text:
Is there enough evidence in this paper that there is a second (mechanical) layer of information in DNA?
The following commentator writes:

Mechanical cues
  Since the mid 80s it has been hypothesized that there is a second layer of information on top of the genetic code: DNA’s mechanical properties. Each of our cells contains two meters of DNA molecules, so these molecules need to be wrapped up tightly to fit inside a single cell. The way in which DNA is folded, determines how the letters are read out, and therefore which proteins are actually made. In each organ, only relevant parts of the genetic information are read, based on how the DNA is folded. The theory goes that mechanical cues within the DNA structures determine how DNA prefers to fold.

My question is: Is there enough evidence in this paper that there is a second (mechanical) layer of information in DNA?

...isn't your question answered in the paragraph following the one you're citing?

I was trying to work out of this paper had any credentials or not. You’re saying it does?

Ah, it isn't clear from your question that you actually want info about this paper. I suggest you to rephrase it to actually include what you ask in the comment. Something like "Is there enough evidence in this paper that there is a second (mechanical) layer of information in DNA?". In the meanwhile I'll check the paper.

I'm voting to close this question as off-topic because SE Biology does not exist to referee scientific papers.

Biologists already know that transcription can be regulated by winding or unwinding DNA.  (This paper might be informative:http://www.cell.com/trends/parasitology/fulltext/S1471-4922(16)30226-4)
But this is hardly the only method of gene regulation.


text:
What insect is this? (Black body two orange lines in its back and six legs)
I found this today in the library while studying. I am very curious to know whether this particular insect has a name that I can look up and find more information about:

Full length is almost one centimeter. It doesn't bite or anything. It has lots of small hairs in its back (similar to cockroaches and ants) and has a tail that a white sticky substance comes out from.

where in the world are you?

Possible duplicate of What is this yellowish insect?

It's a larvae from a ladybird (or ladybug).  Judging by the stripe pattern it is a Common Spotted Ladybird (wiki: Harmonia conformis) and from the body shape & size I'd also say 3rd instar.
The one you have photographed, and the one on flickr, are larval forms of the ladybug, just like when a catepillar becomes a butterfly, the ladybugs also have a larval stage in their life cycle which crawl around and look very different to the adult form.

It is definitely this one: http://www.flickr.com/photos/burtonandy/4628261516/ I just cant understand why the photo of the insect in wikipedia is totally different with this one!

@dane The one you have photographed and the one on flickr are larval forms of the ladybug, just like when a catepillar becomes a butterfly, the ladybugs also have larvae which crawl around and look very different to the adult form. http://www.enchantedlearning.com/subjects/insects/Ladybug.shtml

Wow. I've seen these around a bunch, but I had no clue that they were ladybug larvae. That's wild!

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


text:
What fish (and/or shellfish) species with a multi-year life-cycle, besides salmon, die after spawning?
Most species of salmon die after spawning. Are there any other types of fish that spawn once and then die after a multi-year life-cylce? Is this a rare life history strategy among our human exploited marine species? Googling this question only yields articles about Salmon.

Many species of Eel (order Anguilliformes) have a semelparous life history (most species? all?), i.e. they only reproduce once and then die (as opposed to an iteroparous life history). Many species are now threatened by extinction (e.g. American eel and European eel), since they have been heavily exploited by fisheries and they are also vulnerable to habitat modifications (e.g. hydroelectric dams) and pollution. The nature of their life history was also unknown for a long time, since they migrate and spawn in the Sargasso Sea after living many years in fresh water (so the opposite migration path compared to Salmon), which is called a catadromous life history. However, there are also many species of eel that are strictly marine, for instance the very large Conger conger, but many of these species still migrate long distances before mating.

(American eel, Anguilla rostrata, picture from Wikipedia in public domain)
As a fun sidenote, captive eel can become very old, and earlier this year a more than 155-year-old European eel that was kept in a well died (see newsstory) - the oldest known eel from what I know. Eels were often put in wells because they were believed to keep the well water clean.
Semelpary is also found in other fish species, for instance in the Smelt (Osmeridae) family, where many species are fished commercially. Some (most?) species in the family have multiyear life histories, but some, e.g. the Delta smelt (Hypomesus transpacificus) only live for a single year. Similarly to Salmon, Smelt also migrate from sea to freshwater to spawn, i.e. an anadromous life history.
Overall, less than 1% of teleost fish are semelparous according to Finch (1994) - see link for more examples of semelparous fish species and background. However, this figure is most likely uncertain, given that we know very little about the life history of many marine species. In some cases, you can also find a range of life-history strategies from semelparous to partially or totally iteroparous within the same species, depending on ecological context. Nevertheless, the low overall proportion of semelparous fish means that semelpary is generally a rare life history strategy in human exploited fish species.

(Delta smelt, Hypomesus transpacificus, picture from Wikipedia in public domain)

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
How do I know which alleles the parents have?
I have the following assignment where I am to look at the "tree" (not sure the english word) and assign whether or not they can be autosomal dominant or recessive as well whether they can be X-linked recessive.

My way to try and complete this assignment is by drawing a punnet's square but I quickly run into some confusion. When I draw my square, I know that is I'm checking for autosomal dominant, then I would draw the mother as A'a, the A' denoting the sick dominant allele. What I'm not sure is this: Can't I also draw her as A'A'? That would also mean she would be autosomal dominant but with 2 sick alleles. What about the father? Do I draw him as Aa, aa or AA? I'm a bit confused here!

Let's go step my step here.
Going by your notation I'll call the square as Male and Circle as female.
So from this information I can confidently say that you disease is not X linked dominant.
Why?
Because Females carry XX, that would mean to be X linked dominant she had to be X'X' for the disease allele to manifest it's phenotype. But if it were X'X, it would lead to a loss in fitness. And since the Male is normal and XY he does not carry the disease which tells us that the disease is definitely not X linked dominant.
Therefore in a cross of X'X' and XY you get individuals X'X and X'Y in the ratio 1:1
Coming to AD Autosomal Dominant may mean A'A' as the disease allele is present in homozygous condition. A heterozygous condition would lead to loss in fitness, not necessarily a disease.
A Father may be AA or AA'
so this cross would give you individuals

AA' for A'A' x AA
A'A A'A' for AA' x A'A'

so in this case you always get the disease in autosomal dominant, what remains is recessive.
AA or AA' Father x A'A' Mother
Products AA' for AA x A'A'
or AA' and A'A' for AA' x A'A'
which tells us that the disease is actually Autosomal recessive on the mother.
The father's genotype for the allele is AA or homozygous dominant
and the disease is autosomal recessive for the disease in the mother.

Why can the father not be Aa or aa?

the Aa that you are talking about is the AA' condition and the aa or A'A' cannot exist because in the diagram the father is a normal individual. So he can be either homozygous dominant for the wild type fit allele and heterozygous leading to a loss in fitness.

I don't think loss of fitness is relevant in this situation. In any case, there is nothing in the question to suggest that the disease is incompletely dominant and would result in a loss of fitness in a heterozygote


text:
Difference between thylakoids and lamellae in a chloroplast?
I'm slightly confused as to the difference between thylakoids and lamellae. My understanding was that thylakoids are 'discs' that are stacked into grana and there is a membrane between the grana called the integranal lamellae. However in my text book it says that 'the inner membrane is folded into lamellae, which are stacked up like piles of pennies. Each stack of lamallae is called a granum.' This sounds to me like the description of thylakoids.
It later says 'grana are stacks of flattened membrane compartments, called thylakoids'...
Could someone clarify this?
Thank you in advance :)

The answer above goes in depth so I will try go off that.
Firstly, lamella is the word used to describe plate-like structures. A thylakoid therefore, being a flattened vesicle, would fit this description, so a thylakoid is a type of lamella.
As mentioned earlier, a lamellar system consists of uniform thylakoids, the thylakoids being the individual lamella.
I have the same textbook as you, OCR A2 Biology, and I must admit I had the same confusion. What this textbook fails to mention is the fact that thylakoids are just one type of lamellae.
The textbook also states that the inner membrane of the chloroplast is "folded into lamellae (thin plates)". There are two types of lamellae in the chloroplast, thylakoids and intergranal lamellae, both are stacked, however only thylakoids appear as "piles of pennies" as it states. Intergranal lamellae look nothing like pennies, which is why the textbook is strongly misleading, they are big flattened bits of membrane that connect together different grana (stacks of thylakoids).
Note: my answer comes in 3 years late (I'm currently doing my A2), and the textbook in question will see its last use this year as the current A2 level syllabus is updated, I hope my answer still helps to clear up any confusion should OCR mess up again on this one

can you give some references for additional information and/or to back up your answer? It's something that we always appreciate in this community.


text:
Can we say that microevolution and macroevolution is fundamentally the same thing over different time scales?
This Wikipedia article states:

Macroevolution is evolution on a scale of separated gene pools. Macroevolutionary studies focus on change that occurs at or above the level of species, in contrast with microevolution, which refers to smaller evolutionary changes (typically described as changes in allele frequencies) within a species or population. ... macro and microevolution describe fundamentally identical processes on different time scales.

My question is: Is this a valid claim? Can we say that creating the genetic information for a feather is not qualitatively different from changing the colour of that feather?

This question about the difference between macro- and microevolution might be of interest.

You are mixing up two different things in your question:

the mechanisms (processes) that cause micro- and macroevolution, and
the genetic basis for different types of traits.

