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In life history theory, does trade-off between reproduction and growth and maintenance imply longer health span for a sexually inactive organism?
The life history theory suggests that there exists trade-off between life processes like reproduction and growth and maintenance of the organism.

One significant trade off is between somatic effort (towards growth and maintenance of the body) and reproductive effort (towards producing offspring).

Quoting from wikipedia page Cost of reproduction hypothesis

The traditional view of the cost of reproduction says that a cost is caused by differential allocation of limited internal resources. (...) Reduced immune function and a decreased defense against environment stress are also important factors in the cost of reproduction.

It has been suggested that this kind of trade-off in resource allocation between different life processes has plasticity, that is, the resource allocation between different life processes in a given individual is dependent upon external factors like the absolute amount of nutrient input.

Reduced nutrient availability can substantially magnify, while increased nutrient availability can diminish or obviate an apparent trade-off. (...) For example, in laboratory and field experiments on bivalves, cladoc-
erans, insects, and mammals, allocation to maintenance or storage was found to
take precedence over allocation to reproduction under nutrient-poor or stressful
conditions

So, my question is, what does all this mean? Could sexually inactive life for an organism, for whatever reason, actually correspond to longer health span? (Better immunity, growth and maintenance of the body, etc.)
I know that the rate of deterioration of health with age is hugely determined by the rigid parameters corresponding to the specie the organism belongs to. But for a given organism, the various life processes like reproduction, repair and maintenance, and immune system are fighting for the limited resources available, and it appears that there is some amount of plasticity in how much resource will be allocated to which life process. In other words, the rate of deterioration of health of an individual appears not to be completely written on stone.

I am not sure if life span could be extended in such circumstances but the probability of survival could probably increase, given the high metabolic costs of growing and raising offspring. I work mainly with marine mammals and there are multiple studies showing that the body condition of females following births is much lower (as to be expected), and thus health indices are worse. Therefore, these animals are at greater risk of being severely affected by infections or variable densities of available prey, showing to an extent the high costs of reproduction.
Another thing to consider is the level of stress that any member of the population is exposed to. Whether an individual is sexually active or not, various stressors (i.e., limited prey, pollutants that compromise the immune system) can limit their life span and increase mortality risks. For example, there are various studies on the effects of persistent organic pollutants such as PCBs (i.e., https://pubmed.ncbi.nlm.nih.gov/29096314/) that can be passed down to calves and persist in the body for long periods of time. These substances can compromise the immune system, thus putting animals with high concentrations of these pollutants in their bodies at greater risk irrespective of whether they become sexually active or not. Therefore, there might be a higher likelihood that an animal can live (potentially) longer as a result of the lack of investment in reproductive activities, because the resources can indeed be used for growth and body maintenance, but there are stressors that can limit survival rates before the animals are even born.
Here is a study that is not directly related to the cost of reproduction, but investigated the plasticity of immune investment in individuals exposed to human-generated stressors and limited food availability: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0067132
I hope this answers your question and if you are interested in references to papers that were briefly mentioned but not specifically provided, I am happy to help!

You bring up an important factor with the human generated chemicals likely to contaminate much of what's currently likely to be observed.

I wonder if this also relates to matriarchal societies needing their matriarchs to survive longer (to lead, pass on knowledge, etc) and menopause/cessation of female fertility?

Also keep in mind that females can offload contaminants to offspring via gestation and lactation, therefore reducing the contaminant load of the mother. But whether or not reduced contaminant loads offset the energetic demands of motherhood is another question...


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What mammals can rotate and move their ears the most?
I found out that rabbits can rotate their ears 270 degrees, and also move them up, down and independently. Are there any other mammals that can control their ears' position that well, or even better?

Can't find a study with actual measurements, but from personal experience horses can move their ears through a pretty wide range: tilting about 180 degrees forward & back, and rotating independently about the same angle.

source: Stack Exchange

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

sort: votes


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Is fucus filamentous or colonial algea?
Am a bit new to biology SE. My question is wether fucus is filamentous or collonial form of algea?Does a form of algea have to be collonial or fillamentous or it can be something else?
https://en.m.wikipedia.org/wiki/Fucus_vesiculosus

I would suggest looking up some basic sources on types of algae. For example, that source that I link to says this:

Algae vary considerably in size, shape, and growth form.
They can be:

Single celled
Many celled - either colonially or as filaments of cells; or
Elaborate plant bodies with differentiated cell types

In this case, I believe that Fucus would be in the third category ("elaborate plant bodies").
But note that these are informal categories, they don't really correspond to taxonomy or evolution or anything.

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


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Does the Human Eye White Balance?
OK, this may be a stupid question…but here goes.
Does the human eye “white balance” itself?
I assume that each human perceives colour slightly differently according to the peculiarities of their own eye, but within parameters (notwithstanding colour-blindness).
But does our eye (or brain) white balance? Or do we simply all see our own personal colour balance?
If the eye can white balance in real life, can it also colour balance a photograph that has been taken at the wrong colour temperature.
So, say I shoot and print an image shot at 2000K. The image printed will have its luminance information intact, but colour-wise, it will be very, very orange.
If I could somehow exclude all other vision from my eye and fill my entire viewing capacity with that single image, would my eye balance the colour back to a true white?
If it does not, why not? What goes on in our brain to say “this is an image at a fixed colour temperature, so you will see it as an orange hue”
Please excuse me if this is an eye-roller of a question. I’m not a Biologist, so I am well aware I may be demonstrating my own ignorance in asking the question!

I'm pretty sure any sort of color (or orientation / image / ...) correction happens in the brain. Anecdotally you can test this i.e. by wearing tinted glasses for a while (your vision should adapt to a more normal color up to the point where you take them off and get an opposite color shift for a while). Similar effects happen with other vision distortion effects (i.e. top-down mirroring glasses), which is why I'm pretty sure this happens in the brain & not the eyes.

Hi Nicolai - Thanks for responding! I see your point. And I can get my head round the brain making adjustments to what we see - white balancing on the fly. But are there limits? If the tint is such that, for example, no green information gets through to your eye, does your brain then "invent" the green information in order to render white? So, as per my example, if I was to look at a picture shot at 2000K, to the exclusion of everything else, could my brain invent the colour information missing and render it a "true" white balanced image?

I don't know how this works in detail, so I can't really answer these specific points of the question (which is also why I only wrote a comment and not an answer)

Welcome to Biology.SE! This phenomenon is known as color constancy. Please note that we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

The human brain white balances, the eyes do not, but the process is not instantaneous.
the easiest way to see this is to make a person wear colored lenses they will soon see colors normally again, but will need to readjust, taking a similar length of time,  once the glasses are removed.
Your eyes will balance an image back to white , but it takes time, and may happen faster in a landscape image.
https://www.sciencedaily.com/releases/2005/10/051026082313.htm
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3820566/
there is a great ted talk showing a major aspect of this visually.
https://www.ted.com/talks/beau_lotto_optical_illusions_show_how_we_see?language=en
you can also see it with common photo negative color illusions.
Stare at the center dot on this for a minute then look at the second image.

you will see that the as the brain adjusts color balance you can use the lag as the eye readjusts to see false color in black and white images.

There's an easier, or at least less contrived, way to see the white balancing in action.  Go skiing late in the afternoon when there's a gaudy orange sunset.  Take a picture of the snow that you are perceiving as white.  It'll be orange.

@jamesqf not everyone lives where it snows ;)

Yes, some people are deprived.  But they can do the same experiment with any sort of white or light-colored object.


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What is the difference between Molecular and Cellular tolerance?
Although I've read that there are three types of tolerance, molecular cellular and behavioural, I cannot seem to find any mechanism of cellular other than desensitization of receptors. If someone can clear it up, or inform me that cellular tolerance is not a thing, that would be much appreciated <3

Hi, and welcome to the site!  It would be best if you could include a bit of background research... what have you looked at already?  Please [edit] to clarify what research you have already done and what it is you are not understanding in your sources.  Thanks!

Personally, I find these distinctions a bit silly but I also understand they have some use.
People sometimes divide neuroscience into molecular, cellular, and systems levels of understanding. Molecular covers all the "one cell" phenomenon: expression of particular receptors or related proteins, for example. Cellular is one step above of molecular and considers the collection of all "molecular" entities and also considers a circuit level, recognizing that neurons exist among other neurons. Systems level neuroscience sometimes ignores these low-level interactions and sometimes embraces them, but overall is more connected to the behavior and state of the whole organism, approaching psychology.
The reason I think this separation is a bit silly is because, well, none of these levels of understanding are independent. That said, it's a good framework especially for novices to drive home that stuff happens at different levels of explanation. This is true for drug abuse as it is for many other concepts in neuroscience. It also lets someone that is writing a textbook focus on these different levels of explanation in sequence, in a way that is easier to process. A professional in the field is unlikely to draw the same boundaries, but they also have enough background to consolidate knowledge at all levels of interest.
I included a reference that makes the same distinctions I'm making here, but it's likely to be hard to find a canonical one. Different textbooks are going to draw different boundaries as they explain what we know in their own ways, and that's okay. I hope students recognize that A) There are different levels of explanation for neurobiological phenomenon, and B) These levels are interconnected. It's important to recognize that it's possible to study addiction at these different levels of abstraction; it shouldn't be important to draw boundaries between them, however.

Pietrzykowski, A. Z., & Treistman, S. N. (2008). The molecular basis of tolerance. Alcohol Research & Health, 31(4), 298.


