text:
Can one see flickering of a light bulb at 50 Hz?
Yesterday I had a BBQ with some friends. The sun had already set and the only light source left (besides some ambient light from the world around) was a low energy light bulb.
After a while I started to see lighting changes in the faces of my friends and the number plates of their cars. It felt like someone toggled the light very fast. When looking at the wall or the light directly I didn't notice any flickering.
In my country the power grid is running at 50 Hz. Is it possible that I actually saw the flickering caused by the alterations in the power grid or am I just going insane?

Sub-question - had you been drinking alcohol?  I'd guess that would have slowed down your reactions/perceptions though.

@Criggie No intoxication whatsoever - funcact: my friends asked me the same question when I told them :D

You didn't mention if this was an incandescent bulb. If so, it seems the filament's brightness wouldn't change that much during a 50 hz cycle, but it's possible.

It is actually not hard to detect on-off flicker at 50 Hz with your eyes even in well-lit surroundings. Simply flick your line of sight across the flickering light source, and you will see a regularly spaced sequence of images for a split-second in your visual field. There are even some electrical lights that oscillate between different wavelengths, and such a technique will allow you to see it. Also, even if you do not do this on purpose, you may notice the effects when you shift your gaze or during the natural saccades of your eyes. But incandescent bulbs hardly flicker, as @rcgldr said.

@rcgldr It was some sort of energy saving bulb (Not sure which type, but not LED). Not a incandescent bulb.

@Timo - possibly a CFL (compact fluorescent light) bulb (usually a coiled tube). CFL bulbs could change intensity nearly instantly, but there's usually some capacitance in the circuitry which would reduce flicker.

@user21820: This is quite noticable (at least for me) with LED car tail lights, especially at night when I'm a bit tired.  Sometimes traffic signals & advertising signs, too.  Part of it, I think, is that they often use pulse width modulation to control the light intensity...  Also note that a bad or failing LED or CFL bulb can flicker.

@jamesqf: Yes indeed. Especially those that deliberately pulse on and off, but what I found interesting was that some fluorescent tubes that give 'warm light' are not monochromatic, and I discovered it exactly by flicking my line of sight across them, the first time accidentally.

I seem to recall reading multiple times statements from autistic persons who claimed they could see fluorescent light bulbs flicker. (I have a child on the spectrum. This would have been when he was preschool age, and he is now 18, so it was some time ago.)  IIRC the thinking was, it's not so much that very few people can see this but that most of us have learned to filter/ignore it.  We live in the US so this would have been 60 Hz.

Doesn't appear to be mentioned in the answers: your peripheral vision is much better at noticing movement that your focused/central vision.  This is why you noticed it "out of the corner of your eye" but when you looked at it directly you couldn't see the change.   Old CRTs have been mentioned and it was quite obvious if you put two side-by-side (and 1metre/3feet apart) and looked at one: the other would appear to flicker but not the one you were looking at.

You can definitely see if a lightsource is continuous or flickering, by observing rapid motion. Wave a bright (like, white) object lit by that source in front of your face. With flickering light you'll notice multiple separate images.

It might be that it's a very cheap LED light, and uses only a half wave rectifier instead of a full bridge. This means every other wave is turned off, and the lamp spends at least half its time completely switched off. This also makes it flicker at half the frequency it would with a full bridge rectifier.

Short answer
Yes, the flickering of a light bulb may be noticeable, and yes, that's directly related to the mains frequency. However, since the flickering of a bulb is about two times higher than the temporal limits of our visual system, it is unlikely to be perceivable.
Background
The temporal resolution of the visual system can be quantified in a number of ways. As you are referring to a relatively simple flickering stimulus, the critical flicker fusion frequency is probably the most relevant. At a certain critical frequency, a flickering stimulus will appear as a continuous stimulus. This critical flicker fusion frequency limit is around 50 Hz, but variable between 5 - 50 Hz, dependent on the lighting conditions (Kalloniatis & Luu), see Fig. 1 below.
For example, the turn signal of a car is obviously flickering (flickering in the 1 Hz region). But an object displayed on a standard flat-screen computer seems steady. A monitor's refresh rate is typically 60 Hz, which is indeed above the critical flicker fusion frequency (Holcomb, 2009).
However, the good old CRT screens can sometimes seem to be flickering. The mains, as you indicate, is indeed 50 Hz (Europe, Australia) or 60 Hz (US), and indeed the flickering is at this frequency. Similarly, well functioning fluorescent tubes seem to flicker on occasion (when they are reaching their end they start to flicker too, but that's because of a failure of the device rather than the mains frequency peaking through). Due to a similar effect, light bulbs may seem to flicker too. However, because of the sine wave characteristic of the mains alternative current, featuring two peaks per wavelength (a negative and positive peak, the flickering of a light bulb is actually two times the mains frequency, or 100 - 120 Hz. This is quite far above the critical flicker fusion limit and hence will likely not be noticeable.
It's interesting to see that you mention that it was around sunset. Scotopic vision (night vision) is mediated mainly by the rod photoreceptors. The rod visual system mediates gray scale vision at low-lighting. While spatial resolution is poor, it's very well adapted to process fast-moving stimuli. Hence, the flicker fusion frequency under scotopic viewing conditions may indeed be higher; i.e., flickering of light bulbs may not be perceived during the day (Federov & Mkrticheva, 1938). Nice add-on there.
To add to this as alluded to in the comments, whether the flicker of mains-grid powered appliances are actually visible depends on a lot of factors other than flicker frequency. CRT screens, for instance, may have improved phosphors that have delayed response times, 'smearing' out the flickering into invisibility. In other words, it's not a simple matter of 'ON' and 'OFF'. Likewise, light bulbs heat up and hence the temperature difference might not be noticeable to us, as the temporal flickering depends on heating and cooling of the wire.

Fig. 1. Flicker fusion as a function of stimulus intensity. Note that the shape of this graph means that photopic vision is less sensitive to temporal changes; the intensity scale relates to the stimulus intensity, as alluded to in the other answer. Scotopic vision to promote the temporal resolution of vision in the sense mentioned in this answer alludes to the ambient lighting conditions conditions. source: Kalloniatis & Luu (2007)
References
- Federov & Mkrticheva, Nature; 142: 750–1
- Holcomb, Trends Cog Sci 2009; 13(5): 216-21
- Kalloniatis & Luu, WebVision, chapter "Temporal Resolution" 2007

Great answer, thanks! I think, besides your point, if the sun weren't already set, it would have inferred with the light from the light bulb anyway, making it impossible to notice. Glad I'm not going crazy :D

To add a data point, with CRTs I had to go up to around 80Hz or so - 85 being one "standardised" (VESA) refresh rate. Anything less and I had a sense of the flickering "out of the corner of my eye".

LCDs generally are better, even at 60Hz, but I had the privilege of using three Hanns·G monitors in $JOB[-2]. They would operate at 75Hz, and got rid of the semi-permanent mild headache I'd had previously.

@WillCrawford - Part of the flicker effect from a CRT depends on the persistence of the phosphors. The greater the persistence, the slower the rate at which the phosphors light decays, Greater persistence is good for flicker but, can cause blurring of virtual objects moving across the screen. Some fixed field entry monitors, where scrolling wasn't used, like the green monochrome IBM 3740 terminals, had a persistence around 1 second, which allowed for very crisp fonts and no apparent flicker. For many standard CRT monitors, the flicker goes away at around 75 hz.

@WillCrawford - continuing, CRT televisions with interlace, only update "pixels" about 30 times a second, but flicker is usually not an issue. The persistence of the phosphors used on CRT televisions is designed to avoid flicker at these lower frequencies.

I'm aware of what causes the effect. I think the persistence of my retina (or nervous system) may be a little lower than normal :o) [and I've used terminals like the ones you mentioned]

TV is ~25fps here the other side of the pond, so flicker is more noticeable on older CRT-based equipment.

And however it was designed, I seem to be particularly sensitive to "flicker" (older energy-saving bulbs and many office fluorescent tubes give me headaches, quite apart from the way they exacerbated my impaired colour vision).

It should be noted that the eye's ability to detect flicker (raid movement) also depends on the angle under which light enters the retina, because there are 2 different kinds of detector cells. Cone cells in the center (i.e. under sharp angles, head-on) are good at differentiating color, while rod cells at the outer edge of the retina pick up light from the periphery of the visual field and are better at light/dark differentiation and movement detection. You can test this IRL by looking at a sublty flickering light source - the flicker will be more noticable when viewed from the side.

The measurements shown in the graph are for the fovea. Some people report being able to detect flickering only in their peripheral vision, which is mostly rods, which matches your suspicion that the rods may have higher flicker fusion frequency.

A lamp flickers at 2x the mains frequency, i.e. 100 or 120 Hz, and that is typically not noticeable to human eyes. It is visible to chicken and insects.
That being said, a low quality lamp or a lamp at end-of-life may also flicker at 50 or 60 Hz, and you will notice. It depends on the brightness, so an area illuminated by the lamp may not seem to flicker.
A simple way to suppress the flicker of a 60 Hz CRT is to put on sunglasses. The chemistry in your eyes is slower at low brightness, this makes the flicker less visible. The invention of 100 Hz CRT TV (I was involved) was necessary for allowing higher brightness.

+1 for your A lamp flickers at 2x the mains frequency, i.e. 100 or 120 Hz. Can you add sources? I adapted my answer to allude to this effect too. Thanks.

A 50 Hz true-sine wave will pass through zero amplitude twice per cycle: once going toward its positive extreme (climbing through zero), and once going toward its negative extreme (falling through zero). (I'm ignoring bias voltage here.) The entire cycle is from e.g. zero with slope X all the way to zero with slope X, but two zero-passes happen, at slope X and slope -X. So the instantaneous voltage will be zero 100 times per second for a 50 Hz AC waveform (120 times/second for a 60 Hz AC waveform). I don't know the extent to which this actually impacts the intensity of the lamp's light output.

