How does "be altruist to those who are similar to you" evolve? There are many cases when people commit altruism. One is relationship. I am willing to die for 2 of my children or 8 nieces, say an evolutionary psychologist. Another is reciprocal altruism, which is just a selfish cooperation rather than true altruism.

  In the 1930s J.B.S. Haldane had full grasp of the basic quantities and
  considerations that play a role in kin selection. He famously said
  that, "I would lay down my life for two brothers or eight cousins".[8]
  Kin altruism is the term for altruistic behaviour whose evolution is
  supposed to have been driven by kin selection.

Is it possible that humans may be altruists not for their 2 children or 8 nieces but to say, 1000 people that are similar to them.

If so, how does "Be altruist to 1000 of people similar to you" evolve?

Note: If the answer is negative, then we will have a hard time understanding voting. Why sacrifice your time. However, if the answer is positive that humans do love other humans "a little bit" then voting, or even suicide bombing make sense. Those humans sacrifice their little time to improve reproductive success of those who are similar to them.

Answer DOES NOT have to be about humans. If you can show me why strong/weak chimps tend to help each other or whether alpha males like one another, that'll do. Of course, naturally we would expect that leaders need followers and followers need leaders. But sometimes there are behavior that defy even this complementary nature.

Similarity does not have to be genetic. For example, fellow programmers and fellow engineers tend to be gang up.... Or does it have to be genetic?

This is an important question in evolutionary biology, but you need to distinguish the biological terms 'altruism' vs 'cooperation'.

Altruism in biology means giving up your chance to reproduce so that someone else can more readily.  This is not like a gorilla troop, where only one male breeds, and the rest contribute to mutual security.  A more typical example is a honeybee or an ant, where the vast majority of the hive have no ability to reproduce at all.  This happens in animals, but is relatively rare. Its causes are currently the subject of intense debate but as far as I know, the only cases are where you do this for others who are genetically similar to you.   That logic sort of plays out as you say: "My brother has kids, why do I need to have any? I'll just help out a little bit there."

Cooperation includes forming groups for mutual safety and increased competition for food resources are why you might vote or schlep down to the DMV to get a drivers license when simply getting in your car without might be just as good most of the time.

Cooperation is incredibly common in biology.  It even happens between species.  A dolphin helps a ship navigate submerged rocks, symbiotic bacteria in our gut help us digest food, but also get enough to live and reproduce.  The benefit is always win-win in such situations.

To understand how cooperation occurs spontaneously, one of the best experiments to look at is the Prisoners Dilemma experiment.  If individuals are in a situation where you are likely to see each other again later (like a society).  The most successful ones are the ones who treat each other reasonably well, even if you do look out for less reliable types.  Why do people from Northern climates have strong hospitality traditions?  "Today you (are in trouble) tomorrow me."  As the saying goes.

There are individuals who are not cooperative, but the selection forces are positive enough that those folks will regularly disappear from the group, while more cooperative types will become more numerous.

This is a significant selective pressure that you can train robots with very simple reward mechanisms to cooperate.  http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.144.2881


How many water molecules will be produced starting from acetyl-CoA in citric acid cycle I am puzzeled by the answer. Acetyl-CoA when enter citric acid cycle, it produces 3NADH, 1FADH2, total 4 reducing equivalents. If each one makes 1H2O, then 1acetyl-CoA should make 4H2O. Why some textbooks make it 2H2O. In addition, almost like all (or many) do not balance oxygen; they say entering 16O2 and making 16H2O, so how?

Thank you.

Acetyl-CoA has three carbon-hydrogen and one carbon-carbon bond, and it is electrons 'held' in these bonds that are available for biological oxidation.  Thus we say that acetyl-CoA contributes four reducing equivalents. In the TCA cycle, these are transiently passed to NAD+ (to give NADH) and to FAD (to give FADH2): the cofactors may be considered intermediate electron carriers.

It takes 4 electrons (2 reducing equivalents) to make 2 water molecules from 1 O2 (or 4 electrons to reduce 1 oxygen 'atom' to 1 water molecule), but this takes place in the cytochrome oxidase reaction of the respiratory redox chain (with reduced cytochrome C as electron donor), not in the TCA cycle.

It is important to realize that water contributes no reducing equivalents to cellular respiration, and that hydration reactions are neither oxidation or reductions. For water to contribute reducing equivalents, it would have to be 'split', as it is in photosynthesis.

In addition, oxygen is not consumed or produced in the TCA cycle.

The assertion that water can pass electrons to NAD+ in the TCA cycle is an infamous 'textbook error', notably advocated by Efraim Racker in A New Look at Mechanisms of Bioenergetics, and my opinion on this (for what it is worth) is given in this SE answer.

For the role of water in the TCA cycle and the controversies surrounding it, I would recommend the letters by (i) D.E. Atkinson and (ii) Herreros & Garcia-Sancho on TCA cycle confusion published in TIBS and kindly made available by David.  (These references are not indexed by Pubmed and are apparently not available from the TIBS website)


How easy is it to carry out de novo sequence assembly? Today a colleague of mine asked the following question:

" Assuming I need to build from 0, a chromosome of a fish, with short reads
but no other reference whatsoever [de novo assembly]:

how much work is that?
Is there a generic software (like SAMtools) that will align the reads in a
scaffold one can use?
Basically, given a reasonably clear pipeline in terms of software, is it still blood sweat and tears or is it just a matter of getting it on a cluster?"

Very grateful for any suggestions, sources of information, software etc.

You can try looking around biostars.org, which is like stackexchange, but for bioinformatics.

Velvet is one example of a de novo assembler.

But 30 bp is really short, and animals have big genomes (not as tough as lots of plants and fungi, but still tough)

What you would get is a bazillion short contigs.  It would not be pretty.


Is our color vision calibrated to sky, vegetation, and blood? Our color vision is based on three types of receptors (cones) which are sensitive to three distinct locations on the spectrum:  420–440 nm, 534–555 nm, and 564–580 nm.  We label them "red", "green", and "blue", but these names are arbitrary.  However, their locations on the spectrum may not be arbitrary.

I notice that they correspond to the colors of the three most important things in our natural habitat:  sky (the above), vegetation (the below), and blood (the sign of potential food or alarm, depending upon whether you are the hunter or the prey).

Am I on to something here, or am I just dreaming in technicolor?

Short answer
Color vision is not based on a calibration to the sky, vegetation and blood. The current leading theory of the development of trichromatic vision in humans is based on the foraging of fruit in our primate ancestors.

Background
The places of red, green and blue wavelengths in the spectrum are physically defined and, therefore, not arbitrary; see this question on Biology SE.

Before continuing, it is good to mention that trichromacy (the presence of red, green and blue cones in the retina) is typical for primates. For example, dichromacy (<500 and >500 nm cones) is the most common configuration in mammals. The split in red and green photopigment in primates developed relatively late in evolution (30-40 mln years ago), inferring trichromacy in primates from a dichromatic ancestor. Note that many avian and aquatic species may be tetrachromats or up (4 or more photopigments) (Nathans et al. 1999), with the mantis shrimp featuring no less than 10(!) different photopigments (Cronin & Marshall, 1989).

It is believed that the red-green-blue system in primates has evolved due to its benefits for identifying fruit on a background of foliage, and to assess the ripeness of fruits. The food of monkeys typically consists of fruit, and young leaves. Young leaves are light-green, while ripe fruits are often yellow (e.g., bananas) and orange (e.g. oranges, mangos) (Osorio & Vorobyev, 1996). Unripe fruits typically contain chlorophyll and resemble the color of foliage (green). Hence, to discern ripe, nutritious fruits (yellow-orange or 570-620 nm) from foliage (green or 495-570 nm - frequencies mentioned were copied from wikipedia), it makes sense to have good resolution in the red-green area. The red opsin has its maximum at 530, and the green at 560 nm. The blue has its peak a lot lower at 425 nm (Nathans et al. 1999). Hence, the red and green opsins, which evolved late in evolution, are both right in the "ripe fruit area" and have absorption spectra very close together. Hence, there is a lot of color sensitivity (high color resolution) in the red-green area, which covers reds, oranges, yellows and greenish colors. This gives primates a very high sensitivity to recognize fruits, and especially ripe fruits in a green background. The resolution in the green-blue range is smaller (blues, purples).

As a background: color vision in trichromats works by color opponency, and specifically a yellow-blue and red-green color opponency. This means there exists no yellowish blue hue, or a reddish green (De Valois & De Valois, 1993). The red-green opponency means that we have exquisite sensitivity in the red-green pathway, as red cones suppress green cone output and vice versa. In other words, there is a high color acuity in the red-green area that helps to recognize fruits.

As a side note: The trichromat color vision scenario in primates supports the notion that cats (for example), being predators with dichromatic vision, do not benefit from being able to identify ripe and unripe fruits, as mentioned by @GoodGravy. In contrast, cats need excellent night vision and motion sensitivity, being nocturnal hunters. Indeed, color vision versus night vision, and color vision versus high motion sensitivity are both trade-offs that do not go hand in hand (Kelber et al, 2002).

References
- Cronin & Marshall, Nature (1989); 137-40
- De Valois & De Valois, Vis Res (1993); 33(8): 1053-65
- Kelber et al., Biol Rev (2003); 78: 81–118
- Nathans et al., Neuron (1999); 24(2): 299–312


Does endo- and (or) exocytosis require energy? Do they belong to active / passive transport? I expect vesicle formation and fusion to require energy input; however, I'm not sure about which of endocytosis and exocytosis require energy and how they use the energy input.

Do they belong to active or passive transport?

Wikipedia is your friend:

  Exocytosis... is the durable, energy-consuming process by which a cell directs the contents of secretory vesicles out of the cell membrane and into the extracellular space.

and

  Endocytosis is an energy-using process by which cells absorb molecules (such as proteins) by engulfing them.

Emphasis mine.  Here's a nifty paper which gave some evidence a few decades ago for some basic intracellular thresholds for budding and fusion, and this paper shows that endocytosis definitely requires ATP, using a novel assay.  Check the sources, too, some of them are excellent.


