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Is pyruvate considered a high energy molecule like ATP or NADH?
ATP, NADH and FADH2 are high energy molecules. The second half of glycolysis is known as the pay-off phase, characterised by a net gain of the energy-rich molecules ATP and NADH.
In fermentation, for example, pyruvate still has energy into it. If you had oxygen around, you could have cellular respiration, you could go into the Krebs cycle, the citric acid cycle, and derive more ATP from pyruvate. But the term 'high energy' or 'energy-rich' is not commonly used to describe pyruvate. Is it wrong to use such terms to describe pyruvic acid?

Summary
Do not use the term ‘high-energy’ to refer to biochemical intermediates because many people (including the OP) do not understand what it is supposed to mean. However, if you insist in using it in its historic biochemical sense, pyruvate does not qualify,
The terms ‘high-energy’ and ‘energy-rich’, although traditional in biochemistry, are best avoided. This is because they are meaningless to a chemist and misleadingly imprecise to a biochemist. This question is a good example of the misunderstanding of the term.
What is important is not to stick ‘labels’ on molecules (leave that to undergraduate politics) but to understand and articulate the energetic role molecules have in metabolism. As regards ATP and NADH, I have already provided such an explanation in the answer to another question. I will only summarize here to make a comparison with pyruvate.
However one thing should be emphasized at the start. Statements about molecules containing ‘energy’ are sloppy:

A change in Gibbs Free Energy only occurs when a molecule reacts with other molecules, and the magnitude of this change depends on
which molecule(s) it reacts with.
The biochemical usefulness of a molecule participating in a reaction with a negative change in free energy depends on the availability and ubiquity of
reacting partners and the magnitude of the free energy change compared with that of the reacting partners.

Historic use of the term ‘energy-rich’ with respect ot ATP, NADH and pyruvate

In the case of ATP, the hydrolysis reaction to ADP + Pi has a high enough negative change in Gibbs Free Energy to drive many biochemical reactions that have a positive Gibbs Free Energy change, and enzymes have evolved to couple ATP hydrolysis to such reactions. The latter is key — there must be a way of using this energy!

In the case of NADH, its oxidation to NAD+ has a standard redox potential of +0.32V, which is, in effect, a negative standard free-energy change. However it can only occur in conjunction with another redox ‘half-reaction’ with a redox potential that will result in an overall negative free-energy change. In fact the redox potential of the NADH oxidation half-reaction sufficient to drive many biochemical reductions, and enzymes have evolved to couple NADH (and NADPH) oxidation to such reactions. Furthermore the oxidative phosphorylation system has evolved to allow production of ATP from NADH.

In the case of pyruvate, its reduction to lactate has a standard redox potential of –0.19V, so it has a positive standard free-energy change. Clearly quite a different situation to NADH, with which it reacts to regenerate NAD+. So pyruvate could only be considered in relation to half reactions of even higher redox potential. In fact, it plays no general role in metabolism for driving thermodynamically disfavoured reactions.

The cause of the confusion
The explanation above shows that pyruvate does not conform to the description ‘energy-rich‘ in its (discouraged) historic biochemical usage. What caused the OP to think so? He states:

…pyruvate still has energy into it. If you had oxygen around, you could have cellular respiration, you could go into the Krebs cycle, the citric acid cycle, and derive more ATP from pyruvate.

What this is actually saying is that pyruvate is a metabolic source of energy in the form of ATP because it can be metabolized aerobically (in the pyruvate dehydrogenase reaction) like glucose and a host of other intermediates. This is not the usage of the term ‘energy-rich’. All one is saying here is that when pyruvate, glucose, fatty acids etc. etc. are oxidized to carbon dioxide and water the C–C bond energy etc. can be utilized in biochemical reactions (reductions) rather than being released as heat.
Appendix 1: Other phospho-compounds with a high group-transfer potential
An alternative to ‘energy-rich‘ for compounds such as ATP is that they have a high ‘group-transfer potential‘ — the free energy change in a particular reaction. The student of biochemistry will be aware that particular reactions in glycolysis and the tricarboxylic acid cycle can phosphorylate ADP to ATP, and so must have a high group transfer potential. Some examples (taken from Berg et al.) are listed below. These are all ΔG0′ (kJ/mol) for the hydrolysis of the phospho/phosphate group.
Phosphoenolpyruvate        –61.9
1,3-bisphosphoglycerate    –49.9
Creatine phosphate         –43.1
ATP (to ADP)               –30.5  ------------------
Glucose 1-phosphate        –20.9
Glucose 6-phosphate        –13.8
Glycerol 3-phosphate        –9.2

Thus, phosphoenolpyruvate, 1,3-bisphosphoglycerate and creatine phosphate have a higher group transfer potential than ATP, as expected from their role in phosphorylating ADP. They can be considered ‘energy-rich‘ in the historical usage of the term. However, unlike ATP, they play specific — rather than general — roles in biochemical energy transfer.
Appendix 2: Other biochemical reducing agents
Although biochemical reducing agents play a central role in overcoming the energy barriers to synthesizing reduced compounds such as fatty acids and steroids, the historical term ‘energy-rich‘ has not been applied widely to them. To provide a perspective on the reducing power of different biochemical compounds, some examples (again taken from Berg et al.) are listed below. The standard redox potential (E0′) is expressed in volts, and n is the number of electrons transferred in the oxidation/reduction
OXIDANT             REDUCTANT         n    REDOX POTENTIAL
Succinate (+ CO2)   α-ketoglutarate   2       –0.67
Ferrodoxin (Ox)     Ferrodoxin (Red)  1       –0.43
NAD+                NADH              2       –0.32
Glutathione (Ox)    Glutathione (Red) 2       –0.23
FAD                 FADH2             2       –0.22  ---------
Pyruvate            Lactate           2       –0.19
Cytochrome c (+3)   Cytochrome c (+2) 1       +0.22
Oxygen (O + 2H+)    Water             2       +0.82

Oxygen to water is a 4 electron process

@VincentFourmond — Not with reference to one atom with the product 1 molecule of water. I've clarified. (The problem is that if you try to lay out a table you have to use pre formatting that renders everything literally. Hence you can't use subscripts or superscripts etc.)

This is a related conversation between me and David Harrison, Course Director of Biochemistry for Pharmacy since 2009:
David:

Amir,
There is a problem with your nomenclature. I would describe NADH as an electron carrier not as a high energy molecule. Its reductive potential is only relevant in the presence of a molecule that has oxidative potential (say pyruvate). Similarly, I would say that ATP has a high energy phosphate bond meaning that the free energy of hydrolysis of ATP to ADP and phosphate is -7.3 kcal/mol (-30 kJ/mol) whereas a typical phosphate bond’s hydrolysis (glucose 6-phosphate) is closer -3 kcal/mol (-12 kJ/mol).
Pyruvate has a higher reduction potential (-0.19V) than NAD+ (-0.32V) which explains why it is readily reduced by NADH, but the free energy for the reaction producing lactate is only -2.5 kcal/mol. So, no pyruvate is not a particularly high energy molecule under reductive condition. However, when you consider the reaction of pyruvate and oxygen to give CO2 and water the free energy is huge. But again, if you want to talk about high energy bonds neither pyruvate nor NADH have them.

Amir:

Thank you. I know my question is semantic. I don’t think that terms like ‘energy-rich molecules’ and ‘high energy molecules’ are exclusively used to describe molecules that contain high energy bonds. For example, I read this in Wikipedia: The second half of glycolysis is known as the pay-off phase, characterised by a net gain of the energy-rich molecules ATP and NADH.

David:

The reason the NADH is considered high energy in this context is that, in the presence of oxygen, NADH can be restored to NAD+ via the electron transport system (Complex I, III, and IV) to produce a proton gradient across the inner mitochondrial membrane. That gradient is then responsible for driving the F0F1-ATPase (complex V) to produce ATP from ADP and phosphate. [I should mention that there are two different mechanisms for delivering the reduction potential of NADH from the cytosol to the mitochondrial matrix, but that is a different story] But again, the energy of NADH is dependent on context. In an anaerobic environment, it is the NAD+ that is necessary for the formation of ATP and the NADH is restored to NAD+ by converting pyruvate to waste products (lactate or ethanol).

Three cheers for David Harrison


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How much sunlight is required for photosynthesis to peak?
I've read that photosynthesis peaks at some point over light intensities https://en.wikipedia.org/wiki/PI_curve According to https://www.bbc.co.uk/bitesize/guides/z9pjrwx/revision/5 suggests

At very high light intensities, photosynthesis is slowed and then inhibited, but these light intensities do not occur in nature.

But https://en.wikipedia.org/wiki/Photosynthetic_efficiency seems to suggest otherwise

most plants can only use ~10% of full mid-day sunlight intensity

If plants can only use ~10% of mid-day sunlight, then the intensity of mid-day sunlight would have been too high for the rate of photosynthesis to plateau.
Are the two incompatible or am I missing something?

