text:
Does opening of ion channels alter the membrane potential directly?
Does the opening of a voltage-gated ion channel (i.e. the change of configuration of the protein) by an appropriate local change of the membrane potential directly and significantly alter the membrane potential in turn? Like the influx of ions that was caused by the opening of the channel does directly alter the local membrane potential?
(Assume there were no ions going through the channel: would there nevertheless be a significant change of the membrane potential by the mere opening of the channel?)

Why are you interested in this question? How can you imagine a channel opening but no ions passing through? Even if we could somehow experimentally isolate this effect, why would you expect it to matter enough compared with the voltage changes due to ion flow?

I added "significant" in my question. Because I am not a biophysicist and my physical intuition is not strong enough, I only guess that there might be a significant change. If you say the effect is negligible ("doesn't matter enough"), that's already a valid answer.

Like others said before: if there was such an effect, you would have heard of it. Does this apply here, too?

BTW: Of course I can imagine a channel opening but no ions passing (because there aren't any around). But not under normal circumstances, that's true.

Not in any substantial way from the perspective of the overall membrane potential; it could be possible to measure the charge moving as a way to study channel gating, but that's a completely separate issue (and the scale of measurement would have to be incredibly precise, way more precise than is relevant for neural function).
Although very few ions have to move across the membrane to change the membrane potential, this "very few" is in relationship to the total number of ions present in a solution, which is massive and difficult to imagine. A single ion channel can flux millions of ions per second.

That's the explicit answer I hoped for (and expected) but couldn't get otherwise.

I would like to add a small calculation to this question:
The membrane has a large capacitance (1 uF/cm^2). A 20 um diameter cell will have a capacitance of about 50pF.
The number of charges needed to change the membrane potential in 1 mV can be calculated by:
Q=C*dV
Acording to the fromula you`ll need 0.5 pC or about 3*10^-6 elementary charges to produce a 1 mV change.
A single ion channel such as the Shaker K+ channel can move 12-13 elementary charges during activation link. This would mean activation of 3*10^6 Shaker K+ ion channels.
You can see you`ll need to have a lot of channels to do the trick.
Even though the voltage changes due to these "gating" charges is small, the current generated by the movement of these charges can be measured. They are called "gating currents".


text:
Distribution of synapses of CA1 neurons
In the Wikipedia article on dendritic spikes I read:

In the hippocampus, the CA1 neurons contain two distinctive regions
  that receive excitatory synaptic inputs: the perforant path (PP)
  through the apical dendritic tuft (500-750 μm from soma) and the
  Schaffer-collateral (SC) through the basal and apical dendrites
  (250-500 μm from soma).

I wonder how the distinctiveness of these two regions does appear when plotting the number of synapses as a function of the distance to the soma:

More like the gray, or more like the red, or more like the green curve? Or which other?

One source for this estimate is Megias et al. 2001, an electron microscopy study in CA1 of the rat hippocampus.
I plot their data from Table 3 in the following graph.

The X-axis is not in micrometers. Rather it represents dendritic subclasses. $Ori$ stands for Stratum Oriens, $Rad$ for S. Radiatum, $L-M$ for Lacunosum-Moleculare, $T$ for thick dendrites, $t$ for thin dendrites, $prox/med/dist$ for proximal, medial, and distal, respectively. Stratum Oriens represents basal dendrites that are close to the cell body, stratum Radiatum apical trunks, and stratum Lacunosum-Moleculare the apical tufts. The approximate locations of the layers in reference to the cell body are (in micrometers): $Ori = (-100, 0)$, $Rad = (100, 350)$, $L-M = (350,550)$. The Y-axis represents the total number of synapses, both excitatory and inhibitory.

Isn't it possible to attach rough distances to the dendritic subclasses? Since distance to the soma is important.

What does a  negative distance mean?

If we assign the cell body, or more precisely the stratum pyramidale, at $0$, then stratum oriens is to its dorsal side and stratum radiatum on its ventral side. I've arbitrarily assigned dorsal $\rightarrow$ ventral as the positive direction.

But the effective (physical) distance is still positive, isn't it?

How could the soma distinguish between dorsal and ventral?

I have included direction to help the reader realize where the cell body would lie in the above bar graph, nothing more.

source: Stack Exchange

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

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How can botox cure wrinkels?
How can botox cure wrinkels?
Do wrinkles caused by tension of some muscles in the skin?
Can these muscles be relaxed by hypnosis or training?

To avoid down-voting of your question, perhaps first read about Botulinum toxin and if there's something that you still don't understand come back and amend your question.

@vkehayas you can downvote if you wish; I have read articles about botulinum toxin, but I need positive statement like wrinkles caused by tension of muscles.

I hope you didn't take my comment as a 'threat' but merely as a suggestion to improve the question. Based on your comment I would suggest that you could consider asking that question, i.e. "how do wrinkles form?"

@vkehayas then I would read about collagen, hyaluronic acid and etc loss which I don't want to

@vkehayas i.e. I need to clash the fact that botox works and common theories of skin aging

Botox works by inhibiting signal transmission at the neuromuscular junction preventing the signal sent by the nerve from reaching the muscle through the destruction of the receptors on the surface of the muscle. As the intensity of contractions decreases the overlying skin is able to recover from constant contractions and replenish the lines and wrinkles with collagen. To keep the wrinkles at bay you will have to repeat this every 3-4 months.

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

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


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What is the minimal focal length of the human eye?
What is the minimum length to which the focal length of our eye can go, even when  considering the blurred images too.

Short answer
The focal length of the average, healthy, adult human eye at near-point is about 18.5 mm. Young individuals can accommodate their lenses further to a focal length of around 15.4 mm.
Background
The focal length of the human eye is the distance between the lens and the retina when an object is in focus (Fig. 1). Therefore, the ...even when considering blurred images too part in the question doesn't make much sense. So, I will focus my answer on sharp images only (pun intended).
The lenses of the eye are thicker in the center than at the edges, and hence positive and converging lenses. They form an inverted image on the photosensitive layer in the back of the eye - the retina (Fig. 1) The retinal image is shaped by two lenses: 1) the cornea with a fixed focal length and 2) the eye-lens, which is a lens with variable focal length through shape changes (Fig. 1) called accommodation and is mediated by the ciliary muscles (Kolb, 2012).
When the ciliary muscles are relaxed, the focal length of the eye-lens is maximal and the distant objects are in focus (infinity). When the ciliary muscles contract they shorten the focal length of the eye-lens to bring nearer objects into focus. The two limits of this range are called the far-point, (ciliary muscles relaxed), and the near-point (maximal accommodation) (source: University of Colorado, Boulder).
The distance between the eye-lens and the retina is about 20 mm. When an object is far away from the eye (infinity), the image is located essentially at the focal point. Therefore the focal length of the cornea and the eye-lens should be about 20 mm when the muscles of the eye are relaxed. The lens strength is the reciprocal of its focal length in meters. Hence, the strength of the cornea and the eye-lens at the far-point is about 1/0.020 = 50 diopters (source: University of Colorado, Boulder)..
When an object is located at the near-point (the closest point at which an object can be brought into clear focus on the retina), the focal length of the cornea and the eye-lens must be changed so that the image is formed on the retina, which is still 20 mm away. The typical near-point in an adult is 25 cm, corresponding to a focal length of the cornea and the eye-lens of 18.52 mm using the standard ray-tracing rules of lenses. Hence the strength of the cornea and the eye-lens must now be about 1/0.01852 = 54 diopters. In other words, the muscles of the eye can provide an accommodation range of 4 diopters (source: University of Colorado, Boulder).
Kids can, however focus to points as close as 6.5 cm away, i.e., 15 diopters worth of optical power, i.e., a minimal focal length of 15.39 mm.

Fig. 1. Human eye. Upper panel: non-accomodated relaxed eye. Lower panel: accomodated eye. source: Khan Academy
Reference
- Kolb, Gross Anatomy of the Eye. In: Webvision. The Organization of the Retina and Visual System, Moran Eye Center (2012)


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Can a person die from over exposure to rain?
Is it possible to die from being over exposed to rain? For example, if outside for a long amount of time (days) in a continuous storm?
I searched online but didn't find anything immediately. To me, maybe a really long exposure to rain (water) would cause skin tissue issues, which might then have potentially more serious effects on other body organs/systems.

Now that I think about it.... maybe I didn't find anything because it's never happened before... maybe I'm just not good at searching online. but still, can someone answer this question for me,?

Rain per se? No. But when you are wet, your body looses heat more quickly. If it's near freezing, windy, and raining you are in much more danger of developing hypothermia, or low body temperature. If your body temperature falls low enough, you can die. You may hear references to death from exposure, which is shorthand for "exposure to the elements", but the actual problem is hypothermia. If your feet are continuously wet for days and day, you may develop immersion foot, also called trench foot:

Trench foot is a medical condition caused by prolonged exposure of the
  feet to damp, unsanitary, and cold conditions. The use of the word
  trench in the name of this condition is a reference to trench warfare,
  mainly associated with World War I. Affected feet may become numb,
  affected by erythrosis (turning red) or cyanosis (turning blue) as a
  result of poor vascular supply, and feet may begin to have a decaying
  odour due to the possibility of the early stages of necrosis setting
  in. As the condition worsens, feet may also begin to swell. Advanced
  trench foot often involves blisters and open sores, which lead to
  fungal infections; this is sometimes called tropical ulcer (jungle
  rot).


text:
Why facet cells/umbrella cells of uroepithilium are sometimes multinucleated?
Why do are they multinucleated and why only some cells, why not all?

Can you add a source where you obtained this information? Is it a question on the human urogenital tract or of some other animal?

The source is 'Textbook of HUMAN HISTOLOGY' by Inderber Singh and yes, we are talking on human uroepithilium.


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Camouflage grasshopper identification
I came across the following grasshopper this afternoon while walking to my car. It was initially resting amongst some fallen tree leaves, but as I got closer to my car I must have startled it, as it then ran to the tree, and is also how I noticed it.

It was calm enough for me to temporarily hold it in a cut-in-half water bottle, and I was able to take a few more pictures, and record a brief video. Afterwards, I released the grasshopper back into the grass and it promptly flew away. :)

When searching for its species, I was only able to find a dessert grasshopper, Trimerotropis pallidipennis, but I live in KY, and not out west, so I don't think that's it.
Can someone ID this for me please?
Location: Central KY, USA.

