text:
Can DNA sequencing of food provide quantitatively the fraction of protein from chicken vs soy?
update: New York Times  X, 2021: The Big Tuna Sandwich Mystery:

For about $500, his lab could conduct a PCR test — which rapidly makes millions or billions of copies of a specific DNA sample — and try to tell me whether this substance included one of five different tuna species.

There is some news about a report from Canada's CBC about fast-food chicken items containing as much as 50% soy protein, based on DNA testing. I won't do the report the service of linking to it directly, but you can search for the news "What's in your chicken sandwich? DNA test shows Subway sandwiches could contain just 50% chicken."
Isn't quantifying ratios of various DNA sequences fairly difficult, requiring rigorous sample preparation? Could results vary dramatically by varying cooking times, and the independent processing of the animal protein and the vegetable protein? Is there an reason to expect isolated DNA ratios to be a good indicator of protein ratios?
I'm also curious, is there a better way to at least try to do this study - perhaps search for key sequences of amino acids within the proteins to at least try to distinguish animal from vegetable proteins quantitatively?

edit: Here is a newer, more reliable, independent news item not written by the agency who paid for the testing.
The NPR news article DNA Tests Find Subway Chicken Only 50 Percent Meat, Canadian News Program Reports says:

The tests were conducted by a DNA researcher at Trent University's Wildlife Forensic DNA Laboratory, for a CBC Marketplace episode dedicated to testing fast-food chicken dishes, and have not been independently confirmed.

Later in the same article a strong statement by one of the companies refuting the results has also been provided.

Looking at the article, which didn't provide a link to anything published, they used several control sources (McDonald's, Wendy's, etc.) so assuming their method was truely the same in each case there is reason to suspect it contains significantly less chicken. "Just 50%" might be a stretch, though. It does seem like a good place to start at least, although the lack of actual publication and the rush to the press seems pretty unethical.

@jzx the history of the food - the chicken and any soy could be very different. Quantitative DNA analysis requires very careful and controlled sample preparation. Cooking temperature and time, chemical environment, pH, all these things are totally uncontrolled. Even if they pay lip service to the word "control" the samples are totally uncontrolled in a variety of factors that could impact final DNA concentration, in a way that differs between soy and chicken, for each tested product.

Exactly @uhoh - without a paper outlining their methods and observations it's hard to say. Although I'd have to assume the chicken would be uncooked, possibly frozen.

@jzx I'd guess they are cooked and purchased over the counter, the only caveat is that no sauces were added (e.g. "hold the sauce"). If you read farther down and see the discussion, most of this stuff is "restructured product" - even if it feels like it is cooked muscle, most of this stuff was a slurry or even a liquid at some point. That's how the soy gets mixed into the "meat" - the stuff is usually mixed as a "goo" and then pressed and moulded into suggestive shapes that remind you of real meat. Go look for veins, ligaments, nerves, etc. all you'll find are air bubbles.

@jzx Here is a paper: X. D. Sun (2009) Utilization of restructuring technology in the production of
meat products: a review, CyTA - Journal of Food, 7:2, 153-162, DOI: 10.1080/19476330903010193 here is a pdf: http://www.tandfonline.com/doi/pdf/10.1080/19476330903010193 I have no idea about the level of peer review, but it helps explain what "restructured product" is like and the processes that can be used to prepare it. Not exactly what one would do for a quantitative DNA analysis in an analytical laboratory.

Mm, yes. It would be interesting, then, to repeat with uncooked product. I would hope that any reputable business would want to know if their supplier's meat doesn't match their policy, which they'd have to have agreed on previously.

I'm not saying your question is bad, in fact it's quite interesting. I also agree that methodology of any "study" should be published. But, the way you phrase the question makes it sound like you already have your mind made up on the answer before asking it. Anyways, my previous comment is not particularly relevant, so I have deleted it. Good day to you, sir.

@canadianer I've cleaned up too. For sure i believe that a method that tries  to use chicken/soy DNA ratio as an accurate proxy for chicken/soy protein ratio in restructured meat product is flawed. But instead of making my mind up, I've asked here in bio SE, where science reigns - at least most of the time :)

Importantly, if you look at the lab that did the testing, most of their work seems to involve identification, rather than quantification. Without more insight into their methods I can only say that there is a huge difference between determining whether a steak came from a moose or beef and determining that a hamburger is some % moose...

http://s3.documentcloud.org/documents/3477610/DNA-Report-Chicken.pdf

In reference to the update in the question three years later, I'll include additional quotes from the same New York Times article.

“No amplifiable tuna DNA was present in the sample and so we obtained no amplification products from the DNA,” the email read. “Therefore, we cannot identify the species.”

The spokesman from the lab offered a bit of analysis. “There’s two conclusions,” he said. “One, it’s so heavily processed that whatever we could pull out, we couldn’t make an identification. Or we got some and there’s just nothing there that’s tuna.” (Subway declined to comment on the lab results.)

With all testing, there are major caveats to consider. Once tuna has been cooked, its DNA becomes denatured — meaning that the fish’s characteristic properties have likely been destroyed, making it difficult, if not impossible, to identify.

While this question falls somewhat between biology, chemistry, and food science, the use of quantitative DNA analysis as a proxy for estimation of relative protein fractions from two different species (in this case plant vs mammal) is probably on-topic here considering it is biologists who have invented, use, and interpret results of DNA amplification and sequencing analysis, and can best speak to their correct use and potential problems when used outside their accepted protocols.
I am not a trained biologist myself, so I can not state with authority that starting with a food product whose plant and animal components may have started from different places on Earth, been processed differently, then combined and further processed involving major excursions in heat (cooking) and in pH deviate substantially from accepted protocols for DNA quantitative analysis, but I have a strong hunch that this is probably so.
As @BryanKrause has noted in a comment, the laboratory in question's primary expertise is in animal identification - does a carcass or piece of meat or fish come from the species claimed or not, and this is a laudable service. But using relative fractions of DNA within a single sample of prepared food as proxy for relative contribution of protein is far outside that kind of service, and as far as I know, is not an accepted practice anywhere.
Ars Technica is a popular technical news source that generally does a excellent job of summarizing scientific topics when they do cover them, in my opinion at least. In an update to the article Subway releases data after scientists weigh in on 50% chicken test [Updated] they summarize released information from two independent laboratories using an "ELISA methodology designed for food products to quantify soy in the chicken." ELISA is a quantitative method that can be used to measure the presence of various proteins directly, and does not use DNA as a proxy.

Update, March 6: Subway has released the lab reports from both of its independent tests. Both Maxxam Analytics in Ontario, Canada and Elisa Technologies, Inc. in Florida used enzyme-linked immunosorbent assays (ELISA) designed for food products to quantify soy in the chicken. ELISA's are a standard type of assay that generally detect and quantify substances based on binding by an antibody. In the assay, antibody binding kicks off a detectable chemical reaction, commonly resulting in a color change. In the case of Elisa Technologies, the lab used an antibody that binds to soy flour proteins and the lab used known concentrations of those soy proteins for comparison to determine the quantity of soy protein in Subway's chicken samples.
In all samples, Elisa detected 3 parts-per-million or less of soy proteins, which is well below one percent of the chicken. Maxxam detected 5.3 ppm of soy protein in the chicken, which is still well below one percent. (emphasis added)

The testing by subway only raises more questions since they, too, did not release their methodology. Also, what does ppm mean in this context?

@canadianer these are very good points, thanks! I am not sure how much has been released in toto, this is the best source I could find so far. It is possible a more complete report has been released elsewhere. I'll keep looking.

I'm going to tentatively accept my own answer in this case. Please flag me if there's a change or new information that I've missed, or just leave an improved answer!

I now read the article. They don't include/show a standard curve so take it with a grain of salt.
It's possible to do Carbon Isotope analysis to distinguish plant vs. animal carbon from an isolated protein fraction.
Besides that you could also do quantitative mass-spectrometry and look for animal vs. plant peptides.
If you want both cell number, protein abundance of known targets there's the fancy Mass Cytometry that could do this.
That being said, IMHO: DNA-sequencing is probably fine and definitely robust. If you set-up a standard curve (mix soy and chicken at known ratios and DNA sequence it) then that's probably the easiest/cheapest way to do this. Without a standard curve testing this though you can't draw a definitive conclusion.
Also from the NPR article; analysis from other fast-food sources of meat gave lower Soy DNA ratios with Subway being an outlier. That's an important distinction to make. Subway subsequently claiming that it's 100% chicken appears more misleading after previously saying there was soy as a stabilizer.

Can you provide some evidence to support the "probably fine"? The mix is processed at high temperature with several added chemicals, none of which are directly related to standard laboratory procedures for handling and preserving DNA samples for quantitative analysis. Can you also support that a DNA ratio can serve as a quantitative proxy for a protein ratio? I appreciate your answer, but right now as written, it's looks like an unsupported opinion.

Temperature and chemical treatment wouldn't matter since all the DNA is being treated the same. Maybe if it's heavily degraded the values are low you get into a non-linear problem. One way or another there isn't enough information to say what they did is correct or not, so yeah it is partly based on opinion, the methods I outline are ways to definitively test it. My opinion is also that fast-food places will serve junk if it's cheap, subway chicken in particular barely resembles a chicken breast.

That's not necessarily correct. Animal and plant DNA start out in very different types of cells, with different ratio of protein to DNA. They are processed separately for quite a while before being added together. The chicken will probably be sterilized fairly quickly (compared to soy) due to the risk of salmonella or other dangerous organisms.

Sure, if you want to find flaws in this study they are there I'm not denying it. Is that difference enough to explain the 1.5 order of magnitude discrepancy (1% vs. 50%) between what the company vs. researchers are saying? I'm skeptical.

