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When do the first neurons appear in humans?
According to this
Neural Plate
The neural plate appears in day 18 in humans (very specific).
and according to this
Neural Plate (wiki)

The progenitor cells that make up the precursors to neural tissues in
  the neural plate are called neuroepithelial cells.

And according to this
Neuroepithelial cells

Neuroepithelial cells are the stem cells of the central nervous
  system, known as neural stem cells, and generate the intermediate
  progenitor cells known as radial glial cells, that differentiate into
  neurons and glia in the process of neurogenesis

So, if it's known when the cells which are precursors of neurons appear, I suppose it should be known when the first neurons appear, but I can't find information about it.
When do the first neurons appear in humans?

define a neuron

Apparently, olfactory axons and GnRH producing neurons are among the first neurons that migrate from neural crest at around 39th day of gestation in humans (Cassoni et al., 2016).

In rodents, early GnRH neurons migrate together with a heterogeneous
  coalescence of placode-derived and neural crest-derived migratory
  cells (Forni et al., 2011) and olfactory axons, collectively called
  the ‘migratory mass’ (MM) (Miller et al., 2010; Valverde et al.,
  1992). This cell migration precedes the targeting of olfactory sensory
  axons to the developing olfactory bulb (OB). The existence of a
  similar MM in the human embryo has not yet been described. We thus
  immunolabeled consecutive sagittal sections of a CS 16 embryo† for GnRH
  and doublecortin (DCX) (Fig. 1D,E,G), a marker of immature migratory
  neurons (Gleeson et al., 1999). We identified a very small number (50
  in total) of immature GnRH-expressing cells in the nasal mesenchyme,
  in the medial portion of the olfactory placode (Fig. 1C-E), adjacent
  to the basal lamina of the VNO, showing that the acquisition of cell
  identity occurs outside the VNO between GW 5 and 6. At this stage, we
  observed a mixed mass of immature GnRH neurons expressing DCX (Fig.
  1F,G) or βIII-tubulin (Fig. 1H-J), migrating across the nasal
  mesenchyme towards the telencephalon. As in rodents (Miller et al.,
  2010), GnRH neurons in humans only represented a small proportion of
  the MM (Fig. 1G). Furthermore, these pioneer neurons of the MM
  expressed the delta/notch-like EGF repeat containing (DNER) (Fig.
  1H-J), a transmembrane protein specifically localized in the dendrites
  and cell bodies of postmitotic neurons.

†Carnegie stage (CS) 16 = ∼39th day of gestation


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corse tree identification
My nosy belling-cat was asking itself what kind of mediterranean tree/fruit is seen on the pictures below. Location is Corsica, St. Florent - late June.
Extra points on nutrition factors in case of adability ;)

Looks like a loquat, native to China, family Roseaceae.  Latin binomial is Eriobotrya japonica.

source: Stack Exchange

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

sort: votes


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Determination of the species of a skull
Out here in the mid german woods,  the kids found this skull:

Now we would like to figure out what it is. Started to look at various google image search results for all kinds of animals that came to our mind, but not only due to bad reception this takes long and lead to no result.
So what is a good structured way to start detrmining what this is?

What is the size of the skull? Could you measure it or make a photo with a euro coin next to it? Looking at it's teeth, it looks like a herbivore.

Just to clarify, do you want people here to identify it or do you want to know how to identify an unidentified mammal skull?

@kmm: ideally I would like to have some information that can guide me to do such identification myself in the future; the skull here should serve as a kind of example people could explain some method, so in the end it should be identified here

@RHA: obviously you are right, that information is important. I will try that as soon as I have better network. For now the size is approximately 20cm I length

I usually use an old-fashioned book, but it's in Dutch. I imagine these kind of books exist in English (and German?), but I can't advise you on that.

@AlwaysConfused: fair point being too broad. We could interpret it as identification plus thought process? I really would like to take away more than just the name from it

And about results, it must be a young wild boar (Sus scrofa) or a domestic pig (please notice the very small canine).

Can you add photos of the occlusal surfaces of the teeth?

I changed the title of your question for it was in imperative mode. Hope you don't mind.

If you're serious about this (and it appears you are), you'll benefit by starting with a Comparative Osteology book or webiste that discusses all the various characteristics of skulls that give you clues to exactly what you're dealing with.
This page on Amazon has a variety of such books. Pages such as this one begin with the basics and references help you to pursue the subject further.
On your specimen, although the missing teeth would be very helpful, important identifying features include the very large percentage of the cranium given over to the masseters, the eye socket placement, the size, the jaw shape, etc.

Teeth are really important features for mammal identification.
The types of teeth gives an idea of the kind of food they eat.
In the skull you show, I guess that the tooth surface is far from being a "flat" grinder (which would be typical for an herbivorous, especially if old), but neither is there a sharp scissors-like structure (which would be typical of a carnivore). Therefore I will bet the animal is omnivorous.
The size, number, disposition and diversity of the teeth (dental formula) can further help. Some comments pointed to the presence of small nascent canines.
You can then look at a list of mammals that are living in the region of interest, filter it by size, and check what kind of dental formula they have.

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


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Why can't I swallow the entire (liquid) contents of my mouth at once?
I've tested this out using water - I manage to fit a certain amount of water in my mouth, but if I try to gulp it all at once, I fail: I feel like spitting the water out (gag reflex?) There's a certain limit, say 60%, of the full amount of water, that I can insert into my mouth and then gulp it without drowning myself. Why is that? What sort of muscle coordination causes this?

Normal swallowing triggers a peristaltic motion towards your stomach.
However, as demonstrated by young "scientists" (search "water chugging tutorial"), one can train to  voluntarily keep the esophagus valve open and poor down liquids without triggering peristaltic waves.

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


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Under which conditions is human energy consumption minimized?
Including but not limited to:

body state

consumed food composition
state of the digestive tract
diseases
wounds
sleep
coma, etc.; death excluded

environment state

temperature
light
pressure, etc.

Merely curious. I do not expect to find complete answers, which seems impossible, but all insight is appretiated.

Hi there, I see you're new here, please check out the biology help center (https://biology.stackexchange.com/help) to find out what types of questions are supposed to be asked in the Biology Stack Exchange and edit your question accordingly (https://biology.stackexchange.com/help/dont-ask).
You have an interesting question, just needs some adjusting for this site. Feel free to separate this question into multiple questions after reading the links provided.

come in a warm environment sounds like the most likely factor. light and pressure are negligable. people that are starving also conserve lots of energy.

@com.prehensible Thank you for the insight. I am unsure however what exactly do you mean by your first statement; could you please explain?

coma, sounds like a pretty low energy state, in a warm environment!


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Mitochondrial shape and function
I was wondering how can mitochondria come in different shapes and sizes? And why are they always shown as ovals on textbooks?
p.s. I would appreciate any suggestions for wider reading on mitochondria and cellular biology as well.

Welcome laerningsheep. Please take our [tour] and read-up in the [help], especially the [ask] section, taking particular note of the requirement that questions should show their prior research. You can then [edit] to show us what you searched, found and where you got stuck. Perhaps start with Mitochondrial evolution to get an idea about where we think they come from at present.


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Can anyone identify this please?
I found this in a toilet in the UK. Any ideas what it is please?
Thanks

A Flat-Backed Millipede.
The Woodland Trust has an article that's much more informative than the Wikipedia page:

Via Wikipedia, CC By-SA 3.0, Ratingen, Germany.
They're:

This species has a long, flat, segmented body with a large number of
legs. It is orangey-brown in colour and measures around 2cm in length.

Herbivores, normally found in woodland where they live under leaf-litter.
Widespread throughout the UK.


text:
Why can't the fructose monomer in sucrose be α-fructose?
In all academic sources, sucrose is identified as α−glucose (1-->2) β−fructose. However, I cannot find any explanation anywhere as to why the fructose monomer has to be in the β configuration. Maltose has both α and β anomers, same for lactose. Even trehalose, another non-reducing disaccharide with glycosidic linkage between two anomeric carbons, has α-α, α-β, and even β-β anomers. Why is sucrose special? And is there a disaccharide out there that has α−glucose (1-->2) α−fructose configuration?

Welcome to SE Biology. Please finish reading the [Tour] to learn how this site works. We allow just one question at a time, and if you wish to know whether a particular molecule exists it should be easy enough to determine its systematic name and do an internet search. As for the why question, why questions in biology can relate to either function or mechanics. In the case of disaccharides that function of which is nutrition, the answer is probably mechanical, and I imagine lies in enzyme structure and specificity. Check the structures of the synthases for these disaccharides.


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Insect ID from sound in video
Can you please help identify what insect this might be based on the noise it makes? Video below.
The noise is regular tapping, and can be heard especially at night when everything is quiet. When approached or my footsteps can be heard, the noise stops and starts again when it’s quiet again. I’ve never managed to see what it looks like.
It is only a single source of noise, and on different days comes from different parts of the room. Often can be heard from wooden window frames. This time when I recorded the video it was most likely somewhere in the bag.
I live in Sydney, Australia.
I listened to a number of different bugs (in videos) and can confirm it is not:

Termite
Deathwatch beetle
click beetle

https://youtube.com/shorts/5wf-UhwSEgk?feature=shared

I think that the most likely culprit are the so-called booklice (Psocoptera and Psocodea). These have a world-wide distribution and are a common household pest, eating dust and plant material (including paper)
These are small whitish/transparent insects that you might see scurrying around on recently disturbed surfaces - particularly books, stored boxes or in cupboards where you store flour or similar foods. They are quite small - in the order of 1-2 mm (~1-3/16th inches) long. Some of these species make quiet tapping sounds and they are very common in households - which might explain them being in a bag.
However, I wouldn't be so sure of ruling out deathwatch beetles - there are quite a few species in the group, besides "the" deathwatch beetle (Xestobium rufovillosum), some of which  I believe also make clicking/tapping sounds, though I'm not sure of the species which do and whether they might be present in Australia.

