How many sensory neurons are in the human body? While I understand that there is a wide disparity of precision when it comes to specifying what constitutes "sensory neurons/receptors", I'm trying to find an authoritative source to provide at least a rough order of magnitude estimate on the number of receptors in the human peripheral nervous system (including skin, tongue, eyes, ears; but also mechanoreceptors and proprioceptors as well). The only sources I have found so far (here and here) only provide hints at the answer. I have found estimates as high as 15 billion, and as low as 3,000,000, but none of these guesses cite authoritative sources.
As I'm sure you can tell, I am not a student of anatomy (my interests lie in cognitive science and artificial neural networks), so forgive me if my question is too imprecise.  But to put it simplistically: what I want to know is, roughly how many externally-produced sensory signals (channels) does the human brain have the capacity to process? Again, I am not looking for a precise answer, but I'm hoping to at least reduce the uncertainty to less than four orders of magnitude.

CONTEXT: My purpose in this investigation is to try to quantify the magnitude of the computational capability of the brain with regard to processing external signals. If one were to imagine an "artificial nervous system" (as distinct from an artificial neural network), how many input sensors would it be able to simultaneously process if it were on par with a human brain?

UPDATE: I recognize from the comments the inherent ambiguity of my question, so let me attempt to clarify. Assuming that the number of incoming signals to the brain at any one time is limited by the number of neural connections between the brain stem and the spinal column*, can someone provide an indication of what that number might be.
* (if that assumption is overly simplistic, feel free to enlighten me)

This is a really interesting question.  However, I'm going to try to address the context and update sections of your post rather then attempt to quantify all afferent signals in the nervous system.  This is because quantifying those signals would be an exceedingly difficult task.  It's not only logistically difficult to measure on an individual level, but to say anything definitive regarding the entire species would be superfluous.  The number of signals at any one time is constantly in flux, as not every sensory receptor generates an action potential at the same time.  Even in instances where similar or "competing" receptor types are simultaneously stimulated, those transmissions will be modulated and/or pathways suppressed.  A good example can be found in this editorial article[1] on pain, where inducing painful stimuli can alleviate an itch sensation.  I reference this to illustrate that sensory signals are not entering the brain unchecked. In the most simple of terms, they are heavily regulated.

Based on the context on your question, it seems what you really want to know is what is the maximum threshold.  In an artificial nervous system, how many signals could we pump into it before it becomes inefficient or overwhelmed?  However, what makes the nervous system unique is that it's a living system that adapts to stimuli.  When there's more signals then it can handle or process, it regulates them.  You can read more about the process and its importance in this article on sensory gating[2].  For this reason, a healthy brain that isn't being artificially stimulated shouldn't become overwhelmed.  In fact, this process makes it far more efficient then any super computer.  A fun example of this was the six chess games between Kasporov and Deep Blue in 1996.  Think of the sheer number of moves Deep Blue could calculate compared to Kasporov: hundreds of millions of moves per second.  It lost that match.  Computational capability isn't conditional on the number of inputs the system can receive, it's how that information is processed, utilized, and applied once it's in the system.

I know I didn't answer your question in regards to a hard number, but hopefully it helped give a different perspective.  Please let me know if you'd like anything further clarified.

[1]: Focus on pain.  Nature Neuroscience 17, 145 (2014). doi.org/10.1038/nn.3644

[2]: Sensory gating, inhibition control and gamma oscillations in the human somatosensory cortex.  Scientific Reports 6, Article number: 20437 (2016). doi.org/10.1038/srep20437


What type of cell do you start with in Meiosis? Okay, I was learning about mitosis and meiosis in school and had a question. I know in Mitosis you first start off with a Diploid (2N) cell and then end up with two daughter cells that are also Diploid. However, in Meiosis, I know you end up with four Haploid Cells (N), but what exactly do you start off with? Is it like a single egg makes four more eggs or something? Or does it start off with a Diploid Cell and then end up with the Haploids? If so, what exactly is the starting cell called?

Meiosis starts with a diploid cell and produces four haploid cells.  In animals, the starting diploid cell is usually called a germ cell and the surviving haploid cells become gametes (sperm and ova).  (In animals, the female mitotic sequence produces only one ovum; the other three haploid cells become "polar bodies".)

In other organisms such as plants, the starting diploid cell is typically not called a "germ cell" as it is not distinguished early in the organism's life.  Instead the starting cell can be any undifferentiated diploid cell that finds itself in the appropriate location (e.g. in a flower) at the appropriate time.


Why do we suffer abdominal pain after we get very angry or stress? You also realize probably, when we get so much anger or high levels of stress, after some point we have terrible stomach ache, like really heavy pain. Why is that? How stress or anger can effect our stomach? What is the mechanism?

Cortisol produced from the zona fasciculata of the adrenal cortex is directly caused by stress.

According to http://en.wikipedia.org/wiki/Cortisol

  Cortisol stimulates gastric-acid secretion. Cortisol's only direct effect on the hydrogen ion excretion of the kidneys is to stimulate the excretion of ammonium ions by deactivating the renal glutaminase enzyme. Net chloride secretion in the intestines is inversely decreased by cortisol in vitro.

This increase in gastric-acid secretion can irritate the lining of the GI tract, especially if there are ulcers or inflammation, resulting in pain. In addition, the fight-or-flight response causes

  inhibition of stomach and upper-intestinal action to the point where digestion slows down or stops.

(see http://en.wikipedia.org/wiki/Fight-or-flight_response)

Those things, paired with increased muscle tension and vasoconstriction cause pressure changes in the GI tract, which can cause pain.


Does eating nonsalty food with MSG make you thirsty? Assume that you're thirsty after eating food  that didn't taste salty while you were eating it.
Quora posts and https://msgdish.com/msg-problems-and-answers/ still impute the thirst to salt:

The Problem with MSG Problems - MSGdish
“Chinese food makes me so thirsty—it’s the MSG.” — Well, chances are, if you’re thirsty after eating Chinese food (or any food), you’ve probably consumed a good dose of sodium in the food or you’ve not had enough liquids recently. And, while MSG does contain sodium, it has only 1/3 the sodium of table salt. Chinese food contains a lot of high-sodium ingredients, including soy sauce, broths and other sauces. In fact, there are lots of foods (snack crackers and flavored chips, condiments, soups and sauces, commercially-prepared entrees) we eat all the time that typically contain much more salt than MSG. It’s time to stop blaming Chinese food (and MSG) for your thirst. Many Americans are chronically under-hydrated, and a salty meal of any ethnicity can send us all racing for water afterward.

But Hungry Onion

But since the food didn’t feel overly salty at the time, the only reason I can think of for the thirst is MSG.

and Wired.com impute the thirst to the MSG respectively:

The exact flavor MSG confers is difficult to describe, and many just say it increases the "taste intensity" of food. One thing is certain: It makes people thirsty, encouraging them to eat and drink more. Americans consume about 28,000 tons of MSG per year, according to one estimate reported in the June 1995 Journal of Environmental Health.

MSG (monosodium glutamate) can trigger thirst simply because it's a spice or because foods with MSG often contain other spices.

Relationships between human thirst, hunger, drinking, and feeding (PubMed, 2008)

  Drinking may occur at meal times to facilitate chewing and swallowing,
  improve sensory stimulation and food palatability, reduce aversive
  sensations evoked by irritants such as spices, or in anticipation of
  physiological deprivation.

Thirst after ingestion large amounts of MSG is described here as part of Chinese restaurant syndrome; the mechanism involved is a transient release of acetylcholine:

  symptoms experienced by individuals following intravenous MSG were
  similar to those experienced by individuals following intravenous
  acetylcholine (ACH).

So, does MSG trigger thirst? It may, but not necessary.


Why are some plants frost tender? Why do some plants have the ability to stand frost, while others can't? Does it have to do with the size of the water vacuoles in the plant cells?

All cells are susceptible to cold, but freezing is particularly difficult.  If the water in the cells freeze, it would usually burst the cells (water expands when it turns to ice) and tearing the cell membrane (totally killing it).

Some plants and animals have adapted to colder temperatures by putting antifreeze proteins in their cells.  A lot like adding antifreeze to the radiator of a car, this lowers the freezing temperature of the water in the cell.

So the answer is that some plants have adapted to colder climates with the help of additional genes.  There are other things that have to change too - the chemical reactions in the cell will go haywire when temperature changes too, so lots of genes must make adjustment for a fully cold adapted plant.


Is the function of adjacent genes correlated? Do genes that occupy a similar locus on the genome have correlated function, specifically in human beings? It is my understanding that adjacent genes are inherited together, and so location plays a role there. However it terms of function, I don't know to what extent location plays a role. Furthermore, if say two adjacent genes have the same expression, does this necessarily mean that their function is correlated, or is that interpretation stretch?

In bacteria, this is often true.  This is because more than one gene is often transcribed onto a single RNA.  This grouping of genes is called an operon.  It is usually true that these have a related function because they are being translated to protein in very much the same proportion - a convenient way to regulate the function as a whole.

Once you get into eukaryotes this is no longer true (except for v. rare cases most of which are viral genes), one mRNA transcript contains just one translation region.  This is true even for yeast and other single celled organisms.  Gene regulation can be correlated, but the relationship on the genome has little to do with it.

There is some importance to the genomic relationship of two genes because of the crossing over that occurs in meiosis, but this is more of a relationship that is important in speciation and evolution, it doesn't have any recognized importance to how the genes act within the eukaryotic cell.


What predates on cactus in the Atacama desert? Introduction

Last week, I was in the Atacama desert where I've seen many cacti. Some / many of them were seemingly suffering from predation. Most of predation seemed to be on cardón, often restricted (but not only) at the interface between the woody bottom part and the green spiny part. It looks like a big piece (maybe over 300 $\text{cm}^2$) of the flesh was bitten away. Unfortunately, I do not have a picture.

