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What is the percentage of people living in England in 1500 AD whose lineage is still alive?
This sounds a bit random, but it stems from a lecture in statistical genetics which I attended a while ago. We were shown a population lineage graph from which it was clear that most lineages eventually go extinct. The further you go in to the past, the smaller the percentage of the individuals living at that time whose lineage is still alive today. This probably makes sense in the context of evolution.
So I am curious about the speed of that process in human populations. I am aware that this speed, quite possibly, varies over time and geographically. Are there any estimates about that speed in European populations? To be more specific, I would take England at 1500 AD as a starting point. What is the percentage of the people living in England at that time whose lineage still exists?
EDIT
I am very grateful to @Richard Erickson for the reference to the Galton-Watson process. It is really fascinating that +70% of all known Chinese family names have become extinct. It would be really interesting to know more about the speed of the process of extinction - in particular in European populations.

It totally depends. This is difficult to answer based on just calculations because unless you have exact data for the population dynamics of the region. This is mostly an issue of bookkeeping (census). The further you go in the past the smaller was the percentage of the individuals living at that time whose lineage is still alive.: not necessarily true; imagine population bottlenecks.

@WYSIWYG Out of curiosity: how do bottlenecks change this? The percentage still seems a largely monotonous, if not continuous, function.

Assuming arguendo that a bottleneck killed all except 10 people in the population in 1500, right after your 1500 sample was taken. The percentage of people who still have their lineages extant today would be greatly reduced.

@Nick birth and death are stochastic processes and though the mean behaviour may seem monotonous, there are always fluctuations. Let us assume that there was only one couple left after a mass extinction process. All the subsequent generations would be their descendants. Similarly, during a bottleneck a few individuals give rise to the entire population. Now, if you take generation-0 and any later generation-Y, compared to some generation-X and generation-Y (X<Y) then there the lineage would be intact for the former. Plus there are other factors such as fitness of the starter population.

@March Ho The percentage of the people living at a time point before the bottleneck who have a living lineage would still be lower than for the generations afterwards. I know that a scenario can be constructed in which this is not strictly true but, generally, the rule holds for realistic bottlenecks - at least in species with birth rate not much greater than those of humans. However this point is a bit tangential to what I asked.

Interesting question +1. One can calculate such things using Coalescent Theory but the issue is that it assumes constant effective population size which is obviously very wrong for England. The Coalescence should have very long branches, much longer than expected from constant effective population size. I don't think there is an analytical method for dealing with growing population size. Also, the descendents went through several bottlenecks and rapid expansion so it definitely is not an easy case. I don't think that theory can help here, one will need to analyze data to answer this question.

Check out Galton-Watson branching process models. They area closely related topic that focus on the probability of an individual surname going extinct.

In reaction to @WYSIWYG's comment: The further you go in the past the smaller was the percentage of the individuals living at that time whose lineage is still alive is very likely to be true but not necessarily indeed. However, The further you go in the past the smaller (or equal) was the number of individuals living at that time whose lineage is still alive is always true.

Here is a partial answer that also expands upon a previous comment:
Between 1900 and 2013, 20,000 English surnames had gone extinct according to the Daily Mail's summary of research on surnames. This is a partial answer because it only tells us how many names are gone and is from the wrong time period.
To completely answer your question, I suspect you need to conduct primary research. I would suggest the following broad steps:

Gain access to the data needed to answer your question. British Census records only appear to available from 1841 to 1911 so you most likely need to sample old names (e.g., graveyard based studies).
Use the data to parameterize a statistical model such as a Galton-Watson branching process models.

I doubt the answer to your question can quickly be found unless somebody has already done it. Although, if done well, it could probably be a masters' thesis. However, before embarking on such a project, I would suggest doing a good literature search to make sure it has not been done before.
Note: If anybody finds the answer, please feel free to take content from my answer and include it yours.

Thanks. Daily Mails seems to refer (though not providing a direct link) to research done by ancestry.co.uk. I haven't checked that site yet but it would be another port of call. The thing is that family names are a sort of proxy variable. There was a lot of emigration from the UK. Also, people adjusted the spelling sometimes. More importantly, females traditionally took over the family name of their husband (so their own family name may become extinct while their lineage may continue). The emergence of double-barrelled family can also affect the stats.

You're welcome. I know this data would be hard to come by. An academic researcher might be able to get it from ancestry.com or ancestry.co.uk. I know Google shares information with academics. Otherwise, it might also be machine learning exercise in reading in old church records or something like that. Good luck with the question though!

I realize there it would be a lot easier if only a subgroup of the population is taken into account - the nobelty. I presume good records exist. The question is how to get them.

@Nick, good point. Check out out Galton's work. He was afraid of the "good" aristocratic names going extinct.


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Do birds emit infra-red radiation?
I'm an electronics engineering student and I am going to use a sensor that detects infra-red emitted by birds that invade rice paddies.
Do birds emit infra-red radiation?

Anyone here can correct me, but I think that all living organisms emit infrared, since all organisms undergo metabolism (respiration? converting food to energy? what's the correct term?) which releases heat, and hence infrared radiation.

Some birds emit more infra-red radiation than others so it's worth bearing that in mind and testing sensitivity (likely involving field study - sit and compare what the sensor detects to what a good bird spotter detects). I saw a documentary a while back where they showed ptarmigans through thermal imaging cameras, they were barely visible, I tried to find an image but couldn't. Obviously where there are rice paddies its unlikely that birds will be quite as well insulated though... It's  not just a problem of do they produce heat, but also how well they retain it

Short answer
Birds emit infrared.
Background
Objects with a temperature higher than the background emit detectable infrared (IR). Endothermic (warmblooded) animals keep their body temperatures at around 37oC and given the relatively cool temperatures at the earth's surface, endotherms generally emit more IR than the background. Endothermic animals include the mammals and birds, but also some fish.

Infrared image of a hummingbird. Source: Nature Conservancy.
Note that dinosaurs were probably not ectothermic (coldblooded), but they are believed to have been mesotheroms, that is somewhere in-between ecto- and endothermic (Grady et al., 2014).
Also note your IR recordings will benefit from lower temperatures and reduced light-pollution from the sun, hence your recordings will be better at night than during daytime.
Reference
- Grady et al., Science (2014); 344(6189): 1268-72

Nice Answer. You all but told them they probably would want to use a beam and sensor, sort of like the ones that automatically keep an elevator door from closing when the beam is broken than trying to detect the thermal signature of the birds themselves. They would likely be too fast and too small to register on an infrared sensor, especially considering rice paddies are often associated with hot climates.

@AMR - Thanks for the appreciation and also thanks for an interesting add from an engineering perspective. I think IR sensors come in various flavors. For example, hyperspectral cameras can be able to resolve quite some detail, but I am not sure about how fast they are.

Technically, all objects emit infrared, not just those "with a temperature higher than the background". It's true however, that to photograph such an object with any sort of contrast, one would need the temperature to be higher.

@nbubis thanks for that. I corrected my answer.

I would expect all animals, and possibly all living things, to emit infrared as metabolic reactions tend to be exothermic, even if the animal is ectothermic.  The question is that if the difference between the animal and its environment is enough for you to be able to actually detect it.

Dinosaurs is a very broad term which includes both the ancestors of birds as well as modern reptiles. But that analogy stretches as far to say that a bird is a modern dinosaur and a reptile is a modern dinosaur but a bird is not a reptile. Both of their ancestors lived during the cretaceous period and tend to get lumped together.
Another analogy would be that dolphins, bats, and humans are all modern-day mammals. But a dolphin does not fly and humans do not live underwater, etc.
Modern-day birds descended from a group of dinosaurs called theropods which were warm-blooded dinosaurs.
See here for more information:
http://www.abc.net.au/science/articles/2010/11/23/3073903.htm
To be specific to your question, if it is an endotherm then it will emit some level of infrared radiation, as this is their primary means of avoiding overheating.
Interestingly, some birds are actually warmer than humans at 102-112F:
http://animals.mom.me/signs-parakeet-cockatiel-birds-cold-8448.html

Minor nit - dinosaurs are typically not construed broadly enough to encompass the ancestors of any modern non-avian reptiles. The closest modern reptile to the dinosaurs (and birds) are believed to be the crocodilians, but the non-dinosaur pterosaurs branch between crocodillians and dinosaurs/birds on the evolutionary tree, meaning crocodiles - or any other reptile - aren't descended from anything which would count as a true "dinosaur" to a modern paleontologist.

In current technical usage by people who study these things, birds are dinosaurs. Classics usage now becomes "non-avien dinosaurs".  Reptiles are not dinosaurs.  Reptiles are not a mono-clade and don't follow "always will be" rule.

Typically an animal must be 2.7°C warmer than its surrounding environment, to trigger a detection.
Are you talking about herons that hunt frogs or small birds that forage seeds?
The distance of an animal from the camera’s PIR sensor and its body mass, varies the magnitude of infrared radiation, which affects the ability of the PIR to trigger an image.
So PIR triggers perform well for large and medium sized mammals, but do not reliably detect ectotherms (reptiles, amphibians, and invertebrates) or smaller mammals.
I'm drinking a beer while i write this so I can answer well, and by unabashed plagiarism: here is a complete review of some PIR technologies, which is biased towards their 3mm laser sensor called HALT: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5628828/
Personally i'd say forget about complex electronics for this project! just take a slow exposure image every seconds and pass the image stack through pixel processing code to search for bird sized dots and lines.
Birds in paddies should be easy to detect, because they come down from the sky which has a light background and they move at relatively high speed. So a computer can easily recognize the trails against the sky and classify them by size. You can therefore use a very cheap time lapse camera trap which takes 1000ds of pictures a day, at a cost of perhaps 1 gygabites per day, and do comprehensive statistics on bird movement around the paddy fields. Infra red? home made? i'd say forget about it, image recognition digital signal processing is more thorough.
here are some pics from here

Recently I programmed image stacks, and it was very much fun because it was 2d and 3d graphs. to sequence through an image file is 12 lines in U3D. To loop through the pixels is another 12 lines, so all you have to do is write conditions. to save relevant images to another area. That said, you have 1 minute exposure images all day, you will have 600 images a day to sort through manually.