Varies by plant

^this. Also I would be cautious to assume that 10% of mid-day sunlight energy utilized by a plant translates into 100% energy utilization at a tenth of mid-day lighting conditions.

source: Stack Exchange

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Are ganglion cells in the foveal avascular zone served by choroidal blood supply or diffusion from retinal layer capillary beds?
I am trying to determine which blood supply (choroidal or retinal) serves the retinal ganglion cells that respond to foveal cone stimulation. I know that the fovea is supplied by the choroid, but it is unclear to me if this only applies to the cones in the fovea. The paper I link to below mentions that the choroid serves the fovea, but the choroid also serves the outer retina in total (and the RPE). So is the statement that 'the choroid serves the fovea' extending beyond the observation that the choroid serves the outer retina (since the fovea is mostly cones due to the inner layers being pushed aside)?
Are the ganglion cells that are pushed aside in the fovea served by choroidal vessels, or are they pushed aside far enough to be served by capillaries in the retinal layers? Please provide a paper as a reference.
I've searched google obviously and perused PubMed and I cannot find a clear answer to this.
https://www.ncbi.nlm.nih.gov/books/NBK482301/

I'm sorry if this sounds picky, but did you enter your question into a decent search engine? Also, your title and your actual question don't seem to me to match. You seem aware that there are ganglion cells in the FAZ, and it's the blood supply that you ask about in your final question. Would you please edit for clarity?

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Fossil identification
I recently found a fossil which I am unable to identify. I believe it's a sea creature, but I don't know what kind. my best guess is some kind of shell or a porpita.
I appreciate any help.
this is the image of the fossil.

The features of this fossil that I can describe are :
1- It seems to be circular
2- A pattern of lines which spread from the center
3- It does not seem to be curved (like a shell) — it looks flat
4- Dimensions are about 1.2 cm by 1.2 cm (circular)
5- This fossil was found in Iran/khouzestan
Another thing to mention is that where I found this fossil, I found other sea creature fossils like starfish and shells.

Welcome to the site. Can you please edit into your question the dimensions of the fossil and where in the world the specimen comes from? These will greatly increase your chance of getting an answer.

Thank you so much for your guide. I edited the question and added dims and location of discovery. @bob1

your question is a better fit over at https://earthscience.stackexchange.com/ but you need to provide more information like a more exact location and if possible what other fossils can be found in the area,this is to find what geological time it is from.

without more information, best guess would be a natural cast of a fish vertebra.

Mah Es there is also https://www.reddit.com/r/fossilid/


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Impact of increased sodium conductance at a neuromuscular junction
If trans-epithelial Na+ transport were to increase at the synapse(please consider both pre and post-synaptic membrane situations) in a neuromuscular junction, how would that manifest itself? My guess is that the increased sodium conductance would depolarize the membrane to a higher resting potential.

Would this translate to higher firing rate or result in more frequency of miniature end-plate potentials?
Would this also affect the rise time of action potential? Or its threshold?


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Thermodynamics of passive transport
My question is, where does energy come from for passive translocase's conformational changes? I argue it can't be concentration gradient, as concentration is only statistical phenomenon at micro scale, and has nothing to do with energy of individual molecules and interactions. I also don't want to cover electric gradient, as it involves obvious electric forces.
I couldn't find any diagrams like this about this theme, so I would appreciate very much if someone provides me with one:

I am not sure that the concentration gradient provides the energy for conformation changes in passive protein transporters (or at least the molecular mechanism), but your statement about a concentration gradient being unable to energy is obviously incorrect or Mitchell's hypothesis would have been thrown out years ago. Instead it won a Nobel Prize. (And that involves an electric gradient as well, whether or not you want to cover it.)

@David thank you for your response. concentration of molecules doesn't correlate to energy of each particle, but temperature does. i did not want to cover electric forces as they are already obvious, moreover, not all particles have charge, e.g. glucose.

I said concentration gradient, not concentration. There is a page in Berg et al. that derives the thermodynamic expression for the free energy change represented by a concentration gradient. Unfortunately this is no longer available online.

Type of transport to be considered
The term used in the question — passive translocase — is not a standard description of any transporter protein. From the description I shall assume we are talking about what is called Passive Transport or Facilitated Diffusion. This is defined in the Wikipedia article on the topic as follows:

Facilitated Diffusion… is the process of spontaneous passive transport (as opposed to active transport) of molecules or ions across a biological membrane via specific transmembrane integral proteins. Being passive, facilitated transport does not directly require chemical energy from ATP hydrolysis in the transport step itself; rather, molecules and ions move down their concentration gradient reflecting its diffusive nature.

Although most structural information is available for ion transport, because of the specification of the question, I shall consider the transport of glucose (and other neutral sugars) by the proteins GLUT1 and GLUT3
The molecular concentration gradient supplies the energy for transport
Before considering the molecular interactions between the sugar and the transporter protein, it is necessary (because of the assertion otherwise in the question) to assert that the net difference in concentration of sugar between the two sides of the membrane supplies the overall energy for transport.
The free energy change in transporting a neutral species from one side of a membrane at a concentration c1 to the other side at a concentration c2 is:

ΔG = RTln(c2/c1) = 2.303RTlog10(c2/c1)

For example, if c1 = 10–1 M and c2 = 10–3 M, one can calculate the change in Free Energy as –11.3 kJ/mol.
General aspects of the thermodynamics of conformation changes in proteins
Many protein, e.g. allosteric proteins such as haemoglobin, can adopt two (or more) conformations differing only slightly in Gibbs Free Energy. Clearly, the conformation with the lower free energy will be favoured. However the position of the equilibrium between the two states can be changed by the specific binding of a small molecule which can favour the disfavoured structure, because the protein–ligand complex has a different, and lower, free energy than that of the free protein.

A general alternating model of transporters was proposed by Jardetzky as long ago as 1966, assuming three characteristic features:

A cavity in the transporter to accommodate the substrate
Two different transporter conformations to allow for the molecular cavity to be open to one side of the membrane in one conformation and to the opposite side in the other
A binding site for substrates in the cavity, the substrate affinity of which may be different in the two conformations.

Detailed thermodynamics of the GLUT transporters
Zhang and Han (Biophysics Reports 2016) performed the kind of thermodynamic analysis solicited in the question in the light of structural information on GLUT transporters of the major facilitator superfamily (MFS). They considered two conformation states — Cin and Cout, with and without bound substrate in a four step model:

They also presented a free-energy landscape of the type requested, concluding that the lower free energy of Cout after transport was due to loss of energy as heat.

For a full explanation it is, of course, necessary to consult the original paper.

Thank you very much for your expertize. I wonder weather  lower free energy of Cout after transport increases after regaining thermal energy from surroundings. That should finally answer my question.

@nikopapiashvili — I'm not an expert on transporters, and I do find this a bit puzzling myself. I would need to read and think a bit more about this. There are some protein chemists on the list that are more knowledgeable than me on thermodynamics. Perhaps they will chip in.


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Has anyone who has ever isolated synaptosomes using subcellular fractionation before know what the 'crude/heavy membrane fraction P2' is?
I am reading a journal paper where they analyse the proteome of synaptosomes. In this paper, they isolate synaptosomes from the hippocampi of mice. I know that synaptosomes contain the complete presynaptic terminal along with the postsynaptic membrane and post-synaptic density.
I am trying to understand the subcellular fractionation protocol they used for isolating the synaptosomes in the materials and methods section.
I know that synaptosomes are isolated from the subcellular fractionation of homogenised tissue. What I don't understand is what is meant by the 'crude membrane fraction P2'. I am wondering what exactly this crude membrane fraction P2 is because it is from this fraction that synaptosomes are isolated (via sucrose density gradient centrifugation).
I have read other papers where they also isolated synaptosomes. However in these papers they also mention that they homogenise brain tissue, and isolate the synaptosomes from the crude membrane fraction P2.
Any advice is appreciated.

The first google result I get for the search term "crude membrane fraction P2" is a paper from 2014 with the title Preparation of Synaptic Plasma Membrane and Postsynaptic Density Proteins Using a Discontinuous Sucrose Gradient. It includes a step-by-step protocol; I'll post the most relevant steps here:

Low Speed Centrifugation to Remove the Nuclear Fraction (Yields Supernatant S1)

Centrifuge the homogenate in a fixed angle rotor at 900 x g for 10 min at 4 °C. Transfer the supernatant (S1) to a new, labeled 13 ml tube and resuspend the nuclear fraction pellet (P1) in 500 μl of 0.32 M HEPES-buffered sucrose. NOTE: The (P1) fraction can be stored at -80 °C and used for western blot analysis of the nuclear fraction.

Enrichment of the Crude Synaptosomal Fraction (Yields Pellet P2)

Centrifuge the supernatant (S1) at 10,000 x g for 15 min at 4 °C. Remove the supernatant (S2) and reserve 500 μl in a microcentrifuge tube to store at -80 °C for subsequent protein quantification and western blot analysis of the cytosolic/light membrane fraction. Resuspend the remaining crude synaptosomal fraction pellet (P2) in 1 ml of 0.32 M HEPES-buffered sucrose solution and then add another 3 ml of 0.32 M HEPES-buffered sucrose solution.
Centrifuge at 10,000 x g for 15 min at 4 °C. Remove the supernatant (S2’) and reserve 500 μl in a microcentrifuge tube to store at -80 °C for subsequent protein quantification and western blot analysis of the cytosolic/light membrane fraction. Save the washed crude synaptosomal pellet (P2’) in the polypropylene tube.

