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Definition of semiquantitative
I'd like to understand differences between how biologists and statisticians deal with uncertainty. As a concrete example, I'd like to understand if "semi-quantitative" can be defined in terms of statistics and probability. As a first step, I'd very much appreciate any definition (either statistical or not) of "semi-quantitative". What is the distinction between a "quantitative" and "semi-quantitative" method?
Google scholar has many papers including "semi-quantitative" in the title. As an example, I'll quote a portion of the abstract from Marone, M., Mozzetti, S., De Ritis, D. et al. Semiquantitative RT-PCR analysis to assess the expression levels of multiple transcripts from the same sample. Biol Proced Online 3, 19–25 (2001). https://doi.org/10.1251/bpo20

As for all quantitative techniques, great care must be taken in all optimization steps: the necessary controls to ensure a rough quantitative (semi-quantitative) analysis are described here, together with an example from a study on the effects of TGF-β1 in TF-1 cells.

Caveat:
This answer differs fundamentally from that given by @acvill. I have not provided authoritative support for it — it is merely my understanding of the use of the terms in biological science.
The use of the terms Quantitative and Semi-quantitative in biology refer to measurements, not to statistics, although if the measurements are accurate meaningful statistics can be performed upon them. Nor is the distinction fundamentally to do with accuracy. Both types of measurements can vary in accuracy, depending on the methods used to obtain them.
In the example given, the problem is to measure the quantity of transcripts — RNAs of a particular kind (generally specific mRNAs) — that are present in only small quantities.
Quantitative measurements of such transcripts would determine one of the following:

Their number or molarity (molarity)

Their weight or concentration (grams per litre)

However doing this is difficult in the case of such small quantities of molecules found in a mixture.
Semi-Quantitative measurements of transcripts attempt to measure something indirectly related to their concentration, which, while not producing a number, concentration or amount, gives some value related to these that can be used for comparison with other mRNA transcripts.
In this case the mRNA is copied many times by PCR to eventually give an amount of product that can be measured. As far as I can see from the paper it was intensity of staining with ethidium bromide after gel electrophoresis. However it might have been incorporation of radioactivity or amount of some radioactive probe hybridized to it. In any case the measurement would have arbitrary units which could be used in comparison.
In my opinion it is the fact that the method does not measure the quantity of the mRNA (or whatever) in standard units that makes it semi-quantitative, although the indirectness of the measurement involving several stages can compromise its accuracy.
Addendum: Definition in relation to Covid antibody tests
I am wary about talking about a definition of ‘semi-quantitative’ because the definition in the reputable Merriam-Webster dictionary, citing the first use in 1927:

constituting or involving less than quantitative precision

does not correspond to current biological usage by implying that it relates to the precision of measurements. (See, for example, the Wikipedia entry on Precision to see why.)
It is of interest that the emergency approval by the US Food and Drug Administration of certain SARS-CoV-2 antibody test in late July 2020 specifies explicitly that they are semi-quantitative, and the pharmaceutical company, Roche, provides the following explanation of the term on its website.

A qualitative test determines the “if;” quantitative and semi-quantitative tests answer the question “how much?” By measuring the level of SARS-CoV-2 antibodies in a patient’s blood sample, quantitative and semi-quantitative tests give a more definitive answer about the body’s immune response to the virus. Quantitative tests are traceable to a specific international standard that ensures the result produced correlates to a numeric quantity of antibodies. Due to the current lack of an international standard, the FDA has not granted EUA to any quantitative tests. Semi-quantitative tests estimate an approximate concentration of SARS-CoV-2 antibodies in a patient’s blood sample, and can be traceable to a specific standard to ensure consistent results.

The italicization is my own to indicate the relationship to my explanation, above.

Thank you for your answer. If you have a chance, I'd appreciate hearing a generally applicable definition that captures the key features of what you wrote. Here is one attempt:
Consider an experiment designed to measure a physical quantity. That measurement is quantitative if it can be expressed in the same units as the target physical quantity. All measurements that are not quantitative are semi-quantitative.
I think most people would agree that my attempt needs some modification.

@rileysg — At present I think your definition is on the lines of my standpoint. However I am wary of definitions. In biology things are always a bit less defined than in the physical sciences. I would like time to look at other examples of usage of the term and its application. One problem with my answer is that you can try to calibrate non-standard units against a standard. Another consideration is that the nature of the assay may be internally consistent and usable for comparison in an individual setup, but the values not transferable to another setup.

@rileysg — I decided not to go in quite the direction I mentioned when I discovered the recent application of the term to covid antibody testing. This seemed to me of more contemporary general interest.

There is no strict statistical definition of semi-quantitative. Generally, a quantitative method yields results that can be compared across different experiments, whereas a qualitative method yields results for which comparisons are only meaningful between samples within a single experiment. Per your quote, we can see that the authors are using the semi- prefix to indicate to readers that the technique has not been fully optimized, and therefore any results obtained by their semi-quantitative method should be interpreted with a grain of salt.
In context of RT-PCR methods, quantitative methods typically undergo rigorous optimization to define necessary controls and a strict parameter set. This should include (1) instrument and reagent specification, (2) constraints on primer / probe design, (3) some measurement of expected experimental error, and, most importantly,  (4) use of a well-defined spike-in or control sample. A control sample or set of samples of known concentration is necessary to back-calculate the nucleic acid copy number for your experimental samples, and any RT-PCR without such a control is necessarily qualitative.
By calling their RT-PCR protocol semi-quantitative, the authors are saying to the reader "Hey, we made this method. We think it's pretty good. We tested some things, but not everything. Caveat emptor."

Thank you! Could you give a reference for your definition? Even if it's simply something you learned by working as a biologist, that would be helpful to know.

The definitions I give are just my understanding. I am a biologist.

I think David's answer fits my understanding better, but my bigger quibble with your answer would be the definition of "qualitative". Something qualitative is something that can't be put into numerical representations. It might include comparisons like "more/less" that get closer to "semiquantitative" but also includes things that can't really get any number, like lists of words or semantic relationships.


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Does every person have unique nervous system?
If we had the technology to directly interface electronic devices with the nervous system and we wanted to connect a robotic arm to a person that lost his/her real arm, would we be able to find the same "wires" that control(led) that arm in every person?
Or does every human control their organs in completely unique, "incompatible" way?

Probably the best way to answer this question is with a counterexample to humans: the nematode worm C. elegans has 302 neurons. Every individual has exactly that number, and each is found in the same place with the same function in every individual. This is one of the things that makes C. elegans an attractive model organism for study.
Humans definitely do not develop the same way. There are certainly groups of neurons that are found in every individual, and many of the tracts have at least a typical anatomical course that can be found from individual to individual, but it's not as if you can arrange each of the tens of billions of neurons in a list and find the same "Neuron #10,934,035,587" in two different people.
The most successful prosthetic operation that interfaces with the neuromuscular system these days is through myoelectric control, where rather than using electrical activity from neurons, one uses electrical activity in muscles, such as muscles in the chest and shoulder to control a prosthetic arm or hand.

But when they do things like hand transplants, they connect the patient's nerves to the nerves in the transplanted limb, don't they? People are similar enough for this to be feasible.

@Barmar They can connect nerves, but not neurons. The individual neurons need to re-grow through the nerve structure. "Re-wiring" the hand from that point onward is a result of extensive physical therapy and more about plasticity in the CNS than rewiring in the periphery. A similar process would happen if a nerve were severed and reattached in the same patient without a transplant; it's also somewhat similar to how those connections are developed in the first place. Human infants are born with fairly incomplete motor control and so are an (adorable) excellent insight into this.

The OP didn't specify individual neurons. I think his figurative "wires" equates to nerves.

(it's also worth noting that a lot of hand control occurs outside the hand)

@Barmar That's possible, but then you'd have to also specify the detail of nerve. Everyone has a spinal cord where nerves leave at every vertebral level, sure; from there, variation increases the more distal you get. Hooking things up at the nerve level isn't sufficient to connect electrical devices to the nervous system; the only way to do it is to let the nervous system learn associations with the connections you've made. Every attempted brain-machine-interface or nerve-machine-interface has done this.

My thinking is that the details are unique like fingerprints, but at a higher level it's similar like the general structure of fingers.

@Barmar Sure, but isn't it a bit superficially obvious that if you have a finger, it has to have nervous innervation? "People have fingers" is enough to tell you that; the interesting part would be considering whether there is some one-to-one relationship between the neurons and structure of the finer nerve endings in two people; there isn't.

I guess what I'm saying is that the arteries and veins have direct correspondences that allow you to connect these, and there would be similar correspondences for nerves. There will be minute differences, but not enough to prevent reconnection.

@Barmar Only at a very gross level. For example see this question: https://biology.stackexchange.com/questions/82918/coronary-circulation/ about a common difference in the coronary circulation, and that's in a couple of major vessels together supplying over half of the blood to the heart. Have a look at the superficial veins in your arm that are quite visible from the surface: you'll find they vary quite a lot.

agreed yes you can connect the same nerves but neuron to neuron will be slightly different, especially in the brain, but the person can learn to control the new limb without problem it will just take time.  translpantees will have gross control fairly quickly but precision control takes a long time.

