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Can CRISPR-cas9 be used to insert a large gene?
I would like to insert a 1500 bp or longer gene to the broken site in E.coli (or may be bacillus subtilis which support NHEJ) after cut with Crispr-Cas9. Is this possible for both NHEJ or HDR?

CRIPSR-Cas9 can be used in eukaryotes to insert much larger fragments (using two different sgRNAs and HDR), so in in principle this should be possible - I'm not sure if it will work in bacteria though.

@Nicolai thank you very much, can only one sgRNA work?


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Why do simulations of dichromatic color vision portray medium wavelengths as yellow rather than green?
Please take the time to read & answer this at your own convenient pace.
Is this even the right way to put this?
Do you think this post better belongs in the Physics or Philosophy forums?
This must be part of the old philosophical question of whether you see the same colors as I do.
This is a simple question really, but the description may get a bit technical if your not familiar with the basics. If you find this complicated to read then I can write it more basically if you desire.
It’s important to bear in mind that we shouldn’t equate or compare other animals’ senses & perceptions with our own, such as ‘modified’, ‘enhanced’, ‘dehanced’, ‘reduced’ or ‘increased’ human senses.
We can form educated estimations about how the perception of other animals is through study of their nervous systems, brain & sense organ anatomies & behavioral tests, but have little way of proving how they actually experience things.
The same applies to other humans, only that we have more ways of proving how other humans actually experience things because we have language, but even that’s still very subjective.
It’s a basic fact that unlike shape, dimension & location, sensations are not matter & energy itself, but our brain & mind’s representation of them. For example, how do we know for sure whether other animals even perceive gradients of light as shades of black & white? It could turn out to be something totally different, even uncomparable or unimaginable for us.
This is common sense when mentioned, but many people forget or aren’t aware of this basic fact to keep in mind.
Nevertheless, what I’m wondering is whether the short-medium wavelength dichromats of most mammals & some humans & New World Monkeys, which have two kinds of opsins sensitive to short & medium visible EM wavelengths in constrast to having the extra opsin sensitive to long visible EM wavelength for most humans & anthropoid primates, actually see green or yellow as their primary color representating the middle EM wavelength?
Simulations of dichromatic color vision usually portray them as seeing the primary colors blue & yellow, with the rest being combinations of those primary colors & shades of black, grey & white.
In fact I’ve never come across a dichromatic simulation using green to portray the perception of the middle wavelength color for them.
Its always yellow.
Could it be because we’re not exactly sure whether short-medium dichromats actually see either green or yellow as their primary color for middle wavelength peak, if they even do see those colors for that matter?
However, yellow is not a primary color. It may be in art & design, but it’s not in biology & physics.
Yellow is the extreme end of red & green, & a mixture of red & green.
In biology & physics, red, green & blue are the primary colors.
So what I’m wondering is why do simulations of dichromatic color vision portray the perception of the medium visible EM wavelengths in gradients of yellow rather than green, the actual primary color for middle visible EM wavelength, & how can we know or give the best answer to what color dichromats see as their perception of middle wavelength of Visible EM?
So which color is it? Yellow or green?
& is it the same for all short-medium wavelength dichromats?
How would we know? If we can’t, then what is the best evidence & way to give the best educated guess?
Like why is the dichromatic simulation of the frog & parrots below using yellow & blue to represent their primary colors? Wouldn’t using blue & green be more honest to biology & physics? Isn’t yellow not a primary color but the extreme end of & mixture of both red & green?

which kind of dichromates are you talking about, there are more than one.

Opponent color processing.
https://en.wikipedia.org/wiki/Opponent_process
Studies have shown blue and yellow are opponent colors, as are red and green. We process the colors in opposition, as in perceiving one requires perceiving less of its opponent, equal amounts of both (minus other colors) yields no color in your final visual perception. If you cannot differentiate red and green, than the only two colors you can differentiate reliably are yellow and blue. As a side note this is also why in image processing programs these colors are on paired sliders, it is the simplest way to manipulate color images.
The most common forms of color blindness in humans, and the one all non-primate mammals have prevents them from differentiating red and green.
If you cannot differentiate red and green, and if I show you blue and yellow, you see no color, if I show you red and green you see yellow, becasue your blue cone is not being activated.
The image below is our opponent pairs in our vision.

I just wanted to ask what you mean when you say ‘no color’? Do you actually mean no color at all, or do you specifically mean white, grey or black?

no color would be white, grey, or black, those contain no color at all. Greyscale a colorless scale.

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What are the limiting factors of human stamina?
What are the limiting factors of (human) stamina? Let's define stamina as the capacity to continue doing a physical activity. We clearly have our limits, so what aspects of physiology impose a limit on human physical exertion? How do these aspects work together and interact?
Great detail isn't necessary, but a concise overview is what I am looking for.

I don't have a complete answer but in some ways your question is, as yet, unanswered. It is a bit like asking, "why do we need to sleep?" Also, there are things the body needs for energy that can run out, such as carbohydrates. However, to a limited extent we can increase our "stamina" by taking stimulants such as caffeine.

@takintoolong - An answer based on our best understanding will suffice.

You might start be defining stamina, the word covers a wide variety of factors.

It seems this review has got you covered in pretty good detail: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2375555/

Since your question is being considered too broad by some members of the community, I suggest you narrow it down to "What aspects of physiology impose a limit on human physical exertion?", and/or specifically ask for physiological quantities that correlate with the onset of perceived exhaustion.

Stamina, even if you narrow it down to a capacity to continue a physical activity, is still influenced by diverse factors, including genetic, training, diet, hormonal, psychological, religious, social...It seems that one would need to write almost a book to make "a concise overview" about how various aspects work together. If you are looking for more physical factors, do you maybe want to use the term endurance instead of stamina?

There are multiple factors as already pointed out by others. You should check out a review or a book on muscle physiology. It would be difficult to explain each and every factor that affects muscular performance.

@Jan I believe Justsnilloc is looking for the more proximal factors, what physically is happening when someone reachings their limit.

@John, yes, I get it, but I still have a big problem to decide what to focus on.

It sounds like the OP is asking for an an overview more than anything, I have been looking for my book on kinesiology but have had no luck. I can't remember the actual progression after oxygen debt and running out of glycogen.

A few explanations at the cellular and molecular level:
First, for contraction to happen, muscles need signals from nerves. Replenishing the pool of neurotransmitters (used for each synaptic burst) takes a bit of time, and short-term exhaustion may happen at this level.
In the muscle cells, contraction is caused by a calcium release within the cell, from a cellular compartment called the sarcoplasmic reticulum. This reticulum can only contain so many ions, so if the muscle contracts a lot, it will eventually need to rest for a while to re-accumulate calcium in the sarcoplasmic reticulum to prepare for more contractions.
Muscles need molecular "fuel" (like ATP molecules) to contract/relax. After an intense or sustained effort, these molecules are partially consumed and the muscle simply runs out of energy; it needs a bit of time to resore the pool of metabolites needed to work properly. Conversely, muscle contraction also causes the accumulation of metabolites and ions like potassium, which partially inhibit muscle contraction. Fatigue occurs when these accumulate at high level, and they must be cleared before making new efforts.
For references see:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5668469/ doi:10.1038/emm.2017.194 (general review)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5033663/ doi:10.1249/MSS.0000000000000923 (focuses more on muscle-neuron relationships)
https://www.ncbi.nlm.nih.gov/pubmed/9232550 Green, J Sports Sci. 1997 Jun;15(3):247-56.  (at the cellular scale)
https://www.ncbi.nlm.nih.gov/pubmed/7715628 Williams & Klug, Muscle Nerve. 1995 Apr;18(4):421-34.(more focused on calcium)

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How related do life forms need to be to produce hybrids?
Specifically, I'm asking about infertile hybrids like ligers, mules, camas, etc. How closely related do animals need to be?

Related just enough? There probably isn't a single answer across taxa.

"The number of quantitative trait loci fixed for different alleles in different species should increase with time since speciation" (Genetic distance between species predicts novel trait expression in their hybrids). I suppose that the genetic distance of hybrid parents may be larger in plants than in animals.


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How do adult differentiated somatic cells divide?
My textbook (which is Biotechnology by David P. Clark) states, when talking about fate-mapping potential stem-cells:

"If the marked cell is not a stem cell, the marker will not be passed
  onto descendants since normal differentiated somatic cells do not
  divide by mitosis."

He then goes on to say:

"Most adult differentiated cells do not divide at all and are
  considered postmitotic."

So there are some differentiated somatic cells which divide, but apparently not by mitosis? So what is the technical term for their division?
Here is a screenshot of the passage:

There is no known alternative mechanism of proper cell division apart from mitosis and meiosis in animals. I think this is an unfortunate phrasing where the author is trying to introduce the term "postmitotic". The reason for saying "most  adult differentiated cells" is because some cells in adults are considered differentiated but they still proliferate under certain conditions, like for example the cells of the adaptive immune system.
It could also be that the author is trying to be overly cautious because there are cells that split parts of themselves off and release them. These mechanisms could be considered cell division in some sense but are neither mitosis nor meiosis. Examples of this are the release of platelets by megakaryocytes and the release of extracellular vesicles by cells undergoing apoptosis.

Mammalian cells can do either mitosis or meiosis. Depending on the context, meiosis might be an option but usually this is not the case, and many articles don't explicitly state it when they refer to mitosis.
I do understand your confusion. All I can think of is that perhaps the passage was referring to the fact meiotic cells are not as pluripotent as some other stem cells.


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Hydrophobic interactions in the helix-turn-helix
This slide states that the second helix works to stablize the configuration of the two helixes via hydrophobic interactions. What exactly is this hydrophobic interaction? In other words, what molecular interaction does the second helix have with the recognition helix?

