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Comparison of humans and other primates in milk production amount
Do human females produce more milk (relatively to average child weight weight) than other primate females? Are human females more likely to feed several children through breastfeeding than other primates?

P.S. I am asking this, because it's what my antropologic hypothesis predicts: some women refused to nurse (and breastfeed) children born by them, so "nurses" - other women - fed those children. This, of course, would require those women to have extra (more than needed to feed their own children) amount of milk.

It seems certain. 1)There are twins fed by a single mother. 2)There were mothers who suckled a second child for payment. 3)The suckling period of an infant can be long and suckling of multiple babies can occur. But as the milk is adapted to the baby, the first one, if old enough, often stops, because the flavour changes. At least that’s what mothers say.

@Ludi, seems reasonable and p. 1. is what I already had in mind. However this is not scientific approach, of course. I'm pretty sure other species also can have twins.

I disagree with the close voter that this question has anything to do with personal health. I do think the question could be improved, however. The word "excessively" doesn't help you here, it doesn't seem to be what you are actually asking. What you are actually asking is "Is it typical for a primate mother to produce enough milk to feed more than her own offspring?" I think an edit like that would improve the reception of your question, and you can copy my wording if you'd like but I prefer not to make major edits to peoples' questions without their agreement.

Milk production (in all mammals, as far as I'm aware) is stimulated by suckling, and is limited by the health of the lactating individual, not the number of offspring produced. Provided they let you, you can milk a cow, goat, mouse, marmoset... I would speculate that wet-nurse behavior is more about the social behavior of a species than the maximum milk producing capacity.

@DanHall, I don't say it's limited by the number of offsprings produced. Won't you argue cows (especially on farms) have excessive milk? I'm rather asking if that's limit is higher in humans.

I'd say excess. The farmer certainly doesn't think the cows production is excessive

@DanHall, lol, excessive from the position of feeding it's own offsprings, of course, not the farmer.

I'd add to @BryanKrause 's suggestion. I think close and down voters may be reacting to your use of the word "excessively". It's a little confusing. I like Bryan's wording. You could also use "excess". "excess milk" sounds more neutral than "excessive milk".

The comparison to non-human primates and the behavioral question kind of threw me, but I think this is an X-Y problem. If you're asking:

Are humans capable of producing more milk than they need to feed their own offspring

The answer is yes
There is some data I don't think we'd be able to get anymore, but in Chapter 5 of Nutrition During Lactation, they break it down.

Several studies indicate that potential milk production in humans is considerably higher than the average intake by single infants. Kaucher and colleagues (1945) measured maximum milk output with intrusive and tedious mechanical methods to extract all the mother's milk and reported that production averaged almost 1,200 g/day at 6 to 10 days post partum. This level is much higher than the 500 to 700 g/day consumed by breastfed infants at the same age (Casey et al., 1986; Saint et al., 1984).

Kaucher's methods may not have been particularly good, because others showed limits more than twice that

Women who express surplus milk for a milk bank have been shown to produce as much as 3,000 g/day (Macy et al., 1930).

As my wife and many lactating mothers who use a breast pump will be able to confirm, this isn't a relic of the 30s and 40s. If you keep pumping, you keep getting milk.

In two separate studies, milk production increased by 15 to 40% when a breast pump was used to remove additional milk after feedings (Dewey and Lönnerdal, 1986; Neville and Oliva-Rasbach, 1987).

I'd add that this is how biology does almost everything involving regulating production of something, from small molecules to excreted fluids to tissues: use feedback to know when to increase or decrease production, rather than producing some specific magic amount automatically.

Thanks, this is useful info. Of course, it's not enough for say that women have more milk than primates, which should be true, if, of course, primates did not have such division of labor as humans. And as we know, they don't.

@rus9384 I don't know enough about non-human primates to answer authoritatively. Maybe Bryan does? But I'm not sure we can make a global statement about the social structure of all primates. As far as I remember from school, there's a lot of diversity in social structure across that order.

@DanHall, there is, but division of labor is proposed to be the effect of great level of intelligence. Lower than that of human, yet higher than what any existing primate has.

Well, sure women who produce for a milk bank produce more.  Women who produce less don't donate milk.  Quantifying outliers says nothing about how the data is distributed in the whole population.  If it takes a pump to get the excess milk out, then that milk shouldn't be counted as being available in communities which lack access to that technology.

@swbarnes2 you make a good point

@DanHall At least some non-human primates will foster nurse under certain conditions, so although I'd be very hesitant to make any global claims (especially, as you say, because social structure in different primate species varies dramatically), I'd feel quite confident in saying this is not a human-specific trait within primates. I have no idea if other primates would ever foster nurse in the presence of the natural mother, however.

@rus9384 I'm a bit skeptical that your statement "division of labor is proposed to be the effect of great level of intelligence" is anything besides just that: a proposal. To the contrary, my albeit limited anthropological understanding is that besides for possible male/female division of labor, division of labor among human groups is only understood as a recent cultural phenomenon

@BryanKrause, there always were politicians, warriors, craftsmen etc. as history knows it. So I don't understand that division of labor is somewhat new.

@rus9384 Citation needed if you really want to go the evolutionary psychology route, which based on your collection of questions and comments on SE seems like what you want to do. Evolutionary psychology is making pre-history arguments, not history ones. This is one of the major criticisms of evolutionary psychology and yet another reason I suggest you tread lightly: be wary of the just-so story.

@BryanKrause, as I say, division of labor based on abilities is good for society in all cases. Also, psychologically people already have different interests, which is seen as adaptation by me, while having particular interest in videogames (example) is a byproduct of that adaptation. In either way, I'm seeking arguments for the hypothesis.

Just because you think division of labor is good for society does not mean society has always had division of labor. Eating vegetables is good for me. Want to take a guess how many vegetables I've eaten so far today? You are not using good logic.

The vast majority of human existence is pre-historical.  It's not at all clear to me that there could be "craftpeople' in a hunter-gatherer group, in the sense of people doing nothing but making tools in exchange for everything else they needed.

@swbarnes2, if clothes are tools I see no problem. Except producing tools there are many other deeds like cooking food, cutting meat, etc.

@BryanKrause, division of labor started somewhen and it started prehistorically. Another question is when and the question that can give a clue is "What were the premises for it?". I can see no other premises than see that people developed different skills (varying more in their skills than most other animals) and used them accordingly.

This, of course, would require those women to have excessive (more
  than needed to feed their own children) amount of milk.

No it doesn't.  A wet nurse might be a woman whose infant died, or she might switch her child to all solid food or a milk substitute.

You seem to misunderstand what I mean by nurse. Nurse for me in hunter-gatherer society is somewhat like nurse in ants society, who deliberately cares about children (who are not necessarily her own).

If you are so sure that hunter-gathers and ants work the same way, why are you bothering to ask a question here?

Not the same, but similar. Also, one should not answer here something that is not the part of the question (it is just an explanation for motive) and that's not a part of biology. I don't even see any negative connection between my thoughts (regarding hunter-gatherer society) and the motive to ask.

Alloparenting is what's common in hunter-gatherers, the opposite of the specialization you seem to think is obviously innate and superior.

According to my hypothesis minority (15% or higher) of women did not care about their and others' offsprings in their early childhood preferring typically "mens' work".

I don't think you understand how testing scientific hypotheses works...You don't make a hypothesis and then try to fit every other piece of data to it. You create a hypothesis that you can test somehow. Only once you have an overwhelming amount of support for a theory can you use it to make predictions about novel things.


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What exactly happens during the crossover
My knowledge of biology is rather limited, but I think I have a grasp of some basic concepts. For me (as a person close to math) a chromosome is a sequence of elements from the set {A,C,T,G} of some (arbitrary?) length. In humans, there are 23 pairs of chromosomes, and during meiosis each of these pairs produces a singe "mixed" chromosome.
Q1 In each pair, do chromosomes have to be of the same length? If yes, does it mean that this length is the same for all humans? Do chromosomes in different pairs have different lenghts?
Now, we have two chromosomes from the first pair and they get mixed during the meiosis.
Q2 In which exactly place do they get mixed?

if chromosomes are same length, I expect they exchange pieces of the same length only as well; however, if they are of different length, do they exchange pieces of different lengths? e.g. suppose first chromosome in a pair has length 100, second is 105 (I do understand that in reality the numbers are much bigger). Can that happen that the new chromosome is created using the first 10 elements of the first, and the last 80 of the second (so the first 10 of the first replace the first 25 of the second), with the total length of 90?
how many exchanges may happen in a single meiosis, namely can that happen that chromosomes exchange several separated pieces from the middle?

I guess, that this process may not be understood completely yet, so I'm rather looking for an answer either "No, it can't happen at all, we know that for sure", or "this we don't know yet, perhaps it may happen".  Thanks.

Q1 In each pair, do chromosomes have to be of the same length?

Yes, approximatively.

If yes, does it mean that this length is the same for all humans?

Yes, approximatively.

Do chromosomes in different pairs have different lenghts?

Yes. E.g., in humans, chromosome 1 is 294 millions nucleotides long while the chromosome 22 is only 50 millions nucleotide long.

Q2 In which exactly place do they get mixed?

These crossover can appear pretty much anywhere. The probability of a crossover to happen at a given locus (locus=location on a chromosome) is not a constant throughout the chromosome though. In any case, the crossover always (almost always) happen at the same locus for each pair of the chromosome. In other words, if ~3 millions nucleotides goes from the paternally inherited to the maternally inherited chromosome, then ~3 millions nucleotides goes from the maternally inherited to the paternally inherited chromosome.

