text:
What happens to plants if they are exposed to "sunlight" 24h a day?
I just wondered if one could grow plants faster, if they were exposed to sunlight-like light all the time.
In a similar question which is not the same, I could confirm that plants have different processes going on at day and at night. However, it didn't answer the question about the consequences of permanent exposure to sunlight.
However, I don't understand what would happen if there was light all the time. What would happen to different plants if they are exposed to "sunlight" 24/7?
(Similarly: What is the "optimal" amount of sunlight time for different plants? Is it basically what is common in the environments they typically grow in?)

Possible duplicate of Do plants need sleep?

Look into crop growing in Alaska, Scandinavia, and other places where there is nearly continuous sunlight in summer.

This review (from 2011)1 states that it depends on the plant species and cultivar.

Some continuous light (CL)-grown photosynthetic organisms show
  increased productivity. However, CL also induces negative effects in
  several plant species. The most visible CL-induced negative effects
  are leaf chlorosis and necrosis. CL also lowers photosynthetic
  parameters ... The CL-sensitive species include eggplant, geranium,
  some onion species (Allium fistulosum), peanut, some cultivars of
  potato, tomato, and even lichens (Xanthoria parietina) and mosses
  (Pleurozium schreberi and Ceratodon purpureous).

Among the plants that have better yields under continuous light are lettuce, roses, some potato cultivars, some algae.
The reasons why some plants can be damaged under continuous light aren't completely clear (at least they weren't in 2011). One of the problems is carbon imbalance. Leaves produce too much sucrose and other organs such as roots are not able to process it fast enough. This leads to high sugar concentrations and can cause leaf senescence. Continuous photosynthesis also results in more photo-oxidative damage and plants that better detoxify reactive oxygen species have less negative effects from continuous light.
So look for research on the particular species you want to grow or just experiment with different light conditions.

 1. Velez-Ramirez, A.I., van Ieperen, W., Vreugdenhil, D. and Millenaar, F.F. 2011. Plants under continuous light. Trends in plant science, 16(6):310-318.

Plants - like essentially eukaroytic &/ phototrophic organisms - have circadian clocks, regulating a bunch of cellular processes including the 'light' and 'dark' cycles of photosynthesis. Circadian systems can control a lot different things so disrupting them  can have all sorts of effects - which is probably also why some plant species are affected in different ways than others.


text:
Mushroom Identification (USA)
I would like some help identifying this mushroom I found in my yard.
Location: Southeast Georgia
Near Pine trees after heavy rainfall
Color: Light brown to Dark Red, biggest is about 4 inches in radius

It is some type of boletus. You would need a spore print and a few more examples to decide which one. They are commonly found under conifers.The books say most are editable and good taste. The couple kind I have eaten had no flavor , not worth collecting. The tubes instead of gills on the bottom of the cap are an indicator of boletus group.

I agree it looks like a bolete, but your post needs to provide citations to support your claims and should ideally give a more direct answer as yoru answer currently is conjectural and not actually answering the OP's question. Please do some additional research and [edit] your post with more info. Thanks!

source: Stack Exchange

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

sort: votes


text:
Are controls needed for urine cultures?
If testing for bacteria (gram-negative) in a urine culture, are negative or positive cultures needed?
I could not find anything that says controls are needed unless results seem to be contaminated. I thought since controls are used in Gram stains, they would be used in cultures as well. Thanks!

No, controls aren't needed for a diagnostic test of that kind, since the only concern is about that urine specimen. The result will be either positive or negative; if positive, the urine will be plated and the bacteria will be tested for antibiotic sensitivity. The same is true of blood tests, MRIs, Xrays (although in some pediatric cases, the unaffected side acts as a comparison), etc.

that makes sense, thank you so much!

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


text:
How much variation in the human genome for humans
We are currently learning about the Human Genome Project in high school biology. Wouldn't the human genome that was mapped be different from, say, mine if it was mapped? How much variation is there between individual humans in our genetic sequencing? I'm assuming there is not that much difference since multiple volunteers were used in the project. I did see another question that talked about mutation rate, so I'm not sure if that's the same thing.

Welcome to Biology.SE! This is a very basic question and thus appears to meet this sites criteria for a homework question. In these situations we expect you to do some research on your own and then ask questions informed by what you have learned (ideally with references to reliable sources). For instance the "Related" links led me to this question. ——— Please also take the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site. Thanks!

Possible duplicate of Why are the genomes of Humans 99.5% the same?

Hi Sarah, and welcome to Bio.SE! @tyersome I disagree that this is a "basic" or trivial question. So do the 500K genome project, gnomAD, ClinVar, Genomics England & BioBank, and countless other massive projects. Even post-sequencing, calculating the rate of variation is incredibly challenging. This question clearly is a fundamental question about genetics that has massive ramifications in rare disease, cancers, developmental disorders etc.

@David I think that I side with Sarah on this. Mutability (i.e conservation) and variation are fundementally different principles. Conservation (evolutionary constraint/mutability) are measuring changes of genetic regions over huge timescales by comparing homologous sequences in other species. Variation, however, is snapshot of what is currently varied in the population of a single species. Of course, there is a lot of overlap between constrained genes in gnomAD, for example, and highly conserved regions. Practically I'm not sure if this will be reflected in the answers...

@James — Perhaps we could do with a community wiki (whatever that is) on this whole topic. I think the current dispersed nature of questions relating to it makes it very hard to get a coherent view.

You are correct in saying that the human genome sequenced in the project was contributed by a dozen anonymous volunteers. However, the final sequence that is used as a standard reference is a somewhat arbitrary construct that represents a collection of consecutive segments taken from one or other of the contributors. It is a haploid sequence, plus a Y and an X chromosome.
Now you ask how different are the genomes of any two subjects, taken at random from a population. Imagine for simplicity looking at your own genome. For each of the 22 autosomes, you know you have two copies, one transmitted from your father, the other from your mother (for the X chromosome you have two copies, if you are a girl). Now imagine comparing the sequence of each of your pair of homologous chromosomes side by side; remember that they are derived from very different individuals (unless your parents are close relatives), so that they will not be identical, as they represent independent evolutionary histories.
Then, the question becomes: how much variation is there between the sequences of your paired chromosomes? And the answer is known: approximately every 1,000 base pairs your chromosomes show a base pair in one chromosome and a different base pair in the other; otherwise they are identical. The sites where this variation occurs are called SNP, for Single Nucleotide Polymorphisms (many other kinds of variation exist, but SNPs are the more common). We can generalize this observation, as it remains true for any pair of chromosomes chosen at random from any pair of subjects. Therefore, we can say that humans are identical for 99.9% of their genomes, whereas the genetic variation responsible for the differences that allows us to recognize ourselves as unique are limited to 0.1% of our genome.

I think this answer gives a good basic overview to the question, for further detailed reading it would be helpful to include links about the already mentioned SNPs and also the 1000-genomes project (which is essentially about exactly this question)


text:
Is there any justification for the claim that blood travels 12,000 miles per day?
An oft-quoted "fact" on the internet1,2,3 (and at least once in print4) is the claim:

Your body has about 5.6 liters (6 quarts) of blood. This 5.6 liters of blood circulates through the body three times every minute. In one day, the blood travels a total of 19,000 km (12,000 miles)—that's four times the distance across the US from coast to coast.
Source: https://www.pbs.org/wgbh/nova/heart/heartfacts.html

None of the instances I've found provide any justification for the 12,000 miles figure; nor do they cite any authoritative source.
Although the 12,000 miles figure occurs often, it is fairly obvious that most (if not all) instances are copied from one of the other instances. Sometimes word-for-word, sometimes paraphrased; sometimes with a mention of the other instance, more often with no mention of the source. It is therefore quite possible that someone "plucked a number out of the air" and the meme-dispersal properties of the internet have done the rest.
In trying to justify this claim (see Background and Further Research below), it becomes clear that an awful lot depends on what precisely is meant by "the blood" and – to a lesser extent – what is meant by "the distance traveled". Some plausible definitions could put this figure at anywhere from around 70-90 miles up to around 90 million miles (and, in extremis, even a couple of thousand trillion miles!). It is entirely possible that there is no meaningful answer to the question of how far blood travels in a day.
Question(s)

Is there any extant, authoritative (ideally peer-reviewed) source for the 12,000 miles claim (i.e. that might have been the original source for the above "fact")?

If the 12,000 miles has simply been plucked from the air, is there any extant, authoritative source for a different figure?

If there is no extant authoritative source for any such figure, can someone provide a justifiable and evidence-backed answer to the question "How far does blood travel in a day"? (But see note below.)

Please note: I am slightly hesitant at including the third option above, and may remove it if felt appropriate. I recognize that the underlying question is likely ambiguous, and that any attempt at an answer might well be "opinion based" (as it will probably need to interpret exactly what is meant by "the blood" and "the distance traveled"). At the risk of being over-demanding, any attempt at answering under this option must include fact-backed justification for any such interpretation(s) and ideally would justify why such interpretation(s) are the only valid ones. I an not
looking for speculation along the lines of "If we define "the blood" this way and follow these calculations, we end up with this figure.".

Background
In the pub a while back, someone had the book 1,342 QI Facts To Leave You Flabbergasted4. This was opened at random to the "fact" that in one day, "blood travels 12,000 miles". I don't have the book in front of me to give its exact wording, but the accompanying Source Finder website5 points to the PBS quote at the top of this question.
Our first thought was "that's Quite Interesting" (which, after all, is the point of the show/book). Our second thought was "that sounds very high"... if "the blood" travels 12,000 miles in a day, it travels 500 miles in an hour, and clearly (at least at a simplistic level), blood isn't coursing through our body at 500 mph!
Some further pondering, and a little web-searching on mobiles didn't clarify things: our conclusion  was (as noted above), that too much hinged on what exactly is meant by "the blood" and how you measure "the distance traveled". Some clearly wrong interpretations:

We found a figure of 3-4 mph for the average speed of blood-flow6 . Treating "the blood" as a homogeneous fluid, this would give a "total distance traveled" of between 72 and 96 miles over a 24-hour period.

