text:
Why do I get such a strong background in a detection of DIG-labeled DNA (Southern Blot)?
I have done a Southern Blot Analysis of DNAmt transferred to nylon membranes. The DNA was firstly loaded on a 2% agarose gel. An immunoassay was done to detect the bands using Anti-Digoxigenin antibody with Alkaline Phosphatase which catalyzes a colouring reaction with NBT and BCIP.
The results has a very strong background as you can see in the following pic:

I am not sure about what can be the reason of that background. I have read that thick agarose gels produce strong backgrounds, but I never experienced that before. If somebody has experience on this or alternative explanations, I would thank him/her to share them with me.

Could you please describe your procedure? It is extremely difficult to pick apart what may be wrong here when we have no idea how you made the gel, how long you placed the anti-body on, what you blocked with, etc etc.
2% is not a terribly thick gel. It's higher than the norm (~1%) but I've never had this trouble with them. My guess is you did something weird when placing the antibody or blocking. Perhaps made the buffer improperly.

I agree, try to post the full protocol step-by-step (e.g. 1, 2, 3) since sensitivity can be altered by a number of mishaps that can occur at different steps of the process!

Thanks FrankyG and Kendall. I will write a short traslated version of the protocol and will link it here in a while. It is the first time I follow it but I know it worked fine for other colleagues. Probably I did something wrong and am trying to figure out what. When I tell a thick gel I mean the mm of thicknes. I have read that "The recommended thickness for agarose gel is 3–4 mm; a gel thicker than 5mm will result in fuzzy bands and higher staining background." Source: https://www.thermofisher.com/us/en/home/life-science/pcr/elevate-pcr-research/agarose-content-with-tips-and-tricks.html

The protocol http://bit.ly/1QE3y7z

Offhand, I'd look at the blocking and washing steps (perhaps try a different source of nonfat dry milk). Be careful about contamination (alkaline phosphatase is ubiquitous). Also, you may be over-exposing - reducing reaction time might produce cleaner results. At the extreme end, you might try using peroxidase-linked rather than phophatase-linked antibodies.

I appreciate your suggestions R.M. It makes sense to reduce the reaction time. Over exposure could be the cause. I left it overnight. Next time I will check every couple of hours to find out if we can have a cleaner signal controlling this step. I will try also with another nonfat drymilk. I used a new package and brand, different of this used by colleagues in previous experiments. If nothing works perxidase-linked antibodies can also be a good alternative. Thanks a lot.


text:
How does the body survive Ebola?
Because Ebola takes over the immune system and uses it to replicate more and more of the virus, how does the body survive?
Is it a case of the virus being self-limiting and eventually just getting 'too big for its britches' so to speak? Or does the body somehow eventually start producing antibodies to fight it off?

From your text and the tag "retrovirus", I am wondering whether you are confusing ebola and HIV?

Nope I wasn't mixing up the two, I know that Ebola attacks the dendritic cells, monocytes, and macrophages. But I forgot about the T-cells and how it doesn't do much with them, HIV attacks those.

While the ebola virus infects a lot of human cells, immune system cells it infects are mainly monocytes and macrophages. The cells in our body mainly responsible for adaptive immunity, T cells, are at least not completely infected:

Our data indicate that 20–30% of CD4 and CD8 T cells died during the course of infection1

That's a lot, but the ones that survive get activated and it's apparantly enough that between 80 and 10% of the infected (depending on the strain) can survive the infection. Little is known about the details of the immune reaction to ebola, but the immune system does get activated. The immune system even remains on "high alert" for quite some time after infection and recovery.
And the antibodies do stick around, at least for 10 years. Whether they confer immunity against all strains of ebola, we don't seem to know - ebola isn't very well-researched yet.

So, basically, if you can outlive the initial damage, you'll recover, no? That seems to be the gist of the treatment: keep them alive with fluids and, if necessary, blood. I remember a student nurse saved almost her entire family at home (not hospital) that way.

@anongoodnurse possibly? I think the morbid guideline I heard was that whoever isn't dead 7 days after onset of symptoms will probably make it. CDC says it's a mean of 7 days: http://www.cdc.gov/vhf/ebola/healthcare-us/preparing/clinicians.html with the dehydration being really horrible in the end

source: Stack Exchange

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

sort: votes


text:
What is the advantage of using plant-derived antibacterials rather than bacteria-derived antibacterials?
So obviously we have a big problem with antibiotic resistance. Most of our antibiotics originate from bacteria themselves (or are synthetic variations on scaffolds which originate from bacteria). I have heard it asserted that using antibacterials derived from plants would lessen the problem.
One argument for the use of plants is that the bacteria from which we derive an antibiotic must themselves already be resistant to that antibiotic, meaning that the allele for resistance is already in the bacterial gene pool and when we exert a selection pressure by using the antibiotic, resistance will eventually appear among pathogenic species.
Another argument I have heard is that plants can provide a lot of structurally diverse metabolites from which we might discover new classes of antibacterials.
Is there anything else to this?
(I know I have answered my own question to an extent, but I am wondering whether there are any other good reasons to look to plants for the next generation of antibacterial drugs).
Thank you!

You're right that some antibiotics do originate from fungi e.g. penicillin, cephalosporin. But many antibiotics do come from bacteria (especially Streptomyces spp.) for example: chloramphenicol, erythromycin, kanamycin, streptomycin, tetracycline, vancomycin, gentamycin, rifampicin

Your first argument of use of plants isn't really valid.  Take streptomycin, which is derived from Streptomyces griseus.  If a person had an S. grisues infection, you wouldn't use streptomycin against it of course.  But if they get tuberculosis, you can use streptomycin without worrying the the TB will somehow transfer genetic information from S.g and gain it's "resistance".

I think you raise an interesting point, but I don't think anything is being ignored today as a potential source of antibiotics. Look at that 15th c. ox gall, copper, and this & that recipe to treat chalazions that is effective against MRSA.

@Nathan - If I'm not mistaken, horizontal gene transfer can result in exchange of genetic material between bacteria that are quite distantly related. I think it's possible that a Mycobacterium could acquire streptomycin resistance from Streptomyces.

@DIPEA Not to be cliche, but anything is possible.  But it seems rather unlikely that these two bacteria are going to transfer genetic material given their different native environments.  Also given that one produces a molecule specifically meant to kill, or at least, hamper the other.

@Nathan Here's a reference describing gene transfer between distantly related bacteria: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC284573/?page=1

@anongoodnurse you're probably right; I guess the search for new antibiotics has just broadened its horizons generally

@DIPEA - I think that knowing bacteria (and yeast) compete makes the ease of plating and measuring reaction to discs easy enough guesswork (wasn't penicillin discovered because of clear spots on a plate? I can't remember now.) Doing that with all known plants, though... that's a lot harder. Just my guess. But as I said, I think you raise an interesting and good point.

@anongoodnurse Yup, Alexander Fleming had contaminated Petri dishes and realized some fungi had a clear zone without bacteria around and said "That's funny" - true quote. And boom, pennicillin.

@DartFeld it wasn't quite "And boom, penicillin". More like  "And 12 years later, penicillin"

Bacterial isolates from ancient permafrost and isolated caves allow study of the resistome, or the collection of antibacterial resistance genes, in environments without exposure to modern antibiotics for medical and agricultural use. These samples have genes for resistance to antibiotics derived from a variety of sources, including fungal sources (penicillins, cephalosporins) and synthetic dyes (sulfonamides), as well as bacterial sources (macrolides, aminoglycosides, etc). This finding was surprising, but does help explain the rapid emergence of resistance in response to clinical use. The genes have been there all along.
The OP is correct that a great deal of our current armament of antibiotics were derived from bacterial products, but since fungal and wholly synthetic products don't solve the resistance problem, I don't believe plant products will either.

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

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


text:
sodium chloride and amylase activity
So, I did an experiment on the effect of sodium chloride on amylase. and I found out the higher the concentration, the slower the activity.
Therefore, is it valid to make the assumption that when we consume food with starch and high salt concentration, it can affect our digestion of starch? like slower break down of starch?

I highly suggest you actually look at studies that analyze this and there should be a good number since amylase is a well defined enzyme. (Bailey K, Hopkins RH, Dolby DE)
Not only that but applying this type of logic to any problem results in bad conclusions and therefore is bad science. (Berkeley)
The process of proving something scientifically is something that follows a somewhat predictable route. I only say that because not everything follows this exact path.
There is usually a nicer looking picture though I cannot seem to find it.
(Source)
So to answer bluntly, no. You cannot make that conclusion with any stretch of the imagination.
Being that amylases are so well studied you may have your answer after a few google searches, but the case remains that it took many years of research to reliably say so.

I found that the higher the concentration of NaCl, the higher the rate of reaction
Why is this different to yours?

Welcome to Biology.SE! Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then delete or [edit] your answer accordingly. In particular what you have posted is a comment, but you posted it as an answer. Answer are much more likely to receive a favorable response if they are actually answers and include supporting references (primary literature is best). Without that support, an answer is indistinguishable from opinion. Thanks!


text:
Are surface area or volume conserved during cell division?
I am a student of physics of mathematics with very little knowledge of biology. Nevertheless, I am very keen on biophysics and I'm trying to learn the biological concepts that I need on the way.
I'm preparing now my bachelor thesis (regarding the physics of cell division) and my advisor has recommended me a paper of his where he studies some forces that are relevant in this process.
Under his analysis the constriction of the cell is independent of the area of the cell (the cells constrict on a similar fashion no matter which size they have, the only important parameter is the shape) and he considers several different scenarios. Two of those seemed plausible biologically speaking to me but I don't know if they happen or not in real life. They are to consider the surface of the cell constant during the process or to consider the volume to be constant (during the constriction of the cellular vesicle prior to the division in two new daughter cells).
Are any of these assumptions realistic? Does the area or the volume of the cell undertaking mitosis change drastically during the constriction of the cellular vesicle?

