text:
plant crossing for creating breeding population
I read some material about plant breeding. For a self-incompatible plant with high heterozygosity, it said that after selecting the plant population based on phenotype/desired trait, a cross was done among plant with the desired trait to create the breeding population. However, as far as I know, the breeding population was usually phenotypically selected for desirable traits. I'm not experienced in this field, could you please kindly explain to me why crossing is conducted for creating breeding population?
Thanks in advance

Here, self-incompatible here means that the plant has both anther and pistil, but need pollen of another plant for pollination.

A cross was done among plant with the desired trait to create the breeding population. The breeding population was usually phenotypically selected for desirable traits.
That phrase is confused. To phenotypically select from a breeding population, you first have to generate the breeding population, which requires an initial cross of desired plants. The generations are generally labelled as F1 F2 F3 and checked for statistics. They can back-cross the mother plant onto herself. The selection refines itself as the number of crosses of the most desirable plants increases in generations.
Hybrid populations are often stronger and have a wider gene base, so if you want big fruit for a tree, you can cross an asian one with a european one, it might be more resistant and vigorous, gain stronger roots, better low N performance, and better structre from one plant, which is then mixed with the desirable traits for example of yield or mould resistance. The wider the gene base, the more potential diversity of individuals can be chosen which also contain the alleles from the desired traits, and the selections start with more options. The goal is to maximize the desired pheno's.
http://www.nature.com/nature/journal/v537/n7622/full/nature19433.html?foxtrotcallback=true

What do you call a gene base? Note that definitely not any cross result in hybrid vigour. Some causes hybrid depression.

And in OP it was already said that the initial population before breeding had a high level of heterozygosity?


text:
The source of ABA for inducing stomatal closure in the detached leaves?
As you may know, when leaves detached from the whole plant close their stomata to maintain water and prevent wilting. Could you please let me know what is the mechanism of stomatal closure in the detached leaves? if it is induced by ABA, what is the source of ABA under these conditions?
Please provide me the corresponding links for your answers as I couldn't find an appropriate answer for the question.
Thanks

I think that ABA could be one of the player involved on the stomatal closure in detached leaves. In fact originally it was think that ABA is the main player on abscisic leaf but this in correct only for a small number of plants. Moreover ABA is produce in terminal buds to slow down the plants growth and prepare it for the winter (it is also produce in response to water depravation by roots). So probably ABA could also migrate in leaves and provoke the stomata closure.
This is what wikipedia suggest by looking on Abscisic acid.

ABA was originally believed to be involved in abscission. This is now known to be the case only in a small number of plants. ABA-mediated signaling also plays an important part in plant responses to environmental stress and plant pathogens [...].
Abscisic acid owes its names to its role in the abscission of plant leaves. In preparation for winter, ABA is produced in terminal buds.This slows plant growth and directs leaf primordia to develop scales to protect the dormant buds during the cold season. ABA also inhibits the division of cells in the vascular cambium, adjusting to cold conditions in the winter by suspending primary and secondary growth.

By digging more on internet I found that abscission (the shedding hence the dropping of the plant leaves) occurs after the senescence of the leaf. In fact, before the leaf falling, the plant draws resources out of leaves and degraded the chlorophyll. This will cause also the change of colour (the leaves are green thanks to the presence of chlorophylls).
Finally I think that the stomata closure is also due by the darkness and the senescence. In fact the open or close state of stomata is mediate by guard cell and their state (swollen guard cell stomata is open, shrunken guard cell stomata is closed. Those state are influenced by Temperature, Darkness, Photoperiod, pH and also ABA. Hence when the plant start to take out nutriments from leaves, on leaves there will be a rise on pH and a diminution on water contents that will provoke the closure of stomata. Those two image could maybe help 3.

Hope my answer will help.

source: Stack Exchange

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sort: votes


text:
Background selection and hitchhiking effect
As I read the maintenance or removal of an allele from a population is dependent upon the alleles in its linkage group; so, when an advantageous mutation occurs in the population, variation in nearby alleles that linked to that mutated allele is reduced to fix (maintain) the mutated allele in the population (hitchhiking effect). This is true for deleterious mutations and background selection. But, I cannot understand how background selection can remove the deleterious mutation from the population? Could you please kindly explain to me about it?
Thanks

can you clarify your question at all?  The focal, deleterious mutation is being removed by plain old natural selection (e.g. it would be removed even if it were on a chromosome by itself, unlinked to anything else). "Background selection" is the term for the loss of diversity/alleles in the linked region around the deleterious allele.

The phrasing in your question is a little unclear which makes it hard to know exactly what is unclear to you. But I'll give it a try hoping that it helps.
Background selection (BGS) is the process by which deleterious mutations reduce genetic diversity at nearby loci. When you say

I cannot understand how background selection can remove the deleterious mutation from the population

I would like to highlight that BGS does not remove the deleterious mutations per say. BGS is caused by deleterious mutations and has for consequence to reduce genetic diversity whether this diversity represent any variant for fitness.
An easy way to get an intuition of this effect is to think of the effective population size. In a Wright-Fisher population, where all individuals have the same probability to reproduce, the effective population size is equal to the population size. Imagine now that half of the individuals in the population carry a mutation that make them completely sterile. If this is the case, then the effective population size is reduced to half the population size. As the effective population is smaller, so is the genetic diversity. Hence, deleterious mutations (and fitness variance in general) reduce the effective population (in comparison to the actual population size).
Now, a single deleterious mutation that disappears in the next generation will affect the entire genome equally. However, repetitive deleterious mutations at specific loci (conserved regions) that stay around for a few generations will affect the effective population size at this region more than at other regions. Yes, the effective population size, for a population, can vary along the genome.
The strength of BGS to affect various statistics such as expected heterozygosity, $D_{XY}$ or $F_{ST}$ is hard to estimate as both hitchhiking (selective sweeps) and BGS leave very similar genetic signature. See for example Matthey-Doret and Whitlock (2018; bioRxiv) (shameless self-citation).

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text:
How to interpret the simple sequence repeat (SSR) on the coding sequence, but not the related protein sequence?
I have predicted some SSR repeat on the gene of interest using SSRLocator program, which the result creates a question for me. Please consider the below sequence, which is part of gene sequence of interest (coding sequence):
GGTGATGAGGTAGAGGAAGAGGCTGAGGAACCCTACGAAGAAGCCACAGA
GAGAACCACCAGCATTGCCACCACCACCACCACCACCACAGAGTCTGTGG
AAGAGGTGGTTCGAGAGGTGTGCTCTGAACAAGCCGAGACGGGGCCGTGC
The program reported CCA motif as a repeat; since this repeat located on CDS, I expected to find the related amino acid track (prolin), but I observed the Threonine track in the corresponding protein sequence.Threonine is coded by ACC. Now I would like to know which motif is really a repeat, CCA or ACC. Is it possible to consider CCA as a repeat, but just on the transcript level not protein sequence or the real repeat is ACC and the software didn't work well here? Please share me any your opinion in this regard.
Thanks so much for your help and participation.

SSR searching tools have generally no idea about CDSs: they consider DNA/RNA sequences as strings and search for tandemly repeated patterns, nothing else. It is also important to remember that in many real-life cases different programs with different settings will reports differing results.
[Knowing that you always have two strands in the genomic DNA, one has to bear in mind that also SSRs can be "read" in either direction, such that for a stretch ACCACCACC the unit can be reported as ACC or GGT. Some programs by default will report SSR units sorted according to alphabet: ACC in this case. Now with coding sequences the story is a bit different: RNA has only one strand, i.e. it has a direction, which means that you cannot "flip" RNA sequences.]
mRNA besides having a direction, codes for protein with the protein sequences sometimes showing their own repeated patterns. SSRs in mRNA are mostly tri-nucleotides or with unit lengths divisible by three and coincide with the tandem aminoacid repeats. So, from the functional point it is a ACC|ACC|ACC|ACC|ACC|ACC|ACA (note that the last element is ACA) repeat, which codes for the respective T|T|T|T|T|T|T aminoacid repeat. To formalize this idea you search for SSRs in the RNA sequence and in the protein sequence and try to find the overlap.
From the point of view of the DNA-polymerase [the enzyme which changes the SSR length] it is a perfect CCACCACCACCACCACCACCA repeat: within these limits the fragment is prone to slippage. But for an actual slippage event the unit boundary does not matter. Imagine that the polymerase "skipped" a CAC unit in the middle: CCACCAC[CAC]CACCACCACCA. The outcome for the protein sequence will be the same: minus one threonine.

