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How do birds eliminate oxygen free radicals
Birds breathe in a lot. Do they produce a lot more of oxygen free radicals than mammals? And how do they cope with oxydative stress?
Thanks!

Did you check on google scholar? There are a few papers there

“Birds breath a lot”! Me too.

@user438383 That is not scientific wording. better results from: https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=avian+oxidative+free+radicals+&btnG=

There is some info on that here:
Oxidative stress in ecology and evolution: lessons from avian studies
The article cites enzymes, antioxidants, brood size, serum analysis, body temperature, food types, membrane fatty acid composition, Vitamine E, carotenoids, and many other considerations. Perhaps you can read it and write an answer for us? Here is a summary:

Possible explanations for the higher longevity of birds compared to their mammalian counterparts are that birds have (1) a lower ratio of oxygen radical production and oxygen consumption, (2) an exceptional cellular resistance to oxidative stress, (3) a lower mitochondrial and nuclear DNA oxidative damage, (4) a lower cell membrane unsaturation and (5) a slower life history for a given body size

thanks, this table is wonderful! I will try to find an answer, the article you shared seems to be more complete than what i had found so far. i will share my findings

take it with a big grain of salt "aging rate" is not a well defined thing. There are also big extraneous factors like mammals can run out of new teeth and starve becasue they can't feed, which is a common cause of death among mammals and nothing else. becasue mammals are basically the only group with limited numbers of teeth. and mammals can develop more in utero becasue of the advantage live birth has over eggs.


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Am I reading this respirometer correctly?
I want to double check that I'm reading these respirometer vials correctly. The volume O2 of the following vials should be:
Squirrels in Torpor:
E1: 0.4 E2: 5.0 E3: 0.3 E4: 5.1 E5: 0.4 E6: 0
Squirrles at Stable body temperature in rewarming phase:
E1: 90.3 E2: 85.1 E3: 85.3 E4: 90.4 E5: 90 E6: 0
Right? Image below

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No, you're misreading the scale several times. The scale divisions indicate "tenth of ten" = one, while you sometimes misread them as "tenth of one" = 0.1.
For example:
E2 is correct as 5.0
E1 is just one mark less and should be 4.0 instead of 0.4.
(Remark: I don't know, whether to read the scale at the right or left side of the green part - I trust you using the right side)

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Gibson assembley for small fragments?
I am new to the Gibson assembly, I know how I need my plasmid but main problem is I don't have short tags and linker so I wanted to do Gibson assembly?
5'-TCACTCTCGGCATGGACGAGCTGTACAAGcagcggcagcgaaaccccgggcaccagcgaaagcgcgaccccggaaagcgaaaacctgtactttcagtccgactacaaggaccacgacggtg

Capital letters - my plasmid backbone
Italics - 3xtag
Bold - TEV site

I have plasmid backbone but I dont have 3xtag and TEV site so how can I design the primer so that i can do Gibson assembly to incorporate the sequence?

I assume that your backbone is supposed to continue after the TEV site?

Yes, but due to MCS limitations i decided to go on another plasmid and it is 21nt length so difficult to extract by agarose

Gibson Assembly is not ideal for short fragments; chances are that the T5 Exonuclease will digest your entire fragment before it has the chance to hybridize with the backbone. For fragments shorter than 200 bp NEB recommends a 5-fold excess to compensate for this, but in your case the fragment would only be around 130 bp long. It might work, but efficiency will be very low.
Either way, based on my understanding that you don't have the 3xtag-TEV sequence available as PCR template, what you would need is two long primers designed such that they overlap by 20-25 nt at their 3' ends (orange), and with the backbone at their 5' ends (blue) as shown below:

You would then run PCR cycles with the primers alone to generate your double-stranded fragment, which you can then use in the Gibson Assembly reaction.
If you're not using a commercial Gibson Assembly kit, but instead add the enzymes yourself, you can also try an alternative method called TEDA cloning. The procedure is practically the same as that of Gibson Assembly, but TEDA uses only T5 Exonuclease. Instead of relying on (very expensive!) Phusion DNA Polymerase and Taq DNA Ligase for sealing the plasmid, plasmid repair in TEDA happens after transformation into bacteria, taking advantage of E. coli's own DNA repair machinery.
In your case, the advantage with TEDA is that you can try different incubation times with T5 Exonuclease to find a short enough incubation time such that single-stranded 5' homology ends are generated without digesting your entire fragment; or even incubate your backbone first and add your short fragment later in the TEDA reaction. As an extra bonus, TEDA cloning costs a fraction of the price of a Gibson Assembly reaction.

Great. I will go for long primers which seems to be reliable. In case if i have time i will give a try to TEDA cloning also.

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Will wiping a phone down with isopropyl alcohol daily breed bacteria resistant to disinfectants?
The title says it all. If you disinfect something more regularly, aren't you just selecting for bacteria which are most robust to that method of disinfection? I've heard it said about some medications that they "can't cause antibacterial resistance". In particular I've read that this is claimed about topical benzoyl peroxide in the context of skincare. Do these claims have any weight to them?

Does this answer your question? Why can bacteria resist topical antibiotics, but not compounds like Benzoyl Peroxide?

It is possible to select bacteria in vitro, with some help, to withstand 50 g/L (5% v/v) of isopropanol.   According to this paper, bacteria at hospitals in Peru have a variable but increased resistance to isopropanol.  (That study was preliminary, however)  Since bacteria can produce isopropanol themselves, some degree of resistance is very plausible.  Even so, the fundamental nature of 70% isopropanol's attack on the membrane makes it hard to defeat.  Anything is possible in biology, but the more proper the application of disinfectant in terms of exposure time and concentration, the less plausible the selection of resistant species or strains from the bacterial community will become.


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Blood and plucked-feather sample storage
This next field season I will be collecting both blood and feather samples and I wondered how best to store the samples. The blood samples will be used for microsatellite and/or SNP analysis. The feather samples will be used for genetic sexing and/or microsatellite analysis.
Feathers: can these be stored in envelopes at "room" temperature? I've seen mixed answers in the literature. They are plucked feathers and so may have a bit of blood or tissue at the tip. If they are used for microsatellite analysis, I want to ensure this DNA is not degraded. I will be storing them frozen at my field site, but our partners at other sites may not have access to freezers.
Blood: we will be collecting blood into capillary tubes. I have a few Whatman FTA cards, but not enough. So I'm planning to freeze the blood in the capillary tubes. Are there better options than this? I'm planning to use non-heparinized tubes. Out of curiosity, has anyone used blood from FTA cards for microsatellite or SNP analysis? Can I expect sufficient DNA quantity and quality? Bird DNA is nucleated, so I should get more bang for my buck (volume-wise).
I appreciate your help!

I've always used pure ethanol to store samples in the field before extraction. Is this possible with feathers?

I'm not sure, it seems possible and I can see if there is anything published. Unfortunately we are dealing with international shipping, so that may be difficult (that's a question for my advisor!). So far, for feathers it seems that people freeze them or store them dry. I have seen ethanol recommended for blood samples.


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Why is gyrification advantageous?
Standard 'Explanation':
I've seen countless neuroscience articles and experts explain that 'cortical gyrification is advantageous because it increases surface area which obviously increases your intelligence' (e.g. this wikipedia article).
Question(s):
But this explanation is woefully lacking, why does surface area matter at all? That implies  that somehow empty space is contributing to cognition (since the alternative is that space being filled with brain matter).
My best guess:
The only guesses I have are that perhaps it functions like skip layer connections in Residual ANNs. This section of the wiki page, says it is advantageous because 'it allows neurons to be closer together' which I guess kind of corroborates my idea?
Question(s):
But it is still far too vague and speculative. Why could these same wiring patterns not just emerge within a smooth-surfaced brain without wasting space? Also, does this imply that if you got more brain matter to fill in these spaces later your intelligence would decrease?

Short answer
The structural anatomy of the cerebral cortex is closely related to its functionality. The cortex is a thin sheet of only a few cell layers deep. Expansion of processing power requires enlargement of the surface area of this sheet, and simply increasing its volume doesn't help. As a consequence, gyri and sulci developed during evolution to accommodate this restriction.
Background
The human brain is characterized by a prominent and enlarged cortex, much larger than that of other primates. This is mainly due to the great expansion of the cerebral cortex during evolution. The underlying structures have, however, remained stable (Toro et al., 2008). The cerebral cortex houses the higher cognitive functions that separates us from other animals, allowing us to reason, talk, write books, develop culture and so on. As a result, to allow the development of these higher cognitive functions in man, it was the cortex that needed expansion, and not the deeper more ancient brain structures that govern more basic needs of life (breathing, heart beat etc.).
Because the cortex forms only a thin sheet a few cells thick that overlies the rest of the brain, a solution had to be found when the cortex was expanding in our early hominid ancestors, because the whole brain did not need inflation, just the cortex. Folding of the cortex increases the surface-to-volume ratio such that an expanding cortical surface fits onto a relatively stable base.
To take this a step further - why not increase volume in order to fit those extra neurons in? Since the volume of a ball increases by a third power with radius, why on earth would nature keep holding onto increasing the surface area, and not simply inflate the cortex by enhancing its thickness?
This has to do with the fact that the vertical architecture of the cortex has remained remarkably stable during evolution. In other words, evolution of a bigger cortical area to enhance higher cognitive processes has occurred in the most parsimonious way so typical for evolution: take an existing structure and enlarge it when there is need for more.
The cortex typically consists of a thin sheet covering the brain, and is not more than 3 mm thick. The neocortex represents the great majority of the cerebral cortex. It has six layers and contains between 10 and 14 billion neurons. The six layers of this part of the cortex are numbered with Roman numerals from superficial to deep (Fig. 1). Layer I is the molecular layer, which contains very few neurons; layer II the external granular layer; layer III the external pyramidal layer; layer IV the internal granular layer; layer V the internal pyramidal layer; and layer VI the multiform, or fusiform layer (Review of Clinical and Functional neuroscience, chapter 11).

