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293T safety, transfections with plasmid DNA
I am a little concerned with 293T cell lines, I have been working with this cell line for a few years with less frequency. However there were times that i extracted the proteins from these cell lines outside the hood. I never work with virus, i have only transfected plasmid DNA. can someone help me if there are any chance o exposure, if yes, how dangerous is it.

Exposure to what? The cell line?

293T cells do incorporate partial virus genomes, consisting of about 4000 bases (about 11%, if I remember right) of the adenovirus type 5 genome (Cloning and Sequencing of the Cellular–Viral Junctions from the Human Adenovirus Type 5 Transformed 293 Cell Line).
This amount of DNA is not enough to make a viable virus; it lacks all the structural components of the capsid, for example.
293T cells also include the SV40 Large T antigen, another viral gene. Again, this is not enough to make a replicating virus.
Therefore these cells don't pose any human health hazard aside from the normal almost entirely theoretical risk associated with any transformed human cell line (actually considerably less, since these were never tumor cells but were transformed in the lab, so they have no intrinsic adaptations to replication in humans, unlike say HeLa cells -- which are also demonstrably safe).
293 cells have been continuously cultured in thousands or tens of thousands of labs for over 40 years, and I'm not aware of any safety incidents associated with them.  Of course, you should always handle cultured cells with appropriate precautions and protective wear, but these are not a specific concern.

Washington State has a nice risk assessment out of their biosafety department that outlines the risks associated with 293 cell lines (downloads a docx). The risk in itself is predicated upon poor work practices and the potential for the generation of a live virus in the technician, or the cell line itself (see the special hazard notes in the risk assessment report). However common these events may be I don't know, but in the US, OSHA 29CFR1910.1030 (The Bloodborne Pathogens Standard) sets us up for risk management regardless of the incidence (or frequency) of such events.
The 293 cell line is considered BSL-II, requiring work done in a BSC with a carefully selected PPE ensemble and training for the manipulations being performed. This isn't at the discretion of the lab personnel but rather at the discretion of the EH&S or Biosafety department. OSHA levies heavy fines against institutions for non-compliance and thus decisions regarding compliance are left up to administrative professionals. I would recommend checking out Biosafety in Microbiological and Biomedical Laboratories (BMBL) 5th Edition (link) for guidance.
Ideally, though, check out your institutions written Exposure Control plan, which you're given access to by law for instruction and assessment performed by your own institution with the goal of mitigating exposure events.


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what happens when you put enhancer and caat box in prokaryotes
what happens when you put enhancer and caat box in prokaryotes

I do not think that enchancers do anything in procaryotes since there is no
chromatin spatial organization of DNA involved.

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Can the body always find the right antibodies?
If the body produces random antibodies in order to fight a virus, is there a small chance that the specific antibody needed to fight the virus just won't be randomly generated? Even though it is a common virus that normally doesn't kill people?
For example if you have a common cold, is there a small chance that you could die from this just by probability? Whereas someone else won't because they randomly produced the right antibody?

Yes and no. Yes, it's possible that some individuals won't be able to (or happen to) make antibodies to a specific part of a pathogen. But most pathogens are large and complex enough that they have many different targets for antibodies, and it becomes increasingly unlikely that someone won't be able to target any part of the pathogen.
An example is given in Influence of Immune Priming and Egg Adaptation in the Vaccine on Antibody Responses to Circulating A(H1N1)pdm09 Viruses After Influenza Vaccination in Adults. A subset of adults (who were exposed to a particular influenza virus as children) have poor antibody responses to a vaccine to a different strain of influenza virus:

Significantly reduced antibody reactivity to circulating viruses bearing K163Q was observed only in the USSR/77-primed cohort, whereas significantly lower reactivity caused by egg-adapted Q223R change was detected across all 3 cohorts.

(This is not an argument against vaccination, I feel obliged to point out, because the vaccinated people were still better off than unvaccinated, just not as well protected as they could be.)

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Why don't moles repair their DNA?
Cells have mechanism to repair damaged DNA. So why don't the cells in moles (the spots), repair themselves and the moles dissappear?

What makes you think that moles are caused by DNA damage? Please cite the source of this information.

@David because people get moles from sun damaged skin. So I put 2+2 together.

Let's try again. Are you asking why the known mechanisms of repair of e.g. UV damage to DNA are not 100% efficient, or are you thinking that the DNA repair mechanisms somehow detect that the DNA has been changed in the mutated cells (e.g. the transformed skin cells) and can reverse this ("repair themselves")? If all mutations got repaired there would be no evolution.

@David Let's not.

As is appropriate for a comment on a question that is unclear and lacks detail, I asked for clarification on specific points. If you had made this clarification I would have attempted to answer your question. As you refuse to do without giving any reason I have no option other than to vote to close.

DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome. However it is yet to be linked closely to mammalian moles.
Information here, states:

"Moles are overgrowths of skin cells called melanocytes, but the genetic factors involved in their development are not well understood."

The BRAF gene is one of the most well-studied genes involved with benign moles, if a mutation arises in this gene - there may be a production of an altered protein that causes melanocytes (melanin-producing cells located in the bottom layer of the skin's epidermis) to aggregate into moles.
I cannot answer why DNA repair does not occur. Maybe the cell cannot identify the mutation, maybe the cell cannot corrects the damage, or maybe it is also from environmental factors. This is an active area of research, but receives far less attention compared to cancer or heart disease.

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Does melanin protect against nuclear radiation?
It is known that melanin protects against UV radiation.
But say a nuclear bomb dropped somewhere would more people of dark complexion survive the radiation burns because the melanin would protect them?
Or as another example, suppose there was a meltdown and someone had to swim into the reactor to pull out the core, would it be best to send the light skinned or dark skinned person to ensure maximum chance of survival? All other things being equal.

The absorption of gamma and x-ray radiation by skin is negligible, so the amount of melanin present is irrelevant. Stopping high energy photons requires a lot of mass, not a few microns of melanin.
Edit:
I think a citation that x-rays and gamma rays go through skin is unnecessary (they'd be useless for imaging bones otherwise), but NIST has tabulated values for different tissues as a function of photon energy if anyone wants to double check:
https://physics.nist.gov/PhysRefData/XrayMassCoef/ComTab/tissue.html
As expected, x-rays have absorption path lengths on the order of centimeters to meters in soft tissues, which is why you can use them to image through skin.

interesting. There was an article about a mould that was inside a nuclear reactor, and they said it survived because it had high levels of melanin

@zooby Were you thinking of this? https://en.m.wikipedia.org/wiki/Radiotrophic_fungus

@LifeInTheTrees What is wrong? It seems like you agree with my point that high energy radiation penetrates deep into skin due to low absorption.

Yes sorry I misread the first statement, i'll delete it, i upvoted previously. There is a difference caused by melanin at least for beta radiation.

Ken Mac is correct, melanin has an effect and you should also consider fatty people to be the heroes of your scenario.
Melanin can cause more surface burns compared to a person with light skin and good fat coverage.
Here's a study that states that black people complain of skin problems more often during radiation chemotherapy.
also this research:
Human and animal heterogeneity in terms of skin tissue distribution and impact on radiation dose distribution:
In humans, subcutaneous skin thickness and body fat vary as a function of age, sex and ethnicity. Fat tissue thickness can lead to wound variability, especially in the case of beta radiation, and the presence of MSCs in the adipose tissue could alter the response. Therefore, care must be used in selecting a model that minimizes these variables.
In pig and mouse models, there can be different healing rates based on what part of the skin is irradiated. For example, in the pig, thicker dorsal skin heals differently than the thinner ventral skin. Mice also have similar skin location differences, in that radiation-induced damage can be very different in that of leg skin compared with that of ear skin.
Proximity of the radiation exposure to bone can play a role in the extent of damage.
Effect of skin melanization in view of possible differential radiation responses due to higher levels of melanin, as well as challenges involved in scoring erythema in pigmented skin:
Concerning the use of a pig such as the Duroc, which is more heavily melanized, differential sensitivity to high-energy radiation may be observed due to the presence of melanin.
The physics forum would know, the radiation types are so variable. Older style atomic bombs had flash burn from the explosion and the fallout from the sky aftewards, i.e. in bomb tests near the Marshall islands.
Marshall islands research.

Maybe not much of an immediate advantage, but evolutionarily, I mean...according to the article below, the melanin in frogs with darker skin was enough to sway natural selection and drastically reduce the population of green frogs while the population of black frogs flourished
https://www.livescience.com/black-frogs-evolution-chernobyl?utm_source=facebook&utm_medium=news_tab

An answer should stand of it own and not consist of a link. References are for for further reading. Please edit your answer accordingly.


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Is a butterfly one or two animals?
I have read somewhere that a butterfly might be two animals that combined together. One animal was a worm-like creature and the other an insect.
And the insect basically hatched inside the worm. Somehow they combined into one creature.
Is there any truth in this? Wouldn't this mean a catterpillar and a butterfly would have different DNA?
But in that case why would a butterfly lay eggs that turned into caterpillars?

Can you please provide a link to where you read this from?

From what I remember about the theories of metamorphosis, the butterfly at the worm stage just has underdeveloped wings. Basically all body parts of the butterfly are already present at worm stage.