Can cfDNA testing distinguish results in the case of twins? A fetus can now be screened for some of the more common genetic diseases and its sex determined from just a whole blood sample from the pregnant mother. Fetal DNA is abundant enough in the systemic circuit to be able to be purified and sequences analyzed. Question is, in the case of fraternal twins, could the procedure discern between the two fetus's...

As a clearer example, can it distinguish between:

Scenario 1: if one fetus was male and one fetus female
And scenario 2: both male?

It appears the test would just look for presence of Y chromosome using certain markers. But it could then look at SNP to distinguish individuals.

Looking for clarification here

I think you are overestimating how these cfDNA tests work.  Maybe I read the paper wrong, but from what I read of one technique (Sequenom's MaterniT21 test) there is no purification of fetal DNA.  They do restriction digests to assess the percentage of fetal DNA,  but I don't think they enrich for the fetal DNA when they sequence.  The library they make is mostly maternal, they are just looking for slight deviations in how many reads come from each chromosome, if too many come from chromosome 21, they conclude it's because the fetus has too many copies.

And as for SNPs, coverage is way to low for that.  We're talking about 40 million reads, even if that were mostly fetal DNA, which I don't think it is, that's not enough coverage to call SNPs.

So if there were two fetuses, and they were not identical, then the signal from each would be half what would be expected based on the restriction digests assay. So maybe you would have enough counts that you could tell that the Y chromosome counts were too low, and the X chromosome a bit too high, but since these tests almost certainly have not been clinically tested on multiple fetuses well enough for verify their accuracy, no company is going to report results.


What is the most genetically complex organism? I understand that new genomes are being sequenced ever day and these answers replace themselves often; although as of today, what has been proven to be the most genetically complex organism (Other than a human of course)? I keep getting a multitude of different answers like Daphnia pulex, Axolotl, Paris japonica or Adder’s Tongue all from different dates and sources so it becomes difficult to tell what is the right answer here if any. If this question is not specific enough I would be happy to revise.

Edit: I would define genetic complexity as either genome size or number of genes. Either answer  would work. If you would like give other information like chromosomes or isoforms from any other definition, that would be helpful. Whatever is the best of the best.

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

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

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

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


How is "selection" best defined? There is natural selection but there is also sexual selection which some regard as a category of natural selection.  There is also artificial selection (by humans).  The question is, what is a most appropriate for selection?  What criteria does a  force have to meet in order to be considered to have acted selectively?

My favourite definition

Selection is a fitness differential associated to a genetic variance among individuals in a population.

You might want to have a look at What does fitness really mean?.
What I like about this definition
I personally went with this definition because it is short and clear cut and directly highlight the importance of mathematical statistics in the evolutionary biology literature.
What I don't like about this definition
This definition has the issue that it may be hard to be fully understood to a layman reader. Also, I think my definition lack a mention of the phenotype as being causal to the fitness differential. While such mention is not necessary, I think it would clarify in most minds what selection is really about.

Now, let's consider the definitions that we typically get when we google the question
Wikipedia
Here

Natural selection is the differential survival and reproduction of individuals due to differences in phenotype

I am quite unhappy with this definition. While I like that it highlights the fact that fitness difference is caused via phenotypic difference, it completely lack the idea that for a change in allele frequency to happen, this variation must be correlated to genetic variation.
I would note that the rest of the introduction on the wikipedia article clarify my criticisms. I only attack the short version (one sentence) version of the  definition.
Dictionnary.com
Here

the process by which forms of life having traits that better enable them to adapt to specific environmental pressures, as predators, changes in climate, or competition for food or mates, will tend to survive and reproduce in greater numbers than others of their kind, thus ensuring the perpetuation of those favorable traits in succeeding generations.

There are a few things I don't like about this definition
..traits that better enable them to adapt..
It sounds like they are talking about evolvability. I would just say traits that are better adapted.
..too much emphasis on the role of the environment..
Also, I don't like that it is presented as if all selection pressures where environmental (predators, climate, competition for food, etc...) and completely ignore a very important source of selection which are simply related to the functioning of the body. A mutation that causes an individual to fail copying DNA anymore will obviously be lethal and under very strong purifying selection. Such the "outside-of-the-body environment" is important but it is definitely not the only thing.
It is kind of a common misconception about evolution that selection occurs when there is a climate change and not so necessarily in other case in most people's mind.
..ensuring the perpetuation of those favorable traits in succeeding generations..
Well.. it does not "ensure" that these traits will be kept. First because it only increases the probability of certains allele to be kept or to reach fixation, it does not ensure it. Also, because depending on the genetic framework, once the underlying QTL have reached a given frequency, depending on the actual genetic mechanism (epistasis, dominance and others), traits that are being express might differ quite a bit from those that have been selected for.
Overall, I think the definition lack any notion to genetics.
Biology-online
Here

A process in nature in which organisms possessing certain genotypic characteristics that make them better adjusted to an environment tend to survive, reproduce, increase in number or frequency, and therefore, are able to transmit and perpetuate their essential genotypic qualities to succeeding generations

I like this definition. The only issues in my opinion are very similar to my above opinions

too much emphasis on the environment as done before
it seems that they define more the consequence of natural selection than what it actually really is.

What Google gave me when I entered 'what is natural selection?'

the process whereby organisms better adapted to their environment tend to survive and produce more offspring.

Again there is IMO, too much emphasis on the environment and no mention of thee actual mechanism (fitness - genetics correlation).

Potential confusion
Some people might use the term "selection" to refer to the existence of phenotype - fitness correlation and the "response to selection" as being the effect of such correlation of the population genetics whenever there is a non-zero association between phenotype and genotype. This nomenclature would typically be inspired by the terminology used in the Breeder's equation (see How to interpret the breeders equation?).
However, none of the definitions I could find clearly suggested that selection was nothing but a phenotype - fitness correlation as all of them implied that selection has a long term impact on the population phenotype which such phenotype - fitness correlation would not have in absence of a phenotype - genotype correlation.

Lewontin recipe
I am not sure a recipe count as a definition but Lewontin recipe is a good way to understand the what is natural selection

Individuals in a population varies in terms of a given trait
This trait has some heritability.
The fitness varies (not necessarily linearly) as the trait varies.

The recipe hides the complexities behind the term heritability. You can learn about the math of heritability at Why is a heritability coefficient not an index of how “genetic” something is? .


How to inactivate trypsin permanently by boiling? I have to perform a hydrolysis of BSA with the enzyme trypsin. As a control I want to inactivate the trypsin enzyme. Can I inactivate it permanently by boiling (100oC) for 10 minutes, or does it it require 1 hour of boiling? After inactivation, I have to do a test (with an active enzyme) and a control with BSA at 37oC). At this point the inactivated trypsin (the control) should not be re-activated. So my questions are (1) whether I can irreversibly inactivate trypsin by boiling, (2) how long I have to boil it, and (3) if the boiling process will irreversibly inactivate the trypsin.

In my experience 10min at 100°C are sufficient, this is also supported by the paper linked below. Heat inactivation works by denaturing the protein and is therefore final.
Depending on what you want to do with you sample, it might be problematic, as this is probably also denaturated at least to some degree.

You can also chemically inactivate trypsin, either by adding fetal bovine serum (which is done in cell culture), which contains protease inhibitors as α1-antitrypsin and α2-macroglobulin or by using commercially available inhibitors. Trypsin is also inhibited by calcium and magnesium ions, so your reaction buffers shouldn't contain any of them.

A Simple Procedure for Effective Quenching of Trypsin Activity and
Prevention of 18O-Labeling Back-Exchange


The effect of pH on catalase Why does catalase still produce oxygen when mixed with 1 mL of 0.1M NaOH (pH 13), but not when mixed with 1 mL of 0.1M HCl (pH 1)? Catalase's ideal from what ive researched is 7. In other words, since both are on opposite side of the pH scale and equally distant from catalase's ideal, why does the acid mixture stop working, but the base still function, even if a little slower? Why did the catalase denature after the acid, but not the base? Thanks for any help, I'm pretty curious

The pH profile of an enzyme is not necessarily symmetrical. As random examples, see Figure 7 here, or Figure 5b here. Or if you have access, a pH profile for Magnaporthe grisea catalase can be seen in Figure 7 of http://dx.doi.org/10.1042/BJ20081478

The reasons for this go back to why enzymes are pH dependent in the first place. One of the major reasons for a pH dependence is that key catalytic residues become  (de)protonated as the pH changes. But different residues have different effects and different pKas, so you need to look at the sum of all their effects.

Example:

Imagine that a key catalytic residue must be in a deprotonated form, and has a pKas of 4.0. At any pH above about 5.0, it's all in the deprotonated form, so that residue should work. Any pH below about 3.0 and the enzyme is completely dead.

But an enzyme might have more than one residue that's pH sensitive. So now imagine that there's another residue which in the protonated form helps the reaction, but isn't as critical to catalysis such that the deprotonated still has residual activity. For the sake of argument let's say this residue has a pKa of 9.0.

Now imagine a third pH sensitive residue with a pKa of 6.5, but it's even more removed from the active site and has an even lower effect on catalysis (for example, it's a remote electrostatic effect based on the polarization of the transition state).

What would the pH profile for this enzyme look like? Here's an example:

"Activity" is the estimated total activity, and Residue 1/2/3 are the fractions of "active" form of each residue. - Diagram was made using the Henderson–Hasselbalch equation to determine the fraction of "active" states of each individual residue, and then assuming that the inactive forms are 0%, 80%, and 33% the activity of the fully active form for the pKa 4.0, 6.5, and 9.0 residues, respectively.

Note that the maximal activity occurs at about pH 5.7, but the activity drops off asymmetrically - the enzyme is much more sensitive to low pH than high pH.