Fig. 1. Cortical layers. source: Mental Construction.
Basically, layer IV receives most input from the periphery via the thalamus (visual, auditory, tactile inputs etc.), layer II/III takes care of horizontal projections for further processing, while layer V takes care of the output (motor output etc.). This basic architecture cannot be changed easily without changing the entire core workings of the cortex. As an analogy - to speed up computers in a parsimonious way, one can expand the number of processors quite easily. Coming up with a speedier processor is difficult these days, as evolution of single processor capabilities is pretty much at a dead end.
Thus, to increase the number of cortical neurons, the cortical surface must be enlarged. As the basis (subcortical structures) remain pretty much the same, creating folds (gyri and sulci) is the best way, and perhaps the only way to increase cortical surface area.
Reference
- Toro et al., Cerebral Cortex (2008); 18(10): 2352–7

I appreciate your answer and it does help but some things I still don't understand: why has it remained so stable during evolution? And if as you say evolution likes to take something which already exists and make it larger why not do that vertically instead of horizontally?

Another possible reason occurred to me, is it because of 'brain cleaning' mechanisms when we sleep? I heard once that when you sleep the brain expands & becomes 'loose' to clean itself out. Is this true, do you think its related?

@profPlum why has it remained so stable during evolution? And if as you say evolution likes to take something which already exists and make it larger why not do that vertically instead of horizontally?: because structure is related to function. The second comment you make here seems far fetched to me. No gross structural changes happen overnight.

One last question before I accept your answer, do you suppose that if extra brain matter were to fill-in these gyres after the brain has developed that it could somehow disrupt the proper functioning of the cortex?

@profPlum I can only think of brain tumors as a practical example of your hypothetical situation. Brain tumors are bad, always, as they compete with normal brain tissue for space and disrupt its normal function  for space. This probably doesn't answer your question, but it's too hypothetical to be answered in any conclusive way.


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Which landmark paper first described the differentiation of T-cells?
T-cells are distinguished from B cells in part by their locus of differentiation/maturation (thymus). This is textbook knowledge, but I was wondering which particular person or people were responsible for making this discovery. I'd appreciate any links to their original papers/works. Thanks a lot!

This paper appears to be a history of the discovery of B/T differentiation and the role of the thymus. I believe that you should find a number of important references therein.
It describes specifically a series of publications in the 1950s and 1960s that may be relevant (section "Identification of T and B cells"), such as this one by Gowans.


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Pearl formation process: what is it called? How does it work?
I have heard a pearl is a disease of oysters.
Astonished by the statement, I searched a bit [1] and I discovered that  it is really a protection mechanism of the oyster.
I know this defense mechanism is not unique in nature. E.g. humans can isolate foreign bodies (this happens with not-extractable bullets), as well as bees propolize foreign bodies if they can't eject them.
What is the process, the ability of those organisms, called?
How does it works? E.g. how organisms recognize foreign bodies other than other things?

[1] https://en.wikipedia.org/wiki/Pearl

https://en.wikipedia.org/wiki/Nacre#Formation


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Why didn't Escobar's hippos introduced in a single event die out due to inbreeding
Today I read a BBC Report about how Pablo Escobar had once imported 4 hippos (1 male, 3 female) into his estate in Colombia for his private zoo. After his downfall, while other species were shipped out, hippos were considered too big to move and expected to not survive.
However, to the surprise of all the hippos are thriving and are so numerous that there have been calls to cull them. From the report:

Numbers are projected to only get bigger. [Colombian biologist Nataly] Castelblanco and her
peers say the population will reach over 1,400 specimens as early as
2034 without a cull - all of them descended from the original group of
a male and three females. In the study, they envisaged an ideal
scenario in which 30 animals need to be culled or castrated every year
to stop that happening.

My understanding is that since there was only 1 male, the gene pool would be limited and lead to lot of inbreeding in the descendants. This would cause population to not explode because some individuals would be unfit to survive.
Why has this not happened in case of hippos? Is it because there are 3 females (probably unrelated to each other) which keeps gene pool large enough? Or can mutations explain this phenomenon? Would results have been different if originally 2 females had been moved and only 1 retained?
EDIT - I have just found that current population is maybe less than 100 individuals which though big is not massive.
EDIT2 - I have edited the question title to keep focus on the hippos although a general answer would be welcome.

It is definitely not the case of all invasive species but in sunflowers at least, there is a tendency of invasive lineages to reproduce clonally (Bock et al, 2018)

It happens in other species.  Hamsters, for example.  Every golden hamster alive today is descended from 1 mother and a litter found in Syria in the 1930's, and there's millions (maybe billions?) of them due to their popularity as pets.  And hamsters don't live nearly as long as hippos, so we're talking far more generations, and a longer timespan, and that genetic bottleneck hasn't been a problem yet.

Keep in mind, it usually takes several generations for inbreeding to show its effects. The first couple of generations won't be that inbred at all, but as the inbreeding coefficient rises and the average individual is more and more related to one another they are more likely to show ill effects. Hippos only reach sexual maturity at about age five to six so there have only been a handful of generations born in Colombia as of now.

@DarrelHoffman at least according to wikipedia, that's not quite true about golden hamsters - only domestic ones (maybe only north american? wording unclear) and it also has a glaring "citation needed"

@llama Well, domestic hamsters are by far the majority of them - apparently a few have been found in the wild since, but nowhere near the numbers of domestic ones.  Either way, even if it is only North America, we're still talking about millions of hamsters descended from one litter.

The European royal families handily demonstrate that inbreeding isn't necessarily a showstopper.

I think one of the important things to understand in thinking about this case is that it just hasn't been that long, generationally.
Escobar imported the hippos in the late 1980s. Hippos reach sexual maturity at an average of about 7.5 years old for males and 9.5 years for females, space births about 2 years apart, and live for 40-50 years.  Thirty years out, this means that only about 3 generations have passed for females. Moreover, the dominant males are highly territorial, which means that much of the breeding might even now be still coming from the initial male and not his descendants. Still, the initial male breeding with his own daughters would indeed produce a significant inbreeding coefficient.
The impact of inbreeding, however, is also affected by the density of deleterious alleles. In geographically restricted species, the higher natural level of inbreeding can result in purging selection that leads to a much lower frequency of accumulated deleterious alleles than in highly social and gregarious species like humans and dogs. Hippos appear likely to be such a species, as well as having overall lower genetic variation than other large African mammals, suggesting a fairly recent expansion.
In short: it hasn't been that many generations, and if the inbreeding sensitivity of hippos is indeed fairly low to begin with, it may indeed be that there simply isn't any significant impact from inbreeding at this point in time.

Its also important to understand inbreeding does not guarantee a die out, it increases the chances of it. Its like being a heavy smoker makes lung cancer much more likely but does not guarantee you will get lung cancer.

Note that at least according to the BBC report "Indeed, conditions in their South American home seem so ideal for the hippos that studies show they start reproducing at earlier ages, she said." where "she" refers to Nataly Castelblanco - co-author of the article referenced in MikeSerfas' answer.  So they may well be beyond the 3 generations suggested in this answer.

They often do. You hear a lot about all of the times invasive species succeed in invading a new habitat, because there is a surviving population around for researchers to observe. There are lots of cases where new species are introduced to an environment in a single event but fail to survive. Rabbits and foxes were repeatedly introduced to Australia, only for most of the events to fail. The fact that there are rabbits and foxes there now is a consequence of the sheer number of times Europeans tried to introduce them. There are also many cases where captive animals escape captivity but fail to establish a breeding population, everything from "alien" big cats to coatimundis in Oklahoma.
This has actually been suggested to be one reason you don't see a lot of carnivores on islands. Carnivores might be able to disperse to islands, but they do so infrequently and the islands can't support their population that they end up dying out and we never know there was a dispersal event in the first place.
It's worth mentioning as well that many invasive species events probably aren't a "Noah's ark" type situation where you have only a couple of surviving adults. Many of the fishes that invaded the Great Lakes either did so in large numbers through the Welland Canal or were introduced in large number as eggs (smelt, salmon, some suspect alewives could have been introduced this way). Ballast ships can contain thousands of genetically distinct larvae and propagules of algae, small fishes, and invertebrates. Most deliberate introductions (e.g., rabbits and foxes in Australia) usually try to introduce enough individuals that inbreeding won't be a problem. Many invasive plants or feral domesticates (Asian carp, wild boar) were bred in captivity in large numbers and merely became wild.

