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How is it possible for the absolute fitness to be more than 1?
The wikipedia definition of Absolute fitness is "the ratio between the number of individuals with that genotype after selection to those before selection. It is calculated for a single generation and must be calculated from absolute numbers."
But in one generation there are no reproductive events so it should be theoretically impossible for the population to be larger after the selection event than before it (since no reproduction is taking place).

That definition in the wikipedia is misleading at best. Contrary to what it seems to suggest there, absolute fitness is computed across a single generation, not within a single generation. For simplicity, let's look at an example using asexual haploids with discrete non-overlapping generations. If individuals with the A genotype produce an average of 3 offspring, each of which survive with probability 0.5, the A genotype has an absolute fitness of 1.5. The key is that we've multiplied fecundity (3) by viability (0.5) and this allows us to obtain a value greater than 1.
Things get more complicated if we look at diploid sexuals. The absolute fitness of the Aa genotype is not the ratio of the number of individuals with the Aa genotype at time t+1 to the number of Aa at time t. An easy way to see this: in a population of AA and aa parents only, e.g. as produced by a cross, the ratio of Aa at t+1 to Aa at t is infinite, which would imply infinite fitness if we went this with definition. Rather, the absolute fitness of the Aa genotype is one-half the number of surviving offspring at time t+1 produced by Aa parents at time t. The one-half comes from the fact that a parent individual contributes only one-half of the genetic material of each surviving offspring. For some traits, e.g. those involved in sex ratio determination or parental care, it will not be sufficient to count surviving offspring; in these cases we apply comparable logic to counting grand-offspring.
The wikipedia seems to suggest we are to look only at viability because we are comparing before-selection numbers to after-selection numbers, within a single generation and thus without an opportunity for fecundity to come into play. That is not consistent with the common usage of the term. To be fair, I have on rare occasion seen "absolute fitness" used as a synonym for "viability"--though I cannot think of any good justification for this usage.

That definition is problematic and incomplete. Absolute fitness can be used in different ways, and can be calculated at different levels of organisation (individuals, genes etc). However, absolute fitness always relate to actual growth rate, actual numbers of offspring or other measures of fitness (so an absolute measure), while relative fitness is calculated as a fitness ratio in relation to a specific genotype (so a relative measure).
Absolute fitness is often defined in terms of the per capita growth rate of a genotype (or the intrinsic rate of increase (r) for e.g. bacterial clones), which can clearly be above or below one. However, how to measure this is another thing, and this is where many different metrics are used. In quantitative genetics and life history evolution it is common to use the net reproductive rate (R0) derived from the characteristic equation as a measure of fitness. However, sometimes the number of offspring or other measures are used as proxies for absolute fitness (as fitness components).
The definition of fitness is a tricky subject, and what to use depends on exactly what type of organism you are studying. The Wikipedia definition is clearly inadequate, and I feel that the formulation "...is calculated for a single generation..." is a direct mistake. The section "Measures of fitness" in Roff (1992) and Day & Otto (2001) (chapter on fitness from the Encylopedia of Life Sciences) are both very useful to read to better understand different measures of fitness.

Welcome to Biology.SE!
Definition of Absolute Fitness
Let's forget about the wikipedia definition for a little while. There exists different definitions of fitness. They vary only slightly and usually it does not really matter. Let's talk only about absolute fitness at first. Absolute fitness can be calculated

for a genotype
for a haplotype
for an individual

fitness can be calculated for

for a given period of the lifetime of an individual
for the whole life of an individual.

Also, absolute fitness can be calculated in function of

the number of offsprings
the number of offsprings that survive at a given age (typically age of sexual maturity), that is the number of offsrping after selection on survival.

Very often, when talking about theoretical concepts, we consider exclusively for semelparous species (species that have only one reproductive event and then die like some salmon species for example). In such case, when talking about one generation, we think of a population of adults that gets entirely replaced by a new population of offspring. Thinking about semelparous species has the advantage (among other advantages) to avoid confusion about lifetime reproductive success versus rate at which offsprings are produced. So, yes in one generation there is reproductive events. Even if selection on survival hasn't yet occurred on the offsrpings of the parents in a given generation, the fitness of these parents during this generation is calculated in function of the number of offspring that will survive later. Hope that makes sense.
Relating the above definition to your question
Now, let's relate the above to the wikipedia definition. Absolute fitness is NOT "the ratio between the number of individuals with that genotype after selection to those before selection". It is only the number of offsrpings produced by an individual for a given period (often the whole life of the individual. It can eventually be the number of offsprings that survive to a given age (selection on survival). Wikipedia seems to be wrong unless it has been misquoted. You should indicate where you read that so that one can correct wiki if there is indeed an error.
Relative Fitness
Now, relative fitness of a genotype/haplotype/individual for a given period of time (eventually the whole life of the individuals of interest) is just the absolute fitness of the individuals of interest divided by a standard absolute fitness. This standard absolute fitness is either the maximal absolute fitness observed in the population (or metapopulation) of interest or the maximum theoretical fitness based on some assumptions. For example we may calculate the relative fitness of an individual by dividing the absolute fitness of this individual by the fitness of a theoretical individual that would carry only the best possible mutations even though this individual doesn't exist in the population.

I think that if we want to settle on some definitions we should look into the book: Endler, J.A. (1986) Natural Selection in the Wild
Definition of Relative fitness

Relative fitness can also be measured with reference to a particular
  phenotype (or genotype), in which case $\overline {w}$ is not
  necessarily 1; this is the most common method used for polymorphic
  traits. If the population is sampled twice (or more) within a
  generation so that individuals in the second sample represent a subset
  of those sampled in the first sample (as in a capture-recapture or
  cohort study), then absolute fitnesses can be calculated. Examples are
  the probability of surviving between samples, or the probability of
  mating. On the other hand, if samples are made without replacement, or
  if samples are made of juveniles and adults at a single time, then
  only relative fitness can be calculaqted; information on total numbers
  and mean fitness is lost (see discussions in O'Donald 1971, Horns and
  Harrison 1970, and Manley 1974).)

Definition of Absolute fitness

Adaptedness and Adaptation. Adaptedness is the degree to which an
  organism is able to live and reproduce in a given set of environments:
  the state of being adapted (Dobzhansky 1968a,b). Adaptation is the
  process of becoming adapted or more adapted (ibid.). Unfortunately,
  adaptation.is also used in the sense of an adaptive trait (Lewontin
  1978), confounding the end product with the process (see also Dunbar
  1982). An adaptive trait is "an aspect of the developmental pattern of
  the organism surviving and reproducing" (Dobzhansky 1956, 1968a).
  There are problems in defining precisely what adaptednedd is so that
  it can be measured (Dobzhansky 1956, 1968a,b; Stern 1970; Lewontin
  1978; Dunbar 1982). One solution is to define it in the sense of
  absolute (rather than relative) fitness (Table 2.1). In this case it
  can be measured by the average absolute lifetime contribution to the
  breeding population by a phenotype or a class of phenotypes. It thus
  becomes intimately related to the actual (R) or intrinsic $(r_{m})$
  rate of increase, or "Malthusian parameter," and these have actually
  been used as measures of fitness for populations and species, though
  there are some problems (Fisher 1930; Dobzhansky 1968a,b; Dunbar
  1982). Adaptedness has also been defined as the mean absolute fitness
  (Sober 1984). [...]

Defining Generation
A generation is the interval of time between birth of an organism and the birth of its offsprings (reference from "Biology ninth edition, Rave, Johnson, Mason, Losos and Singer).
So in my interpretation, yes there is a reproductive event in one generation. If some phenotypes or genotypes are producing more offsprings compared to other individuals, and that there is a correlation between their fitness and the trait that hey have, than yes, it is probable that the population could increase. Especially if they survive, and have offsprings, enough resources, etc.


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Why asexual reproduction?
When I took a course on genetics and evolution, I learned that recombination and sexual reproduction is advantageous compared to asexual reproduction. Sexual reproduction allows more combinations of DNA because of recombination, allowing more variations of species, causing natural selection to "choose" different variations of species to reproduce and share their genes to help the species from dying out. On the other hand, asexual reproduction doesn't allow recombination. So species can only rely on mutational changes to keep a species safe from extinction. Therefore, why don't we see more sexually reproducing species than asexually reproducing species? Sexually reproducing species have an advantage, don't they?

The most obvious disadvantage is that of sexually reproducting organisms, since half of the population cannot reproduce directly (i.e. reproduction will be 50% lower compared to an asexual counterpart), which is why "the mystery of sex" has become a issue. So in evolutionary biology, I would argue that explaining the value of sex has been the bigger issue.

There is one thing that both of the answers so far do not say and you kind of have to just think of, but except for the fertilization event, all development in animals anyway is asexual cell division guided by chemical signaling. So even in a human with its trillions of cells, only the fusion of the male and female gamete occurs sexually, the rest of the organism is made through controlled cell division. That program is probably the most important part of the genetic code of an organism, otherwise it will fail to develop.

"Sexually reproducing species have an advantage, don't they?"  - To be corrected to  "A(!)-sexually reproducing..."?

When you say, why don't we see more sexually reproducing species than asexual, I presume you are referring to bacteria, protists, archaea, some fungi, etc.
Most multicellular organisims do reproduce sexually, which makes sense since an organism would need to be multicellular to have cells specialized for gametes. As you stated, the advantage is that sexual reproduction offers an advantage by allowing more rapid generation of genetic diversity, allowing adaptation to changing environments.
However, look at the single-celled organisms that reproduce asexually. Asexual reproduction is beneficial in many circumstances in that it can create individuals rapidly and in large quantities. For example, yeast can duplicate every hour under the proper conditions. For yeast, that means survival by sheer numbers. For us, it means we can make bread in a few hours.
If you believe asexually reproducing organisms are at a disadvantage due to lack of genetic diversity, consider bacteria and antibiotic resistance. The rapid generation times allow mutations to be selected for in particular circumstances. Penicillin was introduced in 1941. Two years after this landmark event, strains of Penicillin-resistant S. aureus had already emerged. Now, perhaps 2% of Staph. aureus (SA) is susceptible to penicillin, and some SA are "superbugs" with multidrug resistance: good for Staph, bad for us.
Also, it is possible for single-celled organisms to "share" DNA through mechanisms sometimes likened to sexual reproduction; lateral gene transfer occurs through conjugation, transformation and transduction.
Thus, both asexually and sexually reproducing organisms are well-suited to their ecological niches.