A similar thing happens with natural enzymes, except that they may have many more residues which have minor contributions. They also may have $\ce{H+}$ and $\ce{OH-}$ playing a role as reactants (thus affecting the intrinsic reaction rate), and pH may play other effects, such a denaturing the enzyme. That's what leads to the complex pH profiles: multiple small effects all adding together.


Slow-oxidative fibres vs fast-glycotic fibres Why do slow oxidative muscle fibres contain more mitochondria compared to fast-glycolytic muscle fibres?

This is well-explained at the Wikipedia page on skeletal striated muscle.

  There are two principal ways to categorize muscle fibers: the type of
  myosin (fast or slow) present, and the degree of oxidative
  phosphorylation that the fiber undergoes. Skeletal muscle can thus be
  broken down into two broad categories: Type I and Type II. Type I
  fibers appear red due to the presence of the oxygen binding protein
  myoglobin. These fibers are suited for endurance and are slow to
  fatigue because they use oxidative metabolism to generate ATP. Type II
  fibers are white due to the absence of myoglobin and a reliance on
  glycolytic enzymes. These fibers are efficient for short bursts of
  speed and power and use both oxidative metabolism and anaerobic
  metabolism depending on the particular sub-type. These fibers are
  quicker to fatigue.

In the terms used in the article, the Type II fibers rely on anaerobic, glycolytic metabolism, whereas the Type I fibers use oxidative metabolism which, of course, requires mitochondria for the TCA cycle and oxidative phosphorylation.The Type I fibers also contain myoglobin which promotes rapid movement of O2 through the cytosol to the mitochondrial ATP synthase.


Origin of term ‘confluency’ in cell culture Since as long as I have been doing cell culture, the word confluency has been used to describe the percentage growth of cells or area covered by them. However, no dictionary that I have found uses this word. I was wondering if anyone could reliably state where the meaning comes from or how the association began, and truly what it means. I don't believe I can post this on another Stack Exchange  because the word doesn't have even a resembling meaning in the dictionary. Cell culture is such an integral part of cell biology, medical research and biological manufacturing. And this term is an integral part of cell culture. I was surprised to be unable to reliably verify its meaning.

Besides the etymologic explanation that @aandreev gave, in cell culture this term is commonly used to describe the density of adherent cells and it is used as a measure of their proliferation. It is usually combined with an estimated (or counted) percentage, so 10% confluency means that 10% of the surface the dish or flask used is covered with cells, 100% means that it is entirely covered. The cells grow twodimensional on the surface of the flask in this case. The picture below (from here) illustrates different levels of confluency:

The level of confluency is important as the cells change their growth with changing densities. Low density cells (10-20%) usually grow slower than 50% confluent cells. If the plate is complete grown by cells, they tend to grow much slower again. This influences their genetic program, behaviour in experiments and transfections.

As @Roland pointed out it is important to say that confluency is not a hard measure, but rather an estimate of the cell density. Different people will get different estimations, but the trend should be the same.


Can viruses that normally infect eukaryotic cells also infect bacteria? Can standard viruses infect bacteria?  I'm not speaking of bacteriophage but typical RNA and DNA virus such as influenza and Ebola.

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

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

Here is a review article about the phage classification.


Dominance coefficient I am trying to understand the meaning of the dominance coefficient. I'll be more specific to what I don't understand, in a moment.
Let $A_{11}$, $A_{12}$ and $A_{22}$ be genotypes with fitnesses $1$, $1-sh$ and $1-s$ respectively. I can understand the meaning of the selection coefficient $s$ as its sign clearly determines which allele is more advantageous.
Though, I cannot figure out the meaning of the dominance coefficient $h$. I understand the following:

if $h>1$ we have underdominance i.e. both homozygotes are more fit than the heterozygote
if $h<0$ we have overdominance i.e. the heterozygote is more fit than the homozygotes
if $0 < h <1$ we have that the heterozygote is only more fit than the deleterious homozygote

The last point is called incomplete dominance as opposed to complete dominance in the cases $h=0$ and $h=1$. Here, I'm having trouble to understand how this is related to dominance. I mean, I can clearly state that $h=0$ implies that the fitnesses of $A_{11}$ and $A_{12}$ are equal, but why does this imply that $A_1$ is dominant and $A_2$ recessive (the situation $h=1$ is symmetrical of course)?

For this terminology, I'm referring to Gillespie's Population Genetics: a concise guide. A table resuming what I'm talking about is also on Wikipedia here.

I'd like to point out that I'm not a biologist, but just a mathematician, so it may be something simple in how dominance works that I'm missing. Also, for the same reason, please, forgive me if I have worded something not appropriately. Thanks to those who will help.

EDIT: I'm not asking what the biological process behind dominance is. I'm just asking how $A_{11}$ and $A_{12}$ having the same fitnesses (which, for me, reads as having the same chance at surviving) relates to $A_1$ being dominant. As it was pointed out in the comments, this is the definition of dominance. Though, I thought that dominance of one allele means only which phenotype will prevail in the heterozygote case and I cannot find the relation between the two definitions.

Thank you for asking such a well-thought out question, I really enjoyed how hard this made me think about the concept. I think there might be an issue here that's quite common to biology, in my experience- poor definition of terminologies.
I think the core question can be summed up by your comment:

I thought dominance was only related to which phenotype will show. If fitnesses of $A_{11}$ and $A_{22}$ are equal, doesn't it mean just that $A_{11}$ and $A_{22}$ have the same chance at surviving?

In my thinking, the definition of dominant could mean two things:

The expression of a particular characteristic
The fitness associated with the expression of a characteristic

Of course, the second definition depends entirely on the first- if the phenotype of the heterozygote ($A_{12}$) is the same as the homozygote ($A_{11}$ or $A_{22}$), then their fitness must be the same- evolution acts on phenotypes, not genotypes.
Let me break this down using Gillespie's tables. For a given value of $s$ (between 0 and 1), we can imagine the following scenarios for the value of $h$:

$h$
Phenotype
$A_1A_2$ fitness
Dominance scenario

h=0
$A_1A_2$ phenotype = $A_1A_1$ phenotype
$1-s\times 0 = 1 = A_1A_1 fitness$
$A_1$ is dominant allele

h=1
$A_1A_2$ phenotype = $A_2A_2$ phenotype
$1-s\times 1 = 1 - s = A_2A_2 fitness$
$A_2$ is dominant allele

This is assuming the phenotype for $A_1A_2$ is the same as the phenotype of the homozygote, in each scenario. It may be possible that the phenotypes are different, but the fitness is the same- what we are actually measuring with $h$ and $s$ are fitness, not phenotypes. But if the phenotypes are the same, the fitnesses must also be the same- natural selection works on phenotypes, not genotypes.
Where the break between fitness and phenotype becomes complete is when $h$ is a value other than 0 or 1 (not complete dominance).

$h$
Dominance Type
Scenario

0<h<1
Incomplete dominance
The heterozygote ($A_1A_2$) more fit than $A_2A_2$ and less fit than $A_1A_1$

h<0
Overdominance
The heterozygote ($A_1A_2$) more fit than homozygotes ($A_1A_1$ and $A_2A_2$)

h>1
Underdominance
The heterozygote ($A_1A_2$) less fit than  homozygotes ($A_1A_1$ and $A_2A_2$)

In each of these cases, the phenotype of the heterozygote is something different than either of the homozygotes (hence the term incomplete dominance). What the value $h$ is measuring here is not the difference in phenotypes, it's the effect it has on fitness- which might be different in different contexts.
Let's think about the classic example of overdominance, sickle cell disease. In terms of fitness, individuals with one copy of the sickle cell allele have the sickle cell trait. The sickle cell trait offers resistance to malaria, and therefore higher fitness in regions with endemic malaria. An individual with two copies of the sickle cell allele are less fit because they have sickle cell disease. An individual with no copies of the sickle cell allele is less fit because they don't have resistance to malaria infection.
But this measure of dominance, where we define dominance as the fitness associated with a the expression of a characteristic, is context-dependent- individuals with the sickle cell trait are prone to other diseases, and in the absence of endemic malaria it might be they have lower fitness than an individual with no copies of the sickle cell allele ($0<h<1$).
If we think about dominance as simply the expression of a characteristic, we would actually describe the sickle cell heterozygote as co-dominant- when you look at the blood of individuals with sickle cell trait (heterozygotes), they have a mix of normal-shaped red blood cells and sickle-shaped red blood cells.
So to conclude:

Dominance sometimes refers to the expression of a trait in relation to an allele, and sometimes refers to the fitness associated with the expression of a trait in relation to an allele.
Differences in fitness imply differences in phenotype (because natural selection acts on phenotypes, not genotypes)
Differences in phenotype do not necessarily imply differences in fitness

I wrote also some notes on the following, but as they're not directly relevant to the question (but might be useful for Googlers later on) I will put them here below the cut:
Table of relative fitness measures with dominance coefficient $h$ and selection coefficient $s$

Genotype
$A_1A_1$
$A_1A_2$
$A_2A2$

Relative fitness
$1$
$1-hs$
$1-s$

The choice of alleles assigned to $A_1$ and $A_2$ are arbitrary- in reality these are As, Ts, Cs, and Gs. By convention the first allele is the dominant one, but if you're not sure which is dominant before you test it may be the second!
Similarly, by convention we assume the individual with $A_2A_2$ is not more fit than individual with $A_1A_1$ (in other words, $0<s<1$). But you might have it backwards!


How will changing the concentration of a Tris buffer affect amylase enzyme activity? For instance if you increase the amount of Tris but pH still does not change then will the enzyme activity still proceed normally?  If it does change the pH will it change enzyme structure and why?

I realize I'm 4 years late, but wanted to give an answer to this. It appears that tris often has inhibitory effects on amylase activity. Adding more Tris will lead to competitive inhibition with the substrate and will skew the results.

Binding of Tris to Bacillus licheniformis alpha-amylase can affect its starch hydrolysis activity
https://www.ncbi.nlm.nih.gov/pubmed/18289113


Why are plasmids called plasmids? I knew from this website (https://www.etymonline.com/word/plasmid) that the word "plasmid" is a combination of "plasma" + "id" , where "id" means: belonging to or connected to.

