Strand representation in the DNA version of the Genetic Code A Wikipedia entry entitled DNA Codon Table states that the codons presented in the table are on the ‘sense strand of the DNA’. But what is the purpose of this, if the sense strand doesn’t code for anything? It stated that it is used a lot in computational biology, what exactly is the use of it in that field?

The sense strand has the same sequence as the transcribed RNA. The antisense strand is read in the other direction. For a particular gene, the sense strand is the genetic code, the other strand is the complementary template used to transcribe the RNA from it. The resultant pre-mRNA molecule (before introns are spliced our) will be single-stranded in the 5’ to 3’ direction with exactly the same sequence as the coding sequence (except for U instead of T). As such, the sense strand is the coding sequence of a gene (as it corresponds directly to the transcribed RNA sequence).

It is important to distinguish the direction of a DNA sequence. Genes can overlap in opposite directions. DNA and RNA molecules can only be synthesised by enzymes in one direction. This is important for DNA synthesis in vivo  (e.g., Okazaki fragments) and molecular biology experiments in vitro (e.g., PCR and NGS). Antisense RNAs are also expressed and are important in regulating cellular functions: this includes enhancers which sometimes express bi-directional RNA and short RNAs involved in RNA interference, microRNA, and CRISPR-Cas).

In molecular, cellular, and computational biology, the sense strand encodes the coding sequence (gene or other transcript). This is the sequence of any resulting RNA. Hence we define a codon as the nucleotide triplet that corresponds to a resulting amino acid. The antisense DNA strand and the tRNAs are complementary to this. Therefore there is an agreed upon convention to determine which strand is “coding” and it is straightforward to derive the resulting amino acid sequence of the encoded peptide given a coding sequence and a start codon (AUG). The antisense strand is the reverse compliment sequence which can also be computed. It is not necessary to store the sequence of both strands of a gene since the coding sequence can be used to infer the sequence of both strands.

See Figure 6-7. Molecular Biology of the Cell. 4th edition. Alberts B, Johnson A, Lewis J, et al. New York: Garland Science; 2002. excerpt online


Did the capacity to be "knocked out" arise because it conferred an evolutionary advantage? From first principles, it seems surprising that a blow to the head would cause unconsciousness rather than just impaired function.

I've heard a lot of analogies to computers -- "Your brain has to reboot." But computers reboot when there is an error because they are explicitly designed to do so, in order to recover and prevent further damage.

So, did we evolve the capacity to get knocked out for similar reasons -- because it helped us recover or prevent further damage? Or is the capacity to get knocked out just an "accident" or an inevitable consequence of the way our brains are designed, without a good evolutionary explanation?

(I realize the answer might be: "we don't know". In that case, I'd wonder what the prevailing opinions are and what if anything we've ruled out).

https://en.wikipedia.org/wiki/Concussion#Mechanism

We did not evolve in order to become knocked out. See the wikipedia link. The "water" in the head is designed to not make us get knocked out that easily. However each dampening system has a limit.


How does the Endoplasmic Reticulum scale with Cell Volume in Epithelial Cells? I am working on a mathematical model of a biological tissue (drosophila pupal notum; an epithelial tissue) where the tissue is built up from cells all described by the same cellular-model. The tissue is generated using a somewhat random process, and so each cell in the tissue has a different size (volume, surface area, etc.)
The model focuses on the movement of particles both between cells as well as between the cytosol of each cell and internal stores (like the Endoplasmic Reticulum (ER)). In order to use the same parameters across the entire tissue, I need to know the ratios of various volumes and surface areas, such as the ratio of the volume of the cell to the volume of the ER, or the ratio of the volume of the cell to the surface area of the ER.
So my question is, if we have a cell of some volume $V_1$, and we look at another cell with volume $V_2$, what can we say about how the volume of the ER of cell $1$, $V_{\text{ER},1}$, or the surface area of the ER of cell $1$, $A_{\text{ER},1}$, compares to the volume and surface area of the ER of cell $2$, $V_{\text{ER},2}$, and $A_{\text{ER},2}$? For example, would we expect $V/V_\text{ER}$ to remain constant across all cells in the tissue? Or maybe we would expect $V/A_\text{ER}$ to be a constant across cells in the tissue? Or maybe both of these ratios follow some other sort of scaling law?

Please consider this "answer" as an enlarged comment. I can't answer your question, but it's possible that my speculations or considerations could be helpful in your particular situation, in the early phase of building a model.
First of all, I doubt that general formulas that link cell-volume to ER-volume of different cell-types can exist. Dependent on the specific cell-type, (dependent of the protein production need in the rough ER), the ER/total ratio can strongly vary (i.e. compare neurons (strongly protruding ER), red-blood cells (no ER), pancreatic cells (large ER), endothelial-cells..). Thus, any correlation may just be chance, without the general meaning that you truly seek.
Therefore, you should focus on such volume-correlations within the same cell-type at different cell-cycle stages.
In this context, I can think of mathematical considerations, that could help your model: When cells divide, they effectively half their membranes (membrane-lipid count). Mathematically, this means that the overall volume of the cell should reduce to around 35%. In contrast, the volume of the ER as a highly condensed structure could scale linear with its surface area, if we see it as a long tube that gets separated. From this, you could build an easy mathematical model, in which ER volumes are relatively bigger, when cells are small.
However, according to cell-size measurements this is not true; cell-volumes get halved [1] when cells divide, which should indicate relative stretching of the membrane. Unfortunately, I could not find any data on how the stretching of the cell-membrane relieves over time. Further, the volume (quite) linearly increases over time until the next division can take place [1].
This means the cell-membrane keeps a constant weight/V before and after cytokinesis, while the surface-area increases by root 2. Given, that the ER-membrane-mass is also halved when the cell divides, and there is no apparent mechanism that should cause swelling, it is still quite difficult to predict how the ER volume would change. Again, the ER is no simple sphere, but has a highly collapsed shape.
However, I found this source, that deals with changes in shape and volume of the ER during the cell-cycle. Apparently, there is a membrane exchange between nucleus and ER and the ratios in volume between ER and nucleus is constant throughout the cell-cycle. You can study this yourself in more detail, but I would take this observation as an indication, that the ER volume behaves as would be inferred from a mathematical standpoint; to the third power of the diameter of the cell.
To sum it up, I initially expected smaller cells seem to have relatively larger ER volumes, and I suspect, that you had a chance to fall for the same trap. However, if the volume-ratios are not constant, they should rather behave the opposite way: ER takes less cell-volume after division, when the cells are small.


Why are Taurine and Arginine essential components of the feline diet? Taurine and arginine play a key role in the feline diet but I am unaware as to where exactly they fit in.

From the Taurine Wikipedia article:

  The absence of taurine causes a cat's retina to slowly degenerate, causing eye problems and (eventually) irreversible blindness – a condition known as central retinal degeneration (CRD), as well as hair loss and tooth decay. Decreased plasma taurine concentration has been demonstrated to be associated with feline dilated cardiomyopathy.

Arginine is an Essential Amino Acid for cats (and many other mammals - including Humans while we're infants). That is, they cannot synthesize it on their own and must obtain it entirely from their diet. A 10lb. (5kg) cat will require about .86g of Arginine - which is abundant in all meats and can be met with a few ounces of food.

I could not find anything particularly special about Arginine as opposed to other EAA's for cats.


Non-descriptive gene nomenclature I formally come from a physics/physical chemistry background, but I have begun to specialize in the area of the biomedical sciences and biomedical engineering. I found myself reading an article which talks about using leukocytes as carriers for targeted cancer drug delivery. One of the frequent adhesion molecules that comes up in the paper is E-selectin, whose wikipedia page I looked up to learn more about the molecule.

On that wikipedia page, it says that E-selectin is encoded by the SELE gene. Now, I can see that the gene is called "SELE" as it abbreviates "Selectin E", but my question is: how did this become the "official" name for the gene? Why doesn't the official name reveal anything about the actual nucleotide sequence of the gene? If someone had never heard of E-selectin before, how is he/she supposed to learn anything about the gene just from the name "SELE" ?

Sorry if this is a very nit-picky question. It's just that most of the substances talked about in chemistry have official names that reveal information about the structure, even if there is a more commonly used "nickname."

Welcome to Biology.SE.

To my knowledge there is no good rule on how to name genes. The first person to name a gene or an allele is free to just pick up a that (s)he finds easy to remember and eventually intuitive. Sometime the author just picks a funny name. Here are a few examples from Drosophila melanogaster data base:

bag of marbles: involved in oogenesis, spermatogenesis.
breathless: involved in development of trachea.
buttonhead: regulates segmentation of the head.
dissatisfaction: involved in many aspects of sexual behavior.
hobo: a mobile genetic element.
Indy: for "I'm not dead yet"; this mutation makes the fly live twice as long.
windbeutel: German for "cream puff".

Did you suggest to name genes based on their sequence? Would be quite painful! One cannot name a gene based on its sequence as the sequence is way too long. The median gene length in humans  is 24,000 base pairs (Fuchs G et al. 2014). You just need to refer to a database to match a sequence to a gene name (see BLAST for example).

How could we improve this system?

Do you have any suggestion on how we should name genes? Should they be named in relation to the phenotype they affect or to the biological pathway that are involved in or maybe something else? The issue is that we often annotate and name a gene before knowing much about its effect.

Note that some genes have several names which is indeed confusing. Would be good to solve this a little bit.


