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How much plant grow is required for a human's oxygen consumption?
I think Plants do:
6CO2 + 6H2O -> C6H12O + 6O2
I'm thinking that plants take 12 + 6 moles of oxygen and give back 12 mols of breathable oxygen and 1 mol of Cellulose.
I've read that a person needs about 550 liters pure oxygen (not air) per day, which I believe is about 785 g of oxygen (1L /22.4 L/g * 32 g/mol * 550 L).
I've read that grass is the most common plant, and is about 85% water.
Cellulose is about 162 g/mol, O2 is 16 g/mol, so for every cycle of photosynthesis, a plant's increase in sugar weight yields about ((6*16)/162) = 59% weight in oxygen. Since this sugar weight is only 15%, a plants total weight in growth will produce .59 * .15 = 8% weight in oxygen.
Does that mean that if a person needs 785 g of oxygen per day, there needs to be 9812.5 g (about 21.6 bl) of new plant growth that same day?


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WHO Essential Medicines vs Essential Medicines for Children
Per the WHO (World Health Organization), there are a list of "Essential Medicines" such as those listed on their Wikipedia page.

Is there a database link for this directly other than Wikipedia?
What is the difference between the "Children" list and the regular list. Is one a complete superset of the other? I noticed the "Children's" list is much larger.

I would like to make an open JSON database of some sort regarding a more easily accessible and organized way of accessing this data in a Postgres database or something. What do you know like this that exists?
https://en.wikipedia.org/wiki/WHO_Model_List_of_Essential_Medicines
https://en.wikipedia.org/wiki/WHO_Model_List_of_Essential_Medicines_for_Children

Wikipedia links to ressources: this is the first references of your linked article: https://www.who.int/medicines/services/essmedicines_def/en/ - it should contain all information that is needed, though arguably not in an easily parseable format

Neither list is a superset of the other.  The children's list is longer but notably lacks medicines for reproductive health and perinatal care.

source: Stack Exchange

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Sorting beads with FACS
Does anyone know if it is possible to sort micro-beads, ideally magnetic, using FACS and if so what diameters can be sorted. I was thinking of using fluorescent beads that might help facilitate this but I have no previous experience with FACS.
Ultimately I want to separate beads into separate wells that can be used for PCR templates.
It would be helpful if anyone knows any studies that have used similar methods.
Cheers!

Just some questions to facilitate a good answer: What sorter do you have access to? Are they the MACS microbeads (Miltenyi GmbH)? What's bound to the beads?

I'm not sure what model the FACS is that I have access to, I can find out on Monday. We haven't decided what beads to use for our experiment yet, this is what I am trying to prepare. We want to isolate Bacteria and Archaea cells from environmental sediments but haven't decided the best way to do this yet either and what to use to bind the cells to the beads. These are all things that I'm currently considering but initially, most crucially, if it is not possible to sort beads using FACS then I will need to look for an alternative approach.

You can sort on a fluorescent signal, though I'd be apprehensive about sorting magnetic beads. The MACS microbeads are 50nm to start, which is probably below detection for sorters not sporting a 405nm small-particle detector, making a gating strategy using scatter difficult. Have you considered a negative magnetic sort where your flow-through is your population of interest, followed by FACS?

The reason I wanted to use magnetic beads is to isolate them easily from an environmental sediment sample, not to use MACS. Therefore I could use beads larger than 50nm, I've seen some available that are several microns in diameter. The beads would just be suspended in some buffer like PBS (or whatever is suitable for FACS). Ultimately I want to then separate these beads so that each is in its own well on a well-plate, I thought maybe FACS could do this?

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How did the nucleus of eukaryotic cells evolve?
What is/are the most popular theory/theories on how the nucleus evolved?
I know mitochondria came from alpha-proteobacteria, chloroplasts from cyanobacteria and that eukaryotes evolved directly from archaea, but what about the nucleus?

Devos et al. 2014 will be of interest as well as wikipedia > Nucleus#evolution.

I hope these papers by Wilson and Dawson (2011) and Devos et al. (2014) will help you.
In summary these two review provide evidence for the following statements:

The nuclear pore complex is well conserved with some regions of divergence.
The nuclear lamina appears quite variable between major supergroups.
Centrosomes are ancient structures but exhibit a complex evolutionary history.
There is evidence for prokaryotic ancestors of some nuclear components.
Analysis of divergent organisms is essential to fully understand nuclear biology and its origins.

But this is not an answer to the question. The poster is clearly asking for theories on the origin of the nucleus (he makes comparison with the origin of mitochondria) but your ‘summary’ of the papers does no more than say “there is evidence fro prokaryotic ancestors of some nuclear components”. Answers need to be self-contained and provide information in response to the question.

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Why don't membrane potentials violate the principle of electroneutrality?
The principle of electroneutrality states that the number of anions and cations in a solution must be the same, i.e., that there will be no charge excess in any side of the membrane separating two solutions.
Despite this, a membrane potential of (e.g., of -70 mV) must mean there must be a charge excess on one side of the membrane.
My texts say that this does not violate the principle of electroneutrality since the number of potassium ions that moves to create the membrane potential is very small. I appreciate this fact,  but it seems unconvincing to respond to "there will be no charge excess" with "there will be, it's just very small".
As a follow up question: when we discuss "injecting Na+ into a cell" does this also not violate electroneutrality? How can we get a solution with only sodium ions dissolved in water in the first place?
Thank you.

Whose principle is this and under what conditions does it hold?

@BryanKrause this is part of my confusion as the principle is mentioned in several of my texts and in places online but I can't find where it comes from. It does seem to hold in macro solutions, e.g., a solution has 140 mM of K+ and 20 mM of Na+ then it would be the case it has 120 mM of some A- ion. But in micro it seems counterintuitive when considering membrane potentials

In bulk aqueous solution, the principle of electrical neutrality strictly requires that the sum of n(i)z(i), summed over all i, be zero.  But is it generally agreed that local violations are allowed.  One the the brickbats aimed at the chemiosmotic theory of Peter Mitchell was (and still is!) that it violated the principle of electrical neutrality. See Analysis of molecular mechanisms of ATP synthesis from the standpoint of the principle of electrical neutrality

There is perhaps Pauling's principle of electroneutrality "each atom in a stable substance has a charge close to zero" - maybe that's the principle referred to in your book? "Close to" is an important part, though, and this is not some law of physics, just an observation of how things tend to be, not how they must be.
Consider also a capacitor - that's how the membrane behaves. A capacitor features charges that are separated by some insulating medium.
Unfortunately, some textbooks do a really terrible job of explaining how membrane potentials work. I recommend starting from imagining no membrane potential at all, just ions of different concentrations, and then think about how those ions would move across the membrane according to those concentration gradients, ignoring charge entirely.
If, say, K+ is high inside a cell and low outside a cell, K+ is going to tend to diffuse out of the cell more often than it diffuses in. No charges needed to understand that so far, just concentration gradients. But, as a consequence of K+ ions tending to move out of the cell, you're creating an electric current: the K+ ions have a positive charge, so if a few more leave the cell than enter, the inside is going to be a little more negative than it was. And since it's a little more negative, there will be a little less tendency for K+ ions that have positive charge to leave that slightly negative space, even if the concentration gradient would make you expect K+ ions to keep moving.
How much more negative? And how many ions will move until it's "negative enough" that the electrical gradient holding K+ ions in is equivalent in strength to the concentration gradient letting K+ ions leak out? I posted some of the math for the number of ions here - as you mentioned, it's very small. Electricity is powerful stuff, and that's why Pauling has that principle that things tend to be roughly equal. For a membrane potential, things are equal enough that if you were just writing down the concentrations it would fit into the measurement error. For the "how much more negative?" question you can use the Nernst equation.
When multiple ions are involved you'll have to weight each of their contributions to calculate the overall membrane potential. Only ions that have some permeability across the membrane contribute to the membrane potential. You can both calculate the membrane potential and also see how ions that don't have any permeability don't contribute from the Goldman equation. You can also see it from the story above: the voltage across the membrane caused by potassium is only happening because potassium is moving.
When someone talks about "injecting Na+", they don't have a vat of sodium ions, rather they're using this for shorthand of "injecting Na+ and an unimportant anion", that is, something that's not important for the membrane potential.
Be careful about trying to add up charges on each side of the membrane to calculate a membrane potential: you want to think about concentration gradients, instead, and how ions move according to those gradients and what consequences that has for the distribution of electrical charge across the membrane. You also shouldn't think about the charge that moves across the membrane as being distributed throughout the cell: it's literally at the membrane. Remember, the membrane is a capacitor: the extra charge exists right along the membrane, and it doesn't just sit there without having an effect on anything, a bit of negative charge inside the membrane is going to pull any positive charges anywhere in the membrane a little closer to the inside, and push any negative charges a little further away.

Thanks, that makes sense. I went down a rabbit hole of some of your responses and they also helped clear things up. In this answer you mentioned you won't do the maths but such a charge separation would boil the apparatus - just for fun what equations would show the energy released?

@TheAnonymous https://en.wikipedia.org/wiki/Electric_potential would probably be a good place to start, it'll be easiest to do the calculations if you make some "uniform spherical cow of charges"-type physics classroom assumptions. Actually, probably easier conceptually to work from https://en.wikipedia.org/wiki/Capacitor

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What is the contribution of respiratory rate to oxygen absorption?
Firstly, I am aware that oxygen absorption in the alveolus is perfusion limited. Apparently, oxygen equilibrates in ~0.25 seconds or 1/3rd of the way along a pulmonary capillary.

However, we are often told that we breathe faster so we can get more oxygen during periods of high activity.
This seems to contradict the first point. If oxygen diffusion is perfusion limited then it makes sense that an increased heart rate will increase the oxygenated blood flow ($\dot{V}_{O_2}$), but an increased $P_{AO_2}$ (due to increased respiratory rate) surely makes no difference as of the blood is already totally saturated at normal $P_{AO_2}$?
What is the mistake in my understanding or analysis? Does an isolated increased respiratory rate (in the absence of increased perfusion) affect oxygen absorption?

