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Why has life evolved around oxygen?
Why has life evolved around oxygen? Many lifeforms require oxygen to breakdown bio-molecules and release energy. I think there are two possibilities:

Reactions with oxygen tend to release more energy, so it is profitable to use oxygen for metabolic activities.
It is chance that it got to be oxygen; it could have been anything.

Which is right? Or is there some other possibility?
Edit: Yes, it is true that there are organisms to which oxygen is toxic. But you can't ignore the large numbers of organisms to which it is absolutely necessary for living. Why could it not have been some other molecule? Which property of oxygen drives it to become the most useful in bio-processes?

Have you done any research before asking this question? If you have, we would like to see it (edit it into your question.) Thanks!

I think you need to consider that oxygen is toxic to large groups of microorganisms, because it poisons their electron transport chains.
Strict anaerobes does not tolerate the presence of oxygen at all and as such I would argue that life can survive and thrive without O2.
Also life on earth evolved under conditions were O2 levels were extremely low, in fact when some organisms started to release oxygen into the atmosphere it caused an extinction event (Great Oxygenation Event).
So I think you need to change your question to why did life adapt to the presence of oxygen?

The reason life adapted to the presence of oxygen is that if it hadn't, it would have died - and so we wouldn't be around to ask the question :-)  Just a larger version of why bacteria become resistant to antibiotics, plants develop resistance to herbicides, insects to insecticides, &c.

@jamesqf You cite the reason why organisms became adapted to the presence of oxygen. But why did oxygen become so vital to a large number of organisms? If it is because of the abundance of oxygen, aren't plants major contributors to stable oxygen levels during the oxygen cycle? So does it not mean that life also contributed to the abundance of oxygen and so it could not be the reason why life evolved around it?

@prlfak1: I think what I'm trying to say is that asking "why" really isn't all that meaningful in evolutionary terms.  Photosynthetic organisms hit on the trick of using light for energy, releasing oxygen.  Then other organisms evolved ways of using this energetic waste product for their metabolism, which allowed them to survive & reproduce.  Lots of photosynthesis eventually meant lots of O2, so lots of O2-using organisms.  But there are other ways, like chemosynthetic bacteria that react CO2 & H2S to produce carbohydrates & sulfur.  It's just that H2S isn't all that plentiful...

The main drive towards oxygen is it's efficiency. When you consider the order in which different energy generation pathways evolved you will see the improvement. Here are the main ones

Glycolysis - produces 2 NADH and 4 ATP. Plus you end up with two pyruvates ()
Pyruvate Decarboxylation - 3 NADH, 1 FADH2, and 1 GTP (equivalent to
12 ATP)
Electron Transport Chain (final electron acceptors other than O2) - 2-36 ATP equivalent. This number varies so much because bacteria have a whole range of different systems and their efficiency varies greatly. However efficiency mostly depends on the final acceptor redox potential which is highest for O2
Oxydative phosphorelation (ETC with O2 as final acceptor) - 10 NADH (equivalent to 30-36 ATP)

In addition to that 2.3 bya Great Oxygenation Event occured. What happened is that cyanobacteria was releasing a lot of oxygen as part of photosynthesis for a while but it was all instantly bound to Iron diluted in ocean waters (and other compounds). Then 2.3 bya, oxygen levels got saturated and atmospheric oxygen levels increased rapidly driving many obligate anaerobes to extinction.

Yes, oxygen is crucial for all of the processes mentioned above, where it is used as electron acceptor. The reason why oxygen was "chosen" over other electron acceptors, which are in fact better electron acceptors, was due to the abundance of water and therefore how easily accessible oxygen is. There are in fact certain organisms, such as lithotrophic bacteria, that instead of oxygen use sulfur.
You can also read up more about when the production of oxygen first occurred on Earth and which were the first organisms to use oxygen here: https://en.wikipedia.org/wiki/Great_Oxygenation_Event.


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Is sex a spectrum?
At the moment I'm especially interested in the question of whether biological sex is really a spectrum. Unfortunately I could not find any good answers on the Internet. Therefore I hope that some of you might be able to present the current state of science here and whether it is already generally accepted in biological science that sex is a spectrum.
What I am confused about here is for something to be a spectrum it must have some some sort of distribution along a parametrised scales. For example, it would be daft to think height to be binary even though there are tall people and short people. Tall and short are relative; height is defined by a continuous factor, length, measured (for example in cm) from foot to head. There is no such parameter that can be used to show that male and female are relative in the way that tall and short are. There is no scale. What I thought is that it relies on the binary to classify gonads as either male or female. So, people with disorders of sex development are still either male or female due to the presence of gonads (which define sex) if I understood correctly. There are only two gonad types since this is the fundamental feature of what sex is. I hope someone can correct me here, if this is wrong.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Sex-determination system and Sexual differentiation in humans might be informative for you and are as good a place to start as any. Read up a bit more on the topic, and then please come back to [edit] your post about what you've learned and by adding a specific biological question about something you still don't understand. Thanks

@theforestecologist So, I edited the question and added from what I understood to be a spectrum. I hope, you can help me out there.

As requested, the assumption in your edit is wrong :p. See the links in my previous comment. Hope this helps.

@theforestecologist I did read those articles already. It didn't really help me though, since they also have not mentioned exactly what sex on a spectrum means. Could you help me out here and explain what exactly is wrong in my edit? This is from what I understood so far.

Also, I am not quite sure why this question was downvoted. :/ It's a fair and crucial question and I hoped that someone could clarify it or at least give a glimpse into what current studies or science says. Just linking to wikipedia articles is not really that much of an helpful answer.

biological sex is based on presence/absence of sex chromosomes and not on anatomical gonads as you mention. Within a species, there is no spectrum (though, there are variations based on chromosomal disorders/abnormalities).

It was downvoted because it doesn't follow the guidelines for writing good questions on our website (specifically, see here). I've already described to you in my first comment what improvements you need to make to have the question receive upvotes and to receive the most helpful answer. your question is currently written in a hypothetical inquisitive manner, whereas we require prior demonstrated research to be explicitly stated in a question. Please take our [tour] to learn more. Thanks

@theforestecologist But wouldn't these variations essentially be on a spectrum then? Why would it be a "chromosomal disorder" for example being a hermaphrodite and not just another sex on the spectrum?

See Chromosome Abnormalities Fact Sheet for a review of chromosomal abnormalities.

To get an idea about the spectrum as it relates to genital development check out the Quigley_scale and the related links on that page. Also note that while hermaphrodism (defined by having both male and female genitalia) does occur in some animals (e.g. slugs) it does not occur in humans.

You're comparing apples to houses. Some things occur on a spectrum (e.g. height or intelligence) because it is multifactorial (genetics, hormone expression, nutrition/genetics, nutrition, environment, opportunity, etc., each factor contributing something) and some things do not (you are either a chromosomal male or a chromosomal female) excluding uncommon genetic abnormalities. @theforestecologist has given you the answer, and Wikipedia is actually a good resource to start at a basic level.

@anongoodnurse I don't believe the OP asked about chromosomal sex. Maybe different medical schools teach this differently, but I was taught that the karyotype is not adequate for defining biological sex.

For what it’s worth, I don’t think your question deserves as much grief as it has gotten. The only critique I’d make is that you should not conflate sex with gender.

@canadianer Just saying, that's not really a fair and reasonable critique since I specifically wrote: "biological gender". So, there has been no conflation between the term sex and gender. But thanks anyway for your input.

This Q/A might be interesting: Whats the difference between male and female

@DeNovosupportsGoFundMonica - The OP specified "biological sex". That is the correct answer to "biological sex." I think you read (as we are wont to do these days) too much into "sex". To quote the OP: "There are only two gonad types since this is the fundamental feature of what sex is." Without defining sex as gender but as "biological", I answered what I thought the OP was asking. N.B. Gender is not necessarily sex. It's all about definitions, wic the OP has not accurately specified.

I, too, commented assuming that the OP had conflated "sex" and "gender" and chose to respond as though the OP simply was referring to biological sex. If that is the case (i.e., if the OP did conflate the two), then (as @anongoodnurse suggests above), we mustn't complicate the biology with conflated social constructs, and we need to emphasize the strictly biological aspect of this question. Which is what I have tried to do.

However, since the OP has suggested in their comment that they intentionally used "biological gender" (gender normally referring to "social and cultural differences rather than biological ones" (Definition 1 here), then I would suggest that either the OP needs to define what they specifically mean by "biological gender" or otherwise this question is off-topic b/c it is not about biology.

@anongoodnurse as i was taught, karyotype is not sufficient for determining biological sex. I mean those terms precisely. Gender is a behavioral category, and not at all what this question or my comment were about. Biological sex is a (complex) question of physical phenotype that depends on a great deal more than the simple presence or absence of a Y chromosome on karyotype.

What is "biological gender"?

@BryanKrause - Exactly. Definitions matter, and the OP provided none. I think, though, you can differentiate between a simple definition of biological sex (female, male, neuter, hermaphrodite, etc.) and phychological/emotional gender.

@DeNovosupportsGoFundMonica - Feel free to tell me your definition of "biological sex." I am not too old to learn. And since I have no dog in this race (not trying to push or support my particular views/biases), I'm open to learning more.

Your question uses the word I very much... sci pubs and research dont communicate journalistically about themselves.

@anongoodnurse as I understand it, "biological sex" = reproductive phenotype, which is determined by the (variable) expression of a heterogeneous set of genes on multiple chromosomes, including autosomes.

@anongoodnurse I'd say whether reproductive phenotype is binary or not depends more on philosophy, politics, and whether you're a lumper or splitter.

Possible duplicate https://biology.stackexchange.com/questions/17327/does-any-animal-species-have-two-sexes-and-more-genders

related question https://biology.stackexchange.com/questions/52149/how-is-trangender-female-different-from-normal-female-biologically

Isn’t that rainbow logo confusing you?

Is the question only referring to the human species or the general case? This is a bit muddled, both in the Q and some comments (and the current answers).