The links you have posted are interesting! If I understood correctly, the second and third paras of the answer deal with overpopulation and multiple introduction events. As the question is specifically about dying out due to inbreeding (not over population) and from a small gene pool (rather than multiple individuals), maybe you would like to tackle those aspects as well?

I have edited the question title to make it clear that I am more interested in why the hippos thrived.

This is answering the opposite question. The question presumes that they should have died out like the examples you give, and asks why they didn't.

I'm almost tempted to purchase the rabbit article (just not $35 worth of tempted), as I was under the impression that a single release was the source of mainland rabbits.

@Barmar It's survivorship bias at work. Most of the introductions do fail, but we pay attention to the few that do succeed due to blind chance because they have a big impact on the local ecology. Thinking they represent the rule rather than the exception is the issue.

I don't think he's thinking they represent the rule, he seems surprised about it. And he's wondering how they achieved this miracle.

There are some references on this: Castelblanco-Martinez, 2021 is a recent one.  There doesn't seem to be much doubt at least that hippopotami are thriving as an invasive species.
I didn't see anything on the genetics, but I will give in to the temptation to speculate even if perhaps I shouldn't.  There are some advantages that are likely working against the effect of inbreeding depression:

being an invasive species with perhaps fewer diseases and predators or more assured access to resources that in their native range.
artificial selection to avoid deleterious alleles, if particularly healthy specimens were chosen for transport to South America by people who really did not want to leave their customer dissatisfied.
outbreeding enhancement ("hybrid vigor"), perhaps, if the founders were brought in from widely separated populations as a collector might tend to prefer.  Since we care about genetic diversity, not the literal number of founders (nor their sex, much) this directly opposes the bottleneck circumstance.
mundane issues: perhaps the females were imported pregnant, or an escaped hippo was surreptitiously replaced by a terrified lieutenant at his own expense.

Given these advantages, the hippos might do at least as well as the wisent, which was already facing extinction (suggesting harsher circumstances) before being reduced to 12 individuals, but has since begun to recover.

To focus on the inbreeding:

Inbreeding in itself is not a factor that would make species die out. Rather, inbreeding increases the risk of genetic diseases, if the deleterious alleles are already present.
Three females do not represent such a large genetic pool, so that inbreeding would still occur.
Given that there have been only few generations since the introduction event, there were obviously no outright deleterious alleles present, while it is too early to talk about dicrease in overall fitness.
Restoration of populations of nearly extinct species from small populations has been the focus of the conservation movement for over several decades. In many of the cases where a species was brought back to life we are talking about severely inbred populations. Notably, the modern population of Przhevalski's horses is claimed to descent from one ancestor.

Animals don't die out from any causes related to themselves, their breeding, or anything like that.  They die out either because their ecological niche goes away (climate change, etc.), because something else outcompetes them in that ecological niche (introduced fish outcompeting cichlids, for example), or because an external force exterminates them (dinosaurs and a damn great rock).
Inbreeding doesn't stop breeding - it just means they're more prone to certain developmental problems.  If you look at pure-breed dogs for example, all breeds are inbred because that's the very definition of a "pure-breed".  The result is that they're all very prone to issues with joints, eyes, arthritis, and more obscure issues like "cocker spaniel rage syndrome" (yes, that's a real thing).  None of this stops dogs from breeding though.
In the case of the hippos, they've been dropped into an ecological niche which is perfect for them, and which has no predators capable of limiting their numbers.  If given time and limited to that area, their numbers will naturally become limited by overgrazing and starvation.  But before that, they'll have made a complete mess of an environment which hasn't evolved to deal with hippos in it. Of course inbreeding means they'll develop some genetic issues which cause many individuals to be unhealthy in various ways, but it won't stop the herd from continuing.

Some individuals being unfit to survive, doesn’t necessarily lead to extinction, it leads to removing the traits that make them unfit to survive from the breeding pool.  From a species POV this is a good thing.
This leading to extinction happens when so many individuals have the trait, that those without it can’t can’t find a breeding partner to have children that don’t have the trait.
Critical in that happening is the trait being present in the breeding pool AND it making them unfit in the their current environment.  For instance, a trait that made them unfit to face off against lions or hyenas wouldn’t matter, if they aren’t fighting something that is at least similar to them.
Take snakes in Guam, lots of them probably came from similar small lots, but without predators, it doesn’t have so much of an immediate impact.  Of course that doesn’t mean they will be successful in the long term either, as they are likely to run out of prey and starve to death.


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Is there any reason to use an upright microscope over an inverted microscope?
I've never actually owned an inverted microscope, but it seems it has only advantages compared to an upright microscope: taller, heavier samples; no crashing the objective into the glass slide; easier to operate, etc.
Why then do people still use regular, upright microscopes? Is there a disadvantage I'm missing?

Cost?  A quick search shows inverted microscopes costing several thousand dollars, while a decent upright can be had for a few hundred.

@jamesqf Yup, seems obvious now... Should I delete the question?

There might be other reasons - I'm certainly not an expert!

For metallurgical microscopes there is little difference. I would say individuals chose on the basis of  quality ( image ,light, and mechanical). We nominally had about a dozen , mostly different , from Leitz to Unitron. Some console types like Richert (?) were only used for special jobs as they tended to be less convenient My boss loved old B & L where you physically removed the objectives - no turret.

As already mentioned in the comments, cost is one of the primary reasons when you're looking at simple light microscopes. Inverted scopes have more complex optics, along with the convenience factor of being able to examine larger samples, generally having a more stable frame, etc. All this leads to higher cost.
An advantage I can think of for smaller upright scopes is the ability to use them as a dissecting scope, where the sample is opaque and you need to see it from above. Another advantage is this:

Many fluorescence microscopes are upright, as there is a significant amount of extra equipment that needs to be mounted in addition to the eyepiece, including lasers, stage motors, and cameras and other detectors. This can take up a lot of room, and for convenience's sake it's often easiest to mount it up top where it is accessible.

Doesn't the extra equipment usually have to be built in, though, or at least have ports & fittings on the microscope to allow it to be added?  Which would raise the cost.

@jamesqf correct, which is why I clarified that the cost argument really only applies for simple "magnification-only" light microscopes. Once you start getting into very high magnification, fluorescence, live sample chambers, etc., cost starts to skyrocket.

Because inverted microscopes use a long working distance condenser (which allows them to fit plates, flasks, roller bottles, etc) - the resolution in transmitted light is inherently limited.  An upright microscope with a standard condenser will deliver much better results at higher magnification when you are imaging slides.
Consider your resolution in transmitted light a function of objective resolution AND condenser resolution.  If you have a high resolution objective but a low resolution condenser then you are inherently limited by the condenser regardless of how good of an objective lens you have.
A typical condenser on an upright microscope has a working distance of 1mm and a numerical aperture of 0.9/1.25.  So the condenser is right on top of your sample delivering the light needed by higher resolution objectives to perform.  A typical condenser on an inverted microscope has a working distance of 72mm and numerical aperture of 0.30 (of course there are alternate choices, this is just the most common).  So on the inverted the microscope the condenser that delivers light into your objective lens is 72mm away and has limited NA/resolving power.  This is just fine for the lower mag and long working distance objectives used for tissue culture because the LD objectives already have limited numerical aperture/resolving power.  But if you were imaging slides with standard working distance objectives which have higher apertures (especially if you are using oil immersion objectives i.e. 100x or 63x) - the condenser on an inverted microscope doesn't cut it and you need an upright microscope.

This looks like a great informative answer, but it would be helped by citing sources.


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What is tissue patterning?
This term gets thrown around sometimes in biology articles, and I have a rough idea of what it is: during embryonic development, the tissue differentiates in a certain spatial configuration. Wikipedia also mentions that its two main mechanisms are regional specification and cell differentiation. However, I would really enjoy a thorough definition of the term (either in the form of an answer or a reference).

I would guess that the term "tissue patterning" could be an umbrella term for multiple different developmental processes. In precise (more modern) developmental terms it could be a old synonym or sub-type for "Regional differentiation"
https://en.wikipedia.org/wiki/Regional_differentiation
It also fits to the concept of X-inactivation in female mammals, but this phenomenon can not be observed by the bald eye.
https://en.wikipedia.org/wiki/X-inactivation
It is quite possible the term originated from pigmentation biology an early genetic discipline. The underlying mechanism are the Pibald mutations , which result in dysfunction in dorso-ventral melanoblast migration , a dominant mutation, that is a source of white spots and patches in many mammals.

These mutations are almost omnipresent in domesticated furry mammals (cows, dogs, cats rats,horses) as well as some wild species where it gives an evolutionary advantage.
You can also check out cat coat genetics its a lot of fun and relative easy classical genetics.
https://en.wikipedia.org/wiki/Cat_coat_genetics

Excurse biological definitions:
Many biological terms originated in the first years of biology as a science (<1820 ) when genetics, microbiology, evolution and developmental biology where not discovered as disciplines yet (Mendel, Pasteur, Darwin&Wallace where born later, Boviery, Speemann even later), so people (zoologists, botanists) just named the thing they observed, without knowing what the underlying mechanism was. So since they did not have the concept of mendelian inheritance, nor embryonic development, they just called it in layman's therms: "patterning".
Nowadays with the term "tissue patterning" is not totally clear anymore what an author means, if it has no proper context, in my opinion. We have clearer defined terms.