These cacti have very long spines and it was unclear to me what predator could maintain selection for cactus lineages to produce that many large spines.

In the desert, I have seen rabbits, guanacos, small birds, vultures, large black coleoptera and butterflies.

Question

In the Atacama region,

What species predate on cacti?
Is there a single species that causes most of the predation on cacti?

Short answer
This type of herbivory is probably from feral livestock, especially donkeys.
Long Answer
There is video footage of guanacos eating flowers off of cacti in the Atacama. For example, an image capture of a Getty Images video:

 Credit: BBC Natural History
This type of florivory has been documented in related species of cacti as well (e.g., see Gomes et al. (2016)1)
However, I could find little evidence about guanacos eating the trunk of these cacti (especially to the degree you describe).
Actual herbivory of Echinopsis cacti has been reported in multiple publications. For example, Peco et al. (2011)2 cite feral livestock as a major source of herbivory in columnar cacti in South America:

Columnar cacti are an important feature of the arid “cardonal” landscape in South America. The predominant columnar cactus in the southern zone is Echinopsis (=Trichocereus) terscheckii. At some sites, the species suffers considerable trunk damage, attributed in previous studies to feral livestock grazing (donkey and cattle).
In a previous study we found that damage intensity on Echinopsis terscheckii trunks correlated with abundance of livestock dung in their surroundings, but not with the abundance of guanaco dung (Lama guanicoe) (Malo et al., 2011; Novillo and Ojeda, 2008). Futhermore, E. terscheckii was found in summer or winter donkey diet but not in guanaco diet in the study area (Reus pers. comm.). Direct observation of donkeys feeding on columnar cacti suggests that this species is the main cause of stem damage

See this National geographic video explaining how camels and other related animals handle eating spiney cacti. (Specifically, they accomplish eating cacti through the use of hardened papillae guiding the spines down the throat vertically).

Works Cited:

 Gomes, V.G.N., Koroiva, R. and Araujo, A.C., 2016. Vertebrate florivory on the short-columnar cactus Echinopsis rhodotricha K. Schum. in the Brazilian Chaco. Plant Ecology, 217(12), pp.1481-1487.

 Peco, B., Borghi, C.E., Malo, J.E., Acebes, P., Almirón, M. and Campos, C.M., 2011. Effects of bark damage by feral herbivores on columnar cactus Echinopsis (= Trichocereus) terscheckii reproductive output. Journal of arid environments, 75(11), pp.981-985.


Hearing system as in visual system: exists well also - in protecting the inner mechanical parts of both sensing systems - a similarity? I prefer answers, not just discussing.

In the mechanical part of the human eye the control system to protect for overload of the diaphragm in the iris with a strong coupling to the light intensity that falls on the retina has his place in the visual system as close as possible to the light source in the chain of control devices of the human visual system. The iris is disk-shaped and consists of two muscles. Like a diaphragm for light, the iris regulates how much light comes into our eyes. In bright conditions, the muscles of the iris limit how much light comes in. In lowlit conditions, the muscles of the iris increase the amount of light comming in.

Basic hypotheses is that the protection device in mammalian human hearing system is based on similarity as in the visual system and therefore should well also be using similar protection tools as used in the visual system and should well also be placed in the chain of control devices as close as possible to the signal source, as an experienced system engineer will always place a protection device in the chain of control devices as close as possible to the signal source.

Exists such an continuous functioning simalarity analogue in the protection system for sound signals ?
Both the iris in the eye (two muscles) and eardrum+ossicular chain in the ear (two muscles): in protection.
Exists that similarity ?

The cooperative functioning of the eardrum and ossicular chain attenuation can be regarded as in this schematic drawing of the ear as an externally activated spring-mass system. Fig. 2.

Ossicular chain and eardrum function, together operating as a continuous sound reduction mechanism for changes in the strength of the offered signal. The tympanic membrane and the ossicular chain can be seen as a spring-mass system with amplification facilities, like it is shown in this figure.

The combined action of the ossicular chain and the eardrum is hypothesized to provide for both permanent volume control of the input sound and for overload protection. The stapedius reflex, evoked by sudden strong sound signal, cannot be seen as anything else than an extreme manifestation of the very mechanism that the schematic drawing of the ear as an externally activated spring-mass system propose.


Is phosphofrucrokinase1 PFK1 found in the liver? I am trying to understand glycolysis control. One thing I am stuck on is whether there is PFK1 in the liver, or only PFK2.

Edit: As far as I am aware, there is no pfk2 in muscle cells, only pfk1. This is entirely under allosteric control of ATP/AMP ratio to control the rate of glycolysis compared with gluconeogenesis. In the liver there is pfk2 which ensures that there is hormonal control of the rate of glycolysis. However is there also pfk1 so that there is a rate of glycolysis sufficient for liver cells to survive, irrespective of the hormone signals?

PFK2 (PFKFB2) doesn't appear to be present in the liver. The two sources I have used agree that PFK1 (PFKL) is present in the liver. They diverge regarding the levels of expression of PFKL.

This is the expression of the three 6-phosphofructo-1-kinase and one 6-phosphofructo-1-kinase genes according to the Human proteome map (mass spectrometry).

I can't see a huge dynamic range across the proteins in the liver, although the liver specfic gene (PFKL) is the 'winner' there.

The Human protein atlas (immunohistochemistry) is also a useful source for information and it provides a very different answer. Using immunohistochemistry it shows robust signal for PFKL but not for PFKFB2 in the liver.


Are there "multi-frequency" signals within a human brain? I know that neurons can exhibit tonic and phasic firing, and also that a neuron is sometimes called an integrator. This makes me interested to know if there are activities in the brain that depend on two or more signals of different frequency occurring at the same time. For example, in a telephone system, two signals with a different frequencies at once(DTMF) are interpreted as 1. Is there anything similar in the human brain?

Remembering that neurons don't generate sinusoids, just spikes (mostly)....

It depends on exactly how you want to define "depend on".  For instance, a downstream neuron receiving inputs from two neurons will be more likely to fire as it spatially/temporally sums the inputs from the two neurons.  Regardless of their specific rates, if their interaction is such that an impulse from each neuron arrives within a certain timing of the other, it may be sufficient to cause the downstream neuron to spike.  In this case, particular sets of frequencies of the two upstream neurons would be more likely to activate the downstream neuron and would do so at a particular rate for the downstream neuron.  Of course, the phase delay between the two neurons would be important too.

In a more general sense, one might consider the binding problem, by which many sensory inputs are bound into a single, higher level experience, such as an object or a biographical memory, which can then later be recalled (and thus activate all the lower sensory regions that encoded the memory in the first place, nearly recreating the experience).


Why does K+ going out of the cell cause hyperpolarization? I'm really  confused by how the terms Hyperpolarization and Depolarization are used in Cell biology and hope somebody can enlighten me hopefully.
Here's what they mean for me so far:

Depolarization means the inner and outer side of the cell membrane become less polarized (so the Nernst potential tends to 0 due to log(1) being 0)

Hyperpolarization that the inner and outer side become more polarized (so the Nernst potential increases).

Assuming I'm not completely wrong until here.
Let me give some examples, so maybe you can see better where the problem lies:

We have a model cell so (K+ internal is 140 mmol/l, K+ external is 4.5 mmol/l) and the external side is increased to 8 mmol/l , then a DEPOLARIZATION occurs because

roughly : $-60 \cdot \log(140/4.5) = -90 mV < -60 \cdot \log(140/8) = -74 mV$ ; or in other words, "energy" was used so a depolarization occurred (so far this seems correct with the solutions I can find to this example)

\
\

Now comes the second example (famous depolarization of a cell with the graph and the peak and repolarization):

Na+ enters the cell : the concentrations im gonna use for this example are inside:$12 mmol/l$ and outside $140 mmol/l$

so before the Na enters we have: $-60 \log(12/140)= 60 mV$

if Na+ enters the Cell, a depolarization should occur (because the difference inside and outside is decreased)

this seems fine with the graph...

the part of the graph which goes over 0 (also called "overshoot"), is it not technically a hyperpolarisation+depolarization?
repolarization: this occurs by K+ ions leaving the cell, but that doesn't make sense according to the Nernst equation?

The concentration inside before the cells leaving is 140, outside 4.5 ; if K+ leave the cell, its simply going to depolarize more... So why does repolarization occur and not depolarization?

It's commonly stated that Hyperpolarization is caused by K+ LEAVING the cell (for example with ion channels) , how does this make sense if the inner concentration is higher than the outer? If anything, this again should lead to depolarization
Same thing with K+ entering the cell, isn't that supposed to cause a hyperpolarization as well?

I appreciate any kind of insight into this matter, since it seems that I'm completely wrong.

Adding K+ on the outside of membrane is not the same as transfering K+ from inside to outside.
When K+ is added to outside(hyperkalemia) the RMP becomes less negative(depolarisation)
When K+ is transfered from in to out RMP becomes more negative(re/hyperpolarisation)
We should not forget that most of the intracellular anions are nonpermeable protiens, so when K+ is transfered to outside they pull harder, and when K+ added outside, the pull decreases


Is it better to receive a certain dose of radition gradually or all at once? Suppose you had to choose between getting exposed to 1000 mSv gradually over the next 5 years, or all at once exactly 5 years from now.

Which one would be the healthiest option? Is the probability of having developed a disease like cancer after those 5 years the same in both cases?

Phrased differently: Are the effects of multiple doses of radiation entirely probabilistic and/or cumulative?

Thanks in advance!

The period of time over which a dosage is given matters critically. You probably have experienced this in your daily life. If you are out in the bright, summer, sun for 8 consecutive hours on a single day, you are likely to get a sunburn. If you are out in the sun for a total of 8 hours spread evenly over a month, you're very unlikely to get sunburned.

