The common repository for affinity purification (CRAPome) contains the results from many tandem affinity experiments and scores them based on their presence in control purifications.
The database can be found here. I did a very quick and dirty comparison of the frequency that human ACSL_1 (Uniprot ID; P33121) and GAPDH were detected in control purifications. The graphs shows that ACSL_1 is not a frequent contaminant (detected in less than 5% of GFP control purifications) whereas GAPDH is frequently detected in control affinity purifications.

You can submit your tandem affinity experiments to the CRAPome and it will  provide quality scores for your hits. It's very well thought out and not difficult to use. You might want to try it if you're still .


Why does sympathetic activity constrict pulmonary vessels?

Short answer
The sympathetic nervous system mediates the fight, flight and fright response. It constricts the arteries and arterioles to increase blood pressure, in turn pushing the blood to the muscles and other organs vital for physical activity.

Background
The sympathetic nervous system functions triggers the fight, fright, flight (FFF) response (Fig. 1). It provides the body with a burst of energy so that it can respond to danger (source: Harvard Medical School).

The FFF response is initiated in the hypothalamus by activating the sympathetic nervous system through the adrenal glands. These glands release epinephrine (adrenaline) into the bloodstream. Epi increases heart rate and blood pressure to push blood to the muscles, heart, and other vital organs. The person also starts to breathe more rapidly and the small airways in the lungs open up. This way, the lungs can take in as much oxygen as possible with each breath. Extra oxygen is sent to the brain, increasing alertness (source: Harvard Medical School).

In blood vessels, as you say, sympathetic activation constricts arteries and arterioles (resistance vessels), which increases vascular resistance and decreases distal blood flow. When this occurs throughout the body, the increased vascular resistance causes arterial pressure to increase (Klabunde, 2012). This enhances the distribution of oxygen already present in the blood.  I don't think the pulmonary circulation responds differently than that in the rest of the body. The stress response is meant to support the evasion of acute dangers. But indeed, chronic exposure to adrenaline may eventually lead to impaired oxygen exchange in the lungs (Krishnamoorthy et al., 2012).

Fig. 1. Fight, flight, fright response. source: Freelap USA

References
-  Klabunde, Cardiovascular Physiology Concepts, 2nd ed. (2012). Lippincott Williams & Wilkins
- Krishnamoorthy et al., Anesthesiology (2012); 117(10): 745-54


Pedigree Probability of Autosomal Recessive Trait

Starting with the left hand side of the diagram:

III:2 is definitely a carrier (Tt) as one parent (II:2) is affected (tt).
III:1 is also definitely a carrier (Tt) as when mating with III:2 they produce an affected (tt) offspring (IV:1)
This means that we can work out the possibilities for IV:4 as we know the parent genotypes.  It follows the standard arrangement for two carrier parents giving the options of:

TT (1/4)
Tt (2/4 = 1/2)
tt (Normally 1/4 but in this case 0 as individual not marked as affected).

Therefore for this scenario, the probabilities for IV:4 are :

TT (1/3)
Tt (2/3)

Now if we look at the right hand side of the diagram.

IV:5 is definitely a carrier (Tt) as one of their parents (III:5) is affected.

This gives two possible Punnett squares to be examined:

|-------------------------------------------------------------------------------|
|                                        ♂ (IV:5)                               |
|                          T                                   t                |
|            -------------------------------------------------------------------|
|           |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
| (IV:4)    |-------------------------------------------------------------------|
|    ♀      |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
|-----------|-------------------------------------------------------------------|

This gives nil affected offspring so we can disregard this option for your question (as we are ONLY looking for scenarios which produce affected individuals).

Therefore the alternative is:

|-------------------------------------------------------------------------------|
|                                        ♂ (IV:5)                               |
|                          T                                   t                |
|            -------------------------------------------------------------------|
|           |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
| (IV:4)    |-------------------------------------------------------------------|
|    ♀      |                                |                                  |
|         t |              TT                |                tt                |
|           |                                |                                  |
|-----------|-------------------------------------------------------------------|

Giving 1/4 affected offspring.

As mentioned above, in order to have affected offspring then IV:4 must be Tt.  There is a 2/3 chance of this being the case.  If this is the case, then there is a 1/4 chance of the child being tt.

Both conditions need to be true for this to happen so we multiply the fractions:

2/3 * 1/4 = 1/6


Poly-symbiosis? What's the name for this?

A mutually beneficial relationship between two species is not called symbiosis, but is rather called "mutualism." The benefit is measured in terms of fitness; a combination of survival and reproduction. Symbiosis is the degree to which species are "together," which is used in terms of physical proximity or degree of dependency. Pathogens, for instance, have a symbiotic relationship with their hosts and physiologically depend on their hosts by feeding on them. Mutualism and symbiosis are often conflated, and should not be.
Let's dissect: "If multiple symbiotic relationships exist with a single common (dominant) species, is this called 'farming'?" It seems like you mean, if members of the same species increase each other's fitness. Reciprocal fitness benefits between species is called mutualism, and within species is cooperation. There are important differences between mutualism and cooperation from evolutionary points of view and they have vastly different intellectual histories. None of this is really called "farming," except for some ant-insect mutualisms, where ants raise and protect aphids for a reward (honeydew; i.e., plant sugars secreted by some insects).


Why don’t different organisms have nucleic acid genomes containing different bases and sugar?

It sounds like you are confused about how Darwinian evolution "works".  For example, as we survey the current life forms in this biosphere there is absolutely no evidence that these species (or their molecules, which you refer to) are optimized in any way, shape, or form.  All we can state with any certainty is that at some time in the past, during one, or more, selective events, all the species that used ribose, deoxyribose, and the five common bases (A, C, G, T, and U) for their genetic material, survived to reproduce, and contribute progeny to the next generation.

If that putative selective event was different, then perhaps all the pentose-based species would have died off, and we would all have hexose-based genetic material.

We don't know how many different genetic material recipes were tried out before this one "won".

Evolution can only work on, or select, or select against, the current batch of organisms.  It is not an optimization algorithm, it is a filter that lets variants through.

It may well be that our genetic material, for example, replicates faster than the other candidates. That could be a selective advantage, but it doesn't have to be.

So what are you really asking here (since your original question contains incorrect assumptions)?


What are these white areas of coronary thrombosis?

Low density lipoproteins can be taken up by the macrophages under a number of circumstances (typically high circulating levels is the most important). These macrophages are called foam cells. The macrophage can then die and deposit this cholesterol and fatty material onto a vessel wall in the context of atherosclerosis. Additionally tissue damage as a result of release of damaging chemicals from the macrophage can induce an inflammatory response recruiting more macrophages (worsening the problem in a cyclical manner) and result in fibrosis and platelet activation. I think this would cause the white stuff you point to.

In summary I think you're right, it's a combination of fat, cholesterol, fibrotic tissue and platelets. 3 is more likely macrophages and platelets whilst 1 and 2 are more likely a combination of all the above.


Identification: creepy dangling spiderthing

It is probably a wasp mud nest with spider bodies (possibly still alive and paralyzed) used to house and grow their larvae.
See https://bugguide.net/node/view/560614
and https://ucanr.edu/blogs/blogcore/postdetail.cfm?postnum=28834
The wasps are commonly called "mud daubers" or "mud wasps."


What allows the hypothalamus to detect a lack of thyroid hormones?

The thyroid hormone, thyroxin has a multitude of effects in various cells of the body. It is a lipophilic hormone and acts via nuclear receptors, i.e. the receptors for the hormone are not on the cell surface but inside it. This hormone-receptor complex then travels into the nucleus to attend to transcriptional changes.

The picture above is for steroid hormones but is almost similar for thyroxin too.

Inside the cell, the effect of the hormone depends on which cell it is in. For thyroxin - in heart muscles, it increases cardiac contractility, in fat cells, increases fat catabolism, and in the very same way, in the hypothalamus, its function is to reduce the production of TRH. And the control of this production is at the level of gene transcription.

Hence there is a lovely feedback loop that is formed. Increased thyroxin would lead to reduced TRH production and vice versa. So the hypothalamus responds to the thyroxin hormone by regulating the production of TRH. There is nothing special that the thyroxin is doing here. It just has different effects in different cells and in this particular cell (the neurons of the hypothalamus), the effect happens to be its own feedback loop regulation (via TRH).

The effect of thyroxin is through its receptor that is an intracellular protein and is more or less the same in all cells.

Chemoreceptors are a different ballgame. They sense changes in pH, pO2, and other biochemical parameters through their direct effect on neurons and their firing. Although their functioning is not particularly clear, they interfere with channel conductivities in particular neurons. There is no receptor and transcriptional changes as in thyroxin.


Why is chlorophyll green? Isn't there a more energetically favorable color?

The reason that chlorophyll is green is because it absorbs other colors of light such as red and blue, so in a way the green light is reflected out since the pigment does not absorb it.
Because life might have been purple:

It is possible that the very first life form to process light may have been purple colored. This would mean it was reflecting red and blue light and absorbing green. In such a scenario this thing if it was the first to produce energy from light would have out competed against everything else. It would have had a population explosion and possibly covered much of the Earth or at least the oceans. Haloarchaea are an example of a simple life form that uses Retinal and Bacteriorhodopsin to produce energy though far less efficiently than photosynthesis. Had this been developed prior to photosynthesis it may have let it spread very far even though it is a less efficient energy production method. A 2% efficiency increase in a market no one has yet tapped is still a huge advantage.
In this scenario because the first thing to use light was using green light it left a niche for another form of life to exploit. That niche would have been absorbtion of the Red and Blue spectrums. Which is the same area plants absorb today. They got so good at their niche that they eventually were able to generate much more energy than the first life form did and eventually out competed for the sun. This niche has worked so well that they never developed a full system for the other spectrums.