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Risk with cultures taken from stagnating water?
Necessary foreword: I'm an amateur and just starting with microscopy and microbiology.
Wanting to observe some protozoa, I collected samples of dirt and water from some pools here in the city and nearby, and started keeping them in jars to see if something changes over time (different protozoa and small animals, quality of water, etc.). Stuff happens, which is great, but also means that a lot is going on in there.
The jars sit mainly indoor and I wonder if I should be more worried about them: apart washing my hands with care after handling them, is there any other measure I should take (some guidelines maybe)? For instance, I will for sure breathe nearby the water when I observe at the microscope.
I hope that your answer will be "take it easy", but you know, safe is better than sorry.

First off, without knowing the specifics, it is very hard to say, but in general, so long as you are careful and don't ingest (i.e. drink) or breathe in aerosols/droplets of the water, it should be OK. Washing your hands and spraying down work surfaces with hand sanitizer after you finish your observations is a good idea too. The risks probably aren't substantially greater than digging in the soil in your garden. Other standard lab practice is also a good idea - don't eat/drink/smoke/apply lip gloss/makeup while doing this, keep your hair tied up, clean up spills immediately, keep your hands off/away your face.
What is in the water strongly depends on your water source. If you got it from the local duck-pond, it could contain all sorts of things associated with bird faeces, such as Avian botulism, Salmonella, Cryptococcosis and Histoplasmosis (though these last two are more associated with soil than water), even viruses, such as avian influenza, though you'd only likely get this by handling sick birds or the feces directly.
Water that runs off a farm, might have a range of bacterial species, such as E. coli, and Brucella, as well as eukaryotic pathogens such as Giardia, Pinworms (we carry these too, 30-60% of children has these at any given time) and a whole range of other parasites.
Water from a puddle in your back-yard, on the street, or an actively flowing stream (collect the water from a still-water spot) is less likely to contain parasites that might harm you, but bacteria will remain in suspension. Again it depends on source - the neighbour's (or your) cat/dog can carry pinworms, tapeworms, even Toxoplasma, as well as a range of bacteria similar to those listed for the farm above. Any wild animal that visits your place can also carry a range of things.
the highest risk places are areas with a lot of people. We carry a huge range of native and non-native pathogens that you can pick up from people's dirty habits and leavings. These include bacterial species (E. coli again, but also several others), viruses such as norovirus and rotavirus, and the aforementioned parasites. However, you are much more likely to catch these sorts of things from shared facilities such as toilets rather than water, unless you are collecting from a high-traffic area such as a popular forest walk which doesn't have toilet facilities nearby.
These are the worst-case scenarios, follow good hygiene practices and good laboratory practice and you should be fine.

Thanks @bob1, this makes me more aware of what I'm handling and what the good practices are


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

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


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Bioavailability -- what is the effect of absorption rate?
I learnt about Bioavailability and this is the definition given by many sources:

...the fraction (%) of an administered drug that reaches the systemic circulation.
(https://en.m.wikipedia.org/wiki/Bioavailability)

In some other places, it was defined as:

Bioavailability (F) is defined as the rate and extent to which the active constituent or active moiety of a drug is absorbed from a drug product and reaches the circulation."

This 2nd definition is supported by sources including:

Essentials of Medical Pharmacology by KD Tripathi; 8th Edition; Page 22 (photo attached)

https://www.sciencedirect.com/topics/medicine-and-dentistry/bioavailability

https://www.msdmanuals.com/professional/clinical-pharmacology/pharmacokinetics/drug-bioavailability

However, I find it very disturbing to accept that the rate of absorption affects Bioavailability. And this is my reasoning:
Let's say you have 2 drugs, A & B
20g of A is administered and a total of 10g is seen in systemic circulation where A is absorbed at a rate of 1g/hr (taking 10hrs to be fully absorbed at 10g)
20g of B is administered and a total of 10g is seen in systemic circulation and B is absorbed at a rate of 2g/hr (taking 5hrs to be fully absorbed at 10g)
I am assuming both drugs experience same degree of 1st pass Metab and that every other factor that affects Bioavailability is constant.
Isn't the bioavailability of both drugs same at 50% irrespective of the difference in rate of absorption?
Please help.
PS: This source, https://www.sciencedirect.com/topics/medicine-and-dentistry/drug-bioavailability#:~:text=Drug%20bioavailability%20is%20the%20fraction,which%20the%20drug%20is%20absorbed , says:

Bioavailability does not take into account the rate at which the drug is absorbed

I am even more confused!

I think you will frequently find that measures in biology are not defined in a consistent manner, largely because experimental constraints often require a different operational definition. People prefer to keep the same term for the underlying concept, but recognize that different operational definitions may give slightly different answers. I'd consider this in the realm of "all models are wrong, but some are useful".
In the case you describe here, I would argue this is a conflict between a theoretical and practical version of the same concept.
For drugs, the concept of bioavailability generally applies to different dosing strategies and contrasts intravenous injection (bioavailability = 100% because the entire injection is immediately introduced to systemic circulation) with other routes (e.g., oral, transdermal).
Operationally, though, people don't typically measure bioavailability by counting individual molecules in the systemic circulation versus not. Instead, they measure serum concentrations at multiple time points, calculate the area under the curve, and use a ratio of area under the curve to determine bioavailability.
Here's an example of how that might look from Wikipedia:

For the IV curve, you just have decay kinetics; for PO you have absorption and decay. To compare them, you integrate to get area under the curve which has units of concentration*time, and look at the ratio of PO to IV to report PO bioavailability.
Sort of the "null hypothesis" or basic assumption for kinetics in pharmacology is that everything is single exponential unless you find otherwise. That is, rates of absorption and clearance are directly proportional to concentration in different compartments, or in other words every molecule behaves independently like you expect for any process driven by diffusion or unsaturated enzyme kinetics. Under that assumption, this AUC ratio is equivalent to "fraction of an administered drug that reaches the systemic circulation" and it's also true that "Bioavailability does not take into account the rate at which the drug is absorbed": it doesn't matter "when" a molecule enters the systemic circulation, if you calculate AUC you will at some point have that molecule enter and then leave and it will spend exactly the same amount of average time in circulation as a molecule entering at any other time.
However, drugs aren't always going to perfectly obey exponential kinetics, and another meaning of bioavailability is just "area under the curve", whatever the contributions to the area under the curve might be. That might include a drug that enters circulation very fast saturating an enzyme that metabolizes it, leading to a slower clearance for a drug absorbed quickly versus slowly. If that's the case, your AUC ratio no longer precisely represents bioavailability in terms of "fraction of an administered drug that reaches the systemic circulation" but it retains a meaning of bioavailability in terms of "dose*time".
Your definition:

Bioavailability (F) is defined as the rate and extent to which the active constituent or active moiety of a drug is absorbed from a drug product and reaches the circulation."

is consistent with this practical measurement issue from AUCs.
In contrast, if you are using some sort of pharmacological model with explicit terms for absorption, decay (including higher-order decay terms), etc, you would want to use the theoretical definition for bioavailability.
I'll add that when you read:

Bioavailability does not take into account the rate at which the drug is absorbed

I would interpret this as trying to emphasize that bioavailability is not about peak concentration. In medical practice, this is very important to understand, whereas in a pharmacokinetic sense the other nuances may also become important.


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Total number of animals in Australia
In the last weeks there have been a lot of news reports about the number of animals that died in the current wild fires. However, I was wondering, what that is as a percentage of overall animal population in Australia. So:
What's the total number of animals living in Australia?

I wasn't sure about the tags, you're of course free to change it to more fitting ones

Hi, and welcome to the site!  It would be best if you could include actual quotes from the news articles you are looking at.  Thanks!

Note that the definition of "animals" behind the "# dead in fires" numbers going around is not the same as a biologist's definition of "animal"


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Human fecal sample storage: Can it be stored temporarily at -20 C before being transferred to -80C deep freezer?
I am trying to analyze human gut microbial composition by 16S sequencing.
There is enough literature saying it is crucial and standard to store the sample at -80 C if it can't be processed in the molecular lab.
Can the hospital ward, that collects the samples, store the sample immediately at -20 C first which can then be transported to the lab on ice and then stored at -80 C ?
Literature also points out that the sample should not undergo more than 4-5 freeze-thaw cycles.
Experts and experienced, any kind of input would be helpful.
Thank you.
R

Welcome. I think it all depends on how long the samples are stored at temps above the recommended temp - can you clarify your question - what microorganisms are you interested in? How long will the samples be stored in -20? etc etc. In addition, we require questions to be accompanied by some evidence of finding a solution to the problem; what have you found so far? Lastly, provide links to the literature you have used as indicated in the post; please edit the question.

If maintaining bacterial viability is not a concern, I would recommend using a nucleic acid preservative like DNA/RNA shield or STAR buffer or RNALater. Some are sold pre-dispensed in specimen tubes with a scoop or swab for stool collection. They're all pretty great for maintaining the composition of the microbiota, but it depends on your storage conditions, specimen types, etc. Plus they tend to inactivate most pathogens, which has saved me some paperwork to do with shipping and receiving certain specimens in the past.


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How I can find the list of transcription factor proteins involved in transcription of a specific gene?
I want to get the list of transcription factor proteins involved in the transcription of the human SIRT1 gene. How can I access that?

Can you tell us what you have tried so far? My first instinct would be to check the literature.