You forgot to mention that one part of the Yeast life cycle is sexual. You can have a mating type cells fusing with alpha mating type cells to produce a diploid cell. When resources are scares the diploid yeast undergo meiosis form an ascus with four haploid spores, two a-type and two alpha. They go through meiotic recombination the same as multicellular organisms. It is felt that this is done to increase genetic diversity and improve survival chances during times of unfavorable growing conditions.

I would also probably bold your entire third paragraph. I know we disagree about paragraph 4, but resistant SA mutants likely already existed in the population well before Fleming worked out how to extract Penicillin. Remember that SA and P. rubens have been an arms race for millions or even billions of years, so if P. rubens had a chemical to defend against SA, there were likely already SA in the population that had resistance to it.

This just in addition to @anongoodnurse's excellent answer. It was mentioned in the OP that asexual organisms do not undergo recombination; this is not true. Recombination is used for integration of foreign DNA into prokaryotic chromosomes and for repair.
Also, don't underestimate the power of mutational change in rapidly reproducing organisms. While mutation rate is low, consider the effect when it is applied to millions of individuals.
Finally, just an interesting example of the ability of bacteria to evolve. Many organisms can rearrange foreign DNA for their benefit. I will mention the specific example (because it's what I work with) of transforming B subtilis with a plasmid containing an antibiotic resistance marker and somewhat toxic gene. Often you will find transformed bacteria that have rearranged the plasmid to delete or inactivate the toxic gene while still retaining the resistance gene. Thus they can still grow in the selective medium and manage to be of no use to me whatsoever!

@anongoodnurse Well I wouldn't say that, but thanks! (I +1'd yours as well)

Good point about mutational change. In multicellular sexual organisms, only mutations that happen in the germ line (relatively few cells) can be useful for evolution, while every single mutation in the entire population can potentially have an evolutionary impact in unicellular, asexual organisms.

Sexual reproduction probably evolved because an asexually reproducing species of bacteria evolved an evolutionary stable strategy and then there was a rapid change in the environment and only the mutant individuals that could reproduce sexually could evolve fast enough to survive which later evolved into sexually reproducing animals. Also, sexually reproducing species are more likely to be able to evolve fast enough to avoid extinction when there's a rapidly changing environment. However, the true evolutionary stable strategy for any species probably has the species reproduce only by parthenogenesis. Indeed, some bacteria probably didn’t evolve to reproduce sexually and then evolved into an asexually reproducing animal species which still exists like the New Mexico whiptail and Mycocepurus smithii.
If an asexually reproducing species happens to have the right genome, it will already be adapted to all those future rapidly changing environments that will happen like the spread of a deadly parasite assuming the Sun won't get brighter or die. The ones with a slightly faster mutation rate will very slowly outcompete the ones with a slower mutation rate because they can evolve the trait that's best for the current environment faster but once the next sudden change in environment occurs, the ones with a lower mutation rate will survive because they remained adapted to the change. After enough sudden changes to the environment occurr, the ones that survived the most recent sudden change in the environment will be the ones that had a genome that prediced that that environment could occur already was adapted to it because it was adapted to the sudden changes that already happened and there is a pattern in which changes in the environment already occurred.
Another advantage in asexual reproduction is that a mutant asexually reproducing individual who happens to have the right genome in a sexually reproducing species could rear 2 kids and pass all their genes onto them if the species was already at an evolutionary stable size. However, once the asexually reproducing individuals outcompete the sexually reproducing ones and reach a new evolutionary stable size, each individual on average could only rear 1 kid.
Another advantage in asexual reproduction is that any mutation that's advantageous for an offspring is also advantageous for their off spring and the mutation rate is very low making the strength of genetic drift very weak so there would probably be less of a tendency that the more of one advantageous trait there's genetic drift against that a species has, the less of another advantageous trait there's genetic drift against it can evolve to have. For example, an asexually reproducing human could outcompete all humans other than her descendants and then evolve a genome that gives them immunity to malaria without the possibility of sickle cell anemia. An sexually reproducing species if it evolved resistance to enough past diseases doesn't necessarily have to be more prone to the spread of a deadly parasite than a sexually reproducing species. Frequency dependent selection could easily select for mutations that make some individuals different from others in order to have resistance to a deadly parasite that already evolved to spread through some individuals.
The smaller an animal is, the faster it can run without ever getting too hot because the faster it can get rid of heat. However if it exceeds the speed it can go without ever getting too hot, then the faster it runs, the shorter the distance it can run before it collapses from heat exhaustion. A larger animal that exceeds the speed it can run without ever getting too hot can run longer at that speed before it gets too hot than a smaller animal running at the same speed.
I read that a wolf never gets too hot in its chase if it's not too hot outside so a mutant asexually reproducing wolf probably would have a huge evolutionary advantage for chasing rabbits as long as the air's not above 30°C. It would be able to evolve into a poikilotherm so that it can do away with having fur so that it can get rid of heat faster so that it can chase rabbits faster so that they'll be less likely to escape and to burn less energy when it's cold out.
A cheetah on the other hand builds up heat way faster than it can get rid of it during a chase so a mutant asexually reproducing cheetah would probably also have a hug advantage. It could evolve to be a poikilotherm so that it can have a lower core temperature at the beginning of a chase during times the air is colder so that it can chase its prey for a longer time before it gets too hot to continue the chase, and also evolve to not have fur so that it can get rid of heat faster after a chase so that if a prey animal happens to come sooner after its chase, it can chase it. That's because the expected amount of energy it will gain from continuing the chase is larger than the expected energy it will burn in continuing the chase. I think they could actually get rid of heat way faster because they could walk to speed up the loss of heat after a chase because the air would be freely circulating around them.

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What are microRNA, siRNA and antisense RNA?
From what I understand, microRNA binds to proteins which can cut certain mRNA strands do that this protein is not synthesised. This seems like gene silencing to me, however I have also come across the term siRNA and antisense RNA...
Would be grateful if someone could explain what these are and how they work, and perhaps how they can be applied to treating diseases... Thank you in advance :)

Can you please clarify your question? At the moment it is hard to understand.

@Chris I am looking for a description of the functions of microRNA, siRNA and antisense RNA and how they carry out these functions. Also, if possible, how they can be applied to treating diseases. I have heard, for example, of microRNA being used to treat cancer, but I don't understand how...

I have edited your question slightly to replace "bones" with "binds". If this was not what you meant, please revert the edit.

Is this from homework or for a class?

There is an entire review on this. Your question is too broad as of now.

@WYSIWYG Neither for homework or class- i'm just really interested!

MicroRNA (miRNA) are gene-regulatory RNAs that are loaded onto the RNA-induced silencing complex (RISC) and interact with partially-complementary targets on mRNA to suppress protein expression.  The miRNA is originally double-stranded and composed of strands about 21 nucleotides long; on loading onto RISC, one strand is degraded and the other, the "guide" strand, is held on the surface of RISC where it can interact with mRNA. The targets recognized by the guide strand are most commonly on the 3'-untranslated region (UTR) of an RNA.  Binding can suppress assembly of an initiation complex on the 5' cap of an mRNA because the mRNA is bound into a circular shape at the initiation of translation, bringing the 3'-UTR and 5'-UTR close together.
If the RISC loads an RNA than then finds a perfectly complementary target, RISC cleaves the target RNA using the activity of one of the protein components of RISC called Argonaute.  This property is exploited experimentally by manufacturing small interfering RNAs (siRNA) intentionally targeted to particular target sequences.  Once loaded into RISC these siRNA might recognize and cleave their perfectly complementary target sequence within an mRNA (though there is a significant failure rate, so several sequences are often tried).  The siRNA will also have miRNA-like effects on some partially-complementary targets on various mRNAs, leading to the observation that a single siRNA sequence can modulate expression of hundreds of off-target genes.
Antisense is a nucleic acid strand (or nucleic acid analog) that is complementary to an mRNA sequence.  Antisense occurs naturally and can trigger RNA degradation by the action of the enzyme RNase H.  Originally natural antisense RNA was tried as a method for silencing a gene, but the poor stability of RNA in cells led to development of nucleic acid analogs that are more nuclease resistant and still activate RNase H (such as phosphorothioate RNA) and other nucleic acid analogs that bind to RNA and sterically inhibit processes without activating RNase H (such as 2'-O-methyl phosphorothioate RNA, Morpholino oligos, locked nucleic acids, or peptide nucleic acids).  These latter RNase-H independent oligos do not trigger degradation of mRNA but they can be used like molecular masking tape to block translation, alter splicing of pre-mRNA, inhibit activity of miRNA, block ribozyme activity, and interfere with various other processes that require some other factor to bind to a particular sequence on an RNA molecule.

Thank you for your reply! So it seems to me like the siRNA is just like microRNA, but we make it ourselves rather than it being a natural cell process like how microRNA is used? And also, is the microRNA code on an intron?

I have looked up more about siRNA and see that mmicroRNA does not have to be 100% specific, but siRNA does. Therefore siRNA only leads to cleavage of the mRNA strand from which it came (so it is complementary to this). Dooes this mean that siRNA is likely to be coded for on an intron in a gene? Also, I have read that microRNA 'inhibits translation of mRNA' and siRNA 'cleaves mRNA', so it seems like they work in two different ways (this is from a website comparing miRNA and siRNA). Could you elaborate on how exactly each works?

