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What is the name of this creature?

What is the name of this creature?
It looks like either a crustacean or a conch.

Nautilus.

Nautilus belauensis. Licenced under CC ASA 3.0 unported, via Wikipedia 2022 from user Manuae.
Mollusca -> Cephalopoda (like squid and octopus) -> Nautilaceae ->  Nautilidae - comprising of six extant species.
They range the 200m to 700m depth of the Indo-Pacific, scavenging carrion.
They seem to have been more-or less the same over the last 500 million years according to the fossil record - then being up to 2.5 metres in shell diameter, being more modest now at a maximum of 22 cm (10 inches) when fully grown.
They move via jet-propulsion by drawing water in through their hyphonome, then expelling it with force, as seen in the "front view" here:

From Profberger at English Wikipedia, freely licensed.


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What came first: the ribosome in which RNA is read, or the RNA to encode for the ribosome proteins?
It's a bit like the chicken-and-egg problem. Ribosomes need proteins because they are partially made of them. Where can they get their proteins? They read the base sequence in mRNA entering them, assemble the amino acids, and spit out the proteins. The problem though is that the proteins needed for the ribosome need a ribosome in the first place.
I realize that it's a highly simplified picture I paint here, but I think its clear what I mean. Did proteins existed before RNA/DNA? Amino acids were created in a lab-soup already many decades ago, back in the previous century, and probably the same holds for RNA-kind of (small) structures. Did one of them come first? Did protein primordial life took advantage of self-replicating structures capable of storing information about proteins, or did the self-replicating structures took advantage of the primordial protein life to facilitate replication?

I suggest — and indeed this list requires — that you do a little reading on this topic, which was first raised over 60 years ago. Of course, we do not (can not) know that answer, but we do know that the ribosomal peptidyl transferase resides in the ribosomal RNA, so it is possible (likely?) that the original ribosome lacked protein, simplifying the question a little.

@David Thanks. That would simplify things. But what should be called life then? Proteins (which I assume were present), or self-replicating RNA-like stuff?

This question has also been asked several times before: see https://biology.stackexchange.com/questions/80603/what-created-the-first-ribosome

source: Stack Exchange

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

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How to distinguish hornbeam from hophornbeam?
The town where I live plants both hornbeam trees (Carpinus betulus) and hophornbeans (Ostrya carpinifolia) as street trees. How can they be reliably distinguished, especially when there is no fruit on the tree? The fruit is different but the leaves are very similar.
To be clear, this question is about the European-native species, not American ones.

There is a German-language article on the topic: https://www.zobodat.at/pdf/Fl-Austr-Novit_4_0032-0040.pdf

Both plants like similar mesic conditions and so can be found in similar locations. However, these plants are actually very easy to tell apart using only a few easily observable characteristics*.
Bark:

Ostrya is peely/shreddy brown

Carpinus is smooth and grey. The bark almost looks sinewy, leading to its much better common name: muscle wood.

Leaves are both doubly serrate and similar in size. However, leaf texture is different:

Ostrya is finely hairy. Best to feel with lips (more sensitive) when 1st getting used to difference.

Carpinus is smooth (glabrous) and even somewhat papery like Fagus.

now, if I could only remember which one had the hop in its name! (this is why I stick to scientific names :p)

I'll update with sources soon.

I took the time to find an Ostrya where I could reach the leaves so I could examine one close up. You are right that it feels hairy, although some Carpinus leaves I got for comparison also feel slightly hairy (if not as much). However, the Carpinus seams to be hairy only on the underside and only along the veins, while the Ostrya is also hairy on the top and inbetween veins. Under a magnifying glass, the Ostrya hairs are shorter than the Carpinus hairs, and this seems to be confirmed by the German article I linked (as far as I can tell, my German is not good).

Two more interesting differences are: The tertiary veins clearly stand out on the Ostrya (like on big-leaf linden), but not so much on the Carpinus (which is more like little-lead linden). This is also confirmed by the German article. Finally, some of the secondary veins branch out on the Ostrya, but not on any of the Carpinus I looked at. This is the easiest to see difference. Do you know if it is a reliable way to distinguish them?

Picture of two Carpinus with Ostrya in the middle

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


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Does refrigerating (but not freezing) bread inhibit mycelium growth?
During COVID, supermarkets struggled to keep things in stock. Bread seemed to be hard to come by for a time. As a result, when I came across the brand I liked, I grabbed a couple extra loaves. I didn't want the extra to go bad, so at first I froze it, but that was harsh on the bread. However, it turned out that simply refrigerating it was amazing! It seems to last indefinitely, although it eventually hardens if left for too long (around a month?). I thought I had found a cool trick, as it takes us a while to go through a loaf of bread.
The other day I watched a YouTube video about mold growth and food safety. From 3:06 to 4:13 in the video, he explains that before bread has visible spores, there are already mycelia in the bread. In other words the bread is already moldy before mold is visible.
I began to wonder: is refrigeration actually preventing mycelium growth, or is it only preventing spores? I noticed a commenter on the video raise the same question.
In case it's relevant: Two meat thermometers sitting on the shelf where I keep my bread read 40 degrees F, as does an IR thermometer pointed at the bread bag. According to a quick Google search, that seems to be an acceptable refrigerator temperature.

Welcome calcmari. This is not simply a Q&A site, here we are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are. You should also take our [tour] and refer to the [help] for guidance as to the ways of any site you post on, see our section on how to ask. There are some things you should investigate: (Cont...)

(Cont) Common bread-mould growth temperatures? What bread? What does the ingredient list say about: ascorbic acid, sulphur dioxide, sulphites, calcium/sodium propionate, ginger, garlic, clove, cinnamon? Does your jurisdiction even require these things to be disclosed on the label?  Or is is fresh from the baker's oven without preservatives? Then you can [edit] your question to include your research in attempting to answer the question and where you got stuck.


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Have any animal been discovered which don't have any kind of symmetry?
Bilateral symmetry is a common feature, yet we come across starfish that has rotational/circular symmetry.
But is there any animal that has no symmetry?

I suspect something like a sea sponge won't have any symmetry.

Starfish are also bilaterally symmetric as larvae and descend from bilateral ancestors.

Maybe the abalone family (Haliotidae), but I don't know whether the animal is symmetrical or life-stages.


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Why are animal's whiskers in a square lattice?
I was observing my cat up close when I noticed his whiskers were in a square lattice as a novice mathematician, took notice of it and wanted to know if any other animal had this peculiar feature, so I went onto my phone and choose a random animal that I knew had whiskers (which was the sea lion), and to my surprise, it had the same grid-like shape of my cat's. This seemingly insignificant question was turned into a very real question that I had no answer to. Plus, the only place where I saw someone mentioning it was on Wikipedia, where it said: "…they form an ordered grid of arcs (columns) and rows…" However, this is the only sentence (besides the caption of the image that the sentence refers to) that takes notice in this lattice, so I'm wondering why (maybe because of evolution?) all whiskers are in this shape.

The question of "why" can have different meanings for different people. You may find an answer by studying how the whiskers develop. Evolutionary explanations are intriguing but hard to prove. You can also look at their functionality.

We know that some nocturnal species use them for navigation. In the case of mice or rats, the tips of the whiskers of a row reach forward, beyond the nose, placed on the same plane. So it helps the animal predict what is coming next as it moves forward. The physical properties of an obstacle appear as a series of row-wise stimuli.

The brain of these species (e.g. the barrel cortex) is certainly set up to process stimuli row-wise, with increased inter-row connectivity and activation flowing row-wise.

Being more specific about what you mean would help, I certainly would not describe whiskers as being in a lattice, they rarely cross over each other. what about the whiskers is in a lattice? maybe include an image.

Whiskers in cats are like little tuned sensory apparatuses that let them feel/handle what they're eating up close, since they don't see very well up close. It could be they're organized in a sort of matrix to get a better feeling of what's close. I personally see rows, and then the two whiskers that are apart (further up the cheek). Also the whiskers in the hind legs can convey meaningful information about the environment before deciding to, for example, perform a jump.


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What types of spider and caterpillar are these, and what are they doing?
What varieties of spider / caterpillar(?) are these?
And what is the spider doing to the caterpillar?
This is in Texas.
This went on for hours, with the spider dancing with the caterpillar in the spider web where the caterpillar was caught. After 10+ hours, this morning, I found the caterpillar -- still intact -- curled up on the ground beneath. Was the spider sucking the juice out of it or something? I don't understand what parts of it, if any, was consumed by the spider.

Are you aware how spiders eat?

@DKNguyen Probably not by sucking the juices/blood out of its prey like a mosquito? Which is why I was particularly confused, as the spider didn't seem to be 'eating' it. Now the caterpillar is just dead. So I'm not sure what the spider did to it..

Not like that no. I assume you're younger if you're not aware, but they do drink their victims. Spiders pump digestive enzymes into the prey to externally digest it then drink it, whereas you ingest your prey and the digestion is done internally.

Thanks! I did not know this. I also looked this up just now, and yes, that's in fact what happened: "When feeding the spider regurgitates enzyme rich stomach fluids over and into its prey. This external digestion... reduces the prey's body and tissues to a chitinous soup. The liquid is sucked up through the spider's tube-like mouth, aided by the action of the pumping stomach, leaving the hard parts behind. Spiders... inject digestive fluids into the bitten prey and suck out its liquefied internal tissues, leaving an almost intact body husk behind." (src: australian.museum) @DKNguyen

The spider is a cobweb weaver - family Therididae (can be determined from the bulbous abdomen, thinness of legs and small cephalothorax) and appears to be Steatoda triangulosa from the brownish colour, white markings on the abdomen, and rings/annulations on the legs. S.triangulosa is found widely across North America and Europe.
The prey is not a caterpillar but a myriapod, I believe in the order of flat-backed millipedes.
As @DKNguyen already answered, the spider was preying on the millipede. The 'dancing around' was the spider trying to subdue the prey by wrapping it up in silk, but for prey that size, it takes a long time to get enough silk on it to hinder its movements.
Once the spider gets a meal out of the prey, they detach it from the web and let it fall to the ground below. This is often a way to detect when you have a cobweb spider in a corner or under a stair or something - when you see a clutter of dead bugs. The clutter also tells you that the spider is helping take care of pest control while staying in one spot.

