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Does a vaccine reduce the contagion "efficiency"?
Note: I am specifically interested in the question in the context of COVID, but general information is welcome as well.
If someone vaccinated still catches the COVID, is their capacity to infect others smaller, the same, or higher compared to someone not vaccinated?
In other words, is there a relationship between the "efficiency" of infecting others and the fact that someone was vaccinated (but still got infected)?

Each individual case will be different, but in general it is useful to ask "why did the vaccinated person still catch the Covid disease?"
If they caught the disease because the vaccine had essentially no effect on them (for example, some immunocomprimised individuals who cannot generate an appropriate immune response), then they are likely to be at least as contagious as an unvaccinated individual. In fact, they may carry a higher viral load and be more infectious because of their underlying impaired immune response.
It's clear now that those who are vaccinated and successfully develop a targeted immune response against the covid virus (almost everyone for the two current mRNA vaccines), tend to have lower viral loads even if they are infected with the covid virus. This is presumably the reason why the incidence and severity of Covid disease is dramatically lower among vaccinees. The lower viral loads do indeed lessen the chance of infecting others with the covid virus, but do not completely eliminate it.

Thank you. What exactly does "virus load" mean? Is it an absolute number of the "amount of viruses" - that is there are fewer individual viruses, which all keep the same capacities of infection (so the lowered contagion is because of fewer viruses, and there are statistically less chances to get in contact with one), OR are the viruses "weakened" (possibly being as numerous as in a normal infection), so the lowered contagion would be because even if they get to the target, they are not as "powerful" as normally? (sorry for the non-technical terms)

@WoJ Your first answer is right -- virus load just means the number of virions (mature, infectious virus particles).  With the immune system responding well, fewer cells get infected, leading to lesser disease symptoms and also to reduced production of new virus particles.


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why do these sounds make a dog unhappy?
Cross-posted from StackOverflow
This is an odd one. I'm not sure it's the right place to ask, but maybe there are some sound / dog experts who can chime in? (no pun intended)
We use two sounds on our website to indicate success and failure on a quiz. Those are very simple and short sounds.
Somehow one of our customers reported that her dog was whimpering and really upset with both of those sounds. He's normally fine with lots of other sounds that dogs are typically unhappy with including loud sounds, hoovers etc. She even said it happens when she uses headphones!
Other than muting, or replacing those sounds (and upsetting other dogs?), is there anything we can do to clean the sound or detect what specifically makes them upset this or other dogs?

Just a note:  I'd recommend deleting the cross-post on SO.  Of course, it will automatically get deleted in a while, but as a general rule, it's better to keep questions on a single site.  Welcome to the site!

Thanks @rotaredom. Good to be here :) I'm still not entirely sure where it fits best... I'm pretty sure it would require some cross-domain knowledge (computer/sound processing, and understanding of animal physiology).

I get a message that "questions with open bounties cannot be deleted", so I am currently unable to delete it...

I just played the sounds on loud with my three dogs, all within a ~3 feet of me (they're sheepherding breeds, so they stay close to their human.) Not a one had a reaction, though I tried several times. My youngest dog, though, a Belgian Tervuren, is very sensitive to sound, and whimpers when I play the live version of Jeff Buckley's "Hallelujah" in the car. Not the regular version, mind you, just the live version, which is much more tender (as if that's possible.) So, my guess is that your main assumption is wrong. One dog only.

P.S. I love your pun!

Thanks for willing to experiment on your three dogs, @anongoodnurse. I thought about doing it, but I don't have a dog, and wasn't so comfortable trying out something weird on strangers' dogs. That's already very useful. At least it's good to know that it's not a widespread issue... at least with the current sample of 1 out of 4, ;-)

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Can the Staph streak method be used for culturing Neisseria on blood agar?
What I learned in class:
Normally chocolate agar is needed to grow Haemophilus and Neisseria. The Staph streak technique can be used for culturing Haemophilus on blood agar by allowing the Staph to hemolyze the blood so Haemophilus can grow around it.
My question:
Is there a reason this method couldn't be used for Neisseria as well?

It depends on your species of Neisseria.
N. meningitidis grows on BAP (Blood Agar Plate), with colonies being grey and unpigmented on  appearing round, smooth, moist, glistening, and convex, with a clearly defined edge
You can read more about that here.

N. gonorrhoeae is known not to grow on BAP.
More on that here.

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White blood: cells concentration
Anyone knows of a table with average concentration that can be found in  white blood?
Something like:

Neutrophils - 80%
Mast cells - ?%
Dendritic cells - ?%
B cells - ?%
Helper T cells - ?%
Killer T cells - ?%
Natural killers - ?%
Others - (whatever is left)
(the sum should be 100%, of course :))

Also: are helper T cells and killer T cells visually different? I can only find pictures of T cells, but not of each. I am also unable to find pictures of natural killers. - Thank you!

You mean the concentration of these cells in the blood of "normal" and healthy people?

Wikipedia to the rescue!

@Luigi, I have looked up wikipedia. It does not discriminate lymphocytes nor does its source.

Here are some figures from Cellular and Molecular Immunology, 8th Edition:

Hopefully they're helpful in some way.

Perfect. That's exactly what I needed - btw, do you know if (and why) it is so rare to find photos of helper T cells, killer T cells and B cells? (I can only seem to find pictures of the lymphocyte class ...)

I'm a little confused as to what you mean by photos. Like bright field, scanning electron, transmission electron, etc?

Yes, pictures of Th, Tc and B cells... I can only find picture of generic lymphocytes. (I am not a biologist!) ps: I know Th,Tc,B,etc are all lymphocytes, but I would like to have pictures of each, if those exist. Do you think they do?


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What allows for no selection pressure against non-coding DNA?
Genomes of prokaryotes tend to have a higher proportion of coding DNA to non-coding DNA in their sequence than eukaryotes.
This means that either eukaryotes accumulated lots of non-coding DNA, much of which is regulatory, in the course of evolution — or that prokaryotes lost this proportion of non-coding DNA.
In order for transcription of a particular gene to occur, it seems that there must be some search performed on the DNA sequence to find the gene to be transcribed.
This search seems to be independent of the sequence length — if it weren't, that could act as a selection pressure, inducing loss of DNA that doesn't do anything. Therefore, it seems that the method by which this search is done must be O(1) — that is, it takes a constant amount of time to complete the search, regardless of the length of the sequence.
Such a method would be most welcome in computational sequence searches (in place of BLAST for example).
My question is, what, if anything, is currently known about the process of transcription that could explain this constant search time?
Or, if I am completely wrong in my assumptions, what are more reasonable assumptions?

can you add some references to the 'facts' you present in the question? (i.e. "genomes of prokaryotes tend to have a higher proportion of coding-DNA")

It doesn't take a constant amount of time, but the deletion of a single non-coding sequence is not going to noticeable change that time. more and more functions for introns are discovered everyday, so their may be far less junk than we think. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3325483/

I know this is a losing battle, but for the record: Very little eukaryotic non-coding DNA is regulatory.  Almost all of it is truly useless, and the simple reason for this is that there are many mechanisms that allow DNA in the genome to expand, and very few mechanisms that can safely remove non-functional DNA; it's therefore more adaptive to ignore the large amounts of harmless but useless DNA than to try to trim down the genome, which would provide very small benefits compared to the risk.

A) Here's the thing about evolution - just because something might have an adaptive benefit does not mean that trait will evolve ; this is contingent on the occurrence of the necessary mutations to produce a phenotype in the first place.
B) There are multiple copies of the transcriptional machinery (RNA pol, Transcription Factors) - numbering in the tens of thousands when you are talking of the core transcriptional machinery.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC84381/
The 3d structure of chromatin , as well as the large amounts of the core transcriptional machinery, prevent there from being too much adaptive benefit to losing large amounts of noncoding DNA.
C) Thirdly, there are suggestions that enhancer promoter contacts, which can greatly facilitate transcription, may be in some part at least determined by sequence motifs in the loops that bring together enhancers and promoters ; so there would be costs associated with losing ncDNA en masse. See www.nature.com/ng/journal/v48/n5/abs/ng.3539.html
D) Indeed, even when one looks at repeat elements derived from endogenous retroviruses, there are those that are of functional significance; Syncitin (which actually codes for a protein) is responsible for trophoblast fusion + placenta formation (See https://www.ncbi.nlm.nih.gov/pubmed/10693809 )  , and there are multiple repeats that themselves serve as enhancers of interferon response genes. See https://www.ncbi.nlm.nih.gov/pubmed/26941318


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FPLC based separation of serum proteins
I am working on a project which involves bio-marker discovery in neuro-developmental disorders. I have an akta-prime FPLC instrument in my lab but I do not know how to use it.
According to theory, plasma, or serum, normally contains numerous proteins of high molecular weight — which might mask the concentration of small-molecular-weight proteins that could be relevant to my study.
I am looking for the abnormal expression, if any, of such protein molecules.
But I am concerned that if I run the serum sample directly, I will get too many bands to allow me to identify my desired molecule.
Which column should be used to separate such masking proteins from serum — or, alternatively, what previous separations should be done?
Also, what reagent concentrations should I use (particularly re: binding buffer and elution buffer)?

Firstly, may I suggest 2D electrophoresis as a technique for identifying differences in protein/marker expression levels. This technique will give you greater resolution and ease of comparing your sample in basically one step/experiment. Added bonus once you determine your protein of interest you can easily excise it and send for mass spec analysis to identify your protein. In short, 2D electrophoresis separates protein based on their pI(isoelectric point) in 1st Dimension and then by their size in the 2nd Dimension. Once you identify the protein of interest you can purify it using the below steps.