You've found a Dissosteira carolina or carolina locust.
I'm not completely sure, but I think this is a male.
They are quite common in North America.

idtools.org/id/grasshoppers/factsheet Dissosteira carolina
uwyo.edu: Dissosteira carolina

Yes, this is it! Thank you.


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Which species has the highest proportion of homosexual individuals?
Are there more homosexual individuals in ducks, humans, or some other species?

100% of male flour beetles are bisexual.

Homosexual behavior have been observed more than 1500 species (according to Museum of Natural History of the University of Oslo). A full comparison between all known species is far beyond the scope of this site, but below I discuss three species of interest. Also, the details of what counts as an homosexual behavior, and also whether you compute incidence or prevalence makes the whole discussion semantically complicated.

According to Simon Levay and Aldo Polani, in domesticated sheep, 10% of the rams (males) prefer mating with other rams than with ewes (females).
About 25% of black swans are homosexuals (Braithwaite, 1981).
In lions, 8% of the mounting is in between two males (Bagemihl 2000)

In humans, around 3%-5% of the surveyed people claim being homosexual or bi-sexual (see wiki > demographics of sexual orientation#Modern_survey_results).

Any evidence (link) for the claim of the 1500? Otherwise nice answer!

@RHA Reference added. I would not call it an evidence as it is not a peer reviewed paper though. Thank you

Good enough (and +1), I just knew you hadn't made that number up yourself.


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How many oxygen atoms are used up in aerobic oxidation of one pyruvate?
Please explain elaborately, if possible using the EMP, Krebs and ETS cycles.


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Saltwater fish identification
Can someone please identify this fish. Someone had asked me to rehome this fish but they were unsure what type of fish it is. Right now I have it in a quarantine tank until I find out what type of fish it is. I know it is some sort of clown but I cannot find the specific type after that. The fish is the one in the foreground of the image being black and white. It is a saltwater fish.

I know it is some sort of clown but I cannot find the specific type after that.

This is a juvenile Plectorhinchus chaetodonoides, which carries the nickname of "Harliquin sweetlips". With respect to the clownfish, they are similar up to the order Perciformes.

Juveniles are brown with large white blotches and mimic the movement of a poisonous flatworm for defence against predators. They gain more spots and the spots reverse from white to black as they age.

Thank you very much! Now I can do research on type compatibility. I appreciate it


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Does exhalation help us speak, and if so, how?
Everyone knows that we breathe in oxygen and breathe out carbon dioxide. That's how the respiratory system works. But we also use the respiratory system to produce sound and language. When we speak or emit sound, our glottis opens up, and depending on whether the sound is vocalized, our vocal chords vibrate. We then use articulators (tongue, lips, teeth) to shape the sound we produce.
But what kind of air is emitted in the first place? When our glottis opens up, what kind of air is passing through, and why does it pass through? The most obvious answer, which is my first guess, is that carbon dioxide is passing through our glottis and our trachea, and that we use this to create sound. In this way we would be using the product of respiration for a separate purpose: to create sound and communicate.
This is only a guess. But a logical one. The question, to put it most simply, would be, do we utilize our natural cycle of exhalation to produce sound and speak? Or is something else going on?

Exhaled air is not changed drastically from inhaled air; it is still mostly nitrogen and oxygen.

@canadianer I see. But would you agree that the air which helps us produce sound is exhaled air? I.e. We take advantage of exhalation in order to speak? It's almost a stupid question, but I would like to get a solid understanding of the mechanism.

Yes, I would agree.

There is a very minimal increase (and I do mean minimal) in the CO2 concentration depending on how fast we speak, how often we stop to take breaths, etc. compared to plain, expired breath. This is because the inhaled air is being held back in the lungs and released more slowly as we speak, giving more time for O2/CO2 exchange to occur. However, it will mostly occur in what's called "dead space" and the %CO2 will be changed for a few breaths thereafter as well.

Not including water vapor, argon and trace elements, inhaled air at sea level: ~79% nitrogen, ~21% O2, ~0.04% CO2. Exhaled air: ~79% nitrogen (the body doesn't "use" inhaled nitrogen), ~16% O2, ~4% CO2
It is this exhaled air we use to speak. However, there is a very minimal increase (and I do mean minimal) in the CO2 concentration and decrease in the O2 depending on how fast we speak, how often we stop to take breaths, etc. compared to plain, expired breath. This is because the inhaled air is being held back in the lungs and released more slowly as we speak, giving more time for O2/CO2 exchange to occur. However, it will mostly occur in what's called "dead space" and the %CO2 will be changed for a few breaths thereafter as well.
To demonstrate this, speaking until we're "out of air" should make us slightly dizzy because maximal exchange will have taken place at a certain point, after which our blood CO2% will rise, and our blood O2% will fall.
After that, the higher serum CO2 will cause us to take a deeper breath, a 'cleansing breath' if you will, to jump start the return to normalcy in blood gasses. It is very, very hard to resist this deep breath (which is why breathing has a voluntary and an involuntary component, i.e. you can't hold your breath until you die.)
Breathing

If an average of 5% of your expired gas changes from 1.45 grams per liter to 1.95 g/L as it goes from O2 to CO2, the total change of mass of expired air is about 1.5 percent. That's countered by warm air which expands so it becomes lighter.
So the fluid physics of the expired air doesn't make a marked octave difference compared to raising the vocal chords.
Air at 0'C is about 5 percent heavier than air at 20 degrees, 20'C incoming air would be 1-2 percent heavier than the same air 30'C.
Another physics thing is that dry air is lighter than moist air.
Oxygen absorption has no major role to play in sound generation, as Nitrogen constitutes 78% of the volume.
why does it pass through? Exhalation contributes to control the volume of the sound output. Air pressure is necessary to cause the vocal chords to vibrate as taught chords that can oscillate continuously when displaced by a constant flow of air.
Quite complex muscle actions of the thorax, rib cage, diaphragm, and abdomen occur during utterances, here are some measurements.
The vocal chords are also known as vocal folds. They narrow during sound production, and are open during respiration. They narrow very thin and vibrate as a direct cause of exhalation. There is a video of vocal folds vibrating, and you can see them vibrate. https://en.wikibooks.org/wiki/Acoustics/Human_Vocal_Fold
http://www.entusa.com/larynx_videos_flash/normal_larynx/normal_larynx_mp4-0.htm
Above them is an air chamber that guides the sound waves into vowels, like A E I O U.
Other mammals don't have a developed air chamber above their vocal chords, and mostly can make screech sounds rather than vowels, however mammals can drink and breathe at the same time, which humans can't. You can study evolution of the voice box on other threads.
It's the same as with a trumpet, if the guy doesnt breathe outwards, sound is not produced, and stronger breathing changes the sound.


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Motifs in undirected networks
I have an undirected network and I am currently analyzing both three and 4 node motifs in the network. However, I can't find any articles which describe the biological significance of 3 of 4 node motifs in my network. Comparing with randomly generated networks, I am able to deduce that the number of three node motifs and 4 node motifs are significantly higher. However, I am unable to infer any biological significance for this finding.

Can you clarify what is your network? Is it a network of genes, protein-protein interactions or something else?
Also do I understand right that you randomly generate networks without considering the fact that most biological networks are actually scale-free networks?

@MaximKuleshov Its a transcriptional regulatory network https://price.systemsbiology.org/research/honeybee-transcriptional-regulatory-network/

@MaximKuleshov  I understand that TRNs are directed and bipartite comprising of transcription factors and the genes they regulate. I was just curious about motifs in co-expression networks.

@MaximKuleshov Also, I understand that Biological networks are scale free networks, I actually split my network into 8 clusters and the whole comparison to random networks is to prove that the clusters in themselves are real.

What is the structure of the 3 of 4 node motifs of your network for which there is no description of biological significance? - Which type of random network did you compare to?

I am not 100% sure that I understand the question, but I am going to try to answer, based on the following assumptions:

The "number of 3 and 4 node motifs" is not very clear. If I understand correctly, it should be a quantity determined in large part by the degree distribution. You could rewire your network to lose all information about the TRN other than degree distribution and this number is probably very similar (or it is a quite weird network, which would make me suspicious of the data).
Therefore, the number of such motifs of size $k$ is not particularly interesting biologically, specifically due to technical issues such as incomplete ascertainment of edges, etc. The true network may have many more edges, and this will change this number, so the degree distribution is not itself interesting- it is in fact the thing you want to control for.
Therefore, when you compare with randomly generated networks and find different numbers of motifs of $k$ nodes, I suspect the random networks were generated with a different degree distribution. (It is pretty easy to generate networks of the same degree distribution, using e.g. the rewire() function in igraph)
Therefore, I interpret the question to be more specifically: "Among all 3 and 4 node motifs, a subset are overrepresented in my TRN compared to randomized graphs of the same degree distribution. What are some ways to interpret these motifs?" This is the kind of question that is traditionally asked with TRNs in my experience.

As an example of how other groups have analyzed TRN motifs, I suggest looking at Figures 5 and 6 of this paper. For instance, the "feed-forward" motif is overrepresented for links involving some TFs. I believe that it is standard to compare motif distributions to other biological networks, such as the C. elegans neural network. There are references in the Cell paper that could probably help you out further. The wikipedia article on network motifs also looks to have some information, and there are other resources on the internet if you google.
While there is not necessarily a strict biological interpretation of such motifs, they nonetheless can be informative in identifying specific patterns peculiar to different TFs or master regulators.
Caveat
It is possible that I have misunderstood the question or made bad assumptions- my graph theory is superficial. But if I am wrong and you are actually interested in the simple number of motifs of size $k$, that observation is of interest as a "I have a weird graph" theoretical problem, not as a "this is biologically interesting" problem. As a biologist I would care much more about which specific motifs of size $k$ you have, rather than the summed count of all motifs of size $k$.
On the other hand, forgetting about motifs for a moment, a "weird" network could be quite topologically interesting biologically. For instance, do your different clustered components associate with different pieces of biology, like sugar metabolism vs. morphogenesis? That would be expected, but it has very little to do with motifs- they may just be a side effect of that functional topology. In that case, it would be not only degree distribution but also that topology that you would have to control for to make interesting statements about motifs.
good luck!


