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Looking for the closest example of life forms similar to some mathematical patterns

Caveat: this is my first question here, it is quite interdisciplinary, but I hope to be in the correct place to ask. I am a user of Mathematics Stack Exchange since some years ago, and this question is related with some questions there (here, here whose general formula is discussed here and here).

Context: I am preparing a mathematical paper regarding a new family of dynamical systems (if you are not familiar with the concept, simplifying the idea it is a mathematical formula in which starting from a initial value, once applied to the formula the resulting value is again applied to the formula, and so on, finally the values are plotted and eventually a -sometimes interesting- pattern emerges) whose attractors (plotted patterns) in the present case seem to have unexpected pareidolic properties.
Basically some of the patterns generated by these systems show similarities with some structures of invertebrate life forms, specially insects, marine jellyfish, and zooplancton and also due to the patterns of the accumulation of points, also with life forms presenting bioluminescence properties.
For each interesting pattern so far I have tried to find the closest life form example, to compare both the model and the life form patterns.
So my target is including in the paper the closest life form similar to each mathematical pattern. Initially it is just a pareidolic coincidence, but it might be interesting if the mathematical formula can resemble models of some organic structures.
These are the ones I have been able to gather, both the model and the closest life form I found.  The pictures I am using at the right side of and below the images are just for the sake of completeness (they belong to their respective owners, I do not own them, if there is any problem I will remove them, so just please let me know). The formula can be verified at the MSE links I have added at the beginning of the question and the Python code to generate them is in this link (please feel free to use it and modify it). The questions are after the examples (click to enlarge):

Patterns similar to thorax and abdomen of Bembicini wasp, head and body of Turritopsis dohrnii (inmortal jellyfish) and Tardigrade limbs:

Patters similar to Drain fly:

Patterns similar to Acherontia atropos (thorax and abdomen and main proportions of body, specially the patterns near the head are interesting):

Patterns similar to Ctenophora (down left) and Mnemiopsis_leidyi (down right):

I would like to ask the following questions:

Are there better examples of life forms for the models I am showing above (1,2,3,4)? If somebody could provide examples or specific names would be very appreciated.

Are there papers or references in the Biology field regarding mathematical models of this kind?

In the case I would like to add images from internet in the paper, I know that in the case of Wikipedia there is a standard way to add the reference in the bibliography. Apart from Wikipedia, are there other sources of images which I could use without problems in a paper (thinking about the kind of life forms that are the target of the patterns)? Thanks in advance.

I have tried to add the tag "mathematical-models" but it is converted into "theoretical-biology". Tried to correct it but it seems I can not do it for some reason.

I think those tags have been merged (with [tag:theoretical-biology] as the main one), which is probably why you cannot change to it.

The question has nothing to do with mathematical modelling or theoretical biology anyway (nor does it have much to do with the other tags).

The question is entirely based upon a personal visual appreciation. I am hence voting to close as opinion-based.

@Remi.b I definitely think it should be open, since Mathematical modelling of biological patterns (using semi-mechanistic models or phenemenological  models) is a valid topic in Mathematical biology. The background to this particular Q could be stronger though (eg links to the research field).

For the second subquestion (papers or references of similar models), it could be useful for you to look at the books by J.D Murray for inspiration; Mathematical Biology, vol I & II. A pdf of volume 1 can be found here, and the second volume here. Even if they are a complete of years old (last edition from 2002 I think) they provide a really nice background to the field of Mathematical biology, and he has quite many examples on pattern formation of different kinds. I don’t remember if dynamics systems are included per se though.
However, several chapters include reaction diffusion systems and wave models, to model e.g. coat/fur patterns and wound healing. It is also packed with references, so you should be able to find lots of classic citations that might be useful.
Some chapters you might find interesting:

Reaction Diffusion, Chemotaxis and Non-local Mechanisms
Travelling Waves in Reaction Diffusion Systems with Weak Diffusion: Analytical Techniques and Results
Animal Coat Patterns and Other Practical Applications of Reaction Diffusion Mechanisms
Mechanical Theory for Generating Pattern and Form in Development
Bacterial Patterns and Chemotaxis

I've mostly looked at population modeling in his books, so I'm not very familier with these topics myself.

thanks for the references! indeed the classical reaction difussion was included in my readings regarding the characterization of these systems. This is very useful.

Good. Sorry for not being able to help more with the specifics. There are probably also more recent books that might be more relevant, but Murray provides a nice overview for those that come from a mathematical background. Since it requires quite alot of mathematics it is probably rather inaccessible for many with a biological background.

hi again, I managed to publish recently an article at Springer Nature CS regarding this matter, thank you for taking time to guide me to the important bibliography of J.D.Murray. Hoping you the best, cheers! https://link.springer.com/article/10.1007/s42979-019-0028-6?fbclid=IwAR0idtC1Lrf2PNWDWImoJi_BdagcUzxcC7YchyOcG-WLuvdK0QWbbhwEw44

@iadvd Great news and I'm glad to hear. I will download and look at the paper later on. Fun to hear that Bio-SE input has made its way into a published paper as well even if it was rather vague in this case). I guess it would be really cool if we eventuelly started to find mentions/references in papers to Bio-SE Qs (or Stack Exchange in general), but we are probably not there yet.


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totaling OTU from 2 or more observations and assign to new observation in OTU table from qiime
I am new to microbiome processing pipeline but I want to ask, How do I combine two observations and assign it to a new single observation in the OTU table resulted from QIIME.
Here is the situation. I am doing river microbiome analysis. I have water sample named A-P, P for particle-attached sample and A for its and A-F for free-living sample for the same site. They are just different in the filter size being used.
I extracted the DNA, sequenced, and processed the raw reads separately using QIIME for all the 110 samples. But now, I am doing analysis on "R" and i need to combine A-F and A-P as one observation, namely only A. It seems simple to do on "R" for only one observation. But, I have 110 observations needed to be merged to 55. Are there any simple ways doing that without doing it one by one either in "R" or QIIME
Thanks,
Bob Adyari

There is no word "wanna" in English. I have changed it to "want to" in your question.

Which is the output you are working on from QIIME? is it biom-format?

sorry for the long missing. I figured it out already in a bit complicated way. So, I ran collapse_samples.py in qiime to merge two samples to one new. Thanks anyway

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Agarose gel electrophoresis - wrong running conditions?
Please have a look at the electrophoregram.
The DNA ladder used is GeneRuler 50bp (loaded according to the instructions), size of the gel is 6*7cm, lane width is 4mm, agarose percentage is 1%, TBE buffer. The power supply is Consort EV243. Running conditions were: 120V, 200mA, 45W, 40'.
What went wrong? The ladder is very far from the lane, and the sample bands look fuzzy. During run voltage remained constant (120 W), while current and power were  slightly changing (56mA and 7W ~in the middle of the run). Should I change running conditions? And/or make a fresh TBE running buffer?

How long did you let it run? I think time is a factor here. I would cut the time down by 15 mins.

@GabrielFair 40’ = 40 minutes.

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What is a good approximate functional form for an equation relating plant growth to sunlight?
Question is in the title.  I've got daily measurements of daily mean shortwave radiation at the surface, and annual measurements of plant growth (some measure, be it height or biomass or something).
I want to fit a statistical model
$$
growth = f(light) + \epsilon
$$
Assume that all other conditions are near-optimal, for simplicity.  What is a good first-order approximation for how to specify $f$?
For example, could it be:

Average daily light over the growing season?
$$
growth = \beta_0 + \beta_1\bar{light} + \epsilon
$$
Average daily light for each month?
$$
growth = \beta_0 + \displaystyle\sum_{months}\beta_m\bar{light_m} + \epsilon
$$
Maybe it's quadratic?

$$
growth = \beta_0 + \beta_1\bar{light} + \beta_2\bar{light}^2 + \epsilon
$$
Obviously something so simplified will never be perfect, but what's a good rule-of-thumb that'd cover most situations reasonably well?

You need to write more about the specific system/plant species you are modelling to get useful answers. Is it a crop plant? Annual or perennial plant? Strongly seasonal environment? Generally, and since it seems like you are not testing a specific hypothesis, you should try several models and see what fits your data best. After all, the goal should be a biological reasonable model that describes the patterns in your data.

Ok, let's say an annual in a temperate climate.

And I take your point that cross-validation is how to do model selection. But domain knowledge is usually the best starting point.


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Overall, for the most part, which is more important--capturing prey or surviving predators or parasites?
For animals in nature, does selection intensity tend to be stronger upon abilities used against parasites or predators or abilities used against prey?  Any empirical reports would be appreciated.
I understand that it would depend somewhat upon the species and the time, but I'm asking about a typical generation in most species.

By strength of selection, I am assuming you mean what it typically means, that is the fitness variance in the population, right? Or do you mean something else like "number of deaths caused by ..."?

@Remi.b I mean that if you were to assign separate numerical values to  an individual's ability to capture prey and to an individual's ability to evade predators or parasites and you were to model that individual's fitness, would the coefficient in front of the ability to capture prey be higher or lower than the coefficient in front of the ability to evade predators or parasites?

The coefficients would depend upon the range of values your metric would take. But the fraction of variance explained by each trait is not. This is the definition I expected. It is likely hard to find such estimates but it is very interesting and it would great to have that. +1


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Why does GLUT2 (With a high Km), bind less glucose at a lower glucose concentration (below Km)?
A text I am reading says
"GLUT2 is a low-affinity transporter in hepatocytes and pancreatic cells.
After a meal, blood travels through the hepatic portal vein and GLUT 2 captures excess glucose for storage.
When concentration drops below Km, much of the remainder bypasses the liver and enters circulation. The Km of GLUT2 is quite high so  the liver will pick up glucose in proportion to its concentration in the blood".
I know Km is a measure indirectly of binding affinity.
Rate also is based on concentration so at a higher concentration the rate is higher.
But the passage seems to be saying that at low Km, most of the glucose will not be transported, while at high glucose concentrations, more will be transported.
But i thought Km was a constant so I am confused.

