text:
How do trees lift water higher than 10 meters?
The atmosphere pressure is 10 meters of water (approx). This means that it is impossible to lift water higher than 10 meters with vacuum or сapillary action (on Earth, under normal conditions).
There are trees higher than 10 meters.
How do they lift water to their tops?
UPDATE
In other words: how cohesion-tension theory can be true if it apparently contradicts the laws of physics?
UPDATE 2
Atmospheric pressure helps to rise the water, not resists rising. What is resisting is water weight. When water column is 10 meters high, then atmospheric pressure can't help anymore.
Any adhesion/cohesion mechanism can't help here too, because it acts only in thin molecular layer. To transfer action force further the pressure is required, which is insufficient at 10 meters.
UPDATE 3
If we had capillary small enough to rise water to 10 meters and then we will build smaller capillary which we expect will rise water higher, we will fail. Water column will break and does not climb higher than 10 meters.

Menisci acts like small piston and can't help rising water higher than 10 meters.
UPDATE 4
Common pressure distribution in capillary is follows:

$P_0$ is atmospheric pressure. As you see, right under menisci, the pressure is lowered by $2 \sigma / R$ where $R$ is the radius of menisci and $\sigma$ is surface tension. The entire term is called "Laplace pressure". As you see, it can't supersede atmospheric pressure, because water continuity will be broken in the case.
I.e. no any menisci can rise water higher than 10 meters.
The existence of higher trees PROVES that there are some other significant mechanisms, not adhesion/cohesion, not capillary.
UPDATE 5
Current version, as I understood it, is based on a declaration, that a water, if put into thin capillary, can behave like a solid body. Particularly, it can resist tension up to minus 15 atmospheres.
This is a tensile strength of concrete, so I don't believe that without additional proofs.
I think it is just not hard to make thin tube, put water into it and check, how high it can climb.
Was it done ever?

It is not the atmospheric pressure alone that pushes the water up to the tops. Have a look at Cohesion-tension-Transpiration pull theory https://www.boundless.com/biology/water-and-solute-management-in-plants/transpiration/the-cohesion-tension-hypothesis-for-pulling-of-xylem-sap/

Possible duplicate of How does water move throughout plants?

@SatwikPasani so this is wrong theory then. "Negative pressure" can't rise water higher than 10 meters. This is more basic law -- physics.

@Amory this is not a duplicate, the linked question is answered by capillary action, this one is asking how that works specifically at great heights.

It seems like you are mixing up three different mechanisms/forces for moving water: 1) pressure, 2) capillary action and 3) cohesion-tension. The 10 m rule is referring specifically to pumping water using vacuum/atmospheric pressure.

Maybe this discussion provides a better explanation of current thinking.

@terdon It boils down to the same thing, really.  The comment there answers this well enough.  I think the underlying problem here is really about physics.

@Amory I hadn't seen the comment, OK, fair enough.

@fileunderwater see my update2

@AlanBoyd point 4 on your link is just completely wrong: no any small menisci can rise water column higher than 10 meters. To rise water on 100 meters, we need to live on Jupiter.

@SuzanCioc The thing is that you do not seem very open to appreciate the complexity of water transport in a plant. There are several forces in play, and we are not talking about a single water column being sucked up 50m. As have been mentioned, capillary forces, cohesion-tension, osmosis and horizontal movement between cells in xylem are all hypothesized to contribute.

@SuzanCioc Also, the first update in your question could just as well be rephrased as: How can the laws of physics be true, since they are obviously contradicted by living trees?. Either your understanding of the physical laws relevant for this case are mistaken, or some very fundamental laws must be revised. That trees are transporting water to their crowns is a fact.

@SuzanCioc I believe Update 3 in your question is wrong. Water can rise over 10m by capillary action though that is not the only thing pulling up water in a plant. The "10m law" is very specific only to a confined column of liquid and is no way related to the physical processes pulling up water in a tree.

@fileunderwater I am open to any answer, including "we don't know". But I can't accept capillary forces and cohesion-tension because they would violate Pascal's law.

@fileunderwater I don't thinks trees contradict physics. I think biologists do, if they think that capillary forces can rise water to 100 meters.

@SuzanCioc Those processes not only do not violate pascal's law but aren't related to them in a way you think are related to them. And I suggest you provide here a quantitative (mathematical) proof to validate your argument about capillary forces and cohesion not being valid for ascent of sap according to physics,

@SatwikPasani suggest any other force that can rise water, this is the question. Menisci can't. If it can, then pumps would not required to water supply buildings. We would use just thin capillary.

My last contribution - try this.. There is a whole literature on this topic out there, and I suggest that you explore it.

@AlanBoyd I explored it, but found no answer; may be I missed it, then, if you didn't, please, answer the question.

@SuzanCioc Really?  "The air–water interfaces in the cell walls of the leaves, where the matrix of cellulose microfibrils is highly wettable and the spacing between them results in effective pore diameters of something like 5 to 10 nm. A wettable capillary with a diameter of 2.91μm pulls on water just strongly enough to balance the 0.1 MPa atmospheric pressure, so the pressure in the water is zero. For smaller diameters, the capillary force is capable of lifting water higher than 10.33m. For example, the maximum height of a water column with a capillary diameter of 10 nm is nearly 3 km."

@Amory capillary with 10nm diameter can't lift the water to 3 km, I already said that. If somebody states this, he or she is just wrong. Of course, I can be wrong too, but I have an explanation of my point (see above), while others just use Jurine's law blindly.

Disclaimer: This is not my field of research.

First, this is not a complete answer to our question. A nice explanation of the current hypothesis of water transport in trees (Dixon-Joly cohesion-tension theory, originally proposed 1894) can be found at The Amazing Physics of Water in Trees but also in Tyree (1997). The key points are that the stoma (leaf surface pores) are so small that the menisci can withstand huge water columns, that water has strong cohesive forces, and that water is transported using the negative pressure that is created by transpiration. The webpage linked above contains a beautiful visualization of how multitudes of stomata and menisci create strong negative pressures:

Second, much of the current discussion in the comments (an indication that the question might be a poor fit for Bio-SE?) revolves around the plausibility of the cohesion-tension theory, and specifically on whether water can sustain strong negative pressures. Caupin & Herbert (2006) review metastability and cavitation in water (in a physics journal), and contains experimental results on negative pressures in water. The paper references a large number of experiments under various experimental setups (I cannot fairly judge these). In their conclusion they state that:

Among the countless cavitation experiments, only the ones with special care about water purity can reach large negative pressures; with a variety of techniques, they all obtain Pcav around −25 MPa at room temperature (see Fig. 3 (b)), which falls far away from the theoretical value (from −120 to −140 MPa). There is a notable exception: experiments with mineral inclusions achieve −140 MPa. The large gap between these data requires special attention.

So basically, the theoretical estimates lie at -130MPa and empirical results at -25MPa (-250 atmospheres), and water can clearly achieve large negative pressures. This would also mean that the current estimates are much larger than what is needed for the cohesion-tension theory to work (atmospheric pressure= 0.1MPa, negative pressure in water column at 50m ~ -0.5MPa).
They also have a section specifically discussing trees:

7.1. Water in nature
  The law of hydrostatics teaches us that the pressure drop in a water column of 10.2 m is 0.1 MPa. This points out that negative pressures can be reached in the ascending sap of tall trees. In fact additional effects (viscous flow, drought) make the pressure in the sap negative even at smaller heights. The cohesion-tension theory, first proposed by Dixon and Jolly [56], explains that the sap column is held at the top by the meniscus in the pore of the leaves: by Laplace’s law, the meniscus curvature allows a pressure jump between the outside air pressure and the negative pressure in the sap. The trees thus contain large amounts of metastable liquids. Cavitation may sometimes occur, disrupting the liquid column and stopping the flow (xylem emboly). The complex hydraulic architecture of trees limits the damage, and strategies exist to refill the embolied xylem channels. Much work has been devoted to this topic, and is reviewed in Refs. [110,111].

There is also evidence that the risk of xylem embolism increases with tree height, and this creates a trade-off between water transport efficiency and structural adaptations to deal with embolism (Domec et al. 2008). This is for instance facilitated by the pit aperture diameter of tracheids, with apertures decreasing with height along a tree, causing increased resistance to embolism but at the same time lower water conductance. This will clearly limit the height of trees, and the paper indicates that the tallest Douglas firs are at the edge of what they can achieve.
Another recently published paper that should be relevant is 'Methods for measuring plant vulnerability to cavitation: a critical review' by Cochard et al. (2013), but I haven't had time to look closely at this. See abstract below:

Abstract:
  Xylem cavitation resistance has profound implications for plant physiology and ecology. This process is characterized by a ‘vulnerability curve’ (VC) showing the variation of the percentage of cavitation as a function of xylem pressure potential. The shape of this VC varies from ‘sigmoidal’ to ‘exponential’. This review provides a panorama of the techniques that have been used to generate such a curve. The techniques differ by (i) the way cavitation is induced (e.g. bench dehydration, centrifugation, or air injection), and (ii) the way cavitation is measured (e.g. percentage loss of conductivity (PLC) or acoustic emission), and a nomenclature is proposed based on these two methods. A survey of the literature of more than 1200 VCs was used to draw statistics on the usage of these methods and on their reliability and validity. Four methods accounted for more than 96% of all curves produced so far: bench dehydration–PLC, centrifugation–PLC, pressure sleeve-PLC, and Cavitron. How the shape of VCs varies across techniques and species xylem anatomy was also analysed. Strikingly, it was found that the vast majority of curves obtained with the reference bench dehydration-PLC method are ‘sigmoidal’. ‘Exponential’ curves were more typical of the three other methods and were remarkably frequent for species having large xylem conduits (ring-porous), leading to a substantial overestimation of the vulnerability of cavitation for this functional group. We suspect that ‘exponential’ curves may reflect an open-vessel artefact and call for more precautions with the usage of the pressure sleeve and centrifugation techniques.

Everybody get plus, but I still can't accept minus 15 atmospheres in trees. Of course I agree that metastable states can exist in principle. Will explore all this...

