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Why does tetracycline have such a broad spectrum of activity?
What are the structural and chemical characteristics that make tetracycline uniquely broad spectrum? I understand it acts on the A-site of the prokaryotic ribosome, but there exist many ribosome-targeted drugs that are relatively narrow spectrum. I assume it has something to do with its permeability in several different classes of bacterial cell walls and/or membranes - but I can't find any literature that links some characteristic part of its structure to this permeability.

This is a tricky question. First of all, I wouldn't call tetracyclines "uniquely" broad spectrum. They are broad spectrum, but there are other drugs with equally broad coverage absent acquired resistance (e.g., imipenem and chloramphenicol), and current clinical use of tetracyclines is limited somewhat by the spread of resistance.  They don't have any major class limitations, though. Again, absent acquired resistance, tetracyclines are effective against gram positive aerobes and anaerobes, and gram negative organisms, as you seem to be aware.
Tetracylines access their target on the 30S subunit of the bacterial ribosome (blocking the A site, as you said) by passive diffusion through porins of the outer membrane of gram negative bacteria, and active transport across the cytoplasmic membrane of gram negative and gram positive bacteria, but the mechanism for that active transport is still unknown. This is quite a good review despite being quite old. Now, some 30 years later, we have still not identified the exact mechanism, as you can read in Goodman & Gillman's most recent edition (13th), Ch. 59, crossing the cytoplasmic membrane requires metabolic energy, but the process is not well understood. Because of this, we can't point to a specific structural or chemical characteristic. For chloramphenicol, it would be the ability to diffuse across the cytoplasmic membrane; for tetracycline, we don't know. I suspect part of the reason for this is that people are now more interested in pumps removing tetracyclines from the cell than those that accumulate it, so it's more of a question about research priorities than some transport mechanism that is particularly difficult to detect.


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Are cryovials really better than regular tubes for cryopreservation?
What is the rationale for using cryovials instead of regular, sterile centrifuge tubes for the storage of mammalian cells?
With a good aseptic technique and without touching the cap directly, there should not be a significant risk of contamination in regular microcentrifuge tubes. Is the plastic quality fundamentally different (in terms of leaching chemicals etc)? Both kinds of tubes are usually made of polypropylene so it's not obvious how they would otherwise differ.
There may be a difference when storing things in direct contact with liquid nitrogen (as regular tubes may leak), but many cells can be stored for years in a -80°C freezer, a temperature at which most molecular biology tubes are perfectly stable.

I feel like the best answer here is application-specific ease of use, but I could be wrong!

I do not have data to back this up, but can say that from experience, cryo vials are a much better solution for storing your valuable cells. First, their plastic is thicker, meaning they’re more sturdy and can handle a deep freeze much better. The killer feature is the screw caps, which means that they will never pop open accidentally due to mishandling or temperature changes (which has happened me with samples in microcentrifuge tubes). These screw caps also allow much more efficient storage in expensive cold conditions (liquid nitrogen will be best for cells long term) and easier retrieval from boxes that are freezing cold.
Microcentrifuge tunes may suffice but cryo vials exist for a reason.

Although, thicker plastic is disadvantageous for flash freezing.

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Why do humpback whales sing songs?
Scientists have documented that it seems to only be male humpback whales who sing structured songs, but do we know what purpose their songs play?

The only way to know in great detail is to translate what they say. Though if they speak in monogrammar, that is only possible if you know a monogrammar language.

There are four hypotheses with varying levels of supporting evidence for why humpback whales sing.
Yes, only males have been shown to sing. It used to be thought that the songs only occurred on breeding grounds and therefore served a reproductive purpose. However, songs have since been recorded on migration routes and feeding grounds, though not as prolifically.
The hypotheses are:

"Mate Attraction" whereby males sing and females approach them to mate. No evidence has ever shown a female humpback whale approach a singing male. Rather, a group of males will swim after a female, vying for position, until she is receptive to mating. Then the closest whale (the primary escort) will be best poised for success. In my opinion, this is the least plausible hypothesis.
"Lekking" whereby a group of males sing to stimulate the females to begin estrus and advertise their body size and health for female mate choice. https://en.wikipedia.org/wiki/Lek_mating This may allow for female selection of choosing a mate later while being pursued as part of competitive group. I am unaware of which articles support this hypothesis and provide evidence. Birds and land mammals are much easier to observe in a lekking behavior than any underwater animal is.
"Territory establishment" whereby males sing to mark their territorial bubble of water. If a male has a larger territory, then it is more likely a female will pass through that larger territory so that the male can respond by pursing her. This could be supported by proving that male humpback whales respect each other's territories and space themselves consistently across their watery world. Refer to http://dx.doi.org/10.1121/1.4962217
"Orientation by echolocation" has recently been put forward by Edward Mercado that song reflects on a broad scale around the whale's environment to provide feedback for navigating the general area. Many researchers argue the plausibility of such low frequencies echoing effectively.

New studies into cultural transmission of parts of songs across ocean basins may suggest the song is not just for reproduction but to fulfill wider communication needs or generate a form of social creativity. See work by Ellen Garland.

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Are there any organisms, extant or extinct, that have only one neuron?
Nervous systems are useful in one way because they allow for integration of complex information. They are also useful because they transmit information very rapidly, over a large distance.
However, that last function can be done without an actual nervous system; presumably, all you need is one cell. Some individual sensory neurons can transmit an impulse at 120 m/s, which in and of itself would be useful in many circumstances.
So, are there any species that have only one neuron? There may have been many one-neuron creatures in the early days of animal evolution, but it's also possible that nerve nets appeared together, as a unit. I also suppose there are some small multicellular organisms that have a single excitable cell, but it's up for debate whether we should call those "neurons" or not.

In evolution things don't just pop into existence. So, it's unlikely that a single neuron originated by itself. The question is, what would that neuron do? It would communicate to at least one other cell, right? Otherwise the transmitted signal would be lost and useless. And where is the signal coming from? Neurons generate signals either by receiving signals from other neurons or, for specialized sensory receptors, through some changes in the environment. The receiving cell could be a muscle cell, so your minimal network would consist of a sensory neuron and a muscle cell. Upon a detected change in the environment, the neuron would signal the muscle to contract.
In evolutionary basic organisms we can find action potential like excitability and synapse-like cell-cell contacts in non-neuronal cell types. This hints towards a step-wise development of these functions before actual neurons arose (wiki, paper). Even one-cell-organisms have neuron-like features (sensory input dependent polarization, intracellular signal propagation, coordinated movement). If cell-cell communication or excitability are not limited to neurons, what makes a neuron a neuron? This is also a matter of definition, as discussed in the paper mentioned above.
What makes neurons unique is their property to propagate signals in a network. That's why the neuronal nets of jellyfish are usually seen as the first appearance of neurons in the evolutionary tree. While organisms without a nervous system are able to respond to their environment by signal transmission between non-neuronal cells, I am not aware of any organism that possess only a single cell which we would now call a neuron. At the stage where neurons arose, animals were already a more complex arrangement of specialized cells for different functions. You would therefore assume, that also the neuronal predecessors were a group of cells within the organism.

Expanding on @Frieke's answer, evolution often adapts old functions for new processes. So, just as how membrane polarization is useful in unicellular organisms (Irazoqui and Lew, 2004) but can be exploited for neuronal depolarization, vesicular release also has unicellular prototypes (Oliveira et al., 2010) that preface eukaryotic neurotransmitter release. And, as (Bucher and Anderson, 2015) in Frieke's answer states, this vesicular release largely uses the same proteins and machinery in prokaryotes and neurons.
Another way that single celled organisms can be thought of like neurons is that, just as how a brain is formed of a network of neurons releasing neurotransmitters onto each other, prokaryotes too can ostensibly form neural networks with individual cells communicating with one another Wiki; (Cohen et al., 1999). Think of a soup of bacteria that receives and integrates information en masse.
But no, I think it would be misguided to say that a single celled organism could be called a neuron but that's not to say it can't have homologous functions and roles.


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Join a linear plasmid just using a primer (without ligase enzyme)
Can I use just a primer and PCR to join the cutted plasmid like this ? without using any further enzyme like ligase.

After the linear dsDNA plasmid annealed into 2 ssDNA, primer will bind to middle. And Taq Polymerase will bind to the 3' and start extend the DNA to join the plasmid. So I don't need a ligase enzyme, is that possible?
Edit: I think the plasmid will be nicked at 2 position with this method but will this plasmid still work in e.coli cell?

Your diagram shows two single-stranded pieces of DNA that are annealed together to form two short regions of dsDNA, but in your description you mention linear dsDNA (which is not shown here).  Assuming that you intend to denature the linear dsDNA, and then add the shorter primer, then yes, adding a suitable DNA polymerase enzyme, proper buffer and reaction conditions, and dNTP substrates, will yield some relaxed (nicked) circular DNA molecules.  If there is a selectable marker on the plasmid then you should be able to transform competent E. coli cells.  NOTE: There is no PCR involved.

@mdperry In all protocol I found. They usually use some extra enzyme. For example Ligase, or exonuclease (Gibsom Assembly), or T4 polymerase. Is there anyway I can use only Taq Polymerase?

It is not clear to me which protocols you are referring to. T4 DNA ligase, Exonuclease (type unspecified), and T4 DNA polymerase are three distinctly different enzymes (and could not be substituted for each other).  The main difference between Taq polymerase and T4 polymerase is the temperature of the reaction.  So I think they can easily be substituted if you change the reaction temperature.  It is quite clear that a dsDNA plasmid does not need to be covalently closed in order to transform E. coli. The cells will repair the nicks after they take up the DNA.

@mdperry "The exonuclease activity of T4 phage DNA polymerase will create overhangs at the ends of your PCR product and within the homologous site of your destination vector, thus allowing your PCR product and vectors to anneal to create a final cloned piece of DNA" - I found it on "Method : Sequence and Ligase Independent Cloning (SLIC)".  I may though like you too but I can't find any evidence on the internet, so it still uncertainty to me.