A good answer until the last paragraph. "the rate of crossover is limited to exactly 1 per chromosome" is wrong: the number per chromosome averages the same as the length in Morgans of the chromosome (higher in females), so more for chr. 1 than chr. 22.  "the crossover happens at the location at which spindle attach during meiosis" is wrong: spindle attaches to the centromere, not the crossing-over chiasma.

Yes, you're right. Thank you. I deleted this last paragraph.... but then I don't fully answer the question anymore...

Thanks for the answer, pretty much comprehensive. The last paragraph is confusing though: you're saying that the crossover can happen at any location of the sequence (with non-uniform probability, fine), but "in other words" you're saying about the length of the exchanged sequences - those two facts are important, but to me they are quite different. Could you elaborate? Also, rephrasing the last part of my question was: during a single meiosis, can crossover happen at two separate locuses?

@Ilya, the process can be thought of as having the two chromosomes laid out parallel to one another and aligned, at a random locus (same in both) both are cut and the loose ends are reattached to the other chromosome.  Hence the pieces exchanged are (approximately) the same size.  And yes, multiple crossovers can occur on a chromosome in one meiosis.  The longest chr., Chr. #1, averages 4 and a quarter crossovers in a human female meiosis (males average 2.9 crossovers on Chr. #1).

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Do beneficial viruses exist? If so, what examples are there?
Typically, people call viruses some kind of organic compounds that cannot reproduce autonomously and which lower the fitness of their hosts. Even the word "virus" means "venom" in Latin.
But from the perspective of natural selection, one would expect those organic compounds that cannot reproduce autonomously, but which would increase the fitness of their hosts, to be more widespread. One can see an analogy with bacteria: people are more aware of harmful bacteria and even such words as "microbe" are perceived as somewhat harmful (among non-biologists for sure). But we know that an animal body contains many more useful bacteria than harmful ones, and animals have their own microflora, which are necessary for survival.
The same must be true for viruses: those viruses which were useful (or at least unharmful) to their hosts would be passed more easily to other organisms since their hosts would have a selective advantage.
So, do such beneficial for their direct hosts viruses exist? If so, what are they called? What are the examples?

Technically, since we do not know if a virus is alive or not, we cannot say it is "good"; akin to not being able to say a rock has good behavior.

@Phil, the question is not about the morality (and I even do not make such a distinction), and this is not a Phi.SE. Under "good" I mean its positive value for its possessor. Just like the water is good for you when you are thirsty.

Someone's been watching Red Dwarf :P

Are you only looking for naturally occurring viruses in your question?  We've engineered a few viruses (from existing viruses) which can overcome certain diseases.

@ReginaldBlue, that's also is interesting topic, would be interesting to read about that.

@russ9384: Well, then do not use the word "good" and keep the focus on fitness as you mentioned or other word like "survival probability" and "probability of passing on its genes"- terms that are objective and focus on things in terms of biology. One would think you are making this a "Phi.SE" discussion, when you throw in "'Phi.SE' terms" into a molecular biology discussion. This is a minor point that contributes littles to your goal. I think we can now end this.

@Phil, I couldn't predict that one would think of the word "good" as only in moral terms. I thought it's common to use the word "good" interchangeable with "useful". Because it's really common in my place to do it. But "useful" would be misleading as then bacteriophages would be useful.

@rus9384 - The word "good" has a variety of meanings. In general, readers will know that many words have multiple meanings. Choosing the intended meaning is often easy, as in this case. Nevertheless, you could substitute the word "beneficial" if you're looking for something more precise.

One of the theories of how viruses came to be in the first place is that they started as symbiotic organisms - perhaps in a similar way that mitochondria or chloroplasts are thought to be. Over time, they lost most of their machinery until possibly only the barest genetic coding remained, and either simply turned parasitic, or left the cell's environment and moved into other cells that weren't quite as welcoming (note how most human plagues are caused by viruses that were transmitted from other animals - the same virus that caused mild symptoms in e.g. a cow would kill a human).

I have gone ahead and made the beneficial edit discussed. We really cannot have questions imputing moral qualities to viruses when a functional descriptive adjective will do. Sloppy writing encourages sloppy thinking.

Even reworded I feel there's still a certain amount of ambiguity to this question.  Contracting Chicken Pox is "beneficial" if you consider the benefit of the immunity you gain.  Regular contact with Influenza is said to benefit the overall strength of the immune system as well, though tbh, I'm not sure if that's a myth or not. I see these types of benefits as analogous to the way lifting weights creates a short detriment but a long term benefit.  I'm not posting this as an answer because I know practically nothing about the subject - more just thinking out loud and wondering here...

@billynoah, I believe the word "good" itself created no much more ambiguity. In either way adding "for their direct hosts" after "beneficial" made it less ambiguous, right?

yes, it's less ambiguous.  do my examples above qualify as "beneficial" according to your intent?

@billynoah, regular pain reduces the sensitivity to pain. I can't say it's really beneficial. The mechanism is beneficial, but that's mechanism, not the disease (in your example) itself.

Do they exist? Yes
What are they called? Marilyn Roossinck calls them viral mutualistic symbiotes. She has an excellent review here.
What are some examples?
My personal favorite is GB-Virus C, or Hepatitis G, which appears to slow the progression of HIV using a number of different mechanisms:

Box 1. Summary of the effects of GBV-C infection in HIV-positive individuals

GBV-C infection downregulates HIV entry co-receptors CCR5 and CXCR4, and increases secretion of their ligands RANTES, MIP-1α, MIP-1β and SDF-1.
In vitro GBV-C NS5A and E2 proteins inhibit X4- and R5-tropic HIV replication, and NS5A protein downregulates CD4 and CXCR4 gene expression.
HIV-infected individuals positive for GBV-C E2 antibodies have survival benefit over HIV-infected individuals with neither GBV-C viremia nor E2 antibodies; in vitro GBV-C E2 antibodies immunoprecipitate HIV particles and inhibit X4- and R5-tropic HIV replication.
GBV-C induces activation of interferon-related genes and pDCs.
GBV-C promotes Th1 polarization and the NS5A protein contributes to this effect.
GBV-C infection reduces surface expression of activation markers on T lymphocytes, suggesting its role in T cell activation signaling pathways.
GBV-C protects the T cell from Fas-mediated apoptosis and as a result of its effect on immune activation may also play a role in protecting lymphocytes from activation-induced cell death.
GBV-C viremia reduces IL-2-mediated T cell proliferation suggesting a significant interaction between GBV-C, IL-2 and IL-2 signaling pathways.

Endogenous retroviruses
As @mbrig recalls in the comments, there are a number of retroviruses that have inserted themselves into the germ line. Those are called endogenous retroviruses, and they interact with the host genome in a number of ways. Some are even translated:

Proteins produced from ERV env genes have also been demonstrated to function as restriction factors against exogenous retroviral infection

Interesting answer. For future reference, it is not ideal to post text as images: it increase page loading time, prevents searching and presents various accessibility problems.

Oh, wow. Now it is interesting to know whether my hypothesis that these viral mutualistic symbiotes are integral part of almost any life form, like how micrpflora is such for animals. And hypothesis there are much more viral mutualistic symbiotes than viruses (which are causing diseases). But this is not within the scope of this question of course and has not been yet investigated, I believe.

@canadianer ok :) i typically post images of figures, and pulled a box instead. You're right this is better as quoted text. Thank you for making the edit.

Though I can't name any off my head, I have fuzzy memories of reading that a number of retroviruses have become permanent (and beneficial/essential?) parts of some species genomes.

@mbrig they're called endogenous retroviruses. They exist in the germ line. Some are beneficial, some are not.

@Mbrig I went ahead and added an example to the answer :)

These retroviruses (or by now also retrotransposons) are so ancient, that by now we have a couple of 'human' (and fly and ...) genes that probably evolved from them. One crazy example is Arc, which is important for brain developement and seems to have a very uncommon mechanism

@Nicolai I think that might have even been the one I read about, thanks! Amazing that a virus ends up not just harmlessly incorporated, but actually useful/needed :)

Endogenius retroviruses part apply perfectly for analogy with microflora.

@rus9384 well, they are germ line viruses (I"m not sure there is consensus on the distinction between an endogenous retrovirus and a retrotransposon), so I don't know if I'd agree that they are perfectly analogous to microflora. The gut virome and skin virome might, but much of that is comprised by phage viruses, so that's not perfect either.

Transposons cannot be passed to other individuals (except offsprings), right? I thought a virus is a virus, because it can be passed.

Another good virus would be a Bacteriophage, a virus that infects and kills illness-causing bacteria.  From Wiki:

A bacteriophage also known informally as a phage, is a virus that infects and replicates within Bacteria and Archaea. The term was derived from "bacteria" and the Greek φαγεῖν (phagein), "to devour". Bacteriophages are composed of proteins that encapsulate a DNA or RNA genome, and may have relatively simple or elaborate structures.
They have been used for over 90 years as an alternative to antibiotics in the former Soviet Union and Central Europe as well as in France. They are seen as a possible therapy against multi-drug-resistant strains of many bacteria.

Intentionally using Bacteriophages medicinally is called phage therapy.

I'm aware of them, but it's not good for its possessor, as its direct possessor is that bacterium itself.

