalized.

From BLAST docs:

  $$E=K.m.n.e^{-\lambda.S}$$

  This formula makes eminently intuitive sense. Doubling the length of
  either sequence should double the number of HSPs attaining a given
  score. Also, for an HSP to attain the score 2x it must attain the
  score x twice in a row, so one expects E to decrease exponentially
  with score. The parameters K and lambda can be thought of simply as
  natural scales for the search space size and the scoring system
  respectively.


Species Identification: Red velvety insect, India

As you might have noticed from its appearance, this is a red velvet mite. This is an arachnid (related to spiders) and not an insect.

The red velvet mite apparently does not bite or sting (according to this website), and it is also used for medicinal purposes in India, according to this Wikipedia image, so it is unlikely to be dangerous.

If you haven't seen it already, the webcomic The Oatmeal has an amusing take on some of the arthropod's mating habits.


Who/where has the advocado genome been sequenced?

You can search for genome sequences at the National Center for Biotechnology Information (NCBI) site.

Here is a link to Persea americana (avocado) from NCBI. It states on the page the submitter for the genome was Hainan University.


These species likely don't see you as a predator, or if they do they don't know if you've seen them yet.

A study indicated that the vision of the White-tailed deer was good;

  As expected for a crepuscularly active prey species, the visual system of white-tailed deer is specialized for sensitivity in low-light conditions and detection of predators.

The observation that many prey species only notice movement may relate to behavioural adaptations that increase their chances against natural predator species. Staying still while monitoring your surrounds decreases the chance of the predator seeing you.
I'll quote D'Angelo et al again;

  The visual streak of deer in combination with
  their wide-set eyes likely provides them with enhanced ability
  to monitor the horizon and to detect movement with a
  wide field of view while keeping their head stationary.

Visual specialization of an herbivore prey species, the white-tailed deer.
G. J. D’Angelo, A. Glasser, M. Wendt, G. A. Williams, D. A. Osborn, G. R. Gallagher, R. J. Warren, K. V. Miller, M. T. Pardue
Canadian Journal of Zoology, 2008, 86:735-743, 10.1139/Z08-050


I think that's more of a matter of linguistics rather than any scientific/physiological reason. For instance, in Portuguese, you wouldn't call legs to a cat or a dog's limbs. You would say they have 4 "patas" (roughly translated as "paws"). And calling them legs, in Portuguese at least, would be weird.

When veterinary doctors refer to animal limbs, they usually use anterior and posterior limbs. In fact, anatomically speaking, anterior limbs in cats and dogs (and probably in other animals too) have more in common with human arms (upper limbs) that with their own posterior limbs.

Also, as rg255 commented, maybe the reason behind the colloquial nomenclature is quite simple...

To (miss)quote Nancy Sinatra:

  These "legs" are made for walking

  And that's just what they'll do


What factors are known to affect evolution?

Evolution is defined as a change in the allele frequency of population through time.  The Hardy-Weinberg model predicts that the allele frequency of a population will not change (i.e., evolution will not occur) if the following conditions are met:

no natural or sexual selection
no gene flow (immigration or emigration from the population)
no mutatation
no genetic drift (changes in allele frequency due to random events)

So we can conclude that if any of the above conditions are not met then there is a change in allele frequency and thus evolution, and thus that factor is the cause of evolution.


It's a (possibly subadult) female Black Widow. Subadult females often have some level of red or red and white markings on the upper surface of the abdomen, and females of some species retain those markings even into adulthood - the notorious Redback (Latrodectus hasselti) being an examnple of that. Black and red is a very common "Danger!" signal in nature, so you should be a little leery when you see it.  This one looks like Latrodectus mirabilis, which Garb, Gonzalez and Gillespie have marked in the area of Bolivia. I know almost nothing of this Widow, but since most Black Widows are pretty similar in their habits and venoms, I feel pretty confident in saying that you probably do not want to get bitten by this spider. It would be extremely painful, and would probably give you a couple of very bad days until the effects eased up. Widows don't usually tend to bite unless physically injured, but you probably want to shake out your boots in the morning before putting them on..

Here's the link to the Garb paper:

Garb, J.E., González, A. and Gillespie, R.G., 2004. The black widow spider genus Latrodectus (Araneae: Theridiidae): phylogeny, biogeography, and invasion history. Molecular phylogenetics and evolution, 31(3), pp.1127-1142.

And here's a nice Spanish language blog
that features this photo of L. mirabilis:


What is the minimal focal length of the human eye?

Short answer
The focal length of the average, healthy, adult human eye at near-point is about 18.5 mm. Young individuals can accommodate their lenses further to a focal length of around 15.4 mm.

Background
The focal length of the human eye is the distance between the lens and the retina when an object is in focus (Fig. 1). Therefore, the ...even when considering blurred images too part in the question doesn't make much sense. So, I will focus my answer on sharp images only (pun intended).

The lenses of the eye are thicker in the center than at the edges, and hence positive and converging lenses. They form an inverted image on the photosensitive layer in the back of the eye - the retina (Fig. 1) The retinal image is shaped by two lenses: 1) the cornea with a fixed focal length and 2) the eye-lens, which is a lens with variable focal length through shape changes (Fig. 1) called accommodation and is mediated by the ciliary muscles (Kolb, 2012).

When the ciliary muscles are relaxed, the focal length of the eye-lens is maximal and the distant objects are in focus (infinity). When the ciliary muscles contract they shorten the focal length of the eye-lens to bring nearer objects into focus. The two limits of this range are called the far-point, (ciliary muscles relaxed), and the near-point (maximal accommodation) (source: University of Colorado, Boulder).

The distance between the eye-lens and the retina is about 20 mm. When an object is far away from the eye (infinity), the image is located essentially at the focal point. Therefore the focal length of the cornea and the eye-lens should be about 20 mm when the muscles of the eye are relaxed. The lens strength is the reciprocal of its focal length in meters. Hence, the strength of the cornea and the eye-lens at the far-point is about 1/0.020 = 50 diopters (source: University of Colorado, Boulder)..

When an object is located at the near-point (the closest point at which an object can be brought into clear focus on the retina), the focal length of the cornea and the eye-lens must be changed so that the image is formed on the retina, which is still 20 mm away. The typical near-point in an adult is 25 cm, corresponding to a focal length of the cornea and the eye-lens of 18.52 mm using the standard ray-tracing rules of lenses. Hence the strength of the cornea and the eye-lens must now be about 1/0.01852 = 54 diopters. In other words, the muscles of the eye can provide an accommodation range of 4 diopters (source: University of Colorado, Boulder).

Kids can, however focus to points as close as 6.5 cm away, i.e., 15 diopters worth of optical power, i.e., a minimal focal length of 15.39 mm.

Fig. 1. Human eye. Upper panel: non-accomodated relaxed eye. Lower panel: accomodated eye. source: Khan Academy

Reference
- Kolb, Gross Anatomy of the Eye. In: Webvision. The Organization of the Retina and Visual System, Moran Eye Center (2012)


How often do retrotransposons jump in human cells?

For just rough order-of-magnitude, try this reference. Their experimental design seems to maximize transpositions so it should be a reasonable upper bound.

There is a lot of variability, but some retrotransposons jumped in ~1000 cells per million, others only a few per million such that they were difficult to detect, after about 1 month in HeLa cells.

The same reference gives an estimate of 10,000 retrotransposon elements in a mammalian genome, though, again, their transposition frequencies vary considerably.


You are mixing different things here: Virus are grouped based on their genetic material (dsDNA, ssDNA ssRNA and so on) into several groups (see here for details), then grouped into families, subgrouped into a genus and then into species.

So it is: Group > Family > Genus > Species.

What you have here are are different positions in this classification.
The names you mention belong all to the same tree:

Group: IV ((+)ssRNA-Viruses) > Family (Caliciviridae) > Genus (Norovirus) > Species (Norwalk Virus).

The Astrovirus belongs into the same group, but then form an own family.
To answer your question: No, since the Norovirus forms its own genus in the caliciviridae family.


Effects of tobacco smoke on plant health

Results from the peppermint plants study show that all the peppermint plants contain minor amounts of nicotine before treatment, but the experiments revealed that the plants also incorporate nicotine considerably from the soil as well as from tobacco smoke. These findings demonstrate for the first time that the reported occurrence of nicotine indeed may originate from tobacco. The incorporated nicotine was subsequently metabolized by the plants.

Effects:
Apart from the nutritional aspects, the results on nicotine uptake may also affect basic plant biology, because they demonstrate that alkaloids can be transferred from one plant, after its death, to another plant species.

  The plants, said Dirk Selmar, the study’s lead author, appeared, at
  first, to be unchanged. “As far as we have seen, there have been no
  negative effects on the growth,” he wrote in an email. Yet, tests for
  nicotine, conducted at various stages in the plants’ life, found that
  they had “tremendously elevated nicotine levels,” Selmar said.

References:

https://link.springer.com/content/pdf/10.1007%2Fs13593-015-0298-x.pdf
http://www.takepart.com/article/2015/04/15/nicotine-plants-second-hand-smoke
https://www.ehow.com/info_7987584_effect-cigarette-smoke-house-plants.html

some anecdotal answers (to be taken with a grain of salt) on your 2nd bonus question: https://www.rollitup.org/t/is-smoking-weed-around-a-growing-plant-bad.182179/


As @WYSIWYG suggested, this is probably more suitable for Math-SE.

From you question, it is unclear exactly what shape you are looking for, and there are many functions that could describe the behaviour you're after, i.e. a continuous, smooth decrease towards an asymptote. However, two possible options could be the negative exponential and a negative gompertz function. Possible forms of these could be:

Negative exponential

$y(x)=e^{−ax+ln(1-b)}+b,$

where $b=0.2$ and a is a rate parameter.