Can cerebrospinal fluid pass through the pia mater or ependymal cells of the ventricles? During a lecture, a professor commented that the cerebrospinal fluid and interstitial fluid of the brain parenchyma have similar composition because they can exchange with one another. This struck me as surprising because I was always under the following impressions:

pia mater is essentially impermeable to fluid (therefore CSF from the subarachnoid space could not penetrate it to be in a passive exchange with the underlying brain tissue)
the ependymal cells of the ventricles (besides the choroid plexus where blood is 'pushed' through) is impermeable to fluid...i.e. CSF cannot leave the ventricles to be in passive exchange with the surrounding brain tissue.

Could someone please confirm if these two impressions are correct, and, further, if they are correct, could someone confirm the accuracy of the professor's claim and by what means it is true?

Both the blood brain barrier and the blood CSF barrier tightly regulate the CNS fluid interstitial fluid environment of the CNS. You, however, are talking about a different barrier, the barrier formed by the pia mater, sometimes called the brain/CSF barrier. This barrier is less well studied. It does appear to prevent transport of particulate matter and red blood cells, but allow the passage of immune cells and small molecules. In addition to your professor's statement that the composition of CSF and brain interstitial fluid is similar, intrathecal injection directly into the CSF in the subarachnoid space provides an effective way to deliver drugs with CNS action, suggesting the pia mater does not effectively restrict small molecules (see Goodman and Gilman's The Pharmacological Basis of Therapeutics Ch 2).


Hayflick's limit and cell division Suppose the Hayflick's limit of a cell is 10 and it divides 10 times.  At this point, it undergoes differentiation.  Is it possible for it to undergo dedifferentiation at this point?

I don't think so naturally. I think the general stream of the progeny goes stem cell => pluripotent cell => progenitor cell => specialised cell.


Mode of inheritance - DYT1 Dystonia Homozygous DYT1 mutation carriers have not been reported in humans.

Does this mean that the mode of inheritance for dystonia (DYT1) is autosomal dominant? This to me implies that if one has both alleles for dystonia, then one must also have the phenotype, as people with both alleles cannot be carriers.

Your description is correct. Most genes do not show complete dominance as outlined in Mendelian genetics and inheritance is almost always more complicated than a simple 1 gene/2 allele system. The mutation you're studying is classified as autosomal dominant but even heterozygotes may not display the phenotype. The proportion of the population that has the mutation AND displays the mutant phenotype is called the penetrance and, for DYT1, has been estimated at around 30%.

http://www.omim.org/entry/128100?search=Dyt1&highlight=dyt1


Does a cell suspend or exit cell cycle at G0? In an exam, there was one question which asked whether the cell exits or suspends cell cycle at G0 phase.

I answered that it exits cell cycle but the official answer key says it suspends cell cycle.

I marked exit because a cell in G0  undergoes differentiation and maturation. Is there a difference between the two terms?

It is actually suspend and yes the words do differ. This is because the cells that enter the G0 stage is not actually exiting the cell cycle because when situation demands it will divide. It is metabolically active and therefore the word suspend suits better


Do eye muscles relax when you close your eyes? I wonder whether the eyes muscle relax when you close them. Common knowledge told us the eyes muscle get tense when you stare at nearby object. If you close your eyes, you eye lids have 0 distance with you eyes. Would the eyes muscle relax in this case?

I would guess that the eye muscle relaxes when the eye is closed. After having the eyes closed, just in the moment after opening them, it seems that the focus is in the distance. It takes a fraction of a second before you can read some text on your computer screen for example . This focusing-duration seems to be shorter when looking into the distance after opening the eyes.

Another effect is when you look at an object in short range for quite a moment and then close your eyes. You can feel the relaxation.


Mystery rodent in Winnipeg I spotted this rodent in Winnipeg, Manitoba, Canada on September 6, 2020.
It is about 10 inches long.

What is it?

That is a Franklin's Ground Squirrel

Winnipeg is part of its range:

Have a look at a gallery of such photos here: https://inaturalist.ca/taxa/179937-Poliocitellus-franklinii/browse_photos


Does the Valsalva maneuver require a completely closed airway? How do the effects compare to exhalation against partial resistance? The Valsalva maneuver is defined as "attempted exhalation against a closed airway", "The effort to breathe out forcibly while the mouth and nose are firmly closed or the vocal cords pressed together", or, colloquially, straining as if you were trying to poop. It can "pop" the eustachian tubes open, stimulate the vagus nerve, and briefly spike blood pressure, occasionally leading to people dying from a burst aneurysm on the toilet.

Some breathing practices involve pushing air out against resistance, such as ujjayi breath in yoga. This can be done by partly closing the glottis while exhaling, or by firmly exhaling through the mouth with lips slightly open, as if one were whistling. It can also happen while forcefully exhaling through a congested nose.

This seems like it should raise eustachian and thoracic pressure in the same way as the "full" Valsalva maneuver, though to a lesser extent. Are the effects of these other breathing practices similar to the Valsalva maneuver, or are there any unique effects of the Valsalva maneuver that only occur with a fully closed airway?

As a second question, would you expect any unique effects exhaling against resistance? It seems different in that the practitioner is still breathing, and that they can continue the practice indefinitely, as opposed to a breath-holding Valsalva.

The eustachian tubes exit into the nasal cavity superior to the glottis.  Thus restricting the glottis while exhaling cannot increase pressure in the nasal cavity / eustachians.  Only by closing the nostrils can that be achieved, and only while exhaling.  Even a technique like circular breathing cannot maintain pressure in the nasal cavity since that's necessarily the entry point for every new breath, be it mouth or nose.


What is the impact of prolonged electromagnetic exposure on human health? What are the health effects of being exposed to a very strong electromagnetic field caused by  two resonating superconductive coils (not static magnets) for a period of years?

Actually the applications of magnetism to organic systems is new to Science.  Duke Univ in NC is currently experimenting with humans sticking their heads into large electromagnetic coils while electrodes are attached to the outside of the skull. A small amount of research has been done with magnetism and plant physiology (my interest), but in the main very little published research is available on the topic.  I might direct you to use Scholar.Google to find more technical articles rather than just using Google itself.


What is the biological principle of this "holotropic breathwork" technique? Holotropic breathwork is a non-drug technique developed by Stanislav Grof used in psychotherapy. The therapy as a whole is usually called holotropic breathwork (at least by Grof himself) and will most probably rely on a range of effects. However, I am mainly concerned about the core technique, which leads to hallucination and a changed state of conciousness (i.e. being half concious and having a distorted perception of time).

As quick googling does not reveal any specific information of the technique, I will describe a demonstration of an amateur enactment of something which was stated to be based on the same principle as holotropic breathwork. (I consider the respective people very irresponsible to have done this without trained assistance, it is probably very dangerous, do NOT try at home!)

A person squats curled near a wall and breaths as quickly and as heavily as possible for a few minutes. After that they quickly stand up in front of the wall and another person pushes them quickly in the chest and presses them strongly against the wall behind them. The pushed person collapses completely, their muscles relaxed, they even don't have the time to close eyes and you can see their eyeballs rolling around freely. They are in this state for about 15 seconds and then wake up reporting vivid hallucinations. Some of the people said that their perception e.g. of sources of light and surfaces were altered for another several hours.

So, what is the biological basis of this collapse and hallucinations? (It would be perhaps good to also comment on the possible risks.)

I think this is mostly caused by hyperventilation. The excessive breathing disturbs the balance between CO$_{2}$ and oxygen in our lungs. This will cause respiratory alkalosis (the blood pH, which is normally strictly regulated, gets higher), which can cause dizziness, headaches and fainting.

The shift in pH can also disturb the eclectrolyte balance, especially the concentration of the free dissolved calcium, as it binds to negatively charged plasma proteins (which release protons into the blood due to the higher pH). This can lead to craps and spasms.
I would be very careful not playing around here, as this can have some severe consequences.


How we can localize sound vertically (up-down) and front-to-back? It is quite simple to understand the concept of lateral localization of sound. It depends upon the loudness and time (and wave phase) difference between 2 ears.

But how can we detect front-back localization (if someone is calling me from my front/back direction) and up-down localization (such as an aeroplane's sound is coming from upper place and a car's whistle is coming from lower-direction of the balcony I'm standing). How does that happen? Or doesn't localization happen at all under these conditions? Is it just an illusion just because we are already aware about the possible source (such as since it is aeroplane's sound then it might coming from upward place, or I can see my friend is talking by standing my front so the sound must coming from front... etc.)

I've searched wikipedia and other sites, but I found nothing that explained the matter sufficiently.

The Wikipedia article is quite good.

In brief, as you state, the wave phase can be used only to localise sounds in the plane of the ears. To have an approximation of the position in the median plane (above-below/front-back), we use asymmetries that distort the sound differently at different frequencies.

In humans, it seems that these asymmetries and their processing are not genetically programmed but evolved by each listener.

This is different in owls, although different species have each a specific asymmetry. https://en.wikipedia.org/wiki/Sound_localization_in_owls


How hard is it to build a promotor in a DNA that initiates DNA transcription when specific hormones are around I have an idea that you could find out which substances are within a sample in vitro that you are investigating by creating DNA that has a bunch of different promotors for different substances you are interested in.

After inserting those DNA strains you could do nucleotide sequencing and as nucleotide sequencing allows you to to read a lot of data you could read the sequencing behind the promotors.

How complicated would it be to build DNA with promotors for dozens of medically relevant substances?

Promoters bind transcription factors (TFs) and RNA polymerase (or a related complex, in the case of eukaryotes).

The substances you are interested in testing would need to bind to DNA in the same way as TFs and RNA polymerase, in order to trigger RNA synthesis (which you might measure with RNA-seq experiments). That would seem to severely limit what you can test the presence of.