So S and P refer to the supernatant and pellet after centrifuging, respectively. P1 and S1 are from the first round of centrifugation; the pellet P1 contains the cell nucleus and the supernatant S1 goes on to the next steps. The second round of centrifuging gives P2 and S2. P2 contains the synaptosomes, but also other membranous material which will need to be removed as S3 in later steps.


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Can anyone identify this woody plant
They were cut a while ago and have paper like bark, the newer bark is a reddish colour and the old is almost black, the leaves are long and slender and it had some yellow flower buds
https://i.stack.imgur.com/uaYM4.jpg
https://i.stack.imgur.com/ARWuG.jpg
https://i.stack.imgur.com/mCPum.jpg

Hello LIam! It would be helpful if you added the location of where you found this plant. Also, I use the iNaturalist app regularly-- and it's auto classifiers are pretty good at helping me identify a plant (immediately), and in my area they are usually followed up by a crowd-sourced (human!) identification within a few days. Plus, these pics can hopefully be used for science! You can add the app to your phone and use in real time. Check it out here: https://www.inaturalist.org/

This one has been bothering me, I keep coming back to it. I'm sure I've seen the plant as a non-native in the UK, perhaps a botanical garden or the like. Bookmarked in case it comes to mind.

This one has been bothering me as well! Perhaps a neighbor has it in their yard? I dropped the picture into two different online databases (https://identify.plantnet.org/ and https://plant.id/ and did not get the correct match. If you have a location, that would help!

Leaves and flowers bring to mind Australian and South African (fynbos) plants. The flower is odd though,

Almost got it, I reckon:
I think that this is one of the Hakea species, but it could be another of similar genera, such as Grevillea. Hakea are moderately diverse group of Australian plants in the Proteaceae. They are hardy and are like places that reach very high temps in the summer, and I think all need fire to open their seed pods. This group of plants have very distinctive flowers, with the stamens sticking out and curling around (OP's second image).
I think this is probably Hakea arborescens, as this has yellow flowers and strap-like leaves, whereas most of the other species have white flowers. H. arborescencs is also one of the more commonly planted species in those areas where it is used as a garden plant. There's also Hakea nodosa with yellow flowers, but it has stick-like leaves.


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Question about manifestation of an X linked disease (homework help)
I am doing some practice exams and came across this question. Perhaps the answer is a lot simpler than my reasoning, but after discussing it with others, I still disagree why the answer is clearly and simply what it is, based on the information given. I apologise that this is quite long.
-- Question starts below --
During very early development of mammalian females, one of the two X-chromosomes normally present in each somatic cell becomes deactivated. Deactivation is random, with maternal and paternal X-chromosomes equally likely to be deactivated. All cells deriving from this cell carry the same deactivated X-chromosome, creating local patches of tissue with either maternal or paternal features.
Anhidrotic ectodermal dysplasia (AED) is an inherited skin condition caused by the recessive allele (s) of a gene that has its locus on the X-chromosome. In some individuals with this condition, sweat gland distribution is patchy, with some areas lacking glands. In other individuals with this condition, all sweat glands are absent.
Q) Which one of the following is consistent with the information given?
A. Patchy sweat gland distribution is found in males and females but is more likely in males with the condition.
B. Patchy sweat gland distribution is equally likely in both males and females with the condition.
C. Only females with the condition exhibit patchy sweat gland distribution.
D. Only males with the condition exhibit patchy sweat gland distribution.
--/ End of question /--
The correct answer is C.
I would like to know why you should be able to tell that only females will manifest or show patchy sweat gland distribution. My reasoning is, individuals with the condition must have the recessive gene. Since it is an X-linked condition, and females have 2 X chromosomes, they must have 2 copies of the recessive gene (little r) to get this condition. Thus, females must be homozygous recessive, or rr. (Males will be just r)
If we define the phenotype of having the recessive gene, we say that it causes the individual to either have patchy sweat glands or no sweat glands at all.
The thing is, they do not tell you under what conditions a person will have patchy sweat glands and when they will have no sweat glands at all.
As an X linked disease, think haemophilia, they should either have the skin condition or they don't: in other words, even though females can be carriers, carrier females will not exhibit the symptoms and the question talks about all humans with the condition (either males or females).
How* the disease manifests isn't made clear, so how are you supposed to know that of those who have patchy sweat glands vs those that have absolutely no sweat glands, females are those who have patchy sweat glands?
*For example: Angelman and Prader-Willi syndromes are both results of errors on the same region of chromosome 15, however, the important how that explains who gets PW and who gets A is, the phenotype depends on whether it was maternal or paternally inherited due to imprinting. By telling you this, if the question told you that males tend to get PWS and females tend to get Angelmann, told you some characteristics of either syndrome, then told you "given that a specific gender is more likely to get a specific symptom", you can determine whether males or females are more likely to have which disorder (PWS or A) based on the symptoms.
The question doesn't have this sort of information. It doesn't tell you how a person tend to get patchy or missing sweat glands and it doesn't tell you anything about incomplete dominance, co dominance, mosaicism etc.
Since both males and females can have the condition but it is X linked, why is it not A, but C? Why can't males have patchy sweat gland distribution too?
One answer I got while discussing this was, the information tells you about random inactivation of the X chromosome. For me, this only further rejects the idea that only females can be patchy: Suppose a female is a heterozygous with XRXr. One X chromosome gets inactivated at random. Let's pretend XR gets inactivated, leaving Xr. This is the recessive gene.
Now, we know the recessive gene produces the skin condition, with could be either patchy or completely absent sweat glands. Sadly, it does not tell you the exact symptoms of the recessive gene, see my point and analogy about PWS and A above. Since it doesn't tell you, I can only assume that like all other X linked diseases, having the recessive gene will cause the individual to show symptoms of that disease, end. of. story.
Usually when you have the recessive gene, you have the disease. Either have or not have. Thus an XRXr female with the first X inactivated will have the recessive disease, and fully show this (no sweat glands at all).
If she was XRXr with the second X inactivated, she would show a normal phenotype and have fully functional in ordinary quantity sweat glands.
Similar case with the males: They either have, or not have the faulty gene due to the fact that they only have 1 X chromosome.
Now, during my discussion with others, someone said, if you assume one copy of AED X (Xr) + one copy of normal X (XR) = carrier, then there is no way to explain how anyone could have patchy glands. They either have normal glands or no glands at all.
But I think this is exactly the point. The question doesn't ask you how anyone could have either patchy or totally absent sweat glands. Why does patchy glands exist? Where is the condition of its existence? It's not told to you in the question. The normal train of thought (at least for me) is therefore, a female either has it or they don't. No where does the text mention anything to do with mosaicism. IF the question TOLD you that AED is inherited the way it is etc, then stated that females have patchy sweat glands while males have none at all, and asked you "what is the most likely reason for this", then you can say mosaicism.
This direction of reasoning would work much more logically.
Otherwise I just don't see this.
Would appreciate input from someone specialising in genetics.

"Since it is an X-linked condition, and females have 2 X chromosomes, they must have 2 copies of the recessive gene (little r) to get this condition." Your reasoning here is wrong. Actually, to have a patchy phenotype, the female must be heterozygous! Therefore, the cell patches where $X^r$ was inactivated exhibit normal phenotype, and cell patches where $X^R$ was inactivated are missing the sweat glands. Men cannot exhibit patchy phenotype because we can only have either $X^r$ (missing glands everywhere) or $X^R$ (normal phenotype everywhere).

@Domen you should write a formal answer

@Domen Thanks but I know that, given the statement, "men cannot have patchy, only females have patchy", then the reasoning is because men only have one X. That's fine. However, in the REVERSE, if they say "some people have patchy, some people have none at all - why?" how do you determine that females have patchy and not men? It makes no sense to me that if a female has XRXr, why would she be patchy, rather than completely normal? Do we assume codominance? I'd like to use hemophilia as a comparison and example -->

@Domen <-- Correct me if I'm wrong: the dominant version of a gene dominates the phenotype, eg in hemophilia, even if the female genotype is XHXh, the female will have a completely normal phenotype because the normal version of the H dominates over the h. Why should AED be any different?
And, if we bring random X inactivation into the picture, does that mean if the X carrying the normal H in a female carrier gets inactivated, then the female will have only the recessive little h, Xh, left, making her fully hemophiliac?

