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Codons at for transcription vs translation
Why are start and stop codons present at translation level but not at transcription level? And how will I obtain a protein at transcription level?
Thanks in advance

After transcription, you don't get a protein but an mRNA. Is this unclear to you or is something else unclear to you?

@Remi.b Ya that's unclear too :(. Why is that the case? And why aren't any start and stop codons present at that time? Thanks

It is hard to know how many things are unclear to you from your question. Hence, the best anyone can do would be to write a whole introduction to the so-called "central dogma of molecular biology", which makes your question too broad, IMO. Plus, many such introductions already exist online. For example, have a look at Khan Academy, wikipedia or many other source of information.

Codons are only meaningful for translation, since that is when the nucleo-based DNA/RNA sequence information is translated into a protein sequence based on the triplet code. Before that step codons don't really have 'meaning'.
During transcription the start & stop codons are already present, but they are ignored by the RNA polymerase, because it works on a single base at a time.
The equivalent 'start' and 'stop' signs for transcription are promoters and poly-adenylation-sites (at least for eukaryotic mRNA). Both are recognised by additional proteins, that help regulate transcription:

transcription factors bind the promoters on the DNA and recruit RNA polymerase to that site so that transcription can start
poly-adenylation-site are specific sequences that lead to the addition of the poly-A tail to the nascent mRNA. This process also leads to termaination of transcription, however the exact mechanism isn't quite clear.

Thanks a lot. It cleared a lot of my concepts. I just have one more specific question. I am given a particular DNA sequence. What will be the mRNA molecule as a result of transcription of that DNA segment?

I hope the question is clear. Please help. I'll be grateful to you!

The mRNA that binds to a template strand will complement the template. For the sequence AATC, the mRNA will be UUAG (remember that in RNA, uracil is used instead of thymine)


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How different is breathing in wildfire smoke in urban areas compared to sitting by a campfire for a night?
The air quality in the Bay Area is currently the worst in the world, due to the devastating Butte County wildfires. I understand smoke inhalation can cause inflammation and respiratory issues, especially with chronic exposure, but I'm wondering in actuality, how different is the exposure to wildfire smoke in urban areas (AQI 100-300) over the course of a few days, compared to sitting by a campfire for a night?

I'm voting to close this question as off-topic because it is not about biology in terms of SE Biology, but about air polution.

The effects of air pollution on the human body seems like biology to me. Plus, it is topical and relevant to every person who has ever been camping. I think it is an interesting question that I would like to know the answer to.

Generally one sits upwind of a campfire, so as not to breathe the smoke.  And if the wind shifts, everyone moves :-)

source: Stack Exchange

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

sort: votes


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Why do we have nerves in our teeth?
Toothache is a useful signal to us as we can visit the dentist who can try to fix any problems with our teeth. But what is the natural biological role of toothache? Does toothache make animals take action that helps them to deal with their dental problem?

Why do you think this is different from pain anywhere else? (that is, could your question be simply "why is pain useful?")

@BryanKrause teeth really due have a unique problem with pain, because for the most part they do not heal.

Because your teeth evolved as a sensory organ.
The material teeth are made of evolved first in placoderms, it existed to sense the electrical current in the water around it, so it has to form around a nerve. in modern animals the nerve mostly functions in sensing stress and thermal stress on the tooth.
And because mammals are weird.
Teeth did not evolve to be permanent, they evolved to be lost and replaced, that is what everything that is not a mammal does. So having a nerve was not a big disadvantage (in say, reptiles) since that nerve would eventually wither and die as the tooth was lost. toothaches were not permanent they were a temporary irritation, and served do dissuade any behavior that caused them, like trying to eat food that was too hard, it was little different than the pain of thorn telling you not to grab sharp things.
Mammals are unique in retaining their teeth throughout their life so now a system shaped by evolution to be temporarily has been dragooned into something permanent. So now what would be a temporary irritation becomes a permanent thing when the tooth is damaged in mammals. Worse permanent teeth means things like stress on the teeth is even more important since you are stuck with damaged teeth so mammals actually make the nerves bigger. The addition risk of a toothache is not an issue because mammals are stuck with that risk anyway because they retain the tooth. The earliest mammals did not have long lifespan so the risk of a debilitating toothache was minimal, however we their descendants live for decades, so a structure evolved to last a year or two now has to survive for decades and it just fails sometimes. Evolution can only change what it has it cannot throw out a problematic system and start over from scratch, so it often gets stuck with such haphard thrown together solutions (kluges) And we unfortunately have to pay the price in this case

Abscesses happen easily in teeth and they are close to the sinuses and the brain. It's important for animals to be wary of permanent tooth damage and abscesses that can lead to death.
Good teeth are crucial for survival and reproduction, to avoid starvation. Nerves prevent animals from being careless with their teeth.
Teeth get chipped from cracking nuts, seashells, marrow, hunting, fighting, kocking a slack jaw, gritty food.
The nerves are pretty well tuned to guide the mammal for safe and proper use of his teeth.

I would guess that humans and "smarter" animals (animals with strong cognition, culture learning etc.) figured out that some kind of oral hygiene and diet helps against toothache. However, it turns out that apparently animals don't get tooth decay and don't need special oral hygiene.
In any case, nerves in teeth cause pain when a tooth breaks. This allows animals to develop an avoidance response in the future: "This kind of nut/bone/bark/root/seed/whatever may seem tasty, but chewing it last time hurt for a long time. Avoid it." It might even prevent any broken teeth in the first place if chewing starts to hurt. As @BryanKrause wrote in the comments, it serves the same purpose as pain anywhere else.

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


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Can anyone tell me what type of fish this is?
Notice the reflective patterns on its underside.  I think it must be a deep water fish.  It was found washed up on the ocean sand in Myrtle Beach, South Carolina (USA) after a hurricane.

Not an expert, but an online search for bioluminscent fish led me to a bioluminescent toadfish called Porichthys porosissimus. The ventral angle of your specimen looks a lot like the photos I could find...

 Source: Robertson, R on Fishbase
Like many midshipman fish, P. porosissimus have photophores (those dots in your specimen) that glow to attract prey:

 Source: W. Ward (Rutgers Center for Research and Education in Bioluminescence and Biotechnology)

This site provides a sightings map, but some of the points are sort of suspect, so I don't know how accurate it is...


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Open Mass Spec Database
Wondering if there is an open (freely available) database of Mass Spec Data, particularly for the Substances/Compounds listed in NCBI.
Specifically, I am not sure if NCBI includes the mass spectrometry data / datafiles in their FTP server related to any of their chemicals. So I am just wondering if there is an open database of mass spec datafiles out there somewhere.

It's unclear what you are looking for, there are many substances/compounds listed in NCBI. Could you clarify this so the question can be answered?

The Human metabolome database (HMDB) contains many MS/MS and NMR spectra for human metabolites. You can acquire the spectra from the downloads section. The HMDB includes external identifiers for each compound. This includes the PubChem Compound IDs that are given on the NCBI database. There are 2 265 compounds with LC-MS/MS spectra in the HMDB.
The excellent MS-DIAL software package also comes with extensive positive and negative ion mode LC-MS/MS and GC-MS/MS spectral libraries in flat text format; that's also worth a look.
A lot of the raw spectral data is restricted due to multi party agreements (NIST, chemspider).


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Can two different species in the same genus generally succeed in the same habitat?
This plant-care website writes

In the context of plant care, usually most plants within the same genus need the same environmental conditions suitable for plant growth. If the genus of a plant is known, the information can be used to apply the appropriate levels of plant care.

I'm wondering if this is true in general. A more general question would be, if I know that two species are in the same genus, what phenotypical similarities will they have?
So far I've only found that genus classification is based on genetic similarity, but that doesn't say anything about what phenotypical similarities there may be between different species in the same genus.

It is not correct to say that genera are based on genetic similarity. Different lineages diverge genetically at highly variable rates, and there is no set cut-off for what defines a genus. Instead, genera are based on publications, which could be over 100 years old. Genera are not a biologically real category the way species are, so one genus may hold hundreds of species, while another, only one. Most of these genera were defined before molecular data was possible. There are no set phenotypic criteria for the definition of a genus, except that a well-described genus should have at least one fixed character that defines it. So in answer to your question, yes, two species in the same genus (congeners) will often exist in the same habitat. There would be selective pressures to separate them in terms of the niche that they occupy. The publication you referred to is simply a best guess: if you don't have information on the habitat requirements of a species, it would most likely share many similarities with its close relatives. Phylogeny is predictive, but different species in the same genus need not be identical in terms of their ecological requirements.

I don't think you can generalize either way.  For an example, take penstemons: https://en.wikipedia.org/wiki/Penstemon  Hereabouts I can find 3 or 4 species growing in the same conditions, within a radius of 3-4 m.  I can also find other species growing in close proximity but very different conditions, e.g. wet meadow vs dry, rocky slope.


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Why do so many parasites infect definitive and intermediate hosts rather than just one host?
Many parasites infect multiple host species, with one host species being the definitive host (where the parasite reproduces), and the other host species being the intermediate host (where the parasite grows to maturity). (Further details described as "complex life cycle" at https://en.wikipedia.org/wiki/Parasitic_life_cycle ) Why is this complex life cycle so common? Why wouldn't more parasites adopt a simpler life cycle of just one host?
I knew that there were some parasites that infected more than one kind of host species, but now that I am looking into it, it seems like a majority of internal parasites have this kind of life cycle. Does anyone know why?

Several reasons have been proposed.

We suggest that complex cycles in helminths without penetrative infective stages evolve by two essentially different processes, depending on where in the cycle a new host is inserted. In ‘upward incorporation’, a new definitive host, typically higher up a food web and which preys on the original definitive host, is added. Advantages to the parasite are avoidance of mortality due to the predator, greater body size at maturity and higher fecundity. The original host typically becomes an intermediate host, in which reproduction is suppressed. In ‘downward incorporation’, a new intermediate host is added at a lower trophic level; this reduces mortality and facilitates transmission to the original definitive host.

