text:
Why is arterial pO2 normal in carbon monoxide poisoning?
Arterial blood gas measurements often show that pO2 is 'normal' even though haemoglobin is bound to carbon monoxide with high affinity.
Is this because there is still oxygen bound to some subunits of the haemoglobin? Surely the CO will displace at least some oxygen, reducing the pO2? As oxygen solubility in plasma is very low, where would oxygen be in the blood if not bound to haemoglobin if there was still high  pO2?

First, let's think about what pO2 means:
pO2 is not the same as "oxygen concentration." pO2 is the partial pressure of oxygen, you can think of it as proportional to the "number of oxygen molecules per unit area leaving the solution" (or colliding with the side of the container). There is also pO2 for the atmosphere, which is going to be approximately 21% * 760mmHg = about 160 mmHg. Partial pressures are often a convenient way to measure gas concentrations, but that only works when there aren't any other interactions happening, so it's not valid for blood.
When blood comes in contact with inspired air, there are >100 mmHg of oxygen molecules hitting the solution and <100 mmHg of oxygen leaving, so there is a net diffusion of oxygen from the inspired air to the blood. If the gas in the alveoli and the blood in the lung capillaries have the same partial pressure of oxygen, there is no more net transfer of oxygen, they are at equilibrium.
Hemoglobin can't do anything to cause the blood to carry more "partial pressure" of oxygen. What hemoglobin does is to "hold on" to oxygen molecules. These "held" molecules can't leave the solution, so they don't "count" as much towards the partial pressure. Hemoglobin instead allows for a higher concentration of oxygen at the same partial pressure of oxygen. Another special thing hemoglobin does is to change its affinity for oxygen in the acidic environment of metabolically active tissue, releasing O2 at a higher partial pressure than it was initially dissolved at.
If you pumped plain saline through the lungs, it would get to about the same partial pressure of oxygen, but it wouldn't have as many oxygen molecules.
If not enough fresh air is entering the lungs, or if the air entering the lungs is low in oxygen, you would expect the blood pO2 to drop, but this isn't what happens in CO poisoning.
There is also the issue that what actually happens in CO poisoning is that affinity of hemoglobin for oxygen increases, but this is actually irrelevant to the pO2 question. The oxygen tightly bound to carboxyhemoglobin (CO-poisoned hemoglobin) doesn't "count" towards the pO2.

Nicely done. I added an answer with some more structure around how we measure and think about total oxygen content that may complement this.

@Bryan's answer is good. I'd like to add a little structure around what seems to be the primary confusion in your question.
There are three important measurements here:

$P_{aO_2}$
$O_2$ saturation
Hemoglobin concentration

$P_{aO_2}$
Arterial $P_{O2}$ ($P_{aO_2}$) is typically expressed in mm Hg. It is very specifically a measurement of the concentration of oxygen dissolved in arterial blood and NOT bound to hemoglobin. Low $P_{aO_2}$ is called hypoxemia.
$O_2$ saturation
$O_2$ saturation is a measurement of the percentage of Hemoglobin binding sites occupied by oxygen. It is expressed as a percentage, e.g., 98%.
Hemoglobin concentration
Hemoglobin concentration is a measurement of the concentration of hemoglobin protein in blood. It is typically expressed in the U.S. in g/dL.
Total oxygen content
Together, these three measurements ($P_{aO_2}$, $O_2$ saturation, and Hb concentration) determine the total oxygen content of arterial blood. Any one or any combination of these three measurements can result in hypoxia (inadequate oxygenation of tissue).
Carbon monoxide poisoning in an otherwise healthy individual is a specific cause of hypoxia that has a characteristic pattern: normal $P_{aO_2}$, normal Hemoglobin concentration, and low $O_2$ saturation. Because there is no problem breathing in oxygen or having it cross the blood gas barrier, there is a normal level of oxygen dissolved in arterial blood. $P_{aO_2}$ is normal. There is no anemia, so Hb concentration is normal. The problem is strictly a matter of $O_2$ saturation.
In many cases of hypoxia, the picture is mixed, but $CO$ poisoning is a classic example where the problem is exclusively one of $O_2$ binding. Anemia is another example. In anemia, $P_{aO_2}$ is normal, $O_2$ saturation is normal, but total oxygen content remains low because there is not enough Hemoglobin.
These are fairly complicated concepts, but covered quite well in West Respiratory Physiology, Ch. 6. The following table may be helpful. Note the footnote for $O_2$ saturation in the row for CO poisoning. Saturation is normal when calculated for Hemoglobin not bound to CO, in other words, there is nothing wrong with the Hb molecule itself. It is simply bound to something else. This is why administration of 100% $O_2$ is a useful treatment.

I like the inclusion of other clinically relevant measures in your answer, +1. I think mine got to be a bit more of a ramble than I intended. Physiology is one of those things that only makes sense once you get it - and then it all clicks. I'm all for trying various ways to getting to the get it step. I'm curious about the O2 saturation measure in the presence of CO... my understanding is that arterial O2 saturation would seem normal in typical CO poisoning, because of high affinity of CO-bound hemoglobin for oxygen.

@BryanKrause the typical bedside measurement is actually not useful in many specific cases, so this is more a physiology teaching concept. I honestly have never seen a CO poisoning patient myself, but in theory you'd have a suggestive history, normal arterial PO2 and normal Hb, and need to have some index of suspicion. Interestingly, another classic teaching about CO poisoning is that you see a cherry red complexion. It turns out, that only happens post mortem, and since we were all taught by pathologists, we passed it along for a number of years.

That last anecdote is both an entertaining and terrifying one.

@DeNovo thank you. I am slightly confused when you say PaO2 is "very specifically a measurement of the concentration of oxygen dissolved in arterial blood". My understanding was that oxygen is relatively insoluble in blood (0.0031 mL / mmHg of oxygen / dL of blood), hence the need for haemoglobin. How can PaO2 therefore reach 100mmHg? Is the /mmHg term in this solubility that of the alveolar air it is exposed to that supplies the oxygen dissolving?

@pincushion44 partial pressure is independent of solubility. Partial pressure in a liquid reflects the amount of gas dissolved in a liquid at equilibrium with a gas at that partial pressure. That's a little confusing, so perhaps it would help to think of it this way: Oxygen is more soluble in freshwater than seawater. Imagine a body of fresh water next to the sea.  More molecules of oxygen will be in a liter of fresh water than a liter of seawater, but both would have the same partial pressure of oxygen, because both are in equilibrium with the same partial pressure of oxygen.

@pincushion44 we use partial pressure to reflect the concentration of oxygen in blood instead of mass or moles per volume because we're not interested in the mass or number of moles dissolved in arterial blood. As you understand, it is not much relative to what is bound to Hb, but O2 dissolves in blood first, before it can bind to Hb. It is important to be able to see if there is a problem getting O2 from the alveoli to the blood, or from the blood to Hb.


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What does the thalamus consist of?
There is a long list of thalamic nuclei which are somehow embedded in the thalamus, a "large mass of gray matter located in the dorsal part of the diencephalon", according to Wikipedia.
I wonder what the nuclei are embedded in:

In a pool of glia cells or of other more or less unspecific "thalamic
neurons"?
Does the thalamus consist mainly of nucleic or of non-nucleic
neurons?
How are the non-nucleic neurons of the thalamus classified?

Edit: In the Scholarpedia article on the thalamus one learns, that thalamic nuclei essentially are relays, and that there are relay neurons and interneurons in the thalamus. Might it be the case, that relay neurons can but interneurons can not be assigned to a specific nucleus (= relay), that means: interneurons build a somehow separate neuronal structure that is somehow interwoven with the nuclei?

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

@BryanKrause: Thank you!

@Hans-PeterStricker That article really gives a good description.

This is an interesting question with good comments. I did medical school, and I am here on unix.se, so let me give some thoughts:
The central nervous system consists of "gray" and "white" matter. In the spinal chord you have this gray butterfly shape, in the neocortex it is "gray matter" (neuron's cell body) and "white matter" (neuron's myelinated axons).
There is no room for a "pool of glia cells" - from tip to tail all the neurons and their axons are highly organised.
Now the brain is already complicated. It is divided into 5 segments, and the Thalamus is quite in the center of everything. Some other nuclei (e.g. the ones connected with the 12 head nerves) have a well defined function, but the Thalamus is hard to define.
The famous "limbic system" is close by, and is also complex.
A high resolution MRI should give a good estimate of neuron/myelin distribution, to the millimeter.  But I am afraid it is not an easy gray-or-white question, but some complicated arrangement, with e.g. short unmyelinated axons.
(The MRIs can look very different)

It is even worse than I thought: this histologic picture shows how hard you have to look to even define a nucleus.

Thalamus Nissl stained
"thalamus histology" give very nice results in google. In the MRIs you can mostly just see that it is something a bit in between gray and white.

First I checked Nissl stain: this really colors neurons (body and dendrites), but not axons.
The stain is labeled "myelin-nissl", and it is blue and magenta, so this must be a combination. But -- I can't even tell which is which!
Well it must be pink is neurons, and thus blue is myelin. This makes sense with the Cn A = cornu ammonis = hippocampus region bottom right, the pink-white spiral, and with the outlining of nuclei. But very counter-intuitive...I trust them it is the appropriate stain.
Keep in mind this is a section to show the nuclei (at their max?), so other parts/sections will look quite different.

Yes, very nice -- there are so many others, too, maybe even better. But this one shows the subtleties well.

wikipedia has some good pics + explanations, but I miss the classical medical neuroanatomic aspect. The "large mass of gray matter" with "nerve fibers projecting out in all directions" is a bit shallow... "lamellae" and "clusters of neurons" are mentioned later.