Km is a constant which follows the unit of substrate concentration.It has a constant value. "Km of GLUT 2 is quite high" which implies that it's substrate affinity is low (inversely related). When the substrate concentration drops below that required for binding with GLUT 2 (Km value) obviously there would be bypass and no uptake by liver.

It would help if you would either copy the text acurately or provide a link. You are obviously a non-native English speaker as you have left out the articles, and probably other things besides. I assume that the sentence actually reads or means "When the concentration of glucose drops below the Km of GLUT2…" Km has units of concentration, so there is no question of the Km changing, it is the concentration of glucose that is changing, and its relationship to the Km of GLUT2 that determines whether this transporter acts on it, in the way described in any text.

I'm voting to close this question as off-topic because it is based on a misreading of a text.

Agree with @David - you're misreading... Km is the concentration that the transporter works at one-half the maximal rate (velocity) of transport. There's nothing in what you type that says anything about changing the Km (Km is a property of the GLUT2 transporter).


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What is this tree and fruits?
Please help me identify this tree and its fruits that have sweet taste and very small soft seeds:

It grows in the Mediterranean region.

Ficus sycomorus possibly...it's a type of fig (Ficus)

@user33690 Why don't you turn your comment to a proper answer?

It's a sycamore fig (Ficus sycomorus)- a type of Mediterranean fig.

For details: see this wiki page


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Why do Pelicans seem to disappear when circling high in the sky on a sunny day
When I watch Pelicans circling high in the sky on a sunny day, at a certain point in that circle, they disappear from view, then reappear again further along in that circle.
Is it something to do with the angle of the sun reflecting off the feathers?


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How does better sperm result in more viable offspring?
Quoting wikipedia:

Greater choice and variety of mates increases a female's chance to produce more viable offspring.

This led me to the question: "How sperm parameters are connected with entity parameters?"
Actually, sperm parameters are usually: motility and morphology. I am speaking about a single sperm, therefore any parameters involving their count or parameters of semen are not included.
On the other hand, what helps a particular entity to survive is determined by many parameters. Some of them are: speed, endurance, strength, agility, stealthiness and savvy. It is hard to find out how strength of being is connected with motility or morphology of sperm it has been conceived. And even less obvious is the connection of stealthiness with such sperm parameters.
But since sperm competition exist, it helps in natural selection, therefore there must be a connection. But how does it really work? How are stronger/faster/stealthier/etc. entities are the product of more motile or better in morphology sperm?
After some thinking about it I think that if there is some correlation between sperm parameters and genome, it can answer the question. E.g. presence of gene that increases fitness of organism makes sperm faster.

Greater choice and variety of mates increases a female's chance to produce more viable offspring.

The claim is a little hard to address because it is vague. However, one can give a simple example to give you a feeling of why this could be the case.
This example is based on Zaahavi handicap principle. Spermatozoids aren't free to produce. A male that can produce more and stronger spermatozoids can do so because he is a healthy males. As many of the traits that determine health, in a general sense are heritable, healthier males tend to have healthier offspring.

On the other hand, what helps a particular entity to survive is determined by many parameters. Some of them are: speed, endurance, strength, agility, stealthiness and savvy.

You are mainly listing traits that are very specific to human's sport ability. In reality, there are loads of other traits that are much more fundamental such as the efficiency of the potassium pump or of the mechanism to produce ATP.

[..] it helps in natural selection [..]

I don't understand what you mean by this sentence.

"I don't understand what you mean by this sentence." This is how biology works. Females who were involved in multiple-male relationships with sperm competition gave birth to more fit offsprings. Otherwise sperm competition would not exist. Also, you are ignoring the principle: why sperm competition is more efficient for females than sexual selection? (And males in many species are more sexually selective when it comes to how female looks).

"healthier males tend to have healthier offspring." Actually this should make female sexual selection superior to sperm competition but somewhy it really isn't. "You are mainly listing traits that are very specific to human's sport ability." Not really, speed is helpful for animal to run away from predator and it is helpful for predator to catch an animal. Same applies to stealthiness, for example. Instead, in humans intelligence massively outweights such parameters (well, strength is needed to make and use tools, but other parameters are not that essential).

@rus9384.Isn't that just biased stats? Ain't it possible that the females gave birth to more fitter offsprings precisely bc they mated with a more fitter guy?I mean they  mated with more people. And in monogamous relationships,you only mate with one person, ofc that one person can be either a very fit guy or a unfit guy. Its all on probability. Females who'll mate more people will have more odds of mating with a fitter guy rather than monogamous folks,I think its just a simple trick of stats you say,fitter here means in the evolutionary context.Sorry if I'm wrong,this is just pure speculation.

And that speed comes from more efficient ATP generation.That strength comes from more efficient potassium ion pumps in nerves and muscle cells.

You are over thinking sperm competition, just like two males can compete for access to a female, multiple sperm compete for access to eggs. If male A's sperm are faster than male B's sperm and both are present in the same female, more of her offspring will be from male A. So male A has advantageous genes. Additionally that female is going to have male offspring that may also engage in sperm competitions so having good genes for sperm competitions benefit her genes in the long run.
It benefits her in the same way having more males compete for her helps her: she is getting the best from a wider selection of individuals thus more likely to carry genes that will benefit her male offspring. Every mating is a roll of dice, those who can play the game more often have a better chance of getting a jackpot. If male A has Gene X and male B has Gene Y the female gets offspring with gene X and some with Gene Y. Since most genes are contextual it increases her chances of getting a better gene into her offspring.
Let's think of an example:
Female A mates once with the best male of 5.
Female B mates 3 times with the best male from three separate competitions of 10 males each.
Female B has an advantage because she not only has taken the best from a wider range of options, Thus by pure chance is more likely to get the best available genes, but also because she had three separate chances vs just one.
Now of course there are thousands of other factors at play like offspring cost this is just for understanding why competition helps both males and females in some cases.

"that female is going to have male offspring that may also engage in sperm competitions" The problem with such reasoning is following: sperm competition is the consequence of sperm competition itself while it can't be true. Females started to be involved in multiple mate sex not because of faster sperm being more competetive. If there are some genes (as I proposed) which both increase fitness of offspring and sperm, than I would like to see any research supporting this.

The gene does not have to make healthier offspring just healthier sperm, There are genes that reproduce themselves at the expense of the organism,(R2D2 in rats), genes do not have ot benefit the organism they just need to spread themselves. . to tweak a famous biology saying, sometimes a man is a just a sperm's way of making another sperm. There is nothing special about males or sperm they are both products of genes.

But how does it justify the sperm competition itself? E.g. if everyone stops sperm competition nothing differs according to your point (which is wrong, females with lesser fitness will give birth to the same amount of children, as opposed to polygamic species).

If peacocks stopped there displays and females stopped preferring displays both would be far better off, the costs are huge, but any adaptation to do so is quickly selected out of the population because it has to deal with all the other females who are looking for the display. sexual selection can be hugely detrimental to an organism as long as it favors the genes. All it takes ot start sperm competition is females who mate with more than one male which is not uncommon in the slightest, in many cases it is not even the females choice.

The reason why peacock females preferred displays is a coincidence of natural selection: it was easier for females to notice those peacocks who had more colorful tails. Therefore, their male offsprings became more colorful through natural selection at first and female offspring became to care about male tails through natural selection. But then they start to choose males who are too noticable. This is what I call sexual selection overkill.

What aren't you understanding about sperm competition then?

Let us continue this discussion in chat.

What part of sperm competition is giving your trouble then, a female mates with more than one male, thats all it takes to start sperm competition selection.

Then the question is: "Why females who mate with more than one male starts to have more offsrpings than ones who don't?"

They don't, they have more successful offspring on average. This is becasue they are using a wider pool of genes. Even this is not necessary, they could just have more successfully MALE offspring that carry whatever gene that let their father's sperm win the sperm competition. There are many genes detrimental to one sex and beneficial to the other. Not all females have a choice in mating with more than one male.

"This is becasue they are using a wider pool of genes." This was my starting point. How wider pool of genes help if we consider better genes do not affect sperm quality? E.g. the slow sperm could become a really fit entity, with the same probability as fast sperm. "Not all females have a choice in mating with more than one male." Some females, I claim, do not even have a chance for a single mate. And this reasoning (that sperm competition indirectly increased species fitness - so that fit females had sex with more males, therefore males would not have sex with less fit females) is more logical

whoa, better genes can absolutely affect sperm quality, better genes is does not mean the gnes have to benefit the individual organism and still be selectively favored. A gene can be beneficial to the sperm and detrimental to the organism. Species fitness is irrelevant to natural selection, natural selection does not occur on the species level, in fact many gene decrease the fitness of the species yet continue to spread. It seems the the source of your confusion is you don't understand how evolution operates.

Hm, but then nothing would favor polyandry. We may assume polyandrous female appeared, her male offsprings would have better sperm and female offsprings would have higher probability of polyandry. But we know there is such thing as inbreeding, therefore here male offsprings would be more likely to have ofssprings from not her female offspings, but other monogamic females. And there those better sperm would never helped. But I'm wondering if multiple-male sex increases birth rates then. Only then it would explain her female offsprings being bred.

inbreeding is pretty small risk, otherwise all non-monogamous animals would not evolve. Like I said not all females have a choice in their mates. but again as I said it can increase the average success of her offspring by producing a wide pool of genes in the offspring. It seems like you may want to aska sperate question about good reading for understanding sexual selection in general.


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What are these Bahrain insects living in a colony?

These insects are in the desert in Bahrain. About 500 in one place both adults and juveniles. Some dung beetle near by. Does anyone know a name?
The adults seem to be protecting the young ?

Welcome to Biology SE! Kindly explain your question further - is it about species identification or what? Currently its hard to get you I am afraid!

Those are hemipterans (true bugs). It is not uncommon for hemipterans to cluster together.


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What advantages do birds gain when they mimic other bird species calls in the wild?
I've read that birds such as crows and blue jays often mimic other bird species calls.  There seems to be evidence that birds do learn and react to other bird species calls, specifically when they relate to danger.  What I'm curious about is what advantages do birds gain when they imitate other species calls?

