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Before Evolution was proposed by Charles Darwin, what were the leading secular theories to explain how life developed?
Outside of evolution, what were the leading scientific schools of thought that Charles Darwin contented with when he published his evolution theory as way of natural selection in 1859?

Hello. I think you'll get the answer to your question on this wiki page. There is probably too much to say in a post. I vote to close because it is too broad. Please let me know if you think the wiki post can't answer your question.

Saltationism maybe?

Darwin stood on the shoulders of giants, most notably Alfred Russel Wallace

@Remi.b I did not know that all theories before Darwinism were listed under the umbrella of evolution. For example the theory of Spontaneous generation, did that ever have any mainstream acceptance within the scientific community?

@GabrielFair absolutely. And it makes total intuitional sense - you take a piece of meat, put it outside, and within a relatively short period of time it has maggots on it. Same thing with hay - cut and dry it in the field, put it on the wagon and bring it back to the barn, and before you know it there are mice in it, which certainly weren't in there before. It feels completely logical. Besides, fresh hay doesn't produce maggots, and rotting meat doesn't produce mice, so the "seeds" of those animals must be within the originating substance.

Of course, not all things behave this way - we know that ducks come from duck eggs, and puppies come from a bitch, and so forth, but when you don't have the knowledge or creativity to set up a completely controlled experiment, it all seems to make a great deal of sense. Remember, the average level of education back then was much lower than today, and most "scientists" (they called themselves natural philosophers) were self-taught.

Most of the evolutionary thoughts presented in the wiki article I linked were build at a time where the word science (and the scientific methodology) didn't even exist, so it is a bit complicated to group those opinions into any category. Lamarckism was clearly an important mode of thinking at the time of Darwin, there are a number of works that kinda anticipated the process of natural selection before Darwin. You can have a look at this history on wiki.

Voted to re-open as it is a valid question with an interesting answer. Broad yes, but philosophical questions such as this one are fundamental to science. Darwin is seen as the founding father of evolution, but some major players pre-dating him set the stage for his appraised evolution theory.

related: How was the resemblance between apes and humans explained in pre-Darwinian biology?

Oh wow, Thanks @fileunderwater, for sharing that.

There were many (more or less) non-theological theories of how life had developed before Darwin, starting at the ancient greeks. Many theories included spontaneous generation but also aspects of modification by descent of existing species (i.e. evolutionary change), but most were not that well developed and complete thought. However, one of the more complete evolutionary theories that pre-dated Darwin was Lamarckism, which claimed that individuals pass on traits that they have acquired during their life time. So the basic idea was that individuals respond and adapt to the environmental conditions they experience, and that these traits are then transferred to their offspring. This is one example of a non-theological theory that pre-dated Darwin, but I cannot really say if it was the leading one. I do know that Lamarck's ideas were relatively ignored during his own lifetime.
Darwin included some aspects of these ideas in his "Origin of Species", but challanged Lamarckism when it came to the main processes of evolution. A weak interpretation of Lamarckism has actually seen a revival after the discovery that epigenetics can be transferred from parents to offspring, see e.g. Heard & Martienssen (2014) and Szyf (2014).

Wow this was really fascinating, I did not know this.

@fileunderwater - shouldn't this question be re-opened? It is a valid question and your answer is great (+1'd fyi)

@AliceD I think the close reason is somewhat valid. You could write a book on this topic. On the other hand, a couple of answers that highlight different theories could probably provide a nice overview for somebody new to evolution.


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What is the most heat-tolerant organism?
What is the most heat-tolerant (or heat loving - hyperthermophile) organism so far identified? What adaptations does this organism have in order to endure such high temperatures?

Methanopyrus kandleri has been able to grow and proliferate at temperatures of up to 122°C when under around 20atm (Takai et. al. 2008).  This was achieved in the lab but the theory should hold true for deep sea thermal vents.  Another strain of M. kandleri survived incubation to 130°C however was unable to reproduce at this temperature.
One of the key adaptions for thermophiles is the selection towards an extremely thermo-stable copy of the enzyme DNA polymerase.  This allows DNA replication at high temperatures and is similar to the 'Taq' polymerase used in the polymer chain reaction in labs, derived from another thermophile, Thermus aquaticus.

References

 Takai K, Nakamura K, Toki T, Tsunogai U, Miyazaki M, Miyazaki J, Hirayama H, Nakagawa S, Nunoura T, Horikoshi K. 2008. Cell Proliferation at 122°C and Isotopically Heavy CH4 Production by a Hyperthermophilic Methanogen Under High-Pressure Cultivation. PNAS 105: 10949–10954.

+1 although Taq is the specific polymerase of T. aquaticus, I am not sure whether there are specific names for M. kandleri polymerase...

I'd add that biochemically speaking, animals and microorganisms from thermal vents tend to have a higher GC content in their genomes, which makes it more thermostable.
All of the proteins are adapted to work at higher temperature.  There are a higher number of salt bridges and specific hydrogen bonds in the proteins to stabilize them - more arginines, more glutamic acids, etc. While this reference says that Cysteine is less common, I imagine anything which is not in a reducing environment will have more disulfide bonds - e.g. for proteins on the cell surface.
Sulferous deep sea vents would tend to be reducing as is the inside of the cell, but maybe in the case of fresh hot water spring extemophiles this may be the case.
Reference:
http://peds.oxfordjournals.org/content/13/3/179.full

What about fire? A grass fire across the prairie or a forest fire generates temperatures in excess of those mentioned here and yet many organisms, mostly plants, need fire to allow for seeds to open and germinate. I know fire is a short-lived situation, but is extreme nonetheless. The bark of the burr oak, for example, is rather resistant to fire.

I was thinking more of organisms which thrive (survive, multiply) in conditions of sustained high temperature. However, you make a good point here!

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DNA synthesis companies: cost per base, turn-around time, codon-optimization algorithms
I would like to synthesize a 3.4kb gene (originally isolated from soil bacteria) and transform it into E. coli. There are several companies (DNA2.0, GeneScript, BlueHeron) which will synthesize the gene for you. I would like to know how these companies (or others) compare with each other in terms of:

Codon optimization - most of the companies are going to codon optimize the sequence and thus increase the protein expression in the desired host. Recently I learned that there are different algorithms that can be applied. I am mostly interested in how the codon-optimization is performed in the different companies and whether there are some direct comparisons of protein expression between them.
cost per base - I would like to find the cheapest one. In general, the cost of gene synthesis usually depends on the size of the fragment, as well as the complexity of the sequence. But on the other hand, DNA2.0 can synthesize 1kb fragment and 5kb fragment for the same price.
Turn-around time - which company will synthesize the fragment the fastest? I think that this mainly depends on size. Of course I have an option of ordering 3 x 1.1kb fragments and joining them myself, but then I have to sequence-verify the final product. So, I need to find the trade-off.

Please, keep in mind that I am not asking about your favorite company, but about specific characteristics of the companies.

The question about price is probably too localized, it changes too fast and those questions are discouraged across the SE network. For the turn-around time you'll only get anecdotes here, which probably won't help much. I'd focus the question on the codon optimization, though I fear the answer will be that the algorithms are prorietary and they won't tell you how they work exactly.

These are good points. I would thing that the information about cost will be valid once you match it with the date on which the answers are posted. As for turn-around time, I came across a blog, where there was a plot of turn-around time vs length of DNA construct for several companies, so average values can be definitely taken into account. But mostly, I really would love to know about their codon-optimization algorithms but perhaps you are right and they are proprietary. Hopefully, the main ideas are not.

Are you working in academia? It might be worthwhile to call the companies directly and see if there is a discounted rate for your institution (another lab or department may have already set something up).
You won't be able to get information on the different algorithms if they are proprietary.  However considering that codon usage data is public and shared knowledge, I can't imagine that the different algorithms are that much different. I think there are some tricks for choosing certain codons near the transcription start site in some organisms? From what I hear, the algorithms are constantly changing. I could tell you how my E. coli optimized gene from GenScript worked two years ago, but they'd probably design it differently now.
Okay - GenScript calls their algorithm "proprietary", so they are not sharing the details. DNA2.0 says their algorithm is patented, so it's out there for inspection. They published a PLOS paper on their E. coli algorithm: Welch et al..
Although, maybe all they do these days is spit out codon sequence randomly:

The results obtained in this study indicate that the codon
  randomization method is a superior strategy for codon optimization. A
  significant improvement in protein expression was obtained for the
  largely established process of chymosin production, showing the power
  of this strategy to reduce production costs of industrial enzymes in
  microbial hosts. (Menzella 2011)

Stitching smaller synthesized fragments works well if you're pressed for time, but it's usually more expensive. However, sometimes these companies do special pricing on synthesis for <1kb, which makes stitching a great choice. Turnaround is generally faster for three 1kb fragments than one 3kb fragment.

Thanks for your answer @Amy. So, you have experience with GenScript. I would like to ask you some specific questions. Would you mind emailing me so that I don't extend my comment into long discussion? My email is gvandova@stanford.edu

Here is a blog post from Ginkgo BioWorks that graphs the turn-times from 3 major suppliers:
http://blog.ginkgobioworks.com/2012/01/14/commercial-gene-synthesis/

Thanks, I already looked at it, but yeah, it is really useful.

And here is a blog post from Reportergene that compares actual prices, even do I agree with Mad Scientist that the question about prize is probably too localized.
http://www.reportergene.com/2011/08/gene-synthesis-review.html

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How does the enzyme ATP Synthase use a proton concentration gradient to make ATP?
I understand what the enzyme ATP synthase does, but I'm not exactly sure how it does it. I've heard that it uses rotary catalysis, but how exactly does this work? How is the energy from the H+ ion harnessed, turned into mechanical energy, and then finally into the chemical energy stored in ATP? Why does the spinning of parts of the enzyme need to occur for this to happen?