But I don't understand how plasmids are connected to plasma even though they exist inside the bacteria cell cytoplasm not inside the blood/plasma

even though they exist inside the bacteria cell cytoplasm

Plasma has several meanings in biology.  Cytoplasm is a type of plasma.

A quick trip to Wikipedia tells us that the term plasmid was first used by Joshua Lederberg in Cell Genetics and Hereditary Symbiosis.  It seems that he coined the term plasmid to reconcile the many terms used to describe extrachromosomal DNA, at the time.

  These discussions have left a plethora of terms adrift: pangenes, bioblasts,
  plasmagenes, plastogenes, chondriogenes, cytogenes and proviruses, which have lost
  their original utility owing to the accretion of vague or contradictory connotations. At the risk of adding to this list, I propose plasmid as a generic term for any extrachromosomal hereditary determinant. The plasmid itself may be genetically simple or complex. On occasion, the nuclear reference of the general term gene will be emphasized as chromogene...


When does exposure to an allergen increase / decrease allergy? In immunotherapy a person is regularly exposed to an allergen to decrease the allergy. Yet apparently "repeated intranasal challenges ... induces robust allergic airway inflammation, " [0]

So when does exposure to an allergen cause allergy induction vs hyposensitization?

[0] http://www.researchgate.net/post/Which_is_the_best_way_to_sensitize_mice_to_house_dust_mites

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

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

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

See these papers for more information:

Allergen immunotherapy.
Allergen-specific immunotherapy


What is different between the pigment of giraffes and the pigment of flowers? I saw this video created by Derek Muller and he says there that it is very unusual to evolutionary develop the colour of the skin without the pigment. That sounds reasonable but if so, what nutrients have to get animals with pigment to get colored? Is it an active job of the cells or skin cells are just full of colorful minerals?

In case of giraffes: How does skin correct the shape of the spots? (For instance in cause of zebras it is clear according to this video)

And what about purposely colorful flowers? What nutrients do they need?

Thank you very much.

Pigmentation in most animals which is between black, brown, red, yellow and which is made up by the mixture of two pigments: Eumelanin (yellow to red) and Pheomelanin (black to brown). The ratio between these two makes a color. These are pigmental colors which are made by a special kind of cells in the skin, in mammals they are called melanocytes (and I will only look into mammals here, as this is already complicated enough). Additionally there are other colors, especially in fish and insects iridescent color play an important role.

This pigmentation is made by a cascade of enzymes from the oxidation and polymerization of the amino acid tyrosinase. So there are no minerals involved in the process. See here for more details.

For the pattern: As far as I know the literature, these pattern by x-inactivation are only present in cats. Here one of the enyzmes which is important for the generation of the dark pigment is encoded on the x-chromosome of the animals. Gene defects on this chromosome then lead to pigmentory defects.

Pigmentation patterns can be explained by a model which was formulated by Alan Turing and which is called "Reaction Diffusion Model". You can find an interesting article about this in reference 1.

Basically two different morphogens (different pigment cells) influence each other with positive and negative signals. If these signals would occur independently, than only relative incomplex two-dimensional colorations would be possible. See the figure from reference 2:

References:

How the zebra got its stripes, with Alan Turing
Reaction-Diffusion Model as a Framework for Understanding Biological
Pattern Formation


Why is the Hydra Biologically Immortal? I have heard that the Hydra organism is biologically immortal (later I found that there are more immortal organisms). Now I know that its immortality is related to its telomerase. The thing is that we all have telomerase, but we age and Hydra don't. What are the proteins (especially telomerase) related to aging in humans and Hydra and how do they work differently?

Hydra are just one of the many organisms which are immortal.  That is to say all their cells divide forever - there is no senescence (planned cell death) in any of their cells. Interestingly Hydrae that reproduce sexually age and die, but asexual reproduction appear to be immortal.  Animals that are immortal more often reproduce asexually... this may only be because immortality became unpopular in evolution early on and may have not developed senescence in the way other animals have, or lost it when it was not so integral to life.

  Although immortal Hydra also appears to share the (TTAGGG)n telomere repeat, there is as yet no data on how or whether they avoid chromosome end depletion. These data suggest the possibility that senescence or death of asexual individuals and colonies may in part result from a failure to maintain chromosome ends that are restored by going through a sexually reproductive cycle .

So its not clear if the telomeres are protected in hydrae and other immortal animals.  I would guess they probably don't have active telomerase if they are truly immortal, though its possible the telomeres are shortened and are repaired.

There are other factors which are supposed to be important for immortality.  Yeast and single eukaryotes are not individually immortal; an individual mother cell can only divide a limited number of times. While hydrae are not a popular focus of research, there has been a concerted effort in trying to understand yeast mortality and there are more than one mechanism being pointed to.

Since there is no germline in single celled organisms, (they only have one copy of their genome to reproduce from) telomeric shortening would not be a useful mechanism for aging; Calorie restriction has been shown to prolong fission and budding yeast by activating pathways which slow aging by protecting against stress, and slowing down reproduction.  All of these findings have strong parallels in work in aging in animals which is a hot topic now.

Finding these pathways is encouraging strong thought that aging and senescence are an evolutionary adaptation rather than a biological necessity.

  Our current knowledge suggests that an apoptotic program has evolved in microorganisms as a survival strategy beneficial to the group. This program is dependent on cellular pathways like the Sch9, Tor1, and Ras/PKA pathways and its activation reduces cell protection and maintenance and raises the level of superoxide production, which in turn contributes to cell damage and death. Superoxide also elevates DNA damage and mutation frequency in the aging cultures ... Aging and apoptosis are intrinsically related in yeast and the mechanisms that cause them have just begun to be elucidated. ...  will provide important information to understand the fundamental biology of aging in other species and investigate the controversial hypothesis that an “aging program” might be conserved in higher eukaryotes.

There is an open question as to whether an immortal yeast could be engineered to be immortal.  A team at Max Planck Institute did a lot of foot work and found a strain which they claim does not seem to experience individual mortality either.

So this does indicates that immortality might not be a necessity for any cell or maybe even for animals.  Occasionally, even animal and human cells can be coaxed to revert to an immortalized state, though usually it is the result of cancerous rearrangements of the genome.

This is a rich field and there are lots of telomerase focused ideas too.  Maybe someone can post something along those lines.


Does melatonin change the appearance of humans? Melatonin (not to be confused with melanin) was sold as a wonder drug during the 90s. I remember images of mice, which supposedly got a more beautiful fur. I would like to know whether the effect is true and whether it also has an effect on humans skin (or appearance in general).

Obviously, googling about melatonin generates a lot of suspicious results.

Melatonin is a hormone produced by the pineal gland located in the brain, and its production is inhibited by light to the retina and permitted by darkness (reference). It has a lot of effects on the body (reference) but I will stick to just discussing its apparent effects on aging and skin.
Melatonin works as an antioxidant and helps in removing free radicals from the body (reference). Research has shown that free radicals could damage the skin (reference), so I would have to conclude that melatonin could have a part to play in maintaining the beauty of your skin.
It is a known fact that melatonin levels in the body decrease from age, and its decrease has been correlated with some of the effects of aging (reference). As you have mentioned in your question, there is research proving that melatonin could decrease the effect of aging in rats (reference). Also melatonin was found to increase the youthful rhythmic activity in a shrew (reference). In the paper titled melatonin and skin aging it has been stated that

In UV-induced solar damage, melatonin distinctly counteracts massive
generation of reactive oxygen species, mitochondrial and DNA damage.
Thus, there is considerable evidence for melatonin to be an effective
anti-skin aging compound.

Moreover in the paper titled "On the Role of Melatonin in Skin Physiology and Pathology", it has been proposed that

Melatonin (synthesized locally or delivered topically) could
counteract or buffer external (environmental) or internal stresses to
preserve the biological integrity of the skin and to maintain its
homeostasis.

So in conclusion, I would have to say that melatonin does have a lot of positive effects on the skin but, given that it is a hormone and there are side effects (reference), it should be used in moderation.


Investigating rare variants in ethnically different populations (European ancestry & African ancestry) If you are investigating low-frequency and rare variants for a complex trait using exome sequencing, why would one consider using different populations (African ancestry and European ancestry) especially considering that the populations have different allele frequencies. Is the main object to see if they're could possibly be novel rare variants in each population at different allele frequencies?

Too long for a comment, but sort of:

Mainly you do this because these populations have segregated long time ago and developed differently, so it is more likely to identify these polymorphisms. It is also helpful to use populations for this which mixed not too much with other populations (thats why north-americans are usually not used here, as America was kind of a melting pot).

You will find rare SNPs for pigmentation in europeans that are not present in the more ancient african population (and must therefore be occured after the populations divided), examples are the so called "golden mutation" in SLC24A5 (rs1426654) or a polymorphism in IRF4 (rs12203592).


Method to inject genes into cells The famous Hershey and Chase Experiment uses phages to inject genes into cells.

In the beginning, Professor Yamanaka injected 24 types of genes into cells to figure out which genes turn a cell into ES cells.

Did he also use phages?

Remember, phages infect bacteria. It looks like he used something called pMXs-based retroviral vectors instead, which is based on the Moloney murine leukemia virus (MMLV).

I have never heard of that virus before, but I do know of others used in vivo to deliver genes, including Lentivirus, Adenovirus, and Adeno-associated virus. All have their strengths and weaknesses. Adenovirus is large so you can fit a big gene inside it, but it tends to illicit a high immune response. AAV, on the other hand, is very small but has a much more mild immune response. It can fit a gene about 4kb long inside or half that if you use a fast expressing form called self-complementary AAV. What is nice about AAV is one of the subtypes (technically callled serotype) can cross the blood brain barrier, so it has already been used in clinical trials to try and treat neurological diseases, including Parkinson’s.