Welcome to SE Biology. The slide does not say anything about "reaction" which involves a change in covalent chemical bonding, but "hydrophobic interactions" which are described here. I have edited your question to fix this.

To quote Sir Max Perutz, in general, the insides of proteins tend to be "waxy", while the outsides of soluble proteins tend to be "soapy."  Those two alpha helices are interacting in a space that is energetically unfavourable for a polar solvent, like water.  Since the outside of the DNA double helix tends to be highly charged, and the edges of the stacked base pairs also have H-bond acceptors and donors, the portion of the alpha helix that interacts with the DNA sequence, will also contain charged amino acid side chains.
In contrast, the portion of the alpha helix that faces inwards, towards the interior of the protein, will have largely non-polar side chains.


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Will our biological bodies be changed after we’ve occupied and settled Mars?
I had this question in mind for very long time, and I could not find a clear answer on the Internet, so I was hoping that you might know the answer.
If we will bring life to planet Mars and a few years later after it turned into a habitable zone, then we will colonize it according to some rumors. But when we colonized Mars after it is turned into a green world like ours, then would our biological body be changed and new origins will be formed? I mean, it will be changed to the point where we will be able to distinguish who’s Martian and who is from Earth? Or, they would still have Earth as their origin?
Just in curiosity.
Can someone please tell me about this matter? I’m trying to understand how things work in our bodies.
Please correct me if I have chosen wrong tags.

We welcome new contributors to SE Biology, but we do ask that they take a moment to read about the scope of the site and the sort of questions that are on-topic here. To quote from the Tour, this "is a question and answer site for biology researchers, academics, and students" — it is not a discussion site. And from the Help "You should only ask practical, answerable questions based on actual problems that you face." So, though perhaps interesting to discuss, your question is off-topic here.

David, the question is not off topic. The question might need to be formed a bit better, however, it is concerning biology, human-biology, and is related to genetics and origins. I think another good tag would be evolution.

The question is making an assumption, that is is certain that humans could establish a self-perpetuating colony on Mars.  (Rather than just research bases, like the ones in Antarctica.)  It would be better asked with a very large IF.  That said, if such a thing happened, and the two populations were reproductively isolated, of course they would diverge, and eventually - a million years or so - become different species.

@takintoolong — It's not explained anywhere obvious, but you should use the @ handle when addressing comments to people other than the poster, otherwise they don't get alerted. As for it not being off-topic, I don't think "we will colonize (Mars)… according to some rumours" represents an "actual problem the poster faces". And really it is not anything that biology researchers, academics, and students are likely to concern themselves with on a serious Q&A site, which  is what this purports to be.

IF we inhabit Mars, it is very likely that our bodies will change. Separation of species is a very common factor for evolution to occur. It is theorized that our continents used to be attached in some places and when they separated animals on each continent evolved differently. There have been other forms of separation which occurred on Earth such as the formation of glaciers, rivers, and mountain ranges. https://www.khanacademy.org/science/biology/her/tree-of-life/a/species-speciation
Although physical changes in our appearance are likely, they would also likely take thousands of years to occur. The differences between "Earthlings" and "Martians" would also depend on how much the two planets interact. It would also be possible for our own future "Earthlings" to look much different than we do today.


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Why are there inverted repeats in response elements?
The following picture shows an inverted repeat sequence in a response element. Response element sequences for glucocorticoids, estrogen, and thyroid hormone show that they all contain inverse repeats. Why do these inverted repeats exist in so many response sequences? In other words, what advantage do they pose to the function of the response element?

Starting with prokaryotic (i.e., bacterial) transcription factors--which were the first to be characterized in depth, this type of pattern was noted.  Even for the "classic" Type II Restriction Endonucleases used for molecular cloning have palindromic recognition sequences.  In all three cases the answer is that the sequence-specific DNA binding protein binds as a dimer, and so each monomer is recognizing a "half-site" (one of the inverted sequences).

Thanks for your answer. We do encourage links to external sources to support assertions in answers. That way the poster or interested readers can check whether or not they are correct, and learn more about a topic than may be appropriate to include in an answer. You can edit your answer at any time.

@RosieF In that case, is it essential that the repeated sequences be inverted? Wouldn't the DNA binding proteins still be able to bind as a dimer if it were just a sequence repeated without inversion?

I think the most important concept here is that by having multiple binding sites concentrated in small region then this will effectively increase the concentration of the transcription factor.  The more sites, the more specificity, and therefore more biological regulation is possible (e.g., ON vs. OFF).  The location of the dimerization interface on the monomer will change if the recognition sites were direct repeats instead of inverted repeats.  There are probably (?) examples of both.  Certainly the first ones characterized were inverted.


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How to promote acorn maturation
I have acorns from an oak tree. They look like:

but I would like to speed up their maturation so they split and I can separate the caps:

How can I speed up this maturation process?

I am not sure but my instinct is to put them in a dry place with a lot of sun.

I would suggest putting them in the ground and watering them (Factors affecting acorn production and germination and early growth of seedlings and seedling sprouts).

Good idea, but in particular I'm not looking to grow a tree, rather to dismantle the acorn.

Sorry. Apparently I misunderstood you. It seems to me that you should leave them to dry (but that's just my feeling). Good luck...


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Skin Colour in "Northern" Regions of The earth
Question: Netflix has recently produced a two-part miniseries, The Evolution of US, that examines the evolution of "man". The topic of of human skin colour was covered and it was stated that 'lighter skin pigmentation was a preferred natural selection for early humans living in the "northern" regions'. The idea being that lighter skin could "absorb" sun-rays; which apparently is necessary for activating vitamin-D. Is this a true statement ? And where might I find good sources of literature to read on this topic ?

Now this particular series does not define "northern" and to be fair neither was the term "lighter skin" . My motivation in asking the question is driven by my own travels in far eastern Russia, Mongolia, Alaska, and parts of Peru and Ecuador. In each of those locations I observed numerous groups of indigenous people with dark brown skin and pitch black straight hair; which seems to contradict the statement in the series.

No "apparently" about sunlight being needed for the formation of Vitamin D. See e.g. [this article]. As regards how much sunlight (UV-B) penetrates the skins of people of different ethnic groups, that I don't know.

@David ; which article are you referring to? Are you sure the link you provided is correct ?

I do apologize — somehow the link never got pasted. Here is is: a review in less-specialized language available from NCBI entitled Vitamin D: The Sunshine Vitamin.

Rather large nitpick here: Equador and Peru are not "northern" (or more accurately, polewards) regions.  In fact (as you might have guessed from the name :-)) the equator passes right through Equador.  As for the indigenous populations of northern Asia & North America, you might ask whether they've lived there long enough to diverge from their ancestral populations.  Evolution takes time.  I might also wonder if the people you saw spent a lot of time outdoors.  Despite a mostly northern European ancestry, I get pretty brown in the summer :-)

Melanin reduces the skin's ability to make Vit D due to reduced UV penetration. This is a disadvantage in northern areas where people get less sun light, and also need to wear heavy cloths to keep warm which adds to the problem. People in Sunny regions have the opposite need as there is more than enough UV light exposure, but they run the risk of developing skin cancer, which is why having melanin provides an evolutionary advantage in these regions.
Interestingly, in the Arabian Gulf region, there is currently an epidemic of Vit D deficiency especially among those with dark skin. Although there is plenty of sun light, people tend to avoid the harsh sun almost completely by commuting strictly in cars and avoiding walking outdoors during the day. Car windows (and glass in general) are opaque to UV rays, therefor reducing the skin's ability to produce Vit D, and forcing many locals who adopt such lifestyle to take oral Vit D supplements.
Here is a link with some references to confirm the medical link between Vit D deficiency and lack of sunlight exposure:
https://www.webmd.com/food-recipes/qa/how-can-dark-skin-lead-to-vitamin-d-deficiency

as a follow up question how might we exlain my observation - the existence of various groups of people living near the arctic regions or at high altitudes and whom have demostrably dark skin colours.

I do not know the specific answer in relation to each of these different groups of people. However I know that in relation to Eskimos, they get their Vit D through diet rather than skin production. Their diet of whale, seal, trout and walrus blubber are all rich in Vit D. I expect you will find the other groups you mentioned have a similar affinity to Vit D rich diets.


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Are there any enzymes without aromatic amino acids?
I'd like to try a new spectroscopic technique to study enzymatic reactions (which reaction doesn't especially matter, something simple and with fast kinetics like catalase would do fine - I'm just trying to test the technique).
Unfortunately, for this technique to work, it is best if there aren't any aromatic amino acids around since it is entirely in the UV range.
I did a quick search in UniProt, and - somewhat surprisingly - there are very few proteins without aromatic amino acids, let alone any enzymes.  The yeast protein sequences database contains zero(!) proteins with no aromatic AAs.  The human database contains a few proteins (~20): for example many metallothioneins, proline-rich proteins, and HMG proteins have no aromatic AAs.  No common enzymes turn up in that search.
Can anyone think of an enzyme - or perhaps a small catalytically active fragment of one - which has no aromatic amino acids?
If not - this is maybe a more general question - what makes aromatic amino acids apparently necessary for most enzymes?
P.S. The yeast results are:
lowest aromatic AA content is 4% in vacuolar ATPase (many DNA/RNA polymerase subunits are also quite low);
median is 11%, many common enzymes eg alcohol dehydrogenase, glutathione oxidoreductase etc fall in that range;
highest is 24% in sterol methyl oxidase
UPDATE A thorough search of the RefSeq NR protein sequence db does turn up a whole lot of stuff, but it tends to be from weird species, mostly bacteria... eg oxaloacetate decarboxylase from Rubrivivax benzoatilyticus (which - maybe no surprise - eats aromatic compounds).  It still seems like there is a strong selective pressure to incorporate aromatic AAs in enzymes

A control for your assumption of selective pressure would be info on proteins that lack other amino acids or groups thereof. I know that is not your particular concern, but…. And out of interest, is it possible to state what replaces the aromatics in the odd-balls you mention — can you do MSAs? If nobody else has done it you might even be able to publish your results.