@BryanKrause Biological gender is sex (and I even wrote it above in brackets. It's absolutely clear what I meant with biological gender). Fairly obvious.

@Tetragrammaton it is absolutely not clear because there is no such thing as "biological gender". As has been made clear multiple times in responses you've received, "gender" (regardless of adjectives you associate with it) is NOT a biological concept. As such, "biological gender" is meaningless and demonstrates a lack of understanding of terminology. Put differently, You cannot equate "sex" and "biological gender" because the latter phrase doesn't make sense. I highly suggest you [edit] your post to remove all mention of "gender" since it is at-best unclear and at worst off-topic.

Scientists Fred P. Thieme and William J. Schull of the University of Michigan wrote about sexing a skeleton in 1957: “Sex, unlike most phenotypic features in which man varies, is not continuously variable but is expressed in a clear bimodal distribution.” The same is true for chromosomes, sex organs and testosterone.

"Variability in size or composition of gonads, genital morphology, chromosomes and/or hormonal physiology"

Specere in latin means to look, that's why it's used for the color spectrum. The rainbow is often used to represent gender-identity to represent the amorphous nature of the mind.

The distribution of fitness effects for genetic mutations of whole genomes and individual genes is frequently found to be a bimodal distribution with most mutations being either neutral or lethal with relatively few having intermediate effect.
Through the process of meiosis and fertilization (with rare exceptions), each individual is created with zero or one Y-chromosome. The complementary result for the X-chromosome follows, either a double or a single X. Therefore, direct sex differences are usually binary in expression, although the deviations in more complex biological processes produce a range of exceptions, resulting in a bimodal graph.
Gender does means biological sex in the context you use.
https://en.wikipedia.org/wiki/Gender

I'd avoid using the term menagerie to describe intersex individuals

Mais pourquoi donc?

Because it contains the implication that intersex people are non-human animals. I'm sure that's not what you intended, but it can read that way.

this really has nothing to do with the question, as the linked article is discussing sex not gender.

@John the OP seems to be misusing the term gender. The edit clarifies the question to be about sex, not gender.

Menage, is a strictly non-zoological term that french proudly use to refer to their household, I 've never heard of a ménage d'animaux, an animal household. Sorry I copied that straight from the wiki because was ona small phone screen. https://en.wikipedia.org/wiki/Sex_differences_in_humans

@john https://en.wikipedia.org/wiki/Sex_differences_in_humans#Physiology besides, it's simple maths like 1+1 =2, if you can read a graph you can understand it john. bimodal distribution is not more complex than a bell curve, it has peaks.

I know what a bimodal distribution is and human gender is not bimodal, even if sex largely is and confusing them makes your answer straight up wrong. Its bad enough the question is using poor terms there is no excuse for an answer to.

Gender is not really an established word, John, it has almost no precedence in scientific literature other than the sense that I use, It's etymology doesn't make sense for science either. Since 1990 there has been a lot of identity hysteria which has seen a new sense attributed to gender, the one that you are militant about: https://books.google.com/ngrams/graph?content=gender&year_start=1800&year_end=2000&corpus=15&smoothing=3&share=&direct_url=t1%3B%2Cgender%3B%2Cc0#t1%3B%2Cgender%3B%2Cc0 and https://www.google.com/search?q=%22gender%22&tbm=bks&tbs=cdr:1,cd_min:1857,cd_max:1995&lr=lang_en

@com.prehensible sounds like even more reason not to use the term. Also what do weaver ants have to do with the question?

@John, No, it's fine to use the word as long as you don't claim there is a precise narrow definition for the word based on your imagination. Your claim that gender is not sex is nonsense according to the wiki page gender, if you read the first phrase of that page it puts your old tutor's quip in the bin.

@com.prehensible have you read the wiki? because the first sentence tells you it is a social construct, and the second paragraph goes on to tell you why sex and gender are not interchangeable terminology.

@DeNovo You are incorrect. I did not misue the term gender and properly differentiated it from the term sex, as can be clearly seen above in my post, if anyone dares to read it.

@com.prehensible Thank you by the way, for answering the question. So, we can conclude that sex is not binary and is in fact bimodal. That's not really on a spectrum, but it definitely means that sex is not that fixed as many falsly claim.

@Tetragrammaton It's usually not good to accept answers with so many downvotes. This answer is bad: it has a graph of a bimodal distribution that is just an illustration and has nothing to do with sex. The rest of the answer talks about sexual orientation and not sex. It then talks about morphology of ants which are not related to sex at all since all the worker ants are sterile females.

Bryan Krause, you are contradicting fact: physical gender is bimodal ... https://en.wikipedia.org/wiki/Sex_differences_in_humans#Physiology There is a list of other bimodal distributions in nature, which includes harvester ants, which are also related to chromosomes.

The answer is bad because you assert that sex is bimodal but provide no evidence to support it.

Scientists Fred P. Thieme and William J. Schull of the University of Michigan wrote about sexing a skeleton in 1957: “Sex, unlike most phenotypic features in which man varies, is not continuously variable but is expressed in a clear bimodal distribution.” Chromosomes, Gamete structure, Hip structure, they graph into two modes.

This is improved.  Are you willing to include the sources for your two figures?

was confused with the downvotes on this answer, until I looked at the edit history.  It's much better now, good job (imo, although I'm by no means an expert)

@bandybabboon Bimodality simply isn't evidence of a trait that is not continuously variable, though. The bimodal plot you've chosen to illustrate the point of non-continuity is clearly labelled as a "continuum", and shows that individuals occupy the entire space between extremes. This is a trait that is both bimodal and continuously variable.

It's amazing to think that the dual bell curve of sexual phenotype applies to most of the animal clades that we see. I was quoting a 1950s scientist who used the words "continuously variable" in the sense of regularity of the variation being a continous spectrum, as opposed to that of a dual gaussian distribution. It's just 2 bell curves, another example from nature is snapdragons. https://www.researchgate.net/figure/Binary-gene-expression-gives-rise-to-a-bimodal-distribution-of-protein-levels-in-a_fig1_230569947

Short answer: it's messy, and probably no answer will satisfy everyone.
I'm only going to consider sex (I'm not going to mess with "gender") in humans.

It's reasonable to consider sex as multidimensional rather than one-dimensional; see the various definitions listed below. The same individual could have different karyotypic, morphological, and endocrinological "sex".
Some but not all of the definitions refer to continuous scales, i.e. if you pick one of the continuous measures below (Quigley scale, circulating testosterone level) you can probably find at least one individual in any not-too-narrow interval on that scale.
It's reasonable to say that many of the continuous measures below are bimodal, i.e. in some random sample of humans there are more people close to 1 or to 6/7 than in the 2-5 range on the Quigley scale; similarly, there would be more people in the ranges of 10-30 ng/dl or 200-500 ng/dl in their testosterone than in between.

Here are some of the possible definitions of sex, drawing on the Wikipedia article mentioned in the comments:

karyotype (chromosal type): this is discrete (XY, XX, XYY, XO, XXY, ...) but not necessarily easy to split into "male" vs "female" except on the basis of what the phenotype (morphology, endocrinology, etc.) looks like. Would "male" mean "has a Y chromosome" (XY, XYY, XXYY)? or "has only one X chromosome" (XY, XYY, X0)? Would female mean "has no Y chromosome" (X0, XX) or "has 2 X chromosomes" (XX, XXY, XXYY)? Non-standard sex karyotypes are rare: e.g X0 1 in 3000 live births, XXY [Klinefelter's syndrome] 1 in 1000 live births; XYY 1 in 1000 live births; XXYY 1 in 20,000 live births (Jarzembowski, J.A. “Sex Chromosome Abnormalities.” In Pathobiology of Human Disease, 185. Elsevier, 2014. https://doi.org/10.1016/B978-0-12-386456-7.01505-7 ; https://rarediseases.org/rare-diseases/xyy-syndrome/)

Below the level of the chromosome, there's lots of genetic and environmental variation that can change the phenotype (e.g. here)

morphology (gonads or internal/external genitalia): the Quigley scale referenced in comments above is one way to describe this variation. The Quigley scale could be used to classify phenotype in cases of

androgen insensitivity syndrome, i.e. someone with at least one Y-chromosome who doesn't respond developmentally in the typical way to androgens such as testosterone
someone with an XX karyotype and congenital adrenal hyperplasia who has become masculinized

(the section on intersex conditions in the Wikipedia article on sexual differentiation links to these among others)

(these are cartoons of external genitalia, in case that's not obvious)
Intermediate morphology can occur in the gonads as well as in the genitalia or internal organs; according to MedLine Plus (US National Library of Medicine), people with "true gonadal intersex" have "[both] ovarian and testicular tissue ... in the same gonad (an ovotestis), or the person might have 1 ovary and 1 testis".

endocrinology (levels of various circulating hormones): researchers most typically consider testosterone (e.g. in this article). This article reports on total serum testosterone in a US health survey. The distribution is indeed bimodal (there's a peak around 10-30 ng/dL for women and 250-600 ng/dL for men), but this article only reports the 10th and 90 percentiles; there could certainly be someone with a circulating testosterone level right in the middle. It's also important to note that a person's phenotype/morphology (musculature etc. as well as gonadal morphology) is not necessarily closely related to their level of circulating testosterone, depending on whether they are androgen sensitive or insensitive ...

In light of recent (August 2024) Olympic boxing controversies, here's some more data on circulating testosterone distributions from Clark et al (2019)

top solid line for each column is the weighted 95% confidence interval for normal men and women, solid line for each study is 95% confidence interval, dotted line is absolute range. Blank spacer line below a study reference indicates an additional subset for that study

[PCOS = polycystic ovary syndrome, 5ARD2 = 5-alpha reductase deficiency, PAIS-CAIS = partial/complete androgen insensitivity syndrome]
So ... the answer to your specific question about being able to classify people based on gonad type is that although it's rare, people with true gonadal intersex as defined above could not be classified as either (exclusively) male or female on the basis of their gonads. Furthermore, it's not obvious which of the many criteria (karyotype, internal/external morphology, endocrinology) would be the "correct" way to define sex in a particular scenario.