WRT C. elegans, neurons are actually a fairly high level of nervous system organization.  Neurons have many dendrites (IIRC something like 1-10K branches in humans) & many synapses whose state changes due to synaptic plasticity.  And researchers keep finding more low-level complexity: https://www.quantamagazine.org/neural-dendrites-reveal-their-computational-power-20200114/

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How can we explain that glucose at its concentration less than a Km for the transporter enters the peripheral circulation?
I'm studying biochemistry from Kaplan's book. In it, I found the following paragraph in the topic on glucose metabolism:
"GLUT 2, a low-affinity transporter, is in hepatocytes. After a meal,
portal blood from the intestine is rich in glucose. GLUT 2 captures the
excess glucose primarily for storage. When the glucose concentration
drops below the Km for the transporter, much of the remainder leaves
the liver and enters the peripheral circulation."
A similar question has already been here, but it didn't help me find an understanding of this. How can we explain that glucose at its concentration less than a Km for the transporter enters the peripheral circulation? Why is this related to Km? I understand, that at glucose concentration equal to a Km, V will be equal to half V max. But even at a low concentration, glucose will still bind to the transporter, although not so actively. Correct me if I'm wrong, but I think that transporting glucose into the hepatocytes at a low speed will be energetically unprofitable or because of the speed of blood flow, it will no longer have time to get into the hepatocytes. Please, give your opinion

I correct you as invited because you are wrong. Please read the sections about enzyme kinetics in your text very carefully. You will find nothing about energetically or “speed” and certainly blood flow is irrelevant as the next unit of blood has the same concentration as the preceding one.

@David Ok, thank you very much

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What is the "anatomy" of transcriptional regulation in Archaea?
I want to know what are the DNA elements that are recognized by transcription factors in Archaea and so what is the "anatomy" of transcriptional regulation in this case.
I found in this paper by Alexandra M. Gehring et al. that the process of initiation of transcription in archaea is governed by TATA-binding protein (TBP), Archaeal transcription factor B (TFB), and Archaeal transcription factor E (TFE). These constitute the basal transcription factors and transcription initiation is regulated by DNA elements that are recognized by basal transcription factors that recruit the enzyme RNA Polymerase (RNAP) that will copy DNA into RNA. There  are  four  DNA  elements  currently  known  to  regulate  archaeal  transcription  initiation: the TATA-box located approximately 25 bp upstream of the site of transcription  initiation;  the TFB  recognition  element  (BRE) located immediately upstream of the TATA box; the initiator element (INR) located  within  the  initially  transcribed  region,  and  the promoter  proximal  element  (PPE) located  between  the  TATA  box and the site of transcription initiation.
This seems very similar to the eukaryotic system and, in fact, also the Wikipedia page tells that  the core machinery is more similar to eukaryotic transcription (with respect to bacteria).
Moreover, the first paper that I linked also tells that it is probable that some archaeon-specific factors await discovery for the elongation and termination steps of transcription.
Now, I started to search if Archaea have enhancers and silencers like the eukaryotic genes but I could not find anything. Since the core machinery is more similar to eukaryotic transcription, can I assume that there are enhancers and repressors and that the main pattern of DNA elements necessary for transcription and transcription regulation is that of eukaryotes? Maybe, the reason why I do not find the answer to my question in Google is that some archaeon-specific factors await discovery. Indeed, Archaea are, in general, often called the "blind spots" of natural diversity because of lack of knowledges about them.
Also if you have a look at the Promoter (genetics) Wikipedia page, there is a list of elements of promoter relative to Eukaryotes and Bacteria, but nothing about Archaea... So is it completely wrong to look at the eukaryotic elements and explanations of this page, for example, as (at least) probably valid also for Archaea ?
Thank you in advance.


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What is this small brown arthropod?
Does anyone have an idea what this arthropod is? I first found one in the bath but have since noticed them on the walls, ceiling and on linen around the house. They are 1mm long, look brown in colour and I think they have 6 legs. Couldn't get a better pic than the one attached.
Size: 1mm
Location: Sussex, UK

Wood framed house by any chance? Sort of looks termite-ish from that angle. I'll let the experts answer though.

It's timber framed, covered with brick. Plasterboard on the inside. Built this year.

Looks more like an insect than a mite.

Welcome to Biology.SE. Six legs is inconsistent with mites (which have eight legs) so I've edited your question to use the more general term arthropod. Please borrow something with better close-up capability and see if you can get better photos — the current photo is so tiny and unfocused I doubt anyone will be able to give you a definitive id.

Thanks for correcting my poor terminology! I'll see if I can get my hands on something with better magnification!

This appears to be a booklouse (psocid). They are tiny, harmless insects that are common in buildings. It is normal to have small numbers of them.

Nice first post neville, welcome to Biology.

Thank you! I have been active over on Reddit's bug ID forums and it only recently occurred to me to check out what's on StackExchange. I am mostly interested in arachnids, but can ID a lot of common insects people find around the house.

Thanks Neville. Yes that looks spot on! Had rather a lot of them! A few hundred. Think we've got a humidity issue so that would make sense based on what I've just read about them.


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The use of the word “canonical” in biological science
What is the meaning of the word canonical in a scientific context? This is an example that I do not understand:

BDNF is a member of the neurotrophin family of growth factors, which
are related to the canonical nerve growth factor.
OR
canonical and non-canonical Wnt signaling pathways.

Though David's answer is technically correct, I offer an alternative for those who struggle with the term in broader contexts.
Definition
Canonical simply means relating to a historically established paradigm, or relating to a common or standard model (which simplifies things!). For example, a biochemical pathway or a mechanism, for example, may be understood to include certain typical players or long-understood elements or interactions. These are canonical elements. They relate to the scientific canon. They depend on the history of discovery and organization of our theories, rather than any biological phenomenon.
Example
For instance, a synapse is canonically composed of a pre-synaptic neuron and a post-synaptic neuron. This has been long known and to this day scientists broadly speak in terms of the two, as a simplification of the system. However, most synapses are tripartite, including a glial cell cradling and modulating the environment between the communicating neurons. The glial cell can be considered to be the non-canonical element, even though it may be essential, or very important in the system. But it hasn't been studied as long, and introduces more considerations and complexities to think about which go beyond a simple way of thinking about it.
The use of the word
Some pathways or mechanisms have been strictly defined and outlined, where one can clearly draw the line between the canonical and non-canonical elements. There is no flexibility in how you use the word. On the other hand, other times the word is used in cases of systems where there is no strict definition dividing the two, it's just a judgment call, of what most scientists consider central, primary and emblematic (as opposed to peripheral, or secondary, or not validated enough 'to have entered the canon') to the system. There the use of the term canonical is colloquial!

Short Answer
The word canonical in this context implies that nerve growth factor is the original, standard or prototype of some sort (in relation to a class of biological agents).
Without knowing details of growth factors I found the sentence slightly ambiguous. As I suspected, it means that NGF is either the original growth factor or the original representative of the “neurotrophin family of growth factors”, which includes BDNF (brain-derived growth factor) — see Wikipedia article. However the use of the word “related” could be interpreted incorrectly to mean that the neurotrophins are in a different family from NGF.
Relationship to the general meaning of the word in English
The excellent Oxford Dictionary, accessible from any iPhone, has this as the first meaning of the word canon:

A general law, rule, principle or criterion by which something is judged.

The appointment violated the canons of fair play and equal opportunity

So its ecclesiastical connotation (in church law) is only one example of the application of the word, and is not intrinsic to it. The word comes from Middle English through Latin from the Greek, kanōn, meaning rule. Hence it has been applied in many spheres to things that are rules or standards.
Another examples of ‘canonical’ in biological science
Perhaps the most well-known usage is in relation to the base-pairing of nucleic acids. A definition by implication can be found in the Wikipedia entry for ‘Non-canonical base pairing’

The standard Watson-Crick base pairs (which are adenine–thymine  in DNA, adenine–uracil in RNA, and guanine–cytosine in both DNA and RNA).

(The non-canonical base-pairs are those that are found outside the context of double-helical DNA–DNA or DNA-RNA duplexes, for example G–U base-pairs in dsRNA, wobble base-pairing between mRNA and tRNA, and other base-pairs in non-duplex components of RNA structure.)


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Can the hippocampus store working memory?
I'm a little bit confused about the role that the hippocampus plays in memory.
I've heard that it stores episodic memories and then consolidates the important ones into long-term memory.
My question is: if it stores episodic memory which is a presumably pretty malleable form of short-term memory why can it not store working memory as well? Also isn't that what 'memory champions' learn to do?
Further: If this is the case then what are the functional differences (e.g. pros / cons) between this and working memory supplied by the prefrontal cortex? ...Is the prefrontal cortex memory even more malleable?

If you "store" working memory, it isn't working memory anymore. Yes, that's how "memory champions" exceed the normal capacity of working memory: they store things as episodic memories to retrieve later.

@BryanKrause Well, that's just semantics...
What I'm really interested in is if it is indeed possible to 'use episodic memory as working memory' then why doesn't the brain do this by default? What draw backs are there? And what is the default way working memory is stored?

Yes, I think your question is also just semantics. Working memory is not stored, that's what separates it from other forms of memory. If you were to store the thing that working memory contains, that would be something else that isn't working memory.

Look technically all memory is stored by definition, working or otherwise. If it were never stored it would be impossible to remember even an instant after it were created. An 'unstored memory' isn't even a memory, it's just external information that you don't know.