This site requires evidence of research in an effort to solve your question. You've assumed - without explanation of why - that PAO2 remains the same with exercise. Please look at an oxygen dissociation curve to see if that helps with your confusion. If it doesn't, edit your question to include links to what you've read regarding the effect of exercise on O2 saturation. Thanks.


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Why are most fishes vertical?
Why do most fishes have a "vertical" body shape instead of a "flat" one ?
Here "vertical" means that the body(from a front view) is roughly orthogonal to the horizontal plane, and a "flat" body shape means something like a frog's or a bird's with spreading wings.
PS: This question was raised when I was thinking how I can swim faster.

Is you question really why is the fish's mass usually distributed into a truck-like shape (rather than into a tank-like shape) or whether they move their fins perpendicular to the direction of gravity?

It is about body shape or mass distribution.

I suspect it has a lot to do with the efficient arrangement  of muscles for propulsion.  The typical fish undulates from side to side, so considering leverage &c, a body that's deeper than it's wide probably works better. Wider fish like rays & anglerfish either use a different propulsion mechanism, or are sedentary.  Whales & dolphins move their flukes vertically, and AFAIK are always more round than tall.

While the most popular image of a fish for many is as you say, a more "vertical" than horizontal body shape, however there are many different adaptations to body shape depending upon the lifestyle of the fish. An ultimate example would be the flat fishes, such as flounder and halibut, which lay on one side essentially flat on the ocean floor or other similar surface. These fish however have adapted to have both eyes on one lateral side. There do exist other fish, such as some angler fish, especially in the family Lophiidae, which are more wide than tall, and they sit on the ocean floor and use a lure like appendage to attract prey so that they can ambush it, using their fins more to walk along the bottom surface. The feeding/hunting style is also highly related to the body shape of a fish, some shapes are more suited for moderate constant speeds, while others are suited for short quick bursts. Generally though, flat fish are not well suited for swimming at the middle of the water column, giving them a smaller habitat in which to live, while the more commonly found fish body shapes are used by much more species throughout the water column.
More information from MEER:
More information regarding Fish locomotion on Wikipedia.

Rays are flat too. Cetaceans also are broad and they are decent swimmers.

The flat fishes seem to be to be sort of an extreme example of a "vertical" body orientation, at least in that their developmental dorsal-ventral axis is the long way, it's just that they live on their sides. Rays of course are quite the opposite.

I think we can all agree that cetaceans are not fish, but their body shapes and locomotion patterns are worth looking at. Unlike most fish, cetaceans use their horizontal caudal fins in an up and down movement, whereas most use their vertical caudal fins for a lateral to lateral movement. I agree that flatfish are an extreme example, however monkfish are a different example, although they are quite sedentary and their fins have developed more to propel them along bottom surfaces like feet than they are adapted for swimming.

The link talks about the balance of stability and speed. I assume the most hydrodynamic shape (eels) is the best for speed so how does the tall shape help the stability? I'd guess "gravitational" stability (the ability to balance gravity) is what we talking about here.

Some fish are built for short rapid movements while some are able sustain fast movements for long periods of time, like tuna. Gravity is not a factor in the sea, but buoyancy is. However buoyancy is controlled with a swim bladder in most fish. Here stability refers to a fish's ability to make angular turns and resist opposing currents etc.

Swimming below the water surface, when you can tune your body density to obtain neutral buoyancy (as fish do), the axis of the swimming motion with respect to vertical is indifferent.
And indeed, there is a very wide variety of orientations of body plan for fish, from the vertical axis dominated body plans and motions (e.g. bream) to the more horizontal body with vertical swimming axis (e.g. monkfish) of mixed motion (e.g. many rays) and down to flatfish. The evolutionary constraints are thus rather on other advantages awarded by specific body plans (e.g. camouflage, angle of vision,...)


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In what ways have plants and animals evolved to support each other throughout history?
I'm curious about how plant and animal life have been able support each other throughout time and how each has evolved in a way that would help the other?
For example I have heard that plants have evolved to attract animals, such as bees in order to allow for pollination.  These plants produce smelly flowers that are usually white....  or colorful, non-smelling flowers.  By allowing bees to collect nectar for themselves and their hive, the plants are able to be pollinated in the process.
Earlier today I was noticing a bird hopping up branches of a tightly branched tree, which made me think of how plants and animals would support each other throughout time.  Trees are usually homes for a lot of animals, including birds, so I was curious about the evolution of trees to allow for tigher canopies to protect animals from the weather/elements.
My question is, how have plants and animals influenced each other's evolution, by helping each other throughout history?

This extremely vague and broad. You are basically asking about all sorts of coevolution and symbiosis, and this is a huge topic within evolutionary ecology.

There are probably a few cases of this and exactly how animals and plants co-evolve probably differs between different scenarios. One 'famous' example I like is between ants and acacia plants. The acacia plant has evolved to produce food for a particular species of ant and in return the ants protect it from the grazing of herbivores.
Explained better here: http://bioblog.biotunes.org/bioblog/2007/10/02/cool-bug-9-acacia-ants/

Thanks for the information.  This actually reminded me of something I heard regarding grass.  It was mentioning the smell that we get from cut grass is apparently a defense mechanism that will alert certain insects to help protect the grass from predators...  I believe there was mention of some sort of sound/vibration that aids this, but I could be wrong and it could just be the smell factor.


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What's the difference between germ line and germ cells?
I'm currently reading some introductory chapters about genetics (in Campbell's book, chapter 13) and I realized that I don't really understand what is the difference between the germ line and the germ cells.
From what I read so far, I understand that germ cells are specialized cells from which gametes are produced, and I suppose that the germ line is the "set" of all germ cells + gametes, but for some reason I couldn't find a good definition of what the germ line is and I was not satisfied with what I found in books and on the internet (because it was not as clear as I thought it could be)...
So, even if I'm ashamed to ask... Could someone explain to me the difference between those two concepts? Thanks in advance!


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What is exactly a phosphoester bond?
I've spent some hours trying to understand what exactly is a phosphoester bond, but I'm still confused and at this point I just want to throw myself out of the window. I've already read that post which treats the question but it doesn't really help me since, according to the link given by WYSIWYG♦:

A phosphoester bond is a bond between the phosphorous atom of a phosphate group and an oxygen atom.

But considering the answer of electronpusher:

Each nucleotide contains one phosphoester bond (between a phosphate O and sugar 5'-C).

It doesn't really make sense to me, since such a bond (in a nucleotide) is not exactly a bond between the phosphorous atom of the phosphate group and an oxygen atom (that is, it's a O-C bond, not a P-O bond).
So, what is exactly a phosphoester bond? Is it a O-glycosidic bond between the sugar (ribose or 2'-deoxyribose, in a nucleotide) and the phosphate group? Or is it the bond that there is between the phosphorous atom of a phosphate group and an oxygen atom of the same phosphate group?
I'm really confused and desperate by all this, so any help would be greatly appreciated. Thanks in advance!

You can find a diagram of the structure of a phospho diester bond in any biochemistry text eg. Lodish et al. and the definition: "A covalent bond in which two hydroxyl groups form ester linkages to the same phosphate group; joins adjacent nucleotides in DNA and RNA". So the question is do you know what an ester linkage is and do you know what a phosphate group is? If not you should try WIkipedia or a basic chemistry book. I shall vote to move to SE Chemistry but you should be able to answer this yourself.


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DNA replication precision
This will sound as a super stupid question, but I just read in the Molecular biology of the gene book (7th edition, Watson, Baker, Bell and al.) that one mistake occurs in 10 million nucleotides added during the replication of DNA.
However, I read in the Campbell's biology book (11th edition) that it is one mistake in 10 billion nucleotides added.
I tried to google it and kept finding these two numbers... probably because people use the same books as I do as sources. So, my question is the following: which book is right about DNA replication precision?
Thanks for your help and sorry if my question isn't very interesting.

Can you provide some longer passages from those books? I suspect one is reporting the number of errors before correction, and the other is reporting the number of errors after. That said, you should consider either number as a very rough approximation to within a couple orders of magnitude to interpret it generally.

Also, what organism are the books considering? Different organisms have different mutation rates. Trying to get something meaningful from these random numbers is useless.


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What species is this bird (found in Cousset, Switzerland)?
A friend of mine saw that bird in Cousset, Switzerland but it doesn't look like anything we know or we've already seen before around here. Does anyone have an idea of what species it could be? Thank you in advance (and sorry for the bad quality of the picture)!

This is really hard to tell given the quality of the picture. What size was it?
Could be Emberiza citrinella, the so-called yellowhammer - a year-long resident in Switzerland. It is about 16 cm in size and its breeding season starts beginning to mid-April and males are advertising for females in a golden plumage.

Again, this is only a best guess and without a better quality image it can never be more. RHA pointed out in the comments that the head of the bird in your image appears to be darker than one would expect in E. citrinella, suggesting it could also be E. melanocephala - the black-headed bunting, Spinus spinus - the Eurasian siskin, or Serinus serinus - the European serin. But consider this:

The bird on your picture appears to have a somewhat dark head but it does not seem to be black (but with the resolution it is hard to tell). E. citrinella males have brown stripes on their head that can be more or less pronounced (see examples in Google search for yellowhammer) - blurred, this fits the brown head in your picture.
In your comment, you give the bird's size as the size of a house sparrow which exactly fits E. citrinella.
E. melanocephala males have a pitch black head and the range it can be found does not fit your location. There are reports of vagrants but in combination with the brownish head in your picture this seems somewhat unlikely to me.
Sp. spinus and Se. serinus are smaller (max. of 12 cm in length) than what you describe.
Se. serinus is a partial migrant in Switzerland which decreases the probability of finding it in April, compared to a year-long resident. Additionally, it also only has brown stripes on its head.

