text:
Evolutionary advantages of gyri
Sulci and gyri are complementary views on the very same brain-anatomical phenomenon

(Note that there is the named concept of gyrification, but not of sulcification, but it's the very same process.)
As the main evolutionary advantage of sulci/gyri stands the enlargement of the surface of the brain, i.e. the neocortex.
As another evolutionary advantage of gyri (not sulci) Wikipedia mentions "increased speed of brain cell communication".
But there seems to be another (as usual: unintended) evolutionary advantage of gyri (not sulci) which I could not find discussed/investigated/analysed in detail: being prerequisite of internal long-range connections of the neocortex in a somehow systematic way (which goes beyond mere "increased speed"):

I am looking for references where this - possible - evolutionary advantage is discussed.

Addendum: In the above mentioned Wikipedia article on gyrification one reads

that axonal tension forces between highly interconnected
  cortical areas pull local cortical areas towards each other, inducing
  folds.

If this was true (it's only stated as a hypothesis), it would suggest that folds are a consequence of such connections, not their prerequisite.

Addendum: In Gray's Anatomy I read:

I wonder why fibers passing the walls of a sulcus and fibers connecting adjacent gyri are explicitely mentioned (BTW: Isn't a fiber passing the wall of a sulcus connecting two adjacent gyri? Don't both of them must have U-shape? Is being intracortical vs. subcortical their only difference?) but not the ones connecting the walls of a gyrus (which would be straight, see above)? Aren't there such fibers?

I think your addendum is a bit misleading; you quote from a source suggesting that it is a known fact, when the source material clearly presents it as one of several hypotheses. The source does not suggest that folds are a consequence, it proposes that they could be. As to the rest of your question, can you not follow the sources linked from wikipedia as a starting point?

I corrected the addendum.


text:
Does ribosome associated with RER separate from RER after finishing protein synthesis?
After ribosome associates with RER because of its specific signal sequence, and then when cotranslation translocation is finished, does ribosome return to free floating ribosome at cytosol? Or does it stay as combined condition?

source: Stack Exchange

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sort: votes


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Aquaporin and the exclusion of $H^+$
As I read in my textbook, aquaporins exclude $H^+$ when absorbing water, but where does this $H^+$ come from? Additionally, is $H_3O^+$ a liquid that looks like regular water?

$\ce{H_3O^+}$ is just representation of acidic water. You'd get much better answers about this on chemistry.SE

It doesn't matter where the $H^+$ comes from in the context of this information. The textbook is just saying that the aquaporin is permeable to $H_2O$ but not to $H_3O^+$ (nor, presumably, to $OH^-$).
In any aqueous solution, especially in the presence of acids, some of the molecules will be $H_3O^+$. The pH tells you how many. It doesn't really make sense to think about what a solution of $H_3O^+$ would look like.

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Breakpoint resolution for copy number variation analysis
I am reading [1].
One limitation of the Read Depth approach is that "the breakpoint resolution is often poor". Which is the meaning of low-resolution breakpoint in this case?
Breakpoint is defined as the sequence breakpoint:

Examples of a structural variation include a large deletion, insertion, duplication and inversion. Each requires the DNA duplex to be broken and rejoined, and this creates a new sequence of bases at the rejoined sites, i.e. the breakpoints.
Sequencing the new breakpoint regions is a good way (perhaps the only way?) to demonstrate an inversion, which does not increase or decrease the amount of DNA.
Original sequence: 123456789
Sequence with inversion: 123765489
Breakpoint sequences are at 37 and 48

[1]: C. Alkan, B. P. Coe, and E. E. Eichler, “Genome structural variation discovery and genotyping,” Nature Publishing Group, vol. 12, no. 5, pp. 363–375, Mar. 2011.

It means that it is hard to tell the precise location on the chromosome where the structural variation event starts and finishes using only read-depth information.
Read depth is measured by counting the number of mapped reads that overlap targeted regions aka bins. These bins are typically many basepairs wide and are used to normalize coverage with respect to various parameters (e.g. GC content). Smaller bins can give better breakpoint resolution but have noisier statistics. Large bins have better statistics but can't be used to precisely call the SV boundaries.
The CNVnator paper discusses the topic
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3106330/


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Cortico-cortical connections
I wonder what the principal ways of (direct) cortico-cortical connections are.
I came up with the following possibilities:

vertical: a cortical neuron connects to another one in roughly the same cortical column, but in another layer
horizontal: a cortical neuron connects to another nearby one, preferably in the same or neighboring layer
"intragyric": a cortical neuron connects to another one in the same gyrus (see here)
interhemispheric: a cortical neuron connects to another one in the same (or neighboring) area of the opposite hemisphere

Are all of these relevant? And/or are there relevant but completely different ways of cortico-cortical connections, e.g. "intergyric"?

Addendum: Maybe too late I found a concise summary in the Wikipedia articles on white matter and association fibers (the latter term I wasn't aware of when I asked my question), which doesn't contradict and complements Bryan's answer:

intracortical (Bryan: "intracolumnar" vs. "horizontal")
short association fibers ("also called arcuate or U-fibers [...]  connect together adjacent gyri")
long association fibers which "connect the more widely separated gyri and are grouped into bundles" (often called fasciculi, but probably not exclusively)
commissural fibers (Bryan: "callosal projections")

There definitely seems to be no reserved name for something like "intragyric" fibers (see second addendum here).

Your question "are all of these relevant" doesn't make much sense to me, but I am going to assume you are talking about it in terms of terminology and answer that way.
The "vertical" connections you describe are usually referred to in the context of cortical "columns" and are therefore referred to as "intracolumnar." Within a column, intralaminar connections by far dominate the total number of synapses, but connections between layers are also important (note that my answer Cortical projections from layers 2/3 back to 4? covers some of this as well, though that question is much more specific).
Horizontal connections refer to connections between cortical columns of the same cortical area (e.g., from V1 to V1 with a different orientation selectivity). These are often stronger between the same layers, but simply saying "horizontal" does not specify that you mean intralaminar horizontal connections.
"Intragyric" is not a word that is used - I think you made it up. Gyri aren't really specialized functional units, and although there may be some brain areas that are localized within a gyrus many span either several gyri or share a gyrus with other areas (for example, "Heschl's gyrus" isn't even just one gyrus). Therefore, you can't really generalize "gyric" connections as being in a particular class, you would have to refer to the specific areas that are connected to understand the nature of those projections.
Interhemispheric connections are fairly ubiquitous in neocortex, and they make up several white matter tracts that connect the hemispheres, most prominently the corpus callosum. As such, those connections are also often referred to as "callosal" projections.
Other terminologies that are used are "top-down" versus "bottom-up" according to the position of areas in the cortical hierarchy. "Lower" areas are considered to be those with primary sensory and motor functions, whereas higher areas are associative/executive areas. The canonical reference for these projections is Felleman, D. J., & Van Essen, D. C. (1991). Distributed hierarchical processing in the primate cerebral cortex. Cerebral cortex (New York, NY: 1991), 1(1), 1-47. The key feature of top-down versus bottom-up projections is a difference in the interlaminar pattern of connectivity between different cortical areas. It can be hard to really parse the precise hierarchical of some of the higher-order cortical areas, and the patterns of top-down and bottom-up are fairly mixed for areas at similar levels of the hierarchy, however.

I guess, it's easier to connect inside a gyrus than across gyri. But I may be wrong.

That's why I put "intragyric" into quotation marks.

How do we know that gyri aren't "really specialized functional units"? We even don't  know it unequivocally for cortical columns: see The cortical column: a structure without a function (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1569491/)

I specified "horizontal" by saying "in the same (or neighboring) layer", i.e. "intralaminar".

I wouldn't rely on that one paper: people still talk and think in terms of columns. I fully agree that they are not as discrete as people once thought, but it still makes sense to talk about intracolumnar units. I totally disagree that it isn't clear that gyri aren't really specialized functional units: there are several dissimilar functions that are held within gyri, and the boundaries of cortical areas often do not stick within a gyrus. This is very clear on any map of the human cortex. And for "horizontal" I was referring to use in the literature rather than how you used it.

I'd say it's also very unclear what you mean by "preferably": biology does what it does, regardless of what is preferable to you. :)

No matter if you say "vertical" or "intracolumnar" resp. "horizontal" or "intralaminar": this is only a trend, but there will be outliers.

I don't understand your latest comment.

Let us continue this discussion in chat.


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Can someone please explain the following jargon to a layman
I was reading an article on a substance called apigenin:

Apigenin can inhibit both aromatase and 17β-hydroxysteroid dehydrogenase (17β-HSD) with the inhibition of 17β-HSD being unique to apigenin and 3 other tested flavonoids (chrysin, genistein and naringenin)[22] and apigenin possessing an IC50 of 300nM (0.3μM). The IC50 of Apigenin on aromatase is approximately 2.9μM (most potent tested flavonoid on aromatase was 7-Hydroxyflavone at 0.21uM, outperforming the reference aminoglutethimide at 1.2uM[22]) and both of these enzymes are involved in testosterone synthesis at different stages.

Does this mean that higher apigenin potentially yields higher or lower levels of testosterone? I guess I'm unsure what the implication of "inhibits" is.

As far as I can tell, aromatase is involved in the conversion of testosterone to estradiol, so it’s inhibition should increase testosterone. However, 17B-HSD is involved in testosterone biosynthesis and its inhibition should have the opposite effect. And there are potentially other pathways that it affects, so you’d probbaly need to find a paper that actually looks at testosterone levels in vivo.

So, to inhibit substance $A$ means to prevent it from reacting with anything else?

It's inhibiting enzymes, which prevents them from catalyzing their reaction(s).