Image Source
Now onto tackling the problem of separating your proteins for analysis. The general outline you can follow to separate a protein, is a follows:

Ion Exchange Column
Hydrophobic Interaction column (HIC)
Size-exclusion Chromatography (SEC)

Ion Exchange first because you elute the protein off the column using increasing concentration of salt (0 --> 1M of NaCl). Whereas you need a high concentration of salt to load the protein onto HIC column. So, the elute from setup 1 can be easily spiked with a 5M (Nh4)2SO4 and loaded onto HIC column (No dialysis). Also, Ion-exchange and HIC are high capacity columns whose resolution can be improved with shallow salt gradients.Hence my recommendation to be used first. However, if you are certain your marker/protein of interest is small you can directly use SEC column
Ion exchange column, as the name suggests, separates protein on the basis of their charge (Least ---> Most Ionic, also note charge +/- of the protein at that pH matters). The buffer to use for Ion exchange would be:
 1. Binding Buffer
    10-50mM Phosphate Buffer pH7.4 (plasma pH)
    0-25mM NaCl
 2. Elution Buffer
    10-50mM Phosphate Buffer pH7.4
    1M NaCl

Use low salt as possible to get the most efficient binding to the column.
Elution is done with a gradient of NACL from 0% of elution buffer to 100% Elution over about ~20 column Volumes.
HIC column separates the protein on the hydrophobicity of the protein. The order of the elution from the column is least --> most hydrophobic.
1. Binding buffer
    10-50mM Phosphate Buffer
    1M (Nh4)2SO4
 2. Elution Buffer
    10-50mM Phosphate Buffer
    (No Salt)

You can find a good protocol for HIC here. The elution is also done over ~20 CV with a gradient of 0-100% elution buffer, similar to Ion exchange elution.
Finally, size Exclusion or SEC separates proteins based on their sizes. The elution order is biggest ---> smallest size. The column is run in an isocratic mode i.e only one buffer used.
Buffer composition:
1. 50-100 mM Phosphate Buffer
2. 150mM NaCL

The salt in buffer is to prevent non-specific interaction of the protein with column, which might result in protein eluting later than necessary. This might result in poor resolution.
The most important thing to realize is each of the above column have their own sets of cavets. 1) Ion exchange columns are specific to the charge of protein, so you will end up having a lot of protein not binding to the column at all based on type (anion/cation) of column used. 2) Similarly, HIC column might not bind well to your protein as well. Also, adding 1M (Nh4)2SO4 will precipitate proteins which might include your protein of interest. 3) SEC columns have an upper limit on protein size they can accept, above which all the protein elute together at the void volume decreasing the resolution(However, this shouldn't be a problem in your case as you trying to separate out the lower molecular weight protein from the higher weight ones.)
Finally, all the above step work great considering you know the protein you are looking to purify(separate). Since that is not the case you will have to collect and run SDS-gel Electrophoresis of the fractions at each column purification stage. Also, run a side by side comparison of control and sample plasma to figure out which protein is being expressed differently.
In closing, I would like to point out that 2D electrophoresis gives you a gel to compare, as shown in the pic, anyway. So it might be a better solution to your problem. However, I do admit you might have to setup purification to confirm your findings.
Hope that helps, good Luck!


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Sterilize/disinfect sugar for lab use
How do I sterilize/disinfect ordinary table sugar for lab use?
I'm using the sugar in an agar and I want it to be as clean as possible. Are there any effective, conventional ways of doing this?

Autoclaving media with carbohydrates (or sugar solutions on its own) is not a good idea for two reasons:

The Maillard reaction: This occurs when you heat mixtures of amino acids and sugars. The amino group of an amino acid reacts with a carbonyl group of a sugar, fusing the two molecules together. This is a common reaction in the kitchen which is for example responsible for making the bread crust brown. It also changes flavors.
Caramellization: This is the heat induced breakdown of sugars - also leading to brown products, but much more undefined than the Maillard reaction. What products arise depends on pH, temperature and other reactands.

Both reactions may lead to products which can be inhibitory to microbe growth and should be avoided. There is also a paper which analyzed the effect of autoclaving on sugars which might be interesting to read in this context (see reference below).
So prepare a higher concentrated stock solution of your sugars, which can then be added under sterile conditions to your autoclaved and cooled down media or the agar solution (still warm enough to pour).
Sterilize this solution by filtrating it through a 0.2µM filter - depending on the volume either through syringe filters or through bottle top filters.
Make sure to maintain sterile conditions.
References:

Sugar degradation during autoclaving: Effects of duration and
solution volume on breakdown of glucose


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Don't the radioactive labeled molecules of dNTPs or DNA harm themselves or their surroundings?
I'm reading some papers for the first generation sequencing methods and some earlier than them, like Ray's Wu first time DNA sequencing from a λ phage virus cohesive 5' ends. Ray Wu, like Maxam-Gilbert and Sanger, used 32P / 3H to label either dNTPs or DNA molecules.
But what happens if you add such radioactive materials inside a test tube with DNA and other molecules like DNA Pol I? For example,  32P emits electrons at 1.709 MeV. Couldn't these high energy electrons harm the DNA or Pol I molecules (bonding destruction), that are present nearby at the time of reaction?

Experimentalists pretend, or act as if, those effects are negligible, or miniscule.  One could calculate the number of DNA or protein molecules that are affected, by plugging in the specific activity of the dNTPs, the concentration of the potential targets, the volume of the reaction, and the time.
Certainly if you create radiolabeled nucleic acids and store them, then over time those strands will undergo scission as the phosphorous emits it's beta particle.  Some of the neighbouring bases might be hit.
If you pulse label growing bacteria or phage you can then mutagenize and select for mutants in interesting pathways (this was called radiosuicide and was invented by Clarence Fuerst).
It is also possible to label bacteria and feed them to C. elegans such that the progeny of those worms will contain new mendelian mutations induced by the radioactive DNA in their mothers' germline.

Thank you very much. Your answer is very informative. I liked the use of "pretend" verb. Do you have any paper in mind "counting" the destroyed molecules from such chemical agents?

It's worth considering how many high energy electrons are actually released compared to the number of molecules in the tube. For instance, I routinely work with $^{32}P$-labeled DNA, and measure the specific activity of samples by scintillation counting. For me, a very hot stock sample of labeled DNA (~1000x more concentrated than I would use in an experiment) will register on the order of $10^8$ disintegrations per minute (dpm). That means each minute, about $10^8$ beta particles are emitted by decaying phosphorous atoms inside the sample. But the amount of DNA molecules in that same tube is about 50 pmol, or about $3 \times 10^{14}$ molecules.
So if each of those beta particles were absorbed by a DNA molecule in the same sample, thus damaging it, that would be a rate of self-damage of $10^{-6} min^{-1}$. Of course, most of those beta particles actually make it out of the tube, so the actual rate of self-damage is much lower still. Since we're probably interested in measuring processes on much shorter time scales than this self-damage rate, it becomes negligible.

Additionally, in an experiment you are generally not looking at the properties of a single molecule. If you were sequencing this DNA, for example, it is exceedingly unlikely, especially given the calculations in your answer, that the majority of bases at a single position would be mutated and therefore affect the result.

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Can fruit fly larvae eat plastic?
I highly doubt that fruit flies or their larvae can digest any plastic used in everyday products. But are there any documented cases where they attempted to eat plastic? I ask this because last Sunday I was setting up a Wii U at my grandparent's house. It had been in this plastic bag that has been sitting in the same room for about three weeks because I only use it at other people's houses and is never set up in my house. This plastic bag was similar in shape and size to many re-suable grocery bags that supermarkets distribute, example Whole Foods. But this bag was made entirely out of plastic. Of course I don't know what type because it wasn't recyclable. It was also more rounded on the edges. Okay, here comes the biology part. I took the Wii out and there were light-brown, rice-shaped and approximately rice-sized "things" on some of the controllers, the power adapter and on the inside of the bag. There were a couple of fruit flies flying around when I took everything out. This immediately led me to believe that the "things" were fruit fly larvae, or dead larvae. I came to this assumption because in the past few weeks there have been more fruit flies than normal in my house, probably because of compost staying inside for too long (in a container in the kitchen sink) and a few too many rotting bananas that weren't eaten or disposed of for a while. And after seeing two or three live flies flying around the controllers I assumed that's what it must be. When searching for fruit fly larvae on Google Images the best picture that represents what I'm describing is this. There were also smaller brown dots where the larvae were and in some places they were not. I don't know what these are. They are smaller than 1mm in diameter. I understand that the flies probably thought that the bag was a dark and safe place to reproduce, but there are two things that I could not figure out, and they seem to be related. One of the Wii remote controller's strings (handles?) was dark brown and slightly wet. It looked like it had been soaking in muddy water. I was very confused by this. I took the bag outside to try and empty it but the supposed larvae were stuck to the inside of the bag. What did fall out of the bag that I missed before was a black ball about two inches in diameter that was also slightly wet upon touching it and was apparently plastic. There were a couple larva on it as well. The bottom of the bag looked like it had some plastic removed from it. This led me to believe that larvae had eaten some of the bag and detached it from the bottom. And somehow this ended up in the form of a ball. (Not a perfect sphere, but round.) I really wish I had taken more time and examined it more to confirm that it was from the bag. I don't have pictures of any of this because everyone was pressuring me to throw out the bag and clean off the equipment, apparently not caring about what actually happened. I also don't have pictures of the Wii remote string because I cut that off and threw it away as well. I later realized that I should have taken pictures because it is so difficult to describe. I began thinking of explanations for each part of what happened. My hypothesis is: Fruit flies in our house reproduced until there were too many to be sustained by the amount of food that was available. This probably happened when there were no bananas left or compost had just been taken outside. Some found the bag which was dark and safe, so they reproduced there. There wasn't any food for the larvae so they tried to eat the plastic that they were on but couldn't digest it, so they died.
This is way longer than I wanted to it to be...
So it comes down to these questions:
1. Would fruit flies lay eggs where there is no food?
2. Would fruit fly larvae attempt to consume something that clearly wasn't food?
3. What are the small dots on the adapter?

the dots look more like the fruit fly poop...

