text:
Why is the threshold between human embryo and human fetus defined as 8 weeks after fertilization?
Why is the threshold between human embryo and human fetus defined as 8 weeks after fertilization? What's happening on the 8th week?

Note: definition of embryo based on Wikipedia's current definition.

Are you seeking for a science article that define the words "baby" and "embryo"?! This is going to be hard to find as these words are so easy and common. Similarly there are probably no science article who define the word "increase" as everybody know what it means. But I don't know maybe someone will find what you're looking for. But you should probably not expect a different definition from the wikipedia ones!

So the question might be "Why did we use the threshold between the definitions of human embryo and human fetus at 8 weeks after fertilization and not at 7 weeks or 9? What's happening at the 8th week?". Is that right?

@Remi.b does my question now appear more clear? Are there any further specifications that I might make?

I would recommend you to just reduce your whole question to what you copy-pasted from my comment (and modify your title accordingly).

@Remi.b done. I'll remove my comments, you might do so as well.

I delete my answer as it does no longer address your question. I don't have enough knowledge in developmental biology in order to answer your question, so I'll let someone else working on your question. You may still receive some comments on your introduction but I think the question will be accepted from now on. You should cite wikipedia for the definition you are using of embryo.

@Remi.b will you vote to re-open? I don't see where any opinion is involved...

An embryo is called a fetus at a more advanced stage of development
  and up until birth or hatching. In humans, this is from the eighth
  week of gestation. However, animals which develop in eggs outside the
  mother's body are usually referred to as embryos throughout
  development; e.g. one would refer to a chick embryo, not a "chick
  fetus" even at late stages.

wikipedia - embryo

I can answer what "more advanced" means with the following 2 pictures. I think you can see the difference. (Real photos were too disgusting for me.)

Figure 1 - 7th week embryo - source

Figure 2 - 8th week fetus - source

For the sake of blind people and google, the 8th week fetus has a face and a human form, while the 7th week embryo doesn't.

From the 10th week of gestation (8th week of development), the
  developing organism is called a fetus.
All major structures are already formed in the fetus, but they
  continue to grow and develop.
Since the precursors of all the major organs are created by this time,
  the fetal period is described both by organ and by a list of changes
  by weeks of gestational age.
Because the precursors of the organs are now formed, the fetus is not
  as sensitive to damage from environmental exposure as the embryo was.
  Instead, toxic exposure often causes physiological abnormalities or
  minor congenital malformation.

wikipedia - prenatal development

So the scientific explanation of the threshold is that the precursors of all the major organs are created by that time.

I don't think this answers the question. That the embryo/fetus becomes more advanced over time is a given, but it does not answer the question of why the 8/9 week divide was chosen as a threshold. A 12 week embryo/fetus also has a more "advanced form" and is more "human-like" than a 11 week embryo/fetus.

@fileunderwater Edited my post.


text:
Can silverfish climb and produce silk?
I am equally disgusted and fascinated by the "Silverfish" (Lepisma saccharina) that we regularly find in our UK home. I tried searching for information on the internet but they seem poorly understood.
We only ever find them on the work surface in the kitchen when we switch on a light at night. They are presumably feeding off food residues - but they never seem to be found in the most obvious place, among the crumbs under the toaster.
When caught by the lights, they run for cover but never, ever climb. You would think them unable to climb at all but then how have they reached the work surface?
The other day there appeared a new twist; 2 "husks" hanging from silk threads between 2 containers, maybe 8cm from the surface. If they were caught and eaten by a spider, why did it take them to a rudimentary web when it (presumably) caught them on the surface? There was no sign of a spider around. The only other possibility I can see is that they somehow suspended THEMSELVES from the silk and this was a moulting behaviour. Thus they now CAN climb - and very well - and also produce silk!
Can anyone explain the mystery?

Hi. Is your question: "What is the function of silk in Silverfish?" (I didn't know they could produce silk).

@Remi.b -  I think POs title question should be "Can silverfish climb and produce silk?"

Modified question title, feel free to rollback if it doesn't match what you are trying to ask. Also, a photo of the aforementioned "husks" would be helpful.

You read my mind @MarchHo

According to a paper by Walker et al. (2013) (found by googling "silverfish + silk", so not very hard to come by), silverfish can indeed produce silk. The paper also mentions that silverfish (Thysanura) and bristletails (Archaeognatha) use silk to transfer their sperm, and they also use it for "...tactile cue during courtship (Sturm, 1956)". This webpage (from NY State University) explains that male silverfish will deposit a spermatophore on a silk thread that is vertically suspended, and the spermatophore is later picked up by a female.

Abstract:
  Silks are semi-crystalline solids in which protein chains are associated by intermolecular hydrogen bonding within ordered crystallites, and by entanglement within unordered regions. By varying the type of protein secondary structure within crystallites and the overall degree of molecular order within fibers, arthropods produce fibers with a variety of physical properties suited to many purposes. We characterized silk produced as a tactile stimulus during mating by the grey silverfish (Ctenolepisma longicaudata) using Fourier transform infrared spectroscopy, polarized Raman spectroscopy, gel electrophoresis and amino acid analysis. Fibers were proteinaceous-the main component being a 220 kDa protein-and were rich in Gln/Glu, Leu, and Lys. The protein structure present was predominantly random coil, with a lesser amount of beta-structure. Silk fibers could readily be solubilized in aqueous solutions of a mild chaotrope, sodium dodecyl sulfate, indicating protein chains were not cross-linked by disulfide or other covalent bonds. We conclude that entanglement is the major mechanism by which these silk proteins cohere into a solid material. We propose silks used as short-term tactile cues are subject to less stringent requirements for molecular order relative to other silks, allowing the random coil structure to be favored as an adaptation promoting maximal entanglement and adhesion.

The linked paper contains several references that should be useful if you want to look deeper into how silverfish use silk.
From what I've seen, they don't use silk for climbing. Silverfish can usually climb rough surfaces, but not smooth surfaces, which is why they are often found trapped in sinks, bathtubs etc.

This species seems to be different to the one we have in the UK and is more an American variant according to Wikipedia. However, it seems strange that a species would develop silk glands simply for such an undefined function - even one related to reproduction.

@Lefty Since the paper seems to claim that the ability of produce silk covers the entire order of Thysanura (along with bristletails, spiders etc), it is unlikley to be specific to their particular study species. To use silk for courtship and sperm transfer is hardly "undefined", since reproduction is essential in the life history of a species.

No, these papers are more interested in the structure of the silk, not the lifestyle of the Silverfish. The only thing it does is to confirm that they do indeed produce silk for the purpose of reproduction - although to transfer sperm packets, not as a "tactile stimulus" in your extract. I'm interested in their reluctance to climb and whether the silk is used in the moulting process.

@Lefty in that case, please edit your question so the actual question being asked is clearer.

It seems pretty clear to me, just read the question text rather than the title.

@Lefty Yes, for tactile cues. Read the entire paper, if you are honestly interested in an answer:   "Approaching the end
of the courtship ritual, which consists of antenna-tapping and
repeated responsive movements between male and female (Sturm,
1956,1987), male L. saccharina cover an area of the substratewith Y-
shaped networks of fibers and deposit a spermatophore nearby.
Detection of the Y-shaped tactile cues by the female induces a
sequence of behaviors that culminates in her uptake of the sper-
matophore (Sturm, 1956)."

@fileunderwater I've never used pubmed and from what I can see, I can't just view this paper without signing-up in some way. If I'm wrong please correct me. Either way, my original question without all the chatter can be condensed into 4 parts: 1) What are they eating if breadcrumbs are not on the menu? 2) Can they climb? 3) Can they produce silk? 4) Do they suspend themselves from silk and moult? From what you've said so far, this paper appears to answer point 3) with "Yes".

@Lefty Sorry, forgot to mention that the paper is available for free here (view/download to the right). 1) dead insects, starch (wallpaper glue), paper, fabric etc. 2) Yes, but not on smooth surfaces, and not using silk from what I know. 3) Yes (see above), 4) I don't know about their molting behaviour, except they molt many times during their lifetime, and the paper linked above doesn't mention molting in relation to their silk.

Thanks @fileunderwater I'll have a read of it then. 1) The Wiki article mentions the same foodstuffs you've listed - none of which would appear to be present on my (tiled) work surface. Nonetheless they would appear to be able to thrive there somehow. 2) Bizarrely, most of the vertical surfaces are actually rough (wood) yet they never appear to climb them but 4) the objects they were hanging from were smooth porcelain containers.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
What is most ancestral: isogamy or anisogamy?
Sexual reproduction can be feasible with anisogamy (gametes of different sizes i.e. genders) or isogamy (gametes of same size i.e. mating types) or with undifferentiated gametes (i.e. true random mating; although I have to confess that I am not aware of such example).
De novo evolution of sexual reproduction happened several times independently. What seem to be the most ancestral states of gamete differentiation (isogamy or anisogamy)?. Does it differ between lineages?

It's not exactly what you're asking, but the recently published "Tree of Sex" might be relevant: http://treeofsex.org ; http://www.nature.com/articles/sdata201415

As stated here the first sexual reproduction seems to be isogamy, which's purpose was likely to repair the DNA, as a damaged cell could repair its' (DNA) strands via recombination with a "healthy" one.
As for lineages, the only thing I could find was also in this book at the very beginning, but there doesn't seem to be a difference as for which is the most ancestral.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Fecundity per woman in early humans
The average fecundity per woman varies a lot from country to country. I call average fecundity per woman the average number of born children per woman. In Homo sapiens, what was the average fecundity per woman during the paleolithic age for example? Is it about 2 offspring per woman or about 12 offsprings per woman?

That goes back about 2.5 Ma - 12k am I right? I'm not an expert, and with all due respect, but my hunch is that the fossil record is very incomplete, and the geologic time frame pretty long. We don't know even how many species of humans there were, let alone reproductive rates during the period.

@ChrisStronks I edited my post to clarify that I talk about Homo sapiens when I say "humans". It is plausible that we don't have the tools to answer this question... But I hope that might be wrong and someone could come up with some rough estimate. An estimate can maybe be derived from the number of surviving kids that can itself eventually be inferred from the increasing population through time (itself inferred from genetic data or from the geographical range over which fossils are found).