A bacteriophage is a virus that infects (not "eats") bacteria. That also doesn't mean they're good for the bacterial host. For instance, V. cholera does not produce the toxin that causes the symptoms of cholera unless it has been infected by the CTXφ bacteriophage. Along with its viral DNA, it also inserts the cholera toxin gene, turning the bacterial host (V. cholera) deadly for its own host (the unfortunate person who contracted the disease). This could arguably be considered "good" for the virus's host, since the definition of "good" seems pretty arbitrary in this context.

Phage therapy is largely ineffective given that not only can it increase the pathogenicity of bacteria (as @kadu points out) and can aid in spreading resistance factors (R plasmids), but because it triggers an extremely strong immune response against the otherwise harmless phage virions.

I would say that if any "good" viruses exist, they are already within us. Retrotransposons are genetic elements in our DNA that were likely ancient viruses and they move around from time to time either by excising themselves and moving somewhere else or by making a copy and inserting it somewhere else in the genome. Even though we are born with them, their activity is similar to modern viruses. When retrotransposons insert themselves in a new place they can cause disease, but the variation they cause likely brought us some beneficial advantage at some point because we have so many of them and they stuck around this long.

Interesting point. I'm just thinking about how plausible would it be to get increased intelligence, for example, from having sex with someone (sounds hilarious, I know), such kind of sexually transmitted advantage.

@rus9384 I don't believe the effects would be immediate, I'm not sure any kind of gene therapy can "increase the intelligence" of an already fully developed brain.

@JamesTrotter, some viruses are known to suppress intellectual functions. Why could they do the opposite?

@rus9384 because it's easier to switch a light off than it is to manufacture and install a circuit, bulb & switch and then switch it on.

@JamesTrotter, better example then could be metabolism... Any person with slow metabolism in developed society (who is either overweight or need to be on diet or go to gym regularly just not to be overweight) would like to get a virus of accelerated metabolism.

@rus9384 Well, now you run into another complex problem - there's no such thing  as "good" or "bad" without context. The same virus that would "cure" your obesity would kill you if you were poor (not to mention that a lot of viruses and bacteria already do that - a serious illness can make you lose quite a bit of weight).

@Luaan, would those people who are skinny even if they eat much, die if they would eat less? I'm pretty sure the mechanisms of those illnesses are different.

@rus9384 There's probably lots of variants. Which comes back to the original intent - context changes everything. I'm pretty sure it's incredibly unlikely for a natural virus to be 100% beneficial - remember, all they can do is make your cells produce proteins. Maybe they could make a diabetic's cells produce insulin in just the right amount - but at the same time being harmless to a non-diabetic? That seems to be stretching the probabilities way too much (unless you look at a population after everyone else was killed off :P). Of course, we might engineer such viruses, possibly.

@Luaan "all they can do is make your cells produce proteins" ... those proteins can do an awful lot, and transcription, translation, processing, distribution, activity, and turnover are all subject to co-evolving regulation.

We have engineered a few good viruses to treat certain diseases
Per my comment and response:
The most current example (at this time and based on my recollection) is the virus we have engineered to treat a certain type of macro degenerative eye condition:
Scientists Have Reversed Age-Related Blindness by Deliberately Infecting Eyes With a Virus
There are a few other cases out there, and, as always, xkcd is there to help:

Cowpox and smallpox viruses are structurally similar, and catching one confers immunity to both by immune system response, but one was a deadly disease and the other almost harmless. Once this was discovered, the days of smallpox were numbered. We had the means and the motivation to stamp it out.
On my last check a few years ago, we are deliberately keeping cowpox alive to ensure that we can kill smallpox should it ever come back.
The virus that ended a plague is a good virus.

So, do such beneficial for their direct hosts viruses exist? If so,
what are they called? What are the examples?

Bacterial viruses, termed bacteriophages or simply phages are normally killers of bacteria and thus occasionally useful for humans (e.g. phage therapy) but not beneficial for their hosts. However, some phages, called temperate phages, have a lysogenic life cycle, where the viral genome can become integrated into the bacterial chromosome and they replicate with the bacteria (at least temporarily) as a prophage. These prophages have a shared evolutionary fate with the bacteria and can be directly beneficial by carrying bacterial fitness factors such as virulence factors or antibiotic resistance genes. You might be interested to read more in our short review.

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What to call a trait that has current utility but unclear evolutionary origin?
I'm looking for a commonly used term to describe a trait that has clear current utility but an evolutionary origin that is uncertain and that we do not necessarily wish to emphasize in our description (e.g. to avoid unnecessary speculation):

Adaptation emphasizes an origin driven by natural selection.
Exaptation emphasizes an origin driven by co-option.
"Aptation" fits the bill, but it seems cryptic and rarely used.

Thank you for your help.

Can you give an example of such a trait? It's not clear to me what you are describing?

I have rephrased the question to make it more precise. A vast number of traits have some function but an uncertain evolutionary history (that we often do not wish to emphasize).

@kmm, maybe woman breasts? It's still unclear why are they prominent. But that's only if "being sexually succesful" counts as current utility.

Intelligent design.

As you point out, people have sampled other terms like "aptation" but these terms are not commonly used.
In order to not imply anything about the evolutionary history, since it is unknown, I think it makes most sense to refer to these simply as traits or phenotypes (or genotype for that matter, depending on the approach you are taking). If you wish to emphasize that these traits are beneficial to the organism, it is sufficient to call them beneficial traits or use other adjectives like useful, positive, etc.


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Difference between reciprocal inhibition and regular muscle movement?
I was looking into a condition I have, anterior pelvic tilt, quite a bit. I ran into a website describing part of the issue as reciprocal inhibition. This was my confusion:
Reciprocal inhibition, defined by just about everyone, is the relaxation of muscles antagonistic to muscles currently contracting, and vice versa. How is this different from regular muscular flex? When we flex a muscle, don't the antagonistic muscles relax to compensate, same as in reciprocal inhibition? Thanks.

What is the difference between reciprocal inhibition and regular muscle movement?

Reciprocal inhibition is part of regular muscle movement. It is controlled by the stretch reflex controlled by the muscle spindle. It's an important part of a functioning muscle and spinal cord, and not pathologic at all. However, this same reflex, in an excessively tight muscle on one end of a joint, would cause an excessively loose muscle on another end of a joint.
Here is an image showing this reflex, from Brust Practice of Neural Science, Chapter 6.

I can't give you any medical advice on this site, so I can't put that in context, but I think that answers your biology question.

Ok, thanks! I just had the thought that the process is in fact pathologic because it was described in correlation with anterior pelvic tilt. Thanks for clearing it up.

@EthanD. Glad to help! If this cleared up your question, you should mark it as the answer by clicking on the gray checkmark. See someone answers


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Flow cytometric counting of apoptotic adhering cells
I have been trying to measure rates of apoptosis in epithelial cells by marking apoptotic cells with annexin V conjugated with phycoerythrin (PE) and sorting using flow cytometry. Unfortunately, the cells are adherent, and have been cultured in a collagen coated plate. Thus, to suspend them for flow cytometry, I have been using a trypsin treatment. Unfortunately, my results have been quite poor. I believe that there are several problems. First, the trypsin treatment is likely to induce the disruption of integral membrane proteins, potentially causing the externalization of phosphatidylserine (PS) (to which the annexin binds) on the outer plasma membrane of cells. Since the cells were incubated with the annexin V following suspension with trypsin, this could have led to a substantial increase in apparent rates of apoptosis, and masked real differences between rates of apoptosis in WT and KO cells. Furthermore, I was informed that epithelial cells, in order to maintain their structural integrity, have a relatively large ratio of cytoplasm to nucleus, and a prominent cytoskeleton resulting in increased background noise (greenish in color). In order to solve these problems I was considering several alternatives, such as changing the fluorescent marker that annexin V is conjugated with to reduce autofluorescent interference, using a different marker of apoptosis (in the place of annexin V), or, if I were to continue using annexin V, I think that incubating with annexin V followed by washing off of excess annexin, followed only then by trypsin treatment could potentially solve one of my various problems (or then again, it might not). Please help me find a suitable protocol for flow cytometric analysis of apoptotic markers in adherent epithelial cells. Additionally, if you know of any studies which utilize such methods, please direct me to them. Thanks in advance.

Consider trypsin is a serine protease and your annexin is a protein.

Here some resources,

Cell harvesting effects on Annexin V staining.
Protocol for apoptotic analysis using Annexin V.
Quite a long discussion about this issue.
Another protocol.

Cheers,
Pedro


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Do mosquitos vary in toxicity?
I already had a question about dealing with mosquitos: Really virulent mosquitos - dealing with them and their bites
But this question is about whether they really do vary in virulence and toxicity. A few people in the other question suggested I am naturally a target and react badly to bites. However:

I haven't in other locations had such big reactions, I get nasty lumps but not swellings several centimetres across
My wife gets even worse reactions, e.g. her whole calf went red and swollen from a single bite - and I currently can't clench my fist because one bite made it swell up!
several other people, including a gardener and a tree surgeon who both deal with such things all the time, have commented they react particularly badly when working in our garden

Interestingly this summer I am reacting differently than this time last year - bigger swellings but less itchy and no weeping wounds. This may be due to the difference between midges and mosquitos.
So - are there a large number of sub-species prevalent in the UK (NE UK specifically) or can a given population become more nasty for some reason?