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Targeted gene sequencing and specialist analysis compared to WGS and DYI searches
There seem to be a lot of "genetic consulting" services that focus on things like cancer, with a modus operandi of:

Do targeted gene sequencing (usually on a few tumor suppressor genes related to cancer the customer is at-risk of)
Analyse the respective data and compile a genetic report outlining risks

The few analyses that I've seen around WGS compared to targeted sequencing claim fairly high accuracy of WGS, including on tumor suppressor genes, sufficient that I wouldn't worry about it, given that TGS will also have some degree of error. So it seems to me like there's little point in using a targeted approach compared to WGS nowadays, given that I can buy a 100x WGS for 1k and some of the targeted tests cost upwards of that.
The other question would be whether the clinics have any "specific" data. I doubt this? I've not heard of a lot of closed-source genetic data, besides maybe that of pharma research companies on a few niche topics. So it seems like a Promethease report could match whatever a specialist would be doing here... or even just searching the variants of concern on clinvar.
Is there any reasons I'm missing why these services still exist? Is it just consumers being misinformed? Or am I glancing over some big problems or benefits?

I guess this might be a bit of a silly question, but hopefully the answers to this will help me elucidate some underlying questions about applied genetics.

Leading question that may help you self-answer: you mention the depth of WGS, but what depth does targeted sequencing (such as these genetic counseling services provide) usually have? With what frequency would you expect to see mutations implicated in cancer risk?

The frequency itself depends since we're not talking single base mutations, the depth for most targeted sequencing offers I could find is unspecified.

First of all: one thing is the cost for research, one is the cost for diagnostic.
Diagnostic tests undergo a series of validation procedures (of which I am not expert) that inevitably lead to an increase in price.
So, the cost of a research WGS can be as low as 1K; the cost of a WGS test validated by FDA would be much higher.
The same is true for targeted. You can sequence an amplicon for 4$. But if you want to use a test that is approved by FDA the price would probably increase.
Also, interpreting variants you get from WGS is not an easy task. There may be false positives, false negatives, difficult situations. It's not that you can do it yourself, unless you are REALLY an expert.
In addition, targeted test are designed to screen for genes responsible of the majority of cases, so in a large majority of cases you would spend more money and still get the same result you would get with amplicon sequencing.
This said, I am sure that the direction we will see in the near future (if personalized medicine stops being a buzzword and starts being reality) is a shift towards more comprehensive screenings such as WGS.


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Does an ORF need a stop codon?
I try to read ORFs from a gene sequence but I am not sure how to interpret a sequence with a start codon but no stop codon. Imagining I have a gene sequence like the following:
atggcagaagaaga
The gene sequence contains a start codon (atg at the beginning) but no stop codon.
Does this count as ORF or not?

Generally speaking, every single ATG..... is not an ORF. That would be a LOT of ORFs in the genome. Not even every ATG.....STOP is an ORF. An ORF has to be transcribed...and spliced into an mRNA. Just looking through an entire genome and finding ATGs is futile for understand gene density.
More practically speaking, a sequence generated from a reverse transcribed library (mRNA to coding DNA, or cDNA) is a good source for ORFs. But, you can still be fooled by the multiple possible reading frames within a cDNA. Using software to convert all 3 possible reading frames of the ORF is an excellent way to start and make predictions. The best way to find out what is really made is to consult the literature OR put the cDNA in an expression vector and translate it in vitro. This tells you the general size of the actual protein and you can compare that kDa value to the expected weight of your ORF. Then, antibodies can be directed against portions of the protein sequence to study it in vivo.

It's actually for an assignment and the task is to read ORFs from DNA. In the assignment every start with stop codon is an ORF. With your answer I am just more unsure yet. Websites like https://web.expasy.org/translate/ also count a dna with no stop codon as ORF.

Darn. I hate it when biology gets confusing like this. Class assignments, depending on the level, can be almost too straightforward. Stick with the straight answer...ATG to STOP codon to find your ORFs. The Web.expasy.org/translate app is pretty weak and just meant to take sequence and find ATGs. Just like I mentioned before...futile. You could get the same answer by taking the sequence into MS Word and using the Find function to search for ATG. The only thing the app gives you is all the additional translation which doesn't mean anything if it's not a real ORF.

Okay. ATG to STOP codon means that ATG without a following STOP codon is no ORF?

Before I definitively say yes, tell me the size of the sequences you are being given to find an ORF. If they are really short, your instructor may just be trying to get you to find an ATG. But if they are long and some ATGs do have an in-frame stop codon and others don't, I'd say the instructor is wanting you to identify an actual ORF...ATG to STOP.

Also, remember that instructors' favorite trick question is find the ORF in an mRNA sequence: A) augccg....stop or B) atgccg...stop...Tricky...tricky


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Actin-myosin cortex stiffness VS elasticity
I have two questions on the mechanics of actin-myosin network:
1- Actomyosin cortex as an elastic material is defined by its elastic modulus $E$. But I know that elasticity would be described by the stiffness of the material!
How do $E$ differ from cortex stiffness $k$ then?
2- What is the difference between passive and active mechanics? In this article, Box 1 page 3 (538), https://www.cell.com/trends/cell-biology/fulltext/S0962-8924(12)00111-0#:~:text=The%20cortex%20is%20a%20thin,role%20in%20cell%20shape%20control., they wrote in the second column "Actin networks differ from passive semiflexible polymers" but they already at the beginning said that "actin filaments are semiflexible polymers". This makes confusion for me in understanding the difference between passive and active properties in cell mechanics.


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Are carrier proteins receptors?
I learnt about carrier proteins; how they bind a substrate/molecule, undergo a conformational change, and release the substrate/molecule on the other side of the membrane.
We can take Glucose transporters(GLUTs) as an example.
I see this "binding" to the carrier protein as something similar to how ligands interact with receptors. However, I don't know whether it is correct to classify carrier proteins as receptors.
Please help.

PS: Carrier proteins don't seem to fall into any of the types of receptors -- ionotropic, G-protein-coupled, or enzyme-linked.

Welcome to SE Biology. Please finish the [Tour] and the Help on asking questions to find out how this site operates. Specifically we expect posters to show that they have researched the question to try to find the answer themselves. If you search for "Receptor" in Wikipedia, taking the Biochemistry variety you will find how the term is used in biological science (rather than general English). Specifically it relates to signal transduction, answering your question in  the negative.


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Confused About Why Red Queen Hypothesis Wouldn't Apply to Deer's Color Vision
In this site,https://www.livescience.com/why-are-tigers-orange, it says ""But there seems to be no evolutionary pressure, particularly for deer, which are the main prey of the tiger, to become trichromatic. That's probably because the tiger doesn't know it's orange either because it, too, is a dichromat."
I am assuming the "evolutionary pressure" refers to the Red Queen Hypothesis. But then why would it matter if the tiger doesn't know its own color? Because it is hiding in the brush anyways, so wouldn't deer who can see red have an advantage over deer who couldn't?
Thank you

"That's probably because the tiger doesn't know it's orange either because it, too, is a dichromat." That phrase right there is garbage. You don't need to know your own weaknesses for someone else to exploit them nor do you need to know why something works for it to work.

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. In general, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, this question demonstrates the value of consulting multiple sources — the quoted statement is as you guessed nonsense. You may find this introduction to evolutionary theory from UC Berkeley useful.

@tyersome That was helpful indeed! Thanks! Also, could you explain how you got the link to the stack exchange link? Was it through a search engine query, saw-the-link before, etc.? Thank you

You're welcome. This type of question comes up quite often, which is why that post was created and why I was already aware that it existed. Due to it being a very general answer it isn't that easy to find when you have specific question like yours in mind, so don't feel bad about not finding it yourself.

what makes you think orange is bad camouflage. in many many environments orange is very good camouflage, no color pattern is good in every environment.


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What are these stinkbug-like insects?
Lots of these insects appeared on a wall in my garden for about a week. I've never seen these before, and they behave like ants. They look like stink bugs and are 2-3mm long.
My search on google lens suggests Nysius Raphanus, but many sources say this species is limited to North America, and I live in south Italy. I think it could still belong to the Nysius genus, though.
Here are a couple of photos I took with my phone (sorry for the bad quality).

Thanks.

Please update with better quality up-close photo.

You are right and these are true bug (Heteroptera) larvae (see this answer on how to recognise them), although not of the familiy "stink bugs", but of the superfamily "seed bugs".
Determining true bug larvea to the species level is tricky and rarely done. But with some experience, it is possible to tell the families apart. Seed bug larvae have elongated, rather flat bodies of brownish colors (which camouflage them on the ground where most of them dwell). Often, they have a pointed nose (a long head) and relatively large eyes.
From their habitus, they could actually belong to the genus Nysius (you could compare with Fauna Europaea which species occur in your region).
But they could also be another species from the seed bug superfamily.
Moreover, identifying Nysius (and most other seed bug) species usually requires a microscopical inspection.

Interesting. Later I discovered that they were coming from and going to a mature Portulaca Oleracea lawn.


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Why do humans see exactly one octave of light?
The visible spectrum of light is often defined as 350nm to 700nm. On Wikipedia, it says 380nm to 750nm. Either way, the upper bound is very close to double the lower bound. This means humans can see exactly one octave of the EM-Spectrum. (By octave, I mean the interval on a logarithmic scale corresponding to 2:1)
Is this a coincidence? Is there an evolutionary advantage to it?
As far as I know, our cone cells work on the principle of resonance. But they do not seem to respond to harmonic frequencies. Why?
To be clear. I am not asking why our vision is in the range it is. I am asking why the bounds are so close to 2:1.
There has been a similar question on Physics StackExchange, but the answer does not address the octave part.

Why do you think there should be a reason?