My question is not semantics, working memory is a faculty of the mind for quickly encoding volatile memories for short-term use. I'm asking if there are any functional draw backs of this 'episodic working memory' compared to 'default working memory'.

The hippocampus is thought to respond to information that is being maintained in working memory in other areas.  Areas that are commonly thought to maintain working memory include prefrontal cortex (reviews: Chai et al 2018 https://doi.org/10.3389/fpsyg.2018.00401) and entorhinal cortex (Fransen 2005; Egorov et al. 2002).  For example, some information about recent trajectory comes to the hippocampus from prefrontal cortex via thalamus (Ito et al. 2015 https://www.nature.com/articles/nature14396).
Critically, episodic memory is not a form of working memory.  Episodic memory refers to the content of memory, not the duration.  Episodic memory storage occurs in different brain areas at different times.  The hippocampus is specialized for rapid acquisition of long-term memories.  Look up "systems consolidation of memory".
Also to address your discussion with Bryan, the general idea is that working memory is "stored" through mechanisms other than changing synaptic weights.  For example, working memory can be "stored" through persistent activity (Sanders, et al. 2013, https://www.jneurosci.org/content/33/2/424.long) or short-term facilitation of synaptic weights (Mongillo, et al., 2008, https://science.sciencemag.org/content/319/5869/1543.abstract).  Review here: https://doi.org/10.1016/j.conb.2013.10.008

So does the hippocampus actually store any memory inside itself (even temporarily)? Also can you address the draw backs of repurposing episodic memory buffers to 'extend working memory', like memory champions do for example, (e.g. is it slower to write too?)

yes, the hippocampus stores memory inside itself.  Look up "systems consolidation of memory".

i don't believe research has been done on the drawbacks of memory champion techniques as the sample size is way too small to make any concrete statements.


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What is the primary purpose of the prefrontal cortex?
I've heard of many functions of the prefrontal cortex (e.g. creativity, working memory, abstract thought, inhibition, planning, executive function, etc...).
But I'd like to know what its primary function is? For example is there any one function it has which facilitates all of its other functions? Or is there a known reason why it evolved in the first place?

Sorry for being such a downer on your last couple questions here, but first "What do you think?" is kind of a flag for the opinion-based questions that are not a good fit for the StackExchange format and are usually voted to be closed. Second, why should there be a one-sentence answer to this question? "Prefrontal cortex" is just a geometric label for a region of the brain, and a pretty arbitrary one at that: it includes 14 different Brodmann areas, and Brodmann areas need not themselves even have a one-sentence function.

I can re-word it but I'm not asking an opinion. I'm asking for science's best approximation of an abstract fact. The reason I'm asking is because information concerning the prefrontal cortex seems a little bit disconnected & sometimes inconsistent.

I'd certainly expect you to get disconnected and inconsistent answers to "what's the one sentence summary of what prefrontal cortex does" because there could be so many and also because most of how the brain works at a high level of organization is not currently understood.

I just want to know what the most fundamental function it serves is.

I don't think that's a factually answerable question any more than "what is the most fundamental sandwich".

Alright... I reworded it so it is more clear what I'm asking. And also clear how the answer is not an opinion.

"To facilitate an organism's survival until it can attain reproductive success and enough to facilitate reproductive success of it's offspring in a varied and challenging environment." - What more than that are you after?

I'm looking for an answer which is as simple as possible, while still being specific enough (i.e. unique to the prefrontal cortex & without ambiguous meaning), and abstract enough (i.e. able to generalize the usual 'laundry list' of functionality people attribute to it).

Attributing purpose to the prefrontal cortex (or really to any biological part) is really the wrong way to look at things.  Ask instead what it does, how it started to evolve in the first place, how it gave the possessors of early versions an evolutionary advantage...

If you want the function of the prefrontal cortex boiled down to a single coarse approximation, the answer is executive function.  That notion of more structured and symbolic cognition encompasses pretty much all of the others on your laundry list.
As with other complex and multifunctional organs in the body, reducing the prefrontal cortex in this manner is a problematic oversimplification, in much the same way as describing the function of the mouth as "getting things in and out of the body".

hm ok fair enough

This brain region's primary activity is orchestration of thoughts, actions, in accordance to internal goals. Many authors have suggested a link between personality and functions of the prefrontal cortex.
This brain region is involved in executive functions such as planning and decision-making, personality expression, moderation of speech and language, controlling certain aspects of speech, and language.

This also looks like it could become a good answer, but in addition to what I said on your other post this is a poor question because it is opinion based (see comments), which is why it has multiple downvotes. Please consider deleting this post as it is encouraging the posting of questions that are not appropriate for this site — from How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here.


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What is the relationship between muscle energy consumption, the period over which the contraction occurs and the mechanical work performed?
I'm asking this question with some basic knowledge of physics and general fitness.
Suppose you are lifting a still object with mass $m$ from height $h_1$ to height $h_2$ with an arbitrary (straight or curved) path. Let's ignore the movement of the body parts during the lift. Suppose you keep the object still at the final height $h_2$.
From physics, the object gains a mechanical energy equal to the variation of the gravitational potential energy during the movement:
$$\Delta E = mg(h_2-h_1)$$  [Joule]
Now, from what I can gather, such a quantity is absolutely not equal to the energy consumption of the muscles performing the lift, as:

Muscles fatigue more if they are shortened for a longer amount of time. That's the reason why lifting an object slowly is harder than lifting it fast. The previous equation does not consider the duration of the lift.

The previous equation ignores the object path because the mechanical energy gained by the object depends only on the vertical distance. But a curved and longer path may mean a longer duration of the lift. Hence it may mean more energy consumption, because of point 1.

Not sure of this, but I suppose muscles aren't 100% efficient. Hence, for each Joule (or Kcal) of input energy (in terms of ATP), they won't provide one Joule (or Kcal) of mechanical energy. I suppose some of that becomes heat.

So, I'd say that the previous equation provides the minimum amount of energy expended by muscles. It ignores the muscles inefficiency and the duration of the movement. But at the same time, the mechanical work does contribute to the energy consumption, since lifting an object is much harder that just keeping the muscles squeezed for the same amount of time.
Do you know some equations which take into account of these factors, and hence relate the mechanical work to these last two variables? Also some papers dealing with t

I suggest also posting this question in physics community

@RogerVadim Cross-posting is typically frowned upon. That said, similar questions have been asked at Physics so I'd strongly suggest OP to look for them there.

Welcome to Biology.SE. I've made some changes that I think make your question clearer, but please check to make sure I've not changed your meaning. In addition, note that your post stops mid-sentence. Also note that this may be too unfocused to be answered here — I would guess that there is a large literature on this subject. Some key words you can try to add to your searches: biophysics, kinematics.

Likewise I have edited your title so it employs standard scientific English. Check whether I have not inadvertently changed your meaning.

Does this answer your question? Why a continuous supply of energy is needed to support a weight?

This is at least partly duplicate from question https://biology.stackexchange.com/questions/35225/why-a-continuous-supply-of-energy-is-needed-to-support-a-weight/35290#35290 , although the question "what equation could model the extra energy spent due to other losses" is not in that one.


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Lowering annealing temperature in PCR
In the book "Lewin's Genes" there is the following quote:

Lowering the Tm of a PCR reaction—in effect, relaxing the reaction stringency and allowing primers to anneal to not quite
perfect hybridization partners — has useful applications, as well, such as in searching a sample for an unknown sequence suspected to be similar to a known one.

Why is this so? That is, why does lowering the annealing temperature in a PCR reaction reduce a specificity of hybridization, more precisely?

https://www.thermofisher.com/us/en/home/life-science/cloning/cloning-learning-center/invitrogen-school-of-molecular-biology/pcr-education/pcr-reagents-enzymes/pcr-cycling-considerations.html, see section "Primer annealing optimization".

Perhaps more specifically, see section "Effect of annealing temperature on primer mismatch" here: https://academic.oup.com/femsec/article/60/2/341/584515

Welcome to Biology.SE. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may be subject to down-voting and closure. Please take the [tour] and consult the [help] starting with [ask] for details.


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Do transcription factors need to undergo extensive post-translational modification?
Some proteins need additional processing to become fully functional, for example NiFe-hydrogenases need to be cleaved by endopeptidases for some of their subunits to be active.
Is it known whether transcription regulators could also, in some cases, need such extensive post-translational modification to be effective?
(I am not talking about possible conformational changes that by specific effectors, but rather an obligatory step in the maturation of the protein, that could also be necessary for other genes' expressions.)
To be a bit more precise, I am thinking about a metabolic system where the expressions of most of the involved genes are regulated by a master transcriptional regulator (SurR, an ArsR-type, redox-active regulator involved in Thermococcales’ (Archaea) energy metabolism).
I am wondering what kind of effects a change in the expression of the regulator-encoding gene could have on the whole system. And before getting to an effect on the regulon, I guess it is a good idea to start with the regulator itself: could it be theoretically fully functional in a greater concentration, if I would only consider overexpressing its gene for example?
One type of heavy post-translational modification is maturation by endopeptidase, which can hamper the correct activity of an enzyme if not considered adequately in a case of, let’s say, overexpression attempt. (this example is particularly important here since several enzymes of the regulon need to be importantly modified post-translationnaly)
Since there does not seem to be enough literature on the particular regulator I am interested about, and since a quick research for answers in other systems was not successful on my side, I am thus asking the SE community if anyone may have known about some kind of maturation-like, post-translational process, which could be needed for a fully functional transcriptional regulator. Would I need to worry about other genes than only the one coding for the regulator, to that extent?

