text:
Why don't mosquitoes evolve towards muting themselves?
Quite certainly, muted mosquitoes would be much more effective as far as their blood-sucking pursuits are concerned, since mosquito sound is predominantly responsible for sealing their fate (between the two palms of the hand). Muting themselves would certainly reduce the chances of being caught in the act. For instance, unless you notice by looking, leeches go undetected for long periods because there isn't any obvious sound emanating from them.
Thus, reasoning says - this should be favorable from the point of view of evolution, unless there is a some indispensable purpose served by this sound, which can not be otherwise served. This page seems to suggest that this is so from the point of view of mating. In fact, quoting verbatim:

Since female mosquitoes are larger, they flap their wings slower, and males know it. They use the distinctive pitch of the females' buzz to recognize them. Louis M. Roth, who studied yellow fever mosquitoes for the U.S. Army during World War II, noticed that males ignored females whenever the females were quietly resting, but whenever the females were flying, and therefore buzzing, the males wanted to mate with them. The males even wanted to mate with recordings of female mosquitoes or tuning forks that vibrated at the same pitch.

But mating signals could also be of other forms, like some chemicals secreted (I envisage something like pheremones). Why is making sound so important? Why can't this noise be either less intense, or lie outside the audio range for humans (their targets)?

Mosquitoes can fly and that is a greatly advantageous. The buzz is a tradeoff for their flying ability. I don't understand what exactly are you getting at.

@WYSIWYG: well, as a colloquial example, gliders, airplanes and choppers both fly, but do not make an equal amount of noise, do they? My point is - why can't the noise be either less intense, or outside the audio range for humans. (Thanks anyways, maybe I'll add this to the question.) :)

Maybe because most mammals are four-legged, thus they can seldom protect themselves against bites. Even though a cow might hear a mosquito land on it's back, can't do much about it. Humans on the other hand, are only here for as little as 200,000 years, which is not enough for much changes to occur.

@FloriOn - That's an interesting perspective. Thanks :)

This question is clear and there is no reason to close it even though the main answer might be pretty straightforward.

this is a frequent sort of question that arises on the site - why doesn't evolution eliminate obvious weaknesses.

Your question is really good, but in actuality, they do evolve towards muting themselves, actually, they have pretty much done "most of the work":
It is assumed that microscopic scales along veins and wind margin
play an important role as a silencer as downs on the flight feather of owl.

From this we can assume that the effectiveness of these scales are high, as they had plenty of time to evolve; thus the other factor they should alter to make them quieter is the frequency of their flapping $f$, which can be calculated from the following equation:
$$f=K m^{-1/6}$$
where $m$ is the mass of the animal and $K$ is the proportionality constant. The resulting number is around several hundred hertz (Remi.b observed a value around 440 Hz)
There are two options for them, either increasing the frequency up until our ear is incapable of hearing it which would be impossible as even the highest flapping frequency can hardly exceed 1000 Hz, which is nowhere near the required 20,000 Hz. By increasing their body mass they could decrease the frequency but the needed 15-20 Hz is pretty low compared to the actual several hundred, thus it would likely need a complete body structure change which is not something to happen in the near-future.
An another solution might be a different strategy in flying. Gliding attacks might pay off really well (that's why owls on the other hand can't be heard during flight), but even though there are some insects capable of such[1], it would need an immerse amount of time, not talking about the problems that might arise from the bumping into of our body.
I don't think that the mating signaling would be indispensable from an evolutionary perspective, but this statement of mine can't be proved.

These are the physical/biological difficulties of the problem, here is one from an evolutionary aspect: They are not likely to have experienced a strong selection against this feature, as most of the possible victims are incapable of doing much against a mosquito due to the absent of hands (and tails are seldom enough to stop them). The first possibly blood-sucking mosquito was found to be living 79 million years ago, while animals that might be able to "seal their fate" are much more recent, while not even having success most of the time.

https://www.jstage.jst.go.jp/article/jsmec1997/43/4/43_4_895/_pdf
http://www.geologica-acta.com/pdf/aghv3501a12.pdf
http://www.physics.emory.edu/faculty/weeks//lab/papers/jwang-arf05.pdf

Thanks, this is a very well researched answer. I'll wait for sometime and hear from others if they have anything to add to this, before accepting.

..they have not experienced strong enough selection to be silent fliers. people can only really hear those things when they fly close to your ears.

Could you please provide the reference for the flapping frequency formula?

@Hans It's in the first cited study, in section 4.1

Gliders do not actively fly and there is no work done by them in producing motion. Other flying machines do make a sound.
If a trait exists then it means that there is not enough pressure against it. You can hear a mosquito only if it flies close to your ears; otherwise, they seem to be undetectable by hearing.
To produce ultrasonic sounds the mosquito has to flap its wings too fast- which is energy intensive. Conversely, to produce just infrasonics, it has to flap the wings too slowly which may not provide it with enough thrust.
A recent study by Bomphrey et al. (2017) suggests that mosquito flight is different from other insects and the aerodynamics are rather complex. Mosquitoes are known to use low amplitude, high-frequency flapping that generates the buzz.
From the abstract:

Mosquitoes exhibit unusual wing kinematics; their long, slender wings
  flap at remarkably high frequencies for their size (>800 Hz)and with
  lower stroke amplitudes than any other insect group1. This shifts
  weight support away from the translation-dominated, aerodynamic
  mechanisms used by most insects2, as well as by helicopters and
  aeroplanes, towards poorly understood rotational mechanisms that occur
  when pitching at the end of each half-stroke. Here we report
  free-flight mosquito wing kinematics, solve the full Navier–Stokes
  equations using computational fluid dynamics with overset grids, and
  validate our results with in vivo flow measurements. We show that,
  although mosquitoes use familiar separated flow patterns, much of the
  aerodynamic force that supports their weight is generated in a manner
  unlike any previously described for a flying animal. There are three
  key features: leading-edge vortices (a well-known mechanism that
  appears to be almost ubiquitous in insect flight), trailing-edge
  vortices caused by a form of wake capture at stroke reversal, and
  rotational drag. The two new elements are largely independent of the
  wing velocity, instead relying on rapid changes in the pitch angle
  (wing rotation) at the end of each half-stroke, and they are therefore
  relatively immune to the shallow flapping amplitude. Moreover, these
  mechanisms are particularly well suited to high aspect ratio mosquito
  wings.

Bottomline is that evolution does not know where the best optimum is and it does not really try to proceed to a global optimum. If a trait is disadvantageous, it is selected against. Neutral mutations stay but do not get amplified unless they have some kind of advantage.

Note that the speed of wing flapping is exactly equal to the frequency of the sound produce. A mosquito flap at about 440 Hz (personal observation during my Bachelor degree). A young and healthy human can hear up to 20000 Hz. The mosquito would need to flap their wings 45 times faster to become inaudible (and would need to adapt its mating behaviour in consequences).

@Remi.b - Wow. That's fabulous information! Any comments about the second proposal (lesser intensity of sound, even though at the same frequency)?

@TheDarkSide for exactly the same reason as explained in the answer - there is no selection pressure to lower the volume. Additionally, since mosquitoes find each other by sound, lowering the intensity would decrease numbers of mating attempts, something that I'm fairly sure would not be advantageous to the species.


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

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

could not access Google book link .

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

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

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

source: Stack Exchange

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sort: votes


text:
Modelling insecticide net efficacy loss
I am currently doing some work on modelling the effects of treated nets usage on mosquito populations. Nets do not retain their maximum efficacy forever. They lose their chemical efficacy after about three years and all that is left is the physical protection offered by the net which I estimate to be 20% of the original efficacy.
I am trying to model this behaviour. I need continuous function over the interval $[0,1095]$ which decreases slowly  from 1 when $x=0$ and asymptotically approaches 0.2 when $x \rightarrow 1095 $.
I tried an ellipse of the form $y=\sqrt{1-\dfrac{x^2}{(1095)^2}}$, but i realized the function is equal to zero when $x=1095$ which is not what i want.
Any help will be appreciated. Thank you.

This is more suited for math-SE. The term "asymptotically" is used to denote value that will be reached in $x\to \infty$. You can rather ask for a condition in which the system reaches within 99% of the desired value i.e. 0.2 at $x=1095$.

Can you describe the shape you are after more clearly, and what you mean with "continuouos cap shaped function"? Would a simple negative exponential function similar to $y(x) = e^{-bx+c}+0.2$ be insufficient? Do you have data that will be used to fit the parameters of the function?

@WYSIWG, I agree the word asymptotic is not appropriate. What I meant was a concave function which has value 1 at $x=0$, and has a value of 0.2 at $x=1095$, beyond 1095, the function should not have a value below 0.15.

@fileunderwater I meant a concave function. I have no data to fit the parameters. I am hoping to generate a function such that the net loses efficacy gradually to about $65%$ in two years, then the chemical protection ebbs  completely over the last year. The remaining protection level is $20%$ of the original protection.

I'm voting to close this question as off-topic because it is about mathematical functions and does not involve any biological principle. Moreover, many functions can be constructed that can fulfil OP's criteria and hence this question is broad.

As @WYSIWYG suggested, this is probably more suitable for Math-SE.
From you question, it is unclear exactly what shape you are looking for, and there are many functions that could describe the behaviour you're after, i.e. a continuous, smooth decrease towards an asymptote. However, two possible options could be the negative exponential and a negative gompertz function. Possible forms of these could be:
Negative exponential
$y(x)=e^{−ax+ln(1-b)}+b,$
where $b=0.2$ and a is a rate parameter.
Negative Gompertz
$y(x) = 1-\alpha e^{-\beta e^{-\gamma x}},$
where $\alpha=0.8$ (describing the asymptote), $\beta$ in an inflection parameter (given a displacement along the x-axis), and $\gamma$ is a rate parameter.
These functions can give results such as:

In these examples, $a = 0.005$ for the negative exponential and $\beta = 150$, $\gamma = 0.008$ for the gompertz v1 and $\beta = 5$, $\gamma = 0.005$ for the gompertz v2.
An alternative parametrization of the Gompertz, which might be easier to understand, is:
$y(x) = 1-\alpha e^{-e^{-\gamma (x-\beta)}},$
where the inflection point ($\beta$) is directly related to the scale of the x-axis (so $\beta = 400$ would give an inflection at x = 400).
Are these examples interesting for your application? Hopefully they can provide a starting point for you.

