X-recessive disorders and genetic markers

Genetic markers don't cut the DNA. They're simply regions of DNA sequence that happen to be variable between individuals (see my answer to your previous question). They might be measured using restriction enzymes (i.e. RFLP) to identify the exact difference, but it's not the marker that's cutting DNA. Furthermore, they don't necessarily cause disease. They're used in pedigree analysis to find regions that are linked with various phenotypes, among which is disease. However, linkage does not imply causation, especially with so few individuals.

To answer your first question II:1 isn't in the affected family - he married into it. In the affected family, A1 has become linked with the disease mutation. It is not necessarily linked with the disease in other families.

This is also the answer to your second question. I:2 has A1 marker on one chromosome associated with the disease allele, and one that's not. II:3 presumably inherited an X chromosome with the disease allele.


Do you know of any disease where HLA / MHC association discovery has led to better treatment or management?

I don't know any true disease associations, but since this question still has no answers, I'll offer one...

One class of associations you might be missing is difference in drug response. Patients with HLA-B*5701 are known to be hypersensitive to abacavir. Genetic screens are available to screen for this allele, and this information is used clinically.


Determining how much energy a plant takes in?

Just a speculation for whether diamond berries could exist or not. This is not an answer for "what is the energy uptake rate of plants" because the actual question tends to be "whether a plant can gather enough energy to form diamonds". For energy uptake rate of plants please see MCM's answer.

Even though enthalpy of formation is same as heat required for destruction, burning a diamond is much easier than creating it (I presume it is easier to generate high temperature compared to high pressure). Natural diamond requires both high pressure and temperature to form. Synthetic diamonds are made by chemical vapour deposition; that also requires high temperature. Such high energies cannot be produced by any known organism (requires devices like arc furnace), and moreover at these temperatures the biological structure will disintegrate.

However there is one possibility of diamond berries; the berries would not be solid diamond though. A plant could be growing in an area where there are a lot of nanodiamonds (meteorite rocks) which could be bioaccumulated in the berries. Living organisms do accumulate nanoparticles [1,2]. There have been studies on biological application and effects of nanodiamonds too [3,4]. However these would not look lustrous like bigger diamonds. Xylem vessels in trees have a mean diameter of 30-40µm; it may be possible that the plant can take up bigger sized diamond particles. Density of diamond is ~3g/cm3 — three times that of water and it would require thrice the force required for water to get diamond to the destination.

For a spherical diamond of diameter 20µm:

Cross sectional Area = 314.15 µm2
Volume = 3351 µm3
Mass = 3×3351×10-12 ≅ 10-8 g
Gravitational force on the diamond = 9.8×10-8 ≅ 10-7 N
Pressure required to counteract gravity = 10-7/314.15×10-12 ≅ 3.18×102 Pa

However, I am not sure if that much of pressure can be generated within a vessel and whether small particles can be lifted like this.

There is another possibility that bigger diamonds are encapsulated by living tissue (not the fruits of course).


Examine the effects of Enzyme A on its own.

Enzyme A performs two cuts that result in 2 fragments that are 5000bp long.
We know that the first cut is made at the 100th bp.  Therefore the second cut is made at the 5100th bp (A2).

You can stop there and determine that the answer is C.  C is the only answer that states A2 = 5100.


Does every mitochondrion in a cell contain the same DNA?

This link seems to have good information that answers most of your questions.

In my mind, there are two types of mitochondria: ones that work and ones that don't. Mitochondria do have DNA but that mDNA is there to encode proteins for their specific functions (e.g. to create ATP). So, although the mDNA may not be uniform for every mitochondrion in your body, it is most likely functional unless you have a mitochondrial disease. If you do have a mitochondrial disease then it suggests that some of your mitochondria are functional and some are not (otherwise you would be inviable).

As discussed in the comments, all DNA undergoes mutations so that even identical mDNA genomes may vary after undergoing some mutations. It's possible that only one genetic line of mitochondria was passed to you from your mom. In this case all the mitochondria in your body would be identical (except for minor mutations). It's also possible that your mom inherited and passed on to you more than one genetic line (as is the case in viable mitochondrial disease).

Mitochondrial repair mechanisms do exist but they differ in various ways from nuclear DNA repair and may be more prone to damage.


Does gross production (P) and biomass (B) mean the same?

Searching for context from what you wrote, I found this which seems to be an original article later introduced to the textbook you are using. I think this other version is more clear; P refers to photosynthesis, which is also gross production of biomass; B/P is the ratio of standing biomass to new photosynthetic product; rate of biomass production seems wrong unless you expand it to "existing biomass relative to rate of biomass production."

In summary, the correct interpretation should be that P is indeed the gross production, but B/P is simply the ratio of biomass to the gross production. If R is the loss of biomass through respiration and R < P, then both B and B/P will increase (i.e., you will accumulate biomass) until P=R. Probably in this process both P and R also increase, but what is important is that B/P is increasing, which means the new biomass isn't as efficient at new photosynthesis (presumably either because light is a limited resource or because more of the biomass is not held in photosynthetic organisms).

P is in units of mass/time; R is in units of mass/time; B is in units of mass. The equation would be dB/dT = P - R, or another way, B(t1) = B(t0) + (P-R) * (t1-t0), where t1 is some time after t0.


In this answer I'm building off of @Fizz's pointer to the nice paper by Laurence Knowles, "The Evolution of Myelin: Theories and Application to Human Disease" [1].

First -- I just want to point out that your question is adaptationist, which means that it assumes that myelin is on some axons and not on others for a reason. Whereas maybe evolution just hasn't gotten around to it yet, even though myelinating all axons would actually be beneficial.

That said, here are two of the main downsides of myelination:

It might cost energy. This one is a bit controversial, but at least one study has found [2] that while myelin decreases the energetic cost of firing an individual action potential, the whole apparatus involved in myelin (e.g., in the CNS, the oligodendrocyte, its processes, and the sheath itself) actually costs more energy than it would cost to just open all of those ion channels without saltatory conduction.
Myelin and its associated oligodendrocytes/Schwann cells take up space. This is likely to be especially important in areas of the nervous system where there are a lot of neurons packed into a small area.

So from the adaptationist perspective, the question is whether the benefits of myelinating an axon, such as increased conduction velocity, increased conduction fidelity, axon protection, and supplying the axon with nutrients, are worth the downsides of taking up space and possibly increasing net energy use.

http://www.ashdin.com/journals/JEM/235996
http://www.jneurosci.org/content/32/1/356


How can you test what color different people perceive?

One way we can get evidence qualia are the same or very similar for different people is by reactions to it, beyond just the word.

For example, beyond the word "pain", we have other strong reactions to pain. So nobody
suspects other people might experience pain as pleasure and vice versa. Obviously not!
There are no obvious signs for colour qualia, so it makes sense to suspect some people experience red as blue and vice versa.

Still, there are weak reactions to colours, like sometimes certain colours are associated with certain emotions. But, this is very weak evidence and could easily mismeasured, or be bound up with culture rather than biology.

We could test it: take pairs of identical twins at birth (so that they haven't learned words for colours yet), re-wire optical nerves of one of each pair so that red and blue receptors were switched (and perform a placebo operation on the other one, so they don't know who is who), and see whether there is any statistically significant change in the attitudes to different colours or the like as they grow up.

The experiment has various technological and ethical problems :-) But it could be done in principle, so to me this shows the question isn't meaningless, just that it's hard to find the answer.


Mixed-mating plants: is the number of mixed mating plants supposed to be trivial?

I think the main message of the quote is

"Many would have expected that mixed mating can only exist as a transitional state and thought that stable equilibriums are either pure selfing or pure mixing (or both). The observation of a non-trivial number of mixed mating populations suggest that our expectations were wrong."

The first sentence of the quote is a statistical detail of their paper and not a premise for the conclusion that there is a non-trivial number of populations that show mixed mating.

The evolution of selfing is a large topic in evolutionary biology and cannot really be summarized in a single post (even more so that many question are still open to debate). Goodwillie et al. 2005 is a review on the subject that will help you understand the work that has been done on the evolution of selfing. Very related is the evolution of hermaphrodism, dioecy and other mating systems in plants. Pannell 2002 is a very good paper on the evolution of androdioecy and the maintenance of these unexpected mating systems.


What limits the size of fish compared to marine mammals?

I'd suggest that one factor could be the difficulties of breathing water - it is highly inefficient. The following is a summary of this response to a TREE article.
Fish spend 10-30% of their energy on breathing because it is so inefficient to use gills because diffusion rates are much slower and oxygen is less abundant. Gills grow in proportionate scales to body size, generally for every 100% increase in body size there is a 50-90% increase in gill size. Thus the larger fish species are working on a lesser body mass/gill size ratio so they can't take up oxygen very easily.
From this I'd suggest it is difficult for fish to grow gill systems much larger than those of a whale shark as it would become to inefficient for them thrive. By comparison whales are air breathers so, despite "breathing" (collecting fresh air) less frequently they can get much more oxygen from it.
I'm sure there is more to it but at least this is a starting idea. If anyone has more then feel free to add to/edit this answer, I merely suggest this as one possible theory and it is not my field.


If someone with "XO" is one of the identical twins with the other twin as male, then what would the sex chromosome of the other twin be?

"XO" (an unpaired X chromosome) is characteristic of Turner syndrome.  The Wikipedia article https://en.wikipedia.org/wiki/Turner_syndrome provides a typical image - a woman with a fairly distinctive broadness of the neck.  The phenotype is described as female, though of course gender identity can be unpredictable for anyone.

For the other monozygotic twin to be phenotypically male, the most likely explanation is a Y chromosome - a Y chromosome that was lost in all or many of the cells of the XO woman.

A set of monozygotic twins with one XXY and one XO would be very surprising - in other words, with the twins differing by two chromosomes - would be very surprising.  But nothing is truly impossible in biology.  And ... this may be such a reference, but I didn't look at the full text to make sure: https://www.ncbi.nlm.nih.gov/pubmed/27315788


In which month should I map maritime vegetation?