Can you elaborate on what behaviour is assumed to be independent of the cell surface area? The review of the entire paper may be considered too broad, so pick up relevant points and add them in your question. The title also seems broad; can you please narrow it down to a specific point; for e.g. the role of surface tension in cell division etc

Cell area and volume should be measurable (over time) with live cell microscopy. Probably there is some data on this.

@WYSIWYG I have changed the title of the question and added a little explanation. I am interested in the behaviour during the constriction of the cell. Thanks.

What cells do you have in mind? Which organism? Which tissue?

Another PLOS One article gives evidence of change both in volume and in surface area, but it is across mitosis phases. It could still be considered constant during cytokinesis only.
It seems that cell shape and size have important function during mitosis, according to this research. It would be interesting to investigate different models from your advisor's paper (constant maximum radius, volume or area) but starting from different shapes and sizes.


text:
Identification of an insect from midwest US
I have been seeing them more and more frequently indoors.  I am currently in the Midwest United States, weather has been unusually warm for December, and there are many trees nearby. Can someone please help identify this?
The pictures are of the same bug, but from different angles.

Brown marmorated stink bug (Halyomorpha halys):

See here, here, here or here for information.
These have become hugely invasive in the Northeast and Mid-Atlantic (and slowly Southeast) portions of the U.S. as well as along the West Coast.
The brown marmorated stink bug (Halyomorpha halys) is native to Eastern Asia, and likely 1st started spreading around the U.S. in Pennsylvania in the early 2000s.

Finally, you can see an image of the life stages of H. halys here.
Update:
Just for clarification, other brown stink bugs do exist and can be easily confused with H. halys. This article from UF IFAS, for example, demonstrates how to differentiate H. halys from Euschistus servus:

See here and here for additional ID tips and further reading.

Though the brown marmorated stink bug is non-native and hugely invasive, the bug's 'ick'  factor is not as bad as the native stink bugs that smell WAY worse! I guess the difference is, people rarely find native species indoors while these Asian ones infest homes  in the winter, bringing them into closer contact with most people.

Also if you see one of these insects, please consider reporting it! Though the battle is likely lost, there are still attempts to actively manage against the spread of these stink bugs. Google "report brown marmorated stink bug" and find a local organization or university that is collecting data in your area /region

I've been seeing them for two decades in the Pacific Northwest!

General info about some common stink bugs foudn in the midwestern US: Stink Bugs of Ohio Soybean

I'm in the middle of Europe and just found one. Great.

@DavidTonhofer a quick search shows this insect was found in Europe as early as 2007 (Wermelinger et al., 2008). Zhu et al. (2012) created predictive models of their range expansion 8 years ago, which predicted spread throughout much of Europe (See Fig 6). Leskey & Nielsen, (2018) confirm that H. halys has established populations in many European countries as of 2018. (See map in Fig 1).

@theforestecologist Thanks. I'm in Luxembourg, 400km northwards even, directly east the yellow blotch covering the Ardennes region in Figure 5 of Zhu et al.. Well done.


text:
Can Biologists identify all viruses?
I went to the doctor today with my girlfriend, and the doctor said that she had a virus but doesn't know which one and she should let the infection heal with some rest.
The fact that the doctor didn't know what type of virus she has bothers me.
Do physicians/biologists not know all the different types of viruses out there? Is it not possible to identify all of them?

Identification of the virus will generally not help the doctor or the patient, just wasting time and money - I'm not sure there's many countries where there is an abundance of doctors and funding for healthcare that this wouldn't be a problem! :) If your Dr had suspected it to be a dangerous virus I'm sure they would have investigated further.

I, for one, certainly cannot. And since viruses recombine and produce new and new variants on a much faster scale than humans do, there is no chance that we can identify all existing viruses in the near future (or ever). Practically speaking, there is an infinite amount of different possible combinations of viral components.

Physicians and biologists are two different groups of people.

As an aside, I would suggest giving the Ted talk "Whats left to explore?" a read/listen. Admittedly its intended for a non-technical audience and may be a bit dated (from 2012). Biological dark matter is the corresponding (rather sparse) wiki page.

Immunity to many pathogens manifests similarly; there's enough evidence to discern viral vs. bacterial most of the time, though. Viruses are often self-limiting at that, and end up clearing after a few days, making it relatively pointless to prescribe an antiviral. Flu is tricky, to make things more complicated, since going with an antiviral is really only helpful soon after onset of symptoms.

To give you a picture of how little we actually know about microorganisms, if you take a soil sample from your back yard you are guaranteed to discover new species of microbes. Someone did this several years back simply to gauge how many more species there are to discover and to his surprise every time he did this experiment he always discover new species. Think about that: always. He could not find any soil sample that only contained known species of microbes.

Do physicians/biologists not know all the different types of viruses out there?

No, Biologists don't know all the viruses that exist out there. There's a lot! We do know many of the ones infecting humans, though, especially the ones leading to the most common diseases.

The fact that the doctor didn't know what type of virus she has bothers me.

Without knowing any symptoms, your girlfriend likely had was some kind of influenza (flu), rhinovirus (cold), norovirus (diarrhea, etc) or respiratory syncytial virus (strong). That's just the most common virus infections. Identifying those is possible (see lab tests for norovirus or influenza), but it's unnecessary in most cases.
The thing is, no matter which of these she has, the medical advice will stay the same - rest and fluids. So identifying them is just going to add time and money.
There are some cases where viral identification is done even for these diseases. For example, before giving an antiviral like Tamiflu, which is for example given to pregnant women with the flu. Before giving an antiviral, it should be established that she is indeed infected with the influenza virus. These tests are also done in patients who are hospitalized. In some countries and years, all influenza cases are screened to later know what strains of the virus infected how many people and how it spread.
As an example, if the result of the test doesn't change the treatment, the influenza test is recommended against by the CDC. With a gastrointestinal issue where norovirus is suspected, nobody is going to make an identification for a straightforward case.

+1 for "There is a lot". It seems that the virus diversity of the oceans is more or less known now, at around ~5500 species: Scientists Map 5,000 New Ocean Viruses. (Most?) of these are not infectious for humans though.

It's a cost/benefit situation.  Yes they could have taken samples, processed them,  teased out the virus, and eventually identified exactly what virus (sort of*) that your girlfriend had by its gene sequence.  But do you want to pay 10k-100k per virus to find that out, or just pay $20-100 and take some fluids and be fine.
I say sort of because viruses tend to mutate quite a bit.  A great example is the influenza virus.  There are many strains, with genotyping you can say this is H5N1 vs H1N1.  But typically the result for a person is going to be "You have the flu. <Insert generic flu advice here.>"
There are some tests specific to families, again flu is a great example.  Because the flu virus can be deadly to certain groups of people, and because it affects a lot of people, it's important to have a rapid test for it.  I just got the test today, only took about 15 minutes, thankfully I do not have the flu.
But for what I will call everyday cold viruses, there's no need for advanced or rapid detection.  And that's where you get the answer you got today.


text:
Does increasing the value of k in k-fold coverage requires more memory?
Study:
Here is what is k-fold coverage which is know as sequence coverage.
According to this, 2-fold coverage means the whole DNA is sequenced more twice in average.
Question:
If I have a genome sequence of length x with 30-fold coverage, then which of the following is correct?

I have to occupy 30x memory for the genome sequence, it means I would be given the genome sequence of length 30x.
It means I would be given the genome sequence of length x, but the sequence is more purified according to the calculation.

By memory you mean RAM or disk storage?

@EliKorvigo Mainly disk storage, you information about RAM is appreciated.

I guess it might increase RAM consumption, but that would not be a 30-fold increase, though that would depend on the genome assembler you use.

In Next Generation Sequencing (or better called 2nd generation sequencing) you are sequencing many many small genome fragments cut from many DNA molecules. Multiplying molecules, cutting them into fragments and amplifying them is known as library preparation (library of fragments to be read). During that process (of which PCR is important procedure) different errors or biases could be introduced.
What you get from a sequencer is many many short reads in form of FASTQ files that you need to assemble into genome sequence (by de novo assembly or more commonly by alignment to reference genome). It is important to know how sure are we for each nucleotide in assembled genome, which depends on how many times (and with what quality score) sequencer read each nucleotide (see image below).

(source: davidson.edu)
Coverage could mean average coverage across whole genome or coverage of some smaller portion of it (different coverage across genome is usually because of mentioned biases introduced in library prep).
To answer question: In final representation you get one whole genome assembled, if all you need is final representation (so answer 2). If you also store reads, then more coverage means more memory, but final genome is of same length.
NOTE: Coverage is even more ambiguous term that I just described, so you should look at this thread for possible different meanings (for example: which portion of whole genome is covered by sequencing).


text:
How can neuronal signals faithfully be reproduced by scalp electrodes?
There is a skull barrier (and possibly other layers too) between the brain and the scalp. I have seen people trying to extract EEG signals from the scalp by connecting electrodes and interface it to other devices. But how do these weak signals pass through these many barriers and reach the scalp electrodes? Also, "scalp cells" will have their own dynamics, right?
I simply don't understand how can we even get a approximate measure of electrical signals inside brain from scalp.

This would probably find better answers on Cognitive Science stack exchange.

@user49102 - it is perfectly on topic here.

Short answer
Small electrical EEG signals need to be amplified and noise-reduced to be detectable. Noise reduction techniques include mathematical averaging and signal processing techniques like filtering.
Background
Neuronal activity is electrical and generates potential differences around each neuron. Potential changes generate electrical fields. These electrical field are what EEG electrodes pick up (Fig. 1).