@SuzanCioc I agree that it is both hard to believe and really cool at the same time. However, with -15atmos you are talking about the tallest trees around. There is also a lot of evidence that at these heights trees are really on the edge of what they can achieve - see e.g. Maximum height in a conifer is associated with conflicting requirements for xylem design.

@SuzanCioc Also, my answer was mainly inspired by your update 5 that questioned if "...water, if put into thin capillary ... can resist tension up to minus 15 atmospheres".

Another disclaimer: this is not my field and I am not competent to judge the content of the paper that I am bringing to your attention.
I said above that I wouldn't make another contribution, but I found something else worth sharing in this context and which complements the answer from @fileunderwater
Wang Z et al. (2012) Capillary Rise in a Microchannel of Arbitrary Shape and Wettability: Hysteresis Loop. Langmuir 28: 16917-16926
This paper includes modelling, free energy calculations and experimentation on this problem. The maths is far beyond me, but they do come to a very interesting conclusion, namely that although a tree cannot start from a position of no liquid in the xylem and then fill up to the top it can start very small and grow beyond the height that can be maintained by simple capillary action and up to 100 m as long as the water column is never broken.
The paper is behind a paywall, but I reproduce below what is essentially the discussion section. Although this gives a flavour of the work, I must emphasise that it presents a very turgid theoretical treatment of the problem and is well worth a look.

V. IMPLICATION FOR WATER TRANSPORT TO THE TOPS OF TALL TREES
  Most plant physiologists accept the “cohesion-tension theory” as the explanation for the ascent of sap.26 In this qualitative theory, the move of water depends upon three important physical-chemical properties of water, which actually corre- spond to capillary rise (cohesion), cavitation (tension), and the hydrated wall (low contact angle), respectively. In this section, we focus only on the implication of the general force balance and loop hysteresis in the capillary rise of a tall tree. The height to which water in a tree rises is dependent on the size of the transport conduits. If one cuts down a tree and looks inside, the capillary dimensions of the relatively large conduits (the xylem tube) are on the order of 100 μm.27 As a result, the capillary rise is about 0.1 m. If capillary pressure alone were to explain the water rise to the treetop of a 100 m tall tree, such as the coastal redwoods of California, a capillary radius of about 100 nm is required. It was suggested that the relevant capillary dimension is the air−water interfaces in the cell walls of the uppermost leaves. The matrix of cellulose microfibrils is highly wettable, and the spacing among them yields effective pore diameters of about 10 nm. It has been pointed out that it is not necessary for the capillary to have a small bore throughout its length. Only the bore at the meniscus (i.e., in the uppermost leaf) is relevant.27 This consequence has been proved in our general expression of force balance, eq 4. Note that a microchannel containing corners or cusps on its cross section is not considered in the derivation of eq 4. Liquid filaments extend to infinity in the corners or cusps.28 Nonetheless, the elevation of the liquid column is still inversely proportional to the characteristic dimension of the cross section of the tube. For the solutions satisfying the force balance, nevertheless, there exists the issue of physical stability.
  A small bore at the uppermost leaf connected to a larger xylem conduit reveals the presence of a convergent micro- channel. As a consequence, multiple stable heights are possible, as described in the aforementioned analyses. However, the final state depends on the initial condition. The liquid will rise to a stable height corresponding to the larger xylem conduit if the microchannel is initially empty. In other words, the liquid will not rise of its own accord to the stable height near the top of the convergent channel because it will not be able to traverse the larger conduit of the channel. This situation is, nonetheless, stable if the liquid is sucked up to the top and then the suction is removed. How does a tall tree acquire such large negative (suction) pressures from above? As demonstrated in our experiments, the gradual rise of an initially immersed cone is able to maintain the stability of the meniscus on the top of the truncated cone as long as the force balance is satisfied. Note that the contact angle in the vicinity of the small pore mouth can be tuned up to fulfill the force balance when the microchannel is not high enough. The slow growth of the tree can be regarded as a gradual rise of the convergent channel. As long as water transport to the pores on the uppermost leaves is not interrupted throughout the entire course of the tree’s growth to 100 m, this stable height can be achieved without resorting to suction.

Now that's an interesting one. What an approach.

Here's Veritasium on youtube has one explanation which is same as @AlanBoyd's comment.

 Meta-stable liquid can have negative pressure.

if your are capable of translating that video into an answer, please do so.  That would get my vote. @suzancioc My understanding before, re-enforced by that video, is that trees are in the amazing field of nano-hydraulics.

So, the point of this video is that water can behave as solid body and express tension up to minus 15 atmospheres if put into small capillary. Can this point be proved by direct experiment? I don't believe it as is. Also I think, that if that would be true, it would have some subsequences. For example, if tree cut at a hight level, we should hear shot sound like taut string cut...

Please see my update. Ability to resist negative pressure is called "tensile strength". And ability to resist minus 15 atmospheres equals to tensile strength of concrete. Do you yourself believe that trees turn water into concrete?

@AtlLED I don't exclude nano hydraulics, but wish to have justified answer.

Thanks for the comments. Since @fileunderwater did a great job, so I won't bother updating my answer. :)

The following paper surveyed work on exploring water at negative pressure, from the first attempt a hundred years ago, when the largest tension reached was -3.4 MPa @ 24 degC, till the most recent measurement of water at room temperature down to -26 MPa:
http://hal.archives-ouvertes.fr/docs/00/72/64/37/PDF/Caupin-JPCondensedMatter-2012.pdf
Therefore trees can lift water higher than 10 meters because water is pulled up by negative pressure at the top (Cohesion-tension theory CTT). The tension needed to lift water to the tallest trees is -1.2MPa, which is very plausible, since it is less than the value measured a hundred years ago.

The same text has also been published in Journal of Physics: Condensed matter.

Good summary, thank you.


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Why was cotton chosen to grow on the moon?
The choice of plants for the first lunar ecosystem is a bit unusual.
They are growing cotton, rapeseed and potatoes.
Why did the Chinese scientists choose them? Is it because of their ability to thrive in such an environment or because of their possible  contribution to sustaining life in long space missions?

China's state-run Xinhua News Agency mentions the reasoning for most of the species they sent:

Why were these species chosen?
Xie [the chief designer of the experiment] said potatoes could be a major source of food for future space travelers. The growth period of Arabidopsis, a small flowering plant related to cabbage and mustard, is short and easy to observe. Yeast could play a role in regulating carbon dioxide and oxygen in the mini biosphere, and the fruit fly would be a consumer of the photosynthesis process.

While this doesn’t mention cotton, it seems very likely to me that, like potatoes, it’s just a very useful crop.
According to another article, the goal for China is a moon research base:

“We’ll use the Chang’e-8 to test certain technologies & do some preliminary exploration for jointly building a research base on the moon,” Wu said.

Arabidopsis, yeast, and fruit flies are also model organisms.

source: Stack Exchange

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sort: votes


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What are these stars in my microscopic image?
I see this very curious patterns on the sun-facing side of a jasmine (probably) leaf - visible with a makeshift microscope (about 50x)
What are them? Pores? Are there other plants with similar textures?
The microscope is made out of a webcam, as described here

really curious. What are these?

Despite low resolution, I'd say those are trichomes. Jasminum is genera that produce essential oils, so it have glandular hairs and other trichomes wich help to rettain the oil layer.

Source: http://cms.herbalgram.org/herbalgram/issue53/article2207.html?ts=1376643526&signature=b4349f7f3ca6f6a47823f4754237eaac
The image displayed above shows glandular and non-glandular trichomes in lavander shown by scanning electron microscopy. I'm afraid I couldn't find anything about Jasminum in particular, but I think it must be the same kind of structure.

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How good are the hematologic parameters (e,g, IL6 or others) in predicting which patients will develop a severe COVID-19 disease?
Clinical implications of the hematologic profile of COVID-19 patients including cytokine storm, coagulation profile and thrombophilic complications are starting to be recognized. Hypercoagulability could be the potential cause of death due to COVID-19:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7585459/
How good is the hematologic profile, including hematologic markers (such as interleukins and others) in predicting if COVID-19 is severe, has mild manifestations or it is asymptomatic?

A recent pre-print has studied this by measuring 86 accredited diagnostic parameters and plasma proteomes at 687 sampling points, in a cohort of 139 patients during hospitalisation.

We identified 26 protein biomarkers and 14 routine diagnostic markers
(Fig. 4a, Supp. Fig. SF20) that correlate with the time between the
first sampling point and release from inpatient care. The proteomic
signature associated with longer duration of inpatient treatment and
hence more severe COVID-19 progression includes upregulated components
of the complement system (C1QA, C1QB, C1QC) and reflects altered
coagulation (KLKB1, PLG, SERPIND1) and inflammation (CD14, B2M,
SERPINA3, CRP, GPLD1, PGLYRP2, AHSG).

They used a learning classifier to then predict survival in critically ill patients:

In a last step, we established a machine learning model based on
parenclitic networks52,53 (Methods) to predict survival in critically
ill patients (WHO grade 7, n=49) from the proteome of the earliest
single time point sample at WHO grade 7 for a particular patient. On
the test subjects (the data of whom were excluded when training the
machine learning model), high prediction accuracy was achieved, with
AUC = 0.81 for the receiver-operating characteristic (ROC) curve. Of
note, the model correctly predicted survival or adverse outcome weeks
in advance (median time from prediction to outcome 39 days,
interquartile range 16 - 64 days).

The 'predictive power' can be captured (not in a perfect way) by the AUC value - a value of 0 has the worst power to separate patients and 1 has perfect power, so 0.81 is pretty good overall. I haven't read the paper fully, but from a brief scan it looks as though their methodology is at least reasonably sound.

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What type of insect is it?
I've found this insect in my apartment and I don't know it could be bed bug or not. Could it be hazardous and what are the ways for getting rid of it?

@PolypipeWrangler Answers should be in answers, not in comments.

Approximately where in the world are you? if you can, a close up photo would be useful.


text:
Can you recognize this larvae that came from a human nose? (probable nasal myiasis?
Those larvae came at least four different times from the nose (inside - from the mucosal) of a 60 year old man from a tropical area in South America. He lives and works in a city with a tropical climate. On another occasion a living insect came out of his nose, the picture is also attached.