The processes of evolution (selection & drift acting on genetic variation) are the same for both micro- and macroevolution, and this what the Wikipedia article is stating. The second question is dealing with the amount of cumulative genetic change that is needed for different types of traits. This naturally differs dramatically between traits (the accumulated genetic change that is), and is also reflected by the different scopes of micro- and macroevolution. Macroevolution is usually studying problems above the species level, and therefore often larger morphological changes, while microevolution is dealing with smaller changes within species and populations. The macro/micro division is also artificial and should be seen as a continuum.


text:
Color perception vs shade perception demo
I can't seem to find one of the best demos I've seen of color vs brightness perception.
It consisted of a rotating animation of earth made of red of bright red points on a dark green background. As the animation plays, the red points slowly get darker while the green background gets brighter. At some point they are of the same brightness (but different colors), which is where something very cool happens; your brain no longer perceives the red points as a 3D object, and they just look like a jumble of points bouncing around the screen. When the red points are darker than the background, the 3D object appears again.
Does anyone know what is this animation called, or where to find it? It's hard to find on google without knowing what to call it.


text:
How do I create a probe for in situ hybridization?
I tried to make the probe several times but it failed again and again. It usually turns out that the probe after hydrolysis is very very short (maybe around 50nt). I did not check the RNA before hydrolysis except last time. However, I saw a band (though very weak) last time, but it still produce very very short probe after hydrolysis.I use Sp6 polymerase to synthesize RNA, and the original length of the DNA is 1.5kb. My expected length after hydrolysis is 500nt.
I'm guessing maybe it's the phenol contamination of the phenol:chloroform extraction step because my 260/280 value is low (around 1.6-1.7), and my 260/230 is also low, which is like 1.6-1.8. Also the peak is not at 260, it's almost at 270.

I'm not all that familiar with in situ hybridization, but I'm missing a few details here. How did you synthesize the RNA probe (PCR, I assume?), and how long should it be? And that RNA is shorter than expected even before you use it in the in situ hybridization, do I understand that correctly?

50bp does not sound that short for in situ...

I had large noise with such probe, but I can see the signal. However, I need to quantify the signal so I need better probe

I dont understand what you mean by hydrolysis in this context.
The way to go about is:

Clone the DNA, that will give rise to the probe, downstream of T7 (or any other) promoter
Linearize this plasmid by digesting at (or ahead of) the 3' of cloning site
Set up an In-vitro Transcription reaction with T7 polymerase (or whatever corresponds to the promoter you used)
Precipitate and purify the RNA (you can use DNAseI to get rid of the DNA).
To check the RNA size: mix ~2$\mu$l of RNA (less or more depending on your yield) with equal volume of 2x RNA loading dye (contains formamide 95%, EDTA, SDS, and the dyes).
Heat at 85⁰C for 5min. Let it cool and run in 1% TAE/TBE-agarose gel (no need to make MOPS-Formaldehyde gel)
dsDNA ladder wont be very accurate but may be used for size estimation (if linear, the mobility of dsDNA and ssDNA/RNA wont be very different. Formamide treatment keeps the RNA linear). Use ssDNA or RNA ladder for better accuracy.

Btw.. the absorbance ratios mentioned are okay.. you don't need an RNA of supreme quality for this application (in fact this suffices for most experiments)

Later I found out that the length of RNA read from the gel is not trustworthy. I guess it's because the RNA is in hybridyzation solution that even when it's running on the gel, it cannot reflect the actually length of the probe. The only way to test the probe quality is to do the in situ.
For the pheno contamination problem, I think it's a separate problem of myself. Once RNA can be synthesized in vitro, it means there should not be pheno contamination.


text:
Does amylolysis occur in vegetables if stored below 0⁰ Celsius?
Assume that we have a plant, e.g. kale, which is prone to amylolysis if not harvested during a frost period.
If it is harvested and put in a household freezer, such that it is frozen solid slowly enough for cell walls to burst, will the amylolysis stop, or will it still occur? Will it occur if it is kept in a fridge in the 0-4 Celsius range? If it does not occur while the vegetable is frozen, will it start after thawing?

I think it will be at least delayed. Enzymes habe an optimal temperature at which they work best. I don't know this for this special amylose, but at 0°C it will definitely be much slower. The rate of the enzyme will not be zero though...

@Chris interesting. I thought that maybe my question is too silly to ask, and half expected to get an answer saying "once the cell plasma is frozen, all biological processes cease because enzymes, hormones etc. can't move around".

I was thinking about 0°C, not freezing. When you freeze the plants, the enzymes will be not functional. The backside is that you probably break cells with the freezing and set free the enzymes.

@Chris what do you mean by "set free the enzymes"? Does this mean that they will start converting the starch upon thawing independent of ambient temperature, because they are free now? I am afraid my mental model of the whole process is very incomplete. You will certainly break cell walls, this is very noticeable with thawed vegetables.

With "set free" I mean that the enzymes can work not only inside the cell but also outside, since the interiour of the broken cells is set free. This is especially a problem when you work with lysed cells and protein degrading enzymes. Its probably no problem here.

Yes. Freezing would practically stop all biochemical reactions. Household freezer can maintain -15⁰C so that would work. However, freezing also damages the cells if cryoprotectants are not used. But I guess that is not your concern.


text:
Where can I get numerical data for the PAR (photosynthetically active radiation) curve?
I'm trying to do some rough figuring to calculating efficiencies of various light sources for growing plants.  I'm hampered, however, by the lack of a curve to multiply by the spectrum of light sources to determine the amount of photosynthetically active radiation that a typical plant will absorb and use.
I can find curves like below all over, but I can't get numerical data in the form of tables. Is there some source from where I can get such data?

plantphysiol.org/content/early/2013/06/28/… is a starting point. He cites a paper of Mcree which may have what you're looking for (pay wall for me). Evans says that photosynthesis for 400-700nm drops off quickly as function of temperature. Red/blue encourage flowering/growth, a gardening truism which may be based on Mcree's paper.

@daniel your link was cut off

This is it---http://www.plantphysiol.org/content/early/2013/06/28/pp.113.219006.full.pdf--except for the standard characters at the beginning ending with the three w's.

@daniel a safer way to provide links in comments is using markdown, e.g. [Google](http://www.google.com/) = Google.  The second link you pasted has a "--except" appended on the end that I had to manually remove.

@NickT sorry for the late comment but what do you mean here, by "numerical"

@WYSIWYG as in a table (spreadsheet, etc) of values with the wavelength then the PAR value for each one.

@NickT Is the table not available from the source of this image?

@NickT I think you should try one of the programs that can be used to extract numerical information from images. I never used one. There is another trick that you can try using Inkscape: import your image → crop to desired region → trace path from the image → Remove unnecessary points → simplify the path → add more nodes if you want to get more datapoints (select all nodes and click add node) → Select all → resize document to selection → save as SVG. SVG doesn't store co-ordinates but you can obtain them using parsers or other tricks.

To know how to extract co-ordinates from SVG see here and here. Since you know the X/Y scale from image you can get the original data points.

This is one paper where you can get that data.

@WYSIWYG that paper just has insolation data over the year, not the spectrum of what PAR is.

@NickT Did you try obtaining the numerical data from this curve?


text:
What is the smallest molecule that can present as an antigen to the immune system in the context of allergies?
People often claim, in a colloquial sense, that they are "allergic to everything".
Is it possible to have a full-fledged IgE mediated allergic response to very small molecules?  I was always under the impression that the smallest antigen was a oligopeptide, but is it possible for someone to be allergic to something like isopropanol, glucose, or another small organic molecule?
How about allergies to metals, as I know those are fairly common, would they be mediated through a similar mechanism?

At one of my previous companies that raised antibodies to proteins and post-translational modifications, we found that 6-8 amino acids was generally the smallest peptide length required for an epitope. Anything much smaller than that won't induce the cross-linking or conformational changes required for signal transduction and an allergic response. As WYSIWYG notes, allergies to small molecules/atoms are formed via hapten-carrier interactions. These can be covalent, as in the nickel-transferrin example, or as a result of denaturation/chemical modification, as likely happens with people who are allergic to things like isopropanol or bleach.
I very much doubt that there can be such a thing as a glucose allergy, as it is so ubiquitous in the body that such antibodies/T-cells would be negatively selected long before they could do any damage.

Yes, the glucose example was a figment of my imagination, I just wondered if it was theoretically possible, but your point about negative selection is surely true.

@jonsca you are correct. However, plasma glucose can spontaneously react with the amine side chains of proteins and form pro-inflammatory advanced glycation endproducts.  Certain immune cells have receptors for AGEs.  So although AGE-drive inflammtion is not an adaptive (antigen driven) immune response, it is immune mediated.

Small molecules do not have antigenic properties but they can elicit immune response by binding to a "carrier" protein. The small molecule is called a Hapten. An epitope forms at the protein-hapten binding interface.
Nickel  acts like a hapten and elicits immune response by binding to proteins like transferrin, albumin etc.
Other metals also cause allergy in a similar way.


text:
Lytic Viruses -- Cell lysis?
So in the video my instructor sent on viruses, he said that for lytic viruses, new viruses manufactured by the host cell could get out of the cell in one of two ways.

The new viruses would leave by exocytosis.
or,
The cell would be "ruptured" and the new viruses would "erupt out of the cell".

