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Force applied to the human body
This is the basic premise of a physics question I have been attempting to solve over on the Physics SE. (I'm working on solving the actual science behind an old movie myth).

How hard a punch hits is determined by your
  hand's momentum, or the combination between mass and velocity. . . . What acceleration would Super Man need to achieve during
  his attack in order to impart enough force to punch his fist
  into/mostly through a human body?

Unfortunately, in order to solve this problem, I somehow need to figure out the amount of force needed for an object to enter/pass through the human body (by either passing through the sternum or directly below it). Since I have so far been unable to find anything helpful in online searches, and naturally I'm not about to test fire an object through human beings until I find the right amount of force, I'm asking for a little help from the experts on human biology... Does anyone know where I can find or how I can figure out this number?

this may be a helpful place to start https://biomechanics.stanford.edu/me338/me338_project02.pdf

As this is homework related I won't help with the math but I can help point you in the right direction.
Basically, you need to find the density of a human chest and then calculate the force required to "break" it. Looking into the average depth of the human chest we can see from this website, It comes out to be about 250 mm for British man.
The density of human muscle tissue  is about 1.06 kg/liter. Average bone density is 1600 kg/m^3.
For now lets just assume that the heart and lungs also have 1.06 kg/liter as the density. This means we can calculate the overall density of the chest and the required force it can withstand.
The average surface area of a mans fist is .043 sq m.
Knowing the size of the fist and how much force the chest can take, we can from here calculate the penetration force needed to pass through the chest.
Granted this is gross approximations and doesn't account for surface area of the fist. You would need to find a better equation to be more accurate.

This actually isn't homework, just a personal project related to a book I'm writing. (I have a superhuman character who was going to perform this feat, and I began to wonder about its plausibility/the related science.) Thank you for these numbers, it's a start, and more than I found on my own. In order to determine the overall density of the chest, do I need to figure out the ratio of bone to muscle and organs in the chest as well?

To be more accurate yes but there are a lot of variables to account for. For instance one assumption being made is that the objects do not compress. Skin and muscles can compress a bit which would increase the amount of force needed to pierce. Ballistics and penetration are rather large topics. Here is a [paper released in 2012 discussing simulations of depth] penetration(https://www.ias.ac.in/article/fulltext/sadh/037/02/0261-0279).

Oh, And in general, the larger the surface area the less likey to pierce. This is becuase more area spread out requires more force to penetrate. One reason why characters in Grapler Biki or Fist of the North star Tended to attack with straight finders for stabbing.

For a very rough upper bound you could assume that the punch force is translated into 100% pressure on the bone, 100% traction on tendons/ligaments (and generally all tissues which contain collagene type 1 and aren't bone) and so on (which is obviously not true in reality where a punch from the side will generate a torque moment rather than a pressure).
The second step would then be finding the numbers for maximal pressure bone can take per mm^2 , maximal traction a tendon can take per mm^2 as well as the numbers for mass and volume of each in the human body.
These number exist so you can find them with enough effort.
The last step would be to decide which ratio you use for each (i.e. in the given area how much does each layer constitute) , this number (in reality) too exists most likely you can find it in some MRI studies.
So while you won't be able to get exact estimates (because they depend on the geometry of the person, constitution and infinite amount of other variables), you can get a very good upper bound by assuming that the force is translated into exactly the type of stress each tissue is supposed to work with!
Note also that you do not need to know the size/area of the attackers hands or the size of the impact area  if you choose this method!


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What properties of the pathogens of infectious diseases make recovered individuals susceptible to the disease?
I was wondering what properties of the pathogens of infectious diseases make these diseases more prone to making recovered individuals immediately susceptible to the disease? I was thinking that with Salmonellosis, for example, there are different variants of the Salmonella type of bacteria, but I'm not sure if having more variants of a pathogen necessarily makes it more difficult for the human body to recognize these pathogens.

gonorrhea is a good example. https://mbio.asm.org/content/2/3/e00095-11

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Why are the other bases not used for RNA capping and tailing?
Why does the addition of a 5' cap and that of a 3' tail involve guanine and adenine respectively? Why aren't any of the other two bases added to an mRNA to protect its ends or act as a signal to transport it to the cytoplasm?

Although I can see why you posed your question in the way you did, it is actually two separate questions. The problem with this is you have received an answer that I regard as a reasonable speculation about the polyadenylation, but not about capping. And as @KaPy3141 makes clear, you should realize that answers to questions of this sort are most often only opinions, and the answer may well be “we don’t know” or “perhaps just chance”.

Yeah, I understood that after reading the answer @KayPy3141 wrote. And, I could make sense of the speculation about polyadenylation alone, not about capping. I was just wondering if there was any explanation to each of the processes. As you said, turns out it may be just chance.

I usually try to alert students to all the possibilities of this sort of thing: chance, some structural feature of the molecule that makes it “better”, or its easier to make because the precursors or enzymes are already there or it involves fewer synthetic steps than alternatives. There’s a common tendency to assume it must do the job better, and answers of that sort tend to get accepted uncritically.

As others have pointed out, any answer to this is speculative, there is no reason why it would be impossible to use some other bases. It might be helpful to point out that there ARE alternative 5' caps that are occasionally used in living cells, based on coenzyme A, NAD, FAD, and others, see for example: https://pubmed.ncbi.nlm.nih.gov/27383794/

As David correctly pointed out, my listed theoretical 'reasons' are purely speculative and come closer to a collection of facts that seem interesting for someone who asks the OPs question. In this context it's hard to not fall in the category of the "chicken-egg problem". In the end, all reasons are pseudo-reasons describing phenomena by other phenomena that cannot be explained and will lead to "because it is like that" after some iterations of "why?".

I don't think definite answers exist but I can think of theoretical reasons:

First, Poly A tail can efficiently be synthesized because ATP is the
most readily available nTP, being the main energy source.

More to the mechanism, but this is no explanation to the evolution:
The termination sequence 'TTTATT' on the DNA template and 'AAUAAA'on the RNA is the start of poly-adenylation. But this falls in the 'chicken-egg problem' category.

As a bioinformatician, I happen to know, that 3'UTR is highest in A-content of the 3 genomic contexts and the 5'UTR is highest in G-content of the 3 contexts, so possibly these post-transcriptional modifications further strengthen the compositional differences of the contexts.

For the poly-A tail it might also be relevant to mention that G or C sequences have higher propensities towards structure due to amount of hydrogen-bonds.

I hope there were some helpful pieces of information.

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What causes bio electricity?
When it is said that “electrical impulses sent from the brain” how is this charge flow produced?

See wikipedia > action potential


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Does turbidometeric method count cell number or cell mass?

Here it says that scattering is inversely proportional to cell number but also says that we can observe greater absorbance as cell number increases.
So does turbidometeric method work on cell mass or number ?

Your text says that scattering is proportional to cell number, which is correct. It is not inversely proportional, as you stated.

But if counts it under measurement of cell mass and not number ?

The spec measures the amount of light scattered by a sample, so increasing the number or size of the cells will increase measured absorbance.

Imagine a room full of flying insects. One could estimate the number of insects in the room by shining a flashlight at one end and observing its brightness at the other end. If the room is densely packed with tiny flies, the flashlight will appear darker from the other side of the room because the flies block the light. A smaller number of butterflies, which make a larger shadow, would block the same amount of light and give the same absorbance. Both the number and size of the insects affect the amount of light transmitted through the room.


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why don't antibiotics reduce our weight?
I know that a significant weight of the human body (in Kgs) is contributed by microbiota. I also know that antibiotics can often be broad spectrum and kill all the bacterias regardless of them being good or bad for us. So why doesn't antibiotic courses reduce our weight as the microbial population must've been demolished?

How do you know for a fact that the weight of the human microbiome is in kgs? Billions of microbial cells of micrometer dimensions still wouldn't weigh a kilogram, let alone a few kgs.

You suppose that antibiotics, even broad spectrum antibiotics, kill a significant fraction of bacteria. This is simply not true. Many species will be unaffected, and even amongst the sensitive ones, many individuals survive. These replicate very quickly to replenish dead ones.

The microbiome isn't simply bacteria. It also comprises fungi and archaea, which are insensitive to antibiotics

First, you present as fact that antibiotics therapy (say AT) does not reduce weight. To show this fact, a study must weigh persons before AT and after. Confounders to this measurement are 1. weight differences because of bladder content (up to around 1 liter urine = 1kg), 2. weight differences because of bowel content (100g-200g), 3. Food weight (up to 2kg and more). High salt foods can cause water retention that can easily reduce your urine output one day by 500-1000ml (=g), increasing it with the same amount the other day. So your confounders can add up to +/- 4kg easily. But what you want to measure is a change of 1kg.
This means that you need to account for all these. I don't know any study that did this. Please cite such a study before presenting as fact that there is no weight loss from AT.
Assuming there is no weight loss, there are several hypotheses that can be advanced: from the fact that no antibiotic (even broadband) can kill all bacteria, the remaining bacteria in the gut may simply feed off the highly nutritional content of those bacteria cells that were killed. Note that although we know which bacteria of those that we can cultivate in a lab are susceptible to AT, we don't know at all about those that we can't grow, and that is the majority of bacteria in the gut.

Other factors are that many diseases cause loss of appetite, vomiting, diarrhea, &c, all of which would cause weight loss.

We do account for all these things during phase I trials, but you're correct that you can't sterilize the gut. See my answer

Antibiotics can cause weight loss, though, especially as they are used in the clinically, they are more likely to cause weight gain than weight loss.
This Lancet Infectious Diseases review is not a very good review in general, but it does catalogue many of the weight related changes in response to antibiotic therapy. You could use the references as a good place to start.
Re: @RStephen's answer:

This means that you need to account for all these. I don't know any study that did this.