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Why do (some) cats chase their own tail?
Is this just playful behaviour or are they unaware that it's their own body part ?

The question is too generic. I have had cats who had no interest in their own tail. The answer would probably have to do with animal psychology. It might even be a bit philosophical.

@takintoolong re: "I have had cats who had no interest in their own tail." thank you. although this is kind of obvious, I will edit the question to reflect your comment, just in case

I will try to answer this. First of all we have to make a claim. This behavior can be found in many animals behaviors but it is much more common in dogs.

In cats there is a few reason for that:
Born hunter
Feline predators have a genetic desire to chase anything what is moving. So the chasing tail behavior can be just game for practising hunting skills.
OCD
But if this behavior doesn't stop after the cat grew up it might be a serious problem.  Just like any compulsion behavior in general it might indicate that your lovely cat has obsessive compulsive disorder. If this is the case, your pet can become much more aggressive, hyperactive.

Source
Perfect Paws: Predatory Behavior of Cats
Psychology Today: It's Alive! Why Cats Love Laser Pointers
Pet Place: Feline Hyperesthesia (FHS)


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Statistical Analysis for Blood Sugar Measurements
I've conducted a lab aimed towards finding the impact of soluble fiber intake on the change in blood sugar levels. Following an 8 hour fast, I had test subjects consume a fixed amount of carbohydrates, with a varying amount of soluble fiber, and measured their blood sugar in 20 minute intervals. This was done for two hours each test, generally until blood sugar levels dropped to normal.
5 test subjects were used for the test, each with individual blood sugar responses - for instance, each had consistently different fasting blood sugar levels before food consumption, each had consistently different blood sugar peaks, and so on. Each test subject was tested 4 times, once with no soluble fiber, and 3 more with varying amounts of soluble fiber. The raw data I am now left with is simply a collection of scatter plot graphs displaying rises in blood sugar from normal condition, a peak, and a subsequent drop to normal condition.
I can visibly see from my graphs that more soluble fiber made blood sugar peaks smaller and longer to reach. Data did not always follow this trend, due to some source of error, but a relationship is nevertheless evident. I hope to make a conclusion from this data. What method of statistical analysis could I use to conclude a relationship from these scatter plots? I would like the method to take into account different individual responses, as well as the few data sets that did not confirm a relationship.
I appreciate your help!

You have a pretty complex experimental design. I think this question is better suited for stats.SE, where there are more likely to be those with expertise.

It would help to see your plots. The way I would imagine to present this data is not scatter plots but line plots:

(Each line would have a confidence interval/standard deviation from your different test subjects. This is just a schematic representation. Color represents different experimental conditions. Let me know if I misunderstood your experiment.)
Now, what is your actual question? Your hypothesis? You want to know if the time or height of the peak of blood sugar levels is different between the different fiber levels, right?
So, why not measure this? At what time do you find the peak for each subject and experimental condition and what's the blood sugar level at that time point? Your null hypothesis would be that there is no difference between the test conditions.

Here some mock data show the data spread from your 5 test subjects of the peak height measurements in the 4 different test conditions. Now you reduced your data to a question, where you could use a statistical test to see if you can reject the null hypothesis.
One thing you could do is to perform an ANOVA with e.g. Dunnett's post hoc test to compare your fiber conditions to the control condition
A problem with that is that your conditions are not really independent. And your actual question is not if any of these conditions is different. Your hypothesis would rather be if there is a relationship between fiber content and peak height/delay (null hypothesis would be: there is no relationship).
Here is the same mock data in a scatter plot (color represents test subjects, they overlap, but let's assume there are 5 data points for each condition) with a trendline showing, that with increasing fiber content there is a reduction in peak height:

You could therefore try a correlation analysis and test the statistical significance of your correlation coefficient.
As you see, the statistical analysis very much depends on your hypothesis and how you analyse your raw measurements. I hope, I have correctly identified the issue and this helps you with your analysis.

Yeah, that makes perfect sense! I very much appreciate your help.


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How does temperature affect photosynthesis?
I am doing a lab for biology and my teacher required me to do this virtual lab. However, it does not make sense when seeing the results of the lab. In 30 second trials, it shows that there are 16 bubbles at 10C, 6 bubbles at 25C and 19 at 40C. This should not happen as 25C is near the optimal temperature (at least in respiration) but it shows the opposite.
Is the site wrong or am I wrong?
Site link: http://www.kscience.co.uk/animations/photolab.htm
Constants: 50 Light intensity, full disolved co2, white light color.

Welcome to SE Biology. I am afraid that questions here have to be self-contained. A link to a reference is OK, but readers cannot be expected to go to another site to  find out what the question is. At present the question is not clear. What is the design of the experiment, what are the bubbles supposed to be, and where is it stated that photosynthesis should be optimal at 25C? You need to clarify your question.

It doesn’t look like the link is working for me on iOS - can you add a bit more information or a screenshot to demonstrate what the lab looks like?

Your experiment should look something like this: The effect of temperature on photosynthetic rate of Elodea (pondweed). I assume you used Elodea canadensis for your test. Maybe the plant is already a bit "exhausted" - try to take a different branch. Or maybe it needs more time to get used to the new temperature.


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Highest bite force of a wolf?
Some sites say wolves can bite around 400 psi. But this site claims that when facing a peril they can deliver upto 1200 ?https://plexidors.com/myths-around-dog-bite-force/(skip to the 'How does that measure compared to cousins in the wild?' portion to save time)
  -That's a huge range, and could in theory put them on par with big cats.Is what the site says true?
-I looked online extensively in the internet but I only came across a reddit post where they discuss this and it wasn't conclusive.Why is there a maximum bite force of other animals like crocodiles,gorillas,hyenas etc but not for wolves?

@Specter writes about other units: PSI (pounds per square inch), but I don't know how it counts to N (newton).

The range from mean to maximum of wolve's bite force is huge.

Is it really? According to this Wikipedia page, (Scully, C. (2003). Oxford Handbook of Applied Dental Sciences. p. 151) claims that human masticatory forces range from 70 N to 700 N. Also, (Kim et al., 2018) claims that domestic dogs have a bite force of (147-3417) N, so I don't think it's too implausible for wolves to have the value of (774-2255) N of wolves that @Olga_Swider claims. We see also, on Table 4 on p. 550 of (Eng et al., 2013), the estimated maximum bite force (MBF) spread over the $M^2$ area of the jaw. Eng claims that Gorillas and Chimpanzees have MBFs of 3200 N and 1800 N respectively. I think there's quite a large degree of control of masticatory muscles, which wouldn't make it too surprising that you can have a large range of forces.

This range of wolves' bite forces could put them on par with big cats.

According to p. 621 of (Wroe et al., 2005), lions have a bite force of around 1768 N, while tigers have a bite force of 1525 N. So, it seems that wolves have a significantly smaller mean bite force than big cats. But bear in mind that while dogs and wolves might have a fairly similar jaw size, lions jaws are much larger so their bite force is spread over a much greater area. So exercise caution when comparing them. Similarly, note that PSI is a unit of pressure (force over area), while newtons are a unit of force.

Why isn't there a maximum bite force for wolves?

Says who? Of course there's a maximum. Wolves can't make arbitrarily large forces with their mouths, that's physically impossible.

I did not carry out these tests. I gave the data after literature. In addition, the values given refer to the mean. In another chart, in the second item I cited, it can be read that the "maximum estimated bite force" does not exceed 3000 N.

By the way: I do not think that we can measure the maximum bite strength. You will not get the animal to do it. Only estimation remains.

@Olga I never said you recorded it, I said you claimed it. Also, it's redundant whether the second paper is claiming that "the value is 2255 N" or "the value is estimated as 2255 N"; it's the same effect. There's tonnes of stuff in science that you can't measure directly but have to estimate.

Re "dogs and wolves might have a fairly similar jaw size", that depends on the breed of dog.  A malamute or husky might have a similar jaw size to a wolf, but a Pekinese or an Irish Wolfhound?  Which probably accounts for the wide variation in dog bite force cited.

@Jam - You wrote that you doubt the presented results. I just made it clea,r that it was difficult for me to discuss it, because I did not estimate or measure it. Have a nice day...

In this article (Bite forces and evolutionary adaptation to feeding ecology in Carnivores) they say, that bite forces of wolf (Canis lupus) is 774 N. Literature (Maximum estimated bite force, skull morphology, and primary prey size in North American Carnivores) gives that: "the wolf had a mean maximum
estimated bite force of 2255 N".


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How do people measure how many calories or proteins/fats/сarbohydrates are in some food?
How is the composition (in fats, proteins or carbohydrates) of a certain food estimated and how is the amount of calories provided by the food calculated?

https://www.scientificamerican.com/article/how-do-food-manufacturers/

https://carolina.com/teacher-resources/Interactive/food-calorimetry+/tr23949.tr

Hi! Welcome to StackExchange. Question is nice but would be better if you add some research you've done

Messured by the amount of energy it will take to raise 1 degree celsius in 1 kg of water. You really can never go by what the packaging says either. All depending on how food is prepared, even your digestion differs the count person to person.


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Loss of function in inflammation
The Wikipedia-article about Inflammation says

The five classical signs of inflammation are heat, pain, redness, swelling, and loss of function (Latin calor, dolor, rubor, tumor, and functio laesa).

What does 'loss of function' mean? And how does it occur?