I am glad i had stings every year aged 1-20, i dont have immunity allergy, stings are always half a lentil and itchy. I recall them being more noticeable when i was young. Different size mozzies may inject different anaesthetics and anticoagulants, but unless you get mozzy diseases in N UK, they orent toxic... you are allergic. I can get 30 stings, not very noticeable. Mozzyland people average 1 2 sting per day.

You should have a serious read about mozzy allergies. They may contain a few bacteria bug no pathogens in the uk. Someone please write bacterial content of harmless mozzies.

I am from Gardening Stackexchange...the thing about mosquitoes that makes them 'harmful' is not the toxicity of the stuff they have to shoot into you before they can take a sample of your blood.  It is not toxic, slightly causes histamines on a different basis for different people.  When they take a drink of your blood (vampire speak) they are taking lots of information from your body and then when they bite another animal they deposit a bit of you into another animal body.  It is the bacteria and virus from other blood systems such as malaria, West Nile Virus that is dangerous.

Bodies don't 'build up' immunity to mosquitoes.  I wish.  I would be protected from mosquito bites.  Not stings...Repellent is disputable, I use 'Skin so Soft' by Avon as do all the wilderness guides and back country people.  Supposedly, I've read, mosquitoes leave a type of pheromone behind after drinking your blood telling other mosquitoes to stay away.  I've not noticed this phenomenon and I've more than most have sat and slept and hiked in clouds of vicious mosquitoes.  Mosquitoes that bite through thick jeans!  I always have mosquito netting.  Two pks. sewed together so two can cuddle.

By the way, whenever you get bit by something that causes major reactions please take Benadryl.  Immediately.  This is an antihistamine that is safe and very effective.  If anything, grins, people who get lots of bites will become MORE sensitive not LESS sensitive unless they take Benadryl.  You want to stop the production of histamines.  They make you far more sensitive and vulnerable for the next bites.  Her calf swelling up like that for a mosquito bite is not something to dismiss.  There aren't virulent mosquitoes, just virulent JUICES from other bodies introduced into yours.

This is more a biological (immunology, serology) question, than one about gardening. It is possible that mosquitoes vary in 'toxicity', however I think the greatest part of the reaction is caused by yourself (no offense, I am prone to allergic reactions to mosquito bites too). So the chemicals that enter your body can vary per mosquito species (or even individual), which can trigger a milder or worst reaction. Just like different pathogens (bacteria, viruses) can also trigger different reactions (influenza can be innocent or deadly). But it is more likely that your own immunological 'state' is causing a worst reaction. For instance if you also have hay fever, levels of immunological molecules (etc. cytokines, chemokines) are already high in your blood and cause a larger or more intense reaction than in periods when less of these molecules are present in your blood.

Mosquito bites absolutely vary in toxicity/danger.
For a start there are multiple different types of mosquito, only some of which carry diseases like Maleria, Dengue, Zika, West Nile, Encphalitis (and different mosquitos carry different virii)   Males, of-course, are non-toxic as they do not bite.
In some ways, Mosquitos are like the Flu - they mutate, and different strains have different characteristics - including when they bite - and most importantly the properties of the anticoagulant (that is what causes bites to itch)

Some references for a difference in anticoagulant properties would be nice.


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Do the centrioles in the centrosome differ in their angle to one another?
The centrioles in the centrosome are often shown at an orthogonal angle, does this arrangement differ between samples, as in, does the daughter centriole show up in different sides of the mother centriole, or on the distal end rather than the proximal end?


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What is the purpose of the “No DNA control”?
What is the purpose of the “No DNA control”?
Recently I have done a forensic DNA lab experiment and I still cannot understand the use of “No DNA control”

No DNA controls (or water control, also "no sample control") are important to rule out false positives results due to contamination.
If your reagents/pipettes/equipment you use is clean, this reaction (I suppose in PCR) gives you no band. If you have a contamination, this will show up where no band should be and shows that you have a problem. In this case you cannot trust the other results as well.

Isn't it to know the protein level backgrounds in the given sample?

This is an instance of the general concept of a negative control -- a very important part of every experiment


text:
Order of samples for RNA extraction
I want to extract RNA from various tissue samples, liver, gut etc, in different treatment groups. Due to the large amount of samples I will extract in sets. I am wondering, in reducing the potential for contamination whether it will be better to extract by tissue type or by treatment?

What you do not want to do is prep all your control samples on one day, and all your treated samples on another day, because you will not be able to separate differences caused by treatment from differences caused by batch effect.  I'd worry more about that than from cross contamination.  Since you probably aren't comparing the different tissues to each other, batch effect between tissues won't be much of a problem.  So do all your spleen samples, treated and untreated, on one day, all your kidney samples the next, etc.


text:
Is it ok to keep primers at 4 degrees?
I reconstitute my primers in nuclease free water ( no sterilised) this morning and I forgot them at 4 degrees, acording to the instructions, they should be storage at -20 after the reconstitution. I am wondering if it will affect to have them overnight at 4 degrees, just for one day.

There is absolutely no problem here. Primers will degrade only very slowly at 4 degrees and even at room temperature leaving them out overnight would not degrade them enough to be of practical consequence. In fact, if you're using them today it's probably better to have stored them at 4 degrees than -20 because repeated freeze/thaw cycles will also degrade primers.

In my experience this is not a problem. I keep my working stocks at 4°C until they are finished to avoid freeze-thaw cycles and better convenience and they work all the time. I also dissolve my primers in pure water, not in TE.
Long-term storage of stocks should be done at -20.


text:
Do cows chew in a preferential chirality?
One of the enduring myths in molecular physics, when talking about chirality as pertains the existence of enantiomers and the differences between them, is that the way cows chew is also chiral, i.e. the up-and-down and the around-in-a-plane movements combine in such a way that you can distinguish a cow chewing from its mirror image. This is mentioned in e.g. Wikipedia, among other resources.
A recent question in the Physics site asked for the source of this factoid, which turns out to be

Movements of the Lower Jaw of Cattle during Mastication. P. Jordan and R. de L. Kronig. Nature 120, 809 (1927),

and this is a rather unsatisfactory source: they report on a survey that finds that 55% of cows chew in a 'right-circular' fashion and 45% chew left-circularly, but they then go on to disavow any statistical significance in the result:

The number of observations was, however, scarcely sufficient to make sure if the deviation [in the ratio of the two kinds] from unity is real.

Given that this isn't a physics question, I thought I'd bounce it over to the mammalian behaviourologists out there: have there been further studies about which way cows chew? I imagine that they're out there, but I wasn't able to find them.

I'd say as a biologist it's almost as interesting if individual cows indeed chew a constant direction (sort of analogous to 'handedness') versus whether there are population-level biases toward chewing a certain direction. If the former is true, regardless of whether the average cow has a biased direction it makes a reasonable entertaining example. Interestingly, Google Scholar notes just 6 citations of the paper you refer to; all 6 are making the chirality connection, none of them have any association with biology whatsoever.

@Bryan That's an interesting distinction I hadn't considered.

It seems there is a commentary on that original article RIEHM, H., & GUGGENHEIM, E. (1928). Movements of the Lower Jaw of Cattle during Mastication. Nature, 121(3045), 357. - they comment that they observe the same direction of chewing in an individual when taking in food and ruminating. They also point out that since the direction of food travel is opposite, the same direction of rotation makes them both left and right handed with respect to food travel. I find that argument a bit silly from a biology perspective but maybe a physicist would appreciate it. :)

Another related example from biology is hand-clasping: when you interlock your fingers together, which thumb is on top? Individuals have a strong bias. Interestingly, this is independent of left/right handedness, and also independent of arm-crossedness: when you cross arms, which hand goes under and which goes above the upper arm? There is some loose correlation with parents for these traits, but in the overall population they are not particularly biased.

This study deals with the chewing direction of cows. It splits the chewing into three phases, the first jaw movement, the middle ones and the last one. It finds out that the first one is always in the opposite direction of the middle ones, that generally the middle ones are usually in the same direction and that seemimgly cows change chewing direction from one middle jaw movement period to another.

@BrianKrause here's a partial answer to your comment, even with a small dataset and no statistics attached to it.


text:
Can something like McDonalds be considered a life form?
"The current definition is that organisms are open systems that maintain homeostasis, are composed of cells, have a life cycle, undergo metabolism, can grow, adapt to their environment, respond to stimuli, reproduce and evolve." (Wikipedia)
Could McDonalds(or any other chain store) be considered a life form according to the current most accepted definition of Life? If not, what am i missing?
It evolves and changes over time; it reproduces by using excess Material to build new stores, it responds to outer stimuli by adapting to them; it grows to a point it is benefical; it starts to function sometime and will eventually stop; it autoregulates it self trying to maintain a stable state and it has a very complex metabolism
Thanks in advance

SE Biology is a question and answer site for real problems in Biology. It is not a philosophical discussion site. Please read the Introduction and Help for the site.

No. First of all, an "organism" is not automatically a "life form". And it is easy to see that McDonald's does not have an information repository in the form of a genome-like structure, where mutations are quantum-acausal, but still have causal consequences on the bearing reproductive units and they trace an evolutionary path all the way down to the ancestor. In your food stores there is no such a thing. Everything is just engineered and organized by us humans. This is "intelligent design" (although fast food is not really an intelligent thing to do) and has nothing to do with evolution in the biological sense.


text:
number of chromatids seen in karyotype
The karyotype is performed on a cell whose cycle has been stopped in metaphase or pro metaphase, using colchicine or by other means. In the textbooks I read that during the S phase each of the 46 chromosomes is duplicated, giving, again, 46 chromosomes, but, and here I am deducing, 92 chromatids. When we perform the karyotype, we only see 23 pairs of chromosomes (46, that is), and, it looks like to me, the same number of chromatids (46 as well). What am I missing? Why can't we see 92 chromatids in the karyotype?
Thanks a lot for your attention.