Booklice are tiny! I can't imagine one making this type of sound. I'm not convinced :p.

@theforestecologist  Surprisingly audible though - I've heard them a few times. I'm guessing it's a drumming effect on a thin surface.

Thanks for the answer. I have in fact seen book lice a few times in the house, however, as mentioned in the comment above, they really are tiny so I can’t imagine them being so loud. It might be though.


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Using autoclaved store-bought distilled water for labwork?
I'm a high school student who's working on a molecular biology project in my school's lab. I need pure water for making culture media, buffers, running a BCA protein assay, running digests, cleaning glassware, etc. I don't have easy access to any professional lab equipment, so I'm looking for an easy way to get "lab-grade" water.
Ideally I'd go to a university and fill up a carboy using a lab's milli-Q system, but this is not easy for me. I also don't want to shell out $$$ to buy ultra-pure water from online suppliers.
Will autoclaving store-bought distilled water (NOT mineral or spring water), suffice for microbiology labwork that needs pure water?

Yes, distilled water would be absolutely fine for your needs. You really don't need ultrapure water except for the most sensitive of applications. You also don't need to autoclave the distilled water before making things like media/buffer/etc; instead you would autoclave/filter them after you make them.
You can take a look at this document for an overview on different grades of water.

Distill your own.
A great excuse to build a distilling apparatus in your high school lab!  Distillation is a valid scientific endeavor it itself, and you can generate fresh distilled water as you need it and be sure of its purity, lack of plastic / metal contaminants etc.

This sounds like a cool project but I doubt I have the time to build and maintain a proper apparatus. More worrying is the amount of contaminants that are in our old, neglected glassware. I need to find a practical protocol for cleaning glassware on a budget...


text:
More efficient method of calculation genotype or phenotype ratios rather than doing a trihybrid punnett square or forked-line method?
Is there any other more efficient method of predicting ratios of offspring phenotypes or genotypes than doing a trihybrid Punnett square or forked-line diagram? Or are those two methods really the only solution. This is for a question dealing with unlinked traits.


text:
What is the meaning of depth relation and EM in this excerpt?
In the excerpt below from Morphology of Invertebrate Neurons and Synapses

For the better part of a century, conclusions were made largely by matching the depth relations between the terminals of input neurons and the dendrites of their presumed targets; this practice became transferred to arthropods and cephalopods. The practice may be true for particular terminals or dendrites, and in vertebrates, but it has been long gainsaid by many examples in invertebrates. In the particular case of Drosophila, now known from dense reconstructions, EM denies any such simple dichotomy in important details, with many terminals having postsynaptic sites and many dendrites that are presynaptic as well as postsynaptic (Takemura et al., 2008).

I'm having trouble understanding what the acronym "EM" stands for, the author seemed to throw it in without prior definition (my guess is it's some neuroscience jargon). I also don't understand what the author means by "depth relation". Could someone explain to me the two terms assuming a college intro level background in neuroscience?

EM is Electron Microscopy; the definition is found earlier in the passage in the normal form where the whole term is given followed by the abbreviation in quotes; you should look for this in the future.

...suited to connectomic approaches using electron microscopy (EM; Lacalli, 2009).

I'm not super familiar with invertebrate morphology, but from context in terms of "depth relation" they are talking about inferring directions of connectivity based on their locations in EM sections. If you find axon terminals from one cell type and dendrites from another at the same depth, you can infer they are likely connected. The passage explains that this doesn't work well in invertebrates that do not have a axon -> dendrite connectivity pattern. Dendrites synapse on other dendrites, and you can't easily tell what the direction of connectivity is from EM alone.


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Origins of transcription factors and RNA Polymerase
I was learning about transcription factors and RNA polymerase from Khan Academy to supplement Dr. Robert Sapolsky's lectures on Human Behavioral Biology. As I understand:

RNA Polymerase transcribes DNA to RNA
Transcription factors are proteins that help the RNA Polymerase bind or inhibit it from binding to the DNA and transcribe it to RNA
Transcription factors called activators help RNA Polymerase bind to the DNA
Transcription factors called repressors prevent RNA Polymerase from binding to the DNA

It seems like we need transcription factors and RNA Polymerase to express genes and produce their corresponding proteins. But transcription factors and RNA Polymerase are proteins themselves. Thus, they must have come from their own respective genes. This seems like a "chicken and egg" problem.
How did early organisms with genetic material get around this problem?

You might look into the transition between the RNA and DNA world: https://www.ncbi.nlm.nih.gov/books/NBK6360/

This is one of the main features of the RNA World.
What I mean by that is, RNA not only acts as a repository of genetic information, it also acts as an enzyme. This enzyme is known as Ribozyme. Ribozyme confers a self-replicating property to RNA, leading to the hypothesis that RNA might be the ancestor to the present day self-replicating genetic material.

The word ribozyme just means “RNA enzyme”. It does not define the catalytic function of the RNA. You are correct in implying that the RNA world hypothesis suggests that an RNA ur-genome might have been able to replicate itself without a protein RNA polymerase. However I am not aware of any contemporary ribozyme with this ability. Are you? Most seem to be nucleases or RNA ligases.


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Could Cyanobacteria farms help dilute pollutants in the atmosphere
If I understand correctly, roughly ~2.8 billion years ago cyanobacteria started pumping large amounts of oxygen into the atmosphere.
Using modern industrial processes could this be emulated by making cyanobacteria farms to help slow down the climate problem?
I also read somewhere that someone was able to genetically (or through other means) turn off the ability of a specific bacteria to reproduce causing it to produce a byproduct much more efficiently. Could this also help these "farms"?
Alternatively could we genetically strip the bacteria of all other functions other than procreating and photosynthesis? Making this bacteria live in a "bubble" would mean it wouldn't need a lot of defense mechanisms. This could make a single purpose bacteria that would be super efficient at doing this single task.

Good question. My gut says that bacteria would be easier to mass produce, to genetically mold into what we would want and are more efficient at doing photosynthesis. To my knowledge cyanobacteria are the only other organism other than humans to have impacted the environment on a global scale.

Plants and algae (including blue green algae, aka Cyanobacteria) sequester CO2 when they grow. But in terms of growing more Cyanobacteria, look up iron fertilisation: the oceans aren't green like a pond because there is not enough iron or phosphate or both. However this means creating new ecosystems as opposed to saving them

Also note that the 'great oxygenation' event was an even more drastic climate change than what we are seeing currently. While it paved the way for most modern lifeforms (who depend on a somewhat narrow O2 concentration) it killed probably more than 90% of what was living back the  (since they couldn't deal with O2 at all).

@Matteo Ferla instead of creating ecosystems could industrialization not just treat them as part of a process in a factory. They wouldn't be introduce into the wild but used in self contained bubbles. Mostly so that all their processes requiring energy to be spent on protecting themselves from the environment and predators could be genetically removed (More efficient and less likely to become an invasive bacteria).

Iron fertilisation (wiki) is at a larger scale and cheaper (a ship releasing a container size of nutrients across an oceanic crossing is sufficient to make a substatial planktonic boom, which when it dies sinks and thus buries the carbon it converted into biomass. If you had a algal farm you would sequester CO2 as biomass, which you would need to bury.

In terms of pollutants, there are several ventures, such as LanzaTech to mention one, who use bioreactors attached to an industrial process to bioremediate it. In their case they use a thermophile who uses carbon monoxyde to make CO2 and biomass (no idea what they do with biomass).

@Matteo Ferla [Joke] Soylent Pink? [/Joke] Thanks for the info, I'll be looking them up.

You have various questions here.

If I understand correctly, roughly ~2.8 billion years ago cyanobacteria started pumping large amounts of oxygen into the atmosphere.

The great oxygenation event was not an instantaneous process and represents a change from one equilibrium (low oxygen) to another (20% oxygen). This abundance of oxygen and organic carbon means that there is "niche" for organisms that burn up pre-existing organic carbon and use oxygen as terminal electron accept. Fermenting organisms use the organic carbon as a feedstock, but don't have oxygen so the use highly reduced organic molecules as terminal electron acceptors (less energetic), making mixed acids (sweat bacteria) or ethanol (yeast).

Using modern industrial processes could this be emulated by making cyanobacteria farms to help slow down the climate problem?

Cyanobacteria and other aerobic phototrophs convert carbon dioxide to oxygen and organic carbon they can use to make biomass. So if you had enough of these you'd need to get rid of the biomass. Responsible forestry for housing actually ticks this box (cf. vs. a mature forest, which is nearly at equilibrium where the biomass gets consumed by other organisms, else you'd had a faster growing topsoil).

I also read somewhere that someone was able to genetically (or through other means) turn off the ability of a specific bacteria to reproduce causing it to produce a byproduct much more efficiently. Could this also help these "farms"?

It is a grand challenge of synthetic biology to stop growth. It is really hard to do as "cheat" (i.e. variant that can grow faster) will dominate. Biofuel research suffers from this as the fatty acid biosynthesis pathway is highly expensive energetically and cheats eventually win despite the most complicated safeguards.

Alternatively could we genetically strip the bacteria of all other functions other than procreating and photosynthesis? Making this bacteria live in a "bubble" would mean it wouldn't need a lot of defense mechanisms. This could make a single purpose bacteria that would be super efficient at doing this single task.

