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Does the lung absorb organic food?
Imagine you swallow something up and not everything gets out of the windpipe (this is possible right?).
Would it be possible for the lung to handle with the rest implying that it is organic? Would it slowing absorb it?

I'd suspect that the bacteria in your lungs would end up with a feast, you'd end up with a major or minor lung infection and hopefully, once the food is gone, the bacteria will go back to their normal population levels and everything will be hunky-dory. Or you could die.

Not well - see aspiration pneumonia - small amounts of food would be dealt with without too much problem, simply being coughed up.  Lung tissue isn't designed to digest or absorb so I can't imagine it being anywhere near effective in this regard

It would also absorb inorganic food by the way, salt for example.

When we eat the architecture makes sure most if not all the food ends up in our foodpipe rather than our windpipe. This is aided by a structure called the epiglottis.
However frequently foods may be inhaled, for example if a drink is sucked through a straw more if it gets into the lungs compared to if we drink it. Occasionally we will inhale a peanut or something else which typically occurs due to abnormal relaxation or muscular problems in the structures involved. This may be due to a neurological disease (e.g. myasthenia gravis) or because simply drinking too much and inhaling peanuts or vomit (aspiration).
If the inhaled substance is small and lipid soluble e.g. alcohol, it can pass through the alveoli at the end of the lung to the rich blood supply. If it doesn't we rely on macrophages to digest the food. They aren't frequent enough to digest anything substantial. Bacteria however are great at munching this up and increase substantially in number. Typically your lowest airways are sterile but food can interfere with clearance mechanisms and provide a home. The part of the lung blocked (distal to the foreign object) can collapse and frequently does. In the long run this may cause bronchiectasis, where an infection recurrently affects the area due to permanent damage done during the initial event resulting in widened airways and an ongoing inflammatory response. The inflammatory response reveals even more receptors for bacteria to latch on to.


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What is the function of PCR in the whole genome sequencing?
Whole genome sequencing (WGS) method is using PCR in one of their steps. In the following page from the CDC, we find this diagram:
It says that the PCR is needed to "make copies of each DNA" but it does not explain specifically why this is needed. Indeed it seems to be clear it is done in order to enlarge the DNA we are after in the sample thus apparently providing easier analyses (at least that was my first thought).
As fat as I understand, PCR in WGS has some disadvantages in this that it is considered "biased" in the sense the target for amplification should be given in advanced, and also this uneven  amplification might result in false positive.
But then there are some "PCR-free" WGS. I tried to understand how having "PCR-free" WGS is even possible? isn't the PCR/step mandatory? if it is not mandatory and better results can be obtained without it, why to include it in the first place?

PCR is used to replicate each isolated genome fragment, yielding several copies of each fragment in your DNA solution (that‘s called a library = a collection of fragments + adapters).
This amplifies the signal of each isolated fragment, since each fragment will be sequenced multiple times. So you get multiple sequence results (called reads) per isolated fragment.
Years ago, the sequencing quality was far worse. You had to amplify the library, so that you can later confidently re-assemble all the sequences of every fragment into one big genome  (fragmentation is necessary, since the sequencing reaction can abort mid-sequence; Shorter sequences are far easier to handle). Also, starts and ends of each read are hard to sequence correctly. Having multiple reads per isolated fragment greatly helps with compensating for sequencing errors.
Also, WGS aims to identify single nucleotide polymorphisms, which can be sequenced more confidently using PCR.
HOWEVER, PCR-free methods seem to have circumvented these problems and have improved so much that they even yield better sequence quality when compared to PCR-dependent protocols Zhou et al. 2022.
I presume that PCR  can be problematic with WGS, because PCR might have trouble with reliably amplifying repetitive sequences, yielding erroneous results.
I also presume that the "PCR-bias" weighs more heavily on RNAseq than on WGS (which is why people talk about PCR-bias in the first place). RNA-seq often aims to quantify the copy number of each transcript, so the sequence itself is less important with RNAseq. However, PCR amplifies different transcripts more efficiently than others, leading to non-linear relations across the read-counts of all transcripts. Still, PCR is essential to RNAseq so that low-copy number transcripts aren't missed. Modern RNAseq technologies use UMIs (unique molecular identifiers) to correct for non-linearities.

Thanks. unfortunately I am not versed in this world, so not sure I fully understand answer. Do you say there is a trade-off between PCR-free and PCR WGS? As each would be a better fit for another use case?

If I understood correctly, there was a trade-off once upon a time.
Now there isn‘t anymore. Still, I might miss some usecases, where PCR is still needed. Please let me know which terms give you trouble and I‘ll gladly explain and further edit my answer

source: Stack Exchange

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Bolete (?) mushroom identification
I'm attempting to identify a gorgeous set of mushrooms.  I'm not anything resembling a mycologist, and I have no intention on consuming these... But for my own curiosity, I'm trying to identify these striking mushrooms.
Some notes:

These mushrooms were found directly under a red oak tree, in central New Hampshire, near Lake Winnipesaukee
The mushrooms were found this morning, on August 2nd
The largest cap was about 6 inches in diameter
The pore surface bruised rapidly (10s of seconds) to a blackish blue, even when lightly bruised.  Harder pressure bruised nearly instantly.
The cap flesh, though, did not.  You can see a slightly more-yellow streak where I rubbed the cap pretty hard.  Even after several minutes, no bruising appeared.
The stipe similarly did not bruise.  In fact, it was quite solid.
When cut in half, no bruising was apparent, even after several minutes (when the picture was taken)

Digging around, I thought maybe it was B. Bicolor, but the cracked appearance of the cap doesn't match basically any photos I can find.  It's not as bruisable as B. sensibilus.
Can anyone help me identify this?  I can run further tests as well.

For even more precision, make a spore print overnight and photograph.

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How does Anabantoideis' labyrinth function? What does it look like?
Anabantoideis are fish with an organ that allows them to take oxygen directly from the air outside of water. However, I cannot find much on how this functions, nor can I find any clear image of what it looks like. Those I do find seems to contradict one another.

This image shows what looks like a bubble flowing into a hollow hole.

This image shows something very different, a mess of flesh, presumably where oxygen is absorbed and expelled from the gills.

This image shows a mess of flesh like before but more similar to intestines, but disconnected to the gills.
What images are most accurate, and how does the labyrinth function?

Welcome to Biology.SE. Have you tried doing an image search and looking for actual images rather than diagrams? ——— You are likely to get a better response if you [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please also take the [tour] and consult the [help] starting with [ask] for details.

@tyersome Yes, I've looked for actual images, but they are even less helpful, usually only showing external anatomy and never the real labyrinth itself.


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can self-fertilization in flowers be called asexual reproduction?
Suppose a flower having both male and female reproductive parts is self-fertilized then can this be called asexual reproduction...?I'm quite confused cause in this case the fusion of male and female gametes do take place but again the gametes are from the same parent....please help.

I'd be interested in your reasoning why some common and known definition that seems to fit still doesn't. What makes you think "sexual" reproduction needs two, not one?

"... from the same parent"... that must stay the same and may not change, may not exchange genes while alife or staying the same... The fact that "mitosis" is not confined to diploid people I find confusing.   It is no trivial thing (to me) to "learn" that it just does not seem to make sense to duplicate some "haplo" in order to exchange genetic information that has got to be identical. Related answer pointing at proof reading as an underlying motif.  What's the sense of exchange if there is some identical copy that 's  being exchanged with.

According to this article from Berkeley, asexual reproduction is:

Any reproductive process that does not involve meiosis or syngamy

Using this definition of asexual reproduction and knowing self-fertilization involves meiosis and syngamy, it is not asexual.

Is there a strict definition of meiosis? If there were no crossing over or mingling  of genes that would still be meiosis? - So only diploids can have sex?


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Can Anyone Tell Me , Which Insect or I think Moth Is This

Region : Asia ( India ) , Size is about : 4 cm . Since yesterday this Insect is in the same place . I don't know any other info , I was just curious to know about this Insect.

This is not a fly! Can you give more information about this individual? Where (what region, what country, what type of ecosystem) did you find it? What is the approximate size? Any behaviour to notice? Did you get a picture where we can see its butt? Any other info?

But it is deffinitly look interesting.

Region : Asia ( India ) , Size is about : 4 cm , Since yesterday this Insect is in the same place . I don't know any other info , I was just curious to know about this Insect.


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Worm in water identification help
I live in Auckland New Zealand. I have been growing Chia seeds in bowls with just water. I noticed after a couple of weeks, these white / transparent worms appeared in the bowl. It seemed that they came out of nowhere? I have seen them crawling in my bathroom before. And the really big ones can get up to a 2-3 cm, so they can't possibly be drain fly larvae as they can grow to a few cm? I also did not see any drain flies nearby. I wonder what type of worm are they? I hope they don't come from tape water, because I have been drinking from it directly.

[EDIT] - Photo of the worm in bigger size (~1.5cm):

Are you sure they're worms? They look like sprouts, either roots or stems.

They look like mosquito larvae, but it is quite hard to be sure: They are so tiny.

Agree with @Astrolamb they are sprout of green grams

@Astrolamb They are moving around!

@bli They are tiny now - but they are growing. I have seen 3cm big ones.

@Astrolamb Yes there are stems and roots in the photo. The other smaller ones are the worms. They are moving and crawling in the water. They can crawl out of water as well. Amphibious?

@JerryH Try to add photos of the larger ones.

@bli - 1.5cm one

In the end, I don't think this looks like a mosquito larva.

They won't be from the tap water, unless you have had something lay eggs in the tap nozzle itself; NZ has high standards of water quality for municipal water and tap water is safe to drink throughout NZ.