TL;DR: It originally referred to abnormality in "secretion" by the inflamed tissue and later became used to mean any abnormality at all.
This fifth cardinal symptom of inflammation seems to be rather mythological as laid out in detail by Rather (1971, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1749862/?page=3). This source explains that the term seems to have been invented at some point in the 19th century without proper definition. Later authors seem to have interpreted it as basically just meaning "not functioning properly" (although this is literally the definition of unhealthy as opposed to healthy, and not specific to inflammation).
According to Rather, the original source of the confusion may have been the phrase: "...heat, redness, tumour and pain; to which should be added an alteration or suspension of the natural secretions of the part." by Macartney in 1838 (page 8 of the same document). Various versions of mentioning a fifth cardinal symptom that involved altered function made their way through pieces of writing, until it received the Latin term "functio laesa" in the late 19th century (Rather cites a piece from 1882), lending it credibility as an established concept. The passage by Macartney was later cited by Marchand in 1924, who was trying to clear up the confusion around who established the four and potentialy fifth cardinal symptoms of inflammation. Marchand rephrased it into a "fifth cardinal symptom the alteration or disappearance of normal secretion (thus a functio laesa)", trying to explain what, according to Macartney, is the fifth symptom, and adding why it could be called a "loss of function".

Usually, loss of function means some sort of limitation in physical performance. Either force, range of motion, or some other aspect of movement. In this context, loss of function can occur by at least two mechanisms:

mechanical loss of function due to swelling of the tissue around the joint
limitation due to pain associated with movement, part of movement, or too high load.


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Fever vs Inflammation
What's the difference between inflammation and fever? And why is fever called an inflammatory response? Does the word inflammation have both a general and a specific meaning?

Inflammation includes accumulation of inflammatory cells, such as neutrophils or macrophags, in a tissue. The typical four local signs of inflammation include redness (Latin rubor), heat (calor), swelling (tumor), and pain (dolor) (Britannica).
Fever is a symptom, which may or may not be present in a certain inflammatory condition. For example, lung inflammation in pneumonia is usually accompanied with fever, while joint inflammation in rheumatoid arthritis is not.


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How to convert enrichment/depletion to frequency for comparing deep sequencing to sequence profile?
I have two datasets, from different sources, that I need to compare.
The first set is deep sequencing results of a directed evolution experiment, where I have the naive library and selected library counts, and have calculated enrichment/depletion (positive and negative values with no upper or lower bound).
The second set is a set of protein sequences for which I calculate amino acid frequencies (positive values from 0-1).
The goal is to calculate a similarity between the two datasets. Typically I have two of the second type of set (protein sequences) and I calculate similarity based on the amino acid frequencies... What's the best way to convert enrichment/depletion to frequency so I can compare?
Example deep sequencing data, for position 77 of the protein:

$$\text{enrichment} = \log_2\left(\frac{F_S}{F_N}\right)$$
Where $F_S$ is selected frequency and $F_N$ is naïve frequency.
I came up with a possible solution for frequency equivalent from enrichment ($F_E$) but am open to thoughts if it's good or not:
$$F_E = \frac{\displaystyle\frac{F_S}{F_N}}{\displaystyle\sum_\text{amino acid}\frac{F_S}{F_N}}$$

Welcome to SE Biology. Your question is unclear to me. It seems like you have RNA or DNA seq quantification and the frequencies that amino acids occur in a set of amino acid sequences. It might help if you clarify what the sets are as well as what you want to achieve by comparing them.

How did you calculate enrichment? Can you [edit] your question to add the formula for enrichment?

@Michael_A, thank you for your response. I edited to add an example of the sequencing data and a possible solution.

@WYSIWYG, I added an example of my data.

Since you have the data, why not compute the actual frequencies? Or you convert frequencies of the second set to enrichment.

Although the question is kind of confusing at some places, what I understood is that you are trying to compare the relative amino acid enrichments in the two datasets.
As far as I know, you could construct the protein sequences from directed evolution experiment (presumably a time series data. Please clarify that.) and make a multiple sequence alignment (MSA) of that. In order to construct the sequences, there would be some technical procedures that would depend on the type of deep sequencing data you have. Factors such as the read length, protein length and coverage would need to be taken into consideration.
You could similarly make MSA for second datasets too.
Then using tools such as Rate4site (https://www.ncbi.nlm.nih.gov/m/pubmed/12169533/) you would be able to get evoutionary rates per site from MSAs. Then compare the evolutionary rates per sites for two datasets by correlating them.
If the correlation is high, the enrichments in both datasets are similar, otherwise not.


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What are the teeth of the viperfish composed of?
One of the viperfish's (genus Chauliodus) most unique traits is the transparent, needle-like teeth. Some other abyssopelagic fish (e.g. certain angler fish) have similar teeth. I'm curious as to what these teeth are actually made of. They clearly aren't made of bone, and from what I can tell from various fish skeletons, they decay fairly quickly with the rest of the fish.

They are not unique
The are made of enamel and dentine just like ours, Even the enamel in human teeth is translucent. Note viper fish are tiny so their teeth are likewise very small, so they can look transparent just by being translucent an small. Hydroxyapatite, the mineral enamel and dentine are made of is translucent. the difference is in the crystal structure,(teeth or often porous which leads to more scattering and less transparency similar to why dry paper is white and wet paper is translucent (also true of teeth)). Impurities or more precisely what else is present in the enamel and dentine are present has an effect as well, as teeth are not just hydroxyapatite.
Source for the composition of teeth.
source for the translucency and microstructure of teeth
Source discussing how translucency changes with mineralization in cow teeth.

This answer would be improved if it contained a citation to anything having to do with the viperfish or a discussion of the translucency of enamel in particular crystal alignments. In other words, I fear that providing a citation implies that the information in the rest of your answer is found in that citation, which it is not.

Viperfish are not alone in having transparent teeth is is very common, but something on transparency and crystalography is a good idea.


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What are the potential dangers (if any) facing the twin girls recently born in China with their CCR5 gene modified?
According to this Nature news article, a Chinese researcher claims to have made the world's first genome-edited baby using the popular CRISPR–Cas9 genome-editing tool. A gene called CCR5 was modified before the embryo was implanted into the mother. The CCR5 gene is known to produce a protein that is utilized by the HIV to enter human immune cells, and the genome editing performed is expected to make the babies HIV-resistant despite their father being HIV positive.
As a Chinese, I am deeply concerned with the ethical consequences and scientific impacts of this highly controversial experiment. However, to form an opinion for myself, I believe that I first need to know the potential dangers, either expected or speculated, that the twin babies might face in their life. Unfortunately I am not familiar enough with molecular biology to be able to know and judge these myself, and the reports in the media seem very vague on this issue.
So please let me ask: What are the potential dangers (if any) facing the twin girls, and how sure are we now about these dangers, their consequences, and possible countermeasures?

None of the research has been published, so nobody can say anything on this specific case, if it is even true.

@canadianer, but the question is pretty general. There has been lot of debate about the dangers of genetically modifying embryos (off-target modifications/unexpected effects of targeted modifications).

@Michael_A Did I say otherwise?

@canadianer I thought your comment could be read as pointing out a problem with the question. My comment was to highlight that there was no need to alter the question. Anyway, this is a secondary discussion. I'm out.

Important notes:
I am not going into the ethical aspects of editing/removing CCR5 in human embryos, neither will I discuss potential effects of introducing that mutation into the human population. Both of these are very important issues, but out of the scope for this answer.
  As of now I'm not aware of any reliable sources of what was actually done in this case, so I will also keep my answer general / hypothetical without going into any specifics of these particular girls.

That out of the way lets get into the potential problems that could be caused by removing the CCR5 gene from  human embryo using the CRISPR-cas9 system. These can mainly be grouped into two classes: off-target or side effects of the procedure itself and any effects of a non-existing/functional CCR5 by itself.
One additional point I want to mention is that removal of CCR5 does not make one completely immune to HIV, because some strains of the virus (can) use the CXCR4 as a co-receptor instead.
1. CRISPR-Cas9 off-target effects
The CRISPR-Cas9 system has become very popular with scientists in the last few years, because it allows genome editing in very many organism with previously unmatched efficiency and speed. However, people only recently  - when the potential medical use of the system was being considered - started to look into the specificity of the system. What they found was, that while CRISPR-Cas9 is supposed to be very sequence specific it often also induces mutations in genes that were not supposed to be targeted.
There is a quite a lot of ongoing research to reduce these off-target effects, one good example being to use two variant copies of the system that each only cut on strand of the DNA at neighbouring sites (instead of cutting both strands at one site as is normally done).
If such mutations occur while genome editing an embryo the possible effects are very hard to predict - it could be anything from completely harmless to cancer inducing. If one wants any reliable estimate for this, it would be necessary to check for any off-target mutations by sequencing the whole genome of the edited embryo. That however requires (even with very modern techniques) removing at least a single cell from the growing embryo before the IVF procedure can take place and might therefore reduce chances of the IVF being successful.
Main source: Extensive review to CRISPR off-target effects
2. Side-effects of CCR5 removal
Normally it would be very hard (read: basically impossible) to predict what potential side effects the removal of a specific gene would have, even if there are e.g. mice where this has already been done but only studied for specific medical aspects. In this particular case however, we are in luck because there is a naturally occurring mutation called CCR5-Δ32 that also renders the protein completely dysfunctional. We can therefore pretty safely assume that the CCR5 removal by CRISPR-Cas9 will have similar effects to this mutation.
Since CCR5 is a gene expressed by immune cells, it  - unsurprisingly - has influences on various immune functions, but mostly seems to be affect infectious diseases. As this review puts it:

In summary, there are ample data to suggest that CCR5 is involved in both positive and negative regulation of immune functions that relate to the regulation of leukocyte trafficking during infectious and postinfectious diseases.

