text:
Is there a molecular basis to intelligence?
Is there any explanation, gene(s) or whatever detected, that are co-related or explicitly related via mechanical bio-molecular (or at any other level) models that explain the higher or lower intelligence found in different individuals of Homo sapiens?
If so, which and how do they work?

Good question. IMHO, I don't think that there's a "intelligence gene". There's a meta-analysis about it here

Just as a potential starting point for your search: this not a review, but it contains a general discussion on the issue of intelligence heredity and underlying mechanisms - Natural history of Ashkenazi intelligence

As a Drosophila biologist, I will attempt to address the above question by giving an examples from the Drosophila field. When this paper (http://www.ncbi.nlm.nih.gov/pubmed/7720066) in Cell came out, it sent shockwaves around the world since it showed a molecular mechanism by which production of cAMP and activation PKA, effects CREB transcriptional activation and in turn formation of the long-term memory (LTM) in flies. Some of these CREB over expressing flies could learn a task after simply one try whereas wild-types had to do it several times! This work was later followed by mouse studies (http://www.pnas.org/content/100/18/10518.full.pdf) and comparisons to RTS patients were made. At that time there were discussions of CREB being responsible for intelligence however now there is nice nature review/meta-analysis paper (http://www.nature.com/srep/2014/140225/srep04176/pdf/srep04176.pdf), which says there are no evidence connecting CREB and IQ. This paper performs a literature based investigation and identifies several candidates that are testable and can act as biomarkers for intelligence related therapeutic approach to mental retardation. According to their screen dopamine and norepinephrine pathways seems to be important in IQ-related biological processes.
Hope this helps!

When doing studies on genome-wide associations, you WILL find an association between a "gene" and pretty much anything (gene A causes preference of vanilla ice cream over chocolate). So, yeah, there are many associations (and correlations), but there is no single "molecular" cause for intelligence; no matter how strong the 'statistical' association is, causality is hardly ever known for complex traits.


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If the top epidermal layer is burned away, what is it replaced with?
If the squamous (top) layer of epidermis, or skin, is burned or damaged in another way, will it then be replaced by the next layer of below?
Also, from where does the basal membrane originate? Does it regenerate from a different layer of cells?

I edited your question so people might find it easier to answer.  hope that's okay - feel free to re-edit.

The epidermis is a four- or five-layered epithelium. The top layers are squamous whereas the bottom ones are more columnar (http://en.wikipedia.org/wiki/Epidermis_(skin)). The lowest layer is separated from the dermis by the basal membrane (a.k.a. basal lamina, basement membrane).
The process of wound healing in skin is extremely complex and obviously depends on the individual wound and how many layers are destroyed. There is a lot of detail on Wikipedia: http://en.wikipedia.org/wiki/Wound_healing.
If the basement membrane is not disrupted, there are two main components as a rule of thumb: 1) outwards-inwards migration, i.e. cells surrounding a wound will migrate into the wound. 2) bottom-upwards differentiation, i.e. the bottom-most layer contains replicating cells which will differentiate and squamify to regenerate upper layers.
Something like this (picture modified from Wikipedia):
If the wound is bleeding, this means the basement membrane is disrupted and the dermis underneath is also wounded (the epidermis itself contains no blood vessels). In this case, the dermis needs to regenerate first, in a process which is probably similar as described above. Simultaneously, the bottom-most epidermal cell layer will proliferate to close the gap, and then deposit new basement membrane. Remember that the basement membrane is a mesh of proteins, not an actual cell layer.

It would first be good to look at the different layers within the skin  as you mentioned in your question.

The skin is made up of:

Epidermis: the outermost layer of skin, provides a waterproof barrier and creates our skin tone
Dermis: beneath the epidermis, contains tough connective tissue, hair follicles, and sweat glands
Hypodermis: deeper subcutaneous tissue is made of fat and connective tissue

Different kinds of damage can occur to the skin, including burns, which have different degrees based on what layer of skin is damaged and how far down the burn goes.  Therefore, it is not as simple as the epidermis itself getting burned, it could also be much worse and the healing process may be hindered if too much damage occurs.

Burns can happen when the skin is exposed to heat (from fire or hot liquids), electricity, corrosive chemicals, or radiation (UV rays from the sun or tanning beds, or radiation treatments).
Burns are classified as follows, according to the severity of tissue damage:

First degree burns: affect only the outer layer of the skin (epidermis), causing pain and redness. The prototype is mild sunburn
Second degree burns: extend to the second layer of the skin (the dermis), causing pain, redness, and blisters that may ooze; deep second degree burns may progress to third degree burns over the course of several days
Third degree burns: involve both layers of the skin and may also damage the underlying bones, muscles, and tendons; the burn site appears pale, charred, or leathery; there is generally no pain in the area because the nerve endings are destroyed.
Fourth degree burns: extend through the skin and subcutaneous fat into the underlying muscle and bone; are stiff and charred

Depending on the type of burn, different skin generation occurs.  If it is a really terrible burn, then a skin graft from another area of the body may be needed, as it cannot regenerate the epidermis layer due to the excessive damage.

First degree burns are the easiest from which to recover [...] the dermis remains intact and can support the regeneration of the epidermis.  It may happen that the skin will get inflamed (due to responses in the underlying dermis) during this time; the inflammation is to encourage clean-up cells (macrophages) and nutrients to reach the damaged area.

It appears as though the dermis itself will help with the regeneration of the epidermal cells.

In a second degree burn, the dermis is also affected, at least partially.   But, with a second-degree burn, most (or at least some) skin accessory organs typically remain in tact.  Remember, these accessory organs (like glands and hairs) are built from invaginations of the epidermis, creating the epithelium of the glands or hair follicles.  If these organs survive the burn, the epithelial cells that remain will begin to divide to regenerate a new epidermis.
Third-degree burns are the worst.  In these, even the accessory organs are destroyed.  How can we recover from this?  Skin grafts are about the best way, but they cannot really be done across one's entire body, so a very widespread third-degree burn is not usually something that a person can recover from.

AND although this is a separate question and topic, the basal membrane is thought to be of epithelial origin, but this is very complex and still not completely known.  There is more information about it in this article; Cellular origin of the dermal-epidermal basement membrane (Marinkovich et al. 1993).  It is a dated article but has some interesting information.

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What is this red liquid produced by a fungal colony?
In a jar, where I had some orchid plants, a fungi start growing few days ago. I removed the plants and let the fungi to expand and grow more.  After some days, red drops started to appear on the surface of the fungal body (images below).
Does anyone know what this probably can be or recognize the fungi? Is it an antibiotic or something else?

Take this with a massive pinch of salt (which is why I'm posting it as a comment) but I guess the reason the colonies have turned red is that the fungi processes Fe(III) so perhaps this review might shed some light as to what it is you are looking at (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC100245/).

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text:
downloading a reference genome for alignment
I am currently working through the code example on the MATLAB website. It requires me to download the reference genome of Arabidopsis thaliana (thale cress) so I can use BowTie2 to align the Chip-Seq experiment data. I need it in a .fa file.
Since I am very very new to this, what is the database where I can use to download this reference genome? How do I search for something like this? Thanks
EDIT: spoke too soon. I think the NCBI website did it for me. Under the Representitive -> Reference genome section. Is this correct?
EDIT2: The answer was in the MATLAB page also. The bioinformatics toolbox provides a function:
% getgenbank('NC_003070','FileFormat','fasta','tofile','ach1.fasta');
% getgenbank('NC_003071','FileFormat','fasta','tofile','ach2.fasta');
% getgenbank('NC_003074','FileFormat','fasta','tofile','ach3.fasta');
% getgenbank('NC_003075','FileFormat','fasta','tofile','ach4.fasta');
% getgenbank('NC_003076','FileFormat','fasta','tofile','ach5.fasta');

Yes, NCBI is fine. So is http://genome.ucsc.edu or http://ensembl.org or genomes online.

Some organisms have special repositories like Drosophila has flybase.

Since you are using Bowtie, you want the indexed genome, see if that's not available here, instead of downloading the fasta and indexing it yourself.
http://support.illumina.com/sequencing/sequencing_software/igenome.ilmn


text:
Why is allolactose the LacI inducer?
For what reason(s) is allolactose, instead of lactose, the "natural" inducer of lac operon repressor?


text:
What does it mean for a distribution to be "consistent with a two rate-limiting stochastic steps"?
I'm reading a study (full text here) that examine the dynamic of nuclear translocation of a transcription factor in budding yeast, in response of calcium stress. They found that it occurs in bursts, which distribution of durations is plotted on this normalized histogram:

In the text they say:

Normalized histograms, $h(t)$, of total burst duration at two calcium concentrations are both well-fit by $h(t)=te^{-t/\tau}$, with $\tau$ = 70 sec (black line).

And also

This distribution was consistent with two rate-limiting stochastic steps, each with a timescale of ~70 sec.

Can someone explain me the second sentence cited?