Thanks a lot for your nice response. As DNA polymerase is often prone to slippage on the repeat sequences, so the repeat unit can be CCA unit as the software predicated. But, how about the situations that the RNA sequence and related protein sequences are matched? the CAG repeat unit is one of famous examples that generated poly-glutamine tract in the protein sequence that resulted in some human disease like Hungtingtun. Could you please help me to figure out what happened, how polymerase slippage occurred here?

If you have a repeated region, re-annealing of the newly synthesized second strand can cause priming of the DNA-polymerase at a different location. Somewhere in the middle it is no longer possible to "tell" whether the first unit started with C, A or G. This logic is implemented for example in Phobos: it can report "alphabetical normal form given by the alphabetically minimal string among all cyclic permutations of the unit", i.e. for SSRs with the first repeat units being AGC, GCA or CAG it will report AGC.

Yes, of course. However, I'm a bit concerned about how I should reported the repeat unit on this sequence?!

As is: "such and such tool identified in this sequence an SSR with the following tri-nucleotide unit: ***, which corresponds to a stretch of seven threonine aminoacids in the translated sequence." The exact formulation for *** depends on the program: SSRLocator reports "CCA", Phobos reports "ACC". In both cases you can mention that the RNA SSR is shifted in relation to the protein repeat (if it is relevant).

By the way, Phobos identifies here (correctly) an SSR with a length of 22: CCACCACCACCACCACCACCAC.

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text:
How is ATP involved in muscle contraction?
The sliding filament mechanism as explained by my text does not elaborate on how ATP is involved in the cross bridge binding and contraction process. How does muscle contraction utilize ATP?
In my text explains this is the procedure for a contraction:

Ach released by motor neuron cross cleft and binds to motor end
plate
AP generated in response to binding of Ach gated channels and propagates down T tuble
T tuble triggers Ca2+ from sarcoplasmic reticulum
Ca2+ binds onto tropinin on actin filament and removes tropomyosin
This opens up sites for myosin to attach to actin using protein heads
Actin filament is pulled toward the center of sarcomere, causing contraction

I see that the action potential definitely needs ATP in order to be generated, aside from that I am surprised that the actual contraction via cross bridge binding does not seem to need ATP.

It is used in the movement of the actin filament.
https://www.youtube.com/watch?v=H6okUPuyby0

ATP prepares myosin for binding with actin by moving it to a
  higher-energy state and a "cocked" position.
Once the myosin forms a cross-bridge with actin, the Pi disassociates
  and the myosin undergoes the power stroke, reaching a lower energy
  state when the sarcomere shortens.
ATP must bind to myosin to break the cross-bridge and enable the
  myosin to rebind to actin at the next muscle contraction.

The muscle contraction cycle is triggered by calcium ions binding to
  the protein complex troponin, exposing the active-binding sites on the
  actin. As soon as the actin-binding sites are uncovered, the
  high-energy myosin head bridges the gap, forming a cross-bridge. Once
  myosin binds to the actin, the Pi is released, and the myosin
  undergoes a conformational change to a lower energy state. As myosin
  expends the energy, it moves through the "power stroke," pulling the
  actin filament toward the M-line. When the actin is pulled
  approximately 10 nm toward the M-line, the sarcomere shortens and the
  muscle contracts. At the end of the power stroke, the myosin is in a
  low-energy position.
After the power stroke, ADP is released, but the cross-bridge formed
  is still in place. ATP then binds to myosin, moving the myosin to its
  high-energy state, releasing the myosin head from the actin active
  site. ATP can then attach to myosin, which allows the cross-bridge
  cycle to start again; further muscle contraction can occur. Therefore,
  without ATP, muscles would remain in their contracted state, rather
  than their relaxed state.

Summary from: https://www.boundless.com/biology/textbooks/boundless-biology-textbook/the-musculoskeletal-system-38/muscle-contraction-and-locomotion-218/atp-and-muscle-contraction-826-12069/
Also this:
Essentially look up the cross bridge cycle (http://muscle.ucsd.edu/musintro/bridge.shtml)
I would also suggest reading it from the master himself here:
Huxley, A. F. "Muscular contraction." The Journal of physiology 243.1 (1974): 1-43.

It begs the question what the mechanism of bending of the myosin head during the power stroke is . Is there any reference for this?

The two links in the question are dead - can you offer us other ones instead?

authors: Екатерина Джонс

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text:
Why are skin tactile receptors considered to be phasic receptors?
A phasic receptor by definition is one that quickly adapts to change. In terms of neuron firing, this means that it does not trigger another firing because the receptors are used to the stimulus.
But when I place my fingers on my arm, I continuously feel pressure. Does this mean that skin receptors are only phasic in the sense that it will fire as soon as it is touched and does not prolong this touching sensation?

Short answer
Slowly adapting mechanoreceptors in the skin mediate the perception of static pressure stimuli, while rapidly adapting skin receptors mediate swiftly changing (e.g., vibratory) stimuli.
Background
There are various skin receptors. Hairy skin, such as that encountered on the arm, contains at least four specialized mechanoreceptors, namely Pacinian corpuscles, hair follicle receptors, Ruffini endings and tactile discs. They can be roughly distinguished by their adaptation rates, namely fast adapting (Pacinian corpuscles and hair follicle receptors) and slowly adapting (Ruffini endings and tactile discs). Rapidly adapting receptors generate robust responses to vibratory stimuli, but respond weakly to static pressures. The opposite is true for slowly adapting receptors (Kaczmarek et al., 1991).
Hence, the static pressure is faithfully registered by static pressure receptors, while the phasic receptors are specialized in vibratory perceptions.
Static receptors fire a continuous train upon a continuous pressure stimulus, phasic receptors do so only at the start and the end of a static pressure stimulus. Hence, when there is a fast vibrating stimulus (say 200 Hz), then the phasic receptors will also fire action potentials each time at onset and offset of a pressure phase, thereby faithfully representing the stimulus. Here follows a picture of various skin receptors and their responses to a static pressure stimulus. Note that only the slowly adapting receptros show a rocust response:

Source: Michael Mann
Reference
Kaczmareck et al., IEEE Trans Biomed Eng 1991;38:1-16


text:
Why can blood vessel contraction be described as a second order system?

Suppose that the x-axis represents time, and the y-axis vessel diameter.
Then this graph is claimed to roughly describe what happens when the blood pressure increases, then decreases.
When the blood pressure first increases, the vessel diameter expands to its maximum radius. Then it contracts. What I don't understand is why it keeps on expanding and contracting after its initial expansion - does this model still make sense after its initial expansion and contraction?
Can anyone explain?

This phenomenon is called damped oscillation. Negative feedbacks sometimes result in such kinds of dynamics. I don't know the physiological mechanism behind it if there is one but I can understand the logic.

In broad terms: pressure causes vessel to dilate, which in turn reduces the pressure, which in turn reduces the diameter, which then leads to increase in pressure. With certain sets of parameters you would get damped oscillation. Can you provide a reference to the model that you mention?

the blood vessels have smooth muscle cells on its walls. One of the property of the smooth muscle cell is that it contracts when stretched. I think this explains the physiology behind damped oscillation

Many systems have this property. The plot you are looking at is the plot of the transfer function for blood vessel diameter vs time. A trick in mathematics or engineering is to understand a system is to sometimes look at at different system with the same properties that you do understand. For instance, a mass springer damper system is similar to a RLC circuit. That is, if we understand the mass spring damper system, we view the RLC circuit as the analog to the mechanical system and vice versa. In the case of blood pressure, we also have a driven force (the heart). Thus, an extremely simple model would be
$$
m\ddot{x} + c\dot{x} + kx = F(t)
$$
As we see below, the mass spring damper model produces the a similar plot of the transfer function. If you understand the mechanical system or RLC circuit, you can look at your plot parameters as an analog to one of these systems to understand the dynamics occurring in the body.

A more interesting question is can we use PID control to manage the overshoot, rise time, and settling time of the vessel diameter in the body?

The differential equation that models this process is probably related to a Bernoulli differential equation.

http://en.wikipedia.org/wiki/Bernoulli%27s_principle
page 15 http://www.physics.usyd.edu.au/~jbryant/Fluids/Fluidslect4.pdf
http://bme.ccny.cuny.edu/faculty/bfu/blood%20flow%20permeability%20in%20microvessels.pdf

A precise differential equation will need to account for pressure (Bernoulli), fluids (Navier-Stokes), and the elasticity of the vessel walls.


text:
Why sympathetic and parasympathetic nerves originate in different parts of CNS?
Curious if there is a reason for having:

parasympathetic nerves originating from brain stem and pelvic part of spinal cord
sympathetic nerves originating from thoracic and lumbar parts

It looks well-organized, so maybe there is a good reason for that.


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

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

@user49102 - it is perfectly on topic here.

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

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

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

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

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

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

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

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

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

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

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

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

Still a good answer.