Clearly 12,000 miles isn't the distance traveled by an individual blood cell, as that would necessitate it traveling at the aforementioned 500 mph.

It's clearly not based on the total distance traveled by all blood cells. An adult male has around 25 trillion (25,000,000,000,000) red blood cells (RBCs)7.  If each is traveling on average at 3-4 mph, the total distance for all cells would be roughly 2,000 trillion miles in a day (or about 350 light-years – a little more than the distance to Canopus, the second brightest star in the sky). Conversely, if the total distance was 12,000 miles, each RBC would travel less than a thousandth of a millimetre (about the wavelength of red light).

We did have some thoughts about trying to account for the multiple paths that "the blood" flows through. In an extremely simplified example, suppose blood from the heart split into two parallel paths, each of which went around the body before merging just before re-entering the heart. It could be argued that "the total distance" was 2 x 4 mph x 24 hours, since "the blood" was going down two channels. However, it could also be argued that what is going down each channel is not "the blood" but "half the blood".
Things get more complicated when more realistic topologies are considered: if the blood flows through a common vessel (e.g. the aorta) before splitting, if you count each path separately (as above), should the shared path count double or only once? You probably want something in between based on the relative lengths of the single path and the multiple paths.
My view is that while this might be a way of deriving a plausible figure, it is not without problems. One is practical: you'd need to map the entire circulatory system in order to correctly assign weights to each branch and arrive at an overall multiplier. Another is numerical: as we scale up to the full system, there is a danger the multiplier grows too quickly (remember: 80% of the system is formed from capillaries, and the smallest of these are no wider than a blood cell... there will be a lot of paths). Finally, what's being measured feels increasingly arbitrary: the contribution from the aorta is from all the blood at once; but from the capillaries it is almost cell-by-cell.
Between the two extremes above – 70-90 miles when treating blood "as a whole", and 2 thousand trillion by counting each cell – you could probably arrive at almost any number for the total distance traveled. Our problem was that we could not think of a natural way of "dividing the blood" and counting "the distance" that would arrive at 12,000 miles. Further research would be required...

Further Research
Over the next couple of days, I did some dedicated web-trawling... with little success.
The 12,000 miles kept cropping up, but with no justification as to where the number came from, and no references to an authoritative source. I also collected the following, potentially relevant "facts" about the heart and circulatory systems (generally, where it matters, for an adult male):

Blood travels an average of 3-4 mph6. Faster in the aorta; slower in the capillaries (where cells need to pass in single-file, and sometimes have to "push" their way through). Another source10 gives a slightly wider range (2.2 to 4.5 mph).

The total length of all arteries, capillaries and veins is about 60,000 miles8,3,9 (with capillaries making up about 80% of this total).

There is about 5.6 litres (6 quarts) of blood in the body1,6,9.

Blood takes about 20 seconds to circulate throughout the entire vascular system1,9.

The only discussion I could find on the subject was a Reddit thread11, which starts:

Does human blood really travel 12,000 miles every day?
Someone posted that on Facebook and I thought it was total bullshit. So I Googled it and it seems it's not bullshit? I guess my real question then would be: isn't there something more to this? That's 500 miles per hour. I can't understand how that wouldn't rip your body apart.

which neatly mirrors our experience: lots of pages quoting 12,000 miles, no references, and a feeling that 500 mph is clearly wrong. There follows some loose speculation, including that the total distance traveled by all blood cells is clearly massively too high; as is a figure of about 90 million miles calculated by multiplying the number of times the blood circulates in a day (1,440) by the total length of the circulatory system (60,000 miles). To me, the most pertinent comment is the closing one from user rm999:

I searched online, there's nothing reputable backing this. The figures I see are closer to <1 mph, which would be on the order of ~20 miles a day.

although rm999's figure for the overall speed is less than the most common figures I saw (although 3 quotes this speed for the aorta).

References
1 Amazing Heart Facts on the Nova section of the PBS website.
2 The Journey of Blood (PDF). Lesson plan on the American Heart Association website.
3 Slideshow on "Circulation" on slideplayer.com by Dwain Gibbs.
4 1,342 QI Facts To Leave You Flabbergasted: a spin-off book from the British TV comedy panel game-show "QI" (for "Quite Interesting") – see entry on Wikipedia. Despite being primarily an entertainment show, it has a pretty good reputation for research, although it does sometimes make mistakes and issue corrections. I suspect the book is less thoroughly researched than items appearing on the TV show.
5 The book lists its sources on https://qi.com/1342/index.php (this can be seen using the Look Inside! feature on the Amazon page above, under "Read This First"). The "12,000" miles fact is the second entry on page 186, leading to the aforementioned http://www.pbs.org/wgbh/nova/heart/heartfacts.html.
6 Our Bodies' Velocities, By the Numbers on the Discover magazine website. Note, though, that after giving the 3-4 mph figure, it goes on to say "But this blood speed is just an average. It starts out by rushing through the aorta at an impressive 15 inches a second, then slows to different rates in various parts of the body." I suspect the "inches" is a mistake: 15 inches/second equates to less than 1 mph; whereas 15 feet/second equates to about 10 mph, which fits better.
7 How many blood cells are in the human body? from the article "How Many Cells Are in the Human Body?" on the Healthline.com website.
8 11 Surprising Facts About the Circulatory System on the Live Science website.
9 Heart Facts on the Health Essentials website of the Cleveland Clinic. The "20 seconds to circulate" fact was originally taken from Amazing Heart Facts on the Arkansas Heart Hospital website, but that link (https://www.arheart.com/heart-health/amazing-heart-facts/) is no longer valid.
10 What is the speed of blood circulation in human body? on Quora.
11 Does human blood really travel 12,000 miles every day? on Reddit.

Welcome to SE Biology. You are to be commended on the thoroughness of your investigation. This sort of question is not the sort of thing that concerns the majority of professional scientists — I personally term it "freak show science" or "Guinness Book of Nonsense" — but there may be someone here interested enough to check your figures. They seem plausible enough to me.

This might be more on-topic at skeptics.SE ? You're asking to confirm a published statement/claim, that happens to be about biology.

A single erythrocite travelling from the heart via the aorta, a certain artery, capillary and vein back to the heart would make about 1 meter in average, I guess.
If the blood volume of an adult is ~5 liters and if the cardiac output is ~5 liters per minute, then "all the blood" travels 1 meter in a minute, which is 60 meters per hour or 1,440 meters (~0.9 miles) per day.
This seems to roughly agree with:

Average peak and mean blood velocities were 66 and 11 cm/sec in the
  ascending aorta, 57 and 10 cm/sec in the pulmonary artery, 28 and 12
  cm/sec in the superior vena cava, and 26 and 13 cm/sec in the inferior
  vena cava. (The blood velocity...(Circulation))

So, if you say that the average blood velocity in big vessels is 12 cm/sec or 432 m/hour and consider that the velocity in smaller vessels is much lower, then it is possible that the average blood velocity in all the vessels could be ~60 m/hour, as I estimated.

But if you took all the blood vessels out of an average child and laid
  them out in one line, the line would stretch over 60,000 miles. An
  adult’s would be closer to 100,000 miles long. (The Franklin Institute)

You can then say that "all separate blood streams" (5 liters in summary) going through all the vessels would make 100,000 miles in a minute or 144,000,000 miles in a day. But not "all the blood" travels all that distance in a day.
I'm not sure how they came to 12,000 miles per day, but this just shows how different the things can look from different perspectives.
EDIT: I just noticed that my "calculation" 144,000,000 miles is 12,000 miles squared.

Just guessing, but I would suppose that someone saw the figure 1200 m(eters) per day, read it as 1200 m(iles) per day, sayd "Oh, wow!", posted about it somewhere, and the post repeatedly got copied without fact-checking.

@jamesqf, such things can happen...Anyway, blood travelling 12,000 or no matter how many miles or meters per day is not really an useful information. I answered just to show how the confusion can develop.

The radius of Earth is ~25,000 miles, so using the center of the earth as a reference frame someone at a moderate latitude would see their blood (and the rest of them) travel about 12,000 miles in a day. I think the 1200 meter explanation is a likely explanation, but overall I think the point that this answer makes (i.e., it totally depends on how you define the trivia) is important, and is consistent with David's point that this sort of estimation isn't really relevant to a biologist.

@BryanKrause, you probably meant circumference...and the blood would then travel 25,000 miles a day...?

@Jan Er, yes of course circumference. Only at the equator would it be 25000, somewhere in the mid latitudes it would be 12000.

@Bryan Krause: But you're still neglecting the motion of the Earth as it revolves around the Sun (about 67,000 mph/107,000 km/h), the Sun moving around the galactic core, our galaxy's motion WRT the local group...

@Jan: The speed of blood flow would be useful information when designing things like stents & replacement heart valves.  E.g. if blood actually did travel 12,000 miles per day, that would be 500 mph, which would cause some serious turbulence, among other problems.

@jamesqf, knowing the speed is useful, of course - and the actual speeds are not calculated but measured. They are all those miles that I don't find useful.

@jamesqf I know, that's why I referred to the center of the earth as a reference frame (I got that detail right even if I misspoke about the radius/circumference ;) ) And yes, knowing the speed of blood flow itself is useful, but the way you'd figure that out is by measuring the speed of blood flow in a vessel of interest. You don't much care about it's velocity elsewhere, and it would likely mislead you if you calculated an average velocity given the differences between capillaries, veins, and arteries.

I tried to come up with an explanation with approximate values. It looks like 12,000 miles is actually milliliter-miles per day. The way to think about is to consider a drop of blood that is part of a heart pump (1 ML) doing roundtrip though the body (say a string of 3.33 meters). There are 56 drops of blood in a heartbeat. If you are to keep 56 strings end to end then the cumulative distance travelled by 56 drops of blood is 3.33*56=186.48 meters. Then if we multiply this distance by number of heart beats per day then we get the 12000 miles number.