Clark, Richard V., Jeffrey A. Wald, Ronald S. Swerdloff, Christina Wang, Frederick C. W. Wu, Larry D. Bowers, and Alvin M. Matsumoto. “Large Divergence in Testosterone Concentrations between Men and Women: Frame of Reference for Elite Athletes in Sex-Specific Competition in Sports, a Narrative Review.” Clinical Endocrinology 90, no. 1 (January 2019): 15–22. https://doi.org/10.1111/cen.13840.

You might consider adding a bullet point for anisogamy, a concept that applies across a wide range of species

But humans are completely anisogamous as far as I know - I'm not aware of any circumstances under which humans produce gametes that are anything other than eggs or sperm. Seems tangential to me.

Since anisogamy is fundamental to the biological definition of "male" and "female" (e.g., Parker et al. 1972, The origin and evolution of gamete dimorphism and the male-female phenomenon), and since the OP's question was "Is sex a spectrum?", doesn't the fact that humans are completely anisogamous provide one important answer?

First gender and sex are not the same thing; as an old teacher of mine glibly put it, "sex is plumbing, gender is clothing," and even that is a gross generalization. The problem you are running into is using imprecise terms to ask a scientific question (sex, gender, and spectrum are all imprecise terms in biology). Precision in language is important in science to avoid confusion. The more vague your terms the less precise an answer can be.
More importantly gender isn't really a biological term; it is a sociological term, in particular it is a form of social construct (like countries, currency, or social class). The closest you get in biology is mating strategy, in which case there are species with multiple alternative mating strategies, including species with more mating strategies than sexes, some that are quite drastically different.  Humans in particular have a very wide range of complex mating strategies, and of course some are more common than others.
Spectrum is also a tricky word in biology; would you call hair color a spectrum even though the distribution is non-uniform? How about handedness or ear lobe shape? They are both multimodal. Quite often in behavior there are evolutionary stable strategies that are only stable as multimodal distributions; are they spectra?
Even sex is tricky in biology. Since you have phenotypic sexes and chromosomal sexes, there are XY females in humans, as well as XX, XO, and XXX females. There are people with neither testes nor ovaries (both are gonads BTW), and humans with both testes and ovaries. So you end up with quite a variety of "sexes". Then you have things like chimerism in which an individual is really two individual cell lines fused together; even the term "individual human" can get tricky if you look close enough because biology is messy and doesn't respect our generalized human categories.
https://www.ncbi.nlm.nih.gov/books/NBK10943/
https://www.who.int/genomics/gender/en/index1.html

Gender is a corruption of the term "gender-identity", which is also "sex-identity", genre in french means "type" and gendre means spouse, so it's a contradiction if you know the etymology.  https://en.wikipedia.org/wiki/Gender#History_of_the_concept https://books.google.com/ngrams/graph?content=gender+identity%2Cgender&year_start=1800&year_end=1990&corpus=15&smoothing=3&share=&direct_url=t1%3B%2Cgender%20identity%3B%2Cc0%3B.t1%3B%2Cgender%3B%2Cc0#t1%3B%2Cgender%20identity%3B%2Cc0%3B.t1%3B%2Cgender%3B%2Cc0

Just a small reminder: Again (and I don't like repeating myself in that matter for the third time) I never said that gender and sex are the same thing, nor did I ever claim so. @John

@Tetragrammaton biological gender isn't a thing, even "biological sex" is not a single thing.  I have have answered the question given, if this is not what you wanted to know then do some research and ask a new question with correct terminology.

@John Again, correct terminology was given. It's written in the question above. I wrote: "biological gender (or sex)". Thus, there's no need to ask a new question. But thanks for your input.

@Tetragrammaton and As I said, biological sex can mean several different things and biological gender is meaningless.

I don't think a random variable has to have a continuous or discrete uniform distribution in order to be a spectrum. Not that the uniformity isn't important, and could be quantified with information entropy.

@LifeInTheTrees Thank you. At least someone here who pays attention.

Summary
The claim that sex is a spectrum is not an accurate conclusion supported by current research and understanding of sex in biology. It is perhaps based on misunderstandings of medical terms and anthropocentric ideas of sex. This answer also points out what I regard as some serious problems with the arguments put forward here by other answers.
Answer
There are a couple of answers here that provide "definitions of sex" and claims about sex being continuous or a bimodal distribution which are not supported at all.
The top answer does not provide any actual definitions of sex and seemingly misunderstands the "definitions" they believe describe sex. To start with, the author gives possible definitions from a wikipedia talk page on sex differentiation in humans, not sex. The claim that definitions of sex were provided here is incorrect. https://en.wikipedia.org/wiki/Sexual_differentiation_in_humans.With regard to sex his first definition, sex has never been defined by karyotype, as plenty of organisms have males and females with different sex chromosome combinations or no sex chromosomes at all. Furthermore, the Karyotypes listed are specific to males or females. His own sources, https://www.sciencedirect.com/science/article/abs/pii/B9780123864567015057?via%3Dihub and https://rarediseases.org/rare-diseases/xyy-syndrome/ not only do not define sex by sex chromosomes but name some of the sex chromosome abnormalities as being sex specific. The Quigly scale in no way or form defines sex, it's just a convenient scale so physicians can describe the appearance of external genitals. There's also the Prader scale. It's categorical with only a set of discrete categories, so I have no idea why it's being claimed to be continuous, let alone why it would define sex. His own citation, https://en.wikipedia.org/wiki/Quigley_scale says does not claim it defines sex and highlights it does not match his description at all. There is no literature that describes a person's sex as "3" on the Quigly scale for example.
Another issue is the answer also provides an "endocrinological" definition using a reference, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6391653/,  that doesn't support it. Said reference does not define sex by hormone levels, in fact I think it bizarre to even claim sex is defined by hormone levels as they constantly change and also vary throughout life. I'd be very interested to hear about the testosterone levels of male ginkgos.
I have no idea why it is being argued that humans have some special definition of sex when sex is not a specifically human thing. Humans have male and female sexes for the same reason all other anisogamous species do. Literature on sex establishes that the sexes are two reproductive roles in anisogamy predicated on two differing types of gamete. This understanding is well demonstrated both in taxonomy and literature (Parker et al. 1972, Lehtonen et al. 2014, "The Biology of Reproduction" pg 112 by Fusco and Minelli, 2019.)
A second answer talks about sex having a bimodal distribution. It includes a graph (Fig.1) from Blackless (2000), but there are several problems with this. First, the graph in question is conceptual in nature and has no real data nor any clear methodology. In fact, looking at the axes, what's being measured doesn't even make sense. Given it says "Variability in size or composition of gonads, genital morphology, chromosomes and/or hormonal physiology", the authors don't even appear to be sure of what is being measured. I've never seen any graph with an "and/or" in it. Also keep in mind this isn't even a conceptual graph of sex but sexual dimorphism. The authors do not argue that sex has a bimodal distribution. Another issue is that it actually isn't even a bimodal distribution but just two normal distributions plotted on a single graph. A bimodal distribution does not have separate curves. Statistically, bimodal distributions require two well separated local maxima, which means the random variable must be quantitative. Sex chromosome combinations therefore cannot have a bimodal distribution, contrary to the assertions in that answer. The distribution the posted of hormones is clearly not a measurement of sex, as it readily recognizes that that there are two separate distributions.
I think a lot of confusion is misunderstandings of medical diagnostic terminology(Money, John; Hampson, Joan G; Hampson, John (October 1955). "An Examination of Some Basic Sexual Concepts: The Evidence of Human Hermaphroditism". Bull. Johns Hopkins Hosp. 97 (4). Johns Hopkins University: 301–19) for describing patients with atypical sex development, etc. You have terms such as "chromosomal sex", etc that are not and never were definitions of sex. There are no such things as "chromosomal sexes" and "phenotypic sexes". Strictly speaking, spectra are measurements along a continuous variable. A continuous variable has infinite possible values, thus if sex was a "spectrum", then each of the infinite points are a different sex. Biology literature does not describe infinite sexes, let alone more than two in anisogamy. Therefore the claim that sex is a spectrum is not supported by research. It is important to distinguish sex from characteristics associated with sex in humans and that while we can describe how those characteristics individually vary that is not the same as sex being a spectrum.

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It's not clear for me the definition you are using for "sex". The closest paragraph I found  is "two reproductive roles in anisogamy predicated on two differing types of gamete". If so, could you please give the definition a more central role in your answer, a short explanation of why it's not a spectrum and the limitation of the definition to expand the conclusion to for example, cariotype and reproductive organs.

What I meant by 'limitation of the definition' is that while sperm and egg can almost certainly belong to two distinct classes, their karyotypes (XX, XY, XXY, XO, etc.) does not, nor does the reproductive organs. If you clearly define your premises, address this and other limitations, and add some references, it could be a valid answer.

@heracho the comment where I explained some misconceptions were deleted. Currently, I do not believe the topics you raised are related to answering the question and do not change the answer. If you wish to discuss, create a chat room and we can.

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What is the probability for an offspring to inherit schizophrenia?
If an European male (i.e. white) is diagnosed with schizophrenia, but an European female (also white) 2-3 years younger than the male is healthy, what is the probability that their first child will:
a) be diagnosed with schizophrenia later in life?
b) have some other mental condition?

I'm not referring to any studies and do not have background in biology/medicine. All I'm trying is to get an answer for my case, because other forums remain silent.

I'm glad that you've made it a tiny bit more specific. The site requirements are that you should show the results of your prior research - perhaps use as a springboard for your researches something like this, this or this. There are indications of a genetic link, but it's far from cut and dry, more like a genetic susceptibility which might get triggered.

https://pubmed.ncbi.nlm.nih.gov/27872260/

Personal medical questions and health advice are off-topic on Biology.SE. We cannot safely answer questions for your specific situation and you should always consult a doctor for medical advice.