Every object hotter than 0K emits infrared radiation. Many object absorb and reflect, re emission infrared radiation (usually lower frequency). For detect bird need some difference with background object's infrared radiation, like different intensity, spectral, phase. One person above show use intensity (at night ground/trees become cool emit less radiation than birds). If need find birds during day, and ground hot, birds appear darker than ground.
Can also use multiple infrared sensors together detect different frequency (like visible light, infrared light have frequency range) different object have different infrared color. Also, if rice paddies have water, reflected infrared light is polarized but reflection from bird is random, maybe can use this help find bird when they fly. I think sky UV and visible light also is polarized (bee use it for navigation), I guess infrared light from sky is polarized too.

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How long do viruses, such as Zika, stay in the body?
Can a virus stay in your body (after recovery) in a concentration that is sufficient to infect someone?
Is it known how long the Zika virus persists in the body?

According to the CDC the zika virus persists in the blood for around a week.

Zika virus usually remains in the blood of an infected person for about a week but it can be found longer in some people. - CDC

I can't find much information on how long the Zika virus specifically can persist after recovery, it seems unknown just now. However, it is advised to be careful about sexual contact after infection, which suggests longer persistence is suspected in other fluids/tissues.

British health authorities have suggested using condoms for at least 28 days. - NYTimes

Some viruses do persist for a while after recovery, including Ebola Virus Disease, which can be sexually transmitted for around three months after recovery:

Some viruses, including Ebola, can linger for some time after recovery in parts of the body (for example, testes, eyes, spinal column fluid) not easily reached by the immune system. - CDC

These parts of the body have immune privilege. This means they can be infected by antigens without producing strong immune responses. This is thought to occur to protect vital tissues/areas which could be damaged by inflamation and the immune response, such as the brain, eyes, spinal column, testes, and fetuses.

Since I wrote this answer there have been several reported cases of sexually transmitted zika, highlighting the problems that can arise from immune privilege.

And the rest of the body?

By coincidence I was making edits at the time of your comment - does that help @Christiaan

Some viruses can stay in your body for your entire life, for example Herpes Simplex Virus.

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Conversion of ATP to NADH without creating a proton motive force?
Is it possible to convert ATP into NADH and vice versa without first creating a proton motive force? If so by what mechanism is it done?

I am not aware of any enzymes that both oxidize NADH and generate ATP.
However, in the absence of oxygen, many bacteria ferment ethanol and acetate (among other products) to oxidize NADH and produce ATP. ATP is produced by acetate kinase and NADH is consumed by dehydrogenases in the parallel ethanol secretion pathway. Together, these pathways consume (or more accurately, recycle) NADH and generate ATP.

http://mmbr.asm.org/content/69/1/124/F6.expansion.html


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Heritability of trait stronger from one sex over another?
Given a trait that can be expressed (and measured) in both parents (e.g weight, height, strength, speed), are there ever traits in the child that correlate better with one sex parent than the other? If so, can you give some examples. This could be in any species.

It has been shown in Drosophila that cross-sex heritability is low for lifespan, where within-sex heritability was three times greater than cross-sex heritability. This means that, sons more closely resemble their fathers and daughters more closely resemble their mothers. This could be considered one such example, if you consider the trait to be a sex-specific thing, i.e. that fathers have a greater influence on lifespan in sons than mothers do.
In humans (and numerous other species, e.g. Indian Meal Moth), it has been shown that several traits have small cross-sex genetic correlations, suggesting that (in such traits) the parent of the same sex is a better predictor of a child's trait value.
It is common (in quantitative genetics circles) to consider homologous traits in two sexes as separate traits (e.g. male lifespan and female lifespan are separate traits), and analyse them in a multivariate framework such as a G-matrix. They often have some genetic covariance between the sexes because of pleiotropy and linkage disequilibrium (though covariance by LD is generally more transient: see books on quantitative genetics by Lynch & Walsh, Falconer & Mackay, or Roff, for more reading).


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Are heterozygotes always fitter than homozygotes? Can inbreeding be beneficial?
Inbreeding is mostly not very good because when there is a 'disease' in one allele, the other could/would take over the function. But when you have two of the same genes/alleles, do they, or could they have advantages? Can inbreeding be beneficial?

Certainly it is not necessarily the case that having two of the same allele is a bad thing - if there is a "bad" allele then there is a "good" allele. It can be that the heterozygote is equal, better than, or worse than either homozygote. When the heterozygote is fitter than both homozygotes it is called heterosis and, when this is the case, outbreeding/hybridisation is advantageous.
The process of inbreeding can actually improve fitness because it increases the rate at which deleterious mutations (bad mutations) are expressed, and therefore the efficacy of selection. If the population avoids fatal inbreeding depression it can have positive effects. This process of removing deleterious variants by inbreeding is called genetic purging.

A good example of homozygotes being more fit might be Polled Cattle. The allele that makes horns on cattle is actually recessive, so a cow needs two copies to have horns. A cow with horns is better able to defend itself in the wild. It also allows them to outcompete other cattle for food on the farm, and can be a safety issue for the farmer. By breeding bulls to be homozygous for the dominant no-horns allele, you can easily remove horns from a herd and avoid costly, and potentially harmful, surgical horn removal.

The phrasing in quite unclear and I would not be able to comment on it.
In short: yes, hybridization can cause offspring to have either particularly low or particularly high fitness. Hybrid depression refers to cases where hybrids have low fitness while heterosis or hybrid vigour refers to cases where hybrids have a higher fitness than any of the two parent lines.


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Biodiversity is restricted by genome combinatorics?
Me and some friends are interested in opinions for the following:
Conjecture

The maximum number of species must be limited by the maximum
  combinatorial/permutational space that can be occupied by DNA. Thus if
  there is a maximum physical genome size this is what will determine
  the maximum number of species that can possibly exist.

Explanation
E.G. say maximum number of DNA base pairs able to fit in a genome was $3$, each base pair can be one of either ${A,G,T,C}$. Then there are $4^3 = 64$ possible combinations of genomes. Extrapolate to genome sizes of $x$ base pairs, then there are $4^x$ combinations.
Questions
Would it be possible to claim that the underlying "blueprint" that codes for living diversity sets the absolute maximum for the total "diversity space"?
**Does it make sense to define the total number of species life can achieve with the simple function:
$S < 4^x$, where X is the maximum genome size measured in DNA base pairs?**
Notable Comments

@Shigeta: for $S<4^x$ the combinations involved quickly dwarf the
  number of atoms in the universe at ~10^80.
@rg255: Even at this simplification of: $S<20^{x/3}$ there are
  $1.024e+13$ possible combinations with just 10 codons, many many more
  than there is likely species in the world.

You would have to alter the current library of amino acids- the 64 nucleotide patterns you mention currently only code for 20 amino acids

Also this is not a question

Please try http://skeptics.stackexchange.com for this kind of discussion. On this page, opinion based questions are not allowed.

@skymninge Such a question would be off-topic on Skeptics, the site requires notable claims for any question.

Issues I have with this idea: 64 nucleotide combinations does not make 64 different results (just 20 amino acids), you assume one nucleotide difference will make a large enough reproductive barrier to create a species (if that were the case almost every individual organism alive could be called a different species), the length of DNA is theoretically infinite so there is no upper bound, environmental effects and gene*environment interactions can bring about differences in phenotype which could make "species" from the same DNA sequence, and not all combinations of DNA will be useful/viable

I don't think hello_there_andy is suggesting something he had thought about and ask for our opinion on his theory. There are several criticism to draw on his theory but this is the whole point of his question. This type of calculations is common in biology and he does not know about it. It is worth answering this question by saying what are the problems with his concept of species and what are the problems with the calculations of DNA capacity to hold information.

This site is not for opinion based answers, the question made little sense - no question was actually asked - and, there are fundamental flaws in the biology of the post

Well, there's a tag theoretical-biology on Biology.SE. This question has to do with theoretical biology. And as @MadScientist said it would be off-topic on skeptics. But anyway. The question is already fully answered!

It is a basic maths exercise put in the background of simply reducing species down to nucleotide differences and ignoring various other biological concepts and principles. I agree that "If the genome is limited to x bases then there is only 4^ x combinations of bases."

Hello, Thank you all. Sorry about not making it sound more like a question, and thank you for editing it to fix that. My honest intention was to learn from criticisms. I have learnt an incredible lot thanks to answers. It is not just a mathematical excercise. I realise the 4^x is a gross over estimation... but I am sure you agree "there cannot be >#species than there are combinations of genomes"

I must say this is my second question so far, and I will be more disciplined now. I did not acknowledge the level of freedom I have till now, please forgive me!

The edits made are good, but the robotics bit is a little out of place, so if that is better expressed as a biological question I will vote to reopen. Just as a note, given that a codon of three bases codes for 1 of 20 amino acids the better simplification would be 20^(x/3) ... at just 6 bases (2 codons) the number of possibilities is 10 times lower (400 vs 4096). Even at this simplification there is  1.024e+13 possible combinations with just 10 codons, many many more than there is species in the world.

Thank you @GriffinEvo I must argue that non-coding DNA has many functions: http://www.genome.gov/10005107

That's a very good point, the possibility the non-coding dna might act on a base-by-base level rather than in triplets is something I hadn't considered

Ah yes, I suppose in all honesty I felt an opportunity to add that diagram since It was something I made for a presentation. I have removed the diagram, hope that would solve the issue!

I have now voted to reopen because I think this is now a question set within a biological framework.

let us continue this discussion in chat

@GriffinEvo Thank you, I have already learned much from the discussion too, cheers. Also I have further edited the question with better organisation and headings.