While you are correct about the sine wave and the math, I dealt with this same issue with a set of LED Christmas lights.  The LED lights are wired in a simple series, and they only get forward voltage 60 times a second (60Hz in my location). Since LEDs only work with voltage flowing one way, the flicker is very noticeable in my peripheral vision, but not straight on.  If the OP was using cheap LED lights, it's possible this same thing was happening.

@JPhi1618: LED drivers can use a diode bridge and a smoothing capacitor. Which means only cheaper LED lamps ought to have significant variation in luminous flux over the mains cycle.

@RedGrittyBrick, oh, yea, of course they can and most LED bulbs I have seen look great with no flicker, but on the extreme cheap end, like the string of lights I have, there is nothing done to smooth out the light or reduce flicker.  Sorry if it seemed like I was talking about all LED bulbs.

Let's say there is a point source of light (it could be a lamp or a highly reflective object) that undergoes large, rapid intensity changes, say 50-100 times a second.
If you quickly move your eyes while it's in your field of vision, it will trace out a path across your retina. Some sections of this path will receive little light, while others will receive a great amount. What you see will look like a dashed line. (The flicker fusion frequency is irrelevant because it refers to fixed points in your field of vision. In this case we are dealing with many spatially distant photoreceptors.)
Let's say it takes 0.15 seconds to "flick" your eyes from right to left. This means a light flickering at 100Hz would be broken up into 30 "off" sections and 30 "on" sections during this time. So in fact you would be able to detect frequencies much higher than 100Hz. (This could make an interesting Arduino experiment.) I have noticed the effect when my laptop varies the brightness of its charging light using PWM. As it "darkens", the dashes in the dashed line get shorter, and vice versa.
But let's put this in context. The conditions you describe mean that:

There is a big contrast between reflective objects and the background
There is a big contrast on some objects when the lamp is at its brightest and at its darkest (assuming a LED lamp without smoothing capacitors, the objects could receive virtually no light from the lamp for certain periods)
The objects are not "point sources"

This means that whenever you move your eyes around, a quick succession of bright "ghost" objects will additively combine in your field of vision. The effect will probably look like a sped-up version of strobe lighting. The same will happen with moving objects (e.g. someone waving a hand). But if you fix your gaze on a stationary object you will probably not see flickering.


text:
Is hydrothorax considered as edema?
In _Robbins Basic Pathology 9th ed., edema is defined as

[E]dema is an accumulation of interstitial fluid within tissues. Extravascular fluid can also
  collect in body cavities such as the pleural cavity (hydrothorax), the pericardial cavity (hydropericardium), or the peritoneal cavity (hydroperitoneum, or ascites).

Though hydrothorax is mentioned here in relation to edema, it is not mentioned explicitly whether it is actually a subtype of edema or not. I also looked into multiple sources for edema definition; “accumulation of fluid in the interstitum”; interstitium refers to the tiny spaces between cells which is not the case for hydrothorax since pleural cavity is not interstitium (right?). So is hydrothorax considered as a subtype of edema?

Welcome. You might wish to consider asking this over at Health.SE. It's best practice not to double-post across the SE network. I'm happy to migrate it for you.

source: Stack Exchange

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

sort: votes


text:
How do we look inside the cell?
My sister is in 9th grade biology and her teacher avoided answering the question of how we actually study the inside of a cell. I haven't taken biology in a while but I'd like to give her an answer.
Can someone roughly summarize how we actually learn about what goes on inside a cell? Just mentioning a few of the most common or used techniques would be fine.
Note: I hope this isn't a bad question. It's a bit vague. But I didn't want to leave her without a decent answer.

Techniques to look at whole cells are: Light microscopy (cells, large organelles), electron microscopy (detailed analysis of subcellular structures and even proteins) and confocal fluorescence miscroscopy (look at particular cellular planes, reconstruct 3D images).
And of course you can analyze the insides by Biochemistry by breaking the cell membranes and look at individual proteins and DNA/RNA by extraction and electrophoresis followed by Western / Northern / Southern blotting, or isolate organelles by centrifugation.
It is a broad question, and I just gave the most obvious examples of techniques (not anywhere near exhaustive). By googling the bold-out terms you may provide some details to your sis.

Beyond the conventional methods listed by Chris Stronks, Berkley Labs have far advanced the state of the art in probing the internal structures of cells using x-ray tomography. See:
http://ncxt.lbl.gov/ . The images obtained are absolutely incredible and allow researchers to probe the cell layer by layer and visually contrast specific organelles for study much in the same manner that organisms are examined using CT scanners.

That was fantastic. Nothing can replace seeing it for yourself!

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


text:
Do potassium channel blockers affect the resting membrane potential?
I am reading about scorpion venoms and toxins for my bio class and they appear to have a variety of potassium channel blockers. My professor asked "What effect would this have on a neuron?" and naturally two things came to mind

Potassium channels are necessary for repolarization
Potassium channels participate in controlling the concentration gradient of the cell.

I have found evidence in articles supporting the first claim, but I don't know much about the second.
Do potassium channel blockers affect the resting membrane potential?  Would they significantly alter the concentration gradient?

If you can access this paper, that would give a great idea how K+ channel blocking affect action potential.

Potassium channels participate in controlling the concentration gradient of the cell.

I would rephrase this to "Sodium/potassium pumps establish the concentration gradients of sodium and potassium across the cell membrane." Potassium channels do not.

I have found evidence in articles supporting the first claim, but I
  don't know much about the second.

Right; because the channels don't set up concentration gradients.

Do potassium channel blockers affect the resting membrane potential?

If they block the resting state "leak" potassium channels, you bet. The resting membrane potential is largely set by the electrical conductance through those channels. Blocking them would greatly depolarize the cell compared to typical resting membrane potential values. But there are many different potassium channels. You may be thinking of blocking the delayed rectifier potassium channel, which shouldn't do much at all to change the resting membrane potential.

Would they significantly alter the concentration gradient?

Probably not, since though the cell would be losing less potassium through this conductance, what matters more to the concentration gradient of potassium are the sodium/potassium pumps.

Short answer
Scorpion venom mostly affects neuronal firing activity by inhibiting recovery.
Background
There are some 100 subtypes of K+ channels and some 120 different scorpion toxins known. Of this host of toxins, the majority were tested on
Shaker-related channels (subfamily KV1.x). Some peptides were shown to act on the Ca2+-activated K+ channels (KCa1.1, KCa3.1, KCa2.x. The family of so-called g-KTx toxins is specific for the ether-a-go-go family of K+ channels (KV11.x) (Rodriguez de la Vega & Possani, 2004).
The Shaker subfamily and the ether-a-go-go family are all voltage-gated channels and hence closely involved in action potential generation (Coleman et al., 1999; Shepard et al., 2007)]; the Ca2+-activated K+ channels are activated when Ca2+ enters the cell, which is an event typically associated with action potentials too.
Hence, based on this information I conclude that scorpion venom mainly blocks the repolarization phase of neurons, meaning the maximum firing rate will be drastically reduced because recovery is blocked. Neurons can fire, but they will not be able to recover from continuous firing.
Scorpion venom is not strongly associated with potassium leak channels (KCNK family). Although other families may also affect the resting membrane potential, it is the KNCK family that is mostly associated with generating the cell resting membrane potential (Cohen et al., 2009). hence, scorpion venom will not affect the resting membrane potential too much.
References
- Coleman et al., J Neurochem (1999); 73: 849–58
- Rodriguez de la Vega & Possani, Toxicon (2004); 43: 865–875
- Shepard et al., Schizophrenia Bulletin; 33(6): 1263–9
- Cohen et al., Eur Biophys J (2009); 39(1): 61-73

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


text:
Are all action potentials the same shape and amplitude when graphed with respect to time?
The most common visualization of an action potential is a graph of the difference in membrane potential (y axis) at a particular time (x axis).
According to my textbook Cognitive Psychology by E. Bruce Goldstein, an action potential sent from neuron down the axon remains the same. That is, if we plot the action potential as described above, then at each as it is propagated down it will have the same shape on the graph (within some range of error obviously, but he is saying the error is trivial).
But he then says on page 34

One way to answer the question of how action potentials determine different qualities [(e.g. taste of something sweet)] is to propose that the action potentials for each quality might look different. However, [Edgar] Adrian rules out that possibility by determining that all action potentials have basically the same height and shape.

My Question
Can someone confirm these two facts:

Once an action potential is sent from a given neuron down the axon, does the shape and amplitude remain constant as it is propagated?
Do all action potentials have the same amplitude and shape?

Generally speaking, yes. For reference see this paper in Nature
This is Fig. 7 from it with comment:

Reason is that most axons are not passive tubes of electrolyte with leakage (in which case AP would be attenuated along it) but rather active media with membrane potential across that have ion channels that reproduce initial action potential along the axon. However, in more passive tubes, like in dendrites, action potentials might be attenuated.

Generally, no. Amplitude of action potential depends on properties of ion channels, at what potential, for example, $K^+$ channels will open to start repolarization (peak of AP). Duration also depends on properties of ion channels. But since there are not a lot of variability in ion channels and extracellular ion composition is mainly same in animals, most of APs will have same shape/duration/amplitude.

Short answer
Action potentials differ in shape between neuronal cell types, and action potentials may even change shapes during action potential propagation within one and the same axon.
Background

Once an action potential is sent from a given neuron down the axon, does the shape and amplitude remain constant as it is propagated?

Although the textbooks will typically say action potentials are transmitted without their amplitude being changed this claim is theoretically virtually impossible due to the many variables encountered in and around the axon. For example, axons in the sciatic nerve may extend to a meter and it is virtually impossible to keep the exact conditions along that length exactly identical. The amplitude of the action potential is mainly dependent on the influx of Na+. Slight variations in membrane potential, concentration of sodium, or channel (subtype) densities may therefore change the amplitude. In addition, temperature affects action potential amplitude (Hodgkin & Katz, 1949) and slight temperature differences along long axons may therefore be expected to alter amplitude. Likewise, shape may alter as well. For example, glutamate released alongside axons of hippocampal pyramidal neurons results in widening of action potentials (Sasaki et al., 2011).