In the rupturing option, is the cell destroyed? The way he phrased it as well as his tone of voice brought to mind an image of the cell bursting and the viruses spilling out....but the diagram showed a little gap in the cell membrane, and the viruses leaving from that one exit point.
Which is more accurate?
Thanks!
evamvid

Yes, ruptured here means that the host cell is destroyed. The virus "hijacks" the cell anyway and uses its protein production machinery to make as much virus particles and its transcription enzymes to makes as many viral genomes as possible. If the ressources of the cell are exhausted, it get destroyed and the viruses are set free.
See this image (from the Wikipedia article on the lytic process). It actually doesn't matter, if the virus infects the cell from the outside or if it comes from the genome.

Adsorption of the virus to the cell.
Injection of its genetic material into the cell.
Production of new viruses (hull and genome).
Rupture of the cell and release of the viruses.

I understand now that the cell is destroyed either way. But is it more likely to be destroyed physically (ruptured) or because of exhaustion of resources?

Rupture and release of the virus happens, when the ressources are exhausted. So one event happens before the next. Then there are phages, which can leave the cell without destroying them before, the phage M13 is such an example. It expresses proteins which make a pore in the cells membrane which the phages can pass.

After the phages leave, what happens to the cell? Does it still have the viral DNA? Does it make more viruses? Or does it carry on with normal business like it was never infected?

Its dead. The membrane is destroyed, and it can not do anything anymore.

I'm confused...I thought you said that some phages can exit without destroying the cell by expressing proteins which basically open a hole in the cell membrane and let the phages out. Is that correct? If so, what I was trying to figure out is, after this process, does the undestroyed cell then carry on with normal business, or does it keep making viruses?

Sorry, I thought you were talking about the burst cells. The M13 infected cells will eventually die as well, since they are busy making viruses. It will probably last a bit longer, but not much. The virus pretty much shuts down everything what he doesn't need.


text:
What are these animals, and what happened here?
While walking along the northern shore of Lake Ontario, I noticed the following strange scene:

Here is a closer angle:

What are these animals, and what is the likeliest cause of this?

Oof! :'-(  Looks more like a raccoon to me. Seeing its head might help...

A picture under the fish's head would help as they could be entangled somehow - fishing line?

This question could focus more on species ID rather than CSI to avoid further close votes. Really interesting albeit disturbing scene though and thanks for asking :)

That's likely a raccoon and a dead fish (salmon, perhaps).
For the animal on the left: notice the ringed tail, foot anatomy, and lighter foot color, and variable (light/dark) fur color:

 University of Arizona

 Furbearer Conservation

 University of Nebraska-Lincoln Extension
Note: Since you mentioned opossums, I include the above to show the vast difference in foot anatomy between a raccoon and and opossum. An opossum's foot is also not white like that.
The fish, in my opinion, is too degraded to get an accurate ID. However, based on size, upper jaw size, and coloration (dark dorsal + tail fin with lighter belly), I think it's quite possible this is a salmon, of which 3 species can be found in Lake Ontario.

 Fishing Booker
Possible species include Atlantic, Chinook, and Coho. See here for descriptions and pictures of each along with many other Lake Ontario fish species. I invite you to stare at your photo longer to convince yourself to which specific species it is.

Oh yeah, and there's just no telling what happened. Though, notice the raccoon's foot is buried. This suggests these animals possibly have either been here for a while and/or were carried here and deposited from wave action. The former seems unlikely given the easy meal both would have provided to some other predator. It may very well be the salmon was caught on fishing line (perhaps snapped by an angler), which caught it up near shore where a raccoon got entangled Then they got swept up, drowned, and then their tied-up carcasses deposited on the beach and covered in moving sand. Who knows...

And in a few 100,000 years they'll dig up the fossils and note the epic battle between the 2 species a la fighting dinosaurs, concluding that racoons were partially aquatic and descended into the depths to hunt their prey.

I was wondering why would a decapitated raccoon end up on beach. Your theory makes sense @theforestecologist

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Are the brains of any herbivorous animals capable of utilising ketone bodies as an energy source?
I ask this question because earlier today I heard from a lecturer at my university that a sheep's brain cannot utilise ketone bodies as an energy source and hence with insufficient glucose supply for their brains they die.

link I think this link provides some relevant information.

My answer is limited to sheep.
Background
The metabolites referred to as ketone bodies (which I will refer to as ketones from now on) are acetoacetate and β-hydroxybutyrate. In humans these are produced in the liver when the amount of acetoacetyl CoA being produced exceeds the capacity of the TCA cycle. These acetyl groups are instead used to produce acetoacetate, and this can be reduced to β-hydroxybutyrate.
The production of significant amounts of ketones occurs during fasting (diabetic ketosis will not be considered here). Once glycogen has run out, the bodies requirement for glucose has to be met by gluconeogenesis (mainly in the liver) - glucose is synthesised from various carbon skeletons including glycerol and the products of amino acid catabolism (coming from muscle protein turnover). This means that in the liver the function of the TCA cycle shifts almost entirely to supplying oxaloacetate for gluconeogenesis, via the activity of phosphoenolpyruvate carboxykinase. Thus there is no oxaloacetate available for citrate synthase, so acetyl CoA cannot enter the TCA cycle. However, because fasting also results in fat mobilisation the level of acetyl CoA in liver cells goes up (acetyl CoA is the end product of fatty acid breakdown).
So what is going on here? During fasting the fuel economy of the body has to switch from being heavily glucose-based to one which uses carbon from fat and from protein. The ketones are the manifestation of this, and many tissues become heavy users of ketones during fasting as blood levels rise to 5 mM within a few days. This means that the glucose being produced by the liver can be directed towards tissues which are more dependent upon glucose. The classic example of such a tissue is the brain, but in humans even the brain begins to use ketones heavily during fasting.
In ruminants the situation is entirely different. Ruminants rely upon the bacteria in the rumen to metabolise carbohydrate in their diet and this results in large amounts of alimentary ketones entering the blood directly. For their glucose supply ruminants rely entirely upon gluconeogenesis, and the substrate for this is propionate, another end product of bacterial metabolism in the rumen: a lactating dairy cow will synthesise over 3 kg of glucose per day.
So, when I read this question my reaction was that the statement must be incorrect - surely it would make sense for sheep to use ketones in all tissues. However my intuition was wrong - according to

Pell JM.& Bergmane N(1983) Cerebral metabolism of amino acids and glucose in fed and fasted sheep. Am. J. Physiol. 244: E282-E289

cited in

Heitmann RN et al. (1987) Hepatic ketogenesis and peripheral ketone body utilization in the ruminant. J. Nutrition 117: 1174-1180
"Although there is some oxidation of ketone bodies by the brain tissues of humans and rats during prolonged fasting, Pell and Bergman ,using an elegant in vivo preparation, have shown no significant uptake or oxidation of ketone bodies by sheep brain."

I don't have access to the Pell & Bergmane paper so I cannot explain what they actually did. What is clear from the review by Heitmann et al. however is that fasting ruminants respond in the same way that we do, switching to hepatic ketogenesis, and presumably they also maintain gluconeogenesis, using not propionate, but amino acid carbon skeletons. The context of the statement quoted above suggests that even in the fasted state the sheep brain doesn't use ketones.


text:
How does the embryo inside a shelled egg get oxygen?
If I'm not mistaken a typical animal in the womb will get oxygen via the umbilical cord from the mother. Thus allowing it to "breathe" in a liquid environment. I thought maybe shells are permeable and allow air to come in through the shell, but then I thought of eggs laid in the ground like turtles do.

How do animals in soft/hard shells get their oxygen?

Both forms are ultimately by diffusion.

The key point in both cases is that the eggshell and membrane are permeable to oxygen, as you thought. There are subtleties - for instance, the oxygen-permeability of avian (hard-shelled) eggshells changes during development.
In the case of eggs laid underground, as in sea turtle eggs, the leathery shell is still permeable to oxygen. The sand restricts oxygen flow, but turtles seem to take care to not bury their eggs too deep for oxygen to diffuse to their developing nest.


text:
What animal has the strongest immune system?
I'm wondering what animal has the strongest immune system. It can be defined as the most evolved immune system or the immune system that can eliminate or tolerate most number of (different) viruses/bacteria/diseases/pathogens/poison (some of which can kill most or many other animals or make them really sick).
I've done some research and found some animals that can be the answer but I couldn't be sure which one. There might be smaller animals that I've missed. There might be studies with more clear results that I've missed. Here are the animals I've found:

Shark
Ostrich
Bat
Alligator
Vulture

Here are some relevant quotes from the articles I've found:

Shark:

The shark's "antiviral defenses have been extraordinary," Zasloff said. "It has adapted a very remarkable immune system and stayed with it." In the study, squalamine thwarted infection of the dengue fever virus in human blood vessel cells and of hepatitis B and D in human liver cells—and with little harm to sharks.
 https://www.nationalgeographic.com/culture/article/110919-sharks-drugs-medicine-viruses-science-health-squalamine

Ostrich:

It is said that ostriches have the strongest immune system of any animal in the world. Because of this, they have shown great promise in preventative healthcare in humans and the beauty industry.
Ostriches strong immune systems make them highly resistant to viral infections. Japanese researchers have discovered how to mass produce natural ostrich antibodies that are effective against influenza, avian flu, MERS, Zika and even the Ebola virus. “The antibodies are resistant to higher pH levels and can remain active even when exposed to heat of up to 100 degrees Celsius.”
 https://pharmaboardroom.com/articles/ostrich-antibodies-a-health-and-beauty-elixir/