If the disorder was an autosomal recessive disorder (and follows the Mendelian dominant/recessive pattern), then your reasoning is correct. Both men and women would either have the disease or not have it at all. If a person has a heterozygous genotype, then they will not have the disease. Only if they have a homozygous recessive genotype will they show any characteristics of the disorder. This is clear for an autosomal recessive disorder. However, for X-linked disorders, things are a bit more complicated. For men, there is no concept of recessive/dominant alleles. They either have the gene or they don't. For women, we need to consider X-inactivation.
When we talk about X-inactivation, the main thing is that it is random. That means that approximately half the cells in the body will contain one copy while the other half will contain the other copy. Some cells will have the recessive allele and some cells will have the dominant allele. In the case of color-blindness, this means that approximately half the cone cells will be defective and the other half will not be. Most of the time, the brain learns to ignore the signals from the defective cells. However, there are cases when the number of defective cells are more than the number of normal cells (due to random inactivation), and the woman experiences Tetrachromacy. You cannot compare these disorders to Angelman and Prader-Willi syndromes because those are on autosomal chromosomes and these are on the sex-chromosomes. You are right that the textbook does not mention anything about which individuals have patchy sweat glands and which do not have them at all. However, the textbook states that the recessive allele on the X-chromosome causes the condition. This means that we can assume both of these things:

The trait is not a polygenic trait - That is, it is only caused by the gene on the X-chromosome
The trait follows Mendelian dominant/recessive pattern

Although we cannot be extremely sure of either of those, we can assume it for sake of this problem. Since the allele is able to cause a complete loss of sweat glands, we can arrive at the conclusion that the recessive gene causes the loss of sweat glands. The reason some women have patchy sweat glands is because of X-inactivation, and the areas in which the recessive copy is activated will have no sweat glands. On the other hand, the areas where the dominant copy is activated will have normal sweat glands. I think that the source of confusion here are the terms dominant and recessive. Although we say that the trait is "recessive", there is no concept of dominance and recession for X-linked traits. For women, half the cells are deactivated whether or not they contain recessive traits. For men, the X-chromosome is used whether or not they contain recessive traits. This means that the even if a dominant gene (in the X-chromosome) was recessive, it would have no consequences on the phenotype. In women, the phenotype (for X-linked traits) is always random (or rather, it's different for each cell - some sweat glands have one phenotype while others have a different phenotype).
Regarding your question on why men can't have patchy sweat glands, consider this. A man would either have the defective copy of the gene or a normal copy of the gene. Normal copy would result in normal sweat glands, so we have to deduce that the defective copy would result in patchy sweat glands. However, this would mean that women with homozygous recessive would still have patchy sweat glands. Hence, nobody would have complete loss of sweat glands. Since the question clearly states that some people have patchy sweat glands while others have a loss of sweat glands, we have to assume that the defective allele causes a complete loss of sweat glands. This makes sense as men would have no sweat glands, homozygous recessive women would still have no sweat glands, and heterozygous women would have patchy sweat glands. Because this is the only answer that makes sense, this must be the correct answer.
Like you said, this isn't guaranteed to be true, especially if the trait is polygenic. However, it's the most plausible answer (and the other three are definitely false), so I think that the question is put in a fairly good manner. Since they have mentioned the trait to be X-linked "recessive" (like I mentioned before, there really isn't a concept of recession for X-linked traits), we can assume that it follows the Mendelian pattern, and making this assumption, arrive at the right answer.
Hope I answered your question!

Thank you for this comprehensive answer. You are right in that my confusion was from the terms dominant and recessive and the lack of this in X-linked traits. I also see why the Angelman and Prader-Willi syndromes are a different case. Thanks!


text:
Can mosquitoes be attracted by our voice?
In the dark, mosquitoes use CO2 to find blood host like us. However, 1) they are known to have excellent auditory organs (ref1, ref2) and 2) sound can be heard from any directions, contrary to odors which follow the wind direction.
Do mosquitoes use our voice to find us?

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

Keep in mind that mosquitoes main food is flower nectar.  Only the females bite for blood and only to feed their eggs.  Humans are not a primary source for such blood so even though they can hear human speech, singling us out specifically would not be evolutionarily advantageous since they can also get blood from many other sources much more easily than from humans.  We get bit as a crime of opportunity, but we're not a consequential source of blood for mosquitoes.  We're also rather more dangerous to bite than other animals because we're quite good at striking back.

@J... - While some of what you say is true, there are anthropophilic mosquitoes - human loving - which prefer human hosts, e.g. Anopheles species, which transmit diseases such as malaria, and some which use humans exclusively.

@anongoodnurse Well, TIL!

Attraction to voice would explain why my significant other is often bitten by mosquitos, and myself far less.

@dotancohen More likely acetone, lactic acid, and estradiol.

Mosquitoes can hear the human voice. If they use human sound to hone in on us as a source of a blood feed is not known at this time, however research into this has just begun. This is especially useful research because of anthropophilic mosquitoes - human loving - which prefer human hosts, e.g. Anopheles species, which transmit diseases such as malaria, and some which use humans exclusively. If disease can be prevented by understanding the role of voice in attracting anthropophilic mosquitoes, it's well worth studying (even if only to develop mosquito traps.).
Until relatively recently, it was thought that a mosquito's acoustic abilities were very limited, and used mainly to detect the correct species and gender to mate with, as there are over 3000 species of mosquito (176+ in the US alone, the CDC states over 200), and they need to be able to determine which other mosquito would be a suitable mate. Most of the research honing in on their acoustic abilities has centered on males and their ability to detect females, e.g. in order to build traps to attract males to determine the efficacy of sterile male release into the wild,  induce sterility in males, capturing and manipulating males genetically to introduce a dominant lethal gene, etc., hopefully limiting the population of those most deadly to humans without harming the environment. From this 2021 paper:

Early studies focused on mate-seeking male mosquito attraction to female wing-beats (Kahn and Offenhauser 1949), and female mosquito responses to male wing-beat frequencies in the laboratory and field (Ikeshoji 1981, Ikeshoji and Ogawa 1988). The fundamental wing-beat frequencies of male and female mosquitoes can vary by species (Table 2), so there has been interest in their use for surveillance and control efforts.

In the last 15 years, however, after studies emerged that some blood-feeding midges focused on host (or prey, if you prefer) vocalizations, some of that attention has turned to the acoustic capabilities of female mosquitoes. Multiple studies have shown that female mosquitoes known to feed on various species of frogs were attracted to traps using recordings of those frogs, and a few have shown the same in attraction of mosquitoes that feed on birds as hosts. Studies have shown that femaqle mosquitoes can detect sounds within the human vocal range at 10 meters away, and males even further (though male mosquitoes do not feed on blood.) But as of this year, no studies have been completed with regard to the response of female mosquitoes to human voive.

"Studies have shown that femaqle mosquitoes can detect sounds within the human vocal range at 10 meters away".
If you refer to Menda et al 2019, it seems that they exposed a male mosquito (not a female) to sound levels of 70 dB SPL located at 10m away from the loudspeaker (which is far louder than normal-speech at 10m away). Or was you referring to another study?

@Noil - OOf, I read a number of papers, I'm not sure which one(s) I read that in. But it's the hot thing to study now, so I saw that claim several times. I'll  have a look when I get the time again, Thanks for asking. :)

"a few have shown the same in attraction of mosquitoes that feed on birds as hosts" Could you give the sources for this please?

I@Noil - I answered this question a year and a half ago. Don't you think asking me to revisit my research now is a little much?

no worry, it was just in case you knew, I'd be interested about it

@Noil - Thanks for understanding. At my age, when something new comes into my memory, something relatively unimportant is tossed... :p

Mosquitos can certainly hear in the range of normal human speech. They are sensitive to the range of around 150-500Hz, and typical human speech is between 100-300Hz depending on your age and sex (DOI: 10.1016/j.cub.2019.01.026). Whether they use that auditory capability to zero in on humans, I do not know (and could find no indication that this is something known in the literature). I do know that the most important sense for mosquitos to find prey is olfaction.
The frequency sensitivity range surprised me actually. I was expecting the frequencies to be much higher. Some insects like moths are sensitive to ultrasound frequencies which helps them detect bats.
Based on the Göpfert et al. paper you listed, it appears that this hearing range tracks nicely with the sound frequency of mosquito flight. Without knowing really anything about the mosquito literature, I would hypothesize that this is no coincidence. I would guess they use hearing to determine the sex of other mosquitos (males and females produce different flight frequencies) for mating purposes. There is also evidence that their auditory abilities can help them in evasion from predators (DOI: 10.1038/s41598-021-81456-5).


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How long can zooxanthellae survive on their own, after being expelled from coral after a bleaching event?
So many sites (and books and journals and such) discuss how long different types of coral can survive without their dinoflagellate algae (zooxanthellae), but...
How long can the poor little symbiotic algae survive on their own after being unceremoniously ejected from their coral hosts?
Aren't most of them (the algae) obligate mutualists?
Can they float around in 'suspended animation' indefinitely?


text:
temperture on rate of mitosis in plants
does an increase in temperature cause an increase/decrease in the rate of mitosis (ie) the rate of cell division increases, more cells are undergoing mitosis at a  higher temperature? mitotic division increase?)