Just wondering...Can there be a new species without a change in coding sequence and only change in regulatory sequences ?

@biogirl yes provided that change brings about a reproductive barrier - up and down regulation of a gene can produce variation in phenotypes

@GriffinEvo WOuld that have any implications on this question ?

It has to be said, the definition of what a species is, or in another way the question: "what is a species" is actually highly controversial... mainly there is a divide among "Niche species" and "Reproductive species" - in the former the critical principle to read about is "Competitive Exclusion Principle" http://bit.ly/cqEkle the one @GriffinEvo hinted is the latter.. which is a more practical definition that is if two organisms fail to make viable offspring they are seperate species - indeed there are at least 20 species definitions e.g. http://en.wikipedia.org/wiki/Species

@biogirl My argument here simply puts an UPPER LIMIT to the whole debate. I have no idea how many species there can be but I can say with some confidence that there cannot be more than 4^X species. That is.. the #species that can ever exist is <4^X

I asked the question in a similar way in the Stack Mathematics forum: http://bit.ly/1bSNwNu

@GriffinEvo There are 22 proteinogenic amino acids (including selenocysteine and pyrrolysine), not 20. Just playing the pedant here but I did my thesis on predicting selenocystein-containing genes so it's kind of a personal issue for me :).

@hello_there_andy you should read Chp 3 of The Blind Watchmaker. I feel it is relevant to your question.

Cheers Biogirl and GriffonEvo, since joining Bio exchange I have collected a big "to read" list :D

Yes, we can say the number of species is limited as you conjecture.  However, quick estimation shows that the limitation has no apparent usefulness:
A reasonable estimate of the largest known genome is 150 GB (150,000,000,000 or 1.5e11 nucleobases).  The limit would be 4 raised to that power.  That limit is so high that it is too large for most calculators to calculate.  For instance. Wolframalpha.com fails to calculate 4 raised to 1e11, its maximum being about 4 raised to 1e9.  The result of 4 to the 1.0e9 power is about 1.0e602059991 or 10 raised to the 602059991'th power.
That rough result, 1.0e602059991, is so enormous that it is exponentially greater than the number of atoms in the universe (which is less than 1.0e100).  Hence, assuming the definition of species requires an organism to use at least one atom for its body, there is no consequence to saying the number of species must be less than this number.
The number of possible combinations of nucleotides is so outrageously large that it does not constrain the number of unique individual organisms or species.

That's an interesting conjecture about the total amount of genetic variation that is possible. I would modify a few things. First, since the size of genomes varies greatly among organisms (from 0.5 Mb to 15 Mb just for prokaryotes), there should be a fifth character in your set, representing the absence of a nucleotide.
There are also issues of whether various combinations are equivalent. For instance, bacterial genomes are often circular, so if we could convert one genome into another simply by rotating it, we would consider those genomes identical. For example, if the genomes each had 99 As and 1 T, it would not be meaningful to say that they are different just because of the location of the T. I think this would require use of the multinomial coefficient to count the number of identical variants.
Regarding your main thesis, your use of the term "species" has no relation to how that term is used among biologists. Biological species include genetic variation, so each of them would include many of your species. Also, one criteria for identifying species is the clustering of these sequences (and the absence of other, intermediate sequences). This implies both that many possible DNA sequences simply cannot produce a viable organism and competition among similar genotypes is an important aspect of species identity.

+1 Very good answer. Of course there is the fact that DNA contains more potential information that what a protein can contain. And therefore, the total space possibility of proteins from x base pairs is lower than $x^4$. the OP might be interested in the [quasi-species theory][http://en.wikipedia.org/wiki/Quasispecies_model] presented in [this book][http://www.amazon.com/Evolutionary-Dynamics-Exploring-Equations-Life/dp/0674023382] for example.

The OP might as well be interested to the concept of robustness ([this book][http://www.amazon.com/Robustness-Evolvability-Living-Systems-Complexity/dp/0691134049] for example)

I'm going to define a species according to the biological species concept, probably the most widely "accepted" species concept where a species is a group of individuals that reproduce, or have the potential to do so. Using a simplified example I will show you that gene*environment interactions affecting phenotype can allow separate species to occur despite being genetically identical.
Imagine a very short section of DNA which affects seminal fluid proteins in a fruit fly. It is  just 10 bases long. The first three triplets of bases code for a protein constructed of three amino acids which affects the females behavior upon receipt of the male ejaculate. The final base regulates the expression of the first codon and is sensitive to developmental environmental factors (let us say nutrient richness). When the development of the male fly is in a nutrient rich background the section of DNA produces all three codons in equal amount to construct a protein and that protein stimulates the female to release eggs for fertilization. If we take a genetically identical male reared in a nutrient poor environment then the regulatory base increases the production of the first codon's amino acid. This makes a different protein structure which no longer stimulates the female in to releasing eggs, therefore the males from nutrient poor backgrounds can not reproduce with the females from a nutrient rich background, and these two genetically identical populations are different species.
Thus I would say, no, the theoretical maximum number of species is not capped by the length of the DNA. However, given that just the potential number of bases (current highest estimates recorded are 150,000,000,000) far far far exceeds the number of species in the world, we can say that the number of base combinations is not the limiting factor on the biodiversity we see. That is down to evolution (selective and neutral processes). Phenotypes determine the ability of two individuals to reproduce, phenotypes are the result of more than just genetics:
$phenotype = genotype + environment + genotype*environment$
Further, as @mgkrebbs has already stated, the number of possible species (given by $4^x$ when $x$ is 150,000,000,000)  is, not only far more than the number of species that do exist, but also far more than the number of atoms in the universe. Assuming each species requires at least one atom then the number of atoms available will halt increasing numbers of species before the number of possible base combinations does.

Coupled with @mgkrebbs answer of atoms in the universe, I have been convinced to a great extent how irrelevant 4^x is. Thank you all for giving me the perspective!

the combinatorics involved quickly dwarf the number of atoms in the universe in fact.  ~10^80

Nobody would consider those flies to be different species. Since there are no females that will mate with the "nutrient poor" (NP) males, those males do not form a separate species -- they just fail to reproduce. Even if the NP males could mate with NP females (to the exclusion of other males), the NP population would not be a separate species because it would still maintain the potential to reproduce with the other members of this species. The isolation of the NP subspopulation from the rest of the species would be transient -- similar to physically separating them.

Maybe you could imagine some sort of feedback loop that would stabilize the mating preferences -- perhaps having been born on a certain type of fruit, they preferentially mate and lay eggs on that fruit. However, I still doubt they would be considered separate species if all that was needed was to transfer larvae between fruit in order to change the preference (which would probably happen on occasion in the wild)

@adam.r sorry, it is a gross over-simplification and to keep it simple I made the (unstated) assumptions that NP females would only be responsive to NP males, and that these environments were isolated during development - artificially bringing adults of the two groups together to mate would then lead to the conclusion that they are separate species as NP<->NP and NR<->NR matings would work... bit of a large jump but, like I say, it is an oversimplification. I should have been clearer in the answer but wanted to keep it simple.

@hello_there_andy this answer may be a little related here... http://biology.stackexchange.com/questions/13834/what-are-some-example-of-genes-that-code-for-multiple-proteins

Well... this is true in the same way that books are constricted by letters. We could have more letters and create more combinations with the same length of DNA. But, like books, there are just so many combinations.

Nice that you spotted the similarity with books. In fact it is more general than that.. it goes for the whole of language, music, computer programs and perhaps all kinds of technology (think about the periodic table).

Well... kind of. With all of those things you are true... except for music. I don't mean to be nitpicky; actually, the science behind the repetitive nature of music is quite fascinating. See this link for more info. http://www.youtube.com/watch?v=DAcjV60RnRw

I guess I simplified music to a string of notes and timings. E.g. the possible number of ways you can create a finitely long sheet of music. More generally I guess there are only a finite number of ways of putting various kinds of sound waves together?

Yes; in the video, it says that in a 5 minute time period (exactly 5 minutes, not a second more), there are about 10^67 different songs.


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Is a fat-soluble vitamin a lipid?
I read in a chemistry book that a steroid is a class of lipids, and that the fat-soluble vitamins like vitamin D are part of steroids. So is a fat-soluble vitamin a lipid?
This makes me confused as the lipid nutrients seems to contain vitamins which make another type of nutrients.

Or maybe simply that book was defining and giving examples of steroids and didn't mean that every example is now a lipid!

Yes steroids are a class of lipids which include cholesterol and sex-hormones such as testosterone and estrogen. Only vitamin-D belongs to the class of steroids.
Vitamins A, E and K are isoprenoids. In fact even steroids are synthesized from simple isoprenoids. You can refer to a standard biochemistry book to understand steroid biosynthesis pathway.
There are other classes of lipids too, such as fatty acids, phospholipids, ceramides etc.
Yes all fat-soluble vitamins are lipids. This is the definition of Lipids from the IUPAC goldbook:

A loosely defined term for substances of biological origin that are
  soluble in nonpolar solvents. They consist of saponifiable lipids,
  such as glycerides (fats and oils) and phospholipids, as well as
  nonsaponifiable lipids, principally steroids.

Both fats and fat-soluble vitamins are nutrients but are functionally different. Fats provide energy whereas vitamins perform regulatory activity and are required in little amounts in the diet compared to essential fatty acids.

The book actually said that fat-soluble vitamins (not just D) are steroids, were they not accurate enough do you think?

@YoussefDir the book is wrong in that case.


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Is it known how human sweat glands evolved?
If human descends from apes than probably we lost our hair. Perhaps in the age of homo erectus we lost our hairs and began transpiring through our skin with sweat glands. But how did these glands evolve? Is it from another kind of cell which is similar?

Welcome to Biology.SE. You probably wan to replace created/evolved by just evolved and replace if humans descends from apes then ... by knowing that humans descend from apes ... or even better, Knowing that humans are apes ....

As a side note: Understanding Evolution (UC Berkeley) is a very introductory online (and free) course to evolutionary biology and you might want to have a look at it.