I think the OP is looking for a concave-down function with no inflections.

@fileunderwater the gompertz look very interesting, v2 especially. Could you please explain to me how the various parameter affect the concavity of the curve?

@canadianer I thought so as well, but this will be very hard to achieve continuously if the loss during the first two years is only 35% and the rest (down to 20% protection) is lost in the last year

@Ozymandais the parameters $\beta$ and $\gamma$ interact to produce the shape. If you increase $\gamma$ the loss is more rapid (almost a step function if $\gamma$ is very large), and $\beta$ sets the inflection point of the function.

Actually one can make many functions that can fulfil the criteria. Because the OP has just mentioned the initial and final behavior of the function, there can be infinitely many shapes. For example one can use a linear combination of polynomials.

@WYSIWYG I agree, and the idea was to give the OP a bit more to work with.

I think, mechanistically, that loss of activity should be negative exponential (assuming first order degradation kinetics).

@WYSIWYG Spontanously, that was my feeling as well (hence my initial comment). However, the OPs description of a 35% loss over two years followed by a further 45% over the third year doesn't fit with this.

@Ozymandais See the updated answer for an alternative parametrization fo the gompertz.

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text:
Is this species a variant of a red flour beetle?
Found this little guy crawling around the back garden - South Coast of the UK.

The closest things I could find online (with an admittedly weak knowledge of where to look up these things, aside a google search for red beetle) were the red flour beetles. However, it doesn't look quite like what we had, this being more stockier, with a dark head, and more splayed feelers.

This does not look like a red flour beetle, but more like some species of Melolontha, possibly a cockchafer. For more specific information, we would need to know, where your back garden is and maybe something to scale the bug. I would go for Melolontha melolontha, the common cockchafer.
Of the two other european species of Melolontha, M. hippocastani usually has a black edge of the elytra (see this picture), which this one doesn't seem to have, and M. pectoralis is very rare and mostly (only?) found in Germany.

I've added some location information - meant to in the original post, but forgot! But I'm on the south coast of the UK

Then it is from my understanding perfectly normal environment for a Melolontha melolontha.

M. hippocastani usually has a black edge of the elytra (which this one doesn't seem to have), which makes M. melolontha even more likely. M. pectoralis is very rare and mostly (only?) found in Germany. I've added this info to your answer and hope you are fine with this.

I totally agree with skymningen, definitely a cockchafer


text:
Is there a karyotype database for human cell lines?
I'm looking for the karyotype of a specific cell line. Some karyotypes are well known, such as HeLa or some carcinomas, but some are very hard to find, such as LG2 (B cells). Is there a database dedicated to karyotypes of human cell lines?

I can't find the LG2 cell line that you mentioned but often times you can find karyotype information on ATCC or COSMIC (for cancer cells)

Have you checked the following link? It is focused on epithelial cells though. http://old-www.path.cam.ac.uk/~pawefish/

As far as I know and have found, there is no one master database for karyotypes of all human cell lines. They are usually grouped into subsets either by some commonality (e.g. being cancers) or simply because of who/where they were developed and how they chose to share the line. Some good databases/resources are:

ATCC - A great repository that has cell line datasheets, references, images, and culturing info. I highly recommend using ATCC as your first stop when looking to learn more about a line.
NIGMS Human Genetic Cell Repository - A very robust repository that contains far more than just cell lines. It's good, but the wealth of info can be a bit difficult to sift through.
COSMIC - A great collection of info on cell lines and mutations found within them. Good if you want to look for/understand particular genetic aspects of a line.
Cellosaurus - A fantastic database on cell lines! I particularly like the info Cellosaurus hosts on different names and common misspellings of names for cell lines. It also provides info on hierarchies of cell lines- that is, when multiple cell lines are derived from a parent line. This is super helpful when trying to parse literature with confusing references to similar lines. It also provides references and cross-references. I cannot recommend this one enough.

To get back to your particular cell line, I have only been able to find one reference to a line called 'LG2'- even with the help of the resources listed above and PubMed, so I, unfortunately, can't give you much info on that specifically. If there really is so little info on this line, I would suggest contacting the source (colleague, lab, excel sheet associated with your storage system, etc.) for your cells to see what info they have. If you can't find anything that way, it may be best to just submit a sample for sequencing yourself and get that info out there.

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text:
How is the subunit molecular weight different from the native molecular weight?
I noticed that the native molecular weight for an enzyme is different from its subunit molecular weight. Why are they different? Aren't the genes needed to express the enzyme the same in the native organism and in the heterologous expression system?
Does the heterologous expression system happen to affect the molecular weight of the final enzyme product? If so, how?

Can you provide a source? It could be listed differently for a number of reasons

Can you please say about which enzyme you are talking? And what is the heterologous expression system in this context?

This paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1065158/ Table 3 in page 3. Please help me. I am very confused with the terminology and how expressing an enzyme from Neurospora crassa in E. coli makes it have a different molecular weight than if it was in its native Neurospora crassa.

Your question is answered in the paper, the protein likely exists as a homodimer in vivo and denaturation (such as performed with SDS PAGE -> Western Blot) separates the dimers into monomers:
"To determine the quaternary structure, size exclusion high-performance liquid chromatography was performed using an Agilent 1100 series high-performance liquid chromatography system with a Bio-Sil SEC-250 column (300 by 7.8 mm) and a mobile phase of 0.1 M Na2PO4, 0.15 M NaCl, and 0.01 M NaN3, pH 6.8. A Bio-Rad standard was used to standardize the column's retention time with respect to molecular mass (supplemental data). All experiments were repeated twice with <0.05 min of deviation in the retention times. The molecular mass of XR was calculated from its retention time to be ∼53 kDa. Monomerization could be induced in the presence of 15% SDS, causing XR to elute as a single peak, with a retention time corresponding to a molecular mass of ∼34 kDa. The data suggest that the native XR is a noncovalently linked dimer. The significant difference between the calculated molecular weight of the dimer and its apparent molecular weight is not uncommon for XRs from other species (7, 21, 33), which also typically exist as dimers. However, to be certain of the protein size, N. crassa XR was subjected to mass analysis by electrospray ionization-quadrupole time of flight mass spectrometry. The highest abundance peak had a value of 38,381 m/z, corresponding exactly with the predicted molecular mass for the His6-tagged XR with the N-terminal fMet removed (supplemental data). Additionally, a 2M+ peak of about 20% abundance at 76,759 m/z corresponds well with the predicted mass of the dimeric form of the enzyme (76,762 Da)."

Also, smaller differences are common when eukaryotic proteins are expressed in bacterial systems due to differences in post-translational modification (esp glycosylation).


text:
What is the impact of sertraline on white blood cells?
This simplified video and RT.com article discusses how the mechanics of the death of a white blood cell can be useful as an "alert mechanism" to other white blood cells of an incoming infection.
Also in the article it describes how this same notification mechanism might enable the transmission of certain types of pathogens and it has the following quote:

"We found that a commonly used antidepressant can block this whole process and an antibiotic can promote this event,” said Ms Atkin-Smith.

The full report is available here.
Can anyone explain, (with a summary in layman terms) the impact of Sertraline on white blood cells?
Does taking Sertraline increase the risk of susceptibility to illness, or decrease it?

Short answer
While sertraline may theoretically affect the immune system, there is no evidence, as far as I know, that it negatively impacts immune status.
Background
In the article (Atkin-Smith et al., 2015) sertraline (a.k.a. Zoloft, an antidepressant) is shown to block the formation of ‘beads-on-a-string’ protrusions and apoptotic bodies after from dying white blood cells.
Generally, when cells die physiologically, they do not just disintegrate, they undergo programmed cell death called apoptosis.

Beads-on-a-string from a apoptotic monocyte. Source: (Atkin-Smith et al., 2015).
The authors hypothesize that these beads-on-a-string and apoptotic bodies may boost immune responses by containing antigenic material, or that they may contain a warning signal for other immune cells that a pathogen is on the loose.
These claims, however, are hypotheses.
There are many reported side effects of sertaline, but immune suppressant effects are not evident. The only side effects reported touching on it are, e.g., a fever and a sore throat. However, such general symptoms can be caused by a variety of causes and were not reported frequently.
Indeed, in a small study in HIV patients, sertraline showed no adverse effects on the immune system (Rabkin et al., 1994).
References
- Atkin-Smith et a. Nat Comm (2015); 6: 7439
- Rabkin et al. J Clin Psychiatry (1994); 55(10):433-9


text:
What does the hominin phylogenetic tree look like?
I'm no biologist, but I'm curious what the rough phylogenetic tree looks like for Hominin.  Could you create a rough sketch that includes:

Homo rudolfensis
Homo ergaster
H. georgicus
H. antecessor
H. cepranensis
H. rhodesiensis
Homo neanderthalensis
Denisova hominin
Homo floresiensis
H. heidelbergensis
H. neanderthalensis
H. sapiens
H. erectus
H. habilus
any others I may have missed

Feel free to correct any incorrect assumptions I may have made here, or clarify anything that could be instructive.

Is this suitable? I am a novice so sorry if it is not: http://humanorigins.si.edu/evidence/human-family-tree                                              I Googled "Hominid tree" to find it.

Gonzalez-Jose et al. (2008) published the following cladograms, based on two analyses (parsimony versus maximum likelihood). The table shows the legend. The interesting case of Homo floriensis, among others are not included, likely because of their recent discoveries and limitations of the study cited.