The historical explanation at the end is pretty cool, after reading up a bit more on it and consulting your links, I tend to agree that regional differentiation is close to what is meant by tissue patterning.


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Why can we eat salty food, but can't stomach salty water?
I know that too much sodium is bad for our health. However, it struck me as odd that we like to add salt to pasta sauce or other foods we eat, yet trying to drink salt water can bring on the gag reflex.
Is this because sea water is many times more salty than the salt we would add to our food? Or is there another reason?

Seawater is equivalent to adding a bit more than an entire tablespoon (17.5 mL) of salt to a 16oz (~500 mL) glass. If you're dumping that much salt onto your pasta sauce, I'd recommend you not skip the annual physical this year :p.

Not sure everyone experience a gag reflex when drinking sea water. Do you have a reference that this (claim) actually happens, before we try to find out why? (That it's unhealthy to drink/eat that much salt is another matter.)

Seawater is many times more salty than the "pinch" of salt that is often recommended to add to cooked dishes.
According to the USGS

the concentration of salt in seawater (salinity) is about 35 parts per thousand. In other words, about 35 of 1,000 (3.5%) of the weight of seawater comes from the dissolved salts

To translate that to a typical glass of water: seawater is equivalent to adding a bit more than an entire tablespoon (17.5 mL) of salt to a 16oz (~500 mL) glass!
By the way, 1 tablespoon of salt is about 7100 mg. To put that into perspective, you'd have to consume almost two entire 8-cut pizzas (using Domino's as a reference) or more than 7 McDonald BigMac cheeseburgers to consume that same amount of salt.
In fact, consuming 7,100 mg of salt would more than triple the recommended amount for daily intake. According to the FDA:

Americans eat on average about 3,400 mg of sodium per day. However, the Dietary Guidelines for Americans recommends limiting sodium intake to less than 2,300 mg per day—that’s equal to about 1 teaspoon of salt!

Thanks for the answer. I would never have guessed seawater had such a high concentration of salt.


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At how low a temperature can a snake like a copperhead survive in winter /
Copperheads were very common here, less so now that more people have moved into the subdivision. My yard is sort of an oasis for them . E. TX is expecting record cold in spite of climate change so I was covering a few things; damn ground orchids are already blooming. I let the camellias take care of themselves; there are too many to cover. I lifted a large plastic tub that was inverted on the ground , a smallish ,dormant copperhead fell out on the leaf covered ground. He did not move so I built a well insulated enclosure over him ( with an exit). Temp is now 40 F but 30 is expected tonight and mid 20's the next two nights. I am wondering at his chances of survival ; I estimate his body temperature will get to mid 30's F. I had thought they went deep into animal boroughs; we have many voles and some moles ( because there are not enough copperheads left to keep them under control). I have a well insulated garden shed that will probably not go below 50 F but I don't want to move him unless it is an emergency.

I will try to write a more detailed answer when I get back to my office, but just quickly, you might find this paper useful: Sanders, J.S. and Jacob, J.S., 1981. Thermal ecology of the copperhead (Agkistrodon contortrix). Herpetologica, pp.264-270.

Generally as long as their tissue does not freeze they are OK, brumation makes snakes pretty cold tolerant, it is more likely to die of dehydration than cold. Moving it to a warm area is not a great idea as it may cause it to come out of brumation early. Some decent cover is all they need, your enclosure should be more than enough as long as it is made of something insulating like wood or plastic, (just don't put it in a metal enclosure. Don't worry if it does not move, in very cold temperatures it may not move for days.

Thanks, helpful. I did not know the name but moving him to a warm location where he could wake seemed like a problem . Actually your comment is an answer.


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How did so many types of larvae become known as worms?
How did it come to be that so many types of creatures typically known as worms are actually insect larvae? Silkworms are not actually worms at all, but larvae of a type of moth. Another example being the Maguey worm, which is supposedly the worm in some types of tequila and also not a worm, actually also a type of moth-larvae?
I find it curious that Wikipedia would have a creature with the word worm in its title, and then the first thing they tell you about it is that it is actually an insect. These are just the two examples I came across, there are probably more.

I’m voting to close this question because it is a language usage question rather than one about a biological concept or mechanism.

Discussion on meta: https://biology.meta.stackexchange.com/q/4178/52598

Excellent question. My zoology professor during biology undergrads explained this by clarifying that "worm" is a term that relates to one type of shape of animals. As such it does not carry any additional information on the relatedness of animals or their developmental stage.
This view also seems to align with wikipedia.

but worms are not insects though, worms have no exoskeleton, breathe trough there skin and dont molt. They are both Invertebrates though. I'm trying to get my head around this.

"worm" is not a word with an exact scientific meaning (like the word insect). It's use colloquially to name any animal that have an elongated cylindrical shape. (Maybe snakes escape from this use today, but not in the 13th century, as you can read in https://en.wikipedia.org/wiki/Worm)

@NeilMeyer It's not too unusual for colloquial terms to not match the scientific counterparts. In some cases the colloquial terms have shifted with science, in other cases not. For example, "fish" once referred to all sorts of non-(biological fish) animals that lived in water, including marine mammals. We still see it used this way in jellyfish, starfish, the more generic "shellfish", etc.

@Bryan Krause: And then there's the silverfish, which doesn't live in water. https://en.wikipedia.org/wiki/Silverfish

In common English, worm is not a precise biological term, and long predates even the idea of precise biological names.  It's a generic descriptor for creatures that are long & skinny, without much in the way of legs.  So we have earthworms, silkworms, tapeworms, &c.  Even dragons can be called worms - or wurms, wyrms, &c, depending on your spelling preferences.  For instance, Old English epic Beowulf https://en.wikipedia.org/wiki/Beowulf ends with Beowulf fighting & being slain by a wyrm or dragon.
PS: Worm is also applied to non-biological things, for instance the worm gear: https://en.wikipedia.org/wiki/Worm_drive

An addition to tsttst answer:
"Worm" can go to very abstract realms, in Neuroethology "Worm" can be a stimulus attribute:
horizontal movement implied:
▄▄▄▄▄▄   would be considered "Worm configuration"

▅
█
█
▀
would be considered "antiworm" (ignore the white stripes)
at this level of abstraction underlying taxa would not matter at all, could be an eel, a snake or a branch , or a piece of cardboard. As long as it triggers the "worm " synapse

This isn't really a matter of biology so much as etymology.
The English word for "worm" was applied to any sort of slithering distasteful creature for centuries before we actually started get our taxonomies properly sorted out. Thus, the word "worm" ended up in the common names for lots of organisms without any real relationship to one another besides their generally cylindrical shape. It's also unsurprising that there are so many different things that have ended up with that shape, because it's a really simple one to grow and thus an easy case for convergent evolution.
In short: "worm" just describes a common shape and isn't really a biological term of art.


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Why is graft-vs-host so selective against phylogenetically close cells?
Is there a well established explanation for the phenomena that graft-vs-host is so much more selective against phylogenetically close cells? See historically significant references below,
"This type of aggression of the immune system is thus particularly directed against allo-antigens and is much less in evidence across two animals species. “ - Jerne, 1971
"Normal lymphoid cells obtained from animals that are phylogenetically unrelated or only distantly related to the chicken do not initiate graft versus host reactions when introduced into chicken embryos. " - Lafferty, 1968
References
Lafferty, K., & Jones, M. (1969). REACTIONS OF THE GRAFT VERSUS HOST (GVH) TYPE. Australian Journal of Experimental Biology and Medical Science, 47(1), 17–54. https://doi.org/10.1038/icb.1969.3
Jerne, N. K. (1971). The somatic generation of immune recognition. European Journal of Immunology, 1(1), 1–9. https://doi.org/10.1002/eji.1830010102

Since this has gone unanswered, I'll give my best guess. My guess is that closely related MHC* can still be recognized by CD4/CD8 (while not in distant relatives phylogenetically), but, the MHC + eventual bound peptide will not be recognized as self (with or without bound peptide), since its structure may differ even when binding self-antigen peptides that were exposed to T-cells during central tolerance "traning".
I am very intersted in what the established explanation is including references, and invite better answers if there is competence to produce that.
*in the context of the question, i.e., at species level, within species sufficiently close MHC genes are not attacked at all and compatible.
I'll attach potential reference to my guess that ability to recognize MHC as... MHC, decreases with phylogenetic distance,
Vignali, D. A., Moreno, J., Schiller, D., & Hämmerling, G. J. (1992). Species-specific binding of CD4 to the beta 2 domain of major histocompatibility complex class II molecules. Journal of Experimental Medicine, 175(4), 925–932. https://doi.org/10.1084/jem.175.4.925
that references this,
Lamarre, D., Ashkenazi, A., Fleury, S., Smith, D., Sekaly, R., & Capon, D. (1989). The MHC-binding and gp120-binding functions of CD4 are separable. Science, 245(4919), 743–746. https://doi.org/10.1126/science.2549633
that says this,

"although human and mouse CD4 share a high degree of amino acid sequence identity (19), the murine homolog does not bind gpl20 (11) and does not interact with the human class II MHC molecule HLA-DP as assessed by functional and adhesion assays (20). "


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How did animals on Earth survive without plants?
Around 500 million years ago, there were animals on earth, but there were no plants yet. How did animals survive? I'm assuming some of the animals ate other animals, but did some animals eat rocks or something?

