text:
Does *E. coli Dh5 Alpha* strain has the ability to degrade polyethylene?
Does E. coli Dh5 Alpha strain has the ability to degrade polyethylene? What are the bacteria that can be used as a control in the research of polyethylene degradation?

I am not aware of any wild E.coli strains that have been described to have the ability to degrade polyethylene. However, work to equip E.coli DH5α with the ability to degrade polyethylene, by means of transformation, has been done in the laboratory (Mahalakshmi 2012, Danso et al 2018)
Microorganisms that can be found in the wild/nature that do have the ability to break down polyethylene include (Source: article):

Pseudomonas spp
Bacillus spp
Staphylococcus spp
Aspergillus nidulans
Aspergillus flavus
Streptomyces spp


text:
can magnesium bicarbonate be absorbed in the mouth?

Can Magnesium Bicarbonate be absorbed in the mouth?"
  Magnesium Bicarbonate occurs naturally in some mineral waters.

Why did you tag this question with "genetics", "evolution" and "cell-biology"? Does this indicate you are expecting answers that are related to these fields?

Is it important for you to know that magnesium bicarbonate is absorbed in the mouth or, for example, in the small intestine, where most of the minerals are usually absorbed? Also, what you have found yourself, so far?

Technically, the human mouth do not absorbed anything. The human mouth is just a first line of defense mechanism against external microbial (In terms of saliva). If in terms of physical aspect, it just helps you to reduce food size and shape it for consumption.
Real absorption do not happen in the stomach neither. Stomach is where acids are used to break down your food and subject to higher lethal effect to kill microbial. The absorption only begins in the small and large intestine. (This is why drug delivery is such a hot topic in research labs).
To answer your question, yes. We need magnesium to survive and so we do absorb magnesium. In fact we can't live without magnesium, we need it for certain vital functions for our body to be normal. (Only in small magnesium amount, we don't need a lot of it).
As for bicarbonate, our body do not need it. In small amount, it is not toxic to our human body but in high volume, this would be a serious issue. When we breath, on cellular level, gas exchange occurs. Oxygen is supplied into our healthy cells while carbon dioxide is removed from our cells into our blood.
This is where it gets tricky, we do not store carbon dioxide in the form of gas when removing it via breathing out. We actually store carbon dioxide in the form of Bicarbonate in the plasma of our blood (Do note that its plasma, not RBC). When it is transported to our lung, this bicarbonate will be converted to CO2 and removed as we breath out. Hence, we do not absorb bicarbonate unless it reacted with some other elements or salt to produce some byproduct that we could use.
I hope you find this useful.
Regards
Price

Thank you. So what about mineral waters containing magnesium bicarbonate?
Duman

source: Stack Exchange

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text:
What's the lowest atmospheric pressure a tardigrade can remain active in?
I'm not asking what atmospheric pressures they can survive (we now they can survive the vacuum of space) I'm wondering at what point a deficit of atmospheric pressure would cause them to enter one of their various states of metabolic suspension.

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


text:
What is this colourful insect?
Found this colourful  insect in our garden. It measures about 1.5cm. I am from Kuching, Sarawak, Malaysiai

Not that colourful IMO! What do you think it could be? Look like some hymenoptera with its apocrita to me

The short orange antennae and the round eyes are those of a Diptera, although I can't tell the family

Check on from yr response i.e. Diptera order, I think it is from Family:Micropezidae.

This looks to me like a stilt-legged fly from the family Micropezidae.
https://www.singaporegeographic.com/insects/insect/stilt-legged-fly-micropezidae
Perhaps, more specifically:  Mimegralla albimana