In some cases, miRNAs are clipped out of introns.  These miRNAs are sometimes called miRtrons. https://en.wikipedia.org/wiki/Mirtron  The mRNA cleavage and the translational inhibition are both mediated by the RISC, using the miRNA as its target-recognition moiety.  The cleavage activity is catalyzed by Argonaute, one of the protein components of RISC.  https://en.wikipedia.org/wiki/Argonaute

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Selection for less efficient egg transfer in Human Botfly life cycle
I have heard that the Human Botfly transfers its eggs through other invertebrates, and it strikes my curiosity that if an insect could simply land on its host directly to deposit its eggs, then why have intermediate hosts?
I have speculated that the vectors may be better specialized for penetrating hosts, and that penetrating hosts may be difficult, or that approaching hosts is risky. Another speculation on my part is that the Human Botfly may be filling a niche where it does not need to compete.

Possibly for the same reason as indicated here https://www.youtube.com/watch?v=a9qtVbgDnsU. Using a smaller intermediary is less noticeable and threatening to the host.

Strange - me neither (I think I could when I tried a couple of months ago, though). I can access the previous page (with the first few lines of the section "Parasitism by courier") which confirms it's the correct link.

I recently could not find the link either, but question is still open for a cited answer.

In multi-host complex life cycles (CLCs), an intermediate host often aids in the dispersal of offspring.
In general terms, an animal, say a botfly, have an ultimate "purpose" or 'goal'  to spread their genetic information as much as possible. This could mean producing a large number of offspring and hoping some survive or it could mean having one offspring, investing a lot of energy and ensuring it does survive. Regardless, spreading genetic information often requires offspring to disperse (or be spread) a great distance, which may allow the individuals' genetic information to dominate an new region.
In the case of botflies, having an intermediate host means the genetic information can be spread a great distance.
If you're looking for a more thorough explanation of complex life cycles, this paper describes it well. There is also this site more specific to the botfly which is not peer reviewed, but well-researched and descriptive.


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Is apparent competition a suitable term in situations where one species is not negatively affected?
When two prey (or resource) species share a common predator (consumer), they can be in apparent competition. An increase in one prey species can increase the common predator density, which negatively influences the other prey species.
A textbook (Molles, Seventh edition, ISBN-10: 0077837282) gives an example of apparent competition that confuses me. It gives another definition "one species facilitating populations of a predator or herbivore of the second species." Thus, one of the species does not have to be consumed by the predator/herbivore.
The specific example is that there are two plant species. Species A becomes the habitat for the herbivore (but is not consumed by the herbivore). Species B is consumed by the herbivore. Therefore, an increase in species A will increase the herbivore density and has negative effects on species B. I thought that to form an apparent competition relationship, it has to be mutually negative relationship (-,-).  In this example, there is no mutually negative relationship. Furthermore, the plants do not share the common herbivore.
This is simply a definition question. Different sources have variable definitions, but is the example really considered an apparent competition?

Competition-like interactions where only one species suffers ([0,-]) are usually labelled amensalism, so a suitable term for the situation you describe should be "apparent amensalism". I hadn't actually seen this term in use from before, but a quick Google search reveals that is in fact used. One example is in Jaworski et al. (2015):

Indirect interactions mediated by shared natural enemies are known as apparent competition, if negative interactions are reciprocal, or apparent amensalism, if one prey suffers from the presence of the other prey (Holt 1977; Holt and Lawton 1994).


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Exact location of E. coli in human body
E. coli lives in lower intestine. But exactly where can we find E. coli, and where is there none (or a really small amount) of it?
I need the exact names of parts of the lower intestine where we can find E. coli.

In Gastrointestinal Tract Location of Escherichia coli O157:H7 in Ruminants (Grauke et al. 2002):

in the lower GIT digesta, specifically the cecum, colon

It's about O157:H7, but I think the standard act a same.

FYI, this study was performed in sheep and cattle, so it may or may not apply to humans.

Yes I saw, not a human and not a standard E.Coli, but it's the best I found. If someone know better source, please share.

Best I could find for humans was Population structure of gut Escherichia coli and its role in development of extra-intestinal infections which says "large intestine"


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Survival curve in early humans
The survival curve/function describes the probability of a given individual to survive to age $x$. In humans, today's survival function is very much influenced by medicine. This leads me to wonder what the survival function looked like before modern medicine. Typically I wonder what the survival function looked like during the paleolithic age.
What did the survival function looked like during the paleolithic age?
Why did the survival function looked like that? What were the major causes of mortality for males and for females?

I posted an answer based on the same info as the answer here, since those papers can be useful for this question as well.

To obtain a full survival curve (basically a full life table) you would need to make quite a number of assumptions, since the data for paleolithic societies is scattered and probably biased. This is however not a field I know well, but I can point you to one recent paper (White, 2014) that explores how the ratio of young and old individuals in a population relates to demographic rates, using agent-based models. Using such a model you can obtain smooth survival curves and also explore how different assumptions will affect the survival curves.
There are also data from recent or current hunter-gatherer societies that can be used to approximate what the survival curves looked like during the paleolithic. For instance,  Hewlett (1991) (pdf here) has compiled survival rate data for individual hunter-gatherer societies (along with other demographic rates and data from other types of pre-industrial societies). The child mortality rate (deaths before age 15) often lie in the range 40-50% in active (mobile) and sedentary hunter-gatherer societies, with an infant mortality rate usually between 10-30% (death before 12 months of age). This indicates a fairly steep survival curve, which is the reason why the average age of paleolithic people is often estimated to ~25 years. This doesn't mean that most people died around the age of 25, just that the distribution of ages was very skewed and non-normal. Many died young, but people that survived to adulthood could become much older than 25.


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Calculation of the bacterial growth rate from a spectrophotomer growth curve
Typically the microbial growth in liquid cultures is monitored by turbidity. Data is obtained with a spectrophotometer to measure optical density at 600nm. The slope of the bacterial kinetic curve in exponential phase is the growth rate.
But I have seen two ways of calculate the growth rate:

Growth rate = Maximum slope value of the Kinetic curve
$Log_{10}$ transformation of the growth data and then calculate the slope.

I think the second one is right if you want to calculate the generation time:
generation time = $\frac{ln(2)}{Growth rate}$.
What is the correct way to calculate the growth rate and then generation time?

This is a common experiment for microbiology courses and you can find instructions on the internet , here is an example from University of Wisconsin: http://inst.bact.wisc.edu/inst/index.php?module=Book&func=displayarticle&art_id=114
But the general method is measure optical density at regular intervals and plot them on a semilog graph, which has the normal linear scale on the X axis for time, but a base 10 log scale on the Y axis for optical density. You can set this up in microsoft excel or libreoffice calc by right clicking the y axis and going to format axis, there should be a logarithmic scale option somewhere depending on the version.
After you have the data plotted, the exponential growth phase should appear as a line with positive slope. The logarithmic scale on the Y axis will automatically transform the exponential curve into a straight line. To determine growth rate in terms of generation per hour, you need to get the optical density at time 0, which is the beginning of the exponential phase, and time t, which is just some other time on the exponential phase. Use this equation to determine growth rate: $k =\frac{log(X_t) - log(X_0)}{0.301t}$
Once you know the growth rate, you can determine the generation time with $t_{gen} = \frac{1}{k}$, which gives time for 1 generation in hours. To convert to minutes, just multiply by 60.
As a side note, remember to blank your spectrophotometer with sterile media. Also, if the optical density goes over 2 it won't be as accurate, so dilute the aliquots to make the optical density go below 2. Remember to record the dilution factor so you can multiply the density by the dilution and get back to the "original" optical density for plotting.


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Why was disease transfer to the Americas one-way?
It is well known that the European colonists brought many infectious diseases to the Americas, and that these had a deadly effect on the native populations, because they had no immunity to them. Were there any local infectious diseases to which the colonists were not immune? I’ve never heard of such. I’m not aware that the colonists suffered any epidemics, or that they brought any new and unusual diseases back to Europe.
Why not? Is this merely an accident of history, that there were no infectious diseases in the Americas which did not already exist in Eurasia? Or is there some explanation?

I assume because if a disease is contracted and mutated at a certain rate, then the chances of it developing further into new strains in a large number of population is faster than lets say the few native colonies, hence if you stretch this through time you can see that even the simplest of viruses that people have build immunity to over say 100 years can be deadly to a few that might have never encountered the virus before. but thats just my guess.

@BenCrowell That malaria may have been carried by the slaves instead of being indigenous in the natives. http://en.wikipedia.org/wiki/History_of_malaria#Spread_to_the_Americas

In "Guns, Germs, and Steel" Jared Diamond includes quite a bit on this topic. His conclusion is that Europeans, and old world humans in general were much more exposed to their farm animals, often living in the same buildings. This allowed a much greater number of diseases to jump from animal to human, forcing us to development immunity against these pathogens.
The native americans never domesticated as many animals, and weren't exposed to as many pathogens. As a result the foreign pathogens could freely move through their populations.
So why did it only go one way? A lot more Europeans came to American than vice-versa, so there just wasn't as much opportunity for American pathogens to move to Europe. Additionally, the Europeans brought a lot of animals here, including cattle, horses, and pigs. These would have carried pathogens as well, again, very few American animals were taken to Europe.

I find this very hard to believe (though I know absolutely nothing about it so I am likely wrong). Surely at least the parasites were a problem for the colonists! We know there are all sorts of parasitic pathogens endemic to the Americas, none of which would be familiar to the European immune systems. Weren't they an issue?