There are a number of reasons birds will mimic other birds mostly for deception, but not always.

Impressing a mate: Songs are a large part of bird courtship behavior, and a more varied song that includes different mimicked tones can help attract a better mate. Because mimicked tones are learned, a bird with more vocal variety is demonstrating its intelligence, ability to survive, and other characteristics a mate would find desirable.
Safeguarding Food: Using a hawk or owl call, or the sound of a cat, dog, or other predator, is an effective way for a bird mimic to claim a food source. When it utters such a call, birds monopolizing feeders or nearby bushes, trees, or other feeding spots may scatter, letting the mimic take advantage of a less crowded food source.
Defending Territory: Songs are crucial for many birds to claim territory, and adding mimicked tones into the song can demonstrate the resident bird's strength. Extra sounds may also trick other interested birds into believing that there are far more birds in the region than there actually are. The newcomers may then simply move along rather than challenge the resident mimic bird.
Social Acceptance: Baby birds learn many songs from their families and other birds of their species, and if mimicked sounds are included, young birds will learn them as part of their initial repertoire. This helps birds fit in with their flocks, which will also help them eventually defend their own territories and attract mates. Many pet birds that mimic speech are doing so for social acceptance, as they consider humans to be their flock.Bird to bird mimicry
I have personal experience with one of these where a Blue Jay would come to our feeder imitating the screech of a hawk and all the other birds would scatter so he/her had the feeder to themselves.


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Is this experiment to check enzyme reaction rate according to substrate concentration correct?
We just had an experiment to check enzyme reaction rate according to it's substrate concentration.
In the experiment, we used a varying amount of substrate and the same amount of enzyme:
(1.5mm enz, 4.0mm water, 0.5mm subs)
(1.5mm enz, 3.5mm water, 1.0mm subs)
(1.5mm enz, 2.5mm water, 2.0mm subs)
(1.5mm enz, 1.5mm water, 3.0mm subs)
(1.5mm enz, 0mm water, 4.5mm subs)
We check the rate by looking at the optical density after 3 minutes.
Upon staring at this, I couldn't help but wonder: We don't only change the substrate concentration! We also change it's amount!
While 3.0/4.5 is a higher concentration than 0.5/4.5, it's also a higher amount resulting in longer reaction time for sure. If we check after 3 minutes, there's a chance that the 0.5mm subs would already be gone.
If we really wished to look at the rate according to concentration, shouldn't we have only changed the amount of water? It also changes the concentration of the enzyme but there is there any way to isolate either of them?

I think there are a few important answers in your question

The concentration of enzyme is the same in each reaction chamber.  The volume of each chamber is 6ml, and you are using 1.5 ml of enzyme in a final volume of 6 ml, so the dilution factor (the same in all chambers) is 1 in 4. So if stock enzyme concentration is 4 micromolar (as an example), the concentration of enzyme is 1 micromolar in each reaction chamber.
The concentration of substrate varies in each reaction chamber.  You MUST take the dilution factor into account when calculating the final substrate concentration.  You do no tell me what the stock substrate concentration is, but if it is 1mM as an example, then in reaction chamber 1 you are taking 0.5 ml of a 1mM solution in a final volume of 6 ml, which is a 1 in 12 dilution.  The substrate concentration in the reaction chamber is therefore 1/12 mM (about 83.33 micromolar).  In a similar way, the concentration in the final reaction chamber (4.5 ml in a final volume of 6 ml, dilution factor of 1.33) is about 750 micromolar.
You are right, measuring the reaction velocity by taking a single time point after 3 minutes is dangerous!  You must of course measure the initial rate if you want to analyze results according to the Michalis-Menten equation. The assumption you are making is that the rate is linear over a period of 3.   minutes for all substrate concentrations.  If this is not so, you will need to redesign your experiment to take a number of time points and take the tangent to the curve. I think you must be interested in determining the Michaelis constant.
In the language of enzyme kinetics you are doing a discontinuous assay with a single time point after 3 minutes as a measure of the initial rate at a series of substrate concentrations.  A better approach if available is to use a continuous assay, for example by continuously monitoring the change of absorbance of NADH with time at 340nm.  But of course continuous assay not always available.
I am surprised that you use water to dilute. Where is the buffer? And how control pH in your chamber?  Maybe the enzyme and substrate stock solutions are made in buffer, is this the explanation?
You should also check that the velocity versus enzyme concentration is linear at all substrate concentrations.


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If it weren't for animals, insects, or people, would plants that produce seeds (nuts, fruit, etc) cease to exist?
I gather that some would or could in theory still be successful, but don't most depend on takers to flourish?

Comments are not for extended discussion; this conversation has been moved to chat.

No
Not all seeds need to be ingested in order to be spread from one place to the other, in fact some won't grow at all if eaten, some need the fruit to help them germinate and sprout after they hit the ground. Nuts simply will not grow at all if you crack them open.
Most plants rely on the wind to disperse their pollen and seed.
Dandelions are a prime example of a plant with wind carried seeds, their seeds can travel for hundreds of kilometres on parachutes before settling down and germinating in the ground, plenty of other weeds and plants go to seed the same way.

Cotton bearing trees produce their cotton so the wind can carry their seeds, like the Cottonwood and many species of Poplar tree.

One of the fun ones is helicopter seeds. Maples, elders and ash trees are among the species that disperse their seeds this way. The seeds will literally helicopter down, and fly great distances on the wind if it's strong enough. Even as an adult it's still fun to pick these seeds up of the ground and drop them just to watch them fly.

Some trees don't even need to go to seed in order to spread and multiply. Poplars are notorious for sending out suckers underground. Their roots systems spread out from the tree near to the surface and sprout suckers that will pop up out of the ground an grow into another tree. Other bushes and plants do this as well, like raspberry plants.
Not even all fruit is intended to be eaten, The fruit of the chestnut tree is sour, and covered in sharp spines that hurt. We used to spin them around and throw them at each other as kids imaging we were medieval warriors wielding maces. The spikes can get rather long and sharp, I've seen them stick to kids that have been hit by them, and after plucking them off they develop a golfball-sized welt covered in lots of tiny puncture marks.

Worst case scenario for plants that spread their seeds via burrs or by being ingested a pooped out elsewhere if animals were to suddenly cease to exist is that they wouldn't be able to disperse their seeds as far. They'd simply drop their seeds beside them, but they would continue to exist.

Thank you, Shem, for your wonderful answer. That puts into perspective fruits and seeds, which I appreciate! :) I had thought of fruits and nuts as being quite dependent on being eaten or carried away, but as you point out, not all are so dependent. Interesting!

I up voted your answer, but since I don't have 15 points yet, I'm not "allowed" to say thank you in such a way. Sorry man

As kids in Hawaii, we had 'burning beans' of this tropic legume tree with beans the size of a quarter that we rubbed on the concrete to get hot and touch another poor kid!  No 1st degree burns at all...

Even edible fruit trees may survive, just look at the osage orange, the only animal that could eat its fruit is long extinct, so not only the fruit that rot away fast enough spread.

A really good book on how trees work is this one:
Trees: Their Natural History 2nd Edition
by Peter A. Thomas
I think pollination would be a bigger issue. There are trees that depend on very specific animals for pollination. Some would probably vanish after existing plants died.
And, yes, there are trees that depend on animals for seed distribution. But, they would probably get by. They would spread a lot slower. But, they also wouldn't have animals around to eat their fruit/seeds/nuts. For example, squirrels and jays cache nuts from various locations and they don't retrieve them all later.
There are also trees totally dependent upon specific animals: There is a South American plant/tree dependent upon the agouti to open the shells of their nuts and bury some. Nothing else can do it. I am not sure if the shells would deteriorate fast enough for the insides to have a chance to grow.

I think this question is wonderful.  This is the kind of thinking everyone should find themselves doing everyday.  And, my answer would be, yes, plants would adapt to other ways to disperse seed.  It would take a long time but you bet, if that method of dispersal stopped plants would evolve to use only wind or water to disperse seed.  The dandelion's method would become the norm.  Maple seeds, the little helicopters would become even more impressive.
The problem with your scenario are insects; bacteria, nematodes, fungi and macro soil organisms the millipedes, earthworms...without these decomposers it would inhibit decomposition and thus no food for all the other soil organisms, some plants are totally reliant upon.  Plants would change, evolve into a more survivable organism.
Plants already communicate via chemistry to protect their own species.  When the antelope and other herd beasts in Africa got overpopulated and started to put major stress on the shrub trees, the shrub trees got together and became poisonous and killed entire herds of animals.
I am wondering when plants will turn on us!  Grins...


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Distribution of the number of clover leaves
Being no expert at all in this field I am just interested in emprical studies of the frequency $f(n)$ of clover plants with a given number $n$ of leaves.
I would suspect naively from general considerations that the frequency follows an exponential distribution.
Any hints are greatly appreciated.

Roughly: You find around 1/10000 four leaves clover. If you want to get into the details, know that each observation isn't independent from the other (as two "clover" are sometimes the same individual sharing the same genetics) and the time of the observation (summer or spring) may change this rate (more four leaves in summer). I advise you to search this website to find good and referenced answers to your questions. If it is not what you were looking for, edit your answer to give  what you understood from other questions and what you are still looking for.

@ Untitpoi Thank you for your comment. I would appreciate if you could be a little more specific which website I should search for what? Neither during the formulation of my question nor in the margin section of related stuff something relvant has popped up.

did you check that answer : https://biology.stackexchange.com/questions/57860/are-four-leaf-clovers-mutations-developmental-errors-or-something-more-complic the Tashiro et al. 2010 reference seems to be a good empirical study on four leaves clover!