Reference
- Gonzalez-Jose et al. Nature (2008); 453 775-79

Great answer, but one thing to note about the upper tree is that the Bremer support values are really really low (0.2 to 0.5) particularly within Homo. So basically there is no resolution at that point. They may as well have a large polytomy at that point. This is not a fault of the authors but of all these fossils being fragmentary.

@kmm - This is pretty much over the top of my head - Please advice, should I crop the image and only show the bottom tree instead? Piece of cake to do so. I simply pasted their complete figure in here without critically assessing their respective merits to the question.

No, it's fine as is. The tree is the tree and is (very likely) technically correct. It's just that the devil is in the details. I'm sure the bottom tree is equally poorly supported.


text:
Punnet Square for Genotype Probabilities
I'm a computational physicist by trade, and today I was working with a student that is coding a simulation that requires the interactions of different genotypes to determine which phenotype will be expressed. This student drew a Punnent Square like so:
$
\begin{equation}
\begin{matrix}
& O & Y \\
\_ &\_ & \_ \\
Y& |YO& YY \\B &|BO & BY
\end{matrix}
\end{equation}
$
and then stated that each genotype should have a 25% probability of being expressed. I remember learning this as well in highschool bio, but since finishing my Bachelor's in Physics (with some focus on complex adaptive systems/chaos theory) I am a bit skeptical that biology really obeys the probabilities of the Punnet Square. Are there examples in biology where the probabilities of the Punnet Square are clearly broken?

Mendelian inheritance is not governed by laws. Mendelian laws are statistically inferred. In reality, by chance it will never be 25% exactly and mutations may mess things up too.

Our germ cells are haploid, while our somatic cells are diploid. The diploid cells of a child result from the fusion of a paternal haploid germ cell and a maternal haploid germ cell. When these germ cells are generated during meiosis, the paired diploid chromosomes of each parent (which they in turn received one of from each parent) are randomly segregated such that for a given chromosomal pair there is an approximately equal chance of a given germ cell containing either member of the pair independent of the what other chromosomes it receives.
In the case of a single gene with a single copy on both the maternal and paternal chromosomes, the Punnet Square accurately estimates the probably of inheriting each possible genotype. (50% chance of getting one of two alleles from dad * 50% chance of getting one of two alleles from mom). In the case of multiple genes on different chromosomes, the 50% chance of any given allele still holds, as all the genes segregate independently. The accuracy of the Punnet Square fails when genes are sufficiently close to each other on the same chromosome. Genes distant from each other on the same chromosome still segregrate independently due to a high level of recombination events between chromosomes in meiosis I, but genes in close physical proximity no longer segregate independently. The closer two genes are physically the more they tend to co-segregate. This tendency is reported empirically as a "distance" in centiMorgans and is related to physical distance in base pairs (kB or mB) but is not completely proportional to physical distance due to the existence of recombination "hot spots."
It's important to note that is accurately predicts genotypic ratios, but not necessarily phenotype. Phenotypes can be less than 100% penetrant, can cause embryonic lethal, epistasis, etc. Such that the observed phenotypic ratio does not match the predicted ratio. (For example, if YY was known to be 100% embryonic lethality, live births -> observed phenotypes instead be expected at 1/3 of each of the remaining genotypes. If Y was instead phenotypically dominant (one copy of Y determines phenotype), then 75% of children would be expected to be phenotypically Y (genotypically, the Y phenotypic children would be expected to distribute evenly between YO, YY, BY).

The clearest example of a Mendelian exception (in my opinion) are lethal alleles.
In your example, let's say that the $YY$ phenotype causes a fatal phenotype in utero (in humans, Achondroplasia is fatal for homozygotes). Your Punnett square might instead look something like this:
$
\begin{equation}
\begin{matrix}
& O & Y \\
\ &\_ & \_ \\
Y& |YO& ☹ \\B &|BO & BY
\end{matrix}
\end{equation}
$
This would also change your observed population proportions, rather than seeing the typical ~25% (1:3 ratio) you'll start to see a ~33% (1:2 ratio) population segmentation, which is a good indication that something fishy is going on. This can happen with both dominant (Achondroplasia) and negative alleles (Hypophosphatasia). In the case of a dominant allele like Achondroplasia, heterozygotes show a phenotype (dwarfism) but only the homozygous genotype is immediately fatal.


text:
Could we slow down life?
As far as I know there is no absolute time measurement (one that would measure time in a non-environment-dependent fashion) in any life form. Only such time measurements exist, which are dependent upon cyclic changes like the strength of the sunlight, heat, amount of water, etc. (In case this assumption of mine is false, than please answer it in mind of life forms which in deed have only relative)
Theoretically, if we could change everything a given life form is dependent upon, could we increase it's entire lifespan?
For example if we were to put a plant inside a manually controllable environment and slow down the day/night cycle to it's third, maybe even decrease air pressure and the strength of gravity(thus eliminating any problem that might arise from the actual transport of water and the solution of organic matters produced in photosynthesizing cells), change (even though I'm not sure if this could be physically possible at all, but my whole question is theoretical, thus it should not cause a problem) the adhesion/cohesion as well (so the speed of transports in the cells would change accordingly) and change other, (for me) unthinkable aspects that, for example, regulates the time between cell divisions, would it live for longer?
Even if we could not change every aspect that regulates a given life form's working, changing many could we (although this time not linearly) increase it's actual lifespan?

I find this too broad, speculative and opinion-based to be suitable for the SE format. You mention a huge number of processes, which will also interact with eachother.

I work in a fly lab, flies kept at 18 degress live longer than those at 25 degrees... though I agree with fileunderwater that this is too broad

I voted to close this question. I think it holds great potential, it just needs some tinkering and especially a narrowing down of the variables as well as species. I think many non-complex life forms adapt to environmental factors by going into some kind of low-metabolic state- a bacterial spore for example. This is not what you are after. Perhaps focus on humans and specify some parameters of interest. As of now it only generates answers that are commented upon with "yes, but no... I want to know this..." Such comments on answers identify it as a poorly defined question.

Short answer: Changing something (instead of everything) yes.
There are several studies on the impact of environmental factors on life span.
Of course it depends from organism to organism. Diet restriction for example has been shown to extend life span of worms and mice. Temperature is also working well, at least with microorganisms, the metabolism of E.coli for example (that usually grows at 37 Celsius) can be greatly slowed down at lower temperatures. Also, there are enzymes involved in the "ageing pathway" some of these enzymes can be promoted or repressed by small molecules, like resveratrol does, and as result you get some increment in life span. The opposite is also true, you can accelerate ageing with external factors. For plants works as well, changing the environment you can definitely have an effect on the life span and the overall metabolism rate, indeed tricking the light cycle is a very well known method to induce flowering for example.
Here some interesting links if you wanna dig more into this topic.
http://web.mit.edu/biology/guarente/
http://genetics.med.harvard.edu/sinclair/
http://www.ted.com/talks/cynthia_kenyon_experiments_that_hint_of_longer_lives?language=en
http://jxb.oxfordjournals.org/content/58/12/3099.full

But these are only defensive reactions to the environment. What I would like to know is how would changing many (as everything is impossible) aspects modify the life span of our average life form.

I don't get what do you mean for "defensive reactions"... The point is that organisms respond to external stimuli and that there is data pointing out that also life span can be influenced by such a stimuli. Isn't that you were looking for? I cannot really answer to "how would changing many (as everything is impossible) aspects modify the life span of our average life form" because is too vague, it depends from the organism and many other factors so there is no simple protocol for that. Have you check the links I posted? The last one is about slowing down plants growth with light.

First, I find this too broad, speculative and opinion-based to be suitable for the SE format. You mention a huge number of processes, which will also interact with eachother.
However, taking a general view, life span and generation time can definitely be increased. Changes in temperature and nutrition will often change the metabolic rates and growth rate of organisms, but the actual effect will depend on which organism you are looking at. For instance, the length of the larval stage of many longhorn beetles can increase by several years in colder climates or site conditions, under shorter growing seasons and/or poor wood substrates, compared to ideal conditions or warmer microclimates. The mechanism here is often lower activity levels or lower nutrient contents, leading to lower growth rates, which means that it will take more time before the larvae reaches maturity. This means that individuals of the same species (also the same genotype) may have a life span of 6 years in one location and 2 ys in another location. This is just a single example, and lots of similar processes can also be found in other organism groups, especially considering the large number of factors that you mention in your question.
References:

Bilý, S. & Mehl, O. 1989. Longhorn Beetles (Coleoptera, Cerambycidae) of Fennoscandia and Denmark. Fauna Ent. Scand. Vol. 22: 47–48.

Cherepanov, A.I. 1990. Cerambycidae of Northern Asia. Leiden, The Netherlands: E.J. Brill Publishing Company.

Quite some experiments like this have been done with C.elegans, also.

That's not actually the same thing I'm interested in. In this case, the given specie is genetically coded to work like that. I would like to know whether this thing works on species which are not supposed to live longer than they do now.

@FloriOn And how are you actually going to determine that? You cannot separate the genetical background of a species and its reaction norms from the equation. If you do, this is pure science fiction and answers will only be based on speculations. Also, how do you determine how long a species is "supposed to live", and under what conditions?


text:
How stable is linear DNA transfected in eukaryotic cells?
I would like to know, with references from the literature, what is the half life of a linear dsDNA transfected in a mammalian cells.
For example, if I transfect human cells with a PCR product (500-2000 bp), that does not contain any replication or transcription signal, how fast will it be degraded by the cell (hours, days, weeks...)? Is there any difference in the half life if the DNA is in the cytosol or in the nucleus?

I would assume that it won't be degraded but will be just diluted out.

I am looking around, I cannot find a clear answer. I would expect foreign DNA to be actively digested by some enzyme rather than having it flowing around...

