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What are the Genes/Enzymes responsible for the supposedly stark between-individual differences in lethargy after eating starches?
Andrew Huberman claims in one if his podcasts episodes that:

[...] because starches cause the release of serotonin in the brain and lend themselves to a state of sleepiness.
Now, I should mention that about about 25% of individuals have genes that encode for enzymes that allow them to eat large amounts of carbohydrate and not suffer from this lethargy.

Timestamped Video: https://youtu.be/aXvDEmo6uS4?t=4333
Sadly he doesn't reference any kind of study or data that this claim is based on.
I am aware that serotonin is involved in digestion and that most serotonin found in the human body is in the gut. Though I do not know what its function is there or if this is even relevant for this question, given that Huberman specifically states

starches cause the release of serotonin in the brain [emphasis mine]

This aligns with my knowledge that Serotonin doesn't cross the blood brain barrier, so the Serotonin released in the gut cannot make its way to the brain somehow. I am also confused how or why Serotonin would cause lethargy, though this still fits with the typically reported side effects of Serotonin Reuptake Inhibtors.
I am also not surprised that this trait varies between individuals, but Huberman's claim is phrased like the difference is not just forming a normal distribution arising from many genes and instead that the distribution seems to be at least bimodal, i.e. "about 25% of people" do not experience this at all.
There are two previous questions on the tiredness after eating,
What is the biological basis for tiredness after eating?
Why do the humans become sleepy after meals?
but neither really discuss anything related to serotonin in the brain, or deal with the factors underlying between-individual differences. One of the answers brings up

Sugary foods lead to the production of insulin. Insulin stimulates cells to take up glucose from blood. It also mobilizes tryptophan to brain. Once in brain, tryptophan triggers formation of serotonin, a hormone involved in controlling mood and slumber.

but this answer only references a blog with no further citations, but is at least some kind of explanation.
My questions is thus:
Is there some well known paper or review underlying this claim that he is implicitly referencing and potentially overly simplifying?
And if this isn't some well known paper, which I can read up on myself, but someone else can answer my more specific questions:
What are the enzymes that influence the "post carb lethargy" in such a strong way and how do they attenuate the serotonin released in the brain?

I don't know about an enzyme that may or may not influence sleepiness after starchy meals, but I do know a fair amount about the physiological effect of somnolence after eating: https://medicalsciences.stackexchange.com/a/1087/169. If there is an enzyme that allows sleepiness after carbohydrate ingestion, I certainly have it. If I can't sleep, a bowl of cereal helps immensely. :)

The video is likely referencing alpha amylase, which is encoded in humans by AMY1A, a gene that is know to have a high level of inter-individual copy number variation. Some scientists have speculated that production of this enzyme in the brain can have an impact on neurotransmitter levels and thus memory in Alzheimer’s Disease (AD)1:

Since we have previously discovered the presence of α-amylase in the brain, we find it tempting to speculate that production of α-amylase is one of these factors. How the very high AMY1A copy number variability (and potentially thereby very high production of brain α-amylase) can be implicated in the lowered AD risk and episodic memory remains to be investigated. But since α-amylase is known to efficiently degrade polysaccharides (such as glycogen) in the periphery, we find it likely that the enzyme has a similar role in the brain. The enzyme might thus be important for the degradation of glycogen in astrocytes and neurons [20, 28], which is known to be crucial for neurotransmitter production and memory formation [21, 29, 30]. The presence of α-amylase in activated astrocytes and neuronal synapses, found in our previous studies [19, 31], supports this idea.

References

Byman E, Nägga K, Gustavsson AM; Netherlands Brain Bank, Andersson-Assarsson J, Hansson O, Sonestedt E, Wennström M. Alpha-amylase 1A copy number variants and the association with memory performance and Alzheimer's dementia. Alzheimers Res Ther. 2020 Nov 21;12(1):158.

My initial reaction was that he must be referring to one of the genes/enzymes that explain the observation that neurotransmitter release by brain neurons may be controlled by carbohydrate (but not protein).  'Carbohydrate consumption--acting via insulin secretion and the "plasma tryptophan ratio"--increases serotonin release; protein intake lacks this effect.' (ref). I have not been able to find the enzyme, but tryptophan hydroxylase must be a likely candidate?

While alpha amylase seems interesting, I am fairly sure that this is not what Professor Huberman was referencing in the podcast. The connection to serotonin specifically seems like a stretch, especially when there are much older results establishing a link to serotonin specifically like @user338907 linked. This would actually be good enough for me to accept as an answer if you want to post it as such, there are enough details in the paper to narrow down the enzymes involved.


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Identify the caterpillars
These are the two caterpillar I found at Taipei, Taiwan. Can anybody help me identify the species. The first caterpillar is about 6-7 cm long and the other one 10-12 cm. Thanks in advance!

This is actually not easy - for the first one I am sure that is a caterpillar from order Orgyia and the family Erebidae, but since there is a vast number of different caterpillars on all continents, I am not sure which one it is exactly.
If you look at this image (from here), you will see a striking resemblance:

A lot more information on these moths can be found here.
The second one is most likely Trabala vishnou ssp. guttata, see the image (from here) for comparision:

There seems to be very little information available, some on the Wikipedia page.

source: Stack Exchange

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

sort: votes


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How it will taste if one puts two substances on tongue simultaneously?
If we put two substances having different taste on tongue simultaneously how it will taste? Does specific part of tongue is sensitive to specific taste?

The popular "tongue map," which depicts the tongue having distinct regions where you can only taste certain tastes, is completely inaccurate and was debunked quite a while ago. There are regions of the tongue that are slightly more sensitive to tastes, however. A google search of "taste map" or "tongue map" will yield links on the origins of the myth.

This would perhaps be more suited for the Cooking site :-)  Though most taste is actually smell.

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


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What "algorithm" are carnivorous larvae using when foraging?
What algorithms are carnivorous larvae (lady bugs like Adalia bipunctata, Coccinella septempunctata, common green lacewing (Chrysoperla carnea) or hoverfly (Syrphus)) using as they are foraging for aphids?
Is it just random walk or something more efficient?

I'm going to assume that when you say algorithms, you mean the forms of innate behavior an organism may have relating to their senses (e.g. when sunlight is detected by a worm through the photoreceptors in their skin, it will move towards the opposite direction of the source of light to stay in their preferred environment).
These mentioned species of insects are very different taxonomically, but their number of sensory organs are for most part similar including during larval stages.
Examples of innate behavioural responses seen in invertebrates include taxis and kinesis.
Taxis is a change in movement in response to an environmental stimulus – either towards (positive) or away (negative)
Kinesis is a change in the rate of activity in response to an environmental stimulus
So, when talking about rough algorithms, when a larva detects a particular stimulus (e.g. chemicals of prey via chemoreceptors),  The organism will either have a 1 or a -1 value for Taxis response (e.g. it runs towards or away from the prey), and a rate of activity relative to taxis which represents kinesis (e.g. it gradually moves faster towards the prey as the chemical stimulus becomes stronger (meters per hour for example).
So, you could say that the theoretical formula/algorithm for hunting prey relating to the chemoreceptors as an example would be:
Taxis ('1' or '-1' to symbolize moving towards or away from a prey) multiplied by the number of 'prey' chemicals received by the chemoreceptors equaling the strength of the larva's response which could be (as an example) translated to the velocity of larva
Of course all the other senses such as photoreceptors and the chordotonal organ (vibration sensor) must be considered and I couldn't find any actual algorithm for how these species hunt. This is just a way to percieve how insects both in and past their larval stages respond to stimuli through their innate behaviour.

By "Algorithm" I mean: Suppose you want to implement an algorithm on a computer that indistinguishably mimics the animal's behaviour provided they get the same input information, i.e. no mathematical / statistical analysis (or other mathematical approaches for that matter) is able to distinguish the outputs of either algorithm. Given such a setting, what algorithm will the programmer get? Just random walk with specific average path length (which may depend on the habitus of the plant being foraged on) or something more or less efficient, and what algorithm is it specifically?

Are you saying that it's not known what algorithm(s) -- with "algorithm" according to your definition or my definition from my other comment at your disposal) -- these animals are "using"? Is it a (current) research topic?

Unfortunately I am not experienced enough to know whether there is an algorithm that can "indistinguishably mimic an animal's behaviour provided they get the same input information" Animals in general have so many senses and chemical reactions that determine what they next action will be. As far as I know, perfectly simulating most if not all organisms is currently not an achieved goal as of yet.
If it's any help... larvae usually wonder randomly at a more or less steady pace until they sense the chemical signature of a prey/food.


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Why is urine acidic (equilibrium of I/O, input <=> output)
Urine pH is on average 6.0, net excretion of acid. Is that in balance with net input of acid?

Welcome to SE Biology. The answer to your question is, of course, no. Have you tried to research this question yourself? Acid–Base balance is an important topic and there are numerous introductory articles such as this one about it on the web. If after doing a little reading, you still have specific problems, repost letting us know precisely what they are. (There's no chemical law of conservation of acidity, you know.)

consumption of meat (acidic) will be handled by increased excretion of acid via the lungs though, carbon dioxide, and since the kidney is the major organ for acid-base regulation, it seems very likely that its normal rate of excretion of acid was a result of equilibrium of "acid-in, acid-out", since it will increase acidity of urine to respond to acidosis, or alkalinity for alkalosis, etc.

Please finish reading the Tour to find out how this site works. If you wish to answer your own question you may do so, but as an answer, not a comment. My own comment was an attempt to improve your question by making it more specific, given that this is such a wide area. Although I expressed an opinion, I was not answering your question (by explaining why) but suggesting where you could read about the counter-view to the one that seemed implicit in your question and may have been the result of erroneous chemical assumptions.

well if average kidney pH has nothing to do with acid-base regulation (while urine pH clearly does often reflect acid-base regulation), and it is more about antibacterial properties or similar, that'd be an answer too. idk if the question is out of place, since clearly acidic diet (or, one that generates surplus acid in body) would tend to acid-base regulation compensation by acidic urine.