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Mitosis does not occur at very low or very high temperatures. Within the ideal temperature range, the rate of mitosis seems to increase linearly with temperature. That is, higher temperature supports a faster rate of mitosis, and a lower temperature results in a slower mitotic rate.
As a side note, I was able to find many sources surprisingly quickly, and it is recommended that you provide your previous research when creating a question on Stack Exchange. Since you are new here, I have decided to assist you by answering, but be warned that plain questions without any prior effort from your side will get no answers and could even be voted to close.
Sources
One:

They [work by Engelberg in 1965] showed that temperature controls the rate and speed at which a cell divides ... mitosis was very sensitive to temperature, and that cell cuture subjected to temperature between 24-31°C exhibited an accumulation of cells in mitosis ... the speed at which cells exit mitosis is temperature dependent (Rieder and Maiato, 2002). M-phase length is dependent on temperature and is longer at low temperature, likely due to a decrease in enzymatic activity. However, at high (42-44°C) temperatures, spindle assembly is also impaired and cells do not meet the requirements to proceed through spindle assembly checkpoint.

Two:

The rate of cell progress, or mitotic rate, throughout the mitotic cycle increases linearly with increase in temperature between the range 3 °C to 25 °C.

Three:

Observation shows that at 0° and at 40° the cells do not go through the cycle at all and that from 10° to 30° the speed increases in almost linear proportion.

Worth noting: This range may be true for many terrestrial plants, aquatic and marine plants have an optimal temperature that's somewhat lower.

@ARogueAnt. that's a great point. Feel free to edit my answer!


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What happens if a population of songbirds increases rapidly without predators?
Suppose there’s an area where there’s a rapid increase in the population of songbirds and no presence of predators.  What type of detrimental effects, if any, would this have on the environment in that area?
I’m guessing at least a reduced insect population but I’m not sure about some of the other effects such as plant life or generally how songbirds function in the predator-pray cycle with respect to any particular environments.

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, your question is 1) unfocused and 2) shows no evidence of prior research. 1) You are asking for a textbook, which is not reasonable (answer will vary with both habitat and bird species). 2) You haven't said where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Both of these are considered to be reasons for down-voting and closure on this site.

I’m voting to close this question because it is much too broad and under researched.

Likely result in an increase in Cooper and Sharp Shin, and possibly other hawks(US). We had hundreds of Goldfinches, Pine Siskins and others at our bird feeders, then Cooper hawks moved in and we see only a small fraction of the number of birds previously here. Most of common song birds eat seeds, not insects. Robins being a notable exception, eating worms and fruit. Warblers are insect eaters but seem to stay rather dispersed and most people would not hear their songs. I have never seen any detrimental environmental affect of song birds; the American Beauty berries, wild grapes, etc slowly disappear over winter. But other than an occasional flock of Cedar Wax Wings, it is not apparent that birds are eating them.


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Thermodynamics of one directional passive membrane transporters
I have read in my biochemistry textbook, that some membrane transporters transport only in one direction, moreover, they don't require ATP energy. I wonder, why these proteins do not act as  Smoluchowski's Trapdoor and break second law of thermodynamics.
It seems that concentration of substance on the "A" side somehow affects protein's ability to pump molecules, even though on that side  protein doesn't bind with former (on the A side protein has conformation with low affinity to the molecule, thus complex disassociates). So I don't understand how this form of Maxwell's demon is countered, or how concentration on the A side affects protein's function.

Can you quote from your textbook where it says "transport only in one direction"?

the transport is only in one direction but only as long as a gradient exists, it is no different than a ball rolling downhill and not back uphill. the gate just stops the gradient working in the opposite direction. think of one way seals

Thank you for your attention. Bryan Krause, my textbook is not in English, so I translated it. @John you confirmed that these kind of proteins exist, thank you. I will soon post my question's improved version and I hope for your help there as well.

I am afraid that this is a biology site, and I, for one, have never heard of Smoluchowski's Trapdoor. You have provided no links to this, and the obscurity and complexity of the thermodynamic ideas are evident from a paper in the journal  Entropy from which your diagram appears to be taken: “Skordos and Zurek [1], in their deliberations on Smoluchowski’s trapdoor, fall into the same syllogistic error as does Feynman [2,3] in his discussions of a ratchet and pawl within the micro- domain.” If Feynman got it wrong, do you expect us to get it right?


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Why isn't pure animal fat appetizing to humans?
When eating beef or lamb, humans almost invariably trim away the gristle. Tastes are a bit more varied with poultry and pork but, there too, most people don't like to eat pure animal fat. (Although bacon is very popular, and some people like to eat pure schmaltz or lard.)
But isn't this strange from an evolutionary sense? The fat is the most calorically dense part of the animal, so shouldn't we have evolved to find it appetizing?

Have you asked most people why they trim away fat? If they didn't like fat, producers of beef would not feed cattle in a way that produced optimal marbling. People would not eat potato chips. French fries would be disgusting. The snack food industry wouldn't be buying millions of tons of palm oi every year. Etc., etc. Your statement isn't founded in science.

Culture plays a strong part in food and taste preferences - it's not all genetic / evolutionary.

This question is based on the false premise that what is prevalent in the tastes of where the OP lives universally true. Go to a country where traditionally people don't have enough to eat like Vietnam and they're all about the lumps of fat. I guess you could compare it to a spoonful of crystal sugar. You probably don't find that very appetizing either because it's quite abundant now and it's better when accompanied by other things which you have been accustomed to. But when it is lacking, the pure stuff is going to seem really attractive.

Not really, in my mind. I see your point, humans love sugary sweets, but why not fatty lumps of lard? Well, humans do love fatty lumps of lard! The American diet consists of disproportionately higher amounts of saturated fatty acids. So, people tend to go for and prefer calorically denser foods anyhow. As you mention, people still use lard for cooking incredibly often, so even pure fat is at least appealing.
However, the gristle we refuse to eat isn't really fatty and is mostly inedible depending on the cut of the meat. There is an incredible amount of sugar when you look at a tree, but do you get hungry? I imagine not, because the tree is mostly inedible. So even if the resources are there, they still have to be edible for anyone to want to eat them in the first place.

Humans love fatty lumps of lard, especially when sugar is added. It's called a cookie.

I have eaten roasted bone marrow, which is basically a lump of fat. then you have fatback, lardo, ect. we don't like almost anything a pure refined state, but as it exists in the wild eating fat is pretty common.

I've just been reading a novel about the Inuit — “De pierre et d’os” by Bérengère Cournut. The Inuit are (or were) very partial to animal fat — raw of course — and much else besides that 21st century urban man would consider unappetizing. If they weren’t, they wouldn’t have been able to survive.
So before talking about human evolution it is advisable to think on a somewhat longer timescale than that of contemporary US urban civilization, and to recognize temporary cultural fads for what they are.


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Does Herpes Simplex Virus induce antibodies which last a lifetime?
Herpes simplex virus (HSV-1) is a virus which produces both lytic and latent infection. In the latter case it persists in a quiescent form in the neural ganglia for the lifetime of its host.
My question is whether the antibodies raised against the virus persist for the lifetime of the individual.
I understand that exposure to the virus again would activate the memory B cells and lead to the elicitation of these antibodies. But in general, what is the scenario with the circulating antibodies?
I found some websites stating that the antibodies persist for the lifetime of the individual, but I could not find any research publications to support this.

@MattDMo Thank you for your response. After the 3-4 weeks, the level of antibodies will deplete unless there is a reinfection. However, it is known that plasma cells residing in bone marrow can secrete antibodies for a long time even after the clearance of the virus. Not sure if it applies to herpes virus infection as well.

Which Herpesvirus are you talking about? Human Herpes Virus Type 1 (HSV1) or what? Until you tell us, nobody can answer your question, and anyone who has has made the same mistake as you.

@David I guess it does not matter as all herpes virus remain in our body for the rest of our life after infection. However, to be specific HSV-1 can be used.

Human herpesviruses range from alpha (HSV1 and 2, varicella zoster), beta (cytomegalovirus) to gamma (Epstein-Barr virus). So I think scientifically it is best to specify. I have edited your question accordingly. It would be helpful if you could give links to the sites you quote as saying that antibodies stay a lifetime.

For the vast majority of a herpesvirus infection, the virus genome is only present in the nucleus of latently-infected neuronal cells; there are no virus particles in the body. My understanding is that there will therefore be no circulating antibodies unless the latently infected neurons reactivate and begin producing viral particles. However, in this 2005 review, "Immunity in latent Herpes simplex virus infection", mouse studies found that infected neurons had CD8+T cells stuck to them that stayed there and secreted interferons for the lifetime of the animal:

In mice, CD8+T cells invade TG ~7 days after HSV-1
infection, reach maximum ~4 days p.i. and are then retained
in a significant number seemingly for the life-time of the
animal. Significantly, HSV-1-specific CD8+T cells are
persistently stimulated within the latently infected TG. ... The steady expression of IFN-γ and TNF-α in latently
infected TG suggests continuous stimulation of the cells
producing these cytokines. Expression of these cytokines is
tightly regulated and subsides within two hours of
withdrawal of the stimulant. Since IFN-γ can block HSV-1
reactivation from latency in sensory neurons, such a CD8+T
cell population is ideally suited to the function of long-term
protection with minimal tissue destruction (Kodukula et al.,
1999; Liu et al., 2000, 2001; Mueller et al., 2003; Stuart et
al., 2004).