56 : milliliters - amount of blood per pump
72 : pumps per minute
56*72 = 4,032  : milliliters per minute
4032*60 = 241,920  : milliliters per hour
241920*24 = 5,806,080  : milliliters per day
1.67 : meters - height of average adult
1.67*2 = 3.33 : meters - roundtrip travelled by blood
5806080*3.33 = 19,353,600 : milliliter-meters per day
19353600/1000 = 19,353 : milliliter-kilometers per day
19353/1.61 = 12,021 : milliliter-miles per day
Note: I am not the person who came up with 12,000 miles per day claim. Since there is no citable source for the claim, I am only trying to come up with a possible explanation for the circulated number.

References:

The web pages below claim that blood travels approximately 12,000 miles per day.
https://www.pbs.org/wgbh/nova/heart/heartfacts.html
https://www.heart.org/idc/groups/heart-public/@wcm/@fc/documents/downloadable/ucm_454347.pdf
The web page below says heart rate range is 60 to 100 beats per minute. I chose 72 which is within the range.
https://www.mayoclinic.org/healthy-lifestyle/fitness/expert-answers/heart-rate/faq-20057979
The web page below says amount of blood per pump is 55-80 milliliters. I chose 56 which is within the range.
https://www.smm.org/heart/lessons/lesson2.htm
The web page below talked about human height. I chose 167 which is within the range.
https://ourworldindata.org/human-height

I'd understand if it got a quarter of the way there with every pump, but that's not what your calculation shows. Do you have a ref. to show that your assumption is correct? I.e. that a particular set of blood goes out the heart, and back again in one beat-cycle?

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.

As blood flows at a rate of 3 to 4 mph or 4.8 to 6.4 kph call it 5kph in 24hours it will have travelled some  120km or 12,000 metres please note METRES not miles.
Too many people misread or misquote things without checking and some actually get printed in quiz books.

Thanks for this, although that should be "120km or 120,000 metres", shouldn't it? However, someone confusing meters and miles and slipping a power of 10 seems a very plausible explanation for where the "12,000 miles" came from (I only ever worked things out in miles, so never spotted the similarity of the "simple" distance in metres).


text:
Cell communication
In some organism we observe that different individual cells organize and form structures. How are these individual cells attaining the information for the grouping? How does these cells communicate?

Welchome to Stack exchange! While this question may seem basic / simple, it is actually a super broad question: Cell communication & organisation encompasses large parts of developmental biology and cell signalling - both of which are very large & active fields of research. You can check the Tour and Help center, which may help you to narrow your question down to a point where we can reasonably answer it.


text:
How do schistosomes find and attach to human skin?
Schistosomes are parasitic flatworms that have a snail intermediate host and a human definitive host.
After developing in the snail, they (cercariae stage) escape into the water and can attach to the skin of a human. Then, it will penetrate the skin and migrate into areas of the human's body.
I have been unable to find any information on the mechanisms related to attachment to the human host's skin. More specifically, my questions are:

Do they attach to whatever they can find, and can only develop into the next stage if they (by chance) attach to the right host?
If they selectively attach to human host skin, how do they detect the skin? What makes the skin distinguishable to them?

Here is a great picture of the life cycle of these parasites, for reference.

Schistosoma recognize human skin by mechanical, thermal and chemical stimuli from host. Attachment of parasite to skin is  stimulated by L-arginine. Schistosomes specifically bind  to L -argine by chemotaxis. L-arginine guides this parasite towards site of penetration. The lipids on the human skin surface also serve as signal for host invasion.
It is also reported that parasite may use L-arginine to synthesize nitric oxide for blood vessel dilation so that it can easily penetrate into the host. Schistosoma may attach to L-arginine of surrounding tissues to escape the cellular immune response from host.
(Via: https://www.ncbi.nlm.nih.gov/pubmed/11860033)
These parasites enter the host through skin by producing several proteolytic enzymes to degarde the host tissue proteins including elastin, condromucoprotein, keratin, fibronectin, laminin and collagens.
Two distant serine proteases are responsible for digesting host tissue. One is Chymotrypsin-like protease which degrades protein with large hydrophobic side chains. And the second one is Trypsin-like protease which prefers proteins with positively charged side chains.
(Via: http://www.jbc.org/content/275/49/38667.full#ref-2)


text:
Original Lotka–Volterra model
I am looking for the articles in which Lotka and Volterra published their original predator prey model. I couldn’t find the model presented in many textbooks in Lotka’s book Elements of Physical Biology or Volterra’s paper Fluctuations in the Abundance of a Species considered Mathematically.
Is there really Lotka–Volterra model for dynamics of two  competing species? On Wikipedia and Murray’s book Mathematical Biology: an Introduction, it is written that it exists but I couldn’t find it in their papers.

Volterra’s Variations and Fluctuations of the Number of Individuals in Animal Species living together features what is nowadays often called the generalised Lotka–Volterra model.
Thus it captures competition between and with populations.
In particular, Section 2 is titled:

Biological Association of two Species which contend for the same Food.


text:
How can we say that a gene is spacio-temporally regulated?
Gene expression is depending on the space and time of the cell. How can we distinguish the function of a gene without a chance of changing its expression? And also how is it possible to find the exact position where the gene is expressed?

The title doesn't seem to fit with the body of the question, which includes two almost completely unrelated subquestions. Can you edit to clarify and reduce your question to one question? It would also help to describe your attempts to answer the question on your own. A typical basic biology textbook would have examples of both testing function and measuring location while teaching other concepts.

Some clarifying questions:  "How can we distinguish the function of a gene without a chance of changing its expression." -- are you asking what the effects of measurement are on transcriptional dynamics? "And also how is it possible to find the exact position where the gene is expressed?" -- by position, are you referring to position in the nucleus / cell?  position along the gene body?


text:
Difference between KEGG Pathway and Module (from KO mapping)
At the KEGG otholog mapping query page I can map pathways and modules. I can't seem to find an extremely low level description of the difference between the two. I think I understand what a pathway is. I can't seem to find any definition or description of what a module is.

A pathway shows all the reactions required for the synthesis / metabolism of a given product.  A module is a functional unit that can be utilized in a pathway, and some modules are common to many pathways.  For example, look at the tetracycline biosynthesis pathway 00253.  This pathway has a description at the top that includes this excerpt:

Tetracyclines contain a linear tetracyclic skeleton, which is formed from a malonamate starter unit and malonyl-CoA extender units through a common polyketide pathway [MD:M00778].

Confusingly, that "common polyketide pathway" is actually a module, Type II polyketide backbone biosynthesis, acyl-CoA + malonyl-CoA => polyketide or M00778.
Note that this module is included in other pathways:

map01056 map00253 map01100 map01130

Looking at the drop down menu at the bottom of the module page, we see that the Reference Module contains multiple different KEGG Orthologs that perform the same function in different systems.

Choosing an organism from the drop down menu, the specific Orthologs used by that species are highlighted.

So, you can see how separating pathways into modules can help in identification of these components in other organisms, even if the full pathway does not exist.


text:
Ideas for microbiology lab. Antimicrobial properties of cutting boards
I am an undergraduate student in Biology and I am trying to design a microbiology lab that will takes 3 weeks to carry out (1-2 day each week). I am going to examine the antimicrobial properties of cutting boards. So far I have determined that I will use bamboo vs plastic and dish-soap vs disinfectants. I will be using two bacterial strains E.coli and S.epidermis.
Week 1: MIC (Minimal Inhibitory Concentration) assay of disinfectants and soap and prepared LBA (lysogenic Broth Agar) plates for viable counts during week 2.
Week 2: Inoculated cutting boards wait 30, 60, and 120 mins wash with various products then swab cutting boards with sterile swab, place swab in test tube with saline vortex and plate the resulting liquid on LBA. Count CFU (colony forming units) during the week.
Week 3: This is where I'm stuck the experiment has to last three weeks but I'm not sure what other tests I could carry out on the third week.
Any advice would be greatly appreciated thank you.

Did you plan on doing statistics to compare your treatments?  Statistical analysis could be your "Week 3"

I do plan on doing statistical analysis but that will be done outside the lab I was looking for another type of assay or different types of treatments I could do in lab. Thanks, @Dirigible

In my experience in biology, usually if everything goes as well as possible then Week 3 is for repeating the thing that went wrong in weeks 1 or 2. If everything goes normally, then Week 3 is for repeating Week 1 and Week 4 is for repeating Week 2.

I am afraid that however much one sympathizes with the problems of setting up laboratory classes for students, that is not included in the remit of this site, which is to answer questions about biology itself.


text:
How does energy conversion happen (chemical to mechanical?) in moving body muscles?
From my understanding, the brain sends electrical pulses through neurons to different part of the body to initiate a movement. My question is, how is the movement realized? For example, in a train, steam engine is used to convert heat energy to mechanical energy to move the engine. Similarly, in the body, I understand the energy is stored in chemical form. How is this converted to the mechanical motion of a body part?

Welcome to Biology.SE!  This is a very basic question and thus appears to meet this sites criteria for a homework question. In these situations we expect you to do some research on your own and then, informed by what you have learned, ask any questions you might still have (ideally with references to reliable sources). ———  Please also take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I do not work in Biology and I'm long out of school,so it is not a homework question. When I searched the above, I didn't get any insight into how the conversions work.Perhaps I didn't use the proper terms involved. My doubts were clarified with Joce's answer.

Questions don't have to be homework assigned for a class to be considered homework on this site — if you wish to understand how this site works please consult the links I provided in my original comment.  If you are interested in brushing up on the basics of biology (or any other subject — they helped me relearn calculus) I recommend Khan Academy.

The conversion from chemical to mechanical energy is in general done by molecular motors which perform a power-stroke, using the hydrolysis of adenosine triphosphate (ATP) or more rarely of GTP to power a change of their conformation while bound to cytoskeletal elements.
Molecular motors include myosins, which is the molecular family powering muscles in interaction with actin filaments but also other cells e.g. for their motility or for morphogenesis. animation  of muscle contraction
There are also kinesins and dyneins, not used for muscle function, but which perform e.g. transport of "cargo" organelles along microtubules.
An alternative way to produce mechanical energy is via ion pumps, as is the case in flagellar rotors.

