Harvest honey without damaging brood cells I want to make a homemade beehive, I want to know how to differentiate honey cells and brood cells, therefore, I'd like to know how can I organize the beehive so bees will create honey and brood cells separately. By this way, I would be able to harvest the honey without killing the larvaes :)

Ancillary issues : Do bees need cells to sleep in ? Can I populate a homemade beehive with several bees caught from my garden ?

Thank you for your attention :)

In domesticated bee hives, this is usually accomplished by excluding the queen from a section of hive frames (by the size of the entrance hole), so that these frames only contain honey and no eggs/larvae.
For instance, this can be achieved using a queen excluder.


Why do spinner dolphins spin? Spinner dolphins have a behavior where they jump out of the water and spin a bunch of times in the air. Wikipedia's article on this just states

  These spins may serve several functions

and doesn't anything. Are there any known reasons for their extreme spinning behavior?

No single factor is considered to be the reason for the aerial spinning behavior (Hester et al., 1963; Norris and Dohl, 1980; Norris et al., 1994). The various factors include leadership or dominance, alertness, acoustic communication, courtship display, defining positions of members in the school, and dislodging ectoparasites. The most notable ectoparasites are remoras and whalesuckers (order Perciformes, family Echeneidae). ... Hester et al. (1963) suggested that the aerial maneuvers executed by spinner dolphins are involved in the removal of remoras. ... While aerial spinning maneuvers may not have developed specifically to remove ectoparasites like remoras, dynamically it is plausible that this proves to be an added benefit.

--Dynamics of the aerial maneuvers of spinner dolphins


Has the protein composition (with identification) in honey and other honeybee byproducts been studied? I am interested in studying honey and other honeybee byproducts.  I have not been able to find sequence or structure records for any of the contents of honey.

In particular, I want to study the protein sequence and structure and the amino acid compositions within honey.

Has any of this data been produced and published in any databases or research papers?

First of all: Honey is not a byproduct of bees - it's their main and most important product which stores energy for the bee hive for the time when no flowers are available.

Honey itself consists (according to the USDA database) to about 99.5% of water and sugars (82.5% sugars, 17% water). The sugars are mostly fructose and glucose, but also some other mono- di and tri-saccherides in traces. See reference 1 for details. It also contains trace amounts of vitamins and minerals, see table from the Wikipedia on Honey:

The protein content varies between honey sample but is somewhere in the range between 0.2 and 0.5% (see also reference 1). The proteins come from flowers (pollen incorporated into the honey) as well as from the bees (see reference 2). Paper 1 lists a number of enzymes as most common bee proteins in the honey, but doesn't go into much more details here. These are invertase, diastase, glucose oxidase and catalase.

You could now go into the sequence databases (Apis mellifera has been complete sequenced) and look up the sequence information of the enzymes. Information can be found here and here.

References:

A review of the analytical methods to determine the geographical and
botanical origin of honey
Source of the honey protein responsible for apple juice
clarification


Do animals with their eyes ~180 degrees apart have depth perception? Lots of animals have their eyes more on the side of their head, like an octopus or a parrot. Are animals with eyes more on the side able to tell the depth of objects at different distances? It seems like the line of sight in each eye wouldn't be able to cross to a singular point to triangulate distance.

Many such creatures do overlap in part of their field of view. Some don't.   Presumably, the former still have some range sense. It's generally accepted that range judgment it's far more valuable to predators while herbivores focus on movement over a wide range. (at least in the sources I've read on this.)

That said:

Focal length can provide some amount of depth information, but not like comparing two angles. ("accommodation " in the wiki article on depth perception)

Parallax can provide some useful depth information. This is a function of basoc geometry. (In the same article, see "motion parallax", "occultation", and "perspective")

Theoretically, if a creature is precisely enough aware of its movement, it could pick up depth by rotating its head. This is because of the previously mentioned geometry. (https://en.wikipedia.org/wiki/Depth_perception#cite_note-5)

Not sure if any animals actually do this, but some birds seem to.

This answer is, fundamentally, just a summary of elementary information. The wiki entry on depth perception chops up the list of factors a lot more fine than I did off the top of my head.

https://en.wikipedia.org/wiki/Depth_perception

https://en.wikipedia.org/wiki/Equine_vision#Visual_field


Are there records of monozygotic twins in which one experiences androgen insensitivity syndrome I have given my high school biology students the thought experiment of "What would happen if a researcher induced twinning of a female zygote and then replaced one of the X Chromosomes with a copy of the father's Y chromosome". In theory you should get what would be about as close as possible to male/female identical (monozygotic twins). However, I don't believe it would be possible for this to occur in nature (feel free to correct this if I am wrong). The closest I am familiar with is "Semi-identical twins in which the egg is fertilized by two sperm and then twinning occurs. However this isn't really the same.
However, I realized that Androgen Insensitivity Syndrome, in which a mutation leads to the body not responding to masculinizing hormones, leads to a male developing as female. Is anyone aware of this ever happening? I realize it would need to occur after the zyote/morula split.

Similarly if the SRY gene (essentially the master control switch for masculinizing an embryo) has ever been transferred on to an early embryo of a pair of female monozygotic twins, essentially inducing one twin to develop male.

In essence I'm asking for evidence of physical manifestations of (near)identical monozygotic twins. Has any of this ever been done in research on other species?

This is an important question to geneticists because monozygotic twins are the only ethically acceptable way to research genetically identical humans.

I'm sure the sort of non-symmetrical fission where specific DNA coding for genes are not present or are modified to completely different phenotype in the formation of the twins probably has happened, but it incredibly rare.  In stem cells, asymmetric division has been observed frequently (warning: google doesn't like PlosOne right now).  In development, unless its actively been activated as an asymmetric division, this would be incredibly rare- this would be akin to a birth defect in a single fetus - how many cases of mixed male and female cells in a single baby. I can't even find a reference for such a thing.  Much more common are semi-identical twins, where two different sperm fertilize a single egg which may have split.  Semi-twins are still vanishingly rare - the first report was in 2007).

  Such twins are probably very rare. Their existence and discovery relies on three unusual, and possibly unlinked, events: first, that an egg fertilized by two sperm develops into a viable embryo; second, that this embryo splits to form twins; and third, that the children come to the attention of science.

This might be the case you are thinking of?  In one case reported there was a gender difference.

  Souter and her colleagues investigated the twins' genetic makeup because one was born with ambiguous genitalia. This twin turned out to be a 'true hermaphrodite', with both ovarian and testicular tissue. The other twin is anatomically male.

They weren't monozygotic though.  Just others from the same mother ;)

Monozygotic twins are not completely identical, epigenetic fingerprinting - including DNA methylation and chromatin DNA binding patterns (pnas - paywall) change while the fetus develops and as the child and adult age.  This can cause quite significant differences as the twins age. Epigenetic markers change the dynamics of brain development and can make a difference in the occurance of leukemia.

There are also modifications to the DNA sequences of cells, copy number variations (CNVs) are multiple (sometimes hundreds or thousands of times over) repeats of short (2+ base pairs) DNA sequences.  These also occur as the cells differentiate and divide to form tissues and organs.  Twins show significant differences there too as this is not a deterministic mechanism in development.

I can't find any references to twins showing asymmetric AIS. but the number of variants requiring this makes it sounds like its possible.  If you have a reference post it and I can have a look?

note added: this paper shows that methylation profiles appear identical at least in utero.


How does a virus reach its host, it is always passive? We know that viruses are non motile and cannot metabolise, and that it enters the host cells via binding to the receptors. But how exactly it reaches the host

(that is, how it go from the transmission medium (e.g. the aerosols) to actually make contact with the cells in the host)

If it rely on simply diffusion to bump into the host cells' receptors, what makes the odds high enough so that such proliferation strategy is efficient enough to ensure the virus to multiply and proliferate?

In addition, once it has released its DNA into the cell, what helps the DNA to reach the nucleus and not drifting randomly within the cell for a long time, that is, is there exist mechanisms or transportation pathways that actually guide the DNA from the perimeter of the cell through the cytoplasm in the middle and towards the area where the nucleus lie?

There are a number of different ways to spread a viral infection. Some viruses sit on surfaces (or infected persons) "waiting" for someone to touch and take them up, this is called smear infection. Other viruses are airborn inside of small droplets distributed by coughing or sneezing. These are inhaled and can then cause a new infection. Other viruses are transmitted through our body fluids (blood, semen) and either need a wound or can be transmitted sexually (for example Herpes or HIV). Other viruses are transmitted by animals which bite humans (Dengue and rabies would be examples here). Have a look into the Wikipedia for more details and examples.

Additionally viruses are produced in vast numbers by their hosts with most viral particles never reaching a new host. This strategy helps a lot to transmit further.s

For entering the nucleus (which is an obstacle) the viruses use the nuclear pore complex (NPC). Depending on what virus tries to enter the nucleus, different strategies are used. Some viruses are too big and release their DNA through the NPC into the nucleus, while others can pass through and some get stuck inside and release their DNA/RNA at this point. A last group uses the time during mitosis when there is no nucleus. See this figure (from here)
and also the references below:

References:

Virus strategies for passing the nuclear envelope barrier.
How viruses access the nucleus.
Viruses challenge selectivity barrier of nuclear pores.


Can you extract specific data from EEG First of all, sorry if this is the wrong place to ask this question, please redirect me if it is so.

I have a project in mind involving and EEG, which is the following :

Using a "consumer-grade" EEG (see this one, for example) I would like to be able to control a binary system with my mind (for example, turning a led on and off). From what I've seen until now, this seems to be possible since the headset is able to detect eye blinks, for example. It also gives access to two variables "focus" and "relaxation", which you can learn to control somewhat accurately (accurately enough for a binary system, at least).

Now here's my problem. While the methods that I described above do work, they would also continuously activate even when I don't want them to. Everytime I blink, my led would turn on, even though my intention wasn't to turn the led on. Everytime the "focus" level goes over 50/100, the led would turn on, even though I'm just focusing on my physics problem.