You body has mechanisms that can repair radiation damage or limit it's effect, but these processes take time. A particularly important processes is apoptosis. A cell can detect if its DNA has been critically damaged, and self-destruct before something else goes wrong. If the exposure is acute, there my not be time for the apoptosis mechanism to take effect before it is damaged itself, possibly transforming the cell into a cancerous state. There is considerable evidence that lower dose rates do give rise to fewer cancers.


Do all sources supply all sinks on a plant? Sources include any exporting organs, typically mature leaves, that
  are capable of producing photosynthete in excess of their own needs.

  Sinks include any nonphotosynthetic organs of the plant and organs
  that do not produce enough photosynthetic products to support their
  own growth or storage needs. Roots, tubers, developing fruits, and
  immature leaves, which must import carbohydrate for normal
  development, are all examples of sink tissues.

Sinks are always supplied by sources. Now, I want to know do all sources transport their photosythetic to all parts of plant or some sources just supply some especial sinks.

This is a question for me:

Do all sources supply all sinks on a plant?

What you think about phloem is not correct, actually there are a lot of phloem which transport the photosynthetic. Although the overall pattern of transport in the phloem can be stated simply as source-to-sink movement, the specific pathways involved are often more complex. Not all sources supply all sinks on a plant; rather, certain sources preferentially supply specific sinks. In the case of herbaceous plants, such as sugar beet and soybean, the following generalizations can be made.

Proximity. The proximity of the source to the sink is a significant factor. The upper mature leaves on a plant usually provide photosynthetic to the growing shoot tip and young, immature leaves; the lower leaves supply predominantly the root system. Intermediate leaves export in both directions, bypassing the intervening mature leaves.
Development. The importance of various sinks may shift during plant development. Whereas the root and shoot
apices are usually the major sinks during vegetative growth, fruits generally become the dominant sinks during
reproductive development, particularly for adjacent and other nearby leaves.
Vascular connections. Source leaves preferentially supply sinks with which they have direct vascular connections. In the shoot system, for example, a given leaf is generally connected via the vascular system to other leaves directly above or below it on the stem. Such a vertical row of leaves is called an orthostichy. The number of internodes between leaves on the same orthostichy varies with the species.
Modification of translocation pathways. Interference with a translocation pathway by wounding or pruning can alter the patterns established by proximity and vascular connections that have been outlined here. In the absence of direct connections between source and sink, vascular interconnections, called anastomoses (singular anastomosis), can provide an alternative pathway. In sugar beet, for example, removing source leaves from one side of the plant can bring about cross-transfer of photosynthetic to young leaves (sink leaves) on the pruned side. Removal of the lower source leaves on a plant can force the upper source leaves to translocate materials to the roots, and removal of the upper source leaves can force lower source leaves to translocate materials to the upper parts of the plant.


How does heart beat faster while doing a strenuous task? I know that when we do tasks which require extra physical effort (like running etc.), our heart beats faster.

I also know that the reason behind this is that these jobs require more energy than usual and, hence, require more oxygen for breaking down food. And, since, oxygen is transported throughout body by blood (by forming compound with Haemoglobin (present in RBCs), called Oxyhaemoglobin), the heart needs to beat faster to pump more blood.

However, I am not aware of how does the heart automatically start beating faster.

Is there any involvement of the Nervous System?
Does the heart have some sort of special mechanism that activates when the body performs a strenuous job?

I am sure that there are many ways that your body can regulate heart rate, but I am going to cover this topic briefly from the perspective of $\ce{CO2}$/$\ce{O2}$ concentrations, and pH.

The medulla oblongata

The medulla oblongata is part of the central nervous system, and makes up the lower portion of the brain stem. It is responsible for performing autonomic functions, including the regulation of heart rate through chemoreceptors. The medulla oblongata receives its blood supply from the vertebral artery and makes both afferent and efferent connections with the vagus nerve.

Chemoreceptors

There are two main types of chemoreceptors in your cells that are responsible for regulating heart rate.

Central chemoreceptors

These are located in the medulla oblongata, and are responsible for measuring the concentration of $\ce{H+}$ ions (ie. pH). When the pH is low, neural cells with these receptors will signal the release of norepinephrine and epinephrine.

Peripheral chemoreceptors

These are located in the carotid and aortic bodies and measure the concentration of $\ce{O2}$. The receptor cells of these structures make connection with afferent nerves, to send a signal to the central nervous system in times of hypoxemia.

$\ce{CO2}$/$\ce{O2}$ Exchange

Blood is the tissue responsible for distributing chemicals around your body. It is therefore also involved in the $\ce{CO2}$/$\ce{O2}$ exchange between tissues. Blood cells use hemoglobin as as a carrier molecule for this exchange.

When $\ce{O2}$ is delivered to tissues, it will be processed by the mitochondria of the cells to synthesise ATP, and $\ce{CO2}$ as a biproduct. ATP is also responsible for muscle contractions, and so, with exercise comes an increased utilisation of ATP. With ATP stores running low, your cells will begin to use more $\ce{O2}$, and therefore, they will produce more $\ce{CO2}$.

$\ce{CO2}$ and Acidity

So, I kinda lied when I said hemoglobin is the carrier of $\ce{CO2}$. This is mostly true, but $\ce{CO2}/$$\ce{O2}$ is also somewhat soluble in blood, and this accounts for changes in blood-pH.

$\ce{CO2 + H2O}$ $\ce{<=>}$ $\ce{H2CO3}$ $\ce{<=>}$ $\ce{HCO3- + H+}$

The above equilibrium is catalysed by carbonic anhydrase, and accounts for a decrease in pH levels.

Signalling in response to pH

So your exercising, your body is using lots of $\ce{O2}$ to produce ATP. Your $\ce{CO2}$ levels have increased, and your internal pH has dropped. Now what?

Well, as I'm sure you have guessed, your nervous system takes over.

The central chemoreceptors of the medulla oblongata send an impulse to  the adrenal glands in response to the decreased pH. This signals the release of the hormones epinephrine and norepinephrine in to the bloodstream. The release of epinephrine and norepinephrine is regulated by the sympathetic nervous system. This accelerates the heart rate by binding β-receptors in your heart tissue. Efferent nerve connections from the vagus nerve also participate in this process (I think).

For mechanisms on heart contration, see here; everything following "excitation contraction coupling" is probably the most relevant.


HELP! How will pH 14 affect enzyme structure? If a substance is very alkaline/ basic, e.g. a pH of 14, does this mean that there are near to zero H+ ions (or it is possible to have such a situation where there are zero H+ ions and it is still alkaline) or does it mean there are lots of OH- ions relative to H+ ions? If so, how will this affect enzyme structure in very alkaline/ acidic conditions?

This is a very chemical explanation. Here goes.

$\ce{pH = -log[H+]}$

$\ce{pOH = -log[OH-]}$

$\ce{pH + pOH = 14}$

Therefore, at a $\ce{pH}$ of $14$, $\ce{pOH}$ is zero, so there is 1 mole of $\ce{OH-}$ and $10^{-14}$ moles of $\ce{H+}$ in a liter of your substance.


How do birds influence brood sex ratios? This paper concludes that birds can adaptively modulate brood sex ratios. How do birds modulate brood sex ratios? Are they somehow able to influence the sex of their young? Or once young are born, do they provision one sex with more food so that the other sex does not survive?

On a more general level it is possible for parents to influence sex-ratio of broods in a number of ways, and there are other reasons why a brood might have a sex ratio distortion. The paper I've been reading this morning is about side-blotched lizards doing just this. I'll give a quick basic answer just from the top of my head and hopefully someone can give some specific examples in birds.

Bias in gamete production

Assuming XY chromosome systems where the males are heterogametic (XY, females XX) the male can influence the brood sex ratio by producing more or less Y-bearing sperm. Sperm carrying an X-chromosome will always produce daughters and sperm carrying a Y- will always produce sons. The opposite would be true for ZZ/ZW where female gamete type determines the sex, they could only produce Z eggs, therefore only having sons.

Female cryptic sperm choice

A fairly modern idea is that females can selectively fertilise eggs with sperm based on the DNA they carry, this could include whether the sperm is Y- or X-bearing. This idea is thought to explain how females produce daughters from small sires and sons from large sires in the paper I mentioned at the start.

Meiotic drive and sex ratio distorters

Meiotic drive elements may be responsible for sex-ratio distortion in broods. Just like the biased sperm production this can alter the sex-ratio at the gamete level. Genetic effects mean that fewer offspring of one sex than the other are produced. Here is one example where suppressors of the distorter have evolved in the autosomes.

Direct selection by the parents

In the paper you mention above, and with most studies, it is possible that the parents are selecting which offspring to raise after they hatch (or as an egg - it may be possible to determine sex at that point) and if females are more costly to raise and conditions are poor, they may kill/neglect the female offspring early on.

Within brood competition

If one sex is stronger as a chick it possible that the broods could become sex biased in certain conditions which consistently favour one over the other.

Consequence of environmental strain

Similarly to the last two points, if conditions are poor it may be harder for one sex to reach maturity than the other which would result in sex-bias. This is the conclusion the authors in your paper seem to come to.

Environmental effects

As with some reptiles, environment can determine the sex of the offspring. For example, incubation temperature in turtles has a considerable effect on offspring sex ratio. Given how close birds and reptiles are in evolutionary time, and the importance of active incubation in birds, I don't see that it's impossible for the parent to vary some kind of environmental factor in order to bias sex-ratio.

There are certainly more potential mechanisms and some of these ideas are fairly new in evolutionary biology research so there are many unanswered questions. I hope I will have time to find some bird specific examples later.


Help to recognize spider It is unusual to see such size spiders in Lithuania, so I was wondering what kind of spider it is and if it is strong enough to bite through humans skin.
I've googled for biggest known spiders in Lithuania, but mentioned few species don't look alike - mine has way thinner legs, but I'm not an expert.
I've placed 1 euro cent coin for size - it's diameter is 16.25mm

The long hairy legs make me think that this might be a spider belonging to the Tegenaria genus, or something related.