Do all action potentials have the same amplitude and shape?

Therefore, given the answer under question 1 no, they do not have to. Even a propagated action potential in a given axon may change amplitude and shape, as said. Most notably, different neuronal types may in fact be classified according to their action potential morphology, such as the various neuronal types in the dorsal root ganglia of the spine that can be differentiated based on their duration (Villiere & McLachlan, 1996).
References
 - Hodgkin & Katz, J Physiol; 109: 240–9
 - Sasaki et al., Science 2011; 331: 599-601
 - Villiere & McLachlan, J Physiol 1996; 76: 1924-41

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


text:
Correct enzyme nomenclature
I notice many wikipedia articles, courses, pathway sites use a different abbreviation for the same enzyme. Eg: Wikipedia lists the abbreviation of phosphoglycerate mutase as PGM, whilst wikipaths lists it as PGAM in the glycolysis pathway. Then there's enzymes like glyceraldehyde 3 phosphate abbreviated either as GAPDH or G3PDH. This has led to many confusions, particularly when the enzyme abbreviation is completely different to the gene abbreviation, eg: protein kinase A (PKA).
For the official names of genes, I'm using genenames.org. I thought it might be common practice to abbreviate an enzyme with its gene abbreviation, but I see this is problematic due to many enzymes being encoded by multiple subunits and genes from different locations.
Is there a site, or a way, to unambiguously know the correct, and most widely recognized, official name/abbreviation for an enzyme, like there is for genes?

No, not that I have ever seen. Classically, the Enzyme Commission (E.C.) identifiers are the only way to be certain that two (or more) abbreviations or acronyms are all referring to the same enzyme activity. Sometimes, when the situation becomes very complicated interested parties will co-author a proposed new naming convention within their subfield. Some journals may require specific abbreviations, but otherwise authors are free to use whatever nomenclature they like.


text:
Why didn't a concept like "pointers" in Computer Science evolve in the genome?
I see that the genome contains large regions of repeating sequences called interspersed or dispersed elements. The long dispersed elements (LINES) such as LINE-1, can reach up to 6-8 kb in length.
I'm wondering, given the amount of repetition that takes place in these regions, wouldn't a system where a pointer (such as in computer programming) existed  be more efficient? For example, instead of including a LINE, include a unique 5 base pair sequence acting as a pointer to that LINE. A separate chromosome (containing one copy of each LINE) would then be read at the correct position once the pointer was read.
Do you think that given enough time in evolution, such a system would be more sustainable? Sort of like using a proper functional language instead of Assembler in computer programming, where f(x) can be defined once, and accessed via pointers, instead of being repeated many times?

Are you sure about what pointer exactly does? As far as my knowledge goes, a pointer stores the address of an object in the RAM. I don't think your analogy is correct. And for function calls: Leave pointers to functions; there are no true equivalents of function calls in biological systems (see this post). It is imperative to understand both the subjects to a basic level before making analogies.

In the question you'll note I asked why a concept "like" pointers "didn't evolve". In this case of "like" the "object" being pointed would be a LINE. Putting semantics aside, I was curious why heavy extended chains of repeating sequences of carbon atoms would be evolutionarily beneficial when those same repeating chains could be just created once, and then activated as needed. Interestingly in the post you reference, you yourself state it's not the physical implementation, but the underlying concept that is important. It was a question regarding concept, as mentioned in the title.

There's not much point in conserving space when at least 50% of your genome doesn't do anything at all. To use a computer science analogy: Disk is cheap. (and all processing is parallel so even I/O isn't a deal)

@Resonating "50% of your genome doesn't do anything at all" is not necessarily true. A large portion of our genome does not have any currently-known function, but that is completely different from saying it has no function whatsoever.

The most generous papers have pegged maybe 80% of the human genome as functional. The average estimate is more like 15% even on the generous side. I gave a bit of a margin because much is not known, but there are ~at least~ 800 million bases that do nothing at all. I'm comfortable with my estimate given what is currently known.

Very important to be absolutely clear what "functional" means. The ENCODE estimate of 80% is based on a definition of functional that basically = "binds to something". Whether these have phenotypic consequences or not does not follow from just that fundamental property.

Short answer: Pointers already exist within the genome, in terms of transcription elements (such as repressor/activator systems). These systems can remotely activate a specific gene for transcription based on concentrations of specific chemicals within the cell.
The problem with LINEs are that they are thought to be ancient retroviruses which lost their capacity to infect other cells, instead jumping around within the genome. They are therefore parasitic in nature, and they reproduce by inserting multiple copies of themselves into the genome. It makes more sense to think of LINEs as nearly inactivated retroviruses instead.


text:
Regarding cryonics, why can't you freeze a living body and then thaw it later, fully functional?
Cryonics is very popular in science fiction today, as a method of preserving animals, including humans, for long time storage and thawing the tissue later in the future. What is the difficulties with this method? Why can't we simply freeze living persons and expect them to be fully functional again later?
I've heard that the membrane potentials get lost in the process and thus all neural activity stops. I've also heard that freezing cells leads to cells imploding, due to the formation of ice crystals, leading to rapid necrosis. Is any of this true or just myths?


text:
Cell-type specific methylation profiles: original reference finding?
This is a general question, and a specific question. I'm looking for the original reference that first talked about how DNA methylation profiles are cell-type specific.  This is specific, because I care about this specific reference paper, but it is general because I don't know how to go about finding original reference papers to begin with.
Any help would be super appreciated!

Note: This is not my field, and only the result from a quick  database search

Doing a quick search in the Web of Knowledge, I found the paper Ehrlich et al (1982), Amount and distribution of 5-methylcytosine in human DNA from different types of tissues of cells, which is relatively well-cited. This in turn mentions that:

Recent studies indicate that for many genes associated with vertebrate development, there are tissue- or cell-specific differences in the extent of DNA methylation.

The oldest studies referenced in this paper that seem to refer to tissue-specific methylation are Vanyushin et al (1970), Rare Bases in Animal DNA, Nature and Vanyushin et al (1973), The content of 5-methylcytosine in animal DNA: The species and tissue specificity, Biochimica et Biophysica Acta. The 1973 paper is also one of the earliest papers cited in another well-cited paper from 1983 (Gama-Sosa et al, 1983)), so it might be the best bet. However, Gama-Sosa et al also mentions Kappler (1971), The 5-methylcytosine content of DNA: Tissue specificity, which is clearly relevant. In total, Gama-Sosa et al has references to 13 early papers on DNa methylation, so you might want to check them all out, and backtrack from there. Also, Vanyushin seems to have published in smaller, more obscure journals around the same time (e.g. DOKLADY AKADEMII NAUK SSSR), so there might be earlier papers that express the same ideas. The earlier papers seems to deal with bacterial DNA methylation though.
A couple of other references are:

Van der Ploeg & Flavell (1980), DNA methylation in the human gamma delta beta-globin locus in erythroid and nonerythroid tissues,
Mandel & Chambon (1981) DNA methylation: organ specific variations in the methylation pattern within and around ovalbumin and other chicken genes
McGhee & Ginder (1981), Specific DNA methylation sites in the vicinity of the chicken beta-globin genes


text:
Walkthrough Illumina Genotyping
I would love help outlining a basic walkthrough of the wet-lab techniques for processing blood samples from patients, all the way to loading a BeadChip, to the part just before Next Generation Sequencing takes place. Here is my basic understanding so far, that I am not 100% certain is accurate. I am not a biologist - I just communicate with them, so I do not need any confusing assay names/specifications that are important only for wet lab biologists.
Steps:
1. Collect blood from patient.
2. Purify DNA by isolating DNA
            (Procedure (?): lyse/sonicate, bind using ethanol, centrifuge,
            wash with buffer, centrifuge again, rinse with water, centrifuge
            again)
3. Cut DNA into 100-150 bp read fragments
            (Procedure (?): with restriction enzymes? how do you determine
            read length with restriction enzymes?)
4. Separate double stranded reads into single stranded reads
            (Procedure (?): denature with heat)
5. Amplify reads via PCR, leaving you with many single stranded reads
6. Disperse sample evenly into all cells on a BeadChip. The BeadChip
      contains bountiful DNA polymerase and fluorescently tagged single nucleotides.
7. Submit the BeadChip to the Next Generation Sequencer for processing.
8. You end up with a BUNCH of images which you can transcribe into sequences
      based on the color illuminated in each photo capture, in each position
      on the BeadChip.

Here's what doesn't make sense to me:
Step 6. You either have to only put one PCR read product in each cell at a time - which would take FOREVER, if you wanted to sequence someone's whole genome... Or you have more than one light going off per cell, per BeadChip, in each photo. If the latter is the case (which it would have to be for high throughput wet lab experiments), how do you determine between photo captures of a given cell in a BeadChip that the nucleotide going off in photo 2 is a part of fragment n or n+k?
Does this make sense? Basically, how are BeadChips loaded with sample reads for NGS genotyping? I know that reads are "anchored", but are they anchored in each cell of the BeadChip? This is the only way this makes sense to me.
Thanks for any insights!

Genotyping and Next Gen Sequencing are two entirely different applications.  If you are using BeadChips, you are genoptying.

The BeadChip is literally a silica chip that holds beads in an array. Each bead contains many copies of a specific oligonucleotide that bind and capture genomic DNA fragments.

@swbarnes2, isn't the input of NGS a beadchip? What is the difference between sequencing and genotyping? NGS is a sequencing technology that gives you the nucleotide sequence of sample DNA. Is this not genotyping?