Negative Gompertz

$y(x) = 1-\alpha e^{-\beta e^{-\gamma x}},$

where $\alpha=0.8$ (describing the asymptote), $\beta$ in an inflection parameter (given a displacement along the x-axis), and $\gamma$ is a rate parameter.

These functions can give results such as:

In these examples, $a = 0.005$ for the negative exponential and $\beta = 150$, $\gamma = 0.008$ for the gompertz v1 and $\beta = 5$, $\gamma = 0.005$ for the gompertz v2.

An alternative parametrization of the Gompertz, which might be easier to understand, is:

$y(x) = 1-\alpha e^{-e^{-\gamma (x-\beta)}},$

where the inflection point ($\beta$) is directly related to the scale of the x-axis (so $\beta = 400$ would give an inflection at x = 400).

Are these examples interesting for your application? Hopefully they can provide a starting point for you.


Wikipedia actually means that being male is a risk factor for sleep apnea, which is a jargony way of saying that males have been observed to develop sleep apnea more often than females.

The article pointed out by com.prehensible suggests that this difference in the prevalence of sleep apnea between genders is due (in part) to a difference pharyngeal airway length (illustrated below), which is longer in men than in women even when corrected for (body) height.

Since the pharyngeal airway lacks any bones or cartilages for structural support, the theory goes that a longer pharyngeal airway is more likely to collapse during sleep, when breathing is reduced via mild to moderate hypoventilation (in everyone). Here's an illustration (3rd one in the set below) what that collapse looks like (source):

Another theory of this structural kind is that the pharyngeal cross-sectional area is smaller in women relative to men, but studies measuring this cross-section didn't all come to the same conclusion.

Finally, an experimentally observed difference between males and females during sleep is the so called "hypocapnic apneic threshold", which means that relative to men, women require a more substantial reduction in PETCO2 (a measurement of carbon dioxide partial pressure during expiration) before they show signs of apnea. A more prosaic way of saying this is that men's bodies are more prone to go into a state where a reduction CO2 in the expiration causes the brain to decide to stop breathing for a bit because it seems it has enough oxygen (based on the lack of CO2). This mechanism is substantially inhibited during wakefulness and least inhibited during NREM sleep (and in REM sleep it's somewhere in between).

Why there's a difference in this threshold between men and women is not known precisely, but another experiment established that giving testosterone to women increased their breathing instability during sleep. And conversely, blocking some of the effects of testosterone by administration of finasteride increased breathing stability in healthy men during sleep. Note that this is a pretty new (2013) study. Neither finasteride nor any other medication is currently FDA-approved for treating sleep apnea.

And one more thing to point out is that there are different types of sleep apnea, so the two mechanisms discussed above are not necessarily contradictory or competing; the first one (airway length and its collapse) is mostly relevant to obstructive sleep apnea, while the second one is more often discussed in the context of the so-called central sleep apnea.


Here's a good summary of knobs, which says that they are "typically telomeric," "tandemly repeated DNA sequences [that] appear as distinct, heteropycnotic regions located at certain sites on specific chromosomes and look much like beads on a string" and are involved in:

increased recombination
neocentromere activity
preferential segregation
chromosome breakage and chromatin loss
sex differences in recombination

The introduction to this paper gives some of the same information.


Are the subordinate genes of a repressed operon really "turned off"?

There are several mechanisms by which the expression of a gene can be completely turned off. Certain network architectures can ensure foolproof repression (for e.g. by using multiple repressors parallely or additional epigenetic silencing mechanisms). Bistable switches can also ensure robustness of expression in a way that small fluctuations in the transcription factor levels do not lead to expression of the gene. Sometimes the activator molecules need to co-operatively activate the expression. In such conditions the activation graph is sigmoidal with respect to activator concentration. All these mechanisms can prevent leaky expression.

Some genes do have a basal expression but it is not necessary for all cases. However, basal expression is absolutely necessary for proper functioning of the lac operon (see this post).

Having said this, there is always some non-zero probability of expression of a gene when it is actually turned off. This probability may be very low but it would not be zero. This small accidental expression may or may not have any significant downstream effects.


You are thinking about something like "compost tea".
http://www.homecompostingmadeeasy.com/composttea.html

The problem is that a random piece of forest soil may or may not be rich in nutrients.  If that soil has water soluble nutrients in it, wouldn't the rain have already rinsed them out?

If you make tea out of compost, there has been no chance for rain to rinse out nutrients because the decomposed stuff has been in your compost bin.

Last piece: if you are making tea out of forest soil or compost, when you are done you will have a soaked clump of wet soil or compost.  What are you going to do with it?  Probably throw it on the ground somewhere.  It might make more sense and be much less messy to skip the tea step, put the forest soil or compost on the ground next to your plants, and then water them.


Can birds touch their wing tips together either in front or behind (not above and below)?

Black herons (Egretta ardesiaca) can overlap their wing tips in front of them while doing what is known as canopy feeding.


Can any one reaction in a cell be at equilibrium?

I think there are a few principles that we need to consider before answering your question.

(a) When a reaction is at equilibrium, the rate of any elementary reaction is exactly balanced by that of the reverse process.  This is an important one.

The above principle follows from transition-state theory, which holds that the activated state for the reaction in one direction is that same for that in the reverse direction.  It also follows from the principle of microscopic reversibility at equilibrium or, more correctly, the principle of detailed balance at equilibrium, which states that “in a system at equilibrium each collision has its exact counterpart in the reverse direction, and that the rate of every chemical process is exactly balanced by that of the reverse process” (my emphasis) [Laidler, 1987, p 130]. It is important to realise that these two points of view are equivalent.  To again quote Laidler (p130), if one is working within the framework of TST “the principle of microscopic reversibility presents nothing new”.

To put it bluntly: a system where any elementary reaction, either explicitly or implicitly, is not exactly balanced by the reverse process is not at equilibrium. By this criteria, the actin example alluded to above cannot, even loosely, be considered at equilibrium.

This principle has many important consequences, even when a system is not at equilibrium.  One is that the the product of the ratios of rate constants around a cycle (closed loop) equal the equilibrium constant for the cycle (see Cornish-Bowden, 2004, p 104). [see Addendum for an example of where this consequence was not adhered to].

(b) When a species is in a steady-state, the rate of formation equals the rate of breakdown. The steady-state concentration may differ markedly from the equilibrium concentration.

(c) As @WYSIWYG has pointed out, an enzyme (catalyst) does not change the equilibrium constant for the uncatalyzed reaction.

(d) When we are dealing with equilibria, we are usually interested in Gibbs free energy changes.  For example (Silbey & Alberty, 2001, p 277).

ΔGo' = -RT ln K’

(In the above equation K’ is the apparent equilibrium constant, that is the equilibrium constant at specified pH, and ΔGo' is the standard transformed Gibbs free energy of a biochemical reaction.  More on this distinction, if you are interested, in the Silbey and Alberty reference quoted above).

The important point is that there is a relatively simple relationship between Gibbs free energy and the equilibrium constant. The Gibbs free energy, of course, gives a measure of the spontaneity of a reaction and also its capacity to do work.

When the transformed Gibbs free energy is of a reaction (ΔG') is zero, the reaction (at specified pH) is at equilibrium and cannot perform useful work, and reactions with negative ΔG' may be considered ‘spontaneous’.  It is also important to realize that equilibrium is a dynamic state: chemical bonds are continuously being broken and energy is continuously being redistributed (with no loss of energy). [I am dealing here with the transformed free energy, ΔG', that is the free energy change at specified pH, rather than ΔG (the pH independent value), as this is the most useful when considering a biochemical reaction.  However, similar conclusions apply to ΔG].

Having got those out of the way, I can now attempt to answer your question (slightly rephrased). Can a reaction in a metabolic pathway be at equilibrium?

To be extremely pedantic, if there is a flux through the pathway (net conversion of first substrate to end product) then the answer is no (Newsholme & Start, 1973, p 11). That is, if there is a flux through the pathway, ΔG' cannot be exactly zero for any individual reaction.   However, reactions in a metabolic pathway may be very close to equilibrium (Newsholme & Start, 1973, chapter 1).

Let’s (once again) rephrase your question.  Are there any examples of reactions in metabolic pathways that are close to equilibrium, and how can we determine this?

To again quote Newsholme & Start (1973, p11)  “In a series of reactions that constitute a metabolic pathway, a few may be displaced far from equilibrium, whereas the majority of reactions may be close to equilibrium”.

So how can this be determined? One way would be to measure the ratio of products to substrates (or the ratio of product to substrate pairs) in the cell, and compare this with the equilibrium constant.  Note that it is only the ratio of substrate/product pairs we are interested in, not the absolute concentrations. We might be interested in the NAD+/NADH ratio in the cell, for example.

That is, we measure the mass action ratio and compare this with the equilibrium constant.

Such measurements are fraught with difficulties, but let’s agree that they can be made. We could rapidly freeze the tissue sample to -190°C (using liquid nitrogen), for example, and then measure the ratio of metabolites.  Finally, it should be pointed out that comparison of mass-action ratio with the equilibrium constant is not the only way of deducing that a reaction is near equilibrium, and agreement between alternative methods is highly desirable before any firm conclusions are drawn.

Let’s consider glycolysis as an example.  It is generally agreed that the reactions catalyzed by phosphoglucoisomerase, phosphoglycerate mutase and enolase are all close to equilibrium: the mass action ratios and the equilibrium constants are about the same (see Newsholme & Start, 1973, p 98).

It is also generally agreed that the reactions catalyzed by phosphofructokinase and pyruvate kinase are far from equilibrium (see Newsholme & Start, 1973, p 98).

What is the rationale? In general, it is control reactions catalyzed by regulatory enzymes that are displaced from equilibrium. (A key property of a regulatory enzyme is that the activity is controlled by factors other than substrate concentration).

The enzyme phosphofructokinase is a good example.  This enzyme plays a key role in the regulation of glycolysis. Measurement of the mass-action ratio for this enzyme gives a value of 0.029, where the equilibrium constant for the reaction is about 1000 (see Newsholme & Start, 1973, p31). It is clear that physiologically this enzyme catalyzes a reaction that is far from equilibrium.