Fig. 1. Electrical field generated by a neuron (top) and the correspodning electromagnetic field (bottom). The former is detected with EEG, the latter with MEG. Source: Picton (2002)
The intervening tissues (dura mater and the skull) are not very conductive and indeed cause those potentials to be weakened. Worse, still, the electrical fields diffuse on their way to the scalp, meaning that adjacent patches of neurons cannot reliably be distinguished at the scalp. In other words, the spatial resolution of the EEG is very poor. The small amplitude of the potentials simply needs signal amplification to make them measurable. However, as @user49102 points out nicely, background noise is amplified with it. Hence, the magic hat of an electrophysiologist may be needed to extract the signal on the scalp from the noise by using noise reduction techniques such as signal averaging and filtering. A notable example where signal averaging is used is the event-related potential, or ERP. A stimulus (e.g. a flash of light) is repeatedly presented and the time-locked EEG is repeatedly measured and averaged offline. The random noise is reduced by the averaging process and neat ERP responses can be extracted without much filtering needed. A specialized example is the visual evoked potential, or VEP (Fig. 2):

VEP. Source Creel (2015)
Your question whether scalp cells (skin cells) have their own electrical responses - Well yes and no. The skin cells do not generate action potentials and feature only steady membrane potentials. Hence, if they are picked up by the electrodes it will only generate a stable offset, i.e., a baseline shift. Nothing to worry about. Neurons feature active potential differences through their action potentials, and that is what is picked up - voltage differences.
The low spatial resolution and weak signal means that the activity of single neurons cannot be measured. Instead, the gross signal from many thousands of neurons is collectively measured. In turn, when those neurons fire randomly, they will cancel each other's responses out and little signal is obtained. The most robust responses are obtained when the brain generates synchronized oscillatory potentials, for example during slow-wave sleep (Roth, 2009).
While EEG has poor spatial resolution of EEG, it excels in the temporal domain. Responses of a few milliseconds can be measured reliably (Fig. 2). As a comparison, fMRI has a temporal resolution in the order of seconds.
References
- Creel, Visual Evoked Potentials, In: Webvision
The Organization of the Retina and Visual System (2015)
- Picton, Int J Bioelectromagnetism (2002); 4(2): 225 - 8
- Roth, J Clin Sleep Med (2009); 5(2 Suppl): S4–S5

"Hence, the magic hat of an electrophysiologist is needed to extract the signal on the scalp from the noise by using noise reduction techniques such as signal averaging and filtering" Don't overstate this - alpha waves are readily observable in raw EEG traces baring any filtering or averaging.

I'd phrase it as saying that to display specific, complex neural patterns, such techniques are necessary; but try to avoid the impression that you could not observe any neural activity at all without them. Alpha is important, clearly neural, and easily observable.

@user49102 - given the level of knowledge of OP I do not think nitpicking about which frequency band can, and which one can't be observed without signal processing.

Nice answer; I like that you discussed the difference between action potentials and gradients across scalp cells. (And if I may say, the way you're wearing the flip-flop hat is exceedingly effective!)

@Christiaan It's not so much which, but that any, oscillations can be observed, readily, without any processing. Processing is only required for observing interesting patterns, not for observing neuronal activity.

It's not a big point, I just wouldn't want anyone getting the impression you can only see neural activity in the EEG if you do preprocessing.

@user49102 Gotcha. However, in the end, EEGs are recorded with differential amplification, which is a very powerful way of excluding noise. Implicitly, one of the most common, but most powerful signal processing strategies is baked into the hardware.

@anongoodnurse - Thanks! But hey, that hat's supposed to be secret :)

"However, in the end, EEGs are recorded with differential amplification, which is a very powerful way of excluding noise" - yes, but Berger could see Alpha, with very rudimentary instruments, in 29, before Tönnies introduced the differential amplifier in the mid-30s. (Berger did almost everything wrong that could be done wrong, and he still saw neural activity.)

Still a good answer.

EEG has been recorded beginning in the late 20s, by people who were fairly clueless about electricity. While the strength of the EEG is indeed weak, it is readily observable with even such comparatively primitive technology.
The first thing you should take note of is that EEG measures the aggregate field. It does not see single neurons. It sees the synchronized activity of large neural populations of neurons - tens, hundreds of thousands of neurons at the very least, and probably more on the order of tens and hundreds of millions of neurons. This aggregate activity creates activity on the order of microvolts. This activity is then relayed (via the differential amplifier technique) to a powerful amplifiers. Modern EEG amplifiers have very large input impedances, and are thus able to amplify these weak signals. However, it still only observes mass action of large groups of neurons, not e.g. single action potentials by single cells.
Next, direct EEG analysis is comparatively uninformative for many reasons, including those you mention: that the scalp, the skull, and the other intervening tissue attenuate the signal. Thus, very often, extensive preprocessing is applied, such as averaging over many recordings. However, at least two features are already visible in the waking EEG. The first is the power-law structure of the frequency spectrum (although this is reinforced by the filtering characteristics of the tissue; the tissue filters higher frequencies more than lower ones). The second is the alpha wave, which is a large activity pattern coming mostly from visual areas. However, this is a very coarse feature; it tells us little beyond if the subject has their eyes open and is attentive, or has them closed/is inattentive.
Lastly, it is indeed generally assumed that deep sources (such as subcortical areas) are not picked up by the EEG (but only by e.g. MEG).
A good introduction to the topic is the book Electroencephalography by Niedermeyer and Lopes da Silva.


text:
Can galls be formed from mutualistic relationships?
According to Wikipedia, galls (cecidia) are formed by parasitic insects and mites like gall wasps (Neuroterus albipes). At some metamorphic stage, these organisms alter cell division processes in meristematic tissues of their host plants, which creates a tumour on (typically) the surface of leaves, branches or roots. These organisms use the galls as their habitat and/or food source (exploiting the sugars present).
However, I also know that bullhorn acacia and ants form an interspecific mutualistic relationship (with galls), so apparently galls don't need to be parasitic. Are there any other specific plant-insect pairs that have the same type of mutualistic gall relationship as the acacia-ant system?

Pardon the initial link and thank you for clarifying the question

Thanks for fixing it. I'll remove the now obsolete comment.

From what I know of ant-Acacia mutualisms, I've never heard of an ant gall in an Acacia. The link in your question also never mentions a gall. You've likely confused either domatia or Beltian bodies as a gall. Both differ greatly from galls in that domatia or Beltian bodies are created by the plant and not by the insect.
Domatia are small plant-made chambers that house mutualistic insects (though are often invaded by non-mutualists).
Beltian bodies are a type of food body (or plant-made structures containing nutritional substances (often high in protein) that attract a mutualist species of ants in Acacia).
See here or here for more info about galls.
To answer your overarching question of whether there are mutualistic galls, I would have to say no. I do not know of any instances of which this is the case. Further, galls are inherently parasitic (not mutualistic). Even if the swollen cells do not interfere with normal plant function (e.g., as is common in Solidago spp.)1, the parasitic insect (or other arthropod) is still required to chew its way out of the gall. Last I checked, chewing on your host's tissues is never very mutualistic.

 1: Crutsinger, G.M., Habenicht, M.N., Classen, A.T., Schweitzer, J.A. and Sanders, N.J., 2008. Galling by Rhopalomyia solidaginis alters Solidago altissima architecture and litter nutrient dynamics in an old-field ecosystem. Plant and soil, 303(1-2), pp.95-103.

Yes, pollinating fig wasps are gall inducing and mutualistic at the same time, and actually essential for the pollination of figs (see e.g Martinson et al., 2015). During the very intricate mutualism, fig wasps deposit eggs in some of the flowers and leave others. The flowers with eggs and later larvae will develop into galls that will produce new wasps but no seeds, while the flowers that lack wasp larvae will produce seeds. However, the hatched females that leave the figs will pick up pollen before leaving, and are essentially the only vector for cross pollinations between fig plants.
(with the aim of expanding the answer later...)

I do not believe that galls are categorically non-mutualistic. However, as noted above, ant domatia (of acacia at least) are not galls, the trees produce them in the absence of ants. However, the size and number of domatia seems to be mildly inducible by the presence of their symbiotic ants.
But back to galls as mutualistic, my argument is that seemingly purely parasitic/herbivorous galls may also provide indirect fitness benefits to their host through their affect on the endophytic community. There is a vastly underappreciated universe of endyphytes, many are commensal and benign, but there undoubtedly parasites among them, and perhaps their predators as well, qualifying those endophytes as 'mutualists', and thus there are nested ecological interactions in many wild plants which are not apparent when we zoom in on two characters in the whole scene. Insects introduce certain hormonal factors, antimicrobials, and other chemicals which directly affect the dynamics of these endophyte communities. Basically the parasite benefits from keeping its host alive, and may provide immune function to its host in order to keep its food source alive longer, increasing the fitness of both the gall-maker and the host plant. Thus, from a somewhat game theory, lesser-of-two-evils kind of argument, this would qualify an apparent herbivore (a gall-making insect) as a mutualist under certain conditions.

Welcome to Biology.SE! Your answer is much more likely to receive a favorable response if you [edit] it to be based on published research rather than personal speculation and included supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and is thus off-topic for this site. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly. Thanks!


text:
Can a reservoir host act as a vector?
Is it possible to get an infection by contact with a reservoir host ?
Can a reservoir host act as a vector ?
What is the distinction between these two concepts (reservoir host vs vector) ?

Female Anopheles mosquito houses plasmodium vivax. But is not affected by the same. So reservoir host. But plasmodium is pathogen to human. So these terms are relative to perspective of viewer.

A reservoir host most obviously is a long-term carrier organism of a given pathogen that doesn't exhibit the disease caused by the pathogen.
A vector is literally any agent that transfers the pathogen to another organism. If you think about it, a reservoir doesn't have to be a vector i.e. there's no route of transmission they participate in, but a vector can certainly be a reservoir, such as bats, who often act as a vector for the pathogens they house (think Rabies). On the flip side, ticks are common vectors for Lyme disease, but small rodents actually act as the reservoir for B. burgdorferi (1).


text:
Why does the kidney of a cow have lobules, why the kidney of a human hasn't any?
The kidney of a cow has lobules, while the kidney of a human hasn't any.
I can't think of any reason why it would be good for a kidney to have lobules. It would be good if the kidney needed to have a large surface area, but I don't see a reason why it would have to, since there is no diffusion or another proces that needs larger area.