Deviations from carefully established protocol can lead to loss of DNA. The stuff that is likely to be most carefully cooked and sterilized is the stuff who's DNA is "low". Cook it long enough and hot enough it could drop much further, and who knows what pH excursions happen during the "restructuring" process. I'm just explaining why I think your answer could use some factual support

I could also imagine different outcomes depending on the standardization procedure. For example, if the products from soy are mostly protein isolates, different procedures might leave more or less DNA intact. If Subway's process left 50x more DNA than the preparation used in the standards, that could also lead to an overestimate. I think overall it is going to be hard to interpret these results without a full publication-style report.


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What is the definition of an opioid, beyond that it's something that stimulates opioid receptors?
At first glance, this looks like a circular definition.
Is there some way to definitively determine if a given molecule is or is not an opioid? (Medically or scientifically, not legally).
I'm hoping for something more scientific than "if it's on this list, it is; and if it's not, it isn't."
Wikipedia's article Opioid receptor:

Opioid receptors are a group of inhibitory G protein-coupled receptors with opioids as ligands. The endogenous opioids are dynorphins, enkephalins, endorphins, endomorphins and nociceptin. The opioid receptors are ~40% identical to somatostatin receptors (SSTRs). Opioid receptors are distributed widely in the brain, and are also found in the spinal cord and digestive tract. (emphasis added)

Wikipedia's article on Opioid:

Opioids are substances that act on opioid receptors to produce morphine-like effects. Medically they are primarily used for pain relief, including anesthesia. Other medical uses include suppression of diarrhea, treating addiction, reversing opioid overdose, suppressing cough, and suppressing opioid induced constipation. Extremely strong opioids are approved only for veterinary use such as immobilizing large mammals. Opioids are also frequently used non-medically for their euphoric effects or to prevent withdrawal. (emphasis added)

The common-sense answer (also given on googling) is: "Opioids are drugs that are either derived from opiates (drugs created directly from opium, such as morphine or codeine) or are chemically related to opiates or opium."

@anongoodnurse thanks, but that just pushes everything under a rug called "chemically related" which is nearly useless. It is a subjective and fluid concept; there is no litmus test for chemically relatedness. There is no common-sense here, just further ambiguity.

It's not "nearly useless" just because it breaks your question. Of course there is a definition for "chemically related". Look at PubChem or ChemIDPlus to see the structure opioids have in common.

@anongoodnurse given molecule X and Y where X is an existing synthetic opioid, and Y is a completely different synthetic opioid, is there a test, with a binary result Yes or No to the question "Is X chemically related to Y?" This needs to be a test that anyone can apply and receive the same answer in all cases. "Chemically related" is a fluid and ambiguous concept, and is not a scientifically well-defined test.

"...Y is a completely different synthetic opioid..." If it was completely different, it would not be an opioid. It might be an analgesic, or a euphoric agent, or an emetic, but it would not be an opioid. I think instead of arguing from opinion, it would help if you gave an example of two molecules classified as opioids that were completely different in structure. Again, I refer you to PubChem, which will give you the chemical structure in all three dimentions of every opioid.

@anongoodnurse Are you sure? Can you express that in clear, unambiguous terms that can be objectively applied by a third party?  What does "completely different" mean? I think if we continue this we will go in semantic circles. In the end you often end up posting excellent answers to my questions, so I'm happy to go along, but it might not be so interesting to others.

You're the one doing the dancing (semantically); I'm standing in the same position. I'm done here.

@anongoodnurse A PubChem list of every opioid was anticipated by my sentence I'm hoping for something more scientific than "if it's on this list, it is; and if it's not, it isn't." I wonder if there is at least a much shorter list of opioid receptors? So any molecule which interacts with those receptors could be classified as an opioid? At least that approach could be codified with some sort of standard procedure and interpretation of result.

I suspect opioid was originally defined to be chemicals derived opium. Then, when the receptors that these chemicals acted on were identified, other molecules were found that also interacted with them. Thus the Wikipedia definition of opioid receptor may be changed to: a group of inhibitory G protein-coupled receptors which have for ligands chemicals derived from opium while the opioid definition would remain the same. Again, this is entirely speculation and well outside my field.

So I wrote that comment while reading the question in the review queue, which doesn't show the answers (like the answer which essentially says the same thing). I'll leave it since it doesn't hurt anything.

@canadianer thanks for your comments, and for the heads-up that there is a close vote. In many SE sites if it is not completely clear what one is asking, someone will first leave a comment asking for clarification, before reaching for the close button. I feel that silent, anonymous "unclear" voting is not productive behavior when the question is in fact fairly clear. One thing that demonstrates that is the lucid answer posted. I am not sure if it is 100% right yet, but it addresses all aspects of my question squarely.

@canadianer great minds...

First there was opium. Then the active components of opium (morphine etc.) were defined and called opiates. Then the receptors for opiates were discovered, along with their endogenous ligands (enkephalins etc.), and since those endogenous ligands were not derived from opium and indeed (being peptides) were not chemically related to opiates, a new term was needed. This term was opioid, and yes, the definition of an opioid is that it is something which binds to an opioid receptor.
The perceived circularity lies in the shift of emphasis from the drug to the receptor as the central player - when the first binding studies were being done in the early 1970s the search was for opiate receptors, not opioid receptors.

The only issue I have with this answer is that endorphins, enkephalins, etc. are not listed as opioids but as "opioid peptides" (most commonly), "opioid neuropeptides", or opiate-like pentapeptides or some such, as far back as 1977. So far, I have not seen them referred to as opioids.

@anongoodnurse Ref 2 of the WP page for opioids is as follows:  Hemmings et al.  (2013). Pharmacology and Physiology for Anesthesia: Foundations and Clinical Application: Expert Consult - Online and Print. Elsevier Health Sciences. p. 253. ISBN 1437716792. "Opiate is the older term classically used in pharmacology to mean a drug derived from opium. Opioid, a more modern term, is used to designate all substances, both natural and synthetic, that bind to opioid receptors (including antagonists)."  [my emphasis] ...

...I think the use of the term 'opioid peptide' is just a way of emphasising what is being discussed in a specific context.

Perhaps, but a Google Scholar search of 2016-2017 Neuropharmacology papers on opioids fails to refer to any endogenous opioid peptides as "opioids".

The introduction to this paper  – Involvement of Endogenous Enkephalins and β-Endorphin in Feeding and Diet-Induced Obesity – refers to opioid peptides as: endogenous opioids (twice); endogenous opioid peptides; endogenous ligands of opioid receptors; endogenous opioid activity; and finally states that 'This study aimed to distinguish the role of the two major classes of endogenous opioids acting at MORs and DORs, namely enkephalins and β-endorphin...'.

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text:
Roughly at least, how many types of cells comprise human blood?
A long time ago there were only three kinds - red, white, and rose platelets. Advances in cell sorters and more recently in genetic techniques and differentiation studies have led to the identification of a wide variety and complex lineage of cells that comprise human blood.
Roughly at least, how many types of cells are currently identified?
I understand that "types" is a non-technical term, and I'll try to better define what I mean. For example, I do not mean to enumerate each antigen specificity separately because that would make the number fairly large and probably dependent on the individual's history.
One possible definition of a "type" would be that it has been given a name.
I don't mean to include cells that are present due to injury, clean-up, trash collection, or foreign cells including bacteria, viruses, parasites etc.
Just for an example, here is an overview of types of hematopoietic stem cells. There may be further recognized subdivisions, I don't know how far it goes. There are certainly other cells that comprise human blood. (From here.)

The short answer is that there are still three "kinds" of blood cells: red (RBCs), white (WBCs) and platelets. The graph above names pretty much all of them.

@anongoodnurse I always liked the sound of T-helper cell - are they not a well-defined type?

Maybe discussing an application or disease could help.
Let's take WBCs as an example. The journal of immunology, which is dedicated to WBCs and immune response, prefers to make sections as innate immunology, allergy, antigen recognition, immune regulation, immune system development, etc.
Same story can happen for thrombocytes and erythrocytes.
The point is discussing an application can help to answer about each cell "kind/type" more precise.

@uhoh Helper T cells are quite well defined but are constantly undergoing subsetting due to advances in phenotyping. CD4 is the classical marker denoting a Th, but on cytokines or receptors you may be Th2, Th2, Th9, Th17, some sort of Treg, or a newer one is Th3. Th cells have also been shown to be cytolytic where they're known to simply "help". If you count lineage plasticity, they can be whatever they want depending on the microenvironment they're in..

@CMosychuk OK great! Cells that have distinct, generally recognized and accepted names among biologists can all be included. I have a hunch the answer will be roughly a few hundred total, but don't know. However if there is so much plasticity in vivo (blood still in a person) that it is impossible to give even an approximate number, that could be the answer. Thanks!

@uhoh I think being less specific here is more informative, since regardless of CD4 or CD8 both are still T cells. Exceptions aside, your circulating subsets will define your blood composition. So RBC, WBC and platelets most broadly, and then probably at a finer level: RBC, platelets, monocytes, granulocytes, and lymphocytes so about 9 cells types just based on your chart. Everything else tends to hang in the bone marrow or tissues and so you wont often or in significant numbers find them in blood.

@CMosychuk Thanks. I'm wondering — do you think this question might be unanswerable? If specifying "human blood" makes an answer difficult because there are so many types with such a wide range in frequency that it is too hard to establish a lower cut-off, then I think that would be a really informative and insightful answer, to me at least. However, if the answer is "about a hundred types of distinctly named cells are usually found in the blood of a healthy human individual" then that would be an informative answer as well.

@uhoh Here's a chart I cited in a different question. I think that's among the better estimations of what you might find, and in what quantity, ignoring unlimited subsetting.