That's what I was thinking. Still doesn't answer if they were eating the plastic though...

Why do you think they eat plastic? I'm not able to find anything about that, I doesn't seems logical for me because the fruit flies lay their eggs in the fruit because their larvae need fermenting fruit to develop.

Can you give a better description of the 'black ball about two inches in diameter'? The most obvious explanation would be that it was a piece of fruit of some sort. It rotted, leaked on the remote before it dried out and the associated fruit fly population then starved (after crapping on everything). The photo definitely shows fly excreta, and flies can't eat plastic, so they were eating something...

arboviral - I think you might be right about the fruit. I don't know why I hadn't thought about that before. It seems so obvious now. There must have been some sort of fruit, probably a piece of a banana that was in the bag and stayed there for a while. It don't remember it smelling like any particular fruit at the time but maybe that's because it had been eaten. And the fruit must have stained the bottom of the bag and that's why it looked damaged. I left a banana in a plastic lunch bag one time for a few days and after it rotted I couldn't get the stain out.

As someone commented, it seems likely that this was just caused by a piece of fruit that had been accidentally left in the bag. It attracted fruit flies and for weeks they were reproducing.


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What is the contribution of the cockroach to the ecological environment?
I've read a lot about cockroaches but was unable to find how they contribute to the ecological environment. Does anyone know?

What do you mean with "contribute"?

They make more cockroaches. They also feed things that eat cockroaches, eat things that are eaten by cockroaches, and transmit microbes that are transmitted by cockroaches. Et cetera.

Their main contribution to my kitchen ecosystem is that they keep the floor clean.They do that mostly at night, a nice example of co-evolution.

Short answer
Cockroaches are an integral part of the food chain.
Background
Cockroaches are an important source of food for a number of organisms, such as arthropods, birds, and mammals. As such, they are an important part of the food chain. Cockroaches also play an important role in nutrient recycling. Most species of cockroach are detritus feeders and with the help of endogenous cellulases play an important role in degrading plant material. Some species, such as Cryptocercus, feed directly on wood and play a major role in lignocellulose digestion in temperate forests.
Reference
 - Bell et al., Integr Comp Biol, 2008; 48(4): 541-3

They don't have to "contribute" as such. All they have to do is survive and pass on their genes to their offspring. Any benefits that they have (in terms of detritus cleaned up, etc.) or harms that they cause is purely coincidental.
There's no "desire" on the behalf of species to make things "better". All they "do" is try to survive in their existing environment but not make it "worse" for themselves. A species wouldn't survive very long if it ate all of the food in an area or if its waste products polluted the area to such an extent that they couldn't survive.
However, that doesn't mean you can simply remove a species from an environment and not cause actual harm to that environment. The environment includes all the other species that co-exist and they have all evolved in the presence of each other. This means that other animals have evolved to cope with the fact that cockroaches prey on them, others have evolved to eat cockroaches. Remove the cockroaches and the population of the first species will explode and that of the second will collapse. This will have knock on effects to other species in that environment and so on.

You must read this article:

“Most cockroaches feed on decaying organic matter, which traps a lot
  of nitrogen,” Kambhampati said. “Cockroach feeding has the effect of
  releasing that nitrogen (in their feces) which then gets into the soil
  and is used by plants. In other words, extinction of cockroaches would
  have a big impact on forest health and therefore indirectly on all the
  species that live there.”

http://www.huffingtonpost.com/2012/06/21/cockroaches-good-environment-nitrogen-cycle_n_1614913.html


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Recessiveness of allele for protection of organism
Heterozygous organisms profit from pairs of gene alleles. Harmful alleles when being recessive can be carried without any harm for the organism. Only when two harmful recessive alleles form a gene the negative effect is produced. As described in wiki article on allele:

A number of genetic disorders are caused when an individual inherits two recessive alleles for a single-gene trait. Recessive genetic disorders include Albinism, Cystic Fibrosis, Galactosemia, Phenylketonuria (PKU), and Tay-Sachs Disease. Other disorders are also due to recessive alleles, but because the gene locus is located on the X chromosome, so that males have only one copy (that is, they are hemizygous), they are more frequent in males than in females. Examples include red-green color blindness and Fragile X syndrome.

But some illnesses are carried by dominant alleles (from the same article):

Other disorders, such as Huntington disease, occur when an individual inherits only one dominant allele.

My questions are:

How does harm from alleles correlate with their recessiveness? Generally speaking, do harmful alleles tend to be more recessive?
How does benefits from alleles correlate with their dominance? Generally speaking, do "beneficial" alleles tend to be more dominant?

Very harmful dominant alleles tend to go extinct --> harmful alleles found in a population are usually recessive.

following up on fileunderwater's comment - dominant alleles (if complete) are exposed to selection every time they occur, recessive only when they are homozygous, which means recessive alleles with deleterious effects can persist at low frequencies easily (see Rice 1984 for a discussion related to X chromosome linkage and hemizygosity in males: http://www.jstor.org/stable/2408385?seq=1#page_scan_tab_contents) Novel deleterious mutations are not necessarily biased to being recessive as far as I know.

Instead of dividing mutations into two classes, dominant vs. recessive, consider categorizing them into classes based on how the mutation affects the gene--or the gene product.  This yields loss-of-function (lf) alleles, that reduce the activity of the gene, or its product, and gain-of-function (gf) alleles that act as if they somehow increase the activity of the gene, or its product.
The logic underlying this classification was described in this classic reference: Muller, H. J. 1932. Further studies on the nature and causes of gene mutations. Proceedings of the 6th International Congress of Genetics, pp. 213–255.  Since this was before DNA had been shown to be the genetic material his arguments are based solely on the phenotype of animals carrying various combinations of chromosomes.  In particular he relies on genetic duplications and deficiencies (or deletions).  In this nomenclature + indicates a chromosome carrying a wild-type (wt) allele of the gene, and m indicates a chromosome carrying a mutant allele of the gene.  So if an +/m animal appears Wild-Type then that allele is recessive.  Similarly, if an +/m animal has a Mutant phenotype then the allele is dominant.
There are two types of lf alleles:

a hypomorph is a partial reduction in function and retains some residual gene function (e.g., a weak missense mutation, or a temperature-sensitive (ts) mutation. A hypomorph is recessive to a wt allele.
an amorph is what we would call a true genetic and molecular null allele, a complete knockout of the gene, where there is no measurable function left (e.g., a nonsense mutation early in the protein coding region, or a small deletion that only removes a single gene).  Amorphs are normally recessive to a wt allele (but see below for an exception)

There are three types of gf alleles:

a hypermorph that elevates the level of the wt gene function (e.g., a promoter mutation that removes a negative regulatory site, leading to increased expression). Hypermorphs are dominant.
an antimorph, or so-called dominant-negative (dn) allele that produces a mutant gene product that somehow interferes with the wt gene product (think poison product as one model). Antimorphs are always dominant over wt.
a neomorph, an allele the results in a completely new gene function (e.g., if a glycolytic enzyme acquired sequence-specific DNA-binding activity, perhaps from a gene fusion event(?)). Neomorphic alleles are extremely rare and almost always dominant over wt.

So we have a straightforward mapping of lf alleles to recessive phenotypes, and gf alleles to dominant phenotypes.  However there is an important exception to this simple scheme for genes that are dose-sensitive, or haploinsufficient. These are dominant lf alleles. For example, when halving the level of the gene product causes a mutant phenotype: +/null. Some well-known examples from the developmental genetics of model organisms are the Ubx gene, and the Notch gene from D. melanogaster.
Further discussion of these terms can also be found in Wikipedia

Can you add references to some of your claims (e.g. "Neomorphic alleles are [...] almost always dominant over wt")?

@fileunderwater Done. As I recall, Muller did not discuss the fabled recessive neomorph as a category in his paper, and it is not clear to me if there are known examples of recessive neomorphic alleles, however my understanding is that this class remains a formal possibility. In general the literature treats all neomorphic alleles as dominant.

Honestly, I think the whole concept of recessive and dominant is unhelpful when trying to understand genetics and we'd be better off teaching the concepts in this answer from the very start.

Harmful alleles can be both recessive or dominant. They do not tend to be more recessive or more dominant. But, you must look at it from a population genetics point of view. When a allele is dominant, it tends to be a highly selected for trait, an analogy of this would be black eyes are a dominant trait compared to blue eyes or green eyes, which is why you see so many people with black eyes in the world than blue.
So therefore dominant alleles are highly selected than recessive ones and when a dominant trait is harmful, the subject tends to get killed off or the line is destroyed in the process by the natural course of reproduction. What remains are recessive alleles which do not get a chance to attain recessiveness and are therefore carried forward by evolution as passenger, never expressing themselves until they get the chance to attain homozygous recessive state.

Welcome to Biology! Could you add a reference or two please?


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How do nuclear membranes form during Telophase of Mitosis/Meiosis?
During Telophase, homologous chromosome pairs reach the poles of the cell with the help of microtubules. From there, nuclear membranes form around each new set of chromosomes.
My confusion originates from a single question: How did these nuclear membranes form around the chromosomes?