I don't know about linear DNA, but plasmid DNA is often detectable in cells after they stop producing detectable amounts of protein. They tend to get transcriptionally silenced, but aren't degraded as quickly. CpG methylation probably affects half-life as well, as normal PCR product DNA is not methylated, and normal eukaryote DNA is methylated.

I am specifically looking for more info about linear DNA especially PCR products. Thanks for your comment, I will search about the effects of CpG methylation as well.

Why do you want to know about linear DNA and PCR products rather than plasmids? Have you tried any literature searches so far?

I am inducing homologous recombination in cells and I am using PCR products as donor templates, but (without getting into details) I need to be sure that the donor template is not in the cells anymore if not integrated. I have looked around but I could not find any paper with clear data. To detect the recombination event I want to amplify back the donor templates from my pool of cells. Now, if the linear DNA is still around I cannot be sure if I am amplifying that one or the integrated one.


text:
Anopheles arabiensis lifespan and sporogony duration
What is the longest observed lifespan of a mosquito, especially of the species Anopheles arabiensis? How long does it take for Plasmodium parasites to develop and move into the salivary glands of these mosquitoes?
I need this information to calibrate my model on malaria transmission.

What is the longest observed lifespan of a mosquito, especially of the species Anopheles arabiensis?
Mean lifespan calculations for Anopheles arabiensis range from 14 days (Karoki, 2013)* to 21 days (Yamada et al. 2014)**
*This Masters thesis tests efficacy of different drugs against An. arabiensis, 14 days is the mean control lifespan.
**These An. arabiensis are of a specific strain but no indication is given that the life span is different than normal An. arabiensis.
The CDC Anopheles mosquito page is another good source for information on Anopheles life spans:

The adult females can live up to a month (or more in captivity) but most probably do not live more than 1-2 weeks in nature.

How long does it take for Plasmodium parasites to develop and move into the salivary glands of these mosquitoes?
US National Institutes of Health:

Growth and division of each oocyst produces thousands of active haploid forms called sporozoites. After 8-15 days, the oocyst bursts, releasing sporozoites into the body cavity of the mosquito, from which they travel to and invade the mosquito salivary glands.

United States Air Force (USAF):

The length of the developmental stage in the mosquito not only depends on the Plasmodium species but also the mosquito host and the ambient temperature.  This may range from eight days in Plasmodium vivax to as long as 30 days in Plasmodium malariae.

Wikipedia (Plasmodium falciparum) :

Over the period of a 1–3 weeks, the oocyst grows to a size of tens to hundreds of micrometres... The sporozoites then migrate to the salivary glands and complete their differentiation. Once mature, the sporozoites can proceed to infect a human host during a subsequent mosquito bite.

US Center for Disease Control:

After 10-18 days, the parasites are found (as "sporozoites") in the mosquito's salivary glands. When the Anopheles mosquito takes a blood meal on another human, the sporozoites are injected with the mosquito's saliva and start another human infection when they parasitize the liver cells.

Overall, it depends who you ask, but especially on the species of Plasmodium you're working with. I'd look for specific papers on the development cycle you're modeling and run with it.


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Normal death experience
Consider a natural cause of death (no car accidents etc) -
Is it true that death is generally preceded by suffering? In other words, are we destined to experience the most severe suffering we could not ever imagine, that will ultimately end with death?
If this is true, is it true for all living things?

I'm voting to close this question as off-topic because it about philosophical musings on death and not biology.

@terdon in my mind this question fits perfectly, since it is asking about workings of the body and its lifecycle. There are similar questions already, like: http://biology.stackexchange.com/questions/14873/death-by-exsanguination-not-painful which is accepted ok.

That is a very different question. It asks whether a specific cause of death is painful, citing a scientific paper that claims it is not. You are asking whether we can say that in general, death is preceded by suffering. That is really not a good question for the site as it has nothing to do with biology. There are several hundred thousand ways to die. Obviously some will be painful and some will not. I don't see what we can add to that.

just a point, I'm going to suggest that "death with a severe blood-loss" is quite painful, no matter how quickly it occurs (given realistic possible bounds of rate of blood loss).

I edited the question by stripping it from its fluff. It seems more like a thought, not a biological question.

@AliceD thank you! :) I really like your edit, you just cut it to the point, this is much better!

No worries, my pleasure :) In this form it may fuel the discussion better as folks are more likely to read a short question than a long one.

No and no.
I'm not sure what is a "natural cause" in this context, but if it's cardiac arrest caused by age-related dystrophy of the cardiac muscles, then no, there is no suffering, at least not universally: Since age-related dystrophy hits all parts of the body, it's likely preceded by increasing amounts of bed rest, leading to quietly drifting off into the great sleep.
Of course, if you add on other natural causes like age-related diseases or being eaten by predators, the suffering can be great indeed, or not: A tiger will sneak up on you and crush your skull without you ever knowing what happened.
Adding on further causes still, like dehydration or hunger, and the suffering is back.
But is suffering a universal fixture of death? Emphatically no.
As for the "all living things" part of the question, the answer isn't just "no"; it's "that's nonsensical".
By individual count, practically no life is complex enough for suffering to be a relevant concept.
I don't have an exact number for you, because how would I get one, but at a rough estimate, bacteria, algae and archea constitute 100% of all individual life forms by count, and suffering is not a concept that makes sense for them.
If we ignore simple life, even among complex life there is so much variety of capabilities that basically nothing universal exists.

I think this answer is low quality as it stands so -1, it is just opinions. It would be very useful to get some science in to it.


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Is it possible that the DNA of an individual changes significantly over a period?
Is it possible that the DNA of an individual changes significantly over a period ?

What do you mean by "significantly"?

Not that significant that changes your identity, but that significant that may change your life.


text:
How to estimate a genome's size?
The genome size of human is 3.000.000.000 bp and for Arabidopsis it is 255.000.000 bp. I know these numbers because their genomes have been published. Which methods are used by scientists to estimate the genome size before they sequence that genome?

A rough estimate can be given using gel/electrophoresis on different chromosomes.

Can U explain more or insert a protocol link, please?

More details and links may help you get better answers.

This is rather broad as there are many ways to do it. I'd speculate that reassociation kinetics was one of the first methods used.

this link from NAR is good but I am looking for an up to date review. http://nar.oxfordjournals.org/content/31/10/e56.full

Gel electrophoresis is a basic lab method to get size info about nucleotide fragments, although one might need to chop up larger DNA to be able to apply this method. The wikipedia page covers the topic well, thus I'd suggest reading it. I'll just give a short outline:

Nucleotide fragments are loaded into a gel (agarose or acrylamide).
The gel is put into a static electric field
Nucleotide fragment move to the positive end, because they have negative charge
larger fragments migrate slower than smaller fragments
standardized DNA ladder can be used to get approx size.

UV fluorescent dye is used to stain the fragments.
Another way, is to check closely related species. Among closely related species it is a fair assumption that they have similar genome size. You can also hybridize the unknown DNA to a DNA of such close relative to see how much of them are similar and you can also make estimates based on the size of the hybridized regions.

Thank you. even I think both methods are not sensitive enough

I find this link: http://nar.oxfordjournals.org/content/31/10/e56.full But I think there most be some better and easier ways.

Well, I just gave some examples, there are many methods if you look around :) Without knowing how much knowledge do you already have, I've tried to give the simplest examples and explanation.

General agarose gel electrophoresis for DNA can not tell chromosome length because it is too big to run. It is tough to run DNA having length more than 100kbp, which is too short to estimate the length of chromosomes. Then how can you tell the chromosome length?

Another way is to digest the DNA and measure the total nucleotide content. I think that's how earlier experiments were done.

In the absence of molecular sequencing data the most accurate estimates are based on reassociation kinetics, more commonly known as Cot curves. Here is a classic paper from 1974 that describes the basic approach. While pulsed field electrophoresis can be used to resolve the chromosomes of species with relatively short chromosomes (like baker's yeast), there are really no suitable size markers that you could use to construct a standard curve for size estimation. C. elegans has six chromosomes, but they are all fairly close to each other in length, and the genome size of 100 Mb is the same as a single long human chromosome.

I guess you could estimate the length various ways. Pulse field electrophoresis could show DNA length, but you need a standard.
When you combine Karyogram and FISH, you would could make a map. By genetical approaches, you could estimate distance on the map by centimorgan. Then you could know how many centimorgan chromosomes are. One centimorgan would be 1 million base pairs.
Oh, I forgot the simplest way. For example, take 1 million cells and estimate how many grams of DNA there.

" One centimorgan would be 1 million base pairs." That is false. Centimorgan is based on recombination frequency and can be very very variable between species (your info is only true for humans at best). It is not an actual distance between genes.

@canadianer I know, my last comment became obsolete after the edit...still that is a very rough estimate in my opinion.

I was not able to tell you I edited. About centimorgan, you can not apply human results to others, but you can apply the methods as they do with human chromosome. And DNA amounts would be a very rough estimation , but I do not know how exactly MySky want to estimate. Rough estimations are still estimations.


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Math behind the Genetic Relationship Matrix

The genetic relationship matrix (GRM) can estimate the genetic relationship between two individuals ($j$ and $k$) over $m$ SNPs and $i$ representing a specific SNP. What I don't understand from their equation is why we divide our summation by $m$ (the number of SNPs). $x_{ij}$ is the number of copies of the minor allele for the $j$-th individual in SNP $i$. $p_i$ is the frequency of the minor allele for SNP $i$.

I do not know anything about this GRM but it seems to me it is divided by m to represent the average relationship over all (m) SNPs.