Having run several phase I trials, I can tell you that we do account for all these factors. These trials are done to demonstrate safety and determine the pharmacokinetic properties of a drug (absorption, distribution, metabolism, and excretion). We keep volunteers in house, and ins and outs are carefully monitored. When we control intake, if weight loss does occur, it's water loss (through diarrhea) or water loss and decreased absorption (again, with diarrhea).
@RStephen was correct, though, that you're not going to get weight loss due to elimination of your microbiota. It is simply impossible to sterilize the gut. You can throw as much heavy artillery as you'd like at it, but the best you can do is change the composition.
Clinically, though most sick patients gain weight when you treat them, weight loss is not uncommon after broad spectrum antibiotic use (often clindamycin or metronidazole) typically with GI side effects (nausea, anorexia, diarrhea). When it's due to changes in the bowel flora, it can be overgrowth but not sterilization. You can read about that in this excellent JAMA review

With a quick read of the first review though, I only found evidence about later weight gain and not short-term, as the OP is asking. Additionally, most human studies cited therein are about correlations between obesity and bacterial concentrations, focused more on what the effect of antibiotics is on obese people (table 2). Perhaps you should also note why there is weight increase (quote from same review): "Beneficial effects of antibiotics in relation to weight gain probably arise through treatment or prevention of disease."

Overall, I am not convinced whether antibiotics intake affects body weight either way in the short-term like the OP is asking, when adjusting for all other factors (previous body weight, condition etc).

@vkehayas I would never quote from that review. It's bad. Part of my job is teaching interpretation of medical literature to medical students and residents. The references, though, are a good place for background reading. The clinical fact that sick people (with infections) gain weight when you treat them (with antibiotics) is from my experience and clinical education. It is so basic, I don't have a reference at hand to cite. It's similar to the fact that a fever will go down (and may actually be mediated by the same factors, e.g., IL-1).

@vkehayas the answer to the OPs question, reformulated, do antibiotics destroy all bacteria in your body and cause weight loss because of it, is categorically no. I'm sick, on leave, and bored. I've found answering these questions helps relieve the boredom, and I hope they're helpful. You'll notice I typically answer questions I have good background knowledge on, and provide additional reading for background. I don't go hunting for sources to support each statement I make. That's boring, and likely to lead to a bad answer. Literature you're unfamiliar with is easy to misinterpret.

@DanHall thanks for answering but the fundamental question of why? is not dealt with here. when antibiotics are known to lay havoc on our microbiota why is the logical argument (i belive it is) is failing ?


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Technique to test antibiotic resistance in a bacteria in presence of another compound
so I have to 'quantitatively' assess a bacterial strain for its antibiotic resistance property (it is a specific antibiotic) in the presence and absence of another compound alongside antibiotic. What technique or protocol can be followed?

It sounds like you might employ a "Disk diffusion test" described in this Wikipedia article.  It could be done with and without the secondary adjuvant compound and be quantified by measurement of the varying diameters of the resulting zones of bacterial inhibition.
https://en.wikipedia.org/wiki/Disk_diffusion_test

thank you that was very helpful but the page does not describe how to add adjuvants in the equation. I googled for it and still couldn't find a satisfactory answer

I suppose you would add them to the mueller-hinton when making the plate, a few for each concentration of the other compound you want to test. Then run the disk diffusion as usual.

Eliane B - obviously.  The question involves the addition of a potential adjuvant (other compound).  It's addition can be determined by the experiment.


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How to convert bwa mem output to BAM format without saving SAM file
I want to go straight from bwa mem alignment to BAM format as I don't need the SAM file and it takes up too much space. How do I achieve this?

For directly outputting a sorted bam file you can use the following:
bwa mem genome.fa reads.fastq | samtools sort -o output.bam -

Optionally using multiple threads:
bwa mem -t 8 genome.fa reads.fastq | samtools sort -@8 -o output.bam -

Ah, great solution if sorting is needed! I had tried this in the past but I was trying to pipe it though samtools view and then into sort. Didn't realise you could go straight into sort.

If you don't need sorting, you can avoid the computational overhead by piping the output from bwa mem into samtools view like so
bwa mem ref.fa in.fq | samtools view -b - > out.bam

The - in samtools view tells it to read from stdin and -b indicates BAM output.
You can also just allow samtools to infer the output format by using the -o option, which will guess the required format based on the file extension given
bwa mem ref.fa in.fq | samtools view -o out.bam -

In my workflow, BWA output goes to MergeBamAlignment, so samtools view seemed lower overhead than samtools sort.  (Directly piping from BWA to MergeBamAlignment, as suggested here, failed for me.)

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In the NCBI Taxonomy tree what does "no rank" mean?
NCBI publish their taxonomy browser at https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi
While many taxa have a well defined rank (Order, Family, Genus etc..), some of them have "no rank".
For example, Amniota:

Taxonomy ID: 32524
Genbank common name: amniotes
Inherited blast name: vertebrates
Rank: no rank
Genetic code: Translation table 1 (Standard)
Mitochondrial genetic code: Translation table 2 (Vertebrate Mitochondrial)

What does "no rank" mean?

Can you quote them? The information in the link can be accessed only when the software is installed. It's not fair to make people do this when you are asking for help.

@Tytoalba point taken.

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Are the Fastq files content is truly random
I'm building a system to generate fastq files as they are being output from HiSeq 3000 and HiSeq 4000. This will serve us to test our internal systems with some gold standards.
As we are working with microbiome a standard sample may contain around 1500 different species, is there a a bias in the output regarding how 'close' each assembly record appear next to each other or is it truly random?
If record 1,1 is from assembly 2913, what are the odds that record 1,2 is of that assembly as well (assuming 1500 species with the same strain length) ?
I couldn't find any paper on that so any help from experience would be great.
Thank,
Eden

I'm a bit confused what you mean by 'close' - is it the order of the entries in the fastq file? I'm pretty sure that is completely random (it should be more or less dependent on the cluster order on the flowcell). Also note that the primary output of the HiSeq (or any Illumina Sequencer) are not fastq files, but bcl files. Most sequencing facilities do the demultiplexing which generates fastq files for you, so you never see the 'raw' sequencing data.

@Nicolai By close I mean records in the fastq file one after another. But by now I think it totally random
I didn't know about the bcl file. I'll check it out. Thanks.

In my experience, the distribution of reads on the flow-cell is pretty much random, but the sequencing errors are not necessarily randomly distributed.  In all Illumina instruments I have seen, it is common to see edge-effects, or other localities on the flow cell where the error profile differs from the rest of the cell, and QC pipelines generally test for this problem.
A particular issue with the HiSeq3000/4000 patterned flow-cells is that, in situations of under-clustered runs, it would be typical to find the same sequence repeated multiple times in nearby 'clusters' - in other words, a clustering of clusters all containing replicates of the same underlying molecule.  Even for runs where there is no severe under-clustering, it might be expected that duplicates would be found in adjacent cells.  qcfail.com has an outline of this phenomenon: https://sequencing.qcfail.com/technologies/hiseq/


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Trypsin and Cell Surface Receptors
Can adding Trypsin to mammalian cells affect the expression of or hydrolyze cell surface receptors?

Yes. Trypsin cleaves proteins and can do so quite indiscriminately if left on for very long. Trypsin is primarily used to cleave the proteins that cells use to adhere to each other and the plate in culture. It can cleave other membrane bound proteins as well, including receptors.
https://jbiomedsci.biomedcentral.com/articles/10.1186/1423-0127-17-36


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How is an RT-PCR representative of the RNA contents in a cell?
For example, we first collect all the RNA contents from a mammalian cell line. Say, for instance, we collect 80 uL of RNA with a concentration of 150 ng/uL. Next, to make cDNA, we take 1,000 ng of the RNA. However, this 1,000 ng is a completely random sampling of the total RNA we had. How is that random sample of RNA representative of the RNA contents originally in our cells?

Are you asking if mRNA molecules that are present in only few copies may be distorted by random sampling?  That's certainly true.

It isn’t really clear exactly what the questioner is asking, but…
...one way of thinking about this is to ask how likely is it that a low-abundance RNA will be absent from the sample taken from the preparation of RNA. This would make the sample non-representative at the qualitative level.
The question states that 12,000 ng of RNA is isolated. Since nothing else is specified I assume this is total RNA. A rough estimate of total RNA per eukaryotic cell is 20 pg.
This means that the preparation came from 6 x 105 cells. (I’m assuming 100% yield, but this won’t really affect the conclusion.)
Now assume that a low-abundance mRNA is present at 10 copies per cell. The total RNA preparation therefore contains 6 x 106 copies of that low-abundance mRNA.
We take a sample of 1,000 ng from the total 12,000 ng. In other words we take 1/12th of the preparation of RNA. If that RNA preparation contains 106 copies of the low abundance mRNA how likely is it that we happen to take a sample which contains no copies of that low abundance mRNA? Here my maths fails me, but intuitively I say that the probability is very very small.
Now, if there are 1,000 different low-abundance mRNAs in the cell the probability of missing each of them is very very small, but the overall probability of missing one of them is 1000 x very very small, so maybe very small.
I'll continue thinking about how to calculate the value of very very small, but if anyone wants to help out - thanks in advance!

To add to my question, what if you are checking the inclusion of an exon and lets say if we assumed that the alternative exon shows up in 15% of gene X. However, if we take a random 12th, couldn't the 12th be non representative and show something like 60% inclusion when it should actually be much lower?

Yes, there are all kinds of ways in which, due to chance, the final cDNA mixture might be a rather skewed reflection of the original mRNA distribution, as Roland said in his comment.


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Is it possible to stop more/extra fat from being stored in the body?
I don't mean simply by restricting eating or upping the activities, but a way to basically stop the body from adding more fat on itself down on the bio level. For example, I'm not too knowledgeable on this, but I believe fat is stored when the body can't make any extended use of extra energy put in to it.
Given such, could we simply direct the body to only use the energy needed and dispose of any "extra" while not storing it as fat/triglycerides? I know there are drugs that can speed up metabolism and etc., but this only heightens the body's ability to remove said fat -- not stop the process at which it is stored
This would be a great thing because then we could assure the body only uses the energy on what can be beneficial to us -- all the "rest" can be removed and not stored on us and being a con instead of a pro.
So in summary: Is there any feasible way this could be theoretically possible, given our biochemistry/physiology?