In conclusion, many reactions in metabolic pathways may be close to equilibrium, but regulatory enzymes almost always catalyze reactions that are displaced from equilibrium.

Finally, if anyone wishes to provide more recent references or to otherwise improve the answer, feel free to edit.

Addendum

For a well-known controversy in the enzyme kinetics field where the requirement that product of the ratios of rate constants around a closed loop equal the equilibrium constant for the cycle was not adhered to, see Selwyn (1993) and Topham & Brocklehurst (1992).  These authors were critizing the work of Varon et al (1992), who made a bit of a hash of things. If you are interested in this area, you may wish to read up on this controversy, which is very informative. (Selwyn’s paper is a great start). [All the above papers are freely available in PubMed Central].

References

Cornish-Bowden, A. (2004) Fundamentals of Enzyme Kinetics. 3rd Edn. Portland Press.

Laidler, K. J. (1987) Chemical Kinetics 3rd Edn. Harper & Row.

Newsholme, E.A. & Start, C (1973) Regulation in Metabolism. John Wiley & Sons.

Silbey, R. J. & Alberty, R.A (2001) Physical Chemistry. 3rd Edn. John Wiley.

Eric Arthur Newsholme (1935–2011) Obituary


Do people with congenital analgesia feel cold?

Interesting question. Here what I think (I am not an expert in congenital analgesia so take it with a grain of salt).

The pain provoked by an high temperature is mainly transmitted via the receptor TRPV1 (a Ca2+-channel nocireceptor) while cold sensation is driven by TRPM8 and possibly, for noxious cold, via TRPA1 (two similar types of Ca2+-channels). Those receptors are known as the temperature sensors. As an anecdote, TRPV1 is what give you a pungency sensation when eating spices while TRPM8/TRPA1 give you the cooling sensation from mint.

Mechanical pain is transmitted via other receptors, including TRP channels, but this is not fully understood at the molecular level.

As far as I know, the encoding of pain, and more generally physiological sensations, in the brain are also not yet fully understood but it is very likely that the pathways taken by TRPV1 differs from the one taken by TRPM8/A1 which would suggest that it is possible that CIPA individuals experience high-temperature pain and cold differently at the molecular level and therefore might respond, to some degree, to one but not the other. This also probably applies to mechanical pain vs temperature-driven pain.

I would actually not be too surprised if CIVA people shiver even if not feeling any temperature sensations. Would be interesting to have the opinion or even better the observations of experts in this field.

P.S. I know this is not a definitive answer but I have not enough reputation to comment.


How does it make thermodynamic sense for photosynthesizers to turn CO₂ into O₂?

Oxygen in photosynthesis does not come from carbon dioxide. It comes from water and this is the step that actually requires light: Photolysis of water.
The proton produced in this process is used to synthesize ATP and NADPH by a chemiosmotic process similar to what happens in mitochondria.
These biochemical pathways are also referred to as Light reactions.

Carbon fixation (or Calvin-Benson Cycle) requires energy (in the from of NADPH) and is therefore dependent on light reactions. The light has no direct role in carbon fixation. Oxygen production also, is not directly coupled to carbon dioxide consumption.


How does geography affect morphological features of the human body

Geography does not typically affect the morphology of the human body.
In certain special cases, there are physiological adaptations, the most obvious being tanning and acclimatization to high altitude, but these aren't changes in body morphology.
So why the difference in children of immigrants?  This is because diet, nutrition, and disease have quite strong effects on children's growth. Kids growing up in a healthier environment with more food get bigger, and those are linked to the wealth of the community where you live.


Why do farts stink, but perfume does not?

Why is it that natural things like farts, poop, halitosis etc., from
  which we are always surrounded smell "bad"; whereas manufactured
  products, such as perfume or glue smell "good" to most of us?

  In my understanding, things smell "bad", because they are not good for
  us. But how are farts not good? And shouldn't artificial things like
  perfume or glue, which are relatively new to us, smell "bad"?

Kind of a strange question but here is a quick and rough answer... There are at least three things to think of here.

Firstly, yes often natural things that are good for you have evolved to smell attractive, but not all natural things are good for you. Therefore a fart should not smell good just because it is natural. And it is likely that breathing farts non stop is not good for you.

Secondly, perfumes etc. have been chemically manipulated or designed to smell nice by human manufacturers - the preference for such smells existed before the specific perfume, the manufacturer simply designed a fragrance that was attractive.

And Finally... Not everything exists because of selection. Farts probably smell as a by-product of process of digestion rather than selection for avoiding them. Gas is produced during the digestion processes, the amount and odor (determined by the constituents of the gas) of gas will likely depend the efficiency of digestion and what is being digested. The dominant selection force affecting the odor is then probably related to digestive efficacy and selection against odor would only be (relatively) very weak.

It's better to digest food and fart a bit than it is to not digest but smell nice, digestion is quite important!


What are the lifetimes of cellular components on organelle or molecular level?

Your question has several parts to it so I will attempt to address them one-by-one.

In terms of protein stability and turnover, this is a nice paper describing how human cell (HeLa) line, although this is a cancerous cell line, is used to measure the turnover of proteins (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3316722/?report=classic). They have used labelled amino acid technique and mass spectrometry (SILAC) to make measurements of protein turnover. It is concluded that on average the turnover is 20 hours, which is correct in my experience when doing gene knockdowns in Drosophila (S2) cells using RNAis as we incubate the RNAi with cells for 72 hours to ensure most proteins that we targeting are degraded and we can see the desired effects in cells.

Now getting to your questions regarding organelle turnover, you have to consider that cellular organells are very precious to the cells as most of them consume a lot of energy to build hence they are maintained unless they suffer critical damage, and they would become detrimental to the cellular integrity. In that case organells such as mitochondria undergo a specific type of degradation called mitophagy, which is a subtype of autophagy. Now I'm sure there are specific average times for the so called turn-over of cellular organelle under "normal" conditions but thats a slightly misleading view since the turnover can be tipped through reactive oxygen species (ROS) or ageing leading to less efficient cellular maintenance and buildup of toxic aggregated proteins or ROS.

Now just to clarify the use of the word half-life in you last paragraph, half-life normally refers to the time it takes for half the molecules in a given system to degrade (or to be more correct Half-life is the amount of time required for a quantity to fall to half its value as measured at the beginning of the time period) so I do not agree with your use of the word half-life in the last paragraph of above question although human DNA does have a replication limit (Hayflick limit) of roughly 40-60 due to telomer shortening and afterwards the cells (due to the DNA) that no longer replicates will enter senescence and eventually die.

Now getting to non-replicating, highly differentiated cells such as neurons, it still remains a mystery as to how neuronal DNA remains so highly stable (although DNA is a highly stable molecule (compared to RNA) and its further stabilised through histones), while undergoing many dynamic processes such as transcription (since if anything goes wrong the cells cannot be replaced at least in CNS) and how axons of some neurone that can reach over a meter in length are maintained so well for decades. There is a lively argument amongst the scientific community about this, which you can find out about if you simply search for axonal maintenance in a search engine.

Hope this answers some of your questions.


How many different chains exist within a specific pdb file?

In the PDB format the lines with atoms can start either with ATOM or HETATM.

Chain ID is in column 22, i.e. it is 22nd character of a line that starts with ATOM or HETATM. (Programs that support 2-character chain IDs use columns 21-22 − it's a popular extension of the PDB format).

Yes, the number of different chain IDs is the same as the number of "chains" in the PDB file.
But note that the "chain" from the PDB format is not necessarily a real chain (polymer). It may be a bunch of water molecules or something else.


Why are H+ ions pumped out instead of in during cellular respiration

Mitochondria pumps out the H+ perhaps just because there is no disadvantage of it. Once they've evolved such a machinery with complex network; they weren't threatened to evolve any opposite-system.

Any opposite system too; would not plausibly disadvantageous; and really happens in case of chloroplast; another sort of cell-organelle.

1: image from Plant Biochemistry, by Hans Walter Heldt, 3rd Edition.

2:  picture including all chloroplast membranes.

But if any organelle used cytosol as the H+ pool; probably that would made cytosol acidic as wel disrupt metabolic processes on cytosol. (usually the cytosol have very mildly alkaline pH.)

  Reference: Plant Biochemistry by Hans Walter Heldt, 3rd Edition, Academic Press.


Looks like shaggy ink cap, Coprinus comatus, to me.

Blacksmith37's answer suggests that shaggy mane is the usual common name. I hadn't heard that name until I looked at the Wikipedia page. In the U.K. it is shaggy ink cap, inkytop, inkhorn or lawyer's wig.

Update

This is a good general source of information. Also comatus (Latin) means hairy.


Can multiple cetacean species communicate?

Do dogs and humans communicate? What about cats and dogs? I think defining "communicate" is the real question here.

This 2012 study claims to show "the first experimental evidence that the interception of heterospecific vocalizations can mediate interactions between different cetacean species in previously unrecognized ways". In other word, one species is recognizing and responding to the vocalizations of another.

This article points out that "...false killer whales and bottlenose dolphins choose to spend time with specific members of the other species rather than randomly mixing or engaging in brief opportunistic encounters" How could this occur without some form of "communication"? I'd argue it couldn't,


How to find a PDB structure of a protease with a peptide like inhibitor

Here's one: http://www.rcsb.org/pdb/explore/explore.do?structureId=2IPH. It was crystallized with the inhibitor bound to the protein.


Difference between aerosol and droplet transmission for airborne diseases

An Aerosol is a suspension of droplets or particles in air. A "suspension" means that the droplets or particles are suspended in the air and do not just fall down with gravity. Very tiny droplets can be suspended in this way by the Brownian motion of the air molecules: The air molecules move around randomly (their speed indicates the air's temperature) and hit these tiny droplets back and forth and prevent them from falling down as they would normally do because of gravity. But larger droplets are too big, the air's Brownian motion is not powerful enough to keep them suspended against gravity, so larger do fall down and do not create an aerosol.