The carbon will be a problem, so you'd need to make biomass or some value added compound.
Three additional points:
Green biotech
There are many "green biotech" companies out there and there is an increasing number of green chemistry awards going to biocatalysis (enzymes for a reaction) and in some cases synthetic biology processes (whole enginereered organisms for a product or intermediate). But the former field is slow at growing because it needs to compete against a century of homo/heterocatalyis (normal chemistry), while the latter needs a lot more technological innovation to improve the production chassis (e.g. cheats, slow reactions, iron-sulfur cluster over-expression and electron balance are common issues: hydrogenase is a classically cited example of a hard target with great potential).
Note that most green biotech uncouple the process and use the biomass from regular algae or plants to feed their engineered organisms, as it is easier and there are less containment issues.
Algal blooms
In the comments I mention, iron fertilisation of the oceans (a ship releasing a container size of nutrients across an oceanic crossing is make a substatial planktonic boom, which either increases fish levels or sinks and thus buries the carbon it converted into biomass). This is a curious case of huge scale and cheap algal farming. But we don't know all the details, yes we'd be turbocharging the oceans (which are barren relative to say a jungle), but we may favour toxin-releasing algae, jellyfish and imbalance fisheries and actually send to extinction others.
Bioreactor in the ISS
The Internation space station splits water to make oxygen, dumps all carbon waste outside (CO2 and ...) and has water and food shipped up. This is odd as you'd expect they would be the first to use algae to scrub CO2! However, things are changing: they are trialing an algal bioreactor, which on a larger scale will result in a near-closed loop system. However, there are many engineering and some biological issues that need to be faced.


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Is gibberlic acid present in monocots or not?
As gibberlic acid is a PGR and helps in elongation of stems like in sugarcane,so,if it is present naturally in monocots then rice should also have.
And on other hand foolish seedling disease is caused by a fungus Gibberla fujikoroi with activated substance Gibberlin,then it should not to be said as a PGR for rice seedlings

What do you mean by PGR? Plant growth regulator, plant growth retardant, or something else?

Plant growth regulator

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Yes, gibberellins (of which gibberellic acid is one member) are present in monocots, which both produce the chemicals and are sensitive to their effects.
In fact, gibberellins are important hormones in all seed plants (and possibly seedless vascular plants). The receptor for gibberellins, GID1, originated with the origin of vascular plants, and one hypothesis is that the canonical gibberellin signalling pathway originated at this time. This study looks at the evolution of the gibberellin signalling pathway.
Gibberella fujikuroi is a fungus that also produces gibberellins (but uses a completely different pathway), and it seems that the fungus takes advantage of the plant's response to gibberellin and the resulting stem lengthening.


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What does 'percentage of participants with Recurrence-Free Survival (RFS)' mean in a cancer clinical trial?
From what I have been reading, in most cases, recurrence-free survival (RFS) is defined as the time from date of randomisation to the date of recurrence of disease (e.g. tumour growth), or death due to any cause.
What about the percentage of participants with RFS?
I have seen clinical trials with primary outcome measures like: 'Percentage of Participants With Recurrence-Free Survival (RFS) At X Months Among All Participants'; let's say that from the result they got a percentage of 80% for Group A and 50% for Group B, what does this '80%' and '50%' exactly mean?
Here is my guess: the higher the percentage of RFS among participants in [a certain time frame], the higher number of participants have not experienced any disease progression / death. Therefore higher % of RFS, the more effective the treatment is. (As for my previous example, Group A would be more effective than Group B).
p.s. I'm a high school student, apologies if I have missed certain information or have misused some medical terms. I would appreciate it if someone can clarify this for me. Thanks :)

Short answer: Yes, your guess is right.
Cancer treatment has the problem that it has to catch all malignant cells. The more effective a treatment is the higher the chance for reaching this goal and the lower are the chances for disease recurrence.
I a clinical study you usually test a new treatment against the current standard (placebo treatments are not seen as ethically justifiable) to see if the new treatment is better. There are different possibilities to test the outcome, recurrence free survival (RFS) is one of them. It marks the time between the treatment until recurrence of the disease (or death occurs).
So if the new treatment has a higher percentage in the PFS for a certain timepoint than the current standard of treatment, it is better in treating the disease, if the percentage is lower, the treatment is worse.

Thank you so much for your answer; it really cleared my doubts :) Do you have any related sources for this question that I can read/cite? It would help me invaluably with my dissertation.


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Does individual differences in pain tolerance impact the pain score rating?
I have been looking at clinical studies due to self interest. In studies where the severity of pain is evaluated, a pain scale with a pain score of 0 to 10 is often used.
However, since different people would likely to have different tolerance to pain as well as difference in describing the sensations they feel, would this impact the pain score given from the patients? If so, would this cause a significant error or bias in research studies where the pain score is used as a measuring outcome?

I think the far greater problem is with the physician's perception of the patient's pain, with underestimation being a major problem.

Short answer: yes. Pain-reporting (especially on the standard 0-10 scale or Wong-Baker Faces) is subject to significant amounts of bias due to a multitude of factors.
In one study (citation below), it was found that people tend to overreport their pain levels due to:

Wanting to enhance the provider's belief and responsiveness
Increasing the likelihood of receiving pain relief
Fear of future pain or potential illness

On the other hand, people underreport pain due to:

Concerns about how their pain affects and is perceived by others
Financial concerns

***But there could be a new way to figure out severity of pain using biomarkers or brain activity (https://www.bbc.com/future/article/20230414-the-search-for-an-objective-measure-of-pain)
Boring, B. L., Walsh, K. T., Nanavaty, N., Ng, B. W., & Mathur, V. A. (2021). How and Why Patient Concerns Influence Pain Reporting: A Qualitative Analysis of Personal Accounts and Perceptions of Others' Use of Numerical Pain Scales. Frontiers in psychology, 12, 663890. https://doi.org/10.3389/fpsyg.2021.663890


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What are the constraints on an operon?
From what I understand, the term operon is loosely defined to be a collection of genes that are found to be in the same proximity in a genome.
Some definitions enforce that an operon is only regulated by a single promoter and all of the genes are transcribed together.
If the above definition is strict, that would imply a couple of things

Genes are opposite strands cannot be in the same operon (since they cannot be transcribed together)
Overlapping genes cannot be in the same operon for the same reason.

I realize that part of the issue with these definitions stems from an ongoing investigation behind this phenomenon.  But are there strict standards surrounding the definition an operon? What is the minimal definition of an operon?
Relevant links

What is an operon?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4161906/pdf/12864_2013_Article_6422.pdf
https://en.wikipedia.org/wiki/Operon

From Henderson's Dictionary of Biology 14 ed. An operon is: a type of gene organization in bacteria, in which the genes coding for the enzymes of a metabolic pathway are clustered together in the DNA and transcribed together into a single mRNA. This mRNA is then translated to give the individual proteins. The expression of all the genes in an operon is controlled by a single promoter.
I'm not sure what an overlapping gene is, but according to this definition, yes genes on opposite directions of a promoter or different loci cannot be a part of an operon because they wouldn't be on the same mRNA.


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Could old-style "inoculation" be used against COVID-19?
Before the first vaccination was invented, for smallpox, there already was a technique called inoculation or https://en.wikipedia.org/wiki/Variolation. Unlike vaccination where dead or modified viruses are introduced to the immune system without causing an illness, in those old-style innoculations, people were infected with real live smallpox viruses, but not through the normal infection mechanism (the mucus membranes) but through scratches in the skin. Apparently when the virus arrives in the "wrong" organ, it can't cause as much damage quickly, but still the immune system gets a chance to prepare antibodies for it - so at the end the individual does get sick, but it's a much milder version and not as deadly.
Could we do something similar for COVID-19, i.e., deliberately infect at-risk individuals in locations far away from the pulmonary system (e.g., scratches in the skin) hoping such innoculation will indeed cause disease but a milder and less deadly version?
Is there any reason, besides the ethical questions of how to test this approach, why such an approach might not work? (again, "work" here means reducing the morbidity rate. It will not reduce the number of people sick, unlike a proper vaccine - it should just reduce the number of critically ill and most importantly, the death rate).

SE Biology is concerned with the mechanisms of biological processes, and questions are generally answered by people with biological rather than medical or epidemiological expertise. Although I understand your concern about the coronavirus outbreak, your question asks for subjective view on a proposal for combating the disease. Such questions are off-topic here. I advise you to consult more appropriate reputable sources for such information, some of which are listed here.

My question is not about epidemiology - the spread of viruses - it is about viruses, the human immune system and the (now considered antiquated) concept of inoculation. I think all are biological concepts, and not "subjective" in any sense, nor "medical" (the question was not about how to treat a certain person given his symptoms).


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Have we found any other life form outside our planet?
I'm not asking about the possibility of formation of life on other planets instead has there been any real evidence of life(such as micro organisms or even very basic structures) that might suggest an evolutionary path(for example from asteroids that hit the earth or planets and other objects in the solar system)?

You really think there might be such evidence, but somebody’s keeping it from you?

@David No not really but I'm trying to get a good grasp of evolution and it seemed only logical that simple life form might exist even in our solar system and no recent exploration mission or revelation came to my mind!

You say you want to get a good grasp of evolution, but your concern seems to have nothing to do with evolution.  In essence you are asking whether life originated from non-living matter (abiogenesis) here on earth or somewhere else in the universe. The latter idea was proposed by astronomers (Bernard Lovell was one I seem to remember) — some would say because it provided an easy way of avoiding a difficult problem they were unable or unwilling to tackle. Do your own homework on that.

No, there has been no evidence found of extraterrestrial or off-Earth life, at least as publicly-shared information. Via NASA:

No life beyond Earth has ever been found; there is no evidence that alien life has ever visited our planet.