I'm not an expert on parasitic diseases, but off the top of my head parasites just don't seem as contagious or as deadly as the viral or bacterial diseases of the time. Some parasitic diseases did slow European colonization of Africa, particularly malaria and sleeping sickness, but these weren't present in the Americas at the time. And the same conditions that exposed Europeans to more viruses and bacteria would have probably exposed them to many common parasites, possibly conferring at least some resistance to the parasites they encountered here.

@user137 - As a small extension of what you've written, I'd suggest pointing out that most Europeans who came over here and got sick probably died here rather than take the disease back to Europe.

Yeah, we don't remember how many people were killed by disease. Cities were so bad that deaths outpaced births until the 19th century, they relied on immigration to sustain themselves.

@Bobson I agree... but at some point in the next centuries, many americans DID visit Europe. Didn't they carry the American diseases?

There is at least one important exception - it is generally thought that syphilis came to Europe from the Americas.

But as far as we know it's the only exception. And the percent of Europeans killed by it was much smaller than the percent of Americans killed by European pathogens. And the 2011 paper that supports an American origin for syphilis analyzed skeletal evidence. I'd like to see PCR evidence for the bacteria in skeletons dating prior to 1492 on either side of the Atlantic, but 600 year old skeletons probably aren't the easiest to get treponema DNA from.

@user137: There's also direct genetic evidence from the bacteria itself the  that modern syphilis descends from a related South American disease.

@slebetman, thanks, that sounds like better evidence.

@caseyr547 I read the article that question refers to, and tried to follow the sources for evidence of those diseases originating in the Americas, and couldn't find anything beyond those assertions. However, wikipedia claims that polio probably occurred in ancient Egypt and Rome, even if not in widespread epidemics. Viral hepatitis is caused by several different viruses, from different families of virus. Encephelitis is similar. Some of these may have originated in America, but probably not all. Part of the problem is that tracking old disease requires those diseases to have symptoms obvious

Comment too long... Obvious and unique enough for ancient physicians to recognize them, and for historians to recognize the description. Polio is kind of like that, with its paralysis. However, syphilis had symptoms similar to other diseases often described as leprosy before 1492. Hepatitis and encephelitis would be very difficult to distinguish from other illnesses, so it would be hard to rule out their presence in Europe before 1492.

@user137 : this paper presents interesting phylogenetics for Treponematoses which suggests the most recent ancestor of venereal syphilis was a central American variety of Yaws (caused by a very similar organism). http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0000148

I want to point something important out and that's why I make it a answer. It is not sufficient explanation (maybe I'm misunderstanding) user137's answer. Let me explain why. He says that not many Americans visited Europe, it was the other way around for a long time, and it's 100% true... but they DID visit Europe after the primary colonization, in the centuries after 1492, a lot of times. Traveling from America to Europe has obviously occurred.
So, at some point there should have been a similar effect to the one occurred in the colonization of Americas with the continents reversed.


text:
Why would an Eadie-Hofstee Plot be non-linear?
Besides cooperativity between multiple active sites on an enzyme, what are the other reasons for the Eadie-Hofstee plot to be non-linear?

Is this an assignment/homework questions?

The reason is that the inhibition models are inherently wrong.
Inhibitors bind to enzymes with the same mass action principles as substrates do so the term that should describe their binding should mirror the form of the MM equation i.e. ([S]/([S]+km)).  However all the traditional equations use (1+([I]/Ki)) rather than ([I]/([I]+ki)).
To compound this problem the (1+([I]/Ki)) term multiplies into the Km in competitive inhibition but divides into the Vmax in the noncompetitive equation.  It is therefore not affecting these terms in the same way in these separate equations and leads to the conclusion it is upside down in the competitive equation.
The plots above are deceiving as they allow the user to look at a linear plot and assume mechanism based on axis intercept pattern without analyzing the actual change in kinetic parameters produced by the inhibitor.  Kinetic models should be only fit using global data fitting to the proposed inhibition model.  This can be done quite easily using excel, for an example of how this can be done check out Kemmer and Keller 2010, or check youtube.
Kemmer G, Keller S. 2010. Nonlinear least-squares data fitting in Excel spreadsheets. Nature Protocols 5:267-281.
By realizing that the change in enzyme kinetic properties relates directly to inhibitor binding the logical hyperbolic shift in values exactly like the hyperbolic curve of the MM equation must be acknowledged and finite changes in the kinetic parameters must be accounted for.
i.e. Km = Km-((delta Km)*([I]/([I]+Ki)))
  Vmax = Vmax-((delta Vmax)*([I]/([I]+Ki)))

While I have been told this may be over fitting as the competitive, noncompetitive, mixed noncompetitive equations define inhibition with one or two inhibition constant (Ki alphaKi), these terms eliminate the need for all of these equations and the family of equations that they spawned as they proved ineffective over the years (such as uncompetitive, partial competitive, partial noncompetitive, partial mixed noncompetitive, I could go on but I think you get the point).
Additionally the competitive, noncompetitive and mixed noncompetitive equations define the effect of the inhibitor with the equilibrium binding constants and do not allow for the possibility that complete inhibition may not occur (no delta terms), leading to the family of equation to try to make up for this, i.e. partial competitive and partial noncompetitive.
Use empirical models and stop trying to force mechanistic models, the data will suggest the mechanism with good experimental design.

"these terms eliminate the need for all of these equations and the family of equations that they spawned as they proved ineffective over the years" - Can you add a reference please!

Walsh R. (2014) Are improper kinetic models hampering drug development? PeerJ 2:e649 http://dx.doi.org/10.7717/peerj.649           http://cdn.intechopen.com/pdfs/36518/InTech-Alternative_perspectives_of_enzyme_kinetic_modeling.pdf

Wikipedia where these equations have been up for several years although people still try to make the old methods coexist side by side http://en.wikipedia.org/wiki/Enzyme_kinetics http://en.wikipedia.org/wiki/Enzyme_inhibitor

One thing I hardly understand, why don't they use the Vmax + (Vmax2-Vmax)*(...) form?! It is much easier to understand x than --x... Btw. nice article, thanks again! :-)

On Eadie-Hofstee plot, you can draw enzyme activity changes for example inhibition in a linear form:

Figure 1 - inhibitions on Eadie-Hofstee plot

left-top: competitive inhibition
right-top: non-competitive inhibition
left-bottom: uncompetitive inhibition
right-bottom: mixed inhibition

(Btw. they are linear on Hanes-Langmuir, Lineweaver-Burk plots too.)
edit:
According to review "enzymatic" linked (2012 - Alternative Perspectives
of Enzyme Kinetic Modeling) these plots were important only before the development of the unified enzymatic activity modulation equation (2007). (I had learned about this topic somewhere between 2004 and 2009 that's why I weren't up to date.)

Can you explain this and not only drop in a image and some links? This will not help someone who is not familiar with the topic.

@Chris The question was very specific so I wrote a very specific answer. For those who did not know the topic I added wikipedia links, so if they are interested they can read a detailed description there. Why should I write more? It wasn't the question to explain how enzyme kinetics work, and how to draw an Eadie-Hofstee plot...


text:
What are the structual differences between DNA and RNA?
How is the structure of DNA different from that of RNA?

This looks like homework. See the homework policy of BioSE.

Seems like an odd homework post though, he answered his own question.

DNA and RNA are similar, but different molecules. Both are made up of nucleic acids attached to a backbone made of phosphate and a sugar forming a nucleotide. DNA uses the nucleic acids Guanine, Cytosine, Adenine, and Thymine, while RNA replaces Thymine with Uridine.

The nucleic acids can form pairs due to hydrogen bonding, which allows the DNA/RNA to store information, if one strand has a C, the other must have a G and vice versa. Same applies for A and T.

While both molecules are capable of forming double helices by hydrogen bonding between G and C or A and T/U, the types of helix tend to be different. DNA prefers to form what is known as a B type helix, while RNA prefers the A type.

The left most helix is A type, the middle is B type, and the right helix is Z type, a highly unusual form found only under certain conditions.
DNA is almost always found as a double stranded molecule, and is primarily responsible for storing the information for making proteins and RNA and regulatory functions in cells. RNA is made by copying information from DNA through a process known as transcription and performs a variety of roles. Messenger RNA, or mRNA, carries information from DNA to ribosomes where it is used to build proteins through translation. Transfer RNA, or tRNA, carries amino acids to ribosomes to build proteins. The ribosome itself is made of RNA, known as rRNA, with proteins to help it function. Even through RNA is usually made up of only 1 strand, it can fold up and form complex shapes, such as the characteristic tRNA structure shown below. Some RNA molecules can even act as catalysts, carrying out chemical reactions such as cutting up other RNAs. These catalytic RNAs are known as ribozymes.

good answer, but could you add some references of where you got the images?

The images all came from the wikipedia pages I link to in the answer. Didn't realize the image URLs get converted to an imgur link so you can't even get the original URL by clicking on edit to look at the source code.


text:
During bridge amplification of DNA sequences, why aren't sequences amplified in both orientations?
During bridge amplification, when sequences attached to adapters on the surface form "bridges" and are replicated, it seems like sequences with either end attached to the surface will be created.
For instance, in this link in figure 7, there are sequences facing both ways on the plate. In step 8, all the sequences are oriented in the same direction (pink end attached to the surface)
How are does this occur? How are the other sequences removed?

See this document on how Illumina sequencing works.
When you are doing a single end sequencing, the reverse strands produced after the bridge amplification + denaturation (step-7) are specifically removed (clipped at the junction of primer and the "insert" region). Furthermore, the free 3' ends are blocked (by chemical modification) to ensure that there is no unwanted priming.
For paired end sequencing, both strands are sequenced; so in one flow cell the forward strand is cleaved while in the other the reverse strand is cleaved.