Welcome to SE Biology. First, it would be useful to know why you are asking this question. As it stands it seems to me, at least, rather arbitrary. Potential responders would have more incentive if you told them why this is important to you. Second I have edited your answer so that it employs standard scientific English terminology. I appreciate this is difficult if you are not a native speaker, but the harsh reality requires all scientists to master this. My approach for other interests is to find a Wikipedia article in my own language and then switch to the foreign language version of it.

In addition to David's excellent advice, please note that this is a very broad question and could be closed due to lack of focus or insufficient prior research. Answers to a question like this are often unsatisfactory (tend to be superficial) because they require enough material for a review article or high-level textbook chapter to answer with any depth. This is not practical on this platform. If you can focus your question then a useful answer may be forthcoming — as it stands the answer is "Yes", which I suspect helps no one.

Thanks David and tyersome for your help and remarks. I have edited my initial post to give a bit more context, hope that’s better.

Notch signaling involves the cleavage of the transmembrane Notch protein. This releases the intracellular domain that then enters the nucleus and modifies gene expression. Does that count? Beyond cleavage reactions there are many examples of transcription factors that need to be phosphorylated (also a post-translational modification) for activation. But in your case you appear to be talking about a repressor, and at least LacI and TetR are both fully active repressors without any need for post-translational modifications. My guess is that it's quite general for at least bacterial repressors.

Your title seems to ask a different question (do [ALL] transcription factors...) than the body of your question (...in some cases...).


text:
What is this water animal in my swimming pool?
I have had a swimming pool (which is salt) for few months. 2 weeks ago I saw this:

I made a quick gif of a video:

Today, I found 4 more of this animal:

All of them that are living I found in the water. I saw one beside, but it was dead.
I'm currently in France (in the middle). Around the swimming pool there is nothing except grass for 5m. Else it's my house, a hedge or just the grass continuing.
What is it? Is that dangerous/bad news that I have some of them?

Note* Saltwater won't do them a lot of good in the long-term as they're adapted to freshwater.

That's a good point, I don't really want them in my swimming pool ...

Welcome to Biology.SE. Species-identification questions should use that tag. Amphibian is used for a group of vertebrates — these are insects so I replaced that tag with entomology. Please [edit] in an approximate size for your new "friends" as this may help with the identification. ——— Also note that whether this is "bad" is a matter of opinion, which is not appropriate for this site. Based on the suggested id (which seems correct to me) you can do some research and decide for yourself if this how you feel about their presence!

Thanks ! Yes, I search for the species-identification tag but i didn't find it. Thanks for edit. Yes, I say something opinion-based, but it's tolerated in comments ?

Corixidae (Water-boatmen).
Aquatic insect comprising 6 subfamilies and 55 genera. (The Wikipedia page's right-hand panel contradicts the detail below that).
Size 2 - 15 mm long (0.1 - 0.6 inches), six legs, the front pair are hairy and shaped like oars. Feeding on aquatic plants and algae they range worldwide except Antarctica.
If I couldn't guess from the picture which of the 55 genera it might be as so many are wide-ranging and have similar morphology.
Edit: in response to bob1's comment, the related family notonectidae (backswimmer) deserves a mention.
Being of the same order as the corixidae above (the neomorpha), the backswimmer is distinguished by ... swimming on it's back. They're slightly bigger on the whole than their cousins and although primarily aquatic are able to migrate through flight. They can inflict a painful bite and are able to pierce with their proboscis - which they use to great effect in hunting tadpoles and small fish.

Thanks, yes it's seems to correspond ! Do you know if it's dangerous ? It seems no but idk

@Elikill58 they are not dangerous but some of them can bite you,it gives a stinging sensation but it only last a very short time.

Thanks that's perfect ! :)

Good answer. You should also include the Notonectidae (back swimmers) which are very similar, and the ones that bite as they are carnivorous. The Corixidae are mostly herbivorous I think.

@bob1 Sure thing, I can't really tell from the picture which way up the thing is. Will edit.


text:
What are the current theories on how baleen whales make whale song?
Wikipedia does not provide many details1 on how baleen whales produce 'whale song', saying it's still a mystery.
The linked Gizmodo article provides these paragraphs:

Humpback whales, for example, do not appear to exhale while singing, and yet their songs are believed to be produced by a phenomenon similar to how humans sing: by air flowing across internal membranes within the respiratory system. In a whale, air could be circulating back and forth between the lungs and another respiratory chamber during 20-minute dives, though this remains speculative.
The researchers argue that "ingressive" and "egressive" air movements may produce different sounds. They also posit that the shifting of the oxygen/carbon dioxide ratio (which must occur during a dive) could be changing the resonant frequency of the singing organ, by changing sound velocity in the gas in the organ.
Both of these physical constraints might contribute to the periodicity (and variability) commonly observed in whale songs. Compare this reading to a hierarchical interpretation of whale singing (which, you'll recall, involves naming the individual components of a song), in which qualities like periodicity and variability might be linked to some function of syntax, rather than physiology.
Mercado and Handel's "heterarchical" model could be empirically tested by linking subtleties of whale songs to their behavior, or their breathing patterns. For instance, this model would be well-validated if the scientists could predict the diving or breathing of a whale based on the spectrotemporal nature of its song.

But I'm not clear exactly what '"ingressive" and "egressive" air movements' these would be? Unlike for Odontocetes, in that wikipedia article, there's not cross section or diagram with any hint of explanation.

1. At least at time of access: 2021/09/23 17:40

releated, but not a dupe (I hope): https://biology.stackexchange.com/q/79858/1270

DId you have a look at reference 14 in the wikipedia article: "Discovery of a low frequency sound source in Mysticeti (baleen whales): anatomical establishment of a vocal fold homolog "

@bob1 I did not, I didn't think the sentence it was attached to was that relevant, but I can just from the paper title it would be worth a read

As you can imagine, it is difficult to study this in baleen whales. There are decades of research on odontocetes (toothed whales) in captivity, but it is much more complicated for baleen whales. The Discovery of Sound in the Sea has great general information and citations for further investigation. They provide the cross sectional image I think you are looking for--- this schematic of a humpback whale that shows the potential mechanism for sound production in a humpback whale.
 (Image credit: Dr. Joy Reidenberg. Adapted from Joy S. Reidenberg and Jeffrey T. Laitman. 2007. Discovery of a low frequency sound source in Mysticeti (baleen whales): Anatomical establishment of a vocal fold homolog. The Anatomical Record. Volume 290, Issue 6, pages 745–759.)
According to Reidenberg and Laitman, 2007: "Ingressive" vocalizations refer to those produced by airflow from the laryngeal sac to the lungs (driven by contraction of laryngeal sac muscles) and "egressive" voclizations are produced by airflow from the lungs to the laryngeal sac, driven by diaphragm contraction. Reidenberg and Laitman, 2007


text:
Do the activity patterns of an owl species determine their eye colour?
Recently I've been thinking about the colour of owl eyes, and trying to figure out if there is a pattern anywhere between species.
I have read for example, that yellow-eyes implies they are day time hunters.
Is this true, and if so what do other owl eye colours indicate about their behaviour?

No, there isn't a perfect link between eye colour and behaviour
The full claim, as reproduced here is as follows:

Yellow eyes point to day-active species, such as little owl.
Orange eyes indicate that the species is active at dusk and dawn, such as
long-eared owl (Asio otus).
Black eyes are for night-active species, such as tawny owl (Strix aluco).

However that same page also provides exceptions:

... a team of Spanish ornithologists gathered data on eye color and activity rhythm for over 200 owl species. The analyses revealed that dark irises were more frequent among strictly nocturnal owls (41 out of 70 nocturnal species) compared to owls that are active during or at the end of the day (37 out of 131 diurnal or crepuscular species). These numbers indicate that the statement from the television show was too general. There are plenty of exceptions to the rule. To name just two: the barn owl (Tyto alba) is diurnal and crepuscular but has pitch-black eyes. And the Sokoke scops owl (Otus ireneae) has bright eyes despite being active at night.

emphasis mine


text:
When recalling the same piece of memory in different times, are the brain activities different?
When we are thinking about the same piece of memory in multiple different times, would the corresponding brain activities always be the same? Or how similar/different can the corresponding brain activities be?

The term for the brain activity that corresponds to an experience is "neural representation".
Neural representations "drift" over time.  From https://elifesciences.org/articles/51121:

Similar ‘representational drift’ has been shown in other neocortical
areas and hippocampus (Attardo et al., 2015; Ziv et al., 2013; Levy et
al., 2019).

So that means that the brain activities corresponding to an experience can change over time.


text:
Extensions of proteins in SARS-CoV-2 variants
What lineages of the coronavirus SARS-CoV-2 occurring in the wild show some extensions, i.e., mutations of the stop codons to codons encoding amino acids (mutations to another stop codon don't count here).
By chance I found that the pango lineage B.1.1.318 has an extension of the accessory protein encoded by ORF7b.
Are there more such cases, and what lineages are affected?