Nope. NGS puts prepared DNA fragments on a flow cell, and gives you millions of short reads.  Genotyping gives you a single letter at a single pre-determined position, or in this case, the single base at a few million chosen locations.  BeadArray technology is genotyping, not sequencing.


text:
What large "package" is carried by this large spider underneath itself?
One night in early May in northern Taiwan a strange looking spider carrying a large white "package" underneath itself ran in front of me and stopped, so I photographed it. The package is roughly the size and shape and color of a round dental floss dispenser that one would carry in one's pocket, perhaps a little smaller, about 2.5 cm in diameter.
I took some photos with a flash and without. The total span of the spider's legs was about 10 cm.
I'm guessing this would be an egg case, but it's surprisingly large, could it be prey? I suppose if a spider didn't have a home of any kind it would have to carry its meals with itself. It seems to be well adapted to this and moved quickly even with the large load.
Question: What kind of spider is this and what is it carrying underneath itself?

It's a Huntsman spider. The genus is  Heteropoda but not sure of the species (pingtungensis?) Yes, it is an egg case she is carrying.
Ask a local if it is the white barred spider, LaYa 喇犽, Mandarin is 白額高腳蛛. If so then it may be veratorias as in below article.
Wikipedia article on one species at
https://en.wikipedia.org/wiki/Heteropoda_venatoria
If you get more good photos, put them on wikipedia or somewhere. Until then, here's Heteropoda venatoria (Fam. Sparassidae) from here:
 click for full size

Oh, comments are on again. I fixed the link thank you, feel free to edit the answers yourself to do so. The good photos can go on wikipedia, and maybe iNaturalist. I dont know any other good place to put them.

Okay this certainly seems close enough for me considering the quality of my snapshots, thanks!


text:
How is silica transported to the leaves of genus Dendrocnide trees to form stinging needles for toxin delivery?
I just read the NYTimes' This Tree’s Leaves Look Soft and Inviting. Please Don’t Touch Them. which mentions the genus Dendrocnide and that Wikipedia section begins with:

Contact with the leaves or twigs causes the hollow, silica-tipped hairs to break off, penetrate the skin and inject the toxins.10 The hairs cause an extremely painful stinging sensation that could last from several hours to 1–2 days, recurring to a lessening degree for several months or more whenever the area is touched, exposed to water, or subjected to temperature change. The injured area becomes covered with small, red spots joining together to form a red, swollen welt. The hairs are also believed to be released to the air when the plant is cut or cleared in large areas. Workers without respiratory protection have reported sneezing, runny noses, mild nasal bleeding and throat irritation while cutting or clearing.
10Hurley, Marina. "'The worst kind of pain you can imagine' – what it's like to be stung by a stinging tree". The Conversation. Retrieved 2020-03-08.

and that article says:

The stinging hair structure is complex and consists of a tip, shaft and bulb composed of silica, calcium carbonate and calcium phosphate.

Reference 5 in Neurotoxic peptides from the venom of the giant Australian stinging tree (open access in Science) is Stinging hair morphology and wall biomineralization across five plant families: Conserved morphology versus divergent cell wall composition and this article contains a lot of information, for example following Figure 2:

Biomineralization
Notable differences were found in the mineralization of stinging hairs. Three zones of the stinging hairs could be distinguished based on their mineralization patterns. The tip regions were generally strongly mineralized with highly concentrated silica or calcium phosphate, except for Cnidoscolus stinging trichomes, which were completely nonmineralized. The shafts were usually mineralized with calcium carbonate, but in some cases with calcium phosphate or silica besides calcium carbonate. Trichome bases showed more irregular mineralization, mainly with calcium carbonate and often additional silica deposits (Fig. 2K, L), or they were not yet completely mineralized (Fig. 2M).

This article primarily addresses structure and morphology, but I'm interested in how silica actually makes its way into a leaf structure. Unlike calcium and phosphorous, neither elemental silicon nor SiO2 readily dissolve in water, so I'd like to ask the following:
Question: Presumably it comes from minerals in the soil, but is it transported as particles of silica, or molecules of SiO2, or by other chemical forms containing silicon and reformed as silica on site, or something else?

I don't see a tag related to transport, and I don't think nutrition applies. Is there a catch-all tag for stinger structures or the mechanical aspects of stinging mechanisms?

Biosilicification is a good search term to use.
The silicic acid present around the roots can be actively transported into roots, and later into specific cells or cell compartments. It is deposited preferentially onto lignin or polysaccharide surfaces.
For free articles giving an overview there is:
Nawaz, Muhammad Amjad et al. “Phytolith Formation in Plants: From Soil to Cell.” Plants (Basel, Switzerland) vol. 8,8 249. 26 Jul. 2019, doi:10.3390/plants8080249
found at:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6724085/
and:
"From biosilicification to tailored materials: Optimizing hydrophobic domains and resistance to protonation of polyamines"
David J. Belton, Siddharth V. Patwardhan, Vadim V. Annenkov, Elena N. Danilovtseva, and Carole C. Perry
PNAS April 22, 2008 105 (16) 5963-5968; first published April 17, 2008 https://doi.org/10.1073/pnas.0710809105
found at:
https://www.pnas.org/content/pnas/105/16/5963.full.pdf
Keywords silaffins, frustulins, pleuralins (used by diatoms) silicatein (used by sponges)

+1 already :-)


text:
The Tun state of a tardigrade
I was wondering How long does it take for a tardigrade to enter and exit the Tun state?
I'm doing a thesis on tardigrades for my B.S in biology and I haven't come along any information in the primary literature talking about how long roughly, it takes to enter the tun state in cryptobiosis. I understand that it takes a couple hours for it to pop back up again, but what about entering?


text:
Allergy desensitization: what is the mechanism? Could it happen with other immune responses?
Allergy is a type of immune response against an otherwise harmless substance. If I understand it well, the aim of allergy immunotherapy is not to stimulate an immune response like the immunotherapy for for other diseases, but to progressively reduce it by controlled exposition to the antigen. Is the mechanism understood? Could the repeated long-term exposition to an antigen reduce other types of immune responses (to virus or bacteria for example?)


text:
Why don't cats have to pant?
I understand why dogs pant and humans transpire, namely for temperature homeostasis. So why don't cats need to do either, even after expending a lot of energy on a hot day?

Do cats ever expend a lot of energy?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site (it is not identical to SO) and [edit] your question accordingly. In particular, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). I believe you have not done this because your question is based on a false premise — google search result. Thanks!

Cats have low endurance, dogs can jog for 20 kilometers, endurance hunting. Besides, check videos of lions on hot days, they pant under a tree.

@aliential: Depending on the breed of dog, a 20 km jog might just be a gentle warmup.  Even my friends' small dogs - not much bigger than a cat - will happily go 10 km or so.  But I don't think I've ever seen a cat run even 100 m.

domestic cats do pant sometimes: https://www.timeforpaws.co.uk/s/cat-panting-should-you-be-worried

The answer to this question should be that cats do pant when overheated. It's a thermoregulation system that they do use in extreme circumstances (aside from paw sweating). Especially after exercise (zooming up and down the stairs). It could also be a sign of disease, though, it should all be taken into context when analyzing panting (or any other behavioral cue) in cats. It's not a frequent thing to see, because of their high tolerance to heat as stated in one of the answers, but only a few days ago with all this heat waves I saw one of my cats precisely panting after a good random run.

My question is why don't you ever see a cat pant when it's hot (or any other time for that matter), while all sizes of dogs pant when it's hot. When they're idle.

Cats are smaller and hotter than dogs and humans, with a temperature  between 100.4°F and 102.5°F (38.1°C to 39.2°C).
Smaller animals have a higher surface-to-volume ratio and so radiate excess heat more efficiently.
Being hotter, cats tolerate higher temperatures.
I could not find an accessible ref for this, please insert some if you can find some.

I've added as source for a cat's core temp. But you say 'Cats are smaller and hotter...' than what? An elephant? And the fact that they are more heat tolerant and that it's due to core temp and size is what really needs a proper source. But in itself a nice answer.

Somebody should do a study correlating the RoP (Rate of Panting - excuse the technical lingo) with dog size! I must say thinking about it - my sausage dogs do indeed pant less than my husky...

Transpiring and panting are ways to regulate body temperature. When sweat evaporates, it cools the skin, and panting releases heat through the mouth. Horses, humans and even plants transpire for this reason, while dogs and birds pant. But how do cats release heat?
In fact, cats sweat through their paws. It appears that a cat after it has been frightened may leave wet pawprints on the floor. Although it's all over the internet, I couldn't find a convincing picture and as a cat lover, I've never noticed this phenomenon. That aside, cat's paws have little surface area, and cannot provide much cooling power. Instead, felines have other, more effective strategies to adjust their core temperature. Like dogs, they often sprawl out on cool surfaces (Fig. 1), or they seek out the shade on hot days. They also tend to sleep a lot, which reduces core temperature and is preferable of being very active in hot times in terms of body temperature (Fig. 2).

Fig. 1. Sprawling cat. source: Columbian blogs

Fig. 2. Cats in the shade. source: Cat memes
Source
- Indiana Public Media

A cat on a hot tin roof is in greater trouble that I always thought! :) I'm having trouble understanding how my cat with thick fur is cooling down through it's paws at the same rate as my short hair dog panting under the same conditions. Maybe a cat's metabolism is much slower so heat buildup is less of a problem.

@HeinduPlessis as said, they keep calm :)

They sure do! I wonder if there's a paper in this?

The second paragraph of this answer is substantially copied from the source you linked to. You should make it clear through quotations when you are using someone else’s writing.

@canadianer it's not quoted though; the text has changed. I can add the source somewhere again, but it's clearly mentioned below? I guess it's fine as is.