But if scientists don't know an answer, how can a doctor know?

It may not be about "don't know" so much as "don't want to be legally responsible for" - in fact, the medical Stack Exchange is sometimes reluctant to answer personal questions about the questioner's own health (or in this case their child's), too.  But also, there is a specific medical Stack Exchange (I don't remember what its exact name is, but it'll be in the list), which may be more applicable to a question about human health than Biology.SE (which covers everything, from tomatoes to amoebas to fish), though I'm not sure.

Doesn't that probability depend on the father's age?

Haven't directly answered this
I found a recent literature review that is relevant to this:
"Gene-Environment Interactions in Schizophrenia: A Literature Review"
by Marah H. Wahbeh and Dimitrios Avramopoulos *Department of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Academic Editor: Sarah Tosato
Genes 2021, 12(12), 1850; https://doi.org/10.3390/genes12121850 (registering DOI)
This article notes that the chance of schizophrenia is more likely to arise if one of a group of conditions is present.
Conditions such as prenatal maternal exposure to some infections, childhood adversity, and cannabis use.
As far as increased chance of other disorders, the below article only uses the measure of first or second degree relatives - not chance of heritability from a parent only. This study uses the entire population of Taiwan.
"Familial Aggregation and Heritability of Schizophrenia and Co-aggregation of Psychiatric Illnesses in Affected Families"
I-Jun Chou,  Chang-Fu Kuo,  Yu-Shu Huang,  Matthew J Grainge,  Ana M Valdes,  Lai-Chu See, Kuang-Hui Yu,  Shue-Fen Luo,  Lu-Shuang Huang,  Wen-Yi Tseng  ...
Schizophrenia Bulletin, Volume 43, Issue 5, September 2017, Pages 1070–1078, https://doi.org/10.1093/schbul/sbw159
"The RR (95% CI) in individuals with a first-degree relative with schizophrenia was 3.49 (3.34–3.64) for mood disorders and 3.91 (3.35–4.57) for delusional disorders."
(RR is relative risk.)

Seems that the first article gives 80% genetic chance for a child to inherit a disease?

@mercury0114 that's the heritability - i.e. how much of the variation between individuals in having schizophrenia is caused by genetics. This isn't the same as the probability of getting it with a first-order relative has it.

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How to calculate information content of a DNA sequence
How does one calculate the information content of DNA sequence like ATCGGCT where mutation rate of G's is 10% and the most common mutation product binds with C and A with equal frequency.
I know that the individual information of a sequence is the dot product of the sequence and the weights matrix for each base. Essentially I = sum (base1xweight + base2xweight + ...)
What I can't figure out is how to determine the the weight of each base so as to incorporate the 10% probability of mutation of G's.. Can anyone help me figure that out
EDITED since wording may be confusing:
Original problem says:
" Spontaneous deamination of exocyclic amine is dG (deoxyguanosine) can occur occasionally in DNA strand. Given probability of this occurring  during the time it takes DNA polymerase to copy DNA is 20% per dG in a particular DNA. Given that most common deamination product pairs with dC and dA with equal frequency calculate information content during DNA replication in the given sequence. "
     As an example I choose ATCGGCT and changed it to 10% deamination of dG.
PROPOSED SOLUTION:
For sequence ATCGGCT,
I am only consider the initial strand bases A,T,C are 2 bits a base, given by I=-1/ln(2)ln(n_before/n_after) ,where n_before = 1, and n_after = 4
In the case of mutated G (Gm) ,
I say, I = -1/ln(2)ln(1/3)= 1.58 bits , n_after=3 since A,C are equivalent to Gm
Perfect copy would give us 7 bases x 2 bits each = 14 bits content of strand.
Since there are 2 G's, with 10% change of mutating --> 0.02 of G in strand will mutate.
Thus I content during replication,
    Information content I(ideal) - I(inc. mutation) = 14-0.03 = 13.97 bits during time of replication

Sounds like a homework question. Have you already tried to solve this yourself? If so then it would help if you show what you have tried and why you think it is incorrect (or correct).

"the mutation rate of G's is 10 %" what does this phrase mean? For example, are you saying that for every cell division a G residue has a 1/10 chance of mutating (and that the other bases have a 0/10 chance of mutating?)? In this model, what base does a G mutate into? One of the other 3 bases, randomly? "The most common mutation product binds with C and A" this phrase does not have a clear sense to me. Since there are only 3 choices, G could mutate into A or C or T, but none of those will bind with C and A with equal frequency, do you see what I mean?

Since DNA is double-stranded, if the sense strand is 5'-ATCGGCT-3' then the antisense strand (or reverse complement) will be 5'-AGCCGAT-3', so there are two G's on the top strand and two more G's on the bottom strand, did you take that into account?

This sounds like computing science/statistics rather than biology. Where does this mathematical formula you quote for information content come from? I've never heard of it and I can't see how it relates to anything 'real' in  genetic information.

I think I have a solution..
I am only considering 1 strand based on original problem wording, however mdperry I did consider the second strand. I am glad you also brought that up.
David the formulas come largely from (https://schneider.ncifcrf.gov/paper/ri/latex/ )
So my soluion

Thanks @Valentin-Angelo Uzunov. More mathematics than computer science even. I'll pass on this one.

So I think you have answered the question yourself. While I am no expert, I think Schneider presents the most thoughtful, and clearest descriptions and explanations in his many publications on this subject. I also appreciate your clarification of the question, and now understand the answers to the points I raised. 14 bits for a 7-mer sounds correct to me.  I don't really understand what a student is supposed to learn from doing this exercise, with the mutations etc. but I suspect you have the answer they are looking for.

I guess we will find out.
Actual sequence was AGCCGATTTGGGAAAAATCG, = 40bits without. 2bit / base.
When 20% mutation of G is taken into account.
If 20% of G will be mutated, then that = 1.2 bses ~ 1 based in the sequence will be likely mutated during replication
The information content of a mutated G = 1.58 bits. thus, deltaI for that bit is 2 - 1.58 = 0.42 bit lost from mutation
Thus information content is 40 - 0.42 = 39.6 bits during replication.
That is my final answer.

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Is insect farming more efficient than shrimp farming?
Insect farming is sometimes advertised as the way to feed the growing global population with animal protein in a way that is more efficient (in terms of protein yielded/feed consumed) than growing cows, sheep, pigs or fish.
Would insect farming be more efficient than shrimp farming, even though these two broad groups of animals share some similarities in terms of "complexity"?

Maybe worth reading this and this

I don't have an answer one way or the other, but from what I've seen, shrimp farms require flooding large patches of land, often in coastal regions where, whereas insects can be grown in self-contained and relative dry environments that should be easier to scale up. It's a topic I've followed for years, but I still haven't seen an insect protein product that's priced competitively with other sources.

efficent at what? calories per acre, calories per kilowatt hour, calories per gram, water usage, cost vs profit, ect.

Insects have a very low feed conversion ratio, which essentially means most of what they're fed turns into edible protein for us. Cows, sheep, pigs, etc. typically have high feed conversion ratios. According to this site: https://in.virbac.com/aqua/health-care/aqua-advice/how-to-get-optimum-fcr-in-shrimp-culture, shrimp have a feed conversion ratio of 1.5 - 1.8., where Acheta domesticus, which is a cricket, is at about 0.9 - 1.1, pork is 5, and beef is around 10 (Huis. A., 2012).. So if we look at feed conversion ratios, they are approximately the same, especially when compared to cows and pigs. What's more efficient to produce depends on the area, and what resources are available. Hope this helps.


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Is there a dominant gene for right-handedness?
Has there been any definitive research about handedness being genetic? Also, why is right-handedness clearly dominant in humans? I'm interested in evolutionary theories, as well as any molecular explanation (if known).

I'd also curious as to what degree other mammals/animals show any handedness. Should it be a different question altogether, or should I edit this one?

You might as well ask a new question.

@LanceLafontaine yeah I'd be inclined to keep them separate :)

There is a lot of information at OMIM  - too much to summarize here - regarding the genetics of handedness and links to which hemisphere of the brain dominates (in an individual), to schizophrenia (slight association with non-right-handedness), and to hair whorl patterns on the scalp. References are provided at the above link. Basically, hand skill appears to be a complex multifactorial phenotype with a heterogeneous background.

OMIM (online mendelian inheritance in man) is a good example to explain how complicated heritability usually is.  Simple Mendelian traits, where smooth or wrinkly peas will have wrinkly offspring, allow us to segregate individuals with pure dominant / heterologous and pure recessive traits.  When we have done so the chance of inheriting the trait can be predicted precisely (i.e. 25/50/25%).
The number of simple mendelian traits which are observed in an individual are pretty doggone rare. Even things that are dominant like dark hair are usually more complex.  I'm of 100% japanese descent, but my son was born with blonde hair and it looks like it won't go darker than mousy brown - black hair is not really dominant, he will have a color between my wife's and mine.
I also need to make a distinction between mendelian traits, which are observed in the individual organsim as opposed to specific DNA variants like a single site mutation (A->T, C->T etc)  which are usually mendelian.
The rarity of mendelian inheritance is because there are so many checks and balances in our gene networks that no single gene is solely responsible for any function.  Medical research has discovered many single mutation (Mendelian) diseases, but they are very rare in practice.  There are single mutations that cause diabetes like systems (called MODY diabetes) for instance, but more than 99% of diabetes are not caused by these mutations.  A single mutation advantage is quickly adapted so that single mutations cannot nullify the advantage.
Common mutations that cause diseases or other disadvantages are likewise relatively quick to disappear through adaptations.
I once saw the old text bound copy of "Mendelian Inheritance in Man" It was not a small book, but it seemed to me that when I paged through it, when you look at traits like 'handedness'. there were only a few hundred simple mendelian traits identified.  Most of what we are is the result of the interplay of several or even many of our ~30,000 genes.
For an example of how this works, see this article about what happens to new fly genes.