Because you could say that good enough is good enough:

The sun puts out a lot of energy. It is possible that there was no need to try and capture all of the spectrum or that it was actually not beneficial to do so. Often too much sun is more an issue than too little. Too much sun and heat can dry out the plant. It is possible that to gain the benefits of photosynthesis there needed to be a reduction in some energy to balance it out. Much like a black car on a hot summer day a black plant might absorb all of the spectrums but also get far too hot. Blue plus red may just be the sweet spot.

However, about your question about colour:

Wouldn't plants get more energy if they absorbed light in the green area of the spectrum instead of the red one?

Plants would probably get more energy if their leaves were black.
Sources:

https://www.quora.com/Why-did-chlorophyl-evolve-to-be-green-as-opposed-to-black-which-would-absorb-more-energy
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691134/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2807594/


This is a Birch tree, Betula sp., probably B. pendula, a common species in Denmark that also has hanging branches. It can be identified by the white bark and the leaves, that are not as long as a willow.


What kind of insect can this be? This appears to be just a shell after and insect went through a metamorphosis process

It's a carpet beetle larvae (family Dermestidae).
See here fore more info.

Example:

 Anthrenus verbasci from Wikipedia


How do tea, coffee, and beer dehydrate you?

Diuretics
These drinks contain minor diuretics. Caffeine is the diuretic found in tea and coffee. Alcohol is the diuretic in beer. Diuretic substances increase the amount of urine produced i.e causes dehydration. This is often offset by the water content of mild diuretics like tea, coffee, and alcoholic drinks.
Tea, coffee, and coke
Caffeine belongs to the xanthines, and inhibits re-absorption of Na+ by cells, and increases flow rate of filtered fluid through the kidneys. This reduces water content in your body. In other words diuretics do dehydrate you, specifically caffeine will. Coffee, coke, and tea (very low doses of caffeine) are mild diuretics.
Beer
On the other hand alcohol is an anti-diuretic hormone inhibitor that inhibits arginine vasopressin.


Are there examples of animals that adapt to their environment very quickly? The phenomenon is called Phenoptic Plasticity

The snake example you provide is a single animal that adapts itself to its surroundings. Adaptation is similar, yet very different from evolution. Adaptation happens on a short timescale (as little as seconds, to perhaps years, but within a single life time, without substantial changes in DNA other than, perhaps, epigenetic ones), while evolution may occur over the course of millions of years or more, and likely involving gross changes in appearance and hereditary material. I am not entirely sure what you are exactly after.

A striking example of adaptation is the fish Tilapia, an invasive species of fish (Fig. 1) that is capable of sustaining fresh water as well as sea water environments. The transition from one medium to the other is mediated by gross changes in endocrinology. Your specific snake example on size adaptation seems, however, unsupported based on non-scientific websites at least.

Fig. 1. Nile Tilapia. Source: Sea EX

If you are after examples of swift evolution -There is a nice example of the Waterlily Beetle, Galerucella nymphaeae (Fig. 2), that shows striking host-race formation, i.e., the same species of beetle shows clear adaptations (on an evolutional scale) dependent on which plant it has been found. It has been shown that these beetles extracted from different plants (Nymphaeaceae versus Polygonaceae) showed strong morphological and ecological differentiation to their different host plant families. Beetles from Nymphaeaceae were significantly larger and had disproportionally larger mandibles than beetles from Polygonaceae. It is argued that these differences are adaptations (on an evolutional scale) to the tougher leaves of the Nymphaeaceae, which has been linked to genetic differences. In addition, females showed a strong oviposition preference, and all beetles showed distinct feeding preferences for the host family from which they originated. Moreover, these host preferences resulted in clear differences in survival: survival was 2 to 11 times higher on the natal host family than on the alternative host family.

Fig. 2. Waterlily Beetle. Source: Wikipedia.

Exactly how fast these beetles have adapted I am unsure of, but the interesting thing is that these beetle races are not geographically separated by a natural barrier like a sea, a mountain range etc. Instead, they live side-by-side, but have adapted to a specific host plant.

Reference
- Pappers, Evolution in action: Host race formation in Galerucella nymphaeae. PhD thesis (2001), Radboud University, Nijmegen, the Netherlands


C. Elegans is the only species with a fully characterized connectome and I don't believe there's been much electrophysiological work done on them. The GEVIs are still being optimized and have their own share of issues particularly with signal resolution - distinguishing between subthreshold changes in membrane potential vs action potential. See the embedded paper. If anything, it will be awhile before the response properties of the neurons in C. elegans are characterized. However, I'm sure you could try modeling smaller circuits where the connectivity and neural properties of the neurons are known.


Why do antacids have a special importance when taking lactulose?

Other laxatives can exacerbate the effects of lactulose, leading to diarrhea, and could eventually lead to dehydration and general GI issues.

Neomycin and antacids in general raise the pH of the gut, making it more basic, and reducing the peristaltic movements. Lactulose, meanwhile, is broken down to primarily lactic acid (if I recall) in the gut, and creates a more acidic environment. The acidic environment increases peristaltic movement in the bowel, and in turn the patient eliminates waste.

If you are on concomitant antacids or other drugs that raise the pH of the lower gut, you are reducing the effects of lactulose, and in a worse case scenario, making the constipation worse.


Does a large effective population size result in faster decay of linkage disequilibrium (LD)?

It is certainly possible as yes, rapid population growth will reduce LD.  From Slatkin, 1994:

  In a rapidly growing population, however, there will be little chance of finding significant nonrandom associations even between completely linked loci if the growth has been sufficiently rapid.

Or Nature Reviews, 2002

  Przeworski... showed that population growth tends to decrease the extent of LD, especially for longer periods of growth. By contrast, population subdivision tends to increase the extent of LD, especially when a sample contains individuals from several strongly differentiated subpopulations.

See also box 1:

  Rapid population growth decreases LD by reducing genetic drift.


What does it mean "specialized populations of neurons"?

It's just a specialized group of neurons. You can call a group of cells a population of cells. They are specialized because those particular neurons carry out a specific function.


What is this strange worm-like creature?

I believe this is some sort of Cranefly larvae, see here:  I've found these guys both directly in streams and along the banks of rivers, but also underneath rocks far away from major sources of water. There are different types of cranefly larvae, but they all have the same characteristics, (bulbous bodies, worm like, not easily noticeable arms, alien encephilization)

It may also be deer fly larvae ( a type of horsefly ) but they typically are more "spiky" on the sides.


What (if any) is the shortest evolutionary process observed by humans?

Definition of evolution

The whole problem boils down to the definition of the term "evolution". Typically, evolution is defined as a change in allele frequency over time. See wikipedia > allele if needed.

Answer with definition "evolution = change in allele frequency over time"

Using this definition, any event of death or birth is an evolutionary event. As such, in the human species, there are about 6 evolutionary events per second! This number will vary a lot among species / lineage of course.

Do you want to consider another definition?

If you are willing to use another definition, I am happy to investigate how common are events matching this definition. Please make sure to clearly define the term so as to leave out possibility for subjective appreciation. If you need inspiration for definitions, you might want to have a look at this post.

Sidenote: Evolutionary experiments

You might be interest in evolutionary experiments. An evolutionary experiment consists at putting individuals in a lab, let them breed under some circumstances and let them evolve. Of course, doing such experiment with elephants would be pointless as the generation time is so long. Common species that we use for such experiments include E.coli, S. cervisae (yeast) and D. melanogaster (fruit fly). Some of these experiments can be as short as a few days while others have been running for decades.

Somewhat related posts

How come most animals never seem to evolve over millenia?
Evolutionary chronology - if any, which species have evolved in the last 100 years
Why don't we keep evolving until we are super-human?

For a very introductive source of information in evolutionary biology, you can have a look at the website that @BryanKrause recommended: evo101


Why humans have the temperature they have?

It's simply not possible for humans to live with an absolute body temperature below 20 C for the simple biophysical reason that it would prevent flux of protein through the Golgi and therefore biosynthetic and secretory pathways, as well as endocytosis. The lipid membranes become too "stiff" to correctly function.

My own sense is that the nominal 37 C body temperature is a result of all of the ATP hydrolysis reactions that happen all the time. The chemical reaction is not efficient, and some of that energy is absorbed, heating the tissue.

There are various grades of hypothermia, from mild (33–35 °C) to severe (< 28 °C). Death from hypothermia results only from prolonged exposure, for example, being in ice-cold water results in death after 50-100 minutes. The basic mechanism is that the body dies from a combination of decreased electrical conductance of pacemaker nerves in the heart, and a slowed heart rate incompatible with sustaining life. Ultimately, hypothermic death is a dysregulation of the body's thermoregulatory mechanism, rather than an immediate biochemical problem as I've pointed out above. For a detailed review, there is an open access article detailing hypothermic etiology and pathophysiology.

M.L. Mallet. Pathophysiology of accidental hypothermia. QJM (2002) 95 (12): 775-785.


How long will a typical bacterial strain keep in a -80°C freezer?

Richard Lenski's lab at Michigan State university has been doing long-term evolutionary research on E. coli and maintaining a "frozen fossil record" of their experimental populations every 500 generations since 1988. They still periodically release research papers comparing the physiology of evolved and ancestral populations. For example, this recent paper looks at populations collected at 2000, 10000, and 50000 generations. According to this timeline, they used populations frozen over 3 decades ago.
This doesn't guarantee that your specific organism will last that long, but it does show that freezer stocks can remain viable for longer than some research labs will even exist. Most of their protocols are on the website. I've had lunch with Dr. Lenski, and he's a pretty approachable guy. I'm sure if you emailed him with specific questions that aren't covered on the website, he'd try to find an answer for you.
References:
Changes in Cell Size and Shape During 50,000 Generations of Experimental Evolution with Escherichia coli. Nkrumah A. Grant, Ali Abdel Magid, Joshua Franklin, Yann Dufour, Richard E. Lenski, Journal of Bacteriology Mar 2021, JB.00469-20; DOI: 10.1128/JB.00469-20
Lenski Lab homepage: http://myxo.css.msu.edu


Passive diffusion.
This question specifically refers to passive diffusion.
Ill reiterate and clarify what was mentioned in the question.
Passive diffusion involves a molecule dissolving into the membrane, diffusing across it, and then dissolves in the aqueous solution on the other side.
The second part of your question can be answered briefly: this diffusion event occurs from time to time, and often at a high rate.