--Evolution of complex life cycles in helminth parasites

Despite these advantages to omitting hosts, the majority of digenean trematodes have a life cycle with three hosts, suggesting strong counteracting forces that maintain hosts in the cycle. Such forces have been proposed to be higher growth and fecundity (Parker et al., 2003), an increased probability of finding a mating partner (Brown et al., 2001), and higher transmission rates (Morand et al., 1995; Choisy et al., 2003; Parker et al., 2003). ... we propose here that maintaining a second intermediate host in the life cycle can be advantageous for the individual parasite to increase the intermixture of different clones and therefore decrease the risk of matings between genetically identical individuals in the definitive host.

--How a complex life cycle can improve a parasite's sex life
Also see The evolutionary ecology of complex lifecycle parasites: linking phenomena with mechanisms.

Thanks for this reply and the great citations. Sorry for not accepting the answer in a prompt manner, but I am accepting it now that I am seeing it. Thanks again!

Alot of lower eukaryotic parasites do infect just one group of hosts and are some, such as malaria, are host specific. Transmission from host to another is not trivial for a large infectious agent and no parasitic agent is associated with aerosol transmission.
In this case, malaria, leishmaniasis, African sleeping sickness amongst others, a vector is required.
Even schistosomiasis, may similarly be viewed as using vectors (snails), so the definitive host, whilst it certainly happens for example Toxoplasma gondii, it is less frequent than widespread than you are inferring in my opinion.

I assume that by internal parasites you mean animals like tapeworms etc?
They can infect several species simply because they are not picky. These parasites do not rely on precise molecular hijacking mechanisms like intracellular parasites (e.g. Apicomplexa).
All they need is a certain amount of heat and humidity (which any host provides) and food pre-digested by the host, which is essentially the same for host species that share the same feeding habits, so there is no reason a priori for them to have a narrow range of hosts.

I've rewritten the question to make it more clear. I am interested in why there is such a common pattern of having a specific complex life cycle of definitive and intermediate hosts. I was thinking this looked more common in what I call "internal" parasites (i.e. endoparasites, like tapeworms, protozoa, etc.), but the question really goes for any parasite with that complex life cycle. (P.S. I apologize for the delay. I guess I shouldn't have posted the question just prior to traveling for Thanksgiving.)

This answer does not have any references, misses the point of the question, and suggests lack of familiarity with parasitology. Many multicellular internal parasites have specific host tropism, corresponding to specific life cycle stages.

In fact, a lot of parasites are very specific. Stating something as general as "They can infect several species simply because they are not picky." is, at best, misleading.


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Are bears related to dogs in a similar way to how cats are related to 'panthers'?
I've tried searching on Wikipedia but I couldn't find what family dogs belonged to. Ursidae is 'bears' and Canis is 'dogs' ; Panthera is big cats like:- tigers and jaguars is what I know.

You will be interested int he ressources from the post The best free and most up to date phylogenetic tree on the internet?

No, because panthers are cats, but bears are not dogs. You can see their phylogeny in a figure from one of my papers here: https://www.researchgate.net/figure/Most-likely-phylogram-derived-from-the-Bayesian-Analysis-ln-533753675-Numerals_fig1_6550244
As you can see, Bears are most closely related to pinneped (seals and sea lions), with dogs as sister to that group.


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How to calculate the turnover number?
I understand that Kcat (turnover number) = Vmax/total enzyme concentration.
However the formula I have been given is Kcat = specific activity/molecular mass of enzyme.
What is the relationship between these two different formulas - why do they give the same answer?
Definition of Kcat that I am using: specific activity * molecular mass of the enzyme
Specific activity = units of enzyme/ mass of protein in mg

Are you sure your formula refers to the molecular weight of the enzyme, and not the total mass of enzyme in the reaction? It would be helpful to post a copy of the question you are working on.

@J-- I've uploaded the formulae

Please do not upload text as images. It is impossible to index and it discriminates against people with sight defects.

Yes, and especially don't post images of sideways text.

Do not post images as questions. There cannot be indexed by the search and pose problems for persons with sight problems. Please correct this to avoid closure and subsequent deletion of the question.

Let's do some unit analysis:
$\pu t$ = time
$\pu U$ = units = $\mathrm{mol_{product}/t}$
$\pu s=$ specific activity $\mathrm{= U/g_{protein}}$
Therefore:
$\mathrm{s = mol_{product} / (g_{protien} \times{t})}$
Your sheet says:
$\mathrm{k_{cat}= s \times MW_{protien}}$
And we know that:
$\mathrm{MW_{protein} = g_{protein} / mol_{protein}}$
Substituting definitions of specific activity and MWprotein:
$\mathrm{k_{cat}= mol_{product} \times g_{protein} / (g_{protien} \times t \times mol_{protein})}$
$\mathrm{k_{cat} = mol_{product} / (mol_{protein} \times t)}$
Cancel out the molar terms:
$\mathrm{k_{cat} = t^{-1}}$
This yields the correct unit for kcat ($t^{-1}$). You can think of this as the number of product molecules formed per enzyme molecule, per unit time.


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mRNA bonding to itself
Does a mRNA molecule bond to itself? I heard that only tRNAs have hydrogen bonds that let them have second structures, but after searching the web i found multiple answers. If yes, does anybody have a credible reference for that?(books, articles etc.)

Welcome to SE Biology. Please quote the source of the extra-ordinary and incorrect statement you quote. This will better allow us to help you. Often students misunderstand the subtlties of a statement and misquote — carefully writing out the quote often makes this obvious or allows us to explain the misunderstanding.

It is very common!
Let's have a look at a few examples.

In bacteria, a lot of the genetic expression is regulated at the mRNA level. Certain mRNAs can form complex secondary structure that prevent or allow translation, and can switch from one structure to another based on the presence or absence of a signal molecule. These structures are called riboswitches; a very well-described example is the riboswitch regulating the expression of genes responsible for the biosynthesis of tryptophan.
For more details see this short article or this one.
Some mRNAs include internal ribosome entry sites (IRES), usually just upstream of coding sequences in mRNAs that code for several distinct proteins (polycistronic RNAs). IRES are highly structured RNA structures recognized by ribosomes that allow translation to start at a point in the middle of the mRNA. They are very widespread, especially in viral genomes. You can find a detailed explanation in the case of viral genes here:
In eukaryotes, mRNA molecules undergo a maturation process called RNA splicing that results in the excision of unnecessary internal sequences. During splicing, the mRNA forms a loop and a covalent bond is created at the future junction point; this bond is very transient but absolutely necessary for mRNA maturation and correct gene expression. See here for more explanations.
What about engineered RNA molecules? Self-hybridization of mRNAs is very useful in biological engineering. People reprogram riboswitches and IRES, but also use very useful tools based on mRNA self-binding. For example: based on a similar principle as the riboswitches, the transcription starting site can be masked by articificially introducing a (fairly simple) secondary structure called toehold switch that hides the ribosome binding site; however when a competing RNA sequence (which nature is specified by the sequence of the toehold) is present it opens and binds a part of the toehold, thereby making the ribosome binding site available for gene expression. This website shows an explanation and a real-life application of toehold switches for diagnostics.

These are only a few examples of mRNA self-binding processes; all of these have been extensively studied and are well described in many articles and books. There are many others types of self-hybridization in mRNA, and in pretty much all other types of RNAs too!


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GC content of a protein-coding region
I have computer science background and I am trying to understand the equation below.
The average value of the G + C content of a protein-coding region is
given by :
(G+C)=  $\sum_{\alpha} (I_\alpha *f _\alpha$ )/3
$I_\alpha$ = Maximum number of nucleotides C and G that appear in one of the
synonomous codons for given amino acid
$f_\alpha$ = Frequency of amino acid α.
Where does the 3 in the denominator come from ?

Each codon codes for one amino acid and every codon contains 3 nucleotides.


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What is the term for a given interpretation of a fossil record?
There exists a term, that I have heard and forgotten it appears, for taking a described species in paleontology and creating a version of what it was like in life.
For example, a prior [insert this term here] for T Rex had it upright and dragging it's tail, while a more recent [insert term again] has shown a much more horizontal and rigid body plan.
I know you 'describe' it formally when you identify it from remains, and 'mount' when you set up a specific set of remains. But what is it when you interpret those remains to a specific form?

Realization? Re-creation? Interpretation? Depiction? Illustration? Imagination?

The term you are looking for is reconstruction (as in
Forensic facial reconstruction).
You can find it used on the wikipedia articles for Fossil cave and for Transitional fossil or in the post In reconstructions, how are various shapes of facial features determined from skull only? for examples.


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How does axon guidance system precisely targets specific axons?
Axons find their way to the terminus by responding to axon guidance molecules (AGMs) that attract and repel growth cones or make them stir. This I understand.
Through a very specific combination of AGMs, a precise path can be layed out that an axon cone will follow even across half the brain. This I also understand.
What I don't understand is that in developing brain, there are millions of axons moving to their termini at the same time, and millions of AGMs released all over the brain. When an axon departs on a journey to reach an AGM at the opposite end of the brain, it will probably pass by thousands of other AGMs and yet ignore them all.
When an AGM is released, there are like thousands of neurons nearby, and yet they all will ignore it but some single neuron across the brain will reach for it.
I can think of two possible explanations:

There are unique AGMs for every neuron that no other neurons will
follow (but it doesn't seem to be the case).
There are somehow very specific instructions wired into EACH neuron aka ignore five netrins, then follow the sixth, then ignore two more, and then follow the ninth one till you reach it (but how is it possible to program every neuron in the brain like that?).

So, how does it work in reality?