Is there any reason why it would be beneficial for a kidney to have
lobules?
Is there a known reason why the kidney of a cow has lobules,
while the kidney of a human hasn't any?

Please edit your questions to provide links that reference the facts you are questioning. This will help future readers of your question that may not be aware of these facts to learn more, should they be interested. Thank you.

@AMR Thank you for your answer. But I am not sure what you meant by your comment. Do you want me to add a link to a picture of a human kidney and a cow's kidney?

I basically meant that you should add the sources of your research. How did you learn that bovine kidneys are lobular? If it was an article or a book you could say something like "The kidney of a cow has lobules, -X..." where X is the title of the article or a link to the source where you read it. I suggest it because it may not be common knowledge and someone may want to read more than your question and my answer on the subject. Also, general guidelines for asking questions on the site can be found here.

It appears that the invagination of the renal kidney is vestigial from development and unlike human and other mammals, the bovine kidney does not form a smooth outer cortex.

The kidneys of the bovine do not lose their foetal lobulation.

-Renal Anatomy - Anatomy & Physiology en.wikivet.net
However this is not related to its function.

Despite what it’s externally lobulated appearance may suggest, the cortex of the bovine kidney is continuous and the kidney is of multipyramidal type.

-Renal Anatomy - Anatomy & Physiology en.wikivet.net
If you want further information on the subject, The bovine kidney as an experimental model in urology: external gross anatomy; Carvalho, et. al. Cells Tissues Organs. 2009;190(1):53-8. doi: 10.1159/000159370 made measurements of the bovine kidneys and compared then to human measurements. This article is unfortunately behind a pay wall, so you will need academic access to Medline to access.
One observation that they do make is that

There are few publications about bovine kidney anatomy. The available information is general, contains little detail and is limited to the classical texts [Bossi et al., 1909; Nickel et al., 1979; Sisson, 1981; Dyce et al., 2004].

The question seems based on a partially incorrect premise (i.e., that human kidneys don't have lobules), but I could not discover any known reason for the variation in external appearance.
To start, all mammal kidneys contain renal lobules that form during fetal development and are necessary for the organ's function; so they are certainly beneficial.
In some mammals the kidney develops a smooth covering cortex that leads to the well-known "kidney bean" shape (as far as I can tell this is the case across all adult primates). Dogs, cats, sheep have the bean shape, and also have thicker kidneys than pigs, who have a more flattened shape. In some animals the left and right kidneys appear nearly "mirror image" in size and shape; in others (such as horses) the left and right are very different in shape. In the context of all this variation, cows are not that unusual among mammals, they do have a larger rumen that can force both kidneys to be on the right side, and the cortex that covers the lobules just doesn't develop to be as smooth as it does in humans. Since the lobules are universal across all the kidney shapes, and are often visible in a fetus with the cortex forming later, it is likely that is the original structure to evolve, whereas the smooth cortex was only selected later in evolution, and only in certain species where it was useful.
source: I have seen a lot of kidneys.


text:
Diffusion approximation to genetic drift
I am reading from the classical textbook Principles of Population Genetics, Hartl and Clark (pdf here).
Introduction
Let $f(p,x,t)$ denote the distribution of allele frequency $x$ at time $t$ knowing that at time $t=0$ the frequency was $p$. One can model the change in this distribution with time using the Kolmogorov forward equation
$$\frac{\partial f(p,x,t)}{\partial t} = -\frac{\partial [M(x) \cdot f(p,x,t)]}{\partial x}+\frac12\,\frac{\partial^2[V(x) \cdot f(p,x,t)]}{\partial x^2}$$
where $M(x)$ is the "drift parameter", which represents natural selection (thus, in the absence of the selection $M(x)=0$), and $V(x)$ is the "diffusion parameter", which represents genetic drift. The diffusion parameter is $V(x) = \frac{x(1-x)}{2N}$, where $N$ is the population size.
Question
Why is it true that $V(x) = \frac{x(1-x)}{2N}$?
I welcome intuitive explanations and mathematical proof.
Thoughts
I would think it derivates from the Wright-Fisher model of genetic drift where the distribution of allele frequency at the next generation is given by a binomial distribution.

What is the definition of N in V(x)?

$N$ is the population size. Thanks for noticing. Question edited.

It does indeed proceed from the Wright-Fisher model, specifically from its diffusion process approximation.
If the population is size $N$, then at generation $t$ the number of alleles is $A(t)$, and so the frequency of alleles is $x(t) = A(t)/(2N)$, assuming the diploid case. Then Wright-Fisher says that:
$$ A(t+1)\mid A(t) \sim \text{Bin}(2N,x(t)) $$
So the distribution of the next generation's count, given the last one, is binomially distributed (under random mating).
One can find that, for a binomially distributed random variable $b\sim \text{Bin}(m,p)$, the mean and variance are given by:
$$ \mathbb{E}[b]=mp\;\;\;\;\;\;\&\;\;\;\;\;\;\mathbb{V}[b]=mp(1-p) $$
Thus, we get that
$$ \mathbb{E}[A(t+1)\mid A(t)] = 2N x(t)
\;\;\;\;\;\;\&\;\;\;\;\;\;
\mathbb{V}[A(t+1)\mid A(t)] = 2N x(t)[1-x(t)] $$
Applying $x(t)=A(t)/(2N)$, we see that
\begin{align}
\mathbb{E}[x(t+1) \mid x(t)]   &= \frac{1}{2N}\mathbb{E}[A(t+1)\mid A(t)]= x(t) \\
\mathbb{V}[x(t+1)\mid x(t)] &= \frac{1}{(2N)^2}\mathbb{V}[A(t+1)\mid A(t)] = \frac{x(t)[1-x(t)]}{2N}
\end{align}
using the fact that $\mathbb{V}[cX]=c^2\mathbb{V}[X]$.
We can relate this to forward Kolmogorov as follows. Recall that the binomial distribution can be approximated by a normal distribution, with mean $\mu$ and variance $\sigma^2$ given by the mean and variance of the binomial. This tells us that: $$ x(t+\delta t)\mid x(t) \sim \mathcal{N}(x(t),(\delta t)x(t)[1-x(t)]/(2N)) $$
The properties of the normal distribution then imply that $$ \Delta x_t=x(t+\delta t) - x(t)\sim\mathcal{N}(0,\sigma^2(x_t)\delta t) $$
where $\sigma^2(x_t) = x(t)[1-x(t)]/(2N)$.
This implies the following equality (in distribution):
$$ \Delta x_t = \sigma(x_t)\Delta W_t $$
where $\Delta W_t\sim \mathcal{N}(0,\delta t)$. As $\delta t\rightarrow 0$, we get a stochastic differential equation,
$$ dx_t = \sigma(x_t)dW_t $$
where the solutions are Markov random processes (unlike e.g. ODEs where there is only one solution and it is a deterministic path; think of it as a noisy ODE), specifically in this case an Ito diffusion. Note the SDE has no $dt$ component since the increment mean was $0$. If we then consider the density function for the random process $p(x,t)$, it must satisfy the Fokker-Planck (Forward Kolmogorov) equation: $$ \partial_t p(x,t) = -\partial_{xx}[p(x,t)\sigma^2(x)/2] $$
which gives a probability distribution over the allelic frequency value at each time point (given some initial value I've not specified here).
Note that $V(x)=\sigma^2(x)$.

In terms of intuition, I'm not really sure. Essentially $V(x)$ measures how much perturbation in the allelic frequency you can expect to happen each generation due to purely random effects, i.e. genetic drift. Notice that there is no perturbation when $x=0$ or $x=1$, i.e. no random changes can happen if no one or everyone has the allele. Notice also that this variance is exactly the variance of a Bernoulli distribution. It's like we've distilled the individual-level model to a population-level model that simply looks at the frequency of the binary choice of allele presence, I guess.
The variance (noise) is maximal when the frequency is $1/2$. It's sort of pushing the allele away from the middle, by increasing noise when one goes there; one might expect that (if run long enough) any such model will hit and get stuck at $0$ or $1$ (not sure if this is true).
I looked a bit if there were any other interesting interpretations of the sde considered here (e.g. in physics), but couldn't find any. Basically, it would be equivalent to a heat equation, spreading under some potential function controlled by $\sigma$.

Your question is closely related to this one. My answer largely follows Tataru et al, Statistical Inference in the Wright–Fisher Model Using Allele Frequency Data.


text:
Do viruses linger/passively transport or attack the body at once?
Do viruses generally attack as soon as they can or do they lie dormant until they reach a cozy spot in the body?
Like is it improbable I have inhaled a virus if I do not feel pain in my lungs?

Different viruses have different "modes of attack". Also, it depends on what you mean with "attack".
As a really short introduction to what viruses are, they are very unlike your body cells or bacteria. They are literally (usually) just genetic information with a kind of shell. The shell allows them to penetrate cells, where they then use the cell itself to produce more viruses. That's all they do, reproduce.
So, what do I mean with different "modes of attack" - well, different viruses lead to different things. For example, infections with Herpes simplex are often asymptotic and many people have no idea that they are infected. If you get the flu, however, you will notice.
Every virus that can infect humans will try to spread as soon as it enters the body. It won't linger around and wait - HIV directly targets immune cells, herpes directly targets nerve cells. The reproduction does takes time, but if they start reproducing and the immune system can't destroy them immediately symptoms can follow soon (think influenza) or late (HIV/AIDS). With most viral infections, the immune system at one point catches up and destroys the virus.

Like is it improbable I have inhaled a virus if I do not feel pain in my lungs?