Spiders pump digestive enzymes into the prey to externally digest it then drink it, whereas you ingest your prey and the digestion is done internally.
That's not even the only way animals eat...starfish bring their stomachs out of their body onto their prey and digest the prey there. Might seem even weirder, but arguably less roundabout than the spider's method.

I dunno about that. Regurgitating your stomach to surround a victim outside of your body would seem to be a very risky proposition; it could be damaged. I’ll take my meal with a straw, please, like the early astronauts.

@anongoodnurse I think it is less like a straw and more like throwing up on your food, letting it sit and then drinking it up.

Ooooo, that does sound awful indeed, but safer for keeping my stomach out of harm’s way. I saw this once at a tiny aquarium in Maine. Fond memories! (Ugh.)


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Can disk diffuson be used, without diluting a broth culture to match a 0.5 McFarland turbidity standard?
In this video, there doesn't seem to be a process of diluting the broth. I'm not looking for extremely accurate test results, all I need is to see if a particular colony is susceptible to the antibiotic. Since it's not a lab project or anything, I only need a Yes or No answer. Does that mean broth dilution can be substituted by making a good lawn? Can I just inoculate my agar that simply?

It depends on what you mean by "susceptible" for the question that you're asking. Fresh broth cultures will likely give you a good lawn, but if you aren't doing anything to standardize the innoculum, it's not really comparable to anything else when you make your determination. So, if you do end up seeing a zone of inhibition, you won't really have any idea if it's actually suceptible in the context of clinical relevance. For that, you'd check a table of clinical breakpoints for that organism, which are determined using standardized protocols most likely involving a McFarland standard. If you look through the linked table of breakpoints, you'll find that some organisms can have a fairly large ZOI diameter and still be considered resistant.
Another consideration is spontaneus plasmid loss. In my experience, passaging a colony into a broth culture overnight is a great way to cure plasmids from their host, plasmids that may carry genes which would otherwise make your isolate resistant to antibiotics. For that reason alone, I think you're better off using some kind of pseudo-McFarland procedure than broth cultures. If you don't have a standard, and don't want to buy one, just pick some colony and mix it up in a mL or so of sterile saline solution until it's a little more turbid than the unadulterated saline solution and make the lawn with that (looking up pictures of the different standards online will probably get you in the ballpark, which is really all the McFarland standard method is anyway).


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Can New Caledonian crows survive on their own in Europe?
Is it possible to insert New Caledonian crow in Europe and have them survive on their own, mate, lay egg, hatch and so on?
The motive for the question is to find cheap labor, highly capable animals similar to working dogs, since the New Caledonian crow is among the ablest land animals known.

This question could be improved by adding in your own research on what introduced bird species are present in Europe.

This question is potentially about invasive species introduction. The motives for the question would be welcome. That species has lived in temperatures always warmer than 15 degrees for many generations and would have some disadvantages, compared to european crows. Yes they can breed a bit, but there is no scientific information to say if they would proliferate.

What kind of work would a New Caledonian crow do?  They're pretty small, couldn't herd sheep or carry anything big.  I suppose they could act as rather unusual service animals - they wouldn't take up much space!  Also, there seems to be a fair bit of research that shows that some of the native crow species in Europe are capable of doing some very clever things - the gap might not be all that big, it might just be that the New Caledonian crows were studied earlier.


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How does a turtle develop inside its egg?
This is related to Cause of premature death in turtle eggs, for those interested.
I have noticed that Kinosternon spp. eggs have three layers:

hard outer shell
white opaque membrane (like the one you see in hard-boiled eggs)
transparent memebrane that completely wraps the baby turtle

Since I am forced to manually open this species' eggs (see the linked question for details), but doing so too early will likely result in the death of the developing turtle, I would like to know more about how turtles develop inside the egg (from a physical/chemical point of view).
I am assuming turtle eggs are permeable to oxygen.

assuming lack of oxygen is the root cause of these deaths, which, out of the three membranes, is more or less permeable to oxygen (in other terms: would breaking just one or two of the egg's layers be enough to let the turtle breathe?)
when do turtles start to breathe with their lungs?
Would it be harmful for the egg to get oxygen too early?
why would a turtle possibly die in the egg if it is opened too early? Could it be because of bacterial infections of some sort? I know for a fact that some breeders hatch turtles with shell-less incubation, the same tecnique used for chickens.

Biology is not really my area of expertise, I am just a passionate turtle breeder and I have not been able to find anything relevant that could shed some light on this issue.
My idea is to get some scientific insights that could possibly lead to a change in the incubation's parameters.
So any help would be greatly appreciated.


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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.


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What is this spider? Found in garage during May in NY
Stands very flat with its legs very outstretched, doubles-up its front legs (first pic looks like it only has 6 legs). Brownish-dark gray, not quite black. It's alive, but it wasn't particular active or spry when I saw it.

Edit: more pictures, with a quarter for scale

Also, sorry for the cup, but I was under strict orders not to lift it.

yikes! There are a lot of spiders who double-up their front legs for some reason so that at first glance it looks like they only have six. I don't know if that's the case here but it certainly might be. Also see google search spider appears to have six legs Have you seen it move and confirm it walks with six (and that it's actually a living thing and not a prank?) Can you also edit your question and add the approximate size? Thanks!

See also Are there any spider species out there that only have 6 legs? and as mentioned on your previous weird looking insect identification question, refer to https://biology.stackexchange.com/tags/species-identification/info

something for scale had been nice,is that thing 2m or 2mm?

@trondhansen and hopefully before I have to go to sleep tonight :-)

I added more pictures with a quarter for scale. @uhoh I had forgotten I had even asked a question before (it was 4 years ago). Forgot about those little beetles!

@trondhansen it's pretty big and seems to have eight legs after all.

It appears to be an American nursery web spider (Pisaurina mira), a species of spider in the family Pisauridae (Nursery web spiders).
They tend to double up the front legs and they can have the dark median band on the abdomen like the one in the photos. They can be found in New York also and it is listed in the spiders found in New York here:
https://spiderid.com/locations/united-states/new-york/
Some fishing spiders look similar but their size and pattern are different.
We can't see in the photos but you can also confirm by checking its eyes. This species has a unique straight anterior row of eyes where they are arranged in two rows.

Here is a similar one with a more clear photo I've found:

Source: https://www.spiderzrule.com/nursery-web-weaver/


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Why is cDNA usually lacking in terminal sequences of the template mRNA?
It appears from presentations I have attended that cDNA often lacks terminal sequences (usually 5′) which have not been copied from the mRNA. This puzzles me a lot, but I have not been able to find the answer as the focus of most of the sources I have consulted seems to be the principle, rather than practicalities.
Does reverse transcriptase just fail to finish copying the mRNA sequence, and if so, why? Or what is there some other problem? ?

I have edited your question to show you the sort of style that is preferred here to help you frame any future questions. First describe the background, and then state the question clearly, indicating why you have been unable to find the answer yourself, as @uhoh has mentioned. Try not to personalize it. Our aim is to provide answers to questions of general interest that will be useful for others besides the poster.

Traditionally cDNA cloning used an oligo(dT) primer that binds to the 3′ poly(A) tail of a mRNA and extends towards the 5′ end of the mRNA.
What makes it difficult for the reverse transcriptase to copy right to the 5′ end is the fact that this has secondary structure which has to be unwound. This is a general feature of eukaryotic mRNAs, as evidenced by the fact that in the initiation of translation during protein biosynthesis there are specific factor(s) to perform the unwinding in an ATP-dependent manner.
In addition, during the subsequent steps to prepare the second cDNA strand, trimming of the 3′end of the single-stranded cDNA can occur. Various strategies are now employed to avoid this.

As far as truncations at the 3′end, I am not sure there is anything specific one can say — at least I do not know of anything.


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Do cochineals ("scale bugs") form aluminium complexes themselves? Where do they get such large quantities so quickly and how do they handle it safely?
Wikipedia's Carmine begins:

Carmine (/ˈkɑːrmən, ˈkɑːrmaɪn/) – also called cochineal (for the insect from which it is extracted), cochineal extract, crimson lake, or carmine lake – is a pigment of a bright-red color obtained from the aluminium complex derived from carminic acid.1 Specific code names for the pigment include natural red 4, C.I. 75470, or E120.
1 Dapson, R. W.; Frank, M.; Penney, D. P.; Kiernan, J. A. (2007). "Revised procedures for the certification of carmine (C.I. 75470, Natural red 4) as a biological stain". Biotechnic & Histochemistry. 82 (1): 13–15. doi:10.1080/10520290701207364

Wikipedia's Dactylopius; Cochineal dye includes the image below of a ~5mm individual Dactylopius confusus that's been squished and a finger covered in a bright red dye thereby "extracted" from it.
And my guess is that the central aluminium may in fact be necessary to produce such a strong absorption of green and blue light (λmax = 530–335 nm).
But it's not yet clear to me where the aluminum for complexing comes from. Is it in the insect's diet and the "aluminium complex derived from carminic acid" is performed inside the insect itself? If so, from where do these insects get their aluminum in such large quantities how do they handle it safely?

video: Why Tiny Cactus Bugs In Red Food Dye Are A $35 Billion Industry | Big Business | Insider Business

Question: Do cochineals ("scale bugs") form aluminium complexes themselves? Where do they get such large quantities so quickly and how do they handle it safely?
"so quickly" because they seem to be pretty short-lived and I'd expect that bio-available aluminum would be pretty scarce.
The reason I ask is because biological aluminum has a toxicity aspect and it doesn't seem to me that it's something you'd particularly get a lot of sucking on plant juice.

Click figures for full size. above first: "Figure 2. Salasaca dyer showing red woollen cloths with modified cochineal red colours. Ecuador. Photo: A. Roquero." from Ana Roquero (2008) Textile Society of America Symposium Proceedings Identification of Red Dyes in Textiles from the Andean Region above second: "Dactylopius confusus crushed scale insect, Fort Collins, Colorado, United States" from Wikimedia. below first: "scale bugs" on my houseplant, perhaps female Dactylopius confusus or Dactylopius coccus, from Are these little white fuzzy insects "scale"? What species and what is their lifecycle like? below second: Structure of carmine from Wikipedia

companion question: Are these little white fuzzy insects "scale"? What species and what is their lifecycle like?