Bat:

The mammals can carry many viruses with the potential to cause serious diseases in people, including rabies, Ebola, Nipah, severe acute respiratory syndrome, or SARS, and others. Bats rarely get sick from those viruses. Why these pathogens tend to be so dangerous when they infect other animals has been a mystery.
Previous work suggests that a bat’s immune system is especially adapted to tolerate viruses, thanks in part to its ability to limit inflammation. Now a study using cells grown in a lab hints that to counter a bat’s immune defenses, these viruses have gotten good at spreading rapidly from cell to cell.
https://www.sciencenews.org/article/bats-immune-system-viruses-ebola-marburg-people

Alligator:

American alligators have an enviable innate immune system, the “primitive” first line of defence that is shared by all vertebrates. In 2008, chemists in Louisiana found that blood serum taken from the reptiles destroyed 23 strains of bacteria and depleted reserves of the HIV virus.
https://www.newscientist.com/article/dn27059-germ-killing-molecules-identified-in-alligator-blood/#:~:text=American%20alligators%20have%20an%20enviable,reserves%20of%20the%20HIV%20virus

Vulture:

Vultures' faces and large intestines are covered with bacteria that is toxic to most other creatures, but these birds of prey have evolved a strong gut that helps them not get sick from feasting on rotting flesh, according to a new study.
"On one hand, vultures have developed an extremely tough digestive system, which simply acts to destroy the majority of the dangerous bacteria they ingest," Roggenbuck said. "On the other hand, vultures also appear to have developed a tolerance toward some of the deadly bacteria — species that would kill other animals actively seem to flourish in the vulture lower intestine."
https://www.livescience.com/48899-vultures-bacteria-microbiome.html

this all depends on how you define strongest, A blue whales immune system can eliminate way more bacteria than a mouse just due to mass.

@John The question has details regarding "strongest immune system" already and the quotes I provided give an idea as well. I've also added: "immune system that can eliminate or tolerate most number of viruses/bacteria/diseases/pathogens". There are studies regarding immune system of animals. I might have missed studies that can provide an answer.

I've added the word "different" in parenthesis before "viruses/bacteria/diseases/pathogens" to make it more clear. I thought It was clear when the word "diseases" was there already and the quotes give a clear idea what the strongest immune system can be.

which really does not help, we don't measure immune systems by how many things they can fight because any immune system can fight a theoretically infinite number of organisms plus how many things an immune system is exposed to varies wildly, terrestrial organisms for instance are subjected to orders of magnitude fewer bacteria.

@John "Fighting" is different though. Immune system can fight many things but might not overcome. We are talking about eliminating or tolerating pathogens that can make animals really sick or kill them. More details are in the examples I gave. For example, vultures seem to be not affected by the bacteria that causes Anthrax which can kill many other animals, so the answer is likely an animal that can eat carrion. It is hard to find studies that compare animals though.

@0.. What if it's not even a matter of fighting? Not all viruses need to be fought because they are incompatible with the host to begin with. To me, this question is like asking who is the strongest fighter when everyone specializes in different styles of combat with dissimilar types of opponents where you can't pit the fighters against each other or the opponents against each other for comparison.

the problem is most infections diseases are specialized to their host very few diseases can infect a very wide range of organisms, anthrax for instance is very rare in predators it mostly infects herbivores. and is extremely rare in birds in general. a disease good at infecting one group of organisms my fair very poorly in another without the immune system coming into play. anthrax again for instance only infects endotherms.

I understand it is not an easy to answer question (hence asking) and might require comparison between studies. Anthrax was just one example of disease that a scavenger can eliminate. We are talking about many diseases/toxin where sum of them can kill many or most animals. Opossum might be the right answer as it is a scavenger and a snake hunter so it is immune many diseases and toxins where sum of these pathogens/toxins can kill many or most number of different species.

From fragmented memory files, I report that an immune system is not just the lymphatic cellular system (WBCs); there's also the acellular components like physical barriers (skin), chemical barriers (stomach acid, tears). Right? If you ask me, the most powerful immune system would belong to the species that's immune to air/water-borne viruses.

Though not strictly pathogenic in nature, Opossums (Didelphis virginiana) are well known to be able to recover from broad range of deadly toxins/venoms due to -- at least in part -- lethal toxin-neutralizing factor (LTNF).
According to Lipps (1999), who tried putting LTNF into mice:

Death due to intraperitoneal (IP) injection of a predetermined lethal dose of venom from major families of snakes, for instance Crotalidae, Elapidae, Viperidae and Hydrophiidae, is prevented in mice by subsequent IP inoculation of LTNF. Furthermore, LTNF neutralizes the lethality of scorpion and bee venoms and toxins from various animals, plants and bacteria. Thus, natural LTNF from opossum serum has potential as a universal therapy for envenomation caused by animals, plants and bacteria.

Also, because of their low body temperature, opossums rarely if ever get rabies unlike all other mammal species.
Opossums have also been known to eat a wide variety of foodstuffs including carrion, bones, and even garbage without getting sick -- suggesting they have strong immune systems associated with their gut.

Thank you, great answer. I've seen opossum mentioned when I searched before but didn't know the details about their immune system and LTNF.

I'm going to accept this answer (till something better comes up). Opossum, as a scavenger and a snake hunter, evolved to be immune to many diseases and toxins/poison where sum of these pathogens/toxins can kill many or most number of different species. Here is a relevant quote also: "They are nearly impervious to rabies because their body temperature is too low to host the rabies virus. They also rarely catch Lyme disease from tick bites, and are immune to the stings of honeybees and scorpions, botulism toxin, and snake venom." https://www.wildlifehc.org/in-defense-of-opossums/

Don't they also play dead when threatened? Thanatosis or something?


text:
Is there "limbic mimicry" in real life to distract animals? (like it was portrayed in "Fantastic Beasts: The Secrets of Dumbledore")
In the movie "Fantastic Beasts: The Secrets of Dumbledore", one of the characters comes up with the idea of "limbic mimicry" to distract dangerous animals from violent behavior. Please see the details below to have a better idea (in a spoiler tag because it contains spoilers from the movie):

  While freeing his brother Theseus Scamander from Erkstag prison used by the German Ministry of Magic, Newt outmaneuvers an army of baby Manticores (scorpion-like creatures) using "limbic mimicry" to distract them from violent behavior, forcing them to copy his dance-like movements that mimic the appearance of the creatures. Theseus begins to copy Newt's movements as well when they were escaping.

Is there an example of this from real life?  Of course, in the movie, it is a bit exaggerated for cinematic effect and they are fantastic animals.
However, I wonder if certain movements can distract animals from violent confrontations and is there a term for this in biology? (it can be animal vs animal also)
I know there is mimicry in biology which is an evolved resemblance between an organism and another object or another species as an anti-predator adaptation. However, it is about appearance. I couldn't find examples related to movements.

There's lots of different behaviours to avoid angering animals and to avoid attack. There are various technical terms for those things, but they aren't a formal field of study as far as I know.
Here is an example of someone with experience interacting with lions. https://www.youtube.com/watch?v=tC7DuEEk-zY I'd say the main reason why the lion stays calm is that the human stays very calm and portrays a sense of absolute certainty in his movements.
Someone in Botswana walked up to a female lion who was keeping some babies, and she looked very angry... So he walked backwards very slowly, maintaining eye contact, trying to appear tall. and everything was fine. If he'd turned his back and run that's is a behaviour that would have provoked an attack. Most carnivores are triggered to attack by flight or fear.
I was confronted with 50 angry bulls in a field once, and having lived near cattle for many years, I could see that they were particularly menacing and angry. I mimicked a different gait than I would normally have to look like a non-menacing animal, and their behaviour changed and the looked at me confused rather than angry, while i walked past them, I noticed the difference because at first they charged towards me, and then they didn't take a single step when I changed my behaviour to look like a weak old human.
Angry predators are particularly difficult to dissuade, i.e. dogs.
As far as scorpions go, they attack pretty much anything that has the right size and movement to represent a prey, i.e. generally a lot smaller than them.

I knew some erudite geek(s) would downvote this so i kindof wrote it for that purpose :)/

+1 I upvoted. Some people don't appreciate interesting/challenging questions (unless it includes some bloated babble perhaps). This is not an easily answerable question as it is in the field of ethology, and possibly a less studied category of mimicry and you tried your best to answer with observational experiences.

Thank you for the lion vs. man video also. It is very much related. I can't believe he did something like this for the sake of science :)

Locomotor mimicry is what I've found while searching and it is very related.

Locomotor mimicry is a subtype of Batesian mimicry in which animals avoid predation by mimicking the movements of another species phylogenetically separated. This can be in the form of mimicking a less desirable species or by mimicking the predator itself. Animals can show similarity in swimming, walking, or flying of their model animals.
https://en.wikipedia.org/wiki/Locomotor_mimicry

There are three types mentioned: Terrestrial, Aerial, Inanimate object. However, the examples include small animals like spiders and insects like butterflies, moths, drone flies.