So, if the coughed-up droplets are big, they will quickly fall down - and as a result the disease will be hard to transmit (the healthy person needs to stand close enough to the infected person to inhale the droplets before they fall down). However, if the droplets are smaller than some size, they form - as I described above - an aerosol. Such an aerosol can be suspended in the air for a long time, which can mean that a person who walks into a room where a person previously sneezed will get infected. It can also mean that the aerosol can float around the room, and infect a person standing pretty far away from the source.


Why can't plasma proteins migrate from capillaries?

Cells of the endothelium are joined by tight cell junctions which are impermeable or selectively permeable. Generally, proteins can only migrate through the endothelium via active transcytosis.
Leukocytes (specifically neutrophils, lymphocytes and monocytes) express various adhesion molecules and cytokine receptors which allow them to interact with endothelial cells and facilitate their movement (diapedesis) either between (paracellular) or through (transcellular) the cells. The process of leukocytes leaving the endothelial lumen is known as extravasation.

Carman CV. 2009. Mechanisms for transcellular diapedesis: probing and pathfinding by `invadosome-like protrusions'. J Cell Sci 122:3025-3035.
(C,D) The process of diapedesis, whether during intravasation or extravasation, can occur by two distinct pathways: paracellular or transcellular. (C) Paracellular diapedesis. Leukocytes and endothelial cells coordinately disassemble endothelial cell-cell junctions and open up a gap between two or more endothelial cells (Muller, 2003). (D) Transcellular diapedesis. Leukocytes migrate directly through individual endothelial cells via a transient transcellular pore that leaves endothelial cell-cell junctions intact. Note that the two individual endothelial cells in C and D are distinguished by different shades of pink.


Can protein precipitate out in alcohol during DNA extraction?

Yes, Ethanol can precipitate proteins during a DNA precipitation as well, although Acetone will be more efficient. Usually you do a proteinase K digest or a proteinase K digest followed by a Phenol/Chloroform extraction to avoid this problem. I was usually doing the later, I can post my protocol if you are interested.


How are the first mammary glands thought to have functioned?

the production of liquids to nourish offspring has evolved separately in several lineages, mammals have simply taken it further than any other group. it is pretty easy to see how it could evolve, any way of providing even trace nutrients or nourishment to young will have an advantage in organisms that are already engaged in child rearing. it means exposing the young to predators less often.

Mammary glands are modified sweat glands.

Monotremes do not have nipples what they have is a cluster of mammary glands on a patch of skin. the young have to suck the milk of the a cluster of hair.

The exact sequence of how lactation evolved is not well known since lactation leaves no fossil evidence.

Sources:

Lefèvre, C.M., Sharp, J.A. and Nicholas, K.R., 2010. Evolution of lactation: ancient origin and extreme adaptations of the lactation system. Annual review of genomics and human genetics, 11, pp.219-238.

Capuco, A.V. and Akers, R.M., 2009. The origin and evolution of lactation. Journal of Biology, 8(4), p.37.


A natural process is something quite vague: this is a natural process, but it's not related to the elephant's ageing. Neither is it (normally) related to fighting.

Those notches and tears are caused by the daily activities of elephants, feeding in the bushes. The longer the ear, the more prone it is to damage. On the other hand, thicker ears are less prone to damage.

Day by day, the number and pattern of tears/notches/holes changes.

Curiously, this pattern of tears/notches/holes is used by researchers to identify individuals. Not only that, but also the pattern of the veins in the ears (you can see them in the left ear):

Thus, the same way the tail of a humpback whale or a human fingerprint is unique to each individual, so are the elephants' ears.

Sources:

http://voices.nationalgeographic.com/2013/08/16/name-that-elephant-how-to-identify-elephants-in-the-wild/
https://www.elephantvoices.org/support-now/814-how-to-use-ear-notches-and-tears-to-id-african-elephants-.html


What happens when the brain is no longer capable of co-ordinating or regulating the heart and breathing rates?

Damage to the brainstem - the part of the brain responsible for controlling breathing and the heart - has different effects on the heart and the lungs.

Every heartbeat is not directed by the brain. Instead, the brain has a "throttle" to the heart, by which it can regulate the heart rate up and down, but the actual heartbeat is initiated by special cells in the heart, called pacemaker cells. In the absence of signals from the brainstem, the heart will continue pumping; this is (one of the reasons) why people who need ventilators to breath for them do not also need their heart pumped for them.

Breathing, however, is directly controlled by the brain. Without signals from the brain, breathing will stop completely (the technical term is "respiratory arrest", but that literally just means "breathing-stuff stopped-ness"). Survival time without breathing depends on a number of factors, but at room temperature, without medical intervention (ie. rescue breaths or a ventilator) and barring any special circumstances, is only a few minutes. Permanent brain damage sets in a few minutes later, even if the person can be resuscitated.

Of course, without any breathing, the heart will stop beating due to a lack of oxygen before long. The general progression will be from sinus ("normal") rhythm, to ventricular tachycardia, to ventricular fibrillation, to asystole ("flatlining").


Are mesophyll cells the same as parenchyma cells?

Despite countless sites and other resources saying otherwise, Mesophyll is not a tissue technically speaking. It's just a place, a specific area. Or you can even think of it as the set of all tissues in a given area.

And that given area is easy to define: the "filling" of the leaf, between the upper and lower epidermis. According to Mauseth (2012), that with Raven is my favourite book on Botany:

  Mesophyll: All tissues of a leaf except the epidermis.

Actually, this is easy to see if you understand the Greek origin of the term: μέσος, meaning "in the middle", and φύλλον, meaning "leaf". Therefore, mesophyll means "in the middle of the leaf".

In a common, regular leaf, most of the mesophyll is made of parenchyma, be it palisade or spongy. As I said before several sources treat these terms (mesophyll and parenchyma) as synonyms, but they are not.

Just for completeness, this is a very simple list of the plant tissues. You'll see that mesophyll is not on it:

Meristems
Dermal tissues

Epidermis
Peridermis

Ground tissues

Parenchyma
Collenchyma
Schlerenchyma

Vascular tissues

Xylem
Phloem

Source: Mauseth, J. (2012). Botany. Sudbury: Jones & Bartlett Learning.


Is it possible for a prey to become its main predator's predator?

Also it should be noted as you move from prey to predator, there is less energy to be had. This is why we often do not have a predator of a predator species. There simply isn't enough food at that level of a predator to support another predator above it.

That said, I am assuming you are thinking of an alien ecosystem. In which case you might be able to sustain such a system if there is a massive flux of bio-matter through the ecosystem. Ie plant food is extremely abundant and animals within it reproduce at an extremely fast pace. We can see such an environment at the bottom of a marine ecosystem in the polar regions during summer (near constant sunshine, and an up welling of minerals from the deep sea.

  If that's not possible, is it at least possible for X to evolve
  adaptations for fighting/killing Y (Not for food)?

Happens all the time. While lions do hunt cape buffalo, cape buffalo can and do kill unwary lions.


Does crude oil or kerogen contain ancient DNA?

According to Live Science, the temperatures are in the 120 to 300 degree-Fahrenheit range (48-148 degree-Celcius) when crude oil is forming. DNA in "dry" conditions completely degrades at temperatures above 190 degree-Celcius. Which means that there could be DNA in the oil itself if there are some surviving cells, however, outside the cells there are DNases which will chew up DNA.

So the DNA they are talking about is like the DNA studied by Gong et. al, where they're looking at the live bacteria in the crude oil, which would be descendants of the bacteria that was around when the oil first began its degradation from organic material.

On both NCBI and PLOS ONE there appear to be a number of papers studying the bacterial growth in crude oil. Which would be why you may have seen articles about DNA in the oil.


What happens to potassium after an action potential?

During the repolarization, relatively few ions need to cross the membrane for the membrane voltage to change and therefore the change in ions concentration outside and inside the cell is neglible. After repolarization, the concentrations are restored by the continuous action of Na⁺/K⁺-ATPase. The same happens for calcium, but I don't know exactly what kind of pump is used.


Does the 1:1 sex ratio at birth apply to every human pregnancy or is it a statistical average?

The ratio you are referring to is indeed computed aggregating multiple observations and thus it is a "statistical average".

Any individual (or couple, in this case) can have a specific ratio that differs from the average one. Many factors may affect sex ratio, among which sperm/egg viability, chromosomal aberrations, and hormones misbalance are the ones usually affecting the fertility of a couple and they can also bias the sex ratio.

Many other factors can play a role.
Different populations have slightly different sex-ratio and even smoking can skew the sex ratio!


Are there any proteins in the body whose surface is hydrophobic?

Sure. Although you are right in thinking that most proteins have hydrophilic surfaces, some are very hydrophobic. My favorite example is Elastin, it is the main component of the skin which grants it elasticity. In fact, the hydrophobic nature of elastin is what confers it its function. The idea, briefly said, is that a insoluble/hydrophobic structure will tend to minimize it's surface area with water, so if you stretch such a substance (i.e. increase the surface area), it will pull back to the minimum surface area state.

Reference: Li, Daggett. Molecular basis for the extensibility of elastin. Journal of Muscle Research & Cell Motility (2002).


How to find suitable qRTPCR reference gene for a inflammatory response experiment?

You don't say how you're measuring but I'll guess that you're using quantitative PCR. A typical approach to handling housekeeping gene normalization in qPCR experiments is described in

Accurate normalization of real-time quantitative RT-PCR data by geometric averaging of multiple internal control genes.