I gather it's in the diet of O. ficus-indica which does the binding, but I can't pin down the mechanism. I'll give it more time tomorrow, see if there's anything more detailed to find on the topic.

Definitely something to do with the Al. You get 2 carminic acids to 1 Al and the colour of the carminic acid alone is not bright red, more a deep orange. See article here

@bob1 Interesting!

Interestingly ionic salts produce other colours - substitute Na and you get indigo/deep blue, K and Ca salts are red to purple (may also contain Al I though) and ammmonium is blueish red. I'm having difficulty finding anything about the salts without Al though.

@bob1 the article I've linked to about dyed wool describes use of wood ash and lemon juice to induce different color changes as well.

pH dependent I would have thought. Wood ash = potassium salts, though I guess others present too.

Aluminium moves within plants as a complex with ligands such as oxalate, malate, and citrate.
Plant cells also hide the aluminium (and other junk) in vacuoles. That is most likely the immediate source for the beetle.
Plant roots exude malate and citrate to neutralise aluminium before it poisons the roots. I got this from The role of solute transporters in aluminium toxicity and tolerance.
The toxicity of aluminium is greatly dependant on its form and what it is complexed with. The more "naked" the ion is, the more toxic.
The toxicity is pretty much confined to the roots, and gets more nasty if the pH gets down to 4.3. Once inside the plant it is usually complexed, and not a big problem.
An easily readable review article on toxicity is Aluminum, a Friend or Foe of Higher Plants in Acid Soils.

This is all really interesting and mostly new to me, thank you!


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Please help identify this plant
This plant/branch was part of a table decoration brought home from La Puente, CA, a week ago. It's been kept in a jar of water. I hope to:

Learn the name(s) of this plant.
Learn the correct morphology terms (not sure if I said that right) that apply to this plant/its leaves (e.g., about its shape, leaf base/tip/veins). I've looked at some leaf identification charts online but the ID'ing process is totally new to me so it's a little confusing.

Some notes about the accompanying images:

Images A and B --- The top leaf is kind of spiraled, and it has 3 "entire" leaf margins (they're smooth) and 3 surfaces. (Is there a morphology term that applies to the 3 surfaces?)

C, D, and E --- The leaf arrangement of the lowest 4 leaves seems to be "opposite" but then the other leaves above them seem to have an "alternate" or "alternate spiral" arrangement.

Here are the images:
Image A and B.

Images C, D, and E.

Regarding Image A: any chance that is 2 leaves that are flattened against each other as they emerge and unfold?

If your goal is to learn the basic parts of a generic vascular plant, this is a bad example.
As @BryanHanson's answer states, the wide, flat surfaces are cladodes, not leaves. The diagram included with the answer shows scale leaves, which can be seen in photos D & E; that means that the cladodes grew from the axillary buds of those scale leaves. Presence of an axiallary bud is normally the best clue to "is this a leaf?", but things get a bit confusing when the shoots take on this unusual morphology.

Since you mentioned it was a table decoration, I searched "florist greenery" and found images very similar to what you have.  Good chance it is from the genus Ruscus but you will have to compare your plant to online images to be sure.  Wikipedia on Ruscus.
Note that Wikipedia mentions that what appears to be leaves are not actually leaves, but cladodes, a type of hybrid tissue.  Wikipedia's entry summarizes a study on Ruscus aculeatus in particular (a molecular biology study, original here).
Looking at the paper linked above, Figure 2 (and others) show tiny "scale leaves" below each apparent leaf, and I think I can see these in your photos, but again, you will need to inspect more closely.

It does look like a Ruscus, they come from Eurasia, and he found  it in the Americas. Tell tale thing is the flower that comes in the middle of the underside of the leaves, so it's definitely a Ruscus variety.

@LifeInTheTrees the tiny white nub not quite mid-point on the underside of the "leaves" - is that a flower bud, or a dried up flower?

here is a bud... https://upload.wikimedia.org/wikipedia/commons/0/01/Ruscus_israeli.JPG and https://commons.wikimedia.org/wiki/File:Ruscus_israeli_cladode.JPG


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Vision and signal through the nervous system: Is it Frequency Shift Keying?
I have questions regarding the signal between the retina and other parts of the brain. There are two types bipolar cells which are excited by light or darkness to the retina.
Question: Do these form different signal frequencies over the nerve channels?
This is my understanding from resources.
Wikipedia states:

Retinal ganglion cells spontaneously fire action potentials at a base rate while at rest. Excitation of retinal ganglion cells results in an increased firing rate while inhibition results in a depressed rate of firing.

It’s my understanding the photoreceptors in the eye have an opsin pigment molecule which experiences a change in geometry when an electromagnetic wave passes through, pushing on the photoreceptor’s body.  A potential difference in voltage occurs which causes the photoreceptor to release glutamate, an exciting neurotransmitter, or GABA an inhibitory one to the electric synapses of the bipolar cells via synapses.
One type of bipolar cell gets excited by light while the other inhibited.  Either one releases a neurotransmitter to the synapses of an ion channel.  The ion channel creates potential difference, sending a signal or action potential through from the soma, to the axon, to dendrites and to its receptor destination. The above quote suggests that the action potential is “frequency shit key” modulated, with a baseline frequency, then a higher or lower frequency depending on presence of a particular light wavelength.  The photoreceptor outputs an exciting neurotransmitter with no light, inhibitory with light.

In the edit, you've added a couple of other questions, we deal with single questions, one per post. Ideally you can place the others in their own threads, and link back here to the place you've shown your researches.

Frequency-shift keying is an electronic communications approach, part of a broader set of frequency modulation strategies for conveying information.
These strategies relate to the difficulty in communicating over what is really a single available physical channel: the electromagnetic spectrum. If you're communicating by radio or other similar frequencies, you can't really sort out an individual signal from all the background except by knowing something about its structure and using that structure to filter out the noise.
It seems like you're trying to apply what you've learned about these forms of electronic communication to brains. However, none of that is necessary in brains, because each neural process represents a separate physical channel. There's no need to encode and decode signals that way: communication within the nervous system is massively parallel.
Sometimes "rates" and "frequencies" are interchangeable concepts, but not here. When people talk about a "firing rate", they literally mean a rate: discrete events. See for example "rate code". More action potentials means more neurotransmitter release at the end of an axon. No frequency encoding or decoding is necessary. Different messages are conveyed through different "cables". This is also called the "labeled line principle" or theory: the idea that information in nervous systems is conveyed largely based on the physical structure of where it comes from and where it transmits to. There is no difference in the electrical properties of an axon conveying information about one part of the visual field versus another, except that they are connected respectively to a part of the retina and a part of the brain each also dedicated to processing information about that part of the visual field.


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What is this insect found in Melbourne, Australia?

This photo was taken a few days ago (late May 2022, during daylight hours) on a timber deck in the northern suburbs of Melbourne, Australia.  The animal is roughly 3cm long.  The photograph shows shed fur from a Jack Russell terrier for size comparison.
When a larger animal moves near these insects or they are disturbed, they react by raising their abdomen with its spike in a manner similar to a scorpion.  Otherwise, they seem sluggish and slow-moving.
There have been a dozen or so of these insects seen in the area over the last few weeks, but they haven't been seen in previous years.
Given its six legs and segmented abdomen, I'm assuming that it is an insect of some sort.
Can anyone identify this animal?

Also, check the gum trees nearby for defoliation. That’s probably their food.

This appears to be a sawfly larva. Sawflies (Hymenoptera) are a widespread group of insects with a few thousand species. However, Australia doesn't have many species, and this one is fairly distinctive. I think it is either a long tailed sawfly larva or a bottlebrush sawfly larva. There are a few pictures of some members of the Australian species at Brisbaneinsects.com. One distinctive feature of many of the species in this family are that the larvae cluster together in large masses. As you are only seeing single ones, it is likely that you are seeing the long tailed species as this one doesn't cluster.
They are related to the wasps, bees and ants, but won't sting. They can release a smelly substance when disturbed.
I found this image at "whatsthatbug.com", which is similar to yours.

I agree that it's a sawfly larva, but it doesn't look like either a long tailed larva or a bottlebrush larva.


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How does hypokalemia antagonize lidocaine's effect?
I was reading the lidocaine user's manual for dentistry use and according to it and I quote "Lidocaine in concomitant use with acetazolamide, thiazides and loop acting diuretics. The hypokalemia ("a low level of potassium (K+) in the blood serum") induced by these drugs, antagonizes the lidocaine effects" which seems a bit weird as a potassium deficit would hyper-polarize the membrane increasing membrane potential making it to hard to get to the threshold potential right?

Thanks for adding the quote; I agree it's odd. I could see systemic concerns with lidocaine reducing heart rate which would be a bad combo with hypokalemia, but antagonism is not the concern there. Is this possibly a bad translation? Is there other context beyond what you quoted?

As a matter of fact, I couldn't find the exact same info in the English version, but I can guarantee you there is no translation error. I could provide you with a copy of it if you wanted to.

Here is the link where you can download the Spanish version of the manual https://zeyco.com/producto/fd/ is the part about drug interactions

Thanks; it's clearly in both English and Spanish inserts. Inserts for similar formulations like https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/021381s006lbl.pdf or https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/006488s097lbl.pdf don't mention any such antagonism. Certainly it makes sense as a possible contraindication for other reasons, but I agree with you that the mechanism and concern they mention isn't making much sense to me.