There was a paper by: Donald I. Williamson, published in the Proceedings of the National Academy of Science (PNAS) August 28, 2009 https://doi.org/10.1073/pnas.0908357106, and communicated by Lynn Margulis.
Lynn Margulis, as a member of the National Academy of Sciences, could publish papers in PNAS without adequate peer review. Members of the academy were afforded this honor, because they have achieved the highest levels of science, and supposedly, have few peers who can review their work.
Margulis was known for her work on the origin of mitochondria from the engulfment of prokaryotes, and also the Gaia hypothesis (that the Earth is itself, a living organism). That may have predisposed her to the ludicrous idea that butterflies were the result of some strange symbiosis from onycophorans (Velvet worms).
The whole thing was a huge embarrassment to PNAS, and Margulis. It would never have been published if it had been objectively peer reviewed, and was formally rebutted as wrong, and without any merit whatsoever. See: https://blogs.scientificamerican.com/observations/controversial-caterpillar-evolution-study-formally-rebutted/

Pity cos it's quite an interesting idea even if it's not true!

Re: "Lynn Margulis, as a member of the National Academy of Sciences, could publish papers in PNAS without peer review": Do you have a source for that statement? The blog post that you link to says something quite different, namely that members could select the reviewers for peer review. (Additionally, per that post, Margulis originally made it sound like she had selected an unnecessarily large number of reviewers and then cherry-picked the few favorable reviews -- which would have been even worse -- but subsequently clarified that that was not actually the case.)

The Scientific American blog you link to is confused and positively misleading. It complains that Margulis "handpick[ed] its peer reviewers." Well, duh. That's just a heavily loaded way of describing exactly what the journal's handling editor would have done with a normal submission. Three people declining to review because they had no time is utterly irrelevant.

@zooby Look at chloroplasts and mitochondria - we're pretty sure the weird kind of symbiosis did happen there. Both still retain their own DNA (though of course, it's only a small fragment of what was there before the endosymbiosis and millions of years of evolution happened). There are also some very interesting colonies of single-celled organisms - e.g. the Portuguese man 'o war; each cell has its own DNA (they're all the same species), but is also differentiated based on its location within the colony. Looks like a potential step between colonial microorganisms and multi-cellular life :)

Good points. I added the modifier "adequate" to peer review. However, I disagree with the idea that editors always "hand pick" editors for the purpose of predicting a desired outcome. I was an editor of Systematic Biology for 15 years, and the only hand-picking I did was to ensure that they were qualified and objective.

Moths also undergo metamorphosis, so this merger would presumably have happened before the divergence between the moth and butterfly species.

@DavidRicherby the journal's handling editor is free to choose reviewers, but that is a very, very different thing to an author (or author's representative as the case may be here) chooses the reviewers. While I can suggest reviewers when I submit, that doesn't mean I get to pick them! So choosing three people who already reviewed positively and then sending the reviews to the editor is a recipe for disaster. I don't see anything wrong in the SciAm blog post.

@KarlKjer Right but "hand-picked" is just a loaded way of saying "picked". It's always "by hand".

@DavidRicherby hand-picked implies they were carefully chosen not because they were experts but because they could be relied upon to give favorable reviews. That seems like a very correct use of the term. It's supposed to be loaded since, apparently, Margulis chose folks who would say the "right thing".

@terdon I think you're confusing "cherry-picked" and "hand-picked". The latter just means chosen by a person, using their skill and judgement, as distinct from being chosen by some automatic system or process.

@DavidRicherby yes, it can mean that. But it also means selected for a special purpose.

@terdon and in addition the linked article stated that the method of publication used by Margulis will be terminated, though it was not in response to this specific incident.  This was back in 2009 so thankfully this weird system is now closed from further errors.

@zooby how to make butterfly-like creatures that are actually symbiotes of two organisms might be a viable question for [worldbuilding.se]

"Pity cos it's quite an interesting idea even if it's not true!" good for sci-fi and fantasy literature, horrible and out of place in science.

What's the definition/role of "communicated"? I guess it's similar to co-authoring.

"Communicated" means that the author contacted Dr. Margoulis, and she submitted the paper under her unique privileges as an academy member. It is not similar to co-authoring. More like sponsoring or promoting.


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Do trees in a forest generally grow in a lattice formation?
The closest arrangement of trees in which they are at least a certain distance away from each other is a triangular lattice, much like a honeycomb. I wonder if you tend to see this sort of arrangement of trees in the wild?
I guess this would actually not be beneficial to the trees since it would mean they would all be lined up in certain directions which might not be good for sunlight etc.
I wonder if there is much research on the pattern of distribution of trees in a forest?

For most trees and plants, distribution is spatially highly variable. Thinking about the lifecycle of plants—their seeds are non-randomly dispersed, the seedlings and saplings grow in different biotic (neighboring trees, distance to herbivores) and abiotic (different soils, shading, etc.) environments, all the plants are at different life/size stages, and that they are highly plastic in their ability to have fluid morphologies in different conditions—it's really difficult to detect a clean lattice pattern with little variance.
Nevertheless, for some species of plants, where the conditions are right (e.g., very limited and highly sought-after resources, species poor areas, synchronicity of generations, strong antagonism), we see some evidence of regular patterns. Ecologists often analyze spatial distributions to see if they are random, clumped, or uniform/regularly distributed (link). We see some distributional uniformity that does resemble lattice-/tiling-like patterns, which you may find in the references from the link above. There is reference to only 1 tree species in that link :/ I can't say that I see ecologists looking for lattices explicitly, but I would be surprised if there isn't a subfield interested in it. HTH.

Good answer. I was surprised that there are actually plants that have regular distributions. I wonder though whether they are categorised as separate plants or are they in fact a giant super organism with a common root structure. In any case it seems like some form of communication between the different out-growths is needed for this arrangement. Also, I would imagine that such arrangement must grow out from a single plant much like how a snowflake crystal grows from a single seed.

Thanks—good question. Some plants that tend to grow regularly distributed, like creosote (Larrea tridentata) some oaks, can reproduce clonally and through seeds. Clonal propagation ought to lead to more regular distributions. Communication in most plants through root exudates are ubiquitous and very poorly understood, but I think you're right on about stronger patterns arising from sensing and responding to local environments. Animals do this well, and many territories (again, in the right conditions) are lattice-like, such as nesting sites of birds that next at high densities in the open.

It would be closer to an irregular Voronoi pattern.
"A certain distance" is imprecise, it would have to be "regular" intervals to give a lattice/matrix.
For trees that grow at the same rate, a square grid arrangement would give square canopy shapes. A triangle lattice would give triangles and honeycomb would give honeycomb canopy units.
For trees that are different sizes, the regularity would be chaotic. Voronoi:

Voronoi can describe a lot of things in nature, bubbles and animal cells, it's one of the fundamental mathematical patterns in nature just like spirals.
And even some arid clay.
Trees have irregular, not straight sides, that's different from voronoi. The trees are spaced irregularly and chaotically, and so it's a chaos of differently sized and irregular cells, rather than a lattics.

I think it would not quite be veronoi because there's only so close trees can get. And trees would tend to overshadow their neighbours and kill them.

I think you have things backwards.  You can make a Voroni diagram for ANY distribution of points, since it's merely the area that's closer to each point than any of the others: https://en.wikipedia.org/wiki/Voronoi_diagram

@zooby You are correct that the points of any distribution can be joined togeter into triangles... Google "Voronoi Forest" you will find lots of images and mathematics forestry research using voronoi... http://revistas.inia.es/index.php/fs/article/view/8021/2913 lattice is a repeating arrangement, i.e it has a symmetry. mathematics research has used voronoi to define plant spaces: https://pdfs.semanticscholar.org/de5a/1e987457ece17f6512e019e88111530d8d4d.pdf

OK, then what's the point in saying it's veronoi? Why not just say it's an irregular distribution of points? I guess you are trying to show how points can form cell like patterns?

Because you talked about geometry of the canopy... you said triangles, much like a honeycomb, and a lattice, all of which are wrong if you do any geometry. I program geometry so i know the technical words very well. So I replied that it is voronoi cells, and technically not a lattice, or a honeycomb, it's a point and cell distrubution simplified to Voronoi. You didn't specify the positions of the trees, you specified the canopy, which is not triangles. the positions of the trees themsevles have not triangular symmetries. They can be represented by single groups, duos, triangles and quads.

@zooby: Re "only so close trees can get", not really.  It's not uncommon to find two trees growing so close together that their trunks meet and sometimes join: https://en.wikipedia.org/wiki/Inosculation

OK. I see what you mean.


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How does DNA still work after recombination?
If you take two computer programs and randomly swapped pieces from each of them. The result is not going to work. It will just be garbage. If you take two novels and randomly swapped chapters the result will be garbage too.
How is it than DNA (which is infinitely more complicated) can be combined, some from the father and some from the mother and yet it still somehow works?
Can you give a simple example?

Actually computer programmers can be made by randomly swapping bits of their programs around if it's set up properly, this is called genetic programming https://en.wikipedia.org/wiki/Genetic_programming

How exactly is DNA infinitely more complicated? It's only got a 4-character alphabet? You may argue that it is more complicated in some specific aspect, but not significantly so, let alone infinitely.

@Thijser. Yeah but genetic programming has never really worked that well as far as I understand for that very reason.

@orangedog computer programs (for the computer POV) has a 2-letter alphabet. The claim that it is infinitely more complicated is a fallacy, but the amount of sigils in an alphabet is not a measurement of complexity.

@OrangeDog Although you might say all genes are separate and generate different proteins. All the proteins must work together. The system it encodes, i.e. a human being is a very complicated interconnected system I think you'd agree.

@zooby I didn't say it wasn't very complicated, I simply contest that human language and computer programs are in fact comparable in complexity to DNA.

@Mindwin yes I know, that's why I was asking what measure zooby thinks they're using

@zooby there are indeed a few ways I can think of where DNA is measurably simpler (as far as current understanding goes). For example the order that genes appear on a chromosome is usually not important, and you can usually pad them with meaningless junk. The only immediate complexity is the feedback loops where some genes express proteins that effect the expression of other genes, but you can write a computer program that does the same thing (dynamically re-writing its own execution, or "machine learning") and it will be similarly hard to understand what it's going to do.