WYSIWYG is almost there, but you need one more piece of information to make this explicit.
The distribution cited in the paper is $h(t)\propto te^{-t/\tau}$ (we're going to ignore normalizing constants today). We can recognize this as a particular case of the Gamma distribution, with PDF:
$$f_{\mathrm{Gamma}}(t\,\big|\,k,\theta)\propto t^{k-1}e^{-t/\theta}.$$
In particular, $h(t)$ looks like the PDF of a $\mathrm{Gamma}(2,\tau)$ random variable,
$$h(t)\propto f_{\mathrm{Gamma}}(t\,\big|\,2,\tau)\propto te^{-t/\tau}.$$
So the authors of the paper are claiming that the burst duration $\tau_{\mathrm{burst}}$ is a random variable with a $\mathrm{Gamma}(2,70\,\mathrm{ sec})$ distribution.
How do we get from that to "This distribution was consistent with two rate-limiting stochastic steps?"
If we recall from our stats class (or look up properties of the Gamma distribution on Wikipedia), a Gamma distribution with integer values of $k$ is the distribution of the waiting time for $k$ events to occur in a Poisson process. The setup of a Poisson process is that you are tracking the occurrence of unlikely/infrequent events in time, so the fact that the distribution $h(t)$ of burst times looks like a $\mathrm{Gamma}(2,\tau)$ suggests that the burst duration $\tau_{\mathrm{burst}}$ is determined by the occurrence of 2 stochastic events (with the same "frequency" $1/\tau$). In other words, this distribution is consistent with the following scenario: a nuclear localization occurs, and then will stop after two particular events, where the timing of the events is governed by a Poisson process (which, as WYSIWYG pointed out, is a reasonable model for the occurrence of chemical reactions with reasonably slow kinetics, i.e. you can count individual reactions in time). If this is true, the distribution of $\tau_{\mathrm{burst}}$ will look like $te^{-t/\tau}$.
The authors generalize that statement somewhat by saying that technically there could be more events/reactions required to terminate a localization burst, but all but 2 of those reactions happen extremely rapidly, i.e. there are 2 rate-limiting steps in the decision process (both of which happen to have the same value for $\tau$).

Edit: I realized that one more mathematical point might make this more clear: The statement about the Gamma distribution and Poisson processes above is equivalent to the statement that the sum of $k$ iid random variables with distribution $\mathrm{Exponential}(\tau)$ is a random variable with a $\mathrm{Gamma}(k,\tau)$ distribution. Thus $h(t)$ is literally (up to normalization) the distribution of a sum of 2 independent exponential random variables. If you read up on the connection between the exponential distribution and waiting times that might make the claim in the paper seem more transparent.
Source: https://en.wikipedia.org/wiki/Gamma_distribution#Special_cases
http://en.wikipedia.org/wiki/Exponential_distribution

A very thorough answer, now is truly clear. Thank you!

Do you have any speculations about the identity of the two rate determining steps? Is it plausible that one of them is the binding of the molecule at the DNA (it's a transcription factor) and the other is the translocation process itself?

The article mentions that Crz1 nuclear localization is controlled by phosphorylation and dephosphorylation. If I had to speculate I'd hazard that at least one of the steps is based on phosphorylation (see well-studied examples like the Pho2/Pho4 system in yeast). But I would caution against reading too much into this statement in the paper; without more rigorous tests of the properties of the empirical distribution, it's quite possible that this distribution that fits well "by eye" is not at all related to the process generating the empirical distribution.

The rate limiting step of a reaction is the slowest component of the reaction. So if there are two steps in a reaction, each of these steps will have a rate, and the slowest of those two rates will determine the overall rate of the whole reaction.
As a simple example, consider the equation
$A + B + C\rightarrow AB+C\rightarrow ABC$
If the rate of $A+B \rightarrow AB$ is fast, but the rate of $AB+C \rightarrow ABC$ is slow, then the overall reaction will still be slow.
The figure in your question is showing the distribution of the burst durations, and highlighting the fact that the calcium level has no effect on the burst duration. The second quote is a bit confusing, this is my interpretation:
The functional form which they fitted to the distribution indicates that the expected burst duration is about 70 seconds. I'm not completely sure which stochastic steps they are referring to, maybe translation and subsequent localisation (I think transcription would happen on a different timescale and so could be ignored in this case).
By the way, this paper is a really excellent example of an organism harnessing stochasticity to its advantage in order to synchronise its response to a stimulus (calcium in this case). I just think that it is so cool that the mean response to the signal level can be different to the response to the mean signal level - so counter-intuitive to me. And so much fun!!

Well.. First assume the chemical reactions to be a Poisson's process (which is a right stochastic approximation for processes such as chemical reactions and radioactive decay etc).
While the event of a burst follows a Poisson's distribution, the time interval between two reaction events follows an exponential distribution. (See wikipedia page on Poisson's distribution for details)
Since the both two mentioned steps have approximately equal time scale of ~70 sec we can expect that the mean delay between two reaction events to be equal to 70 sec.
The exponential distribution with a mean τ is:
p(t)=e^(-t/τ)


text:
Why do doctors do chemo or transplantation for cancers that don't respond well to these treatments?
From the UpToDate article on multiple myeloma:

In most people, chemotherapy partially controls multiple myeloma;
  rarely, chemotherapy leads to complete remission.

Also:

Transplantation, when successful, prolongs survival, leads to a
  remission, and, infrequently, cures multiple myeloma. However,
  transplantation has several limitations. The high-dose chemotherapy
  given before transplantation usually fails to kill all of the plasma
  cells, allowing the condition to relapse after transplantation. Such
  treatment also puts the patient at risk for serious infections and
  bleeding, which can be fatal.

UpToDate is used by 700,000+ physicians worldwide; it's not alternative medicine. Thus, if even mainstream medicine recognizes the relative ineffectiveness of chemo and transplantation for multiple myeloma, why do they do it?

This is really a question about healthcare, not about biology and it is off-topic here.

@MadScientist Is there a healthcare StackExchange or something equivalent? thanks

To long for a comment: Its more an ethical thing I would say.
I do research which is connected to melanoma - a cancer which is notoriously treatment resistant, once it started moving. Until very recently there was only one chemotherapeuticum which has pretty low (around 20%) response rates. It was usually tried anyway because its possible that the patients belong to this 20% which respond. If not, treatment was usually not prolonged.
I think its something similiar here. The other problem for chemotherapy is that it is cytotoxic (until we got the small molecule inhibitors which are tested and used today) and the problem is to kill the cancer cells (all when possible) while you leave the rest of the body as unaffected as possible. To get this balance is hard (people tend to react differently to chemotherapy). The other problem is that cancers are not homogenous. So its possible that 99.9% of the cells present respond to chemotherapy and get killed, while a few acquired an additional mutation, which gives them an advantage. The conditions of chemotherapy are very selective.

I know that 97% of multiple myeloma patients have anemia, but do you know if chemo causes anemia?


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What is immunosuppression? Why would one use it?
What is immunosuppression? I know it is used in cancer patients, but why would one want to suppress the immune system?
Do homeopathic physicians ever use immunosuppression, or do only allopathic doctors practice this?

Have you read the Widipedia article or done a simple Google search? Please read up on the vast array of publicly available data, then either [edit] your question to make it more specific, or ask a new question.

You should edit your question and delete the reference to homoepath as this is not medicine but pseudomedicine (or add a real reference for that). Than remove "allopathic" as this is also homeopathic terminology. There is simply medicine (which is all that works) and pseudomedicine (all that claims to work but fails to proof it).

Please look up on immunosuppressants.. you'll find all the reasons on why they are used

Immunosuppression is not used in cancer, in fact it is typically harmful unless of course the cancer is a immune or white blood cell cancer where suppressing their growth may be helpful. What you are perhaps alluding to is that an adverse effect of cytotoxic chemotherapy used in the medical treatment of cancer can cause immunosuppression.
Immunosuppression is helpful when it is causing more harm than good. The immune system is powerful and sometimes when its fighting an infection it can go a little overboard and cause enough damage to harm someone in the long term. In this case immunosuppression is helpful in preventing too high a response. For example in an organ transplant the recipient's immune system may destroy the new organ, but immunosuppression can prevent rejection.
Another case is when there is an autoimmune or inflammatory condition occurring. Rheumatoid arthritis being an example of the former and asthma being an example of the latter. In these diseases inflammation due to the immune system perhaps targeting our own body cells causes damage to our organs or cells and causes the disease. Immunosuppression here can limit or prevent further degradation or sometimes even reverse damage due to inappropriate immune responses.
Interestingly the human body must keep a good balance between being under and overactive. Certain individuals with better ability to control HIV infections or other infections are genetically more likely to also get autoimmune conditions.

Referring to immunosuppression in cancer, I would expect him to be thinking of leukaemias or lymphomas. Immunosuppression is actually quite common there firstly because the cancerous cells are most often (in lymphomas always) themselves immune cells and directly affected by immunosuppressive treatment - on the other hand it is a typical part of bone marrow transplantation procedures, which are sometimes the best or only treatment for these conditions.

Excellent point Armatus. That's what I was referring to in my first sentence but thank you for elaborating it.


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A mutation question from the Indian National Biology Olympiad

DNA was isolated from wild type (Gal+) and mutant (Gal-) E. coli cells and separated by density gradient centrifugation technique. DNA from Gal- strain acquired a lower position. This indicates that the mutation is caused by:
(a) deletion (b) insertion (c) mis-sense mutation (d) point mutation

Me and my friends had an extended discussion on this question and we all agreed that since the Gal- strain acquired a lower position, it was obviously more dense than Gal+ strain. Now, one of them claimed that if the volume were to remain constant, then mass is directly proportional to density hence the insertion mutation should cause increase in mass corresponding to a similar increase in density. I am not convinced by this explanation. They also said that, "Keeping the volume constant is a necessity since the experiment would lose its meaning otherwise". I am curious to know how far these assertions are correct.
After doing some research on this topic on the internet, I found a paper related to this question :
Mutations caused by the insertion of genetic material into the galactose operon of Escherichia coli
The answer given by the organizing committee of the 2nd Indian National Biology Olympiad was (b) insertion.
What could be the possible explanation for such an occurrence? Me and my friends are still unable to grasp the logic behind it even after going through different papers and books.

Volume is not kept constant as adding an insertion will definitely increase volume. In fact the volume of the object does not even matter much in density gradient centrifugation.
https://www.sigmaaldrich.com/technical-documents/articles/biofiles/centrifugation-separations.html. Look at isopycnic centrifugation in this sheet.

@RoniSaiba Yes. I get your point. It makes sense.

Would you want to win a competition run by people who are stupid enough to set this question? It’s complete and utter nonsense to imagine that the increase in mass of DNA caused by an insertion in a gene could have a significant effect on the sedimentation of bacterial DNA of 4 million base pairs, even if it is partially fragmented.

