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What does it mean to be a fully human monoclonal antibody?
I somewhat understand that some monoclonal antibodies are developed from the cells of mice, or a fusion of human and mice genes.
When something is a fully human monoclonal antibody does that mean it came from some person? What type of human cell did it come from? Will the drug always be from that original human?
I read that they're derived from something called a phage display technique. I'm guessing this is another type of way to fuse genes together, but with all human cells.
Where do the cells come from?

Following technquies are used for developing fully human monoclonal antibodies:

Complementarity-determining region (CDR) engraftment: This method is
performed by preparing  cDNA library. CDRs are amplified from a mouse
hybridoma cell line, and later these sequences are engineered  into
the human variable light and heavy chains.
Using transgenic mice with human Immunoglobulin genes:  Hybridoma fusion
technique is used to synthesize human monoclonal antibody. The
transgenic mice expresses DNA encoding human immunoglobulin genes.
Display technologies using phage, yeast, and ribosome:  Heavy and
light chain cDNA from human B-cells is used to construct a library.
Various  heavy and light chain pairs are expressed on the phage.
These phage are screened for antigen binding. Further this
recombinant monoclonal antibody is synthesized using prokaryotic,
yeast expression system, insect or mammalian cell expression system.

Display technique uses the  principle of specific antibody production but employ micro-organisms in case of phage display and cell free extracts in case of ribosome display. These systems depend on  creation of gene libraries  constructed using peripheral blood from humans. The  products synthesized in this procedure are antibody fragments of Antigen binding (Fab) or  Single-chain variable (scFvs), having complete human sequence.
Via:
http://www.pharmtech.com/novel-process-developing-fully-human-monoclonal-antibodies?id=&sk=&date=&pageID=3

Took a while to do some additional reading, but thank you. I think I better understand. Would you mind letting me know if you don't fully understand this though?

Also, Link seems dead.

I found this small article that seems to cover all your questions:
https://www.sciencedirect.com/topics/medicine-and-dentistry/human-monoclonal-antibody
Summary:
Being considered a human monoclonal (many of the identical antibody, as opposed to different antibodies for the same target) antibody does not mean it is produced by a human body; it means that the fc-region of the antibody is human-like, which aims at avoiding immune reactions against that antibody if injected into humans.
So the human antibody can originate from animals (e.g. rats or rabbits) with humanized antibody genes or from immortalized human cell-lines (lymphocytes).

Thank you. I was able to access the full article, and was surprised to see it's from 1998. It has some sections on general approaches to making monoclonal antibodies and human monoclonal antibodies. The 1998 article explains that for ethical reasons it's not possible to "hyperimmunize humans and typically the only source of B lymphocytes is peripherial blood ... less suitable for fusion." It then goes on to discuss workarounds. The only human work around is to "immortalize" the B lymphocytes with the Epstein-Barr virus.

The link you shared has newer information, and talks about using "bacteriophage display library of human variable region sequences and selects for antigen binding in vitro. The selected genes are then combined with human constant region genes to reconstitute a complete IgG antibody." This sounds like the current state of the art. Doesn't sound fully human either!

Link-only answers are generally not acceptable on Stack Exchange sites. The link may change or become unreachable in the future, and without a summary of what the link contains this answer would be useless. Please summarize what is in the link (don't just copy and paste) and use the link solely for reference. If you remove the link and the answer cannot stand on its own, it is not a good answer.

Sorry, I didn't know that and obviously just tried to help.

@KaPy3141 That's fine - my comment is one of the standard ones and is intended to help you know so you can improve your answer, since you can edit it to fix the problems. Welcome to Biology.SE!


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Does specific immunity affect the incubation period of viruses?
My interest was inspired by the observed variation in incubation times for different strains of Covid-19, however I ask the question in the broader sense as it seems hard to find an answer in general.
Does the presence of immunity affect the duration of incubation period? I would have thought the body's ready ability to identify and defend against a virus may mean that it is identified sooner following infection. But I can't find evidence to confirm or refute this idea. Would really appreciate any thoughts!
Thanks

Sorry - I'm not sure on the question here - once a virus enters a cell it will replicate at approx the same rate no matter whether there is an immune response. Immune response could prevent infection/limit infection, but won't affect replication kinetics.

I feel contradiction: if there is "incubation" there is bound to be "no immunity".

@bob1 It was a question of what is really happening during incubation. During incubation the virus is replicating undetected, but at some point it becomes detected and is no longer in the incubation phase. So I'm curious whether having a better immunity to a particular virus would result in a quicker detection in this phase, therefore shortening the incubation phase. Thanks for your answer

@PeterBernhard that's not true at all. The evidence is all around you - people who have been vaccinated are still getting sick with the omicron variant. Granted, not as sick as with other well-publicized strains, but sick nonetheless. The same thing happens with delta, to a lesser extent. So clearly, people with (good) immunity can still have virus incubation and eventually illness.

@MattDMo Thanks to your comment I now feel better ... with the question that seems to have incubated on me, just as your comment seems to have.
I will delete that expression of my feelings up above, as it hurts. Sure, me too, I have been misunderstood:  it's in your parenthesis, what I was up to, i.e. how can you use the word well - immunity - if incubation is evidence for its failure which is non existence. That is a debate on words and definition. Maybe more, though. (What is: symptomless infection) I feel understood. Still, I will delete my comment. I always did agree with all you say.

@MattDMo Amending my comment with the help of your comment I would say that the phrasing of the question "specific immunity" makes you think - first guess - of a kind of immunity that is effectiv (again, your parenthesis, to me are of importance).
The phrasing does not immediately let youknow what the point is: does specific immunity as a very good immunity shorten or prolong incubation  in cases that you list, i.e. in cases of break through infection, vaccine failure. That word vaccine failure does not go well with "specific immunity" in a head line. I still insist, but will delete.

The wording of the question does not seem convey what it is about: If there is enhanced, "specific" immunity, the incubation period of a  break through infection (vaccine failure might be  some inappropriate term) should be prolonged

as with specific immunity which is good ammunition the fight should last longer before it is lost and incubation becomes "success".
By intuition, the answer should run: yes, immunity affects the incubation period, the more  specific and thus the better the immunity the longer the fight, the longer the breakin' the immunity, the longer the  incubation time.

Does this question also refer to "symptomless infection"? I think it is important to be clear about definition of word: can there be spoken of "incubation" if there will never by any "symptoms"? Interestingly, your question is of practical relevance: thanks to vaccination people might either prolong their being infective to some indefinite point in the future - good to know -- and, counterintuitively, it is not at all trivially clear that (specific) immunity does not shorten the incubation - "period" :-) Seriously: it does not occur easily that good immunity just cannot shorten incubation.

You refer to "symptomless infection", too?  Can there be spoken of "incubation" if there will never by any "symptoms" (two terms mutually defined)? Of practical relevance: Thanks to vaccination people might either prolong their becoming infective to some indefinite point in the future - good to know.
It is not at all trivially clear that (specific) immunity does not SHORTEN - just cannot -  the incubation - "period" :-) Seriously: it does not occur easily that good, specific immunity just cannot shorten incubation time. @Bob: no "influence" of immunity on "virus as is"?

@PeterBernhard, I think you need to have a good look at the role of immunity in infection. Good immunity means infection is limited in some way. This will not prolong their being infective indefinitely. Either the virus will enter the cell and replicate, or it will not enter and no infection results. Replication kinetics of the virus are key. Good immunity results in lower levels of infection because virus that exits the cell will be absorbed by the immune response faster and to greater levels than with poor immunity. Not longer infection!

@PeterBernhard In fact, it is the other way around: Prior immunity shortens the observed incubation period. See my (now edited) answer to the question.

There are two effects that can shorten the observed incubation period in presence of prior partial immunity

Symptoms are caused mainly by the reaction of the body, not by the virus itself. When there is some prior immunity, the immune response kicks in faster, leading to an earlier onset of symptoms. This effect is genuine.
When the infection proceeds somewhat slowly, it may be completely terminated by the immune response without any symptoms occurring. This effect cuts off the long tail of slow infections, leading to a shorter average incubation period.

EDIT: Not a publication but a Twitter thread by a renowned scientist (Micheal Mina) confirming shortening of incubation period by immunity.

source: Stack Exchange

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sort: votes


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vocalizations meaning for rats/mice
Rats (rattus norvegicus) vocalizations are said (in the literature) to have some positive or negative meaning, mostly 22kHz vs 50 to 80kHz. Some papers hints to nearly syllables, describing a number of different class of vocalizations depending on their spectrogram shapes.
Could we give any meaning to those "syllables" ? Couldnt find any specific answer.

What did you find during your research?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site — saying you couldn't find an answer is not sufficient. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

When searching, also try the term “DeepSqueak”. This delightfully named software is for analysing ultrasonic vocalisations.