In a nutshell, I would say neurons do have "specific instructions."  However, it isn't so much "ignore netrin X amount then stop."  It's more like "express receptors 1, 30, 48, and 62" which as a unique combination gets the growth cone where its going and prevents it from forming an erroneous connection along the way.  I've provided more context below that might help this make more sense.
A number of factors come into play with proper axon pathfinding and guidance, but I think the two below are sufficient for this:

There are different receptors present or absent on the cell surface depending on what cell type it is, which allows different cell types to respond only to specific cues. However, most developing axons express multiple types of receptors, so they can respond to multiple guidance cues (or respond to a cocktail of different cues).
There are non-diffusible signals present along the path in which the axon is growing.  You can read about one type here: https://www.nature.com/articles/nn.2231.  The main point about non-diffusible cues is that they can either stabilize the growth cone (which might promote growth or initiate the formation of a synapse) or they can repel the growth cone.  Therefore, they play an important role in informing the growth cone what is and is not the proper target.

There are now two things from your question should bring it all together.  First, you state that the precise path comes from a "specific combination of AGMs."  Exactly! The key word here is "combination."  Because there are so many AGMs that can affect the growth cone in so many ways, the combination of receptors (and intracellular secondary messengers) expressed on the growth cone and how they work in concert is what's critical.  Second, you state that growth cones will "ignore" potential targets as they pass them by.  That might sort of be the case (i.e., if a growth cone doesn't have a receptor for something the target is expressing, it won't "grab onto" or respond much to its presence).  However, it may also be that these potential targets express some non-diffusible cue that repels the growth cone, and it doesn't recognize that spot as a its final destination.
This article can also help provide more insight on the nuances of axon guidance:  https://dev.biologists.org/content/145/10/dev151415.long


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Do green algae form obligate symbioses with fungi?
I understand that obligate symbioses means that the two organisms cannot live without each other and are in a symbiotic relationship, but do green algae from this with fungi?

Yes, Lichen are composite organisms of green algae (or cyanobacteria) living togther with fungi.
In most cases the fungi-part is completely dependent on that symbioses and is completely dependent on the symbiosis. For the algae it seems that some species can survive on their own, but not necessarily in the same enviroment as the lichen, while other species may again be completely depedent on the symbiosis (see also the comments).

The wiki page you quoted states "The photosynthetic partner [so the algae] can exist in nature independently of the fungal partner, but not vice versa." That contradicts your answer, don't you agree?

@RHA, this quote does indeed contradict my takeaway from the part/quote is was focusing on: "Although some photosynthetic partners in a lichen can survive outside the lichen, the lichen symbiotic association extends the ecological range of both partners, whereby most descriptions of lichen associations describe them as symbiotic". I guess for the algae/cyanobacteria it really depends on the exact species and environment whether they'd be able to survive on their own.

It seems that way, but it might also be unknown. Maybe add some doubt to your answer?

@RHA I (hopefully) clarified it a bit


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Is it possible to grow brain tissue in vitro? Can we make a super-brain this way?
I wonder whether such experiments were conducted? Is it possible to create a "biological super-computer" this way?

Hi, this is John from the ethics committee at your local university. Please meet me tomorrow at 9 PM at my office so that we can further discuss the details of your oncoming experiment.

can you specify what you mean by "brain tissue"? it is possible to culture stem cells to neurons. It is possible to create organoids (artificial collection of several tissues).

More importantly, you currently asking two questions: is it possible to create artificial brain, and is it possible to use such brain as super computer. COnsider asking two separate questions instead

This is actually not an unheard of idea among neuroscientists and is an aspect of much research.  Brains in general have amazing computational powers and abilities that allow them to circumvent the limitations of computation which is usually based on a Turing Machine. Neurons pursue highly parallel architectures and exhibit cognition or even emotions or do highly sensitive signal processing, which has heretofore been unapproachable with computational methods such as Machine Learning.
As such many researchers are focused on understanding the brain or at least the brain's structure to augment or produce computation.  Here are a couple of examples of neuron arrays flying virtual or real drones....
The ethical issues aren't great concerns because neural cell networks can be encouraged to grow differentiating from easy to grow cell lines like fibroblasts.
Another approach to augmented computing is to interface directly into a living brain. Model brain organoids are a popular topic of interest and could one day be used to interface to other computational systems.  There are of course many devices that try to interface to the brain via electrical fields in the same way EEGs work.
there are connectome projects that are trying to understand the neural connections between cells that are so important to brain development, with the theory that the topology of these networks might enable even computers to perform like brains.

Moore's Law of computation (which was in no way a law) was an observation of a trend in the fabrication of computor memory). Unless your brain is receiving upgrades from Intel every two years, your statement would seem difficult to understand.

fixed this in edit


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Can neurons take oxygen from air?
Why can't/don't neurons take up atmospheric oxygen or at-least dissolved oxygen (like amoeba does) to survive and do all life processes outside animal body ???

Does an amoeba (or other microorganisms) actually take up oxygen directly from the air?  My impression is that most if not all actually live in water, so they take up dissolved oxygen (and avoid drying out through loss of their internal water).

Short answer
Neurons, and in fact all cells in the body, utilize water-dissolved oxygen to fuel their energy metabolism.
Background
The brain, and tissues in general, obtain their oxygen through passive diffusion (Fig. 1). Water, carbon dioxide, and oxygen are among the few simple molecules that can cross the cell membrane by passive diffusion,  or osmosis (source: Estrella Mountain Community College).
The body uses hemoglobin to transport oxygen (Fig. 1), because passive diffusion would take too long, especially in oxygen-hungry warm-blooded animals like humans.

Gaseous exchange in fluid medium is mediated by hemoglobin. source: Kokyo

Thanks
but can neurons survive outside body ? by breathing from atmosphere ?? or swim freely in water like amoeba ??

No. Neurons are incredibly dependent on their micro-environment and require many cells to keep them alive. In many labs, neurons can be cultured outside the body but this requires very specific conditions and they do not live long.

A brief addendum: not all gas exchange in the body uses haemoglobin/blood. In fact a portion of the oxygen the cells in the cornea of the eye receive is absorbed from the air into the tear film Intro of (Leung, 2011). But note that AliceD's point about dissolved oxygen still applies in that case. Also, (Stuecker, 2004) describes how the skin can take up atmospheric oxygen but that's not to say they haven't got an oxygen supply from vasculature too.


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Looking for realistic representation of angiosperm sperm cells during pollination
I've scoured Youtube, google, and a handful of my botany textbooks for a cellular-scale photo, animation, or video illustrating an angiosperm sperm cell during pollination/fertilization.
Unfortunately, other than an unclear glimpse of one in this video I've had essentially no luck.
Ideally, I'd like a microscope recording or a realistically-animated video demonstrating the accurate shape and movement of sperm along the pollen tube and into the ovary.
I think a video will better allow my botany students to visualize this process.
Please let me know if you can find or are aware of any such video or animation from any textbook supplemental materials, journal supplement, or via some reputable online resource.


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Are there any viruses that integrate their DNA into organellar DNA?
It is known that many viruses (e.g. retroviridae) integrate in the nuclear genome of their host as part of their cycle. However, I'd like to know if integration can happen in organellar DNA (cpDNA and mtDNA) as well.
I've found a paper proposing that some chloroplast genes have a viral origin; however, the virus would have been present into the ancestral alpha-proteobacterium that later became the chloroplast, so no direct chloroplast infection is involved.
There is also this almost identical question on ResearchGate, but frankly the answers there are not satisfactory.

Mitoviruses have been reported to replicate within the mitochondria of certain fungi, though integration was not observed.
https://www.sciencedirect.com/science/article/pii/B9780123943156000064?via%3Dihub

Oh, I forgot the juicy tidbit here about DNA!  The virologists have this theory about Mimi?  This massive huge virus...that came from asteroids and meteors.  That this virus caused life to start (some used to call this the God virus but I gag) and inserted some basic DNA.  How else would we share DNA with plants?  Hello?  Fascinating stuff!

I'm only aware of one paper that claims to show regular viral integration into mitochondrial DNA, and even there they suggest it might be a host defense rather than a viral life cycle thing:

Interestingly, 69.4% (50/72) of HBV integration sites were observed in human mitochondrial DNA (mtDNA) (Supplementary Table 2). ... However, 32% of HBV integration sites in mtDNA (16/50) were in the displacement loop (D-loop) region, which is known as the major control site for mtDNA expression as it contains the origin of replication for the heavy DNA strand and the major promoters of transcription (Figure 1B). Of note, we repeatedly detected mtDNA integration events through the same micro-homology site in independent mice, indicating the hotspot for HBV integration in mtDNA, which is probably related to replication or transcription. ...
We found that HBV integrations were mediated through MMEJ, which is known as an alternative DNA double-strand break (DSB) repair system and reported as a principal mediator during mitochondrial DNA lesions. This suggests that early-phase HBV integration occurred in mtDNA. Damage in mtDNA is known to induce autophagy and was removed in C. elegans, therefore it is possible that integration of HBV DNA into mtDNA might be a defensive mechanism to protect the nucleus from HBV integration.

--Characterization of HBV integration patterns and timing in liver cancer and HBV-infected livers
I would like to see this replicated and extended before I spent too much time wondering about functions and mechanisms.


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Why is wombat scat (feces) shaped like cubes?
I've heard that wombat scat is cube shaped, but I don't understand how that can happen. Has anyone studied the phenomenon? What would the evolutionary pressure have been to cause this?

How do wombats poop cubes? Scientists get to the bottom of the mystery

Although the OP might no longer be active, I'm comming back to this question, because there is a new study on this released in "Soft Matter". With simulations Yang et al., 2021, describe how corners of these almost perfect cubes might be formed. From the abstract:

Using histology and tensile testing, we discover that the
cross-section of the intestine exhibits regions with a two-fold
increase in thickness and a four-fold increase in stiffness, which we
hypothesize facilitates the formation of corners by contractions of
the intestine. Using a mathematical model, we simulate a series of
azimuthal contractions of a damped elastic ring composed of
alternating stiff and soft regions. Increased stiffness ratio and
higher Reynolds number yield shapes that are more square. The corners
arise from faster contraction in the stiff regions and relatively
slower movement in the center of the soft regions.