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Why are GC-rich regions less condensed than GC-poor regions?
As far as I know, chromatin consists of two kinds:
Heterochromatin is more condensed so translational factors have less access to this region, and this region is poor in GC.
Euchromatin is less condensed so translational factors have more access to this region, and this region is rich in GC.
I wonder how GC content affects the condensation status of the chromosome? What is the mechanism behind this relationship?
It is well known that GC and AT pairs differ in the number of their hydrogen bonds. Does this hydrogen bonding play the key role in condensation of chromosomes?

@ThoH.Ho and @Thawn. When banding chromosomes they are first treated with trypsin before staining with Giemsa dye. My understanding, and I have worked in the field of cytogenetics for quite a while, is that chromatin condensation due to gene content IS the reason for differential banding patterns. Gene rich/ high GC content areas, with more open chromatin, are more readily digested by the trypsin enzyme and therefore less protein is then present to stain with Giemsa. Vice versa for the gene poor/ low GC content regions. This is why non coding regions such as heterochromatin stain very dark and gene rich chromosomes such as chromosome 19 are pale. So although chromosomes may be at their most condensed stage of the cell cycle in pro metaphase, there is obviously still a relative difference between chromatin condensation of the GC rich and GC poor regions.

Chromosome condensation seems to be primarily driven by epigenetic factors like methylation and histone modifications, not GC content. However, high GC content is associated with gene rich regions and gene expression generally requires open chromatin. In other words high GC content correlates with genes, and genes being expressed correlate with open chromatin, so high GC content correlates with open chromatin, but isn't necessarily causal.

Thank you. I highly appreciate your point of view. There's only one thing, I'd like to hear your opinion on this, that the reason I asked this question is because of the G-banding. When people stain the chromosome using Giemsa solution, the cell is mostly in prometaphase or metaphase. Expression regulation should be very low at this stage, chromosomes should be condensed at a same level. So why they are stained differently while they are all condensed (metaphase)?

@ThoH.Ho The question you ask in the comment is a completely different one from the question you originally posted. I suggest you ask a new question and specifically mention the giemsa stain. The dye used for the giemsa stain specifically binds to AT base pairs and this creates the banding. This has nothing to do with chromatin condensation.


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Pseudomonas aeruginosa biofilms grows stronger after 95 % ethanol treatment
I used 95 % ethanol to disinfect Pseudomonas aeruginosa biofilms from titanium discs and compared it to disinfection with water and hydrogen peroxide. The strange thing was that when examining in SEM, roughly ten times more bacteria was present in the ethanol treated samples than the water treated samples hydrogen peroxide treated samples showed no bacteria. Metabolic activity assay showed however more bacterial activity from the water treated samples than the ethanol treated, hydrogen peroxide showed least. Anyone have any theory why ethanol seamed to increase the bacterial biofilm compared to water? Ethanol are regarded as an effective disinfectant on bacteria.

95% Ethanol does not work as a disinfectant. You need to dilute it to around 70% to be effective.

@Chris while that is true, wouldn't you still expect it to be better than water?

@Chris is right. ~70% ethanol is the way to go.
From a discussion here :

The effectivity of ethanol as e.g. desinfectant or antiseptic agent depends on the concentration of ethanol-water-mixture: An ethanol percentage of 50-80% destroys the cell wall/membrane of bacteria by denaturing their proteins and dissolving their lipids (effective against most bacteria, fungi and some viruses; ineffective against bacterial spores). Therefore, the ethanol has to pass the bacterial membrane/wall to get into the bacteria - if you use 100% ethanol instead, the bacteria get 'sealed' and they will survive... An other mechanism is the high osmotic pressure of ethanol/water-mixtures; and the 70% has the highest one.

By using a high ethanol concentration, you're effectively creating a layer of coagulated protein on the surface of the biofilm, "sealing" the bacteria in below that top layer.
As to why water seemed more effective than alcohol, I would venture a guess that some of the bacteria from the biofilm was flushed off. Maybe check the water for bacterial count to verify? :)


text:
most different human tissues with respect to gene expression profiling
Is there a PCA showing the relative distance in terms of gene expression / functional genomics among the different human tissue types?
So far I have found:
(1) A paper based on gene expression with some tissues/tissue groups, not many:
https://genomebiology.biomedcentral.com/articles/10.1186/gb-2010-11-12-r124
(2) A paper based on gene expression signatures and aging:
https://www.nature.com/articles/npjamd201614/figures/1
(3) A paper on Gene and Protein Expression in Normal and Cancer Tissues:
https://www.nature.com/articles/srep24799/figures/3

Assuming you know what distance measure you want to use, I think the best approch is download a tissue data set such as GTEX yourself and compute the pairwise distance matrix. If you're a bioinformatics person this is should be straightforward. PCA projection to 2D (or even 3D) is only an approximation of the actual pairwise distances, and for tissue gene expression that approximation tends to be poor, in my experience.

You can navigate the GTEX project. PCA section.
https://www.gtexportal.org/home/histologyPage?tab=PCA
You have different samples for many tissues. Currently you can navigate it tissue by tissue but perhaps there's a way of visualizing the whole dataset (or you can ask for it).

The website looks very promising, but it seems, as you say, that you can only PCA tissue by tissue.


text:
what species of ant is this?

I found this queen ant on the pavement (in Adelaide) its about 1 cm long and I am not sure what species it is, is someone able to help me?

Probably a Ponerinae.
(Wikipedia, AntWiki)
It's not the easiest picture to work with, but here's what I did.
Going by the location we have the following distribution of ant species in South Australia (see below, or here).
A critical identification point is the petiole, bumpy segments on the thin part of the back of the ant. Your specimen appears to have none or one.
This excludes Dolichoderinae and Mymicinae, who both have two clearly distinguishable petioles (or rather, a petiole and a post-petiole).
Myrmeciinae have different colours and/or mandibles, leaving the following three likely candidates:

Formicinae
Ectatomminae
Ponerinae

Ponerinae are distinguishable by a constricted gaster, so an impression in the posterior section, which is quite clearly visible in the picture.
(This is technically only an identification to subfamily level, if anybody wants to take a shot at species, feel free)

This is wrong, the first segment of the gaster is not elongated here.

This is a Formicinae or a Dolichoderinae.
Myrmeciinae and Myrmicinae have two segments between the thorax and the abdomen, it is not the case here. The first segment of the gaster is elongated in Ponerinae and Ectatomminae, which is not the case here (the physogastry is confusing, the abdomen is distended because of the pressure induced by the development of the eggs in the ovaries).


text:
Name of neurons affecting or being affected by a neuron?
This question is about terminology:

By which established and catchy terms are the sets of neurons with
  respect to a given neuron $N$ called which

directly affect $N$ synaptically
are directly affected by $N$ synaptically?

These terms came to my mind, but I am not sure which ones are most commonly used:

the presynaptic/postsynaptic neurons of $N$
the afferent/efferent neighbours of $N$
the afferents/efferents of $N$
the incoming/outgoing neurons of $N$
the neurons projecting on/to $N$ vs. the neurons projected on/to by $N$

Or is there no such established term, and anything goes, depending on the context?

At the simplest level, the terms 'pre-synaptic'/'post-synaptic' neurons should cover what you wish to describe.
'Afferent'/'efferent' are usually used to refer to axonal projections, usually between functionally distinct areas, or nerves. However, I wouldn't be too surprised if someone used these terms to refer to synaptically connected populations although I would consider it unusual. Simply, 'connected neurons' is also a term frequently used.

I will now go into a tangent to give you some background that should help you formulate an informed view about the vocabulary being used:
In areas that display a high degree of local connectivity, like the cerebral cortex and the hippocampus, any given neuron is connected with many different neurons. Hebb's theory of cell assemblies posits that a group of highly connected neurons may form over time in order to subsist a specific function. Given the high degree of connectivity, any given neuron will be able to participate in many different assemblies. It is often thought that these assemblies constitute the substrate of engrams, the physiological correlates of memory, at the level of the neuronal network. Hence, the concept of cell assemblies is prominent in our thinking about groups of synaptically connected neurons.
Setting aside the questions of the definition of the engram, recent efforts have claimed to identify engram cells under this or that experimental paradigm, although the connectivity of those cells has not been established. While we know that functionally similar neurons display a higher degree of connectivity and that groups of cells with correlated activity patterns can be formed by artifically-induced synchrony, the direct link between increased connectivity and behaviourally relevance has not been established.
On the other hand, only a handful of studies have directly measured the connectivity between more than two neurons (Song et al., Perin et al.), revealing the intricate properties of neuronal network structure. Depending on the level of description they may refer to distributed cell assemblies, synaptic clusters of neurons, $n$-vertex cliques, and motifs.
All this is to say that as soon as you start considering more than a pair of neurons, it makes little sense to talk about neurons that are exclusively connected with each other. As every neuron is connected to almost all other neurons in its immediate neighbourhood we often focus on the functional implications of their connectivity. Under this light, the concept of cell assemblies is central in modern neuroscience.

I added "directly" to modify "affect" in the original question.

Sorry for the inconvenience.

I think the only way to reasonably answer this question is to say: "read some papers and follow their conventions" - it's much too hard to develop an exhaustive description of how all of those terms are used without creating an answer that's much too broad. I'll give some comments, though:
Presynaptic/postsynaptic is most often used in the context of synaptic transmission/plasticity/etc where the subject is a synapse. You would not typically say presynaptic neurons to N when you are really just talking about a network from A to N.
Afferent/efferent 'neighbors' I have never heard used, won't claim it never is but it seems completely wrong to me.
As for afferents/efferents these refer to the fibers primarily. Those terms are most appropriate when you are talking about something like the spinal cord, where afferent projections head toward the CNS/brain and efferent projections head toward the periphery; in the brain I find them often confusing or incorrectly used. This is because the terms afferent and efferent don't actually refer to inputs and outputs, but rather to inward versus outward direction. Defining "direction" in the brain gets pretty ambiguous if you aren't talking specifically about primary sensory or motor areas.
Incoming/outgoing I rarely if ever hear.
In the context of "projecting" usually the noun form is used: projections, as in "thalamocortical projections" or "projections from V1 to V2." I'd say this is the least ambiguous/best terminology if you are talking about connections between different brain areas. Within a local brain area (i.e., a given nucleus or a region of neocortex) you would be less likely to use the term "projection" though it wouldn't necessarily be wrong.