You can juggle around things in a computer program too. Some languages lets you define functions and classes in arbitrary order, for instance. You can also pad with useless junk (as long as it's syntactically correct), like defining functions that no one will ever use, or performing the calculation 5+5 without storing the value anywhere.

If you're a computer programmer, this page on computer analogies to DNA might provide you some inspiration.

For an example, homologous recombination is like swapping chapters between different editions of the same book; it would still make sense.

I'm voting to close this question as off-topic because it is based on the false premise that DNA is comparable to a computer program.

Homologous DNA recombination does not swap parts randomly in the sense that any two bits of DNA can swap places. DNA recombination is random in the sense that it may or may not occur. In fact DNA homologous recombination is highly specific and its specificity is what it makes a great tool to study genetics in organisms like yeast by swapping a gene of interest with something else.
In your example of meiotic recombination between the sister chromatids can swap  DNA between different alleles. Alleles are genes that encode for a protein with the same general function, but have some variability in sequence that gives them slightly different properties. The reason why it only occurs between alleles, is because homologous recombination requires regions of homology, in a laboratory experiment this can occur with 20 to 40 base pairs in length and the low likelihood that a 20 base pair sequence is found anywhere else in the genome is why you don't get a chaotic mix and match of genes that you suggested would happen.

Very interesting - and to extend the software analogy this sounds very similar to how patches/diffs work. They also require an identical section before and after the piece of code that is to be swapped with an updated version.

The definition of allele here is a little misleading. An allele is a variant at a locus. Most often people consider loci that are genes but this is not necessarily the case. A sentence like "it only occurs between alleles" is a bit misleading. It would be better to say "it only occurs between variable regions". Also, just to avoid that the reader gets mislead, there are other things that affect variation in recombination rate than polymorphism.

Another software analogy might be something like taking some program with hundreds of shared library dependencies and randomly swapping some of the library versions with versions used in a different release of the overall software. It might make certain things start crashing, or it might make that mysterious bug you started seeing in the latest version go away. ;-)

One must always be careful not to stretch an analogy further than it can withstand, but since you started these analogies, I will follow up on them and explain the small mistake you've done in their representations.
The two books are not as different as you have in mind. You are not pasting the beginning of Uncle Tom's Cabin with the ending of Harry Potter but only the beginning of Harry Potter with the ending of another Harry Potter in which Ravenclaw is renamed Eagleclaw.
Also, unlike in books, there is no beginning-to-end reading frame for the entire chromosome. There are just genes randomly placed along chromosomes. The reality is that the placing is actually not that random but assuming it is can give you a sense of why it can often be fine to recombine two chromosomes and end up with still functional chromosomes.
For the computer program analogy, it would be like swapping files between branches of the same project (thanks @IronSean for his comment).

But what I don't understand is if the genes encode for proteins, how is it that if you have different genes the proteins still all work together? Well I guess then those genes would die out quite quickly unless they worked well with all the other proteins.

Yes, selection does its job at ensuring that only alleles which phenotypic effects are well integrated within the actions of the other genes remain. Also, while there is a level of interdependence, it does not mean you cannot just modify things. In fact, you can often add a new gene in an organism and this organism may well just do fine. We might be more resilient than you would assume at first.

Hmm.. I guess that's why most animals have the same basic layout because that's hard to change whereas eye colour is easy to change without affecting too much else. It sounds like the more complicated we get the harder it is too evolve.

Let's not forget that even after successful fertilization (merging of egg and sperm), many embryos die because of incompatibilities in the genomes.

@Thawn that's a good point. That would `weed out' a lot of unsuccessful combinations.

In the Computer Program example it would be more accurate to say swapping files between branches in the same project, not randomly mixing and matching lines of code. In most cases, swapping some files between branches won't break the whole program.

@IronSean Ah nice. I could not find a good analogy for the computer programs. The one you're giving is perfect and I've added it in the post.

It's also key that unlike most examples of computer code you might look at, DNA is not executed in order but all of it in parallel. So long as your DNA contains the full string for a single protein in tact, it doesn't matter much where in your chromosomes it is. And for some genes, you might have several copies in your genome and losing or gaining a single copy might only have minor affects such as making a dog's nose just a little bit shorter or longer.

Also adding to the book anology, it is more like an library where you exchange, add or remove books. At first glance, it does not change much, but essentially it can change the structure (order) of the books and as library you want all 'important' writework, for it to work.

Can you give a simple example?

Yes. A mother is an entire codebase of Android OS, that boots with a dark blue background and where initial language is set to English (US).
A father is an entire codebase of Andoroid OS, that boots with a dark green background and where initial language is set to English (UK).
Other than that their codebases are exactly identical line-to-line. Recombination: each code line has a chance to be swapped to the code line at the same position.
A child might have a dark green background and English (US) and it will work mostly flawlessly.
You grossly overestimate how different the humans are from each other. (You're biased because you are a human.) Any single species is a group of nearly identical individuals. If the codebases are not very much identical, yes, the result will be garbage, both in programming and in biology. Exactly the same as trying to recombine rabbit's DNA with ant's DNA.
Rabbit and ant are considered different species not because they look differently; but because the codebases after recombination do not work at all.
(Another thing - the codebases over the generations evolved "programming patterns" that made them vastly more tolerant to glitches that typically happen during the recombination. A very very defensive kind of programming, that is really ugly and nearly impossible for a human to read or understand.)

I'd also add that large swaths of the code is functions that are dead and non-functional.  So if the flip-flop happens in them (and they make up the majority of the file), the working functions are intact.

Genomic structure, gene structure, and the structure of human culture are quite plastic, and when parts of it get messed up there is usually excess capacity somewhere that keeps the system operating.

Stories, books, tales, songs, etc. are both mutable and recombinable.  From the party game of "telephone" to the creation of new works of art, sections of one work are replaced intentionally or by accident either with original contributions or with pieces from other works. These new works are then selected for fitness for the intended purpose by the creator or by other social mechanisms. The only ones you ever observe are not complete failures by those criteria. This is a pretty good analogy for the type of recombination you are talking about.
If a genetic recombination event ends up making a gene that no longer serves its original function, that is usually OK and the organism will have another way to survive. It may even be more fit (always in a particular context) without the working gene. The non-functional gene may acquire a new function (by further recombination or mutation) over generations. [a paper of mine where we show, that many genes reduce fitness https://www.ncbi.nlm.nih.gov/pubmed/23990803 in particular environments]
You absolutely can "rearrange a gene", some genes anyway, and have it make sense. One example: many genes can be "circularly permuted", the beginning (N-terminus) of the protein can be moved to various positions. [a paper of mine where we do that: https://www.ncbi.nlm.nih.gov/pubmed/12149462]

The English language has 26 letters which can be rearranged in combinations of open-ended length, giving colossal variability. According to the Oxford English Dictionary, there are about 170,000 words in current use.
Programming languages are based very loosely on human language structures. Although the pool of "words" is much smaller, they are also open-ended in the sense that the programmer is free to create words or function names.
Both are also sequential - if you do anything other than follow them in the order they were designed to work, you will get gibberish.
Although DNA can be understood as a language it is much simpler than your other examples. It has four letters and all of its words are 3 letters long. That gives you a hard maximum of 64 words. In point of fact, nature only uses 21 of these words, and there is a great deal of redundancy built in.
A "book" in DNA sense is a single gene. The length of a gene varies enormously but the average is about 480 "words". Although the DNA in a book does need to be read sequentially, all the "books" in a chromosome or a genome do not. So long as each "book" is read in order, the "books" themselves can be read individually and still make sense.
So: all recombination needs to do is ensure that the combination occurs in a break between two "books", and everything will work fine. As @user40949 mentioned above, there are processes to ensure that recombination does indeed occur within specific regions between "books". And even if it didn't, a failure would only invalidate a single "book".

perhaps the analogy would be improved by having gene = paragraph, chromosome = chapter, and genome = book?

@JCRM I went with book = gene because the OP was specifically making a comparison about rearranging a book and it making sense. You can't rearrange a gene and have it make sense, but you can certainly rearrange genes on a chromosome and have them still readable, providing there aren't multiple reading frames.

you're absolutely right, I'd forgotten the precise question by the time I'd finished your answer.

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Is there a name for survival of the fittest in a single family?
Imagine a case where the children of a bird each have a 50% chance of being born blind.
But the bird always has on average 4 chicks. So on average 2 will be blind and 2 sighted.
(Perhaps this could evolve if the energy needed to create a chick with 100% probability of being sighted is more than the energy needed to create two chicks each with 50% probability of being sighted. The eye being a very complicated organ).
Now, the mother brings food to the chicks and only the sighted children eat the food. The blind chicks (the 'runts') are thrown out of the nest. (It is common there being a 'runt' of the litter. So this scenario has some truth in it.)
Thus all adult birds of this species are sighted. (The 'fittest' birds).
(This is a kind of surival of the fittest but in a family setting.)
Is there a name for this kind of process? This could happen in any animal that has on average more than 2 children. Where it might be cost effective not to make sure that 100% of the children are fit, because the weakest will die anyway.
Secondly, imagine a scenario, where there is a surplus of food one year, so that even the 'runts' make it to adulthood. Now, 50% of the adult birds will be blind. And people might say "There is an epidemic of blind birds". Can we make comparrisons with the theory that there is "an epidemic of myopia" in modern human populations, possibly due to modern medicine decreasing childhood mortality?