One way to approach this problem would be to look at herbarium collections of the taxa that you're interested in. Usually, a flowering or fruiting specimen is easiest to identify; but no matter what character is best for your taxon, if you look at the herbarium collections and see that
-most of the collections identified to species, or
-the especially good-looking collections, or
-flowering/fruiting collections,
were made in a certain month or season, that could help you to narrow down your time window.

As a bonus, in reviewing herbarium collections, you'll have given yourself a step towards being able to identify the species.

Some herbaria have some collections online; here, for instance, are records and images for online Puccinellia collections at a number of UK herbaria.


How does residual chlorine in tap water work?

Actually, I think that to qualify this statment, you should use about a 3.33% solution of household (5%) bleach for disinfecting. So that's actually, 0.15% sodium hypochlorite solution.

Also, time and pH are factors. A 0.15% bleach solution will kill many bacteria within 5 minutes. But after a few days, a more dilute solution will also have killed many bacteria.

Also, given that household bleach has a pH of around 11, a 1% solution will have a pH of about 9. The optimal pH is about 6, where all of the -OCl is converted to HOCl which is roughly 80x more effective as a germicide.

So, I realize that 0.5mg/L is still about 3000 times less than 1.5g/L (= 0.15%), and that's the real question. The real answer is that the place where the bleach is added (in a municipal supply) is at the filter, where bacteria collect. Once the old filter has been bleached the fresh water supply is allowed to resume which flushes the bleach along (at tolerable levels). Also, they often use other oxidizing agent which are synergistic with HOCl, so that they can reduce their cost and improve the function.


Double use of ATP in relaxing myosin & active transportation of calcium?

ATP is used (hydrolyzed) by ion pumps to transport ions such as calcium against their concentration gradient.

Molecular motors (such as myosin and kinesin) also couple ATP hydrolysis with movement.

However both these processes are separate and just because calcium flux changes happen during muscle contraction doesn't mean that it is the same ATP that drives some kind of a bifuntional enzyme to perform both tasks.

Moreover calcium is released during the contraction phase from the sarcoplasmic reticulum (SR); pumping back the calcium to the SR happens during the repolarization (there is no myosin movement at this stage).


Identifying a creature that appears to be a worm wrapped in a cocoon

I think it's just a case bearing moth larva (Tinea pellionella).

Source: http://www.hantsmoths.org.uk/


Does covariance and phenotypic variance have to be for the same trait to calculate narrow-sense heritability?

Yes. See below for more information.

  Can I still calculate the narrow-sense heritability of AA [..] even though they're different traits?

No, you can't. A measure of heritability makes sense only for

a given trait
a given population
at a given time
in a given environment

  [I'm also told that if any resemblance between parents and offspring is completely due to genetics, ie. without environmental effects, then $h^2$ is 0.5, but I'm a little confused with it.]

The above is not a exact quote from you but the original sentence made no sense. I rephrase what I suppose you tried to say.

The formulation is inaccurate and could therefore be misleading. It is wrong to say that any covariance between parent and offspring is only due to genetics. In reality, environments between parent and offspring often covary. There might also have covariance due to epigenetic reasons and potentially many other reasons.

You cannot make any claim about what value should $h^2$ takes for the special case where covariance between parent and offspring is solely due to genetic variance (or any other special case considering only genetic variance). You still need to know the relative importance of the genetic variance to the total phenotypic variance. If any of this is unclear, then you should keep on with the recommended reading below.

Reading Recommendation

I recommend that you have a look at Why is a heritability coefficient not an index of “how genetic” something is? for an overview of the concept of heritability and common misconceptions.


The one I found is Ovomucin,though it's not a pure carbohydrate.

Ovomucin is a highly glycosylated protein and approximately 33% of ovomucin is made up of carbohydrates.

Nutritional Values of Egg White Proteins paragraph of
http://ps.oxfordjournals.org/content/92/12/3292.full
So you can see it's mostly a protein.

Ovomucin is a trypsin inhibitor found in raw egg white.
Ovomucin is responsible for the gel properties of fresh egg white and is believed to be involved in egg white thinning. Ovomucin is composed of two subunits:

α-ovomucin - carbohydrate-poor with a molecular mass of 254kDa

β-ovomucin - carbohydrate-rich with a molecular mass of 400-610kDa

Souce: Wikipedia


How to evaluate the efficacy of an antibody for fluorescence microscopy?

When testing an antibody for an imaging application, it is almost always a good idea to test it in another application like ELISA or Western blotting to see if it binds the target of interest. For example, try to find high- and low-expressing cell lines, load equal amounts, and see if there is a difference in signal at the expected molecular weight. Check the company's literature or contact their technical support to see if they have tested the antibody by immunofluorescence (IF), and if so what their results were and how they validated them. Check the literature to see if other people have published with this product. http://highwire.stanford.edu is a pretty good full-text search engine, but they don't have all journals in their database. Google Scholar can help, too.

You can also use your high- and low-expressing cell lines to see if there is a stronger IF signal in the high-expressing line. Look at your images to see if the signal is localizing where you expect it to, and do co-staining with antibodies to other proteins that should co-localize with your target of interest. For example, if your target is expected to localize to mitochondria, co-stain with COX-IV. A quick Google search found this Cellular Localization IF Antibody Sampler Kit that has controls for several different organelles and other specific locations.

Make sure you are following the manufacturer's recommended protocol. Don't crank the gain up too high on the scope, because non-specific background goes up, too. Look at the induction of signal between high- and low-expressing cell lines. Generally you would want at least a 2-3 fold shift, especially if you see a strong change in signal intensity by Western. Try using siRNA or similar silencing technology to knock down the signal in your cells, and validate using Western and IF.

Ultimately, you can never be absolutely 100% certain that an antibody is binding a certain target, and only that target, but you can accumulate a lot of evidence to show that it is likely. Try to put yourself in the mindset of a reviewer, and objectively convince yourself that the signal is real. If you can't, then shop around and try something else. Good luck!


Is there an absolute minimum intensity level to the stimuli we can perceive?

There are limits to what a sensory system can detect, which is called the detection threshold. To determine the detection threshold psychophysical methods can be used. A straightforward way to determine the detection threshold is with a yes/no task, where the subject receives stimuli with various intensities. An arbitrary point, mostly the 50% correct-rate, is then defined as the detection threshold. At this point, the subject correctly detects the stimulus 50% of the times. The response curve in a psychophysical task typically takes the shape of a cumulative function such as the one shown in Fig. 1.

Hence, the detection threshold is an arbitrary point, because people are not machines and show variability in their decisions. The detection limit of, e.g., electronic devices is much more precisely defined. The exact values of the detection limits depend on the exact stimulus (visual, tactile etc.) and depend highly on the exact stimulus. For example, in the visual domain the detection limit of light depends on the color, the location in the retina tested, dark adaptation etc etc, and in the tactile domain static pressure stimuli have a different threshold than vibratory, different body parts have different thresholds etc. etc.

Fig. 1. Psychometric curve showing 50% threshold of a visual stimulus. source: Webvision

Training to lower the detection threshold (i.e. improve detection limits) is indeed possible (Sterr et al., 1998).

Reference
Sterr et al., J Neurosci (1998), 18: 4417-23


How can i confirm that the given pedigree chart is of an autosomal dominant trait?

Sure, both are possible here!

Your book probably makes an implicit assumption of low frequency for the "red allele".

Assuming, "red" means "disease", it is quite standard to assume that the "red allele" is at low frequency in the population. If this is the case, then it is unlikely that partners of the members of the main family being represented in the tree carry this allele. It is therefore quite standard to assume that partners does not carry the "red allele". If this assumption is made, then recessive autosomal cannot explain the observed tree.


What is the difference between "dikaryotic" and "heterokaryotic" states in the sexual lifecyles of fungi?

A heterokaryon is a fungal cell which has two or more genetically-distinct but allelically-compatible nuclei, as suggested by this resource, as well as this Wikipedia article.

A dikaryon is a fungal cell which has precisely two genetically-distinct but allelically-compatible nuclei, as shown here and here.

In this sense,  a heterokaryon is a general term, whereas a dikaryon is a specific term. A dikaryon and a trikaryon (although not often seen in literature) are both heterokaryons.


Why can't the brain and red blood cells use fuels other than glucose?

In the case of red blood cells: human erythrocytes (red blood cells) have no mitochondria. Since the mitochondria are the cellular site for oxidative metabolism of fatty acids, erythrocytes cannot oxidise fatty acids to release energy. The erythrocytes also cannot fully oxidise glucose (to carbon dioxide and water) because this is also a mitochondrial process, so they have to rely upon anaerobic glycolysis. The end product of anaerobic glycolysis is pyruvate, and erythrocytes reduce this to lactate (to recycle the NADH that is produced during glycolysis) and then export this lactate into the blood for further metabolism by the liver.


Why do bacteria die in a high sugar content environment?

In (very) short: enzymes are necessary for life. Cytoplasm is necessary for enzymes to function. Water is necessary for cytoplasm to exist. Cells have osmotic membranes.

Given a cell in a solution (even a goopy one, like jam) with a very high concentration of sugar, water will move along a gradient of low to high sugar concentration, in other words, water will move out of the cell and into the jam, thus stopping all major activity in the bacterium (basically stopping it from reproducing, if not exactly killing it. The killing actually comes from heating the jam and canning it while still hot enough to kill most bacteria.)

Plasmolysis: The shrinking of protoplasm away from the cell wall of a plant or bacterium due to water loss from osmosis.


First, it's not true that all animals have two eyes. For example many spiders have four, six or eight eyes whilst worms have none, but all are animals.

In simple terms, the reason typical mammals have two eyes is probably similar to the reason that cars usually have four wheels, the reason houses keep out the rain and why coffee cups have handles. It's because that's what works.