Plants evolved around a billion years ago, land plants evolved at least ~800 millions years ago, likely closer to 1200 million years.

Maybe if you cite a source for the claim about particular years that could help someone write an answer explaining where the discrepancy is?

They ate grass, since grass was not classified as a plant back then :)

Since you're a new contributor, I'm going to go ahead and answer this despite the flaws in the question that have caused it to be at -4 when I write this answer (skip to the last paragraph to see what I have to say about that).  The major reason the answer isn't more obvious is that your assumptions about how long plants and animals have been around is incorrect.  Or rather is based on when a particular type of animal life (sea life with hard parts) arose 500 million years ago and comparing it to when complex plant life was able to colonize dry land (about 475 million years ago). Besides the obvious point that animal life in the oceans is  not directly dependent on eating plant life on dry land, there  a larger problem.  You are treating complex multicellular life as the only type of life. It is not.
When most people think of 'animals' and 'plants' they are thinking about complex multicellular life.  Things we can see with our own eyes.  The problem is that this type of life is quite recent.  For most of the history of life on earth, living creatures have been single celled.  While composed of only one cell, these creatures (like animals and plants) could be divided into two groups based on how they got their food: heterotrophs that consumed other things (like animals do) and autotrophs that make their own food (like plants do)
The oldest fossils of single celled life date back to about 3.5 billion years ago. Since these fossils suggest relatively complex communities of multiple types of living creatures, including both heterotrophs (that ate autotrophs or other heterotrophs)  and photosynthetic autotrophs (albeit using a less efficient form  that did not make oxygen but otherwise lived much like plants do today).   We think life originated before that, probably abut 3.8 billion years ago.   Mostly because before 3.8 billion years ago, the earths surface was repeatedly blasted with meteorites and comets sent crashing through the inner solar system by the orbits of the outer planets shifting into their current positions (see https://en.wikipedia.org/wiki/Late_Heavy_Bombardment  )
I draw your attention to the timeline of life on earth within that article and follow it to the article: https://en.wikipedia.org/wiki/Timeline_of_the_evolutionary_history_of_life
By 3 billion years ago, long before multicellular plants and animals, single celled autotrophs were engaging in photosynthesis essentially identical to how plants do today. Even at 3.5 billion years ago,  there were single celled plant-like organisms for animal-like organisms to eat.
Before that?  Classically, it has been thought that the first living creatures consumed the 'soup' of organic (carbon containing) molecules that made the first simple informational and catalytic macromolecules that were the likely basis for early protolife (or one well established idea, read about the "RNA world hypothesis" https://en.wikipedia.org/wiki/RNA_world). Either right about this time or soon thereafter, protocells that could make their own food evolved. Similar to very primitive life living in extreme ecological niches today, these chemoautotrophs likely made food from high energy chemical reactions that take place as a result of geothermal activity.  In places like "black smoker" deep sea vents where single celled organisms use the boiling hot water and highly reactive chemicals dissolved in it to make food that is even today the basis for ecosystems that do not depend on the light of the sun (see https://en.wikipedia.org/wiki/Chemotroph).  In a manner of speaking, these did sort of eat rocks.
By the time complex multicellular heterotrophic life (animals) had evolved hard bits that fossilize well about 500 million years ago (when you incorrectly have animals first evolving),  animals without hard bits had existed for about  500 million more years.  Even when they evolved, there was a 2.5 billion year history of single celled things to eat.  When complex multicellular photosynthetic autotrophs (plants) first colonized dry land about 475 million years ago, some single celled photosynthetic autotrophs had been living there in or near fresh water for about 400 million years  (https://en.wikipedia.org/wiki/Evolutionary_history_of_plants).  And the most basic complex multicellular photosynthetic autotrophs (similar to simple seaweeds today) had been living is marine environments for a billion years (https://www.eurekalert.org/pub_releases/2020-02/vt-1bg022120.php)
So you can see, your question is predicted on incorrect assumptions.  When these are corrected, there is no question at all.  As to why this question is downvoted, the incorrect assumptions likely are a big part of it.  But you may notice that all the key citations I make are from one source.  Wikipedia.  I could easily have made it from primary sources or college level textbooks.  But I used wikipedia for a reason.  You could have done it too. Before asking your question, you probably should have checked to see if what you thought was the timeline of animal and planet development was correct.  You would quickly have found it was not. Stack Exchange, as I understand it, really isn't for asking questions that can be quickly answered with a wikipedia search. And that, I think, is why the question has been downvoted so much.  As to why I answered it anyway, the question seemed genuine and it didn't seem like you were just trying to lazily answer a question from class.  Besides,  I think even a question that isn't ideal can teach.  By answering, I show my reasoning which may help teach a reader how to answer questions themselves or ask a better question next time.
That and I think the issue of people forgetting that most of the history of life on earth is unicellular is widespread and deserves more consideration.  For example,  most alien life we are likely to encounter will look like slime on rocks.  Just like it would have looked to a visitor to Earth for most of our history.  So I rarely pass of a chance to make the point that life is mostly unicellular.

DrRadium. Nice attitude, and spot on about your Wikipedia paragraph. Thanks for contributing here. Hope you stick around and get more involved here.


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How does the shoulder joint stay in place?
I read that a human shoulder is a ball and socket joint, but when looking at a picture of a shoulder the socket part seemed way too small to hold the ball in place like a ball and socket joint. Usually the socket covers a little over half the ball and the shoulder socket covers almost none. How does the shoulder stay connected? Are the illustrations wrong?

Because it's

held together by muscles, tendons, and ligaments.

(image from Wikipedia.)
It's somewhat complicated how all these parts contribute to holding the joint in place because it depends on the position of the joint. E.g.

Shoulder muscle forces are usually powerful stabilizers of the glenohumeral joint, especially in mid-range positions when the passive stabilizers are lax. However, muscle forces can contribute to instability as well. Certain muscle forces decrease glenohumeral joint stability in end-range positions. We found this to be the case with both active and passive pectoralis major forces.

That study has some data based on computational models and actual tests on cadavers.


text:
Need help designing an enzyme immunoassay (EIA)
I have a FITC-labelled DNA sequence and an anti-FITC antibody, however this antibody is not conjugated with HRP or any other enzyme. I work in a lab with limited finances, so is there a way I could make use of these without having to order an HRP conjugated antibody to be used in a detection assay?

Could you make this a fluorescent assay and simply detect the FITC itself? Do you have a fluorescent plate reader? Or won't the FITC be at high enough levels to detect on its own, and you need the signal amplification of primary and secondary antibodies?

Thanks Matt! I have already done this, i.e. use a fluorescent plate reader to detect the FITC labelled DNA Seq. However, I was trying to find a way to design an ELISA assay without needing a conjugated antibody. But thanks for your suggestion, i'll keep searching!


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

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

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

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

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


text:
Common ancestry of our cells to the first unicellular cell
If we start the chapter of life with low fidelity self replicating RNAs forming exactly identical copies of themselves,  which then later evolved to form the first primordial basic cells which further reproduced, and formed identical daughter cells and so on ... besides mutation and other factors that might affect gene expression, our genome must still be derived from the very first RNA strand.
So is it too far fetched to say that in our bodies, our cells are the primordial cells themselves, as reproduction happens either by mitosis and meiosis (which keep the integrity of the first cell genome besides factors like mutation, etc.)?

I think it is too far-fetched to say so. It bounds a bit on philosophy: in what sense the modern sense are primordial cells? It do not consist of the very same molecules, and they do not resemble the primordial cells in terms of their RNA/DNA sequence, protein sequences, etc.

What it seems you're struggling with here is a lack of clear definitions.
Yes, the unity of core cellular mechanisms implies an unbroken line of descent back to the origins of life. But that does not in any way mean the cells are actually the same. I think that you would find it instructive to learn about the puzzle of the Ship of Theseus, which is the essence of the issue you are dealing with. In short, once changes can happen (e.g., mutation, as you note), it's possible to have both continuity and a fundamentally different item.
Beyond this, it's also worth noting that at every step we are dealing not with individuals but populations, even likely back into the murk of abiogenesis (when the populations would be various chemicals and protocells of some sort), and that genomes are also modified in a much wilder variety of ways, e.g., all the various forms of horizontal gene transfer.


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

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


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Can Inositol triphosphate (IP3)-mediated Calcium release on its own cause membrane depolarization?
This is about smooth muscles.
I know that the Voltage-operated Ca²+ channels on the smooth muscle membrane can be opened by membrane depolarization to threshold. I also know
that this depolarization in question can be brought about by opening of receptor-operated calcium channels on the plasma membrane.(1) What I am curious to know, however, is whether the Ca²+ released into the cytoplasm (sarcoplasm) when say IP3 binds to its receptor on the Sarcoplasmic reticulum can (on its own, without any other thing happening) cause depolarization of the membrane potential to threshold and subsequently lead to opening of
the Voltage-operated Ca²+ channels on the muscle cell plasma membrane.
I am asking this because most often, the IP3-mediated Calcium release is discussed almost entirely as an accessory pathway for Calcium release, being only able to supplement an existing Calcium current.
(1) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652144/#!po=4.24837

The membrane potential is not determined by ionic concentrations but by ionic permeability, so I would assume that it doesn't change.