  We outline a robust and innovative strategy to identify the most stably expressed control genes in a given set of tissues, and to determine the minimum number of genes required to calculate a reliable normalization factor. We have evaluated ten housekeeping genes from different abundance and functional classes in various human tissues, and demonstrated that the conventional use of a single gene for normalization leads to relatively large errors in a significant proportion of samples tested. The geometric mean of multiple carefully selected housekeeping genes was validated as an accurate normalization factor by analyzing publicly available microarray data.

There is an R package called NormqPCR that implements this approach (publication here).

Briefly, the approach required measuring multiple housekeeping genes and iteratively removing the ones that are most variable, ending up with two genes that are jointly least variable, and making a sort of pseudo-housekeeping gene from them with which to normalize your other genes.

This doesn't magically turn bad data into good data, but it helps clean up some intrinsic problems with housekeeping genes.


How to determine if two mutations in a gene are on the same or different alleles?

Yes, it can be determined by sequencing but the sequencing read has to be long enough to span both the mutations. PacBio sequencing allows long reads but it also has higher error rate than the short read sequencing platforms like Illumina. If you know the gene locus then you can amplify the region using PCR and use Sanger sequencing too (for this the amplicon has to be cloned in a plasmid, transformed into bacteria and then single colonies must be sequenced; see Why does one combine PCR and cloning as ways for amplification of sequences?).

Another possibility is to look at the RNAs from this gene. If the two alleles have different expression then comparing the number of reads for each mutation might tell if they occur together. However, as I said it already depends on the two conditions: expression and dissimilar expression.


Where does female ejaculate actually originate from?

According to this article female ejaculate is produced by the Skene glands.


What is the difference between the Modern Synthesis and the Extended Synthesis?

The term Extended Synthesis has been invented very recently and the concept was defended in these two papers

Laland et al. 2014
Laland et al. 2015

I read each paper when it came out and haven't reread them since. Here is a short summary of what I remember.

Those who want to use term Extended Synthesis

In short, they are arguing new findings have extended our understanding of evolutionary biology so much so that we should rename our theory of evolution. The main findings they are talking about concern the field of evo-devo (merging Evolutionary biology and Developmental biology). The subjects that they consider having radically advanced our understanding of evolutionary biology include niche construction and inheritance of niche, developmental bias, plasticity, cultural evolution and epigenetics.

Those who do not want to use term Extended Synthesis

We have discussed both papers in groups in my department and in short, we pretty much all ended up saying that:

It is true that our understanding of evolutionary processes have advanced a lot since the time of Wright, Fisher, Muller, Kimura, and others. However...

There is no important enough rethinking that deserves a renaming of our Theory of Evolution
Most arguments are based on rephrasing of old concept without bringing anything new. This is especially obvious when reading the 2015 paper.
Do we really care about this debate anyway? It is just a name!

Reading

I recommend reading the 2014 paper as 1) offer both point of views and 2) is pretty short.

Note

I do not know your level of knowledge in evolutionary biology but it might be a pretty bad idea to start with complicated subjects such as evo-devo, niche construction, epigenetics, developmental bias, etc...


Do common terms for animals such as amphibian or reptile fall somewhere in taxonomy levels?

This is all a matter of how we define terms, and which definitions are scientifically useful.

Traditionally (since Linnaean times), organisms were classified based on their outward similarities (phenetic systematics). As such, the traditional definition of reptile, which is the same as any common usage that I've heard, includes organisms like snakes, lizards, turtles and crocodiles but does not include birds. This is the class Reptilia. As evolutionary understanding increased, however, it was found that some reptiles, like crocodiles, are actually more closely related to birds than to other reptiles. This makes the common use of reptile a paraphyletic classification.

In modern phylogenetic systematics, organisms are classified in monophyletic groups, or clades, that include an ancestor and all of its decedents (ie it is based on evolutionary relationships). Thus the class Reptilia, since it is paraphyletic, is essentially meaningless in this system. In order to have consistent nomenclature, you could either say that birds are reptiles (a new, cladistic meaning of the term, but which contradicts traditional/common usage) or come up with a new name that includes all traditional reptiles and birds. Taxonomists taking the latter approach use the term Sauropsida for this clade. Sauropsida does not have a taxonomic rank like class because such ranks are useless in cladistics (and actually quite arbitrary even in the traditional system).

So, to specifically address your question:

In phenetics, both Reptilia and Amphibia have the taxonomic rank of class.

In phylogenetics, what we commonly consider reptiles and birds are grouped in a single clade that can be called Sauropsida or Reptilia (re-defined to include the clade Aves) depending on who you ask or which paper you read. Amphibia form a clade.

Perhaps the most important take-away message is that taxonomy is largely un-standardized.


what would be the scientific name of this variety of dove

It's a rock pigeons (Columba livia).

The Color coding of Pigeon

There are three genes responsible for pigmentation in pigeons.

  – Tyrp1 gene produces a protein that helps make the pigment eumelanin.
  Pigeons with blue-black feathers have normal Tyrp1. Ash-red and brown
  birds pigeons contain different mutations in the Tyrp1 gene, which
  leads to less or different pigmentation.

  – Mutations that affect the Sox10 gene override colors determined by
  various versions of the Tyrp1 gene. Regardless of whether the Tyrp1
  version makes pigeons blue-black, ash-red or brown, mutations that
  regulate the Sox10 gene result in red pigeons.

  – Mutation of the Slc45a2 gene decreases the intensity of colors
  determined by Tyrp1, Sox10 and their mutants. Depending on the version
  of the Tyrp1 gene – blue-black, ash-red, and brown − pigeons harboring
  the mutant Slc45a2 gene still display the same colors, but in
  watered-down or diluted versions, less intense than those with normal
  Slc45a2. For example, a pigeon with both the ash-red version of Tyrp1
  and the mutant Slc45a2 gene has ash-yellow feathers. Pigeons with
  Sox10 and Slc45a2 mutations are yellow, which is the dilute form of
  red.

Source: http://unews.utah.edu/news_releases/birds-of-a-different-color/

Source: University of Utah


After looking it up, I can, with some confidence, confirm that this is a book louse in the larval stage, as seen in this picture:
https://bpca.org.uk/write/MediaUploads/Pages/A-Z/Booklice/booklice-1.jpg
I hope this answers your question!


Do Schwann cells have Na+/K+ ATPase pump?

Yes. Although utilizing the action potential is not in their function, Schwann cells do have Na/K ATPases. In fact all animal cells do. It contributes to the resting membrane potential in neural networks, with regards to Schwann cells, and prevent differences in osmotic pressure from disrupting the cells.

As for your second question, action potentials do not occur in Schwann cells as there is nowhere for this "impulse" to travel to. A localized depolarization is not an action potential. Papers such as this, and this suggest that voltage-gated ion channels in Schwann cells serve complex and specific purposes such as inducing myelin formation.


How high into the air are spores of molds commonly occurring?

Air currents can carry bacteria and mold spores into stratospheric altitudes.  Early balloon collections found bacteria and mold in air samples at a little above 71 thousand feet altitude.  There were only a few colonies, but we also know that our bacterial media often do not allow many microorganisms to grow.

More recent studies of the atmospheric microbiome have indicated that a wide variety of bacteria and fungi can routinely be found in the atmosphere thousands of feet up.  Modern measurements find about 10 million living microbes per cubic meter.

Sandstorms or jet streams are known to be able to move living bacteria long distances.  Spores are often of about the same size and I see no reason why we will not find that they do the same.


How to select genes before log2 ratio on a RNASeq gene expression matrix, based on signal median

There is no rule for fixing t and p. It depends on the level of stringency you expect. Value of t depends on what is considered to be an active concentration; this need not be same for all genes.

This is an RNAseq data; I don't understand what is the "median" signal you are talking about. For each sample a gene would have a normalized expression value which is typically RPKM (Reads Per Kilobase per Million mapped reads). If you have replicates for each sample then take the mean not the median.

Regarding calculation of log-ratios: Always be careful with this especially in case of zeros. Instead of log ratios you may use some sort of a gain metric:

if
ratio = x/y
then
gain = (x-y)/y

You can also do a principal component analysis on the data and select first n principal components.


Im struggling to see how these are presynaptic terminals/knobs and not post synaptic

The fibers in green are axons and axon terminals from other neurons, not the one colored orange.

Yes, there would be post-synaptic structures associated with these but those are not drawn in this cartoon.


Under what conditions do laboratories have the need to perform both, colony counting and cell counting?

Any lab that would like to make the distinction between live and dead cells in a cheap way would use both techniques. You count colonies on petri dishes to get the number of living cells, and count in counting chambers under the microscope to get the total number of cells.

There are easier ways to do this though, for example using this: https://www.thermofisher.com/de/de/home/brands/molecular-probes/key-molecular-probes-products/live-dead-viability-brand-page.html in a flow cytometer. That's not that cheap though.


I can see why you might be confused! The authors chose bad notation, since the way they wrote it $w_i$ clearly depends not just on the choice of anenomefish species $i$ but also on the choice of anenome species $j$. And it is not clear how exactly they are performing their sum in the definition of SSR: sum over all possible anenome-anenomefish species pairs or only over all anenomefish species? The former makes sense but is extremely unclear, and the latter doesn't make sense because there's no way to interpret that as a probability that an anenomefish will choose a particular anenome because the sum of the SSR for all the different anenome species would not necessarily be 1, so the probability of an anenomefish species choosing some species of anenome would not be 1!

NOTE: The reference to Manly 1993 was incorrect (you cited a 1995 paper); they actually cite a book: Manly B, McDonald L, Thomas D (1993) Resource selection by animals. Statistical design and analysis for field studies. Chapman and Hall, London. This would probably be the best place to look to get an exact answer to your question. I think that would be the best place to look first.


What is the mechanism of action of lithium-induced polyuria?