Due to a 15nt deletion around the ORF7b stop codon B.1.1.318 has a merge of ORF7b and ORF8 giving ORF8: MKF 1:3 MIELSLIDFYLCFLAFLLFLVLIMLIIFWFSLELQDHNETCHAY


text:
How many signals can one neuron send and/or receive simultaneously?
I've been researching this question online and finding opposing answers. Some articles say that one neuron can only send one signal at a time while others says that one neuron can send more than one signal.
What is the the exact answer, if it is a known fact in biology? If both cases are there, is a typical neuron in our brain sending one signal at this time or "multitasking"? Does the answer depend on the type of neuron?
Even further, if each neuron is sending more than one signal at a time, what would that imply to our current medical detections of brain? Can different signals happening at the same time be distinguished at all with our technology of detection and brain scanning?

It would be helpful if you provided more information about what you read - where did you read it, and can you provide a short quote of what was said?

I'd also ask you to clarify what you mean by "medical detections of brain"... no clinical uses of brain activity care about single-neuron stuff.

You're asking a pretty broad question here. Basically it's asking for a mini-course on how the different types of neurons work. Please narrow it down to a specific question, and your last question as already been answered by @BryanKrause. While every neuron is important, we can only examine/detect large groups of neurons at work.

A typical neuron receives in parallel many signals, both excitatory and inhibitory, from many different sources (usually other neurons). At any given time, if excitation exceeds a certain threshold, the neuron fires a single outgoing signal (the so-called action potential).
Thus, the simplest possible answer to the first part of your question is that neurons can only send out a single signal at a time. However,

each action potential is distributed to many targets at once (usually other neurons)
a single action potential is hardly meaningful as a signal; instead, the firing rate, i.e. the frequency of outgoing signals, is regarded as the most fundamental (but not the only) neural code.

For example, a neuron along a sensory pathway might respond with a barrage of several hundred action potentials to the onset of an appropriate stimulus (a sound, a blinking light, a touch on the skin, etc.). In turn, these signals would be transmitted to many other neurons, and so on.
Mind you, this concise description barely scratches the surface of an immensely complex topic. As mentioned in the comments, the question as a whole is too broad and ill-defined.


text:
How related are trees?
I was surprised to see how far apart macadamia and hazelnuts are from each other. I always thought all trees had a common ancestor that was also a tree. But that doesn't seem to be the case? Did wood evolve multiple times?

Welcome to Biology.SE. You seem to be assuming that the first flowering plant wasn't a woody plant. IIRC at least one hypothesis about the origin of angiosperms contradicts this assumption. Wikipedia looks like a reasonable place to start checking what the latest thinking on this is, but if that is correct then herbaceous angiosperms have lost "treeness". Also, please edit your title — it doesn't seem to reflect your actual question because trees occur outside the angiosperms!

WRT evolving multiple times, consider bamboo, which is botanically a grass, even though some varieties can be tree-sized, and the stems are to all appearances a kind of wood.

The word "tree" is a not a taxonomic classification, but a human perceptual clustering based on form and size. The word "fish" has a similar problem, covering a vast collection of taxa, some of which are less closely related to one another than they are to us.
Becoming tree-like often has a strong evolutionary value, because plants compete for sunlight and taller plants shade shorter plants. Thus, we should not be surprised that "tree" forms have evolved independently in a number of different lineages.
The common evolutionary lineage for all of these, however, is tracheophyta, the vascular plants.  These are plants that have differentiated xylem (which is the wood of a tree) and phloem tissues for transport of water and minerals. Most such plants are not trees, of course, but these tissues provide an effective means of vertical transport and the basis for hard woody material, which  appears to have been the key differentiator between plants capable of evolving into trees and plants that are not able do to so.


text:
meaning of the name "Dictyostelium discoideum"
Dictyostelium discoideum is a well-known species of slime mould.
Does anyone know what the name means?
Here's my best guess.
I found the 1935 article in which it was first described, but there doesn't seem to be an explanation for the species name 'discoideum'.
It might mean 'disk shaped', as in disk+oid plus an agreement morpheme -eum, because in Picture A in plate I, the sorocarp is described as having an 'expanded basal disk'.
The genus name 'dictyostelium' seems to be a reference to the stalk of the sorocarp, and how it resembles a 'dictyostele' or fern stem ('dictyo' meaning 'mesh' + 'stele' meaning upright stone),
which seems plausible but strange, because I don't think the stalk has any internal structure like an actual dictyostele.
So if that's right, the overall name would be a physical description of the fruiting body, something like 'thing with a fern-like stem on a disk-like base'.
Is any of that even close?

Brefeld described Dictyostelium in 1869. The book/article is viewable here

I worked through the article as best I could. (I don't speak German.) Unfortunately, Brefeld doesn't say why he chose the name Dictyostelium, just "it may be called Dictyostelium mucoroides" (p15) The article suggests he thought it might be a primitive mushroom, or something between amoeba and true fungus. "Mucoroides" seems to mean "like the mucor species," which are fungi that produce a tiny stem with a spore. It sounds like he was using analogies with other species to choose the name.

I think your analysis is correct.
Dictyostelium generally means net-like pillar. Dictyo references a net or mesh, and stele originates from the Greek stēlē: to stand or pillar. However, as you point out, "stele" is also the word for the central vascular tissue in vascular plants. The stele can take on several different architectural arrangements, including a net, or dictyostele, in some ferns.
As I don't read German either, it's unclear to me if Brefeld was referencing the structure in ferns, or just describing D. mucoroides on its own terms, perhaps envisioning the gathering of cells to form the stalk as being like a net. See, for example, this image of a Dictyostelium aggregation.

"Discoideum," as you note, means "disk-shaped," and Raper in his description references "expanded disklike bases" and "basal disks."

Dyctio means to throw, to cast [a net], stellum is star shape, discoideum is a grammatical varian of disk / disk shaped.


text:
What is the mathematical relationship between selection coefficient and dN/dS
dN/dS is often used as a measure of the intensity of selective pressure on a mutation or gene, but I'm curious about how it can be written as a function of the selection coefficient. I'm specifically interested in the scenario of somatic mutations in human cells; suppose there's a gene, and all non-silent mutations in the gene are equivalent (such as if they're all loss of function mutations). The mutation rate is μ mutations per bp per cell division and once both alleles are (nonsilently) mutated, there's no fitness gain (or loss) from additional mutations. The selection coefficient for mutations in the gene for homozygous mutations is:
w_hom = 1 + s

and for heterozygous:
w_het = 1 + hs

How would one derive the expected dN/dS ratio (where the selection coefficient of a silent mutation is 0)? I realize there are a few questions for which answers must be assumed to begin to answer this question, such as:

Is population static, or growing?
Is dN/dS only including clonal/fixed mutations, or perhaps all mutations with a frequency in the population greater than or equal to some value?

I'd be interested in what the relationship with dN/dS is even under the simplest assumptions, e.g. h = 1, only considering clonal mutations, and static population. I've found one paper that posits such a formula, citing a finding from another paper, but I don't think either shows all the math.

Are you suggesting that all non-synonimous mutations have the same fitness? Also, I think homo vs. heterozygocity is not really the issue here, unless we also need to account for recombination.

All non-synonymous mutations might have the same marginal effect fitness, in that they all just break the copy that gets mutated, but having a cell with one remaining functional copy may be more/less fit than one with no functional copies remaining.

Now you seem to suggest that these mutations are wekly deleterious. Perhaps, you could add a reference to what you consider standard use if dn/ds - we might be talking about different things.

dN/dS is usually calculated for an alignment or a phylogenetic tree as if the gene is haploid. Dioloidy is an interesting complication, since it can render deleterious mutations neutral. Selection coefficient can be calculated, if we make additional assimptions about the population growth, etc., as suggested in the OP. However, ut would limit the applicability of the method to the situations covered by these assumptions.

References
Perhaps this article is relevant, as it associates the fitness edge (i.e. accumulation of multiple beneficial mutations) with dN/dS:
Predicting evolution from the shape of genealogical trees

I think an example of it being used in this kind of context is in this paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5720395/. They're using dN/dS to assess selective advantage/disadvantage of mutations in cancer.


text:
How do I classify cytotoxicity values, whether a sample is mildly, moderately, or highly cytotoxic?
I used LDH assay for cytotoxicity testing. I have a plant extract which I tested against HepG2 cancer cells. I did three trials, my results were 2%, 6%, and 8% cytotoxicity, respectively.
How do I classify these values?
I was wondering if these values are low/mild, moderate, or high cytotoxicity. Someone told me that anything higher than 10% is already highly cytotoxic; however, I cannot find any reference that stated this.

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, you should tell us: 1) what the LDH cytotoxicity assay is and what LDH stands for; and 2) if you are using a kit — from what company or if not, what protocol are you following (summarize and then provide references). Finally, please tell us what you have done to find the answer — as  it stands this seems under researched and possibly opinion-based, both of which are grounds for closure.

I hope the results are compared with the effects of the solvent alone on the cancer cells. For example, Ethanol kills cells...

I’m voting to close this question because it is unclear (e.g. unexplained abbreviations), under researched, and possibly opinion-based.