Oh! Yes. You're right


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Are the "cocaine hippos" suffering from noticeable inbreeding depression?
Colombia has a population of about 100 "cocaine hippos" founded from a group of one male and three females, which escaped from a drug kingpin's private zoo; it's even estimated that this population could grow to over 1,000 in the next two decades or so:

The rise of the so-called "cocaine hippos" began in 1993 after authorities killed Pablo Escobar and seized his luxury estate Hacienda Napoles, about 250km (155 miles) north-west of the capital Bogotá.
Animals found there were distributed to zoos across the country, but not the hippos. "It was logistically difficult to move them around, so the authorities just left them there, probably thinking the animals would die," Ms Castelblanco said.
Instead, they thrived.
Over the years, scientists have tried to calculate how many hippos are living in Colombia's waterways, with estimates ranging from 80 to 120 animals. "It is the biggest hippo herd outside Africa, which is their native region," veterinarian and conservationist Carlos Valderrama told the BBC. [...]
Ms Castelblanco and her peers say the population will reach over 1,400 specimens as early as 2034 without a cull - all of them descended from the original group of a male and three females.

I'm curious however if these "cocaine hippos" don't show any signs of inbreeding depression given how small the founding group was. Are there any studies/articles on this aspect in that Colombian hippo population?

I found one publication of Hippo population genetics from 2015 in Mol. Ecol. but they sadly didn't feature the Columbian population, actually it seems there is very little research going on regarding this Cartel-neozoa -bloat. Sadly some people are trying to get them on birth control https://www.animalbalance.org/hippos . They could be of great value for the fields of population genetics, evolution, invasive species ecology, as well as ecosystem engineers ecology.

Well, is there a report that they don't suffer from inbreeding depression?

@user12256545 *Colombian. Columbian is the exchange.

@pascal no, but since the founder group consisted of a male and three females, its likely they do.

https://biology.stackexchange.com/q/98252/27148 seems like approximately the same question asked a different way.

It then seems you gave yourself an answer.

Answer: Its highly likely they are suffering from inbreeding depression,or will be at least soon, since the founder population size (n=4) is three magnitudes low of the literature value for the minimal viable population size. Even if there is no genetic evidence in form of a published study, this is a super clear case with such a restricted gene pool.

An MVP of 500 to 1,000 has often been given as an average for terrestrial vertebrates when inbreeding or genetic variability is ignored. When inbreeding effects are included, estimates of MVP for many species are in the thousands. Based on a meta-analysis of reported values in the literature for many species, Traill et al. reported concerning vertebrates "a cross-species frequency distribution of MVP with a median of 4169 individuals (95% CI = 3577–5129)."

source:

https://en.wikipedia.org/wiki/Minimum_viable_population
https://www.sciencedirect.com/science/article/abs/pii/S0006320707002534?via%3Dihub


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How is the glycemic index computed from a blood sugar curve?
The definition of the glycemic index is often given as the area under curve (AUC) of their two-hour blood sugar response. However, it's essentially meant to be a measure of whether food causes a fast or slow rise in blood sugar level. Why is the two-hour AUC a good measure of the speed of the rise?
When ingesting the "same" amount of sugar, no matter the form, the AUC should be the same, right? The only explanation I can find is that the two-hour cutoff means some carbohydrates are metabolized beyond that cutoff, so their AUC and hence their GI is lower, is that what's happening?
The reason I'm a bit confused is that all of the images of blood sugar curves illustrating low & high GI seem to show two curves with the same AUC, both going to 0 before the two-hour cutoff.

First of all, yes, the cut-off at 2 hours will make most of the difference. But I think your question asks about what would happen without that 2h cut-off, e.g. measuring 10 hours instead.
In theory, the AUC of identical dosages of sugar can vary, dependent on the kinetics of how sugar is removed from the blood stream.
Mathematically, if sugar exponentially decayed in a first order rate, which seems true during the initial insulin spike, then the long-time AUC would be identical, independent of the digestion speed.
If we assumed that some aspects don't fully scale-up (less than first-order), e.g. alcohol is mostly metabolized in a 0 order reaction rate  [2], then even the long-term the AUC would be lower if digestion was slower.
However, reality is complicated. Looking at an example insulin and glucose day-curve [3], you can see, that lower insulin levels drastically reduce the glucose elimination (via uptake by cells). From this, it's not clear how long-term AUC would look like and one could actually speculate, that actually slowly digested food could have a higher long term AUC, given its glucose acts during smaller concentrations of insulin.


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What is meant by the term synaptic targeting?
I am studying whether a protein interacts with the mitochondria in the synapses of neurons and I have come across the term "synaptic targeting". I am reading this paper and I have come across the following:

During synaptic development, proteins aggregate at specialized pre-
and postsynaptic structures. Mechanisms that mediate protein
clustering at these sites remain unknown. To investigate this process,
we analyzed synaptic targeting of a postsynaptic density protein,
PSD-95, by expressing green fluorescent protein– (GFP-) tagged PSD-95
in cultured hippocampal neurons.

I am not sure what exactly is meant by the term "synaptic targeting". I have tried Googling the definition but all I get are links to journal papers. I think that synaptic targeting refers to where in the synapse (e.g. presynaptic or postsynaptic ending) a protein is located, but I am not certain. Any insights are appreciated.

PSD-95 is a protein located in the post-synaptic region inside a cell. In fact it's named for this, "post synaptic density-95" referring to the dense appearance of the post synaptic area on an EM microscope and this protein's presence there.
"Synaptic targeting" in this context refers to how that protein gets to where it belongs (the synapse) in the cell, rather than just floating around in the cytoplasm by simple diffusion.


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Are synaptic boutons always located on axons?
I am learning about the protein Synaptophysin and I have read that it is an integral membrane protein localised to synaptic vesicles. I have also read that it is a specific and sensitive marker for synaptic terminals. On this site, I have read that synaptic terminals are the presynaptic endings and on Wikipedia that the presynaptic axon terminal is also known as the synaptic bouton. From what I have read online it seems to me that synaptic boutons are located only on axons.
However, I have found out about dendrodendritic synapses which are connections between the dendrites of two different neurons. Can the presynaptic ending of a dendrodendritic synapse be referred to as a synaptic bouton or are synaptic boutons only located on axons? Any insights are appreciated.

Axonal boutons are named as such due to their shape. Dendro-dendritic synapses do not resemble this shape and are never referred to as boutons. It does not appear that synaptophysin is expressed on dendrites (Fletcher et al. 1991), but I am unaware of a study that targeted dendro-dendritic synapses specifically.

References
Fletcher, TL, P Cameron, P De Camilli, and G Banker. ‘The Distribution of Synapsin I and Synaptophysin in Hippocampal Neurons Developing in Culture’. The Journal of Neuroscience 11, no. 6 (1 June 1991): 1617. https://doi.org/10.1523/JNEUROSCI.11-06-01617.1991.


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How does the social structure of lion prides prevent incest?
I assume that lions don't have a concept of incest and they will just mate with any adult lioness in heat, daughter or not.
If so, is incest inevitable as the female cubs will grow up and remain in the pride? Their brothers will be kicked out as they reach mating age. But the females stay, so what is the mechanism that will prevent their fathers from mating with them?
I suppose that their fathers will be driven out of the pride by incoming males sooner or later. But if it doesn't happen soon enough, then what prevents them from mating with their daughters?

It is true that African lions have recently become more prone to inbreeding, largely due to human actions (reasons include limited dispersal and at least temporarily reduced pride sizes). see here
Generally though, lions likely avoid mating with close relatives innately as most animal species do. see e.g. here
A few things about the social structures of lions (ref.):

First, many prides are not controlled by a single male. Although the males might often be related to one another.

A single male might often not be in control for long enough to mate with his grown daughters.

Females do not only mate with the leader of their pride, but mate sometimes with males from outside of the pride.


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Is the General Cirrate Octopus Form the Basalmost Octopoda Morphology?
The reason I ask this is due to the distinctive internal mantle shells of cirrina, of which the incerrata have stylets that are a remnant of the cirrate shell. Along with this, both cirrate octopuses and Vampyroteuthis have a gladius (although with different morphologies) with fins upon their mantles, which incirrate octopuses lack.
Also, a relatively recent study presents a view that cirrate octopuses are actually paraphyletic, being an evolutionary grade rather than a monophyletic group. Can it be inferred then that the basalmost octopus form is then a pelagic form with a gladius that uses mantle fins as the primary form of locomotion, and the incirrate form normally associated with octopuses is a drastic deviation?


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What is disease risk?
I would like to find an accurate definition of disease risk for virus ecology.
I am searching in articles and in none of them this term is defined, they only mention it.
Schematic of the relationship between habitat heterogeneity and disease risk.
Disease is greatest in fully cultivated plants, intermediate in wild plants
that are tended by humans in anthropic habitats, and lowest in fully wild plants.
On the other hand, biodiversity is highest in the habitats of wild plants, and
lowest in those of cultivated plants.