Lithium changes the effect of at least three substances that play a role in diuresis:

aldosterone:  lithium partially inhibits its ability to increase the expression of ENaC receptors on apical membrane thus increasing sodium losses [1].
arginine vasopressin (AVP): because lithium can induce hyperparathyroidism, parathyroid hormone can act as partial agonist to AVP, inhibiting its hydroosmotic action [2].
antidiuretic hormone (ADH): lithium blocks its stimulatory effect on adenilate cyclase. The result is a decrease of cAMP levels in the cells from collecting tubules. cAMP promotes formation of water channels, thus improving absorption from collecting tubules. Because lithium decreases cAMP levels, diuresis is stimulated [1].

All these result in polyuria.

Lithium levels can be determined from the blood. Usually the test should be performed 12 hours after last dose of Lithium [3].

References:

Eleanor Lederer, MD; Lithium Nephropathy on http://emedicine.medscape.com/article/242772-overview#a0104
Carney SL, Ray C, Gillies AH. Mechanism of lithium-induced polyuria in the rat. Kidney Int. 1996 Aug;50(2):377-83.
http://labtestsonline.org/understanding/analytes/lithium/tab/sample/


How can a two genera share a latin name?

No, not an error. Plants, Animals and Bacteria each have their own independent nomenclatural codes. So while it is not advised, it is not forbidden by the code to have the same genera. It would be forbidden to have the same genus within one of the three codes. As a side issue, don't forget that the species ALWAYS includes the genus. Species are always binomens. The species epithet is the second word in the species binomen. Thus our species is Homo sapiens, not sapiens.


In practice, subspecies are often fairly loosely-defined, reflecting a degree of uncertainty and ambiguity at this level of taxonomy. There are systematists who take the view that subspecies-level classifications should not be used as they are not rigidly definable.

In general, a subspecies will fulfil the following criteria:

it will occupy a distinct geographic range from other subspecies
within its species,
it will have limited gene flow to other subspecies within its species, while still being capable of interbreeding
it will have some recognizable shared character, used to distinguish it from other subspecies within its species

Subspecies classifications, and their usefulness, are discussed in the Turtle Taxonomy Working Group's 'Turtle Taxonomy: Methodology, Recommendations, and Guidelines', for those interested in further reading.


Why boys who inherit more genes of their mother are not born as girls and girls who inherit more genes of their father not born as boys?

Most genes are not male or female, so receiving more genes from a father or mother would not make a child more male or female. Whether a mammalian embryo grows to be male or female is pretty much determined by a single gene that's found on the Y chromosome. Called the "Testis-determining factor" (TDF), it triggers the development of male characteristics. TDF is a regulatory gene, and its effect is to switch on other genes, which result in the development of testis. All embryos would become female without the intervention of this gene.

The gene TDF is found on the Y chromosome. Male mammals have one Y chromosome and one X chromosome, females have two X. So there's a 50% chance a fertilised egg will inherent an X, and a 50% chance it will inherit a Y chromosome from it's father, which determines its sex.

References:

Testis determining factor, https://en.wikipedia.org/wiki/Testis-determining_factor

General info about sex determination in different animals (it varies a lot),
 https://www.nature.com/scitable/topicpage/genetic-mechanisms-of-sex-determination-314


You've found a Dissosteira carolina or carolina locust.
I'm not completely sure, but I think this is a male.
They are quite common in North America.

idtools.org/id/grasshoppers/factsheet Dissosteira carolina
uwyo.edu: Dissosteira carolina


Is receptor antagonism just long-term binding?

The details of activation vary by receptor of course, but talking in the popular key-lock picture:

An agonist is a key, that fits the lock and opens ("activates") it.
An antagonist is a key that you can put into the keyhole, but it does not open the lock. What this means is: while the "wrong" key is in the keyhole, you won't be able to open the door, even if you have the correct key, as long as the wrong key is in the keyhole.

As far as Wikipedia goes, the articles for Agonist (and the links contained therein) might be more informative than the one you quoted.

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


The fatty acids within micelles are taken up by enterocytes in the upper/middle part of the small intestine (duodenum/jejunum) through selective transporters in their plasma membrane, which do not accept bile acids. The SLC27A4 protein is thought to be the principal transporter for fatty acids in enterocytes, although there has been some controversy about this.

As a result of this selective uptake of fatty acids in this part of the intestine, the bile acids are left behind in the micelles, as they are emptied of fatty acids. They travel down the small intestine until they reach the ileum, where enterocytes express a bile acid transporter, SLC10A2, which performs active uptake of the bile acids. The bile acids are then secreted on the opposite (basolateral) side of these enterocytes; enter the portal vein; and travel back to the liver, where they are reused. This is known as the enterohepatic circulation. A review of these mechanisms is found here.

So the uptake of fatty acids and bile acids differs by location in the intestine. First the emulsified fatty acids are extracted, then the bile acids are recovered in the ileum. There is also some passive transport (diffusion) of bile acids into enterocytes throughout the intestine, but this is considered a minor mechanism.


Can siRNA induce DNA methylation in mammalian cells?

From a brief survey of the literature, it seems Kawasaki and Taira have been largely vindicated by the community before and since their paper. The retraction was by Taira alone, Kawasaki refused to co-sign because he maintained the data were valid. From the retraction it seems the reason for the retraction was a lost lab book.

Prior to the Kawasaki and Taiga paper, there were already several other papers describing RNAi-induced epigenetic modification in mammals:

Castanotto, D., Tommasi, S., Li, M., Li, H., Yanow, S., Pfeifer, G.P. & Rossi, J.J. (2005) Short hairpin RNA-directed cytosine (CpG) methylation of the RASSF1A gene promoter in HeLa cells. Mol Ther. 12 (1), 179–183.
Morris, K.V., Chan, S.W.-L., Jacobsen, S.E. & Looney, D.J. (2004) Small Interfering RNA-Induced Transcriptional Gene Silencing in Human Cells. Science. [Online] 305 (5688), 1289 –1292.

Then there was another paper the next year by Kawasaki & Taira, which was not retracted:

Kawasaki, H. & Taira, K. (2005) siRNA Induced Transcriptional Gene Silencing in Mammalian Cells. Cell Cycle. [Online] 4 (3), 442–448.

And it seems the idea is now generally accepted and supported by quite a few other studies, mainly looking at germline cells. For example:

Carmell, M.A., Girard, A., Kant, H.J.G. van de, Bourc’his, D., Bestor, T.H., Rooij, D.G. de & Hannon, G.J. (2007) MIWI2 Is Essential for Spermatogenesis and Repression of Transposons in the Mouse Male Germline. Developmental Cell. [Online] 12 (4), 503–514.

There is no review that I could find which really ties it all together convincingly, but there are several reviews on RNAi directed histone and chromatin modification in general which mention that the fact is now established in mammals:

Joshua-Tor, L. & Hannon, G.J. (2010) Ancestral Roles of Small RNAs: An Ago-Centric Perspective. Cold Spring Harbor Perspectives in Biology.
Volpe, T. & Martienssen, R.A. (2011) RNA Interference and Heterochromatin Assembly. Cold Spring Harbor Perspectives in Biology. 3 (9).


How do neurons form new connections in brain plasticity?

I haven't read anything particularly about dendrites being reshaped, though I would expect them to be as flexible as other parts of the cells.

The more commonly discussed topic (in my literary experience) is reshaping of the axon's branches before forming synaptic terminals. These branches are not fixed even in adults - neurons can grow new and retract old branches, attaching (synapsing) to other cells in new places and removing old connections (see Wikipedia: Synaptogenesis).

Additionally to this actual change in the number of synapses, individual synapses can be regulated in their signal strength by adjusting the number of neurotransmitter receptors in the postsynaptic membrane (Gerrow&Triller, 2010, also see Wikipedia: Synaptic plasticity)


There are quite a lot drug databases. I think DGIbd is a good place to start (see below). Further there are a lot of databases which describe drugs and their targets, take a look at these (and the links at the bottom) hopefully you can use several of these in your implementation.

SIDER

  SIDER contains information on marketed medicines and their recorded
  adverse drug reactions. The information is extracted from public
  documents and package inserts. The available information include side
  effect frequency, drug and side effect classifications as well as
  links to further information, for example drug–target relations.

DrugCentral

  DrugCentral provides information on active ingredients chemical
  entities, pharmaceutical products, drug mode of action, indications,
  pharmacologic action. We monitor FDA, EMA, and PMDA for new drug
  approval on regular basis to ensure currency of the resource. Limited
  information on discontinued and drugs approved outside US is also
  available however regulatory approval information can't be verified.

Therapeutic Target Database

  Therapeutic Target Database (TTD) is a database to provide information
  about the known and explored therapeutic protein and nucleic acid
  targets, the targeted disease, pathway information and the
  corresponding drugs directed at each of these targets. Also included
  in this database are links to relevant databases containing
  information about target function, sequence, 3D structure, ligand
  binding properties, enzyme nomenclature and drug structure,
  therapeutic class, clinical development status. All information
  provided are fully referenced.

Potential drug target database (PDTD)
NOTE: I think this one is coupled to DrugBank however you can take a look here

  PDTD is a dual function database that associates an informatics
  database to a structural database of known and potential drug targets.
  PDTD is a comprehensive, web-accessible database of drug targets, and
  focuses on those drug targets with known 3D-structures.

PharmGKB

  The PharmGKB is a pharmacogenomics knowledge resource that encompasses
  clinical information including dosing guidelines and drug labels,
  potentially clinically actionable gene-drug associations and
  genotype-phenotype relationships. PharmGKB collects, curates and
  disseminates knowledge about the impact of human genetic variation on
  drug responses through the following activities: Annotate genetic
  variants and gene-drug-disease relationships via literature reviews
  Summarize important pharmacogenomic genes, associations between
  genetic variants and drugs, and drug pathways Curate FDA drug labels
  containing pharmacogenomic information Enable consortia examining
  important questions in pharmacogenomics Curate and participate in
  writing pharmacogenomic-based drug dosing guidelines Contribute to
  clinical implementation projects for pharmacogenomics through
  collaborations Publish pharmacogenomic-based drug dosing guidelines,
  very important pharmacogene summaries and drug-centered pathways
  Display all information on the website and provide comprehensive
  downloads

STITCH

  To facilitate access to this data, STITCH (‘search tool for
  interactions of chemicals’) integrates information about interactions
  from metabolic pathways, crystal structures, binding experiments and
  drug–target relationships. Inferred information from phenotypic
  effects, text mining and chemical structure similarity is used to
  predict relations between chemicals. STITCH further allows exploring
  the network of chemical relations, also in the context of associated
  binding proteins. Each proposed interaction can be traced back to the
  original data sources. Our database contains interaction information
  for over 68 000 different chemicals, including 2200 drugs, and
  connects them to 1.5 million genes across 373 genomes and their
  interactions contained in the STRING database.