I have found a study [1] of 2017 (http://www.sharetheluck.ch/single-post/How-rare-are-four-leaf-clovers-really) which answers a great part my question, and I'd like to show those results together with some additional evaluation.
They have counted 5.7 million clovers and found the following numbers compared to 3-leaflet clover:
4-leaflet clover    1 in 5,076
5-leaflet clover    1 in 24,390
6-leaflet clover    1 in 312,500
For the 4-leaflet clover they have corrected appreciably the common figure of 1 in 10,000 (see e.g. the comment of Untitpoi here).
A logartihmic plot of these relative frequencies shows interesting features
(i) a fairly regular exponential decay of the frequency in the range n=4,5,6
(ii)    a significant "exception" from this rule is the "normal" clover with n=3

How can these observations be explained?
It would also be interesting to extend the study to n>6, and maybe also to the range of "deficient" clover which posesses only one or two leaflets. The latter are most probably very rare so that the complete log-plot would resemble an inverted letter V.
The question of 2-leaflet clover was raised here [2] https://www.quora.com/What-are-the-chances-of-me-finding-a-two-leafed-clover. But no quantitative answer was given.
References
[1] http://www.sharetheluck.ch/single-post/How-rare-are-four-leaf-clovers-really
[2] https://www.quora.com/What-are-the-chances-of-me-finding-a-two-leafed-clover
[3] https://en.wikipedia.org/wiki/Four-leaf_clover#cite_note-auto-6
A comprehensive reference which I have only partially explored up to now

Thank you, Dr. Hintze, for citing our work (http://www.sharetheluck.ch/single-post/How-rare-are-four-leaf-clovers-really). We were frustrated about the lack of a reliable source for the '1 in 10'000' estimation of the prevalence of 4-leaf clovers (it is most likely a circular reference that was once started simply by guessing), so we started our own research (complementing the philantropic side of our project www.sharetheluck.ch). This let us come up with the below-mentioned numbers.
We do keep record of clovers with 7 and 8 leaflets, but we believe that the numbers are too small (yet) to be of significance.
Substantially higher numbers of leaflets have beeen obeserved only after inbreeding, to our knowledge.

@ U Sperling Could you provide the numbers for 7 and 8 even though they are not reliable enough? I'd like to put them into my graph and see if the rule continues approximately.


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What determines the physical location of differentiated cells in an organism?
Exposition:
As a little kid, I always thought of DNA as being a description of how to build an organism. For example a human DNA would have "Add two legs and two arms", a dogs DNA would have something like "put a tail here". Now, at school, I have learned that DNA codes for proteins, for structural proteins, enzymes etc. But how does a growing fetus actually know where to put the different parts of the body?

Examples:
For example, why don't I have retinal cells growing on my feet? Why is my cerebral cortex not in my mouth? And where is the information stored that humans do not have tails, or that elephants have trunks?

Summary:
What determines where different cells should be located, and how is that information stored?

I have edited your question to remove the anthropomorphic implications. Cells do not ‘know’ anything — they are not sentinent beings, and it encourages sloppy thinking to use this term, even in quotation marks. Otherwise, the scope of your question is huge — it is not my field but it would seem to cover the whole area of embryology and determination of cell fate, which is only partly understood. Perhaps someone else can point you to the chapter of a basic biology text where this is covered, but I doubt whether this question can be answered here.

Which organisms? There are several very different answer across life. nematodes and houseflies use very very different methods. For humans and houseflies you may want to look into hox genes or just embryology in general.

Cool question. As the other answer mentions, the process is very complex, and we are still learning the relevant mechanisms in organisms other than the fruit fly. But it is considerably well described in the fruit fly which merits a brief summary.
Since a lot of asymmetric (A-P axis, for our purposes) development occurs pretty early in embryonic growth, whatever drives this pole-specific differentiation must act early. As it happens, it begins as early as maternal ovum (Bicoid mRNA). Using cellular machinery (microtubules, motor proteins), these are concentrated towards one end of the egg and subsequently of the early embryo. Once such an asymmetry in the concentration is achieved, further development genes can take advantage of this patterning by being influenced by downstream signalling. Hence there is a cascade of gene activation downstream, which involve Gap genes, Pair-rule genes and several homeotic genes (see Hox genes) which are also differentially expressed along the A-P axis. They directly control patterns of the organs formed from there. Using a gradient of these genes, further patterning of organs can be similarly achieved (the retina gene would be activated only at a concentration of these genes which is found only at the top and so on).

Developmental biology is a huge field, and we are still learning a lot.
But a basic principle would be "The cells in the developing embryo develop differently depending on where they are".
We understand fairly well how fruit fly embryos figure out their head-to-tail axis; it starts with the fly ova having an asymmetrical distribution of maternal mRNAs
https://en.wikipedia.org/wiki/Drosophila_embryogenesis


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Neutral genetic mutations in eukaryotic cells
Why are most mutations in eukaryotic cells neutral? i.e. have no effect on the phenotype.

Your premise that most mutations in eukaryotic cells are neutral is dependent on where in the genome the mutations occur. Most of the genome of eukaryotes is non-coding, so mutations are frequently neutral unless they occur in some signaling region. In protein coding genes, all mutations in 2nd codon positions, and about half of the mutations in 3rd and 1st codon positions change the amino acid, and this is most often deleterious. It is informative to distinguish between mutations and substitutions. Many mutations are never observed because they are lethal. Substitutions are mutations that have survived the filter of selection long enough to be observed. Lethal mutations are never observed because they kill the embryo before it is born. And seriously deleterious mutations are removed from the population quickly as well. So selection acts to favor the observation of neutral substitutions, but most mutations are deleterious.


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When you lose weight, how does the mass exit your body?
As a thought experiment, consider the case of Angus Barbiery, who allegedly lost almost 200kg in about a year by not eating at all, save for necessary nutrients provided as supplements.
My question is, where did those 200 kilograms go.
And please, don't suggest that it was "converted to energy". 200 kilograms of mass would be approximately equivalent to 1.8*1016 joules. For comparison, Czech nuclear power-plant Temelín generates approximately  4.3*1016 joules of energy.
So how does the mass exit the body after the glucose is metabolized?

I suggest you consult a text book to find out the chemical products of the metabolism of glucose (or fat). Then blush and withdraw your question.

Closely related/possible duplicate of: Breathing faster to lose more weight

To burn fat it needs to be aerobically.  Cardiovascular exercise is critical...steady state heart rate 65 to 85% of max heart rate using large muscles.  After 10 to 15 minutes, THEN one is burning fat.  So holding onto that rate of exercise for another 30 minutes means major burning of actual body fat calories.  Figure out how much you would be able to lose per day walking for an hour.  Don't be discouraged, you are also changing your body to BURN fat more readily like a race car versus a volvo.  People who are more muscle than fat NEED calories regularly.  Fasting is just stupid and stupider.

Nobody except you is suggesting that the human body is a nuclear reactor, so the strident tone in your question is unfortunate. And what is presented is a calculation, not a thought experiment. (You owe Schrödinger an apology, I think — or at least his cat.)  Energy and matter may be interchangable, but before this was discovered there was a law of conservation of matter based on general everyday experience of how one form of matter is converted into another.

@David I was googling this before asking and a great amount of people have written things like "he converted the fat to energy". The thought experiment goes before the calculation, hence new paragraph.

Possible duplicate of Breathing faster to lose (more) weight?

as CO2 and water
in respiration sugar (or fat) is combined with oxygen to produce energy(ATP and heat), water, and CO2.

fats are converted to Acetyl Co-A just like glucose is, the rest of the metabolic pathway is exactly the same.

Well, you can indulge those who are too lazy to do the required research before asking a question, or you teach them how to find out things for themselves. However I suspect the poster hasn't even the chemistry to understand your first diagram, nevermind the bizarre construct that follows.

Not everyone see the need to mock laymen who are lacking a key piece of information but obviously put some though into their question.

Biology Stack Exchange is a question and answer site for biology researchers, academics, and students. It is not for laymen, although the poster is certainly not a layman, but clearly has an education in physics. Regardless, he should follow the guidelines about posting: "Have you thoroughly searched for an answer before asking your question?". I just suggested that he blush when he realized that metabolism involves chemistry rather than nuclear physics, and a calculation is not a thought experiment.

Let me explain my criticism of your answer.Here is a question about metabolism from a physics student who has forgotten his school biology basics; that glucose is metabolized to carbon dioxide and water. You provide a diagram with terms like "Glycolysis", "Krebs Cycle","Chemiosmosis" — only comprehensible to someone who is already familar with biochemistry. You also use logically inconsistent representations with arrows between an explanation (aa group removed), a compound (urea) and a milieu (urine). Your answer is at the wrong level, and for more detail a link to a text would be far better.

Or was never taught it in the first place, or is lacking a key piece of information, such as that fat are converted into something that can undergo the same process as sugars, which is something few people are ever taught. Additionally a Phd in one subject can be a laymen in another.  Also I did include links.

I think it would be more truthful and interesting to add "and heat and ketones" to your bolded answer of CO2 and water. It's not all just CO2 and water. There are other metabolites excreted in urine as well. It's not a lot every day, but over time, it adds up.


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In ketogenesis, why is acetacetyl-CoA not directly hydrolized to acetoacetate in ketogenesis?
Ketogenesis pathway maps show acetoacetyl-CoA converted to HMG-CoA and only then to the first ketone body acetoacetate. Why this detour instead of directly hydrolyzing off the CoA to get there in a single step? Is it possible that some ketone bodies are made by direct conversion? The enzyme acetoacetyl-CoA hydrolase to do this job exists and can be found in rats.

I've been Googling this a bit and the trail seems to run dry for the acetoacetylCoA hydrolase after about 1980. I suspect that there is something fishy about it. I notice that the acetyCoA hydrolase turned out to be an alternative activity of the thiolase, and wonder if it is something similar and is not active under the appropriate physiological conditions. There aren’t many biochemists around these days that know about this stuff, and I don’t rate your chances of finding one on this list, but I hope I am proved wrong. Fair question, though.

Thanks David for researching this. Too bad we both came up short so far. A future research project hopefully.

The answer I would give here is because HMG-CoA is a key intermediate not only in ketogenesis but also in cholesterol (isoprenoid) biosynthesis. The 'starting intermediate' may be considered to be  HMG-CoA for both pathways. (An example of what Lehninger called 'the molecular logic of living organisms' perhaps)

I believe it is related to the fact that the enzyme HMG-CoA lyase is regulated by glucagon (activates) and insulin (inactivates). It appears that this extra step was added so the pathway can be hormonally regulated.