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Help to identify a odd skull
I found this skull in the woods, I came across an old stable that the roof was falling in. In the corner there was tree limbs stacked neatly as if something stacked them and the limbs were no bigger than a broomstick. The skull was laying on top of the ground not far from the neatly piled limbs.
I have google photo searched it in several different angles and found nothing similar.
I am at a loss as to what type of animal this could be. It is just very oddly Proportioned.
It does not resemble anything I have reached. Please help I identifying this skull.

I live in oklahoma by the way

Welcome to the Outdoors SE. If you could provide photos for other angles and higher resolution for each, that would help with ID. You could also request migration to the Biology SE, which has ID tags too.

Also, would need some sense of scale - is this 2 inches or two feet long; can't tell from the photo.

It is 6 to 8 inches long

Very hard to say from the shape it is in.
Some observations:

The molars suggest it's a herbivore, the teeth look similar to what I know from the skulls of sheep/goats/roe/deer/...
Seems to have no signs of horns or antlers.
From the size I would say it is about the size of a roe/sheep/goat.

My best guess:
Since roe deer only live in Eurasia and not Oklahoma US I'd figure this skull could be from a small (young?) female deer or similar, or - if livestock is more likely - a variant of goat or sheep without horns.

I think White tailed deer juvenile or doe. No sign of antlers, teeth look right (curved row rather than straight) and cranium is about right too.


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How well are we able to determine diet of an animal based on teeth?
Just by looking at teeth and jaws of extinct are we able to say what specifically species was eating? For example gray wolves eat mainly large herbivores like deer compared to red foxes who in addition to hunting eat fruits, eggs grain and other. But when I look at replica of grey wolf jaw and replica of red fox jaw I don't see many differences.
What other factors are taken in when determining diet besides direct observation?

Maybe a combined approach of jaw morphology + metagenomic analysis? We can tell an animal is a predator or not based on how the eyes are positioned, so maybe the big plus the subtle differences in jaw morphology and a genomic validation could shed light on your question. The accuracy is another story!

Pretty well.
you don't see many diffrences between wolves and foxes because there is not much diffrence in their diet. During the parts of the year where they are avialiable fruit makes up a majority of a wolfs diet. the trick is that is only a small part of the year. Somthing like a encyclopedia is only going to give you a breif overview not a detailed breakdown of an animals diet.
More detailed source
for instance we can see a shift in diet to more grain in early dogs due both to dental anatomy and genetics (digestive enzymes) https://www.jstor.org/stable/29775234
https://www.sciencedirect.com/science/article/abs/pii/0305440392900499
The biggest limitation is for teeth that don't match any living animal, this can be much more difficult, we see this is some dinosaur groups. Although you can still say, primary herbivore, primarily carnivore, or the like. you also combine teeth and jaw morphology with the rest of the anatomy. For instance the neck anatomy (specificaly the size and shape of the supporting nuchal ligment) can tell you whether an herbivore is primarily a ground feeder or a browser. This matches what we see in living antelope so again living animals are the  best measure.

I didn't know that wolves have similar diet, so far on internet I've only seen articles talking about wolves eating meat and no mention of fruits etc.
(And the first link says Access Denied)

@Graphenjoyer the problem you have is the word "articles", not great sources for detailed science. I suggest searching google scholar. but here are a few more sources. https://wildlife.onlinelibrary.wiley.com/doi/10.1002/wsb.1065 and https://rcin.org.pl/ibs/dlibra/publication/27793?tab=1&language=en obligate carnivores are extrememly rare.

@Graphenjoyer Dont feel bad even searching papers can be confusing since a paper about prey selection may barely mention plant matter if they include it at all even when talking about diet. wplves eating berries is not sexy enough to make it into common articles with only a few exceptions and then only for the shock value , https://wildlife.org/wsb-blueberries-surprisingly-important-in-wolf-diet/

wikipedia is a rare exception and can be a good start. https://en.wikipedia.org/wiki/Wolf


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Glucose to Glucose-6-phosphate
What does actually occur- ATP is hydrolysed and esterification between glucose and HPO4^2- (formed as a result of hydrolysis) take place to form Glucose-6-phosphate or nucleophilic attack of O- of glucose on ATP leads to formation of ADP and Glucose-6-phosphate?

I think since this is about chemical reaction mechanisms, it will be better suited at chemistry.stackexchange.

Duplicate of http://biology.stackexchange.com/q/10938/3340

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Can an enzyme be activated without allosteric inhibition or activation?
Are there ways by which an enzyme may be activated or inhibited by non substrate molecules other than allosteric activation or inhibition?

Apart from what Phototroph mentioned in their answer (competitive and non-competitive inhibition), an enzyme can be activated/inhibited via covalent modification of the protein (post-translational modification) such as phosphorylation by protein kinases (phosphorylation is the most common modification).

Yes, competitive inhibition is another form of enzyme inhibition. The inhibitor binds to the active site here, as opposed to allosteric inhibition, where it binds to a secondary site. An example of an inhibitor would be the cyanide ion (CN-), which inhibits Cytochrome C oxidase, preventing electron chain transport and thus ATP production. Note this ion is different from the substrate, oxygen.

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Why are the organs for reproduction and urinary excretion combined?
We eat food for getting energy to our body parts, and we excrete the wastes through urine, feces, and perspiration.
Why has nature combined the urinary tract with the genital system (urogenital system) in humans?

they really don't. Only overlap, i guess, is in urethra

I edited your question to remove textual ambiguities.

I think this is a question open for much debate, but part of the answer may be that sharing functions reduces anatomical complexity. In other words, adding functions to existing structures is one of the essences of evolution; complexity through parsimony.

@AliceD thanks for editing the question the right way and properly.

Actually it is there in all mammals (in fact most vertebrates), not just humans afaik. It is better to not limit the question to just humans. Related post.

It is surprising that "urogenital system evolution" is not giving any decent hit in google scholar!!!

@WYSIWYG Can't it be considered as nature's mistake
of combining truly liked and truly disliked
things (of most humans) together?

@AliceD  Can't it be considered as nature's mistake
of combining truly liked and truly disliked
things (of most humans) together?

@AliceD sir,I think no one will love to eat food in the toilet room

@sagar "nature" doesn't make mistakes, because there is no conscious thought involved. Evolution produces changes in DNA that accumulate over time and lead to new phenotypes. Those phenotypes either give a reproductive advantage, a disadvantage, or are neutral. These either allow a population to survive/flourish in a particular ecological niche, or not. Generally, traits that negatively impact a population's likelihood of survival are selected against, and tend to disappear over time. Since this combination you are interested in is widely spread across species, it likely confers an advantage.

Don't use terms like "nature's mistake" and all. I rolled back the title edit.

Developmentally, the urinary and genital systems (typically you will hear them referred to as "urogenital system") are derived from the same embryonic tissue, the intermediate mesoderm. The embryonic kidneys are drained by the mesonephric duct in both females and males. This embryonic tissue also gives rise to the ovaries and testes. The mesonephric duct degenerates in females, and becomes the ductus deferens in males. A second tube, the paramesonephric duct develops in both, but degenerates in males. The female paramesonephric duct becomes the uterine (Fallopian) tube.
Embryonically, the ureter, which drains the adult kidney is connected to the mesonephric duct. This connection is maintained in males, so that both urine and semen share a tube (urethra) for some of their exit pathway. In females, the paramesonephric duct and urethra are separate, so there are two openings.
In males, sphincter muscles and autonomic control prevent the simultaneous expulsion of urine and semen.

This system has worked acceptably well in mammals for at least about 200 million years (and in humans for the last 4 million or so), so I think it's not correct to call it a mistake. It's not how you would consciously design such a system, but evolution doesn't have a conscious designer.
Here are some slides that cover the embryology of the human urogenital system.

Excellent answer, well done!

Evolution has no conscious designer?? What about the great architect?

I would just modify the excellent previous by pointing out that the embryology describes a local maxima of fitness whose barrier to change is higher than any selective pressure.  The re-use of the "logic" of the intermediate mesoderm was either initially a bifurcation from one or the other, or, was of enough selective advantage to have the two developmental processes and the resultant physical systems folded together.

Can you please make your answer clearer? I don't understand what you try to say.

Any relatively stable developmental process has some selective advantage, but is not necessarily the best - like if you could only walk upward, and you had to pick a hill to climb.  You might not end up on the highest peak.
Embryonic processes are often "hijacked" for other purposes, through mutation and selection
It's possible that these two functions were at one time separate, separate "hills", but again through mutation and selection, merged embryonically.

@Abram You can just edit your answer to include more information.

kmm gives what is likely the best possible answer, as it is argued from causality rather than teleology. As my ninth grade biology teacher used to say, "there is no 'why' in biology, only 'how'".
On the other hand, it is fun to speculate! Here's my two cents in the form of a Bad ad hoc Hypothesis:

Holes going into the body are an expensive and risky prospect at best for any animal. In order to maintain homeostasis they need to keep any holes constantly supplied with fresh mucus and a ton of antibodies. Total orifice count tends to be kept to a highly conserved minimum along evolutionary lineages. Thus, the reason why urinary and genital systems are merged along a single urogential tract is so that they can both efficiently share the same hole. As evidence for this view, consider the reptile: they manage to use their holes even more efficiently than we do, mating and excreting both liquid and solid waste out of their single cloaca.

I think the orifice count reduction that led to eating and talking at the same time out of the same hole was a mistake.


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Comparing the amount of domestic animals and wild animals?
From some material, I read about the ammonia (NH3) emission from animal waste.
I found that the emission from domestic animals are greater than wild animals.
Then, I can't help wondering the amount of wild animals and domestic animals(cow, pig, chicken, etc). Which has the greater amount on Earth? And how to estimate the amount approximately?

You may find this interesting: https://xkcd.com/1338/

Can you please link and cite your source? That would definitely help.

The comparing of NH3 emission was from a textbook named Atmospheric Science by Hobbs.Link

And how to estimate the amount approximately?