@CMosychuk please consider posting this an answer! You have a great way of explaining/summarizing the big picture in short comments, and I think future readers can benefit better from this as an accepted answer than as a comment. Thanks!

I think any answer will be subjective, depending on what you consider to be distinct cell types --- how detailed should the classification be. As you already mentioned, if you consider all cell populations that can be separated by surface antigens, that's already a pretty large number. Also, what previously was thought to be terminally differentiated cell types are increasingly found to be more like cell "states" that can change over time, so-called "plasticity" (see for example http://www.nature.com/ni/journal/v11/n8/abs/ni.1899.html). This makes it hard to even uniquely define a cell type.

@Roland can you consider expanding that explanation into an answer? I would be happy accepting a thoughtful answer that explains why the concept of "number of cell types" is simply problematic, and I'd be interested to find out if it's problematic particularly in blood cells, or for many categories of human cells. There are a number of thoughtful comments here but so far nobody's chosen to pen an answer. I'm here to learn!

I think any answer to this question will be subjective, depending on what you consider to be distinct cell types --- how detailed the classification should be.
As you mentioned, if you consider all immune cell populations that can be separated by surface antigens, that's already a pretty large number. In 2013, the Immunological Genome (Immgen) project reported characterization of 249 immune cell types, and I think they are still working on expanding their catalogue (see immgen.org). One can argue about which of these are really different enough to be called "cell types", but I think it gives a pretty good ballpark number.
At some level of resolution though, the notion of "cell type" itself becomes slippery. While previously it was thought that many cell types were terminally differentiated (unable to change back to more primitive forms), we now increasingly find that these "cell types" are more like temporary "cell states", or phenotypes, that can change over time. For immune cells, this phenomenon is often called "plasticity"; for more information, see for example this paper. The advent of single-cell genomics has further strengthened this view, demonstrating that individual cells can dynamically change their gene expression pattens. These issues makes it hard to uniquely define and count cell types, and it might be more useful to reason quantitatively in terms of the phenotypes and behavior we can measure --- expression patterns, signalling molecules, metabolism and so on.

Nice answer!...

When I started to write this question, I chose blood instead of a solid organ (e.g. liver, heart, kidney) because its natural state is individual cells in fluid and so it lends itself more naturally to some types of cell characterization. I'd thought that a 3D organ would have to be sectioned or destructively disturbed before individual cells could be separated and "typed" and that would still be difficult to do without bias. Now I'm wondering if I should ask a new, similar question using one of those solid organs where the "slippery slope" is not so steep.

The abstract of your linked Genome Research paper Trapnell 2015 is really well written and works hard to explain the "landscape" well. It turns out "how many kinds of cells are there" in the human body is a 60 year old question, and the historical answer used to be "210". I wonder if a block quote or two from that paper in your answer might be informative to future readers. I certainly found it helpful. Thank you very much for taking the time to post a well-written answer my question and to use the space to teach some important points!

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text:
How did the "serendipitous rediscovery" of Sulfasalazine as an antirheumatic agent after 30 years happen?
This excellent answer describes the history of the ~50 year old drug Sulfasalazine, and it's worthwhile to take a moment and read through the answer now.
Roughly speaking the drug is an antibiotic molecule linked to a molecule of aspirin, developed at a time when rheumatoid arthritis inflammation was assumed to be caused by an infection. Ironically the drug is now widely used as a treatment for RA, but its mechanism of action does not seem to be related to the way that it was originally designed to work.
Sulfasalazine is on the World Health Organization's Model List of Essential Medicines. See section 17.3, Anti-inflammatory medicines.
Within one of the block quotes in that answer from a publication by the Department of Medicine at Princeton can be found:

[...] Early therapeutic results were encouraging, but the drug was discarded as an antirheumatic agent for 30 years, until its serendipitous rediscovery (emphasis added).

Pubmed shows this to be Pinals R.S., J Rheumatol Suppl. 1988 Sep;16:1-4., PMID: 2903922, but I can't find access to the Journal of Rheumatology Supplements that far back in time.
Can somebody track this down and relate the "serendipitous rediscovery" story here? Or perhaps find a link to another author's version of the story I can read? What was the serendipitous biological evidence that led to rediscovery of Sulfasalazine as a disease-modifying anti-rheumatic drug? (DMARD, see also arthritis.org)

Your question led me to:
Pinals, RS (1988) Sulfasalazine in the Rheumatic Disease. Seminars in Arthritis and Rheumatism 17:246-259. I reproduce the introduction to this paper below:

Most physicians are familiar with sulfasalazine (SSZ) as an agent commonly used to treat inflammatory bowel disease for more than 40 years. In 1978, McConkey et al reported preliminary studies suggesting that this sulfonamide might be effective in rheumatoid arthritis (RA).1 The use of SSZ arose from earlier open and controlled trials with a sulfone, dapsone, which had demonstrable efficacy in RA, but the benefits were accompanied by relatively frequent, often unacceptable adverse effects.2 Dapsone was effective in dermatitis herpetiformis, presumably because of immunosuppressive activity. Another therapeutic agent for this skin disorder was sulfapyridine (SP), a drug with a poor record of gastric tolerance. Therefore, McConkey et al elected to try SSZ, a compound that released sulfapyridine in the bowel after passage through the stomach. Ironically, McConkey was initially unaware that SSZ had been synthesized specifically to treat RA in the late 1930s. In 1980, McConkey et al reported their open experience with SSZ in 74 patients treated for up to 1 year.3 The improvement in erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and clinical score (a global evaluation) was similar to that achieved with the disease-modifying antirheumatic drugs (DMARDs), and appeared somewhat sooner, often within 2 months. Moreover, although adverse effects were frequent, they were seldom of sufficient severity to discontinue treatment. This encouraging report led to several controlled trials in the United Kingdom and elsewhere, all confirming the efficacy of this interesting agent. The first study in the United States has been reported4 and, although SSZ has not been approved by the Food and Drug Administration for use in RA, many rheumatologists have used it as an alternative DMARD because of its availability and long record of safety and efficacy in inflammatory bowel disease.

What I have gleaned from this and a couple of papers cited there is that B McConkey, working at a hospital in Birmingham in the UK became interested in developing methods of clinical assessment of rheumatoid arthritis (RA) in the 1960s and this led eventually to the discovery that the drug dapsone is effective as a treatment but with an unacceptable level of adverse side effects. Then, to quote McConkey:

We had studied dapsone partly because of its effect in leprosy and dermatitis herpetiformis; its mode of action in those diseases may be through its immunosuppressant properties. Another drug used in dermatitis herpetiformis is sulphapyridine;it did not attract us as a contender but it is a constituent of salicyl-azo-sulphapyridine (sulphasalazine), a compound originally formulated for RA and latterly found to have immunosuppressant properties.
McConkey et al (1980) Sulphasalazine in rheumatoid arthritis. British Medical Journal 1: 442-444
(This is ref 3 in the Pinals introduction.)

So clearly there was a strand of chemical logic in the rediscovery of the drug; the only serendipitous aspect was that McConkey did not at first know that sulfasalazine was originally designed as a treatment for RA.

Wow, thank you for both taking the time to put together this material and for sorting things out re the serendipity angle. A quick glance as the structures of Sulfapyridine and its more symmetrical cousin Dapsone makes it even clearer.

fyi I've just asked Considering its salicylate component, is Sulfasalazine contraindicated when aspirin is? Can it have similar therapeutic benefits? in Medical Sciences SE

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text:
Is brain transplantation possible?
Many organs can be transplanted nowadays, including the liver, lungs and kidneys.
Can the brain be transplanted?

@ChrisStronks Now I think it's too broad, unfortunately. There's a laundry list of assumptions that have to be built into any answer, and so narrowing it down to whether one would want the CNS to be functional, be able to vascularize itself, or to maintain histocompatibility would be helpful, but even bearing that narrowing of the question, this is still really a fanciful idea.

@jonsca - I disagree - it is not too broad as it is a specific, quite technical question now. It is fanciful, yes, but it has been tried in the past. A quick search on the web brought me to some interesting stuff going on recently as well. I'd like to answer this question by giving a short review on what has been done and these few studies obviously ran into all the issues you are describing. Nothing fancy, not too broad at all.

@ChrisStronks go for it, it's been reopened.

Short answer
Yes, brain transplantation is technically possible, but only for short periods of time, and only in experimental settings.

Background
In terms of a full-brain transplant there has been only one group that have made serious attempts in doing this (according to wikipedia and a literature search on my end). In the 1960's White and colleagues transplanted canine brains from one animal to another (White et al., 1965). In total 6 brains were transplanted. However, the recipients' brains were not removed and the brains were merely surgically transplanted into the neck region of the recipient animal, and connected to the recipient's cervical vasculature (carotide arteries and jugular vein). Hence, the recipient canines ended up with two brains. The authors, however showed with these experiments that the transplantation of brains was feasible, and that the transplants survived and remained functional, which was evidenced by EEG activity. The brains survived from 6 hours up to two days.
Later, White and colleagues worked out a way to keep an isolated (but blood-perfused) monkey brain alive outside the skull, potentially allowing for a primate brain to be transplanted (White et al, 1975). The procedure could include longer-term 'storage' of the brain by cooling it, making the possibility of transplantation more feasible. However, White realized the difficulties with this approach, since, and I quote:

[...] by definition the brain must be isolated before the transplantation, and thus requiring all nervous tissue connections to be severed (e.g. cranial nerves and spinal cord), the isolated transplanted monkey brain is without a mechanism to receive or transmit information.