Maybe related: https://biology.stackexchange.com/q/57708/27148

trivial answer: it is the most intense portion of the spectrum that we experience.

It isn't really true that the human eye sees "exactly one octave of light".
The visible spectrum does not have precise boundaries, so the choice of "350-700 nm" is a bit arbitrary and might even just reflect a human bias towards integer ratios.  Wikipedia gives "380-750 nm" as the typical range for the human eye, and if you look around online you'll see lower limits that range from 350 to 400 nm, and upper limits from 700 to 830 nm.
For sufficiently bright sources, human perception may actually extend down to 310 nm and up to 1100 nm.
Humans can see the spectrum they do because of a combination of eyes being optimized for seeing in sunlight and avoiding the biochemical and biophysical challenges of detecting longer and shorter wavelengths.
Visible and near-visible light is the "sweet spot" for biological vision on Earth. The human eye could probably not operate over a much larger wavelength range, and a range much less would inefficiently waste available light. There is no reason for the visible range to be precisely a factor of 2, but it would be surprising if the range was very much larger.
As noted in the comments, the range of human vision almost exactly matches the wavelength region of peak solar irradiance on the Earth's surface. The full width at half maximum range for sunlight is about 300-900 nm.
As noted in the answers to "What is the biological potential for vision of wavelengths outside the human visual range?", shorter wavelengths tend to destroy biological structures and longer wavelength photons don't have enough energy to be easily detected individually.
The human eye doesn't "respond to harmonic frequencies" because it it detects light via quantum processes, which are not the same as the classical resonances such as a vibrating string. Just because a molecule absorbs photons of a given frequency, doesn't mean it will absorb photons of twice that frequency.
Another issue is that if you double the frequency of light, you double its photon energy, which for visible light takes into dangerous wavelengths.
Even for creatures whose eyes work into the ultraviolet, their range doesn't go much below 300 nm, which is not surprising since 300 nm (4 eV) photons can break carbon bonds and 250 nm (4.5 eV) photons can break C-H bonds.
Interestingly, however, the eye has been observed to respond to sub-harmonic frequencies. Intense infra-red light can be seen as green, because two infra-red photons can activate the rhodopsin receptor that normally is activated by a single green photon.  This requires very bright infra-red light since such two-photon processes happen rarely.


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In this representation of the tree of life, what are the lateral connections?

I found this simple representation of the tree of life in a wikipedia article, and I was curious what these horizontal connections shown here are supposed to be, like the ones between plants and protists, or bacteria and protists going to plants. Do they represent things like lateral gene transfer or potential endosymbiotic origin relationships? (like the theory that eucaryotes came from a merging of a bacteria with an archae).

they likely represent the inclusion of mitochondria and chloroplasts into eukaryotic cells.

thanks john, that makes sense :)

Yes, pretty much! Lateral branches here indicate endosymbiotic events and major horizontal gene transfers.
I'd warn though that the diagram is not very accurate, and additions I'd make would complicate it further as a bush (rather than a tree). Each branch root itself is an instance of cladogenesis, and for this reason the diagram is not very accurate (e.g. fungi and metazoans seem to arise within the same "branch"), and also misses a few lateral branches that otherwise exist. My favorite example of atypical horizontal gene transfer is that of prokaryote-insect transfers which occur frequently. This has been known for some time; many insects contain genes of Wolbachia origin and some (not all) are definitively functional, and are understood to facilitate obligate (fully-dependent) mutualisms.

Thank you so much for your detailed answer! Very interesting stuff. You mind if I bother you for a recommendation for a book reference on this topic? I've been reading "Assembling the tree of life" which I'm really enjoying, but I was curious if there was a newer reference (the book is from the early 2000s), that is as large in scope as this one, since from what I've heard phylogenetics has grown quite a lot with computational models in the last 20 years.

Unfortunately I don't think I am familiar with the most recent literature on the most comprehensive phylogeny of all life available. Perhaps you could take a look at the Tree of Life Explorer OneZoom, maintained for years and most recently a publication with plenty of explanations was made about it in 2021. You're right, we still catalogue new species and next-gen sequencing and related tools are helping resolve a lot of phylogenenies quickly. To compile all this is a mammoth task, and is of course ever-ongoing.


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Is harmonic resonance in Photoreceptors explored?
Look at the resonance curves of the L-cone (OPN1LW) in humans, it has its peak at ~570nm and rises up in the lower wavelength (higher frequency) area. For me as a musician, that looks like a natural harmonic 2/3 response – the fifths – of the frequency. But all spectral response charts I've found so far for the different receptors in humans don't really go beyond the borders of the range visible to humans.
Has someone a link to a study that tested for harmonic responses or general response in a field extending at least one octave in both directions, hence about 200nm - 1600nm, for the actual receptors (rods/cones) without surrounding effects like the lense being a low-pass-filter etc.

See https://physics.stackexchange.com/questions/229046/why-do-we-see-just-one-octave-of-light and https://biology.stackexchange.com/questions/57708/what-is-the-biological-potential-for-vision-of-wavelengths-outside-the-human-vis.

I’m voting to close this question because a request for a link is not a question about Biology in terms of SE Biology.

I think a few things are muddled here. The frequency response profile of a cone (which is an entire cell) is a functional response to excitation of that cell's photoreceptors. It's easy to show that these cells only function over the range of wavelengths that are considered "visible range." So that's why you won't readily locate experiments that address your query. (I think a link to the data you're asking about would help.)
Since the underlying light-detection event here is the photo-isomerization of rhodopsin, there's no reason to think the process (at that scale) would occur at harmonics you're familiar with from music theory. That's because electronic transitions correspond to well-defined frequencies (as with the photoelectric effect). The rhodopsin molecule, like most pigments, isn't well-approximated as a harmonic oscillator (unlike, say, a guitar string) which is the whole reason classical electromagnetic theories failed to predict the emission spectrum of hydrogen.
So you're mixing-up your natural phenomena; biological photoreceptors behave somewhat-like the hydrogen atom, not like a guitar string. As you can see, the emission or absorbtion spectra of hydrogen do not have simple overtones of a fundamental frequency.

Vision works by a pigment molecules changing conformation by absorbing a photon. A certain range of energies is necessary for this conformation change.
More generally, molecules can potentially absorb multiple photons simultaneously rather than individual photons, and the combined energy of multiple lower-energy photons can excite the molecule to the same state as a single higher-energy photon. This is commonly utilized in biological experiments via 2-photon microscopy. Because 2-photon excitation requires simultaneous arrival of two photons, you need much higher intensities of light.
Here's an example of a paper discussing this in rhodopsin:
Palczewska, G., Vinberg, F., Stremplewski, P., Bircher, M. P., Salom, D., Komar, K., ... & Palczewski, K. (2014). Human infrared vision is triggered by two-photon chromophore isomerization. Proceedings of the National Academy of Sciences, 111(50), E5445-E5454.


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Was Spinosaurus bipedal or quadrupedal?
Different sites told me different things. I tried looking it up but I haven’t found anything. So which was it? Was Spinosaurus quadrupedal or bipedal like all other theropods? Either seems possible.

The Wikipedia page is pretty thorough on the subject. Is there a particular point you needed clarifying?


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Sigmoidal Curve in Geometric Growth
Here is an excerpt from my textbook:

Let us now see what happens in geometrical
growth. In most systems, the initial growth is slow
(lag phase), and it increases rapidly thereafter – at
an exponential rate (log or exponential phase). Here,
both the progeny cells following mitotic cell division
retain the ability to divide and continue to do so.
However, with limited nutrient supply, the growth
slows down leading to a stationary phase. If we plot
the parameter of growth against time, we get a typical
sigmoid or S-curve.

The exponential growth can be expressed as  $W_1 = W_oe^r{^t}$

$W_1$ = final size (weight, height, number etc.)
$W_0$  = initial size at the beginning of the period
$r$ = growth rate
$t$ = time of growth
$e$ = base of natural logarithms

The first paragraph makes perfect sense to me, but what bothers me is the formula given. When I plot the given equation $W_1 = W_oe^r{^t}$, this is what I get;

Which is clearly not sigmoidal (s-shaped) as my textbook says.
What I think should be the correct equation is:
$$W_1 = \frac{W_o}{1+e^-{^r{^t}}}$$
When I plot this equation, this is what I get:

Which is slightly better than the previous plot. Though this formula might also be erroneous as I just made it up from the general formula of a sigmoid function $S(x) = \frac {1}{1+e^-{^r{^t}}}$
Why is there a discrepancy between the in-text statement and the plot of the mentioned formula and is there any better formula to depict this growth?
Also, I have referred to various sites but could not find any satisfactory answer.
Any help is appreciated. Thanks!

If this statement is true (The exponential growth can be expressed as 1=^^), which seems to be the case, then this is a mathematics question. Probably acceptable on Mathematics.SE. I'd love to help, but I stink at math, and am exceedingly impressed that you even bothered to plot this out. I predict you have a bright future in STEM fields!

I’m voting to close this question because it's a mathematics question. (I did upvote you, though, because wow!)

It is presented confusingly, but they aren’t giving you the equation for the sigmoidal curve. They are giving you the equation for the exponential phase of the sigmoidal curve (Fig 15.6). See wikipedia for the sigmoidal (logistic) growth curve equation.

@canadianer - D'oh! I even stated that, but didn't see it.

I agree with @canadier. The formula given corresponds only to the exponential phase of the growth curve, which is also clearly indicated on the corresponding figure 15.6.