One particular risk that seems to correlate with non-functional CCR5 is both initial infection and disease progression by flaviviruses. It has been reported that the CCR5-Δ32 mutation increases the risk of being affected by both the Tickborne encephalitis (TBE) virus and West Nile Virus, both of which can affect the nervous system if the diseases progresses far.

Nice and detailed answer that raised a question for me: First, as a side note, is there today an update to add to this question? For example, it appears from my readings in 2022 that single-strand cut is a "feature" operationnal in CRISPR. Second, would there be a possibility to gene-edit a human organism AFTER it has born (and thus reducing the potential side effects during pregnancy)

2019-09-29 update: the answer below is based on a scientific paper that seems to have a major flaw, see https://www.statnews.com/2019/09/27/major-error-undermines-study-suggesting-change-introduced-in-the-crispr-babies-experiment-shortens-lives/ (mirror): the 2 authors have requested that the journal that published their study, Nature Medicine, retract the paper.

The study {1} was published earlier this month and pointed out some side effects of the CCR5-∆ 32 mutation:

Abstract: We use the genotyping and death register information of 409,693 individuals of British
  ancestry to investigate fitness effects of the CCR5-∆ 32 mutation. We estimate a 21%
  increase in the all-cause mortality rate in individuals who are homozygous for the∆ 32 allele.
  A deleterious effect of the∆ 32/∆ 32 mutation is also independently supported by a significant
  deviation from the Hardy–Weinberg equilibrium (HWE) due to a deficiency of∆ 32/∆ 32
  individuals at the time of recruitment.

The article {2} gives an interesting overview of the challenges to use CRISPR gene editing on embryos.

References:

{1} Wei, Xinzhu, and Rasmus Nielsen. "CCR5-∆ 32 is deleterious in the homozygous state in humans." Nature medicine (2019): 1. https://doi.org/10.1038/s41591-019-0459-6 ; Open access through: https://www.nature.com/articles/s41591-019-0459-6.epdf?referrer_access_token=WPFpaFyStI8YbTTEMfC_ttRgN0jAjWel9jnR3ZoTv0Oj3tn20k72VWFe-jjXtNEJHlLKXYkKaqGD9skHjnGnvJUTVNbCDm7LZzwrct9UdoYEGjuFiNmdY_PBv1mOtejfdSOBNIfiYYPHQKxPBPquqX2okvaHuqrbH-cPOgidfYQQoHehy580Z2p1e1IWOQCICnlOBtWq97g3ThPRT3rg3zh0Xu3TB1_y4uDZyqTR0sI3w-e2BhL5AOM01Ot08-PkdJ-2aNqhmxMR6DJJtSfoBfxwDFzkQT_EkudaLLr7jixVT1WokrmAXf_uU6A8hxuZ5-0c1tjYXcnq7amqV7lPTw%3D%3D&tracking_referrer=www.theatlantic.com
{2} Heidi Ledford. CRISPR babies: when will the world be ready? Nature 570, 293-296 (2019). https://doi.org/10.1038/d41586-019-01906-z (mirror)


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Jellyfish gulf of Thailand
I found may such jellyfishes on the Hua Hin beach in 27.11.2018. They measure around 25 cm.
Since I'm more botanist, I have big problem to identify it. Google doesn't help me a lot (spent 3 hours googling and nothing).
Anyone know latin name?

So in a 3 minute search for blue-rimmed Thai jellyfish...Doesn't look like Rhizostoma pulmo, Aequorea, or Cyanea lamarckii,

However,  others have seen similar specimens to yours: see here, here, and here. I'll sleuth a bit more for you in a little bit....


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Centrifuge after sonication
I follow a protocol to get protein from E.coli cells after sonication.
I used to grow 6 litres of large cultures and add IPTG to express the protein. I centrifuge for 10 mins at 8,000 rpm and get the pellets.
Then I do sonication and centrifuge again at 20,000 for 1 hr.
My question is: can I do the last step of centrifugation at 4000 rpm for 2 hr? The centrifuge is no longer working at high speed (20,000rpm)
Thanks

It is better to indicate centrifugation speeds in terms of g instead of RPM. We basically want to know the centrifugal force acting on the sample. The RPM required for a particular amount of centrifugal force depends on the rotor radius.

No, if you use only centrifugation to separate proteins from other parts of the (bacterial) cell, you need very high centrifugal forces. The actual speed (in rpm) you need to separate soluble proteins from the rest of the cell is mostly dependent on the rotor of the centrifuge, because both together determine the acceleration you get, which should be
in the order of at least 10,000 - 100,000 g.
If you do not have a (working) ultracentrifuge available, you could try to precipitate your proteins from the lysate, which would allow you to use a normal centrifuge to collect it. However, this won't be an option if your protein can't be properly re-folded and you need it functional.


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Is a species lifespan affected by meat consumption?
I read a review-like article about the hypothesis of Caleb E. Finch  in a science magazine. The article of interest engages with the idea of Finch

"[arguing] that immune functions and nutrition have been of major importance in the evolution of aging and longevity."

According to this, humans started to regularly consume meat. Meat itself, carrion or injuries during hunting have chances of getting infected and thereby causing death to humans. A strong defensive system against infections lets you survive and its coming into existence may be accompanied by an elongation of our lifespan.
I find myself now asking two questions:
(1) Because the whole article is only about the primate branch, I wonder, whether there are other omnivores that drifted apart concerning their eating habits and if now there is a more carnivorous, longer-living genus?
(2) Do carnivores, in general, have a long lifespan (or is their lifespan highly dependent on a healthy predator–prey equation)? I tried googling, but could not find a relevant scientific resource on this topic.

A major flaw is chimps also eat meat, often other primates, they even hunt for it.  This will put even more stress on the immune system than what we had. The invention of cooking is a more likely suspect, that basically doubled our calorie intake.

Also keep in mind chimps can live for 50 years, which is not much longer than us prior to the invention of medical technology. This sounds like an answer to a question nobody asked.

welcome to Stack Exchange. Maybe for your question it will be useful to search scholar.google.com That engine focuses on scientific literature

The title of your question is a statement. I have converted it into a question, although I doubt whether it can be answered here or anywhere else.

You are going to find too many confounding factors to get ans answer about carnivore lifespan, there are plenty of predatory carnivores that evolved from omnivores but in most cases one or the other side of the split is extinct.

You may have better results asking about Finch's hypothesis, their are plenty of competing ones, one is that humans increased ability to breakdown maillard compounds may be a factors (something we evolved for after we started cooking, or simply that higher intelligence makes longer lifespan more useful, after all evolutionarily speaking longer lifespan is not inherently better.

@John I really hope that somebody posts an example where "the other side of the split" is not extinct. But more importantly: Can you link my to an article, that focuses on the topic of how "higher intelligence makes longer lifespan more useful"?

Its simple, the real benefit of intelligence is learning and learning takes time, longer lived creatures can learn more, many tribal cultures use their elderly for as repositories of knowledge for rare events.

The stated theory is easy to prove with prevalent zoo and other statistics... its just a vague theory.

I don't think that the theory is very reasonable, because animals drink from stagnant ponds (i.e. savanna wells , forest puddles) and have lots of vectors of infection other than rotten meat: cuts and grazes, tract infections, parasites like mosquitoes and nematodes.
The olfactory sense is also very sharp in many carnivores and they can gage the decomposition state of meats. Even humans have a very strong sense of the age of meat using smell, although I can't find  research on it.
The fun thing is to see the age of other animals, i.e. birds and bears. The oldest zoo birds:
Flamingoes, seagulls, vultures, 50-70
parrots 90-120 years.
the oldest panda: 37
the oldest grizzly and polar bear: 40 and 42
Oldest reptiles:
lizards crocodiles and tortoises: 50-100 years
giant tortoise: 150-250 years.
Other herbivores with slow senescence: donkey 60, bison 50, gorilla 60...
research papers don't include any evidence to correlate carnivory and lifespan. It's mostly body mass and ecology, i.e. predation rate.
Carnivores have must stronger stomach acid also which mitigates some of the risk.

Study by Loma Linda showed that 1) a very low meat intake was associated with a significant decrease in risk of death in 4 studies, a nonsignificant decrease in risk of death in the fifth study, and virtually no association in the sixth study; 2) 2 of the studies in which a low meat intake significantly decreased mortality risk also indicated that a longer duration (>/= 2 decades) of adherence to this diet contributed to a significant decrease in mortality risk and a significant 3.6-y (95% CI: 1.4, 5.8 y) increase in life expectancy; and 3) the protective effect of a very low meat intake seems to attenuate after the ninth decade. Some of the variation in the survival advantage in vegetarians may have been due to marked differences between studies in adjustment for confounders, the definition of vegetarian, measurement error, age distribution, the healthy volunteer effect, and intake of specific plant foods by the vegetarians.
CONCLUSION:
Current prospective cohort data from adults in North America and Europe raise the possibility that a lifestyle pattern that includes a very low meat intake is associated with greater longevity.
This study can be read at https://www.ncbi.nlm.nih.gov/pubmed/12936945.

That study has way to many flaws to be useful, it does not differentiate low meat intake and no meat intake, and only compares a dichotomy, so someone who eats nothing but meat and someone who eats meat 1/week are classified together. secondly there is no linkage to the immune system shown nor does it answer any of the OP's questions.

I think this is irrelevant, because (if I understood correctly) the OP is asking about species' lifespans, not the lifespan of individuals within a species.


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How much of my ancestry will match with my brother?
Recently, my brother (full sibling) got his ancestry checked from MyHeritageDNA. They have a similar service like 23 and me and I've found out that both companies are offering the basic service almost the same, with some add-ons which are different.
My question is that if I (I'm a male) send my DNA sample to either organization, how different should I expect the results to be?