Image from wikipedia page on ATP synthase
In brief, the addition and release of protons to the structure cause a conformational change that leads to another conformational change.  This series of conformational changes occurs in such a way that it induces a rotational motion.
The rotation of the central axel that extends through both hemispheres of this large complex is driven by the proton gradient.  Specific residues in the c12 ring are protonated in order to drive this rotation.  A high concentration of protons (in this picture the high concentration is found above the complex) allows each of the subunits in the membrane to be constantly loaded with H+ ammunition, ready to fire when it comes to be their turn.
The function of this axel is to slightly but significantly change the shape of one subunit at at a time in the red part.
Changing the conformation of subunits in the red part is what allows for the three steps in ATP synthesis to occur: binding of ADP and Pi, catalysis of the formation of ATP, and release of ATP.
All of these changes occur at the molecular level.  The proton forms a bond with a single amino acid of the entire protein complex, but this is sufficient to cause a difference in the most stable 3-dimensional structure of the whole.  This could cause either a cascade of changes that result in a net rotation or it could cause a re-stabilization of the structure due to electrostatic forces.
According to Vinit K. Rastogi & Mark E. Girvin in their 1999 Nature paper on the subject, it's more like the former:

Earlier models proposed simple rotational diffusion of a rigid c12 ring, possibly driven by electrostatic forces. The structural data on protonation-linked conformational changes in subunit c indicate that the process may be more mechanical, with local rotations within subunit c driving larger-scale rotations of the c12 oligomer as a whole, in a `wheels within wheels' type of mechanism.

The whole paper's a good read.  But this is as current as I am on the topic, and it's likely that a more detailed mechanism has been determined for the action of ATP synthase since 1999.


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What is the advantage of using starter cultures for growing bacteria?
Many DNA isolation and protein expression protocols contain instructions to use a starter culture of E. coli that is then used to inoculate the main culture.
What are the advantages of using starter cultures compared to just let the bacteria grow in the same medium for a longer time? When should one use starter cultures and when can one safely skip that first culture?

Growth can be quite slow for some species under certain conditions when the concentration of cells is too low. Log-phase growth is powerful, and so one would like to keep cells in this state for the experiment at hand. Different genes are expressed then compared to a stationary phase.
In addition, you'd like your culture to out-compete a contaminant if there is one. That is more easily accomplished with a starter culture, which is then used to inoculate a larger culture for scale-up. Inoculating directing into the large-sized flask may allow your bacteria to enter a stationary phase, thus giving an opportunity for other species to out-compete your bacteria.

I'm not sure if I'm reading into this incorrectly, but does E. coli (or monocultures in general) function commensally?  e.g., if I inoculate 5 mL or 1 L with the same number of cells, will the 5 mL produce more cells (not density) faster?

If a culture is too dilute, it can have a reduced doubling time.

I agree that a starter culture would out-comete a contaminant (especially if there is no antibiotic in the media).
Another advantage of inoculating with starter culture is that your results concerning plasmid preps or preparing competent cells will be easily reproducible. By inoculating with a colony, the starter number of cells is different each time you do that, so you might not know how long your cells have to grow to reach a certain OD (e.g. for preparing competent cells) or you have to measure the OD before you isolate DNA to be sure that your yields are comparable with your previous ones.


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For how long and how cold should I perform ethanol/isopropanol precipitations of RNA or DNA?
Precipitating nucleic acids using either isopropanol or ethanol is a very common operation, and I've read some very different protocols on the duration and temperature the precipitation should be performed.
I've seen anything from precipitating at room-temperature and centrifugating immediately without any delay to precipitating at -20 °C over night in various protocols.
Is there any published data about the influence of duration and temperature on the yield of the nucleic acid precipitation?

I think the folklore is influenced by how much nucleic acid you are working with. As @Daniel Standage suggests, some conditions wouldn't be influenced by anything.

I always did mine at -80 C, but I never compared the results to other protocols (I don't fix what's not broken). But, I was curious about the same thing, so I looked around. I found one paper discussing this: Paithankar and Prasad, Nuc Acids Res 19(6):1346 (1991)
It shows that at low concentrations, EtOH at RT actually outperforms the precipitations at both 4 C and  dry ice/ethanol bath. That difference is quite big at 100ng/ml DNA and lost when there is more than 10 ug/ml DNA. For typical extractions, based on this data, I'd do it at RT.
On the other hand, Hilario and Mackay say in their book that:

for genomic DNA isolation, different DNA precipitation temperatures
  and incubation times have little effect on recovery rates. One can
  directly centrifuge after adding ethanol without the -20 C incubation,
  and, it -20 C ethanol is not available, room temperature ethanol can
  be used.

They do not, however, provide any citation for that statement.

As a first year molecular biology student, I did a class project on this very question:  trying to see if buffer temperature had an effect on yield during DNA precipitation. This is a far cry from peer reviewed research, but my finding was that there was no significant effect for a wide range of temperatures.


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How do I deal with sticky and viscous samples from cell lysates?
To check a protein expression I pelleted a small amount of E. coli before and after induction and lysed them by redissolving them in SDS-PAGE loading buffer and heating them to 95 °C for 1 minute.
This lead to a solution with some very sticky and viscous parts in it, that make pipetting the sample into the gel wells extremely annoying. As far as I heard, this is probably genomic DNA, and my usual way to deal with this is to centrifuge the samples and only pipet a small part out from the top. This does seem to help sometimes, but not always.
How can I avoid the formation of that sticky and viscious stuff or how can I avoid pipetting that stuff into my wells?

Just to say I have the same problem! So I look forward to the answer.

Yes, it is the genomic DNA that is causing you trouble. Although a brief 1000g spin should bring it all down, the pellet is never tight and you almost always are going to pull up some gunk with the clear supernatant. A better solution is to include a quick sonication step (5-10s) before the 1000g spin. That way, the DNA is sheared and it should pellet better. It has worked for me most times. Also, remember to use a reasonable volume of SDS buffer when you lyse the cells. Too little buffer and its always going to be hard. For comparison, I use about 200ul per 1ml culture pellet and this volume works well for both pre- and post-induced cells.

In addition to gkadam's suggestion, for my protein gels, I heat my samples at 95C for 10 minutes. I would also look into different lysing conditions. Rather than using SDS loading buffer, look into more vigorous lysing steps either with a kit like bug-buster or using a homogenizer. When pelleting your lysate, I've traditionally done a 10,000g spin for 10 minutes.
Maybe I just work with really soluble proteins...

Definitely your suggestions will make things much better. I think Mad Scientist was looking for a quick and dirty way to do it when doing small scale checks for protein expression from a new construct.


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NADH vs. NADPH: Where is each one used and why that instead of the other?
I know NADH is used in cellular respiration and NADPH is used in photosynthesis. What difference does the phosphate group make that the same one isn't or can't be used for both? Is there a greater reason for this separation or is it just coincidental? Why can't the two be interchanged?

The phosphate group in NADPH doesn't affect the redox abilities of the molecule, it is too far away from the part of the molecule involved in the electron transfer. What the phosphate group does is to allow enzymes to discriminate between NADH and NADPH, which allows the cell to regulate both independently.
The ratio of NAD+ to NADH inside the cell is high, while the ratio of NADP+ to NADPH is kept low. The role of NADPH is mostly anabolic reactions, where NADPH is needed as a reducing agent, the role of NADH is mostly in catabolic reactions, where NAD+ is needed as a oxidizing agent.
You'll find some more information about this in chapter 2 of "Molecular Biology of the Cell by Alberts et al.

too bad I only have one upvote to give. A direct link to the section in Alberts that talks about NADH/NADPH was great!

Great use of the link to the chapter - I wish more authors did this.

I personally do not think Alberts et al is a very good reference for this as they do not mention a single anabolic reaction. The supplementary answer by @user9778 does this, and I would suggest the student consult a textbook of biochemistry to find out about biochemistry, not one about cell biology (or biology or molecular biology).

Just to clear out some things:
As stateted above, NADH is produced in catabolic reactions and is later used in the electron transport chain to obtain energy by converting NADH back to NAD+.
NADPH is primarily produced in the oxidative part of the pentose phosphate pathway. NADPH is used in
a) anabolic syntheses to produce cholesterol, fatty acids, transmittor substances and nucleotides.
b) detoxifying processes as an antioxidant. NADPH is for example an essential part of CYP450 in the liver and rereduces gluthatione (one of the most potent antioxidants in nature) in order to make it active once again.

It would be great if you provided some references for your response!

NADPH is found in the cytosol and stroma (chloroplast) of eukaryotes. NADH is more ubiquitous, but mostly found in bacteria and in mitichondria, possibly evidence for the endosymbosis of bacteria in eukaryotes. Neither can pass easily through a membrane.

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Is there are evolutionary explanation for why humans and primates are ticklish? How might it have evolved?
Tickling is a rather interesting phenomenon: When humans or apes are touched in certain areas like the armpits or sides, we respond with laughter AND frantic attempts to stop the assault. Obviously our ticklish areas tend to be very vulnerable, so it makes sense that we would want to protect ourselves, but why do we respond with laughter? How might both of these reactions to tickling have evolved? Do they have the same evolutionary purpose or different ones?

I have heard that rats are also ticklish, so apparently it is not limited to primates.

Tickling probably evolved from a defense mechanism but then gradually changed into a more social action, as explained in Provine, 2005 (PDF):

The neurological mechanism of tickling probably evolved from a reﬂex defense mechanism that protects our body’s surface from external, moving stimuli, probably predators or parasites. Our response to tickle is more varied and complex than the typical reﬂex, but it has some stereotypic, reﬂex-like properties (i.e., we laugh when tickled, struggle to escape the tickler, huddle, fend off the tickling hand). Although you can be tickled to laughter by a machine (Harris, 1999) (PDF), most everyday tickle is yet another social context for laughter and a form of communication.

Actually I find the phenomenon of laughing itself a bit intriguing. Does anyone know how laughing evolved? I think we need to understand that before trying to find an explanation for how why tickling needs to laughter.