Having said that, I was wondering if it is possible to pick up more subtle and "controlled" information on the EEG. One thing I was thinking about is, if I think and visualise the color red, maybe that could cause a signal that can be picked up ?(Of course the led would activate when I look at something red, but that's still an improvement) Or even looking at the led I want to turn on, would that have any discernable effect on the EEG ? My guess is that those "thoughts" are way to subtle to be picked up by an EEG, which is just an average of the brain activity, but I'm not an expert on the subject !

So I guess my question is : what are the "kind" of thoughts that I can somewhat reliably see on the EEG data ? For example, I know I can reliably pick up a eye-blink. Are there any thoughts that are not related to muscle movement that can also be reliably read on a EEG ?

Short answer
The key word in EEG-driven mind control is brain-computer interface (BCI). In contrast, eye blinks can simply be detected with an eye tracker.

Background
As far as I know, EEG-driven computer control (The force is strong in you) is based on recording the EEG while thinking of certain actions, or simply doing them. As you likely understand by now, thinking of moving your arm activates much of the same brain circuitry as actually making the move, up until the pre-motor cortex. The motor cortex itself stays silent (otherwise you would actually make the move (Griggs, 2013).

So EEG correlates of motor activity can be translated into digitized electrical brain activity. In turn, these brain waves can be put to use from playing pong by mind force, to state-of-the-art applications like driving artificial (bionic) limbs for the lame. By using artificial neural networks / deep learning techniques / and multiple EEG electrodes, the combined activity can be registered of many brain regions and certain signatures may pop out and be trained for a computer to learn them. In tun, that can be used to, say, play a computer game.

For a commercial alternative, delivered with an SDK, check out (Pogue, 2012):

Emotiv's EPOC

References
- Griggs, New Scientist, January 2013
- Pogue, Sci Am, December 2012)


Meaning of the word "targeted" in a description of chromatin immunoprecipitation From a research paper:

The ChIP assay demonstrated that CIC physically binds to the promoter region of FOLR1, PCFT and RFC1.
Compared with IgG control antibody, CIC antibody enriched 4.1-fold more targeted FOLR1 promoter DNA, 13.8-fold more targeted PCFT promoter DNA and 4.2-fold more targeted RFC1 promoter DNA (figure 3B).

As far as I understand, the authors used chromatin immunoprecipitation to look whether and to what extent the CIC gene influences the promoters of folate-related genes (FOLR1, PCFT, and RFC1). And well enough, they discovered that the antibody to CIC precipitates more "promoter sequences" compared with the control antibody (IgG).
What does the word "targeted" mean here? If I remove this word, the meaning seems unaffected to me. In my Russian translation, I just omitted this word, because it does not seem to bear any additional meaning, but I'm not sure.
Can one simply omit "targeted" or does it have a meaning?

Looking at the article, I think they could leave out the word "targeted".
I think they used it because what is being enriched is not a promoter DNA, but the section of promoter DNA bound to the protein and antibody.
I suppose they could use  "...enriched 4.1-fold more FOLR1 Promoter DNA-CIC protein complex,..."
It is a little awkward or clumsy because the protein targets the DNA, and the antibody targets the protein.
So it is not always very obvious what the word "targeted" is referring to.
But without "targeted" I think the meaning is still clear enough.


Regarding tumors and their developement If certain cells or tissue in a specific part of the body are for some reason overworked; like the cases of severe acid reflux damaging the throat repeatedly and the cells in the throat having to do growth and repair a lot more than they would with a healthy person -- or problems in the stomach attacking the stomach lining a lot, causing 'extra' growth and repair; could these situations of 'extra' growth and repair cause various cells used in these processes to mutate with all the cellular division and replication required? And maybe some of these extra-growth-and-repair induced mutations might cause the apoptosis mechanisms to malfunction?

There is indeed a positive correlation between gastric reflux disease and esophageal cancer, and also between stomach ulcerations and stomach cancer. There are more than one possible mechanisms for these correlations to arise, but what you are proposing is definitely a prime suspect.

http://www.webmd.com/heartburn-gerd/news/20130523/chronic-heartburn-may-raise-odds-for-throat-cancer-study

http://www.ncbi.nlm.nih.gov/pubmed/10658066


Can a Turner syndrome patient develop male characteristics artificially? From an answer to the question Can stem cells from male convert to cells of female-only organs, and vice versa?

  Y chromosome is the sex determining chromosome with SRY gene that determines testes development. Absence of the Y chromosome leads to female development by default. That is why XX forms women and there are people with only one X chromosome which are women. (Turner's syndrome)

and Why are mice with a single X chromosome and no Y chromosome males?

  The Y has only a few genes (less than all other chromosomes), but it has genes that occur only on the Y. One of these in particular, the one called SRY, is the main gene that causes the individual to develop male characteristics. It mostly does its job indirectly, by making a protein that affects many other genes on other chromosomes that in turn do the work of building and maintaining the male form... they managed to cause mice without a Y chromosome to develop many male characteristics. They did this by faking one or two of the actions of SRY. One of the many actions of SRY is to turn on a gene called Sox9 (which is on a non-Y chromosome), and it turns out Sox9 causes most of the things that make the male mouse form.

My question: Is it possible to make a Turner syndrome patient develop male characteristics by artificial stimulation? Has it ever been tried?

After a lot of research, I've finally found an answer.

In the case of humans, it is practically impossible. See this article from wikipedia:

  During gestation, the cells of the primordial gonad that lie along the urogenital ridge are in a bipotential state, meaning they possess the ability to become either male cells (Sertoli and Leydig cells) or female cells (follicle cells and Theca cells)...Once proper SOX9 levels are reached, the bipotential cells of the gonad begin to differentiate into Sertoli cells.

This part is just to clarify why it is not possible. In embryonic stage in turner syndrome patients (and females), since SOX9 is not expressed (due to absence of SRY), the bipotential gonad cells in the urogenital ridge (Müllerian/paramesonephric ducts) of embryo develop into female reproductive system i.e. become mature into that state. After this has happened, any amount of SRY cannot develop male reproductive system as all bipotential cells have differentiated into female reproductive system.

It is practically impossible, but virtually it can happen if you can insert Y chromosome or TDF in the bipotential cells of embryo. Practically, doing such experiments on embryo might not be possible (at least for now).

Source

Source

However, it only means that they can't develop primary sexual characters. Secondary sexual characters can, obviously, be developed by efforts as small as hormone injections. In fact, hirsutism is a condition in which females devlop hairs on chest, face, etc. and even beards! Its causes are as common as obesity. See this article:

  Some medications can cause hirsutism. These include danazol, which is used to treat women with endometriosis; systemic corticosteroids and fluoxetine (Prozac) for depression...Being obese causes increased androgen production, which can worsen hirsutism.

So, if a Turner syndrome patient wants a moustache or beard (just in case), it can be achieved by androgen injections too.


Why is the brain white? I have read many articles about how the brain is the most power-hungry organ in any living complex organism, requiring about 70% of it's oxygen supplies in the resting state.

Since the usual medium of oxygen delivery is through respiration, this should mean that a lot of blood is supplied to (and hence present in) the brain.

Why then is the color of the brain almost always white? There is usually a little red tainting on the exterior and that's it, you can see the interior is still white. Should it not be red? Presuming that for a higher surface area to volume ratio, most of the brain cells are in direct contact with the bloodstream.

The brain is indeed stacked with blood vessels, as shown in a 3D model in Fig. 1.

Fig. 1. 3D-printed model of blood vaculature. Source: Biobots.

The blood supply on the surface of a live brain is readily seen during a craniotomy (Fig. 2.)

Fig. 2. Surface of the brain. Source: The Sterile Eye.

When freshly prepared, the interior of the brain appears pink, indicative of the presence of blood (Fig. 3):

Fig. 3. Coronal sections of a non-fixated brain. Source: Documenting Reality.

Mostly, images of the brain are taken after fixation of the brain. The fixation process includes removal of the blood in the brain and the fixative pales the color of the tissue markedly. Fixation results in the more familiar pale-appearing pictures of the brain as shown in Fig. 4.

Fig. 4. Coronal section through a fixated brain. Source: Wikimedia.

Also note that the blood supply mainly targets the areas where the cell bodies are located, i.e., the gray matter. The white matter is pretty much devoid of blood supply and mainly consists of heavily myelinated, fatty tissue supporting axonal fiber tracts (Fig. 5).

Fig. 5. Arterial innervation of the brain. Source: Human Physiology Academy.


Can mosquitos bite in self-defense? When chasing away wasps or bees there is a danger of them stinging us in self-defense.
Can a similar danger arise when chasing away a mosquito which is otherwise not hungry? I understand that mosquitoes bite to feed (by sucking blood), but do they use their bites in self-defense against large targets, like humans? Mosquito bites can be somewhat painful or at least uncomfortable, and can carry dangerous diseases, making them theoretically viable as a self-defense weapon.

Probably not. An immediate defense against predators requires an immediate response. The sting of Hymenoptera like the wasps and bees has an immediately painful reaction.  In addition, in the eusocial (colony-forming) species, multiple individuals typically contribute to defense of their nest. One sting may not deter a predator or invader but dozens or hundreds of stings would create an immediate deterrent.  See for example this paper by [Breed et al. (2004)] on the defense behavior of honey bees.  Animal bites that are immediately painful, such as an ant bite or dog bite create an immediate response in the organism being bitten. Spines and thorns on plants deter organisms from biting the plant. Odors released by skunks and some insect provide an immediate response.

The bite of blood-sucking mosquitoes does not provide an immediate deterrent. (Not all mosquitoes suck blood.) This paper by Ramasubramanian et al. (2008) provides a detailed explanation of how a mosquito penetrates the skin.  The paper is related to microneedle design but they are using the mosquito as a comparison for painless needle design. Go to page 3 to get a description of the mosquito anatomy and piercing behavior. Comparison of painless microneedle design to the mosquito's proboscis is instructive.