Okay, yes, that is true, IF: you add T4 DNA polymerase IN THE ABSENCE OF dNTPs then there is a 3’ -> 5’ exonuclease activity that we used to use to turn a 3’-overhang into a blunt end.  As I recall, this is not a very processive activity, and difficult to control, but maybe there are newer applications I a, not aware of.  Anyway, you don’t need it for the picture you drew above.  What you described is if you have the same short sequence on both ends of the two blunt fragments (based on the quotation).

Anyway, bottom line: what are you afraid of? Just try it (denature, anneal, extend, transform).  You could even compare +/- ligase to see for yourself if it makes a difference.  What’s the big deal? Don’t you have somebody local to bounce your ideas off of?

@mdperry Thank you very much, May be I will try. I just want to know if someone tried it before so we can save time and cost for doing other things.


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Can multiple cetacean species communicate?
It seems that individuals within the same species have their own communication, but is there evidence to suggest that individuals from different species are able to communicate?

We are starting a Bioacoustics Stack Exchange for people interested in the studies of non-human animal sounds and the impacts of sounds on animals. Please join us! https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680

Do dogs and humans communicate? What about cats and dogs? I think defining "communicate" is the real question here.
This 2012 study claims to show "the first experimental evidence that the interception of heterospecific vocalizations can mediate interactions between different cetacean species in previously unrecognized ways". In other word, one species is recognizing and responding to the vocalizations of another.
This article points out that "...false killer whales and bottlenose dolphins choose to spend time with specific members of the other species rather than randomly mixing or engaging in brief opportunistic encounters" How could this occur without some form of "communication"? I'd argue it couldn't,

to be fair the second one does not require communication just the ability to recognize individuals in the other species.

It's a reciprocal relationship that involves interpreting signs and signals from the other. What is the threshold at which "recognition" becomes "communication"?

I can avoid riding ornery horses a second time that does not mean I was communicating with the horse, I can prefer my cat to my neighbors cat that pisses on my car, but again it does not mean I am communicating with it.  Favoritism is not necessarily communication.

"I can avoid riding ornery horses a second time that does not mean I was communicating with the horse" Is not the horse's "orneriness" a non-verbal form of communication that it does not want to be ridden? It's not Shakespeare but the threshold in biology for "communication" is quite basic--if a cell emits a signaling molecule and another cell receives it, we call that communication even thought it's nothing more than "recognition".

If you define communication that broadly then the question more or less breaks down, any behavior that impacts another organisms can be communication. Communication does not have only a single biological definition.

And if you proscribe communication so broadly then the question likewise breaks down.FWIW, saying that interspecific congregation behaviors mediated through vocal cues is definitively NOT a form of communication is refuted by the opening sentence from Wikipedia's definition of Animal communication.

making a big leap from what I said to that, interspecific congregation behaviors mediated through vocal cues is definitively not what I was referring to, it is neither of my examples. Also wikipedia is not a scientific source.

I have been trying to have a discussion here but you appear refractory to much beyond defending your ego. I cited WIkipedia because the claim you are making is so fundamentally wrong that I thought a more general source might help you. Guess not. Okay, here's a recent peer reviewed paper discussing a terrestrial analog to the whale example that you took issue with. Unsurprisingly, they consider this to be a form of "communication" as well.


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Are STOP codons impacted by base insertion or deletion mutation?
I am learning about base insertion and deletion mutations. An example in my textbook is given below.
GUU CCA CAU AUC.
So if there is an insertion (of guanine):
GUU GCC ACA UAU C_ _ (there will be a detrimental effect on the protein created).
I'm a bit confused about how the stop codon will be read. If we have a new example with a stop codon:
GUU CCA CAU AUC UAG
When the mutation occurs (insertion of guanine) will it become:
1) GUU GCC ACA UAU CUA G
OR
2) GUU GCC ACA UAU C_ _ UAG
If mutation 1) occurs, there would be no stop codon, but mutation 2) looks strange to me. So which is the right one?
Thanks

Yes. Mutations can affect STOP codons and they do relatively commonly. These are important because they can lead to significant changes in the resulting peptide and are likely to affect protein functions or phenotype.
For a point mutation (a single base substitution), there are several possible effects:

silent mutation is a synonymous base substitution which does not change the encoded amino acids (this is neutral variation).
missense mutation is a non-synonymous bass substitution which changes only one amino acid in the protein (these can affect protein functions but do not always).
nonsense mutation is a change in a coding codon to a STOP codon (this truncates the encoded amino acid sequence prematurely resulting in a shorter peptide).
nonstop mutation is a change from a STOP codon to a coding codon (this means the amino acid sequence will continue to the next STOP codon resulting in a longer peptide).

Insertions and Deletions in DNA sequence (InDels) are important because they change all codons that follow it (not just the base substituted):

frameshift mutation adds or removes a base which resulting in a change in the reading frame: all bases following will result in new codons, including STOP codons (this commonly results in entirely new protein domains and proteins of different lengths as STOP codons will also be changed. They are encoded in the reading frame like all other codons.

As you can see, mutations which affect STOP codons are very important as they drastically change the protein sequence. This usually disrupts the protein function and causes diseases or inviable embryos. Most of these are removed from populations long-term by natural selection. However, it can rarely lead to entirely new proteins beneficial to the organism and evolutionary changes. This is more likely with duplicated genes where one can change while the other retains the original function.
As such, mutations involving STOP codons are among the most biologically important.  Another important case is splice functions. Point mutations and frameshifts can also affect intron-exon boundaries, resulting in new splice variants, skipped exons, and reading further into introns (which may contain splice junctions or STOP codons).

Let's start with your example:
Wild-type gene looks like:

GUU CCA CAU AUC UAG*

After G insertion, you end up with

GUU GCC ACA UAU CUA G

There are 3 stop codons: UAG*, UAA*, UGA*
You don't see those in your mutated gene, because you truncated sequence. Let's imagine that gene actually goes like this:

WT: GUU CCA CAU AUC UAG* GCG UCU AAA ACG CUA
Mut: GUU GCC ACA UAU CUA GGC GUC UAA* AAC GCU A...

In mutant you got now new stop codon created
Gene, transcribed into mRNA doesn't stop at stop codon, there is whole bunch of sequence after it too (3'-UTR and poly-A tail for Eukaryotas)


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(secondary) human/primate advantages over other animals?
I am trying to understand the advantages that humans have over other species, besides what you could call 'sentience-critical'.
What I mean by this is, the first set of answers you'll get is "more capable brains (in general), opposable thumbs, tools, comunication". But all that is core to sentience and civilization, not primates. I am more interested in the second set of answers, such as 'better temperature management'.
I suppose the question is, what advantages do primates have over other animals? Or, what traits are likely to be missing, compared to humans, from a hypothetical non-primate sentient creature?

Primates in general, or humans in particular?  I think the temperature management (which isn't necessarily better, just different to allow extended exercise in hot climates) is unique to humans among primates.  Otherwise the only things I can think of are trichromatic vision, and a forelimb structure that allows throwing.

Both work, and I'm actually interested in humand in particular, but since the line between what we can do as species and as sentiences is not too clear, I figured comparing our cultureless relatives to other animals could help. But those two examples are wonderful!

Pure speculation on my part but walking upright seems important as it frees up our hands for not only using tools or carry things, but it helps us stay clean because we can reach more of our body to remove unwanted pests.

@Cell that is interesting! I guess walking upright IS a primate trait! By my criteria, it'd be a trait I shouldn't demand from a civilised species... Well, that's surprising!


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What anatomical structures do baleen whales use to vocalize?
What anatomical structures do baleen whales use to vocalize? How does this differ between species?

Look at there they don't give a definitive answer but it's already something https://en.wikipedia.org/wiki/Whale_vocalization (Baleen whales are called Mysticete whales)

They use larynx and folds in the larynx for underwater vocalizations. Source and details: https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/baleen-whale

Discovery of Sound in the Sea (dosits.org) provides good general information on these topics.
According to DOSITs,
Marine mammals produce vocalizations using mechanisms similar those of land mammals. Pinnipeds (seals and sea lions) have a larynx similar to that of humans. Baleen whales also use a larynx to produce sounds. Toothed whales can produce sounds using their larynx as well as specialized air sacs near their blowhole. The larynx is used to produce whistles, while the air sacs are used to produce high frequency echolocation signals.
See https://dosits.org/animals/sound-production/how-do-marine-mammals-produce-sounds/ for more information and additional citations

The DOSITs website is a great resource with many links to scientific studies, but I believe they made an error in their description of toothed whale sound production. Toothed whales produce both echolocation clicks and communication whistles using the phonic lips in their nasal passages.

Not much is known about the exact method of sound production in baleen whales and current knowledge is mostly based on dissections of dead animals.
Reidenberg and Laitman (2007) examined 6 baleen whale species (37 animals in total) and they identified a structure in the larynx, which they called the "U-fold"1. This U-fold is supported by cartilages and the shape and tension seem to be controlled by skeletal muscles, which might then control the sounds produced. Based on various features, Reidenberg and Laitman suggest that the U-fold is homolog to the laryngeal folds in other mammals. A key difference between the U-fold of baleen whales and the vocal folds of terrestrial mammals is that air flows in parallel with the U-fold, whereas airflow across the vocal folds is perpendicular in terrestrial mammals. Baleen whales also have a laryngeal air sac, which is homolog to the laryngeal ventricles of terrestrial mammals, which captures air as it is used during vocalisations, and allow air to be recycled back to the lungs in-between vocalisations1,2.
To my knowledge, there is no evidence that toothed whales produce any sound in the larynx. Toothed whales produce both echolocation clicks and so-called “whistles” by creating an airflow across phonic lips in their nasal passages, and the resulting tissue vibrations produce the sound, which is then guided into the water via a fatty organ called the melon3. Toothed whales have a pair of phonic lips in each nasal passage, and it seems that echolocation clicks are produced using the phonic lips in the right nasal passage and communication whistles are produced with the phonic lips in the left nasal passage4,5.
References:

Reidenberg, J. S., & Laitman, J. T. (2007). Discovery of a low frequency sound source in Mysticeti (baleen whales): anatomical establishment of a vocal fold homolog. The Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology: Advances in Integrative Anatomy and Evolutionary Biology, 290(6), 745-759. DOI: 10.1002/ar.20544.
Reidenberg, J. S., & Laitman, J. T. (2018). Anatomy of underwater sound production with a focus on ultrasonic vocalization in toothed whales including dolphins and porpoises. In Handbook of behavioral neuroscience (Vol. 25, pp. 509-519). Elsevier. DOI: 10.1016/B978-0-12-809600-0.00047-0.
Madsen, P. T., Jensen, F. H., Carder, D., & Ridgway, S. (2012). Dolphin whistles: a functional misnomer revealed by heliox breathing. Biology letters, 8(2), 211-213. DOI: 10.1098/rsbl.2011.0701.
Madsen, P. T., Wisniewska, D., & Beedholm, K. (2010). Single source sound production and dynamic beam formation in echolocating harbour porpoises (Phocoena phocoena). Journal of Experimental Biology, 213(18), 3105-3110. DOI: 10.1242/jeb.044420.
Madsen, P. T., Lammers, M., Wisniewska, D., & Beedholm, K. (2013). Nasal sound production in echolocating delphinids (Tursiops truncatus and Pseudorca crassidens) is dynamic, but unilateral: clicking on the right side and whistling on the left side. Journal of experimental biology, 216(21), 4091-4102. DOI: 10.1242/jeb.091306.