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Bats, bees and nectar
I have been thinking about this for a long time and your thoughts would really help. Since it's known that bats spread Covid 19, I studied more about places that they may have contacted. The first place that I came across was how they feed. Bats usually feed on nectar, now say that the bat is tested positive for covid 19. This may lead in others animals like bees getting their nectar contaminated. Now when these bees use the nectar to produce honey, and then the beekeepers collect the honey.
This may cause us humans getting positive for covid 19 when we eat honey. So why haven't we already tested positive for covid a long time back? It would be great if you can help me out over here.
Pardon my English, for it's my second language.

There are a number of incorrect assumptions here, including the basic premise of your question: bats absolutely do not spread COVID-19. This is a misunderstanding that has unfortunately gained a lot of traction amid the pandemic hysteria, and one that only serves to deepen the public's mistrust of bats and encourage people to harm or kill wildlife that pose no threat to anyone.
It's true that SARS-CoV-2 is similar to other bat coronaviruses, and it's not implausible that it could have originated there, but that's literally all we know at this point - we haven't even definitively established the true origin of the virus, much less unraveled the mystery of how it spread to humans.
What is clear, though, is that it's not being spread by bats. If nothing else, the rampant speculation about possible intermediate hosts suggests that it didn't come about merely as a result of direct contact between humans and bats, but through a much more circuitous pathway involving a specific combination of hosts and conditions that favored the jump to humans. Going beyond that, the idea that nectar-feeding bats could somehow "contaminate" the flowers, and that this in turn could somehow lead to live viruses showing up in honey produced by bees that visited those flowers, is mistaken on several levels.
You might be interested in this article, which gives an overview of what we currently know about the virus' origins: https://www.nature.com/articles/d41586-020-01449-8.
In short, there are a lot of things to be concerned about when it comes to the spread of the pandemic, but one thing you definitely don't need to worry about is the possibility of contracting SARS-CoV-2 from bat-pollinated flowers.


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Is this a black carpet beetle and how do I keep it alive?

About 3mm in length, location Hong Kong. Is it possible to keep it as a pet? I currently have it in a clear plastic case (kinda cubic, 6.5cm per side) with a piece of moist paper. It rarely flies.


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Definition of synaptic strength
The canonical definition of action potentials found in textbooks states that action potentials are all alike in shape.
From techniques such as spike sorting which are used to attribute electrophysiological recordings to individual cells, we know, however, that shapes and amplitudes of action potentials vary.
Synaptic strength is defined as the average amplitude of postsynaptic potential evoked following a presynaptic action potential.
Given that the incoming action potentials might differ for different synapses (and for instance lead to more or less vesicles being released), how can we hence have a uniform definition of synaptic strength?

What do you mean by uniform definition of synaptic strength? Synaptic strength has nothing to do with shape or amplitude of action potentials so why do you think that is relevant?

Why not? Say the amplitude of an AP is larger, then could it not be that the number of vesicles being released at the axon terminal is larger as well, hence leading to a larger PSP by a stronger depolarization at the axon terminal?

"action potentials might differ for different synapses" and synaptic strength can be different at different synapses. The latter says nothing about the cause. It remains unclear where your confusion lies, maybe setting up a specific scenario where you think the synaptic strength has a different definition than the one you gave ("average amplitude of postsynaptic potential").

I see - I think the confusion was that synaptic strength could be distilled to structural properties of the synapse (such as area of the postsynaptic density). But as you mention the definition is independent of the cause (e.g. effect of APs of different amplitudes), right? Thank you for the clarification

Ok, if that's your confusion I understand now, I'll move my comments into a short answer. Let me know if this covers it.

Although action potentials do vary from neuron to neuron between different classes of neurons and neurons from different areas, the differences that appear in extracellular recordings are due to recording conditions, such as the distance of the electrode from the neuron and the part of the neuron that is being recorded. Hence, the different action potential shapes observed in extracellular recordings are not inherent to the neurons. Spike sorting takes advantage of the different conditions that each neuron is recorded in an attempt to separate them into different units, i.e. candidate neurons.

Thank you @vkehayas this distinction is extremely helpful

@vkehayas Some of those AP characteristics can also be measured extracellularly, in particular the spike width differences between cortical pyramidal cells and fast spiking interneurons.

Do spike width differences correspond to different ion channel kinetics?@BryanKrause

Synaptic strength is defined as the average amplitude of postsynaptic potential evoked following a presynaptic action potential.

This is a correct definition. Synaptic strength is a fairly abstracted measure. It can be influenced by both presynaptic (for example: number of vesicles/concentration of neurotransmitter per vesicle) and postsynaptic effects (for example: receptor number and composition). So yes, changes presynaptically such as the character of an action potential can influence synaptic strength, but that isn't a problem: we still represent this as part of the synaptic strength if it affects the average postsynaptic potential.
Biologically, action potential amplitude in the axon does not really matter much for synaptic release, but local conditions in the presynaptic terminal that influence calcium influx do. The section on presynaptic inhibition in the answer here may help a bit.


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Synapses of inhibitory neurons
I sometimes read of "inhibitory synapses". But I understand that when the neuron is inhibitory, all of its synapses will be inhibitory (so it is a property of the neuron, not only the synapse) - is that correct?
How is this experimentally tested? I did not find an estimate of how many outgoing synapses inhibitory neurons typically have, but I assume that it might be thousands. So how do we know for all of its synapses that they are inhibitory?

I think the definitions of inhibitory and excitatory neurons are currently defined as a matter of convenience based on observations made by synaptic staining, electrical feature and its morphology.
In other words, neurons with more inhibitory synapses are inhibitory neurons, and neurons with more excitatory synapses are excitatory neurons, and so on.
By detecting inhibitory and excitatory synaptic-specific staining in different colors on the same section, we may be able to determine whether all synapses in a single neuron are inhibitory or excitatory.
Also, I think there are events happening in the process of neural differentiation that distinguish excitability/inhibition, but we don't seem to know how they are happening.
It may be determined by signals from neighboring neurons, Ca++ concentration, etc.
If, at the neuronal precursor stage, the differentiation mechanism that determines excitability/inhibition could be confirmed at the level of gene expression, it might explain why inhibitory neurons only make inhibitory synapses.
22th June 2020 added;
I find a good example of Excitatory synaptogenesis on dendrites of hippocampal-mediated (inhibitory) neurons, here;
https://www.nature.com/articles/ncomms1736
In short, this article shows what will occur after generating spine on inhibitory neuron.
(A)The synapses move along the microtubule from the tip of the process to the shaft. (B) Morphological changes in parallel fibers of cerebellar granule cells during synapse formation. When the parallel fibers come into contact with Purkinje cells, the neurexin-Cbln1-δ2 glutamate receptors A complex of synaptic vesicles is formed and synaptic vesicle accumulation occurs. Synapse matures after microprojections extend from the parallel fibers and encircle the spine to form an annular structure. (C) In early postnatal hippocampal pyramidal cells, DCLK1 accumulates at the tip of the process to promote process elongation and Inhibition of synaptic maturation.

Thank you! So the classification of a neuron as inhibitor or excitatory is based on its neurotransmitter - say a neuron is GABAergic - how could it then have an excitatory synapse?

I find a good example about your question, here;
https://www.nature.com/articles/ncomms1736
This article shows the process of generating excitatory synapse on inhibitory neuron.
I Added the brief to my answer.


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Why is there no herd immunity against common cold coronaviruses?
In discussions of herd immunity against SARS-CoV-2 the underlying assumption usually appears to be that the virus basically stops spreading once a sufficient percentage of the population has overcome an infection.
My understanding is that this approach does not work for the seasonal flu, for instance, because the flu virus mutates too quickly. Since coronaviruses do not mutate so quickly, herd immunity "can work" for them.
Question: Given how long common cold coronaviruses have been spreading in the human population, why does there not appear to be herd immunity against the common cold coronaviruses? To what extend can we expect herd immunity to SARS-CoV-2 if there is no herd immunity against common cold coronaviruses?

The following review has extensive answers to the complex of this question. They also include MERS and SARS-Cov-1 in their discussion, as there is good data on them.
Huang et al., A systematic review of antibody mediated immunity to coronaviruses: antibody kinetics, correlates of protection, and association of antibody responses with severity of disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217088/
The best data comes from challenge experiments which, with common-cold CoV, are not ethically problematic. They write:

Several studies exposed volunteers to two challenges of virus, some months apart. Reed re-challenged 6 volunteers who had been experimentally infected 8–12 months previously(ref.9). On the first challenge, all 6 developed symptoms and detectable viruses and 5 of 6 experienced significant rise in titer. In the second, 0/6 experienced illness, detectable virus or significant rise in titer. Callow et al re-challenged volunteers with the same dose of coronavirus, one year apart(ref.8). Of 9 volunteers who were infected in the first exposure, 6 (67%) were infected in the second exposure. However, none of these individuals developed respiratory illness symptoms and they experienced a mean duration of detectable virus of 2 days compared to a mean of 5.6 in the initial challenge.

So, reinfection can occur even after 1 year with HCoV 229E, and this does not support the idea of herd immunity against that virus.
Note however that it is not known to date if, when reinfected after some years, you will also shed active 229E virus. If not, this would be just as good as neutralizing immunity and would support herd immunity.


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What fraction of human cells gets infected during a viral infection?
As I understand, if a cell gets infected during a viral infection then it eventually dies. If an individual does not die of an infection, the percentage of cells that gets infected in the course of the infection must be quite low.
Are there any estimates available on how many cells get infected during a viral infection? (say, an influenza infection)?
(A very similar question was asked five years ago but unfortunately received no answers.)