Fat storage comes from conversion of glycogen (a glucose polymer) to triglycerides (fats).  (source: https://en.wikipedia.org/wiki/Glycogen).
Intuitively, the simplest way to prevent fat storage is to block conversion of glycogen to fats. Unfortunately, this will cause a glut of glycogen which can cause an entirely different set of problems (see https://www.hopkinsmedicine.org/health/conditions-and-diseases/glycogen-storage-disease ), so you would want to couple this with a mechanism to eject excess glycogen.
Referencing what user1136 posted: uncoupling oxidation from phosphorylation is a really bad idea. That would basically "burn" fuel while blocking the expected ATP outlet. This will cause a dangerous energy buildup in the mitochondria which has to be unloaded somewhere - provable simply by conservation of energy. Energy can be converted to other forms of energy, but it is never destroyed. Physics is the ultimate anti-cheat tool.
Blocking expected energy outlets is almost always a bad idea in practice. Just to name some practical examples:

In archery class, instructors will warn you never to "dry-fire" a bow (draw the string back and release with no arrow). This can compromise the bow's structural integrity, causing it to splinter, snap, or explode later.
Microwave ovens should never be operated empty with no sink for the electromagnetic radiation they produce - this can damage them. See https://physics.stackexchange.com/questions/309154/what-happens-in-an-empty-microwave-oven for more info.
If you jam the pistons in a standard cylinder-based combustion engine (prevent them from moving), you end up with a lot of energy that needs to go somewhere, which will end up as massive vibration and extra heat - either of which could damage the engine as the design never expected this to happen.


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Could certain drugs enable one to consistently eat above TDEE or BMR without fat gains?
I heard anabolic steroids and stuff like DNP and ephedrine and etc. can somewhat enable one to eat more and get away with it without much or any fat gain, despite eating more than the body would normally use.
Is this true? Can hormones, AAS, HGH and other fat burning drugs or stimulants or etc. enable one to consistently eat more than their basal metabolic rate without becoming fat?

Do you remember where you heard this


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What is inside digestive system while it's empty?
Up to this point, all my life I assumed that stomach and intestines are filled with air. I got this impression from all the anatomic drawings in schoolbooks and encyclopedias that show empty stomach and intestines like a big sacks, with only small amount of digestive fluids in stomach at the bottom of it.
But getting some in-depth knowledges of scuba/free diving, it seems that it was a lie, all along! If it would have been filled with air, divers would need to "equalise" it, like they do with middle ears, sinuses, mask and lungs. Otherwise, they would face pretty serious barotrauma.
So, if it's not filled with air... Is it filled with liquid? I don't think it's likely, in this case we would always feel "fullness" and it would add too much weight.
My current hypothesis is, that stomach and intestines are so stretchy (distendable?), that it just collapses naturally, when empty, and maybe only contains small amount of mucus on it's walls to decrease friction of the walls. Is this correct? I couldn't find this information anywhere on the internet, strangely. Maybe it's so obvious that nobody writes about it?
I can imagine intestines shrinking, but stomach? It's kind of hard to imagine how such a big "bag" can shrink so much to not contain any gas/liquid in it...

When empty there is almost nothing in them. However one is frequently swallowing sinus mucus and saliva.  My doctor told me a couple gallons in 24 hours; but I have no internet source so not an answer.

"Is it filled with liquid? I don't think it's likely, in this case we would always feel "fullness" and it would add too much weight" How would you know this if it's the normal state of being? If it were this way since infancy or before? You would feel "normal". Which is normal. Also, your urinary bladder shrinks when empty. Why not your stomach?

As far as barotrauma goes, how distensible are the sinuses, the middle ear, the lungs and the diving mask? Not very. But the intestines? Very. If you're absolutely full of gas, you'll get gas pains (not the bends) on ascending, but you don't need to equalize something that you can't possibly equalize. Barotrauma of the GI tract is rare; much more commonly, the lungs are involved. I wrote a full answer including Xrays, but got the erroneous message that your Q was deleted, so my answer was discarded. Sorry.

@anongoodnurse That's true, I meant filled with liquid to the extent that is shown on all the anatomy pictures in encyclopedias.

@anongoodnurse NP, your comment is good enough for my understanding! I think that probably one possibility of barotrauma is when diver swallows some high pressure breathing gas on very deep depth, so that it would greatly extend when coming back to surface quickly (for example in an emergency assent).

As I said, barotrauma to the GI tract is rare. Even when there is free air in the abdominal cavity, and the GI tract is imaged for perforation, it usually is found to come from trauma to the lungs and damage to the diaphragm. "I think that probably one possibility of barotrauma is when..." Imagining something doesn't make it so.

There is nothing. The tissue compresses together.
The entire digestive tract, including the esophagus, is pressurized by muscles.
Gases do get produced by digestion (and disfunctionally by air swallowing) and those gases must be removed from the body.
A small amount of air and carbon dioxide can naturally exist in the stomach, but if this increases it will rapidly cause disomfort or other symptoms, such as burping.

A rapid transit time is 24 hours; more normal is 36-40, and even 72 hours is still considered normal. Unless you're NPO for >72 hours or you've undergone a rigorous bowel prep (ugh!), there's almost no time that the entire GI tract is empty. Also, I can't recall ever seeing an upright abdominal film where there wasn't an air-fluid level in the stomach. Air (and saliva) in the stomach is the norm.

@anongoodnurse The OP is asking about gases, not fluids. Obviously the digestive tract has fluids.

It's not obvious from your answer. "There is nothing." That's not quite the extent of it.

If by "nothing" he meant air, then I'm fine with it!


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How lungs can inhale and exhale?
I know that lungs are extended and compacted by muscles to create partial vacuum to breath in, or to create elevated pressure to breath out. But one thing seems not right to me...
As far as I know, air comes through bronchi airways (like pipes) then branch like twigs and end up in tiny berry-like alveoli where gas actually exchanged... That's all clear, but I can't connect this 2 things together.
It seems to me, that bronchi + alveoli is a closed system. So how by creating partial vacuum inside lungs themselves (like in bags) makes air come into alveoli if it's a closed system and the air pressure outside alveoli does not has access to outside air at all (as it seems to me).

I hope this image will make it a little bit clearer...
So does bronchi have some kind of openings in them to let pressure inside "bags" connect to outside world or does alveoli walls are so thin, that it actually allows gas to flow freely? What am I missing here?

this may help your understanding. https://www.youtube.com/watch?v=H62wTF9vKPQ one video is worth a thousand words.I recommend turning the sound off.

Why do you say the "bronchi + alveoli is a closed system"?  The bronchi are open to the atmosphere through the mouth and nose.

No, I'm 27 y.o.


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Is DNA actually like source code repository?
So after reading articles like "People Use Just 8.2% of Their DNA" etc., and thinking a bit... I got this idea:
What if DNA is actually like a software source code repository? You know, it has "master" branch - which is most stable and up-to-date version of program but also it has other branches, experimental ones and of course it has huge amount of "junk" - i.e. backed up version of files from previous changes to code that is not used in any way in actual program.
So what if first primitive single-cellar organisms had super primitive and very short DNA, then it got improved, but original DNA was not erased, but backed up every time new mutation (commit in software SCCS) appeared.
Theoretically, the more primitive organism is, the shorter DNA it should have. For example, some very old sharks that still survive from Mesozoic era should have shorter DNA than modern sharks... Is this confirmed by actual experiments?
This explains why human DNA is mostly so similar to dog DNA, fish DNA etc. Because we all evolved from same primitive cells! Base of our "repository" was same!
Also this explains why human embryo come though all this steps of been single cell, multi-cell, fish, amphibian, mammal etc.
I'm no expert in biology by any means, and I suspect that this idea was around for long time, but I'm not sure... What do you think?

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@BryanKrause — Let’s make it clear. I have no wish to discuss anything, only to use the comment box for it’s correct purpose to ask the poster for clarification: What is your biological question?

that seems to me like a very open-ended "discussion"-type question right now. How is it about biology?

@David umm... this hardly seems like the place to discuss it. Please take it to meta if you feel it's important.

@rotaredom — “Discuss”? I’m asking the poster to clarify his question. Poster, are you asking what junk DNA is, whether it’s the decaying remnants of duplicated genes, whether the expansion of the gene repertoire of organisms occurs/ed by duplication, whether duplicated genes can acquire different functions or what? But just one at a time, please. Biology is an experimental science. A lot of genomes have been sequenced and analysed and we can attempt to answer questions on the basis of this analysis. Proposition of theories by people, however much biology they know, is not a question.

I think this analogy is not actually that bad, but you are making some incorrect conclusions from it especially regarding 'junk' DNA and which parts of a repository DNA holds (which shows the limits of analogy!). Think instead of the DNA of an organism as a single local copy of a particular commit.
There is no remote to compare to and no list of historical changes, each organism just has its own local copy of the most recent source that can sometimes be merged with other local copies via sexual reproduction or horizontal gene transfer.
What you need to drop from the analogy
Get rid of any thought of a master branch or ideas that the repository contains backups of previous versions. These thoughts will only mislead you.
This statement:

original DNA was not erased, but backed up every time new mutation (commit in software SCCS) appeared.

makes little to no sense in biology. There is no backup, except in that each organism is a branch of it's parent(s) source.
Where the analogy could work
Genomes of different species are all branches from some original source code. Therefore, you find a lot of commonality when you compare even very distantly related life, especially in the most key libraries that are involved. There is a ton of conserved sequence in the basic machinery for replicating DNA and producing proteins, for example.
This is why your statement:

This explains why human DNA is mostly so similar to dog DNA, fish DNA etc. Because we all evolved from same primitive cells! Base of our "repository" was same!

is mostly correct.
Length of source
Your analogy has gotten some criticism for your conclusion:

Theoretically, the more primitive organism is, the shorter DNA it should have.

but I would argue this is actually a way in which your analogy works, yet your conclusion from it does not. Software development involves both adding new code and deleting obsolete code. Lines of code is a poor measure of how primitive some code is. Biology shows this well: all life is equally primitive in terms of years of existence, and single-celled organisms are much more advanced in terms of numbers of generations. If organisms contained some log of all the past changes (which they do not), the repository would be way way bigger in bacteria than in animals because of that large number of generations.
Summary
In summary, analogy can be helpful to wrap your head around some information, but be careful in taking it too far. Sometimes analogy is good for generating new hypotheses and for guiding your learning, but you need to verify those hypotheses in the actual biology (see Richland and Simms 2015 for one take on the usefulness of analogy as an educational tool).
I disagree strongly with the comment by @SPr stating "The analogy between the genome and source code repository is unhelpful and poor": even the imperfection in an analogy can be very helpful in that they help you build a relational map of the world by finding where analogies work and where they conflict.