In summary, I think the the most parsimonious call is that the bird on your picture is E. citrinella. However, keep in mind that it could also be one of the other species mentioned above, with E. melanocephala - given your size description and the dark head - perhaps being the second most likely identification.

My friend says it was as big as a house sparrow... We think he escaped from somewhere and I thought of an american goldfinch first, but I don't really see why a goldfinch should escape from somewhere in Europe.

@AlissaDeschamps: That fits the size of E. citrinella as well.

I know, I was just reporting the exact words of my friend ;) Thanks for your help anyway :)

The bird in the (vague) picture clearly shows a black head, that lacks in E. citrinella. Can you explain how you can rule out other species that have a dark head, for example Carduelis spinus, Emberiza melanocephala and Serinus serinus? @AllisaDeschamps

@RHA: I mentioned the bad quality in the picture. There is a reason why I think it is most likely E. citrinella. I'll edit the answer to make that more clear.

Thanks for your edit. I am still not convinced it is E. citrinella, but your answer reflects the doubts now well enough IMHO.


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Why is it unlikely that bathroom smells can pose health risks?
Based on a little bit of internet reading, it appears that odor molecules that enter your nose from human feces are of little concern to your health because the harmful stuff, like the pathogens, are not likely to be picked up and carried through the air.
This seems to make sense, however due to my limited knowledge of biology, I am having a difficult time distinguishing WHY the bad stuff is not likely to become airborne whereas other molecules can, and will cause damage by smell. Chlorine, for instance, will cause some significant damage simply by smelling the airborne fumes (which I assume are the molecules doing the damage).
I have to assume it is a natural defense mechanism that something that smells bad is not something you want to be around (CO being a major exception) but it seems that feces molecules are not a concern. Why?

Being around excreta is bad for health, because of the pathogens that breed in it. As a result, due to natural selection, we have developed an aversion to being around excreta, for safety reasons. Chlorine on the other hand, reacts with moisture in your nose/lungs and becomes HCl, which is never good to have inside your respiratory system.

So can we conclude that you can indeed get sick from simply being in bathroom that 'smells' foul, or does our aversion protect us from this?

@JAlecksen I think the point is that there are (roughly) two reasons to evolve an aversion to a smell: 1) The compound smelled is/can be harmful, or 2) The compound smelled is a marker for something that is/can be harmful. In case (2), it isn't the compounds you actually smell that are harmful, it is the presence of potentially harmful bacteria, etc. Chlorine is an example of (1); bathroom odors are an example of (2).

You can't fall ill from being in a modern sanitized toilet. You can fall ill from hanging around feces in your day to day life, and not being clean about handling it.

Mostly, what you're smelling are volatile small molecules: stuff like butyrate, indole, mercaptans, hydrogen sulfide, etc. These molecules are thousands of times smaller than even the smallest pathogens, being measured in Angstrom vs. nanometer scales. Pathogens are just too large to be actually volatile, in the sense of freely escaping into the air. And fortunately, these volatile organics are not nearly as reactive as something like chlorine gas. (If they were, imagine the damage they would do, at a much higher concentration, to the person they were just inside.)
Now, if someone had literally just projectile-vomited (or if excreta were churned around, e.g., by flushing), it's possible that a very small pathogen like norovirus could spray outwards in an aerosol. Since norovirus has a very small infectious dose (on the orders of tens of viral particles) this could be enough to make you sick, and indeed, aerosols have been implicated in norovirus transmission, though it's not that common. But the smell would remain long after any viral particles in aerosols had settled down onto surfaces.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4692156/

Great answer, of course it also makes me wonder why our bodies have not evolved to recognize the bad pathogens as smelling bad. This seems like it would be a good defense mechanism...

@JAlecksen I think one issue might be that by the time there's enough pathogen in your nasal passages to be able to detect it as a "smell", you're hopelessly contaminated. Far better to be able to detect pathogen-associated volatiles which can be detected before you get close enough  to pick up the pathogens. That way you can keep your distance. The smell molecules themselves are not harmful, they just indicate that harmful things are nearby, and you should keep your distance.


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What does "sect." mean?
For example, Centaurea sect. Microlophus

Section, a taxonomic level. In plants it's a possible level between genus and species.
See also https://en.wikipedia.org/wiki/Section_(biology) as the term is used differently in zoology.

So in my example above Microlophus is a Section? And is this different from Genus - Species - Subspecies?

@AlLelopath Yes. It's different because Microlophus is a group of species within a genus. If you have subspecies, those are within a species. All of the levels are quite arbitrary, but are used to avoid having to rename things every time you discover or want to emphasize some particular aspect of taxonomy.


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Test for e. coli in murky water
We had some tests done on some stream water. In the results report, the lab said:
The coliform/e. coli test was requested and [we] attempted to test for the bacteria but the sample was too dark in color to run the test, therefore, a result for coliform/e.coli is not available. This test requires a sample with little or no sample color to successfully read the color change that is performed during the test.
The test method is SM 9223B
Is there an e. coli test that can be done on murky water?


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Would a clone of myself have exactly the same development (character, appearance) as me?
If I'd have a clone of myself (with my DNA) and I would record the development of that person, would I be able see exactly the same development as myself (same personality, appearance)? For example that at a certain time, that clone would look how I looked like when I was 8?

Appearance, personality etc. are also influenced by the environment (persons around your clone, geographic location, eating, sporting etc). So there are a lot of other factors which need to be the same. Further not only the sequence is important but also  epigenetics ( like methylation of DNA)

No, your clone would differ from you. Actually such clones exist in humans also. Monozygotic twins are clones. They certainly look alike but they definitely differ in some respects.
Understanding why this is true require one to understand the concept of heritability from the field of quantitative genetics. You should definitely have a look at the post Why is a heritability coefficient not an index of how "genetic" something is?. The main reason why you would differ is because our phenotype (personality, appearance, etc...) also depends on the environment we experience.

your come would be even more different becasue it would have a very different in utero environment, this can have a rather strong effect. You how to wonder how different monozygotic twins would be if they did not share the same womb.

@John I don't fully understand your comment due to the typos. Yes, of course, the correlation coefficient between twins depends on whether they share the same environment (again, see Why is a heritability coefficient not an index of how "genetic" something is?) which includes the uterine environment.

Sorry, that should say "Your clone" I was pointing out that the clone of an adult would have a drastically different in utero environment. This could lead to some surprising differences, in some organisms (not humans that we know of) it could even mean your clone is a diffrent sex. http://onlinelibrary.wiley.com/doi/10.1002/dvdy.23924/full

In eutherian mammals, sex is determined by sexual chromosomes though, not so much by the uterine environment. But it is true that the uterine environment can be very influential. It is also true that many species that do not have a uterus, parental care will affect sex determinism.

I did say not in humans, I should have moved that to the end so you knew I was referring to sex specifically. Now epigenetics may affect sex in humans by modulating the gametes but that will not have an effect on your clone.

Yes, not in humans and not in any species that have a uterus I would think as all uterian mammals have sexual chromosomes to determine sex. But I might be wrong. I have not read the paper.


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How do we know we have to use the mouth for eating and drinking?
I have a question that I am very curious to: how do we know we have to use the mouth for eating and drinking? Because we have multiple openings where, if we didn't know better, could put food and drinks in. So there must be someone who started with eating via the mouth and started to teach their children.
I spent many hours on the internet, but did not find any answer.

It's an instinct, there's no teaching involved. You're better off asking about the biology of this instinct.

The people who fed themselves through their other orifices died out, leaving only that minority who used that crying orifice. As they survived, it was taught to subsequent generations. Now it seems everybody does it that way.

Excuse me, I heard that this kind of logic is prevalent in the knowledge of sects and cities where artwork and nudity is banned. People become very confused... I also would not breathe with my head if no one told me. I would breathe with my armpits or something. You don't have to... If you put a some small foods in the other way round, and you stay upside down, you can regurgitate it and it will still be digested backwards through your digestive tract... try it at home one day. so you don't have to use your mouth if you dont want to. the world is an illusion anyway. why listen to reason?

Food doesn't taste good when you put it in your ear. It does when you put it in your mouth. So every baby who experiments with stuffing food into places, will quickly find that it's much nicer when put in the mouth. Not really much to it.

Quite frankly we don't, eating is instinctual, only later as we grow up do we learn why we do it. It is reinforced with learning later but that is a minor effect. Eating is one of the most basic of animal instincts.
The association "hungry > eating > not hungry" this could reinforce the behavior, but the instinct is present first. infants will learn eating stops hunger long before their brains have have even developed the capacity for abstract thought, and they will latch and feed long before that.
No human "figured out" or "started" eating, eating existed before brains existed. And every single organism between that first feeding organsm and you and me ate. Eating was hardwired into the genome long before parental care existed.

There are several reflexes that are hard-wired and present in newborns. The root reflex and suck reflex are two of them, among others. An infant doesn't have to know how to feed, it will automatically do that.
Once it is feeding through the mouth, the growing baby will have no reason to change its habit when starting on solid foods. Besides, its parents will start to spoon feed the baby by presenting food to the mouth. The parents will do the best they can to comfort the baby when its crying because of hunger. Stuffing the food in the wrong place won't aid that purpose.


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Is it possible to color sperm cells so they look more clear under a microscope?
Im working on something that requires me to check the velocity of a sperm cell under a microscope but I imagine it would be very hard for a program to keep track of the sperm cells.

You can check this http://www.vivo.colostate.edu/hbooks/pathphys/reprod/semeneval/morph.html


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What type of animation software is used to create these molecular motor motions?
Recently, I came across this video on molecular motor motion. Can someone suggest software that can do similar animations? I am not sure what they (at Harvard Medical School) used but the animations are really cool.

I'm voting to close this question as off-topic because it is not about biology.