No digested product bands, but markers are visible. What could be the reasons? I had to digest my insert containing plasmid and another vector into which my insert has to be ligated, each with BamHI and NotI.

Upon digestion, I ran the gel to check for results. The digestion seemed to be ok the first time with reasonably good bands. Since I needed more concentration I ran the gel with the same reaction setup (30microL) for the second time.

Well 1 - 100bp marker

Well 2 - Insert in a vector (820 ng/microL, 3microL)

Well 3- Plasmid vector into which the insert has to be ligated (1000 ng/microL, 2microL)

The marker bands were faint while there were absolutely no bands in the other wells. What could be the reason for failure during the second run? I've performed the second time digestion in a span of 40 min after the first one.

Usually there is no issue of mixing. One possible reason is degradation. But you say marker is faint (marker wont get degraded). Stain the gel with extra EtBr and see again. If you reused the gel then definitely stain it again because EtBr migrates towards the cathode.

It doesn't seem like degradation to me but to be cautious for the next time:

Use freshly autoclaved water. If you are not sure then filter using syringe and keep some 10ml for yourself
Ensure that the plasticware are also autoclaved properly.
Use endo - plasmid extraction kits, if available
Dissolve the plasmid in TE (only if conc is high and you need not put much in the reaction mix else EDTA interferes in the reactions. In that case use Tris-Cl pH-7.6 ).
If you have to digest a lot of DNA then set up small reactions in many tubes.
Do not incubate the reaction for a very long time (>6h).
Inactivate the enzyme by heating if you are not running the gel immediately.
Ensure that the gel running buffers are not too old.


Relationship between mN and mg in vessel contraction studies? What is the relationship between mN and mg as the units involved to measure the changes in contraction?  A tool most widely used is an instrument called myograph. In these exoeriments, either units of mg or mN is used without any mention of why. Note that the first two examples use an experimental tool called a myograph - used to measure the force produced by a muscle (in this case muscular blood vessels) when under contraction. Both examples mention tension. Wether these myograph experiments are completely different i'm unsure.

This example shows force as 'mN' from this paper Fig 1A a.
Those who are interested the caption is as follows
"Effects of Li+-PSS and NMDG-PSS in PGF2α-preconstricted pulmonary arteries. Intrapulmonary arteries (IPA) were first exposed to 80 mM K+, and endothelial function was assessed by relaxation of PGF2α contractions (10 μM) to acetylcholine (10 μM). Following a period of recovery, IPA were preconstricted to 10–15% 80K using PGF2α, and then physiological saline solution (PSS) was replaced by Li+-PSS in the continuing presence of the same concentration of PGF2α in endothelium-intact IPA"

This example shows units as 'g'. note that some examples from other papers also use units of mg essentiall x1000 similar to other unit conversions from
this paper Fig 1a.
The caption is pretty much the same as 1. Particularly thromboxane A2 (TXA2) is a pharmacological agent affecting a set of ion channels:
"Requirement of thromboxane A2 (TXA2) for hypoxic pulmonary vasoconstriction (HPV) in rat pulmonary arteries (PAs). A: hypoxia alone (3% PO2) did not induce contraction of PA (left). In the presence of 10 nM U46619, hypoxia induced a strong contraction equivalent with the response to high K+ (80K, right)"

For a third example click here. It does interestingly state "The PA rings were stretched to a predetermined optimal passive tension of 750 mg". As such mg (or g) is an alternative representation of a unit of force as presumed. Figure 1 in this link again demonstrates mg as an y-axis unit of measurement under myograph experiment

The difference between above two units is a matter of metric systems used:
The newton (symbol: N) is the International System of Units (SI) derived unit of force. One newton is the force needed to accelerate one kilogram of mass at the rate of one metre per second squared.

Another system:  kilogram (gram, milligram)-force
The kilogram-force (kgf or kgF) is a gravitational metric unit of force. It is equal to the magnitude of the force exerted by one kilogram of mass in a 9.80665 m/s2 gravitational field (standard gravity, a conventional value approximating the average magnitude of gravity on Earth). Therefore one kilogram-force is by definition equal to 9.80665 N. Similarly, a gram-force is 9.80665 mN, and a milligram-force is 9.80665 µN.
Kilogram-force is a non-standard unit and does not comply with the SI Metric System.
See:
http://www.sengpielaudio.com/ConvForce.htm


Hardy Weinberg Equilibrium problem In a small tribal population, the frequencies of two alleles A and a
  at a particular locus were 0.3 and 0.7, respectively. However, not all
  the individuals with genotype aa could live up to the reproductive age
  and the relative fitness of this genotype was found to be 0.5. The
  remaining genotypes had a relative fitness of 1. What is the expected
  percentage of heterozygotes among newborns in the next generation?

My answer is : 37 % but the answer given 43.52 %

I did the following : First I assumed the population to be of 100 individuals and then I counted the no of individuals with respective genotypes. Then I assumed that each person leaves 1 offspring except the aa ones which leave 0.5 offsprings and then I calculated the new genotype frequency from this.

This is basically the same solution as @AlanBoyd's answer, but since he asked me to, I will post my solution as well (also a reason to try out $\mathcal{MathJax}$ a bit more).

Assuming:

$f(A)=p=0.3, \\f(a)=q=0.7$

and the standard formulas:

$f(AA)=p^2\\
f(Aa)=2pq\\
f(aa)=q^2$

gives these genotypes in the parental generation (G1), before and after selection (using the fitness vector $w$):

$$
\begin{array}{c|cccc}
\text{genotype} & \text{freq G1} & w & \text{freq breed.pop} & \text{freq breed. rescaled}\\
\hline
AA & 0.09 & 1 & f(AA)\cdot w_{AA}=0.09 & 0.119\\
Aa & 0.42 & 1 & f(Aa)\cdot w_{Aa}=0.42 & 0.556 \\
aa & 0.49 & 0.5 & f(aa)\cdot w_{aa}=0.245 & 0.325\\
\text{sum} & 1 & & 0.755 & 1
\end{array}
$$

The genotype frequencies in the breeding population (rescaled so that they sum to one) are then used to calculate allele frequencies as:

$$f(A)=f(AA)+\frac{f(Aa)}{2} = 0.397\\
f(a)=f(aa)+\frac{f(Aa)}{2} = 0.603$$

These are then used to calculate the genotype frequencies in the next generation (G2), using the same HW-equations as in the beginning:

$$\begin{align}
f(AA)&=0.397^2=0.158 \\
f(Aa)&=2\cdot0.397\cdot0.603=0.479 \\
f(aa)&=0.603^2=0.363 \\
\end{align}
$$

I do not understand where the given answer $f(Aa)=0.435$ is coming from.


Why are there no known animals with an odd number of legs? In my 6th grade science book it is said that there are no three legged animals, and that no animal with an odd number of limbs exists. I checked Wikipedia and could confirm this:

  There are no known naturally occurring three-legged animals

On yahoo it is said that

  When an embryo is developing, it grows by cell division - the first single cell divides into two, then four, then eight etc. It doesnt' divide into odd numbers - each cell divides in half. So, this means that every creature develops the same on each side of it's body - same number of limbs per side.

It seems to be a valid explanation. So is it true that any organ in any living organism is either one in amount or is in even number? And the explanation of yahoo.com is fine?

I am a beginner in Biology. Please explain in simple terms.

It depends what you mean by 'leg'.

The instinctive way to define a 'leg' is based on its functional use: we use legs to walk on. But if we adopt that definition of 'leg' then there certainly are animals with odd numbers of legs: kangaroos, for instance, have a five-legged gait, functionally using their tail as a fifth leg. There is no developmental process that stops an animal from growing an odd number of appendages, and if one of those appendages happens to be used as a leg, evolution and development will have no problem with that.

However, there is another way to define 'leg', and that is by homology - 'legs' are the appendages derived by evolution from the legs of a common ancestor. Under this definition, (for vertebrates, at least) you're a bit more hard-pressed to find examples of animals with an odd number. This is because those legs are paired appendages, and the developmental pathways for the leg on one side of the body are tied into the developmental pathways for the leg on the other side of the body, so it is hard to evolve an odd number of legs from these appendages.

Hard is not the same as impossible, though. A comparable piece of evolution is the severe reduction in size of fins from one side of the body in flatfishes (flounders, sole, etc). I am struggling to think of terrestrial examples, but it is certainly evolutionarily possible to lose one appendage from a pair but keep the other.


Does PCR amplification affect microarray or DNA biosensor results? I've noticed that PCR amplification is commonly done before analyzing the DNA sample with microarrays or biosensors.

However, won't amplification biases or errors mess up the gene expression profile results you get from a microarray? Secondly, does that mean amplification only allows you to get qualitative information from say an electrochemical biosensor? (rather than actual quantitative information about DNA concentration)

Anytime you have PCR in a protocol, yes, you might mess up the quantification.  So you do as little PCR as you can, so that it stays in the linear range, preserving the different abundances of templates  (qPCR after all is the gold standard for quantifying expression), and you hope that there are minimal PCR biases between templates.


Is there a medical condition in which you can't cut your hair? Just curious, does there exist a medical condition in which a patient is advised not to or simply cannot cut their (head) hair?

Alopecia and balding, these individual experience hair loss, thus nothing to cut


How can co-dominant alleles work in flower petals? I am studying gene inheritance, and I understand complete dominance/co-dominance and incomplete dominant penetrance in flowers. I know how to recognize each case.

However, how does co-dominance work? If I understand correctly: when a gene is transcribed, both alleles are transcribed. Hence, for flower petals, if I have a "red" allele and "white" allele, and there is incomplete dominant penetrance, I get rose petals. However, if both alleles are co-dominant, why are petals either red or white? Aren't both alleles transcribed? Or perhaps, in the case of co-dominance, heterochromatin is responsible for shutting down one allele in lineage cells?

I hope that I am expressing myself correctly. Thank you very much for your time!

We tend to use "incomplete dominance" to describes situation of haplo-insufficiency.  The white flower petal has two broken alleles for making pigment, and one working copy doesn't yield enough pigment to make the flower look as red as it would if it had two working red pigment alleles.