As described by the previous answer, there are apperently two stiffer regions opposite of each other in the last intestinal section, seen in the longitudinal direction. These press inward more strongly during intestinal peristalsis, i.e., repeated contraction, thus flattening the material further and further on opposite sides, so to speak.
Similarly, we form a cube from a spherical piece of plasticine by pressing inward with two parallel fingers on each side, doing so sequentially from different sides. In the wombat intestine, however, there is no change in the direction of indentation, so the researchers assume that the more elastic intestinal strips are pulled inward in the middle and in this way flatten the missing sides.
As @anudder already pointed out, the last author commented on this in "Science": How do wombats poop cubes? Scientists get to the bottom of the mystery

The stiffer portions are “like a stiff rubber band—[they’re] going to
contract faster than the soft regions,” says David Hu, a biomechanics
researcher at the Georgia Institute of Technology and author on the
study. Softer intestinal regions squeeze slowly and mold the final
corners of the cube, the team found. In other mammals, the wavelike
peristalsis of the intestinal muscles are consistent in all
directions. But in the wombat, the grooved tissue and the irregular
contractions over many cycles shape firm, flat-sided cubes.

Why?
It is not yet proven, but they suspect that it has a purely practical reason. Like many other animals, wombats mark their territory with excrement. They often choose stones as a place to lay their excrement, from which cube-shaped piles roll down and away less easily than round specimens would.

I'm almost certain that your question is based on the press that Patricia J Yang's research is receiving (e.g., here and here).
Yang and her co-authors examined the structure and mechanics of some dead wombats to investigate this question further. They found that varying degrees of pressure in the latter portion of the wombat's intestines (in conjunction with a dehydrating of the fecal matter) led to the characteristic cube shape:
From their abstract:

In the final 8 percent of the intestine, feces changed from a liquid-like state into a solid state composed of separated cubes of length 2 cm. This shape change was due to the azimuthally varying elastic properties of the intestinal wall. By emptying the intestine and inflating it with a long balloon, we found that the local strain varies from 20 percent at the cube's corners to 75 percent at its edges. Thus, the intestine stretches preferentially at the walls to facilitate cube formation.

Why do this?
There seems to be two major reasons:

Mark territory
Attract mates

For example, see Wells 19891:

The rubbing of posts, logs and overhanging branches with their backs and rumps and deposition of faeces along trails may be a means of olfactory communication used in the maintenance of territories

One hypothesis is that by being square, the droppings don't roll as easily and therefore stay in the place that the wombat intended to mark.
I've also seen hypotheses about wombats stacking their square feces as some sort of signaling, but I couldn't find any reputable literature sources that make this suggestion.

1: Wells, R.T., 1989. Vombatidae. Fauna of Australia, 1, pp.755-768.

The "Why do this?" part doesn't really explain why. Plenty of other creatures mark territory and attract mates, and they don't have square poops. Similarly the Wells quote seems unrelated.

@Parrotmaster: As nature continually proves, multiple solutions to the same problem exist. Plenty of creatures are land-based animals but that doesn't prove that birds shouldn't have evolved to have wings. Recognizability of feces may not have been the reason for its inception (random mutations tend to be the reason for the inception of a trait), but the subsequent benefit of recognizability of the uniquely shaped droppings may explain why the trait persisted.

@Parrotmaster take a look at Wells's paper for number of citations regarding the ethology and social-ecology of wombats

"Thus, the intestine stretches preferentially at the walls to facilitate cube formation." Sooo...the intestines are square?

probably means there are 4 muscles around the intestine that form a square.

@GraphTheory, no. The intestine supposedly just squeezes differentially due to varying elastic properties of the intestinal wall.

@gunfulker no. There aren't 4 muscles surrounding intestines. Rather, the intestines are composed of their own tubular smooth muscles which periodically squeeze (causing peristaltic movements of the contents)

On a more serious note than my comment, and as a supplement to theforestecologist's answer, it's worth pointing out that a cube with rounded corners and edges has larger surface area to volume ratio than a spherical dropping, making it more efficient for the reabsorbtion of moisture, which would be an evolutionary advantage in a place where water is in short supply (as it is in large parts of Australia).
Additionally, in respect of the claim made here that droppings are used for marking, it may be advantageous to have a dropping that doesn't roll, if it's important some subsequent visitor can identify the precise spot the droppings were dropped, especially if one inhabits sloped terrain (which a wombat does - mountainous areas of Australia) where a round dropping might roll and mark an ambiguous spot.

Why would feces reabsorbing moisture be an advantage? Do wombats eat their droppings?

@Paul I guess he meant colon absorbing moisture from feces to conserve water.

@Paul a standard function of the colon in all animals is to reabsorb nutrients and fluid from doo doo before it's expelled.


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Can turkeys run around when their head is cut off like chickens do?
Chickens may run around after their head is cut off if the head is severed near the base of the skull leaving the brain stem intact and missing the jugular vein.  This usually only lasts for a few minutes, however there is the case of Miracle Mike that survived for 18 months after his head was cut off.  Do turkeys also exhibit this same behavior and if not, what makes this possible in a chicken but not a turkey?

The brain does not control all bodily movements. Some movements are to a great extent controlled by neural networks in the spinal cord. The spine contains a network which is pre-programmed to control the muscles in frequently-used movements such as running or swimming in chickens. This is why a chicken can run away after you chop its head off. Likewise, turtles swim using their a spinal neural network. As long as a signal is received somewhere in this network, the network will activate the swimming movements. Such a system is coined an ‘attractor network’ (source: Science Nordic). A similar system has been shown to occur in a sea slug. I couldn't find similar information in the turkey though. Happy Thanksgiving :)
Note that walking and running in higher animals (mammals) is controlled by the motor cortex higher up in the brain, involving a more complex system including the pyramidal system. Reflexes, however are controlled by quick, short spinal relay circuits in higher animals as well.

Wow, attractor networks are fascinating.  I thought for sure turkeys would display the same behavior but could not find any supporting evidence either.  Happy Thanksgiving indeed.


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Why does pyruvate from lactate and pyruvate from other sources follow different pathways in gluconeogenesis?

My teacher taught me in a lecture that PEP forms from Pyruvate by two ways, based on their sources, that is -
1. If the Pyruvate was from lactate (by lactate dehydrogenase action), it gets shuttled into mitochondria and is successively converted to OAA and PEP, by enzymes PC and PEPCK(mitochondrial) respectively. This PEP is then shuttled to cytosol for rest of gluconeogenic steps to take place.
2. Whereas, if the Pyruvate was from any other source, it is shuttled to the mitochondria, where it is converted to OAA by PC. It is then shuttled to cytosol by malate shuttle and then converted to PEP by PEPCK (cytosolic).
Why the difference in mechanism?
Please correct me if any of these steps are wrong.

Thanks for the corrections. But my main doubt was that why does the Pyruvate from lactate follow a different way to become PEP rather than the other way (when Pyruvate is produced from other sources), or vice versa. The question could also be framed this way - 'why does two mechanisms exist for conversion of Pyruvate to PEP?' Thanks.

What is the basis of the right portion of your diagram which is new to me? The vast majority of the PEP used for gluconeogenesis is generally thought to occur in the cytoplasm from oxaloacetate made in the mitochondrion and shuttled out via malate as indicated in the left of your diagram. Even though there is evidence for a mitochondrial PEPCK, this has no known role in gluconeogenesis. Even if it did, how could it distinguish pyruvate from different sources?

In any case, please rewrite your question so that  your diagram is only an illustration of the text. The question should not rely on text on an image as it is not possible to index it and it discriminates against people with sight problems. You can do this by carefully describing the key steps in words. Please quote the source for your diagram or explain if it is from notes taken at a lecture.

Sorry mate. Did not think of that while posting the diagram. The diagram and source of the content was from a biochemistry lecture. But, I found other sources (like this one: https://www.ncbi.nlm.nih.gov/m/pubmed/24497630/) where mitochondrial PEPCK was linked to lactate (Here, silencing of mit. PEPCK in rats was seen to increase lactate and lower plasma glucose). Thanks.

According to this research paper (http://m.jbc.org/content/284/40/27025), the presence of two different PEPCK's may have to do with the 'cytosolic redox state' because both pathways result in production of one NADH + H+ in cytosol. Although I didn't get the clear picture, I got a superficial idea why this stuff is like this. Wow, the human body is truly wonderful.

That's interesting. If you like I'll set that out clearly in an answer when I have a moment. It's worth putting on file.


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What is the maximum electric potential that can occur in the human body?
Neurons can generate a voltage, if there is an action potential. Also, membranes where an ion concentration gradient is present, generate some membrane potential.
What I wish to know is, which cellular element in the human body creates the greatest potential differences? And how high can they be so high? Are there also biochemical reactions, where significantly high electric/electrostatic voltages are important? How strong are these?

What do you mean by "cellular element"? Do you mean different types of cells, or something else?

I mean any microbiological Entity like membranes, ribosomes, Golgi-apparatus, etc.

To the best of my knowledge, the potential difference across the hair cells in the inner ear (cochlea) (Fig. 1) is the highest in the (human) body. It is about 120 mV, mainly due to the exceptionally high positive potential of the scala media as provided by the stria vascularis, referred to as the endocochlear potential. This potential is mainly built up by the high amount of K+ pumped into the scala media by ion pumps located in the marginal cells and basal cells (Salt et al, 1987) in the stria vascularis. Adding the potential difference of -40 mV of the hair cell it yields a total difference of 120 mV (Fig. 2).
References
- Morrill & He, J Otology (2017); 12: 151-64
- Salt et al., Laryngoscope (1987); 97(8 Pt 1): 984-91

Fig. 1. The cochlea. source: Morrill & He (2017)

Fig. 2. The potential difference across the hair cells is 120 mV, due to the endocochlear potential of +80 mV in the scala media. source: University of Minnesota Dulluth

As excellent as this answer is, if you look at the comments in the OP, the asker wants to know about voltage differences within an individual cell

@Astrolamb the question title tells me differently, but you might be right. W'll see if OP updates the Q. I might have been too fast answering.