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What is the thickness of the biosphere?
In other words, what is the vertical distance between the deepest and highest point on Earth where life is found?
Life has been discovered at the bottom of the Mariana Trench, 13 km below sea level. It's hard to get deeper than this, but I'm not sure if this really represents the bottom of the biosphere. Elsewhere at sea, microbes can be found many kilometers below the sea floor -- would we expect to find life far below the Mariana Trench?
In the other direction, the biosphere arguably reaches as high as 435 km, the maximum altitude of the International Space Station. If the ISS is disqualified, then that number would be much lower, but again I'm not sure exactly what it would be. The highest recorded bird flight clocks in at 11 km, though it's possible that microbes regularly get dragged up higher than this by wind.

Nice question, welcome!

You might also note that life is found in rocks several miles/km below the surface: http://www.bbc.com/earth/story/20151124-meet-the-strange-creatures-that-live-in-solid-rock-deep-underground

Relevant paper, referring to the 8-15 km range in the atmosphere: Microbiome of the upper troposphere: Species composition and prevalence, effects of tropical storms, and atmospheric implications.


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What is meant with “the chest wall and lungs are coupled together”?

Since the lung and chest are elastic, we can represent them with springs. Under normal conditions, they are coupled together: the “lung” springs are stretched and the “chest” springs are compressed. During a pneumothorax, the lungs and chest are independent and the springs representing them go to their relaxed positions, causing the lung to collapse and the chest wall to enlarge.

This analogy is honestly completely flying over my head. How are the lung and chest wall “coupled”? Heck, earlier in this book it’s mentioned that one of the two forces keeping the lungs from collapsing is “the surface tension between the lungs and the chest wall” (the other being the intrapulmonary pressure).
This and the said analogy make it sound like there is a physical-contact adhesion force between the lungs and the chest wall, which, from what I’ve looked into (and several other analogical figures the book has provided), seems to not be the case.
I believe this analogy of “coupling” is probably related to pressure relations, but I don’t understand how those are exactly set up either, and why during a pneumothorax they just cease as the two become “uncoupled”.
For those interested, the book is Medical Physics by John R. Cameron.

Then add how the diaphragm functions : the chest (ribs etc) can stay stationary and xou can breathe via the diaphragm...

@SolarMike this question isn't really about that (the dynamics of breathing). It's about the coupling of the chest wall and lungs. Of note: if the chest wall and lungs are decoupled (as in a pneumothorax or hemothorax, breathing via the diaphragm isn't effective.

How are the lung and chest wall coupled?

You have your answer in the text:

the surface tension between the lungs and the chest wall

And as you say, it is very much

like there is a physical-contact adhesion force between the lungs and the chest wall

A good, medical school level anatomy textbook will walk you through this. Moore's Clinically Oriented Anatomy gives the appropriate level of detail. Lets refer to Fig 1.30 (pg 107 of the 6th edition):
Below, you can see that there is a bag of fluid (the pleura) around the lung itself, like an under inflated balloon wrapped around the lung (see the picture of the fist, representing the lung, wrapped in a balloon, representing the pleural sac). The space inside the bag of fluid is very small, very thin, in a normal lung. The size of that space is exaggerated in the figure below in order to show the layers more clearly. In fact, in medical images of a healthy chest, it doesn't even appear as a space. The thin layer of fluid provides surface tension, keeping the two pleural walls close together. Since the chest and lungs are physically attached to the pleural walls on either side, that surface tension pulls the elastic lung outward (expanding it), and the chest wall inward (collapsing it, slightly). If the pleura is punctured, blood or air can enter, surface tension can no longer keep the two pleural walls next to each other, the chest wall returns to its preferred state (slightly more expanded than it would otherwise be), and the lung returns to its preferred state (substantially more collapsed than it would otherwise be).


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Pre-linnaean names, where can I ask about current IDs?
I run a large website with lots of historical herb books. For the older ones, finding out current botanical names is very difficult.
Can I ask here? If not, does anybody know where I could ask what any given plant is, with or without images, usually with descriptions and pre-Linnaean names?

Where are you located geographically? Your best bet might be to get in touch with local botanists who are likely familiar with the local flora mentioned in the herb books. If you’re in the US, an organization like the Smithsonian Transcription Centre might be able to help you out: https://en.wikipedia.org/wiki/Smithsonian_Transcription_Center

I'm in Northern Europe. The old books are from Europe or the US, variously. I'll try the Smithsonian, thanks!

Ooo, nice! There’s a ton of biodiversity resources in Europe. I’m not sure who’d be best to approach first here (and I hope someone who does posts an answer to your question!), but this might be a good place to start: https://www.kew.org/blogs/kew-science/celebrating-50-years-of-library-collaboration

Kew isn't interested in pre-Linnaean, I've asked them. Or at least, I asked their "current botanical name database" people.

The Smithsonian botany set is complete, looks to be mostly herbarium specimens, with current botanical names. I don't think they do pre-Linnaean. (I do have Linné's works, of course, which helps a little.)

In case you're not aware, a late 19th century edition of Culpeper's complete herbal gives binomial names for many of the entries, and is freely available at archive.org

Culpeper is easy: http://medherb.com/culpeper_names.html
Salmon's Botanologia 1710 is difficult, here, for instance:
"Of Water Agrimony the Male Kind"
In Latin, Eupatorium aquaticum mas, Eupatorium Cannabinum mas, Agrimonia aquatica mas
It is ... the Genus to three other Kinds:

Our English Male Water Agrimony.
The New-England, or Hemp-like Agrimony.
The Virginian Kind.

I think #1 is Eupatorium cannabinum, #2 Eupatorium maculatum, and #3 could be Acnida cannabina or Amaranthus cannabinus.
Alas, Salmon has hundreds of such entries. Other old herbals can be as cryptic.


text:
Does applying a sedative via hypodermic needle anywhere in the body really work?
Bad Guy is fighting the Good Guy. Good guy miraculously produces a syringe and rams it into the Bad Guy's neck.
Cut,
  From my middle school biology I aware that capillaries are present throughout the body but I severely doubt that sedatives work by using them anywhere and everywhere. If so we're the case then why would doctors need to find my vein to give me a shot for flu?

 Yes, I'm not fun to watch movies with.

At least in my experience, having recieved a number of vaccinations over my life, they're almost always given intramuscularly, rather than intravenously.  You may be confusing vaccinations with the drawing a blood sample from a vein, where you want to draw out a relatively large quantity of blood.

On further thought, the fact that sedatives will work (almost) anywhere is demonstrated by the wide use of tranquilizer guns in wildlife management: https://en.wikipedia.org/wiki/Tranquillizer_gun

There are three basic types of injections:

intravenous (IV): An injection straight into the blood stream. Fast, but as you pointed out, one needs to find the vein first. If you are hospitalized, you will likely have a catheter in your vein already, so that you can be given drugs rapidly if needed.
intramuscular (IM): This is your second best option for fast effect. There is plenty of capilary vessels in your muscles because they need a good circulation to function (get oxygen in & carbondioxide out). This helps your body also to take up drug injected in your muscle and there is little delay until they enter the blood stream.
subcutan: this is used when you are aiming for slow uptake.

Assuming that you envision some sort of combat situation where good guy cannot just start looking for a vein on bad guy's arm, IM seems to be a reasonable choice. If they are in a fight, Bad guy will have a high pulse, so the drugs should get into the blood stream fairly quickly.
See further: https://en.wikipedia.org/wiki/Injection_(medicine)


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Can diet, supplementation and/or drugs affect sexual dimorphism?
After puberty, can certain diets, exercise, and/or possible drugs affect masculine/feminine dimorphism in adults? We know dimorphism and/or morphology is a product of genes, but to what extent can this be altered through environment? Like, can chewing more give a more masculine jaw shape/angle? Can talking a certain way make a more deep, manlier voice? Can squinting give hunter eyes?
For women, can eating soy-based products increase hip-to-waist ratio? Estradiol?  Feminization of the face, cheeks and etc.? Likewise, in males, can vigorous exercise, drugs/diet and etc. masculinize?
Sexual dimorphism I mean as in how they look and what makes assure genetic/reproductive value.
Aside from genes, basically, what extent can diet, foods, exercise and etc. affect epigenetics, morphology and sexual dimorphism in animals, namely humans? Any evidence/studies/work on this?
This isn't intended to be a medical/personal question thing -- more so, broad on any means a human and/or animal may use their environment to try and improve dimorphism and morphology/phenotype.

There is a slight inaccuracy in your title question. Let's clarify to begin with:
I think you are asking whether environmental factors can affect sexually dimorphic traits. I don't think you are aiming to ask about dimorphism itself (i.e. the presence of apparent differences between the sexes) specifically. You're not interested in whether, say, food will affect sex dimorphism in humans but rather whether it can affect phenotypes which are sex-specific. It's a good correction to start with.