@David Sure, but the question is right:  Four gal negative mutations, which affect the expression of the gal operon severely as described in the preceding paper (Saedler et al.), are characterized as insertions of DNA by CsCl density gradient centrifugation... from https://link.springer.com/article/10.1007/BF00268890

@Bipasha — OK. But poor terminology in the question. "Density gradient centrifugation" comes in different flavours. The isopycnic flavour is something of an experimental rarity these days. There was a question on CsCl centrifugation that I intended to answer by surveying the different types of centrifugation, but I am still too busy.

@David Right, I understand, but please keep an open mind while looking at INBO questions- they are set by professors at HBCSE- the premier institution in the country for research in science. They can make mistakes, sure, but they are definitely not stupid.

Now, one of them claimed that if the volume were to remain constant,
then mass is directly proportional to density hence the insertion
mutation should cause increase in mass corresponding to a similar
increase in density.

I don't think that's quite how it works.  You don't worry about the volumes being used.  In those experiments (I don't know that anyone does them anymore)  the DNA is in a solution of really salty water.  Larger molecules get pushed more to the bottom of the tube, so the mutant DNA is larger, since it was close to the bottom.
https://embryo.asu.edu/pages/equilibrium-density-gradient-centrifugation-cesium-chloride-solutions-developed-matthew#:~:text=Density%20gradient%20centrifugation%20enables%20scientists,molecules%20based%20on%20density%20alone.

Thus, centrifugal force pushes the larger components of a mixture
farther from the rotor and closer to the bottom of the tube.

Larger DNA means an insertion.  Point mutations are not detectable with this method.

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What is this insect? Possible assassin bug? or kissing bug?
I saw this bug (around 2 cm) in the front of the balcony door inside the room.

I googled and found two same insects- Assassin bug and Kissing bug. Could they hide their eggs inside the room? Should I be worried?
I live in Vienna, Austria
Thanks in advance
Update: I found this bug here https://www.massaudubon.org/learn/nature-wildlife/insects-arachnids/western-conifer-seed-bugs
The bug that I saw looks like a Western Conifer Seed Bugs! Do you agree?

I found this bug here https://www.massaudubon.org/learn/nature-wildlife/insects-arachnids/western-conifer-seed-bugs

Kissing bug that carries Chagas disease is in the Americas.

Yes, it does seem to be a Western Conifer Seed Bug (Leptoglossus occidentalis). Not a hazard to people.
Photos from Italian language wikipedia.

This ref below suggests it may be looking for somewhere indoors to wait out the winter. It lays eggs on conifer leaves.
http://www.zin.ru/animalia/coleoptera/pdf/steyrer_perny_2008_new_insect_species_in_austria.pdf
"Two New Insect Species in Austria: One Established, the Other One Not (Yet)" by
Gottfried Steyrer and Berhard Perny,
Forstschutz Aktuell, num 44, 2008

Thank so much for your help. Now I can calm myself down. It sounds harmless. Blaming myself for killing a harmless creature.

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text:
Why is the food we consume right from birth not immunogenic to elicit an immune response?
Excluding the hypersensitive reactions which are individual specific, how is  food we consume considered safe by the immune system?

Actually for few food items we do develop some sort of immunity. Let me give an example—
Suppose in an individual's RBC membrane, there's a specific ABO antigen (let's say the subject has "A" blood group).
Now in that individual, how do you think anti B antibodies will be formed?
It will essentially be due to some food intake and subsequent exposure to 'B Antigen'. Hence we usually tend to say that 'blood group—A' has anti-B antibody.
This article might be helpful (See the section: Basic Biochemistry$>$ABO Phenotype--4th paragraph)

https://www.ncbi.nlm.nih.gov/books/NBK2267/

Can you link to some literature that shows we are exposed to ABO antigens through food?

Yes, sure. I have added  an article.

That's interesting, I never knew that before. Or, if I was taught it once I forgot :)


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How is cognitive ability linked to the presence of sex chromosomes?
Most cases of sex chromosomal abnormalities in humans have a case of learning disability or less developed cognitive abilities. Wikipedia says:

When additional X and/or Y chromosomes are present in 48,XXXY, 48,XXYY, or 49,XXXXY, developmental delays and cognitive difficulties can be more severe and mild intellectual disability may be present

So, the question is simply this: How is cognitive ability linked to the presence of sex chromosomes?

Cognitive impairment does not have to do anything in particular with the sex chromosomes. Downs syndrome results because of trisomy of an autosome and it also results in cognitive impairment.
So, cognitive impairment is associated with incorrect gene dosage. As mentioned in the other answer, most aneuploidies are lethal.
Persons affected by aneuploidies do not just suffer cognitive impairment but also some other physiological problems. It is just very easy for us to notice the cognitive defects. Moreover, brain is a complex organ and neuro-development has a complex regulatory network. So dysregulation of common pathways is likely to affect brain development in a noticeable manner.

There's also the family of https://en.wikipedia.org/wiki/X-linked_intellectual_disability which I think is fair to say is less about the sex chromosomes being important for cognitive ability and more that, like other X-linked genetic disorders, males with a single X chromosome are more likely to show symptoms/stronger symptoms because they have a single copy.

If you are thinking that, say, a chromosome 1 triploidy will not result in cognitive impairment... that's not quite right.  Almost all triploidies result in death.   Same with chr2, chr3, chr4...just about every chromosome is lethal if there are extras.
It's not so much that having extra sex chromosomes is bad for cognitive function, it's that having extra chromosomes is usually lethal, only a few triploidies are even survivable, and they all cause lots and lots of problems, including cognitive impairment.  Having extra sex chromosomes is the mildest one, and it results in lots of comparatively mild problems.


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Are endorphins addictive?
Endorphins are among the brain chemicals known as neurotransmitters, which function to transmit electrical signals within the nervous system. Stress and pain are the two most common factors leading to the release of endorphins. I wanted to know if they are addictive, and found some contradicting answers:

If people can get addicted to risky sports just for the thrills they
  provide, they can also get addicted to painful activities where
  endorphins provide relief, "despite the harm to self and/or others,"
  says Dr. Anna Lembke, chief of addiction medicine at Stanford
  University School of Medicine in an email interview. "For example,
  someone who compulsively cuts herself for the endorphin release is
  causing self-harm. Someone who compulsively runs, even to the point of
  causing musculoskeletal injury, is causing self-harm."

Source:
https://science.howstuffworks.com/life/inside-the-mind/human-brain/can-be-addicted-to-endorphins.htm

In contrast to the opiate drugs, however, activation of the opiate receptors by the body's endorphins does not lead to addiction or dependence.

Source: https://www.medicinenet.com/endorphins_natural_pain_and_stress_fighters/views.htm#
If they are not, how can we explain the 'love' for pain in (this content might be sensitive for some of you) some people?

Wiki suggests that they haven't found a root cause for exercise addiction: https://en.wikipedia.org/wiki/Exercise_addiction#Mechanisms

Addiction specialists and others who study human behavior often catageorize addiction into the two broad categories of physical dependence and psycological dependence. They are not always mutually exclusive, and they can both manifest in serious or mild cases of addiction depending on the person and a number of other factors.
What differentiates them is how they affect your physiology. A person severly addicted to alcohol or opioids can become extremely ill or even die from the withdrawl of those substances, due to the strong physical dependence their body has developed. To my knowledge, people do not experience a physical withdrawl after cessation of compulsive pain seeking behaviors. Since they didn't cite any source, we can only guess as to the intended meaning of your second source, but it's probably related to this lack of withdrawl. A quick search on PubMed shows publications referring to certain endorphins as mediating this type of addiction. Meaning that the endorphin is not addictive per se, but a compulsive or addictive behavior can be communicated to the brain in terms of a native neurochemical pathway which is otherwise a normal part of a healthy brain.
I think the lesson here is to be somewhat skeptical of online sources that don't link to peer-reviewed science. Attempts to simplify a topic for the purposes of communicating with a lay audience often result in more confusion than clarity. And if you search something on PubMed or google scholar, you'll probably find an answer in the same amount of time it took you to post your question here.

Pain is not an endorphin but p substance triggers reactions to form opioids and those are endorphins. There is a lot of research about serotonin and dopamine being highly addictive.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4028699/
Here they review this and explain it a little bit
From a psychological point of view people harm them self because they want to sentence themselves, but there are very much deviations and you can not put anybody in the same pot...

Hi and welcome to biology.se. Answers are expected to explain and give an answer to the question, not mainly link to another source. Please edit your question accordingly to avoid its deletion. Also please have a look into the Help center on answering questions.

I have huge problems dealing with you guys here, there is the explanation Substance P triggers opioid secretion, what else do you need?

It‘s now 2020 and before 1970 they already knew the biomolecular way how pain triggers addiction, and you can not take my 3 words - opioid - substance p - secretion and make a quick google research it‘s awful how you guys are here on this channels.

If you like it or not - in this community an answer is expected to answer something and not point to another resource or a google search only.

Anyway I gave an accurate answer  substance p leads to expression of opioids. Opioids make addictive what do you need more? All the stuff after is just some other stuff to read because it‘s interesting for me and has not a real link to the question above... his question is inaccurate pointing to an interview and not to science, so what do you want from me?

I will review how to answer questions and try to change it I try to help not to disturb threads. And Itms not my goal you feel disappointed by my answers


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Can someone provide resources on human electromagnetic frequencies?
Pardon all of my questions below.  I'm basically looking to find online resources regarding my inquiry.  If you can answer any of them off the bat, that would be awesome!!
It seems that humans and mammals give off certain frequencies from our nervous systems.  For example, dogs are able to sense when their master is coming home, even when their distance is close to a mile away.  Also, cats are able to sense when a human is about to die.  They can feel the frequency the person is giving off, and react differently.

Where can I learn more about this frequency that humans give off?
Has anyone ever done research on this subject?
Is this electromagnetic frequency or something else?
Are there devices that can measure this frequency that the human nervous system gives off?
Are there devices that can generate this frequency that the human nervous system gives off?

http://www.ncbi.nlm.nih.gov/pubmed/15197761

" For example, dogs are able to sense when their master is coming home, even when their distance is close to a mile away."  Do you have a citation for that?