Richland, L. E., & Simms, N. (2015). Analogy, higher order thinking, and education. Wiley Interdisciplinary Reviews: Cognitive Science, 6(2), 177-192.

Watch out with analogies. Even when they are somewhat helpful, they are only analogies. That being said, unfortunately, your analogy is completely unhelpful!

What if DNA is actually like a software source code repository? You know, it has "master" branch - which is most stable and up-to-date version of program but also it has other branches, experimental ones and of course it has huge amount of "junk" - i.e. backed up version of files from previous changes to code that is not used in any way in actual program.

It is unclear what you would call "junk" here. Typically, if you include regulatory sequences in "junk" as it is often done by lay people (see @iayork comments below for more information), clearly they are being used and are essential. But anyway, seeing non-coding, non-regulatory sequences (such as the ALU sequences) as experiments would be very misleading. Large amount of repetitive DNA usually comes to existence through the work of transposons and retrotransposons. They are not attempts (clearly not with an intuition but even without intuition in mind) to make something "better"

So what if first primitive single-cellar organisms had super primitive and very short DNA, then it got improved, but original DNA was not erased, but backed up every time new mutation (commit in software SCCS) appeared.

DNA get lost all the time. A mutation can alter the code, it can also duplicate sequences (or even whole chromosome or whole genome) and it can "remove" sequences (even "remove" whole chromosomes). Genome reduction is indeed not that uncommon.

Theoretically, the more primitive organism is, the shorter DNA it should have. For example, some very old sharks that still survive from Mesozoic era should have shorter DNA than modern sharks... Is this confirmed by actual experiments?

"Old sharks that still survived from the Mesozoic era" are not more primitive than humans, E.coli or than the European green lizard. At least not in any way that "primitive" is easy or intuitive to define. Please have a look at the post Are we “more evolved” than present-day bacteria? for more information.

This explains why human DNA is mostly so similar to dog DNA, fish DNA etc. Because we all evolved from same primitive cells! Base of our "repository" was same!

I am not sure I understand what you have in mind here.
Any two extant lineage share a common ancestor at some point in the past. Depending upon how recent is their Most Recent Common Ancestor (usually abbreviated MRCA), they are more or less likely to have similar genome.

Also this explains why human embryo come though all this steps of been single
  cell, multi-cell, fish, amphibian, mammal etc.

I am not sure I understand what you have in mind here.
There is MRCA of all living creatures on earth is called LUCA (Last Unversal Common Ancestor). We don't know much about LUCA but it was pretty clearly single celled and had a relatively short genome. Note btw that LUCA itself is not the very first cell though but that does not matter much for our discussion.

Typically, if you include regulatory sequences in "junk" (as it is generally done, I think) Not so. Although there are a lot of people who attack the concept of junk DNA with this as a straw man, regulatory sequences are not and never have been considered part of junk DNA. Doesn't change the rest of the argument, just a caution

I don't know what meant the first people who coined this term but my first 5 google results for "junk DNA" define it as "non-coding DNA". But yes, let's be cautious that it might not be what everyone mean at least. Answer edited. Thanks

The original definition did not use that - I agree it's often used that way, but actual researchers on the field are much more strict. See The Case for Junk DNA, especially the section The origin of “junk DNA”

I would compare DNA to a computer filesystem rather than a source code repository. Coding sections are "programs" that can be run to produce a protein product. An important difference, however, is alternative splicing, where a gene can code for multiple products. This serves as a form of "compression on disk", where repeated regions can be represented by a copy and pointers wherever the region is required.
The vast majority of what was previously called "junk" DNA instead turned out to be important for other purposes. For example, some serve as regulators or recombination faciliators (source - https://www.scientificamerican.com/article/what-is-junk-dna-and-what/), some serve important structural purposes (source - https://www.sciencedaily.com/releases/2018/04/180411131659.htm), and others serve as important binding sites for transcription control (source - https://ghr.nlm.nih.gov/primer/basics/noncodingdna)
Think of noncoding DNA as filesystem metadata - stuff like file allocation tables, master file tables, journaling, and the master boot record that doesn't represent actual data - although your computer will probably break if this data disappears. Again, the analogy doesn't fit too well considering only about 1.2% of the human genome is coding regions (source - https://www.bing.com/search?q=what+percentage+of+the+human+genome+is+noncoding&pc=MOZI&form=MOZSBR ). On the other hand, computer filesystems are generally designed to minimize the amount of metadata overhead since that costs you an extra storage space that could otherwise be used for files.
Further reading on "junk" DNA that really isn't garbage:
https://www.scientificamerican.com/article/what-is-junk-dna-and-what/
https://www.sciencedaily.com/releases/2018/04/180411131659.htm
https://ghr.nlm.nih.gov/primer/basics/noncodingdna


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How protozoa spawns in newly formed ponds?
How big protozoa like Paramecium caudatum, Amoeba proteus, Euglena viridis etc. appear in newly created ponds of water? Suppose there was rain, and pond was formed. Or earth, dead leaves, live leaves and wood was added to bottle like in this video:
https://www.youtube.com/watch?v=j2T__l7FgU4
She says in this video that paramecium "should spawn from the dirt", but this makes no sense to me... Do they magically recombine from inorganic elements? Doubtful. Or maybe they are just scattered in every grain of dirt, everywhere, in a form of microbial cyst? Seems not very realistic either...
P.S. I'm mostly interested how Paramecium caudatum get in there, but if other protozoa have some other means, that would be interesting too.


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How much MPa of pressure can human cells survive?
Is there any research on this topic with concrete numbers? I found some papers of high pressure tests on microbes, but not on human/mammal cells. What I want to find is true "crush depth" for a human (assuming full liquid breathing and CO2 scrubbing from veins).
One in one Youtube video author claimed that 1000 m (10 MPa/100 Bar) is maximum depth human can reach, because at such pressure human cells will fail. Membranes will get so stiff, that it will fail to exchange oxygen/nutrients/energy, so, effectively, neurons will die at such depth. Author didn't provide any sources whatsoever for such claims, though. He just provided Blobfish (Psychrolutes marcidus) example. It has jelly-like, very soft cell membranes that at 1.6 km depth are as rigid as our own membranes at sea level, but when brought to sea level pressure loose structural integrity.
Yet, I highly doubt this claim, considering that Sperm Whales casually dive to 2 km depth and Cuvier's beaked whale dives 3 km. They do not turn into jelly like Blobfish at the surface, yet still manage to remain at such huge pressure as 30 MPa for hours. Of-course, they don't live permanently at such depths, but human diver is not required to live there too - just survive and go back without major trauma.
So if a Sperm whale can do it, can't we too? Or can we? At what pressure our cells will fail?

How do you propose the research be conducted? On paid volunteers? Prisoners? Illegal immigrants? What difference does knowing this make, practically (or scientifically)? If people need to go deeper, they get into mini subs that can withstand great pressures now. Nobody dies finding the answer. (This kind of extreems of endurance research was done, oh, 70-80 years ago...)

Well, with modern technology there is no need to even go into the ocean. And this is very cheap experiment for somebody with required tech. Just get some human liver or neuron cells, put them into pressure chamber and start increasing pressure while monitoring their status. As simple as that. It is really weird that nobody don this yet, as it is very important to know our theoretical limits so that we can improve our exoskeletons (yes I call body exoskeleton, because the human is neuron connections and currents within them, and body is just an external structure that supports this system).

Seems like nobody in the World can provide any information on this topic. I will assume, for now, hard limit of 3 km depth, judging from deep diving whales. I don't know why they don't dive deeper, maybe there is no food there, but maybe they actually reached hard limit of what surface mammal can achieve in terms of cell membrane pressure.

@anongoodnurse at the very least, tests on mice might give pretty accurate results for surface optimised organism's crush depth.

Why kill a mouse for such useless information?


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Is it feasible to grow edible crops for lawns?
Is it possible to grow some type of plant that functions well as a lawn (e.g. is somewhat grass like), but that is humanly edible?  Would anything that currently exists fit this role?  For example possibly spinach or lettuce might work somewhat, but probably wouldn't be ideal.  If not, could we bioengineer something to fit that role?  I am thinking if we can, this could solve world hunger!

It's a bit off-topic for biology, but there are a lot of economic problems with distribution rather than scarcity of food. In many places where hunger is a problem, it is more profitable to sell cash crops to developed countries or to use crops as animal feed than to sell to impoverished neighbors. Grasses are probably as good as anything to grow in a lawn, if those grasses were fed to animals to free up other space for people. That isn't really the problem, though.

@Brian Krause as far as the distribution problem goes, I wonder if this could be grown anywhere in the world?  Different plants would probably be required in different environments.  Even in deserts, cacti can grow, but they would not make for a good lawn unless significantly bioengineered.

@canadianer Chives is definitely on the right track!  I think of chives more of a spice, but it certainly is grass like and edible.  Now, question would be if it is edible in large quantities, like the majority of a person's food intake?