So this implies it's the presence of T-cells in the trigeminal ganglion (TG in the above quote) that keeps infected neurons from reactivating and producing new virus. Since the T-cells are apparently being continuously stimulated, it seems possible that B-cells could also be getting stimulated and secrete antibodies, but I haven't seen that possibility addressed anywhere. Also, this continuous stimulation of the immune cells may only happen in mice, not in human infections:

In contrast to latently HSV-1-infected mice,
the frequent reactivation of HSV-1 in human TG may reflect
a less efficient CD8+T cell recognition. This would be
compatible with the fact that HSV-1 ICP47 protein inhibits
TAP-mediated transport of antigenic peptides more
efficiently in human than in mouse cells.

Mice with suppressed B-cells were not found to be less effective at preventing reactivation of latent HSV-1 infections.
Finally, the viral antigen that most of the reactivation-inhibiting T-cells were found to be going after was a fragment of gB, an envelope glycoprotein somewhat similar to the famous coronavirus spike protein. I would expect this antigen to also be a major target for antibodies.

Thank you for your response. Here is the a publication: http://dx.doi.org/10.1128/mBio.00678-17
Like T cells in trigeminal ganglion (TG) gets stimulated, the antibodies also increases after infection and persisted 8 months after infection (latest time studied). IgG concentrations were significantly increased in the TG and brain but not in the lung or liver. They persisted for long in human and murine TG.
The data in the paper shows that TG IgG originates both from locally antibody-secreting cells and from circulation.


text:
Can distilled / deionized / demineralized water "attack" teeth?
Demineralized water is claimed by some resources to be highly aggressive (due to their lack of minerals) and to attack all sorts of materials. From the World Health Organization website:

Demineralised water is highly aggressive and if untreated, its
distribution through pipes and storage tanks would not be possible.
The aggressive water attacks the water distribution piping and leaches
metals and other materials from the pipes and associated plumbing
materials.

Teeth are constantly going through remineralization and demineralization processes and demineralized water has neutral pH in room temperature which is positive for promoting teeth remineralization.
However I wonder if such water in practice rather promote demineralization when in contact with teeth by means of leaching of minerals from teeth to water due to their lack of minerals?

Interesting question.  My first thought is how does demineralised water "attack" materials?  Other web sites claim it, but I have not found one that provides a mechanism.

From a corrosion perspective , "pure" water is considered a problem for common pipe metals.

If you read your source all the way through, the answer would/should be, "Of course! It's pretty awful stuff!" If you search for reliable sources, you won't find too much literature on the subject, but you will find more on the effect of soft and hard water on health (soft = low levels of Mg/Ca; hard is opposite.) I'm not completely disagreeing with the author, but people need clean water however they can get it. I would not drink distilled water, mostly because it tastes awful, it's expensive, and I have access to safe drinking water. I doubt it's an idea liquid.

@User65535 - Water is a solvent. It will leach metals from metal pipes (like lead, causing lead poisoning) or other elements from other surfaces. If you want to know more, read about problems associated with reverse osmosis in home water treatment systems. Or study chemistry. Or something.

I’m voting to close this question because as other users have already indicated this: 1) lacks evidence of prior research, 2) is phrased as a personal medical question, and 3) is primarily a chemistry question. Please take the [tour] and consult the [help] starting with [ask] for details and [edit] or delete your question accordingly.

@tyersome For me the subject is pure curiosity. I've edited the question to emphasis it's relation to the biological processes, changed wording to "claimed by some resources" and to be more "neutral" (sound less like medical question).

Here is a list of mineral dissolution rates in pure water. they ALL dissolve, even quartz. The figure for quartz is 4 × 10−14 mol/m2s at 25'C:
https://pubs.usgs.gov/of/2004/1068/pdf/OFR_2004_1068.pdf
There's carbonate rocks and phosphate rocks including fluorapatite at the end of the study, it's quite complicated, although they do weather in pure water.
Rain is demineralized water which has had time to take in carbonic acid from CO2.
Teeth can actually become stronger and remineralize when the mouth has a pH of 7.5 or above. ref. Demineralized water contains no minerals though, so it will only erode the teeth.
Up to pH 9 is the highest range recommended by the health authorities locally where I live, and it's quite common to have tap water at pH 8 that leaves white residues on taps. It may be annoying, it's very healthy.
If the local water leaves limestone flakes, that's ideal for teeth. If it doesn't it's not very good. Fluorapatite has a pH of 4.5, it comes from fluorine toothpaste, it has higher acid resistance comparatively.


text:
Why are bacterial genomes limited in size compared to eukaryotic ones?
I was looking at this graph that shows that the eukaryotic genome has "no size limit" whilst the bacterial one does. Unfortunately the graph has no reference but essentially the idea is that most bacterial genomes are in the roughly 10^5 - 10^7.5 base pair range whilst eukaryotic genomes can be anything from 10^7 t 10^12 base pairs long for example and there is a lot more variation in genome size.
I was wandering where this limit for bacteria comes from? Specifically is eukaryotic DNA packing more efficient in eukaryotes than in bacteria and therefore more genetic material can be safely carried? Or does this have more to do with evolutionary constraints on bacterial genome size with smaller genomes being selected for?


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Ventral View VS Dorsal View in cell experiments
I am trying to understand the difference between ventral and dorsal view of "cell spreading on a substrate" experiment in this article https://rupress.org/jcb/article/205/1/83/37623/A-contractile-and-counterbalancing-adhesion-system. Consider figure 1:

How could I understand the way the image was taken and analyzed? Is it by taking image C and looking from above to get A?
If we rotate image A 90 degrees to the left we get image C? but that seems to be quite different from what is presenting lamella.
And what then are the broken yellow lines with respect to image C?
I think that the ventral view and dorsal view are just opposites. Why then we don't get the same resolutions in A and B? Because of the substrate?
Maybe very stupid questions, but I know nothing about experiments!


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Why does damage to myelin sheath in multiple sclerosis lead to a decrease in information reaching the brain from sensory receptors?
In multiple sclerosis(MS), myelin sheath is attacked and damaged. When this happens, there is a decrease in the amount of information reaching the brain from sensory receptors. How and why does a decrease in the amount of information occur?
I know that myelin sheath speeds up the conduction of nerves by which the action potentials can jump from node to node by saltatory conduction by their local circuits; but how when this stops happening action potentials and information can be lost (I believe that it must have not decreased in information but the whole amount of information will reach the brain but slowly because of lower speed of conduction)?
I got more mixed up when I saw on a website that:

The myelin sheath prevents these impulses from escaping from the nerve
at the wrong point.

Can please someone tell me how this happens? And how in the absence of myelin sheath or it being damaged, how the nerve impulse can escape from the nerve?
Reference:
https://www.emedicinehealth.com/myelin_and_the_central_nervous_system/article_em.htm

Related: Why is saltatory conduction in myelinated axons faster than continuous conduction in unmyelinated axons?

As you write in your question, myelin is an insulating sheath that speeds neuronal transmission.
However, the mechanism for transmission in myelinated axons is very different from unmyelinated fibers. In an unmyelinated axon, voltage-gated channels are present along the entire length of the axons; in a myelinated axon, these channels are concentrated and only present at nodes of Ranvier.
The way that myelination speeds up transmission is by not allowing ions to leak out along the distance between nodes of Ranvier. More accurately, myelination reduces the capacitance (see cable theory) of the membrane. However, electrical transmission in neurons is still ultimately driven by ions moving across membranes, so the nodes of Ranvier are the locations where that movement can happen at gaps in the myelin sheath. This is called saltatory conduction.
The fastest possible conduction velocity would be for nodes of Ranvier to be as far apart as possible without the signal from one node failing to reach the next one. Nodes of Ranvier are roughly spaced according to this distance, with a bit of safety margin built in. However, if the integrity of the myelin sheath is damaged, the distance that an action potential can propagate in that damaged stretch of axon may be shorter than the actual distance between nodes of Ranvier. In that case, there is not sufficient depolarization at the next node to trigger voltage-gated channels to open. This causes a "failure" in transmission.

I will try to explain in layman's terms
Myelin sheath is the protective covering which basically works like the rubber insulation of a typical electrical wire.
Now here's how the impulse in neuron network works - I tried to explain in points

In the normal condition, the outer side of neuron has Sodium ion i.e. positive charge and the inside of neuron has negative charge. This phase is called the resting phase and the neuron is said to be polarized

On stimulation, this polarization breaks and the axon membrane (myelin sheath) becomes more permeable to sodium ions. This is called depolarized state

This depolarized spot becomes stimulation for the immediate next spot and it follows so on.