Each time an organism develops, there is a high chance that the genetic information that built it will include something new. When that happens, most often the phenotype (essentially, the organism's appearance, such as how many eyes it has) does not change. The organism looks the same as its parent(s) did. If something significant does change, it is most likely to be bad news for the new organism. The chances are the organism will not survive and the particular genetic information that built it will not used again. Hence, organisms don't tend to be that different to their parent(s). Dogs don't give birth to cats.

But just rarely, this new combination produces something different and useful - useful enough that the organism is particularly successful and a good fit for its environment. In that case, simply because it can, the organism has more offspring and more of those offspring themselves survive to have offspring of their own. The genetic information that built the organism is thus used to create more, similar organisms.

So, the first eyes were produced by accident. When eyes turned out to be useful, subsequent generations from the first organism with eyes were more likely to have eyes themselves. As it turns out, analysis of genomes shows that eyes have evolved like this multiple times.

We can only assume that since mammals typically have two eyes, either the random genetic accident that would produce different numbers of eyes in mammals has never happened, or if it did happen, the result was not a good fit to the environment.

Why not no eyes? Human beings are occasionally born without eyes and the cause may be genetically inherited. One might reasonably imagine that for much of human history such a child would be unlikely to survive into adulthood and thus pass on this mutation.

Why not one eye? One reason in the case of primates is that two eyes are useful for estimating distance, which is difficult with one eye. A two-eyed animal has an advantage against predators, making it more likely the next generation is going to have two eyes.

Why not more than two eyes? Perhaps a larger number of eyes requires a larger head making childbirth impossible, or perhaps it requires too much energy to sustain. Who knows? What we observe today - humans typically have two eyes - means that, if that mutation for more than two eyes did happen at some stage, then more than two eyes wasn't optimal for the environment in which the resulting organism found itself, so it didn't get passed on to the next generation.


No, you don't. Having the DNA in your hand means that you have access to a macromolecule, not more.

Think of the DNA as a book (or a library). From holding the book in your hands, you don't know what the content is. You have to actively read the book to get this information.

Sequencing a piece of DNA is basically the same. Your readout is the sequence of the bases which is essential to understand (or do research on it) a certain piece of DNA. With this knowledge you can see where genes start and end, define introns and exons (for eukaroytes) and so on.


I can't think of any way to start with an intestinal "blank slate", so to speak, except with antibiotics.

Perhaps it's possible to at least partially homogenize/standardize a sample group's biota with probiotics?

If it's ethics you're worried about, perhaps draw experimental subjects from a pool already being treated with antibiotics (although this, I suppose, introduces it's own biases?).


Is human vision sensitive to frequency or wavelength?

It is not the wavelength or frequency that determines light absorption- it is the energy of the photon that matters. The energy of incident light should match the excitation energy of the chromophore. The medium itself can also affect light absorption by electronically interacting with the chromophore. Frequency is proportional to the energy (given by the relationship $E=h\nu$); while wavelength and velocity change in different media, frequency and energy remain constant.

The chromophore in the opsins (retinal) absorb energy to become active and you can say that they detect the frequency. However, sufficient number of opsins have to become active for the retinal cells to transmit the signal. So the overall light flux is also important. An interesting thing to note is that activation of the opsins hyperpolarizes the photoreceptor cell and reduces its tendency to fire.

Wavelength plays a role in diffraction and therefore diffraction is less in a medium with higher refractive index. Wavelength also determines scattering. So, while the opsins actually detect frequency, the wavelength can slightly affect the overall "vision" because of scattering/diffraction effects.


A research, detailed in a 2012 issue of the journal PLoS Biology, suggests the fish do indeed take naps and can experience sleepless nights.

Another research with Pacific sand lance species, found them utilize a one of a kind methodology of tunneling into sand to rest and moderate vitality, and to maintain a strategic distance from predation.

Therefore, we can assume that fish sleep cannot be related to a terrestrial. As @Zxyrra has mentioned, with the currents being random in their direction, we can connect the reasoning of the continuous movement of the fishes as an effort to stabilize themselves.

On the aspect of any evolution or biological reasoning, fish sleep is still an ongoing research in marine biology. An interesting research have opened up a case in which through evolution, cavefishes have lost sleep. Information from this research could help you understand the evolutionary relationship of fish and sleep, in atleast, a broad scale.

UPDATE: Unique method of sleep in dolphins.

At the point when it's an ideal opportunity to rest, a dolphin will close down just a single side of the equator of its mind, and close the inverse eye (the left eye will be shut when the correct portion of the cerebrum dozes, and the other way around). Amid this time, the other portion of the cerebrum screens what's going in nature and controls breathing capacities. This process is termed as unihemispheric slow-wave sleep.


If due to some reasons a small portion of our neurons die, how does our body remake them?

Evolution set us humans up to not regenerate our neurons on the whole, which is a pity since we can regenerate our liver cells, so it's not an impossible feat. If neurons die because you drank too much, banged your head, or just because they got old, they are gone. If this death is accelerated like in Alzheimer's disease, you can literally see holes in the brain autopsy. That said, we now know that in a few exceptional areas of the brain, neurons do regenerate. It's not many cells but it's something. The two areas known to date are the dentate gyrus of the hippocampus (DG below) and the subventricular zone of the lateral ventricles (LV). See the green zones in the image below.

From Ernst & Frisen PLoS Biology 2015 (CC-by)
In those areas, like elsewhere in the body, new cells are made from stem cells, that is infant-like cells that have the potential to become many cell types. If we could only understand why some cells regenerate and others do not, we might be able to promote this. Alas, our current understanding is woefully incomplete. We'll need more research # # # before we can dream of regenerating our neurons.


Who are humans' closest relatives, after primates?

Short answer

It is a flying lemur (there exist only 2 species). Flying lemurs and primates are together a sister clade to treeshrews.

Easy source of information

Have a look at the post The best free and most up to date phylogenetic tree on the internet?.

In short, you can have a look at onezoom.org, tolweb.org or opentreeoflife.org by yourself!

Tree of life of placental mammals

Here is a screenshot coming from tolweb.org.

In this tree, there are polytomies showing everything that is unknown. This tree was last updated in 1995 and there are also clades that we now know were misplaced including the bats (as commented by @NoahSnyder). It is not handy to make a good screenshot from onezoom.org or opentreeoflife.org so I just welcome you to explore the tree of life by yourself on onezoom.org or opentreeoflife.org to get a better representation of the reality.

Tree of Supraprimates

Supraprimates (=Euarchontoglires) include all primates and a few of the most related clades. Stealing the tree from @Gwenn's answer, here is the tree of Supraprimates

[

Here is the original tree from Janecka et al. (2007)

Here we see that flying lemurs (=Dermoptera) is a sister clade of primates (ignoring the extinct plesiadapiformes) and treeshrews (=Scandentia) are a sister clade of flying lemurs and primates together. Below I briefly talk about these three clades and about their position on the phylogenetic tree.

Flying lemurs

Flying lemurs is a small clade that contains only two extant species, both found in the family of colugos. Note that flying lemurs are not lemurs (which is confusing). Here is what a flying lemur look like

The position of flying lemurs on the phylogenetic tree has always been quite uncertain. In the tolweb.org screenshot above, flying lemurs (=Dermoptera) is a sister clade to bats (=Chiroptera) and together they are sister clade to treeshrews and primates. However, Janecka et al. (2007) placed flying lemurs as the sister clade to primates. Together flying lemurs and primates are a sister clade to tree shrews.

Tree shrews

Treeshrews is a clade of 20 species native from southeast Asia. Before, the era of phylogenetic comparisons, treeshrews were mistakenly thought to be part of the Insectivora.

Extinct clade of Plesiadapiforms

Although they are represented above as a sister clade of primates, it is possible that they the fossil we found are just individuals coming from the lineage giving rise to primates. As such, they would not be a clade aside from primates. Below is an artistic representation of what they may have looked like.

Introduction on phylogenetic trees

As the question is quite introductory, I presume you might want to improve your understanding of phylogenetic trees. You might want to make sure, you understand what a monophyletic group (=clade) is and understand why a chimpanzee and a human are both equally related to any species of treeshrews.

Here are two sources of information for you:

Understanding Evolution (UC Berkeley) > The history of life
This answer on Biology.SE


In general, sweating is caused by too much heat, even if you're not aware of the heat. This can happen if the bowel moves and so raises the core temperature. Such movement is often accompanied with sweating, and since you only feel the normal temperature on the skin, it is cold sweat. But at the same time your core is hot so you think it's cold, but it will later mix to normal.

Anyway, it points to unusual bowel movement. This can be due to food allergy or, in a milder form, in food intolerances which are quite common. When it comes to sour ingredients, they are often in fruits, so I'll make a shot in the blue and say that you have a food intolerance against some fruits. You can check this hypothesis by trying chemically pure acetic acid to sour your food. If that doesn't result in sweat/hotness then it's probably the fruits.

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

The Wikipedia points even directly to salicylate in fruits but I think you cannot exclude allergies against essential oils like limonene and such. Plants are really chemistry factories and not all is well that you can get with them.


There are a few reasons for not feeding cooked foods to worms (Eisenia spp.) in a smaller household size worm farm. It's not because the food is cooked but what it often contains.

The earthworm used in vermiculture is usually Eisenia fetida (red wigglers) though other Eisenia species are sometimes used. All Eisenia are epigeic species meaning they live in the junction of decomposing organic matter (such as leaf litter, aging manure, rotted fallen trees) and their natural food is decaying plant matter and bacteria that are also digesting the organic matter. They don't make use of small dead animals (meat and fat).

In large scale commercial vermiculture operations, leftover and past-due-date foods from restaurants, institutions, nursing homes and schools are used along with plant matter and carboard and paper. I'm not sure how they balance cooked foods but possibly much less is used than plant matter.