Green leafy vegetables tend not to have much in the way of usable calories, so spinach and lettuce wouldn't work, However I think what you are going for is rice... it is the seed of a type of grass and is a staple in much of the world's diets. Now if I can toss my opinion in here, we would be even better off if we stopped fearing GMOs, as we could grow rice that had more nutritive value, such as golden rice, or strains of rice that required far less water to cultivate.

@Bryan Krause: Also hunger tends to be a localized, sporadic thing, often caused by drought or other unusual weather.  That would affect the edible lawn as severely as the field crops.  Also most people with lawns and a disinclination to use large amounts of herbicides seem to have a pretty good crop of dandelions, which are edible.

There are lots of things that you can eat that you could grow as a lawn.  That probably are growing in your lawn now.  My yard is about half violets and they are edible.  Purslane is a delicious succulent lawn weed.  Grab some, rinse it off and eat it.  It is crunchy!  I am telling you from experience you can eat a lot of it and you will not get sick.

Purslane image from here.
http://www.livescience.com/15322-healthiest-backyard-weeds.html
This backyard weeds link says lambs quarters are edible and I did not know that.  They are also volunteers but I did not know they were good for anything and so I was pulling them up.
We are surrounded by things we could eat and which our ancestors ate all the time but which we do not eat.  If you are in school, Johnathan, and this sort of thing interests you it would be a stellar project.  You have all summer to grow weeds in pots and then at the science fair you could have people taste them.

Very nice!  Looks like there are several good candidates here and that such a thing might be feasible, thank you for your answer!


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Is it possible to consume O2 via a pill form to inhibit the need to breathe?
Just wondering if it would be theoretically possible to consume oxygen via O2 pills, in the effort of being able to hold one's breath without limit.
Totally just curious.

Ask yourself two questions: where do pills go when swallowed and where does gas exchange occur?

No, then add more 'no's. The change from solid to gas would explode whatever structure it was in.

You mean solid oxygen exists?! Even if it does, you won't be able to hold it in your hands, leave 'eating' it for future. Also, you need to note that the urge to breath comes from increased CO2 concentration in blood, its got nothing to do with oxygen.

The problem is volume and surface area for gas exchange.  The volume in a pill is puny compared to the amounts you pull in and out breathing.
But could you use something other than the lung for gas exchange?  The colon has a lot of surface area and the small intestine even more.  Maybe if you flooded your gut with an oxygenated fluid like that liquid fluorocarbon the mice breathe, or even oxygen saturated water you could get some of that out via your intestinal villi.  Dragonfly larvae do something like that, performing gas exchange with their rectums.  You would need to exchange the liquid at least as fast as you breathe, getting all the depleted liquid out and new oxygenated liquid in.
Some of those high colonic machines work like that, as I understand: fast in and fast out.  People might not notice you were holding your breath because they were distracted by the churning machine with the hose up your trouser leg.  Maybe you could pass out cards or wear a T-shirt explaining what was going on because you would still have to breathe to talk and that would ruin it.  If you do this would you please post video and link it up here?  Thanks.

The volume of gaseous O2 compressed into a solid the size of a pill would be awesome indeed.


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How the electrons from electrode play a role in stimulating the neuron?
I am trying to understand how a neuron fires action potential after being stimulated via electrode (extracellular stimulation). GHK equation gives the membrane potential,which is -70 mV when neuron is at rest. When the membrane potential increases to -55 mV, it fires AP. But then an electrode gives electrons, which do not appear in the equation. Then how the electrons from electrode play a role in stimulating the neuron? Also,   is there a way to calculate how many electrons or how much current would be required to stimulate a  neuron?

You might be interested in this.


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Temperature threshold of a cell
While human body as a whole will find a increase in temperature by 2 C fatal, what about individual cells? If temperature of a cell or tissue is maintained at higher temperature via external mechanism , say a sophisticated heating rod, how much temperature rise it can take before dieing? Say, endothelial cells lining blood vessels. Or,any other cell.

different cells and tissues have different tolerances, so you will have to be more specific.

A core body temperature of 39°C is far from fatal, so you are starting from an incorrect assumption.

Talking about cells in general, the main problem about higher temperatures is the denaturation of proteins (when proteins lose their structure and then they don't work anymore), and every organism has a specific range of temperatures in which its proteins have evolved to work in that determined range.
The most common example of bacteria living at high temperatures is Thermus aquaticus (or others) which proteins are widely used in laboratories for their peculiarity to be able to work at more than 70 °C (e.g. polymerase chain reaction).
In humans the mean temperature is 37 °C, and it's not unusual during severe fevers to get it rising to 39-40 °C (so the assumption that over 39 °C occurs death is incorrect). Of course you can reach higher temperatures but reaching 43-44 °C leads to multi-organ damages. You can find out more in this review.
Another thing to take in consideration is that cells must contain water in liquid phase, so over the 100 °C limit (at atmospheric pressure, so the limit can increase alongside pressure) it's kind of impossible to find living cells.

The highest I found is 122 °C (http://www.pnas.org/content/105/31/10949) but you have to consider the high pressure that keeps water a liquid and not a gas.

I think the question was about the temperature tolerance of human cells, not extreme thermophile bacteria, so this seems to be veering off topic ...

Reading the question and the comment wrote by John I thought it was clearer to take them as example, anyway the thermophile-related sentences can be easily deleted.


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In the event of an abrasion, do mast cells cause vasodilation or vascular constriction?
Or both? I am unsure as to what mast cells will do in the event of a wound either on the epidermis or the epithelial. I know they secrete factors that mediate vascular constriction / dilation, but I can't find information anywhere as to what they do in the area where the wound is located.
Based off my current understanding, this is what I think happens:
Wound. Mast cells release mediators that cause constriction around the area of the wound, but dilation further upstream to increase the delivery of essential leukocytes (white blood cells), plasma and red blood cells.
Any help is greatly appreciated!


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Does orgasm cause a dopamine crash?
There's some theory around that orgasm will cause a dopamine surge and drop, and that this can lead to a period of low mood or depression. A come down.
Is this true, does orgasm have a negative psychological consequence ?

To answer your last question, I very much doubt it's true in general. It does have unplesant effects in some people though. Form a popsci account

He [a psychoanalyst] was puzzled about a 24-year-old man whom he viewed as psychiatrically healthy except for intense depression that lasted for several hours after sex. [...] Could it be that some patients have particularly strong rebound activity in the amygdala after orgasm that makes them feel bad?

And this post-coital dysphoria can happen to women too, for which there is some prevalence data:

Forty‐six percent of respondents reported experiencing PCD symptoms at least once in their lifetime with 5.1% experiencing PCD symptoms a few times within the past 4 weeks.

"No sex before game day" was a tenet in some sports psychology/physiology corners, but more recent research failed to find significant differences of sex acts on mental performance... at least in (healthy) athletes. A 2016 review notes

Despite the major differences found in the recovery phase, where higher values of HR [heart rate] were found 2 h after sexual intercourse, no significant differences were found in workload achieved and in mental concentration of the athletes.

And, yeah, I know sex doesn't necessarily mean orgasm, but it seems close enough to mention.


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Do hedonic chemicals in humans work as anhedonic in other organisms?
We have various neurotransmitters that cause pleasure or feelings of love in humans. Do they work in this way for all other animals and organisms ?
What about reptiles, insects, crustaceans ?
I don't know how far science is assuming the state of subjective experience in other organisms, but how far can we say that other organisms would feel the effects of neurotransmitters in ways that we would recognise from our own experience ?
For instance, we could assume that another primate experiences dopamine in a similar thing to humans, but what about non-mammals, animals of other classes ?


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What's the best way to measure biodiversity?
As I understand it there are various ways biodiversity is measured, with varying results. From what I have been told on these boards, part of the difficulty is because it's hard to define a species exactly, so it's hard to count them.
What I really want to know is whether genetically engineered organisms count towards increased biodiversity but my last attempt at asking that question foundered on the rocks of species definition.

Could you narrow your question? Biodiversity is not just the number of species, but also the phylogenetic range of diversity. For example, a Tuatara is the only representative of its kind. Does one Platypus species count the same as one Drosophila species? But if you want to know if genetically engineered organisms count as species; No, they don't. They are not different species, but simply have a gene inserted to provide some trait like herbicide resistance. If that is the question, then ask that.

Hi I'd like to narrow the question and agree that a gene inserted isn't a new species, and there are those definitional problems as people have pointed out to me. But I think that genetic engineering is going to soon be more than just tinkering with genes but designing whole new organisms. So I'm trying to look into the future a bit here.
So I could rephrase as "If in the future new species are engineered, will that count as an increase in biodiversity, and will it be a significant increase ?"

If genetic engineering actually does create new species, they would be counted in biodiversity studies. I am not an expert, but I do not think that these "new species" could ever be approved for release into the environment. There are pretty strict rules about this. They would also need to be formally described. I don't know where you are getting your information, but I am skeptical that there will be a significant flood of human-engineered new species.

Well, I'm speculating in a science-fictiony way somewhat, and looking at efforts like Craig Ventors to synthesize genomes, and other stuff like this
https://www.technologyreview.com/s/610180/why-redesigning-the-humble-yeast-could-kick-off-the-next-industrial-revolution/
"Instead of engineering or even editing the DNA of an organism, it could become easier to just print out a fresh copy. Imagine designer algae that make fuel; disease-proof organs; even extinct species resurrected."
So if that industrial revolution does take off, does that mean more biodiversity ?

OK, well that is not happening now, and if it ever did, it would need to be under tight regulatory control. Estimates are that there are at least 10 million species. A couple of engineered organisms, even if they were approved for release into the environment would do nothing to increase estimates of biodiversity. Could you modify your question? As written, it is not clear what you want to know.

I disagree with a couple of things there Karl. The environment in this case is a lab. It's not environment just because it isn't a forest or ocean. There's a history of new species arising in human made environs and these will be more. As to how many organisms there will be, I can imagine a lot, even just from what articles on MIT Review say. They're talking about a biotech revolution. Regulation is also only part of the story, lots of unregulated things happen, presumably they always will, though I think regulation is pretty important here.