Presumably they removed one set of fragments from their figures for clarity of demonstration. In reality, both fragments remain immobilized on the chip. The sequencing primer only anneals to one adapter which allows selective extension of one of the sets in each run. For fragments of sufficient length, this provides an easy mechanism for creating paired end sequence reads as you can use one primer to read one strand and, subsequently, another primer to read the other strand.


text:
Do metastatic cells still have their parent's identity?
If a liver cancer, for example, gives metastases. Will metastatic cells still have liver identity? I mean, if we mark liver cells, will we see the cancer cells too?
Thanks a lot!

Welcome to biology stack exchange. This is an interesting question and could be important in certain cancer research. I suspect the answer is highly dependent on what you're using to label the liver cells and how the cancer cells have mutated as they migrated throughout the body, but don't know of any specific examples. You might want to consider some edits to grammar and wording to make this a little more readable.

My English grammar is really bad, sorry. I tried to edit a little. Thank you for the answer!

I made an attempt to improve the grammar.

Welcome to stack. This is a good question.
To answer your question: Generally, yes.
Howeve like @user137 stated below it can depend on many factors most notably how many division cycles they go through, and also where they metastasize to. The immediate environment of a cell is very effective at altering gene expression.
I use Hepg2 cells regularly. These are hepatocellular carcinoma cells that can be cultured. These cells are known to express 3-hydroxy-3-methylglutaryl-CoA reductase and hepatic triglyceride lipase, two enzymes characteristically highly expressed in liver cells. If we want to do a quick quality control typing we will perform rtPCR for those enzymes. I have seen the expression drop off after about 4 months (~35 passages).
Looking at gene expression (ideally through microarray) is a very valid way to identify/type a cells tissue of origin.

I used to use HepG2 cells a lot too, but we never looked at gene expression and would pass them for months until they died, usually when we forgot to pass them. How do you get "new" HepG2 cells? We'd just ask the university cell repository, but I never bothered to ask where they got them.

ATCC has the lowest passage number, for most every cell line. Your looking at about $400 a line though- reficulous if you ask me but I believe they take qc pretty seriously. Hepg2 cells are pretty stable so your probably ok. If your validating a cell line (not submitters question) it's better to type it by polymorphism. http://www.promega.com/products/str-analysis/cell-line-authentication/cell-line-authentication-service/


text:
Our muscles give us the ability to move our arms but....?
I have a strange question, but let me tell you something first.
If you think of this carefully, then you realize something, please try this right now:
Contract your muscles only so that your arms move without you doing it. You can't.
The way it happens is that you move your arm (or you do something or whatever you call it), then your muscles contract.
If our muscles weren't there, then we wouldn't be able to move our arms.
We don't contract our muscles, we move our arms, then our muscles contract automatically. So the muscles contract themselves, but what gives us the ability to make our arms move after deciding when we want to move our arm?
We can't contract our muscles so that our arm moves, we make that movement, then our muscles contract, but you can't even feel it because it's so light.
This is hard to explain.
So what gives us the ability to make our arms move, but not the muscles? I'm telling you, some people won't even understand, but this is real.
Thank you.

I have tried to edit your question for language and grammar. I tried to keep the revised text as close to your original intent as possible, but if I have made a mistake, feel free to revert the edit or edit it yourself.

Your brain is responsible for interpreting your spatial "I want to reach that way" and converting it into the proper muscle contractions. You're pretty good at it because you've had a lot of practice, you started working on that skill when you were a baby.

This question sounds more like philosophy than biology.

You are trying to connect two neural circuits which are not linked. The muscles act due to discharge from the motor cortex (which gets input from the frontal and prefrontal cortex) which is not directly involved with thought process.

I am a bit confused as to what you are asking. You don't move your arm, like your suggesting, ever. No one does, and no one can. You contract your muscles which happen to move your arm. The movement of the arm is the result of your muscles contracting, not the cause.
How it happens is that your brain sends a signal to your muscles (which you cant feel). The muscles get excited and they contract. The instant your muscle contracts your hand begins to move. In the end your bones are like sticks, and your muscles are the ones that pull the stick in different directions, in order to achieve flexion and extension.
Might i suggest you read up on the musculoskeletal system (http://kidshealth.org/teen/your_body/body_basics/bones_muscles_joints.html) ?

I understand what my question is now, what causes the signals to be sent, how are the signals sent, before the muscles are even contracted.

If I have satisfactorily answered your question, please click the green tick mark to accept my answer, and if you found it helpful, please do consider upvoting the answer also.

your answer is not answered im afraid lets see if you can answer the above.

Can you please be specific as to what exactly you are asking please?

my question is now,  what causes the brain to send signals. what do we do to cause the brain to send signals, so if I want o lift my arm, then what is it that gives the brain to send signals. what comes after the intention to lift arm, and before the brain sending signals.

This is quite different to your first question which you asked. Please start a new question for this.


text:
Difference in reptile inner ear and otosclerosis
In reptiles, the sound is conducted from the tympanic membrane to the inner ear by a single bone.
In the disease otosclerosis the stapes of humans become fused to the other middle ear bones( or to the oval window ). This disease leads to the loss of hearing.
My question is - From what seems like superficial resemblance between otosclerosis and having one bone in reptiles, what is the difference between the two that leads to loss of hearing in one case but not in another ?

Good question. To understand it perfectly, you'll need a good reference to a text on detailed explanation of sound conduction by the ear ossicles in reptiles and humans. I couldn't find anything better than these here and here.
But these are partly inadequate in addressing your questions and are a bit involved in the physics used.
But, if we leave the physical details aside below is the possible reason as to why a single bone in case of reptile conducts just fine but in humans fails to conduct.
 The reptile ear has evolved such that it uses a single bone for conduction, while the human ear is functioning with three transmitting ossicles (the only example i could think of). This is similar to the working of a watch. You can create a time-keeping device by using a combination of three gears (old play watches) or a combination of a large number of gears (my Timex Retrogade). Both have the same function, but if we fuse several gears in the second case to equal the number in the first (hypothetically only), it will obviously stop working. In our analogy, the ear has evolved such that the sound is optimally transmitted due to several effects like, resonance, impedance, transformation and simple amplification along the ossicles, and all these functions depend very specifically on the shape and orientation of the various conducting elements of the system. And therefore, even a slight disfigurement might severely impair the conduction of sound. Therefore, had the human ear system evolved to work with one ossicle, it would have evaded osteosclerosis by being able to conduct with one ossicle also.


text:
What effect does the Barr body have, in relation to female Turner syndrome?
Why do persons with Turner syndrome have  developmental abnormalities, when normal XX-females do not, even though they only have 1 active X chromosome? From what I know, one X-chromosome is inactivated into a Barr body in normal XX-females, but these obviously don't show the symptoms of Turner syndrome. What function does the inactive chromosome have?

The reason is that X-inactivation is not complete (Carrell & Willard, 2005; Ahn & Lee, 2008), and as many as 15-25% of X-linked genes escape silencing (Carrell & Willard, 2005; Cheng et al, 2005). This means that some genes on the Barr body are expressed in XX-females, although often at lower levels compared to the active X-chromosome, and this is part of the normal gene dosage. The "purpose" of X-inactivation is usually dosage compensation, so that genes are expressed equally in males and females (and then actually upregulated in both sexes to balance autosomal genes, see e.g. Dementyeva et al, 2009). However, this is not true for all genes, and the ones that normally escape X-inactivation will be expressed in the incorrect dosage in X0 females. Some of these genes are thought to contribute to the symptoms of Turner syndrome.
It is also likely that the genes that escape silencing are involved in sex-linked traits, as stated in Carrell & Willard (2005):

Such genes are potential contributors to sexually dimorphic traits, to phenotypic variability among females heterozygous for X-linked conditions, and to clinical abnormalities in patients with abnormal X chromosomes.
  ... ...
  However, as many of the genes that escape from inactivation do not have Y-linked homologues, strict dosage compensation may not be necessary for all genes on the chromosome. Such characteristic genomic differences should be recognized as a factor for explaining sex-specific phenotypes both in complex disease as well as in normal, sexually dimorphic traits.

Cheng et al (2005) also point out that the expression of the genes that escape silencing is tissue-dependent, which suggests that the role these genes play in the symptoms of Turner syndrome is also tissue dependent.

Very interesting question!
And I don't think either that the linked Wikipedia article answers the question.
Unfortunately I do not know the answer for sure, but I might have some relevant information to add. So, from my studies I know that Barr-bodies are not totally inactive, they, in fact, do have some very limited transcriptional activity. It might be low in intensity, but still vital? I'm just guessing.
My other guess is linked to the development of a Barr-body in a cell with two active XX chromosomes early during fetal development. So this happens via a process called X-inactivation in which a gene called Xist becomes active on both X chromosomes, then another gene, the Tsix also becomes active on one of the chromosomes and suppresses Xist on the other. The one with the suppressed Xist remains active, the other becomes the Barr-body (the process of selecting which chromosome becomes the Barr-body is random, hence female mosaicism). So, the point is, that for correct X-inactivation, the interplay of two X chromosomes are needed, and people with Turner syndrome have only one. That might be the problem, e.g. the Xist becomes active on the one X they have and starts interfering with the normal functioning of the chromosome, and there's no Tsix to suppress it.
But, again, I'm just making educated guesses here.

Thank you for your concern. Your question fits; however, it doesn't expain the case of Triple-X female, they also express some different symptoms, it means the Barr body really plays some role but not just in early fetal development. Today I see fileunserwater's that satisfies me the most. Hope you would agree if you were interested in this issue too.


text:
How to statistically test the predictability of evolution?
Can anyone recommend me an experimental study which tries to test the predictability of evolution? The closest works I found are the studies of fluctuation tests (f.e. classical study of Luria & Delbrück, 1943) which demonstrates that in bacteria, genetic mutations arise in the absence of selection, rather than being a response to selection. Is there any other point of view from which the predictability of evolution can be studied?

Luria & Delbrück (1943) Mutations of bacteria from virus
  sensitivity to virus resistance. Genetics 28: 491–511.