There is some debate about this, but there's a chance that we have found alien microbial fossils.  In 1984, a meteorite that originated on Mars was found in Antarctica.  In 1996, odd microscopic formations were found inside that resemble known fossils of bacteria.
The visual resemblance to fossils alone is not enough to prove it is truly evidence of alien life, but it's the most compelling piece of evidence we have now.

It seems controversial since there isn't just much data to support it but can we assume that further exploration on Mars could actually reveal the existence of extraterrestrial life?

@Matt It's possible, but currently there's no concrete evidence.


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Is there a way to compare two treatments with no shared outcome measures?
For context, I am performing a comparative effectiveness research study on Drug A, Drug B and Drug C. I want to identify the drug with highest efficacy, out of the three drugs.
Let's say that from three separate clinical trial results, I have reached to the conclusion that:

Drug A > Drug B (i.e. Drug A is more effective than Drug B)
Drug C > Drug B

Now, I have to compare Drug A and Drug C. However, I cannot find any shared primary/secondary outcome measures from the trials I am looking at, therefore I cannot make a indirect comparison.
My question: Is there a way that I can approach the comparison of Drug A and Drug C, given that they do not share any common outcome measures? I do not have advanced statistical knowledge, so my only shot to attempt this comparison through a simple indirect comparison, therefore I am aiming to make an approximation only.

Even comparisons with the same outcomes across studies are fraught: the groups studied are not the same, even if inclusion criteria are similar.

Combining results from different clinical trials is called meta analysis. You say "I do not have advanced statistical knowledge" and yet you're attempting to do what is arguably the most difficult type of statistical analysis.

I'm glad you got a comment on this. I've been trying to come up with any criteria for "effective" that doesn't need to be followed with "for..." and I can't. Even if a drug (A) were 100% effective at .1 mg/kg for the treatment of (condition X) while another drug (B) was 100% effective at .15 mg/kg for (condition Y), what would that even mean? If drug A treated runny noses and drug B treated psoriatic arthritis, should a drug company pursue development and marketing of drug A over drug B? The reason for the drug needs to be considered.


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Calculating F_IS, F_IT on ancient DNA
I am trying to calculate genetic diversity within a handful of ancient communities. I have 1240K genotype data (made pseudohaploid), and I need to generate statistics to estimate the levels of genetic diversity within these populations.
I was looking at F_IS and F_IT. Does anyone have any recommendations on how to calculate these on pseudohaploid aDNA. I have the data in Plink format.


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Skeletal remains on the beach
We were walking along the beach in FL and came across this skull and we’re wondering if anyone e could help identify it!


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Does sectioning of sporangia of ferns kill the spores inside the sporangia?
In certain religions like Jainism, killing, or eating of seeds or unicellular microorganisms is banned. Does sectioning of sporangia kill all the spores? And by the way do the spores form a part of parent generation, or the offspring generation? Are the spores fully developed in the strobilus before dehiscence?

Welcome. In general, focused questions are best and a great way of doing this is by asking a single question per post (not 3 as here) and to add your research efforts so far; the second question seems readily answerable with an internet search. Further, if this Q pertains to adhering to religious values and norms, I would strongly recommend to ask this question on another stack and delete it here. Perhaps the site on vegetarianism and veganism can be of help.


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How do Ocean Ecosystems support high trophic level predators?
Ocean Ecosystems have carnivores that can exclusively hunt other carnivores. We know that Otodus Megalodon occupied such a high tropic level that it ate animals that would've eaten today's orcas.
In terrestrial ecosystems, large carnivores hardly ever target smaller ones, rather opting to target herbivores. Of course, in rare instances, a lion would target an adult cheetah, but ocean carnivores have adaptations to target others (eg. Orca's using waves to knock a seal into the ice, Great White Sharks leaping out the water to ambush a seal)
I'm wondering how oceans can support so many carnivores at higher tropic levels and what environmental conditions make carnivore hunting carnivores less common in terrestrial ecosystems. (The Morrison Formation had a lot of carnivores but Ceratosaurus and Saurophaganax aren't believed to have had a predator prey relationship like Brygmophyster and Megalodon)

Welcome. I think your question contains some mistaken assumptions and some conflated ideas. 1) terrestrial carnivores do eat other carnivores (e.g., multiple vertebrate groups including many canines, snakes, raptors, and even felines and primates). 2) big size is not automatically the most important/relevant indicator of trophic level (e.g., bats, ocelots). 3) your ultimate question is really framed as 2  (site policy is that posts should ask only 1 question, so please edit) -- 1 is about abundance (despite the rest of your post focusing on size or frequency)  and 2 is about frequency again.

I would suggest 1) editing your post to focus on one concept/question and 2) if possible, trying to look into and include any support for your underlying premises (e.g.,that higher trophic level consumption is rarer on land). Both will improve your question and will help any potential answer writer provide a more directed response to address your core interest. As of now, I think any potential answer would have to first address some of the issues I have laid out. So, please [edit] as you're able, and if you haven't already check out our [tour] and [help] pages. Thanks!

look up secondary consumer, tertiary consumer, quaternery consumer, and apex predator. because your assumptions about the land is just wrong.


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What kind of bug it is?
I saw dozens of this bug in my kitchen. They are smaller than one millimeter and they crawl and jump. Can someone help me please. Thanks

Welcome mohammad. Could you add the detail of your location for reference.

Thanks. I live in Iran, Tehran.


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Research databases
So I'm just a lay person who likes to read about human biology/medical research but I dislike reading what so and so thinks of certain studies from pop articles. I like reading them for myself and I was just wondering which peer reviewed databases are the most reliable and accessable in your guys opinions?  I think researchgate is pretty good but I find navigating around the sign up inconvenient since you have to be working with a relevant company to join.  I hope I worded this specific enough thank you all who answer much appreciated!

Too much informality and opinion in the question for the forum ( i didn';t downvote as you have 1, other humans delight in downvoting cos their innately apathetic) ... I check https://scholar.google.fr/ and i check  "abstract" with the keywords in google search.

So post with more formality and less opinion next time?

Yes it's good to practice writing same as the articles that you like to read rather than the pop articles than you dislike reading :) when someone downvotes you you get -20 and fast you are restricted from the website.

Your title is confusing. Databases are a resource for research but not research, and are not peer reviewed as such. You are not asking about databases but scientific research. This is likely to be voted as off topic because opinions are subjective (I wouldn't recommend you follow the advice of tsttst if you are a lay person.) Is Scientific American or New Scientist what you are after? The News and Views section of Nature and the corresponding section of Science are also good. But you get what you pay for, and journalism costs.

Mendeley database repository, which is driven by an Editorial Company (Elsevier) and is free-access even as plug-in for citation in word, which is highly convenient: https://www.elsevier.com/products/mendeley

Pubmed is the major database for biomedical research articles. Especially if you know what you're looking for, it should be easy to find.
Google scholar will also compile things that are not peer-reviewed journal articles. Sometimes that's useful (e.g. PhD theses) but you will have to be a little careful.

Google Scholar is good, since it searches all kinds of databases and gives you different options to view full articles.  If you use Mendeley and get Mendeley Desktop, you can import articles that you like and it will often suggest other articles you might like as well.  I know what you mean about the pop articles, they're often misleading ;)

I've known about Scholar for awhile and never checked it out till last night I only spent a couple  minutes on but it does seem pretty good. I've spent the last half hour on Mendeley on your recommend and I like it alot so far very organized and easy to use in my opinion thank you very much.

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


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Use lab agar for cooking
Our lab manager suspect that something wrong with our lab Bacto agar (Difco). So she decide to throw it to the garbage. I think that it's just a waste to throw that thing.
Can someone think of reason why don't use that agar for molecular cooking in my kitchen?
(My lab manager think that i am totally crazy without give any reason)

I'm voting to close this question as off-topic because it has nothing to do with either biology or biological techniques. There may be some other SE site (Health, Domestic Science?) where it is appropriate, but that's for the poster to find out.

If there are reasons to not use it for lab stuff, maybe there are reasons for not using it for cooking either.

Technically agar has first been used (and still is) in the kitchen and then adopted to the lab.
In the 19th century, gelatin was used in the microbial laboratory. The problem is that gelatin is much less thermostable than agar and at higher cultivation temperatures plates will melt and get liquid again.
In 1882 the german microbiologistt Walther Hesse (at that time an assistant in Robert Kochs laboratory) followed the suggestion of his wife Fannie Hesse to use Agar instead of gelatin. See the two references for some interesting details.
I personally would never use anything which comes from the lab in my kitchen since you never know if there are any contaminants in there. This is also probably the reason, why your lab manager doesn't want you to have it.
References:

Walther   and   Angelina  Hesse-Early Contributors  to  Bacteriology
History of the agar plate

What kind of contamination should I suspect? We use specific spoon to take out the agar from the box that used only for this.

The agar doesn't care where it is prepared, however, I am 100% with Chris on this one, I wouldn't use any coming from the lab for fear of contamination. I don't know what kind of organisms you work with and what you may find in your environment but generally it is not a good idea to mix things that were used in the lab with things that you use in your kitchen.

I don't think that I need to worry from the bacteria that I have in my lab more then the normal bacteria that I (probably the same) have in my kitchen. I am more worried if they use something in the production of the Agar that is toxic to people.

@Moshe I think more about lab chemicals which are present where agar gels are prepared like Ethidiumbromide. Or people using dirty spoons/spatulas before going into the agar. The agar itself is prepared from algae and my guess (although I don't know for sure) is that the lab agar is pretty clean.