The fact food is cooked isn't the problem but what's in it and/or what happens to it when added to the bin. If you have leftover vegetables and fruit that's been cooked with no added salt, it's perfectly acceptable. A certain amount of sweetened cooked fruit is also fine as the worms will eat that too. But ready-made foods usually have preservatives, salt, fats and spices added. Either worms won't eat it, leading to odour caused by mouldy rotten food, or it can make them unthrifty and even killing off your worms if it's fed them repeatedly.

Fats and meat along with cheeses and dairy products will also not be eaten so shouldn't be used. Sites about vermiculture say onions and garlic can 'burn' the worms skin which is the problem with citrus fruit. They can be used but in very small amounts and should be mixed well with their other food.

Vermicomposting for Business, Farms, Institutions & Municipalities

Wormy FACTS and Interesting Tidbits about Eisenia fedita


Can genetically engineering the DNA of a human zygote, make it a twin of another human in entirety?

The answer is no, and it is because sequence of the genome is not all information that is required for gene expression and development, there are also epigenetic factors.

A lot of patterns of epigenetic marks, such as most of DNA methylation and some histone modification patterns, are set during parental germline development, and these marks are transmitted to the zygote by gamets (except paternal histones, those are not transmitted because they are temporarily substituted for protamines in sperm for greater compaction). Therefore, the naked DNA inserted into zygotic nucleus will not have access to the machinery that established epigenome during development of the gametes.

And even though nucleosomes may assemble in the zygote on the naked DNA and histones may acquire post-translational modifications, and cytosines may get methylated, but most definitely the zygote is going to have no means to correctly set distinct patterns of epigenetic marks at alleles that are normally imprinted, i.e. those alleles whose epigenetic state depends on the gender of the organism that produced the gamete.

Therefore, the twin created in this way will have the same DNA sequence, but it will be a  subject to disorders associated with imprinting


In summary, cellular respiration and thermogenin.

Most of the energy in our body comes from cellular respiration. Cellular respiration is how ATP, the major source of cellular energy, is made from glucose. Cellular respiration generates heat mo matter what because not all of the energy from glucose is converted to ATP.

In certain cells, a protein known as thermogenin allows the protons in the cellular respiration to flow from the inner membrane to the matrix (the protons are in the inner membrane of the mitochondria as the electrons from glucose were used to pump them). This generates heat. In regular cellular respiration, the proton gradient is used to make ATP, but now, it juet generates heat.

Also, ATP can be hydrolyzed directly in brown fat cells and muscle cells to produce heat along with inorganic phosphate and ADP.


Eventually, I've stumbled upon an article which calls it a cigar jellyfish.

Further research even shows a very empty entry on Wiki about it, which consists of the single line entry:

  The cigar jellyfish (Olindias phosphorica) is a species of jellyfish from the Central and East Atlantic, and the Mediterranean Sea, including off Malta.[2]

Also an interesting article about it being 'rare' in Malta (despite the above information)


How long can a naked human survive on Mars?

Long story short, the astronaut probably wouldn't make it, and would first loose consciousness then suffocate.

There is a lot of myth and hollywood dramatization regarding this kind of thing. Here are some:

You will explode. This is just ridiculous. The skin is air tight (relatively speaking). It is also very elastic and can pull and bend quite a great deal before tearing. Through quite a few, equally durable, tissues, it is connected to the bones, which are unaffected by negative air pressure.
Your blood will boil. The circulatory system is also a closed system. It is not directly exposed to the environment. Also, the blood pressure in a healthy person is averaged around 100 mmHg and Earth's atmosphere at sea level is 700 mmHg. There is already a massive disparity, yet Earth's atmosphere doesn't go pouring into our veins at random. Likewise, the blood in a person's veins won't go pouring out into the atmosphere simply because the pressure is extremely low.
Any air in your lungs will be forcibly sucked out of you. Again, this is a closed system, if you hold your breath. As long as you don't try to breathe there is nothing forcing the air from your lungs.
Your eyes will be sucked from their sockets. Thank you Total Recall (the original) for this myth. The eyes are very firmly in place. You might feel a pull on them, but they aren't going anywhere.

Absolutely none of these would happen in the vacuum of space and certainly not on the Martian surface.

Here's what will happen:

Any liquid material on the surface of your body will vaporize. All sweat, saliva (if you open your mouth), water in the mucous, and tears on the eyes, will nearly instantly vaporize. It would be quite uncomfortable, especially the eyes, but very survivable. Long term exposure to a vacuum might damage the eyes eventually, but in this scenario there are far more pressing matters.

The negative pressure may also cause your eardrums to rupture. Try to imagine the feeling your ears get on the plane at 30 thousand feet times about 100. Since you can't close your ears, plugging them with your fingers may help, but likely just postpone the inevitable pressure disparity, which will lead to at least great discomfort and possible drum rupture.

If you had the chance, you should take a deep breath before jumping out and avoid trying to breathe at all costs. Opening your lungs for a breath would very quickly draw whatever breath you had in them out into the atmosphere and also vaporize any fluid that was in them. Considering the rapid pace of this event, you would surely have permanent damage from this and begin suffocating and will die in a minute or two unless you get medical attention. There seems to be conflict in the procedure for this, with some sources suggesting that emptying your lungs would be better to avoid this. Considering the astronaut in your example is about to do a 200 meter dash he is going to need all the O2 he can get.

The cold is also a treacherous factor. At -50C the heat from your body would dissipate so rapidly that it would likely be very debilitating, perhaps causing you to seize up and clutch your extremities to your chest. It would also be excruciatingly painful. It might cause you to fall into shock. In a total vacuum however, this does not exist. A vacuum is actually very insulating, but on Mars' what little atmosphere is there is enough for you to feel the chill.

The lack of oxygen and high CO2 would be what would eventually kill you. You would eventually try to breathe and loose consciousness within a breath or two (or you might loose consciousness first then your body would try to breathe naturally). Your body would try to keep you alive as long as possible by pumping your heart faster and increasing your blood pressure, but your heart would eventually fail and you would die within seconds after that.

Evaluating your particular scenario

There are first a few things about the scenario that seem unlikely.

The astronaut would not be naked. They remain in some of their protective gear in case of emergencies like this. He would have some protection against the cold if he had to run out without it.
Certain things like extinguishers are always nearby. The idea that one was unreachable is a little silly.
Space vehicles, shuttles, and buildings all are compartmentalized like a submarine. They could simply close off the affected areas.
Fire only burns in the presence of oxygen (with few exceptions). After being closed off, compartments can be decompressed, halting the fire immediately. They can then begin refilling them with breathable atmosphere. This poses the same vacuum problem if the astronaut is in the affected area, but he won't be trying to run across the surface naked. People have survived rapid decompressions before without a single injury, as listed in my second source, however, others have never regained consciousness.
Assuming you made it to the other building, they usually only open from the inside. So unless someone saw you coming and opened the door for you, your last minutes would be better spent desperately fighting the fire until it consumed you rather than banging on the neighbor's door.

But let's say all of this breaks down and poor Astronaut Joe finds himself making a mad, streaker's dash across the Martian surface.

We should assume that our astronaut is both quite athletic and knowledgeable about the environment outside of his shelter, knowing that he should take a deep breath before heading out, but literally has no time to grab a shirt, goggles, breathing mask, or anything. Just him and Mars.

If he's lucky, it's not too cold and he doesn't seize up and fall into the fetal position within a few steps. Let's say it's -20C, which is pretty darn cold, but tolerable for a minute or two. I next see him flailing across the surface, trying to run in Mars' low gravity (no easy task). He begins to loose vision as a cloud of steam of what should be tears pours from his dry eyes. His eyelids then begin to stick to his eyeballs because there is no longer any lubrication. He is desperate to reach the other building, and his movements get more and more erratic, as his body is rapidly using all of the available oxygen. All the while, he is still holding his breath, knowing that if he attempts to breathe he will likely collapse within seconds and perish. But the more he struggles to make it, the more his innate urge to breathe overpowers his conscious thought to prevent it. Eventually, against his own willpower, he gasps and attempts to inhale deeply. He takes two or three dying breaths, if they can be called that, then falls to the ground unconscious. He dies shortly after when his heart stops and his brain tissues die.

The whole ordeal lasts under 30 seconds and he is 100 meters at most away from his shelter. If he did get lucky and actually made it to the other building, he would likely have frostbite over much of his body, permanent damage to his eyes and ears, and possibly deadly exposure to cosmic rays.

The event would be very similar to being drug by a fishing line to the bottom of the sea and drowning.

Sources:

A fun questionnaire to see how long you would last in space
What really happens in a vacuum


Although current research has little to say about the effects of exercise on personality, there has been recent correlations demonstrated between personality and the "drive" to exercise--specifically, aggression as a personality trait has been linked to higher metabolic rate. See http://phys.org/news206006380.html for more information about this.

The causation in exercise-induced neurogenesis is not well understood. A correlation that has been found (in mice) is the presence of a hormone called beta-endorphin, which is attributed to positive affect (a boost in mood). Exercising mice that demonstrated the presence of beta-endorphin in their hippocampal region did experience exercise-induced neurogenesis, while those that naturally lacked beta-endorphin did not experience neurogenesis.

The basic worth of circulation should not be overlooked, either. Anything that gets your blood pumping more efficiently means that the more distal parts of the body will appreciate an influx of nutrients. A smoker with poor circulation (as a result of lowered oxygen in the blood -- carbon monoxide competes for hemoglobin-binding) will have cold hands and brittle fingernails, and this is just a simple example of this phenomenon. The value of increased circulation to the brain shouldn't be overlooked -- the blood is our main transportation system, and the brain gets nothing that is not delivered via circulation. It's akin to watering a plant -- sure, it may grow it you give it 30 minutes of sunlight and 1/4 cup of water a day, but it will certainly grow to its full potential if it is fed as much as it needs.