I am not familiar with it either, sources would be very useful. But, this may answer your question, if it does let me know and I will post it as an answer... Summing over $m$ SNPs would give a result for a pair of individuals. But if you want a result which is comparable to other GRM's then you need an average which accounts for the number of SNPs measured, hence $1/m$ times the summation. Otherwise you two GRMs could have different scores purely because of the number of SNPs included.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3014363/   This is a link to the paper I am studying hope it helps fill in any missing information you need.

did my comment answer your question (does it make sense?) 2) could you also edit the question to include the article link and explain what each term is e.g. $m$ denotes the number of loci, $i$ is ... $j$ is ... $k$ is.. $x$ is... and $p$ is... The question would be most valuable if it is able to stand alone (not require going to external sites/papers for definitions)

This expression is a mean
$$\frac{1}{m}\sum_{i=1}^m ...$$
($m$ is the number of SNPs) of the ratio
$$\frac{numerator}{denominator}$$
where the numerator is a covariance
$$(a_i-C)(b_i-C)$$
and the denominator is the expected heterozygosity (it is also the variance of binomial distribution with n=2)
$$2p_i(1-p_i)$$
Therefore, it represents how much do two individuals covary $(x_{ij})(x_{ik}-p_i)$ respectively to what is expected on average $2p_i(1-p_i)$ averaged over all SNPs $\frac{1}{m}\sum_{i=1}^m...$, where $m$ is the number of SNPs.
It is a relative measure (relative to the expected heterozygosity) of covariance between each individual (averaged over all SNPs).
Does it help?

Evaluating it this way gives us the average correlation per SNP between two individuals which considering the amount of SNPs it will be a very small value and considering the the correlation will be between -1 and 1 i dont see the intuition behind dividing by the number of SNPs (m). Also does anyone know other methods of estimating the genetic relationship between two individuals?

I am not sure what confuses you with this division by $m$. When you calculated your average grade at school, you added all the grades and divide the whole think by the number of grades. This is what this division is. You add all the relative covariances for each SNPs (relative the expected heterozygosity) and you divide the whole thing by the number of SNPs.

Does it make sense? You might just want to read about the arithmetic mean.

A little complex but I will try to get it. Thanks for sharing a detailed analysis.

$2p_i$ is the expectation of $SNP_i$:
$$E(SNP_i) = 0 \times (1-p_i)^2 + 1 \times 2p_i(1 - p_i) + 2 \times p_i^2 = 2 p_i$$
$(x_{ij} - 2p_i)(x_{ik} - 2p_i)$ measures how the two SNPs covary. I have no idea why they divide it by $2p_i(1 - p_i)$, but if you leave that one out, you have the plain definition of covariance.
Further readings:
https://en.wikipedia.org/wiki/Expected_value
https://en.wikipedia.org/wiki/Covariance

interesting... can you add a reference to link to your answer that others can read further for more information?

Though the question was posted a long ago, I feel that a clarification could be beneficial.
Heterozygosity / gene diversity
The factor in the denominator is twice the variance of the number of major alleles at site $i$, also known as heterozygosity or gene diversity:
$$
H_i = 2p_i(1-p_i).
$$
What might appear confusing here is the factor $1-p_i$ that is explicitly written instead of traditional $q_i=1-p_i$: $$H=2pq$$ (since the probabilities of minor and major alleles sum to $1$).
Covariance
In statistical terms this factor can be interpreted as twice the variance of the average number of major/minor alleles on the site, which is the motivation for including it in the denominator of the covariance function, as, e.g., when converting covariance to a correlation coefficient. It is necessary however to note that this inclusion can be done in different ways, depending on what statistical aspects one wants to emphasize.

In particular, the equation given in the question, taken from this paper (referenced in the comments), is the covariance of a standartized genotype matrix, defined as
$$
W_{ij} = \frac{x_{ij}-2p_i}{\sqrt{2p_i(1-p_i)}}.
$$
In other words the standartization is done prior to calculating the covariance
$$
cov_{jk} = \frac{1}{m}\sum_i W_{ij}W_{ik}.
$$

This is however different from a more traditional definition of Genetic relationship matrix, as in VanRaden's work, where such division is done after calculating the covariance:
$$
G_{jk} = \frac{\frac{1}{m}\sum_i(x_{ij}-2p_i)(x_{ik}-2p_i)}{\frac{1}{m}\sum_i 2p_i(1-p_i)}
=
\frac{\sum_i(x_{ij}-2p_i)(x_{ik}-2p_i)}{\sum_i 2p_i(1-p_i)}.
$$
Finally, as a word of caution, let me mention that $x_{ij}, x_{ik}$ in these expressions can take only values $0$ or $1$.

The matrix gives you an estimate of the average linear relationship between any two individuals genomes, it's essentially taking the average of the betas (like linear regression betas) across each locus. One of the formulas for 'beta' is covariance divided by the sample variance, which is exactly what is happening. Each locus beta predicts the state of a person's genome at that locus from another person's genome at the same locus. Taking the average of these betas across the entire genome gives you a coefficient that can be thought of as a measure of how well we can predict one person's genome from another.


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Why is human vision restricted to 400-700 nm?
Across the electromagnetic spectrum, 400-700 nm is a narrow spectrum of frequencies and focused in the region of short wavelengths. For example, radio waves cover a large range of frequencies unexploited by the visual system. So what biological reason is there that evolved us to use such a small frequency bandwidth for vision?

We can only answer "how" or "how come"? "Why" actually is quite speculative and philosophical. Why human are the way they are? Why didn't humans evolve to swim naturally or run fast (very favourable attributes)? We can just guess the "why". :)

Short answer
The visible spectrum has the highest energy in sunlight at the earth's surface, explaining the gross location of the visible spectrum in life on earth. The specific frequency range varies across species and can be explained by species-specific survival strategies.
Background
When you look at the solar light spectrum at the earth's surface the visible spectrum has the highest intensity (fig. 1).

Solar irradiation. Source: University of California.
So it makes sense to use the range of frequencies that is represented most in sunlight as a starting point.
Then the question becomes, why do humans utilize approximately 400 to 700 nm, and not infrared or UV? That can be explained because we do not need it. Our range has been hypothesized to be related to foraging behaviors and our visual system is particularly sensitive in the frequency range of the coloring of (ripe) fruits, which is thought to have been of great benefit to our hominid ancestors (Osorio & Vorobyev, 1996).
Why then do animals extend their vision into UV? Many fish, amphibian, reptilian, avian, and some mammalian species use UV vision. Many birds can identify UV-reflected nectar and berries, and UV-reflecting plumages in birds, and scales in fishes are used for recognition (Shi & Yokoyama, 2003). Moreover, some arthropod species are know to use UV vision to reduce light-reflection distortions under water, such as in the mantis shrimp that features 12 photoreceptor types (as opposed to four in humans) (Thoen et al., 2014).
Why then do animals extend their dynamic range into the infrared? A notable beneficial effect of perceiving infrared is the detection of body heat. The generation of heat is accompanied by the generation of infrared light. The detection of this emitted light is highly useful for nocturnal predators, like the rattle snake (Hartline & Newman, 1982).
References
- Hartline & Newman, Sci Am (1982); 246(3): 116-27
- Osorio & Vorobyev, Proc Roc Soc B (1996); 263(1370)
- Shi & Yokoyama, PNAS (2003); 100(142003): 8308-13
- Thoen et al., Science (2014); 343(6169): 411-3
Further Reading
1. Is our color vision calibrated to sky, vegetation, and blood?
2. Is there a physical reason for colors to be located in a very narrow band of the EM spectrum?

Not that you said it was, but I'm not sure if snakes detecting IR light can be classified as vision. Anyways, nice answer +1

@canadianer - I classify vision as light perception. People classified as having ultra-low vision (near-blindness) sometimes have not much more than bare light perception (light on or off).

It's largely a semantics issue I think and I don't really know why I even brought it up ;) A plant can perceive light, thought I wouldn't say it has vision.

@canadianer - plus I never said that snakes had IR vision in my answer in the first place lol. I used perception

Most of the light from the sun doesn't actually reach the earth's surface due to the atmosphere.

[source]
So the light reaching earth includes near-UV, visible, near-IR and a band of radio waves. Seeing any other part of the spectrum would be impossible since it doesn't reach earth.
You asked why we only see in the visible light range; this is due to evolution. Birds, among other animals, can see UV light. In fact, all vertebrates have the potential for near-UV vision. Humans, as vertebrates, also have UV-sensitive photoreceptors. However, our lens is opaque to UV light:

[from Clinical Ocular Anatomy and Physiology via this website]
Just speculating, it would seem that the ability to see near-UV is an ancestral condition which we lost at some point; either it provided no significant advantage (neutral regression) or there was some advantage provided by a UV-opaque lens, either directly (such as protection from UVB light) or indirectly (through pleiotropic antagonism).
On the other hand, human photoreceptors cannot detect IR light. Again, this is a product of evolution.  These researchers hypothesize that the longer the wavelength of light detected, the more noise is produced. This noise is due to activation of the pigment molecule by heat. Or, it could just be that never happened. An IR-sensitive photoreceptor might be possible, but evolution doesn't lead to perfect adaptation. In other words, there isn't necessarily a reason why.
As for radio waves, they are too low energy to interact appreciably with matter, at least as far as vision is concerned.

Most photoreceptors, the way they work, cannot absorb IR because IR is too low in energy to cause electronic transitions. Regarding false alarms; yes heat can generate false alarms but that doesn't mean noisy (in fact IR scatterance is much less. Rayleigh scattering reduces with wavelength). I would reason that diurnal habit and temperate habitat of humans does makes IR sensing not very useful.

While it is true humans do have some marginal sensitively to UV (basically spillover) we have no UV focused receptors like many other animals. this is true of Mammals in general so the group as a whole seems ot have have lost UV sensitivity. A major problem with infrared is water is not very transparent to infrared, and what are eyes made of. this is why pit vipers have open air filled pits for infrared detection.

Its not really
That is only the human visible spectrum.
Humans actually have a reduced spectrum compared to many animals. Mammals in particular have a reduced spectrum compared ot non-mammals. Reptiles and birds have 4 color sensitive cell types (cones) and can see into the ultraviolet. Many invertebrates can see an even wider spectrum. Mammals lost two of these cells. Modern mammals are descended from early mammals who were nocturnal Thus color vision was less useful. Primates evolved a third cone, (a mutant variant of one of the two they had before) Primates did this because many are frugivores and color is excellent for determining when fruit is ripe.