text:
How is a specific fragment isolated for PCR amplification?
For background I am interested in studying engineering applications of a specific protein, which is not commercially available. My end goal is to express the gene for the protein in bacterial cells, most likely E. Coli, if that is a feasible procedure. I am mostly familiar the process of forming recombinant DNA, and though our lab does not specialize in Biology, we will be working with another lab in our Biomedical department which can provide necessary equipment and some advise.
The last time I did a lab where we expressed a new gene in E. Coli cells was a biotechnology class in high school, though much of the set up was done for us. I recall that our first step was amplifying the desired DNA fragment through PCR, but what I don't know is how the fragment was initially isolated. I know the primers help by essentially setting the start and end positions for the DNA cloning, but if you were to use an entire chromosome that contains the desired gene, it would seem likely that there would be many possible sites that the primers could attach besides the desired region. So if the DNA sequence for the protein I want is already known, how would I get a fragment that contains the gene I want?
Additionally, how difficult will this process be? Since the end goal is actually to study the protein, I do not want this step to turn into a full thesis on its own. For some specific proteins, the process seems well documented and can be done using relatively common materials and by following simple instructions, but how much should I expect the procedure to diverge for attempting this with gene that has not been specifically done before?

There are a number of primer testing tools that will compare primer sequences against the genome to ensure specificity, or help you design specific primers to amplify a specific region. One place to start is NCBI Primer BLAST; the linked page explains how to use it to generate primers to amplify a specific gene.
Doing PCR on genomic DNA can be a bit tricky, though, since you have to deal with a lot of confounding factors like DNA accessibility, contamination, and PCR inhibitors that get through your purification procedure. In addition, genes often contain huge introns, so you're going to end up doing PCR on an extremely long template (which is very hard or even impossible, depending on the size of the gene) and you'll end up with the whole gene sequence with introns which is not what you need in order to express it as a transgene.
Instead, I'd recommend purchasing a cDNA clone of your gene of interest and amplifying it from that. cDNA is made from the spliced mRNA sequence, so it will be a much more managable length and will prevent problems with alternate splicing.
If you go to the NCBI page for a gene, on the right sidebar under "Related Information" you'll see a link to Order cDNA clone. This will give you a few options to purchase a purified plasmid containing that gene for around \$60 - \$90. It will be much easier to work with this plasmid than genomic DNA and it will definitely save you time and money, especially if you're still inexperienced at molecular cloning.

Of course, it's not 2003 anymore and there's a good argument to be made that the whole idea of doing molecular cloning yourself is a waste of time and money. If your budget allows it, the easiest and fastest way is to pay a company to synthesize your gene for you. Genewiz, for example, offers snythesis for $0.28/bp, but you can probably get a better deal if you shop around.
The advantage of synthesis is that you can get the exact sequence you want cloned into exactly the right vector done perfectly the first time. If you don't have experience with it, trying to clone a gene yourself will take longer and cost more money than you think. It's better to just get it synthesized so you can move onto your real experiment.

I was going to suggest getting a synthetic gene, but now I’ll just second your answer. Some (most?) companies will even correct for codon bias, etc if you so desire.

@canadianer That's a good point. Since the asker mentions "engineering applications", they're probably going to care about getting good levels of expression.

but if you were to use an entire chromosome that contains the desired
  gene, it would seem likely that there would be many possible sites
  that the primers could attach besides the desired region.

No.  The point of the primers is that they should be long enough to bind to one specific locus (or at least, there is only one place where the two primers bind close enough to each other and in the right orientation for PCR to happen)


text:
What's the lowest temperature a tardigrade can remain active at?
There's a lot of information floating around the net about how tough they are & what they can survive, like "We now know that some tardigrades can tolerate being frozen to -272.8 °C".
But any details on the environmental ranges they can actually be active in rather than what extremes they can survive in one or other of their various states of metabolic suspension seem entirely absent for the casual (& not so casual, I've spent hours looking for these details) surfer.
So does anyone out there know what the temperature range of an active (rather than dormant) tardigrade is, with specific reference to the lower end of the scale.


text:
Why do neurons have long axons but short dendrites?
Cian O'Donnell, a British neuroscientist, originally asked this question on Twitter: https://twitter.com/cian_neuro/status/1075432086692089857. I am not a biophysicist by training but I wonder whether there might be existing publications that have shed light on this question.
My primitive back-of-the-envelope analysis involves the following:

If we suppose that most neurons are limited to a volume V, give or take epsilon volume, and the function of axons is to carry a signal over a large distance whereas the function of dendrites is to integrate information from different sources then a semi-spherical radiation of dendrites should be the norm.
This becomes an extremal optimisation problem where there are specific constraints on the minimal axon thickness, the minimal dendrite thickness and an upper-bound on the average number of dendrites that fan out of a given axon.
This becomes an extremal optimisation problem where there are specific constraints on the minimal axon thickness, the minimal dendrite thickness and an upper-bound on the average number of dendrites that fan out of a given axon.