To address this issue White et al. set out to transfer  the entire cephalon (head) of a monkey to the body of a recipient whose own cephalon had been removed at a mid-cervical
level. Under these circumstances the brain, being within its own cephalon, still connects to the cranial nerves:

source: University of washington
White et al. succeeded in transplanting a head, but the preparation rarely survived longer than three days due to haemorrhagic shock (White et al, 1975). Basically the recipient was quadriplegic, as the face was fully functional and White comments, and I quote:

Observe the wakeful appearance of the cephalon and the obvious movement of the facial musculature with open mouth and eyes. This preparation gives every evidence of being in intelligent contact with its environment. [...] Cortical [EEG] activity in this preparation demonstrates awake recordings.

Hence, with the current available technology it does not make much sense to perform a brain transplant, as the transplanted brain cannot be functionally (neurally) connected to recipient body. However, strides are being made in re-connecting a severed spinal cord (Canavero, 2013), endeavors that could bring head transplants a little closer.
Quadriplegic people obviously face extreme psychological challenges (Sane Australia). However, even when they have become quadriplegic due to an event later in life, they are not mentally changed, in that they are still 'themselves'. Therefore, although human transplants never have been done, I dare to say that the transplanted head will determine the psychological 'self' of the recipient body, which includes memory and personal traits. At least, assuming the brain can be transplanted without inflicting neuronal damage.

References
- White et al. Science 1965;150:779-81
- White et al. Resuscitation 1975;4,197-210
- Canavero et al. Surg Neurol Int 2013;4:S335–S42

Further reading
- CBS News

Wow! This is amazing. Though I feel sad for the animals used in experiments.

@CRags - when I first read about these (horrific) experiments, I couldn't help myself and felt a certain thrill. Obviously, and luckily, these kinds of experiments would never pass any ethical committee as of now.  At least not until functional re-connection with the peripheral nervous system can be potentially made.

authors: เด็กชายวรภัทร อุประวรรณา

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


text:
Why does a light object appear lighter in your peripheral vision when it's dark?
So, I am not sure I can reproduce it via images, but the steps are:
1) At night, open a window and have a look at the surface of the earth
2) Suppose there's an object that reflects a tiny amount of light
3) When you actually try to focus your eyes at this object, you either don't see anything (depends on the amount of light it reflects) or you can hardly see it
4) When you focus your eyes on something that is 3-10 metres away, you can easily see this object with your ambient vision. Not the details, but it seems that it reflects more light.
Why does it happen?

An evolutionary development to 'see' better in the dark, not only light objects but movement!

Short answer
Peripheral vision is more light-sensitive than central vision.
Background
When you look directly at an object the image is projected onto the fovea. The fovea has maximal visual acuity (high resolution) and a high density of cones, which are specialized photoreceptors to sense colors. However, cones are not very sensitive to light.
Here is a picture showing the foveal field of view:

Source: Pinhole Eyeglasses
If you look at the same object using peripheral vision, the image is formed more eccentrically on the retina. Here, cones are sparse, but high densities of rods are present. Rods do not detect color, but are much more sensitive to light than cones. In fact, they can faithfully detect a single photon! (Webvision) Moreover, many rods converge onto a single ganglion cell, and rod responses are therefore summated. This spatial  summation further increases light sensitivity in the periphery, but degrades spatial resolution.
Here is an image on rod and cone distributions on the retina, showing a high cone-density in the fovea and a high rod density more eccentrically:

Source: Webvision
And here is an image showing the higher light sensitivity of rods over cones:

Source: Webvision
Hence, peripheral vision is more light sensitive because: (1) there are more rods in the peripheral retina; (2) rods are more light sensitive; and (3) eccentric retinal rod circuitry further amplifies the rod responses. However, color perception and spatial resolution are better developed in the central field of view.

Further reading (Cognitive Sciences.SE)

Rod and cone distributions: "Why can we not see around our point of focus of our eyes?"
Visual acuity as a function of retinal eccentricity: "Visual acuity and offset stimuli"

One of the absolute best answers ever, Alice!  I just wanted to add that peripheral vision is a critical survival mechanism that humans have forgotten how to access and use.  Like you have explained so perfectly, we are able to see more in the dark using our peripheral eyesight as well as detect movement far better.  People need to learn "owl eyes" versus "eagle eyes".  Focusing on one spot is eagle eye.  When focusing on one spot one loses their peripheral vision to a large extent.  By allowing one's focus to soften changes eye sight into 'owl eyes'...they use their peripheral vision better.

@stormy - thanks a lot for your words and your comment.


text:
Why do flies "rub" their front legs when resting?
I've noted that every time a house fly is resting on a surface, it appears to "rub" or "scrub" its front legs in a repetitive movement. And they do it continuously. Why?

Flies rubbing their legs are cleaning themselves. They can also often be seen rubbing their back legs often. Additionally, flies also often clean their wings, compound eyes and bodily bristles. Legs and wings are used as a primary means of locomotion and means of escape. Eyes and bristles are sensory organs and hence also essential for their survival.
Below a picture of a tachinid fly showing the bristles and compound eyes:

The eyes need to be clean as they are essential for the detection of visual stimuli. The bristles, as a commenter rightfully stated, contain chemoreceptors reminiscent of receptors on the human tongue that sense sweet and bitter tastes. These taste receptors alert the fly for sweet (food) and bitter (poisons) substances. Hence, cleaning of the legs may not only serve hygienic purposes, but may well be important for keeping the bristles and hence the associated sensory organs clean and free of prior encountered substances.


text:
What equipment is needed to perform simple plant electrophysiology?
What is the minimum needed equipment to perform simple plant electrophysiology? I am looking for some simple experiments that I could run at home for learning. Ideally, I would transfer the skills to stud neuroscience later on (the skills could be related to operating a microscope, doing recordings with microelectrodes, signal processing, statistics, etc). How expensive this would be?

I think it will be difficult to do at home. You would need to dissolve the cell wall first, to do electrophysiology. You would need cellulase+pectinase.

@WYSIWYG dissolve the cell wall? I don't know about plants, but the popular methods in neuroscience, such as patch clamp, measure the voltage between the plasma and the environment. The membrane has to stay intact so you can measure the current which depolarises (and sometimes hyperpolarises) the cell.

@rumtscho In neuroscience methods the clamp is fixed on the membrane. In this case there is an additional layer of cell wall that is quite permeable. IMO you won't be able to attach the clamp on the membrane properly.

Electrophysiology on plant cells means single-cell recordings, as there are no gross compound action potentials.  As you correctly say, this means micro-electrodes; this in turn means computerized manipulation of the pipettes, a decent microscope, signal amplifier, recording software, stimulator slash voltage/current control, Faraday cage, analysis software (Matlab), and not unimportantly a vibration-free workbench (whole departments have moved house due to micrometer vibrations in the building). I guess you should think anywhere between 10k - 100k (dollars, euros whatever) as a reasonable estimate.
A student internship would be advisable finance-wise, but especially because single cell recordings, and electrophysiological skills in general, are relatively difficult to master.


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Why do we only initially feel the bending of a hair?
In my neurobiology class, my professor prompted us to take the tip of our pencil and fold or push down a single strand of hair on our arm or leg in the opposite direction that it grows in. He then commented on how we are able to detect the initial stimulus, but how after a while we no longer feel the hair being bent.
My question is thus, why does this occur? Why would we suddenly no longer be able to feel the stimulus of the hair being forced back?

Short answer
Touch receptors become unresponsive after continuous stimulation, a process called neural adaptation.
Background
There are various touch receptors in the skin (Fig. 1). One of them is the hair follicle receptor. These receptors form sensory nerve fibers that wrap around each hair bulb. Bending the hair stimulates the nerve endings.
All the afferent fibers of the skin receptors in the skin show neural adaptation. A rough classification of the various skin receptors is grouping them in rapidly and slowly adapting fibers.
Rapidly adapting fibers respond mainly to pressure changes. Typical examples are the Pacinian and Meissner's corpuscles, but also the hair follicle receptor.
Fig. 1. shows a static stimulation of the various receptors. Upon initial stimulation, the hair follicle receptor (Fig. 1a) vigorously fires action potentials. Because the hair follicle receptor rapidly adapts, however, it soon stops responding when the hair is continuously, statically bent in that same direction. Once the stimulus is removed it fires another volley of action potentials because the hair moves again.
In other words, the hair follicle receptor responds to strokes, stretch and skin vibrations, as it is a novelty detector; it detects change, just like Pacinian and Meissner's corpuscles do (Fig. 1b,c). This opposed to Merkel cells and Ruffini endings (Fig.1d,e) - these receptors are designed to continuously fire action potentials upon a static pressure stimulus (Fig. 1), although even these receptors eventually give up and become unresponsive.

Fig. 1. The skin receptors and neural adaptation. source: Delmas et al., (2011)
Reference
- Delmas et al., Nature Rev Neurosci (2011); 12: 139-15


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What is it that creates that wonderful smell after a fresh rain?
I've heard that the wonderful smell of a fresh rain is actually chemicals  released from the trees and grass and other plants.

What is the process that allows these chemicals to be released?
What are the chemicals that create that smell?
How is it advantageous for the plant to release the chemicals rather than hold onto them?

The fancy word for it seems to be petrichor. It has a nice wikipedia article which might lead you to some of the relevant publications. https://en.wikipedia.org/wiki/Petrichor

Yeah, +1 and you go 2000+ :D Petrichor ;)

That molecule is called Geosmin. It is mainly produced 1 by Actinomycetes such as Streptomyces which are filamentous bacteria that live in soil. Other organisms also produce geosmin:

Cyanobacteria
Certain fungi
An amoeba called Vanella
A liverwort

It is an intracellular metabolite and cell damage is the primary reason attributed to its release. However oxidant exposure and transmembrane pressure also causes geosmin release in cyanobacteria. It seems that the release is triggered by some kind of stress.
I am not quite sure about their advantage to the host species.

1 or perhaps the most well-studied in

Interesting answer!

What about Petrichor that @skymningen suggested in the comments?