After trying to answer this for a while, I've reached the conclusion that the information needed to answer it satisfactorily doesn't exist. I'll go ahead and summarize my findings here for you though, hopefully it's informative.
Different viruses infect different cells, and different people's immune systems are more or less successful at limiting infection, so the number of cells that get infected also varies a lot. A useful way to narrow your question might be "What is the maximum fraction of virally infected cells that can be survived?". All infections will vary between this maximum and 0%, with milder disease being associated with lower % cells infected.
I looked at Ebola as a candidate because it can infect a wide variety of cell types and a lot of research has been published on it.
From J Virol. 2004 Apr; 78(8): 4330–4341.:

Notably, 20 (91%) of 22 nonsurvivors had viral loads that reached ≥10^8 RNA copies/ml within the first 8 days after the onset of symptoms, thus suggesting that 10^8 RNA copies/ml can be considered an approximate threshold that predicts a fatal outcome with a positive predictive capability of >90%.

So, for about 3 L of blood serum in a person, that's 3 * 10^11 copies of the viral genome in the blood as a threshold for survival. I couldn't find useful information about viral load in organs and other tissue, but since blood has been claimed to have much higher concentration of virus than saliva or other fluids, we can assume this number is a significant portion of the total load. I'll assume about a third, so we get 10 ^ 12 genome copies. Some or even most of these RNA genomes might not be incorporated into viral particles but counting actual viral particles is very difficult, so no-one has published a correlation between Q-RT-PCR results and infectious particle counts as far as I could find.
Next, we need to estimate the number of progeny viruses that each infected cell produces. In Clin Diagn Lab Immunol. 2002 Jan; 9(1): 19–27. , researchers got about 2 * 10^4 PFU from wells containing 2-4 * 10^6 alveolar macrophage cells each. In these wells, 50-60% of the cells had detached from the walls, compared to 0 in non-infected wells. This implies that, for macrophages at least, about 100 infected cells make enough virus to create one plaque in the assay they used. In J Virol. 2015 Jul 1; 89(13): 6773–6781. about 1000 particles per PFU are reported for the 12th passage of virus in their Vero cell assay system, so 10 virus particles per infected cell. We estimated 10^12 virus particles earlier, so that implies about 10^11 cells were infected. That's a similar number as estimated for HIV in the comments of that question you linked. At about 3 * 10^13 human cells in the body, that's about 0.3 % of all cells.
Each of the studies I've linked here is quite different from the other, so plugging results from one into the other is introducing a lot of error, but hopefully the process was informative.

Thank you for this answer!


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Do any animals mix porphyrins and carotenoids in their pigmentation?
Many animals (particularly birds) use carotenoids or porphyrins in their diet to contribute to the brilliance of their skin/fur/feather coloration. A few even mix melanin in with carotenoids to get more complex colors. But are there any animals that mix a porphyrin with a carotenoid to make their color?

Yes. Here is one example of an annelid worm that does this:

Altogether, the endogenous porphyrinoid pigments of E. viridis appear to be similar in function and origin to the coloured bile pigments of H. diversicolor. It must be noted that biliverdin in this latter species is described as a secondary pigment, since the green coloration is only noticeable when the presence of the worm’s main pigments, namely carotenoids, decline during the reproductive phase and/or in starving individuals7. However, in E. viridis, green pigments are unequivocally predominant, likely being homologous to biliverdin, whereas yellow pigments may be more similar to another product of haem breakdown known as bilirubin (also yellow), rather than carotenoids. In fact, the yellow pigments found in the proboscis and epidermis (see Fig. 2) have quite distinct spectra from carotenoids36.

It seems that the original reference that they refer to is here, performing a relatively straightforward organic extraction and spectrographic analysis of pigments, stating:

Worms thus owe their green appearance to biliverdin, while the yellow, brown and orange pigments also present in the epidermis in most worms are carotenoids.

Biliverdin is a porphyrin.


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What is the actual mechanism by which ApoA-1 Milano exhibits its phenotype?
ApoA-1Milano is a variant of the apolipoprotein A-I protein that was discovered by the University of Milan when sequencing the genome of those native to the village Limone sul Garda. The mutation has been shown to dramatically reduce the occurrence of cardiovascular disease for those who carry it. There has been much research invested into developing a means of delivering a synthetic version of this protein to the tissues of people already suffering from cardiovascular disease.
Typically with protein variants as high profile as this one there'd be some consensus or theory as to why the variant performs in the way that it does. For instance, the G171V mutation in the LRP5 gene results in a variant LRP5 protein receptor that reduces the ability of the DKK1 inhibitor to bind to it, resulting in greater LRP5-induced canonical Wnt signaling, which augments load-induced bone formation, which increases bone mass/density.
So a known mutation with a known protein variant as a consequence, the exact structural difference of which is known, and the exact intermolecular consequence of this difference is known, and finally the resulting phenotype is also known.
But in the case of ApoA-1Milano I can't find any literature regarding what the specific intermolecular consequence of this variant is that confers the reduced risk of cardiovascular disease phenotype. Big pharma has gone so far as to inject the variant protein into living human beings since the beneficial nature of it is so definitive but there doesn't seem to be any consensus as to how this variant is beneficial?


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Why do bees fly inside the gaps between the decoration on the exterior wall of a building and the wall?
My house has decorations around the windows on the exterior wall:
There are gaps between those decorations and the bricks of the building:
During the summer, there are always bees looking for those gaps so they could fly into them while I rarely caught them flying out. I wonder why do they do that? What do they do inside? Is there anything I should do about this situation?
I guess that maybe they want to stay in a cooler place since it's quite hot outside? However, it's also worth noting that they seem to be interested in only one particular side of one particular window since I have never seen this happening to other windows of my house.

Bees often nest in rocks and in soil, i.e. cliffs and rodents nests. Those gaps are a good shelter for a bee, from sun and rain.

@DeltaEnfieldWaid that sounds like the start of an answer.


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Do viruses do anything other than multiply?
Viruses are "on the edge of life ". They infect the cells and use it for multiplication of themselves  but other than that do they do anything else like "eat food" like an amoeba or move on their own like Euglena ? Do they share any other characteristics with living things other than being able to reproduce ?

To be clear, the OP's question is not about classification per se, but about function, motivation—perhaps even purpose—and properties.

@RyanG viruses do not have motivation or purpose. One can speak of their function as a part of an ecosystem, and sometimes viruses are co-opted by organisms, in which case they stop being viruses.

The way I understand the question, it is about comparing fubctioning of a virus with that of a living organism (in simplest case a cell). It doesn't really invoke the virus role in ecosystems.

They can also divide

@RogerVadim ".. is about comparing fubctioning of a virus with that of a living organism.." absolutely correct. I want to know whether a virus has ANY resemblance with ANY other organism other than being able to multiply. What is the purpose of its multiplication is whole another topic, I think.

look up giruses AKA giant viruses.

Skirting the Question's fringe, and too long for a comment:
On symbiosis with viruses, from some science magazine:

Most viruses are harmful, but some viruses have a mutually beneficial
relationship with their hosts. A lot of viruses help their hosts by
attacking their competition. For example, the hepatitis G virus slows
down the growth of HIV, the virus that causes AIDS, in humans.
Bacteria grow viruses inside their cells and infect competitors with
those viruses. Other viruses are needed for their host's physical
development. When wasps lay eggs inside other insects, their eggs are
equipped with viruses. These viruses fight off the infected insect's
defenses and guarantee the eggs' survival.

This doesn't appear to answer the question, which is about mechanism, what viruses do — not what role they play, but what routines their "firmware" implements.

@Ruslan that was my original thinking as well. But the question also asks whether viruses "share any other characteristics with living things other than being able to reproduce", which can be interpreted rather generally.

They infect the cells and use it for multiplication of themselves but other than that do they do anything else like "eat food" like an amoeba or move on their own like Euglena ? Do they share any other characteristics with living things other than being able to reproduce ?

Individual level
No, viruses are not considered living entities, because they do not extract energy from the environment (aka eating) and do not do any active work like moving or constructing themselves. They entirely rely for these functions on their hosts or random influences (like being carried by air in droplets).
Maximum of what some viruses are known to do are attaching to a cell and a simple one-time syringe-like movement to penetrate it.
Part of ecosystem
Being obligatory parazites, viruses certainly play a role as a part of their ecosystem: e.g., limiting the population of their hosts or even being in symbiosis with them (as pointed in the other answer). It is necessary to note in this respect that a "successful" virus is not the one that causes the maximum damage to its host, but rather the one that most efficiently uses the host to replicate and spread itself. This drives viruses towards co-existence with their hosts, since the extinction of the host would also mean the extinction of the virus.
Wandering genes
It has been argued that viruses play a role in horizontal gene transfer, gene duplication, etc. Some parts of mammalian genomes are identified as deactivated ancient viruses, which continue producing proteins essential for the functioning of the host organism. See, e.g., here.


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If Covid antibodies disappear after 2-3 months, will a vaccine still be effective?
It looks like there have been studies in China and also in Spain that suggest antibodies don't last very long or could disappear after some time. What does this mean for the effectiveness of a potential vaccine? Could the effects wear off after a few months? Is this different from other diseases we get vaccinated for? I know we need to update the flu vaccine every year, but I thought that was due to mutations in the virus, not from antibodies breaking down. I am not a scientist, can anyone ELI5?

Humans don't constantly produce antibodies for a pathogen when the pathogen has been gone for a while. They just store the 'recipe' for making the particular antibody in memory T cells.
If the antigens that the virus contains mutate enough to not work for the antibodies an immune person has developed. Then the process starts over and the immune system will have to 'create a new recipe'.
Each new host creates a possible scenario for a coronavirus such as the current SARS-CoV-2 to mutate and develop different antigens that may cause a second wave requiring humans to develop new antibodies in our immune system and new vaccines to be distributed.
Though coronaviruses do not mutate as quickly as other viruses such as the influenza virus. It is still possible that SARS-CoV-2 having caused such a large pandemic, may develop a new strain.