That does not change the fact that your question does not ask what you want to know. It seems you already know the answer.

Sure it asks what I want to know. I'm only speculating, so I want to see if people more knowledgable than I can let me know if it's reasonable speculation ?

"If genetic engineering actually does create new species, they would be counted in biodiversity studies."
Karl, Ventor says he has created a new species. I know people debate what counts as a species. If that IS a new species, then has he increased Earth biodiversity by one bacterium ?
https://www.scientificamerican.com/article/scientists-synthesize-bacteria-with-smallest-genome-yet/
"the genome of the minimal cells is like nothing in nature. Venter says that the cell, which is described in a paper released on March 24in Science, constitutes a brand new, artificial species."

A very good way to measure biodiversity would be to do environmental barcoding with high-throughput sequencing methods, and then use an algorithm that estimates genetic distance to get both species count estimates, and then calculate higher-level diversity, such as genera and families. Then you would repeat this procedure over several collections to obtain a species accumulation curve, so you could then estimate the asymptote. The future possibility of biogenereed organisms would not be worth reporting among the thousands of species at a given location.

OK, but what about by methods used now, particularly the ones that are used to tell Joe Public like me what the state of the world is in a typical news outlet ?
Currently the news is that biodiversity is on the slide due to human activity. I've no doubt it is. But, counting all organisms including ones that may be man made, will this always be the case ?
It may or may not reflect a pleasant planet to live on, but will it be the case ?

No. You seem fixated on a hypothetical that somebody used to sell magazines. Not going to happen. And if it ever did, it would be such a tiny fraction of biodiversity, that it would not be significant in the counts.

Why won't it happen ? Why would it be a tiny fraction ? How much is significant ?


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Did any warm blooded animals evolve back into cold blooded?
Pretty much as title says - wondering if evolution can go from mammal back to reptile - either in theory or practice.

The terms "warm-blooded" and "cold-blooded" are very undefined.Please have a look at this post or this post for the correct terms and concepts. I suppose that you meant "endothermy" and "exothermy" instead of "warm-blooded" and "cold-blooded" but I am not 100% sure.

I think your question will be improved by doing some reading on thermoregulation and then incorporating that knowledge to create a better defined question. For example you could start with this wikipedia article and the associated articles.  ——— You also seem to be confusing taxonomic groupings (e.g. mammals) with types of thermoregulation (e.g. "warm bloodedness), which is likely to get a negative response ...

Secondary ectothermy has been suggested in living crocodylians by Seymour et al. (2004). Their rationale is based on:

Presence of a 4 chambered heart (otherwise only found in endotherms)
Post-cardiac shunting via the foramen of Panizza and "cog-tooth" valve, which develop secondarily in crocodylians
Lung structure and ventilation during locomotion

Thus ectothermy in extant crocodylians is associated with being aquatic or semiaquatic. These authors suggest that endothermy may have been ancestral for dinosaurs as well.
Seymour RS, Bennett-Stamper CL, Johnston SD, Carrier DR, Grigg GC. 2004. Evidence for endothermic ancestors of crocodiles at the stem of archosaur evolution. Physiol Biochem Zool 77:1051–1067.

There is no evolutionary "ratchet" that prevents a life form from evolving "backwards".  However, it is statistically unlikely because it would pretty much require all of the environmental factors that changed during the transition from "cold blooded" to "warm-blooded" to change back in the reverse order, because all of those factors contributed to the selection pressures that caused the "forward" evolution.
It would be analogous to getting a set of moving billiard ball to reverse direction and re-form an earlier pattern: reversing any one ball's velocity would be fairly easy, but getting all of the balls to cooperate to re-form a static pattern that ends up shooting out the queue ball is so unlikely as to be effectively impossible.
That said, for a modern form (B) to evolve into another form (C) that resembles an archaic form (A) without actually being that archaic form would "only" require a sequence of environmental changes that leads to the evolution of (B) from (A).  It just wouldn't actually be the archaic form.  It would be a process analogous to convergent evolution.


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Why do chain identifiers in PDB have no standard starting chain id type?
At first I assumed that PDB chain identifiers are just uppercase letters (A, B, C,..) but found out there are protein chain ids that are numbers (0-9) and lowercase letters as well.
For example,

1NAL only has chain ids (1 - 4). It starts with chain '1' (number).
103L has chain identfier 'A'. It starts with chain 'A' (uppercase letter).
5afi's chain id's range from [a-zA-Z0-6] since it has 52 unique protein chains. It starts with chain 'a' (lowercase letter)

Can someone please explain? Or are id's just arbitrarily assigned?

Chain IDs are assigned by authors who submit the structure to the wwPDB.
According to the PDB spec:

Non-blank alphanumerical character is used for chain identifier.

Usually, the chains are assigned uppercase letters.
But since digits and lowercase letters are also allowed, some people will use it.
And a good reason to allow more characters is to accommodate for structures that have more polymer chains than there are letters in English alphabet. With lowercase letters and digits the limit is 62 chains.
Which is still not enough for some structures.
(Many programs can handle two-character chain IDs, but this common extension has not been embraced by the wwPDB.)


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DNA replication in $ E.coli $
$ E.coli $ has circular DNA which I guess implies one strand forms the outer circle and the other the inner one. So, is there a way to know if the replicated DNA forms the outer or inner circle?
In the image attached it is seen that the replicated DNA forms the inner circle. Also mentioned is the fact that it is not possible to make out individual strands by TEM.

The picture on the bottom is a simplified cartoon. The two strands make a double helix so they both alternate between top strand and bottom strand. Also plasmids aren't 2D circles in the cell; they twist and turn and rotate.


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Can endometriosis be considered a form of cancer?
In endometriosis the lesions form their own vasculature and compromise organs, arteries, and nerves. It can spread and embed throughout the body. It's difficult to treat as the adhesions resulting from repeated surgeries can cause the same symptoms as the lesions. Treatment often leaves patients with the original level of disability after the 2 year mark.
My question is, for these reasons could one treat and research endometriosis as if it were a form of cancer?
Could the immune system be utilized in treatment as the lesions induce high levels of certain cytokines?
Why or why not?

According to Endometriosis: benign, malignant, or something in between? (PubMed, 2017), endometriosis is not considered cancerous because:

Does not appear as an expansille tumor mass
Is not destructive
The cells in the lesions are normal, like in the uteral endometrium
Is not lethal

Immunotherapy of endometriosis is in the experimental phase - you can read more here: Novel Therapies Targeting Endometriosis (PubMed, 2011). Other treatments mentioned are anti-inflammatory drugs, selective estrogen or progesterone modulators, statins and antiangiogenic agents. There is also a study Open Label Immunotherapy of Endometriosis running - it is briefly described on ClinicalTrials.gov.
Chemotherapy, which is effective in some cancers, is based on killing quickly-dividing cells, but cells in endometriosis do not divide so quickly, so you can't treat it by chemotherapy in the same way.

It is important to note that cancer includes loss of the property of contact inhibition in cells. This leads to uncontrolled divisions in cancerous cells. Although endometriosis includes cells dividing at ectopic locations, they still possess the property of contact inhibition. So, endometriosis can't be called a form of cancer.
For information on Contact inhibition, visit the following link:
https://en.m.wikipedia.org/wiki/Contact_inhibition


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Can you identify this bug

This was found in my home in Mojave county Arizona. It was about 1/8 inch long. I have a cat. Hoping not a flea.

Definitely not a flea. It has the mouthparts of a true bug, order Hemiptera. I can't tell beyond that.

If the specimen is still at hand, adding a top view photo would help get an answer as to what true bug we're seeing here (but if the primary concern was flea or not, that's been dealt with).

I don't have it anymore. I Would like to know what it is, but yes my concern was flea. Me and my cat keep getting bit up. I have seen lacewing and thrips in house and on me. I know the larvae stage of both feed on blood. Also thrips are known to lay eggs under people skins. Pretty sure all these stupid little bugs are tearing us up. Just trying to identify  everything I see. So I can prevent as much as possible


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Why does K+ going out of the cell cause hyperpolarization?
I'm really  confused by how the terms Hyperpolarization and Depolarization are used in Cell biology and hope somebody can enlighten me hopefully.
Here's what they mean for me so far:
Depolarization means the inner and outer side of the cell membrane become less polarized (so the Nernst potential tends to 0 due to log(1) being 0)
Hyperpolarization that the inner and outer side become more polarized (so the Nernst potential increases).
Assuming I'm not completely wrong until here.
Let me give some examples, so maybe you can see better where the problem lies:

We have a model cell so (K+ internal is 140 mmol/l, K+ external is 4.5 mmol/l) and the external side is increased to 8 mmol/l , then a DEPOLARIZATION occurs because

roughly : $-60 \cdot \log(140/4.5) = -90 mV < -60 \cdot \log(140/8) = -74 mV$ ; or in other words, "energy" was used so a depolarization occurred (so far this seems correct with the solutions I can find to this example)
\
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Now comes the second example (famous depolarization of a cell with the graph and the peak and repolarization):

Na+ enters the cell : the concentrations im gonna use for this example are inside:$12 mmol/l$ and outside $140 mmol/l$

so before the Na enters we have: $-60 \log(12/140)= 60 mV$
if Na+ enters the Cell, a depolarization should occur (because the difference inside and outside is decreased)
this seems fine with the graph...

the part of the graph which goes over 0 (also called "overshoot"), is it not technically a hyperpolarisation+depolarization?
repolarization: this occurs by K+ ions leaving the cell, but that doesn't make sense according to the Nernst equation?

The concentration inside before the cells leaving is 140, outside 4.5 ; if K+ leave the cell, its simply going to depolarize more... So why does repolarization occur and not depolarization?

It's commonly stated that Hyperpolarization is caused by K+ LEAVING the cell (for example with ion channels) , how does this make sense if the inner concentration is higher than the outer? If anything, this again should lead to depolarization
Same thing with K+ entering the cell, isn't that supposed to cause a hyperpolarization as well?