@Chris TNX. like I said before we dedicate special spoon for each reagent in the lab. so i don't think that i need to worry from that (BTW the box is open but i pretty sure that they used it only once or twice). PS - ethidium bromide have very bad reputation compare to the risk that it made https://bitesizebio.com/95/ethidium-bromide-a-reality-check/

If we are worried about stuff from the lab being so contamined that it could be unhealthy, shouldn't be worried about that same stuff contamining other experiments? I would expect some experiments to be even more sensitive to contaminants than our dishes are.

@Pere In general you are right. But: This is a general precaution to avoid harm. We have a number of substances in the lab that can be nasty.


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Why does a stronger heart cause blood pressure go down
Intuitively, why does a stronger heart cause blood pressure to go down? The answers I've found from a cursory google search seem to indicate that it has to "work less hard" to pump the blood and that it "beats more slowly," but I do not immediately understand the implications of this.
Furthermore, if it is due to a slower heart beat in a stronger heart that blood pressure is lower, then how does (/is it true that) blood pressure remains lower in those with a stronger heart during exercise? Wouldn't a stronger heart beating just as fast as a weaker heart lead to higher blood pressure?
Thanks for any help. :)

Welcome to Biology.SE! I think this might be a better fit for [medicalsciences.se]. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

My intuition may be wrong, but see Bernoulli’s equation for an incompressible fluid. Modeling the circulatory system as a closed loop, the pressure exerted on arterial walls by blood decreases with increasing blood velocity. Assuming a stronger heart pumps blood faster, a stronger heart should reduce blood pressure compared to a weaker heart and slower blood flow.

Use of the word “stronger” is not clear. The flow rate needs to be considered and those who are very fit have a lower resting heart rate, a higher maximum and tend to need a lower beats per minute when doing the same exercise level as an unfit person.

A heart that is stronger (bigger; thicker walls) does not need to work stronger. In usual circumstances, the strength of a healthy heart has nothing to do with blood pressure.


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Why is the body not able to "detect" imbalances and defects on its own?
We all know, our body is able to roughly localize pain sources or react to imbalances or defects:

the stomach hurts because we may have eaten something spoiled,
muscles hurts after exercising too much,
we feel dizzy after we drank too much alcohol, and so on.

However, the body is not able to "detect" most of the  imbalances and their causes on its own. We certainly do not know why exactly we feel in a certain way, or which current issue is causing pain. We can't "listen" to our body to find out why we feel uncomfortable.
Let me give you some examples:

Our hand hurts because of the carpal tunnel syndrome, but we only receive the information that our hand hurts.
We feel tired, dizzy and suffer from headaches because of a vitamin D deficiency, but we only feel tired and dizzy instead of knowing that we are missing on the vitamin.
Our body reacts to a virus like influenza with the typical flu symptoms. But the body does not tell us, that it's a virus infection right now.
Rather hard example: we experience pain the left arm and feel uncomfortable around the heart area, and we can only assume that it's a heart attack. But the body does not tell us that the heart is having issues right now.

Why, from a biological perspective, can't we "listen" to our body to find out the real causes for our issues, and not only experience some symptoms? What would our body need to actually be able to tell us what's wrong?

People can have issues growing and developing properly as children, yet you can see at 2 kids who didn't grow properly, see that they have the exact size yet realize one didn't grow because of problems related to growth hormones while the other's issue is related to the thyroid gland.
Your body can have a great understanding of itself and what it needs. It will tell you when to drink, when to eat and even what to eat depending on what you need, because, for example, it can feel if you're going a bit low on sodium, and so causes a craving for saltier foods it knows will fix that.
That said your body isn't perfect. Let's go for your examples:
Why can't my brain detect my pain is because of carpal tunnel syndrome?
Well it is simple: carpal tunnel syndrome isn't the only reason your hand can hurt. Hell, the only reason it hurts is because the nerves are being compressed, and the signal they can send as a result of that can be caused by a myriad of factors, like inflammation of nearby muscles, excessive cartilage growth in cases like acromegaly, or even other issues such as nerve damage. Which is it? It can't know, but it Can tell you something is wrong and that you probably should go easy on that hand for a while.
Why is my body not telling me I'm having a heart attack instead of saying "hey my arm hurts"?
Here's an easy exercise you shouldn't engage in: spin in circles until you're very dizzy then book it towards an open door. You hitting your face or other parts of your body on the sides of the door is basically the you equivalent of irradiated pain. Your heart has both pain receptors and a Bunch of specialized built in reserves and mechanisms that exist solely so it can resist not having oxigenatd blood pumping through it for a time until things hopefully fix themselves. That said the same nerves that provide information from the heart provide it to other parts, and so the pain stimulus coming from your chest can get confused by your brain for pain in other more superficial parts of the body. Other than that, there's not much you can do other than going to a hospital anyways (and I'll get to this part in a bit).
Why won't my body tell me I have influenza?
Honestly, how could it? Until you develop proper antibodies that target that virus specifically, your body isn't even sure what it is fighting, just that it is causing issues to you (many of the symptoms you feel a direct consequence of your immune system trying to eliminate the threat). Add to that how influenza isn't just a stagnant virus, but one that mutates so violently there's essentially a new strain every year and its impossible for your body to tell you "hey by the way, we got influenza", because in practice, its not influenza, or at least its not the same influenza as last year. Your body knows this (though it has no clue what "influenza" is), but you may not.
For your body to be able to identify a virus or a bacteria, it'd need to somehow be able to interpret all you know about these and compare it to each microorganism it has a track record of in the form of the immune memory it has stored, and even if it could, it probably would only be able to tell you "hey by the way the thing we just fought looks like it was some kind of bacteria". You don't know every single type of virus and bacteria or how each works or how they do on a chemical level (the one your body mostly deals in), and these types of organisms are constantly changing, so what defines a certain virus today may not define it in a week (see HIV).
So why can't your or my body just tell us what's wrong?
To put it simply: because hospitals weren't a thing while we evolved into what we are.
It is easy to look at this from a perspective of "if my stupid body would tell me what's wrong I could get help from a doctor or treat it with the right medication", but throughout most of your evolutionary history, your body was on its own, at best being helped to maintain itself by your gut bacteria and other mutualisitc microorganisms. If it is facing is a weak virus or a potent bacteria isn't the main concern. Hell, there are times where Even if it could tell what's wrong, it wouldnt change a thing. Even if you're a trained doctor with full knowledge of what to do, if you have a heart attack or a stroke while alone in a field with no immediate help around, its over for you.
To better illustrate this: If I were to put you on a battlefield where you're suddenly bombarded by enemies, does it matter what flag they bear or what they're known as? Sure, your superiors would probably want to know what you're fighting right now, but right now what matters is figuring out where they are and how they work so you can eliminate them before they can eliminate you. AHell, once you know who you're fighting you tell your bosses, but they may not know the enemy by the name you gave them. What if, let's say, the enemies drop a bomb right on you? or if the place you're fighting in is hit by an avalanche? well, let's just say knowing how strong is the bomb or what caused the avalanche won't really change the outcome.
With all that said, under normal circunstances our bodies have an absurd amount of processes constantly regulating everything and making sure we have everything we need to survive and keep going, processes that, from an evolutionary perspective, you don't need to worry about or even be aware of, because you're already subtly told what to do all the time: Your brain constantly receives and sends messages on how everything is working. Dozens of minuscule operations rid you of would-be tumors daily, and your levels of calcium (a substance crucial for several crutial biological processes to function) are quite literally managed by the minute. Your cravings, apetite, actions and desires (be it to sleep, to do something, etc) also often reflect your needs to various degrees, as your body can  and does subtly induce you to act in ways it thinks will cause you to do what it at least thinks it needs you to do to keep yourself safe, healthy and happy.
Your body talks to you all the time, but your body isn't a doctor, nor does it really understand what a doctor is. It is also not infallible in its objective to preserve itself, but those 2 issues is what we have hospitals for.

Thank you very much for this thorough answer. Very helpful in understanding the reasoning.

As cooperative entities (cells) form a larger body, the larger body takes up functions that are beyond the scope of an individual cell. This involves storing and processing information at a higher level of abstraction and quantity. Your blood cell wouldn't be able to understand what a computer is, in the same way your blood cell doesn't expect you to understand how it recognizes a virus, because as a large body, you cannot see the virus.
This is very similar to how a Prime Minister may not be able to understand all the complexities of building a rocket, but he/she can direct a space agency to build one. If there any problems, the space agency can convey that to the Prime Minister without going into detailed explanations, because he doesn't need to know anything about the equations of the rocket's trajectory. He just needs to know information at a larger scale.
So the answer to your question is that we can't "listen" to our body because everything is happening on a microscopic scale, while our large body is tuned to have senses which "listen" to macroscopic phenomena.


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What kind of mushroom is this? Found in SF
We found this on a trail in San Francisco. Could someone please tell me what kind of mushroom this is?