Maybe you want to have a look at the edit I made to the original question.

source: Stack Exchange

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Umbrella term for "parts of the brain"
I am looking for an umbrella term for general "parts of the brain", esp. for (somehow arbitrary) "subsets of neurons".
For the tree of life there is an umbrella term for all kinds of taxonomic groups all down the tree. They are called taxa.
Domains, kingdoms, phylums all down to families, genus, and species are taxa:

In brain sciences there seems to be no such umbrella term which is generally agreed upon.
Which term would best include all of the following?

brain hemispheres
coarse brain subdivisions (cerebellum, cerebrum, ...)
cerebral lobes (frontal, parietal, ...)
the thalamus („a large mass of gray matter“)
nuclei (thalamic, ...)
Brodman areas
cortical layers
cortical columns
the limbic system
regions of interest (in fMRI)

All of these immediate suggestions don't fit perfectly:

(brain) region
(brain) division
(brain) area
(brain) volume
(neural) group
(functional) system

When you just want to list the components of the brain, that is to say what the brain consists of from the gross anatomy perspective, you can say that the main parts of the brain are:

cerebrum
cerebellum
brainstem

You can also say that the parts of the brain are some smaller, but anatomically well defined components, such as the pineal gland and pituitary gland.
When you intend to describe the functions of anatomically well defined brain areas, you can say that the brain structures are cerebral lobes, thalamus, hypothalamus, hypocampus, amygdala, putamen, corpus callosum, cyngulate gyrus, etc.
A part is "a portion or division of a whole that is separate or distinct; piece. A structure is "mode of building, construction, or organization; arrangement of parts, elements, or constituents." So, it's not about what "it is," but about how you look at it. A thalamus is a part of brain and is a structure made of several nuclei...
You can see these terms used very differently in various texts, but a short overview of brain anatomy by Mayfield clinic use them in the same way as I did. These terms are not a part of any official classification in neurology.

This fits perfectly, for the moment. So, to call a cortical column a (anatomical) "part" would be OK, but also to call it a (functional) "structure"? I can go on with this, thanks for your "opinion", which surely is not an arbitrary one.

It's nothing written in stone here. My impression is that "parts" are used to describe anatomy and "structures" to describe physiology.  To me, it sounds fine if you say that a hemisphere is a part; saying it's a structure sounds awkward, because a hemisphere as such does not really "do" anything. Thalamus can be both a part and a structure if you want.

And what about cortical columns being a part? How does this sound in your ears?

Interesting enough, thank you for the clarification - even though it still might be not written in stone, right? And why do you say cortical columns are not "(functional) structures". At least they are considered "functional units", aren't they?

OK, particular cortical columns can be associated with particular functions, so if you insist, they could be brain structures. A "part" is a "piece" in the sense that you can disassemble a complex thing, lie a car, into clearly defined pieces. When it comes to brain, you can say something is a part when you just want to mention it as part of the bigger brain. If you want to describe it from inside, you can say a structure. It's about the perspective not what "it is."

Gerstner et al. in their splendid book Neuronal Dynamics use the term neuronal populations as a synonym for "groups of neurons", e.g. in chapter 12:

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Why are plasmids called plasmids?
I knew from this website (https://www.etymonline.com/word/plasmid) that the word "plasmid" is a combination of "plasma" + "id" , where "id" means: belonging to or connected to.
But I don't understand how plasmids are connected to plasma even though they exist inside the bacteria cell cytoplasm not inside the blood/plasma

even though they exist inside the bacteria cell cytoplasm

Plasma has several meanings in biology.  Cytoplasm is a type of plasma.
A quick trip to Wikipedia tells us that the term plasmid was first used by Joshua Lederberg in Cell Genetics and Hereditary Symbiosis.  It seems that he coined the term plasmid to reconcile the many terms used to describe extrachromosomal DNA, at the time.

These discussions have left a plethora of terms adrift: pangenes, bioblasts,
  plasmagenes, plastogenes, chondriogenes, cytogenes and proviruses, which have lost
  their original utility owing to the accretion of vague or contradictory connotations. At the risk of adding to this list, I propose plasmid as a generic term for any extrachromosomal hereditary determinant. The plasmid itself may be genetically simple or complex. On occasion, the nuclear reference of the general term gene will be emphasized as chromogene...


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What's the purpose of segregating a virus from the blood and growing it in the lab?
I heard that the scientist in Australia found a way to segregate the 2019 NovCoronovirus from the blood. Does this mean they are one step closer to the cure? Why is virus segregation crucial in finding a cure for a viral infection?

Isolating virus particles is important for accurate genomic sequencing, which in turn enables study of mutation rates and determination of hotspots, locations in the genome where mutations occur at higher rates:

“Sorting individual viral particles makes it possible to identify and sequence the genomes of viruses one by one,” states Òscar Fornàs, head of the Flow Cytometry Unit of Pompeu Fabra University and the Centre for Genomic Regulation.

Researchers attempting to create vaccines need to know this information about the viral sequence, in order to make a functional vaccine:

Dr. Corbett and others had studied the spike proteins on SARS and MERS viruses in detail, using them to develop experimental vaccines. The vaccines never made it to market because SARS was successfully contained with public health measures before the vaccine was ready and preliminary human trials for the MERS vaccine showed success last year.
But the scientists had a method for developing vaccines that could help them fast-track production for the new coronavirus. They used the template for the SARS vaccine and swapped in just enough genetic code that would make it work for the new virus. “I call it plug and play,” Dr. Corbett said.

Characterizing how quickly a virus mutates, and where, can decide the effectiveness of a vaccine.
In the United States, for example, this year's batch of influenza vaccine did not match up well with the strain of flu virus that ended up becoming dominant:

An unusual viral strain is dominating flu activity across the United States and may be one reason for the severe infections in children so far, according to a new report from the Centers for Disease Control and Prevention, and this season’s influenza vaccine is not a close match for the virus.

There are limited resources to allocate to vaccine development. Faster and more accurate sequencing can help with a more targeted and effective response.

It is also important for testing treatments, developing diagnostic tools, and even just determining what kind of virus it is, sequencing a RNA virus is quite different than doing so on a DNA virus for instance.

2019-NCoV was first cultured by a Chinese group, as published here on January 24. China has not shared samples, but did share sequencing data in the linked paper and via GISAID. The Australian group at the Doherty Institute hasn't published yet, but did put out a press release today (January 29), and appears to be the first group outside of China to have cultured 2019-NCoV.
Viral isolation, and in particular, culture, is an important, and often difficult step in characterizing a novel virus. Once characterized, viral culture serves as a gold standard for diagnosis. Generally speaking, the ability to grow virus in cell culture allows for a broad range of pre-clinical studies that can lead to clinical advances including prevention, diagnosis, and treatment. Consider how difficult it may be to study a pathogen if you are not able to manipulate it in a living culture. You can read about this in Murray Medical Microbiology, Ch 50. This article, which does not require a subscription, may also be of interest. The article describes a variety of historical and modern methods, but also includes some discussion about the use of viral culture.


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Why do vaccines sometimes induce a fever?
How does a vaccine cause an immune response such as fever? Why do only some people experience these reactions? Why might those reactions change upon subsequent doses of the same or similar vaccines?

Does this related question help?: https://biology.stackexchange.com/questions/855/how-does-the-immune-system-learn-from-a-vaccine?rq=1

Yes, that's a useful link!  Wish there were something about side-effects like fevers, though.


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Have we found any other life form outside our planet?
I'm not asking about the possibility of formation of life on other planets instead has there been any real evidence of life(such as micro organisms or even very basic structures) that might suggest an evolutionary path(for example from asteroids that hit the earth or planets and other objects in the solar system)?

You really think there might be such evidence, but somebody’s keeping it from you?

@David No not really but I'm trying to get a good grasp of evolution and it seemed only logical that simple life form might exist even in our solar system and no recent exploration mission or revelation came to my mind!

You say you want to get a good grasp of evolution, but your concern seems to have nothing to do with evolution.  In essence you are asking whether life originated from non-living matter (abiogenesis) here on earth or somewhere else in the universe. The latter idea was proposed by astronomers (Bernard Lovell was one I seem to remember) — some would say because it provided an easy way of avoiding a difficult problem they were unable or unwilling to tackle. Do your own homework on that.

No, there has been no evidence found of extraterrestrial or off-Earth life, at least as publicly-shared information. Via NASA:

No life beyond Earth has ever been found; there is no evidence that alien life has ever visited our planet.

There is some debate about this, but there's a chance that we have found alien microbial fossils.  In 1984, a meteorite that originated on Mars was found in Antarctica.  In 1996, odd microscopic formations were found inside that resemble known fossils of bacteria.
The visual resemblance to fossils alone is not enough to prove it is truly evidence of alien life, but it's the most compelling piece of evidence we have now.

It seems controversial since there isn't just much data to support it but can we assume that further exploration on Mars could actually reveal the existence of extraterrestrial life?

@Matt It's possible, but currently there's no concrete evidence.


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Why is therapeutic index a ratio instead of an interval?
The therapeutic index of a drug is defined as its toxic dose ($TD_{50}$) divided by its effective dose ($ED_{50}$).  Why is it defined as a ratio rather than the difference $TD_{50} - ED_{50}$?
For example, if drug A has an effective dose of 1 ml and a toxic dose of 2 ml, and drug B has an effective dose of 50 ml and a toxic dose of 100 ml, then they both have the same therapeutic index (2), but intuitively, I would say drug A is much more dangerous, which is reflected if we take the difference instead.