But isn't the concept of "the set of neurons which directly affect neuron N synaptically" a very clear one, and would deserve a name? (And I did read more than just some papers, and didn't come up with a convention. Maybe because these sets aren't interesting and/or dealt with?)

It depends on context, but there's also no strict rules. If you are talking about just one cell in a computational fashion, you would probably just say "the inputs to cell X" but people would understand if you used some other terminology. I'd say this is typical of English in general, and maybe that gets carried over into scientific fields where English is the main lingua franca.

"Inputs to cell X" sounds good. Does "outputs from cell X" sounds good to you, too?

That's fine if you are talking about the outputs themselves; you could also use "targets of cell A" to describe the population that receives inputs from cell A.

You have to admit: terminology and wording is not very controlled and unequivocal in neurosciences.

.. which doesn't make life easier for the novices;-)

"Incoming/outgoing? I rarely if ever hear."
I found this wording here.

@BryanKrrause: Just to let you  know: I feel offended and censored by you and your actions (e.g. closing my questions without giving me good reasons and opportunities to react). I find it indiscriminating and would like to flag it - but I can't because you are a moderator.

@Hans-PeterStricker I explained to you why your last question was deleted in a comment on that question (cross-posting), including a link to the relevant discussion on Meta. If you prefer to delete your question at Psych&Neuro instead, ping me here and I'll undelete. I downvoted rather than closing your question so as to not unilaterally close it; the deletion is separate from my reason for downvoting. If you have issue with my actions you can post to Meta, or see https://meta.stackexchange.com/questions/28867/what-recourse-do-i-have-if-i-believe-a-moderator-has-abused-their-privileges

Cross-posting is not prohibited per se, is it? The distinction between Biology and Psych&Neuro is hard to make, and how can I consider it beforehand? Why is it bad to post the same question twice when it is not clear where to find the better audience? Why is it to be "punished"?

@Hans-PeterStricker Deleting a question doesn't "punish" anyone. Please read the meta I linked to you; I can link it again here: https://meta.stackexchange.com/questions/64068/is-cross-posting-a-question-on-multiple-stack-exchange-sites-permitted-if-the-qu I find it very rude to cross-post, because if a question is answered on one site, someone might still answer it on the other site despite it already having an answer. These sites have high bars for answers, and it often takes a lot of work to answer a question. It's rude to have someone take the time to answer an already-answered question.

Especially reference requests are not so hard to answer: If anyone knows a reference he/she just can give it. I deliberately did not ask for elaborate answers but just for a link. Personally, I cannot see anything rude in cross-posting reference requests. Finally and generally: What is bad with having two (independent) answers? Do you believe, every question can have only one correct answer?

@Hans-PeterStricker The problem is not having two independent answers, but having two independent questions that are the same question. In this case, the different answers end up in different places rather than the same place. Please please read the well-reasoned answers in the meta post I linked and don't make me rehash the entire discussion here, that's why I linked it for you.

But why not accept that there are questions that can equally well be posted at two SE sites? Why to force to ask them only at one site? Isn't it in turn a good opportunity to bridge gaps? (I understand your point better with respect to more or less eduacted SE sites like MathOverflow SE and Mathematics SE. But Biology and Psych&Neuro are on the same level.)

And be assured: Whenever I get an answer on one of the sites, I'll share it on the other - to the benefit of all!


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How effective is it to rinse fruit, lettuce, tomato, ... with water?
The general rule I've seen stated is that to get rid of some nasty bacteria, one should rinse fruit and vegetable under running water before using them, especially if eaten raw.
Most likely the effectiveness of such a measure depends significantly on the details of how this rinsing happens.  So, by how much is the risk of health problems reduced in different cases (e.g. just bath the fruit&vegetable in a water bowl, pass them quickly under running water, bath them and scrub them, keep them for a minute under running water (moving them around and scrubbing them at the same time), ...).
Of course, assuming those fruit&vegetable have already been washed earlier (e.g. before we bought them).

I suggest reading this FDA page. See "Prepare Safely".

@Charles: This page is the kind of example I mention that gives general rules, but without detailing the actual effect on the probability of getting ill, nor discussing how that probability is affected by the various rules they propose and how we choose to follow them.

I strongly doubt that studies have been conducted which test the rates of individuals falling ill from food-borne bacteria with respect to varying degrees of wash for fruit & vegetables. I do however believe though that there were initial studies which established how long a fruit/vegetable should be washed, as to sufficiently remove pesticides, bacteria, and any other undesired substance(s).

@Charles: Could you give me some pointers to those studies?


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Why does DNA need to be pure for restriction enzymes to act on it?
My textbook states: “In order to cut the DNA with restriction enzymes, it needs to be in pure form, free from other macromolecules. Therefore DNA isolated from other chemicals of the protoplasm like carbohydrates, lipids and proteins via techniques of DNA isolation.”
My question is, why does DNA need to be alone? Won’t restriction enzymes work if there were a DNA molecule in a sugar solution? I understand that the DNA has to be freed from cell membranes and walls for restriction enzymes reach the DNA but how does the presence of other macromolecules hinder DNA’s digestion of a restriction enzyme?

AFAIK its not that other macromolecules hinder the activity of restriction enzymes, its just that we don't want other macromolecules in the solution, we want pure DNA for our job. I might be wrong though...

Some other macromolecules or other solutes may be present that could interfere with the affinity of the restriction enzyme. For example, there could be salts that denature or modify the conformation of the enzyme or inhibitors present that may interfere with the enzyme. Hope this helps.

Welcome to Biology.SE! Could you please add some references?

No Problem! https://www.promega.com/-/media/files/resources/protocols/technical-manuals/101/restriction-enzymes-protocol.pdf


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What kind of larve is this? Found in shed on terracotta pot in Northwest Oregon
Found this on a terracotta pot in my shed

They look like the nest and pupae of a mud dauber wasp; the black and yellow mud dauber is a common species to your area and elsewhere, though I can't personally identify the species clearly from the larvae themselves they certainly are consistent.
A nice view of the nest building process

These wasps have a characteristic very skinny abdomen, and they pack their nests with spiders before laying an egg there. They aren't typically a bother to people because they don't have any communal nest to defend, except for building nests on troublesome places like airplanes.

This is a good ID, +1. I'm curious though -- was there anything specific that tipped you off in order to properly ID, or were you already familiar with this wasp?

@Charles Those nests are pretty distinctive, though I see the blue variety more often than the black and yellow where I am (OP's nest could easily be a blue mud dauber as well).


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What is the difference between the otolith membrane and the endolymph?
The human vestibular system contains otoliths to sense acceleration in the vertical and horizontal plane. I cannot find what the difference is between the otolith membrane and the endolymph?
Can anyone show them where they are located in a picture?
It seems they are different as wikipedia has two different entries for them. See for example the two pictures here and here - I cannot pick the difference.

Instead of downvote, please explain what is wrong with the question. My background is math not biology.

I suspect it is because it's not clear why you think they are the same thing, so the question is whether you have adequately tried to understand them before asking.

@kmm, I understand nothing from biology and anatomy and I will not understand them later too. It is like asking you to try understanding optimal control theory or Algebraic Riccati Equations. I just would like to make sure I am not writing a wrong annotation in a report which contains a human anatomy. This is totally irrelevant to my topic.

@kmm, These photos A and B cause I feel they are the same things.

Don't blame me. I was just speculating as to the downvote. You say you will never understand biology, but you are trying to do just that right now. So I think it is incumbent on you to do what you say you won't do. I actually do understand optimal control theory, because I needed to for a project I was working on. I didn't know anything about it, so I did my "homework" to learn what I needed to learn. I suspect the downvoter expected the same of you.

The two pictures you provide in the question (Fig. 2 and 3 below) actually show it all. You just didn't got the scale right. The question shows prior research effort and the inner ear is a complex organ indeed.
Fig. 1 shows a macro-scale overview image of the inner ear, or the labyrinth. The two otoliths are called the sacculus & utriculus, who sense accelerations in the horizontal and vertical planes.
Now if we zoom in on the sacculus you get Fig. 2, which you provided in the question (comment). Here you can see that the hair cells (the sensory cells) are bathed in endolymph, which is the fluid contained in the membranous labyrinth of the inner ear.
Now if we zoom in further to the cellular level we can see the sensory parts of the sacculus (Fig. 3). In the figure you will recognize the other structure you are referring to, namely the otolithic membrane. The otoliths contain small grainy crystalline structures called otoconia. Otoconia move in response to acceleration, because of their inertia. When they move with respect of their surroundings they activate the hair cells. The otoconia are embedded in a jelly like matrix, called otolithic membrane. the endolymph surrounds the region above the otoconia in Fig. 3.

Fig. 1. Overview of the inner ear. source: Dizziness & Balance

Fig. 2. Sacculus. source: Wikimedia

Fig. 3. Sacculus - close up sensory structures. source: Wikimedia

Many thanks. Just another question. Is otoconia the same bone people take out of fish and call it otolith?


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Transposons, Viruses and RNA interference
My textbook says that in RNAi, a complementary double stranded RNA sequence attaches to an mRNA and silences it using a protein machinery. I Googled and read about this so now I know what siRNA and RISC and microRNA are. But the next thing my book says is

“the source of these complementary double stranded RNA
  sequence [obviously my textbook means siRNA] may be viruses and
  transposable elements.”

What does this mean? Do transposons make siRNA? I thought transposons were non-coding except when they travel via the retrotransposon mechanism.
Do viruses that infect eukaryotic cells donate their own RNA genetic material for the cell to use in RNAi? But I thought RNAi was a cellular defence against viruses, how can viruses help give the dsRNA that’s supposed to fight the viruses? A number of sites online simply state that siRNA is exogenous is origin; do they mean that it comes from viruses?
I would greatly appreciate it if someone could take the time to answer each of my questions one by one or even recommend a site that answers them all.