@VinayakPathak - This answer talks about that.


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Are some virus loads introduced to human cell but never triggered?
Is there a term or any evidence of phage DNA integrating into chromosomes/ DNA but never being triggered?
For example, could a virus that affected Neanderthals still infect human cells today but is never expressed, triggered, or executed?
How often is latent viral DNA ignored by the host?

There is viral DNA within our genomes. Embedded in the genomes of all vertebrates are the proviral remnants of previous retroviral infections. It is possible that some have conferred biological benefits.
Human endogenous retroviruses (HERVs) represent the proviral phase of exogenous retroviruses that have integrated into the germ line of their host. They are transmitted vertically through the germline and are thus inherited by successive generations in a Mendelian manner.
HERVs possess a similar genomic organisation to present day exogenous retroviruses such as human immunodeficiency virus (HIV) and human T cell leukaemia virus.
Although many are defective through the accumulation of mutations, deletions, and termination signals, some HERVs have been implicated in certain autoimmune diseases and cancers and might have a role in the etiology and pathology of disease.

Within humans, the most recently active ERVs are members of the HERV-K (HML2) family. This family first integrated into the genome of the common ancestor of humans and Old World monkeys at least 30 million years ago, and it contains >12 elements that have integrated since the divergence of humans and chimpanzees, as well as at least two that are polymorphic among humans.
Here we show that the HERV-K (HML2) family has increased in copy number predominantly via reinfection, and that the family has probably retained replication-competent and infectious members for >30 million years. We also present evidence for persistent reinfection by other ERV families within the human genome, and suggest that endogenous retrovirus families are often capable of extremely long periods of smoldering infection.

Long-term reinfection of the human genome by endogenous retroviruses
The viruses in all of us: characteristics and biological significance of human endogenous retrovirus sequences
Demystified . . . Human endogenous retroviruses


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Can elements of one's environment act directly as hormones?
Can pollution and things in an organism's environment serve as hormones?

A hormone is defined as "a chemical released by a cell or a gland in one part of the body that sends out messages that affect cells in other parts of the organism" (I'm just taking Wikipedia definition).
Hormones work by binding to specific receptors present on their target cells so, if there is something in the environment that mimics the hormone, by binding to the same receptor they can act as hormones: these substances are called xenohormones and can often act as endocrine disruptors compounds (EDC), by acting on various organs in the body.
Probably the most known xenohormones are xenoestrogens that are been studied as possibly harmful for human health (e.g. linked to breast cancer), and as an environmental hazards, as they can, for instance, cause reproductive problems in fish.
Xenohormones are not necessarily bad, though. Some analogs of human hormones are used in therapy, having being synthesised specifically, for instance, to have higher potency then their natural counterparts.

Yes, they can.
An example of a man-made chemical byproduct affecting hormone signaling is Bisphenol A (BPA).
There is a vast body of evidence linking BPA to all manners of hormonal misregulation.
It would be impossible to try and enumerate all of the studies, and specific mechanisms or the extent of the signaling pathways impacted by BPA have yet to be clarified, however you can have a look to the huge amount of papers on the matter that you can find on Pubmed.

Now that's concise. :)

Perhaps too concise. Can you elaborate?

answers should contain enough information to stand on their own w/o links.  Links should only be used to support the info in the answer

@KAM I think it may be time to either expand on or remove your answer :)

@KAM: there is no need to take it personally... I suggested an edit to your answer that says pretty much the same thing, but in a more self sufficient way...


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Will a bone marrow transplant change one's blood type?
Will a bone marrow transplant change one's blood type?
Or is the donor blood type matched with the person before transplant?

Bone Marrow transplants are extensively matched in order to prevent rejection. Current matching methodology is HLA matching: Stanford Children's Hospital Guidelines

How are a donor and recipient matched?
  Matching involves typing human leukocyte antigen (HLA) tissue. The antigens on the surface of these special white blood cells determine the genetic make-up of a person's immune system. There are at least 100 HLA antigens; however, it is believed that there are a few major antigens that determine whether a donor and recipient match. The others are considered minor and their effect on a successful transplant is not as well defined.
Medical research is still investigating the role all antigens play in the process of a bone marrow transplant. The more antigens that match, the better the engraftment of donated marrow. Engraftment of the stem cells occurs when the donated cells make their way to the marrow and begin reproducing new blood cells.

However, because the HLA matching doesn't utilize blood-type and the recipient's marrow is destroyed in the process, then if the donor's marrow produces different red blood cells - then so will the recipient with time:

Does my blood type change after SCT or [Bone Marrow Transplant]?
Yes.  The recipients blood type eventually changes to the donor type.  That means if you had a blood type of A+ prior to transplant and your donor had a blood type of O, eventually your blood type would become O.  I may take several weeks, possibly months for your original blood type to disappear, but eventually it will.

What's interesting is that blood-typing is not be expressly necessary with the modern bone marrow transplant process. The danger of mixing two antagonistic blood types in vivo is that the recipient's immune system attacks the foreign red blood cells resulting in body-wide rejection. However, because the immune system's response capabilities are decimated by the destruction of the recipient's bone marrow (usually accomplished via chemotherapy or radiation), it can't mount much of an attack in the first place. That's not to say the body can't mount an attack, or that the donor's tissue can't mount an attack on the recipient (Graft-Versus-Host-Disease [GVHD]) - but the better the HLA match the less likely issues are to arise, which is why we do the more accurate and relevant HLA matching instead of blood-typing.

Great answer. And it's pretty amazing that blood type can change, I never would've thought of that!


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Coincidence that navel is near the womb?
The attachment point of the umbilical cord in a baby girl is very close to where her own baby would develop. Is there something in the evolutionary history of mammals that explains this, or some anatomical constraint? Or is it just a coincidence?

I would say that they are not that close. Yes they are both around the abdomen, but the navel is central to the abdominal cavity and the uterus is quite low in the pelvic cavity, in a non-pregnant woman, (it is even below the pelvic brim, and not even in the peritoneum).

I would say it is a coincidence because:

the navel is in the same place in males, so if it was there for some evolutionary advantage the charachter would be sexually dymorphic, which clearly is not the case.
I cannot think of any specific function of the navel that is related to pregnancy or delivery (or of a specific function of the navel at all for that matters)

Why would it be dimorphic even if it didn't carry an advantage? Usually, sexual dimorphism has to be selected for. Even if the advantage was only to the female, why would the SRY gene code for anyplace else?

@C. Lawrence Wenham: I'm not sure I follow you... what I meant is that if the position of the navel was selected because it was somehow advantageous for pregnancy I would expect the selection pressure not to exist in males...

@nico unless the locus for naval position wasn't sex linked, in which case males would have it in the same place as a side effect of selection for that location in females...


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What exothermic reaction distinguishes warm blooded animals?
I would appreciate an answer specifically in the form of an exothermic chemical reaction. Namely, the one primarily responsible for generating heat in warm blooded animals that does not take place in cold blooded animals.

Don't have time for an answer, but see here, where someone asked a similar question: http://en.m.wikipedia.org/wiki/Wikipedia:Reference_desk/Archives/Science/2011_October_2#section_13. If it's not complete, it should at least get you started.

The first link on that page takes you to an explanation.  One reason is that shivering produces heat in warm blooded animals.  In mammals, which have brown adipose tissue, uncoupling protein 1 disrupts the protein gradient in the mitochondria, leading to release of some energy as heat rather than ATP.

Related: https://biology.stackexchange.com/questions/2503/is-there-a-relationship-between-efficiency-of-cellular-metabolism-and-warm-blood

Brown adipose tissue or brown fat is one of the primary ways of generating body heat, and it is only found in warm-blooded animals. It is brown due to the high numbers of mitochondria, and heat is generated by uncoupling the electron transport chain from ATP synthesis by oxidative phosphorylation.
In the typical (ATP-producing) mitochondria, an energy gradient is formed by storing protons within the inter-membrane space, and these then flow through the ATP synthase to power the generation of ATP from ADP and phosphate. In brown fat mitochondria, Uncoupling Protein 1 (UCP1 or thermogenin) forms a pore in the inner membrane, allowing the proton/electron ratio to reach equilibrium and robbing ATP synthase of its motive power. This is what generates the heat.

From Wikipedia

The heat comes from the release of the proton gradient - it's just being changed from electrical energy to heat energy. I don't know if there's a specific chemical reaction going on...

Kind of like why resistors get hot (though with them, it's electron traffic)?

@Pete - Exactly.

While all animals and even plants generate heat from chemical reactions or mechanical motion of their tissues (like muscle tissues), warm blooded animals have brown fat which has the unusual ability to generate heat directly from metabolic energy.
The particular chemical process you are looking for is performed by uncoupling proteins (UCPs).  They reside in the mitochondria and rather than use the proton gradient in the mitochondria to generate ATP, UCPs pass protons through the membrane and generate heat.
Brown fat is brown because of a relatively large iron content associated with many extra mitochondria (brown adipose tissue appears to be derived from muscle cells and not white adipose tissue).  Its a heat generating organ in humans, particularly infants.


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How was the first ribosome theorized to have been made?
Seeing as ribosomes are what help perform the act of translation itself, and the blueprints for they themselves are in nucleotide sequences, how was the first ribosome theorized to have been made? Also, before there were any ribosome, how was translation theorized to have taken place?