The following is a suggested answer only -- and is NOT intended to be authoritative; since it is not clear from the literature on Lidocaine why its efficacy is reduced in hypokalemia.
While it is true that hypokalemia will tend to induce hyperpolarisation of cell membranes, which in the case of neurons inhibits the elaboration of the action potential (by increasing membrane potential), other effects should also be considered, in the first instance that the concomitant tendency for K+ to flow out of cells generally also implies the countervailing tendency for Na+ channels to promote the transport of Na+ into cells -- more channels operating with greater facility.
Since Lidocaine is a sodium channel blocker -- which prolongs the inactivation of voltage-gated Na+ channels -- then prima facie, a generalised condition of hypokalemia suggests that the associated operation of more sodium channels will tend to antagonise its action.
At the same time, since the Na+/K+ ATPase would be operating to maintain homeostasis of intracellular cations (K+ in particular) in the face of any such efflux of K+ from cells, this effect would likely be accentuated by virtue of the corresponding efflux of Na+ from the same cells; notwithstanding the findings cited in the study below [1] concentrating on myocardial activity, that ''hypokalemia significantly inhibits Na+/K+-ATPase pump activity causing intracellular Na+ and Ca2+ accumulation''.  In that case, it is presumably the implication of the Na+/Ca2+ pump which complicates any effect on Na+ channels.
Additionally, the finding that hypokalemia inhibits the Na+/K+ pump would imply a tendency to recalcitrance in the opening and function of sodium channels which, since that would favour the action of Lidocaine (as a sodium channel blocker), contradicts the premise of the question.
[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5399982/
https://en.wikipedia.org/wiki/Sodium%E2%80%93potassium_pump

@Bryan Krause (or whoever down-voted the answer) Please indicate what is wrong with the reasoning. I think any objection deserves explanation. While I don't KNOW that this answer is correct, whatever the answer is, presuming the premise of the question is valid, almost certainly involves some effect of hypokalemia on Na+ channels presumably as a consequence of changes in IC K+. If it is true that the Na+/K+ pump is inhibited in hypokalemia, it would suggest recalcitrance in the opening of Na+ channels favouring the action of Lidocaine which contradicts the premise of the question.

Thank you very much! Although I wonder why hipokalemia improves sodium channels activity.

@Quique I'm not sure that it does -- it was merely a suggestion based on the idea that since K+ will flow out of cells in order to redress a condition of hypokalemia, then it is likely that Na+ will flow into the same cells via the most efficient mechanism, which would be sodium channels. However, my answer was not well-received so there is probably some more obvious effect which I'm overlooking. There still doesn't seem to be any explanation for the effect you cite on Lidocaine activity. The consensus among the erudite here seems to be, ''We dunno and it's not really important''. Fair enough.


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Vision System: neural activity is modulated using FSK?
I’m learning about the human vision system and signaling. Does anyone know if the signaling used by the vision system is modulated at the neuron using amplitude frequency shift keying?
I present my understanding of this below.
It’s my understanding that the rods and cones of the retina have a mechanism involving opsin and a geometry change which ultimately causes neurotransmitters to signal. This signal is an action potential over an axon ion channel.  The neurotransmitters in the vision signal path excite, inhibit or neither. This results in three frequencies of signal over the ion channel corresponding to the retina receiving light (20 Hz), no light (1.7 Hz) or unknown/baseline (.19 Hz). The light intensity changes the amplitude or voltage of the signal.

I think this is a case where you're much better off learning about how neurons work first, and then much later trying to relate this to other things you already know about, say, technological radio communication. It'll be way less confusing that way. There are definitely not only 3 possible firing frequencies, though; neurons can fire at any frequency from never up to a maximum governed by the kinetics of their ion channels (100 Hz would be a reasonable expected maximum for a typical neuron).

A good place to start might be understanding the individual figures in your links.


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Neurons: how does the brain reduce electromagnetic interference?
I read that the frequency of signal over neural ion channels in the brain can range from .19 Hz - 30 Hz at low voltage. For an interference example, AC electricity is 60 Hz at high voltage and generates an electrical field. From cited research below, it appears neural activity is impacted by EMR/RFI. Question: does the brain have some process it uses to reduce this interference? Forward error correction?
It seems that if there is an electrical field, force will be placed on these charges traveling over the ion channels and as a result lots of interference.
Research:
Electromagnetic waves, particularly RF-EMFs emitted by mobile phones are absorbed into the brain to such an extent that it can affect the activity of neurons (Kleinlogel et al., 2008; Hinrikus et al., 2018). Also, in 2011 World Health Organization’s designated mobile phone RF-EMFs as Group 2B, that is, possibly carcinogenic to humans. Recent studies show that RF-EMFs emitted by cellular phones are absorbed into the brain, to a degree, that can affect neuronal activity (Kleinlogel et al., 2008; Jeong et al., 2015; Jiang et al., 2016). physiological changes in cell membranes and ion channels at cellular levels have been reported (Pall, 2013; Buckner et al., 2015). Changes in cell membranes and ion channels induce alterations in the electrical activity of neurons, and these changes stimulate or inhibit neuronal activity through interaction with voltage-gated ion channels (Nanou and Catterall, 2018).

Take the easy data. Check the thickness of a neuron's cell membrane, and the voltage across it. Calculate the Volts per metre. Compare this with any external influences.

There is an extensive Q&A about the difference between brain waves and EM waves over on our sister site Psychology & Neuroscience: https://psychology.stackexchange.com/q/15222/14382 (though some of the answerers beyond the first two are a bit confused)
In summary, the brain doesn't care about EM in that range at all.
Light travels about 300,000,000 meters per second, so a 30 Hz electrical signal has a wavelength of about 10,000,000 meters. Nothing in a brain is long enough to resolve that length of wave. All electricity in the brain is via potential differences over membranes; a wave that long is almost exactly the same amplitude on both sides of the membrane so there is no consequence.
Yes, 30 Hz is a common neuronal firing frequency, but that has little to do with EM waves. Neurons don't communicate with each other through EM waves, but through release of neurotransmitter and opening/closing of ion channels. It becomes a problem for recording neuronal activity, but that's it.

I'm still confused why a 60 Hz signal has no impact on the potential voltage difference of the ION channel.  Even if the wave is long, it is still oscillating at 30 or 60 Hz, which would induce current on the ION channel due to the Lorentz Force.  Why would the length of the wave have anything to do with this?  It's the time of rise and fall of the EMF that is located along the ION channel isn't it?  The neurotransmitters (glutamate, dopamine, GABA, norepinephrine, etc) are released at the terminals of the ION channels, so would be effected by the ION channels and induced EMF.

I also read another article from NIH https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6025786/.  It states that "several studies have reported that exposure to EMF results in oxidative stress in many tissues of the body. Exposure to EMF is known to increase free radical concentrations and traceability and can affect the radical couple recombination."

@Nick That's an NIH site that indexes journals. Saying it's from NIH is like saying that Google said something because you found it on a Google search. Try out what Polypipe suggested in a comment.

There are two aspects to this question.  The first, dealing with EMR associated with AC generated in the usual range is already properly answered.  However, in the case of mobile phone radio and wifi frequencies of the order of 2 to 4 Ghz for example, the wavelengths are precisely in the range of the internal dimensions of the human calvarium: e.g. at 2 Ghz, the wavelength is ~15 cm.
Now whether this correspondence implies any physiological effect in the brain -- if you can imagine microwaves of that frequency rattling around the brain, being variously reflected and refracted by the calcific structures of the skull -- is another question, possibly worthy of specific research.
However, in the instance in which such microwaves might be slightly refracted or reflected within the calvarium, there will certainly arise a beat frequency deriving in any interference effect between those refracted or reflected components which is conceivably of the order of the so-called frequency of 'brain waves', which as noted are not really 'waves' in the ordinary sense -- rather an integrated effect deriving in the more-or-less synchronised signaling or 'firing' of myriad neurons.
Again, whether wave interference resultants arising with these comparable frequencies imply any actual physical effect which is directly dependent on those hypothetical beat frequencies is a further question.  Perhaps the brain becomes confused about the origin of these 'beats'.
To address your central question, perhaps the brain even learns to interpret not only this interference effect, but given the correspondence mentioned between radio and microwave wavelengths and the dimensions of the brain, perhaps it is in fact learning through the endless and inexorable processes of adaptation how to decode the information transmitted through such EMR.  All the more wondrous then, all the more tantalising and seductive that one should then hear and see this data in full flower slightly delayed in the devices themselves, on screens and in speakers.  Perhaps somebody will devise an appropriate experiment (if the whole thing isn't already an experiment).


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Why is African hair different in texture to European or Asian hair?
Most Africans with the exception of Ethiopians and Somalians have relatively kinky/coiled hair. The texture is very different to that of Europeans or Asians. Why is that?
I've heard it has to do with the shape of the hair follicle which is flat but also the thickness of the hair itself. Is this true?

As this article details, the texture of hair is influenced by many aspects of the hair follicle, primarily the follicle shape (curved or not, angle relative to scalp), distribution of particular cells within the follicle, and the coordination of cellular activity in the follicle (symmetrical or asymmetrical activity).
The article also confirms, as the question recognizes, that a great variety of hair textures are found in all parts of the world, so that categorizing hair by country or continent of origin is specious.


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Optic Nerve: neurons/area and bit rate?
Does anyone know the number of neurons adjoining a cross sectional area of the optic nerve and the theoretical bit rate of the nerve?
I read that the ON cross sectional radius is 3-5 mm and the diameter of a neuron is .004 - .1 mm. Area of cross section: (5 mm)^2 * pi = 75 mm. 75 mm / .004 = 18,750 neurons/cross section. The average action potential of a neuron is 1 ms in duration, making maximum signal rate of 1,000 Hz.  The action potential is both a frequency (on/off/unk) and amplitude (intensity).
I read that light at min intensity signals at 0-1 Hz and max at 30 Hz. At 30 Hz that’s 18,750 * 30 Hz = 562,500 bits/sec or 562 kB/sec or .5 mB/sec.  at 15 frames per second that’s 37.5kB/frame.  Now I think something is wrong because this is very slow considering all three cones and rods must signal over this slow bandwidth.
They are also orders of magnitude off from the 576 MB image calculated for the human eye. I read that the nerves are really signaling contrast changes, but it seems like a large amount of bits just for contrast.

Neurons are not encoding a digital signal in the sense of computers, so it may not make any sense to think about it that way. Neurons can't fire at 1000 Hz, even if an AP is 1 ms wide. Like I've suggested elsewhere, start by just learning about neuroscience. Read a whole undergraduate-level neuroscience textbook. Purves' "Neuroscience" or Kandel's "Principles of Neural Science" are good options. I know, it seems like a lot of work, but it will save you a ton of time wasted.