Transposons and viruses don't "make siRNA". However, an endonuclease called Dicer can process dsRNA from these sources to produce siRNA which is then loaded to the RNA-induced silencing complex (RISC) to suppress propagation of viruses and transposons. The following papers provide a good overview:
Buchon N, Vaury C. 2006. RNAi: a defensive RNA-silencing against viruses and transposable elements. Heredity 96:195-202.
van Rij RP, Andino R. 2006. The silent treatment: RNAi as a defense against virus infection in mammals. Trends Biotechnol 24:186-193.


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Why are only 6 water molecules formed in the aerobic degradation of glucose?
I am studying the aerobic degradation of glucose and it seems that for every glucose molecule we should obtain $\ce{10H2O}$ molecules. However, it is known that we only obtain 6.
$\ce{C6H12O6 + 6O2 -> 6CO2 + 6H2O}$
(I am not going to focus in all products and reactants, but just in the important ones for the formation of water molecules)
First, in the glycolysis, for each molecule of glucose we obtain two water molecules, $\ce{2NADH+}$ and 2 pyruvate molecules. By the oxidation of two pyruvate molecules we obtain $\ce{2NADH+}$ and 2 acetyl Co-A molecules. So we are going to pass twice through the Krebs cycle, obtaining $\ce{6NADH+}$ and $\ce{2FADH2}$, and requiring 4 water molecules.
So, when we arrive to the electron transport chain, we have a negative balance of 2 water molecules, and we have $\ce{10NADH+}$ and $\ce{2FADH2}$. We have been told that for every of these molecules 2 electrons go to the electron transport chain, that means that a total of 24 electrons go to the system. The problem comes here:
$\ce{4e- + 4H+ + O2 = 2H2O}$
So, bearing in mind that we have $24e^-$, 12 water molecules should be formed, so at the end, we have gained 10 water molecules, but we know that the number of water molecules formed should be 6. So, clearly there is something wrong in my explanation. I would be very pleased if you could tell me what is wrong.

Your confusion comes entirely from this equation:
$\ce{C6H12O6 + 6O2 -> 6CO2 + 6H2O}$
This reaction is the combustion of glucose. This is not how glucose is oxidized in cells! Why so many biology texts and courses present this equation when introducing metabolism is beyond me.
Indeed, your tracking of water molecules is correct: starting with one glucose molecule, 2 waters are produced in glycolysis, 4 are consumed in the tricarboxylic acid cycle and 12 are produced during oxidation of NADH/QH2 (ie FADH2). This gives a net total of 10 produced.
Why is this different from the combustion of glucose? The answer lies in the oxygens introduced by inorganic phosphate during substrate level phosphorylation. Consider the balanced net reaction for the biological oxidation of glucose (simplified by ignoring ATP produced by oxidative phosphorylation and substituting ADP/ATP for GDP/GTP):
$\ce{C6H12O6 + 6O2 + 4ADP + 4P_i + 4H+ -> 6CO2 + 4ATP + 10H2O}$
In particular, consider the formation of ATP from ADP and Pi (HPO42-). In both substrate level phosphorylation reactions (catalyzed by GADPH/PGK in glycolysis and succinate-CoA ligase in the tricarboxylic acid cycle), inorganic phosphate nucleophilically attacks the activated carbonyl (thioester) of the substrate and is then transferred to ADP (to form ATP):

The oxygens of the original inorganic phosphate are coloured red. The key point is that an oxygen atom from HPO42- is transferred to the substrate. This oxygen is later removed in the form of carbon dioxide, via oxidative decarboxylation, during the conversion of pyruvate to acetyl-CoA and in the tricarboxylic acid cycle. This occurs four times for each glucose molecule entering glycolysis and is accompanied by the reduction of NAD+ to NADH. Given that NADH is used to reduce molecular oxygen during the electron transport chain:
$\ce{NADH + H+ + 1/2O2 -> NAD+ + H2O}$
...this explains where the four, apparently extra, water molecules come from when comparing the combustion of glucose with its biological oxidation.

Good answer, but I would contest that the plain combustion reaction is actually very useful, even if it does not reflect the mechanism that cells use. The reason is that, if you balance your reaction involving substrate-level phosphorylation with ATP hydrolysis -- which always occurs alongside ATP synthesis in cells -- then you will get back the simple combustion equation exactly. And this must always be the case. So comparison with simple combustion helps us verify that we understand biochemistry correctly.

@Roland Thanks! And good point. I find that it often causes a lot of confusion, but that may be more from poor explanation or comprehension.

@Roland, I am a high school student, I also had the same confusion, that why do so many textbooks compares combustion with respiration? in respiration 10 H20 are released, and I look upto the answer, but it seems like, i don't have enough knowledge to grasp it, can you explain it to me in simple terms? should I say that the other 4 H2O molecules are used somewhere else?

@ArunBhardwaj, This is an old post, but as I mentioned in other comments, it's important to distinguish between (1) H2O derived from glucose oxidation and (2) H2O from ATP synthesis (respiration). Glucose oxidation in cells is always coupled with ATP hydrolysis to provide energy (for example, in muscle contraction). The ATP hydrolysis reaction is ATP + H2O --> ADP + H+ + Pi. So if you balance the the first reaction equation in this answer with 4 x ATP hydrolysis, the extra 4 ATP will cancel out and you get back the basic glucose oxidation reaction. So this is where the extra 4 ATP are used.

@ArunBhardwaj, (continued)  The H2O formed during respiration is very different. Respiration is not even a pure chemical reaction, it's a physical process -- ATP synthase is actually more like a turbine!  In respiration, the number of ATP formed by respiration is not fixed, but varies depending on conditions. It's usually somewhere between 2--3 ATP per NADH, but there are exceptions: some cells don't produce any ATP at all, but instead use all the energy in NADH to produce heat.  So there is no single, exact chemical reaction formula for respiration.

@Roland,I am a high school student, and only knows the various steps involved in respiration, I was confused that if the combustion reaction and respiration gives the same results then why do we have 10 h20 formed in respiration as OP have calculated, but it seems like you are cancelling out ATP to form 6H20 ,,,i.e if we consider ideal cases for calculating each thing formed, we will see that 38 ATP/36 ATP are getting formed in respiration,,but it seems like you have hydrolysed 4 ATP from them just to make 6 H20 molecules? correct me if I am worng.,,and I don't know why u have said extra 4 ATP

In total there are 38 ATP formed by biological oxidation of 1 glucose, 4 from substrate level phosphorylation and 34 By oxidative phosphorylation,,what do you mean by extra 4ATP hydrolysis?

@ArunBhardwaj, sorry, I meant to say "extra 4 H2O" in the comment above. I was trying to address your question of where "the other 4 H2O molecules" go, and the answer is that they are accounted for when the ATP formed is hydrolyzes (used for energy). Respiration is a separate problem, and again, there is no exact number for how many ATP values are formed from respiration (the textbook value 34 is just one possibel scenario). But I think this is too much to deal with in the comment field -- we should probably move this discussion to chat.

how to continue in chat? and again I know that there is no exact no. of ATP formed, but if we consider ideal scenerio than 38 ATP are formed not 34 , it seems like you are hydrolysing 4 ATP just to form 6  water molecules?

I think you are misconceiving the intent assumed within the statement "6 H20 generated from glycolysis". The number 6 is simply in relation to the number of carbons oxidized to CO2 within the TCA..which generates an electron at each oxidative occurance, in which the 6 electrons are then shuttled to OXPHOS requiring 3 O2 to form 6 H20. ... In short: Whenever they say 6 H20 are produced "aerobically"  they are specifically referencing the simplified OXPHOS component (or simply: C6H12O6 + 6 O2 → 6 CO2 + 6 H2O).
Of note:

Stoichometry is relatively useless in real research. Don't overthink it. Metabolism is incredibly dynamic.
Real life H20 involvement within complete glucose oxidation is much more complex: Two turns of the TCA cycle generate: 4 CO2 from 2 acetyl CoA which requires 4+ H20 in total, but only has a net H20 loss of 4. Citrate synthase and fumerase both consume 2 H20 apiece to allow production of 4 CO2. The remaining H20 is used at aconitase, but no loss nor gain of H20 occurs in this reaction. Pyruvate dehydrogenase produces the other 2 CO2's making 6 CO2 in total, but does not require H20 at this step.   ... OXPHOS activity: (following 2 turns of TCA) results in 48 total H20 produced between ATP synthase, cytochrome oxidase, and enolase - and being that 4H20 are consumed in the TCA, the net H20 production per glucose is actually 44 H20.

Don't understand the comment that "Stoichometry is relatively useless in real research". I find it incredibly useful, and I like to think of myself as a real researcher. Admittedly, I've never had to carefully balance waters, but if you do it right, it works out.

This doesn't answer the question. The H2O produced in ATP synthesis is not relevant here, since those H2O molecules originate from the phosphate groups and are recovered during ATP hydrolysis. Also, ATP synthesis is not stoichiometrically fixed to glucose oxidation since chemiosmosis is a stochastic process, so it is not even possible to give an integer coefficient for H2O if you would involve ATP synthase.

@VictorChubukov my apologies, my intention of saying "real" was not to contrast paid vs non-paid research, I meant it only as when looking at real-life biological systems, in vivo. Regarding the stoichometry, I was trying to imply that there can be multiple different reactions in the same place at the same time, that all produce the same product; and trying to break down those dynamics into an equation is impossible as of this moment; I guess I should of clarified what I meant as 'systems stoichometry'. Equation stoichometry itself is very usefull. Cheers.

Two waters come in at each turn of the TCA cycle, one at citrate synthase and one at fumarase. Additionally, I don't think it's right to say that you get a net water from glycolysis (in fact if you look at what you wrote, the oxygens don't balance). I think what you're missing is you also get an ATP, and the water you do get at the 2PG->PEP step is really part of the net reaction ADP + phosphate -> ATP + water.
To really balance the waters you have to consider all the substrates and byproducts of glucose oxidation, including the ATP/GTP.

Thank you very much. However, this only works if the ATP produced in the ATP-synthase does not need water to be formed. Why by this way (with ATP-synthase) the formation of ATP doesn't need water, but if is done in any other way, water is required?