Possible duplicate of Karyotypes Appearance

See this question. Karyotypes do not show the entire structure. It's a good question, though, and shows you've been putting some thought into this.

As you noted, karyotypes are prepared from cells halted in metaphase or prometaphase.  In either of these phases, the chromosomes will have two chromatids bound together at the centromere with the chromatid arms lying parallel to each other.
The difficulty in seeing the chromatids in most karyotypes is due to the way they are prepared. Most karyotypes are prepared using Giemsa staining which causes contrasting bands to appear on the arms.  These bands have patterns characteristic for each chromosome type and thus allow the chromosome images to be identified and sorted into pairs.  Between the stain, lighting and exposure used to show the banding, the images don't show the separate forms of the chromatids well.
With alternative staining and lighting, the chromatids can stand out (all images from commons.wikimedia.org):

Still, in typical karotype photographs of sufficient resolution you can at times make out the separate forms of chromotid arms, or perhaps the "pinched waist" shape where the centromere draws the chromotid arms together:

So, yes, a normal human karyotype has 92 chromatids present; they just tend not to be apparent due to the preparation done to show banding.

Chromosomes and chromatides are referring to the same physical objects, although a chromatid is mostly referring to the DNA strand, and chromosome to the "colored object" (chromo=color, some=body) that people first saw under a microscope. So, yeah, don't get confused by that, it is just that biologists like to coin terms for specific contexts.
You can see a detailed explanation here.
Cheers,
Pedro

I'm familiar with the difference between chromosomes and chromatids, what I don't get is why we see 46 objects in metaphase, and not 92 (and by objects I mean independent molecules and also molecules linked at the center, so that two sister chromatids count as two objects, even though they are linked, by this definition)? If the chromosomes duplicate in the S phase, my reasoning goes, even though the copies may be 'linked' to the original in some way, shouldn't we still be able to distinguish them clearly (and thus distinguish 92 molecules, however they may be connected to each other)?


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Is this a Tsetse fly?
I found this on my back while looking in the mirror.It took me 10 minutes to kill it.I hit it well at least 5 times before it died.It kept flying to me every time i tried to hit it,trying to go under my shorts
Is this a TseTse fly?

what fly is this?

Why the downvote?

This is a species of Hippobosca, looks like H. equina. There aren't too many species of this genus, so the species may be this one, which is rather common in Europe, Africa and parts of Asia - see https://www.biodiversidadvirtual.org/insectarium/Hippobosca-equina-Linnaeus-1758-img485046.html. Since you suggested it could be a tsetse fly, I assume you are in Africa. Hippobosca equina occurs in Africa as well. Other hippoboscids are not as strong fliers as Hippobosca species, which would explain its flying back to you over and over.

Thanks a lot Steve.I am actually from Greece.The title was for click-bait and the suspense :P ! The smartest fly i have ever seen.


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How close are we to having phages take over the role of infection control from antibiotics? What developments need to occur?
The discovery of, and research in, the field of phages was overshadowed by the discovery and implementation of antibiotic treatments for infectious disease control.  With the rising concern of antibiotic-resistant microbes, is there a serious effort to refocus research and development to master the science and technology of phages?

Welcome to Biology.SE! This is a good first question. I suggest you to make the tour in order to learn more about this site and earn yourself your first barge. Have a good stay!

This is a very interesting topic. Indeed, historically, it might seem that "phage therapy" research is in a dormant state. But there are some groups actively doing theoretical research on the synergy between phage treatments and the immune system, as well as research on how the appearance of antibiotic resistance could be attenuated by the use of phages.
Nevertheless, this research is not what the field is trending towards, since there is still hope to find new antibiotics (for which, then, we will see other types of resistance evolving), and most of the funding agencies are still privileging this instead of the alternatives.
A colleage of mine is working on this very same theme. Here is one of his recent research papers on a specific type of infection.
Cheers,
Pedro


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Do marsupials ever die in childbirth?
Question: Do marsupials ever die in childbirth?
Obviously the notion of there being a linear ordering of "least advanced" to "most advanced" life forms isn't correct. Still, often marsupials are depicted as relic or archaic creatures with an inferior reproductive strategy, since besides possums they are restricted to Australia and New Guinea.
However, compared to some placental mammals, like the spotted hyena and humans, the marsupial method of always giving birth to very small young, who can finish developing outside of the mother's body, seems to be more sensible.
If there haven't been enough field observations of marsupials, then of course this is an unanswerable question, but I was wondering if anyone knew anything about papers or other materials which discuss the advantages of the marsupial reproductive strategy.


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Are there limits to drug resistance?
It's well-known that indiscriminate use of a drug leads to resistance. My question is what the limits on resistance are. It seems obvious that there must be limits: for example I can hardly imagine a tiger evolving "resistance to bullets", and similarly I can hardly imagine a microorganism evolving resistance to heat treatment @ 1000 degrees celsius (surely its proteins must long denature before then).
Are there methods of killing microbes that cannot be resisted? If so, can we make similar cannot-be-resisted drugs?

You mean drugs that eliminate bacteria without killing the host, right? Otherwise every strong enough poison is a candidate drug :D

There are physical limits to the existance of life forms, wether temperature, pressure, osmolarity, etc. But these are usually physicochemical fields acting over a wide spatial structure. In the case of drugs, they are physically localized molecular entities. They are usually very tiny, even compared to the smallest microbes. Even though the genome of any microbe is finite and they could not, in theory, recognize the infinitely many drugs we can synthesize (assuming the simple case they need one gene per drug resisted), they can just evolve very generic mechanisms like preventing these molecules to get into the microbe, pumping them out of the cell, or other generic mechanism; with the same overall effect: preventing the drug from acting in the desired way.
The question you ask is very interesting, and it is the focus of some recent efforts and discussions among academics. Here you can find a recent article discussing the possibility of "evolution-proof" drugs. As you can see, the subject is not trivial.
Cheers,
Pedro

The article you link to discusses a very important and basic principle that you might include in your answer. In the absence of selecting pressure, the frequency of resistance shouldn't increase. Theoretically.

The link's dead ... any idea what the title was so I can try to find it?

I just updated the link. Depending on your situation, you might need to access it through SciHub (using its DOI).

In case I need it again, the paper title is "Targeting virulence: can we make evolution-proof drugs?" by Richard C. Allen, Roman Popat, Stephen P. Diggle & Sam P. Brown.


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How do retroviruses exit the cell
Do they just pass through the membrane? Is there some specific transporter or mechanism? Does it vary?
I've seen pictures if retroviruses outside the cell but no details

Retroviruses, like many other enveloped viruses, exit the cell by a process called budding. The virus uses the host machinery for producing transmembrane proteins to enrich areas of the host cell membrane in viral transmembrane proteins, and co-opts a host process for releasing vesicles.  You can see budding illustrated in the context of the life cycle of HIV in this figure from Murray Medical Microbiology.

The process has been studied in some detail in HIV and other retroviruses.

They would have to exit the bud as well and the bud would have to accept the virus which is unlikely.


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due to hypersecretion of growth hormone why only terminal growth takes place?
why only terminal growth takes place in acromegaly and gagiantism, due hypersecretion of GH?


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Is this tree poisonous?

I touched this tree on my visit to South Africa and a huge rash developed on my body,please help,what is the name of this

Welcome to Biology.SE! That picture looks like a screenshot of a previous question. Is that question yours? Consider editing it instead of post a duplicate question.


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Can you accelerate the growth of a plant by accelerating its surroundings?
I had this weird idea of making plants grow faster when I first visited an indoor nursery which used floodlights instead of sunlight. They turned on during the day and went off during night in cycles.

If the time period of the cycles are decreased, it would seem to the plants that the earth just switched to fast-motion. Will this trick the plants into growing faster?
If not the current generation, would the later generations of plants grown like this adapt to the new rhythm ?
(Given that the plant is provided with surplus nutrients to meet the new requirements.)
I would love to do the experiment myself if it would actually work!

Hello, This is an interesting question. I'm sure there is an effect of day-length on growth (number of hours of light). However your question is more about effect of  whole day-night cycle modification? like a cycle of 30h (15day/15night) or a shorter cycle? I would see that more like an adaptation to a whole new planet where the length of a day is not anymore 24h (climatic change won't affect that).

@Untitpoi Hello there! I meant a decrease in day-length, for your information.

How can altering the clock prevent global warming? If plants grow faster, they will also die sooner, releasing all their saved carbon to the environment. The long term effect will be close to none.

@jmster  I googled how to decelerate plant growth. It is possible with a method called Topping. So, you can slow down the growth after it has reached full growth. This should decrease global warming, or at least provide some shade!

"We can fight global warming like never before!" You have to take into account the energy and infrastructure you're expending to know how much net CO2 you're sequestring or releasing. Not to mention scaling - how much plant mass could we do this for ? What percentage of the Earth's surface would we be covering in indoor nurseries or floodlights, and how much of Earth's vegetation would we be replacing with the accelerated version ? And how much more carbon would those plants sequester than ordinary plants do in the first place?