Check your citations.  How do they use this assay?
I am not familiar with the assay you used, but you are.  Probably it is used to evaluate other plant extracts.  How do those authors do it?   When other people use this assay to look at plant extracts, how do they classify their results?
Consider what has been done in the past using this assay.  Then put your results in the context of what has gone before.


text:
How does Propionibacterium acnes survive the antibacterial effects of sebum?
Sebum has antibacterial properties due to sapienic acid and oleic acid according to this article on sebum. According to the same article, desaturation of fatty acids increases acne development. Another article, also suggests that the free fatty acids contribute to the antibacterial properties of sebum.
How does Propionibacterium acnes survive the antibacterial effects of sebum? Does it lack the enzymes to break down lipids in the sebum to form the antibacterial free fatty acids?
Also why are certain acne medications are so effective simply by inhibiting sebum production? Is sebum actually metabolic fuel for Propionibacterium acnes?

Welcome to Biology.SE. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may be subject to down-voting and closure. Please take the [tour] and consult the [help] starting with [ask] for details.

In particular, how do you know sebum has antibacterial properties — providing references supporting such statements will greatly improve your question. Also note that you seem to have multiple loosely related questions — please post each question separately as this makes it easier to index (and find) answers on the site and also greatly improves your chances of getting all your questions answered.


text:
Can we view the cross section of dna using electronmicroscope?
Is it possible to find how the cross section of DNA looks using without computer simulations ? All pictures I find on the internet are mainly computer simulations.

Note that electron microscope, scanning electron microscope (STM) and atomic force microscope (AFM) are three very different types of devices, imposing very different constraints on the sample type and preparation - even though all of them have, in principle, sufficient resolution. Important limitation for biology is that the sample has to be in vacuum. And, of course, the image is in false color, since these are not light microscopes.

Yes. We can use some specialist applications of electron microscopy to do this. This does rely on a computer to do some of the imaging (think very fancy camera).
There is an open access article at Science Advances that has images from transmission electron microscopy of DNA, specifically figures 1 and 3. Note: As mentioned by @timeskull figure 3 is a simulation of the HRTEM method that they used. Real HRTEM images are in figure 1.
Ref: Marini et al.,  2015. The structure of DNA by direct imaging. Science Advances vol 1, issue 7.

Wow fig 3 is incredible.

bear in mind that figure 3 is a simulation, figure 1 is actual data.

@timeskull good point. I'll edit that in.

And despite the fact that you have found a very pertinent paper, none of the images are the “cross-section” requested. Your answer would be much more useful to SE Biology if you expanded it to describe what is actually visualized and how the resolution compares with X-ray crystallography, which provides an electron density image.

@david I agree I could expand the answer, and I may have time to later. I disagree that it isn't sectional - longitudinal section rather than transverse, but the OP doesn't specify which they want. I've found a better paper with another visualization which is clearer and may be more useful.

I appreciate the demands on people’s time. I have my own backlog of unfulfilled promises to answer. But I think this would be worthwhile when you have a moment.


text:
Limitations of 16S rRNA sequencing
Looking at the microbiome analysis literature there seems to have been a shift away from 16S rRNA sequencing analysis toward shotgun sequencing of the whole genome. While the motivation given is typically that there is more information obtained by the latter, I am curious about the actual limitation of 16S rRNA analysis. Is the problem that:

There is simply no variation in the 16S rRNA gene between different species/strains that it would be useful to tell apart for a more accurate analysis.
There is some variation that would be useful, but the noise in the current sequencing methods and the capacity of the current computational analytic techniques are not able to capture it.
There is some variation that would be useful, but it is not clear how this correlates with the phenotype it would predict therefore scientists prefer to use shotgun sequencing to investigate causal relationships between genome and phenotype.
Something else (please explain!)

Thank you very much

Ask yourself and then tell us what the objective is of the sequencing in the two cases? Is it the same in the two cases? You should also find out how long the two techniques have been available. This will provide a better basis for your attempts at an explanation.

There is simply no variation in the 16S rRNA gene between different species/strains that it would be useful to tell apart for a more accurate analysis.

The amount of sequence variation depends on the region of the 16S rRNA gene amplified, and the choice of region depends on the desired universality of your primers as well as the read length constraints of the sequencing platform. Put simply, choice of target for 16S amplicon sequencing is a tradeoff between breadth and specificity. Typically, 16S sequencing connotes the use of primers targeting the V3, V4, and/or V5 regions of the 16S gene. Such primers are often optimized for taxonomic breadth (i.e. to differentiate as many organisms as possible) and designed to create amplicons that are readily sequenced on an Illumina platform.1 Thus, strain-level differentiation is limited in vanilla 16S analyses, though use of a multi-region framework can greatly increase phylogenetic resolution.2

There is some variation that would be useful, but the noise in the current sequencing methods and the capacity of the current computational analytic techniques are not able to capture it.

Modern short-read sequencing platforms (primarily Illumina) are considered quite robust in terms of sequencing error rates. However, for amplicon sequencing techniques like 16S, the per-base error rate might exceed the expected relative abundance of low-abundance organisms, making their detection and differentiation tricky.3

There is some variation that would be useful, but it is not clear how this correlates with the phenotype it would predict therefore scientists prefer to use shotgun sequencing to investigate causal relationships between genome and phenotype.

You've identified the major benefit of metagenomic / shotgun sequencing over 16S amplicon sequencing. When you are trying to extrapolate microbiome functions from 16S data, you are constrained by the existing phenotype-to-phylogeny mappings that are present in your databases. With databases of sufficient size, such analyses can give very good estimates of microbiome function.4,5 That said, strains that are closely related at the 16S level may have very different functional profiles due the inherent flexibility of bacterial genomes. Increasingly, pan-genomics is revealing that the so-called "peripheral genome" carries genes of consequential function, and the carriage of such genes in a particular strain cannot be detected by 16S amplicon sequencing alone.6

References

Caporaso JG, Lauber CL, Walters WA, Berg-Lyons D, Lozupone CA, Turnbaugh PJ, Fierer N, Knight R. Global patterns of 16S rRNA diversity at a depth of millions of sequences per sample. Proc Natl Acad Sci U S A. 2011 Mar 15;108 Suppl 1(Suppl 1):4516-22.
Fuks G, Elgart M, Amir A, Zeisel A, Turnbaugh PJ, Soen Y, Shental N. Combining 16S rRNA gene variable regions enables high-resolution microbial community profiling. Microbiome. 2018 Jan 26;6(1):17.
Schirmer M, Ijaz UZ, D'Amore R, Hall N, Sloan WT, Quince C. Insight into biases and sequencing errors for amplicon sequencing with the Illumina MiSeq platform. Nucleic Acids Res. 2015 Mar 31;43(6):e37.
Langille MG, Zaneveld J, Caporaso JG, McDonald D, Knights D, Reyes JA, Clemente JC, Burkepile DE, Vega Thurber RL, Knight R, Beiko RG, Huttenhower C. Predictive functional profiling of microbial communities using 16S rRNA marker gene sequences. Nat Biotechnol. 2013 Sep;31(9):814-21.
Wemheuer F, Taylor JA, Daniel R, Johnston E, Meinicke P, Thomas T, Wemheuer B. Tax4Fun2: prediction of habitat-specific functional profiles and functional redundancy based on 16S rRNA gene sequences. Environ Microbiome. 2020 May 18;15(1):11.
Gordienko EN, Kazanov MD, Gelfand MS. Evolution of pan-genomes of Escherichia coli, Shigella spp., and Salmonella enterica. J Bacteriol. 2013 Jun;195(12):2786-92.

In my experience, the primary impetus is number 3 on your list, but it's also related to number 1. There's a lot you can learn from 16s sequencing, but reviewers want functional data that can help elucidate causal mechanisms. 16s is mostly limited to providing information about the taxonomy of a community. While there are ways of "predicting" the functional capacity of a metagenome from 16s sequences, like PICRUSt, these approaches are reliant on a some shaky assumptions that are baked in to the predictions. This is where it relates back to number 1 on your list. When I was doing my first 16s run on a 454 platform, I recall reading about different E. coli isolates that could have identical 16s genes but genomes that shared less that 50% sequence similarity (don't have source on hand, but will edit post if I find it). So, effectively two strains with identical 16s genes could have substantially different functional capacities, and there's only so much a prediction algorithm can do with that.
Another big driver is the lower cost and improved efficiency of newer sequencing technologies and bioinformatic analysis pipelines. The cost of getting a plate of 16s sequencing done ten years ago was probably comparable to the cost of doing as many high-quality shotgun metagenomes today.

In addition to the points raised in the other answers, organisms like bacteria frequently engage in horizontal transfer of genetic material.
This means that the relationships between organisms are more complex  than the relationships between the stable core elements like ribosomal RNA (see, for example the mosaic genome of Rickettsia felis). Focusing on only 16S rRNA thus gives only part of the story and can be highly misleading.

But horizontal transfer never affects ribosomal RNA, which is why it is suited for phylogeny. However as the poster doesn’t say we don’t know whether that is what he is talking about, and it would be better to ignore his question until it becomes worth answering.

@David My point is that phylogeny itself can become a fuzzy notion for microbes. I've added a linked example to illustrate the point.

@David: HGT does seem to affect the 16S (not at as high a rate as other loci, of course). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC296235/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4558861/, https://www.frontiersin.org/articles/10.3389/fmicb.2017.02225/full

I think that the HGT fuzziness is a good thing to keep in mind, however this is not really solved by shotgun metagenomics! You are still kind of trusting the central tendency of the tree for each gene independently.