Most drugs are measured by mass - they are then dissolved in some solution or incorporated with fillers into pill form.
If you are worried only about a difference, say from measuring out a volume to be given intravenously, then it would be trivial to solve that issue by dilution: you could take your drug that was dissolved in 1 mL, dilute it so that you are giving 50 mL instead, and make the difference unimportant. The ratio, however, stays the same, regardless of formulation.
A ratio is also much more likely to come up in clinical practice. Take your example, where the toxic dose is only 2X the effective dose. That means that an error where a drug is accidentally given twice could be a serious problem. It doesn't really matter if the volume delivered is small or large, just that someone doesn't realize the drug was already given.


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How can a disease be transmissible animal-to-human but not human-to-human?
I have heard some debate about whether or not the Wuhan virus can be transmitted human-to-human, but this doesn't make sense to me.  Why wouldn't it be able to?  Are there diseases that can only be transmitted from animals, not humans?

Does this answer your question? Viruses: Adaptation to a new host through repeated host jumps

I have heard some debate about whether or not the Wuhan virus can be transmitted human-to-human, but this doesn't make sense to me. Why wouldn't it be able to?

A virus has to be able to physically get out of one person and then into another in order to infect them.  If it can't do that, it can't spread between people.  Just because you can get a virus by (for example) eating an infected animal doesn't mean you'll be able to spread it to other people, at least without them eating you.

Are there diseases that can only be transmitted from animals, not humans?

Yes, and this is very common.  Rabies for instance can be transmitted from hundreds or maybe even thousands of animals to humans, but is virtually incapable of moving between people because it infects the nervous system which severely limits the ability of the virus to get into another host.

I would think (though I'm far from an expert) that rabies is a bad example.  A person with rabies might well be able to infect another person if, like other animal vectors, they bit that person.  Better examples might be insect-borne diseases.

@jamesqf There are no documented cases of human transmission of rabies, so while it could in theory happen, it doesn't appear to in practice. It is possible viral shedding is too low in human saliva, or that paralysis sets in too quickly in people vs other animals.

Sorry, I mean human transmission through bites. People have gotten it from organ transplants if the donar was infected.

Though I would wonder if it's a matter of humans being unable to transmit rabies via bites, or of infected people being kept from biting others, or perhaps not having the instinct to bite.


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Is there a Zipf law in epidemiology?
Are there cases where Zipf Law appears in epidemiology?
I ranked provinces of China by their coronavirus confirmed cases (2020-01-30 14:29):

4586, 428, 311, 278, 277, 200, 165, 162, 145, 142, 129, 114, 101, 101, 78, 70, 65, 63
  ...

Then I tried fitting the Zipf Law to it. I managed to get a good fit for a segment of it by using $x_n = 1600/n$:

4586, 428, 311, 278, 277, 200, 165, 162, 145, 142, 129, 114, 101, 101, 78, 70, 65, 63 ...
1600, 800, 533, 400, 320, 266, 229, 200, 178, 160, 146, 133, 123, 114, 107, 100, 94, 89 ...

The fit isn't very good, but good enough to be interesting. It makes me think there might be situations in infectious diseases where a Zipf Law appears. And by (Cristelli et al, 2012), I expect this situation to be particularly likely in places with a lot of economic and social integration.
I searched on Google Scholar with phrases like "Zipf infectious disease", but did not get anything interesting.

I am now aware of Zipf Law and its applications in biology but I want to ask what exactly are you trying to model? There are some well know modelling approaches for epidemiological data.

@WYSIWYG I'm just trying to figure out if Zipf's Law applies to this dataset. What it actually models, I'm not sure, but Zipf's Law applies to many phenomena for unknown reasons, so I think it'd be cool to see if it applies to epidemiological data.


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How do I identify and then isolate a Gene that codes for a particular observable phenotype
How do I identify and then isolate a Gene that codes for a particular observable phenotype. It is a novel bacteria and I do not know the gene sequence or the protein that it codes for.

This sounds like a homework question. Finish reading the Tour (you haven’t) and read our policy on homework questions. The repost when you can satisfy the criteria for allowable homework questions.

https://en.m.wikipedia.org/wiki/Forward_genetics


text:
How was 2019-nCoV (Wuhan coronavirus) identified so quickly?
It seems that from the first few cases to identifying 2019-nCoV as a new disease happened very quickly. How were they able to identify this as a new disease and not an outbreak of a previously known but rare disease so quickly? Side question: How many patients were needed to identify this new strain of coronavirus?
If this question can be answered in the generic case as well (how do any new diseases get identified quickly), that would be good too!

I'm voting to close this question as off-topic because this is not a question about a biological problem that can be answered objectively, which is what this site is about, but a question about historic public health measures taken in China.

@David See https://biology.meta.stackexchange.com/a/4040/10204

Your question has come back because of an edit. The meta link you posted over a month ago is irrelevant to whether a question is off-topic or not. It just expresses the view of individuals who have not backed up their opinions by answering your question. Since your original post there is a resource on information about the coronavirus on meta as a community wiki, which you can find here.

Thanks @David. That meta link doesn't answer my question. It's possible the information is in one of the further links somewhere, but then it's a link only answer. "Please provide the relevant details here."


text:
Why does a stronger heart cause blood pressure go down
Intuitively, why does a stronger heart cause blood pressure to go down? The answers I've found from a cursory google search seem to indicate that it has to "work less hard" to pump the blood and that it "beats more slowly," but I do not immediately understand the implications of this.
Furthermore, if it is due to a slower heart beat in a stronger heart that blood pressure is lower, then how does (/is it true that) blood pressure remains lower in those with a stronger heart during exercise? Wouldn't a stronger heart beating just as fast as a weaker heart lead to higher blood pressure?
Thanks for any help. :)

Welcome to Biology.SE! I think this might be a better fit for [medicalsciences.se]. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

My intuition may be wrong, but see Bernoulli’s equation for an incompressible fluid. Modeling the circulatory system as a closed loop, the pressure exerted on arterial walls by blood decreases with increasing blood velocity. Assuming a stronger heart pumps blood faster, a stronger heart should reduce blood pressure compared to a weaker heart and slower blood flow.

Use of the word “stronger” is not clear. The flow rate needs to be considered and those who are very fit have a lower resting heart rate, a higher maximum and tend to need a lower beats per minute when doing the same exercise level as an unfit person.

A heart that is stronger (bigger; thicker walls) does not need to work stronger. In usual circumstances, the strength of a healthy heart has nothing to do with blood pressure.


text:
What animal is this?
I have seen this bug/worm twice on my dog's leg after taking him for a walk this week. I think that this is a leech, but my mom disagrees because she says leeches are not found where we live but are found around beaches. We live in Carmel Mountain San Diego: Google Maps.
The closest beach is around 15 minutes away.
The bug is approximately the size of a fingernail, and it did not do anything when I picked it up.

EDIT: We were just walking around my neighborhood, nowhere jungle-ish at all.

Welcome to Biology.SE! What kind of environment(s) are you walking through? There are definitely leeches in California, but leeches are typically associated with wetlands ...

I added an edit, with details about the environment of the walks.

Leeches are found other places than beaches. Some live in streams, lakes, rainforests, mountains, and even aquatic locations in deserts

@theforestecologist interesting. I guess San Diego can be considered a Desert, but I do not think there are any aquatic locations around where we live.


text:
Provisional vaccine for fast spreeding new viruses?
Developing a standard vaccine for coronavirus will take at least a few months - what might be too late:

However, its sequence is already known, and is nearly identical - suggesting a recent single point of origin for human host, e.g.

"The researchers also found that the eight complete 2019-nCoV genomes were more than 99.98 percent identical" https://www.genomeweb.com/genetic-research/coronavirus-genome-sequencing-finds-distinct-genetic-differences-2003-sars-virus

So the question is if/how there could be quickly started production of some provisional vaccine - not perfect but fast to introduce? Also exploiting the fact that these viruses are now nearly identical.
For example synthesizing its outside proteins and putting them on liposomes - would its introduction to blood have a chance to prepare immune system for the real virus?

I think the main issue about developing a new vaccine is not that it it's supposed to be perfect - but that it's safe. You can just quickly put out medicine without rigorously testing for any side effects

Fake virus: e.g. liposome exposing some material of the virus, seems easy to synthesize and safe(?) - definitely safer than the real virus, and preparation of the immune system it could provide(?) might be a matter of life and death (?) Sure, in normal situation there are needed time consuming clinical tests, but the question here is about situation when time is literally translated into deaths, and it is approximately known where the virus will strike?

Perhaps you should address yourself to sites or texts related to clinical virology. People spend their lives working in this area. This site does not exist to solicit the opinions of people whose expertise you know nothing about theories of curing diseases based on no expertise whatever. If you think you are in “A race to save mankind from destruction” you may have been watching too many movies.

I have added the exponential growth plot to remind how serious this situation is, and generally ask if there is some "provisional vaccine" - not perfect, but which could be introduced before it spreads over the world. The comments suggest the answer is 'no', but could anybody elaborate with support of some materials?

Some discussion: https://www.scienceforums.net/topic/121181-provisional-vaccine-for-fast-spreading-new-viruses/

Stack Exchange Biology does not have the remit or expertise to answer questions about coronaviruses relating to the recent 2019-nCoV outbreak. We have compiled a list of what we regard as reputable external sources of such information. Please consult that.