Most any reasonable animation/modeling software can handle this sort of animation. I have developed an educational iOS app with interactive biological macromolecules, including several animations. Here is how I would approach this, I suspect something similar was done here.
The models are likely built up from PDB files, or equivalent. These files allow viewing and manipulating large molecules in 3D with special viewers.  Many 3D modeling/animation apps can also view and convert these molecules into polygonal models that can be used as components and then animated within the app. I use Cinema 4D, not cheap. There is a free, downloadable program called Blender. I'm sure Blender can handle the animation but not certain whether it can read and convert the PDB file. If not, there may be other options for this.
This is not a challenge to be taken lightly. The person doing the animation you reference also knew how to assemble the parts as well as how the movement is effected. There is also a steep learning curve to using this type of software.

Thank you for the suggestion about Blender. I did a search on importing PDB files into Blender. It seems like there is an extension called atomic blender that does just this.


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Can an octopus survive if one of its three hearts stops working?
While reading the book "The Soul of an Octopus" by Sy Montgomery, I learnt that Octopuses have three hearts. This is very fascinating. According to a Wikipedia article,  two of the three are used to  pump blood through each of the two gills while the third pumps blood through the body.
So, my question is can an Octopus survive if one of these hearts stops functioning?

This is not he definitive answer, but a comparison. Your own heart has two sides, one to pump blood to the lungs (for oxygen exchange, much like the function of gills), one to pump blood to the rest of the body. If one side of your heart stopped working, do you think you would survive? The question is whether an octopus can survive on one gill alone. In either case, it's survival would be severely compromised if at all possible.

I thought many people live with partially functioning hearts. Is that not true?

Not in the way I described. A poorly functioning heart still sends blood to both the lungs and the body but does each less well. There is right and left sided heart failure, but it's a relative failure, not full failure. Full failure of either side = death.

I heard that when some octopuses swim, their third heart (which pumps blood through the body) stops, which is why they tend to crawl.
I only heard it, though, and I haven't verified.


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Why does the scalp hair become grey first?
I understand that when the hair follicles produce less melanin or stop producing melanin altogether, hair becomes grey. But it seems like it is the scalp hair that becomes grey first. If follicles are producing less and less melanin, shouldn't the hair everywhere become gradually grey? Why is it that the scalp hair greys first?

Did you do any searching for an answer? What did you find? Please share, as per our guidelines on showing your research. Thanks.

I didn't do much research for an answer. Prior to posting the question, all I read was an article (https://medlineplus.gov/ency/article/004005.htm) that didn't explain it other than saying that it is usually the scalp hair that becomes grey first. Will research more. Should have researched more.  Thanks.

The answer is right in the article: "Graying is largely determined by your genes." Scalp hair is genetically programmed to go grey first if a person's hair will go grey.

What do you mean "scalp hair"? The hair on top of the head? As far as I know, it's the temple hair (above the ears) that usually go gray first. But in different people the exact place may differ, I've seen right above the forehead, as I've seen the beard too.

From my own observation, it's usually the chin & jaw that goes gray first, not the scalp.

@anongoodnurse "Determined by your genes" doesn't come anywhere close to providing an answer about a mechanism. Presumably the "genes" are the same in all parts of the skin.

@BryanKrause - why would you think that regulation of hair on the scalp and hair on the mons pubis are exactly alike? Skin cells have the same genes; some skin is thick, some is thin (and it's not solely due to use.)

@anongoodnurse I don't think all hairs are identical, just that all of the cells have the same genes - that isn't the same as expression. Saying "it is because of different expression of gene XYZ" is a good mechanism answer. Saying something "is determined by your genes" suggests you are talking about differences between individuals, which is not what the question is about.

@BryanKrause - A kinda fine line which I accept. Thanks.


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Is it better to maximize sleep, or align to ~1.5 hr cycles
What is better for the body, to sleep 6 hours (4 deep sleep cycles) or to sleep 7 hours, but interrupting the last sleep cycle. I know I feel a lot better with 6, but am curious as to its medical consequences. Does the brain have a chance to repair/clean itself properly with this lesser amount?

Personally speaking, I feel very tired if I have only 6 hours of sleep, but am totally ok with 7. Is this sleep cycle theory correct?

Neither
Sleep cycles do not have a set length.
sleep for 7 hours every night and you won't interrupt a sleep cycle. 6 hours may be fine for a person but it is unlikely.
You feel tired when you interrupt a sleep cycle becasue many of the sleep inducing hormones are still present in your system.
http://apsychoserver.psych.arizona.edu/jjbareprints/psyc501a/readings/Carskadon%20Dement%202011.pdf
If you are sleeping different lengths every night (or say sleeping longer on the weekend) that will also make you feel tired. Normally your body adjusts the length of your sleep cycle to how long it predicts you will sleep for, if that is constantly changing however it cannot do this and you often wake up in the middle of a cycle making you feel tired. Sleep the same length of time for ~14 days and you will see your sleep cycle stabilize.
http://journals.sagepub.com/doi/abs/10.1177/1534650103259743
https://www.researchgate.net/profile/Martin_Moore-ede/publication/15765130_Human_Sleep_Its_Duration_and_Organization_Depend_on_its_Circadian_Phase/links/557881b308aeb6d8c01f1715.pdf
http://healthysleep.med.harvard.edu/healthy/science/what/sleep-patterns-rem-nrem

The thing about sleep is that there is no "one size fits all". Think about it, if we are all biochemical different, then why would we all need the same amount of sleep? Why would all of our sleep cycles last the same amount of time?
I was once a severely insomniatic person. I would worry about not getting that perfect eight hours of sleep that everyone talks about being so important, and despite trying my hardest to get eight hours of sleep it would never happen. I would either get no sleep at all, or I'd sleep in and get over twelve hours of sleep.
One day I was talking with my professor who specialized in sleep, and he suggested that I aim for four or five hours of sleep and to see how I start to feel. He also said to pick a specific time that I want to wake up everyday. Oddly enough, it fixed my problems. I can now go an entire day without thinking about how tired and fatigued I am.
So to answer your question, it does not matter. Wake up when you need to wake up, and go to bed when you are feeling tired. If you find that you feel good throughout the day having only slept 6 hours, then only sleep six hours. If you feel tired throughout the day, then you might need more sleep.
Your body will "tell" you if you need more or less sleep. But you need to listen to it.
*Edit
What I'm saying plays in to what Raja's comment is getting at, "is sleep cycle theory correct"?


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Tissues in plants and animals

What is the equivalent connective tissue in plants?

Connective tissue in animals are mostly made up of collagen.

What about in plants?


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Ethics in Paleontology
Ethics in Paleontology
Fossils help researchers understand the evolution of many lineages of plants and animals. But, who actually owns fossils? What if an important fossil (say a transitional fossil like Tiktaalik or Basilosaurus) were found by an amateur fossil hunter and sold to a private collector? Should there be regulation of fossil hunting to prevent loss of scientific information? Should all "important" fossils be turned over to museums?

I'm voting to close this question as off-topic because it is not about biology.

It depends entirely on where the fossils were dug up. In the US fossils on private land belong to whomever owns the mineral rights to the land, that landowner can do with the fossils as they will. On public land the fossils belong to the government and to get a permit to dig them a paleontologist must have a place to store them, this is part of the permitting process (digging on public land without a permit is a felony). Most of the time this place is something called a repository, a public institution that has facilities to store and care for fossils, usually a museum or university and has contingencies so that the fossils will not be lost if the facility were to fail or close. Now this is for vertebrate fossils becasue of the nature of invertebrate fossils (chalk for instance is made entirely of fossils) the laws can be a bit more lax.
Private collectors can only collect on private land, which usually involves making an agreement with the landowner. Keeping collection records is always a good idea if for no other reason than to show where a fossil was found.
I have worked with both types of collectors private and public, good private fossil hunters will differentiate rare fossils and common ones and will donate rare ones to museums while selling common ones. Bad one will sell everything, which often does lead to fossils disappearing or in some cases being outright destroyed by those who disapprove of evolution and the fossil evidence for it. For this reason most journals will not accept publication made using private collections, becasue it makes repeatability impossible.
Now this is all in the US, other countries have different laws some more strict some less so.


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Why is there no U3 snRNP in the spliceosome complex of transcription initiation?
snRNP U1,U2,U4,U5,U6 are present in the spliceosome but there is no mention of U3.

U3 RNA with its proteins forming a complex is localized at nucleolar. The box C'/D motif in U3 snRNA is responsible for this localization. Therefore U3 snRNA does not have a chance to go to mRNA transcription active sites. Instead, U3 snRNP play important roles in ribosomal-RNA processing.
Because of necleolar localization, U3 snRNA is called U3 snoRNA alternatively.
https://en.wikipedia.org/wiki/Small_nucleolar_RNA_U3


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What is responsible for soft rot of organic matter?
In soft foods, for example, why is there a limited amount of time before consumption is no longer safe due to soft rotting of material.

Are you asking about why food becomes dangerous to eat or about why food becomes softer? They are related but some food softens without becoming dangerous or becomes dangerous without softening.

Both. Why some foods become dangerous to eat and also what makes the food become soft? Is it the decay of the organic matter inside the apple or is it a breakdown of the structural proteins on the surface?


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How do you calculate the charge on a polypeptide chain with changing pH?
I understand the charge placement on the N & C-terminus and also the utilization of the R-side groups in the amino acids.
For example,
What is the overall charge for a chain Glu-Cys-Arg-Asp with pH 11.0 buffer?

In theory, you can calculate the charge on every individual ionizable group (i.e. looking up their pKa and calculating charge by henderson hasselbalch) and just add them up to get the total net charge.
In practice you would need to measure it with something like isoelectric focusing, since polypeptides fold and certain groups end up interacting with other groups/being shielded from solvent, meaning you really can't calculate it accurately unless you had structural data and even then it would be extremely difficult.