Can diet affect sexual dimorphism?

Of course. This is the case with all sexually dimorphic animals. A good example is nutritional deficiency, sub-optimal calorie intake or ingesting hormones or metabolically-active natural products from food. For instance, a male stag's antlers will not grow very much if the stag does not ingest enough phosphorus or calcium. This has drastic effects on its ability to reproduce, as often antlers are a key element in sexual selection in deer species.
Also, in some nutrient deficiencies, the body's ability to produce sex hormones is affected, which in turn affects secondary sexual characteristics such as jaw shape and the storage of fat. In bulimia and anorexia, periods become irregular due to the body's state of chronic starvation and inability to regulate menstruation with hormone cycles. Thirdly, diet can affect the ethology of disease (diabetes is a good example) which can indirectly affect sexual characteristics. There are many complex examples in which disease has an endocrinological (hormonal) component.
In addition, regular exercise, for instance, is well-demonstrated to affect testosterone levels.
It's important to keep in mind that not all traits which are sexually dimorphic are visible. For instance, smoking has an effect on sperm count, which is something not visible but still constitutes a sex-specific phenotype.

Can supplementation and drug-use affect sexual dimorphism?

Of course. I think taking steroids and hormones is an obvious example. I don't think this one needs explaining - a search engine can help here.

Of course. I think taking steroids and hormones is an obvious example. < But I've seen people -- guys in particular -- who've used steroids and it didn't seem to affect dimorphism of the face. It builds more muscle, but doesn't necessarily create masculine dimorphism face-wise (i.e., stronger jaw; wider face; larger warrior skull; powerful brow ridge and etc.). If this was true then virtually every guy who's used steroids would look/have some kind of highly masculine, dimorphic, cro magnon-esque face, which we know doesn't happen to most male steroid users at least (but female maybe).

I don't think facial features are as 'plastic' in adulthood. Once they are set up, they change relatively little in shape compared to musculature, i.e. overall skeletal shape can't be changed much. The obvious changes that steroids induce are not skeletal, they are most obviously related to connective tissue, muscle, skin, fat storage, etc. Also, transgender individuals who have 'transitioned completely' with the help of sex hormones tend to have distinct facial features that are not typical of their biological sex. You can certainly masculinize or feminize faces artificially with hormones.

Then wouldn't your point be rendered invalid then? If you're a man with bad, non-dimorphic male bone structure and hormones do not make a difference in this way, how would they affect dimorphism then? A non-dimorphic face is bound by bones primarily. How would fat/skin/etc. matter if the overall structure of the hard tissue is what appears non-masculine? In fact you agree yourself with the "distinct facial features that are not typical of their biological sex" part you mentioned. It seems hormone manipulation post-puberty barely affects dimorphism.

You're using the word dimorphic incorrectly. I wouldn't use terms like bad either, it's not clear what you mean. I don't think you appreciate the diversity of things taking place when you introduce steroids. If a man takes estrogen, he will grow soft tissues on his breast region. Breasts are not typical male characteristics. If a woman takes testosterone, she will find an increase in muscle mass, changes in fat storage and a deeper voice. Muscle tone or body shape are very typical indicators of sex-specific traits. Your last statement that hormones barely affect dimorphism is thus incorrect.

Can diet, supplements, drugs or exercise improve masculine appearance in men and feminine appearance in women?
In short, some of the mentioned factors can affect the appearance of the muscles and fat tissue but not the bones, face or genital organs. I'm not discussing about hormonal treatment here.
MUSCLES
Resistant exercise in combination with sufficient calorie and protein intake can significantly increase the muscle mass (Essays in Biochemistry, 2008) in the limbs, torso and neck. You can't realistically expect that chewing or other facial exercises will significantly change the shape of your facial muscles.
FAT
If overweight, a hypocaloric diet can make you lose body fat and thus:

make you look more fit
make your jaw angle more prominent
reduce your breast fat (gynecomastia)
decrease your waist-hip ratio

A diet can result in increase or decrease, but not redistribution, of body fat, which is genetically determined (Diabetologia, 2014).
BONES
There seems to be no natural and healthy way by which you could increase the thickness or length of your bones or change their shape in adulthood.
Bone thickness
Exercise does not significantly increase the thickness of your bones - only 1-2 mm increase was observed in one study in tennis players (American Journal of Sports Medicine, 1994).
High intake of calcium, vitamin D, other nutrients or supplements in adulthood also does not likely visibly increase the diameter of your bones (it may increase bone cortical thickness or bone density, though).
Bone length
I haven't found any studies that would show how exercise or diet could increase bone length or shape in adults.
Jawline
The shape of jawline is mainly determined by the shape of the jaw bone. While the jaw angle can be affected by the genetically determined thickness of the chewing muscles (Scientific Reports, 2018), it does not sound realistic to change the jaw angle by chewing or other exercise.
Shoulder and hip wideness
The shoulder and hip wideness is genetically determined by the length and width of the bones in the shoulder and pelvic girdle and cannot be significantly increased by exercise or diet.
GENITALIA
I'm not aware of any exercise, diet or supplements that would significantly change the shape of genital organs.
VOICE
There are psychological factors, attitudes, conscious effort and exercises that can significantly affect someones voice.

Hormones found in food
Soy and some other foods are high in phytoestrogens that can have some pro-estrogen activity, but do not likely significantly affect the appearance of the muscles or bones.

Nevertheless, the only positive effects of phytoestrogens on bone
  observed so far in post-menopausal women have been small and limited
  to the lumbar vertebrae. (Baillière's Clinical Endocrinology and
  Metabolism, 1998)
Estrogen or soy isoflavones given to postmenopausal women results in a
  small increase in lean tissue mass. (Appl Physiol Nutr Metab.
  2008)

Hormonal drugs
Estrogen, testosterone, corticosteroids and other steroids and growth hormone can affectsome of the following features: the morphology of genitalia, muscle mass, body fat distribution, facial appearance and voice.


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How do these triplets code for these proteins?

I am slightly confused by the diagram above.
The first codon of the unaltered DNA is AAG. During transcription, isn't this coverted to UUC (mRNA). So doesn't UUC code for phe and not Lys?
Likewise, how does TAG code for a stop codon? Isn't it transcibed to AUC, which codes for ile?
Also, is that the coding strand or template strand? If there is a mutation in the coding strand, is there any impact on the protein?

translation is making protein out of mRNA. Transcription is making mRNA (UUC) out of DNA (AAG). TAG transcribes to UAG. Check wikipedia page for https://en.wikipedia.org/wiki/Transcription_(biology)

Isn't there complementary base parigng for the template strand? So won't AAG become UUC as A pairs with U and C pairs with G?

codons are defined by mRNA sequence, defined by gene sequence. Correspondence is 1:1 except Ts become Us. What materials you are using? Do you have access to some Cell Bio textbook?

@aaaaaa thanks so much for replying. I uploaded what my textbook said about transcription. When mRNA is formed from AAG, won't the mRNA have the code UUC due to complementary base pairing. That's what I'm believing as that is what my textbook says. So doesn't UUC code for a different amino acid, not Lys?

@ChristopherU'Ren you're correct: transcription is complimentary. ATGC in DNA becomes UACG in RNA (except we think in terms of 3-base codons). What I think is confusing aaaaaa is that there are 2 strands of DNA: the coding strand and the template strand  (see here for explanation). The coding strand is the same as the mRNA (except for U vs T), but mRNA is actually transcribed from the template strand (which is complimentary to the mRNA).

@theforestecologist so is the first picture incorrect? Isn't AAG transcribed into UUC which codes for the amino acid Phe?

@ChristopherU'Ren it's not lysosomes, but "lysine." Also, no, AAG would be transcribed as UUC which is translated to Phenylalanine. See a codon chart (source: here).

However, if the book was showing you the coding strand of DNA (i.e., the strand not actually being used in transcription), then they're correct -- the coding strand triplet that is complimentary to the base triplet on the template strand used in transcription is going to be AAG when the resulting amino acid is lysine (and the codon in AAG). To summarize how the coding DNA strand, template DNA strand, and mRNA strand compare, see the link in my previous comment.

Note: In my experience, it's much less common for a textbook to show you the triplet on the coding strand (vs the template strand), but perhaps your book's authors/editors simply did not catch this mistake or preferred to illustrate this concept in this way.

In the first image, AAG is the true codon for Lysine.  So when the ribosome hits "AAG" in the mRNA it recruits a Lysine-tRNA.
What can be confusing is the use of the term "coding strand" when talking about the DNA. The coding strand is illustrated in the second image you posted, and it is the coding strand of DNA that the first image is depicting. What "coding strand" means here is, this is the strand that looks like the mRNA will look. Depicting the DNA coding strand like this--i.e. as a series of codons--can be slightly misleading since we know codons really only mean anything when in the form of mRNA. Nevertheless, it is a common way of thinking about DNA.
Back to the first image. Because it is showing the "coding strand" of DNA, the "template strand" for 5'-AAG-3' then must be 5'-CTT-3'. Hence, when this strand is transcribed by RNA polymerase, the 5'-CTT-3'(DNA) becomes 5'-AAG-3'(mRNA).

Why does CTT become AAG? Isn't it GAA?

You need to always be thinking about this in terms of 5'-to-3'.  I indicted this above and I think that may be why you are getting confused.

Please provide support for your answer. Preferably, cite or link to reputable sources that back-up the claims you make. Thanks


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Strand representation in the DNA version of the Genetic Code
A Wikipedia entry entitled DNA Codon Table states that the codons presented in the table are on the ‘sense strand of the DNA’. But what is the purpose of this, if the sense strand doesn’t code for anything? It stated that it is used a lot in computational biology, what exactly is the use of it in that field?

@David https://en.wikipedia.org/wiki/DNA_codon_table

@Remi.b your answer would have been fine with a minor edit

Thanks for the ref. You will see that I have suggested better terminology in my own answer. Also I have modified your title to make it more informative and less adversorial. Questions that say "what is the point of" tend to antagonize people.