In any case, if you could make that happen for your substances of interest, you would probably also want to make sure to avoid degradation effects of short-length RNA, by removing associated proteins.

https://en.m.wikipedia.org/wiki/Promoter_(genetics)

https://en.m.wikipedia.org/wiki/RNA-Seq

https://en.m.wikipedia.org/wiki/Small_RNA


What percent of your blood can you lose before you need a transfusion Losing a little blood is okay. If your a normal healthy person, and got into an accident, how do they know if you need a transfusion or if you'll be okay? This is hypothetical.

Typically transfusions are indicated for hemoglobin < 7 g/dL (for adults normally: 12-15 grams per deciliter [1]) or < 8-10 g/dL if there is cardiac disease where diminished oxygen carrying capacity cannot be compensated by increased cardiac output.

The answer above is theoretical because there is no accurate way to measure blood loss in the clinical setting - it's usually a mess.

The most useful parameter to assess intravascular volume in the immediate term is blood pressure. Again, the actual number is variable but a 30% drop from baseline in the acute setting is bad.

Another less acute indicator of hypovolemia is urine output (normal is .5-1 ml/kg body weight/hr, dropping below ~35 ml/hr therefore is an indicator of hypovolemia.)[2] Hypovolemia is often corrected with sterile saline fluid and adding packed red blood cells only as needed to keep hemoglobin in the above required range, unless someone is actively bleeding (trauma, bleeding ulcer, etc.) in which case "whole blood" (or packed red blood cells, fresh-frozen plasma and platelets) is given.[3]

[1] McPherson: Henry's Clinical Diagnosis and Management by Laboratory Methods, 22nd ed.
[2] Oliguria &  Volume Depletion
[3] Fluid Resuscitation and Volume Assessment


Why does vacuum sealing of foods prevent spoilage from anaerobic bacteria? I have noted that many purchased food items in containers only require refrigeration after they have been opened, thus eliminating the vacuum seal.  Air contains bacteria and fungus spores that enter the food container and if not refrigerated, the aerobic micro-organisms will proliferate, thus altering and rotting the food.  The air also allows any dormant micro-organisms that survived the factory sterilization process already in the food to come back to life and proliferate.
However I do not understand why anaerobic bacteria, that don't require and cannot survive in air, do not proliferate and thrive in the vacuum sealed food containers.  That plus the fact that we can leave already opened food items such as honey, jams, and peanut butter out of the refrigerator for weeks but they do not spoil.

I do not understand why anaerobic bacteria, that don't require and cannot survive in air, do not proliferate and thrive in the vacuum sealed food containers

They do. Vacuum sealing can prevent aerobic bacterial growth but does not prevent anaerobic growth.
Botulism is a particularly dangerous consequence. If food containing C. botulinum spores is sealed without being properly treated (usually by heating) or otherwise by being inhospitable to bacterial growth (often due to acidity or salt), dangerous botulinum toxin can accumulate and be dangerous or fatal when the food is later eaten.


Can I safely handle this caterpillar? I just found this caterpillar in my garden. I’m about to mow the grass for the first time. Can I safely handle it? What type of caterpillar is it?
For reference, I’m in Leeds, UK. Here are some pictures:

It’s about 5cm long and 1cm wide. Thanks

After a bit of Googling I think I found it. It’s a pale tussock moth caterpillar. https://butterfly-conservation.org/moths/pale-tussock
It says it irritates the skin and can cause a nasty rash so I’m staying away for now.
I might risk moving it with a trowel and small tub though.


Why does temperature shock kill fish? As is advised with most fish you should avoid sudden changes in water temperature (for example by introducing new water that hasn't been left to come to room temperature). I have, however, never understood why that is the case, in particular given that most fish are cold blooded so there is no issue with needing to "ramp up" the metabolism when in cold water.

Say a particular species of fish can survive in water between 20°C and 30°C what causes a fish that was previously in 30°C water to die when suddenly plunged into 20°C water? I understand this effect is called "shock" but I'm looking for the biological reason for it.

To be clear I'm not looking for "chemical x is released and that leads to the fish dying,  I'm looking for why these chemicals are released at all. So to give an example if my question had of been "why does adrenaline shock kill" I'd be looking for "adrenaline release is usually a good thing, it's released in response to a fright and prepares the body for a fight or flight response. However this heightend preparedness can cause additional strain on the body which can cause death in some cases"

This due to a phenomenon called "cold shock". This induces a number of physiological changes in the fishs metabolism and also in its behaviour and can lead to death.

The first paper cites some reasons in table 1:

Brain and central nervous system response: Changes in neuronal
activity
Catecholamine and corticosteroid response: Release of hormones due to
the shock.
Haematological and metabolic response: Changes in red and white blood
cells and lactic acid in the blood.
Protein expression and molecular responses: Changes in the expression
of proteins of the heat shock family.

These changes (especially in brain and nerves and also the hormones) can deregulate the fishs metabolism so much that it can die. Shock is a critical condition. Obviously a lot of research is going on, but I recommend reading the two articles below for further details.

References:

Cold shock and fish
Physiological stress responses in the warm-water fish matrinxã
(Brycon amazonicus ) subjected to a sudden cold shock


Why was cotton chosen to grow on the moon? The choice of plants for the first lunar ecosystem is a bit unusual.

They are growing cotton, rapeseed and potatoes.

Why did the Chinese scientists choose them? Is it because of their ability to thrive in such an environment or because of their possible  contribution to sustaining life in long space missions?

China's state-run Xinhua News Agency mentions the reasoning for most of the species they sent:

Why were these species chosen?
Xie [the chief designer of the experiment] said potatoes could be a major source of food for future space travelers. The growth period of Arabidopsis, a small flowering plant related to cabbage and mustard, is short and easy to observe. Yeast could play a role in regulating carbon dioxide and oxygen in the mini biosphere, and the fruit fly would be a consumer of the photosynthesis process.

While this doesn’t mention cotton, it seems very likely to me that, like potatoes, it’s just a very useful crop.
According to another article, the goal for China is a moon research base:

“We’ll use the Chang’e-8 to test certain technologies & do some preliminary exploration for jointly building a research base on the moon,” Wu said.


What is the mass of a single erythrocyte? I really have been searching through internet on different languages, but can’t find any article that answers on the question what is the single erythrocyte mass. I don’t know, I think it’s pretty easy to calculate experimentally, but I didn’t find anything.

Has anyone measured single erythrocyte mass, and if yes, what is the value?

My try

Experimentally

I am not biologist or medical student. What do I know: blood consists of liquid part(water, salt) and solid part(red blood cells, white blood cells and thrombocytes). If It is possible, the white cells and thrombocytes can be moved off the blood in some test tube, so that will left only erythrocytes. Then, there should be medical statistical value like erythrocyte density or number of erythrocytes per liter.

We have some blood with only erythrocytes, we know how many erythrocyte are there. We can measure that blood weight, substrate the liquid weight(somehow), divide by erythrocyte number and will get the mass of a single erythrocyte.

Theoretically

About 90% of erythrocyte mass is hemoglobin. Hemoglobin is a molecule. Molecule is a countable thing, so, perhaps there is information about how many hemoglobin molecules, in average, is in one erythrocyte.

According to Angelo D’Alessandro, Monika Dzieciatkowska, Travis Nemkov, and Kirk C. Hansen article Red blood cell proteomics update: is there more to discover? it is about 270 millions per red blood cell. Molecular mass of hemoglobin is about $64 kDa$, absolute mass equals $1.106*10^{-22} kg$.

If my assumptions are correct, then 90% of erythrocyte mass is about
$$2.97*10^{-14} kg$$

It’s not my kind of biology, and I tend to make mistakes in arithmetic, I’ll have a go…

I found a paper by Leblond and Shoucri published in the Journal of Microscopy (1978) 113, 161-170, entitled Calculation of surface area and volume of human erythrocytes from scanning electron micrographs. You need institutional access to read it, but for the human erythrocyte shown below they calculated:

Volume = 85.5 μm3

They found a range of sizes (65 μm3 in another image) so I shall take an average value of 75 μm3.

75 μm3 =  75 × 10–18 m3

Assuming a density of 1.1 g/cm3 for erythrocytes, i.e. 1.1 × 106 g/m3

Mass of an erythrocyte = 83 × 10–12 g (0.08 ng)

This is the same order of magnitude as that calculated later by the poster.

(Apologies for initially quoting the volume in pm3. No idea how I did that — it’s clearly μm3.)


Lack of yolk in mammalian oocytes as compared to other vertebrates? Why do mammalian oocytes have little to no yolk? How does it compare to other vertebrates such as frogs, fish, and birds?

In oviparous animals (those that lay eggs which hatch outside the body), the eggs need to be provided nutrition for embryonic growth, which is the main function of yolk.

In placental mammals, the embryo is provided nutrition directly from the mother via the placenta.

Therefore, most mammalian oocytes do not need to develop large quantities of yolk to support the embryo in the way the eggs of most birds, reptiles, amphibians and fish do.


What makes a cancer contagious? Most human cancers are not (very?) contagious (perhaps besides a couple of incidents). But the Tasmanian devil seems to have a form of cancer which is contagious. Now what makes the difference between a contagious cancer and a non contagious cancer in the DNA mutations of a cell?

There are two relatively common contagious cancers: Tasmanian Devil Facial Tumor, and Canine Transmissible Venereal Tumor.  Both are truly contagious cancers, in that the cancer cells themselves are transmitted from one host to the next, and expand and cause disease in each successive host.  (There was also a contagious cancer of hamsters, which has long since gone extinct, and there are some transmissible tumors in clams and oysters; the latter don't have immune systems that are remotely similar to dogs, Devils, or humans.)