You cannot. Most of the earth is water, and fauna diversity is highest in water. We are still tagging and tracking the movement and reproduction cycles of animals, and that is a never ending task. I say we cannot reach an accurate approximation because of how these projects work. They are targeted towards the monitoring of specific species. Next, different countries have different approaches towards conservation of the same species, and above all this many countries choose not to report numbers. The example which comes to mind is the Red panda. As many animals come inside the radar of active conservation efforts, even more remain outside it.
In fact, some time ago I read a compelling article about why the WWF should change their logo to a Red panda (or known as the lesser panda) rather than the giant panda, the argument being that awareness about the giant panda is very high while red pandas are still misunderstood as pandas. Unfortunately I cannot find that article now, but you can visit the red panda network to find out more.

Which has the greater amount on Earth?

Second, what do you consider as a wild animal? are insects included? are gutter rats included? Is the infestation of wild boars near the now defunct Fukushima plant included? If yes then they outnumber domesticated animals by a long shot. I would dare to say that cities are habitats more for members belonging to Animalia but not belonging to Homo.


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Is there a better lysis buffer than this for fungal DNA extraction?
I've being using this lysis buffer for fungal DNA extraction,lysis buffer - 400mM TRis-HCl(pH8.0), 60mM EDTA(pH8.0), 150mM NaCl, 1% SDS and containing 40microgram/ml RnaseA.
It is keep giving very light bands on 1% agarose gel and shear appearence. After extraction I have to follow PCR and sequencing. If there are inhibitors, how can I get rid of those ?

Do you Fungi contain pigment, especially melanin? This is a potent inhibitor for PCR. If not, you could start by trying a phenol/chloroform extraction.

yeah they have pigments,one sample was a penicillium,  i did PCR for these DNA extractions (didn't make any changes to the lysis buffer) but I got good bands after PCR,my primers were ITS1 and ITS4. But I didn't get PCR results for extractions I did more than 4 days ago. thank you for the answer.


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Does chromosome cross occur over male and female or vice versa?
My understanding is homologous chromosome pair, which means male and female chromosome inside the DNA. So if that's homologous how does male do with female? Does it flip over and change direction, that could not happen as male chromosome 1 (say) is indistinguishable from female?
And what about the XY chromosome in male,say?
I know some are pseudoautosomal, but most are normal sex chromosome nucleotides.
So what about them?

The question is unclear to me but hopefully that will help a little bit.

My understanding is homologous chromosome pair, which means male and female chromosome

There is no male and female chromosome. Chromosomes have no sex. In humans, to the exception of chromosome Y all chromosome can be found in individuals of any sex.
There are paternally inherited chromosomes and maternally inherited chromosomes though. As you said the maternally inherited chromosome is indistinguishable from the paternally inherited chromosome when comparing their sequence (they may well differ in terms of epigenetic changes).

chromosome inside the DNA.

A chromosome is not inside the DNA. DNA is the name of the very long molecule from which a chromosome is (mainly) made of. DNA can be organized in different forms one of which is into chromosomes (another one would be a plasmid for example). While it would still sound funny, it is more correct to talk about DNA inside a chromosome than talking about chromosome inside DNA.

So if that's homologous how does male do with female?

This is very unclear...do what? Why would the paternally inherited chromosome (assuming this is what you mean by male chromosome) do anything with the maternally inherited chromosome rather than the other way around? While it is clear from the what follows that you would like to talk about recombination, I don't get where you're heading.

does it flip over and change direction, that could not happen as male chromosome 1(say) is indistinguishable from female?

I don't get what kind of "flip" you are thinking about. You probably should have a look at the wikipedia article for cross-over.
In short, synapsis are formed during prophase I of meiosis and when segregation happen synapsis are resolved with a probability of $\frac{1}{2}$ of causing a recombination event. Synapsis occur as they allow matching pairs of homologous chromosomes together that will ensure their separation during anaphase 1. You should probably take some time to review the meaning of this paragraph.

And what about the XY chromosome in male,say?

Sorry, that's a bit unclear too.

I know some are pseudoautosomal, but most are normal sex chromosome nucleotides. So what about them?

Sounds like you misunderstand what a sex chromosome is and what pseudoautosomal mean.
In short, in humans, there is only one pair of sex chromosomes (XX or XY depending on the sex). The other 22 pairs of chromosomes are autosomes. There is no such thing as a pseudo-autosomal chromosome in humans but there is a pseudo-autosomal region on the Y-chromosome.
Most of the Y chromosome never recombine (while the X chromosome recombine in females only) as it is never present with another Y chromosome in the same cell. There is only a short sequence on top of the Y chromosome that recombines with the X chromosome, this region is called the pseudo-autosomal region. This region probably still exist to allow separation of X and Y chromosomes during anaphase I.

Please also note that you seem very focus on humans (without saying it and maybe without realizing it). The diversity of sex-determination is huge. You might want to have a look at Do males of all sexual species have Y chromosomes?

There is a difference between the processes of meioses and mitoses. Meiosis typically leads to 23 chromosomes in a new cell while mitoses typically leads to 46 chromosomes in a new cell. Because every normal human being must have 46 chromosomes, you need to get 23 from your father and 23 from your mother. Meiosis creates cells that are necessary for humans to procreate. Mitosis creates cells that help an individual grow.
Almost every cell in your body has its own 46 chromosomes. Red blood cells, for example, are cells that don't have chromosomes. When a cell has 23 chromosomes it is called a haploid cell, and when it has twice that much it's called a diploid cell.
Chromosomes are not specific to a gender. The sex chromosomes only confer gender depending on whether you get one copy of each of X and Y, or two copies of the X chromosome. So you could have a man passing 23 genes to his daughter and then the daughter passes some of those chromosomes ,after genetic recombination, to her son or daughter. It doesn't matter. The separation is more or less random.
During genetic recombination the homologous chromosomes cross-over by DNA strands being cut by biomolecule processes. The image of this process is called a Holliday junction. So they do flip over and change direction, but they are only strands (aka strings) of DNA.


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Chimera in bacteria
Would you please define me the chimera in bacteria? Some sequences are clustered as a chimera table in metagenomics analysis, I know OTU table is used for clustering bacteria based on 16S rRNA, but I cannot find out the chimera? What is the difference between chimera and OTU table exactly?


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How the size of ribosomes are calculated?
When I was studying microbiology, something didn't make sense to me. We all know ribosomes have two subunits; the large subunit and the small subunit. Such as for eukaryotic cells, the large subunit has 60 S (svedberg) and  small subunit has 40 S. When they combine with each other they are considered as 80 S. Why it is 80 S instead 100 S?

Because Svedberg is not a measure of weight, but it is a measure of a relative sedimentation after centrifugation.
"It is defined as the ratio of a particle's sedimentation velocity to the acceleration that is applied to it (causing the sedimentation)."
The high number of S are correlated to the shape of the particles as well.
https://en.wikipedia.org/wiki/Sedimentation_coefficient

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Can there be forced evolution
Can we force a species to evolve through a mixture of natural and artificial selection in a closed environment?

Maybe pose a more specific scenario and we can suggest whether this would be feasible experimentally.  Purely artificial selection, as was used to generate basically all of the food we eat, for example, is definitely a form of forced evolution but it happened in a somewhat-poorly controlled environment (a farm over a long period of time, in the case of plant or animal breeding).

Exactly what are you asking? Artificial selection clearly exists, as does the combined effects of natural and artificial selection. How does "forced evolution" different from this?

I don't think this question shows much research effort on the part of the OP. The OP acknowledges the existence of Artificial Selection so has even answered their own query surely?

Selection (whether natural or artificial) is one of the force causing evolution. So yes, artificial selection is one way to 'force' evolution to happen in a specific way. One could select trees for bigger fruits or dogs for longer fur for example. One cannot force "Natural Selection", as "forced natural selection" is defined as "artificial selection".
You might want to have a look at an intro to evolutionary biology such as Understanding Evolution by UC Berkeley for example

In addition to what others have replied, perhaps what you're referring to is speciation, i.e. can you force a species to evolve into a new one that is a distinct species from the original one? I'd say yes, but if you wanted to be quick about it then you'd have to choose an organism with a very short generation time, subject them to different selective pressures than the original population are subjected to and prevent the two populations from mixing and interbreeding. I guess you could say a new species had evolved when they can no longer produce viable offspring with the original population. Might take a while though. In fact maybe this would work better/be quicker with an asexual organism but it would be more difficult to identify the point at which a new species had evolved.

Yes, we can. One example is pushing bacteria to evolve antibiotic resistance by putting them under artificial selective pressure, i.e. adding antibiotics in the medium.
You can find it here http://gizmodo.com/watch-as-bacteria-evolve-antibiotic-resistance-in-a-gig-1786389688


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Inheritance patterns in individuals with triploidy
If you search on the genetics of Down's Syndrome, you'll find plenty of results explaining the genetic mechanisms which can result in triploidy. However, I can't find any information on the inheritance combinations of triploidy - i.e. what are the possible genetic outcomes in the event that an individual with triploidy should reproduce.
It might seem unlikely, which is presumably why it's glossed over. However, I'm just curious about it from an academic standpoint.
So: how does one calculate the inheritance probabilities for a trait associated with triploidy, and what are the outcomes?