Don't have time to write a complete answer, but you may want to start by reading about the RNA world hypothesis, ribozymes and the central dogma of molecular biology

An interesting take on this question is addressed in Bokov and Steinberg's hypothesis.
They have proposed the ribosome has evolved from a short length (~110bp) of RNA that did not have the translational activity that we associate with ribosomes today.
Instead this short length of RNA carried out alternative functions on RNA in RNA based life. Then overtime the accumulation of mutations occurred, such as duplication events that allowed the RNA strands to fold around one another forming a larger unit. This larger unit may have been able to add building blocks together. Over time natural selection will have guided these strands to be more precise in their building actions.
The details of course aren't entirely filled in yet (it's difficult to do because how long ribosomes have been a staple of life), but it's important to take any seemingly complex structure in organisms, and break them down into potentially useful intermediate evolutionary steps.
Some more reading on this subject here -

An article giving a background of Bokov and Steinberg
Bokov and Steinberg's 2009 paper (believe it's paywalled)
Origin and Evolution of the Ribosome (paper)


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Is it possible for any animals today to have more than one brain?
Is it possible for any organisms in the animal kingdom to have more than one brain?

Do siamese twins count?

Would siamese twins count as two organisms?

"Is it possible" and "does it occur" are different questions. Which one are you interested in?

Oh I thought if someone could show me where it occurs, then it would be possible. I am interested in either.

To some degree the answer depends on your definition of what counts as a brain.
Bilaterally symmetrical organisms tend to have some level of cephalization, which involves the concentration of sensory and inter-neurons at one end of the organism (the head).
This aggregation of neurons at the head is typically more complex than aggregations of neurons elsewhere in the body and so it gets designated as a brain whereas the others are designated as ganglia (if they are outside the central nervous system or nuclei if they are within the central nervous system).
In vertebrates, cephalization is very well developed so the brain is typically much more complex than the ganglia (although the enteric nervous system is pretty awesome, its not the brain). However in many invertebrates, the ganglia at the head of the organism (its brain) is not much more complex than the other ganglia around the body.
For this reason, many invertebrates can survive decapitation (at least for a while) and some like the flat worm, can famously survive and regenerate their head after decapitation.

Spot on. Great answer.

It may be interesting to add that the octopus has a central brain and eight rather autonomous brains per leg, the legs can do things by themselves that the main brain doesn't know, but they follow its instructions. The octopus is widely considered one of the most intelligent and far developed species, with almost no common dna with humans (it split 600mln years ago) and some consider it therefor the most 'alien' organism known to man.


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What are the biochemical interactions between human body and Polyethylene?
Our waterways and oceans are showing increased levels of plastic contamination. These plastics are breaking down into smaller pieces. When one goes to the beach and plays in the surf they often swallow some seawater and thus some amounts of plastics, including Polyethylene.
What are the biochemical pathways or effects of plastic, specifically Polyethylene, in the human body? I am looking for toxicity of both a large amount scenario (plastic bag milkshake) and a small amount (some in ocean water).

PE is not bothered by acids and there is no way humans have a pathway for it, except that for choking or being obstipated. But neither do bacteria or fungi make a dent in the molecule. That's why it's not degraded and collects in the oceans.


text:
How would our vision be improved if our photoreceptors were not backwards?
I'm curious to how much better human eyesight would be if the nerves from our rods and cones were correctly placed behind the receptors?
Are there any Animal Models with correctly placed photoreceptors that we can use as a benchmark?

Octopuses have nerves in the arrangement you want. However I do not know any more detail. Please see if you can find some literature on this topic.

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


text:
Would butterflies prefer drinking blood over nectar?
Knowing that butterflies will drink carrion blood and nectar, I wonder if they would prefer one over the other? The blood has more nutrients like iron and copper that the nectar would not have. Or do they not need nutrients outside of what is found in nectar?

Well nectar contains a lot of sugars which provide a quick fix of energy. It is quite similar to humans in which our bodies much prefer the breakdown of sugars rather than protein or fat breakdown. Blood may provide important nutrients but it lacks a lot of the sugars that nectar has, like fructose, glucose, and sucrose.


text:
What nutrition do flies find in feces?
How are flies able to extract nutrition in feces when the originating animal wasn't able to? What makes flies more capable?

I wonder how much (by percentage) of feces consists of bacteria. These would be added nutrients, wouldn't they? Also, feces are not entirely digested, so even if bacteria provided nothing extra, there would still be nutrition for the taking, with the right enzymes.


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What is a normal healthy amount of Titratable acid in a person's blood?
A person's normal pH for arterial blood is 7.41 and venous blood is 7.36.
But I am curious to what is a normal amount of Titratable Acid in someone's blood?

As you say yourself blood is kept in a slightly basic range (and this is tightly controlled). Why do you think there should be free acid present here?

There are proton pumps involved with pH regulation, right?

@GabrielFair yes, what's your point? Just because there is a proton pump doesn't mean there's free hydronium ion (or any other type of acid ion) in circulation. In fact, in vivo it's exactly the opposite.

Isn't titratable acidity expressed as percent lactic acid? Isn't there lactic acid in the blood?


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Why do live crabs in a bucket prevent each other from escaping?
It has been observed that crabs in a bucket will stop others from easily escaping. This observation has lead to the English language colloquialism crabs in a bucket. Has this phenomena been studied? What are some animal psychology explanations of this?

you might want to either explain the behavior in more detail or cite a source showing it actually occurs, otherwise this is likely to be closed as unclear.

Yeah human beings have always been randomly ascribing human psychology to animal/plant behaviors, which simply makes no scientific sense. Don't think one should treat such interpretations too seriously. They're more of a means to reflect on human beings themselves.

There should be a dictum somewhere that states, "Never ascribe to psychology what is caused by instinct."
By that I mean, the captured crab has a survival instinct. It's not going anywhere on the bottom of the bucket; it needs (I don't even know if I would say, "It wants") to get out. Out means "up", since "sideways" doesn't get them out, which doesn't prevent them from trying that as well (as shown by scuttling around the bottom repeatedly.)
The sides of the bucket are slick; there's nothing to grab onto. So if one crab climbs atop another, suddenly there's something "above" (a shadow? An outcropping? Another crab?) to grab onto to hoist itself up the side. So the crab instinctually grabs onto something above it. Unfortunately for the higher crab, there's nothing for it to hold onto above it, so he falls back into the bucket.
If only they would work together, a few of them might make it out. If they were chivalrous, the females and the young ("women and children") would go first.
I don't really know crab psychology, nor do I know any crustacean psychologists. All kidding aside, however, there have been some attempts to study stress in crustaceans. Science Daily published an article about stress in declawed crabs. What you and I think of as "stress" may be different than how the author thinks of it, but from the article, it's pretty clear that Dr. Elwood means psychological stress. However, there is no evidence to support that; the increased mortality of declawed crabs is more likely to be due to physiological stress (as in the second cited paper.) He has been called out on this by fellow biologists.
Crabs are invertebrates. If you want to learn about invertebrate psychology, the octopus is your animal.
Declawing Crabs May Lead To Their Death
Assessing Stress and Predicting Mortality in Economically Significant Crustaceans


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Is Batesian Mimicry a form a parasitism? To what extent is the species with real defenses harmed by the defenceless species?
It seems like Müllerian mimicry would be an example of mutualism because both species would end up being eaten less by predators that only have to learn one pattern of warning symbols. But to what extent is Batesian mimicry a form a parasitism? It seems like predators who ended up consuming the harmless species would lose some of their conditioning to not eat prey that resembled it, thus harming the species that is actually protected.
How often might this happen in ecosystems where Batesian mimicry is present? Does the presence of a similar unprotected species cause the protected species to be a more common target for predators?
Difference between Batesian and Mullerian mimicry on wikipedia

In my own opinion, I would not classify this as parasitism, as more unpalatable species are eaten with Batesian mimicry (and eating causes death). Parasitic organisms often do not kill the host, whereas in this case, it does. However, you are correct in stating that a unpalatable species with aposematic coloring is detrimented by the presence of a palatable Batesian mimic.
Predators often recognize the aposematic coloring of an unpalatable or dangerous species. They "train" themselves not to eat that particular prey, as it is detrimental. The presence of a Batesian mimic which is palatable or not harmful, in simple terms, "untrains" predators of the harmful nature of that particular aposematic coloring. Predators are "confused", and are thus more likely to eat preys with that aposematic coloring, and results in more death of the species being mimicked, while providing protection to the species that is mimicking.
As far as I'm concerned, within an ecosystem, this phenomenon happens with any Batesian mimicry to some degree. Factors that may influence this degree is the recognizability of the aposematic coloring, as well as the ability of a predator to recognize this coloring.
I hope this clears things up.


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Alternatives to TBE buffer for denaturing polyacrylamide gel electrophoresis of DNA and RNA?
I just stumbled upon an article promoting 10 mM sodium borate as an alternative to the well-known TAE and TBE buffers for agarose gel electrophoresis of DNA (Brody & Kern, 2004). They claim that sodium borate outperforms TBE and TAE at high-voltage conditions due to the significantly lower heat development.
I'm currently using TBE buffer and gels with 7M urea for my denaturing PAA gels, and I'm wondering if there are similar alternative conditions for those denaturing PAA gels of nucleic acids?
I couldn't find anything on using sodium borate for denaturing PAA gels, so I'm wondering if it should work the same as for the agarose gels or if it just isn't a good buffer for that kind of gel.

Brody, J. R. & Kern, S. E. Sodium boric acid: a Tris-free, cooler conductive medium for DNA electrophoresis. BioTechniques 36, 214–216 (2004).

Not related to your question but what voltage are you running your gels? It seems as if your having all sorts of issues with over-heating.

250V (results in ~30-35mA), I'm having no significant overheating problems, but if I could just run the gels faster at higher voltages it might be useful.

@bobthejoe PAGE and PAA gel electrophoresis are the same thing, if you mean a discontinuous gel like SDS-PAGE for proteins that doesn't exist for nucleic acids as far as I know.

@leonardo, I've always heard that its the other way. CE  is run at a high temperature to improve resolution. This is worth a question...

I've used Lithium Borate with an agarose gel and high voltages (>200). Didn't turn out as well as advertised the few times I tried it though - worse than TAE.  If I had to try it again I would definitely lower the voltage.

As you don't have sufficient reputation to post comments everywhere yet, I have converted this for you as it is more a comment than an answer to the question.