Approximately how big are the larvae and (presumably adult) insect? Did he find all of these around the same time (over the span of hours/days) or were there longer intervals between them?


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A level 2022 Biology percentage increase question

In January 2022 WBI12/01 they asked:

9c. In 1963, there were only three males and 12 females of
C. hoodensis left in the wild.  These 15 tortoises were used in a
breeding programme.
ii.The wild population of C. hoodensis is now 1800 individuals.
Calculate the percentage increase in the wild population of
C. hoodensis tortoises.  Give your answer to one decimal place.

I did the calculation 1800-15
(new-original value)
Then divided the difference by 15 (the original value) times 100 and got 11900.0%
But the mark scheme says
1800-15 = 1785
(1785÷1800)x100% = 99.2%
So I don't understand why they divided by the new value 1800, not the old one 15, since this was a percentage increase calculation.

I’m voting to close this question because, in addition to being a "homework"question — see link for an explanation and expectations, it is not primarily about biology as defined in the [help]. Please take the [tour] and consult the [help] starting with [ask] for details.

15 to 1800 is a 11,900% increase (= form A)
or
12,000% of the initial 15 (= form B).
They asked you for a percent increase, so they want the answer in (A) form.
The correct working:
Take the new value 1800, divide by the original 15, and multiply by 100 to get a percentage: (1800/15)*100=12000 and thus you have a percentage answer in form (B). From this, to get form (A), subtract 100 at the end to get a percentage increase: ((1800/15)*100)-100=11900.
You have to remember to distinguish forms A and B. To illustrate, 100% of 10 is 10, and 11 is a 10% increase from 10 (form A), but it is 110% of 10 (form B).
In other words... the marking scheme is woefully wrong. It claims the correct percentage increase in the wild population is 99.2%. That means it's below 100% increase (i.e. below doubling). A 100% increase from a starting 15 tortoises means there would be 30 tortoises. Not 1800. So the mark scheme is hilariously incorrect.


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How do I know if the claims of a scientific paper are generally accepted?
I am looking for information about the use of glucosamine and  chondroitin for treatment of back pain and disc degeneration. A paper published in Military Medicine in 1999 reported some beneficial effects, but newer papers (references needed) do not support these conclusions.
How do I search for more recent papers that cite this older paper, to decide what the current medical consensus is?
Glucosamine trial (negative results):
https://smallpdf.com/result#r=a595b512d3b25e41aabe7f3179ba8a4b&t=share-document
Chondroitin Sulfate trial (negative results):
https://smallpdf.com/result#r=b82b6b31030bfb6dffd6261a48153fe7&t=share-document
Glucosamine and Chondroitin Sulfate(good results but not conclusive)
https://smallpdf.com/result#r=626038b39e87cc64baab274e1d053871&t=share-document
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC165439/

It might be beneficial to also link to the more recent studies that contradict the older one.

Welcome to SE Biology. Please finish reading the [Tour]. I appreciate that your first language is English, but I think you should reconsider the use of the word "debunk. Do you want to know whether anyone has published a critical analysis of the paper showing that it is flawed — that is what I would take "debunk" to mean — or do you want to know what the current scientific/medical consensus is? People can disregard the conclusions of a paper without proving it flawed. I've cleaned up your presentation a bit.

Use the word “review” in the search terms. A review article will have references to all the useful papers.

@AgnesianOperator you are right sorry I've added the sources of the conflict, Thank you

@David Thank you David for the correction, it is a way more properly to ask, but what I would like to know, if there is a study that take that as a reference (because it is one of the oldest of this topic) and claims like ("We have followed the methods of this papers in a large trial but the outcome its different")

Papers provide evidence for or against various hypotheses, but no one paper is ever a definitive statement on an issue. It is expected that different trials will have different outcomes, both due to differences in the studies themselves (different inclusion/exclusion criteria, different study population, different dose/procedure, etc) and random statistical variation.
It's also very important to recognize that most studies are designed to test whether there is sufficient evidence to reject a null hypothesis of no effect. Failure to reject that null hypothesis does not mean that there is no effect, it means that the results aren't different enough from what you'd expect to see if there was no effect. It may be that there is a smaller effect than the study was powered to detect. Also, consider that a properly powered study generally has a true-positive detection rate of somewhere between 80 and 90%; that means, 10-20% of the time when there's a real effect of the expected size, the study won't be able to conclude there is a significant difference.
So, when there are multiple studies with different results, how do we decide what is "right"? Well, scientific consensus is built over many studies. In clinical research, the best evidence is when you have not only clinical evidence of an effect, but also an understood biological mechanism. At just the clinical level, though, studies can be combined through techniques of meta-analysis. Meta-analysis combines results from multiple studies, weights them by the size/quality of the study, and makes a comprehensive quantitative estimate from the covered literature. If you want to look for scientific consensus on something, you often want to look for recent meta analyses of that topic. In the medical field, there are also often consensus papers written on particular topics. Here's an example:
Priori, S. G., Wilde, A. A., Horie, M., Cho, Y., Behr, E. R., Berul, C., ... & Tracy, C. (2013). HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes: document endorsed by HRS, EHRA, and APHRS in May 2013 and by ACCF, AHA, PACES, and AEPC in June 2013. Heart rhythm, 10(12), 1932-1963.
These statements are written by a bunch of scientists/physicians gathering together and comprehensively reviewing literature on some topic. They typically will weigh not only evidence for effect like in meta analysis, but also consider the implications of treatment options including costs, side effects, and the consequences of getting it wrong (for example, if a treatment following a wrong diagnosis masks some other condition that then goes untreated).

@BryanKrause has given a good general answer to this question.
One specific approach (which the poster may or may not already have taken) is to look for links on the publisher’s webpage to subsequent papers that have cited the one of interest. In this case the page shows that there are 107 papers in Web of Science citing the article in question. It also gives direct access to Google Scholar and Crossref. Click and go. Happy reading!

Thanks David, you do answers the originally question but, Bryan answer's is the apparently correct for the new question

@RodParedes — no problem. Better to accept his answer. But a gentle suggestion about your English. You have a peculiar tendency (as I’ve never met it before) to put the letter “s” at the end of verbs. I realize it’s tough, but if you are going to communicate in science you need to improve your English. Or cheat, like I do in Italian. Prepare your text in a word processor. Select the text and set the language to English, and then run a grammar test. Think about the errors flagged (the suggestions may not always be right) and check in your basic language reference.

Use google scholar and have a look at the papers that have recently cited it by filtering for the year the citing paper was published.
https://scholar.google.com/scholar?cites=17068797659415407733&as_sdt=2005&sciodt=0,5&hl=en
More broadly it's often taken that more citations is a positive, though this is impacted by all manner of phenomena and a high citation count could be due to papers negatively reviewing it!

PubMed has a similar feature (https://pubmed.ncbi.nlm.nih.gov/?linkname=pubmed_pubmed_citedin&from_uid=10050562)


text:
Does regulate always mean suppress when it comes to heteroreceptors?
Do heteroreceptors always suppress the release of the neurotransmitter they regulate upon their (the heteroreceptor's) activation?

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text:
Which of the nicotinic acetylcholine receptors (nAChRs) catalyse the release of the neuromodulators mentioned below that's caused by nicotine?
Neuromodulators: acetylcholine, norepinephrine, epinephrine, vasopressin, histamine, arginine, serotonin, dopamine, autocrine agents, and $\beta$-endorphin.
I am aware that agonists of the $\alpha_7 $ nAChRs improve cognition in Schizophrenia, presumably by catalysing the release of histamine, norepinephrine and/or acetylcholine.1,2 I also know that $\alpha_7 $ nAChRs antagonists reduce $\Delta^9$-tetrahydrocannabinol (THC) self-administration in mice presumably by suppressing dopaminergic activity in the nucleus accumbens or by inhibiting the activity of the CB1 receptor.3 Selective CB1 antagonists also manage to reduce nicotine dependence.4 Also I know that the activation of the $ \alpha_3 \beta_4 $ nAChRs in the adrenal medulla catalyses an epinephrine and norepinephrine release.

Reference List (Oxford Style)

M Hajós, BN Rogers, 'Targeting alpha7 nicotinic acetylcholine receptors in the treatment of schizophrenia.', Current Pharmaceutical Design, 16/5 (2010), 538-554.
LF Martin, WR Kem, R Freedman, 'Alpha-7 nicotinic receptor agonists: potential new candidates for the treatment of schizophrenia', Psychopharmacology, 174/1 (2004), 54-64.
M Solinas, M Scherma, L Fattore, J Stroik, C Wertheim, G Tanda, W Fratta, SR Goldberg, 'Nicotinic α7 Receptors as a New Target for Treatment of Cannabis Abuse', The Journal of Neuroscience, 27/21 (2007), 5615-5620.
C Cohen, E Kodas, G Griebel, 'CB1 receptor antagonists for the treatment of nicotine addiction.', Pharmacology, Biochemistry and Behavior, 81/2 (2005), 387-395.


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Is urethra a part of male accessory duct system?
In my textbook it is written that male accessory duct system constitutes the rete testis , vasa efferentia , epididymis and the vas deferens . Can urethra be also included here ?

Did you consider exploring what these other structures are accessory to? This line of thinking might help here.

Thank you for your suggestion. But is it because that urethra has only role in providing a comman passage for urine and sperm , but it doesn't have any role in functional maturation of spermatozoa , so it's not part of accessory duct system ?

I don't really find this terminology occurring very frequently, so it seems mostly something special to your textbook and others like it. Really the primary content I find online about this particular accessory duct is in the form of multiple-choice homework cheat sites. For example, this search for "accessory duct" epididymis vas deferens includes very few results and some are false-positives.
That said, a duct is:

a bodily tube or vessel especially when carrying the secretion of a gland

Accessory, in this context, has meaning along the lines of additional/supplementary/auxiliary, or not the main/primary, as in the accessory duct of the pancreas. So, an "accessory duct", where the adjective "accessory" modifies "duct", is "another duct in addition to the primary/main one".
The main duct, in this case, would seem to be the urethra itself, something common with the female urogenital anatomy, whereas the male accessory duct is the additional ductwork needed to attach the sperm-producing testis to the outside world. So, no, if you're taking the urethra to be the main duct, it doesn't make sense for it to be an accessory to itself.