"Survival of the fittest" is a flawed summary of natural selection that covers up some nuance in the theory (and was not originally used by Darwin but rather a phrase used to try to explain the theory, and then, probably unfortunately, edited into Darwin's own work). Your question seems to lack a basic understanding of heritability and evolution. In particular, your model seems to not involve a heritable trait.

Is there a name for this kind of process? You described a non-heritable lethal trait with a prevalence of 0.5 (which is very unlikely). Does this answer your first question? I don't understand what you mean by Where it might be cost effective not to make sure that 100% of the children are fit, because the weakest will die anyway.. Can you please clarify what is on your mind?

Your second question starts with Can we make comparrisons. One can only compare whatever they want to compare. One can even make analogies. But that does not mean there is much to be taken from it. Can you please write a clearly defined question or, otherwise, maybe just remove this second point.

@Remi.b Yes, the biology needed to grow a bird with 50% likely of being blind might cost 3 units of energy. But the biology needed to grow a bird with excellent vision might cost 500 units of energy. (Think of buying two cheap cameras vs buying one expensive one.) It might be more cost effective to buy the cheap cameras even though they are likely to be defective. As long as you buy enough of them so that at least some of them work.

@Bryan. Yes I understand evolution. That is why I asked is there a name for this process. Which is not standard evolution.

@zooby I understand evolution Take no offense but the phrasing of everything in your post strongly suggests that you don't have much knowledge in evolutionary biology.

@zooby You will probably want to have a look at wikipedia > siblicide. A famous example of siblicide (not listed in the wikipedia article) is the case of shark that kill each other in the mother's womb (see this popular article)

@Remi Of course i'm no expert. I will look at the shark thing. sounds intriguing.

I've read The Selfish Gene and Darwin's book. I don't know what else you want from me? Since I wasn't talking about evolutionary biology I don't know how you came to that conclusion.

This competitive relationship often goes by the simple and intuitive name of sibling rivalry, and its closely related idea of parent-offspring conflict.  While it may seem counter-intuitive for evolution, you must remember that while it's better for the parents to have multiple surviving chicks, it's better for the chick to have less siblings to compete with for insufficient food.
We do in fact, see this type of behavior amongst humans as well: who amongst us with a sibling has not competed for parental resources and affection? Fatalities, though, are much rarer than in birds that routinely have more chicks than they can support, because our species are different.

Yes, "sibling rivalry" is probably the right phrase. By question is really, whether there is a name for an animal deliberately making children compete in order to weed out the most fittest or healthiest and discard the runts of the litter. (And also since humans used to have lots of children, whether this sibling rivalry is good for health of a population.)

Also, I make a side point, that if an animal was to stop having lots of children and so there was less sibling rivalry, would this be bad for the health of the species?

@zooby In general, there's no "deliberately" involved, since you're not talking about animals with sufficient cognitive faculties to make such a choice.  Even with humans, how often do you think that a parent deliberately makes their children compete, vs. falling into it as a side effect of their own choices and patterns?  As for whether it's "good" for the population---it doesn't have to be, it just has to be a stable equilibrium.

Well I mean deliberate in the sense of a stable equilibrium, like you say, that has evolved over thousands of years. Perhaps birds evolved under the assumption their chicks compete. Perhaps humans evolved to have their children compete, and stopping the children compete will upset the equilibrium and be bad for the population's health however one might define it. Perhaps it is "natural" for humans to have 10 children who fight to the death leaving only the two fittest to reproduce.

What I'm trying to say is, whether there is reasearch into how much "sibling rivalry" is essential for maintaing the health of a population. Or having enough children incase some of them are weak is important vs having only two children and hoping they are both strong.

@zooby It's a spectrum, and species can end up at different set-points along it.  See, for example the notion of r-selection vs k-selection: https://en.wikipedia.org/wiki/R/K_selection_theory

I think "r-selection vs k-selection" is pretty much an answer to the question.


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Indirect lineage sorting between human, gorilla and chimpanzee, does it exclude loci reversals (for example on chromosome 12?)
Insights into hominid evolution from the gorilla genome sequence looks at shared genes across human (H), gorilla (G) and chimpanzee (C), and that indirect lineage sorting led to 15% of the gorilla genome being closer to humans, and 15% of the genome being closer to chimpanzees.
In that study or similar studies, is for example the reversed loci in the image below treated as a genetic sequence shared between gorilla and chimpanzee and not with human, or is the specific genes being looked at, so that their position in the genome does not matter?


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Does dreaming have any physiological impact on our body?
Personally speaking, when I wake up after a really good dream, I feel really happy, similar to how I would feel if something good has happened in reality. This makes me wonder if we are actually going through stress when we are having a nightmare. Is there an increase of epinephrine in our body when we dream about being in trouble or running away from a scary situation? Similarly, are endorphins released when we are experience a happy moment in our dreams?


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What does the nucleus look like in S phase of Meiosis?
I was watching an animation video about Meiosis and this is what the video shows (pics attached.)
It shows that before synthesis, each chromosome exists as single chromatid and then after replication, it has a sister chromatid. I am confused because germ cells are diploid, so shouldn't the S phase look like this?
It should start with 23 chromosomes (46 different DNA's) and then replicated to 46 chromosomes (92 different DNA) which then get assorted into 4 different cells?

In terms of chromosome number
During meiosis, the meiocyte is a diploid cell ( 46 chromosomes for human). So during the S-phase , the meiocyte would contain 46 chromosomes.
At the end of meiosis I, the divided meiocyte contains 23 chromosomes so it's called the reductional division
At the end of meiosis II each cell contains 23 chromosomes.
In terms of chromatid number and number of DNA molecules
Meiocyte in S phase contains 2 chromatid in each chromosome, so the number of DNA molecules is doubled (if you consider that each chromatid is composed of a pair of DNA strands like in Watson Crick Model, then each chromosome of S phase contains 4 strands... So 46×4 strands of DNA is present. Often each helix / duplex is considered one DNA molecule , so in that case you have 46×2 molecules. So you have to be careful with the terminology mentioned.
After meiosis I there are 23 chromosomes in each divided cell with 2 chromatids in each chromosome...So there are 23×2 DNA molecules.
After meiosis II there are 23 chromosomes with 1 chromatid...So they contain only 23 DNA molecules.

It states mitosis here but it is the same for meiosis at this stage. What you have drawn for the inside of the first cell is already 44 chromosomes.
Hope this helps

At the beginning, germ cells are diploid and as far as I know they are the cells that give rise to gametes which are haploid.
Here how it goes, the germ cell is containing 46 chromosomes and in S phase, these chromosomes replicate so that each chromosome will be made of 2 chromatids resulting in 92 chromatid.
In meiosis I, the germ cell divides and the 46 chromosomes divide as well giving two cells each containing 23 chromosomes and 46 chromatid.
The meiosis yet hasn’t finished. In meiosis II, each daughter cell containing 23 chromosomes will divide to two daughter cells. In this division, the chromatids in each chromosome will separate. In other words, the 46 chromatids in each cell will divide and each cell from the new daughter cells will be containing 23 chromatids. So now we have 4 haploid cells each one containing 23 CHROMATIDS ( a gamete ) all coming form one original diploid germ cell.
Those chromatids will then be referred to as chromosomes.


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High Blood Pressure - Na or NaCl?
What is the cause of high blood pressure? or, Which foods can cause high blood pressure?
Is it just sodium, or sodium chloride? I'm confused because sodium chloride should ionise in the aqueous medium of the stomach.
It'd be great if someone could share the working details/mechanism of the same. Thanks in advance!

Welcome to Biology.SE! What research have you done before asking it here?

High blood pressure is caused by an excessive amount of fluid circulating in the blood vessels, or an excessively small mean blood vessel diameter. The later is more associated with stress situations and stressful lives, while the former is more related to the theme of your question: electrolyte balance.
An electrolyte is any molecule that produces an electrically conducting solution when dissolved in water (http://www.medicalnewstoday.com/articles/153188.php). In other words, they are or give rise to ions or charged molecules when dissolved in water. Examples are sodium, potassium, calcium, magnesium, chloride, phosphate, bicarbonate, ...
Water, even though on its own is a neutral molecule, it is still polar. This means that it has parts which are more negatively charged (in concrete, the oxygen atom) and parts that are more positively charged (the hydrogen atoms). These are called poles, and are due to different electronegativities.
The result of this is that water will form electrostatic bonds with charged molecules such as ions, or, in other words, which causes salts to be soluble in water. This also means that water is attracted to places with a lot of charged molecules - places with higher osmolarity. The travelling of water from places with lower to higher osmolarity is called osmosis.
That's what happens when the blood has an excess of ions (and thus higher osmolarity) when compared to the rest of the body and the normal, healthy values. Water starts travelling from the different parts of the body to the blood, being attracted by the extra concentration of salts, and pushing the blood volume over the healthy limits. This also makes it harder for the kidneys to excrete water from the blood, increasing further blood volume and giving rise to hypertension.
As you can see, any charged molecule in excess in the blood can increase blood volume (through higher plasma osmolarity) and create hypertension. In our bodies, the most common and impactful electrolytes are ions, being Sodium the most abundant.

Because sodium is the most abundant in the blood and the most ingested electrolyte, it is usually referred as its excess being the cause of hypertension. The common salt we use to cook comes in the form of NaCl, containing Sodium and Chloride, both electrolytes. They are very useful and fundamental to our organism, but in excess can cause diseases such as this.


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What type of insect is this?
ery bug 1]1
What insect are these? Found them indoors. No wings, just crawling on the walls.

Where was the photo taken (geographically), at what time of the year, and how large are they (can you include a scale bar in the photo)? All will be useful for answering this question.

Looks like a termite; male; after loss of wings.

This answer could be improved by explaining why you think so - for example find a picture of a male termite with its wings and explain what body parts you compare with the insect in the photo to reach that conclusion.