Welcome to SE Biology. We expect posters to do some research of their own before posting. Have you considered the genetics and tried to work this out yourself? What do you expect? If you tell us we can tell you if your logic is correct or not.

Should match pretty well. Are you a boy or a girl?

As both you and your full sibling are males, it means that you share the exact same Y chromosome. You also share the same mtDNA as you have the same mother. All the rest is just a bit of segregation and recombination that will lead to minor differences but generally speaking, your ancestry data should be very similar. Specific disease related data might vary though.


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Where is ethanol detoxified? peroxisomes or smooth ER? Or both?
I am reading the textbook Biology (Campbell et al, 2005), and I am confused.
In Chapter 6.4, on page 104, it says that "In the smooth ER,  other enzymes help detoxify drugs <...>", and alcohol is mentioned later.
In Chapter 6.5, on page 111, it says "Peroxisomes in the liver detoxify alcohol <...>"
Googling the question also brought me mixed results.
As I understand it, alcohol detoxification happens in two stages, first oxidising ethanol to the also toxic ethanal, and then oxidising ethanal to acetic acid.
Do these processes happen in different organelles? Is that the reason that both of them are mentioned? Or do they both detoxify alcohol completely, but do it in different circumstances?

It seems that there are multiple (oxidative) pathways.
If you look here, there are multiple references showing how ethanol (alcohol) is detoxified.
Alcohol dehydrogenase (ADH) is found in the stomach and starts breaking down ethanol (see first-pass effect, see also the article Gastric alcohol dehydrogenase activity in man: influence of gender, age, alcohol consumption and smoking in a caucasian population). But it is further detoxified elsewhere like the liver cells where the smooth endoplasmic reticulum contains cytochrome P450 2E1 (CYP2E1) and ADH inside the cytosol. The peroxisome also contains catalase which can use peroxide ($H_2O_2$) to oxidize ethanol to acetaldehyde.
This article (Determinants of Alcohol Use and Abuse: Impact of Quantity and Frequency Patterns on Liver Disease) contains a nice figure (2), which shows the pathways which was reproduced here.
Check out this reference also for more details about the pathways.


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Why is there such a large evening rise of temperature and night sweats in certain diseases like TB, lymphoma etc?
I've heard that it's got to do something with the levels of cortisol which usually dampens the effects of IL-1, but when it's night time the cortisol levels are usually low so IL-1 response is exaggerated.
But why does it occur to a greater extent in diseases like TB and lymphoma? Why is the interleukin 1 effect during night so much greater in these diseases than in case of other viral and bacterial infections?

Where are you getting the idea that temperature doesn't tend to increase at night with other illnesses?

@BryanKrause night sweats are a typical, and at times dramatic symptom characteristic (but not diagnostic) of TB, endocarditis, and certain cancers. I'm not aware of data on the how the mechanism is different from typical fever produced by IL-1 myself. I would say this is a good question.

Of note, there are other instances where fever has a periodicity to it. The quotidian fever of malaria comes to mind, but if I recall, that's associated with the life cycle of the parasite.

@DeNovo But isnt body temperature itself also circadian, with fevers from just about every cause following this cycle (exceptions being anything with an onset or resolution too fast to see it)?

@BryanKrause you're right, body temperature is circadian. I remember a 4th year medical student asking me if a regular increase in temperature by 0.5 C every night meant his patient might have malaria. It didn't. The difference is a matter of degree, but it's a significant degree. Drenching night sweats will make any good clinician immediately suspicious of some specific causes. As to the periodicity of fevers in malaria, the pattern is an increase of 3-4C at regular intervals (the specific interval depends on the species).

@DeNovo I don't doubt that malaria, TB, or lymphoma could have a particularly strong periodicity, but my understanding is that fever of all cause follows a circadian rhythm (again, excluding cases where pyrogen levels are either increasing so rapidly or dispersing quickly, in which case that time course would overwhelm a circadian rhythm, I'm referring to cases where fever is persisting on the order of at least days), whereas OP suggests that this is limited to TB and lymphoma, which seems to be a similar misconception shared by your med student.

OP, I've edited this question to focus on why the nightly increase in temperature is exaggerated in these particular disease (rather than why it occurs at all, since you seem to already have a handle on why it occurs in the general case). @BryanKrause I see your point. I've edited to make it a better question.

I beleive sweating is a sign of Fall in temperature and not Rise?? Am I wrong?

As for some parasitic infections like Wucheria, filarial worms were shed during night, so fever at night. In certain other conditions, temperature outside in daytime is already hot, so body does not need to rise core temperature to kill virus/org ,but need to do say at nights.


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Rejection of valid theories of biology on theoretical grounds
Is there a theory in biology that was initially disregarded as false (because of critical or contrasting perspectives) and only recognized as important after a considerable time, possibly only in recent years, thus significantly impeding its development?

Welcome to SE Biology. Because I assume your first language is not English and because the question relates to ideas (where language is important) I have rewritten it and made the title fit the question. Could you check that this is what you meant. There is one phrase that is unclear to me — "because of critical or contrasting perspectives". Do you mean "because it went against the prevailing ideas of the time"? If so, substitute that as it would clarify. If not, explain what you mean so we can phrase it better.

Extinction was rejected by many on religious grounds until science gained sufficient power and acceptance that the religious opinion no longer mattered. Not a theory though.

I took the liberty to modify @David 's edit and add back in part of the original phrasing that mentioned an interest in only recently accepted previously controversial theories.

I don't think this is a good question for the SE format. There are too many possible answers, and most answers will lead to a discussion of opinion over whether or not that example is an ideal example (and the meanings of words like "theory" "initially" "false" "important" "impeding") rather than anything concrete.

The idea that organisms with mitochondria derive energy from respiration through a proton motive force was considered controversial at the time.
This is the best reference I could find at the time:

His theory explained that it was the energy captured from those protons
  returning to the matrix and not energy stored in an undefined
  high-energy covalent chemical intermediate that was then used to drive
  ATP synthesis. This Nobel Prize-worthy concept (1978) was so counter
  to the leading theories of the day that the field spurned it for the
  better part of a decade.

Pagliarini, D.J., Rutter J. Hallmarks of a new era in mitochondrial biochemistry 2013  Genes Dev.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3877752/

This is a good example of a hypothesis that was not accepted initially. What took it so long to be accepted? Experimental Support! Once someone else had conducted the "acid bath" experiment (or whatever was the first piece of supporting evidence — I'm just going on Stryer) in support, the X~P intermediate that had never been found faded into obscurity. So it is arguable whether the acceptance of the hypothesis/theory without the experimental systems to study it would have made much difference.

I notice from his bio, that the poster is a mathematician, so I have chosen to answer this question as an experimental scientist (a molecular biologist with a chemical education) to a non-experimental scientist:

In my view, for biology, the acceptance or rejection of hypotheses plays only a minor role on the development of the science. This is because actions speak louder than words — it is the experimental validation or support of a hypothesis that is important. If the hypothesis is correct, but the technical or theoretical basis does not exist to test it, then that basis is also lacking to exploit the idea.

This only applies to an open society. An example of the damaging effects of false theory can be seen in the rejection of genetics by the Soviet Union in the 30s (and later) on political grounds (Lysenkoism), a rejection that did not affect science in the West, but was responsible for thousands, if not millions, of deaths by starvation because of its influence on Soviet agricultural practice.
Let us consider the two answers already given (both of which I have upvoted). First @Mowgli on Pasteur and ‘germ theory’. I would maintain that it was only when a mode of killing ‘germs’ by heat was suggested, that practical demonstrations of the effectiveness of measures to prevent spoilage of food and drink (and to prevent sepsis) was possible. And it was these practical demonstrations that overturned the prevailing theories, not the strength of the intellectual arguments against.
The case made by @Cell for the rejection of Mitchell’s hypothesis is perhaps more pertinent. Certainly Oxford biochemists were still taking about X~P (an unidentified ‘high-energy’ phosphorylated intermediate) in the mid 60s, five years after the hypothesis was published in Nature. But the key — and unusual — thing was that this was specifically a hypothesis. It was supported by a variety of arguments and equations, the latter of which would cause many to shrug their shoulders. Clearly some scientists were attracted to the idea, but it took a system with photosynthetic bacteria to provide practical evidence, as well as improved characterization of the membrane ATP-synthase (which was generally referred to as an ATPase, because that was all it could do in vitro). So the maximum of a 10-year lag in acceptance was not caused by the rejection of the idea, but the lack of a means to prove it.
Similar arguments may be made about the non-acceptances of the idea of Avery (1944) that DNA was the genetic material. Although this was based on experiments, one could argue against the experiments. It was only with the determination of the structure of DNA and the development of phage and isotopes, that the means to confirm this idea and develop the field further arose.
That’s how I see it. However I would be interested for suggestions of any other examples (template theory of antibodies?).

Germs
The idea that life is not spontaneously created, but always develops from... well, something.
For decades, centuries even, the notion that invisible micro-organisms were responsible for diseases, mold etc. was controversial.
Louis Pasteur's swan necked flask experiment (in the 1860's!) is one of the last and most famous demonstrations that sterile media must be contaminated and cannot generate life from scratch. He showed that a sterile broth communicating with the outside world through a single aperture was not contaminated if the aperture was long enough to prevent accidental contact with ambient micro-organisms, whereas the broth grew turbid quickly after being directly exposed to air by removing the swan neck.
Before this theory was accepted, the notion that sterility is important notably in hospital settings was often challenged, leading to thousands of people dying of nosocomial infections.