The proboscis is the set of modified mouth parts the mosquito uses to penetrate the skin and suck the blood.  The study states that microneedles that penetrate human skin less than 1.5mm is usually painless or effectively so. These needles have a very small diameter, only about 40-100 micrometers in diameter, similar to the width of a human hair. The mosquito's proboscis is about 1.5-2.0 mm long. The diameter of the various structures used to cut through the skin and suck the blood are all less than 40 micrometers in diameter. Thus, the size of the mosquito's proboscis is so small that it does not cause immediate pain, or the pain is so little that it is an annoyance at best. In addition, the proboscis is weak enough that the moquito may have to probe the skin several times before a spot suitable for penetration can be found.

Finally, only the females of blood-sucking mosquitoes feed on blood and have the penetrating mouth parts. Males do not. They feed entirely on nectar and water. Males would thus not be capable of such defense.


What is this red mushroom with the "inverted" cap? Picture taken on 29 March 2020, Czech Republic (Middle Europe). The cap is red, and its shape is "inverted". It is quite tough, first I thought it was a piece of plastic, but apparently it is growing from the ground.

What is the mushroom - if it is a mushroom :) ?

Looks like Sarcoscypha Austriaca (scarlet elfcup). It's actually used in many textbooks as a representative species for the Ascomycetes.

Details from Wikipedia and Messiah.edu both confirm that this species is found in Europe and that it is typically found either as solitary or clustered fruiting bodies (2-5 cm wide) growing among rotting wood matter in damp wooded floors in the spring.

Photos below:

 Source: Wikimedia

 Credit: William Roody; Source: Messiah.edu

Read more at MushroomExpert.com.


Why are people unable to develop lasting immunity against Norovirus? Infection with many viruses will result in decades-long if not lifetime immunity, for example chicken pox.

Because of the large number of viruses responsible for the common cold, lifelong immunity to the common cold isn't possible; we will still be susceptible to those we haven't encountered before. But we do develop immunity to those we've been exposed to.

Influenza virus mutates quickly enough that there will nearly always be strains which will be new to us. Immunity to HIV is difficult because of the particular cells the virus attacks (as well as mutations).

However, Norovirus, while there are many strains, is particularly problematic because immunity to a strain lasts less than a year, making reinfection with the same strain repeatedly possible.

Is the reason Norovirus infection doesn't confer longer-lasting immunity known?

So the direct mechanisms of norovirus immunity aren't well understood - the shortage of straightforward animal models, and the extreme difficulty in culturing the virus make mechanistic studies really rather hard.

A modeling study pegged the duration of immunity at 4.1 to 8.7 years when talking about symptomatic disease, which is much higher than many of the estimate's you've encountered, and isn't actually all that fast. The older estimates were built off human challenge studies, which involved massive doses of norovirus, rather than the normal exposure you'd have. Now that is for a single strain, but immune cross-reactivity for strains isn't well understood. There's also several efforts to develop norovirus vaccines, which suggests some duration of immunity is at least possible. It's also possible that a proportion of the population (~20%) is simply immune due to the absence of the FUT2 gene, which acts as a receptor for the virus in the intestines.

In addition, there's definitely some antigenic drift, where mutations in the primary antigens negate previous immunity to the disease (the same mechanism that causes you to eventually lose immunity to a particular strain of influenza).

This paper is a pretty brief review of all these factors, written by some norovirus experts.


Integration of several environmental signals I am looking for examples of different functions that are good fit to how signals are computed in order to respond to the environment. Let's make my question more copmrehensible with an example...

One example

I have been told (I haven't found an article yet) that in plants, in order to know if it is overshadowed by a big tree, the plant computes that ratio of two signals (UV intensity over Infrared intensity or something similar) so that it can decide whether or not it should grow bigger leaves or other attributes.

This plant radiation example would be an example of a species that computes the function $\frac{S_1}{S_2}$ (where $S_1$ and $S_2$ are two types of signals) in order to take decisions about their response to the environment.

Question

Can you please give me examples (examples with a diversity different functions, with different numbers of different signals) of organism using environmental signals to adaptively respond to their environment?

For example, can you give me examples of the adaptive response to the environment is giving by the following functions of 2 signals:

Continuous traits:

$f(S_1, S_2)= S_1 + S_2$

Produce a trait value at $K_1 + K_2\cdot \left(S_1 + S_2\right)$

$f(S_1, S_2)= \frac{S_1}{S_2}$

Produce a trait value at $K_1 + K_2\cdot \frac{S_1}{S_2}$

$f(S_1, S_2)= S_1^2 \cdot S_2$

Produce a trait value at $K_1 + K_2\cdot \left(S_1^2 \cdot S_2\right)$

$f(S_1, S_2)= funA(S_1, S_2)$

Produce a trait value at $K_1 + K_2\cdot S_1$ iff $S_1$ is detected.

$f(S_1, S_2)= funB(S_1, S_2)$

Produce a trait value at $K_1 + K_2\cdot S_1$ iff $S_1 < S_2$.

Boolean traits:

$f(S_1, S_2)= OR(S_1, S_2)$

Iff signal 1 or signal 2 is detected, produce the trait

$f(S_1, S_2)= AND(S_1, S_2)$

Iff signal 1 and signal 2 are detected, produce the trait

$f(S_1, S_2)= FunA(S_1, S_2)$

Iff $S_1$ < $S_2$, produce the trait

, where iff means if and only if and $K_1$ and $K_2$ are constant values.

What I am NOT asking

I am NOT interested in the accurate description of the signal transduction (Description of the kinase cascade and names of the genes and transcriptions factors). I am interested in having examples of mathematical functions that are computed by the cell in order to take decision about which phenotype to produce (plasticity).

What you are looking for sounds like the mechanism for a fold-change detector. I would recommend looking at these two papers:

The incoherent feedforward loop can provide fold-change detection in gene regulation

As an example of this working in a real system, I recommend looking at the NFkB pathway, as recently detailed by Suzanne Gaudet:

Fold Change of Nuclear NF-κB Determines TNF-Induced Transcription in Single Cells

Here are a few others that I found just by searching for "Fold change detection"

Comparing Apples and Oranges: Fold-Change Detection of Multiple Simultaneous Inputs

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0057455

Efficient fold-change detection based on protein-protein interactions

I'm sure by looking at the referenced papers in the above you can find more examples as well.


What is the exact principle of capillary isotachophoresis? I know it's a type of capillary electrophoresis, but I don't get how does the separation happen exactly.

Many of us are using isotachophoresis all the time without even realising it. The explanation that follows may not be exact, but I hope that it helps.

Firstly, think about a simple electrophoresis set-up - in agarose electrophoresis of DNA we have a uniformly distributed buffer such as Tris-borate. The current is carried by the borate ions and the DNA molecules run through the homogeneous electric field towards the anode. They separate by size because of the sieving effect of the agarose matrix.

Now let's think about what is happening in an SDS-PAGE separation (a Laemmli gel). Just to remind you:

The running (or reservoir)  buffer is Tris-glycine pH 8.3
The stacking gel is in Tris.HCl pH 6.8
The separating gel is in Tris.HCl pH 8.8

When the power supply is turned on, the glycinate ion in the top reservoir begins to move into the stacking gel. When it hits the zone of pH = 6.8 it is much closer to its pKa and so is now only weakly charged. Consequently it slows down. Meanwhile the chloride ions in the stacking gel have begun to move rapidly down through the stacking gel (towards the anode). This creates a discontinuous electric field: the chloride zone has a lower resistance than the glycinate zone so the field strength in the chloride zone is weaker than the field strength in the glycinate zone. This is a stable situation because the ions cannot stray into each other's zones: if a glycinate ion happens to diffuse forwards into the chloride zone it will experience a weaker field and slow down, whereas if a chloride ion diffuses back into the glycinate zone it will hit the stronger field and quickly move ahead again.

What about the SDS-protein complexes that were in the well? (I'll just refer to these as proteins from now on.) Their ionic properties lie between the glycinate and the chloride, and so they eventually end up moving through the stacking gel between the trailing zone of glycinate and the leading zone of chloride. Any protein that finds itself in the glycinate zone will move quickly forward (due to the higher field strength) and any protein that moves ahead by chance into the chloride zone will slow down due to the weak field strength, falling back into the protein zone. And in this way these zones move in a procession through the stacking gel, with the proteins being focussed into a very narrow region in the middle. The glycinate, the proteins and the chloride are all moving at the same speed, and so this is an example of isotachophoresis (isotacho- = "same speed"). The polyacrylamide gel matrix in the stacking gel has no separating function - its role is simply to stabilise against convective effects. The proteins can reach very high local concentrations in the stacking gel, and if you look carefully you will often see refractive effects as your sample runs through the stacking gel. In this way the protein sample is "applied" to the separating gel in a very tight band, perfect for achieving high resolution separation (bands broaden by diffusion in the separating gel so the tighter the bands ar eat the point of loading, the better the final result.)

Once the sample hits the separating gel, all of this breaks down: the pH is now 8.8 so the glycinate becomes strongly charged and zooms off ahead with the chloride through the gel, leaving the proteins to move more slowly due to the sieving effect of the polyacrylamide matrix.

It is possible to set up an isotachophoresis as described above in isolation. Individual proteins will have slightly different ionic properties and will line up in the region between the two buffer ions, allowing for their separation.


What happens between two nodes in an evolutionary tree? Hey guys can you help me with this one!?

What happens between two nodes (in an evolutionary tree) or a between a node and a tip?

A) at least one character changes

B) all organisms die

C) Nothing can happen between two nodes

D) Monophyly, Paraphyly, Polyphyly

E) None of the above

I came down to E) and C). Since B) doesnt even make sense, organisms don't die among two nodes- they evolve. D) it is irrelevant to the question asked A) I think that probably is wrong as well, since among a node and a tip, the organism stays the same and finally I thought C) could be the answer, but at the same time a new trait could be formed,

Your answer is A. for one simple reason, two different nodes represent at least one notable/measurable difference between groups, so between any two nodes there must be at least one difference.