As far as I have followed the papers, the genetic stability of SARS-CoV-2 seems pretty high. Can you please add some ressources to back your claim?

Thank you! This is so helpful. So vaccines help create memory T cells. But why would normal antibodies not be stored in T cells? Are they only activated when there are a certain number or strength of virus?

When a recognized virus has been detected by the immune system, the memory T-cells multiply into more memory T-cells as well as plasma B cells which are able to actually use the 'recipe' to produce antibodies that flow freely in the blood and neutralize their target antigen. For each immunity you have developed, you have specific memory T-cells that store the 'recipe' for that one antigen. eventually over a long amount of time these memory T-cells may die which is why people need to take a tetanus vaccine around every 10 years (as an example)


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Expected number of times a mosquito bites (per night)?
Imagine you are sleeping alone in your bedroom and there is a (female) mosquito in the room wanting to feed on your blood. I read here the mosquito will try to keep biting and feeding on you until its belly is full.
Question: What are the expected number of times the mosquito will bite you if you do not actively avoid it? (For example, in the case you were sleeping). However, I imagine this might vary with the mosquito species.
In particular, I am thinking about strategies aiming for minimizing the number of the mosquito bites: would it be feasible to let the mosquito bite you once and suck your blood until becoming fully feed?

as far as i know mosquitos bite only once,if they get disturbed before they are full they will not bite again.

@trondhansen Best to answer in a supported answer rather than a comment.

@BryanKrause i know too little about mosquitos to make an answer,my comment is more an asumption about mosquitos not taking the risk again if they got some blood the fist time.

Your answer is here: https://www.google.com/search?q=how+many+times+do+moskitoes+bite There is no limit to the number of mosquito bites one of the insects can inflict. A female mosquito will continue to bite and feed on blood until she is full. After they have consumed enough blood, the mosquito will rest for a couple of days (usually between 2-3) before laying her eggs.

@com.prehensible That is not the answer to my question. The number of times a mosquito bites a sleeping person (or a person actively not avoiding the bites) will typically follow some distribution; I am asking about the expected value of this distribution (and possibly its standard deviation). However, I understand probably this has not been studied.

There are many variables to your question then... 3000 species of mosquitoes, dozens commonly drink human blood. A sleeping person, what are they wearing, what are they covering up? how much the person stirs if they are bitten? What time of night bitten,,, deep sleep? That is the science you want, human physiology of stirring in response to bites. mostly she will find a spot with enough bloodflow to fill up, and only sting  once. thats why no research is that general.

quote:... In particular, I am thinking about strategies aiming for minimizing the number of the mosquito bites: would it be feasible to let the mosquito bite you once and suck your blood until becoming fully feed? ... it does answer your question in particular.

@com.prehensible mostly she will find a spot with enough bloodflow to fill up, and only sting once. could you provide some source for this? (And maybe write it in an answer)

No. I just linked the NYT science post on it, check the google search to find references yourself: It is also possible that some blood types are not as easily thinned by the anticoagulant in the mosquito’s saliva, so the mosquito has to make more tries to get a satisfying meal. Another factor may be...

From a couple of species (Culex quinquefasciatus, Anopheles gambiae) I rear and feed in laboratory, I can tell that if the female is not disturbed, she will bite only once, untill her belly if full, as you said.
So the best to minimize the number of bites (and to get rid of the disturbing mosquito noise while trying to sleep!!) is to let you be bitten once to be alright the rest of the night. This is easier to say than to achieve, but this should be the best, provided on:

filling all the largest holes of your room to be sure that mosquitoes cannot enter (use mosquito nets!)
switching off the main light to encourage the mosquito to come quickly (for night species). The mosquito will be attracted to your breath, then to your heat at close proximity.
offer the back of your arm where the skin is the thinnest, that may be less scratchy
after the bite, you can put some water gently on the bite to avoid any body response against mosquito saliva, but don't touch it otherwise you may elicit  the scratching feeling.

Then, you should sleep peacefully for the rest of the night, except if a mosquito gang is around.

Nice answer haha Though I tend to go with the more destructive alternative: eradicate the little monster (at the cost of losing my sleep).


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Why is it that only humans are ashamed of certain critical biological activities
Humans are ashamed of certain activities that are critical to our survival.
Examples: mating, defecation, exposing certain parts of our bodies
This restricts some activities from being performed while others are around (usually only if others are also humans).
Perhaps it is because we are the only species who is capable of feeling ashamed?
What are the advantages of this mechanism in terms of survival as a species?

Welcome to SE Biology. In my opinion this is not the kind of practical biological question that can be answered in an objective manner, but is one the answers to which will be opinions and lie in the area of psychology or sociology. That is why I have voted to close it.

I think there is certainly an interesting biological question underlying the evolution of e.g. fecal avoidance, which has been studied in a variety of organisms (e.g. https://pubmed.ncbi.nlm.nih.gov/24027342/). Unfortunately, when such questions are applied to humans, they often end up descending into telling just-so stories about human evolution.

Some humans are, not all humans, nudity for instance is definitely cultural. Don't confuse your cultures behavior  with universal human behavior.

@John Can't culture have a genetic component?

@RodrigodeAzevedo cultural behaviors generally have no genetic component they are purely learned behaviors. This is easily seen by the behaviors of people raised in drastically different cultures than their ancestry. Humans in general have so little genetic variation claiming anything cultural has a genetic component would require a great deal of evidence.

@John Studies involving identical twins adopted by different families would suggest that it is more complicated than that. A proper definition of "cultural" would be the starting point.


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Absorption of glucose in small intestine
During the absorption of glucose in the small intestine, glucose enters the epithelium by Na+/glucose co-transporter by the concentration gradient of Na+. The gradient is generated by pumping 3Na+ out each time and the entrance of 2K+ by Na+/K+ pump. The K+ is then removed by the concentration gradient via the potassium channel protein.
My question is is it more favorable to use a Na+ channel protein to pump Na+ out of the cell to generate the concentration gradient? Or there are some biological significance for K+ to enter the cell and leave again repeatedly (e.g. maintain stable charge distribution in and out of the cells? Thank you.

Na+ channel proteins would not be able to generate a concentration gradient, as they are passive transporters, not pumps. They essentially can only facilitate diffusion of Na+ down a gradient. The Na+/K+ pump is ATP-driven, providing active transport needed to establish or maintain a concentration gradient.


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Question on thick filaments

In this photo, I know that the arrows pointing towards the M-line of sarcomere on actin filaments are due to the power strokes of myosin heads. However, what I don't understand are the arrows on the myosin filaments pointing away from the M-line.
Are they the reaction forces (action-reaction pair, where the action force is power stroke)? Also, will this force (pointing away from M-line) 'tear apart' the myosin filaments on M-line? If not, how can the filament withstand this force?

Yes, they are action-reaction pair.( Newton’s third law).
No, it won’t tear under normal circumstances. The filament withstands all that force because the attractive force between its constituents is far more than the force generated by myosin actin cycle.

Thank a lot. For (2), for the attractive force, do you mean the force between the myosin filament and the M-disc?

@234ff yes. That’s it.


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Taking cold shower / drinking cold water after / during training
(I am a new-comer in biology SE so sorry if violated any rules)
Effect of cold showers after intense training
I have read the answer to this question, but it seems there are discussions on the validity there so I am still confused. For me,
Benefits: increase heat loss by conduction on the skin surface, prevent heatstroke.
Disadvantages: thermoreceptors in the skin detect a drop in skin temperature, sending nerve impulses to the hypothalamus. Then the heat gain center is activated and causes vasoconstriction, reducing blood flow just under the skin hence reduce heat loss (&dangerous for patients with heart disease like the answer says). This also reduces sweat production by sweat glands.
Won't this 'chain' of physiological actions reduce heat loss (which is needed after exercise), hence trapping more heat inside the body instead of cooling in the long run? Or am I wrong when deducing the disadvantages?

You're right, It will reduce heat loss.

@ArkLomas OK thanks this means taking a warm shower can make the body return to normal core temperature even faster?

not necessarily, your body has natural methods of cooling and heating itself to stabilize body temperature.
If you have just done exercise, your body will naturally try to cool itself, taking a warm shower to make your body cool itself quicker (via vasodilation etc...)  is less efficient than taking a cold shower.
that said, drinking warm liquids also causes your body to sweat which can serve as a cooling mechanism to counteract the heat conducted from the liquid. but If your body is dangerously warm, a cool drink will probably be better especially if your sweat can't evaporate.


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Population Genetics Using WGS: How do I know when I have enough individuals?
I am having a difficult time finding information about a minimum threshold for number of individuals to use in wgs pop gen analyses. Are there software or formulas/theory available to determine what number total number of haplotypes/individuals you need to get theta estimates, make a linkage map, run mk tests etc based on inputs such as genome size, read depth per individual, sequencing platform? Obviously there can be financial constraints and considerations to make for non-model organisms when choosing how many individuals to sequence. Any advice would be appreciated. Thanks!

I think that many of the applications that you mention require wildly different numbers of individuals. It would help to know more about goals, questions, organism details, etc.
For example, for simple population statistic estimates, you can depend on the large number of sites in the genome to get an accurate estimates (such as Watterson) from a single individual, if you are working in a diploid organism, as you can use heterozygosity. See the first Neandertal genome paper for what you can do with one single not very good sequence.
For applications such as linkage maps, you will need a rather larger number of individuals, as you need to sample a large number of recombinations. However, "large" is relative, as a centimorgan-level resolution of the human genome was achieved with a mere 110 humans and ~6000 loci. For finer linkage analysis you may need more individuals; however, with WGS your loci will be much less limited.
For McDonald-Kreitman tests or such-like, it is possibly more important to have more individuals. But you don't need WGS of every individual, in principle you could just find the gene(s) of interest and Sanger it for every individual, which is in most cases still much cheaper.
Obviously each of these has its own power and precision added by more samples, more could be said of each. General resources can be found here and here and here and here, in case it is helpful.