Thanks you all for your comments. The thing is I have done a few year of academic research on the subject and where I state 'couldn't find any specific answer' I mean papers are only describing the USV but usually don't go as far as giving any meaning nor studying their occurrence in time mostly they correlate pitch with positive or negative behaviours / environement such as stress, eating ... and mostly with very young individuals

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can mammalian expression vector be used in e coli to produce plasmid
I would like to use this plasmid (mammalian expression Flag-HA-USP53 (Plasmid #22606) - Addgene) to produce plasmid in e coli to purify plasmid. Would this work? I am starting out with this vector because it is already available and has the insert I need.

Short answer: Looking at the plasmid map, yes, this should work.
Long answer: It depends on the plasmid. To be able to replicate a plasmid in bacteria, you need a origin of replication (ori). To find out if this is present, have a look at the vector map provided by Addgene:

It shows the ori on the left side of the map. Additionally an antibiotic resistance gene is helpful to be able to select for bacterial cells whic have taken up the plasmid in the transformation, which is also present in form of the ampicillin resistance gene.
Generally speaking most expression plasmids will carry both feature since bacterial transformation, growth in culture and mini (or midi or maxi) prep it is by far the fastest, easiest and cheapest method to produce large amounts of plasmid.

To add to this, note that the linked Addgene page has a section titled "Growth in Bacteria" with specific instructions for growth temperature, strain, and selection

Thank you. Very helpful.


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Is it possible to identify secreted metabolites or secondary metabolites from a gene list?
So I have a gene list obtained from differential gene expression analysis of a metabolic disease model, and I was wondering if I can identify metabolites or secondary metabolites that may be produced by some of enzymes or reactions modulated by these genes by bulk.
For example, I know that Ptgds synthesises prostaglandin D2 and it is secreted in urine and plasma, and so on.
However, I don't want to do a whole research on each and every gene separately, rather like a database or a tool that can identify them by just inserting a gene list!

Obtaining the specific metabolites from genome-wide measurements of transcripts can be somewhat possible, but remains quite challenging, and might not be possible for many organisms because too little is known about them. If the purpose is to get a better idea of the changes in transcriptome without needing to infer specific metabolites (e.g.: if it is sufficient to know if some pathway is up or down regulated) you could do functional gene enrichment analysis instead. Latter can be adopted widely and there are nice tools such as the web-based https://david-d.ncifcrf.gov

The problem is that we want to identify some biomarkers that are steadily found in urine, plsama or other easily attainable fluids. I already did enrichment analysis and gene ontology along with many others.

I am currently going through each gene and looking into their pathways to find whether they produce metabolites. It's time consuming and not efficienct I'm afraid.


text:
What does this jawbone belong to?
I found this specimen in a rock garden near St. Louis Mo. I believe it to be the posterior portion af a lower mandible of a mammal. The photos I am including seem to me to show;b[!broken teeth, ]2:tooth roots, blood vessel fossa. I could be seeing things but can somebody support my theory?
It measures 4cm in length,4cm in width, and 4 cm tall.

That's most likely quartz, which isn't generally found in fossils. High quality photos with the whole specimen in focus (i.e depth of field increased - use a higher f-stop) from several angles would be required for us to make any identification. We would also need a location (approximate, nearest city would probably work).

this is likely quartz,it had probably been better to ask what is this than it is to state what you think it might be.if rock id questions had been on topic over at https://earthscience.stackexchange.com/ it could have been migrated but rock id is off topic there.


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Do bees use their ovipositors for egg-laying?
I'd always assumed that, since bee stings are 'modified ovipositors', queen bees couldn't sting. But apparently they can.
What is going on with bees' ovipositors? Are they capable of injecting both venom and eggs?

Hi and welcome! This is easy enough to google. Did you try, and if yes, what did you find? You might wonder what kind of Q&A site this is, being asked to show your search results; shouldn't we just answer your question? Actually, no. We're expected to help if we so choose. We're scientists or people interested in science, a lot of us teach, practice, or research some aspect of Biology. We expect some meaningful degree of research; not a ton, but not nothing, either. Consider this kind of like a classroom, not a chat room. You'll get a (better) response with a better effort on your part.

Googling didn't turn up anything useful for me, but if you know the magic phrase to google for, let me know, and I'll finish the research and answer the question myself!

Try some combination of your own words: ovipositors, stingers, queen bee, eggs.

So, from the first page of hits for "ovipositors, stingers, queen bee, eggs", I have : "However, in virtually all stinging Hymenoptera, the ovipositor is no longer used for egg-laying."  and "Queen bees can use their ovipositors to lay eggs and to sting but worker bees only use it to sting as they are infertile and don't lay eggs." That sort of thing is why I asked the damned question here, where I thought an actual biologist might answer it.

OK, so you think all Biologists know about queen bee ovipositors/stingers? An etymologist would probably know, or an apiarist. Don't know if we have either one on this site; I'd be surprised if we didn't have an apiarist or two. I have two advanced degrees in Biology, and I didn't know off the top of my head, but I did google it and found the answer. You also found the answer: your two statements are not mutually exclusive. Think about the statements and tell me why you think they don't answer your question, and I'll answer the damned question personally! ;)

So, if 'virtually all stinging hymenoptera' doesn't include the canonical example of stinging hymenoptera, then yes, clear. Queen bees lay eggs through their stingers. As implied by the unlikely conjunction of two random things on the internet. But the only reason I think that might be true now is because you've just elliptically told me this and you claim to have appropriate knowledge. I was hoping that someone might actually answer the question, maybe with a link to a trustworthy source. A man can dream. Don't worry, I won't be troubling your website with my half-wit questions again.

I'm not going to feel sorry for you for labeling your own question as "half-wit". Your feelings are what they are, and I have no control over that. It's not a bad question; hover over the downvote arrow and note that "contains no research" is a reason to DV  and to close. You were welcomed, up voted, no one down voted you, not even me. Think what you will. Btw, virtually is just shy of "all (full stop.)"

If you still want an answer, I will provide a definitive one tomorrow. It might surprise you to learn that even someone with two advanced degrees in Biology can be wrong. Maybe your question was better than your last assessment.


text:
How do I help an injured plant avoid infection?
A hail storm came through my town while I was at work and my innocent cactus was outside! I'm pretty sure this exists, but is there something I can put on these open wounds to stop them from rotting/getting infected?

I would like to point out that I did try to google this, and I was unable to find an answer, which is why I'm here.

I think this would be a better fit for [Gardening.SE]. If you agree that is a better site for your question, please delete your post from here before reposting there because cross-posting is impolite. Alternatively, you can request migration of this question by flagging your post for moderator intervention and explaining what you want and why.

Petroleum jelly thin coat with clean fingers would work in my opinion.


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What were the mammal ancestors like 65 million years ago?
What we know about our mammal ancestors that were alive (and survived) at the extinction event 65 million years ago?

Many of them looked like little rodents. However, several distinct mammalian lineages were already present, including Monotremes, marsupials and placental mammals. Throughout the whole Mesozoic era, mammals were already quite diversified! Also, even though most of the mammals that survived the K/T boundary were rather small, there were already some larger mammals around in the Cretaceous.
Here is a nice picture of a symmetrodont:

See a nice page on early mammals.

A recent genetic analysis suggests that they were probably bigger that we thought before :
http://www.newscientist.com/article/dn22343-mammals-ancestor-was-not-as-puny-as-we-thought.html

In a 2013 study, that combined genetic data and morphological data, the last common ancestor of placental mammals was estimated to be a four-legged creature likely ate insects, weighed from 6 grams (about the weight of some shrews) up to 245 grams — and was more adapted for general scampering.  Also, its cerebral cortex — the part of the brain linked to higher mental processes — was probably convoluted, folds linked with greater brain activity, http://www.livescience.com/26929-mama-first-ancestor-placental-mammals.html
The same study estimates that this ancestral creature arose some 200,000 to 400,000 years after the end of the age of dinosaurs. This is in line with what paleontology suggest... but is in contrast with other studies based purely on genetic data, which puts the last common ancestor of placental mammals 36 million year before the dinosaur extinction. (which depends on how accurate you can estimate the speed of the genetic clock which is dependent on number of generations and thus the lifespan of the animal...faster in fast breeding, short lived animal. Slower in long lived, slow breeding animals)

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Cambrian explosion and evolutionary arms race
I've seen many times mentioned in textbooks and popular articles that a reason of the Cambrian explosion is an 'evolutionary arms race' between predators and prey. But this isn't really a sufficient reason, since that happens all the time, but evolution seems to happen only at brief intervals separated with long intervals of stasis, which is described extensively in the Punctuated equilibrium hypothesis.
So, my question is, what made the evolutionary arms race of the Cambrian possible?

Lots of things happened during the Cambrian explosion, and I do not think that anyone believes that it was only due to predator-prey arms races. The wikipedia page has a summary of hypotheses, and as you can see the arms race theory is just one of many. It is also likely that there is no single cause, but several interacting factors.

I think it is really wrong to assume that evolution occurs only in punctuated way. Evolution is a continuous process.

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text:
Is Nerve Growth Factor (NGF) commercially available?
I'm curious if NGF, or Neurotrophins in general is available commercially. Can I order it online? If not, what are the medical/biological reasons. Does it breakdown quickly after synthesis/capture? Is it a regulated protein?