Someone appears to have used sodium borate for denaturing acrylamide gels, with no issues: http://www.protocol-online.org/biology-forums/posts/17703.html (no detail on the exact conditions, though).

You can try SB (sodium boric acid), LA (lithum acetate) or LB (lithium boric acid) buffers. Thex generate must less heat then TAE or TBE buffers and can be run on much higher voltages and are much cheaper than TAE or TBE. Also they do not interfere with standard applications such as band excision and they last longer.
For more info try this sites:
http://www.fasterbettermedia.com/products.html
http://ddgehelp.blogspot.com/2008/01/alternative-electrophoresis-buffer-to.html


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How do migrating geese handle hurricanes?
I live on the East coast of the United States, where we are in hurricane season. This week during my morning bike rides in Charlotte, North Carolina, I have seen migrating Canadian geese.
I'm curious if migrating geese have any adaptations for sensing and dealing with hurricanes? Do they treat it like any other rain and wait it out or are there observations of them avoiding a storm?
Here is the range of the Canada Goose.

Do geese migrate far enough south during hurricane season, so that they'd be likely to encounter hurricanes?

yes. I see them overhead now and there is a hurricane coming my way.

Are they actually migrating, or just flying around?  It seems way too early for migration.  And would they have specific adaptations for hurricanes, as opposed to storms in general?

Strongly related question


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Why is there more female mortality in the middle of pregnancy?
NPR writes in Why Are More Baby Boys Born Than Girls? :

Scientists have found some unexpected clues that could help explain
why 51 percent of the babies born in the United States are male.
[...]
So that must mean the skewed sex ratio at birth happens during
pregnancy. Looking deeper, the researchers found that in the very
first week of pregnancy, more male embryos died, possibly as a result
of serious chromosomal abnormalities, which they also documented.
"When that settles out, it looks like there starts to be an excess of
female mortality," Orzack says. "And in the third trimester, as has
been known for a long time, there is a slight excess of male
mortality."

I suggest that you move this question to SE Medical Sciences, which seems to me both more appropriate and a place you are more likely to get an authoritative answer.

If you read the journal article referenced by NPR, the authors give some possible explanations for this phenomenon, including skewed X-inactivation and developmental retardation by the paternal X chromosome. See the second paragraph of the section titled "Overview".

It's worthwhile to note that the researchers were not able to assemble a uniform and random sample spanning all of pregnancy. Their information came from different sources during different stages of pregnancy and so is not directly comparable. Some of the sources are likely to be biased, e.g. amniocentesis is more likely to be performed if a problem is suspected.

The statement quoted in the question is hedging, a clear sign that its authors are uncertain of the reasons for the gender imbalance at birth.  As with anything in the scientific realm, there are usually more variables than can easily be considered or even filtered.
It used to be that about 106 boys were born for every 100 girls.  The numbers of boys are in the decline, a sign of loss in fertility.  This is most probably a result of environmental toxins, but may involve other lifestyle factors as well.
WebMD has a page HERE that details some of this (and the CDC concurs).  As its author points out, new mothers and young fathers tend to conceive more boys than girls--a clear sign that fertility is involved.
One theory, believed by many but still questioned by others, was promoted by Dr. Valerie Grant, Mr. David Rorvik, and Dr. Landrum Shettles (one article HERE).  It involves the physiology of sperm.  Biologically speaking, because the female X chromosome is very large, relative to the Y chromosome, "female" sperm are also claimed to be somewhat larger.  Their advantage is said to be endurance--being likely to survive in the womb longer than the "male" sperm.  But they are thought slower at swimming, particularly given certain environments.  Younger couples tend to be more active, and are more likely to have coitus near the time of ovulation, giving the advantage to the "male" sperm.  There are other factors involved, however, including the levels of acidity in the birth canal, and even how the mother's body protects and nourishes the sperm while waiting for ovulation.
As to why more females are thought to perish mid-pregnancy, the answer may be as boring as that it simply appears to be so because the mortality of boys at both the early stages and the late stages is higher.  Could it be, for example, that boys are more prone to getting strangled by the umbilical cord?  There are some distinct gender differences with respect to the development of the umbilical cord and placenta, including increased risks for boys in the latter period of gestation, as noted HERE.
Even though more boys are born, boys have a lower survival rate.  They can be more accident prone, more likely to succumb to sickness, or to have more impairments from birth defects.  By the early teen years, the male-to-female ratio has usually corrected itself, and by the twenties there are more females in the population.  One chart providing a quick overview of this information for US populations can be seen HERE.

I'd suggest deleting everything after the first paragraph. The 1st paragraph is good, but the rest is not really scientific.  What exactly is meant by a "loss in fertility" and why would that affect the sex ratio at birth? There's no verified link to "environmental toxins" whatever they might be, and so forth.

@Armand If you had followed the links I included, some of your questions might have been answered.  Environmental toxins include elemental toxins like lead, cadmium, mercury, arsenic, bismuth, and antimony as well as biotoxins from other sources.  They come into our environment in many ways, and there are studies showing how they affect fertility.  Toxicologists can quantify the levels of toxins in the body through laboratory tests like a provocative urine test, a hair-mineral analysis, and a newer technology that uses a laser to scan the skin and spectrum analyze it with computer support.

my point is that such "explanations" are so nonspecific as to not be scientific. There is no credible science that I'm aware of indicating that typical exposure levels of any "environmental toxin" affects the sex ratio at birth in the US. Again, the answer says "fertility is involved" - what does that mean? The sperm X or Y content affecting fertilization rate has no credible evidence. The umbilical cord and last paragraph issues seem out of the scope of the question, and the increased mortality rate in the 1st half of pregnancy is real, not an illusion, according to the data shown.


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What protein or other process does the peptide BPC-157 come from?
BPC-157 is a peptide for which there were some studies that suggest that it can help with wound healing and gastrointestinal problems in some animal models. In 2022 the World Anti-Doping Agency added it as a forbidden substance.
A patent suggests that it can be extracted from human and animal gastric juice, but it was from the time before the human genome project, so they don't mention the actual protein it comes from.
My attempts at running BLAST only bring me to the synthetic Usp-BPC-157 and not to any protein that could plausibly be the source in humans or other animals.
Can someone tell me how the body creates BPC-157 naturally, either from what protein it's a breakdown product or otherwise how it gets into human gastric juice?

As far as I can tell, it's a made-up scam.
Almost all of the research on this peptide is done by one person, Predrag Sikirić, who also discovered and patented it.
The claim is that this is the "important part" of some other, larger protein that he claims to have isolated from the gut. E.g. from Jelovac, N., Sikiric, P., Rucman, R., Petek, M., Marovic, A., Perovic, D., ... & Prkacin, I. (1999). Pentadecapeptide BPC 157 attenuates disturbances induced by neuroleptics: the effect on catalepsy and gastric ulcers in mice and rats. European journal of pharmacology, 379(1), 19-31.:

We have identified a new human gastric juice protein with mucosal protective properties and a huge range of organoprotective effects, and with MW 40,000 (determined by gel chromatography), code-named BPC.
...
In line with this, a 15-amino acid fragment (BPC 157), with amino acid sequence, Gly–Glu–Pro–Pro–Pro–Gly–Lys–Pro–Ala–Asp–Asp–Ala–Gly–Leu–Val, MW 1419, and apparently no sequence homology to known gut peptides, thought to be essential for activity of an entire peptide, was characterized and synthesized

Okay, so apparently this MW 40,000 protein has a "huge range of organoprotective effects", except... it doesn't seem it's actually been studied, ever. Let us follow some citations... The earliest paper those passages refer to is this one:
Sikirić, P., Petek, M., Ručman, R., Seiwerth, S., Grabarević, Z., Rotkvić, I., ... & Karakas, I. (1993). A new gastric juice peptide, BPC. An overview of the stomach-stress-organoprotection hypothesis and beneficial effects of BPC. Journal of Physiology-Paris, 87(5), 313-327.
From the paper:

A new gastric juice peptide, Mr 40000, named
BPC has recently been isolated (in preparation)
and its huge range of organoprotective effects has
been described. In this, a 15 amino acid fragment
(BPC 157) thought to be essential for its activity
has been characterized (Sikiri6 et al, 1991a,b,
c,d,e,f,g, 1992a,b).

Okay, so they've already got this peptide from gastric juice, already found and "fully characterized" (quote from the abstract) it, all in just 2 years. I can't think of anything in biology that is fully characterized and it takes decades to do this kind of work with modern methods, yet this was done by one group in a couple years! Within just those a,b,c,d,e,f,g references in 1991 they've already shown that this peptide cures kidney lesions, pancreatitis, colon hypersensitivity, diabetes, liver lesions, and stomach ulcers. And all of this work on the peptide was completed and published before the discovery of the original MW 40,000 protein was ever published (that's the "in preparation" note from the quote; I can't find evidence that the "in preparation" manuscript was ever published). All of these papers with the same lead author. This is not credible, at all: no one can perform all this work. My best guess is that it is made up entirely. The "1991a" reference is this one:
Sikiric, P., Petek, M., Rucman, R., Rotkvic, I., Seiwerth, S., Grabarevic, Z., ... & Udovicic, I. (1991). Hypothesis: Stomach stress response, diagnostic and therapeutical value: a new approach in organoprotection. Exp Clin Gastroenterol, 1, 15-16.
Along with several of these other papers, it makes up the first volume of the journal "Exp Clin Gastroenterol", which appears to have been created solely to host this new, influential work. I can't really find any trace of it. Google Scholar can't find any of these papers. There is an (also sketchy) journal with a similar name hosted at "gastrossr (dot) org" that only took that name in 2002 but does not seem to have any relation.
So, let's review...
A larger protein, never before described but supposedly isolated from the stomach, cures everything. Before this protein is described in the literature (nothing published on it at all), one person has already identified and synthesized the important 15 amino acids from it that are responsible for all of its activities across all body systems. All further research is done with this peptide.
The peptide and precursor protein are unrelated to any other protein (e.g.: your BLAST attempt; also, there is no mention of any related protein in any of these papers, including recent ones).
The peptide is patented by the person who publishes all the papers about it's benefits.
The original work describing the peptide was published in a brand-new journal; I haven't found any evidence that the journal actually exists. I suspect it's a creation of the person who "published" all of its content, including a dozen first-authored papers in the first year that this peptide was discovered.
The name: BPC, stands for "Body Protective Compound". So, before doing this research categorizing all the ways that it protects the body, it was already pre-ordained with the name "body protective compound". I assume this is because the author already knew what his results were going to show, because he planned to make it all up.