Thick waist, straight antennae, head position are all consistent with a male termite.

Edit your answer to include that and provide a reference or picture for the question author to check up themselves and I would say this is a perfectly sufficient answer :)


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Has it been enough time for evolution through simple natural selection?
Let first state that I understand natural selection. I am not asking if evolution happened. I see evolution as a fact, but I do not assume the current theory of natural selection as fact.
I wonder if there has been enough "time", or number of generations, needed to create enough mutations that lead to the known genetic complexity of all species today (or even just until dinosaurs), since the Last Universal Ancestor.
Is it possible to prove, or estimate this time?
Note: There was obviously enough time for evolution to occur. My question is if, the known mechanisms of mutation and theory of natural selection, are enough to justify the evolution in this amount of time.

The evolution to the current state of life on earth has occurred through some 3.8 billion years. During this time it has gone from the most basic forms of life, simple self-replicating units, to the complex beings we see today. Evolution, the process of change within a collection of units, is caused by 4 factors, mutation, selection, drift, and gene flow. So firstly, the current state is not thought to just be the result of natural selection but instead a result of all the mechanisms of evolution.
Selection can itself be subdivided in to two types, natural and sexual selection. Therefore "natural selection" does not even contain all types of selection. Selection is not a simple process, but occurs in a very complex manner, simultaneously affecting the many levels upon which selection can act (nucleotide, gene, organelle, cell, organs, organism, population, species, ecosystem etc.).
There are a number of things to consider when discussing whether enough time has elapsed for the mechanisms of evolution to produce the variation we see today, a primary concern is quantifying how much variation there is in the world that has evolved. Here are some other factors which would determine the likelihood at arriving at that level of genetic variation:

Mutation rates (per generation)
Generation times
Offspring per generation (affects the number of potentially new lineages per generation)
Genome size (number of potential sites)
Complexity and strength of selection
Population size (affecting drift and the efficacy of selection)
Genetic admixture/inbreeding/potential gene flow
Recombination rates
Social structure
Environmental variation

These all vary wildly in contemporary populations and would also have varied in ancestral lineages too, this makes it, in my opinion, near impossible to even get a rough estimate of how likely our current state of variation evolved via the known mechanisms of evolution. But there is a simple answer, all variation you see today arose from simple life and evolved in the last 4 billion years via the four known mechanisms of evolution - which, in part, includes natural selection. The proof is in its existence and the absence of other possible (plausible) mechanisms.
To illustrate the complexity of the problem and the high likelihood of these mechanisms leading to substantial genetic variation (this is highly unscientific):
I'd suggest a very conservative estimate of just mutation rates and time since life began (3.8 billion years, Last universal common ancestor [LUCA]), using approximate human mutation rates (175 per generation and 25 years per generation = 7 bp mutations per year), would suggest a single lineage from LUCA to now could have had some 26 billion mutations, an average of 8 mutations per site in the human genome (this would assume constant mutation and generation rates, and starting genome size of 3 billion BP in LUCA - obviously completely ridiculous, but it's just an illustration and assumes evolution purely by drift and mutation).

" the absence of other possible (plausible) mechanisms" - who is to decide what is plausible? what i cannot see cannot exist?

Whatever there isn't evidence for might as well be treated as non-existent.
If your preferred theory is that an invisible dragon is secretly directing mutations in order to reach a desired outcome then show me evidence for that. Without evidence for this dragon or even a hypothesis for how it might work in the world while simultaneously avoiding detection then this theory isn't anything more than an unsubstantiated hypothesis.

"The proof is in its existence and the absence of other possible (plausible) mechanisms." This is precisely the same argument religious people use for God.

As in, the existence of so much diversity, which we know came about by evolution, is proof that there has been enough time for evolution of so much diversity.

There was a paper that attempted to assess this published in 2010
There’s plenty of time for evolution - Herbert S. Wilf and Warren J. Ewens
There is also a layman's explanation of this here
Basically when we account for the fact that genes evolve in parallel under a number of simultaneous trials, it appears that there is indeed enough time for species to have evolved as far as they have.

What's your average contemporary DNA pol error rate? Something like 10^-9 errors per bp? Your average prokaryote generation time is maybe something like 10 days. LUCA is thought to be about 3.5 billion years old. However, it would be expected that DNA pol error rates were far higher in the past. In fact, if RNA + protein world existed (I think a strong case can be made for it), we're looking at multiple orders of magnitude faster change. Eukaryotes with their longer generation times don't pose much problems to the calculations, since the vast majority of domains in Eukaryote proteins were prokaryotic inventions and Eukaryote proteins are mostly just prokaryotic domains shuffled around. I agree with the above answer of there being way too many variables involved (that we would basically have to guess) for robust calculations..

-1. This doesn't actually answer the question.


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Can UV radiation be safe for the skin?
It is well known that UV radiation can damage the DNA and generally harm our skin.
We also know that UV radiation helps on the production of melanin and Vitamin D.
From what I could find, the DNA absorption spectrum goes to almost zero for wavelengths higher than 300 nm. This seems to suggest that we would be safe to use UV radiation between 300 and 340 nm in our skin (as long as the power or exposure is not too high/long to make burns), for therapeutic purposes such as the stimulation of Vitamin D production.
Is this assumption correct? Are there any evidences that we could use this UV wavelength range safely?

Remember that UV can damage DNA indirectly by creating ROS.

You're talking about long-wave UV, or UV-A radiation. In the 80s, experts claimed that this was a safe wavelength. Protection against UV-A was not part of sunscreen in the early days. Consequently, UV-A was (and still is) used in tanning beds due to its perceived safety over UV-B. However, a lot of research has been done since.
UV-A is well understood now to also be unsafe in unreasonable amounts. Currently, UV-A protection is a typical feature of sunscreen and tanning beds are still not a healthy alternative to moderate, healthy doses of sun. Here is a recent review covering some of the aspects comparing different UV range effects on skin. I really suggest you put a search engine to good use here; it makes little sense for us to expound on the literature when it is so clear and easily available.
In summary,

UVA certainly contributes to the development of skin cancer.
UVA penetrates deeper into the skin than UV-B (which is largely responsible for 'burning' of the topmost layer of skin, without directly affecting the deeper layers). For this reason, UV-B is associated primarily with burning and UV-A is primarily associated with aging and aging diseases like cancer.
It is important to note that 95% of UV light in every day life is UV-A, because it does not vary seasonally and can penetrate clouds and windows. Therefore, in spite of the fact that short wavelengths carry more energy per photon, the ratios of UV-A and UV-B exposure are far from equal.

These are only a few of the explanations as to why we observe an incidence of aging and skin damage and disease upon UV-A exposure.

Great answer. Thank you. Your literature suggestions have shown that, despite many evidences that UV-A and UV-B being harmful, some authors seem to point out that "moderate" exposure brings many benefits (not only Vitamin D). Apparently, it's not clear yet what "moderate exposure" is, or if there is such win-win scenario regarding UV exposure. Interesting stuff...

Just to add a nice reference, following my comment, for those who might be interested: https://onlinelibrary.wiley.com/doi/epdf/10.1111/bjd.17992/

So, no benefits to being out in the sun then...

There are (at least) two sides to this story. One is direct DNA damage being caused by UV-B light which happens to have photons with just the right amount of energy to interact with thymine. This has been known, and assumed not just during the 80s, but until the late 2000s to be The One major thing that causes cancer, or trouble in general (there's papers from ~2008 claiming that).
Meanwhile, it is known that UV-A can excite an electron in a chromophore (i.e. some more or less random unspecified molecule, or part of it) in a way which turns out being less desirable than one would wish.
Photons exciting electrons isn't something particularly new or stunning (think photosynthesis or our ability to see), it happens all the time, almost every time a photon hits something. But some molecules react more favorably, and some... don't.
For example, melanin happens to be our "sun protector" molecule because it has the property that it almost instantly drops its excitement into heat, which is quite harmless.
Other "random" molecules do not necessarily have such favorable properties and may either form radicals or stay excited for a long time until they finally bump into something and interact with it in some way, giving off that energy in some unspecified, haphazard manner. When that happens, well, things happen, whatever they may be. The damage, finally, doesn't even have to be at the exact location where the sun was shining.


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What are the ways to test for protein in the canine urine?
I know that one way is to use the reagent sticks and the refractometer, but this is inaccurate. Is protein distinguishable when using a microscope? Is it time sensitive(i.e. have to test it right away)?

After some research, I could primarily find two tests for testing the protein content in dog urine.
1) The Urinalysis dipstick test (reference) which has a chance of giving false positive results (reference). Here is the link to a lab test done using the dipstick method and the results that the researchers got.

A sample Dipstick (reference)
2) The second test would be the benzethonium chloride test (reference).

This test precipitates the protein and increases the turbidity of the
  sample. The turbidity is proportional to the protein concentration.
  This technique is very sensitive and can yield accurate results in
  samples with very low protein concentrations (< 20 mg/dL).

A lab study done using this procedure to precipitate protein (reference).

The urine sample is best read within 30 minutes of collection
  otherwise certain factors (like crystals, bacteria and cells) may
  alter their composition (dissolve or multiply) over time. If you
  collect a urine sample at home, please drop it off at your veterinary
  clinic as soon as possible (reference).

Reasons for excess protein if present in the urine of your pet is listed in this article.

Sorry to bother again, did you find out by chance whether the upc ratio test is time sensitive or not?

@shooting-squirrel Since the quality of the sample is what could be affected after the aforesaid time period. I believe that the quality of any urine related test after that time period could be skewed.

@shooting-squirrel I just found an article which said that if sufficiently refrigerated, the sample should be alright for maybe even 24 hours. Don't worry about it if you handed over the sample to the lab.