Welcome to Biology.SE! I could see this as a mechanism for maintaining a step, but I don't see how adding an extra step to an existing pathway could be selected for especially to allow future regulation. In addition, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion.  ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and [edit] your answer accordingly. Thank you!

This is a good example of how to format references.

After further checking, I found that HMG-CoA synthase rather than HMG-CoA lyase is the enzyme which is regulated. This enzyme also plays a vital role in cholesterol synthesis. HMG so produced can either form mevalonate, which leads to cholesterol synthesis, or form acetoacetate. Therefore if acetoacetyl CoA were directly hydrolyzed, it would short circuit the cholesterol pathway.
The enzyme can be regulated by succinylation. Its synthesis can be regulated by several transcription factors. Evidence suggests that hormones play a role in each of these processes. References: Harris, et al., Journal of Investigative Dermatology 114(1) 83-87 (2001); F.G. Haggart, Biochem. J. Mar. 5, 338 (pt. 3) 569-582 (1999); Quant, P.A. et al. Eur. J. Biochem. 187, 169-174 (1987)
Most Biochemistry texts today list HMG-CoA as the source of acetoacetate with no mention of direct hydrolysis of acetoacetyl-CoA. This suggests that if direct hydrolysis of acetoacetyl-CoA does occur, it probably plays a very minor role.

If you wish to post a second answer to a question it should stand alone and not refer to a first one you have (or should have) reservations about. You are able to edit or delete any answer you post, so I would suggest you do this to consolidate them into a single answer, comprehensible in itself. (And as one of the few people who answer questions on biochemical metabolism I’ll have a look at it when I have a moment.)

Since you now seem to be posting using two separate accounts, you may find this information on merging accounts to be of interest ...


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Coefficient of relatedness for a locus on the Z chromosome
So i know that the ZW determination system is the equivalent for XY in birds. Moreover, I know that the coefficient of relatedness between siblings for the X chromosome is 0.5 so im guessing that the coefficient of relatedness between siblings for the Z chromosome is the same ??

Yes it would be .5 Due to reasons you correctly deduced

but isnt it different between brother and sister and between sisters and between brothers. Isnt the Z chromosome considered as haploidiploid ?


text:
Are longer and shorter DNA similarly charged?
A longer DNA molecule would have more phosphate groups, so it should have a greater negative charge, right? It was taught in my class that only terminal ends of DNA are charged and all the phosphates in the middle are not charged.
My teacher said that this is the reason that Electrophoresis separates the fragments. All DNA have same charge and so same force on all of them. Then difference in masses would give different acceleration and thus separation of fragments according to size. But isn’t Gel Electrophoresis more like a sieve where longer molecules move slowly and shorter pass through easily?

Each phosphate group has a single negative charge. Not just the terminals. The reason gel electrophoresis works so well with DNA is that charge is linearly proportional to size. The longer the fragment, the slower it moves. A double stranded DNA molecule with 100 nucleotides has a charge of -200. If it were twice as long, it would have twice as many, just as if it were 3.4 times longer, it would have 3.4 times as many negative charges. This way, charge is essentially ignored, so DNA migrates through the gel at a rate inversely proportional to its size.


text:
Why isn’t Haemoglobin a plasma protein, rather than being encompassed by the erythrocyte?
Erythrocytes (red blood cells) are a common feature of almost all vertebrates. What evolutionary advantage do they provide in containing haemoglobin, rather than it being just a plasma protein? In fact, haemoglobin is dissolved in plasma in a few annelids and haemocyanin in cephalopods.
The only reason I can think of is that haemoglobin is small enough to get filtered into the tubules of the kidney and is renotoxic. Maybe that's why it had to be packaged into erythrocytes. But isn't this a greater cost than reducing the pore size to prevent it being filtered out? Also, doesn't haemoglobin or haemocyanin get filtered into the primitive kidneys of annelids and cephalopods?

I have edited your question a little. Note that haemoglobin may be coloured, but is not classified as a pigment. Also it is a reasonable sized protein (four chains of about 100+ amino acids), although I have not edited that part.

To the man with a hammer, everything looks like a nail.

The poster’s hammer seems to be kidney function. Mine is the biochemistry of the erythrocyte (red blood cell). Others, no doubt will be able to provide yet different perspectives.
From a biochemical point of view the erythrocyte has a limited repertoire of metabolic pathways compared with other tissues. However it does have an extremely active pentose phosphate pathway (not universally found in tissues) and the function of this is to provide the reducing cofactor NADPH, which is needed to maintain glutathione in a reduced state. The importance of reduced glutathione in these oxygen-carrying cells is that it provides protection against reactive oxygen species — something that could not be done — or at least not controlled so well — in the blood plasma.
Another feature of haemoglobin is that the equilibrium between the oxy- and deoxy- forms involves the small triose molecule, 2,3-bisphophoglycerate. This is described in the answer to another question. The ability of the erythrocyte to synthesize this molecule allows the sophistication of this control.
I imagine there are many more examples. (Any added in comments will be added.)
One could argue that these metabolites are not indispensable for organisms (glucose phosphate dehydrogenase deficiency does cause haemolytic anaemia in man), and this presumably explains why the simpler organisms you mention (and about which I know little) can dispense with red cells.
But a question certainly worth asking.

Cool! I'd thought of compartmentalization giving some biochemical advantage but couldn't think of how since G6PD as you mentioned isn't indispensable. But after a little search I found out - absolute deficiency of the enzyme <10% activity leads to chronic hemolytic anemia. Only the moderate deficiencies are 'stressor' induced hemolyses.

But it is important to note that a G6PD deficiency causes anemia by hemolysis - bursting of the RBC. But we are talking of a case when there is no RBC, so the argument doesn't make much sense. Bt yeah 23bpg might play an important role...

@Polisetty — The argument makes a lot of sense. As a medical student you are only thinking about diseases, not the underlying biochemistry. The anaemia is just the end result of the damage caused by active oxygen species resulting from oxygen transport by Hb. In the plasma they would affect the walls of the veins and arteries (or whatever — I don't do cellular stuff) and other proteins.

An additional aspect is that the availability of iron usually constrains the growth of pathogens. Cassat and Skaar in "Iron in Infection and Immunity" state:

Iron is an essential nutrient for both humans and pathogenic microbes.... Given the absolute requirement for iron by virtually all human pathogens, an important facet of the innate immune system is to limit iron availability to invading microbes in a process termed nutritional immunity. Successful human pathogens must therefore possess mechanisms to circumvent nutritional immunity in order to cause disease.

Later they say:

Even in the absence of infection, several facets of human iron metabolism ensure that iron is scarcely accessible to pathogenic microorganisms. First, the majority of iron in humans is sequestered intracellularly, complexed within hemoglobin inside erythrocytes. Some pathogens have therefore evolved mechanisms to liberate hemoglobin by lysing erythrocytes to ultimately extract iron from heme.

Thus, one advantage of sequestering hemoglobin within erythrocytes is that it slows the growth of invading pathogens by making necessary iron more difficult for the pathogen to obtain.

Interesting. I never knew that.

Some pathogens have therefore evolved mechanisms to liberate hemoglobin by lysing erythrocytes to ultimately extract iron from heme.I'm just taking a shot in the dark here but is plasmodium part of these pathogens?


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Do fallen leaves produce oxygen?
After a leaf has fallen from a tree, if it is still green and hasn't dried out, is it still converting CO2 into O2 if not put in water?
Can anyone find any data showing how long any different species of leaf will continue to produce oxygen after fallen?

Short answer
It all depends on the time window you are talking about. After having been detached from the mother plant, a leaf will typically keep on photosynthesizing for a few hours or so.
Background
Cutting of the stalk of the leaf results in impaired water flow and wilting. As soon as a leaf is detached from the plant, it will also be cut off from hormones, minerals and other nutrients. The result of this is that senescence (and death) sets in straight away. However, leaves will typically stay green and moist for hours or even days, dependent on the conditions it is stored. Hence, in practice, photosynthesis can be measures at least a few hours after a typical leaf is picked (source: Science and Plants for Schools).

Thanks so much. Any more-detailed information showing exactly how long they will continue to photosynthesize?

@Johan88 - depends on species, and conditions (heat, humidity and so forth)

that's exactly what I'm thinking, but I hope I can get some data from some studies, but have not been able to find any such studies.

It would be a nice experiment to use CO_2 with radioactive C14 isotope in an artificial atmosphere to measure it, or you can measure the increase of humidity (much easier, but less crazy scientisty and accurate). btw. the saddest biology question ever :( poor leaves...

Note that there are many plants where if you cut off some part of it and leave it lying on the ground, it will grow roots and become a new plant.

@atevm Hahaha. The saddest Biology question Kakaka. Well, the leaves fall around me all the time, and I like to pick them up and put them in a bowl in the hopes they can still create oxygen for a while and their life isn't over yet  :)

@Johan88, seriously, you are not kidding?  There is plenty of O2 and as long as things like CO2 concentrations stay stable or better RISE in ppm plants and the ocean will continually make O2.  There are far better ways to expend your energies!

Every single thing that was once alive, once dead, once cut off begins to decompose immediately.  Fully is the temperature is correct.  O2 is produced during the day as long as there is CO2, tiny tiny amounts of chemistry (NOT NUTRIENTS), water, drainage in the soil medium, ventilation...actively photosynthesizing chlorophyll produces oxygen, 'sinking' the CO2 within its biomass.  Just like the ocean.

https://www.youtube.com/watch?v=CrrSAc-vjG4 This would be fun for you to watch if you've not watched already.  When they say the words, 'food for plants' I want you to hear me scream!!  Otherwise, great documentary.