Can someone tell me how the body creates BPC-157 naturally, either from what protein it's a breakdown product or otherwise how it gets into human gastric juice?

I can't find any evidence that it does; in a 'research' context it's an entirely synthetic peptide. The papers supporting it seem to be entirely synthetic, as well. As of now there is only one result for a search of "BPC 157" as a treatment/intervention on clinicaltrials.gov; this was a Phase I study that was cancelled; it's not clear whether a single patient was ever enrolled. You can find sources that sell or claim to sell it, in some cases labeled as "for horses", in others as a dietary supplement for humans while repeating some of the dodgy claims in these papers, despite never being studied in people. I won't link to any of these sources for what I think are obvious reasons.

Nice work Bryan!

Even when I hoped for a different kind of answer, this is likely the right one. I sent Examine.com a message over their contact and it will be interesting to see whether they retract their claims.

@Christian I'm not familiar with that website, I don't think I've encountered it before your link here, but I would not really consider it a reliable source, though I'm also not immediately seeing anything there that is wrong, rather that it's misleading merely because it does not provide sufficient context. That's why we have regulatory authorities rather than letting patients decide from direct marketing based on studies: the quality of published evidence requires professional expertise to interpret.

Wow, such a rabbit hole to fall down. I don't understand the economics of all this. This person has published an article about this made up peptide every month for 4 months straight in an MDPI journal this year. They seem to make the rounds every year to different open access publishers.

@IanCampbell It's pretty remarkable, isn't it? And the papers will claim "no conflict of interest" when the author is the guy who has a patent on the main study ingredient... It must be sold by someone for it to catch WADA's attention enough to make a banned list, but it doesn't seem popular enough that anyone reputable has gone after it. I didn't find any press about any accusations of fraud or similar though I didn't look extensively.

I was also surprised by the WADA's action. Could it be guerilla marketing? Fake peptide person convinces friend on WADA to add it to the banned list. Potential customer sees that it is banned and so must be useful and then buys it to get ahead?

@BryanKrause : Examine.com is an independent subscription-based website that hires people with professional expertise. That makes it business-model very different than all those websites that make money with affiliate commissions to sell supplements. The particular article was written by someone with a MS in nutrition and fact-checked by two other people who also have credentials. When it comes to nutritional supplements it's normally one of the better sources. That's why I cite it in the OP instead of citing on of the supplement sale websites.

@Christian Still, their business model sounds like it favors selling supplements: if people subscribe to find out "none of these supplements are supported by actual evidence; if they were, they'd be sold as medications and recommended by doctors", they're not going to hold a subscriber very long who is convinced these things work and looking for someone to tell them that.

@BryanKrause : There's a market for people who do believe that some supplements work and at the same time there's a lot of crap in the supplement market and who want someone they can trust instead of listening to Mercola.

While the concentration of publications from Predrag Sikirić and his group is reason for caution, I can easily find a number of papers from seemingly unrelated groups; not necessarily direct replication papers, but papers that do find effects of a similar type. If its a scam, it sure is an elaborate one. More often than not, individual molecules are the hobby horse of individual researchers for decades; and it has only been in recent years that it has recieved wider attention as far as I am aware.

@EelcoHoogendoorn I'm not really seeing any, but I wouldn't be too surprised that they exist. Doesn't mean that there is any actual science behind the drug. Unfortunately, academic systems are susceptible to this sort of scam. The academic has a huge productive research program: he can point to funding agencies and say look at all these many publications I have about this miracle compound, I must do more experiments! Then, instead of spending the money on actual experiments, they spend the money on publication fees for more publications.

No country is immune to this sort of fraud, and Alzheimer's research in particular has been at the center of major fraud by big names in the US in past years. But countries with less advanced academic systems may be even more susceptible. India and China have each become quite worried lately about the growing poor reputation of their science. Eastern and Southern Europe have had similar issues as they try to compete with their richer neighbors.

With the level of claims being made, if anyone else thought this was a fruitful area of research, there would be dozens or more other labs working extensively on this new miracle peptide and all producing similar results. There aren't, because it's junk, there is nothing to build on, and it's patently obvious to anyone with a biology background. The origin story doesn't make any sense at all. The broad efficacy doesn't make any sense at all. There is no mechanism that makes any sense.

I had another look for Exp Clin Gastroenterol and there is such a journal... Ėksperimental'nai︠a︡ i klinicheskai︠a︡ gastroėnterologii︠a︡ but the earliest date is 2002. There are articles on BPC157 not from Sikiric, but they are few and far between and all in low impact journals with very poor methodology as far as I can see.

Sure, low-to-negative quality publications arnt exactly rare. And replication is known to be an unpopular business. Still, the kind of effects claimed for BPC on simple mouse experiments are amongst the simplest to replicate; nothing like following alzheimer patients for a decade and getting approval for an experimental trial. Just as I am skeptical that bad papers will get negatively replicated quickly, I am not too sure that good ideas can't linger in the margin for decades, while getting sneered at by people who massaged their data into higher impact journals.

https://journals.physiology.org/doi/full/10.1152/japplphysiol.00945.2010
Here is one example, of a taiwanese group with positive findings, with no obvious links to Predrag, published in what appears to be a non-fictional journal.

The patents I can find on the topic seem to be expired. The general thesis that peptide chains of this type can have important regulatory functions is nothing controversial per se; I tend to see a lot of critiques of ozempic, but nobody seems to be disputing people are losing weight. That peptide was being messed around with in labs by just a few people since 1970 before it blew up commercially in recent years. All the while you could have argued 'why doesnt anybody care if this has such a sought after effect and could be the most profitable drug ever'. Well; it wasnt; until it became that.

Nice bunch of work there on the validity of BPC157! But while I personally remain very skeptical, or let's say "cautious" on what's real or not, I think with all respect the main answer here leaves out a bunch of other clinical evidence. YES, the original discoverer of the "supposed" BPC, Sikiric, does appear to be citing his work to validate his work all over the place, which I agree is highly questionable, as is the time frame in which claims are made ..... But, you have either left out or missed the fact that since, there has been a whole bunch of others that have done really in depth studies on BPC and the 157 peptide fraction. There are numerous NLM.NIH.GOV articles citing these studies that most notably do not list Sikiric or any of the other eastern euro named researchers that you see in the earlier references. In particular there is a host of Chinese researchers that have put their names to these studies. Now I certainly agree that this doesn't necessarily "prove" the presence of an actual compound, and even more so any of it's potential benefits, but it does appear to confirm that there are other researchers that studied what they apparently believe to be BPC157. It would be hard to assume anyone would get into examining rat tendon fibroblasts and the effects of a compound that doesn't exist...... I mean I suppose it's possible that THEY are in on promoting a scam as well, but I find it unlikely that that kind of endeavor would go beyond the sole originator and perhaps his inner circle at best. So my research tells me that there are just too many different people that have conducted studies involving BPC157 for it to be a complete scam as far as its very existence. It obviously IS an identified oligopeptide chain, that can be isolated or synthesized. What remains to be seen tho is if it has any actual efficacy that can be proven. Unfortunately because it involves a fairly complex compounding, and the US FDA's ban on any US compounding labs making it for a medicine or supplement, people are left with no way to really know exactly what they are buying and taking without spending all the money to have it analyzed. I immediately became skeptical when researching who sells supposed BPC157 and came to the conclusion that most of them are not actual BPC157, they are Arginate salt "versions" often with SNAC added to make up for assimilation deficiencies. Others try and trick you further and sell you something they call BPC 159.....  in most of them they either list the ingredients as (BPC157) which to me means who knows what it actually is, or they list the 15 amino acid chain...... I can only assume they may just be selling you a capsule full of 15 amino acids and not a peptide at all...... I found one company that at least mentions their ingredient as a "naturally occurring acetylated and amidated form of BPC157" ..... which both of those terms are directly involved in making amino acids into peptides..... So who knows. I guess we wait and see.


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Amount of neurons in the heart
Finding numbers for the amount of neurons in the brain is quite easy. Finding them for other human organs is harder. How many neurons are there in the human heart?

In terms of cell bodies? Zero.  There are autonomic projections from the spinal cord (sympathetic) and vagus nerve (parasympathetic) to the sinoatrial node, the atrioventricular node, and at discrete points in the atria and ventricles.

How can the sinoatrial node fulfill it's function if it doesn't have neurons inside itself? It creates action potentials. Isn't that what being a neuron is about?

@Christian Apologies if my answer was a bit terse.  While the tissue of the SA node is excitable (has channels, etc.) I believe it is still considered to be part of the cardiac musculature.  Some refer to the activity in heart as action potentials, but really it is the effect of passing the electrical excitation along the membrane (in the case of the heart, the musculature) rather than along an axon.


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Is the mesenterium a synonym for the mesocolon?
On biodigital anatomy browser I found a structure called the mesocolon. I didn't find the term in Uberon and I'm unclear whether it's simply a synonym for mesenterium or whether it's a separate concept.