I appreciate any kind of insight into this matter, since it seems that I'm completely wrong.

Why do you think that K+ leaving the cell is going to depolarise more? When Na+ enters the cell, it affects the total ionic concentration inside the cell, so that Na+ entering the cell (depolarisation) is “balanced” by K+ leaving the cell (repolarization). You also have to consider that a lot of channels are voltage-gated, so they regulate ionic transport based on a change in total membrane potential, regardless of which ion concentrations caused the change in potential.

considering the Na+ entering is probably smart BUT for example; if you have a cell why is it said that K+ leaving the cell will cause hyperpolarization? if it is not true due to the Nernst equation ? Same with K+ entering the cell ; regardless of whether Na enters or not ; if K+ leaves the cell potential from nernst will go towards 0 ; yet it is still claimed that this will cause a hyperpolarization? Is my understanding of depolarization and hyperpolarization incorrect?

since cell membranes are normally polarised at a resting potential of -70 mV, hyperpolarisation refers to any event that polarises the membrane even more, making the cell interior more negative beyond -70 mV (so the opposite of depolarisation). Hyperpolarisation is not specific to K+, and K+ leaving the cell doesn’t necessarily cause hyperpolarisation: it only does so when potassium channels stay open for a longer duration, allowing more K+ to leave the cell than needed to repolarise the cell back to -70mV.

The extra efflux of K+ and hyperpolarisation are important concepts in neurons, because nerve cells can only be excited (depolarised) from their resting potential. Going from a hyperpolarised state to the resting potential of -70mV allows a gap in time between excitation events. Because you wouldn’t want neurons firing constantly! :)

How does that relate to the simplified Nernst equation? I don't really see how your comment answers my question: $\frac{-60}{k} \log (C_{in}/C_{out})$. If you go from 140 inner  and increase the concentration outside, then according to the equation it's going to go towards 0 ; this by definition is a depolarization ??????

K+ and Na+ movements across the membrane are coupled in cells, so I think you need to use the Goldman equation instead of the Nernst in order to account for both ions.

So when somebody says K+ is leaving the cell, what they really mean is Na+ is entering at the same time which in total causes a hyperpolarization?

Yes, that is exactly my reasoning.

Here is how I think of the issue. First, keep in mind over the course of the action potential, ion concentrations on both the outside and inside of the neuron remain relatively unchanged.  You can think of the Nernst potential as a charged battery, and they keep their concentrations relatively constant. Currents will flow, and the voltage will change, but this effects very few ions at a time, and does not effect the bulk concentration (See section 2.6 here). This is because any small change in concentration near the membrane (where voltage is measured) will quickly equalize with the surrounding bulk solution via diffusion.
Second keep in mind that the Nernst potential is an electro-chemical potential. Thus for potassium in particular, the chemical potential will overpower the electric potential driving potassium out of the cell, making the driving voltage of potassium negative.
So, as you state, the Nernst potential of sodium is $60$ $mV$ and for potassium is $-90$ $mV$. In your example there is a rest potential of $-70$ $mV$ this is given by the GHK potential mentioned in the comments. That means at rest, the balance between the sodium and potassium potentials is $-70$ $mV$. Here is the equation for reference. Note that this equation reduces to the Nernst potential when we consider only one ion.
$$ V = \frac{RT}{F} \ln(\frac{g_{Na}[Na_{out}]+g_{K}[K_{out}]}{g_{Na}[Na_{in}]+g_{K}[K_{in}]})$$
When the action potential starts, the depolarization is driven by the opening of sodium channels, that is $g_{Na}$ gets larger. Thus, when these channels open sodium rushes out and the cell voltage attempts to become more like the sodium Nernst potential, not zero. You can see that in the equation for the GHK voltage equation as the sodium conductance dominates the equation.
Near the peak of the action potential, the sodium channels close, and the potassium channels open. That is $g_{Na}$ gets small, and $g_{K}$ gets large. This means that now the potassium conductance dominates the equation, and the neuron's voltage becomes more like the $-90$ $mV$ Nernst potential. Then the repolarization occurs when the potassium channels close, and $g_{Na}$ and $g_K$ are back to there intial closed values, bring the rest potential back to $-70$ $mV$.
**note I am oversimplifying how the gates change in time, but I think this will help clear up your confusions.

My answer: it's not the concentration change that causes repolarization, it's the permeability change.
The relevant equation here is the Goldman-Hodgkin-Katz equation, which entails that transmembrane voltage V_m is proportional to the ratio of [K]_o/[K]_i times permeability P_K:

[K]_i is always higher than [K]_o, so the ratio of [K]_o/[K]_i is always providing a negative contribution to V_m. During repolarization, the contribution from this ratio becomes less negative as its electrochemical gradient evens out, and if this was all that was happening then V_m would increase. However, there is a second relevant term that changes upon repolarization: potassium's permeability. P_K increases dramatically during repolarization, providing a negative contribution to V_m.
Note 1: Because potassium is positive and the cytoplasm is negative, the electrochemical gradient favors [K]_i > [K]_o. This explains why the transmembrane voltage decreases to -90 mV instead of 0 mV.
Note 2: The only reason why Vm is positive during an action potential in the first place is because there exists a high resting [Na]_o, and so a step change increase in sodium's permeability P_Na is what's driving the AP Phase 0 increase. As soon as P_Na drops, we would expect V_m to drop too regardless of what's happening with potassium.
Note 3: While I think your definitions make more sense (i.e. they're more literal), this quote (from Raz 2013: "depolarization is a positive change from the resting membrane potential") implies to me that "depolarization" has shifted from its historical definition to now just mean "an increase in transmembrane voltage".

Welcome to the site!  References would be appreciated.  Thanks!

With respect to "note 3", there's really nothing biologically meaningful or special about the potential "0 mV", hence the use for "depolarization" meaning "any positive change from rest", sometimes including overshoot.

Adding K+ on the outside of membrane is not the same as transfering K+ from inside to outside.
When K+ is added to outside(hyperkalemia) the RMP becomes less negative(depolarisation)
When K+ is transfered from in to out RMP becomes more negative(re/hyperpolarisation)
We should not forget that most of the intracellular anions are nonpermeable protiens, so when K+ is transfered to outside they pull harder, and when K+ added outside, the pull decreases

Can you expand your explanation a bit, as well as expanding the acronyms?


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Are chromosomal microdeletions passed on?
I've been looking around but can't find a clear answer: are chromosomal micro-deletions passed on (hereditary) or not?

Of course. Just like any other type of mutation.
If a mutation (incl. a chromosomal microdeletion) happens in the germ line, then the mutation can be passed on.

another question I may add/ask: if a parent has a chromosomal micro deletion, and uniparental disomy happens, then the child will inherit the deletion as well , right? Thanks for answering

Yes, necessarily. As both chromosome are passed (uniparental disomy), the one carrying the microdeletion will necessary be passed.

To be clear, microdeletion is the term for when a gene on one chromosome replaces its counterpart, yes?

@TheNate I think (but might be wrong) it is a term mainly used in the medical field. I think it refers to a small chromosome deletion (a few kb say) that is too small to be detected by the simple colouring methods (such as FISH or G-banding) often used in medicine.

Thanks. I'll go start some reading, then.


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Is all of the DNA used by genes (encoding DNA)?
My intuition tells me no, since only 1.5-2% consists of exons, so this statement would be wrong.
The correct statement would have to be: only about 1.5-2% of the whole DNA is used by genes (encoding DNA).
Am I correct in this assumption?

Possible duplicate of Is most of the human genome functionless “junk DNA”?

The ENCODE consortium classifies human and mouse genome elements to try to answer this very question.
Work by ENCODE suggested up to 80% of the genome is functional in some way. In other words, by that upper-bound measurement, there is apparently more to DNA's role in biology than just encoding genes — there's a lot going on under the hood.

Case for Abundant Functional Genomic Elements.
Genome-wide biochemical studies, including recent reports from ENCODE, have revealed pervasive activity over an unexpectedly large fraction of the genome, including noncoding and nonconserved regions and repeat elements (58⇓–60). Such results greatly increase upper bound estimates of candidate functional sequences (Fig. 2 and Fig. S2). Many human genomic regions previously assumed to be nonfunctional have recently been found to be teeming with biochemical activity, including portions of repeat elements, which can be bound by transcription factors and transcribed (79, 80), and are thought to sometimes be exapted into novel regulatory regions (81⇓⇓–84). Outside the 1.5% of the genome covered by protein-coding sequence, 11% of the genome is associated with motifs in transcription factor-bound regions or high-resolution DNase footprints in one or more cell types (Fig. 2), indicative of direct contact by regulatory proteins. Transcription factor occupancy and nucleosome-resolution DNase hypersensitivity maps overlap greatly and each cover approximately 15% of the genome. In aggregate, histone modifications associated with promoters or enhancers mark ∼20% of the genome, whereas a third of the genome is marked by modifications associated with transcriptional elongation. Over half of the genome has at least one repressive histone mark. In agreement with prior findings of pervasive transcription (85, 86), ENCODE maps of polyadenylated and total RNA cover in total more than 75% of the genome. [emph. added]

However, people outside the ENCODE consortium have criticised this research with very strong language, such as in this article by noted critic Dan Graur:

Actually, the ENCODE authors could have chosen any of a number of arbitrary percentages as “functional,” and … they did! In their scientific publications, ENCODE promoted the idea that 80% of the human genome was functional. The scientific commentators followed, and proclaimed that at least 80% of the genome is “active and needed” (Kolata 2012). Subsequently, one of the lead authors of ENCODE admitted that the press conference mislead people by claiming that 80% of our genome was “essential and useful.” He put that number at 40% (Gregory 2012), although another lead author reduced the fraction of the genome that is devoted to function to merely 20% (Hall 2012). Interestingly, even when a lead author of ENCODE reduced the functional genomic fraction to 20%, he continued to insist that the term “junk DNA” needs “to be totally expunged from the lexicon,” inventing a new arithmetic according to which 20% > 80%. In its synopsis of the year 2012, the journal Nature adopted the more modest estimate, and summarized the findings of ENCODE by stating that “at least 20% of the genome can influence gene expression” (Van Noorden 2012). Science stuck to its maximalist guns, and its summary of 2012 repeated the claim that the “functional portion” of the human genome equals 80% (Anonymous 2012). Unfortunately, neither 80% nor 20% are based on actual evidence.