It's believed that one key aspect of the Devil Facial Tumor is that Tasmanian Devils are immunologically closely related.  Normally, cancer cells from one host would be a tissue graft in a different individual and would be rapidly rejected as with any allograft.  However, immunologically closely related individuals can tolerate each others' grafts, and it's believed that this is part of what allows the Devil tumor to spread -- a lack of genetic diversity among Tasmanian Devils.

  Major histocompatibility complex class I and class II genes have extremely low levels of sequence divergence in the devil population from the Tasmanian east coast (Siddle et al., 2007a, 2007b). ... The lack of diversity at MHC loci, coupled with weak responses of east coast devils to allogeneic mixed lymphocyte culture, has led to the suggestion that this population may be functionally identical at MHC loci, thus permitting the spread of DFTD as an allograft.

--Clonally transmissible cancers in dogs and Tasmanian devils

The genetic diversity explanation is widely accepted, but it hasn't been formally proven and there are a number of points that suggest that it isn't the whole story.  There are several other molecular features of the tumor that probably make it less immunogenic (see the review The role of MHC genes in contagious cancer: the story of Tasmanian devils) and the full story probably involves a combination of these things.

CTVT is different.  It's astonishingly ancient (it apparently arose in a dog, or a wolf, 11,000 years ago and has been passed from dog to dog continuously since), so it's obviously very successful at what it does, but it's not at all understood how it does it. Dogs are genetically pretty diverse and definitely don't tolerate arbitrary grafts from each other, so that's not the explanation. Lots of other possible explanations have been put forward, most of which point to various immunological features of the tumor; however, while that's clearly an important point, none of the things people have implicated are unique to CTVT -- tumors invariably have immune suppressive abilities and don't have the same ability to spread. (Going back to the Devil tumors, the low expression of MHC molecules on the cancer cells is probably a factor there too, but it's important to understand that low MHC expression is almost universal among tumors, including the vast, vast majority that can't transmit.)

Summary:

There do exist a very small number of truly contagious cancers.
The reasons for their transmissibility are not fully understood.
Genetic diversity and immune evasion are probably two of the causes.


What are the consequences of inbreeding? Inbreeding increases the risk of getting two identical recessive genes, alleles, that cause a disease which wouldn't have been activated with mixed genes. That's how I understand it anyway. But I sometimes read and hear that inbreeding among humans also causes decreased intelligence, especially emotional and social intelligence. Is there any support for such claims, and if so how does that work?

You are right. Inbreeding strongly increases overall homozygosity which subjects inbred individuals to diseases caused by rare recessive alleles. In non-inbred individuals the chance is quite low to receive those because many deleterious variants (and in fact, most segregating alleles we can observe) are recessive. Most often, but depending on the dominance coefficient, these 'hide' in healthy heterozygous carriers and when very closely related individuals breed (with a lot of variants that are identical by descent) there is a high chance that some of the 'hidden' deleterious variants are passed to the offspring.

You have to be aware that there are in fact two conceptually different processes that can be both be referred to as inbreeding but are also somewhat continuously linked (see below):

Mating systems that allow offspring between actually related individuals (measured by the degree of relatedness), what in humans often is referred to as incest or consanguinity.
Populations with very low effective population size $N_e$ generally exhibit higher relatedness due to lack of genetic diversity (excess of homozygous sites). Therefore, populations with low $N_e$ are referred to as inbred even if no actually related individuals are mating.

There is some evidence that inbreeding in the first sense is linked to cognitive abilities in humans:

Bashi (1977) investigated the effect of offspring having first-cousin (i.e. between children of siblings) and double first-cousin (i.e. between children of siblings and unrelated siblings, sharing as much variants as half-siblings but with more recombination events) parents while (at least somewhat) correcting for socioeconomic effects. He found an inbreeding depression with respect to cognition that could

  result either from the general increase in homozygosity [...] or from decrease in performance resulting from homozygosity for specific recessive alleles (highlighted by me). The higher variance of the double cousin group in some of the tests favours the second interpretation.

Woodley (2012) presents evidence for slightly lower IQs caused by inbreeding, however, he also mentions that the effect is way smaller than socioeconomic effects:

  Consanguinity could subtly influence IQ at larger scales as a result of small IQ handicaps bought about through inbreeding being amplified into much larger differences through their effect on factors that maximize IQ such as access to education and adequate nutrition.

Fareed and Afzal (2014) investigated verbal IQ, performance IQ, and full-scale IQ and found that all of these IQ parameters are significantly lower in inbred children compared to non-inbred children - actually the difference increases significantly with the degree of relatedness. They conclude that there is

  evidence for inbreeding depression on cognitive abilities among children.

Please keep in mind that, for for sociological/ethical reasons, this is highly controversial, especially when the two concepts above are intermixed - human populations underwent differential and variably strong periods of low $N_e$, i.e. were subject to stronger or weaker inbreeding in the second sense. When reading the citation of Bashi (1977) above carefully, you will notice that he takes good care not to intermix those. Inbreeding in the first sense leaves large runs of homozygosity (ROH, blocks without heterozygous sites, i.e. a clustered and local lack of variation) whereas inbreeding in the second sense increases homozygosity in the genome less selectively. Therefore, the distribution of homozygous sites can be used to infer whether inbreeding is recent (first sense) or old (second sense) (see for example McQuillan et al. (2008) - here you see that both concepts form a continuum: where do you set the cutoff between recent and old? what is an appropriate threshold size for ROH? ...). Regardless, Bashi's findings indicate that effects of inbreeding are caused by recent inbreeding as he presents evidence that his results are rather driven by specific deleterious recessive variants than overall excess homozygosity. Finally, even though the study by Fareed and Afzal (2014) shows rather large effects of recent inbreeding in IQ measures, the results from Woodley (2012) show that one needs to be really careful to separate genetic from environmental components as his study suggests that the latter contribute more to the observed decrease in IQ.


Help identify this Caribbean plant Could you please help me identify this plant. I think it grew from some seeds we brought from Cuba (I might be mistaken though).

The plant in the picture is about 1.5 years old; it stands about 50 cm/20 in. tall. The leaf shown seems pretty large compared to the plant height, it's about 20 cm/8 in. long.

Leafs though appear shiny are rough to the touch on both sides, like very fine sandpaper.

Finally I think I can answer my own question. Having spent the summer outside in full sun, the tree has produced flowers that helped us identify it.

It appears to be Cordia sebestena


Confusion over equations for population's heterozygosity vs. heterozygous individuals On page 24 of Gillespie's Population Genetics, 2nd ed, an equation for $H$, the probability that two randomly drawn alleles are different by state, is given.

$H$ is stated to be similar to the heterozygosity of the population, which I guess is expected to be $2pq$, where $p$ and $q$ are frequencies for different alleles. $ H′=(1−1/2N)×H$

On page 23, $H_t$, the probability that an individual chosen at random from the population after $t$ generations of random mating is heterozygous, is given :
$$H_t = H_0 \times (1-\frac{1}{2N})^t$$

For a current time $t$, are $H$ and $H_t$ measurements of the same thing, or are they different ?

I interpreted them as being the same, because drawing two alleles at random is similar to drawing a diploid individual at random.

One is a recurrence equation and the other is a general solution. These are basic concepts of mathematical modelling.

Reccurence equation

A recurrent equation describes the state of a system (here, heterozygosity $H$) at the next time step given the state in the previous time step. The recurrence relation is $H' = (1-1/2N)\times H$. Given the state $H$, at a given generation, one can know the state $H'$ at the following generation (given the population size $N$).

General solution

A general solution describes the state of a system at any time step given an initial state. Not all recurrence relation have a general solution. Here there is a general solution and it is $H_t = H_0 \times (1-\frac{1}{2N})^t$. Given the initial state $H_0$, one can know the state $H_t$ after $t$ generations (given the population size $N$).

Two equations for the same model

The two equations both refer to the same model and therefore the same statistic of expected heterozygosity which, as you said, is $H = 2 p (1-p)$ (for a bi-allelic locus) by definition.

Understanding the basics of mathematical modeling in ecology and evolution

Have a look at A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by S. Otto for an introduction into mathematical modeling in the field of interest.


Evolutionary origin and exogenous cues of ~28 day infradian rhythm? The most obvious example of an approximately monthly biological cycle is the human menstrual cycle. My questions are the following:

Is it known when and where this cycle or one like it arose?
What exogenous cue(s) (if any) is/are this cycle based on? The moon's
orbit around the earth is seemingly obvious however the only cue that
I can think of that would be easily sensed by organisms is variance
in night-time illumination, which seems like a very weak phenomenon
when compared to day/night and seasonal cycles. King and neap tides may be a suitable cue however they have a half-monthly modulation.
The moon has been steadily retreating from the earth over the course
of its history, which means that months have been slowly getting
longer. Is there any fossil (e.g. biogeochemical) evidence of
organisms with biological cycles in synchrony with a 'short month'?

A double-blind, prospective study during the fall of 1979 investigated
  the association between the menstrual cycles of 305 Brooklyn College
  undergraduates and their associates and the lunar cycles.

  .... Approximately 1/3 of the subjects had lunar period cycles, i.e.
  a mean cycle length of 29.5 ± 1 day. Almost 2/3 of the subjects
  started their October cycle in the light 1/2 of the lunar cycle,
  significantly more than would be expected by random distribution. The
  author concludes that there is a lunar influence on ovulation.