Exercise is important, but it's easier to think about the questions you pose if you consider exercise more as a physiological stressor on the body. Muscle tissues are torn and damaged by exercise, but the body recognizes that it must need these resources (because of some present danger in the environment that caused you to run/strain yourself) so you begin to see the typical skeletal muscle hypertrophy. The heart is also made stronger through this strain, which is why regular exercisers have a lower resting heart rate -- it takes their heart less effort to pump the same amount of blood.


Pathogenesis of chronic venous congestion in skin?

Probably so simple answer is enough

acrocyanosis (manifestation of heart failure) which lead to distant (acro - distant) cyanosis, bluish skin.


Help with analogy: Competition among similar species

Here are some definitions of interest to you

Ecological succession is the process of change in the species structure of an ecological community over time. The time scale can be decades (for example, after a wildfire), or even millions of years after a mass extinction.
A seral community (or sere) is an intermediate stage found in ecological succession in an ecosystem advancing towards its climax community. In many cases more than one seral stage evolves until climax conditions are attained.1 A prisere is a collection of seres making up the development of an area from non-vegetated surfaces to a climax community.
In biology, a disturbance is a temporary change in environmental conditions that causes a pronounced change in an ecosystem. [..]  Because of these and the impacts on populations, disturbance determines the future shifts in dominance, various species successively becoming dominant as their life history characteristics, and associated life-forms, are exhibited over time.
Ecological facilitation or probiosis describes species interactions that benefit at least one of the participants and cause harm to neither.1 Facilitations can be categorized as mutualisms, in which both species benefit, or commensalisms, in which one species benefits and the other is unaffected. Much of classic ecological theory (e.g., natural selection, niche separation, metapopulation dynamics) has focused on negative interactions such as predation and competition, but positive interactions (facilitation) are receiving increasing focus in ecological research.


The Semi-Conservative Model of DNA Replication: Question

I believe the reason you are having trouble understanding the concept is due to a poor usage of colors in the diagram. Don't focus on the colors, but on the concept. It's the same for both replication events. Each strand of a double helix is used as a template to make a new complimentary strand, giving rise to two new DNA helices from the original. In each new double helix, one strand should match that of the double helix it came from before, as it was the template and is the same strand. While the other strand, the complimentary strand, has been newly synthesized to match the complimentary strand. In this diagram, every newly synthesized strand is shown in light blue.

Start by looking at the first double-helix of DNA (navy blue). During replication, the DNA is unwound and each navy strand is used as a template to create the newly synthesized (complimentary) strand, which is shown in light blue. In this first all navy double helix, you have two navy strands that are each used as a template strand and new complimentary strands (light blue) are synthesized to match . This produces the second two helices (navy and light blue). They each have one strand from the original helix (navy), and one new strand (light blue).

The process is exactly the same for the second replication event, only, a new color was not introduced to show a newly synthesized strand, so one cannot differentiate between the original (template) strand and the new complimentary strand. Both are pictured as light blue.

For the final replication event, only focus on the top navy and light blue helix first. Just as before, the two strands are separated from each other and are both used as templates to create a new strand. The navy blue strand is used as a template for a new light blue strand to be transcribed. This produces the top-most helix, where the original strand is shown as navy and the newly transcribed (complimentary) strand is light blue.

Just as the navy strand was a template, the light blue strand from the bicolored helix is used as a template strand as well to create the second all light blue helix. This light blue template strand is used to synthesize a new light blue strand, creating the all light blue helix. One of the strands is the original light blue one from the navy and light blue helix, while the other strand is the newly synthesized one.

It might've been easier if they had used a different color for the final round of replication, like orange. Then to show the newly synthesized strands in the final round, the 1st and 4th double helix would consist of a navy (original) strand and an orange (newly synthesized) strand. The second and third double helices would then have each had a light blue (original) strand and an orange (newly synthesized) strand. This would have made it easier to understand where each strand originally came from.


Can nociceptors die because of too much mechanical stress?

As far as I know, adaptation of peripheral receptors, including pain receptors, is transient (Giniatullin & Nistri, 2013)

Instead, my educated guess is that the increase in subjective pain threshold plays an important role. Pain thresholds differ between the sexes (Chesterton et al., 2003), and depend on disease and physical status (Kosak et al., 1996). Repeated exposure to painful stimuli hardens one mentally (I have practiced martial arts for two decades ).

Morever, there is an interesting answer on Martial Arts SE on the question How should I expect my fist to change over time from punching? Here it is shown that extensive training stimulates the growth of additional skin and bone. Extra skin (calluses) may dampen the impact of painful pressure stimuli.

References
- Chesterton et al., pain (2003); 101(3): 259–66
- Giniatullin & Nistri, Front Cell Neurosci (2013); 7(245): 1-9
- Kosak et al., pain (1996); 64(3): 415–23


What are mast cell membranes made out of?

Although the Wikipedia page on dermatographism refers to "weak membranes" it cites no source for this, and like Chris, I haven't found any mention of this in a quick look at the literature.

Histamine is usually released from mast cells in response to specific stimuli by a degranulation reaction (internal vesicles fusing with the surface membrane to release their contents) and I would guess that abnormal degranulation is a more likely cause than cell lysis.

In a recent paper (Ralph, JW (2013) Evidence for a role of neural pathways in dermographism. Brit. J. Dermatology 169, 1357–1374) a case is reported of a man who combines dermatographism with a syndrome called "stocking-glove neuropathy". This latter syndrome results in a pattern of loss of sensation in the lower arm. When the dermatographic reaction is triggered in this patient the resulting weal does not extend into the affected part of the arm, suggesting that neural activity is part of the trigger for dermatographism. In other words, in those suffering from dermatographism, sensory nerve activation would somehow result in cross-talk into the pathway for stimulating mast cell degranulation.


Do local field potentials (LFP) create waves on the surfaces of nerve cells?

A LFP can be measured at any point in space and is just the sum of all the fields generated by nearby charges.  Conventionally, it's assumed to be some distance from a cluster of neurons, but you technically could measure the LFP near the external surface of a neuron (but that would bias your signal towards the reading of that one neuron).

LFP's are relatively weak, but have some small influence on the neighboring cells:

Modeling the coupling of single neuron activity to local field potentials


Where can I find resources of the biological processes occurring after death of a mammal at various temperatures?

I believe William Bass has written on this, probably in the Journal of Forensic Sciences, but no specific articles come to mind. I'd start by looking for his articles, then probably with a variety of search terms using a filter for that journal. It's not open access, so you'll need to use a library or institution that has a subscription.


Paralogous genes in genome-wide association studies?

There is no literature report saying such a thing. However, I did a cursory check for GWAS study on neuroblastoma.

Selected SNPs with p-value>0.05
Converted p-values to a score —  -log10(p-value)
Mapped the SNPs to genes while calculating cumulative score for a gene

I just sorted the genes based on their names, assuming that many paralogs have similar names. I know it is not the right way to go about it. However, I found many similar named groups in the list.

Now the next step is find actual paralogs and to score the cumulative score for a paralog-group. This is a little task:

Get sequences of the genes
Run a BLAST search to find paralogs
Assign genes to groups and find scores

I can share the file with genes and scores. I would, however, continue only if someone is actually interested in pursuing this — this could be a research paper.

PS: If you want the file just comment your email id. Some IT admin idiot has blocked rapidshare/4shared etc


How do I make conclusions from the autoradiograph of a Southern blot?

As @canadianer pointed out in the comments section flanking sequence is a sequence that is immediately near the target on either side. Since chimps and humans are closely related and the sequence different is minimal (according to this paper its approx 4% for the entire genome)  so using human primers is totally fine.  Now if take a look at the picture of the gel:
 The answer is 2. only A because only this offspring has a variant in large amount (that can be determined from the width of the band) that can be acquired from both parents and in this case chimp A actually did inherit the 136bp variant from both parents.

For chimp 4 either parent can be the same (as for chimp A) from the two because it has the 136bp variant as well ( that can be inherited either chimp one or two), but has a different one that cannot come from chimps 1 and 2.

As you said chimp 5 can be ruled out instantly because it has a large band that cannot be found in either of the two parents.


It looks most like a common Green Lacewing larva - Chrysoperla rufilabris. Lacewings are considered a benefit in the garden because they effectively feed on aphids and other soft bodied garden pests. Here are some links that may be of further help.

https://bugguide.net/node/view/16103

http://www.uky.edu/Ag/CritterFiles/casefile/insects/lacewings/lacewings.htm

https://greenmethods.com/chrysoperla/


How does the modern synthesis theory explain the evolution of birds from dinosaurs?

First of all, dinosaurs did not evolve to birds. A better way of saying it is that modern birds evolved from a particular type of dinosaur. That, however, is not the same as the blanket statement "dinosaurs evolved to birds". The latter implies that dinosaurs somehow morphed into birds and stopped being dinosaurs. What actually happens is that a species starts changing and, eventually, a sub-population of that species has changed so much that we call it a new species. It is a subtle distinction but important.

As for a specific paper, no we don't have anything like that for any specific examples. What we have is a huge collection of observations all of which point to the process of speciation occurring via the processes of mutation and natural selection. It's impossible to know the precise series of mutations that led to the creation of a new species for a variety of reasons.

All we have is the current species. If we know an ancestor, we can deduce a possible path that leads from the genome of the ancestor to the genome of the target species but we have no way of knowing whether that specific path was followed. For an analogy, consider computers. If I were to give you a modern desktop PC and one of the first computers:

You might be able to guess certain changes that were made to the old ones in order to build something like the new ones but would you be able to figure out every single step along the way? How would you detect all the attempts that failed? The ideas that didn't pan out? Would you be able to infer the existence of floppy disks, for example?

The same problem applies to species. It is essentially impossible to infer the precise series of mutations that led species B to split from species A. Especially since, usually, this happens through species A.1, A.2, A.2.1, A.3 etc, and all we have is species B.