Well, upon some simplification, we're talking digital vs. analog information. An 8-bit digital image can distinguish between 256 tonal values. The exact amplitude of a neuron action potential along an axon is continuous ("analog"), and perhaps more importantly, the summation/integration of electrical information along any point in the neuronal soma and dendritic regions, before the axon hillock, is entirely continuous, and as such is theoretically "infinite-bit" in "infinite locations", digitally speaking. So bandwidth is infinity. That's what you get when you compare digital and analog.

@SPr It seems you are implying the amplitude of the signal has infinite states.  That makes sense.  I think in OP I confused intensity and amplitude.  Am I correct saying the signal amplitude is intensity and the frequency is on/off/unknown?  Or is it the other way around?

Start with basic neuroscientific principles such as action potentials as suggested above. An action potential is a signal propagated through an axon of a neuron, that's the most basic idea to grasp as to how neurons send information down the 'wire'. Here, the exact amplitude doesn't correspond to intensity, either there's a signal propagating or not, so it's binary in that sense; usually signal intensity is coded for in part by frequency of action potentials and is limited by its input (stimulus) and other things like their refractory period.


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What results would come from DNA analysis of several different types of DNA mixed together?
By "types," I mean several different species of animals. If, post extraction, the pure, isolated DNA of several different animals were mixed together and run through DNA analysis, I know the results would be inconclusive, but would there be any usable information returned at all? Would any species be individually identifiable?
The scenario is hypothetical and for a TTRPG plot; the players procured samples of a substance that they don't yet know are isolated DNA polymers (think the "extracting strawberry DNA" science experiment for children) from several different species of animals and a couple of humans, which was mixed together post-extraction. They'd like to have the DNA samples analyzed. Handwaving turnaround time (I know this process would realistically take weeks to months at the bare minimum, but if crime procedurals can deus-ex analysis results in 48 hours, so can my players), what would that analysis turn up?
Would they be able to parse specific species, or the ratio of one species to another (ie the sample only containing one or two dogs, but many, many small birds and squirrels)? They almost certainly wouldn't be able to turn up any kind of identifiable information on the human DNA, even with an uncontaminated reference sample, right?

I'd push back on your turnaround time in the real world; depending on the technique, the motivation of the people involved, and access to equipment/reagents, this could be accomplished in a couple hours (PCR assays) to a couple days (DNA sequencing+analysis).

In your TTRPG you can kind of do whatever you want, but I guess I'd keep in mind that there isn't a "ANALYZE DNA"  button you push on some biology machine in the real world; what you output very much depends on what you go about trying to accomplish.

You may be interested in commercially available meat testing kits - DNA kits have been widely used to detect what certain food products are actually (or are actually not) made of. Some kits are designed to identify the presence/absence of a dozen or more animal species, which can be reliably detected at proportions even less than 1% of the total sample. There have been some high-profile cases of meats labelled beef or pork actually turning out to be horse, for example, which was revealed by DNA testing. It is quite routine to be able to identify what species of animal are present in a mixed DNA sample, and to estimate their contribution to the mix.
At a practical level, this gets more difficult the more species you have in the mix, the less you know about what's in the mix, and as the concentration of any contributor decreases. But in principal, if the DNA is there, it can be sequenced and identified bioinformatically. It would be feasible to isolate human DNA from a mix of many animals, although you'd have a harder time with highly conserved genomic regions that are consistent across many species. But there are some regions of the genome that are uniquely human, which could be used positively ID a particular human's DNA among a mix of different species.
Overall, you can in theory learn a lot from a mixed-DNA sample, including the species present, their relative contribution, and even tell apart individuals within a species and identify whether any of the DNA matches the reference of a particular individual.

Minor criticism: while I expect there to be readily google-able support for this answer, it's handy to have a specific trustworthy source linked in an answer.


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What is this colorful bug from Germany?
a friend found this little fella just outside of Berlin and managed to snap a blurry picture.

This boy or girl is probably the size of a finger nail and features fly like skin wings with no hard cover. There are thin curved antennas at the head.
On the internet I found the same color scheme in "Festive Tiger Beetle (Cicindela scutellaris)", but the shape doesn't seem to match.
Can you identify this creature?
(surely not spider, right?)
Thanks

Welcome to the site. Could you please provide some sense of scale - approximately how big do you think the insect is? With the poor photo, it is hard to tell if it is winged, or any features besides the distinctive colouration. Any further details you could provide would be useful in ID.

Festive tiger beetle seems to be only north America, though I am no expert.

It could be a ruby-tailed wasp.

That sounds indeed quite possible

Perhaps it's some form of jewel beetle. Their wings are traditionally used in jewel and clothesmaking and some of them are detrimental invasive species.
It will be nearly impossible to say which species based on that photo, which is too blurry.
https://www.lsuagcenter.com/profiles/lbenedict/articles/page1590086881287
https://en.wikipedia.org/wiki/Buprestidae


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Does succinic acid provide any caloric value in humans?
Would the ingestion of pure succinic acid provide any caloric value in humans? I couldn’t find any nutritional information about it via Googling, but I read on Wikipedia that it’s converted into fumaric acid, which after Googling I found does have a caloric value of around 2.74 Kcal/g.
I don’t fully understand exactly how succinic acid is metabolised though, be it where it’s metabolised or the amount of it that can be metabolised, so I’m simply lost with the numbers.


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Heart rate and Metabolic rate relationship
Metabolic rate in humans can be approximated using the Penn State equation.
It can also be estimated using direct and indirect calorimetry.
According to Kleiber's law, metabolism scales across species proportionally to the mass by a power of 3/4 (also by 2/3 or the [2/3, 3/4] range for other models).
Now, despite the known relationship between temperature, mass and metabolism, the relationship between heart rate and metabolism is less clear. Heart rate also scales with body mass approximately by a power of -1/4.
Usually, as a human ages, both its metabolic rate and heart rate decrease. Also, there are many examples of animals with a very high metabolism that have a very fast heart rate, like the hummingbird or the etruscan shrew.
I want to know if metabolism, after controlling for mass, is related to heart rate. I find it suprising that nobody has studied this relationship. I guess more data is needed to generate a model (I found this site, which could be useful, beats-per-life).
Heart rate is related to the distribution of nutrients and oxygen to all organs in the body. I think a faster metabolism would require/imply a faster distribution. We know this is true at least within the same individual organism, for example, during the elevated metabolic demands of exercise. Despite all of this, I haven´t found examples of it being used in relation to metabolism.
Any ideas about why this might be the case? What's the relationship between metabolic rate after controlling for mass, and heart rate, if there is any?
What about cardiac output? Cardiac output is stroke volume times heart rate. A bigger body tends to have a bigger heart, a bigger heart likely implies a greater stroke volume. Maybe if you adjust stroke volume by weight, and combine it with heart rate, you get an even better indicator of metabolism.

I think this is correct, the relationship between heart rate and metabolism exists, and can be explained by oxygen consumption. This is given by the Fick principle. That is:
$$ VO_2 = CO (C_a-C_v)$$
Where $(C_a-C_v)$ is the arteriovenous oxygen difference. So:
$$ VO_2 = (HR·SV)(C_a-C_v)$$
$$ MR ∝ VO_2$$
$$ MR ∝ (HR·SV)$$
Given that:
$$ SV ∝ Weight$$
You could estimate Metabolic rate using a combination of Weight and Heart rate.  Let's assume the stroke volume follows an allometric power law given by the exponent $e_{SV}$. Then:
$$ SV≈ a_1+b_1M^{e_{SV}}$$
(I guess lean body mass is more related to organ size than just Mass, so you probably could use it instead of Weight to estimate the Stroke volume)
$$ MR ∝ a_1+b_1M^{e_{SV}}·HR$$
Alternatively:
$$ MR ∝ LBM·HR$$
So, to summarize, I think Heart rate, through its effect on cardiac output and oxygen consumption, gives information about the metabolic rate that goes beyond mass, and can be used in combination to estimate it. The specific model type (logarithmic, linear, exponential...) that uses $ a_1+b_1M^{e_{SV}}$ and $HR$ is unclear but It might still work.

Please make sure to readers where Fick's principle ends and your personal assumptions start. While your assumed correlations individually seem plausible, they are presented without any source whatsoever. Especially, the step from ∝2 to ∝(·) seems dubious. Sure, there is a correlation between cardiac output and metabolic rate, but what is the margin of error? The OP, based on their research, asked the question WHY the heart rate is NOT used in the literature to determine MR.


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What does rescue mean in the context of biological experiments?
I have come across the term 'rescue' in biological contexts a lot recently and despite reading multiple definitions online cannot seem to get my head around what the word means on its own, and what it means in biology generally.
The definition differs depending on the context... 'genetic rescue' is a a mitigation strategy, 'synthetic rescue' is a gene alteration that counteracts the deleterious effects of another gene alteration etc.
Could anybody please explain what this means simply and in a way that could apply to different contexts like, for example, virology.

"Rescue" in an experimental context means you're capable of undoing some experimental manipulation. It's considered evidence towards identifying a causal mechanism or verifying that your manipulation does what you think it did.
For example, let's say you think secretion of molecule ABC is key towards mounting an immune response to MouseKiller virus. You test this by creating a knockout mouse that lacks the enzyme that synthesizes ABC, let's called it Alphabet Synthase, and find out that all the mice die when exposed to MouseKiller virus.
However, maybe you got it wrong. Maybe ABC isn't the key, but actually Alphabet Synthase is involved in some other pathway independent of ABC. You do an experiment where you produce some ABC in the lab, inject it intravenously to your Alphabet Synthase-knockout mice, and find these mice no longer die when infected with MouseKiller. You can say that you've "rescued" the ability of the mice to survive MouseKiller, and now have better evidence that indeed ABC is the key factor.
Another example of a rescue experiment would be that you think specifically Alphabet Synthase in B-cells is important for defense against MouseKiller. It's not very easy to knock out Alphabet Synthase in B-cells specifically, but you can 1) knock out Alphabet Synthase entirely in some mice, and 2) introduce a new version of Alphabet Synthase specifically in B-cells (for example, using a Cre-dependent expression vector with a B-cell-specific promoter). Experiment (1) shows the knockout is susceptible to death from MouseKiller, experiment (2) shows you can rescue the immune defense if B-cells specifically express Alphabet Synthase.
The precise experimental manipulation described as a "rescue" is completely dependent on the research question being asked: you'll have to read specific papers to know what exactly they are doing as a "rescue".