The inner membrane of the mitochondria has a huge membrane potential generated by the pumping of protons as part of the respiratory chain.
In rat cortical neurons this value is around -140 mV and can variate between -108 and -158 depending on the metabolic activity of the cell.
Ref: J Physiol. 2012 Jun 15; 590(Pt 12): 2845–2871.


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How to perform cell biology research without lab affiliation
Related to this question, I am wondering just generally how one can do cell biology research without being part of an already well-established University laboratory. I am not doing this myself but am just curious what the process is like for somehow getting to be one of the ones to be approved to do such research, approved to buy cells or other things like that.
The only places I know of currently that are approved are well-established Universities. That makes sense because they have good intentions and they probably have a lot of manual contracts or inspections and that sort of thing. But then at a second level of approval, there are big private companies like Genetech that probably also have approval of some sort (although maybe they "started at the beginning" by building their own cells from scratch sort of things, and so never needed approval). Then at a third layer are smaller private companies that either buy cells for research, or make their own somehow. I don't know of any examples of this but there's probably some less well known 10-20 person companies that have access to cells for research somehow, at least I would imagine. If there are not any examples of that it would be interesting to know.
But say you are either a nonprofit or a private company just starting out, and you would like to do research or provide some service that requires expressing DNA at large scales and requires a streaming supply of cells to do that. I wonder what your options are just generally (to keep this question focused not on specific companies that offer solutions to this, but on the general process). Maybe it requires you have 1 person on the team with a PhD of some sort. Or perhaps a Masters degree is acceptable. Or maybe you can get by just a Bachelors degree in Biology. Or maybe just a college degree in any major. I wonder if you can go further and, no one on the team has graduated from college (if they are young and in college), or they are older and no one went to college, they are just self-taught. So part of this question is if there is a degree requirement to being approved to buy cells (and other stuff).
So as a new company or non-profit, you start "establishing a lab" from scratch. You invest in some machines somehow. You either have some PhD's, or no one even graduated from college, but in both cases you have the same level of expertise. The part here is how you, as someone working for this "new lab", can express to some company like ATCC that sells cells, that you are affiliated with a lab doing ethical research or work for expressing DNA for some service.
Basically the question is, how a newcomer breaks into the space and can start either doing research or performing a service that requires having access to cell lines and such. What the general requirements are (such as (1), must have at least 1 PhD, (2) PhD must be affiliated with a University laboratory (i.e. they must have been a PostDoc for x years at that University, or must currently be partially employed there), and (3) you must have some sort of legal "Code of Conduct" or some guidelines for good ethics). Currently, I can't see how any new lab can be established, unless it is established as a branch/offshoot of an already existing lab.
The only example I can think of as a startup that might've been in this situation is like 23andMe, founded in April 2006 (12 years ago) by Linda Avey who only had a Bachelor's degree in Biology it looks like, and Anne Wojcicki, who also just had a Bachelor's degree in Bio but looks like they worked at some well established labs for a while (National Institutes of Health and the University of California, San Diego). I don't know if they need cells or anything, not too familiar with all that, but it seems like they probably do. "Wojcicki was married to Google co-founder Sergey Brin at the time", well that would be helpful funding-wise lol. Some helpful info:

According to Anne Wojcicki, 23andMe had been in dialogue with the FDA since 2008.[31] In 2010, the FDA notified several genetic testing companies, including 23andMe, that their genetic tests are considered medical devices and federal approval is required to market them; a similar letter was sent to Illumina, which makes the instruments and chips used by 23andMe in providing its service.[29][35][36] 23andMe first submitted applications for FDA clearance in July and September 2012.

But it's like, you need to have all these tests and results to demonstrate to regulators that this is ethical and not a health issue and whatnot. But I don't see how you can even perform those tests and get those results in the first place, since you don't have access to anything. Someone is doing lab work in private somewhere, pre-regulation. Or perhaps you have to submit proposals that need to be approved first before even embarking on initial experimental tests to get initial basic results. But if you have the funding (without needing to write grants, like 23andMe), it seems you don't need to get any approval first.

23andMe began offering direct-to-consumer genetic testing in November 2007. Customers provide a saliva testing sample that is partially single nucleotide polymorphism (SNP) genotyped and results are posted online.[13][57][58] In 2008, when the company was offering estimates of "predisposition for more than 90 traits and conditions ranging from baldness to blindness", Time magazine named the product "Invention of the Year."[10]
After the sample is received by the lab, the DNA is extracted from the saliva and amplified so that there is enough to be genotyped. The DNA is then cut into small pieces, and applied to a glass microarray chip... If the sample has a match in the microarray, the sequences will hybridize, or bind together, letting researchers know that this variant is present in the customer's genome by a fluorescent label located on the probes.

So maybe 23andMe had PhDs who did all the communication or something with the companies to get the cells for these experiments.
Also to just throw it out there, I am not really sure what "lab affiliation" means. If it means (a) you are actively employed at the lab, or (b) were employed at some point in the past, (c) for how long does it matter you were employed, and (d) if you need to have been working at that lab with a PhD, or if being an undergrad or other sort of helper counts. Not sure if clarifying that would help answer the question.
I ask because there is no place online where you can just click "S. cerevisiae, Strain A -> Add to Cart -> Checkout -> [Enter credit card info and press Buy now]" and get cells delivered to your door the next day. Something is in the way there (obviously not talking about the physical aspect of transporting the chilled cells and such). Something is going on in between an individual/new organization, and getting the cells. I'm not sure what it is (if it purely just laws, or what it is). If it is purely just laws, then that is good to know and the answer to this question is "It is purely the laws that govern this, it doesn't matter your degree or lab affiliation" is a good one sentence answer. Otherwise maybe it is some other social contracts like forming good B2B relationships over time, or knowing a friend-of-a-friend sort of thing. Or perhaps something else like degree requirements, etc..

Your answer will be very different if you want to work with cell lines or with human samples (like 23andMe). There's not a whole lot of unethical things you can do with cell lines, but human samples will have a much higher bar in terms of ethics, privacy, and medical intervention.

An answer containing the situation with the lowest bar would be the most helpful (so just with cell lines), as that would set the foundation for understanding how to handle the higher-bar situations.

I think your question is off-topic because it is not about biology in terms of SE Biology, but I am curious why you think it is not possible to buy cells and other biological supplies without some sort of approval. Obviously this relates to the laws of the country you are in — in your case the US, where I would imagine it is under state juristriction. Have you tried to buy biologicals? Presumably poisons might be under a different category, although you might regard this as the "right to bear arms".

I'm voting to close this question as off-topic because it is about US State laws.

No but the linked question I proposed at the top was closed and the comments said basically that you need approval.

I am not wondering about state laws, that is the details of how to actually do stuff. I am wondering about the general process instead of the specific details. After knowing the general process, then I would be prepared to know what to consider in terms of laws, and could ask on law.stackexchange.com. Just stating as one of the steps "Find out the regulatory laws" would be enough legal stuff for me.

This question is on topic: "questions about techniques in a biological or biochemical laboratory".

I think there are just too many different questions here and as @David pointed out it isn't really about biology but rather a legal question. You aren't asking about techniques from a biology perspective, at best you are asking about regulatory compliance for which the answer is always going to be "it depends" and "we can't offer legal advice." In addition, your question covers a whole scope from regulatory approval for medical device marketing to experimental biology.

Ah, maybe this question simply boils down to "How to build a new lab", in which case this and this about Biosafety Levels and permits is pretty much all you need to know. So it doesn't seem to require PhDs or anything so far.

@LancePollard I am thinking you need to know about your closest available University that offers Cooperative Extension Services!  Yes!  I tried to read through to see if anyone picked up on this!  Your best bet is to go find your closest Cooperative Extension Service!  Oh my.  they offer Joe Blow classes to become a Master Gardener, a Master Composter, a Master Food Preserver as well as Master pruner!  They are the ones to get to know like NOW!  They also have (used to be free) soil testing.  They might allow you to use their labs or direct their techs for studies, perhaps if you landed grants

@stormy what you wrote sounds a bit like spam so I can't tell if you're serious. Maybe if you wouldn't mind posting a link to an example or something perhaps.

The resource I am talking about is a State's University (one of them) Cooperative Extension Service.  It is almost FREE.  This extension service is non profit.  I took their Master Gardener Course 3 times, Priceless.  They KNOW your locality, the zones, the soils the special differences for your locality...to not know about this service is a shame.  Check it out.  Spam?  Are you kidding me?  Please, let me know....

One needs to be part of the University to do purchase orders within the University.  That makes the most sense.  Otherwise someone outside the realm of the University needs to learn about University outreach programs such as Vocational Education and the Cooperative Extension Service or be privately funded.

In general, I think that degrees would not matter. PhD is not a license (compared to licensed medical doctor) but a scientific degree, reflecting some amount of education and achievement.
There are many governmental regulations that apply to organization that seeks to work with human tissues, import/export biological samples, order regulated substances et cetera. There are review papers, for example "Guidelines for the use of cell lines in biomedical research"
Another layer of regulations, that universities are particularly prone to, are ethical guidelines established by funding sources. For example, NIH have specific guidelines for work with human subjects and specimens. You will have to pay attention and comply, if you want to get their funding. Universities have dedicated groups of people who are in charge of making sure that these policies are followed, you don't want your organization to fall out of favor with funding agencies.
All together, it seems that establishment of private lab is logistics problem. Compared to research universities, you lack legal and operational teams that know all the caveats of the regulations, as well as just plain handling of materials. You need Purchase Orders most of the time, not credit card, to buy something from ThermoFisher or Sigma-Aldrich, and that is done via purchasing departments at universities.