I'm not sure Pasteur's work influenced hospital procedure. I think that the success rate of surgeons that adopted it (in Britain initially I believe) was key. And remember, Pasteur's work was extremely applied: he consulted with the brewing industry, for example. If his advice worked for the brewers it saved them lots of money, and this encouraged others to consider his approach.

I think it did, although not directly. Pasteur's work was a demonstration that there are germs everywhere - regardless of the setting. Pasteur's work was the primary source of Joseph Lister's inspiration to promote aseptic techniques. Pasteur did not make any specific point about hospital acquired infections (Lister did) but he was the starting point of a progressive realization that germs were the prinicpal cause of hospital deaths. An excellent article by Pitt & Aubin (Canadian Journal of Surgery, 2012) tells the full story in greater detail


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Why is there such in interest in antibiotics against Pseudomonas?
I keep finding information on anti-pseudomonal antibiotics, or information specifying the antibiotic has anti-pseudomonal activity. Is there anything peculiar to this bacterium when compared with other gram negative bacteria?

Pseudomonas aeruginosa is versatile (growth requirements) and recalcitrant (biofilm formation).

Indeed Pseudomonas is a very peculiar (and concerning) genus in clinical microbiology, specially P. aeruginosa. The reason why you keep finding emphasis on antibiotics that have pseudomonal activity is because this organism is the model of bacterial antibiotic resistance. It is often considered more deathly than other important multi-resistant bacteria such as S. aureus, Acinetobacter or Enterobacter.
P. aeruginosa is responsible for multi-resistant nosocomial diseases (a basic definition of nosocomial is an infection acquired inside a hospital) that have really high mortality rates. It is not uncommon to see hospital antibiogram results for this bacteria informing about resistance for all the commmonly used classes of antibiotics for Pseudomonas infections including 3rd and 4th generation cephalosporins, fluoroquinolones and carbapenems.
Reference: Evolution of Pseudomonas aeruginosa Antimicrobial Resistance and Fitness under Low and High Mutation Rates
There are LOADS of articles and info to read about P. aeruginosa antibiotic resistance, but I like this one since it tries to explain how the problem appeared from a genomic point of view.


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Berries ID - Can someone help us identify this plant?
Found it in the hilly areas of Meghalaya - a state of India.
Not sure if is edible or not, we haven't tried it but it gives a beautiful blue color when used for dying.
The seeds are big and there is not enough fruit except its like the skin covering the seeds.


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When consuming carbohydrates and fats together, why are the fats caloric?
If I understand things, and I most likely don't: mammals primarily use carbohydrates to produce metabolic energy when there are sufficient carbohydrates to do so.  The use of fats for fuel requires the organism to break down the fat into constituent parts and from there produce either glucose (right?) or ketone bodies.  Presuming that the organism is not in ketosis, it seems that its body would preferentially use carbohydrates for fuel.
This is where my confusion comes in: why would the mammal's body use fats for fuel if its diet contain sufficient carbohydrates?  The real underlying layman's question is: why is that when I eat fat, I have to count those calories, if my body preferentially uses carbohydrates for fuel?

The only way you wouldn't have to count calories from fat is if your digestive system wouldn't absorb them. Fat might not be used immediately as metabolic fuel but it will still be stored as adipose tissue in your body.

So you're saying that the fats are presumably broken into their constituent parts and will be stored as fat tissue if I'm in a caloric surplus, yes?  If so, then to change the question slightly, when I consume a deficit of carbohydrates compared to my base metabolic requirements, and consume the rest as fat (for simplicity), does the fat get turned into adipose tissue and then to fuel, or is it converted directly?

Yes, fat is not turned directly into energy and it is stored first before its usage. If you undergo a carbohydrate deficit you would first make use of your glycogen stored in the liver and muscles before proceeding to use fat for fuel via beta oxidation. I can try to provide a more detailed answer once I get off work later.

@MikeKatz45, it seems that now the question is getting clear and you seem to be able to make an answer. If not an excessive effort for you, I'd love to read a simple explanation about how carbs and fats are consumed at the same time are used for current metabolic needs. Mainly how fats are converted into energy.

To expand on my comments:
Just like you mentioned in your question, carbohydrates (mostly glucose) is used as the primary source of energy when available to satisfy metabolic needs in human cells, however lipids and even proteins will be used if required, in order to produce energy. Since all these biomolecules (carbs, lipids and proteins) can actually be used to sustain the metabolic activity of cells, that means all of them store energy to a greater or lesser extent (which we can quantify in a practical way as food calories). Other things that we eat or drink such as vitamins, cofactors, water, etc. are not accounted for in the calorie count because they can't be broken down to produce energy for metabolism.
Dietary carbohydrates are easily digested into smaller blocks (mostly glucose) and absorbed directly into the bloodstream, afterwards glucose is taken rapidly from the bloodstream by human cells and processed via glycolysis and lactic acid fermentation or the citric acid cycle (all these are metabolic pathways for glucose in humans). Each gram consumed of carbs yields approximately 4 calories of energy.
Lipids on the other hand undergo a more complex process of usage after their slower digestion compared to carbs since after their absorption they have to be transported in special molecules across the lymph, then into the bloodstream and then they can be taken by various kinds of cells. Considering just this, we can start seeing why lipids aren't a fast source of energy (they take long to be available as potential energy sources). Furthermore, the main destination of dietary lipids is the adipose tissue which constitutes a special tissue in which fatty acids can be stored for latter usage. Fatty acids not being used immediately to provide metabolic energy doesn't mean they lose their stored energy (doesn't mean they have no caloric intake value), its just "quiescent" for when its needed (when exercising or when fasting for example).
Each gram of consumed fat yields approximately 9 calories of energy, this quantity is higher compared to that of glucose because the metabolic pathway that breaks down fatty acids (beta-oxidation) in combination with the citric acid cycle produces more metabolic energy (ATP) compared to glycolysis in combination with the same citric acid cycle. However such amounts of energy are not usually required in rest.
It is important to mention that glucose can also be stored in the form of glycogen or even fat since it will be converted to these molecules if there is more glucose available compared to what the cell needs in a given moment. This glucose converted to glycogen or fat also has to be accounted for in the calorie count because its still a potential energy source (just not used right now).
References:
Dietary Carbohydrates - National Agricultural Library
Dietary Lipids - National Agricultural Library
Insights into digestion and absorption of major nutrients in humans - Goodman, B. E.
Food calories per gram of biomolecule - National Agricultural Library

I'm tempted to suggest you to copy-paste the first two paragraphs from p. 430 from your 2nd link https://www.nap.edu/read/10490/chapter/10#430 , which clearly explain how fats are metabolized and why are metabolized after carbs.


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How do we know that mild forms of rabies are nonexistent?
Wikipedia's rabies article says: "Death usually occurs 2 to 10 days after first symptoms. Survival is almost unknown once symptoms have presented, even with the administration of proper and intensive care."
I am wondering why we exclude the possibility of bite victims developing a mild form of rabies, in the same way that influenza can be mild or asymptomatic depending on the individual and the season. I noticed that rabies vaccines use an inactivated (killed) virus, while influenza vaccines can be attenuated, for example cold-adapted, so that a live virus may be used causing minimal symptoms. Clearly, for these vaccines to work, influenza infection must be able to proceed without symptoms. Similarly, the bubonic plague bacillus Yersinia pestis is endemic in many regions and presumably spread through asymptomatic carriers. Rabies vaccines are made from viruses whose infectivity upon intracranial injection is titrated according to a method of serial dilutions, suggesting that a harmless live vaccine would also be feasible at some level of dilution (barring, perhaps, the infeasibility of intracranial administration of such a vaccine).
What evidence do we have to suggest that rabies is different from influenza or plague, i.e. that it is not possible to have an infectious case of rabies with no or with mild symptoms?

There are many people worldwide who are exposed to rabies and don't die (they get treatment), but there are very few of these cases where people don't die after rabies has entered the central nervous system, and even fewer who didn't receive post exposure prophylaxis before the virus reached the central nervous system. Rabies isn't as rare as many would like to believe, unfortunately, with approximately 15 million exposures and 59,000 deaths a year, so data is available.
"Once symptoms have presented" in the Wikipedia article should probably be edited to "once central nervous system symptoms have presented". As discussed in this review rabies entry to the central nervous system is typically the "point of no return". One of the main challenges of rabies is that the virus hides from the immune system inside cells, making its way from muscle to peripheral nerves to the central nervous system before the immune system can mount a response. Once in the central nervous system, it has special protection from immune surveillance. The goal of post exposure prophylaxis is to allow the body to generate an immune response clear the virus before it gets to the central nervous system.
Generally, we say that central nervous system rabies is almost uniformly fatal without treatment because that is what has been observed and reported. *I'm not aware of any published epidemiologic survey looking for anti rabies antibody in healthy non-immunized adults. I know it's not very satisfying, but I would strongly suspect that someone has done a seroepidemiologic study and not published these results, since they're exactly what physicians have been taught since before Hippocrates: a dog bite followed by the characteristic illness leads (almost inevitably) to death. Other illnesses, on the other hand are observed to produce an antibody response in individuals' with mild disease. It is possible that there are unknown cases of mild non-encephalitic rabies that are self limited, but given the 150 years of intense study, I don't think it is likely there is a major aspect of the disease's natural history that hasn't been observed and reported.
Re: your idea about dilution of the vaccine suggesting you could dilute the virus, I think you may have a misconception about what that method actually involves. A killed virus vaccine cannot replicate, and so cannot cause rabies (though some forms of rabies vaccines used in the developing world have fairly high rates of nasty side effects).
Pasteur's risky rabies vaccine trial in 1885 may have involved a live vaccine, but he was notorious for incomplete documentation on his methods. It was essentially, a specimen of air dried rabbit spinal cord that didn't cause rabies in dogs. Here, his method was reported as drying spinal cord segments for longer and longer periods of time until the specimen did not produce rabies in dogs. This isn't a method that "dilutes the virus", but rather a method that attenuates the virus, making it less virulent. Pasteur didn't have methods for detecting what exactly that meant, other than that it didn't cause rabies, but did prevent the animal (or human child) from developing rabies after exposure to a virulent sample.
You can read more about rabies in Murray Medical Microbiology, Ch. 60
*Please see the link in @iayork's comment for a very interesting example of rabies serology in members of two communities in the Peruvian Amazon.