Triploids are characteristically sterile, but people with Down's Syndrome aren't triploid(they're anueploid technically). There's only one chromosome duplicated, and it's the smallest one. Women with Down's can have kids just fine, but men tend to be sterile(according to WebMD at least).
See here for a full coverage of triploid genetics and why triploids are nearly always sterile. In short: gametes formed during meiosis pair off but there's always one copy of each chromosome that chooses a daughter cell at random. If one daughter cell gets none of the extra copies, you have a haploid gamete and a diploid zygote and everything goes according to plan. If one daughter cell gets all of the copies you have a diploid gamete and you'll have a triploid zygote and everything will be fine-ish, but you'll have another triploid generation.
Statistically this happens for 2(1 for females with asymmetric gametes, but let's fudge it a little) of the possible sorting patterns, of which there are 2^n where n is the number of chromosomes. For a triploid human male(bear with me) mating with a diploid female(the best possible combination mathematically) instead of the more typical 200 million viable sperm he would produce about 50 viable sperm(About 2 in 8 million sperm have a chance.). If you account for 23-triploidy that number goes up to about 100, but that's still worse than a millionth of the fertility.
Other combinations are vastly worse. A human female only has about 2 million eggs lifetime total, so even in the best of circumstances a triploid female has maybe a fifty fifty shot at having a single viable egg in her entire life. The calculation for the probability of a two triploid humans(or any n=23 organism) breeding successfully is left as an exercise for the reader but it's very low indeed.
If you were working in some other organism with maybe n=2 chromosomes the numbers would be more forgiving and it might be worth thinking about making Punnet squares. They'd work much like Punnet squares for diploid creatures, but the sides would be a little longer to accommodate the larger number of gamete genotypes, and you'd have to adjust the probability of some of the squares to account for aneuploidy-related fatalities and other weirdness. For instance, with two triploid parents the probability of getting a successful triploid zygote from any random pair of zygotes is something like 1/2^n instead of the 4/2^2n or whatever it is for diploid or quadruploid offspring. This is counterbalanced by aneuploid gametes perhaps dying(or even being slightly less fit).
If n=1 the math is more tractable, however(surprisingly, this exists. haplodiploidy complicates triploidy considerations so I'm pretending it doesn't exist). Examples like AAaxAa give strange results(only 1/12 are recessively phenotyped) but AaaxAa produces 1/4 recessive phenotypes and 3/4 dominant ones, just like AaxAa.
In sum, I see why triploids are just declared infertile and not dealt with in the fullest, most complex sense.


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What's the fastest legal way for the nutrients in a dead body to re-enter the ecosystem?
Apologies for weirdness.
Of the various legal methods of disposing of a human corpse, which one ensures the nutrients which compose the body get back into the wider ecosystem the fastest?
Unless I've overlooked something (which is likely) the answer would seem to boil down to:

Burial, in which case soil microbes have relatively free access to the body but will initially restrict their nutrients to the sub-soil ecosystem.
Cremation, in which case most of the nutrients are converted into heat and light energy by the furnace, although this energy, and the remaining nutrients, are then made available to the wider environment much more rapidly.

In terms of cremation: Which remaining nutrients?

No idea. I presumed that not everything in the human body was easily oxidized?

Well, we are talking about 60-90 min (if I remember correctly) at temperatures of 900°C. There nothing carbon based will survive. The remains are basically the mineral parts of the body.

Perhaps you can remove the word "legal" from the question. I think there is no law on how to deal with a corpse. Even if there is one it will not be universal.

The Parsis and other Zoroastrians dispose of their dead in a so-called Tower of Silence, where the body is left on a raised platform to be eaten by scavengers, particularly birds such as vultures.
This is possibly (probably?) the quickest way for nutrients to re-enter the wider ecosystem, as scavengers usually work a whole lot quicker than microbes.
Tibetan tradition also contains a ritual known as the Sky Burial, which achieves the same sort of thing. The Tibetan version may be even quicker, as once the scavengers have stripped the body, the bones are ground into a paste along with flour and yak's milk/butter to be fed to a second round of scavenging birds.

Well, with cremation comes also a lot of harmful gasses entering the atmosphere as well, and from your question, I'm assuming you're interested in eco-friendly alternatives.
I've heard of organic embalming fluids, so it might be interesting to you to look into that. Also a lot of steel and cement go into a traditional burial; if you were to be buried in a plain pine box with no fancy coatings or finishings, that would certainly speed up decomposition. If you look at traditional Jewish burial customs, you may find a bit of what you're looking for.


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What are the benefits of statins in terms of prolonging life?
Recently the UK government suggested that all adults over the age of 50, without exception, would benefit from taking statins.
I have an elderly female relative who may, or may not have had a minor cardiac event (the diagnosis is still out) and low blood pressure. It has been suggested to them that they would benefit from statins and have asked me (a former biologist) to find out more.
I've had a look at the mechanisms of action, which seem clear. But the clinical data is somewhat confusing.
It seems we can state with certainty that a small but significant number of users report relatively minor side effects, and a very tiny minority have serious ones.
In term of the benefits, however, the picture is much less clear. I have found a variety of statistics about how they reduce cardiac events but what this translates to in terms of length of life and quality of life is not stated.
One article I looked at suggested that on average, someone at high risk of heart disease taking statins for 30 years would only live an extra 9 months.
The author of that site has a book to sell, and may have an axe to grind. But there are several other articles out there - such as this, and this and this - which make worrying claims about statins being both more unsafe and less beneficial than clinical trials suggest. In particular there seems very limited evidence of any benefits to women.
I am inclined to treat these as alarmist nonsense - they have that sense of hysteria about them. But given that the authors look legitimate, that clinical trials data do not appear to agree with one another (widely varying in the percentage of users reporting side effects, for example), and that this is a relative, I wanted to get a second opinion.
So - can someone please crunch the numbers and tell me what the benefits of statin use are in terms of life years and quality of life? Is there any benefit for women with or without heart disease? And is there any basis to some of the alarmism around their use?

I suspect I won't be crunching as much numbers as you'd want me to, however here are some basic points:

Statins have shown a clear ability to improve the blood llipid profile.
Their use in primary/secondary prevention for cardiac events is justified by the belief that less blood lipid will leave less lipids to clog the arteries with. This is an old paradigm, and it is debated, even if we nowadays indeed give statins to all (potential) cardiac patients. There is evidence for a positive effect of those drugs, but it is not undisputable.
An enormous amount of money is made from statins, and the pharma pushes very hard for their use.
They do have undesirable effects, but those appear mostly early, so patients are usually well monitored for them and they mostly pose no real threat.

On the subject of women: women before menopause are protected from cardiac events by their hormone profile, and would therefore likely benefit very little from statins at that time. After menopause, women present the same cardiac risk as men do. I do not know if studies have shown a difference in outcome for statins in postmenopausal women. If you want to know more, I advise you to go searching for it on Pubmed
DISCLAIMER: The above does not represent professional medical advice, and is subject to debate.

Wouldn't this paper be helpful?https://www.tandfonline.com/doi/full/10.1080/17512433.2018.1519391


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distribution of some injected materials/medicines through blood vessels
Fastest distribution of some injected materials/medicines & with no risk of any kind can be achieved by injecting it into - artery or vein?

it depends on where you are injecting it or what is the target organ, etc. In general terms, it'll be artery because arterial blood flows with more pressure and venous blood has to be pumped before being circulated in the body.

It depends on what your target tissue is, as @another 'Homo sapien' stated.
If you want to get something to the hand, for instance, injecting it into the brachial artery will get it there "faster" than injecting it into the cephalic vein.
However,

Fastest distribution of some injected materials/medicines & with no risk of any kind

does not exist. There are risks with any invasive proceedure, and invading arteries is riskier than invading veins. Unless the risk outweighs the benefit, substances which cannot be administered orally are given intravenously. Arterial lines are usually used for purposes other than injecting substances.
Arterial Line Placement


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Are there animals that are present in two different classes?
Are there animals that are present in two different classes, like amphibian and bird, reptile and mammal etc.?

Like mammals also being vertebrates?

@WYSIWYG FOR EXAMPLE frog is an amphibian and a mammal (this is not correct it's just an EXAMPLE)..Are there animals present in two different classes?

@WYSIWYG Wouldn't taxonomist propose a new class if some species (somehow) showed characteristics of 2 close classes?

Short answer: No. Taxonomy is about categorizing and an organism cannot be placed to different taxa.

@WYSIWYG Mammals are a class, vertebrates compose a subphylum.

An organism is not placed into two classes, an amphibia is very different from a mammal. During classification the characters of an organism are considered before it is placed in a particular taxon. You may read ncert class XI biology(the chapters are available online), the concept is explained in the most comprehensible way.

Classes are a holdover from Linnean classification that don't have any real taxonomic meaning in modern systematics.


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Detecting nuclear DNA in suspension of mitochondria
Is there a way to detect nuclear DNA in a suspension of mitochondria extracted from leukocytes? I need to make sure there is no nuclear DNA in the suspension before extracting mtDNA from the mitochondria.

Centrifuge the suspension in Cesium Chloride solution at a particular g value which causes the mitochondria to settle to the bottom of the centrifuge tube but leaves nuclear DNA forming a layer near the top of the centrifuge tube. This is since the nuclear DNA is less dense than the mitochondria. Using a needle syringe, extract a small part of the centrifuged suspension from the very bottom of the centrifuge tube. This extract is most likely to contain no nuclear DNA. Hope this helps :).


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What is this beautiful pink flower plant seen at Bodnant Gardens?

Seen at Bodnant Gardens, North Wales UK.

Please include as many details as possible. I can't tell if it's a tree, a shrub, or a tall plant. It certainly is beautiful, though!


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Can a broken thumb/finger bone not require realignment of the bone?
Is it possible that a finger/thumb bone fracture is so superficial, that the doctor does not need to realign (re-set) the bone before applying the cast? Or does it always require for even a finger/thumb broken bone to be put back in place before applying the cast?

It is possible for bones to be broken and heal without any intervention, but it's rare. This is anecdotal, but my grandfather fell out of a barn and broke the top of his femur without knowing it. He kept walking on it, and a few years later he needed 2 canes to walk ( was in his 30s ). He saw a doctor, and X-rays showed he had broke his hip and when it healed it misaligned and caused wear to the hip socket. That also eventually healed after he was told not to put so much pressure on it. So if a hip can do it, fingers probably can too, but I don't recommend it.