Thank you, this is nice. This answered pretty much everything, thank you. I have never heard of Purchase Orders, good to know.

I'd also like to point out on that very note @LancePollard that setting up an account with a scientific vendor often requires a commercial credit application, because POs are executed on a net-15 or net-30 days regimen, i.e. they don't take your money immediately, so you need to be credit-worthy.


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Can Tajima's D and other population genetic tools be used to copare Arabidopsis ecotypes?
I am currently investigating 2 genes in Arabidopsis taliana that are a product of a recent duplication even (observable from synteny and phylogenetic analysis). In addition to the molecular and biochemical functions of these genes, I was wondering how evolution is acting on them at the population level. There the genome sequence of 1300 ecotypes of Arabidopsis from all around the globe available. So, I was wondering if I could use all these sequences to quantify nucleotide diversity and/or Tajima´s D? However, I am not sure if this is conceptually right, since I am not using an actual population, but I am just aligning 1300 sequences as "global population". what do you think?  is this a good approach to see the level of variation for each gene "globally"? is this "global" view scientifically and statistically relevant?
Regards


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What kind of insect can this be? This appears to be just a shell after and insect went through a metamorphosis process
What kind of insect can this be? This appears to be just a shell after an insect went through a metamorphosis process.

Related: Can anyone help confirm this tiny insect larvae?, Bug Identification: Is this small tubular, black bug..., How to protect my mounted insect specimens..., Varied Carpet Beetle Larvae, What is the name of the critter depicted..., What small insect is this?, What bug is this...

It's a carpet beetle larvae (family Dermestidae).
See here fore more info.
Example:

 Anthrenus verbasci from Wikipedia


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Is it possible for a fire to start inside of a live human body?
Over the years, I've read about spontaneous combustion in the news, but now I am wondering if it's possible.

I'm voting to close this question as off-topic. We welcome new users to SE Biology but expect them to read about the site first. The tour explains that this is a "site for biology researchers, academics, and students".  This implies a certain standard that unfortunately this question does not reach.

Like any community, this one has rules. If you join you are expected to read the rules and abide by them. The community is self-regulating, and requires the votes of five members of sufficient experience before a question is closed. It is generally thought helpful to explain why one has voted in a particular way. I am afraid that it is your response rather than the explanation of my vote that is rude.

@WillyA - Do not call people a troll who are trying to guide you through the site's conventions. David's investing time and effort in your question. I concur that the question is underresearched. If you could provide a web-link and explain why you doubt the process of spontaneous combustion that would be helpful.

Willy, please stop flagging every comment that you don't like. Secondly, FYI, the diamond behind a name means they're a mod - flagging comments from such a user doesn't make too much sense, as they are the ones handling flags :)

@AliceD please note that this user may be an attempt to get around a 10 year suspension by this user.  The user has asked and had closed and deleted the same question that he was repeatedly posting as willy150. He is also engaging in the same behavior of posting questions on multiple stacks (see the aspiration pneumonia question).

@AliceD see this meta discussion.  The repeat aquagenic urticaria question link is here

@DeNovo thanks heaps for your vigilance. However, I am unsure at this stage whether it is actually the same user.

@AliceD yep, could be another Willy who is also interested in aquagenic urticaria :) But yes, I suppose you'd need more than a similar user name and similar behavior to take any action. I just wanted to alert people that this may be an attempt to get around an account suspension

@DeNovo - I checked it out and I can't find any evidence, unfortunately, because I understand your hunch.

Short answer: No, there is no evidence that this is possible. Reported cases can usually be explained by an external source of ignition (https://en.wikipedia.org/wiki/Spontaneous_human_combustion)
Edit: ok, let's add some more information..
The human body consists mainly of water and is therefore hard to burn. It nevertheless contains burnable material such as fat. Not to forget the easily ignitable hair and of course clothing.
If a body (or its surrounding textiles) is burning long enough, its body fat can liquefy and keep burning even on lower temperatures. This is called the candle effect. Like with a candle, the fire does not easily travel horizontally and can keep the surrounding furniture intact. In many cases, arms and legs remain mostly intact, which is probably due to temperature gradients in the limbs and a lower mass of burnable material.
It is though that in most cases the victims were already dead or unconscious due to e.g. drug intake before their body started burning. Often they were smokers or found in a room with an open fire place, which are possible sources of ignition.
Since victims often were alcoholic, one theory was brought forward that the flammable alcohol was causing an ignition within the body. But to bring the alcohol content of a body to a flammable amount, you would die of intoxication long before that..
This study posted by user1136 also mentions the points made above: https://www.jflmjournal.org/article/S1353-1131(00)90353-5/abstract
Yes, a body can burn. But there is no evidence that it can ignite spontaneously without an external source. There might be a few cases where no source was found, but that doesn't mean it wasn't there (a cigarette fallen onto the clothes would be burned). The media likes to push sensational news on "mystery cases", but that doesn't mean that humans just spontaneously turn into walking torches for no reason.

+1 for your reference - I've cleaned up the chit chat


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Who cleans the cleaner fish?
Cleaner fish are those fish that eat the dead skin cells and parasites off from other usually larger fish.
( such cleaners include wrasse, cichlids, catfish, shrimp etc )
I wondered if the cleaner fish themselves ever receive this service from others, though understandably it is an added benefit rather than a necessary one for health.


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What is the benefit of reducing inflammation when producing antibodies?
We just learned in lecture that IL-10 promotes the formation of plasma cells over memory cells. Which seemed strange to me as IL-10 also reduces inflammation, and I figure you would want inflammation as it will help antibodies reach the site of infection.
My question is, why would the body want to reduce inflammation and produce more antibodies at the same time?


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Is it possible that there are unknown vitamins?
Is it possible that there are vitamins or other essential nutrients about which we still do not know?

This question is tending to be POB. There is always a possibility that we don't know the mechanism of every enzyme. You should add some rationale behind your question so that it becomes useful to everyone. A point to note is that if someone acquires a mutation which prevents the formation of a metabolite that humans can normally produce then they would need it in the diet.

@WYSIWYG — Which one of the 39 possibilities for the acronym POB had you in mind? But I agree. I would think most "Is X possible" questions are matters of opinion and off topic. They assume that X currently does not exist/happen/has been observed, so unless your attitude is that all things are possible, the answer has to be a matter of opinion. And, indeed, such questions are can only rarely be "practical, answerable questions based on actual problems that (people) face.".

Yes, it is possible that there is a vitamin or other essential nutrient that has not been identified so far.
Essential nutrient means any substance normally consumed as a constituent of food which is needed for growth and development and/or the maintenance of life and which cannot be synthesized in adequate amounts by the body (fao.org). Essential nutrients include vitamins and some minerals, fatty and amino acids.
Choline: An Essential Nutrient for Public Health (PubMed, 2009):

Choline was officially recognized as an essential nutrient by the
  Institute of Medicine (IOM) in 1998.

The fact that choline has been recognized an essential nutrient relatively late suggests that there may be other nutrients that are not recognized as essential today but may be in the future, for example:

Aluminum (Biocyclopedia)
Boron (PubMed)
Nickel (WebMD)
Silicon (PubMed)
Vanadium (PubMed)

Please not that term Vitamin excludes essential minerals, fatty acids or amino acids. So the other examples you listed - even if considered essential - would unlike Choline never be a vitamin.

I'm not sure if I understand your comment. Essential nutrients include vitamins, some minerals and some amino and fatty acids.

Thats correct of course, I was mostly going from the fact that the OP used the word vitamin the title but then used "essential food components" in the body text. Maybe adding a short comment about the distinction might improve the answer.

Russian wikipedia says choline is vitamin B4 (since the 1930s) and in modern view is not a vitamin.

@Anixx, I'm not saying choline is a vitamin, but it is sometimes described as a vitamin-like substance. The source I provided in my answer and Office of Dietary Supplements by National Institute of Health in the US, among other say choline is essential.

https://iubmb.onlinelibrary.wiley.com/doi/pdf/10.1080/15216540500078939 says vitamin B4 can refer to many things


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Name of dsRNA (or dsDNA) where all strands are identical
What is the name of dsRNA (or DNA) where all component strands are identical (i.e. where the complex consists of multiple copies of the same ssRNA)?
Example: 2 identical ssRNAs forming a dsRNA
C C G C G G C G G
| | | | . | | | |
G G C G G C G C C

Furthermore, is there a different name for it depending on the degree of complementarity (full Watson-Crick complementarity vs. full complementarity with non-Watson-Crick basepairs vs. lower complementarity due to bulges etc)?
My thoughts
You probably wouldn't say "RNA homo n-mer" (for the example above "homo dimer/2-mer") since I assume that would be referring to a 2-nucleotide long ssRNA?
Can you use the terms dimer, trimer, tetramer, 5-mer, 6-mer etc in multiple ways; (a) referring to the binding of nucleotides to each other to form a polymer/n-mer of nucleotides i.e. polyribonucleic acid, and (b) to whole ssRNA or dsRNA binding to each other to form a "dimer"?
You also probably wouldn't refer to it as a "homo duplex" since that refers to  something related to chromosomal crossover.

Welcome to Biology.SE! A few comment to your questions: 1) dsRNA is very rare, afaik it only occurs almost exclusively in some viral genomes; unless you include self-basepairing in structural elemnts 2) As long as there is complete base pairing something like this would be a palindromic sequence, however that term is also used for short elements within a long DNA strand, and doesn't necessarily imply that actual DNA molecule is double stranded.

Such a nucleic acid sequence is described as a palindrome or palindromic.
Wikipedia has an entry for palindromic sequence in which it is defined as:

A palindromic sequence is a nucleic acid sequence on double-stranded DNA or RNA wherein reading 5′ (five-prime) to 3′ (three prime) forward on one strand matches the sequence reading 5′ to 3′ on the complementary strand with which it forms a double helix. This definition of palindrome thus depends on complementary strands being palindromic of each other.