I suggest that "rescue" is an informal term used in the place of "complementation" in a genetics context. For example, that wiki page has a sentence that reads:

Another exception is transvection, in which the heterozygous combination of two alleles with mutations in different parts of the gene complement each other to rescue a wild type phenotype.

I would suggest that the complementation interpretation means that rescue could be read as: "the restoration of a wild-type phenotype that is otherwise expected to be altered by some insult (genetic or otherwise)".
For example, ura3 yeast have a ura- phenotype such that they cannot grow without provided uracil. However, this growth defect can be complemented or rescued by a plasmid carrying a functional URA3 gene.
I imagine that the word could be used slightly differently in a variety of contexts as biology is a large field. In genetics at least, I would say that the term is used informally and we should not pretend that it has a very specific meaning.


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How to make predictions on genes not involved in a particular disease
I have one set of genes which counts about 100 such that every gene of that set is evidence based involved in a particular disease. Let's call this set A. For a machine learning project I need a set of genes that is with high probability not involved in that particular disease. Let's call this set B. Usually in science one focuses on finding a gene that is involved in a pathology and not the opposite,i.e. finding a gene that is not involved in that particular pathology. But one can eventually make predictions based on some strategy in creating the set B. Knowing the genes of set A in terms of their identity, location in the genome, expression profile in a certain tissue where the pathology arises etc., how could one propose the set B ? Can one indicate a paper or present his/her own experience with a similar question ?
Many thanks.

Simple idea: find a GWAS for the trait you’re interested in, aggregate p values across genes and take a random set of the genes with the lowest highest p-value

Thanks. The set A is not based on GWAS. It is difficult to find GWAS studies in this case.


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Why are RNA nucleotides added first, only to be replaced by DNA nucleotides during DNA replication?
I am not asking why RNA primer needs to be added, but rather why RNA nucleotides are added as a primer by Primase and replaced by DNA polymerase I? It seems very inefficient to first insert RNA nucleotides and then add DNA nucleotides when you could have evolved to just add DNA nucleotides directly, without having to add RNA nucleotides.
Perhaps, it is an evolutionary remnant? Proof that DNA arised RNA? What do you guys think?

Does this answer your question? What is the function of the RNA primer in DNA replication?

Welcome to SE Biology. At root, your question is a good one, but I have voted to close it as a  duplicate for the following reason. You say you are not asking why an RNA primer is needed, but that is the self-same reason why the primer is RNA and needs to be replaced. In short only DNA-dependent RNA polymerases (of which primase is an example) can operate without a primer —DNA polymerases cannot. If they could there would be no need for a primer, the lagging strand could just be copied. WHY this difference is a matter for conjecture. The answers in the original question only make suggestions.


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Which statistical test should be used for GC-content comparison?
I'm predicting that certain genes (n=20) are more GC rich than expected in all protein-coding genes. How can I test this hypothesis efficiently?
I generated the same number of random genes (also n=20) and calculated GC content for them. After using the t-test (2-tailed, two-sample unequal variance) it shows a significant P < 0.005 result. But I'm not sure that I can interpret it with high confidence.

Crossposted https://www.biostars.org/p/9525660/

You could try a permutation test. These are a kind of non-parametric statistical test which involve creating your own null distribution from your data.
Your hypothesis $H_{1}$ in this case, is that your gene set has a higher GC content than expected by chance. Similarly, your null hypothesis, $H_{0}$ is that there is there is no difference between your set a random set of gene from the population. You are interested in a p-value, which simply asks what the probability of obtaining  a test result at least as extreme as the result actually observed, under the assumption that the null hypothesis is correct.
So thus to obtain a p-value and take say, 1000 random samples of protein-coding genes and calculate their GC content to obtain a null distribution. Then to obtain a p-value that your gene set has a higher GC content than expected under the null, take the proportion of the null distribution greater than your gene set.

I feel you should be comparing your 20 genes against all other protein coding genes in the same organism.
A statistical test comparing the proportion of GC nucleotides in your sample to the rest may be the one to use.


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Is this a worker, or something else?
As far as I understand, this is a buff-tailed bumble bee (Bombus terrestris). It was collected (dying) inside my house in Santiago, Chile. The species was intentionally introduced not far away, for agriculture, some years ago.
Looking for descriptions, I see it is huge for its species, queens reportedly being 20-22 mm (1, 2). I also learned that workers span a wide range of sizes, depending on age (but not this large, supposedly.)
Now, for the caste/sex, I'm stuck due to lack of experience. This site suggests looking at pollen baskets in the hind legs for females (I think I see one, but can't be sure since I don't know exactly what to look at, despite browsing some example photos), but then hairy hind legs (again, I think I might see them, but I'm much less confident) and facial hair for males (I don't really have a point of comparison, but it has some short, black hair in the frons: see expanded photo). Common descriptions also suggests buff color for the tails for queens, but I have seen white-tailed queens around too.
I'd really like to acquire the experience needed.
Is this an old worker, or something else?

this is very likely a queen as they are 20-23mm long but to give a definitive answer you need to measure the lenght of the wings,if they are 38-43 mm it is a queen.the body of a male is 14-16mm the lenght of the wings are 30-33mm and the workers are 11-17mm long and the wings are 22-34 mm long.this is not an answer only some easy to find information.

@trondhansen, thank you! I also read that queens are supposed to have a shorter tongue, which doesn't seem to be the case. I was wondering if there could have been a selective pressure towards larger individuals, vaguely analogous to leg length in cane toads in Australia

I mean, introduction is still relatively recent. Wingspan is about 45 mm BTW (about twice the body length, like all three queens, workers and males)


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How does the researcher deal with new data different of what they have learned?
I am currently studying the book Alberts 5 edition 2016. I was wondering how much of the info will remaining vigent in 10 years.
How does the researcher deal with this kind of things? Do they have to relearn, every new edition of every book that they have learned related to his work?

Life is their book.

Papers.... type a topic of interest: Pubmed

Most of what makes it into a textbook is fairly settled knowledge; there are always minor exceptions being found to whatever rule you think you're sure of in biology (we're not physics), but paradigm shifts make news at scale appropriate to their disruption.


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Single flowers and double flowers on the same plant?
A friend of mine found a strange plant of begonia that at first had regular flowers. After a while it started producing double flowers and has now a mixed inflorescence:

The double flowers look like a result of a homeotic mutant that are also known for begonia, but in this case it is as if such a mutation was somatically "unstable". What might be the mechanism of this abnormality?

I’m unsure of the mechanism, but there are a number of common flowers that change like this. Often it is “age” related:  the young plant gives single flowers, and as it matures, it starts giving double (or more). Some doubles if undernourished will only produce singles. On cosmos, seeing singles and doubles on the same plant is common on plants that are hybridized to be doubles, but not vs. versa. Some sunflowers give doubles on the early buds, but drop to singles on later axillary buds. Your begonia, if healthy, should start producing more doubles.

@anongoodnurse Thanks for the insight. I feel like we might mean different phenomena though. I'm referring to the homeotic mutation that causes stamens to be replaced with petals. Do you mean the same thing for your Asteraceae examples?

I did say that I didn’t know the mechanism, so could not have meant that. Maybe you should clarify your post?

I've updated the question


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conduction in unmyelinated axons
(Not a specialist here) Several questions touch the voltage propagation along an unmyelinated axon, but I'd like to focus on the following.
How fast does the voltage of a sub-threshold perturbation propagate?
More specifically, as in the picture, consider two positions $x_0$ and $x_1$ along an unmyelinated axon. At time $t_0$, a current step is injected at $x_0$.
My understanding is that, at every position $x$ the voltage will charge up with a characteristic time given by the (local) RC value, up to a value that will build, in space, an exponentially decaying profile, with characteristic length given by the resistances of the system.
At position $x_0$ the charging starts at time $t_0$, and at position $x_1$ it starts at time $t_1$.
How much is $t_1$? Is $t_1=t_0$, as suggested here, and probably by cable theory? Does the voltage propagate at, or close to, the speed of light? Doesn't diffusion of ions enter into the picture at all?
And, importantly, can you give me references where I can learn more about this aspect?


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How does the exposure time affect the potencies of antibodies?
The potency of neutralizing antibodies is commonly represented by their binding affinity for their targets. However, binding affinity is based on the dissociation constants at equilibrium, which can’t accurately predict the potency against intracellular parasites (viruses, bacteria and some eukaryotes). These organisms primarily multiply inside the host cells beyond the reach of antibodies, and are only accessible when new offsprings are released from infected cells, which exposes them to antibodies in the bodily fluids. As a result, the time it takes on average for a new offspring to find another target cell (the exposure time) should have a direct impact on the potency of antibodies.
Here are several good examples. HPV is a sluggish virus. Newly released HPV particles have to spend hours in the bodily fluid to undergo complex conformational changes and enzymic activation to become infectious, which gives ample time for antibodies and phagocytes to neutralize and destroy them. As a result, even a very low antibody titer can provide sterilizing protection. Malaria parasites are on the opposite end. It takes only 30 seconds for a newborn parasite to latch onto a RBC and invade it. As a result, antibody concentration needs to be several orders of magnitude higher to stop them. HIV can spread via cell-free particles or close contact between infected and uninfected cells (virological synapses). The amounts of antibodies required to neutralize direct cell-to-cell transfer are also much higher. So is there a more detailed mathematical model to describe the relation between exposure time and neutralizing potency?

Citations:
Explanations for the high potency of HPV prophylactic vaccines
The RH5-CyRPA-Ripr Complex as a Malaria Vaccine Target


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Which spider(?) is this hanging out on my seaside daisy?
The title says it all... location: Switzerland

These things are very shy (of humans, anyway), but great ambush hunters.  I watched one wait patiently on one side while a hoverfly explored the (comparatively) vast surface on the other side of a gaillardia, until the hoverfly chanced within range of the crab spider, whereupon it pounced with great rapidity.