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Tiny insect identification in potted plants
Unfortunately, the new potted soil I've bought seems to be heavily infested with insects. Firstly, I have had a fight with fungus gnats. After using parasitic nematodes about 10 days ago, I no longer see them flying around, but there are still a lot of unwanted guests that I see moving around in the pot.
Can you tell what those could be? I live in Central Europe. The pests are quite small (ca. 1 mm in length) and are running quite quickly around the pot. They don't seem to be able to jump around. Unfortunately, due to their size and quite fast movement I was not able to take a good picture, but here are two specimens, marked with red arrows. Could those be the same or different species?

They might not be insects, but more basal hexapods like springtails.

Also, they are not necessarily pests. They have a pretty high change of being detritivores that break down waste, not really getting in anything's way and being more helpful than harmful.

These are a type of hexapod called springtails (Collembola).

 Common Soil springtails. Source: UMN Extension
Springtails vary in size, shape, and color, but most are < 6 mm long (as low as ~1 mm) and many tend to be dull white/grey/yellow in color.
Many species are omnivorous soil-dwellers preferring moist and organically-rich soils.

You will find them more frequently in over-watered plants.

For reference, I've had concurrent fungus gnat and springtail populations in my house plants before.
According to UMN Extension:

Springtails do not have wings and cannot fly. But they can jump up to several inches using a special forked structure under the abdomen

But these insects would very unlikely survive a jump out of your plant, nor do they want to do so -- they want to be near the moist soil. I would not worry about it. (though you could water less frequently to cause their population to drop if you're concerned -- but these animals are harmless and will often help with the breakdown of the soil or removal of some soil pests depending on species and ecology).
Sources:

Wikipedia

UMN Extension

FES Summaries

The variety in sizes in that photo is intriguing. Do you have any idea what that depends on? Is this a species that will continue growing for as long as it has food, perhaps, so larger ones are older? Is it some sort of sexual dimorphism? Something else?


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Can jellyfish improve the Black Sea ecosystem?
According to this study, cited by many popular science magazines, jellyfish and other, smaller animals can contribute to the vertical ocean stir as much as currents do.
Black Sea chemistry and biodiversity is highly coupled with the lack of vertical currents, present in oceans or bigger seas. Some of the effects are low salinity in the top layers - many ocean fish species cannot tolerate the Black Sea salinity, and limited space for life (below 50 meters there is no oxygen)
Can the jellyfish population (which is exploding now) change the stratification of water layers enough that the highly saline waters from bottom go up, and oxygen goes to the deeper layers, allowing a completely new ecosystem here?
If yes, what are the outcomes of such prospects? Besides the potentially catastrophic release of hydrogen sulphide form the bottom, can it be an improvement for the biodiversity here?

At least they have an influence in the sense of butterfly effect. Which can be small, or huge. http://en.wikipedia.org/wiki/Butterfly_effect

To quote the PI from the BBC article:

But, Dr Dabiri explained, the jellyfish were unlikely to be the "primary ocean mixers".  "Crustaceans - like copepods and krill - are likely the primary biogenic mixers, because there are so many of them," he explained.
"But much of the open ocean is like desert," he added, "and the density of these animals is unlikely to be sufficient (to cause mixing)."

My guess therefore is no, jellyfish would not be sufficient to dramatically change the current structure of ocean layers.  Animals in general, as the paper and its references suggest, do contribute significantly, on-par with tides and wind.

While in the ocean they are not the primary mixers, their influence is not negligible. My questions is about their effect in a sea where other vertical movement vectors are missing. A change of 10% in water movement is not much in an ocean, but in a closed sea may mean a dramatic change.


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Cannot see images beyond a certain magnification with a microscope
Using a new microscope with my son, we cannot see images beyond a certain magnification:
Eyepiece: 25x - Objective lens: 4x   --> OK
Eyepiece: 25x - Objective lens: 10x  --> OK
Eyepiece: 25x - Objective lens: 40x  --> not focused
Eyepiece: 25x - Objective lens: 100x --> not focused

In the last two cases, we try moving the stage along all its range, without getting anything.
Same issue using a 10x eyepiece.
On the 100x objective lens "OIL" is written; does it mean the observation needs to be done through oil instead of air? Or just that oil is used inside the objective?
We did not prepare the leaf; we just put a small piece of it between two slides.
Are we doing anything wrong?
Observing a leaf at 250x, we can see tiny round structures (I think barely bigger than what can be possibly seen by our eye): are those the cells?

Can you tell us the other writings on the objective lenses ? Do you also have a 10x ocular in your kit ? How are you preparing the leaf for observation ?

Generally speaking, strong objective will focus very close to the sample. (Be careful of lens-sample collision though)

It's been thousands of years since I've used a microscope, but shouldn't 100x be an oil-immersion magnification? Also, looking at a pre-fixed set of slides first should help you to get the hang of things. Looking at cells takes practice. If you have none, buy some. The very thin skin between two layers of an onion needs little preparation, and is a great home-made intro to plant cells. A scraping of the inside of your cheek mixed with saline (easy to make) is also a good home-made intro to animal cells.

Oh, btw, it's possible that the things you're seeing at 250x are chloroplasts. Round and green and very small.

60x has already entered oil immersion range.

I updated my question with more details. Thank you.

Just a guess, but putting the piece of leaf between two slides may not let the objective get close enough to focus at higher magnification.  There are cover slips made of much thinner glass that are used for this purpose.

This is probably the problem: "We did not prepare the leaf; we just put a small piece of it between two slides.".
I suppose you mean you put a leaf fragment between two regular microscope slides, those measuring 26mm * 76mm (1in. * 3in.)?
That won't work. Long story short: microscope optics/objectives are designed with a specific working distance in mind, which is not an entiraly free choice, but dictated by the laws of physics/optics. An average achromat 40/0.65 has a working distance of about 0.6 mm. An average achromat 100/1.25 has a working distance of about 0.2 mm. An average microscope slide has a thickness of about 1 - 1.2 mm...
In the... well... regular microtechnique, a specimen is put on a slide and covered with a very thin coverslip, having a thickness of around 0.15 - 0.17 mm.
Also, as others mentioned, using a 25x eyepiece in combination with a 40/0.65 or a 100/1.25 is kind of overkill. With that combination, you enter the realm of "empty magnification". In short: structures appear larger, but no new structures are revealed and the image becomes more and more fuzzy.
And yes: you need to use immersion oil with the 100x objective, but keep in mind this is a very demanding objective to be used, on the part of the microscopist as well as on the part of the slide preparer.
Using a microscope is not all that simple for novices, but there's an easy way to find out -if no image can be produced-, if it's a microscope problem or an inexperienced user problem: take as a specimen an as thin as possible large object, such as a leaf of cigarette paper, and try to focus on it, using low power and gradually use stronger objectives up to 40/0.65. If an image can be produced, even if it's rather blurred at 40/0.65, the microscope is okay.

Sorry. I'm not a native English speaker, but in Dutch and, as far as I know, in French and German as well, any object put on a slide for microscopic examination is considered "prepared" for -, being it as a temporary mount. Ah well, I'm not a linguist, unfortunatly.

25X is a mighty strong ocular (eyepiece) lens, certainly for home use. This means with the 40X objective you are already at 1000X overall. It would take a seriously thin, well mounted and well lit specimen for you to see a good image. This assumes the optics are of sufficient quality.
I recommend using a 10X objective. This will give you 400X with the 40X objective. To use the 100X objective, you will need to insert a drop of oil between the objective and the slide. "Immersion oil" is made especially for this purpose.
At the 400X, or higher, magnification you will need to slice tissue very thin. But there are a couple ways to view cells without the knowledge or tools for preparing sections. To view plant cells, do an internet search for "onion cell wet mount". To view some animal cells (your son's), search "cheek cell slide".


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What Conditions must Drugs satisfy for them to be Deliverable via the Transdermal route?
What Conditions must Drugs satisfy for them to be Deliverable via the Transdermal route? I assume a high $\log{P}$ (lipophilicity) would be one, are there any others?

Whether a drug can be delivered transdermally?  I think that carriers can be formulated to carry a small molecule through the skin into circulation, so I don't even know about lipophilicity. I believe if you spend enough money, you can overcome many of these problems.  I think that pharmacology might be just as important.
I think the first condition of a transdermal administration is that the drug cannot be effectively administered orally.  This is the most cost effective route go get a pharma compound into the body. It requires no devices, no fancy coatings or vaporizors.
Reasons that a pill (or its less popular cousins the suppository and sublingual tablet) cannot be used as the delivery system for a drug include effect of pH and other degradation of the compound in the GI tract, absorption rate from the GI tract and other factors such as effect of food in the system, other drugs which might interact in the system.
Another advantage of absorption through the GI tract is that this is the physiological system which is meant to be ingested and introduced into the body - its relatively fault tolerant, even if less of the drug actually reaches the blood stream.  There's more, but that's not a bad outline.
After pills and the like, the second choice is intravenous administration, which puts 100% of the drug into the circulatory system.   This has its own disadvantages, requires a clinical setting and the needle and breaking of the skin are not ideal in many cases.
If the drug needs continuous and non clinical administration there are many other means of drug delivery, including transdermal administration.  Differentiating these methods often includes making sure the drug is available specifically to the part of the body that needs it.  E.g. topical administration; putting on a medicated cream for a skin condition or use of an inhaler which delivers the drug directly to the lung for an asthmatic condition.
Transdermal administration has its own specific advantages; continuous distribution of the compound over long periods of time.  Disadvantages include: poor ADME properties for biologicals like antibodies and other proteins, low delivery concentrations where you need a large amount added (epinephrine, and maybe antibiotics come to mind).
Examples of successful transdermal delivery are testosterone gels and the nicotine patch.  Both of which apply continuous controlled low dosage that is important there.
There are three typical routes of drug absorption in transdermal delivery.  The drugs can diffuse through the membranes of dead cells of the stratum corneum, which works if the drugs are lipophilic enough.  They can diffuse around these cells, through the intercellular spaces, which can work for more polar drugs although this path is not usually as efficient.  The most extreme means are patches which contain tiny needles that can deliver straight through the protective layer of the skin.  With enough economic investment probably any sort of compound could be introduced through a patch.
Most of this is just cribbing off the notes from this lecture on coursera: Fundamentals of Pharmacology.  Its probably outlined on any pharmacology text.