The most common form of locomotor terrestrial mimicry is found in ant-mimicking spiders. These mimics are capable of antennal illusions and similar gait patterns as an ant, which is shown in the jumping spider family (Araneae, Salticidae).
https://en.wikipedia.org/wiki/Locomotor_mimicry

The ghost pipefish is the only bigger animal mentioned as an example of inanimate object locomotor mimicry and they resemble sea vegetation and also sway in water like them.

Good call, was about to add locomotor mimicry and you noted it first. Most weird locomotion dissuasion i've seen this year is a stack of 50 processionary caterpillars in the grass, all twitching together in sychronous waves 1-2 times per second. Looked very extraterrestrial. Same as this with 50 of them https://youtu.be/mzhGebtRmgI


text:
How many times did terrestrial life emerge from the ocean?
Evolution is often mistakenly depicted as linear in popular culture. One main feature of this depiction in popular culture, but even in science popularisation, is that some ocean-dwelling animal sheds its scales and fins and crawls onto land.
Of course, this showcases only one ancestral lineage for one specific species (Homo sapiens). My question is: Where else did life evolve out of water onto land?
Intuitively, this seems like a huge leap to take (adapting to a fundamentally alien environment) but it still must have happend several times (separately at least for plants, insects and chordates, since their respective most recent common ancestor is sea-dwelling). In fact, the more I think of it the more examples I find.

I doubt we know the precise number, or even anywhere near it. But there are several well-supported theorised colonisations which might interest you and help to build up a picture of just how common it was for life to transition to land. We can also use known facts about when different evolutionary lineages diverged, along with knowledge about the earlier colonisations of land, to work some events out for ourselves. I've done it here for broad taxonomic clades at different scales - if interested you could do the same thing again for lower sub-clades.
As you rightly point out, there must have been at least one colonisation event for each lineage present on land which diverged from other land-present lineages before the colonisation of land. Using the evidence and reasoning I give below, at the very least, the following 9 independent colonisations occurred:

bacteria
cyanobacteria
archaea
protists
fungi
algae
plants
nematodes
arthropods
vertebrates

Bacterial and archaean colonisation
The first evidence of life on land seems to originate from 2.6 (Watanabe et al., 2000) to 3.1 (Battistuzzi et al., 2004) billion years ago. Since molecular evidence points to bacteria and archaea diverging between 3.2-3.8 billion years ago (Feng et al.,1997 - a classic paper), and since both bacteria and archaea are found on land (e.g. Taketani & Tsai, 2010), they must have colonised land independently. I would suggest there would have been many different bacterial colonisations, too. One at least is certain - cyanobacteria must have colonised independently from some other forms, since they evolved after the first bacterial colonisation (Tomitani et al., 2006), and are now found on land, e.g. in lichens.
Protistan, fungal, algal, plant and animal colonisation
Protists are a polyphyletic group of simple eukaryotes, and since fungal divergence from them (Wang et al., 1999 - another classic) predates fungal emergence from the ocean (Taylor & Osborn, 1996), they must have emerged separately. Then, since plants and fungi diverged whilst fungi were still in the ocean (Wang et al., 1999), plants must have colonised separately. Actually, it has been explicitly discovered in various ways (e.g. molecular clock methods, Heckman et al., 2001) that plants must have left the ocean separately to fungi, but probably relied upon them to be able to do it (Brundrett, 2002 - see note at bottom about this paper). Next, simple animals... Arthropods colonised the land independently (Pisani et al, 2004), and since nematodes diverged before arthropods (Wang et al., 1999), they too must have independently found land. Then, lumbering along at the end, came the tetrapods (Long & Gordon, 2004).
Note about the Brundrett paper: it has OVER 300 REFERENCES! That guy must have been hoping for some sort of prize.
References

 Battistuzzi FU, Feijao A, Hedges SB. 2004. A genomic timescale of prokaryote evolution: insights into the origin of methanogenesis, phototrophy, and the colonization of land. BMC Evol Biol 4: 44.
 Brundrett MC. 2002. Coevolution of roots and mycorrhizas of land plants. New Phytologist 154: 275–304.
Feng D-F, Cho G, Doolittle RF. 1997. Determining divergence times with a protein clock: Update and reevaluation. Proceedings of the National Academy of Sciences 94: 13028 –13033.
 Heckman DS, Geiser DM, Eidell BR, Stauffer RL, Kardos NL, Hedges SB. 2001. Molecular Evidence for the Early Colonization of Land by Fungi and Plants. Science 293: 1129 –1133.
Long JA, Gordon MS. 2004. The Greatest Step in Vertebrate History: A Paleobiological Review of the Fish‐Tetrapod Transition. Physiological and Biochemical Zoology 77: 700–719.
 Pisani D, Poling LL, Lyons-Weiler M, Hedges SB. 2004. The colonization of land by animals: molecular phylogeny and divergence times among arthropods. BMC Biol 2: 1.
 Taketani RG, Tsai SM. 2010. The influence of different land uses on the structure of archaeal communities in Amazonian anthrosols based on 16S rRNA and amoA genes. Microb Ecol 59: 734–743.
 Taylor TN, Osborn JM. 1996. The importance of fungi in shaping the paleoecosystem. Review of Palaeobotany and Palynology 90: 249–262.
Wang DY, Kumar S, Hedges SB. 1999. Divergence time estimates for the early history of animal phyla and the origin of plants, animals and fungi. Proc Biol Sci 266: 163–171.
 Watanabe Y, Martini JEJ, Ohmoto H. 2000. Geochemical evidence for terrestrial ecosystems 2.6 billion years ago. Nature 408: 574–578.

This is explained at the linked paper, but it's interesting to notice that there are four different arthropod colonizations of land: myriapods, insects, arachnids, and isopods.

What is also cool is that some animals (pulmonate molluscs, mammals, etc) have re-colonized the ocean back from the land.

@NoahSnyder, also Brachyura, it seems?

Richard's answer is fantastic, and I'm not going to be as thorough.  But here's some other examples:

Turtles (which did sea to land to sea back to land!)
Gastropoda (snails and slugs)
Tardigrada (water bears)
Onychophora (velvet worms)
Planaria (flatworms)
Annelida (annelid worms)

Together with Richard's examples that includes all the examples of terrestrial animals given at wikipedia.

75% of questions about the awesomeness of life, the answer includes tardigrades.

The venomous snakes of Australia are all in a single family, Elapidae. These are thought to have descended from a single sea-snake colonization event, so the sequence would be sea->land->sea->land.

@ChinmayKanchi Fascinating!  If it turns out snakes originally emerged in the sea that'd be sea->land->sea->land->sea->land!  (Though my understanding is that currently early snakes being burrowers is more likely.)

It's highly likely that all extant reptiles derive from a terrestrial ancestor because of the egg physiology. As far as I'm aware, not a single reptile lays eggs that can hatch in water.

@ChinmayKanchi: I'm not sure how that's relevant.  Certainly basal amniotes were land-dwellers (that's the first land).  But early snakes may have been aquatic (and closely related to Mosasaurs) which would give the second sea.  Then basal Elapids would then give the second land, the sea snakes the third sea, and the Australian Elapids the third land.  Anyway, as I said current evidence is towards a fossorial origin of snakes against an aquatic origin.

Ah, now I understand. Almost a shame snakes are thought to have originated fossorially, really.


text:
Question regarding Rate of Photosynthesis AP Biology Lab
We are doing a lab on the effects of light intensity/wavelength on the rate of photosynthesis in AP bio and we were asked to visit this website here: http://mhhe.com/biosci/genbio/biolink/j_explorations/ch09expl.htm
The link takes you to a shockwave applet in which you can change the wavelength/intensity and record the ATP production (%). We were supposed to try out as many different combinations of intensity/wavelength and record the respective intensity, wavelength and ATP production (%) in a chart. Now the problem I'm having is that we are to graph this data. How should I go about graphing this? One problem is that for some values in the data, the intensity might be the same with different wavelengths or the wavelength maybe the same with different intensities. Can I do two graphs? One graph? Which one would be best and how should I go about doing so? And here is the chart just in case you want to see the data:
https://drive.google.com/file/d/0B4A27kix-0naMk4wNmNQejd3cGc/edit?usp=sharing

Why ecology tag? Come to think about it, why energy tag? To be completely honest with you, it is not strictly a photosynthesis question either, and I think you could have asked this question on stats SE or math SE too, because the question is "how to plot?" rather than about photosynthesis. Personally, I still think it's an okay question to ask on biology SE, but maybe we should edit the tags a little. Anyway, I'm happy to help you to the best of my ability, welcome to biology SE :-)

Ty for the welcome and I have not posted this question on any other stackexchange sites. And yes I agree that the question really is about graphing but still the graphing is directly related to biology and so I thought it would be reasonable to post this here. Also I couldn't find any other related tags; these were the ones that came closest to the question =S.

Your task is to determine how light intensity and wavelength affect ATP production. Therefore, we know for sure that your dependent variable (or response variable) should be ATP production. It is customary to depict the response variable on the vertical axis (Y-axis), so let's trying doing this.
Now we need to sort the other two variables. I suggest that you make one variable a control variable -- a variable that you don't change and keep constant, and the other then will be an independent variable (or explanatory variable). Then you swap them around, producing at least two plots.
In a nutshell:

You pick one value of wavelength and don't change it. Then you change the light intensity and record ATP with constant wavelength. You plot ATP (vertical axis) vs the light intensity (horizontal axis).
You pick one value of light intensity and don't change it. Then you change the wavelength and record ATP with constant light intensity. You plot ATP (vertical axis) vs the wavelength (horizontal axis).