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Are quaternary protein monomers unique to a particular protein complex?
I know that quaternary protein structures are formed exclusively via non-covalent bonds. My biochemistry professor discussed a viral capsid that is essentially one quaternary structure with 240 individual monomers of 4 kinds. I suspect that for this protein coat to be stable, the non-covalent bonds holding it together must be rather stable. He also mentioned that different monomers can join to form the functional protein complex from relatively far distances, like across an entire cell, which once again leads me to believe that both monomers must be interacting with each other very strongly.
My question is: Since a strong non-covalent interaction is required between (at least) two protein monomers to form the functional quaternary structure, can one particular protein be a monomer to an array of different quaternary complexes? Are there any examples of this?

I realize that this question isn't exactly "precise", and I might be using the wrong terminology. Feel free to edit or let me know how I can improve the question.

Are you limiting this to protein complexes which assemble irreversibly? Otherwise anything where two proteins attach temporarily to form an active enzyme would be an example. E.g. cyclin-dependent kinase (CDK) and the different cyclins.

I had originally asked this question with irreversability in mind, but just activation would make a great addition to the answer.

I would say that there are quite a few quaternary protein structures that are connected by intermolecular cystine bonds.

If I understand the question correctly, you're thinking something along the lines of modular tertiary domains, but in a quaternary sense?
For a reversible interaction, heterotrimeric G proteins spring to mind. Once activated by a G protein coupled receptor (GPCR), the alpha subunit and the beta-gamma complex dissociate from the receptor and from each other. They can both go on to affect signaling by binding to various effector proteins, depending on the particular pathway in which they are involved, and their activities can be mediated by other proteins (e.g. the alpha subunit GTPase regulated by GAP proteins).
I spoke to my Protein Engineering professor, and she also directed me to a few examples, although I'm not sure they're quite what you're looking for in the strictest sense.

Cyclin-dependent kinases, as @Armatus mentioned, bind to all sorts of different cyclins. (I get the sense that subunits found in multiple protein complexes will probably be more common in signal cascades. I don't have any real data on that, but it makes sense that a signal protein could interact with two or more protein complexes and even have slightly different functions in each.)
Alcohol dehydrogenase (ADH) is an example of a protein with different quaternary structures between species. According to my professor, it occurs as a homodimer in mammals, but as a tetramer with some slightly different residues in budding yeast. I can't say whether the sequence changes are what affect the oligomerization, although my prof also mentioned "oligomerization domains" that could mediate protein-protein interactions.
She also directed me toward a slightly more interesting example (in my opinion), though, again, it's also more along the lines of oligomerization. Small heat shock proteins (sHSPs) undergo something called "dynamic subunit exchange" and can take on a wide variety of oligomeric architectures. Binding is transient, but it's still kind of neat. There's a review here: http://www.sciencedirect.com/science/article/pii/S0968000411001903. Figure 3 shows different oligomeric architectures from the one monomer.

It seems that pretty much any protein that interacts with two or more separate protein complexes could be considered an answer. Neither I nor my professor have managed to come up with an example of an irreversible assembly of common subunits, but she is of the opinion that, in all the different possible protein structures, there is probably at least one example of everything, no matter how outlandish it seems.


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What controls the southern range of willows?
Many willows (Salix spp.) grow in northern states but do not grow in southern states, for example Salix viminalis.
What mechanisms control the southern range of temperate hardwoods such as willow? Is it disease? Temperature sensitivity of respiration? Water use efficiency?

The distribution of temperate hardwood forests, as well as deserts, tundras, savannahs, and other ecosystems, is determined primarily by average climate conditions, specifically average annual temperature and precipitation. You can see how biomes are related to climate in this figure, taken from Whittaker (1975):

Temperate forests tend to be between 2.5-17°C, and between 800-2500 mm precipation. These are not exact boundaries but reflect long-term climate conditions. As climate changes, so will the distribution of the biomes.
Temperature is important in many ways.  For example, most temperate trees go dormant during the winter. This requires metabolic preparation by the tree. If the weather turns cold too fast, then the trees may be be properly prepared. Alternatively, if the weather warms to quickly the trees may not be able to come out of dormancy properly. This technical report (Coder 2011) provides more detail.
The precise mechanism that restricts the distribution of any one species would require experimental determination. As it turns out, Populus trichocarpa (black cottonwood), plus other Populus and Salix (all in the family Salicaceae) are quickly becoming model organisms for study. This should shed more light on specific distribution limitations, such as changes in soil nutrients, light intensity, or other environmental parameters. There are now regular symposia held on these model organisms. You can read an introduction to one symposium here (Tognetti et al. 2011).
As a side note: One must be careful about the mapped distributions of popular trees like willows. Many species, including Salix viminalis, have been introduced far outside their native range, including through out the eastern United States, as shown by the map you linked to. The native distribution of the species is the Palearctic (Eurasia), shown here.
Literature Cited
Coder, K.D. 2011. Trees & cold temperatures. Environmental Tolerance Series WSFNR11-12, Warnell School of Forestry and Natural Resources, University of Georgia, USA.
Tognetti, R. et al. 2011. Fifth international poplar symposium: Poplars and willows: From research to multipurpose trees for a bio-based society.
Whittaker, R.H. 1975. Communities and Ecosystems. MacMillan Publishing, New York, USA.

little typo: 80-250 mm --> 800-2500 mm. +1 for this broad nice answer.

@Hav0k - Little typo, big difference. Thanks for catching it.


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What is this strange mantis-like coral reef dwelling creature?
On the first episode of BBC's Blue Planet II they visited a coral reef and showed some odd reef-dwelling creatures as part of their establishing shots, but did not name the creatures.
In particular creature that resembles a mantis:

I tried a Google reverse image search and it very 'helpfully' identified it as "Documentary film". So close, yet so far.

The first one seems to be a mantis shrimp. No clue about the other one.

@JAB I've decided that I might have better luck if I split this into two questions. If you make that comment into an answer first I'll make sure to accept it when I do the split.

The specimen is indeed a mantis shrimp (to be specific, a peacock mantis shrimp).

These predators have highly sophisticated vision and, depending on the species, either spearlike limbs or clubs that move so fast the water can't keep up, causing dangerous cavitational effects that can even break glass.


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multiple HIV infection in same T cell
I was wondering can multiple HIV virus infecting same T cell ?
Coz in flu virus they have SA to cleave of those sialic acid residue preventing re-infection of the same cell by other viruses to maximize the amount of cell get infected.
I was wondering is there any mechanism found in HIV virus like what found in flu virus to prevent re-infection of an already HIV-infected T cell.
(little bit more about HIV virus that is irrelevant to the question, coz i was told that there is some HIV possible to hide in our body, but then i don't understand what it is the meaning of this hiding? Q1:Is the "hiding" refer to the genome of HIV that integrated into T cell. some of these infected T cells circulating in the blood Q2: will some of them reside in lymph node? Q3: and what make these infected B cell proliferate so to keep these B cell with the hiv genome long existing? will the virus transform these T cells into self proliferating? but will that be like cancer cell uncontrollably proliferating or well controlled?)
Thank you everybody

HIV doesn't infect B-cell as far as I remember

Oops~ hahahah really thanks for reminding me of that.Omg so embarrassing. Thank you

Yes, HIV does attempt to prevent multiple infection of the same cell. Once a T cell or other cells are infected, HIV downregulates the CD4 receptor which it uses to gain entry. Because of this, there are less receptors so another HIV is less likely to infect that cell. Meanwhile, the infection itself upregulates CD4 receptors on other cells which means the downregulation is even more effective. There are other mechanisms but this is a major one.
Hiding means it is somewhere where we don't know where it is and it isn't that active. When HIV is active it is destructive but also the cell is aware it is there. The cell can then try to alert other cells that it is infected. If HIV isn't active but instead hiding, it can stay where it is without really being detected. Even the drugs we use usually only affect HIV whilst it is replicating. So again if it's in a cell that's long lasting and the HIV is not replicating then it is essentially hiding. Such a cell includes macrophages and memory cells when we are just talking about the immune system.
Will HIV reside in the lymph node? Well yes, this is an exciting place for it. There's loads of exposed CD4 receptors and lot's of it's favourite T cells about. An infected cell will transmit HIV to other cells when they are signalling to each other. Even worse is when a dendritic cell is infected. Instead of instructing the immune system how to detect HIV infected cells, it is infecting them.
HIV is an infection. As soon as the body detects it, it goes into overdrive trying to eradicate it. This means there are more cells for HIV to infect. More foreign material means the immune system is even further stimulated to make even more cells. However it doesn't want CD8 cells to proliferate too much nor too many HIV specific cells so driving too much proliferation is a bad idea. What HIV does do is make lots and lots of useless copies of itself. HIV particles that are so badly made they aren't functional. The body tries to fight these and makes more cells to combat these but there's no point because they aren't the problem. But this immune diversion and a larger target number of cells is exactly what HIV wants. Proliferation of HIV specific cells, particular CD8, is associated with delayed disease progression or control.
Usually the cancers caused by HIV are because of other viruses running unchecked. Kaposi's sarcoma or lymphomas for example.

Though at the same time, i have some questions coming up in my mind. The first one is i was wondering is that T cell the only cell get affected by HIV coz macrophages and dendritic cell are mentioned in the answer. mmmm...i wonder how can the HIV get into these non-T cell by skipping the part that they requires CD4 for entry or actually CD4 is also present in these cell besides T cell as well?? 2nd one is what makes HIV prefer to infect memory cell?

3rd one is about the upregulation of CD4 cell in other yet infected T cell, is there anything to do with the HIV itself, like the hiv bears some genes to selectively upregulate the CD4 receptor on other unifected T cell or it is the feedback system of the immune system while the HIV has no direct role in the upregulation of CD4?