Could it be that the formation of ATP by the ATP-synthase uses PO3 instead of HPO4 + H+?

Every phosphate fixation reaction will release a water molecule and every atp hydrolysis reaction will use a water molecule. That includes ATP synthase.

But then we have 40 water molecules, since in the electron transport chain 34 ATP are formed.

Sure. But then you have to write the equation as 1 glucose + 6 O2 + 34 PO4 + 34 ADP -> 6 CO2 + 34 ATP + 40 H2O. I think that balances.

It should be 38, since 4 ATP are produced before the electron transport chain, but that is not important at all. The problem is that as you pointed out, 6 extra water molecules are formed (40-34), so those 6 waters do not come from ATP formation, at least that is what I understand. My question is were those waters come from.

So talking about water molecules that don't have anything to do with ATP formation we only have: in the glycolysis two Phosphoglycerate are transformed to Phosphoenolpyruvate, producing 2 water molecules in total. In the TCA cycle 2 hydrogenations take place, as it is done twice we have a loss of 4 water molecules. At the moment we have just lost 2 water molecules. Finally at the electron transport chain, oxygen is used as an electron captor, producing 12 water molecules. So at the end we have gained 10 water molecules, but it should be 6. What happens with those 4 water molecules?

Try writing down the entire mass balance equation, not just the reactions that you think are important. Water is a tough one to track because it's used in so many processes (balancing carbons is a lot easier). I think you'll find that the glycolysis water works the way I described, and your other missing water might have to do with a similar thing happening at the succinyl-coa step (fixing phosphate into GTP).

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


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genetic difference subpopulations vs movement rate
Someone told me that if a geneticist finds no significant difference between 2 subpopulations that have temporal spatial overlap it might be that they are still almost closed (no connection). Is this right?
Can I deduce anything about the individual exchange rate between populations and the genetic similarity/difference? For instance, one would need 5% of individuals to switch populations to keep them almost genetically identical. Does this differ between species (let's say fish and mammals)?
Thanks.
ps: any references to this would be great

[..] if a geneticist finds no significant difference between 2 subpopulations that have temporal spatial overlap

This isn't clear. Significance difference between what? What statistical hypothesis are you testing for which one would found no signicant difference (accepted the null hypothesis). Are you maybe thinking about a t-test between testing difference between the average phenotypic traits?

it might be that they are still almost closed (no connection). Is this right?

Do you mean no gene flow (aka. no migration)?

Can I deduce anything about the individual exchange rate between populations and the genetic similarity/difference?

"Individual exchange rate" is typically "called migration" or "gene flow".
At some extend, yes you can. But the question is really broad and will be hard to answer in the general sense. I will just provide a very common methodology here.
You can compute $F_{ST}$, a statistic of population divergence. A very good paper explaining the math of $F_{ST}$ is Nei (1973). I recommend computing $F_{ST}$ following Weir and Cockerham (1984). Then, if you can assume a finite island model (equal migration rate $m$ between any two population) and a constant and known population size $N$, then
$$F_{St} = \frac{1}{1 + 4N(m+\mu) \frac{d}{d-1}}$$
, where $d$ is the number of demes (number of islands)This equation can be found at many places. Slatkin (1995) is a very good paper but note that its final solution differs a little bit from the one I presented (by a square term) for reasons explained in Charlesworth (1998). You can solve for $m$ and plug the observed $F_{ST}$ and $N$. Note that depending on the markers used, $\mu$ will be negligible in comparison to $m$.
You might want to have a look at the very related post How could one calculate the gene flow between two populations?

@Wave Did it answer your question?


text:
What species are these juvenile birds?
What species are these juvenile birds found at São José dos Campos, Brazil?

A puppy is a young dog. There exist a number of correct terms for birds (chick, hatchling , nestling, fledgling and other species specific terms). See here for more information

@Remi.b Excuse me. I'm Brazilian and I wrote wrong.

@LCarvalho No worries. I make plenty of english mistakes myself. Can you please add the location where you took that picture?

From São José dos Campos

I am flattered by my question having had so much attention from reputed people. Well, I found the right site to ask. I did not expect it to be like this.

The birds in question appear to be fledgling eared doves, which belong to the species Zenaida auriculata. The beak color, eye markings, and overall feather coloration were most indicative when IDing.
Here's a few images of what the doves may look like once matured:

The OP is from Brazil, so assuming he saw them in Brazil, could it be Zenaida auriculata?

@Remi.b Yes, after doing a bit of reading, I agree. I've updated my response to Z. auriculata instead of Z. macroura. Thank you.

Sounds right esp. now that we know the location. +1


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How the glycogen accumulate intracellularly in the reversible cell injury?
As we know in reversible cell injury as the most common cause is ischemia decreases oxidative phosphorylation which decrease ATP & increase anaerobic glycolysis which depleting glycogen !!? But one of the intracellular accumulation in addition to lipid , hyaline, pigments and calcium is glycogen So how this occurs ?


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What is the difference between average sperm epimutations and intersection sperm epimutations, in the context of the attached article?
The paper of interest is Manikkam et al. (2014).
In research for a school Year 10 Science project, I came upon this article and the following two graphics. I don’t quite understand the difference between the two graphics in the context of the article: what is the difference between average and insertion epimutations? Also, what do the Mb’s along the x-axis mean? Is it in a reference to genetic information size, like megabytes? And how does it refer to the loci of the epigenetic changes? I want to be able to interpret and explain this graph, so could someone provide an analysis and explanation of these graphics.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0102091

Welcome to Biology.SE. I added the link in the post. It has no good reason to be in a comment. Maybe you did not know how to add a link in a post.

Yeah, it wouldn’t let me add more than 2 links to a page, and I think the images counted as links.

Oh indeed users with less than 10 points of reputations are limited to two links apparently. I'm not sure why this restriction though!


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Gel electrophoresis bands
Is there any way to calculate the number of bands formed due to sodium dodecyl sulphate-polyacrylamide gel electrophoresis for a particular compound of group of proteins? For example, how could I calculate the number of bad formed after electrophoresis of IgG (immunoglobulin G) under oxidizing or reducing conditions?

This sounds like a homework question, which are not allowed unless you show your attempt at the answer. Do you know what reducing conditions will do to a protein? Do you know the structure of immunoglobulins?

Okay, so I think I figured out what was required. Immunoglobulins have 2 light chains and 2 heavy chains. So 2 distinct bands would be formed (the heavier one at the back and the lighter one in the front) I suppose.


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Do the individual claws of a bear have names?
The question seems pretty self-explanatory (if perhaps a little odd). Anatomical names or colloquial names are both appreciated, especially the latter if they exist.

I would be surprised if they do!
Bears have 5 clearly visible toes per paw. You could just name the claws based on the fingers it is on (thumb, index, middle, ring, pinky).


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What is this stinging/biting insect?
The missus was bitten/stung in the palm by this (we think) in NE Scotland this morning. Pain was immediate, described as like getting a pin stuck in her hand. Apparently her first attempt to flick it away failed, and it took her second attempt to remove it. Afterwards, a short black stinger appear to remain embedded and had to be removed with tweezers.
She got fairly immediate swelling (white circle around the site, and red swelling further out). Even 20 minutes later, the swelling and pain remain.
This may or may not be the entirety of the insect.

Location: NE Scotland (indoors)

Time of Year: Early October
Size: Very small. Few mm long at most

So, we just found a dead wasp nearby. Could this just be it's stinger?

Yes, this appears to be the stinger of a wasp. Typically though, wasps are able to keep intact their stinger after an attack, whereas bees aren't so successful. Also, did the wasp that you found not have it's stinger? I would think that would solve the case, should the stinger not be present.

@Charles I didn't notice it having a stinger, but it's rear segment appeared intact. I'm no expert though, so it sounds like mystery solved. ;)

The stinger that got stuck in your partner's skin isn't completely black. Its coloration shifts from dark brown near the abdomen to black to dark brown again at the tip of the stinger.
This identifies the stinger as one belonging to Vespula vulgaris, the common wasp as the stinger of the other most common stinging insect in Scotland (Apis mellifera or European honey bee) is honey brown to brown.
Once in a while a wasp can happen to get its stinger torn of when it's flicked away during its sting. Obviously it dies afterwards as also part of its intestines are torn.
Pictures of both stingers can be found below.

Thanks. Strangely, the item I pulled from her hand was more like a small black hair (we found the stinger on the bed afterwards).


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Warburg effect in lung carcinoma, the logic?
Outside of 'purposefully' removing mitochondria to diffuse cytochrome C's apoptotic threat, I would assume that lung carcinomas, and their proximity to high oxygen levels, would have the lowest rate of cells entering the Warburg effect. Would this be a correct assumption?
Thanks

As far as I can tell, there are no data to support your hypothesis. Someone correct me if I'm wrong.
There's actually some data to support that aerobic glycolysis occurs in lung carcinomas despite their proximity to oxygen (ref). There's even an article on the prolifertative pathway behind lung microvascular endothelial cells (ref), alluding to this requirement for anaerobic glycolysis in rapid proliferation.
T cells exhibit a similar pathway, switching to aerobic glycolysis in the effector phase where T cells are rapidly expanding (see clonal expansion). The general trend is that the Warburg effect lends itself to the rapid accumulation of biomass, supporting rapid cell division, instead of energy production to support cell survival (ref). You could rationalize it like cancer is already a failure in cell death, and so the cancer cells need to worry more about carbon compounds that support rapid division. There was also a paper by Cai et al. in 2014 that described their hypothesis behind aerobic glycolysis in cancer, whereby the Warburg effect helps tumors resist anoikis and thereby promote metastasis (ref).
It may be that the Warburg effect is a means to a required end for cancer cells, but as far as I know there's is no correlation between proximity to oxygen and incidence of Warburg metabolism. There are papers out there that continue to ask: is the Warburg effect a cause or consequence of cancer (ref? My thought is that cancer cells will undergo the Warburg effect at a given stage regardless of histology or behavior because it's beneficial.