This is about as straightforward as you can get for addressing a homework problem. For this, though, I think you can just eyeball the net charge if you know the R groups and pKa values: NH2(-1)(-1)(+1)(0)COO- = -2, for example. This may get a close vote due to the homework nature of the OP question, however.


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what benefits does lab procedure Realtime PCR have in gene silencing experiments?
RT-PCR performed in gene silencing but mechanistically what are the benefits of this procedure?

Can you please re-phrase your question? At the moment it is a bit unclear what you want to know exacty.

RT-qPCR amplifies mRNA molecules present in a cell, if you have the right primers for it. The whole point of RNAi (the "gene silencing" that I think you're referring to) is downregulating the expression of a specific gene, so you'd expect the mRNA transcript of said gene to be not present (rather, present at very low concentrations at any given timepoint) if indeed the interference has worked.
Therefore, after RNAi has been performed, you can check by qPCR that there are indeed very low levels of the specific mRNA present in the cell. You might want to also perform a Western Blot against control cells transfected with scramble siRNA (where nothing should be downregulated, think of it as an "empty" siRNA), to check that protein levels are indeed much lower than in "regular" cells.


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Does the assembly of the PLC transcription complex utilize phosphorylation in binding of the GTFs?
in the recruitment of general transcription factors during transcription initiation is phosphorylation utilized?


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gene duplicated on genome but is different
I've been looking at a miRNA cluster on a genome and I found it three times. The first two are right next to each other and look exactly the same, the third sequences is on a different scaffold of the genome and is both shorter and has a number of mismatches with the first two sequences.
Is there a particular name for this? The first two are most likely some sort of gene duplication, but I'm not too sure on what to call the third,
Thanks

That sounds line one of two things. Either a sequencing or assembly error (quite likely since you're talking about scaffolds so, presumably, not a completely assembled genome) or duplication and subsequent pseudogenization.
It is relatively common for genes to be duplicated and then to be rendered inactive by a mutation event. Such genes can still be detected in the genome and are called pseudogenes. The process of their creation is, unsurprisingly, called pseudogenization. You can think of such genes as fossils. They often have significant sequence similarity to the original and can even be transcribed.
A quick search brought up a couple of articles discussing the pseudogenization of specific genes:

Pseudogenization of CCL14 in the Ochotonidae (pika) family.
Pseudogenization of sopA and sopE2 is functionally linked and contributes to virulence of Salmonella enterica serovar Typhi.

That said, is also quite possible that what you describe is a simple duplicate that has diverged without becoming a pseudogene. The details will depend on the particular sequence. Are there in-frame STOP codons? Can the gene still be transcribed? Such duplication events give rise to paralogs (note that all three of the genes you mention would be paralogs of each other, it's just that one has diverged more than the others). You can read more about those here: What is the difference between orthologs, paralogs and homologs?


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How to start learning disease profiling?
I am student of Biological Sciences and interested to learn profiling in order to characterize the state of organisms (especially diseases). You know that there are different types of profiling like, Genome, Proteome, Metabolic and many more.
I am confused from where should I learn in order to understand principles of profiling.
Kindly, guide me.
Thank you!

Are you asking about various classifications of diseases?

Sort of! But characterizing diseases with molecular profiling. Likewise, all skin cancers are not equal but through profiling, we can classify.

I am focusing more on profiling. It's technique.

There are many results for the search "disease profiling." You can try this and ask what remains unclear.

Are there any books related to it?

Okay! I'll try.


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Why are there so many different humans yet chimpanzees are just chimpanzees?
There are two species belonging to the Pan genus (Pan troglodytes and Pan paniscus). That's just two.
I mean, humans have changed radically since we split from chimpanzees, we have Australopithecus afarensis, africanus, anamensis, Paranthropus robustus and boisei, Homo erectus, habillis and so on.
A chimpanzee fossil that is 2 millions years old should be pretty different from a modern one, why aren't they considered another species?

The rest you listed that are not Homo sapiens are evolutionary ancestors of humans. Not humans. Close to humans? Sure, some of them. But not humans.

@MCM Yeah, but my question stills stands even if they are not called humans.

Could you re-phrase your question? Are you asking why we don't find/identify more fossils of Pan ancestors?

There really is only one species "human" (Homo sapiens). I guess you want to know why "our" branch brought up a lot of species, whereas the "chimpanzees" branch remained nearly "untouched" since the last common ancestor? I'd say this is due to an greater expansion of our ancestors across a wide variety of different terrains.

@AstronAUT But what about those that stayed? Here's a modern Chadian (there are a lot of ethnic groups, but whatever), and heres a reconstruction of a Sahelanthropus Tchadensis/Toumai.

And to the wide variety of different terrains and climates, one might consider the possible impact of the genetic drift due to population bottlenecks that seem to have been significant in the history of human expansion.

I'd guess it is just sampling bias. Humans are dis-proportionally interested in humans so they spend more time looking for human fossils than Chimpanzee fossils. In addition there is the lure of declaring you found a new Homo species instead of declaring you found one weird-looking part of a known Homo-species.

There is an inherent flaw in your question. Humans did not split from chimpanzees. Humans and chimpanzees descended from a common ancestor. The modern chimpanzee lineage has made a similar number of evolutionary steps since the branching from the last common ancestor as the modern human lineage has. Australopithecus is an entirely different genus in the lineage that lead to modern human. Similar changes happened in the Chimpanzee, Bonobo, Orangutans, and Gorilla lines, until we reach the modern day lines that are examples of the survivors of the split millions of years ago.

The first chimpanzee fossils were found in 2005 http://www.nature.com/nature/journal/v437/n7055/full/nature04008.html and date back to ~500K years ago... the have been very few fossil finds for the chimp lineage, so unlike with Lucy which gets us back to about 3.3 million years ago for humans, we have not uncovered the same artifacts for Chimpanzees. It could be that the range of the Chimpanzees was not conducive to the fossilization and preservation of bones that the human lineage was afforded.

There's also a question of perception. As humans, our brain is very good at distinguishing other humans, so we see enormous variety whereas we are not good at seeing differences in chimpanzees, so they all look alike. In reality, present day humans are all one species; I don't know if the variability in humans is actually larger than in chimpanzees (or any other species), considering there are about 30000 times as many humans as chimps. There's a similar argument about human fossils if we classify them in far too many distinct species or if it's individual variability.

For fossils the answer is simple chimps live in forests and forest are really bad at preserving fossils, we lived in savannah which include some floodplains which are really good at preserving fossils. Thus we find a lot more human fossils than chimp fossils.
Otherwise Chimps exhibit far more genetic diversity than humans. humans are just a weird branch of chimp.consider the genetic diversity below. If we were not so  morphologically biased we sould easily conclude all hominids as just one species based on genetics.Chimps actually have quite a wide morphological variation its just we as humans are far better at noticing human variation.

Can you please give the reference for this graph?

Its from this royal society publication http://rstb.royalsocietypublishing.org/content/366/1567/1080 a more detailed and updated version is available here http://ucsdnews.ucsd.edu/archive/graphics/images/Gagneux_et_al_PNAS_1.jpg

Cool +1 I am surprised there is really so little genetic diversity in humans despite our gigantic population size. I suppose we only very recently went through population expansion and still have the genetic diversity of a small population. But chimpanzees typically have rather small populations...

It could also be that humans keep killing of entire bloodlines and tribes, technology makes conquest easier. This is just an idea however.

That's just two [species of chimpanzees]

C'mon!
There is a huge behavioral gap between the two species. I get your point that the human lineage had several, not just two, forms. Yet these two chimpanzee species are so brutally different that they make most of our "human diversity" seem so regularly the same.
About your question - it seems obvious to me the point brought by @Pete: That we, humans, came from the forests to the open land, which brought the seas and continents to us. Many different habitats would lead to wider variation.

A chimpanzee fossil that is 2 millions years old should be pretty
  different from a modern one

Why should it? The African Forests changed drastically in the last 2 million years? If not, then why should chimpanzees have changed? Take a look at the horseshoe crabs (Xiphosura, Limulidae): they've been that way for hundreds of millions of years! The punctuated equilibrium seems to be the norm, more than the exception, doesn't it? (I remember the horse evolution through the Mesozoic, apparently linear, but in a closer look there ain't some teeth in the line? Aren't there plateaus - long periods of stability - among the high precipices of sudden genetic/form/function change?

I think this is the first answer that looks like an answer, but it still needs to more clearly deconstruct the question. 1-The difference is greater than the species count suggests; we're missing chimp data. 2-Humans are more similar than you think, but they have had more dynamic geographical selection pressures to amplify their differences. 3-It's common for much less change to occur than what we see in both these examples.

Chimpanzees are relatively isolated and confined in so far as their environment, it's all much the same... forest. They haven't been subject to the environmental factors humans have... arctic, tropics, deserts, mountains etc. Therefore there hasn't been the need to change as much. Animals adapt to their environments, chimpanzees only have one, humans have hundreds.
If you have a look at the humans living in the same distribution area as compared to chimpanzees then you'll see that they don't have much variation either for that area.

Chimps haven't been subjected to tropics and mountains?

They certainly have

@AliceD I think Pete is trying to say that humans cover a much more varied ecological environment  due to our greater expansion. This is a good point.

Chimpanzees have only been subjected to a specific type of mountain and tropical environment. Humans have inhabited every type of mountain range and tropical environment there is... Hence our greater adaptive variations.

@Alex This is a good comment that Pete has made, but it's not an answer.