Inoculating agar plates with microbes suspended in sterilised water? We were having a problem with our experiment (culturing microbes on homemade nutri agar) so we decided to change our set-up. It already cost us quite some money. So, we saw this procedure. Can anyone tell if this is legit? Thank you!

It would be great if you could provide more information with regards to what you have done already and what the problems were that you observed. That being said, yes, the "protocol" you found should work.

I am assuming that this is some kind of homework / school project so you don't actually need to know what organisms you are inoculating with and at what levels.

One thing I would recommend is that when you take your swab sample, wet your swab by dipping it into the sterilised water first and then swab a predefined area of about 10cm x 10cm (4in x 4in) very thoroughly before putting the swab back into the test tube. Once back in the test tubes make sure that you swirl the swab around for a sufficient length of time (~30s) and press the swab against the inside of the test tube to allow as much liquid as possible to run out of the swab. The last step is important in order to maximise the yield of bacteria, yeasts and moulds that you might find in your sample.


Relationship between our microbiome and personalized nutrition Recently, it has been asked whether there are 'metabolic types' between humans that can benefit from a sort of personalized nutrition. One answer suggested that one discerning factor could be the human microbiome. It is known that host–microbial symbiotic states might respond differently to diet and drug intake, but whether this can be useful for personalized nutrition is less clear to me. I wonder:

does the microbiome affect food metabolism? (useful for personalized nutrition)

OR

is the food that we eat affecting the microbiome? (less useful for personalized nutrition)

I know the answer is probably both, but there are examples causally demonstrating one branch and excluding the other?

does the microbiome affect food metabolism?

Most definitely (and not surprisingly). The Arumugam paper [1] notes that

The drivers of [enterotype 1] seem to derive energy primarily from carbohydrates and proteins through fermentation, … because genes encoding enzymes involved in the degradation of these substrates (galactosidases, hexosaminidases, proteases) along with glycolysis and pentose phosphate pathways are enriched in this enterotype […]
Enterotype 2 … is enriched in Prevotella … and the co-occurring Desulfovibrio, which can act in synergy to degrade mucin glycoproteins present in the mucosal layer of the gut […]
Enterotype 3 is […] enriched in membrane transporters, mostly of sugars, indicating the efficient binding of mucin and its subsequent hydrolysis as well as uptake of the resulting simple sugars by these genera. […]
The enriched genera indicate that enterotypes use different routes to generate energy from fermentable substrates available in the colon, reminiscent of a potential specialization in ecological niches or guilds. In addition to the conversion of complex carbohydrates into absorbable substrates, the gut microbiota is also beneficial to the human host by producing vitamins. Although all the vitamin metabolism pathways are represented in all samples, enterotypes 1 and 2 were enriched in biosynthesis of different vitamins […]

[All emphasis mine.]

is the food that we eat affecting the microbiome?

Yes, just as certainly. I don’t have a publication handy but it should be obvious that our food influences our gut microbiome – in the extreme case, it can kill it (consider antibiotics side effects).
[1] Manimozhiyan Arumuga, Jeroen Raes & al., Enterotypes of the human gut microbiome, Nature 473, 174–180, May 2011.


What is the maximum number of babies a human woman can have? I know you could divide the female fertility period (~40 years, right?) by 9 months which would give something like ~50 kids (with no multiple kids per pregnancy). The limiting factor in this calculation is time but is there a biological upper limit as well?

How do you define the biological limit?

It very much depends on how you define a biological limit. If you prefer, it very much depends on how you define a human! Some women are completely sterile while others are highly fertile and there is genetic predisposition to that.  How much "perfect" should the genotype of an individual be so that it is still considered as a human? There is genetic variance underlying fecundity that is important to consider. For example, in your calculation you took lifespan as a constant but it obviously is not a constant. Fecundity is reduced by all these small mutations segregating in the human populations that reduce the fecundity of any single human. There exist no human that is free from all deleterious alleles. Imagine a giant woman with 10 independent reproductive system! Would she still be a human? That was probably kind of a too extreme thought experiment. Imagine a woman that can have a reproductive lifespan of 100 years. Would it still be a human? The issue behind this question reminds me an old post (now closed, I can't find it anymore) that asked whether a leopard would run faster if it had more legs. Well... one can imagine something running faster than a leopard, but it would not be a leopard anymore. So how many changes from a leopard are we allowed to make to answer the question. So I had to chose a definition of what a "perfect woman" is. Or a definition of a woman that would set this so called biological limit.

The definition I am using to answer this question

In the below answer, I will assume that by biological limit you mean the expected fitness of a female that would live in the same environment than we live in today but would not carry any single of the deleterious locus that are segregating in the human population. In other words I assume that you accept that the "perfect woman", that is a woman that would not carry any single of the deleterious mutations that segregate in the populations will set this biological limit to woman maximal fecundity.

Mutation load Theory

The decrease in the mean fitness of an idealized population where no deleterious mutations would exist compared to the realized mean fitness of a population is called the mutation load. The mutation (in an infinite population) is a function of the genome-wide mutation rate only. Let the genome-wide mutation rate in human be $U=2.2$, the mutation load $L$ in the human population is equal to $L=1-e^{-2.2}=0.89$. The estimates are taken from this video. You may want to have a look to the video in order to have a better understanding of why $L=1-e^{-U}$ and what are the assumptions of these calculations. The main assumptions are 1) infinite population size, 2) multiplicity of fitness effects at different loci and 3) additivity of fitness effect between alleles at the same locus.

So what does mutation load theory predicts?

The above calculation means that segregating deleterious allele reduce the fitness of the average woman by 89%! If we assume that an average woman can have 10 babies (this number is just a random guess) if she wants to, then the maximum biological limit of a "perfect woman" (in a world where there is no more competition than the one in which we are living) is $\frac{10}{1-0.89}≈91$  babies!

According to wikipedia, the world record is 69 and is owned by Mrs. Vassilyev. It is reasuring to see that the observed world record (69) is lower than the the biological limit we just calculated (91). If we were to know the distribution of maximal number of babies per woman (not to be confused with the realized number of babies), we could calculate the probability to have 69 or more babies and compare this probability to the total number of females that has ever lived (or the total number of females that would have never had the idea to have so many babies). Always according to wikipedia, the world record for men would be 867 and is owned by Ismail Ibn Sharif. However, sounds possible to me (but I really have no idea) that some sperm donor may have overshoot this number today.


Exhaled air and lung capacity I wonder if there is any connection between exhaled air and lung capacity. I need to implement some algorithm in my game to calculate points of how much time you blow and compare it maybe with some sportsman.

There is.

At a first approximation the total lung capacity is the anatomical dead space(the volume of your trachea, more or less) + the tidal volume(the volume of each breath). It's slightly more complicated than that based on the differences in how deep you breathe and how often you can breathe, but at a first approximation exhaled air + half a liter(plusminus) = lung capacity.


What kind of tree is this — why do its huge leaves change shape and "grow fingers"? Edit 2: Confirmation that it's one tree!

Surrounding trees on either side along the sidewalk are completely different, and the ones on the other side of the fence are short and have rounded but far smaller, as well as thicker, dark leaves.

I've taken a 180 degree vertical "panoramic" photograph to show that there are no encroachments from trees with large leaves from behind. I've also included a few more photos of small clusters of leaves coming from a single large branch, again showing all three types of leaves.

Note some of the photos are large, and if you open them in a separate tab or window you can zoom in for additional detail.

I was riding a bike in Taipei recently (November 2017, location in google maps - more views of trees: https://goo.gl/oXPHr3) and I saw two huge leaves on the sidewalk. I stopped to photograph them and realized that they were very different shapes but otherwise looked quite similar. They are both over 40 cm long broad leaves, but while one has smooth edges and is "leaf-shaped", the other has long serrations (roughly 10 cm deep, 5-7cm spacing) on each edge.

I took some more photos of the leaves and branches of this very large tree, and one of the trunk, which looks quite gnarly.

Edit 1: I've cropped and lightened sections of two of the photos where I believe I can show examples where leaves on the same branch exhibit continuous change from smoothed edges to serrated edges. I've used 1 to denote smooth-edged leaves, 2 to denote leaves that show a few "digits" at the far end of the leaf, and 3 to denote leaves that exhibit full "digitization". In each case I think it's pretty clear that they connect to the same branch, and are not from different trees as suggested in the answer. This is strongly (if superficially) reminiscent of the sassafras leave differences.

Question: What kind of tree is this, and why do its huge leaves change shape and "grow fingers"?

It was pointed out to me that Sassafras leaves also come in different shapes with "fingers", I've included one image of those below as well for comparison.

For comparison, here's an image of Sassafras leaves with "fingers", from Landscape Plants, Oregon State University.

I'm going to take a stab here.  It looks a lot like Artocarpus altilis or breadfruit.  However, the trunk is a bit gnarly for breadfruit, but maybe that is the result of being a street tree.  Also, I can't find any reliable information about the variation in the leaves (heterophylly) for this species.  However, other species in the genus have entire leaves, so perhaps this is hybrid.  Also, Artocarpus chaplasha does show heterophylly related to light intensity and leaf position (online images suggest your tree is not A. chaplasha however).  I think the climate in Taipei is consistent with Artocarpus too.  If it's not breadfruit, I imagine it is a species from the Moraceae.  Finally, in some of your pictures it looks like there is an adjacent tree (possibly a Ficus or Clusia) mixing in -- those leaves are obtuse rather than acute at the tip.
EDIT:
I'm including one of your photos with the leaves of the tree in question circled in yellow, and what I believe to be the leaves of a different tree circled in red (in case my earlier comments were too cryptic).