@SolarLunix I guess that is the name of the smell, not the molecule itself

The Wikipedia article on Petrichor mentions geosmin, and indicates it is a compound different than petrichor.

@mgkrebbs Yes I checked that but I did not find much info on what petrichor really is. Moreover the wiki article does not have much info.

The aerosol generation by the rain droplet impact on wettable surface being the mechanism releasing geosmin from the soil into the air completes the story. The paper is at https://www.nature.com/articles/ncomms7083, together with a PDF version of the paper.


text:
What motivates birds to make birdsong?
I was pondering the question "Why do humans make music?" and on an intuitive level, my answer was "because of the feelings it evokes of course!"
But I then wondered, what about songbirds? Does a songbird have a feeling that compels it to make songs? I know there are plenty of instances of birds dancing and singing (at least, some call it that), but what motives does a songbird have to make birdsong?  How does this compare to the emotions and motives humans feel?

Why do bird sing?
The main reason, male bird sing to attract mates (often, only males sing). Birds may also sing to communicate to their peers. For example a song can mean "This is my territory, you'd better not approach!". There are other reasons birds can sing (although I think I cited the two most important ones); you'll find much more information if you just google why do birds sing?, there are plenty of very accessible online articles on the subject. Here is one such article that you may like reading
Talking about emotions is always difficult due to the absence of a good definition of what an emotion is. But anyway... yes, if females are attracted to the mates that sing well, it probably (depending on your definition) means it cause them to feel some emotions (sexual excitement for example).
Evolution of music in birds and humans
Bird song to attract mate (sexual selection). Humans, on the other hand, have evolved music production for different reasons (or at least this is what we think). The field of evolutionary musicology is a field in the junction between evolutionary psychology and biomusicology. In evolutionary musicology (and in evolutionary psychology) empirical testing is very complicated and therefore, today we can only think and make hypotheses but we can't test them. So always take with a grain of salt what you read in those fields.

+1 As a side note, like AliceD you are good at formatting. I'd give an extra +1 for style if I could. I also did not know biomusicology was a thing! Very interesting. I will have to read my songbird books and consider what you say about emotions. Maybe I should look more carefully at how they define the term.


text:
Are the sympathetic and parasympathetic nervous systems exact opposites?
Suppose mechanism existed that could block function of the PNS. Would this just mean then the sympathetic nervous system would become overly active?
Do the sympathetic and parasympathetic systems act as opposing forces?

The Autonomic Nervous System is composed of the sympathetic and parasympathetic nervous systems. Each are dominant under different conditions - both are always active but one is dominant.
An important way to understand the the autonomic nervous system is in considering the effects of pharmaceutical drugs.
Sympathomimetic drugs enhance adrenergic function.
Sympatholytic drugs interrupt adrenergic function.
Parasympathomimetic drugs enhance cholinergic effects.
Anticholinergic drugs inhibit cholinergic effects.
For example:
Muscarinic antagonists are parasympatholytic (Anticholinergic) drugs - which reduce the effects of parasympathetic system.
But it is not that simple. They also increase sympathetic tone.
But again it is not always that simple. E.g. for sympathomimetic drugs (enhance adrenergic function) - there is no parasympathetic nervous system effect.
To answer your question, the sympathetic and parasympathetic nervous systems oppose each other sometimes. It depends on which receptors are activated and where.
(E.g.Alpha 1 receptors, Alpha 2 receptors, Beta 1 receptors & Beta 2 receptors).
Source & further reading on pharmaceutical interventions
Source & further reading on receptors


text:
Are there emotions that motivate pattern completion? If so, where in the brain are they located?
I have been studying musical "tension." Musical tension essentially refers to the "expectations" one builds up in a melody that are then "released" when a stimulus matching the expectation occurs. For example, if you play the white notes on a piano in order CDEFGAB, you have a "tension" that motivates you to finish the scale and play C to complete the pattern.
I am aware pattern completion occurs in the brain and have seen a few biological models of this. For example, with attractor network models of human memory. So I am not surprised obviously that pattern completion occurs. But this example with musical tension highlights how there is an emotion (aka drive or motivation) that compels me to complete the pattern. When I hear the sequence CDEFGAB, I am compelled to finish the sequence.
My Question
Can someone provide me of examples of canonical models of emotions influence on pattern completion? I would like to learn example mechanisms as to how, on a circuit level, emotion would influence pattern completion.  I am particularly interested in examples relating to common forms of human creativity like visual art, problem-solving, etc., but any examples will do.

This question should also be suitable for http://cogsci.stackexchange.com/, and users there might be able to offer a different perspective.

This "tension" is actually called anticipation in neurobiology and related fields. Whole purpose of this is to get higher reward. This is generally happens because of dopamine release. Many musicians have utilized this 'anticipation' technique in their compositions. Famous example is Led Zeppelin's stairways to heaven in which audience is 'anticipating' third part of song where Page's guitar in high tempo. Anatomically distinct dopamine release happens during anticipation and one will experience of peak emotion to music. You can read this paper for experiments related to this. This paper's introduction has given reference to many of such research papers. Go through it's references.


text:
What keeps organs suspended in the body?
I'm a bit confused what prevents our organs from not collapsing into a heap or putting pressure on each other. I have a 3D anatomy app and have been studying the relationship between the organs. According to the models, the organs are remarkably complementary in geometry and compact, but this still doesn't explain what prevents gravity from distorting them or squishing them.
My Question
What keeps organs suspended in the body?

Organs have internal structure to support them, and are attached to other organs and the various linings of the compartments in which they reside. They have many blood and lymph vessels going in and out of them as well. They do move somewhat with gravity, as the simple (for most people) experiment of standing on your head or laying backwards off an elevated surface will tell you. The body has evolved to contain them in a certain, not terribly flexible volume, so there's not much room for them to move around.

Most of the organs are attached to the abdominal wall by a fold of peritonium called mesentary.
Mesentary is a membranous tissue arising from the posterior wall of the peritoneal cavity and is responsible for keeping the organs at their designated places.Mesentary wiki


text:
How much force can connective tissue withstand?
I have been studying a 3D anatomy model. Based on visual observation,  it doesn't look like the bones would be able to stabilize themselves at all without the connective tissue like ligaments. In the model I have been studying, i've noticed that all the ligaments are clustered around joints or areas where the bones connect and it looks like it they act as a kind of glue to in essence keep the joints intact. However, I don't really understand how much force connected tissue must withstand on a regular basis.
How hard is it to keep bones aligned and confined enough that the bodies overall shape remains pretty constant? Is this the role of connective tissue? if so, how much force does such tissue need to withstand on a regular basis?

Do you have a specific connective tissue in mind? I'm guessing you are thinking of cartilage and ligament (blood is technically a connective tissue). Also in what orientation are the loads you are thinking of? Compression is very different from tension.

Ligaments and cartilage. Isn't that all there is? Is blood actually a significant player as a connective tissue?


text:
How does loss of the electrochemical gradient result in heat production?
As far as I understand, uncoupling of the flow of protons and ATP-synthase  provides a bypass for protons between the outer and the inner membrane of mitochondria so that the protons don't have to go through the ATP-synthase on their way to the matrix. I see how it results in loss of electrochemical gradient. But why is heat produced?

The same reason as what happens when you short-circuit a battery :) Same principle, same effect.

ALiceD's comment is perfectly true. (Though in real cases, the short circuiting is seldom absolute as there is usually some finite resistance in the short circuiting wire.)
You can understand this in two ways.
Intuitively, the uncoupling provides a channel for the hydrogen ions to move across the membrane in the direction of their electrochemical gradient without having to do any work. Therefore, the energy it gains by traversing a potential difference, can be thought of as being converted to kinetic energy, i.e. the hydrogen ions are accelerated by the potential difference which causes them to gain speed and hence move at a higher speed than the average in the final compartment. This will cause increased collisions (and more energetic) with the surrounding molecules, slightly increasing their kinetic energy too, which will ultimately increase the average kinetic energy, the measure of which is called temperature. If it was coupled, the hydrogen ions would not have gained the kinetic energy, as the energy they gain by traversing the potential difference would have been used to do work in the ATP synthase machinery.
Rigorously, you can show this using some chemical thermodynamics which includes using $\Delta G$ functions, $\mu$ functions and some related thermodynamic variables. Let me know if you want that explanation.(though I stand the risk of having lost the touch to the mathematical aspect of thermodynamics)
PS:- While the thermodynamic explanation also accounts for the increase in temperature due to obliterated concentration gradient, it is difficult to explain with the former model. You can think of this, as the neutralising of the concentration gradient changes the number of collisions per unit volume (and time), and hence also contributes to the observed temperature change.

The way that you have explained the mechanism is very nice +1

Thank you for your answer. I am quite happy with the intuitive approach for now. I am not sure I would be able to fully understand the strict mathematical explantion at this point, I feel I have to do some reading first.


text:
Why are vertebrae, specifically, so important in classification?
A fundamental level of animal classification is the distinction between vertebrates and invertebrates.  The vertebrata are, arguably, often classified as higher life forms than the invertebrata.  But why is the presence of the spine so important?  Why not use the simpler concept of internal bones as a classifier?
I might be missing something, but I can't think of any creature that has an endoskeleton but no spine.  Do any such creatures exist?  If not, why does classification focus on the spine and not the endoskeleton?

"If you have a spine, you're a higher form of life than things that don't." This is not true. Terms like "higher form of life" are meaningless

@CactusWoman You could say these stratospheric bacteria are literally higher forms of life!