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Would modifying the human microbiome to digest cellulose be worth it?
I've read that cellulose has a lot of calories that go unused. I was wondering how practical it would be to incorporate a bacteria capable of suggesting cellulose into the human gut.
I would say that it is worth it if a human could gain a substantial amount of calories by digesting cellulose in a "normal" diet. To compute the amount of calories, I would like estimates for how fast bacteria can process the cellulose (like half life per billion bacteria) and how efficient the process would be.
Then given the average duration of the digestive process and a reasonable bacteria population, estimates could be made on how much energy could be gained by digesting the cellulose in an average diet.

It looks like you are confounding the verb suggest with the verb digest! Also, instead of practically, you probably meant practicality

Possible duplicate of Human Digestion of Cellulose?

@Remi.b Auto-correct likes to type for me! I'd say this isn't a duplicate because I am more interested in the economics of it. In the sense of "Can we get enough energy from the cellulose to make it worth it?". I'll edit the questions to make that clear.

Given the answer at the linked post, it seems like talking about engineering is way too early as we have not quite been to the stage of whether it is possible yet. But I'll let other users give their opinion on the post.

If you plan to alter the human microbiome, you should investigate the effect in an animal model, first. The human gut microbiome is largely important on an organismal basis.

Cellulose constitutes a major part of our dietary roughage.  If you plan to modify the microbiome in the gut to break down the cellulose for us, it would result in the decrease of the bulk fiber, which increases the stool volume and finally result into constipation and painful mornings. I am not saying that cellulose is the only bulk fiber, but it does constitute a major part of it.

You really need to understand how cellulase would effect metabolic systemic homeostasis before anyone can answer that. It's an interesting question. At first glance, one could consider that cellulase would allow disproportionate glucose intake, ultimately making fat a smaller % part of the diet. If unchecked, this could lead to a reverse Randal effect inhibiting fatty acid metabolism thus altering adipokine synthesis leading to a range of negative, if not, species detrimental effects such as reduced capacity for reproduction (as an example between altered biosynthesis and crosstalk between leptin and estrogen). This may have presented a problem for early humans, because in essence, cellulose could have acted as the very first mcdonalds convienience if we were capable of digesting it. I'm sure I'm missing many complications that would have occurred if early humans had this capacity, but it's a nice thought experiment.
And regarding the mathematical induction, forget about it, you can't induce a conclusion on potential alterations within the mammalian digestive system from only the enzyme kinetics of cellulase found in bacteria.

When you say you can't do the math induction, why can't you just put upper bounds on the energy intake? I've done this for things like having chlorophyll in our skin. With chlorophyll, it was something like you'd need to spend >24hrs in bright sunlight to get 200kcal around 95% confidence. Clearly not worth it. I thought cows have a bacteria that digests bacteria. Can't you make estimates using that as a model?

It's quite complicated to explain actually. Your best bet would be to somehow model the ruminant 24-hour diet AND digestive system required to extract enough energy from low-efficiency fibers (cellulose containing) as an equivalent human model. But dang, you're gonna have a lot of caveats and complications to make a useable conclusion, not to mention cows can digest meats as humans do, making their similarity more of an systems biology obstacle. Also, you have to consider the location and distribution of all the enzymes within the digestive tract; and the differences in analogue

efficiency - I know it doesn't sound so important at first but enzyme location in the gut can dramatically effect metabolite uptake and usability. My best guess would be to identify if anyone has measured blood glucose levels of a human who mimicked a cow for 24-72 hours; & from there you could somehow create a type of weighting to better interpret cow digestion to human applicability, at a high level.

Or just create your own hypothetical human scenario, with enzyme density and tract location, but this could easily be done simply by giving someone an equivalent X amount of glucose that mimics the amount of to be digested cellulose (kinetics shouldn't be a major burden here). But still, the many biological optimization per species will create caveats in the conclusion; tho id still read about it lol


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What is this tree that displays sycamore like characteristics but appears to be too small?
I have been wondering about this tree:

It's bark/leaves make me think it's a sycamore, but it seems too puny. I don't think they'd plant a sycamore there... What is it?
The tree is in a park/residential area in Orange County, Southern California.
Reasons I think it looks Sycamorish:

Alternate leaves
3 lobes
Mottled/patchy/peely bark

https://www.thoughtco.com/identify-maple-sycamore-yellow-poplar-sweetgum-leaves-1343480

When dealing with species ID, Africans indicate the country and the continent, Americans indicate the county and an abbreviation to indicate a region within the state (now corrected) $\ddot \smile$ I personnaly did not know SoCal meant South California. +1 otherwise!

probably the london planetree. that is my best guess

Adding photos of bark, and fruits/flowers if available might help.

"Mottled/patchy/peely bark" suggests me https://en.wikipedia.org/wiki/Platanus

This is very likely a London planetree (Platanus × acerifolia), a hybrid species of Platanus often planted in cities.

 Source: Cuyamaca College

 Source: Wikimedia
The tree is a hybrid between Platanus orientalis and Platanus occidentalis (the sycamore tree), and has characteristics intermediate between the two species.

Smaller (heights of only 20-30 m vs 30-40+ m for parent species).
More deeply lobed leaf than P. occidentalis but less so than P. orientalis
Seed balls typically two per stem (one in P. occidentalis, 3-6 in P. orientalis)

Note: seed "balls" = aggregate of many small seed-like fruits called achenes

VERY OFTEN PLANTED IN URBAN AREAS

Because it's very tolerant of atmospheric pollution and root compaction

Description:

Leaves: alternate, simple, 3-5 lobes, maple-shaped, 10–20 cm long, 12–25 cm wide
Bark: pale grey-green (or brown), smooth and peeling (sometimes not peeling)


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Do plants sleep under ultaviolent rays?
I observed Phyllanthus reticulatus is sleeping during nights. I want to plant this species indoor under a UV device.  Do these plants sleep under ultraviolent rays?
(Sleeping means leaves are close to each other)

For this answer, I'm going to assume that by "sleep" you mean that it maintains a circadian rhythm/photoperiod. Recent unpublished research indicates that even protoplasts maintain their circadian rhythm under UV lights so the UV light isn't the problem. In order for the plant to "sleep" like you mention, the photoperiod needs to be maintained. The UV light needs to be on during the day and off at night. If you leave the UV light on all the time you would actually perturb the plant's photoperiod and it would be very unhealthy. Plant metabolism and photosynthesis requires both dark and light reactions. In summary...yes, the plant will sleep but you must maintatain the photoperiod by switching the UV light off and on.


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Histidine protonation
In histidine structure , full protonation gives a structure with only the double bonded nitrogen having been protonated in the ring and not the single bonded nitrogen. Why is that?

I think this question may be better received at Chemistry.SE.

Textbooks tend to report structures as relatively static, whereas advanced biochemistry texts explore structural tautomerism. In essence, the histidine imidazole sidecvhain may move around it's protons and electrons when pH is roughly equal to pKa. Thus, the sidechain exists as two tautomers where the two nitrogens sort of "share" the double-bond character and the proton, like so:

And it's even more accurate to depict that the double-bond character is like so:


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What is the name of this species which I found in an Epipremnum (Money Plant)?
I found a very rare specie (at least from my knowledge of species and research) today in a money plant (Epipremnum plant) in my kitchen garden. This caterpillar was on it. Please help me with the name of this species and any information about it.

Can you add size and location?

The caterpillar in question is a kind of hawk moth caterpillar, most easily noticed by the pair of "eyes" on the thorax. From my experience with hawk moth caterpillars though, they generally have multiple sets of eyes, and so, this one was somewhat difficult for me to ID (not to mention a location has yet to be provided).
Looking at the OP, other defining features include: unique pattern on thorax; repeating triangular pattern on dorsal; a single tail; stripe along each side of the abdomen; overall coloration.
That being said, I believe this caterpillar is of the genus Eupanacra, and is most likely of the species E. elegantulus.

Such well defined patterns on the OP suggests full maturity. Consider the following instar sequence, and notice how the emergent patterns converge to the OPs.

images source
After undergoing pupation, the caterpillar will transform into the following:

And then, here's a distribution map.

source


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Terminology for parts of the leg
Going out on a limb here (pun intended)...I'm writing a paper in which I need to refer to various sections of the human leg from upper thigh to knee to calf and ankle. However, "calf" covers a fairly large area. Without having to go into specific leg muscle identification (semitendinosus, biceps femoris, etc.) which could be confusing as they overlap and can be found with Google.
Is there a (standard) anatomical way to describe (cylindrical) sections of the leg from top to bottom?

This should be what you need, http://johnhawks.net/explainer/laboratory/anatomical-directions/

The lower leg is anatomically called the crus1 and you can refer to the area above the knee as the thigh.

Sural refers to the calf region of the crus, while Peroneal refers to the side of the leg2.
The front (anterior) side of the crus is called the shin.

Patellar and Popliteal refer to areas associated with the front and back of the knee, respectively2.
You can see a summary of regional leg and other body terms here. (Below is a chart from the site):

Alternatively, you can refer to the regions of the leg using relative anatomical directional terms:

 Sources:
 1. Wikipedia;
 2. Rutgers

There's also "proximal, distal, medial, and lateral" for relative positions.

@fredsbend I was just giving some examples in my post, but you're certainly right. Thanks.

Yes, there are ways to refer specifically to regions of the lower limb.

Lower limb: everything from the hip to the toes. "Leg" has a different, specific meaning. Lower limb includes all the sections below.
Hip: the area comprising the proximal femur and attachments to the pelvis.
Thigh: Femur and associated musculature from the hip to the knee.
Leg: From the knee to the ankle. "Calf" is often used colloquially to refer to the posterior leg.
Foot: Ankle to the digits

From your description, you would use thigh and leg. "Leg" (in the usual vernacular sense) is not correctly used to describe the entire lower limb.
This is drawn from 20 years of anatomy teaching. A reference with more references is here.


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Help identify this Caribbean plant
Could you please help me identify this plant. I think it grew from some seeds we brought from Cuba (I might be mistaken though).
The plant in the picture is about 1.5 years old; it stands about 50 cm/20 in. tall. The leaf shown seems pretty large compared to the plant height, it's about 20 cm/8 in. long.
Leafs though appear shiny are rough to the touch on both sides, like very fine sandpaper.

The leafs remind me be a bit to a cocoa tree, but I am no expert on identification.

@Marzipanherz Thanks for the comment, I agree there is some similarity, but my tree's leaves seem wider and have those little teeth, while cocoa leaves don't seem to have teeth.