Yes. You can figure that yourself if you look a bit at the types of fractures on Wikipedia, the Bone Fracture page:

Other considerations in fracture care are displacement (fracture gap) and angulation. If angulation or displacement is large, reduction (manipulation) of the bone may be required and, in adults, frequently requires surgical care.
[...]
Other types of fracture are:

Complete fracture: A fracture in which bone fragments separate completely.
Incomplete fracture: A fracture in which the bone fragments are still partially joined. In such cases, there is a crack in the osseous tissue that does not completely traverse the width of the bone.
[...]

Incomplete fractures and fractures with less or no displacement may heal correctly in some situations without needing realignment.

Most finger fractures (including the thumb) and, for that matter, hand fractures will not need to be "reset" before applying a cast, as most fractures are simple and non-displaced. More serious fractures (displaced, involving an articular surface, and many comminuted fractures) will need manipulation and possibly pinning.
But to answer your question, the fracture need not be incomplete to be casted/immobilized without manipulation. It is not rare, but common.


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If everybody DNA is different then how blood can match even with matching blood group?
We know that everybody's DNA pattern is different in the world. Then how can ´we transfer blood from one person to another person and this person can survive ?

A few components to my answer.

Red blood cells do not contain a nucleus, therefore, they do not harbour DNA.
The major determinant of blood compatibility is the blood antigen. There are only 4 types: O, A, B, AB. This is genetically encoded, and is expressed as a set of sugar coats on the blood cell membrane. However, the enzymes that encode for A or B should be identical from person to person.

I hope this gives you a preliminary answer to work off.

Because one's DNA doesn't have to exactly match another person at all 3 billion locations for the transfusion to be successful.  As it turns out, there are only a few proteins that determine whether a person's blood is a match to someone else's.  And as it turns out, in the vast majority of the human population, there are only three alleles of the ABO gene, and only two alleles for the Rh gene, and for the vast majority of cases, compatibility of those two proteins is all that you need.

It is critical for you to realize that one's DNA is not the determining factor when it comes to a blood transfusion. Rather, what you have to look at is the proteins being expressed by the DNA coding for blood-associated proteins, as it is these proteins that are the determinant of blood acception or rejection.In other words, the key question is whether or not the blood being transfused harbors antigens -- specific blood proteins associated with a given blood genotype like A & B -- that are foreign to the recipient.
Individuals that have type A blood express A-type antigens, but also house anti-B antibodies which specifically bind to blood with the B antigen. For a person with type A blood (AO or AA), transfusing either AB or A type blood would be dangerous. The RBC in both cases would house B antigens, which the recipient would respond to the transfusion by initiation an immune response against the blood.
I want to touch up one more time on your connection of DNA to rejection of blood. Please be careful with this as different DNA really does not mean much in this case OR in many other biological cases. You have to be much more specific and ask what is the DNA encoding, what is is transcribing and eventually translating and how that relates to the biological process in question. For blood type, although every individual has 'different' DNA, their DNA for blood type has 3 distinct alleles to consider --iO, iA and iB. These alleles are located only within a small region of a person's overall DNA and the difference are 3 discrete categories, as opposed to every person having a different allele and expressing a different protein. If every person different over this small segment of DNA, in the DNA coding for blood type, then indeed it would be possible for each person to make unique antigens and thus for all transfusions to be rejected.
However, since the differences  encompass only 3 allele types, people can only have a limited range of genotypes (aO, aa, bo, bb, ab, oo) which connect to only 4 distinct phenotypes (A, B, AB, O). So there is different in DNA, but the difference is defined and limited, so that overlap of genotypes between is possible and compatibility is quite common. So yes people differ in that DNA, but you have to ask if those differences are significant for a particular biological phenomenon.

Welcome to the site. I appreciate your effort in answering the question; it would be even better if you can make your answer more precise by avoiding repetition of previous answers.

Since the antigens are genetically encoded DNA IS  the determining factor when it comes to a blood transfusion. Just not all of it.


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What is the purposes of these sugars?
What is the function of $\alpha$-D-glucofuranose and $\beta$-D-glucofuranose?
Are they both converted into energy? Or are they just different variations with no particular difference in function?
I tried searching but found nothing on the web except chemical structures.

What do you mean by purpose or function?

You see, there are types of glucose. And I want to know what a-d-glucofuranose and b-d-glucofuranose does in the cell.

I think you can ask that without referring to purpose or function, as these imply that  someone designed it that way versus being sort of an organic chemistry curiosity about glucose.

Please provide some context and describe the results of your own research. Why do you want to know about these compounds? Where have you read about them? Do they occur in the certain foodstuffs — or have you just seen their names in a chemical classification of sugars, and have no idea whether or not they occur in nature? I find nothing on the web except chemical structures.

So whats the problem about this question?

What makes you think they're found in cells? There are lots of things that turn-up in a biochem. lab which aren't found in nature, but are used in synthesis. Or just held onto for future use.

So are these found in cells of living things or not? Im very confused just give me the answer "they arent found in living things"

As a new user to this site "for biology researchers, academics, and students" you seem not to understand how this site or science works. You are supposed to post about a biological problem that you have encountered, and if anyone knows the answer they provide it with evidence or links to support. As far as I can tell — you still haven't told us — you have discovered a classification of sugars somewhere, and because glucose is a natural sugar you have assumed all other chemicals of this category are. This is not so, and chemists traditionally synthesize and describe any compound possible...

...You then ask us to tell you "they aren't found in living things", without understanding that we have no knowledge, evidence of other basis for saying that, so as scientists we cannot. The fact that we have never encountered them doesn't mean that some plant somewhere doesn't produce them. Chemists have synthesized thousands of compounds, so how should anyone here know which existe in nature (and why should we care)? We would assume that you would know something about them to go to the trouble of posting, but it seems not, or you are not going to tell us, so I suggest your post be removed.

Im sorry, im deleting this post.


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Sleep stages and rythm
I would like to get a rough understanding of sleep stages and their rythm, especially in relation to my experiences with sleep.
Disclaimer: I hope to get explanations to my experiences with this post. I do not seek medical advice here, for this i consulted a medical professional. But they couldn't give me satisfying explanations.
If i sleep 6 hours (+- 30 min) i have an easy time getting out of bed, feel well rested and energetic throughout my day. 6 hours has been my average for the past half year or so.
If i sleep more (e.g. 8 hours) i experience the opposite. I have to drag my self out of bed and feel tired for hours to come. I also don't "fully recover" to the point i feel like with 6 hours of sleep. In the past i used to have an 8 hour schedule. But i was aware of the 6 hour behavior and abused it on days i needed an energy boost.
If i sleep until i wake up by my self (10-12 hours usually) i do feel well rested, but have a slower start in the day than with 6 hours. I usually try to avoid sleeping in this long.
From what i understood this experience is related to the sleep stage i am in when i wake and 6 hours seems to hit the "sweet spot" for me. Altho i don't know any other span that would result in the same experience. So im asking my self the following questions

Which sleep stages are there and how do they influence you when you wake during them?
Are there ways to "schedule" these stages to shift my 6 hour cycle to 8 hours?

Sorry if this post isn't in the right place here. Let me know and i will remove it.

The background information you give and your second question place this post in the "medical advice" category, even though that may not have been the intent. If you remove all that, it boils down to a very broad question that shows no evidence of research, something this site strongly advises in order to get an answer. Sleep is complicated; you can start here. You can change your sleep pattern for the better, but you need a good sleep specialist's help.

I think there are some good questions in there but as anongoodnurse says you'll need to separate them from medical advice and also separate them from "tutorial":: Stack Exchange is for specific questions with specific answers, there are entire books written about sleep stages and their rhythms. It would be better to start reading about this on your own (Wikipedia is a decent starting place) and then as you come across things that are unclear you can ask questions here about those.


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How many Type II restrictions enzymes are currently available (commercially)
How many Type II restrictions enzymes are currently available (commercially) for purchase as of the date of this posting (September 1, 2014)

A lot. Why do you need to know? It would be very difficult to inventory every enzyme from every manufacturer out there...

I'm  an exercise for UGR studentS and was trying to stress the diversity out there with an accurate number. Figured this would be a tough one. NEB has always been the most pioneering company for these but I know they don't own all the patents.

This question appears to be off-topic because it is basically a "shopping-list" question, see Why are “shopping list” questions bad? and Q&A is Hard, Let’s Go Shopping!.

This question appears to be off-topic because it is not about biology per se, is extremely difficult to answer, and has no use whatsoever to the users of this website (and it seems very little use to the OP as well)

I disagree @Raoul ! Respectfully. If one is planning a cloning experiment a comprehensive list is the very thing he/she needs. This ? Explores just that. This is one of the most diverse enzymes in nature as well, knowledge about which ones have had their synthesis mastered and an appreciation if that is  perfectly relevant I believe. You can find the reason for this question above, for education.  I don't think it's an answer is impossible either. I will remove the date from the question but I figured it would allow future readers to easily gauge the accuracy of any answers.

@rhill45 I did not mean any disrespect. It may be that I have a skewed point of view, not being a fundamentalist. I however suggest not to remove the date, since its presence makes your question more compliant with site policies.

A quick look in REBASE finds 15999 type II restriction enzymes of which 616 are listed as having suppliers. Obviously some of these will share recognition and cut sites.

The Restriction Enzymes section at Biocompare is likely not comprehensive, but short of contacting every single molecular biology company and merging all their inventories into a master list, it's probably the best you can do on short notice. They currently list 289 uniquely-named enzymes, but I'm not enough of an expert to say how many are similar in activity/recognition sequence, or whether they might also be known by other names not currently listed. For your purposes, however, it'd probably be enough to tell your students that there are on the order of 300 common commercially-available enzymes. Hope this helps.

downvoter care to comment?