Add to that the fact that evolution is not a linear process, there are many dead ends (way more than in computers), and the story gets even harder to understand. This graphic illustrates it quite well:

Obviously, if you have the first red dot on the far left and the last blue on on the far right, it will be impossible to infer the entire evolutionary history linking these species.

So, with this in mind, given that dinosaurs and birds share a common ancestor, it is essentially impossible to get the full, true, path that led from that ancestor to either dinosaurs or birds. More importantly, as shown in the image above, dinosaurs did not evolve into birds in the first place so the question is moot.


How do mutations of viruses lead to drug resistance?

It doesn't. Viruses don't "know" anything. Mutations occur at random. Most of them don't do anything, or have a slight negative effect on the ability of the virus to infect and reproduce. However, there are billions and billions of viruses. Once in a while a random mutation will offer a significant advantage like immunity to an anti-viral drug. The viruses that have that beneficial mutation will then massively out-reproduce the viruses that don't have it. Eventually the population of viruses will consist mostly of individual viruses that have that mutation.


How many cells does the smallest animal have?

Rotifers are microscopic protostomes with around 1000 cells apiece.  This website claims the smallest rotifers have less than 100 cells, but I couldn't confirm this.  Most rotifers are eutelic — within a given species, each adult individual has the same number of cells (Encyclopeia of Life: Rotifers).

(Source)

Edit: Myxozoans might be even smaller.  These are microcsopic parasites that have been classified as cnidarians based on molecular studies.  They have complicated life cycles including a single-celled stage.

(Source)


Does ChEMBL have a specific definition for what they mean with "Max phase for indication"?

This refers to the phase a compound has "achieved" in a clinical trial.

Phases are typically ordered from 1 to 4
(although phases 1-3 are most talked about, as they are needed to bring a drug to market):

  Phase 1: Testing of drug on healthy volunteers for dose-ranging

  Phase 2: Initial testing of drug on patients to assess efficacy and
  safety

  Phase 3: Testing of drug on patients to assess efficacy, effectiveness
  and safety (larger test group)

  Finally, there is Phase 4 (referred to in your example), which is
  after a drug has been approved (by e.g. the FDA or the EMEA): here,
  the effects of a drug while used on the general patient population are
  monitored.

See also https://en.wikipedia.org/wiki/Phases_of_clinical_research

Your example has been approved (i.e. it can be brought to market, or might already be available), while others might still be in ongoing clinical trials. Others might have been "killed" earlier due to e.g. toxicity or side effects. Or have not even entered clinical trials (which would be the majority of compounds).

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


Is it possible to use virus for genetic modification of embryos during the fetus stage

Zika doesn't alter the host genome at all.

  Since Zika can alter the genome of a baby to cause deformities

Zika virus is incapable of altering the host genome. The exact mechanism by which Zika virus infection causes microcephaly is still unclear, but basically it depletes the neural stem cells at a point when the brain is developing, meaning brain development is more limited (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5516183/).

Some viruses do alter the host genome and are candidate technologies for gene therapy

Retroviruses are RNA viruses that copy their genetic material into DNA which is then integrated into a host genome. As such, and as you note, this can potentially be exploited to deliver new genetic material into an organism's genome. I'm not sure what you meant by transduction above, but the term is 'retroviral vector-mediated gene delivery'.

Retroviruses have been trialled for gene therapy for decades. See this sad report on a 2002 trial that apparently succeeded but had unexpected side effects here. However, CRISPR is probably an easier method to use.

You wouldn't attempt to modify a fetus

Some terminology here: a fetus is what an embryo grows into; it's getting bigger and more complex. And as illustrated by Zika-related microcephaly, any messing about with fetal development can have nasty side effects. There are also more cells to modify and you're likely to end up with a 'mosaic' where some cells are genetically different to others within the same organism. If you're attempting to modify the somatic cells of one organ, you might as well do it after the baby is born; if you're attempting to modify every cell in a human (including germ line cells) you'd do it to an egg or embryo.

This study describes a successful attempt to modify embryos using CRISPR. They saw only 1 mosaic in 58 embryos.


What's a "constitutionally small penis"?

"Constitutional" refers to the physical state of the concerned individual (Merriam-Webster).

In biology, it most probably means a trait that is not pathological or environment induced.

This is in the context of size of babies:

  Small for gestational age (SGA) can occur following a pathological
  process or may represent constitutionally small fetuses.

  From: Ananth & Vintzileos (2009)

  Between18-22% of infants SGA by population
  standards are reclassified as normally grown by customized standards
  and as the perinatal mortality of these reclassified babies is similar
  to those who are normally grown they can be considered to be
  "constitutionally  small.".

  From: McCowan et al. (2018)

  In most cases, it is difficult to differentiate between
  constitutionally small head size vs pathologic microcephaly, and
  available data regarding prenatal diagnosis of microcephaly are based
  on small numbers of cases of varying etiologies.

  From: Ultrasound screening for fetal microcephaly following Zika virus exposure.
   American Journal of Obstetrics & Gynecology, Volume 214, Issue 6, B2 - B4

Regarding constitutionally small penis: Since the article you mentioned is the only source (scientific or otherwise) of this term, I would believe that it is based on the population average (of possibly South Korea from where the authors are). Moreover, since it is not defined rigorously, it is most likely an arbitrary classification.


SARS-CoV-2 : does vaccination provide a better immunity than being sick and recover?

As @MikeyC and @jamesqf pointed in the comments, vaccines are better documented than the actual cases, whereas qualifying the immunity conferred by having recovered from Covid-19 would require large cohort studies.
However, one can follow up thir argument in many ways:

It would be reallys urprizing, if large-scale cohort studies have not been udnerway or already available by now: while nationwide testing may still be lacking in many countries, masive and repeated testing campaigns in specific regions are not a rarity by now. (see, e.g., here and here)
Hospitalization is not a necessary requirement for attesting a covid case - one could test unvaccinated persons for the presence of the Covid-specific antibodies.
There is much still unknown about the vaccines themselves - particularly about whether the immunity conferred is a lasting one, and whether.
Moreover, the fact that many people might have lived light cases of Covid does not make it easier for attesting the efficacy of the vaccines. Public authorities openly warn that the vaccine might be inefficient and a vaccinated person might be still a carrier of the disease.

In other words, "we don't know" is the most likely answer.
As the OP, I forgo the ethical issues raised by the "green passport" - these are not only those related to the restrictions on the individual freedom, but also the discrimination against the individuals to whom the vaccine is counter-indicated (e.g., allergics, pregnant women, people with weakened immunity, etc.)


The question is a bit vague but I will take it to mean the following

  Why does it (the body) stop in terms of height or physical mass when it can still keep on growing?

The answer is physics, specifically the ability for a body of a specific shape and structure to support itself and move itself, followed by the energy requirement to feed all those cells.

Strength of a bone scales with its cross sectional area, similar to muscle. Mean while mass scales with its volume. As a result, mass increases faster than bone strength. So the bigger your are, the weaker your bones become if all proportions are maintained. As a result for a certain design of animal there is an upper limit of how big it can become before it unable to support its own weight or able to move.

Next comes energy requirement. In general the more living bio mass you have, the more energy you require to keep it alive. The scaling isn't proportional but there is a general trend. And the more energy required the more food is needed, and given the habitat an animal lives in, there is only so much food around. And this places a limit on how big an animal can grow. An animal living in its niche has an energy budget.

Associated with energy budget, we meet biology and natural selection. Energy placed into growing, isn't energy placed into reproducing. All animals eventually die, either by predator or bad climate (winter, drought, even bad luck) . So it becomes a balance, given the amount of energy available, how much energy should be put into growth to give a more robust structure to survive vs how much energy should be put into reproduction so that the organism can multiply.

Put too much energy into growing bigger, your probability of dying before reproducing increases as you take too much time growing before becoming sexually mature. Put too much energy into reproducing, upon sexual maturity your body is small and weak and your die before you spend much time reproducing.

The ultimate right answer is dependent on the animal's niche, the physical environment around it, its biology, and the predators around it.


Comment: this question is a bit confusing, since none of the answers seems to directly explain how a shift to the right in the dissociation curve results in more oxygen delivered to tissue. Therefore, we'll try to choose the least wrong option...

This answer came out a bit long, so here's a TL;DR for you. I chose

   Option A

and here's why:

Although not stated explicitly, the pH in question is most probably the blood pH (this is a rather well-known graph from biochemistry undergrad studies). It shows that when blood pH drops or rises, the amount of %O2 saturation of hemoglobin deviates from the norm accordingly.

First of all, regarding your rule-of-thumb, it might be misleading in this context, since it may be true in both normal conditions and pathological conditions, depending on the site of measurement:

Under normal conditions, general blood pH is around 7.4 (7.35-7.45), blood pH in the tissues is around 7.2 (due to increased pCO2 resulting from cellular metabolism), and blood pH in the lungs is around 7.6 (due to the release of CO2 in the lungs for expiration, which results in lower pCO2 in the lungs) - see this reference and its references.
Under pathological conditions, general blood pH may rise above 7.45 (alkalosis) or fall under 7.35 (acidosis), regardless of the site of measurement [reference]. This means that a dissociation curve under abnormal blood pH value does not necessarily relate to normal conditions in a certain body site, but may also relate to a pathological condition in which blood pH is abnormal in general.

I believe the graph represents the latter situation, i.e. how hemoglobin behaves under the pathological states of acidosis (lower blood pH = right-shift) and alkalosis (higher blood pH = left-shift) compared to the normal state, since it depicts the change in %O2 saturation over the physiological range of pO2 and the curve is continuous (a depiction of blood pH only in the tissues or the lungs would not have resulted in a curve, since pO2 does not change significantly in each site, certainly not over the physiological range).