Look at this example, whether A and B represents Mammals and Birds or two subspecies of chimp, or two strains of virus the fact they are two separate nodes means there is some difference between them. When constructing a tree there has to be at least one character difference to have more than one node. A tree with no differences is just a dot by itself.

Also an organisms does not stay the same between a node an the tip (the tip is a node) to use the below example the starred node between A and B is the most recent common ancestor of A and B which is not the same thing as A or B.


How would i describe a Cladogram as paragraph? I have this paragraph that i have halfway finished, but i do not know what to put in the spaces.

A Cladogram is a branching diagram that represents the proposed phylogeny or evolution of a species or a group. The groups used in Cladograms are called clades.. To construct a cladogram, two characters are defined. Then the outgroup of various species are identified based on the sequencing or closeness of the derived characters in the clades. In making a cladogram, ______ assume that groups that _____ more derived characters have a more close common ancestor.

The letters that are italicized are words that i think are correct. This paragraph is needed for part of a recite that i have to do in front of my class. The prof. gave me a page like this. And  I don't know what those spaces are. Can someone help me.. please?

I provided some edits in my comment -- hope the following clarifies things for you a little bit.

  To construct a cladogram, two characters are defined.

You may be confusing character and character state. It's valid to have a cladogram with a single character (e.g. the single character, "warm-blooded"), but you will need at least two character states to infer a non-trivial cladogram. The states for the character warm-blooded would be Yes or No.

A molecular example would be a cladogram inferred from a column of a sequence alignment. That column is the character, and for, say, DNA, the character states are the set {A,C,G,T}.

  Then the outgroup of various species are identified based on the sequencing or closeness of the derived characters in the clades.

The outgroup is specified by you, the investigator. It's typically a hypothesis (viz. model parameter), which is either a guess or is based on some external evidence.

In short, the analysis starts from character-state data for some number of taxa ("species" in your paragraph). From this data you are selecting (constructing) a tree-topology that best fits this data.

E.g. for four taxa, labeled A,B,C,D, with D the outgroup, the process is like:

 start  --> cladogram
 ABC(D)     A  B C (D)
             \/ / /
              \/ /
               \/

There are many different methods to construct the cladogram. One popular method is  maximum parsimony, but the assumptions of that model are severe. However, any method is effectively selecting a tree topology out of all the finitely-many possible tree topologies over N leaves, where N is the number of taxa (species) in your investigation.

  In making a cladogram, ______ assume that groups that _____ more derived characters have a more close common ancestor.

In this sentence, you seem to be expressing a relationship between the number of shared derived characters (synapomorphies) for a given clade, and the common ancestor of that clade.

This can be very confusing, maybe an example will help. Let me annotate the above tree with a binary character, having states + and -.

            +   +  -   -
            A   B  C  (D)
             \ /  /   /
              +  /   /
               \/   /
                -  /
                 \/
                  -

The idea is that the ancestral state for the entire group is -, as was the state for the ancestor of {A,B,C}. However, the + state was derived after the ancestor of {A,B,C} but before (or "in") the ancestor of {A,B}. Then it was passed to the terminal units, A and B. (Note: typically you don't have this ancestral-state information, only the information at the tips of the tree. You're actually inferring the ancestral states and topology from the data at the tips.)

I would claim that, in general, taxa that share more derived character (states) have a more recent common ancestor than taxa that do not. Although, this can be confounded by homoplasy.


Schedules of mating for men It’s simple deductive logic to follow that for a species to survive it must provide it’s offspring with the best possible conditions to ensure it’s survival – either that or to reproduce in such quantity that it ensures survival. The obvious application of this for women is sharing parental investment with the best possible mate her own genetics allow her to attract and who can provide long term security for her and any potential offspring.

  Thus women are biologically, psychologically and sociologically the filters of their own reproduction, where as men’s reproductive methodology is to scatter as much of his genetic material as humanly possible to the widest available quantity of sexually available females. He of course has his own criteria for mating selection and determining the best genetic pairing for his reproduction. This is evidenced in our own hormonal biology; men possess between 12 and 17 times the amount of testosterone (the primary hormone in sexual arousal) women do and women produce substantially more estrogen (instrumental in sexual caution) and oxytocin (fostering feelings of security and nurturing) than men.

From a biological point of view, is the bold sentence correct? And is the quantity of hormonal differences the only explanation of this?

Link to article: http://therationalmale.com/2011/08/23/schedules-of-mating/

Females are defined as the sex that produces that bigger gamete (ovule) while the males are those from the gender that produce the smaller gametes (spermatozoid). Because producing big gametes is costly, the number of females fix the reproductive limit in the population and in other words the variance in reproductive success in males is higher than in females. In the same logic, because females fix the reproductive limit in the population, males have to compete to access the females while the females are choosy. You may want to have a look at the wikipedia articles for Bateman's principle and Parental Investment.

The conclusions of Bateman's principle holds in general but not systematically. In some species males produce huge amount of parental care and therefore, the females become choosy for example.

  [..] men’s reproductive methodology is to scatter as much of his genetic material as humanly possible to the widest available quantity of sexually available females.

Yes, in many cases but not everytime. Human are an example of the cases where this statement is wrong.

  [..] for a species to survive it must provide it’s offspring with the best possible conditions to ensure it’s survival – either that or to reproduce in such quantity that it ensures survival.

It sounds a bit weird! The reason is that the sentence almost implies that individual's strategy evolved in order to increase the probability of survival of the species which is totally wrong. By the mechanisms of natural selection a population evolve in the direction so that each individual favors its number of offsprings which can be in some cases very detrimental to the species as a whole.

Reading some bits of what I found no the webpage you linked i your question, it doesn't seem to me that the author is a good evolutionary biologist…but I haven't read much.


Why does spiral or annular thickening occur in water conducting plant vessels? From what I behold, spiral and annular thickening of xylem and trachied cell walls leaves a lot of not thickened regions of cell wall. Lignin is the material which prevents water from escaping these water conduits. If lignin is absent from certain regions, does not that mean that water flows out of the xylem vessels and trachieds through their cell walls? If so, is not this disadvantageous to a plant? Why can't a plant simply thicken the cell walls with uniform lignin deposition, only sparing pits to allow lateral flow into the required tissue? I would appreciate your kind response.

Non uniform lignification of xylem vessels is beneficial to a plant in that it enables growth. It is at the unlignified parts of plants that growth occurs since fully lignified tissues are dead and so can not grow. Spiral and annular thickening allows for vessels to elongate and thus allows tissues to expand without breaking the vessel walls.

Water cannot just go on flowing from plant cells because they are not lignified, plant cells have cellulose cell walls and cell membranes which prevent water loss. In addition, water in the xylem is not under pressure so I do not think water would be able to flow out of the xylem vessels except in cases where water is forced to move to adjacent phloem tissues by osmosis during phloem translocation.


Why is it that bacteria and fungi cannot develop resistance against essential oils? I wonder why bacteria and fungi cannot develop resistance and mutate agains essential oils?

For example, some fungi get killed by oregano oil.

Being not a biologist, I hope my question is not so stupid..

Thank you!

Here are my thoughts on this, taking your example, oregano oil.

The active anti-microbial ingredient in this essential oil is carvacrol. The WP article states that it probably acts by disruption of the membrane.
 There appear to be no examples of carvacrol resistance, as suggested by your question. In mammals the compound is detoxified in the liver via esterification to increase solubilty, thus promoting excretion.

Assuming that we can create a situation with a strong selective pressure for the development of resistance in a microbe, what would that resistance look like? If the carvacrol does indeed disrupt the membrane, then it is probably useless to develop intracellular degradation - what is needed is the secretion of an enzyme that is able to inactivate the compound, analogous to the β-lactamases that inactivate antibiotics like penicillin (which also has an extracellular mode of activity).

Furthermore, unlike β-lactams, carvacrol is insoluble in water. This suggests to me that most of the time, in the natural environment, free-living bacteria will not experience significant levels of the compound.

In summary - it may be difficult to evolve a system for the degradation of a lipophilic compound, and because it is lipophilic it may be that it is rarely a problem for bacteria unless they are being subjected to laboratory tests for antimicrobial activity.


can the face of a person be accurately predicted from DNA information? http://blogs.smithsonianmag.com/artscience/2013/05/creepy-or-cool-portraits-derived-from-the-dna-in-hair-and-gum-found-in-public-places/?utm_source=plus.google.com&utm_medium=socialmedia&utm_campaign=20130503&utm_content=collageartdna

Can the face of a person be accurately rendered just from analysing a DNA sample of that individual?

Not accurately. Assuming the DNA information is the DNA sequence, you can't tell which genes are being expressed and which are being silenced. These are through chemical groups on the DNA which aren't generally picked up.

Also there's the environment that grossly affects what you look like, how much you weigh, your skin colour and cosmetic surgery.


Fixation rate at neutral loci It is a classical result that the expected time for a neutral mutation to occur and to get fixed is $2 N \mu \frac{1}{2N} = \mu$, where $N$ is the population size and $\mu$ is the neutral mutation rate (wiki).

I am not sure I understand what this actually mean. What is the probability of (at least) one fixation event to occur in $\frac{1}{\mu}$ generations? Is it 0.5? Could we calculate the probability that (at least) one fixation event occurs in $n$ generations? For example after $n=\frac{\mu}{10}$ generations, is the probability of observing (at least) one fixation event equal to $0.1$ or is it more complicated?

UPDATE

Following @DanielWeissman comments:

Let's consider we are starting with an initially monomorphic population (population of clones). In addition to that, let's consider that the population is relatively small $N\mu < 1$

First of all, the $\mu$ is not expected time for a mutation to occur and get fixed; it is the rate at which mutations are fixed in the population. The basic result states that if neutral mutations arise at a locus at rate $\mu$ within individuals, mutations at this locus will be fixed in the population at rate $\mu$ as well.

The expected time for a given neutral mutation to fix after arising, given that it is not lost from the population, is approximately $4N_e$, where $N_e$ is the effective population size. Kimura and Ohta (1969) derive this result using a diffusion approximation; Kingman (1982) develops coalescent theory and in the process obtains what in my opinion is a more elegant derivation of the same approximation.