Copying the phrasing of others, even if you change some words, is plagiarism regardless of whether you cite the source. You might consider consulting some academic guidelines on plagiarism, for example: https://integrity.mit.edu/handbook/academic-writing/avoiding-plagiarism-paraphrasing or https://www.ox.ac.uk/students/academic/guidance/skills/plagiarism

@canadianer - I'm aware of the rules, and normally I'm always really careful. I've edited the text.


text:
A colony of humans are sent to an alien world, at what point would the descendants evolve to be genetically incompatible with Earth humans?
I recently heard about the evolution of the London Underground mosquitoes, and how they have changed genetically enough that they almost can no longer reproduce with above ground mosquitos. Since this change in the mosquitos occurred over a relatively short time frame, how many years/generations would it take for a similar process to happen with humans?
The thought experiment that comes to mind is this. Assuming we sent a colony of humans to a distant planet and didn't have any physical contact with them for x number of years, how many years would it take for the colony of humans to branch off enough genetically to be no longer be able to reproduce with Earth humans? This is assuming the planet is habitable but different enough to change the course of human evolution.
In other words, what would be an expected minimum number of years it would take for this colony's descendants to be removed from Earth humans to one day again be reunited and not be able to produce offspring between the now different species?
In other words, what would be an expected minimum number of years the would need to pass before they are reunited and are no longer enough of the same species to produce offspring together?

Welcome to Biology SE! Very interesting question! Although I am not an evolutionist, and I may be wrong here, but I think this question will likely yield only speculative answers. Perhaps it could be rationalized by stating the question as "how long did it take our earthly homo forebears to evolve into species that were genetically incompatible with their predecessors?"

Chris, good point! I realize it is very theoretical, and I assume that the past evolution of our species would be a good indicator of how long this process would take. I suppose the difference here is that it would be an instant separation of the species, rather than a slow migration like our past homo forebears. And there also would be no cross-breading during this time, like it has been expected to have happened with various homo species of the past (slowing down the branching of evolution).

Ah, I understand your point now. Interesting addition to your question.

If Australian Aborigines are any indication, it would take a long time. They arrived in Australia on the order of 50,000 years ago and were still genetically compatible with other humans when settlers arrived within the last 500 years. Prior to exploration in the last few centuries travel to and from Australia would have been pretty negligible.

I think there are 2 solutions to answer this question. If we assume that the environment did not change, one can calculate the number of mutations that accumulates through drift in both lineages. ....

... I am not sure how from this info we can infer any level of reproductive isolation. Eventually, this can be done based on observations of slight level of outbreeding depression in humans today (assuming this exists, see this post) or with known past reproductive isolation in the human history and their genetic distinctiveness (assuming we have these informations).

Better on Skeptics.se?

There's an interesting question (yes hypothetical, but is that bad?), and an interesting upvoted answer. Why close? Astrobiology is serious business!

but it's impossible to answer without using a great degree of speculation

and is that bad? In this field (Astrobiology) I would definitely allow it, as of course no one knows the answer, since no one put a population outside earth's confines. This is a well-thought question and science is there to ponder about and explore the unknown.

that would mean answers would tend to be almost entirely based on opinions, rather than facts, references, or specific expertise

@ChrisStronks I think it need to be narrowed down to be suitable, even though it would still be based mostly on speculation. Whole books have been written on the mechanisms of reproductive isolation. Some relate to differences in environments (selection pressures) while others do not (drift). Some take place prebreeding and others postbreeding. Other mechanisms are behavioural, and in this human scenario these would only be based on speculation. I agree that a narrowed down version that builds on e.g. the average time to reprodutive isolation in mammals could be interesting.

@fileunderwater: that is indeed a valid and very acceptable reason for closure (although I still vote for re-opening :-). However, the closure because of speculation I still disagree with. It is just that I think, in general, too many questions are closed on questionable grounds. But that's probably something to discuss elsewhere. Thank you!!

@ChrisStronks about closing questions on questionable grounds. Chris and I had discussed this on chat that this is same as cleaning the lab fridge. Lots of junk is cleared but sometimes a somewhat important stuff is also gone. That is one tradeoff. We can have meta discussion on deciding whether to reopen those questions or not (as such those questions are not that common). It took quite some effort to clean up the site.

@WYSIWYG - And you guys did a wonderful job! I don't want to undermine your efforts, but it's just that in some (indeed not too common) cases I think babies are thrown away with the bath water. This is one of them. The closing should be balanced and even unanswerable questions deserve the right to exist, let alone answered and upvoted answers like this one (!!). Thanks again.

@ChrisStronks I voted to reopen.

I don't get the votes to reopen, since it hasn't even been edited after it was closed (besides a retag). At least give the original poster a chance to respond to the suggestions/criticism and maybe clarify before voting to reopen. What's the hurry?

I appreciate the honest meta discussion on the nature of this question. I don't think it's necessarily unsolvable, but understand that it seems difficult for one field to give a real answer without some speculation or hand-waving. I can see that genetics are needed to determine the rate at which our genes would change given the environment. Astrobiology would provide that data on the environment to determine the effects it would have (change in gravity, planets rotation, solar energy, etc). Applied mathematics to work out the models. Biology to use past knowledge on evolution. And so on.

I can imagine this would be a very real question if we were to send an "ark" of sorts to another planet, without guarantee of being reunited in any given timeframe. Of course our civilization has never been this concerned with future generations more than 100 years out, I mean just look at global warming and how difficult of time some people have caring about that. But being able to model how [human] life would change in a different isolated environment over thousands/millions of years could be invaluable to many different scientific fields, no?

I do understand (as fileunderwater mentioned) that perhaps this question needs to be narrowed down. There are a lot of variables, and some we may need to resort to hypothetical models or deep speculation. This is an answer for many fields, but biology/astrobiology seems to be at the core. Given my inexperience in the field, I'm mostly curious whether the branching off of the species would even occur (with or without a drastic change in environment). Even if it would take millions of years, it'd still be a fascinating realization given that is a relatively short time.

That's an interesting model, because mosquitoes are vectors for serious illnesses, so are pretty well studied.  One team of scientists are working on genetically altering mosquitoes in Africa to make them unable to transmit the parasite that causes malaria. As the mosquitoes breed, it spreads through the population. In an interview, the lead researcher stated:

In the lab, we saw the mutation spread to more than half the population of mosquitoes we had living in cages. This happened in a time span of 12 to 16 generations of mosquitoes (each generation being between 18 to 30 days in the wild). So it's quite efficient.

12 to 16 generations for one mutation to spread to half of a contained population. In human generations, 16 = 320 years, and that doesn't take into account fertility rates, miscarriages, etc. (Not a problem for mosquitoes, I presume).
How many mutations would it take to make two humans incapable of reproducing without endangering their own health or fertility? Excluding all of the harmful mutations that might just result in disease or decreased fertility? And add to that that the males need to change as well as the females? No one knows.
Imagine a cystic-fibrosis type mutation (one gene) that increased the viscosity of cervical mucus such that normal sperm could not fertilize the egg. There would need to be another mutation in males that would make sperm stronger, or secrete an enzyme that breaks down mucus, or something to that effect. However, look at Cystic Fibrosis. People used to die before adulthood. Most men with CF are sterile. Women with CF, living longer now because of better care and treatment, are getting pregnant, but many have a decreased lifespan post-pregnancy, and almost all the babies are premature. You can't predict "when" a series of beneficial mutations so dramatic as to change a being so dramatically. The answer might be never.
Try to give me a single or a few mutations that would prevent the ability of people from one population and another to mate. Say one mutation led to a smaller pelvis. Most women with that mutation would die in childbirth before a mutation arose to make smaller babies (which would most likely be a deleterious mutation as well).
I am not a geneticist (which is really the person who should be answering this question) but I think the odds of this scenario ever occurring are very low. I just can't imagine mutations making reproduction impossible between two populations being beneficial and selected in one population rather than harmful. Keep in mind that different humans from populations that were isolated for many thousands of years have no problem reproducing.

just out of curiosity - why answer and vote to close?

@ChrisStronks - ethical standards. :D


text:
How can a brainless Cnidarian hunt and defend itself?
Cnidaria, such as jelly fish and sea anemones are radial symmetric en feature a simple body plan. One notable aspect is the lack of a brain. Hence, there is no central guiding structure, no mind or will if you like. Nonetheless, they are known to be predatory (such as the sea anemones), and are quite effective in defending themselves as well (such as stinging jelly fish). How does a diffuse nervous system allow Cnidaria to feed and defend themselves?
Sea anemone devouring a crab:

Sea anemones CAN move around.

Sea anemones are members of the phylum of Cnidaria. Distinguishing features of this phylum are radial symmetry and the presence of cnidocytes, or stinging cells (like the ones found in jelly fish). These cells have a mechanical trigger and if activated a subcellular harpoon is fired and paralyzing and painful toxin is injected. A cnidocyte diagram is shown below (from Wikipedia):

The Cnidarian nervous system is relatively simple indeed. The Cnidarian nervous system is decentralized and diffuse, and it basically consists of reflex arches. It is referred to as a "nerve net" as shown in the following schematic of a sea-anemone's nervous system (picture from Florida Int. University):

The presence of cnidocytes and a mesh nervous system basically answer your question:
1) Feeding: Whenever a prey touches the sting cells, it gets harpooned and paralyzed. The mechano-sensory cells sense touch, and drive nervous cells in the mesh. The nervous cells activate contractile epithelial cells in the arms of the anemone that push the prey inside the mouth. Then digestion takes place and the mouth serves as anus once digestion is complete.
2) Defense: the cnidocytes operate by mechanical triggering and no nerve cells are necessary.

Lol, its nerve cells not nervous cells! Beautiful answer though

Are all toxins from Cnderians actually powerful for every creature?

@vajra78: no, e.g. some fishes are resistant and actually live in anemones as a safe home.


text:
Is there a difference between human neuron cells compared to those of other animals?
Thanks for looking.
Firstly, I am nowhere near biologist, just a student, so my apologies if this isn't a "good" question.
Background:
So I was searching about intelligence, brains and computers, and noted 2 videos, one where a person tries growing human neurons to be connected to a computer, and a mouse brain connected to a supposed robot car.
It made me curious, if there's any major difference between neurons between species.
Question
Is there a difference between a human's brain cells compared to other species?
For the sake of the question, it will be limited to a mouse or a dolphin's, but if you can bring more info from another kingdom, it would be really welcomed.
I'll be really grateful if you coupled it with some illustrations!
Note:
This question is NOT about brain-size, but rather, a single unit of whatever that makes a brain, brain.