Mind you, I would not object to the phrasing "What is the point of a Wikipedia entry" for something which is just the standard Genetic code with U changed to T. Almost everyone analysing data will be using a computer program and any computer program for DNA analysis will have it — and variants — encoded in a suitable format. Marginally useful for somebody somewhere, but a Wikipedia entry — really?

The genetic code was a seminal discovery in the field of molecular biology. The experiments leading to the results in this table have lead to the existence of the field as we know it today. It's been important reference material for interpreting mutations in disease and evolutionary biology for decades. Asking why there is a page for this is misunderstanding it's importance in biology, there is a wikipedia page for it for the same reason there is a Wikipedia page the atom and periodic table. It's fundamental knowledge in Genetics.

The sense strand has the same sequence as the transcribed RNA. The antisense strand is read in the other direction. For a particular gene, the sense strand is the genetic code, the other strand is the complementary template used to transcribe the RNA from it. The resultant pre-mRNA molecule (before introns are spliced our) will be single-stranded in the 5’ to 3’ direction with exactly the same sequence as the coding sequence (except for U instead of T). As such, the sense strand is the coding sequence of a gene (as it corresponds directly to the transcribed RNA sequence).
It is important to distinguish the direction of a DNA sequence. Genes can overlap in opposite directions. DNA and RNA molecules can only be synthesised by enzymes in one direction. This is important for DNA synthesis in vivo  (e.g., Okazaki fragments) and molecular biology experiments in vitro (e.g., PCR and NGS). Antisense RNAs are also expressed and are important in regulating cellular functions: this includes enhancers which sometimes express bi-directional RNA and short RNAs involved in RNA interference, microRNA, and CRISPR-Cas).
In molecular, cellular, and computational biology, the sense strand encodes the coding sequence (gene or other transcript). This is the sequence of any resulting RNA. Hence we define a codon as the nucleotide triplet that corresponds to a resulting amino acid. The antisense DNA strand and the tRNAs are complementary to this. Therefore there is an agreed upon convention to determine which strand is “coding” and it is straightforward to derive the resulting amino acid sequence of the encoded peptide given a coding sequence and a start codon (AUG). The antisense strand is the reverse compliment sequence which can also be computed. It is not necessary to store the sequence of both strands of a gene since the coding sequence can be used to infer the sequence of both strands.

See Figure 6-7. Molecular Biology of the Cell. 4th edition. Alberts B, Johnson A, Lewis J, et al. New York: Garland Science; 2002. excerpt online

You say "It is important to distinguish the direction of a DNA sequence. ... DNA and RNA molecules can only be synthesised by enzymes in one direction." - That could be a great start-up for learners. Does RNA-polymerase (that does the m-RNA read only from 3'to5'? -  Rarely will I find "negative RNA" in humans declared in that context, thank you!

Generally no, RNA and DNA polymerases both synthesize a new strand from a template strand in the same direction. It is possible there are exceptions in prokaryotes. Anti-sense RNA is usually transcribed independently (not in the opposite direction) by using different primers or promoters on the opposite strand of DNA. Long non-coding RNAs are regulated and expressed separately, they are not simply genes in reverse.

The Problem is in the Terminology
There have been several variants of questions of this type relating to the DNA strands in genes. In my opinion the reason that this is a common problem for students first encountering the topic is poor or ambiguous terminology.

In science loose expression reflects and/or encourages loose thinking.

This answer attempts not only to answer the question, but to encourage both the inexperienced and experienced to communicate with more clarity and less ambiguity.
It is the Genetic Code, not the DNA code
If the genetic code is related to any particular nucleic acid it is to mRNA. It is a table indicating which amino acids correspond to (are inserted in protein in response to) mRNA codons made up of triplets of the ribonucleotides corresponding to the bases, A, U, G and C. It does not include the DNA base thymidine.
The Genetic Code was established using artificial mRNAs and triplet oligonucleotides. Not DNA was used. It was further confirmed using translatable RNAs from the genomes of bacteriophages and eukaryotic viruses the genetic material of which is RNA, not DNA. Not only is there no reason to mention DNA when discussing the genetic code, but for the majority of scientists who believe that RNA preceded DNA, DNA was not even present when the genetic code emerged. Indeed, the title of a 1965 paper by Nirenberg et. al. (who were major contributors to deciphering the genetic code) was:

“RNA codewords and protein synthesis, VII. On the general nature of
  the RNA code”

Another reason for not referring to the “DNA Code” is that genomic DNA contains encoded other information (e.g. transcription start sites) besides the sequence of amino acids.
DNA sequencing and the presentation of genetic information
What, then, is the table presented in the question which — containing T, instead of U — clearly relates to DNA? It is a reflection of the fact that about ten years after the genetic code was deciphered it became possible to sequence DNA with much greater ease than RNA, so that the sequences of fragments of the genome were determined, annotated, and deposited in databases. When users researched and retrieved such sequences, they obviously wanted them presented in a manner that most clearly communicated those annotated features that related to the function of the genomic fragment (or later, whole genome). One of the most important features for users was obviously the sequence of the protein which the gene specified. In addition, because of the complementarily of the two strands of double-stranded DNA genomes, it was not necessary to present both strands, and presenting one strand would increase clarity. Therefore, the databanks adopted the following policies:

Only a single strand of the DNA was presented (in the 5ʹ to 3ʹ direction, as the convention for chemical abbreviation assumes).
Where the DNA fragment contained a single gene, the strand presented was that which could be interpreted by the scientist as if he were reading a strand of mRNA, but with U replaced by T.

To aid such interpretation (or for human or computer analysis — the latter mentioned in the question — of both strands of DNA to identify potential protein-coding regions) tables of the type in the question are produced. They are perhaps best referred to as ‘DNA versions of the genetic code’ or the like.
How to refer to the two DNA strands?
When referring to a segment of DNA containing a single gene, I think the most unequivocal way to refer to the two strands is:

The transcribed strand, and the non-transcribed strand.

This relates to the actual event — transcription — that produces the mRNA. I would advise its use by those teaching and writing on the subject.
Alternatives to the term non-transcribed strand
Unfortunately the strand presented in sequences of genes retrieved from the databases, as described above, is the non-transcribed strand. Perhaps from a reluctance to give a word with negative connotations to something of semantic importance, this term is very rarely used and is never likely to be generally adopted. Instead the following are often employed for the non-transcribed strand — the name of the transcribed strand is given in parentheses.

coding (non-coding)
non-template (template)
plus (minus) or positive (negative)
sense (anti-sense)

I have already discussed the problems with these terms in more detail in answer to a related question, where I explained why I discourage the use of  any of these other than sense/anti-sense — the sense strand conveys the sense of information of the mRNA. Coding/non-coding causes confusion because the naïve student may well assume that the transcribed strand holds the genetic information and feel that the term ‘coding’ should apply to it. (In fact both strands hold the information, as the existence of single-stranded negative-strand (here the terminology is correct) viruses attests.
RNA polymerase-recognition sites
A related problem has been the source of a question as to why CAAT boxes — recognized by RNA polymerase — are named for the non-transcribed strand. The answer is that having developed a convention to represent the strand of a gene that allows us to discern the protein product and the features of mRNA and mRNA precursor, the main concern of the scientist is to see the transcription features in relation to this, rather than to another strand, with A/T, G/C and 3ʹ/5ʹ mental conversions.
Remaining Problems
As discussed in the answer to another question, the use of any description — even non-transcribed — with the unqualified noun strand is a problem because it suggests that the genome as a whole has one transcribed and one untranscribed strand, whereas almost always there are genes with both orientations, and hence transcribed from different strands. It is perhaps better, therefore, to refer to the strands of a gene, except in those cases (generally bacteria or viruses) where two genes overlap in opposite directions. But Biology is not Physics, and sometimes nomenclature has to be descriptive rather than definitive.

This is incorrect. The sense strand is coding and the antisense stand is the template. Non-coding does not refer to DNA strands, it refers to RNAs (which are transcribed) that are not translated into proteins. The “transcribed strand” is not terminology used in this field, learning it is unhelpful and counterproductive.

@TomKelly It should be clear that I am not advocating anyone learn the term transcribed because there is no need for anyone to learn it. Once a student understands DNA replication, transcription and translation, the term is descriptive of one of the strands of a gene in an unambiguous definitive manner, which all other designations are not. Even if you have never heard it used before you know which strand I mean. Hence it can be used as a reference point for explaning the meaning of terms that are in use, but are not self-explanatory. It would be helpful for explaining template.

@TomKelly Thank you for pointing out that the transcribed strand is sometimes referred to as the template strand, a most ambiguous term because the DNA strands are both templates in replication and I would reserver template for mRNA. I have corrected my answer accordingly. I would never use coding or non-coding for DNA strands (I am familiar with its uses in relation to RNA), but the Wikipedia entry for Coding Strand in which the use of template strand is explained uses both coding and non-coding. I am only listing the terms in use.

Since the terminology has been corrected, this should cause less confusion. The terms themselves make sense to me but I have am very familiar with them as a Geneticist (some are used more often than others). Still to avoid any misunderstanding, we frequently use diagrams to show this sort of thing.

Since I started to assume (skipping the Okazaki-part) that RNA-polymerase knows only one "direction" (see above) I feel better,  further assuming "negative"  is synonym to "transcribing", and "negative" is from '3 to '5.  Indeed, I came across "coding strand" not being used according to convention.  - Also, negative RNA (not DNA) does exist und must be coded. - Moreover, I believe in "coding" refering to DNA, by convention. "Transcribing" instead of non-coding is a helpful idea, but it needed to become convention,  isn't it ironic.

Here is the entry in ensembl for the human transferrin gene.  In real life, people look at cDNA sequences, not RNA sequence, and don't see the U's, just T's
http://uswest.ensembl.org/Homo_sapiens/Transcript/Exons?db=core;g=ENSG00000091513;r=3:133745956-133796640;t=ENST00000402696
Look at that first exon, which starts 5'-GGGCTTTGCCTGTCATT.  Look at the DNA sequence in that region.  It's the same.  The template stand for this gene runs reverse, which makes the strand itself look just like the DNA sequence in the forward direction.