Importantly only small, relatively hydrophobic molecules are able to diffuse across a phospholipid bilayer at significant rates. Thus, gases (such as O2 and CO2), hydrophobic molecules (such as benzene), and small polar but uncharged molecules (such as H2O and ethanol) are able to diffuse across the plasma membrane. Other biological molecules, however, are unable to dissolve in the hydrophobic interior of the phospholipid bilayer. Consequently, larger uncharged polar molecules such as glucose are unable to cross the plasma membrane by passive diffusion, as are charged molecules of any size (including small ions such as H+, Na+, K+, and Cl-).
-Cooper, 2000

Hydrophobic fatty acids repel charge.
The additional or missing electron gives the ion its charge. The hydrophilic head groups of the bilayer are charged, but the fatty acid chains are not, and these repel charge.
There are also repulsive forces between hydrophobic and polar residues (hence the bilayer exists in water), however polarity is essentially a spectrum. A small relatively non-polar polar molecule will not experience enough repulsion to stop diffusion, but a larger, or more polar molecule might.
Active and passive transport.
Although not mentioned in the question, these ions and other molecules can permeate the membrane via protein channels that allow, often with great specificity, ions and large molecules to traverse the membrane.


Low migration rate in Papadopoulou et al. (2008)

After a quick look-up, they don't seem to comment much on this choice of parameter unfortunately. Here are my quick thoughts.

They are dealing with quasi isolated species. They explored a range of values and I would like to assume that made sure that more extreme values won't yield to drastically different results.

These simulations can be pretty computationally intensive, it is possible that they considered $Nm$ to be the important statistic but they would assume that the results could scale up and down for different $N$ and $m$ values. In fact, they almost systematically refer to their migration rate as $Nm$.


Looks like a dye blob.  A better job of clean up might help.

https://www.nucleics.com/DNA_sequencing_support/DNA-sequencing-dye-blobs.html


Which diagram correctly describe an effect of tar entering lungs?

COPD is not caused by an infection (which would require a pathogen) but by the inflammation reaction the body triggers because of the tar particles. Thus the statement "mucus accumulated causing infection" does not correctly describe the effect of tar on the lung. Consequently, B and C are incorrect.


Speciation and Phylogeny of Lactobacillus

generally, lactic acid bacteria (LAB) are the ones you should be looking at for milk-based fermentation products. although sometimes species like bifidobacterium are added, which is of a completely different phylum. also, for cheese production, or the Dutch variety I am familiar with anyway, you would need fungi as well.

the lactobacillales order is not monophyletic, as you can see on the wiki page there are at least two different clades.

the wikipedia page 'Yogurt' speculates on the ecological niche of LAB: "Analysis of the L. delbrueckii subsp. bulgaricus genome indicates that the bacterium may have originated on the surface of a plant. Milk may have become spontaneously and unintentionally infected through contact with plants, or bacteria may have been transferred via the udder of domestic milk-producing animals." (source)

EDIT: the LAB are an order, they have been around for quite some time before the humans showed up.


Do people with colorblindness have less cones or no cones of a certain type?

This is a complicated case, as it can have multiple causes.
The genes which are coding for the long (L, yellow) and medium (M, green) wavelength photopigments are located head-to-tail on the X chromosome. This is the reason why this colors are affected much more and especially in men (which only have one copy of this chromosome).

What seems to happen mostly is that the photopigment of one type of cone cells (and their neuronal connectivity) is missing, while the density of the cone cells is still the same. This means that the cells are they, but are not functioning. See these publications (when you have problems getting the articles, let me know in the comments, I can help):

The density of cones in the fovea centralis of the human dichromat
Color-deficient cone mosaics associated with Xq28 opsin mutations: a
stop codon versus gene deletions.
Functional photoreceptor loss revealed with adaptive optics: an
alternate cause of color blindness.

What can additionally happen in some cases is that these cones have a different pigment than they should have. See the third paper above for details.


Supply of cells growing in adherent culture is unproblematic, as long as you don't fill too much media in the petri dish/cell culture flask.

Oxygen supply here work by diffusion which is getting more problematic if the layer of media covering the cells gets to thick. I usually follow the recommendations of Corning for the amount of media to be used in the flasks/dishes:

The complete information can be found here, other companies have similar data sheets available. With these amounts I do a lot of cell culture work and I have no growth problems.


What does these $\Delta \Delta G$ numbers signify?

Very basically, what they've done in the paper was incubate different DNA sequences with histone octamers which were then separated on a gel. From this they could measure the ratio between nucleosomal and free DNA, which represents an equilibrium constant. This can then be expressed as a change in free energy ($\Delta G=-RTln(K)$), which is what the table shows. A lower (more negative) free energy change corresponds to a higher equilibrium constant which represents a greater proportion of DNA bound to histones. In other words, the free energy change quantifies the propensity of these different DNA sequences to form nucleosomes.


The most important features are the eyes, followed by the nose and mouth, respectively.

An elaborate answer can be found on the duplicate question on Cognitive Sciences SE:

Are some facial features more important than others in human facial recognition?


Sources of phenotypic variance

There is phenotypic variance in height in the human population. This phenotypic variance is in part explained by genetic variation, but there are also non-genetic variations, incl environmental variation (what you eat, your physical activity among many other things). See this post for more information.

Sampling error

On top of that, those measures of "genetic height" are based upon a limited number of SNPs and a limited number of individuals sampled. There is therefore a bit of room for a little bit of sampling error here. Note sampling error is not a mistake. It is just the fact that parameters estimated from a sample don't necessarily match perfectly the population parameters.

Training data set

Finally, the estimate is based upon correlation made from previous people. There might have a generational gap in height, typically present in countries that have recently largely changed their diets, such as many Asian countries.

For all of the above reasons, there might have a gap between your actual height and what has been predicted by some genetic testing. In short, yes your nutrition might part of the reason for this gap.


Why Do Healing Wounds Feel Warmer To The Touch?

This is a normal part of the inflammatory process. Inflammation is your body's localised defensive response to tissue injury of any kind, and it is characterised by four cardinal signs- redness, swelling, heat and pain (severe inflammation involves a fifth, loss of function).

Your body is performing three main processes here:

Mobilisation of the body's defences.

Involves release of vasoactive chemicals, which cause the blood vessels to dilate and increase blood flow to the area. This causes the pain and heat, The blood vessels also produce cell-adhesion molecules which make immune cells (leukocytes) stick to the walls of the your blood vessels.
Containment and destruction of pathogens.

The immune system then goes to work clearing up any bacteria which have got into the wound. The leukocytes release chemicals called cytokines to attract more immune cells, to contain and destroy bacteria.
Tissue cleanup and repair.

Dead cells, cell fluid and other debris (pus) is then absorbed by the lymphatic system. Platelets and endothelial cells then secrete growth factors which stimulate cells called fibroblasts to multiply and produce collagen. The heat also increases metabolic rate and increases the rate of tissue repair.


Simultaneously using both hands - How does that work?

I am not sure I fully understand your question, it's a little unclear. But if I understand the question correctly it is how to we coordinate movement on both sides of the body?

Well this can occur because we have connections between both hemispheres of the brain. The major connection is called the corpus collosum, this is a white matter tract that allows signals from one side of the body to pass to the other side of the body.

In some rare cases there have been individuals who have had this connection severed, for these individuals each side of the body may perform tasks of which there other side of the body is unaware.


Could humans choose to establish fibre digesting colonies in our guts?

Probably not without some substantial evolution to change our physiology, depending on what you are wanting.  If you just want to digest fibre, that might be done, but if you wanted to see nutritional value out of it, its not clear that's going to be worth it..

Soluable fibre is currently used by the human body, so you are probably be asking about insoluble fibre.

It might be possible to do a little of this experimentation - I'm not recommending this - but there would be several likely issues depending on your goals in such a project, which could vary.

the human gut microenvironment probably will not accommodate the bacteria you need and they might not grow in significant quantity.
the human gut is not physiologically arranged for digesting such fibre - ungulates generally have four stomach chambers that they can use to store some of the hard for the longer time it takes to break the fibre down.
the nutritional value of plant fibre is low XKCD has some numbers on this and a cow can eat 10kg of plant matter a day and in doing so they don't tend to move that much.  Humans have to eat a greater volume of vegetables to get the calories they need.  Is getting that last 2-5% or so of the energy from digesting fibre worth the trouble? Eat one more apple or a handful of grain.

Lastly, there would likely be some impact on human health - if you succeed then you would be modifying fibre's role in human diet as it stands - which is to help keep the intestines cleaned out.


GENETICS: Analysis and Principles, 4th edition, Robert J. Booker

This book is used in my school's ( NYU Poly) undergraduate genetics class.


Why do surface mole tunnels follow directly below the electric fenceline

Rumor has it that some moles, such as the star nosed mole, have electroreceptors in their nose.

  In 1993, Gould and colleagues proposed that the star-like proboscis had electroreceptors and that the mole was therefore able to sense the electrical field of its prey[24] prior to mechanical inspection by its appendages. Through behavioral experiments, they demonstrated that moles preferred an artificial worm with the simulated electrical field of a live earthworm to an identical arrangement without the electrical field.

They may thus be sensing the electrical field of the fence, and interpreting it as a nearby tasty worm.


Characteristics of radius of blood vessel

The radius of a blood vessel is entirely defined by only two parameters:

1.blood pressure

2.compliance of the vessel walls

Of course, active contraction can decrease the vessel radius. Physically, this is a decrease in compliance, so the above relation always remains true.