@CactusWoman - I edited the question to make it less emphasizing on the higher/lower aspect

Short answer
The term vertebrata stems from grouping animals according to obvious gross anatomical distinguishing features as typically used in the early days of taxonomy. However, from a phylogenetic point of view, the presence of the neural crest during embryonic development, which is unique to this subset of animals in the phylum chordata, is a much more important distinguishing feature than the presence of vertebrae.
Background
Vertebrates belong to the phylum chordata, but share some characters that make them unique. Chordates, with a few exceptions, are active animals with bilaterally symmetric bodies that are longitudinally differentiated into head, trunk and tail. The most distinctive morphological features of chordates are the notochord, nerve cord, and visceral clefts and arches.
Vertebrates feature neural crest cells, which sets them apart from any other group. These cells appear early in development, and only vertebrates have them. Neural crest cells form the skull and jaw bones.
The neural crest has sometimes been called the fourth germ layer because of its importance (Fig. 1). The neural crest cells produce a variety of  cell types, including (1) the neurons and glial cells of the sensory, sympathetic, and parasympathetic nervous systems, (2) the epinephrine-producing (medulla) cells of the adrenal gland, (3) the pigment-containing cells of the epidermis, and (4) many of the skeletal and connective tissue components of the head (Gilbert, 2000).

Fig. 1. Regions of the neural crest. The cranial neural formt the bones and cartilage of the face and neck. It also produces pigment and cranial nerves. The vagal neural crest (near somites 1–7) and the sacral neural crest (posterior to somite 28) form the parasympathetic nerves of the gut. The cardiac neural crest cells arise from the neural crest by somites 1–3. Neural crest cells of the trunk (about somite 6 through the tail) make the sympathetic neurons, and a subset of these (at the level of somites 18–24) form the medulla portion of the adrenal gland. Source: Gilbert (2000)
In all, the term vertebrates is just a reflection of an apparent and obvious marker of this group of animals, namely the presence of vertebrae, but their distinguishing most important feature is the presence of the neural crest during development.
Reference
- Gilbert. Developmental Biology, 6th ed. Sunderland (MA): Sinauer Associates (2000)


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What evolutionary advantages are provided by ovoviviparity?
I read that some sharks are ovoviviparous.  What advantages and disadvantages are provided by this type of reproduction as opposed to egg laying and live birth?

Reading this website (www.sharks-world.com/shark_reproduction) it seems that for most sharks the eggs develop inside the mother (ovoviviparity), and the young sharks ("pups") are born fully functional, but this is not true for all sharks (as you mention in your question).
This persons blog (morgana249/modern reptiles give birth to live young) discusses evolution of ovoviviparity in some reptiles, but not others. In some species this seems to have gone back and forth in their evolutionary history, which suggests that changing conditions favour one then the other at different times, possibly influenced by temperature, among other things.

The researchers stated, "These results suggest that parity mode is a labile trait that shifts frequently in response to ecological conditions."

This could be similar for sharks, although I could not find an article postulating this.
Alternatively, this could be because the mother does no "parenting"; the pups are immediately independent. Because sharks do not have many eggs at a time (according to the sharks-world website) each individual egg/pup has a higher "value" than each individual offspring in other fish species, which often lay many hundreds of eggs at once outside their body (oviparity). Therefore sharks that evolved this trait may have been selected because the offspring are more likely to survive if they are protected until fully functional within the parent.
No doubt there are other possible explanations, but as with all these questions along the lines of "What are the evolutionary reasons..." we cannot ever actually know, only suggest.


text:
Latency differences between our senses
I would be interested in knowing how long it takes between the moment something touches our skin and the moment something is activated in the brain. Also how long does it take in total until we subjectively perceive something? And I would like to know whether this is dependent on which part of the body was stimulated (same latency for foot and neck?), or if it is dependent on the nature of stimuli (heat or mechanical). I would also be interested in that latency in the auditory and visual system. I tried searching for that but could not find what I needed due to the lack of the correct terminology.

Given your questions taken together and your comment It would be interesting to know how much delay the brain can handle in understanding causality and associating events I think you are interested in intersensory asynchrony. A well-known example where two stimulus modalities are perceived as separate while they are in fact coming from the same event is a thunder heard after lightning. This is caused by the fact that sound travels at a speed much slower than light, and hence a thunder can lag lightning by seconds.

source: NASA
In many instances, however, one event generating perceptions across stimulus modalities are actually perceived as synchronous while they are in fact offset in time due to differences in physical characteristics of the stimuli. Taking the storm as an example - when it is far away, the thunder is perceived as separate because the thunder lags by seconds. But when the thunderstorm is close enough, the auditory crack and visual lightning are actually perceived as synchronous, while in fact they are still offset because of the sound travelling so much slower than light.
So the question becomes, as you rightfully ask, what are the margins in which stimuli across modalities can be asynchronous while perceived as one event? In other words, what is the window of integration?
A review by Vroomen and Keetels (2010) describes various psychophysical studies that have examined what the minimal asynchrony is between two stimuli of different modality that lead to a synchronized percept. The following values are for simple stimuli, such as tactile taps, auditory beeps and visual flashes.

Auditory and tactile stimuli: 80 ms
Auditory beeps and visual flashes: 25 - 50 ms
Visual and tactile stimili: 35 - 65 ms

Note that these lag differences are relatively large, given the speed of peripheral neural transduction (see the other answer of Nandor Poka below). Moreover, the window of integration between more complex stimuli can be much greater. For example, the window for speech and visual information can be as large as 203 ms.  Such large windows of integration point toward higher processes playing a role in the brain.
Note that only temporal lags below 20 msec are expected to go unnoticed because of hard-wired limitations on the resolution power of the individual senses,
Hence, Vroomen and Keetels (2010) argue there must be higher processes at work in the brain that actively synchronize percepts that are offset in time, but seem to belong to one and the same event. One such mechanism is referred to as temporal ventriloquism, which means that one perceptual modality is actively shifted in time to match it with another. This effect is most pronounced in visual stimuli, in that a visual percept is actively adjusted in time to match a sound or tactile stimulus. Likely visual percepts are shifted preferably by the brain, because the visual system is the slowest of all the senses.
Reference
- Vroomen & Keetels, Att Percept Psychophys 2010; 72(4): 871-84

This is a really interesting set of questions and I'll try to answer all yet keep it compact. So first of all let's see the nerve classes and conduction speed from this and this wikipedia pages:
Peripherial nerves can be classified into three groups A, B, and C (based on their diameter).
Group A are the thickest (largest in diameter), are myelinated and have high conduction velocity.
Group A can be divided to subclasses:

'A' alpha nerves are 13-20um (micrometer) thick and have 80-120m/s
conduction velocity (this equals 288-432km/h (meter/s * 3,6) or
180-270mph (khm/h / 1,6)). These are associated with proprioception (this
subconscious sensation is responsible for us knowing how our body is positioned in 3D and where are our limbs compared to our body)

This means that in a fairly average 180 cm (approx 6 feet) tall human a stimulus on such nerve can travel the whole body of the person in 0,018s (with an average of 100m/s conduction velocity) How ever this is not the real case, I'll discuss that later.

'A' beta nerves are about half as thick as 'A' alpha (6-12um) and
conduct stimulus with 33-75m/s. Among others these are linked to cutaneous mechano receptors

Alpha and beta fibers can be both afferent (sensory) or efferent (motor)

'A' delta nerves are thinly myelinated and far slower than the
previous nerves with 3-30m/s velocity. These type of nerves are linked to nociception, cold thermoreceptors and make up the free nerve endings for touch and pressure.
'A' gamma fibers are efferent fibers and with 4-34m/s velocity.

Group B nerves are preganglionic fibers (ganglions are hubs of neurons of the autonomic nervous system) and conduct stimuli with 3-15m/s velocity. Thes are 1-5um thick and myelinated.
Group C are post ganglionic fibers (leading to the organs) and belong to nociceptors and warmth receptors They're thin (0.2 - 1.5um) and non myelinated. Their conduction speed is 0.5-2m/s.
So different sensory types have different nerves associated to them, and this results in different conduction velocity of that stimuli. Thus the answer is yes there is difference in sensation lag times to different types of stimuli.
In this paper scientist tested reaction lag time to heat caused pain and found the following:

Researchers stimulated two different parts of the hand of test subjects, the thenar eminence - that is the base of the thumb, and the volar forearm - that is the same side of the forearm as the palm ( the lower part of your forearm if you imagine your hands palms down). As you can see on the graph the volar forearm has lower lag times that the base of the thumb after a certain level of stimulus.
These authors also made a control experiment to:

estimate the sum total of time necessary for central sensory processing, the decision making plus motor execution times were measured in one subject for responses to suprathreshold auditory stimuli. Auditory stimuli were chosen because primary afferent conduction time is negligible. Latencies were measured in the same way as with the thermal stimuli. The tenth percentile (point at which 10 ~ of the latencies were faster and 90 ~ were
  slower) was near 0.19 s.

So response to sound is pretty fast, but this as with the heat experiment includes the measurable response of the test subject, thus the value is higher than the actual sensation.
For the heat-pain experiment the authors concluded :

The conduction distance from the area stimulated to the spinal cord was 0.78 m in this subject. If receptor utilization time, rise time, and conduction time in the cervical spinal cord are ignored, then primary afferents that signal first pain must have a conduction velocity of at
  least 0.78 m/ (0.33 --0.19) s, or 6 m/s.