What about fentanyl? Fentanyl can be delivered orally yet it is also available in transdermal patches. Nicotine is water soluble but it is also lipophilic which is how it manages to cross the BBB so easily.

I tried to address this in edits.  I don't claim to cover all transdermal delivery, just trying to answer the question at the fairly general level it was being asked.  I would have to do some digging re: fentenyl.  I might have time tonight.


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How long does it take for the Opioids listed in the Description to induce Analgesia when Administered via IV?
How long does it take for the Opioids listed in the Description to induce Analgesia when Administered via IV? Now I don't mean how long it takes for euphoria to come on but analgesia.
The opioids I would like to know this information to include:

Buprenorphine
Butorphanol
Fentanyl
Hydromorphone
Methadone
Morphine
Oxycodone
Pentazocine
Pethidine (meperidine)
Sufentanil
Tramadol

These are 'peak' values when administered via IV, with the exception of oxycodone. There will be some variation person to person depending on their opioid tolerance and any concomitantly administered medications.
Buprenorphine: 60m
Butorphanol: 5m
Fentanyl: 5m
Hydromorphone: 30-90m
Methadone: 1-2h
Morphine: 20m
Oxycodone: Not administered intravenously
Pentazocine: 15m
Sufentanil: 3m
Tramadol: 2h


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Which Enzymes are Responsible for the Biodegradation of Noladin Ether?
Which enzymes degrade the CB1-specific endogenous cannabinoid 2-arachidonyl glyceryl ether? (Noladin ether)

Noladin is an endocannabinoid. The best-characterised members of this family of molecules are Arachidonoylethanolamine (AEA; anandamide) and 2-arachidonoylglycerol (2-AG). The degradation of these endocannabinoids is reviewed in:

Pamplona, FA et al. (2012) Psychopharmacology of the endocannabinoids: far beyond anandamide. Journal of Psychopharmacology 26:7-22

These endocannabinoids are inactivated via a reuptake system that is present in both neuronal and glial cells, although the protein responsible has apparently not been identified.
AEA is then metabolised to arachidonic acid and ethanolamine by fatty acid amide hydrolase, while 2-AG is converted to arachidonic acid and glycerol by monoacylglycerol lipase.
Because of its ether linkage, noladin cannot be a substrate for either of these enzymes. However the review also describes other possible pathways of endocannabinoid metabolism involving oxidation by cyclooxygenases, lipoxygenases and P450 cytochromes. These are the best candidates for the further metabolism of noladin, but there is apparently no direct evidence for this.


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How do paper wasp larvae not fall from their nest?
There is now a paper wasp nest hanging from the eaves of my bedroom. Not very big, I supposed about a hundred chambers and about 7 to 10 adults in total. I observe it every now and then.
It just occurred to me that when the larvae first hatch, they are so small compared to the chamber diameter. So here are two questions:

How do they not fall off, being suspended and all?
Is there any known statistics of how often larvae fall off (for a particular species, let's say)?

Social wasp larvae hatch from an overhanging egg, and they grow up through a series of skin moults, typically 5 in number. The shed skins accumulate terminally behind their pointed anus, where the egg chorion peduncule remain. These wasps have a special body construction and skin texture (e.g. abdominal lobes, numerous spikes) that allows for pressing against the cell walls.
You can see these traits from high-resolution images shown in the larval descriptions:
Florida Entomologist, 95(4):890-899 (2012) https://doi.org/10.1653/024.095.0411
Sociobiology 63(3): 998-1004 (2016) http://dx.doi.org/10.13102/sociobiology.v63i3.988
Finally, it should be minded that gravity doesn't affect small insects in the same way it affect larger mammals like humans. This means it way takes less effort and sticky secretions for these bugs to hang onto walls than we typically imagine by common sense.
I don't know of any dedicated estimations on fallen larvae, but I guess the event isn't common, unless perhaps in abnormally structurally-challenged nests.

What I can say from observing an abandoned nest, larvae have a connection to the chamber ceiling. I don't know what it is, exactly, but looks like some form of glue.


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How does a jumping spider manage to "jump" on the ceiling?
I just witnessed a small jumping spider jump on some kind of louse or bed bug on the ceiling. How does it do that without falling? I have yet to find a high-speed-camera video of a jumping spider jumping on a ceiling.
My hypothesis is that the spider would spit silk and anchor it on the ceiling, then jump, and allow itself to be swung by the silk onto the prey. But I don't have a high speed camera to prove that.
EDIT:
I now have some evidence that supports my hypothesis: I just saw a jumping spider attempt to jump on a prey and failing to land properly. It didn't fall directly to the floor. Instead, it dangled from its own silk, at about 2 cm from the ceiling, then climbed right back up the thread of silk, onto the ceiling.

Whilst I've seen no evidence either, your hypothesis that the spider uses its silk seems highly likely; small spiders are known to 'balloon', using their silk to float through the air  http://en.wikipedia.org/wiki/Ballooning_(spider). Using their silk to 'pounce' on prey seems very plausible.

good work using observation btw... that's how all science starts...

You are right - most jumping spiders have draglines they secure to the surface before they jump.  They can't defy gravity, but they can recover from a miss if they do this.

Disturb a jumping spider on a wall, and watch it seemingly defy gravity: it will jump horizontally out into the air, then return to the wall.  This seems fantastic until you spot the major ampullate dragline.  It essentially becomes the bob at the end of a pendulum string.

the book goes on to explain that the dragline is used as an airbrake and a spring to help the spider control the jump, which might make it seem to do unnatural things when jumping from a ceiling.  You might want to get a video of this if you can.
Some of the references in another book here, point to other uses of draglines - the spiders can tell each other's species by them, attract a mate.


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How to determine if a plant is autotrophic or heterotrophic?
How do you determine if a plant is autotrophic or heterotrophic, and are there any traits in particular that can be used to classify species?
As two examples, how should Melampyrum pratense and Orobanche be classified?

It is difficult to understand what you are asking. Please elaborate.

What is you overall reason for asking? Are you interested in these species in particular or for a more general application?

This in part depends on how you define heterotrophic. The most common definition is the inability to synthesise energy-containing molecules, most commonly by fixing carbon through photosynthesis (but dont forget chemotrophs). However, I've sometimes seen definitions that also include dependency on external sources for nutrition (e.g. nitrogen) but also to supplement carbon sources.
Using the first, main definition a lack of chlorophyll is a sufficient trait to define heterotrophic plants, which clearly places Orobanche (lacks chlorophyll) in the heterotroph category. If you use the second definition you will include more species, but it also becomes much more tricky to draw the line between autotrophs and heterotrophs. I know that Melampyrum pratense is a hemiparasite, but don't know exactly to what extent, and therefore cannot say if it is accurate to label it as heterotrophic (using the second looser definition - it has fully functional photosynthesis). Checking whether a hemiparasitic plant can establish, survive and reproduce without its host should be a useful way to establish if it is a obligate or facultative hemiparasite (I suspect that Melampyrum pratense will be found in the latter category). Myco-heterotrophy can also be obligate and facultative, and can involve transfer of both carbon sources and nutrients, see Merckx et al (2009) for a review. Insect-eating plants such as the Venus flytrap are however sometimes called partial heterotrophs, based on the fact that they get part/most of their nitrogen from insect trapping, while still obtaining their energy from photosynthesis.


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How common is complete heterochromia?
How common is complete heterochromia? (One iris is a different color from the other)
Are there any statistics available for this? If no, why not?

Note: not my area of expertise

First of all, heterochromia can be congenital (found at birth) or acquired, and from your question it is not clear if you are asking about one specific type or the overall frequency (if so, at what age?). Since acquired heterochromia is often due to injury or disease, the overall frequency is likely to increase with age. Also see answers to the question "Is it biologically possible for an adult's eye color to change?" for more on reasons for acquired heterochromia.
According to an Austrian study (Stelzer, 1979), the overall frequency in the Vienna population was 0.26% (males: 0.16; females: 0.37). However, Medicine.net reports a frequency of 0.6% for only congenial heterochromia, but this number lacks a clear reference. A thorough review of different reasons for heterochomia can be found in Rennie (2012).


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Spread of malaria from an infected person
If a person is infected with malaria, how can that person be a part of spreading malaria? As in, if a female anopheles mosquito sucks blood out of that infected individual, how is it possible that malarial schizonts will be only sucked by the mosquito and not pure blood? The point is, out of such a huge volume of blood, how can only malarial parasites enter the suckling mosquito?

With humans infected with malaria, the parasite load in the blood can be quite high. It ranges from 10 to 108 Plasmodium falciparum parasites per ml .
When a female Anopheles mosquito bites an infected human, they take in infected blood, not just the parasite. They take in a few micro liters of blood, which in usually enough to get themselves infected, and the next time they bite a human (about one week later), the infection is spread.
You can learn more at the CDC malaria FAQ and their overview of the malaria transmission cycle.


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What is a subspecies?
Within a species there may be subspecies that are named using trinomial nomenclautre. For example the Grizzly Bear, Ursus arctos horribilis is a subspecies of the Brown Bear Ursus arctos.
The dictionary definitions of subspecies seldom expand beyond this:

A taxonomic category that ranks below species, usually a fairly permanent geographically isolated race.

I'm assuming redefining species into subspecies is not a completely arbitrary process as the definitions would imply, but is based on biology. What are the biological criteria for a group within a species to be "upgraded" to a subspecies?