SuperTarget and Metador

  An easy-to-use query interface enables the user to pose complex
  queries, for example to find drugs that target a certain pathway,
  interacting drugs that are metabolized by the same cytochrome P450 or
  drugs that target the same protein but are metabolized by different
  enzymes. Furthermore, we provide tools for 2D drug screening and
  sequence comparison of the targets. The database contains more than
  2500 target proteins, which are annotated with about 7300 relations to
  1500 drugs; the vast majority of entries have pointers to the
  respective literature source. A subset of these drugs has been
  annotated with additional binding information and indirect
  interactions and is available as a separate resource called Matador.

Pharos

  Pharos is the user interface to the Knowledge Management Center (KMC)
  for the Illuminating the Druggable Genome (IDG) program funded by the
  National Institutes of Health (NIH) Common Fund. (Grant No.
  5U54CA189205-02). The goal of KMC is to develop a comprehensive,
  integrated knowledge-base for the Druggable Genome (DG) to illuminate
  the uncharacterized and/or poorly annotated portion of the DG,
  focusing on four of the most commonly drug-targeted protein families:
   G-protein-coupled receptors (GPCRs); nuclear receptors (NRs); ion
  channels (ICs); and kinases. For more information on opportunities in
  the druggable human genome see this poster

KEGG drug

  KEGG DRUG is a comprehensive drug information resource for approved
  drugs in Japan, USA, and Europe unified based on the chemical
  structures and/or the chemical components, and associated with target,
  metabolizing enzyme, and other molecular interaction network
  information. All the marketed drugs in Japan, not only the
  prescription drugs but also the OTC drugs, are fully represented in
  KEGG DRUG and integrated with the package insert information (labels
  information). These include crude drugs and TCM (Tradictional Chinese
  Medicine) drugs.

The IUPHAR/BPS Guide to PHARMACOLOGY (database)

  The information in the database is presented at two levels: the
  initial view or landing pages for each target family provide
  expert-curated overviews of the key properties and selective ligands
  and tool compounds available. For selected targets more detailed
  introductory chapters for each family are available along with curated
  information on the pharmacological, physiological, structural, genetic
  and pathophysiogical properties of each target. The database is
  enhanced with hyperlinks to additional information in other databases
  including Ensembl, UniProt, PubChem, ChEMBL and DrugBank, as well as
  curated chemical information and literature citations in PubMed.

DGIbd

  The druggable genome can be defined as the genes or gene products that
  are known or predicted to interact with drugs, ideally with a
  therapeutic benefit to the patient. Such genes are of particular
  interest to large-scale cancer profiling efforts such as TCGA, ICGC
  and others that identify lists of potential cancer driver genes from
  high-throughput sequence and other genome-wide data. In cancer
  therapy, the increasing number of targeted drugs--those designed to
  inactivate proteins carrying activating amino acid changes as
  determined by mutational analyses--make more compelling the need for a
  searchable database of drug-gene interactions, available here.

There are a lot more databases, maybe these links will help you:

Drug to Target/Gene/Protein Interaction Databases
Question: Database Of Drugs Targeting Genes
Drug Databases


What are sources for learning bioinformatics for self-learning?

Learning a language such as python or perl is almost necessary.

You might have a look at coursera.

There are quite some bioinformatics-oriented courses:

https://www.coursera.org/courses?query=bioinformatics&languages=en

University of California San Diego has a series of bioinformatics courses, with one that seems made for beginners in programming:

https://www.coursera.org/course/algobioprogramming

I haven't had a detailed look at this one, but I liked their more advanced courses.

In coursera, the courses are often organized in so-called "specializations" which give you a certificate, but are not free. However, you can normally enroll to individual courses without paying.

I would also advise learning how to use a UNIX-like command-line environment, and tools such as sed, awk, grep.

The following sites might be good for this:

http://www.grymoire.com/Unix/

http://software-carpentry.org/lessons/

The scope of the latter is broader, and the things they teach could be valuable if you want to do scientific programming in general.


How to calculate the quantification of qPCR to the equivalent of the number of nuclei in fungi?

From your comment:

  "As few as 148 fg of Verticillium dahliae DNA were detected and quantified (through qPCR), which is equivalent to five nuclei". How is possible to make this convertion?

The Verticillium dahliae JR2 genome is 36.2 Mb.  Assuming this organism is haploid and dsDNA has an average mass of 660 g/mol per base pair, that means the molar mass of the genome is 2.40 × 1010 g/mol.  Therefore, 5 nuclei will contain 8.30 × 10-24 mol of your genome.  Multiplying the molar mass by the number of moles gives us a mass of 1.99 × 10-13 g, or 199 fg, which is close to your cited value.


What do ants do with human finger nails?

I believe that MattDMo's hypothesis is incorrect.  Only one group of ants, the Attini tribe, cultivates fungus as a food source.  This group is exclusively a New World group, thought to have originated in the Amazon rainforest and spread out from there.  I see from your profile that you are located in India, which is outside the range of the fungus-cultivating ants.

So if the ants aren't using your fingernails for fungus cultivation, what are they doing with them?  Fingernails are primarily composed of keratin, a very tough protein which ants cannot digest.  However, it is likely that the clippings also contain materials like dead skin, nail fungus, or other organic substances that the ants can eat, making them worthwhile for the ants to collect.

References:

U.G. Mueller, T.R. Schultz, C.R. Currie, R.M.M. Adams, & D. Malloch (2001). "The origin of the attine ant-fungus mutualism". Quarterly Review of Biology 76 (2): 169–197. doi:10.1086/393867


It is a bit ironic that you phrase your question with 'in the first place'. There is a parsimonious explanation for the effect: Dominant deleterious variants are quickly removed by purifying selection whereas recessive deleterious variants can "hide" in individuals that carry a dominant neutral/advantageous variant.

You can think about it this way: In heterozygous carriers (in which the other variant has a neutral or positive fitness effect), a recessive deleterious variant has no (strong, depending on the dominance coefficient) negative effect on fitness and therefore, in those heterozygotes, purifying selection will not remove the variant (efficiently, again depending on the degree of dominance) - it can only act on homozygous carriers of the recessive variant. A consequence of that is that the recessive deleterious allele usually segregates at low frequency with most carriers being heterozygous.

In short: This probably has little to do with there being more recessive deleterious variants per se (even though that might also be the case due to the mechanisms you described in your question). In the snapshot we are looking at when we investigate genetic data, the likelihood of finding dominant deleterious alleles is way lower than finding recessive deleterious alleles as the latter usually just persist for a way longer period of time.


Are all tastes just a combination of sour, sweet, bitter, etc.?

Interesting question.

  The brain perceives taste or flavor as a combination of input from taste buds, the olfactory system, and even pain receptors (spicy foods). Other food contents, such as metal, spice, fat, pH, and even dissolved gas content seem to contribute.

While there are 5 types of taste receptor, there are some 2000 olfactory bulbs encoded by 1000s of gene.  As such, it is not possible to predict how something will taste in a simplistic 5-taste combo.  However, this is an area of active research, such that structural models are used to develop taste enhancers, artificial sweeteners etc.

Sources:

http://www.sciencedirect.com/science/article/pii/S0976120913000041
http://health.howstuffworks.com/mental-health/human-nature/perception/taste.htm
http://www.livescience.com/17684-sixth-basic-taste.html


When does exposure to an allergen increase / decrease allergy?

Small or relatively small amounts of the antigen can cause an allergy, when you have IgE antibodies which fit to this antigen. They will then cause a local immune reaction and cause the secretion of histamine.

For the desensitation therapy large amounts of antigen are given (which is not without risk). The mechanism behind this therapy is not completely understood, but there are some good points.

The immunetherapy seems to induce class switching from the IgE antibodies which can trigger allergic reaction to IgG who can not do this. Furthermore the IgG will mark the antigen for uptake and degradation by the mast cells.
This seems to be induced by a shift from a Th2 immune response over to a Th1 response. This also leads to the production of a different set of cytokines which are anti-inflammatory (IL-10 for example) and the already mentioned different secondary immune response. The immunetherapy reduces the amount of mast cells, basophils and eosinophils which are recruited into skin, nose, eye and the bronchial mucosa. These cell usually support the reaction to allergens in this tissues after the exposure.

See these papers for more information:

Allergen immunotherapy.
Allergen-specific immunotherapy


The following paper answers your question in detail:

  http://www.ncbi.nlm.nih.gov/pubmed/18568020

It seems like the following aa are responsible for the binding, but please refer to the paper for more details:

  Val152,Tyr156,Asn157,Ser422,(Asp79)


microscopic slide cleaning and maintenance

An old technique to clean used slides is to just toss them in a jar containing equal volumes of distilled water, ethyl alcohol 95% and xylene. Shake from time to time. When needed wipe them dry using a clean, lint free cloth and use.

The techique was at the time (1930's?) in use in the lab of prof. Baudet (Veterinary parasitologist, Utrecht University) and is mentioned in several editions of the "Précis de Microscopie" by Maurice Langeron.

Langeron mentioned that the slides treated that way were "perfectly grease-free".

Another method is to wash the slides, rinse in distilled water and store for some time in a mixture of ethyl alcohol and acetic acid.