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

It appears to be Cordia sebestena


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Spores bacillus subtilis in milk
I need to inoculate spores into milk and then count on the plate. I never see a spore, so how i recognize it from the germ cell? does anyone know the procedure and if there are differences from a normal count in agar colonies?

If you need to inoculate milk with a known number of Bacillus subtilis spores then you will have to go follow a "sporulation" protocol - (going by your question I am not 100% certain whether this is what you want to do).
However, please find a sporulation protocol, developed by the Universities of Bonn and Freiburg, below:
Sporulation

Overnight culture

Inoculate your culture of Bacillus subtilis in 4 ml LB-medium
Let them grow overnight at 37°C, 200 rpm

Exponential growth

Measure the OD600 of your overnight culture and dilute it in LB-medium to an
OD600 off around 0.1-0.2/ml in 10 ml LB
Let the cells grow to an OD600 of 0,8/ml (37°C, 200 rpm)

Sporulation

Centrifuge 10 ml of the cells at 13,000 x g for 1 minute
Wash the pellet with 1 x PBS
Re-suspend the pellet in 5 ml DSM (Difco Sporulation Medium)
Let the cells grow for 24 hours at 37°C (200 rpm)

Lysozyme treatment (additional for spore purification)

Treat the samples with lysozyme (15 mg/ml) at a dilution of 1:6
Incubate for 1 h at room temperature
Wash 6 times with 1 x PBS

Additional:

count spores using a Neubauer improved counting chamber and make aliquots
with a defined number of spores per aliquot (e.g. 100 Million spores per 500 μl)

(Note: always use fresh DSM since the FeSO4 is rusting when it is in dilution)
May I make special mention of the Bacillus subtilis Manual here which was put together by the iGEM team and has proved as an excellent resource. The protocol above was taken from it.
Once you have your spore counts you can then inoculate the milk to your liking. However, please be aware that milk, unless completely pasteurised prior to inoculation, is not a sterile product. This means that other organisms might grow on whatever agar you decide to plate out on.

Thank you, but i have already a culture of b.subtilis spores (10^8), i have only to put into milk. Then this milk (+spore) will be treated (temperature etc) to try to kill the spores. After treatment i have to.count how much we have reduced the number of spores. I put 1 ml for inclusion in petri plate with pca+skim milk. Now, how i count spores? As a common colonies? Or are different? If there are spore and germinative in the same plate how i recognize spores?

Ah, OK. I'm with you now @StarChips. I don't think there's a way to detect spores as such on agar plates. They are easy to small. You would rather operate on the assumption that all the colonies that you can see on your PCA plates stem from spores. Given that you only inoculate with spores. So at the end you just count the colonies.

Yes, but i don't know if the condition of treatment could cause sporulation. I want to be sure to count only spores

Chances are that the treatment will cause sporulation given that some live, vegetative Bacillus subtilis cells are present in the sample. If you really want to be 100% certain that all you count are spores or colonies from spores then you have to go through far more effort. This can't be done on agar plates only. Unfortunately this article is behind a paywall but in its abstract it outlines a wee bit what is required to get an accurate answer on spore counts in your sample: http://www.sciencedirect.com/science/article/pii/S0167701211003526?via%3Dihub


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Is there a surface or body cavity that does not have epithelium?
Is there any surface in the (human) body that is not covered with epithelium?

Can you narrow down what you mean by "surface"? It might matter.

@kmm - It doesn't matter, really.

I don't know if I'm missing the point but I thougt that there is no epithelium on the surface of the teeth and the joints.

@mioppli nobody seems to be refuting this - I'd post it as an answer, maybe.

Are you referring to body cavity in the medical sense of the term (https://en.wikipedia.org/wiki/Body_cavity) or something more colloquial like e.g. a skin fold? (Asking "in the body" sounds like you mean the medical sense to me.)

Short answer
Edit with credits to anongoodnurse: As far as I know, every bodily surface and cavity is covered by epithelia.
Background
Epithelial tissue is a sheet of cells that covers a body surface or lines a body cavity. There are two types of epithelium in the human body:

Covering and lining epithelium forms the outer layer of the skin; lines open cavities of the digestive and respiratory systems; covers the walls of organs of the closed ventral body cavity.
Glandular epithelium surrounds glandular tissue.

Hence, the entire the bodily surface is covered by some sort of epithelium. Even the eye is covered with squamous epithelia (thanks to anongoodnurse for pointing this out).
And while acknowledging that an absence of evidence is not evidence of absence, I believe that there is no surface on, or cavity in the body not lined with epithelium.

Fig. 1. Epithelial lining of bodily surfaces. source: Ternopil State Medical University

I wonder if there is any body cavity which is not connected with the outside of body and also it doesn't have epithelium.

@SepehrM Depends on your definitions of "cavity" and "connected", I guess. I mean, would the ventricles of the brain count? They're full of CSF but typically described as cavities, and connected to each other but not to the outside (although this wouldn't answer your question directly, since they have epithelium).


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Are there foods which not only prevent but help fighting cancer?
I was reading a probably not to serious webpage and I found this quote

" Certain types of vegetables, such as the cruciferous variety, are
  not only nutrient-dense but contain compounds that may fight cancer,
  according to the National Cancer Institute."

Then I looked more information about this, but I can only find references to foods helping prevent cancer but they dont seem to say they help fight cancer when it's already present.
This page says the following foods help prevent cancer, but later make an ambiguos statement that you could think they imply those foods help fighting cancer when it's presented

The following is a list of foods that have been shown to have
  cancer-fighting properties. While some are well-known super foods,
  others may surprise you. You won’t find a burger or fries on this list
  – when it comes to cancer prevention, clean eating prevails:

http://www.cancercenter.com/community/newsletter/article/Foods-that-have-cancer-fighting-properties/
So, my question is, are there foods which not only prevent but help fighting cancer when it already exists?

Short answer: No, for neither of the two questions.

What about this, is not serious or fake? "In conclusion, the results from our laboratory and from others provide ample evidence for the benefit of I3C and DIM for the prevention and the treatment of prostate cancer."  https://www.ncbi.nlm.nih.gov/pubmed/15570059  (sorry for insisting, just looking to understand why there are some aparently real sources which seems to claim so)

It seriously shows that you can put chemicals in a petri dish and kill cells from cell cancer lines.  That is not evidence that the chemical would do the same thing in a person.  The "MAY fight cancer" (emphasis mine) is doing a lot of work there.

Lack of evidence of foods that prevent or fight cancer is not the same as there being no foods that prevent or fight cancer.  There are logistical issues and lack of monetary incentives associated with running clinical trials to test the efficacy of foods in preventing or fighting cancer.

@swbarnes2 so to summarize, it's doubtful.

Lack of evidence when one has looked certainly doesn't make the proposition more likely.  Food companies would LOVE to have evidence that their products inhibit cancer.  Pharma didn't prevent people from testing the heck out of resveratrol;

The short answer is, no.  There really isn't any good evidence that a person can eat enough of any chemical to have a clinically detectable effect on cancer.
Note that any study that shows an effect on cancer cells in a petri dish doesn't count as demonstrating that it would do anything in a person with cancer.  It might be that the chemical would not work the same in the body, or would not work the same on real cancer cells growing in a person (not cells cultivated to grow in a petri dish for 30 years).  And even if they did kill cancers like in a petri dish, that doesn't mean that you can actually eat enough of the chemical to get a high enough concentration to have that effect.
That link is pretty much click-bait, and nothing more.

Cryptotanshinone is a good example. Exhibiting anti-cancer effects against cancerous cell lines such as LOVO cells, the bio-availability through oral administration in rats was found to be less than 10% (ref1, ref2). The oral dose was 100mg/kg of HPLC-purified CT in the rat model. A separate production paper was able to produce 23.2mg of CT per gram of inoculum (Salvia miltiorrhiza root cells) (ref).

And the half-life is ~6.67 hours in the rat model, from the 1st reference. So just imagine: You're 88kg and need to consume 100mg/kg every 12-18 hours. That means eating 0.85lb of root material. Never mind poisoning from accessory compounds in the roots, among a list of other potential problems, such as even lower bioavailability in an impure form.

I've received an email from a cancer researcher from Denmark. I asked her if it was true she stated a chemical component of carrots delay cancer development in rats. She gave me some links and stated yes.

What cancer researcher?  Where are her findings published?  No matter what nonsense you propose, you can find a quack willing to support it.


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phosphorylation of Glyceraldehyde 3-phosphate
This question is related to something that happens when 3-phosphoglyceraldehyde is converted to 1,3-bisphosphoglycerate during glycolysis.
As I understand it, 3-phosphoglyceraldehyde is deprotonated by NAD+ and phosphorylated by a Pi group, which results in NADH + H. The extra H apparently comes from the Pi group (which I believe is called orthophosphate [1]).
Now, where does the Pi come from? is it just sitting in the cytosol?, does all Pi have a hydrogen? can someone clarify what an orthophosphate is, I never heard of that term.

You can google orthophosphoric acid. Pi is the acronym of inorganic phosphate.

Yes, the cytosol contains a high concentration of orthophosphate (in yeast, between 10--75 mM) so it is readily available for this reaction. The notation P$_i$ is commonly used because the orthophosphate ion can exist in multiple forms in water solution:
H$_3$PO$_4$ $\leftrightarrow$ H$_2$PO$_4^{-}$ + H$^+$ $\leftrightarrow$ HPO$_4^{2-}$ + 2H$^+$$\leftrightarrow$ PO$_4^{3-}$ + 3H$^+$
When we don't need to specify an exact form, P$_i$ is convenient as a shorthand for "some phosphate ion".
At the cytosolic pH (about 7.2), almost all orthophosphate is in the H$_2$PO$_4^{-}$ and HPO$_4^{2-}$ forms, which are roughly equally abundant. So yes, there is (at least) one hydrogen on orthophosphate available for the enzymatic reaction.
The term "orthophosphate" rather than just "phosphate" is common in biochemistry because phosphate also exists as polymers, including the di- and triphophates (in nucleotides, for example) as well as longer polyphosphate chains. These form are all referred to as "phosphates", while "orthophophate" specifically means the "monomer" P$_i$.