This is the definition by ICZN which is equally un-informative "The species-group rank below species; the lowest rank at which names are regulated by the Code. (2) A taxon at the rank of subspecies."

@WYSIWYG The definitions are all very tortological rather than insightful. Of course it's below a species rank! What else could 'sub' mean in this context? There must be criteria that make some strains, or groups biologically different enough to be subspecies, but that threshold is apparently hard to come by if you're not 'in the know'.

The wikipedia article is more helpful, if accurate: "a polytypic species has two or more subspecies, races, or more generally speaking, populations that need a separate description" and "A monotypic species has no distinct population or races, or rather one race comprising the whole species. A taxonomist would not name a subspecies within such a species."

@jzx It sounds better until you realise that it's still missing that nugget of information; specifically what factors warrant the 'need' to be separately described?

To clarify, it might be better to refer to subspecies on equal footing as Ursus Arctos Brunneis (brown) and Ursus Arctos Horribilis, both of which would be members of species Ursus arctos.

I think the answer is that it is whatever taxonomists agree to. So we have Canis lupus familiaris to identify our lovable friends and C. lupus dingo for the baby eaters. These are holdovers from Linnaeus et.al. But in all seriousness, this comes from an eLS article on genetic differences of Chimpanzees. "The researchers also used demographic history models to identify the values of different population and evolutionary parameters for all four populations of subspecies (i.e. effective population size, divergence and rates and directions of migration)." It sounds like there are a lot of factors.

There are likely many changes to come, and a rethinking of classifications, as we learn more about genomes and have access to whole sequences for organisms, tools that were not available to taxonomists when many of the classifications were first made.

Your assumption is wrong. Subspecies taxonomy is highly arbitrary. There are no clear criteria. On the other hand species are frequently constituted by an array of loosely defined races.

@RobertMcFetridge - Welcome to Biology.SE. Please provide references for your claims and explain answers in good detail. You can take a look at what is considered a good answer on this site here.

@RobertMcFetridge - Welcome to Bio. I've converted this answer into a comment. AlexDeLarge has given fruitful details on how to improve your post.

This post is related as it talks about the concept of species.

In practice, subspecies are often fairly loosely-defined, reflecting a degree of uncertainty and ambiguity at this level of taxonomy. There are systematists who take the view that subspecies-level classifications should not be used as they are not rigidly definable.
In general, a subspecies will fulfil the following criteria:

it will occupy a distinct geographic range from other subspecies
within its species,
it will have limited gene flow to other subspecies within its species, while still being capable of interbreeding
it will have some recognizable shared character, used to distinguish it from other subspecies within its species

Subspecies classifications, and their usefulness, are discussed in the Turtle Taxonomy Working Group's 'Turtle Taxonomy: Methodology, Recommendations, and Guidelines', for those interested in further reading.

Great answer, albeit not what I was hoping for! I'm with the systemists on this one. I can't understand the usefulness of unsystematic subspecies nomenclature.

There can be good pragmatic reasons to hold on to subspecies labels. For instance, imagine you're after old DNA samples from museum specimens, and the species falls into two subspecies, one in the Pacific Ocean and one in the Indian Ocean. However, the old specimens do not have a lat/long of collection associated with them. In that case, you can get geographic subsets of the museum's catalogue by searching based on subspecies, and there may not be any other useful way to get that geographic subset.

There are also conservation reasons for wanting a "subspecies" designation. If a species is cosmopolitan, but a local unique population is threatened, being a "subspecies" may provide for governmental protection. For instance, many freshwater fish species on the US endangered species list are subspecies.

Subspecies are useful becasue species are not uniform homogenous populations, subspecies, may gave different behaviors, gene ratios, morphology, ect. For example there are several subspecies of Canus lupus including dogs, dingoes, and a variety of wolves ranging from the high tundra to the equatorial desert with adaptations to those environments.


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How can a YAC be screened against a cDNA library and a cosmid library of genomic DNA to find a gene?
I am reading fw2.2: A Quantitative Trait Locus Key to the Evolution of Tomato Fruit Size (doi: 10.1126/science.289.5476.85).
The authors are trying to find the gene that makes tomatoes bigger. As far as I understand, previous research had narrowed it down to "something" in the region of the genome called fw2.2. They are trying to determine the actual genetic elements responsible (which turns out to be a gene similar to human HRAS).
Supposedly, the big-fruit allele is recessive and the small-fruit allele is dominant.
They say (in section Genetic complementation with fw2.2) that:

They got a YAC containing the fw2.2.
They "screened a cDNA library" with the YAC to find transcripts that were potentially relevant. (How?)
They "screened a cosmid library" of genomic fragments to find the stretch of genome that the cosmid came from. (How?)

It is unclear to me how steps 2 and 3 work. Can someone explain how you can take a YAC, cDNA library and cosmid library to find the gene inside the region responsible for your trait, as these researchers describe?

The YAC contains a segment of chromosomal DNA. By using it as a probe they could screen the cDNA library to find cDNAs derived from that genomic region. This would be done by plaque or colony hybridisation. The cDNA clones thus identified represent the "candidate genes" .
The last step is a little unclear. Clearly they are identifying cosmid clones that map to the segment of interest, but they could be using either the YAC or relevant cDNA clones (could be pooled for this step depending upon their aim) as probes. My guess is that they used individual cDNA clones to find corresponding cosmid fragments so that they could home in on the regions encoding the identified cDNAs.

I am skeptical because firstly the YAC contains one allele, while the cDNA comes from an organism that has the other allele (a detail in the paper). Secondly, this becomes dubious if the gene on the ORF is spliced (like this one). For hybridizing cDNA to cosmids, there is again the potential issue of exons/introns. Or are you saying the cDNA would still hybridize if only a small part of it was complementary?

@Superbest - hybridisation of probe to clone will occur if there is shared sequence. The fact that there might be small differences in sequence (alleles) or missing sequence (no introns in cDNA clone) will be irrelevant. Before transcriptomics this was the standard way to relate genomic DNA mapping to information about transcripts coming from cDNA cloning.


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What's a good and reliable database on the pharmacodynamic and pharmacokinetic data of drugs both approved and unapproved?
What's a good and reliable database for the pharmacodynamic and pharmacokinetic data of drugs both approved (in the US and elsewhere) and unapproved?

For approved drugs, the Drugs @FDA database at CDER (Center for Drug Evaluation and Research) aggregates labeling information (which includes at least a cursory PD explanation and a listing of or reference to common PK data for the substance) for most modern drugs.
Unapproved drugs may be a bit trickier to find out about, but the FDA maintains a list of contract research organizations (CROs) who are running trials here, and the actual trials can be found on http://www.clinicaltrials.gov/, which will have citations for the papers that have been published.
Drugs in their earliest stages of development, i.e., internal to a pharma company, are likely to be kept pretty tightly under wraps.
I don't know enough about the governing bodies in other countries to know where any international data would be, but I assume you can find published papers for substances in those countries as well.

Where exactly on this site do you find the PD and PK data? I looked up sertraline all I got was these sort of pages...http://www.accessdata.fda.gov/scripts/cder/drugsatfda/index.cfm?fuseaction=Search.Overview

If you go to the brand for the drug (Zoloft), click on the pill form, and then click on the "label data", it will come up.  On the main screen with the brand drugs, it also has a link that says "label available"  (they aren't labels any longer, but those inserts that manufacturers put in, but they retain the old name).

@BrentonHorne The generics don't need labeling info, only bioequivalence, so I think the information for PK is retained with the original IND number.

If you haven't already, I'd recommend volunteering in a university lab, because you clearly have a strong passion for this with all of your questions!

Before I asked this question I knew of a website that provides reliable (from the US government) pharmacodynamic and pharmacokinetic data for FDA-approved drugs: DailyMed. I didn't accept it as an answer because of the fact that it is just FDA-approved drugs but I'm interested in other drugs like moclobemide, tianeptine, piracetam, aniracetam, nefopam, flupirtine and levomepromazine too.


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Horizontal gene transfer from humans
It is known that some viruses embed themselves in the human genome. Is there a mechanism by which human genes can be transferred to other animals or plants by means of viruses shuttling them from humans to other organisms?

Yes, Horizontal gene transfer (HGT) can happen in both ways, from prokaryotes to eukaryotes and vice versa. So far less attension is given to from eukaryotes to prokaryotes HGT. It has played very important role in eukaryotic evolution also. Following figure from (Patrick and Palmer 2008) shows some potential cases in eukaryotic phylogeny.

You can find many such examples from above reference. Coming to human part, there are few cases like From Humans to Plasmodium vivax and From human to Neisseria gonorrhoeae , where researchers have shown evidence of HGT from humans to prokaryotes. Unfortunately , there is very little on mechanism by which they transfer. It is matter of speculation right now as these studies are controversial.

Is this only about organelle genes?

No, even nuclear genes undergo HGT as mentioned in reference articles. You can check that paper, it has few examples.


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Are fish and reptilian scales homologous?
Wikipedia:

Fish scales are dermally derived, specifically in the mesoderm. This
  fact distinguishes them from reptile scales paleontologically.

So aren't reptilia scales also dermally derived?

No, fish scales are dermal (= formed in derma) bones like skull roof bones. Scales in reptiles are formed by epidermis and are made primarily of protein (from keratinocytes), being similar in derivation to hair, feather and nails.
On the other hand, in reptiles one must differentiate between scales and osteoderms (= scutes). Scutes are widespread among reptiles and they are similar to fish scales in that they are produced in derma and are ossified. Similar structures are found in some amphibians and in armadillo. Nevertheless, different types of osteoderms are currently considered as converges: "it is essential to recognize that osteoderms represent non-homologous structures that have been independently evolved a number of times" and have no direct homology with fish scales.

Do u mean fish scales disappeared and then reptilie scales re-emerged?

@Anixx I don't know anything about reptile and fish evolutionary history, but it's also possible that both developed after divergence. According to wikipedia, scales have evolved multiple times. Also, some reptiles have scutes which are derived from the dermis, like fish scales.