Roossinck, M. J., & García-Arenal, F. (2015). Ecosystem simplification, biodiversity loss and plant virus emergence. Current opinion in virology, 10, 56-62.
I have defined it as the probability of a host to develop a disease. However, I have the feeling that this definition is somewhat lax.

To my knowledge disease risk is not a generally acepted epidemiological term. You may want to look at the incidence rate or prevalence and follow the suggestions from the "See also" section.

Thank you @Vadim for your answer. However as you see in many papers disease risk is introduced as a term:  The ecology of infectious disease: effects of host diversity and community composition on Lyme disease risk. Proceedings of the National Academy of Sciences, 100(2), 567-571.  I defined it as the probability of a host to develop a disease, I have the feeling that this definition is somewhat lax

Perhaps you should edit your question to make it more specific: pointing that you are discussing ecology (rather than epidemiology), and perhaps giving examples of the articles.

I have changed it. Thank you for your support


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Using punnett squares to express sex/gene linkage and recombination frequency
I have been using punnett squares to visualize mating experiments. I am looking at a pairing which is known to have a crossover event occur. I know from empirically collected data the recombination frequency is ~3%. Can punnett squares be used to express the results bearing the recombination frequency in mind or should I consider a different visualisation technique?
The end result of what I want to achieve is the expected genotypic/phenotypic outcomes taking recombination into account.
In addition the pairing has a sex-linked mutation which further complicates things e.g. aB/Ab x Ab/Y
Here is an example punnett square:
 a-B/A-b x A-b/Y
 -------------------------
 | x   | A-b     | Y     |
 -------------------------
 | a-B | A-b/a-B | a-B/Y |
 -------------------------
 | A-b | A-b/A-b | A-b/Y |
 -------------------------

If a want to represent a recombination event in the punnett square (e.g. to produce a-b/A-b and a-b/Y does this mean I would  need to add a-b as an additional trait to the punnett square like so?
a-B/A-b/a-b x A-b/Y
 -------------------------
 | x   | A-b     | Y     |
 -------------------------
 | a-B | A-b/a-B | a-B/Y |
 -------------------------
 | A-b | A-b/A-b | A-b/Y |
 -------------------------
 | a-b | A-b/a-b | a-b/Y |
 -------------------------

If that is the case, that would give me a frequency of 16.666666% for each.

Although generally Punnet square is used to show the expected progeny in case of validity of Mendel's laws of segregation and/or of independent assortment, you definitely can represent the outcome of any cross using Punnet square. It would be useful if you drew the square of your results and posted it here sharing your doubts with the community.

Thanks @FabioMarroni, I have modified my original question with example punnetts.

Punnett squares show the possible gametes from each parent.  I suppose you could write out all the possible recombined gametes with their frequency in the same format, explicitly stating the percentage of each (usually 50% or 25% is assumed but not written).  So if you have the female at the top of the table (sorry, I tried some html tags but they're not taking; I should RTFM)
........ AB - Ab - aB - ab
....... 48.5 1.5 1.5 48.5 %
ab 50%:  24.25 0.75 0.75 24.25 %
Y 50%:   24.25 0.75 0.75 24.25 %
Per your last sentence, the male can only pass on its X genotype, which I've assumed as ab for a backcross, or Y - no crossover - so this would be a 4x2 Punnett square.  The odds of each box in the square (not considering lethality) are still found by multiplying the odds of each allele as ratios, then converting to percentage.  You have to add up all the percentages that match a phenotype as you score it to find phenotypic ratios.
This page explains this idea with better formatting, but not for a sex-linked trait.

The Punnett squares are a general way to visualize the product of any two polynomials; for example, you know that the result of (a + b)(c + d) is the sum of the four terms ab, ac, bc, bd. You may put it this way:
  | a   b
----------
c | ac  bc
d | ad  bd

Suppose that the female sex gametes are of two types, X1 and X2, which are transmitted with probabilities 0.9 and 0.1; suppose that males form three types of gametes, X1, X2, and Y, with probabilities 0.45, 0.05 and 0.5. Then, you may visualize the outcome of a general population mating this way:
    |Fem   X1   X2
    |      .9  .1
--------------------
Male|
X1  |     X1X1  X1X2
.45 |     .405  .045
    |
X2  |     X1X2  X2X2
.05 |     .045  .005
    |
Y   |     X1 Y  X2 Y
.5  |     .45   .05

(You may note that this situation roughly depicts the population genetics of color blindness)


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Using BLAST for molecular replacement in structural biology
This is my first time trying to do molecular replacement to solve a protein structure. I am using the NCBI blastp program to find suitable search models. When choosing a search model, I understand that sequence identity is the most important -- but should I also take into account e-values or query coverage (i.e, what % of my query sequence is in the alignment) or any other factors for the purpose of molecular replacement? Thank you for your help!

Identity, Similarity, E-value are the key numbers, for the prediction of the 3D structure of proteins. The Length of the query and selected results should also be close to each other.
E-value:
The first value to look at is indeed the E-value.
For the most accurate predictions, E-values less than $10^{-100}$ are of extreme importance While E-values ranging between $10^{-50}$ to $10^{-100}$ come as the second priority. E-values less than $10^{-20}$ or so, should not be trusted. (As you know the larger amount of E-value accounts for random hits which may not have any evolutionary background with your query)
Similarity and Identity:
The ranges for these amounts differ for each survey and should be assessed with other statistics. Needless to say, Identities below 5% for amino acid blasts and below 25% for nucleotide blasts are useless. For proteins identity above 25% is acceptable and 35-50% (and more) are of greater importance. Similarity plays a more important role in the overall shape and structure of the protein. "Total score" in Blast NCBI should suffice for these evaluations.
Length:
The sequence length of your results should be reasonably near to one another. For example, having a sequence of 600 amino acids as your query, the acceptable range for the selected results (to eventually predict 3D structure with) should be 600 $\pm$ 30. Five percent difference is usually enough. Deviation from this would result in extra 3rd and 4th structures induced by other subunits.
Other considerations: In the case that your organism is known, pick the sequences which share a common evolutionary history with your organism of interest See Tree of life. The number of subunits and Symmetry types might be useful in some cases. Avoid selecting ab-initio based 3D structures in your results all the time and focus mainly on X-ray diffraction-based structures. If you're using the PDB website for data retrieval, Refinement Resolution is also extremely important. Try both CIF and PDB formats as input, as the results may sometimes improve.
At last but not least, try blasting using curated databases. In blastp, refseq_protein , swissprot , pdb , refseq_select are ideal.
This is just a rule of thumb and should not be generalized as the exact numbers differ substantially from one query to another.


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Why do genes, encoding the same proteins and in the same conditions, have different expression?
Is it possible that two genes, which come from two different cell cultures and which encodes the same protein, produces different quantity of mRNA? If yes, why?
My question comes from the fact that I am doing statistical analysis of a microarray dataset for the hyperthermophilic archaeon Pyrococcus furiosus exposed to gamma irradiation. Microarray experiments measure relative quantities of mRNA in a cell. My file has values, for each gene of the genome, that are positive or negative since the scientists who performed the experiment made the log10 ratio between the fluorescence intensity of the sample that was irradiated and the reference sample (not irradiated). Indeed, in the microarray experiment we have two channels that typically are one for the "controls" and the other for the cells which are stimulated by an event (in this case the event is gamma irradiation), in order to make a comparison.
In my dataset there are two columns (that are indicated as "reference") that refer to the case in which they should have put the cell cultures not irradiated in both the two channels. I would expect that the values in the file corresponding to these two columns are 0 (since they are the log10 ratio between the intensities of the signals of the genes which encode the same protein and that are in the same conditions). Instead they are different from 0. Therefore I wonder what is the reason for which there is different quantity of mRNA produced from two equal genes?
I made a graph of relative mRNA produced (calculated as I explained before) vs time, in which you can notice that the relative mRNA produced of the reference  (I called them as "Ref" on the horizonal axis) is not 0.

Is it only due to some noise or are there biological reasons ? (the picture refers to a gene which encodes Ferritin-like proteins but it is the same story also for other genes).
Even though I think that my interpretation of the data is correct, I tell you that the dataset I am talking about is here, if you want to have a look.

Please edit your post to make it clear what you mean by "which are equal". More importantly how are these "equal" genes different — is the mRNA labeled differently? If so, does that give you any clues as to why you might see differences? In addition, I have edited your post to try to make your question clearer — please check to make sure I have not broken anything. Finally, please proofread your future posts and also use a spelling and grammar checker — this should help you improve your writing. Thanks!

@tyersome the fact is that it is not easy to explain but I will do the best say it better. Thank you anyway.

I agree I had a bit of trouble following this. Is it that there is a systematic difference, or that there is variability? In biological experiments measurement error and trial-to-trial variance are often relatively large compared to signals of interest.

@tyersome I tried to make it clearer and your edits are ok.