I'm going to assume you mean either the virus responsible for colds (rhinovirus) or the flu (influenza) here. No, it's perfectly normal to be exposed to either of these viruses without noticing anything. Many people come into contact with infected people without ever showing any symptoms, because their immune system takes care of the infection before any symptoms show up. If it does show up, it will be within a matter of days, though. The flu virus won't stay in your lungs for weeks waiting, it has no way of doing that (viruses are... very simple in that regard).

Like your answer but I am still wondering something: Say you know you are infected. Say you remember the times and the places where you felt pain. Is this a reliable time log/trace of how the virus entered/spread throughout your body? Maybe for some sorts of viruses?

@Emil It takes a certain so-called infectious dose of a given causative agent to become symptomatic of it's disease. The paradigm is that you normally get infected long before you experience symptoms, and by then the virus has rather nicely spread itself around in advance!


text:
What is the difference between "gene delivery" and "gene therapy"?
What is the specific difference between gene delivery and gene therapy?
As far as I understand, gene delivery is the first step of gene therapy, but where does gene delivery end and gene therapy begin?
Does gene therapy necessarily imply that the host DNA is itself changed, or is it just that there is "extra" DNA floating around with the host DNA that also gets replicated?

Citing wikipedia:

Gene delivery is the process of introducing foreign DNA into host cells.
Gene therapy is the therapeutic delivery of nucleic acid polymers into a patient's cells as a drug to treat disease.

In other words, 'gene therapy' refers to the use of 'gene delivery' for therapeutic goals.

So you're saying that literally the only difference is the purpose? It seemed to me (indeed, from the Wikipedia article) that Gene Therapy goes far beyond just delivery into the cell and includes the processes involved in getting the DNA into the nucleus and accepted by the host cell.

In my opinion the terms are interchangeable. The only difference I see is that "Gene Therapy" could be limited to therapeutic proteins, while "Gene Delivery" could be any gene, such as luciferase or GFP. Nuclear entry and transcription are still necessary by both, because even simple reporter genes won't do anything if they can't get into the nucleus or make mRNA. If you want to avoid nuclear uptake, look into mRNA delivery. Nuclear uptake is hard.

Gene therapy is not just delivery of genetic material into the cell. There are processes such as homologous recombination and reverse mutation that are also a part of Gene therapy that helps in correcting the genetic makeup so as to cure disorders.
Gene delivery is delivery of gene into the cell where as Gene therapy has an objective of correcting the genetic make up by inserting or correcting the defective gene. I hope that helps.

I dont understand. How and why could you deliver a gene to a cell not for the specific purposes of correcting a genetic makeup?

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


text:
Why do humans have 46 chromosomes?
Humans have approximately 25000 genes. Why are these genes on 46 chromosomes? Why not 40 or 50?

In general, the chromosome number has to be even because each set of chromosomes comes from 1 parent, so 2 x N is always even. But different species have different chromosome numbers. No real reason why humans have to be at 46. There are plenty of people who survive with 47.

Chromosome rearrangements are just a type of mutations, hence the process is stochastic. Some chromosomes split, some merge, some duplicate etc. These events are very rare, though. Like all mutations these influence fit to some extent, since karyotype structure is known to play important role in epigenetic regulation.

user137 and @EliKorvigo I think one of you can extend your comment into an answer.


text:
Why are fifth order Markov Models, the ones most often used for gene prediction?
As far as we know that smallest polypeptide chain length is 60 amino acids - so if we found an Open Reading Frame (ORF) of about 60 codons without the interruption of stop codon we can consider it to be a possible coding region or gene.
The fifth order Markov Model uses hexameric frequency to predict coding regions, however this doesn't seem very specific.
Why wouldn't we use higher order Markov Models with higher frequencies and more specificity? Wouldn't increasing the order of Markov models prevent false positive results?

We do not, in fact, know that "the smallest polypeptide chain length is 60 amino acids".  That is a purely artificial cutoff, not a biologically meaningful one.  There are undoubtedly many, many functional polypeptides that are much smaller but that have not been correctly annotated.

You also have to remember that higher order Eukaryotic genes are interrupted. If the exons in the gene you are looking for are all less than 180 nucleotides, then you are going to miss it. you also have to factor in splice acceptor and splice donor sites, alternate splice forms, codons for methionine that do not indicate the start of the reading frame, etc. Think of it this way; by increasing the stringency, you are throwing out more information. Most of that information is bad, but not all of it, which means that you are creating the situation where you miss things you want.

Why are you so sure that people stick to 5-order Marcov Chains? 2. This boils down to training the state transition matrix, i.e. increasing order leads to increasing the number of possible k-mers exponentially, hence at some point your sample becomes insufficient to estimate transition rates with enough confidence, let alone the computational complexity.

The problem with increasingly complex HMMs is that their parameter space tends to explode with the nth-order of the HMMs. Higher number of parameters is often not great because it reduces the possible number of observations that go into training each parameter and can increase overfitting of the model.
From the information that you are providing it is possible that the 5th order model reaches the sweet spot of having great performance with a reasonably contained parameter space.
It is not clear how your model also works.
Is each state a single nucleotide or a single KMER?
Is it a generalized HMM with separate states for exons and introns with the KMERs being observations?
Work by the Bier lab has shown that 5-mers are very good at telling apart enhancers from background using a SVM model for classification. In your context it seems pretty reasonable to use 6-mers to find genes given this finding.
For more details please check "Biological Sequence Analysis" by Sean Eddy and the work of Dr. Michael Brent @ Washington University in Saint Louis (his lab has done a lot of research on HMMs for gene finding).
It'd be useful to have one or few paper references behind your question.


text:
Why is the penicillin/ceftriaxone hypersensitivity test only done once?
I have had a severe bacterial infection. I was prescribed ceftriaxone, and when the time came for injecting it the nurse asked me whether I have an allergy to ceftriaxone. I answered that it's my first time, so she did the test and it was negative.
I was expecting a second test because as far as I know from type 1 hypersensitivity the body -  even if it is sensitive to an allergen - won't show a reaction the first time. The body makes the particular IgE and in the next exposure of same allergen it will have an allergic reaction.
So why is only one test done, considering the first two columns of the following picture?

From: Harsh Mohan's Pathology textbook 7E

When were you expecting a second test? Directly afterwards? After taking the antibiotic?

If you are not allergic, you are not allergic, and it's unnecessary to do the test more than once. If, on subsequent treatment with the same (or similar) antibiotic,you do develop an allergy, you'll know from then on, and they'll know not to give it to you. Finally, it's not necessary to test for every allergy that might possibly be present. Most allergies are not life threatening, and if you don't have a history of allergy, that's a good enough reason to believe it won't be a problem.

Can you please specify the time frame you were expecting the second test to occur? Were you treated at a later date with ceftriaxone, or were you expecting the nurse to give you a second test after she had just performed the first test? It is unclear from your question what the timeline was and what your expectations was.

You are misinterpreting that table. Peak action time refers the time after exposure if you have already been exposed to the antigen. Raising the adaptive response to the first exposure to that antigen will then take 8 to 14 days. Even if you are genetically predisposed, you need to activate that B-Cell to make IgE which acts as the Mast Cell receptor and triggers the degranulation that triggers anaphylaxis.

Please somebody read the first column (features) and it's first row (definitation). it says crystal clear what i want to know

I did read it and you are misinterpreting it. "...previously sensitized person" does not mean sensitized 5 minutes ago or an hour ago. It means weeks, months, or years prior. Reaction to humoral antibodies, means that you would have had to make the antibodies first from a prior exposure. That would be at the minimum 8 days to two weeks after exposure.

ok then why the nurse or doctor didn't recommend me to take a second test 2weeks or one month later if not directly (based on your explaination which is right )? because you too said that in your comment that the body first should be sensitized (making IgE's) in order to create allergy!

Was it a single bolus? You said it was by injection, so were they treating you over a period of more than two weeks? Or was it one and done? They aren't going to tell you to come in for a second test if you aren't receiving the drug, because you might develop a sensitivity to it. They would cross that bridge if and when they ever got to it. For the most part, you do not test healthy people for anything more than vital signs unless they are at risk or they have a complaint. Do you have other allergies, to other drugs or are you healthy? If you are healthy, then there is no point to test you.

The caveat to that is if that healthy person will be going someplace where they will not have ready access to medical care, such as an Antarctic research station or the International Space Station. Then you would give then a complete battery of tests, because there is no way to get to them with trained staff if something happens. The only other reason would be if there is something that suggest that their might be some problem. Like they warn you about the flu shot if you have allergies to eggs. Etc.

Because developing a hypersensitivity takes time. If you get exposed to an allergen, the body first has to produce those antibodies that then get used in the hypersensitivity response at the second, or subsequent, exposure.
If you are talking about taking a second test just minutes after the first one, how would your body even "know" that this is a second exposure? Two exposures within minutes are not distinguishable from one exposure for the body.
Usually, an allergic reaction shows the second time a patient takes a full course of antibiotics. It does not show at the second oral dose or injection, which are way too close to the first dose to have already lead to the developing of a hypersensitivity.
So, why test you in the first place? Because you might have been exposed previously without remembering it - people misremember what medication they got during their childhood all the time, I imagine, and your doctor/nurse seem to just routinely do the test before giving these antibiotics.
Sources/Reading
Drug allergies
Update on the Management of Antibiotic Allergy

Personally, my amoxicillin allergy decided to show itself on day 8 of a 10 day treatment, the first time taking it.

I'm not sure of something you assume in your answer  (because the question is unclear): I don't think the OP is talking about the second dose (though he might be), but rather the second course of antibiotics (at least, I hope that's what was meant.) Also, you might want to read about amoxicillin-associated rashes.

@anongoodnurse I thought he was talking about the course of antibiotics being the second exposure, the first being the skin test. But it's unclear. What do you mean with those rashes? Or rather, what do you mean with them in relation to this question/answer?