I am not sure exactly what you are after when asking "how did these glands came?". It seems that you wrongly believe that similar glands do not exist in other primates. Here is a short answer that will help you to search for more information about the evolution of these glands.
Chimpanzees and Gorilla also have sweat glands. The use of sweat gland in thermoregulation is however quite unique to humans and is thought to have evolved in parallel of hair loss and bipedism. See The evolution of sweat glands (Fold and Semken 1991) for more information.


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How long can you effectively store a glycerol stock at -20 degrees Celsius?
I know that glycerol stocks are typically kept in a -80 °C freezer, however there are some people who do not have access to such equipment. How long would you be able to keep a glycerol stock at around -20 °C (typical household freezer temperature). I would like to create a new stock before anything goes amiss.

-20 is also good enough.. I have revived 1 year old cultures..

I have successfully used own stocks that were about 5 years old and stocks from a colleague which where about 10 years old. So they are pretty stable.

While I believe that it is possible to keep a bacterial culture viable while frozen in glycerol stock at around -20 °C, as attested to by WYSIWYG, it is important to note that your "typical household freezer" may not be suitable for such a purpose.
This is because household freezers usually have an "auto-defrost" function. This makes it temporarily thaw out to remove the frost that condenses from atmospheric moisture. If storing sensitive materials such as bacterial/cell culture frozen stocks, this would lead to repeated freeze-thaw cycles which would damage the viability of the stocks.
For that reason, almost all laboratory freezers do not have that function, and instead need to be manually defrosted routinely.


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Why did the yeast rise?
Here are the notes I made for an experiment I was doing (I didn't put it here as it is too long)
(please ignore the numbers at the end of the pdf file)
The graph looks like this:

As you see on the graph, the numbers are the same as the ones below
1. The effect running out of glucose has on the yeast growth
Our yeast increased in number by dividing rapidly. They use glucose to respire and release energy. They need energy to grow.
2. Why the yeast starts to grow again
The yeast  starts to decrease in volume when they ran out of glucose.
3. Describing patterns in graphs
The yeast breaks down the starch to glucose
The problem is, why did the yeast rise at the end, I forgot?
Thanks in advance

I just would like to say that the teacher never talked about the production of Co2

What did your growth medium contain? Only glucose? Or other substances as well?

@Chris only glucose

So you added glucose and some salts into the medium? Or did it also contain some complex materials like yeast or tryptone extract?

What do you mean by Volume. Volume occupied by yeasts? Then it is not the cell number.

First, the glucose is reduced by anaerobic fermentation to ethanol and carbon dioxide. The yeast uses the produced energy for a fast growth and division (1). As soon as all glucose is consumed the metabolism of the yeast changes from anerobic fermentation to aerobic respiration (oxygen is required). This is called diauxic shift. During this time the yeast stops growing (2). After this shift the yeast further reduces the ethanol to carbon dioxide and water. The generated energy is used for the second growth phase (3).
Hope this answers your question.
Best
Vanessa

Ethanol is toxic for yeast, it cannot metabolize the large amounts produced during fermentation. This is the reason why most wines are not stronger than 12-14% alcohol.

Welcome to Bio. Some references would be appreciated.


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How can a blood test give information about rickets?
Can we detect rickets from a blood test? What  evidence pf rickets is in the blood and how is the blood treated to detect rickets?

o one to answer :-( ?

Confirming a suspected phenotype with an emperical test helps us determine the provenance of a disease. Coincidently, here's an easy to read article about Rickets I found some time ago:

Welcome to Biology.SE. Blood is part of the phenotype. So you question (in the title) boils down to How can we infer anything about the phenotype by looking at it? The question can only be answered for a specific case (and you gave one so that's great). I would suggest to edit the title

From the Wikipedia article I linked to in your question:

Serum calcium may show low levels of calcium, serum phosphorus may be low, and serum alkaline phosphatase may be high from bones or changes in the shape or structure of the bones.

There is also a rare genetic form of rickets called Vitamin D-resistant rickets or X-linked hypophosphatemia that can be diagnosed by DNA sequencing of cells collected by a blood draw.
It should be noted that, at least in the case of rickets, blood tests alone will not diagnose the disease. There are many other possible symptoms of the disease, so a patient presenting with one or more of these symptoms may also be subjected to a blood test to confirm the diagnosis, not just make it on its own.


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Enzymes and plasmids
A high school class has analyzed plasmids by the help of restriction enzymes and electrophoresis.
The class got delivered two different plasmids, pBR 322 and pC 508. These two plasmids were going to be clipped by EcoR I and Hind III.
Figure 1 shows the two plasmids with specification of the two cutting points for EcoR I and Hind III.
Furthermore, the cutting points are also shown for the enzyme Pst I.
In figure 2 you can see the result of the restriction analysis.

Questions:
1) Analyze and explain the results in figure 2
2)  What DNA-pieces would be formed if you had clipped with Pst I ?
1) You can see that the figure is showing the result of the restriction-analyzis. As for the plasmid pBR 322, you see that the result of the cutting of Hind III and EcoR I, is that both enzymes have the same size. Figure one shows that Hind III cuts over 0 bases and EcoR I cuts at 0 bases.
In pC508 you see that both enzymes have cut two times. EcoR I have cut at 1200 and 5800 bases, which you can see on figure 1. You can see the result of this in figure 2 (the gel electrophoresis). Hind III cuts at 6400 and 1200 bases, which again is an explanation as why the DNA-molecyles (figure 2) have different size.
2) If Pst I was used instead on the plasmid pBR 322, you would get the same size as Eco and Hind, because they all cut one place. If you had cut in pC508 you would get the bases 4800 and 6700 (as figure 1 shows)
Are these questions correctly answered?

Your estimation of the sizes of the fragments for pC508 are incorrect.
Look at the size of the plasmid at the center of the circle.The size of your fragments has to add up to that number. So if you were sure that one fragment was 1000bp, then the other fragment would need to be 6300bp.
You should also notice that fragment sizes for EcoR1 and HindIII digests should not be the same size.
You also need to say something about the type of DNA you have in the pBR322 lanes. Is it linear, circular, supercoiled?
For question 2, your explanation for pBR322 is okay, you should still mention the type of DNA you have in those lanes.
You need to explain not only where PSTI cut but also the size of the fragments that it produces.
A place where a restriction enzyme cuts is called the restrictions site, so instead of saying cuts in one place, or two places, you should say at a single restriction site, etc.

Thank you, but what do you mean by:
"You should also notice that fragment sizes for EcoR1 and HindIII digests should not be the same size.
"You also need to say something about the type of DNA you have in the pBR322 lanes. Is it linear, circular, supercoiled?"
As for 2) its obviously circular? but, maybe i dont understand what you mean?

Do the math to figure out the length of each fragment. Also look carefully at your Gel for pC508 digestions. Are those fragments the same number of basepairs? As for '2)', really? What have you done to the pBR322 plasmid before loading it onto the Gel, and what does that do to DNA?


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Blood testing for chlamydia
I am working with the bacterium Chlamydia trachomatis.
The main test for this species is the naat test, which is based on amplification. But I would like to know how the bacteria affects the blood composition, and if there is a method of diagnosing it from the blood.

Blood antibody tests for Chlamydia trachomatis can be done, but they are far less reliable than amplification:

According to our results, serologic testing for Chlamydia can exclude active infection of the lower genital tract with a high reliability (> or = 95%). However, detection of C. trachomatis can only be reliably achieved by nucleic acid amplification assays.

Low correlation of serology with detection of Chlamydia trachomatis by ligase chain reaction and antigen EIA

Well, I checked your question about chlamydia and there is a way to check if someone has chlamydia from his blood. They take some blood and after they check if there is the Chlamydia bacteria. If they are not sure they simple do a NAAT test. The NAAT test will sure sow if there is chlamydia or something else.


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autosomal recessive population numbers
This question is background research for a science fiction / fantasy novel, my knowledge of genetic is very basic.
It seems obvious to me that for genetic disorders that are autosomal recessive, if those disorders prevent affected individuals from reproducing, the carrier and affected rates in a population will naturally be smaller. I'm not sure if this is the entire reason why say, blue eyes are more common that cystic fibrosis, but it definitely seems to be a contributing factor.
My question is this: say you have a (fictional) autosomal recessive trait that does not prevent reproduction. Let's call the initial carrier rate in the population for this trait C and the initial affected rate A.
In case it matters, the fictional trait I'm considering might reduce the chance of reproduction (as the people may be shunned, or considered less desirable as a mate) but there is nothing preventing reproduction. Something like "bright purple hair" where there is a stigma against affected individuals -- "your hair marks you as tainted" or something. I'm thinking A is around 0.1% (1 in 1000 births). (And if I understand the math right, C would then be around 6%, or 1 in 16 -- so that C * C / 4 gives A.)
Now let's say an oppressive government decides to prevent all affected individuals from reproducing (but carriers are left alone). Let's assume a 100% success rate for the government at rendering affected people infertile thus preventing their reproduction. What will happen to C and A over time? Is there some simple way to estimate how they will trend over several generations?
I don't need exact numbers but I'm having trouble with even coming up with a guess.

Welcome to Biology.SE. I am not sure I understand your C and A correctly. Is it true that C+A=1?

Sorry @Remi.b, my terms come from common stuff like literature given to family members of babies born with a genetic disorder (I have some personal experience there). C is what they call the "carrier rate", the proportion of the population that is a carrier. I'm not sure if "affected rate" is a real term, but I mean the proportion of the population born with the disorder.

Oh ok... so any individual that carry the recessive allele counts in the frequency C regardless of whether it has the disease, is that right? Btw, red hair is not a disease, as you said they can procreate!

Oh so maybe the terms I used like 'carrier' are more appropriate to disorders/diseases? I thought they were generic enough to apply to any trait!!