Other critics, including Sean Eddy, focus a great deal on what is called the C-value paradox: Given a genome of a certain size, if it was all functional — or a lot of it functional, as the ENCODE consortium has claimed — then it would all be under evolutionary pressure, i.e., you'd expect certain mutation rates to occur, but they don't. Evolutionary biology would say about 5-10% is functional, I believe, based on how much selection takes place and where. So those critics would say (and have had indeed said) a lot of negative things about results reported by ENCODE.
I suspect that the true answer, if there is one, depends on what one defines as functional and as evolutionarily conserved, by what means you measure it, and what the balance is between functionality and conservation. You pick your definitions and processes, and you accept the compromises and limitations that go along with those choices.
Caveat: I am a contributing author to ENCODE papers released in Nature in 2012.

It's good that people of your experience are contributing to SE Biology, although you may do better to transfer your answer to one of the previous questions on this topic if it is judged a duplicate. Although your answer is extensive and interesting, I do feel that it might help readers if you summarized the way the ENCODE data supports a larger proportion of functional DNA. I believe that the data were mainly RNAseq, so would I be right in thinking the argument is based on the portion of the genome transcribed, together, perhaps with data on conservation?


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How does a nerve cell adjust if O2 diffusion is interrupted?
What effects would it have on a nerve if the oxygen supply is cut off? Is there any data on this?
Does the nerve conductance velocity increase? What about the Amplitude and receptor-channels on/in the nerve?
Funnily enough it's insanely hard to come by an answer to this question, or maybe I'm just searching at the wrong places....

There should be plenty of studies on this topic. At least it is quite a well known fact that brain is one of the first organs to be affected by of oxygen deprivation.

If Oxygen diffusion is interrupted, there is a serious problem. Neurons inside of the brain slowly start to die, many other things like change in personality or the inability to process pain impulses occur if the brain is deprived of oxygen.If this is not fixed within 15 minutes it is impossible to survive.
The actual effects on the neurons are as follows:
Like in most cells the first solution to this kind of circumstance is anaerobic metabolism, the same happens in neurons but it does not last long and it is inefficient. As far as i'm concerned nerve conductance decreases in this kind of scenario and the receptors shrivel.
Well if the receptors are shriveling, they shouldn't be able to transfer impulses meaning that nerve conductance should stop.
This link to an article on the effects on the brain from oxygen deprivation.
https://www.livestrong.com/article/106179-effects-lack-oxygen-brain/

Thanks, that's what I was also thinking, I'm gonna leave the question open for a bit longer, maybe somebody can add more information, hope you don't mind.

Brian, it would be great if you can add some references to support your answer and explain a bit on how lack of oxygen affects the conductance. (Hint: ATP synthesis, Na/K pumps, Neurotransmitter release/re-uptake).

@WYSIWYG please elaborate, all I can find are general impacts on the whole human, not a single cell lol

@schokakola then I can write a new answer myself. I need some time for it. Brian is almost there. But there needs to be better referencing.

@brian please try to cite more authoritative references like peer-reviewed articles or books. Blogs are just slightly more than opinions. They are not rigourous and can miss important details. You need to find articles on effects of hypoxia on neurons which is not a very difficult to search topic. Also, you haven't taken my hint on the effects of loss of ATP on different neurological processes.

Ok I will try to find some better references and talk bout ATP synthesis.

By the end of tomorrow I will try to complete my explanation.

Also thanks for the feedback on my answer

lol thanks , also i don't care about citations, i just want to know whats true

@schokakola it does not matter whether you care or not. Citing proper references is essential as per the site policy. Answer are not supposed to be just for the satisfaction of one user; it should be useful to anyone who wants to know about the particular topic.


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I did an agar gel electrophoresis but I could not see DNA, why?
After performing a PCR, I ran the products (700 bp) in an agar gel electrophoresis along with a Genedirex ladder (100 bp), but the transilluminator did not reveal them.

Please give us information as to how your prep was done, because otherwise our guess is as good as yours.

Assuming you loaded everything correctly, if you CANNOT see the ladder, you forgot to add EtBr. If you can see ladder but no product, then there is no product, or at least not enough. You can try to concentrate or amplify your DNA sample to increase the signal, if you have anything.

I think you should check if you added following two before loading on a gel

EtBr
Loading dye

Since you can't see the ladder either, amount of PCR products may not be the reason.

The same thing happened with me again this time i could see the loading dye but not the pcr product and ladder.

One common reason you can't see your DNA is because you didn't put any EtBr / GelRed into your gel. Do you have enough PCR product to run it on another agarose gel?

When i ran the same ladder(100 bp) again on the same gel i got ladder on the gel.


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Database of colors mapped to species
I was wondering about the physics of color, and now am interested in finding out if there are any resources (databases, text files, html tables, or pdf listings) of species and their associated colors or (ideally) color wavelength spectrum.
For example, a rose bush might have a pink (flower) color spectrum and a green (leaf) and brown (stem) color spectrum. A worm might have a brown and pink color spectrum. A lion might have a yellow and brown and gold color spectrum. Wondering (a) if any of this information is captured in any form on the web (such as 1 journal article per species), and (b) if it is aggregated into a database, text file, table, or other sort of list which includes lots of species (animals, plants, fungi, rocks, etc.), so it would say the wavelength of visible light that it emits, or some ranges of it, or even a hex color range.

would be unbelievably difficult as not only do many species have multiple colors in a single individual  or change color over time but many species also vary in color from individual to individual, then you have the species that cn voluntarily change color. You might be able to find a database of pigments but not one of colors.

Pigments would work too.

I have rose bushes with flower colors ranging from white through dark yellow, pale pink to a very dark red, and a couple of rather lavender-ish ones - and that's just in my own garden.  Then there are the multi-hued flowers of e.g. iris, particularly aril iris: https://www.google.com/search?complete=0&q=aril+iris&tbm=isch&source=hp&sa=X&ved=2ahUKEwionsub3sPiAhUpJzQIHaZ9DGYQsAR6BAgHEAE&biw=1311&bih=946

FYI there is a very simple and clear answer to this in regards to minerals - https://earthscience.stackexchange.com/questions/17081/database-of-color-wavelengths-of-minerals


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Dinosaurs vs. humans
If dinosaurs were here so much longer than humans, why did their natural selection not account for higher intelligence, as is the case in humans?

Perhaps this is already answered here: https://biology.stackexchange.com/questions/11254/why-were-dinosaurs-not-as-smart-as-we-are?rq=1

Some dinosaurs are extremely intelligent, being able to use tools and make tools. However, this is a duplicate question, VTC

Welcome to Biology.SE. Even if the question is short, it is sufficient to show a good number of common misconception about evolutionary processes. I'll be brief in commenting on them and will invite you to seek for more knowledge in an intro course and related posts.
Phrasing

their natural selection

Natural selection is a concept (the concept of fitness variance in the population correlated with an additive genetic variance). Natural selection is not a thing that is owned be a population. It is not "theirs"
Your misunderstandings
Evolutionary time
Any living species on earth has 3.5 billion years of evolutionary time. There is no exception to that as we all share a common ancestor. Humans are not less evolved than a crocodile or a bacteria. We all have the exact same evolutionary time.
Evolution of intelligence
Higher intelligence is NOT what natural selection will tend to. Having high intelligence is most often rather negatively correlated with fitness.
Related posts:

Why evolution should not be equated with progress?
Why were dinosaurs not as smart as we are?

Source of information
You would make good use of a very short and very introductory course to evolutionary biology. There is a large number of free ressources online. You might want for example to consider Understanding Evolution by UC Berkeley.


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how do microtubules polymerize?
given that micro tubules are involved in so many processes in cells, it seems that such a complex "highway" would require some advanced underlying mechanism to orchestrate its assembly in a direction needed for the cell, such as towards a kinetochore. multiple search results on google and textbooks simply just state polymerization as is without explaining how these events happen. so how are microtubules polymerized and how is this polymerization oriented directionally ?

Microtubules are made up by $\alpha$- and $\beta$-tubulin units, the wiki page for this will link you to a short section on microtubule dynamics, which is the basis of how the growth & shrinking of microtubules is controlled:
Microtubules grow (by addition of $\alpha\beta$-units) and shrink (by dissociation of these units) primarily at the '+ end', which is the one in the cell periphery not at the centriole. Actually both of these reactions (growing/polymerisation and shrinking/de-polymerisation) usually happen at the same time but with different speeds. These speeds depend on whether GDP or GTP is bound by the $\beta$-tubulin at the + end, the (relative) concentration of GTP-bound free monomers and other structural proteins. Except for the GTP/GDP bound state in the mircotubule all of these factors can be controlled (or altered) by the cell through various mechanisms (some are listed on the 2nd wiki page I linked; I may add some specific ones if I have more time).

the wiki page you listed mentions MAPs and plus end tracking proteins, if a cell needed to, for example, send a mircotubule to attach to a kinetochore or orient its Golgi bodies to a specific side of a cell (like how a t cell orients its own golgi bodies before releasing its effector molecules ), would the directionality of this polymerization use a concentration gradient ? or perhaps a series of signal proteins in a cascade?       edit: just trying to get a good conceptual framework of cystoskeleton protein interactions


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What is the difference between phylogenetic tree "construction" and "reconstruction"?
When I look through papers, there are two terms

Phylogenetic tree construction
Phylogenetic tree "Re"construction

What is the difference between phylogenetic tree "construction" and "reconstruction" ?

There is no difference! In both cases, they refer to the building of a phylogenetic tree from data.
The expression 'phylogenetic tree construction' is less common.