This is my speculation, but there are no or few organic chemicals which can absorb radio waves having longer wave lengths. Eyes sense lights by absorbing light with organic chemicals, but to sense longer wave length, eyes might need more sophisticated devices like tuners.
In addition, less than 100nm radio waves from the outer space are absorbed by the atmosphere, so even if eyes could sense such radio waves, you don't see any signals on the earth.

This answer holds great potential, especially the radio wave part. Elaborating on that may get you your deserved upvotes.

"Visible light" is the wavelength of the light that we can see, if human beings could see UV or IR, those wavelengths had been included in the "visible light" definition.
Now, our Sun is brightest in yellow-green light, which (you guess?) is right in the midle of the "visible light" spectrum. So the only remaining question is: "Why can we only see that short spectrum?" The answer is EVOLUTION.
The same reason that made us to have only 5 fingers in our hands, only 2 eyes and only two kidneys.
The bandwith of the "visible spectrum" is enough to make the human beings (as specie) survive.

Every question can be answered by 'this is EVOLUTION'. I do acknowledge the inherent problematic nature of the why questions, but they nevertheless form an interesting class of questions in the light of speciation. Further, the capitalization should be used with caution as it implies yelling at OP. It is a legitimate question.

it is also a bad answer using evolution, since there are some pretty solid evolutionary artifacts that make human vision very limited.

These wavelengths happen to satisfy two conditions.
First, shorter wavelength photons (EM radiation) tend to be dangerous for biology. Even UV light (<350nm) is already can damage DNA. That is due to the fact that bond energies in biological molecules tend to have values close to energy of short-wavelength EM radiation. These is why high-energy particles called ionizing radiation. For reference, see this paper. ionization energy for DNA estimated in 4-5eV range, which is 300-250nm.
Secondly, on low-energy hand of spectrum, water absorbs a lot of IR radiation:

So, as you can see, what we see aka visible spectrum is sitting nicely in valley of water absorption but does not extend to area of harsh UV light that will damage chemicals of your body.
Now, why is that so? Because atoms have these masses and electrons around them have these energies. So bonds and molecular interactions have these values.
(In radio range of frequencies you, opposite to UV, have not enough energy to elicit any significant molecular changes, which is why you can't perceive WiFi)

The reasoning that UV shouldn't be visible because it is dangerous makes no sense. Along that reasoning the visual system should be filtering out predators, guys with guns etc. as well. Moreover, there are classes of critters that sense UV and use it for meaningful purposes.

Essentially none of the UV light that reaches the surface is ionizing. Lower wavelength UVB light can damage DNA, but this is hitting our body and eye whether we can see it or not. About 95% of UV light that reaches the surface is non-damaging UVA.

@AliceD My reasoning is following: UV is dangerous hence it is/should be filtered before it reaches anything sensitive. Animals don't really need retinal cancer.

Reasoning is one thing, claiming it to be so is another, especially since many species actually use UV. Oxygen is highly toxic. Should we therefore neutralize it before we breath?


text:
Is Araucaria fruit toxic?
I've had an Araucaria tree in my garden for more than 30 years.
Today a fruit fell off the tree. It looks just like this one:

I want to know if it is toxic?
Can I eat it? If so, how?

A very simple Google search should have told you that the seeds are edible.

Araucaria araucana is an evergreen. The pictured "fruit" is actually more of a cone (which I don't think you'd want to eat). However, the seeds are edible, and look like this:

Let the cone dry and it should open up.


text:
Why are oceans carbon sinks?
Building on this question,
I understand pretty clearly why forests are carbon sinks (trees grow, and there is carbon stored in soil and biomass).
What about the oceans, though? Are underwater plants the real actors here?

https://en.wikipedia.org/wiki/Carbon_cycle#/media/File:Carbon_cycle.jpg
Look at the white number in parentheses labelled "deep ocean". Solubility is the biggest actor of them all

@Luigi You should make that an answer.

Check out the excellent Wikimedia picture of the carbon cycle:

All the numbers are in billions of tons of carbon: white = stored, yellow = natural flux, red = human contribution. Notice that the deep ocean stores much more accessible carbon than any other carbon cycle source, and is only surpassed by the lithosphere* in overall quantity of carbon stored on the planet. Some is stored by algae/sea plants, but the vast majority is stored as dissolved CO2.
*The lithosphere (crust and upper mantle) is not involved in the carbon cycle, and is therefore not shown in the above image.

The diagram in the answer by @Luigi does a great job describing how oceans operate as both short-term and long-term carbon sinks. Where phytoplankton can immediately uptake carbon and then upon their demise (as well as the demise of other marine organisms), the action of their sinking to the ocean floor transmits carbon to the deep ocean, where carbon is stored for decades to centuries (based on where in the ocean this occurs).
The second question you ask about underwater plants is especially interesting and an area of active research! For example, the Blue Carbon Initiative is trying to evaluate the global potential of "blue carbon ecosystems", that is coastal photosynthetic systems (i.e., Mangroves, Salt Marshes, and Seagrasses), to sequester carbon in their soils.
In addition to carbon seqeuestration, there is also the problem of ocean acidification, where the absorption of CO2 in seawater is making the ocean more acidic. Under those circumstances, both seagrasses and kelp forests are being considered as potential "ocean acidification refugia".
And, the state of California recently passed legislation to understand the role of eelgrass, a specific type of seagrass, in sequestering carbon and reducing the impacts of ocean acidification.


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Has anyone tried to prepare chemically competent Mycobacteria?
Bacterial species like E. coli are easy to transform using a variety of methods, including both chemical transformation and electroporation. Chemical transformation is especially nice to use as it can be done in high throughput. I'd like to start working with Mycobacterium smegmatis, though, and have only been able to find electroporation-based transformation methods like the one described here. Can chemically-competent mycobacteria be prepared? If so, are they just very inefficient? Is it worth testing some E. coli-specific methods with mycobacteria?

There was no link to the paper. So I added one.

Mycobacteria are very different from E. coli. I would be rather surprised if you could adapt the methods without a lot of customization. What's wrong with electroporation?


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Characters do not make the genus, but the genus gives the characters?
In his Origin of species, in the chapter entitled 'Mutual Affinities of Organic Beings: Morphology: Embryology: Rudimentary Organs', Darwin, speaking of the nature of classification systems of living organisms, writes:

Such expressions as that famous one of Linnaeus, and which we often meet with in a more or less concealed form, that the characters do not make the genus, but that the genus gives the characters, seem to imply that something more is included in our classification, than mere resemblance. I believe that something more is included; and that propinquity of descent, the only known cause of the similarity of organic beings, is the bond, hidden as it is by various degrees of modification, which is partially revealed to us by our classifications.

What does he mean by  "that the characters do not make the genus, but that the genus gives the characters"?

I cannot really know what Darwin intended to say but I guess this statement means that two distant species may look similar but they are actually evolutionarily distant.

It sounds like the intent of the phrase is to suggest that the presence of similar characteristics in two species do not imply that they are related, but that related species would be expected to share characteristics.
I.e. that similar characteristics do not imply relatedness, but relatedness implies similar characteristics. Genus -> Characteristics, rather than Characteristics -> Genus. These two possibilities are logically distinct.

@InactionPotential I think you can make an answer out of your comment.

I am doing research in marine benthic ecology and taxonomy. I think the above sentence denote that one species is originated from a single ancestor,but they have different characters for adaptation in a particular environment. that mean they have similarity in morphological characters,but genetically different.

It has been a long time since, I've read The Origin of Species, but it sounds like the intent of the phrase is to suggest that the presence of similar characteristics in two species do not imply that they are related, but that related species would be expected to share characteristics. I.e. that similar characteristics do not imply relatedness, but relatedness implies similar characteristics. Genus -> Characteristics, rather than Characteristics -> Genus. These two possibilities are logically distinct.
The assumption that Genus -> Characteristics segues into the key concept of his theory of evolution, that related species (a genus) arise from the descent with modification of an shared ancestral population. Remember that Darwin wrote long before we understand the role of DNA as the carrier of genetic information. He knew nothing about the physical substance or the mechanism of transmission that passed characteristics to offspring, but through his observations built a strong case that such a substance exists and that gradual changes in this substance occur over time in a population. He later posits that natural selection leads to the accumulation subsets of descendants with modifications that are advantageous in their environment. Thus the species within a genus could arise, their similarities the result of their shared ancestry, their differences that result of descent with modification and selection.

I'm not sure when the concept first arose but I would assume it was after Darwin had come up with the Theory of Evolution.  The concept I am talking about is "Convergent Evolution" which in essence explains "characteristics do not make the genus".
Convergent Evolution is the concept that two completely different organisms, given the same selection pressures, may, independent evolve to exhibit similar characteristics.  If one was to assume "characteristics makes the genus" one would think these two must be genetically similar when they are not.
One example I found illustrated from link is:

If you look at the external characteristics, we would say the 3 must be closely related - tail fin, dorsal fin, pectoral fins all pretty much the same.  But looking at the bones and others we know that they each evolved from very different species.  Not only are they from different genus, their divergence goes all the way up to the class level (Kingdom, Phylum, Class, Order, Genus Species).
Why then do they all look similar?  The reason is they all have to deal with the common selection pressure of water.  Living in water, moving efficiently in water to be able to catch prey and evade predators.  Separately, they all gradually evolved fins because the ones that did not, were out competed by there "better finned" peers.  The better finned shark ancestor out bred the poorer finned sharks, the better finned porpoise ancestor out bred the poorer finned porpoise.  The ichthyosaur too except it finally did not evolve sufficiently and became extinct.


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What is this droplet of liquid that comes out of a mosquito?
I have been looking at pictures of different species of mosquito and several times I came across pictures where the mosquito seems to be secreting some kind of fluid.
In the pictures one can clearly see that the mosquito both secretes transparent fluid and blood.