So I can definitely explain what "inhibits" means and what that implies, but I think the answer as to what apigenin is actually doing to testosterone levels is somewhat complicated. I wasn't able to find a study looking at steroid levels in vivo following apigenin administration, so this is based solely on a quick look through the biochemistry and cells biology available.
17β-HSD is an enzyme that catalyzes a reaction (meaning it makes the chemical reaction happen more quickly than it would by itself) that converts androstenedione to testosterone. If it is inhibited, that means that the enzyme is no longer able to catalyze the reaction. Therefore, inhibition of this enzyme should prevent the synthesis testosterone, and reduce its levels, since less testosterone will be made.
On the other hand, aromatase is an enzyme that converts androgens, namely testosterone and its aforementioned precursor androstenedione, into estrogens. So, one would expect inhibition of this enzyme to lead to increased testosterone levels, as less testosterone and androstenedione would be converted to estrogens, meaning more testosterone and its precursor are left unchanged.
So, it seems we have some competing actions. Based on the paragraph in your question, apigenin's IC50 for 17β-HSD is 0.3 μM, and its IC50 for aromatase is about 2.9 μM. That means that when the concentration of apigenin is 0.3  μM, the enzyme activity of 17β-HSD is cut in half, but it must be at a concentration of 2.9 μM to do the same to aromatse's activity. So, it is about ten-fold more potent at inhibiting 17β-HSD than aromatase, at least in the assays used above. That would suggest that at concentrations significantly below 2.9 μM, apigenin would inhibit 17β-HSD but not aromatase, resulting in a decrease in testosterone. However, once concentrations became sufficiently high to allow for inhibition of both enzymes, things would get more complicated. Depending on the relative amounts of both enzymes, how much access apigenin was able to get to each, and what the cellular steroid composition was prior to inhibition, you could imagine relative testosterone levels to go either up or down. However, I would be inclined to suspect that testosterone levels would in fact decrease in the long run, since eventually existing testosterone stores would be depleted, and the inhibition of 17β-HSD would prevent the creation of new testosterone.
However, if we look at the paragraph in the article immediately following the one you quoted, there is a summary of a study done in cells that found that apigenin actually increased testosterone levels by blocking the TBXA2 receptor. This inhibited a signaling cascade that normally decreases testosterone synthesis, so the end result was an increase in steroidogenesis/testosterone production.
So, I suspect things are actually somewhat complicated and the best way to know would be to test in vivo


text:
How to differentiate male and female mosquitoes at pupal stage?
There are many differences between male and female mosquitoes in their adult stage. But for my experiment, I need mosquitoes before they mate. So I need to sort them before they develop in to an adult. The best option is to sort them in their pupal or larval stage. I tried to search the differences, but most of them were very general. So, if someone knows about it, please share your answers.

Male and female pupae are consistently slightly different sizes. This isn't particularly obvious to look at them, but allows them to be sorted mechanically by using two sheets of rigid, waterproof material (aluminium, glass or acrylic) fixed at a slight angle to each other, and washing the pupae down between them until they get stuck. The pupal sorter in most common use is described in this paper and you can buy one commercially here:
http://johnwhock.com/products/laboratory-equipment/larval-pupal-separator/
I think I've seen a video of one in use at Virginia Tech somewhere online but I can't find it right now; I'll edit it in later.


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What is this New Zealand insect and what is it in?
What kind of insect is this?

Found in Early September at Jubilee Park, Dunedin, New Zealand. It was suspended from a silk thread (quite long, a few meters) to a tree above. It was climbing the thread, balling the thread as it went up. It looks like a caterpillar. What species is this and what is it inside of?

The quality of the pictures is not the best one, but due to the fact that this is NZ, it's probably a moth from the species Liothula omnivora.
It's a kiwi insect (that is, endemic to New Zealand). Its English common name is bagworm, and its Maori common name is pū a Raukatauri. The English name explains your question ("what is it in?"). According to Farm Forestry New Zealand:

The common name of this insect refers to the strong silk bag made as a refuge by the caterpillar. The bag is brown to greyish, often covered with fragments of vegetation, and so tough it cannot be torn open.

Here is a picture of it:

And here is the adult, for comparison:


text:
Can anyone help confirm this tiny insect larvae?
Can anyone help identify this insect larvae?
Found: UK, autumn, in a bed.
Size: less than 2mm

The bed was searched thoroughly and no others were found, but is there likely to be more of them?
Thanks!

Related: What kind of insect can this be?..., Bug Identification: Is this small tubular, black bug a bed bug?, How to protect my mounted insect specimens..., Varied Carpet Beetle Larvae, What is the name of the critter depicted..., What small insect is this?, What bug is this...

Can anyone help identify this insect larvae?

This is a varied carpet beetle larva, which belongs to the species Anthrenus verbasci.

A. verbasci. larval form, left; matured beetle, right.

The bed was searched thoroughly and no others were found, but is there likely to be more of them?

It's difficult to say, though, generally, ~40 eggs are produced at a time, and they can remain in the larval stage for 8 months to almost two years.
At any rate, the University of California Agriculture & Natural Resources, and this website, both provide solid information about this insect, and outline measurements that can be taken to protect your home from it.

It's also called a buffalo beetle. This is the varied [or also called variegated] form; there are other forms like the black carpet beetle.


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Do corresponding areas in the two hemispheres arise from the same stem cells?
After having asked this question about the connectivity between clonal cortical neurons, I'd like to know:

Do corresponding areas in the two hemispheres arise mainly from the same stem
  cells, such that these areas connect to each other more strongly than to others?

I answered this question, but I strongly advise you to do more research before asking some of the questions you are posing here. Ask yourself questions and look for answers like "where are the stem cells that give rise to neocortex located" and you will easily answer these questions. I think you are having a tendency to find one piece of information and try to connect it to too many other things without reading intervening information.

I'll try to take your advice.

No, they don't. The stem cells of each cortical hemisphere are located far from each other, in the subplate below the developing cortex.


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Identify these hinged barbed bones
My daughter Stella and I found these bones on the shore of Port Phillip Bay, Victoria, Australia.
The smaller, barbed bone is attached by a hinged joint that allows it to move through just over 90 degrees. The photos show it at its two extreme positions.
The photos include an Australian 20 cent coin for scale (29mm diameter).
Can anyone identify what kind of bones these are, and which species they come from?

Looks like one of the scorpionfishes.

I think it is part of a Australian trigger fish skull. check the pictures below, unfortunately someone sawed off most of the spine on the skull photo, but you can see the base of it, it is probably not the exact same species, but it is certainly part of a triggerfish skull. There are a half dozen species in Australia.

Cool find.


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Where did H2 come from at pyruvate oxidation?
After pyruvate oxidation, H2 come out by pyruvate dehydrogenase. Does this mean H2 is from C3H4O3 (pyruvate)?
But then it makes no sense that numbers of pyruvate (C3H4O3) 's H and acetic acid (C2H4O2) 's H is same.
How can this happen if H is from pyruvate?

It's not clear what enzymatic reaction you mean, but since you mention acetic acid, I would guess it's the quinone-coupled pyruvate dehydrogenase (EC 1.2.5.1, also known as pyruvate oxidase). It would help if you write out the entire reaction.


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What happens to those molecules that are not received by receptor proteins on the cell membrane?
I am studying cell communication and come to know that proteins from outside environment gets received by receptors on the cellular membrane and then the signal is transduced inside the cell. My question is given a certain concentration of proteins are disseminated in the environment what happens to those protein which are not received by any receptor molecule, are they denatured and get destroyed in the extracellular environment after some time in case if the answer is yes can one provide a reference for the same Are they bounce back or absorbed by cell membrane?

For that matter, what about those that do attach to a receptor? Do they stay there forevermore?

This is a HUGE topic which deserves a comprehensive answer, but here's a basic summary while I have time. 1) often, these signals are degraded over time, e.g. by things the cell secretes [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1783984/]. 2) ligands can attach and unbind repeatedly; mostly they cannot pass through the membrane, though receptor endocytosis can take them into the cell: https://en.wikipedia.org/wiki/Receptor-mediated_endocytosis

Probably some of these things are covered better in more physics- or modeling- oriented textbooks; I have not read it, but I have heard good things about Lauffenberger + Linderman's "Receptors: Models for Binding, Trafficking, and Signaling"

@AJK the link you mentioned gives this error: The web page address (URL) that you used may be incorrect, can you please provide me reference name or another link?

It included a bracket by mistake: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1783984/


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Hand-washing resistant bacteria. Will they evolve one day?
I know that soap kills bacteria by dissolving their membrane. But it is not 100% effective. A small portion of bacteria which survive replicates and I have to wash my hands again.
Will this cycle lead to evolution of soap-resistant bacteria with insoluble membranes?

Different from common believe, handwashing will only reduce the number of bacteria on your hands but not eliminate them. Have a look on surgeons and their practice to wash hands and sterilize them. And this is not a problem, bacteria live normally on our skin and belong there.

soap isn't a germ killer.
soap is a germ REMOVER. it is basically made of things a lot like phospholipids, that bury their fat loving tails into germs, and their water loving heads stick into the water, making whatever is in the capsule called a "micelle" super slippery,and they wash away.
the cool thing about this is it removes even non living gunk (sometimes).

Not all soap kills bacteria, not all soaps work the same
actually, the rinsing, rubbing, and temperature of the water significantly contribute the removal and termination of bacteria even then this is not 100%.
I wouldn't want to touch blood with AIDS virus or Ebola and rely solely on soap and hand washing to save the day.
Some soaps work by raising the PH and there are already a category of organisms called Alkaliphiles which thrive in high PH environments. To my knowledge these cant really harm you as you are a low PH organism.
But yes theoretically if you use the same measure against a bacterium long enough and constantly give it a chance to succeed, eventually it will.


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What spider is that in south of Brazil?
I'd like to know if it is possible to identify the spider in the photo below.

In fact, as shown in the next picture, it is very small.

Location: South of Brazil.

I've seen a very similar cephalothorax pattern before, but I'm not sure where. Perhaps in the Zoropsidae, but I'll have to go look through my books and get back to you.

It would help if you could see how many eyes it have. It helps a lot in spider identification.

This is Arachosia praesignis, a kind of ghost spider from the Anyphaenidae family.

(Photo source: https://inaturalist.ca/observations/150348963 )
See this paper for representatives of both the male and female specimen of this species, plus additional species of the Arachosia genus:
https://www.biotaxa.org/Zootaxa/article/view/zootaxa.3932.1.1
(Available free on ResearchGate: https://www.researchgate.net/publication/273951397_Taxonomic_revision_of_the_American_spider_genus_Arachosia_Araneae_Anyphaenidae#fullTextFileContent )
The paper reports the distribution consistent with where you found it:

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What is the identity of this spider from India?