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Are any biology research journals free to publish in?
The research journals Ive published in require significant financial cost to publish. On top of that many require a membership to the society the journal is associated with, in addition to publication fees. I was wondering if anyone is familiar with any journals (reputable hopefully) that do not require fees like this to publish a research article?

I'm not sure if this is on-topic here. Perhaps Academia SE would be a better fit.

Many biology journals are free to publish in. As a rule of thumb:

Most journals from for-profit publishers such as Elsevier, Wiley, etc. charge nothing to the author (but of course bill the libraries handsomely).
Many but by no means all society journals charge page charges even if they are not open access.
Most but not all open access journals charge substantial publication fees. You could try this website to search for open access journals that do not charge publication fees.


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How can paleontologists identify morphologically different fossils as members of the same species?
I recently saw a documentary about Tyrannosaurus rex, which detailed the growth stages of the dinosaur. Apparently, it underwent a huge growth spurt at around 14 years of age, growing into the massive predator so well known in the popular imagination. From what else I've read, this much seems uncontroversial.
However, it made another claim which is that pre-teen Tyrannosaurs had a radically different morphology from adults. The skull was smaller, the legs much longer and the two-fingered forearms far larger in proportion to the rest of the body.
Given that there is some limited evidence for the animal living and hunting in social groups, the program speculated animals of different ages may have filled different hunting roles. The faster, more agile teens driving prey toward the massive, slower adults which then tackled the actual killing. Lions in Africa hunt in packs in this way, but whether Tyrannosaurs did remains speculative.
Anyway, on seeing the body plan of the young Tyrannosaur, I immediately wondered at how any palaeontologist could identify it as the same species as the adult. And lo, the documentary went on to say that, for some years, it was presumed to be a different species.
So the question is: given the radically different body shapes of these two forms and the limited evidence one can glean from the fossil record, how were scientists able to conclusively identify that young and adult tyrannosaurs were, in fact, members of the same species?

Just to be pedantic about the scientific method, scientists seldom "conclude" anything. They propose a hypothesis, and then collect data to see if their hypothesis can be falsified. Paleontological species hypotheses are frequently overturned as more or better fossils are discovered.

Radically different body shapes and sizes represent overall phenotype. Overall phenotype was used briefly in the 1960s and 1970s for species identification under a statistical distance method called "phenetics". However, phenetics has been rejected as a valid method of species identification. Similarly, although ecologists widely use the Biological Species Concept (Mayr) based on reproduction, taxonomists generally prefer some form of the Phylogenetic Species Concept. In addition, paleontologists find species concepts that require assumptions about reproduction in fossils to be difficult. The phylogenetic species concept uses the presence of fixed morphological characters to identify individuals as members of a species. Fixed characters need not be major, obvious differences. They need only be present in all members of a hypothesized species, and absent outside the species. That they are fixed in all members of a species implies a lack of gene flow, but the definition does not require that. So in the example you gave, juvenile T-rex must have some unique characteristic morphological feature that define them as members of the species (a synapomorphy). In addition, when there are a series of intermediate juvenile fossils, it becomes possible to link them together.


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Does drinking spoiled milk that has been boiled upset the GI tract?
With water, boiling will kill harmful pathogens. Does this also hold true for milk ? If it does not, what in the milk will continue to cause gatrointestinal distress ? Shouldn't boiling kill the harmful bacteria ?
I'd rather not get into a discussion whether animal milk should be consumed by humans. I am asking about a typical person who is not lactose intolerant and does not have any milk allergies.

Toxins could be produced by the bacteria that spoiled the milk that wouldn't be destroyed by boiling. Similarly, spores could be formed that are impervious to boiling as well.

@MattDMo If you would like to create an answer out of this I will mark this thread as answered. BTW out of curiosity, which toxins are they and how do spores upset the GI tract ?


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Multiplication to formalize Microbiological Processes
I am not from the field, but have a question regarding modeling in biology:

I know that some processes can be modeled with the mathematical multiplication operation, and wondered if anyone could give me an example (or examples).
Especially with regards to axonal growth and the chemical (de-)stabilization taking place which involve microtubuli and actin, I was wondering if these processes again could be formalized mathematically as multiplication of (several) variables.

I have looked through the internet but did not find anything so far,
any help is appreciated

there are mathematical models for each of these things, but i don't think they usually incorporate all possible parameters and its unlikely they are all linear (i.e. resulting from multiplication alone).

can you give me some link, some example of a multiplication?

Here's the quick answer you asked for, too big for comments so sorry if this is not a full answer either.
This paper is an example of cytoskeletal modelling.  the equations are not simple products (that is to say they have exponentials, derivatives and other non- multiplication operations in them).
This example reference is a simple axonal growth model.  You will see derivatives being modeled as products.  Not sure if this is what you are looking for.

oh good - glad that worked for you.


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Cell culture experiments, technical or biological replicates?
Experimental design:
Cells are grown, counted, and seeded in 96-well plates.
Cells recover 24 hours.
Cells are treated with different doses of a drug, 3x per treatment.
Cell survival read via MTT.
This is repeated twice, on two additional times.
In other words, on three independent days, we seed out this plate and measure it one day afterwards (measurement kills the cells):

A
B
C
D

1
1 µM
2 µM
5 µM
10 µM

2
1 µM
2 µM
5 µM
10 µM

3
1 µM
2 µM
5 µM
10 µM

Each Dosage (columns) is measured in triplicates (rows). This is repeated three times, so in the end, each dosage has a total of nine datapoints.
Does this experiment have 3 biological replicates, each of which has 3 technical replicates or is there another way to group this?
My inclination is to use a mixed-level model where each of the plates is a level in a random variable.

I don't think your description of the experiment is very clear.

@ Bryan Krause: I disagree, I understand his setup very clearly, it‘s a standard procedure in cell culture. Also, this question should  not have been closed, since these matters aren‘t trivial and their impact is often underestimated

@markur Disagree, it's still unclear. It may be standard, but it's unclear.

@BryanKrause please specify what exactly is not clear. I have ideas how to improve this post, but I don‘t want to change things that you already understand.

@markur How the replications are administered: what is measured in the same wells and what is measured in different wells. Total N is important too.

@BrianKrause ok I applied some edits

It's a bit complicated, because your cells at each replicate are single source, so biological replicates are not truly replicates - but it gets very difficult to escape that when you consider that most established cell lines are from a single source. If you want to do it as close to properly as you can, you should get up 3 separate vials of your cells and maintain/use them individually.
In your case you can consider that different repeats are biological replicates (so you have initial with 2 repeats? so 3 replicates total(?)) - your wording is unclear here, I interpreted it to mean you have done the experiment twice, not an initial with two additional repeats, but the next line says "3 biological replicates". These give you information about the biological variation in your cells over time.
The replicates at each repeat are technical replicates and provide information about how well you are able to do things like pipetting or making dilutions.

The experiment was done three times. Regarding cell lines, yes, all the cells came from the same lot of the same ATCC catalogue entry (albeit different "break-outs" from frozen stocks). So, there are actually zero biological replicates?

@Bryan it's a philosophical debate as to whether they are biological or not. Most would consider them to be biological replicates, because if you reductio ad absurdum the argument, it makes it impossible to ever have biological replicates in a cell line.

It is not philosophical. Technical replicates measure technical variance while keeping biological variance as low as possible. Hence, you measure technical replicates on the same day. Biological variance is introduced by prolonged culturing (react to differences of FCS, culture flasks, Selection by splitting, etc.). To display biological variance, you measure at different timepoints and minimize technical variance by taking the mean of tech replicates. Even if the cells have the same background, some cell lines do have great internal time-dependent variance, like the ones I work on.

Also, it‘s important to never mix technical and biological variance. If you measure triplicates on three different days, show technical variance by plotting three separated groups, each group consisting of the three technical replicates, (not one group with nine datapoints). To show biological variance, take the mean of the triplicates and display the three means, each mean measured on a different day (not as a ‚time series‘, just on a different random day). If you mix technical and biological variance (n=9) , that‘s pseudo-replication and and bad practice.

Source: Harvey Motulsky (the CEO of Graphpad Prism), Intuitive Biostatistics


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What controls the size of breasts?
I am not a biology student, just a curious person. To be specific, I'm talking about female humans. I know that it might apply to other mammals.
What controls the size of breasts?
I have heard about progesterone hormone.

Is it just progesterone?

Are there any other factors?

I have seen a movie in which couple talks about breast size increases after sex. Is it true?

Can somebody give more info on this?

Prolactin may be a good candidate.

The known factors seem to be mainly oestrogen and genetic (although I haven't been able whatsoever to find detail on what genes):
Manning et al (1997): Breast asymmetry and phenotypic quality in women. Evolution and Human Behavior, 17 (2): 129–143.

Our data support the thesis that mammotropic hormones, particularly estrogen, are harmful because they suppress the immune system. Heavy women with high levels of body fat produce more estrogen and, therefore, bigger breasts. However, more estrogen leads to an increase in breast asymmetry. Women with “good genes” are able to produce symmetric breasts despite the presence of large quantities of estrogen. Large and symmetric breasts are therefore honest signals of high phenotypic quality in women.

The first signs of breast growth begin as a girl reaches her teens. The fat in the connective tissues starts to accumulate when the ovaries begin to secrete (express) estrogen. The breasts will then grow. Also, the duct system begins to grow. These breast changes often occur at the same time as pubic hair and armpit growth.
After menstruation and ovulation, maturing begins in the breasts with the formation of secretory glands near the milk ducts. With the development of many glands, lobules, and breasts that continue to mature and grow, the duct system and breasts also continue to develop. Each woman's breast growth rate is different.
In the end it's estrogen and the amount of fat that accumulate in the breast, that are largely responsible for the size of the breasts.