Do you mean offspring as in individuals reaching reproductive age or as in born children? If the latter it was certainly not 2, since disease, violent death etc were common. If it was close to 2, H. sapiens would have been extinct and we wouldn't be here.

I meant offspring = born children. I edited my post. THanks

Infant mortality was high during the paleolithic, so the fecundity of females had to be quite a bit higher than 2 to sustain viable populations.
A recent paper by White (2014) that explores how the ratio of young and old individuals in a population relates to demographic rates compiles data on hunter-gatherer societies from previous studies that you will probably find useful. Among other statistics, that paper reports a range in total fertility of 2.6–8.0. One of the source papers (Hewlett, 1991, pdf here) has data for individual hunter-gatherer societies (along with data from other types of pre-industrial societies). Many populations lie in the range 4-7 offspring. Note however that most (all?) of these values are from current or recent hunter-gatherer societies and not paleolithic societies. However, to give a ballpark estimate they are probably useful and fairly accurate. Also note that the child mortality rate of these societies are often between 40-50% (infant mortality ~10-30%)


text:
Powdered meal replacement vs regular meal
Can a person live with this alternative nutrition? Of course, assuming that eating pleasure is assumed the same.
The nutrients that contain are far better than average meal a person eats the majority of times, al least me. However, since is not solid food, do our digestive system need to work harder?
Scientific reports would be appreciated, comparing these two modes of feeding.

Are you referring to the Sci-Fi Classic movie Soylent Green?

Soylent is a powdered meal replacement product, advertised as a "staple meal" that meets all nutritional requirements for an average adult.

Probably yes, but I wouldn't look forward to bowel movements without any fiber in my diet

I've lived on it for a month with no ill impacts (sample of 1!) The bigger issue with Soylent is the protein in it is dried soy beans. I love soy beans fresh, but anyone who cooks knows that if you don't soak dried beans before cooking them you get gas. Horrible gas. Which can be corrected by taking "beano" but it makes me wonder about long-term nutritional impacts.

Thanks @futurebird, It would be great to know what were the main differences you noticed during this month. Did you miss real food? Maybe the ritual associated with eating? Let us know your experiences.

Yes you could live off a protein shake type supplement if it had the vitamins, minerals, protein, carbohydrates, and fats you would need. Would you want to? Probably not.
First thing we must determine is the protein whey or soy? If a male is consuming this meal replacement and the only protein is from soy, their estrogen levels will be elevated. In Soy Protein Isolate Increases Urinary Estrogens and the Ratio of 2:16α-Hydroxyestrone in Men at High Risk of Prostate Cancer, Dr.s Jill M. Hamilton-Reeves, Salome A. Rebello, William Thomas, Joel W. Slaton, and Mindy S. Kurzer concluded that soy does elevated estrogen in men which helped with the reduction of prostate cancer [1], but as a male, you wouldn't want to have a lifetime of increased estrogen [2].

Infertility. Estrogen is partly responsible for creating healthy
sperm. When estrogen levels are high, sperm levels in semen may fall.
This can lead to fertility issues.
Gynecomastia. Estrogen may stimulate breast tissue growth. Men with
too much estrogen may start developing larger breasts.
Erectile dysfunction. A balance of both testosterone and estrogen is
important for healthy sexual growth and development. Sexual function
may be impacted when these hormones become imbalanced. Men with high
levels of estrogen may have difficulty getting or maintaining an
erection.

So to be on the safe side, let's assume that the protein is from whey and we have one less thing to worry about. Now as for the vitamins and minerals, the Mayo Clinic states that [3]:

Supplements aren't intended to be a food substitute because they can't replicate all of the nutrients and benefits of whole foods, such as fruits and vegetables.

and there are three main differences:

Greater nutrition. Whole foods are complex, containing a variety of
the micronutrients your body needs — not just one. An orange, for
example, provides vitamin C plus some beta carotene, calcium and
other nutrients. It's likely these compounds work together to produce
their beneficial effect.
Essential fiber. Whole foods, such as whole grains, fruits,
vegetables and legumes, provide dietary fiber. Most high-fiber foods
are also packed with other essential nutrients. Fiber, as part of a
healthy diet, can help prevent certain diseases, such as type 2
diabetes and heart disease, and it can also help manage constipation.
Protective substances. Whole foods contain other substances important
for good health. Fruits and vegetables, for example, contain
naturally occurring substances called phytochemicals, which may help
protect you against cancer, heart disease, diabetes and high blood
pressure. Many are also good sources of antioxidants — substances
that slow down oxidation, a natural process that leads to cell and
tissue damage.

So you could live off of some meal replacement shake for the rest of your life but should you? Probably not.

Suggested edit: answer the question with facts, and leave out the opinion at the end. It doesn't contribute anything useful.


text:
Time required for RNA precipitation in ethanol
I precipitated bacterial RNA during 1 hour at -80ºC after depleting rRNA with Ribo-Zero kit.
Does more time lead to better results?

I typically leave my mRNA in isopropanol at -70C overnight, but that's because I usually get to that step at the end of the day and I'm lazy. I would also like to know the optimal precipitation time in case I'm hurting my yield. Note that I'm not using ethanol, and different solvents may have different optimal times.

With isopropanol even keeping for 15-20 min at room temperature is sufficient. With ethanol you can keep at -20⁰C for 1-1.5-hours. Keeping at -80⁰C is not required.

You should also consider what is occurring during this precipitation step. The monovalent cations are performing two functions: (1) they are shielding the negative charges from the phosphate on the nucleic acid backbone, those negative charges would ordinarily repel each other. (2) they are decreasing the chemical potential of the water molecules in the solvent (by ordering them), so this is a dehydration effect. The alcohol also has a dehydrating effect. So if the RNA is in solution and the water is the solvent, then by dehydrating the RNA it will precipitate. When it's complete its done

As far as I know this has never been thoroughly analyzed for RNA, but there is an excellent paper on the precipitation of DNA and the usual conditions in BRL Focus by Zeugin (see below for the paper). Since DNA and RNA are pretty much the same (except for one OH-Group) and the conditions used for precipitation are also similar, I think we can use this for a very close estimate.
Interestingly neither the time nor the temperature of a precipitation have a great influence on the outcome - they change the yield only by a few percent. If you look on figure 2 from the paper mentioned, you see the following:

This subfigure shows that the recovery is almost not influenced by the temperature, but only by the conconcentration of the DNA (or RNA). Depending on how much RNA you expect (how much cells did you use for the isolation) I would add a co-precipitation agent when you have only very small amounts on RNA. Glycogen works very well here. Otherwise I wouldn't worry.

This figure shows that the incubation time has only an influence on the percentage of the recovery when then time is too short. If you incubate for an hour, you are on the safe side.
Reference:

Ethanol Precipitation of DNA.

Since I usually get 100ug of mRNA from an in vitro transcription, I probably don't have to worry about time or temperature too much then? Unless isopropanol is totally different ethanol, but I doubt it.

I wouldn't worry about this. Follow your protocol and you should have plenty of yield.

As many kits suggest, RNA concentration has the most profound influence on precipitation efficiency / recovery fraction. Time, temperature and precipitation agent concentration has lesser effect. See for example instruction by Life Technologies on LiCl precipitation:
The Use of LiCl Precipitation for RNA Purification

N.B. Precipitation of RNA by 4 M LiCl does not include any type of alcohol (as I recall), will not work on DNA (as I recall), and is usually performed when there is still tons of rRNA present (i.e., not just mRNA)


text:
Is viral protein expression important for peptide vaccine?
I would like to know if proteins expressed in higher quantities, such as DNA polymerase, would be better vaccine candidates for a T-cell based vaccine.

To find candidate proteins which can be used as peptide vaccine, these need to fulfill some criteria:

The most important is that the peptide (or protein) used for
vaccination shall not have a closely relate sequence in the organism
in which the vaccination shall occur. Otherwise either no reaction
(due to immunologic tolerance to self) or an autoimmune reaction
might happen.
The peptide/protein need to be expressed on the surface of the
microbe (either virus or bacteria) since otherwise it will not be
recognized by the immune system. Also domains of a potential vaccine
candidate which are inside of membrane are not useful.
The epitope needs to be stable enough to be used as a vaccine and
also be present on the microbe (otherwise there is no immune
reaction).

If you want to read further on this topic, there is an interesting Paper from the WHO available, which gives a nice introduction:

Guidelines for the production and quality control of synthetic
peptide vaccines

To answer your question: No, these proteins cannot be used for this purpose, as they are relatively closely related to the same proteins in the human body. This will probably lead to no immunologic reaction at all. Additionally, these proteins are located inside of cells and thus not exposed to the immune system.

I have doubts about the second statement. If virus replicates inside the cell, virus will let some proteins located inside cells to proteasome degradation and thus will be exposed via MHC, thus revealing to CD8+ cells that has been infected.

@Bernardo When a virus infects a cell it basically takes over. In most cases the cell is lost and destroyed when the viruses are set free. Additionally you want to find and inhibit the virus when it enters the body, not when it already had time to replicate. This is something you will achieve only when you recognize the virus.

I agree that neutralizing antibodies are a good strategy to prevent a new cell infection. But, why are T cell-based epitops have that hype? http://www.ncbi.nlm.nih.gov/pubmed/22044118    http://www.ncbi.nlm.nih.gov/pubmed/24358361

I don't understand this either - this approach always needs the professional antigen presenting cells which present the antigen on their MHC-molecules. So T cells do not stand alone.

@Bernardo Chris is right, you are not able to activate CD8+ T-cells without APC. So you need a badly infected APC or an APC presenting your protein on MHC1/MHC2 and a CD4+ T-cell which verifies that it is really a pathogen. I am not certain whether it is possible to achieve T-cell response by vaccination, but it is certainly harder than to achieve B-cell response...

@Bernardo For me your link means that we need more research to create T-cell vaccines... I can agree with your point of view, I think the answer should be extended with the term B-cell vaccines. So it is just partially valid in this context.