EDIT 2:
Here is an excerpt of Fig 1 from Jones et al. "Morphological diversity in breadfruit (Artocarpus, Moraceae): insights into domestication, conservation, and cultivar identification" Genetic Resources and Crop Evolution vol 60 no 1 pgs 175-192 (2013) which shows the diversity of leaf morphology in Artocarpus including some hybrids.  I'm convinced you are looking at one of the species in this genus or a hybrid, and looking at the leaves in the panel for A. altilis there is considerable diversity (phenotypic plasticity) w/i that species, so that may be as close as it can be nailed down.
Finally, I can't run it but apparently there is graphical key to Artocarpus species which might be fun to try.

EDIT 3:
@uhoh has verified that all the leaves in the pictures belong to the same tree, so, it's likely we are seeing heterophylly based on the age of the leaves.  I went back to the reference above, and found this sentence would would seem to be consistent with the young leaves being entire and obtuse (and we've already established that the more mature leaves show a lot of variation): "Leaf characteristics, such as the number of lobes, degree of dissection, size, and shape can vary between young shoots and older branches".  So I think all the observations and literature point in the same direction, namely good 'ol breadfruit.


Why I don't feel pain when I press the skin on my knee and elbow? Does the muscle on our knee and elbow have some speciality ? Why are we unable to feel any sort of pain when I pinch it ? I also did it with my Mom and Dad and result was same .

There is several types of nerves in the body.
Some nerves are specialized in sensing cold or hot temperature, some other to cuts and cell damage and others feel pressure and touch.

The answer to your question is that the nerves in your elbows and knees have less pain detectors and are in fewer number, thus with they are less sensitive.

Here's a funny little poster on BBC: Can you pinch yourself without it hurting?


Do HIV particles die without host cells? When a person is on antiretroviral therapy (ART) which blocks HIV particles from infecting cells, where do those particles go? Do they die out while floating in the bloodstream? I particularly want to understand if this is the reason viral loads go down once a person starts ART.

I've learnt that our circulatory system can clear foreign matters from blood stream. Phagocytes can engulf and breakdown virions. Our liver and spleen is the blood filter system, which sequesters foreign matters all the time. So free floating HIV virions can't stay indefinitely in our blood stream.

However, without an effective adaptive immune response, these mechanisms are still unable to suppress viral replication. That's why HIV patients still have high viral load if untreated.


What kind of spider is this, please? I've found this spider in my bathroom today, never seen one like this, especially since I'm living in part of Europe ( Bosnia, Balkans ) that isn't known for being promised land for spiders. This one was somehow aggressive, when I touched him with an object, he immediately launched himself from the roof using his net, and when landed, he raised his "bottom"?! I've sprayed him with some water, and removed him as seen on picture, didn't want to kill him, but I'm interested if this is some venomous kind, because his head was blood red, and I've never seen this in my region

To me it seems to be an Araniella Cucurbitina ,also called a cucumber spider. It grows upto 4mm to 6mm. This type is native to the UK and they have venom which is not considered dangerous to humans.


What is an efficient way to spike 10-50 cells to a culture I'm trying to add on the order of 10-50 mammalian cells to a mixture of other cells (order of 1e6 cells). What is the best way to do this?

(edit) I guess this wasn't clear. I would really like to emphasize how to sort 10-50 cells to give me an precise (not necessarily accurate but that would be nice too) method of getting a desired number of cells.

If you are you working with primary cell cultures or cell lines may be you could do this when cells are in suspension, after tripsinization, mix them well with a 5mL serologial pipete in a falcon 50mL tube and plate to a 100mm2 with a final volume of 7mL. And finaly draw an eight with the plate in the hood more than 3 times to mix them well.

Edit: For the addition of 10-50 cells, count these cells with trypan blue, and do a 1:100 dilution, for example if you have 1e6 cells in 10mL you could take 0.01 mL (10 microliters) to get 1, 000 cells

And then you add the 0.01mL into 1mL of cell media to get 1 cell per 1 microliter, and then if you wanna get 10 cells, take 10 microliters, and so on


Authority on Microbiological Definitions Is there an authority on definitions for molecular microbiology concepts, like an IUPAC book for chemical definitions?

The particular definition I am debating is chromatin. Some say it encompasses DNA, RNA and protein, whilst others say that it contains DNA and only during the mitotic interphase can it transcribe to produce RNA and protein.

So in a very broad definition, yes, chromatin encompasses DNA, RNA and protein. The primary function of chromatin is to provide a method to effectively package all the DNA in a cell. This packaging is dynamic, and it's constantly regulated in a cell type-specific manner. We can see the broad interactions of protein and DNA in this cartoon representation from wikipedia:

Combined with histone-modifying complexes, and chromatin remodeling complexes, we obtain the aforementioned mode of regulation. Histone protein can be modified (acetylation, methylation, glycosylation, phosphorylation, etc.), they can also be moved, substituted in their subunits for specific pruposes (think H3.3 or H2A.X). We can also end up with varying regions of dsDNA, 10nm or 30nm fiber.

The RNA comes in as a structural and functional components of the chromatin, participating in many controls as noncoding RNAs.

I believe most of the method in defining chromatin comes in very much as the amassed literature on the subject to-date. You'd even consider it "common knowledge" entering the field (i.e. a quick google search can return you the right definition).

  "only during the mitotic interphase can it transcribe to produce RNA and protein."

Transcription halts entering M phase or mitosis, transcription may occur during G1, S, G2, or "interphase."


Snake with strange head This snake was killed in graveyard Peshawar (Pakistan). I just wonder what is this? Is it a snake? Baby crying sounds were reportedly heard from graveyard in Peshawar after months of search the sounds of baby crying were identified and this snake was killed. I have a video. I just want to know what is this?

The picture looks like it's from the Cerastes genus. It looks similar to a head shot of Cerastes Cerastes (Saharan horned viper) shown on Wikipedia:

In fact, the incident you describe is also reported in Wikipedia's Cerastes Cerastes article since it could be the first sighting in Pakistan. However, I sincerely (and respectfully) doubt that this snake was producing the "baby crying sounds". According to Wikipedia they produce a "rasping sound" when threatened.

I'm not sure that the specimen in your photograph is actually Cerastes Cerastes but the genus should be correct.


What is this mushroom? I found a singular mushroom in my back yard,  It is jet black, seems to have gills and looks somewhat like a flower do to it's upturned-ness. Sorry for not having spore colors, but I didn't want to disturb it. I will post a picture soon. I found this mushroom at 4/11/15 and it disappeared the next day. I'm just south of San Antonio.

The mushroom suggestive for one of the inki ones of Coprinus family, especially Coprinus comatus. The black color can be very intensive in some stage of their development, since it is a part of the spread mechanism.

"Members of the genus Coprinus have been collectively known as the "inky caps" because of the curious character of autodeliquescence of their gills-- in other words self-digestion to release their basidiospores. Most of these species have gills that are very thin and very close to one another, which does not allow for easy release of the spores. Moreover the elongated shape of mushroom does not allow for the spores to be shot off the basidia and get caught in air currents as in most other mushrooms. Coprinus species "compensate" for this by a sequential maturation of the spores from the bottom of the gill towards the top. After the spores have matured and been released, the gill tissue digests itself and begins to curl up, allowing easy release of the basidiospores above. In other words, the digestion opens up the fruiting body so that spores from further up the gills become exposed to the air and a clear path of spore release. The self-digestion continues until the entire fruiting body has turned to black ink. In the olden days this ink was actually used for writing. The self-digestion is also a way of releasing the spores over a longer period of time, and allowing the release of spores from very closely spaced narrow gills borne inside a longitudinally tall pileus. If any Coprinus species are collected for eating or for scientific study, they must be cooked or dried right away, since the self-digesting enzymes seem to kick into high gear after the mushroom is removed from its substrate. They're pretty easy to find too-- the genus name Coprinus gives you a pretty good idea where to look for these mushrooms-- in dung or very rich organic soil."

examples:
1.

2.

3.


What is this bird - sound attached - (Atlanta Georgia)? We live in Atlanta Georgia (northern suburb) & this bird starts singing in the middle of the night !!

And goes on for almost 2 hours without stopping.

Here is the link to it :

https://drive.google.com/open?id=0B3WzrpCj4uKeQ3l5MnJPY1RfcUpiVzkxRHBsWEN4RnYtTlNB

Any way to politely ask him/her to stop singing at night ? :)

Would highly appreciate any help in this regard !

It sounds like a Chuck-will's-widow; click the "sound" icon in that link for the song. They're native to Georgia and sing interminably at night, so the story checks out.


Found this bug in my apartment in New York. Does anyone know what it is? It was around 2-4 mm in length.

It's probably just the second instar (nymph) of a cockroach (Periplaneta americana).

Compare with this image of the instars:

Source: http://entnemdept.ufl.edu/creatures/urban/roaches/american_cockroach.htm


How do you know which organisms are keystone species? I know that keystone species are those that play a crucial role in an ecosystem, but since all species are interdependent upon each other and each occupy their own niche, aren't they all important?

How do you know which organisms are keystone species?

According to the wikipedia page, a keystone species is:

  A keystone species is a species that has a disproportionately large effect on its environment relative to its abundance.

Thus, you could work out the keystone species in an ecosystem by sampling population size and and what size 'effect' the removal of the species from the ecosystem would have. If you standardised the units of 'effect' for all species in the ecosytem, the keystone species would be those with the highest effect/population fraction. I don't know if there's a critical size of this fraction for a species to be determined 'keystone', but if there is it would allow you to explicitly define a keystone species. This would rule out the problem of interdependency as you mention.


Why do children prefer sweeter foods? As we get older, we tend to lose our sweet tooth and become more tolerant to bitter foods, like vegetables. However, I never understood how this works. Why is it that children prefer sweeter foods, even some that adults may consider "too sweet"? In fact, is there any reason they would also dislike bitter foods, even when they can be beneficial to their health?

This just seems bizarre to me that the body would start out craving sweets and lose this later on. Are only humans like this? Is there anything suggesting that younger animals prefer sweet foods too, but like them less as they get older? Does this have any biological advantage or is it just random?