(Menstrual and Lunar Cycles, Friedmann E., American Journal of Obstetrics and Gynecology, 1981)

Another source supports this conclusion, finding that "a large proportion of menstruations occurred around the new moon."

Somewhat related, this study found that light exposure shortened menstruation cycles.

In summary, there seems to be a good amount of data suggesting that lunar cycles do in fact calibrate the length of human menstrual cycles to some degree.


What species is this aromatic plant found in a mountainous region of Greece? This plant was found in the Taygetos mountains, Greece, and had a lemony smell.

Small plant about a foot high.

The shiny recurved leaves are reminiscent of rosemary, and the dry seed-heads seem rather distinctive.

Any ideas of Genus or species most welcome!

A type of greek lavender with no blossoms anymore?
https://www.florealpes.com/photos/lavandulastoechias_5.jpg?PHPSESSID=0a72039f5036d91c7df80dd406b795b0


How much of my ancestry will match with my brother? Recently, my brother (full sibling) got his ancestry checked from MyHeritageDNA. They have a similar service like 23 and me and I've found out that both companies are offering the basic service almost the same, with some add-ons which are different.

My question is that if I (I'm a male) send my DNA sample to either organization, how different should I expect the results to be?

As both you and your full sibling are males, it means that you share the exact same Y chromosome. You also share the same mtDNA as you have the same mother. All the rest is just a bit of segregation and recombination that will lead to minor differences but generally speaking, your ancestry data should be very similar. Specific disease related data might vary though.


Effect of single-gene overexpression in the cell's response Which are the factors that modify the overall gene differential expression by introducing a vector for single-gene overexpression?

If you overexpress a gene for a protein involved in signal transduction (e.g., a kinase, scaffold, or receptor) by vector cell transfection, then you overdrive the cell using this signaling pathway, it's useful to isolate the pathway and study them.

Is there any way to modify the overall gene expression or cell differential expression pattern by gene transfection? I think this would work if you delivered a gene for overexpression in proteins involved for RNA processing (e.g., splicing, ribosomal proteins, etc.), RNA transcription (e.g., TFs) or protein translation.

Which are the factors that modify the overall gene differential
  expression by introducing a vector for single-gene overexpression

This is a very relevant question and the field of experimental biology needs to revisit the experimental strategies.

One of the explanations that you gave is correct- that the overexpressed protein might override the cellular processes.

Another problem that this practice gives rise to is incorrect inference. We are mostly interested in knowing what a protein does in a cell at general physiological conditions. If the stoichiometry is altered wrong results will definitely pop up.
For example in the case of a repressor/activator with multiple targets: At its general physiological concentration it may not really activate gene-X because of low affinity but in high concentrations it just may, and we end up concluding that gene-x is a target of repressor-1 by an OVEREXPRESSION experiment.

A synthetic biological approach is very good in studying small signaling/transcriptional modules. The entire module can be cloned and expressed in a cell under an inducible/constitutive promoter. This can be implemented in a heterologous cell also. A mathematical model generally helps in making certain predictions.

Other strategies which can be used instead of overexpression:

using sensor constructs harboring a functional or non-functional
target sites instead of overexpressing the upstream protein
downregulation experiments


What fraction of human cells gets infected during a viral infection? As I understand, if a cell gets infected during a viral infection then it eventually dies. If an individual does not die of an infection, the percentage of cells that gets infected in the course of the infection must be quite low.

Are there any estimates available on how many cells get infected during a viral infection? (say, an influenza infection)?

(A very similar question was asked five years ago but unfortunately received no answers.)

After trying to answer this for a while, I've reached the conclusion that the information needed to answer it satisfactorily doesn't exist. I'll go ahead and summarize my findings here for you though, hopefully it's informative.

Different viruses infect different cells, and different people's immune systems are more or less successful at limiting infection, so the number of cells that get infected also varies a lot. A useful way to narrow your question might be "What is the maximum fraction of virally infected cells that can be survived?". All infections will vary between this maximum and 0%, with milder disease being associated with lower % cells infected.

I looked at Ebola as a candidate because it can infect a wide variety of cell types and a lot of research has been published on it.

From J Virol. 2004 Apr; 78(8): 4330–4341.:

  Notably, 20 (91%) of 22 nonsurvivors had viral loads that reached ≥10^8 RNA copies/ml within the first 8 days after the onset of symptoms, thus suggesting that 10^8 RNA copies/ml can be considered an approximate threshold that predicts a fatal outcome with a positive predictive capability of >90%.

So, for about 3 L of blood serum in a person, that's 3 * 10^11 copies of the viral genome in the blood as a threshold for survival. I couldn't find useful information about viral load in organs and other tissue, but since blood has been claimed to have much higher concentration of virus than saliva or other fluids, we can assume this number is a significant portion of the total load. I'll assume about a third, so we get 10 ^ 12 genome copies. Some or even most of these RNA genomes might not be incorporated into viral particles but counting actual viral particles is very difficult, so no-one has published a correlation between Q-RT-PCR results and infectious particle counts as far as I could find.

Next, we need to estimate the number of progeny viruses that each infected cell produces. In Clin Diagn Lab Immunol. 2002 Jan; 9(1): 19–27. , researchers got about 2 * 10^4 PFU from wells containing 2-4 * 10^6 alveolar macrophage cells each. In these wells, 50-60% of the cells had detached from the walls, compared to 0 in non-infected wells. This implies that, for macrophages at least, about 100 infected cells make enough virus to create one plaque in the assay they used. In J Virol. 2015 Jul 1; 89(13): 6773–6781. about 1000 particles per PFU are reported for the 12th passage of virus in their Vero cell assay system, so 10 virus particles per infected cell. We estimated 10^12 virus particles earlier, so that implies about 10^11 cells were infected. That's a similar number as estimated for HIV in the comments of that question you linked. At about 3 * 10^13 human cells in the body, that's about 0.3 % of all cells.

Each of the studies I've linked here is quite different from the other, so plugging results from one into the other is introducing a lot of error, but hopefully the process was informative.


Has the gestation (pregnancy) period for humans always been 9 months? At this point in our evolutionary progress, the expected human gestation period is (roughly) nine months long. My question is, has this duration of time always been the same for homo sapiens? Or, are pregnancies getting longer/shorter?

My attempts so far: upon searching online, I was only able to find a single reddit thread, of which didn't provide much of anything. And then, on Wiki's page for gestation it provides a link that should contain content on the "evolution of gestation related features for mammals", however, the link revealed itself to just be a page that outlines all mammalian evolutionary developments, and I'm not able to find the forementioned gestation specific information within it.

human gestation period

According to the link gestation period doesn't vary much between great apes.

I don't see any signs that human are becoming "more complex". In fact human babies are uniquely underdeveloped compared with other mammals (large brain size, upright posture)


Books for biology,popular but rigorous? There are very goods in physics and mathematics (like Feynman lectures for exemple) that give an elementry but but broad view of their,therefore I'd like for help to find help to find a biology book that:
-Covers a variety of subject in an elementary fashion.
-Is written for the non-specialist.

Where I studied, every undergrad read Campbell Biology. You can start it as a non-specialist but you will not be one at the end..


The protostome/deuterostome distinction and why it is important As I unerstand it, at some point an embryo develops a hole; this hole continues to punch through, and eventually makes an opening at the other side of the embryo. If the original hole becomes the mouth, then the organism is called a protostome. If the second opening becomes a mouth, then the animal is called a deuterotome.

My first question is, is this distinction made only for organisms who have two openings? In other words, would an organism with only one orifice be called a protostome, or would it be neither?

Why is the protostome/deuterostome distinction important? Why does it matter whether embryo develops a mouth from the first or second orifice?

The terminology is really just describing the process in embryonic development that you describe: deuterostome means "second mouth"; protostome means "first mouth."

The significance of these groups is in evolutionary history and cladistics. All of the deuterostomes have a shared common ancestor that is not shared with any protostomes, and vice versa. Regardless of developmental pattern or number of openings during development, no other organism should be given these names (and if it is, and the correct ancestry is determined later, they would be moved out of those categories accordingly).

This is actually really important in biological classification of organisms, and before modern genetic techniques these types of shared characteristics were the best way to determine shared ancestry. Think a bit about what it means for an organism with two openings to differentiate one as mouth and the other as anus: once they are strongly differentiated, there is a huge barrier towards going "backward" and "switching" openings because mouth and anus have very different functions. However, if you go from having one or no openings to having two, before there is specialization, the distinction of which one develops first isn't likely to be that advantageous one way or the other.

Nephrozoa contains the deuterostomes and protostomes, consisting of almost all extant animals. However there are also other animals that are neither. For example, Xenacoelomorpha might be the closest thing to a bilateral animal with only one orifice, though they don't really have a true gut at all.


How do SDS-PAGE gels differ in a Bis-Tris system vs. a Tris-Glycine system? Protein migrate differently in Bis-Tris and Tris-Glycine gels. I was curious about the actual reasons why. Do certain gel systems result in a tighter resolution than others?

SDS PAGE system rely on the fact that protein is denatured and surrounded by the SDS negatively charged detergent micelle.  This eliminates most of the charge and idiosyncratic solubility differences from one protein to another and gives a reasonable separation based only on size of the protein which is related to the size of the SDS micelle around each molecule.

Bis-Tris and Tris-glycine buffers have quite different charge shielding characteristics.  Bis (also known as 2-[Bis(2-hydroxyethyl)amino]-2-(hydroxymethyl)-1,3-propanediol) has a tertiary amine with a pKa of 6.46 and a pKb of 7.54.  glycine is a zwitterion at any pH between 2.3 and 9.6.  This creates a difference in the way that the buffer shields the SDS PAGE micelles from the rest of the electrical field, slowing down (probably glycine slows things down a bit) the time to resolution, but also giving the micelles more time to migrate.