I came across this strange guy today at my classroom in Tamil Nadu, India. It is a spider which is not very much bigger than an ant but with an artistic body. He has 8 legs, but the two on the front are raised above his head, just like a crab does. Can anyone identify this little guy?

Anyone identify this little guy?

That is a Siler semiglaucus, which is a type of jumping spider. It has the nickname of "metallic jumper", and can be found all throughout India, Indonesia, Philippines, and Thailand.

He has 8 legs, but the two on the front is raised above his head, just like a crab does.

Here is a wonderful collection of more images, which also includes locations of discovery.


text:
How can rhodobacter possess a single 'PS-II' like reaction center?
I recently came across an information in my book Trueman's Elementary Biology ,  a popular text in India, that photosynthetic bacteria like Rhodobacter, Rhodopseudomonas etc. possess a single photosystem where the reaction center is PS-II like. Now how can PS-II work as a single unit? As far as I know, PS-I can operate singly in cyclic mode generating ATP only. But PS-II works in conjunction with PS-I to generate ATP, $\ce{O2} $ and $\ce{NADPH} + \ce{H^+} $. So how can PS-II work as a single unit in this case?

McEwan (1994) Photosynthetic electron transport and anaerobic metabolism in purple non-sulfur phototrophic bacteria. Antonie Van Leeuwenhoek 66: 151-164.
...The purple non-sulfur bacteria ... carry out photosynthesis under anaerobic conditions. Photosynthetic electron transport is cyclic and involves ... two redox complexes ... reaction center (RC) [and] cytochrome bc1 complex. ... This cycle of electron transfer, [mediated
by ubiquinone (UQ) and a c-type cytochrome,] is linked to the generation of a proton motive force ... across the cytoplasmic membrane.

That means, the PS II in case of Rhodopseudomonas is a bit different from that found in a typical chloroplast.

TL,DR: I think you've just swapped PS-I and PS-II.
Recall the differences between PS-I and PS-II.  Bear in mind that PS-I and PS-II were not so named because of the order they run in, but rather because of the order in which they were discovered.  PS-II comes before PS-I chronologically.
PS-II basically takes in water, breaks it down into $H+$, $\ce{O2} $, and a spare electron.  The hydrogen ions are sent inside the thylakoid space, creating a concentration gradient between the stroma and the thylakoid space.  Since the ions cannot cross the thylakoid membrane, they must have a transport channel of some sort.  This channel is known as an ATP synthase, and ATP is synthesized from ADP and a phosphate group using the energy created by the hydrogen ion moving down the concentration gradient.  You are then left with an O2 group in the stroma, and an electron in the ETC.
PS-I takes that electron and basically just boosts its energy to produce NADPH using the H+ ion sent out of the thylakoid space during ATP synthesis.
In other words, PS-I cannot take place without the H+ and the electron from PS-II.  However, if PS-II were to run alone, it would simply mean that somewhere along the way either the oxygen would bind back to the H+ and electron to form water, or else the electron and H+ would be used elsewhere in the cell.  Thus it would be PS-II running in cyclic mode producing ATP.

But I think u swapped b/w ps I and ps II. As I'm sure it is ps I which runs in cyclic mode.


text:
Explanation of the results of Warburg's Flashing Light experiment?
Between 1919 and 1920† Warburg obtained a higher rate of photosynthesis in Chlorella, exposed to rapid alternating periods of light and darkness, than when exposed to constant illumination.  I would expect the opposite — that continuous illumination would generate more ATP and $\ce{NADPH}+ \ce{H+}$ in the light reaction, and thus give a higher rate of photosynthesis. In the light of what we now know about photosynthesis, is there any obvious explanation for Warburg’s results?
†Cited by Emerson, Robert and Arnold, William (1932)

Can you pls put a link to his paper?

I cannot comment so I write here. Besides details that I let to people with better knowledge than me, it seems you compare or "equate" amount of product and rate. That is not correct. Think of a sprinter (that actually stop, breath and eventually restart) and a marathon runner. Who is going faster and who is covering the longer distance? Indeed I suspect that a kind of fatigue is at play, like inhibition, saturation of some path. However this latter is just me speculating. I wanted to point out the difference above. It might help.

Your justification was indeed a help.  I read this logic somewhere, but want to know precisely what the inhibitory factor is. Besides it may seem that I'm confusing rate and yield, due to my last line, but actually I'm talking about rate and not yield..

I have taken the liberty to gut this question of the references to a possible effect of the light on the 'dark' reactions of photosynthesis as the poster provided no reason or logic to make such a connection and there is no reason to make such a connection. Warburg was not in a position to deduce anything much from the original experiment, but I think it is still of interest (5 votes) to ask if his observations can be rationalized in terms of today's knowledge of photosynthesis. So I have recast it with that single focus. There seems to be literature out there discussing it.

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text:
Selective breeding and Mutagenesis
I am writing an argumentative essay in which I claim that GMOs are safe. I know, it is not proved, but for the sake of my course I want to prove it. The counterargument that my professor said to me is that genetic modification is not like selective breeding. GM brings changes faster and most of the cases it is inevitable. We don’t know the consequences and they can be bad. On the other side selective breeding is changing the organism slowly and something bad can be prevented in the start of its development. What are disadvantages of selective breeding to compare with genetic modification? Can I use the mutagenesis as the example of selective breeding and use its cons?

Yes, GMO are safe to consume! See Is Genetically Modified food safe to consume?. Now, there are other (potential or real) issues related to the use of GMOs such as for example a loss of genetic diversity if every farmer plant the exact same strain. Talking about such issues will require talking about ethics, economy and sociology and it can therefore not be answered in a science website only.
Your teacher's argument does not make much sense (although a direct quote would have been helpful). GM plants also have to develop. They are organisms too!

[W]hat are disadvantages of selective breeding to compare with genetic modification?

Keep in mind that it is practically impossible to define GMO. Many of the things that we would call GMO actually don't result from much more than just selective breeding. Following this logic corn, wheat, sunflower oil, lettuce, broccoli, cauliflower, peanuts and pretty much everything else you eat is a GMO.
Attempting to let aside the semantic issue a comme argument is a lack of lack of familiarity and this is why extra precautions and testing must be done. See What risks exist with GMO, but not with selective breeding?

can I use the mutagenesis as the example of selective breeding [..]?

Mutagenesis and selective breeding are two different processes (although often used together). One is not an example of the other.


text:
Screening Enzymes?
I wish to obtain a list of all known enzymes and then get rid of the ones that use cofactors, the ones that use ATP, and a few others. What is the easiest way to do this?

You should be able to filter the UniProt database for this. For example, this search query:
ec:* NOT cofactor:(chebi:*) NOT annotation:(type:"catalytic activity" atp) AND reviewed:yes
...gives you all manually curated (reviewed:yes) enzymes (ec:*) that don't have a cofactor (NOT cofactor:(chebi:*)) and don't catalyze reactions with ATP (NOT annotation:(type:"catalytic activity" atp)).


text:
How can Giant squid have $20,000 mm^{-2}$ photoreceptor cells, but no cones?
According to this post, Cephalopods have about $20,000 mm^{-2}$ photoreceptors in there eyes. However, Cephalopods (in my case, the Giant Squid) aren't born with cones (cells that dictate which colours you see). So are they born with about 20,000 rods (cells that help detect movement), or is there another type of cell involved?

How do you get from 20,000 $mm^2$ to 20,000 cells? Note also that in the title you said 20,000 $m^2$.

You are missing a "/". The number in that post is 20,000 PER mm2. Overall though I think you need to do some more research on this on your own... rods are not only used for detecting movement, for example. Even that post you linked has a lot of information that you seem to be lacking.

First squid lack both cones and rods, they evolved their eyes independently, the cells they use most closely resemble rods but they are by no means identical.
In vertebrates there are two types of cells rods and cones both of which can be used to see movement (movement is just detecting changes in the visual field). rods are better at it becasue they are smaller so they can be packed tighter, thus they can detect smaller changes, but that is by no means their primary function. Rods detect luminosity, that is the intensity of light, but react to light from all parts of the visual spectrum.
There is a lot of debate about how much color squid and octopi can see. behaviorally they appear to recognize color, but they don't have differentiated cells or opsins to detect them.
I appears they have stumbled on a completely different way to achieve color vision, they appear to use weird shaped pupils and chromatic aberration.
I suggest reading the linked paper as you have to dive pretty deep into the physics of optics to understand. Basically different colors of light are bend by slightly different amounts by a lens, and they are using the multiple images of their U shaped pupils to gain color information.


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the range of interleukin 2 and 12 that can be used to activate nk-92 cells
I am one of the biotech students. I want to know the dynamic ranges of interleukin 2 and 12 that i can use to activate the NK-92 Cells.
    thank you

If you have the resources you should ideally titrate your cytokines. You'll find that cytokines from different vendors may exhibit varying stability or availability in vitro, but also that you obtain varying levels of activation. Standard NK-92 culture conditions are 100-300 IU/mL IL-2 in RPMI1640 medium, 10% serum and 2mM L-glutamine (or 1X GlutaMAX, life technologies). Activation levels depend on how much you want to activate them. Interleukin-12 I'm fairly certain is standard at 10 ng/mL, but should also be titrated.
There's actually a relevant paper with a fair titration looking at granzyme expression at different concentrations of IL2, IL12 and IL15, and different timepoints. They note that NK92 cells show response at 100, 500 and 1000 IU/mL IL2, and at 10-30ng IL12.


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Mathematical relationship between membrane conductance and conduction velocity?
By what factor would the myelin need to decrease membrane conductance (gm) if you wanted conduction velocity in a 10 μm myelinated mouse axon to be 100 times faster than in a 10 μm unmyelinated mouse axon?
This is a question from a homework set. I understand WHY myelin decreases membrane conductance, and WHY decreasing membrane conductance would increase conduction velocity. I just do not understand how to calculate what factor specifically the myelin would need to decrease membrane conductance by.

See also https://biology.stackexchange.com/questions/53003/what-is-the-mechanism-by-which-myelination-reduces-the-capacitance-of-the-axon-m/53007#53007 tl;dr: capacitance matters too

The conduction velocity is inversely proportional to the membrane time constant $\tau_m$ and proportional to the length constant $\lambda$. Membrane time constant is proportional to membrane resistance (inverse of membrane conductance), and the length constant is proportional to the square root of membrane resistance.