Not really.
There really is little difference in neurons in mammal and indeed not much change across vertebrates. You have to go back all the way to jellyfish before you find major differences in neurons.
https://pubmed.ncbi.nlm.nih.gov/30826503/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159607/

As you mentioned yourself, there are differences in brain size, form and structure. This difference also affects the size and shape of cells, i.e. you won't find meter-long neurons in mice, but rather in bigger animals. However, the types of cells are overall the same among the mentioned species. It was found that the ratio of glia cells to neurons greatly varies between species and follows a function of overall body mass, i.e. blue whales have an increase glia cell ratio.
https://www.pnas.org/content/103/37/13606

The basic structure of a neuron is conserved across animal species. This is what is taught at universities and can be found in most textbooks. This does not mean that there are no differences, it just means that we do not have any clear/good evidence of any major differences.
There have been some recent studies suggesting that there may be subtle differences between a typical human neuron and that of another mammal e.g. longer dendrites, differences in the electrical properties of the neuron, differences in cell-signalling within the neuron, more compartmentalisation within the dendrites etc. Here is an example of one such study:
https://www.cell.com/cell/fulltext/S0092-8674(18)31106-1


text:
when does an erythrocyte start carrying oxygen molecules and what is the binding capacity
As it is in the title, I am just wondering when does an erythrocyte (especially Reticulocyte) start carrying oxygen molecules and what is the binding capacity for oxygen.
That is, Under normal conditions, reticulocytes are the youngest erythrocytes released from the bone marrow into circulating blood. They mature for 1-3 days within the bone marrow and circulate for 1-2 days before becoming mature erythrocytes. How much oxygen molecule a reticulocytes can carry ?
I mean, I need an approximation of the number of O2 molecules bound to hemoglobin per reticulocyte

Erythrocytes contain many hemoglobin proteins. Each protein has 4 haem groups, and oxygen molecules bind to in porrin ring inside these haem groups. The binding capacity is the affinity each haem group has for oxygen. This changes depending on the external conditions, for example PH.
For example, when the ph is quite low (acidic), this is often due to CO2 build up in the local area, dissolving in the blood to form carbonic acid. This means that there is anaerobic activity happening in the area so it needs more oxygen. The oxygen associated with the hemoglobin will disassociate making it available for the surrounding tissue. It is important to remember that the process is not concrete and is always fluctuating. There are many curves that show the likelihood of association and disassociation. I would recommend looking at these disassociation curves to understand.
Erythrocytes are typically oxygenated in the lungs (supplied by the pulmonary artery from the heart). After oxygenation, the blood goes back to the heart via the pulmonary vein in order to be sent round the body. Reticulocytes are immature erythrocytes and will be carrying increased amounts of haemoglobin as they develop it. The following link leads to a paper which approximates haemoglobin content in reticulocytes.

https://www.ncbi.nlm.nih.gov/pubmed/18027835

Thank you for your answer and the link. I updated my question

@bantandor what specifically about this answer and the linked paper don't answer your question, or give you the tools to find the answer on your own? Are you looking for an approximation of the number of $O_2$ molecules bound to hemoglobin per reticulocyte? You need to be clear about what you're asking for, and be willing to do some research on your own.

Actually, yes I am looking for an approximation of the number of O2 molecules bound to hemoglobin per reticulocyte


text:
CNS memory structure
I'm new in biology. could you please let me know if the following 2 assumptions are correct
A nerve cell in the CNS along with its loop back neurons (Collaterals) is a memory unit. It will trigger per given spikes pattern (example – from the PNS). The said pattern should be “close enough” to enable the memory unit to resonate.
A memory unit is a cyclic sub-graph with its “root neuron”. An inhibitory neuron eliminates multi resonance of the memory unit.

These things could be correct in a very specific implementation of biologically-inspired neurons for an artificial neural network, and might be reasonable assumptions to taking a graph-theory approach to understanding biological neural networks, but they don't capture the known subtleties in our actual biological understanding of how brain networks work.

For example, "memories" as abstract concepts are held in populations, not single cells, though single cells can have "some memory" - pattern completion can be performed by networks, as well. Neurons may resonate in some contexts but resonance is not necessary for recall or encoding of memories. Inhibition has many roles: it can prevent unwanted resonance (for example, seizures), help discriminate similar stimuli, control gain, suppress expected outcomes to highly unexpected events, etc.

Thanks Bryan. Let me ask you, given arbitrary episode how does the brain determine its start & end ? or when does brain conclude "I do not know" / "i do not remember" / "I do not recognize" ?

We don't know :) There are many studies that use psychophysical tasks to begin to answer some of these questions. Some have shown that estimates of confidence can be derived from activity in the prefrontal cortex - answers like "I don't know" require a bit of metacognition so it is somewhat difficult to study. It's actually quite a big deal to be able to recognize when you know and don't know, and one could imagine a fully functional animal/robot without those abilities.

i assume that the answer to this question may address my question  (though it's chicken  - egg  issue)

The concepts you raise in your question are not founded in neurobiology. We do not know what the biological correlates of a "unit of memory" are in the central nervous system.
Although oscillations are widespread in the brain, the relationship between oscillations and memory storage and recall is a subject of active research. The way you state this process in your question is not justified by any experimental evidence that I am aware of.
Memories do not have a "root neuron" — as I wrote above, we do not know how memories relate to neurons. Inhibitory neurons simply provide inhibitory input currents to their post-synaptic targets. Any relationship with "resonance" or oscillations relies on explicit assumptions about emergent network properties, and these are currently unfounded.


text:
Why are human mothers told to "push" out a baby?
I've always wondered why human mothers are instructed to "push" when giving birth.
Every other animal just gives birth of it's own accord. Albeit perhaps from a different position with the help of gravity. You don't have to tell a giraffe to push.
But for some reason humans feel like mothers can only give birth through conscious will power.
Surely, if the mother just let the body do it's natural thing, the baby would come out just the same.
What's more, I would expect that if the mother was consciously "pushing" using the wrong muscles this would hinder rather than help the birth. (Does a woman even have mental control over this?)
Also, what's the rush? As long as the umblical cord is still attached, should it matter how long the birth takes?
When did this idea of telling the mother to "push" first start, and is it common practice around the world?
Here is an article which questions this idea: https://curiosity.com/topics/should-we-stop-telling-women-to-push-during-labor-curiosity/

Also like telling the husband to go out and chop wood - keeps the attention where it is needed...

@Solar But I've read that no attention is needed. As animals can give birth even if unconscious. Actually I read that a hospital in Kent England, has recently stopped telling mothers to push and it actually has reduced stiches and such-like and that this only started in the 1920's as more mothers gave birth in hospitals.

Now you should update your question...

@arsak https://curiosity.com/topics/should-we-stop-telling-women-to-push-during-labor-curiosity/


text:
What are the differences between internal organs between sub-saharan Africans and Northern Europeans
Lets take as examples a typical Norwegian and a typical Nigerian.
In terms of human anatonomy the outer differences are more obvious e.g. (on average)

White skin vs dark skin
Pointy nose vs broad nose
Thin lips vs thicker lips
Straight hair vs tight curly hair
Different skull shape
Height differences
Different colour eyes or eyelids.

In fact there is almost a difference in every external organ.
There are also some invisible differences such as propensity to sickle cell disease.
But what I hear less about is the differences (in general) between internal organs between populations. Some people even suggest that differences are only "skin deep" between human populations. Which I think goes against evolutionary theory. As why would natural selection stop at skin level? Also, there is a lot of research into skeletal differences but that's easier to do since we can look at a skeletons.
Therefor it seems fairly logical to assume that there would be fairly apparent differences in internal organs between these populations. (I hesitate to use the word 'races') i.e. as apparant as different hair types, or different nose shapes.
I don't mean that one population will have 3 kidneys for example, but I would expect that there would be an obvious shape or size difference between most, if not all internal organs, just as there is a shape, colour or size difference between most external organs.
Is there some research done on this, e.g. a catalogue of differences in internal organs morphology between different populations? Or is it taboo to even ask such questions perhaps?
Edit: One might say, "how would anyone know? Or care?" But, for example, a heart surgeon might find they need different sized instruments dealing with different people. Or surgeons from different continents might compare notes on anatomy. And anatomy textbooks based on just one population might not be representative. Surgeries working on one "race" might not work on others. e.g. if the heart wall was thinner or the colon was longer.

Why was this downvoted? Is it a taboo subject? I thought it might be. Pity societal pressure gets in the way of science.

I don't know about organ sizes, but it is known that certain population are more prone to develop certain diseases than others. One famous example I'm aware of are the Pima, who developed a very efficient metabolism in response to the available food in their  traditional environment. However, this efficient metabolism in combination with nowadays western diet makes them prone to overweight and related diseases like type two diabetes. There is research in that field, but it's far from being complete.

I won't consider it a taboo but you must understand that the traditional concept of races is based on superficial appearances. For example it would put all black skinned African people in one group (and so on with other people). Certainly there are differences in different human populations (morphological, anatomical and metabolic). You may rephrase your question on these lines and narrow it down. Be precise and avoid unnecessary explanation of things that you are not interested in.

@WYSIWYG Well if you say straight hair vs. african curly hair is "superficial" then you might say there would also be "superficial" differences in organs. However, it easy to tell by sight the differences. No-one would mistake a native Nigerian for a native Norwegian. I did narrow it down to Norwegians vs Nigerians. In that case the question is "what are the superficial differences in internal organs between these two people." Sounds like a worrying lack of research in this area!

@zooby By superficial, I meant what is easily observable (like skin color or hair shape). The easy-to-tell-by-sight differences were the basis of race. Research has found that just because two people look similar doesn't mean that they are genetically more similar. Anyway, by narrowing down I meant that you can make you question precise. I would rephrase the title on the lines of "are there significant differences in the internal anatomy of different human population groups" (and edit the body accordingly). You don't have to narrow it down to the level of comparing Norwegians and Nigerians.