Misumena vatia. (Crab spider, female specimen.)

OZGUR KEREM BULUR / SCIENCE PHOTO LIBRARY 2022, fair usage.
Size: Females can reach 1 cm at maturity, males half that size.
Comprising more than 2000 species, crab spiders can be found all over the world, with the Mitsumena Vatia being confined exclusively to Europe and North America.
A kind of active camouflage allows them to change colour with each moult in response to their surroundings. Colours and intensity of marking varies, the body being yellow or white, the markings pale through intense red and green.
Females are mostly static and wait to catch prey on flowers, trailing a silken line which the males follow to find them.


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What are the mechanical properties of human skeletal muscle?
TL;DR: I need more information on the mechanical properties of human skeletal muscle; if you have such information, please give it to me.
I'm writing something on how much more effective (or otherwise) spider silk would be as a muscle and/or connective tissue in prosthetics in in comparison to human skeletal muscle and connective tissues. As such, I need information on several of the mechanical properties of human skeletal muscle, such as its:

fatigue limit; this is particularly irritating to attempt to find info on; looking it up instead gets returns on the entirely unrelated concept of muscle fatigue, even with very specific search terms.
ultimate tensile strength; while I have sources for this, they're inconsistent, giving me values between 0.44 MPa and 5.3 MPa - more than an order of magnitude in difference!
tensile and/or compressive (i.e. end-to-end/lengthwise) Young's modulus; I already have information on its transversal (i.e. perpendicular to a strand) Young's modulus, which, from what I can tell, is another word for shear modulus, and therefore is useless for my purposes; after all, good muscles are, AFAIK, supposed to withstand tensile or compressive loads, not the shear ones discussed in that source.
elastic modulus; I already have information on it after 8 days of cell differentiation (45.3 ± 4.0 kPa), or the elastic modulus of the rectus femoris in particular (16.67 to 85.31 kPa, depending on pressure applied), but these sources contrast with one of my sources for skeletal muscle's ultimate tensile strength, which states that this figure is 36 ± 19 MPa.

I was also able to find another source on its Young's modulus, but it doesn't specify the direction the Young's modulus was measured in.
One of the few sources I currently cannot find problems with are this one, on how much a strand of muscle can elongate before it fails - and that's because I can't find any other sources which could contradict it - and this one, on how much force a longitudinal muscle of a certain cross-sectional area can contract with: ~30 newtons per square centimetre, or 300 kPa.
There's also the content of and source of this Biology Stack Exchange answer by WYSIWYG, especially the image displayed:

...although I'm still trying to figure out which parts of it correspond to which points on a stress-strain curve.
The unifying factor here, however, is that I don't have enough sources - so few, in fact, that I have no reliable information on the fatigue limit. Please give me more.

Muscle by itself is very weak, all the strength is in the fascia (the tissue around the muscle).
You can see a review here, the muscle itself is negligible strength while the fascia is in the megapascal range.


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How does the female body sense its own pregnancy?
I understand that after the fertilized ovum attached in the uterus the female body will not produce the required hormone surge for ovulation the next month. Therefore no new ovum will be sent down the fallopian tubes during pregnancy. My question is how does the body sense that there is a fertilized ovum in the uterus? Are there some kind of sensors for this? Is the ovum it self producing hormones which can be detected by the body? Does the brain combine a lot of "hints" to infer that there is pregnancy?
Originally the question came about in the context of chickens and how their body detects if new eggs should be produced based on if they are already sitting on an egg.

Just a nit-picky bit of info: it’s different in chickens. Chickens don’t go broody on one egg. They wait for a clutch of eggs. Women don’t wait for several zygotes to start gestation. Also, some research on your part must be attempted and shown in your post, otherwise it will probably be closed. Seems odd for a Q&A site, but it’s still the norm. Thanks.

Interesting! Thanks for the pointer. The research about how this works in chickens turned out to be difficult as most of the internet is apparently just concerned with preventing chickens from going broody. I will try to add some more info about my research anyway. Thanks!


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How is the biggest animal ever existed measured?
Blue whales are considered the biggest animal ever lived with maximum confirmed length nearing 30 meters. While some titanosaurs reportedly were somewhat longer (up to 40 meters for Argentinosaurus and up to 37 meters for Patagotitan).
It's obvious that size constitutes not just length, but I don't quite understand how one can be certain that the said sauropods were smaller provided that they are about 1.5 ~1.33 times longer?

Just look at the body structure of a blue whale vs a sauropod. Whales are round/elliptical in cross-section, and their width is larger proportional to their length than sauropods. Put simply, they just have more volume, even though they may be somewhat shorter. BTW, 40:30 is not 1.5x.

@MattDMo you are right, but I believe there should be more precise way to say that than just raw approximation based on the body structure

We'd also be forgetting about the largest animal ever recorded which is a syphonophore at 46 meters, a spagetti jellyfish.
A blue whale can weigh 196 tons. Argentinosaurus could weigh in at 77 tons:
Initial estimates placed it at 40 meters (131 feet) long with a weight of 77 tons. This makes it comparable to the next largest titanosaur, Puertasaurus (which has been estimated at 73-83 tons by some studies), and thus one of the largest land animals in Earth's history.
People can confuse voluminous, massive, largest, and longest. Scientists will generally not agree about the best way to measure he largest animal, whether it is the syphonophore or the whale.


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Do cheetahs compete with lions?
Do cheetahs compete with lions for the same prey?
A quick Google search says the answer is no:

Lions hunt big animals such as buffalo, giraffe, wildebeest, and zebra. What prey do cheetahs hunt? Cheetahs hunt small animals such as gazelles, hares, and impalas.

Such videos I have seen of the two species hunting, appear to confirm the above.
But I've also heard and seen multiple accounts of lions killing cheetah cubs. Why would they do that, if there is no competition? If another predator eats different herbivore species than you do, their existence is good for you, not bad; by reducing the number of their prey species, they reduce the herbivore competition, thereby increasing the number of your prey species.
A bit more searching found this paper: https://journals.co.za/doi/pdf/10.10520/EJC117300

Based on
actual diet, lions exhibited the least amount of
overlap with wild dogs (31.6%), leopards (39.1%)
and cheetahs (42.5%; Table 2)...  Lions exhibited
the least amount of overlap of preferred prey with
wild dogs (41.0%), cheetahs (43.7%) and leopards
(48.3%).

'Least amount' notwithstanding, that claims more than 40% overlap, in other words a very high degree of competition between lions and cheetahs, in direct contradiction to the story I had previously understood.
Which of these claims is true? And if the two species do compete, how does that work? Which prey species do they both eat?

Yes, cheetahs do compete with lions. Cheetahs can share the same habitat with lions; however, they actively avoid lions (and also hyenas and leopards). They are smaller carnivores/predators than their competitors and they are non-confrontational in nature. They would avoid unnecessary injuries at all costs because they rely on speed to hunt and survive. An injury that can slow them down is potentially life threatening.

Cheetahs have been reported to suffer from intraguild competition by lions Panthera leo, spotted hyenas Crocuta crocuta and occasionally leopards Panthera pardus. These larger predators represent a threat to the smaller-bodied cheetahs as they can affect their food intake by limiting access to high resource areas or kleptoparasitism (e.g. 10–12% of kills are kleptoparasitized in Serengeti National Park (SNP)), and reduce population sizes via increased cub mortality (e.g. 73% of cub mortality was due to predation in the SNP). In response, cheetahs often demonstrate avoidance behavior to minimize interactions with dominant carnivores , with spatial and temporal partitioning regarded as the principal behavioral mechanisms by which this is achieved. Accordingly, cheetahs have been described as a refugial species that seeks competition refuges within the landscape with low densities of lions and spotted hyenas.
Rostro-García S, Kamler JF, Hunter LT. To kill, stay or flee: the effects of lions and landscape factors on habitat and kill site selection of cheetahs in South Africa. PLoS One. 2015;10(2):e0117743. Published 2015 Feb 18. doi:10.1371/journal.pone.0117743

 (removed the citations)
The definition of the terms used in the above citation:

Intraguild predation, or IGP, is the killing and sometimes eating of a potential competitor of a different species. This interaction represents a combination of predation and competition, because both species rely on the same prey resources and also benefit from preying upon one another. - Wikipedia
Kleptoparasitism, literally meaning parasitism by theft, is a form of resource acquisition where one animal takes resources from another. Although kleptoparasitism of food (i.e., kleptoparasitic foraging) is the best known example, the stolen resources may be food or another resource such as nesting materials. - Sciencedirect.com

One of the prey species that cheetahs and lions both eat is Thomson's gazelle (Eudorcas thomsonii). Thomson's gazelle is the primary prey of cheetahs. Probably, the most amount of overlap in their diet comes from eating this prey. However, lions would hunt them less or just steal them from cheetahs.

The prey species included buffalo (Syncerus caffer), wildebeest (Connochaetes taurinus), and Thomson's gazelle (Eudorcas thomsonii) as the three main prey species of Serengeti lions, hyenas, and cheetahs, respectively (Schaller, 1972; Sinclair & Norton‐Griffiths, 1979).
Swanson A, Arnold T, Kosmala M, Forester J, Packer C. In the absence of a "landscape of fear": How lions, hyenas, and cheetahs coexist. Ecol Evol. 2016;6(23):8534-8545. Published 2016 Nov 6. doi:10.1002/ece3.2569

The same paper (cited above) talks about the coexistence of lions, hyenas and cheetahs in Serengeti National Park, Tanzania and provides analysis on the avoidance behavior among the predators. It has the conclusion that despite cheetahs avoid lions, they are not displaced from their habitats and they don't lose access to their prey. In contrast, African wild dogs are displaced from their habitats by lions.

Competition describes where two species have negative effects on each others fitness. But what is sounds like is described here is amensalism, where one species has a negative effect and one has no effect on the other. If cheetahs don't have a negative fitness effect on lions, then the ecological and evolutionary consequences are different for this case amensalism compared with competition.