For Penicillin Binding Proteins, why is the enzyme-peptide complex less stable than the enzyme-β-lactam complex?

According to Foyes Principle of Medicinal Chemistry, the significant difference is the crowding of the active site by the cycle next to the lactam ring, which prevent attack on the ester and release of the drug from the PBP.

Reversing the reaction to the beta-lactam is unfavorable given the resulting ring strain.

I would personally expect the ester to be hydrolysable (water being much smaller), but not very rapidly given the active site somewhat shields the complex from water. Foyes disagrees on that. ("Water is also an insufficiently effective nucleophile and cannot hydrolyze the complex either.")


I would rather think about regulatory differences instead of biological ones. (Edit, as also Rory M highlighted in a comment)

Extended shelf life can be obtained through microbial ultrafiltration. However in Europe, ultrafiltration labelling is not mandatory, so it is difficult to distinguish if a milk product was simply pasteurized or also ultrafiltrated. The converse case, biologically speaking, two milk products could be generally the same but one country could be more stricter than the other on shelf-life legislation. (The shelf-life relates more to the unsuitability for sale rather than for consumption).


How can a species switch from r to K - reproductive strategy in a single generation?

The issue in your reasoning is to associate a $r$ or $K$ as being a property intrinsic of the species which, while not entirely wrong, is rather misleading.

The classical and simplistic model of population growth is the model of logistic growth

$$n(t+1) = n(t) + rn(t)\left(1-\frac{n(t)}{K}\right)$$

, where $n(t)$ is the population size (number of individuals in the population) at time $t$, $r$ is the growth rate and $K$ is the carrying capacity. Of course, there exist also continuous time equivalent of this discrete time recursion equation. Here is a quick and dirty R code to compute this recursion equation

r = 0.0004
K = 1e4
f = function(n) {return(n + r * n * (1-(n/K)))}

nbGenerations = 1e5
n = numeric(nbGenerations)
n[1] = 1
for (t in 2:nbGenerations)
{
    n[t] = f(n[t-1])
}

plot(y=n,x=1:nbGenerations)

If you want to compute such function fast you can look for the general solution of the recursion equation (it is a good exercice if you are a little uneasy with recursion equations).

As you can see, the population grows exponentially until some point and then the growth is slower and slower until reaching the carrying capacity. If you look at this species at $t=2000$, then you will deduce that it is a r-strategy species because its growth is dictated by the parameter $r$ (the growth rate). If you look at the same species at generation $t=6000$, then you will deduce that it is a K-strategy species as the population dynamic is dictated by the parameter $K$. Yet, the species has not changed so much.

Being r or K strategic is not a intrinsic characteristic of the species as much as it is a characteristic of the species population size in a given environment.

Now, in my example I chose $r=0.0004$, just pick some greater $r$ value and you'll see that such change from being a r- to being a K- strategy species can change very quickly. Consider for example

r = 0.02 # growth rate
K = 1e10 # carrying capacity
f = function(n) {return(n + r * n * (1-(n/K)))} # recursion function

nbGenerations = 1e3    # number of generations to computer
n = numeric(nbGenerations)
n[1] = 1e7             # starting population size
for (t in 2:nbGenerations)
{
    n[t] = f(n[t-1])
}

plot(y=n,x=1:nbGenerations)

You can now look for realistic estimates of $r$ and $K$ for humans (data from after the industrial revolution), plug them in this equation and see what you get! You can also try to estimate $r$ and $K$ from data (from after the industrial revolution only) of population size over time.

If you play with high values of $r$, you can get overshooting and you can even get chaotic population dynamic.

  Are there other species which can change their entire reproductive strategy when the population approaches its carrying capacity?

Of course, this change in a conscious. It is not a decision of the species. It is not either so much an evolutionary process. It is just a consequence of their environment. Yes, all species follow some kind of model of population growth. The famous example of logistic population growth comes from daphnia which growth dynamic has been highly studied. Daphnia can have quite a high $r$ value (depending on the environment) and they can typically show overshooting behaviour of the carrying capacity before settling down back to the carrying capacity.


Why is chloride ion classed as a cofactor for amylase rather than as a coenzyme?

On the wikipedia page (en.wikipedia.org/wiki/Cofactor_(biochemistry)) a coenzyme is defined as a complex organic cofactor, so Cl⁻ doesn't count. Another thing that disqualifies it as a coenzyme is that the ion is not directly involved in the catalyzed reaction. This amylase contains both a calcium ion, involved in catalysis. The chloride is speculated only to be involved in differentiation between substrates, and is absent in other structures.


What does "Activation" refer to in the context of the symptoms of Schizophrenia and Schizoaffective Disorder?

The authors use the Positive and Negative Syndrome Scale (PANSS) to assess symptoms.  One of its cluster scores is activation factor.

Summary:
http://en.wikipedia.org/wiki/Positive_and_Negative_Syndrome_Scale

Original publication of the article, which doesn't list activation factors:
http://schizophreniabulletin.oxfordjournals.org/content/13/2/261.long

Marketed currently here:
http://www.mhs.com/product.aspx?gr=cli&id=overview&prod=panss

None of the sources I saw specified what is meant by activation factor, and many didn't even mention it. It's possible that it's the hyperactivity mentioned in the original publication.  Also, it's possible that it's a modified category in the version sold at the last link. Hopefully this is enough information to get you started, if you want to hunt down the details.


I'm not an expert in functional paleontology, but it has been suggested that the specific shape of heteromorph ammonites could be related to hooking on to macrophytes or branched animals:

Examination of ribbing pattern and its resolution in various parts of
the living chamber in 11 species revealed that the ribs were less
developed and had some traces of wear on the inner surface of the
hooked chamber, being well developed both on the lateral and outer
lower parts. This could indicate that the adult animals were
semi-loosely hooked (Ancyloceras, Macroscaphites) or permanently
clipped (Scaphites, Hoploscaphites) onto either horizontal or upwardly
angled stipes of non-calcified algal macrophytes or branched animals.
Comparison of the adult mode of life with those of modern cephalopods
suggested that ammonites of the suborder Ancyloceratina had developed
a stationary brooding phase that could have several ecological
advantages over free-swimming monomorph ammonites.


That's a marsupial, the spotted cuscus, Spilocuscus maculatus.

Here is another image:

By the way, the same individual in your photo can be found in this site about Australian animals, still eating that starfruit:


What is the contribution of viruses to the evolution of mankind?

The processes that control the germline of metazoans (multicellular animals) are highly regulated compared to single cell bacteria and eukaryotes as well as plants.

At this point there are no clear stories of gene transfer into a complex animal, though there are some for plants:

"animals and fungi seem to be largely unaffected, with a few exceptions, while lateral gene transfer frequently occurs in protists with phagotrophic lifestyles, possibly with rates comparable to prokaryotic organisms."

Bacteria fungi and plants are more permissive and more susceptible to gene transfer and it probably is more important to their evolutionary path.

Its been estimated that as much as eight percent of the human genome has been affected by viral integration.  But viral genomes are highly selected against carrying non essential material - other genes rarely come along for the ride it seems.  What is probably more influential is that viral insertions could participate in rewiring the regulatory network of animal cells, not adding genes, but modifying the conditions under which they are active.


Why do 60S & 40S ribosomal subunits make an 80S ribosome (not 100S)?

That's not a simple mathematical addition!

If those units were mass, for instance, you could (and should) add them: a 60g Lego piece combined with a 40g Lego piece will, of course, form a combo that has 100g.

However, those numbers are Svedberg units, which is...

  a non-metric unit for sedimentation rate [...] The Svedberg coefficient is a nonlinear function. A particle's mass, density, and shape will determine its S value. (emphasis mine)

Funnily enough, most of my students thought that that S stands for Sedimentation. However, it's a tribute to Theodor Svedberg, winner of the Nobel Prize for Chemistry in 1926.

Thus, in a oversimplified explanation, the prokaryotic ribosome has two sub-units. The large sub-unit sediments at 50s, the small sub-unit sediments at 30s, but the two together (that is, the whole ribosome) sediments at 70s, not 80s.

The same way an eukaryotic ribosome has a large sub-unit that sediments at 60s, a small one that sediments at 40s, but the whole structure sediments at 80s, not 100s.

Also, the rRNAs that constitute the sub-units have their own sedimentation rates (in svedberg units) as well:

For a detailed explanation with all math you need, the other answers here and here explain it beautifully.


Does osmosis take place in prokaryotic cells?

Osmosis works across every cell membrane along a concentration gradient as its a physico-chemical principle. Water can cross the membrane (or cell wall), while the substance dissolved in it (for example salts) can not. Because eukaryotic cells only have a cell membrane, they will burst eventually, while bacteria (and also plant cells) have a more rigid cell wall, which will mostly prevent bursting. However the influx (or outflux) of water creates a pressure which is called turgor pressure. How this works is shown below (figure from here), bacterial cells and plant cells work pretty much the same way:


If the jellyfish your friends saw actually look like this and if they were small (Wikipedia says they're usually less than 7 cm in length), they're likely Vellela vellela or sometimes called By-the-wind Sailors for the way the raised part catches the wind and is blown along the ocean's surface.

Wikipedia writes

  ...all possess nematocysts, in some species the nematocysts and toxins
  therein are more powerful than other species. V. velella's nematocysts
  are relatively benign to humans, although each person may respond
  differently to contact with the nematocyst toxin. It is wise to avoid
  touching one's face or eyes after handling V. velella, and itching may
  develop on parts of the skin that have been exposed to V. velella
  nematocysts.

Some photos.

Source

Source


Question is: If an Ashkenazi(1/30) and(multiply) French-Canadian(1/30) ....
Where 1/300 came from ?

I duno, I may missing something - but may it be like  that

Parrent1(=1/30 * 1/2)*Parrent2(=1/30 * 1/2) = P(child with both mutations)


Which parts of the cerebral cortex don't belong to the neocortex?