I think that is a great question, but as far as I know not a great deal is known about the process. The nuclear membrane, as depicted in textbooks, is contiguous with the endoplasmic reticulum. So when the nuclear envelope breaks down it would seem like the membrane components join a pool of structures poised to reform. In the first published experiments using nuclear extracts from the eggs of X. laevis, just adding purified DNA from bacteriophage lambda could enucleate membrane formation.

According to this book, during disassembly of the nuclear envelope, the nuclear membranes are broken down into vesicles. The nuclear membranes reform at the end of mitosis as the vesicles bind to the surface of chromosomes and fuse with each other to form a double membrane around the chromosomes (how this happens is not clear, except that integral membrane proteins and lamins may be involved, but physical contact is supposedly the first step).


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When we laugh or run for sport which autonomic system works?
When we laugh or run for sport which autonomic system takes place in this time?
While I am not sure what happens in heart while laughing (tachycardia or bradycardia), but for sport running I'm sure that the heart has tachycardia. Does it mean that the sympathetic system works there (or there isn't relation between them)? If it does, then I really don't understand why being anger cause damage to the cardiovascular while sport running said to be healthy for the cardiovascular system, here are both activate the sympathetic system. Isn't it?

For laughing, our parasympathetic system works: "Breathing is the only function of the autonomic nervous system that can be consciously regulated or changed. It encourages deep diaphragmatic breathing, which stimulates the parasympathetic nervous system. This is the cooling branch of the autonomic nervous system and is the opposite of the sympathetic stress arousal system. This helps in relaxing the aroused state of a person and provides a sense of calmness." (See here: https://www.laughteronlineuniversity.com/laughter-good-nervous-system/)

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


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What's unique for vitamin B-12 group?
I've been trying to figure out what makes the vitamin B group really big with 8 vitamins.
Chemically they have different structures.
Solubility: not only vitamins from this group are water soluble vitamins (also vitamin C).
Function: not only this group of vitamins are cofactors for metabolic processes.
So what's the reason for this grouping, or why we can't include other vitamins in this group?
Also, what does the letter B stands for?

Related: https://chemistry.stackexchange.com/questions/63956/why-is-the-vitamin-b-complex-a-complex

The common scientific belief around 1900 was that the only dietary components needed to support life were protein, fats, carbohydrates, and salts.[1]  In 1912 Hopkins reported on experiments showing that "accessory factors" seemed to be needed.[1]  In 1916, some of the factors began to be characterized in the paper "The Relation of the Unidentified Dietary Factors, the Fat-Soluble A, and Water-Soluble B, of the Diet to the Growth Promoting Properties of Milk."[2]  The title itself designates two factors as A and B.  Lack of factor A seemed to be associated with various problems particularly with the eyes, and factor B with a condition similar to beriberi.  Before long, another factor was found that was associated with scurvy. In 1920, the literature had a confusion of terminology in use, and Drummond, using a variant of Funk's word, proposed:

that the substances be spoken of as Vitamin A, B, C, etc. This simplified scheme should be quite sufficient until such time as the factors are isolated, and their true nature identified.[3]

It was only later that the factors became well characterized. Vitamin B came to be known to be a complex mixture, and its components took decades to be characterized.(Wikipedia)  As components of Vitamin B came to be known, subscripts were assigned.  Some of the subscripts were assigned to compounds that later turned out to not to be fundamental and essential, and so are no longer used. Vitamin B12 took a particularly long time to characterize.(Wikipedia)
The vitamins are now well understood, and each has a specific name unrelated to the vitamin naming scheme, yet the vitamin terminology continues to be used because it is well known and useful to people at many different levels of technical knowledge. The significance of the name of the B group of vitamins is that "B" follows "A" and precedes "C" in the alphabet, and the history of discovery is still embedded in the names we use.
[1]  Hopkins FG. Feeding experiments illustrating the importance of accessory factors in normal dietaries. J Physiol. 1912 Jul 15;44(5-6):425-60. doi: 10.1113/jphysiol.1912.sp001524. PMID: 16993143; PMCID: PMC1512834.
[2] EV McCollum, N Simmonds, W Pitz. The Relation of the Unidentified Dietary Factors, the Fat-Soluble A, and Water-Soluble B, of the Diet to the Growth Promoting Properties of Milk - Journal of Biological Chemistry, 1916
[3] Drummond JC. The Nomenclature of the so-called Accessory Food Factors (Vitamins). Biochem J. 1920 Oct;14(5):660. doi: 10.1042/bj0140660. PMID: 16742922; PMCID: PMC1258930.

According to PeaceHealth:

The vitamin B-complex refers to all of the known essential
  water-soluble vitamins except for vitamin C.
Vitamin B was once thought to be a single nutrient. Researchers later
  discovered these extracts contained several vitamins.
Each member of the B-complex has a unique structure and performs
  unique functions in the human body. Vitamins B1, B2, B3, and biotin
  participate in different aspects of energy production, vitamin B6 is
  essential for amino acid metabolism, and vitamin B12 and folic acid
  facilitate steps required for cell division.

So, vitamins B have different functions, but most of them appear to be involved in the metabolism, especially of carbohydrates (Medical Libre Texts).

B doesn't stand for anything. Originally, the vitamins were name alphabetically which can be traced to Cornelia Kennedy's 1916 Master's Thesis. What separates B-vitamins (and all vitamins) is there function. The function of B-vitamins is in metabolism and certain metabolic cycles, such as the Citric Acid Cycle.
Citations:
http://vc.bridgew.edu/cgi/viewcontent.cgi?article=1029&context=mahpls_fac
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772032/

Please cite a reference in support of this assertion about B vitamins being classified as such because of an involvement in metabolism. It may be true, but I find it strange as the requirement for a vitamin must have been established before its function was known.


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Is it possible to stop yourself from going into shock?
https://en.wikipedia.org/wiki/Shock_(circulatory)
I was helping someone move a refrigerator down steps and it slipped while I was holding a sharp corner and it sliced my finger and there was continuous blood flow. Soon after, I started feeling light-headed and was shaking and felt like I was about to pass out or have an attack, but I could not allow myself to appear weak, so I fought against it mentally and I got past it without anyone observing any signs. Did I avoid circulatory shock? Did pure mental dedication allow me to surpass such a thing?

Is it possible to stop yourself from going into shock?

There are different types of shock: hypovolemic, cardiogenic, anaphylactic, septic, neurogenic, etc.
Can you prevent yourself from going into shock by virtue of pure willpower? No. You cannot override the body's reactions to decreased oxygen to the brain any more than you can will yourself out of the flu.
The early signs of hypovolemia (blood loss), though, can be confused with those of vasovagal syncope (simple fainting). Both involve dizziness/lightheadedness, cool or clammy skin, and a decrease in blood pressure. However, with hypovolemia, your heart rate increases to compensate for the lowering of blood pressure (which eventually leads to shock), whereas with vasovagal syncope - which can occur with sudden fear - your heart rate drops, which is what causes your blood pressure to fall.
Passing out due to blood loss depends in part on how rapid the blood loss is (the more rapid, the earlier on might pass out) and the volume lost. To lose enough blood to pass out, a healthy, normally hydrated person would need to lose about 2 liters of blood (or 20% of one's blood volume); maybe 1.5 liters if it happens quickly enough.
Regardless of whether it happens slowly or quickly, if enough blood is lost, shock will ensue. No amount of willpower will stop it.
Interestingly, the sight of blood or having your blood drawn are frequent triggers of vaso-vagal syncope.
What you experienced is commonly called pre-syncope: the feeling of lightheadedness as though one might blackout, but consciousness is preserved.
Vasovagal syncope
Hypovolemic shock
HEMORRHAGIC SHOCK

+1, but I have heard an MD telling that she would faint when blood loss occurred with herself/her loved ones while she wouldn't faint when performing surgery in the OR. I guess I have the same thing - I fainted when a doctor drew blood from my baby, but I am totally sure I could draw blood without problems from someone else I didn't know. I don't faint when they do it to me either. There is something going on in terms of will power / professionalism /emotional involvement that may keep one from fainting.

There was a fellow medical student in my class who would faint at the site of anyone's blood, his or someone else's, every. single. time. Unfortunately, the profs had no sympathy, and we witnessed him pass out during most of our hematology labs where pinpricks were needed. The thing with you is emotional - you are more concerned about your child than yourself. That's not at all uncommon in parents. We often tell parents to avert their eyes when doing bloody procedures on kids. (My adult friend passed out when I was ministering to her daughter's cut in my kitchen. And she's stoic.)

@AliceD, Fainting due to a small loss of blood (50 mL?) during blood drawing is not caused by shock, but by a vasovagal syncope triggered by pain and looking at blood. In this reaction, the vagus nerve temporarilly slows down the heart rate, which causes a drop of blood pressure and hence fainting. You may be able to learn to prevent such a reaction. In hypovolemic shock, you lose a lot of blood (700 mL+), which again causes a drop of blood pressure. You can't convince yourself that you did not lose blood; still your psychological reaction to blood loss may aggravate or postpone shock a bit.

I seriously doubt you lost 750mL of blood, the 15% where they wouldn't even treat you, according to your linked article, which is the equivalent of a full bottle of wine, from that cut. Even if you had sliced your finger off completely, I doubt that you would have lost that much blood. You would need to sever an artery...
750mL is less than two units of blood that you would give donating blood, and they are hardly concerned with putting anyone into shock at a blood drive.
You likely had a vasovagal response (syncope) to the sight of the blood.
Now if you were in a car accident and the guard rail had impaled you....


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Typical neuronal firing rates across the human cerebral cortex
I would like to find a scientific article (or articles), which would summarize typical neuronal firing rates in different parts of the human cerebral cortex.
Any good references on this?