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Are the cpli and ctli tests time senstive(i.e. is it needed to test right away in order to get accurate results)?
I'm sending the blood samples to a lab and this takes some time until the actual testing.
Some information on the tests.
TLI : http://www.vcahospitals.com/main/pet-health-information/article/animal-health/trypsin-like-immunoreactivity/405
CPLI : https://www.vetstream.com/canis/Content/Lab_test/lab00522

From doing a bit of research, I quote

The various analytes have different stability in serum. Serum TLI and
  PLI are stable for up to 2 weeks at room temperature. However, serum
  folate shows limited stability at room temperature. Therefore, serum
  samples for folate analysis should be kept at 4ºC for not longer than
  48 hours, but freezing is preferred. Furthermore, folate is light
  sensitive and samples should be stored in the dark or wrapped in foil (reference).

So, it should be fine if the tests are conducted in two weeks.


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What are the reactions in the body that triggers dizziness after cigar(nicotine) smoking in non-smokers?
Suppose there is a person that has never used nicotine in any form in his/her life. Why does the person get dizzy after a few "shots" from a cigar(nicotine)? What's the difference between using other plants(e.g. marijuana)?

It's all about the synapses, the places where separate neurons connect to one another. All psychoactive drugs act in some way so as to modulate the signals that are passed from one neuron to another. Nicotine acts by increasing the effect of signals that pass through a particular type of synaptic receptor called nicotinic acetylcholine receptors (they're named after the fact that they're affected by nicotine). The dizziness and other effects of nicotine are caused by this interference with normal neuronal communications.
The reason why regular users of nicotine don't get dizzy is because they've gained a tolerance to the drug. Tolerance isn't super well understood at the molecular level, but it has been associated with long term changes in the quantities and types of receptors that are present at synapses in certain regions of the brain, it particular the nucleus accumbens.
Marijuana is similar to tobacco, only its main psychoactive component, THC, acts on the cannabinoid receptors.


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What does NaOH do for the plating of Bacillus subtilis?
A book called Molecular Biological Methods for Bacillus called for plating Bacillus subtilis cells on LB-agar plates with the following components:

A general-purpose medium containing per litre:
Bacto-tryptone 10 g
Bacto-yeast extract 5 g
NaCl 10 g
1 M NaOH 1.0 ml
Autoclave (151b/in^2, 30 min). For LB agar plates solidify with 1.5% (w/v)
  agar; for LB overlay use 0.7% agar.

The first three components and their corresponding amounts are the same as what I normally work with, but I usually add distilled water for plating E. coli instead of NaOH. According to Wikipedia's entry on lysogeny broth, NaOH can be added to adjust LB's pH. But the protocol here mentions nothing of that sort. In other protocols of the book, at least it would say "adjust to pH -- with 10 M NaOH" or 1 M NaOH, etc. So if it is not to adjust the pH for the growth of Bacillus subtilis, what other purpose does NaOH do for the bacteria?
Also, I usually autoclave my LB or LB-agar for 2 hours instead of 30 minutes. Would autoclaving at 2 hours instead of 30 minutes affect NaOH?

The NaOH is to adjust pH. They must have determined that that much NaOH with those ingredients makes a suitable pH, but I think your much safer to titrate.

Why 2 hrs? Why change the recipe? @canadianer is quite correct, per usual, the only reason to add a small amount of extremely strong base to your media is to adjust the pH. And yes, if the pH of the broth and the plates is crucial for your experiment it would be much wiser to titrate the solution. The distilled water pH will vary, as will the agar and the other ingredients (slightly, from batch to batch). also, I would be concerned that autoclaving for extended periods of time could also affect pH by breaking down the ingredients in the complex mixtures

http://www.ncbi.nlm.nih.gov/pubmed/11700343

I think NaOH is added to bring up pH not to get too acidic. I feel autoclaving LB or LB-agar for 2 hours is too long. During autoclaving, some components are gradually degraded.


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How is the volume of the dialysis buffer decided?
Is there a specific ratio between the volume of enzyme solution in semipermeable membrane bag and the volume of the buffer outside the membrane bag? I have been looking for a specific formula or general rules to decide on the volume of the buffer outside the membrane bag but to no avail. There must be general rules to determine the volume. It can't be come up with out of thin air. What common criteria are there to determine the volume as well as the time for the dialysis?

You can calculate the final concentrations of solutes in your sample after dialysis, assuming complete equilibration, with C₁V₁=C₂V₂. This formula also tells you that it is more efficient to dialyze, say, twice in 500 mL instead of once in 1 L. I typically dialyze several times in 500 mL because it seems like a reasonable beaker size.

In case I wasn't clear: you can calculate solute concentrations as mentioned above and then use this information to plan the volume(s) to use in your dialysis, depending on your specific needs.

By "solute", do you mean the enzyme, imidazole, salt, or something else?

A solute is anything dissolved in a solvent, so all of the above and more. The point of dialysis is to remove something unwanted from your sample. You decide what concentration of that something is tolerable for your experiment and dialyze accordingly.


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Are amantadine and rimantadine MOAs unknown to evolution?
Are any natural (human or otherwise) antiviral mechanisms similar to the antiviral mechanisms of amantadine and rimantadine, or are these mechanisms undiscovered by evolution? Are drug researchers discovering completely new mechanisms to attack viruses?
http://www.rapidreferenceinfluenza.com/chapter/B978-0-7234-3433-7.50014-1/aim/mechanisms-of-action-of-antivirals
The mechanism by which antiviral drugs (amantadine and rimantadine) interrupt the replicative cycle of influenza is illustrated. M2 inhibitors prevent the M2-mediated acidification of the interior of the virus while it resides in endosomes and the subsequent uncoating of the viral genome, thus inhibiting viral replication. Neuraminidase inhibitors (NAIs) prevent cleavage of sialic acid residues and thus newly formed virus cannot be released from the cell surface to infect adjacent cells; also, virus particles remain associated to one another.

Welcome to Biology SE. It is an interesting question, but I don't know if there are any experts on animal virus life-cycles in this group. In terms of evolution and discovery, there are definitely pharmaceutical companies (the ones I've heard of were based in Japan) who maintain cultures of purified soil microbes, and then assay the microbes' used culture media for "natural" compounds that affect a lucrative biological process.


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Can suppression of the immune system help cure chronic diseases?
I am not a biologist, but recently while reading an article on Scholarpedia about self-organization I encountered a fascinating biological observation concerning immune response to infections.  To quote the article:

Whether the resulting patterns are stable or oscillating depends on the relation of the time constants. If the antagonistic reaction has a longer time constant than the self-enhancing reaction, oscillations or burst-like activations will occur. An example is the time course of an infection: The infection with few viruses could be sufficient to trigger a sickness since the viruses replicate themselves (self-enhancement). The antagonistic reaction, mediated by the immune system, is much slower. It takes a day to become sick, but a week to become healthy again. (What appears on a first inspection as a disadvantage is in fact a good strategy. If the immune system would be much faster, an equilibrium between virus production and virus removal would be established. After a single infection we would fight for the rest of our life against the virus. However, due to the burst mode, we become sick for a short while but the virus is subsequently completely eliminated).

Since the quote may be hard to parse out of context, I'll recapitulate: The writer is asserting that the immune system's response to infections is slower than might be physically possible because such slowness actually makes the response more effective.  By waiting a few days, the patient is sick for longer than they might be happy about, but when the infection goes away, it's gone for good.  If the immune system responded immediately to an infection, it might result in a low-level infection that persists indefinitely.
This makes me wonder: For chronic diseases, is the reason they are chronic related to the time scale of the infection vs. that of the immune system's response?  Could such diseases possibly be cured by suppressing the immune system for a time so as to get the "burst" effect alluded to in the quote above?

I fail to follow the logic of that quote. Furthermore, components of the immune system are active as soon as an infection is recognized.

@canadianer I'm not an expert, so I can't say with authority, but as I understand it the implication is not that the immune system waits before taking any action, but rather that the time scale for the overall response is "intentionally" longer than the time scale for the infection itself, the idea being that the delay in response can make it more effective in eradicating the infection.

It's entirely possible that I'm missing something, but why would a delayed response be more effective?

@canadianer That's exactly the point, and it's why I found this so surprising! :)  I don't claim to know why it should be true in the case of infections, but I can believe it based on analogies from other systems with multiple competing agents.

@canadianer Here's a basic way of rationalizing it to myself: The immune system will take some minimum time to prepare a counter-offensive against the infection.  If it were to start attacking the infection before it was completely prepared, perhaps the infection would be able to adapt and reach a stand-off.  On the other hand, if the immune system delays, it will be able to wipe out the infection entirely before it can adapt.  I don't claim this explanation is right--I only propose it as a heuristic for why it might be advantageous to delay response.

I can not answer clearly, so I write comment here. Take vaccination for example. Some virus infection causes acute symptoms, but if you are vaccinated, you do not get any symptoms. This means your immune-system is fully functional to eliminate viruses as soon as viruses are invaded. You do not need to wait propagation of virus to eliminate them.

What should be the benefit of this delay? It raises the chances that our body is overwhelmed by the virus and dies. The delay of the adaptive immune system is simply caused by the fact that it needs some time to launch a highly specific immune response. The innate immune system (you could call this our first line of defense if you like) acts very fast and almost immediately. Additionally viruses get used to our immune system and adapt, see HIV for example. I can make this into a full answer later today.

@Chris is right here.  The quote is both wrong and misleading.  The immune system clears an infection after a delay because the adaptive immune response takes a few days to develop.  Chronic diseases almost always are due to an ineffectiveness of the immune system or inability to respond appropriately.