@Joce, your answer is exactly what I was looking for. I mentioned brain and neurons only to clarify that I had an idea about how those are involved, but that was not what I wanted to be answered. I thought it would be pretty clear. Sorry for the misunderstanding.


text:
Why are bees "committing suicide" in my house?
There is a beehive about 500-1000 meters away from my house.
During the last years, almost every day, one or more bees enter from the window, "dance" for an hour or two, and then drop dead on the floor. Some more details:

The bees may come in every hour of the day, but most of them come just before sunrise. This morning about 20 of them came in; now they are all dead on the floor near the window:

Often, the bees prefer to make their "dance" near the lamp. But this is not always the case.
They usually do not sting me; I was stung only twice, the bee died immediately afterwards, I took the sting out with tweezers, and it did not hurt too much.
I did not use pesticides or any other stuff that could kill the bees.

Why are they doing this? How can I stop them from coming?
I read that bees are disappearing; maybe it's because they all come to my house to die? :-)

How can we possibly know?

Welcome to Biology.SE! This is probably not an answerable question on this site since there could be many different reasons. To get an answer try contacting a local agricultural extension agent or entomology department and see whether you can get someone local interested to check for toxins and pathogens. ——— Please take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Abnormal behavior could be explained by use of pesticides, such as neonicotinoids. You may not be using pesticides, but agricultural companies around your place of residence may be using them. Hard to say for sure in the regulatory vacuum we live in, where our environment is concerned. https://en.m.wikipedia.org/wiki/Colony_collapse_disorder

@tyersome thanks for the welcome. I thought that maybe this phoenomenon has been observed in other places too, so maybe there is some research about it.

As @AlexReynolds indicated bee loss has been linked to neonicotinoids (a class of pesticides often used as a seed treatment), but many pesticides and pathogens can have neurological effects.  Consequently, I wouldn't believe any diagnosis made that didn't involve inspection for parasites and a toxicological workup ... Also getting someone local involved could result in the problem being solved!

@tyersome thanks! Following your advice I contacted the bee department in the ministry of agriculture in my country. I hope they will have a solution.

It's possible that there's something confusing them about the light. Does the window face the rising sun?  I've read that at twilight, bees get confused by nearby lights; maybe this happens at dawn as well. In one particular case, a beekeeper's porch light. The beekeeper moved the hive and it helped. Not a terribly helpful comment, but if the window does, in fact, face the rising sun, that might have something to do with it. Try having the hive moved.

Kind of a possibility: https://www.beebestinc.com/are-bees-attracted-to-light/

@David - Just because you don't know doesn't mean no one can know. forestecologist might know; a bee keeper might know; who knows who might kniow, but someone might. You should be less dismissive.

@anongoodnurse — No. The question relates to a particular circumstance, rather than a generality —  my house. How can anyone know the particulars of this, or even if the poster’s observations are reliable?

@anongoodnurse your guess was correct - my window does indeed face the rising sun. And the link you gave indeed describes a situation very similar to mine. Thanks!

After years of struggling with the bees, I finally found a solution. I put in my window a lot of pots with various flowers, including some vegetable plants with flowers. Now, instead of entering my house, the bees go to the flowers.
As a bonus, I get wonderful scents and some fresh cucumbers - pollinated by the bees. I have learned that bees are not a nuisance - they are an asset!

Don't forget to mark your answer as best answer.

Fragrances inside your house were probably attracting them then. I just use nets to keep out lots of curious insects. Bees and wasps, for no discernible reasons, sometimes investigate the nets pretty thoroughly... almost certainly looking for a way in, either to nest or who knows what.

Also, based on your location: in arid/desert areas bee colonies send out more scouts.

By the way, bees can see UV and of all the frequencies this is the most attractive to them https://www.nature.com/articles/s41598-020-64782-y. So it's possible the bulbs you were using, e.g. if CFL, were attracting them.

I found another solution, for a season when the flowers on the window are insufficient. I have noticed that bees are attracted to my light bulbs, especially in the early morning when it is dark outside. I have also read that bees cannot see red light - it is beyond their visibility spectrum.
So, I bought some RGB bulbs - bulbs with a remote control for changing colors. These are surprisingly cheap. Now, whenever the bees approach, I switch the light to red, and they go away.


text:
Prokaryotes Genome

What function of repetitive sequences of Prokaryote?
I see a gap (intergenic region) between 2 coding strand. But just only a single origin region in Prokaryotes. How it can transcription coding strands after the intergenic region?
I read documents say the genome of Prokaryote is small. So it needs to overlapping transcription in a chromosome. How its works with a single origin region?

A google search resulted in finding this site, which I believe explains a lot about the prokaryotic genome: https://courses.lumenlearning.com/boundless-microbiology/chapter/prokaryotic-genomes/

An additional resource for making sure you understand the basics of biology is Khan Academy. The reason I'm suggesting that site is because your questions reveal that you are confused about some the difference between transcription and replication. ——— Please also take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!


text:
Effect on gene loss because of compartmentalisation of plastids/mitochondria/endosymbiont?
Considering the transfer of genes during endosymbiosis a gene transfer event (at least fundamentally, even if it's a special case), how does the fact that in this case the genes are inside a compartment, affect their gene loss, or incorporation into the host/recipient's genome (in context of gene transfer)?
I would imagine that the loss would be slower, recombination with other transferred genes less probable. But I can't find literature on the same. Any leads?

Could you clarify? What systems are you thinking of? Slower compared with what?

Slower compared to gene loss if the genes are in the nucleus.

Still don’t follow. Can you give some examples of the two?

I don't know if it's true or not. I am assuming that because of compartmentalisation there should be a significant difference in the rate of loss between the two compartments. But I may be very naive and maybe it's trivial that it's not true. What I am asking is for evidence or scientific literature on this topic (because i couldn't find much).

Here is an extreme example of rapid total loss of photosynthetic genes from a now parasitic organism. Compare that to the rate of loss (or lack of it) for photosynthetic genes in common photosynthetic plants. Now what I am thinking about is a comparison of this rate of loss in plastid genes, to that of genes incorporated into the nucleus. Think about a situation if those photosynthetic genes were incorporated into the nucleus somehow, directly, instead of being in a endosymbiotic compartment (giving rise to a plastid).

OK. I'm not helping. Perhaps it would be better for someone familiar with this sort of paratism to comment. My own observation is that gene loss is just loss. Gene transfer from organelle to nucleus would seem more complex, but the extent to which it has ocurred in different eukaryotes differs widely.

The parasite example was just to give an idea of how varied the rate of gene loss can be in general and to provide some context. But I need information on a more general perspective on gene loss. I'll even find it helpful if it's about pressures of natural selection acting differently (or not) on genes in nucleus vs other organelles, which would be something related to gene loss.
Thanks for the comments anyways.


text:
Why, when someone eats food, and he/she directly checks his body weight, why it seems to be no changes in body weight?
Why, when someone eats food, and he/she directly checks his body weight on balance, why it seems to be no changes in body weight and there wasn't any execration, I want to know where did food weight went?

How accurate is your scale? How big is the meal?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you might still have (ideally with references to reliable sources). ——— Please also take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

This question is wrong. If you eat some food, that extra mass goes straight into your belly and has to show up on the scale. Conservation of mass.

Compared to their body weight, humans don't really eat that much
Where I live, the typical serving at a restaurant is 150g or 200g of meat, plus about the same amount of side dish. Even if your test subject is a big eater, that's just 300 + ~200g of biomass. Eating that much food without drinking is difficult, so you allow your subject one beer, or about 500g of liquids.
Even with generous assumptions, an intake of more than half a kilogram of food in one go is unusual.
If you live in a country where this specific figure is higher than that, please adjust the value accordingly, and the next figure in the same ratio.
I could perform a scientific measurement of an average human mass based on a sample size of two people, but the more rigorous way to do it is to open a random web page on the topic and use the number stated there, up to 80kg for a healthy male.
Therefore, a person's weight after one meal will typically increase by, Fermi estimate, 1% of their body weight. Compare that to the common shrew, which eats 125% of its body weight per day. Source: Google
A scale I have available at home is graded at 5kg, so an increase of 0.5 kg is difficult to notice. The only scientifically valid test would be to have two different people read the scale reading and only communicate their values after the experiment. A single person taking two readings is likely to introduce a bias.
A typical digital scale, however, should be able to pick up the difference.
Be sure the "no excretion" criterion is met. A human body is able to dispose of just as much mass in one go.
The other answer beat me to this figure, but the amount of perspiration cited by Wikipedia is up to 2-4 liters per hour. So, if you've just been working out or if your AC is broken, You can actually sweat faster than you eat. That's the maximum rate of perspiration, though, and far from the typical situation.
Finding the typical rates is much more difficult. Every article I've checked boils down to "how much you sweat varies wildly, and if you think you sweat too much, go find a doctor".
For perspiration, Science Alert suggests 2.3 lb (1 kg) of carbon dioxide per day as the usual amount. If your meal takes 15 minutes, that amounts to about 10 grams of mass loss due to breathing while eating.

To make a proper evaluation of the immediate effect of food on your weight you need to:

Have a sensitive (optimally: digital) and properly working scale that shows the same value when you weigh yourself few times in a row
Wear the same clothes during the pre- and post-meal measurement
Not vomit, urinate, defecate or sweat significantly between the 2 measurements

How much weight you can GAIN by having a meal?
An average main meal for an adult consisting of a soup, potatoes, steak, sauce, salad and compote could weigh, let's say 500 grams (0.5 kg). Such a meal should contribute about 500 grams to your weight (let's say in 30 minutes between your pre- and post-meal measurement), because no significant weight of food is lost during digestion and absorption of nutrients and because no significant metabolism that "burns" the nutrients occurs within 30 minutes of starting a meal.
How much weight you can LOSE during a meal?
If there is no vomiting, defecation and urination between the pre- and post-meal weight measurements, you can lose  a significant amount of weight only by sweating. In one study, the sweat rate of athletes during training was 1.2 liters/hour in average, but up to 5.7 liters/hour (see Fig 1). In another study, young males sitting in the sauna at 95 °C 2 x for 10 minutes with a 5 minute break resulted in 0.2-1.1 kg loss of weight (check Table 1, the BML column). So, it might be theoretically possible that a person with a very high sweat rate would lose 500 mL of sweat (and hence 500 g of body weight) just by sweating when eating for 30 minutes in a hot environment. This seems to be the only possible explanation for "no weight gain after a meal" when the measurements have been done properly.


text:
Does food grade diatomaceous earth contain mercury
Not sure if this is the right site to ask this question, but since diatomes are or once were biological creatures it seemed to fit this one more than any of the others. I have been supplementing my food, and my cats food occasionally, with food grade diatomaceous earth which is supposed to be healthy and good for bones, teath, skin, hair and cell growth among other things, it is inhert & has no known side effects, its is used regularly as a cattle feed additive & also as a pesticide or anti-parasite treatment to kill worms, fluke and other critters.. I only started doing this as a supplement as i do not generally eat alot of vegtables or fruit & am more of a snacking person.. However I just seen an article that say's beer, wine and many other beverages contain mercury as many of them are filtered using diatomaceous earth (Which pressumably would have to be Food Grade). If there are any minerologist/biologist's is this true? Where does the mercury come from? is it safe? Can the human body filter this out?