What kind of fluid is the transparent stuff? Could it be plasma from the host's blood?
Why does the mosquito do it?

Short answer
Excretion of blood and urine may prevent overheating by reducing body temperature through evaporative coolong (akin to perspiration). Excretion of blood and urine also concentrates the ingested blood.
Background
Female Anopheles mosquitoes seek blood for nutrients necessary to egg production. The cold-blooded insects may excrete some freshly ingested blood as a way to avoid overheating when consuming blood as warm as 104 degrees Fahrenheit (40°C). It is thought that excretion of a droplet of fluid aids in evaporative cooling, similar to perspiration in humans, to reduce the animal's temperature. The excretion of urine may serve a similar purpose, namely avoiding overheating during blood ingestion. By keeping the urine or blood droplet attached to the abdomen, excessive heat can be eliminated (Lahonde & Lazarri, 2012).
In the malaria mosquito (Anopheles stephens) the excretion of fluids has been investigated in detail. Females ingest blood meals that are equivalent to more than twice their unfed body mass. Engorged animals can fly only with great difficulty, making them more prone to predation. The blood meal serves primarily as a source of protein for egg development, but it also contains considerable amounts of unwanted salts and water that threaten haemolymph homeostasis. To counter this, a rapid natriuresis and diuresis commences even before the blood meal is completed, and ∼40% of the imbibed plasma volume and salt are voided within 1–2 h of feeding (Coast et al., 2005).
References
- Coast et al. Exp Biol (2005); 208: 3281-91
- Lahonde & Lazarri, Curr Biol (2012); 22: 40–5
Further readings
- Do mosquitoes urinate on you when they bite you?

I used to think that they do that to concentrate the nutrients from the blood. I have also seen this in Anopheles only. Do other mosquitos not show this behaviour?


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What comes out of this bump in this vegetable?
I live in Denmark, Europe and I have in my garden this gigantic vegetable.
It has a big bump on the top and i was wondering about what comes out of it?

Where is the plant located?

I just edited my question and put in it's location which is Denmark, Europe.

@WYSIWYG. I accidentally used the danish word for the vegetable. I do not know the english name for it so i just changed it to vegetable.

I think your vegetable is a leek, or a closely related allium. If this is the case, you are seeing its flowerbud. Congratulations, it will become quite pretty in some days, I know people who use leeks as decoration plants instead of vegetables.

Thank you very much for enlightening me. Im carefully following the process of this plant. Nature is amazing!

@Lanka did you ever get a photo of the plant in flower? It would be neat to see that added as an update to your question.

Hi:) I never got another pic from it and now I moved to Greenland so I dont have the garden anymore. Hopefully Ill get one when I move back to Denmark again. Thanks for asking btw.


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Does level of bats activity differs from day to day?
Say we measure bats activity as number of passes through given area. Can it differ significantly depending from day to day or it stays on average roughly the same? I am wondering whether the following might have an effect:

Weather conditions (wind or rain). I do not mean here heavy conditions (strong wind or rain), those understandably will affect bats eagerness to fly
Moon cycle
Mating
For insect-easting bats: the prey not being active every night

I would welcome some good reading on the subject.
My question stems from the following problem. Say I have one detector and want to measure activity in three locations. If I rotate it between them, will I get unbiased result?


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How can I keep pond water "alive"?
I've been preparing wet slides for my kids to look at from pond water. I have a mason jar of pond water. What can I do to keep the microbes in the jar alive going forward so that we can look at it any time we want without having to go back to get more pond water.
I remember we did something like this in 7th grade biology, it seems like we put in sugar, or oatmeal, or something. I can't quite remember that though, it's been over 30 years. Thanks!

Thanks for the comments. The pond water I get keeps for a couple of days easily. I can always get more at the pond.
If I want amoebas, I go near dark and get them at the bottom of the pond. If I just want paramecia and other critters, I grab some scum and fill the rest of the jar up with water.
The paramecia water I give moderate sunlight. The amoeba sample I keep in the dark. And I just pitch it after a few days. No Legionella for my family, please and thank you.

How long do you want to keep it. I think the water will have a sustainable microecosystem if it is kept open.

Is there anything in particular in the pond water you want to look at specifically? Do you want to look at microbes, or more tardigrades and daphnia, etc? You could always fix the slides. Sunshine should keep it going on a microscale, but stuff like brine shrimp or around that size require snacks.

I'd like to keep it alive indefinitely. As far as tardigrades/daphnia/microbes, yes, yes, and yes!

And how open would it need to be? I have the mason lid sealed on it, but with a bunch of holes in the lid.

You want to keep live water indefinitely? I don't know if you'll be able to tell if it gets colonized by Legionella.

Yikes. Maybe I'll just go back to the well then. Or the pond, in this case.

The answer will be to replicate the conditions as best possible, given the biotic and abiotic variables it could be very difficult to answer this.

"No Legionella for my family, please and thank you.".

"No Legionella for my family, please and thank you.". Legionella pneumophila ocurs in oxygen rich, fresh, standing water, maintained at temperatures between 30 and 50°C (86 - 122°F). Infection occurs trough the air, by inhaling water droplets from aerosols (drinking Legionella containing water is harmless). Unlikely to become infected by a jar of pond water, I would say... There's nothing wrong with being cautious, but there's no need to exaggerate...


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If dinosaurs could have feathers, would they still be reptiles?
I just finished watching a video where it was mentioned that nowadays birds are dinosaurs and non-avians dinosaurs could have feathers.
I confirmed this from wikipedia:

Birds are highly advanced theropod dinosaurs, characterised
  by feathers, a beak with no teeth, the laying of hard-shelled eggs, a
  high metabolic rate, a four-chambered heart, and a lightweight but
  strong skeleton.

And:

Direct fossil evidence of feathers or feather-like structures has
  been discovered in a diverse array of species in many non-avian
  dinosaur groups, both among saurischians and ornithischians.

And this family tree of reptiles mentions:

Archosauriformes (crocodiles, birds, dinosaurs and extinct relatives)

And later in the Mesozoic era:

The dinosaurs also developed smaller forms, including the feather-bearing smaller theropods.

So, were these non-avian dinosaurs with feathers actually reptiles?

No.  Dinosaurs were never reptiles, they evolved from reptiles.  Nor are birds dinosaurs, they likewise evolved from dinosaurs, just as mammals evolved from reptiles, and all of those evolved from fish.  It all depends on which branch of the tree you look at, and what forks you decide are important.

@jamesqf So in your opinion Wikipedia is wrong (and also the scientists who accepted the possibility that birds are dinosaurs). How would you classify these particular dinosaurs? Can you detail in an answer, possibly with references (through cladistics)?

@jamessqf Birds are reptiles as are dinosaurs.  http://biology.stackexchange.com/questions/17546/were-there-any-flying-dinosaurs

@Kmm thanks for the link! Your answer provides a good explanation :)

"Reptile" is not a clade. It is a paraphyletic group.

@Armfoot: Yes, Wikipedia is sometimes wrong (and not just about this).  Likewise, the scientists who jumped on the "birds are dinosaurs" bandwagon for the sake of publicity are wrong.  As Remi.b says, it's to some extent a question of semantics, but the principle is that we group things that have similar characteristics under names.  Birds have characteristics that dinosaurs don't (adaptations for flight), just as mammals have characteristics (hair, milk glands) that reptiles don't, so we call them by different names.

@kmm birds are not reptiles. Sauropsids other than birds are generally considered as reptiles.

@WYSIWYG No, birds are within the clade Reptilia, and thus are reptiles.

@kmm birds are specifically excluded from reptilia afaik. If they were included reptilia would have been monophyletic. Sauropsida is the clade that contains both reptiles and birds

@kmm: But as a reductio ad absurdum, would not cladistics define all of these - dinosaurs, birds, reptiles, mammals, &c - as just members of the fish clade?

@jamesqf Actually, yes. Successively broader clades are Sauropsida, Amniota, Tetrapoda, Rhipidistia, Sarcopyerygii, Osteichthyes, Ganthostoma, and Chordata to name a few. The closest thing to a "fish" clade is Osteichthyes. Birds only fall within Sauropsida, as they do their more inclusive clades Dinosauria and Reptilia).

reptiles and dinosaurs and birds are a bit like sharks, fish and bony fish in terms of family groupings.

Taxonomy is dynamic, and conforms to new findings. That birds are nested inside therapod dinosaurs renders Dinosauria paraphyletic. The way you fix this error is to include birds as dinosaurs. Same with reptiles. Birds are reptiles or the taxon "Reptilia" needs to be eliminated. Both are solutions.

Source of information on Biology.SE
This answer offers an introduction to phylogeny on the case study of dinosaurs and birds. If you are not at ease with the concept of monophyletic group, you should definitely have started with this introduction.
This post is somewhat related.
Origin of your misunderstanding
The question is all about nomenclature (and a little bit of semantics). One can call reptiles whatever (s)he wants. The question is what do we define as being a reptile? And the answer is that there are two possible definitions, a common "bad" definition (Definition 1) and a phylogenetic-based "good" definition (definition 2). I think your confusion comes from the use of the same term to mean two different (but related) things.
Definition 1: reptiles
In general, when people talk about reptiles, they talk about turtles, Rhynchocephalia, Squamata and Crocodilia. In this sense, the term reptile is NOT a monophyletic group. In other words, all species being called reptiles (according to this definition) do not share a common ancestor who has no other descendants than the species being called reptiles.
Definition 2: Reptilia
There is a defined monophyletic group called Reptilia. Reptilia is a group that contains all Amniota except the Synapsida (mammals and their extinct close relatives). In other words, Reptilia contains all generally called reptiles (as defined above) and all birds as well as all extinct species that are descendent from this same common ancestor.
Exploring the tree of life by yourself
You will find the tree of life on tolweb.org or on onezoom.org (see The best free and most up to date phylogenetic tree on the internet? for more info).
Using tolweb.org: here are the roots of the tree of the Amniota. And you will probably want to search for the Dinosauria (there) and see how closely related they are to the birds but not so much to the turtles.
Addressing your question directly

If dinosaurs could have feathers, would they still be reptiles?