So for SDS PAGE systems, the resolution of the gel has at least as much to do with the size of the gel pores (based on the acrylamide and bis-acrylamide percentages), the amount of protein you are putting into a given volume of loading well, and the size differences of the bands you are tying to separate. (you need to get pretty lucky to separate a 100.54 kda band from a 100.85 kDa band, but 1.5 to 1.8 kDa is easier 10 to 14 kDa is even easier). Also consider adjusting the current or voltage of the power supply.  The buffer system is only one consideration in planning your experiment and often not the primary factor of quality.


What does 'per capita births and deaths' mean? My book says,

  If in a pond there are 20 lotus plants last year and through reproduction 8 new plants are added, taking the current population to 28, we calculate the birth rate as 8/20 = 0.4 offspring per lotus per year.

..

  If 4 individuals in a laboratory population of 40 fruitflies died during a specified time interval, say a week, the death rate in the population during that period is 4/40 = 0.1 individuals per fruitfly per week.

What does per lotus per year, and, per fruitfly per week imply?

I will use an ever so slightly more specific scenario than what your book offers.

At the beginning of 2017, there were twenty lotus plants in a pond. By the first day of 2018, eight of those twenty lotus plants reproduced. Using this information, we now want to describe the birth rate of lotus plant population.

To do this, we need the number of plants that produced offspring, and, the population size at the beginning of 2017.

$$\frac{no. \ of \ parent \ lotus \ plants}{initial \ population \ size} = \frac{8}{20} = .4$$

This means that, when considering the twenty lotus plants that first existed at the beginning of 2017, each of those twenty plants contributed an average of 4/10s of a lotus plant offspring for that year.

To generalize this, we say, "a birth rate of .4 offspring per lotus plant per year."

The same method and persective can also be applied to the fruitflies, however, they're considering death rate.


Are oxygen and carbon dioxide simultaneously present in red blood cells during gas exchange? From my understanding, the process that displaces the carbon dioxide and oxygen in our erythrocytes and lungs is diffusion. I've been taught that diffusion is the net movement of particles from a region of higher concentration to a region of lower concentration, until an equillibrium is reached.

For there to be an equillibrium in carbon dioxide and oxygen, doesn't that mean that there should be equal portions of those elements present at all times? So therefore, erythrocytes should contain both of those chemicals simultaneously. Am I correct in assuming this? If I am, then I have a follow-up question: wouldn't carbon dioxide floating about in our blood indefinitely cause some unhealthy side effects, and is there something that prevents it from doing so?

I'm currently only in GCSEs, so apologies if this question might actually have a very simple answer.

Thanks

For diffusion to occur there must be a "concentration gradient", that is one area where the substance that is diffusing from, to where it is diffusing to. Where the substance is diffusing from, the concentration is high and where it is going to, the concentration is low. Our bodies continually use up oxygen and produces carbon dioxide. Carbon dioxide is generally carried in the blood plasma, and oxygen is generally carried by the red blood cell (erythrocytes).
Whereas, it is true that in diffusion an equilibrium is usually achieved, in this case you mention there is no equilibrium. Our physiological processes (respiration) continually maintains that concentration gradient and so carbon dioxide always flows out and oxygen always comes in. Too much carbon dioxide in the blood will raise the pH and cause serious metabolic problems with enzymes and their efficient function.


How do I find the number of child terms associated with a specific GO term? I am trying to figure out how to find the number of child terms associated with a specific Gene Ontology (GO) term using QuickGO, without just counting the amount of terms in a list. For example when I want to find the number of child terms associated with the GO term 'heart development'.

I could just click on the tab 'Child Terms' and count, but what if it would be a very long list, how can I find the correct amount?

I assume there is some way to do this by going to Protein Annotation and applying a filter, but I do not know how to do this.

Any help?

I don't think it's possible to do this via QuickGO. You can, however, do it from GO's website, using their GOOSE tool. This offers an interface to the GO SQL database and lets you run queries. It also offers example searches, one of which ("Find descendants of the node 'nucleus'") can easily be modified to return what you are asking for:

SELECT COUNT(*)
FROM
 term
 INNER JOIN graph_path ON (term.id=graph_path.term1_id)
 INNER JOIN term AS descendant ON (descendant.id=graph_path.term2_id)
WHERE term.name='heart development' AND distance = 1 ;

In the query above, I modified the example and changed 'nucleus' to 'heart development' (GO:0007507) and changed distance <> 0 to distance = 1 to make it list only direct descendants. Finally, I also changed SELECT DISTINCT descendant.acc, descendant.name, descendant.term_type to simply SELECT COUNT(*) since all we are interested in is the number of descendants. If you also want their names, leave the SELECT line as is. That will show both the list of names and the total in the output.

The modified query shows us that this term has 30 descendants:


(How) Does the human digestive system process petroleum jelly, aka petrolatum? Does the human digestive system processes petroleum jelly? In other words, does it pass through the digestive system without any interaction, or is it absorbed and/or metabolized?

There are controversial case reports about systemic absorption of paraffin used for constipation. These reports mention systemic effects of paraffin absorption and one of them report liquid paraffin accumulations in
abdominal visceral organs. (full text article about paraffin)

  Liquid paraffin is indigestible and is absorbed only to a limited
  extent following ingestion.

+

  As inert substances the ingested mineral oils mostly are excreted
  intact in feces and to some degree in urine. However, some absorption
  form the small intestine has been observed (Stryker 1941). Using
  radiolabeled mineral oil, it was established that the amount absorbed
  in rat was appr. 1.5 % (Ebert  et al. 1966).

  (full text article)


What is the animal in Nosferatu movie? I was watching Nosferatu, and this dog-like animal appeared, with very curious stripes. I was wondering if this is clearly a specific animal, and which one it is, or if it's too mixed up and low resolution to tell. You can see in this video, at 11:43 and 12:22 (close up) to 12:33.
https://www.youtube.com/watch?v=PH7L4V-3VxA&t=703
Sorry about my lack of a more scientific research, but I couldn't be farther from being a biologist. This is all I got: from the stripes, it immediately brought to my mind a Thylacine (which is what caught my attention), but even though it would not me an anacronism (it was extinct in 1936, the movie is from 1922), the movie is European (filmed in Germany, Slovakia and Romenia) and the story happens in Europe too, so it wouldn't make sense to be a Thylacine (not to mention that in 1922, you wouldn't find them right around the corner ;) ). Further investigation confirmed the already almost obvious, the stripes are too in the front in their body to be a Thylacine. My second thought, from the apparent big head and the way it moves (hips lowered), it resembled a hyena to me. But it doesn't seem to have ears big enough, they also wouldn't make sense in context of the movie, and hyenas usually have spots instead of stripes. A quick search showed me that there are striped hyenas, and from pictures it looks kind of similar, but the snout doesn't seem to match. Also, they don't occur in Europe, according to Wikipedia.
So at this point I'm in doubt if it's a striped hyena (that doesn't seem to make sense to me), another real animal that I don't know, or if it's a fictional creature, some animal "modified" specifically for the movie (painted, extra/less fur, artificial modifications in height, body size, ear size, etc). Although that also doesn't make sense.
Any pointers appreciated, sorry if this should belong in scifi or another SE.

It's a striped hyena, it is relatively rare/endangered these days. Hyenas are closer to cats/felines than to dogs. They are in the suborder Feliformia.
https://en.wikipedia.org/wiki/Striped_hyena
some images here


Identify this black dragonfly with a bright bluish-white band around its body I took these photos around noon in late July in Hsinchu county Taiwan. This particular stick in this particular pond is visited by many dragonfly species. This one was very high energy and nervous but taking my time and waiting for it to return each time I spooked it I eventually got almost (but not quite) close enough to take a decent photo with my phone.
Its body is about 5 cm long and mostly jet-black. However it has a bright, solid white or blue-white band about 1 cm long behind the fat part of it's body along the long "tail section".
I'm showing the two best photos below, for the darker one I lowered the brightness of the photo on my phone before taking it so that the band wouldn't be saturated but it is still extremely bright. It may in fact be slightly blue-hued or that could be an effect of the phone's camera.
Is it possible to identify this particular species of dragonfly?

The closest match I can find is Pseudothemis jorina:

It's very similar to your pictures in regards of body shape and the light distinct band, although I'm not sure it would normally be found in Taiwan. It's more common further south like Thailand and Malaysia.


Organism identification, what is this? Im trying to find out what this is, see image below.

Im thinking these are either some insect eggs or some sort of mosslike plant.
The substance is stuck to a steel pillar, outside, about 5 feet above the ground.
The substance is found in the Netherlands in a wet meadow area.

The substance has multiple tiny cells or eggs, seems to be only 1 layer thick and has a soft/smooth feel to it.

Excuse me for the bad picture, my camera would not focus better because of the reflective surface of the pillar.

What we have here appears to be clustered insect eggs, and examples such as this tend to have some type of moth or butterfly as the culprit. It appears similar to moth eggs that I have observed on surfaces. See this page with information and this page with an example that look vaguely similar to your photograph. You would need an expert to identify a specific species though, if it's possible.