I saw it on a documentary, but I cannot recall which one it was.  It might not have been one mile, but it was a long distance.

I'm sorry, but much of this is pseudoscience. While animals do release electromagnetic radiation, mammals are not capable of detecting it. For example, cats may be able to sense that someone is about to die because they have an excellent sense of smell.

For a start, you could learn about Bioelectromagnetics which is the study of the interaction between electromagnetic fields and biological entities (reference). Electro-magnetic fields are generated by the heart, brain, tissues and cells. These fields are in-turn affected by temperature and the overall mood of a person (reference).
There is a lot of research that is being conducted in the field. You can find a lot of papers relating to the field with a simple search on Google Scholar.
Well technically electromagnetic fields.
There are instruments to measure EMF which are detailed in the Wikipedia page. Here is an article on an instrument made to measure the electromagnetic field of the heart (reference).
Generally, if you have measured the electromagnetic fields in different parts of the body (eg: this article states that the electric field of the heart is up to 50 mV/m, and that of the brain and other vital organs up to 5 mV/m) then it shouldn't be too hard to generate them seeing that EMF generated is a low value (reference).


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Is the book "Bioinformatics for Geneticists" outdated?
I am going to be working with genetics data in my organization's data warehouse next year and helping our biotechnology department.  I work in academic research, but I have very little genomics background.  I was able to find the book called "Bioinformatics for Geneticists" (Edited by Michael R. Barnes & Ian C. Gray) at a used book store for a couple dollars.  It looks like it was published in 2003.  Do you think this book is too outdated, or would I still get a good introduction to the subject?  If you think it's too outdated, what book(s) do you recommend?

I haven't read through all of it, but from the second edition, which I found available online here, it seems to me that it might be a good introduction, but (as expected from the publishing date) it is really missing out on all the next generation sequencing stuff. Which is important, not only because it is my favourite field.
I am not sure what you want to get from it? You say you have little genomics background, but then you got a book that expects you to know the genetics, but explains the bioinformatics.
There's a basic description of the background of sequencing at the NIH website, maybe that helps.

The hyperlink of "here" is not working for me.  Which country are you in?

Germany. It is loading slowly,though. But it works, and I checked, it is not as site we might have some kind of paid subscription for.

After it downloaded, I got an exe.  What happens when you run it?  I didn't want to open it at work, so I will wait until I get home and test it.

Well, for me it's just a pdf. Maybe you got an exe for a pdf-reader? I was looking at it from a Mac, so no exe at all.

Yah, maybe.  I'll try it tonight.  Yep, this was Windows.  I'm in the US by the way, but that shouldn't matter.  I was asking because of the latency.  It took several minutes to download.

Well, it is a whole book, with graphs and all. I guess you just need to be more patient or find a faster internet connection. ;-)


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What hair do aquatic mammals have?
I'm reading an essay on the creating of the Mammalia zoological classification (Londa Schiebinger, The American Historical Review, Vol. 98, No. 2 (Apr., 1993), pp. 382-411).
It contains the statement (page 386)

All mammals (including the whale) have hair, and it is still today considered a distinguishing characteristic of mammals.

Is that statement correct? Do all known species of whale and dolphin have hair? If so, where is it? You can't see it on the surface of the animal, is it internal like we have nostril hair?

Well, technically yes, but most adult dolphins do not have hair:

Unlike most mammals, dolphins do not have hair, except for a few hairs around the tip of their rostrum (beak) which they lose shortly before or after birth. The only exception to this is the Boto river dolphin, which has persistent small hairs on the rostrum.

Whales do, and depending on your definition of "hair" - that includes Baleen - which is composed of fine keratin fibers, much like normal fur/hair, which is the distinguishing characteristic of "Baleen whales" (like the Blue Whale).

What about orca or other whales with teeth?

Yes and yes. A lot of marine mammals lose the hair before birth or shortly after, including orcas and many whales. However, because it is present during development, they can be classified as mammals if no other traits are present.

Orcas are dolphins by the way, not whales.

@terdon A lot of 'whales' are actually dolphins, which would be an interesting discussion on it's own.

I'll echo what others have said here. It is a characteristic of marine mammals as mammals. But not something you'd obviously see on adult whales. Humpback whales do have visible hair follicles. Another example where you can see hairs well are on gray whale calves. If you zoom in on this photo, you can actually see a few! This was taken in San Ignacio Lagoon, Baja, California Sur, Mexico.


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Virucides - Herbal and otherwise, for HHV6 type virus or any inner-cell virus
Does anyone know where I can find a reliable list of virucides (not anti-virus) that can be used by humans? This virucide must be able to affect viruses that are already inside the cells. St John's Wort is considered a virucide along with it's other properties, for example.


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Mammary gland development and lactation
I was reading on mammary gland development, and I found this (1):

As a girl approaches her teen years, the first visible signs of breast development begin. When the ovaries start to produce and release (secrete) estrogen, fat in the connective tissue starts to collect. This causes the breasts to enlarge. The duct system also starts to grow.

Wikipedia has an article about the duct system(2):

The development of the mammary gland occurs mainly after birth. During puberty, tubule formation is coupled with branching morphogenesis which establishes the basic arboreal network of ducts emanating from the nipple.

It goes on to say, developmentally, mammary gland epithelium is constantly produced and maintained by rare epithelial cells.

By the pubertal stage, the mammary ducts have invaded to the end of the mammary fat pad. At this point, the terminal end buds become less proliferative and decrease in size. Side branches form from the primary ducts and begin to fill the mammary fat pad.

In the end, I understood that the mammary alveoli (containing milk) are not formed during this. During pregnancy, the ductal systems undergo rapid proliferation and form alveolar structures within the branches to be used for milk production.
And from where is the milk produced? (Just for some more detail)

After delivery, lactation occurs within the mammary gland; lactation involves the secretion of milk by the luminal cells in the alveoli. Contraction of the myoepithelial cells surrounding the alveoli will cause the milk to be ejected through the ducts and into the nipple for the nursing infant.

Three questions:
An interesting case is one of neonatal milk.(3)

It is thought to be caused by a combination of the effects of maternal hormones before birth, prolactin, and growth hormone passed through breastfeeding and the postnatal pituitary and thyroid hormone surge in the infant.

The article doesn't mention anything about developement of mammary alveoli, though. How does that happen, then?

I know milk formation primary requires prolactin, oxytocin and indirectly, estrogen.(4) So does this process wait till pregnancy?(If yes, then the lobes and branches are devoid of any lumen, and they remain empty until pregnancy, which seems skeptical to me.)

Can lactation occur without alveoli formation?

1-
www.hopkinsmedicine.org/health/conditions-and-diseases/normal-breast-development-and-changes%3famp=true
2- https://en.m.wikipedia.org/wiki/Mammary_gland
3- https://en.m.wikipedia.org/wiki/Witch%27s_milk#:~:text=Breast%20milk%20production%20occurs%20in,not%20by%20prematurely%20born%20infants.
4- https://www.ncbi.nlm.nih.gov/books/NBK148970/#:~:text=Hormonal%20control%20of%20milk%20production,indirectly%20in%20lactation%20(2).

You take a long time to ask your questions, and should really restrict yourself to one. But am I to understand that all three relate specifically to the phenomenon of lactation in the neonate and what you want to know about the cells responsible for this? Or are you asking also about the general development and role of alveoli in the pregnant female?

I sure do, but I want the question to reflect what I understand as well- that takes time to write. The questions were related, so I clubbed them and added a bounty; I'll make sure to not repeat this, thanks. Only the first question relates to the neonate.

There is a comprehensive 2012 review of the development of the mammary gland by Macias and Hinck which covers the poster’s question(s). I shall try to summarize the points they make regarding the development of alveoli and their role in milk secretion, ‘borrowing’ two of their illustrations to do so.
Development of mammary gland and role of hormones

At birth there is a rudimentary system consisting of a few rudimentary ductal system.

Until puberty this system grows along with the rest of the organism, under the same hormonal influences that affect other tissues.

At puberty oestrogen — in concert with growth hormone and insulin-like growth factor — accelerates the growth of this ductal system, and its branching is subsequently stimulated by progesterone.

It is only in pregnancy that alveoli form, with a continued requirement for progesterone (perhaps partially indirect) and a specific requirement for a prolactin — which is secreted both from pituitary and — as a different molecule, placental lactogen — from the placenta. The alveoli express the genes for the synthesis of specific milk proteins such as casein, α-lactalbumin and β-lactoglobulin.

[Lactating Mammary Gland: Alveolar cells shown in pink (nuclei blue and milk droplets white) with surrounding adipose tissue yellow]
Oxytocin does not affect the development of the mammary gland (as is made clear in the reference cited by the poster). After parturition it is released from the pituitary in response to the nervous stimulus of suckling and causes the myoepithelial cells around the alveoli to contract causing ejection of the milk.
It should be mentioned that the alveolar cells apoptose on weaning, being replaced by adipocytes. However new alveolar can develop from undifferentiated epithelial cells during a subsequent pregnancy.
Regarding the poster’s specific questions
Q1 The article doesn’t mention anything about development of mammary alveoli, though. How does that happen, then?
A1 The development of the mammary alveoli occurs during pregnancy, under the influence of prolactin/placental lactogen and progesterone.
Q2 I know milk formation primary requires prolactin, oxytocin and indirectly, oestrogen.(4) So does this process wait till pregnancy?(If yes, then the lobes and branches are devoid of any lumen, and they remain empty until pregnancy, which seems skeptical to me.)
A2 The poster’s statements are not completely accurate. Milk formation does not require oestrogen, and oxytocin only affects it in so far as failure to remove milk causes involution. The ducts are indeed devoid of the alveolar lumen until pregnancy, and return to this state on weaning. It is not clear why you are sceptical that this is so. The mammary gland development after puberty prepares the ductal network, but alveolar cells only arise when they are required. Pregnancy is quite long enough for them to develop.
Q3 Can lactation occur without alveoli formation?
A3 I would think not, although the situation regarding neonatal milk secretion (witch’s milk) is unclear because of the obvious ethical barriers to its study in humans. The increase in breast nodule size is suggestive of development. So my opinion is primarily based on argument. The formation of milk requires cells with a specific pattern of gene expression, i.e. of milk proteins and metabolic enzymes that are required for fat formation. It also needs a structure and organization that allows the milk to be secreted into a duct. That is what an alveolus is. Therefore I would imagine that in these circumstances the rudimentary mammary ducts of a new-born infant develop alveoli under maternal hormonal influence.
Postscript
This is a topic I worked on for my doctorate, but have not had contact with for many, many years. It was interesting reading the review — how the technology has changed! I also find it curious that the review makes no mention of corticosterone, as one of the earliest systems for observing alveolar development in vitro was in explants of mammary gland from pregnant mice cultured in defined medium with insulin, prolactin and corticosterone. Perhaps the corticosterone was mimicking what is now known to be the effect of progesterone in vivo.