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Which parts of the cerebral cortex don't belong to the neocortex?
In the Wikipedia article on the cerebral cortex one reads:

»Most of the cerebral cortex consists of the six-layered neocortex.«

Accordingly, in the Wikipedia list of regions in the human brain, one finds "cerebral cortex" and "neocortex" as almost synonyms.
But assuming that they are not perfect synonyms – but that there are some parts of the cerebral cortex that are not part of the neocortex – I wonder which parts this might specifically be.
To make my question specific, I list here all parts of the cerebral cortex as listed at Wikipedia:
Cerebral cortex (neocortex)
Frontal lobe
    Primary motor cortex
    Supplementary motor cortex
    Premotor cortex
    Prefrontal cortex
    Orbitofrontal cortex
    Dorsolateral prefrontal cortex
    Superior frontal gyrus
    Middle frontal gyrus
    Inf. frontal gyrus
    Brodmann areas
Parietal lobe
    Primary somatosensory cortex (S1)
    Secondary somatosensory cortex (S2)
    Posterior parietal cortex
    Postcentral gyrus (Primary somesthetic area)
    Precuneus
    Brodmann areas
Occipital lobe
    Primary visual cortex (V1)
    V2
    V3
    V4
    V5/MT
    Lateral occipital gyrus
    Cuneus
    Brodmann areas
Temporal lobe
    Primary auditory cortex (A1)
    secondary auditory cortex (A2)
    Inf. temporal cortex
    Posterior Inf. temporal cortex
    Superior temporal gyrus
    Middle temporal gyrus
    Inf. temporal gyrus
    Entorhinal cortex
    Perirhinal cortex
    Parahippocampal gyrus
    Fusiform gyrus
    Brodmann areas
    Medial superior temporal area (MST)
Insular cortex
Cingulate cortex
    Anterior cingulate
    Posterior cingulate
    Retrosplenial cortex
    Indusium griseum
    Subgenual area 25
    Brodmann areas

If there are parts of the cerebral cortex missing here, a hint would be welcome!

The hippocampus is considered archicortex rather than neocortex. Sometimes hippocampus is considered "sub-cortical" but I think this is only really fair if you really mean "sub-neocortical"; it's common for "cortical" to be used as a shorthand for neocortex in human neurobiology. Writers will be more specific when necessary.
The piriform cortex and related olfactory structures are considered paleocortex.
Some also delineate an in-between periallocortex that includes entorhinal cortex and limbic structures around the hippocampus.
Neocortex is mostly a six-layered structure and found only in mammals. The other, non-neocortical types of cortex have fewer layers, and are shared by an older common ancestor that includes other vertebrates.


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Why is angiotensin converting enzyme localized in the lungs
I understand that it's also found elsewhere, such as in renal capillaries, but I can't see logic behind it being located in the lungs. Isn't ACE's function, through making more angiotensin II, causing increased fluid and sodium retention and increasing peripheral resistance? What benefit does that purpose get from ACE being mainly in the lungs?

I guess you do mean ACE, i.e you do not mean ACE2.
It looks like some  coincidence that you started your question when "Corona" began.  ACE2 (in spite of homology: not ACE)  is target receptor of CoV and COV-2  in lung: Pneumocytes type II. - Your question makes me re-research on ACE not ACE2 in lung epithelia.  In fact, as answered: ACE2 but not ACE in lung epithelia.
Highly interesting: in evolution, ACE2 might have mutated from ACE as both receptors are almost identical. ACE might be  the more ubiquitious protein in the sense of answer given.

ACE is present on the luminal surface of vascular endothelia throughout the body and is abundantly present in the endothelium-rich lungs.
ACE in the kidney—particularly in the endothelial cells of the afferent and efferent arterioles—
can produce enough ANG II to exert local vascular effects.
Thus, the kidney receives ANG II from two sources:
✓ Systemic ANG II comes from the general circulation and originates largely from the pulmonary region, and
✓ Local ANG II forms from the renal conversion of systemic ANG I.
• In addition, the proximal tubule secretes ANG II into its lumen and thus achieves intraluminal concentrations in excess of
those in the general circulation. ANG II in the circulation has a short half-life (~2 min).

Oh, so the reason ACE is abundant in the lungs is simply a product of the fact that the lung has a lot of endothelium?

Yes, you are right.


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What is Balbiani's vitelline body function?
I tried searching on Google Scholar but I found little to no information about this Balbiani's vitelline body.
I don't even know why it is called vitelline...I've been taught that it can be seen under the electron microscope, is perinuclear, made of mitochondria and lamelle anulatae (I don't know what these are) and you can see it only in primordial follicles.
I initially thought it was involved in protein synthesis, but primordial follicles should be biologically quiescent until they 'wake up' and begin folliculogenesis.

Did you read this section in Wikipedia?

No, I didn't.I'm reading it now for the first time.So this vitelline body silences transposons?

We can close this question as solved.


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Are there land animals that use gill-like organs instead of lungs?
Among aquatic, water-breathing animals, gills and other continuous-flow breathing methods dominate over lungs and other storage-based breathing methods as in land animals. Notably, axolotls have gill-like structures around their heads which use a high surface-area structure heavily vascularized with capillaries to breathe water.
However, it seems all air-breathing organisms use storage-based breathing, air-breathing fish included, as lungfish use their swim bladders as lungs, a clear example of storage-based breathing.
Are there any land organisms that use continuous-flow breathing methods over lungs?

That emphasizes that fish with only gills would have had much difficulty in adapting to land for the same reason that electric tyre pumps and manual tyre pumps are different.

Terrestrial crustaceans are land animals that use gills (or gill-like structures) for gas exchange, though these gills must be kept moist for efficient respiration.
Specifically, animals like hermit crabs have a branchiostegal lung that looks like gill tissue but is better adapted for absorption of oxygen from air instead of water.

Some terrestrial hermit crabs (genus Coenobita) have gills, but these are only partially responsible for their respiration1. These animals carry around water with them in the snail shell they 'wear'.
Amphibious land snails in the genus Pomatiopsis have gills2.
Finally, a terrestrial amphipod known as a "sand hopper" Talitrus saltator also has gills3.
References:
1: Farrelly, C. A., & Greenaway, P. (2005). The morphology and vasculature of the respiratory organs of terrestrial hermit crabs (Coenobita and Birgus): gills, branchiostegal lungs and abdominal lungs. Arthropod Structure & Development, 34(1), 63-87.
2: Burch, J. B., & Van Devender, A. S. (1980). Identification of eastern North American land snails: The Prosobranchia, Opisthobranchia and Pulmonata (Actophila). Museum of Zoology and Department of Ecology and Evolutionary Biology, The University of Michigan.
3: Ungherese, G., Mengoni, A., Somigli, S., Baroni, D., Focardi, S., & Ugolini, A. (2010). Relationship between heavy metals pollution and genetic diversity in Mediterranean populations of the sandhopper Talitrus saltator (Montagu)(Crustacea, Amphipoda). Environmental Pollution, 158(5), 1638-1643.

Modern reptiles (including birds, but possibly excluding turtles) have a continuous flow system of lungs. In birds, the lungs have air pushed over their lungs by larg air-sacs, similarly to how water is pumped over gills by the mouth in fish


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How does an antisense RNA molecule restore protein function in CF patients?
I am researching a treatment for cystic fibrosis (CF) called Eluforsen and I am trying to understand the mechanism by which an RNA molecule can restore proper protein function. In many research articles I come across the same sentence:
"Eluforsen, is an antisense RNA oligonucleotide designed to bind specifically to the mRNA region around the F508-encoding deletion and to restore CFTR protein function."
But I cant find any literature explaining how an antisense RNA molecule can restore function of a protein on its own. When I think of antisense RNA I think of  RNA interference not restoring protein function.

Please [edit] your question to include information for at least one of the references for the quote. This is expected on this site, is generally considered good practice in scientific communication, and will help other users understand the context for the quote. ——— In general, it might be beneficial for you to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

https://www.nature.com/articles/nbt0102-47

The root of the problem for a majority of cystic fibrosis patients is that they have two defective genes for a particular protein and at least one of these genes is defective because it is missing a 3-base codon for the amino acid at position 508 of the protein.
Eluforsen, also known as QR-010, is a somewhat modified 33-base RNA molecule.  The bases in it are complementary to an area centered on the codon for amino acid 508 of the normal mRNA (messenger RNA) for the protein. Since the defective mRNA is missing 3 bases in the middle of this sequence, eluforsen binds to only 30 bases of the mRNA and has an unbound loop of three bases in the middle, as suggested by the wiggle in this diagram:

[image from SEC]
Such a double-stranded stretch of mRNA is abnormal, of course, but the effect of its presence at least some of the time is to cause the mRNA to undergo repair in the duplex area in a manner which makes a break in the main strand opposite the loop and inserts RNA bases that are complementary to the three "excess" bases present in the eluforsen loop.  Since these three bases are complementary to the normal mRNA bases at that point, the effect is to transform the defective mRNA into a normal mRNA.  When the repaired mRNA is translated by a ribosome, a normal protein is produced, and some of the symptoms of the CF condition are reduced because of the presence of normal protein.
The mechanism which causes the mRNA to be repaired in this manner is not yet well understood(1).  The condition improvement from a complementary mRNA fragment was noted back in 2004.(2)  One hypothesis is that RNAse H is involved in the repair.(1)  Some further information about QR‐010 effects can be found towards the end of reference (3).
(1) Matos & Matos, 2018
(2) Zamecnik et al., 2004
(3) Alton et al., 2016


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Virus Mortality Selection
This question is related to the recent Wuhan outbreak. Currently, mortality rate for the virus is somewhere around 2-3%. This is much lower than say, SARS (9.5%) and MERS (34.5%).
As a thought experiment, the main cause of death of the above viruses tends to be pneumonia (direct and secondary). If pneumonia leads to a higher rate of infection, then (indirectly) would such a virus would become much more deadly over time?
Do viruses such as the coronavirus self-select for higher rates of mortality, e.g. by leading to pneumonia, thus causing more phlegm and coughing?
Related to the above, how quickly can such mutations arise?
Sources would be really appreciated!