Make sure to generate enough data points in order to be able to fit a smooth curve.

Another option would be to make a 3-D graph, with 3 axes: Y for ATP, X for wavelength and Z for light intensity. Initially, this might seem like a better approach, however 3-D graphs are not very common in science, and maybe there is a reason for it. Your goal is to make your data intuitive, easy to read and straight to the point. Science can be rather complex even without additional effort to complicate it with confusing graphs.
I would try it out as well, and see which one of two approaches shows you the trend more clearly. If I had to pick one straightaway -- I would probably go with the previous option that included a control variable.

This is a great idea and this is how I initially thought I should do it but I actually ended up doing it differently and handed the lab in today =]

@genius12, did I overlook a better solution? Do you mind sharing it? Good luck with you report.


text:
Circular mRNA to produce long proteins
Ribosomes can read mRNA and produce proteins, if we somehow make a circular mRNA for the ribosome to bind onto, it will make infinitely long "proteins", (since ribosomes can make very big proteins, I assume they can bind long enough before disassociating)
However after doing some search on this topic, it seems that I am able to find only about 2 related papers. One of them seems to be from 1998, while the other one is more recent.
These articles suggest that it's doable. If this works, we'll be able to produce biopolymers with the sequence exactly as we designed, there would be massive applications, but I'm curious why it's not getting much attention, or why aren't there more papers related to this area?

Non-covalent circularization is known to increase the protein steady state levels by increasing mRNA stability and translation efficiency. But certainly no long proteins are made by such a process. If there is no stop codon then the non-stop decay mechanism eliminates the mRNA. I am not sure how it works out in this case. I guess it may work out to some extent but is not very reliable.

If you read the two papers, in fact long proteins are made. They stated that they constructed a circular mRNA with infinite open reading frame. The 1998 papers makes poly-GFP 5~6 times long than the GFP (if i remember correctly). The 2013 paper makes very large proteins as can be seen on the southern blotting figures (i didn't find the numbers though).
I'm however curious about how the non-stop decay mechanism works. In the paper they used the PURE system, which is an artificially constructed reaction vessel that mimics the environment within the cell, but eliminates the decay mechanisms.

Yes I did see the paper; I found it interesting. But I am not sure if this can be reliably replicated and how the length of the product can be controlled. Perhaps those are the aspects that you are interested in when you plan to use the system to synthesize your biopolymer. (PS: it is the western blotting that is used for detecting the protein)

Yeah, western blotting, sorry for the mistake.

I'm familiar with those papers, and they were dissapointed in the yields. The issue seems to be that ribosome binding is the slow step, and the ribosomes don't stay on the mRNA forever. Made me wonder if you could tie the ribosome around the mRNA strand to lock it in place.

@user137 It looks like they were disappointed in the yields and then stopped doing further research!

non-stop decay in my understanding is probability of ribosome to unbind RNA (half-life time of RNA-ribosome complex is finite). The longer transcript, the higher is chance that ribosome will fall off and product will not be functional or will be degraded.

@user137 Some cysteines strategically placed in each subunit might do the trick.

In vitro translation is not as efficient as other chemical polymer reactions. For example, when proteins are synthesized using in vitro translation systems, many researchers have been using radio-labeling to see the products because the yield is too low to detect them by other methods, although few small proteins have been successfully produced at a microgram level. It should be noted that it is also difficult to produce exogenous long peptides at sizes more than 100kDa in E coli in vivo expression system.


text:
Can viruses be used to extract oil from algae?
I read that one hard step in algae oil extraction is to rupture (or fracture) the cell walls to get the contents inside. Some people use chemical methods; some use sonication or mechanical forces.
I wonder why nobody is talking about using viruses to accomplish this task? Viruses destroy the cells and release clones of itself. Some article states that there are plenty of unknown viruses in seawater. I'm sure a major part of it infects algae.

Another major concern would be containment. Let's say you start producing industrial amounts of virus that you engineer to quickly causes the lysis of algae (we'll ignore mutations).  Where are you going to grow that where it wouldn't also be open to insects, birds, or even wind.  You could move this entire operation in a green house, but then you start to loose your major provider of energy in the first place--the sun! Again it could work, but is unlikely to yield what you want.

Viruses hijack the hosts translational machinery, forcing the host to downregulate translation of other proteins in favor of viral proteins. Your cells will eventually lyse, but in the meantime they would not be producing the enzymes required to make whatever product it is you're trying to get, likely resulting in low yields that are contaminated with virus.

A virus has to infect the cell, take over the cell machinery to make more virus, and then is might lyse the cell.  And then you have to wait for more virus to do that again to more cells, and you have to keep the algae alive all that time.
Chemical or mechanical shearing would be much faster, and you don't have to run the risk of virus floating around and getting into stocks that you don't want to kill right now.

But we could use a lot of virus to shorten the time it takes for all the cells to get infected, the virus can just be reused from a previous batch so it's cheap to produce.
Mechanical shearing would be inefficient if you want to fracture cells that small, and chemical methods require recycling and they are expensive in the first place. Virus is using the energy of the cell itself to do the fracture, and afterall the purpose of making oil from algae is to use the cell to produce energy, it's still a net gain.

Consider where you'd get all that virus. Purify it out of the lysed cultures you just made? The viral lysis takes longer, results in less product, and requires an additional virus recovery step. If you're making energy, it's probably more efficient to run the sonicator off the extra yields you get from sonicating your algae instead of using viruses.


text:
Why do provitamins-A do not cause Vitamin-A toxicity?
Why do beta-carotene and other provitamins like alpha-carotene not cause vitamin-A toxicity but rather carotenosis (Orange skin) whereas retinal, retinol, and retinoic acid cause vitamin A toxicity with dosage as low as 4000 IU?

Retinoic acid is a signalling molecule whereas the provitamins are merely precursors.

Since, you didn't state whether you were referring to a concentrate or not, i'm assuming the following forms of Vitamin A were obtained via pill or topical suspension - except for the Carotenoid.
α-carotene and β-carotene are (primary) precursors to Vitamin A. Likewise with, Retinal, Retinol but not with Retinoic Acid (irreversibly metabolized/end point) however, i'm assuming that these first generation Retinoids are produced via ex situ (a facility) metabolism and hence, they do not contain the carotenoid component that cause yellowing of the skin due to the absence of lipid soluble orange/yellow pigments (Xanthaemia). Albeit, the color of the aforementioned FG retinoids when in a concentrated solid state are all yellow still due to molecular structure - explained in midsection.
For example:
Retinal:  Otherwise known as Retinaldehyde, is ingested via meat (as a single/complete molecule) or produced by ingestion of carotenoid containing food-stuff (e.g. carots). The pigment causing the color are, Carotenes. Carotene is a component of the Carotenoid molecule; α-carotene and β-carotene.
Alternatively, Retinal can be produced from the metabolism of β-cryptoxanthin, a Xanthophyll containing compound. Xanthophyll and Carotene are similar in terms of molecular structure, however, a Xanthophyll molecule contains Hydroxyl groups and hence, Oxygen atoms - Carotenes are hydrocarbons.
On that note, hypervitaminosis A can be caused by an over ingestion of α-carotene and β-carotene sources e.g. Carrots, due to the process of metabolism; over an extended period of time.
Generally;
Retinyl ester <=> Retinol <=>  Retinal => Retinoic acid

What causes Xanthemia in this context?
α-carotene and β-carotene, are absorbed via (passive) diffusion within the gastrointestinal tract. From there, they are metabolized (not fully/partially) at the the mucousal layer of the intestine for the substance to be transported into the liver. Next, the metabolite is diffused into the peripheral tissues by the blood plasma. This is were the "issue" is: Excretion. Carotenoids are excreted via bowel movements (gastrointestinal secretions), Urination, through the secretion of sebum and by sweating.
If very high levels of Carotenoids are being ingested, the pigment tends to show itself when a "build up" occurs, in the sweet glands of our dermis and more noticeably, in areas of which there are a large amount of sweat glands e.g. nasolabial folds.
The orange color is defined is due to the classification of what Carotenoids are. All carotenoids are tetraterpenoids: essentially being tetraterpenes that have been modified by chemical transformations such as oxidation or cyclization. Furtherly, tetraterpenoids are made up 40 carbon atoms and contain 8 isoprene molecules. α-carotene and β-carotene, are bicylcic tetraterpenoids. This molecular classification may have an affect on the amount of energy that the molecule can absorb, and more formally, the colour. Albeit, the greatest majority of reasoning in regards to the orange color, is in favor of the long conjugated chain'ed structure of the molecule.
Carotenoids absorb light in the blue-green and violet region and reflect the longer yellow, red, and orange wavelengths; these pigments also dispose excess energy out of the cell.