"Co-dominance" is for two functioning alleles when the effect is that you can see them each, and the result is not an intermediate blend.  Like having a working A antigen and a working B antigen. A blood will not clot when mixed with A blood.  AB blood doesn't halfway clot, it also won't clot at all, just like A blood.


Can I relocate bird's nest? Doing a deck project and found a bird's nest.  Can I safely move it in order to continue working?

Think they'll fledge soon?
This is in New Jersey.

You can move it but the parents will likely not return to it or care for the chicks.  If they are nearly ready to leave the nest, perhaps you might wait a bit until that happens.
I'd say put things back the way they were and keep an eye on the nest.  If the parents don't return there is nothing more you can do.


Is there a standard reference for the importance of tumor heterogeneity? In a recent post, Philip Gerlee highlighted the two biggest contributions of mathematical oncology to cancer research: (1) increasing focus on the progress of cancer as an evolutionary process, and (2) looking at the importance of tumor heterogeneity.

For the first point, the standard historical reference is: Nowell, P. C. (1976). The clonal evolution of tumor cell populations. Science, 194(4260): 23-28.

However, for the second point, although I am vaguely familiar with modern work, I don't know of a historical reference. When was tumour heterogeneity first recognized as important to cancer dynamics and treatment? Was this work related to mathematical or other modeling insights? If not, what is the first important mathematical (or computational) modeling work on tumour heterogeneity?

It's quite interesting that the first reference that come to mind is not a mathematical/theoretical one (which is, in all likelihood, going to be a lot older than the one I am going to mention) but a clinical one. That would be Gerlinger and Swanton and their paper in the New England Journal of Medicine.


Photosynthesis Equation The equation for photosynthesis is

$\ce{6CO2 + 6H2O + Energy -> C6H12O6 + 6O2}$

My confusion rests in the following: during the photolysis (water-splitting) step of the light reactions that occur in Photosystem II, water gets split into 2 H+ ions, 2 electrons (which enter the photosystem), and one Oxygen ion. But if Oxygen ($O_2$) is comprised of two oxygen ions covalently bonded to each other, doesn't this mean that

$\ce{6H2O -> 3O2}$  ?

Could someone please clarify this for me?

Equation you have mentioned is balanced chemical equation. In reality these are series of Redox reactions, major two as follows,

Oxidation of oxygen from water in presence of light (energy from photon),

$ 2H_2O  \xrightarrow{Photons} O_2 + 4H^*$

Ions produced from above reaction reduces carbon dioxide ,

$4H^* + CO_2 \rightarrow (CH_2O) + H_2O$

So both equations combined, we can write general form as

$nCO_2 + nH_2O \xrightarrow{Photons} (CH_2O)n + nO_2$

In simple words to answer your doubt, in final equation 2 oxygen molecule coming from per 2 $H_2O$ molecules and 1 coming from per $CO_2$ molecule. Hence final balanced equation is

$6CO_2 + 6H_2O \xrightarrow{Photons} 6(CH_2O) + 6O_2$


What is this stinging/biting insect? The missus was bitten/stung in the palm by this (we think) in NE Scotland this morning. Pain was immediate, described as like getting a pin stuck in her hand. Apparently her first attempt to flick it away failed, and it took her second attempt to remove it. Afterwards, a short black stinger appear to remain embedded and had to be removed with tweezers.

She got fairly immediate swelling (white circle around the site, and red swelling further out). Even 20 minutes later, the swelling and pain remain.

This may or may not be the entirety of the insect.

Location: NE Scotland (indoors)

Time of Year: Early October
Size: Very small. Few mm long at most

The stinger that got stuck in your partner's skin isn't completely black. Its coloration shifts from dark brown near the abdomen to black to dark brown again at the tip of the stinger.

This identifies the stinger as one belonging to Vespula vulgaris, the common wasp as the stinger of the other most common stinging insect in Scotland (Apis mellifera or European honey bee) is honey brown to brown.

Once in a while a wasp can happen to get its stinger torn of when it's flicked away during its sting. Obviously it dies afterwards as also part of its intestines are torn.

Pictures of both stingers can be found below.


The selective pressure of contraceptives Is it possible that the use of contraceptives will produce evolution humans? Contraceptives can reduce reproductive success, so shouldn't selection favour resistance to them?

In this case it might be useful to think of evolution as a "black box", an information processing mechanism  where only input and output is relevant. From this point of view, we would expect the box to produce an output comparable to the resistance that evolution will produce in a population experiencing a poisoning effect which seriously damages its reproduction mechanism.

The evolutionary "output" from such poisoning  has been studied in great detail. Are there any lessons relevant to future human evolution in these studies?

Interesting question, but the answer is simpler than you might think.

Antibiotics put selective pressure on bacteria. Bacteria resistant to that antibiotic evolve as only the resistant ones survive. But this is the key, there has to be at least some already resistant bacteria from which the new (resistant) population will emerge.

With contraception, this is not the case. There are no spermatozoids capable of penetrating condoms, for example, and you should also bear in mind that in most cases mild hormonal disbalance is enough to prevent conception. It's a very delicate process, and contraception is basically an overkill.

Even if some spermatozoids could penetrate condoms, that trait would have to be hereditary in order for evolution to occur.

If you'd want to prove that contraception constitutes selective pressure on humans you'd first have to prove that there are spermatozoids and egg cells that can beat contraception, and that it's hereditary.

Evolution doesn't work the way you think it does. If you kill a random person, even if you kill a million people, it's not necessarily selective pressure. There are rules to evolution, and one of them is that it has to be hereditary.

This is not.

It wouldn't even come close to being artificial selection, let alone natural selection.

Besides, there's 7.3 billion of us. More than ever. We can hardly say contraception is reducing the world's population.

You also fail to see one thing, that a person who uses contraception in teenage years still has kids as a young adult. Contraception just delays pregnancy until you're ready. In evolution, there's a concept of "surviving long enough to reproduce". You can both use contraception and be an organism with 10 kids - though not at the same time.


What happens if a speciation event causes the new species to evolve out its clade's defining trait? If a speciation event occurs to a member of the strepsirrhine clade in such a way that its rhinarium is selected out, would it stay a strepsirrhine?

Yes, it would. A clade is defined as an ancestor and all of its descendants regardless of whether they look alike or not. Now, it is of course up to us (humans) to decide what we want to call strepsirrhine. If we decide that the new species that has no rhinarium is not a strepsirrhine, then strepsirrhine will stop being the name of a clade but will be the name for a paraphyletic group (and we would probably need a new name for the current clade of strepsirrhine).

You can get more information about phylogeny in this post and much more info in an intro class to evolutionary biology such as Understanding Evolution for example.


Chiasmata and Adaptation We know that during the crossing over of meiosis II, some portions of the paternal chromosome recombine with the maternal chromosome along the  chiasmata. And the number of chiasmata varies.
My question is this: If the crossing over is responsible for genetic variation, then does the number of chiasmata increase in the same chromosome in the same species for the sake of the species' survival? And if so, what factors contribute towards increasing that number?

The number of recombination events (chiasmata) varies dramatically from species to species.
It is also unlikely that this number has any universal relationship to selection, though for specific cases it has been shown that selection can change recombination frequency.
For some more information about the processes controlling this in present-day species and the inferred mechanisms driving among-species variation in recombination frequency, you might see this paper.


Differentiation of norepinephrine and epinephrine in indications Norepinephrine is less beta2 adrenomimetic than epinephrine so more selective so less bronchospasm so may be therofore better in treatment of cardiac failure and different shocks.

However, I am not sure.

I have some intuition that some of them is somehow analog of the other one.

PubMed about norepinephrine in Pharmacology

Sympathomimetics
Adrenergic alpha-Agonists
Vasoconstrictor Agents

PubMed about epinephrine in Pharmacology

Bronchodilator Agents (beta2)
Mydriatics (beta2)
Adrenergic alpha-Agonists
Sympathomimetics
Adrenergic beta-Agonists (this causes those two first indications)
Vasoconstrictor Agents

which is logical because epinephrine is nonselective beta2.
However, I am not sure if those properties include all accepted indications.

This proposes me that norepinephrine can be used better in acute situations.
However, I know that epinephrine injections are more given to allergic people to carry for anaphylactic shock.
Why so?
Probably, because of price.
How does the indications of norepinephrine differ from those in epinephrine?

The differences in the action/indication is because of differential affinity of the two molecules to different adrenergic receptors. The wikipedia page on Ardenergic receptor has a table which summarizes this.

Wikipedia doesn't cite references for it. You may have a look at some of the following old articles.

α- and β-Adrenergic Receptor Subtypes

  In the periphery, α1-receptors are located postsynaptically, mediating the excitatory effects of catecholamines at α-receptors. α2-Adrenoceptors, on the other hand, are autoreceptors involved in the regulation of noradrenaline (norepinephrine) release. In the central nervous system, both α1- and α2-receptors exist on postsynaptic cells; there are also 2 principal subtypes of β-adrenoceptors. β1-Receptors have a high affinity for both noradrenaline and adrenaline (epinephrine) and are found in the heart, brain, and adipose tissue. β2-Receptors have a low affinity for noradrenaline and are involved in mediation of relaxation of vascular and other smooth muscles and in many of the metabolic effects of catecholamines.

β-Adrenergic Receptor Subtypes: Properties, Distribution, and Regulation

                  NE=Norepinephrine, EPI=Epinephrine, ISO=Isoprenaline


What biological specimen is this? Seed? Excrement? Fungal form? Hundreds of these 1-3 mm "seeds" have been found a couple of times this summer on my deck shaded by a large oak tree. But, they are not seeds with typical seed parts.  Too small to be pollen or spores.  I am baffled. They each have one or more deep crevices or slits longitudinally. Structurally, they appear to be composed of tiny (almost microscopic) wood chips. (Though I am sure this is just the appearance they have.) The first time I found them was after a rain and they had absorbed water and swelled to twice or three times their size and had become gooey and almost gelatinous to the touch. Almost looked like hundreds of little piles of brown poop on our deck. This time the weather was dry and they look as pictured in the photo.  I swept up hundreds in a four-foot diameter area.  Another area of the deck had a similar amount.  None on the rest of our deck or any noticed in other areas under the oak tree. My biologist friend was also baffled.  Please help identify

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


Why does chromosome inversion happen? I read that chromosome inversion is a type of genetic mutation.