Thank you this was very helpful. New to the MK and Watterson stuff. I've built linkage maps with roughly thirty haploid individuals before (drones), but that was with radseq and individuals all from the same diploid parent (queen  bee), so a different approach was taken. Yeah for the linkage map stuff now I'm using population genetic data, just not sure how many are two few using software like ldhat. I suppose, in theory two unrelated individuals could give you estimates, because with 4 haplotypes you can catch recombination events. However, I know I'd want more than that of course. Thanks!


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Are there any thermogenic plants which are suitable as houseplants?
I have been wanting to supplement my heating system with some plants that produce heat! I have become aware that there are around 14 species which generate significant amounts of heat for example the eastern skunk cabbage.
However I have also read that many species which are thermogenic release odours such as the smell of rotting flesh. I would rather avoid plants which will make my house smell like this!
Are there any plants which produce heat which would be suitable for storing in my house?

I never knew there were such plants, thank you for educating me! Insulating the walls with plants or moss might be the most effective way, though. You want any structure that creates cusions of small air pockets along a surface. Like wall carpets that are used in some cultures, but green and pretty and happy.

I doubt this would work, the cooling effect of transpiration would likely outweigh the thermogenesis

Philodendron bipinnatifidum is a thermogenic houseplant. It is somewhat toxic, so not pet- or small-child-friendly, but commonly grown as a houseplant. However, I do not know if the heat generated would be enough to significantly impact your house; my impression is that most thermogenic plants merely warm their immediate surroundings (so you may need a LOT of plants). As a side note, your scheme to use plant-based-heating would probably also have good effects on air quality :)

Well, this is really more of a fun experiment than a serious project but I am not opposed to having many plants! I will investigate this species further thank you.

The heat the plant produces ultimately comes from the light it uses. Unless the plant produces heat just in the wanted time (winter?) from light absorbed another time; then you would be just as warm by letting the light directly warm your environment regardless of plants.

I don't see how this can be true. Light reflected off my white walls could be better spent absorbed by the plants and used to generate heat.

Yes basically I believe they do not release heat immediately after obtaining the energy from the sun so they would be "smoothing" variation in temperature in the room by releasing heat e.g. at night. From what I understand some species are capable of melting snow in this way.


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What is a subgenomic promotor?
I am looking for a good definition of the term "subgenomic promotor". Can someone help me out?

Welcome to SE Biology. Please read the [tour] and the Help on asking questions. Note that you are expected to research a problem first before posting here. Where are you looking, or, more precisely, where have you looked for this term? I find an immediate hit to a Wikipedia entry on Googling. If that did not solve your problem you need to explain why and describe (preferably link to) the context in which you met the term so we can check out the context.

The spelling promoter is most common in this context, which is important if your search mechanism does not return both spellings.

Can it be a DNA motif where the RNA polymerase will bind to create a subgenomic (m)RNA ?

A subgenomic promoter is a promoter added to a virus for a specific heterologous gene, resulting in the formation of mRNA for that gene alone. Many positive-sense RNA viruses produce these subgenomic mRNAs (sgRNA) as one of the common infection techniques used by these viruses and generally transcribe late viral genes. From doi:10.1128/jvi.74.13.5988-5996.2000
So it seems to be an added promoter that helps express certain genes. Often useful in viral engineering.


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Bougainvillea flowering problem
My bougainvillea plant hardly flowers and only at the tips. It has one very long vertically growing stem(if I may call it so).

Is this an example of apical dominance.
If so how is it to be corrected?
Do I have to cut the long step?

what is the water regime? what is the climate (day length and heat)? how much sun does it get?

@Hachiloni Everyday a lot of water is added to it. It receives continuous fresh air, but direct sunshine for nearly 3 hours in the morning. In August, days are long with rain as it is monsoon here in India.

This question and others like it are much better suited to [gardening.se].

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, I'm voting to close this question because it would be a better fit for [Gardening.SE], but please don't repost (instead request migration). Thanks!

bougainvillea is a qualitative short day plant meaning that it needs long, uninterrupted nights to flower. Most flowring accours when it gets 8hrs of light (=16 hrs of night).
India is a huge country so you need to be more specific or tell us how many hours of light the plant gets. Note that if it's exposed to light from the house/street it may not flower as the light intensity for photoperiod is much smaller than that of photosynthesys.
Flowering requires a lot of energy, even if all conditions are met not enough sunlight might prevent flowering. bougainvillea loves sun, give it as much direct light as possible.
According to fao, Paclobutrazol shortens the time to flowering in long day conditions, meaning that GA might delay flowering. Another way to prevent GA synthesis is to stop watering the plant. Once the leaf start to fall give it water again.
Don't water too much:

these plants need full sun & well-drained soils. After establishing,
minimal watering is needed. Two or more irrigations with 3/4 – 1″ of
water per week would provide too much water for the bougainvillea to
bloom well.

What to do:

Give it more sun
Give it less water
Induce water stress to prevent GA synthesis
shorten the day, you may cover the plant with a dark cloth from the late afternoon to the morning

Yes, too frequent watering is what I have seen stopping flowering. I have seen them flower even growing with only indirect light. The gardening and landscaping SE is also a good place to ask. If your plant has been grown from seed, that may account for slower flowering also.


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What is the relationship between the oxygen affinity of hemoglobin and the maximal oxygen uptake (VO₂ max) of the human body?
I was curious about whether any of the numerous documented human hemoglobin variants conferred a quantifiable athletic advantage but the only thing I've found of any relevance is the relative oxygen affinity of each hemoglobin variant. From the bit of research I've done it seems to be the case that a higher oxygen affinity causes the hemoglobin to hold onto oxygen more tightly and not release it into the plasma at the same rate as normal hemoglobin, leading to the body overproducing red blood cells to compensate for this (erythrocytosis). On the other hand, lower oxygen affinity causes the hemoglobin to release oxygen more readily, leading to the underproduction of red blood cells (anemia).
Assuming the quantity of blood cells were normalized between the two (so the consequent erythrocytosis/anemia is mitigated) would the lower oxygen affinity confer an increase in maximal oxygen uptake? How about higher oxygen affinity?


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Do "basal" clades tend to be more similar than "derived" clades to their common ancestor?
I often hear certain clades described as "basal", "lower", or "less evolved", or "less recently diverging", and others described as "derived", "higher", "more evolved", "more recently diverging". These "basal" clades seem to be ones with few species compared to their sister clades. For example, within Gymnosperms, I've often heard ginkos and cycads described as being "ancient" plants. Sometimes the differences between more and less recently diverging clades are used to make arguments about broad evolutionary trends within a group (e.g., Ma et al. 2018).
However, as Krell and Cranston (2004) point out, which clade appears to one side of a phylogenetic tree is based on the arbitrary rotation of nodes, and they argue that therefore "basal" and "derived" are imprecise terms. Which clade is more or less recently diverging seems to me to be less arbitrary, but I still do not understand why it would serve as a measure of how primitive a clade is.
My question is, do the species in basal clades / less recently diverging clades tend to be more similar (molecularly or morphologically) than their sister clades to the common ancestor of the two? If so, why does similarity with the common ancestor correspond to less or less recent divergence within the clade?

From Forest et al. (2018)

I think there's a risk of tautology here; you're right, the drawing/ordering of a tree is not meaningful. But, if we label "basal" to be one that is most similar (perhaps superficially) to an inferred ancestral state, then of course basal is more similar to ancestral.

@BryanKrause I think you're right overall, but this is also a pretty common way of talking about taxonomy! I think it is worth sussing out whether this highly subjective but very common way of thinking about taxonomies does have any empirical validity. I bet it does!

@MaximilianPress Yeah, I think the "molecular" question is a more interesting and is non-tautological if "basal" is determined by (typically gross) morphology. The tautology comes up if your assessment and categorization use the same criteria.


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If coral didn't exist, would jellyfish not exist either? (Or vice versa)
Is the evolution of corals, sea anenomes and jellyfish intrinsically linked to the point where if say corals did not evolve, neither would jellyfish? Or vice versa.

Hello and welcome Jefferey. How did you come to the conclusion coral & Jelly fish are reliant on each other?

They both evolved around the same time and are part of the same phylum. Do they have a common ancestor? I'm not saying their reliant per say.

Poor wording on my behalf. But is seems although the relationship is not clear. https://www.britannica.com/animal/cnidarian/Evolution

Welcome to Biology.SE! I don't think I understand your question — can you clarify what it is that you are asking?. Are you thinking that different lineages within a group are somehow dependent after they've separated from each other? If so why? If not, then why would the extinction of corals (or their failure to ever form a separate lineage) have any effect on jellies? ——— As an analogy, does the failure of the hominid lineage to form trolls have any effect on humans or the other great apes? What does that question even mean?

I was a little tired when I wrote this. I think the answer provided understood what I was getting at, though even in hindsight I can barely grasp what 1AM me was getting at. Heh, sorry for the confusion.

I found this article with phylogenetic trees of Cnidaria answering your question.
You should note that phylogenetic tress are statistical models based on sequencing. They may change depending on the methods used, the organismed sampled and the genes used for comparison
I translated the groups you mentioned to the following biological names:
Corals - Hexocorallia and Octocorallia
Sea anenomes - Actinaria (Hexocorallia)
Jellyfish - Medusozoa
(Not the same levels)
Judging by Figure 3 (don't know if I'm allowed to post the figure to this site)
And my limited knowledge in the subjet they each group could've evolve seperatley with a higher linkage between jellyfish & corals(octocorallia) than to sea anenomas.
Sea anenomas and corals(hexocorallia) are very closly linked and sea anenomas appear at the first junction of the tree which means that if sea anenomas did not exists neither the rest of the group.