The original question asks about vaccine development against a virus. Most effective anti-viral vaccines elicit antibody responses that presumably protect via neutralization of viruses as they enter the body. Bob Seder has a good review on this - you may find a discussion relevant to this topic in the section titled "Viral targets for the induction of humoral immunity". These vaccines would not necessarily be leading to the destruction of infected cells as this is a CTL function.
I think the hype that biotech is referring to is in relation to therapeutic vaccines against cancer, etc. that elicit CTL responses capable of destroying cancer cells. However, it is also important to keep in mind that both CTLs and B Cells need CD4 T Cell help in order to develop - nothing stands alone in the immune system.


text:
Western blot alternatives
Given an in vivo sample from an experimental infection, I would like to see if a bacterial protein is present.
I've been thinking about Western Blot using sera from animals infected with the bacteria. However, this strategy needs a positive control that requires prior gene cloning and expression.
There is maybe a shorter path.
Thanks

Is the antibody against your protein commercially available?

No, they are hypothetical proteins, not common ones.

People asking same thing here: https://www.physicsforums.com/threads/western-blot-alternatives.642444/

I think that enzyme-linked immunosorbent assay (or ELISA) is the best way to do so, given you have an antibody against the protein to coat the sample wells with... You could use mice to create polyclonal antibodies against your protein by injecting the protein and collecting the serum and purifying it...as long as there isn't similar proteins to the bacterial one in the sample you are testing for...but to diagnose an infection you could use something like q-PCR assuming you can get the bacterial DNA from the sample (you could use typical bacterial DNA extraction techniques).
For more on ELISA go here. Here is a good animation on ELISA:
http://highered.mheducation.com/sites/0072556781/student_view0/chapter33/animation_quiz_1.html

You don't have to use PCR to diagnose diseases, ELISA or western blot is routinely used for this purpose.

@chris well... it depends on the disease too...


text:
Publicly available resources for learning metagenomics
We are starting a metagenomics project in our research group to study microbiota in the respiratory tract. Since the are no books yet about metagenomics, seems reading some reviews and online tutorials is the only alternative.
Could you suggest me essential papers, websites or other resources useful for my purpose.
Thanks

You can have a look at some of the lecture slides of previous years' EBI-Metagenomics course.

The Coursera Bioinformatic Methods courses include classes on metagenomics and, more importantly, tools to use when applying these methods. I have not taken this particular course, but Coursera is generally very good with getting hands-on experience using computational tools. A course-like setting may also be conducive to group learning.

In the paper here compared lots of different tools for the different parts of the anlysis in metagenomics. It is a comprehensive study in which several labs participated.
You need to take into account that not necessarily the most popular tools are the best. And in the end it will depend on what you want to and how you do it.

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


text:
RT-qPCR of selected differential expressed genes: which dilutions in calibration curve?
I've seen in MIQE guidelines that calibration curves a needed when performing RT-qPCR. I'll use genomic DNA to perform these calibration curves.
My question is that I don't know the range of concentrations to test.
The genes I will check for differential expression have logFC between 2-8 (base 2 log).
50 ng/μL is the sample concentration I will have when performing the Comparative CT Experiment, but 98% is ribosomal RNA.
Please let me know you suggestions and possible reference books/papers to revise.

I am not sure what you're trying to do. I think you want to measure gene expression level (amount of transcript), but then why would you use DNA as your reference? What do you want to calibrate with the DNA?

Are you doing a gene expression analysis by relative quantification of cDNA? Or are you looking for copy-numbers of a gene in genomic DNA?
In either case, you need the same type of template in both the standards and samples, and that your curve must cover the whole range of Ct's in the sample set for the most trustworthy results.
For cDNA, I usually get a purified and concentrated cDNA from the same cell/tissue/etc. and do 1/4 dilutions for 5 points (every dilution giving roughly +2Ct)


text:
How long can C. Tetani survive in soil?
Clostridium tetani (C. tetani) is a bacterium commonly found in soil and is excreted in the faeces of many animals (both mammals and birds) and serves, by means of the exotoxin, tetanospasmin, causes the life-threatening condition tetanus.

Soon after asking this question I found a reliable source, the National Institutes of Health. It can survive for over 40 years.

Clostridia form endospores and can survive for years as a dormant spore. You can check this article about viability of clostridial endospores but it doesn't really talk about how long it can survive.

The paper however includes a general passage on endospores saying that: Once they are formed, endospores can stay dormant for extended periods of time, from thousands (8, 13, 20, 25, 33) to millions (3, 35) of years, although for the more extreme claims of longevity it is difficult to rule out modern contamination (37). So apparently the potentially survial is extremely long.

yeah.. i did read that statement but thought that it is too hyperbolic :P


text:
How Common are Paraneoplastic Syndromes in Cancer Patients?
I recall reading around one in four cancer patients will suffer a paraneoplastic syndrome during the course of their illness but I can't find where I read this and I can't find any reliable sources to back this up.

The incidence of paraneoplastic syndromes appears to be variable and dependent on the kind of cancer. Estimates by Baijens and Manni (2006; Eur Arch Otorhinolaryngol 263: 32–36) are 1% to 7.4% of all cancer patients, however they are citing Gulya (1993; Laryngoscope 103: 754–761) and Zuffa et al. (1984; Neoplasma 31: 231–236) for the data.
Pelosof and Gerber (2010; Mayo Clin Proc 85: 838–854) make the particularly salient observation that

As patients with cancer live longer, and as diagnostic methods
  improve, this prevalence will likely increase.


text:
Do Fatty Acid Synthase Inhibitors Selectively induce Apoptosis in Cancer cells without inducing the same in healthy human cells?
Do Fatty Acid Synthase (FAS) Inhibitors (e.g. cerulenin) selectively induce apoptosis in cancer cells without inducing the same in healthy human cells?

"Inhibition of fatty acid synthase (FAS) suppresses HER2/neu (erbB-2) oncogene overexpression in cancer cells" http://www.ncbi.nlm.nih.gov/pmc/articles/PMC490000/

I found this reference: "Inhibition of fatty acid synthase (FAS) suppresses HER2/neu (erbB-2) oncogene overexpression in cancer cells".   Cerulenin is not a magic bullet, but in some cases it may help.


text:
Why Do Most Humans & Cats Have Blue/Bluish Eyes At Birth?
I've read that the eye color at birth for most humans and for cats may not always be the the true genetic color at first. This is due to the lack of melanin in the iris. This makes sense as there is no light in the womb to stimulate the production of melanin.
My question(s) though is:

Why does the lack of said melanin produce a blue/bluish colored iris?
Why is it not say green, red, clear, etc?

The blue colour is an example of structural colour, caused by light interacting physically with something. Some examples of structural colour are the iridescence of insect wings and body surfaces (usually caused by repeating chitinous structures), and of certain birds feathers, as well as the non-iridescent colours of the blue and yellow macaw.
In the case of the eye it is the stroma of the iris that is responsible. This is a network of fibrous tissue which scatters light. When light is scattered in this way (Rayleigh scattering) it is the short wavelengths which are most scattered. So when you look at the sky (away from the sun) you are seeing diffuse blue light created by this scattering in the atmosphere. In the case of the iris what you are seeing is light reflected from the eye being scattered within the iris, creating the diffuse blue colour. As you say in the question, everything else is down to melanin.

The generation of iris color is quite complex and the exact color of the eyes depends upon many different factors, not just melanin. In fact, blue coloration does not depend on a specific chemical, but on the structure of the eye itself.
This very nice review (free) summarizes our current understanding:
Genetics of human iris colour and patterns - Sturm and Larsson, 2009
From the Introduction (bold is mine)

In the brown iris there is an abundance of melanocytes and melanin in the  anterior border layer and stroma whereas in the blue iris these layers contain very little melanin. As light traverses these relatively melanin-free layers, collagen fibrils of the iris scatter the short blue wavelengths to the surface, thus a blue iris is a consequence of structure not of major differences in chemical composition. Different shades of blue, and in irises with a limited amount of melanin, different shades of grey, green and hazel, are determined
  by the thickness and density of the iris itself and the extent of accumulation of white collagen fibres, as well as patches of tissue loss in the anterior border layer and stroma.
  However, a careful examination of people’s irises makes it clear that there are characteristics other than eye colour that present in the human iris. The iris has been analysed to show that it can display a degree of complexity encompassing over 240 degrees of freedom (Daugman, 2003).

Thanks for the edit @Alan... too early in the morning to speak proper English :P

Mammals are born with blue eyes because the melanin level has not yet been established to give brown/yellow. Blue is the absence of melanin, so that eyes reflect outside light which is seen as blue. Melanocyte cells respond to light and will start to make melanin in the first few weeks after birth. Melanocyte cells have a range of activity and will produce roughly the same amount of melanin that the parents had.

Welcome to Biology.SE! Your answer sounds reasonable and, if correct, it better addresses the original question than the existing answers. However, it is much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support non-specialists will have difficulty in evaluating your claims. ——— You may also want to take the [tour] and consult the help pages for additional advice on [Answer] effectively on this site. Thanks!


text:
What Makes A Pet Hypoallergenic
I know you can purchase dog and cat breeds that are hypoallergenic so those who are prone to pet allergies will have reduced allergies or none at all. These breeds are specifically bred for that trait, and as a result are typically pricey compared to another breed. These breeds are not necessarily hairless or short-haired, so I do not think it has to do with the amount of fur shed.

What makes these animals different from other breeds in their inability to cause allergies?