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular note that speculative questions (i.e. thought experiments) are not appropriate for this site. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

Stack Exchange Biology does not have the remit or expertise to answer most questions about coronaviruses relating to the recent 2019-nCoV outbreak. A list of what are regarded as reputable external sources of such information has been posted on Biology Meta. Please consult that.


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Coronavirus origin could be bat, why this happen while people have been eating bats for centuries?
Sorry for my lack of understanding, Why now, when people been eating bats for centuries? If bats are simply a vector, where does that virus come from?

Please see the meta discussion and contribute. I thoroughly disagree that biology.SE doesn't have the expertise to answer questions about biological concepts and disease mechanisms as they relate to virology. They are, in fact, explicitly on topic. This question's problems are related to the lack of prior research. Address that issue and I will vote to re-open.

Bats are reservoirs of many important human pathogens, some are emerging infections (e.g., 2019-NCoV, the coronavirus in the news recently), and some are not (e.g., rabies).
Contact between humans and bats is certainly not a new phenomena, but there is more required for an emerging infection than a reservoir and a new host. There must be some bridge that allows a virus to cross a previously effective species barrier. For SARS, there was an intervening amplifying host, the palm civet.  We've now had long enough to study the molecular biology, so this is now quite well described:

Once SARS-CoV had jumped from bats to civets, it underwent further mutations in civets. The first K479N mutation allowed SARS-CoV to jump from civets to humans and the second S487T mutation allowed SARS-CoV to transmit from human to human, leading to the severe SARS outbreak in 2002–2003.

It may be useful to understand that, as they are RNA viruses, coronaviridae have a high error rate, increasing the rate of mutation. Additionally, making a species jump may allow for novel recombination.

I think you could expand a bit on the lack of stability in viral populations.

@BryanKrause done. Feel free to expand further if you'd like.

The four endemic human coronaviruses are all bat-origin coronaviruses that have jumped into humans in the past 100 years, so the premise of the question is wrong.

@iayork that's fascinating. For some reason I was remembering bovine coronavirus, rather than bat as a source for human coronaviruses.

A more recent study suggests that two of them may have passed through livestock first (https://www.ncbi.nlm.nih.gov/m/pubmed/29551135/) and may or may not have started in rodents


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What are the differences between internal organs between sub-saharan Africans and Northern Europeans
Lets take as examples a typical Norwegian and a typical Nigerian.
In terms of human anatonomy the outer differences are more obvious e.g. (on average)

White skin vs dark skin
Pointy nose vs broad nose
Thin lips vs thicker lips
Straight hair vs tight curly hair
Different skull shape
Height differences
Different colour eyes or eyelids.

In fact there is almost a difference in every external organ.
There are also some invisible differences such as propensity to sickle cell disease.
But what I hear less about is the differences (in general) between internal organs between populations. Some people even suggest that differences are only "skin deep" between human populations. Which I think goes against evolutionary theory. As why would natural selection stop at skin level? Also, there is a lot of research into skeletal differences but that's easier to do since we can look at a skeletons.
Therefor it seems fairly logical to assume that there would be fairly apparent differences in internal organs between these populations. (I hesitate to use the word 'races') i.e. as apparant as different hair types, or different nose shapes.
I don't mean that one population will have 3 kidneys for example, but I would expect that there would be an obvious shape or size difference between most, if not all internal organs, just as there is a shape, colour or size difference between most external organs.
Is there some research done on this, e.g. a catalogue of differences in internal organs morphology between different populations? Or is it taboo to even ask such questions perhaps?
Edit: One might say, "how would anyone know? Or care?" But, for example, a heart surgeon might find they need different sized instruments dealing with different people. Or surgeons from different continents might compare notes on anatomy. And anatomy textbooks based on just one population might not be representative. Surgeries working on one "race" might not work on others. e.g. if the heart wall was thinner or the colon was longer.

Why was this downvoted? Is it a taboo subject? I thought it might be. Pity societal pressure gets in the way of science.

I don't know about organ sizes, but it is known that certain population are more prone to develop certain diseases than others. One famous example I'm aware of are the Pima, who developed a very efficient metabolism in response to the available food in their  traditional environment. However, this efficient metabolism in combination with nowadays western diet makes them prone to overweight and related diseases like type two diabetes. There is research in that field, but it's far from being complete.

I won't consider it a taboo but you must understand that the traditional concept of races is based on superficial appearances. For example it would put all black skinned African people in one group (and so on with other people). Certainly there are differences in different human populations (morphological, anatomical and metabolic). You may rephrase your question on these lines and narrow it down. Be precise and avoid unnecessary explanation of things that you are not interested in.

@WYSIWYG Well if you say straight hair vs. african curly hair is "superficial" then you might say there would also be "superficial" differences in organs. However, it easy to tell by sight the differences. No-one would mistake a native Nigerian for a native Norwegian. I did narrow it down to Norwegians vs Nigerians. In that case the question is "what are the superficial differences in internal organs between these two people." Sounds like a worrying lack of research in this area!

@zooby By superficial, I meant what is easily observable (like skin color or hair shape). The easy-to-tell-by-sight differences were the basis of race. Research has found that just because two people look similar doesn't mean that they are genetically more similar. Anyway, by narrowing down I meant that you can make you question precise. I would rephrase the title on the lines of "are there significant differences in the internal anatomy of different human population groups" (and edit the body accordingly). You don't have to narrow it down to the level of comparing Norwegians and Nigerians.

@WYSIWYG. I think by writing it like that it would make it so vague it would lose most of its meaning unfortunately. Is there anything wrong with asking about 2 specific populations?

“Propensity to sickle cell disease” is a misleading description of the fact that specific individuals in a population have a mutation that renders them less susceptible to malaria. Sicilians also have individuals in their population with a different mutation that serves the same function, although causes a different disease in homozygotes. In neither case is this a universal feature of the populations like skin pigmentation.

@zooby nothing wrong in asking about these specific groups. However, your actual question can be answered with respect to any two groups (not necessarily the ones you mentioned). Also note that lifestyle will also affect the organ sizes. There is some correlation between body weight and size of some organs (studies done in different populatins). However, I don't think anyone has investigated if these relationships are significantly different between different populations (after accounting for factors such as lifestyle and diet).

Yes, but I was just interested in these two particular groups as they have more obvious outward differences than, say, a the differences beteween Sweden and Norway, for example. So the differences should be more pronounced. It would be fascinating if it was found, for example, that in one population the left ventricle was larger than the right and other populations the reverse was true (as a made up example). In a similar manner that a nose might be wider than it is tall or vice versa.

Perhaps you should ask on a medical site. Someone doing autopsies in a country with a population of diverse origins would know. I imagine the answer is no or it would have been observed and reported. I see nothing wrong with your question, just that you are addressing it to a group that is unlikely to have experience in this area.

@David. Thanks, I might try.


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Non specific band in EMSA gel?
I am doing EMSA with Thermo LightShift Kit. I have a 150 bp biotin labeled probe which has been PCR amplified, gel eluted and sequenced. When I load samples on 5% native polyacrylamide gel, I see a non specific band in my control and samples along with suspected shift. Can anybody please help with an explanation of this band and possible troubleshooting?
Image Details:
Lane 1 and 3 are controls rest are samples

My binding reaction has HEPES ph 7.9, KCl, DTT, Glycerol, MgCL2, Poly (dI.dC) and NP-40
Lane 1 and 3 are my negative controls ie binding reaction mix + labelled probe
Rest are binding reaction components mix + probe + nuclear extract
Nuclear extract was made using Thermo NE-PER kit
Thanks!

Can you provide more details on what your controls and samples contain? Are they positive or negative controls? Have you run DNA-only?

My binding reaction has HEPES ph 7.9, KCl, DTT, Glycerol, MgCL2, Poly (dI.dC) and NP-40 Lane 1 and 3 are my negative controls ie binding reaction mix + labelled probe Rest are binding reaction components mix + probe + nuclear extract Nuclear extract was made using Thermo NE-PER kit.

You could try running your probe on a gel by itself to make sure it only contains one species. Your labeling may not be uniform. You could acrylamide gel purify it before running your EMSA if it contains a secondary band. This should make the assay cleaner.

I did run just the probe and did not see this extra band. I ran the probe without poly (dI.dC) too and did not get any band as well. I am only get this when I run the probe with all components of binding reactions. I ran them alone without probe too to rule out contamination. Do you think it might be due to poly (dI.dC)?

Yes, my guess would be that your probe is non-specifically binding with the poly (dI.dC). You can probably eliminate this by playing with the salt concentration, adding 1% DMSO, or adding more detergent to your buffer.


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Genes associated with human female breast size
What are the genes associated with female breast size and natural variation thereof in human beings?

Welcome to Biology.SE! This seems like a valid question to me, but please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). The lack of evidence in your post for any effort at prior research may be why some people have downvoted your post. Thanks!

It's frequently helpful to do a little research with e.g. Google before asking questions here. I searched "human breast size genetics" and found a lot of information.
Also note that in genetics it is usually misleading to say "the genes for X" or similar constructions. We can point to specific genetic variants (e.g. DNA variations, which are not genes) that have a statistical association with some phenotype (such as breast size). This is the best we can do here.
To directly answer your question, looking at some of the papers there is not strong evidence for any specific gene being associated with breast size. The total proportion of variation explained by all the variants detected is on the order of 2%-3%. In other words, those genes don't seem to be very important for breast size. You can read more about these variants here or here, and in other similar papers that you can find on google scholar.
Some (such as those papers) have estimated that variation in breast size is up to 50% due to genetics, which is to say that "heritability" is 30%-50%. Some people interpret this to mean that we just need to look harder to find more variants. However heritability is a notoriously unreliable estimator, so it may be truly a much smaller percentage of breast size variation that is heritable. To read more about how to interpret this try this paper.
Hope that helps.