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How to troubleshoot islet isolation
I have been getting very low yield from islet isolations from rats.
My procedure is as follows:
Inject the pancreas with 5mL Liberase (1 wunch unit/ml) in HBSS + HEPES through the CBD (decent inflation, atleast of the frontal part of the pancreas) and excise it to an Erlenmeyer flask with 5mL Liberase in HBSS + HEPES on ice (takes ~10 minutes).
Once all animals have been processed, I incubate for 21 minutes at 37C.
After incubation, I shake for 5 seconds and stop digestion using HBSS + 10% FBS. I sediment for 20 minutes and homegenize again using a wide-tipped pipette.
The tissue is pelleted and dissolved in 20mL Histopaque gradient. Spun at 380g for 20min at RT.
Wash twice in culture media and handpick islets.
Can anyone flaw my procedure or give me some clues as to what might cause very low yields in general? I've read somewhere that blood and fat tissues might inhibit digestion. Does anyone have any experience with this?
My current concern is that the islets are over digested.
Thanks in advance.
Jesper


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What will happen if the biceps stop contracting and instead triceps contract?
For example if i bend my arm the biceps contract and triceps relax but if I bend my arm and the triceps contract instead of biceps what effect would it have?

your arm wouldn't bend...

I'm voting to close this question as off-topic because this question is too trivial

When your triceps contract your arm straightens out.

This can be termed co-contraction of antagonist muscles, and it can occur in several pathologic processes. It essentially results in a spastic state.
Yelnik et al. describe the state as:

Spastic co-contraction is defined as an "unwanted, excessive, level of
  antagonistic muscle activity during voluntary command on an agonist
  muscle, which is aggravated by tonic stretch in the co-contracting
  muscle" (2, 8). Spastic co-contraction in patients with spastic
  paresis is a descending phenomenon, most probably due to misdirection
  of the supraspinal drive. It may be facilitated by increased recurrent
  inhibition, causing loss of reciprocal inhibition during voluntary
  command (2, 9).

For example, this can occur with perinatal brain damage. See a study by O'Sullivan et al. titled "Abnormal development of biceps brachii phasic stretch reflex and persistence of short latency heteronymous reflexes from biceps to triceps brachii in spastic cerebral palsy."
The state of co-contraction can be produced in healthy individuals as well, and studies on joint biomechanics under these conditions have been done. See Wise et al.


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Are oxygen and carbon dioxide simultaneously present in red blood cells during gas exchange?
From my understanding, the process that displaces the carbon dioxide and oxygen in our erythrocytes and lungs is diffusion. I've been taught that diffusion is the net movement of particles from a region of higher concentration to a region of lower concentration, until an equillibrium is reached.
For there to be an equillibrium in carbon dioxide and oxygen, doesn't that mean that there should be equal portions of those elements present at all times? So therefore, erythrocytes should contain both of those chemicals simultaneously. Am I correct in assuming this? If I am, then I have a follow-up question: wouldn't carbon dioxide floating about in our blood indefinitely cause some unhealthy side effects, and is there something that prevents it from doing so?
I'm currently only in GCSEs, so apologies if this question might actually have a very simple answer.
Thanks

There in fact typically is an equilibrium of diffusion for both oxygen and for carbon dioxide by the time the blood finishes gas exchange in the alveoli of the lung. One confusion in the OP is that there is no real meaning for a chemical equilibrium between carbon dioxide and oxygen, as they are separate chemical entities. Carbon dioxide in the lung capillary blood equilibrates with carbon dioxide in the lung alveolar gas; oxygen similarly equilibrates between blood and gas. Each effectively on its own.
Yes, oxygen is continually being consumed and carbon dioxide being produced by the body, so from that perspective we have a whole body steady state. At overall equilibrium we are dead. But at the site of gas exchange in the lung, there is generally no difference in the chemical activity of either gas between the alveolar air and the capillary blood leaving the alveolus. So from a chemical perspective there is generally local equilibrium of both gases at that point.
In some circumstances this local equilibrium is not reached. The transport of carbon dioxide is very complicated, as it exists in several inter-convertible forms: dissolved carbon dioxide gas, a form called carbonic acid where it has chemically reacted with water, the bicarbonate and carbonate ions that come from dissociation of carbonic acid, and a carbamate form that is a reversible chemical bond with amino groups on proteins. The reaction with water is slow on its own; it is catalyzed by the enzyme carbonic anhydrase in red cells. If that enzyme is inhibited (for example, by the drug acetazolamide) then there might not be chemical equilibrium of total carbon dioxide between alveolar air and capillary blood as there might not be enough time, as blood flows through the alveolus, for all the other forms to convert to the dissolved gas that can diffuse from blood into alveolar air.
Another complication is that transport of oxygen and carbon dioxide in the blood are somewhat interdependent. Acidification by carbon dioxide (lower pH is more acid) affects the ability of hemoglobin to bind oxygen, tending to release more oxygen. Nevertheless, in most circumstances in humans, both gases are individually at equilibrium between alveolar air and the blood that leaves the alveolus.
Finally, the continued presence of carbon dioxide in the body is a normal, healthy part of physiologic functioning. It does have to be kept in balance, but it does have to be there.

For diffusion to occur there must be a "concentration gradient", that is one area where the substance that is diffusing from, to where it is diffusing to. Where the substance is diffusing from, the concentration is high and where it is going to, the concentration is low. Our bodies continually use up oxygen and produces carbon dioxide. Carbon dioxide is generally carried in the blood plasma, and oxygen is generally carried by the red blood cell (erythrocytes).
Whereas, it is true that in diffusion an equilibrium is usually achieved, in this case you mention there is no equilibrium. Our physiological processes (respiration) continually maintains that concentration gradient and so carbon dioxide always flows out and oxygen always comes in. Too much carbon dioxide in the blood will raise the pH and cause serious metabolic problems with enzymes and their efficient function.

Diffusion can (and in this case, typically does) lead to local equilibrium in lung gas exchange. This was determined by extensive work during the first 3/4 of the 20th century. Also, increasing carbon dioxide lowers rather than raises blood pH; acidification is a lowering of pH.


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trp operon repressor
Does trp repressor form a tetramer or a dimer before it binds to its corepressor tryptophan?
I've been reading BIOS Molecular biology it says that it is a dimer

The repressor is a dimer of two subunits that have structural similarity to the CAP protein and lac repressor.

but according to wikipedia it is tetramer. What is correct?

Revised answer summary
My original answer provided evidence that the trp repressor is a dimer, and that conclusion stands, especially as regards its functional form. I still regard the statement in Wikipedia that it is a tetramer as incorrect, although I now see how it might have arisen. It seems to be a misinterpretation of results in vitro that show an equilibrium can exist between dimer and tetramer (not tetramer only). I have expanded on this in an additional section.
A functional dimer
The functional form of the is certainly a dimer, as originally reported by Schievitz et al. (1985). The summary of this paper includes the statement:

“The crystal structure of the Escherichia coli trp repressor has been solved to atomic resolution. The dimeric protein has a remarkable subunit interface in which five of each subunit's six helices are interlinked.”

It was crystallized in combination with the operator DNA, and the structure deposited in the Protein Database (PDB) as 1TRO. I reproduce an image from the PDB entry below. Many other DNA-binding proteins also have dimeric structures.

A dimer–tetramer equilibrium observed in solution
The statement in Wikipedia probably arises from a report by Fernando and Royer (1992) — subsequently confirmed — that in solution there is an equilibrium between the dimer and higher oligomers (the tetramer predominating). Tryptophan was found to shift the equilibrium to the dimer. The authors claim that this has physiological relevance, although this still seems a moot point.

I have revised my answer, explaining the situation with the tetramer. Wikipedia is incorrect, but it is important to realize that Wikipedia consists entirely of the voluntary work of people like us. It doesn't claim to be correct, only correctable. I feel that it is an obligation of those who find mistakes to correct them (if they can do it easily and with authority) and I shall do so myself in this case. I encourage others to do likewise.

I have now edited the Wikipedia page. I also deleted a reference to nucleoplasm in this section, which should have been removed long ago. Needless to say, bacteria have no nuclei and no nucleoplasm.

I saw you editing today. The original article was poorly written.

@SanjuktaGhosh — Unfortunately many of the articles on transcription  in WIkipedia are poor or out of date. The main article is terrible, failing to distinguish between eukaryotic and prokaryotic systems. The problem seems to be that when Wikipedia started there was an initial surge in enthusiasm, but the updating has been very uneven across topics. Younger people who try to help are often brought up on eukaryotic molecular biology and are unaware of the older work on what then were the only tractable systems — prokaryotes. Specialists generally have little time or incentive to contribute.


text:
Origin of the double membrane of mitochondria and chloroplasts
Most websites and textbooks say that the double membrane of mitochondria and chloroplasts are a result of the endocytosis of ancient prokaryotes (the outer membrane is from the vesicle containing the prokaryote, the inner membrane is from the prokaryote itself).
However, some sources say that this is not the case. The precursor to the mitochondrion (alphaproteobacteria) was a gram-negative bacteria, which has a double membrane. This site says that the reasoning for the double membrane that is often taught is a lie, and that the mitochondrial precursor had a double membrane already to generate ATP through the ETC.
So, if this is the case, why do mitochondria now have two membranes, and not three (two from the prokaryote and one from the vesicle)?

This is a genuine question about your question; why would the Gram negative bacteria need to have a vesicle? Perhaps it the case of Gram positive and vesicle versus Gram negative only.

@James How would the Gram negative bacteria (or any bacteria) be endocytosed or enter the cytoplasm of the proto-eukaryotic cell if it's not surrounded by a vesicle?

From the link you shared "It's simply not true that the double membranes of bacteria and chloroplasts were the result of endocytosis." After a brief bit of googling and reading some comments by internet folk I am convinced that the third membrane could be lost. I still can't answer the question though. Very interesting!