Mesentery is the name of a whole set of tissues attaching the intestines to the abdominal wall.
In human anatomy, there are three different portions of the mesentery:

Mesenterium sensu strictu, also called Meso
Mesocolon transversum
Mesocolon sigmoideum, also called Mesosigmoideum

Two smaller mesenteries can be found at the appendix (Mesoappendix), and at the cranial part of the rectum (Mesorectum)
So... Mesocolon is a part of the mesentery, but no synonym.

Could you specify what the term Mesocolon includes?

Mesocolon includes all mesenteries of only the pelvic colon (Sigmoid colon) and transverse colon. All other parts of the intenstine are held in place either by the Meso or the smaller mesenteries named above.


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Do Alzheimer's patients have spaces in their brain with low interstitial space?
Lulu Xie et al write in their paper Sleep Drives Metabolite Clearance from the Adult Brain:

Using real-time assessments of tetramethylammonium diffusion and two-photon imaging in live mice, we show that natural sleep or anesthesia are associated with a 60% increase in the interstitial space, resulting in a striking increase in convective exchange of cerebrospinal fluid with interstitial fluid. In turn, convective fluxes of interstitial fluid increased the rate of β-amyloid clearance during sleep.

Given that Alzheimer's patients have more β-amyloid in their brains, do they also have less interstitial space?

It's hard to judge whether interstitial space changes are due to beta amyloid accumulation or because the Alzheimer's brain has suffered such profound cell loss and neurodegeneration as a result.
The Nedergaard paper you quote is more about a daily cycle of increase/decrease in interstitial space related to the sleep/wake cycle [Ref 1]. Specifically, that during sleep, there is more space to flush out the brain including beta-amyloid.  One interesting hypothesis from that being that perhaps the accumulation of these aggregates is actually due to inefficient sleep -> inefficient flushing of plaques which go on to give symptoms.  So even if the interstitial space in what's left of the Alzheimer's brain remained the same as a healthy brain, the problem of beta amyloid clearance could still be present.  It remains to be seen if one could restore normal clearance whether degeneration could be slowed and symptoms abated.
[Ref. 1]: Paper from Nedergaard group


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When did CRISPR/Cas9 evolve and what is the likelihood that a superior system for live cell genome editing has already evolved on earth since then?
I've read that CRISPR/Cas9 is currently being implemented and tested for its ability to edit genomes in live cells, and that it is supplanting other genome editing tools in labs, such as TALENs and Zinc finger nucleases.
I understand that there may be a few metrics used for analyzing any genome editing system.  One is the efficiency, which could be measured perhaps in edits per time or edits per molecule.  Another metric might be error-rate.  What is the probability that a genome is altered in something other than the intended way?  Another metric might be the length of the genome that may be edited at once.
I've also read that CRISPR/Cas9 evolved in bacteria.  When did CRISPR/Cas9 evolve in the history of life on earth?
If CRISPR/Cas9 evolved in bacteria, and before other evolutionary advances, including some of those that may have enabled certain multiceullar forms of life, I have to wonder if other systems like CRISPR/Cas9 but superior to it in some metric evolved as well.
How does recombination in sexual reproduction work?  Might it involve biomolecular machinery like that of CRISPR/Cas9?
How does the adaptive immune system work?  How does VDJ recombination work?  Does it involve an advanced (relative to CRISPR/Cas9) genome editing system?
How might one estimate the probability that a system superior to CRISPR/Cas9 exists already?

could you further expand on the question and set out some parameters or perhaps share your thoughts or work on the matter so that any input is constructive.

Lots of interesting questions! Let me try to address a few of them as I don't think I am qualified to answer them all but hopefully I can get this thread started. I am a graduate student in the biophysical chemistry field and have been following a little bit of the Crispr Cas9 craze in the last couple of years. So I am not an expert on Cas9 by any means but I do find it interesting.
Many speculate that as long as their have been cellular life, viruses or some obligate parasites have existed as well. This stems from the idea that viruses perhaps are not "non-self" but rather are parts of the host that happen to become inanimate particles that escape the cell and then find another suitable host. Some viruses have co-evolved with the host, perhaps to prevent other viruses from invading its "home/birth mother". Again, much of this paragraph is just speculation, but it is likely that CRISPR systems, or an adaptive immune systems like it have existed as long as viruses/obligate parasites have.
Error rates, you can look at some of the papers that have come out recently but the idea is that there are a lot of error rates, especially if the RNA is constitutively transcribed from a plasmid. Some people have suggested delivering, not the plasmids for the guide RNAs and the Cas9 protein, but instead, the Cas9 protein complexed to the RNA itself. Other ways to control the amount you deliver to a cell include delivering the RNA for the Cas9 protein so it is eventually degraded. This avoids the complication of delivering DNA which can be transcribed multiple times potentially flooding your cell with cas9 protein or guide RNAs, increasing the likelihood of off target effects. Or you can have the cas9 protein and the guide RNA plasmids under inducible promoters, so you only get expression say if you introduce a small molecule to your cultured organism and limit the amount you deliver of it.
As to if there are other systems "superior" to it, and by superior you mean more efficient, and has less off targeting effects? Sure those things may very well exist, since we haven't sequenced the entire planet yet! All joking aside, maybe start looking around at research groups that do adaptive immunity in prokaryotes, you might find some interesting ideas...
VDJ is a very cool system that I know only a little about but this review might be worth checking out:
"Mechanism and Control of V(D)J Recombination versus ClassSwitch Recombination: Similarities and Differences", which can be found here.
Also recombination in meiotic versus mitotic replication is covered in this review: "Meiotic versus Mitotic Recombination: Two Different Routes for Double-Strand Break Repair", which is available here.
So to answer your question, I will have to defer to someone else!
My question to you is what is "advanced"? Life as we understand it has been evolving for about 3-4 billion years. "Advanced" suggests that one organism has evolved better or faster. I don't know if I would call anything more advanced per se, but maybe more complicated and more capable of rapidly adapting to new environmental pressures? Bacteria have us trumped if there were rapid changes to the environment, global warming, asteroids careening into the planet etc.
Estimating this probability requires knowing how large the entire sequence space of the Earth is, some have estimated 5-50 million eukaryotic species but depends on what metric you would use to define a new species. It is unknown for prokaryotes. My guess is that you have 100's of millions of different organisms that are capable of having some type of adaptive immune system that may be inherently different from CRISPR/Cas9 system but still use some similar elements, like nucleic acid complementation, as a mode of defending against obligate parasites. Then the questions are how many of those organisms have we sequenced and how many proteins do we have any idea how they function based on sequence similarities to other proteins? Or if we have directly characterized their 3D structure based on Cryogenic Transmission Electron Microscopy (Cryo EM), NMR or X-ray crystallography. So, I imagine we have just hit the tip of the iceberg in finding natural enzymes that can function as gene editing and gene locating tools. Plus, we may start designing our own enzymes like what Professor David Baker at UW works on. Huge ocean to go exploring, bring a molecular fishing pole :-)

Thank you for getting the thread started with this interesting response.  To respond to your question about what I mean by "advanced," I suppose I've conflated two separate meanings in the term.  On one hand I am interested in whether a substantially different genome altering system evolved (I suppose that is true with VDJ?) after CRISPR/Cas9, and on the other I am interested in whether any such system provides a measurably "superior" genome editing system.  So I conflated "advanced" in evolutionary time with some practical and measurable superiority for intentional genome editing by humans.

Well you could look at systems like the RISC complex in eukaryotes (RNA interference), or the other Cas9 based systems that function using different PAM recognition motifs or the Cas6 Endonuclease complex which supposedly cuts foreign RNA. Not sure what else may be available, obviously the TALENs systems and Zinc finger nucleases may still be useful tools as they become more high throughput in design.
I think at the moment the type II cas9 system from Streptococcus pyogenes is pretty robust and decently well characterized. So far its a good platform to modify and optimize for exogenous hosts.


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Which protein complex is composed of the greatest number of different kinds of proteins, and how many types are involved?
Why are some protein complexes composed of many different types of proteins? How many different types are they composed of? In particular, which protein complex has the greater number of different types of proteins in it?
For example, I've read that the ribosome consists of 70-80 different types of proteins.
How many different types of proteins are in the spliceosome for example?
I'm using the phrasing "types of proteins" to distinguish aggregates/complexes composed of many different copies of the same protein (i.e. some viral capsids) from those composed of many different kinds (i.e. ribosome, exosome complex, spliceosome).

it is better to say "70-80 different proteins". Saying types impose that there is a classification. They are just different proteins aka polypeptides

I've edited your question to include suggestion by @aandreev. Please feel free to revert at any time.

thanks for the criticism @aandreev. I edited the question to try to clarify why I used "types." Is there a more appropriate terminology to use?

In this paper detailed analysis has been made on spliceosome (U2-type) composition. It should be noted that this complex has dynamic composition. In the paper authors state that up to 170 proteins may associate to a metozoan spliceosome during its course of action. Individual assemblies contain approx 110 proteins (human). Similar complex of the yeast contains approx 60 proteins (precatalytic B complex), while C complexes have 50 proteins, altogether 90 different were identified in yeast. See the linked paper for details.


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Phenotypic Variation of cattle - looking for academic sources
Can someone please point me in the direction of a good academic article on the following:
What are possible sources of phenotypic variation of different 400 day weights of cattle?
Furthermore how much variation is likely to be due to each contributing source?
I have tried the following searches in google scholar:

Phenotypic, genetic, environmental cattle weight
Phenotypic variation cattle weight
Phenotypic variation
Phenotypic variation, genetic
genetic variation, dam, sire

this is a subject that has been well understood by cattle breeders but is not an academic research topic I think.  This is not my field, but this article might point you in the right direction http://www.theatlantic.com/technology/archive/2012/05/the-perfect-milk-machine-how-big-data-transformed-the-dairy-industry/256423/

Online Mendelian Inheritance in Animals (OMIA) is a database of genes, inherited disorders and traits in more than 135 animal species (other than human and mouse). At the moment, it has about 400 entries for Bos taurus, mostly disease phenotypes. This is probably the only attempt to exhaustively list such phenotypes.