Here's a good reference to start you off where you can access an atlas of different properties of neurons.
Cell types from the Allen Brain Institute
Remember that when you say typical firing rates you have to specify what kind of cells you are talking about because interneurons can fire faster for example than pyramidal cells. Also there are differences in basal vs active firing rates.


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Is there any websites that provide the DNA sequences of food samples?
We can get many DNA sequences at NCBI websites for free. Is there any websites that provide the DNA sequences of food especially meat, for free?
When I read papers regarding food authentication, they only stated the exact DNA sequence for the primers only, not the DNA sequence of their food samples. Why primers? Is it because scientists from the same field can guess what the sample's sequence will be?
Alternatively, if there's no site that shares the DNA sequence of food samples, is there any other place where I can get DNA sequence of mixed species or mutation? For free.

They use primers because the DNA of an animal is enormous and they only want to amplify a certain part of the DNA that can help them distinguish one species from another. As far as I am aware, for food fraud purposes DNA sequencing is not routinely done (just because it is quite a resource-intensive process), instead simple electrophoresis is used to separate fragment size. So the sequence itself doesn't matter - it's the fragment length that is used to distinguish species and detect meat/dairy fraud. However I'm sure sequencing will be used more commonly for this purpose in the future.

Thank you for your valuable explanation. Just to clarify that I understand the big picture : first, use primer just for amplification - then amplify (PCR) - then use electrophoresis -  then bands appear - results: band with length A belongs to species X, if length B then species Y, and so on. If wrong please correct me. So they don't need compare the amplification product with any database of species' DNA sequence? That seems nice..or maybe I dont understand its drawback. Why do you said sequencing will be common for food fraud in the future? I'm interested in knowing that.

Yes, you can compare the length of the PCR product to a known database of species, presumably knowing what species to expect. Sequencing is still a relatively expensive and intensive technique, but as it becomes cheaper and easier it will probably become more popular since it's more sensitive than electrophoresis and gives you more information. There are other genetic technologies used in food fraud as well. I don't have time to write this up as an answer now, but will do so later and add more details if nobody beats me to it.

Thank you so much! In my opinion i've read many papers and some books on dna-based food authentication and dna sequencing, but without basic knowledge on biotech (only high school bio). i got confused thus mixed them up..thanks for clearing me up. other than drawbacks, i am interested in how PCR product is compared with the database part also.. thank you for sharing your knowledge even in your busiest time.

I am not aware of any websites that provide full DNA sequences for food products specifically. In the context of your question, by "food samples" I am assuming you are chiefly referring to meat, fish, and dairy products (the headline-making categories of food fraud), although similar principles are applied to plant products, oils, rice, and other natural products.
PCR
There are a wide variety of genetic techniques used to detect food fraud or adulteration. These techniques do not look at the entire genome of the animal or plant from which it is derived – that would be extremely expensive and unnecessary. Instead, scientists look at particular parts of the genome that they know will likely help them distinguish one species from another.
This is where the primers come in. DNA primers are short segments of DNA that are used to initiate replication of segment of DNA, and is the vital component of PCR that determines which part of the genome will be amplified. Once the PCR product is amplified, it can be analysed by a variety of techniques. For instance, if the PCR products of various species are known, they can simply be run on gel electrophoresis which separates the DNA products by size. Thus if a band of an unexpected size appears on the gel you know there has been some contamination. There are also more automated methods of detecting fragment size via electrophoresis.
Examples of where these techniques has been used has been to detect:

cow's milk in buffalo mozzarella cheese (López-Calleja et al., 2004)
king bolete mushrooms potentially mislabelled as slippery jack mushrooms (Moor et al., 2002)
domestic pig meat in wild boar products (Conyers et al., 2012)

From the López-Calleja study on mozzarella, one of the gels looked like this:

The PCR was run to detect cow's milk in buffalo cheese. Lane 1 corresponds to 100% cow's milk (it is a very bright band), lane 2 is 10% cow's milk, ranging down to lane 6 which has 0.1% cow's milk (a very faint band), and lane 7 is the pure buffalo cheese which shows no band. Therefore, this assay could be useful to rule out contamination with cow's milk.
Real-time PCR
Running gels is a somewhat old-fashioned way of doing things, and there are better ways to make use of PCR technologies on a larger scale. Real-time PCR is the technique now routinely done to detect food fraud. This is a variant of PCR, which (as the name suggests) allows one to quickly see which PCR products are being produced, in what quantity, and there is no need to run a gel.
For example, real-time PCR has been used to detect:

horse and donkey DNA in otherwise-labelled meat products (Chisholm et al., 2005)
pork adulteration in commercial beef burgers (Ali et al., 2011)
Atlantic cod, Atlantic salmon, and European plaice in fish products (Hird et al., 2012)
honey containing pollen from a specific region (Laube et al., 2010)

An example of what the read-out from the real-time PCR is given below. This example is from the Ali study on beef burger adulteration. The letter A was 100% adulterated (i.e. contained 100% pork instead of beef), letter B contained 10% pork, and so-on to E which contained 0.01% pork. F had no pork. The more pork contamination there was, the sooner on the plot (in PCR cycles) the contaminant reached detectable levels:

About the sequence
As you will see from reading about these techniques, it is not so much the sequence itself which is important – it is fragment size or other properties of the region analysed by PCR that is most practically useful. Sometimes the PCR product may be sequenced for comparison purposes, although I do not believe this is done as a routine screening for food fraud.
Keep in mind that PCR is just one of a number of genetic techniques used in food safety. For example, DNA barcoding and SNPs are also useful techniques that are used in this field. The technology is constantly improving and evolving and no doubt more refined and efficient methods are being developed to detect food fraud.

This is much better than what I read by myself. Having a great teacher really makes differences. Particularly on how the fraud is detected by each technique. Thank you very much!


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Dehydration Synthesis: Why does a monomer contribute a -H instead of an H atom?
My Campbell's Biology 9th edition textbook says that a dehydration synthesis is a reaction in which water is produced while two monomers are joined together. Specifically, it makes the following statement:

One monomer provides a hydroxyl group (-OH), while the other provides a hydrogen (-H).

Sorry if this is a silly question to ask, but what I'm wondering is how exactly a Hydrogen electron joined with a Hydroxyl will create H2O? Why isn't it a Hydrogen atom (1 proton and 1 electron) rather than just the electron which moves?

The dash ("-") does not represent a negative charge or an electron.  It simply indicates that the group of atoms ( -OH or -H ) are attached (covalently bonded) to other atoms in a molecule.  So they are saying one monomer (molecule) contributes OH to the reaction and the other H.  (A charge is indicated by a trailing superscript minus sign.)

That's what I suspected, thanks for the response and for clarifying!


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What distinguishes Mendelian Inheritance from Non-Mendelian Inheritance?
I'm having some trouble determining what exactly is the difference between Mendelian inheritance and non-Mendelian inheritance. For instance, I understand that chromosomal abnormalities such as Down's Syndrome fall under non-Mendelian inheritance because they concern chromosomes, not single genes. And I also understand that Mendelian inheritance concerns single genes, as in Sickle-cell anemia (which is an autosomal recessive disorder).
What confuses me is the fact that our textbook discusses dihybrid and trihybrid (concerning 2 genes and 3 genes, respectively) crosses under the Mendelian inheritance chapter, when to me it seems like these crosses are non-Mendelian because they deal with multiple genes. However, Gregor Mendel did in fact use the dihybrid cross to deduce the law of independent assortment, so I'm completely confused. Could someone please clarify this for me? I'm afraid that I'm maybe misinterpreting something.

You can discuss multiple genes within the framework of Mendelian inheritance; what you're probably thinking of, though, is the fact that Mendelian inheritance doesn't recognize the idea of multiple genes that contribute to a single trait.
For example, if there is a gene that controls petal color (blue vs. white, with blue = dominant) and a gene that controls height (short vs. tall, with tall = dominant), then Mendelian inheritance predicts that two short plants with white flowers will only produce short plants with white flowers.
But if there are multiple genes that interact to determine height in a complex way, that's outside the scope of Mendelian inheritance.

Let me know if I understand this correctly: so dihybrid crosses in which the genes contribute to different traits are still within the scope of Mendelian inheritance, correct? And so things like epistasis fall outside of the scope?

@AleksandrH: Correct.

Okay, and so what about things like Incomplete Dominance and Codominance--are those still a part of Mendelian Inheritance or are they within the separate branch of non-Mendelian inheritance? That was also one of the things that was confusing me

@AleksandrH: Those are non-Mendelian. ("Mendelian inheritance" specifically describes traits that are controlled by a single autosomal gene with exactly two alleles, one of which is dominant and one of which is recessive.)

Thanks again for responding. So if I understand this correctly, then non-Mendelian genetics is everything else, like polygenic inheritance, epistasis, incomplete and co-dominance, poly allelic traits, sex-linked traits, mitochondrial inheritance, linked genes, etc?

@AleksandrH: Yes, exactly. :-)


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The Semi-Conservative Model of DNA Replication: Question
My Campbell's Biology textbook contains the following diagram related to the semi-conservative model of DNA replication proposed by Watson and Crick. I have highlighted where my confusion arises in red:

So, I understand what goes on in the first replication--that's pretty much straightforward. However, what I don't understand is why in the second replication, the light blue strand isn't paired with a dark blue strand. After all, aren't the light blue strand and dark blue strand complementary, per the results of the first replication?
After the light blue and dark blue DNA strands separate to serve as templates in Replication #2, why don't we see two dark+light double-helices?

A small note for the future. Ending the title by : question is really not informative as the post will obviously contain a question.