The answer lies in the protein composition of mitochondrial membranes, which undoubtedly prove that the outer membrane (OM) is of alphaproteobacterial origin, and the phagosomal membrane (if there was any) is lost. Though the endosymbiotic origin is without question, bear in mind that the phagocytotic origin is still debated (cf. López-García & Moreira 2015). And if the symbiont has entered the host some other ways than phagocytosis (cf. papers of Tom Cavalier-Smith) or syntrophic engulfment (cf. papers by Bill Martin; Searcy; López-García & Moreira) (e.g. puncturing the plasma membrane as a pathogen), then there never was a third membrane.
From Symbiogenesis Wikipedia:

Porins (transport proteins) are found in the OM of mitochondria and
  chloroplasts, are also found in bacterial cell membrane (Fischer et
  al. 1994Zeth & Thein 2010Fairman et al. 2011). The
  membrane lipid cardiolipin is exclusively found in the inner membrane
  of mitochondria and bacterial cell membrane Mleykovskaya & Dowhan
  2009.

According to many (Cavalier-Smith 2002, Cavalier-Smith 2006, Zeth 2010), the presence of β-barrel transport proteins proves that the OM evolved from the bacterial OM, not from the host food vacuole membrane. Both mitochondria and plastids contain in their OM β-barrel proteins (e.g. Tom40, Sam50 and porins in mitochondria, Toc75 homologue of Sam50 and their joint negibacterial ancestor Omp85 in chloroplasts) and these are only present in the OMs of gram-negative bacteria (cf. Schleiff & Soll 2005). All Alphaproteobacteria are gram-negative, hence the ancestor of mitochondria originating from the Rickettsiales or very close was also.
Note, that many secondary and tertiary plastids still retain their third, outermoest phagosomal membrane originating from the host's plasma membrane (cf. Keeling 2010).


text:
Machine-readable APG III trees?
Does anyone know where I can find a machine-readable version of the phylogenetic trees from APG III?  I'm looking for something that contains the full tree structure, including unnamed branches.  (i.e. not merely a list of which families are contained in which orders.)
The trees at the APG III site are graphic images -- not easy to turn into a data structure.

Just email the curators. peter.stevens@mobot.org (Missouri Botanical Garden), or stevensp@umsl.edu (University of Missouri, St Louis)


text:
What is this insect found in Melbourne, Australia?

This photo was taken a few days ago (late May 2022, during daylight hours) on a timber deck in the northern suburbs of Melbourne, Australia.  The animal is roughly 3cm long.  The photograph shows shed fur from a Jack Russell terrier for size comparison.
When a larger animal moves near these insects or they are disturbed, they react by raising their abdomen with its spike in a manner similar to a scorpion.  Otherwise, they seem sluggish and slow-moving.
There have been a dozen or so of these insects seen in the area over the last few weeks, but they haven't been seen in previous years.
Given its six legs and segmented abdomen, I'm assuming that it is an insect of some sort.
Can anyone identify this animal?

Also, check the gum trees nearby for defoliation. That’s probably their food.

This appears to be a sawfly larva. Sawflies (Hymenoptera) are a widespread group of insects with a few thousand species. However, Australia doesn't have many species, and this one is fairly distinctive. I think it is either a long tailed sawfly larva or a bottlebrush sawfly larva. There are a few pictures of some members of the Australian species at Brisbaneinsects.com. One distinctive feature of many of the species in this family are that the larvae cluster together in large masses. As you are only seeing single ones, it is likely that you are seeing the long tailed species as this one doesn't cluster.
They are related to the wasps, bees and ants, but won't sting. They can release a smelly substance when disturbed.
I found this image at "whatsthatbug.com", which is similar to yours.

I agree that it's a sawfly larva, but it doesn't look like either a long tailed larva or a bottlebrush larva.


text:
Why human skin colour disprove natural selection?
Amount of melanin decides the darkness and fairness of skin.
The darker the skin is, larger the heat energy it will absorb from sunlight.
The lighter the skin is, less will be the heat energy absorbed.
The people in cold regions of world should have darker skin to absorb much heat available. And people in hot climate should have reflexive white skin to reflect much heat from sunlight.
But here's exactly opposite of it. Why?

Melanin is there to protect skin cells (their DNA) from UV light, not to "absorb heat".

Also, even having traits that are not beneficial does not "disprove natural selection". If our own skin color would disprove such a fundamental part of the theory of evolution, it really wouldn't be around anymore ;-)

Your conclusion is actually the exact opposite of the reality.
Light skin in colder climates (i.e. climates that have short winter days) is selected for because melanin blocks the absorption of 310nm UV light which is needed to produce vitamin D.
The evolutionary significance of vitamin D, skin pigment, and ultraviolet light; RM Neer,
Am J Phys Anthropol. 1975 Nov;43(3):409-16.
The less melanin you have, the more UV you absorb, the more Vitamin D you produce. As Neer says, "Vitamin D deficiency can cause death, immobilization, or pelvic deformities which prevent normal childbirth." Vitamin D deficiency can be fatal, so the harder it is to produce, the harder it is to produce Vitamin D, the less likely you will be to survive and reproduce in areas where days shorten for 6 months out of the year as a result of the tilt of the earth.
This can be witnessed in the lengths that societies living closer to the poles go to to supplement natural Vitamin D production, adding Vitamin D to dairy products or as this famous National Geographic photo shows , exposing children to doses of UV light.

- Ultraviolet Bath, Russia by Joe McNally

http://photography.nationalgeographic.com/photography/photo-of-the-day/ultraviolet-bath-mcnally-pod/

This article, The evolution of human skin coloration by Jablonski and Chaplin gives a review of the how skin color is an adaptation "related to the regulation of ultraviolet (UV) radiation penetration in the integument and its direct and indirect effects on fitness."

Your underlying assertion of the purpose of melanin is incorrect.  Although we need sun exposure for production of things like vitamin D, it doesn't take much to do this.  You're correct that lighter materials will reflect more light, but that's not enough to prevent UV damage.  So there's no advantage for being able to absorb more sunlight for energy or protein production.
Instead look at it as a protective mechanism.  People with light skin suffer from UV burns in shorter time than those with darker skin.  People in cooler climates are typically in the sun less, or at least more of their body is covered when they are in the sun.  They don't need as much protection from the sun as do people where it is warmer that are typically out more with less clothing needed to feel comfortable.
Many times the claims that "disprove natural selection" are just because they're being viewed from the wrong vantage point.


text:
Anabolic reactions and reaction energy
My textbook says,

In general, the formation of a [chemical] bond releases energy

and continues to state,

Anabolic reactions (collectively called anabolism) link simple molecules to form more complex molecules. Anabolic reactions require an input of energy because strong bonds within the smaller molecules must be broken to form the more complex molecules.

Do these two statements contradict each other? The first statement says that when two chemicals combine to form a bond, energy is released; the second statement says that when simple molecules are linked, presumably through a bond, an input of energy is required.
Any help is appreciated.

Both statements are correct, but an understanding of why they are not contradictory requires a bit of explanation.
For "spontaneous" reactions, those which occur naturally, entropy must always increase.  As a general rule, one of the easiest ways to increase entropy is to release energy, so we generally find that spontaneous reactions release energy.*  It's a pretty decent rule of thumb to use.
In the case of an anabolic reaction, we're putting together complex molecules from simple ones, and for these particular reactions we see they don't release energy.  They in fact "consume" energy in their formation.  This is reasonable, so what we find is that such reactions are not "spontaneous."  We don't see them just occurring on their own.
To make an anabolic reaction occur, we need to change the environment such that the reaction becomes spontaneous. We need to change the environment such that the reaction releases energy.  To do that, we start off with inputs which have even more energy than the final product should (such as extra kinetic energy from heat, or a strong oxidizer to reduce one of the reagents, or any one of a number of chemical and mechanical approaches).  Now the formation of the complex molecule can release energy, so it can occur spontaneously.  When we do this, we release some energy, but not all of it.  The rest of the energy is consumed in building the bonds of this molecule that would not otherwise have spontaneously come into being.  The released energy is typically seen as waste, and the energy pent up in the molecule is your desired product.
So in the end, the reason why there's no conflict is the "In general..." bit in the first quote.  You can cause a reaction to occur that consumes energy, but you typically have to do some clever things to put the energy into it.  Reactions which release energy occur spontaneously.  In general, we find "spontaneous" reactions occur far more often, hence the rule of thumb.
* I'm pretty loose with energy and entropy here to try to paint a simple picture without all of the confusion that entropy always brings to a discussion.  As you learn more, do expect to need to be more precise than I am here.

Thanks for your answer, but I'm still a little confused on the concept. Take, for example, the following reaction: $\ce{2H_{2}+O_{2} \rightarrow 2H_{2}O+heat}$. Is this an example of an anabolic reaction that is exergonic? Or are anabolic reactions a special type of endergonic reaction, to which the above reaction is not classified as?

Ahh, I see the confusion.  Anabolic and catabolic are terms typically used when talking about complex molecules like protiens and other polymers, where the term "complex" is more easily meaningful.  Adding amino acids to a protein, for example, is anabolic.  When you get to the small reactions, like your redox of hydrogen example, our intuitive concept of "complex" gives way to basic chemistry rules.  I could argue that maintaining a mixture of hydrogen and oxygen is actually more complex than maintaining a body of water, and thus it was not anabolic, but really, I'd be better to say...

... it' just a "simple" reaction which doesn't easily fit the mold used for more complicated reactions.

Although the answer from @CortAmmon is generally admirable, I think there needs to be a distinction between the type of veracity of the two statements. I would say that:

Statement 1 (bond formation releases energy) is a fundamental truth which emerges from the definition of bond energy.
Statement 2 (anabolic reactions require energy) is a generalization
  that is true in most circumstances but is not a fundamental truth, as
  illustrated by exceptions.