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how to estimate phylogeny without using DNA sequences?
I am new to bioinformatics, I am reading ‘Analysis of Phylogenetics Second Edition and Evolution with R’ from Emmanuel Paradis.
I can create phylogeny from DNA sequences, by first calculating the distances and then using (ie nj() function).
My question is: if instead of DNA I have trait data (ie height and weight of species), how can I estimate a phylogeny? (is the same process valid? somehow calculate distances and pass that to nj()?)

You want to make a phylogeny with only two non-independant data points per species?

let's say I have 20 data points for weight and length, and 3 or 4 species, is it doable? (I am curious how, either using R or paper...)

Morphological taxonomies are typically based on presence or absence of different anatomical traits. While you could technically calculate a phylogeny based on size and weight, it seems unlikely to produce an accurate or valid phylogeny. Sometimes distantly related species have similar body sizes (raccoons and opossums). In other cases, related species might have dramatically different sizes. For example, the round-eared elephant shrew (Macroscelides micus) resembles a small mouse (weighing around 28g), but it is more closely related to elephants than rodents.

https://www.khanacademy.org/science/biology/her/tree-of-life/a/building-an-evolutionary-tree


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What's the opposite of a thermophile?
Thermophiles, heat-loving organisms, have been a popular topic of research for decades due in large part to the utility of their enzymes in various chemical reactions (Taq Pol single-enzymedly made PCR practical). One of the signatures of thermophiles is that their proteins resist heat denaturation up to much higher temperatures than their mesophilic (middle-loving) homologs.
Is there a corresponding group of extremophiles whose proteins resist cold denaturation down to much lower temperature than their mesophilic homologs? If so, could someone please point me towards a few good literature reviews on the topic? Or at least give me the proper name for this group of cold-loving extremophiles?

there are organisms that survive in cold temperatures - like arctic plankton and fish...don't know their names, but their adaptations tend to be the production of antifreeze proteins.

The term you are looking for is psychrophile or cryophile. There are examples of microbes adapted to very cold conditions in Bacteria, Archaea, and Eukarya. There are also fairly complex animals capable of surviving very low temperatures -  Tardigrades, for example. There are multiple issues that organisms face in withstanding extremely low temperatures - protein denaturation, membrane fluidity, intracellular ice-formation, just to name a few.
There is this review that might be useful to you.

D'Amico, S., Collins, T., Marx, J.-C., Feller, G., Gerday, C. Psychrophilic microorganisms: Challenges for life (2006) EMBO Reports, 7 (4), pp. 385-389. link

You beat me by 20 seconds! I shall defer to you.

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


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Does probiotics bacteria from yogurt live in the mouth too? Does it populate the mouth/throat or just the gut?
Yes I was basically just wondered this as I've taken probiotics in a pill form but those only go to the gut. I guessed the mouth needs probiotics too and I wondered if yogurt can accomplish that.
I also found conflicting stuff on the internet: some say enzymes in the mouth kill the bacteria in yogurt, others say yogurt helps bad breath for example which means it does have beneficial bacteria that live there in the mouth probably.

of course they do... the question is for how long.
Probiotics will tend only to affect the microbiome in the digestive tract for a while.  For yogurt supplemented with probiotics subjects microbiomes drifted back within 48 hours.  Depending on your diet the individuals can hang out for a while or persist.  Children, who tend to drink more dairy have a more persistent Lactobacillus signature.


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Meaning of "acute LSD"
I am currently reading this research paper: https://www.nature.com/articles/1395848, and I'm confused by this line: "Serotonin Receptor mRNA Levels Are Unchanged by Acute LSD".
What is the exact meaning of this sentence? I could probably understand it as "immediate", that it doesn't pertain to long-term effect instead of short-term.

In the abstract they refer to "acute LSD administration" (emphasis mine), and in the next section of the results after the one you mention in your question, they clarify it as "Acute LSD administration (1.0 mg/kg, 90 min)".
(That seems like an awful lot to me, as I understand typical recreational doses for humans are in the tens to hundreds of micrograms range.)

Thanks for the answer! Just realized it now. 1.0 mg by itself is a lot, not even talking about 1.0 mg/kg.

@TimotejLeginus Though these are rats so 1 mg/kg is probably about a 0.2-0.3 mg dose (the paper probably gives specific mass ranges for their animals but I'm just going by my memory of common sizes). Still a lot.

@TimotejLeginus Just a small addition: the term acute generally means that a phenomenon/effect lasts for a short time period, in contrast to chronic which refers to a phenomenon that continues over a long period. This doesn't mean long term responses. There can be long term effects of an acute phenomenon.

thanks for the explanation! well I wasn't so sure about that, haven't found it anywhere, so I had to ask :)


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Does LSD "stay" in your fat storage and then "returns" back?
This rumor was told me by a very anti-drug person. A stance I agree with only lightly.
The rumor was that when you take LSD, it stores itself in your fat storage, and then returns back in 3-6 months, returning back meaning there would be another series of effects of LSD (the trip).
Is this true? I highly doubt it. However, what I don't know, if the body is processing (burning?) fat and then processing substances (such as the rumoured LSD) found in fat stores.

Welcome to SE.biology. I downvoted because questions based on rumours from other people don't tend to encourage speculative and non-evidence based answers. Take a read of the help-centre to find advice on how to ask a good question. Thanks!

@user438383 This is actually a very widely-spread idea (with several variations) amongst the drug and hallucinogenic community. The version I've heard most is that it accumulates in CSF or just "the spine", however as I reference in my answer, it's not true.

@user438383 I haven't found much evidence on the web about this, so I had to ask here.

@TimotejLeginus showing a little research would probably keep your question from being closed. Alternatively you may want to drop this question the skeptic stack, urban legends like this area better fit there. I know a lot of scientists who believe this urban legend, until today myself included, so it deserves a little attention.

@John kind of interesting that sciencists believe these things too! I would have done some research, but before this, I would be unsure where to start, now I would be sure where to :p

@TimotejLeginus a scientist outside their specialty is not much better than a layman, and paleontology does not involve much pharmacology.

I've heard this rumor for years, both from pro- and anti-drug people, and it is not true. According to this review of LSD's pharmacology, its half-life in the body is about 5 hours, with it being completely cleared within about 15-28 hours. There is no evidence that it accumulates long-term in fat, cerebrospinal fluid (CSF), or anywhere else in any pharmacologically significant quantity.
Reference:
"The Pharmacology of Lysergic Acid Diethylamide: A Review" CNS Neurosci Ther. 2008 Winter; 14(4): 295–314. PMID: 19040555 DOI: 10.1111/j.1755-5949.2008.00059.x

My guess is that flashbacks are almost or entirely psychological, where the brain and the rest of the CNS somehow gets triggered in a similar way that acid does. Also, hallucinations can occur in a number of severe psychiatric diseases, independently of past drug use, so that likely has a role, too.


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How do prodrugs exactly work? Are there multiple varieties of prodrugs?
I have been reading about a (new?) prodrug of LSD, 1CP-LSD, which is being synthesized in the body to LSD.
However, I don't know how exactly. I read somewhere, that another prodrug of LSD, 1P-LSD was put  into a vial of human blood, and it was synthesized to LSD. Which is kind of hard to belive, that just exposure in blood synthesizes 1P-LSD to LSD. What processes in the body are responsible for this, are there another processes for synthesizing another prodrugs to their respective drugs?
Are there multiple varieties of prodrugs? By that I mean that they synthesize themselves using another method instead of one another.

Prodrugs are extremely common; we often don't even think of some of them as prodrugs unless we're also familiar with the metabolite. Psilocybin, for example, is a prodrug; the active molecule is psilocin. Aspirin is a prodrug of salicylic acid (though there are also other active metabolites).
Prodrugs can be categorized according to where they are converted to active forms: intracellularly in target tissue or other organs like the liver, or extracellularly like in the gut or in the bloodstream. The Wikipedia link at the beginning of this answer includes a table with some examples.
Prodrugs may be converted to active forms by enzymes or by environmental conditions in the body, like pH. I'd argue they are diverse enough that it doesn't make all that much sense to study them as a category, rather that in any pharmacological class of drugs you should be aware that they may be administered in a modified form, often to improve bioavailability or storage stability.

So it is indeed true that prodrugs can be synthesized to drugs within blood too? That's cool!


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Near-infrared EM spectrum and uses in biology (specifically in botany/vegetation)
A little explanation for my problem:
I have a large dataset - images of aerial scans of my country. These images are available in both RGB and RGBN colors - N specifying the near-infrared color channel. I plan to  use this data/images to make a computer-simulated realistic landscape game. However, the data has a resolution of around 15cm, which means I can't really expect realistic depictions of individual blades of grass. I will need some kind of interpolation.
I could manage pretty well with the RGB colors, but I would like to know some uses of the near-infrared color channel for this kind of problem - which is analysing vegetation, ground, etc. - and how could it help me with this kind of project.
I did try doing some research: I found this neat little picture that illustrates how we can analyze if a plant is healthy or not.

Green vegetation (left) absorbs visible light and reflects near-infrared light; Sparse vegetation (right) reflects more visible light and less near-infrared light. (source)

Thank you for any help.

Sorry, I can't see what your question is here - are you looking for data on how to resolve types of plants based on NIR or something else? The GIS Stack might be more help. There's also some info in the original publication for your image here, which you incidentally should attribute correctly!

To be fair, it's a very general question. I am looking for a botanist's view on this - I am not very well versed in botany nor biology. I'm just looking for some resources as to how to approach this issue. The GIS StackExchange users are not biologists - I believe I'd be redirected to the Biology StackExchange and so on again.

There's quite a bit of information on this topic around - try this search at Pubmed


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What data would Meselson and Stahl have expected if DNA replication was dispersive rather than semiconservative?