@canadianer and everybody wondering about the logic behind the q: this type of equilibrium is best known to biologists from the Lotka Volterra rule. Start out with a balanced ecosystem, say 100 rabbits and 10 wolves, and you'll have rabbits and wolves forever, in changing ratios. But if you start with 100 rabbits and 50 wolves, you'll run out of rabbits before the wolf number goes down. The assumption behind the q is that waiting for a large virus population elicits an overproportionally "large" immune response which kills all viruses instead of the supposedly "small" response to few viruses.

@rumtscho I understand what the quote is saying, but the immune system does not follow a predator-prey relationship. The quote suggests that a delayed immune response is an adaptive advantage rather than a mechanistic requirement. That is the logic I did not follow, with the implication that it is incorrect.

@canadianer I see. Then I had misunderstood your first comment - it now seems we agree on what the exact problem is with the quote. I thought it important to write it out explicitly, because when somebody presents with a wrong idea, it is frequently best to hunt down the exact place where a wrong assumption is used, else he is unlikely to understand the correct explanation. And sometimes the experts have the hardest time to spot the problem in understanding, because they know the subject so well, they can't imagine that somebody will make an "obviously" wrong assumption.

@rumtscho Your comment was good, I just wanted to clarify mine to avoid looking like a complete dolt ;)

No, this wouldn't happen. The logic of your proposition assumes that chronic diseases are caused by the strength of the immune response being insufficient to kill off the virus, resulting in a long-term equilibrium between the amount of virus particles produced and the amount of virus particles killed.
In reality, this is not how chronic diseases work. Only a small amount of chronic diseases are caused by viruses. There are many which have other causes, not all of which can be defended against by the immune system - e.g. chronic depression is not curable by immune response.
But even if we focus on chronic virus infections such as herpes simplex, they are not sustained by the mechanism you describe. They happen due to the fact that our immune system simply does not know how to get them out of their new home within our body, they are just that good at hiding during latency. So even if you could cause a strong immune response all at once, it wouldn't kill all viruses at once.
Even if we have viruses whose serum presence depends on a constant growth vs. destruction dynamic (I don't know if these exist at all), an overly strong immune response won't be that good for the human host. Inflammation is a dangerous state, most of the unpleasant feeling you get when you are sick is not due to the virus itself but due to your own immune response, which causes the fever, muscle pains etc. associated with many acute infectious diseases. If we were to ramp this up, you'd probably get a fever high enough to cook you alive, or some other undesirable effects.

On a side note, I also doubt the author's argument which suggests that long-ish convalescence times evolved because shorter ones would leave the system in an undesirable equilibrium. Sure, an alternative reality is thinkable where the innate and adaptive responses described by Chris occur much stronger at the beginning, leading to steeper curves and shorter healing times. But the simpler explanation for that is that 1) our immune system is not perfect, and it evolved to the highest healing speed it could achieve, and 2) an immune system with higher acceleration would have been way too costly in terms of resources available to the body. An evolutionary advantage in having a low-acceleration immune system is a strong assumption for which I see no support, especially considering that the residual immunity provided by the adaptive immune system would prevent the dynamic equilibrium suggested in your quote.

I think the person who wrote the quote does not really understand how an immune response is happening. There is no real "waiting period" until the immune system starts attacking the virus (or bacteria or whatever), this happens instantaneously when the virus is recognized.
To do so, we have two, independent systems, the innate immune system and the adaptive immune system. The innate imune system reacts immediately and launches a unspecific, but still very effective answer to a virus. The adaptive immune system delivers a highly specific (via antibodies) immune response, which takes a while since the generation of specific antibodies takes some time (the body produces antibodies which are then matched against the virus). It works like shown in the figure (from here):

It is also the adaptive immune system which mediates the long-lived immunity against pathogens which have triggered a immune response. Once you get in contact with such a pathogen again, the adaptive immune system can react immediately and protect you. This is also how vaccinations work.
Both immune answers start immediately upon pathogen recognition, there is not benefit in delaying (or suppressing) this immune response. In contrary, this is highly dangerous for the individual, as you can see in persons, which have received a transplant. These need to suppress their immune system in order to prevent a transplant rejection, but at the price that they get sick a lot easier.
However, there are some diseases, where a partly modulation of the immune system is beneficial. These are autoimmune diseases where the immune system is directed against the own body. Examples would be rheumatoid and reactive athritis.


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How many animals inhabit the United States?
How many animals inhabit the United States and its waters? Not the number of species, but the number of individual animals. And since animals are diverse, maybe we can limit the estimate to just vertebrates - domesticated and wild. I totally get that nobody knows the answer to this, but I'm wondering if anyone has made an estimate, or if there are sources from which I could piecemeal an estimate.
Thank you!

Perhaps you could try here to start calculating a rough estimate.

Related post: How many organisms have ever lived on Earth?

If you are interested in the number of pets, this can be found here: http://www.aspca.org/animal-homelessness/shelter-intake-and-surrender/pet-statistics (e.g.:It's estimated that 70-80 million dogs and 74-96 million cats are owned in the United States.)

Do humans count?


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Identify this black dragonfly with bluish coloration along its flat top, yellow on it's mid-body and green on its head
I took these photos around noon in late July in Hsinchu county Taiwan. This particular stick in this particular pond is visited by many dragonfly species. I have seen this kind of dragonfly very regularly, in different nearby ponds, they seem to me to be far more active than other dragonfly species in the same area at the same time.
Its body is about 5 cm long and mostly black. However it has light "power blue" to white markings on the flat top surface of its "tail" and "mid" sections and the front part of its body before the head, and it seems to have some smaller yellow bands on the sides of its fore body and greenish markings on its head.
Wings are mostly transparent but are tinged orange or brown near the body.
Question: Is it possible to identify this particular species of dragonfly?

This species of dragonfly is Brachydiplax chalybea. Colloquially known as blue dasher.
General information
More information

can you confirm that it's not this instead? https://biology.stackexchange.com/a/94939

The colour and placement of colour - blue and it is located on the dragon fly thorax. Also the dragon fly in your link has a distinction of where the colour ends, unlike your image and the blue dasher. Whereby the colour is 'smudged' along the abdominal segments.

Care to try another? Identify these two big, beautiful dragonflies in Taiwan?


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Why do wasps have "wasp waists"? What's been optimized?
I photographed these (unidentified) wasps on a sunny but cool winter day in northern Taiwan because they were conspicuously hanging out on a hand railing and had much lighter coloring than I'd ever seen before.
But after I took the time to look at a close-up I realized "Wow, they really have long, very thin waists!" Mechanically, it looks like they are two large masses connected by a very long thin beam, which must have quite a tiny canal in the center to let all the "juices" flow through.
While other insects and spiders may have segments separated by a tiny connection, this one is both small in diameter and quite long.
Why? Does this specific configuration provide some benefits to them?

 click for full size

companion question: What are the three dots (eyes?) on the top of this wasp's head? What species might it be?

Note that mechanically, the required slenderness ratio of a self-supporting beam is inversely proportional to scale. So this feature is much less costly for insects than it seems to be from macro photos.

@Therac agreed for sure - but... why? The reason I mentioned that it looks like two masses connected by a beam (and with wings attached to one of them) is that I wondered if this configuration has some mechanical advantage - perhaps during flight. As you suggest, it can be small in diameter and still plenty strong for the job, but I also wonder why it's so... long.

Why do humans have such a flexible shoulder?  Our ancestors relied on throwing things so the ones who could throw things better did better.  What is the wasp's equivalent weapon?  The stinger.  Wasps have such thin "waists" to facilitate maneuverability of the stinger.  This is especially important in wasps because for many, and for the ancestors who first evolved this feature, a flexible thorax with an ovipositor capable of depositing eggs into grubs and caterpillars was fundamental to their reproduction.  The path to their current form seems to have been as follows:  1) early stingless wasps develop an ovipositor and begin implanting their eggs into other insects, 2) the thorax evolves to be thin and flexible to facilitate this method of reproduction, 3) the ovipositor modifies into a stinger and, combined with that flexible thorax, the wasp becomes the Zorro of the skies.
See New Scientist's 20 November 2019 Hourglass figure: Why do wasps have such narrow waists?

I had also thought about that, but for the specific types I wonder whether it could also have aerodynamic reasons (in terms of efficiency and balance).

The ovipositor argument sounds (to me) like special pleading.  While the wasp-waist may make ovipositoring somewhat more efficient it seems unlikely that this is of such major selection advantage to drive such a change in so many wasp variants. || Stinging flexibility as suggested by one respondent in your link sounds more likely. But even that seems an unlikely selection driver.

@RussellMcMahon hmm... we have to remember that the stinger is a modified ovipositor, so only females can sting or "oviposit". In Sexing a Black & Yellow Mud Dauber Wasp "abdomen (A) to petiole (B) length ratio (A/B) - (male = 0.6 to 1.3, female = 1.5 to 1.9)" the abdomen is significantly longer for females. That's one species only, and I don't know if males have different aerodynamic requirements...


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What are the three dots (eyes?) on the top of this wasp's head? What species might it be?
I photographed these (unidentified) wasps on a sunny but cool winter day in northern Taiwan because they were conspicuously hanging out on a hand railing and had much lighter coloring than I'd ever seen before.
But after I took the time to look at a close-up I realized "Wow, this wasp has three dots on the top of it's head!"
If it was a spider I'd assume they were eyes, but like many insects these wasps already have to large wrap-around eyes that extend towards the top of the head already?
Question: What are the three dots (eyes?) on the top of this wasp's head?

 click for full size

companion question: Why do wasps have "wasp waists"? What's been optimized?