I'm sorry but I think the idea of preventing global warming is not the principal point! The question is can we accelerate the growth using in-vitro technics (related to day-length). Whether it could be used to prevent global warming is another issue.

@Untitpoi If preventing global warming had been the principal point of the question, all those comments would have been answers! As it is, given how preventing global warming was emphasized in the question in a way that suggested a misunderstanding of the magnitude of the different phenomena involved, I think the comments were justified. I think editing that passage out of the question was a good idea, it distracted from the main question which is interesting in its own right.

they have evolved for 24/24 for billions of years. there's not a mechanical reason they perform better at 12/12.. It's been tried and studied and measured, but only to see the reaction, I don't think that the plant photosynthesized more if the same amount of light was given at different times.

@Untitpoi Don't consider it as a knowledgeable answer, but I have posted an account of the experiment  below; I don't know if it's appropriate !

This is not the best answer, but see that as a starter! Feel free to use my answer to build yours!
I have found a so-called professor speaking of advantages to go on a 24h light/12h dark cycle (36h cycle) to accelerate the growth of cannabis. I'm not sure of the reliability of this source.
I think the main problem we will encounter with that reduction of cycle would be the trouble with the circadian clock inside the plant. This clock is quite stable and I suspect some deregulation would happen if you desynchronize your day-night cycle with that clock.
See the effects we show on humans in the section Enforced longer cycles of
 Wikipedia or this stack question

Researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions - both physiological, behavioral, and cognitive.

Do you think this clock inside plants would itself get altered, in the new generations at least?

The circadian clock seems to be complex, it is highly improbable that it will change in one generation. But I think some arabidopsis mutant showing an absence of circadian clock exists and show a high suspeptibility to diseases. You could be interested in that article https://theconversation.com/studying-circadian-rhythms-in-plants-and-their-pathogens-might-lead-to-precision-medicine-for-people-84024

Note that many plants grow north of the Arctic Circle, where they get continuous sunlight for part of the summer.  (And very long days in subarctic latitudes.)  The same varieties of (domestic) plants grow in more southerly latitudes.  For instance https://sites.google.com/site/alaskafruittrees/

I'm not sure if it's right to post an answer like this but anyway, seeing is believing!
Three days ago, I (finally) gathered enough resources to do this experiment.
I'm testing on a pea plant as it comes in handy. I have set up two samples, one for the test and the other for reference.

Today's Day 3, and the results have started to show up. I thought it would be nice for you to see it yourself. The experiment is not over, it's still going on; so I would update the news every three days from now on.
Everything was done in my study room, which is not a laboratory, so the results may not be accurate. I have tried to bring uniformity in the amount and type of soil used, water content, no. of seeds in each sample, seed spacing and other parameters.
I'm providing the link here.
EDIT: Today's only day 5, but the test plant has grown out of my simulator box!
I have modified the setup and started a fresh experiment.
The updated record here.
UPDATE
Maybe I should give an update for future readers. I asked this question a couple of years ago and forgot about it. I did this experiment when I was in high school, and I am currently an undergrad in science :).
I can confirm that this experiment was seriously flawed, be it the control parameters or the theory used. The plants grew bigger just because they received more light.
My past self was too enthusiastic about the results that he forgot to think about any of these. I am not deleting this answer as I want it to serve as a reminder for myself how not to do an experiment.

Interesting input, Are you trying a 30 seconds day-length there? It seems rather fast. In your document it is not clear what is the day-length for your reference. It seems more like your control had less light than your tested peas, but I am just guessing.

@Untitpoi My reference sample is sitting in bright sunlight right now ! I am not sure of the previous days, as I was out of station.Today the seeds has just  begun to open up. But the test seeds are on its own legs already! But the initial results cannot be depended upon. I am looking forward to day 6!

Maybe I misunderstood, but your control should also be in a box similar to your test with the same length of light exposition. If you don't do that, we can't know for sure if the effect you are measuring is not due to the quality of light (sun VS articifial light) or the total amount of light.

@Untitpoi Do you mean to place the reference sample in another test environment with a 12-hour on and off period?

Yes that's exactly what I mean.

@Untitpoi I will consider that. Thank you for the input!


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Osmosis in red blood cells and bacteria
This is a question from an exam in my biology course.
Bacterial cells and human red blood cells were inserted into one solution. Upon testing one hour later the blood cells exploded, while the bacterial cells stayed intact. What answer explains the findings:
A. The bacteria cell walls prevented their explosion.
B. The blood cell walls didn't prevent their explosion.
C. solute concentration in the solution is equal to the blood cells and bacteria solute concentration.
D. solute concentration in the solution is higher than the blood cells solute concentration.
My lecturer said the right answer is B. I thought the right answer is A.
What would be the correct answer and why?
To my understanding, red blood cells don't have a cell wall, but rather a membrane, which is why in my opinion you can't say that it prevented the explosion if it doesn't exist. On the other hand, bacteria does have cell wall, that's why I thought this answer is the correct one.

Do you have any proposals for what would distinguish the two answers?

To my understanding, red blood cells don't have a cell wall, but rather a membrane, which is why in my opinion you can't say that it prevented the explosion if it doesn't exist. On the other hand, bacteria does have cell wall, that's why I thought this answer is the correct one.

I edited your question to include your reasoning. When you have a homework or exam related question, you should include this kind of information in your question

Absent a very specific learning objective, if (B) is correct, this is a poor question. In a high-school or undergraduate introductory biology course, I would say:

(A) The bacteria cell walls prevented their explosion

Would be the correct answer, because of exactly your reasoning. This is what you're taught in introductory biology. You're taught that animal cells don't have cell walls. Bacteria and plant cells do have cell walls.
See The Cell

animal cells are not surrounded by cell walls

Under this concept of a cell wall, red blood cells certainly don't have them.
However, red cell osmotic fragility testing comes out of a tradition that uses the phrase cell wall strength to describe the response of a red cell to osmotic stress. See Orcutt

It appeared logical to us that a model based on a distribution of cellular wall strengths ought to reproduce the experimentally observed variation of degree of hemolysis as a function of osmotic stress.

All the same, if you were operating from that perspective, how would you distinguish between (A) and (B)? Here, we're not even taking into account the fact the primary mechanism for responding to osmotic stress in most animal cells, including the human erythrocyte, is regulation of ion flow, not the pressure of a rigid extracellular matrix. If the solution contained ouabain, which certainly does lyse human RBCs, would it be best to characterize the problem as "The blood cell walls didn't prevent their explosion"?
I would ask your lecturer to clarify the learning objective behind the question. As an interpersonal note, I'd point out that this is very different from asking him or her to justify the correct answer. Some (many...) teachers are oddly sensitive to any suggestion that they need to justify their expertise, especially when it comes to exam questions. If you make it a question about the learning objective, this should help you avoid triggering that particular sensitivity.


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What is the relationship between induction of cell differentiation and DNA methylation status?
This may sound like a broad question to ask, but I am working on interpreting a review article for my epigenetics course and I'm having trouble reconciling two seemingly contradictory things this review is saying.
Ehrlich, M., & Lacey, M. (2013). DNA methylation and differentiation: Silencing, upregulation and modulation of gene expression. Epigenomics, 5(5), 553-568. doi:10.2217/epi.13.43
On page 554,

Constantinides
  et al. found that treatment of an embryonic
  fibroblast cell line with 5-azacytidine (5azaCR),
  an inhibitor of DNA methylation, induces the
  formation of [myotubes] [35].

and

Treatment with DNA demethylating agents
  can not only convert non-myogenic progenitor cells to Mt, but also can induce other cell-
  type interconversions in progenitor cells. For
  example, with 5azaCR treatment, the C2C12
  Mb cell line can be induced to express genes for
  key osteogenic transcription factors as well as
  adipocyte markers [40]. The outcome of DNA
  demethylation treatment is dependent upon the
  cell type as well as the treatment and growth
  conditions [41].

and

The conversion of a multipotent adult stem
  cell to dissimilar differentiation products by
  treatment with DNA demethylating agents
  can be explained by the hypothesis that some
  genomic methylation restricts the differentiation
  potential of progenitor cells [40].

These three quotes, all on the same page, seem to indicate that at the very least, induction of differentiation is contingent on demethylation. More specifically, DNA methylation restricts the possible differentiation activity that a progenitor cell can undergo. However, just a little further down,

Terminal
  differentiation predominantly led to increases
  in DNA methylation and both increases and
  decreases in H3K27me3, depending on the
  gene involved.

and

[...] to
  hypothesize that changing the DNA methylation status of pluripotency genes in vivo is critical to their function [43]. DNA methylation is
  considered a more stable repressive mark than
  repression-associated histone modifications [42].
  The association of differentiation and the loss of
  pluripotency with DNA methylation at previously unmethylated sites (de novo methylation)is consistent with the inability of ESCs to differentiate when Dnmt1, the most abundantly
  expressed DNA methyltransferase gene, is
  homozygously knocked out [44].

I'm working on a presentation on DNA methylation and gene silencing, and I want to make an accurate portrayal of the role of DNA methylation in cell differentiation, and this is only a portion of the whole presentation, so I am not including a lot of data on this topic. However, I want whatever I do present to be self-consistent and accurate. How do I reconcile these two phenomena? From what I can tell, there is no explanation in the intervening text between these passages about how these two phenomena are similar but distinct. Am I accurate in determining that this is a difference between induction of differentiation and terminal methylation status? If so, how is it that ESCs can be differentiated with demethylating agents, but also ESCs have trouble differentiating when Dmnt1, which promotes methylation, is knocked out?