Um, hmm yes I think individuals with the trait do count as part of frequency C. But if it made explanation/calculation easier it would be fine if you want to redefine the terms so that C does not include the "affected" individuals.

In population genetics, with a simple one-locus two-allele model, we consider the frequency of the two alleles to be $p$ and $q$ where $p + q = 1$ (and thus $1-p=q$ and $1-q=p$). When an allele is recessive it is only expressed at the phenotypic level when the individual carries two copies of the allele.
Following from your example, gene $A$ might be responsible for hair colour, with alleles $A_1$ and $A_2$ where $A_2$ is a recessive allele responsible for purple hair. I will denote the frequency of $A_1$ with $p$ and frequency $A_2$ with $q$. This means that the frequency of individuals with purple  hair ($f_{A_2A_2}$) is $q^2$ and the frequency of people with not-purple hair is $p^2 + 2pq$ (assuming an idealised population). As such, a population of 500 diploid individuals* where there is 100 copies of the $A_2$ allele would have the following genotypic (& phenotypic) frequencies:
$$f_{A_1 A_1} = p^2 = 0.9^2 = 0.81$$
$$f_{A_1 A_2} = 2pq = 2 \times 0.9 \times 0.1 = 0.18$$
$$f_{A_2 A_2} = q^2 = 0.1^2 = 0.01$$
So the allele for purple hair would be present in 19% of the population, but the trait would only manifest in 1% (only ~5.3%, $\frac{1}{19}$, of the people that carry the purple hair allele exhibit the trait). Therefore selection would be quite inefficient at removing this allele from the population, even if you could prevent all purple-haired individuals from reproducing. To find the frequency of $q$ required to give a genotypic/phenotypic frequency where 1 in $x$ individuals have purple hair just take the square root of $1/x$. E.g. to get 1 in 1000 individuals expressing purple hair
$$q = \sqrt{q^2} = \sqrt{(1/1000)}$$
What does this mean for evolution? Alleles that are recessive deleterious are very hard to remove from the population because, at low frequencies, they rarely produce the detrimental effect. Assuming complete dominance ($A_1 A_2$ = exactly like $A_1 A_1$), denoted by $h = 0$, selection only acts on $A_2 A_2$ homozygotes. The frequency of the $A_1$ allele increases at the rate $1/(1-sq)$ where $s$ is the relative fitness advantage. Mutation can also introduce more copies of the $A_2$ allele to the population such that there will be an equilibrium, balanced by the rate of loss due to selection, and rate of gain by mutation. Furthermore, to further build on your analogy, a neighbouring population, where purple-hair is not selected against, may bring copies of the allele in by migration.

Suggested further reading on evolution here and reading on eugenics would likely be of interest to you.
* 500 diploid individuals = 1000 gene copies. Thus $q = 100/(500 \times 2) = 0.1$

That helps immensely. And even better, one of your links led me to find the free PopG program which seems to provide a way of exploring these values over time, while doing the calculations and graphing for me!

Just noted a couple minor correction -- in the third equation I think you mean q-squared not p-squared is 0.01. (sorry I don't know how to write equations)
Also after you define the rate 1/(1-sq), I think you meant "where 1-sq is the relative fitness advantage" but I'm not sure.


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How to introduce predators to a simulated ecosystem?
I made an evolution simulator and observed that when a marginally competent predator appears, it quickly multiplies and hunts down all of the prey animals, which leads to their own extinction soon after. This seem unlike the real world.
About the simulator
The animals are controlled by neural networks, herbivores must consume spontaneously generated food particles to obtain energy, predators can sap energy out of a prey without killing it, but this significantly hinders the prey's well-being. Animals reproduce asexually with mutations.
There are about 50 animals when the predator appears. All herbivores tend to resemble one another.
The ideal result
This simulator was initially meant to explore the development of individual organism through evolution, but the phenomenon I observed made me aware of the importance of whole ecosystems. I want a modified simulator to produce a ecosystems with multiple niches and stable final state, in short, I want biodiversity.
Some proposed modification

Add different habitats: different habitats vary in naturally spawned food particle, and their difference can be detected by the animals
larger population
arbitrarily increase the reproductive period of predators (?)

Please inform me if more information about the simulator is needed, I will also accept general guide lines to such a simulator.

have you set up so that individuals (both predator and prey) need to gather energy above a set rate to reproduce and survive? In the real world many predators would die of starvation as the prey population shrinks so dramatically, this allows the prey population to recover, and the predator population will recover with some lag

Just a point of ecology: a predator that "can sap energy out of a prey without killing it, but this significantly hinders the prey's well-being" sounds like a micropredator to me. Generally an organism will have one or the other feeding mode, it can't choose between them (although you could have a fixed probability of a mutation evolving that switches feeding mode)

I may write a full answer at some point but you definitely need larger populations. It depends on the range they can move over, but if I put fifty rabbits into a sealed empty warehouse with randomly-placed bowls of food and then added a fox, I wouldn't expect the rabbits to last long.

Don't forget parasites and disease. I took an ecology course and the that we used simulator was underwhelming... but the net result was that predator/prey population lags. Predators kill prey, until there are not enough to sustain the poulation. The fewer the prey, the more difficult they are to capture. After the predators population declines (starvation), the prey population blooms... and then the predator population increases again, like two sinusoidal waves with the predator population a couple years behind.

@rg255: Yes, all animals slowly lose energy overtime, and predators especially.

You may be able to take some insight from the Madingley Model, which is very similar to what your doing but on a global scale. http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001841

What you're trying to do sounds really cool. I feel that you can do the following:
1) Increase reproductive period of predators
2) Increase prey to predator ratio (see Lotka-Volterra equation)
3) Make the reproductive speed/ ability of an individual to be in relation with the number of energy 'points'
What kind of set-up are you working with, a unicellular model or a larger scale?
Maybe you could start with a solely herbivorous setup, but give all individuals the ability to harm/sap a small amount of energy out of another individual.
Is there some way you could send me your project? I want to have a look at it

I think the first thing to consider is adding immigration of prey animals from outside populations. In the real world if a predator hunts it's prey to extinction (or close to it), the predator will slowly die off. In that time period of low/no prey species and low predator density is a perfect opportunity for outsiders of the prey species to come in a fill that empty niche in that area.
Another thing is that predators eating prey is easy at first because prey numbers are large. As prey becomes rare they become harder to find and potentially smarter, so harder to catch once you do find them.
Also the fact that predators can "sap energy" out of prey makes them more of a parasite, not a predator. Just something to consider when you read about predator/prey dynamics.

You have a parasite or parasitoid, since they dont kill and eat preys. Assuming real predators,I think that these need too:

add some kind of defense behavior or defense structure to preys. in real world this occurs as potential prey is capable to run, or have a thick skin.
add variation in both prey and predator, things like individuals faster then others, etc
Good evolutionary novelties for predators (biger claws) drives selection of good evolutionary novelties for preys (thicker skin), that drives  again selection of good evolutionary novelties for predators (group hunting), that selects good evolutionary novelties for preys (big horns and agressive behaviour) and so on...
add diseases, death and life spam to preys and predators

Add the option of cannibalism and maybe increase predator mutation rate such that new species that feed of each other quickly evolve. Also insure that herbivores have the capacity to evolve defense mechanisms such as speed herd protection or the ability to harm predators back.


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Conservation Ex Situ
This came up in my biology diversity course and I wanted to raise a question about it.
On the topic of ex situ, one of the presentations that a speaker mentioned that one of its disadvantages is that 'endangered habitats may be fragmented and each small area may not be large enough to ensure survival'. Unfortunately, she left before I could ask anything of this statement.
Can anyone clarify what this means?

She was probably referring to ex-situ conservation as a way to complement in-situ conservation. Indeed, if a population is endangered and fragmentation it thought to be one of the main factors causing the decline, it can sometime be hard to restore the habitat in a way that would permit the population reestablishment (in-situ conservation). Ex-situ conservation can therefore permit to protect some individuals. Then, we could reintroduce individuals to their natural habitats later on, and this could give us more time to restore the habitat.
If you want a good example of how hard it can be to restore the habitat to permit population reestablishment, have a look a the Caribou situation in the north of Québec.
If your question is about how fragmentation is affecting species then it's a very very large subject... it can reduce gene flow, induce stress that could leads to lower reproductive success, etc.
Hope this helps.


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Identification of a mammal in cage
This unidentified animal was trapped in northern part of Kerala State India and images circulated through social media. Doea anyone know what species this is?

Normal animals can look really strange if they lose all their hair. It looks like this one might have lost its hair due to disease. I don't know enough about what animals are native the area to make any suggestions.

Looks like a lemur to me, due to the long tail and finger-like front digits.

@C_Z_ Agreed. If you compare this image to that of a healthy lemur, you can see identical paws, teeth, ears, tail and hind legs.

On a net search Lemurs are seen only in Madagascar. The tail appears to be longer than the body. Can it be a Toddy cat (Palm Civet) with loss of hair?

@RamManoharM it can be a palm civet. This seems like a picture of another semi-hairless palm civet in Kerala.

@WYSIWYG  I didn't even think about the bio geography of it/ This looks like a fat version of the OP picture, so I think you're right.

Could be a civet.

To me it looks like some kind of feline with mange.
It is unlikely to be a Lemur given the lack of thumbs on said animal. And this is India not Madagascar. Lemurs are only found on Madagascar.