If I understand your question and graph correctly, your Y-axis is log(x/REF), where REF is some external standard. Your "Ref" on the x-axis you expect to be the same as REF, so that log(Ref/REF) "should be" zero, but you find it is not.
However, it looks like the mean(log(Ref/REF)) is still approximately zero. This is what I would expect: values that deviate a bit from perfectly 0, but having an average around 0 (and this average should approach 0 the more samples you have per the law of large numbers). You don't expect to have zero variance in data like this, which is why you repeat the experiment a number of times. You'll notice you have variance in all of your categories.

Ok thank you, indeed now I notice that they are close to 0. But the variability is due to noise due to experimental setup or something like this for instance ?

@Manuela Unclear, but there are lots of places where "noise" is possible in this setup: in production and degradation of mRNA, which are going to be stochastic processes, in imaging of the microarrays themselves which are subject to noise in the camera and digitization, any optical aberrations, stochastic bleaching of fluorescent molecules to non-fluorescent compounds, etc.

Another source of noise is hybridization of labeled cDNA to the microarray chip. It should happen under standard conditions and evenly across the chip - but in physical world nothing is realy ever exactly even. If you have the raw data with coordinates of the probes you should be able to display fluorescence intensities across 2D chip (There are R libraries for that). I once analyzed a chip with what looked like bubble in one corner. Even without bubbles one side could be warmer during hybridisation or other things.

It is entirely possible that different cell-lines express the same genes at drastically different levels.
The proteinatlas provides data and analyses on differences between certain tissues or cell types / cell-lines.
If your cells are of the same line/tissue, then they might still differ dependent on the cell-cycle, age and external factors. There are chemicals that facilitate cell-cycle synchronization.
But I agree to the other answer, that your observations could be within margin of error.


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

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

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


text:
Why do animal cells "mistake" rubidium ions for potassium ions?
So, I was browsing the Wikipedia article for rubidium, and came across this interesting tidbit:

Rubidium is not a known nutrient for any living organisms. However, rubidium ions have the same charge as potassium ions and are actively taken up and treated by animal cells in similar ways.

This immediately struck me as interesting, and a completely wrong explanation, as all singly-ionized ions have the same net charge.
Now, from my basic understanding of chemistry, elements of the same group have the same valence electron structure, which accounts for much of the element's chemical effects. And if you look at the periodic table, sure enough, rubidium falls below potassium, in the Group 1 alkali metals.

But, from my old memories of basic biology, even saying "these elements are vertically adjacent on the periodic table" is an incomplete explanation, because, for example, the body has no problem "telling apart" sodium from potassium, or plenty of other vertically adjacent elements.
A survey of other potentially relevant features reveals the calculated radius of rubidium (265 pm) is relatively close to the radius of potassium (243 pm), and the first ionization energy of rubidium (403.0 kJ/mol) is also pretty close to that of potassium (418.8 kJ/mol). So they do seem fairly similar, but question still remains, how "similar" does an element need to be to become a biological proxy?
This leads to me to the following questions:

Why does rubidium act as a biological proxy for potassium? Also:

Why is cesium also a decent, but less good, biological proxy for potassium?
Why is potassium not a biological proxy for sodium?

If rubidium acts as a biological proxy, why is it still not a "nutrient" and not considered to play a biological "role"?
Which other sets of elements can act as biological proxies for each other? (I presume expanding this question to molecules yields too many answers to be useful.)
Is this rubidium-potassium proxy effect specific to animals or to all life?

Some good references I've found, skimming the literature (I started by looking at some references in this article):

Relman AS. The physiological behavior of rubidium and cesium in relation to that of potassium. Yale J Biol Med. 1956;29(3):248–62.

Relman notes that this phenomenon was first noted by Sydney Ringer in experiments begun 1882, published in the Journal of Physiology in the year 1884 (or so).

Fieve RR, Meltzer H, Dunner DL, Levitt M, Mendlewicz J, Thomas A. Rubidium: biochemical, behavioral, and metabolic studies in humans. Am J Psychiatry. 1973;130(1):55–61.

But I'd rather someone present an intuitive explanation for this before or after I attempt to dive in.

Not what you'd call a useful proxy, but arsenic is poisonous because it's similar enough to phosphorus to act as a substitute in the ADP/ATP cycle, but then fails to provide energy to cells the way ATP does.

To be fair, the Wikipedia article does not actually say that rubidium ions are taken up in the same way as potassium BECAUSE they have the same charge. It just says that they have the same charge AND are taken up in the same way, which is true. A similar statement appears at the end of the article.

@barbecue Yes, I realized this later on. Still, I think that sentence in Wikipedia could have been phrased more clearly.

@JonathanJeffrey someone seems to have updated the article to make it clearer, was that you?

@barbecue No, it wasn't me! But I'm glad that someone got around to it (probably after reading this question).

As a side note, we use this property in nuclear medicine. Rb-82 is radioactive and can be used in heart studies - myocardial PET scans - as it enters the myocardial cells in a similar way to potassium. Pertechnetate - TcO^-4 is similar to iodine, and there are a lot of other examples.

The Na⁺/K⁺ pump discriminates sodium ions by their smaller size – that’s why in no way can (a larger) Rb⁺ pass for Na⁺ in this important application. But obviously Rb⁺ can pass for K⁺ there, and does it.

There are multiple biological mechanisms that can be brought to bear for distinguishing between atoms. In addition to binding properties (e.g., ionic charge, electronegativity, bond strength), there is also the size of the atoms and even their vibrational properties.
For one of these mechanisms to actually be used, however, it needs to be evolutionarily selected for in some way. The binding properties are by far the simplest to select for, since they are fairly local and permissive in nature, while the others require much more carefully tuned mechanisms.
Thus, we should expect to see most biological selectivity to be developed in terms of binding properties, as seems to be the case. For same-group covalent-binding such as one encounters with oxygen vs. sulfur, there are major differences in the properties of the bonds, giving ample opportunity for biological selectivity.
For Group 1 alkali metals like sodium, potassium, and rubidium, however, ionic bonding is much more uniform. Thus, we should expect mechanisms that apply to one to apply to all unless strongly selected for distinguishing.  In the case of potassium versus sodium, which are both very important in biochemistry, a recently discovered mechanism in sodium-potassium pumps uses binding properties to grab both, then atomic size (via steric hindrance) to distinguish sodium versus potassium as described nicely in the answers to this question.
Presumably, there simply has not been sufficient evolutionary pressure to establish mechanisms for distinguishing rubidium from potassium in the same way.  While sodium and potassium have approximately equal abundance, rubidium is approximately two orders of magnitude less abundant than either. Cesium, in turn, is nearly two orders of magnitude less than rubidium, and rapidly decaying francium mostly doesn't exist.
Thus, unless there is a particularly problematic effect of occasional incorporation of rubidium or cesium, then, we should expect these elements to be essentially indistinguishable from potassium biologically, but not from sodium, since sodium/potassium distinguishing mechanisms will reject them all along with potassium into the "not the right size to be sodium" bin.

@user338907 That's fascinating about lithium... do you have any information about mechanism? To me, that would suggest that the sodium selectivity is not just "small enough" but "just the right size", which would cause lithium to not work right either. It sounds like we're getting to the edge of known science here, however.

Excellent answer. I have to say, the pore selectivity in (for example) voltage-gated channels permeable to sodium or potassium but not both is something that I find to be one of the most remarkable feats in evolution.

Nice answer. Upon looking at things more, it appears the verdict is out on whether rubidium is an essential nutritional element (i.e. a mineral) or not for humans and other animals. How that ongoing research bears with the question of how animals evolved rubidium-potassium compatibility is an interesting question.

Although I accepted this answer, I think there are still lots of interesting insights and questions in this area, so I welcome others to write their own answers. (I myself am currently being quite fascinated by this paper that describes how some bacteria require lathanides, but can't tell them apart!)

I've just asked Help understanding how "steric effects" are distinct from "electronic effects"?


text:
How does this small brown crescent-headed land planarian(?) "look around" and sense its envirnoment?
This 2-3 cm long, thin brown worm with a wide "anchor" or hammer or crescent shaped head was seen in northern Taiwan slowly moving along a damp tile outdoor surface. It moved by contraction/extension and regularly lifted its head appearing to explore its environment, as if to say "where should I go next"?
Comments suggest that this is a land planarian.
Question: Is it possible to confirm that this is a land planarian and to understand what sensory organs it has on its head in order to "look around" and decide where to go next?

Related: https://biology.stackexchange.com/q/55054/16866

@theforestecologist yes, it does indeed look like a land planarian and the hammer-shaped head was my first clue, thanks! (see also here from here) So all that's left now is the part about how it senses its environment.

Edited to reinforce that this is not a duplicate because what's still asked here is the part about how it senses the environment

Given that "hammerhead worms" are Bipaliinae, I expect you can find your species from this bibliography1.  Bipalium or Diversibipalium ruteofulvum and cosmopolitan Bipalium kewense are mentioned, but I did not find images of these species online just now.
A paper about the sense organs of B. kewense (Abdel-Haleem, 2014) mentions many small pigment cup eyespots, as well as papillae and pits that may be chemosensory in nature.

1Kawakatsu et al. 2004 An Annotated Bibliography of Taiwan Land Planarians, with Lists of Linked Papers on This Animal Group

Thanks for your answer! The historical bibliography is intriguing, and also provides a historical view to the colonial rule period.