What data would Meselson and Stahl have expected if DNA replication was conservative rather than semiconservative?

Answer:
In the first generation, there would be two bands, one of light density and one of heavy density. In the second generation there would still be two bands, one of light density and one of heavy density.
Question 1:
In the second generation, are the heavy-density bands getting closer to the end of the test tube, and the light-density bands closer to the top of the tube, than the first generation? (due to the larger number of DNA molecules)

What data would Meselson and Stahl have expected if DNA replication was dispersive rather than semiconservative?

Answer:
In the first generation, there would be one band, one of intermediate density. In the second generation there would still be one band, one of intermediate density.
Question 2:
Are the bands closer to the top of the test tube in the second generation than the first generation?
(Because DNA molecules would become lighter)
If this model was approved, could we see this change in the test tube? (Between first and second generation)

A few baseline ideas should be understood. 1. The assumption is made that Meselson and Stahl's cell line at the start of the experiment contains DNA composed entirely of the $N_{15}$ isotope. 2. DNA with a greater proportion of $N_{15}$ isotope is denser than DNA with lesser proportion of $N_{15}$ isotope. 3. Higher density DNA sinks lower in the test tube than lighter density DNA. (Same density DNA sinks to the same level.)
Q1: Let's follow 100 parent (generation 0) cells. If DNA replication was conservative, after they first replication (generation 1), we would expect 200 DNA strands. 100 strands come from the "parent" cells and are entirely composed of $N_{15}$ isotope (the conserved template strand). The other 100 strands come from "daughter" cells and are entirely composed of $N_{14}$ isotope (the newly synthesized strand). After the second replication then, we would expect 400 DNA strands. 200 strands come from the "generation 1" cells and share their DNA composition: 100 strands of $N_{15}$ isotope and 100 strands of $N_{14}$ isotope. The other 200 strands come from "daughter" cells and are entirely composed of $N_{14}$ isotope. Thus, in both generations, there are only DNA strands of 100% $N_{15}$ isotope and 100% $N_{14}$ isotope. The only difference is that the second generation has proportionally more DNA STRANDS composed entirely $N_{14}$ isotope than the first. Because the proportion of $N_{15}$ isotope and $N_{14}$ isotope in an INDIVIDUAL strand determines the strand's density, and because the strands in both generations comprise of 100% $N_{14}$ isotope strands and 100% $N_{15}$ isotope strands, the bands visible in the two test tubes are at the same level. They do not move closer to the ends of tube.
Q2: Yes this is correct. The first generation's DNA would all be ~50% $N_{15}$ isotope/~50% $N_{14}$ isotope strands. The second generation's DNA would all be ~25% $N_{15}$ isotope/~75% $N_{14}$ isotope strands. Strands of proportionally less $N_{15}$ isotope are lighter and thus closer to the top of the test tube.


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What are the differences between white and brown adipose tissue?
What are the differences between white and brown adipose tissue? Here are some that I have come across:
Brown Adipose Tissue                        White Adipose Tissue

Thermogenic                                 Non-thermogenic
Multilocular                                Unilocular
Relatively many mitochondria                Relatively few mitochondria
Vascularised                                Relatively few capillaries
characterized by the presence of leptin     characterized by the presence of UCP-1

I think Shep had more of the right idea in his answer to your Meta question about this, I don't know how you can maneuver this to make it more constructive.  In its current form, it's still asking for a list.

but Kevin's answer on meta wasn't shot down, so I assumed it would be OK....

Well, see what everyone else thinks about it, but list questions are normally closed as "not constructive".  Is there anything in particular you are looking for in terms of the relationship between the two types?  That would make a much stronger question and would probably get a better answer, anyway.

My suggestion was to just ask the question. I didn't think you would answer it in the question.

there are a lot of differences between brown and white fat (and don't forget beige fat - that's a 'thing' now too) - anatomic differences, physiologic differences, biochemical differences, etc, etc...

Not sure what you are asking, except to add to the list?
Its worth mentioning that brown adipose tissue is the only organ in the human body whose primary purpose is to generate heat.  We are warm blooded, but the body temperature is regulated by other organs generating heat while they do work (like muscles or I suppose the stomach, kidney, etc).
Brown Tissue is supposed to not a juvenile attribute - doesn't show up in adults to the same extent (usually being limited to neck and upper chest.
Brown Tissue is thought to be present in only critical areas of the body - even in infants.  Its found in the inner body cavity around vital organs.
The color comes from the large number of mitochondria in the cells, which is where the heat is generated via uncoupling protein 1 (UCP1).
White adipose tissue is what we more commonly call fat tissue - its primary function is to store energy in the chemical form of long chain fats.  Fat tissue as it grows can inhibit the function of insulin in the body, increasing insulin resistance.
You could almost call them 'good fat' and 'bad fat'

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


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Is there a database containing sequences of human cell lines?
I'm looking for the whole genome sequences of several human cell lines, e.g., A549 or Ea.hy.926. Is there a database specifically dedicated to human cell lines?

Is this what you are looking for? http://cancer.sanger.ac.uk/cancergenome/projects/cell_lines/

Thank you, I found this one already. Is this the only one?

As pointed out by @kmm (http://cancer.sanger.ac.uk/cancergenome/projects/cell_lines/) is an excellent database. Alternatively you can look at the broad institute page (http://www.broadinstitute.org/software/cprg/?q=data-resource) in the cancer cell line encyclopedia section, then go to the browse tab and select the cell line for a very comprehensive list of cell lines.


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Material on the analysis of (micro)array data
I'm at the moment analyzing cytokine array data. The available material on the statistical analysis of these data is more than unsatisfactory. Since a lot of effort is being made in the analysis of gene microarray and MALDI-TOF proteome data, I seek to apply these methods on my cytokine arrays.
What is a good introductory text on microarray analysis, especially quality control and error estimation?

A good place to start would be Statistical Methods for Microarray Data Analysis. I'd also suggest papers from the labs of Terry Speed, Gary Churchill, John Quackenbush, and Gordon Smyth.
Also, I found some papers that specifically reflect on your exact issue: how to apply the methods developed for DNA microarrays to analyze protein arrays.

Eckel-Passow et al. Experimental design and analysis of antibody microarrays: applying methods from cDNA arrays. Cancer Res. 2005 Apr 15;65(8):2985-9.
Royce et al. Extrapolating traditional DNA microarray statistics to tiling and protein microarray technologies. Methods Enzymol. 2006;411:282-311.


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How are vaccines mass-produced?
I have a background in product design and so am familiar with with how most things are mass-produced — food, machines, etc.  But I've been able to find very little information on how vaccines are mass-produced.
It looks like there are 4 types of vaccines, all of which include pieces or byproducts of the virus they're intended to counteract.
If you're producing billions of vaccines, I imagine you need a tremendous amount of the virus.
How is such a mass of virus obtained? Do they just fill up tanks with a culturing agent and a sample of the virus and wait for it to grow, like a giant petri dish? Are there big vats of Coronavirus sitting in factories somewhere?

Did you read the part of the page you linked about the mRNA vaccines for covid-19?

I’m voting to close this question because it is about industrial pharmaceutical practice, not biology.

@David I would disagree with that assessment. This seems to me to be very much about "techniques in a biological ... laboratory" just for higher scale operations.  Or is this site intending to exclude all discussion of bio work beyond MRL 3?  Scale-up is a massively important part of biotech R&D.

@jakebeal — No. Industrial biotechnology is not laboratory biology, and the people who are able to answer questions on biology based on their biological education and research and teaching experience seldom know any more about it than an educated non-biologist with access to the Internet. And I emphasize that this is not a discussion site — it is a question and answer site. If the question is such that it is unlikely to attract objective expert answers on a SE site is should be neither asked nor answered there.

@David Your response assumes that experts from industry should not be interested in this site, not to mention experts from academia who interact with industry.

@jakebeal — "should not be interested in this site"? Not unless they have questions about problems in biology of the type this site was set up to answer. If you mean contribute answers, their historical lack of participation speaks for itself. But even if this question were on topic, it is so vague and its scope so wide that I regard it as unsuitable. There is a Help entry somewhere about answers that require a book chapter to answer.

@David I'm currently working with algae, scaling up and investigating mass production is a big part of the area and a follow up research we must do. This will give me enough information and experience to answer this kind of questions in the context of algae, so I think this question should stay open

@Hachiloni — "This will give me enough information…"? What do you mean by this. There is only one answer which in my opinion provides no information. You may well be interested in the question, but if it is on the wrong list it won't get any answers. Wishing that experts in this area visited this list to provide their expertise is unrealistic.

@David I mean that this kind of questions can be answered on this site, so closing this question will give a bad precedent. I gave an example how I could answer a question of this kind with my knowledge

@Hachiloni I'd like to invite you to commit to the proposed Synthetic Biology site, where questions like this will be clearly on-topic and welcomed: https://area51.stackexchange.com/proposals/125068/synthetic-biology?referrer=MjE2YzEyZjY2NGZiZjQyMmQxNjM4YzE1ZTgyMTBjM2M1ZThhODIyZjc0OGY4MjUwNjQzYWUyYjcxYzdjNjgyZWgojuPHgTg3aSlhs7HovzJGQ8mR63x7oTvvqF7pWvWl0

Per Wikipedia, typically when one needs a lot of virus, it is grown in a controlled cell environment. This used to be eggs, but is moving toward cell cultures instead.  So basically yes, factories full of virus (though more like in nice discrete bioreactors than big Joker-friendly vats).
Synthetic vaccines, such as the mRNA vaccines for COVID, do not need this step at all, since they do not actually use the virus, but can be done through cell-free biochemical reactions that replicate the mRNA directly.

I used to work in a flu vaccine manufacturing facility, and we would go through millions and millions of eggs each season, sourced from local farms. It was quite a sight to behold...