This does not look like a lemur at all. This creature has whiskers... lemurs do not have whiskers.. More telling is the lack of tumbs. Lemurs have that... weird looking thumbs but thumbs. this animal does not. .https://www.google.com/search?q=lemur&biw=1252&bih=567&source=lnms&tbm=isch&sa=X&sqi=2&ved=0ahUKEwj0toOc7YjPAhUG4yYKHYFCDToQ_AUIBigB#tbm=isch&q=lemur+paws

Agreed, it's probably a cat, perhaps this https://www.google.com/search?q=Asian+Golden+Cat&sxsrf=ALeKk03eXvY-h6N7Ibq_GgdkzQej4BkQcA:1616468088878&source=lnms&tbm=isch&sa=X&ved=2ahUKEwi4kunxtMXvAhUQnxQKHfhkDuMQ_AUoAXoECA8QAw&biw=1267&bih=711#imgrc=4RDO6Zd8sVUI0M


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Evolution of insects, spiders and jellyfish
Well we all learned at school the classic evolutionarily theory
From:          To:
fish           amphibian
amphibian      reptile
reptile        mammal
reptile        bird

But what always interested me:
What about invertebrates?
Do they also have some evolutionary table like vertebrates or was there evolution never that interesting to begin with?
I can roughly imagine that there are giant evolutionary gaps between an insect and a jellifish but is there any common ancestor of all of them?
So my question has essentially two parts:
1. What is the common ancester between vertebrates, arthropods and molluscs
2. Is there an evolutionary Tree for the last two like for the vertebrates

Have a look at this post

Welcome to Biology.SE
Answering your question fully will require to write a whole book. Evolutionary Biology is a big field and I would recommend that your take some time to get an introduction (slightly more advanced than what you received in school). I am suggesting you take advantage of this free online resource.
I am briefly making comments and answering your question(s) below. They may be hard (or easy, I don't know) to understand but for more info you should really get to the above free online resource.
Species A evolved from species B
Evolution did not make mammals out of reptiles, mammals are reptiles. Evolution did not make birds out of reptiles, birds are reptiles as well (I am using here the phylogenetic definition of reptiles (Reptilia), more info there). It is wrong to think of any two extant species as one having evolved from the other one. But it is correct to understand how closely related are two extant species. It is also correct to make predictions about how the most recent common ancestor (MRCA) look like and it is true the the MRCA might look more like one of its descendents than like another.
We talk about clade as a lineage including many species. In these terms both any lizard species and any given bird species belong to the same clade, the Reptilia, they are both reptiles. They are also both vertebrates (Vertebrata) and animals (Metazoa) and eukaryotes (Eukaryota).
If the statements of the kind "mammals evolved from reptiles" are very misleading the statement "amphibians evolved from reptiles" is simply wrong. The MRCA of reptiles and amphibians was not a reptile (neither an amphibian), it was a tetrapoda (vertebrate).
I can roughly imagine that there are giant evolutionary gaps between an insect and a jellyfish but is there any common ancestor of all of them?
Any two species on earth have a common ancestor. The universal common ancestor, that is the common ancestor that any living thing (bacteria, plants, lizard, human, fungi, jellyfish, Archea, etc...) is called LUCA (Last Universal Common Ancestor). So yes, jellyfish and insects have a common ancestor. LUCA is one of them. Their MRCA is the same guy as the MRCA between jellyfish and you, as insects and primates are more closely related than are insects and jellyfish. This MRCA is an animal (a metazoa) and therefore is also a eukaryote (Eukaryota).
Do they also have some evolutionary table like vertebrates or was there evolution never that interesting to begin with?
Evolution occurs in every single living population. So yes, evolution occurs in jellyfish as it occurs in insects. The clade of jellyfish contains several thousands of species (most of them belong to the clade Hydrozoa). There are almost a million species of insects.
Here are just a few fun facts that come to my mind when I think about jellyfish:

Some species have tentacles, some don't.
Some species have alternance of generation (a given individual is either a sticking thing on the ground while its descendent is swimming).
Size of jellyfish vary wildly

And a few fun facts about insects:

Some have evolved 3 pairs of wings to fly (we think it evolved from gills but it might have evolved from the exoskeleton as well).
Some live in water, some not, some live in water in the larvea stage and not in their adult stage.
They have all sorts of diet
When flight evolved at first, they had 3 pairs of wings. All extant species (who are descendents of this species that evolved flight) have now lost at least one pair of wings, the one closest to the head.
Some species have lost flight.
Some species have lost a second pair of wings (diptera)
Some have evolved crazy mimetism and defense mechanism from the developmental pathway of the third pair of wings.
Eusociality (which is arguably one of the most mind boggling things in evolutionary biology) has evolved several times in insects.
Some species have sex that is determined the ploidy (number of sets of chromosomes) level (it is the case in many eusocial species).

1. What is the common ancestor between vertebrates, arthropods and molluscs?
You can explore the tree of life by yourself on tolweb.org. Arthropods and molluscs are more closely related than any of them are to vertebrates. The MRCA of vertebrates, arthropods and molluscs was a Bilateria (animal, eukaryote). You can see this bifurcation here on tolweb.org. I'd recommend to explore a bit this tree of life, it is pretty fun to do.
2. Is there an evolutionary tree for the last two like for the vertebrates?
Yes, see above.
BTW, I noticed that you talk about spiders in your title but not in your post. You'll find the spiders here on tolweb.org.

You have to be very careful when saying what evolved into what.
In fact you can only say that e.g. ancestors of modern amphibians evolved from the ancestors of modern fish.
Ad. 1 Have a look at this simplified picture of the evolutionary tree of life
Ad. 2 Yes all living organism including plants, bacteria, fungi, and animals can be placed on one evolutionary tree goverened by the same principles of evolution


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Chromosomomal walking
I'm having a great deal of trouble understanding chromosomal walking, especially in regards to this article:
Control of male sexual behavior and sexual orientation in Drosophila by the fruitless gene.
I can get the fact that you can use recombination frequency analysis with chromosomal markers to assess the relative position of a gene, but I'm just stumped as to what it exactly it means when they say that they cloned the gene using DNA segments flanking the two insertions (fru3 and fru4) as a basis for the chromosomal walk.

How to perform a chromosomal walk
I believe that the first publication to describe this approach was Bender et al., Science, 1983.  In that paper they explain how they "walked" along the chromosome to reach the Bithorax Complex (BX-C).
This approach requires two reagents:

a cloned DNA fragment that you have mapped to a defined genetic interval, and possibly to a cytogenetic interval as well (this is only possible if the organism in question has cytogenetic tools).
a genomic library of larger cloned DNA fragments.

Step 1. Use the DNA fragment to screen the library and isolate genomic clones.
Step 2. Purify each genomic clone and prepare enough DNA to construct a restriction map of the foreign insert (N.B., Bender et al., actually used heteroduplex mapping--an EM-based technique--as well) in each clone.
Step 3. Isolate a suitable DNA fragment, devoid of repetitive DNA, from one end of the clone that extends the farthest along the genome in the direction in which you wish to "walk".
Step 4. Congratulations, you have taken one "step." Now use the new DNA fragment as a probe and screen the genomic library again.  Each time you screen the library you will recover all of the genomic clones that hybridize, or overlap, with the fragment you are using as a probe.
Step 5. --> go back to Step 2. above.
Each time you take another "step" you are isolating cloned DNA that is taking you closer to your target (the gene of interest).  For the very first step you will not know which clone is extending in the desired direction (typically) so you need some type of complementary assay to decide which end of the overlapping clones' restriction map is the direction you want to pursue. In other words, you need to align the physical map to the genetic map. In Drosophila one can use  in situ hybridization to polytene chromosome squashes to visualize where the genomic clones are derived from in the genome, and this lets you pick the correct clone at that first step.
Periodically during the walk you will need to test the new genomic clones by in situ to find out when you are getting close to your target (or if you have even walked past your destination).
Ideally you will have some chromosomal rearrangements that alter the physical and genetic maps, and let you unambiguously determine when the chromosomal walk has reached, or entered, the locus.  Alternatively, a strong loss-of-function mutation in your target gene might be a deletion or deficiency that causes a RFLP, and isolating genomic DNA from such a mutant will let you use a Southern Blot to confirm that you have reached the gene.

Thanks for your answer, but can you also explain what it means when they write that they used DNA flanking the fru4 and fru3 insertion alleles as starting points for the walk?
Does it mean that these DNA segments had already been isolated and sequenced by others beforehand?

I have not read the entire methods section of the paper you cited, but presumably further specific details are in there. The authors state that fru4 and fru3 are independent insertions of the P-element transposon. As described by Gerry Rubin (I think it is Bingham et al., Cell, 1982), if you have a cloned DNA fragment that hybridizes to a transposable element, then all you need to do is construct a genomic library from a strain carrying the insert and probe the library to isolate clones containing P-elements. One of those clones contains the fragment(s) used to start the walk.

Okay, a more detailed scan reveals several more germane facts. Figure 1 is your friend. When coupled with the methods section "Molecular Cloning" you have all of the facts at hand. Their task was even simpler than I described because all four of the P-element insertions they describe, fru1, fru2, fru3, and fru4 are loss-of-function alleles of the fruitless gene, so they knew they had knock-outs. They were not walking to they gene, they were walking to recover all of the gene--it is huge (compared to an average fly gene).

Thanks! Now it all starts to make sense. I have one more question though, if you don't mind.
In the "Molecular Cloning" section they say that "The positions of the fru mutants were determined by Southern analysis and in situ hybridization to salivary gland chromosomes in the case of the fru1 inversion and the Df(3R)P14 and Df(3R)ChaM5 deficiency breakpoints." - I don't quite understand how they did this and how they mapped it. Did they make a genomic library of the particular mutant and probe it or something?


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Current human behavior as a genetic heritage
People: I have doubts about genetic heritage, but let me explain the context which has shown up this doubt for you: I was debating about sexism and the following question were put on the discussion: What kind of behavior, most of them come from men, is cultural and social, and what is a genetical heritage from our ancestry? Because I have a feeling that plenty of these behaviors that can be considered, maybe not correct, but at least justifiable. If you have some literature about this subject I would greatly appreciate it.