I believe the reason you are having trouble understanding the concept is due to a poor usage of colors in the diagram. Don't focus on the colors, but on the concept. It's the same for both replication events. Each strand of a double helix is used as a template to make a new complimentary strand, giving rise to two new DNA helices from the original. In each new double helix, one strand should match that of the double helix it came from before, as it was the template and is the same strand. While the other strand, the complimentary strand, has been newly synthesized to match the complimentary strand. In this diagram, every newly synthesized strand is shown in light blue.
Start by looking at the first double-helix of DNA (navy blue). During replication, the DNA is unwound and each navy strand is used as a template to create the newly synthesized (complimentary) strand, which is shown in light blue. In this first all navy double helix, you have two navy strands that are each used as a template strand and new complimentary strands (light blue) are synthesized to match . This produces the second two helices (navy and light blue). They each have one strand from the original helix (navy), and one new strand (light blue).
The process is exactly the same for the second replication event, only, a new color was not introduced to show a newly synthesized strand, so one cannot differentiate between the original (template) strand and the new complimentary strand. Both are pictured as light blue.
For the final replication event, only focus on the top navy and light blue helix first. Just as before, the two strands are separated from each other and are both used as templates to create a new strand. The navy blue strand is used as a template for a new light blue strand to be transcribed. This produces the top-most helix, where the original strand is shown as navy and the newly transcribed (complimentary) strand is light blue.
Just as the navy strand was a template, the light blue strand from the bicolored helix is used as a template strand as well to create the second all light blue helix. This light blue template strand is used to synthesize a new light blue strand, creating the all light blue helix. One of the strands is the original light blue one from the navy and light blue helix, while the other strand is the newly synthesized one.
It might've been easier if they had used a different color for the final round of replication, like orange. Then to show the newly synthesized strands in the final round, the 1st and 4th double helix would consist of a navy (original) strand and an orange (newly synthesized) strand. The second and third double helices would then have each had a light blue (original) strand and an orange (newly synthesized) strand. This would have made it easier to understand where each strand originally came from.

Thanks for your thorough response. But in the second round of replication, why isn't the light blue template strand's complementary strand just another navy blue strand? I would imagine the base pairs of the complementary strand would be the same as those of the navy blue strand. Does it have to do with 5' and 3' arrangements?

Ah, I see. This diagram is set up so that you can easily follow which strand was the original template strand that is from the original helix. The navy color is not signifying whether a strand is 5'-3' or 3'-5'. If you want to think about it like that then, yes, one of the light blue strands for the final helix, IS exactly the same as a navy strand, so it could be shown as navy.  But really, navy is used to signify the original strands of the first helix so you can follow the movement of original strands started out with. Try drawing your own replication event of a double helix to help. :)

Yep, I took your advice and drew a diagram using 5'___3' and the parental DNA does in fact end up in all of the "daughter" strands. Not sure why the book writers didn't use the navy after replication #2. EDIT: nevermind, I see what you mean. So they just represented the original parent strands with navy rather than using navy for any strand that matches the parental sequence, right?

Exactly!! In the EDIT, you have it! That's all they were trying to do.


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What's the difference between the *types* of tissue dissociation enzymes?
I'm trying to dissociate a tumor, and most protocols like NCI/NIH recommend a 10X triple enzyme digestion stock consisting of: collagenase type IV, DNase I type IV and hyaluronidase type V in HBSS. This goes all the way back to the 90s, and the recipe varies between papers (dispase, papain, neutral protease, elastases, etc.). The so-called official recipe that I've been tasked to use is composed of the above, however, mostly from Sigma-Aldrich (C5138, D5025, H6254)
I can't really find anything that says what the real differences are between these types of enzyme are, however. Or why for example type IV DNase works better than type II, and so forth. Is it perhaps that the recipe just happened to stick?

It’s years since I looked at a Sigma catalogue (before it became Sigma-Aldrich) but as I remember, these designations are arbitrary proprietary ones used by Sigma to distinguish different sources — the key point being that Sigma didn’t generally manufacture all of these themselves, but obtained the from third parties.
The other point to note is that these enzyme preparations were/are generally impure,  but to differing extents, so the type designations allowed you to re-order a particular preparation that worked, and also to specify the actual grade you used when you published so that other people could repeat your work. More expensive grades would, no doubt, also work in the sort of crude application you describe, but they would be a waste of money.
I thought the catalogues used to give you some information (organism/tissue at least), but, as I said, it’s been a long time (although be careful with your “way back to the ’90s”, young man).

Regardless of your age, 17 years is a fairly significant amount of time. Old fart.

This is kind of what im getting out of their catalog. I saw one source that said something like DNase IV works better on DNA containing lots of repeats, but I couldn't find anything else to back that up. Cost vs. activity/purity seems to be the case.

And to be fair, reading "Cancer Research 54" circa 1994 is a bit like reading a history book about T cell-based therapies.

But there's some stuff of that vintage and earlier that has hardly been added to since, especially in very chemical areas. I was trying to find info (for a SE Biology question) on sugar ring conformation in different helices and had to walk over to the library to get a book published in the 80s.


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Garden weed identification
I'd like to identify this weed found in a garden in northern England at this time of year (March).
It reproduces using underground roots rather than flowers - so if you dig it up and leave any behind it grows again.
EDIT: here's a photo with the bulb cleaned a bit.

if the leaves are cylindrical, with pointed tips, maybe Juncus spp. If you want info on how to grow (or get rid of) then ask to have the question moved to Gardening (or move yourself).

This certainly looks like a graminoid, but my guess would be a species of Poa. Very common for lawn grass, and when it doesn't get mowed they can get tall like this.

Is it possible to clean the roots in water to see the "bulb"?


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What kind of bug is this? I’m not sure if it’s a cockroach
Found this bug in my home. Is this a roach?

Welcome to the site. It is almost impossible to say from your photo as the main features are obscured, the subject is badly lit and the body is distorted (crushed?) If you had better photos we might be able to tell. Would also need a location in the world to help ID.

Rove beetle possibly.  Not sure though, and if so it's not clear what kind of rove beetle - it's a large and varied family, and the picture is a bit smudgy.  They seem to usually be harmless/not a pest species, and occasionally wander into houses from outside.  https://en.wikipedia.org/wiki/Rove_beetle
Doesn't look like any of the types of cockroach I found pictures of on a quick search.  It seems that there are several unrelated species called "cockroaches", but all of them seem to have plain antennae, not "beaded" ones like the insect in your picture, their heads are a different shape, and most of them aren't visibly segmented like that.  https://en.wikipedia.org/wiki/Cockroach
You might have more chance of finding out whether it's a cockroach just by typing "cockroach" into a search engine and looking at some of the image results than by posting here.  I mean, you've got the insect (or had at the time) and we haven't, so you can see it better.

My impression is also Rove Beetle of some kind.  The big beetle head and mandibles. the smallish partially deployed wings, exposed abdomen and "hunchbacked" look lean in that direction.  However, it's not clear if some of these apparent points are simply artifacts of the squashing it underwent, so that's just an impression.


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Understanding why the definition of life is so challenging
The Wikipedia article on the definition of life states that there is no consensus for the definition of life with at least 123 definitions being proposed.
I am unclear why this is the case.

It's really the same as https://xkcd.com/927/ - every definition has problems. Yours has problems too, such as everything most biological life does is "script-based" - possibly some emergent behavior occurs when those scripts are sufficiently complex.

"Behaviors such as avoidance and targeting." Missiles do this this and it's scripted and they aren't living. Your definition basically defines something living if it has having free will. We don't even know if humans have free will. You're going to need to implement a physical way to measure that and after you do it will eliminate a lot, if not all living things as living things. Plants, bacteria, lichen, fungi, jellyfish, insects...all non-living.

@DKNguyen Missiles in my mind fit in Algorithm (3) so would not be alive.  :-)  I am not making any statement about free will here.  :-)  Bryan Krause makes a great point.  Is there such a thing as unscripted information processing?  My suspicion is that "pain" and "pleasure" are unscripted phenomena that are still information processing at say the cell level.  I will need to read up more to better understand if this idea makes ANY sense at all.  :-)  It may not.  You make a strong case that it is hard to distinguish between (3) and (4).  Thanks for your points.

@LarryFreeman You don't mean to make statements about free will but that's what you're doing when you throw around terms like "unscripted" and "information processing at the cell level" without rigorously defining exactly what it is you mean by that. As far as can be discerned when you say unscripted you are referring to something that is not deterministic and free will is the quintessential example of that.

The other thing that should be noted about classification is that classifications are arbitrary. Humans use classification because they simplify communication and we try to make them rigorous but ultimately, things that exist don't need to follow any classification. Things are what they are. A classification that is not accurate 100% of the time is still useful if it simplifies communication 99% of the time.

You are right. My statements require rigorous definitions which I have not provided.  I need to be clear on these definitions to be clearer on my question.  Great point.  I will spend time reading existing definitions to better understand the current thinking on the topic.  :-)  On your second point, a classification is meant as a pathway to understanding.  If it doesn't help with understanding, then it serves no value since, as you point out, it is independent of the phenomena itself.  :-)

I do not see this as a question about biology, or indeed a valid question for this site. A valid question (although one that must have been asked before) is “what is the definition of life”. You seem to be asking for comments on your own answer to the latter question, which in my opinion is off-topic for a Q&A site about problems in biology. (In the Help on the type of questions not to answer it would seem to fit “I think this, am I right?”.)

Hi @David I have updated my question.  Hopefully, it is now a better question which maintains my intent and also is on-topic to the site.  :-)

Doesn't the Wikipedia page you linked already have a discussion of this? What about that is unclear?