The hippocampus is considered archicortex rather than neocortex. Sometimes hippocampus is considered "sub-cortical" but I think this is only really fair if you really mean "sub-neocortical"; it's common for "cortical" to be used as a shorthand for neocortex in human neurobiology. Writers will be more specific when necessary.

The piriform cortex and related olfactory structures are considered paleocortex.

Some also delineate an in-between periallocortex that includes entorhinal cortex and limbic structures around the hippocampus.

Neocortex is mostly a six-layered structure and found only in mammals. The other, non-neocortical types of cortex have fewer layers, and are shared by an older common ancestor that includes other vertebrates.


How to create a phylogenetic tree (using Maximum Likelihood method) in newick format for a Multiple Sequence Alignment file in FASTA format?

RAxML (Stamatakis, 2014) would be a good place to start.


What we have here appears to be clustered insect eggs, and examples such as this tend to have some type of moth or butterfly as the culprit. It appears similar to moth eggs that I have observed on surfaces. See this page with information and this page with an example that look vaguely similar to your photograph. You would need an expert to identify a specific species though, if it's possible.


Is there a good explanation for this swarming pattern?

I watched some youtube videos but couldn't find any swarming that looked like rotated sinc function.

The following is nothing but the guesses of someone who doesn't know much about swarming!

One pattern that is often found (through computer simulation and empirical observation) in swarming is a simple 2D rotation.

Let's first consider only the static form of the shape you observed. This shape might be the consequences of multiple rotating layers. Do you remember what kind of dynamic had the individuals within your sinc function?

Oscillation is a pattern that is also sometimes observed in swarming. The oscillating behavior might be the result of inertia. Just like a pendulum, individuals that are far away from the group accelerate continuously in the same direction up to the point they reach the middle of the group. Then they undergo a inverse acceleration up to the point they reach a null speed and then start their cycle again. This inertia depend on the number of neighbors they align their movement on are low. For example, it has been shown in I don't remember which species of birds (I can't find the reference) that each individual align their movement according to only the 6th closest neighbors.

For more information about the 3 basic rules (separation, alignment, cohesion) that allow swarming behavior, have a look to the wiki page

In short, I hypothesize that thanks to the underlying 3 basic rules of swarming, the patterns of rotations and inertia together allow to explain your observations.


Why are centrioles aligned at 90 degree with each other?

As far as I know, the function is not truly known, although there are some seriously interesting guesses.  Part of the problem seems, from scanning the literature, to be that it's not easy or obvious to disrupt centriole orientation.  This paper in PLoS Biology presents some really interesting results, in particular two piece of evidence:

Centriole orientation, to some degree, is dictated by the "mother" centriole during centriole division and is thus passed on from cell to (daughter) cell.
Defects in centriole orientation can result in organelle localization defects in the cell (e.g. nuclear orientation), and at least some of these defects are genetic.

So it seems that orientation is, in some part, a product simply of centriole division, but that there are some gene products that do help determine orientation and localization.  This paper puts forth the hypothesis that centriole orientation determines the axis of cell division which can affect embryo orientation, whereas this suggests that external environmental factors could translate into altered centriole, and therefore cellular, orientation.


What are some examples of non-homologous sequences having similar functions?

Serine Protease Catalytic Triad
This is classic example of convergent evolution in catalytic mechanisms. Shown below are chymotrypsin (4CHA, green) and subtilisin (1ST2, blue) aligned on their catalytic triads (Ser/His/Asp, darker colours). There is no obvious sequence or structural similarity.

You can check out the MEROPS database for a list of protease clans ("represents one or more families that show evidence of their evolutionary relationship") and this paper for a discussion on convergent evolution of the catalytic triad:

Although the biophysics of rate acceleration are intricate and sensitive to even minor structural perturbations, evolution has converged on a catalytic triad (or diad) with a reactive Ser, Cys, or Thr nucleophile more than 25 separate times to facilitate central biochemical reactions such as hydrolysis, transacylation, and phosphorylation.


Neither is "more advanced" than the other, they are separately evolved mechanisms to form a gut.

You may be misled by a human-centric view that treats humans and animals more humanlike as more advanced or "more evolved" than other animals but this is not true: all life has been evolving for the same length of time.


What is the difference between intrinsic and extrinsic apoptosis?

In both pathways 'the cell does itself' the difference is in the reason.

In short:
Intrinsic apoptosis is a response to 'internal damage' eg. damaged DNA, chromosom rearrangement, hang ups in division, hypoxia, etc. that the cell senses itself and 'decides to commit suicide'. This is done by the mitochondrial pathway - release of cytochrome C from the mitochondria activates the caspase cascade that results in programmed cell death. This is like "I'm too damaged, I must die".

In the extrinsic pathway as you have mentioned is indeed related to the FAS ligand (and Fas/FasL being the main pathway for apoptosis), but that is not the only external signal as TNF (also known as TNA-alpha) binding to TNF-R1 (tumor necrosis factor receptor 1) may also lead to apoptosis. These pathways are usually activated by the immune system for example in cellular immune response. This is like "You're abnormal / dangerous / infected, you must die".

Both pathways activates the caspase cascade at some point that results in apoptosis. Either way the actual process of apoptosis is carried out by the cell itself in a programmed, regulated manner.

Source: http://en.wikipedia.org/wiki/Apoptosis
This papaer offers a great review on the topic, including both pathways:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2117903/

I'd like to quote few  important parts to support my answer:

  The extrinsic, intrinsic, and granzyme B pathways converge on the same terminal, or execution pathway. This pathway is initiated by the cleavage of caspase-3 and results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells.

(...)

  The extrinsic signaling pathways that initiate apoptosis involve transmembrane receptor-mediated interactions. These involve death receptors that are members of the tumor necrosis factor (TNF) receptor gene superfamily

(...)

  The intrinsic signaling pathways that initiate apoptosis involve a diverse array of non-receptor-mediated stimuli that produce intracellular signals that act directly on targets within the cell and are mitochondrial-initiated events.


Predicting and identifying microbes and enzymes DNA sequence with metabolic prediction

The first step after sequencing is finding probable genes. After that, genes and their proteins can be classified to belong to protein classes. This is the most what you can do with completely unknown genes. It's possible nowadays to predict the final structure using contact maps (if there is no homologous structure known) but this will still leave you unclear on ligands in many cases. So, the final step is to clarify the function with biochemical lab methods.

So, if you are stuck with a huge sequence, first try to find the genes in it.

http://en.wikipedia.org/wiki/Gene_prediction

For subsequent annotation/classification, I recommend InterPro and PROSITE.

http://www.ebi.ac.uk/Tools/pfa/iprscan/

http://prosite.expasy.org/scanprosite/


Comparing Shine Dalgarno scores, creating a distribution

I would expect to see if every gene has a strong SDS, and that every strong SDS is in a gene (and if not, an explanation of why).

Mathematically, that can be calculated using Fisher's Exact Test (since I don't see any p-values for your scores).

You should also provide a diagram of the genome showing coding sequences or genes, and mark each SDS on it.


In males, why it is difficult to control orgasm?

The sphincter of the bladder is under voluntary control (that's what toilet training is about). That's why you can hold your urine even when the stretched bladder is sending messages to your brain that you really have to go. That's not to say there aren't involuntary effects on the bladder during orgasm.

Orgasm is a separate entity. It is a complex neurological response with four stages. Orgasm is controlled by the autonomic nervous system and is a response that can be controlled as easily as pupillary dilation/contraction in response to light (that is, not at all). However, there is some measure of voluntary control over the plateau phase of orgasm.

In a bit more detail,

  expulsion is a spinal cord reflex that occurs as the ejaculatory process reaches a ‘point of no return’. During expulsion, the smooth muscle fibers of the bladder neck contract to prevent the backward flow of semen into the bladder; the pelvic floor muscles, along with the bulbospongiosus and ischiocavernosus muscles, have primary roles in this function, and display stereotypical rhythmic contractions to propel semen distally throughout the bulbar and penile urethra. During this process, the external urinary sphincter is normally relaxed. The bladder neck and proximal portion of the urethra, which both contain abundant smooth muscle fibers, receive dual sympathetic and parasympathetic innervation. Besides the cholinergic and noradrenergic components, the principal mediators found in these nerve terminals are NPY, VIP, and NO. The external urethral sphincter and pelvic floor striated muscles are solely regulated by the somatic nervous system, but there is no definitive evidence that a voluntary control of the expulsion phase exists in humans.[1]

Human sexual response cycle
Physiology of male sexual function
[1] Ejaculatory Disorders: Pathophysiology and Management: Physiology of Ejaculation


Can carnivores survive on a (processed) vegetarian diet? Why or why not?

With arbitrarily broad meaning of "processed", yes. If absolutely nothing else, elemental purification and inorganic synthesis of something chemically resembling meat in nutrition is possible. Prohibitively expensive and stupid, yes, but possible. So then the question becomes exactly how much processing you need to do. Without clear bounds on that question and inadequate research on the metabolism of obligate carnivores, nothing closer than a broad stab at an answer makes sense. That said, here's a broad stab.

For instance, you'd probably need to synthesize vitamin D3, carnosine, DHA, and a handful of other things from plant extract, which is possible but difficult. Carnivores often have carnosine synthases, for instance. Cats have two distinct carnosine synthases. In terms of dietary sufficiency, that may or may not be enough. To be sure, you'd have to break it down to amino acids and build it back up again, essentially. Obligate carnivores are likely to have a number of other metabolic needs that aren't met with, for instance, pulverized soybeans. You're going to need at least one vat for fermenting raw amino acids into carnosine, and probably another for vitamin D3. Seawater microalgae contain lots of DHA, so that is probably something to look into. You could oversupplement alpha-linolenic acid instead of supplementing DHA, which might or might not work. There's not a lot of study into carnivore metabolism, so prepare to make some discoveries the hard way. Genetic studies can only take you so far, so don't try this on your favorite pet first.