Meanwhile, the previous spot regains its polarity because sodium ions are "pumped" out using energy from ATP

This simply means that damage to myelin sheath will sure cause disturbances in polarization and depolarization, which means improper impulse or may be delay in transmission time.
Hope I could help


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What does genetic diversity in one species have to do with survival rate when an epidemic spreads?
I was studying about genes, and soon remembered that the more diverse the genetics of one species, the less the chance of the species to go extinct from natural disaster.
One instance was an epidemic spreads.I don't fully understand why that happens, so I searched for it in Google and books, but all of them only told me that it is true, not why or how.
So my question is : why and how genetic diversity in one species affects the chance of the species's extinction?
I mean, for example, does it relate to antibodies or something else?

you might need to change some key words when you search the net for information i found this https://en.wikipedia.org/wiki/Genetic_diversity and this https://www.biologyonline.com/dictionary/genetic-diversity by searching for "what is genetic diversity"

If everyone has the same weakness, then one thing targeting that weakness can wipe everyone out. If everyone has different weaknesses, then that is no longer the case.

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I would recommend looking at the "Evolutionary diversity" section of this page. (for vertebrates, at least)

Genetic diversity could be understood as a variation in alleles (gene variants) and their frequencies in a population. Due to these allelic variations, we would expect an inherent variability in individual genotypes (or genetic codes). Phenotypes (or traits) can and do vary with changes in underlying genotype. (In simple terms: if you change the underlying genetic code, it could result in changes to an individual's traits).
Changes in traits (e.g., color, size, speed, temperature regulation, mobility, etc.) could lead to a variation in energy conservation, survival, reproductive success, and ultimately fitness.
If any member of a population is more fit given a set of environmental circumstances, it is morel likely that they will survive and pass on their genes to subsequent generations.

You would benefit from reviewing evolution and natural selection. (Sexual selection and genetic drift are relevant, too, of course).

However, the environment and resulting ecologies are always changing, and so there is never an "endpoint" of this process. I.e., there's never a perfectly fit individual that will survive all future environmental changes better than all other variants. In fact, all organisms can only tolerate stressful environmental conditions to a point. (See, e.g., principle of allocation).

As a result, any given individual is limited in its ability to survive various environmental conditions, and no individual organism can survive all possible environmental conditions.

With genetic diversity (and therefore the resulting variability in traits), a given population has members that may be better suited to survive a broad[er] range of environmental situations/changes/outcomes.
Therefore, it's less of an issue of survival rate and instead sustainability of the genetics of that population and life in general.

If a population lacks genetic diversity, then there is a greater chance that the population as a whole goes extinct.

Example:
Population of rabbits that have variability in their alleles dictating fur length. If there was no variability in their genes (the extreme case being that they're all clones), then any massive shift in climatic conditions (e.g., temperature) may decrease their entire population to 0. If, however, we have some rabbits with alleles that could now or in later combinations result in longer fur, that would enable some members to survive very cold years. This population would be in trouble if it suddenly turned very warm. But if our population's initial gene pool also contained alleles that could now or later result in a short fur phenotype, then the population is even better protected from extinction in these various scenarios.
I think you could figure out how this applies to pathogens in the context of an epidemic...

Hint: traits could also include metabolic rates, biochemical processes, cell-surface proteins, etc.)

 This could get much more complicated, but this gives you the introductory understanding I think you're looking for.


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What are the possible causes of Lactase persistence?
Lactase enzyme which is responsible for the digestion lactose (a disaccharide milk sugar) normally its production decreases when a young mammal is weaned but mostly Humens continue to produce this enzyme throughout adulthood, this ability is termed as lactase persistence.
What is the reason and mechanism of this phenomenon?
what are the evolutionary basis of lactase persistence?

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Interesting question. This paper, Evolution of lactase persistence: an example of human niche construction, published in a very reliable source, argues that lactase persistence is an example of niche construction: "Niche  construction  is the  process by  which organisms construct important components  of their local environment in ways that introduce novel selection pressures. Lactase persistence is one of the clearest examples of niche construction in humans".  The pdf seems to be freely available from the journal site


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Why is NAD used mainly for catabolic reactions and NADP used mainly for anabolic reactions?
NADH is used mainly in cellular respiration and the NAD+ to NADH ratio inside the cell is kept high, but NADPH is mainly used in photosynthesis and the NADPH to NADP+ ratio is kept low in animal cells.
Why is this?

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Does this answer your question? NADH vs. NADPH: Where is each one used and why that instead of the other?. ——— Please note that one part of the expected prior research on this site is that you look for previous questions and answers..

[1] For a very interesting perspective on a slightly different question, "why are there two almost identical cofactors (NAD and NADP) anyway?" see Why NADP by B.T. Kaufman, who argues that phosphorylation on the 2'-position of the ribose may be protective "from the drastic
effects of the ribosylation reactions" and other non-redox reactions that NAD is involved in. ...

[2]  He points out that (only?) NADP and DNA are modified on the 2'-position of ribose, but Coenzyme-A, cyclic-AMP and PAPS are all modified at the 3'-position

NADPH is first generated in the light reactions of photosynthesis before it is used in the reductive synthesis of sugars. But this would seem irrelevant to mammalian systems. NADPH is used in mammalian cells for reductive synthetic reactions, e.g. fatty acid and steroid synthesis.
Although it is merely an opinion, it would seem to me advantageous to separate pools of reducing power for energy generation and synthesis so as to allow regulatory prioritization of the former over the latter. And, incidentally, the generation of NADPH in mammalian cells is independent of that of NADH, being primarily in the pentose phosphate shunt, a pathway found particularly in tissues like adipose tissue, mammary gland, liver and steroid-synthesizing tissues.
Although I now see that a similar question has been asked before the most voted answer repeats the somewhat unsatisfactory statement of the question (to be found in Albers et al.):
“The ratio of NAD+ to NADH inside the cell is high, while the ratio of NADP+ to NADPH is kept low.”
The reason I consider this unsatisfactory is, as just stated, some tissues are specialized for reductive synthesis of fatty acids and steroids, whereas others are not. Their need for NADPH will obviously differ, as will the redox ratio. Remarks about “the cell” are unfortunately typical of texts generalizing metabolism from bacteria.

@user338907 — Yes, of course you are right. I'm afraid I always tend to focus on the actual energy generation aspects of photosynthesis (the light reactions) — the dark reactions being of less fundamental interest to me. I'll correct my answer.


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How can I confirm that this pedigree is of a pseudodominant trait?

This is an example of an autosomal recessive trait masquerading as autosomal dominant.  I carried out genetic analysis for each generation as if the trait was either recessive or dominant, and both modes of inheritance seem to fit the pattern observed. Does the pedigree have any defining features that might indicate that it is indeed autosomal recessive? Or would we simply have to carry out further analysis with other pedigrees?
Thanks to anyone that can help

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What kind of deciduous tree is this?
This image was captured on October 10th, 2020 in Haliburton, Ontario, Canada. Any help identifying the tree species is greatly appreciated. Rob.

I think it's a poplar tree, very fast growing, light wood, often used for matches, very often has a white saprophytic tea color mushroom growing on the tree stumps. https://en.wikipedia.org/wiki/Cyclocybe_aegerita
The description is missing bark photos and leaf anatomy photos. It can also be a birch or a willow, very difficult to ID from just that photo.

Are you sure it isn't quaking aspen (Populus tremuloides), which is in the Poplar family, but called aspens in North America.

He can tell by comparing the bark which is a lot whiter on tremuloides.


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Surface Area to Volume Ratio and Ice Baths
Hi I was taking a practice test and stumbled across this question. I couldn't find information about this on the internet. Does anyone know why B is the answer? Thanks

Please [edit] your question to include the full text of the image you posted. Images are not searchable, and are incompatible with screen readers for those with visual impairments.

At present there's insufficient information to determine if b. has merit, you would need to specify a timescale for measurement. As MattDMo says, please provide us with the full information.

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look up the square cube law in reference to heat.

@ARogueAnt. - I don't understand your comment either. Why do you need a timescale for measurement for this very basic Physics question? (Please answer me; when I ask you something in comments, I can't remember you ever answering me.)

@anongoodnurse This is the first time I recall you asking me anything. Apologies if I've been unintentionally rude. 1) We don't know what organisms are being referred to and if metabolic processes continue at ice-bath temperatures, 2) the square cube law's effect will be short-lived in such small organisms if their metabolism ceases for temperature/lack of energy as they will quickly asymptote to ambient temperature (timescale). We need more info to answer without making assumptions that may be unwarranted. That's it.

@anongoodnurse I agree that a. c. and d. are impossible (assuming sphericity), but the practice-test is not a good one if the "correct" answer is only findable by exclusion of other answers - as opposed to findable by deduction from the information supplied, i.e. b. must be right, but there's only the evidence that the others are wrong to support it - e. or f. might be a better answer, but the nature of the multiple choice format is such that often it's not a good teaching aid.  I believe my concern was valid.

BTW. I had previously (mosquito hearing), but the comment was deleted. Just because something is common and seems "common sense" - doesn't inherently make it good quality. I've seen the same thing here (UK). Perhaps it might make a useful question on another site, [academia.se] or [psychology.se] regarding effective teaching/assessment.

Last comment on the issue, @ARogueAnt: I never said I liked the question or that it was good. I said it was common, and the fact that it's not a good question does not give validity to your request for more information. I use logic, and that it's common = it's good is a fallacy. It is common and it does not test all understanding; it tests the ability to deduce the correct answer using the information at hand, that's all it does. Well, also basic principles of Physics in this case.