No.  Any use in humans is strictly experimental and should only be done by physicians.  Using it like a nutritional supplement wouldn't do anything for the body anyway.

Nobel prize Rita Levi-Montalcini begs to differ: http://www.independent.co.uk/news/science/is-this-the-secret-of-eternal-life-1674005.html

It's awful hard to study something with an N=1.  Given that she put it in her eyes in the form of drops, it probably just degraded away.

(also, she is a physician)

I'm voting to close this question as off-topic because it’s not about biology but commerce, and is intrinsically temporarily transient.

recombinant human NGF is available for purchase.  You might not be able to buy it without some sort of a research lab affiliation.
http://products.creative-biolabs.com/symbolsearch_NGF_1.htm


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What does this statement pertaining to fission mean?
I was reading about fission on Wikipedia when I encountered the following statement under Fission of prokaryotes section.

Like in mitosis (and unlike in meiosis), the parental identity is lost.

What does 'parental identity' mean here?
From what I understand it to be, it possibly means that the parental form is no longer present after mitosis as it is divided to form new individuals in the process, thus the 'parental identity' is lost. If I am right, isn't parental identity lost in meiosis also?

You're right, this makes no sense or at least is misleading. It seems the edit was introduced in March 2019, after another mistaken edit that suggested parental identity was preserved in binary fission.
I agree with Douglas that this phrase "parental identity" seems to have been invented in some study guide, so I wouldn't dwell on it. It does not seem to be used by scientists in science. From context, though, they seem to intend to distinguish with budding, where you can clearly identify one cell as the (larger) "parent", and the other distinctly as a "daughter" copy. You can tell which one is the parent, aka, "parent identity" is preserved. In binary fission, there is no such asymmetry, and you can't really consider either cell the "parent" of the other.
With respect to meiosis, the editor may have been thinking of genetic imprinting where the parent is marked in gametes epigenetically, but this doesn't have much to do with "parental identity" in terms of cell division. The only similarly is that people do use "parental identity" to refer to chromosomes marked by whether they came from the female or male parent. I think the author just got confused by reading that term in two places, not realizing the meaning was totally different, and trying to make sense of the two together. Wikipedia is great and I rely on it a lot as a basic reference that anyone can use, but this is one of the occasional examples where it falls short!

In fission, each daughter cell gets a full copy of the parental genome. But "parental identity" doesn't seem to be a standard term.

What does 'parental identity' mean here?

You're not alone; I don't get it either. At first, I assumed it was jargon specific to molecular biology or microbiology.
But, parental identity doesn't appear to be a standard term in biology.
A Google search returns exclusively online study guides, textbook exercise answers, and your own question :)

From what I understand it to be, it possibly means that the parental form is no longer present after mitosis as it is divided to form new individuals in the process, thus the 'parental identity' is lost.

Though I don't know what exactly was intended, I think the author meant the genetic material, not the cell body. That is, "parental identity" is said to be "preserved" if the daughter cell contains a complete copy of the parent cell's genome.

If I am right, isn't parental identity lost in meiosis also?

In both cases, the cell bodies are split -- so, yes.
But meiosis results in very different genetics.
In both fission and mitosis, each daughter cell (2 total) retains a complete copy of the parent cell's genome. But in meiosis, each daughter cell (4 total) retains only half parent cell's genome.
(This distinction is the ploidy of the cells.)


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Does technology exist to represent cell biology in a bona fide fashion?
I have been teaching life sciences for nearly a decade now. Still something keeps giving me mental distress each time I think of it. I feel no representations of cell biology can convey information in a truly bona fide fashion.
Think about the following example. If I want to know about tigers, a text description will help.

Many tigers possess stripes on their face, sides, legs and stomach. The striping is varied in width, length, whether they are single or double-looped, coloration from a light brown to dark black and are not symmetrical from one side of the tiger to the other. (source: https://seaworld.org/animals/all-about/tiger/characteristics)

But no matter how useful this text is, it does not give me as much intuition as a painting does.
Still, a much better representation of a tiger is a photograph, as it gives much more direct knowledge about a tiger. Before the invention of full-color photography, the best thing I could get was below.

This black-and-white photo is even worse than the painting, because it removes the essential colors. It is the invention of full-color photography and videos that would eventually give me the most direct knowledge about a tiger.

With the analogy of a tiger, I can better describe limitations of information carried by existing forms of life sciences materials. For example, one day I want to learn transcription factors and their control of gene expression. I can find a piece of text on this topic:

Some transcription factors bind to a DNA promoter sequence near the transcription start site and help form the transcription initiation complex. Other transcription factors bind to regulatory sequences, such as enhancer sequences, and can either stimulate or repress transcription of the related gene. (source: https://www.nature.com/scitable/definition/transcription-factor-167/#:~:text=Some%20transcription%20factors%20bind%20to,transcription%20of%20the%20related%20gene.)

But I feel this is not enough to give me an intuition about TF. I then found an image representation of the process.

This abstract image is a complement to the text. But I don't feel it insightful enough. The next helpful thing I found was a video https://www.youtube.com/watch?v=MkUgkDLp2iE. And the searching process stopped there.
Does current technology allow for truly bona fide representation of cell biology in the same sense as a tiger is represented by a full-color photograph? For students who have strong imaginations, they don't find learning cell biology too much of a trouble. For those that lack imagination, I must strive to find something that gives them as much of an intuition as possible.
The ideal tool to represent cell biology is something that presents the products of imagination for the strong minds in a directly accessible manner. I'm afraid this goes far beyond current technologies. Is it so?

Are you ever going to find better things than animations of molecular machinery? Because your tiger analogy only works because you can perceive a tiger with your senses.  I also argue that an image of a tiger only seems more bona fide because it is heavily augmented by your real world experience with similar things. Seems very similar to math equations versus graphs. The graphs don't embody the existence of what is there. Even animations for higher level stuff don't make sense unless you already know what you're looking at, if they can even be animated at all.

Or are you just asking if electron microscopic motion cameras exist that work on living samples?

Hi @DKNguyen, thanks for bringing up electron microscopic motion cameras. I did a bit research on my own and found this type of technology can allow up to 1600 fps. That's a fantastic tool for my teaching purpose. And it is vastly better than the abstract images or animations for cells.

I think they don't work on living samples though. But maybe still life photos are better for you than generated animations.

Does current technology allow for truly bona fide representation of
cell biology in the same sense as a tiger is represented by a
full-color photograph?

There is no way, that any cell-biological depictions will ever reach the level of intuitive understanding, that is conveyed by such a picture of a tiger.
Next to the tigers image, you see every-day objects like trees and grass, that give immediate sense of the scale. Also, the tiger is a mammal, just as you are, and you have multiple close references at your disposal, like other mammals or cats, which you can immediately extrapolate to gain insights about the tiger. Besides obvious aspects, like the knowledge of anatomical structures, that one effortlessly recognizes, e.g. the tigers eyes, and what seeing or breathing means, you also have a detailed model of the physics of objects at your scale of mass.
On the contrary, being confronted with 2d depictions of molecules, most people would find it hard to guess how the missing information in the 3rd dimension would look like. Also, they lack an intuition of the physics at these small scales.
You would need to be a biological molecule yourself and spend all your 'life' at these scales to understand and feel what it means to be a bio-molecule, and your "molecule brain" must have evolved with pressure to recognize predatory tiger-molecules at first sight, which would otherwise mean your death; only then would you have any chance to come close to achieving the intuitive understanding of such a magnitude.


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Is the human mouth more burn-resistant than other animals which don't eat cooked food?
I burnt my mouth on some hot pizza and it got me wondering if we have been eating cooked food long enough to have evolved a better resistance to oral burns than other species. Have there been any studies on this?

Possible duplicate of https://biology.stackexchange.com/q/35532/27148 - to evolve a trait by selection it has to have some fitness benefit. For humans to evolve protection against pizza burns it would have to afford a survival/reproductive benefit, not just be a "nice to have".

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site (also see: "homework"). Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

Does this answer your question? Why do some bad traits evolve, and good ones don't?


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Can antibiotic resistant bacteria compete with normal one in an antibiotic free environment?
The question is based on an intuition that antibiotic resistance can't come along. This mutation will probably make bacteria less tenacious. Is there any research how AR bacteria compete with normal one in an antibiotic free environment? Because if them generally lose to normal bacteria then AR bacteria is not a big threat and they can't spread to much.

They CAN spread like wild fire when an antibiotic is introduced in their environment.

The antibiotic resistance adds to growth cost. In an antibiotic free medium the antibiotic-susceptible strains will outgrow the resistant ones. See this

So it is a myth that antibiotic resistant bacteria is somehow dangerous? You will not catch this AR infection if you are not using antibiotic. Normal bacteria will outgrow it.

Well..no.. Your immune system acts as a barrier to both strains (both are pathogenic)... Then you take antibiotics to control the infection. In this condition the resistant ones thrive.

AR bacteria is less viable it will not be present if I didn't use antibiotic. Both this infections fight not only with immune system but also with eachother and AR lose.