If by reptiles you mean Reptilia, then whether a given dinosaur has feathers, endothermy, or an exoskeleton (!) doesn't change anything to the fact that this dinosaur is a reptile.
If by reptiles you mean turtles, Rhynchocephalia, Squamata and Crocodilia, then whether a given dinosaur has feathers or not doesn't change anything to the fact that this dinosaur is NOT a reptile!
Known Dinosaurs with feathers?
Given that birds are the only animals that have feathers and that birds are dinosaurs, we don't know of any species that has feathers and that is not a dinosaur! However, when we think of dinosaurs, we usually don't think about a pigeon.
Of course, the Archaeopteryx had feathers too. Archaeopteryx is an avian (bird-like) dinosaur.

But even non-avian dinosaurs such as Velociraptor probably had feathers as well. More info about how closely related is Velociraptor to the birds (Aves) there on tolweb.org. You probably remember the so-called Velociraptor from Jurassic Park movie (on the left) but here is what a Velociraptor probably really looked like (on the right).

The "velociraptors" from Jurassic park actually look more like a large Deinonychus without feathers than a Velociraptor (Thank you @Gaurav in the comments). I suspect because they chose Velociraptor because Deinonychus is much harder to pronounce and way less sexy sounding. Like this, tThe movie Jurassic Park deceived an entire generation about what a Velociraptor is! More information about what the species of Dinosaurs the Jurassic Park movie features in the fun video (in French) Le Vélociraptor from Max Bird.
You might want to have a look at the post Were there any flying dinosaurs? that is very related.
At least, all these big and extinct things with scales are dinosaurs, right?
Well.... not exactly. There are species that many would call dinosaurs that are typically not considered as dinosaurs. Have a look at the MinuteEarth video called "What makes a dinosaur?" for more information in this regard.
Fun and instructive videos

Les dinosaures ont disparu ? from Max Bird and Jamy (in french)

Le Vélociraptor from Max Bird (in French)

What makes a dinosaur? from MinuteEarth

What a great answer!

I believe the "velociraptors" from Jurassic Park are really Deinonychus, not Velociraptor (the dinosaur on the right). Great point about them having feathers, though!

You say "Some dinosaurs actually had feathers". I'd go further and say that every taxon that we know of that has or had feathers is a dinosaur.

I meant dinosaur in the common sense and not Dinosauria. In the core of the paragraph I talk about non-avian dinosaur to make the distinction. I'' edit to really clarify my point and to add the idea that we don't know any animal species that has feather but is not a dinosaur Thnks

The first ever feathered dinosaur tail preserved in amber was found fairly recently. See here for the story!!

Feathers are pretty widespread in therapods, therizinosaurids and tyrannosaurids are known ot have feathers. Even ornithischians dinosaurs may have had feathers.

There have been some good answers here, but I think some information could be added.
Willi Hennig introduced modern phylogenetic systematics, which is sometimes conflicting with traditional taxonomy.
Hennig's important insight was that one should only use synapomorphies (shared derived traits) as the evidence for identifying relative recency of common ancestry within and among groups.
However, many groups, reptiles, fish, invertebrates, etc., are based on symplesiomorphies (shared ancestral traits).
The original question posted above can be addressed with the stem-crown group concept.
Considering the relationship of fossil taxa with living ones, we can ask the following question: do all fossil taxa fit into living clades?
Crocodiles and birds are an excellent example to address this question:
From a cladistic perspective, members of each of the two clades have three types of traits: symplesiomorphies (shared ancestral), synapomorphies (shared derived), and autapomorphies (unique traits).
Where would these traits appear on a phylogenetic tree?
Let us have a look at a bird with a very distinctive bill, the Shoebill (Wikipedia):

This can be considered a unique trait, thus an autapomorphy.
The feathers of the shoebill is a trait it shares with other birds, thus a synapomorphy.
While the shoebill's legs is a trait shared with crocodiles (the sister clade of birds) and many other vertebrates and therefore is a symplesiomorphy.
Thus, autapomorphies appear within the clade, synapomorphies are traits primitively shared by all the members of the clade of interest, but not by members of its sister clade. They are shared but relatively new traits: these traits must have appeared further down the clade, but not below the split between the two sister clades.
Symplesiomorphies are traits shared by the sister clade, or even more distant clades. These traits must have appeared deeper down the tree.
Another question: what sort of organism was the last common ancestor of birds and crocodiles? Was it a bird, a crocodile, or neither? What traits would it have?
By definition of our question, these two groups (crocodiles and birds) are both monophyletic, therefore, one did not give rise to the other. It did not have any of the synapomorphies or autapomorphies in either clade, only their shared symplesiomorphies, and therefore did not lie in either modern clade.
By definition, the organisms that make up the lineage of birds, appearing after the split between the clades of crocodiles and birds, but apart from living birds, must be extinct. We call this the stem group of birds.
The last common ancestor of all living birds, plus all its descendants make up the crown-group of birds. The total group of birds is the crown group and stem group together.
Stem and crown groups are hierarchical, and some crown group taxa have gone extinct, for example, the dodo. The dodo, therefore, belongs in the stem group of pigeons and doves.
By definition, all stem groups are paraphyletic, as they give rise to their crown group. All fossils fall into one or another stem group.
The original question can thus be answered appropriately: dinosaurs are stem-birds and belong in the total group of birds.


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Cell Line With DNMT3a Mutation
I am looking for a cell line (preferably hematopoietic) that has an inactivating DNMT3a mutation. I have checked the Cancer Cell Line Encyclopedia but of all the hematopoietic cell lines I know I can't find any with a DNMT3a mutation.
It would be great if somebody knows of a cell line with a DNMT3a mutation, but it would also be helpful if somebody knows of a database that I could use to find this information in the future. Thanks.

Why not just induce one? There are quite easy-to-use CRISPR/Cas kits available nowadays.

While that would work, it would be much cheaper and easier to identify which of the cell lines at my disposal contain such a mutation.

All I'm saying is if you can't find a cell line that meets your needs, it would be quite cost-effective to generate one on your own. There are some extra costs outside of the kit, but this Life Technologies kit is only US$514, whereas purchasing a new cell line from ATCC not in your collection may cost an approximately equivalent amount, depending on the line, what kind of institution you're at, etc. Worth thinking about.

For CRISPR-Cas you don't even need the kit. Just have a plasmid for containing the Cas9 gene from where you can IVT the Cas9 mRNA. Co-transfect this with the donor plasmid.

Or for only $60 from AddGene


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Leptin and fat mass?
I am interested in the relationship between blood leptin concentration and fat mass.  It is well known that as fat mass increases, leptin increases.
Have there been studies that look into whether the relationship is linear, or perhaps as fat mass increases, the level of leptin increases at a decreasing rate (e.g. logarithmic relationship) or an increasing rate (exponential) etc.
Furthermore, for two individuals with identical fat mass, is there a high variance of leptin concentration?

The obese gene (OB gene) secretes a protein that functions in the signaling pathway of adipose tissue and adipocytes (fat cells) produce the hormone leptin (reference).

When the amount of fat in the body increases, the amount of leptin
  released into the blood also increases and signals to the brain that
  the body has enough to eat (reference). Inversely, studies in rodents suggest
  that a reduction in leptin level during weight loss signals to the brain
  to increase feeding and decrease energy expenditure (reference).

Other molecules have a role to play in the ratio of BMI to leptin like the ghrelin hormone (reference). The genetic and environmental factors other than overall adiposity may also regulate leptin concentrations (reference) which is why individuals with the same weight may have different leptin concentrations.
A study has reported finding a strong exponential relationship for leptin levels with body mass index (BMI) (reference). Hope that answers both your questions.

The over-simplified answer to the question: "Have studies examined the linearity or non-linearity of leptin concentrations in the blood and body fat?" - is "yes".
Leptin (the product of the ob gene - that is, the obese gene) is typically thought of as being secreted in proportion to the amount of adipose (fat) tissue that an organism (mice, rats, primates, humans) has overall. Like most things in biology, though, it's likely not a perfect linear relationship across species or across a wide range of individual body weights within a particular species.
Even the plasma concentrations across individuals within a particular species with the exact (or very close) body weight is still different. In my own experience, when trying to "normalize" or "adjust" the estimated fat mass based on the leptin concentration there's still a good amount of variability between individuals. The leptin concentrations for a number of individuals at one specific body fat percentage are not identical - which could be due to some error in the measurement, but also due to biologic variability from other sources (for a example of this variability in animals matched for body weight see here). This is probably because there are a lot of other modifying factors or variables within the body that can affect leptin concentrations in the plasma (like other hormones or nutrients from the gastrointestinal tract). So yes, these other hormonal and/or nutrient signals probably contribute to the high variance of plasma leptin concentration for individuals with the same fat mass for all of the reasons listed above (I don't have any references that examine this specific question, though).
To my knowledge there are no studies that have examined leptin concentrations across multiple species or even within a large cohort of one species. Even though this might be interesting from a scientific perspective, it's not really necessary to be able to predict fat mass from leptin concentrations (or vice versa) for medical purposes, because we have 'good enough' methods for accurately determining fat mass in patients or animals.
Overall leptin is an adipose tissue hormone thought to be involved in control of body weight over long-term (weeks to months) time courses. For a good review of the long-term actions of leptin and other hormones controlling body weight see a great review on CNS control of body weight that discusses leptin and other factors that modify leptin and body weight regulation.
Additionally, Dr. Jeffrey Flier in Boston is a senior physician-scientist at Harvard Univeristy and has studied leptin biology and has some very nice articles on leptin including this review on leptin in energy balance and long term control of fat mass.