Pet allergy is an allergic reaction to proteins found not only in the
  animals' fur or hair but also in saliva, urine, mucous, and hair roots
  and in the dander sloughed from the animals' skin. Thus, the
  widespread idea that "hypoallergenic pets" are those that have less
  hair or shed less is a myth.
Most often, pet allergy is triggered by exposure to the dead flakes of
  skin (dander) a pet sheds. Any animal with fur can be a source of pet
  allergy, but pet allergies are most commonly associated with cats,
  dogs, rodents and horses.
Some dog breeds have been promoted as hypoallergenic because they do
  not shed their hair, shed very little, or have the same pH as human
  hair. However, no canine is known to be completely non-allergenic.
Some cat breeds, especially females are likely to have low levels of
  Fel d 1, the main allergenic protein.
There is only one known hypoallergenic horse breed. The Bashkir Curly
  horse has a uniquely textured coat that lacks the protein (present in
  all other horse fur) believed to be the source of allergic reactions
  to equines.

via

Quotes should be clearly indicated using the quotation formatting and should support your answer rather than form it


text:
Why Do Ruminants Require A Multi-Compartment Stomach To Digest Food?
Cows, camels, sheep, goats, etc being ruminants must chew their food repeatedly by regurgitating their food from their first stomach compartment and chewing their 'cud'. This then finer chewed material makes its way to the various stomach compartments to be digested.
These animals are eating plant material, the same plant material animals such as elephants, horses and hippos eat as well. However, these animals only have one stomach compartment.

Why does one need a multi-compartment stomach and one does not if they are all eating the same/similar food?

There is more difference than just the parts of plants that are eaten.
Two of their stomachs - rumen and reticulum are not used for digesting food at all. Multiple rounds of chewing and mixing with saliva, wich result in very small particles of undigested food help the bacteria in those stomachs reach, digest and use that cellulose-rich plant material. Cows "eat" the bacteria from their stomachs and the grass is just food for these bacteria. You could say that cows are not herbivores but secondary consumers.
Look at this picture (from Wikipedia article on ruminants, a good place to check all this in more detail but still simpler than most professional books):

See that the ruminants have the same second and third part of their digestive system (though the bacteria use up most of carbohydrates, so some difference in absorbed material), but have an additional part in the front - where the microbes digest and ferment the food, that the ruminant has provived them. The reticulorumen needs to be large in order to provide space for all that plant material and bacteria.

It is not a biology question but simply a logistic problem. The digestion of cellulose just because of the presence of celluase producing microbes. Rumination itself, by the action of chewing, can enhance the cellulose digestion efficiency by incresing the surface area. Still nothing related to the multiple compartments of the ruminant stomach.
Actually, the multiple compartments allowed the anti-directional peristalysis and multi-tasking of the stomach. That is Ruminants need A Multi-Compartment Stomach to perform rumination for the reason of logistic.

If you ever look at a huge pile of elephant/horse dung you will see it is full of poorly digested vegetation. I had an (unfortunate) 4 day project on a field trip in south africa which involved handling a lot of elephant s***, more than once I found whole amarula fruits!
Think about this in comparison to ruminants which have a much better digested pile of dung, e.g. a cow-pat. The ruminant digestive system allows them to digest cellulose (found in plant material) much more efficiently than other vertebrates thanks to a specialized gut flora. You may want to look at this and this for more details.

They are not all eating the same/similar food.
Elephants, horses and hippos are herbivores that have different diet to ruminants. Elephants, for example, have trunk to access fruits that is less difficult to digest.

100 kg for a 5000 kg elephant is 2% of body mass.

ok, i have edited.


text:
Temperature Tolerance In Relationship To Body Temperature
A humans body temperature averages at around 98.6°F
A dog's body temperature averages at around 101.5°F

If the temperature outside is 45°F who would feel colder?

The dog's temperature is higher than the human. So you would assume since its temperature is higher it would feel warmer than the human.
However, the temperature difference between the body and the external temperature is the following:
Difference in humans internal and ambient temperate: 52.6°F
Difference in dog's internal and ambient temperate: 56.5°F
I'd like to know as I keep telling my mom that the dogs feel hot when she puts on doggy sweaters for them when its slightly cold for us humans.

Things other than the temperature that could affect whether or not the coat is necessary: Is it raining? a wet dog will get cold quicker. How long/thick is the fur? thin coats of fur will be less efficient at keeping the dog warm than thick. Is it windy? Wind blows warm air out of the fur. How big is the dog? Size & body fat will affect the rate of heat loss. How active is the dog? A dog doing lots of fetching will keep warmer than a dog ambling along the pavement

Clues as to whether the coats are necessary: Is the dog shivering? if yes, give it a coat. Is the dog panting? yes, take the coat off before you bake the thing!

@rg255 would you like to post your comments as an answer?

done (and here's some extra characters to let me post this comment)

Things other than the temperature that could affect whether or not the coat is necessary: Is it raining? a wet dog will get cold quicker. How long/thick is the fur? thin coats of fur will be less efficient at keeping the dog warm than thick. Is it windy? Wind blows warm air out of the fur. How big is the dog? Size & body fat will affect the rate of heat loss. How active is the dog? A dog doing lots of fetching will keep warmer than a dog ambling along the pavement.
Clues as to whether the coats are necessary: Is the dog shivering? if yes, give it a coat. Is the dog panting? yes, take the coat off before you bake the thing!
this probably does not fully answer the question "If the temperature outside is 45°F who would feel colder?" but as requested by the OP I have posted my comments as an answer. I would expect a dog without a "doggy sweater" to be better able to cope with the cold than a human not wearing a "people sweater" or any clothes, just like the dog, if you want to make it a fair test!


text:
Why Is The Toughness Of Skin Different On Different Parts Of The Body?
My cat was licking my arm with his sandpaper like tongue. It hurt and the area he was licking was slightly smarting afterwards. However, when he licks the palm of my hand the feeling is rather ticklish and results in no pain during or after.
We can pick up sharp, prickly, abrasive objects with our hands (palms/fingers) and even rub against them and have little to no damage incurred. However, if we do the same with say the back of our hand we are more likely to be injured.
I thought maybe the skin is thicker in our palms and that is resulting in our palms being more resilient. But, our palms are so sensitive to touch that it makes me think the skin is thinner to allow the nerves closer access to our environment.

Why is there such a stark difference in different areas of skin on our body when it comes to feeling pain and being susceptible to injury from scrapes, bruises, cuts, etc?

Sensitivity to touch depends on the density of mechanoreceptors.

@WYSIWYG do you want to post that as a more detailed answer so I can accept and close this?

As dd3 said the density of mechanoreceptors dictates skin sensitivity to touch (also look at penfield map. It is a nice illustration of how different senses are mapped to the brain and to what extent each region is sensitive to stimulus). Skin thickness is also different in different regions. This article says that Dikkopf1 (a Wnt pathway antagonist) controls skin thickness.

There are different receptors and different forces at play here.
Skin thickness depends primarily on frictional forces and is determined by the thickness of the epidermis, which is made up of 5 layers of keratinocytes:

Stratum basale
Stratum spinosum
Stratum granulosum
Stratum lucidum
Stratum corneum

The areas that are subjected to high frictional forces have the thickest epidermal layers, such as palmar surfaces of the hands vs the dorsal aspect of the hand (the back of the hand)which is significantly thinner.
The actual thickness of the skin doesn't always correlate with how tactile or painful stimuli are perceived. The receptors can be very sensitive even where stratum corneum is the thickest and vice versa.

Your links are for specific epidermal layers vs providing adequate citations for the claims you make throughout. Please edit.


text:
Why we aren't making Darwin's theory a Law
I was wandering about darwin's theory which is controversial theory and there are no enough evidence to prove it right or falsify it, since I'm a biology student so i studied basic way of a hypothesis going to be a law ,the last thing to be a law is theory...am i right?
Hmmm if yes then it's been about more than 130 years since darwin died and there is still no response to his theory?why this taking so long? Are we supporting Darwin because if we don't then we gonna recreate our basic embryology and evolution? If no then why we aren't making it a scientific law?

We have Newton's laws and Theory of relativity, but we still don't have Einstein's laws. I personally think it isn't a law because we cannot practically prove it yet.

Sorry i didn't got your point...Do you mean that the theory of relativity is also pending?

Yes. Theory of relatility is controversial. It needs some more modifications to be completed, as well as Darwin's theory.

Yes it needs but darwin's theory is based on fossil records and till date we have found fossils of a million years ago dino but not the fossils of humans completely even about 30%

In my opinion, Darwinian theory is like a naive approach, a kind of "-ism" to explain evolution. We also have Lamarck's theory, Kimura's theory and a lot of modern adjustments. None of these are able to fully explain the high diversity of the nature. Maybe we can never prove it, maybe eventually we might be able to prove it, but for now there is not enough evidence and too many opposite critics to make it a law.

I'm voting to close this question as off-topic because the definitions of terms such as hypothesis, evidence, theory, law, axiome belong to the field of philosophy of science. You should give it a try at Philosophy.SE.

Despite being a subject of philosophy, we already have a post that answer your question here. The post could as well be close as a duplicate.

Tho H. Ho is very obviously wrong! I would love to be able to down vote his comments! The theory of evolution (often called "modern evolutionary synthesis") is a theory. A theory is a a set of hypoteses extremely strongly supported by evidences. There is nothing controversial about the theory of evolution, just like there is nothing controversial about the theory of gravity. None of these theories will ever become laws because a law is just something different from a theory (not something better).

Thank you for your helpful clarification, except your love to voting down my wrong opinion couldn't make anything better.

Possible duplicate of How do we know that humans and chimpanzees evolved from a common ape ancestor?

To me, this is mainly a semantic issue (scientific theory vs scientific law, especially in lack of a clear definition of a scientific 'law'), and therefore opinion-based.  As @Remi.b writes, the Q is a bettet fit for philosophy-SE, but too vague for that site as well.

@ThoH.Ho I hope you did not take it with too much offense. If you just google hypothesis, evidence, theory, law you'll get many websites that make short intro to the semantic of these terms. These definitions are a matter of philosophy of science (a very interesting field of philosophy IMO).

Don't tell me you came here from zakir naik! ;)

@polisetty why? What he have done to you?