@stormy truth be told, I'm not allowed to bring plants where I work: boss would consider it inappropriate. Modern decor: the air REEKS of plastic and fumes and I absolutely hate it and feel nauseous. I pick up fallen leaves in the morning and stuff them where they have some light and won't be seen. Hope it improves oxygen. Certainly has a placebo effect if it doesn't. Need some damn green! :P I dump em when they're dried out since decomposition does the opposite I think: O2 to CO2

Ah, Johan, you are describing a true nightmare.  Decomposing leaves don't provide oxygen.  The smell of earth, of rot and decay, 'centers' you.  Something like that. Sigh and major sigh.  I would be working on a major change for you...I hate money. Anyway, You need to get your hands in the dirt after and before work.  You need to 'work out'...cardiovascular mostly.  Walking, running, bicycling.  That will help you keep your objectivity.  I get it, I do!  You are the only one who decides the directions of your life.  You be honest with you and take care of you firstus!

@stormy Thanks. When I said "Need some green" I meant need some green life, plants, even if it's just a few leaves I pluck each day, despite my modern square plastic concrete boss and her rules. Lol, she caught a sight of a small leaf pile the other day and was like, "What's that?" "It's my oxygen machine. Cannot?" "Really?" "Cannot?" "REALLY?" "The air quality is so bad. Cannot?" "Get rid of it on your lunch break." Currently I'm hiding an airplant somewhere. Lol. Good things my boss's boss likes me, otherwise my little quirks would not be tolerated.

Johann...it is nice your boss likes you, needs you.  You sound as if you need to be self employed.  Photosynthesis produces oxygen but there is plenty of it around, you don't need to make anymore.  Decomposition doesn't produce O2 it uses it during aerobic decomposition.  You are so dang cute.  Hiding an air plant.  Seriously, life is too wonderful to waste a single minute working FOR someone else in an environment that is driving you nuts.  Huggs.  You and your little quirks need to find a new home where appreciated!

https://www.researchgate.net/profile/Rien_Aerts/publication/216809762_Climate_Leaf_Litter_Chemistry_and_Leaf_Litter_Decomposition_in_Terrestrial_Ecosystems_A_Triangular_Relationship/links/54412b640cf2e6f0c0f60201.pdf

@stormy self employment is the plan. In HK, in the heart of the city, kilometers of concrete and asphalt all around me in every direction, air pollution is terrible. I want the plants for air cleaning (fumes and chemicals) more then oxygen. My boss doesn't like me. She fears me. Because her boss fears me. Because the former boss of the boss of my boss loves me. It's complicated. I'm aiming to launch my own business. I'm not against hierarchy at all, in principle. The problem is toxic personalities when you encounter them. And I want to employ people below me, and be a great boss. Thankyou hug!

You said the magic words, "they fear you"....this is a good thing as well as very bad.  If you are unable to get support, you've been boycotted.  Try to become less visible.  Less, grins, scary?  You will have to lead, and the more experience you've had with other humans the better a leader you will be.  Toxic personalities is not a helpful perspective.  As a leader you will be making these 'toxic' people into productive happy people, all part of a team.  Objectivity is a crucial skill. Sit down or lie down and imagine where you want to live and how you want to affect the world around you.


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Which gene regulatory network is the largest in human?
What is the maximum number of nodes involved in any gene regulatory network and which network is it, provided its from human?

Your questions come across rather strangely. You don't explain why you would want to know something like this. I gather from your bio that it is related to your PhD project, so I imagine you have a reason. However I would suggest you are more likely to get a response on SE Bioinformatics. There are more people there who know what a node is.

It is not quite my field and I don't know how to answer this question but it strikes me as it is likely that the definition about what type of interactions you would consider to deserve being represented by an edge between the two genes (genes are nodes in this network) would matter a lot.

@David i did not know there is SE Bioinformatics,... thanks!


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What are these little leaves growing on these other leaves? (plant growing near the ocean)
I saw many of these plants while hiking on a hill facing the ocean in northern Taiwan. I've included a snapshot of a nearby part of the same trail to show it's rugged, wet, green, and rocky, and another photo of some what looks to be the same kind of plant without these things, and one that has a reddish coloring.
Any idea what these little (~10 mm long) "leaf-shaped" brown/orangish things are, growing from points along two regular rows of bumps that are repeated everywhere? Is this reproduction, if so how does it work?
Also curious, any thoughts on what kind of plant to call this? I don't need a species identification necessarily, but is it a kind of fern?

below: Additional photos, click for full size.

These are really cool, and I am absolutely not certain of this, but I would hazard that they might be some kind of bulbil? Ferns (if I have started my ID correctly) can use them to asexually reproduce. For example the New Zealand endemic Asplenium bulbiferum grows little bulbils on the adaxial surface of its frond.

Thank you for that term! With it, one can search and find all kinds of crazy/weird looking things growing out of other things. Search for it along with fern and photos on pages like this and especially this and this show structures somewhat reminiscent of what I saw. I wish I could go back to the same site and see how those have grown, but that's not going to happen any time soon.

Also this and this and this and this!

@uhoh no problem, glad I could help


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Biological contamination from ground
I took samples of tapwater in order to examine concentrations of escherichia coli and enterococcus, in a rural area. I was told, by the analytical lab, to take samples in four sterilized vessels bought from pharmacy. The problem is that at the completion of the last vessel, its cap fell frοm my hand down to the soil and some grains of sand stack on the inner surface of the cap. As fast as I could, I picked it up and washed it off totally with the water of the sampling tap. After that I closed my last sampling vessel with it and this was the completion of the sampling. How great is the possibility my sample has a serious contamination of these twο biological pollutants after this incident?
Thanks and sorry for the long story and bad english

Document the incident and notify your supervisor. For environmental testing where SOP is involved, this would count as an incident, i.e. anything that falls outside SOP. Whether the incident is a non-conformance, deviation or nothing at all is up to your quality team. You can always take another sample, supplies withstanding, too.

I would say there is a pretty big chance that you sample is contaminated. Maybe by washing most of the bacteria or fungi are removed. It would be very difficult to stick on the lid when you washed it but still. Wash the sampling tap distillate water or just tap water. If so you don't have to worry much normally it has to be free from bacteria. But, At school we did an experiment to demonstrate the present from bacteria in this water and we found bacteria. Because you took it with you and bottle opening isn't sterile. There is a big chance on contamination. But the greatest contamination would probably be the air. I think it's best to not use the data you will gain from this sample. It wouldn't be representative for you experiment. My English isn't that good either so don't worry about that.


text:
UV-lamp, DNA and RNA extraction lab
I'm equipping a lab room (~3x5 meters) that's supposed to be used for DNA and RNA extractions. I know  about the basic safety precautions when working with RNA and DNA extraction (fresh gloves, labcoat, separate workstations/pipettes, RNase-free workspace etc), but it is my first time seting up this sort of things
so I'm a bit unsure how strict I have to be about some of these things, so my question might seem a bit silly/stupid to some but here it goes anyways.
The question; I want to buy UV-lamps to clean out old DNA in the environment so I don't contaminate my fresh samples. I don't work in any hoods. I have a downdraft ventilation table and a bench that both stands along one wall on which I'll be Working on. I wonder if it is enough to just have one UV-lamp that covers my working area, or should I buy enough UV-lamps that cover the entire room (since I'm not working in any hood -> risk for airborne contamination)? Or is it over-kill to cover the entire room? I don't want to spend to much money.


text:
What are the types of interactions in biological network (protein networks)?
In the KGML files, the types of relations between genes or proteins are precisely activation, inhibition, expression, repression, indirect effect, state change, binding/association, dissociation, phosphorylation, dephosphorylation, glycosylation, ubiquitination, and methylation. I want to know more about these interactions. Is there a particular source from where I would understand what these interactions mean in depth?

Most of them are pretty self-explanatory. KEGG pathways are often vague, as a lot of the specific biology for some proteins has yet to be properly investigated - sometimes you only know that two proteins associate, not what they actually do.
The relationship between the two is easier to predict when you know the function of one, e.g. a protein interacting with a kinase is likely phosphorylated by said kinase. A lot of those relationships correlate to post-translational modifications (glycosylation, phosphorylation, ubiquitination, acetylation, methylation, etc) made to one protein by another. Wikipedia actually has a decent overview of these with lots of examples.
Several of the other relationships have to do with regulating protein activity or expression. This goes somewhat hand in hand with what I stated above. Some proteins are only activated once phosphorylated or demethylated, etc. Other enzymes may remove phospho groups, leading to repression. Others still may interact directly with a protein, inhibiting it from binding its substrate or target. Maybe the binding induces a conformational change in one protein that allows it to bind its substrate when it can't normally. Some proteins function as transcription factors that activate or repress the expression of certain genes, indirectly affecting protein levels.
There are all sorts of possibilities - the KGML files try to represent them in a way that at least gives some indication of how the interactions between two proteins may affect each. I hope that provides some insight.


text:
Easy derivation of Kimura's approximation for the probability of fixation of a mutation
Kimura's approximation for the probability of fixation of a mutation under selection finds recurrent use in population genetics models till date. I am trying to understand the mathematical basis of this equation but none of the textbooks or online resources that I have checked, provide an easy derivation of this approximation but rather simply cite Kimura's 1962 paper.
$$P_\text{fix} \approx \frac{1-e^{-4Nsp} }{1-e^{-4Ns}} \qquad (1)$$
So, I was reading the original paper but the provided derivation doesn't appear clear to me.