When on a tight budget, used Carnoy fixative was (is?) used.

This is a trick that was (is?) in use at some botanical labs in Eastern Europe.

It's mentioned in some of the German literature on microtechnique, if memory serves me right in Braune, Leman and Taubert's "Pflanzenanatomisches Praktikum".


What does the 34/70 in Saccharomyces pastorianus Weihenstephan 34/70 stand for?

I went to the Yeastbank website at Weihenstephan for some info. The keyword here is "Stamm," which is German for stem, clade, clan, or strain. So, I would take this to mean that the 34/70 is an isolate (#70) of strain 34. Two of 34/70's strengths, according to the link above are it makes clean beer and gives a pleasant taste profile due to its low yeast-like aroma in the finished beer. I can attest to that firsthand, having had on numerous occasions the pleasure of partaking of Weihenstephaner beer in its home city of Freising.


How much of the weight of yoghurt is due to bacteria?

Interesting question and it will only be possible to do some estimation. The problem is to know the exact bacterial composition as well as the mass of the bacteria. To start, it is necessary to know the number of bacteria in a defined amount of yoghurt. There are scientific publications on this topic, but the numbers in fresh produced yoghurt are in the area of 108 bacteria per gram yoghurt and declines over time. Based on the numbers in  reference 1 and 2 I use 2x108 bacteria per gram fresh yoghurt.

The other number we need is the mass of one bacterium. This is complicated, as bacteria are very light due to their size and cannot be easily weighted. There are some numbers available (we imply here that all bacteria weight the same, which is of course not the case), and according to them, one bacterium weighs about 1x10-12 grams.

Mutiplying both numbers gives the amount of bacteria in one gram of yoghurt, around 0.0002 gram or 0.2mg. One typical sized yoghurt of 150 gram therefore contains about 30mg of bacteria. The weight of the bacteria can thus be neglected against the total weight.

References:

Survival of Yogurt Bacteria in the Human Gut
Handbook of Food and Beverage Fermentation Technology
Mass of a Bacterium


At what stage is the nervous system developed enough to interpret neuronal signals as 'pain'?

First, there is some confusion on your part about heart cells and pain perception. Heart cells generate an action potential intrinsically; they do not need the central nervous system to beat (your second article explains this; read the part about the importance of calcium.) So yes, long before a fetus can feel pain, the heart is beating, because there must be circulation of nutrients throughout the embryo.
Secondly, the vagus nerve and sympathetic nerves can affect heart rate (the former by slowing it down when firing). These nerves start to reach their endpoints late in week 4 of development. So 19 days is not correct.

Cardiac sympathetic system
Although the primitive human heart starts to beat at 21 to 22 d, heart development continues to day 50, and it is near the end of this period, during the fifth week, that thoracic neural crest cells migrate from the neural tube through the somites and form aggregations (ganglia) near the dorsal aorta. [emphasis mine]

To experience pain, however, requires maturation of certain parts of the brain, most importantly, part of the thalamus and the cerebral cortex:

Current theories of pain consider an intact cortical system to be both necessary and sufficient for pain experience. In support are functional imaging studies showing that activation within a network of cortical regions correlate with reported pain experience. Furthermore, cortical activation can generate the experience of pain even in the absence of actual noxious stimulation. These observations suggest thalamic projections into the cortical plate are the minimal necessary anatomy for pain experience. These projections are complete at 23 weeks' gestation.  [emphasis mine]

Fetal surgeons and anesthesiologists often use 20 weeks as the time at which a fetus can start to feel pain, because that is when the fetus reacts to stimuli that would be recognized as pain if applied to adults (e.g. recoiling from noxious stimuli.)
One must recognize that recoiling from noxious stimuli does not prove what the fetus is perceiving. But it's a step in the direction of protecting the fetus from unnecessary pain.
Autonomic cardiac innervation: Development and adult plasticity
Can fetuses feel pain?


How closely related will your descendants be to you?

For how genetically related to you your  my grand-grand-children will be....

Well on the surface the answer is simple. Your grand grand children will 12.5% of your DNA.

Dig a little deeper... the question becomes a bit more difficult to answer.

(1) Humans do cheat a small but significantly amount of time. On average about 0.7-3% of all children are unknowingly raised by men who are not their biological father http://theconversation.com/what-are-the-chances-that-your-dad-isnt-your-father-24802. This is less than the 9-30% which has been reported. The reason appears to be that the data was derived from paternity clinics where  there was already suspicion on paternity of the child. Not the best data set to represent the population, even if the data set was large and mostly free to researchers.

So which that factored in... it depend on what gender you are, and how said grand grand child is related to you. Are you a woman? Is that grand grand child, the child of your daughter's daughter. A pure maternal descended would guarantee a 12.5% genetic relatedness.

But if you are a man, and the grand grand child, is the child of your son's, son... on average genetic relatedness falls to 11-12% (on average). But since a person is related to your or not, there is a 3%-10% that your grand grand child is not related to you if that child is your son's son's child.

(2)Rural (old world) populations tend to share more genetic material since they have had less outside influence into the genepool. This is a reflection of history, where mobility was limited and families tend to stay for generations. In these places, a random stranger isn't that random after all. In which case genetic relatedness calculations become more complicated. Terms to look up are founder effect, population structure. Large cities, with massive influx of people moving in and out tend to be more mixed. Also note isolation, can also because by social stratification. The nobility is a great example where two random nobles are not as random as you think.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1685612/pdf/ajhg00202-0030.pdf
http://link.springer.com/article/10.1007/BF02442864
http://www.nytimes.com/2004/07/31/us/by-accident-utah-is-proving-an-ideal-genetic-laboratory.html rare american example.
https://en.wikipedia.org/wiki/Stoccareddo
http://gizmodo.com/5882644/iceland-is-so-inbred-it-needs-a-website-to-avoid-incest

  And I also once heard that even though the share of my genes will be
  descreasing, the mutations unique to me will stay. Is that so and how
  is that possible?

Not quite. A mutation unique to you has only 50% chance of passing on to a child. (Or a 50% chance of not passing to a child.) So if you have 2 children, that mutation will have a (0.5*0.5=0.25) 25% chance of failing to pass to the next generation. In fact unless that mutation has some sort of selective advantage (awesome X-men powers), or your family has really big families for several generation or you and your families becomes a founder of a new colony/town (founder effect), your unique mutation will likely fallout after a few generations.

  And what about all-males descendants? Like, if I have a son and he has
  XY, then if there always will be a son down the line then Y chromosome
  is going to stay the same, being the one from me?

yeah they will inherit your Y chromosome.. which will change very little over the generations. It will accumulate a few mutations but that is over thousands of years.


NMR spectroscopy detection methods for proteins

In most cases when you perform NMR experiments on proteins you detect the signal on the protons. Even if you're looking at other nuclei, in the end you transfer the magnetization to a proton and detect that signal. This is simply the most sensitive method due to the high gyromagnetic ratio of 1H, and this is the method that is labeled "inverse" in your figure. This is pretty much the default way to measure heteronuclear spectra.

Direct detection means that you directly observe the less sensitive nucleus like 13C. This has certain advantages especially for large proteins where you often have to deuterate the protons to be able to measure anything useful.

DEPT is a type of experiment where magnetization is transferred from the directly attached protons to the heteronucleus. This increases the sensitivity and allows to distinguish CH and CH3 groups from CH2 groups


While its possible humans could speciate into two distinct groups at some point in the future, it hasn't happened recently (100 kya) and it doesn't seem to be happening now. If it were happening we would see two or more distinct populations that didn't interbreed and over time accumulated increasing differences.

These skin colors track most of the evolution we've done in the last hundred thousand years or so, and none of the people from different parts of the globe have any difficulty reproducing with any of the others. If speciation is happening it hasn't happened yet. I doubt speciation could happen given how much gene transfer there was between populations just on foot and boat, never mind planes and trains. Although, speciation does not require physical isolation to occur. See Wallace Effect and sympatric speciation. If there's enough pressure agaist hybridization, human speciation could occur. Think blue collar versus white collar worker and the disappearing middle class.

Speciation has certainly happened with humans before. Not with 'evolutionarily modern' humans, but 'evolutionarily modern' is mostly defined as 'humans since the last speciation event', so that's tautological. But Homo erectus, the neanderthals, the denisovans, et cetera(seriously, there's a lot of Homo species) were all descendants from one common ancestor.

As for the idea that Chinese people are a different species, or descended from Homo erectus? See the geneticist from the documentary who mapped out the genetics of the Chinese population. Archeological and skeletal evidence is easily blurred, but the genetics can't be explained without an out of africa theory.


What sections of the brain can be removed without causing instant death?

Many areas of the cerebral cortex aren't essential to life/consciousness, damaging/removing them will only destroy the function associated with that area, e.g. visual cortex in the occipital lobe, auditory cortex in the temporal lobe etc. The Corpus Callosum can sometimes be bissected without any major detrimental effects to the "patient/victim".

Edit: The point here is that what appears to be a major link between the hemispheres of the cerebral cortex can be destroyed without necessarily killing the patient. Whether it falls under the same surgical category as a frontal lobotomy or not, I don't know.

Generally the "lower" portions of the brain, midbrain and brainstem are more important as regulatory centres. However these are each made up of multiple smaller regions, each involved in multiple functions, e.g. the Pons, medulla, thalamus. Removing any of these could have wide-ranging consequences, e.g. the thalamus is important for integrating multisensory information.

So, broadly speaking, cortex damage is OK, midbrain/brainstem, probably not unless you only removed very small regions (e.g. removing the cochlear nuclei from the Pons would probably only affect hearing).

If you use the added image, you can predict what removing each brain area would affect, removing the brainstem would remove respiratory centres, certain death. Removing visual areas would lead to blindness, but probably not death.

Fully answering your question would probably require an entire book to list all of the known brain regions and the implications of removing them.