The 6/ms velocity correlates well with the A-delta nerve's conduction speed.
Also here's another diagram on the distribution of lag times to different level of stimulus:

The difference of lag times can result from the activation of differrent receptors. Temperatures around 40 degrees Celsius are more likely to activate warmth receptors only that have lower conduction velocity. The high numbers of slow (1-1,5s) response to these stimuli correlate well with the group C fibers for warmth reception. On the other hand, responses to higher and potentially more damaging temperatures, nociceptors are more likely to be activated and faster conduction of these stimuli result in lower latencies. Also the transition from high latency to low is quite smooth with increase of the temperature.
Difference in nerve conduction values are not the only thing that occurs lag in sensation. These stimuli do not travel directly to the brain from receptors, but have to be transmitted to a sensory neuron, then these have connections in the spinal cord before stimulus can be transmitted to the adequate part of the brain, and then these neurons of the brain still have to process the signal. It is important to note that lag times are different from individual to individual. Authors of this paper conducted a great series of measurements to find out effects of age, sex and height on nerve conduction velocity and it turns out that for example:

Controlling for age and temperature, the 0.17 m/s decrease in sural  conduction velocity per centimeter increase in height (0.44 m/s per inch)
  was somewhat larger than previously reported.

Also this last article has many good comparison tables of different nerves and conditions.


text:
How can insects survive without an adaptive immune system?
How can insects survive in a world full of pathogens that are able to defeat the innate immune system?

As mentioned by InactionPotential, organisms and their parasites are caught in an arms race. When an organism develops a new defense, the parasites with traits that allow them to survive those defenses excel and vice versa. Parasites must balance their survival and reproduction with that of their hosts or go extinct. Over time they may become commensal/symbiotic, transfer to another species, and/or eradicate its host species.
Invertebrates' immune systems (including insects) as a whole are quite complicated. Because of the diversity of these systems we may not have anywhere near a complete understanding of them for decades. Some species intentionally upregulate their immune systems in anticipation of events that may expose them to pathogens. Social insect species, like ants, have evolved specialized immunities that take advantage of individual sacrifice, situational recognition, and colony health. Fruit flies possess radically expressive immunoglobulin receptors (IgSF), similar in some ways to the vertebrate major histocompatibility complex.
This diversity is key: the world is full of pathogens capable of defeating certain innate immune systems to some degree. However, the variety of challenges presented by even two different species usually prevents a pathogen from killing all of either species. As a pathogen becomes adapted to one species, it may lose its fitness for the other. If a pathogen is limited to one species, it has to make do with what it has or it will disappear with its host.
References and further reading

The Evolution of Adaptive Immune Systems
Social Immunity
Extensive Diversity of Ig-Superfamily Proteins in the Immune System of Insects
Biology of the Bed Bugs
Immunoglobulin superfamily members play an important role in the mosquito immune system

There is not really a definitive explanation for why, although it's important to note that many mammalian pathogens are not adapted to insects and vice-versa. Insects need to survive insect pathogens, and they have a number of defenses for this purpose. Animals and their pathogens co-evolve and exert selection pressures on each other.
Killing the host (or killing the host quickly) is often not in the pathogen's best interest. Pathogens evolve towards their own successful reproduction as much as animals do. Success may ultimately mean evolving towards a less pathogenic state that improves a pathogen's chances of being transmitted.
As animals develop new defenses, they gain an advantage (relative to others of their own species) in surviving various pathogens. Pathogens evolve to escape these defenses, and a new equilibrium is established. An animal lacking this defenses is likely to be more susceptible to dying of infection, as the new equilibrium is dependent on them having these protections.
Here is an interesting paper on this view: http://hedricklab.ucsd.edu/PDF/HEDRICKImmunity113.pdf

I think this is more of a comment than an answer.The question, to me, boils down to "why can insects suffice with an innate immune system (i.e. lacking an acquired immune system)?" This answer, although in itself valid and interesting, poses not more than a general view on  the co-evolution of pathogen and host.

I was debating between posting it as a comment and as an answer. Like most evolutionary questions, I don't think there really is a clear right answer.

You are probably right, but I thought it might be possible to answer this one without an evolutionary perspective. After all, evolution is not mentioned in the question, although it may implicity be tied to it. One way or another, fine enough. Downvote retracted :) [had to make a slight edit to do so - feel free  to roll back]

In the innate immune reponse, pathogens are recognized by a fixed repetoire of cell-surface receptors and soluble effector molecules. These receptors have evolved to recognize pathogens over hundreds of millions of years and provide a formidable defense against a wide range of pathogens.
Adaptive immunity has evolved only in vertebrates and complements the innate system with a very different strategy that allows for an almost infinite number of adaptations in the production of B and T cells.
That lower life forms survive without this adaptation is probably just a testimony to the efficiency of the innate system. Much of this answer must be credited to Peter Parham's text,The Immune System.

Insects have generally shorter life spans than many vertebrates, and since they are smaller they also have a lesser amounted of invested energy in the generation of individual members of the species.  A large number of animals have nervous systems and are capable of movement, and can thus actively avoid environments that might be harmful to them and have predators that are either orders of magnitude greater or smaller in size than the organism in question.
If they have variation among individuals for self recognition and complement, then a greater ability to reproduce more different individuals quickly with a lesser amount of food may help fill the relative deficit in disease resistance from not having adaptive immunity.
For vertebrates that is generally not an option due to the longer life cycles of each individual organism in comparison with either insects or bacteria or viruses.

Please add some references


text:
Why doesn't the ambient lighting condition change the perception of colors we see on a monitor?
Suppose that I take a picture of an object illuminated by an incandescent light bulb and I choose the daylight white balance setting. The picture I then get will display a white object as looking yellow, which is how the object would look had my brain not processed the image according to the ambient lighting conditions.
The question is then why the way the picture looks doesn't change depending on the ambient lighting conditions. If a white piece of paper continues to look white when illuminated by an incandescent light bulb, then why would that same piece of paper displayed on a computer monitor look yellow when I'm viewing it in a room illuminated by incandescent light bulbs?

Because actual reality and our ability to perceive reality are very different. Or brain is predictive and will predict white for a piece of paper under variable light color temperatures. But the context of the paper on the screen is different, as that is transmitted light and not reflected light. Your brain hasn't predicted that paper color by adjusting to the ambient light in the room. I would however say that you can perceive the differences in the reflected light coming off a piece of paper when you change the light source.

@AMR Can you please not answer questions in the comments section?

@Chris, but that isn't an answer. An answer would either from the standpoint of providing expert knowledge, i.e. in my field of study, or would be well referenced, neither of which my comments are. This reflects a comment, based on my general understanding that I feel adds to the discussion but does not rise to the standards of an answer.

The best ever answer is here: https://www.robotbutt.com/wp-content/uploads/2017/03/Calvin-Hobbes-Strip.png - that's a pity I have to keep it as a comment only :)

The phenomenon you are referring to is color constancy: The apparent hue of a reflective surface remains constant even when changes in the spectral power distribution of the illuminant alter the wavelengths reflected from it (Mather, 2008). In other words, despite substantial changes in illumination, we usually experience the color of an object as being constant.
The spectrum of wavelengths that enter our eyes is jointly determined by 1) the spectrum of the illuminating source (a variable), and 2) The spectral reflectance properties of the object (a constant).
To achieve color constancy, an object's spectral reflectance is the constant color parameter that needs to be evaluated.
Any information that better characterizes an object's spectral reflectance is a cue to colour constancy. This includes (Mather, 2008):

Local color contrast. Cone excitation levels of one surface relative to another remains constant when both surfaces experience the same change in illumination. Relative cone excitation levels are invariant ratios useful for achieving colour constancy.
Color adaptation. Adaptation reduces the contribution from the source illumination by lowering activity in the most highly active cone classes.
Global contrast. Global spectral changes generally represent changes in the illuminant; localised differences usually correspond to reflectance differences.
Luminance highlights. Glossy surfaces offer near-perfect reflections of the illuminant, which can then be factored from the rest of the scene.
Mutual reflections. The pattern of reflections that arise from different surfaces, under the same illumination, carries valuable information about the reflectance properties of each surface.
Range of reflected spectrum. This gives an indication of the breadth of the illuminating spectrum.

A graphical example of the effect of lighting conditions is found below (Fig. 1.)

Bowl of fruit photographed under artificial daylight (left), hazy day light (middle) and clear blue skies (right. Source: Mather (2008)
The most powerful cue to constancy is thought to be local color contrast (Mather, 2008). In other words, the relative contribution of the different cone classes stays constant, despite differences in the spectrum of the illuminant.
In your example, the object (paper) is not represented by a reflectance, but as an image; a representation taken out of its context, and it will appear yellow. Even if the ambient lighting is the same, as in your example, the monitor displays a 'real' yellow color, which has a different spectrum, because it is not a reflectance, but it is generated by a light source: your monitor; as mentioned in the excellent comment of @AMR. The real sheet of paper will have a different reflectance spectrum. Hence, both photo and real sheet will be interpreted as a function of ambient lighting by your visual system and they will appear different.
Even when your image was printed as a photo, the color is obviously different from the white sheet of paper. So the ambient light has a different effect on the reflectance spectrum of the photo and the real sheet.
Also the global contrast is different: the photo with a different spectral content than the real sheet is re-placed into the context of ambient lighting. Hence, the photo it is out of context and will be re-interpreted.
Reference
- Mather, Foundations of perception and sensation 2nd ed. Psychology Press 2008


text:
Why do I feel funny in my tummy when riding a virtual roller coaster?
I've ridden a virtual roller coaster on an Oculus Rift. I felt tension as I went up to the top, but more interestingly I actually felt my stomach drop when I went down the steep drop on the other side. Why can I feel this, when no forces are actually being applied to my stomach?
A bonus question: If you took someone that had never ridden a roller coaster, or even been exposed to rapid acceleration, and had them try a virtual one - would they feel the same stomach lurch as I did?

Why can I feel this, when no forces are actually being applied to my
stomach?