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


text:
Are these lovebugs?
I used to see these insects frequently in Chennai and Bangalore (South India). I just would like to know if this is a kind of lovebug. The lovebug as mentioned in the Wikipedia page is, however, different in appearance, although they too are walking as pairs.
Why are they always walking as attached pairs? It also seems to me that the bigger one drives the motion and decides the direction. Is that true?

I believe this is a member of the family of Phyrrocoridae also called firebugs. A more detailed identification would require a more high resolution image of the head and also an image of the ventral (belly) side. However, they are certainly not lovebugs.
Edit: As PhilipC pointed out, they are probably from the genus Melamphaus.

Taking a more high resolution picture is only necessary if you need to know to which subfamily or species of phyrrocoridae this bug belongs. However this classification will require a lot of detailed information (there are more than 300 species in the family of phyrrocoridae world wide), maybe even about the larval stages and thus a lot of work on your side and on the side of an expert doing the classification. Thus if you are satisfied with the information that this is a firebug, the picture is perfectly fine.

There's a pretty reasonable chance they are Melamphaus looking at the picture on Wikipedia, and that Bangalore is mentioned on that page.

As to them 'always' walking in pairs:
I had a different firebug (Pyrrhocoris apterus) living around my previous house. They do not always walk in pairs, especially early in spring i've often seen them walking alone. In summer pairs become more common indeed.
You will probably have guessed that the pairing has to do with sexual reproduction. The question however is why they stay together so long, as mating in insects usually takes no more then a few minutes. This is called mate-guarding, the male wants to make sure that the female deposits eggs with his sperm and stays with her until she has layed her eggs, as shown Shöfl & Taborsky 2002 (thanks to @fileunderwater for this reference.)
This behaviour is not uncommon for insects, and is also well documented for dragonflies (odonata, e.g. Corbet 1962).

Indeed so, see e.g. Schöfl & Taborsky. 2002. Prolonged tandem formation in firebugs (Pyrrhocoris apterus) serves mate-guarding

I agree with Phillip C's comment – this pretty much seems to look like a melamphaus

Melamphaus Stål, 1868
kingdom Animalia
phylum Arthropoda
class Insecta
order Hemiptera
suborder Heteroptera
superfamily Pyrrhocoroidea
family Pyrrhocoridae

Descriptive features

Body large (15–30 mm), elongate oval. Colour usually dark with different pattern on dorsum and venter; abdominal venter never with alternating black and light transverse stripes. Integument dull, covered by very short but distinct, dense pubescence. Head (Fig. 25) triangular, as wide as anterior margin of pronotum, postocular part gradually narrowing posteriad, eyes medium-sized, not stalked, remote from anterior margin of pronotum. Antenna relatively long, second segment distinctly longer than third. Labium long and gracile, surpassing posterior margin of metasternum, first segment surpassing base of head. Thorax: pronotum (Fig. 25) subtrapezoid, relatively elongate, lateral margins not explanate and reflexed. Metathoracic scent gland ostiole with well-developed peritreme (Fig. 20). Fore wing: apical angle of corium narrowly rounded. Abdomen: intersegmental sutures between abdominal sternites 4/5 and 5/6 laterally strongly curved anteriad. Legs: fore femora with small denticles ventrally.

Sources:
http://psybugs.biota.biodiv.tw/files/biota_psybugs/fig.1-2.jpg
http://psybugs.biota.biodiv.tw/pages/598


text:
Would symptoms differ from eating virus contaminated food versus breathing in virus?
Would symptoms differ from eating virus contaminated food versus breathing in virus?
The COVID-19 causes respiratory symptoms and I guess that is because people are breathing in virus droplets in their lungs.
But if you would swallow COVID-19 contaminated food and avoid breathing in the virus would that cause other symptoms like stomach pain or diarrhea?

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. For one of these reasons I think  that your question on the coronavirus outbreak is off-topic here. Question of a medical nature might be on-topic at SE Medical Sciences. Otherwise you are advised to consult more appropriate reputable sources for such information, some of which are listed here.

@David Can I remove the COVID-19 from my question and only keep "Would symptoms differ from eating virus contaminated food versus breathing in virus?". I believe that question is about biology but I could be wrong.

Does the virus genetic code decide which organs to infect or does it depend where it infects initially?

Please transfer your question to a site that deals with medical questions. Or read the Sources I suggested. And the virus uses the same genetic code as its host. The complete genetic information for an organism is termed the genome. The genetic code is a 64-word cypher used to transcribe the mRNA for that portion of the genome that encodes protein. Check it out on Wikipedia.

@David I posted the question now at https://medicalsciences.stackexchange.com/questions/21741/would-symptoms-differ-from-eating-virus-contaminated-food-versus-breathing-in-vi but I need to think how I can make this question non medical and more biology oriented.

If you have posted it on Medical Sciences you should now delete it from here according to SE policy.


text:
Is Zeiss Primo Start microscope worth the price for student use?
I study physics but I have got interested about biology too. Surfing around the web, I have found out that in buying microscopes one needs to decide between the cheaper no-name brands vs. the four big ones: Zeiss, Nikon, Leica, and Olympus.
From the four big ones, only Zeiss delivers directly to my country. The price for Primo Star with phototube and Full-Kohler illumination is 1.8k euro or 2.3k usd. It has only bright-field optics but dark-field (if I got it correctly) is easy to add, as well as phase-contrast.
Anyway, I was wondering how much I would get out of the scope as a home user. I would probably do plant biology. I would also like to learn some staining techniques.
How difficult it would be to run some mini-studies at home? Do research? I would know about imaging quite a lot..
(There was some other similar questions but they did not mention home use.)

What kind of research are you thinking about? You might find the magnification/resolution of a bright field microscope limiting.

It doesn't matter whether you're using your microscope in a 2 billion dollar building or a garden shed, a microscope is a microscope. Either way you'll want a clean work area, isolated from the rest of your living space (especially depending on what you plan to stain with). You'll get out what you put in. Is the opportunity worth $2300 USD to you?

I'm defenitly no fan of the Primostar. It's made to order for Zeiss, probably by Meji.
It's a fine microscope allright, but compared to the gray and beige Standards, it's a toy.
And those gray and beige Standards were already kind of toys, compared to the former black GF stands...
Being a "home user" there are far better and at the same time much cheaper  alternatives availlable on the second-hand market.
In Europe, a Standard 14, basicaly equipped (4,10,40,100 achromats, 0.9 condenser, build in 6V/10W HAL illuminator, binocular) can be bought for anything between 100 and 200 Euro.
This is a universal platform, designed with flexibility regarding applications such as DF, FC, DIC, fluorescense... in mind. The same can't be said to that extend regarding the Primostar.


text:
Are bleach solutions still routinely used in biochemistry laboratories to rid surfaces of bacteria, viruses, certain enzymes, and nucleic acids?
Decades ago I would stop by biology and biochemistry laboratories to see what was up, and I noticed a ubiquitous presence of a squirt bottle of bleach solution. When I asked what it was for I would get different answers in different laboratories. They ranged from disinfection of surfaces by accidental bacteria or phage contamination to denaturing of certain specific proteins or nucleic acids thought to be threatening to certain types of experiments.
Experimental techniques have developed dramatically over the subsequent decades.
Question: Are bleach solutions still routinely used in biology and biochemistry laboratories to rid experimental surfaces of bacteria, viruses, certain enzymes, and nucleic acids? If so, how can one solution be so reliably useful across all of these cases?

Does nobody use the ubiquitous Virkon?

@DDuck Virkon has a wide spectrum of activity against viruses, some fungi, and bacteria... However, it is less effective against spores and fungi than some alternative disinfectants See Assessment of in-vitro efficacy of 1% Virkon® against bacteria, fungi, viruses and spores by means of AFNOR guidelines

Don't forget hydrochloric acid, still used a lot for cleaning purposes in food production industry (like milk & cheese).

@PeterMortensen — I agree with your suggested edits, but I wonder why you are trying to include links in your editing comments? Links don't work in that context and just make the summary of your edit hard to read!

I'm a research post-doc working in a US-based microbiology research lab. We still use a relatively low-concentration bleach solution to decontaminate most liquid cultures before disposing of them, but most of our surface and equipment decontamination is accomplished with alcohol (either ethanol or isopropyl alcohol (IPA)). We do work with some organisms that are not effectively killed by alcohol, such as C. difficile. C. difficile makes endospores which are very resistant to alcohol-based agents, but they are readily killed by bleach.
So after working with C. diff and other spore-forming bacteria we decontaminate with commercial wipes containing a stabilized sodium hypochlorite solution at a little less than 1%, which isn't even enough to give off a strong bleach odor. On metallic surfaces and some kinds of rubber, we follow up with an alcohol wipe to prevent corrosion from the bleach.
We do have other sporicidal agents that are used for specific applications where bleach isn't suitable, but most of them are much more harsh (requiring use of respirators), require a longer contact time, and have a substantially shorter shelf life at the effective concentration (sometimes just days or hours, vs. months with bleach).
Bleach is also good for destroying DNA and RNA in clean areas used for PCR setup, but there are some commercial products specifically designed to do this along inactivating nucleases that might degrade a sample, so I personally use those products. (Note that ethanol and IPA solutions can actually precipitate nucleic acids, leaving them behind after the solution evaporates.)