Scientific Laws differ from Scientific Theories in that Laws do not posit a mechanism or explanation of phenomena. Scientific Laws are merely distillations of the results of repeated observation. As such, a law is limited in applicability to circumstances resembling those already observed, and may be found false when extrapolated.
Examples are like
Ohm's law only applies to linear networks, Newton's law of universal gravitation only applies in weak gravitational fields, the early laws of aerodynamics such as Bernoulli's principle do not apply in case of compressible flow such as occurs in transonic and supersonic flight, Hooke's law only applies to strain below the elastic limit, etc. These laws remain useful, but only under the conditions where they apply. Such laws do not explain how and why they work.
https://en.wikipedia.org/wiki/Scientific_law
Darwin's Theory of Evolution in contrast contains both observation, and a proposes an explanation of the phenomena of species formation.


text:
How large is the variability in human bone thickness, and is "big boned" a real thing or not?
My girlfriend is arguing that there are "big boned" people, I read some articles that there is no such thing but she still didn't believe in me because she saw some articles too that big boned people exist. Am I missing something and is my girlfriend correct?
I know that some tall people or some people living in Europe or US have of course bigger bones that in some Asian countries because some Asians are really small. However, this is not how most people understand "big boned".
How large is the variability in human bone thickness in persons of the same height? Could this variation mean that a person might appear overweight, when they in reality are only having relatively thick bones (large diameter), so that the expression "big boned" might have some truth to it?
UPDATED
I'm asking about the most people perceive about the "big boned" thingy. Most people (like my girlfriend) sometimes touch chubby people and when they feel like it's not fat, they say "ohh, you're not fat, you're just 'BIG BONED'". I'm asking if there is a real health/scientific basis for that. Personally, I don't believe that 'big boned' is a real thing. However, it's hard to find information about this on the web.

Do you mean whether bone size varies across humans, or whether this has a significant effect on weight, with people of the same height having different weights because some of them have bigger bones? Those are two very different questions.

Not sure this is the correct site, as there is not a health question here.

Yeah, either way, as @JohnP said, this is not about health.

Try asking at http://skeptics.stackexchange.com/

Then migrate instead of close.

@FranckDernoncourt since this is a beta site none of us can vote to migrate to anywhere except for the Meta site. Also, in its current form Skeptics would just put it on hold. It needs links to notable sources claiming something in order to be on-topic there. It's also still unclear to me what the OP is actually asking.

Please do not answer in comments.

@JohnP This is not on-topic for Biology, and the only time I have ever heard mention of Human Frame Size is in a Doctor's office, as you will see from this article on MedLinePlus https://www.nlm.nih.gov/medlineplus/ency/imagepages/17182.htm . That being said the question is either primarily opinion based and should have been closed on Health or it is on topic on Health, at least from the perspective of the American Accreditation HealthCare Commission as they accredited A.D.A.M where the article is published.

I'm voting to close this question as off-topic because it's a Health or Sceptics question.

@Christiaan this was from Health

seems like this is best in skeptics. can someone move this?

@Ceeee I am pretty sure it needs editing before moving it over to skeptics since it will otherwise be closed there.

@Chris Thanks bud, will check to make this question suitable for skeptics

"I'm not fat, I'm big boned"

To make this question more suitable for Bio-SE I think you should frame it in terms of variability of bone diameter in persons of the same height, e.g. "How much does the thickness of human bones vary in persons of the same height, so that some people could appear overweight when only having very thick bones?"

Since the argument with my girlfriend was finished days after this was posted(sadly we were waiting for this but it took so long, we posted this question to have an answer right away) I'll just post here what I conclude about the "big-boned theory" based on searching through internet.
Let me site this link; that says,
"However, the initial findings of this study show that having big bones does not make you fat, being fat gives you big bones". What the link says, having more fats forced our body to increase the size of our bones for it to endure the stress brought by having heavier weight. Which means big-boned really do exists. (Damn lost the argument with my girlfriend because of this link)
Another site that says, "If your scale weight indicates that you’re overweight, it’s most likely because you’re carrying too much body fat.   Not because you’ve got 'big bones'". This site says that we cannot use the "big-bone theory" to reason out being fat. In the article, The heavier weight was caused mostly by fats and not by bones. Also the article says that tall person having 6'2 height will have of course bigger bones that a person with height of 4'2. Also the article says that "Still others definitely seem to have a larger “frame” as evidenced by a larger circumference of the wrist and ankles.  [NOTE:  The wrist and ankle joints typically do not have much fat or muscle, it’s mostly skin and bone.  So a person with a larger wrist would most likely have a larger bone circumference.]" (My girlfriend's face would be so happy to read this)
The last site that I would like to post here have chart to know if you're big-boned or not. The site also agrees that there is big boned

TL;DR
I lost, "Big-boned theory" is real but having heavier weight not mean your big-boned.
P.S. : Also instead of saying "ohh, you're not fat, you're just 'BIG BONED'" to someone just to make their feelings well, you're not doing it right! Just tell them the truth and tell them to do more exercise and have healthy lifestyle. :)


text:
Fisher's Fundamental Theorem of Natural Selection
Ronald Fisher discovered what he, with humility, called the Fundamental Theorem of Natural Selection. This theorem says (in its modern terminology):

The rate of increase in the mean fitness of any organism at any time ascribable to natural selection acting through changes in gene frequencies is exactly equal to its genetic variance in fitness at that time.

As I understand it, it sounds alike the standard equation that we learn in the first class of Introduction to evolutionary biology
$$R = S \cdot \frac{V_G}{V_p}$$
In words: the response to selection equals the selection differential times the genetic variance of the trait under consideration divided by the total phenotypic variance of the trait under consideration
But how can we prove/demonstrate that Fisher's fundamental theorem of natural selection holds true?
I don't ask for empirical evidences that support this claim but for a theoretical/mathematical proof/demonstration of this claim.

Can the term "selection differential" be used in contexts other than breeding?  Like to say that some traits have a "selection differential" that is higher than other traits in some time-steps and lower than other traits in other time-steps.  For example, if an individual is better than a second individual at capturing prey, while the second individual is better than the first at evading predators, the first individual has more of an advantage when prey are scarce and the second individual has more of an advantage when predators have proliferated.

The following answer is not complete and only give some intuitive grasp on Fisher's fundamental theorem of Natural Selection. A better devlopment can be found in Ewen's book
Let's first define what is the Additive Genetic Variance
Consider a quantitative character that is determined entirely by a locus $A$ which two alleles are $A_1$ and $A_2$. the measurement $m$ of this quantitative character for an individual is given by their genotypes so that the genotypes $A_1A_1$, $A_1A_2$ and $A_2A_2$ have measurements $m_{11}$, $m_{12}$ and $m_{22}$ respectively. Suppose that random mating obtains with respect to this character and that the frequencies of $A_1A_1$, $A_1A_2$ and $A_2A_2$ are $x^2$, $2x(1-x)$ and $(1-x)^2$, respectively. Then, the mean value $\bar m$ of this measurement is
$$\bar m = x^2m_{11} + 2x(1-x)m_{12} + (1-x)^2m_{22}$$
and the variance in the measurement is
$$\sigma ^2 = x^2(m_{11} - \bar m) + 2x(1-x) (m_{12} - \bar m) + (1-x)^2 (m_{22} - \bar m)$$
The covariance between the fathers and the sons (assuming no change in allele frequency) is
$$x(1-x)\left(xm_{11} + (1-2x)m_{12} - (1-x)m_{22}\right)^2$$
The correlation between the fathers and the sons is found by dividing the covariance by the variance (since the variance of fathers equal the variance of sons) is
$$\frac{x(1-x)\left(xm_{11} + (1-2x)m_{12} - (1-x)m_{22}\right)^2}{\sigma ^2}$$
which can be decomposed into dominance and additive variance
$$\sigma _A ^2 = 2x(1-x) (xm_{11} + (1-2x)m_{12} - (1-x)m_{22})^2$$
$$\sigma _D ^2 = x^2(1-x)^2 (2xm_{12} - m_{11} - m_{22})^2$$
Replacing the measurement by the fitness, you get the additive genetic variance in fitness.
$$\sigma _A ^2 = 2x(1-x) (xw_{11} + (1-2x)w_{12} - (1-x)w_{22})^2$$
$$\sigma _D ^2 = x^2(1-x)^2 (2xw_{12} - w_{11} - w_{22})^2$$

Now, the mean fitness in the population is given by (as already said)
$$\bar w = x^2w_{11} + 2x(1-x)w_{12} + (1-x)^2w_{22}$$
Using Wright-Fisher equation, the change in mean fitness is
$$\Delta \bar w = 2x(1-x) (xw_{11} + (1-2x)w_{12} - (1-x)w_{22})^2 \cdot (w_{11}x^2 + (w_{12} + \frac{w_{11} + w_{22}}{2})x(1-x) + w_{22}(1-x)^2)\bar w ^{-2}$$
which can be approximated
$$\Delta \bar w ≈ 2x(1-x) (xw_{11} + (1-2x)w_{12} - (1-x)w_{22})^2 = \sigma _A ^2$$

Reference

I don't think that you need to look further than the Price equation, which is basically a proof of a generalized version of Fisher's fundamental theorem. Price had a series of papers in the 70's that derived and applied the Price equation (e.g. Price, 1970; Price, 1972a), but most relevant for your question in probably Price (1972b).
A nice summary of Price's legacy can be found in Frank (1995).

There's a Frank paper from JEB (2007?) on it too which is good - we have an ongoing discussion group of the price equation here at the moment. (Any good suggestions of papers with quantitative genetic applications of price equation?)

Good to know. I've seen this one as well, but haven't read it: Frank. 2012. Natural selection. IV. The Price equation

That's the one, why did I think it was 2007?? I only read it last week!

Here's a paper with an historical bibliography of mathematical analyses in the introduction.
As you can see when you demand a mathematical treatment of something as poorly understood as the genetic inheritance of traits, the word proof is to be used in a qualified way.  In this case a multilocus fitness with variation in the population with no linkage between the alleles.  Its probably a case that shows up frequently enough, but how many alleles are we talking about?  With large numbers of alleles which are scrambled randomly at each generation (zero linkage) I would imagine that the number of individuals that contain a lot of diversity.
Most GWAS studies show lots of less probable variants may contribute to many genetic traits (like height, diabetes, etc).  So this is quite a reasonable number of the cases.
The fundamental theorem is true for any number of variants involved though, so hopefully this helps.