The last question is that really bother me is that cant we activate those provirus and force them into actively proliferating form. Then, large dose of antiviral drug are introduced to the system to prevent the newly produced HIV from infecting those uninfected target cell as to completely eradicate the provirus in our cell. I was wondering is it possible.Oh before that, have the mechanism of those pro-HIV been found out yet?

OH this one is really the last one. I was wondering what is the route for HIV to get into macrophage and other non T cell cell, by recognizing CD4 receptor or other protein?

Make another question. There's so much to write to answer all those. Add a comment here linking me to them and I'll try to answer


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Why isn't Bubonic Plague as virulent as it once was?
Although I am admittedly not anywhere near an expert on any topic, I still have a hard time understanding how Black Death and Bubonic plague are one in the same. Since plague still exists, with news stories about it every once in a while, and especially in places like India, why doesn't it spread with anywhere near the rate it did during the Middle Ages?
Obviously global society in general is much more sanitary than it was then, people also tend not to live in close quarters with animals today as they did then, however in places like rural India and China this lifestyle still takes place and plague still exists, so why aren't there large out breaks of plague in these areas if it indeed is Black Death?
Is it possible that Black Death has been miscategorised due to various historical circumstances and scholarly errors?

To answer your first question, just search "plague" in Google News: "Just last month the Chinese government sealed off a city of more than 100,000 people, fearing the spread of a plague outbreak.", and even "Struggling Liberia creates 'plague villages' in Ebola epicentre". The way poor people deal with plague changed from the times they thought the miasma is to blame, to the point that it is a model for fighting other epidemics. Also, the antibiotics are only 70 years old: old enough to be patent free and easily manufactured. China and India are in fact top manufacturers for such drugs.

@simontemplar I think you have answered your own question. sanitary practices, quarantine techniques and improved diagnosis and fast communication of such events prevents their rapid spread.

The identification of the Black Death with plague is now fairly well-established - see this paper (open access) in which PCR and protein detection were used to detect the presence of Yersina pestis in human skeletons from plague-related mass graves across Europe.
Outbreaks of plague do occur in rural environments, see this WHO page for some details. The WHO plays a role in responding to these outbreaks, as long as they are notified by the relevant countries. Plague infections respond well to antibiotic treatment.
There has also been a recent outbreak in Madagascar. According to the epidemiologists we are still in the midst of the 3rd plague pandemic, which started in China in the mid 19th century.

Thank you for all of that. It's still unclear to me, though, how it managed to spread so incredibly fast during the time of Black Death, but subsequent outbreaks didn't spread as far and wide even in the Middle Age Europe, or rather that seems to be what I've inferred. I realise the population was much smaller, but even after it bounced back a lot, it still didn't seem to be as dangerous. Did people learn something or change something about their lives?

An addition to Alan's answer:
Some sort of selection for more resistant genotypes inevitably did take place and left distinct footprints in the human populations1.
Specifically, the paper linked above presents evidence that Toll-like receptors, which are immune system proteins that recognize molecular patterns of pathogens, likely adapted to better recognize the plague bacterium Yersinia pestis:

Reconstruction of evolutionary history of European populations has identified Toll-like receptor 1 (TLR1)/TLR6/TLR10 as a pattern recognition pathway shaped by convergent evolution by infections, among which plague is a likely cause...

Reference:

Laayouni, H., Oosting, M., Luisi, P., Ioana, M., Alonso, S., Ricaño-Ponce, I., ... & Netea, M. G. (2014). Convergent evolution in European and Rroma populations reveals pressure exerted by plague on Toll-like receptors. Proceedings of the National Academy of Sciences, 111(7), 2668-2673.


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What does rescue mean in the context of biological experiments?
I have come across the term 'rescue' in biological contexts a lot recently and despite reading multiple definitions online cannot seem to get my head around what the word means on its own, and what it means in biology generally.
The definition differs depending on the context... 'genetic rescue' is a a mitigation strategy, 'synthetic rescue' is a gene alteration that counteracts the deleterious effects of another gene alteration etc.
Could anybody please explain what this means simply and in a way that could apply to different contexts like, for example, virology.

"Rescue" in an experimental context means you're capable of undoing some experimental manipulation. It's considered evidence towards identifying a causal mechanism or verifying that your manipulation does what you think it did.
For example, let's say you think secretion of molecule ABC is key towards mounting an immune response to MouseKiller virus. You test this by creating a knockout mouse that lacks the enzyme that synthesizes ABC, let's called it Alphabet Synthase, and find out that all the mice die when exposed to MouseKiller virus.
However, maybe you got it wrong. Maybe ABC isn't the key, but actually Alphabet Synthase is involved in some other pathway independent of ABC. You do an experiment where you produce some ABC in the lab, inject it intravenously to your Alphabet Synthase-knockout mice, and find these mice no longer die when infected with MouseKiller. You can say that you've "rescued" the ability of the mice to survive MouseKiller, and now have better evidence that indeed ABC is the key factor.
Another example of a rescue experiment would be that you think specifically Alphabet Synthase in B-cells is important for defense against MouseKiller. It's not very easy to knock out Alphabet Synthase in B-cells specifically, but you can 1) knock out Alphabet Synthase entirely in some mice, and 2) introduce a new version of Alphabet Synthase specifically in B-cells (for example, using a Cre-dependent expression vector with a B-cell-specific promoter). Experiment (1) shows the knockout is susceptible to death from MouseKiller, experiment (2) shows you can rescue the immune defense if B-cells specifically express Alphabet Synthase.
The precise experimental manipulation described as a "rescue" is completely dependent on the research question being asked: you'll have to read specific papers to know what exactly they are doing as a "rescue".

I suggest that "rescue" is an informal term used in the place of "complementation" in a genetics context. For example, that wiki page has a sentence that reads:

Another exception is transvection, in which the heterozygous combination of two alleles with mutations in different parts of the gene complement each other to rescue a wild type phenotype.

I would suggest that the complementation interpretation means that rescue could be read as: "the restoration of a wild-type phenotype that is otherwise expected to be altered by some insult (genetic or otherwise)".
For example, ura3 yeast have a ura- phenotype such that they cannot grow without provided uracil. However, this growth defect can be complemented or rescued by a plasmid carrying a functional URA3 gene.
I imagine that the word could be used slightly differently in a variety of contexts as biology is a large field. In genetics at least, I would say that the term is used informally and we should not pretend that it has a very specific meaning.


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Could this Francobelgian comic book woman really have these 4 diseases at the same time?
I'm doing an archive binge of a paper comic "The Kiekeboes". One of the characters is an elderly woman currently at the doctor, and she says the has the following illnesses:

Erythema Exsudativum Multiforme;
Necrobiosis Lipoïdica;
Phlegmasia Alba Dolens;
and Metropathia Haemorrhagica.

now, I googled these, and these are apparently real diseases (which actually makes sense, since she said she found them in her medical dictionary), namely 3 skin diseases and 1 menstruation problem. However, I find it hard to believe an elderly woman could have 3 different skin diseases and a menstrual disorder at the same time, especially since she already stopped menstruating.
Is it possible for a patient to have all 4 of these illnesses at the same time? Or do the causes interfere with each other too much for that? I don't want to know how to cure it, I just wonder how much they're talking out of their anuses.

Image I just took with my camera:

Kiekeboe 21: the Piri-Piri Pills, Page 17, strip 30. Author: Merho. Publisher: J.Hoste NV (currently part of Standaard Uitgeverij). Picture taken by Nate Kerkhofs on 16 september 2014.
It is in Dutch, but the names of the illenesses are clearly readable (since they're Latin anyway).
The doctor asks "what are you here for, madame? a cold, reumathism, headache?" right before this. The woman answers "no, doctor, I'm struggling with ... and also ... not to mention ... and a really annoying .... The doctor then replies "but madame, where did you get all those illnesses?" the woman replies "in my medical encyclopaedia!".

I hope this question isn't too off-topic. I understand that Medical questions are somewhat iffy, but since this isn't about a personal situation, I assume it's on-topic?

This is fine for the site.  The disease process is definitely a part of the biology.  We're more concerned about people asking for personal treatment advice than anything.

Erythema multiforme (minor) can and does occur in a lot of people; while it is usually self-limited, it can recur, especially when the trigger is an unsuspected food.[1] How common is it? It is very common.
Necrobiosis Lipoidica is not uncommon in diabetics, less common but still found in non-diabetics. It can occur at any age, including the eighth decade. It also shows a sex predilection, being 3 times more common in women than in men.[2] How common is it? It is not rare.
Phlegmasia Alba and Cerulea Dolens[3] is serious and associated with deep vein thrombosis, which is an acute event. It is not uncommon, but it's not chronic. (More than 600,000 cases of venous thromboembolism are estimated to occur each year in the United States, all of which can lead to Phlegmasia Alba and Cerulea Dolens. How common is it? Luckily, not very. If the author is referring to garden-variety thrombophlebitis, though, that's a chronic problem, and not uncommon in the elderly. Thrombophlebitis is chronic and common enough.
I'm not going to address Metropathia Haemorrhagica, because, as you have noted, it's found in menstruating women.
Diseases generally don't really interfere with each other; some diseases can't co-exist (you can't have hyperthyroidism and hypothyroidism at the same time, for example, or have an active pituitary gland tumor and empty sella syndrome at the same time), but diseases don't interfere with each other exactly. Some diseases have common underlying foundations, so can occur co-morbidly, for example collagen vascular diseases can manifest with skin, joint, and lung findings, which might not be diagnosed as several manifestations of one disorder if it's not obvious. A better example might be diabetes, where similar underlying pathologies cause, say, heart disease, skin disease, eye-problems and kidney disease together.
Whatever, the likelihood of a little old lady having all four of your diseases are nil. The first three all the time (assuming not garden variety thrombophlebitis) - nil. Once, not impossible once, but not chronically. Of the first two - not far fetched. The first - common as dirt (comes and goes, though.)
I hope this helped.
[1] Erythema Multiforme on Medscape
[2] Necrobiosis Lipoidica on Medscape
[3] Phlegmasia Alba and Cerulea Dolens on Medscape

@anongoodnurse Insulting other users is not acceptable, and I expect that this won't happen again. @caseyr547 It is not your job to enforce any laws here, I'm removing the entire conversation, the tone was inappropriate.