I can only speak from my experience in many labs in different countries: We never used bleach for cleaning or disinfecting surfaces like cell culture hoods or lab benches. For this purpose we routinely used 70% Ethanol or commercial alcohol based disinfectants. Bleach was only used to inactivate culture media (cell culture and also bacterial cultures) so we could later discard it in the sink without the need to autoclave it (we usually had enough trash that needed this kind of treatment, so we didn't want to increase the amount further).
I think alcoholic solutions are used because they are more friendly to the skin if spilled, residues evaporate relatively fast and also because bleach is pretty aggressive to the surface, which can alter them possibly. There is also no need to remove residual bleach afterwards. However, for treating liquid waste, it was favorable.
Bleach can be used ultmatively because of its mechanism of action. It disrupts the cells and oxidizes its contents, so contaminants have no chance of reproducing anymore.

Thanks! From what I gathered in answers to How exactly does alcohol solution kill or neutralize viruses? (my own humble there in particular) alcohols are particularly good against viruses whose envelope includes lipids from the host's membrane, but may not be so effective against viruses that don't. But maybe those are not stable in the environment in general anyway?

@uhoh They are at least not a general problem you encounter in the lab. If you suspect something like that, you would use a more suitable disinfection agent.

I work in a C. diff lab where we have to decon benches and hoods with bleach wipes, as alcohol does not kill C. diff spores. We usually follow any bleach application with an alcohol wipe-down to prevent corrosion of stainless steel surfaces, like in a biosafety cabinet.

@MikeyC As I wrote, this is my experience. Since I never worked with spores, this might be the reason. Maybe make this into another answer?

@uhoh the point isn't that the lipids come from the host, it's only that they are lipids. Their origin is irrelevant, all lipid membranes are susceptible to detergents or alcohol or other disinfectants.

@terdon there's no such thing as an objective "the point". I could correct your statement and say "the point is that the envelope has soluble components, that they are lipids is irrelevant." We all write our own sentences and choose what to share in them. I like SE because it's a place to share what we know. I don't know much about viruses but I find them fascinating, and won't apologize for my enthusiasm.

@uhoh apologize? What in the world for? You didn't do anything wrong! I just thought that you had understood that the reason alcohol is effective against membrane-bound viruses is because they incorporate the host's lipids and I didn't want you to come away with that misunderstanding since alcohol would be effective against any lipid membrane whether it came from the host or not.

@terdon okay got it, thanks!

Bleach also destroys DNA/RNA, and kills bacteria, making it useful in an area where PCRs are done. 70% ethanol is very friendly to DNA, but it kills bacteria well enough. My guess for the preference of 70% ethanol is that it is not as corrosive as bleach. Best would be bleach, and then a wipe of ethanol.
References
Use of bleach to eliminate contaminating DNA from the surface of bones and teeth
Improved ethanol precipitation of DNA

Best would be bleach, and then a wipe of ethanol. If you do this (the genetics lab I work in does), do a water rinse in between. Otherwise, ethanol and bleach can react to produce chloroform, which you don't want to breathe. Whether or not it would produce a dangerous amount, I don't know, but there's definitely no harm in reducing the risk

I was associated with a lab in 2015 that used a lot of Streptococcus pneumoniae. They had ethanol squirt bottles to clean certain surfaces and in case of a spill. This was intended to kill that bacteria. In other labs previously I had seen bottles of hypochlorite (bleach) - but it was comical to see fungal growth in some of them due to the hypochlorite having decayed over time.
With regard to enzymes, (RNase particularly) the laminar flow cabinet stainless steel was wiped down with ethanol - not to denature any enzyme, but just to remove it and prevent remaining enzyme from becoming airborne.
Sorry for lack of refs yet

Yeah, people don't realize that hypochlorite is light-sensitive. I've fought a losing battle in a couple labs to store bleach solutions at least wrapped in foil or paper tape, if not in an entirely opaque container. I've found 1:10 bleach solutions dated several years previous that didn't even smell like bleach...


text:
How widespread among mammals is the glymphatic system's metabolite clearance in the brain during sleep currently known to be?
The glymphatic system and "brain washing" (metabolite clearance) during mammalian sleep:
Xie et al. (2013) Sleep Drives Metabolite Clearance from the Adult Brain (also here) has been cited over 3,000 times. It describes in-vivo brain imaging and radio-labeled β-amyloid techniques to document sleep-correlated modulation of interstitial space and β-amyloid clearance rate. If I understand correctly the Glymphatic system was first named in this work by corresponding author Maiken Nedergaard.

Abstract:
The conservation of sleep across all animal species suggests that sleep serves a vital function. We here report that sleep has a critical function in ensuring metabolic homeostasis. Using real-time assessments of tetramethylammonium diffusion and two-photon imaging in live mice, we show that natural sleep or anesthesia are associated with a 60% increase in the interstitial space, resulting in a striking increase in convective exchange of cerebrospinal fluid with interstitial fluid. In turn, convective fluxes of interstitial fluid increased the rate of β-amyloid clearance during sleep. Thus, the restorative function of sleep may be a consequence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake central nervous system.

From Wikipedia's Glymphatic system:

The glymphatic system (or glymphatic clearance pathway, or paravascular system) was described and named in 2013 as a system for waste clearance in the central nervous system (CNS) of vertebrates. According to this model, cerebrospinal fluid (CSF) flows into the paravascular space around cerebral arteries, combining with interstitial fluid (ISF) and parenchymal solutes, and exiting down venous paravascular spaces.1 The pathway consists of a para-arterial influx route for CSF to enter the brain parenchyma, coupled to a clearance mechanism for the removal of interstitial fluid (ISF) and extracellular solutes from the interstitial compartments of the brain and spinal cord. Exchange of solutes between CSF and ISF is driven primarily by arterial pulsation2 and regulated during sleep by the expansion and contraction of brain extracellular space. Clearance of soluble proteins, waste products, and excess extracellular fluid is accomplished through convective bulk flow of ISF, facilitated by astrocytic aquaporin 4 (AQP4) water channels.
The name "glymphatic system" was coined by the Danish neuroscientist Maiken Nedergaard in recognition of its dependence upon glial cells and the similarity of its functions to those of the peripheral lymphatic system.
1Bacyinski A, Xu M, Wang W, Hu J (2017). "The Paravascular Pathway for Brain Waste Clearance: Current Understanding, Significance and Controversy". Frontiers in Neuroanatomy. 11: 101.
2Kiviniemi V, Wang X, Korhonen V, Keinänen T, Tuovinen T, Autio J, et al. (June 2016). "Ultra-fast magnetic resonance encephalography of physiological brain activity - Glymphatic pulsation mechanisms?". Journal of Cerebral Blood Flow and Metabolism. 36 (6): 1033–45.
3Konnikova M (11 January 2014). "Goodnight. Sleep Clean". The New York Times. Retrieved 18 February 2014. She called it the glymphatic system, a nod to its dependence on glial cells"

Cetacean sleep and conscious breathing:
Wikipedia's Dolpin; Sleeping and Whales; Sleep indicate many species of each type of mammal are conscious breathers i.e. many are not thought to be able to go somewhere safe and undisturbed and enter extended periods of unconscious sleep.
Question:
How widespread among mammals is the glymphatic system's metabolite clearance in the brain during sleep currently known to be?
I've mentioned conscious breathing in cetacean sleep as an example of both how challenging it may be to investigate some mammals and of where it might be less likely to be found. Since Xie et al. (2013) there must have been a substantial investigation in humans not only to address the "Why we absolutely must sleep?" question but due to the significant place that Amyloid beta holds in the investigations of human disease, including Alzheimer's disease.
Potentially helpful:

This extensive answer to What is happening physically when I get sleepy and when I wake up?
This answer to Do all mammals have a Ventricular system? says "The ventricular system is common to vertebrates." and links to Lowery and Sive (2009) Totally Tubular: The Mystery behind Function and Origin of the Brain Ventricular System
Jessen et al. (2015) The Glymphatic System: A Beginner’s Guide (also here)

in meta: Should the glymphatic system be covered by extending the lymphatic system tag? Does it warrant a separate tag? . The different way that dolphins sleep was brought to my attention in the NPR podcast The Extraordinary Lives Of Migratory Birds some of which may fly continuously for 7 to eleven days without stopping!