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What is Pan for in pan-caspase?
A simple question (I could not find it on internet): What is Pan for in pan-caspase? Is it any different from the term 'caspase' ?

can you tell the context of that phrase? If in case of inhibitor it could mean that it inhibits all caspases. Similarly with antibodies: a pan-caspase antibody would bind to all caspases.

there is no specific context but i now realized that it is usually used as pan-caspase inhibitor in the articles i was looking at. just to be sure: can we then say that pan is the opposite of specific?

yes you can say that.. but we generally use the term "caspase-x inhibitor", where x is that specific caspase

The term pan, in my opinion, is perhaps one of the most vague that exists in science! I can partley answer this question (ironically as vague as the term pan) by referring you to the term pan-neuronal. A pan neuronally expressed genes has features, which include the expression of many "generic" genes required non-specifically for neuronal function, such as components of the synaptic vesicle machinery, so pan-neuronal genes are not neurone class specific (http://www.wormbook.org/chapters/www_specnervsys/specnervsys.html). So with that token pan-caspases are a term referring to a general caspase activity/function/structure and not a specific caspase type activity but I would welcome any corrections or edits to this response.

Pan is referring to all. So a pan-caspase inhibitor is a molecule that inhibits all caspases indiscriminately.
Note that pan means all in Greek.


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Does the DNA of a tadpole change after it becomes a frog?
Does the DNA of a tadpole change after it becomes a frog? In other words what changes take place as a tadpole becomes a frog, and does this metamorphosis affect the DNA in any way?
I would appreciate your help. I am doing research for a book I'm in the process of writing. If you can refer me to research material, I would appreciate that also.

Welcome at Biology SE! Your question in the title is valid, but your second question is, I beg your pardon, so unscientific that I think this question will be closed. I suggest to read basic biology textbooks to get basic understanding why organism transform from one to another in an instance. in short it does not work like that.

Is your question a better fit for worldbuilding.SE? If so, we can migrate it there.

Thanks for your reference to the world-building site. I have posted my 2nd question there. Enjoy your day--CC

I'm voting to close this question as off-topic because it has no biological basis.

the question has been edited to probably fit the rules... should we conider reopening this?

Your germline DNA remains the same no matter what you do in the growth process (The DNA of a child is the same as the DNA of the adult). What does change is the expression of the DNA (transcriptomic profile), other regulatory factors (Epigenetic modifications), alternative forms of the same DNA expressed differently (splice site variations and alternative promoters) things like that.
Your somatic DNA does undergo small changes, caused by (retro) transposons, and in a few cells, like the mature B and T cells, they contain only a small subset of a few essential genes (that give them their specificity to an antigen), and other small changes like that (credit: mdperry, see comments).

Thank you for answering my 1st question in layman's terms. I appreciate your time. As for the 2nd part, which is basically a "what if", I will try your world building site.--Best regards, CC

DNA gets methylated in certain places.. That is the only "change" that happens with DNA.

We need to make a distinction between somatic DNA and germline DNA. In vertebrates with an immune system, the B-cells that produce antibodies all contain rearranged DNA in their antibody light chain and heavy chain genes (for example). Similarly the T-cells contain rearranged T-cell receptor genes. These are all somatic cells. In contrast, the germline DNA remains intact and identical until meiosis and the recombination that accompanies crossing over. This fundamental observation (somatic rearrangement) was shown in 1975 by Susumu Tonegawa and Noburo Hozumi.

Also, transposable elements are active in somatic cells of many species and introduce DNA rearrangements.


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What happens when we stretch?
From the wikipedia page on stretching:

Stretching is a form of physical exercise in which a specific muscle or tendon (or muscle group) is deliberately flexed or stretched in order to improve the muscle's felt elasticity and achieve comfortable muscle tone.

How is this improvement of elasticity achieved, at the physiological level?
Searching around on this topic brings a lot of articles about the types of stretches (e.g. again, wikipedia) and what are their benefits and disadvantages.
But how do they differ at the biological level?

here is a youtube video on how stretching work

Short answer: Due to habituation. You do something enough number of times, then that event ceases to be something new, and your body adapts to it.
In this case, you train your body to accept more risks allowing greater lengthening, before it begins to internally signal the muscles that an injury is incoming.
Read below for the slightly longer version:

The stretching of a muscle fiber begins with the sarcomere, the basic unit of contraction in the muscle fiber. As the sarcomere contracts, the area of overlap between the thick and thin myofilaments increases. As it stretches, this area of overlap decreases, allowing the muscle fiber to elongate. Once the muscle fiber is at its maximum resting length (all the sarcomeres are fully stretched), additional stretching places force on the surrounding connective tissue.
There are two kinds of muscle fibers: intrafusal muscle fibers and extrafusal muscle fibers. Extrafusil fibers are the ones that contain myofibrils. Intrafusal fibers are also called muscle spindles and lie parallel to the extrafusal fibers and are the primary proprioceptors in the muscle.
When the muscle is stretched, so is the muscle spindle. The muscle spindle records the change in length (and how fast) and sends signals to the spine which convey this information. This triggers the stretch reflex (also called the myotatic reflex) which attempts to resist the change in muscle length by causing the stretched muscle to contract. The more sudden the change in muscle length, the stronger the muscle contractions will be (plyometric, or "jump", training is based on this fact). This basic function of the muscle spindle helps to maintain muscle tone and to protect the body from injury.
One of the reasons for holding a stretch for a prolonged period of time is that as you hold the muscle in a stretched position, the muscle spindle habituates (becomes accustomed to the new length) and reduces its signaling. Gradually, you can train your stretch receptors to allow greater lengthening of the muscles.

You can read more about it (including the role of the lengthening reaction by the gogli tendon organs) here: http://people.bath.ac.uk/masrjb/Stretch/stretching_2.html#SEC13
It has also been published in a short section in this paper. I am sure you can follow the reference chain if you need to.
Smith, Craig A. "The warm-up procedure: to stretch or not to stretch. A brief review." Journal of Orthopaedic & Sports Physical Therapy 19.1 (1994): 12-17.


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What is the developmental basis of the placental sac?
The placental sac is the organ that provides nutrients to the embryo from the mother.
My question is that, since this obviously involves a lot of complexity, where does the sac originate from  (maternal / embryonic) ?
Also, what is the genetic basis of the above? do the genes intercommunicate between the embryo and the mother ?

I edited your question for it to be more in line with what you are after. I also updated the answer for the same.

We used to spend a few days studying the placenta in our embryology course. The short answer is, both.
Organ level embryogenesis:
The placenta connects the fetus to the uterine wall, and is the organ by means of which the nutritive, respiratory, and excretory functions of the fetus are carried on. It is composed of both fetal and maternal portions. The placenta can be traced right from the moment when the blastocyst is implanted into the uterine wall, though it takes a good portion of 12 weeks to develop.

After this adhesion, the invasion process starts, during which the cytotrophoblast cells from the trophoblast layer migrate deeper into the decidual layer. The formed vacuoles of the embryo become confluent to the uterus with the formation of the lacunar space 13 days after fertilization. The lacunar space will develop into the intervillous space for blood circulation a few weeks later. The placental progenitor stem cell is the cytotrophoblast cell. These cells are responsible for the cellular growth of the placenta, and they have the ability to proliferate and differentiate throughout gestation. The proliferating cytotrophoblast cells provide, after differentiation, the villous syncytiotrophoblasts as the outer cellular layer of the placenta.

I took the above paragraph from here (http://www.medscape.com/viewarticle/780615_2).You can read more about it here (https://embryology.med.unsw.edu.au/embryology/index.php?title=Placenta_Development.)
But for a serious scholarly study, you might be better off using textbooks.
Genetic basis of placental development:
As for the second part of your question, that is the genetic basis of development for a placenta, allow me to lift a paragraph from a book. You must remember that the embryo as it were, is not a distinct entity genetically, in that it contains half of the genes of the mother, and half of the genes from the father. And this is where biology becomes more complex, beautiful and truly mind boggling. It involves intricate interactions between evolution, organogenesis and developmental biology.

These results [in mice] led to an extraordinary conclusion. Paternal genes, inherited from the father, are responsible for making the placenta – maternal genes, inherited from the mother, are responsible for making the greater part of the embryo, especially its head and brain…
David Haig had begun to reinterpret the mammalian placenta, not as a maternal organ designed to give sustenance to the foetus, but more as a foetal organ designed to parasitise the maternal blood supply and brook no opposition in the process. He noted that the placenta literally bores its way into the mother’s vessels, forcing them to dilate, and then proceeds to produce hormones which raise the mother’s blood pressure and blood sugar. The mother responds by raising her insulin levels to combat this invasion, yet, if for some reason the foetal hormone is missing, the mother does not need to raise her insulin levels and a normal pregnancy ensues.
In other words, although mother and foetus have a common purpose, they argue fiercely about the details of how much of the mother’s resources the foetus may have - exactly as they will later during weaning. But the foetus is built partly with maternal genes, so it would not be surprising  if these genes found themselves with, as it were, a conflict of interest. The father’s genes in the foetus have no such worries. They do not have the mother’s interest at heart, except insofar as she provides a home for them.
The father’s genes do not trust the mother’s genes to make a sufficiently invasive placenta; so they do the job themselves…. Modern evolutionary theorists, led by David Haig, now think of the placenta as more like a parasitic takeover of the mother’s body by paternal genes in the foetus. The placenta tries, against maternal resistance, to control her blood-sugar levels and blood pressure to the benefit of the foetus.