You've been busy! Unfortunately this doesn't seem to provide any new information and most of it is not actually answering the original question. Please focus on providing high quality answers rather than quantity.


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Does an antibiotic that inhibits protein synthesis delay bone generation?
After removal of a femoral intramedullary nail the bone needs to generate in the intramedullary canal and bone generation to take place at the screw sites. Would an antibiotic which inhibits protein synthesis, such as Clindamycin delay bone generation?

No, this cannot happen, because the ribosomes of prokaryotes (bacteria) and eukaryotes (mammals) are build differently. Ribosomes of prokaryotes consist of two subunits, the so-called 30S and 50S units, while the ribosomes of eukaryotes consist of one 40S and one 60S subunit.
Clindamycin works by inhibiting the 50S subunit of the bacterial ribosome and since inhibition is highly specific and the subunit is not present in mammals there is no inhibition of protein biosynthesis.

Mitochondrial ribosomes are similar to prokaryotic ribosomes and some antibiotics can indeed affect them. However, mitochondria are also "protected" because they are inside the cell. The linked paper also shows that mitochondrial ribosome is sensitive to some antibiotics but resistant to to others. (also this)


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Does a bigger breast give creamier milk?
It is fairly common for a woman to have one breast larger than the other.  I have also heard that, for a breastfeeding mother it is common for one of the breasts to yield a creamier milk whilst the other is more watery and has less nutritional value.
Is there any correlation between the larger of the two breasts and the one which yields the fattier milk?

Can you please supply a link to support your claim of breast milk production differentiation?

Because mammary glands define us (mammals), the genetics of the ability to make milk has been of interest.[1] Because we consume milk, we have a dairy industry. Because the industry places a monetary value to certain milk constituents, the genetics of milk component production has been a viable area of study[2]. Since you are talking of cream production, we'll stick to that.
The effect of nutrition and the environment (e.g. temperature) on milk fat production has long been known, and the ability to selectively breed for higher fat content has been exercised for decades if not longer[3][4], But the molecular genetics of milk fat production is only recently starting to be understood.
Mammals with the highest fat content are those in cold environments where an insulating layer of fat is required, such as gray seal milk (53.2% fat), whale milk (34.8%), and polar bear (31%). Humans and cows have approximately the same milk fat percentage (~4.5% fat).[5]  The gene most studied to date is the DTAG1 allele[6] on chromosome 14.[7]
It is very clear that genetically milkfat production is under the governance of part of chromosome 14.[7][8] Since this chromosome is identical in both breasts, genetically one breast cannot make milk with a higher fat content than the other. Environmental and nutritional factors affect both breasts equally, so those can be ruled out as a source of fat percentage differences. The only factors left that can be variables are 1) fat content of one breast over the other, and 2) demand from one breast over the other.
In cows, more frequent milking increased milk production but decreased fat percentage; in the end, the effect on fat in milk was the least influenced by frequency of milking (significance questionable).[9]
Triglycerides in milk are synthesized in the smooth endoplasmic reticulum of the mammary alveolar cell from precursor fatty acids and glycerol (obtained from blood nutrients), and while other cell types are involved in milk let down, etc., there is no known function of interstitial adipocytes (fat cells).[10]
That was the long answer. The short answer is: no[11].
[1] The origin and evolution of lactation
[2] Milk Components: Understanding the Causes and Importance of Milk Fat and Protein Variation in Your Dairy Herd
[3] A review of nutritional and physiological factors affecting goat milk lipid synthesis and lipolysis
[4] Factors affecting milk composition
[5] The Highest Percentage of Fat in the Milk of an Animal
[6] Evidence for multiple alleles at the DGAT1 locus better explains a quantitative trait locus with major effect on milk fat content in cattle.
[7] Identification of novel single nucleotide polymorphisms in the DGAT1 gene of buffaloes by PCR-SSCP
[8] Scientists pinpoint gene linked to fat in cow’s milk
[9] Covariance among milking frequency, milk yield, and milk
composition from automatically milked cows
[10] MILK SECRETION: AN OVERVIEW
[11] Does a bigger breast give creamier milk?

Please add a reference link to support your short answer. :D

You should move your tl;dr to the top.

"Since this chromosome is identical in both breasts, genetically one breast cannot make milk with a higher fat content than the other. Environmental and nutritional factors affect both breasts equally, so those can be ruled out as a source of fat percentage differences.".. I don't think so. Environment, which also includes artificial environments such as clothing can affect "symmetric" parts asymmetrically. There is an inherent asymmetry as well. All these can result in different tissue efficiency- just like vision or hearing or muscle strength in limbs etc

However, I cannot comment on correlation of breast size and milk composition.

+1, but I partially agree with @WYSIWYG: fluctuating asymmetry should have its own component in the differences in fat content (although, seemingly less important than that of the main factor).

@WYSIWYG - I don't think that even extreme differences, such as keeping one breast bared to the winds, would affect milk composition. Lots of other things, God help the poor woman, but I disagree with you. I didn't say different breast sizes don't result in different amounts of milk; the amount of milk would vary based on the number of alveolar units in each breast, which, judging from the size discrepancies in women's breasts (as opposed to their eyes or their ears) varies considerably. Quantity, yes. Composition, no. All those alveolar cells are under the same governance.

@anongoodnurse I didn't mean such subtle effects.. I meant things like exposure to heat, mechanical stress etc. What I meant is that it is possible that environment can have assymetric effects. Or some other factor that causes assymetric development. These can affect the composition of the milk.

@WYSIWYG - I might be more convinced if I hadn't read so much about what governs fat composition in milk. To get more fat, you need to feed optimally and breed optimally. None of the papers discuss "bag size" as a factor. The increased bloodflow to, and increased adiposity/insulation around, alveolar units would mitigate most any natural effect, I would think. If you don't think keeping one breast exposed to the wind is too subtle, please tell me exactly what effects you're referring to. I'm open to considering them.

@WYSIWYG - Finally, I had milk goats for many years, which I hand milked twice a day while they were lactating. Bag size varies considerably. I could not see a difference between the milk from each udder.

@anongoodnurse true then, perhaps.. As I said I am not too sure about it.. and I didn't know really that wind exposure does have any effect


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Is this maritime plant a species of zostera?
This photograph was taken on the intertidal mudflats at Lindisfarne, Northumberland, UK today. It was about 40m from the shoreline at low tide. Is the green plant a species of zostera? Can anyone help with the identification?

This question appears to be off-topic because it is about plant identification. These questions are usually asked on Gardening and Landscaping Stack Exchange. This topic is not found in the following appropriate topics listing in the Help center: 1) General questions about biological concepts 2) Questions about the biological mechanisms behind medical conditions 3) Questions about techniques in a biological or biochemical laboratory


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Why prefer $MgSO_4$ over $MgCl_2$ in recipies
Many molecular biology recipes use MgSO4 (and not MgCl2). Is there indeed a preference? If so, why?

Can you specify which recipes you mean? I am aware of a number of polymerases like Pfu which prefer $ MgSO_4 $. I haven't found a reference for that now, but its probably the same: The chloride ion interferes with the enzymes reaction.

My guess is its the solubility properties of the anions.
Chloride ions can precipitate with some metals that might appear in a complicated buffer or medium. And yes they could even compete with enzyme binding.  Sulfate will remain in solution with just about anything.
There are exceptions, but if you're making a buffer you're probably going to do better if you use the general solubility rules.

Are you sure about the insoluble chloride salts? I recall only a handfull of them, mostly with ions, which are not common in cells like titanium or silver. For sulphate I agree completely.

Although calcium sulphate is only sparingly soluble.

added a link... this is chem 101 so nearly every book has a mention of some form of counter-ion solubility rules.

@AlanBoyd A number of sulphates is nearly insoluble.


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Biological investigations or Biochemical investigations
I am working on phytochemicals and their antimicrobial and antioxidant activities.
Are these activities investigations called Biological investigations or Biochemical investigations?
What is the difference between them?

For what purpose do you want to use one of these labels?

As the name implies, biochemical relates to the chemical reactions in biological processes. If that is your focus, fine, if you are only interested in the events, inappropriate. But you don’t say, and if you check the meaning of these terms, you don’t need to post here.


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Origin of enzyme names
Sometimes I get confused about why this or that enzyme was named in this or that particular way.
1) TCA: Why was not isocitrate dehydrogenase named isocitrate decarboxylase?
Wouldn't it have been at least as accurate to name the enzyme in question isocitrate decarboxylase as to call it isocitrate dehydrogenase? It does remove the -COOH, doesn't it?
2) Glycolysis: PEP (phosphoenolpyruvate) carboxykinase. Why isn't it oxaloacetate carboxykinase? Isn't it agreed upon that enzyme substrate be used in the name of enzyme?
3) Why name enzymes by reverse reactions (especially when the reaction is irreversible)? Pyruvatekinase makes pyruvate from PEP. Why not use another name, PEP phosphatase, for example?
I understand that this is the way the enzymes were named and I just have to accept it. But I would also like to understand the logic behind these names.

I don't have a proof for this right now, but since the enzymes usually work in both directions (although under physiological conditions only one direction usually is happening), it is possible that the (for the physiological pathway) reverse reaction was classified and analyzed first.

Sonic Hedgehog, and his arch nemesis, robotnikinin.