Comments are not for extended discussion; this conversation has been moved to chat.


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How much is known about dinosaur DNA condensation and crosslinking?
The conclusion section of Bailleul et al. (2020) Evidence of proteins, chromosomes and chemical markers of DNA in exceptionally preserved dinosaur cartilage is:

The identification of chemical markers of DNA in Hypacrosaurus suggest it may preserve much longer than originally proposed [30,31]. Even though it is clear that contamination does exist in fossil material and complicates identifications of original organic molecules, it can be accounted for with proper controls. Contamination is not a plausible explanation in this case, and to this date, the possible preservation of original proteins and DNA in deep time has not been convincingly eliminated with data. Although extensive research and sequencing is required to further understand DNA preservation in Mesozoic material, along with its chemical and molecular alterations, our data suggest the preserved nuclear material in Hypacrosaurus was in a condensed state at the time of the death of the organism, which may have contributed to its stability. We propose that DNA condensation may be a favorable process to its fossilization. Additionally, as was suggested for protein fossilization [20,45,46], crosslinking may be another mechanism involved in the preservation of DNA in deep time.

The last three sentences highlight that "the preservation of DNA in deep time" may be aided by both DNA condensation and crosslinking.
Wikipedia's DNA condensation; in eukaryotes links to Chromatin
If I had to bet I'd say dinosaurs had chromatin but I could not defend it. If one of the conclusions of this paper was that the DNA was in a condensed state, then it sounds like they are not taking it for granted either.
Is this paper the full extent of what's known about DNA condensation in dinosaurs?
Together with condensation, crosslinking is mentioned in the conclusion, but a text search for "crossl" finds no other instances. As it seems closely related to condensation but there's no further information I don't see how to break that out as a separate question yet.
Question: How much is known about dinosaur DNA condensation and crosslinking?
Potentially related and/or helpful:

Zheng et al. (2021) Nuclear preservation in the cartilage of the Jehol dinosaur Caudipteryx
Wikipedia: Hypacrosaurus; cells

Biology SE:

Was 14,000+ year old DNA "laying around in cave dirt" protected from degradation, or is it just naturally this robust?
Roughly speaking how stable are short sections of single-stranded RNA in exposed environments compared to double-stranded DNA?

I'd say about as much as is known in birds...

@bob1 actually known?

Well, no, not actually known, given that there's 65 My between then and now, but I doubt such important mechanisms have changed much in the intervening time.

@LifeInTheTrees It can not fail if it does not try. It does not try because as far as I can understand (not being a molecular biologists) they simply did not search for DNA. This is in fact what makes the paper so intriguing and tantalizing! However, my question is not about this paper specifically (it's provided as evidence of prior research and what got me interested in this. There is likely more known on the topic (I have linked to a second paper just as an example) but probably not much more, and so I've simply asked "How much is known...?"

Of course dinosaurs had chromatin. Histones — a key constituent of chromatin — are present in eukaryotes as primitive as yeast. I am not aware of any way to establish the condensation state of fossil chromatin, nor would I imagine it to attract much interest, but I may be wrong.

phylogenic bracketing is your friend, if crocodilians and birds both have it non-avian dinosaurs would have almost certainly have had it.

@John I think a short answer based on that would be well received. It's not exactly "known" in the same way that we know what their bones look like, but I think if you qualify it, it's certainly helpful! I'd rather have phylogenic bracketing as my friends than crocodiles and dinosaurs :-)

@uhoh Phylogenetic bracketing was what my first comment was about (more or less) - look at closely related species and work from there. I know hardly anything about DNA condensation, so I won't attempt an answer myself at this point.


text:
Can nociceptors die because of too much mechanical stress?
In martial art people hit their body (e.g., with small bean bags) to become more insensitive to pain. Can the sensory neurons die during this procedure? I think this is just an urban legend. Instead, I think the skin receptors desensitize, but they don't degenerate by the constant mechanical stress. However, I cannot find any research in the topic.

As far as I know, adaptation of peripheral receptors, including pain receptors, is transient (Giniatullin & Nistri, 2013)
Instead, my educated guess is that the increase in subjective pain threshold plays an important role. Pain thresholds differ between the sexes (Chesterton et al., 2003), and depend on disease and physical status (Kosak et al., 1996). Repeated exposure to painful stimuli hardens one mentally (I have practiced martial arts for two decades ).
Morever, there is an interesting answer on Martial Arts SE on the question How should I expect my fist to change over time from punching? Here it is shown that extensive training stimulates the growth of additional skin and bone. Extra skin (calluses) may dampen the impact of painful pressure stimuli.
References
- Chesterton et al., pain (2003); 101(3): 259–66
- Giniatullin & Nistri, Front Cell Neurosci (2013); 7(245): 1-9
- Kosak et al., pain (1996); 64(3): 415–23

Ok. I can accept this. Btw. the technique I referred is called as "bone hardening". I have found a lot of interesting articles about bone remodeling. It appears to depend on mechanoreceptors. http://www.researchgate.net/publication/239942205_Osteocytes_are_not_only_mechanoreceptive_cells http://www.bme.sunysb.edu/people/faculty/documents/2012-gene-mechanotransduction.pdf http://www.sciencedirect.com/science/article/pii/S1063458412000192 http://link.springer.com/article/10.1007/s00018-005-5175-3


text:
How does the frequency of a visual stimulus affect the steady-state visually evoked potential?
I want to design a project for EEG signal processing. In my research I found the concept of SSVEP. SSVEPs represent the electrical activity of the brain as measured via EEG, and are evoked by visual stimuli with low frequency applied to the eye.
My question is whether it is known how the electric activity of brain will change? And a second thing, does it mean that each frequency applied to the eye has a fixed reaction for the brain?

Explained perfectly in http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1880883

I corrected your title since the SSVEP is the pattern in the EEG activity and is not the stimulus for it.

I slightly modified question wording. Feel free to roll back.

Short answer
SSVEP frequency corresponds to stimulus frequency and SSVEP amplitude decreases with stimulus frequency.
Background
The simplest form of steady state visual-evoked potentials (SSVEPs) are those to flash stimuli. Herrmann (2001) studied the SSVEP by recording the EEG from the visual cortex at various flash frequencies. He found that SSVEPs occurred at a frequency corresponding to the flicker stimulus. Amplitudes decreased steadily with frequency and SSVEPs could be recorded up to ~90 Hz flicker frequencies. The shape and frequency following of SSVEPs are shown in Fig. 1.

Fig. 1. SSVEPs and FFT spectra at various frequencies. Source: Herrmann (2001)
Interestingly, SSVEPs in response to some frequencies showed resonance phenomena, indicating a selective frequency preference of the neural oscillators. Specifically, SSVEPs at around 10, 20, 40 and 80 Hz resulted in higher amplitudes than stimuli flickering at adjacent frequencies (Fig. 2).

Fig. 2. SSVEPs showing resonance at 80 Hz. Source: Herrmann (2001)
Reference
Herrmann, Exp Brain Res (2001); 137: 346–353


text:
Neuron stimulation experiments
Has anyone extracted a class of neurons (or a connected set of neurons) and stimulated them electrically to get an understanding of their behavior?
If so, could someone point me to papers along these lines? If not, do people have an idea of why this is not been technically feasible yet? As I would imagine this would be tremendously useful in building neuron models.

Have you heard of optogenetics? For single neurons though there are classic experiments involving electrical stimulation. To me it seems like this question lacks any background study which makes it impossible to answer reasonably.

Short answer
Although outside my direct area of expertise, there is quite a lot of literature on the topic. The trick often is to use the correct keywords. Key in "recording + stimulating + ensemble + neurons", or "Utah + neuron + implant".
Background
There is quite some literature on this topic. For instance, a much used device in this arena is the Utah implant (Fig. 1), which can be used to record and also stimulate neurons (e.g., Nordhausen et al. (1994)). It has 100 penetrating electrodes and is even used in humans. There are also other approaches, e.g. by implanting a bunch of microwires (e.g., Nocolelis et al (1997)). In scientific jargon, the recording of multiple neurons simultaneously is often referred to as 'ensemble recording' (Nicolelis, 2008).