It should be noted that this is a description (rather than a name) that is usually applied to segments of larger nucleic acid molecules or to synthetic constructs. I am not aware of a generic name for short dsRNA (or dsDNA) like the one in the question as they are not, to my knowledge, found in Nature and so there has been no reason to devise a name for them. Thus, there are no names for variants either. If you wish to write an article about such things you would need to invent your own terms, but keep well clear of ‘-mers’ (see use of e.g. tetramer).
The sequence presented in the question does not conform to the Wikipedia definition, above, as it has a central mismatch and is therefore not a perfect double-helix. However, as the use of the term palindrome for nucleic acids is a somewhat cavalier extension of the general use of the English word palindrome (an example of which is “ABLE WAS I ERE I SAW ELBA”), I would regard a further minor modification of the Wikipedia author’s definition as unexceptionable.

Note that the biological palindromic sequence does not quite match the general meaning of palindrome.  The DNA sequence is complementary to its reverse, whereas the normal palindrome is the same as its reverse.

@mgkrebbs — Yes. But I did note that, didn't I? I wrote "the use of the term palindrome for nucleic acids is an extension of the general meaning of the English word palindrome" and gave a reference to and example of the general meaning of the word, that can be compared to the example in the question for NAs and the reference I provided for that. However, it is worth emphasizing to those not familiar with Napoleonic English.

I don't agree that palindromic sequence is an extension of the normal word meaning of palindromic because it (in general) violates the one central meaning of palindrome, that its reverse is the same.  Since it completely throws out the core meaning and is in conflict with the normal meaning, it is not an extension but rather an alternative meaning.  (Palindromes of course have no known biological significance, unlike palindromic sequences.)

@mgkrebbs —  From a linguistic point of view the "use" of the word has certainly been "extended" — from a single string of characters to two strings having special properties in two-dimensions. Only if the 3' end of the first string is joined to the 5' end of the second string do you have a palindrome.in the original sense. I've tried a modification of my own in this spirit, but do suggest alternatives.

The specific sequence you have posted is not strictly a palindrome since the reverse complement of the top strand is not the same as the bottom strand. Although there is no central body making these definitions, a better term, in my opinion, would be inverted repeat, of which palindromes are a subset (inverted repeats with no intervening sequence). Of course, the final say would be its predominant usage in the literature (of which I am not overly familiar).
Furthermore, the specific sequence you have shown forms an internal loop, though there is no requirement that internal loops be formed from inverted repeats.

Yes. That's another way of looking at it.

…although the description "inverted repeat with intervening sequence" does not capture the mismatch of identical bases in the intervening sequence, which palindrome actually does.


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Protein electrophoresis
Three proteins A, B and C of equal molecular weight are being investigated in a study. They contain six, four and four cysteine residues respectively. Only Proteins A and B were treated with β-mercaptoethanol (which reduces disulphide bond) and heated in boiling water bath for a few minutes. Which of the following is expected in the SDS PAGE gel run?
a. Protein C will move fastest.
b. Protein B will move fastest.
c. Proteins A and B will move at the same speed but faster than C.
d. Proteins B and C will move at the same speed.
Before knowing the answer the I thought the answer would be b. Because as Protein A has the most no. of amino acids so it will be behind Protein B and C for sure. And for protein B and C, as Protein B has been in a reducing environment it will not form disulfide bridges but Protein C will, so it will be billore and hence will be behind Protein B. So B will be fastest?
But the answer key says C, I am not really sure how?
So the answer is C . Before knowing the answer I thought the answer would be b. Because as Protein A has the most no. of amino acids so it will be behind Protein B and C for sure. And for protein b and c as Protein B has been in a reducing environment it will not form disulfide bridges but Protein C will so it will be billore and hence will be behind Protein B. So B will be fastest? But the answer key says C

Welcome to Biology.SE. Please note that [tag:homework] questions are only on-topic here, if you show that and how you have tried to answer the question yourself. We'll gladly help you with understanding a problem, but we won't just answer it. Please add your own try to answer this question.

I did try it. Sorry I am new to stack exchange. So the answer is C . Before knowing the answer the i thought the answer would be b. Because as Protein A has the most no. of amino acids so it will be behind Protein B and C for sure. And for protein b and c as Protein B has been in a reducing environment it will not form disulfide bridges but Protein C will so it will be billore and hence will be behind Protein B. So B will be fastest?    But the answer key says C

I've made an edit to add your description to the answer (people won't always read the comments, so it's better to update the question), you can accept that edit (I think?) or also add something by yourself.

The problem statement says all the proteins have the same molecular weight but does not say how many amino acids they have.  It does say how many cysteine amino acids each has, but not how many other kinds they have.  Cysteine forms disulfide bonds, holding bends in the protein structure.
BiteSizeBio says:

SDS is a detergent that is present in the SDS-PAGE sample buffer where, along with a bit of boiling, and a reducing agent (normally DTT or B-ME to break down protein-protein disulphide bonds), it disrupts the tertiary structure of proteins. This brings the folded proteins down to linear molecules. SDS also coats the protein with a uniform negative charge, which masks the intrinsic charges on the R-groups.

So the point to SDS-PAGE is to have proteins migrate in the gel according to molecular weight without regard to the natural charges carried by the various component amino acids.  The three proteins should thus migrate at the same rates in SDS-PAGE (not A being slower than B and C, as OP thought).
However, protein C is not treated with β-mercaptoethanol (B-ME) which is an important part of SDS-PAGE, so it retains the disulfide cross-links and thus is not a linear string of amino acids.  Hence C will migrate more slowly than A and B, and the expected result is as stated in choice (c.).


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Mushroom Identificaton(USA)
I need help identifying a perculiar species of mushroom found in my yard today. Color is orange-yellow, around 3-4 inches total radius, its a cluster of tiny to medium mushrooms. They were found near an oak tree. Location is southern Georgia, USa.

These could be specimens of Omphalotus Illudens based on the orange/yellow color, the time of the year, their association with decaying wood (an oak in this case) and your location (eastern North America)
You can read more about these species in this reference: Messiah College

I did some research on Omphalotus Illudens (Jack-o-lanterns) and found that they were bioluminescent. The mushrooms i found are not. Is there a possibility that there is a subspecies of Illundens that are not bioluminescent?

You are right about the claimed bioluminescent properties, however this phenomena is not always happening. Apparently some people that study these mushrooms sometimes have to wait hours in the dark to be able to see the glowing and some even say the bioluminescent claims are completely false ( like this reference: mushroom expert ). I unfortunately lack the expertise to say for sure if they are bioluminescent or not.

MikeKatz45, I had cut down a tree about a month ah go, about a foot away from the clusters location. I noticed that the post said "Occurrence on wood substrate: or on the ground from decaying underground roots; ". This somewhat fits in with this type since of the location and the surroundings. Could it be possible that it might actually be it?


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Why does the HLA show a high degree of polymorphism?
I know how the HLA undergoes high degree of polymorphism (random genetic rearrangements), but I have not understood why it undergoes rearrangements. What is the advantage offered when HLA shows a high degree of polymorphism? What would have happen if all individuals had the same HLA?

There are multiple explanations for the enormous polymorphism in major histocompatibility complex (MHC -- the general term for the equivalent of HLA in all species) proteins. In general they reflect resistance to infectious disease, with the details being mildly debated, and usually not mutually exclusive -- multiple reasons probably apply.
The overall phenomenon is called balancing selection (Wikipedia link), and the most common explanations for the phenomenon in MHC are heterozygote advantage (which is not quite the same as overdominance), frequency-dependent selection, disease-specific selection, sexual selection, maternal-fetal interactions, and drift.
Simplistically, since MHC molecules are involved in protection against infectious disease, if there was only one MHC type then infectious agents that developed resistance to that type would be able to spread throughout the entire population readily. That means you as an individual are better off if your MHC is different from your neighbors', since you're likely to be more resistant to whatever pathogen is infecting them.
Many years ago I wrote a series of blog posts discussing the various evolutionary explanations in some detail, including dozens of references. The posts include:

Evolution of MHC: Elimination round
SEX! (… and MHC diversity)
Heavyweight championship: Overdominance vs. frequency-dependent selection
Testing overdominance in MHC: Can it be done?


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What is the meaning of 'state of nature' in On the Origin of species by Charles Darwin?
I have started reading "On the origin of species" by Charles Darwin.
The beginning paragraph is:

When we look to the individuals of the same variety or sub-variety of our older cultivated plants and animals, one of the first points which strikes us, is, that they generally differ much more from each other, than do the individuals of any one species or variety in a state of nature.

What does he mean by state of nature here?
Note:
The term state of nature is very often used in this book, so for anyone reading this book my question would be helpful for greater understanding.
Edit: One user has requested for more context for better understanding...I would like to provide the next paragraph and also a related paragraph.

When we look to the individuals of the same variety or sub-variety of our older cultivated plants and animals, one of the first points which strikes us, is, that they generally differ much more from each other, than do the individuals of any one species or variety in a state of nature.
When we reflect on the vast diversity of the plants and animals which have been cultivated, and which have varied during all ages under the most different climates and treatment, I think we are driven to conclude that this greater variability is simply due to our domestic productions having been raised under conditions of life not so uniform as, and somewhat different from, those to which the parent-species have been exposed under nature. "

Another paragraph in which State of nature has been used:

Sterility has been said to be the bane of horticulture; but on this view we owe variability to the same cause which produces sterility; and variability is the source of all the choicest productions of the garden. I may add, that as some organisms will breed most freely under the most unnatural conditions (for instance, the rabbit and ferret kept in hutches), showing that their reproductive system has not been thus affected; so will some animals and plants withstand domestication or cultivation, and vary very slightly—perhaps hardly more than in a state of nature.

Doesn't the second paragraph explain exactly what Darwin means?  "State of nature" = things that are not cultivated.