This is a good question. I'm not as steeped in this literature as I'd like, but here is my understanding of the process:
Methylation is one of the key methods by which cell fate is restricted. The review you're reading is giving specific examples of cell lines that are at least partially restricted into cells that are of an entirely different type. Thus de-methylation is a method for de-differentiation, which then allows differentiation along a different line.
Your three examples that it sounds like you're interpreting as induction of differentiation, are actually examples of that effect -- de-differentiation that then allows for differentiation to a different fate. Constantinides work, for example, showed the conversion of a non-myoblast precursor into functional striated muscle cells. Not only can fibroblasts be turned into muscle cells, myoblast cell lines can be made to look like bone cells or fat cells. None of these things would happen without re-programming the cell fate by de-differentiating the cell lines to form dis-similar differentiation products.
This is consistent with other findings about de-methylation in vivo. An important example is the global de-methylation of primordial germ cells, as demonstrated in this figure from the linked review, summarizing the methylation state of the germ line in mice. Pay particular attention to the blue line. The pronucleus of the highly differentiated spermatazoon (along with its highly methylated DNA and histones) undergoes global de-methylation. Its products include the primordial germ cells of the developing mouse, the most de-differentiated state, which, in the case that it is a male, then become methylated as they become primed to differentiate, and then differentiate.

Thank you for your help, I actually found a diagram that answered my question but your comment reinforced my understanding.


text:
Could higher carbon dioxide levels be beneficial to plants?
C4 plants take ATP-expensive routes to ensure photorespiration does not occur.
They minimise oxygen concentration in cells where the Krebs cycle occurs and cart carbon dioxide into these same cells. To over-simplify, they increase the carbon dioxide concentration and decrease the oxygen concentration in these cells.
Despite the ATP this costs them they are enormously successful (in hot areas at least).
Considering this, would human-caused carbon dioxide emissions, i.e. increased concentration in environmental carbon dioxide, be beneficial to plants?
Considering @Cell's comment: I mean beneficial from the 'plant's point of view', i.e. the plant can grow faster-reproduce sooner or less photorespiration occurs; due to the higher level of carbon dioxide. I think we can disregard ocean acidification for now, climate change is relavent but perhaps it could be disregarded initially? Especially as climate change effects different areas differently.
Please note: I am not encouraging or supporting human caused carbon emissions; this is a genuine question asked out of curiosity.

Don't worry this is a standard question asked in most intro to biology classes. So you will find it welcomed here

Except that it seems to show a lack of prior research.  Google Scholar shows about 1.8 million hits on "CO2 concentration plant growth".

I think it might be helpful if you describe in more detail what you mean by beneficial. Anthropogenic climate change entails more than just increase in CO2 levels, for example drought and ocean acidification. It would be like me eating nothing but cheesecake everyday. Sure it makes me happy and it's an energy source, but there are other factors that can make it an overall unhealthy habit.

I have made some minor corrections. Note especially 'Krebs', named after Nobel lauriate, Hans A. Krebs, is not a possessive. Krebs is a German singular noun meaning 'crab' (and also 'cancer').


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Human genome, chromosomes
I have a very basic question, but it seems the hardest to me.
So we have 46 chromosomes (23, 2 copies of each). Do all chromosomes have the same DNA? If so, does it mean that in different cells with different functions some genes are expressed and some aren't? Also, if each chromosome has different lets say "fragment" of the genome, how is the genome interconnected?

Welcome to SE Biology. Please take the time to read the tour and, especially how to ask questions here. One key point is that you are expected to research  questions before asking. What texts have you consulted. Have you looked at pictures of human chromosomes and observed whether they are of similar size, for example? Try searching NCBI bookshelf, e.g. Molecular Biology of the Cell

Do all chromosomes have the same DNA?

No.  Not any more than each chapter of a book has the same words in the same order.

If so, does it mean that in different cells with different functions
  some genes are expressed and some aren't?

Yes.  In general, all cells in your body have all the same DNA; what makes your retina cells function differently from your pancreatic beta cells is which genes they express.  Like if every chef in a restaurant had the same recipe book which had every recipe the restaurant can make, but the pastry chef only makes pastries.

Also, if each chromosome has different lets say "fragment" of the
  genome, how is the genome interconnected?

The genome is not physically connected except for all the genes on a chromosome being physically connected.  But a gene product from one  chromosome might control expression of another gene by physically binding to the DNA close to it, which can affect its expression.  But most gene-gene interactions are really protein-protein interactions.  (Or in some cases, RNA interacting with RNA)

Well used analogies and nice short answers to simple, broad intro questions! +1


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Where can I find a picture of the inflorescence of Epipremnum aureum (golden pothos)?
Epipremnum aureum (golden pothos) is a very popular house plant - attractive and almost impossible to kill.
Also, it is a flowering plant with flowers produced in a spathe up to 23 cm (9 in) long, according to Wikipedia.
I have been trying to find further documentation of these flowers, in particular a picture, without success. Can anyone help?
(Google image search produces some stock photos that claim to show E. aureum flowers but I am skeptical about these.)

Figure 4d on page 6 of (Hung, 2016) shows a flower the authors managed to induce in E. aureum (This is one of the papers that mgkrebbs cited in his answer).

Hung, 2016 - Chiu-Yueh Hung, Jie Qiu, et al., "Gibberellin deficiency is responsible for shy-flowering nature of Epipremnum aureum", Scientific Reports 27 June 2016, DOI: 10.1038/srep28598 Creative Commons Attribution 4.0

You may find it quite hard to find an image of the flower of Epipremnum aureum as it is almost always described as "shy flowering".  Here "shy" seems to be an understatement, as the first recorded flowering was reported in 1962, and the latest report of flowering I found mentioned was from 1964 (Boyce, 2004).  Chiu-Yueh Hung et al say "Since 1962 there is no report of E. aureum flowering both in wild as well as in cultivation" (Hung, 2016).
Even though the name Epipremnum aureum was assigned in 1964, one still encounters it under several other names, including binomial names using the genus names of Pothos, Scindapsus, and Rhaphidophora.  Perhaps most problematically, one finds some use of Epipremnum pinnatum for it, as for some time it was considered a cultivar of that species based on the form of the flower. Consult Boyce for a good overview.
Boyce, 2004 - P. Boyce, "A review of Epipremnum (Araceae) in cultivation", Aroideana 27:205 (2004) [PDF].
Hung, 2016 - Chiu-Yueh Hung, Jie Qiu, et al., "Gibberellin deficiency is responsible for shy-flowering nature of Epipremnum aureum", Scientific Reports 27 June 2016, DOI: 10.1038/srep28598, [PDF].


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Can the human gut work with other type of gut bacteria?
I was wondering if the human body would be capable of functioning with, say, cellulolytic bacteria in their gut (instead of or in addition of their current bacteria), like that of ruminants and if they'd be able to digest cellulose thanks to it.
Couldn't find any papers on that, only on the implantation of faecal matter from a healthy gut to a sick one, nothing interspecific.

interspecies transfer of fecal material occurs often enough, but we usually study it in terms of pathogens and parasite life cycles. Interesting question. Probably tough to get IRB approval for that one, though.

@DanHall hahaha, bet. It'd definitely be interesting though! I'd like to hear the point of view of someone who's done human-human faecal transfers and what they think would happen!


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Is there any data to explore the heterozygosity of the South African lion over the last 18 years?
Background:
I need to find data on the heterozygosity of the south African lion over the last 18 years... and I'm struggling: so far I have found a single data point.
Question:
Where can I find data to help me explore changes in the heterozygosity of Lions living in South Africa?


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If fully colorblind people only see shades of white,gray, and black, does that mean that the colors black, white, gray are colors humans can’t see?
And since the brain can be tricked to thinking that objects with mostly black and grey gradients are moving, like optical illusions, does that mean motion has a color?

According to your title you should consider a repetition from optics.  But anyway it is quite interesting question.

Based on your question: if fully color-blind people see whites, blacks, and greys, that means that humans can see them colors. After all, aren't color-blind people humans?
If you actually think about it, is color just created by evolved cells? If so, should we not see just black, grey, and white?


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What is the name of this tiny creature? It looks like a tiny piece of moving cotton?
By chance, I saw this tiny insect on my bag a few days ago in Sydney. Am I the first person who has pinpointed this animal?! If not can you please let me know its name?

From your image, it looks like it might be a woolly aphid. I just did a bit of cursory research, and it looks like they're often described as floating pieces of fluff, that seem to wander instead of directly heading somewhere. The fluff on their back is actually wax produced as a defense mechanism from predators and the like. I hope this is what you were looking for!

Welcome to Biology.SE! Nice first answer. Take the tour to earn your first badge and edit your answer with a link to the species description or a picture to get another one! Have a nice stay!

Though I agree this is some species of woolly aphid, you need to update your answer as suggested by LinuxBlanket. Please provide links/citations to support your answer. Species ID answers require you to show support since incorrect identification is so prevalent...Providing a picture is also always helpful for species ID answers. thanks.