Fig. 1. Utah Implant. Source: WebVision
References
- Fernandez & Normann, Introduction to Visual Prostheses. In: WebVision, online book
- Nicolelis, Methods for Neural Ensemble Recordings, 2nd ed., Front Neurosci, CRC Press/Taylor & Francis; 2008
- Nicolelis et al. Neuron (1997); 18(4): 529-37
- Nordhausen et al., Brain Res (1994); 637: 27-36


text:
What keeps the resting potential of neurons constant at -70 mV?
I know the sodium-potassium pump pumps out 3 Na+ ions and pumps in 2 K+ ions per reaction so the negative charge in the axon increases. However, once the voltage (difference of charge inside and outside of the neuron) gets down to -70 mV, this stops going further below. Why?
I know that this is because of other transport proteins and the presence of anions and cations in the axon, but what are those proteins and ions precisely? There are always negatively charged proteins inside a cell, including a neuron, so I assume there must be a strong force which keeps the voltage from going down.
By the way, is the opening and closing of an ion channel triggered by the voltage of the neuron or the concentration of the ion?

Take a look at the wiki article for Resting Potential: http://en.wikipedia.org/wiki/Resting_potential. Essentially, you form a balance between the electrical force pushing ions through the channels and the force caused by an imbalance in chemical concentration in ions across the membrane.

What about the mitochondrial inner membrane potential of neurons? Does this even have to be more negative for mitochondria to work?

Potassium tends to leak out of the cell via "Potassium leak channel" - These are passive potassium channels that do not require ATP or energy. Potassium flows along the concentration gradient - from inside to outside.

The neuronal cell membrane is quite permeable to K+. Because the Na+,K+-ATPase pumps K+ inside of the cell, K+ tends to diffuse outward again, thereby taking positive charge outside the cell and making it negative inside (see Further Reading 1). This outward flow of K+ stops at a certain point, because the driving force of K+ diffusion out of the cell along with its concentration gradient, equals the charge gradient, which becomes more and more negative inside the cell as more K+ diffuses out (see Further Reading 2). Hence an equilibrium is reached which is close to the resting membrane potential of -70 mV. Other ions such as Cl- are also relatively permeable and affect the resting membrane potential (see Further Reading 1). Ions such as Na+ and Ca2+ are typically highly impermeable and do not substantially affect the resting potential.
As to your second sub-question:voltage-gated channels are gated through voltage differences (Purves et al., 2001), not ion concentration differences.
Further Readings
1. If the average resting potential of a neuron is -70 mV, why is there such a high ratio of K+ ions inside relative to out?
2. Why do negative ions flow into a cell in an inhibitory synapse, even though a neuron has a negative resting potential?
Reference
- Purves et al., Neuroscience (2001). 2nd ed. Sunderland (MA): Sinauer Associates


text:
Why does it hurt more when you touch a nerve directly?
I am not a biologist nor know much about biology (so please explain in layman's terms) however I have always been curious as to why this is.
What causes the difference in pain between touching an open wound and pushing down on your skin? In both circumstances you are applying pressure to the nerves except one is a foreign object touching the nerve and the other is the nerve's natural surroundings in your body.
Why is it that a foreign object causes so much more pain?

see this post. Similar kind of question

I answered the other question and it is similar. However, this one is different enough that I will give a slightly more simple explanation.
Nerves transmit messages using electrical current, more specifically the flow of sodium and potassium. Just remember that it's electricity. When you have any sort of cut or damage, your body recruits white blood cells which protect you from any bacteria that might enter. They also cause inflammation to prevent those bacteria from spreading (and to warn other cells that they may become infected). It is also important that we feel pain, so we know something is wrong (because we have the ability to do something about it). That's why inflammation causes pain. It does this by lowering our threshold so our nerves are more sensitive. In other words, it takes less damage, pressure etc. to cause our nerves to send the pain signal. Normally, it is set higher, so we don't suffer too much pain. Naturally if you want clarification on anything just ask.


text:
What are the functions and differences between axons and dendrites?
My textbook doesn't do a very good job of pointing out what the differences between the two are. It basically mentions axons only in the same breath as the synapse (that synapses are the endings/tips of axons).

how about some other textbook, wiki, google? how is this question OK for Bio@SE?

Dendrites

Means Trees in Greek;
Are the input of the neuron;
Receive information from other neurons or the external environment;
Transfer information to the cell body and axons;
Are numerous, relatively short, and branch extensively in a tree-like fashion
May have numerous spines on them to provide a greater surface area for other neurons to synapse on;
Receive information from other cells at these synapses. This makes dendrites postsynaptic.
The connection between axons that synapse on dendrites is called axodendritic;
The connection between dendrites that synapse on other dendrites is called dendrodendritic.

Axon
 - Means axis in Greek

The output of the neuron;
Transfers information to other neurons;
Begins at the axon hillock, which is a swelling at the junction of the axon and soma where there are many Na+ channels and the action potential starts;
Is relatively long (some reaching several feet);
Has terminal boutons at the end where the synapse is located. This makes axons presynaptic. These swellings at the terminal bouton is where the neuron synapses with another neuron;
Contains numerous vesicles which hold neurotransmitter;
Has many Ca2+ channels in the membrane;
The space between the terminal boutons and the next cell is known as the synaptic cleft, and is approximately 20 nm thick;
Most are myelinated, i.e., have myelin sheaths that are made by Schwann cells or oligodendrocytes. Myelin acts as insulator to help conduction of action potential. There are openings between the Schwann cells called Nodes of Ranvier. These help with the conduction of action potentials.
Synapse on other cells in various forms;
Axoaxonal: Axon is connected to another neuron’s axon;
Axodendritic: Axon is connected to another neuron’s dendrites
Axosomatic: Axon is connected directly to another neuron’s soma
In neuromuscular junctions, axons synapse directly on muscles.

Presynaptic and postsynaptic neuron. The synapse is shown enlarged in the inset. Source: Rowland Hall.


text:
Concentration of caffeine in physiologically relevant setting
Caffeine is known to overcome G2/M (and possibly other types of) cell cycle arrest through its effects on DNA repair machinery and is used as a positive control in studies of cell cycle arrest. In this paper, for example, researchers use concentrations of caffeine in the 1-4 mM range to overcome nocodazole-mediated arrest. Is this a physiologically relevant concentration?
I found a lot of interesting caffeine data including the LD50 (estimated to be around 150-200 mg/kg) but have not been able to turn up any good numbers on reasonable concentrations that might be found in a human.

To make sure I understand your question right: You are looking for the physiologically occurring caffeine concentrations in the human body? For example after consuming coffee?

Yes, that is correct

Let's figure it out. Suppose an adult with an average blood volume of 5 L (5000 mL) drinks a cup of strong coffee with 100 mg of caffeine in it. Given caffeine's formula weight of 194.19 g/mol, and assuming 100% of the caffeine is in the blood stream, its concentration (from this awesome calculator page from Graphpad, the makers of Prism) would be approximately 103 µM, or 10-40 times less than what's being used in the experiments you cite.
Of course, this is overcoming drug-mediated cell cycle arrest, so its possible that a lower concentration is needed to jump-start physiologically-arrested cells.


text:
Is the ratio Brain Mass/Total Mass still considered a valid indicator of intelligence?
I was reading this(1) and it led me back to ask a very basic question (I'm not a neuroscientist).  All the way back to undergrad anthropology and neuroscience courses I remember being taught the general rule of relative intelligence was that one looked at the ratio of the brain mass over the total mass of the animal (or the estimations therein from let's say fossils).
I know a lot of the interesting neuroscience research going on these days does looks into bird brains, particularly within Corvidae.  It would seem that birds are often much more efficient in the abilities they seem to show with considerably less brain mass.  I do realize that birds often weigh very little as well, so perhaps the ratio is preserved?
I also realize that within birds, they see better ratios in more intelligent birds.  But what about the comparison from mammals to birds?
Dinosaurs are often predicted to not be intelligent because of the enormous body size and small cavities for a brain.  Now I realize that some dinosaurs were actually quite tiny, but this is just an example.
Given birds' close genetic link to dinosaurs, could it simply be that they were just doing more with less?  The mammalian brain is a huge caloric burden, so perhaps this would show an efficiency that could be selected for?
Thus as the title suggests, my main question:
Is the ratio of brain mass to body mass still considered to be a valid indication of intelligence of a species in modern (current) neuroscience?  Certainly there are exceptions, but is it still considered the rule of thumb?
EDIT: I also wanted to point out the first article(2) I started to read after formulating the question.  It made me question the usefulness of encephalization in addressing this issue at all, but I don't/didn't feel adequately trained to evaluate the conclusions of the meta study.
Again, this still leaves us comparing within primates, which still leaves me feeling that Corvidae have some really impressive efficiency going on with their overall brain mass.  Which then leads to hope that some dinosaurs could be at least equally intelligent, if not more so (noted that this is complete conjecture).

(1) Front Hum Neurosci. 2013 Jun 6;7:245. doi:10.3389/fnhum.2013.00245. Print 2013.
(2) Brain Behav Evol. 2007;70(2):115-24. Epub 2007 May 18.