Taken from: Matt Ridley, Genome: The Autobiography of a Species in 23 Chapters, Fourth Estate, 2000
For a more scientific explanation, I'd suggest reading the following papers.
Wang, Xu, et al. "Paternally expressed genes predominate in the placenta." Proceedings of the National Academy of Sciences 110.26 (2013): 10705-10710.
Hemberger, Myriam, and James C. Cross. "Genes governing placental development." Trends in Endocrinology & Metabolism 12.4 (2001): 162-168.

Does that mean that the DNA instructions as it were (sorry, not a biologist or scientist of any description) for the development of the sac come from both the mother and the embryo/fetus together? (When/if I get enough rep I'll up-vote your answer! Thank you :) )

Thanks for such a thoughtful and well written answer.  I take it from the Ridley excerpt that, effectively, the placenta is "organised" by the paternal genes of the embryo? I think that maybe my/our (am asking along with a group of pregnant English language teachers) biology defecit prevents us from understanding the finer points (that's probably  a massive understatement), so I hope that the last question doesn't sound silly. EDIT: have been advised to add that some are ex-biologists, of sorts.

@Bob If you are satisfied with my answer, please check the green box next to my answer to accept the same.

I certainly will! I'm a linguist and post a bit on SE EL&U. If it's ok with you, I'll wait a wee bit and see if any answers match your fantastic one? ... and then up-vote your answer!


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Enzyme Inhibition by alpha-2 macroglobulin
Alpha-2 macroglobulin is a plasma protein which acts as an anti-protease. It does so by a "bait mechanism" - the protease cleaves the bait domain, following which a conformational change causes binding of alpha2-macroglobulin with the protease, and consequent irreversible inhibition of the protease.
This seems to be very similar to "suicide inhibition" or "mechanism based inhibition" - when an enzyme catalyses a substrate analog's conversion to an active inhibitor, which subsequently binds strongly to the enzyme to inactivate it.
Is alpha2-macroglobulin's inhibition of proteases a case of suicide inhibition then? If it is, why is not more commonly described as that (I have not come across any description of alpha2-macroglobulin as a suicide inhibitor)?

Lets first see the proper definition of Suicide Inhibition as given by Wikipedia (emphasis mine):

In biochemistry, suicide inhibition, also known as suicide inactivation or mechanism-based inhibition, is an irreversible form of enzyme inhibition that occurs when an enzyme binds $\alpha$ substrate analogue and forms an irreversible complex with it through a covalent bond during the "normal" catalysis reaction. The inhibitor binds to the active site where it is modified by the enzyme to produce a reactive group that reacts irreversibly to form a stable inhibitor-enzyme complex. This usually uses a prosthetic group or a coenzyme, forming electrophilic alpha and beta unsaturated carbonyl compounds and imines.

Now, lets see how $\alpha$-2-Macroglobulin works, again by Wikipedia (emphasis mine):

$\alpha$M protease inhibitors inhibit by steric hindrance. The mechanism involves protease cleavage of the bait region, a segment of the $\alpha$M that is particularly susceptible to proteolytic cleavage, which initiates a conformational change such that the $\alpha$M collapses about the protease. In the resulting $\alpha$M-protease complex, the active site of the protease is sterically shielded, thus substantially decreasing access to protein substrates. Two additional events occur as a consequence of bait region cleavage, namely (i) the h-cysteinyl-g-glutamyl thiol ester becomes highly reactive and (ii) a major conformational change exposes a conserved COOH-terminal receptor binding domain (RBD). RBD exposure allows the $\alpha$M protease complex to bind to clearance receptors and be removed from circulation.

So, clearly, it is not suicide inhibition as:

$\alpha$M protease inhibitor does not form an irreversible complex with the protease, instead it uses steric hindrance to prevent protease from binding any substrate.
this inhibition does not occur during the "normal" catalysis reaction, it is after the protease has catalyzed a reaction that the inhibitor covers it up, more like the consequence of catalysis.
the inhibitor does not bind to protease active site, it covers the active site like a shield.

Putative mechanism of protease entrapment and inhibition by ECAM (Escherichia coli Alpha-2 Macroglobulin)
References:

Suicide Inhibition
$\alpha$-2 Macroglobulin
Structure of protease-cleaved Escherichia coli $\alpha$-2 macroglobulin reveals a putative mechanism of conformational activation for protease entrapment (PDF)


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What makes a strong polyadenylation signal a strong signal?
I was wondering why is it that "AAUAAA" is a strong Polyadenylation signal whereas the rest of the polyadenylation signals show reduced cleavage and polyadenylation efficiency?

because enzymes, responsible for these reactions recognize strong signal more readily?...

Just expanding on aandreev's comment.

Polyadenylation is initiated by binding of CPSF (Cleavage and Polyadenylation specificity factor) after its binding to the AAUAAA motif.
From the introduction of this article:

CPSF (cleavage and polyadenylation specificityfactor) binds to the
  AAUAAA hexamer via its 160-kDa subunit and possibly its 30-kDa subunit
  (Keller et al., 1991; Murthy & Manley,1992; Jenny et al.,1994;
  Barabino et al.,1997). CstF (cleavage  stimulation  factor) binds to
  the U- or G/U-rich element downstream of the cleavage site, and
  stabilizes the binding of CPSF to the AAUAAA sequence of the pre-mRNA
  (reviewed in Colgan & Manley,1997; Wahle & Kuhn,1997).

Any alteration in the CPSF binding site will lead to reduced polyadenylation efficiency. Polyadenylation efficiency also depends on other factors such as secondary structure and presence of proximal CstF sites.


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Why do new atypical antipsychotics like Zyprexa cause TD at lower rates?
When the d2 receptors are blocked for long periods of time they tend to up regulate.  This is what causes tardive dyskinesia.

Why do the newer atypical anti psychotics cause such at a lower rate?  Added tables for clarification of receptors I am referring to.
Zyprexa
D1  35–118  Antagonist
D2  3.00–106    Antagonist
D2L 31–38   Antagonist
D2S 21–52   Antagonist
D3  7.8–91  Antagonist
D4  1.6–50  Antagonist
D4.2    17–102  Antagonist
D4.4    21–60   Antagonist
D5  74–90   Antagonist

Abilify
D1  265–1,170   ND
D2  0.45–3.3    Partial agonist
D2L 0.34–0.74   Partial agonist
D3  0.8–9.7 Partial agonist
D4  44–514  Partial agonist
D5  95–2,590    ND

Haldol(typical antipsychotic)
D1 (silent antagonist) — Unknown efficiency[citation needed]
D5 (silent antagonist) — Unknown efficiency[citation needed]
D2 (inverse agonist) — 1.55 nM
D3 (inverse agonist) — 0.74 nM

If we compare the Haldol to the abilify for example, we see that Haldol is an inverse agonist, which means it turns receptor activity down below baseline. This is more than simply antagonist activity. While abilify is a partial agonist, it can activate the dopamine receptors to some extent, while preventing full activation. Perhaps this is part of the explanation. Haldol really turns down receptor activity, while abilify only partially turns it down. So the cells are less likely to respond to abilify by upregulating dopamine receptor levels. Just a guess, so not an answer.

@user137 that was my guess as well, but then I would assume abilify would have lower TD rates then the other drugs which no literature seems to suggest

So I'm leaving this as comment for now because it isn't well the perfect source.  According to Dr. Peter Breggins book he says they are using lower doses in comparison to the older typical anti psychotics.


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Species that have evolved to be near identical?
Are there any species that are near identical in outward appearance but are separate species?
When I say species I mean can’t interbreed.

I don't know bro. If we cannot identify them so we cannot talk about them, can we? (This definition "Species that have evolved to be near identical" is somehow an identification itself.)

Define your criteria for being identical: outward appearance, similar ecological niches, or what?  My personal favorite are the ichthyosaurs & dolphins, and hummingbirds & hawk moths, but there are many others.

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Differing species of nematodes can be difficult to distinguish.

Simple answer: yes, an uncounted number of them.  You need to read up on two topics: convergent evolution and mimicry.
Convergent evolution is when environmental factors cause different creatures to evolve similar appearance and lifestyle.  Perhaps the classic example of this are the dolphins and ichthyosaurs.  Despite being of different groups - mammals vs reptiles - they both evolved from land-dwelling creatures that adopted a marine lifestyle, and as a consequence a similiar appearance.
Mimicry is when one creature evolves to appear similar to another because that gives them some advantage.  Here the classic example is the viceroy butterfly, which supposedly evolved a similar appearance to the monarch because the latter tastes bad, so that birds avoid eating it.

Can the Monarch & Viceroy interbred?

@William: Not as far as I know, and I would strongly doubt it. (But I'm not an expert lepidopterist.)


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Inverse Agonist vs Neutral Antagonist
Could somebody explain in simplest terms the difference between inverse agonist and neutral antagonist?
Which one is more well natural and less likely to cause pathways to rebound?
Does neutral mean less effect such that stepping from an inverse agonist to neutral is the best idea to avoid withdrawal?
Edit: I am trying to determine how quickly the pathways rebound when stopped during withdrawal.  I would assume this might vary between inverse agonist and neutral antagonist.  I am not asking about actual withdrawal symptoms.

Where did you find these terms?