We are talking about the condition in which the immune system requires drug supplementation. For example in the case of tuberculosis.. The drug resistant strains are a major issue of concern

I am interesting how AR strains are able to spread. If they can't compete with normal bacteria then worst possible scenario is to ban antibiotics worldwide for a year. Wait while AR bacteria instinct in a competition with normal one and remove the ban. Or better to switch between two types of antibiotics on odd and even years. If AR bacteria really lose to normal one then the issue is not as bad as it depicted in mass media.

It is not that easy as it seems. Indiscriminate use of antibiotics should be controlled to prevent evolution of resistant strains. However, infections which evade immune system naturally are a matter of concern and the technique that you suggest wont work.

@ZAB Before a century, antibiotics were not used but the AR bacteria WERE present. So, even if we stop use of antibiotics there will be certain bacteria which have resistance to it. One more thing, DO NOT take this thing so LIGHTLY. Antibiotic resistance IS creating problems. If there were an easy and feasible way to tackle it, agencies like CDC would definitely have implemented it.

In general, antibiotic resistant strains may be a little less fit than sensitive strains in the absence of the antibiotic.  But that doesn't mean they are at all times and places instantly competed out of existence.  Once you apply the antibiotic, the resistant organisms grow from resistant organisms that were in the population to start with.
Ad of course once you have a large number of resistant organisms in the population, selection might encourage the increase in organisms bearing compensatory mutations, such that the growth of those organisms is closer to the growth level of sensitive organisms.
Your premise is a little weird.  Resistant organisms are out there.  XDR tuberculosis, MSRA Staph...why would you assert that those can't be problems when empirically, they obviously are?

Totally agree with the last sentence. They ARE there and they ARE bad.

How long will XDR tuberculosis and MSRA Staph last if we ban antibiotics or if we will globally alter one antibiotic with another once in a decade? That is a question. If resistant stains are less fit then normal stains then they will extinct.

Ban all antibiotics all together?  Do you understand that the idea is for people to not die from infectious diseases?  Sitting back and watching someone die from a drug-sensitive strain because you are banned from using antibiotics is not an improvement over watching someone die because you don't have a useful antibiotic to use.

You do not listen. Ban penicillin worldwide and treat people with metronidazole. Then switch. Stain resistant to both of them will not survive in competition. After a year of penicillin treatment all metronidazole resistant stains will extinct. And so on.

You can't treat everything with one antibiotic.  For one thing, there are people who are allergic to penicililn.  And I'm sorry, but there are such things as compensatory mutations, it certainly is possible for resistant organism to compete with sensitive ones.  Just repeating over and over again that that's not true isn't helpful.

In short, yes. Perhaps the best way of thinking about antibiotic resistance is not to think of there being 'antibiotic resistance' genes at all, but rather ordinary alleles that are vertically transferred in the typical fashion until at a certain time a deleterious chemical agent is introduced and one specific allele just happens to mitigate the effects of that chemical. It is less a matter of competition than it is of blind chance. Now of course, in principle, the lucky genetic element that will ensure survival may come with an increased energy cost as opposed to the 'wild-type' genome expression, but considering the general mechanisms of antibiotic resistance, one or two extra gene products, maybe a slightly less active enzyme, an extra membrane transporter, the cost is typically not excessive. In culture, antibiotic-resistant bacterial strains grow essentially as fast as non-resistant strains.
Now concerning the retaining of the resistance after removal of the antibiotic, if the gene is integrated into the genome with the proper regulatory apparatus, it can remain in the species essentially forever. In the case of plasmids or other mobile genetic elements, bacteria do tend to lose these through random processes between divisions, however, many of these elements do have mechanisms to preserve (plasmid addiction) and propagate themselves (horizontal gene transfer).
The most important thing to remember about resistance, however, is that only an infinitesimally small proportion of the population actually needs the resistance genetic element to actually start a new resistant population upon antibiotic introduction.

" In culture, antibiotic-resistant bacterial strains grow essentially as fast as non-resistant strains.".. Antibiotic resistance does pose and additional cost on growth.. It might be difficult to observe it in a gross scale.. However it is true that that resistant strains must have optimized the protein synthesis machinery as much as possible to minimize cost.


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Why does plucking nose hair cause tears in the eyes?
It's not a particularly sad or painful thing to pluck a few nose hairs, but it's common for the tear ducts to wet up when doing this.
I would like to know the physiological reason for the correlation, how/why are the tear ducts and nose hairs related in the human body?

unreferenced, but here you go: http://answers.yahoo.com/question/index?qid=20061231043153AAaJdCT

Is this for real?

Although I'm not sure, here's a working theory. The tear collection ducts feed into the nose. That's why when you cry you have a runny nose. When you pluck nose hairs you irritate the nasal mucosa, so that causes a reflex which attempts to flush out whatever might be causing a problem.

It might be an overstimulation of the sneeze reflex neural circuit, which causes tearing instead of sneezing. I do get a feeling similar to the "I'm about to sneeze" along with lacrimation.

Also, tears are an intrinsic pain response and considering the dermal-derivative nature of hair, there are loose nerve endings ensnaring the follicular area, so the sensory neurons detect pain and tears are a physical manifestation of the pain, cuing the body to avoid that stimulus again.

+1. Innervation of the nose is extremely sensitive.  It's primarily a combination of this and what Armatus said above, plus the fact that AndroidPenguin mentioned of the connection between the nose and tear ducts.


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What's the difference between a plant and an animal?
Are there some living things where the distinction between plant and animal is blurry or unclear?  I wouldn't know where to put something like yeast.  I also thought of photosynthesis, but then I heard that some salamanders have photosynthetic cells.  So, what's the difference between a plant and an animal, formally?

Yeast are neither plants nor animals; they are fungi. The old classification where things were lumped into only two buckets - plants or animals - has long since broken down. In fact, even things you might think of as plants, like algae or most seaweed are no longer classified as plants. Under the old system, plants and animals were considered kingdoms, and the latest classifications now divide the Eukaryotes into six kingdoms, but even this is poorly evidenced and facing challenge.
The best method of classification is probably cladistics which is based on the evolutionary history of organisms - but even it has problems when you start considering what to do with horizontal gene transfer and endosymbiosis. Because under a cladistic view, plants and animals are defined not by their features but by their ancestors your question becomes moot, I think.

Just a small addition (with some few examples): According to the new classification by Cavalier-Smith fungi and animals are in the same clade -opisthokonta, whereas plants and some protists like plasmodium, are in another clade called bikonta.
Some unicellular lifeforms have been called algae for a long time but they are close to plasmodium and have obtained their chloroplasts from a secondary endosymbiosis (they actually captured an alga which in turn has a cholorplast). Same is the case with diatoms.

That "photosynthetic" salamander is clearly an animal, with smaller photosynthetic organism living in it symbiotically.
And yeah, cladistis is the way to go.  You build your tree based on DNA, and see if the data lets you group organisms in a useful way. You might find a few organisms whose genome makes them edge cases, but this salamander is not one of them.  Yeast very clearly falls way outside both categories.

Classification is not only based on one or a few features, but you have to consider lots of features in classification of livings. for example plant cells globally have chloroplast, cell wall, and vacuole and have not centrioles. Animals are different in all this features with plants. furtherly plants are autotroph and steady while animals are not. Other organisms are also different in these features or other features with plants and animals.


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Why do sneezes come in pairs or more?
I very rarely sneeze just once, usually there's two coming in a row, and I've noticed the same thing in other people and even in animals.  Is there any reason for this?

The very simple answer is that the causal factor or trigger hasn't disappeared after the first sneeze. Sneezing is a reflex, partially autonomous, to clear the nasal cavity of particles that don't belong there. As long as the trigger is not removed, the reflex is repeated.
This is also one of the reasons that allergies that cause sneezing, such as hay fever, continue as long as the factor causing the allergy is present.


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What does 'pedigree information' mean?
This paper uses Pied Flycatcher as a study species. For the population of Pied Flycatchers they studied, 'pedigree information' was available. What exactly does this 'pedigree information' mean?

It means that they recorded family information for the traits that they were investigating in the paper, i.e., they had plumage characteristics for siblings or parent-offspring pairs. Look for this phrase in the paper: "phenotypic data usually available for one or two generations, mostly from parent-offspring pairs or siblings."


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How does the ideal free distribution work?
I have recently completed a study on Brent Goose. I found that Brent Geese occupy high quality habitat first then once this is full of geese, they fill up low quality habitat. However, there were always fewer geese in the low quality habitat.
This pattern therefore seems like a good match for the ideal free distribution…but is it?
Under the ideal free distribution, do birds fill up high quality first, then low quality habitat second?
Or do birds fill up both high and low quality habitats simultaneously, but fill up high quality at a faster rate?
Or does the ideal free distribution not make explicit the order/rate at which birds fill up high and low quality habitats?