I don't know about brain mass to body size, but ratio of neocortex to brain volume is correlated with primate evolution (Figure 3, here). If you subscribe to the view that humans and more closely related primates are more intelligent than more distantly related primates, then that is an important correlate.
I think the issue with this question is that we're still having trouble defining intelligence.

+1 I certainly agree that we have problems with defining intelligence, and that even getting theory of mind levels poses problems.  I also enjoyed the reference.  Is the issue then, that across higher taxa (say class) we can't rigorously compare intelligence.

@AtlLED: I would say, yes.  Even if you want to talk about temperament, there's a lot to debate. Here's a review: http://homepage.psy.utexas.edu/homepage/faculty/Gosling/reprints/CDPS99Xspeciesreview.pdf

Short answer
It is mainly synaptic connectivity that determines intelligence, rather than brain size per se.
Background

For a starters, Albert Einstein, considered to have been a reasonable intelligent person, had an average sized brain (Sukel, 2009).
Secondly, there are not only neurons in a brain that determine its size. The brain contains a relative large proportion of glial cells, which perform mainly a supportive function and are not part of the main neural network in the brain. A brain with a larger proportion of glial cells can thus be bigger than another equally sized brain with a higher proportion of neurons (Sukel, 2009).
Thirdly, even the number of neurons per se is not a valid indicator of intelligence. Of course, in the very extreme, an organism with a few hundred neurons like C. elegans (Jabr, 2012) has hard-wired cognitive limitations due to the low number of processing units available to it, as opposed to, e.g., the human brain with some 100 billion neurons. However, scientific studies across several animal species, including humans, have shown that brain size alone is not a valid measure of intelligence. For example, birds with tiny brains have shown to be capable of some remarkable clever stuff, including the use of tools to obtain food. Rather, scientists now argue, it is the number of connections in the brain that matter, i.e., the organization and molecular activity at the level of the synapses is the main determinant of intelligence (Sukel, 2009).
Lastly, as mentioned by others, intelligence is notoriously hard to measure. Species evolved in different environments. Learning to use a tool to dig up ants by chimpanzees is quite a clever thing, but makes absolutely no sense for a humpback whale diving 3 kilometers below sea level in search of giant squid. Intelligence is a relative thing.

References
- Jabr, Sci Am (October, 2012)
- Sukel, Sci Am (October, 2009)

I always heard Einstein's brain was bigger than normal

Considering that as humans had larger brains in prehistoric times, then no, brain size doesn't mean more intelligent.
I aren't well versed into this subject, so I don't particularly know if they could learn better than us, but there are speculations of why their brains were larger than ours.
The most primitive humans, had to deal with a lot of predators, and unnatural things in their environment. Mist of them contained a vast amount of knowledge of what is "bad" or "good", and that was a requirement if they wanted to survive in that period.
As we settled down, and our natural predators became our food, such needs became less and less important.
Maybe they were actually smarter than us.

Welcome to Bio. This is a scientific stack where sources and preferably references to credible papers are considered mandatory. Apart from that your answer seems incomplete as it is commonly accepted that at least part of intelligence is determined by the number of connections present in the brain.


text:
How can electric fields inhibit tumor growth?
In MIT's Technology review it is explained that electric fields can cause dividing cancer cells to explode, while these fields have no significant impact on non-dividing tissues. The original research was done by Palti et al.
What is the mechanism behind this? It does not seem to be related to thermal effects.
Edit: The treatment in question seems controversial. A clinical trial showed improvement but it is not rock-solid data.

Could you link to the trial paper?

@RoryM http://www.ncbi.nlm.nih.gov/m/pubmed/15126372/

http://en.m.wikipedia.org/wiki/Alternating_electric_field_therapy

I am deeply suspicious of this. It's not theoretically impossible but if it worked the way it is supposed to work patients should experience hair loss.   It's been shown to be not worse than chemo for treating recurrent glioblastoma, but that's a far cry from a real benefit.

I edited your question somewhat in terms of style. Please feel free to roll back.

@Resonating: Even if it is only as good as chemo that would still be great news since it can adjunct on top of chemo with negligible side-effects.

In a PNAS paper by Palti's group (2007) they explain the hypothesis behind the technique:
They reason alternating currents of 100 kHz to 1 MHz specifically affects dividing cells and thereby targets cancer cells. Note that this is the same basic idea as chemotherapy and radiotherapy, which also target dividing cells mostly. The mechanism of action of alternating electric fields on dividing cells is though to be the result of a specific effect on the  bridge separating the daughter (cancer) cells during cell division (Fig. 1). They think it interferes with spindle tubulin orientation and induces electrophoretic effects (Kirson et al., 2007), resulting in a pile-up of cytoplasmatic organelles at the cleavage furrow. This is thought to interfere with cytokinesis, and to lead to cell destruction** (Kirson et al., 2004).
Note it is the frequency that differentiates between the various effects of current stimuli. At very low frequencies (1 KHz) electric fields stimulate excitable tissues through membrane depolarization. At higher frequencies this excitatory effect is lost. At very high frequencies (>1 MHz) tissue heating results (e.g., microwave ovens).  Hence, alternating electric fields of intermediate frequencies (10 kHz to 1 MHz) were considered not to have any meaningful thermal effects (Kirson et al., 2004).

Fig. 1. Palti's electric field hypothesis. Source: Kirson et al. (2007)
References
- Kirson et al., Cancer Res (2004); 64: 3288-95
- Kirson et al., PNAS (2007); 104(24): 10152–57

This is just a hypothesis, there are unanswered questions such as why does it have little/no side effects like hair loss that normal anti-mitotics do.

@KevinKostlan correct, it's a hypothesis. The reason why there is no hair loss is that the electrical field was applied locally via electrodes, so there were no systemic side effects reported.

@AliceD The missing hair loss is kind of strange. We expect an effect on the deeper lying brain but see no effect on the hair bulbs which are located directly in the skin? I don't believe this.


text:
Why is LH level much higher than FSH level at ovulation?
My teacher showed us an elaborate collection of graphs with one of them showing FSH and LH plasma levels during the menstrual cycle. LH level was almost 3 times higher than FSH level. Why?
Does this have anything to do with their synthesis or cellular responses?

It is not the absolute plasma levels that are important, it is about their relative differences during the cycle. The steep rise in FSH during the first days induces follicle stimulation. The LH surge at day 12 induces maturation of the egg and stimulates its release (see wiki page). The fact that LH's absolute plasma levels are higher may theoretically have to do with the fact that more LH is needed to elicit its physiolocal response. However, the differences of their relative levels is way more important from a physiological point of view.

The LH receptors are not less sensitive...instead they are more sensitive, than FSH receptors...so the same amount of GNRH which affects those receptors, LH secretion is increased almost by 3x, than FSH...

Ah, thanks@souvik bhattacharya, I'll adapt my answer. My point still stands though.


text:
How does the "heat vision" of some snakes work?
Some snakes have an infrared sense which is used to track warmblooded animals.
How does that organ work? And would a similar organ be possible in a warmblooded animal?

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

Vipers, pythons and boas have holes on their faces called pit organs (Moon, 2011), which contain a membrane that can detect infrared radiation from warm bodies up to one meter away (Fig. 1). At night, the pit organs allow snakes to sense an image of their predator or prey (Source: Nature).

Fig. 1. Pit organs in python (top) and viper (bottom) as indicated by arrows. Source: Wikipedia
Nerve cells in the pit organ contain an ion channel called TRPA1, which detects infrared radiation as heat. The pit organ is part of the snake's somatosensory system, which detects touch, temperature and pain. It does not receive signals from the eyes. Hence, snakes sense infrared by detecting heat, not photons of light. Infrared radiation heats up the pit membrane tissue, and TRPA1 channels open when a threshold temperature is reached, allowing ions to flow into the nerve cells and triggering an electrical signal (Gracheva et al., 2010). Rattlesnake TRPA1 is activated by temperatures higher than about 28 °C — roughly the temperature a snake would 'feel' from a mouse or a squirrel about a meter away (Source: Nature).
Hence, this organ works best in cold environments where temperatures are low so that warmblooded prey stands out. Further, warmblooded animals won't be able to use this organ, as the pit would be ~37oC and not be able to detect anything below that temperature.
References
- Gracheva et al., Nature (2010); 464: 1006-11
- Moon, Anat Cell Biol (2011); 44(1): 8–13

To my surprise, these are heat sensitive channels :o

I've just asked How do snakes determine the direction of prey from their thermal infrared sensing pit organs?

@uhoh - nice one! +1'd


text:
Do we know a complete list of nutrients that humans must ingest to live?
When the people who are making "nutritionally complete" foods like Soylent are developing their product, how do they know that they've covered all their bases? You need to have protein, carbohydrates, fats etc., but what about vitamins or minerals?
Has science produced a commonly accepted list of all the nutrients that humans need to live?