Although the bulk of the explanation is done in the other answer, my answer will focus on the observations in Serengeti national park and the studies made.
Lions in fact kills cheetah cubs. In the 1990s, a researcher documented lions attacking and killing up to 57% of cheetah cubs (kleptoparasitism) in Serengeti National Park but they rarely ate the cubs completely; the cheetah mothers often consumed the remains of their offspring after the lions had left. However, the increasing lion population has not triggered a drop in cheetah numbers. They have remained stable, despite losing many of their cubs. They are apparently able to compensate for the loss of their cubs because females become fertile within 2 weeks of losing their offspring.
Cheetahs also adopted different strategies to deal with threats from lions. Cheetah females were found to set up their dens precisely where there are the most lions. Researchers says it is counterintuitive but their study offers a plausible mechanism for this and they called it "fine scale behavioral avoidance of the lions, a sort of carnivorous ballet". Male cheetahs and single females eat their prey as quickly as possible. Mothers with cubs, on the other hand, watch out for possible threats while their young are eating in order to give them enough time to eat their fill. Cheetahs do not have the strength to haul their kills up trees to keep them safe from scavengers as a leopard does, nor can they physically defend themselves against a lion. They therefore tend to hunt when larger predators are away or less active and eat their prey as quickly as possible before it can be snatched away from them.
References

https://www.science.org/content/article/carnivorous-ballet-helps-cheetahs-coexist-lions
https://www.springer.com/gp/about-springer/media/research-news/all-english-research-news/how-cheetahs-outsmart-lions-and-hyenas/15602738


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Identification of Mold / Fungus
I am working with some old plaster powder, and a few days after it set (mixed with water), I found that pink mold / fungus appears to be growing on it. See attached photo.
Please help me identify what type of mold this is and if it is dangerous to my health.
Thank you.

Welcome to SE Biology. Personal medical questions are off-topic here..  It would be useful to include your geographic location.


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How does a stimulus causes a voltage change in nerve cell?
I know about the opening of voltage gated sodium channels and then how the membrane becomes depolarized when the rise of potential greater than threshold occurs.
But what happens initially after the stimulus that causes a change in potential and makes it reach up to the level of threshold?
Like what that light, touch or chemical did?

Ligand-gated ion channels, mainly. Ligands can be neurotransmitters like glutamate or acetylcholine, or extraneous chemicals. TRP channels can also be sensitive to things like temperature. Mechanoreceptors and hair cells in the cochlea used in audition are gated mechanically. Gating can be direct or via a second messenger; photoreceptor cells use a chemical conformation change triggered by photons to detect light, but the actual voltage change comes by a channel gated by cyclic GMP.


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Ecosystem Control Theory
I've used EcoNet online tool to analyze an ecosystem. You can run the default model by pressing "run model" in order to follow my question.
Among the extended results there are 2 'Control Matrix' but unfortunately they don't state the source for the calculations in their documentation. In the documentation, right below Utility Analysis, there's a blank paragraph intended for Control Analysis.
I'm looking for someone that knows some articles explaining the math behind those matrixes and also their interpretation.
I'd be really glad if you could help me.


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What decomposes the decomposers?
Decomposers feed on dead organisms. What feeds on them? In particular:

What decomposes mold?
If fly larvae feed on animal dung, what eats their dung?
Are all fungi eaten by animals? If not, what decomposes them?

Just think of it like scavengers but at the microscopic level. Microorganisms can scavenge each other just like larger animals can.

Maybe your thinking on a "food chain" paradigm. So, who eat the specie that are at the end of the chain?. In a "food web" paradigm there is not such a problem.

Probably (1) "fungi and other decomposers", (2) "fungi and other decomposers", (3) "fungi and other decomposers".
If you're interested in precise answers ("exactly which taxa are responsible for the decomposition of some particular type of dead tissue?") you probably won't get an answer. In general the answer is "detritivores chew on it, break it down, extract some of the useful material, poop it out; then a broad spectrum of other decomposers (fungi, bacteria, protozoans) do the rest of the job".


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Arachnid identification request
Every so often I come across one of these (presumably) spiders, but haven't been able to find out what species it is.
It is black, ~7mm in length, has a long and narrow body and relatively short legs, and seems to be able to spin threads. I came across it indoors in South-Western Germany in early Summer. The closest match I could find is the Zebra jumping spider, but "mine" has no stripes. Could it be another species of jumping spider?
I realize the picture quality isn't great, but it's all I have:

Not a zebra jumping spider - but it is in the same family of jumping spiders.
It is a kind of ant-mimic jumping spider. Possible genuses (genera) are: Synageles, Myrmarachne, Leptorchestes, which are present in Europe.
Micaria is another genus in Europe but this does not look like one of those.
There are other similar-looking genera Peckhamia, Sarinda, Synemosyna, but these are mainly found in the Americas and not in Europe.
--
(EDIT) the most observed species in Germany from these genera are (in order):

Synageles venator
Leptorchestes berolinensis
Myrmarachne formicaria

(according to iNaturalist)

Thanks very much! I can't verify for sure, but Leptorchestes berolinensis looks like a very close match.


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How can I easily distinguish between eukaryotic and prokaryotic cells using flow cytometry?
I am trying to count populations of cells in a co-culture. One organism is Pichia pastoris and the other organism is a gram-negative bacterium. Pichia stains gram-positive using crystal violet and the bacterium is negative. These two populations are reasonably distinct in front and side scatter but not so much that I can gate the entire population. I can pick a region in FSC-SCC for each organism that I know will only include that organism, which is 'good enough' for my purposes, but I'd love to know if there is a quick, easy, cheap way to distinguish these two populations more decisively. To clarify my requirements:

Cheap: Ideally something widely available in the price range of <$1/sample e.g. Hoechst/Van-Bodipy/WGA-647
No processing steps: I just want to add the dye/stain to my sample automatically using the flow cytometer before running the samples

Things I have considered but have ruled out:

Antibodies: They are too expensive for my case. I would need a custom conjugated antibody or to add processing steps between primary and secondary antibody that is too complicated.
Tracker/tracer dyes (add to one cell population before mixing the co-culture together): Also expensive, and I will probably want to track my population over more generations than most of these dyes work for.
Intracellular markers that require permeabilisation: I don't want to do any processing

Things I'm considering and would welcome input on:

Conjugated lectins, specific to glycoproteins on Pichia pastoris
DNA dyes, using the fact that Pichia genome is approx 2x larger than the bacterial genome
Differing autofluorescence: There's nothing obviously different here from my data so far, but I will go back and tweak the voltages etc. if this is a very promising avenue
Any combination of stains/techniques that are not specific alone, but then the populations can be separated using e.g. PCA

Is there anything out there that will work for me? It seems to me that the cell types are so different there must be an easier solution here than expensive antibodies etc. An answer of "No" would be just as valid as yes! I can continue just using front and side scatter if the only solutions are going to be too complicated.

Acridine orange might work for nucleic acid content. You might want to check out the Molecular Probes Handbook for some options Ch8 and 15.

Ok to kill the cells you are counting?

@PolypipeWrangler Sure, but only if it's not too complicated/doesn't involve too much waiting

What about using cell size? The prokaryotes should be much smaller.

@Chris Yes, I do see a difference in forward scatter on the flow cytometer, which correlates with cell size, and it's 'good enough' when combined with a difference in side scatter. I'm wondering if there's a third dimension that I can separate them on that will make it totally unambiguous.

If you kill one population, the dead cells will be easily permeable to various dyes.


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Why does photosynthesis specifically produce glucose?
Why not a pentose? Or a tetrose? Or a deoxy sugar? Or just some other hexose, like fructose?
Is there some chemical reason life should have settled on glucose as the standard photosynthetic output, or is it just random? It seems very suspicious that this ubiquitous molecule nicely break down into exactly 3CO2 + 3CH4, or 6CO2 + 6H2O - 6O2, or 6H2CO, when such convenient formulas are not true of the actual immediate products of carbon fixation.

Or why a sugar at all?  CO(2) is the most oxidized form of a single carbon atom, and in photosynthesis carbon is reduced (where water is the source of electrons), but not fully reduced: the most reduced form of a C-6 compound is hexane, not glucose (and the most reduced form of a single carbon atom is methane)

@user338907 The plants use the glucose too. It's not (just) a waste product. It isn't particularly helpful to extract the most amount of energy out of photosynthesis just to then waste way more than that when trying to build e.g. cellulose. Evolution doesn't select the "best" process in isolation, it's always part of a specific environment. Mind, that's not knowing where glucose came from - it's very likely that was long before photosynthesis developed. And of course, photosynthesis doesn't actually produce glucose - it produces GAP/G3P. That's quickly turned into glucose, usually.

Glucose is such a ubiquitous energy storage molecule, that we show the simple photosynthetic chemical equation to include the capture of six CO2 molecules to create one glucose molecule. However, the steps specific to photosynthesis, the light-dependent and light-independent reactions, don't produce glucose directly. Instead, they produce an intermediary molecule, the 3-carbon D-glyceraldehyde 3-phosphate (G3P), which can directly enter the general metabolic cycle, which includes gluconeogenesis. Gluconeogenesis includes a pathway from G3P to glucose.
So, photosynthesis itself doesn't produce glucose, but can be considered to add to the production of glucose because it is integrated into ubiquitous metabolic cycles.
There are existing hypotheses as to why glucose is so ubiquitous. One hypothesis is that glucose is less likely to nonspecifically interact with proteins than other molecules of its kind (aldohexoses) because it is more stable in its cyclic form (instead of the open-chain form) compared to other aldohexoses. Another hypothesis is that β-D-glucose has all five of its hydroxy groups in the equatorial position, making them more accessible to chemical modification, such as esterification, acetal formation, and linkage into polysaccharides.

Excellent answer. I would just emphasize that cellular life existed on Earth existed for at least a billion years before the evolution of photosynthesis. That's a long time for organisms to have refined the storage and utilization of organic molecules for energy. It makes a lot of sense that photosynthesis would evolve in a way that most efficiently feeds into these existing metabolic cycles.

I'd always assumed that being a precursor for handy molecules like starch and cellulose would have made it quite an attractive choice for plants as well