  Why does inversion happen? What is the purpose?

I also read that if genes do not match up during cross over between inverted chromosome and non-inverted chromosome could cause birth defect.

  Then would that make chromosome inversion fall under harmful mutation?

In addition, there are two types of inversions: paracentric and pericentric. The difference between these two inversions is that one of them invovles centromere and the other one does not.

  What is so important about centromere?

And lastly,

  Does inversion happen before humans are born, or after they are born? When does it happen?

I apologize if my questions are vague. I do not have much background information on chromosomes.

Why does inversion happen? What is its purpose?

Like many other mutations, inversion is generally a neutral mutation. Many inversions, especially those which are between small, intergenic regions, evolve neutrally by drift alone. However, selection can, and does, occur when:

inverions create structural problems with meiosis, like pericentric inversions
a breakpoint disrupts open reading frame or alters gene expression
inversion carries one or more selected alleles

Thus, inversion does not necessarily yield any advantage, but it usually does not cause any harm either (Kirkpatrick, 2010).

  Can chromosome inversion fall under harmful mutation.

No mutation is useful or harmful by default. It depends on what effect it gives in every case. Similar is the case with chromosome inversion. It is mostly a nuetral mutation, occasionally harmful, and rarely useful for the individual. Thus, in a way, it can be classified as a neutral mutation.

  What is so important about centromere?

The main point to ponder is how the two types of inversion affect daughter cells, especially during meiosis. For introduction, in a paracentric inversion, the centromere is not involved, while it is in pericentric inversion.

Now consider paracentric inversion during meiosis. Start with a diagram:

Due to a paracentric inversion during a crossover, formation of a dicentric bridge and an acentric fragment takes place. While the acentric fragment, due to lack of a centromere, is lost from the genome, the dicentric bridge forms such structure that the two remaining chromatins lie farthest apart. Eventually, due to tension, the homologous chromosomes break apart, leading to formation of chromosomes lacking certain genes. This makes the gamete and/or the zygote inviable, and reduces the recombination frequency.

Now, while very similar thing happens in pericentric inversion, the mechanism is a bit different. Again, see the diagram first:

Since the centromere is also involved in inversion, the genes on both arms of chromosomes are, as a result, inverted. When crossover takes place, both homologous chromosomes receive two copies of one fragment and no copies of the other. As a result, again, the gamete and/or zygote is inviable and the recombinant frequency is reduced (Griffiths et al, 2000).

  When does chromosome inversion happen?

Just like all other mutations, chromosome inversion can occur at any stage of life in an individual. It is not limited to meiosis, it can occur in any replicating cell in the body. However, the phenotypic effects are most prevelant when it occurs during meiosis, since it can easily lead to defected or inviable progeny.

References:

Kirkpatrick M (2010) How and Why Chromosome Inversions Evolve. PLoS Biol 8(9): e1000501. doi:10.1371/journal.pbio.1000501
Griffiths AJF, Miller JH, Suzuki DT, et al. An Introduction to Genetic Analysis. 7th edition. New York: W. H. Freeman; 2000. Inversions. Available from: https://www.ncbi.nlm.nih.gov/books/NBK22042/


Resource for finding what proteins bind? I have two lists of proteins (including phosphorylated forms). I want to determine which members of each list act on which members of the other list. What online resources exist for finding out what a given protein binds or otherwise interacts with?

I am aware of Uniprot and Phosphosite which have proved useful but I am wondering if there are others that I am not aware of.

Again: the question I am trying to answer is "which proteins from list A interact with proteins from list B and vice-versa?"

Go to the NAR database site and look for protein domain databases. You have multiple options. Here is the link.


Can protein precipitate out in alcohol during DNA extraction? In common lab sessions to extract DNA from strawberry or cheek cells, will there be protein contaminating the DNA extract in alcohol? If so, how can we prevent protein from precipitating out of the solution?

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


Why does this illusion work? This is another image I found on Google+

All lines are absolutely straight, parallel and perpendicular but why does it appear to have a curvature?

  Related: How does this illusion work?

Like these questions :) Many of these illusions come from Prof. Akiyoshi Kitaoka, a japanese Psychologist and expert for Gestalt Psychology. On his website you'll find some more fascinating illusions and questions to ask here ;)

The illusion above is named Cafe Wall illusion and the newest model to explain those illusions is the contrast-polarity model. Short explanation from his webpage:

The paper explained it better to me:

  Kitaoka, Pinna, and Brelstaff (2004) proposed a phenomenal model to
  explain the Café Wall illusion, which stressed the importance of
  contrast polarities of a solid square and its adjacent line segment.
  When a dark/light square is accompanied by a dark/light line segment,
  the apparent tilt is the direction of contraction of  the square angle
  (Figure 18a,b). In contrast, when a dark/ light square is accompanied
  by a light /dark line segment, the apparent tilt is the direction of
  expansion of the square angle (Figure 18c,d).

This explains why you perceive a tilt. If you position the smaller squares now in distinct edges of the big squares, you can achieve 2- and 3-dimenional illusions. Here you see a increasing of the tilt due to more smaller squares:

Here you can see that the positioning of the smaller squares is critical to achieve the 3D effect of the orignial bulge effect in your question:

Notice that Gestalt Psychology is a non-reductionistic theory approach and investigates mainly the phenomenology and underlying Gestalt Laws of visual perception. How these Gestalt Laws developed on a deeper level is a question of neurobiological evolution similar to, "why have some species of apes color-vision and some not". The ellipses in the explaining picture above show you, that our cognitive visual machine somehow tries to group divided objects (square and line of same contrast/brightness) in one line and we see a tilt. I'm guessing here, but this is probably due to cognitive brain algorithm that saves things and objects we see and perceive mainly by countor and shapes, rather than pixel by pixel like a computer and digital camera do it, which of course don't perceive any tilt or 3D illusion in any of those trick images :)

Read the papers for more explanations and examples, not behind a paywall:

Apparent contraction of edge angles, A Kitaoks, Perception, 1998
Tilt illusions after Oyama (1960): A review. Kitaoka, A,  Japanese Psychological Research, 49, 7-19.


Do puffin beaks have vertical slits or cracks? I have seen a photo where puffins seem to have vertical lines on their beaks.  It is uncertain if those are just line or actual slits or cracks in the beaks.  Do puffin beaks have 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)


Blood Vessels (Artery Vs Arterioles) I just have a quick question regarding what my textbook says. I have tried searching online but I have failed to find an answer. Basically, my textbook states that arterioles are smaller in diameter compared to arteries but have a larger lumen. Isn't the diameter measured across the lumen? So how can the artery have a smaller lumen but be larger in diameter?

Thank you

The key word you are missing is "relatively": I'm not clear what they mean "relatively" to based on where you cut off the passage, but they probably mean relative to the entire diameter of the vessel; the statement is probably not true for area but you would have to choose a particular artery and arteriole to compare, and both categories have a lot of variation in size within and between organisms.

Arterioles do have a "relatively" thicker muscle layer than the great arteries because they are the place where most of the contraction takes place that regulates the resistance of different vascular beds. Because of that, though, their lumen size varies quite a bit depending on the state of the muscle. When the smooth muscle in the vessel wall is relaxed, arterioles are much larger than when contracted. Even if the book is correct that according to whatever measure of "relative" they are using, arterioles have a wider lumen, I have a hard time believing this would be true over the entire range of contraction.


Wasp nest destroyed by some big wasp like insect: is that the queen? I had a small wasp nest in my bathroom. Initially there were only two to three wasps but the number increased to eight.

Today morning a big wasp-like insect (shown in the image below) came to the nest. I thought that it was the queen but it ate all the larvae and destroyed the nest.

Can someone please tell me if this is a normal behavior of a wasp? Is the "big wasp" their queen or another species?

The wasp is a Ropalidia marginata

The assailant is a greater banded hornet .
There is a video of one attacking a wasp nest here: https://www.youtube.com/watch?v=BPLRpEkNv8Q

Hornets can attack wasp and bee hives and decimate them. In europe there is an invasive species of hornet from japan which is twice as big as the european hornet.

The abdomen of the hornet is about half of the size of the animal. The abdomen of the queen Ropalidia marginata is about 1/3rd of the animal, she has very similar markings as the hornet, it seems to have evolved as a copy cat that consumes larvae. http://drkrishi.com/ropalidia-social-wasp/

You must add location information to search for animals by region and find the species. I only knew it was india/pak because of the avatar.


Can something cause both breaks and cross-links in DNA? A double strand break in DNA is exactly that: the strands of DNA are severed. A cross-linkage occurs when something forms a covalent bond between two nucleotides in DNA. However, is it possible for something to form both a cross-linkage and a double-strand (or single-strand) break? For instance, could one part of a molecule cause a break while another reacts to form a cross-linkage?

For the purposes of this question, enzymes or proteins which do this (If there are any) also count.

Cisplatin forms DNA-protein crosslinks (so DNA-protein-DNA by extension) in vitro [1] and a review [2] says that cisplatin leads to DSBs (although I can't access the primary source at the moment). But you know, with the exception of ionizing radiation, mutagens usually don't directly cause DSBs. It's caused by repair processes or things like stalling at replication forks because of the mutagen.