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Blood Group Notation
In a textbook, I encountered a notation used when writing blood groups down, which was "I" with the blood group type as a superscript. I was curious as to why the letter "I" is used in this notation and what it means. E.g. Iᴬ and Iᴮ.
Thanks.

Those are names of alleles involved in the ABO blood group system. The “I” stands for isoagglutinogen which is an antigen that causes agglutination of blood cells when reacting with a specific antibody (an isoagglutinin).


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Do blood vessels expand during angiogenesis?
I know that there are two usual ways of creating new blood vessels:

A new vessel sprouts from the wall of an old one,
A wall of cells grows down the middle of a vessel, splitting it into two.

I also know that capillaries are all the same size (about wide enough for a single red blood cell to get through). I also know that in between the major blood vessels and the capillaries, you have a hierarchical branching of differently sized tubes.
So my question is to do with, like. So if a new blood vessel starts to sprout, does it start off as wide at the base, as it's always going to be? (E.g. does it already know how many times it'll have to branch before getting to the capillaries, and choose its width accordingly?) Or does it start off smaller, but widen at the base as its ends keep branching?


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Which factors dictate the mineral composition in plants\vegetables?
Here's a table of vegetables mineral composition (one of many), just as an example. Each vegetable contains different amounts of minerals, and my question is why is that, or in other words: Which factors dictate the mineral composition of different vegetables, since the diffusion process by which the minerals are absorbed from the ground into the root is essentially the same for all plants\vegetables?


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S.pyogenes binary fission rate/speed
For my Math IA (IB SL) I want to calculate the average amount of time that one viable S.pyogenes bacteria will need to create an ID50. I cannot find the average speed for the divison of any Streptococcus anywhere.

Hi @Jakub. Welcome to Biology S.E. I would highly recommend to take the tour (https://biology.stackexchange.com/tour) to know how a Stack Exchange site works. Also, you will earn a badge for reading the tour. As you will see, research effort prior to asking a question as well as using the correct tags will make sure that you can enjoy and use this site to its full extent.

Growth rates are largely temperature-dependent. According to this study (Growth rates of Streptococcus pyogenes and derived L form at various temperatures) the growth / doubling rates for Streptococcus pyogenes are as follows:


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"Twig-with-leaf"-like insect in central Mexico
What's that?! I have googled around and found insects that looks like a twig, and others that look like a leaf, but this one looks deceptively like a leaf at the end of a twig (I swear it's a real living thing despite the appearances: it has legs and moves around!). As you can see from my hand on the photo it is also fairly big (well, at least for my European standards...).

Location: Morelia, Mexico (about 2000m high, in the tropics)
Time: October (humid season), in the morning

And about your European standards: the European praying mantis is up to 9 cm and occurs all over Southern Europe and even at isolated locations in Germany. See Though I admit I was startled too when I encountered one.

That is a Mexican/Texas unicorn mantis, which is of the species Phyllovates chlorophaea.


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Spider Species Identification
Can anyone identify this species of spider and whether or not is is venomous?
Location: South Carolina, USA.

Hi Jody.. based on your profile, I added your location to be SC, USA. If this is incorrect, please edit.

Also the size and the habitat might help

That is a Nephila clavipes, a.k.a, "golden silk spider". According to Wiki, this is the only golden web-orb species that's indigenous to America.

Can anyone identify this species of spider and whether or not it is venomous?

"..there is little real danger from an encounter with the golden silk spider. The spider will bite only if held or pinched, and the bite itself will produce only localized pain with a slight redness, which quickly goes away. On the whole, the bite is much less severe than a bee string." (source)


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What kind of spider is this from Nova Scotia, Canada?

What kind of spider is this? It was found in Nova Scotia, Canada and is about the size of a quarter.

That is an Araneus diadematus, a kind of garden orb-web spider.

Orb-weaving spiders are quite common, and can be found nearly anywhere in the world, excluding Greenland. The following is a distribution map for the species A. diadematus, of which, as you can see, is mostly contained to North America & Canada.

Dark gray: present; Light gray: no record. (source)


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What is the minimum caloric intake for a truly starving adult
What is the minimum caloric intake for an adult?  I'm not talking about a healthy diet.  There's plenty of advice on that.  I'm wondering what the absolute limits of H. sapiens are.  When there's a multi-year famine, and the body is willing to shut down as much of its capacity as possible without actually failing to function for years at a time, how much energy is it consuming?
I know the Basal Metabolic Rate is a key factor to this, but the numbers I have seen for it are all "healthy" BMRs.  I'm interested in the unhealthy numbers.  For example, I'd consider maintenance of temperature optional for these circumstances (assume we have a temperate enough climate), and I presume heart rate and breathing will go down, decreasing those loads.  Obviously there's limits as to how many environmental constraints can be addressed (if I knew what environments this was studied in, I'd likely know which studies to look for!).  And obviously not everyone is the same, but that's an issue in every human study ever completed.

Threr's no single answer to this question, just generalizations. It depends on the person, their state of health when starvation starts, and what you mean by "truly starving". To me, truly starving means no food whatsoever. If you want an answer, there's only one place to get it, and it's not here. Hint: these experiments were done in the 40's.

http://jn.nutrition.org/content/135/6/1347.full

How much water does it take for a plant to keep some leaves? how long is a piece of string?

@anongoodnurse The existence of variation does not make the question less amenable to scientific analysis. The confounding factors you mention, along with many other relevant factors, I'm sure, as well as the problem of defining the outcome variable can all be in principle addressed empirically. Although doing experiments on the subject is unethical, naturally occurring events of famine or voluntary starvation can be also studied. Surely we all agree that qualified generalisations and statistical analysis are the bedrock of biological research.

@anongoodnurse The challenge of defining starving is why I started with my first paragraph defining the term as I use it.  I specifically wanted to step away from the anorexia/bulimia related content because the focus there is how to make those people healthy, not just continue functioning.

you need to define the mass, age, and activity level of the individual to get a reasonable answer. You also need to better define your ending conditions does the person to recover completely or can they suffer permanent damage from the starvation.

A better example is the stories of tibetan monks who wrote accounts of their experience to survive for months or years on faith alone, and watch their hair and nails fall out in the search for wisdom. they could tell you how fast a coma arrives from eating just 300 calories per day.
There isn't a minimum amount though, because it's all subjective for time until, temperature, survival chores, time until coma, time until difficulty moving... you can probably keep someone in an emaciated coma with intravenous injections, or someone could stay awake with high exposure risk to illness, hair loss, nail loss. The question is vague, and there are 100 scientific studies about calorie restriction, so you are hoping someone will read 10-20 pages until they find some information for you.
It also depends how many watts the human needs to use in that situation to stay alive.
In 30'C you probably need 30 watts to stay warm, and 20 degrees about 60 watts, so the value can double based on temperature, you must change your question a bit.
60 watts basal metabolic rate body temperature would use 70 calories per hour, about a slice of bread, so 1400 calories per day without bedcovers. It depends a lot on ambient temperature and exercise, for example 1 mile of walking uses 100 calories. At less than 1000 calories per day, exercise becomes difficult and the person gets thin. Jogging uses about 250 watts. Extreme athletes and triathletes peak at about 650 watts for sprinting.
There are 100ds of citations on caloric defficiency and restriction, with values around 350 - 700 per day, which change metabolism considerably:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3014770/
https://www.ncbi.nlm.nih.gov/pubmed/2718912

I don't think it answers the question.

I'm not reading through 20 pages of rambling science articles to find out that there isn't an answer! There isn't an absolute minimum, same as there isn't a minimum amount of water for a plant to survive, and people don't starve for years.


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Why do erythrocytes have no MHC1 but platelets do?
Red blood cells do not have a considerable number of MHC1 through their membranes, and that's explained by them not having a nucleus. But why do platelets have MHC1s if they have no nucleus either? I don't think that lifespan is a good enough explanation since that would mean young red blood cells have MHC1s and old platelets don't, since the latter can last over a week in circulation. Megakaryocytes do have MHC1s, but that means nothing, since red blood cell percursors also have them.

There's actually a good answer to this on Quora.


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Can CRISPR-Cas9 make changes on a living organism?
Can CRISPR-Cas9 make changes on a living organism? What's the limit here? E.g. reversing/restoring hearing loss in a living adult mice.

Hearing loss is a particularly tricky phenotype to mention, because a) hearing loss has many many, sometimes unrelated, causes, and b) because hearing loss is often associated with death of cells that do not reproduce in adults.

Answer is yes, but it depends on which kind of phenotype you're going to restore/change. As you can imagine, using crispr cas9 on an high amount of cells require one condition: edited cells need to have a clear advantage in surviving besides the previous.
Here's an example of a crispr-cas9 protocol followed to restore a wildtype phenotype in adult mice.


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Hammerhead worm

Which Bipalium is this worm? It has no tripe. Nor head collar. It is dark brown as can be seen in the image. This worm is right now in Mauritius. Please help me recognise this Hammerhead worm. Thanks

I am not completely sure, but I think that this is a Hammerhead that comes from Asia: the Humbertum Covidum. It is a new, invasive species, hence the name. I am not sure because the Humbertum Covidum tends to be "Fatter", and your Hammerhead is longer. Another reason why I am not sure about this is that the Humbertum Covidum is a Asiatic species, which is very rare in Mauritius. However, I think this is the most accurate response, and I hope this helped!


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Genotype result of double fertilization

So, clearly, the endosperm would be a fusion of the polar nuclei and one male gamete. Does this mean that each male gamete would have a T allele on it?
I can't seem to figure out a way to predict the allele distribution between the 2 polar nuclei since the flower has a Tt genotype.
Along the same lines, how can I predict what alleles the haploid egg would have? T or t? So, in that case, there would be a 50% chance of the embryo being TT and 50% chance of it being Tt (I didn't understand what the plus sign signifies).
The correct option is D, but I can't figure out how to get to that answer with absolute certainty.

The question is unclear to me. I understand we expect a triploid nucleus plus a diploid zygote (double fertilization) but I don't understand what (TTT + TTt), TT means.