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A question about dna triplex
Short DNA triplex strands have been identified in various organsims. But, would injecting a single strand of DNA or RNA (with its bases complementary to the bases of DNA found in the major groove of a certain gene ) cause it to form a DNA triplex   at that gene?

Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. ——— We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, are you sure you understand how triplexes form? The third strand interacts with the others through Hoogsteen base pairs, which is different from complementary (Watson-Crick) base pairing ... Thanks!

@tyersome Yes i understand this, I meant is triplex formation a spontaneous interaction that occurs at physiological state when the needed strand is present?

Possibly, yes, but there are complications.
There are other conditions that help create the energetically-favorable conditions for bases to bind in a way to form a triplex, including acidity and presence of magnesium ions.
The region of DNA where your gene of interest lies (or its regulatory regions, depending on what you're trying to do) would need to be unpacked, as well. DNA is usually packaged into chromatin. Histone complexes, which wrap up DNA, provide some measure of protection of the major groove. To make a triplex, you'd need biochemical conditions that unwrap histones and support triplex formation, generally.
Use of RNA, specifically, could be complicated if it is or could be processed into a short- or microRNA element, which could be consumed in downregulating the population of mRNA molecules (which, in turn, ultimately regulates gene expression). It isn't helpful if it gets used up before it binds to your triplex of interest.
There is some pharmaceutical interest in TFOs (triplex-forming oligonucleotides) as a drug-delivery mechanism.
If some gene is broken and implicated in a genetic disease, say, and its DNA or nearby regulatory regions can be made accessible, perhaps a TFO can be administered that would help turn up or down the expression of that gene's protein product.
Papers on TFOs could probably point you to other engineering problems that researchers have encountered and would need to overcome in order to create an effective medicine.


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Calculating Rate of Growth without a Population
Lets say that by studying individuals of a rare species, you have determined that species gestation period, age of sexual maturity, average time between pregnancies, maximum lifespan, and average number of individuals born per pregnancy. However, you have never had enough specimens at the same time to establish a breeding population.
How can you calculate the maximum rate of growth of a population from just the information already gathered? If not, what other information would be needed?

is this a homework question?  Given this information, you can write down a life table and calculate a growth rate: http://web.mit.edu/7.01x/7.014/documents/populations.pdf

The breeding lifespan of an individual is (maximum life span $L$ - age of sexual maturity $M$).
Call the time between pregnancies $\tau$ and the gestation period $g$. Then the average number of pregnancies per (female) individual is then $(L-M)/(\tau+g)$.
If the average number of individuals per pregnancy is $N$, then each reproducing individual produces $N(L-M)/(\tau+g)$ offspring in their lifetime.

If this species has males and females (gonochoric/dioecious), and a 50/50 sex ratio, then the number of females per female is $N(L-M)/(2(\tau+g))$.
This is a growth rate per generation: the generation time is approximately (mean time between birth of mother and birth of offspring) = $(M+(L-M)/2)$ (it's a little more complicated than this); the growth rate per unit time would be approximately equal to the ratio (growth rate per generation)/(generation time).
Other things you might need to take into account: survival of juveniles up to $M$; menopause (unusual).


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Is it possible for an immune host to be reinfected and show symptom before swift recovery?
For example, let's say the pathogen is a virus, and the host was infected once but recovered purely on its own and thus retained a highly effective adapted immunity.
However, if we IV inject the the host with an overwhelming dose of virus, is it possible to infect some cells, cause some cell death before the immunity taking over and the host recovery? Is it possible to completely overwhelm the immune system and kill the host anyway?


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What is "irrational" drug/molecule design?
Both the papers "Directed evolution: the 'rational' basis for 'irrational' design" by Tobin et al. and "Rational and 'Irrational' Design of Proteins and Their Use in Biotechnology" by Nixon et al. reference the concept of "irrational" drug design, but never formally define it in their text.
Is there a formal definition of what makes a drug design process "irrational"? What is the meaning of the term "irrational" in this context?

Nixon AE, Firestine SM. Rational and "irrational" design of proteins and their use in biotechnology. IUBMB Life. 2000;49(3):181-187.
Tobin MB, Gustafsson C, Huisman GW. Directed evolution: the 'rational' basis for 'irrational' design. Curr Opin Struct Biol. 2000;10(4):421-427.

"Irrational" design in these papers refers to combinatorial mutagenesis, which is put forward as the alternative to "rational" protein design.
Rational design involves using existing information about a protein to choose residues to mutate.
From Nixon et al.:

Alteration of function by rational approaches can be achieved through single-point mutation, exchange of elements of secondary structure, exchange of whole domains, or generation of fusion proteins

Whereas irrational design uses random mutations to gain insight into the functional capacity of specific residues or domains, which may then be further manipulated by rational approaches.
From Tobin et al.:

‘Irrational’ protein design using directed evolution methods relying on entirely random mutagenesis techniques has also had its successes, particularly in cases in which sequential rounds of mutagenesis have been pursued.

According to "Drugs: From Discovery to Approval" by Rick Ng. The "rationality" of drug design refers to whether structure is used to inform the design.
The Irrational approach:

involves empirical observations of the pharmacological effects from
  screening of many chemical compounds, mainly those from natural
  products. The active component that gives rise to the observed effects
  is isolated. The chemical formula is determined, and modifications are
  made to improve its properties.

Whereas the Rational approach:

Requires three-dimensional knowledge of the target structure
  involved in the disease. Drugs are designed to interact with this
  target structure to create a beneficial response.


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Does photosynthesis begin instantly when a plant is exposed to light?
I'm curious to know if the process of photosynthesis has a "ramp-up" time to become useful to a plant, or if it begins instantaneously when the plant is exposed to light after a period of darkness.
For example, if I'm growing a plant indoors using artificial light, does the plant start converting CO2 the very moment I switch on the light, or does it take a certain period of time for the reaction to reach a critical momentum for the plant to be able to produce sugars?
Or, as a thought experiment, if I turned on the light for 10 minutes, would the plant produce roughly the same amount of sugars as if I toggled the light on for 1 minute, then off for 10 minutes, 10 times in a row?

This is a really interesting question! It gets to the heart of how photosynthesis works.
First, note that whether or not the plant will immediately start producing glucose depends on a variety of factors (what type of plant, what type of light). For example, many succulents undergo CAM photosynthesis (Crassulacean Acid Metabolism) in which light capture and CO2 fixation are temporally separated (the former during daylight hours and the latter at night). Additionally, artificial light comes with different wavelength compositions (ratio of red to far-red light  can differ) and photosynthesis rates will change accordingly read more here.
But I haven't yet addressed the heart of your question: how long does it take for a plant to start photosynthesizing once it is exposed to light? To think about this, consider what is actually happening when light hits a leaf. Light energy is absorbed by pigments in the chloroplasts, which transfer energy to neighboring pigments until an electron is transferred to a reaction center. From here, "light reactions" of photosynthesis continue and usable chemical energy is obtained. From there, the CBB cycle (sometimes called the Calvin Cycle, Calvin-Benson, or "dark" reaction) continues, which is where the CO2 from your question comes into play, and 6-carbon sugars are produced. It isn't a matter of "ramping up", so much as completing this series of chemical reactions.
So now, it is time to consider your thought experiment. Let's say that you have a bean plant in your kitchen (C3 photosynthesizer), and you conduct your experiment shining a white-light lamp on the plant with the experimental conditions as described. I believe that you would produce roughly the same amount of sugars in each because glucose synthesis occurs on the order of seconds (~30s). If you exposed your bean plant to white light for only 5-second increments, there would not be time to produce the energy needed to complete the CBB cycle.
Aside: the experiments that first elucidated the CBB cycle were conducted by exposing cyanobacteria (a photosynthetic bacteria) to labeled (heavy) carbon, and exposing it to light for a few seconds, and characterizing which compounds were produced from that heavy carbon within that few-second time frame. Read more about that experiment in the previous link. It sounds like Calvin himself wondered the same thing you did!
For further reading on the basics of plant physiology, including photosynthesis, I always recommend the plant bio "bible": Plant Physiology and Development by Taiz L., Zeiger E., 2010. I still consult it often.
Hope this helps. Stay inquisitive!

This is a fantastic answer! Thanks so much for taking the time to write it. Very interesting.


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In the notch signaling pathway, what is Fringe activating?
Take a look at the notch signaling pathway in human from KEGG : https://www.genome.jp/kegg-bin/show_pathway?hsa04330

I want to know what is Fringe activating. It is not pointing to another gene or protein, it is pointing to an interaction. What does that mean?