In short: yes, you can raise carnivores on a diet made from plants and plant material. Rhetorical you, as in it is possible. It's probably not something you can do at home, even if you're wealthy.

(I'm assuming "feeding the vegetable matter to chickens" falls outside the domain of "processed" but it would be much easier than large-scale amino acid purification and fermentation.)


Why are ducks more cautious than pigeons?

A possible reason is that pigeons in a city live there year around, while urban ducks often migrate, or their populations are refreshed by new "recruits" from wild populations ; so pigeons have more opportunity to adapt to being close to people.  Another possible reason is that pigeons are more agile than ducks on land and are more able to escape if you decide to grab one for dinner.


Based on the body structure and double pair of legs per body segment, this is a millipede.

Based on the small size and spacing between body segments, it could possibly be in the Paradoxosomatidae family. You could check by examining the specimen more closely:

  Most species possess a groove or furrow ("sulcus") on the dorsal surface between the keels (paranota) on each segment.

Although the color is wrong, this millipede reminds me of the somewhat-cosmopolitan invasive, the Green house millipede (Oxidus gracilis), which is about 1.8 to 2.3 mm long.

 Source: NCSU Plant Disease and Insect Clinic; Credit: Matt Bertone

Due to the color difference, I cannot tell definitively whether this is your species or not. Your poor picture quality makes this more difficult. However, I thought I'd provide this post for you as a jumping off point. good luck!


Is there really a clear distinction between dinosaurs and birds?

The placement of the bird clade within the dinosaur clade is based on much more than just "having feathers and being warm-blooded"; paleontologists have discovered many, many ancient bird and theropod fossils, and as a result their understanding of what the theropod clade was like overall and how the bird clade developed within it is precise enough that discovering another group of dinosaurs was warm-blooded or even had feathers won't result in the conclusion "wow that dinosaur was closer to birds than we thought", but "wow feathers were a much more common feature among dinosaurs than we thought".

If you look at the Wikipedia page you can see there are many "bird-related" clade names that cover different levels of similarity to modern birds. From "Neornithes", which is defined as the clade containing all modern birds, to "Paraves", defined as the group containing all organisms closer to modern birds than to Oviraptors, which are all within Maniraptorans, which is itself pretty deeply nested within the Theropod clade...

So basically what I am trying to say is, our understanding of where birds fit within Dinosauria is precise enough at this point that no discovery about a single trait is going to "blur the distinction between bird and dinosaur"; it might change our idea of dinosaurs in general to be more bird-like, meaning that traits we thought were bird innovations might have been standard-issue in dinosaurs for a long time before, but it will not necessarily change our whole understanding of how birds and dinosaurs are related.

As for this :

  With recent discoveries, isn't this the definition of what a bird is rather than a fact about the extinction?

It isn't; the paleontological definition of what a bird is is not at this point an ad-hoc definition related to "whatever survived the K/Pg extinction". Even Neornithes, the crown group of all living birds, originates to before the K/Pg extinction. For example, the splits between ostriches and other birds and within that latter group, of ducks and geese from other birds are thought to have happened during the Cretaceous. And there are some researchers who argue that a few fossils indicate that some non-avian dinosaurs survived the extinction; the consensus view is that those fossils are dated wrong, but that this position exists shows that "non-avian dinosaurs went extinct at the K/Pg boundary" is a fact-based question, not a definitional one.


When might an inhibitor of bacterial transformation be useful?

In the research lab? I thought about it for a while and found no usage. But it could be interesting for clinical applications to prevent bacteria spreading their resistance genes (which are usually organized on extra chromosomal plasmids) and thus preventing multi-resistant bacteria.


Is there an advantage to linear chromosomes?

I think it is the wrong question. You assume that eukaryotes developed from a single-cell organism with circular DNA. Then, clearly, there must have been an advantage of (newly) developing a linear genome. But eukaryotes could have developed from an organism with linear DNA, too. There are still a few bacterial species with linear chromosomes, so this is not unlikely. We don't know, however.

On the other hand, if linearisation developed independently, you can learn from bacteria why it might have occurred:

J. N. Volff, J. Altenbuchner: A new beginning with new ends: linearisation of circular chromosomes during bacterial evolution. In: FEMS microbiology letters. 186, 2, May 2000, 143–150, PMID 10802162. (Review).

Abstract:

  Bacterial circular chromosomes have sporadically become linearised
  during prokaryote evolution. Unrelated bacteria, including the
  spirochete Borrelia burgdorferi and the actinomycete Streptomyces,
  have linear chromosomes. Linear chromosomes may have been formed
  through integration of linear plasmids. Linear chromosomes use linear
  plasmid strategies to resolve the 'end-of-replication problem', but
  they have generally retained from their circular ancestors a central
  origin of replication. Streptomyces linear chromosomes are very
  unstable and at high frequency undergo amplifications and large
  deletions, often removing the telomeres. At least in Streptomyces,
  chromosome linearity is reversible: circular chromosomes arise
  spontaneously as products of genetic instability or can be generated
  artificially by targeted recombination. Streptomyces circularised
  chromosomes are very unstable as well, indicating that genetic
  instability is not confined to the linearised chromosomes. Bacterial
  linear chromosomes may contain telomere-linked regions of enhanced
  genomic plasticity, which undergo more frequent genetic exchanges and
  rearrangements and allow differential evolution of genes, depending on
  their chromosomal location.


What kind of factors determine how someone looks according to their race or ethnicity?

Concept of race

The concept of race often poorly represent the genetic structure of populations. There is therefore an important socio-cultural aspect to the concept of race. The first sentences from wikipedia > race make this point clear

  Race is a concept used in the categorization of humans into groups, called races or racial groups, based on combinations of shared physical traits, ancestry, genetics, and social or cultural traits. Although such groupings lack a firm basis in modern biology, they continue to have a strong influence over contemporary social relations.

What explain why people of different race look different?

You should most definitely have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?

Your question can therefore be rephrased as "What is the heritability of the phenotypic trait X in humans?", where trait X could be anything of interest such as hair colour for example.

The answer for such question is always the same. It goes in three points

It depends upon which phenotypic trait you are looking at
For whichever trait you consider, it will most certainly be a combination of both genetic and environmental factor.
The evolutionary reasons for the existence of such distinction among groups will again depend upon which trait you're looking at.

If there is one particular trait that is of interest to you, you might want to open a new post to ask what is the heritability of this trait and whether there is any selective reasons for why different ethnic group differ for this trait.

You might be interested in a short and easy intro course to evolutionary biology such as Evo101 by UC Berkeley


How Much DNA do Siblings whose Parents are First Cousins Share?

Before I actually answer your question, let us clear up some problems in your assumptions. The fact that you expect 50% similarity in siblings is a full of several assumptions.

Imagine a case of a simple diploid organism with 2 traits. To restate your assumption, if both the parents are heterozygous in either of the two traits, and the alleles present in either parent for each trait are different (four different alleles possible for each trait), then the probability of getting two children who share 50% of the same alleles is more than any other percentage sharing.

Let us break this down. We'll gradually add complications.

For the 2-trait organisms, let us assume the genotype of the parents to be $\text{AB,EF}$ and $\text{CD, GH}$ where $\text{A,B,C,D}$ are the alleles controlling trait 1. Hence, for their first child, the possible genotypes are $\text{ACEG, BCEG, ADEG, BDEG, }$ and so on.... Since there was no allele match in the parents, each of these genotypes is equally likely.

For the second child, the same possibilities with equal probabilities exist. Now, I computed a matrix which has each possible genotype for child 1 as rows, that of child 2 as columns and the values are the proportion of alleles shared (i.e. common between the two). .

So, all proportions of the sharing is possible between the two kids. But, to find out the most probable configuration, we plot another kind of plot.

Technical note: Although the barplot has frequencies of appearing in the above similarity-matrix, it is equivalent to the probabilities since each genotype was equally likely.

Hence, the case with the two siblings sharing 50% of the genome is most likely for this case. Now, if we expand to 3 alleles, here's the corresponding plot.

It shows, that even if we increase the number of traits (as we gradually approach the human case), the maximum likelihood still includes the sibling-organisms sharing 50% of the genome.

Now, what if the parents already shared some genome? Let us say, the 2 trait organisms already shared 50% of the genome. It is equivalent to say that in the genotypes elucidated above, $\text{A=C, E=G}$. With this assumption, I ran the same kind of simulation to get the following graph.

Another technical note: Although the plot still shows frequencies of appearing in the matrix,the repeats of the same genotype along rows/columns in proportion to their probability of forming will make these frequencies equivalent to probabilities.

So now, the siblings with 75% similarities are the most likely outcome.

Let us now ask, for the 2 trait organisms we are working with, that if the grandparents had zero genomic similarities, and their two kids in-breed, what will their two kids share? For this, we take the probabilities of the first generation (children of the grandparents, sorry for the semantic mashup) for each %overlap, and multiply it with the probabilities of their kids having the various overlaps and plot a final graph.

This shows that they will most likely share 50% or 75% of their genome.

Limitations of this analysis:
 It does not account for linkage of genes. It assumes totally independent assortment of the alleles. It models all similarities to be in alleles of different traits initially and then allows for same diploid pairs, i.e. it does not allow for the observed probabilities of forming a same diploid pair, i.e. case where the similarity (genomic sharing) between two individuals is because of two same alleles for the same trait. It is also blind to any parental imprinting. Homozygosity is not yet incorporated in the simulation, will do in a while.

Below is the two-generation probability simulation for an organism with 4 and 5 traits.

The maximum likelihood of %similarities in genome, as you can appreciate, for a large number of traits would be somewhere around 63-64%.

I shall post the R code in a while, after I format it properly. For computations for greater than 5 traits, I shall write a better engine in a day. Sorry for the improper formatting of the question. Shall rectify in a while.