@caseyr547 I don't care what you report to anyone, I don't see any malpractice here, but I'm neither a laywer nor a US citizen anyway. This doesn't belong in the comments here, but on meta.

@MadScientist - I did take it to meta.

All these are possible side effects of oral estrogen progesterone pills used in perimenopausal or postmenopausal in Hormonal Replacement Therapy(HRT) by a diabetic female.
Irregular bleeding and endometrial carcinoma are known adverse effects of HRT.
Hence, Metropathia Haemorrhagica is quite possible.
Any drug given is usually liable to produce signs of allergy and hypersensitivity, especially in women (more prone to immune disorders).So, the skin disorders, Erythema multiforme is quite possible, if the women suffers from diabetes mellitus type 2, Necrobiosis Lipoidica is quite possible and could ve worsen by Erythema multiforme.
HRT and venous thrombosis
This article from NCBI tells how HRT increase risk of deep venous thrombosis by 2 to 5 fold compared to those not taking.
So, Plegmasia Alba is quite possible.

So, the Answer is HRT in postmenopausal Diabetic female, quite common these days, especially countries trying to copy west.


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What is the difference between a predator and a parasite?
A human encountering a tiger or a malaria plasmodium is likely to suffer, and the tiger/plasmodium is likely to gain from the transaction. Not necessarily a good example, and I am aware that a successful parasite avoids prematurely killing its host, but I can't see any fundamental difference.
Of course it's like pornography: "we know it when we see it". But is there a formal, generally-accepted distinction?

An even better comparison might be between humans and plants: do humans parasitise apple tree when we eat its fruits?

Good question.
There is no fundamental difference between parasites and predators.
Ecological Interaction
In terms of ecological interaction, they are both defined as an interaction where one species benefits and the other suffers from the interaction.
Intuition parasite vs predator

In general predation is viewed as a big individual eating a smaller one while parasitism is when a small individual eats a bigger one. These general intuition however fails to consider a number of cases. Here some cases I can think of
Examples when intuition don't match the above picture
Generally considered as predation but does not fit the above picture-based definition:

social animals attacking in groups preys that are much larger than themselves - non-social animal attacking prey larger than themselves
herbivores browsing on large trees

Generally considered as parasitism but does not fit the above picture-based definition:

indirect effect of habitat modification that would rather be considered as parasitism.
Species that take advantage of parental care of another species by mimicking babies (but being larger)
Individuals of large species stealing the habitat built by a smaller species
Batesian mimicry (see this post; Thank you @WYSIWYG and @NL_Derek for the comments)

Population culture vs science literature
In the popular culture, some people call parasites only endoparasites. This concept is also misleading and not so much in accordance with the general literature in biology.

As we had discussed in another post, Batesian mimicry has also been considered a parasitic interaction.

Thanks Remi; it seems that there is a continuum parasite-predator and no real dividing line. @JordiZambrino's answer was also excellent (therefore +1 from me) but as kevbonham pointed out only tangentially relevant.

Parasitism – a parasite that lives on or in an host, obtaining food from the host and harming it.
Example: Ixodes ticks use white tailed deer as a host

Parasite is smaller and weaker than the host
Parasite may feed over the host from outside or inside
In parasite-host relationship a weaker organism is benefitted
Host specificity is more common
The host is most likely alive when nourished on

Predation – predators benefit as they feed on prey; predation affects numbers and behaviour of prey
Example: Coyotes are predators of white tailed deer

Predators are generally larger than their prey
There is progressive development of characters or evolution
In predator-prey relationship the stronger organism is benefitted
Prey specificity is not very common
Predator usually feeds on prey from the "outside"
The prey is usually dead when consumed

This is a great answer, but doesn't directly address the stated question (what's the distinction?). I think the living vs dead is probably the most consistent. I can't think of any predator/prey relationship where the prey stays alive for very long, nor any parasite that immediately kills its host.

It seems like the difference is that predators feed on most or all of their prey individual, whereas parasites feed on a fraction of the resources of their host.  This distinction explains a lot of the six distinctions given in the above answer.  e.g., predators are larger and therefore require a greater portion of energy of their prey; prey specificity is less common because a fraction of prey does not suffice; the prey cannot survive having most of its resources consumed.  Question:  What do you mean by "progressive development of characters or evolution"??

Previous answers to the question seem to originate from one misunderstanding.  Of course, the large-small distinction between predators and parasites is easily observed by anyone, like the fact that predators kill their prey while parasites only sap the strength of their hosts.
But parasites do not actually attack a host.  Parasites attack only a TINY component of the host. The parasite and that tiny component then develop what is fundamentally a predator-prey relationship.  Whether the host is significantly affected or not depends upon the role of the component in the host’s overall health, and the size of the infection or wound.  Exactly the same could be said about an attack by a predator on its prey.  The actual significance of the attack comes down to the size of the wound and the significance of the wounded body part to the health of the prey.
To sum this up in a few words, the methods and logic of a parasite are the same as those of a predator. Their size difference is not critical; not all parasites are small, and not all predators are large.  The size of the host or prey is not the critical issue, either.
I think the biggest PRACTICAL difference between predators and parasites are the methods used to defeat them. Weapons like spears and guns for predators; nutrition, soap and science for parasites.  Avoidance — aided by brainpower— is the best defense of all

A parasite may or may not kill the host. It's basic motive is to constantly derive nutrition from the host. More a sort of one time investment and as an interest you keep getting the nutrition.
Whereas a predator's motive is to kill the host to satisfy it's hunger. One kill and eat can be a taken as a case of consideration here.


text:
LCMS/MS versus Western Blot
I have a general question regarding which method would you recommend me to use if I would like to investigate the difference in the level of several proteins in tissue samples and compare different treatment groups. I could either do an LCMS/MS or a Western blot. Which one would you recommend and would you do both for validation? I am looking for time- and cost-effective techniques.
I'll appreciate any suggestions.
Thanks!

How would you prep the tissue for LCMS/MS? That read out would totally look like garbage. There are all sorts of tricks for western blot that you could get an accurate measure. Personally, I would do ELISA to quantitate how much protein you actually have.

Which quantification do you need, absolute,  relative, or semi? Usually semi-quantification would be enough.

Related post

Western blot, though is a commonly used technique and is relatively simple to do, has some issues:

Low throughput: it is difficult to analyse multiple proteins simultaneously
Limited cross comparability: since antibodies to different proteins can have different affinities, they cannot be compared with each other.
Low sensitivity
Not very quantitative

LCMS addresses all the above limitations of western blot. It is also possible to do targeted proteomics i.e. study just some few proteins instead of the entire proteome.
An LCMS system has a high initial setting up cost but a relatively lower run cost. However, the mass spectrometer has to be maintained and it is not an easy job; you basically need a facility and a dedicated technical staff.

Which one would you recommend and would you do both for validation?

Which technique to use depends on what you really want to see and what resources you have at hand. It is a commonly practised approach to do a western blot for re-validating a few selected genes identified from LCMS experiment, which is just to prove that the result can be obtained using another technique too.

Although quantitative methods using MS have been developed, MS is not inherently quantitative. Quantification with MS could be quite tricky. Therefore, it is not the first choice. But, if you do not know which protein levels change and want to find proteins the expression levels of which are different between your samples you are going to compare, MS is not bad idea. In this case, validation is necessary. In other words, MS is not used to validate WB results in general.
In your case, you know which proteins you want to see. Therefore, I would suggest WB. This is a more direct way. Validation of WB may not be necessary, but it is better to get some supportive data: the protein activities in lysates, mRNA levels, etc.

MS=Mass Spectrometry; the name itself implies quantification. When you say it is not so quantitative, what are you comparing it with?

Peptides are ionized to determine the mass and ionization efficiency is not predictable. It would depend on peptide sequences and probably environments surrounding peptides. I think the word spectrometry in MS is used because you can see spectrum of molecular mass.

Ionization and fragmentation techniques are quite standardized. All quantification techniques suffer from some kind of bias. Western blot also suffers from biases.

Western blotting and mass spec each have their pros and cons. If you're doing a targeted analysis of a particular protein and have antibodies available (especially commercially available antibodies) I would suggest doing a Western blot. This is a much older technique and people are likely more comfortable with it. In my opinion, it's also much more comforting being able to compare relative densities on a blot visually than looking at mass spec output.

@VanceAlbaugh The only advantage of western blot is that it is easier to do and most people are comfortable with it. As you said, it is certainly cost-efficient and easy when only a few proteins are to be studied. However, even in this case cross comparisons are difficult. Antibody-protein interactions for different pairs are not comparable. It can be much more biased than fragmentation/ionization bias in MS.

@ WYSIWYG ionization efficiencies for fragmented peptides also vary very much. I though this makes cross comparisons difficult as well.

@WYSIWYG Although ionization techniques are standardized, comparison of two samples would be difficult when MS is performed in the same way but separately. Even if solution eluted at the same time from LC, ionization efficiency seems to vary. To improve this, mixing both sample to analyze them in same solution is designed. I'll write it in the next comment.

To improve this, mixing both sample to analyze them in same solution is designed. This ways, everything is the same exactly except for from which sample the peptides derived from. To recognize peptides from which sample, samples has to be labeled. Stable isotope labeling metabolically results in several molecular mass shift (or depend on which isotope and how many atoms)mass shift). This makes comparison more reliable. There are other ways to label, but they seem less quantitative.

What I am saying is that, despite all the possible problems you that mention, western blot is much more unreliable than MS. In MS ionization efficiency may vary but there are ways to detect multiply charged species (it also depends on ionization method and IMO only ESI has a high likelihood of producing multiply charged species). In western there is no way to compare two antibodies unless you make a standard curve (which I don't think anyone does).