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Is there a biological or technical reason for a 40 Ct cutoff in nucleic acid detection assay?
I have developed and validated a modified a nucleic acid test (NAT) for SARS-COV-2 detection using real-time RT-PCR (aka rRT-PCR, aka RT-qPCR). My assay is not for diagnostic use, but for donor screening (which are similar, but different enough to require independent validations). The PCR step is sensitive enough to detect a roughly a single gene copy per reaction, but not always with a sub 40 Ct (which may or may not be an issue).
You see, the protocol is built around the primer/probe sets first published by the US CDC, so I initially adopted the criteria in the CDC EUA protocol, which stipulate a Ct value < 40.00 to classify a target as positive. This means is that amplification with a Ct value of 39.99 is classified as positive, while a nearly identical amplification curve with a Ct of 40.01 is classified as negative. Looking at similar NATs for in vitro diagnostics, most use this same cutoff. It seems fairly common with tests for other pathogens too.
For a little background, using a cutoff like this reduces the potential for subjective classification errors between users by providing a qualitative, binary interpretation for an ostensibly quantitative data readout. The trade-off is that an improperly assigned cutoff can result in systematic classification errors that are universal among all users. Anyone who has used one of the protocols based on the CDC probes has noticed that the two primer/probes sets targeting the SARS-CoV-2 viral genome do not perform equally well. It's common for test results to be classified as "inconclusive" when one viral target is positive, but the other is "negative" because of a Ct value just above the 40Ct cutoff. (I've already tweaked my protocol to reduce this kind of error, but could not eliminate it completely).
As I am writing this up for publication, I'm wondering if it would be better (more honest) to recommend a Ct cutoff that reflects the empirical range of Ct values in my validation studies, as opposed to keeping it at some seemingly arbitrary round number (even if it is almost universal among similar tests). Doing so would not change any of the major findings I report (sensitivity, specificity, etc.), but would change some of the numeric values. More importantly, I think it could help prevent misclassification of late-amplifying samples as negative.
Does anyone know of a biological or technical reason why this cutoff should not exceed a Ct of 40? Maybe this is just some convention that is blindly carried forward; or maybe there's some quirk of TaqMan chemistry to justify this value that I'm just not aware of.

This is done because at some point you start amplifying nonsense and not get a meaningful signal. If (and this is most often not the case) you have the ideal doubling of you DNA template in each cycle, you can calculate how little DNA you start with to detect it only around cycle 40 - or the other way round: What you will amplify and see as a "signal" by then.
If you have templates which always really come this late, I would use more DNA (and probably more RNA to start the rtPCR) until this comes at least 2-3 cycles earlier and then do serial dilutions of your template to see if this signal is real or not. If so, you should see a relation between Ct and dilution.
For doing this you need a negative control which stays really negative until your sample signal shows up - which is tricky on its own because at some point you will see some kind of primer self-amplification. If this occurs in the same range as your sample, your signal cannot be used. If no other primers can be used for technical reasons, sometimes nested PCR has to be considered.
And last but not least all your reagents degrade over time by cycling them 40 times through the PCR program (also the polymerase), which affects the efficiency of the reaction.

I know this applies to SybrGreen assays, where fluroescence is a measure of total DNA present, but with TaqMan chemistry, fluorescence should only increase when both probe and primers match. My NTCs and negative specimen controls never come above baseline over 45 cycles (have run literally dozens of plates at this point).

The signal is definitely real. Have done 10-fold and 2-fold dilution to extinction series in my reference matrix to establish the LOD (20 independent reps per dilution in the 2-fold series). Viral copy numbers quantified via digital PCR. Plus, each sample is assayed with two different primer/probe sets targeting the viral genome plus an internal amplification control. The more efficient of the two viral targets maxes out around Ct 37-38, while the other set lags by ~2-4 Ct (max around 42.5).


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Methods for getting clean C. difficile spore preps without spores clumping together
I'm a microbiologist recently who recently started working on an ongoing C. difficile project for the first time. One of the things I need to do is verify the lower detection limit of my qPCR detection assay (C. diff Toxin B gene) using C. difficile spores spiked into negative clinical specimens. I also need to obtain accurate viable spore CFU counts in order to generate the appropriate spore titers for animal experiments. I'm trying to get a clean spore prep free of vegetative cells (for the spore detection assay), and minimize the number of spores clumping together to obtain more accurate CFU counts (via plating heat-treated spore dilutions on BHIS+taurocholate germination plates).
I'm working with the C. difficile strain 630 (ATCC BAA-1382), a lab strain that's notoriously not the best sporulator (we use 630 because it's toxigenic and infectious, but not highly virulent. This helps minimize animal suffering in simple infection models where we don't need to look at toxicity).
There are a few commonly cited C. difficile spore prep methods that I've been working from, and in some cases trying to mix and match possible solutions from different protocols, but none of them were use this particular strain in the methods papers. Our lab SOP uses Clospore medium, and that seems to give me the best sporulation rates compared to the solid 70/30 medium used in the STAR protocols paper. But when I follow the rest of the Clospore protocol for spore collection and purification I end up with highly concentrated vegetative cells and am getting lower viable spore titers in the "concentrated" spore prep than there are in the unconcentrated cultures (by multiple orders of magnitude). The spores I do recover are mostly clumped together into large clusters when viewed under phase contrast microscopy (possibly explaining the lower spore CFU titers).
If anyone has experience with getting really clean C. difficile spore preps with minimal spore clumping (especially in 630), I would love any tips or advice.
Potential solutions that I've tried without success:

Saving the pellet wash supernatants and re-pelleting with a longer centrifugation: This does recover some spores with almost no vegetative cells, but they are very low titers and still have clumping issues.
Using room temperature water instead of cold water for washing the spore pellet, (it's been reported that cold-water wash induces more clumping): Mine still clump with room temperature water, and there's no difference in terms of vegetative cells.
Separation of spores from vegetative cells using a 50% sucrose gradient centrifugation: This does separate out a lot of cellular debris, but the intact vegetative cells pellet out with the spores, and still has spore clumping issues. Plus I'm losing a lot of spores when I do this (possibly due to extra wash steps needed).
Washing with 0.05% TWEEN/Polysorbate (nonionic surfactant): This actually helps to free up spores sticking to the culture tubes, but they still clump together when washed to remove the TWEEN (polysorbate has toxic effects in mice, so washing it away in not optional).

I’ve had similar poor luck getting sufficient spore concentrations following this protocol and using ATCC strain 9689. Lots of vegetative cells, few spores. One recommendation from that protocol is to use PBS + 1% (w/v) BSA to resuspend spores after washing to prevent clumping, per Edwards et al.

@acvill Thanks! I'll will try that for sure.


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Would this be classified as a cross-sectional study design?
Let's say I'm conducting a study in which persons recently diagnosed with an infectious disease were recruited to provide a variety of different specimens and answer standardized clinical survey questions (with minimal follow up and no additional timepoints collected). The purpose is to study potential modes of transmission by correlating relevant clinical factors with quantitative infectious pathogen load found in different specimen types.
What's the most appropriate description of this study/recruitment design in the context of epidemiology or public health research?
I'm not epidemiologist by training, but I think I can rule out prospective recruitment along with longitudinal, cohort, and experimental study designs. It's not really a case-control study since there is no control group (hard with pathogen load as the primary outcome of interest). Basically leaves a cross-sectional observational study (unless my thinking is way off here).

Seems like this question would fit better on Stats.SE, though I personally feel like most of the study design terminology has little real use even though people in the medical field love to put those words first in their abstract.

generally cohort means you do your measurements (in each subject) at multiple points in time. Merely asking them to provide their own disease history etc. is still just cross-sectional.

IF the sample is representative of a population in some way, authors tend to add that to the title... so you see something like "representative cross-sectional". When it's a convenience sample though, they don't emphasize that :D

@Fizz - Thanks for helping to confirm my initial conclusion Fizz. Glad I'm not totally mistaken. I mostly asked so that I can provide some appropriate feedback to a colleague who asked me for edits on a manuscript.


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Would a size-specific, electrophoresis-based RNA quantification kit work for ssDNA as well?
I'm using a custom library of ssDNA oligos to test the performance of some qPCR assays with mismatched bases in various primer and probe regions, and I'm trying to come up with a good way to verify whether or not my results are due to differences in assay performance or differences in the copy number of fully synthesized templates.
Basically, the fragments I was asked to order were only available with the most basic desalting purification protocol, which does not include any fragment size selection and can therefore include incomplete or degraded templates. After verifying quantifications with absorbance- and fluorescence-based methods, there's not enough of a difference to explain my qPCR results. But, again, this doesn't account for any potential differences in fragment length/completeness.
I have access to an instrument that provides size-specific quantification and integrity assessment based on electrophoretic separation. But the available DNA kits use SYBR Green I, which is really a dsDNA dye and only weakly interacts with ssDNA. They sell RNA quantification kits using SYBR Gold, a better choice for ssDNA, but when I called tech support to ask about ssDNA, I got the boilerplate response. They haven't tested their kits for that application so they can't recommend it or comment on whether or not it will provide good results.
So I'm just here asking if there's some difference in buffer or gel properties that would prevent ssDNA from properly running on an RNA-specific electrophoresis platform. I've looked up a few standard RNA gel electrophoresis protocols and they all seem similar enough to DNA gels, so I'm assuming the instrument's RNA kit would probably work for DNA as well. Just wanted to see if anyone on here had specific experience that might contradict that assessment.


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Can the innate immune system defeat a pathogen by itself? Fast enough that we don't develop antibodies, etc.?
Would we have any way of knowing if our innate immune system destroyed a pathogen without involving the adaptive?
Could a symptomless person who tests positive for COVID-19 with the RNA test, e.g., later test 'negative' for exposure on the antibody test?

Generally antibodies are formed, but it is possible that innate immune system has cleared out the pathogen. But antibodies will be formed even after that, as adaptive immune system has received  the stimulating signals from helper T cells, which are matured during the innate immune responses triggered by an infection.
This signal triggers B cells to produce antibodies. Antibody production is activated because of signals from innate immune system.
So, even if infection is cleared by innate immune system, still antibodies will be synthesized.
Reference:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399021/
https://medicalxpress.com/news/2020-05-dont-antibodies-immunity.html

If the innate system is very fast at clearing the pathogen out, the memory B cells, responsible for antibodies production won't be numerous enough to provide with a good immunity.
Reference:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159104/


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What is the word for a group of genes inherited together?
I know the words haplotype and haplogroup, as well as genetic linkage, but...
I recently came across a new phrase describing genes which tend to be inherited as a group, and wrote it down, but now cannot find it...
Also, is there a word or phrase for genes which are expressed together?