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Does your blood stop moving in between heart beats?
Does blood stop moving in between heart beats or does it move continuously?

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I couldnt find the answer fairly simply on google, so i wrote one here, so that it exists on the web. Agreed the question looks like a homework query without prior investigation.

I think there is a difference whether you mean veins or arteries, and which ones.


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What kind of purple flower is this?
Shot in a garden in Haliburton, Ontario, Canada on June 18th, 2020. Flowerhead size approx. 1 1/4" diameter across.

Identifications questions should also include: 1) habitat information — e.g. was this growing in a marsh? were there any other plants nearby that you could identify?; and 2) an estimate of the size of the organism. Please [edit] your post to include this essential information. ——— Also note that such questions should be given the species-identification tag and that thanks/signatures etc. should not be included in SE posts.

fyi, Google Lens is pretty good at identifying plants.

How nice it would be if all images of flowers were stereographic like this (from here). =)

That looks like it could be a cultivar of Geranium sanguineum (Bloody crane's-bill or Bloody geranium) or something closely related.

Image source: Keith Weller, USDA Agricultural Research Service, Bugwood.org — CCA3.0.
Some features that are consistent with this id are: the five identical bilobed petals, flower size and shape, hairy stems, and leaf form (palmate with five lobes each with three large 'teeth'). The flower features I can distinguish rule out related genera such as Pelargonium and Erodium, which have flowers that are not radially symmetrical. If this is a Geranium, then there should be 10 free stamens and the stigma should have a style with 5 branches.
This species is cultivated and typically blooms from June to August, which fits your described location and time.


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Does technology exist to represent cell biology in a bona fide fashion?
I have been teaching life sciences for nearly a decade now. Still something keeps giving me mental distress each time I think of it. I feel no representations of cell biology can convey information in a truly bona fide fashion.
Think about the following example. If I want to know about tigers, a text description will help.

Many tigers possess stripes on their face, sides, legs and stomach. The striping is varied in width, length, whether they are single or double-looped, coloration from a light brown to dark black and are not symmetrical from one side of the tiger to the other. (source: https://seaworld.org/animals/all-about/tiger/characteristics)

But no matter how useful this text is, it does not give me as much intuition as a painting does.
Still, a much better representation of a tiger is a photograph, as it gives much more direct knowledge about a tiger. Before the invention of full-color photography, the best thing I could get was below.

This black-and-white photo is even worse than the painting, because it removes the essential colors. It is the invention of full-color photography and videos that would eventually give me the most direct knowledge about a tiger.

With the analogy of a tiger, I can better describe limitations of information carried by existing forms of life sciences materials. For example, one day I want to learn transcription factors and their control of gene expression. I can find a piece of text on this topic:

Some transcription factors bind to a DNA promoter sequence near the transcription start site and help form the transcription initiation complex. Other transcription factors bind to regulatory sequences, such as enhancer sequences, and can either stimulate or repress transcription of the related gene. (source: https://www.nature.com/scitable/definition/transcription-factor-167/#:~:text=Some%20transcription%20factors%20bind%20to,transcription%20of%20the%20related%20gene.)

But I feel this is not enough to give me an intuition about TF. I then found an image representation of the process.

This abstract image is a complement to the text. But I don't feel it insightful enough. The next helpful thing I found was a video https://www.youtube.com/watch?v=MkUgkDLp2iE. And the searching process stopped there.
Does current technology allow for truly bona fide representation of cell biology in the same sense as a tiger is represented by a full-color photograph? For students who have strong imaginations, they don't find learning cell biology too much of a trouble. For those that lack imagination, I must strive to find something that gives them as much of an intuition as possible.
The ideal tool to represent cell biology is something that presents the products of imagination for the strong minds in a directly accessible manner. I'm afraid this goes far beyond current technologies. Is it so?

Are you ever going to find better things than animations of molecular machinery? Because your tiger analogy only works because you can perceive a tiger with your senses.  I also argue that an image of a tiger only seems more bona fide because it is heavily augmented by your real world experience with similar things. Seems very similar to math equations versus graphs. The graphs don't embody the existence of what is there. Even animations for higher level stuff don't make sense unless you already know what you're looking at, if they can even be animated at all.

Or are you just asking if electron microscopic motion cameras exist that work on living samples?

Hi @DKNguyen, thanks for bringing up electron microscopic motion cameras. I did a bit research on my own and found this type of technology can allow up to 1600 fps. That's a fantastic tool for my teaching purpose. And it is vastly better than the abstract images or animations for cells.

I think they don't work on living samples though. But maybe still life photos are better for you than generated animations.

Does current technology allow for truly bona fide representation of
cell biology in the same sense as a tiger is represented by a
full-color photograph?

There is no way, that any cell-biological depictions will ever reach the level of intuitive understanding, that is conveyed by such a picture of a tiger.
Next to the tigers image, you see every-day objects like trees and grass, that give immediate sense of the scale. Also, the tiger is a mammal, just as you are, and you have multiple close references at your disposal, like other mammals or cats, which you can immediately extrapolate to gain insights about the tiger. Besides obvious aspects, like the knowledge of anatomical structures, that one effortlessly recognizes, e.g. the tigers eyes, and what seeing or breathing means, you also have a detailed model of the physics of objects at your scale of mass.
On the contrary, being confronted with 2d depictions of molecules, most people would find it hard to guess how the missing information in the 3rd dimension would look like. Also, they lack an intuition of the physics at these small scales.
You would need to be a biological molecule yourself and spend all your 'life' at these scales to understand and feel what it means to be a bio-molecule, and your "molecule brain" must have evolved with pressure to recognize predatory tiger-molecules at first sight, which would otherwise mean your death; only then would you have any chance to come close to achieving the intuitive understanding of such a magnitude.


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How does Heat Fixing make cells stick to a slide?
Regarding Gram Straining, my college instructor told us how we pass the slide with the bacteria on a bunsen burner 3-4 times and it fixes the bacteria so that they don't get washed away with water. How does the heat fix the bacteria that on the slide?

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Have you ever put a peice of meat into a searing hot pan and had it stick? That piece of meat is thick, yet it still sticks, Imagine if it were only a few cells thick, What are the odds it would wash off with water?

I haven't done that but yeah I have seen the meat stick to the pan but why does that happen? Why does the meat or the cells stick to the surface because of heat? What is the science behind it?

It's because meat and skin and cells are made of (not exclusively but enough) protein, and heat denatures protein.

So why does it stick because of the denaturing of the protein?

I grasped this concept from bob1, a notable member of this site , that the term heat fixation is misleading, as heat is not what actually fixes cells in this method, it's dryness that does. In other words, anything that will get these cells to dry will fix them.
I add that generally, the actual culmination for cell fixation resides in denaturing and precipitating proteins. Drying does that. So does methanol.
Now you have two options:
1- Drying: The most reliable way to do that is air-drying, that is, leaving the slide anywhere for atleast 20 minutes or 30 minutes to be sure.
2- Methanol fixation
Heat fixation, or to say it correctly dry fixation by direct heat, is a bad method because you can easily pass the endpoint and the result of doing so is disastrous [*].
--
[*] https://pubmed.ncbi.nlm.nih.gov/6201316/


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Why can SPRITE measure many simultaneous interactions?
Why is the SPRITE method not limited to a number of simultaneous interactions that can be measured, while microscopy and proximity ligation are limited to 2-3 interactions?

You list three methods for determining the pairwise interactions of DNA loci.

SPRITE is a split-pool sequencing technique. First, samples are crosslinked to preserve DNA-protein-DNA interactions. Then, DNA is enzymatically digested to create free ends for barcoded adapter ligation. Crosslinked globules are "split" into many wells for barcode ligation, then "pooled" together again in a single tube. After iterative rounds of "splitting" and "pooling", DNA molecules are sequenced. Pieces that are covalently associated by crosslinking will have the same set of barcode sequences, implying that those loci are spatially associated in situ.
Like SPRITE, proximity ligation techniques start with chemical crosslinking and enzymatic cutting to create free DNA ends. In "all-against-all" proximity ligation (Hi-C), free DNA ends are joined together in a dilute ligation reaction. Paired-end sequencing of DNA molecules containing ligation junctions reveals interactions between distal loci. Taking into account distance-dependent interaction decay, the contact frequency of locus pairs can be used to identify potentially meaningful DNA-DNA interactions.
Microscopy-based methods are limited by spatial resolution and the number of fluorophores (colors) available on a given platform. However, clever multiplexing may be able to overcome the fluorophore problem.

In short-read proximity ligation sequencing, it is true that a single DNA molecule can only ligate to one other DNA molecule, whereas SPRITE allows association of a single DNA molecule with one or more other DNA molecules – however many were crosslinked in the same globule. In practice, however, Hi-C is performed on bulk cells, and therefore the same locus may associate with multiple different loci across the contexts of different cells. Moreover, long-read sequencing can capture multiple ligation junctions in a single read, allowing for the inference of primary, secondary, tertiary, etc. contacts.