Now let us consider the possible answers:

Option A - The distance between the curves at 100 mmHg is less than the distance at 40 mmHg. This seems to be true in it's own right. However, other than describing the situation, it does not explain explicitly anything. It essentially says that the difference between oxygen release in the tissues is more pronounced than the difference in oxygen binding in the lungs, when comparing normal blood pH and acidosis. We can infer that if the right-shifted curve is below the normal and left-shifted curve, it means that less Oxygen is bound in the tissues (and also everywhere else, since this trend is consistent), i.e. Hemoglobin is less saturated, i.e. more Oxygen is released in the tissues in a state of acidosis than in any other state.
Option B - The distance between the curves at 100 mmHg is more than the distance at 40 mmHg. This is merely the opposite of A, and therefore is untrue by the same amount that A is true.
Option C - On the right-shifted curve, Hb will pick up more O2 in the lungs. This is a bit trickier. This option suggests that when pH is lower-than-normal (acidosis), more Oxygen will bond to Hemoglobin in the lungs. However, by observing the graph, we can see that the right-shifted curve is always below the other curves (both the normal and the alkalosis curves). This is also true in high values of pO2, which are present in the lungs. This renders this statement incorrect in itself, and it also does not explain why more oxygen is released in the tissues.
Option D - On the right-shifted curve, Hb will pick up less O2 in the lungs. Based on the analysis of option C, it should be rather evident that the opposite must be true. That is, if the right-shifted curve is always below the other curves, including in high pO2 values, then under this condition Hemoglobin is bound to pick up less oxygen in the lungs than in any of the other conditions. Therefore, this statement is correct, but it does not explain why more oxygen is released in the tissues.

According to the section titled The influence of pH on oxygen-hemoglobin binding in this excellent reference, "the presence of a low pH locks it [hemoglobin] in an unreceptive state, preventing it from binding oxygen molecules". This means that Hemoglobin's affinity to oxygen will be reduced, so that more oxygen will be released (in other words, less will be bound) in the tissues and less oxygen will be bound in the lungs. The two "less" in the previous sentence are in accordance with the curve of pH=7.2 being below the other two curves over the entire range of pO2. I highly recommend reading the above reference through and observing the figures.

To sum up, none of the possible options is satisfying enough, but option A seems to be the least wrong or unrelated to the situation described, so I would choose it.


There are many things going into the evolution of our face. It is not as simple as discussing a single trait. Your question is therefore quite broad. So I will just pick up three different traits and talk a little bit about them. Those traits are

hairs
size of the jaw
cranial capacity

As I will only say a few words, you will have to look for more advanced information by yourself if you want to deepen your knowledge.
But first, let me make a few other comments
A few comments
Panselectionist view of evolution
When you say what advantage did nature selected our present face?, you seem to assume that any evolutionary had to be brought about via a selective pressures. Yet, there is so much more to evolution than just natural selection. Not every trait has been selected for (otherwise we would not have any genetic disease). There is for example genetic drift who is also a very important evolutionary force.
On this subject, you might want to have a look at the paragraph Did you say Natural Selection? of this answer to Why don't mammals have more than 4 limbs? and to Why do some bad traits evolve, and good ones don't?
Accuracy of your Australopithecus's face
In the reconstruction of the appearance of a extinct lineage, there is always some part of artistic representation to fill the gap of what we don't know. One should investigate the exact method used to recreate this image before assuming that Australopithecus looked exactly like that.
For more information have a look at In reconstructions, how are various shapes of facial features determined from skull only?
On top of that, please note that there is variation in faces within a species. This is true for Homo sapiens today and it was true for other great ape lineage. More importantly, there were at least 6 species of Australopithecus (see wiki > Australopithecus).
Human species or hominini lineage?
Your question is

Why did the face of human species changed so much during the course of its evolution?

When we say "human species", we typically refer to H. sapiens (or even H. sapiens sapiens). Based on your images, you seem to rather ask about the evolution of faces in the hominini lineage and not only in H. sapiens as Australopithecus is not the same species as us. Australopithecus is actually a genus (other than Homo) containing several species.
Evolution of a few facial traits
Hairs
We've lost plenty of hairs! Have a look at the post Why did humans lose their fur? to understand why.
Size of the jaw
Here is a timeline of evolution of hominini

As you can see, Australopithecus did not know how to cook. They did not know how to control fire. The first to have a good control of fire were probably Homo erectus.
By cooking, we pre-digest our food, leaving much less work for our digestive system, including the physical mastication performed by our jaws and teeth. As a consequence our jaws reduced in size (Wrangham and Conklin-Brittain 2003, Lucas et al. 2006; See also this book from Lucas).
Size of the brain
H. sapiens cranium is about 3 times the size of Australipithecus cranium (Leigh 1992 and Smith et al. 1995).
Cooking allowed us to save much energy, which could then be used for higher cognitive abilities. Without cooking, it is likely that our brain would never has gotten to the size it has today. Our brain consumes about 20% of our energy today (which is very unusual if you compare to other species). Cooking therefore also lead to an increase in brain size.


At what substrate concentration will an enzyme work at 40% of its maximum rate if its Km = 0.095M?

To be honest I know very few about enzymes and absolutely nothing about Michaelis–Menten.

However, when I "took the Michaelis-Menten equation, replaced v with 0.4Vmax, canceled the Vmaxes (one on each side), and solved for [S]", my result is positive:

0.4 * Vmax = S * Vmax / ( Km + S )
0.4 = S / ( Km + S )
S = 0.4 * Km + 0.4 * S
0.6 * S = 0.4 * Km
S = Km * 2 / 3.


Is there a formal definition of `nature` in Biology?

Is there a definition of "nature"?

I don't think there is any commonly accepted definition of "nature" in biology. To my experience, the term "nature" is actually relatively rarely used in conferences or peer-reviewed papers.

Why is there no formal definition of nature?

The concept of "nature" has been developed outside the field of science or philosophy. As often concepts in the popular culture are used without a proper, complete definition. Even if there is an vague intuition that correspond to a concept, it does not mean that there is any way to make an objective definition of this concept. I think the absence of formal definition of nature mainly come from the fact that nature as used in the population culture does not mean much.

Is the term "nature" used in Biology and with which definition?

I just did a quick review of the use of the term "nature" in peer-reviewed articles. It seems that the term "nature" is rarely used or only in the abstract r in the first two paragraphs of the introduction to convey very general (and somewhat inaccurate) ideas.

Often, the term "nature" holds for "essence", "origin" or "intrinsic characteristic" rather than referring to "outside the lab", "landscape" or "ecosystems". Here are some examples of where I found the term nature

"Nature" as "Essence"

From the abstract of Gibson and Dworkin 2004

  [..] we highlight recent progress in determining the nature and identity of genes that underlie cryptic genetic effects [..]

From the first paragraph of Woolhouse et al. 2002

  Failure to recognize the dynamic nature of the interaction could result in misinterpretation [..]

"Nature" as "outside the lab"

First sentence of the second paragraph of Elena and Lenski 2003

  Since Darwin’s day, many examples of evolution in action have been studied in nature [..]

Note btw that there is no good (objective) definition of life either. One might want to have a look at Why isn't a virus alive? for a discussion on the definition of life.


Ratio of bleach to water required to disinfect COVID-19?

I have also been frustrated by use of percentages in protocols when making dilutions of stock bleach.  It's helpful to look at the product labels, as they often have dilution factors for different uses as well as concentrations in parts per million.

I have a bottle of Clorox brand concentrated bleach sitting next to me, and the label says this solution is 8.25% sodium hypochlorite.  The label also says that 8.25% sodium hypochlorite yields 7.85% available chlorine, and that 4 oz. of this product in 1 gallon of water yields 2,400 ppm chlorine, implying that the stock concentration is 76,800 ppm if 1 gallon (128 oz.) is the total volume or 79,200 ppm if the 1 gallon is added to 4 oz. (that is, 132 oz. total).  For simplicity, let's say that the stock solution is 78,500 ppm so that 1% available chlorine is exactly 10,000 ppm chlorine.

The CDC website cites a study that states 200 ppm chlorine is sufficient to inactivate 25 different viruses.  Sadly, I cannot find the text of that study.  Here's the citation:

Klein M, DeForest A. The inactivation of viruses by germicides. Chem. Specialists Manuf. Assoc. Proc. 1963;49:116-8.

So, using the low end of your given values, a 3% stock solution of bleach will have ~2.85% available chlorine, following the yield ratio above.  Diluting 5 tbsp. (2.5 oz.) of this stock in 1 gallon of water (total volume 130.5 oz.), as recommended, will yield ~0.05% available chlorine, or 500 ppm, which is sufficient for viral inactivation.

Edit - a bulletin from Clorox (PDF, cached HTML) states that 2400 ppm available chlorine is recommended for disinfecting hard, nonporous surfaces.  The bulletin also lists enveloped and non-enveloped viruses against which this product is effective (at the "99.9%" level), including Human Coronavirus (Strain 229E, ATCC VR-740)


Are boat-tailed grackles efficient flyers?

I don't know of studies specifically of boat-tailed grackle flight, so I'll focus on elongated tails in general and come back to grackles at the end.

Long tails in birds are obviously interesting from the standpoint of sexual selection. Going all the way back to Darwin, one hypothesis has been that females prefer males with long tails. There seems to be evidence for this, although experimental reduction or elongation of tail feathers is perhaps of questionable success. See this back and forth in Behavioral Ecology.

Those interested in the study of flight have also studied elongate tail feathers to get at the questions you ask: are long tail feathers aerodynamically costly?

Balmford (1993) compared the aerodynamic properties of different tail shapes. He found that:

  A forked tail that has a triangular planform when spread to just over 120° gives the best aerodynamic performance and this may be close to a universal optimum, in terms of aerodynamic efficiency, for a means to control pitch and yaw.

But the results were more complicated. Forked tails are only used in extreme maneuvers, they are more unstable, and suffer from greater loss of performance when damaged. He leaves open the possibility that natural selection, rather than or in addition to sexual selection, has played a role in shaping bird tails, possibly for increased aerodynamic performance.