There's an interesting treatment of this theorem in the Journal of Mathematical Biology (late 2017), which supposedly accounts for ongoing mutations in the population (not accounted for in Fisher's original).
https://link.springer.com/article/10.1007/s00285-017-1190-x
They show how their modifications produce the same results as Fisher's original when ongoing mutations are assumed to be non-existent.  They also show some results of simulations based on different ongoing mutational distributions.  They discuss which distribution is most reasonable based on observation.
Although this is a mathematical treatment, I think the trustworthiness of the theorem would ultimately be tied to empirical evidence, as I hinted at above.


text:
What triggers the migration of robins?
I live in central Massachusetts, and have begun seeing robins, as we generally do in early March. The temperature is well below normal, though, and three feet of snow are covering the still-frozen ground from which they usually feed. We were expecting them to arrive late, when conditions would seem more conducive to survival.
What triggers their migration process?

I don't know about the specific cues that American robins use for migration. This species is also both a short range (e.g. between states or to lower altitudes) and long range migrant (e.g. Florida & Mexico), so the cues that they use can probably differ between overwintering populations. There are also year-round populations of robins in the US, but probably not many (if any) in Massachusetts. There are however at least two papers that show that American robins are arriving earlier and earlier, at least in Wisconsin and Colorado (Inouye et al, 2000 and Jones et al, 2012). The studies find that arrivals dates have shifted ~13 days earlier between 1990 and 2010 in Wisconsin and 14 days earlier between 1981 and 2000 in Colorado. The study from Colorado also shows that the first date of bare ground has not changed, so snow melt has not changed over the time period. As a consequence, the interval between arrival and bare ground has grown by 18 days. This could indicate a phenological mismatch between spring arrival and the resources used by robins, and your observations seems to agree with this pattern.
This are at least some comments and a couple of papers that could be useful for your question. Sorry I cannot say more about the actual cues used for their migration.

I'm not a specialist in this area, but I would guess that the length of day-light periods compared to night time could be a good trigger. This is quite independent of the weather, is quite constant (even though length of days is known to have changed through over the millions of years past since the formation of earth).

I live in Boston, Massachusetts. At the Back Bay Fens, a couple of miles from downtown, the Muddy River is partly bordered with dense stands of Phragmites reeds. Back in the 1990s I discovered that robins nest among these reeds in spring. According to Cornell University's Laboratory of Ornithology, this is the only place in North America where robins are known to do this. (Phragmites are loathed by conservationists and wildlife officials because they are supposedly worthless as habitat.) In late autumn large flocks of robins roost in those same reeds at night, flying out and dispersing to feed every morning. On a number of occasions I made careful counts of the robin flocks leaving the reeds during November and December. The count was well up in the thousands of birds on several December mornings. On calm sunny mild winter days a few robins can be heard singing very softly---the so-called whisper song---at the Fens and elsewhere in Boston.

Please add some references to your answer.

Thank you for these answers. My robin sightings decreased over the first few weeks since I wrote this, however they're back in full force now. This made me curious enough to do further research, and I happened upon two fact sheets about American Robins, whose scientific name is Turdis Migratorius, meaning Migrating Thrush.
I've extrapolated data from a series published by Learner.org entitled Journey North, and will be referring to and quoting sections of this and this.
As indicated by the thorough sources referenced in @fileunderwater's excellent answer, it's clear that not all robins migrate, and among those that do, there are a number of variables, many of which are not fully understood. Robins are considered nomadic, meaning they travel in many different directions, and, unlike other species, they don't necessarily come and go from the same location, further complicating the study of migration.
In general, food supply is the robin's most important consideration, and weather controls the availability of that food, so a complex combination of the two appears to be the main migration trigger.

Migrators rely heavily on earthworms, caterpillars and other insects for the bulk of their diet.
In the fall, they fly south because the ground freezes, locking them out from their favorite food, earthworms, and because winter weather makes it impossible to find juicy caterpillars and other insect food.
The same theory applies in their motivation to return from the south. Soils in the south can get so warm and dry that worms retreat deeper into their burrows during hot, dry spells, making them harder for robins to find.
Robins are easily overheated, so they become stressed and restless when the southern temperatures remain high for an extended period of time.

The south to north migrators are programmed to follow something called a 37-degree isotope. They move ahead of warm fronts, the intention being to settle down where the temperature averages 37 degrees or more. That weather pattern also brings spring rains, causing the ground thaw that triggers the end of earthworm hibernation.
The male robin migrates first. He bulks up by eating more than usual to sustain him through the arduous journey, which is why the first robins we see are generally chubby! (The male also has a much darker head than the female.) As @fileunderwater pointed out, in some areas robins have begun to arrive significantly earlier, while the ground is still frozen, so that extra preparation helps them survive for a time by eating berries and insects found in trees. If all else fails, some will re-join a flock and fly to a warmer area for a few days or weeks, which supports my recent observation.
Upon arrival, the male's job is to stake out a territory conducive to good breeding conditions. Once he finds an area that has a good feeding source, a safe place for breeding, and the right materials for the female to create a nest, he spends most of his time in a nearby tree singing. It's a unique sound rarely used at any other time, and it lets other males in the area know to stay away.
A few weeks later, the female arrives. Her trigger seems to be related to  ideal nesting conditions.

She has no urgent need to return early, since there is nothing important for her to do until there is a good mud supply for building her nest. As a matter of fact, if she builds too early, hard frosts at night can weaken her nest. And if she runs out of food too soon before the nesting season, it can make it hard for her body to produce eggs. So she waits until conditions are more favorable and she can continue to get a reliable winter diet as long as necessary.

A few other fun facts about migration:

Robins migrate mostly at night.

They fly at speeds of 30-36 mph, traveling between 100 and 200 miles per day.

To keep from getting lost, they figure out their location on the planet in much the way sailors on the high seas once did--using the angle of the sun in relation to the time of day. If blown off course, they fly to where the sun will be at the proper angle.

Flock sizes during migration vary greatly. Although groups of 10-50 are the most commonly seen, they'll fly in groups as few as three or four, and I (the author of one of these articles) once counted 60,000 robins flying along Lake Superior in just 5 hours!

For various reasons, many robins don't survive migration. Scientists estimate that only 25% of fledglings born in the summer survive until November, and even many experienced adults die during migration.


text:
How to evaluate the efficacy of an antibody for fluorescence microscopy?
I'm trying to evaluate data taken from fluorescence microscopy with antibody staining, and am wondering whether there is any standard way to evaluate the specificity of the antibody for such measurements? In particular, I am interested in evaluating whether there is specific binding of the antibody to the cells in the experiment, or only unspecific binding.
By leaving out the primary antibody or taking a control antibody without specific binding, I can compare fluorescence intensity, and an increase in intensity in the actual experiment towards this control will indicate qualitatively that the antibody binds specifically. But I wonder whether there is a standard statistical test or something to get such a result in a more quantitative way?

When testing an antibody for an imaging application, it is almost always a good idea to test it in another application like ELISA or Western blotting to see if it binds the target of interest. For example, try to find high- and low-expressing cell lines, load equal amounts, and see if there is a difference in signal at the expected molecular weight. Check the company's literature or contact their technical support to see if they have tested the antibody by immunofluorescence (IF), and if so what their results were and how they validated them. Check the literature to see if other people have published with this product. http://highwire.stanford.edu is a pretty good full-text search engine, but they don't have all journals in their database. Google Scholar can help, too.
You can also use your high- and low-expressing cell lines to see if there is a stronger IF signal in the high-expressing line. Look at your images to see if the signal is localizing where you expect it to, and do co-staining with antibodies to other proteins that should co-localize with your target of interest. For example, if your target is expected to localize to mitochondria, co-stain with COX-IV. A quick Google search found this Cellular Localization IF Antibody Sampler Kit that has controls for several different organelles and other specific locations.
Make sure you are following the manufacturer's recommended protocol. Don't crank the gain up too high on the scope, because non-specific background goes up, too. Look at the induction of signal between high- and low-expressing cell lines. Generally you would want at least a 2-3 fold shift, especially if you see a strong change in signal intensity by Western. Try using siRNA or similar silencing technology to knock down the signal in your cells, and validate using Western and IF.
Ultimately, you can never be absolutely 100% certain that an antibody is binding a certain target, and only that target, but you can accumulate a lot of evidence to show that it is likely. Try to put yourself in the mindset of a reviewer, and objectively convince yourself that the signal is real. If you can't, then shop around and try something else. Good luck!

Don't really know if the first point is really so useful... Most of the time antibodies work in IHC but not in WB or vice-versa and not having a signal in WB does not mean that your IHC signal is aspecific. Also, if you are working on tissue (rather than cell cultures) you have many different cell types which may complicate things a lot.

@nico - In my experience (at a certain antibody company) it is perfectly possible to have a great IF or IHC antibody work well in WB, and vice versa. It all depends on how the Ab is screened, and the nature of its epitope. I agree that not having a WB signal would not necessarily disqualify its staining capacity, so that's why I put in the other options like differentially-expressing cell lines and siRNA. It seemed like the questioner was talking about cells, and my mind differentiated that from tissue, which may not have been a correct assumption...

Hmmm... in my experience (in the lab) that is not that common when working with tissue. I don't work on cell culture, so maybe that is different.

Tissue makes for dirty WBs in general, which is why we tried to do as much validation on cell lines (and paraffin-embedded cell pellets for IHC) so we could be sure before moving on to tissue. We wanted to be as damn sure as possible we were staining the right thing before releasing something to market. That meant we didn't quite have the product diversity that some other companies might have had, but the quality and level of trust were a lot higher, overall. If you haven't used their stuff before, I highly recommend it, even though I'm not there anymore.


text:
Need for two oxygen sensors in E. coli
E. coli has two oxygen sensors: FNR (fumarate-nitrate reductase) and ArcBA (Anoxic Redox Control, two component control systems). FNR directly senses the oxygen, while the interaction of ArcB with oxygen is indirect one via quinone pool. Out of theree quionones in E. coli, which one (oxidized and reduced forms of all three types)  play roles to what extent in what direction (inhibiting/activating) is much debatable. I would like to see some intuitive level arguments for why a cell, even in principle, need to have two sensors for oxygen?