IMO, the question is unclear
The question is unclear to me. I understand we expect a triploid nucleus plus a diploid zygote (double fertilization) but I don't understand what (TTT + TTt), TT means.

Which book did the question come from?
Is there any preamble to this question?

Double fertilization
I am not so used to thinking about double fertilization in plants. In short, two pollens are involved. One fertilize a haploid gamete from the mother and the other fuse with two haploid gamete (polar nuclei) from the mother (triple fusion) resulting in a triploid "individual".
In my below answer, I am assuming that any two polar nuclei can fuse with the pollen. I am not sure this is true. If it is systematically polar nuclei resulting from the same meiosis II (that is they have the same parent cell after meiosis I), then t story is a little different.
How I understand the question
In my understanding, we are talking about a single locus with two alleles T and t. Both pollens are T. The mother is Tt.
Answer
There are two possible gametes from the female side T and t. Only one possible gamete from the male side T. Therefore, the diploid zygote is either

$\frac{1}{2}$ TT
$\frac{1}{2}$ Tt

, where the numbers indicate probabilities
Now, for the triploid nucleus resulting from the fertilisation of two polar nucleus from the mother and one pollen grain can be either

$\frac{1}{4}$ TTT
$\frac{1}{2}$ TtT or tTT
$\frac{1}{4}$ ttT

Now, I have no idea how that matches to the possible answers as I don't understand the notation.


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Confusion on polarity and hydrophobicity of Proline, Tyrosine and Cysteine?
I will list here several sources that state differently on the polarity and hydrophobicity of Proline and Tyrosine:
From the article Amino Acid on Wikipedia, it states that Proline is a special case, Tyrosine is hydrophobic and Cysteine is also a special case.
From Khan academy, it also states that Proline is polar, Tyrosine is nonpolar and Cysteine is polar.
However,
From Pearson Prentice Hall's Biological Science, it states that Proline is nonpolar, Tyrosine is polar and Cystein is polar.
From BioNinja, it states that Proline is nonpolar, Tyrosine is polar and Cysteine is nonpolar.
On Wikipedia,
The article Proline supports Proline is nonpolar.
The articleTyrosine supports Tyrosine is polar and hydrophilic.
The article Cysteine states that Cysteine is polar and hydrophobic, AS WELL AS Tyrosine.
To summarize the result, I'll put them in the following table

Please help me to clear out the confusion, why the polarity and hydrophobicity of these amino acid are not agreed with each other?

Cysteine shouldn't be considered polar as the difference in electronegativity is lower than 0.4 between Carbon (2.58) and Sulfur (2.55) or between Sulfur and Hydrogen (2,20). The difference is higher in the C-H bond. That's also the reason why Methionine is nonpolar.

TL/DR: these are borderline, complicated cases. There is no broad consensus on whether cysteine and tyrosine should be considered hydrophobic or polar. Proline is clearly nonpolar though.
The reason for the confusion is that are there several ways to define and measure polarity and hydrophobicity for amino acids. First, the polarity and hydrophobicity of the free amino acid is very different from that of the amino acid side chain in the context of a peptide (protein). I assume you are interested in the latter.
Polarity is rather difficult to define for amino acids. The dipole moment is the usual measure of polarity, but this depends on the molecule's geometry, and consequently is only well-defined for small molecules that cannot "wiggle" around, such as water. Larger amino acids side chains can wiggle quite a bit, and their dipole moment is difficult to define. Instead, polarity is usually given by rules of thumb like "hydroxy groups are polar" and "aromatic rings are nonpolar. But then there are borderline cases like tyrosine that has both an aromatic ring and a hydroxy group.
Hydrophobicity is related to polarity, but it is an experimentally measured quantity, usually determined by how an amino acid partitions between water and nonpolar solvents, or by observing how it orients in folded proteins (towards or against the water solvent). More detailed information is found here. But the results of such experiments don't always agree, and so amino acids which are borderline hydrophobic/hydrophilic can be difficult to classify. For example, for two amino acids X and Y, we might find that X dissolves better in water than Y, so X appears more hydrophilic in this sense; but at the same time, X could also partition better into a lipid bilayer, so in this sense X appears more hydrophobic than Y. In such cases, the various scales of hydrophobicity will differ.
For these reasons, there is disagreement on whether some amino acids are polar/hydrophobic. With this in mind, here's my two cents on the amino acids you mention:
Proline is a bit special in that it does not have an -NH3 group; the amine nitrogen binds to the side chain -- it is more of a "loop" than a chain -- and the peptide bond is different. But this "side loop" clearly has no polar group, and I think there is good agreement that proline should be considered nonpolar. The Khan Academy page is probably mistaken on this one. Proline is intermediate in hydrophobicity.
Tyrosine: As mentioned, polarity of the tyrosine side chain is unclear since it is quite large and has both polar and nonpolar groups. Tyrosine is somewhat hydrophobic, but among the amino acids, it places itself near the middle on most hydrophobicity scales. So tyrosine is a borderline case, which explains why different sources disagree.
Cysteine is special in the context of proteins, since cysteine residues often pair up via disulfide bonds, and this changes its properties. By itself, the -SH group is polar (although less so than an -OH group) so the cysteine side chain is somewhat polar. It is intermediate in hydrophobicity as measured by solvent partitioning. Cysteine was considered hydrophobic based on the observation that cysteine is often found in the interior of proteins, away from the water solvent; but this is largely due to its ability to form disulfide bonds.

Thank you. Very insightful and detailed explanation. Accepted and upvoted.


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Can someone identify this spider?
Saw this on the street in the UK. To my eyes it looked and moved distinctly tarantula-y (although I don't have any firsthand experience with them) which I'm pretty sure we don't have any of natively. Most of the spiders you commonly see here are thinner generally and move much faster. This guy lumbered.
For scale, it didn't span more than a couple of inches.

That is a kind of orb weaver.

@Charles Did you want to post this as an answer? Having researched more thoroughly, I think you probably linked the exact species.

Yes, the species that I suggested, Araneus diadematus, is most likely the correct ID. And yes, I suppose I can turn this into an answer. Originally that day I had already provided an ID for someone else that was of an orb weaver, and so, I was giving someone else a chance to ID. Since it's been a few days and still nobody has seized the opportunity, I'll provide an answer within the next few hours. Thanks for following up. :)


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Do oranges have traces of starch?
This is for a chemistry experiment, so I just want to know if there are small traces of starch in oranges, and not whether or not I should eat an orange for its starch content, or something to that extent.

If it is related to chemistry, it would belong to Chemistry.SE

According to Healthy Eating, oranges contain 8.98g of sugar but does not contain any starch:

The natural sugar found in fruits doesn’t create such a big response
  because it's balanced by the fruit's fiber content. One banana has
  14.43 grams of sugar, compared to only 8.98 grams in an orange. The biggest difference between the two is in the amount of starch each
  contains. The orange doesn’t have any, while the banana has 9.42 grams
  of starch.

I’m not sure how trustworthy these websites are. This one, for example, says that oranges do have starch.

Sources are varied. This paper studies starch in oranges (I can't access full paper). However, here authors mention that oranges contain practically no starch (beware, images are upside down). They refer to work by
Stahl A.L., Maturity studies of citrus fruits, 1938

and quote this work saying "starch content was measured to be 0.07-0.13%" in pulp of Pineapple oranges. Compare that to 22% of potato starch amount (dry mass).


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Normalizing Metabolomics data
First time posting. I recently started working in the field of metabolomics. I have semi-quantitative (not absolute concentration) LC-MS data from in-vitro cell experiments under different experimental conditions.
What is the best way to normalize the data so that I can compare across experimental conditions correctly ( + across different cell types)? I've found many people scale their data using different methods (pareto scale, auto scale, zero mean)  each of these leads to different results when I run something like a PCA between experimental groups.
Thanks.
Jon

Scaling is not the same as normalization.  You have empirically discovered how scaling affects PCA, and it's purpose is to control whether large peaks dominate the analysis or not.
Normalization on the other hand is typically done when samples were in a solvent and the concentration could vary due to the extraction method, the hydration of the tissues etc.  So normalization tries to compensate for these varying concentrations.
Normalization would normally be applied across the peak intensity vs time dimension.  Two typical normalization schemes are 1) normalization to constant sum (usually 1) and 2) Probabalistic Quotient Normalization which uses a slightly more complex approach (and is frequently preferred).  I don't work with LC-MS data, there may be other methods that are preferred with this type of data.  Whatever software you are using probably has several options built-in.
Probabalistic Quotient Normalization is reported in F. Dieterle et. al. Analytical Chemistry vol. 78 pages 4281-4290 (2006). The exact same mathematics are called "median fold change normalization" by Nicholson's group, reported in K. A. Veselkov et. al. Analytical Chemistry vol. 83 pages 5864-5872 (2011).


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Calcium concentration in activated dendritic spines?
What are the typical calcium levels reached in single postsynaptic spines following activation of NMDA receptors by an EPSP or backpropagating spike? Everyone seems to refer to that one Neuron paper (Sabatini et al. 2002) which reports experimental estimates of around 1 uM following single synaptic stimulation in CA1 neuron spines. However, most computational papers on LTP (even biophysically detailed models) work with much lower values for Ca2+ transients that do not seem to have concrete experimental support. I am trying to put together a realistic model for hippocampal spine calcium signaling, and would really appreciate it if anyone can point out other relevant experimental papers that provide estimates for spine calcium transients.