More relevant here, Balmford et al. (1993) studied pairs of species, one with a long tail and one without, to assess the aerodynamic cost of long tail feathers. They studied ~600 specimens and used aerodynamic modeling to predict cost. Their results are summarized in this figure:

Graduated (rounded) tails are costliest over all lengths. Forked tails are notably less costly over all lengths, and shallow forks more efficient than deep forks (but there the difference is not great).

They conclude:

  Our model suggests that as long forked tails deepen, it becomes more likely that they are aerodynamically costly..., and therefore increasingly probable that sexual rather than natural selection explains their evolution.

And of the species pairs:

  ... then among species with long forked tails, sexual dimorphism in tail length should increase with fork depth. Pairwise comparisons of closely related species support this prediction.

What of boat-tail grackles then?

From what images I could find, it looks like boat-tailed grackles appear to have graduated tails when spread. If so, then these tails would be very inefficient and males with longer tails would incur a proportionately higher cost of flight than males with shorter tails.

Balmford, A., A. L. R. Thomas, and I. Jones. 1993. Aerodynamics and the evolution of long tails in birds. Nature 361:628–631.

Thomas, A. L. R. 1993. On the Aerodynamics of Birds' Tails. Philosophical Transactions of the Royal Society of London B: Biological Sciences 340:361–380.


If you keep reading the next sentence it makes clear what is meant (emphasis mine):

  Crocodiles (subfamily Crocodylinae) or true crocodiles are large semiaquatic reptiles that live throughout the tropics in Africa, Asia, the Americas and Australia. Crocodylinae, all of whose members are considered true crocodiles, is classified as a biological subfamily. A broader sense of the term crocodile, Crocodylidae that includes Tomistoma, is not used in this article

So, the Crocodylidae family refers to crocodiles, the Crocodylinae subfamily are the true crocodiles which includes almost everything known as a crocodile, and indeed, you found the one that gets left out:

  The crocodylian family Crocodylidae includes the true crocodiles, which are the members of the subfamily Crocodylinae, as well as potentially the false gharial, the only extant member of the subfamily Tomistominae. The latter is a subject of controversy as to whether it is a crocodile or actually belongs in the family Gavialidae.

(via Wikipedia)

Wikipedia further states:

  Gavialidae have conventionally consisted of only one surviving species, the gharial (Gavialis gangeticus), which is native to India and Nepal. Many extinct species are also known

and also

  Tomistominae is a subfamily of crocodylians that includes one living species, the false gharial. Many more extinct species are known, extending the range of the subfamily back to the Eocene epoch. In contrast to the false gharial, which is a freshwater species that lives only in southeast Asia, extinct tomistomines had a global distribution and lived in estuaries and along coastlines.

So there are many other extinct relatives of crocodiles in these groups; the question is to which the extant false gharial belongs. In either case, the other Tomistominae would be non-true crocodiles, according to a definition that subfamily Crocodylinae are the true crocodiles.

The words "true" and "false" are not necessarily used in their boolean meaning here, but rather, "true" in taxonomy fits better with other definitions, for example from Merriam-Webster: "typical" (Merriam-Webster explicitly references the "true cats" as a use for this meaning). A synonym would be more like "archetypal" or refer to a clade or other more robust grouping, rather than a linguistic/non-scientific grouping.


Databases for metabolic pathways of human disease

NCBI BioSystems help file contains a list of their sources:

http://www.ncbi.nlm.nih.gov/Structure/biosystems/docs/biosystems_help.html#SourceDatabases

Please specify what you need as stated in the comments as it is almost impossible to give you more (relevant) information then this.


It's important to note the difference in mechanism between cocaine and meth. While cocaine blocks reuptake, meth makes VMAT - vesicular monoamine transport - leaky and actually reverses the transportation of dopamine, so that instead of transporting dopamine into the axon terminal, it actually transports dopamine out as it leaks from the vesicle that carry it. This is what is meant when referring to 'reverse transport' of dopamine through DAT. Feel free to read this abstract and the sources it cites (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2631950/).

Regarding the possibility of a DAT agonist of sorts, looks like current research has identified some potential targets. One of which seems to be luteolin and its derivatives (http://www.ncbi.nlm.nih.gov/pubmed/20971650). Current studies find new derivatives and test the EC50 to assess pharmacological efficacy.


Can you help with insect identification? (Outback Australia)

This is a member of the family Anostostomatidae, but given its sex is unlikely to be placed further (many Orthoptera are best identified on the basis of males, including this family).  There don't seem to be internet-based identification tools for the group (but the page http://bie.ala.org.au/species/urn:lsid:biodiversity.org.au:afd.taxon:a8042a0a-f34e-4ae3-ab86-5306b9176774#gallery shows a number of specimens and living examples, the latter usually taken only to family); Chapter 5, "Australian king crickets: distribution, habitats and biology (Orthoptera: Anostostomatidae)" in the book The biology of wetas, king crickets and their allies appears to be the best option I've seen that might allow a further identification.


How is incomplete dominance different from codominance?

Certainly if you are talking about signals, red, white, and pink phenotypes are distinguishable rather than intermediates...

But inheriting a character is far away from the concept of distinguishing signals. As genotype of an organism decides its phenotype, you should know that in a hybrid both the paternal and maternal traits would exist. If one is dominant then it is expressed and the recessive is not.

However if the dominant gene is unable to express itself independently in presence of the recessive and if the recessive is partially expressed, then both the dominant and recessive give rise to an intermediate phenotype which "only one of them cannot produce"

This is what we call blending. In case of Snapdragons, pink is a phenotype that allele responsible for red or white alone could not have produced.

In case of co dominance you can notice multiple dominance. i.e., no recessive character is there. All alleles are expressed "independently of one another" in an organism.

Eg:- AB blood group.

Also consider cross between black coat coloured cat and white cat. The offspring produced has black and white patched coat colour. i.e., Black and white didnt blend to give rise to grey. I mean, alleles responsible for these traits are independently expressed.

Hope that clears your doubt. :-)


How does the genetic material differ between dizygotic twins and ordinary siblings?

Differences in genetic material between dizygotic twins and siblings are likely to be very similar.

  Dizygotic twins, or so-called fraternal twins, on the other hand, are no more genetically similar than any other set of siblings. - Utah.edu

Since all oocytes are all synthesized during fetal development, dizygotic twins are no more likely to come from a single mitotic division than siblings are.

Also note that in human females, only one egg comes from the a full mitotic division:


Do free computer programs exist that can simulate drug permeability in bacterial membranes?

I currently work alongside many biologists that are working on simulations of anti-microbial peptides in the membrane. These seem to have a similar mechanism to what you're aiming for — permeating the lipid bilayer.

Presumably you have already come to the conclusion that molecular dynamic simulations are probably a good shot for exploring what may happen at an atomistic and energetic level. Software does exist, but an accurate answer from a project like this may take months of work and time on an HPC cluster.

The only software recommended by PDB (trustworthy) explicitly for membrane systems is GROMACS (and it's free!). This has documentation on membrane simulation which I have used in the past. However you will need to be very careful in both designing the simulation and analyzing the output, and an expert guiding hand may be required.


Can animals train to be noticeably stronger, faster, more agile... than other animals of the same species?

Can animals train to be noticeably stronger, faster, more agile.. than other animals of the same species?

Yes, of course!

Humans are animals, so yes! But even in non-human animals. You can look for example in a tutorial on how to train a dog (or a horse) for specific skills (speed, high jump, long jump, etc...).

  It seems that variation in animals is very small

Such a general statement can only be wrong. Consider dogs as an example. The fastest dogs go at 72 km/h (~45 mph) while many dog breeds barely reach 5 km/h (~3 mph; and they're all considered as the same species). So, there is a lot of genetic variation among dogs.

Now when it comes to variation caused by training it is a little harder to estimate. Consider having a look at Guy and Snow (1977), McKeever et al. (1987), Evans and Rose (1987) and Rivero and Piercy (2008). For what it is worth, note for example that trained racing horse can go up to 70km/h while most horses can go only up to 40-45 km/h. There are a number of studies showing the effect of training on horses.


Identification of protozoa under microscope

At first glance, the organisms may hold the appearance of protozoans like ciliates. However, I am of the belief that these 'totally tubular' micro organisms are in fact diatoms.

The diatoms are a diverse range of eucaryotic microalgae which comprise a large percentage of the phytoplankton group. (Diatomaceous earth is the residual remains of their calcareous walls)

They are likely diatoms because of their apparent hard membrane, and slight brown-green pigment, typical of heterokont diatoms.

I would be unable to specify the organism to family level. However, you may wish to complete your investigation by looking under the order 'Pennales'.

For general information regarding the Diatoms, you may visit https://en.wikipedia.org/wiki/Diatom
Morphology and description available from: https://books.google.co.uk/books?id=xhLJvNa3hw0C&printsec=frontcover&source=gbs_ge_summary_r&cad=0#v=onepage&q&f=false

Good luck


What are the advantages of blood's redness?

The reason why blood is red is rather simple: It is the iron atom in the middle of the heme, which plays the central part in binding oxygen. Depending on the oxidation state the blood looks either dark or light red. The structure is the following (taken from here):

That the color only depends on the coordinated metal atom is shown by another related molecule, the hemocyanin, which is the oxygen carrying molecule in the hemolymph of insects. It contains copper which is colorless in one oxidation state and blue-green in the other. The function is the same, the color is different.


Do puffin beaks have vertical slits or cracks?

No, as far as I am concerned a healthy puffin hasn't got any slits or cracks in its beak. The lines that you see are literally just that - or little grooves. Obviously, beaks might show signs of wear and tear, so cracks may be observed. However, there are no genes in a puffin's genome that would lead to the expression of slits and cracks in its beak.

I think the photos below might help visualising.

(Photo: Tycho Anker-Nilssen, NINA)

(Photo: Will Nicholls)