This is the subject of an entire field - evolutionary psychology http://en.wikipedia.org/wiki/Evolutionary_psychologist

All phenotypic traits have some part of the variance which is explained by the environment and  some part that is explained by the genes. The heritability is then defined as:
$$H_N = \frac{V_{genetic}}{V_{phenotype}} = \frac{V_{genetic}}{V_{genetic}+V_{environment}+V_{interaction. gene.environment}}$$
where $V_{genetic}$ is the Variance in phenotypic traits due to genes, $V_{phenotype}$ is the total phenotypic variance, $V_{environment}$ is the variance due to environment and $V_{interaction. gene.environment}$ is the variance due to interaction between genes and environment.
So your question (if I understand it correctly) should rather be a list of phenotypic traits (behavior) and ask what is the heritability of each trait in the world-wide human population (or on a given subset of the human population).
I think, there is no objective manner of defining a given phenotypic trait. You should chose subjectively, some behavior, define it accurately and then ask the question what is it's heritability.
Moreover, it is quite hard to measure a behavior. It is much easier to estimate the heritability of height in humans.
There are several different methods in order to estimate heritability of a trait. See this wikipedia article
Some of these experiments are not feasible on humans for ethical reasons. Some others are quite limited and are quite expensive. I don't think we have many studies that quantify the heritability of behavioral traits in humans but I might be mistaken.
As said by @AlanBoyd, there is a field called evolutionary psychology that deal with this kind of question. To my knowledge this field is mostly a purely theoretical field and therefore, it does not quite allow to measure heritability.
A good start into this science would be the wikipedia article which seems quite complete.  I can give you some books but I haven't read most of them. Here and here are introductory books in the field. I think this book is a classic in the field. I read this book and it is quite interesting. There are actually many books in this field. The best think you can do is maybe to typewrite "evolutionary psychology" in amazon.
As a sidenote: If you enter in the field of evolutionary psychology you might as well be interested by memetic evolution (evolution of culture). Here is a classic book on the subject.
Be careful in these fields, I think that some ideas do not deserve to be considered as part of science while other do!

Thank you, it helped a lot. Those articles and books that you recommended will be a good start. As i'm not from the biological field of science, so these kind of subjects makes me a little bit confused. I'd ask more especifc questions, but i'll read those material first, maybe it will clear some things to me. Thank you again, guys.


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Is this a crayfish hole? or wasp nest?
I'm suspicious that it might be crayfish, which I'd think was insane (I still kind of do), if I hadn't found a dead one around  my house earlier this summer.
Is that definitely what it is, or do I have to worry it might be wasps?
I'm located in Michigan.

This is the nest of a cicada killer wasp, Sphecius speciosus.

Harmless, solitary and  Cicada-killer wasp holes are ½ half to 1-inch around with thinly scattered loose soil, usually where there is no grass. Cicada-killer burrows have a U-shaped mound of soil at the entrance. Adults emerge June/July.

Source: All the Dirt on Gardening blog
According to the Wikipedia article linked above:

this species occurs in the eastern and midwest U.S. and southwards into Mexico and Central America.

so being in Michigan, you are certainly within the region in which the insect is found.
Parenthetically, also according to the blog from above:

Crayfish holes are 1-inch wide, 2-inches high and made of mud balls.

and the texture of that hole looks more even.

Related Bio.SE question:  Cicada Killer Behavior

Great answer! Perhaps I should change my last name...

Interestingly, I have some experience with Cicada Killers ... See http://biology.stackexchange.com/questions/9830/bee-identification.   I haven't seen any around and I suspect I would've noticed.

@vallismortis. That is smart.  I have a heavy clay based soil with sod on top.


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How does a seed determine when to start germination?
I'm sure there are many different ways for seeds of different species, but what is a general rule? Is it some kind of ideal temperature & wetness that triggers a chemical reaction? What factors stimulate seeds to germinate?

Temperature and humidity are factors. Germination is also controlled by some hormones including Abscissic acid (ABA) and Cytokinins. With sufficient humidity ABA is dissolved and washed away and germination pathway is de-repressed. I had read this long-long time back; I'll verify this and post an actual answer.

Certain conditions are necessary for seed germination:

Moisture — seeds dry out during dispersal, but at germination the cells need to absorb water in order to rehydrate so that metabolic reactions can take place, which will eventually lead to the growth of the embryo tops and shoot. Furthermore, some seeds contain a hormone that inhibits germination and water is needed in order to wash it out of the seed. The water needed for these processes is absorbed by the micropyle.
Warmth —  many of the metabolic events of germination use enzymes, and these are sensitive to temperatures. Temperature will often be used as a trigger for germination.
Oxygen — many of the metabolic events that occur during germination use energy. This energy is produced by aerobic respiration.

Many metabolic processes take place at the start of germination, such as the synthesis  of giberrellin, this is a plant hormone that stimulates mitosis and cell division in the embryo. Other plant hormones include Abscisic acid (ABA), which regulates seed dormancy and germination. It has been found to stop germination once it has been placed in the soil, it causes the seed to enter a period of dormancy. This allows the seed to remain dormant until when the conditions are more favorable for the seed to grow.


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Is there a database providing information about optimum temperature and inactive temperature of enzymes?
I want to know optimum and inactive temperature of some enzyme, but I can't find these information in NCBI, wiki or UniProt. So I want to know if there are some database which provide these information?
Thanks for help.

UniProtKB has annotations for biophysical and chemical properties, such as maximal absorption, kinetic parameters, pH dependence, redox potentials and temperature dependence.
http://www.uniprot.org/help/biophysicochemical_properties
Such annotations are currently available for about 6800 reviewed entries: http://www.uniprot.org/uniprot/?query=annotation%3A%28type%3Abiophysicochemical_properties%29&sort=score
More specifically, temperature dependences is annotated in about 2000 entries: http://www.uniprot.org/uniprot/?query=annotation%3A%28type%3A%22temperature+dependence%22%29&sort=score

Yes, there is a database. It is called 'BRENDA' and can be found here. It doesn't have all the information you are looking for, but it always has the links to the relevant literature, so you can look it up.

您好, you can find more information about optimal temperatures on Uniprot. Look under section 5 and 我爱你.


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Autotrophic and heterotrophic organisms in anaerobic condition
Can both heterotrophic and autotrophic organism survive in anaerobic conditions? If an autotrophic organism does not produce carbon dioxide but requires oxygen, it should not be present in anaerobic conditions, instead the heterotrophic organism can develop. Is this correct?

I am confused by your question ;) Can you clarify what exactly you wish to know?

Whether in anaerobic conditions both auto and heterotroph organisms exist. Actually I am too confused, but I have tried to answer my question by myself, but I am not sure about it. My guess is that because the autotrophic organism requires oxygen even though does not produce CO2, should not survive in anaerobic conditions; instead, the heterotrophic organisms can adapt.

You can edit your question to clarify instead of saying it in the comments.

It is not necessary that all heterotrophs are aerobic. Many are anaerobes (yeast etc.)
Anaerobic Heterotrophs
These anaerobes live on glycolysis and fermentation (as far as I know). These two processes don't require Oxygen for release of energy.
Glycolysis
Alcohol Fermentation
Lactic Acid Fermentation
Alcohol Fermentation takes place in yeast (just an example) and Lactic Acid Fermentation in Muscle Cells.
The autotrophs will take care of themselves as photosynthesis require no Oxygen. If place in correct conditions (light and water are available), then they will thrive.
So, the answer to your question would be that both can survive. It varies from species to species. If you select the correct one then, both would survive or only one of them.

Autotrophs: Organisms that can synthesize organic carbon from inorganic carbon (carbon fixation). Nitrogen fixation is not considered an essential condition to qualify as autotrophs. True autotrophs can fix both carbon and nitrogen (Some algae. This true autotrophs is not an actual terminology).
Aerobes are organism that require oxygen for metabolism; it is not really dependent on whether the organism is autotrophic or heterotrophic. Anaerobes do not use oxygen for metabolism. Some anaerobes are aerotolerant i.e. they can tolerate oxygen (oxygen is highly reactive and can damage tissues) while others are not.
You can have a look at this post for some basics on aerobic and anaerobic respiration.
Examples of anaerobic autotroph include Ferrobacillus sulfooxidans and Methanobacterium thermoautotrophicus.
Some organisms are called microaerophilic i.e. they need oxygen but not in high concentrations.


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How prevalent is sexual dimorphism?
I'm writing a lab on sexual dimorphism (sex differences in phenotypic traits) and I want to include a sentence in the abstract that states how prevalent sexual dimorphism is. However, I can't find any figures that pertain to organisms generally (or even for a clade).
How prevalent is sexual dimorphism in nature? How frequent is sexual dimorphism beyond primary sexual traits (gonads, gametes etc.)?

Ubiquitous to all anisogamous species - gametes (eggs and sperm) at least are sexually dimorphic

You need to clarify exactly what kind of sexual dimorphisms you are thinking about (or define 'sexual dimorphism'). One common reason that sexual dimorphisms occur is sexual selection - which by definition is affecting reproduction - so to say that sexual dimorphisms are sex differences that don't affect reproduction doesn't make much sense to me.

@fileunderwater all dimorphisms outside of the sex organs.

You might consider the possibility that all species have sexual dimorphisms, even if they aren't readily apparent to our limited and prejudiced by anthropomorphism perceptions, since males and females are able to tell each other apart.

I hope something comes up, but without a clear definition this is a matter of opinion.