Conclusion
Retinal and Retinal are preformed retinoids and are not obtained by means of carotenoid metabolism so, they won't contain the the yellow/orange dark pigment that is found within some plant-based food (Carotene).
Retinoic Acid, is a retinoid although it's function is as a cell signalling molecule. The difference between it and the other retinoids is the functional group present of the tail of the carbon-carbon backbone
Theoretically, speaking, and due to retinoids having a shorter/less extended  conjugated system with less unsaturated (multiple) bonds in the molecules it will have shifted the absorption to shorter wavelengths (The two carotene precursors have 11 conjugated bonds and the latter retinoids contain 5).
Furtherly, I don't think that the carboxyl group attached to the Retinoic acid molecule could be classed as an Auxochrome although the remainder of the retinoic acids carbon-carbon chain is still the molecules Chromophore - likewise with the other retinoids.  For example, this would mean that there is possibility that the retinoic acid molecule will be more inclined to absorb shorter wavelengths and hence, less orange/yellow. This is relevant as, you will often find retinoic acid in topical preparations that are used to treat certain dermatological conditions.
I don't think that there is a 100% correct answer for this question as there is no evidence to prove that it would be true in this particular case.
So, you are susceptible to toxicity at lower levels in regards to retinol, retinal and retinoic acid because, of the fact that they are metabolites/concentrates and you need ingest less in order to get to the same point of toxicity. Carotenoids are "raw" in contrast to the preformed retinoids   and require breakdown. Look at the image below to get an idea of how much the molecular mass will have reduced when the carotenoid is metabolized into a useful form of Vitamin A.
Another example would be, you needing to eat more daffodil bulbs to get the required dose of Galantamine hydrobromide (used in Alzheimer's disease treatment) - that's a bit different though, to be fair.


text:
What is the evolutionary tradeoff against primates producing multiple offsprings (litter)?
If we evolved to have multiples all the time we would more likely have extended families living together in 1 house. This would be better than the spouses by themselves for multiple reasons including money.
And during prehistoric times it would have been better for several reasons including that 1 would be more likely to survive than if it was born without any siblings.
Most mammals have litters of at least 2. An extreme of this is the cheetah which has litters of up to 9 cubs. They evolved to have litters because they were in conditions where 1 is likely to starve. Lions evolved this for a different reason since lions are not likely to starve. They evolved it because of the fact that they live in prides.
So for primates including us wouldn't it be better if they had litters often instead of single babies?

No. Primate babies require a lot of care, as a significant amount of development occurs post-partum. Even though, say, a lion cub requires care and teaching, they are born mobile and with the ability to see and hear fairly well, if not very well. Human babies, on the other hand, are completely helpless. Please remember that money is an extremely recent invention in the span of human evolution, and plays no selective pressure whatsoever. Families choosing to have a limited number of children are also an incredibly recent phenomenon (really, in the last 100 years or so).

This is not a duplicate. The answer here is not simply "because not everything advantageous will evolve", this question involves the classic tradeoff between litter/offspring size and the energy expended to care for them. It would not actually be beneficial for primates to have larger litter sizes.

@terdon I am reopening this. If you have an answer for this question then please post it.

There is a tradeoff between having multiple progeny, with relatively low parental investment in each, and few progeny, with high investment in each.  This used to be called "r" and "K" selection respectively, though the terms are now used less.  Very simplistically speaking, long-lived species within a fairly stable environment tend to produce few offspring and invest large amounts of care in each; this description fits primates very well, and so it's not surprising that they follow this paradigm.  The bottom line is that because of primate life history, having small litters is a more successful evolutionary strategy.
The Wikipedia article on r/K selection theory is reasonably good and points to updates and some further reading on the subject.

But some big cats have long lives and large litters. Lions are a great example because lions live for up to 15 years in the wild and have litters of up to 6 cubs.  Likewise some animals with short lives have small litters. So the r/K selection theory isn't completely accurate.

The r/K selection theory is not completely accurate (as I noted, the terms are being used less; and the link I included points out the same thing), but lions are not a good counterexample.  For one thing, lions are often used as examples of K strategists -- the average litter size is closer to 2 than 6, and a typical interval between litters is closer to two years than one.  Three or four offspring every couple years is certainly K-strategy, since with r strategists we're often talking about thousands (or millions) of offspring per year. But as I said, and repeat, K/r is oversimplified.


text:
Evolution of plants and chloroplasts?
I am considering the evolution of plants, specifically considering the chloroplast. I am getting slightly confused and cannot seem to find the information I need to build a coherent picture in my head. Specifically, I have the following questions:

Is the defining feature of a plant cell that it has, or once had, chloroplasts? Is the group of plants all of the species which came from the single common ancestor eukaryotic cell which first acquired a photosynthesising bacterium as an endosymbiont?
In that case, the plants Alectoria sarmentosa (witch's hair lichen) and Monotropa uniflora (Indian Pipe), which are non-photosynthesising plants and do not have chlorophyll, must have some remanant of a chloroplast inside of them (unless they are not actually plants and are just plant-like fungi). My question here is, are these really plants? If so and it is true that plants are defined as all being descendant from this first photosynthesising eukaryote ancestor, then what is their 'remnant chloroplast'? I.e. what organelle do they have that used to be a chloroplast.
If it is true that there are plants which have organelles that used to be chloroplasts but not longer have chlorophyll and photosynthesise, then it is almost certainly the case that the chloroplasts carry out some function other than photosynthesis that is beneficial to the plant's survival (e.g. I know that remnant mitochondria- hydrogenosomes and mitosomes- are useful for fixing iron although they do not carry out respiration). What are the other functions of chloroplast-like organelles?

Modern biology attempts to group organisms by clades, that is, into groups that contain all descendants of a particular organism and no others.  A clade may be associated with characteristics that most or all members of the clade possess, but those characteristics do not define the clade.  Previously it was common to describe biological groups by particular defining characteristics, but that has been largely abandoned because it often does not reflect true relationships.
"Plants" (or Plantae) is a term that can mean several different things, which are outlined in this Wikipedia table.  In short, it might be (approximately) the clade of "land plants", the clade of "green plants", which includes land plants and green algae, or the clade containing those plus the red algae and the glaucophyte algae.  That last clade, also known as the Archaeplastida, is thought to include all descendant species of the initial organism which initially established the symbiosis leading to chloroplasts (although not some organisms that acquired chloroplasts by secondary ingestion of archaeplastida).  It seems like you are most concerned with that third group.
Alectoria sarmentosa (witch's hair lichen) is not a plant by any of these definitions.  It is a lichen, which are symbioses of a fungi with a cyanobacterium or a green algae.  Green algae of course have chloroplasts.
Monotropa uniflora (Indian Pipe) is a member of the heather family and so is a plant by any of the above three definitions.  It does not have chlorophyll; my guess is that it likely has degenerate chloroplasts.
I think a separate question would be appropriate to inquire about the chloroplast remnants of non-photosynthesizing plants like Monotropa uniflora.

Moreover, even among archaeplastida, the chloroplasts don't seem have the same evolutionary origin. I am not too sure about it though.


text:
Why does temperature shock kill fish?
As is advised with most fish you should avoid sudden changes in water temperature (for example by introducing new water that hasn't been left to come to room temperature). I have, however, never understood why that is the case, in particular given that most fish are cold blooded so there is no issue with needing to "ramp up" the metabolism when in cold water.
Say a particular species of fish can survive in water between 20°C and 30°C what causes a fish that was previously in 30°C water to die when suddenly plunged into 20°C water? I understand this effect is called "shock" but I'm looking for the biological reason for it.
To be clear I'm not looking for "chemical x is released and that leads to the fish dying,  I'm looking for why these chemicals are released at all. So to give an example if my question had of been "why does adrenaline shock kill" I'd be looking for "adrenaline release is usually a good thing, it's released in response to a fright and prepares the body for a fight or flight response. However this heightend preparedness can cause additional strain on the body which can cause death in some cases"

As others have said fish can die from an overload of hormones or muscle exaustionn. Mammals are likely to get hypothermia from the dramatic temperature drop killing them.

How fast can a lake or a river change from 20-30 degrees? 2 days. Inevitable thermal shock is not something fish dealt with a single time in the last 300 million years.  Every chemical reaction in the fishes body suddenly goes at 1/2 speed if you cool it from 30 to 20. some fish can go easily from 15 to 25, they can dive for cover one hour and then bask at the top where they can grow faster.

The question that you're posing isn't "why does temperature changes kill Fish", but why these physiological responses exist in the first place. The above answers clearly explained what the effects are of temperature shock, and what biological responses can occur that can harm the fish. I suggest you research and ask people the rephrased question "Why do these processes occur in fish?" Maybe check this article about metabolic rate and oxygen consumption to start your research: http://fishbio.com/field-notes/the-fish-report/fuel-for-thought-studying-fish-metabolism

You might have an easier time if you look at the reverse question, sudden temperature changes are pretty hard on living things, even something as simple as membrane permeability can be drastically changed by temperature. We don't think about it becasue we are descended from terrestrial organisms, and air can and does change temprature quickly unlike water, so our ancestors had to develop defenses against these sudden swings. most fish never had to bother.

This due to a phenomenon called "cold shock". This induces a number of physiological changes in the fishs metabolism and also in its behaviour and can lead to death.
The first paper cites some reasons in table 1:

Brain and central nervous system response: Changes in neuronal
activity
Catecholamine and corticosteroid response: Release of hormones due to
the shock.
Haematological and metabolic response: Changes in red and white blood
cells and lactic acid in the blood.
Protein expression and molecular responses: Changes in the expression
of proteins of the heat shock family.

These changes (especially in brain and nerves and also the hormones) can deregulate the fishs metabolism so much that it can die. Shock is a critical condition. Obviously a lot of research is going on, but I recommend reading the two articles below for further details.