@anongoodnurse Thank you for your comment. Before even posting the question, I knew it was borderline Math-Biology, though I chose to ask here since it was from my Biology textbook  (ps: I'm aspiring to be a doctor, but I'm interested in a whole lot of other things too :)

@canadianer Yeah, that seems to be it, I think. Maybe the authors thought a sigmoidal function would be too complex for the grade level?

I discussed this question with my biology teacher and he confirmed that the equation $W_1 = W_oe^r{^t}$ just represents the exponential phase of the sigmoidal growth, but not the entire growth period. This was also helpfully pointed out in the comments.
Though I did find an article talking about the mathematical functions of sigmoidal growth which includes both the exponential and linear phases of growth.

Within the life cycle of an organ, a plant or a crop, the total growth duration can be divided into three sub‐phases: an early accelerating phase; a linear phase; and a saturation phase for ripening (Goudriaan and van Laar, 1994). Therefore, the growth pattern typically follows a sigmoid curve, and the growth rate a bell‐shaped curve. While the sigmoid pattern can be represented piecewise using an exponential, a linear and a convex equation sequentially (e.g. Lieth et al., 1996), a more elegant way is to use a curvilinear equation which gives a gradual transition from one phase to the next. For example, based on principles of light interception and leaf area expansion, Goudriaan and Monteith (1990) derived a single equation, the expolinear equation, for both the exponential and linear phases of crop growth:
$$w=\frac{c_m}{r_m} ln [1+e^{r_m(t-t_o)}] \tag{1}$$
where $w$ is mass, $t$ is time, to is the moment at which the linear phase effectively begins, $c_m$ and $r_m$ are maximum growth rate in the ‘linear phase’ and maximum relative growth rate (RGR) in the ‘exponential phase’, respectively.

YIN, XINYOU, GOUDRIAAN, JAN, LANTINGA, EGBERT A., VOS, JAN, and HUUB J. SPIERTZ. "A Flexible Sigmoid Function of Determinate Growth." Annals of Botany 91, no. 3 (2003): 361-371. Accessed February 26, 2023. https://doi.org/10.1093/aob/mcg029.

But, this equation too does not achieve the smooth sigmoid curve I wanted to see. With this equation you get a plot like the following:

The equation I suggested is almost close to an equation mentioned in the paper and is not entirely incorrect. The equation uses the logistics function and gets the smooth sigmoidal curve I was hoping to see on the plot.

Alternative, but simpler, functions that can produce two smooth transitions in a single formula are the classical growth functions. The first is the well‐known logistic function (Verhulst, 1838):
$$w = \frac {w_{max}}{1+e^{-k(t-t_m)}} \tag{3}$$
where $k$ is a constant that determines the curvature of the growth pattern, and $t_m$ is the inflection point at which the growth rate reaches its maximum value. At time $t_m$, the RGR is $\dfrac{k}{2}$. As can be seen from eqn (3), the weight at $t_m$ is half of its maximum value, $w_{max}$.

Now, when I plot equation $(3)$, I get what I was hoping for! The smooth sigmoidal growth curve:

NOTE: All the graphs in this Q&A take the growth to be on the y-axis and the time duration to be on the x-axis. The values on the graphs are completely arbitrary.
27-02-2023 EDIT: Added equation which depicts sigmoidal growth.


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Why does nitrification -oxidation consume organic matter?
I want to express some doubts regarding autotroph bacteria.
The question I want to ask is relative to wastewater treatment plants, more precisely at the nitrification/denitrification step.
I've studied that nitrification doesn't need organic matter, in fact the latter is an inhibitor of the process. In addition, there are autotrophs bacteria employed, which comsume inorganic carbon for the processes.
But books of environmental engineering also mention that denitrification, if preceded by nitrification -oxidation, can present the issue of not having enough organic carbon for their processes, and that's the main reason we use post-denitrification systems today. Isn't it a contradiction? Why is organic carbon consumed by nitrification -oxidation, if they are autotroph bacteria? What am I missing in my reasoning? Do autotrophs in reality need organic carbon for their vital functions , and that was just omitted in calculations?
Thank you in advance


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What colour skin would the child of someone with albinism have?
My question is assuming the baby doesn't have albinism. If the mother has albinism and her family all has dark skin and the father doesn't have albinism and has light skin, would the baby just get the father's skin colour, or would they get the gene for dark skin from the mother? Or if the mother would have dark hair if it weren't for her albinism, and the father has light hair, would it be possible for the baby to have dark hair?
I guess another way to ask this question would be, does albinism cover up the genes that give you pigment, or does it cause you to not have those genes at all?

A lot of use with guinea pigs and similar animals have seen that happen. it's a complex mostly recessive and sometimes co-dominant.

To answer the question we first have to take a look what albinism is and how it is caused.
Albinism is an inherited genetic condition that reduces the amount of melanin pigment formed in the skin, hair and/or eyes.It is characterized by the absence of pigment in the eyes, skin, hair, and other parts of the body. Albinism affects the production of melanin, which is responsible for coloring these areas. Symptoms may include vision problems and light sensitivity. See references 1 and 2 for more background information.
Mutations in several genes, including TYR, OCA2, TYRP1, and SLC45A2, are associated with albinism (references 3 and 4). These genes give instructions for making proteins involved in producing melanin, which is made by cells called melanocytes. Melanin is responsible for coloring the skin, hair and eyes. The most important gene is TYR (or tyrosinase) being resposible for the initial step in melanin biosynthesis.
Albinism is inherited in an autosomal recessive pattern, meaning a child must receive two copies of the gene that causes albinism (one from each parent) to have the condition. This means both parents must carry the gene for their child to be born with albinism. See reference 5.
To answer the question: If the mother has albinism, she has two non-functional copies of one of the genes mentioned above, otherwise she wouldn't be albinistic. If the father has two intact copies of the same gene, the kid will have normal pigmentation. However, as kids mixed from parents with a light and a strong pigmentation background it will most likely be darker than the father and lighter than his mother would be without albinism.
If the father carries a mutation on one allel of the genes which cause albinism for the mother and the other is normal, than there is a 50% chance that the kid is also albinistic.
References:

Information Bulletin – What is Albinism?
Albinism
Oculocutaneous albinism
Molecular basis of albinism: mutations and polymorphisms of
pigmentation genes associated with albinism
Albinism

Skin color in humans is mainly determined by a pigment called Melanin. Melanin is produced by cells called melanocytes present in the epidermis of the skin. Melanin production rates are determined both by genetic and environmental factors. A high production of Melanin will result in what we call "dark skin color", and a low production will result in what we call "light skin color".
From the Wikipedia page for Albinism,

Albinism is the congenital absence of melanin in an animal or plant resulting in white hair, feathers, scales and skin and pink or blue eyes.

This means that in an individual with Albinism, Melanin production is extremely low.
Albinism is usually caused by genetic mutations to some of the hundreds of genes that affect Melanin production. As Wikipedia quotes,

All the genetic traits for albinism are recessive traits. This means that their influence is hidden when paired with stronger traits. For the recessive albino trait to be expressed in a mammal, the offspring must inherit a recessive gene from both parents.

You ask about a baby getting the gene for dark skin color from an albino mother. What's important in understanding here is that the mother doesn't have a gene for dark skin color. Albinism is caused by mutations to genes, so an albino's genes encode for albinism, meaning they don't have any genes for "dark" or "light" skin color.
Albinism is recessive, meaning that an individual with only one copy of a gene for albinism will not exhibit albinism. So if the father of the baby in the situation you mention does not have a hidden gene for albinism, the baby will likely exhibit the father's skin color. The same is true if the father has a hidden gene for albinism, but doesn't give this gene to the baby. If the father passes on a gene for albinism to the baby, however, the baby will likely be an albino, considering the recessive allele it receives from both parents.

Sorry, but this answer is wrong. Neither are there "hundrets of gene that affect melanin production" nor is there only one gene for albinism. Please correct this answer.

Hi @Chris, thanks for your feedback. I would like to understand where I went wrong with this answer. The Wikipedia page for Albinism says that "in mice, a total of 100 genes are known to affect albinism". While humans are different from mice in a lot of aspects, I'm assuming something as fundamental as skin color will have its similarities between the two species. If around 100 genes affect Albinism, won't it be correct to say that a 100 genes affect melanin production? Please let me know where I went wrong in my reasoning!

Mice are not humans. They can serve as a model organism to some degree but there are differences. For example: Mice do not pigment their skin. Additionally the Wikipedia article does not give a scientific reference. So be careful to make assumptions about field in which you have no experience.

@Chris you're right. I will put more research into my answers in the future!


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Do all plants have meristems?
Are there any plants that lack a meristem (at any phase in their lifecycle)?
Searching for it on the web, the materials I find seem to assume no, but none say it explicitly.

Welcome to SE Biology! It might be handy to look at the tour and check out other materials provided about the community. With regard to your question: can you please directly show the information that you found so that we can evaluate it? Where have you looked? What do you mean by "meristem"? Note that there are unicellular plants.

If you consider plants to be photosynthetic eukaryotes, some of them have shapes that wouldn't require a meristem in the same sense as the plants we commonly see. i.e
Volvox is spherical. Cells in all organized structure communicate with each other by chemical signals that diffuse through neighbour cells and give knowledge of orientation and distance from neighbours.
All plants with organized structures that grow against gravity would probably have reduced fitness if they lacked meristems.
It's a good idea to read about the evolution of meristems to find out what recent research has found.
Meristems are often the apical cells, so free plants in the water and at smaller sizes, plants don't have a right way up.