Can Eskimos be regarded a distinct species from Kalahari Bushmen based on morphological differences & geographic isolation?

I think that species delimitation is not a science, or at least not a coherent one. Different fields use different criteria, for practical or historical reasons. For instance, in plants, loads of fertile hybrids exist between species. It seems that botanists do not split based on the traditional biological definition of what a species is: they apparently tend to split more (see the splitters and lumpers notion).

My intuition is that humans are generally interfertile. There even seems to have been interfertility between H. sapiens and H. neandertalensis which have been (or maybe still are?) considered as distinct species. But how are the actual genetic exchanges across the human populations?

In my opinion, if it were proven that genetic exchanges between human populations living very far apart and having evolved very different ecological adaptations (like populations from the arctic and from the Kalahari) were almost reduced to zero, then it would not be absurd to call them different species. Humans would form a continuum that can be considered a unique species (if interfertility is to be taken as a criterion), but with isolated extremes being in the process of forming separate species, somewhat like the extremes of a ring species. Maybe there even is some degree of reproductive incompatibility between very divergent human populations. The thing is that it is not ethically acceptable to experiment with this. We need to rely on "natural" experiments happening. Globalization could potentially tell us in the future, by facilitating encounters between individuals from very distant populations, whether such reproductive incompatibilities exist or not. That said, I doubt that the origins of parents are recorded in a scientifically usable manner when a couple has problems having children.


In the context of heterotrophic theory of abiogenesis, what is an organism that eats other organisms called?

@Artem, it's been a while! Good to see you back on Biology.SE.

I doubt that any rigorous terminology exist to describe these "type-0 heterotrophs" living on "non-organismic" organic compounds.

You might be assuming that early organic matters can naturally be categorized as being fundamentally alive vs fundamentally non-living. It is more a question of philosophy of the definition of life than anything else but, to my experience, most authors who wrote about the definition of life tend to consider early life as a spectrum from "definitely not living" to "definitely a living thing". The existence of this spectrum questions the need for the terminology you are looking for.


Endocytosis (specifically you asked about clathrin-mediated endocytosis) is indeed an energy consuming process. the coating of the vesicle may be "spontaneous", but the pinching off of the vesicle, the uncoating of the clathrin, and the transportaion of the vasicle inside the cell all require ATP/GTP hydrolysis.

Dynamin - dynamin forms a spiral around the neck of the vesicle, and uses GTP hydrolysis which in order tighten the coil around the vesicle neck causes it to break and results in the pinching off of the vesicle from the parent membrane.

The uncoating of the clathrin is also ATP/GTP consuming. proteins such as hsp70 chaperon and auxilin is thought to be involved in the ATP hydrolysis. the uncoating process starts after the pinching off of the vesicle.

the tranportation of the vesicle will also cost energy, proteins such as the Myosin family are considered to transport endocytic vesicles into the cell, and use ATP hydrolysis.

Dynamin - Wiki

Myosin  - Wiki

Uncoating process - Molecular Biology Of The Cell ed.6 p.701


Why are so many recreational drugs serotonin 5-HT1A partial agonists?

Interesting notion. However, the main effects of the indoleamine-class of psychoactive compounds, including psilocybin and LSD (Shulgin, 1997), are generally ascribed to 5-HT2A receptors and the glutamatergic system (Aghajanian & Marek, 1999). The stimulant effects of the phenetylamines (PEAs) such as amphetamine and related compounds (Shulgin, 1991) mainly target the dopamine (DA) and noradrenergic (NE) systems. I reckon that the 5HT1A effects are 'side effects', or secondary effects.

Antidepressants, such as the selective serotonin-reuptake inhibitors,  target the 5HT1A system and mainly do so by downregulating the pre-synaptic variant of the 5HT1A receptors, which have a regulatory role by decreasing 5HT release. Downregulating them takes about 2 weeks. After that time 5HT release is disinhibited and 5HT release is enhanced, which has antidepressant actions (source: Sci Am, 2013). Because many recreational drugs are not taken that long, my educated guess is that acute activation of 5HT1A by recreational drugs limits the drug's effect more than anything else.

Why are they partial agonists? Because they target other receptors better; the main effects of e.g., PEAs as described above shows you why. Many of those compounds mainly target the DA and NE system. Because they are aspecific ('dirty') drugs, they also target a variety of other receptor systems. Perhaps altering the main effect, perhaps not doing anything substantial to the trip.

Note that the PEA MDMA is kind of a one-of-a-kind psychoactive compound (Shulgin, 1991) that releases massive amounts of 5HT (Gartside et al., 1997).

On a side note, Wikipedia tends to list all available information on an item in a cluttered way that obscures the relevance of that information to the global picture.

References
- Aghajanian & Marek, Neuropsychopharmacology (1999); 21(2 Suppl): 16S-23S
- Gartside et al., Neuropharmacology (1997); 36(11-12): 1697-703
- Shulgin, Pihkal (1991), Transform Press
- Shulgin, Tihkal (1997), Transform Press


In my DNA sequence for one sampling site there're W's; Y's; R's and K's?

These are the so called "DNA ambiguity codes", when the sequencing result allows to bases at the position but it cannot be decided which. This can happen for example when you sequence genomic DNA and you have two different alleles present.

The code is the following (taken from this website):


What is the state of actin-myosin in my biceps after I have flexed my arm?

When I've totally flexed my arm, are the actinomyosin left in this contracted state?

Yes, the sum of the length of all sarcomeres in series determine the length of the muscle.

So do they remain in this contracted state? Does the myosin head attach to the actin all this time?

Yes, it stays attached.

If it leave the actin, does the myosin snap back to its original position and relieve the tension/comeback to original length?

It doesn't really 'snap' back, it 'walks' back over the actin.

Does it require any energy expenditure?

Yes, the myosin heads require ATP to 'walk' back as well. If ATP is depleted cannot walk back, as is the case with rigor mortis (https://en.wikipedia.org/wiki/Rigor_mortis).

What is the state of the actinomyosin if left in a half flexed state? By state, I mean, the stage of the cross-bridge cycle

Myosin will partly overlap with the actin, but not completely. But this has nothing to do with the cross-bridge cycle. The myosin heads need to complete several cross-bridge cycles to fully contract the sarcomere.

For further reading, the Wikipedia page on the sliding filament model is a good start: https://en.wikipedia.org/wiki/Sliding_filament_theory


Why do plants have green leaves and not red?

Surely it would be even more beneficial for plants to be black instead of red or green, from an energy absorption point of view. And Solar cells are indeed pretty dark.

But, as Rory indicated, higher energy photons will only produce heat. This is because the chemical reactions powered by photosynthesis require only a certain amount of energy, and any excessive amount delivered by higher-energy photons cannot be simply used for another reaction1 but will yield heat. I don't know how much trouble that actually causes, but there is another point:

As explained, what determines the efficiency of solar energy conversion is not the energy per photon, but the amount of photons available. So you should take a look at the sunlight spectrum:

The Irradiance is an energy density, however we are interested in photon density, so you have to divide this curve by the energy per photon, which means multiply it by λ/(hc) (that is higher wavelengths need more photons to achieve the same Irradiance). If you compare that curve integrated over the high energy photons (say, λ < 580 nm) to the integration over the the low energy ones, you'll notice that despite the atmospheric losses (the red curve is what is left of the sunlight at sea level) there are a lot more "red" photons than "green" ones, so making leaves red would waste a lot of potentially converted energy2.

Of course, this is still no explanation why leaves are not simply black — absorbing all light is surely even more effective, no? I don't know enough about organic chemistry, but my guess would be that there are no organic substances with such a broad absorption spectrum and adding another kind of pigment might not pay off.3

1) Theoretically that is possible, but it's a highly non-linear process and thus too unlikely to be of real use (in plant medium at least)
2) Since water absorbs red light stronger than green and blue light deep sea plants are indeed better off being red, as Marta Cz-C mentioned.
3  And other alternatives, like the semiconductors used in Solar cells, are rather unlikely to be encountered in plants...

Additional reading, proposed by Dave Jarvis:

http://pcp.oxfordjournals.org/content/50/4/684.full
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691134/
http://www.life.illinois.edu/govindjee/photosynBook/Chapter11.pdf
https://www.heliospectra.com/sites/default/files/general/What%20light%20do%20plants%20need_5.pdf


What chemicals and structures control the *direction* of plant growth in leaves, stems and roots?

PART 1 : Phototropism

The movement of plant shoot towards light is called phototropism. This process is mainly stimulated by the blue light. The photoreceptor involved is called Phot1 (Phototropin 1) or JK244.

Auxins such as IAA (indole acetic acid) are plant hormones, expressed highly in meristem, which cause shoot growth. On illumination this phototropin, through currently unknown messengers, causes inhibition of polar Auxin transport in the illuminated side. This causes the non-illuminated side to grow more and thus bending the plant towards light.

The image represents an older model which proposed lateral movement of auxin. The mechanism mentioned in last paragraph is the currently accepted model. The below figure illustrates 'polar auxin transport'

For details refer to this nice review on phototropism.

PART 2 : Geotropism and Hydrotropism

Geotropism or gravitropism is movement of roots towards earth (gravity) and hydrotropism is movement of roots towards water. Both phenomena interact with each other and share some common pathways. But hydrotropsim can inhibit geotropism and it is evident in conditions when root goes towards an adjacent water source.

Ethylene and Auxin signaling is involved in root growth both in geotropism and hydrotropism. In geotropism the auxin is stimulated by statoliths (clustered and membrane bound grains of starch) in the amyloplasts- the organelles which store starch. The model suggests that amyloplst sediments under the influence of gravity and thereby affect auxin polar transport (the second figure co-incidentally illustrates polar auxin transport in geotropism).

The exact moisture sensor is unknown but Abscissic acid (ABA), which is well known for its involvement in drought tolerance, is known to affect hydrotropism.