References:

Cold shock and fish
Physiological stress responses in the warm-water fish matrinxã
(Brycon amazonicus ) subjected to a sudden cold shock

So, would it be correct to say in terms of points 1 and 3 that although the fish's overall metabolism isn't ramped up/down (being cold blooded) there are other processes that are ramped up/down to cope with the current temperature so if those "settings" are in the wrong place for the suddenly changed temperature then the fish will die (as it takes time to ramp up/down the processes). Basically I understand that the fish dies because "This process occurs which leads to the fishes death" I'm looking for why those processes even exist in the first place

e.g. A sudden fright can kill people because adrenalin is released which stimulates the heart rate etc to increase. Usually this would be beneficial giving a "fight or fright" response but in extremes can be lethal (in particular to a weakened system)


text:
How does isopropyl alcohol disinfect less in higher concentration?
Isopropyl alcohol (2-propanol) can be used as disinfectant.
For increasing concentration of it in water, the effect as disinfectant increases, and then decreases again.
Typical concentrations for use as disinfectant seem to be 60-75% isopropyl alcohol in water.
Wikipedia: Isopropyl alcohol - Medical mentions membrane pores of bacteria that will not open without water.
That does not feel like the full explanation to me; I expect there are bacteria with membrane pores of diverse kind.
Does 100% isopropyl alcohol not disinfect at all - or just more slowly? What abour the effect on other pathogens?

The main reason why alcohols (isopropanol and ethanol mostly) can be used as disinfectants is that they denature (bacterial) proteins. This is also the reason why they work on such a broad spectrum of microorganisms (bacteria, fungi, viruses), but not on spores, as these are better protected.
The higher the concentration of the alcohol is, the faster this denaturation is happening. And this can cause problems: When you denature the proteins of the bacterial cell wall, they will form some kind of protective layer around some of the cells which allows their survival. Diluting the alcohols makes the disinfection happening slower and thus gives the alcohols more time to get into the cell.
For more information about concentrations and also for a ton of references, have a look into the CDC's disinfection guidelines in the subchapter on alcohols.
More details can be found in this review:

Antiseptics and Disinfectants: Activity, Action, and Resistance

So this is a good question.
70% is optimal for most cell types, especially those with a cell wall like prokaryotes.
Wikipedia is a little off here. The reason you add water is to make the solution hypotonic.
The alcohol disrupts the hydrophobic forces holding the phospholipids of the membrane while dehydrating any peptidogylcan of the wall enough to cause it to become less fluid/more brittle.
Now that you have essentially made the protection of the cell like brittle glass, the hypotonicity causes the cell to swell and now easily burst.
Bacteria aren't going to last long in 100% either. They fix instead, which although irreversible takes a little longer to occur.
It's also a little more economical and less wasteful to use 70% if it's just as, if not a little more, effective

Can you please add some references?

The sentence "They fix instead..." - it that related to nitrogen fixation? I don't understand that part.

Or do they just get immobile with no way to recover?

@VolkerSiegel Fixation in this context is referring to histological fixation, which can actually be one of several chemical processes. This Wikipedia page is a good starting place.


text:
How are proteins reused in the body?
Part of what we eat are proteins,
and our body is in part build of proteins.
Are the proteins of the body build based on proteins in food at all?
Are proteins in food directly reused in the body,
or are proteins first disassembled?
How far are they disassembled, randomly in various pieces, or systematically to keep what can optimally be used to build new proteins, while nothing is wasted for energy?
(The question Can proteins/peptides pass through the intestine? and it's answers are related, and provide some context and relevant parts, but is not a duplicate.)

Does this answer your question? Can proteins/peptides pass through the intestine?

@tyersome Not sure that's the best dupe, since it doesn't cover the "normal" way of business. I know variations of this question have come up before, though.

@tyersome It gives some insight about part of the answer, so it is good that it is linked.

It's not a duplicate of " Can proteins/peptides pass through the intestine?"

Short answer: Indeed the proteins in our body are based on amino acids from external food sources. BUT, proteins up-taken from food are ALWAYS disassembled first into amino acids, through specialized enzymes, proteases, (for instance Pepsin in the stomach's gastric juices and Tripsin in the pancreatic juices), during digestion, in the alimentary canal, (gut). This enables the body's liver to build the proteins most needed by the organism itself, through the processes of transamination, that allows conversion betwixt amino acids, and deamination, that removes N2 from the amino acid, (let's say the "amino" part is removed, and then expelled as urea), to excrete amino acids in excess. In addition this breaking down of external proteins is necessary, since they can act as labels for pathogens, and external organisms in general, and thus would soon be destroyed by the immune system if reused straight away.


text:
Does the body use radio frequencies in the range of frequencies used in mobile phone networks?
I read something related to the biological effects of "mobile phone radiation". It was not as far from reality as one might expect with this topic. The context was about the acceptable distance of mobile phones to the human body. Mobile network operators specify minimal distances of some cm.
I was surprised to read that the human body actively uses electromagnetic waves in or near the frequencies used by mobile phone networks.
Is that true?
Or partially true?
Or at least plausible?

German source: https://www.diagnose-funk.org/themen/mobilfunk-anwendungen/mobiltelefone/smartphone-nicht-in-koerpernaehe-benutzen
Relevant section translated (paragraph above the image):

Human body cells also communicate via electromagnetic vibrations, such currents are measured, for example, in the case of a cardiac ECG or brain EEG. The mobile radio signals are in the frequency range of the body's own vibrations. It is therefore not surprising that electromagnetic radiation can disrupt brain waves, heartbeat and other body functions. The health risks posed by high-frequency electromagnetic fields (EMF) have been sufficiently researched and documented. Diagnosis: Radio documents this on the website www.mobilfunkstudien.org

The body doesn’t use electromagnetic radiation (other than sunlight) as far as I am aware, but the reference in your original question didn’t say that, it said it could affect cells and cause them to become cancerous, like other radiation — e.g. ionizing radiation — that the body doesn’t use. Why did you remove the reference?

@David I added my original reference

Sorry about that. Must be confusing your post with another. Anyway, I was going to make some general observations but I’ll have a glance at the original first. I can read German.

Following the trail I ended up with an English-language paper by Yu et al. in a Elsevier journal I had not previously encountered, Science of the Total Environment. This claimed to show an effect of 4G radiofrequency radiation on rat testis and rat fertility. I can find nothing in the paper corresponding to the section you translate, or on the Diagnose: Funk report page you provide a link for. The only electromagnetic radiation that the human body uses to communicate as far as I am aware is electric currents.

The claims in the quote seem pretty vague to me. "Human body cells also communicate via electromagnetic vibrations" isn't really accurate, and if you wanted to stretch it to be accurate you'd have frequencies that are nowhere near the ballpark of those used in cellular communications. The conclusion "The health risks posed by high-frequency electromagnetic fields (EMF) have been sufficiently researched and documented" is laughably false, and I think a good cue to distrust the whole source.


text:
What happens to the language processing brain part if no language is ever learned?
Language is processed in the human brain in multiple regions.
Some of them seem to be used exclusively or mainly for language processing,
other regions are distributed overlapping with other functions.
If a feral child is never exposed to any language, and therefore never
learns one: What happens to the language related parts of the brain,
like the ones exclusively used for language?
The language processing is not the central point - so feel free to use analogous examples of brain regions that are unused based on exceptional circumstances. Blindness from birth on comes to mind. Also, no need to base examples on homo sapiens.

Although this specific experiment wouldn't be done, similar experiments have been done in experiments in animal models where a sensory input is removed/altered. These experiments show that if you remove some sort of sensory input, the parts of the brain originally responding to that input will take on other tasks. There have been many studies that show this, but the canonical reference is often this one, where the part of the brain previously responding to sensory input to a finger instead responds to stimulation of another finger after the original finger is amputated:
Merzenich, M. M., Nelson, R. J., Stryker, M. P., Cynader, M. S., Schoppmann, A., & Zook, J. M. (1984). Somatosensory cortical map changes following digit amputation in adult monkeys. Journal of comparative neurology, 224(4), 591-605.
There have also been studies of humans with sensory deficits like blindness or deafness that show similar reorganization, depending on the age the deficit is acquired. For examples, see:
Finney, E. M., Fine, I., & Dobkins, K. R. (2001). Visual stimuli activate auditory cortex in the deaf. Nature neuroscience, 4(12), 1171-1173.
Kujala, T., Huotilainen, M., Sinkkonen, J., Ahonen, A. I., Alho, K., Hämälä, M. S., ... & Salonen, O. (1995). Visual cortex activation in blind humans during sound discrimination. Neuroscience letters, 183(1), 143-146.
In summary, the result is that the neocortex is a very flexible, adaptable structure, and if inputs of a certain type are impoverished, that region of the cortex is used for other purposes. Essentially, neighboring functions creep in to that space.
Language processing in humans includes both auditory areas that respond to the sounds made by language, and premotor processing areas that seem to be important both for understanding the semantic content of language and for producing verbal output. None of these areas are truly language-unique, though, they are just regions that are active more than other areas when language-based tasks are occurring. In a person not exposed to a language, it's likely they would develop some rudimentary language-based skills anyways unless they were truly raised in some sort of sensory deprivation context - at this point an answer would get too far into speculation. Besides that, those areas would probably be re-purposed for other types of sensory processing and other types of motor planning.

Using these analogous examples is perfectly fine. Interesting...