[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1874601/

[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4047912/#!po=11.9919


How does pressure travel through the cochlea exactly? I cannot find this answer anywhere.
What I do know is that the stapes pounds on the round window of the cochlea and this causes the fluid to move inside the cochlea itself, which has the three chambers (the scala vestibuli, the scala media, and the scala tympani), where the basilar membrane between the scala media and scala tympani is what fluctuates with pressure. This leads to the sound processing in the scala media and the organ of Corti due to the shearing motion of the hair cells against the tectorial membrane, and so on and so forth.
But I don't understand the pathway of the pressure. A lot of resources show the pressure wave moving front-to-back (towards the apex), making the basilar membrane move simultaneously. But at the same time, they also show that the full pathway through the cochlea goes front-to-back through the scala vestibuli, turns around at the apex, and then goes back-to-front through the scala tympani where the basilar membrane is located. So how can the basilar membrane be moving front-to-back when it's stretching along the latter half of this cochlear pathway, way over on the other side of the scala media?
Therefore I am unclear if (1), (2), or both of the following are true:
(1): Does the pressure somehow permeate through Reissner's membrane (between the scala vestibuli and scala media), move through the scala media (without disturbing any hairs in the organ of Corti), and then push on the basilar membrane from above, which would allow for this front-to-back wave motion?
(2): Does the pressure move the basilar membrane from below during its "return trip" going back-to-front through the scala tympani?

Short answer
The pressure wave through the scala vestibuli drives the basilar membrane response (BM). Your option (1) is correct, (2) is not. The pressure not really permeates or penetrates Reissner's membrane though; it is the pressure differential across the scala vestibuli and scala tympani that is the driving force for the BM movement.
Background
The most accepted way of viewing acoustic activation of the auditory system is the traveling wave theory (Fig. 1) as posed by the famous experiments of Georg von Békésy in the 1960's. These experiments showed, basically, that the basal part of the basilar membrane (BM) starts vibrating first (near the cochlear 'entrance' at the round window) and as the wave travels through the scala vestibuli, more apical parts get activated (Fig 2). This phenomenon explains the cochlear delay that's seen, i.e., that low frequencies tend to activate hair cells later than high-pitched sounds do (He and Ren 2013).
Reissner's membrane separates the scala vestibuli from the scala media. The traveling wave generates a pressure difference between the scala vestibuli and scala tympani. As you rightfully say, this pressure difference is established across Reissner's membrane and across the BM (Fig. 3). It is the movement of the BM that ultimately results in the sensation of sound (source: Ento Key). In fact, the movement of Reissner's membrane is comparable to that of the BM (Reichenbach et al., 2012). However, Reissner's membrane is not tuned and contains no neural elements involved in hearing. The stereocilia of the hair cells are embedded in the tectorial membrane. The shearing forces between the BM and tectorial membrane eventually result in mechanotransduction (Fig. 3). See Fig. 12.5 on this web page from Neuroscience online textbook for an informative video on the BM movement relative to the tectotial membrane.
The traveling wave is basically confined from base  to apex. Because of the tuning of the basilar membrane, high frequencies resonate the basal part (because the BM is stiff and narrow) and low frequencies the apical part (because the BM is wide and floppy). Each time a resonant frequency is met, the BM starts vibrating maximally and basically the frequency cannot go further and its energy is dissipated. Thus, along the way, sound traveling through the scala vestibuli  to the helicotrema (the boundary of the scala vestibulu and tympani) more and more energy is used up from the pressure wave. Thus, the basilar membrane is set in motion primarily by the pressure differences occurring in the scala vestibuli and by the time the traveling wave reaches the helicotrema no appreciable energy is left as all auditory frequencies have been filtered out. Remaining energy containing frequencies outside the audible range (roughly 20 - 20,000 Hz) continue to travel to the scala tympani (think of static pressure during a deep dive) and therefore the round window is necessary to act as a buffer (Robles & Rugggero, 2001).
However, there are other theories, notably one from Hermann von Helmholtz, a brilliant scientist of the 1800's that has revolutionized sensory sciences. It is called the 'sympathetic resonance' theory. I am not at all familiar with this theory, as it has been largely abandoned, at least as far as I know. The theory from Von Békésy assumes that the basilar membrane is a place-to-frequency converter that acts like a Fourier transformer, known as the place coding theory. Basically, the traveling wave dissects complex acoustic stimuli into different acoustic frequencies by menas of frequency tuning of the BM (Fig. 2). By contrast, Helmholtz assumed there are tiny tuned elements positioned in the cochlea that basically perform the Fourier transform (not shown here). If you wish to read more of the latter theory, I happily refer you to Bell, 2004).

Fig. 1. Traveling wave. source: NY University

Fig. 2. Basilar membrane movement. source: NY University

Fig. 3. cross section through cochlear duct. source: Psychology Wiki
References
- Bell, Plos Biology (2004); 2(10):e337
- He & Ren, Scientific Reports (2013); 3: 1874
- Purves et al. (eds), Neuroscience (2001) 2nd ed. Sunderland (MA): Sinauer Associates
- Reichenbach et al., Cell Rep (2012); 1(4): 374–84
- Robles & Rugggero, Phys Rev (2001); 81(3): 1306-43


Was Dr. Livesey's treatment a valid one in the Treasure Islands? Here is that incident from Treasure Island by Robert Louis Stevenson, where Billy Bones had a 'minor' heart attack or a stroke (according to R.L. Stevenson).

To give a little background about Billy Bones, he was a pirate, a toughened and hardened person who has gone through the deadly and unethical ordeals of life. He was an alcoholic and used to drink rum a lot. Dr. Livesey had previously warned him of taking any rum at all. But its quite a daunting task to let go a life long bad habit. Another thing worthy to be mentioned is that (to me it felt) Billy Bones had a very short temper which is indicative that he is a very likely candidate of high blood pressure.

In one incident, Billy Bones had a fight with an old foe of him. His foe escaped after collecting some major injuries caused by Billy Bones namely known as the Captain in Admiral Benbow inn. As the fugitive left the vicinity, Billy Bones gasping called out for rum and immediately he fainted.

  I heard a loud fall in the parlour, and running in, beheld the captain lying full length upon the floor. ...He was breathing very loud and hard, but his eyes were closed and his face a horrible colour.

Jim called in Dr. Livesey downstairs who was treating Jim's father upstairs.

  “Oh, doctor,” we cried, “what shall we do? Where is he wounded?”

  “Wounded? A fiddle-stick's end!” said Dr. Livesey. “No more wounded
  than you or I. The man has had a stroke, as I warned him... I must do my best to save this fellow's terribly worthless life; Jim, you get me a basin.”

  When I got back with the basin, the doctor had already ripped up the captain's sleeve and exposed his great sinewy arm. It was tattooed in several places...

  “Prophetic,” said the doctor, touching this picture with his finger.
  “And now, Master Billy Bones, if that be your name, we'll have a look
  at the colour of your blood. Jim,” he said, “are you afraid of blood?”

  “No, sir,” said I.

  “Well, then,” said he, “you hold the basin”; and with that he took his lancet and opened a vein.

My question is about Dr. Livesey's little surgery. R.L. Stevenson writes after this 'surgery',

  A great deal of blood was taken before the captain opened his eyes and looked mistily about him.

It almost had an immediate positive effect on the patient. My question is about Dr. Livesey's little surgery. What did he do here? Was it any form of valid treatment?

The procedure described here is called venesection. It is no longer standard of care, but was when Treasure Island was written.

Here is an excerpt from the first edition of Cecil's Textbook of Medicine (1927):

  During the acute apoplectic attack the following therapy may be employed: The patient should be put to bed with the head elevated. If he has fallen to the ground the clothing around the neck must be loosened. Difficulty in swallowing contraindicates the administration of nourishment by mouth. An enema may be given. When the face is puffy, the pulse full and strong, and there is reason to suspect hemorrhage, venesection is advisable. It should be employed only for plethoric individuals, not for patients who seem asthenic or arouse suspicion of thrombosis. Usually 250 to 300 cc. of blood are removed.


What makes certain obligate anaerobes viable in fermentation starter cultures? If Propionibacterium are obligate anaerobes (to wit, poisoned by oxygen), what makes 'Dairy' or classical propionibacteria (e.g. P. shermanii, P. jensenii, P. acidicpropionici, et al) viable in Fermentation starter cultures?

Here (mic.sgmjournals.org/content/127/1/121.full.pdf) is a link to a paper in which P. shermanii is grown in flask culture. Although the conditions are clearly designed to achieve low oxygen concentrations in the culture (the flask is almost full and is only shaken occasionally), they also indicate that oxygen is not toxic for this organism.

Also, this is from the WP page you linked to:

  Obligate anaerobes are microorganisms that are killed by normal atmospheric concentrations of oxygen (21% O2). Oxygen tolerance varies between species, some capable of surviving in up to 8% oxygen, others losing viability unless the oxygen concentration is less than 0.5%.


How do exon tandem exon duplications occur in the genome? By this I mean in cases where tandem exons are introduced by replication slippage how would a DNA polymerase by chance duplicate an entire exon cleanly (i.e. from exact start to exact end) when it doesn't even know what an exon is?

There is a section in the Human Molecular Genetics textbook about how such repeats do occur. Like the commentor said, it is likely a result of recombination. If there are repeats flanking a gene or an exon there can be paring between sister chromatids / chromosomes, which can result in the duplication. See Figure 9.7 here http://www.ncbi.nlm.nih.gov/books/NBK7566/#A1095

As for how does it "know": It doesnt. Its not just the exon that is duplicated though. It is also the DNA before and after the exon, which contains cis-elements that splicing factors bind to, which results in the exon being spliced into the transcript.

Splicing is pretty complicated but if just 50 bp upstream and downstream of the exon was also duplicated, it would probably be enough to cause some splicing of the exon. U1 and U2 snRNP bind immediately at the exon-intron junction, and the polypyrimadine tract is about 30 bp or so upstream from the exon. U1 and U2 and the polypyrimadine tract are all vital to splicing. I dont know of any work that shows the minimum requirement for splicing but if you have those 3 you will probably splice the exon at least part of the time. So in sum, its probably not just the exon that is duplicated. It is probably the exon plus the cis elements involved in splicing.