Now what is the probability that some mutation goes to fixation in the population as a function of time? Even though the fixation rate in the population is $\mu$, this does not mean that with probability 0.5 some mutation fixes within $1/\mu$ time units. That probability will depend on the distribution of fixation events in the population. Here's a good way to think about it. If fixation events were evenly spaced and occurred at rate $\mu$, then with probability 1 you would have a mutation within an interval of length $1/\mu$. If fixation events were highly clumped, then you would have a very low probability of having a fixation event within an interval of length $1/\mu$ -- but if you did have one event, you would probably have many. If fixation events are distributed as a Poisson process--which I suspect they would be in a purely neutral model--the probability of having a fixation event within a time interval $1/\mu$ would be given by a (negative) exponential distribution and thus the probability of having at least one fixation event in a time interval of length $1/\mu$ would be $1-\frac{1}{e}$.


Resource for learning analysis of sequence data via QIIME 2 I am trying to study/learn metagenomics through 16s rRNA microbial data and I want to teach myself/review core biology concepts while also learning the QIIME 2 analysis pipeline, as the website suggests learning it instead of QIIME for beginners.

I found a great source : http://www.science.smith.edu/cmbs/wp-content/uploads/sites/36/2015/09/Tutorial-from-sample-to-analyzed-data-using-Qiime-for-analysis.pdf
but was hoping for something with an analysis I could actually work through on my own, as this one involves the use of a cluster, where as I only have access to a laptop of moderate power and also one that involves QIIME 2.

Also something free and maybe as hand-holding as possible would be ideal too.

As for the platform I am learning on, it is a virtual box instance of Ubuntu.

The QIIME 2 tutorials are the place to get started - see here.


Help me understand how the thyroid secretes Please have a look at this close up light microscopic image of a thyroid gland:

So I'm guessing the cubic epithelial cells surrounding this big red pulp are the secreting cells...? If so, is the red pulp a blood vessel that they are secreting into?

Am I misunderstanding?

That "red pulp" spaces you're referring are not blood vessels but, in fact, thyroid follicles that selectively absorb iodine from the blood for production of thyroid hormones and storage of thyroglobuline. So, they act as a reservoir of the materials used by the thyroid's epithelial cells, also called follicular cells, to produce thyroid hormones (T3 and T4).


Why does the intensity of an action potential once generated at the trigger zone remain undistured throught the axon? What causes this consistency?
I read the previously asked questions on this site none of them carry an answer to this question.

Actually, it would be better to say that action potential does not travel but is regenerated anew in a sequence along the axon.

I would like to elaborate how this happens and why this is the reason why the action potential stays constant:

In rest state, there is an ion gradient across the membrane of each cell. This causes a small voltage between the outside and the inside of the membrane, the so called transmembrane potential.
Once the cell membrane becomes permeable for ions (normally this occurs when an ion channel is opened), the potential causes ions to flow across the membrane, the membrane becomes depolarized.

In the axon, the membrane contains so called voltage-gated ion channels. As soon as the membrane is depolarized at the trigger zone, the depolarization of the adjacent membrane causes voltage gated ion channels to open in that adjacent memrane as well, causing ions to flow also across the adjacent piece of membrane. This process continues in a wave along the whole membrane, this is what we call the action potential. Because the ion gradient across the membrane and the density of ion channels is constant along the whole axon, the amplitude of the action potential stays constant along the whole length of the axon.


Why do we suddenly forget things, like PIN or phone numbers, that we've known for years? Is it common to forget a 4 or 5 numeric code which has been used extensively for months and well remembered?

There's an article on the guardian describing this phenomenon and by the number of comments it seems quite common yet no scientific aspect trying to solve the mistery.

Is it some common phenomenon of the brain? Some erasing of irrelevant numeric things happening during sleep?

Forgetfulness is a common phenomenon that tends to increase with age. It usually affects short term memories but it can affect long term ones too. Here are some possible causes which I quote from Healthline (the full list available at that link):

  sleep deprivation
  use of alcohol or drugs and some prescription medications
  lack of oxygen to the brain
  migraine

It can happen at any age and it is normal if (quoting Deane Alban, Memory Loss: When It’s Normal and When It’s Serious):

  Are you overworked and stressed out? Are you eating poorly? Are you on a low-fat diet or skipping meals to lose weight?  Do you struggle with insomnia? Do you drink too much?

  If you answer “yes” to any of these questions, it’s likely you are losing your memory because your lifestyle is catching up with you.

You mention loss during sleep in your question. Sleep affects memories (see WebMD and Wikipedia):

deprivation of sleep leads to memory loss
during sleep brain selects relevant information gathered during the day and turns it into memories
certain stages of sleep improve memories


How valid are Koestler’s criticism of evolutionary theory? I recently read Arthur Koestler's 1967 book The Ghost in the Machine. In it, Koestler criticises the neo-Darwinian theory of evolution—beneficial random mutations preserved by natural seleciton—as insufficient to explain the formation of complex forms like eyes and eggs. The issues Koestler has with the theory are ones that I've been trying to wrap my head around since before I read the book, but I'm aware that:

a) the book is half a century old;

b) Koestler was not a biologist or scientist; and

c) neo-Darwinian theory/the modern synthesis seems to have stood the test of time

so I'm wondering how accurate Koestler's account of the theory is, and if he is wrong what the retorts to his claims are. Here are two examples he gives of complex forms:

  [The giant panda] has on its forelimbs an added sixth finger, which comes in very ‘handy’ for manipulating the bamboo-shoots which are its principal food [but] that added finger would be a useless appendage without the proper muscles and nerves [and t]he chances that among all possible mutations those which produced the additional bones, muscles and nerves should have occurred independently are of course infinitesimally small.

and

  The decisive novelty of the reptiles was that, unlike amphibians, they laid their eggs on dry land...[b]ut the unborn reptile inside the egg still needed an aquatic environment...[i]t also needed a lot of food...[s]o the reptilian egg had to be provided with a large mass of yolk for food, and also with albumen—the white of egg—to provide the water. Neither the yolk by itself, nor the egg-white itself, would have had any selective value...[e]ach change, taken in isolation, would be harmful, and work against survival.

Instead of random mutations and external selection, he suggests that ‘internal selection’ works at all levels, from chemical upwards, to correct ‘misprints’ long before the developed organism is exposed to any sort of external selection. The implication that there must therefore be some plan towards which embryonic development works is supported by two examples:

  the growing eye-bud of the embryo is an autonomous holon, which, if part of its tissue is taken away, will nevertheless develop into a normal eye

and

  [the fruit fly has a recessive gene that when paired with another in a fertilised egg will produce an eyeless fly.] If now a pure stock of eyeless flies is made to inbreed, then the whole stock will have only the ‘eyeless’ mutant gene, because no normal gene can enter the stock to bring light into their darkness...within a few generations, flies appear in the inbred ‘eyeless’ stock with eyes that are perfectly normal.

His other main point is that evolution takes a zig-zag path, evolving down until reaching an evolutionary dead-ends before retracting to ‘an earlier or more primitive, but also more plastic and less committed stage—followed by a sudden advance in a new direction’. For example:

  [A]mphibian...ancestry...goes back to the most primitive type of lung-breathing fish; whereas the apparently more successful later lines of highly specialised gill-breathing fishes all came to a dead end.

and

  ...the human adult resembles more the embryo of an ape than an adult ape

Is Koestler's science just faulty, or are these valid criticisms that've been resolved since?

Maybe both. Certainly his understanding of limb developement doesn't match modern understanding. The quote you provide seems to indicate that he thought the appearance of an additional digit would require a multitude of coordinated mutations. Our current understanding seems to indicate that it's all about changes in the regulation of genes. For example in fruit flies mutations in the antennapedia gene can cause antenna to grow where legs should be or visa versa. Another example is polydactyly(extra toes) in cats which be be caused by mutations to a single regulatory region.

  within a few generations, flies appear in the inbred ‘eyeless’ stock
  with eyes that are perfectly normal.

I'm not a fruit fly expert, but this seems highly dubious to me. There is a well studied eyeless mutation, but it's dominant, not recessive. Furthermore getting two copies of this mutant eyeless gene is lethal at the embryonic stage. This means that a colony of adult eyeless flys are necessarily all heterozygous. That is, they have one copy of the mutated eyeless gene, and one copy of the normal eyeless gene. By Mendel's laws, a quarter of the offspring from the completely eyeless generation are going to have two copies of the normal eyeless gene, and so will have normal eyes. I wouldn't be surprised if the flies with normal eyes outcompete the flies without eyes, so eventually the eyeless flies will disappear from the colony. I can't tell you whether Koestler has mis-characterized this gene, or is talking about some other gene all together. Citation needed.


Why we need a plasmid for r-DNA technology Recently I was studying Biotechnology. When I went through the texts, I had a doubt: both plasmids and gene of interest are made of DNA stretches and bacteria directly absorb plasmids in a test tube (where reactions take place). Why is the gene of interest not directly put in the test tube instead of recombinant DNA Technology (using Edited plasmids), so that it gets absorbed by bacteria?

A plasmid has a site necessary for replication of genetic material know as the origin of replication (ori) since gene of interest (GOI) is just a segment of DNA it only posseses the sequence of interest and lacks an ori site, due to this it will not be able to replicate by itself. Replication of GOI is important for product formation in r-DNA technology (mostly protien) as when the host cells divides the GOI is duplicated and is transferred to both daughter cells. This way the number of recombinant cells will increase hence producing more of the final product.


How do we feel sensations from a tooth surface that is made up of enamel? If enamel does not have any sensory receptors, how do we feel the tactile sensations when we touch our teeth with an object/finger nail?

How do we feel the tactile sensations when we touch our teeth

The same way you feel tactile sensations when you tap a bicycle helmet on you head: the motion (or vibration) is transferred through the material to your head & the nerve endings in your scalp the same as tapping a tooth sends vibrations to the nerves in & at the base of the tooth.