An earlier source for an estimate of ${[Ca]_{i}}^{+2}$ in spines comes from hippocampal slices of P13-P19 rats (Majewska et al. 2000). The resting ${[Ca]_{i}}^{+2}$ in this paper was ~80 nM and a back-propagating action potential (AP) elicited a response up to ~250 nM (change of ~170 nM). They included $F_{min}$ and $F_{max}$, the minimum and maximum fluorescence signal from a single AP, as parameters in the equation they used to estimate ${[Ca]_{i}}^{+2}$. This paper may be where the models you mention got their numbers from.
The resting ${[Ca]_{i}}^{+2}$ estimated in Sabatini et al. (2002), where they also used rat hippocampal slices from P14-P20, matches that found in Majewska et al. as it was ~70 nM. For the estimation of the evoked change in ${[Ca]_{i}}^{+2}$ after a single AP they used the maximum fluorescence increase from trains of action potentials at 62.5 Hz and 83.3 Hz as a parameter in their estimator equation, assuming that the calcium indicator was fully saturated at those stimulation frequencies. Their estimate for the change in ${[Ca]_{i}}^{+2}$ per AP was about 530 nM. They then reasoned that the buffering properties of the calcium indicator itself could reduce the change in ${[Ca]_{i}}^{+2}$. Thus they loaded several different calcium indicators with different affinities and at different concentrations, in order to manipulate the $\kappa_b$, the buffer capacity, of the calcium indicator. They observed a very strong linear relationship between $\kappa _b$ and the change in ${[Ca]_{i}}^{+2}$. By extrapolating from a linear fit on these data, they concluded that in the case where there was no calcium indicator in the cell —i.e. when $\kappa _b = 0$— the change in ${[Ca]_{i}}^{+2}$ per AP would be approximately 1 $\mu$M.
So the difference between these studies is that in Majewska et al. they used the maximum observed fluorescence of the calcium indicator in their data after single APs, whereas in Sabatini et al. they attempted to saturate the calcium indicator with high-frequency trains of APs. Furthermore, in Sabatini et al. they attempted to account for the buffering capacity of the calcium indicator itself, thus arriving at a more unbiased estimate.
Reassuringly, later work from the Yuste lab (the same lab as in the Majewska et al. study) could replicate the results of Sabatini et al. when they used similar methodology (Cornelisse et al. 2007). Their estimate for $\Delta{[Ca]_{i}}^{+2}$ for a single AP was also ~1 $\mu$M.


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Can neurons be inhibited with electric current?
It is well known the electricity can be used to fire neurons. But can it be used to inhibit neuronal firing? This is in the context of extracellular stimulation. In extracellular stimulation, it is known that there is a threshold for stimulation and a threshold for damage(electroporation). Is there a threshold in between these two which inhibits neuron firing without any damage? Please provide reference for your answer.

Generally it's not appreciated to edit the question such that an exisiting answer becomes obsolete.  -1

I apologize, but your answer made me realize the incompleteness of my question. Thanks.

Yes, but maybe not how you think.
It is important to recognize that voltages refer to potential differences. When we say the "a cell is at -65mV" for example, we mean "The potential difference across the cell's membrane to the extracellular space is -65mV." When you stimulate electrically, you create a transient electric field, whereby the extracellular space is no longer effectively isopotential.
Let's imagine for the sake of some neuron that this field strength is on the order of 40 mV across the membrane. If this electric field is perpendicular to some neuronal process, the voltage across the membrane will be about -105mV on one side, and -25mV on the other side. The -25mV side is now depolarized enough to open voltage gated sodium channels, and some current is flowing into the cell. Once the shock has passed, positive current will continue to flow through those open channels and open more channels. It doesn't matter much that the other side is transiently at -105mV, all that matters is that you opened a bunch of voltage gated sodium channels which starts a positive feedback loop.
Therefore, transient electrical simulation will almost always be excitatory. There are two exceptions:
1) Neurochemical inhibition. If you excite a particular brain region that is specifically inhabited by inhibitory projection neurons, you will primarily excite those inhibitory cells and therefore cause excitation elsewhere. Of course, in this case, the electrical stimulation itself is still directly exciting cells, they just happen to have inhibitory effects elsewhere.
2) Depolarization block. If you continually stimulate the same population of neurons with a high-frequency stimulation, you can put neurons in a state called "depolarization block." Voltage-gated sodium channels have a chance to inactivate whenever they are activated. If you inactivate enough channels, there aren't enough available to produce an action potential. Therefore, if you can keep a cell pretty much constantly depolarized by continually stimulating, you can prevent action potential propagation because too many of the voltage gated channels in the axon initial segment are inactivated.

In practice, focal electrical stimulation of the brain can be used to prevent or abrogate seizures.  There is a device marketed for this.
from https://www.scientificamerican.com/article/implant-epilepsy-seizure/

NeuroPace's Responsive Neurostimulation System (RNS), an
  electrical-stimulation implant with two leads, each containing four
  electrodes, placed in the brain at the seizure focus. The RNS detects
  electrical activity that denotes the start of a seizure and delivers
  direct electrical stimulation to interrupt the activity and normalize
  the area.

It is not immediately obvious to me why this would work.  The linked review describes how this was first observed empirically.  My understanding is that the electrical stimulation causes polarization such that the nerve cannot immediately fire again as part of the epileptic focus.  Sort of like a counter burn if you are fighting a wildfire.
Sun FT et al.  Responsive cortical stimulation for the treatment of epilepsy.Neurotherapeutics. 2008 Jan;5(1):68-74.

In the 1990s, Durand and colleagues demonstrated success in
  suppressing spontaneous inter- ictal bursts in vitro by providing
  responsive stimulation directly in the epileptogenic region. Their
  result sug- gested that the mechanism for suppression is an inhibi-
  tory polarization caused by the transmembrane currents generated by
  the applied pulse. These trials in animals laid the groundwork for
  responsive stimulation therapy for epilepsy.

My answer explains how this would work - via depolarization block.

Short answer
Yes.
Long answer
Neuron activity can indeed be inhibited with the correct type of electrical input stimulus.
In fact you can play around with various electrical signalling stimuli yourself, and observe the results not just for a single neuron but the entire network, yourself:
https://www.neuron.yale.edu/neuron/
The link above is a simulation environment that tried to emulate neuronal activity based on user defined signalling stimuli. Not only can you inhibit signals, but you can totally control macroscopic behaviors: e.g. excitation of entire regions of a prototypical neuronal pathway.

Are you referring to injecting current into a cell directly? That isn't what the OP asked.

Oh my bad... ty


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Why do we need to close eyes to sleep?
Out of all our sensory organs, we need to stop taking signals explicitly only from eyes in order to sleep. Even interestingly, those who are not able to receive signals from eyes (i.e., the visually challenged people) also need to close their eyes in order to sleep. I wonder what is the relation of closing eyes with sleeping. I think the reason might be related to the state of the muscles related to the eyes. Of course, even if it were the case that one could keep her eyes open while sleeping, the brain would stop paying attention to the signals received by the eyes -- just like the brain stops paying much attention to the signals received by the nose or the ears while sleeping even if these organs are not physically closed or prevented from receiving signals. But in the case of the eyes, they are physically closed while sleeping,  which makes me curious.

Possible duplicate of Why do our eyes close when we sleep.

Unlike our underwater ancestors, land animals have evolved eye lids or nictitating membranes to protect our eyes and keep them moist periodically by blinking. During the sleep state, closing our lids protects the eyes from drying out and getting damaged while unconscious.  In addition to the lids themselves blocking light stimulus (not totally), our eyes also roll back to attenuate light stimulation.  Fish also sleep and don't need eyelids to do so, thus closing eyes is not a prerequisite for the sleep state.
Textbook Source: Butler, Ann B.; Hodos, William (2 September 2005). Comparative Vertebrate Neuroanatomy: Evolution and Adaptation. John Wiley & Sons. p. 215. ISBN 978-0-471-73383-6.


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Is the Insulin Receptor Considered an Enzyme?
Can we consider insulin receptor an enzyme? In other words, does the insulin receptor have enzymatic characteristics?

For a better understanding. you can refer to :
https://blog.udemy.com/types-of-enzymes/ http://www.diabetes.co.uk/body/insulin.html

Yes, the insulin receptor can be viewed as an enzyme, since it catalyzes a reaction -- phosphorylation of tyrosine residues on its substrates. But since the protein has multiple functions, it's probably better to say that the insulin receptor "has enzymatic activity", rather than "is an enzyme".
The notion "enzyme" is not restricted to catalysis of reactions involving small molecules, like those in central metabolism. The IUPAC definition of an enzyme reads: "Macromolecules, mostly of protein nature, that function as (bio)catalysts by increasing the reaction rates". So "enzyme" is a broad term, including catalysis of all chemical reactions. DNA replication, mRNA transcription, protein synthesis and posttranslational modifications all involve enzymes. Those enzymes that act on small metabolites can be called "metabolic enzymes" to clarify their function.

Insulin receptor tyrosine kinase, is for all intends and purposes an enzyme. It catalyzes the transfer of a Gamma phosphate from ATP to its substrates (a tyrosine), require divalent metal ions (Mg2+) and have maximal activity when bound to an activator such as Insulin. As such it is perfectly acceptable to call it an enzyme.

Also what other activities are you talking about? The insulin receptor to my knowledge bind extracellular insulin or closely related hormones, become activated and start phohorylation of intracellular substrates. Which substrates and adaptor proteins that are present and their concentrations are what determine downstream signalling.

@JeppeNielsen  I only meant that the protein has multiple functions since it is both receptor and an enzyme. I agree it's fine to call it an enzyme, but it can be useful to indicate that it's not only an enzyme.


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About which cells in the human body do we know most?
Are there model cells (in the sense of model organisms) in the human body (other than E.coli) about which is known most (with respect to structure, function, metabolism, gene expression, ...) and to which I can refer when asking questions about "typical cells" (which per se don't exist). The other way around:

About which cells (added: normal and mature) in the human body do we know most?

(Maybe there's a cell in the rat we know more about, but also know/believe that it is very similar to a human cell? Which one, then?)
Having asked this, I'd also like to know, about which neurons in the human brain is known most, e.g. about "pyramidal cells in cortical layer IV"?

Related question: Are all functions of a human cell known?

HeLa cells (from a cervical cancer) are probably the most studied human cells : https://en.wikipedia.org/wiki/HeLa.   Because these cells are cancerous and are "immortal" I don't know if any knowledge gained is that useful, so I'll post as a comment.

@VonBeche - The knowledge gained from study of HeLa cells is incalculable. Just one result - the polio vaccine - should give you an indication of their worth. However, it is not a normal human cell, so...

I would argue that HEK293 cells might be a contender against HeLa for the price of the most studied cells.

We know most about corneal epithelial cells because we see right through them.

@Gaurav: seriously or just joking?