It is not uncommon for cells to have parallel pathways for same outcome. This ensures foolproof response and makes the system robust. E.coli also has another sensor for aerotaxis (Aer and Tsr proteins). See my answer on your previous post and the linked paper.
Also look for coherent feed forward network motifs.


text:
Referencing the homologous chromosomes
There exist a co-ordinate system from chromosomes like "12p11.3". In this system, first integer range from 1 to 23 i.e it takes homologous chromosomes as a pair. If we want to distinguish among homologous chromosomes, how do we refer to each on of the pair? Is it possible to determine if one chromosome from a pair of homologous chromosomes is from father or mother?

The cytogenetic notation seems to refer to parts of the chromosome when they're being karyotyped when the chromsomes are condensed in metaphase. If so, I think you might be able to use FISH to look for pieces of maternal or paternal genetic content on the chromosome. It looks like you can use mat and pat to refer to a maternal or paternal chromosome.

It is not possible to know in most cases whether a chromosome is maternal or paternal without knowing the genome sequence of both mother and father (with some additional effort; see below).
There are certain exceptions and these include chromosomes that bear imprinted genes. For example H19 gene on chromosome-1 is maternally imprinted i.e. the paternal copy is silenced by DNA methylation. Likewise there are many imprinted genes; a list of imprinted genes could be found here.
A technique called bisulphite sequencing (also MeDIP-seq) can be used to find methylated regions in the genome but to map chromosomes using this methylation information is not straightforward. You have to do either of these two:

Segregate chromosomes before checking for methylation
Identify a variable region, proximal to the methylation site, that can be detected by FISH. (It is difficult to find such regions in homologous chromosomes because the differences are small that FISH cannot resolve.)

With X-chromosome it is possible to find out which one is paternal in relatively easy way but this check has to be done at neonatal stage (when placenta is still present). See this post.


text:
Breathing water vapour
Normal air consist of oxygen, CO₂ and nitrogen, with traces of water etc.
Now imagine displacing all gasses except oxygen with water vapour. By water vapour I don't mean hot steam or fog. Just gaseous water.
The question is would it be beneficial or harmful to human, and how much so?
And assuming it's not deadly, in which circumstances could it be useful?
One thing I am wondering in particular is deep dive and high altitude applications. Having no/low content of nitrogen in such an artificial air mixture would help to avoid decompression sickness. And one would think water vapour is at least cheaper than pure oxygen (also might be safer and have less side effects).

Just because you have removed the Nitrogen and CO₂ won't help you keep a higher vapour pressure of H₂O in the air. You Could REMOVE all the other gasses and just have O₂ at its normal partial pressure at 1/5 bar total pressure and breath fine, but there would be a fire risk in this environment due to no non O₂ molecules to quench excited O₂.
The only way to have a high enough vapour pressure of H₂O for something like diving would be to heat it, but I don't think a lungful of very hot water vapour would be terribly good for you.
You can't just pressurise water vapour to any pressure you feel like; it will condense fairly easily.
To avoid Nitrogen's toxic effects, divers often use Helium to replace it as pure Oxygen is deadly at high pressures.

If $O_2$ is at its normal partial pressure, that means there is still the same amount of "non-$O_2$" molecules. Can you expand on how there would be a fire risk despite having the same amount of $O_2$?

Indeed, it was pretty stupid question now that I've recalled some physics :-/

What if we consider saunas? From some off-the-cuff calculations it appears water vapour can actually fully displace nitrogen and CO2 at about 60°. So bring down temperature a bit, bump up oxygen -- would it be a usable sauna option?


text:
A photosynthesizing mouse?
N. Shubin's Your Inner Fish makes the point several times that there is a lot of functional similarity between some seemingly remote gene cousins. If that needed reinforcing we have the spider-goat, whose milk contains spider's silk, and a knock-in mouse whose vision resembles that of humans.
The last two examples are interesting because, as I recall, nothing beyond the gene insertion (already a feat) had to be done to confer the extra/new capability. The machinery at the cellular level (for the mouse to perceive a new color or for the goat to somehow process the milk) already existed.
My question is whether it might not be possible in theory to create a mammal with the ability to photosynthesize? If this is a polygenic trait perhaps it would be accomplished in multiple stages. I realize an answer here would be highly speculative but a careful answer might cast some light on the process of conferring new traits/abilities in this way.
While I see no obvious benefit of creating a photosynthesizing mouse, at least the food bills for their maintenance might be low. This sounds like a joke but it's not a trivial benefit.
Thanks for any insights.

Maybe the answer is, "This is not possible because..." That would also be interesting to me.

also read about kleptoplasty

It is almost impossible for following reasons:

For photosynthesis you need chloroplasts
To maintain chloroplasts you need many genes in the nucleus that will support its endosymbiosis

I said almost impossible because there are some natural examples of what you are asking. A sea slug called Elysia  acquires choloplasts from green algae on which it feeds. However, it cannot maintain the chloroplasts and pass them on to the next generation but it acquires enough to appear green and survive on photosynthesis when there is no food.
Another example is that of the protist, Rhopalodia gibba, which acquired a cyanobacteria like organism. This protist already had a red alga derived secondary plastid before it acquired a "green" cyanobacteria. This acquisition gave the host the ability to fix nitrogen in the presence of light.
The case of Paulinella chromatophora is very interesting because the acquisition of an endosymbiont happened very recently. The endosymbiont is close to Synechococcus clade of cyanobacteria.
Intuitively, it can be understood that these kinds of acquisitions would be quite difficult for a multicellular organism.
ADDENDUM
Photosynthesis is a complex reaction which requires a dedicated compartment which not only harvests light and produces ATP but also has enzyme complexes required for anabolism (carbon fixation etc).
For now we can accept the hypothesis that it would not be possible for a huge eukaryotic cell to perform these functions in absence of a dedicated organelle. For a discussion on why this is so, you can refer this post.
Having said that, there is an easy way to impart partial photosynthetic ability to a eukaryotic cell. Some archaea and bacteria employ rhodopsin to pump out protons against its gradient, in the presence of light; this is coupled with ATP-synthase just like the complexes of ETC in mitochondria. In this study, Hara et al have expressed delta-rhodopsin in mammalian mitochondia which now makes the mitochondria generate ATP in presence of light. Furthermore, these cells were immune to mitochondrial toxins that affect complex-I activity.
PS: thanks biogirl. I almost forgot about this and I just remembered when I was reading about something else

Chloroplast isn't a necessity for photosynthesis. It takes place without it in many prokaryotes. So although I agree with most of your answer, if someone does try to make photosynthesizing mammals I don't think it would be necessary to make chloroplast.

A question : Would it be easier to incorporate so many genes for all the photosynthesis procedures or to try to insert a chloroplast and then maintain it ?

yes I agree that there are other mechanisms of photosynthesis (non cyanobacterial like) but i was referring to the one that is most common in eukaryotes. Having said so there are different kinds of chloroplasts in eukaryotes too (red algae vs green algae). Plus prokaryotes cannot have chloroplasts- no explanation required. In short plastids are more diverse than mitochondria and chloroplast is just a term for an organelle which can have diverse evolutionary origins.

@biogirl see the edit.. I have added some more information. Nonetheless, chloroplast (and its ancestral free living cyanobacteria) with its light harvesting photosystems, is still one of the most efficient photosynthetic apparatus in nature.

Wow the last study cited sounds really cool ! And yes the original photosynthesizing organisms are very efficient...afterall they are products of millions of years of evolution ! Humans will have to work really hard to replicate them..

Also chloroplast photosystem has higher efficiency than rhodopsin based systems


text:
Effective population size when the population sizes varies from season to season
Let's think of a species which has four generations per year and which population size changes from season to season so that the population size is 100 in summer, 200 in spring, 50 in autumn and 20 in winter for example. In such case, the effective population size $N_e$ can be calculated by:
$$N_e = \frac{n}{\sum_{i=1}^n\frac{1}{N_i}}$$
where $n$ is the number of generation per year (4 in my example) and each $N_i$ correspond to the population size in one season.
My question
Can you please provide an explanation of why this formula (based on the harmonic mean) holds true to define the effective population size?

source

This is derived from studying how heterozygosity changes over time. The standard equation for change in heterozygosity ($H$) with constant population size ($N$) is:
$H_t = \left(1 - \frac{1}{2N}\right)^tH_0$
When $N$ varies between generations you use the product of this formula:
$H_t = \left(1 - \frac{1}{2N_0}\right)\left(1 - \frac{1}{2N_1}\right)...\left(1 - \frac{1}{2N_{t-1}}\right)H_0 = \prod_{i=0}^{t-1}\left(1 - \frac{1}{2N_{i}}\right)H_0$
To get the overall $N_e$ you need to find the population size that gives the corresponding decrease in heterozygocity over t generations i.e:
$\left(1 - \frac{1}{2N_{e}}\right)^t = \prod_{i=0}^{t-1}\left(1 - \frac{1}{2N_{i}}\right)$
Rearranging gives:
$N_e = \frac{1}{2\left[1-\left[\prod_{i=0}^{t-1}\left(1 -\frac{1}{2N_{i}}\right)\right]^{1/t}\right]}$
This expression can be approximated by the harmonic mean, which is easy to verify with some toy data (you get small deviations if yearly population sizes are very small). The explanation given above can also be found in Hedrick (2009, p217ff), along with some nice examples that integrates the effects on effective population size from several factors.

That was simple! Thanks a lot for this very good answer!

Yes, and not very difficult to instead use the exact expression to calculate Ne when you have yearly population sizes.


text:
The effect of depth on net primary production in aquatic ecosystems
The figure shows the relationship between the water depth and net primary production (=P-R). I want to know why the production (P) initially increases with water depth near the surface? I have seen similar relationships from other sources but never seen a clear explanation.

Is the figure referring to gross primary production or primary production per capita?