The order of settling depends on the resource availability in different patches (in your case the difference between high and low quality habitat), but generally speaking, the pattern you observe conforms to the ideal free distribution.
The key factor in the ideal free distribution is that habitat patches are filled according to the current resource availablity (~per capita resource access), given the current density of individuals in the patch (so the marginal resource availability). If the high quality patch has much higher resource levels than the low quality patch, this means that many individuals can settle in the high quality patch before the marginal resource availability becomes equal to the resource availability in the low quality patch, at which point individuals will start settling in both patches. Therefore, the two observations you make; 1) lower overall density in low quality habitat and 2) the high quality patch being settled first, both agree with the ideal free distribution.
This graph (from wikipedia.org) illustrates this pattern nicely, for the standard version of the ideal free distribution:

Here, the marginal, apparent value of a patch is shown on the y-axis and the number of individuals in the patch on the x-axis, and the numbers refer to the order that individuals will settle in the two patches (so the first 6 settle in the high-quality Patch B, ind. 7-9 in Patch A, ind. 10 in Patch B etc).
However, I encourage you to read about other theories on habitat choice, and the pattern you describe can probably be explained by other processes as well. The ideal free distribution also has some rather restrictive assumptions (e.g. equal quality of individuals and no dominance/territorial/interference behaviours among individuals), which you have have to consider.


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How precise does a 1:1 ratio PCR sample mixture (microliters) have to be for the liquid amount ratio to not have any effect on results
Amount of liquid:
5 micro liters master mix
5 micro liters of patient sample

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Welcome to the site - can you please let us know what sort of PCR you are doing. Regular PCR with a gel as end-point, it might not matter too much (i.e. you just want a band), but for qPCR it will make all the difference.

If your pipets are calibrated and your technique is good, you shouldn't have issues with those volumes. Using a p10 instead of a p20 might reduce pipetting error a bit. Low-binding tips can help too, but marginally. If running reactions in duplicate or triplicate you can mix them all in one tube first, and dispense the 10 ul reactions out from that; just make them around 10% or so bigger than what you need to account for dead volume, and wet your tips before dispensing.

Pipetting PCR reactions should be done as precise as possible - since relatively small deviations can effect the reaction. Pipetting 4 instead of 5µl results in a 10% error which for example leads to a higher magnesium concentration which may effect the reaction efficiency.
I would try to use bigger volumes (25µl is pretty common for PCR reactions) to minimize such effects, but of course smaller reactions save material and costs. You could run a few tests to see how big the effect is for different reaction volumes and if the possible error is acceptable for you.

Could you clarify more on what would be an acceptable range of deviation in that it wouldn't effect the reaction or provide me please with any reference I could view? For example if I had a total mixture of 20µl.

@Nicole you can work out the error by yourself fairly easily - it's simply your pipetting volume error divided by the expected total volume (e.g if you had a 1 ul error in expected volume 20 ul - 1/20 = 0.05 = 5%)

thank you all for the input


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What Produces the Postive Potenial in the lumen of the thick ascending loop of Henle?

In the Thick Ascending Loop of Henle, Paracellular diffusion of certain Solutes like magnesium and calcium takes place. Such diffusion is a result of the positive lumen potential.
Looking at the image above from "Berne & Levy physiology" both sides should produce similar charge when cancelling charges out. I don't understand what exactly produces the positive potential on the lumen side.
I believe the caption attempts to explain it referring to differences in conductivity between the apical and basal membrane but I couldn't understand how they came to the conclusion.

Don't pay attention to the stoichiometry of the pumps, that will only fool you! The charge is due to passive movement through open channels. This is shown as the "yellow tubes" with dotted lines in the diagram. Students of neuroscience are often confused by a very similar thing, as the resting potential of neurons (as well as voltage during action potentials, for that matter) is determined the same way.
The explanation is in the caption text, quoting from your figure:

Because the apical membrane is conductive primarily to K+, the apical membrane voltage is more negative than the basolateral membrane voltage, which is conductive to K+ and Cl-

The other missing piece of information is that the outside space is (relatively) low in potassium. That means that, given an available path for potassium to diffuse across the membrane, there will be a net flow of potassium out of the cell. That flow causes a negative charge to develop inside, because the potassium diffusing out is positively charged. Very few ions have to actually move to develop a biologically relevant potential (see explanations in other answers involving neurons: https://biology.stackexchange.com/a/76167/27148 and https://biology.stackexchange.com/a/57066/27148), so you can treat the ion concentrations as unchanged (and they will be, out to a fraction of a percentage point) despite this movement.
At some voltage, the negative charge inside the cell will counteract the movement of potassium, so it's not like this is a constant deluge of potassium flowing out, it's more of a maintenance trickle. You can calculate this "reversal/equilibrium voltage" using the Nernst equation.
When you have multiple ion species involved, the equation to use is the Goldman equation which is related to the Nernst equation but involves a relative weighting of different ions by their concentrations and permeabilities. As in the textbook description, adding chloride conductance makes the basolateral membrane less negative than if there was only a potassium conductance, because chloride moves out of the cell as the inside becomes more negative.

But what makes the lumen potential positive relative to the extracellular space on the basolateral side? as shown in the image, the paracellular diffusion is driven by that potential difference. yes chloride exits on basolateral side, but looking at the rest of the transporters it seems like the charges should balances out on each side of the cell. Am i missing something?

@OmarShahaltough Read the explanation in my answer; don't pay attention to the movement shown in the pumps and co-transporters, those don't matter.

im sorry if i misunderstood but im not seeming to understand two things: 1. the relevance of the potential inside the cell when it comes to the potential outside of the cell, and 2. What exactly does "makes the basolateral membrane less negative mean"?

@OmarShahaltough All potentials are relative; the potential inside the membrane and potential outside it are the same, just opposite sign. The apical membrane (left side) has an electrical gradient that is more negative inside, so pulls positive charge in. The basolateral membrane is the one on the right hand side of the diagram; since chloride can move freely on that side, there isn't the same negative gradient into the cell. If you sum these in series, the net result is a pumping of positive ions from the left side through to the right (paracellular diffusion).


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Do plants digest substances they ingest?
I was thinking about plants having no digestion system (is that true at all?) and my conclusion was that they only ingest substances that they can use like that or that they can transform into usable ones (which then would maybe something similar to digestion).
So my question is:
Do plants "digest" substances that they ingested and then egest the "garbage"?
Also: can someone give me some hints where I can read about plant metabolism?

Welcome Chris. This is not simply a Q&A site, here we are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are. You should also take our [tour] and refer to the [help] for guidance as to the ways of any site you post on, see our section on how to ask and see our homework-question policy.

As a starting-point, try plant-fungal-symbiosis and take a look at carnivorous plants for the other end of the spectrum.

for a starter, you might define (and possibly refine) what you mean by "digest" in the question.

Perhaps Plants can use protein as a nitrogen source without assistance from other organisms would also be of interest. This paper shows that roots have proteases that can digest (that is, breakdown by hydrolysis of the peptide bond) proteins

It's unclear to me if the question is asking generally about all plants, or only refers to digestion of food items by carnivorous plants.
If asking about plants generally, they don't to my knowledge perform any internal digestion. Non-carnivorous land plants take in materials in two ways, through their roots and through their leaves.
The roots take in water, along with molecules dissolved in the water. These include molecules containing nitrogen, phosphorous, and potassium, as well as other trace elements. Plants employ various strategies to enhance their uptake of water or nutrients, including pairing up with fungi or bacteria. Some also release low levels of acid to dissolve minerals for uptake. This could be considered a form of external digestion.
Leaves take in carbon dioxide. The CO2 is the primary source of carbon for the plant, and in turn is the main source of a growing plant's mass.
The waste that plants release is primarily O2, which exits the leaves through the same pores the CO2 enters. While roots release many types of molecules, these mainly have a functional purpose and aren't generally considered waste. Plants in salty environments also have mechanisms to expel salts.
So, no, plants in general do not perform internal digestion.
Now, carnivorous plants do capture and digest prey. This digestion is performed either by enzymes produced by the plant itself, or by microorganisms living in the environment of the trap. This would still probably be considered external digestion since it occurs either in open, liquid-filled pitchers, or on leaf surfaces that have folded over. The two sides of Venus fly trap traps do press together to form something of a seal while the prey is digested, but they open again when the meal is digested. The bladderworts, Utricularia spp., maybe have the best claim to "internal" digestion, with prey being dissolved inside small bladders covered by a trap-door mechanism. But these, too, originate from modified leaves or foliar structures.
Since the undigested parts of carnivorous plant meals are never really injested, they are not expelled.


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Really having problem comprehending this Hardy-Weinberg example from biology textbook

Genetic equilibrium is a hypothetical state, but it is often used as a benchmark. Consider how the Hardy–Weinberg equations were used in early studies of an allele that causes hereditary hemochromatosis. Individuals affected by this disorder absorb too much iron from their food, and the excess accumulates in tissues and organs. Untreated, the iron overload results in fatigue and pain; in serious cases, cirrhosis of the liver, heart disease, diabetes, and other problems can occur.