That's an earth sciences question or a food forum question. google will research better than we can. first result http://www.vitaletherapeutics.org/deanlsbw.htm

You are more likely to find mercury in natural gas ( before the gas plant filters it out).

Thank you for the reference com.prehensible, thats exactly what i was looking for. if this question is not suited here please can someone migrate it to earth science or similar...


text:
Effect of angle of light on flowering of plants
I understand that the angle of light changes the direction of growth in plants (phototropism), but would the angle of light have any effect as such on the flowering of plants?
Thank you!


text:
Which white beans have phosphatidylserine?
Many articles online say that plant foods are poor sources of phosphatidylserine, except for white beans, which have 107 mg per 100 g.¹ ² ⁴ Honestly though, I think they might just be repeating a claim from Wikipedia, which cites "Souci SW, Fachmann E, Kraut H (2008). Food Composition and Nutrition Tables. Medpharm Scientific Publishers Stuttgart." I wasn't able to find this source freely available online. Examine.com mentions that "Phosphatidylserine (PS) is found in Soy Lecithin at around 3% of total phospholipids"⁵, citing https://www.ncbi.nlm.nih.gov/pubmed/18846580.
I haven't been able to find any (reliable) sources that say which kind of white bean is being referred to here: is it navy beans, cannellini beans, great northern beans, runner beans, or marrow beans? There are some that say navy beans,³, but I believe that information is derived from the Wikipedia article on phosphatidylserine, plus some speculation based on what the writer of the article thinks "white bean" refers to.

Use sci-hub to get the article? You probably know this by now though since this question is old.


text:
Does increasing contractility increase LV ESP?
I see many PV diagrams showing a negligible difference in the ESP when contractility increases. I'm wondering why this is the case, because if more blood is being pumped out into the aorta, the MAP should increase, which should subsequently increase the ESP.

LV, ESP, MAP, PV? Well I do know what ESP means — Extra-sensory perception, which is presumably what is needed to understand the question.

LV = left ventricle, ESP = end systolic pressure, MAP = mean arterial pressure, PV = pressure-volume

Then edit the question to make it intelligible, especially the title. You might also give an example (with source) of the type of diagram you are referring to. The purpose of comments is to suggest improvements or clarification of questions, not for a dialogue.


text:
quantification of glucose utilization in different metabolic processes
Glucose is commonly associated with ATP production. However, only a small fraction of glucose is utilized this way.
The intermediates of glycolysis, TCA cycle, etc. are precursors to various anabolic pathways and are ultimately involved in amino acid synthesis, nucleotide synthesis, fatty acid synthesis, etc.
Has glucose utilization in different pathways been quantified? What approximate percentage of glucose is used in different pathways?
Certainly, the numbers could vary between organisms, different cell types, cell microenvironment, etc. It helps to have an intuition of how much glucose is used where.

A general answer to this question is not possible because of the difference in organisms and cell types mentioned. However there are some more basic problems with the question. 1. Where is the glucose coming from? Assuming even a single organism such as man, there are a variety of possible diets. 2. The extent of synthesis depends on the nutritional state of the animal and whether cells are dividing. 3. In the paragraph "Has glucose utilization…", the second sentence is incomplete and meaning of the first sentence is unclear.

My question originated while reading a paper which claimed that only a small fraction of glucose eventually ends up undergoing oxidative phosphorylation. Most of the intermediates of the glycolysis and TCA cycle are precursors for biosynthesis of amino acids, nucleotides, etc. I naturally wondered how much of glucose is used where to garner an intuition.

Well give us the reference. Then we can see what the system is.


text:
How does an electrical impulse spread in a muscle fiber spread from the motor end plate?
Does this impulse in skeletal muscle spread much in the same way it does in neurons, with an initial potential change that spreads to its immediate surroundings and is then re-amplified or is it the case that in muscle fibers, the initially produced end plate potential must be "enough" to depolarize the whole muscle fiber?
My issue is with this bit in a lecture about NMJs I took:

Because the ACh-gated ion channels are localized to the end plate membrane, the End Plate Potential (EPP) is generated at and confined to the end plate region only and, therefore, the amplitude of EPP declines progressively with increasing distance from the end plate region.

I only found this site which talked about something similar, and there it talked about it in the context of a muscle fiber that's been blocked by a non-depolarizing neuromuscular blocker, i.e., no contraction occurs, it's just a measurement of how the EPP changes by itself, so perhaps the lecture was talking about something similar?
So, to put it simply, do electrical signals in skeletal muscles get re-amplified as they travel along the fiber, like they do with neuronal action potentials, or is the initial membrane potential sufficient and it just "spreads around"?

Skeletal muscle cells are excitable, like neurons. Enough summation of end-plate potentials causes the cell to reach threshold and fire an action potential (which then spreads throughout the cell membrane through positive feedback, just like a neuronal action potential).
There are some differences between skeletal muscle and typical neurons, like greater importance of chloride in setting resting potential in muscles, but otherwise their action potentials are driven by voltage-gated sodium channels, just like typical neurons.
You quote:

the amplitude of EPP declines progressively with increasing distance from the end plate region.

which is true as long as the threshold potential isn't reached, and would also be true for subthreshold receptor potentials or post-synaptic potentials in neurons.
In the reference you link to, I assume you are referring to the mention of curare. Curare blocks the nicotinic acetylcholine receptor, so it is interfering with the end-plate potentials themselves, rather than the intrinsic excitability of the muscle.

See:
Philip M Hopkins, Skeletal muscle physiology, Continuing Education in Anaesthesia Critical Care & Pain, Volume 6, Issue 1, February 2006, Pages 1–6, https://doi.org/10.1093/bjaceaccp/mki062


text:
How do homologous pairs find each other
If I'm not mistaken the only time homologous pairs of chromosomes need to find each other is during gamete formation in preparation for crossover recombination.
How do they find each other?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you might still have (ideally with references to reliable sources). ——— Please also take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I found this review from 1999.  From the abstract:

It is concluded that DNA-DNA interactions cannot bridge the distances between homologous chromosomes in the nucleus, and it is suggested that protein chains are formed between homologous segments. These attach to homologous chains emanating from homologous sequences in other chromosomes, and the chains move along each other until the homologous DNA sequences meet.

For more recent publications, you can search the citing articles here.


text:
Confusion about Lotka_Volterra model for two competing species
Lotka-Volterra model for two competing species in Boyce's Elementary Differential Equations and Boundary Value problems' is given by:
\begin{align*}
   \frac{dx_{1}(t)}{dt}&=r_{1}x_{1}-a_{11}x_{1}x_{1}-a_{12}x_{1}x_{2} \\
&=r_{1}x_{1}(1-\frac{a_{11}}{r_{1}}x_{1})-a_{12}x_{1}x_{2} \\
&=r_{1}x_{1}(1-\frac{x_{1}}{K_{1}})-a_{12}x_{1}x_{2},\quad x_{1}(0)>0 \\
   \frac{dx_{2}(t)}{dt}&=r_{2}x_{2}-a_{22}x_{2}x_{2}-a_{21}x_{1}x_{2} \\
&=r_{2}x_{2}(1-\frac{a_{22}}{r_{2}}x_{2})-a_{21}x_{1}x_{2} \\
&=r_{2}x_{2}(1-\frac{x_{2}}{K_{2}})-a_{21}x_{1}x_{2},\quad x_{2}(0)>0 \\
K_{1}= \frac{r_{1}}{a_{11}}\\
K_{2}= \frac{r_{2}}{a_{22}}
\end{align*}
$ r_{i}, i=1, 2 $:is the intrinsic growth rate for prey species.
$ a_{ii} $ :are intra-species interference coefficient of the two prey species.
$ K_{i}, i=1, 2 $ : the environmental carrying capacity for ith prey species.
$ a_{ij} $:  are inter-species interference coefficient of the two prey species.
While in the book by Murray 'Mathematical Biology: I. An Introduction' is given by:
\begin{align*}
   \frac{dx_{1}(t)}{dt}&=r_{1}x_{1}\left(1-\frac{x_{1}}{K_{1}}-\frac{a_{12}}{K_{1}}x_{2}\right),\quad x_{1}(0)>0\\
   \frac{dx_{2}(t)}{dt}&=r_{2}x_{2}\left(1-\frac{x_{2}}{K_{2}}-\frac{a_{21}}{K_{2}}x_{1}\right),\quad x_{2}(0)>0\\
\end{align*}
Trying to match them I get
\begin{align*}
   \frac{dx_{1}(t)}{dt}&=r_{1}x_{1}\left(1-\frac{x_{1}}{K_{1}}-\frac{a_{12}}{K_{1}}x_{2}\right) \\
&=r_{1}x_{1}- \frac{r_{1}}{K_{1}}x_{1}x_{1}- \frac{r_{1}}{K_{1}}a_{12}x_{1}x_{2} \\
&=r_{1}x_{1}- a_{11}x_{1}x_{1}- a_{11}a_{12}x_{1}x_{2},\quad x_{1}(0)>0\\
   \frac{dx_{2}(t)}{dt}&=r_{2}x_{2}\left(1-\frac{x_{2}}{K_{2}}-\frac{a_{21}}{K_{2}}x_{1}\right) \\
&=r_{2}x_{2}- \frac{r_{2}}{K_{2}}x_{2}x_{2}- \frac{r_{2}}{K_{2}}a_{21}x_{2}x_{1} \\
&=r_{2}x_{2}- a_{22}x_{2}x_{2}- a_{22}a_{21}x_{2}x_{1},\quad x_{2}(0)>0\\
K_{1}= \frac{r_{1}}{a_{11}}\\
K_{2}= \frac{r_{2}}{a_{22}}
\end{align*}
so here we have an extra factor in the inter-species terms.
How they are equivalent?