Details
Kimura starts with definition of probability of change in allele frequency as:
$$u(p,t+\delta t) = \int f(p+\delta p; \delta t)\ u(p+\delta p,t)\ d(\delta p) \qquad (2)$$
where (quoted exactly)

$u(p,t)$ is the probability that an allele will be fixed in a time interval $t$ given that it's initial frequency is $p$.
$f(p+\delta p; \delta t)$ is the probability density of the change from $p$ to $p+\delta p$

Then he uses Taylor series approximation to obtain an equation of this form:
$$\frac{\partial u(p,t)}{\partial t}= \frac{V}{2}\frac{\partial ^2u}{\partial p^2}+M\frac{\partial u}{\partial p} \qquad (3)$$
He defines $M$ and $V$ as mean and variance of change of $p$ per generation. These are formally defined as:
$$M=\lim_{\delta t \to 0} \frac{1}{\delta t}\int (\delta p).\ f(p+\delta p; \delta t).\ d(\delta p)$$
$$V=\lim_{\delta t \to 0} \frac{1}{\delta t}\int (\delta p)^2.\ f(p+\delta p; \delta t).\ d(\delta p)$$
($V$ actually should be just the second moment as per the mathematical definition and not variance)
Then he solves equation 3 at steady state with boundary conditions $u(0,t)=0$ and $u(1,t)=1$ to obtain this:
$$u(p)=\frac{\displaystyle\int_0 ^p G(x) dx}{\displaystyle\int_0 ^1 G(x) dx} \qquad (4)$$
where:
$$G(x)=\exp\left(-\int \frac{2M}{V}dx\right)$$
I understood the derivation till this point.
Then he just puts:
$$M=sx(1-x)$$
$$V=x(1-x)/2N$$
and obtains equation 1.

In short
Is there an easy derivation for equation 1?
If not, can someone explain me how M and V were approximated as above?

nice question! It might be worth tyring to ask this on math stackexchange (or whatever its called), since most biologists probably don't get the math behind this (I'm including myself here, and I probably have more math background than the average)

@Nicolai Perhaps the mathematicians may know these methods really well but I am afraid without context, just knowing the mathematical methods won't be of any use. I'm trying to read Kimura's book which is more detailed. I think I'll find an answer there. When I find it, I'll post it.

Presumably you've solved this, but, in case not, it's because the PDE is a Kolmogorov backward equation, so the first and second order coefficients are the mean and variance of the underlying stochastic process being modeled.
In detail, consider a stochastic differential equation (which has a solution given by an Ito diffusion process):
$$ dp_t = \mu(p_t,t) dt + \sigma(p_t,t) dW_t $$
then the following system holds (under some conditions):
$$ -\frac{\partial}{\partial t} u(p,t) = \mu(p,t)\frac{\partial}{\partial p}u(p,t) + \frac{1}{2}\sigma^2(p,t)\frac{\partial^2}{\partial p^2} u(p,t) $$
where $u$ is the density of $p$ at $t$.
Note that the drift (infinitesimal mean) $M=\mu(p,t)$ and diffusion coefficient (infinitesimal variance) $V=\sigma^2(p,t)$ are as in the paper (except for the negative sign, which I assume is ignorable since he mostly seems to care only about the case when $\partial_t u\approx 0$ anyway).
Indeed, they are equivalently written:
\begin{align}
\mu(p,t) &= \lim_{\delta t\rightarrow 0}\frac{1}{\delta t} \mathbb{E}\left[ p_{t + \delta t} - p_t \mid p_t=p \right] =: M \\
\sigma^2(p,t) &= \lim_{\delta t\rightarrow 0}\frac{1}{\delta t} \mathbb{E}\left[ (p_{t + \delta t} - p_t)^2 \mid p_t=p \right] =: V  \\
\end{align}
as Kimura writes.
Note that a useful approximation of the transition density is given by:
$$ \mathbb{P}[p_{t+\delta t} \mid p_t] \approx
\mathcal{N}(p_{t+\delta t}\mid p_t + \mu(p_t,t)\,\delta t, \sigma^2(p_t,t) \,\delta t) \tag{TD} $$
Ok, so everything above is just basic stochastic processes theory. Thus, if we have a stochastic model for the population dynamics, we can derive values for $M$ and $V$ from it (by computing its moments), and those will carry over to the backward Kolmogorov equation, upon which Kimura's work rests.
Here is where my ignorance of population dynamics shows. However, since Kimura mentions Fisher and Wright, I looked up the Wright-Fisher model.
It seems like Kimura is using the diffusion process approximation of the Wright-Fisher model.
This appears to be a well-studied and storied model that I cannot fully describe here; instead, I found the work by Tataru et al, Statistical Inference in the Wright–Fisher Model Using Allele Frequency Data to be an excellent description of it, though I do not pretend to understand much of it.
What's important, however, is that the change in genes (transition density) can be described by a binomial distribution. This can be approximated by a normal distribution:
$$ \mathbb{P}[p_{t+\delta t} \mid p_t] \approx \mathcal{N}(p_{t+\delta t}\mid p_t + a(p_t) \delta t,\, p_t (1-p_t) \delta t ) $$
using the standard approximation to the binomial.
This then gives us a forward Kolomogorov equation (not backward) written:
$$
\frac{\partial}{\partial t} u
=
- \frac{\partial}{\partial p}\left[a(p_t) u(p_t) \right]
+
\frac{1}{2}\frac{\partial^2}{\partial p^2} \left[ p_t(1-p_t)u(p_t) \right]
$$
This basically implies that $V=p(1-p)$.
( I noticed that another way to prove this is to notice that the Wright-Fisher approximate diffusion (without any selections, etc... so $a\equiv 0$) has an infinitesimal generator given by: $ \mathfrak{G} f(p) = p(1-p)\partial_{tt} f(p) / 2 $. This immediately implies $V=p(1-p)$. But may be less straightforward to understand. )
Confusingly, however, the paper has changed timescales (variables), so that $\delta t \leftarrow \Delta t / (2N)$, and then set $\delta t$ to $1$ (probably so that they would not have to write $2N$ everywhere).
If we undo this transform, we get
$$ \mathbb{P}[p_{t+\delta t} \mid p_t] \approx \mathcal{N}(p_{t+\delta t}\mid p_t + a(p_t) \delta t,\, p_t (1-p_t) \delta t/(2N) ) $$
If you compare this to our approximate transition density above (equation (TD)), you will see that this implies: $$ \sigma^2 = V = p(1-p)/[2N] $$
as desired.
Now, what is the infinitesimal mean, i.e. $a$ or $M$? Clearly this depends on the selection model, since it controls how the "environment" deterministically affects the process. Kimura describes this as a "constant selection advantage" with coefficient $s$.
The Tataru paper notes that the diffusion approximation to Wright-Fisher under genetic drift, mutation, and selection is given by:
$$
a(p) = -\nu p + \xi(1-p) + 2N\tau p(1-p)[h-(1-2h)p]
$$
If we (1) ignore mutation by setting $\nu=\xi=0$, (2) remove allelic dominance effects by setting $h=1/2$, and (3) define $s:= N\tau$, we get:
$$
a(p) = s p(1-p) =: M
$$
which of course we see by noting $M=a(p)$ matches $\mu$ in the equation (TD) above. (Note that the $2N$ transform also occurred here, but it was hidden inside $s$).
Thus, we have derived where Kimura's $M$ and $V$ come from, albeit probably not in the simplest possible manner.
All that remains is to derive the (steady-state) equation for $u$. I guess I'll do it for completeness.
Ignoring the steady-state subscripts, we get:
\begin{align}
G(x) &= \exp\left( -\int \frac{2M}{V} dx \right)
     = \exp\left( -\int 4sN dx \right)
     = \exp\left( -4sNx\right) \\[0.15cm]
u(p) &= \frac{\displaystyle \int_0^p G(x) dx}{\displaystyle \int_0^1 G(x) dx}
     = \frac{\displaystyle \frac{1}{4Ns}\left[ \exp\left( -4sNx\right) \right]_0^p}{\displaystyle \frac{1}{4Ns}\left[ \exp\left( -4sNx\right)
\right]_0^1}
     = \frac{\displaystyle -\left[ \exp\left( -4sNp\right) - 1 \right]}{\displaystyle -\left[ \exp\left( -4sN\right) -1
\right]} \\
&= \frac{1 - \exp(-4Nsp)}{1 - \exp(-4Ns)}
\end{align}
as required.

Apologies for any errors. (I am neither a population dynamics modeler nor a mathematician, so please point out any problems).

Thank you very much. I don't really understand KBE very well. I remember reading about Fokker-Plank equation but I am not familiar with it in the context of diffusion. I have no background in SDE, so it may take me a while to understand.

@WYSIWYG No problem. The main idea I think is that the allele freq can be modeled by a differential eq with noise (SDE), which approximates Wright-Fisher, then the KBE falls out of that. Let me know if there's anything I can expand on.


text:
Regarding Passive Aritficial Immunity: Why does the concentration of the foreign antibodies decrease over time?
So, like suggested in question, I am extremely confused about this one concept. That whether or not the injection of foreign antibodies ( passive artificial immunity ) triggers an immune response.
From what I have learnt, the general idea is that the antibodies injected into humans, which may have been extracted from another animal or synthesized artificially using hybridoma cells, act as foreign antigens to the body and trigger the cells of the immune system such as neutrophils to engulf and destroy these antibodies and anything they are binded to it ( bacteria or viruses ).
But I was doing some CAIE past papers and got confused by a question and the answers provided in marking scheme;
Question:
"Two people took part in a study to find out the effectiveness of two types of immunization. Person A received an injection of antibodies against tetanus and person B received a tetanus vaccination.
Over the new few weeks the blood from these two people were analysed for the presence of antibodies to tetanus. The results are shown in figure 5.1A and 5.1B
(b) Explain why the antibody concentration in person A,
(I) decreased during the study period,
(II) did not increase. "
The graph provided is similar to that shown in https://i.stack.imgur.com/obZ8V.png except that the rise is not seen (instantaneous) and that the x axis is in days, and most IMPORTANTLY the graph depicts concentration of antibodies to tetanus (as injected earlier).
Now the marking scheme for this question has the following guidelines for marking:
" mark (I) and (II) togeather...
(I) antibody destroyed/broken down;
    antibody excreted;
(II) no antigen entered body;
     no immune response;
     no (active) B Cells/plasma cells/memory cells;
     no antibody made; "
Now, the reason I don't understand this is because it doesn't quite align with what I have learnt. Wouldn't a foreign antibody trigger an immune response causing the neutrophils to engulf and break the antibody down.
And wouldn't the reasoning for it not increasing be that it is simply an antibody that cannot produce copies of itself as it lacks the machinery and only injection was provided, followed by its removal by the immune system?
Even lets suppose if there was an immune response, why would the concentration of TETANUS antibodies, which were injected, increase?
This is on an AS (Advanced Subsidiary Level) for CAIE.
Please, if someone can explain this concept and the answer suggested by the marking scheme, I will be extremely grateful.