I would say that anisogamy, the different gametes such as sperm and eggs, is itself, a form of sexual dimorphism. However, you've since stipulated that you want to know the prevalence of sexual dimorphism beyond sex organs/gametes.
Sexual dimorphism occurs in a vast plethora of traits, at a variety of levels, and in almost all known dioecious species. It occurs even at the level of gene expression in, for example, mice, birds, mosquitoes, fruit flies, nematode worms, humans, and much more. Sexual dimorphism is prevalent and obvious in morphology such as peafowl, red deer, mallards, humans, guppies, fruit flies, horned flour beetles, and much more. It also occurs in physiology, behaviour, and life history traits (e.g. lifespan, ageing).
Simply put, sexual dimorphism is extremely common. It is hard to put a number on it, any studies of sexual dimorphism are likely to be focussed on sexually dimorphic traits (so a meta analysis will likely suffer from publication bias), and not all traits can be easily measured. However, gene expression is a good place to look because many traits (expression level of each gene is a trait) can be sampled simultaneously. This study found that 18% of genes were significantly sex-biased in any one tissue, while this suggests that at various developmental stages it was between approximately (based on table 1) 13% and 61%. Note again, there's not much literature which actually puts numbers on the general frequency and extent of sexual dimorphism. That is generally because, in the relevant research community, the gonads and gametes are included as sexual dimorphisms.*
Also, despite the frequency of sexual dimorphism, it is thought that the evolution of sexual dimorphism is severely constrained by the sexes working from the same genome (links: 1, 2, 3, 4, 5, 6, 7) and sexually antagonistic selection could readily favour further evolution of sexual dimorphism.
In terms of your report, I don't think you would need firm numbers or a citation; it's a well accepted fact that sexual dimorphism is common.* You would be more than fine to say something along the lines of:

"Sexual dimorphism is extremely prevalent in nature, found in a
  range of taxa, and found in a variety of traits."

* These points are based on my experience, I did my phd thesis on the evolution of sexual dimorphism so I've read quite a substantial component of the relevant literature.

I second the comment. Any species that reproduces sexually presents dimorphism. Even S.caerevisiae produces haploid spores with MatA and MatAlpha. Although otherwise indistinguishable, they are dimorphic from a molecular point of view (the expression of the receptor).
Here is a set of figures:
https://en.wikipedia.org/wiki/Mating_of_yeast
"The MATα allele of MAT encodes the α1 and α2 genes, which in haploids direct the transcription of the α-specific transcriptional program (such as expressing STE3, repressing STE2) which causes the cell to be an α cell."

This needs work to be considered as an answer. It's more suited to a comment as it does not attempt to answer the question.

It does as "Any species that reproduces sexually presents dimorphism" and I also mentioned that it traces back to S.caerevisiae, which is one of the simplest model organisms.

The user specified that they want sex differences beyond primary sex traits (gametes, gonads etc.)


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What will happen if a foetus is Rh- and the mother is Rh+?
If a mother has Rh-negative blood and her foetus has Rh-positive blood it will result in rhesus incompatibility and lead to erythroblastosis fetalis. What will happen if the reverse occurs, when a mother is Rh+ and the foetus is Rh-?

Nothing. Rhesus incompatibility results when people who are Rh- develop antibodies against Rh+ blood after exposure. People with Rh+ blood do not show any such reaction to Rh- blood.
In a way, it's comparable to blood types in that regard. People with the blood group O can develop antibodies against type (for example) B blood. People with type B don't develop antibodies against type O blood, and can thus receive blood donations of type O.
Also, rhesus incompatibility during pregnancy is only a concern in second or subsequent pregnancies (or after miscarriages). The antibodies develop through the blood being "mixed" during the birth (or miscarriage) and are then an issue if the next fetus also has Rh+ blood, which is just assumed if the father is Rh+ or has an unknown blood type to be on the safe side, and can be addressed medically.

Injections of a medicine called Rh immune globulin can keep your body from making Rh antibodies. This medicine helps prevent the problems of Rh incompatibility. If you're Rh-negative, you'll need this medicine every time you have a baby with Rh-positive blood.

-What is Rh Incompatibility
Also, as you can read in my answer to a similar question about blood groups and pregnancy
How does a fetus retain a blood group different from its mother? the maternal and fetal blood usually only mix during birth due to the placental blood barrier. If you are wondering whether the fetus should have a reaction, the immediate functions necessary for that don't develop until more than six months after birth.

Does it warrant stating explicitly that the foetus does not (for practical purposes relating to the rejection of Rh+ blood) get exposed to the mother's blood in utero? The questioner might be imagining that the Rh- foetus "should" reject the Rh+ mother. And even if the blood were mixed, I'm not sure whether a foetus has the antibody mechanism for Rh+ rejection active yet.

@SteveJessop good idea, added a paragraph

Steve: that would be specific immunity, so your hunch is correct: it isn't developed yet at that stage.


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Humans genetic/phylogenetic "next relative" in central Europe?
What species in central Europe in the phylogenetic tree shows the closest difference in time to the most recent common ancestor with Homo sapiens?

Could you define central Europe?

What do you mean by "next relative"?

I am not sure I understood the question. Is the following your question?

Among all species living in central Europe, which one is the most closely related to homo sapiens?

Source of information
opentreeoflife.org (nice vizualisation on OneZoom.org) is one of the most update synthesis of existing research inn phylogenetic reconstruction. I base my answer in consideration of the tree on OneZoom.org.
Answer
Outside Homo sapiens, there is no living primates (or any other Euarchonta) in Central Europe. The sister branch of primates include Lagomorpha (Hares and Rabbits) and Rodents (mice, rats, squirrels, prairie dogs, porcupines, beavers, guinea pigs, hamsters, and capybaras). In other words, any Lagomorpha and any Rodents are all equally related to any Primate (incl. Homo sapiens). Their Most Recent Common Ancestor (MRCA) lived about 75 millions years ago.
Examples of species of lagormorpha and rodents that live in Europe include Mus musculus, Rattus norvegicus, Lepus europeanus and Sciurus vulgaris.
How about Hedgehogs?
Hedghogs are Insectivora and they are a sister group to all primates, lagomorpha and rodents. Their MRCA lived about 80 million years ago. So, no there are species currently living in Europe that are more closely related to us than hedgehogs.
Note
The term "next relative" does not mean anything! You might want to understand your understanding of phylogeny with an introductory course.

Yes this was my question. Would it "theoretically" be possible to measure the individual distances of each Lagomorph or Rodent species to the MRCA? I mean it is for instance known that some are more "archaic" then others. So that the question would be what is the most archaic of all Lagomorpha and Rodents? I see that the answer ideally would theoretically require a complete knowledge of the MRCA, nut maybe some guess is possible?

For example Aplodontia rufa
(if it only lived in Centraleurope) would be a candidate in the sense of my question.

Aplodontia rufa lives in north America (California, Oregon, Washington and British Columbia). I added examples of species in my answer.

Nice answer. I would just note that OneZoom.org doesn't assemble the data themselves; they get it from http://www.opentreeoflife.org/ (as acknowledged in http://www.onezoom.org/about.html). They do a nice job of presenting it though, which is also important!

I have updated the question and choose one possible specification of the heuristic term "next relative".

Shortest distance is still very unclear. Do you mean minimum number of average genetic pairwise differences on putatively neutral sequences (which result will slightly depends on the alignment methods and consideration of gene/chromosome duplication/deletion)? Maybe you are referring to some other measure such as chosing a number of quantative traits and compute the average (over all traits) difference between species average trait value.

As you used the term "phylogenetic" in your question, it totally makes sense to consider the time to the MRCA as a measure of distance. It is what we mean when we talk about how closely related are two different lineages/species anyway. It will be a very very good proxy for the number of pairwise differences at neutral sequences also.

Is it better now?

by "time of branching", I suppose the oly thing you can mean is "time to the most recent common ancestor", which is exactly what I answered. Do you feel like my answer does not answer your question?

It doesn't answer, because it implies that all recent rodents and lagomorphs  "to a very good approximation" show the same number of pairwise differences at neutral sequences. Since this is counterintuitive (see my example of an "archaic" rodent (it does not live in Central Europe but just for the sake of this argument)). So the intermediate question would be: What kind of measure would allow us to make a distinction is distance between the relation between an "archaic" rodent and a more evolved one? Is the simplest answer already "number of pairwise differences at neutral sequences"?

The terms "archaic" and "more evolved" make little sense. You seem to assume there is a thing such as "distance between species" and then we try to estimate it with different statistics. The reality is that the term "distance between species" is undefined and you have to chose a statistics and make sense for your particular interest. The very standard is to consider the time to MRCA which is a very proxy anyway to many other statistics of species divergence such as typically the number of pairwise differences at neutral sequences. By the term "relatedness", we also refer to time to MRCA only.

If things are still unclear, I invite you to (1) follow an introductory course to phylogenetics and (2) ask your question regarding your misunderstanding about phylogenetics in a separate post as such discussion would be off-topic here. I you clarify your post by rewriting the question I suggested at the top of my answer (and remove the unclear concept of "next relative"), then you will be able to consider your question has been answered (and your post could well be re-opened).


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Using only one antibody to detect COX-2 enzyme
If I wanted to detect COX-2 from a western blot test, would only a primary antibody work? I'm on a budget so does anyone know of relatively cheap COX-2 antibodies?

Considering that you would need to conjugate the primary antibody to HRP or fluorophores (depending on what detection method you're using), it may well be cheaper to use a secondary antibody.

Unfortunately, you'll often find a relationship between cost and quality in antibodies. Sure, there's lots of cheap Abs on the market, but is it really worth saving $50 on the Ab if you have to repeat your western 6 or 8 times to get an image-quality result? I used to do tech support for a reagent company, and I've heard lots of stories....


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Species Identification: Coniferous tree, Italy
I noticed it close to the place where I work, I live in Italy
Could you tell me the complete name of this tree?
Particular of the leaves

To me, it looks like a species of Taxus (Yew), for instance Taxus baccata. This is based on the flat needles, "flat" apparence/growth of the branches and the red berries. It's a bit hard to see what the red things are in your 3rd picture though (berries, shoots, flowers??). It should also have reddish bark where you can easily peal of loose scales. They can become very old (>1000y), have been used for many human purposes (woodcarving, medical purposes, bows), and all parts except for the berries are toxic.
Abies alba might be an alternative (if the red things are flowers), but then the needle underside should be relatively white and they also look to broad, soft and shiny to me.
Some pictures:

(from wikipedia)

(from http://linnaeus.nrm.se/flora/barr/taxa/taxus/taxubac.html)

(from wikipedia, a 1200-year-old tree in Poland)