Do you use upper and lower case ‘k’ by purpose for Murray’s version?

Sorry for the mistanke it is upper case K in all , the environmental  capacity.

This is probably not a very satisfactory answer. The very next step in Murray's book (3rd Ed) there is a non-dimensionalised version of the model (eq 3.32) which looks like the one given in Boyce's book (10th Ed) except $\epsilon_i$ and $\sigma_i$ (eq 2, Ch 9). If you plug in $\epsilon_i = \sigma_i = 1$ in Boyce's book you get the same fixed point expression (eq 36) as Murray's book.
The idea is: in the RHS of a $\frac{dx_i}{dt}$ term the $x_i x_i$ represents intra-specific interaction and the $x_i x_j$ represents inter-specific interaction between species $i$ and $j$. You can put constants wherever you like to scale these terms with an interpretation. But the qualitative behavior of the system doesn't change and the coefficients persist in algebra, based on how you plugged them.
But to literally interpret the extra factor in the second set of equations: you can think of them like if $a_{ii}$ is the scaling of intra-specific interference, then $a_{ij}$ is a scaling of $a_{ii}$ for inter-species interaction, i.e. the species $j$ interfere with species $i$ with $a_{ij} a_{ii}$.

Thanks for the contribution. The problem is that both books define the parameters biologically in similar way which doesn’t make sense for me. I think $a_{ij} $ is scaled with $a_{ii} $ and not the opposite without any explanation given.

I agree with @Cheesebread I think that one of the books misdefines the parameters because rescaling is super common and often times mathematically-oriented authors more easily forget about the underlying biological interpretation. This is especially true, as pointed out in this answer, when the qualitative behavior is the same.


text:
What is the substance that tumors release that stimulates growth of blood vessels but suppresses its release from other tumors?
I'm currently in high school and I am working on a cancer research project. My project consists of a cancer, and different ways to treat it. I have a set of benign tumor and I was thinking of immediate way of treating it without using a drug like Taxol to destroy parts of the cell is to simply remove the tumor.
However, I remembered learning about a 1 1/2 years ago about a substance that tumors release to stimulate the growth of blood vessels towards them, but this same substance suppresses the release of itself by another tumor (hopefully this makes some sense). I made some drawings that are attached here:
Scenario 1: The 1st tumor in the blood flow releases an unknown substance, which promotes blood vessel growth, but suppresses the release of the same substance from another tumor behind it.

Scenario 2: The 1st tumor is removed, and now the 2nd tumor starts to release the substance, because the 1st tumor's release is not suppressing the 2nd tumor's release anymore.

Does anyone know the name of this substance, and can someone help me learn more about it? Thanks.

One very important signal for angiogenesis are the Vascular endothelial growth factors (VEGF)  (a small group of ~5 similar proteins). They generally promote generation of new blood vessels & migration of these towards the source of VEGF expression.
Blocking VEGF signalling (mostly be blocking the receptors with antibodies) has been a pretty good strategy in cancer treatment, since tumors can't grow over a certain size without blood supply by new grown vessels.
However, I am not aware of any blood-vessel specific signalling mechanism that stops it's own expression at a secondary site. (This may be possible though, especially for specific signals)

Galectins are family of beta-galactoside-binding proteins implicated in modulating cell-cell and cell-matrix interactions. These proteins are produced by tumor cells and promote angiogenesis.
These secreted Galectins are used by endothelial cells to enhance migration and proliferation. And play various roles during development of tumor such as cellular adhesion, cell mobility,  tumor-induced angiogenesis, and apoptosis.
Via:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5855652/
https://www.ncbi.nlm.nih.gov/pubmed/27649167


text:
Why does the liver produce ketone bodies instead of exporting acetyl-CoA from beta-oxidation for use elsewhere?
Under conditions of low oxaloacetate in the liver, acetyl-CoA that cannot be oxidised in the TCA cycle is converted to ketone bodies, which can then be exported for use as fuel in non-gluconeogenetic tissues (e.g. heart, brain).
To avoid this pathway, and the additional enzymes it requires, as well as the enzymes in the receptive tissues which are needed to reverse the pathway and re-produce acetyl-CoA, why does the liver not just export acetyl-CoA directly?
One consideration is an inability to transport acetyl-CoA across membranes, but fatty acyl-CoAs deal with this using a carnitine shuttle across the mitochondrial membrane. Would developing a transport system not, evolutionarily, be a more efficient solution?

Think. What are the conditions you describe as “low oxaloacetate”? What is the source of the acetylCoA and why is it being produced (rather than stored as fat, for example)? What are the needs of the organism in these circumstances? In other circumstances where acetylCoA might be useful to other tissues, how is the molecule from which it arises exported from the liver? Look at the big picture.

"Low oxaloacetate" will presumably occur mainly when it is being taken out of the TCA cycle, for gluconeogenesis (i.e. in the fasted state). The excess acetyl-CoA in this instance is being produced from beta-oxidation of fatty acids, since lipogenesis is inhibited (high glucagon, low insulin in this state). The organism needs to produce glucose, but also maintain a supply of ATP.
Acetyl-CoA can also derive from pyruvate (via pyruvate dehydrogenase). Do you refer to the Cori Cycle, where lactate is returned to the liver, oxidised to pyruvate, and then converted to glucose?

— Ok. You’ve thought about it, but don’t see what I’m driving at. I’ll try to answer your question later today (in a different time zone).

This is simplified version of a complex situation, but in summary:

A key role of liver is to control the distribution of metabolic fuel
for the other tissues (it always has enough for its own
requirements).
The way it behaves differs in the fed and fasted states (because of control by hormones and the concentration of metabolites).
In the fed state (after storing some sugars as glycogen) the liver will synthesize triglycerides and export them as lipoproteins to the adipose tissue, which will take them up and store them. (Other tissues in the fed state will be able to obtain glucose or fatty acids from the blood.)
In fasting and starvation the triglycerides in the adipose tissue will be broken down to fatty acids and glycerol, much of which will be used by tissues such as muscle.
The priority of the liver in starvation is to provide fuel for the
brain and nervous tissues in the form of glucose, by gluconeogenesis. The substrates for net gluconeogenesis under these conditions include glycerol and some amino acids derived from breakdown of protein.
Other amino acids, produced in protein breakdown lead to acetyl CoA,
which cannot serve as a precursor for gluconeogenesis. However it can
be converted to ketone bodies (acetoacetate and β-hydroxybutyrate)
that the brain can use to replace some of its glucose requirement.

With this in mind, it can be seen that the reason for producing ketone bodies is not to generate a molecule that can cross the cell membrane into the blood, but to generate a molecule with special properties, lacking in fatty acids or acetyl CoA, that allows its use by the brain in life-threatening circumstances.
Of less importance, but worth mentioning, is the fact that citrate is used as an export form of acetyl CoA (when there is sufficient oxaloacetate available), a surrogate role it plays in any case in the transfer of acetyl CoA across the mitochondrial membrane for fatty acid synthesis. So it is not necessary to export acetyl CoA, and perhaps preferable to it keep intracellular.
A more detailed account of this is available at NCBI bookshelf online in Berg et al. sections 30.2 and 30.3


text:
Do carrier proteins constantly open and close or do they only work when a substance binds to them?

What causes carrier proteins to change shape ?
Do they need energy to change shape? If that is true, how are they involved in Facilitated diffusion ?
By changing shape, do we always mean opens from one side and closes from another ? (they all work by changing shape right ?)
once they transport a molecule from inside to outside, do they return to their original shape instantly or do they need to transport a substance from inside to the outside to return to their original shape ?
and finally, are all co-transport proteins carrier proteins ?


text:
Why is sedimentation rate significant for a ribsome
When we take a look at biology textbooks (Campbell,  Pearson etc), they will only mention the difference between eukaryotic and prokaryotic ribosome sedimentation rates. Why is sedimentation rate numerically important for ribosomes and not for other organelles like the mitochondria or the nucleus?

It’s important insofar as the ribosomes are named after their sedimentation rate.

Summary

Ultracentrifugation was necessary to identify and ribosomes, and characterize them on the basis of their size. The method does not allow an absolute measurement of molecular mass, but uses a relative quantitation as sedimentation coefficient, expressed in Svedberg Units (S).
Nuclei and mitochondria were characterized by light microscopy and, being much larger than ribosomes, sediment at speeds which do not require an ultracentrifuge and would not be resolved in an ultracentrifuge.
Nuclei and mitochondria vary in size, so their size is not a defining property for them. Ribosomes from one source all have the same size, which may differ from that of ribosomes from other sources in a definitive manner.
Ribosomes are composed of smaller subunits, which are assembled from precursor particles of a different size. They occur in larger complexes on mRNA (polysomes). These forms of different but specific size can be separated and characterized by on the basis of size in the ultracentrifuge — i.e. by their sedimentation coefficient.

Amplification and examples

Prokaryotic monoribosomes (e.g. E. coli) have a sedimentation value
of 70S, the cytoplasmic monoribosomes of eukaryotes (e.g. rat) 80S,
and those of mammalian mitochondria between 50 and 60S. The values may differ for different eukaryotes and prokaryotes, but are constant for one species, reflecting the constant ribonucleoprotein composition of the particles.
All ribosomes have two subunits — a large subunit (50S and 60S for the prokaryotes and eukaryotes mentioned, respectively) and a small subunit (30S and 40S). The subunits are identified by ultracentrifugation, which is also used to separate them preparatively. Hence it is natural that their S values should be used to name them.
The formation of ribosomal subunits from RNA and protein involves sequential addition of proteins. The different sized intermediates at different stages can be differentiated by their sedimentation, and it is natural to refer to them by their S values.
Ultracentrifugation is also used to separate and characterize the ribosomal RNAs in a similar manner.