@WYSIWYG. I think by writing it like that it would make it so vague it would lose most of its meaning unfortunately. Is there anything wrong with asking about 2 specific populations?

“Propensity to sickle cell disease” is a misleading description of the fact that specific individuals in a population have a mutation that renders them less susceptible to malaria. Sicilians also have individuals in their population with a different mutation that serves the same function, although causes a different disease in homozygotes. In neither case is this a universal feature of the populations like skin pigmentation.

@zooby nothing wrong in asking about these specific groups. However, your actual question can be answered with respect to any two groups (not necessarily the ones you mentioned). Also note that lifestyle will also affect the organ sizes. There is some correlation between body weight and size of some organs (studies done in different populatins). However, I don't think anyone has investigated if these relationships are significantly different between different populations (after accounting for factors such as lifestyle and diet).

Yes, but I was just interested in these two particular groups as they have more obvious outward differences than, say, a the differences beteween Sweden and Norway, for example. So the differences should be more pronounced. It would be fascinating if it was found, for example, that in one population the left ventricle was larger than the right and other populations the reverse was true (as a made up example). In a similar manner that a nose might be wider than it is tall or vice versa.

Perhaps you should ask on a medical site. Someone doing autopsies in a country with a population of diverse origins would know. I imagine the answer is no or it would have been observed and reported. I see nothing wrong with your question, just that you are addressing it to a group that is unlikely to have experience in this area.

@David. Thanks, I might try.


text:
Can I dry digested protein sample over weekend in a vacuum concentrator?
I have digested with trypsin the tissue protein extract for mass spectrometry, and forgot to transfer the sample from the SpeedVac to the -80C freezer. As I did this on Friday, I can transfer the samples only on Monday. Will this temper with my sample and subsequent protein identification?

I doubt there is any quality literature on this question, so the only way to find out is to try it. I suspect it would be fine but you should do some kind of risk analysis to determine whether you should just start again (ie the hassle of preparing a new sample versus the hassle of failed mass spec).

If your sample dried in the speed-vac then it should not cause to much damage to the sample. But if Speed Vac stopped and there was some liquid left, then incubation at room temperature would result in hydrolysis and sample degradation ( also depends on the pH, neutral would be slower). Also you would have modifications to the amino acid side chains like oxidation and deamidation


text:
Why do my peptide samples turn yellow and red?
The protocols for (brain) tissue digestion I am trying out are: lysis (buffer containing 0.1% SDC or SDS in 100mM TEAB + phosphatase inhibitor which is sort of yellow), reduction with TCEP, alkylation with iodoacetamide, digestion with trypsin, and acidification with trifluoroacetic acid (TFA) to deactivate trypsin. After that I usually dry the sample and do a C18 clean-up.
For some reason my samples become yellow after the addition  of TFA (and this was also the case with lysis buffers with SDS or SDC so I don't think it is detergent related). As this happened to a colleague who didn't use the phosphatase inhibitor, I don't think it's related to it either. When I do the C18 clean-up this yellow goes to the eluate (elutes with peptides). Would anyone know why this yellow colour occurs? The most disturbing thing for me is that it does not always happen to every sample, as you can see in the photo 0.1%SDC is clear.
Moreover, for the last digestion, I decided to try out Rapigest (0.1% in 50mM TEAB). When I added the TFA for acidification step, the sample was still clear, but after a while drying it in SpeedVac, when I checked up on it, it had a bloody red pellet-like oddity as you can see in the photo. I left it in the SpeedVac to dry out completely, and when I checked it again, the red colour disappeared and it was clear-whitish again. Would anyone know why this happens and if it interferes with subsequent steps such as C18 clean-up or LC-MS identification? So far, I have asked my colleagues, but they have never seen it before and are calling it magic.

Is your preparation of TFA fresh and protected from light?

Do you mean is it kept protected from light after it is diluted and added to the sample? Because TFA usually comes in dark bottles, but then when we dilute it to 0.5 or 5% it is kept in light in transparent ones. Once a dilution is prepared, it is used for a long time (couple of months) in our laboratory. Does this usually cause problems?

After a few months or if the solution begins to take on a yellow hue I'd discard it. TFA on its own is light sensitive, however, and personally I'd try to store it out of direct light. It could also be a reaction breaking down the TFA, but im not sure. In the rapigest tube I'm 100% not sure. I actually saw a protocol somewhere though, if your solution turns yellow you can add some 1% v/v TFA to make it clear again. I'll keep looking into it.

The TFA solution I used was still clear. However, when this happened I made a fresh one, so I will let you know if it happens again. Thank you I will try that next time.

@E.T., Rapigest is an acid-cleavavble detergent which precipitates after cleavage, because of which it can be removed before LC-MS analysis. After digestion, TFA would acidify it and you should keep the sample at 37 ºC for 30 min to cleave all Rapigest that then would precipitate and should be removed by centrifugation.

Also, after lysis and before reduction/alkylation/digestion, do you remove insoluble cellular debris by centrifugation? I would always denature a protein sample before starting  reduction/alkylation/digestion procedure, by 2% SDS or 8 M urea or TCA precipitation.


text:
Reason for hiccups?
I recently fed my axolotyl an earthworm, which is good for them. I was rather kind and made sure that the said earthworm was quickly despatched beforehand. Now, watching the axolotyl whilst swallowing the worm, he exhibited a series of rhythmic "hiccups". It got me thinking. Maybe hiccups are an ancient evolutionary means of ensuring that live prey are killed by the movements of the diaphragm muscle to protect the ingestor, whether the prey is eaten on purpose, or by error. Even herbivores may have hiccups because they may swallow, say a snake or something by accident. A horrible thought, I know, but it may make evolutionary sense ! Although I understand that only mammals have diaphragms, perhaps this is an evolutionary muscular trait which stems from a common anscestor which has been refined in animals. I would be very interested to hear anyone else's thoughts. Many thanks, Donna Skelly.

This phenomenon seems to be typical to mammals only.

Non-mammals don't have a diaphragm.

This paper, linked from the Wikipedia page that Sanjuka linked, suggests an older evolutionary role for hiccups, but I think this is all quite controversial and not well worked out. I'd also caution that hiccups are using machinery that exists for other purposes, so there might not be a great evolutionary reason or origin besides "it wasn't harmful enough to be selected against."


text:
Is this a dust mite?
I dropped my phone onto the carpet and picked it up and saw this tiny mite crawling around on the screen.
It is too small to be a bed bug, but perhaps too big to be a dust mite (and doesn't look like the images I found).
Main image is an out of focus image with an iphone simtray for size comparison (the mite about 0.5mm).
The second picture from the left is the only one where I seemed to be able to get its head; all others it was moving away from my camera. I couldn't take any better photos so you'll need to click the image to see the mite in detail.
EDIT: I am in the UK

Dust mites are microscopic, and have 8 legs only.  You probably have a picture of a carpet beetle larva ('hairy').

Looks mite-like to me. Definitely doesn't look like any  carpet beetle larvae I've ever seen.  It doesn't  have  clear segments like the  larvae typical  of  beetle species...

@theforestecologist - I defer to your superior knowledge of insects. Carpet larvae was the only thing I could think of. But they certainly aren't the typical dust mite.


text:
What is this apple's abnormality?
The apple pictured is a of the Gala variety,typically striped.The stripes swirl around a brown protrusion. The protrusion is flexible,in the way a leaf is flexible. The flesh underneath is not discolored or soft. The apple is not misshapen,the seeds are not un-developed or underdeveloped. What is this brown protrusion called and what causes it?

Did it grow on/next to a branch?

I don't know. It was sold loose it a supermarket. I only saw it after it was picked.

I take it that the question is about the mis-shapenness of the apple, that the stick we see in the dip is the core. The morphology (shape) of fruits such as apple and pear are very sensitive to how well the fruit was pollinated. As we know there can be a variable number of seeds in an apple, but the important fact determining shape is that there should be viable seed develop in each of the five seed pockets resulting in balanced development of the fruit. If the pollination is poor and only a few embryo seeds are fertilized, then the development of the surrounding flesh will favour the pockets that contain viable seed, resulting in possibly mis-shapen fruit. Once you have wondered enough and decide to eat, cut open carefully and on the small side you should see that the seeds are either too few, non-existent or failed to develop.

Thats right, Lorel C. My question is about the brown thing on the side of the apple, not misshapeness.

I don't know what part of the tree it grew on.It was sold loose,in the supermarket.


text:
How to calculate the percent of mitochondrial heteroplasmy
How do people calculate the percent of mtDNA heteroplasmy?
Does 7% heteroplasmy out of 10 cells, represent a mutation found in the same position on the genome among 700 mtDNA genomes out of 10,000 mtDNA genomes assuming there are 1,000 genomes per cell?
Thanks for helping me understand this concept a little better.

I emailed the authors of the paper "Age-Related Accumulation of Somatic Mitochondrial DNA Mutations in Adult-Derived Human iPSCs" and they confirmed that they calculated the % of mtDNA heteroplasmy by the following:
Aligned all mtDNA genomes against the reference sequence. Any deviance at a specific position from the reference was a "mutation". The % heteroplasmy was calculated by dividing the total number of mutations at a certain nucleotide position by the total number of genomes represented at the position multiplied 100.
So in other words, to go back to my original question- if there were 10,000 genomes aligned and there were 700 mutations at the same position, that mutation would have 7% heteroplasmy.


text:
Save endangered parasitic species?
It seems to be an important issue the parasitic control and even some pursue the eradication of some species. Most of the researchers in parasitology are focused on the host damage and population regulation. How do we perceive and value the function of parasites? Is it really needed a change in paradigms and views of dependent species? How important is to conserve them?

are there any parasites that are endangered of extinction? Even smallpox is extinct only in the wild.

This is an interesting subject but it sounds like you're focusing on the ethical aspects, which are probably too opinion-based to be a good fit for this site. Can you clarify what you're looking for a bit more?