I found the wikipedia article unclear which is why I posted the question.  Its seemed to be superficial to me.  It didn't dive into the details enough for me to what was inadequate about common definitions.  I did find the article referenced by wikipedia which I link to is an excellent answer to the question.  I thought it would be helpful to others so I added it.

Hi @LarryFreeman please don't answer the question in the original question - if you think the article you shared answers the question, summarise it and add it as an answer. Thanks.

@user438383, I respectfully disagree with your suggestion and your action.  The article provides a detailed analysis of 100+ definitions in 50 pages.  It is a great analysis.  I'm not sure that a summary would be worth it.  I like the answer that I accepted.  :-)  I will not add the link back.  I thought the link well worth reading if anyone wanted to provide an additional answer or understand the controversy on the question.

@LarryFreeman _ I found the (now deleted) link to be interesting reading and helpful. Thanks for posting it. Sorry you met with some difficulties on this site, but every site has a culture that works best when it is adhered to. Again, though, I thought the article was interesting. I'm not sure anyone benefits from its removal. :(

@LarryFreeman, sorry, didn't meant to vandalise your post - it's yours and you are always welcome to roll back any edits you don't like! The article was definitely interesting, and I think that's why it's good to have the information summarised in an answer - there's a general rule about not answering the question in the original question or in comments here - it makes the process of finding an answer much easier for visitors :)

Thanks @user438383 I believe you are right on the site policy.  I will do as you suggest.  I will post an answer to my question and reference the article.

Here is a question, at what point in organisation, from molecules to cells, does 'life' suddenly appear?
We can rephrase the question, what is the difference between 'life' and 'non-life'?
The takeaway is, that the definition of 'life', and its distinction between 'non-life', like all definitions (i.e., words and concepts) and distinctions, is based on human whim. In other words, all definitions (i.e., words and concepts) are arbitrary, and are abstractions derived from reality.
Here is another question, if we are constantly replacing the matter, that composes 'us', how do we define or distinguish an individual organism? Furthermore, how do we define an atom, in a non-arbitrary way?
These questions arise, because the distinctions we make between any two things are based on personal choice and because, we do not understand our 'reality' or universe, therefore, we cannot answer these questions.

May I add, do understand that this response may contain some errors, due to my lack of experience: I am a 21 year old, 2nd year Biology student.

I have to say that this question is really why I love learning about biology.  Despite all of our progress, there are still mysteries and still disagreements on fundamentals.  I suspect that as we build consensus on the fundamental questions such as: what is the definition of life, we will do so only after making further great breakthroughs.
I posed this question because I was told when I was in school (a very long time ago) that the definition of life was the ability to reproduce. This bothered me because it seemed obvious that mules were alive and because it misses, as per my perception, the essence of what it means to be alive.
I thought that there was an obvious definition which I posted in my original question. It is now removed because not only was it naive but it also was not actionable: it had too many ambiguities to be useful as a definition.  So, the experience of proposing a definition and failing miserably was very helpful to appreciate the difficulty in building a consensus for any given definition.
I found this article which goes through the 100+ definitions and which discusses in detail why each of the definitions has not succeeded to build a consensus.

Nice article, +1.

The Stanford Encyclopedia of Philosophy has an article on Life and gives two broad reasons for why the definition of life has been so hard to agree upon.
First, many people trying to define life are not aware that there are several different types of definitions with different uses. An example the article gives is that NASA's astrobiology lab defines life as, "a self-sustaining chemical system capable of Darwinian evolution". Some people may criticize this definition because it does not include sterile hybrids (e.g. mules, ligers). However, these people do not realize that this is an operational definition, a definition intended to help explain what a project is about. Since NASA's astrobiology lab is only studying reproducing entities, the fact its definition excludes sterile hybrids is a feature, not a bug.
Second, people disagree on is and is not alive, so they build definitions that include and exclude different entities. The original article explains it really well:

Many scientists disagree as to the
phenomena a definition of life is intended to unify. Some scientists
would include prions, viruses, and entities only hypothesized to exist
in the origin of life, while others would completely reject them. Some
might accept digital organisms as alive, others would deny this
approach.

Because life is just one type of chemical process.
There is a whole spectrum of chemical processes with complex life on one end of it and simple one way one off reactions on the other. Where a humans choose to draw a line and say "life above this line" is very arbitrary. Because of the huge variety of chemical processes it must include many factors, thus it becomes imprecise on a the finest scales because many thing fulfill some and not other parts of the definition. Worse many aspects of a definitions can be vague in and of themselves.
No matter what definition you use you can find things that could be exceptions, gray areas; small viruses that need other cells to replicate, giant viruses that have metabolisms, nucleus-less cells, self replicating polymers, sterile individual organisms.
we can all agree a sterile human is alive, but that means reproduction does not work, but a self stabilizing chemical reaction is not, yet they are both just ongoing chemical processes the only difference is how complex and how many feedback loops they have.
Life and therefore biology is a mess, different branches of biology use whichever definition works best for their purposes. This is actually very common in biology and makes sense when you consider you could be talking about extinct fossil organisms, tiny barely functional microorganisms, huge complex animals, from point of view as divergent as diagnostic medical biology, to evolutionary paleobiology, to extreme condition biochemistry. Just like no one definition of species is going to work for all of these, different definitions of life will work better for some and worse for others.
to put it a different way chemical life will keep finding any way it can to work and it does not care if a few apes can easily wrap their brains around it. this is a common issue in most sciences, humans categories don't always fit nature all that well. Is ice a rock? Is a binary planet a planet? ect.


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How to Resuspend cells at cell density of 8 log CFU/ml of bacterial culture whose CFU/ml i don't know at 600nm, also it doesn't grow well on MRS agar?
According to procedure after 24 hr growth of Lactobacillus delbruckii subsp lactis in MRS broth, I have to resuspend it at 10 raise to power 8 CFU/ml and then inoculate it further. But it doesn't grow well on MRS agar and I haven't observed its proper colonies. Is there a way by spectrophotometer that I can know how to determine its CFU at 600nm after 24 hr without having to do spread plating?

Hi and welcome. I think you might be in a pickle, but I may well be wrong. I am NOTNOTNOT a pathologist or a microbiologist, not even close, but... I think a CFU has to be a viable cell capable of forming a colony, and doesn't include cells that can't form colonies (I may well be wrong!) So visualization might be inaccurate. Are you familiar with Modified Fishman Units?nI hope someone who knows more about this than I do posts a suggestion for researching this issue.

You should be able to get colonies on various types of agar, but particularly MRS under anaerobic conditions. What are your growth conditions? There is no way to determine the CFU without doing the plating as you will find variations based on exactly which strain you have and your growth conditions, media variations etc.


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What type of beetle is this? It was on the wall in my backyard
This insect was on the wall in my backyard. I live in Southern California. Does anyone know what is is?

Welcome to the site. We would need at least 1 picture, preferably high quality and close-up of the insect/beetle in question to identify.


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Need help identifying insects in home, Morgan Hill CA
The creature in the attached photos just started appearing in small numbers in various locations inside my home. Would like to positively identify.

Yeah, I think you've got it. Lots of farmland around here, and it has been very hot lately (like everywhere else).

This is a true bug (Heteroptera), likely a nymph of the family Rhyparochromidae. Until recently, this family was part of the Lygaeidea ("seed bugs"). As their colloquial name reveals, they (mostly) feed on seeds (one exception would be the predatory Geocoridae).
Distinctive characteristics of (almost) all true bugs which are visible on the photos, are the rostrum and the scent glands (which are located dorsally in nymphs and abdominally in adults). The position of the scent glands, thus, indicates that it must be a larvae. Another indication is that its wings are still in pockets.
Determining true bug larvea to the species level is tricky and rarely done. But with some experience, it is possible to tell the families apart. Lygaeid bugs (and thus, also rhyparochromid bugs) are elongated with compact legs and antennas. Often, they have a pointed nose (a long head) and relatively large eyes. All charactericstics match with the specimen on the photo, which makes me think it must be a rhyparochromid bug.


text:
Is natural selection a tautology, and therefore not truly falsifiable?
I've heard the argument from a lot of creationists that all the evidence for natural selection (and by extension, evolution) in general is worthless because natural selection is so flexible that it could cover all the data, no matter what we discovered. In essence, that natural selection is a tautology:

Survival of the fittest. What is 'fit'? What survives.

There are other creationists, however, that admit that natural selection could be falsified. These are split into two groups:

The ones that say, if you rephrase natural selection as a non-tautology, it becomes obvious that it doesn't work:

Natural selection has been criticized as a tautology. This would be a major problem for evolutionary biology, if true, because tautological statements can't be falsified and, therefore, can't be scientific. There is merit to this critique insofar as the theory of natural selection is indeed generally described in a tautological manner. However, natural selection can be described non-tautologically if we’re careful. Natural selection should be defined as the theory that attempts to predict and retrodict evolutionary change through environmental forces acting upon organisms. However, this re-framing comes at a cost: it reveals, based on our current knowledge of evolutionary forces, the lack of ability to make accurate predictions about expected changes except in the most simple of circumstances.

And those that say that the falsifying options provided by natural science are impossible to actually use. Here are some of those falsifying options:

Charles Darwin himself proposed a rather strong test of evolution: "If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down." [Darwin1859, pg. 175]. This is the basis of claims by various intelligent design writers that various biological structures, such as the vertebrate immune system or the bacterial flagellum, are "irreducibly complex" -- they consist of multiple components that could not develop in the absence of the others. However, these structures have been exhaustively studied in the scientific literature, and scientists have demonstrated entirely plausible evolutionary pathways. See Complexity.