There already has been an answer but I'd still like to clarify further. I'm assuming the OP was expecting a second skin test because type 1 hypersensitivity requires a repeat exposure. Getting exposed to the antigen will just get you sensitized but will not precipitate the reaction.
What I want to clarify is that the skin test doesn't test whether you are allergic to a medication but if you are already sensitized to it. It is important to get the difference.
If you have. never been exposed (hence sensitized) to ceftriaxone before, the test would be negative even if you are actually allergic. And as sensitization needs time, you wouldn't be getting tested right afterwards (as mentioned in the comments). Instead, you'll be given the dose.
So why skin tests? That's because the dose is low and intradermal - chances of a full blown anaphylaxis are lower (not zero) even if the pt. is previously sensitized.
So, to conclude, as mentioned in the previous answer, the skin test is done just once to check if you've already sensitized, since rarely do people precisely remember the medications they have been previously exposed to.


text:
Is there any mechanical digestion that occurs once food/chyme enters the small intestine?
Does mechanical digestion occur in small intestines and, if so, how does it occur? I found some sources that say digestion happens mechanically and chemically in the small bowel, and others that say it only happens chemically? Also, does chemical digestion only occur with acids (e.g. HCl) instead of enzymes, or does it occur with enzymes?

I believe in small intestine peristalsis is sometimes counted as mechanical digestion as the food is moved along the digestive tract. Chemical digestion occurs with enzymes secreted from the pancreas.
https://www.smartlivingnetwork.com/digestive/b/mechanical-and-chemical-digestion/ - source


text:
Why human skin colour disprove natural selection?
Amount of melanin decides the darkness and fairness of skin.
The darker the skin is, larger the heat energy it will absorb from sunlight.
The lighter the skin is, less will be the heat energy absorbed.
The people in cold regions of world should have darker skin to absorb much heat available. And people in hot climate should have reflexive white skin to reflect much heat from sunlight.
But here's exactly opposite of it. Why?

Melanin is there to protect skin cells (their DNA) from UV light, not to "absorb heat".

Also, even having traits that are not beneficial does not "disprove natural selection". If our own skin color would disprove such a fundamental part of the theory of evolution, it really wouldn't be around anymore ;-)

Your conclusion is actually the exact opposite of the reality.
Light skin in colder climates (i.e. climates that have short winter days) is selected for because melanin blocks the absorption of 310nm UV light which is needed to produce vitamin D.
The evolutionary significance of vitamin D, skin pigment, and ultraviolet light; RM Neer,
Am J Phys Anthropol. 1975 Nov;43(3):409-16.
The less melanin you have, the more UV you absorb, the more Vitamin D you produce. As Neer says, "Vitamin D deficiency can cause death, immobilization, or pelvic deformities which prevent normal childbirth." Vitamin D deficiency can be fatal, so the harder it is to produce, the harder it is to produce Vitamin D, the less likely you will be to survive and reproduce in areas where days shorten for 6 months out of the year as a result of the tilt of the earth.
This can be witnessed in the lengths that societies living closer to the poles go to to supplement natural Vitamin D production, adding Vitamin D to dairy products or as this famous National Geographic photo shows , exposing children to doses of UV light.

- Ultraviolet Bath, Russia by Joe McNally

http://photography.nationalgeographic.com/photography/photo-of-the-day/ultraviolet-bath-mcnally-pod/

This article, The evolution of human skin coloration by Jablonski and Chaplin gives a review of the how skin color is an adaptation "related to the regulation of ultraviolet (UV) radiation penetration in the integument and its direct and indirect effects on fitness."

Your underlying assertion of the purpose of melanin is incorrect.  Although we need sun exposure for production of things like vitamin D, it doesn't take much to do this.  You're correct that lighter materials will reflect more light, but that's not enough to prevent UV damage.  So there's no advantage for being able to absorb more sunlight for energy or protein production.
Instead look at it as a protective mechanism.  People with light skin suffer from UV burns in shorter time than those with darker skin.  People in cooler climates are typically in the sun less, or at least more of their body is covered when they are in the sun.  They don't need as much protection from the sun as do people where it is warmer that are typically out more with less clothing needed to feel comfortable.
Many times the claims that "disprove natural selection" are just because they're being viewed from the wrong vantage point.


text:
Immunotherapy for tumours which do not have TSA
Is immunotherapy possible for tumours which do not have Tumour Specific Antigens (TSA)? If so, doesn't targeting those tumour cells also target other healthy cells, thus causing autoimmunity ?

chemotherapy kills a lot of cells, but tumorigenic cells die first. Same can be true with immunotherapy

During chemotherapy , it is true because tumour cells have weaker dna repair system compared to healthy cells.  But when it comes to immunotherapy, cancer cells are good at immune evasion.

Yes, in some circumstances.
In some cases the antigen being targeted, even if it leads to loss of normal cells, can be targeted. This is most evident in the targeting of CD19 to treat various forms of B-cell derived tumours. Example of such an application and response biomarkers are described here
https://www.ncbi.nlm.nih.gov/pubmed/28291388
Secondly, opportunities may be created by the generation of epigenetic states. Cancer-germline antigens are usually only expressed in gonad tissues (which enjoy immune privilege) but are often aberrantly reactivated in tumours, but not in other somatic tissues. This too can create specificity to immunotherapy even if the antigen is not truly tumour-specific, and is rather striking as a phenomenon in testicular cancer.
https://www.ncbi.nlm.nih.gov/pubmed/28555838

Monoclonal antibodies can have a range of uses: Avastin (Bevacizumab) directly targets VEGF to inhibit angiogenesis (with obvious side effects). Some mAbs are chemolabeled with a cytotoxic drug that can be delivered to tumor based on normal antigens, but the obvious downside is healthy tissue expression.
There's a fair overview of immunotherapies available here.


text:
Understanding the brain: how are neurotransmitters released in the brain?
I have a basic knowledge of how neural networks work. A potential difference is created that forces sodium, potassium, chloride, and calcium ions to flow which carries an electrical signal to the end of a synapse. From there, the presynaptic neuron releases neurotransmitters creating a potential difference to the postsynaptic neuron.
What I don't understand yet are the mechanics of which neurotransmitter will be released. Do the vesicles of each type of neurotransmitter have an energy threshold? If yes, when the highest energy threshold of a vesicle is achieved, does this mean all the other vesicles will release the encapsulated neurotransmitters?

The vesicles are associated with a calcium-sensitive membrane complex composed of quite a few proteins, some details here. (I'll try to detail an answer when time permits)

Have you heard of SNARE proteins?

The release of neurotransmitters is a very specific type of SNARE mediated exocytosis. The action potential from the influx of sodium propagates along the axon and reaches the axon terminal, containing the calcium channels. This causes the calcium cations (ions) to travel down the electrochemical gradient. The Ca2+ then binds to a protein. The vesicles containing the neurotransmitter called synaptotagmin (Ca sensors), would cause conformational changes leading to the formation of a SNARE complex. Some good animations can be seen here and here.
Regarding whether there is an energy threshold: there is a threshold on the amount of Calcium needed to cause the activation of synaptotagmin, as with all types of SNAREs.
See this article: http://www.pnas.org/content/93/23/13327.full.pdf
Past a certain calcium threshold, all the neurotransmitter should in theory be released, but whether they cause a response would depend on the receptor and on the postsynaptic membrane, as each synapse is specific in the neurotransmitters and receptors it expresses.

The mechanism was nicely described by FZG, I'd just like to add:

the mechanics of which neurotransmitter will be released. Do the vesicles of each type of neurotransmitter have an energy threshold?

According to this book, one such mechanism is frequency of stimulation (low frequency of action potentials) and subsequent Ca2+ distribution. With low frequency of stimulation, channels closer to the cleft are open, which means, there is higher concentration in the proximity of the cleft. With higher frequency, the concentration in the terminal bud is more equal in the proximity and further away from the synaptic membrane.
Since small neurotransmitters are usually docked closer to the synaptical membrane, low frequencies of stimulation are sufficient to increase Ca2+ in this area and release them, without changing the concentration of Ca2+ farther from the membrane, where the bigger neuropeptides are docked. They need therefore higher frequencies (as described above) to be released too. Picture.

If yes, when the highest energy threshold of a vesicle is achieved, does this mean all the other vesicles will release the encapsulated neurotransmitters?

As for the threshold, there has to be enough Ca2+ cations to activate the synaptotagmin, which is why the mechanism described above is working. However, there are few types of synaptotagmins, which have different affinities to Ca2+, which could be a another mechanism, if vesicles containing different neurotransmitter bound different synaptotagmins, but this is just a hypothesis as far as I know, maybe someone will know better here :)

The model in Fig. 3proposes that at least Syts 1, 2, 3, 6, and 7 perform complementary functions in Ca2+-triggered exocytosis whereby Ca2+ binding to each class of synaptotagmins contributes differently to triggering exocytosis

Source


text:
Basic Local Alignment Search Tool (BLAST)
Why would BLASTP (Basic Local Alignment Search Tool) be a poor tool to search for motifs in protein sequences?

This question needs more research shown. As it stands, it looks more like a homework question that should be closed.

BlastP carries out a search for sequence similarity to infer function by comparing an unknown sequence with a sequence that has already been annotated with a function, but structurally similar proteins with different sequences can have the same function because function can be mimicked if the replacing amino acid falls into a similar category as the substituted amino acid. The four major categories of amino acids are: negative charged, positively charged, polar and hydrophobic.
Proteins have many shapes, while the double helix in DNA is the form in which DNA is most often found. Therefore, the structure of DNA is not as important for function as the structure of proteins are for protein function. So you need a tool that can compare the three dimensional shape of one protein to another (in addition to sequence comparison) to make an estimate of how likely there is going to be a similarity in function. The Research Collaboratory for Structural Bioinformatics offers a tool that can compare proteins by sequence as well as by structure. The following screenshot shows the options for comparison under each of these two categories:

This doesn't really answer the question at all.