Evidence of Rabies Virus Exposure among Humans in the Peruvian Amazon found serological evidence of rabies exposure in people repeatedly exposed to vampire bats; other papers have found rare seropositive individuals among cavers and raccoon hunters, etc. However, that's not evidence of infection (could be exposure to inactivated rabies antigen floating in the air) or for that matter to rabies (could be a related lyssavirus with lower virulence, especially with the Peruvians and cavers).

@iayork fascinating read. Thank you for that!

Exposure events are very clear in the case of rabies. Unlike the flu, that one may catch without even knowing how or when, individuals at risk of developing rabies are usually clearly identified (for instance, people bitten by wild animals) and as a consequence they are carefully monitored. If they were to occasionally develop mild symptoms like fever, these would not go unnoticed.
In addition, it is very easy to take biological samples from these patients and check for the presence of virus using sensitive detection techniques; it turns out that no case of asymptomatic infection was ever documented, and at this stage it is reasonable to assume that if it had a signifiant risk of happening, we would have seen it by now.

Please would you provide references for your claims. Speaking personally, of the half dozen or so times I've been bitten by wild animals - and not felt well the next day - i ve not reported to anyone. Could you please be specific as to the provenance of your study?

Thanks @Duckisaduckisaduck. I have had similar experiences, but didn't want to describe them in the question, as I worried this would distract people from the question itself and make them want to blame me for not seeking out a painful course of rabies shots.


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Can I get 1% of my one of my great great grandparents genes?
I basically took a 23andme test and found out genetically I was 1% African. The weird part though is that family records shows that my father's mother's grandmother was African, making me 1/16 African. Shouldn't it be closer to 6%?

hi Ray. Nice question. I would suggest you think about some additional question (and maybe 23andme explains it or you might have to search internet). For example, what doe it mean to be 1% African? Technically, all people are from what is currently known as Africa. Also, for example, a lot of people from South Africa have predominantly European ancestry. Finally, when someone says 1%, what is the uncertainty of this number? There is no precise measurement in science, it is always 15.5±0.3 or something

it's a bit like shuffling 16 packs of cards into 1 as far as I know...  That should have a quantitative answer giving the probability of having less than 50% of a parents, less than 25% of a grandparents and less than 6% of a great great GP's genes.  After 4 generations I expect there's a 20% chance that one grandparent has only 1% of genes in an offspring.

The science behind "being X % from a certain place" based on genetic analyses is... approximative at best. It relies on the assumption that some genetic traits are only found in certain (narrow) regions of the planet - which for most of them, is not really true.
Additionally, did your test provide any confidence metric for this result? If not, it may mean that it may be derived from a statistically unsignificant number of traits (and the number could therefore mean anything) or maybe it's simply something like 1% with a confidence interval of several points, in which case the result could be a compatibe the mathematical truth. Genomes are large and have complex dynamics, it it probably difficult to get a precise estimate.
On a side note, there is more genetic diversity in native African populations than on any other continent (for reasons pertaining to Homo sapiens history) so "African" does not describe a homogeneous population.
Source: https://www.nature.com/articles/nature13997 doi:10.1038/nature13997


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Is it possible to deduce facts about a person's parents just by studying his/her genome?
As an example, suppose Anne had abusive parents. Is it theoretically possible to deduce this from her genome even if she didn't inherit this quality (of being an abusive parent)?

Is there any evidence at all that being an abusive parent has a genetic component?

@jamesqf It's likely to have some genetic component, as do most things in life, I guess.

It might seem pernickety but you often can't deduce from a genome; you can only infer from it. For many characteristics about a person, there are only rough, probabilistic associations between genotype and phenotype. Not one-to-one relationships.
You can take an educated guess that someone with a certain genotype could be a social person of European ethnicity with a low risk of psychosis, which might suggest things about their parents. But there are likely many genes that influence those characteristics and still more non-genetic factors. So you couldn't be certain.
For a factor like whether the persons parents had abusive personalities, I think the genetic differences would be so subtle (if existent) and there would be so many other factors (such as the habits and choices of the parents) that you would be very unlikely to be able to draw any conclusive associations. Articles and studies about linking human genetics with a person's characteristics are listed below. If any of the genes in question are linked with those characteristics then the parents of someone with the gene could possibly have those genes and characteristics too.

Personality types including belligerence, charisma, cynicism, housekeeping, lack of personality, obsessive-compulsive behaviour and gullibility.
Psychosis and Schizophrenia risks.
Ethnicity and European ethnicity, which in turn correlate with geographical location, language and certain phenotypes.
Height.

If anyone would like to suggest additions to that list, I'll happily add them.

Not the kind of complex phenotype that you describe (because nobody knows for example if/how "being abusive" is written in the genome), but yes, some things can be determined.
The easiest is through sex chromosomes.
For example: if you look at the X chromosome of a man, you can tell for sure that it comes from his mother (because the Y can only come from the father, quite logically) so any allele that you see there is also part of the mother's genome - but since she has a second copy, maybe it does not translate into a phenotype.
Sometimes you can even guess the phenotype of one of the parents: if you study a woman's X chromosomes and see that both have alleles that cause color-blindness (encoded on this chromosome) it means that the only X chromosome of the father has this allele, so the father is probably color-blind.
See: https://ghr.nlm.nih.gov/condition/color-vision-deficiency


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Is there any relationship between the height of a tree and the number of branches emerging from the main stem?
Is there any relationship between the height of a tree and the number of branches emerging from the main stem?
I am particular interested in spruce or fir.

The height is only one of a few factors; also the species and environment are more significant. A spruce growing in unshaded location may have branches to ground level while the same species in a dense woods will only have branches at the top. A southern pine ( in the US) is often 100 ft tall with all the branches in the top 30 ft ; these trees drop the lower branches because of limited light and because various vines climb into the lower branches ( until the branches die and fall).

My own observation is that most conifers (at least those growing in the western US), and at least some deciduous trees, seem to form a new set of branches each year as the tip grows.  (And likewise with sub-branches.)  How far that growing tip extends during the year depends on species, weather, &c.  So if you counted branch sets (and the knots where low branches had died back), you might have a good estimate of the tree's age.

Not exactly about height-to-branch ratio but an answer more about branching geometry in general.
This is my interpretation of a related question on Reddit, "What determines when/where a branch will grow on a tree?" especially from one answer which I've quoted below. It clarifies a primary mechanism involved. The apical meristem (leader branch / tip of the trunk) releases a hormone, auxin, and as it grows generally upward the concentration of auxin decreases. Too close to the apical meristem and too high auxin, no grow; just the right concentration will generate new branches.
As for the arrangement of hotspots which generate new growth, here's an interesting video on the geometry of plant growth. Not so much about height-to-branch relationship, but it does share important concepts about branch geometry. Basically, branches are forming so as to maximize distance from nearby, previously established branches. All of this seems to be a way to optimize space.
In reality, there are other factors like competition and damage which factor into tree growth. A pristine spruce or fir will have a distinct Phi-like arrangement of branch nodes, as the video linked above describes. How well each branch grows, if at all, will be more complicated.

Basically what you're talking about is phyllotaxy, or the patterning of lateral organs (leaves, branches, etc.) around the axis of growth.
  Some plants will arrange organs in a spiral around the stem as it
  grows, or others will alternate from side to side. This varies a lot,
  but always follows a fairly simple geometric pattern. This will
  produce buds in specific areas, and is the basis for the patterning of
  branches that you see in mature trees. The actual biophysical process
  that arranges this patterning relies on the concept of a morphogen.
  These are chemicals that can exist in greater or lesser concentrations
  across a plant tissue. Specifically, we're talking about the
  distribution of auxin across the surface of the shoot apical meristem.
  The details are quite complex (and the details super controversial!)
  but suffice it to say that the plant cells transport auxin to
  neighboring cells based on feedback loops that produce spots of high
  auxin concentration. The spots with high auxin develop into lateral
  organs (leaves). You can model with computers and recapitulate
  observed phyllotaxy seen in nature.
Now, I'm sure you've noticed that trees don't have well-patterned
  branches. Still, this very well organized structure is the basis for
  plant architecture. Look at young tissue or flowers, and you'll easily
  see these patterns. But back to branches.
When a lateral organ is formed, it is accompanied with an axillary
  meristem and a segment of stem. This basic structural unit of plants
  is called a phytomer. Now, the axillary meristem can do a few things.
  For trees, it can produce leaves, a flower, and/or make a branch. The
  'algorithm' that determines what happens will vary from species to
  species and depend on things like apical dominance and environmental
  factors (e.g exposure to light in that area). Some of these axillary
  meristems will become branch meristems, and this is somewhat random
  from a patterning perspective. This is why most trees don't follow
  strict patterns. Over time, some branches will grow at different
  rates, others will terminate, and successive branching decisions will
  determine it's overall form.
Most trees can also form meristems de novo from tissues. If you've
  ever seen a forest tree suddenly exposed to light (from a neighbor
  falling down) you'll know what I'm talking about, as the trunk might
  be covered in leaves. I haven't ever studied this, but I presume that
  this process is quite random, but I also don't think that it's a major
  influence on tree architecture.

via Reddit user Sluisifer