The allele is inherited in an autosomal recessive pattern, so carriers (people heterozygous for the allele) have no symptoms. People of northern European descent have a very high risk of hereditary hemochromatosis compared with other populations; about 1 in 83 people of Irish descent have the disorder. Researchers discovered that about 28% of normal (unaffected) Irish individuals were carriers, which means the frequency of the allele among members of the Irish population (q) is 0.14. Thus, the frequency of Irish people who are homozygous for the allele (q2) is 0.0196, or 1 in 51 individuals. This calculated frequency is higher than the observed prevalence of the disorder,
so the researchers concluded (correctly) that other factors probably contribute to the progression of symptoms.

I'm really having problem on understanding what the last paragraph is trying to say. It says if (1/83) have the disorder, that means q^2 = (1/83), and q = 0.11
That means p = 0.89, since p+q = 1. That also means that the heterozygous population is 2pq = 2(0.89)(0.11) = 0.20, or 20%.
I'm having trouble comprehending how they figured out q=0.14. I don't even get what "28% of normal individuals were carriers" mean. Does it mean 28% of homozygous dominant and heterozygous individuals combined? If so, how do you get q = 0.14 from that?
I just do not get what this is trying to say.
Please help.

You get off track when you state:

(1/83) have the disorder, that means q^2 = (1/83), and q = 0.11

For that to be correct, each and every person who is homozygous for the problem allele must show symptoms of the disorder and no others can do so.  When they stated "have the disorder" they meant have clinical symptoms of the disorder, and nothing about knowledge of the frequency of the problem allele in the population.  Hence, you shouldn't have jumped to that conclusion and knew from that what q was.
The text says:

Researchers discovered that about 28% of normal (unaffected) Irish individuals were carriers, which means the frequency of the allele among members of the Irish population (q) is 0.14.

Here they are talking about results from genetic testing of normal individuals.  The tests revealed that 28% were heterozygous, having both a normal allele and a problem allele.  This is talking about the frequency of the alleles, and so this 0.28 should be the sum of the probabilities for the two heterozygous areas of the Punnett square, that is 2pq.  When I solve that I get q ≈ 0.168 whereas the text shows 0.14.  Whichever it is, the final sentence in the text excerpt would still apply.

Here the discussion is highlighting the subtlety between disease 'prevalence' and the 'penetrance' of the mutation causing the disease.  The prevalence is an estimated value for the fraction of the population afflicted by the disease (which really should have statistical errors associated with it based on the sample size of their data).  Even if the disease only occurs due to a genetic mutation, not all individuals with the mutation necessarily have symptoms. This is due to incomplete penetrance of the mutation.  Think of penetrance like some probability that the genetic component wins over the environmental component, epistatic interactions based on the rest of the genome, and any other complicating factors you can think of that disrupt genetic determinism for Mendelian disorders.  If the probability that having the mutation causes the disease is 1, and as mgkrebbs said no other mutations or environmental factors cause the disease, then the mutation is completely penetrant.  In that case, and in that case only, you can (post-hoc) infer the allele frequency from the disease prevalence, which is what you tried to do.  That said, measuring the penetrance virtually always requires knowing the allele frequency of the mutation, so this isn't how we figure out allele frequencies in human disease genetics.  (As an aside, penetrance is still really hard to measure, and estimates in the current literature disagree depending on if they condition on having affected family members or if they use an unbiased sample.)
As for the allele frequency itself, the authors of your textbook made a small mistake in the calculation, as mgkrebbs pointed out.  $2p(1-p)=0.28$ (again missing error bars), which can be solved to find $p\approx0.17$. There is another issue here, which is that there is very little information given about the allele itself with respect to the mode of inheritance (and other normal things to check).  The author's claim it is autosomal recessive (which is not necessarily $h=0$, since the medical definition only requires unaffected homozygote individuals, and that assertion is based on the sample size of heterozygote carriers assessed; they may have other medical conditions that are not the same as the homozygote-induced medical conditions).  I just looked up a few of the mutations responsible for hemochromatosis in OMIM (Online Mendelian Inheritance in Man, which is a database of genetic disease status, including mode of inheritance) and here are the results:
https://www.omim.org/search?index=entry&start=1&limit=10&sort=score+desc%2C+prefix_sort+desc&search=%22hemochromatosis%22.
If you click on any of the entries, they mention that compound heterozygous mutations (one mutation from the mother, one from the father, in different locations but both in the same gene) can also cause the disease.  This means that assuming it is a single mutant allele with a single frequency $p$ is incorrect (unless they included that in their estimates of the carrier frequencies via sequencing). If other mutations in the same gene can cause this disease, then one needs to compute both the carrier frequency over all possible mutations and then check the prevalence to see if the additional target size for compound hets is sufficient to explain the epidemiology. The allele frequency for compound hets if there are two alleles is $p_{c.h.} =  p_1^2 + 2p_1p_2 + p_2^2$.  If there are more than two alleles, this becomes a binomial expansion $(\sum p_i)^2$, which can grow quite quickly due to the cross terms $2p_i p_j$.  This could be part of the issue between the discrepancy in disease prevalence and homozygote status, but it goes in the wrong direction!  This likely means that there is a larger environmental component at work (back to this in a bit).
Looking more into this specific disease, here is an article about hemochromatosis in Ireland: https://www.liebertpub.com/doi/10.1089/109065701753145583, which cites the following statistic in the abstract:
"Over 93% of Irish HH patients are homozygous for the $HFE$ gene $C282Y$ mutation, providing a reliable diagnostic marker of the disease in this population. However, the prevalence of the $C282Y$ mutation and that of the second $HFE$ gene mutation, $H63D$, have yet to be determined within the Irish population. ".  Granted, this paper is from 2004, but I couldn't quickly find a more recent statistic on the allele composition of affected individuals. This means that there are not only multiple alleles involved, albeit with one responsible for the vast majority of Irish cases, but also that there are multiple genes involved (again increasing the target size).
So what's going on?  The key is environment and one other factor: sex.  "[A]pproximately 50% of women and
20% of men do not have an increase in serum ferritin
level", cited here: https://www.sciencedirect.com/science/article/pii/S1542356505004131.  Serum ferritin is responsible for the adverse component of the disease, so this paper tells us that women are a coin flip away from not having the disease even if they are homozygotes for the most common mutation causing the the disease in the Irish population.  Additionally, they measure the 'heritability' (https://medlineplus.gov/genetics/understanding/inheritance/heritability/), which is the fraction of the variance in the population explained by genetics.  They find that the heritability is $0.35\pm0.1$ (error bars, finally!!) out of a maximum 1.  This means that 35% of the distribution of disease in the population can be explained by genetics alone (indicating something about how likely you are to get the disease if your parents are both carriers), and the remaining fraction is unexplained!  Usually, we blame this on a number of environmental factors, but in this case, male/female status plays a major role (though not enough to explain 65% of the variance).  Compound hets are likely involved in the remaining "missing" heritability (I honestly can't guess to what extent), and the rest could be from a number of things that are too far removed from the topic.
So there is your answer: compute the homozygote frequency from the carrier frequency (properly) and the difference between that and the disease prevalence is wrapped up in all of the human genetic considerations I outlined.  So sorry this turned into a novel, but I wanted to address some of the details that go into the genetics of human disease!


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Can somebody explain why mouse and cow are the least related based on this sequenece alignment?

Answer key says out of the choices, the mouse and cow and the least related. Is it because they have the most number of differences out of the four choices? (Hedgehog/Horse is 5, dog/horse is 3, mouse/cow is 7, and mouse/dog is 3). I know there are more complex ways to make the tree, as shown in this video: https://www.youtube.com/watch?v=09eD4A_HxVQ, but I just wanted to know if my logic is correct here. This is for AP biology and we did not learn anything about the technique used in the video. Thank you.

Welcome to the site. The image is confusing as there is no reference sequence - normally you would have a sequence to compare them all to. As this is clearly homework - what do you know about genetic difference; how might we measure this? Do you think having a greater number of differences leads to more or less similarity?

I would think having a greater number of differences would lead to less similarity. The video I referenced also didn't have a reference sequence, but I don't think we're supposed to do it that way.

So, you have your answer, and you knew it all along. The reference sequence makes it easier for multiple comparisons, but as the answers in your question are binary, you take one as reference and calculate the numbers of differences between the two, then do the same for the next pair (as you obviously did).

That sounds good. I guess my problem is dog/cow and cow/horse both have eight differences, so I'm guessing the only way to tell would be to do the complex way to actually make up the phylogenetic tree?

The problem there only exists in your mind - those weren't part of the options you were given, so you don't have to worry about that part. No need for a tree.

Yep I'm just trying to understand it the best I can. I don't think what we learn in school tells us the whole picture. I tried the method and what I got is this: https://imgur.com/a/4CA13aI  I'm not sure if it's right, but this would say that cow/mouse and cow/hedgehog are the most distantly related, which is different from dog/cow and dog/horse if you just go by how many different nucleotides. So it's like you get different answers by using different methods.