The link you gave doesn't seem to bring up exons. - Can it be true that the template for the non-template has got the same row of nucleic acids? It's got to be complementary, not just the other way round.


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Could bone marrow transplants help make xenotransplants viable?

So the immune system doesn't calibrate (for want of a better euphemism) to recognize it's own cells until fairly well along in fetal development & the major components of the immune system (antibodies, white blood cells, etc) are all produced by the bone marrow.

Those are the known details that cause me to wonder if this (below) might not be a viable approach.

Introduce the patients cells to a pig fetus before it's immune system has been set & it will be born with an immune system that recognizes both it's own cells & the patients cells as it's own.
Kill the patients own marrow (as per a normal bone marrow transplant) & transplant the pigs bone marrow into him giving him an immune system that recognizes both his cells & the pigs as it's own.

If my understanding is correct you should then be able to transplant any other organs from the pig into the patient without any tissue rejection issues.
I am only interested in the science so (any legal & moral issues aside) are there any major factors I'm unaware of to suggest this approach is a non-starter?

See Xeno: The Promise of Transplanting Animal Organs into Humans By David K. C. Cooper M.D., Robert P. Lanza M.D. Published 23 March 2000 by Oxford University Press, specifically the section on "The Induction of Chimerism Before Birth" from page 117 onward in this link.
That talks about my suggested first step (though in reverse), creating a human with immunity to cell rejection of a donor animals cells, which isn't much use to anyone who's already been born.
So I flipped the idea.

A Thymus transplant might be needed as well.

Comments are not for extended discussion; this conversation has been moved to chat.

I feel I've enough sources & data to venture an answer on this one myself now, so here goes.
Step one: Can we produce the pig in the first place?

Fetal Inoculation With Donor Cells in Cardiac
Xenotransplantation 1996
Perinatal induction of immunotolerance to cardiac and pulmonary allografts July 1997
Induction of donor-specific tolerance to cardiac xenografts in utero: 1998 Sep
Cell Transplantation January 1 2003
IMMUNO-INTERVENTION FOR THE INDUCTION OF TRANSPLANTATION TOLERANCE THROUGH MIXED CHIMERISM: 2011 Aug 11
In utero hematopoietic cell transplantation: induction of donor specific immune tolerance and postnatal transplants: 2014 Nov 12

another link to the same article
In utero hematopoietic cell transplantation: induction of donor specific immune tolerance and postnatal transplants 12 November 2014

First human-pig 'chimera' created in milestone study 26 Jan 2017
Interspecies Chimerism with Mammalian Pluripotent Stem Cells 2018 Jan 26
Interspecies Chimeras and the Generation of Humanized Organs 3 Jan 2019

Yes, an animal can be produced with donor specific tolerance to the patients organs, it's a known procedure & observed effect that has been replicated numerous times in experiments, its immune system would not attack either the patients cells or its own.
Step two : Can we transplant this animals bone marrow to the patient?

Stem cell and bone marrow transplants

Yes, bone marrow transplants involving the complete removal of the original bone marrow is a long established procedure for the treatment of leukaemia.

And now being used for treatment of other severe autoimmune diseases in a way which may make this idea moot, I'll have to look into that further, not read that article in full yet.

Step three : Will we then be able to transplant other organs from this (or a genetically identical) animal to the patient without tissue rejection?
The immune system isn't seated entirely in the bone marrow & its products (the thymus, spleen & lymphatic system also have roles) so for best results some of these may also need to be replaced.
If so it must be hopped the lymph nodes play no role in in the development & tuning of the immune system, there are 500-600 of them around the body so replacing them all would be no small task.
Conclusion :
Still in progress / just saving work so far

No, this will likely never work - but chimeric trans plantations of 'humanised' organs might become possible.
Firstly, the process of injecting human/patient cells into an embryo would - if it works - create a chimera. Experiments of creating pig-human chimeras have (to my surprise) actually been performed, however the amount of humans cells that didn't immediately kill the embryos was very low (~0.001%), so even if they embryos would be able to reach adulthood (which the researchers didn't test) the organs wouldn't be human-like enough to allow transplantation. (source1, source2)
If the chimeric embryo's indeed survive then it might be possible to create animals that have a completely 'human' bone marrow that can be transplanted, by removing part of the pig genome that allows for the generation of bone marrow so that the injected human cells take over that role (this technique has been used successfully in rats & mice for other organs). If organs other than the bone marrow could be 'humanised' this way in pig chimeras is probably unclear since the difference between pig and human is much larger than mice and rat and might cause immune rejection issues.
Transplanting actual chimeric organs will likely never be done, since some of the cells will always be of the 'wrong' species, which would cause a lot of immune issues in some way.
Since chimeras unlike hybrids will never have individual cells that combine two species, it will also not be possible to make a thymus that 'trains' the whole immune system against two species - individual T-cells might only see one type of species during maturation and therefore cause immune reactions later on.

"ethics" please read the question again.

@Pelinore: I read the question, and my answer is a clear NO irregardless of the ethics aspect

"otherwise the pig will die" can you explain why pigs with humanized organs don't die then, we've almost two decades of experimentation doing just that and I don't recall ever reading anything about a problem with pig mortality arising from that?

@Nicolai your post could be improved with more thorough references. Right now you've just linked to the wikipedia page on T-cells, but you make very specific statements about what would or couldn't happen in various experiments.

@DeNovo I'll try to see if I can find some references but it wont be easy since these are mostly hypothetical experiments that noone would actually do (and therefore write about), like injecting adult cells into an embryo.

@DeNovosupportsGoFundMonica I edited (or rather rewrote) my answer with a better sourced foundation.


text:
In what fluid does the sperm swim in the oviduct?
We know that after sexual intercourse, sperm enters the female body and continues to pass through the oviduct by swimming. "Swimming" implies the presence of fluid.
I want to know what that fluid is called. Also could you please tell me the color of that fluid? Is it yellow/off-white?

Specifically in the fallopian tubes, the fluid is called tubal fluid, and is produced by the innermost mucosal layer of the tubes (specifically, the peg cells in the epitelium)

In the follicles, there is the follicular fluid, liquor folliculi.
In the uterus, the endometrial fluid.
In the cervix, cervical fluid.

I don't know about the color. For what it's worth, cervical fluid varies from white to yellowish, but it's transparent when it's best for spermatozoa to swim.


text:
Are there examples of Apis mellifera of different colors?
Re: my previous species-identification question,  What species is this gray bee? I'm still curious: Are there any recorded/reported cases of either albino Apis mellifera, or at least with substantially different pigmentation/color? Is it possible that only part of a colony gets this trait?

In conjunction with your other question, I wanted to let you know that there is a huge variety of species of bees found in the wild, especially in more rural areas. See this link for example that has some bee genera found in Chile: https://www.yorku.ca/bugsrus/resources/galleries/bgoc I think your picture with that earlier question is too unclear to answer but I think the simplest answer is that you have found a bee of a species that is not Apis mellifera.

@BryanKrause Thanks! I really appreciate any info. If you could write that as an answer to the original question, I'd be grateful

I don't think it could really serve as an answer because your picture is too unclear to identify, and just providing a link to the first Google result for "bee species Chile" is not really enough research effort to warrant an answer, just wanted to help point you in the right direction for the future :)

I've been reading a little more, and found a partial answer.
Not sure about albinoes, but Wikipedia lists a few different colors, arguably substantially different:
Under Apis mellifera subsp. ligustica (the Italian honeybee),

Leather
Bright yellow (golden)
Very pale yellow

Under Apis mellifera caucasia (Caucasian honeybee),

Dark with brown spots at times

In fact, both photos below are reported as Apis mellifera, here and here respectively.


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Inhibition of beta-oxidation by acetyl- or malonyl-CoA

Which molecule, in excess, inhibits beta-oxidation?
a. Acetyl-CoA
b. Malonyl-CoA

The answer to this question seems debatable to me, as I think both are correct.  However, according to my professor, only one is correct — which one I  don’t know because it was a question from the final exam.
Acety-CoA can inhibit thiolase, and malonyl-CoA can inhibit CAT I (Carnitine- acyltransferase), both of which lead to the same outcome — inhibiting beta-oxidation

Mammalian $\beta$-oxidation occurs in the mitochondrion, whereas fatty acid biosynthesis is cytoplasmic.

The rate-limiting in mammalian fatty acid oxidation is considered to be carnitine palmitoyltransferase (CAT), a key enzyme in the transport of acetyl-CoA across the inner mitochondrial membrane.  This enzyme is inhibited by low micromolar concentrations of malonyl-CoA (see Beta oxidation of fatty acids by H. Schulz).

Malonyl-CoA, of course, is a key intermediate in fatty acid biosynthesis.  Salih Wakil showed that CO2  is required for fatty acid biosynthesis, but that carbon atoms from CO2  do not appear in fatty acids, and it is now known that this is due to the formation of .malonyl-CoA by acetyI-CoA carboxylase, the rate-limiting reaction of fatty acid synthesis.

Thus when fatty acid biosynthesis is taking place, the concentration of malonyl-CoA is high and CAT (and therefore $\beta$-oxidation) is inhibited (Schulz, 1991).

However, as the OP points out, micromolar concentrations of acetyl-CoA inhibit 3-ketoacyI-CoA thiolase when the concentration of CoASH is low, and the Acetyl-CoA/CoASH ratio within the mitochondrion may also play a role in the regulation of beta-oxidation (Schulz, 1991).
As the OP says, it is a debatable point, and it seems to me, an example of a badly worded exam question.  I think the 'expected' answer is probably malonyl-CoA, and there is no doubt that this molecule plays a key role in the regulation of both fatty acid oxidation and fatty acid biosynthesis.  Nevertheless, the inhibition of thiolase by Acetyl-CoA may also play a role in the regulation of beta-oxidation.
Perhaps your Professor is an example of the type that Warburg told Hans Krebs to attach himself to? :-)

Your Google books link tells me I have reached a page I cannot access. Perhaps you can give us the Warburg quotation, in the German original if possible.