Bibliography
The Wikipedia entry on ribosomes corroborates some of the factual data I have presented.

The Svedberg unit is measurement used to characterize the ribosomal subunits. And it represents  rate of sedimentation in centrifugation process instead of size.
But every organelle and sub-cellular material has its own sedimentation rate. On basis of this characteristic, differential centrifugation technique works.
In case of ribosomes, it may be used so that it becomes easy to differentiate between different subunits.
(Via:  https://www.britannica.com/science/ribosome)


text:
How to design a permanent vaccine to cholera using CRISPR?
I know that Vibrio Cholerae infects the body through the GM1 ganglioside. So, would it be possible to engineer a CRISPR gene editing tool to prevent Vibrio Cholerae from getting into our cells?
Specifically, would it be possible to insert a piece of DNA into our genes that allow the synthesis of cholera toxin-suspressing protein shown  here (Pubmed link).
The reason I ask this question is that there are obvious benefits to being immune to cholera from birth. While I'm definitely not planning on being the next He Jiankui, I find the prospect of such a vaccine highly intriguing.
Edit: changed link because I posted the wrong link.

So, would it be possible to engineer a CRISPR gene editing tool to
  prevent Vibrio Cholerae from getting into our cells?

Vibrio Cholerae doesn't get into our cells.
Did you observe that your paper has no in vitro experiments?
It's going to be tough to get a cell to transcribe and translate something so small, and will the peptide work if it needs a leader sequence to be exported out of the cell?
Its much much easier to break a gene in every cell than to add a new gene and have just a small subset of cell types make large quantities of that gene product.


text:
Have there been multiple aboriginal species of dogs?
In "Variation under Domestication", Darwin writes that:

I may here state, that, looking to the domestic dogs of the whole world, I have, after a laborious collection of all known facts, come to the conclusion that several wild species of Canidae have been tamed, and that their blood, in some cases mingled together, flows in the veins of our domestic breeds.

From this, I understand that several species of dogs evolved independently and half-civilised man tamed them later on, but I want to confirm this. Does Darwin argue that there have been multiple species of beings that resemble the shape of what we now call "dogs", or that there has been one meta-species of aboriginal dogs, which branched off into several wild varieties?

Are you asking what actually happened, or what Darwin thought happened?

Both, I guess. It'd be interesting to know what he thought back then and clear that up with the knowledge we have today.

Most likely we should interpret Darwin as meaning the latter.  Animals that arrived at the shape of wild dogs via substantially different evolutionary routes (that is, via convergent evolution starting with distinct, non-interbreedable species) would be unable to interbreed.

That's one of — quite a few, we have to say — the mistakes Darwin made in his edition from 1859 (I have to confess that this is the only edition I've read, and I reckon this is the only edition anyone should read). This mistake is even more contrasting if you realize that he failed to apply the very same reasoning he had made just a few pages earlier, when discussing variation in pigeons: he explained that, even if counterintuitive, all different pigeons with all different features descend from the same wild species. Then, when he talks about dogs a few pages later, he incomprehensibly makes the same mistake he had just accused his readers of commiting.
Darwin is not the only one: Lorenz made the same unfounded claim, namely that the domestic dog would have two different origins, one from Canis lupus and another one from Canis latrans. We have to agree that Lorenz was way more bold than Darwin when it comes to making unfounded claims.
The fact is that, today, we're pretty sure (the scientific and statistical meaning of sure is being used here) that all domestic dogs (Canis lupus), from the chihuahua to the german shepherd, descend from a population of wolves (also Canis lupus) from east Asia.
Here is a Nature paper from Peter Savolainen, one of the best researchers on this subject: Wang, G., Zhai, W., Yang, H. et al. Out of southern East Asia: the natural history of domestic dogs across the world. Cell Res 26, 21–33 (2016) doi:10.1038/cr.2015.147

My understanding is that two domestication events from two separate populations of wolves is the current theory? obviously the products of those two domestication events (coming from the same species as they did) would have been compatible for breeding so would have become completely intermixed by now.


text:
Can citric acid be used as fungicide in banana based fly (Drosophila melanogaster) food?
I am experimenting with a banana based fly food for better larval synchronization. Instead of propionic acid, I am going to use (added) citric acid as fungicide. Is there any downside to this approach?

I have no data on the fungicidal and insecticidal properties of citric acid at various concentrations (and you may be hard pressed to find a good study on this), but I have worked in some fly labs and I understand the composition of fly food only peripherally. The most commonly and most abundantly used fungicide in a lot of fly labs is methylparaben (trade names Tegosept or Nipagin in Europe). I imagine food recipe-makers have arrived at this solution through trial and error over the years; this is as much an art as it is a science, in balancing the ingredients with humidity, temperature, species and genotype with desired generation time. Methylparaben is used with and without propionic acid for Drosophila melanogaster. Do you have methylparaben in your fly food? Also, I think citric acid is not commonly used, again I imagine because technicians probably found it inferior to its alternatives.
The National Drosophila Species Stock Center at Cornell uses methylparaben with its banana food recipe.
Alternatively, please take a look at the variety of recipes Bloomington Drosophila Stock Center uses. To my knowledge they supply and stock the largest collection using the most recipes.

Fly foods
Alternative recipes

I have used methylparaben (with propionic) acid in past while preparing the corn flour based fly food. We used same preservatives for banana based fly food and larval growth was not satisfactory. That's why I was considering alternatives.

There is still some dispute over the exact cause of the antimicrobial effects seen with organic acid. One of the theories is that the protonized acid crosses the cell-membrane and destroys the pH-balance inside the cell.
This would explain why these acids are more effective at low pH (a higher fraction will be protonized).
Citric acid is a significantly stronger acid (pK = 3.1 for the most acid proton) than propionic acid (pK = 4.87), meaning that the pH of the food has to be around 2 units lower to obtain the same fraction of uncharged molecules.


text:
Why does atrazine kill photosynthetic bacteria and not nonphotosynthetic bacteria?
Atrazine was found to bind to Qb, which is involved in electron transport to create ATP in photosynthetic bacteria.
Why does this herbicide kill photosynthetic bacteria, while having little to no effect in nonphotosynthetic?

Is this possibly just because electron cycling creates energy in photosynthetic, and non-photosynthetic heterotrophs use a different mechanism to create ATP?


text:
ELI5 what is true breeding?
In "Variation under Domestication", Darwin makes several references to the concept of true breeding:

They believe that every race which breeds true, let the distinctive characters be ever so slight, has had its wild prototype.

And:

I crossed some white fantails, which breed very true, with some black barbs.

Before diving into the book, I never heard of the term, so I looked it up and found this definition in the Wikipedia article on Zygosity:

A cell is said to be homozygous for a particular gene when identical alleles of the gene are present on both homologous chromosomes. The cell or organism in question is called a homozygote. True breeding organisms are always homozygous for the traits that are to be held constant.

But this is rather technical and it's not the kind of explanation I would give to a child.
What is true breeding, in simple terms? When is breeding not considered true?

In the context of Darwin's Variation under Domestication, "true breeding" is a phenotypic characteristic rather than a genetic one.  True-breeding organisms produce offspring that are identical to themselves, concerning some trait -- i.e. white fantails, when bred with white fantails, produce characteristically white offspring.  For diploid organisms, true-breeding typically implies that the parents are homozygous at the locus conferring the trait of interest.

Case A: Not Breeding True
If you cross-breed two random dogs, the offspring are likely to only vaguely resemble either parent.  If you could clone a random dog to obtain two genetically identical dogs with different sex, you would likely still only get offspring that vaguely resemble their parents, because the chromosomes of the parents would come in pairs composed of chromosomes from the grandparents; but which grandparent contributed each chromosome in the offspring would be random.  There is of course a very small probability that an occasional puppy would be identical to its parents — about 1 in 278.
Case B: Breeding True
On the other hand, if both chromosomes in each pair were identical for both parents (a situation that can be approached via a long series of inbreedings and selection, or could probably be obtained artificially in the lab), all the randomness would be eliminated and the offspring would be identical to the parents, if we neglect the likelihood of mutations and other genetic novelties.
So, in fact "breeding true" is just one end of a spectrum that is determined both by the amount of similarity between the parents' genetics, and by the amount of homozygosity in each parent.  This whole concept goes right over the head of the majority of adults, so getting it across to a child could be a serious challenge.  So to simplify: "Breeding True" means that the parents are identical and all the kids are identical to the parents.  It happens only very, very rarely.

In farming, "breeding true" is common. For example, "heirloom" plant strains are almost always ones that have been inbred for many generations to the point where they "breed true".


text:
How widespread in the Animal Kingdom is Aromatization as the Process that Determines an Animal's Sex?
I shall summarize my lay understanding of my question before going into details. To my lay reading, the sex of a vast diversity of animal kingdom species can be thought of as arising from the extent that the process of Aromatization - the catalyic conversion of testosterone produced by the gonads to oestrogen - happens. This extent of aromatization can be egg temperature determine, or genetically determined.
The German "Aromatase" Wikipedia page makes the following curious, unsubstantiated claim (translation mine, so apologies in advance):
"Aromatase (aka CYP19A1) is the Enzyme that in backboned animals catalyses the conversion from testosterone to oestradiol ....[emphasis mine]"
Which raises the question in the title. My understanding was that the aromatization process as the sex determining process was wider spread in the animal kingdom than backboned animals, at least as wide as chordates. Since the claim is unsubstantiated, i put the question in my title to this community.
Another take on the question: Can anyone give me examples of animals which are not backboned animals and for whom sex is determined by the extent of the aromatization reaction?

What non-vertebrate chordates do you have in mind? In any case, the claim does not say "only backboned animals" so it doesn't seem like finding a non-vertebrate example would disprove the claim (nor does it say "all" vertebrates).

@BryanKrause agreed. But the naming of a restriction like this got me thinking. I guess there aren't many non vertebrate chordates, but as ascidians spring to mind, for example.  Anyhow, as someone undergoing hormone therapy, the process fascinates me.there seems to be a great deal of lay info on the process in humans, but not to much on fellow animals and indeed how the process cake into being.