Although we think of parasites as harmful and tend not to consider them for conservation, they do peform valuable functions including population regulation and the development of immune systems. More philosophically, under the 'intrinsic value' argument sometimes used for conservation, every species should be considered to have an intrinsic right to existence, regardless of its ecosystem function, harmful effects on other species or appeal to humans.
Conveniently, this article has just been published on this very subject. :)


text:
Why do we die of old age?
Not sure where to ask this question and thought this would the best place.
I am not after any opinion or theological, philosophical answers.
I am after the science or biology research, experiments or facts.
I would like the answer to be focused on the following:
Why do we die? With the condition that there are no diseases or any outside factors contributing to death.
In a simpler way, what makes us die biologically, physiologically. Is there a trigger? Is it cellular?.... and so on
As per suggested comment, I have researched genetics such as cell regeneration dynamics, Organ's lives studies.
Yet I find very little on the brains involvement, nervous system, chemical or anything else on the multitude of systems we have including triggers or irreversible messages from any or these systems

Possible duplicate of What evolutionary explanations are there for death?

These answers are not what I am looking for! I need a scientific explanation on any level, like cellular or brain chemistry or how many heartbeats there is in a human... that sort of thing

here is a good answer about the scientific explanation: https://www.reddit.com/r/askscience/comments/3fmle0/what_really_causes_death_when_you_die_of_old_age/

This answer is too partial and diverges into diseases. Many people just die of old age without diseases and relatively well balanced, yet they still die.

What research have you done so far to answer your question?

Genetics: at one point, our cells regenerate less than what we lose: we get old! Is there a link? There's research on hearts: apparently, they have a certain amount of beats.... that sort of things. Yet I cannot find a complete explanation possibly linking all these factors, or is there another avenue I haven't found yet!

Possible duplicate of Why does evolution not make our life longer?

Again, these answers focus on specific issues of dying old, not the pure biology of what I am asking!

In the absence of disease (including starvation, electrolyte imbalance, etc.), there is no death. Old people die of diseases, even if those diseases went undiagnosed while alive.

A possible answer (plus probably a bunch of other factors) is the rate of cell death/damage exceeds that of cell repair as one ages. Search on google for 'The impact of aging on kidney repair' if you want to read more (EDIT: Here's the link https://www.ncbi.nlm.nih.gov/pubmed/18287400 )

We die of old age because the biological cost of making us live forever does not improve our chances of passing on our genes. In nature something else would kill us eventually so there was never a reason to evolve the ability to live indefinitely. There are multicellular organism  that are biologically immortal(all unicellular are), they live slow low activity lives. A lot of the evolution of more "advanced" life is trading regeneration or longevity for higher activity. Literally live fast die young, leave more offspring.


text:
Why do we see a different color when we mix two colors?
The compounds responsible for a color do not change when they are mixed with another material. The same compounds are there after mixing. However, when we mix colors such as blue and yellow we see green.
BUT we are able to tell where a color starts and ends in pictures. For example, if we hold a yellow piece of paper up to the sky, we can tell that the paper is yellow and the sky is blue. We can distinguish where the paper ends. And where the sky starts. We do not see a green outline near the paper.
I believe that  how we perceive colors may explain this. But I am not sure how. Is it because how the brain integrates information. Or is it because of how the cones cannot register two signals at the same time. Why do we see green instead of a blue and yellow?

Assuming you're correct (and I'm not sure you are), most likely because of the size of the particles mixed is too small to differentiate with the naked eye. Consider: Mix blue and yellow M&Ms and you'll have no trouble distinguishing the colors. Keep halving their size (pretend there's no chocolate) and at some point, the whole group will look green. They'd have to be quite small, though.

Are you asking why eyes don't have microscopic resolution or how color vision works?

I don't seem to understand the question either. Could you be more specific?

@John  I am asking whether it is the inability of microscopic resolution that makes us see a different color when two colors are mixed OR whether it is how color vision works that makes us see a different color OR something else.

well it depends on whether you are talking about mixing pigments or light. For pigments it is basically resolution. for light is how we see color. here is a great ted talk about color vision research. http://www.ted.com/talks/beau_lotto_optical_illusions_show_how_we_see

I am not sure if this is entirely correct, its just a scientific guess. But it might actually play some role in this phenomenon. This is actually the physics part part of answer rather than the biology part.
Rayleigh criterion for angular resolution is the minimum angle which two bodies should subtend on an object so that they can be viewed as distinct bodies by that object.

Suppose there are 2 bodies, (right now) with same color of wavelength $\lambda$. Now, they are viewed from a lens of aperture $d$. Thus, from Rayleigh's equation, the minimum angle which these bodies should subtend with each other on the lens is given by:
$\theta = 1.22 \lambda/d$
Now I'm not sure if this is correct, but if the 2 bodies have different colors, of wavelengths $\lambda_1$ and $\lambda_2$ then the equation becomes:
$\theta = 1.22\times (\lambda_2 - \lambda_1)/d$
$\theta = 1.22 \times \Delta\lambda/d$
Now, putting values in this equation:
$\lambda_2 = 597 nm$
$\lambda_1 = 492 nm$
$d = 5 mm = 5 \times 10^{-3} m$
Answer comes out as:
$\theta = \underline{1.22 \times 105 \times 10^{-9}}$
$\hspace{15mm}5 \times 10^{-3}$
$\theta = 2.56 \times 10^{-5} rad = 1.4 6\times 10^{-3\circ}$
So, if these 2 bodies subtend an angle less than $2.56\times10^{-5}$ radian, then they will appear as a single object with green color.
Now, solving it by a common formula:
$\theta = a/l$
$l = a/\theta$
$l = \underline{\hspace{7mm}10^{-2}\hspace{7mm}}$
$\hspace{8mm}2.56 \times 10^{-5}$
$l = 390.625 m$
It means if yould hold two 5 cm x 2 cm papers together (i.e. total 10 cm2), one with blue color and the other with yellow color, then you would see a single paper of green color if you keep these papers $\approx$391 m away (if my calculations are correct ;).
This, in part, explains that it is not the fault of only our eyes, but of light and physical laws too.
References:

Angular resolution
Wavelengths of different colors
Resolving power of imaging instruments

The geometry part at the end with theta = a / L ...  is not clear. From the  figure it should be tan (theta) = a/2 / L, to be precise.  But I guess theta = a/2 / L is a good approximation since the angle is so small.

@Roland I don't understand that one, why would it be  a/2? If you take the eye at origin and bottom line at x-axis, then $\theta$ has to be a/l. I suppose a/2l would give $\theta/2$.

My mistake. I read the figure wrong, you're right.


text:
How does the body make sure that Vasoactive Intestinal Protein reaches only the target tissue?
Vasoactive Intestinal Protein (VIP) is a 28 amino acid neuropeptide that has several effects in several systems. These include the cardiovascular system, respiratory systerm, urinary system, immune system, etc. Furthermore, some of the effects appear to clash with each other. For example, studies have shown that VIP can have an antidipsogenic effect, while some have shown that it induces the secretion of vasopressin. Vasopressin is usually secreted when there is not enough water in the body. Thus, it seems contradictory that the hormone would induce cessation of thirst and secretion of vasopressin.
The hormone is  a paracrine mediator. This makes sense since limiting the distance that VIP travels allows for the hormone to only reach the intended tissues. However, it is also a neurohormone. Which means that it travels through blood and I would assume that it causes a myriad of effects. My question is, how does the body make sure that VIP does what is intended to do?

Do you mean vasoactive intestinal peptide?

@BryanKrause Yes. Sorry. I will edit the question

Vasoactive intestinal peptide (VIP) acts in the intestine, brain, kidneys, lungs, heart, blood vessels, etc. (Cardiovasc Res) and its effects all lead to the same goal: to improve the delivery of blood, glucose and oxygen to the tissues, so it's not a problem if it acts on different tissues simultaneously. Specifically, VIP stimulates thirst, water retention and blood flow through the coronary and pulmonary arteries, dilates bronchi and breaks down glycogen to glucose, among other.
VIP can act via the nerves as a neurotransmitter or via the blood as a hormone:

In research animals and in humans, VIP, administered into the coronary
  artery or intravenously, increases the epicardial coronary artery
  cross-sectional area, decreases coronary vascular resistance, and
  significantly increases coronary artery blood flow. High frequency
  parasympathetic (vagal) nerve stimulation also releases endogenous VIP
  in the coronary vessels and heart and significantly increases coronary
  artery blood flow. (Cardiovasc Res)

In humans, VIP stimulates water retention and thirst:
1) VIP stimulates the secretion of renin:

VIP has now been shown to produce an increase in renin release in a
  number of species, including humans. (Ann N Y Acad Sci)

The activation of renin-angiotensin-aldosteron system results in water retention.
2) VIP stimulates the secretion of vasopressin (Cardiovascular
Research). Vasopressin stimulates water retention. Since vasopressin (arginin-vasopressin or AVP) is dipsogenic (stimulating thirst):

given the established dipsogenic effect of AVP in the nonpregnant
  state... (JCI Insight)

and since VIP stimulates the secretion of vasopressin, VIP is also dipsogenic.
Now, there seems to be some conflict in the studies about VIP being dipsogenic or anti-dipsogenic in rats:

VIP was found to have no effect on drinking when injected centrally
  and peripherally in the eel, although it is dipsogenic in the rat
  after central injection. (ResearchGate)
Intracerebroventricular administration of vasoactive intestinal
  peptide strongly inhibited drinking in rats deprived of water...
  (Neuropharmacology)

Not to go in the details, but there may be different circumstances, for example, the level of dehydration, in which VIP can act differently...


text:
Can someone please identify this plant?
Photo taken April 27 in Savannah Georgia

Do you know anything about the flowers?

I'm not sure that it has flowers, I think it might just be a leafy shrub. That's why I'm having such a hard time figuring out what it is. :(

It looks a lot like a Muehlenbeckia species to me. More commonly known as the Australian Wire Vine.

@MrG That looks exactly right! Thank you so much!!