Textbooks don't give details. At first, I thought the pattern of the productivity correlates with the abundance of phytoplankton. But because the rate of respiration is constant, now I think it is the per capita effect. If it is not the per capita effect, I like to know why the total respiration is constant.

But the texts in the figure (and other similar figuers from different sources) imply that the figure shows NPP = P - R. So I think it is probably not the per-capita effect. But this figure (http://www.jochemnet.de/fiu/Ink1.jpg) shows that the pattern does not emerge from difference in the concentration of phytoplankton.

Ok, a bit hard to answer if it is unclear whether the effect is per capita or the total productivity. For experts in the field I suspect it is obvious though (I'm not an aquatic ecologist). My initial guess was however that the graph showed total primary productivity (for the entire "ecosystem"), and that the dip towards the surface is related to the density of primary producers. Lower density at the surface could then be related to both turbulence (waves) and predator avoidance (among other things).

It looks like the result like the one shown in the figure is based on a controlled experiment using the dark/like bottle method (http://www.jochemnet.de/fiu/Ink1.jpg). Because the density of phytoplankton is controlled in each bottle, we can qualitatively interpret the result as the per-capita effect too. Because of this, the effect should be entirely based on physical factors (e.g., there are no predators in the bottles). Turbulence can still influence the bottles, though.

What book is the figure in the question from, and the figure you link to in the comments? This would be useful to know, so that people can read for themselves and get some context.

After a quick glance at the book "Light and Photosynthesis in Aquatic Ecosystems" by Kirk (2010), I think that the cause for the productivity dip towards the surface partially lies in photoinhibition, due to high light intensities at the surface. Here are a couple of relevant quotes from the book (Google books: p. 371):

In this light saturated state, the electron transport and/or CO2 fixing enzymes (most likely, the latter) are working as fast as they are capable, and so any additional absorbed quanta are not used for photosynthesis at all. From the end of the linear region through to the light-saturated region ([i.e. close to the surface, my addition]), since photosynthetic rate does not increase in proportion to irradiance, (P/Ed steadily falls, see Fig. 10.3) the quantum yield and conversion efficiency necessarily undergoes a progressive fall in value. This is accentuated further if, at even higher light intensities, photoinhibition sets in. If the cells contain photoprotective carotenoids, in which absorbed light energy is dissipated as heat rather than being transferred to the reaction centre...

However, the suspended bottle methods often used to estimate these depth gradients might be part of the problem, by overestimating the effect of photoinhibition, by forcing plancton to stay at the same depth (p 358):

Depth profiles of phytoplancton photosynthesis, such as those in Fig. 10.4, determined by the suspended bottle method, tend to overestimate the extent to which photoinhibition diminished primary production. In nature, the phytoplancton are not forced to remain at the same depth for prolonged periods. Some, such as dinoflagellates and blue-green algae, can migrate to a depth where light intensity is more suitable. Even non-motile algae will only remain at the same depth for extended periods under rather still conditions.

I hope I got the quotes right (quick manual retyping). There are many more relevant sections in the book as well, which seems to cover all kinds of aspects of aquatic photosynthetic efficiency and how this can be a function of depth.

I think it has to do with what wavelength of light is absorbed by photosynthetic organisms at what depth.
Ultraviolet light with short wavelength is absorbed closest to the surface. Red light (which is responsible for photosynthesis) is absorbed at a deeper point in aquatic systems by the primary producers like phytoplankton and metaphyta which increase the productivity of that particular depth.
[I'll include citations, references and diagrams as soon as I find enough time]

The amount of red light monotonically decreases with the depth. So it still does not explain the hump shaped productivity pattern.

Compared to the surface, slightly below the surface in the water column the availability of nutrients increases as winds and ocean currents cause increased mixing of nutrient rich deep water. The photic zone of the water column is quick to use up the macronutrients necessary to sustain primary production, however upwelling of nutrient rich deep water becomes a significant factor in determining an area's production.
[ I will provide citation later. ]

But according to this figure (http://www.jochemnet.de/fiu/Ink1.jpg), the result is based on controlled experiments (the dark/light bottle method). Therefore, the available nutrients are the same along the depth (even if they are naturally variable).

If this is the experiment I believe it is, then the bottles filled at different depths and returned to the same depth they were filled at. This would have a difference in available macronutrients. However this article about the experiment also details that primary production increases just deeper than the surface because "Primary production is usually suppressed just at the surface because the light is too strong there, but reaches a maximum just below the surface because this is where the light optimum occurs. Below the light optimum, production declines rapidly with light."

Article location: http://www-personal.umich.edu/~gwk/teaching/limno/lab/onlinemanual/primaryoxy.html


text:
Statistical method for characterizing the relationship between body mass and metabolic rate
There is a dataset that contains body mass ($x$) and metabolic rate ($y$) from many different organisms. It is common to fit the data to the model of the form $y=ax^b$ and estimate the parameters $a$ and $b$ (see Kleiber's law and The Metabolic theory of ecology). In doing so, it is also common to log transform $y$ and $x$ and create the linear relationship log($y$)=log($a$)+$b$log($x$) and perform linear regression analysis based on the log transformed data. Is this approach better than directly estimating $a$ and $b$ based on nonlinear regression for $y=ax^b$ (because results are different)?

This is more a statistics than biology question, but before choosing a statistical test it is essential to visually inspect your raw data. Is your data skewed at all? BMI in the normal population already has a Gaussian distribution, and I expect metabolic rate also would - so unless you have a reason to log-transform I would not do this. For me there is nothing wrong with performing a linear regression to test the linear association between these traits, and then also test for any non-linear effects (perhaps by including an interaction term between them).

Are you saying that you've tried both and that the results are different (more than the margin of error from the different methods would suggest)? There shouldn't be a difference, as long as the relationship is linear on a log-log scale, beside the uncertainly that lies in the different estimation proceedures (traditionally, a linear regression has been easier to perform)

When you have a nonlinear curve then you should do a non-linear regression and correlation analysis. You can interpolate an exponential function. People are often more comfortable with linear analysis and that is the reason the curve is plotted in a log scale.

Yes, estimated parameters are different in important ways (not negligible numerical errors). I think this is a biology question but am not sure. I am asking analyzing the data based on minimizing the sum of squares (regardless of linearized or nonlinear models). I think the question is in what (biological) space we want to minimize the sum of squares, which depends on, perhaps, the biological understanding of the metabolic theory, which I don't have.

One thing I can think of is that between-individual variation in metabolic rate would be larger for large (mass) individuals. Taking log will stabilize the variance. This kind of explanation is more of statistics than biology. However, this does not happen all the time, especially when we are studying a single species.

I would post this question to the statistics group on StackExchange (Cross Validated) under the "regression" tag.  Dr. Frank Harrell, Professor of Biostatistics and Internationally Recognized leader in regression modeling is on that community. He's a phenomenal teacher and would easily be able to compare and contrast the statistical pitfalls of linear vs. nonlinear regression for that type of problem.

Short answer: The results of the two approaches (linear versus non-linear model) do not match because the relationship between body mass and basal metabolic rate does not strictly follow a power law.

It is indeed the case that if the relationship between two variables follows a power law the two approaches should provide comparable results, but important differences could arise due to Jensen's inequality. In order to test whether the reported differences between the two approaches are due to Jensen's inequality or to some biological factor I obtained data from Kolokotrones et al. (2010) who have in turn taken them from McNab (2008). Kolokotrones et al. (2010) investigated the issue of whether a power law is appropriate by performing linear regression on log-transformed data but they did not attempt to fit the data with non-linear regression.
I've fitted a non-linear model of the form:
$$ B = \alpha M^b$$ , where $M$ the body mass (in grams) and $B$ the basal metabolic rate (in Watts),
which gave coefficients $\alpha = 0.005$ and $b = 0.87$.
I also fitted a linear model of the form:
$$ log_{10}(B) = blog_{10}(M) + log_{10}(\alpha) $$
which gave coefficients $ \alpha = -1.7 $ and $ b = 0.72 $.
It appears that the results of the two approaches are indeed different. Below I plot the results of the two fits. On the variables' original scale we see that the linear model fails to predict observations from species with large mass and that the non-linear model does much better in this respect (upper left). However, when we look at the two models after log-transform, it is clear that the non-linear model fails to predict many observations from species with low mass (upper right). Looking at the residuals of the non-linear model we see that the errors are multiplicative as the variance of the residuals is increasing with (log-transformed) fitted values (bottom left). This indicates that fitting with a linear model on log-transformed data is warranted. However, the plot of linear model's residuals over log-transformed fitted values (bottom right) confirms that the linearity assumption is violated. Thus, neither method is appropriate for this dataset and the quadratic term the authors of the cited paper added in the linear model fitted on the log-transformed variables appears to be warranted in order to account for the observed convexity.

We can conclude that for this dataset the results of the linear model approach do not match those of the non-linear model approach because the data do not strictly follow a power law. Rather, the megafauna appears to follow a different trend compared to smaller animals. Kolokotrones et al. (2010) found that adjusting for temperature improved the linear fit, in addition to the inclusion of the quadratic term. The resulting model was:
$$ log_{10}B = \beta_0 + \beta_1log_{10}M + \beta_2(log_{10}M)^2 + \frac{\beta_T}{T} + \epsilon $$

The R code used to generate the results for this answer along with the data used can be found in the following git repository in GitLab:
https://gitlab.com/vkehayas-public/metabolic_scaling
 References
Kolokotrones, T., Van Savage, Deeds, E. J., & Fontana, W. (2010).
Curvature in metabolic scaling. Nature, 464:7289, 753–756. https://doi.org/10.1038/nature08920
McNab, B.K. (2008). An analysis of the factors that influence the level and scaling of mammalian BMR. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 151:1, 5-28. https://doi.org/10.1016/j.cbpa.2008.05.008.

What will happen during log-conversion is that the large scale variation that happens in data points with high value will be compressed. This will actually produce an estimate that should be more robust toward outliers (because their deviation from the mean will be compressed).
If the data was perfectly modeled (i.e. no or few errors) then it should not matter.
With that said, I don't expect major differences between the two approaches.