I would think that by "state of nature", he probably referred to any non-cultivated species. As @David suggested in the comments, the expression "in the wild" could also be a good replacement for "in a state of nature".
I think that the first paragraph you quote could be rephrased in the short sentence

There is more phenotypic variation in cultivated species than in non-cultivated species.

My sentence is more concise but of course, is quite a bit less pleasant to read. Darwin was a very good writer after all.

I have provided some more details.Please have a look at them!

I concur with this interpretation. It's his way of saying "wild-type".

@ayc Your edits comforted me in my interpretation. Thanks

This seems correct. @vkehayas — "Wild type" has a specific genetic connotation and even today would not be comprehensible by the layman. The English expression that is applicable and would be understood is "in the wild" (although this does bring up an image of Victorian explorers in pith helmets shooting tigers, rather than Victorian vicars sketching primroses on the Downs).

... one of the first points which strikes us, is, that they generally differ much more from each other, than do the individuals of any one species or variety in a state of nature.

Can be easily re-written as

...in their natural state.

Which is the most minimalistic change to the original text, that still makes the sentence more easily accessible, as its less formal and less old-fashioned language use.


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Why doesn't our immune system react to infused antibodies produced in a horse?
Calmette tried injecting horses with snake venom and then taking out the serum which has produced antibodies against the venom and injecting in the snake-bitten human.
Shouldn't our immune system recognize this exogenous protein and try to eliminate it as it's a non-self protein?

Our immune system does react to horse antibodies, but as with any adaptive immune response it takes some time for the response to develop. In the weeks before our immune response fully responds to the horse antibodies, the infused antibodies can have their effect.
If you then have a second infusion of horse antibodies, the immune response would not only prevent them from having their beneficial effect, but it might case serious adverse effects.  This serum sickness (Wikipedia link) has been known for over a century; here is a paper from 1918 discussing it as a well-known issue:

The injection of horse serum either in small or in large amounts in human beings is always followed sooner or later by the development of hypersensitiveness of the skin to subsequent injections of horse serum. For the development of this reaction serum disease is not essential.

--THE RELATION OF CIRCULATING ANTIBODIES TO SERUM DISEASE. J. Exp. Med. Published March 1, 1918
Although there aren't many modern situations in which horse (or other non-human species) serum is injected into humans, when it is (as with anti-venom, which is generally produced in non-human animals) serum sickness is still a concern.

Serum sickness is a delayed immune reaction resulting from the injection of foreign protein or serum. Antivenom is known to cause serum sickness but the incidence and characteristics are poorly defined. ... The primary outcome was the proportion with serum sickness, pre-defined as three or more of: fever, erythematous rash/urticaria, myalgia/arthralgia, headache, malaise, nausea/vomiting 5–20 days post-antivenom.

--Incidence of serum sickness after the administration of Australian snake antivenom (ASP-22). Clinical Toxicology. Published  2016

Human/mammalian immune system do not react to everything foreign that enters the body. This foreign substances are called "antigens". Instead, the host [i.e. body] reacts to "immunogens" - these are antigens, that CAN elicit immune reaction. Microbes are immunogens, for instance. They don't only consist of microbe proteins, but also of so-called PAMPs, pathogen-associated microbial particles. This can be a bacterial cell wall or "peculiar" DNA and double-stranded RNA, that are definitely cannot be found in mammalian tissue. And these PAMPs are recognized by PRRs, pattern recognition receptors, that are found on innate immune cells, such as dendritic cells and macrophages. WITHOUT activation of innate immune cells, without, basically, INFLAMMATION, the overall immune reaction is not possible. At least, this is a current concept.
So, horse antibodies are not sufficient to elicit immune reaction.
In order to induce immune reaction, these antibodies should be injected with something, that can activate PRRs or cause tissue damage, like aluminum dioxide. The latter substance is largely used in formulation of vaccines. Guess, why ;-)
Of course, there are immune reactions to proteins or harmless xeno-antibodies, but this is usually not physiological, if the manifested reaction is severe. Example: food allergy to egg protein, ovalbumin.
Hope, it helped.
Best,
S

Horse antibodies DO cause an immune reaction, it is just mild and therefore not perceptible as an adverse effect (just like our body reacts to and eliminates thousands of bugs every day).


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Why do musk deer have the smallest red blood cells and amphibians have the largest?
What is the reason that musk deer have the smallest red blood cells and amphibians have the largest? Should they not be proportionate to the size of the organism?

It would be good if you included a reference to your claim that this is, in fact, the case (I personally know nothing about it).

A start would be amphibian red blood cells have a nucleus while mammals do not, removing one of the largest parts of a cell allow it to be much smaller.

In the abstract of (Duke, 1963) we see that mouse deer (Tragulus) have the smallest erythrocytes, not musk deer (Moschus). The paper also explains the origin of the confusion. Mouse deer have 1.5 µm erythrocytes but those of musk deer are 3.6 µm (p. 240). In fact musk deer erythrocytes are the same size as goat erythrocytes at (2.5-3.9) µm (Weiss, D. (2010). Schalm's Veterinary Hematology. 6th ed. pp. 836–842). Whether smaller erythrocytes have since been found, I can't say.
I don't have a definite answer why mouse deer erythrocytes are the size they are but I'd posit a few factors. The size of the erythrocyte needs to approximately match the size of the capillaries so they can press tightly to the epithelium and increase the efficiency of gas exchange. Another factor affecting erythrocyte size is cell number. If you have smaller cells, you need a larger number of them to keep the same sum total volume (as in the figure below). So then factors affecting blood vessel size and the rate of erythrocyte production could possibly affect erythrocyte size.

Size also changes surface area to volume ratio (sa/vol) by the square-cube law and this changes characteristics of diffusion over the cell membrane. A larger erythrocyte may have more plasma membrane, which would allow more diffusion and transporter activity but this may also increase the erythrocyte's volume, which would limit the rate of gas exchange due to solutes needing to work their way out of the middle of the cell. Having a high sa/vol is dependent on morphology (hence, our erythrocytes are biconcave) but Duke claims that mouse deer erythrocytes are actually spherical. So, in theory, the cells' small size could be a compensation to keep their sa/vol high, despite not being biconcave.
Interestingly the size of the cells might not affect the sum total intracellular volume of the cells. In fact, sphere packing density is independent of the size of the spheres. If the cells were made larger, this would increase the size of the gaps between them by the same amount. This could indicate that the the total amount of solutes in the blood is independent of the size of the cells, which could explain the great variation in the size of erythrocytes.


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Why is "VOLVOX" not considered to be in PROTOZA?
Volovox is an Algae, but it moves with the help of Flagella. Protozoa has members that move by Flagella. Why is Volovox taxonomically in the Algae instead of Protozoa?

Algae are also not a taxa (it is an ecological group)

Protozoa is an archaic term that is no longer taxonomically valid because it is paraphyletic. A "protozoan" may be used as a generalized descriptive term of a motile single celled eukaryote, but Protozoa is not a taxon.


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Virus plaque assay, pfu/ml calculation on plates with too little plaques formed
I am a student, so I hope it is okay to put this question here. I've done the virus plaque assay in a practical recently and have a few questions regarding the plaque count for pfu calculation.
In the plates corresponding to times 0 and 10 mins, a few plaques formed (less than 5 plaques in every plate where plaques could be seen) Should I still calculate pfu with those results, or should I leave it as 0 pfu, and use only plaque counts that are at least more than 10?

Wouldn't the actual number of plaque forming units be more precise? Would it make any if your following steps more difficult or why do you want to simplify it?

http://www.microbiol.org/resources/monographswhite-papers/counting-colonies/

Sorry, I don't understand what you mean by simplyging? We were told to count the plaques we could see in the petri dishes and calculate pfu from there. What I don't understand if I should calculate pfu even when there's only one plaque in the plate. The protocol says we should choose the plate that has 20 to 300 plaques for the calculation, but I cannot do that with the plates for time 0 and time 10, because all plates have less than 10 plaques in them. In plates of time 0 the maximum I have is 2 plaques. So I don't know whether it's okay to calculate pfu of 2 plaques or it is usually left out

What is the virus?  If, for example, it is a bacteriophage, then you would not expect any virus particles to be produced at those early time points, right?


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What's the real meaning of "brain shrinkage"?
It is known that some pathologies cause brain shrinkage, for example, it is said that depression causes shrinkage in the hippocampus.
My problem to understand the statement, is that I don't undestand exactly how a brain region shrinks, or what they mean when they say that some pathology causes a brain region to shrink. Does the neurons and everything in them become smaller? Do the cellular membranes become shrink somehow and make the intracellular space smaller? or is it just that a large part of neurons stop firing and they say the brain has "shrinked" because the activity region has become smaller.
Basically, I want to know what happens or what is required in order to have a brain region shrink.

You are trying to get a specific mechanical answer for an observational descriptor that can have multiple mechanisms. Imagine asking the same question about the phrase " tissue damage" There is no single mechanical cause. the brain or an area of the brain is smaller than it was prior, that can have many causes, especially given many contextual uses.

Brain shrinkage = brain atrophy, which means a decrease in volume of the brain tissue, which involves different types of degeneration on the cellular level.
Here is a Wikipedia article about cerebral atrophy with a list of ~30 causes, such as Alzheimer's disease, stroke, cerebral palsy, malnutrition, AIDS, etc. Mechanisms can involve: loss of cytoplasmatic proteins, loss of complete neurons or connections between them, etc.
Alcohol consumption and frontal lobe shrinkage: study of 1432 non-alcoholic subjects (BMJ):

The brain tends to shrink physiologically with age. Heavy alcohol
  consumption seems to exaggerate this shrinkage in social drinkers.
  Moderate alcohol consumption does not seem to affect brain volume.

Vitamin B12, cognition, and brain MRI measures (Neurology):

Methylmalonate, a specific marker of B12 deficiency, may affect
  cognition by reducing total brain volume...