To those that are reading there are similar questions on this site https://biology.stackexchange.com/questions/6972/do-serotonergic-5-ht2a-mediated-psychedelics-elicit-stimulant-effects  https://biology.stackexchange.com/questions/66394/do-enzyme-inhibitors-change-equilibrium?s=2|40.7686

I will assume you are referring to these terms as used in molecular biology and pharmacology then. Have you looked at the wikipedia pages inverse agonist and receptor antagonist?

Many receptors have a natural constitutive, or "baseline", amount of response that they generate, they're not just an on-off switch. At baseline, many receptors will generate a partial response, which means that certain things binding to them can either increase or decrease their response.
A neutral antagonist is one that causes no change in the signaling response of the thing that it's binding to. It simply stays the same. Note that this can still be important, because a neutral antagonist can block the binding of other agonists, ones that would have generated a change in response, even if the antagonist itself doesn't cause a response.
An inverse agonist is something that decreases the response of the receptor from its baseline all by itself. Often, this is caused by stabilizing the receptor in it's "off" state. If the receptor has some degree of constitutive activity, an inverse agonist will decrease its activity.
See this graph from this wikipedia page for a good explanation:

@William Please stop using the term "brain shock" - if you mean "withdrawal" then use the term others use: withdrawal. Knowing whether a something is an inverse agonist or an antagonist is not sufficient information to predict the extent of withdrawal symptoms.

@Bryan to repeat my question which one is "more natural?"

@William That term doesn't have any meaning outside of pseudoscience unless you give it a particular definition.

@BryanKrause I am trying to understand the long term impact and withdrawal effects of inverse agonists and neutral antagonists.  I can ask another question if mine isn't clear.  You are correct my question is not strictly using scientific terminology because I have found little information understanding differentiating the 2's impact.  What in my question isn't clear?  How quickly do pathways rebound?

@William I thought I already made clear in my comment: Knowing whether a something is an inverse agonist or an antagonist is not sufficient information to predict the extent of withdrawal symptoms.

@BryanKrause Are pathways ability to rebound not independent of their use case?  When I am implying rebound I am implying the restoration of the pathways not the actual withdrawal symptoms.

@William Binding affinity is probably closer to what you are looking for.

What is the horizontal drug column mean?

Why are antagonist listed if they don't do anything?

@William the horizontal axis is drug concentration. This is a particular type of receptor, that does something whether or not a drug or endogenous (thing the body produces) compound is bound to the receptor. Like the answer says, antagonists definitely do something. They compete with other compounds at the binding site. The change in activity of the receptor is only seen when you have two  compounds present. This is not shown in the figure.

@William think about what would happen if you had a neutral antagonist bound to a receptor and you added a full agonist. How would this be different from just adding a full agonist with no antagonist?  Then think about what would happen if you had a neutral antagonist bound to a receptor and you added an inverse agonist. How would this be different from just adding an inverse agonist?


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Compare affinity to potency h1 receptor
This quote from Miller (2004) makes it clear that the affinity of drugs for the H1 receptor does not correlate to sedation:

Although both dosage and affinity for histamine H1 receptors play a part in the sedative effect of a medication, what ultimately determines sedative effect is the amount of the drug reaching the histamine H1 receptors in the central nervous system. For example, quetiapine, which has little affinity for the histamine H1 receptors, is a less potent antipsychotic medication and requires many more milligrams to be effective than do higher-potency medications such as risperidone and ziprasidone. Because of this, quetiapine has a greater sedative effect on patients in clinical use than do risperidone and ziprasidone.

Is there a mathematical way to compare affinity to potency between different drugs?

There are a few important things to consider as you interpret these data.
Here potency means Chlorpromazine equivalents
When your linked review refers to potency, it is likely referring to the old concept of chlorpromazine equivalents. The table in the article cites Jibson and Tandon in a review in CNS news special report from 2001. This is not a standard peer reviewed article, and I can't access it, but it lists relative potency in mg, with chlorpromazine set at 100mg and haloperidol at 2mg:

This is almost certainly chlorpromazine equivalents. You can read a discussion of the limitations of this understanding of antipsychotic potency here, but these numbers are not based on a mathematically rigorous pharmacodynamic analysis. They are not consistent, especially for atypical antipsychotics, and are estimated based on clinical data of the minimum effective dose among other methods.
So, where the affinity in this article, $\frac{1}{K_D}$, has a rigorous pharmacodynamic definition, potency does not. Here it is, effectively, shorthand for how much of a drug you have to administer in order to get a therapeutic effect.
Antipsychotic drugs act at many CNS receptors
To understand exactly what Miller means when he says:

For example, quetiapine, which has little affinity for the histamine H1 receptors, is a less potent antipsychotic medication and requires many more milligrams to be effective than do higher-potency medications such as risperidone and ziprasidone.

You need to understand that $H_1$ receptors do not mediate the primary clinical target. So the lower potency of quetiapine means you have to give more of it to have a clinical effect. Because of the higher typical dose of quetiapine, even though the affinity for $H_1$ receptors is relatively low, you're going to get more binding to $H_1$ than with, e.g., risperidone, which requires a lower dose.
Take a look at the chart in the Richelson and Souder article Miller cites to see the different receptor targets for these antipsychotic drugs.

The primary therapeutic targets (used to characterize the general clinical potency) are (probably) the $D_2$, $5HT_{1A}$, and $5HT_{2A}$ receptors. The action at the $H_1$ receptor is primarily an adverse effect. Miller is trying to say that the sedation effect does depend on affinity at $H_1$, but you also have to consider the dose required to get an effect at $D_2$ and the relevant $5HT$ receptors.
A rigorous definition of potency involves simplification
There is a rigorous definition of potency for an agonist (and also of inhibition for an antagonist, and antipsychotic drugs are antagonists). Potency is both distinct from and dependent on affinity.  I'd recommend Goodman and Gillman Chapter 3, if you'd like to learn more. It's not particularly relevant to understanding this article, in part because Miller doesn't use this definition of potency, and in part because the model involves a single ligand-receptor interaction that directly mediates a desired effect. It's based on the following equation, where $LR^*$ is an activated ligand-receptor: $L + R \rightleftharpoons LR \rightleftharpoons LR^*$.  Because both desired and adverse effects of antipsychotics involve actions at many different receptors even beyond those in Richelson and Souder, the simple model falls short.

Thank you for the response.  I just saw your comment.  I need to get a hold of the book to try to understand more before I assume you explanation isn't adequate.

@William what do you need help understanding?

@William the basic idea here is that the article is talking about a general clinical concept of potency, and the clinical (side) effect of sedation for drugs that are given in very different doses. This is not a single receptor system, and Miller is not talking about the relationship between affinity for $H_1$ and potency at $H_1$. I've studied this a good deal, in and beyond medical school. I'm happy to help answer your questions about it if you need more help. Just ask.

I'm trying to compare the drugs and from what I have gathered from reading your post is that there is no way to rank their sedation except with clinical trials and comparing sedation described by the patient.

I am asking for an equation I don't see where potency is plugged into the equation. Can you please post a Mathematical example walking though either Zyprexa or Seroquel.

Hi @William. If your goal is to understand this article, there is no equation that is going to relate chlorpromazine equivalents (potency in this article) to affinity, $\frac{1}{K_D}$ at the $H_1$ receptor. They are different things all together, with no known mathematical model connecting them. If your goal is to understand potency, olanzapine and quetiapine are not very good places to start. They are inhibitors at  many different receptors. I'm not sure what you would want in a mathematical example walking through either of them. Were you able to get a copy of Goodman and Gillman?

Okay ignore my last question.  According to Wikipedia the h1 receptor of seroquel is a neutral antagonist which means it does nothing on the receptors which seems to be at odds with miller?

@William all of these antipsychotics are antagonist, as I've said, and this is not at odds with miller at all. Affinity has to do with the strength of binding, not with the downstream effect. It seems like someone may have taught you something different along the way.

I guess I assumed h1 antagonist mean neutral antagonist and this answer states neutral antongists bind but don't alter the response https://biology.stackexchange.com/questions/73706/inverse-agonist-vs-neutral-antagonist

@William Affinity describes binding, not the effect of binding. Anything that binds will have a dissociation constant, no matter how binding effects the receptor, and the inverse of that dissociation constant is the affinity. Also, neutral antagonists do have an effect on the receptor. They prevent binding and activation by an agonist.

"In each of these studies, the atypical antipsychotic (risperidone, olanzapine, quetiapine, and ziprasidone) caused less sedation than did the conventional antipsychotic used for comparison, haloperidol, except in the highest doses. " This seems contrary to evidence in the article"


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Why does (insulin induced) hypoglycemia stimulate ADH secretion?
Intuitively, I understand that ADH (Anti Diuretic Hormone) is responsible for maintaining osmolarity, and increased serum osmolarity is a stimulatory factor for its release-- ADH increases water reabsorbtion in the collecting ducts and DCT (Distal Convoluted tubule) of nephrons, thus decreasing the osmolarity back to normal.
But, apparently, (insulin induced) hypoglycemia also stimulates ADH secretion.
If it were hyperglycemia, it could be explained on the basis of increased osmolarity, as I have done above. I originally assumed it was a mistake in the standard book, but a quick Google search revealed several papers confirming what the book states. I still couldn't find an explanation though, most of these articles just state the observation.
Here are two of them:

https://www.jci.org/articles/view/114626#:~:text=JCI%20-%20Insulin-induced%20hypoglycemia%20stimulates,blood%20of%20conscious%2C%20unrestrained%20rams.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC296631/

Both of these also point out that Insulin Induced Hypoglycemia causes an increase in ACTH secretion. (I am not sure if that is relevant here, though.)
Also, does "insulin induced" hypoglycemia have an added significance over hypoglycemia?