Acceleration sensors are in the ears and are part of the vestibular system. The vestibular nuclei in the brain uses acceleration- and visual signals to decide what happens to your body. It can be fooled by visual signals without the presence of acceleration signals. The role of the vestibulo-autonomic reflex - you feel in your stomach - is probably to protect your inner organs from the damage they can possibly suffer by acceleration.
The same can happen by watching films with fast camera movements on a monoscopic display (e.g. normal films in the cinema or video games on an average LCD monitor, etc...), however not so often than by stereoscopic displays (e.g. 3d films in the cinema, stereoscopic video games on a head-mounted display like Oculus Rift, etc...). This is because stereoscopic displays create the perfect illusion of depth (e.g. they can even be used by a therapy to overcome acrophobia), while monoscopic displays don't. So your vestibular nuclei is fooled much easier by stereoscopic displays.
References:

These data show that a subset of PBN/KF neurons, whose activity is
altered by a nauseogenic stimulus also respond to body motion and that
irritation of the stomach lining can either cause an amplification or
reduction in the sensitivity of the units to vestibular inputs. The
findings imply that nausea and affective responses to vestibular
stimuli may be modified by the presence of emetic signals from the GI
system.

2011 - Integrative responses of neurons in parabrachial nuclei to a nauseogenic gastrointestinal stimulus and vestibular stimulation in vertical planes

1995 - Study on vomiting related to the vestibulo-autonomic reflex.

This study describes the relation between the vection produced by
optical flow and that created by galvanic vestibular stimulation.
Vection is the illusion of self motion and is most often experienced
when an observer views a large screen display containing a translating
pattern. This illusion has only limited fidelity and duration unless
it is reinforced by confirming vestibular information. Galvanic
vestibular stimulation (GVS) can directly produce the sensation of
vection.

2005 - Virtual acceleration with galvanic vestibular stimulation in a virtual reality environment

Neurons in the vestibular nuclei are not only activated by vestibular
signals, but also by visual information. Consequently, the sensations
of body motion derived from visual and vestibular signals are
indistinguishable.
Sensations of body movement can also be generated by visual signals
arriving at the vestibular nuclei. During unnatural movements of the
body, conflict between visual and vestibular information leads to
disorientation and nausea, as in the oculogyral illusion, the Coriolis
effect, and vection.

Foundations of Perception - The body senses - The vestibular system

Three-dimensional movies presented via stereoscopic displays have
become more popular in recent years aiming at a more engaging viewing
experience. However, neurocognitive processes associated with the
perception of stereoscopic depth in complex and dynamic visual stimuli
remain understudied. Here, we investigate the influence of
stereoscopic depth on both neurophysiology and subjective experience.
Using multivariate statistical learning methods, we compare the brain
activity of subjects when freely watching the same movies in 2D and in
3D. Subjective reports indicate that 3D movies are more strongly
experienced than 2D movies. On the neural level, we observe
significantly higher intersubject correlations of cortical networks
when subjects are watching 3D movies relative to the same movies in
2D. We demonstrate that increases in intersubject correlations of
brain networks can serve as neurophysiological marker for stereoscopic
depth and for the strength of the viewing experience.

2014 - Stereoscopic depth increases intersubject correlations of brain networks

Statistical differences in theta activity showed that the real and 3D
environments caused similar cognitive processes, while the 2D caused
an increase of anxiety indicating that perhaps participants were
looking for the third dimension. Beta and gamma activity showed that
participants perceived the third dimension of the stereoscopic
environment as in the real one, something that did not happen in the
2D environment. Our findings indicate that stereoscopic 3D virtual
environments seem to approximate the real ones as far as it regards
the cognitive processes they cause. Three dimensional stereoscopic
environments increase users’ attention over the 2D and cause less
mental effort.

2013 - Stereoscopic perception of women in real and virtual environments: A study towards educational neuroscience

2001 - Human Cortical Activity Correlates With Stereoscopic Depth Perception

In this study the effects of virtual reality exposure therapy (VRET)
were investigated in patients with acrophobia. Feelings of presence in
VRET were systematically varied by using either a head-mounted display
(HMD) (low presence) or a computer automatic virtual environment
(CAVE) (high presence). VRET in general was found to be more effective
than no treatment. No differences were found in effectiveness between
VRET using an HMD or CAVE. Results were maintained at 6 months
follow-up. Results of VRET were comparable with those of exposure in
vivo (Cyberpsychology and Behavior 4 (2001) 335). In treatment
completers no relationship was found between presence and anxiety.
Early drop-outs experienced less acrophobic complaints and
psychopathology in general at pre-test. They also experienced less
presence and anxiety in the virtual environment used in session one as
compared to patients that completed VRET.

2004 - Treatment of acrophobia in virtual reality: The role of immersion and presence

Despite the increasing use of virtual reality, the impact on cerebral
representation of topographical knowledge of learning by virtual
reality rather than by actual locomotion has never been investigated.
To tackle this challenging issue, we conducted an experiment wherein
participants learned an immersive virtual environment using a
joystick. The following day, participants' brain activity was
monitored by functional magnetic resonance imaging while they mentally
estimated distances in this environment. Results were compared with
that of participants performing the same task but having learned the
real version of the environment by actual walking. We detected a large
set of areas shared by both groups including the parieto-frontal areas
and the parahippocampal gyrus. More importantly, although participants
of both groups performed the same mental task and exhibited similar
behavioral performances, they differed at the brain activity level.
Unlike real learners, virtual learners activated a left-lateralized
network associated with tool manipulation and action semantics. This
demonstrated that a neural fingerprint distinguishing virtual from
real learning persists when subjects use a mental representation of
the learnt environment with equivalent performances.

2009 - Impact of the virtual reality on the neural representation of an environment

Our main results are (1) stereoscopy in games increased experienced
immersion, spatial presence, and simulator sickness; (2) the eff ects
strongly differed across the three games and for both ge nders,
indicating more affect on male users and with games involving depth
animations; (3) results related to attention and cognitive involvement
indicate more direct and less thoughtful interactions with
stereoscopic games, pointing towards a more natural experience through
stereoscopy.

2012 - Understanding User Experience in Stereoscopic 3D Games

The results indicate that in a 2D movie viewers tended to look at the
actors, as most of the eye movements were clustered there. The
significance of the actors started at the beginning of a shot, as the
eyes of the viewer focused almost immediately to them. In S3D movie
the eye movement patterns were more widely distributed to other
targets. For example, complex stereoscopic structures and objects
nearer than the actor captured the interest and eye movements of the
participants. Also, the tendency to first look at the actors was
diminished in the S3D shots.

2014 - What do people look at when they watch stereoscopic movies?

For the correlation between anxiety and presence, the results show
very low correlation between anxiety and presence.

2009 - Using augmented and virtual reality for the development of acrophobic scenarios. Comparison of the levels of presence and anxiety

Stereoscopic visualization in cinematography and VR creates an
illusion of depth by means of two bidimensional images corresponding
to different views of a scene. This perceptual “trick” is used to
enhance the emotional response and the sense of presence and
immersivity of the observers. An interesting question is if and how is
possible to measure and analyze the level of emotional involvment of
the observers during a stereoscopic visualization of a movie or of a
virtual environment. The final goal of this research is a challenge,
due to the large number of sensorial, physiological and cognitive
stimuli involved. In this paper we begin this research by analyzing
eventual differences in the brain activity of subjects during the
observation of monoscopic or stereoscopic contents. To this aim, we
have performed some experiments collecting EEG data using a
Brain-Computer Interface device from two groups of users, during the
observation of stereoscopic and monoscopic short movies inside the
Virtual Theater of the University of Milan. From the analysis of the
collected data, it seems that interesting differences are present in
the average brain activity among the observers in the two groups, with
a significative effect of stereoscopic visualization.

2012 - Analysis of brain activity and response during monoscopic and stereoscopic visualization

If you took someone that had never ridden a roller coaster, or even been exposed to rapid acceleration, and had them try a virtual one - would they feel the same stomach lurch as I did?

Probably not. A congenitally blind person, who can distinguish between a globe and a cube by her touch, is not able to tell which one is which (without touching) when given sight. For details see the article "The newly sighted fail to match seen with felt" from Nature: http://www.nature.com/neuro/journal/v14/n5/abs/nn.2795.html.


text:
How to inactivate trypsin permanently by boiling?
I have to perform a hydrolysis of BSA with the enzyme trypsin. As a control I want to inactivate the trypsin enzyme. Can I inactivate it permanently by boiling (100oC) for 10 minutes, or does it it require 1 hour of boiling? After inactivation, I have to do a test (with an active enzyme) and a control with BSA at 37oC). At this point the inactivated trypsin (the control) should not be re-activated. So my questions are (1) whether I can irreversibly inactivate trypsin by boiling, (2) how long I have to boil it, and (3) if the boiling process will irreversibly inactivate the trypsin.

In my experience 10min at 100°C are sufficient, this is also supported by the paper linked below. Heat inactivation works by denaturing the protein and is therefore final.
Depending on what you want to do with you sample, it might be problematic, as this is probably also denaturated at least to some degree.
You can also chemically inactivate trypsin, either by adding fetal bovine serum (which is done in cell culture), which contains protease inhibitors as α1-antitrypsin and α2-macroglobulin or by using commercially available inhibitors. Trypsin is also inhibited by calcium and magnesium ions, so your reaction buffers shouldn't contain any of them.

A Simple Procedure for Effective Quenching of Trypsin Activity and
Prevention of 18O-Labeling Back-Exchange

The loading buffer for SDS-PAGE + heat(without dye) can also be used if little bit of SDS is okay. Or simply 2-mercaptoethanol + heat will also do [ref].

Since the purpose of this buffer is the denaturation of proteins, this will definitively work. The color helps during the loading and also forms the "running front" in the gel later.

You can consider these also:

Add 2-mercaptoethanol and heat at 95⁰ for 10 min [ref]
Add PMSF, incubate for some time and then heat for some time (lets say 70⁰ for 10min) to inactivate residual PMSF.