Taken me a while to get to it, but I finally found the quotation in Krebs’ (English language) autobiography of 1981, Reminiscences and Reflections. On p. 26 he gives this account of his interview with Warburg “I could learn a lot in his laboratory, he said, but if it were my aim to make a university career, ‘Then you had better attach yourself to some old ass of a professor.’” He goes on to write: “Warburg kept his word on both counts: he taught me a great deal, and he did not actively help me find a post…”


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Balancing selection vs introgression?
Balancing selection can maintain polymorphisms in natural populations for extended periods of evolutionary time. However, in this paper, Dannemann et al. 2016 identify three archaic haplotypes in the modern human genome that are due to adaptive introgression. Why can we exclude that haplotypes III, IV and VII (the introgressed haplotypes) have remained in the human gene pool since the split between modern humans and Neanderthals because of balancing selection?

I'm closing this question because based on a discussion in the comments it seems that the premise of the question is a homework assignment that isn't reproduced here.

Balancing selection and positive selection are not mutually exclusive. Neither are balancing selection and negative selection. Sickle cell is a classic example where there is negative selection against the homozygote for the sickling mutation, and positive selection for the heterozygote. The result is that there both alleles are maintained in the population under balancing selection.

Thank you. I understand that both balancing and positive selection can occur together (along with introgression). In the paper, the authors present evidence for positive selection of the archaic haplotypes. However, I'm wondering if there is conclusive evidence to exclude balancing selection in this case? (The question comes from a homework assignment, so balancing selection is already presumed to be excluded...)

There is nothing in the paper about balancing selection being excluded. Are you saying that the only reason you think it's excluded is because a homework assignment is telling you this?  Also, you keep mentioning introgression along with selection--those two terms need not be related at all. Introgression in the absence of selective signatures is common.

Yes, the question assumes it's excluded which is why I'm wondering what evidence can be drawn from the paper for that? From what I understand, introgression and balancing selection can leave similar genomic signatures so it would be difficult to distinguish between the two of them.


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Can light function as a neurotransmitter?
Any animal with an eye has photoreceptors, which are essentially light-sensitive neurons. Green algae have channelrhodopsin, which are ion channels that open and close in response to light. Clearly, the nervous system and its molecular components have evolved to use light effectively.
I'm wondering if light can act as a neurotransmitter in the classical sense; that is, the presynaptic cell releases a photon, which travels across the synaptic cleft and interacts with a receptor, depolarizing the postsynaptic cell. Light can be generated in vivo through chemiluminescence, and as with channelrhodopsin, different proteins can activate in response to different wavelengths or intensities. I suspect this would be much faster than traditional chemical signaling.

I'd be hesitant about using the term 'neurotransmitter' as it specifically refers to a chemical synthesised by the presynaptic neuron. But I see no reason why a neuron couldn't transfer electromagnetic radiation that is then picked up by another neuron (possibly via rhodopsin). Imo you could probably have a functioning signalling network with bioluminescent/light-sensitive cells but whether that actually occurs in nature, I'm not sure.

Hmmm i feel like a paper was just published about this. Let me go digging around to see if i can find it

I don't think there is a theoretical reason why this wouldn't be possible.  However, I think there might be some practical problems with a system that relied upon light signaling.
1) It would be susceptible to interference.  Many bio-luminescent organisms are transparent, so other sources of light could depolarize a post-synaptic cell.  Light also penetrates tissue in organisms that are not transparent.  Blue light can penetrate 2 mm of human tissue and higher wavelengths like red can more than double that.  I could see light acting to replace signal molecules in quorum sensing though.
2) Neurotransmitters aren't really much of a limiting factor in nervous system speed. A monosynaptic reflex travelling a short distance might take 30 milliseconds, but neurotransmitter transmission is only 1 of those milliseconds.  In more complicated neural pathways, the speed of neurotransmitters might only account for 1/100th of the time.  So, if we're just imagining time-saving nervous system improvement, fiber optic neurons are the way to go.

An emitted photon could go any direction, also go "inwards'. Indeed an optics would be needed.

Adding to the list of why it might be practically infeasible: it might be less energetically favourable for cells to create light than for them to keep using chemical transmitters. Also, it would require the ability of the organism to evolve a specialised way mechanism of bioluminescence, which might not confer any advantage to the organism.

There are four main criteria for identifying neurotransmitters, these are very strict for the definition of something as a neurotransmitter or not.

The chemical (in your case light) must be synthesized in the neuron or otherwise be present in it.
When the neuron is active, the chemical must be released and produce a response in some target.
The same response must be obtained when the chemical is experimentally placed on the target.
A mechanism must exist for removing the chemical from its site of activation after its work is done.

I'm currently not aware of light fulfilling these criteria so it cannot be cataloged as a neurotransmitter. This is the definition I found in wikipedia, but you'll also find it in any neuroscience textbook like Kandel or Purves

The markup you used is reserved for program code. I deleted it and replaced it with bullets. Can you add references?


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Does a mutation in the sense strand of a particular gene affect the polypeptide formed?

Recently, I came across this picture which represents the DNA sense strand of a gene.
The ‘Altered’ picture shows a (frameshift) mutation in the nucleotide sequence in which a T base is deleted.
The sense strand is not transcribed — the anti-sense strand is transcribed. So why is there a change in the amino acids of the translation product when a mutation occurs in the sense strand, if the sense strand does not produce amino acids? Does a mutation in the sense strand change the nucleotide sequence of the transcribed sense strand?

I have edited your question so that it uses only unambiguous strand designations as discussed in my answer to your recent related question.

We’re doing it for the children!
The basic misconception in this question is that the important effects of mutations are seen in the cell that undergoes mutation. This is not the case. So focusing on the whether the strand that receives a mutation is the non-transcribed, sense, strand or the transcribed (anti-sense) strand is of little relevance.

What is important is whether or not the mutation is passed on to the progeny.

Don’t we have a life too?
Why isn’t it important? Consider a mutation occurring in a single E. coli cell in a population of millions of E. coli, or a single muscle cell in a human muscle. Even if there is a mutation in the strand that is transcribed into mRNA and translated into protein, the change in that one cell will not have a significant effect on the overall population.
The birds and the bees
The way in which a mutation — on sense or anti-sense strand — can affect a population of bacterial cells or whole tissue in an organism is:

(For bacteria or in tumour cells) if the mutation is passed on to some of progeny, which then have a selective advantage so that they can outgrow the wild-type population
(For normal tissues in animals) if the mutation is passed on to the progeny through the germ line so that it is present in all (e.g. muscle) cells

Still harking on about sex (Yawn)
The key point is easier to explain with bacteria. Consider a simplistic situation in which a mutation occurs on one strand (and is not corrected by the DNA-repair mechanisms). Before the cells divide into two daughter cells the double-stranded DNA replicates — each strand is the template for a complementary strand in a daughter double-stranded DNA. One cell will have the daughter dsDNA (double-stranded DNA) copied from the unmutated strand and the other will have the daughter dsDNA copied from the mutated strand.

In the case of the dsDNA copied from the mutated strand, both
  strands will clearly carry the mutation, so it is irrelevant whether
  the mutated strand in the parent was sense or anti-sense.

If the mutation is advantageous these cells will grow and divide and out-compete the other bacteria in the population.
A similar explanation holds for tumour cells in a differentiated animal tissue.
In the case of germ-line cells in animal tissues the situation is slightly different — the mutation either will be present or absent in both strands of the dsDNA in the fertilized egg, and so will affect all of the cells in the tissues of the progeny in which it is expressed.

Thank a lot. The mutation doesn't always occur in the original DNA strands, right? Can there be mistakes in the replicating strand? For example, if there is an A nucleotide on one original DNA strand, can the replicating strand accidentally bring a C? Not sure if the term replicating strand is correct.

I'm not quite sure what you mean. Both strands are replicated in ds genomes. There are several different types of mutation with different mechanisms and consequences. I suggest you look at the Nature Scitable article which covers them quite well.

Does a mutation in the coding strand change the base sequence of the template strand?

The DNA molecule is composed of two paired, complementary strands of DNA which--by definition--must be paired and complementary. A deletion of a base on one strand would be replicated such that the new DNA molecule would be deficient at that position on both strands. Here's a nice summary that also includes animations.
And, if you are instead asking whether there are ever exceptions to this very basic rule of molecular biology, then yes, so-called "bulged bases" have been reported (e.g.here) but they are still considered anomalous.

Sorry, but what does deficient mean in a biological sense?

@ChristopherU'Ren — It has no special biological meaning. DavidR clearly meant "deficient in a base" in the sense of lacking or missing a base — the base that was deleted in the first strand.


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E. Coli growth inhibited in Powdered Honey
I ran into problem with my method validation since the E. Coli that I've spiked into my Honey Powder sample can't grow in the media. The media I've used is Merck CCA (Chromogenic Coliform Agar). I've also used the MPN method (3 tubes) using LST Broth with the same result.
Really appreciate if someone Can  lead me into why would this happen and give any suggestion on how to troubleshoot this?
Regards.

If I understood correctly you want to grow E. coli in the presence of honey, right?
This migth be the problem as honey inhibits bacterial grow. See here. Therefore, it also doesn't matter which medium you are using.


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McFarland or O.D of culture what to use and what is the difference?
I am working on gram positive bacteria for which OD was reported and some reported mcfarland value. I am new to microbiology. i want to confirm the only thing that matters is cfu. please reply for what shoul I prefer
thank you.


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What is the name of the species of this butterfly?
Well,I am from India and live in the northern part of the country.I commonly find these butterflies during winter or spring seasons.

The original image shot is:

Welcome to the site! What size is it?

I'm not an expert, but it looks like a male "common mormon" or Papilio polytes romulus

https://species.wikimedia.org/wiki/Papilio_polytes_romulus

The image of the species on the left looks quite identical and accurate.And also,it’s written on Wikipedia that the species is found in Nepal which is the country lying just above the border our state.Thanks.

Those two butterflies are the same species.  The one on the left is a male.  The one on the right is the female.


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Is there a name for the use of sunlight in metabolic processes?
"Photosynthesis" is what is used to describe how plants use sunlight to synthesize sugars, but, I also heard some animals like humans use sunlight in the process of creating vitamin D. Is there a comparable name for when sunlight is used by animals in a metabolic process?