@Colombo explains one reason that I think is obvious. However, there has been some research done on this.

One other reason is because it would provide an evolutionary advantage in environments where calories are scarce. Also, sugar actually acts like a pain reliever. Studies show that giving sugar to babies and children during surgery act like a pain reliever.

The sweet tooth could be controlled by hormones secreted from the growing bones. Some common hormones like insulin also affect sensory centers in the brain. This explains why the sweet tooth goes away as an adult.

Reference

NPR -http://www.npr.org/sections/thesalt/2011/09/26/140753048/kids-sugar-cravings-might-be-biological


Why does the T7 RNA Polymerase require a reducing environment ie. DTT Every bloody protocol suggests adding in DTT when doing in vitro RNA transcription. Why? The rationale seems to be that the cytoplasm traditionally has a reducing environment but as the only protein we care about is the T7 polymerase, why is this necessary.

A quick search on T7 cysteines gave some clues:

  Bacteriophage T7-induced DNA polymerase is composed of a 1: 1
  complex of phage-induced gene 5 protein  and Escherichia coli
  thioredoxin. Preparation of active  subunits in the absence of
  sulfhydryl  reagents  indicates  the reduced form of thioredoxin  is
  sufficient for formation of  the  active holoenzyme. The oxidized
  form of  thioredoxin, thioredoxin modified  at  one  active  site
  sulfhydryl by iodoacetate or methyl iodide, or thioredoxin modified
  at both  active  site  sulfhydryls  by N-ethylmaleimide,  are  all
  inactive,  being  defective  in  complex formation with  gene 5
  protein.

Adler and Modrich, J Biol Chem 258:6956 (1983)

There's a more recent paper (Aguirre et al, Inorganic Chemistry 48:4425 (2009)) that mentions the "the enzyme critical sulfhydryl cysteine groups", but unfortunately I only have access to the abstract.

Update: It seems to be an old finding, rather than a rationale concerning the cytoplasmic redox state. According to Chamberlin and Ring, JBC 248:2235 (1973),

  General Requirements-The general requirements for T7 RNA
  synthesis directed by T7 DNA polymerase are shown in Table
  I. As expected for a template directed polymerase, RNA
  synthesis shows an absolute requirement for DNA, the 4
  ribonucleoside triphosphates and Mg++.

(no surprises there ;)

  The activity of the
  enzyme is reduced significantly if a sulfhydryl reducing
  agent such as b-mercapto-ethanol is omitted from  the
  reaction. The addition of 10^-5 M p-hydroxymercuribenzoate to
  the assay system in the absence of b-mercaptoethanol
  abolished all activity, indicating that the enzyme contains a
  sulfhydryl group necessary for activity.

However, if you see the table I, the remaining activity after removing bme is still 74%

There seems to be 7 exposed cysteines (Mukherjee et al, Cell 110:81 (2002)), but I could not find any paper discussing their roles.


How do amino acids become attached to tRNA? Is there a protein that catalyzes this or does it happen spontaneously?

In which part of the cell does this happen?

The process to which you refer is called tRNA charging and is catalyzed in the cytosol by a class of enzymes called aminoacyl tRNA synthetases.


Is there a biological basis for race (re: Nicholas Wade's article) I just recently read this article by Nicholas Wade on Time Magazine's website about a biological basis for race.  It all sounded very racist, but of course my Western liberal attitudes about racism shouldn't cloud my stronger Western liberal convictions about Science giving every empirical claim a fair hearing.

So, that said, where can I learn more about the evidence supporting and contradicting this view?  I found on his Wikipedia page that a number of scientists have condemned his work, but I'd like to actually know the evidence and arguments underneath all this.

I suppose I should also ask more generally about the state of biological evidence for the reality of race.  I had heard in college that there is no biological basis for race, but I'm wondering if that is an out-dated view in light of recent work in genomics.  I read this stack exchange question but it had more to do with whether there is a consensus rather than on the arguments surrounding the issue.

I think it's best if you check out Wikipedia article on Race. Race is not a taxonomic term. In a nutshell, you can't define it in a useful way that has anything to do with the usual associations of the word, or gives it a practical value in science.

The problem with arguing about the existence of races in humans is that this is an argument about a word without an agreed definition, so there's never a true or false. This author is merely making some controversial extrapolations from quite obvious biology: Of course human genomes change over time, and it is also possible to an (impressive) extent to trace genetic lineages geographically. Of course there are subgroups that share a small set of characteristics not found in the rest of the human population. Some of these subgroupings are for example medically relevant.

Essentially, "race" ends up a loosely defined term that has something to do with subgrouping a species based on whatever criteria chosen. The reason why it's not a useful word to argue about in humans is because whatever subgrouping you might make, and for whatever purpose you are subgrouping, there are better, more meaningful (and quite importantly, less controversial) terms to describe those subgroups.


Vaccination and Immunisation Why are oral polio vaccines advantageous over the killed ones?  I was told that the orally given polio vaccine prevents infection by causing intestinal immunity. How does it do that? Also, how does this make it superior over the intravenously injected polio vaccine?

Oral polio vaccines are delivered in the site of the potential infection. You may think about them as about a realistic simulation of the infection. As it is not scientifically sound explanation, please see the answer about whether intramuscular vaccination leads to intestinal IgA secretion which protects against intestinal route of infection.
Oral polio vaccine (Sabina) contains attenuated (alive but weakened) polio virus, which can proliferate and compete in the environment with the really dangerous wild polio virus. That way also people which has not been  directly vaccinated may be protected - both by development of immunity after less severe infection, and by reduction of exposure to the wild virus.
The route of delivery is much more acceptable by children.


Klenow fragment does not seem to have 5->3 exonuclease activity, but it can still displace nucleotides in front of him - How? Klenow fragment does not seem to have 5->3 exonuclease activity, but it can still displace nucleotides in front of him - How? How would this displacement mechanism differ. My first guess is that exonuclease activity actually digests upcomming strand into single nucleotides, but how come the displacement activity not get in the way for lab work? :
"The 5' -> 3' exonuclease activity of E. coli's DNA polymerase I makes it unsuitable for many applications. "

Why doesn't the 5->3' displacement activity make the applications troublesome then? What would those applications be.

I've spend a long time looking for these answers, but unfortunately I've found nothing.

Maybe someone has any idea:)

Cheers!

References:
Image - http://www.vivo.colostate.edu/hbooks/genetics/biotech/enzymes/klenow.html

Generally, the New England Biolabs website is a great resource for this sort of information.  Maybe you already know this: Klenow fragment is widely used in molecular biology today. The broad use of Klenow fragment is because it will remove 3' overhangs, thereby 'polishing' or 'blunting' the DNA.  See the famous cloning techniques manual for additional information.

It is a polymerase, though, and it does perform 5-->3' elongation in the presence of dNTPs.  (sidenote: Klenow was initially used in polymerase chain reaction (PCR) development, and later replaced with heat-stable Taq pol.)

The so-called 'strand displacement' activity of the enzyme allows the 5-->3 elongation of the new strand to occur even in the presence of an existing, annealed strand ahead of the advancing polymerase, as you say.  This may seem problematic at first glance, but the job of polymerase is to make a complete, templated copy of DNA -- that is why reseachers use it, and that is its job in nature too!  Stand displacement is really convenient for scientists when using random primers, for instance.  The DNA polymerization can continue unimpeded despite the presence of a 'downstream' barrier.  This is also why not having 5'-->3' exonuclease activity is helpful in this context.  (sidenote: pol I is not the main replicative polymerase in E. coli. and its discovery is one of the great stories of post-war biology).

I hope this addresses your question(s).


Do histones constitute the largest proportion of the protein in chromosomes at mitosis? Do histones contribute more (by mass) than non-histone proteins in the chromosomes formed during mitosis?

If you are asking if histone mass represents a larger percentage of total chromosome mass then the answer is yes when considered at the level of the nucleosome. Each histone-octamer wraps ~147 base pairs of dna around 1.7 turns. The histone-octamer consists of  two copies of each of the four structural core proteins (H2A, H2B, H3 and H4). The sequence encoding for H2A histone family member B1 (H2AFB1) is 517 nucleotides long (RefSeq). Based on nucleotide length alone and inferring a consistent contribution to mass from nucleotides at the single base level and in triplet at the amino acid level, each nucleosome should be roughly 95% histone by mass. But this doesnt account for stochasticity in the mass and density due to DNA-methylation and to heterochromatin and euchromatin along the genome, respectively.

Consider DNA methylation, these features represent a non-zero contribution to total chromosomal mass that would decrease histone mass as a portion of the total and would not be considered if whole genome sequencing of a single organism was employed to answer this question at the genome level for a single sample. Now consider histone acetylation, this is another feature that represents a non-zero contribution to mass but swings the pendulum in the other direction. Beyond a local calculation at the nucleosome level this relationship would be nearly impossible to quantify.

During replication specifically, histone translation seems to be as tightly regulated as DNA replication.

Ma Y, Kanakousaki K, Buttitta L. How the cell cycle impacts chromatin architecture and influences cell fate. Front Genet. 2015;6:19. Published 2015 Feb 3. doi:10.3389/fgene.2015.00019
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315090/

nature has a great open source overview related this topic.

https://www.nature.com/scitable/topicpage/chromatin-remodeling-in-eukaryotes-1082


Resolution of X-ray crystallography A structure determined by X-ray crystallography has a resolution of 1.5 Å. When I look at the coordinates, I find every backbone C-N distance is 1.32 Å.i.e. Accurately predicted. If resolution is not good why every C-N bond distance is accurately predicted?

The structural model of a protein is obtained using both experimental data and prior knowledge about geometry of macromolecules. As a structural model is refined, interatomic distances are also restrained. So, the C-N distance isn't really predicted. Alternatively, knowledge about this distance is used to construct reasonable model.