The question says nothing about phylogenetic trees and nor should you as it would be absurd to try to construct one from these contrived data. I loath and detest MCQs in teaching, but the question is clearly testing one idea — that the longer evolutionary time there is between the organisms from which sequences have been derived, the greater chance there is of mutations occurring. You would do better to ponder the simplification in the scoring system — why is a transition scored the same as a transversion (not to mention the convenient absence of insertions and deletions).

By asking about the "least closely related" the question is implicitly asking about a phylogeny—one cannot answer properly without one. While your general statement about time and mutations is true, the seemingly logical corollary, that the most differences means least related or the fewest means most related, is not. I agree this isn't a great question, but mostly because it's conflating the issues of character similarity and relatedness, and it's relying on the simplicity of the example to lead to the correct answer just by eyeballing the count of differences.

@Darlingtonia sure you can. which of these 4000 species is least related to X, based on data given,  only one share's no common sites in the sequence, no need to build a tree of all 4000 species, heck you might not even be able to build a tree with the data given, but you can answer the question.

@John That's incorrect because character similarity isn't the same as relatedness. Imagine species A with sequence GGGG, species B with GGGT, and species C with TTTT. The tree would be ((A,B),C). Species A and B are sister to each other, so they are equally related to species C, even though B has higher sequence similarity to C than A to C. Furthermore, sometimes there can be one species that is "least related to X" (but certainly not always), but across any phylogenetic tree there is never a single pair of species that is "least related", there's always multiple equally-related pairs.

@Darlingtonia Sure there are single species that are most distally related, do you know what an outgroup is?  Also species are not always split into two species equally, a species could for instant spawn multiple species or fuse from multiple species, phylogenetic trees are way of organizing and understanding relatedness they are not actual phylogenesis. Don't confuse the model for reality.  Of course character similarity isn't the same as relatedness, its only a predictor, note the questions asks about classification not true relatedness.

An outgroup (assuming it was just one species) would be in the same position as Cow in the example. It would be equally related to all members of the ingroup, so there would be no single pair of species that is "least related". Phylogenies can support hybrid speciation, and this highlights the need to use robust models when inferring relationships from characters; indeed, the complexities you cite highlight the need to construct a tree rather than eyeballing the answer.

Well the mouse has 7 differences and the horse has 8, compared to the cow, on that sequence.

Answer C (Mouse and Cow) is the correct answer to the question, because among the four answer choices, mouse and cow share the earliest common ancestor*.
OP developed this tree** by following the method in the YouTube tutorial.
Under this tree, mouse and cow are more distantly related than the other provided answers because the common ancestor of mouse and cow is deeper in the tree than the common ancestors of the other answer pairs.
However, mouse and cow are not the most distantly related pair across the entire tree. The tree OP constructed*** shows that cow is equally related to each of the four other species. This is because the common ancestor between cow and any other species is the same. Cow/horse are just as distantly-related as cow/mouse, cow/dog, or cow/hedgehog, because each of those pairs diverged at the same point in the tree (with the most recent common ancestor of all five species).
Finally, the algorithm used to construct the tree can make a difference, so it's a little unfair to provide a set of sequences and have someone think up the tree. In this case the question author probably just expected the student to count up the nucleotide differences and select the pair with the most (which most of the time will be the most phylogenetically distant).

*Edit: This originally stated that they were "farthest apart in the tree", but I thought this would lead to confusion with OP's drawing where Cow and Mouse are separated by the greatest horizontal distance in the diagram. To be clear, horizontal distance in the drawing is essentially uninformative to relatedness. One could draw a tree with the same topology as OP's where Cow and Mouse are right next to each other, and it would not change the interpretation.
**I didn't confirm if this is a correct application of that method, but we can assume it is.
***This tree is not accurate to reality. Our best understanding of relationships among these species would put cow sister to horse, who are both sister to dog, who are all sister to hedgehog, who are all sister to mouse. So, basically the exact opposite of this tree. (Although I believe OP correctly constructed their version based on the provided sequences.)

Thank you for the answer. I have a question about how you said the cow is equally related to all four based on the cladogram I drew. I uploaded another one with some characters added on it. https://imgur.com/7Ffr5iK So based on what I understand, you said the cow is equally related to all four have the shared character "red" right? But you would say the hedgehog and the mouse are the most closely related to each other because they share the most number of characters. Thank you.

Not exactly. To talk about relatedness, you need to have the tree, because the shape of the tree (called the topology) shows you which common ancestor is shared by certain species. Now in order to make the tree, we do use characters, but 1) hopefully we have a lot 2) they're usually not as well-behaved as yours 3) if we're asking how a character evolved it hopefully wasn't used to build the tree, and 4) there are many methods of constructing a tree from the characters. Methods like the video just use simple similarity, but really, some evolutionary model should be applied to the characters.

But, yes, mouse and hedgehog are most closely related in that tree. We know that because they share a more recent common ancestor than other pairs; not because their "color" character is most similar. If you added another species, like zebra, you wouldn't be able to say if mouse/hedgehog or horse/zebra we more closely related (although some types of phylogenetic trees do use informative branch lengths, so that could maybe tell you).


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Why do larger neurons have less cytoplasmic resistance?
I'm studying neuron electrochemistry rn and my book basically says that the more the cytoplasm impedes the flow of ions, the slower conduction will be, therefore larger neurons will have lower cytoplasmic resistance. Can someone explain this to me?
I'm confused why a larger neuron would mean less cytoplasmic resistance...wouldn't it be more since there is more cytoplasm? And the ratio of cytoplasm : ion channels in membrane would increase with size as volume : surface area ratio increases, so it's not that. I thought maybe it has to do with the diameter of the axon since larger diameter tubes have less resistance, but the flow of an action potential down the axon isn't really like a liquid flowing down a tube...
Thanks for any help you can give.

Does this answer your question? Why do larger diameter myelinated axons have greater conduction velocities than small diameter myelinated axons?

Neurons are like leaky cables. If you make them longer, the resistance increase (along the long axis); if you make them thicker (larger cross-sectional area), the resistance decrease. The word "larger" is quite ambiguous here. However if we assume the neuron grows evenly along all axis by a factor of k, the theory goes that
$R_{k} = \rho  \frac{kl}{k^2A} = \rho  \frac{l}{kA} = \frac{1}{k} * \rho \frac{l}{A}$
where l is the original length and A is the original cross-sectional area, so the resistance is 1/k of the original value. If k is greater than 1, the resistence is reduced.

Hi @X, can I changed your equation to latex format - can you double check I've preserved the original meaning?

@user438383 thanks, it looks very pretty. Today I learned latex in comments on cell biology ;-)


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Would viral diversity result in a change in the effectiveness of CRISPR systems in a population of bacteria, within a closed system?
I have here my hypothesis, does this make scientific sense? Assume this situation is occurring in a closed environment with only bacteria and bacteriophages.
The effectiveness of CRISPR/Cas9, being an adaptive defence system, is heavily reliant on the phages that it, or its ancestor has previously hosted. This is because Cas proteins require the virus’s physical presence in order to extract spacers from the virus’s genome and implement them into the CRISPR locus. Therefore, an environment bearing a smaller number of different virus types should theoretically lead to a higher degree of effectiveness for CRISPR systems. Low quantitative viral diversity should lead an influx in CRISPR’s effectiveness as, over time, a population of bacteria and its offspring should gain possession of spacers that provide them with a competitive advantage within their given environment. Hypothetically, this should lead to an increased bacterial population size as bacteria are now more easily able to ward-off viral infections. Consequently, this would most likely lead to a relative decrease in the viral population as the abundance of relevant spacers in the bacterial population will lead to a lower successful infection rate, causing an increased number of viruses to die upon the unsuccessful infection of a host bacterium, preventing induced viral lysis of the host, a process consisting of the disruption of the cellular membrane, resulting in the death of the host cell and the release of cytoplasmic compounds, including a large quantity of additional viral particles into the given medium, leading to a steep rise of the viral population. In contrast, CRISPR’s effectiveness should be diminished in an environment containing high levels of viral diversity as it would be far more difficult for bacteria to obtain the necessary spacers for CRISPR to be effective against the vast variety of bacteriophages in the given environment. Due to the decreased effectiveness of CRISPR systems, it would be more strenuous for bacteria to fight of viral infections, leading to a decrease in the bacterial population or a more moderate reproductive rate. Inversely, it is likely that viral population will flourish due to the scarcity of relevant spacers. This shortage in relevant spacers would result in an increased rate of infection of host cells, causing an increase in lysis and a rapidly multiplying viral population. Fluctuations in the bacterial population can be a strong indicator of the current effectiveness and efficiency of CRISPR systems as its main purpose is to aid bacteria in their survival. Quantitively, a good representation of the fluctuations in bacterial population size is percentage (%) rate of change. Percentage rate of change of a population provides a concise value that indicates whether the population in question is stagnant, increasing, or decreasing.
To me, it makes perfect sense, but I am not an expert in this field, just a high school student.
When I plugged this relationship into an online simulation, found here, I obtained a trend that suggested there is no correlation between viral diversity and the size of a bacteria or virus populations. I'll attach below a graph that shows the relationship I obtained.
Figure 4: Scatter plot graph showing the relationship between viral diversity (maximum virus types | 20, 40, 60, 80, 100) and the percentage (%) rate of change for both the bacterial and viral populations over a period of 500 ticks, within a closed environment. Graph includes two trendlines for each dependent variable, along with an equation for each line, a R2 value, and a R value.