Thanks; I wonder whether there are larger photosynthetic eukaryotes than volvox w/o meristems. Maybe I should ask that as a separate question.

Also maybe you should add a note about unicellular plants in your answer (see the first (and as of writing only) comment on the question).


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What is the difference between monoclonal and polyclonal antibodies?
I'm having trouble to see a difference between monoclonal and polyclonal antibodies. The way I understand it:

Monoclonal antibodies are produced by the same "clone" or "line" of B-cells and, thus, can bind to a single epitope for some antigen.
Polyclonal antibodies are produced by multiple "clones" or "lines" of B-cells and, thus, can bind to different epitopes for the same antigen.

However, it is also my understanding that:

Every B-cell can produce only one kind of antibodies; i.e., the antibody molecules produced by an individual B-cell can all bind to only one epitope.

And so, when combining all these concepts, I can't really find any fundamental difference between monoclonal and polyclonal antibodies. To me, the distinction is only applicable when one is discribing the composition of a given substance (i.e. if such a substance contains Abs produced by a single line of B-cells or by multiple lines), but otherwise there's no difference between an individual "monoclonal" Ab molecule and an individual "polyclonal" Ab molecule; i.e., they'd both have the same general properties and functions.
I'd like to know if there is something I'm misunderstanding or if there's some information I'm missing.

I'd recommend looking into VDJ recombination to learn more about the underlying means by which antibody specificity / identity is defined. A clone of mature B cells derives from a single recombination event.

Welcome to SE Biology. Please do us the courtesy of finishing the [Tour] and then read the Help on asking questions, from which you will see that we require you to show the research you have done before posting. Wikipedia and a hundred other sites on the web explain the difference between monoclonal and polyclonal antibodies.  Read them carefully.

@David I'm aware that there are many sites on the Internet that explain the differences between these concepts, but I just like posting questions publicly so that fellow humans can condenscendingly and unhelpfuly answer to them. I also believe that I've clearly summerized in my question all the relevant information I've gathered so far from what I've read; please do me the courtesy of reading my question carefully. Thank you.

On reflection, I think that a lot of this question comes down to the meaning of the word "clone". Re: David's note about triviality, it is only trivial if you have a very clear idea of what this word means, as the root of polyclonal (many clones) vs. monoclonal (one clone).

Let me start again. You write "I'd like to know if there is something I'm misunderstanding". The answer is yes. You are thinking that the term "monoclonal antibody" is a description of an individual protein molecule, and implies that that individual protein molecule is chemically or structurally different from an individual protein molecule designated "polyclonal antibody". Antibodies are important tools in biological research, and for which they are generated artificially. Polyclonal and monoclonal refers to the heterogeneity or otherwise of the generated populations…

(cont)…So, as many accounts make clear, the key thing about monoclonal antibodies is that they are preparations (mixtures) in which all antibodies are identical in amino acid sequence (and which can continue to be generated to sustain research). This homogeneity of monoclonal antibody preparations allows applications/uses that are not possible with polyclonal antibodies, in which the individual molecules, although binding to the same epitope, have different aa sequences (and affinities and specificities). The applications/uses of monoclonals are many, and are amply described in the literature.

Monoclonal antibodies are like having a bag of tennis balls. They're all tennis balls.
Polyclonal antibodies are like having a bag of sports balls. If some of them are tennis balls, yes, they're the same as the monoclonal antibody tennis balls. But, the polyclonal antibody bag also contains baseballs and ping pong balls and basketballs. And there are far more possibly antibodies than there are sports balls, so it's most likely that your sports ball bag of antibodies doesn't have any tennis balls or any other specific ball you'd have thought of ahead of time, rather just a bunch of things that vaguely serve the purpose of being ball-like.
So yes, you're right, for an individual antibody, it's the same substance whether it's in a bag with only other identical antibodies or if it's in a bag with a bunch of other antibodies, but it still matters whether you have a bag of one antibody type versus a bag of lots of antibody types. The former is more standardized, you "get what you get" and it always will work the same; the latter is more diverse and binds multiple targets which in some sense makes it more robust (e.g., a small change in the target may prevent binding with one clone but not other clones).
Production is also different. Simplifying things a bit, for monoclonal antibodies, you produce the antibodies by isolating an antibody-producing cell and making lots of copies of that cell to make lots of that same antibody. There can be some variation in production but generally they are thought of as "one antibody".
For polyclonal antibodies, you inject an animal with an antigen, and collect the antibodies that are produced. You expect to get different specific antibodies each time, the only thing standardized is the antigen presented. (you can also do this with cell culture like monoclonal antibodies, except using a culture derived from lots of different cells)

I'd add an important distinction is often that monoclonal Abs have often only been presented with a short fragments which is approximately the length of an epitope, whereas polyclonal have often been given larger fragments or even full-length proteins to target, resulting in a diversity of epitopes.

@Bryan Krause Thank you for your easily digestable explanation. I was wondering, if there was maybe genetic factors that would make monoclonal and polyclonal Ab molecules different in some small but important way (like differences in their binding sites or in their backbone structures).

@OldCrow No, it's all in the name: mono-clonal "one clone", poly-clonal "more than one clone", where "clone" means "line of antibody-producing cells".


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How to store chlorella for a long time at room temperature?
Is it possible to store chlorella for a long time (6 months) at room temperature? I was thinking about desiccation and looked for some studies on it, but I only found this study (https://www.sciencedirect.com/science/article/pii/S0168945298000557), which is about a specific strain.


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How can I find out where the holotype of a species is?
When I visit the Wikispecies page for Synapturanus zombie, it tells me where the holotype is, as does the paper which describes the species. But on visiting the page for Quercus gambelii, the holotype is not listed and the article where the species is described is not named (though I am given the journal, author, and year of publication). Can I find out where the holotype for this species is without hunting down the journal article in person?
Q: What's the process in general for me to find out where the holotype is stored for an organism?

In general, one would hope to find the depository that holds the holotype as a part of the formal description article published. However, with many, especially older (1800's or earlier) descriptions, this isn't necessarily the case. Often major collections, such as Kew (UK) or the National Academy of Sciences (USA) will hold collections from important researchers, but this is not always the case. Nowadays, you often have to do a bit of searching to find this information. I've put a description of my process below.
The Journal article in question is:

Nuttall, T. 1848. J. Acad. Nat. Sci. Philadelphia ser. 2, 1(2): 179.

The link provided on the Wikispecies page doesn't take you to the article directly, only to a page for the journal, which links to series 1, volume 1.
I did a bit of link sleuthing and was able to link from the wikispecies page, through the International Plant Names Index (click on the top listing to take you to this page, where you click on nomenclatural link to this page, click on publication, which takes you to this page, where you need to click read this publication under heading BHL). All this finally takes you to the Biodiversity Heritage Library listing for the journal, where you need to access the right volume there (Volume: ser.2:v.1 (1847-1850)), listed as 1847, but covering 1847-1850. You want to look at page 179 under the heading Quercus for the description.
The article doesn't provide any information on the location of the holotype, so a bit more, very easy, sleuthing and you will find that Thomas Nuttall, the descriptor, worked at the Academy of Natural Sciences Philadelphia (now Academy of Natural Sciences of Drexel University), and unsurprisingly published in their periodical. This makes it highly likely he deposited his material with them.  From a quick search of their site, it seems they do indeed hold some 4,000 samples from Nuttall.
They also hold some records from W. Gambel, in their Historical collections. Nuttall's article in the Journal of the National Academy of Sciences, Philadelphia was a description of samples collected by Gambel, and Quercus gambelii is named for him, so they should(!) be with either Nuttall's or Gambel's collections.
So, long story short: The specimen is likely to be at Drexel University in Philadelphia.
I say "should(!)" because things get lost, sent off to other places and not returned etc. Nuttall also worked in the UK from 1842 onwards until his death, as he inherited property from an uncle, under whose will, Nuttall had to spend at least 9 months of each year in England. I don't know enough about the chap to say whether he still continued to work in Philadelphia, but he certainly continued to publish there, as evidenced by the article for the species in question. This could mean that some of his specimens are in the UK. There doesn't seem to be at Kew, at least not digitized, but there are quite a few other sites they could be in the UK.

thank you, you are awesome

Here is one specimen, from Harvard's Gray Herbarium, that is probably a type of Q. gambelii. Because the specimen doesn't have a collector's number (common for that era) and because Nutall didn't say anything about which specimen he used for the description, there's still some uncertainty. Note that L. R. Landrum, who studied this specimen, only says it is a probable isotype (an isotype is another specimen from the same collection as the holotype, called a "duplicate").

We know the above specimen was collected by Gambel in the right area. There might exist other duplicates of this collection at other herbaria, one of which might have a better claim to be the actual one Nuttall used for the description. If someone could convincingly argue that point, they could designate that specimen as the "lectotype", and it would have priority over other isotypes.

@Darlingtonia Kew has a specimen from 1847, A. Fendler collection it seems. Doesn't mention if isotypic or not though.

Since the Kew specimen was collected by Fendler, and Nuttall doesn't mention Fendler, that wouldn't be a type of Q. gambelii. (Well, theoretically, if you could show that Nuttall actually meant Fendler when talking about Gambel, maybe it would have a chance. Like, if Fendler was the botanist on the hypothetical Gambel Expedition to New Mexico, that could maybe be argued.) If one could show that Nuttall consulted the Fendler specimen when writing the description, and then all of the existing Gambel specimens were lost, one could then designate the Fendler specimen as a lectotype.