The first problem is the definition of anabolism. Let us take an uncontraversial one from an internet site:
“Anabolism is… the generation of complex molecule from simple molecules”
or, as in Berg et al. Biochemistry, “Biosynthetic processes”.
It is immediately obvious that this is a much less precise concept than bond energy, and and the distinction arises between anabolism as a whole (e.g. the overall synthesis of glucose from pyruvate in gluconeogenesis) and individual anabolic reactions (e.g. the aldolase reaction in gluconeogenesis).
Now in anabolism in biology we are generally concerned with the the creation of complex molecules containing new carbon–carbon bonds, peptide bonds, glycosidic bonds, phospho-diester bonds and the like. As @CortAmmon makes clear, the second statement is valid because (I would say “if”) the bonds in the molecules that have to be broken for the likage to occur have a greater total bond energy than that of the new bond in the product. This depends on the particular chemistries involved, and may turn out to be true for the whole process, but there seems to be no fundamental reason why it should be so.
Certainly, it need not be true for individual anabolic reactions, as illustrated by the aldolase reaction, mentioned above:

This is a reversible reaction, which in the anabolic direction forms a C–C bond between two trioses. The standard free energy change in this reaction is near zero.
If the poster’s textbook had made this distinction, the poster’s confusion on the matter need not have arisen.

This is old news, and so will likely never be seen by the original poster. However, it came up recently because of a new answer, and I found the question intriguing and felt there was unfinished business here that was worth addressing.

I think both statements are correct.When they consider the entlapy change they consider the overall change. Energy is needed for the reaction to start for breaking old bonds allowing new bonds to form hence on the other hand when bond forms energy is released. The energy released is more as compared to energy absorbed hence bond formation releases energy.

It would be helpful if you could perhaps add some sources that can back up your answer. That way the person who asked the question is able to go and look at those sources as well.


text:
Do proteins generally contain phosphorus and sulfur?
I've heard that proteins generally contain six main elements - carbon, hydrogen, nitrogen, oxygen, phosphorus, and sulfur.
I know that proteins are made from amino acids. Amino acids are composed of an amino group, a carboxyl group, a lone hydrogen atom, and a side chain that varies between amino acids. Of the 20 major amino acids, none of them have a side chain that contains phosphorus. Only cysteine and methionine contain sulfur.
So, are sulfur and phosphorus atoms really characteristic in the structure of a protein?

Well, phosphorus is only present in some proteins which are subject to post translational modifications, such as phosphorylation. Sulphur can originate from either cystein or methionine present in the protein. So only proteins that are modified after translation will contain phosphorus.

So, phosphorus is not characteristic in the structure of a protein, right?

Both phosphorus and sulfur are important to the functional structure of many proteins, even if phosphorylation happens later.

Bryan that is wrong, show me a source on that please. As the asker points out, phosphorus is not present in the amino acids which make up the protein. The phosphor present will have been added after translation by the ribosome, thus as post translational modifications. PTMs typically occur after folding. That phosphorylation occurs is true, but it is usually not essential for protein structures, unless it changes the conformation of the protein significantly.

@JeppeNielsen "Bryan that is wrong" - your own comment contradicts that: "unless it changes the conformation of the protein significantly" - this is precisely what I mean. And many proteins are constituitively phosphorylated at certain residues, rather than the impression that new biology students get (like the people often asking questions here) that phosphorylation is usually a sort of on/off switch. That was my point.

And for how many proteins have it been proven that phosphorylations are essential for stability.

@JeppeNielsen I don't think you understand what he is saying.

@JeppeNielsen I didn't mention stability, though phosphorylation state can be a marker for degradation (the tau protein is an example). In terms of structure, one example mechanism is that some proteins are only functional in a dimerized form, formation of which can depend on phosphorylation. Phosphorylation completely changes the chemical properties of the modified residue. Base substitution is sometimes used experimentally to approximate "permanently phosphorylated" residues, which suggests that phosphorylation is of similar importance to base substitition in structure.

Of the 22 known proteinogenic amino acids, all contain hydrogen, carbon, nitrogen and oxygen. Some (methionine and cysteine) contain sulfur while one (selenocysteine) contains selenium. None contain phosphorus, but this element can be incorporated by:

Post translational phosphorylation of various residues. This often allows/prevents binding of other proteins and/or triggers a conformational change in the target protein. It is also necessary for proper folding of some proteins (example). Sulfur can also be incorporated in a similar manner (sulfation).

Incorporation of phosphorus containing prosthetic groups. This can occur covalently and is necessary for the function of some proteins. Sulfur can also be incorporated as part of prosthetic groups.

You may also consider the other elements necessary for the structure/function of many proteins: iodine in thyroglobulin, iron in hemoglobin, etc...


text:
Can you knockout specific receptors in an adult?
Sorry I don't have a good understanding of this topic, but I'm guessing that "receptor knockout" is related to/a part of "gene knockout"?
And If I understand correctly, gene knockout is currently not yet possible to do in an adult (maybe possible in a small area/specific organ, but not systemically) ?
So does that mean a systemic receptor knockout is not possible and maybe possible in small specific areas?

Short answer: yes, it is possible.
But there are some requirements for your delivery system. "Gene knockout" ("gene KO") means such DNA modification that is permanent (get inherited by cell's progeny) and deleterious to gene function (e.g. protein no longer get produced).
So your system must deliver DNA "mutation agent" to all cells (of organism or small specific area). This can be done by using viruses and, for example, CRISPR/Cas9 system for genome editing. Idea  is that virus will get in the cell, start expressing component for genome editing, multiply and infect neighboring cells. Modification in virus can make it non-lethal and less harmful, so you don't kill tissue in process. Virus delivery can be site-specific (e.g. direct injection into the area), it also might be cell-type specific if virus is tailor accordingly.
Also, remember that CRISPR/Cas9 and other similar techniques have efficiency well below 100% and also that you often have two copies of the same gene. This means that total KO probability goes as square of single copy KO probability. If for one event probability is 50%, for both it will be 25%; 10% becomes 1%.
So, all principle component for such experiment already exist.


text:
Is it possible to have cancer and normal blood count at the same time?
Does cancer always cause abnormal full blood count? I've read on the internet that some people who had advanced cancer, also had normal blood count. I can't find anything on the internet about this topic.

Cancer doesn't have to have a profound effect on the blood. Remember that a cancer generally starts off as an abnormal tissue growth or a neoplasm. As the tumor progresses into a malignancy, it has the potential to gain or lose functions, develop new cell types that shouldn't be present in a given organ, invade other tissues, etc. Because of this, in some cases of cancer patients may be subject to paraneoplastic syndrome, or cross-reactivity between something the cancer is doing and the normal tissues.
In the above-linked source, some hematologic paraneoplastic syndromes include (1) eosinophilia, commonly associated with a number of cancers, (2) granulocytosis, often associated w/ lung cancer, (3) Pure Red Cell Aplasia, commonly associated w/ thymomas. The list goes on, but in some cases blood testing is capable of assisting in diagnosis, especially in cases where cancer of the blood is the culprit (very obviously). To also be kept in mind, they note paraneoplastic syndrome only affects around 8% of all cancer patients.
In other cases, you'll be monitoring treatment. As we know, chemotherapy is destructive, and can cause a depletion of platelets or neutrophils, damage organs, etc. Complete blood count (CBC) testing will help oncologists monitor treatments in cancer patients.
Being said: Because individuals with a tumor/cancer may fall within normal ranges in a CBC test, and because these tests must be analyzed scrupulously due to several factors that influence them such as diet, multiple tests are often needed to arrive at a meaningful conclusion. On the basis of cancer itself, however, if it's a solid mass lodged in the liver for example, it's completely possible that blood counts are normal. What you may find, however, are biomarkers in the blood that are saying "hey, the liver is being damaged or dying" such as the enzyme aspartate transaminase. If the tumors are currently small, you may not find anything meaningful in blood tests, or that the blood is "normal." (the possibilities aren't exhaustive)
As a matter of real data I was able to find, Spell et al. was at least able to find some efficacy in CBC testing for colon cancer, to 84% sensitivity and 88% specificity, but you should suspect that individuals may still be asymptomatic under such tests regardless.


text:
Can you grow more Biomass in a brickhouse only powered by solar cells than in a greenhouse? Will we ever be able to?
So I asked following question some physicists but they couldn't really help me though:

Right now I read that 1m² of solar cells generates roughly 100Watts of
  energy. There are really efficient Grow LEDs that use only two spikes
  in the lightspectrum to make plants
  grow.
I have seen some graphs like the Quantum Efficiency of Sola
  Cells
  that suggest that solar cells can absorb energy in the range of 400nm
  up to 1200nm (in varying degrees of efficiency).
By my logic (given a high enough overall efficiency of the solar
  cell), a solar cell can make light that is most of the time reflected
  by plants in the range of e.g. 500nm-600nm / or 800nm+, into
  electrical energy, and that electrical energy can be used, in turn, to
  produce light in the range of 400nm and 700nm that the plants can use
  again for photosynthesis.
Additionally, i could imagine that the sun sometimes hits the range of
  diminishing returns in terms of brightness (lux, lumen?) when it's
  really really bright and hot and shining directly on the plants.
  Instead it would maybe be more efficient to capture that energy
  (photon) and convert them only to the wavelength needed in enough
  brightness that plants can grow (again, given a high enough solar cell
  efficiency, right now it's 20%, i heard 40% is a theoretical limit?)
You could phrase the question a little bit different: I have 1m² of
  land and two possibilities:

build a greenhouse and plant 1m² of crops
build a brickhouse as high as I want with as many layers of 1m² levels. But they are only allowed to be lighted with LEDs and no
  direct sunlight. And the LEDs are only allowed to be powered by 1m² of
  solar cell on the roof.

What is the needed solar cell efficiency (generated watts/m²) for the
  solar cell to reach the break even point of total biomass production /
  timeunit between case 1. and 2.
If there are other environmental conditions that would benefit only
  one of these cases, assume in favor of case 2 and mention the
  variable.
I was in a heated discussion about this yesterday and I would love for
  someone who knows more then me to help me wrap my head around this.

So, to give some extra Information for you guys or to rephrase it again to increase the chance to get an answer: current solar cells operate anywhere from 100W-200W/m² with an upper limit somewhere around 400W to 450W for the way we do it right now. (100W is 10% efficiency, 20% are high quality PVCells right now)
Thanks a lot!