Do lobsters possess a nervous system to feel pain? I was reading an article, which it mentions that lobsters do not have a nervous system:

  Lobsters have very poor eyesight and no nervous system. They walk slowly
  on the sea floor but are capable of swimming backwards by the curling
  and uncurling movement of their abdomen.

But in Wikipedia, I read that only 3 types of multi cellular animals do not posses a nervous system:

  The only multicellular animals that have no nervous system at all are
  sponges, placozoans, and mesozoans, which have very simple body plans.

Which none of them seemed like a lobster to me. In this answer, it is claimed that every living organism feels pain somehow.

Now I would like to know the answers of these questions:

Is the article about the lobsters true? They have no nervous system which means they feel no pain even if killed?
Is the claim in the answer true? Literally one of the claims must be wrong, since they conflict with each other somehow.

Yes they feel pain, at least in certain areas of their body without a doubt. Research has been done to test whether they feel pain consciously (a signal to the brain that is perceived allows for learned response) or if it is just a reflex response (Nociception), and there is good evidence they actually perceive it especially in the antenna.

source

Source 2


How are monocytes larger than capillaries? I have read that the average size of a capillary is about 8 micrometers. How is it possible that the 15 micrometer or so monocytes in blood do not block these vessels?

https://en.m.wikipedia.org/wiki/Blood_vessel#Vessel_size

https://www.britannica.com/science/monocyte

They aren't completely rigid and can change shape to squeeze through (see Downey et al).

If they are activated, monocytes can get stuck in capillaries and block them, which contributes to poor circulation following reperfusion after an ischemic blockage (see Engler et al).

Downey, G. P., Doherty, D. E., Schwab 3rd, B., Elson, E. L., Henson, P. M., & Worthen, G. S. (1990). Retention of leukocytes in capillaries: role of cell size and deformability. Journal of applied physiology, 69(5), 1767-1778.

Engler, R. L., Schmid-Schönbein, G. W., & Pavelec, R. S. (1983). Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog. The American journal of pathology, 111(1), 98.


Vesicular and non vesicular transport I have to classify them either as transported in vesicles or without vesicles.

What I think -

Non-vesicular

2.vesicular

3.vesicular

4.vesicular

5.non-vesicular

6.vesicular

7.vesicular

8.vesicular

9.vesicular

Am I right ? Is it true that a  protein transported by vesicles is made on ER ribosomes ?
How are proteins transported non-vesicular transport ?

Any protein which enters the secretory pathway will proceed via vesicular transport to some point on that pathway. That includes lysosomal proteins, integral plasma membrane proteins and secreted proteins (also, not on your list, resident proteins of the ER, Golgi proteins, some endosomal proteins).

Cytoskeletal proteins are cytoplasmic: I suppose you could argue they are 'transported' sometimes, e.g. tubulin treadmilling, motors etc., but no vesicles are involved. Nuclear proteins enter the nucleus from the cytoplasm through nuclear pores. They have nuclear localisation signals; vesicles aren't involved. Mitochondria, chloroplasts and peroxisomes all have their own protein import systems with associated unique signals; again no vesicles are involved.


Why is the resting membrane potential of excitable tissue not affected by the extracellular sodium concentration? I know that the resting membrane potential for excitable tissue (eg, nerve) is primarily determined by the electronegative difference between the inside and the outside of the membrane for potassium ions, as they are most permeate ion by far. And since the membrane is largely impermeable to sodium, it's diffusion potential is insignificant, as such it does not contribute much to the resting membrane potential.
However, is it not correct to think that if the concentration of sodium ions in the extracellular fluid drops, outward diffusion of the positive potassium ions will increase, because the outside of the membrane is now less positive (more negative), subsequently making the diffusion potential of potassium and the resting membrane potential more on the negative side and further from the action potential threshold. I am asking this because my professor was mentioning factors that affect the resting membrane potential, and he mentioned that the ECF concentration of sodium has no effect on the resting membrane potential.

I cannot imagine anyone being able to explain it more clearly than this webpage. Your question is addressed in the middle of the page.

It's easier to split the idea into two separate, but parallel ideas: electrical potential and chemical potential. Both sodium and potassium contribute to resting potential. Sodium affects the voltage (electric potential) across the membrane. However, their chemical potentials (difference-across-membrane) are separate. The key idea is that there is a difference between resting membrane potential and potassium equilibrium potential.

I quote a helpful thing to keep in mind:

In a neuron, the resting membrane potential is closer to the potassium equilibrium potential than it is to the sodium equilibrium potential. That's because the resting membrane is much more permeable to K+ than to Na+.

    If more potassium channels were to open up—making it even easier for K+ to cross the cell membrane—the membrane would hyperpolarize, getting even closer to the potassium equilibrium potential.
    If, on the other hand, additional sodium channels were to open up—making it easier for Na+ to cross the membrane—the cell membrane would depolarize toward the sodium equilibrium potential.


How many honeybees are there, and how has the number changed across time? How would you begin to estimate the world population of the European Honeybee (Apis mellifera)? Would recent colony collapse disorder show up as a blip? How about the spread of A. mellifera from Europe to Asia and the New World?

Ideally, I'd love to see a chart with estimates of the kept and feral populations of A. mellifera across time. I realize that this is a tall order; but given that we have available to us:

the complete genome,
current data from agricultural organizations, and
historical and archaeological records,

it seeems that with a combination of genetic and historical methods this shouldn't be impossible. Or is it? There seem to be plenty of articles arguing about A. mellifera's African or European origin, but none that I see that mention actual population sizes.

1 billion hives
(at 10,000-50,000 bees/hive this is 10-50 trillion bees)

Managed: 100 million hives

Based on country-level data from FAO, supplemented  for a few countries with Apiservices, in 2011 there were about 80 million managed hives. Because FAO lacks any data for some countries, and other countries under-report (for instance US figures don't include hives kept for pollination service and hives kept by small-scale operators) a reasonable round estimate of managed hives in the world is 100 million. (This implies a 128% correction to the FAO numbers). (Aizen and Harder 2009 give context on FAO figures).

Wild/Feral: 900 million hives

Wild/feral hives of Apis mellifera are difficult to count via direct observation. Jaffe et al 2010 use a genetic sampling method, and also report a reasonably strong correlation between the total number of hives (managed and wild) per square kilometer and the mean annual temperature of the area.
I used the best fit line from their data to estimate the "hive-carrying-capacity" by country using (the admittedly very general) land area and mean annual temperature. Then I subtracted the number of managed hives from the carrying capacity to estimate wild hives.

Although this formula probably overestimates large, cold countries and underestimates Africa (the formula gives 211 million feral hives in Africa when literature suggests closer to 300 million), in general, it seems to give not unreasonable estimates in comparison to the literature. Globally, this formula gives an estimate of 984 million wild hives. Given that land area included desert and other unsuitable habitat, it seemed reasonable to round down, and I took 900 million as my estimate.

Historical Populations

1961-2011
FAO statistics date to 1961. I plotted their numbers, with the 128% correction for each year. I assumed that during this time the number of wild bees has remained virtually unchanged, at 900 million, because it was defined by mean temperature and land area, which have not changed.*

1650-1961
This period represents the globalization of Apis mellifera. Before 1600, there were no European honey bees beyond their native range (Western Eurasia and Africa). However, once established in new areas (the usually cited first beehive in the USA in 1622), Apis mellifera rapidly spread in both managed and feral populations, in North America (17th c), South America (18th c), Australia (19th c) and East Asia (20th c) (Crane 1999)
.

I used carrying capacity of native range countries (just about 35% of the carrying capacity of the globe, or 350 million hives) as a before-1650 estimate,  and then assumed a geometric increase of about 2% per decade in available land area (ALA), as Apis mellifera bees and beekeeping made their way around the globe.

To estimate the number of managed bees during this period, I assumed a human:hive ratio of 35:1**, and modelled hives based on historical estimates of human population, multiplied by the ALA for the decade. The 1650 estimate was 5 million managed hives.

*Although diseases, pests, and pesticides have been reported to affect feral populations, I didn't find any solid information on this. For instance, feral populations of Apis mellifera mellifera and A. m ligustica have been widely reported to be in decline in the USA, but at the same time, feral populations of Africanized honeybees (Apis mellifera hybrids) have been rapidly spreading. Even with 90% losses in the USA, Canada, Japan, and Europe (areas affected by varroa) my estimates would only be decreased about 10%. However, it's also possible that land-use change has greatly affected feral bee populations (Moritz et al 2007).

**This wasn't a totally wild guess. I first calculated the human:hive ratio for 1961-2011. This ratio was increasing - there were 71 people / hive in 2011, and 47 in 1961. Initially, I assumed the rate of change in the ratio to be constant, but this led to unrealistically large estimates for historically managed hives. However, the rate was clearly increasing (just, perhaps in a nonlinear way I didn't want to estimate), so I decided instead to compromise on a number less than 47 and greater than 4. I decided on 35, as it produced what seemed like a realistic estimate of 5 million hives in 1650, compared to around 20 million today for Eurasia and North Africa (excluding sub-saharan Africa where wild-harvest remains important and likely was even more so in the past).

 Aizen MA, Harder LD. 2009. The Global Stock of Domesticated Honey Bees Is Growing Slower Than Agricultural Demand for Pollination. Current Biology 19: 4–4.
 Crane E. 1999. The World History of Beekeeping and Honey Hunting. Taylor & Francis. (Chapter 12).
 Jaffé RR, Dietemann VV, Allsopp MHM, Costa CC, Crewe RMR, Dall'olio RR, Rúa PPDL, El-Niweiri MAAM, Fries II, Kezic NN, et al.. 2010. Estimating the density of honeybee colonies across their natural range to fill the gap in pollinator decline censuses. Conservation Biology 24: 583–593.
Moritz R, Kraus FB, Kryger P, Crewe RM. 2007. The size of wild honeybee populations (Apis mellifera) and its implications for the conservation of honeybees. Journal of Insect Conservation


peptide MHC microarray "The recent technology is peptide–MHC microarray or artificial antigen-presenting chip.
  In this technique, recombinant peptide–MHC complexes and co-stimulatory molecules are immobilized on a surface, and population of T cells is incubated with the microarray. The T cell spots act as artificial antigen-presenting cells containing a defined MHC-restricted peptides. The advantage of using peptide–MHC is that it can map MHC-restricted T cell epitope."