@WYSIWYG (which I don't think anyone does)>It is because they do not think it is necessary. Because different proteins have different activities. Comparison of the actual amounts between different proteins is less informative unless you are studying stoichemistry of components in some protein complexes. Even if cell lysates has protein complexes and you want to see one of the components, cells may not form the complexes by some regulations.

@WYSIWYG (In MS ionization efficiency may vary but there are ways to detect multiply charged species> Ok, then here is my question. Then why scientists have to desperately develop quantification methods, utilizing stable isotopes etc.

Western blot is an old technique. MS has been relatively recently developed for proteomics so a lot of advancement is still going on. Stable isotope labelling helps in differentiating samples  quantified in the same run (test vs treated). At least I know this is so for SILAC and ITRAQ. I said standard curve is necessary for WB because there is no way you can compare two different antibody labels from the same blot. This is turning into a huge discussion and perhaps we should discuss this in chat.

Thanks for your answers. So I have access to both techniques, for LCMS there is a trained technician that could sort out any problems arising from the procedure. It is not clear yet whether it would be better to use one or the other, or necessarily both. I will need to detect changes in targeted proteins but also it would be nice to see changes in other unknown proteins. So with LCMS I could achieve this, but would it be necessary to confirm it with Western blot? Thanks!

Many people use LCMS for comprehensive, exhaustive  proteome analyses then assess the results with some other ways. Especially WB is popular for this assessment. Various steps are involved in MS data process because coverage of peptides is not 100%, some proteins share the same peptides, and modification disturbs peptide identification. I would say MS is not straightforward. WYSIWYG may know the way using only MS. You could also ask people in the facility you are going to use if the ability of the MS there could achieve satisfactory results to publish only MS.

If you are going to do bioinformatic analyses using whole data, you do not need to assess all proteins. But you might want to pick up several to show the MS is working well.

@Mary It is good to confirm the results using another technique and I guess there is no other technique that is more popular/easy-to-do than westerns. MS is data intensive and doing replicates would be time consuming. You can do multiple replicates in WB. So the general idea is: do LCMS → identify important proteins → Do WB for them.

@243 I am not disagreeing with you. MS analysis has problems and new algorithms are being developed for better reliability. What I am saying is that WB does not necessarily address the issues that MS has. The only advantage is that it is easy to do (sometimes that also can be problematic if you don't have the antibodies).

@Mary If you found your answer then please accept it. In general if you find a post useful then you can upvote it. (Check the buttons on the top left side  of the posts)

Both LC/MS/MS and Western Blot methods can be applied to compare protein level changes in tissue samples across different treatment groups. Each method has pros and cons, as described below:
Pros:
•   LC/MS/MS
o   High throughput: Multiple proteins can be identified and quantified simultaneously. MS/MS data are used for identification, and the peak areas of extracted ion chromatograms (EICs) are used for quantitation.
o   Fast turnaround: A typical LC/MS/MS run takes about 2-3 hours, and multiple runs over fractionated complex samples can take 12-24 hours.
o   High sensitivity: Targeted methods such as SRM (selected reaction monitoring) and PRM (parallel reaction monitoring) are highly sensitive, with the detection limit as low as at the femtomole level.
o   High specificity and selectivity: The protein identification is based on the MS/MS sequence data of two or more peptides with a low false discovery rate. Further, it is highly specific and selective for the quantitation of the target protein using full MS/MS data of each target ion acquired at high resolution and high mass accuracy.
•   Western blot
o   Low cost: Initial setup for Western blot, including SDS-PAGE, blot transfer apparatus, and imager, is much less expensive compared to an LC/MS instrument.
o   Orthogonal validation: It is an orthogonal method to LC/MS/MS and can be used to validate LC/MS/MS results.
Cons:
•   LC/MS/MS
o   High cost: The LC/MS instruments are expensive, requiring significant funding/capital equipment budget (ranging from 0.5-1.0 million dollars) for purchase and setup.
o   High complexity: The instruments are highly complex and require expertise and dedicated staff for operation.
•   Western Blot
o   Low throughput: Each blot can analyze only one target protein.
o   Cross-reactivity:  Cross-reactivity happens when the antibody binds to nontarget proteins, leading to high background, non-specific binding, low sensitivity, and inaccurate quantitation.
Given the high cost of LC/MS instruments, not every lab can afford them. However, many mass spectrometry facilities provide the service for LC/MS/MS analysis at reasonable costs. In your case, to investigate the level changes for several proteins in tissue samples, the multiplexed targeted proteomics method using PRM can be applied. To improve the quantitation accuracy, an internal standard can be spiked in all the samples for normalization.  If needed, Western blot is an excellent method for validating the results obtained from LC/MS/MS analysis.

I wrote this post myself. Please keep my post here. If you have any questions, please let me know.

It's not entirely true that one blot per protein. It is certainly possible to multiplex antibodies (you do need to ensure no cross-reactivity though) or even do them sequentially. IR labeled antibodies with different colour spectra have been around for quite some time now for use with instruments like LiCor Odyssey.

That is a good point. Each target protein needs an antibody with high specificity. Thus, we do need multiple primary antibodies. Cross-reactivity is a major concern. When we perform IP/MS experiments, in addition to the target protein, we always observe many other proteins due to non-specific bindings, even after negative control subtraction.

The best way is to use FPLC if you know what kind of protein you're looking for.in case you don't know what are you looking for,then you can run a 2D-PAGE and after analyzing spots then use LC MS/MS to identify your proteins and then continue with FPLC ( for record FPLC is a method of HPLC or LC which is protein friendly and even you can use it to isolate and purify your chosen protein )


text:
Why are nitrogenous bases of DNA hydrophobic if they can hydrogen bond?
Why are nitrogenous bases of DNA hydrophobic if they can hydrogen bond?
Is it that they are only relatively hydrophobic?
This forum explains it but does not give an example of the structure.

This is better off at Chemistry.SE and I voted to close.

They are not hydrophobic.. They are quite water soluble. See this data sheet for adenine.

@AliceD This is about biological molecules, I see no reason why it would be off-topic here.

@MadScientist But this is about solubility, so these are physical properties of the molecule. This fits better into chemistry or physics.

@MadScientist - I don't see any clue to any biological compound in the Q. I know, implicitly I can autocomplete this question with amino acids etc etc, but I don't see it in the Q. Until placed in a Bio framework, I leave my close-vote where it is :) Plus, the link to a physics forum speaks for itself.

Definitely more of a chemistry question. Short version: In addition to hydrogen bonds between pairs of bases, interactions between stacked aromatic purine and pyrimidine rings of nucleotides stabilize DNA molecules.
https://en.wikipedia.org/wiki/Stacking_(chemistry)

@AliceD Nitrogenous base generally refers to the nucleobases in RNA and DNA, and those are certainly biological molecules. The question about hydrophobicity and hydrogen bonding also have biological implications.

@AliceD The question was asked in the biology section of physicsforums.com ;) I think this is on-topic here. Plus there are plenty of question on DNA and more that chemistry SE doesn't send our way.

The term "nitrogenous bases" was confusing; so I fixed it. This is a question on biochemistry and most biochemists would know the answer. I would not consider this off-topic. Note that questions should be pushed to chemistry SE only if they concern certain advanced concepts that are not generally covered in basic biochemistry.

These two concepts are not mutually exclusive. You have constructed a false dichotomy.  Both of these facts are true:

The electrons in the pi orbitals of the conjugated double bonds in the planar rings are hydrophobic and can "stack" on each other as shown in this drawing of a DNA helix where the bases are shown as planar rectangles:

The nitrogen and oxygen molecules (either in the rings, or as substituents on the rings) can participate in hydrogen bonds (H-bonds):

There are other examples of hydrophobicity and H-bonds co-existing.  For example on the interior of proteins.

I am sorry, I don't understand the answer. Why are both the facts true? I think that is what I want to understand more.

Hydrophobicity and and hydrophilicity aren't yes/no things, they're gradients.

@Whitecat Most detergents are also hydrophobic and hydrophilic at the same time.

I think the confusion here is that no, the DNA bases aren't in themselves completely hydrophobic, but in the region of the planar face of each base is a zone of hydrophobicity. In this way, base stacking becomes favorable where water molecules would otherwise attempt to order themselves to maximize hydrogen bonding with each other.

@Kendall Can you add that to the the answer?


text:
Is there some research paper which focus on the influence of using cancer cell as experimental materials on experimental result?
Cancer cell is unstable cell and high variation, but there are many experiment use cancer cell as experimental materials. I always wonder how much influence can using cancer cell as experimental materials exert over experimental result?
Is there any study about this? If any, please give me the study paper.
Thanks for any help.

Depends on what is the objective of the experiment. In some cases the cancer cells are decent models while they are poor for others. You need to specify what kind of experimental objectives you are interested in. You should also remember that no model is perfect. They are useful and good approximations for certain conditions and you need to know these conditions beforehand.

Sorry, I didn't make it clear. What interests me is evaluating existing result which have been published. Not the experiment design.

That is just too broad. We cannot evaluate all the published literature for problems in the experimental design. Do you mean to ask if there are studies that have done this kind of survey? Again there are many articles on this topic. Did you try a google search?

I have tried scholar. I didn't get satisfied answer, can you give some paper  that focus on this topic?

There are several articles on this. You may look at these for a start:

Masters, John RW. "Human cancer cell lines: fact and fantasy." Nature reviews Molecular cell biology 1.3 (2000): 233-236.
Masters, John R. “False Cell Lines: The Problem and a Solution.” Cytotechnology 39.2 (2002): 69–74.
Masters, John R. "HeLa cells 50 years on: the good, the bad and the ugly." Nature Reviews Cancer 2.4 (2002): 315-319.
Holliday, Deborah L., and Valerie Speirs. "Choosing the right cell line for breast cancer research." Breast Cancer Res 13.4 (2011): 215.
Lacroix, Marc. "Persistent use of “false” cell lines." International journal of cancer 122.1 (2008): 1-4.