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Is it possible to prove that a hand sanitizer can kill 100% of a person's germs?
We have a project for Economics, and we need to advertise something that consumers will be willing to buy. My group thought of "improved" hand sanitizer. So, instead of it killing 99.9% germs, we would make it kill 100% germs. Although, we are having a hard time trying to prove that our hand sanitizer can, but we can't change what our product is anymore, since we only have a couple more weeks until we pass the commercial.
Can anyone help us? Thank you in advance.

Its been found that women have more varieties of bacteria because the wash more and men have higher quantities

I.e. women have morevspecies due to hygiene, men have more quantity. If you use alcohil, there still will be 1 or 2 of every 1000/5000 alive.

Related: https://biology.stackexchange.com/questions/61059/why-dont-antiseptic-agents-kill-100-germs

There's no realistic way to prove that your hand sanitizer can kill 100% of a person's germs. In fact there's probably no realistic hand sanitizer that can do that. The reason is that there are just so many germs. There are billions of germs on your hands. To compare, there were only a few hundred thousand people in Hiroshima when it was hit by the atomic bomb in 1945, and even that did not reach 100% fatality.
It's because it's hard to kill all germs that antibiotic resistance is a problem.

First part of the answer isn't correct at all. You could do metagenomics analysis to say if there's presence of bacteria (or other organism) into your hand sample.

@Shred not an expert on that so if you write that as an answer I'll delete this one.

As others have pointed out, you can't claim your sanitizer kills 100% of whatever, because it just isn't true. However, you could claim, "Product X kills nearly 100% of bacteria." Many readers will key in on "100%" and gloss over "nearly." Advertisers do this all the time.Another alternative is to do an experiment that has an extremely small bacteria population, apply the hand sanitizer then claim 100% effectiveness. And yet another, is to conduct several experiments with different bacterial strains, find one result where 100% of the population was killed, and then make your 100% effectiveness claim. The FDA will probably come down on you hard, but my then you've probably made more than enough profit to cover the fines.

Alternatively, you could adapt your claim to state that "sanitizer X kills 100% of bacterium Y"

As pointed by Allure, there's no way to say that a chemical agent is 100% efficient against all kind of microrganism . That's because of high rate of mutations by these, and a strong evolutionary pressure made by the use of this hand sanitizier.
To do an example: you'll make the first traitment using the hand sanitizier, and a rate of 99,9% will be killed. The remaining 0,01% will proliferate because of the ability to live and division under the hand sanitizier traitment. Consider that SDS is often used into detergent, and some strain of bacteria are capable to make the compound totally ineffective.


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Can you recognize this grape?
This gorgeous and sweet grape I collected in central Italy. I would like to know the name of this variety to get more information about it. I tried to compare with some pictures in Google but I am no grape/wine expert so it's really hard to figure it out for me.

I'm Italian, and that's an example of what we called uva da tavola , so these grapes aren't used for wine production. I think is the crimson variety.

Not sure at all.

@Marzipanherz — Because a proper answer would specify the grape variety in a scientific manner. The answer just makes the point that this is a table grape (uva da tavola in Italian), not a wine grape (which are not generally particularly sweet) and that it is sold under the name "Crimson". He also provides no evidence for his assignation (photo). Crimson appears to be an example of Vitis labrusca but may be an interspecies hybrid. However I am not competent to say if this is indeed Crimson.


text:
Why don't we hear all the processes in our body and what prevents us from doing so?
Why don't we hear all the processes in our body (like the rushing of our bloodcells through our arteries, the pumping of our heart, the electricity of neurotransmitters or our brain cells, etc.)
Is it only because the sound is too low for us to hear?

The issue here is with the definition of the word "hear". We do hear most of this, that is our ears actually pick up and transmit this sound. But we don't hear it in the sense that our brain ignores it and filters it out of what we are aware of. Only a very small fraction of all the sensory data that comes into the brain ever gets processed. The brain does something called sensory modulation it filters through all the sensory data and decides what is worth paying attention too.
This happens at several levels, not surprising since we see these same levels of filtering in animals, as soon as you evolve sensory organs the ability to filter sensory information is an advantage. Some happens directly at the sensory organ, many have a threshold before a signal is sent. In the brain the reticular formation is responsible for much of it. But each sensory processing area also does some of its own filtering. Basically each portion of the brain contributes in some way. Attention and how it is controlled is greatly studied as it is central to how consciousness functions. A complete rundown of all sensory processing is tricky since some senses (like smell) skip some parts of the process, and there are so many ways it can be filtered. you can find a more detailed breakdown here.

It's still very mysterious how Allah made us hear like we consider as normal and how did He make us not here the processes. And what part of the brain regulates that specific task? The auditory cortex in the temporal lobe? I'd prefer medical terms, I'm used to remembering Latin names. So go ahead please ;)

The sound is mostly drowned out by all the other sounds in your environment. The environment is just too noisy. However you can hear it if you are place in sensory deprivation chamber. You can hear stuff like your heart beat, the eyelids moving, joints creaking, muscles tensing and even the movement of blood in the arteries within your ear.
You cannot hear neurotransmitter diffusion because it is a movement of chemicals, which do not generate a pressure wave and is thus soundless.
But there are sounds that you hear. You can hear yourself breathing and chewing your food.


text:
is it possible to use electroshock to temporary stop gross motor functions directly on the neural pathway?
Is it possible to modify that procedure and use it to send a small electroshock on the specific neural pathway and temporarily stop that gross motor function?

When the microphone detects unwanted noise—such as a humming airplane engine—it sends a sound wave into the headphone speakers that is 180 degrees out of phase with the bothersome sound. Consequently, the two waves cancel each other out, resulting in silence._

i would like to know if that procedure can be modified with electric currents in the human nervous system, so body movement is stopped, without stopping organs and damaging the body by sending the current directly in the nerve, canceling out the signal.

You can usually just say "cease all motor functions"

But seriously, this is an interesting question I may answer in detail later. A major challenge would be distinguishing between motor outflow to the diaphragm and to other skeletal muscle. Paralytic drugs require manual or mechanical ventilation. Paralytic electromagnetic stimulation would have the same challenge. That's if you could isolate motor outflow to skeletal muscle in the first place


text:
Can someone help me identify this queen ant?
I found this queen ant near a river on the 14 july in Braga-Portugal, it was on a river bank, and it measures around 8 mm. Can someone help me identifying the species? thank you for your time :)

The small space between the thorax and the abdomen indicates this queen has only one petiole segment (no post-petiole). The large size and absence of an elongated first abdominal segment indicates the subfamily Formicinae. The morphological features necessary to go further with a formal identification are not visible, but from the general aspect of the ant it is likely to be a Lasius or a Formica.
See ref below:

Seifert, Bernhard. Die Ameisen Mittel-und Nordeuropas. Lutra Verlag-u.
  Vertriebsges., 2007.


text:
Regarding detection of pregnancy during post mortem
Is it possible to detect pregnancy in a woman who is dead considering the fact that she did not a have a showing belly.

Answer is obviously yes. Here's an article reporting a forensic method used to detect pregnancy using placental markers in a Reverse Transcriptase PCR from a DNA sample. It could be applied in a death body, when it's possible to get a DNA sample from a tissue.

Could you please specify, whether the DNA sample can be from any tissue or only from certain tissues?

You could certainly do this as part of a postmortem examination, but it's not how it's actually done.

As a general rule, there are more diagnostic options available in a postmortem than in a living subject. While there are some diagnostic tests that aren't as helpful postmortem as they are in the living subject, the additional tests you can do are more definitive rather than less.
Early presumptive diagnosis of a pregnancy in living subjects is through $\beta$-hCG. Definitive diagnosis of an intrauterine pregnancy is through sonographic visualization of a gestational sac. In postmortem $\beta-hCG$ can be done on samples of blood, urine, vitreous humor (fluid in the eyeball), and bile. $\beta$-hCG is pretty routinely included in a postmortem for a woman of child bearing age. Examination of the uterus and intrauterine contents is considerably easier and more thorough postmortem, because, well, you can examine it directly instead of through external imaging.
You can't, of course, detect fetal heart tones or fetal movements if the fetus is dead but this is no different from an examination of a live mother.


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Is a large tumor is more likely to develop hypoxic regions?
It is known that cancerous tumors in humans can develop hypoxic regions where no blood nor oxygen arrive to some volume of its cells, creating a dead lump inside or around the tumor.
See Wikipedia - Tumor hypoxia.

Are hypoxic regions and regions without blood supply are more common in large tumors than in small tumors?
What is the likelyhood or frequency of hypoxic regions in small (< 2 cm) and large (> 4 cm) tumors?
What is the typical size of an hypoxic region within a tumor?

The article in Wikipedia is too techincal and very hard to be read and understood, and doesn't have an explicit answer to my question.

This isn't a direct answer because it's more of a model system in vitro, and wouldn't model in the in vivo microenvironment, but it's interesting to look at Table 1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4764677/

The prescence of hypoxia is independent of size, grade, or histology. It occurs due to a cut off in blood supply to the tumour. Or insufficient vasculature systems, meaning the oxygen cannot diffuse all the way into the tumour. Aberrant growth of tumours can increase the likelyhood of tumours developing hypoxic regions.

Hypoxic region can be formed in any tumor, big or small. But does large tumor have significantly larger hypoxic regions?

Not necessarily. Its all tumour dependant.

And statistically?

There is no relationship. The paper titled: "Detection and Characterization of Tumor Hypoxia Using pO2 Histography," looked at several tumor types none of which have a correlation between size and hypoxia.