The Fendler specimen is a type in its own right, but for a different taxon. That specimen, and a few others, are syntypes of Q. douglasii var. novomexicana. A syntype is a specimen listed in the original description, but where none was designated as a holotype. It looks as though taxonomists generally consider this taxon to actually be a part of Q. gambelii, meaning they just don't think that it's distinct enough to be called a separate species. Other taxonomists may disagree, and if they were to use the name Q. douglasii var. novomexicana, then that specimen would be the syntype.

Incidentally, JSTOR Global Plants helped me track down the Gambel specimen.

@Darlingtonia Sounds like you can write a better answer than me - please do! It's only a hobby for me now (since >20 years ago), so I don't know much of how it is done these days.


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Are stable isotopes ever used in pharmaceuticals?
Carbon has two stable isotopes, C-12 and C-13. Since they both have the same electronic structure they can both make up the same molecules, but presumably they may perform different functions in biochemistry due to different mass.
Q: Have various stable isotopes of the same atom ever been put to use in pharmacology?
Basic internet research only yielded information about unstable, or radioactive isotopes.

I think you'll find that the chemistry is more important than the mass,  but I don't know if there has been any pharmaceutical made that that specifically used a stable isotope, so not writing this as an answer.

@bob1 MRI works on precession of the nuclear spin, and that varies dramatically. Consider 12C (spin 0, no (useful) magnetic moment) vs 13C (spin 1/2 like a proton, but heavier) Now whether medically approved contrast agents used in human MRI are considered a pharmaceutical per se or not is a different question.

29Si Isotope-Enriched Silicon Nanoparticles for an Efficient Hyperpolarized Magnetic Resonance Imaging Probe and Use of 13C Isotopes in MR Research and MRI/MRS: Use of Isotopes in Hyperpolarization

@uhoh It looks as if the FDA considers them to be  intravenous drugs, so, yes, pharmaceuticals

@SimonCrase excellent! The last task of showing that stable isotopes are used as pharmaceuticals (rather than just explored as possible candidates) remains and I'm probably not quailed to assert that with supporting sources. Perhaps someone else can/will. Thanks!

@uhoh I didn't think of contrast agents; wouldn't have thought they are pharma, but apparently they are.

@bob1 well if someone is going to inject a substance into your blood, you'd like it to be safe, and therefore its manufacture and distribution carefully regulated. Doesn't really matter whether it's for diagnosis or treatment.

Could you change the actual Question title to reflect the explanation in the exposition, Q: Have various stable isotopes of the same atom ever been put to use in pharmacology?
Either way, isn't the real Question, 'Have different isotopes of the same atoms been used in pharmacology?' and isn't the different wording in both title and exposition simply confusing?

You should check the Wiki articles:

Isotopes in Medicine
Radiopharmaceutical

If we solely focus on carbon-13 based drugs then there is carbon-13 labeled ibrutinib, carbon-13 labeled midazolam/1′-hydroxymidazolam, carbon-13 labelled aspirin.
Lastly, you can reads this papers:

Schellekens RC, Stellaard F, Woerdenbag HJ, Frijlink HW, Kosterink JG. Applications of stable isotopes in clinical pharmacology. Br J Clin Pharmacol. 2011 Dec;72(6):879-97. doi: 10.1111/j.1365-2125.2011
Gregg, C.T. Some application of stable isotopes in clinical pharmacology. Eur J Clin Pharmacol 7, 315–319 (1974). DOI: 10.1007/BF00560350
Bodamer OAF, Halliday D, Uses of stable isotopes in clinical diagnosis and research in the paediatric population, Archives of Disease in Childhood 2001;84:444-448, DOI: 10.1136/adc.84.5.444

Deutetrabenazine.
As the linked article from Wikipedia notes:

Deutetrabenazine (trade name Austedo) is a vesicular monoamine
transporter 2 inhibitor which is used for the treatment of chorea
associated with Huntington's disease and tardive dyskinesia.
Chemically, deutetrabenazine is an isotopic isomer of tetrabenazine in
which six hydrogen atoms have been replaced by deuterium atoms. The
incorporation of deuterium slows the rate of drug metabolism, allowing
less frequent dosing.

Whilst what you have in the above is an isotope of hydrogen, the effect this gives is seen in other compounds belonging to the bioisosteres (chemical substituents or groups with similar physical or chemical properties which produce broadly similar biological properties in the same chemical compound), the purpose being to:

enhance the desired biological or physical properties of a compound
without making significant changes in chemical structure

The different mass of the deuterium in the case of deutetrabenzine is thought to tweak the chemistry in useful ways:

However, the C–D bond is a bit shorter, and it has reduced
electronic polarizability and less hyperconjugative stabilization of
adjacent bonds, including developing an anti-bonding orbital as part
of the newly formed bond. This can potentially result in weaker van
der Waals stabilization, and can produce other changes in properties
that are difficult to predict, including changes in the intramolecular
volume and the transition state volume

The urea breath test for Helicobacter pylori uses urea labelled with carbon-13 or carbon-14 to detect the presence of the bacteria, which would metabolize it to carbon dioxide and be exhaled.


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Can plants be pathogenic towards humans?
In googling this question you’ll only find articles about plant pathogens jumping over to humans eg candida auris and pseudomonas aeruginosa.
My question is, like fungi can be infectious to humans (aspergillus, candida, tinea corporis), could a plant infect us?

Yes: Protothecosis is infection of the bloodstream by a genus of non-green algae. There are also odd reports of infection by green algae, such as this one.


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Is there a comprehensive Taxonomical ID database?
I know there are resources that outline the latest taxa, such as wikispecies or Kew Gardens. However, I have not found any resources which detail the defining features of each taxa. Are there any resources someone like me could consult?

Who are you? (because of Are there any resources someone like me could consult) Do you mean outside paywall? In any case Kew Gardens is the place (directly or indirectly it is involved). E.g. POWO has descriptions. Else you need an university library.

I'm unaffiliated with any academic or research institutions @GiacomoCatenazzi. If there's no resource outside paywall, I'm open to paying

@imrobert The latest taxonomical descriptions are in the scientific literature. There are committees for naming a number of different groups of organisms, such as the International Committee for Nomeclature of Viruses, which have literature around the naming etc. You could try those. Also, you can often enter university libraries just off the street as it were, and some will even let you subscribe to issue books etc. as an outside person.

The NCBI Taxonomy database is probably a good place to start.
You can look at their taxonomy ID resources and their FTP (linked therein) which includes large datasets.
They also link out to a number of other taxonomy resources.


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Who put Cephalopoda in Mollusca?
Cephalopods are considered mollusks due to homologies such as a shell, a muscular foot, and a mantle. But, they also have closed circulatory systems, two giant eyes, and eight prehensile legs. When did Cephalopoda get classified as part of Mollusca? Also, in a case like this, is there a way to quantify homologies pointing to one classification vs. another?
In researching this question I came across this blog that states Linnaeus taxonomized Octopus and Octopoda in 1758, though there is conflicting information on Wikispecies here and here

The title of your question, asks “who”, its text asks “when”, but then answers that, but you actually seem to want to know “why”. It would be good if you could edit your question to clarify.

This seems more suitable for our sister-site, [hsm.se] as it's not about the biology itself, but about an action taken in times past by a person, committee or other body of people. Flagging for migration.

why focus on the differences and not the similarities like radula or circular brains, of course it hard to see how groups are related if you only look at the apomorphys.

Modern classification (cladistics) is according to common descent as the backbone for our entire understanding of biology, superseding previous classification schemes based on observed traits/features.
Cephalopods are mollusks because they share a common ancestor with other mollusks; if we want Mollusca to be a clade, it must include the cephalopods. If we didn't treat cephalopods as mollusks, we'd be missing part of the "family tree" and it wouldn't be a clade. We already have a separate name for them if we want to distinguish them from other mollusks based on the properties you describe: cephalopod.
Sharing features like a shell, muscular foot, and mantle are hints that there may be common descent rather than a means for classification by themselves in modern taxonomy.

cephalopods are inferred to share a common ancestor with mollusks due to evidence like homologies, or as you say, hints. i'm asking for the basis of that classification, who placed cephalopoda within mollusca, and when

@imrobert If you literally mean who, Cuvier: https://hsm.stackexchange.com/q/13664/13861 that question has already been asked and answered on the history of science site.


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What is a fungus formally?
Fungi are immotile eukaryotes that do not have chloroplasts or perform photosynthesis. Yet there are other organisms that fit this definition that are not fungi, for example slime molds. What is the formal definition of a fungus? Wiktionary, Wikipedia, and other dictionaries provide informal definitions.

Some fungi produce zoospores, which are motile.

A fungus is formally a fungus, a base divergence of Eukaryote, a plant is a plant. An animal is an animal.

Formal definitions aren't really a thing in Biology or anywhere outside of mathematics.
For cladistics, the closest you will get is that species are arranged based on common ancestry. Fungi are a group of organisms sharing a common ancestor. This is present, not absent, in the definition on Wikipedia:

These and other differences place fungi in a single group of related organisms, named the Eumycota (true fungi or Eumycetes), that share a common ancestor (i.e. they form a monophyletic group), an interpretation that is also strongly supported by molecular phylogenetics.