MIZ1/2 are some proteins uniquely involved in hyrdotropism.

Both pathways are dependent on Calcium as a secondary messenger.
To conclude, these pathways are not as clear as those of phototropism.

Reference:

http://www.academicjournals.org/ajar/pdf/Pdf2006/Nov/Dexian%20and%20South.pdf
http://www.sciencedirect.com/science/article/pii/S1360138504002717
http://www.plantphysiol.org/content/133/4/1677.full


Phase-locking can occur at very high frequencies at the early stages of a sensory system. In addition to the answer provided in your previous question, let me offer an illustrative example from single neurons in the somatosensory system.

Deschênes, Timofeeva and Lavallée (2003), have stimulated the whiskers of an anesthetized rat with a sinusoidal stimulus while recording extracellularly in the main feed-forward brainstem nucleus of this system (Pr5). Practically all neurons responded with at least one action potential to all cycles of a stimulus up to a stimulation frequency of $300Hz$. Neurons always fired an action potential at first cycle up to the maximum frequency tested, $400Hz$, and ~$30\%$ fewer spikes upon subsequent stimulation (questions 2 and 3). The extend of coupling to the stimulation frequency depended on the amplitude, velocity, and direction of the stimulation.

 Encoding of high-frequency whisker deflections by primary afferent axons
(Figure 6 from Deschênes, Timofeeva and Lavallée (2003))

Given the physical limitations of the stimulation device (piezoelectric element) it was not possible to directly stimulate at higher frequencies. However, the authors took advantage of the harmonic oscillations of the stimulator to look at the phase-coupling of spiking to higher frequencies of stimulations. Remarkably, units that were sensitive to small displacements of the whisker were able to follow the harmonic oscillations of the stimulator up to at least $1kHz$ (see Figure above).

  What happens beyond? Does the neuron follow a virtual stimulus of 1/n of the original frequency (which would be in phase with the original stimulus)? Or does chaotic firing take over?

It is important to note that $1kHz$ is very close to the refractory period of most neurons, thus I would predict that this could be the only limiting factor in these cells. Of course, different types of cells will show different responses to high-frequency stimulation based on their intrinsic properties, the degree of short-term synaptic plasticity of the activated synapses, and/or the filtering of the incoming inputs by upstream circuits.

  Does this maximal frequency count as a characteristic of a neuron (type of neuron), and what is its name?

I am not aware of something like this. Stimulation at such high frequencies is not typically used to classify neurons as it is rather non-physiological for neurons beyond those receiving direct inputs from the sensory receptors. Most often researchers apply a DC pulse and observe the degree of spiking adaptation.

Reference
Deschênes, M., Timofeeva, E., & Lavallée, P. (2003). The relay of high-frequency sensory signals in the Whisker-to-barreloid pathway. The Journal of Neuroscience : The Official Journal of the Society for Neuroscience, 23(17), 6778–87. https://doi.org/23/17/6778


What is the basis of the endocochlear potential?

About biological electrical potentials generally

Biological potentials on the order of tens of millivolts depend on very very few ions moving (about 1/100,000 of the potassium concentration, for example, for a typical neuronal potential).

Therefore, the sum of positive and negative charges in any compartment is always almost zero (to several decimal places and beyond measurement; if you say a ). Electrical forces are very powerful, and

Some previous answers that are related:

https://biology.stackexchange.com/a/57066/27148

https://biology.stackexchange.com/a/77925/27148

https://biology.stackexchange.com/a/81571/27148

The endocochlear potential in particular - this is really cool

Everything I said above basically can be summarized in a quick statement: you can't figure out potentials just by measuring ion concentrations and summing them up. If you counted all the ions (including charged proteins, etc), you'd get ~0 in any biological solution. Instead, you have to think about where the concentration gradients are and how particular ions are moving. Let's tackle the endocochlear potential... Hibino et al 2010 has an excellent diagram, adapted from their previous 2008 paper:

Let's walk through the key features here, focusing on panel (b). First, the general structure: there are three extracellular spaces, which are all electrically isolated from each other. Between these extracellular spaces, there are two layers of cells where all the business happens.

Between the perilymph and intrastria space, there are a collection of cell types all connected via gap junctions. We can treat them sort of like one big cell, I'll call it the syncytium. A sodium-potassium ATPase uses energy to pump potassium into the syncytium and sodium out (upper left of [b]). Additionally, because there is now low sodium in the syncytium, more potassium enters through NKCC channels, which are symporters that move 1 sodium, 1 potassium, and 2 chloride ions together.

Potassium  would accumulate in the syncytium, except there are Kir4.1 channels permeable to potassium on the other side of these cells, open to the intrastria space. So, potassium flows down its concentration gradient into the intrastria space. This also creates an electrical potential and makes the intrastria space very positively charged (shown as +90mV on the diagram; the syncytium would similarly get a negative charge from the flowing potassium, but that isn't shown).

Normally, not many ions would actually flow to create this potential (on the order of the 1/100,000 I mentioned above) and everything would stop there. However, there are another set of pumps and channels in the marginal cells. The marginal cells also pump potassium in, via the sodium-potassium ATPase and NKCC channels, keeping potassium concentrations in the intrastria space low, such that potassium continues to flow down its concentration gradient from the syncytium.

The marginal cells also have potassium channels on their opposite face, and these are open to the endolymph. The high concentration of potassium ions in the marginal cells and the positive charge in the intrastria space gives the necessary drive to push the concentration of potassium in the endolymph high.

Ultimately, there is a full circuit of potassium because potassium is flowing into hair cells from the endolymph, and then back out to the perilymph. The sodium-potassium pumps use energy in the form of ATP to maintain the imbalance between perilymph and endolymph.

Hibino, H., Nin, F., Tsuzuki, C., & Kurachi, Y. (2010). How is the highly positive endocochlear potential formed? The specific architecture of the stria vascularis and the roles of the ion-transport apparatus. Pflügers Archiv-European Journal of Physiology, 459(4), 521-533.

Nin, F., Hibino, H., Doi, K., Suzuki, T., Hisa, Y., & Kurachi, Y. (2008). The endocochlear potential depends on two K+ diffusion potentials and an electrical barrier in the stria vascularis of the inner ear. Proceedings of the National Academy of Sciences, 105(5), 1751-1756.


1) Yes, that's correct.

2) This is just a simple matter of applying the equation $C_1V_1=C_2V_2$. For congo red:

$C_1=20\frac{mg}{mL}$
$C_2=0.04\frac{mg}{mL}$
$V_2=500\ mL$

I'm sure you and a calculator can figure the rest out.


In your 5 points you basically cover several concepts of evolutionary biology.

1) The number of mutations depend on mutation rate. The mutation rate varies along genome sequences, species and individuals. According to the recent DECODE study (Kong et al., 2012) a human mother transmit on average 15 mutations to her offspring and a human father transmit on average $25 + 2(g-20)$ mutations to his offsprings, where $g$ is the age of the father and where the formula stands only for father older than 20 years old.

2) Mutations happen by chance and are not directed toward creating some specific feature. But it is much more likely to create a round of color on the wings of a butterfly than creating the picture of Tom Sellek. The reason has to do with the developmental and biochemical pathways linking the given mutation to its phenotypic effect. Looking at a given mutation, you can understand how it yield to the modification of some phenotypic trait by looking at the biochemical and devlopmental pathways.

3,4) The third point that you raise is called "genetic drift". Shortly speaking the concept of genetic drift may be called the good luck/bad luck effects. Stating differently genetic drift is the random sampling of alleles (gene variant) from a population. If some alleles are favored over some others at a given locus, then sampling is not 100% random but is not either 100% deterministic. The only case where genetic drift is absent is in infinite population (which is obviously an unrealistic case). Genetic drift is inversely propotional to population size and you'll understand it better by reading this post.

5) When the mutation is at very low frequency, the mutation needs to be dominant in order to be expressed, this is true. But an allele may increase in frequency due to genetic drift up to the point that some individuals are homozygous for this allele and therefore express the trait. Dominance and recessivity are just extreme case of a continuum and most often alleles have intermediate level of dominance. Pleiotropy is also something to consider. Note also thaat the frequency of the three possible genotypes $AA$, $AB$ and $BB$ are given by Hardy-Weinberg law (under some assumptions) $x^2$, $2x(1-x)$ and $(1-x)^2$ respectively, where $x$ is the frequency of the allele $A$.

Hope that helps!


It means "vegetable".
I think it's because people use those plants for food


Difference between KEGG Pathway and Module (from KO mapping)

A pathway shows all the reactions required for the synthesis / metabolism of a given product.  A module is a functional unit that can be utilized in a pathway, and some modules are common to many pathways.  For example, look at the tetracycline biosynthesis pathway 00253.  This pathway has a description at the top that includes this excerpt:

  Tetracyclines contain a linear tetracyclic skeleton, which is formed from a malonamate starter unit and malonyl-CoA extender units through a common polyketide pathway [MD:M00778].

Confusingly, that "common polyketide pathway" is actually a module, Type II polyketide backbone biosynthesis, acyl-CoA + malonyl-CoA => polyketide or M00778.

Note that this module is included in other pathways:

  map01056 map00253 map01100 map01130

Looking at the drop down menu at the bottom of the module page, we see that the Reference Module contains multiple different KEGG Orthologs that perform the same function in different systems.

Choosing an organism from the drop down menu, the specific Orthologs used by that species are highlighted.

So, you can see how separating pathways into modules can help in identification of these components in other organisms, even if the full pathway does not exist.


Sickle cells usually die after about 10 to 20 days, compared to normal red blood cells, which live an average of 120 days. The bone marrow can't make new red blood cells fast enough to replace all the dying ones which causes anemia,low blood count that results in fatigue,shortness of breath and related symptoms.As the cells are made normally but die too rapidly,this is termed as haemolytic.