For babies there is certainly a formula available for a complete menu for survival: formula*
Here are the nutrition facts from Nestlé's "Good Start":

Formula nutrition facts. source: Nestlé
Comparable lists are available for people that cannot eat normally (e.g. people in a comatose state) and are fed enteral or parenteral nutrition.
*. Remember though, breast is best :)

Turning to Nestlé for advice on healthy eating is like turning to Marlboro for advice on how to stop smoking.

@FelixDombek - it's not an advise on a healthy diet, it's a reference to the composition of baby formula. The *endnote is a dietary advice for infants though!

Is the answer to this specific question (let alone this forum) really the place for "parenting wars" fodder?

@RozennKeribin - this is not a parenting wars fodder at all. FelixDombek questions the credibility of my source and that's perfectly fine. In turn they wrote a new answer, which is even better! This is not a war nor fodder, it's called a discussion.

The most complete list of essential nutrients that I have found is here, together with some scientific references and some more "conditionally essential nutrients":
http://www.nutrientsreview.com/glossary/essential-nutrients
I'll reproduce the main list here:

Water
Vitamins
Vitamin A (retinol)
Vitamin B1 (thiamin)
Vitamin B2 (riboflavin)
Vitamin B3 (niacin)
Vitamin B5 (panthotenic acid)
Vitamin B6 (pyridoxin)
Vitamin B7 (biotin)
Vitamin B9 (folic acid, folate)
Vitamin B12 (cobalamin)
Vitamin C (ascorbic acid)
Vitamin D (vitamin D2 or ergocalciferol, and vitamin D3 or
  cholecalciferol)
Vitamin E (tocopherol)
Vitamin K (naphthoquinones)
Choline (vitamin Bp)
Minerals
Calcium
Chloride
Chromium
Copper
Iodine
Iron
Magnesium
Manganese
Molybdenum
Phosphorus
Potassium
Selenium
Sodium
Zinc
Amino acids
Isoleucine
Histidine
Leucine
Lysine
Methionine
Phenylalanine
Taurine
Tryptophan
Threonine
Valine
Fatty acids
Alpha-linolenic acid (ALA)
Linoleic acid


text:
Why might dogs get sick less frequently than their owners?
An article I was reading cited this study result "A comparison of 2473 pairs of dogs and their owners found that dogs were about 50 per cent less likely to have had two or more acute illnesses in the previous year than their human family members (p < 0.01, preliminary data)." The article is here http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189355/.
In the absence of any species specific reasons, we would not only expect rates of sickness to be similar, but in fact, owing to dogs' extremely poor hygiene standards relative to humans, we would expect them to be sick vastly more often.
I have read a number questions on the general subject of humans appearing to get sick more than animals, but most have ended with a presumption (but without any evidence cited) that animals do get sick as often but we just don't see it. This study is the first I've seen on the subject and seems to demonstrate that it is a real phenomenon after all.
The author's explanation seems entirely based on meat-eating, which seems plausible, but perhaps a bit narrow. I wonder if anyone could offer any alternative explanation?

The article is hypothetical. It's written as a discourse trying to explain why pets are sick less than their owners, while the foundation of that hypothesis is not founded: see section 4 of your linked paper:

A hypothesis put forth in this discourse is that humans get sick more often than animals and, correspondingly, typically engage in medical practices more frequently than animals. There is relatively little direct evidence that might firmly refute or confirm this hypothesis.

So your question why

humans appear [to] get sick more than animals

is more a question of if, rather than why.
I think the major problem with this article is that there is not a strict definition of 'sick'. What we may experience as being 'sick' may not be recognizable to us when an animal is in a physiological comparable state.

Thanks for your response, but I wasn't really asking for an review of the article itself, more a comment on the study it cites. The article might have been hypothetical in nature, but the study actually took place and got the results it did. It's these results I was interested in. I presume the uncertainty about observed 'sickness' is why the study chose dogs. It seems unlikely that such beloved pets were actually acutely ill without their owners knowing, and if they were that just means the question becomes 'why do humans exhibit more visible symptoms than animals?', hardly much different.

If your  question is on cited studies - cite those. The linked article is quite poor in its scope. What I mean is that the assumption of the article is iffy. I don't buy it.

Do women get "sick" more frequently than men? I bet a study would find that men do have fewer acute illnesses than women. But do they really? We know that men tend to go to the doctor much less than women for a number of reasons, ranging from laziness to stoicism to expense. Similar reasons apply to dogs and their owners, therefore I also strongly question the premise of this article.

Also, the population dynamics of pet dogs would be quite different from their human owners.

I agree with the above three comments. Dogs get sick, and probably on the same order of magnitude as humans. More than one human disease (like narcolepsy) has been solved because of canine conditions, and with genetic studies, more are certain to come. "...such beloved pets were actually acutely ill without their owners knowing..." How would their owners know? My dogs are quite beloved, but they just can't complain about certain illnesses. They get over it with time, or it becomes vet-worthy.

I don't mean to offend, but I originally asked about a study mentioned in a perfectly legitimate scientific journal. I was hoping someone might either offer an explanation or perhaps some evidence to the contrary. I'm not sure I see the sense, on a science site, of people adding comments that they 'reckon' it's probably not true. If anyone has any scientific, evidence based opinion, it would be good to hear. If you think dogs do get sick as much as humans then perhaps some studies showing this would be a useful contribution.

I hadn't realised I had come up against such a wall of preconception. According to Occam's Razor, if a study seems to show that dogs get sick less than humans, then we should presume that they do and then look for evidence to the contrary, not presume they don't because we don't like the conclusion and proceed to make up reasons why the study might be wrong. This is exactly the sort of confirmation bias that holds scientific investigation back, people decide on a world view and only accept evidence which supports it, anything that doesn't gets picked apart until it can be safely swept away.

I'm not quite sure where the vitriol is coming from, I did not say that any study proved it conclusively, but was careful to use 'might' in my question and 'seems to show' in my comments, please don't put words in my mouth. If mentioning an analytical axiom by name constitutes a 'lecture', then I'm not sure there is any value to continued discussion. I asked the question 'Why might dogs get sick more than their owners?' An answer would be a scientific reason why they do or a study showing they don't, I did not ask for a personal opinion about the value of the article.

Your question finishes with: "The author's explanation seems entirely based on meat-eating, which seems plausible, but perhaps a bit narrow. I wonder if anyone could offer any alternative explanation? It implies you take the finding for granted. The question you now pose in your comment is different than the one in your question body.

I presume you have deleted your previous comments? It looks like I'm having a conversation with myself which is misleading to anyone reading this. With regards to your remaining comments, I did indeed take the finding for granted, for the time-being, it was published in a reputable journal and I had no evidence to the contrary (and still don't), it seemed entirely the rational thing to do. All I did in my comment is flip it on it's head, it's the same question either way, what scientific, evidence based, explanation could there be for the results of this study?


text:
Do gastropelecid hatchet fish have powered flight?
These sites contradict each other:
Source 1 claims that hatchet fish do not fly, but simply jump out of the water instead:

'Species that were once thought to have powered flight, the
Pantodontidae and the Gasteropelecidae. The Pantodontidae currently
contains only one species, Pantodon buchholizi, the African Butterfly
Fish while the Gasteropelecide contains nine species including the
Marbled Hatchet Fish, Carnegiella strigata. Both these species have
deep bodies with a lot of muscular support for their enlarged pectoral
fins, or in the case of Pantodon, pectoral and pelvic fins. It is now
considered that both these species simply jump, if somewhat
spectacularly, out of the water.'

whereas Source 2 says they fly with their tail:

'Investigations using high-speed cameras have since shown that this supposed ‘flight’ is in fact initially a jump which then becomes true powered flight... The buzzing noise, previously wrongly interpreted as the sound of flapping pectoral fins, in fact comes from the tail fin as it beats around 40 times a second during flight!'

and Source 3, finally, claims that they fly with their pectoral fins:

'So while there are many fish that can glide if they jump out of the water at speed, not least of all the celebrated marine flying fish, only the hatchets have true, powered flight. By rapidly fluttering their pectoral fins, they can extend their jumps out of the water to cover several meters.'

Do not worry, I won’t delete my comments

I can add to @JiminyCricket 's comments that comments are volatile; they can be deleted without further notice (I just did so for a bunch of them because they were obsolete); I have added the links and quotations you provided in the comments to your post. Excellent research +1

Although I think, in the end, it comes down to the definition of flight: what is flight? As discussed previously, the difference between powered flight and gliding is the flight stroke, which produces thrust in true flyers. Gliders, then, do not produce thrust; they do not flap their wings. This link differentiates between flyers, gliders and parachuters in terms of terrestrial critters. In fish, a more specific search for terminology is needed