Because it has a poor statistical model. It's basically a local alignment tool aided by a fixed-length k-mer index. It estimates homology in terms of sequence identity and while this is often enough to find homology in relatively conservative sequences, the heuristic scoring model doesn't really allow to search motifs. A motif in terms of bioinformatics can be seen as a series of state-switch events, hence you need a model that estimates similarity in terms of likelihood of observing such a sequence of state switches under  your prior state-switch matrix (inferred from a training sample). These models are known as Markov models and people usually utilize Hidden Markov Models to find motifs. There are good popular tools, such as HMMER
EDIT as per OP's comment

As motifs are locally conserved regions & BLAST also performs local
  alignment then why it should not be able to search for motifs?

A motif is not just a "locally conserved region", it's a specific sequence profile. BLAST doesn't extract any sequence profiles, it wasn't created for that. Given a pair of sequences it simply shows you similar patches. Hence BLAST is simply not the right tool for the task. They made PSI-BLAST for that very sake.
Moreover, many motifs comprise amino acids or nucleotides that can be quite separated in a primary sequence and only get close in a folded (secondary or tertiary) structure. Here your definition of "locally conserved region" fails as does BLAST.
As I've already mentioned, BLAST performs a heuristic local alignment, that is it assumes that two related sequences must contain at least one common k-mer (word) of specific length. This, given a precomputed word index, significantly increases performance in terms of speed and RAM consumption. But similar motifs can be present in non-homologous sequences or in highly divergent sequences that hardly evince any homology, and BLAST won't find anything at all.

As motifs are locally conserved regions & BLAST also performs local alignment then why it should not be able to search for motifs?

@katherinebridges I've edited my post.


text:
What are the hairs/spikes on the edges of these leaves for?
Windows 7 has a wallpaper/background which shows an attractive, leafy plant with fine hairs or spikes on the edges. What might these be for, and what sort of plant is it?
My initial (uneducated) guess is some species of Sempervivum, with the hairs serving some purpose like water-collection?
Windows 7 leaf background http://p1.pichost.me/i/32/1555532.jpg

I believe the hairs are known as trichomes. They can be uni- or multicellular. Depending on the plant and type of hair, they can serve one or more of several purposes. They may interfere with feeding by small and/or large herbivores, depending on how annoying to the palate they are. Some plants use hairs to keep frost away from the surface of the leaf. They can serve as nucleation points for water droplets in areas where the plant's primary source of water is fog. On the other hand, they can also help reduce transpiration in windy areas by breaking up the flow of air across the leaf. Finally, in hot/dry areas, they can reflect some sunlight to protect the leaf's tissues.
So, the function really depends on the type of plant and its habitat. I'm not a botanist, so I can't confirm whether or not your guess of Sempervivum is correct, but if it is, then the hairs would likely help reduce transpiration in hot, dry, windy areas, and possibly block some sunlight.


text:
Is there a model perennial plant species?
Most of plant science is conducted on small annual species with short life cycles; predominantly Arabidopsis thaliana, but also a handful of others like Oryza sativa and Medicago truncatula etc.
Is there a model perennial species? And, if not, is there a good candidate that is relatively small but fast growing and able to be grown in lab/glass house environments that someone could recommend?

To my knowledge, Populus is one of the main model species when it comes to perennials and trees. It is for instance used in several sequencing projects, and to study accelerated breeding in strains that are promoted to flower at a very early age.
Excluding trees, other perennial species that has been described as model species are Panicum virgatum (Switchgrass) (see Lu et al. 2013. Plos Genetics) and Solanum lycopersicum (Tomato) (see Sato et al. 2012. Nature.
For a closer description, and arguments for Populus as a model species, see e.g. Taylor (2002. Populus: Arabidopsis for Forestry. Do We Need a Model Tree?. Ann. Bot.) or Jansson & Douglas (2007. Populus: A Model System for Plant Biology. Ann. Rev. Plant Bot).

Here it is argued that Populus is rapidly becoming accepted as the ‘model’ woody plant and that such a ‘model’ tree is necessary to complement the genetic resource being developed in arabidopsis. The genus Populus (poplars, cottonwoods and aspens) contains approx. 30 species of woody plant, all found in the Northern hemisphere and exhibiting some of the fastest growth rates observed in temperate trees. Populus is fulfilling the ‘model’ role for a number of reasons. First, and most important, is the very recent commitment to sequence the Populus genome, a project initiated in February 2002. This will be the first woody plant to be sequenced. Other reasons include the relatively small genome size (450–550 Mbp) of Populus, the large number of molecular genetic maps and the ease of genetic transformation. Populus may also be propagated vegetatively, making mapping populations immortal and facilitating the production of large amounts of clonal material for experimentation. Hybridization occurs routinely and, in these respects, Populus has many similarities to arabidopsis.

(from Taylor, 2002))

With the completion of the Populus trichocarpa genome sequence and the development of various genetic, genomic, and biochemical tools, Populus now offers many possibilities to study questions that cannot be as easily addressed in Arabidopsis and rice, the two prime model systems of plant biology and genomics. Tree-specific traits such as wood formation, long-term perennial growth, and seasonality are obvious areas of research, but research in other areas such as control of flowering, biotic interactions, and evolution of adaptive traits is enriched by adding a tree to the suite of model systems.
  ...
  The development of Populus as a model system for tree and woody perennial plant biology has been largely driven by the rapid development of genomic and molecular biology resources for this genus, as discussed below, culminating in the completion of a draft sequence of the Populus trichocarpa (black cottonwood) genome (106). This information will facilitate studies on the comparative biology of Arabidopsis and Populus as representatives of two angiosperm extremes, enabling discovery of mechanisms conserved among eudicots.

(from Jansson & Douglas, 2007)

Thank-you for your answer, and yes Populus trichocarpa is an interesting species. However its not quite what I'm looking for as it is difficult to study it like one would study Arabidopsis.

Being a large tree and (relatively) slow to reproduce mean that you cant control enviromental variables (light duration, quality, temperature, humidity, etc) to a satisfactory level of accuracy to avoid systemic noise in any molecular experiments and genetics can't be done very quickly. I'm looking for an Arabidopsis type plant amenable to such experimental approaches.

@G_T I've now added two non-tree examples as well. However, note that you cannot find a long-lived perennial that is as as easy to study on a short timeframe as an annual such as Arabidopsis (almost by definition). This is sort of the point of looking into perennials as well, to get a different perspective and a comparison to short-lived annuals.


text:
What is the origin of prions?
We know something about the origin of the first cell. But what do we know about prions? How did they originate?

Well, it's not like we know the origin of cells.

@Bird - I agree with Eli... what do you mean by "we know the origin of the first cell"?

The computational study by Ehsani et al., 2011, argues that an ancestor metal-ion transporter gene ZIP served as the initial template for the prion founder gene, where the same author produced a 2012 paper that said this was probably a product of a spliced LIV-1 ZIP transcript that became reverse transcribed and inserted into the host genome. Thus, evidence in part points to a retrogene origin for prions (mediated by a retrovirus, especially since the gene is integrated into the host w/ no introns). They go on to state that two genomic rearrangements spanning hundreds of millions of years serve as the basis for the prion founder gene: A cysteine flanked core element inserted into the ZIP ectodomain, and then the insertion of a spliced, C-truncated ZIP transcript.
I don't think the evolutionary origin of prions are very well understood, yet, but I will try to find more recent data on the subject.


text:
What are the effects of non-ultraviolet light radiation on DNA?
I am trying better understand the effects of varying the frequency of light on DNA, however, most of what comes up is "UV light" and how it is damaging to DNA (presumably by ionization). Have there been any studies on radiation on DNA at lower frequencies of light?

have you tried googling?

yes that's why i'm here. everything i get keeps going back to uv light on dna.

Visible light aids DNA reparation after UV exposure (in prokaryotes at least) by activating the machinery. High-energy radiation (x-ray, gamma) causes double-strand DNA breakage (i.e. tears DNA into pieces).

@EliKorvigo any reference?

@aaaaaa Sure, this is for the visible light part, this is for the double-strand breaks

@EliKorvigo I think this is a good answer to OP if you format it as such

@EliKorvigo I'm unable to look at the full article, but I want to know what spectrum of light they used, and what sort of dependence on the frequency is observed in terms of the repairs that take place. Is this the only study that has been done or is there a broader field of study that this topic heads under?


text:
What are allogametes? please explain
Allo means different or unrelated I guess.Please clear me the meaning with some examples.

Where did you read the term allogamete? I dont think I've ever encountered this term. I would guess it applies to species that have a double nucleus such as many fungi species.

Here are a few notes on how to ask a question: 1) When asking for a definition, please provide the context in which you found the word to be defined 2) writing please explain in the title is useless 3) Add a space after the . at the end of a sentence.

I vote to close as unclear until your provided where you encountered this term.

@Remi.b I think you are being unnecessarily harsh. This is an example of a poorly asked question that leads to an interesting and informative answer.

@AMR I think it is still unclear whether the OP was meaning allogamy or allogamete. Simple edits would much improve the clarity of the question. Good answer though (+1)

I vote to close as it shows absolutely no research effort.

@rg255 Have you actually tried to research "allogametes?" Google scholar has 2 hits, one being a Science article from 1911. Google comes back with related hits, but none that specifically mention "allogametes." The OPs profile says that they are from India. If they are not well versed in science writing in English, then it may have been difficult to evaluate what they were seeing when not finding an exact hit. 1911 science writing would be difficult for most American science students not familiar with reading texts from the turn of the last century.

It's a poorly formulated question that would benefit greatly if the user made greater research effort, in my opinion

And....the OP should have said something by now. We've been discussing the meaning of its question for 2 days.