"inherited together" (e.g. in linkage) or "expressed together" (e.g. coexpressed)? These are two different situations

@FabioMarroni — He wrote inherited. He is talking about genetic linkage. Why don’t you believe he means what he says? He asks a second question about expression, which is against the rules and also unclear because he doesn’t say whether he’s talking about eukaryotes and prokaryotes. That affects whether the one answer so far to that question is correct or not.

@David, you're right, I didn't understand that the second question was a separate question.

I believe you are referring to operon?

In genetics, an operon is a functioning unit of DNA containing a cluster of genes under the control of a single promoter. The genes are transcribed together into an mRNA strand and either translated together in the cytoplasm, or undergo splicing to create monocistronic mRNAs that are translated separately, i.e. several strands of mRNA that each encode a single gene product.

There is also a term called supergene which is in a way a less strict grouping, suggesting close genetic linkage and possible functional relationship.


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Where does free ammonium in peripheral tissues come from if oxidative deamination occurs in the liver?
I have a misunderstanding regarding how some claims about amino acids catabolism make sense together. Maybe one of the claims is incorrect by itself so I'd be happy to be corrected. Here is what I don't get:
It is said that in amino acids catablosim, first the amino acids in peripheral tissues transfer their ammonium to alpha-keto-glutarate to form glutamate (with the help of aminotransferase), and that the deamination of the ammonium from the glutamate is carried by glutamate dehydrogenase in the mitochondria. But it is also said that this second step occurs in liver, and that in order to transport glutamate do the liver, it should be converted to glutamine using free ammonium by glutamine synthase.
If so, where is that free ammonium in peripheral tissues come from, if oxidative deamination by glutamate dehydrogenase occurs in the liver? why do we even say that free ammonium is generated in peripheral tissues in the first place?
I thought that the free ammonium come from other processes, but it is generally said that the whole point of this process is to clean free ammonium from peripheral cells. Also I tried looking the internet but I found only more contradictions. I'm sure I have some misconception here and hope for a clarification, thanks in advance

Welcome to SE. Biology. Please do us the courtesy of finishing the [Tour]. Your question is full of statements about vague “claims” you have read and things that “are said”, but the world is full of nonsense, so if you want a response here, you need to document your questions by quoting the sources verbatim, and stating where they are from. This helps us see their context and also makes you reflect on what is actually written.


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Finding antibodies sequence online
Not sure if this is the right section to ask this question but here we go.
I want to find human GPCR antibody sequences online and download them. I had some trouble finding good platforms with good filters and downloading the results.
How do you go about finding protein/antibody sequences online? Is there a universal database for proteins? Are there different smaller databases that specialize in antibodies?
How should I go about this?
Thank you!

I don't know for Abs but proteins can be found on several NCBI sites as well as SwissProt, PDB and quite a few others.

I would suggest looking here at the PLAbDAb database, this appears to be an up-to-date antibody database including sequences.
I ran a quick query for "GPCR" and got a number of results including protein sequences.


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What is crawling on my curtain in the kitchen?
I found one of these crawling on my curtain.

Most likely a small beetle - which one would need better photos and a general location in the world as there are many many thousands (IIRC about 400,000) of beetle species world-wide.

I found out it's a biscuit beetle, a pest. Thank you for the advice: I'll be more specific next time.


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Are the Tm and Ta values of PCR primers based on entire sequences or just annealing portions?
I am trying to use the Q5 mutagenesis kit to produce an indel mutation in my protein.
I used the NEB BaseChanger interface to design my primers (https://nebasechanger.neb.com/). However, I am confused about the way NEB BaseChanger calculates the Tm and Ta of these primers. When it generates the primers, it indicates the Tm and Ta are in the low 60s. However, when I put the same primers into the NEB Tm calculator, I found that their Tm is in the high 80s.
I suspect this is because the NEB BaseChanger is not counting non-annealing bases (bases that encode the inserted amino acids). I am wondering which website to trust - I understand that if the Tm and Ta are what the NEB Tm calculator suggests they are, my PCR will likely not work. But if the Tm and Ta are what the BaseChanger suggests, the reaction should run.
Thanks for any and all advice!

The insertions don't count towards the annealing temperature, at least for the first and most critical cycle of the PCR. After the first cycle, where the bases get incorporated into the product, for the second and subsequent cycles these bases should matter, but the primers should match the target 100% (because of the incorporated primer) and a lack of efficiency caused by the high Tm doesn't matter because of the binding specificity.
Remove the non-annealing insertion bases before calculating the annealing temp.


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


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Why don't we find animal corpses and skeletons all throughout the woods?
Where in the forest do wild animals die?  I rarely (occasionally, but rarely) come across animal bodies.
Where are the large skeletons of bears and deer?
Detectives often investigate human bodies that were dumped months earlier.  They've partially decomposed, but are still mostly there.  Why?

Perhaps because very few animals die naturally.  They are killed and eaten.  I (or more often my dogs) often find bones of deer &c that have been killed and largely eaten by mountain lions or other predators.

Large predators can break up the bones to get at the marrow. This disperses the skeletons. But for the most part, bones are a good source of calcium, and are eaten by rodents. You can see evidence of this when you come across the gnaw marks that rodents make on the plastic boards made from recycled milk cartons. As for the reason that human skeletons are particularly resistant to this destruction, I have only a guess. Perhaps the first stage of destruction, the dispersal by large predators, is less common because these predators have been trained to avoid humans. I would also guess that many murder victims are concealed by the murderer.


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Why are O-antigens and H-antigens on (certain) bacteria called O and H?
Somehow, despite extensive searching, I cannot find an answer....
Does O stand for oxygen and H signify hydrogen?

The "H" and "O" identifiers first appeared in German-language publications around 1920 to describe different forms of disease-causing bacilli. Thankfully, Arkwright and Goyle provide an English explanation of the terms in their 1924 review.1

These writers called the two forms, which they described, the "H" and the "O" form, because in the case of B. proteus, the first bacillus investigated, the "H" form was represented by the normal, which grew with a spreading film (Hauch) on the surface of agar, whilst the "O" form, which occurred as a variant, grew in isolated colonies without any film (ohne Hauch).

The literal translation of Hauch is "breath", and ohne Hauch is "without breath", though some sources translate Hauch as "thin layer", which is probably the intended meaning.

References

Arkwright JA, Goyle AN. The Relation of the “Smooth” and “Rough” Forms of Intestinal Bacteria to the “O” and “H” Forms of Weil and Felix. Br J Exp Pathol. 1924;5(2):104-114.

As a German speaker, "Hauch" idiomatically means something like "a touch of ...", so "thin layer" is indeed an appropriate translation in this context.


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Why are odd numbers of chromosomes (triploidy, pentaploidy) less common than even ones (tetraploidy, hexaploidy)?
Perhaps there is an obvious reason, and I know that most organisms that are either exclusively sexual or at least capable of sexual reproduction are diploid, but....
Is there a specific reason triploidy seems to be less common than tetraploidy?
It seems like a weird coincidence for a normally diploid organism to produce two rare gametes with extra chromosome(s) at the same time, or to do so at the same time a neighbor does so....

Sexual reproduction means taking chromosomes from two parents. Most commonly, that means that each parent gives just half their chromosomes to their gametes, such that the offspring will have a full complement.
As such, at some point you have to multiply h*2, where h is the number of chromosomes that one parent donates, the "haploid", and 2 is the number of parents. It's possible that 'h' could be some odd number, like if each parent contributes 3 copies in the haploid case, but multiplying by 2 parents always gives you an even number in the offspring.
From there, it's straightforward to either get an extra or lose a chromosome somewhere, but improbable for it to happen for all chromosomes at once.
The Wikipedia page on ploidy is a good place to read about these sorts of things.


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Does feeding livestock antibiotics reduce their methane output?
Feeding antimicrobial to livestock willy-nilly to enhance growth and feeding 'efficiency' (or 'conversion') is controversial, of course, but....
Does this have the positive side effect of reducing the microbe-produced gases that the livestock expel via flatulence and education, such as methane?

“education”? Did your spellchecker dream this one up?

No “of course”. Only in countries where the interests of mega-agriculture outweigh those of public health.

There seems little evidence that it does, for if it did it would hardly enhance the growth of the livestock. It’s the methanogenic bacteria that enable ruminant digestion in the first place!
Biochemistry
The biochemistry of methane production in ruminant digestion is well described in a freely accessible review by Mackie et al. (2024). Although there are many different bacteria involved and a variety of pathways and intermediates, the important point is that methane production results from two separate processes, conducted by different bacteria. The first is the anaerobic fermentation of organic foodstuffs, which produces hydrogen gas. The second is the reaction of the hydrogen gas with carbon dioxide to form methane. This is summarized in this figure from the review:

The biochemical rationale for this is that the second step (methanogenesis) reoxidizes that NADH produced in fermentation to NAD+, allowing the first step to continue. The hydrogen is a necessary reducing agent in processes by which the methanogenic bacteria generate energy as ATP, methane being an unneeded byproduct.


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Why doesn't the immune system ever destroy the glucagon-producing alpha cells in the pancreas? Why only insulin-making beta cells?
Our pancreas does multiple thing, yet I only ever hear of the beta cells in the Islets of Langerhans being annihilated.
Why is this?
Hmmmm.....

I just now came across a very similar question... after I posted.... Still, it hasn't been updated, and I wonder if anything new is been discovered...

You should link the similar question so the readers can take a look.