This is a very long question relating to an examination for which there is presumably a syllabus, nobody here is likely to be familiar with. We really prefer real questions people have encountered that have definite answers.


text:
Best colour for a dog to track an object against green background
As dogs have limited colour perception, what colour would appear with most contrast against a green background for a dog? I understand that red and green are very close in a dog's colour perception, so would blue offer better contrast?

Dogs are a dichromatic species, featuring only a long wavelength (L) and a short wavelength (S) cone (source: Smithsonian). As such, they are thought to perceive mainly blues and yellowish hues (Fig. 1). This is unlike trichromatic species like humans, who are able to distinguish red and greens as well (Fig. 2). Whether dogs perceive greens or yellows is hard to say, but either way, they see those longer wavelengths (red, green, yellow) as one hue (say, yellowish).
Hence, in dogs, green hues are basically seen as yellow (or vice versa) and indeed blue (short wavelengths) are best to create a good color contrast.
Of course, brightness contrast will work fine too (white and black).

Fig.1. Dichromatic (dog) color spectrum. source: Dog Vision

Fig. 2. Trichromatic (human) color spectrum. source: Dog Vision


text:
Why can a zygote develop into all different types of cell, whereas a differentiated cell cannot?
A cell formed by the fertilization between two gametes has all the DNA and can lead the development of a human person (or other animals in other species). But other cells in a human person has also all the DNA (like skin cells), yet they don't lead the development of organs, bones, etc. What is the difference between the zygote and cells from any part of the body from a developed person that one can lead to the development of a person and the others can't in spite of all of them have all the DNA? Does it have to do with the enviroment/surrounding those cells are in, is there any structural difference between the zygote and the other cells or how is it?

You may want to ask for basic sources/reading for embryology and development, since answering this question will require restating everything about cell differentiation. As it is it will be flagged as too broad becasue you are asking many different questions.

I disagree that answering this question requires anything as complicated as that; I think swbarnes has already answered the question sufficiently in just a few sentences.

Developmental biology is a huge field that we are still working on a lot.
DNA is only half the story.  The other half is gene expression; what subset of the DNA a cell is using at any time.  Your lung cells have the gene for insulin, but in lung cells, that gene is dormant.
The short answer is that in general, a mature cell is using the subset of its DNA that it needs to do its job and can't just change its gene expression to become a different kind of cell.   Cells that do become less like adult cells and less specialized can become cancerous.

The question in the title — too broad for SE Biology in my opinion — is "Why", not what happens. Saying genes get switched off in differentiated cells doesn't explain why, or why one cell becomes liver and another muscle. Better just to comment if this is all you have to say.

@David I don't think the OP was going for an existential "why" here: see the two questions that are the last two sentences of the OP. This answer, while simplified and missing other special attributes of a zygote, I think does answer those questions succinctly, especially the original title before you edited it which was directed toward the presence of the same overall DNA.


text:
What genes are the muscles, nerves, bones and blood?
I have a question about genes. The question is that bones, muscles, nerves and blood are each made on which genes. Father or mother genes? Does the person take any of the characteristics of the mother or father? Thank you.

The question is very unclear. I don't know either what you mean by mother and father gene. You are maybe referring to maternally vs paternally inherited chromosomes. Then, the answer would be both. You should just have a look to a intro to genetics.

Most genes case:
Let's state back what a gene is: it is a portion of the genome, numerous versions of a gene exists (called alleles). But one individual can only have two alleles in the same time (one from his mother and one from his father). So gene coding for nerve, muscles are present in both your mom and dad, and you will inherit of half of their allele (1 from each). There it is 50/50!
The exception
You maybe know women and men have a slight difference in genome: the sexual chromosome, men have XY and women XX. So the only case I could see a gene only inherited by your father would be that this particular gene is present on the Y chromosome.


text:
Minimum number of cycles for effective qPCR quantification?
I have been having an apparent problem with gDNA contamination in my no-reverse transcriptase (NRT) controls by the appearance of fluorescence peaks in my qPCR data.
I have/am trying multiple DNase treatments (Turbo DNase, Life Technologies) and RNA-clean up (Qiagen, RNeasy). The limiting factor I am worried about is that I am going to destroy all my available mRNA with multiple treatments/clean-ups.
My question is - can I lower the number of cycles I use to measure fluorescence? Is there an aspect that will go awry (in terms of the experiment itself to data analysis) if, let's say, I lower the number of cycles to 25-30? All of my contaminations start to appear within the range of roughly 30 cycles and above (as determined by the Ct values).
Please let me know if you need any other information that could help for an answer!
Best

Are your targets getting into the exponential phase above background before your contaminants are?


text:
What is this 2-3cm insect found in Slovakia?
Noted in the West Slovakia at the garden

You have with you a Carpenter bee, which are species of the genus Xylocopa  of the subfamily Xylocopinae
Xylocopa violacea, the violet carpenter bee, is the common European species of carpenter bee, and one of the largest bees in Europe. It is also native to Asia.

Here is a link to a youtube video documentary about the bees.


text:
Interesting Insect, possibly a beetle (Northern Indiana)
I happened across an interesting looking insect, that I've never seen before.  In Northern Indiana, late spring around 5 PM CST.  I tried a reverse image search, with no luck.  It is approximately 3/4 inch long.
Any ideas?

That is a carrion beetle. Family Silphidae, in the genus Necrophila
https://www.insectidentification.org/insect-description.asp?identification=American-Carrion-Beetle

Ugh.  After reading the linked page, I'm sorry I asked.  ;)


text:
Which comes first, PCR or Gel electrophoresis?
If I want to find out wither a group of patients have the abnormal BCR-ABL cancer gene, how do I benefit from the PCR and the gel electrophoresis techniques? I'm kinda lost trying to determine which comes first and what is the exact function of each device, I have read the whole gene cloning process in my biology book but couldn't absorb it because it's so complex.

PCR comes first. If PCR works right, then a specific product will be amplified. But you cannot see it in the little plastic Eppendorf PCR tube. That is what the electrophoresis is for. After you run PCR, you run the products on an agarose gel to visualize it (with the help of some flourescent dye). The agarose gel is just to see if the PCR worked.


text:
Can someone tell me what kind of reptile is this?

It was found in El Paso Texas. It was very scared and weak when I found it. But I bought it a small aquarium and some food to make sure it’s ok before I let it go. It’s tail is broken off. It have blue and yellow dots on top of it and I think it’s a male. Can someone tell me about this lizard?

Yeah, I agree that it looks like a Fence Lizard.  The "scared and weak" is almost certainly related to the missing tail - indications that it had a close encounter with a predator like a house cat or maybe a bird.

My guess is that you have in your a hand a lizard of the Genus Sceloporus , and perhaps Sceloporus occidentalis longipes.
Commonly called the Great Basin fence lizard is a subspecies of the western fence lizard . It is genrally found in the western part of North America

Here is  a link to a guide of small spiny lizards .


text:
Which blood craving bug is this?
While sleeping in a Tajik homestay these guys have been feasting on my blood and left (they didn't bother to hang around in my skin). The bite marks are pretty nasty, this one is 5 days old. Locals say they come out of the ceiling, that it is normal and we shouldn't worry. Are they right? (https://i.stack.imgur.com/slA9L.jpg)
Bite mark (https://i.stack.imgur.com/Mx33E.jpg)

Those are ticks. You should check the internet for tick-bourne diseases in Tajik.

Hi Arjan! Those do look like ticks, as @KarlKjer said. I'm in America, so I can't say for sure if you should worry, but there are vector-borne diseases in Tajik, some of which are from ticks.  I strongly recommend having a doctor look at that bite, just in case. If possible, bring a bug or two with you. The doctor can identify it and test it for disease if they feel it's necessary. Hopefully the locals are right and it's just uncomfortable.

Thanks! We have contacted a doctor and were recommended to wait and contact again when we develop fever. After 6 days we are still allright. We only took pictures and threw them away but we should have collected them in a jar or so...  good idea for next time (but hopefully there will be none).

Some sort of soft tick, as you've already heard.  Here's a paper on tick-transmitted diseases in the are, for your amusement..  https://www.acq.osd.mil/eie/afpmb/docs/dveps/tajikistan.pdf


text:
How is each region of the DNA replicated only once?
In "Molecular Biology of THE CELL" 3rd Edition, 1994, by Alberts, Et al. (Yes I know there is a newer edition)
the question is posed on page 362

How is each region of the DNA replicated only once?

Two suggestions are offered:

Inhibitor-addition model
Initiation-removal model

Since the 3rd edition of the book is now 24 years old, has the answer been discovered and if so what is it?
I am reading the 3rd edition now because that is what I have and plan to buy the newer 6th edition if a 7th edition will not be out in the next few months. This is for self-study so no need for me to rush or have the latest and greatest info for the first pass of learning as I am only reading.

Replication licensing: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688777/#!po=24.2574

Of interest: Cell Cycle

DNA Replication ensures it only occurs once by the use of licensing factors. These factors are released and bind to the origins of replication during one distinct phase. After the factors have been released and the first phase has ended, the actual replication initiates.
Information on the licensing factors:
The licensing factors used to create the pre-replication complex is the Minichromosome Maintenance (Mcm2-7) protein, Cdc6, and Cdt1. The Cdc6 and Cdt1 are required to load the Mcm’s onto the DNA and therefore, are highly controlled during the cell cycle. The Mcm2-7 hexamer is the actual DNA helicase that is used during DNA replication.
The way that the re-replication of DNA is prevented is that when the DNA replication starts, the Mcm helicase moves away from the ORC and the newly replicated DNA, meaning it then cannot be reinitiated. Along with the physical moving of the helicase, Cdt1’s activity is suppressed by the protein Geminin, which prevents the licensing of the helicase during times of non-replication.
Image from the article on the licensing.

More information on this topic:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688777/#!po=21.8085