What does "intentionally occuring mutations" even mean?

Hi @fileunderwater! Thank you for your comment. My question has been rephrased for better clarity.

There are things we are good at predicting and things we are not good at. Predictability of evolution is too a vast subject. You should refine it to a specific evolutionary process.

Are you interested in determining our predicitve power of a given evolutionary process or in demonstrating that mutations don't occur in response but is a (mainly) independent process? I think I don't fully understand your question.

Thank you @Remi.b for your comments. The reason for this question is that laymens often ask whether the "evolution has some final goal" (and then stops). I was just wondering, if such question could be tested by some simple experiment (simple enough for approx. 12 years old kids).

The issue with this kind of statement is that it is poorly defined and it is hard to know what experience would be considered as a good contradiction. I suppose that if you consider any experimental evolution experiment that has some replicates, you can show that they all end up a little (or completely) different. A famous example is the one of citrate usage in E. col by Lenski. Among hundreds of lines only one evolved the ability to synthetize citrate (after more than 30,000 generations)

You can consider mutation accumulation experiment showing that different mutations accumulate in different lines that are subject to the same conditions. You also may want to consider short term evolution showing the effect of genetic drift on allele frequencies. There are hundreds of study who would more or less address but the statement is too uncear to understand which one is of interest.

Predictable Evolution Trumps Randomness of Mutations
http://www.scientificamerican.com/article/predictable-evolution-trumps-randomness-of-mutations/

I think Lenski's evolutionary long-term experiment should be a good example, without being familiar with Luria & Delbrück (1943). There they use replicated populations of E-coli to study (among other things) the "repeatability" (historical contingency) of evolutionary changes. Nice overviews of the project are given in Blount et al. (2008) and Philippe et al (2008), where they study to what extent certain mutations are repeated in replicate populations, in relation to citrate metabolism and size/shape.
References:

Blount, Borland & Lenski. 2008. Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli. PNAS vol. 105 no. 23
Philippe et al (2008). Evolution of Penicillin-Binding Protein 2 Concentration and Cell Shape during a Long-Term Experiment with Escherichia coli. Journal of Bacteriology 191(3):909-21

I second this.  I think with a Galaxy account, you could do the alignments and SNP calling yourself, if you so desired.


text:
How do you estimate global species richness?
I know how estimates of species richness in a small area are made. But how do you estimate the total number of species on a global scale?
One example of such a method can be found in Mora et al. 2011.

Do you mainly want examples of other methods, or a clarification of the linked article?

@fileunderwater I want examples of other methods.

You might be interested in the below works as well as the references that they cite.
May, R. M. (1988). How many species are there on Earth? Science, 241(4872), 1441–1449.
Millennium Ecosystem Assessment. (2005). Ecosystems and Human Well-Being: Synthesis (p. 137). Washington, D.C.: Island Press.
It's worth noting that many estimates of species richness at large scales are based on the use of the species-area relationship to upscale richness measurements from small scales to large scales.


text:
What is the scientific name of this butterfly?
I have this  butterfly but I don't know its scientific name. I think that it's a common butterfly which can be seen everywhere (btw, I'm in Taiwan.) Thanks for your help :D

Could you give us an indication of the size of the butterfly and the time of year you saw it?

If it's a common butterfly, can you ask locals for the common name? That will give us more to go on.

Your specimen is in very poor shape. did the inner lower wings have have a small 'eye' two thirds of the way down? It may be very insignificant, or difficult to find, on some specimens.

With the information given, I have to say I think it's a Spangle, Papilio protenor, of the swallowtail family, probably a male.
It also is listed on the butterflies of Taiwan.
See pictures for comparison:

........................Male...............................................female............................................................................


text:
Why our bees might have suddenly disappeared
We have a large garden in Bedfordshire, UK, next to woods and to arable fields currently planted with intensively farmed rape. We usually have many bees in the garden. Earlier this year, things were humming along as usual. A cotoneaster bush in flower had perhaps a hundred bees on it at once, of at least 6 different species.
Now, in July, we have lavender and clover in full bloom, normally swarming with bees. But, not now. This morning (overcast and warm) there were two bees on a lavender bush covering two square metres. I can walk for minutes in the garden without seeing a single bee. The leafcutter bees have left no holes in our rose leaves this year.
The nearest managed hives are about 800m away. It's not just a managed hive that has gone, the bumblebees that nest in our garden have gone too.
The rape flowers are long past. I don't know what might have been sprayed on the rape.  Our garden is organic.
Wasps are down too. This is the first year in the last twenty that there are no wasp nests in our outbuildings. There are, however, plenty of flies.
What might have caused such a sudden and unusual population change? Among multiple species of bee from multiple sources, between April and July?
Could it be our globally-warmed weather? June and July have been wetter and warmer than usual, although not exceptionally so.
Are UK farmers allowed to use an insecticide on rape that could kill most bees?
Or is a dramatic in-year population change in bees a routine, if uncommon, event?
Thanks!
Update August 17 2016
Our garden bees do seem to be gradually recovering - nothing like most years, but a few bees are coming back. Other nearby houses, at least 400m from the nearest rape field, have plenty of bees.

Welcome to BiologySE - thanks for your question... though I think there could be numerous reasons and it may be very difficult to answer in this format. Do you have any specific ideas that someone could address in an answer?

This does seem to be a global phenomenon. In Poland, I was recently surprised to find a beekeeper travel across half the country to pick up a colony from a tree in an orchard. Said there were very few this year. I'd say I've observed fewer yellowjackets, too, but I could be mistaken. See Remi.b's answer about CCD.

relevant article in today's PloS Pathogens, oddly enough: http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1005757

We call it Colony Collapse Disorder (CCD).
Consequences
The phenomenon is observed worldwide and is pretty serious. Northern Ireland lost 50% of its beehives for example. Between 1997 and 2003, 10 millions beehives were lost. Many cultivated crops are pollinated by bees and we don't quite have an alternative today. In 2005 a study showed that the worth of crops that are pollinated by bees is around 200 billions dollars.
Causes
Why? The short answer is "we don't know". There are a number of possible factors and the general consensus is to think that there is not a single factor that is causing the decline but it is a combination of different factors. Possible factors include:

Pesticides
Pathogens
Fungicides
Antibiotics
Miticides
Climate Change
migratory beekeeping
loss of genetic diversity through too intense selective breeeding
malnutrition
parasitic phlorid fly

More information
The wikipedia article for CCD is very complete. You should have a look at it!

I'm familiar with CCD, but can that affect all species of bees, multiple swarms of multiple species, in a small area, from a healthy population in spring to a low population in summer? Plus, I'm guessing that the population has dropped to a few percent of its usual value. Wouldn't that be extreme for CCD?

The first reference cited by the Wikipedia page (http://dx.doi.org/10.1371/journal.pbio.0050168) is a very accessible (though now slightly outdated) review of possible explanations for CCD. PloS Biology Unsolved Mysteries are a really interesting article format and mostly quite readable, even if you don't normally read primary scientific papers (and of course are all open access!).

Insecticides in the form of neonicotinoids (and possibly similar substances) can certainly be a factor, and they can affect a wide range of pollinating insects. It is also commonly used on rape seed. Have a look at this paper for some background:
Rundlöf et al. 2015. Seed coating with a neonicotinoid insecticide negatively affects wild bees. Nature (written partly by people from my department).
In it, they report that honey bees, solitary wild bees and bumble bees all are negatively effected by neonicotinoid-treated fields nearby, using paired fields in replicated landscapes. The effects could be seen in both population density, colony growth and reproductive success.
Much more has been written about this (check out references in paper above), and sorry for the short answer, but I don't have time for more at the moment. Other factors (weather, natural fluctuations etc) are certainly relevant as well. Also, from what I know, there is a neonicotinoid moratorium in the EU, so this might not be an issue where you live. I don't know if the ban is absolute, and to what extent it is enforced.

It's going to be hard to prove anything, but I am leaning towards this conclusion. These links: Independent, Nature show that neonicotinoids on rape are particularly harmful. Spraying this year seems to be illegal, but, who knows? Local bees about 800m distant from the nearest rape fields seem to be OK.

The causes are multi factorial. Sick bees usually leave the hive and this behaviour may explain some cases of CCD, where a small number of bees and the queen are found with all other colony members missing. A colony can also leave "en masse" if they are about to starve in a last resort to find better forage. Pollinators are no longer able to adapt rapidly to the numerous threats facing them in 2017.
The human activities listed in previous posts have caused the massive decline in all pollinators. Monoculture and pesticide useage being the main contributory factors. As a child I recall many dead insect on the car windscreen on weekend car journeys, this is a rare today.

as before - can you add some references so that others can read more about your answer and this topic in general?


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Escaping resource limitations during tumor evolution
In their discussion of the importance of r- and K-selection on tumors, Aktipis et al. (2013; figure 3) provide the following illustration of a hypothetical cancer growth curve:

In it, you can see alternations between selection for proliferation and selection for survival as the populations breaks through one carrying capacity after another. Of interest to me, is the overall shape of the growth curve as several sigmoids -- with each corresponding to a different serial resource limitation. However, this growth curve is a cartoon and not a measurement of some empirical system. Are there examples of such growth curves in the empirical literature on cancer?
An ideal case would be in a well studied animal model (or humans), with a corresponding analysis of which resource limitation was overcome at each step. With at least two, but preferably more, resource limitations in series. However, I will also be satisfied with answers from cell lines grown in vitro, since growth curves are usually easier to measure there.
Aktipis, C. A., Boddy, A. M., Gatenby, R. A., Brown, J. S., & Maley, C. C. (2013). Life history trade-offs in cancer evolution. Nature Reviews Cancer, 13(12): 883-892.