@the put-on-hold voters: Is the extent of knowledge about a cell (type) really a matter of opinion?

I admit, an "extent of knowledge" might be hard to define and measure, but it doesn't seem impossible, does it?


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How do infants get their very first gut bacteria?
First of all, I'm a complete layman in Biology. Recently I read "The evidence for evolution" by Richard Dawkins. Pondering about this matter, I wondered about the origin of human gut bacteria (could be more generalized to mammal gut bacteria).
Generally, I see two possibilities:
These bacteria are

acquired later on through the environment (probably after birth) or
they are produced by the organism itself

The former option seems to me a little bit too vulnerable to be true (different food, different bacteria due to geographical location, etc.)
The latter option seems baffling to me. Bacteria are, as far as I know, independent lifeforms. Is it possible, that our DNA contains the information for other lifeforms as well?

30 percent of the beneficial bacteria in a baby's intestinal tract come directly from mother's milk, and an additional 10 percent comes from skin on the mother's breast.... google search breastfeeding and gut bacteria, it's a fascinating topic. that's the temporal origin. the evolution origin, well, ants have gut bacteria too.

Humans do not "generate" bacteria. Spontaneous generation was disproved by Louis Pasteur in the 1800s.

Well, the former is exclusively the answer. Humans (or other mammals, or any species in general) cannot give birth to new species (of bacteria, here); they have to be acquired from the environment at all costs. However, the environment does vary, leading to variance in gut microbiome, as will be discussed later.
First of all, gut microbiome is only a part of the total microbiome of humans (Sherwood et al, 2013). Now, usually, gut bacteria are acquired by a person within one to two years of birth (Sommer et al, 2013), while the gut of a fetus is considered as sterile. However, microbial colonization in a fetus is possible (Matamoros et al, 2013). For example, species of Lactobacillus and Bifidobacterium were found in biopsies of placenta in one study (Mueller et al, 2017).
During birth and rapidly thereafter, bacteria from the mother and the surrounding environment colonize the infant's gut. Infants born by caesarean section may also be exposed to their mothers' microflora, but the initial exposure is most likely to be from the surrounding environment such as the air, other infants, and the nursing staff, which serve as vectors for transfer. During the first year of life, the composition of the gut flora is generally simple and it changes a great deal with time and is not the same across individuals (Sommer et al, 2013).
Now lets talk about variation in gut microbiome among individuals. The gut microbiome of an individual may vary depend mainly due to:

Age:  the diversity of microbiota composition of fecal samples is significantly higher in adults than in children, although interpersonal differences are higher in children than in adults. Much of the maturation of microbiota into an adult-like configuration happens during the three first years of life.
As the microbiome composition changes, so does the composition of bacterial proteins produced in the gut. In adult microbiomes, a high prevalence of enzymes involved in fermentation, methanogenesis and the metabolism of arginine, glutamate, aspartate and lysine have been found. In contrast, in infant microbiomes the dominant enzymes are involved in cysteine metabolism and fermentation pathways (Yatsunenko et al, 2012).

Diet: Gut microflora is mainly composed of Prevotella, Bacteroides, and Ruminococcus. There is an association between the concentration of each microbial community and diet. Prevotella is related to carbohydrates and simple sugars, while Bacteroides is associated with proteins, amino acids, and saturated fats. Specialist microbes that break down mucin, survive on their host's carbohydrate excretions. One enterotype will dominate depending on the diet. Altering the diet will result in a corresponding change in the numbers of species (Wu et al, 2011).

Geography: In simple terms, gut microbiome composition depends on the geographic origin of populations. For example, the US population has a high representation of enzymes encoding the degradation of glutamine and enzymes involved in vitamin and lipoic acid biosynthesis; whereas Malawi and Amerindian populations have a high representation of enzymes encoding glutamate synthase and they also have an overrepresentation of $\alpha$-amylase in their microbiomes. As the US population has a diet richer in fats than Amerindian or Malawian populations which have a corn-rich diet, the diet is probably a main determinant of gut bacterial composition (Yatsunenko et al, 2012).
Further studies have indicated a large difference in the composition of microbiota between European and rural African children. The fecal bacteria of children from Florence were compared to that of children from the small rural village of Boulpon in Burkina Faso. The diet of a typical child living in this village is largely lacking in fats and animal proteins and rich in polysaccharides and plant proteins. The fecal bacteria of European children was dominated by Firmicutes and showed a marked reduction in biodiversity, while the fecal bacteria of the Boulpon children was dominated by Bacteroidetes. The increased biodiversity and different composition of gut flora in African populations may aid in the digestion of normally indigestible plant polysaccharides and also may result in a reduced incidence of non-infectious colonic diseases (de Filippo et al, 2010).

Also, as @com.prehens.ible says in comments, there are various other modes through which an infant may acquire bacteria to give rise to their gut microbiome. For more information, you can also read the Wikipedia page on Gut Flora.
References:

Sherwood, Linda; Willey, Joanne; Woolverton, Christopher (2013). Prescott's Microbiology (9th ed.). New York: McGraw Hill. pp. 713–721. ISBN 9780073402406.

Sommer F, Bäckhed F (2013). "The gut microbiota—masters of host development and physiology". Nat Rev Microbiol. 11 (4): 227–38. PMID 23435359.

Matamoros S; et al. (2013). "Development of intestinal microbiota in infants and its impact on health.". Trends Microbiol. 21 (4): 167–73. PMID 23332725. doi:10.1016/j.tim.2012.12.001.

Mueller, Noel T.; Bakacs, Elizabeth; Combellick, Joan; Grigoryan, Zoya; Dominguez-Bello, Maria G. (2017-04-08). "The infant microbiome development: mom matters". Trends in molecular medicine. 21 (2): 109–117. ISSN 1471-4914. PMC 4464665 . PMID 25578246. doi:10.1016/j.molmed.2014.12.002.

Yatsunenko, T.; Rey, F. E.; Manary, M. J.; Trehan, I.; Dominguez-Bello, M. G.; Contreras, M.; Magris, M.; Hidalgo, G.; Baldassano, R. N.; Anokhin, A. P.; Heath, A. C.; Warner, B.; Reeder, J.; Kuczynski, J.; Caporaso, J. G.; Lozupone, C. A.; Lauber, C.; Clemente, J. C.; Knights, D.; Knight, R.; Gordon, J. I. (2012). "Human gut microbiome viewed across age and geography". Nature. 486 (7402): 222–227. Bibcode:2012Natur.486..222Y. PMC 3376388 . PMID 22699611. doi:10.1038/nature11053.

Wu, G. D.; Chen, J.; Hoffmann, C.; Bittinger, K.; Chen, Y.-Y.; Keilbaugh, S. A.; Bewtra, M.; Knights, D.; Walters, W. A.; Knight, R.; Sinha, R.; Gilroy, E.; Gupta, K.; Baldassano, R.; Nessel, L.; Li, H.; Bushman, F. D.; Lewis, J. D. (2011). "Linking Long-Term Dietary Patterns with Gut Microbial Enterotypes". Science. 334 (6052): 105–8. Bibcode:2011Sci...334..105W. PMC 3368382 . PMID 21885731. doi:10.1126/science.1208344.

De Filippo, C.; Cavalieri, D.; Di Paola, M.; Ramazzotti, M.; Poullet, J. B.; Massart, S.; Collini, S.; Pieraccini, G.; Lionetti, P. (2010). "Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa". Proc. Natl. Acad. Sci. U.S.A. 107 (33): 14691–14696. Bibcode:2010PNAS..10714691D. PMC 2930426 . PMID 20679230. doi:10.1073/pnas.1005963107.

There is also evidence that exposure of the newborn to the vaginal microbiota of the mother during delivery might be important for the establishment of its own gut, oral and skin microbiota (Dominguez-Bello et al. 2016):

Exposure of newborns to the maternal vaginal microbiota is interrupted with cesarean birthing. Babies delivered by Cesarean section (C-section) acquire a microbiota that differs from that of vaginally delivered infants, and C-section delivery has been associated with increased risk for immune and metabolic disorders


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Have we ever observed fertile offspring with a different number of chromosomes than the parents?
Chimpanzees are supposedly the closest relative of humans from a DNA perspective, they are both diploid, and they both undergo meiosis. However, chimpanzees have 24 chromosome pairs while humans have 23.
Have we ever observed a situation where the offspring of meiosis has a different number of chromosome pairs than the parents, the offspring lived, and the offspring was not sterile? How does evolution explain the shifting of chromosome pair counts?

Welcome to the site! That's a good question, and although I don't have time to write a full answer at the moment there's actually a good explanation of this here that you might find helpful: http://scienceblogs.com/pharyngula/2008/04/21/basics-how-can-chromosome-numb/

This is possibly a duplicate of https://biology.stackexchange.com/questions/16533/evolution-of-chromosome-numbers or https://biology.stackexchange.com/questions/16625/how-are-new-chromosomes-replicated-into-the-next-generation-via-sexual-reproduct, but the accepted answer for the latter is basically an edited version of the blogpost I linked above.

I actually attended a seminar by Mike Barker (http://eeb.arizona.edu/people/dr-michael-barker) on this yesterday; he mainly studies plant systems but has also looked at other groups (such as insects).

Thanks. I will look into the articles you post which I have not already read. I am familiar with aberrant euploidy and chromosome duplication. I am tring to understand if we have just theorized this or if it has been observed. The literature I have read at NCBI stated that no offspring of different chromosome pair counts ever survive. Not a polyploidy transfer error, but where the parent had 24 chromosome pairs and the child had 23 chromosome pairs.

In the title you are asking for "different number of chromosomes", while the final paragraph is about "different number of chromosome pairs". Could you please clarify, which is the actual question?

It is actually quite common in plant breeding (Google gets about 460K hits on "plant breeding chromosome duplication") to try to induce chromosome doubling/ltripling by exposure to such things as colchicine, which generally (at least in my understanding: I'm not an expert) produces stronger plants, larger flowers, &c.

[..] have we ever observed a situation where the offspring of meiosis has a different number of chromosome pairs than the parents, the offspring lived, and the offspring was not sterile?