In response to the comment below I'll cite Rupp's Biomolecular Crystallography, the most comprehensive book on this subject. Refinement and restraints are covered in Chapter 12, Model building and refinement.

  An observation does not have to be an experimental observation
  (measured data) specific to the particular structure, but can be any
  type of general prior knowledge regarding molecular stereochemistry.
  Known stereochemistry can be exploited and implemented in
  macromolecular refinement in the form of geometric constraints and
  restraints. [...]

  We know from accurate and precise small molecule and peptide fragment
  structures [...] that bond lengths and bond angles show distinct and
  relatively narrow distributions around their mean positions. [...]

  Refinement programs read restraint target values specific for each
  residue and each ligand molecule from restraint library files, which
  are subject to continuous empirical update.

The value given in this book (Table 12-1) for peptide bond C-N is 1.336 Å with variance 0.023 Å.


Why is xylem a tissue and not an organ? My textbook "CGP AS-Level Biology Exam Board: Edexcel Complete Revision & Practice" says xylem is a tissue.

Then I read from this website that "[Xylem's] major components include xylem parenchyma, xylem fibers, tracheids, and xylem vessels." Therefore, from my understanding, xylem is made up of multiple tissues including xylem parenchyma tissues, xylem vessel tissues and etc to carry out the functions of transporting water and nutrients in plants? Therefore that would make xylem an organ instead of a tissue?

In plants, there are three types of tissue: meristematic, simple, and complex.

Meristematic (embryonic and totipotent)

Simple (composed of only one type of cell), such as

parenchyma
collenchyma
sclerenchyma

Complex (composed of more than one type of cell), such as

dermal (protective covering)
vascular (conducting tissue)
xylem (conducts water and dissolved minerals)
phloem (conducts water and dissolved organics)
ground (bulk of the body; primarily parenchyma, collenchyma &
sclerenchyma)

With this information in mind, let's take a look at what the source you provided says that makes up Xylem tissue.

  "[Xylem's] major components include xylem parenchyma, xylem fibers, tracheids, and xylem vessels

Here are the roles of said cells in Xylem:

Xylem parenchyma are cells specific to storage and short distance transport.
Sclerenchyma Cells (xylem fibers) are specific to support and protection.
Vessel Members (which are conducting cells) are specific to water, mineral transport, and support mostly in advanced angiosperms.
Tracheids (which are also conducting cells) are specific to water, mineral transport, and support mostly in gymnosperms and lower angiosperms.

I hope this information helped you understand why Xylem is not an organ, but rather a complex tissue of plant.

References:

http://facweb.furman.edu/~lthompson/bgy34/plantanatomy/plant_cells.htm

http://www.bio.miami.edu/dana/226/226F09_5.html


Is there a measure of human genetic variation, where human genetic variation can differ more than 1%? According to this

Neardenthal genetics

  The proportion of Neanderthal-inherited genetic material is about 1 to
  4 percent[12] [later refined to 1.5 to 2.1 percent[11]] and is found
  in all non-African populations

And according to this

Interbreeding between archaic and modern humans

  Neanderthal-derived ancestry is absent from most modern populations in
  sub-Saharan Africa

Now, human genetic variation is usually said to be between 0,1% to 0,5%

Genetics

  While the genetic difference between individual humans today is
  minuscule – about 0.1%, on average

Why are the genomes of humans 99,5% the same

  Human's DNA sequence is said to be roughly 99.5% equal

But here,

Human genetic variation

There are at least 6 different ways to measure human genetic variation and

  human-to-human genetic variation is estimated to be at least 0.5%

Does this last affirmation and the first two articles tell us that the difference in human genetic variation, according to some measures of variation, it's actually more than 1% ? (larger than some ways to measure our genetical differences with other animals like chimps for example that are usually mentioned to highlight our similatiries) Or are there things missinterpreted in all this?

The question makes it clear that the poster is aware of the different ways of estimating human genetic variation, and he is also no doubt aware of the fact that Wikipedia is written by “people like you” who may not be experts in the field or have updated an old entry based on limited data. Let me address what appears to be the cause of confusion in this question — certainly in other questions on this topic.

For simplicity let us take a suitable round number for the Human/Neanderthal relatedness. Then the poster’s first quotation can be simplified as:

  The proportion of Neanderthal-inherited genetic material in modern Europeans is 2%.

and his second quotation simplified as:

  Neanderthal-inherited genetic material is absent from modern Africans.

A common conclusion drawn from this is:

  The genetic variation between modern Europeans and Africans must therefore
  exceed 2%, rather than being only ca. 0.5%.

Why is this wrong?

This conclusion is wrong because the 2% and 0.5% are measures of different things.

For simplicity, a value of human genetic variation of 0.5% can be regarded as the extent by which the DNA of the coding regions of the genes of two humans differ because of single nucleotide polymorphisms (SNPs) — single base changes in the same gene (that may or may not affect the gene function). This assumes all humans have the same 20,000 or so genes.

Now let us make an overall comparison of the genes of humans and Neanderthals. Since they diverged from a common ancestor their genomes underwent changes due to point mutations, but, as far as I am aware, they maintained the same set of genes. Even if I am wrong on this latter point, the vast majority of genes — and the ones that we are concerned with are common: they both have/had a gene for myosin, for hexokinase 1, for chymotrypsin etc.

Examination of the majority of such homologous genes reveals single base differences, which must have arisen since the divergence. A combination of such Neanderthal variants in one gene — never seen as human SNPs — and the converse situation allow one to designate a chymotrypsin gene, for example, as human or Neanderthal, even though the overall DNA sequence of the chymotrypsin gene may be 95% identical (to conjure a figure out of the air).

Now consider the European/Neanderthal comparison. It turns out that a small number of genes show no (or almost no) variation between the two, but that most of these show the standard ca. 95% difference between Africans and Neanderthals (and hence between Africans and Europeans). These, then, are the 2% of genes that arose from interbreeding of Europeans and Neanderthals, after the exodus from Africa.

But 2% of genes of different origin which still retain 95% sequence identity would only add 0.1% to the modern human variation, cited at ca. 0.5%.

Disclaimer

I do not know the actual extent of variation between most human and Neanderthal genes or the details of the non-African genes of Neanderthal origin. I will be happy to edit this answer if anyone has that detail. I apologize for the geographical generalizations not present in the question, but my concern was to convey the argument without burdening it with continued qualifications.


What do biologists mean when they use the term "biological distance"? Here is its usage.

"there is sufﬁcient genetic control to make nonmetric traits useful in anthropological work, and such variables have successfully assigned individuals from distinct geographic regions to their correct groups (for example, ... As such, nonmetric traits are an appropriate means for studying biological distances"

Source:https://www.academia.edu/5201951/Sahara_Barrier_or_corridor_Nonmetric_cranial_traits_and_biological_affinities_of_North_African_Late_Holocene_populations

Biological distance is pretty much what you'd guess: how closely related are x and y based on genetic (phenotype or genotype) studies?

There is zero biological distance between identical twins. There is extremely little biological distance between family members (for most intents and purposes, none, no matter where they live). It goes on and on in this manner.

  Biological distance, or degree of genetic relatedness, will be assessed by a comparison of dental nonmetric trait frequencies.1

The phrase has been used in Theoretical Population Biology for decades. Back then, they had phenotypes to measure the degree of biological distance.2 Today, actual genetic determination of kinship is possible.

  Biological distance, or biodistance, is the measure of biological relatedness (or divergence) between and within human groups, living and past, based on human skeletal and dental variation.3

1 Dental Variation of Prehistoric Amerindian Populations
from Eastern Tennessee
2 Kinship, information and biological distance
3 Biological Distance in Bioarchaeology and Human Osteology


What kind of bug/insect is this? photo attached This morning (a few hours after sunrise) I saw this insect running over the blanket.
I'm thinking what it is, if it's a bed bug that missed feeding time and is out of schedule (as i thought that they come out just before sunrise). And I thought they were brown, too but upon research found that they could (colorwise) look similar to this one too. Also, I have not found another one of these and my wife and I both don't find any bite marks on our bodies.  Our matress is packed in a plastic hull to not allow bed bugs to start living in it. What might this be?
Thanks!

I have a doubt we can answer this question with a high level of accuracy: the sample image is very blurred, it is unclear if there are posterior/lower body elements like forceps as well as other significant features which could help with the identification.

My best guess it is baby of Earwig (2000 species): If I look at the posterior part of the body I can "see" the preliminary forceps as well as other similar features, but still the accuracy of the ID is limited.

Enhanced image:

Baby Earwig:


If a gene is missing from an operon that structures a protein, then would that protein not be made properly? From my understanding, operon is a series of genes that are regulated by a single promotor. In many cases genes in an operon form subunits of a protein.

I obtained a genome in my study and looked for genes that constitutes part of a metabolic pathway, and ended up finding that one of the genes in an operon was missing.

Does that imply the protein made from those genes in the operon will not be made properly or other genes will compensate for the loss?

From my understanding, operon is a series of genes that are regulated by a single promotor. In many cases genes in an operon form subunits of a protein.

Genes in an operon can code for protein subunits, but they can also code for separate proteins. Often an operon will have a few genes responsible for one core function, with other accessory genes that may help regulate or enhance that function is some way. Sometime genes are fused, combining multiple subunits into a single gene. In other cases, subunits can have related functions in the absence of other units.
For example, The ArsAB complex uses ATP to pump arsenic from bacterial cells, conferring resistance. But many bacterial Ars operons lack the arsA gene. Minus this subunit, the ArsB transporter still functions to efflux arsenic from the cell, just less efficiently, harnessing the proton motive force instead of burning ATP.

... ended up finding that one of the genes in an operon was missing.
Does that imply the protein made from those genes in the operon will not be made properly or other genes will compensate for the loss?