Time is the limiting factor here for in vivo studies. Normally the growth curves you can actually find span about 1-2 months tops, many between 7 and 30 days (mouse model). At the very least this webpage offers some models incl. growth curves for a number of cancers.


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Is a novel homozygous SNV reasonable?
I'm doing some variant discovery in a human trio (affected child, non-affected mother, non-affected father) and I have found what looks like a homozygous novel mutation. All of the aligned reads in the child have the same nucleotide in that position, but neither of the parents do.
In looking at a small handful of variants, I've seen plenty of novel heterozygous SNVs. But on first blush a novel homozygous SNV seems extremely unlikely. Two independent germline mutations at the same position on both paternal chromosomes is all but impossible, right? Are there other mechanisms by which a novel mutation would become homozygous? Or am I right to be skeptical here?

I was going to make a hilarious joke, but then I thought some modicum of tact may be prudent. Is it possible that one of the parents isn't actually a parent?

What technology are you using.  Illumina?  Sanger?  Have you "eyeballed" the variant?

A heterozygous allele can become a homozygous via homologous recombination. You can check if the region around the SNV is also homozygous.

@WYSIWYG But remember, this isn't a heterozygous allele. It's a novel allele that didn't exist in either parent. Although from the context of homologous recombination, it the novel mutation had already occurred by that point it would be considered heterozygous. But could you clarify how heterozygous alleles can become homozygous? I'm rusty with my molecular genetics, but I thought homologous recombination swaps DNA between paired chromosomes, not copy from one to the other.

@DanielStandage https://en.wikipedia.org/wiki/Gene_conversion


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How do I import FASTA files into Haploview?
I'm trying to produce a haplotype network and so have decided to use the software haploview. However I'm having some problems importing my sequences into the software.
I Have my sequences in a FASTA format but I can't find a way to convert this into a format that haploview accepts.
Does anyone have any ideas how I can get from a FASTA format file (e.g. >Az01|Female|Azores AGGATCT...) to a phased haplotype format (Az01    Azores    0    4    2    2)?

You should let us know how your fasta files are like. What is your reference etc? These are the reads or assembled genomes?

@Luigi Collapser would just collapse redundant reads to a single sequence.

Shoot, I linked to the wrong tool!

What are your sequences? PED format is for SNP data, but I suspect you have a single gene.

I'm rather new to bioinformatics, so please excuse me if I'm a bit slow. They are reads of the ITS region of a shark species, and they're 910 bps long. I did produce a haplotype diagram in TCS, but I was told haploview was better. I'm looking at haplotypes from different geographic regions.

@WillPerry You can try this: Align reads → Get BAM → Get VCF (with GATK or something similar) → Convert to PED (VCFtools). There should be a better way; I am not aware of it.

@WYSIWYG Thanks, I've converted the aligned reads to a BAM file but when trying to produce the VCF file I was asked for a reference file. Do you know what this reference file is meant to be comprised of? I'm using PGDSpider with samtools and bcftools extensions.

@WYSIWYG Also, when I opened the BAM file in notepad it was unreadable; "‹     ÿ BC ÚUÖÍnÓ@ÅqW,ÀH¼Jå{çÎ... etc". Is this normal?

Yes you would need a reference. Your reads also have to be mapped to the genome first, to generate the BAM, so that you know the positions where the reads align. Reference is fasta file for the genome. BAM is binary; it won't be readable. You can use samtools to read it. For more info on VCF see here

@WillPerry When I read your previous comment carefully I realized that you actually need not use haploview. You can try this: Collapse redundant reads (while keeping a count) → do multiple sequence alignment. I am suggesting this because you are interested in just one region. You don't need haploview and all.


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What regulates cyclic AMP?
After reading a textbook chapter on GPCRs I am still confused by what regulates cAMP.
I took in my notes that cAMP is made by adenylyl cyclase and destroyed by cAMP phosphodiesterases (also another question within a question, are phosphodiesterases the same as phosphatases?)
So is cAMP regulated by GPCRs or is it regulated by cyclic AMP dependent Kinase A (PKA)?
I did find this article, but I'm not sure if I am understanding this correctly to answer my own question, but it seems like they are saying GPCRs regulate cAMP?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720142/
Thanks

Phosphodiesterases are not necessarily the same as the phosphatases. A phosphodiester has 2 ester linkages, like in DNA. So a phosphatase could specifically cut off phosphates with a single ester linkage while ignoring the phosphodiesters.

Have you consulted a basic biochemistry text such as Berg et al (available on NCBI Bookshelf)? Start there.

Not helpful as you do not provide a direct answer to my question or even provide the link to the text you are referencing. Here is a google search of Berg et al:
https://www.google.com/search?ei=v46SXPWTNqqMggeL4ZUo&q=berg+et+al&oq=berg+et+al&gs_l=psy-ab.3..35i39j0l9.3621.4609..5211...0.0..0.92.752.10......0....1..gws-wiz.......0i71j0i67j0i131j0i20i263j0i10i67j0i10.4283tGmD09U

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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What is the purpose of using two layers of gel in SDS- PAGE?
I just made a SDS-PAGE with a top layer of stacking gel and a bottom layer of separating gel with different pH values of 0.5M Tris-HCl. The stacking was 6.8 and the separating gel was 8.8. What about this pH change makes the gels different? What effect does this have on the proteins that I ran?

The stacking gel concentrates proteins loaded into the sample wells so that they are resolved as a unified "line" once they enter the stacking gel.  The reason for the lower pH is that this "lower ionic strength implies higher electrical resistance and consequently a higher electric field, provoking the faster movement of the proteins and of every other charged particle in the gel. Such a high electric field coupled with the glycine in the running buffer (that will not go into the resolving gel due to the pH), helps to clean the sample from the Cl- ions from the Tris-HCl buffer. That concludes in a stack of clean, denatured, and equally charged proteins in the boundary with the resolving gel; this will account for a good quality PAGE."
Bassically, in the stacking gel the pore size is larger so it gives a chance for the larger proteins and smaller proteins to equalize with each other.
"As the proteins are denatured and linearized by heating, SDS and dithiothreitol (if there is any di-sulfide bond), the proteins are loaded onto the wells on the stacking gel. The denatured proteins have a uniform mass to negative charge ratio. Since the current run from negative (top) to positive (bottom), the proteins move toward the bottom. When the electricity is turned on, the proteins and Tris-glycine enter the stacking gel. In stacking gel with pH 6.8, the N-terminal amino group of the proteins and amino acids are protonated at equilibrium which makes them less negative. The average electrophoretic mobility is very slow. A Gly-chloride ion boundary is formed since glycine moves slower than chloride ion. However, glycine still runs slightly faster than other proteins. As a result, the glycine keeps pushing the protein towards the chloride ion. In other words, the proteins are trapped between glycine and chloride ion. The proteins form a very tight band inside the stacking gel.
Once the protein reaches the resolving gel, the pH changes from 6.8 to 8.8 and the pores are smaller. As pH increases, the N-terminal amino groups are deprotonated. Amino acids and proteins are more negatively charged at equilibrium than in stacking gel. As a result, glycine moves faster than proteins. Glycine and chloride ions move ahead of the proteins. As the pores are smaller in the resolving gel, the size of the protein determines the mobility (speed). So the smaller the protein is, the faster it will reach the bottom."
SDS-PAGE stacking gel

The other major difference between the two is the amount of acrylamide in the upper (stacking) gel - it's generally around 4%, while the lower (resolving) gel can vary from 6 or 8% to 20%, depending on the size of the protein(s) you're looking for.
When you load your samples in the wells at the top of the gel, then start the current, not all of the sample enters the gel at the same time. The purpose of the stacking gel, with its lower pH and low acrylamide percentage, is to "stack" all of the proteins in your sample into as narrow of a band as possible, so that they all enter the resolving gel at essentially the same time. If you didn't have that stacking gel, your band(s) of interest could be very diffuse, and may not match up with your molecular weight marker.


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Identification of insect
I am trying to identify this insect on a hibiscus plant. Google googles is unable to identify it.

Google "Japanese Beetles".

Can you please specify where you found the insect?

Found in toronto canada

It's a Japanese Beetle Popillia japonica - they are invasive in most of North America and some of Europe now.
https://en.wikipedia.org/wiki/Japanese_beetle

They are spreading rapidly west in the United States and many areas are reporting the largest numbers ever observed, for example:
http://www.wisconsinrapidstribune.com/story/life/2017/07/19/japanese-beetles-invade-central-wisconsin/490140001/
http://www.omaha.com/living/japanese-beetle-swarms-are-worse-than-ever-this-year-and/article_77257d36-6c28-11e7-839a-877ff3c8538b.html
For control around your plants, it is recommended to manually remove them; brushing or placing them in water with some dish soap works well. They tend to congregate with other individuals of the species, so if you take them off your plants that will tend to limit the numbers that join them. However, they likely do the most damage to gardens etc as larvae, and there doesn't seem to be a good, specific way to control them at that stage.


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What are the identifying characteristics of a Jellyfish?
I was walking down the beach today (Wollongong Australia, near Sydney) and saw this Jellyfish washed up on the beach.

Then I saw another.

I wanted to work out what type it was but didn't know where to start.  I'm looking for a process to determine the category of Jellyfish this is.
I've had a look at this chart:

which tells me it is probably a Catastylus Mosaicus (Blubber fish).
I've also looked at this chart:

which tells me it is probably a Rhizostoma Octopus - Barrel or Root Mouth JellyFish (name only - still a jellyfish).
The biggest identifying characteristic seems to be the eight legs. (Clearly a jelly fish - but still a very confusing trait).
My question is: What are the identifying characteristics of a Jellyfish?

Did you do any research at all about jellyfish? What did you find? What was confusing?

@anongoodnurse I am wondering if they are using "category" in the colloquial sense and what they really mean is that they are interested in finding out how you can look at a jellyfish and visually identify its species.