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Type B Nerve fibres cause exactly what kind of autonomic sensation to the preganglionic neurons?
Ganong's Review of Medical Physiology (25th ed) presents the Erlanger and Gasser classification of mammalian Nerve Fibres as such:

Type B Fibres are concerned with Preganglionic autonomic sensations, but there is no mention of this being sympathetic or parasympathetic. Does it mean that it is both?
The table does specify it as sympathetic for the Type C Fibres, though.
(I have tried searching this on google, but I can't seem to find anything specific.)


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Is the colour of a chrysalis predetermined?
Usually, chrysalis of butterflies camouflages with the surface it is attached to, for protection, as I understand it. There are exceptions, though; For example, the golden chrysalis of Euploea core is reflective and literally pops out of its background. My point is, what is the evolutionary advantage of that?

Edit: user -personjerry pointed out that shiny colours indicate poison.
So the main question now is,  if the aim was to scare off predators, why aren't they red/black in colour (as red means impending danger in the animal world)? Also, wouldn't developing a red pigment be much easier?  In these cases, is the colour predetermined?

Flashy colours are often an indicator of poison

Hi. Thanks for the information. I edited my answer to include your comment. I hope you are fine with that. :)

Generally, in biology nothing is designed but if something is working it is saved for the future generations. Chemistry of colors is a complicated field, you can't just slightly modify single "color" molecule to get any color you want. Maybe in chemical sense the material of this shell can be easily modified to get shiny. Suppose it happened occasionally once due to sporadic mutation and no one dared to eat this chrysalis, which gave abundant progeny.


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What arthropod with a distinctive yellow and black colored body is this?
I found this outside my window, today morning, on a clothes peg;

I live on the eighteenth floor, so it probably is a good flyer.
I have noticed that the antennae are almost as long as its body and the legs are yellow, not dark.
Nothing peculiar about the behavior-- it moved around on the peg, for a while, and then flew away.
Location- Bangalore, India.
Length - ~2cm

This appears to be a Glenea multiguttata, a beetle species found in India.
Compare:  from https://commons.wikimedia.org/wiki/File:Black_and_Yellow_Longhorn_Beetle_005.JPG


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BLASTn vs ORF tools
Sequencing projects sequence one strand and call that the + strand and then extrapolate the sequence of the - strand. This means that sometimes the genomic sequence that you download from a database might be the complement of the actual sequence you are looking for.ORF tools like exonerate and genewise takes this into account and thereby look for six possible reading frames.Do sequence similarity tools like blastn take this into account and do pairwise alignment for complement of the actual sequence also?

It depends on the flavor of BLAST you are using. Some do, some don't. Specifically, the classic BLAST flavors are:

blastp :
compares an amino acid query sequence against a protein sequence database
blastn :
compares a nucleotide query sequence against a nucleotide sequence database
blastx :
compares the six-frame conceptual translation products of a nucleotide query sequence (both strands) against a protein sequence database
tblastn :
compares a protein query sequence against a nucleotide sequence database dynamically translated in all six reading frames (both strands).
tblastx :
compares the six-frame translations of a nucleotide query sequence against the six-frame translations of a nucleotide sequence database. (Due to the nature of tblastx, gapped alignments are not available with this option)

Of these, tblastn, tblastx and blastx all check the 6 possible reading frames (both strands). This only makes sense for protein searches since that's the only case where the reading frame is relevant. The simple blastn does not deal with reading frames but it does deal with hits against the reverse strand. The matching strand is highlighted in the output and the numbers in the HSP reflect that.
For example, these are the first and last lines of one of the hits when blasting the reverse complement of the human tP53 gene against the human sequences of the nr database:
Range 1: 1 to 2591GenBankGraphics Next Match Previous Match
Alignment statistics for match #1 Score Expect  Identities  Gaps    Strand
4673 bits(5182)     0.0     2591/2591(100%)     0/2591(0%)  Plus/Minus

Query  1     CACCCCTCAGACACACAGGTGGCAGCAAAGTTTTATTGTAAAATAAGAGATCGATATAAA  60
             ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Sbjct  2591  CACCCCTCAGACACACAGGTGGCAGCAAAGTTTTATTGTAAAATAAGAGATCGATATAAA  2532

[...]

Query  2521  AGACTTTTGAGAAGCTCAAAACTTTTAGCGCCAGTCTTGAGCACATGGGAGGGGAAAACC  2580
             ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Sbjct  71    AGACTTTTGAGAAGCTCAAAACTTTTAGCGCCAGTCTTGAGCACATGGGAGGGGAAAACC  12

Query  2581  CCAATCCCATC  2591
             |||||||||||
Sbjct  11    CCAATCCCATC  1

Note that 1) the strands are given as "Plus/Minus" which means that the query sequence is aligned against the - strand of the target and 2) that the coordinates of the subject sequence start from the end (2591) and go to the beginning (1).
So yes, even simple tools like untranslated BLAST take the two strands into account.

Sometimes the hits could also be "false positives" if the sequence is aligned against the - strand.In that case,what is the solution?

@Raghavakrishna why would they be false positives because they align against the - strand?

If the negative strand sequence is not the actual sequence that codes for,sometimes it might be equivalent to some other sequence(false positive?)

@Raghavakrishna I'm sorry but I still don't understand. The details always depend on what you're actually doing. If BLAST gives you a hit, then that's a hit. Whether or not that is biologically relevant is another question and I can't answer that unless I know what question you are asking.


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Is it possible to establish a newer animal model completely based on Bioinformatics studies?
I wanted to know, if it is possible to prove a new organism as an animal model for any human disease by only Bioinformatics methods like NGS and Structural bioinformatics.
For Example, let's say Drosophila is an animal model for Disease X as it have some 60-70% similarity in the gene and protein structure. Can we prove, a newer organism is a better model for X, if it shows a higher similarity, let's say 80-85%, to gene and protein structure of human?
UPDATE
(First I posted it as comment! But I think, this is suited here best!)
@David: Thanks for your answer! Actually, I did looked into it, Large animal models of rare genetic disorders: sheep as phenotypically relevant models of human genetic disease. I am more interested in listing down the problems if we do start this kind of project in our lab. Do NGS is a solution or what part of biology we need to focus so, that we can be more accurate.

The general problem of predicting the effects [of variation] of sequence on phenotype is far from being solved, so i'd say no. But still, that could be an encouraging signal to pursue experimentation on the new organism.

It is naïve to think that the extent of protein similarity is sufficient to determine what is the best animal model for a human disease. The physiology of the animal and the question of compensatory genes are all factors that contribute.
Indeed, if the protein is functionally similar, it may be irrelevant if it has diverged in other regions. And, of course, there are ethical and cost considerations — the animals closest to humans are the apes!
I suggest you search for literature on the subject. It’s not my field, but Googling brought up this paper discussing models for kidney disease, and no doubt you could find much more yourself.


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What Type of Color Vision do Mantises have?
I am trying to figure out what type of color vision mantises have, but stuff about mantis shrimp keeps coming up instead. All I was able to find was this one paper from 1971. It found evidence that the ocellus have 2 photoreceptor and the compound eyes have 1 photoreceptor, but acknowledges that more could still exist:

Although a second or third receptor type (blue or ultraviolet) was not established as present in the mantis compound eye in these studies, this lack of experimental evidence does not preclude the possibility that a second or third receptor type exists.

Have anything more definitive been done regarding mantis color vision?


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Why Account for Phylogeny when using Relative Brain Size as a Surragate for Intelligence
This paper tries to relate intelligence, life history, and urban fitness of birds. They use relative brain size of each species as a surrogate measure of intelligence. Although this may not be the most accurate method, I understand why they used it. What I do not understand is why they used the method to calculate relative brain size that they did.
Rather than using the absolute relative brain size, they used "residual from a log-log phylogenetic Generalized Least Square regression... of absolute brain size against body mass". This means that relative brain size of a species is regarded as how large its brain is compared to its body size, compared to other species in its taxon. So if a species has a large brain and is part of a taxon that in general has larger brains could get a lower score than a species that has a small brain and is part of a taxon that in general has smaller brains.
Why is this not a problem?

It seems they were attempting to correct for other behaviors/ecological niches that were correlated with brain size, but were not related to "urban tolerance". Their work includes much data on niches, behaviors, breeding strategies, etc, not just "urban tolerance".  Presumably, related species would share similar brain-size effects from these confounders, so residual differences could be correlated more specifically with "urban tolerance".
The authors comment:

Because brain size correlates with these traits, failure to properly
account for such additional drivers may mask the effect of brain size
on urban tolerance. For example, if a large brain affects tolerance to
urbanization by facilitating broader niches (Ducatez et al., 2015; Sol
et al., 2016), including a measure of niche generalism in the model
can block the effect of the brain on urban tolerance.

They are trying to correlate a quite crude measure (brain size) with a specific behavior ("urban tolerance"), which as you suggest raises all sorts of methodological questions.

I understand why they included factors such as niche breath in their model, but that does not explain why they used this calculation of relative brain size during data collection. I see no reason they could not have used absolute relative brain size and these other factors in their models.

I would think it's because they wanted to account for even unknown factors, but am not sure. Why not write the authors and ask? Researchers usually welcome intelligent questions about their work.


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Empirical Measurements of Barr Body Ratio
'Both X-chromosomes in a female have an equal chance of becomes a Barr body in each cell.' Every source I can find on Barr bodies claims this and I can think of no reason for why it may be wrong. What I want to know is if anyone has empirically tested this. Has anyone ever taken a model organism, measured the distribution of Barr bodies, and calculated exactly how far the result is from the 1:1 ratio that the theory predicts? Has anyone ever tested the Null Hypothesis of this statement, or has it just been accepted based on the theory alone?

Generally in science, accepted theories are not simply based on a presumption of accuracy just because it sounds right. While I don't have the citations you're looking for (this would be a good place to start looking), I'm certain it's based on strong empirical evidence, not guessing.

That is why I asked my question. Considering how wide-spread this claim is, there should be empirical evidence, but as far as I can tell there is none.

Did you start looking through the PubMed search I linked to? You can reverse-sort it by date published and start looking at the oldest papers first, as they're the ones most likely to have direct citations of the original work.