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What does entering of sex chromosomes to gametes mean during meiosis I?
I am reading one answer about meiosis:

During meiosis I, the sex chromosomes separate and enter different
  sperm or egg cells (gametes).

I assume that sex chromosomes refer here to homologous chromosomes that experience crossing-over after meiosis that is exchange of genetical information.
Meiosis I refers here to female meiosis I and to male meiosis I.
In both cases, homologous chromosomes separate resulting in haploid cells after meiosis I.
These homologous chromosomes enter sperm or egg cells according to the writer, which I cannot understand, since the given chromosomes, now sister chromatids after meiosis I, do not enter physically anything, they just divide into haploid cells, gametes, after meiosis II.
What is the meaning of the word "enter" in the given sentence?
I am confused by the word "enter".
I am assuming that the word refers to enter something physically which is not the case in my opinion here.

After meiosis I, the resulting cells are haploid, not diploid, but they have 2n chromosomes.

@GerganaVandova So meiosis I is the stage where male (XY -> X and Y) and female (XX -> active X and inactive X). So the resulting cells are haploid.

So that mean that there is no halving of chromosomes anymore in meiosis II, since it is done in meiosis I. Cells are throughout meiosis I haploid, while haploid only after anaphase in meiosis I.

Ok, I am not sure anymore whether the inactivation of the female X chromosome happens right away from anaphase I.

X-inactivation occurs post-fertilization, only if fertilized by a X-carrying sperm. In meiosis I, HOMOLOGOUS chromosomes (meaning your mom and dad's copy of your genes) separate. In meiosis II, SISTER CHROMATIDS (i.e. copies of your mom's or your dad's chromosomes) separate.

@jp89 X-inactivation seems to happen in two places: at the end of meiosis I and then somewhere during meiosis II. - In the former case, there are two daughter cells. The other of the cells gain very little cytoplasm, while the other much. The other with very little cytoplasm will be the polar body.

And then finally the polar body from meiosis I divides to two new polar bodies while the secondary oocyte divides to ovum and one new polar body. So one ovum and three polar bodies. - Ok, the main question still unanswered. - Ok, I will do it, since the answer seems to be that "become" different sperm or egg cells.

@Masi You have some flaws in your logic here. The first polar body does not divide into more polar bodies. Once a polar body, always a polar body. At the end of female meiosis II, your total products is 2 polar bodies and 1 mature ovum.

@Masi And to address the question of X-inactivation, x-inactivation only occurs in diploid XX cells under regulation of the XIST gene from the non-inactivated X chromosome. When homologous chromosomes separate in meiosis I, x-inactivation cannot occur since the XIST gene product from either the paternal or maternal chromosome cannot act on the other X chromosome because they're simply not in the same cell anymore.

@jp89 Are you sure about polar bodies? - If so, then this must a mistake again in Wikipedia and in my lecture materials too: http://en.wikipedia.org/wiki/File:Gray5.svg The picture suggests for instance that the primary polar body can divide again to two polar bodies.

@jp89 The thing does not seem to be so simple: "Sometimes the first polar body undergoes the second meiotic cell division." - Ok, but how that is possible? - The primary polar body is haploid. How can it divide again meiotically and be still haploid? - I would think that mitotic division is needed to have two more polar bodies from the primary polar body.

@Masi See here (http://www.uic.edu/classes/bms/bms655/lesson9.html), here (http://www.ncbi.nlm.nih.gov/books/NBK10008/#A4696) and here (http://faculty.stcc.edu/AandP/AP/AP2pages/reprod/oogenesi.htm). There's also a great diagram in my medical genetics book but it's not on the internet.

@Masi Even if the first polar body divides, it still divides meiotically. It retains it's haploid nature because in meiosis II, sister chromatids separate rather than homologous chromosomes. It is separation of homologous chromosomes (in MI) that results in reduction of ploidy.

I seem to now understand the sentence. I read the clause in other words:

During meiosis I, the sex chromosomes of the gametogonia separate in
  anaphase I and II and become eventually different sperm or egg cells
  after cell differentiation and maturation: male spermiogenesis and
  female maturation into ovum.

Female thing does not seem to have a special name for the maturation thing.
Female does not seem to have differentiation part at the last part similarly as male, since only one ovum is formed after the sequence of events.
Sex chromosomes refer to your parents genotypes. [jg89]
Problem seems to be solved now.
I would not personally use the word "enter" in a such sequence. It is a shortcut. Better would be "enter eventually" or "enter after a sequence of events". I prefer explicity instead of implicity.

Ok, I am not sure whether the last female step has anything to do with differentiation. It seems that it just a maturation step, since there will only be one ovum, while 4 male spermatozoa where the differentiation makes sense. I will fix it. Please, reply if I am wrong.


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Does Human Female Meiosis II occur after fertilization with sperm?
I am reading the answer and I am getting confused by the sentence:

At the end of meiosis I females have two daughter cells and meiosis II
  only occurs if and when fertilization occurs by a sperm cell.

The clause suggests me that meiosis II starts after the sperm has ignited the fertilization process in female: I do not know how that exactly works.
Wikipedia says:

The process of fertilization involves a sperm fusing with an ovum.

So female meiosis II must happen before the sperm fuses with the ovum.
Sperm must ignite some process in female that puts female meiosis II going on before sperm can fuse with egg. Is that right? How is that going to happen?

Primary oocytes are formed prenatally and reain suspended in prophase of meiosis I for years until the onset of puberty. An oocyte completes meiosis I as its follicle matures (during ovulation) resulting in a secondary oocyte and the FIRST polar body. After ovulation, each oocyte continues to metaphase of meiosis II. Meiosis II is completed only if fertilization occurs, resulting in a fertilized mature ovum and the second polar body.
So in short, the egg is stuck in metaphase II until fertilization.

Do you mean that the egg is stuck in metaphase II already before the sperm comes? - Does the egg remain in metaphase II a couple of days each month?

Yes, the secondary oocyte stays in metaphase II throughout ovulation until fertilization. Upon fertilization, the ovum and the third polar body form. If no fertilization occurs, the secondary oocyte (still in meiosis II) is expelled via menstruation.

I am considering know which follicle is at metaphase II here http://biology.stackexchange.com/questions/1205/is-secondary-follicle-or-graafian-follicle-arrested-in-the-second-metaphase-of-o

Meiosis, as you know, have two stages, Meiosis I and II. The oocyte is arrested during metaphase II of MEOISIS II. This arrest is facilitated by a complex called "Cytostatic Factor" (CSF).
After fertilization, the sperm induces a rise in intracellular calcium ion which activates and enzyme, Calmodulin Kinase II. This complex, through a series of phosphorylation and ubiquitination, degrades the CSF comples and in turn, activates APC (Anaphase Promoting Complex). APC will then degrades cyclins, securins and this will promotes the completion of Meiois II.

Sperm must ignite some process in female that puts female meiosis II going on before sperm can fuse with egg.

I think the statement is a bit incorrect. The sperm will ignite (I prefer induce) the above changes and fuse at the same time. Because, what starts all the process above is part of the sperm's cytoplasm that need to be assimilated into the oocyte's cytoplasm.
I hope this clears it all up. Or if you are interested, I can provide the long list of signalling pathways that leads to zygotic development.

Provide a link to the long list?By the way: crossing over is in the "grandma's womb"?

Did you mean "long pathway" or long list? I'd still be interested.  Without knowing I guess induction means setting apart one "haploid" single strand of the egg - must be  - diploid, double strand. As I am into viral infection and how that relates to multi cellularism (CoV-19 induces Syncytia!) this to me as if some "single stranded" "haplo" transfects a regular double stranded host and puts itself in place of the regular second strand. -- So, what happens to the second DNA strand of the female egg DNA? It should "budd off" as a haploid cell with a membrane.

Untill puberty the follicles grown from primordial to antral stage (secondary folliccle) and oocytes are arrested in diplotene of profase I of meiosis I, without polar body, with a nucleous called germinative vesicle. After puberty, with gonadotrophis, they can grow more and ovulate. With LH surge they are stimulated to continuing meiosis and they lose the nucleous and became metafase I oocytes (MI) and extrude the first polar body to became secondary oocytes (MII oocytes) just before ovulation. So, the Graaf folicle, last stage of follicular development, has a secondary oocyte arrested in metafase II. Only after ovulation and with fecundation it is possible to escape from MII arrest and extrude the second polar body.

Nice answer. +1. A referencecwould be nice.


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Do nerve cells cause action potential in cardiac muscle?
I think the answer is no, but I am not 100% sure.
If it was yes, then the dendrite of the nerve cell should each time receive a stimulus causing Na+ channels to open, when the contraction happen.
Also, then it would mean that outside events could alter the function of hearth, which would be dangerous.
The heart has a special excitatory system and a contractile system - Sinoatrial node and Pacemaker cells, which control the action potentials in different portions of the heart.
So heart and primarily myocardium i.e. cardiac muscle can depolarise without any external influence with a slow, positive increase in voltage across the cell's membrane.
Do nerve cells cause action potential in cardiac muscle?

The vagus nerve controls heart rate. This is the best example of a direct nerve action potential impacting cardiac muscle, although one could argue the adrenaline system to be an indirect mechanism.
The vagus nerve is part of the parasympathetic system, it acts to decrease heart rate. Resting heart rate is maintained by permanent vagal stimulation/tone by the release of acetylcholine.

Heart cells will contract on their own without the presence of nervous tissue. If you place small pieces of fresh heart tissue in a Petri dish in a proper solution, they will contract on their own at a frequency somewhat slower than a regular heartbeat. But the pieces may contract independently of one another.
The purpose of stimulation from the vagus nerve is to act like an orchestra conductor causing the contractions of individual cells to act in a coordinated manner.

Can you provide any sources and/or data sets about your claims? It would be great to study basic ECG signals or similar things of such experiments.