@AMR - I think you're right, but it's kind of broad. Intro to jelly fish is better approached on one's own, and this site can help with the difficulties. Just my opinion.

Thanks that's helpful. I've added some comments on my own personal investigation.

Blubber fish is far more likely. https://en.wikipedia.org/wiki/Rhizostoma_pulmo and http://oceanaddicts.ie/blog/rhizostoma-octopus-barrel-jellyfish

Thanks @AMR - can you expand that into an answer?

On that @AMR - the linked article implies it is not common in the Pacific ocean (although my feeling is the article is incorrect) could you comment on that?

All I was showing you was that the Barrell or Root Mouth doesn't appear to be endemic to your area, so it is more likely your first choice, the Catastylus Mosaicus (Blubber fish).


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Is there any evidence to suggest that exercise reduces the side effects of caffeine?
I heard a friend say:

I'm not drinking coffee this week. My body can only process the caffeine if I run at least 15km a week.

I found this claim fascinating - that exercise temporarily increases the caffeine tolerance of the body.
Caffeine side effects include:

Sleeplessness
Additional grogginess when waking up
Withdrawal headaches
Decreased empathy
A decreased ability to listen to orally spoken detail
A decreased ability to calmly think

My question is: Is there any evidence to suggest that exercise reduces the side effects of caffeine?

What side effects?

There are many things that they could mean, some of which even make sense. Exercise could help lower blood sugar, and so help consume the increased glycogen caffeine triggers. It could also help if the person is getting jittery from increased respiration. Finally, increasing metabolism will flush the stuff faster. Beyond those, I can't think of anything off the top of my head.

Can you please reference where you got your side effects list from.

Hi @AMR - I've referenced it - does that help you out?


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Can the human body create glucose out of fat?
I read conflicting views about whether or not the human body can create glucose out of fat. Can it?

Odd chain fatty acids can, via propionyl CoA. There is a computational predicton that even acetyl-CoA can generate glucose. I don't think this is experimentally verified.

Only about 5–6% of triglyceride (fat) can be converted to glucose in humans.
This is because triglyceride is made up of one 3-carbon glycerol molecule and three 16- or 18-carbon fatty acids. The glycerol (3/51-to-57 = 5.2–5.9%) can be converted to glucose in the liver by gluconeogenesis (after conversion to dihydroxyacetone phosphate).
The fatty acid chains, however, are oxidized to acetyl-CoA, which cannot be converted to glucose in humans. Acetyl-CoA is a source of ATP when oxidized in the tricarboxylic acid cycle, but the carbon goes to carbon dioxide. (The molecule of oxaloacetate produced in the cycle only balances the one acetyl-CoA condenses with to enter the cycle, and so cannot be tapped off to gluconeogenesis.)
So triglyceride is a poor source of glucose in starvation, and that is not its primary function. Some Acetyl-CoA is converted to ketone bodies (acetoacetate and β-hydroxybutyrate) in starvation, which can replace part — but not all — of the brain’s requirement for glucose.
Plants and some bacteria can convert fatty acids to glucose because they possess the glyoxylate shunt enzymes that allow two molecules of Acetyl-CoA to be converted into malate and then oxaloacetate. This is generally lacking in mammals, although it has been reported in hibernating animals (thanks to @Roland for the last piece of info).

Good answer.  Some mammals do have the glyoxylate shunt though; hibernating animals use this to maintain blood glucose from fat reserves. See for example: http://www.ncbi.nlm.nih.gov/pubmed/2310778

@Roland — Very interesting — so the genes are present in the bear genome? (I found out by chance that the glyoxylate shunt genes were present in nematodes some years ago and got Kegg to correct their page, but was unaware of this.)

I'm not sure if the encoding genes in mammals have been identified, they may not be obvious homologs of the plant / bacteria / nematode genes. There are a only a few studies of this in mammals (bears, some hibernating rodents I think) and it's mainly by assays for the enzymatic activity or isotope tracing, if I remember correctly.

To be more detailed it is the irreversibly of the reaction carried by Pyruvate dehydrogenase that makes the conversion of the fatty acid chains to glucose impossible.
The fatty acids chains are converted to acetyl-CoA.
Acetyl-CoA to be converted into pyruvate need an enzyme that can do the Pyruvate Dehydrogenase's inverse reaction (in humans there is no such enzyme).
Than the pyruvete inside the mitochondria is converted into glucose(gluconeogenesis).


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Why was it so hard to decode the corn genome?
My teachers growing up told me it was impossible to decode the maize genome. But yet its been done.
Why was decoding the genome so significant, and what made it so difficult?

If I remember correctly : it's huge and has lots of repetitive regions.   It's very hard to accurately sequence repeats de novo with high fidelity.

The short answer is that corn genome is large and has a huge amount of duplication events. Around 80% of the genome are repeated. It's hard to assemble genomes with large amount of duplications because our sequencing technology, practically, at best can give ~500 base pairs. Figuring out the ordering of duplicated regions relies on scaffold sequences or comparative assembly to rice genome.

Why was decoding the genome so significant?
Because decoding the genome gives us a complete picture of the genetic makeup of an organism.
What made it so difficult?
The repetitive sequences as mentioned by other people is a main problem. Imaging you are trying to complete a big puzzle with millions of pieces. Each piece represents a sequencing reads that we get from the experiment. If there are repetitive sequences in the genome, basically the pieces that representing these regions would look very similar (or even entirely identical). Undoubtedly, this would make the puzzle very difficult to finish. To give a scale, the maize genome is ~2.3 billion base pairs and each sequencing reads is <1,000 base pairs.


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What beetle is this?
I've found it in my kitchen. It seems to be that he flew through the window from the street.
The country is Russia.

What size was this specimen?

This is Mealworm beetle, Tenebrio molitor, a species of darkling beetle.
http://en.wikipedia.org/wiki/Mealworm

Thank you @terdon for help!

I am not an entomologist, I just happen to have worked on the genome of the red flour beetle, Tribolium castaneum and this looks very similar. A quick wikipedia search turned up the amusingly named "confused flour beetle", Tribolium confusa, which looks almost exactly like what you have photographed:

So, I would guess (I stress that I don't really know) that this is some sort of Tribolium species and, by now, is thoroughly confused even if it was not to begin with.

Thank you very much for the answer. I've just read about this on Wikipedia and found that this is a Mealworm —  http://en.wikipedia.org/wiki/Mealworm — a bigger version of a Tribolium.

@SunnyRebornPony well done! Could you please post that as an answer and accept it? The species name is mealworm beetle, Tenebrio molitor, mealworms are the larval (apparently edible!) stage.


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Are the cells (structures) of deep sea fish different? And can they survive in shallow water?
In the deep oceans the pressure is enormous. But still there are fish living. But are the cells of them different from fish who just live at the surface of waters?
For example, are the cells smaller because of the pressure? And if so, does that influence the inner metabolism? If not, how do they succeed in maintaining their size?

Yes there can be differences in biochemical composition if that is what you are asking for. Please clarify your question.

Pressure equilibrates: it will be the same inside the cell as outside in the ocean. As said by Thawn in his response, the water inside the cell will not vayr much its volume even with enormous pressure, so the volume will not vary. This would of course be different if there was some air or other gas somewhere in the organism, which would both reduce dramatically in volume and dissolve much more into water.

Cells consist mainly of water and the compressibility of water is very low. Wikipedia states:

The low compressibility of water means that even in the deep oceans at 4 km depth, where pressures are 40 MPa, there is only a 1.8% decrease in volume.

This means that the pressure alone does not affect the size of the cells much. However, the pressure affects the cells and the metabolism of organism living in extreme depths in other ways:

Under pressure, the folding and unfolding kinetics of proteins can change drastically. Which means, that the protein structures may need adaptation to great pressures.
Under pressure the fluidity of the cell membrane lipids changes, requiring adaptations in membrane lipid composition.

In conclusion, I would say that the pressure in the deep sea does not directly affect the size of cells but rather their metabolism.
Edit: I just saw the second part in the heading of your question ("and can they survive in shallow water?"). Again, I'll quote Wikipedia:

The extreme difference in pressure between the sea floor and the surface makes the creature's survival on the surface near impossible;

The reason for this is that pressure works thermodynamically in many ways similar to temperature: As explained above, changing the pressure significantly alters reaction kinetics and phase transitions. Thus, the whole metabolism has to adapt to increased pressure (similarly to the adaptation to increased temperature).
However, at least some deep sea creatures seem to be able to adapt to surface pressure if the transition is not too abrupt (from the same wikipedia article as above):

A marine biologist, Jeffery Drazen, has explored a solution, a pressurized fish trap. This captures a deep-water creature, and adjusts its internal pressure slowly to surface level as the creature is brought to the surface, in the hope that the creature can adjust.


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Textbook for quantitative biochemistry with thermodynamics, as an alternative to Voet, Voet & Pratt (Fundamentals of Biochemistry)?
I'm looking for a great textbook on biochemistry that covers core topics: relevant aspects of thermodynamics, reaction kinetics, metabolism (e.g. krebs cycle, respiration, etc.). Ideally it would also be quantitative in its approach and use mathematical models where relevant.
The classic textbook is Voet & Voet & Pratt (Fundamentals of Biochemistry) and I think that's a horribly written textbook. It uses concepts before actually defining them (and when it does define them the definitions are obtuse and have no conceptual motivation). Is there an alternative to this? Any recommendations?

Stryer?? As far as I remember it had the most thermodynamics of all other books. Example section. You should add more details on what exactly you are looking for. What level of thermodynamics you want etc. See the tag wiki for [tag:book-recommendation]

I've always liked Lehninger Principles of Biochemistry. Seems like it would be a good book for you.

I would also vote for Stryer. But none of the biochem books do the technical stuff (kinetics, thermodynamics) properly I think. For this, get a copy of Atkins' Physical Chemistry.