Usually, in such depictions where a species is pointing to a reaction or an interaction, the arrows mean that the species affects that reaction (for example, catalysis by an enzyme ). Generally pointy arrow heads denote positive effect (enhancing the reaction, for example an enzyme) and flat heads denote a negative interaction (repression). An arrow from one molecule to another can be used to depict a conversion (like glucose converting to glucose 6 phosphate).
There are no real standards on how to depict a pathway. So, it can be confusing.
In this case, Fringe actually alters Notch signalling (see below). So the arrow makes sense. However, the figure also has an arrow from Delta to Notch which can be interpreted as Delta getting converted to Notch. They also show an arrow from Notch to NICD which actually means a conversion. I would say that the depictions in this figure are inconsistent.
From NCBI Gene entry on Human homolog of Fringe, LFNG:

This gene is a member of the glycosyltransferase 31 gene family.
  Members of this gene family, which also includes the MFNG (GeneID:
  4242) and RFNG (GeneID: 5986) genes, encode evolutionarily conserved
  glycosyltransferases that act in the Notch signaling pathway to define
  boundaries during embryonic development. While their genomic structure
  is distinct from other glycosyltransferases, these proteins have a
  fucose-specific beta-1,3-N-acetylglucosaminyltransferase activity that
  leads to elongation of O-linked fucose residues on Notch, which alters
  Notch signaling. The protein encoded by this gene is predicted to be a
  single-pass type II Golgi membrane protein but it may also be secreted
  and proteolytically processed like the related proteins in mouse and
  Drosophila (PMID: 9187150). Mutations in this gene have been
  associated with autosomal recessive spondylocostal dysostosis 3.
  [provided by RefSeq, May 2018]

From Shao et al (2002):

Recent studies have demonstrated that O-fucose modifications play an
  essential role in Notch function. Reduction of O-fucosyltransferase
  expression in Drosophila using RNAi (11) or in mice by gene ablation2
  causes Notch-like phenotypes, suggesting that O-fucose modifications
  are essential for Notch function. In addition, we and others have
  shown that Notch activation is modulated by extension of O-fucose on
  Notch with the fucose-specific β1,3-N-acetylglucosaminyltransferase
  Fringe (for recent reviews, see Refs. 12 and 13). Fringe was first
  identified in Drosophila and shown to inhibit Notch's ability to
  respond to Serrate but to potentiate its ability to respond to Delta
  (14). Three Drosophila Fringe homologues have been identified in
  mammals: Lunatic fringe (Lfng), Manic fringe (Mfng), and Radical
  fringe (Rfng) (15). The β1,3-N-acetylglucosaminyltransferase activity
  of Fringe proteins is essential for their biological activity in
  Drosophila (16-18) and in cell-based Notch signaling assays (19), and
  the O-fucose residues are required for Fringe to modulate Notch
  activity (16, 19). Thus, Fringe mediates its effects on Notch
  signaling by the addition of GlcNAc to O-fucose moieties. Nonetheless,
  neither the specific role ofO-fucose in Notch function nor the
  mechanism of how a change in sugar structure alters Notch function is
  known.


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Paper shows 2 hours of high humidity and hot temperatures kills corona virus, does this stop the spread of the virus?
I found this paper (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2863430/) which says these corona virus strains live for months at 4 degrees C, 20% relative humidity. But at 40 degrees C and 80% relative humidity, 90% of it dies in 2 hours.
For example, if people set the furnace to 40 degrees and humidifier to 80% relative humidity for a couple hours each day, does this stop the spread of the virus?

There's a lot of outdoors, in which many people spend a good deal of their time.  2) The virus exists inside people, where the temperature is fairly well regulated.  As soon as the external temperature is decreased, the virus they shed will survive.  3) If 90% is killed, 10% will survive.  The 10% will presumably reproduce, passing along whatever characteristic made them more tolerent of higher temperatures.

Hi Mark, and welcome to Biology SE. Your question is very similar, but not syntactically a duplicate of this question/answer.

Your proposal is still interesting, because based on that, one may speculate if it would be possible to artificially induce a fever to 40°C in a controlled manner such that it would weaken the virus in most of the body.

SE Biology is concerned with the mechanisms of biological processes, and questions are generally answered by people with biological rather than medical or epidemiological expertise. It is possible, therefore, that some questions about coronaviruses relating to the recent 2019-nCoV outbreak may not receive a satisfactory answer. You may therefore wish to consult this list of reputable external sources of such information.

It's probably easier/more efficient to use standard cleaning/disinfection practices on surfaces ... COVID-19 (as far as we know) isn't hanging around in airborne particles.


text:
What is allosteric regulation?
I've found multiple definitions for allosteric regulation and struggling to understand which one is correct. My text book says:
'Another way of regulating enzyme activity is through allosteric regulation. This is where an
inhibitor binds to a different part of the enzyme, called an effector site, which changes the
shape of the enzyme. This binding can occur at any time. Product can only be formed (and
released) if the inhibitor, I is not bound to the enzyme, E. Assume that binding of the enzyme
to the substrate or the inhibitor is independent of one another so that the inhibitor, I, can bind
to both the free enzyme, E and the enzyme-substrate complex, C1, and the substrate, S, can
bind to both the free enzyme and the enzyme-inhibitor'
What I'm struggling with is if the inhibitor changes shape of the enzyme then how can the substrate still bind to the enzyme-inhibitor complex? Or does it just change the enzyme so that no reaction can occur and the substrate can still bind to it?
Thanks

The topic of allosteric regulation is well covered in reputable text and articles available on line. Berg et al. has a summary at the start of Ch 10 and a more detailed section 10.1 on aspartate transcarbamoylase.

This question really boils down to semantics, and the definition can be clarified by discussing enzyme regulation in general.  The 3 main ways that enzymes can be inhibited are through the following mechanisms: competitive inhibition, non-competitive inhibition, and uncompetitive inhibition.  In competitive inhibition, the inhibitor binds directly to the active site and blocks the substrate from binding (so they are "competing" for the active site, hence "competitive inhibition").  Non-competitive and uncompetitive both involve the inhibitor binding to a separate regulatory site on the enzyme that is different from the active site (the second sentence of your book's definition of allosteric regulation).  However, we have to differentiate between the two, and a nice, concise delineation can be found here.  This page states:

While uncompetitive inhibition requires that an enzyme-substrate complex must be formed, non-competitive inhibition can occur with or without the substrate present.

Therefore, your book's definition is more in-line with non-competitive inhibition.  I'd encourage you to look at this page for a more thorough read, and because they have a nice simple illustration that might help put it in perspective.
Here's a more abbreviated answer:
Inhibitors may change the active site to prevent substrate binding, but that's not the only mechanism of inhibition. Specifically, non-competitive inhibitors may limit the ability of the enzyme to carry out its action without changing the shape of the substrate binding site (see this figure).
Final thought
If you actually look at the etymology of the word "allosteric," its word roots come from the Greek allos that means "other or another" and from the Greek stereos that just means "solid or object."  So in actual etymological terms, it's a more general term that should apply to both uncompetitive and non-competitive inhibitors because both bind at some other or allosteric site on the enzyme.  However, the way your book defines it is more like the definition of a non-competitive inhibitor.

I downvoted this answer because it does not refute the poster's book's definition of allosteric regulation being exclusively to do with inhibition and focuses purely on different types of inhibition. Hence it does not answer the question in the title, which, in any case, is well answered online. I would also add that the etymology cited in terms of "solid or object" is unhelpful as the actual usage of stereos in English and especially chemistry is to do with shape or structure: "…two, stereospecifically different, non-overlapping receptor sites…" (Monod et al.  J.Mol.Biol. (1963) 6, 306--329)


text:
Are blue feathers better insulators?
I recently found an article talking about the colors of bird feathers. https://www.smithsonianmag.com/science-nature/why-are-some-feathers-blue-100492890/
Apparently, unlike other colors, where pigmentation is at fault, blue feathers are actually blue thanks to their unique structure. According to the article, when the feathers grow, they form air pockets, which then form a pattern that just so happens to cancel out the red and yellow wavelenghts, leaving us with blue.
Now, of course, all feathers have the ability to trap air. It's what makes them such excellent insulators, as air conducts heat very poorly. Bonus points if the air is contained in very small cells, as that increases a materials insulation qualities. It's for the very same reason we also use foam for this. Now my question is: As the blue feathers contain miniature air pockets to give them their color, would that make them, in essence, better heat insulators than the ones of other colors, or do all feathers have such pockets, and the blue birds just so happen to be arranged differently, without actually changing any insulation capabilities?

This article https://www.nature.com/articles/s41467-018-05898-8 is likely relevant to an answer, though it deals with the impacts of reflectance on thermal loads, rather than insulation. In short, other attributes of feathers have large effects on their thermal properties, and can be evolved independently of visible colour. Any direct impact of colouration on insulation might be lost in the noise from these other factors.

As an aside (and from memory), a colleague of mine looking at the costs of sexual ornamentation in blue wrens (Malurus cyaneus) was convinced that blue feathers are worse insulators, based on behavioural observations of males that had molted into blue feathers and others that had not. There was an experimental intervention using testosterone implants, which would cause a male to molt into blue if it wasn't in blue already. I can't find a paper detailing the findings though, so she might not have published them.


text:
Will a less favorable allele's frequency go to 0?
For example, a pond is dark in color. There are two alleles. The dark color allele is dominant over the light color one. Let's assume that the relative fitness of both the homozygous dominant and heterozygous is 1, and the relative fitness of the homozygous recessive is 0.5. When I ran the simulation, I changed no other values.  My data after 251 generations is this:  My question is that being homozygous recessive is clearly less favorable, and even though being homozygous dominant and heterozygous carry the same advantage instead of heterozygote advantage, why wouldn't the recessive allele disappear?

You only run your simulation for ~250 generations - what makes you think that this is enough to generalize the results. I honestly don't myself how many generations are 'enough' to be sure that the results won't change anymore (you'd probably have to check if your model converges to a stable state with your given parameters).