Perhaps you would want to replace "animals" with "organisms". I don't think there would be a special term just for animals.

Photometabolism or photocatalysis would be apt terms and the former would specifically refer to biochemical reactions.
Photometabolism is also used in the context of the light dependent conversion of 7-dehydrocholesterol to Vitamin-D.
A google scholar search with photometabolism returns many peer-reviewed articles that have used this term. Some examples:

Photometabolism of 7-dehydrocholesterol to previtamin D3 in skin.
The photometabolism of glucose by an hydrogen-adapted alga
Photometabolism of Heterocyclic Aromatic Compounds by Rhodopseudomonas palustris OU 11.

"photo-metabolism" also, e.g.here.


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How does the intracellular accumulation of cyclic AMP cause edema in case of anthrax?
Edema factor is adenyl cyclase which is activated only inside the target cell. It leads to intracellular accumulation of cyclic AMP resulting in edema. How?

Welcome to SE Biology. This appears to be a homework question and you need to show that you've made an effort to answer it yourself.

@Michael_A This doesn't sound like a homework question to me. First of all, the answer is that it's poorly understood, so a full answer would require a substantial grant and a lab. Second of all, the research is right there in the question: What does edema factor do?  This is what the OP found out: what edema factor is, where it acts, what the immediate molecular effect is, and the clinical result. You may be unfamiliar with this, so it may appear to be poorly researched, but it's actually asked quite well, and succinctly, though probably by someone who's native language isn't English.

Edema factor is a high efficiency adenylyl cyclase, an enzyme that converts ATP to cyclic AMP (cAMP). cAMP is an important second messenger in many pathways, which you can read about in Albert's Molecular Biology of the Cell. In order to be an effective second messenger, it must be tightly regulated. Several bacterial toxins disrupt this regulation, by creating an excessive amount of cAMP directly (B. anthracis EF), forcing the local activator of adenylyl cyclase to stay on (V. cholerae CT), or preventing the local inactivator of adenylyl cyclase from turning it off (B. pertussis). Some of these pathways are well understood. The pathway between cholera toxin and lethal loss of intestinal fluid, as mediated by elevated cAMP, is particularly well understood. The pathway between edema factor, edema toxin, cAMP, and tissue/organ edema is not well understood, as illustrated by this lovely figure, from this review:

Note the nice question mark between Edema Toxin and Edema
It could be mediated by protein kinase A (PKA), and probably is at least partially. It could also be mediated by EPAC and the small G-proteins Rap-1 and Rap-2 (and probably is, at least partially). It could even be mediated by the loss of ATP, since the anthrax ET is so efficient at catalyzing the conversion of ATP to cAMP.


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How does further hybridization affect fertility?
Numeruous scientific sites state that hybrids (like mules) are infertile. On the other hand, ligers are known to mate with both tigers and lions and still have viable offspring.
So my question is: if the hybrid is fertile in the first generation, does further mating with either of the parents' species somehow affect its offsping's fertility?
For example: if liger mates with tiger let the odds to produce viable offsping be 50%. If this offsping further mates with tiger, are odds the same or are they lower / higher?

Some first generation hybrids[f1] are viable and fertile, but when they mate with each other or back to either parental species[P}, the successive generations[f2] are sterile or feeble.  this concept is known as hybrid breakdown.  This is often seen in hybridized forms of domestic crops.  I am aware that some female tiger/lion hybrids are fertile, but I'm unaware of successful breeding of the f2 generations.  It could be a case of hybrid breakdown.
Article about hybrid breakdown in rice
Hybrid breakdown in Cichlid Fish


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What is the meaning of the following: " completion of open rounds of DNA replication"?
I am studying a paper about the relation between polyP granule and cell cycle exit. As the author explained the four general steps for cell cycle exit, the second step is" the completion of open rounds of DNA replication". But I really can't figure out the meaning of this sentence. I hope that someone can explain this to me. Thank you!

From the context of the article I found from an internet search:

Cell cycle exit in bacteria encompass four general steps:
(i) inhibition of inappropriate reinitiation of DNA replication,
(ii) completion of open rounds of DNA replication,
(iii) segregation and compaction of daughter chromosomes, and
(iv) septation.

I would assume that ‘open rounds’ means ‘DNA replication that has already been started’ (‘open’ signifying already started, and a ‘round’ has the sense of one event of a series). ‘Completion’ is obviously ‘finishing’, ‘ending’ — the cell cycle doesn’t end until all the replication that has started has finished.
I have not seen the adjective ‘open’ used in this way previously, and suspect it is uncommon, but as this is not my field I stand to be corrected.

Oh, I see. So, I may translate it into  the last round of DNA replication before entering the cell cycle exit?


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What M9 stands for
Can anyone tell me what M9 stands for in M9 medium?
I have tried googling but I still cannot find it.

I wasn't able to find an original source either but I wouldn't be surprised if it was the 9th version of some minimal medium that was used; M could be minimal or medium or a non-English equivalent. That doesn't mean the history isn't interesting for curiosity's sake but it won't tell you anything else. In any case, the modern M9 has multiple recipes that deviate slightly from one another anyways.

https://www.thermofisher.com/order/catalog/product/A1374401

Original usage seems to be Miller J.H. (1972) Experiments in Molecular Genetics.


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What is a synonym of the word design that can be used in context of evolution?
For example let's take two sentences; "engineer made a design for camera", "evolution made an X for eye". What is the best X that could be used?
I need it for an essay about evolution.

If not already very clear in Bryan's answer... Evolution made X is pretty much never a good phrasing. Instead, say X has evolved. Otherwise, it feels like evolution is a thinking individual with a goal in mind (which would be very wrong). Similarly, don't say, X has been designed but X is an adaptation (assuming X is indeed an adaptation for whatever X stands for).

Although not ideal, "adaptation" is more appropriate than "design" as a noun describing something that has come about in an evolutionary context, even though not all evolution is adaptive.
In writing, though, I would not phrase it as you have, rather I would change the agency from something evolution does as some sort of "entity" which makes it sound like a goal-driven "designer" with whatever words you use, and instead say that "Eyes evolved from simpler photosensitive groups of cells." Eyes deserve the agency, because having eyes is what would improve the survival of an organism versus eyeless conspecifics and increase the proportion of eyed individuals in the next generation (I hope my simplification of the eye-evolving process as if eyes are a simple Mendelian trait isn't too distracting here, I mean it mostly as metaphor), rather than eyes being a "goal" of something called evolution.
Similarly, you would not say "Chemistry makes water from hydrogen and oxygen," rather you would say something like "Hydrogen gas reacts exothermically in the presence of oxygen gas to produce water." There is no agent "chemistry," that is just the word we use to describe the set of processes in the universe that govern how molecules/atoms/subatomic particles interact. Similarly, "evolution" is not an agent who does things.
One place I would differ in this guidance is in talking very big picture, such as saying that "evolution produced the wide variety of species present today"; in that example, there isn't anything more local to act as an agent, and it's appropriate to refer to the evolutionary process as a whole.

Nice answer that highlights the likely mistaken representation the OP had when trying to find a synonym of design as if the concept would apply. +1

@Remi.b Thanks; I'm not sure if OP's representation was mistaken or not, however; I've often seen people who understand evolution very clearly make similar slips, especially when they are assuming their audience will see between the lines and understand what they mean. Sometimes being more correct also means being more verbose, unfortunately.

The closes I can think of is "Shaped" or "Favors". I see that most often when talking about side effects or a suite of features or for comparing alternative constructions. There is no agency any more than erosion has agency if you said "erosion shaped a rock outcrop". You could say "evolution shaped the eye such that ...." A cleaner usage would be "evolution favores eyes with X under Y conditions" I do agree giving agency to the eye is probably cleaner.

How about "strategy"?  For example, elephants, giraffes and koalas all need to eat leaves from tall trees, but they have evolved very different strategies to accomplish that goal.

I think that "adaptation" would be the most appropriate term, since they are all those adaptative strategies (ecological, physiological, morphological, behavioral and reproductive) fixed in populations by the action of evolutionary forces, which guarantee the survival and perpetuation of species..

Welcome to Biology.SE! This seems like a less sophisticated version of  the answer by @BryanKrause. Please only post answers if you have something new to add. ——— Thank you for taking the [tour], but please also consult the help pages for additional advice on [Answer] effectively on this site. Thanks!


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Do blood cells immediately die after leaving the body?
I am wondering, do blood cells die right after they leave the body?

Reasonable question, but it could use some clarification re: what you mean by "die".

Hi C. Jordan, wlecome to Bio.SE. What research did you do to try to answer this question on your own? We ask that all question askers on Bio.SE try to answer their own questions and then ask questions only about specific details they cannot find an answer to or that they do not understand. Please update this question with evidence of such prior research, and please be mindful of this as you continue to interact with this community. thanks!

@theforestecologist I was looking up on a website about refrigerating blood samples, but got varying results.

No. If they did, blood transfusions wouldn't be possible (or they would require some sort of direct body-to-body system).
Red cells collected can be stored under refrigeration for over a month. See for example the description of what happens to donated blood from the Red Cross. Platelets don't last quite as long, but they also survive for some time in the right conditions. Of course, some cells die during storage, but there is no instantaneous die-off once cells leave the body.

+1, though this is perhaps a philosophical question

Blood cells do not die immediately because they still have some amount of nutrients in them that they can use until it finishes.
They only die when they lose their source of nutrients after using up all that is in them.
Cells in blood still have access to nutrients due the presence of plasma which helps keep them alive for while.
Put in a fridge(4-18°C), the temperature slows their rate of metabolism allows which further extends their lifespan. But can die of heat shock if frozen and thawed.
You can read more on it in;
Effect of Blood Storage on Complete Biochemistry
Effect of Specimen Collection and Storage on Blood...
The pathophysiology and consequences of red blood cell storage
Red blood cell storage time and transfusion: current practice, concerns and future perspectives

Please provide support for your answer. Cite at least one reputable source that backs up your claim. Thanks