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Why does high blood pressure not damage the body during exercise?
Exercise is commonly understood to lower blood pressure by making the heart stronger. Mayo Clinic says,

Regular physical activity makes your heart stronger. A stronger heart can pump more blood with less effort. If your heart can work less to pump, the force on your arteries decreases, lowering your blood pressure.

While exercising, though, systolic blood pressure will often go up significantly.
Why does this dramatic increase in blood pressure not damage the cardiovascular system? Stress, for example, can damage the blood vessels,

Increases in blood pressure related to stress can be dramatic. But when your stress goes away, your blood pressure returns to normal. However, even frequent, temporary spikes in blood pressure can damage your blood vessels, heart and kidneys in a way similar to long-term high blood pressure. (Mayo Clinic)

Does daily exercise, for example, not cause "frequent, temporary spikes in blood pressure"?
Why does a blood pressure increase from exercise not damage the cardiovascular system as a similar blood pressure increase from stress (or other sources)?

Actually it can. See https://clinicalhypertension.biomedcentral.com/articles/10.1186/s40885-016-0052-y for instance:

Deleterious effects of HRE [hypertensive response to exercise] on structure and function of left ventricle (LV) has been reported consistently. Theoretically, individuals with HRE would be exposed to abnormally high pressure loads to left ventricle (LV), which may result in global subendocardial ischemia due to mismatch between demand and supply from excessive rate-pressure stress. Indeed, a previous study demonstrated a greater likelihood of new or worsening abnormalities of wall motions from echocardiography in individuals with HRE, even in the absence of angiographically significant coronary artery stenosis.

The issue is that you're confusing somewhat high blood pressure with abnormally high blood pressure during/after exercise, i.e.

Thank you, that's useful. Even a healthy response to exercise, e.g. 160 mm Hg systolic, would damage the heart over long periods, though, so I guess it's just the fact that exercise lasts a relatively short period of time is the reason it's beneficial? I suppose, say, exercising 8 hours a day (or, for that matter, being stressed for 8 hours a day), would be damaging?


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Looking for a biological/physiological mechanism ... effect of diet on those who exercise vs those who don't
I'm researching the effect of adherence to Mediterranean diet on levels of inflammation in the body (C-reactive protein & a couple of other markers).  I want to stratify participants over levels of exercise (which I believe is an effect modifier) and need to come up with a biological/physiological mechanism whereby the Mediterranean diet would have a different effect on CRP in people who exercise versus those who don't?
Would really appreciate any pointers here.

I don't quite follow. You say you are trying to investigate the levels of CRP when on a specific diet. Is the logical course of investigation not (do experiment + collect data on exercise habits --> see if exercise habits made a difference, and if so what kind of difference)? You're jumping the gun trying to come up with mechanisms differentiating an unestablished link. Perhaps baseline levels of CRP in those who exercise would also differ. In that case you should probably treat the cases separately, because it's not obvious what kind of normalisation to use to account for these effects.

I agree that would be the logical course of action BUT I have to use an existing data base - I am not collecting new data.  The supervisor says I have to suggest a biological mechanism to justify why I want to stratify according to exercise and I have to specify this  in my proposal up front...  But maybe that is sufficient to say that I expect baseline CRP to be lower in those who exercise

OK! I don't know much about the effects of exercise on CRP though- I'll try to look it up myself, but what is your reasoning behind thinking that baseline levels of CRP are lower in individuals who exercise? I know there is a lot of talk of exercise being helpful in health conditions characterised by high levels of inflammation, but exercise itself induces micro-tears in muscles, which should lead to elevation fo some inflammatory markers. This would probably be a short-lived effect after strenuous exercise, but again I dont't quite know the balanace of these effects and how CRP

specifically is effected. But at least that's more of a biologicial-mechanism explanation than hearsay about the benefits of exercise!


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Why does a caloric reflex test induce sideways movement of the eyes?
By my understanding the semi-circle canals in the inner ear are oriented in each of the 3 dimensional planes to sense rotation of the head. When the head moves, the fluid inside of the canals does not move with it causing relative motion (like the objects inside of a suddenly breaking car), moving hairs on the walls of the canal.
In the caloric test we inject cold water into the ear which causes a convection current in the canals hence moving the hairs and mimicking head movement. However, I can't understand why the horizontal canal is disrupted, since convection currents move in the direction of gravity. It seems logical that the canal oriented up/down would be most affected. The cold causing water to move downwards, mimicking rotation about the anterior/posterior axis.

The horizontal (= lateral) semicircular canal isn't truly horizontal.  Have a look at this lovely image from Wikipedia, which gives a nice explanation.  If you keep track of the helicotrema of the cochlea there, which is on the lateral aspect, you can see that the horizontal semicircular canal connects with the utricle higher laterally than medially.
This is somewhat confirmed in Maxwell, 2016 Figure 1 which illustrates that the "horizontal" semicircular canal is only horizontal when the eyes are lowered by 30 degrees from a standard anatomical position.  (Bearing in mind that the two lateral semicircular canals are not coplanar, but diverge by 15 degrees).  That paper also confirms that buoyancy is a key mechanism in the caloric test.
Because the lateral end of the horizontal canal is higher, treatment with cold water will draw the endolymph away from it to the medial end, and hence away from the ampulla ("ampullofugal lymphokinesis").  The patient would feel they were turning laterally relative to the the position of the fluid (taken to be fixed in space).  This leads to two types of eye motion - the vestibulo-ocular reflex to maintain fixation by moving the eyes medially, and saccades to follow the position of the "moving" stationary object that the patient is trying to focus on by moving the eyes rapidly laterally.


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How are thoughts biologicaly generated?
I want to know how thoughts are biologicaly generated. I know that electrical impulses can trigger formed memories in the brain but what I want to know is how the electrical impulse is generated in the first place. I don't have a background in biology or neurology but I think it's probably one of the three options:

Impulses are generated randomly at parts where there are stronger connections.
We have loops in our neural network, electrical impulses stay and go around the brain to trigger memories and thoughts.
We are deterministic and only react to impulses from the outside.

Any reading suggestions about this topic are also highly appreciated. I want to understand the human brain a little more to compare it to artifical neural networks.

Hi! It's an interesting question, though I would caution you to narrow down your question, it's very broad. I also warn you to not confuse thoughts or memories with neur(ologic)al activity, this will run you into the hard problem of consciousness. Please also show some effort in trying to answer your own question; for instance, what exactly is it that you don't understand? You will have to show some independent effort for your question not to be closed or marked as a homework question.

An addendum: since neural circuitry is extremely varied, you will find many examples of all sorts of circuits, including those you list. For instance, there exist neurons with a pace-making activity that generate their own activity from within, as well as neurons that only respond to outside stimuli, such as many kinds of sensory neurons. And everything in between... including neurological dysfunctions. You MUST narrow your question and also be very cautious about comparing all of that to artificial neural networks (the analogy is full of common pitfalls and frequent misunderstandings).

Thank you for your answer! Although not posted as an answer your response did help me out. Do you have a resource suggestion where I can deepen my knowledge about different neural activities and differences? I know that artifical neural networks in the current state are completly different from how our brains work. I do believe though that a lot can be learned from our human brains for AI. I think my question can be closed now. And sorry again for the form of my question.

Please take a look here and try searching "how are biological and artificial neural networks different" in a search engine. There are many duplicate answers on psychology.SE and biology.SE and so many more answers and posts about it elsewhere. Good luck!


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Relationship between BMI and age?
I'm trying to study how age as a confounder may affect the relationship between commute mode and BMI (and design a research proposal).
To explain age as a potential confounder, I compared age to commute mode and then age to BMI. I found a weak association between age and BMI in my data.
In the literature does anyone know if BMI is expected to change with age? Is there a linear/ other relationship form? Please could someone attach any papers/ links for help.
Also, does anyone know what a clinically meaningful BMI is too? Would a change of 1-2 be important?

interesting - well thought! whether "important" could depend on what interests you, and may could only be answered after your model is complete. from the perspective of study design, you might run into the question of how sensitive your study / model should be (e.g.: should it be able to possibly be able to measure whether a BMI difference of 1-2 should have an impact on the entity you are interested). The relationship between BMI and age might depend on country etc, but at least in the USA is not linear (https://dqydj.com/bmi-distribution-by-age-calculator-for-the-united-states/ )

In (US) NHANES 2011-2012 data there is a significant quadratic relationship for 16+year olds:  males:  E(BMI) ~ 21.26 + 0.03age - 0.003age^2, females:  E(BMI) ~ 18.2 + 0.47age - 0.004age^2, highly statistically significant.  But the R^2 are not large (3% and 5%).  This is with around n=3000 in each group.  (I just pulled the NHANES data and ran the regression, so I don't have a citation).


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Is publication an important criteria to get a post doc in microbial ecology?
I am a researcher in microbial ecology , currently searching for post doc in European countries. I have publication less than 1 impact factor. Will this hinder my chances of getting selected . Please suggest?

Welcome! You might get a good answer (or find a similar one answered) on http://academia.stackexchange.com ; Personally, I would recommend to rephrase your question slightly to invite recommendations that will help you further (rather than getting a yes/no answer), e.g.: "Only published in low impact journals - how to maximize chance to do a PostDoc position in Europe?". You could possibly also add other information (e.g.: whether other students in your current department publish similarly).

We can also migrate the question to academia, if you want to.

I agree that this is not the best community for this question, since it is not really about biology. But to give a glimpse of an answer:

Having publications in high rated journals certainly increases your chances of getting a postdoc position.
It also depends on the general level/rate of publications in your field: in some fields having a few publications after a PhD is normal, while in the others the first publication may appear in press years after you graduate (not counting the thesis).
Then again, a publication in a top journal does not necessarily testify to one's abilities - e.g., if you are one among a few dozens of authors.
Networking and personal recommendations are often as important in getting positions as having publications.