If you have a way to run a deterministic model that calculates the expected allele frequency over time, that would probably clarify things (e.g., I agree with @Nicolai that you probably just haven't run the simulation long enough)

Welcome to Biology.SE! Have you thought about what happens as the frequency of of the "r" allele drops? Take the extreme example of a population with only a single heterozygous individual being present in the population — how much selection would there be at that point against the "r" allele? ——— You may also want to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!


text:
Inability of vultures to digest diclofenac
The population of Indian vultures has been rapidly declining since 2003. This is attributed to the diclofenac present in the carcasses which the vultures eat. Vultures seem to digest all sorts of food items but why can't they digest diclofenac? What is the mechanism which causes this?

Via: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1618889/

Post-mortem examination revealed extensive visceral gout in all diclofenac-treated birds (see electronic supplementary material). Histological examination revealed significant lesions in the kidneys, liver and spleen with extensive uric acid crystal deposition.

Via: https://repository.up.ac.za/bitstream/handle/2263/26027/Complete.pdf?sequence=7

From the mechanistic studies both diclofenac and meloxicam were directly toxic to chicken and vulture renal tubular epithelial cells following 48h of incubation. It was later shown that this toxicity was associated with an increased production of reactive oxygen species (ROS), which could be temporarily ameliorated by pre-incubation with uric acid due to its anti-oxidant activity. When cultures were incubated with either drug for only two hours, meloxicam showed no toxicity in contrast to the cellular toxicity present for diclofenac. In both cases no increase in ROS production was evident. In addition, diclofenac influenced the excretion of uric acid by interfering with p-amino-hippuric acid channels. The effect on uric acid excretion persisted after the removal of the diclofenac. It was therefore concluded that vulture susceptibility to diclofenac results from a combination of an increase in cellular ROS, a depletion of intracellular uric acid concentration and most importantly the drug’s long half-life in the vulture.

The second link posits three mechanisms for the cause of renal failure in vultures (ref., pg. 26):

Ischaemic nephropathy with secondary visceral gout
Organic Anion Transporter antagonism
Secondary renal toxicity with or without toxic activation

I'm just coming across this post now and I don't see any downvotes. As such, I'm going to remove your last comment as no longer necessary. Your post is well-linked/supported, so that aspect is great (thanks!) and should discourage downvoters. However, to further discourage downvoting, I would also encourage (if you'd like) to add a bit more non-quote context to your post. Some users downvote due to seeing answers that are primarily quotes of other sources. But as I said, you don't currently have any downvotes so you might be ok as is. Thanks!

I just seem to be the victim of some drive-by downvoters, lately, and am trying to head it off at the pass. Sorry if this annoys some.

Everyone is a "drive-by downvoter" by your definition. No one is ever supposed to comment on how they voted; votes are anonymous, and disclosing how you voted would defeat the anonymity of the system. Leaving comments does nothing to "head off" the problem because it isn't a problem. A downvote means someone who read your answer thought it was unclear or not useful. That's all.


text:
sperm reaction of virus infected
we know when a human body cell infected by a virus , create interferon 1 to call other cells that surrounded it  , but red blood cells couldn't do this because they loose their nuclear and other organelles . I have a question about sperms , can sperms produce interferon 1 when they infected with viruses?

Could you please be a little more precise and specify the virus that you have in mind that infects sperm?

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

well David I don't have any special virus just I ask this in general


text:
Average Nucleus size of human skeletal muscle cell
I’ve been struggling the last couple of days to find reliable data on the average nucleus size of a human skeletal muscle cell. If I deduce it from pictures it should be in the range of 20 micrometers long and 3 micrometers in diameter but I need reliable data and a proper source.
Could anyone help me with this?

Welcome to Biology.SE! You may find it beneficial to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

The average "length" for normal human myonuclei is 11.75 µm according to the abstract for:
Watkins, S. C., & Culien, M. J. (1988). A quantitative study of myonuclear and satellite cell nuclear size in Duchenne's muscular dystrophy, polymyositis and normal human skeletal muscle. The Anatomical Record, 222(1), 6-11.
If you can get access to this paper it should have more information for you.

If I am correct, the myoblast are combined into myocytes. Do you think I can assume that the nuclei stay the same size?

Sorry — I messed up. The results were for myonuclei in myocytes (I have no idea what I was thinking when I wrote myoblasts). Now corrected.


text:
What is this sea shell?
Found in Belgrade, possibly carried back from the Mediterranean or Aegean coast.

It is not /Bolma rugosa/, but in fact /Angaria delphinus/, from the Indo-Pacific.
Listing on gastropods.com

Welcome to Biology.SE! You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. (Answers must also be self-sufficient, not just links.) Without this your answer is indistinguishable from opinion and instead should be a comment on another answer. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

This ID seems accurate. The species varies a lot and it's often like the one from the OP.


text:
When does the vertebral column finish chondrifying and begin to ossify?
I have read many articles on vertebral column development in embryos on the internet.
Different articles give different time periods for the end of chondrification of the vertebral column and the beginning of ossification.
Some websites and books(like The Developing Human: Clinically Orientd Embryology 10th edition) say that 'the 2 centers in each centrum fuse at the end of the embryonic period to form a cartilaginous centrum', which is rather confusing since they also say that ossification begins in the 7th week. How can ossification in the centrum begin when the chondrification centers in the centrum have not even fused yet? Why does it takes so long(2 weeks) for the chondrification centers to fuse?
When is the chondrification of the vertebral column complete and when does ossification start?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, including references to your conflicting sources will improve your chances of getting a useful answer. In addition, please specify the organism for which you want an answer. ——— This is a good example of how to format references. Thanks!

I've made some edits that I hope clarify your question, but I think it would be helpful if you could elaborate on why you think the quote (BTW: you must add a reference for that quote) conflicts with "ossification begins in the 7th week".


text:
What are good techniques for determining direct maps of proteins?
I am looking for which techniques to explore to determine electron density maps (or Fourier maps) for a protein (possibly using an assumed model).
In particular, I want to avoid techniques that create difference maps like Fo - Fc, and I think this means I also want to avoid 2Fo - Fc or other types of "sigma_A" maps, which all (I think?) contain data indicating the difference/discrepancy between observed and modeled densities. I believe what I am referring to is a "direct map."
While I'm open to techniques that are informed by a candidate model, I don't want F_calc to show up in the actual output. Also, I'd like to reduce model bias as much as possible while still arriving at a direct map (assuming that is the correct nomenclature).
I've seen references to "Iterative OMIT" and various other "OMIT" maps, but could not determine whether those gave the output I'm looking for.
Ideally, I'd like to use techniques that are implemented in open-source libraries, though that may not be an absolute requirement.

The 2mFo-DFc map is considered to be least biased by the model. Reportedly, it was shown to be least biased in a paper from 1986.

Unrelatedly, I am not certain about it but should this be migrated to SO bioinformatics?

@marcin, I believe the 2mFo-DFc is still a difference map. Its values (if I understand it correctly) are not intended to be an image of the actual electron density.

@DavidR they are. 2-1 map looks like direct map, but is less biased. You can google to find various presentations (from lectures and MX workshops) that cover map types. Books such as Biomolecular Crystallography probably also cover it.


text:
How do big cats perceive objects, specifically vehicles?
Right so we have been on safari in South Africa recently and before encountering big cats (lions) we have been told to hold still and not reach out beyond the boundaries of our safari vehicle because the cats would see it as uninteresting "object", unless something sticks out or moves.
Having a bit of background in biology I tried to map this to a more "scientific" explanation but wasn't successful so far. How would you describe the cognitve perception of vehicles by big cats (or lions specifically)?

It's basically the same as humans, they include higher predatory associations and less logical and word associations. The neural circuits study all the images received from the eye and compare new objects to previously learnt categories: Bird/Log/Horn/flailing upside down limb/face/car/rhino... You can feel your own neural networks at work when you focus on an unidentified detail (bird/branch/rock) and class them into right and wrong results. Moving objects occupy a moving class of their own, i.e. in your garden, they are a potential threat or a prey.
When the truck is rolling along normally, the cat has extensively studied this kind of object already and has made these associations: Glass windows he can't get into, faces inside glasses, rubber tires, slight smell of humans, major smell of petrol and artificial stuff, indestructible, square and round bits, sees it every day from all angles and has interacted with trucks plenty of times. He rarely gets any food from safari trucks, they all look a bit the same. A truck occupy the same prey opportunity as birds in trees which can just fly away.
The brain behaves differently towards known objects and movements and new, unknown animate objects, the unknown animate things result in: the capture of attention.
When there is an arm waving out of the window, the cat's brain is receiving an unidentified living thing attached to the truck, perhaps some kind of living meat! A living thing, a prey. Is it a leg of lamb? is it inside or behind the box? Can he get into this truck? Is it a bird? The cat will be interested in the unidentified, new kind of living thing until he has figured it out.
general reading.
visual cortex of monkeys and cats.
Activation of the hypothalamic feeding centre upon visual prey detection
other research.

Any animal may see something moving in its territory as a challenge.  Big cats and other predators are very intelligent and have an excellent sense of smell. Just because you're not sticking your arm out, doesn't mean that they don't know you are in there.  Lions are basically lazy and will rarely attack people in a car, but it would depend on the animal's prior experience with other vehicles. If they have been harassed or fed by tourists trying to get a photo, big cats (and other predators like bears) are more likely to approach a car. I have seen cheetahs and leopards jump through an open window into a Jeep.  You can watch this video or search youtube.com for others.  https://www.youtube.com/watch?v=-LFTJ-BFWms
Hippos, elephants and rhinos have attacked cars for no apparent reason, especially during breeding season.  Best advice? Stay in the car with your windows all the way up!

Right - that's exactly what you hear when talking to guides etc. I am interested in the scientific answer to why? Is being lazy the real reason for lions etc not showing interest people in cars? And btw. windows up is a nice advice - most safari vehicles are complete open...