These few lines are from Chapter 3 of Immunoinformatics, De, Rajat K., Tomar, Namrata (Eds.).

What is recombinant peptide MHC? What is MHC restricted peptide? How did the advantage get derived?

According to this paper (Yoav Soen et al. PLoS Biology 2003), peptide:MHC microarrays are a type of cellular microarray (a microarray designed to identify cell types; Wikipedia). These microarrays have attached a MHC molecule bound to a peptide, which allows them to work as artificial antigen presenting cells (APCs) that activate specific subpopulations of T cells.

Another recent paper is here where they specifically use the word recombinant peptide:MHC.

The expression MHC restricted refers to the positive selection (in the thymus) of T cells that recognize MHC molecules of the host but not other self-antigens (Wikipedia).


Excretion and metabolic waste? I know there is a difference between digestive and metabolic waste, but which one is called excretion? And what's the other one called? Thanks!

Egestion is the expulsion of undigested food which occurs typically via the anus. Although, interestingly or maybe just gross, flatworms must use their mouth has they have no anus. This is the non-metabolised material.

Excretion is the transfer of any metabolised material to the environment, including urine or carbon dioxide.


Are there U-rich transcriptional pause sites? I've heard a statement in a talk that U-rich sequences cause transcriptional pausing. The intuitive explanation for this was that the UTP concentration is lower in the cell than the ATP concentration. Reducing the concentration of an educt obviously reduces the reaction rate, leading to pausing of the RNA polymerase.

After reading up on transcriptional pausing, I haven't found any literature that shares this view. The recent papers I found don't show U-rich sequences and have completely different explanations on how pausing works. Those explanations mainly concern interactions at the edges of the transcription bubble.

Now, I guess that there might be multiple mechanisms of transcriptional pausing. But I couldn't find any references in the literature to U-rich pause sites and how they could work. Is there any literature on this? Either on the fact that U-rich sequences tend to be pause sites, or that the concentration difference in NTPs leads to pausing at certain sites.

Yes, there are: this is a feature of bacterial intrinsic termination. The mechanism of pausing is not as you describe, though.
In bacterial transcription, two forms of termination are recognised (to my knowledge):

Intrinsic termination, consisting of a hairpin and a stretch of Uridines.
Rho-dependent termination, consisting of a 'loading' site for termination protein Rho, and a pausing site, but not the stretch of Uridines you refer to.

If you were reading up on transcription in eukaryotes, or were reading about rho-dependent termination, that would explain why you found no mention of polyU tracts. When evolution provides many solutions to a problem, it can get tricky to keep on top of it all!
This lists a few types of termination, including attenuation which is fascinating, and does involve regulation dependent on the concentration of a substrate.
Intrinsic Termination
A palindromic sequence situated just before the termination site causes a hairpin to form in the nascent RNA inside the exit channel of RNA polymerase, if given time (and if anti-termination factors do not bind the RNA to suppress hairpin formation). It appears that formation of this hairpin "destabilises the elongation complex [RNA polymerase + elongation factors]", and is an irreversible step towards collapse of the transcription bubble and dissociation of the transcription machinery.
The polyU tract (~8nt long) proceeding the hairpin seems to have dual function: the A:U basepairing in the DNA:RNA hybrid is weak; the hybrid becomes less favourable. Since the hairpin (which is an RNA:RNA duplex) is adjacent to the RNA:DNA hybrid duplex in the bubble, they experience competition for formation. Weakening the hybrid duplex favours hairpin formation, which acts like a switch that separates most of the RNA:DNA duplex in the bubble - synthesis cannot proceed, and the unstable complex dissociates.
Also, the ployU seems to be responsible for pausing which allows time for the hairpin to form, but not for the reason you suggest:
The concentration of UTP in the cell is not unusually low. ATP concentrations are higher than other ribonucleotides since it is the cell's major 'energy currency', quite apart from nucleic acid synthesis. Hence I don't believe pausing can be explained as the polymerase waiting for UTP. The polyU tract probably acts as a 'back-tracking signal' to the polymerase, since the hybrid duplex in the catalytic site is weakened, and the repeated nature may be "slippery"(?). This back-tracking pauses the polymerase.

To summarise: The elongation complex passes the palindrome and reaches the polyU tract, where the hybrid duplex in the bubble is weak and tends to cause back-tracking/pausing. This allows time for the hairpin to form in the exit channel, which both unwinds the hybrid duplex further, and destabilises the elongation complex. The transcriptional machinery is now destined to dissociate and the bubble collapse: RNA is released from the DNA duplex.
It is interesting to note that intrinsic termination can be suppressed by proteins that bind the hairpin. In bacterial operons, where sets of (almost) concatenated genes are separated by intrinsic termination signals, the amount of read-through at each termination site determines the relative expression levels of each gene.
Rho-dependent Termination
Rho is a hexameric protein complex that is loaded on to the nascent RNA at a loading sequence. It hydrolyses ATP to move along the emerging RNA - apparently it "races" with the polymerase, and when it catches up to the polymerase, it causes termination. There are pause sites in the RNA which allow rho to catch up - these sites tend to be rich in A and U, so perhaps polymerase is slowed by destabilisation of the hybrid duplex - but it is nothing like the intrinsic terminator, since it depends completely on rho for termination.


What is the function of the polar bodies produced during oogenesis? Why are polar bodies produced during oogenesis in human females?

I read that polar bodies are produced during meiosis so that the oogonium (or gamete mother cell) can be converted into a haploid female gamete or ovum by getting rid of the extra genetic material.

So, it is pretty clear that one follicle (containing one gamete mother cell) produces only one ovum.

So what is the point of producing polar bodies? Isn't it just a better mechanism over all for the meiotic devision of the oogonium to result in equal distribution of the cytoplasmic content to both daughter cells? That way, one oogonium can produce four ova, not just one. Th entire process of DNA replication during the synthesis phase (S phase) of the meiotic cell cycle seems like such a waste if 75% of the total genetic material produced is going to be expelled as polar bodies.

There is also the argument that since the ovum is non-motile and always within the female body, it need not be produced in large numbers as it is in a safe and protected environment. But, in that case, would it not be a better system is fewer follicles were produced, but each follicle divided to give four ova? This mechanism would end up producing the same amount of ova, but with lesser labour (such as DNA replication) going waste.

So, taking these arguments into consideration, what exactly is the function of the polar bodies produced?

"In other animals and some plants, polar bodies give rise to vital tissues that protect and nourish the embryo " ( http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164815/). This could be the same fucntion to humans since we are all eukaryote.

Polar bodies are not waste. They sacrifice themselves after giving their energy to the embryo, completing development and differentiation into a baby.


Question about phylogenies and DNA sequencing I'm reading this web page which talks about phylogenies and DNA sequencing:

https://bioinf.comav.upv.es/courses/biotech3/theory/phylogeny.html

A certain sentence says, "If we consider dolphins and sharks to be closely related because they share a similar shape we would be mistaken."

If we were to take the DNA sequence of the dolphins and sharks and compare the genes encoding for shape, wouldn't they be very similar? Wouldn't we then be able to conclude that dolphins and sharks are similar?

Or is the workaround that we would examine the entire genome, i.e. the entire DNA sequence, to see if that's the only similarity they have?

Genes reflect a phylogeny of their own. So no, the genes for "shape" (if they existed) would be very different between dolphins and sharks. Every single gene in a dolphin is more similar to its homologous counterpart in a cow than to any gene in a shark. Gene by gene, or with the entire genome, it would not matter. The similarities between sharks and dolphins are due to convergence. Convergence make sense in that there is selective pressure to have streamlines bodies to swim through the water. It is possible for genes to converge as well, but the nucleotides would differ, just as the fins on sharks and dolphins differ.


What are evolutionary implications of contraception and reduced childhood mortality rates worldwide? I've heard the following idea this morning: Before the introduction of contraception, humans conceived quite a lot of babies (there was little to do to avoid that), but the population was kept in check by very high childhood mortality rates. This mortality rate ensured that only the fittest survived.

The idea seems common sense, but I decided to investigate if this is really true. I know that for evolution, even 2000 years should be an instant.

I did some research, for example the worst childhood mortality rate currently in the world is around 17.5%, which is still about half of what it was in "developed" countries during the 1700s, according to the table below. But looking at the wikipedia map of childhood mortality, it seems that a baby nowadays has only around 1-3% chance of dying before adulthood, because even the weakest baby can be kept on life support long enough for the danger to pass.

What are the implications of reducing childhood mortality rates worldwide on human evolution? Maybe evolution is a wrong term to use here. Would it be fitness as species? I'm particularly interested in how this relates to developmental defects and genetic disorders. Is there any evidence that people who lived in a world without contraception and with high childhood mortality rate were more physically or mentally fit?

Here's an paper that deals with the subject and the table is from the paper below:

IS CHILD DEATH THE CRUCIBLE OF HUMAN
EVOLUTION?

Before the introduction of contraception, humans conceived quite a lot of babies (there was little to do to avoid that), but the population was kept in check by very high childhood mortality rates. This mortality rate ensured that only the fittest survived.

Woh! Let me stop you there. No, high rates of childhood mortality do not ensure that whom Natural Selection is acting upon are the "most fit." That title is given to individuals who are able to survive long enough to breed.

Many, many conditions that affect humans do not interfere with a person's growth or ability to perform physical or intellectual feats - but can definitely reduce or completely eradicate a person's ability to reproduce. These individuals are evolutionary dead-ends, and thus - while they survive in the environment - are not "fit" in the context of this topic.

  What are the implications of reducing childhood mortality rates worldwide on human evolution? Maybe evolution is a wrong term to use here. Would it be fitness as species?