Yes!
While it may seem a detail, the difficulty is to know what exactly you mean by observation. Chromosomal abnormalities, gene duplication, chromosomal duplication, robertsonian translocations, whole genome duplication are not super common but common enough to be seen repeatedly. We see them happen again and again in different lineages, we can even investigate how our environment affect such chromosomal abnormalities (Merkatz et al. 1984). So below, I am citing a few papers that I more or less randomly selected among the decently large amount of work on the subject.
Chromosomal rearrangements are sometimes involve in speciation (Rieseberg 2001).
There are many genetic disease in humans that are related to such chromosomal duplication (e.g. Down Syndrome) and de novo mutations for these mutations, while rare, are not so rare that we can witness them only on geological time scale (Veltman and Brunner, 2012)
There are soo many articles on the question that I don't really know what to cite. Of course, there are reviews that can be of interest to you (such as Zhang 2003). I tried to find a video showing a meiosis leading to chromosomal duplication but unfortunately, I have failed to find that.
The mechanisms of these mutations leading to chromosomal rearrangements are pretty well understood. You should probably start with wikipedia > gene duplication # Mechanisms of duplication for an intro.
As you talk about the difference between the number of chromosomes in chimpanzee and humans, you might want to have a look at the post Evolutionarily speaking, why do humans have 46 chromosomes where it is explains (with plenty of citations) how did the change in chromosome number occurred in our lineage.

I have read a lot about the idea of evolution

I do not want to seem pedantic but given that the vocabulary that you are using (change in kind,  concepts of transfer errors, concept of gradual change) it really suggests that all you read comes from the creationist propaganda and not from the evolution literature. Indeed nobody use these terms in the research. Those terms are mainly used as straw man from the creationist propaganda.
There are many free intro courses to evolutionary biology. You might want to have a look at Understanding Evolution by UC Berkeley.

This does not answer the question.

@Will Why not? Could you please leave a comment on what you think is missing?

@Marzipanherz :  I was looking for "yes" or "no", with examples.

The entire text is a series of examples and the first paragraph make it clear that it is a 'yes'. But just to highlight it, I will write a big 'yes' directly after me quoting the question.

Down syndrome is an example of fertile offspring with a different chromosomal number than the parents.  Persons with Down syndrome have an extra copy of chromosome 21, and so have 47 chromosomes instead of the normal 46.  Fertility is lower in persons with Down syndrome but they are not invariably infertile.  Wikipedia gives fertility for women at 50%.  Some of the children of these women also have Down syndrome.
Another example is Turner's syndrome.  Affected women lack an X chromosome and so have 45 chromosomes.  Fertility is lower in these women but some can get pregnant and bear children.
Bernard V et al. Spontaneous fertility and pregnancy outcomes amongst 480 women with Turner syndrome. Hum Reprod. 2016 Apr;31(4):782-8.
It may be that some of these persons who have different chromosomal numbers in sampled cell populations (usually blood) but are still fertile are actually [mosaics](https://en.wikipedia.org/wiki/Mosaic_(genetics).  These individuals have different populations of cells comprising them.  Perhaps the mutation leading to trisomy or monosomy occurred in one cell after the embryo was already comprised of several cells.  Cells from that lineage will show the phenotype associated with the mutation but if the germ cells are descended from cells which did not have that mutation, they would be normal and so be associated with normal fertility.

This only answers the question regarding different number of chromosomes, but not regarding a different number of chromosome pairs.

Plants are particularly well know n for this, polyploidy (duplicate sets of chromosomes) are rampart across plants and is often exploited by humans to increase fruit yields. Strawberries for instance vary from 14 to 56 chromosomes and remain cross fertile. In plants they can still be cross fertile however in animals this is has never been seen and all known polyploid animals are believed to be the result of multiple individuals having the same duplication.
Sturgeons, show various degrees of Aneuploidy (different numbers not due to duplication), and it has been studied by crossing sturgeons with different numbers of chromosomes, many of the offspring are fertile.
chromosome fusion has be observed in horses, cows, sheep, lab mice, and fruit flies, and there varying degrees of fertility. Basically the animals that we pay very close attention to the genes of have shown it, meaning it should be relatively common. The university of indiana provides a more complete list.
Insects, many insects are haplodiploidy which means males anf females have vastly different numbers of chromosomes.
Indian Muntjac (see picture) actually have different numbers of chromosomes between males and females, 7 and 6 respectively. they share this trait with wallaby and echidna.

crossbreeding of scarlet macaw with different numbers of chromosomes to reintroduce genetic diversity has been shown to be successful.
The blue butterfly is the all time winner however as the chromosome count varies wildly, without polyploidy no less. They have so many chromosomes 448-452 that the loss or fusion of some just has little effect.
A 44 chromosome human exists, who appears normal, this number is due to chromosome fusion, since he has not bred we don't know about his fertility.
As has been mentioned humans can have different numbers of chromosomes and while most or lethal some are not and those with them can remain fertile. changes in chromosomes in particular seem to be the most tolerable biologically.


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How interrelated are computational biology and biophysics?
I am considering applying to Ph.D. programs, and am not sure what direction to take. I'm hoping you all can help me out.
I have a background in both biology (molecular focus) and physics (condensed matter and math, heavy on theory). Several years industry experience working in labs doing molecular biology and genetics research.
My primary interest is in mathematical modeling of biological systems, and taking this knowledge to then engineer function. Essentially, what I view as a combination of biophysics, systems biology, and synthetic biology.
Here is the dilemma. It is important for me, should I pursue a Ph.D., to have a solid foundation and training in fundamental principles in physics and math, because I want to be able to derive new theories, models, and methods when needed. This leads me to think biophysics or applied math is the "right" area to do my Ph.D in. But biophysics is very broad and systems biology is only a small part. It is also removed from applications in bioengineering.
I know computational and systems biology intermingles biophysics, applied math, genetics, computer science, and various other fields. It also seems like the type of research I am interested in is typically done in computational and systems biology groups. But I'd like to know if computational biologists, aside from doing simulations, also commonly do work in deriving new models/theories in biophysics. Or do they generally apply this knowledge to build simulations and understand data sets (i.e. removed from fundamental biophysics research)? I don't want to be a programmer -- I want to be a theorist who uses computational tools (and only programs when it's needed to simulate something) to solve problems that can't be solved analytically.
Is computational and systems biology an appropriate "umbrella term" for what I'd like to do? Or would I be better suited in a physics Ph.D. program, and attempt to bridge that training towards systems biology research?
Also, how difficult is it to change to a related field if the opportunity arises? Can computational biologists, who are also interested in engineering work, build a model of a system and then work with others to help engineer it?
My overall concern is pigeonholing myself into a field that I don't want to spend decades working in. I want to maintain flexibility along the range of biophysics to bioengineering, and work on problems when the need arises. Also, what field do my research interests actually fall under? I find it often depends on the university and specific department, so it's a hard question for me to answer myself....
Thanks in advance for any input.

Computational Biology is just the application of computers to solve problems in biology. It may mean using machine learning to identify regulatory regions in DNA or it may be solving a complex system of differential equations to model chemical reactions in some metabolic pathway. Whether a background in physics, chemistry, biology, math, or computer science is more central depends on the exact problem you want to work on,  and in fact which aspect of the problem you want to work on.

Also, what field do my research interests actually fall under? I find
  it often depends on the university and specific department,

Bingo! Your interests are clearly cross-disciplinary, so for any given research question, different researchers in different fields will all be working on different aspects of the problem. Academic disciplines don't get to declare monopolies on research problems!
You Ph.D. is going to require you to spend 4-6 years working on a VERY specific problem. It would be wonderful if you could figure out exactly which research problem you wanted to dedicate the next 6 years to, and then choose the Ph.D. program based on their research program on that problem. This is rare though. More typically Ph.D. students have to spend a year or two doing rotations and talking to potential mentors before picking a research problem. In that case you are going to have to decide which academic discipline attracts you more, and then find a department in that discipline that seems to have a lot of collaborations with the other disciplines that attract you. See Buridan's Ass;

Thank you! Just the response I was looking for. I actually do know the problem I want to work on. I want to take a biological system (currently working in the agriculture industry; so take plants in this case, but I am open to others) and apply systems biology methods to better predict phenotype, and figure out what parts need to be changed/engineered/modified to drive the plant (or other system) to a desired state (e.g. disease resistance). But, a "big picture" answer to this may require new applied math (graph theory) or biophysical (statistical mechanics) methods that aren't known yet.

But I "don't yet know what I don't yet know", if that makes sense. So is it better to go more fundamental? (biophysics --> statistical mechanics, applied math --> graph theory, group theory) Or more applied (computational biology, systems biology)? Intellectually I think I'd rather go more fundamental and transition to applied/computational (I think it's harder to do the converse). But I really think this may be limiting future job opportunities (who would hire a biophysics phd for a computational job when you have a computational biologist phd to choose from)?

(i.e. it's not just a "what am I interested in" question, but also "how do I get a stable job at the end of my Ph.D. question) Which makes it way more complicated. :(

'So is it better to go more fundamental? (biophysics --> statistical mechanics, applied math --> graph theory, group theory)' There is no general answer to this. It depends entirely on the problem and your personal tastes.

"it's not just a "what am I interested in question, but also but also 'how do I get a stable job at the end of my Ph.D. question) Which makes it way more complicated. ' That's a separate question from the one you asked. Keep in mind that Stackexchange is a Q&A forum, not an open-ended discussion forum. Use the chat facility for open-ended discussions. Right now demand is high for machine learning and 'data science' experts across a variety of industries. Whether that will be true in 6 years, no one knows. No one can give you guarantees on this, other than that jobs in academia will be tight.

"That's a separate question from the one you asked. Keep in mind that Stackexchange is a Q&A forum, not an open-ended discussion forum. Use the chat facility for open-ended discussions." Yes -- sorry about that. Wasn't aware of the chat facility. The "can I get a job doing this" was an important corollary to my question. I want whatever I choose as a dissertation and subfield to be employable in the range of research fields I'm interested in, if that makes sense.

I feel like systems biology, and by extension (since they're often grouped together in a department) computational biology, makes the most sense. As I don't necessarily even know what new models or mathematics needs to be used or created until I get to that point in systems biology. Putting the cart before the horse and all that. Anyway, thanks for the help and sorry for the segue into the open-ended discussion.