This is like the mud dauber wasp

They're called 'Ocelli,' other posts have outlined their function.

I don't know what species this is but a lot of bees and wasps have those three dots on their head.  They are sort of eyes, but they can't actually make out images.  They basically just detect light above the wasp's head.  By having three there in a triangular configuration, the wasp can determine the direction of any shadow that appears overhead, like a bird swooping down for a snack.

University of Houston - What Bees See
Wikipedia: Simple eye in invertebrates; Dorsal ocelli

Neat. We often forget as mammals with a paltry two eyes that in other creatures, different eyes may have different purposes and be more highly specialized.

If I recall, these might be horizon sensors or sky polarization compasses.

I recently purchased a Giant Asian Hornet and noticed them -On your example the Executioner Wasp they’re also present . These are not eyes but an organ used for navigation so to speak . Used for sorting out direction and light

Great, and welcome to Stack Exchange! In this site, answers should support their assertions with links or references. Can you add something telling us what makes you think that they are "not eyes but an organ used for navigation so to speak . Used for sorting out direction and light" If you read it somewhere, please mention where. Thanks!

According to the OP, the pictures were taken in Taiwan. The executioner wasp, however, is native to Central and South America...


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Why is thrombin time (TT) normal range longer than prothrombin time (PT)?
Reference range for the TT is longer than that of the PT.

This is a great question.
I'm going to hypothesize here because I haven't had a chance to test my theory and I'm afraid that by the time I get around to it, I may forget about this question.
The real question is, what is the variable that makes the thrombin time act differently than what you would assume? I’d wager the answer is temperature.
Protimes are performed at 37 degrees in order to simulate the in vivo environment, but also because most coagulation factors aren't active at room temp, or at least they are very slow-acting at room temp. Heating the environment speeds this process up so the test doesn't take all day.
Now, we know if you take a tube of warm normal plasma and add calcium and thrombin to it, it clots right away, right? But this is a problem because the thrombin time is a quantitative assay and we need it to be sensitive, especially for those super old-school clinicians who use it to monitor heparin instead of a more modern test like the APTT or Xa inhibition. We need to be able to tell the difference between a patient that’s gotten a bolus of heparin and a direct thrombin inhibitor. So, if you remove the heat, you slow down the conversion of fibrinogen to fibrin, and in the process you stretch the calibration curve, effectively increasing the sensitivity of the test. But this also has the effect of slowing down the conversion to where it takes 14–18 seconds rather than one or two.
If you change your test setup to have the thrombin reagent heated, my hunch is that your analyzer will give an error because the sample will have clotted by the time the analyzer reaches minimum threshold time. Or better yet, try this experiment on a fibrometer. I don’t have access to one so I can’t try it out as I’d like to.
I’d be interested in discussing this with any other experts out there, especially those that have played around in the coag lab. I may have occasion to test this out in the coming weeks; I’ll try to do it and update my answer with my results.


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Why sea water fish can't survive in Fresh water?
Why the sea water fish can't survive in fresh water?
What really happens to the fish if it get into fresh water from sea water.
What are the possible reason...

Does it really depends osmotic pressure on the cell of the fish?
It depends on the buoyancy of the fish?
The bacteria content in water?
The temperature of the water?

homework questions should be tagged as such. They should also show some effort on your part to find an answer.

Osmosis:
In case you didn't know, osmosis is the flow of solvent (here its water) across a semipermeable membrane from lower concentration of solutes to a higher concentration.
Freshwater fishes have their bodies with body fluids isotonic, or same concentration, with the surrounding freshwater body. If you throw such a fish into seawater, considering that seawater has a lot more solutes dissolved in it, water will flow from the fish into the seawater. The fish would get deprived of water and will most probably die.
Note: Certain fishes like Sockeye Salmon can survive both saltwater and freshwater. Sockeye in particular usually lives in marine habitats, but returns to freshwater for spawning (egg laying). This fish overcomes the osmotic problem, by staying in the intertidal zone for a while, thus adjusting it's body fluids to the intertidal zone, and then finally moves to the freshwater. Yet, some others have non-permeable membranes as skins, so that osmosis isn't a problem for them.


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Is there any possibility that gender is determined by Temperature?
One day I was watching TV show. It was based on Fire Dragon. They stated that if the dragon provide greater warmth to the egg, then a male Dragon will hatch. And if the Dragon provide less warmth to the egg it will be female Dragon.
This was totally Science Fiction!!
But is there any possibility that, the Temperature decides the Gender of progeny.

Not exactly a duplicate but the answer to this question is in the background of the linked question.

It is definitely more than science fiction. Many species have sex determination that depend upon the temperature.
As a rule of thumb, when it comes to sex, not much has been invented in fictions. The diversity of reproductive system is HUGE! I will not mention 1% of the existing complexity in sex systems. For simplicity, below I will limit my concepts and examples to big animals only. I won't talk about

double fertilization
cloning
parthenogenesis
dosage compensation
Mating types
Cases of multinucleated cells typically in fungi but not only
Asexual reproduction
Systems with more that two genders or with coexisting hermaphrodite along with a single other gender
Liability factor
Reaction norms for sex determination
How reproduction relate to all that
How dosage compensation relate to all that
How the concept of individual relate to all that
etc...

Sex Determination System: GSD vs ESD
There is a great diversity of sex determination system. The standard is to classify them in two

Environment Sec Determation (ESD)
Genetic Sec Determation (GSD)

Of course, the reality is more complex. In many species a mixture of both genetics and environment clues matter.
Within ESD species, there is quite a bit of variety. Some species use temperature (e.g. crocodiles, Nile tilapia, Australian skink lizard), others use social cues (e.g. clownfish, swordfish, boa constrictor).
Within GSD, there is also a great deal of diversity. By far not all species use the XY system used in mammals.
Related post

Do males of all sexual species have Y chromosomes?
Have there been any theories put forward as to the reasons behind Temperature-Dependant Sex Determination in reptiles?


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Is Dioxin causing Diabetes Mellitus?

Today I was watching a show on Discovery Science (Everything You Need to Know About). In that show they were talking about toxins and venom.
In that they mentioned Dioxin and its effect. And suddenly I heard the unexpected, that Dioxin damages Pancreas!!
Dioxin spreads due to contamination by food & mainly beef (as mentioned in the show).
It is produced mainly because of (chlorinated) burning of fossil fuel, coal,trees,PVC, plastic.
As there is a spike in the diabetes in recent years. And there was a increase in pollution from last few decades.

It looks like Dioxin is culprit which is lurking behind to attack people and causing Diabetes.
Am I thinking right?

Correlation is not causation.  There has, for instance, been a large increase in the consumption of soft drinks in recent years.  There's also been a large increase in the number of personal computers, and of solar panels on rooftops.  Of those four correlations (and there are many others), which is most plausibly linked to diabetes?

Valuable information:- https://www.who.int/news-room/fact-sheets/detail/dioxins-and-their-effects-on-human-health


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Can a lion be fed cat food?
Is there a correlation between eating raw meat and aggressiveness in felines and canines?
Growing up, I was always told to cook the meat I gave to my dogs and cats so as not to give them the "taste for blood". Is there truth in this myth?
And if that's the case, wouldn't the same food have the same effect on "bigger cats" ? Wouldn't it safer to feed Zoo animals cooked meat ?

I read once (I don't remember where), that captive big cats' food has to be prepared in a way similar to how they would eat in the wild. e.g. cheetahs will only eat extremely fresh meat (in the wild, they have to eat quickly because their kills are often stolen), but leopards prefer meat that's almost rotten (in the wild, they store their kills in trees for days before eating it). In other words, I suspect the reason zoos don't cook meat for big cats is because they want to mimic the animals' natural diet.

I'm voting to close this question as off-topic because it looks pob and better suited for skeptics. Issue with this kind of question is that the answer-er needs to prove or debunk the theory first and then start explaining why; basically a double answer imo. Better split it up I guess; prove or debunk @ skeptics and come back here with a more educated question.


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non-coding RNA modelling in silico
I've been trying to model a non-coding RNA molecule which binds to a RNA binding protein. I found the DNA sequence for ncRNA from NCBI. I did not find the RNA seq of the same. Hence my doubt is, whether we should take the DNA seq and convert all the thymidine to uridine and then take that sequence for RNA modelling. Also, I wanted know if there is any kind of splicing occurring in case of ncRNA formation. Thank you in Advance.


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Why can't dopamine cross the blood brain barrier but l-dopa can?
Levodopa can cross the BBB and is less lipid soluble then dopamine, so dopamine should be able to cross the BBB more easily then l-dopa, but for some reason dopamine cant cross the BBB. Both dl-methamphetamine and levomethamphetamine can cross the blood brain barrier, but why not dl-dopamine?

Both L-Dopa and Dopamine are polar molecules and thus hydrophilic. They are solvable in water but not in lipids, so they are not able to cross the Blood-brain barrier on their own.
The difference is that L-Dopa has a transport protein (SLC7A5) that allows it to pass through the Blood-brain barrier, whereas dopamine doesn't.

Yeah, that's LAT1, but why doesn't DAT1 have any effect?

If you look at the distribution of LAT1 versus the distribution of DAT you can see that LAT1 is distributed in the blood-brain barrier, whereas DAT is not.


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What is the name of cell structures that have an adaptation to increase their surface area?
Epithelial cells that line the small intestine have an adaptation to increase their surface area - what is the name of these structures? And why would the small intestine require a large surface area?

What research have you done before asking it here?

@another'Homosapien' I already found microvillus before coming on here, just to confirm.

The small intestine requires a high surface area in order to increase the rate of absorption of digested food.

The greater surface area also provides for more secretion of the "brush border" enzymes responsible for the finishing touches of digestion.