What it means is that populations will rise. As populations rise and intermingle, alleles get spread around. Perhaps rarer alleles become more common, or more common alleles become rarer. We're talking about Hardy-Weinberg equilibriums in the allele frequencies. However, with populations large enough true equilibriums are impractical to reach.

The more pragmatic explanation is that more mutations will arise, they'll be passed around, rare mutations will see more exposure, and humanity - in a very general sense - becomes more diverse genetically until a Selective Pressure is applied. Until there's a detriment to having a particular gene, there isn't a need to eliminate it from the population.

Your example is children who are too weak at birth to live outside of an NICU for their first few months - well, because we're capable of providing such care, until that care goes away it's not negatively affecting us. If it comes with an additional cost - say that, for whatever reason, premies can't digest mother's milk until the 8-month mark, then Natural Selection would pressure humans to evolve so that only 8+ month or older babies are born.

There's no evidence of significant pressures in human populations at this time, though. At least not in politically stable and technologically apt countries, although in areas undergoing long-time drought or other dangers it is seen. Sickle-Cell Anemia is though to be an adaptation to rising Malaria rates - which was quite fatal until medication was devised to treat it in the last 50 years or so (not even a blip in evolutionary terms).

  Is there any evidence that people who lived in a world without contraception and with high childhood mortality rate were more physically or mentally fit?

Not that I can think of or find easily. While there are detriments associated with being born prematurely, and some evidence that women waiting until they're late 30's and men until they're 60 or older can negatively affect their gametes and consequently the development of any children born from them - it's been such a short time since the introduction of hormonal contraception and modern medicine that we may not see results tangible results for hundreds of years. Although condoms have been around for several hundred years, and there's been no associations with condom use that I can think of.

In the short term, what it has done is affect the ethnic diversity of countries. For the first time ever, Hispanic births have outnumbered Caucasian births in 2012 in the United States. Other countries, mostly European countries, are seeing declines in birth rates - which means their populations will decline with age or be compensated for by immigration. Higher birth rates, however, are associated with lower income brackets or very religious communities - both of which are associated with ethnic Minorities, at least in the United States. So while minority populations have more kids, they do so on fewer resources which may negatively affect their children in the long-term, whereas higher-earning segments of the population might have fewer children later in their lives, but can provide a much more stable environment and opportunities to continue that success.

One thing that hormone-centered birth control has done, however, is eliminate rape as a viable form of passing on one's genes. As gruesome as it might be to consider, pregnancies as a result of rape can produce "fit" offspring. It is a legitimate reproductive strategy in nature, and is in humans... unless the woman is using contraception. In the long-term this will probably show some interesting results (nominally an enhanced "Female Choice" effect - which is already evident in human evolution), but nothing right now.

It's also worth considering the ability for humans' increasing abilities to manipulate our own genome. At this point, we're nearly able to remove detrimental genes at-will and replace them with more effective versions. Because of this bio-engineering ability, the generations after ours might never be susceptible to inherited diseases - or they might all hop on the trendy "genes" and end up completely identical to each other. That's part of the fun of being human, though; we're very messy when it comes to Evolution. We tend to muck things but up good. :)


What is this part of blastula called and how is endoderm formed? Could you tell me what the yellow mass within the blastocoel is called ?
I know that blastocoel is a fluid filled cavity, so are the yellow coloured cells the inner part of blastoderm or are they some other cells ?

If they are the part of blastoderm itself, why is it not in the same colour of light-orange as the blastoderm, or is it the mesoderm, or the inner cell mass  ?

And is it the blastoderm that forms ectoderm , and endoderm pinches  off the ectoderm during gastrula phase? And could you also explain how the orange mesoderm formed ?

The blastocoel, as you say yourself, is a fluid-filled cavity (wikipedia) so it has no cells. Fig. 1 shows cellular and non-cellular regions of the blastocyst.

Your questions on the formation of the three germ layers during germination are nicely shown in the illustration in Fig. 2, right two panels.

Fig. 1. Blastocyst. source: wikipedia

Fig. 2. Formation of the germ layers. source: Class Connection


what is this marine creature? I found this creature floating in the Mediterranean Sea, probably dead.
I tried looking it up in the Marine Species Identification Portal but I couldn't find anything like that. It looks like some kind of jellyfish or hydrozoan.

This is a blue button jellyfish! they eat zooplankton and are usually found drifting along on currents
they aren't true jellyfish and just like a jellyfish have no blood, brain or nervous system. they aren't usually toxic enough to hurt but can cause irritation to the skin.
they live in warm waters off of Europe and in the golf of Mexico and the Mediterranean.
they are hermaphrodites and have both male and female reproductive parts. they lay eggs which turn into polyps
here is a website I found all about them as I'm not extremely knowledgeable on this species.
https://www.thoughtco.com/blue-button-jelly-porpita-porpita-2291819


Does the Rayleigh formula apply to electron microscopes or only light microscopes? I am asked to determine the resolving power of both a TEM (transmission electron microscope) and a SEM (scanning electron microscope) and given the Rayleigh formula below.

$$Resolution=\frac{0.61\lambda}{N.A.}$$
Where $\lambda=0.0039$nm since the wavelength of an electron is $0.039$ angstroms and $1Å=0.1$nm.

I am also told that the N.A. the numerical aperture for the TEM is $0.01$

So, $$Resolution=\frac{0.61(0.0039nm)}{0.01}=0.24nm$$

For the SEM I am not given the N.A. but I am told that the resolution is $10$nm

My problem is if I use the Rayleigh formula  $$Resolution=\frac{0.61\lambda}{N.A.}=10nm$$ I get $$N.A.=0.0002379$$ Which would imply that the aperture for the SEM is greater than that of TEM since N.A for TEM is $0.01$ and SEM is $0.00023$ $$0.01>0.00023$$.

My problem is that I'm told the greater the aperture (smaller value of aperture) the greater the resolution but as you can see from the equations above this doesn't seem to make sense, The only explanation I can think of is that the Rayleigh formula does not apply to electron microscopes. Any advice would be greatly appreciated thank you.

This is more than likely better asked in physics SE, however since you contextualized it biologically somewhat I will answer it here.

You are correct in your concern. The Rayleigh Criterion and the associated calculations(Rayleigh Scattering) are talking about the minimum separation of 2 light sources to resolve a given object. From this we are able to derive nice metrics like resolution and so forth. As you say, this describes the resolving of light wrt to the diffraction limit.

In order to calculate the resolving power of an SEM or TEM you need to do a different set of calculations.

First, the theoretical limit of EM microscope resolution is given by the De Broglie Wavelength of the accelerated electrons. However, as with the calculations for the Rayleigh Criterion, there are other factors to consider. For a full walkthrough see this. You take Abbe's equation for resolution in a perfect optical system, and take account of the other factors at play(optics for example).


What is the meaning of the word "Ligandable" in "ligandable proteome"? I see "ligandable proteome", "ligandable proteins" and "ligandable targets" an awful lot.

But really I don't know what exactly the word "ligandable" means?

Is that it means, for example, "ligandable proteins" means proteins have ligands?

Thank for your help.

In biochemistry, ligand is usually taken to mean a substance which binds to a larger molecule such as an enzyme or other protein, thereby forming a larger complex.  The study of ligand binding has been important for pharmaceuticals, particularly in ligand-based drug design.

The term ligandability (and hence ligandable) seems to have come into significant use with a paper by Edfeldt, Folmer, and Breeze in which they say:

  In recent years, the term druggability has increasingly been adopted to describe the ability of a protein target to bind small molecules with high affinity; however, we believe the term ‘ligandability’ is more appropriate for this purpose. Although ligandability is a requirement for finding drugs for a particular target, it is not a guarantee that such ligands will make good drugs.

So, ligandable usually refers to the capability of a molecular target of drug design to bind small molecules.  A ligandable proteome would then be a set of proteins capable of binding small molecules.


What kind of insect is this and what is it doing? I live in Denmark and found these two insects on a tree. I'm interested in the big fly and have the following questions:

What kind of fly is it?
What is it doing with the little fly?

I think it's a Robber Fly. Those are predatory.


Using a Sphygmomanometer If you were to use an older sphygmomanometer and a stethoscope to record blood pressure, why would you hear no sound when the cuff was inflated to 160mmHg

The measured blood pressure is the radial pressure exerted by the blood column againt the arterial wall.

In a normal patient, this pressure varies between 120 mm of Hg and 80 mm of Hg.

click on the image to go to the source

When a cuff is inflated to 160 mm of Hg, the arteries collapse and circulation is temporarily suspended. As blood flow does not occur, no sound is audible.

The korotkoff sounds that are heard while measuring BP are due to disturbance in the streamlined flow of blood. When auscultating an artery without applying pressure no sounds should be heard in a normal person. Generally they are heard when blood flow occurs in spurts. This occurs when the cuff pressure is lesser than the systolic pressure but more than the diastolic pressure.


Reading an amino acid physicochemical properties diagram I want to know if I am reading the venn diagram correctly and why there are discrepancies in the diagrams.

I'm trying to determine which amino acids are considered hydrophobic and I am using this diagram suggested by my teacher from Amino acid properties and consequences of subsitutions.

From the diagram I've determined that A, G, C, T, V, I, L, F, W, Y, H, K, M are hydrophobic.

My problem is when I visit other sources I do not get the same results. Using Amino Acid Table I determines that A, G, I, L, M, F, P, W, Y, V were hydrophobic:

Furthermore, there is even another different venn diagram from Decoding the Building Blocks of Life from the Perspective of Quantum Information

Polarity and hydrophobicity are not discrete phenomena and, therefore, categorizing amino acids as such has some measure of arbitrariness, especially at edge cases. It all depends on one’s definition.

Other properties have similar problems. Charge depends on pH. And what is the cut-off between “large” and “medium” sides chains?

What is, in my opinion, more important than memorizing charts/diagrams/etc (unless you have an exam) is understanding why different amino acids have these properties. For example, why can threonine or tyrosine be classified as both hydrophobic and polar? Why can cysteine or serine, which are classified as uncharged, act as strong nucleophiles in enzymatic reactions?