As @Chris commented, when assayed in vitro with a single substrate (which may not even be the physiological one) most enzymes can catalyse a reaction in either direction. And enzymes such as pyruvate kinase were discovered before the pathways they are constituents of were worked out in full. Furthermore, the ways of naming enzymes only became more sophisticated as more were discovered and characterized. (Try googling for ‘old yellow enzyme’.)
Let us take pyruvate kinase as an example. The name kinase is clearly not chemically descriptive but was applied to any reaction using ATP. But, never mind, go to the Wikipedia page for pyruvate kinase and click on the EC (Enzyme Commission) number — 2.7.1.40 — in the box on the right. You will come to a page where you will see that, like TS Eliot’s cat, the enzyme has three different names:
Accepted Name: pyruvate kinase
(because that’s what everyone uses and is in all the text books)
Other names: phosphoenolpyruvate kinase; phosphoenol transphosphorylase
pyruvate kinase (phosphorylating); fluorokinase; fluorokinase (phosphorylating); pyruvic kinase; pyruvate phosphotransferase
(note these include naming it for the reverse reaction)
Systematic name  ATP:pyruvate 2-O-phosphotransferase
So why is that the systematic name? If you click back from this page to the group EC 2.7.1 to which this belongs, you will find that this group is of ‘Phosphotransferases with an Alcohol Group as Acceptor’, itself a subgroup of phosphotransferases.
So, to summarize, there is a systematic name that have been arrived at after long and careful deliberation and appears in the introductory paragraphs of scientific publications. Thereafter the common name is used, which although sometimes now recognized as a misnomer, seemed most appropriate at the time.


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How do female hormones cause blood to clot?
On most female-hormone supplements you get a warning that is something like this:

The use of a combination hormonal contraceptives (CHC), like NuvaRing, is associated with increased risks of several serious side effects, including blood clots, stroke, or heart attack. (Nuvaring)

The use of a CHC, like NuvaRing, is associated with increased risks of several serious side effects, including blood clots, stroke, or heart attack.
It also goes onto state that smoking can increase these risks.

What makes these hormones so dangerous (prone to clotting)?
If a person is naturally high in these hormones are they at a higher risk of blood clots?
Why/How does smoking affect the hormones - or is the increase risk just due to the natural risk of smoking?

These combination contraceptives contain two substances: Estrogen and progestin (a synthetic progesterone). Both are used together to overcome the negative effects of single substance drugs as acne or sickness.
The risk for blood clots has been known for quite a while (see reference 1 and 2) and is generally caused by raised levels of clotting factors (especially VII and X), increased plasma fibrinogen, increased platelet aggregation in the blood and reduced activity of antithrombin III (which inhibits coagulation). This can happen as well in pregnancy when the factors are naturally elevated (that's the way these contraceptives simulate pregnancy to the body). The paper shows this nicely for two of the factors of the blood coagulation cascade (factor VII and X):

This risk is relatively rare, it affects only about 1-5 in 10.000 women, but is still not negligible. The risk is much higher in persons with defects in the blood coagulation cascade. Compared to this, pregnant women have a risk for blood clots of 5-20 per 10.000 women (for details see here).
Blood coagulation is really fine tuned to ensure proper function when necessary but no blood clotting when not. Basically activating and deactivating hold a balance, as depicted in figure 1 from reference 3:

Smoking now disturbs this balance by inhibiting fibrinolysis and promoting the accumulation of fibrin and pushes it more to the site of coagulation. What causes the problem here is the elevation of clotting factors in combination with the disturbance of the balance between activation and inhibition of clotting. See reference 3 for the details.
This effect seems to be limited to high concentration single estrogen and estrogen/progestin combination preparations, while there seems to be no such effect in progestin single preparations (although data is limited here). There is also a significant difference in the type of estrogen used. See references 4 and 5 for more details.
The mechanism of how this works is relatively straightforward. The estrogen binds to the estrogen receptor on the cell surface and forms a receptor-ligand complex. This leads to signalling inside the cells which finally results in changed gene expression. Additionally the complex can be internalized by the cell. Inside the cell this complex can bind to the so-called "hormone response element" and also regulate the expression of genes. This is explained in detail for Factor XII in reference 6 (and works like this for other parts as well). See the image for illustration (from reference 7):

References:

Relation between oral contraceptive hormones and blood clotting
Use of combined oral contraceptives and risk of venous
thromboembolism: nested case-control studies using the QResearch and
CPRD databases
Hemostatic effects of smoking and oral contraceptive use
Coagulation effects of oral contraception.
Lower Risk of Cardiovascular Events in Postmenopausal Women Taking
Oral Estradiol Compared With Oral Conjugated Equine Estrogens
Molecular basis of estrogen regulation of Hageman factor XII gene
expression.
Estrogen synthesis and signaling pathways during aging: from
periphery to brain

This particular product contains estradiol. Are these findings true for only progesterone or are they applicable for estradiol as well?

The info on estrogen signaling is great. Can you emphasize on the pathways that would lead to regulation of hemostasis.

@WYSIWYG I am not exactly sure which information you are looking for.

The relationship between estrogen signaling and blood clotting

I am not sure, if this has been researched in all detail, at least I haven't found a paper right now. I will have a look into it.


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Insect identification request - Is this a bed bug?
I live in Spain and today I found several of these in my son's jacket. I am afraid they are bed bugs nymphs because last year we had a bedbug epidemic in some neighborhood houses.
The insect in the photo is about 1mm and has green spots in his body. Maybe they are just aphids that have been brought from the park.

Green spots? Probably not a bedbug, then. Bedbugs feed exclusively on blood meals, which means that any coloring you spot in the nymph would be brown or red.

As the answer suggests, I do not think that bed bugs would have green spots.

I got curious and after some image search I got two candidates:

Plagiognathus repetitus

Mullein Bug

Great that you answered your own question! Can you add links to e.g. Wikipedia pages or other sources about these insects?


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Nei's gene diversity - calculation
I am completely new to biodiversity.
I have a question: how do I calculate Nei's gene diversity?
The formula I was given is H = 1 – Σpi2
I have an excel file with 3 different loci (Pgi-2, Pgd-2, Pgm-1). I will attach a screenshot of the table as I have no idea what I have to do. How do I calculate H for the loci?
Thank you!

Welcome to Biology.SE. Please take the [tour] and consult the [help] starting with [ask] for details and then delete or [edit] your post accordingly. In particular, this doesn't seem to be a question about biology as defined in the help — instead you appear to be asking about how to apply a formula. Who gave you the formula and is there some reason why you haven't asked them? Note that prior research is expected for all questions on this site, so this seems to be doubly off-topic.

It seems like you need to determine the value of $\pi^2$ for each locus, sum them, and subtract from 1. For ideas of how to estimate nucleotide diversity ($\pi$) see here. Also: your question would be significantly easier to understand if you used the built-in LaTeX math tools, or really any unambiguous math notation.

I’m voting to close this question because it is: 1) not about biology as defined in the help; 2) shows insufficient  evidence of prior research; and 3) lacks clarity.

The formula you were given is not Nei's genetic diversity.

Rather $$1 - \sum_{i=1}^R p_i^2$$ is the Gini-Simpson index. $R$ is the richness, or equivalently the number of genotypes in the data. Each $p_i$ is the frequency probability of the $i$th genotype.

You can find a description of Nei's genetic score here.

What are the integers in row 3 of the spreadsheet? Different alleles of the same gene?

Please use markdown instead of images to show us tables. It takes up less server space, and makes it easier for us to show you the calculation on your data. You can copy-paste your data into a table generator, such as here and just copy paste into your question.

Do you want to calculate Nei's score, or Gini-Simpson's score? They are not the same.


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How do atherinidae survive the drought?
I found isolated pools in which there are Atherinidae, through the pebbly shores of Piave River (North-East Italy, Europe - in attachment there is a picture of the remainder of shores, after the drought of this year, to let you see it context. Isolated ponds were found about 20m close to the shores, where you can see the vegetation - picture not mine ).

The pools are isolated (, there is no inflowing or outflowing water.
Water seems also stagnant. The distance of some pools is also very large (dozens of meters, in some occasion a hundred).
The drought here was extreme.
When I observed these ponds, it only had rained for a few days (about 3 in a week) after months without no rain: there were not conditions to have inflow of water, because around the ponds is completely dry, and my hypothesis was the ponds may not necessarily be remainders of evaporation of larger volume of waters that resisted months of drought, but originated after rain fall.
There are small fishes in the pools I thought were previously dry.
I think they may be Atherinidae, because they are small and resistent to salinisation of water.
I wonder how they made it to get here.
Could the eggs be preserved?
--
I'd like to learn more about these fishes, I love to explore their habitat.

Thank you David. Awesome that I see you are biochemist! If you would like to explain how to these fishes' metabolism  cope with saline water and extreme variability of their habitats, I'd love to hear!
I can think of at high variability of salinity, and high variability of available oxygen in water also for formation of algae, probably for eutrophysation due to type of agriculture in these area.

The question seems more biology (which I never studied) than biochemistry (although there will surely be a biochemical basis). There is presumably a literature on this sort of thing. Not sure what the technical terms are to use. You might experiment with Google.


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Identification of butterfly from caterpillar
i visited a butterfly house and they didn't know which butterfly will be the caterpillars in the picture, my first guess is 'papilio aegeus'. I think the eggs/ caterpillars were on a 'paulownia tomentosa' plant, but i'm not sure. (Identified with the app 'flora incognita)
My first guess would be papilio aegeus.
Thanks to all answering and helping me out.

I'm sure you meant to add the picture (it's surprising how often people forget). Please take our [tour] and refer to the [help] as and when. It'd be helpful if there's some idea of scale to the creature if possible.

Yes the pictures are missing, i deleted them on accident, but added them now. I'm sorry and thank you for telling me. For scale i just can say they are 2-5 mm.

Where and when were these pictures taken? What is the size of the critter?

Like i wrote the pictures are taken in a butterfly house and the caterpillar is 5mm. It was 4 days ago.
Butterfly houses mainly don't have food plants for the caterpillars, so the butterflies are laying eggs on not suitable plants.