If the gene is truly missing, it's can't be transcribed, and the subsequent protein can't be made, but the remaining genes will probably still work. I would start by asking what the operon's function is, and then consider whether the missing gene is essential for that function (hint: If it's missing and the rest of the operon is still there, it's probably not essential). If it is essential, then consider whether it's truly missing. Are there other open reading frames in the operon that could encode something with similar function? Could the organism have multiple copies of the same operon (possibly found on a plasmid)?


What are the ants underneath leafs in my garden doing? So a few days ago I spotted a couple of ants underneath some leafs of a major branch of a tree in my garden. Yesterday I had the impression the amount of leafs being occupied by ants has increased a lot what then made me curious. So I spent quite some time yesterday observing one of the minor branches the ants had been very active on by that time. What I figured so far:
Underneath each leaf the ants are gathering, is an insect that looks sort of similar to a fruit fly (gonna call it fruit fly for simplicity, despite it certainly is something different).
Around that insect are varying amounts of dots, which could be eggs or larvae. The ants seem to collect something from the larvae and also seem to be interacting with the fruitfly.

At some point I spotted on the far end of the minor branch 2 living fruitfly. They seemed to be not capable of flight despite having wings. So I concluded they must just have been hatched. They seemed to try escaping the branch, as they pretty directly were just running up all the branch. Having almost made it from the minor to the major branch, the 2 fruitfly came across an ant, which immediately attacked both of them on contact. I was expecting the ant to carry them away then. While being attacked, both fruit fly tried to hide in the attatchment point of a leaf. The ant was circling around the attatchment point of the first fruitfly I was wondering why it did not carry that fly away, since it could clearly geto to that fly. After roughly a minute the ant turned back to their hide, having fully ignored the second fly, after attacking it once, and also leaving the first fly motionless at the attatchment point it was trying to find cover in.
But what happened a few minutes later is what left me astonished.
A few minutes after the 2 fruitfly had been attacked, roughly at the same time, they started moving again. But different then before (kinda looked as if they had been injured but not killed by the ant). They did not seem like trying to escape the branch anymore. But just slowly moving to the next leaf in range continuing for 1 to 2 centimeters going underneath the leaf and then stopping there. Pretty much being in a position, as a fruitfly is positioned underneath the other leafs, where the ants are gathering .
After like 4 or 5 hours 1 ant for the first time scouted the leaf these 2 flys went on. And in fact, other than attacking them again, this ant interacted with the 2 fruitfly1 like the ants under the other leaves interact with the fruitfly positioned on those leaves.

By now (over 12 hours later) the 2 fruitfly are still there I just checked and the small fruitfly that was only being attacked once, disappeared. The other one still being at the very same spot it moved to yesterday, tho. I would consider them being dead. But I am not even sure about that.
So what exactly are the ants I observed there doing?
If any other pictures would be helpful ask for it, I can take them later today.
Also I have a speculation what it could be that was going on here, but not sure if that would anyhow improve this OP.
Oh, since I can't identify the species, it might be useful to know at least: this is happening in Bavaria - Germany

1 well with 1 of them, the other that had just been attacked once, was simply being ignored

From what you described, it seems to me the "fruitflies" are aphids and the ants are farming them. This is a widespread and common phenomenon known as ants-aphid mutualism.
P.S.
I elaborate a bit. Aphids feed on plant sap, rich in sugar, which they don't digest completely. The excretions (poop) are thus still rich in sugar (you may have noticed how your car windows get sticky sometimes under tress - that's aphids poop, I believe). Some ant species co-evolved with particular aphids and collect their excretions, a valuable sugary energy source. In turn, ants protect aphids from predators and they move them around to cover other good plant spots for aphids to suck sap and even move them to different plant individuals. This mutualistic interaction between aphids and ants is quite common and causes a lot of economic losses to the agriculture sector.
The behavior you observed of an ant attacking aphids was probably more the ant checking them and trying to evoke a pooping response. Sometimes they get them between their jaws and carry them around. Aphids also have quite complex social structure, with an optimal spatial organization. Hard to say if ants are moving them around to reach this optimal "farm density" or for other reasons.
TL;DR ants farm aphids as humans farm cows. When ants interact with aphids they are mostly checking them and trying to get their sugary poop.
/Emilio


Is there a difference between any of these terms for proteins: "crystal structure," "NMR structure," "solution structure," and "complex structure"? My homework wants me to plot all crystal structures determined per year, but when I search on PDB for all structures, many of the articles say "crystal structure," but some say "solution structure" or even "complex structure." Are all of these considered to be subsets of "crystal structure"?

Depending on who you talk to (typically laymen and scientists who are not structural biochemists), the term "crystal structure" is frequently taken to mean "some determination of molecular structure, whether by actual crystallography or some other means".

For example, a graduate student is talking to her adviser, an immunologist, about the structure-function relationship between a certain viral capsid protein and the peptide antigens they are using to create families of antibodies to the virus. The adviser consistently refers to the recently-published "crystal structure" of the protein, even though the actual study was performed using a combination of NMR spectra obtained from solution, electron microscopy, and quantum mechanical computational chemistry modeling techniques, and no crystals were actually studied.

So, you probably want to talk to your teacher/professor and clarify what s/he is looking for. Most likely, if you're in some sort of undergrad or first-year graduate class, they're just looking for "structural determination" in general, but they may specifically be looking for those models that were generated using actual crystals, so asking is always best.

I should note that there are significant methodological and computational differences when determining structure via X-ray crystallography, various types of NMR, electron microscopy (with or without crystals as the target), so-called "complex" determinations, etc. Find a structural biologist to learn much, much more.


Identification of snake Can someone identify this snake? Photographed in a home in Los Lunas, NM, USA.

Check out the Desert Kingsnake (Lampropeltis getula splendida).  It is native to New Mexico.

Source: Desert Kingsnake (wikipedia)


Is the masking effect of sound related to action potentials or to mechanical aspects of hearing? I am an applied mathematics / signal processing engineer who wants to learn more and I have a question that has been bugging me for some time. It is known in audio coding circles that human hearing is masked both in the frequency and temporal domain. This means that when two sounds of almost the same frequency are presented, the loudest will overshadow the weakest for short periods of time.

I was thinking that maybe here on Biology.SE I can get some explanation of this phenomenon. Is this masking effect caused by properties of human neurons, or is it mediated by processes earlier than the neurons, i.e.., due to the mechanical aspects of hearing while the sound is entering the ear and hitting the eardrum, or one of the tools behind the drum?

Short answer
Both - masking occurs through neural effects, as well as via mechanical effects in the inner ear.

Background
First off, there are basically three types of masking, namely simultaneous, forward and backward masking.

Simultaneous masking experiments are the most basic and likely the most widely used. The most basic type of experiment is listening to tonal stimuli in static (white) noise. In this case, the inner ear is busy processing noise and acoustic probe stimuli (tones) are not perceived by the subject, while loud probe stimuli are noticeable. A more relevant test for everyday functioning is the speech-in-noise test, where speech stimuli are presented in noise. It appears that hearing loss causes folks to have impaired hearing in noise. The amount of impairment in speech understanding in noise exceeds by far the simple decrease in hearing sensitivity. Anyway, I'm drifting off.

Forward masking experiments present a masker before the probe.

Backward masking experiments present the probe before the masker.

To take a step back - the auditory system consists of the peripheral end organ, namely the hair cells in the inner ear (Fig. 1). Those hair cells translate acoustic physical stimuli into electrical currents. These are currents are fed to the spiral ganglion cells in the inner ear. Their axons bundle up in the auditory nerve which innervates the brain stem and ultimately the auditory cortex in the brain.

Now - forward masking experiments are generally regarded to target the peripheral structures, while backward masking experiments target the central structures at a higher level.

Peripheral masking effects occur at the level of

the basilar membrane (e.g. Zwicker (1977)
the auditory nerve (e.g. Stronks et al. (2012)

The basilar membrane is the structure that mediates the (traveling) wave that sounds generate and that traveling wave is the very basis of the frequency analysis in the cochlea, akin to a place-dependent Fourier transform. It is the basilar membrane that separates frequencies from high at the base to low frequencies in the apex due to its physical properties. Now, when the basilar membrane is busy moving in response to a masker presented at 1 kHz at 100 dB SPL, a probe tone of 1 kHz presented at hearing threshold (0 dB HL) will be totally swamped, simply because the amplitude of basilar membrane movement will be changed by next to nothing.

The auditory nerve is also an important neural site where masking occurs (e.g., Stronks (2010). This has to do with the fact that neurons fire action potentials. After a neuron has fired an action potential, there is an absolute refractory period that takes several ms to resolve. In that time, ion channels previously engaged in firing are re-opened and up and ready for the next action potential. Within the absolute refractory period, no stimulus, whatever its strength, can evoke another response in that neuron. Following that, a relative refractory period follows in which its firing threshold is increased, but strong enough stimuli can evoke a response. If a neuron is busy firing after chronic stimulation, it gets tired and a state of adaptation follows. Further stimulation results in fatigue, in which the neuron gets tired and has exhausted its resources to fire. All these processes can result in masking of simultaneously presented stimuli (simultaneous masking), but notably also in stimuli presented after the masker has subsided (forward masking).

Now, all these processes will not affect backward masking, where a short probe stimulus is swamped by a following masker (e.g., Oxenham & Moore (1995). This is caused by more central, higher-level processes that include attention processes, i.e.,

the brain

In other words, the following masker distracts the attention of the subject that in turn fails to notice the probe. It's thought to depend on central processes as peripheral processes can't be 'fooled' and faithfully transmit the stimulus to the brain, whatever comes next.

Fig. 1. The inner ear (cochlea) features hair cells that are actiovated by sound waves traveling through the basilar membrane. source: Modesto Junior College

References
- Oxenham & Moore, JASA (1995): 98; 1921
- Stronks, PhD thesis, 2010, University of Utrecht
- Stronks et al., Otol Neurotol (2012); 33: 35-42
- Zwicker, JASA (1977); 61: 1031