As a result of differences in antigen presentation and recognition, the immune system targets the insulin-producing beta cells selectively within the pancreas, while the alpha cells that produce glucagon are left largely unaffected. There are a number of reasons why this might happen:

Autoimmune Targeting: The most important antigens implicated in the autoimmune response to Type 1 Diabetes (T1D) are major antigens such as insulin and its precursors. Beta cells express these antigens and therefore are the major target of immune cells (see reference 1 for more details).

Immune Cell Infiltration: Although numerous studies have shown that the immune cells that predominantly infiltrate pancreatic islets in T1D are biased towards CD8+ T cells against beta cells, the precise mechanisms that result in such selective targeting remain incompletely understood but are thought to include the unique antigenic properties of beta cells (see reference 2 for more details).

The Islet Cell Composition: Alpha cells are less affected by the autoimmune process. This may be due to their different location within the islet and their lower expression of the antigens that trigger the autoimmune response (see reference 3 for more details).

Conclusion: The specific antigenic properties of the beta cell and the targeting mechanisms of the immune system will explain why, in T1D, such selective beta-cell destruction occurs without a similar involvement of the alpha cells.
References

Beyond the Hormone: Insulin as an Autoimmune Target in Type 1
Diabetes
Characterization of resident lymphocytes in human pancreatic islets
Islet Remodeling in Female Mice with Spontaneous Autoimmune and
Streptozotocin-Induced Diabetes

The short answer is that it is these beta cells which produce Insulin, and since this may appear to be begging the question, consider the following argument in explanation.  Call it the 'Starving Queen Bee Hypothesis' of Type 1 Diabetes Mellitus.

Approaching the conundrum of type 1 Diabetes Mellitus that the body initiates or permits the so-called autoimmune destruction of insulin producing pancreatic beta islet cells, therefore effectively starving the body of glucose, as a detective story, in which one attempts first both to discern some underlying motive for such an assault -- and here it is further necessary to indulge the philosophical heresy that some deeper intention resides beneath such pathologies, that such disease syndromes as Diabetes Mellitus are responses to what may be regarded as more fundamental metabolic defects (not haphazard derangements or 'mistakes' in nature, rather variant configurations within it serving some more fundamental evolutionary purpose) --, and to ascertain which suspects or parties stand to benefit from it, consider as the first clue that as opposed to peripheral somatic tissue, the brain itself does not require Insulin in order to take up glucose; notwithstanding that glucose uptake by neurons is not entirely independent of Insulin, as was once thought, since GLUT-4 which transports glucose across the blood-brain barrier [BBB] is in fact Insulin-dependent.
Moreover Insulin itself is now known to cross the BBB, particularly in conditions in which the BBB is rendered more porous by various factors: systemic inflammation, certain EMR frequencies etc.  At the same time, it is not yet empirically clear whether Insulin detected within the brain and CNS, including in the CSF, is primarily or predominantly of peripheral or CNS origin, particularly in the context of the widespread distribution of Insulin Receptors in the brain.  In addition, given that there remains some scientific dispute about whether Insulin is synthesised in the brain, it is reasonable to ask whether such Insulin of CNS origin differs conformationally or otherwise at a molecular level from Insulin of pancreatic origin and is therefore potentially capable of being recognised as 'foreign' by immune cells.  This conjecture is potentially important in determining the mechanism of the autoimmune process, since it may conceivably be supposed that Insulin of peripheral origin is regarded as antigenically 'foreign' by immune cells within the CNS.
Continuing the argument then, imagine that in some critical group of neurons, some incapacity to metabolise glucose is inherent or innate, either congenitally or as a consequence of some early toxic insult to which given individuals are peculiarly susceptible, and that this intrinsic condition inevitably induces an insatiable craving for glucose, to the extent that in order to maintain what those cells perceive as a perpetually inadequate supply of glucose, the brain itself effectively orchestrates the immune-mediated destruction of pancreatic beta cells in order to circumvent the supply of that critical glucose to somatic cells necessarily mediated by Insulin.
Herein a motive is suggested simply by virtue of the observation that, as opposed to somatic cells, neurons do not require Insulin in order to transport glucose across their membranes; and it is in this sense that such a scenario may be considered analogous to that of a 'Queen Bee' starved of honey produced by the collective, and upon whose survival the life of the entire hive depends: in other words, if the Queen whose nutrition takes precedence is not receiving honey, no other bee will be permitted to receive it either, and the hive will die.
With respect to the identity of those critical cells in which disruption of glucose metabolism, innate or induced, threatens the entire human being, this depends on some inevitably speculative consideration of the precise mechanism by which such an autoimmune response is induced.  The most likely candidates are cells in the hypothalamus or possibly the brain stem depending on how the presence of Insulin Receptors and their role in the brain is to be understood, since for example, according to a number of studies, Insulin Receptors are most densely distributed in the hypothalamus and olfactory bulb, and least densely distributed in the brain stem; that is, sensitivity of Insulin Receptors to Insulin of CNS origin is likely to be greater in the hypothalamus and olfactory bulb; conversely, for those receptors in the brain stem. [3].
Accordingly, to take the argument further, it may even be that the critical cells in which this fundamental defect in glucose metabolism is present are indeed peculiarly susceptible even in normal circumstances to what would amount to the toxic effect of such peripheral Insulin; that is, presuming that these receptors are exclusively sensitive to Insulin of brain origin -- assuming that Insulin is indeed synthesised in certain neurons --, it may be that Insulin of peripheral pancreatic origin is forbidden in certain locations, such as the hypothalamus or olfactory bulb, and that its presence at that site would induce an immune response ultimately directed at pancreatic beta cells.
(Evidence of CNS control of peripheral glucose metabolism via activity of Insulin at CNS Insulin Receptors [1] may suggest the implication of the CNS in the autoimmune destruction of pancreatic beta cells).
To summarise, since this initial fundamental craving for glucose integral to CNS metabolism and energy demands induces transient hyperinsulinaemia peripherally in response to persistent hyperglycaemia arising from dietary excess, then in the presence of an associated condition of generalised systemic inflammation arising as the consequence of that excessive blood glucose (and saturated fatty acids) which presumably renders the BBB more porous and thus permeable to Insulin itself* (generally exacerbated by the ingestion of 'ultra processed foods'), an excess of Insulin effectively floods the brain.  The presence of such excessive Insulin of peripheral origin in the brain may represent the circumstance that it is regarded by local immune cells, particularly at certain critical sites -- around the 'Queen Bee Cells' themselves -- as effectively 'foreign', so that the concomitant presence of T-cells, including those admitted across the same inflamed and consequently more porous BBB, arguably induces the autoimmune effect, not upon Insulin itself, but as indicated in the previous answer, on the beta cells themselves expressing these antigens on their surfaces.

The mere condition of systemic inflammation itself is found to increase Insulin transport across the BBB, evidently separate from such increased permeability (although this effect of a so-called 'sickness syndrome' in such a condition of systemic inflammation raises the question whether the symptoms characteristic of that syndrome are not those of prodromal Diabetes Mellitus itself). [2].

Alternatively -- or even in conjunction with the above --, since beta islet cells are subject to neural control, both Vagal and sympathetic, and bearing in mind that the Vagus nerve is effectively part of CNS (with its cell body in the medulla), then it may also be presumed that the cell body of that nerve is to some more-or-less critical degree sensitive to glucose, and possibly to pancreatic Insulin itself, and that some loss of such sensitivity is implicated in the initiation of a cycle of hyperglycaemia/hyperinsulinaemia -- which is also to say that since such sensitivity to circulating glucose including in beta islet cells themselves under normal conditions is qualitatively equivalent to a condition of glucose toxicity, then the ensuing syndrome of autoimmune type 1 DM may be characterised as a condition of Insulin toxicity.
It may also be supposed that it is what amounts to an insatiable craving for glucose in somatic cells in which mitochondrial processes of glucose metabolism have become deranged -- viz, there is an increasing body of evidence and scientific opinion that this is due to the inflammatory effects of sugars and fats generally, and of these ingredients of 'ultra processed foods' in particular -- which is at the root of 'insulin resistance', the definitive condition in type 2 Diabetes in which cells become decreasingly responsive to Insulin synthesised and secreted in response to hyperglycaemia, exacerbating the latter and implying the tendency to fat accumulation in adipose tissue: in other words, in such conditions of 'insulin resistance', somatic cells are effectively starving: viz, obesity is a form of starvation.
[1] Insulin Action in the Brain [2021]: American Journal of Physiology [Endocrinology and Metabolism].
https://doi.org/10.1152/ajpendo.00642.2020 T
[2] Factors Influencing BBB Permeability.
https://doi.org/10.1016/j.brainres.2022.147937
[3] Insulin in the Brain.
https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2014.00161/full


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How did hydrophilic plants become established on an isolated island with an arid coastal zone?
I find unconvincing the existing explanation of how several hydrophilic endemic plants became established at St Helena. This is one of the most isolated islands in the world, has an arid semi-desert coastline and moist and humid highlands where endemic hydrophilic plants grow. It has been suggested that plants originally arrived either as driftwood from the beaches or arrived inland because occasional birds accidentally blown to the island had seeds on their foliage or claws. However, not only would the brushwood of these hydrophilic plants be unlikely to propagate or survive the arid conditions of the coastal region, these plants normally propagate by root, not by seed.
Has the following third mechanism ever been suggested for the establishment of plants on an isolated island? I wonder whether brushwood fortuitously arrived at the point where streams were discharging into the sea. Despite the arid conditions at all other coastal regions, some plants could take root at these wet beach areas and then spread along the streams growing in the damp alluvial soil into the interior heights of the island. I know the migration of plants along the length of a stream or river (riparian zones) have been studied but I can find no reference to the idea that this can also explain the presence of hydrophilic plants in damp highland regions of an island with a surrounding arid coastal region.

there is an important distinction between normally and only.