You may be getting confused with the term Allogamy.
Humans most higher animals are allogamous, which means that the ovum from one organism is fertilized by spermatozoa of a different organisms.
If you read the term allogametes somewhere, then the reference likely means spermatozoa from one organism of a species and ova from another organism of the same species. There were two references on Google Scholar to allogametes. This reference is in Science from 1911, no that is not a typo.
Dimorphism of the Gametes of Œnothera by Walter T. Swingle.
Species that have hermaphrodites, such as nematodes and other types of worms can be autogamous, meaning that the organism produces both the ova and spermatozoa and self-fertilize. In this case the offspring of this organism are clones of the hermaphrodite, which can come in handy in genetics experiments. Basically you are doing a self-cross.
Many of these species can also be allogamous. In the case of the nematode you usually have the Hermaphrodite, which is XX and the male which is XO. The male only produces spermatozoa and when mating with the hermaphrodite, their sperm takes precedence over that of the hermaphrodite. This is likely due to a last in first out situation in the spermatheca of the hermaphrodite. Sperm develops in the hermaphrodite first and are deposited in the spermatheca, then the ova form. If a male mates with the hermaphrodite, 'his' sperm is deposited in the spermatheca of the hermaphrodite and then as the ova pass the spermatheca on their way to the vulva they are fertilized by the sperm.
Edit
The Urologic and Cutaneous Review: Technical supplement, Volume 2 from 1914 on a section on the origin of sexual reproduction (The Origin of Amphigony), also makes mention of the term "allogametes" in reference to protist cells which are able to differentiate and fuse and then divide asexually after the fusion even. The key in this text is made from differentiated cells, allogametes, or similar cells, isogametes, that are capable of fusing and producing a new cell capable of cell division.

It is also possible that the OP is referring to allopolyploids, in which case the gametes come from two different species with different genomes that produce an offspring that can lead to a new species. This is seen in plant breeding. If OP responds with clarification I will attempt to expand on that.


text:
Why do we get sleeply after we eat?
After we have eaten, we feel cold and sleepy. I think it's because the maximum blood supply is transferred towards the digestive system so that digestion is done, and therefore the brain to does not get adequate blood supply. Am i right about this?
Also, why do they suggest to take a short walk after dinner especially?

Who are "they" advising naps after lunch and walks after dinner?

"...that's why we feel cold and sleepy too because the brain to does not get adequate blood supply." That's a very, very common myth, but it is a myth.

@Roland my grandmothers? Maybe the OP knows them ;-)

After we have eaten... the maximum blood supply is transferred towards the digestive system so that digestion is done, and therefore the brain to does not get adequate blood supply. Am I right about this?

This is a very, very common myth, but it is a myth. Because blood flow and oxygen delivery to the brain is critical for survival, cerebral circulation is one of the most tightly regulated systems in the body. Blood is not shunted from the brain to the gut for digestion.

In a normal physiological state, total blood flow to the brain is remarkably constant due in part to the prominent contribution of large arteries to vascular resistance.

Eating, sleeping, walking, etc. are all normal physiological states. If we had blood shunted away from our brains after eating, we'd literally collapse after every meal.

In normotensive adults, cerebral blood flow is maintained at ~50 mL per 100 g of brain tissue per minute, provided CPP is in the range of ~60 to 160 mmHg.

As eating alone doesn't normally cause our blood pressure to rise or fall, cerebral perfusion is constant regardless of what is or isn't in our digestive systems.
Blood flow to the gastrointestinal system (or GI tract) is also regulated, but the flow varies widely:

Estimates of blood flow (in ml /min × 100 g) to the quiescent gastrointestinal tract of dogs and cats range from 15 to 100 for the stomach, 35–120 for the small intestine, and 10–74 for the colon. Somewhat lower values for resting blood flow to the stomach, small intestine, and colon have been reported for man.

So, the basic answer is that, yes, blood flow to the gastrointestinal tract varies, but blood is not shunted from the brain in favor of the GI tract.
So why do we get sleepy after a meal?
Sleepiness after a meal is caused by the level of peptides in your brain called orexins (aka hypocretins).
In 1998, two groups of researchers simultaneously discovered 2 small neuropeptide hormones that regulate, among other things, wakefulness and feeding behavior.
One group discovered them while searching for molecules that could bind to "orphan" receptors, that is, a brain receptor with an unknown "binding" molecule (called a ligand). They found that the prohormone prepro-orexin was found in a very small area of the hypothalamus which had been implicated in the regulation of feeding behavior and energy homeostasis; this suggested the possibility that the neuropeptides might be involved in the regulation of food intake. When administered into free-feeding rats' brains, one of these peptides (orexin A/hypocretin 1) stimulated food consumption in a dose-dependent manner (with attention to light and dark periods, i.e. the circadian rhythm), with a lower dose increasing rat feeding about 2-fold, and the higher dose inducing a 3+-fold increase in feeding compared to rats injected with a solution without the peptide (the other stimulated feeding to a lesser degree). The effect persisted for 4 hours. Furthermore, fasting rats produced more than twice as much orexins as rats feeding freely. For this reason, the molecules were names "orexins", after the Greek word orexis, which means "appetite". They speculated that the orexin-secreting neurons might somehow be modulated by glucose.
At the same time, another group of researchers using a completely different approach found that the same group of hypothalamic neurons were stimulated by a peptide hormone similar in composition to the gut hormone secretin. They identified the same prohormone and its two peptides, naming them hypocretins for "hypothalamus" and "secretin". They found that at least one of the peptides had a neuroexcitatory activity in specific areas of the brain (they mapped effects in the hypothalamic neurons, the posterior hypothalamus, the septal nuclei in the basal forebrain, the preoptic area, the paraventricular nucleus of the thalamus, the central gray, the locus coeruleus, the colliculi, the laterodorsal tegmental nucleus, and the nucleus of the solitary tract) suggesting that the peptides acted within the central nervous system as homeostatic regulators with a role in nutritional homeostasis.
Scientists have not decided on whether to call them orexins or hypocretins yet, so both are used. They are found in all vertebrates.

Mammalian orexin A sequences thus far identified (human, rat, mouse, pig, dog, sheep, and cow) are all identical, whereas the sequences of orexin B show some differences among species. From Orexin/Hypocretin: A Neuropeptide at the Interface of Sleep, Energy Homeostasis, and Reward System, Natsuko Tsujino and Takeshi Sakurai
In 1999, a group of scientists found that narcolepsy (a sleep disorder characterized by extreme daytime sleepiness) was caused by a lack of a hypocretin/orexin receptor 2 gene in certain dogs, therefore establishing that they play a very important part in the regulation of wakefulness.*
Since then, an enormous body of work has shown that orexins/hypocretins (O/H from here on in) are involved in the regulation of a wide range of behaviors, including wakefulness and vigilance (needed to find food), systems that regulate emotion and reward (including drug-seeking behavior when stressed and eating for pleasure - "consumption beyond homeostatic needs" - leading to obesity), and more.
What does eating have to do with sleepiness?
Several studies report that the firing rates of O/H neurons are influenced by serum glucose, triglycerides and amino acids.
In English: You are awake (O/H is being secreted by O/H neurons in your hypothalamus). You eat. Your serum glucose rises. The elevated glucose causes depolarization of inhibitory neurons that hyperpolarize O/H neurons decreasing the amount of O/H. released. Result: wakefulness decreases.
Control of Cerebral Blood Flow
The Gastrointestinal Circulation.
Comparing these two papers - the first and second references - is a wonderful example of the completely different methods used by scientists to investigate unknowns and up with the same basic conclusion.
Orexins and orexin receptors: a family of hypothalamic neuropeptides and G protein-coupled receptors that regulate feeding behavior, Cell 92 (4): 573–85
The hypocretins: Hypothalamus-specific peptides with neuroexcitatory activity Proc. Natl. Acad. Sci. U.S.A. 95 (1): 322–7
The Sleep Disorder Canine Narcolepsy Is Caused by a Mutation in the Hypocretin (Orexin) Receptor 2 Gene
The role of orexin in motivated behaviours A Nature Neuroscience Review
The role of orexin-A in food motivation, reward-based feeding behavior and food-induced neuronal activation in rats
*Human narcolepsy - caused by a destruction of O/H neurons - also is associated with metabolic abnormalities, including increased frequency of non-insulin-dependent diabetes mellitus and increased body mass index.
Hypothalamic Orexin Neurons Regulate Arousal According to Energy Balance in Mice
Orexin/Hypocretin: A Neuropeptide at the Interface of Sleep, Energy Homeostasis, and Reward System

A plus one seems so insufficient. Where did you find the time for this answer?

@AMR - That is so kind of you! :) Actually, I wrote most of this answer for another SE site. The myth of blood being diverted from the brain after eating is so prevalent, and the reality so much more interesting that I really like sharing about it.

What would be interesting (to me at least) whether napping after meal is beneficial for digestion etc.


text:
Are all tastes just a combination of sour, sweet, bitter, etc.?
For example, can the taste of pineapple be isolated to just a certain amount of "salty-taste-triggering-molecules" and "sweet-taste-triggering-molecules" etc.? Can our current understanding of the gustatory system predict the taste of a new substance (for example we could predict it tastes like chocolate) just based on the amount and ratios of these molecules?

Interesting question.

The brain perceives taste or flavor as a combination of input from taste buds, the olfactory system, and even pain receptors (spicy foods). Other food contents, such as metal, spice, fat, pH, and even dissolved gas content seem to contribute.

While there are 5 types of taste receptor, there are some 2000 olfactory bulbs encoded by 1000s of gene.  As such, it is not possible to predict how something will taste in a simplistic 5-taste combo.  However, this is an area of active research, such that structural models are used to develop taste enhancers, artificial sweeteners etc.
Sources:

http://www.sciencedirect.com/science/article/pii/S0976120913000041
http://health.howstuffworks.com/mental-health/human-nature/perception/taste.htm
http://www.livescience.com/17684-sixth-basic-taste.html