Do male humans have a mons pubis? Wikipedia writes:

  In human anatomy, and in mammals in general, the mons pubis (also known simply as the mons, and known specifically in females as the mons Venus or mons veneris), is a rounded mass of fatty tissue found over the pubic symphysis of the pubic bones. In human females, the mons pubis forms the anterior portion of the vulva. It divides into the labia majora (literally "larger lips"), on either side of the furrow known as the pudendal cleft, that surrounds the labia minora, clitoris, urethra, vaginal opening, and other structures of the vulval vestibule.

The Foundational Model of Anatomy suggests that the feature also exist in the non-gender specific pelvis concept. Does it?

Technically men do have a mons pubis but it is less pronounced. With increased estrogen in females it becomes more pronounced.

Wikipedia


How to prevent HL-60 cell contamination? I have thawed Hl-60 cells from liquid nitrogen chamber two times in RPMI 1640 media (containing 10% FBS, L glutamin, penicillin/streptomycin). In the first day the cells remain okay. But when subcultured from the first flask to new flasks (cell solution : media= 1:3) all the flasks became contaminated on the 2nd day of culture. Cloud was found in both time. It can be mentioned that I used sterile one-time usable pipettes and uncoated flask for growth. All the transfers to other flasks and media addition were done very carefully and done inside clean bench. Before using clean bench, it was sprayed by 70% EtOH.

Has anyone experienced like this problem?  Please share and if have, please give some valuable suggestions or references.

Thanks

The single most likely reason for the contamination is that your frozen stock is contaminated. Assuming you've been properly trained in cell culture, you're working in a correctly-maintained biosafety cabinet, your reagents are all sterile (has your media been sterile-filtered after adding FBS, etc.?), and the incubator is clean (water bath pan has been autoclaved, sterile water with biocide/fungicide added to it, entire incubator wiped down and all removable parts autoclaved periodically, etc.), then stock contamination is the most reasonable answer. Try thawing earlier passages than you have been working with, or order a new vial or two from ATCC or whoever your cell vendor is. Make sure your pipetors are clean, and you're using sterile filtered pipet tips.


Is it possible that there are two people in the world who belong to a different species? There're over 7 billion people in the world and every one of them is different from everyone else. Is it possible that there are two people so different that they belong to different species (in the sense that they cannot reproduce to produce fertile offspring)?

This doesn't have to mean that there's someone in the world who's completely unable to reproduce with everyone else, just that these two individuals are so different that they can't reproduce with each other (they can still reproduce with other people who can reproduce with the other individual - a ring species system).

I'm particularly interested in an answer based on how much the genome varies between people vs. how much they vary against our closest relatives (such as Neanderthals). For example if humans and Neanderthals share 99% of their genes, and the largest variation among current humans is 0.001% of genes, then the answer to this question would be "no".

At the beginning, the population of the parents who we are talking about should be made more specific. Let's limit it to adult, healthy individuals (let's skip pathologies, various kinds of random body injuries, personal sexual preferences and close relatives).

From the descendants group, let's also exclude children who would die from random causes, body injuries (unintentional :-( and intended :-((( ), genetic diseases, etc.In addition to the genetic variation (A global reference for human genetic variation), epigenetic variability (Worldwide patterns of human epigenetic variation) should also be taken into account.

If we give the most popular definition of a species (and there are very many of them), as individuals capable of giving fertile offspring, of course all humans belong to one species. Contrary to popular opinion, we are similar to one another like drops of water.


What are some characteristics of venules and arterioles? I know that the vascular system of the human body is organized in the
two, "ever branching", structures of the veins and the arteries. These two
structures stem from their connections to the heart and stretch and
branch throughout the body.

The two structures are interconnected through capillary beds,
responsible for the interactions between the blood and the
extracellular liquid, surrounding the tissue cells of the body.

The capillary beds are connected to the arteries and the veins through
small vessels, venules, branching out from veins and arterioles,
branching out from the arteries.

The capillary beds consist of a web of capillaries, vessels small and
thin enough to allow exchange of nutrients and waste between the blood
in the vessels and the extracellular liquid surrounding the vessels as
well as the cells of the body.

Now, I realize that the capillary beds must be ubiquitous throughout
the body, sustaining every part of the body but the circulatory system
itself.

I am eager to find out more about the venules and arterioles. Looking
at the structure of veins and arteries, how prevalent are the smaller
blood vessels? Are the arteries and veins "fuzzy" with arteriole and venules or are the small vessels more sparse? Do they emanate from large vessels as well as smaller ones? How do their presence interfere with vascular interventions or
even drawing blood for blood tests?

I'd be happy for information in these matters.
Cheers
Mats

I think this question is a bit too broad to write a comprehensive answer to, and there will certainly be some variation between tissues.

However, here is one reference that might give you what you are looking for.

I used to make acrylic arterial casts, mostly of coronary arteries but also some dabbling in the pulmonary, renal, and hepatic systems. My experience with the coronary system is that most of the arterioles come off in a tree-like branching pattern from quite small arteries, but there are always exceptions. I think the "fuzziness" you refer to definitely depends on the scale of observation: the further away you are, the more "fuzzy" arterioles look: of course they will never be as "fuzzy" as capillaries, but certainly once you enter the muscles themselves there is a lot of branching, but that branching isn't necessarily uniform. That is, there may be larger branches running in one dimension, and smaller branches in another dimension.

In larger vessels you also have the vasa vasorum: arteries that feed the large arteries and veins themselves. Some of those vessels are certainly the same size as arterioles, and some branch directly off the main vessel, but I am not sure whether anatomists always consider those to be arterioles or if they are considered separate.

From the perspective of interventions such as surgery, etc, smaller arterioles aren't really any different from capillaries, and larger arterioles might need to be clamped off or cauterized, but there isn't really any way to avoid them if you are cutting into a vascularized tissue. One wouldn't avoid these vessels they way they might avoid larger vessels.


Is there any relationship between the height of a tree and the number of branches emerging from the main stem? Is there any relationship between the height of a tree and the number of branches emerging from the main stem?

I am particular interested in spruce or fir.

The height is only one of a few factors; also the species and environment are more significant. A spruce growing in unshaded location may have branches to ground level while the same species in a dense woods will only have branches at the top. A southern pine ( in the US) is often 100 ft tall with all the branches in the top 30 ft ; these trees drop the lower branches because of limited light and because various vines climb into the lower branches ( until the branches die and fall).


Alignment of sequenced fragments in Next Generation sequencing (sequence assembly) The NGS (Next Generation Sequencing) involves fragmenting the DNA to be sequenced. This is followed by attachment to beads or flow cells and then a localized PCR is conducted. Modified bases are added and with addition of each base, a detection is made (by fluorescence for instance) for the type of base bonded. After complete sequencing of all the fragments, how are these reads of fragments assembled in the way they were in the original non-fragmented DNA? (in short: How sequence assembly works?)

Assembly and alignment are generally used to refer to two different algorithms that work in two different ways.

Alignment takes your sequence fragments, and compares them to a reference genome, and tells you where that read aligns and how closely it aligns.  For a while, popular aligners used Burrows-Wheeler transform algorithms to make special indexed versions of the genome, this made alignment to the index far faster.

Assembly is when you have no reference, and use the overlap of the reads to build large contigs.  For a while De Brujin graphs were a popular algorithm for that.


What is genodiversity good for? I saw some documents which were trying to say that they can prove via sweat smell selected by women that humans are developed to find a partner with similar genes. At the first glance, I refused it as absurd for many examples of organisms behaving in reverse but then I realized that I don't know any satisfying evolutionary explanation for this (and more: I could even explain the contrary: If less developed and more developed human had a baby, the better genes could be maybe annulled by the worse genes, on the contrary two very developed partners would have not only a lot of descendants, but their descendants would have also lot of descendants and so on.)

And more thing: if genetic diversity is truly evolutionary practical, could for example even people with genetically transmitted disease help our gene pool?

Thanks a lot.

Genetic diversity is indeed very important for many reasons, most notably resistance to diseases.

The Gros Michel banana used to be the most cultivated banana, until it was almost completely wiped out by a fungal disease due to lack of resistance in the genetically homogenous cultivars grown in plantations. As a result, it had to be replaced by the Cavendish banana across most of its former range by banana growers.

Furthermore, the answer is a definite "yes" to people with genetically transmitted diseases helping the gene pool.

For example, the case of sickle cell anemia clearly shows why even people with genetic diseases can help the gene pool by providing useful alleles. Heterozygotes for the sickle cell allele are resistant to malaria. This has led to the allele having a high propensity in subsaharan Africa, where malaria is endemic.

  The first example of genetically controlled innate resistance to human malaria was the demonstration in 1954 that sickle-cell heterozygotes have less severe Plasmodium falciparum infections than do children with normal adult hemoglobin. This observation has been repeatedly confirmed, most recently by independent studies of genome-wide associations in severe falciparum malaria, which have identified the HBB locus as the major signal of association.

Additional examples are the cystic fibrosis gene, which confers resistance to cholera, and thalassemia, which confers resistance to heart attacks.


Why is it unlikely that bathroom smells can pose health risks? Based on a little bit of internet reading, it appears that odor molecules that enter your nose from human feces are of little concern to your health because the harmful stuff, like the pathogens, are not likely to be picked up and carried through the air.

This seems to make sense, however due to my limited knowledge of biology, I am having a difficult time distinguishing WHY the bad stuff is not likely to become airborne whereas other molecules can, and will cause damage by smell. Chlorine, for instance, will cause some significant damage simply by smelling the airborne fumes (which I assume are the molecules doing the damage).

I have to assume it is a natural defense mechanism that something that smells bad is not something you want to be around (CO being a major exception) but it seems that feces molecules are not a concern. Why?