Famed biologist J. B. S. Haldane, when asked what evidence could disprove evolution, mentioned "fossil rabbits in the Precambrian era" [Ridley2004, pg. 66]. This is because mammals, according to current scientific analysis, did not emerge until approximately 40 million years ago, whereas the Precambrian era is prior to approximately 570 million years, when only the most primitive organisms existed on earth.
Biologists had long conjectured that human chromosome number two was the result of a fusion of two corresponding chromosomes in most other primates. If DNA analysis of these chromosomes had shown that this was not the case, then modern evolutionary theory would indeed be drawn into question. This "fusion hypothesis" was indeed confirmed, rather dramatically, in 1993 (and further in 2005), by the identification of the exact point of fusion. For additional details see DNA.
Modern DNA sequencing technology has provided a rigorous test of evolution, far beyond the wildest dreams of Charles Darwin. In particular, comparison of DNA sequences between organisms can be used as a measure of relatedness, and can further be used to actually construct the most likely "family tree" hierarchical relationship between a set of organisms. Such analyses have been done, and the results so far dramatically confirm the family tree that had been earlier constructed solely based on comparisons of body structure and biochemistry. For additional details see DNA.

Is there any way to save natural selection? To do so, we need to:

Prove it can be explained non-tautologically
Prove that it does make useful predictions
Give falsifying experiments that are reproducable and actually possible.

I'm voting to close this question as off-topic because it is not a question about biology in the terms of SE Biology, but an attempt to initiate discussion about the provability of the theory of evolution by natural selection, a topic that must have been discussed ad nauseam.

Welcome to Biology SE! Please have a look at these closely related questions: https://biology.stackexchange.com/questions/64688/the-falsifiability-of-natural-selection and https://biology.stackexchange.com/questions/40579/is-evolution-a-fact. You will find many more by using the search bar at the top of the page. If there's still something that you need to ask, please edit your question to specify exactly what is still unclear to you.

Ah, thank you. The first one I've already looked at, and while helpful was not exactly what I needed and the second I will look at. In any case, I know how to use a search bar, thanks. @David, if this topic has been discussed ad nauseam (which I'm sure it has!), could you please point me to some resources on it? Aside from one article, I'm having a hard time using Google to find anything useful.

There is a helpful discussion along these lines in Dawkins' The Extended Phenotype, chapter 10.

Fossil rabbits in the Precambrian are hardly a disproof of the theory.  It could be some rare collapse of more modern rock into an older layer ... time travel ... convergent evolution ... a spacefaring species of alien bunnies! :)  Really, as we glumly watch COVID evolving before our eyes to come back and perhaps evade our vaccines, it is hard to imagine any single piece of fossil data strong enough to disprove the whole theory.

I think @Remi.b's answer is great and really the only way to answer your questions is with a comprehensive introduction to evolution. However, I wanted to address the tautology issue more directly.
First, the "survival of the fittest" seems like a tautology with "natural selection" because it is not a description of how natural selection works, rather, it is a phrase meant as a synonym for natural selection, to help describe the result to someone unfamiliar with the phrase.
Let me use an analogy: it would be like if you were a very new learner of English, and I told you "Joe's truck has more mass than an elephant!"
If you aren't really familiar with the term "mass" in English, this phrase could be confusing. So I explain instead that "Joe's truck is heavier than an elephant." If you know the word "heavy" this is easier to understand.
However, there is a tautology there! the car is actually heavier because it has more mass, but that does not make either phrase untrue or untestable: it's just another way of saying the same thing within a context (i.e., those statements are the same if they are exposed to the same gravity).
The testable hypothesis that natural selection makes is that, given 2 things: 1) a population where individuals have traits that give them different chances of survival, and 2) some way for offspring to inherit traits from their parent(s), then the population over time will consist of individuals who are more likely to possess the traits that gave a high chance of survival.
Following this, should the environment change in some way such that a different trait is now beneficial, that trait will increase in prevalence.
There are way too many experiments to summarize here that show 1), 2), and a combination of 1) and 2), as well as experiments that show that indeed, when you have 1) and 2) you get natural selection.

Since this post just got bumped to the top of the active question list, I've got to poke. I know it'll be a pain, but I think your answer would be made even stronger for those coming across it if you can actually cite one or two or three papers that you allude to in your final paragraph. Not a must, as the rest of your answer makes your point well. But, if you have time, link/cite something here...+1 btw for simple explanation

The tautology argument is an attack on a rare phrasing and not on the nature of the theory of evolution.
First, the theory of evolution is way more than just natural selection but let's ignore that for the moment.
The phrasing 'Survival of the Fittest' was first suggested by Herbert Spencer and was later used by Darwin when he changed the title of the fourth chapter from "NATURAL SELECTION" to "NATURAL SELECTION; OR THE SURVIVAL OF THE FITTEST" (Thanks @BryanKrause for his comment).
It is before all a labelling. A catchy sentence to refer to the process of Natural Selection. In no way does it mean that Natural Selection is a non-sensical explanation.
Natural Selection is easy enough to understand for a layman that you can make you own opinion
Luckily, the concept of Natural Selection is really easy to understand. It does not take any a priori knowledge in Science to understand it and if you have a look at any intro course to evolutionary biology you will understand it yourself.
There are thousands of good sources of information on the subject online. If you want to learn about it, do not look at straw man and other fake explanations from creationist (and other religious extremist) websites! Consider for example Understanding Evolution or many of our posts on Biology.SE such as this one for example. You can also get any intro text book (see here for recommendations).
How does natural selection work?
Here is a copy paste of my answer here. It explains the very basic concept of natural selection through the so-called Lewontin recipe and gives a somewhat silly, but easy, example with a population of pens!
The Lewontin recipe says that natural selection occurs whenever:

Individuals in a population varies in terms of a given trait
This trait has some (additive) heritability. Here is one of the several posts that explain the concept of heritability. It might be slightly a post that is a bit advanced for you though but shortly speaking it means that offspring are more similar to their parents more than they are to other non-kin individuals in the population.
The fitness varies (not necessarily linearly) as the trait varies.

Simple example:

In a population, there are blue pens and red pens
Reproduction is asexual and blue pens create other blue pens while red pens create other red pens.
blue pens make more offspring than red pens.

Of course, there exist strict mathematical formulations of this process that you can learn in any introduction to evolutionary genetics.
Your questions
Note that your questions are all way too broad for a single post (and your question could be closed as too broad) but I wanted to try to give you a hand anyway.

Prove it can be explained non-tautologically

There is no "proof" in science, only evidence. But let's ignore that for the moment.
Please have a look at any intro course to evolutionary biology (see above).

Prove that it does make useful predictions

Please have a look at any intro course to evolutionary biology (see above). Afterward, you can eventually have a look at Is evolution a predictive theory?.

Give falsifying experiments that are reproducable and actually possible.

Please have a look at Demonstrable and repeatable examples of evolution which lists thousands of evidences explained in layman terms.
There are thousands (tens of thousands maybe?) of papers published every year extending our understanding of evolutionary processes! It is hard to know which one you would be interested in!
Related post
You should have a look at Is evolution a fact?

"Survival of the fittest" was Herbert Spencer's term, not Darwin's, though Darwin later referred to and used that phrasing.

@BryanKrause Thank you for correcting me. I knew it but somehow managed to got it wrong when writing! I've corrected this mistake.

I'm really interested in the history of science and it's really interesting when a rhetorical choice like "survival of the fittest" comes back to haunt a bit. It was really taken as a nice, simple way to convey what selection meant but it has been so contorted since. There are a lots of other examples of where this has happened in science (our insistence on using the word 'theory' in english, is one other example, to mean 'stuff we have figured out' instead of the colloquial 'random idea I just came up with').

Natural selection is an observation, not a tautology.  We can certainly imagine worlds - call them Disney ecologies (or for the religiously inclined, Gardens of Eden) - in which natural selection simply doesn't happen.  E.g. each species is independently created, and each pair of a species has exactly two offspring before dying of old age.
This is easy enough to imagine, just as it's easy to imagine a flat Earth enclosed in a dome of "firmament" but it simply doesn't match what we observe happening in the world we live in.

The "survival of the fittest" statement which Darwin recommended as the best formulation of his idea of "natural selection" is definitely a tautology because there is no other operational definition of fitness besides survival (or reproduction). So, survive (reproduce) are those who survive(reproduce).
Darwin naively attempted to imitate the process of selection of domesticated species assuming that new species are produced by "natural selection" in the same way as dogs are produced from wolves. The poor guy was probably not familiar with the facts: the species produced by selection are inferior to the original ones. Dogs are inferior to wolves since they lost a lot of vital features. Moreover, this loss of information is irreversible: you cannot produce a wolf from a spaniel by selection.
In an abstract form, it is quite simple. There is a law: the complexity of a result of a selection algorithm cannot exceed the complexity of the algorithm. Therefore, any selection results in the information loss, and no new information can be produced by selection.

I'm not clear what you are trying to explain here. It is true that selection itself would lead to loss of diversity (information, in other words) but you are forgetting that mutation (and other processes that cause genetic alteration) keep adding more information. Although, the phrase "survival of the fittest" may seem tautological, it is not really so. Fitness is the ability to survive a condition. Although it depends on the condition, it is a property that existed in a population prior to the selection. After the selection, these fit individuals are the ones that survive.

So, it would be great if you can clarify what you are really saying. BTW, it is not impossible to make a wolf from a spaniel considering the fact that humans (or any complex multicellular organism) evolved from a unicellular ancestor.

If  "Fitness is the ability to survive a condition" then the fittest are those who survive. Survival of those who survive. Anything else?

And it is not a fact that humans (or any complex organisms) evolved as a result of (whatever) selection. It is an opinion, and it is logically faulty.