Other answers are excellent by and large.
One point that is left out: 16S copy number itself varies among organisms, which leads to significant analytic complexity for trying to really estimate relative organismal abundance.
As this is the main use case for 16S analysis (using relative 16S OTU/whatever abundance to describe communities), you can see that there are issues with it.
You can still likely learn something from e.g. distance analysis between samples, PCoA plots, etc. Different communities will still look different by these measures. But the copy number itself is not directly interpretable.

This is a good and necessary addition to the existing answers. An important caveat to 16S

"As this is the main use case for 16S analysis…". Really? What is your basis for saying that? And please don't use terms like "use case" that are borrowed from computing science where more straightforward English would be more accurate and more comprehensible to biologists.

@David As someone in the field, I can affirm Maximilian’s statement that 16S amplicon sequencing is most commonly used to estimate species relative abundance in environmental and host-associated samples. Though if you have insight into it’s historical use for other analyses, I think that would be good to add.


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Explain why bones cannot undergo interstitial growth as cartilage does
I got a question from a textbook <<Seeley's Anatomy & Physiology Twelfth Edition>> that does not have an answer at the back of the book (only odd numbered questions do have an answer and this question is even):

Explain why bones cannot undergo interstitial growth as cartilage does.

i can only think of two reasons:

In bones, calcification causes the chondrocytes to die, so cartilage cannot form in the bone, leading to no interstitial growth in the bone.

Cartilages are usually only found at the tip of the bones, so its growth can cause the bone to lengthen, which is interstitial growth.

I got a nagging feeling that there is got to be more. Did i miss any other reason? (Also are my reasons correct?)

While mature cartilage is solid, the extracellular matrix secreted by chondroblasts during cartilage formation is soft enough to allow for both cell division and tissue expansion. This is interstitial growth.
As the matrix hardens, secretion and proliferation slow down and then stop altogether. Isogenous groups are a testimony of the last cell divisions before the surrounding matrix turns solid. From this point on, further growth can only take place by apposition, i.e. new cartilage matrix is secreted by chondroblasts found in the perichondrium.
Bone matrix becomes mineralized (and therefore very hard) soon after its organic components are secreted by osteoblasts. Osteoblasts that get trapped in the matrix shrink and become quiescent. Thus, there can be no expansion from within, i.e. no interstitial growth.
Bone grows exclusively by apposition, where further osteoblasts differentiate from precursors and deposit new matrix on top of the existing bone.
While this is the answer to the original question, your tentative responses suggest that you need to do some further reading. You seem to refer to the interaction between the two tissues during endochondral ossification, which is a separate, more complex topic.


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Why don't we use hybridization instead of PCR?
So, I would like to ask, why don't we use just DNA hybridization instead of PCR primer amplification to diagnise some illness?
I know, when you have a really small amount of DNA from virus or cell you need to amplifie it, so you can do some hybridizations. But I cannot find out, why you need to amplifie it when you have like 10 ml of substance, where the amount of cells or viruses can be really high.
For instance, when you are trying to diagnose some chromosomal aberation you don't amplifie the DNA, so you do just hybridization, but when you are trying to detect coronavirus you use PCR, why?
I have all the information from Genetics by Eduard Kočárek (Scientina 2008) - so now you know the literature my question is based on.

Could you be more specific about what you mean by "hybridization", e.g. Southern blot? I can assure you that Southern blots are extremely slow and laborious compared to PCR (1-2 days vs. 1-2 hours), more of the time is hands-on work, the technique is more difficult, and Southerns generally involve radioisotopes, which are complex to work with. https://blog.addgene.org/evolution-of-lab-techniques#:~:text=Whereas%20Southern%20blotting%20is%20labor,time%20and%20resources%20(3).

I’m afraid you really need to do some more reading and then edit your question so that it addresses the use of PCR in the diagnosis a specific disease or disease agent. Without that we can’t answer sensibly, as different diseases are diagnosed in different ways.

To add to the other excellent comments, think about what exactly you mean by "diagnose some illness". For example, looking for a genomic chromosomal aberration is very different than trying to determine what bacterium is present. What factors might vary between different types of diagnoses?

From comment.
Could you be more specific about what you mean by "hybridization", e.g. Southern blot? This is the old-fashioned technique that I believe is closest to what you mean. Slot blots are also possible but somewhat less interpretable.
Both are still used occasionally for various reasons but each is much, much more work than PCR. Southern blots specifically are extremely slow and laborious compared to PCR (1-2 days vs. 1-2 hours), more of the time is hands-on work, the technique is more difficult, and Southerns (also slot blots) generally involve radioisotopes, which are complex to work with.


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Why are we more sensitive to green light when 65% of our cone cells are red cone cells?
I read, "human eyes are most sensitive in 555nm which is green. Human eyes are more sensitive to green than to red, and in low-light conditions even more to cyan than to green."
But it doesn't explain: Why are we more sensitive to green light when 65% of our cone cells are red cone cells?


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Is it possible to assert who is the parent/child by looking at DNA sequence only?
Suppose I have whole genome sequences for two people of the same sex. I know one person is the parent of the other, but I do not know who is the parent and who is the child. Is it possible to determine with certainty the direction of descent using the sequencing information alone? Assume that the individuals were sampled at the same age so that you can't tell parentage from telomeres or other age-related markers.

Isn't this the same as asking if DNA testing can identify parentage? (I think you know the answer to that) And isn't this assuming that the genetic material somehow survived for longer than the Carbon 14 did?

@DKNguyen I don't think it is the same, no. I don't care to look if they are relative here, I care to know which one engendered the other, only by looking at their genes. And yes, it is by assuming I have the full knowledge of both genetic codes. I picked 100 k years as an example to remove C14 possibility out of the question, but if you prefer, make it, say, 5000 years ago or even a decade ago (but then please don't cheat using C14 :) ).

What do you mean by 'only looking at the chromosomes'? Staring at them down a microscope? Sequencing them?

@AccidentalBismuthTransform I've edited your question for clarity and to incorporate the information from the comments. Feel free to roll back my edits if you feel they change the spirit of your question.

Take a chromosome of individual A. For each gene check if an identical copy is found in individual B. If it is the case then B is the parent of A.

@rerus if the gene is identical in both, why does that rule out A being the parent of B?

@swbarnes2 B is the parent iff for one of two chromosomes 1 of individual A, all the genes alleles are found in B. This is a naive model due to intragenic crossover, mutations, and mitosis crossover, so you'll need to compute a B->A inheritance score for each chromosome of A.

My main source is https://www.ncbi.nlm.nih.gov/books/NBK21438/ "Mitotic crossing-over is rare" as it is the main thing that can mess entirely what I'm saying.

If one chromosome is identical between A and B, how can that possibly distinguish anything at all between them?  If two students in a class turn in identical papers, how is that evidence that A must have copied from B, and that B could not have copied from A?

@swbarnes2 ... meiotic crossover
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC4353236/ https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC3478297/

@reuns I had to read your comment twice to realize what you mean and that you are right and swbarnes2 just didn't understand you. It would recommend you to turn your comment into answer with diagram. The point is that one chromosome in A is identical to parts of two chromosomes in B. This is not a symmetrical pattern. Another way to look at it is that out of 4 homologous chromosomes involved 3 have at least some part not identical to anything. Problem with this approach is that with current methods we can't get full chromosome haplotypes.

If A is XY and B is XX, if A is the parent, A should pass on their X chromosome intact to the offspring.  If B is the parent, than the X chromosome A receives would have undergone crossing over with B's other X chromosome before being passed to A.
Otherwise, I don't think you could do it from sequence alone.
I guess if the circumstances were right, you could include haplotpye information, and you could tell; if one person had top to bottom haplotypes only found in China, and the other was half Chinese haplotypes and half African haplotypes, the simplest explanation is that the person with one ethnic origin is the parent, and the person with two is the offspring


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Evolutionary advantage of the nutrient played by the chicken
What is the evolutionary advantage of the chicken throwing out so much nutrient ovulating all the time?
Is there a clear advantage to this? Chickens ovulate all the time for the same reason human females do, when the egg is not fertilized it is discarded, in the case of the hen it lays an egg, in the human case menstruation occurs. This is due to the rhythm of reproduction of each species, if the egg is fertilized, it is an advantage that it can fertilize all the time.

First, most chickens will not naturally lay an egg every day. (I raised hundreds - yes, hundreds - of chickens.) It varies, with some breeds (selected over many decades, some hundreds of years) being "heavy layers" and others absolutely not. Also, artificial light and heat is needed to produce eggs year round. If there are roosters around, trust me, almost all (if not all) of the eggs will be fertilized. I used to hatch out my own chicks from fresh eggs collected in no particular manner. I never had a dud. Today's commercial and farm chickens are not the "originals".

@anongoodnurse in the end is it useful to lay a lot of eggs by artificial selection, in short?

Be careful you aren't doing something akin to asking what the evolutionary advantage of a seedless orange or grocery store banana is.

It is useful to humans selling and buying them for chickens to be forced to lay eggs every day, yes. Does that take a toll on chickens' lives? Yes, a great toll. My chickens did not lay eggs every day, and were not killed when production decreased. In return for having been selectively bred for egg laying, and doing so for me, I gave them a good life. I did not force them to lay eggs in any way.

@DKNguyen but seedless fruit only exists transgenic, no?