Just looking for some insight, have I got this all wrong?
(This is a repost as I deleted the other variation of this question due to improper formatting)

Bear in mind that CRISPR is just one of many defenses bacteria use against phage. There is a diverse range of Restriction-Modification systems that also identify and disable foreign DNA, cell surface receptors can be mutated so the phage can't bind, etc. So I wouldn't expect a very tight relationship between CRISPR and phage pressure.


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Why can $\alpha$- and $\beta$-glucose molecules not link together?
My textbook states that for two glucose molecues to link together, they must be of the same form, i.e. they must both be either $\alpha$-glucose or $\beta$-glucose molecules.
Why is that the case?

What precisely does your textbook say? Can you quote and cite? What is your thinking on the matter/best guess from what you know?

You tag your question organic chemistry, and perhaps you are thinking of it from that angle. Think of it as biochemistry.

@BryanKrause my textbook says: "Although some chains of sugars store energy, others serve as structural material for cells. For two glucose molecules to link together, the glucose subunits must be of the same form. Cellulose is a polymer of $\beta$-glucose." I don't see any reason why an $\alpha$- and a $\beta$-glucose molecule shouldn't be able to link together, chemically. The only other idea I have is that maybe there are no cells/enzymes that can facilitate a dehydration reaction between the two - which would fit David's hint.

It would indeed fit because enzymes only evolve and “stick” if they catalyse a reaction of use to an organism. Your textbook should have made that clear.


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Does centrifuging the bacteria culture removes bacteria leftovers?
Usually, we centrifuge bacteria culture to either replace the media, control its density (OD), ..etc. I know that when centrifuging the cells are pushed to the bottom while the media (solution) remains at the top. However, let's say the bacteria was left to culture for a few days and the bacteria metabolism releases some carbohydrates as an output (e.g. Cyanobacteria).
Would those carbohydrates remain at the bottom with the bacteria cells or will they stay with media at the top where we can pour them?

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Centrifugal pelleting is density based. Under general media conditions and centrifugation, most secreted carbs will remain in the supernatant.

Correct answer, +1. The only way to pellet ("precipitate") dissolved compounds is a low enough temperatures, in conditions where sugars would crystallize out of solution. It would then be possible to centrifuge them into a pellet. Also, routine centrifugation in my experience leaves some viable bacteria in the supernatant, so if you wish to have a cell-free supernatant, it is always good practice to additionally filter it post-centrifugation. PS. I see you've been downvoted, likely by someone looking for the addition of credible reference/citations.

@SPr There are methods to pellet dissolved compounds.


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Why is the sex ratio of male and female cats close to 50/50 (with males actually being more prevalent)?
According to this study from 1970, cats are about 50% male and 50% female. Furthermore, there appear to be about 100 male pedigree cats born for every 92 female cats.
I couldn't find any info about sex ratios for cats that aren't adapted to live closely with humans. My understanding is that female cats occasionally live in colonies and work together to guard each other and their kittens. Female cats who do not live in colonies still hunt for themselves and their own offspring and protect their offspring.
Male cats...impregnate female cats?
It would take very few male cats to keep the species going. It seems like male cats don't do anything else beneficial to the species besides donate cat sperm to the females who take it from there.
I am wondering why, from an evolutionary perspective, so many male cats would continue to be born.  Is this purely for genetic diversity purposes?

Don't forget that while species evolve, it is individuals that are acted on by selection. Individuals that are successful cause more of their genetic material to be present in the next generation.
Your question is addressed by Fisher's principle.
For an example, imagine you do have a scenario like you describe, where there are fewer males and more females. Let's say, 90 females and 10 males. In the next generation of 100 cats, each female is responsible for on average 100/90 ~= 1.1 offspring per female cat. However, each male cat is responsible for on average 100/10 = 10 offspring per male cat.
Now, imagine some female cats produce 50:50 males:females, and other female cats produce all females. The latter group will have 1.1 x 1.1 ~= 1.2 grandchildren; the former will have (1.1 x 1.1)/2 + (1.1 x 10)/2 = 6.1 grandchildren. In a world where males are rare, it pays to be a female that produces male children.
These are some extreme examples, but in general you'll always have a pressure towards balanced sexes as long as both sexes are required to produce a child.

I remember figuring this out in SimLife many many years go.  You can start out by setting the organism to have a skewed ratio, but over time, they evolve to go to 50:50

Thanks for writing such a concise and clear answer! It seems so obvious now


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Position of vascular bundles in angiosperm leaves
In both isobilateral and dorsiventral types of leaf, xylem is present near the upper (adaxial) epidermis and phloem towards the lower (abaxial) epidermis.
Why is this so?


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How could microplastics accumulate in the bodies of marine mammals?
I have read several literature reviews and studies on the effects of microplastic particles on fish and invertebrates (one example includes the review by Franzellitti et al. (2019)) and there are multiple instances where these particles where found in the nervous system, lymph, and other organs following controlled exposures.
There are also multiple studies that looked at microplastics in marine mammals, but usually they focus on the contents of the gastro-intestinal tract. My question is: how these particles are likely to accumulate in the bodies marine mammals compared to smaller organisms - could the size of the blood vessels of larger whales influence the uptake of microplastics? Some researchers recommend studying this by using marine mammal cell cultures, but I am wondering how well the results of such studies can reproduce what might be happening at a full-body scale. (I study mainly ecology and the behaviour of marine mammals, so my knowledge of differences between various organisms at a cellular level is limited).
Thank you!

Microplastics are bioavailable to marine organisms, through direct ingestion and/or via trophic transfer. Most studies of microplastics in marine mammals only analysed microplastics in the digestive tract and scats (see Zantis et al. 2021 for a review) and thus, at this stage, there is no evidence that microplastics can cross the intestine barrier and/or enter the blood stream and accumulate in different organs in marine mammals. However, in some marine vertebrates (fish), microplastics have been found in other organs (e.g., brain, liver).The small size of microplastic might allow them to pass through the intestinal epithelium barrier through cell internalization and possible subsequent translocation. However, information concerning the extent of ingestion, accumulation, translocation into organs and possible pathways of transition into cells is still unclear (Wright et al. 2013).
Interestingly, it has been very recently demonstrated that microplastics are found in human bloodstream (Leslie et al. 2022). It is scientifically plausible that plastic particles may be transported to organs via the bloodstream. Regarding your question, "how these particles are likely to accumulate in the bodies marine mammals compared to smaller organisms", it's a difficult one. You need to consider the exposure route (direct ingestion and/or via trophic transfer) and the particle size (and the bioaccumulation and biomagnification processes).


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How can you diagnose albinism in a naturally light-colored person?
Not all albinos have white hair. There is a type of albinism where the affected person has light yellow hair and the skin color can be the same as a normal North European person.
How can you diagnose this type of albinism in a person who would naturally have very light blonde hair and pale skin, even if they didn't have albinism?
I mean, Boris Johnson isn't an albino, but there are albinos who have exactly the same hair and skin color as him.

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Short answer
Due to the considerable phenotypic overlap of different types of Oculocutaneous Albinism (OCA), molecular testing using a multigene panel or comprehensive genome sequencing is generally preferred for a precise diagnosis and is available for most types of OCA.
Using family tree combined with a clinical assessment can get you close. But a targeted sequencing panel looking for mutations in known genes that cause albinism would be the best way to do this.
More Info
Melanin, a black or brown pigment formed from tyrosine, is responsible for the color of skin and hair. Melanin is synthesized in melanocytes, which are specialized, dendritic secretory cells derived from the neural crest. These cells migrate to the basal layer of the epidermis during embryogenesis. The presence of melanin in the epidermis helps provide protection from ultraviolet radiation.
Disorders include decreased and excessive pigmentation.
Oculocutaneous albinism is a group of rare disorders caused by various gene mutations, but the most well known is the gene encoding tyrosinase, which catalyzes several steps in the production of melanin. Obviously in OCA, you'll have less melanin and this gives people with the disease the characteristic depigmented appearance. The disease is inherited in an autosomal recessive pattern (so both parents must have at least one of the mutated alleles).
Source: "UpToDate.com"

Typically the eyes are affected.
"Oculocutaneous" albinism affects both eyes and skin.  On this page the effects on iris and retina/choroid are illustrated.  While I could find a type of albinism in OMIM for which "Nystagmus, photophobia, and marked visual defect were not features", that entry still describes depigmented irides.  I have a hard time picturing a variation in which the eyes would have full pigmentation throughout, which would not be described as a skin color variation.  (That doesn't mean there isn't one!)

You could either look at the family history and see if there were any individuals with albinism or contact a gene counsellor. Here is an extract from the healthline website: "The most accurate way to diagnose albinism is through genetic testing to detect defective genes related to albinism." (https://www.healthline.com/health/albinism#symptoms)
I hope this helps!