Scales must have been present in the ancestor of Tetrapoda. Actinistia (like Latimeria), for example, had/have cosmoid scales. Other elements of dermal ossification are skull roof bones and teeth, and only they are found in Tetrapoda. Hair, reptile scales (and feather on their basis) have absolutely no relation to dermal bony elements.

@canadianer can scales develop into scutes ever rather than other way around?

@har-wradim I thought skull originates as several vertebrae.

No, the bones of the skull roof have a completely different origin.

@canadianer Indeed, we have a terminological problem scales != scutes. I have modified my answer.

Are teeth bones?

The scales of reptiles are made of proteins not present in fish, and are regulated by genes not present in fish.
Proteins produced in the skin prevent amniotes from drying out. A specific kind of springy protein (corneous beta protein) produced by sauropsids (lizards, crocs, birds, etc.) produces what we now look at and call scales. This protein makes tiny springy bits that are ~50% smaller than the smallest bits in keratin proteins that we mammals make, so it may be critical for allowing the evolution of fancy feathers. Sauropsida mix these springy proteins into their hard skin bits to control how flexible, strong, etc. the pieces are.
I find this recent review paper super-helpful:
https://onlinelibrary.wiley.com/doi/epdf/10.1002/jez.b.22840
To summarize, the last common ancestor of a tuatara and a sparrow probably had some resistant skin material made with corneous beta proteins that formed in the upper layer of skin. Crown-groups evolved increasingly complex assignments for this material: claws, scales, shell, feathers, rhamphotheca.
I'm glad to see this review paper, because this makes the springy protein inside the scales of lizards and birds another good synapomorphy of sauropsids, which is easier for college freshman to see on the first week of class than the wacky regrown history of diapsid skulls.


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Can sexual reproduction create new genetic information?
Is there a small chance that in sexual reproduction a new allele forms in the off-spring that was not present in either of the parents, or are the alleles in the offspring always from at least one of the parents?
Is new genetic information ever created during sexual reproduction, or only through mutations during an organisms life time?

Only gamete genes can be passed on from the organism, they are transient. it is estimated that 2/3rd of the mouse genome has been completely rewritten since 65mn years. mice only have 1/3rd of their original genome since that time. https://www.wired.com/story/shrinking-bat-genomes-spark-a-new-model-of-evolution/ gene variants only occur during transcription, i.e. the gametogenesis.

Homologous Recombination not only shuffles different mutations together, but similar sequences near each other from gene duplication events and from regions with highly repetitive sequences can recombine and cause gross changes in the sequence of the genome in hot spots.

That'd be any different in mitosis? I'd like to get a hold on what is specific to crossing over - what kind of mutations are specific to maiotic crossing (over)?

mitosis pretty much just duplicates the chromosomes in the cell.  (some changes do happen but not on the scale of meiosis).  In Meiosis the two chromosomes mix and mutations on the different copies of the two chromosomes can end up in the same chromosome.  the ends of genes can be changed to kill or activate the gene. lots more can happen than mitosis

An interesting question! During homologous recombinations many mutations are actually fixed (here meaning that those that have accumulated over time can be restored) as both chromosomes are condensed and can be compared by the DNA repair enzymes. However additionally mutations can occur and be passed on. As gametocytes primarily do not have to do much more than housekeeping (energy metabolism, basic cellular processes etc) genes they do not rely on can mutate and become dysfunctional. This frequently causes miscarriages, if you check the chromosomes there can be massive errors due to deletions or translocations in miscarried fetuses. Specifically the ova, as these are made before the female is born and then are "revived" as needed they carry the burden of mutations throughout life and this causes the increased rate of genetic diseases (particularly Down's syndrome) observed in later pregnancies.
tl;dr
Mutations can continue if they're not deleterious. Those that are particularly common that lie in "functional" genes are the ones that lie in HLA. These genes are involved in the immune system, and differences across generations are frequently observed. This is because there are many and if one fails, another can take its place. Mutations that are neutral occur the most frequently (i.e. don't affect offspring at all). But new alleles can most definitely be generated, and is the whole basis of evolution.

Many mutations occur during DNA replication (or when a mutagen is around, but that also largely affects replication).
Mutations occurring "during sexual reproduction" might occur during gametogenesis, when the eggs and sperm are developing in the parents. If a mutation were to occur during these processes, it could be that the alleles in the offspring are different from that of both parents.  Alternatively, an intragenic crossover during synapsis might produce new alleles (if the parent is heterozygous).

"Alternatively, an intragenic crossover during synapsis might produce new alleles (if the parent is heterozygous)"  - There seems to be some concept of allele that encompasses the exchange of parts thereof. I mean, allele can be shifted, but can parts of alleles be shifted, too? That, indeed, would be different from creation of new alleles by mutation and transcription, the latter I read of as being excluded from "allelic variation".

I know of some discussion about "what is a gene?". - What is in a gene that might be exchanged means, what is a gene, in an allelic approach.

Biological information has several hierarchies is ambiguous between syntactic information in a hierarchical modular system, and functional information, without a particular context[1].
Out of necessity the DNA is sequence is generally highly conserved, but small changes can easily lead to gross changes in folding, function and the minimum energy states of the protein. (Proteins are ultimately dynamic systems, with many constantly sampling their minimum energy conformation structures - the static pictures on magazine and book covers are misleading)
Additionally an allele, by definition, is a gene variant that occurs in at least 1% of the population - by consensus (and and sufficient statistical power). As such the term is part of population genetics. For instance, for a 400AA long protein, that would mean that a particular homologous recombination event has to occur very frequently and be favored by at least one of many (known) mechanisms.
Is new genetic information ever created during sexual reproduction, or only through mutations during an organisms life time?
Yes. Recombination has several mechanisms, is not a perfect event, and shows different efficiencies depending on the type of mechanism and "helpers"/helper-types as well as helper concentrations involved, - notwithstanding cofactor-concentrations.
[1]John Collier, Hierarchical Dynamical Information Systems With a Focus on
Biology, Entropy 2003, 5, pg. 100-124


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What is needed for a G-matrix?
I have been doing a lot of reading on quantitative genetics and the G- (and B-) matrix lately. I get the principle behind performing the analysis now but I am still not sure how to do it. I'd like to be able to try it out with some dummy/old data in R to see how it is done.
Let's pretend I have measured 5 traits of Drosophila (Wing length, lifespan, eye pigmentation, bristle number, and fitness). Could I construct a G-matrix for the population from this data and also get a B-matrix to measure the selection on the traits?
Aims of the post:
1) What information (trait measurements, fitness scores etc.) is needed to construct G- and B- matrices?
2) I would like to find print or online material that would guide me in actually implementing this method. It seems like there is an awful lot of papers saying that G-matrices are great, but no one actually says how to do them in real life...

Your link talk about G-matrix only. I don't know what a B-matrix is. Do you have a link that explain what is a B-matrix? Thks

@Remi.b The b-matrix is a sub matrix within the g-matrix (the g matrix is constructed of four sub matrices, Gm [male genetic variance and covariance] Gf for female too, B (and B transposed) with the cross sex genetic covariance

A short description of what is a G-matrix can be found in this question

To construct the G-matrix you need additive genetic variances and covariances for all traits, so you normally need results from breeding experiments (e.g. phenotypic midparent-offspring data), that you can do parent-offspring regressions on. Don't know any good online sources but see Balding et al. 2007 p. 534ff for some info. I've seen methods that claim that the G-matrix can be estimated directly from phenotypic data from unrelated individuals (e.g. Zintzaras 2011) or from genomic info e.g. SNPs (Vattikuti et al. 2013), but are not familiar with these and do not know how reliable they are.
A clear background on using mixed models to estimate the G-matrix, including examples/tutorials, can be found in Wilson et al (2009).
Or did you have something else/something more specific in mind?

There is really two aspects to this for me I guess. Firstly, I'd like to know how they can be done. Secondly I am trying to figure if I could do them using trait values from hemiclonal lines of drosophila such that I get sex specific trait values for each haplotype and can therefore make a B matrix.

Well, you should be able to get genetic variances from hemiclonal lines - you need to carefully consider exactly how to calculate them and the amount of heritability captured though. What do you mean with: "Firstly, I'd like to know how they can be done". What the matrices contain, how to technically peform the regressions or something else? I suspected that you were after something more specific, but you should update the question to make it less unclear.

Also, have you looked at Animal models (statistical mixed models), where the entire pedigree can be used to estimate components of the G-matrix?

what I mean by "how they can be done" is what sort of data do I need, what needs to be measured, as it already says in the question

@GriffinEvo I guess this is what is unclear to me; in the simple case, what you need for a G-matrix is phenotypic data on the traits of interest and a known relationship between individuals (e.g. parent-offspring). I also wrote this in my answer, but apparently you are looking for something else. To account for e.g. environmental factors, sex or a known pedigree you need a more complex statistical model, e.g. Animal models. I have updated my answer with a paper that might be of use.


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What is the best way to clean plastic flasks that have been used for cell cultures - is virkon a good idea?
When you use cultures e.g. insect cells, which are infected with virus one way to clean the (plastics) shake flasks is with virkon. Which is the most effective way to clean your flasks in order to extinguish the virus?
Also, is it effective to use SDS in order to denatured the virus proteins?

I've always cultured either in disposable plastic vessels, or in glass flasks, so that they can be autoclaved and run through a depyrogenation oven. SDS will likely disrupt the virus particles, but it won't do anything about leftover DNA/RNA, which could still be infective/pathogenic.

I use a disinfectant solution of such as lizol (popular floor/toilet disinfectant).

Just to be clear, when you say clean, do you mean to disinfect to throw away, or do you plan on reusing them?  I would certainly not reuse.  Bleach is always a good idea, and when I did more serious BSL 3 work we had to use PAA.

I use virkon for cell cultures, but for viruses I tended to use standard bleach during the time I worked in a virology lab.


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Why do people and animals stretch out their bodies and what is causing this behaviour?
I noticed that my cat which is only 6 months old has started stretching its body from time to time. Then I thought that this motion doesn't seem very natural from another cat's viewpoint, so my cat probably didn't try to imitate some other cat all of a sudden and learned it like that. This action must have been caused by something else then. Or at least that's what I think.
Both animals and people stretch their muscles from time to time, but it doesn't seem to be caused by memory of others doing it. So how does this action originate in them?

stretching also occurs in animals that wake up and when yawning.