@Behemooth Not transgenic. Seedless fruits are a naturally occurring mutation that would have otherwise died out but was found and artificially propagated. Think about it...what organism would you even get a seedless gene from to insert it into something to begin with?


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I found this tiny transparent creature in my aquarium - what is it?

Please help me identify this 1-2 mm nearly transparent animal which I found in my salt water aquarium.

Can you give some kind of indication of size, is it a freshwater or salt aquarium?

Can you say also if it's moving or not, is there any sign of a rudimentary (presumably transparent) shell? (I'm thinking freshwater limpet, but the symmetry may not be right).

Hi.. It may be in 1 Or 2 mm and i just 2days back only bought the aquarium and filled with salted tap water.. It's moving and it's walking with it's legs by walls only.

It's very transparent like water..

Oh, those things are legs, that's a whole different thing. Now I'm thinking some kind of arthropod, perhaps a parasite, will look into it.

I thought it might be a turtle or crab

I moved it small glass jar today morning only. Can I put it ian that har for some days.. Do you have any idea approximately how many days it will takes to find out what it would be...

with a good picture i could tell you what it is right now,please take a better picture by turning off the light in the room so only the water in the tank is lit and be sure to focus the camera properly.

Welcome to Biology.SE! Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible); 2) the location (e.g. country and region — the more specific the better) where you observed this organism; and 3) an estimate of the size of the organism. Please [edit] your post to include this essential information as comments are ephemeral and so should only be used to communicate about the post. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site.

Initial thought was a Triops species. But your specimen is too small for that. Likely some kind of crustacean.

i had that with my tropical fish, i found 2-3 it wasn't too much of a contagion though it was not good.

Now THAT is a fish louse in the Argulidae family. They are bloodsucking parasites that attach themselves to fish with those round suckers near their head and feed with needle-like mouthparts. Needless to say, I'd advise you to find and eliminate as many as you can, as they'll be harming your fish with their bites.

Time to him read on all the fish parasites that affect common goldfish and tropical fish and see what to be wary of.


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Are fully vaccinated people more likely to not get infected at all with COVID-19?
I've found some papers which describe that the viral shedding does not decrease during infection (for fully vaccinated people). But the overall shedding time does decrease. Therefore it is possible to say, that the vaccines could have a positive effect on the whole pandemic. (They lead to a reduced spread of the disease.)
My question is now: are vaccinated people more likely to not get infected at all?
I've read that the vaccines lead to a shift from severe cases to mild cases, but is there evidence that the vaccines can actually protect people from getting infected?
If someone knows more, could you provide me a source?

You need to define "not get infected at all" more precisely.  Being vaccinated does not stop the virus from entering your body, and may not prevent some of your cells from being infected. However, it (almost always) ensures that enough targeted anti-viral molecules and cells are circulating in your body that they can quickly clear virions and infected cells, resulting in no noticeable illness.

@Armand Wouldn't it be safe to assume he means not get an active infection?

The CDC puts the rate as 5x more likely to be infected if unvaccinated: https://www.cdc.gov/mmwr/volumes/70/wr/mm7037e1.htm

@Armandt, its hard to come up with a definition. But than I would say something like "not beeing able to infect other people, because the virus is not able to increase within the host."

Yes, this is the effect of the vaccine. A reduction of infections of over 88%, a reduction of severe cases and death by 95% and higher. See reference 1 for the details. Data from the ReCoVAM Study from Malaysia (unfortunately only not yet published, so see here) shows a reduction of infection by 88% and a reduction of admission to ICU/death by up to 96%. So yes, the vaccination works pretty well.
Although symptomatic cases have a comparable viral load in the first four days of their infection this decreases very fast after day four. The figure below (from reference 2) shows this nicely.

The curves show the Ct-values of the PCR from infected patients. The Ct value is the cycle at which the PCR machine can detect a signal from the amplification reaction for the first time. Due to the nature of PCR, the Ct value is inversely proportional to the log of the amount of DNA set into the reaction. The lower the Ct value (the fewer cycles to first detection), the higher the amount of target DNA originally in the sample.
Please note that this comparison is done by PCR and does not give any evidence how infectious the virus from vaccinated people really is. There is evidence (unfortunately from an underpowered study, so results should still be taken with care) that the viruses coming from symptomatic vaccinated people are not as infectious as from unvaccinated persons. See reference 3.
References:

Impact and effectiveness of mRNA BNT162b2 vaccine against SARS-CoV-2
infections and COVID-19 cases, hospitalisations, and deaths
following a nationwide vaccination campaign in Israel: an
observational study using national surveillance data
Virological and serological kinetics of SARS-CoV-2 Delta variant
vaccine-breakthrough infections: a multi-center cohort study
Longitudinal analysis of SARS-CoV-2 vaccine breakthrough infections
reveal limited infectious virus shedding and restricted tissue
distribution

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


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homologous recombination and non-homologous recombination ratio during S-phase
Can I assume that it is easier to do targeted gene knock-in in rapidly dividing cells because they should have a short period of G1? Is there an easy way to measure the relative amounts of homologous recombination (HR) and non-homologous end joining (NHEJ) during the S and G2 phases? Is HR favored over NHEJ during S-phase for all cell types?


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What evolutionary advantage do separate teeth have compared to a single piece of bone?
Humans and many animals have multiple teeth consisting of separate pieces of bone embedded in the jaw. For humans, this arrangement has some disadvantages:

teeth are quite fragile when impacted and break easily
gaps between teeth are difficult to clean and risk decay

Why don't we have a single piece of bone in our mouth (possibily with an uneven surface to aid crushing food)? Is there any evolutionary advantage to having multiple separate teeth, or does it simply not matter because by the time problems arise we have already reproduced?

teeth are used to crush bones,so they are significantly stronger than any of the bones in the body.

When discussing evolution, it's important to remember that forces of selection work by affecting reproductive fitness, i.e., the viability and number of offspring. So yes, as you point out in your last sentence, likely our teeth work well enough for us because their potential drawbacks don't significantly affect reproductive fitness. Also, as a matter of theoretical exercise, there is likely a redundancy benefit to having multiple teeth - if one is diseased, the others are still usable. I also wonder if there are any animals that do have one single bone as you describe.

Consider that many animals (sharks, for instance), have teeth that are continuously replaced.  So a better question might be to ask what caused humans (and I think most mammals) to lose this useful trait?

One broken tooth doesn't really affect the strength of the others.  A crack in a single long tooth would damage the structural integrity of the whole chewing surface.

There are significant differences between teeth and bone, for example teeth are much harder than bone, teeth are replaceable, teeth are directly exposed to the outside environment, not covered by tissue, and so forth. Perhaps some more research into teeth would be useful.

@Armand i know there are differences. My question was maybe a bit unclear. I didn't want to ask why there are teeth instead of bones, but why there are multiple teeth instead of one large spanning the entire jaw. Besides, parts of teeth (dentin, cementum) are not that different from bones. I never questioned the presence of the harder parts (enamel).

That would be a hell of a root canal...

@jamesqf Mammalian teeth are like mammalian hearing: sacrificing long term regeneration for short term performance because breeding is the only thing that matters,

You should check and see if an question has been asked before you post https://biology.stackexchange.com/questions/104682/what-evolutionary-advantage-do-separate-teeth-have-compared-to-a-single-piece-of/104721#104721 and https://biology.stackexchange.com/questions/8302/what-is-the-evolutionary-reason-behind-the-fragility-of-teeth/53692#53692

@DKNguyen: But it's difficult to see any short-term performance benefit from not replacing teeth.

@jamesqf I think I read somewhere it might have something to do with the specialization of teeth in mammals. They work better but their arrangement and alignment matters more.

It also has some advantages, although some of these have been mostly lost in humans.
In sharks for example teeth get continuously replaced, so losing one is much less of deal for them. This true in reptiles too, e.g. a lowly gecko can have 1,000 new teeth their lifetime. (The more technical term is polyphyodont.)
It is somewhat of a mystery why mammals lost most of this ability, but it is thought  to be related to the specialization in the shape of the teeth. Species that have little differentiation between teeth [types] are most prolific at replacing them. (I guess you're ware that humans get two sets, but this is driven by age rather than by a loss process.) There are few polyphyodont mammals as well: elephants, kangaroos, and "sea cows".
Being able to replace teeth in smaller increments (i.e. individual teeth) is probably an advantage as at any given time only a small proportion would be missing... although as with other things in evolution there are some exceptions. Piranhas actually have quadrant-fused teeth (which basically act like larger serrated knives)... and they replace them in whole quadrant increments. (They also grow the replacements in such a way that it takes only about a day for the new set to replace a lost quadrant.) However this is almost certainly energetically expensive, which is probably why few other species have this feature.

i know there are differences. My question was maybe a bit unclear. I didn't want to ask why there are teeth instead of bones, but why there are multiple teeth instead of one large spanning the entire jaw. Besides, parts of teeth (dentin, cementum) are not that different from bones. I never questioned the presence of the harder parts (enamel).

For one thing, multiple teeth can adjusted individually for wear and alignment.
However that clarification in the comments conflicts with with points in your question which could be construed intended as the argument against teeth of any kind, singular or multiple, especially singular.

teeth are quite fragile when impacted and break easily
gaps between teeth are difficult to clean and risk decay

Can you imagine what would happen if your ONE tooth broke or decayed?