I think most ascidians are hermaphrodites (possibly all but I don't know nearly enough to make that statement). If you want to know about sex differentiation more broadly it might make more sense to focus on further flung species that have been well studied, like drosophila, and contrast between humans and flies.

@BryanKrause Interesting. I don't know much about ascidians, aside from that they taste really good, at least the ones on the shores of my home state Victoria do. See also the Japanese dish kenned as "Hoya". See the "other" take on my question. I completely disagree with the Wikipedia description of the taste of sea pineapple BTW - the Japanese and Victorian edible ones taste almost identical and like salted sour cream with a sweet aftertaste, but with a soft meaty texture. Most peculiar but thoroughly ambrosial nonetheless.


text:
What kind of leafy house plant is this?
I was given the plant as a gift.  Started out small and has grown to almost 6 1/2 feet tall and has sprouted off spring.
Original

Offspring:

Google reverse image search resulted in "Houseplant".  Not very helpful.
I have since removed the dead leaves from the plant.

Future visitors might appreciate for reference the somewhat similar (though different) species found in this post: What is difference between “Syngonium” & “Pothos”?

I believe it's a Dieffenbachia, see also this question & answer from Gardening.SE:
https://gardening.stackexchange.com/questions/9765/what-is-this-thick-stemmed-houseplant-with-variegated-leaves
though I am not sure of the species, it could be Dieffenbachia seguine which shows a similar coloration and is one of the taller species (I believe some of the others stay bushy).
On the linked answer, @TeresaMcgH warns:

By the way, one of the common names for this plant is "dumb cane" because the sap can cause numbness and swelling in the mouth and throat if ingested. So watch pets and small kids around it if you have such at home.

Bryan is correct: this is a Dieffenbachia. Also, I would like to emphasize the warning: it may not only cause numbness, but can be dangerously toxic. If you search scientific literature, several serious cases are documented. Those include necrotic tissue (fingers, to the bone!) and other severe systemic health issues.


text:
Where in this photo can I find archaea?
This photo is from Guide to the Six Kingdoms of Life under Archaebacteria:

It's not obvious to me where I can find archaea in this photo, although the website seems to indicate it's clear.
Question: Where in this photo can I find archaea?

It's probably the yellow bacterial mats, which are rich in life. The mats are a stratified ecology which varies with distance from the surface, so they are rich in many species of algea, procarote and eukariote. In Yellowstone,  the bacterial mats can range in color including brown, green, yellow and orange. They are different to precipitated minerals.
You can say "The photographer contains archaea"! So, no need to search very far.
Here is a pic of an bacterial mat habitat: https://www.sciencedirect.com/science/article/pii/S0717345817300738
You can see in some videos. Ideally we would have a a biology video demonstrating the stuff at Yellowstone to show if it's squishy, slimy, spongey, has growth rings, colord layers, cross sections... although it's only tourist videos for the moment.


text:
Does my nearsightedness come into play when creating light outlines in the distance?
After looking at a light and closing your eyes, you see an outline of the light. I was curious how my nearsightedness would come into play. I look at a light in the distance without my glasses on and close my eyes, would I be able to distinguish the light shape better than if directly looking at the light?

Welcome to Biology.SE! Since this is a question about your personal response to light is there something stopping you from testing this yourself? Note that we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you might still have (ideally with references to reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

Not likely.  The afterimage you see when you close your eyes is an effect dependent upon which light-receiving cells in the retina (rods and cones) saw light when your eyes were open.  The blurry image you saw when your eyes were open has the same size and shape as the afterimage you see when you see when you close your eyes.  Because the afterimage has less detail, perhaps you would be less distracted by detail and be able to pay more attention to shape, but it seems unlikely that would noticeably help your idea of the shape.


text:
Effect of myelination on inteligence in cephalopods
Cephalopods are known for their unique intelligence compared to other invertebrates.
The number of neurons of cephalopods is of the order $5*10^8$, similar to dogs. Humans have about $10^{11}$ neurons.
However, a major difference between cephalopods and humans and most vertebrates is the lack of myelination of their axons. Instead, to quickly transmit signals, cephalopod axons are much larger, reaching sizes of up to 1mm.
If we could edit the genome of an octopus, so that its axons are coated in myelin similar to a humans axon, whilst retaining their size, would this change the intelligence or behaviour of the octopus because of the increased processing speed?
Edit:
This is a repost of my original questions, to better conform with the guidelines of this forum. I am new to both this site and biology. Thank you very much for reading.


text:
life based on different elements
It is commonly proposed to look for life based on silicon, based on it's relative abundance and similarity to carbon. However, carbon and silicon are not completely interchangeable. The bond strength between carbon or silicon and itself is different, thus, some molecules with high chain length can not be replicated with silicone. Similarely, molecules such as proteins, for which all carbon atoms are replaced with silicon, would not retain their form and thus not their function.
Is life based on silicone still possible, just under a different environment?
This would affect how we should look for aliens. Also, if silicon based life is unlikely, is there some other element that could lead to life?

A couple references might give you pointers to work of interest: 1) https://science.sciencemag.org/content/332/6034/1163; 2) Rampelotto, P. Henrique (2010). The Search for life on other planets : Sulfur-based, silicon-based, ammonia-based. The Journal of Cosmology, 5, 818-827.

Welcome to SE Biology. The Tour makes it plain that this is is a question and answer site, not a discussion forum. As the Help states  "You should only ask practical, answerable questions based on actual problems that you face". The only responses to the present question are speculation and discussion, which is why I have voted to close it as off-topic. (Oh, and you might check the difference between silicon and silicone.)


text:
What is the human energy consumption by organ?
The human brain uses about 25% of the human body's metabolic energy. How are the other 75% spent, in terms of portioning to its various systems?
I thought this could be answered by a simple search, but I can't find the answer after searching very hard. I only got dieting advices.
I am envisioning the best answer to look like

You presumably didnʼt find an easy answer because, unlike for the brain, the metabolic expenditure of other organs varies dramatically based on their need. In this context, basal rates are only so useful.

Your vision of an answer seems to me more of a nightmare. This is an example of a representation that would be totally inappropriate to the question you ask. Why do you think that the different coloured items (energy/tissue?) need to be shown leading into something (Total) and what is the equivalent of the traces moving up or down or splitting? Sorry to sound severe, but there is a general problem that people do not think what graphical representations are appropriate for a particular data set. A pie chart will do, but the danger is thinking this is absolute, as @KonradRudolph points out.

Woah, 25% of the energy is lost to distribution? That's a lot. I cannot understand the other 29.52% because the graph is really messy there.

Percent of basal metabolic rate by organ (BC Campus Open Education):

Liver and spleen : 27%
Brain: 19%
Skeletal muscle: 18%
Kidneys: 10%
Heart: 7%
Other tissues (lungs, intestine, skin, bone, fat tissue, glands...): 19%

Basal metabolic rate by 1 kg of specific organ tissue (kcal/kg of organ/day) (Table 5 from American Journal of Clinical Nutrition, 2010):

Heart: 440 kcal/kg
Kidneys: 440 kcal/kg
Brain: 240 kcal/kg
Liver: 200 kcal/kg
Skeletal muscle: 13 kcal/kg
Adipose tissue: 4.5 kcal/kg
Residual tissues (lungs, intestine, skin, bone...): 12 kcal/kg

Why are liver and spleen aggregated?

@MJD, It's them (BC Campus) that merged them, not me. "Liver and spleen" are often mentioned together because they share some functions.

Where is the stomach and intestines? They utilize so much energy in the digestion process.

@Loren, stomach and intestine are active only during digestion, while the heart, kidneys and liver work all the time...I mentioned intestine under "other tissues" - I'll see if I can find some more specific data.

Based on the per-weight list (and this paper), if we separated the liver from the spleen, the liver would represent ~17%, lower than the brain.


text:
Can a drug induce specific mechanism of resistance in tumors?
For example, can a drug that targets a given protein induce overexpression of that protein or increase the copy number of the gene coding that protein?
I strongly suspect that antineoplastic resistance happens due to natural selection alone but I was wondering if there are examples that suggest otherwise.

Yes.
There is a lot of literature on cancer evolution and now several countries have genome sequencing programs for "pharmacogenomics", for example Genomics England, specifically to see which cancers are likely to evolve resistance to which drugs.
One small detail is that mutation exists before treatment in a subset of the cancer population —as happens with evolution normally. That mutation is neutral for the fitness of the cancer before, but is advantageous during treatment.

Thanks, the last phrase is especially useful


text:
Helix aspersa or Cornu aspersum
The common garden snail was originally assigned as Helix aspersa and stayed that way for over 200 years. Recently, some biologists assigned it to the genus or subgenus Cornu renaming it to Cornu aspersum, yet other researchers assigned it to Cantareus. Still, many texts still use the name Helix aspersa.
My question is what is the correct or official binomial nomenclature (scientific name) of the garden snail as for 2019?
Remark: I read Wikipedia but even there there are inconsistencies about it. E.g. Wikispecies.

I consulted with Prof. Henk Mienis, the curator of the Israeli Mollusca Collection, and the valid name is Cornu aspersum. The Israeli subspecies is Cornu aspersum megalostomum.


text:
Can Darkling Beetles Fly?
I searched the internet on the question whether darkling beetles can fly, and I read mixed results to it. Some say they can, there are even videos about it, but then again they say that they cannot, due to fused wings or the like.
I am currently interested in mealworms, and plan to farm some myself, and some people show their containers without covers, even though the beetles should be able to fly out then, shouldnt they?
This is really confusing to me, thanks for the awnsers.

Short answer; It depends. Darkling beetles is a very large family of beetles (Tenebrionidae) where some species can fly and some do not. Looking more narrowly at the genus Tribolium (i.e. mealworms), which many people refer to when they talk about darkling beetles, it also differs. The common Tribolium castaneum (red flour beetle) as well as T. molitor are good fliers, while T. destructor does not fly. The same goes for the confused flour beetle (T. confusum), which is not know to fly from what I know.

Ah I see, I really gotta start using the Latin-Names, that makes life easier..