Mostly, what you're smelling are volatile small molecules: stuff like butyrate, indole, mercaptans, hydrogen sulfide, etc. These molecules are thousands of times smaller than even the smallest pathogens, being measured in Angstrom vs. nanometer scales. Pathogens are just too large to be actually volatile, in the sense of freely escaping into the air. And fortunately, these volatile organics are not nearly as reactive as something like chlorine gas. (If they were, imagine the damage they would do, at a much higher concentration, to the person they were just inside.)

Now, if someone had literally just projectile-vomited (or if excreta were churned around, e.g., by flushing), it's possible that a very small pathogen like norovirus could spray outwards in an aerosol. Since norovirus has a very small infectious dose (on the orders of tens of viral particles) this could be enough to make you sick, and indeed, aerosols have been implicated in norovirus transmission, though it's not that common. But the smell would remain long after any viral particles in aerosols had settled down onto surfaces.


Making sense out of the visual representation of transcription Most people are familiar with the following diagram. Some genomic DNA with a promoter region, exons and introns. This is transcribed into RNA that is then translated into a polypeptide.

When we look closer at the strand that is being transcribed we can distinguish between the two as the sense and anti-sense strands.

So the transcription factors and RNA polymerase bind and begins transcribing mRNA in the 5' to 3' direction and thus reading the anti-sense strand in the 3' to 5' direction and have the same sequence as the sense DNA strand, substituting U for T in the mRNA.

My question would be, shouldn't the exons be numbered in the reverse order as shown in the first picture I provided. So instead of Promoter -> Exon1 -> Intron -> Exon 2, should it be, Promoter -> Exon N -> Intron -> Exon N-1?

Also, in bioinformatic sites are the gene sequences listed in the sense or anti-sense strand? I have noticed in some bioinformatic tools, to determine what polypeptide will result from a DNA sequence, one must input the sense strand in 5'to 3' orientation and not the anti-sense strand.

Gene sequences are annotated in the sense strand. So, these diagrams are correct.


What are the major causes of mutations in DNA? I know that point mutations can change the base sequence of a gene by altering a specific codon that codes for a particular amino acid. Are these mutations purely random events that occur when DNA is being copied into a cell? Furthermore, can environmental factors play a role in the amount of mutations that occur?

Welcome to Biology.SE!

  can environmental factors play a role in the amount of mutations that occur?

Yes! The environmental factors that increase the mutation rate are called mutagens. You will definitely want to have a look in the wikipedia article. You may also want to read the wikipedia page on mutagenesis

Some chemicals increase the mutation rate, physical agents such as radiation also increase the mutation rate. There are viruses that are mutagens as well. Also, the number of mutations that an organism produce can also be phenotypically plastic. For example, plants have been shown to increase thee number of mutations they produced in response to stressing environment. The reason (or at least the commonly stated reason) is that they produce many mutations, "hoping" that at least one of the offsprings will carry a beneficial mutation and will be very fit even in this environment that is stressing for the parents. Many viruses and some bacteria also act as mutagens.

  Are these mutations purely random events that occur when DNA is being copied into a cell?

Mutations are random in the sense that it is impossible to predict with certitude that a given mutation will occur at a given locus (locus=position in the genome). As a consequence, it is also true that mutations are random in the sense that it is impossible to predict the effect on the phenotype (and on the fitness) of a future mutation. Mutation rate varies throughout the genome. Typically, repeated DNA sequence tend to have higher mutation rate. Also, transposons causes many mutations and regions in the vicinity of transposons have higher mutation rate. But again, you should have a close look to the wikipedia pages I linked above.

Note that a full answer would require going into the terminology of the term "random" which itself is a question of philosophy. When using the term random, it is always important to specify what is meant exactly (which is not done in the question) as one may argue that since the Big Bang happened everything has been deterministic.


Why does too much candy cause nausea? As I sit here after eating too much chocolate, I wonder:

What are the biological mechanisms behind eating too much candy candy causing nausea in a healthy individual?  Is it a spike in blood sugar, or does the stomach run out of a particular chemical, or is it a pH shift?

Is it the same reason that greasy meals can cause nausea?

From an evolutionary perspective, candy causing nausea seems counter-intuitive since candy is easy calories.  Then again, candy and concentrated carbs are modern inventions...

There can be many reasons about why too much candy (chocolate) can cause nausea. Lets talk about them one by one.

Hyperglycemia - chocolate contains sugar, and too much sugar consumption can cause high blood sugar levels i.e. hyperglycemia. When blood sugar levels remain high for some time, it can cause nausea and vomiting, among many other symptoms including dizziness, itchy skin, dry mouth, thirst, etc. If left untreated, it can lead to diabetic ketoacidosis or diabetic coma. See this article for more information.
Artificial Sweeteners - often chocolates contain artificial sweeteners instead of table sugar or glucose to prevent risk of hyperglycemia without compromising with taste. But many times, these artificial sweeteners can cause side-effects too. For example, there have been reports that sucralose causes nausea and vomiting in some people. Other alernatives, like mannitol, sorbitol, xylitol, maltitol, isomalt, etc. can also cause nausea and similar symptoms.
Dumping Syndrome - sweet foods, like chocolate, are hyperosmolar i.e. have high osmolarity. When these are ingested in large amounts, they cause the small intestine to expand quickly, due to which the ingested food passes too quickly through the stomach, largely in undigested form. This condition is called Rapid Gastric Emptying (RGE) or Dumping Syndrome. The initial symptoms of dumping syndrome include nausea, dizziness, diarrhea, fatigue, etc. See the Wikipedia page for more information.
Fats - chocolate contains cocoa butter, and cocoa butter is a source of saturated fats. Ingestion of large amounts of fats can lead to indigestion, and indigestion can become a cause of nausea and vomiting. This also explains why greasy foods can cause nausea; because they have high fat content.

Some other factors could include candy allergy, pregnancy, etc. or something I failed to mention. But I hope this much would help too.


Why is the pressure pulse bigger after exercise? Right after exercise, is the amplitude of the pulse smaller or bigger than resting period? And why is that ?

I would guess that pulse pressure increases after exercise. As I understand it,

Systolic pressure is simply resistance against the pressure wave of the ejected blood. Since the stroke volume is increased in exercise to deliver more blood, systolic pressure will be definitely be increased.
During diastole, the major resistance to flow is due to peripheral resistance (major arteries now assist flow by releasing stored energy), and this is reduced in exercise due to vasodilation. Although there is more flow, since the resistance is markedly reduced, diastolic pressure may drop.

Hence, pulse pressure should increase.


How can the organic mercury compound Thiomersal be not dangerously toxic? My intuition tells me that organic mercury compounds are absolutely toxic. Unimaginably, fundamentally, extremely and uncompromisingly toxic.

I know that is not true for all doses.

Thiomersal is the organomercury compound that was used in vaccines as preservative. It's use has been controversial outside of the scientific community.

I am not asking whether the use in vaccines is dangerous, to be clear:

The use of mercury as Thiomersal in vaccines it is not dangerous.

That is well-established beyond reasonable doubt. Far beyond.

My intuition tells me that any organomercury compound it so mind-blowingly toxic that I feel cognitive dissonance if I try to accept that, at some dose, it's not.

I'm totally aware that toxicity depends on dose, that the compound is toxic at higher doses, and the dose used is just low enough that it is not toxic.

But the dose used is still antiseptic and antifungal, and having anything in my body that contains mercury and carbon in a dose high enough to kill a form of life feels just not right.

I would not worry at all to get vaccinated with a vaccine containing Thiomersal, and if a physician would ask me whether I prefer a vaccine with or without it, I would answer "Whatever you think is best."

But still, on the abstract level, the feeling of "That can't be right" to have an organomercury compound in my body it pretty strong.

I know it is not dangerous, but:

How is that even possible?

Thiomersal is broken down into two compounds, thiosalicylate and ethylmercury (Ensink 2015).  The thiosalicylate it is relatively non-toxic, and there is even some evidence that this compound could counteract some of the effects of mercury poisoining (Asadi et al 2010), though the mechanism of this inhibition has yet to be elucidated.
Although they have similar names, methylmercury and ethylmercury have very different levels of toxicity.  Methylmercury has long been known to be highly toxic, producing high levels of cell death in the brain, particularly in the cerebellum and the visual cortex (Ceccatelli et al 2010).
Unlike methylmercury, ethylmercury appears unable to cross the blood-brain barrier as fast as it is eliminated in the stool.  Consequently, small quantities of ethylmercury have been shown to be non-toxic, resulting in the relative non-toxicity of thiomersal (Pichichero et al 2002).

Sources:

Asadi S, Zhang B, Weng Z, Angelidou A, Kempuraj D, Alysandratos KD, Theoharides TC. 2010. Luteolin and thiosalicylate inhibit HgCl(2) and thimerosal-induced VEGF release from human mast cells. Int J Immunopathol Pharmacol 23(4): 1015-1020.

Ceccatelli S, Daré E, Moors M. 2010. Methylmercury-induced neurotoxicity and apoptosis. Chemico-Biological Interactions 188(2): 301-308. doi:10.1016/j.cbi.2010.04.007

Ensink E. 2015. Preservative or poison? The science behind Thimerosal. The Substrate (online): http://substrate.asbmb.org/2015/05/15/preservative-or-poison-the-science-behind-thimerosal/

Pichichero ME, Cernichiari E, Lopreiato J, Treanor J. 2002. Mercury concentrations and metabolism in infants receiving vaccines containing thiomersal: a descriptive study. The Lanclet 360(9347): 1737-1741. doi:10.1016/S0140-6736(02)11682-5