Humans and other animals have lots of innate behaviors that are not learned from observation, i.e. behaviors that are hard-wired into our nervous system, and this is one of them. Suckling reflexes in mammals and the Moro reflex is human babies (which we grow out of) are other simple examples.
The stretching behaviours you are referring to are usually labelled pandiculation in humans (defined as involuntary stretching of the soft tissues), and yawning is often considered a special case of this. These kinds of behaviours are also normally related to transition periods between high-low activity in animals (Walusinskie, 2006). In practice, stretching functions as a way to reverse the muscular atonia during REM sleep, and is in this sense a way to restore homeostatic functions (Fraser, 1989; Walusinskie, 2006).
A paper by Rial et al (2010) deals with the evolution of sleep and wakefulness in mammals from our reptile predecessors, and indicates that stretching behaviours might have originated/evolved from post-basking activities, more specifically risk-assessment behaviours, such as:

...risk assessment behaviour (RAB) and consists of the suspension of current behaviour, to be replaced by head dipping movements, eye scanning, rearing and
  adopting stretch attending postures...

There is most likely much more to be said about this, and the paper cited above contains many references that can provide further clarification and evidence. A short comparative discussion of pandiculation is found in Frasier (1989).


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How should I put a large phylogeny into a scientific paper?
I've been trying to put a phylogeny tree into a scientific paper. This tree includes ~220 species, which is too too large for one page for journal articles (Letter or A4 size). But in my paper it is crucial to show the whole tree on which the among-species distribution of a characteristic is indicated. I have looked up some journal issues but so far haven't found any similarly large phylogeny in one article. How do people usually treat this kind of situation in scientific papers? Could anybody tell me how to do it, or show me examples? Thank you so much.

Which journal and article type are you thinking of? I'd probably suggest it would have to be a supplement if it's too large for a page - is it also possible to simplify the graphic you are trying to display, perhaps by grouping?

Have you tried contactating the editors about this problem? Usually they are helpful.

Also, don't forget that you can deposit your full tree in treebase. So you can show the collapsed tree in the paper, and give a link to the full tree somewhere in the text.

The simplest way of course is to add it to the supplementary materials. However, 220 species are not that many, you should be able to fit that into a page. You have not shown us your tree so it is kind of hard to give specific advice but I am guessing that you have a linear rather than circular tree. If you convert it to a circular tree you should be able to fit it on a single page.
Here are a few random examples of large circular trees I found on the internet:

If you update your question to show us the actual tree I might be able to give you more specific advice. For example, you could split the tree into smaller ones, each showing a specific order or class or whatever resolution you are working on. There are various tricks you can try but they all depend on the details.

A circular tree is basically the only way to fit a large number of species onto a single page. Obviously, there is a tradeoff between being able to read each of the species names and the number of species you have in your tree. If the big pattern is important, rather than individual names, then you should be fine. Just make the species names as small as they need to be to fit. You can also include an arbitrarily large PDF of your tree with legible names as a supplement.

It is not always essential to show a big tree.
My opinion might be biased but it seems to me that huge figures with illegible labels are just a gimmick to make the reader feel that it is a great analysis (another case is that of networks).
First of all it is important to decide what is that you really want to convey from your figure. For example if your comparing some species with different clades then you can show the last common ancestor instead of showing all members of the clade.
As far as 220 species are concerned it will be tough to fit all of them stacked. But if you split them into two stacks it would be possible to fit with all labels legible (Paper=A4, Fontsize=6pt).

Agreed about people just wanting to make it look fancy - I often see people making figures (using R they have been to me for help with coding) and once they've put a lot of effort in to a figure they realize it doesn't really show the point but have become to attached to it because it was so hard to make. Wish more would think, before starting to make the figure, about what they want their figure to show - would save a lot of time and hassle!

LOL @GriffinEvo "become too attached to it because it was so hard to make".. This can become a PhD comics strip :)


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Why do some ant workers still wander at night?
As far as I have seen, the vast majority of workers in colonies of diurnal, non-nomadic species return to their nests and remain there at night. The colonies seem to forage largely during the day. However, a few individuals of said colonies would still wander far from the nest at night. I don’t believe they are lost because they still seem to be following pheromone tracks.
Why do they do that? What drives them to still come out at night and not remain in the nest like most other workers do? Are they any different in terms of caste? Are they always the same individuals? Is there a selection process to decide who will wander off at night? Are they somehow invalid and can't tell day from night? Is that somehow evolutionarily advantageous (e.g. having a few workers take some risk at night, maintaining the pheromone tracks throughout the night so that the other workers don't have to start all over the next morning)?
Someone (jokingly) told me those ants must still be hungry, but I don't immediately buy that explanation because my understanding is that most species will store food in the nest in one form or another anyway, or they just share food by trophollaxis.

I wonder if the nocturnal ones might have been affected by the Dicrocoelium dendriticum parasite. Can you take a look at https://biology.stackexchange.com/a/89248/55929 and let me know if the ant behaviour matches that given in Example 3 there?


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Can Infant Crocodiles digest Bread?
I'm just curious as to whether crocodiles and if you require specifics, saltwater crocodiles, could eat bread as infants. I was watching Lake Placid and I was curious as to whether infant saltwater crocodiles could even digest bread.

From a quick search it seems that amylase production in reptiles is highly variable and is generally a function of the eating habits. According to that logic crocodiles shouldnt produce amylase. Therefore I shall guess that crocs cant digest bread

This question seems more suitable for Pets-SE

If @WYSIWYG could convert his comment in an answer I think this is an OK question. I haven't seen much folks holding a croc as pet ;)


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Are simple esters like those used as flavouring agents metabolised into their constituent carboxylic acids and alcohols in the human body?
By this I mean to ask whether say ethyl butanoate is hydrolysed in humans into ethanol and butyric (butanoic) acid. This is of interest to me as a pharmacology researcher because butyric acid, for instance, serves as a potent histone deacetylase (HDAC) inhibitor and hence increases gene expression but it has very poor oral bioavailability and I am curious as to whether there's any theoretical basis for suspecting that using butyric acid esters as prodrugs would be a more efficient way of delivering butyric acid.
Here is the molecular structure of ethyl butanoate:


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Why is a nicotinamide-tryptophan combination used to treat affective episodes in a few older clinical trials?
At least one of the journal articles that reported on such clinical trials allured to the nicotinamide-tryptophan pathway that I assume must be related to the metabolism of tryptophan into serotonin since at least one of these journal articles placed some emphasis on the serotonin hypothesis of depression.


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Are there any enzymes synthesised by humans that specifically catalyse the hydrolysis of non-cyclic Imides?
Imides or dicarbonyl amides are an interesting class of compounds that includes the pharmaceuticals thalidomide, aniracetam and a few other drugs. These compounds, however, are cyclic and I'm wondering whether there's an enzyme found in the human body that specifically catalyses the degradation of non-cyclic imides. I'm thinking that fatty acid amide hydrolase (FAAH) may catalyse the hydrolysis of non-cyclic imides at least as a minor metabolic pathway.


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How do prokaryotes perform cellular respiration without membrane-bound organelles?
In order to survive, prokaryotes such as bacteria need to produce energy from food such as glucose. In eukaryotic cells, respiration is performed by mitochondria, but prokaryotic cells do not have membrane-enclosed organelles. How do prokaryotic cells respirate without mitochondria?

This Wikipedia page has information on endosymbiosis a.k.a symbiogenesis https://en.wikipedia.org/wiki/Symbiogenesis

Mitochondria are very similar to bacteria and are thought to have originated from bacteria. This points you to the answer: bacteria produce ATPs the same way mitochondria do, with the oxidation machinery place in their plasma membrane (analogous to the mitochondrial membrane).

If you could add a diagram or a reference then it would be great.


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How extensive is CD47?
CD47 aka the "don't eat me" signal has recently been claimed to be expressed on all tumor cells. This doesn't seem to corroborate with other cell-biology experiments. On what other cells is CD47 expressed?

I don't know how extensive. Let's run a simple data query and find out: Go to GEO at NCBI. In the "Gene profiles" window, type CD47, and hit enter to launch the query. At the top of the resulting page, use the link labeled "Limits" to restrict the 7000+ results to human by entering the term "human" in the "DataSet organism" window. So, there are 3700+ results. Look through them to get an idea of which cell types and under which conditions CD47 is expressed.
Let's try a second method. Go to the BioGPS portal. Enter CD47 in the appropriate window and run the query. From the results, select the row with ID # 961 as this represents the human gene CD47. The resulting gene expression/activity chart for Hs (human) will show you in more general terms where CD47 is expressed.

I can't give a comprehensive answer to this, but the CD proteins are found on white blood cells of various types.  If you think about it its impossible that a surface protein could be only observed on cancer cells as cancer is a cell line which is a reproductive dead end.   You can see on the geneatlas box on the lower right side of the page - its gene is expressed, at least to a small amount, on nearly every major tissue type.


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Where can I find histograms and tables of prevalence of mutations in cancer?
At some point in the past I found a cancer portal site which had aggregated data for the relationships between various mutations and their prevalence in cancer types and tumor data. The data was presented in various pleasantly coloured interactive histograms and you could search per-gene or per-disease.
However after spending a few hours, I cannot find the site again. Though I have found many sites with a great deal of data and nice visualizations.
The nearest looking site, was this one:
http://plugins.biogps.org/data_chart/data_chart.cgi?id=673
But that doesn't have the level of detail that I remember.

Perhaps you mean COSMIC? The EBI Gene Expression Atlas also has pretty charts, but now mutations.

Your description sounds a lot like the International Cancer Genome Consortium's website. Choose a cancer and click your way to "Project Data" and you'll see some nicely covered histograms describing disease prevalence. You can also get mutation data among other things
Another good bet is the cBio Portal. If you click on "Data Sets" at the main page, you can choose a cancer and get various data in the "Study Summary" section including the prevalence of mutations within the study dataset.