If you have some organism and you want to convince other biologists that it should or should not be classified as a fungus, you would want to make arguments about its ancestry.
Before modern molecular biology techniques, these groupings were entirely based on phenotype. Linnaeus is the individual most recognized for classifying organisms this way and many of his conventions and groupings are still used today (though many others have changed, as well). Darwin's contribution to biology was recognizing that the groupings based on phenotypic similarity originate from common descent (that is, shared ancestry). But, even with that knowledge, it's possible to make mistakes in classification based on phenotype alone. When you hear about some organism previously classified one way whose classification has changed, it's likely that the previous classification was based on assumed relationship based on phenotype, but molecular phylogenetic methods have since suggested a different ancestry and therefore a different classification is more appropriate. Because we do not have all the ancestors (or, really, any of them) to examine, these relationships have to be inferred.

So if I find a new mold, how am I supposed to know if it's a fungus or something else?

@imrobert New to you, or new to science? How do you know it's a mold? If you're sure it's a mold, for whatever reason, then congratulations, you have a fungus! If it's a slime mold, well, that isn't a mold at all, any more than a bat is a bird.

If I find an organism of any kind that I suspect to be a fungus, how am I supposed to determine whether it is or not...

@imrobert You can probably assume it's a fungus if it shares the phenotypic characteristics of other fungi. It's helpful to know about other types of organisms that you might possibly confuse with a fungus so you can consider or dismiss those alternatives. If you have a key for identifying species, and you can use it to classify what you've observed, you'll have a better answer. If a definitive answer is critical you could sequence the genome and use that to either identify the species or find which known species it is most closely related to.

@imrobert: It might be worth asking a followup question, something like “What phenotypic characteristics distinguish fungi from other similar organisms?”  This answer gives the correct theoretical answer to your original question as written — that the formal definition of fungi is cladistic, not phenotypic.  But asking about distinguishing characteristics is also a valid and important question, and it sounds like that’s more the question you care about and maybe meant to originally ask, you just didn’t quite hit a technically correct phrasing of it.

@PLL I'd like to leave my question open to a cladistic definition but "The monophyletic group where true fungi go" is obviously not a definition

@imrobert "Fungi" is the name for that monophyletic group; that's the definition.

@BryanKrause What defines that monophyletic group?

@imrobert Phylogenetics: common descent. They share an ancestor. That's what "monophyletic" means.

Not liking an answer doesn't make it wrong... Life evolves from previous life. We can organize all life into a "tree" of related organisms. It's useful to name parts of that tree to refer to groups of organisms together. Fungi are one of those groups. There are no features that make something a fungus or not besides being in that related part of the tree. If you find something that seems to share every characteristic you can think of, but then find out it's not actually related, then it's not in that group.

Similarly, if you find a member of that "family tree" of organisms within that group that has some feature that you didn't think any fungus has, you wouldn't declare it "not a fungus", instead you would say "aha, this particular fungus has a new feature we didn't think any fungi had". There is no definition, besides membership in that clade, that describes it and would not change with new discovery.

If you want a definition, here is a not very formal cladistic one: If you found an organism and determine that the most recent common ancestor of that organism and a mushroom is neither your ancestor nor the ancestor of a potato, that organism is a fungus (probably the potato part of the definition can be discarded as redundant).

Thanks guys, I understand the concept of a monophyletic group. My question is, how can I determine if an organism is inside the group Eumycota? If you don't know it's okay

It's hard to be sure.  You need to reconstruct a tree using the available features of that organism and other members of the taxon (and also other non-member), and that features can be of all kinds, although nowadays genetic ones are the most useful when available. From here: https://evolution.berkeley.edu/phylogenetic-systematics/reconstructing-trees-cladistics/reconstructing-trees-parsimony/

Of course, if the organism you found is of a known species or at related to know taxa, it becomes a lot easier. For example, if you found a mushroom with all the parts mushrooms usually have, you can be sure that it's a fungus.

@imrobert You can see my comment above about using phenotype to get a pretty good idea but if a definitive answer is needed you'll need to look at the genome. As far as which phenotypic characteristics, the Wikipedia page you previously rejected is a good place to start (for example the "characteristics" section). Fungi are a huge group with a lot of variety, so it's not as if you'll be able to just check one or two boxes to decide. Like Pere suggests it might make more sense to start more focused e.g. to ask "is this a mushroom?" - if yes, it's a fungus, too.

@BryanKrause "how am I supposed to determine whether it is (a fungus) or not"?  Didn't there used to be books where they asked questions about what you saw, and it sent you to a different page?  Eventually, after X number of questions, you got your answer.  I remember doing this once in high school at an insectarium: catch a bug, and then identify it using a huge book.

@RonJohn Sounds like a "dichotomous key". It's a lot like following a phylogenetic tree: each time the tree branches, there is some characteristic that is different in one branch from the other, though as a practical tool they don't necessarily need to follow phylogeny at all, just go through enough characteristics within a limited group (usually limited by geography as well as overall "type" of organism, a literal tree perhaps). The thing is, fungi are a huge group many many steps removed from the common ancestor, so they don't necessarily look very much like that ancestor.

@RonJohn at the end of the day, the ancestry-based definition means that kind of thing only works as an approximation. If it walks like a duck, talks like a duck, but (e.g.) its DNA tells us its ancestry branched off earlier, when then, its not a duck.

@mbrig in practice, how far does DNA move creatures?  For example, moving the Giant Panda from Ursidae to Ailuridae then back again seems reasonable, but "We thought this was a really weird bat, but DNA says it's really a bird" seems a bit extreme.

@RonJohn I think that's partly a question of how "bad" the initial identification is and partly how close convergent evolution comes. You could imagine that somebody guessing that some Multituberculata is part of Rodentia, but obviously people try not to make that kind of mistake (and its harder when the thing is extinct and you have less evidence to go off of). Maybe more realisticly, I could definitely see some kind of bacteria getting reassigned to Archaea based on DNA, and that's a whole nother domain!

@RonJohn Adding to what mbrig wrote, some initial classifications were extremely wrong (eg: archaea used to be classified as bacteria), and have been revised substantially as various new information is available, and there are still open debates about fairly substantial parts of the overall tree, especially around microorganisms. But, mostly what keeps things consistent are the closer relatives; every time you discover a new bat, you can see how it relates to other bats and that immediately tells you roughly where it falls, you don't have to start from scratch.

does anyone know the genetic data required to classify something as a fungus, or where i can find out?

@imrobert: As per my first comment, I really suggest asking that as a new followup question.  I appreciate your disappointment with this answer — it’s technically absolutely correct, but it’s also kind of a gotcha, saying “you phrased your question technically wrong” and explaining how, but never answering the actual question you wanted an answer to.  But you’re much more likely to get a useful answer by asking a new question, now you know a technically more correct wording for it, rather than going on in comments here.

thanks @PLL i'm going to ask a new question. do you have a suggestion on specific wording to include to make sure i get what i'm looking for in the answers


text:
Can Sleeping With Reptiles Reduce Excess Body Heat from Your Partner?
I'm an engineer and biology is my weakest point, so please forgive if this question is dumb.
My wife always complains that I set the air temperature too cold at night. She's exothermic in a number of good ways, but she also radiates too many literal Watts. It's like sleeping with a space heater. She wants to get a pet and has been asking me what kind of dog I want, and that got me thinking...
What if a pet could solve our sleep problems?
Sure, they might strangle you in your sleep and then eat you, so this probably isn't the most practical solution. But snakes and other reptiles might make the perfect heat absorbent bedding!
All kidding aside, I'm truly curious. My incredibly shallow bio class gave me the idea that warm blooded animals are exothermic and cold blooded animals are endothermic. But is that right? And if so, does it follow that sleeping with reptiles would cool your bed down to some temperature more hospitable than Mordor?

Reptiles are generally ectothermic or "cold-blooded", not to be confused with exothermic. This means they largely use environmental heat sources to get their heat, rather than generating it themselves
The same limits apply here as you might find in any other system - once they reach your body heat, they won't get any warmer and will not appreciably draw any additional heat. They will likely also get more active with the additional heat, which I suspect is not exactly what you want in the middle of the night. This might depend on whether you have a nocturnal species or not.
you'd also need to consider the mass of reptile you might need in the bed to provide any substantial cooling - a wee gecko ain't gonna to do much, but you also probably don't want a Komodo dragon hogging the bed covers for a variety of reasons.
I'd suggest you get one of those bed-covers (duvet/comforter/quilt/doona) that is capable of holding two different insulating thicknesses, or simply have a lighter cover for both with an additional blanket for your wife. You can also put a standard two-person insulating duvet and a single inside the one cover.
On second-thoughts, perhaps you are on to something here. Get the all new RepiCoolTM It's 100 finest quality Tokay geckos in one easy to use system of convenient mesh pockets. Too Hot??? simply add an extra gecko or two for that great cooling effect; too cold? simply take geckos out as you need and allow the fantastic warming effect of the bags to keep you "just right" all night long!!! But that's not all!! Also included at no extra charge; fall asleep to the soothing sounds of the gecko and you'll never have problems sleeping again! geckos not included, get geckos for a one-off additional payment of only $99.99, each sold separately

100 geckos making that sound at night (lol) would also affect (soothe?) the sleep of the neighbors. I am always curious why people don't use the blankets with different levels of warmth on either side, or just use an extra blanket on one side.

@anongoodnurse Deliberately chose that species for that feature; most aren't quite as noisy, but plenty do make similar noises and are nocturnal. I'm glad it amused someone.

It sure amused me! I'm certain it has amused/will amuse others who haven't/won't post a comment. I'm a bit chatty. :)


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what chaetoceros species can this be?

the object on the picture (which isn't mine) was found at upper newport bay, orange county, california. it looks a lot like what I saw at the white sea, which is what I wish to identify