This is a very sloppy analysis which ignores biophysical constraints but I think that we have an extremal optimisation problem here.

Axons are used to transfer electrical signals from Point A to Point B.
Dendrites are for receiving electrical signals from different neuron cells via their respective Axons.
There are mainly two different types of Axons, insulated and non-insulated.
Insulated Axons allows extremely high velocity of electrical signals to propagate from Point A to Point B. Please note that insulated axons are not entirely insulated, the axons are only insulated at every given interval for a certain length (in measurement of distance). This forces the electrical signal to jump from one gap to another gap between insulation and result in extreme speed of electrical signal propagation down the axon.
Non-insulated axons still allow high velocity of electrical signal propagation but it is very much slower as compared to insulated axons. This is why when you have a stomach ache, its a slow and dull pain due to non-insulated axons which gives you prolonged pain signal. However, if you accidentally knock into a sharp object, you receive an instant sharp pain for a split second for you to react at that instant (Its a biological life saving function) due to insulated axons that gives you extreme speed of pain signal propagation.
On the other hand, dendrites are not built for signal transmitting but for signal receiving. Dendrites comes in different configurations, one such examples are your color sensory cells in your retina.
This is why dendrites are short while axons are long. They are configured for different purpose. Just a bit more information, electrical signal in biofluid are actually ionic current. Ionic current are different from electron current, the charge carrier are different. Lastly, electrical signal are generated due to electrochemical gradient on cellular level. When a certain membrane potential threshold is reached, action potential will be triggered and they resulted in the firing of electrical signal down the axons.
I hope you find these useful.
Best Regards
Price

To me it makes sense. Axons are optimized for speed, dendrites are optimized for networks. It explains why the size is different in the "typical" neuron.

I'm not sure that statement holds true. Pyramidal cells are one of the primary excitatory cells in the cortex and are characterized by their long apical dendrites.


text:
How far does eardrum move?
Sound waves move human eardrum back and forth, like the peak to peak excursion of speaker driver, how much is it though? Ofcourse this movement depends on sound pressure, frequency and even location on eardrum, the edge moves less than center just like rubber surround around driver diaphragm.
I am interested in center of eardrum, the part of it that moves the furthest. The SPL is 100db at the eardrum and I would like to know how far it moves at 20 Hz and 20 KHz. I know this is hard question without specific answer becose every person have different eardrum but I believe there must be some rough average, some decent estimation about how much is it.
Is it micrometers? Is it nanometers? Or does it exceed 1 milimeter?

Tympanic displacement measurement (TMD) is a well studied field using hi-tech tools (i.e. stroboscopic holography), and complex units:
Vm = volume displacement in nl nanoLiters.
μm/pa (UDTF) = Linear tympanic membrane displacement is known as the umbo displacement transfer function.
The graph on the left gives you a value of 0.8-0.6 = 0.2 microns:

The graph above can be seen as resonances in an images sequence of stroboscopic holograms of tympanum (cool name to call your band) https://i.stack.imgur.com/fD6E9.jpg
According to this graph a 94dB sound wave gives you 0.1 micron displacement and a 100dB sine wave gives you 2pa, 0.2 microns.
https://i.stack.imgur.com/O7nQL.jpg
The first research document on google gave me a volume displacement from -120 to -700 nl.
1000 nano Liter = 1mm3
So the TMD volume displacement when very loud can be 1-2mm3, and eardrum rupture probably occurs from 10 to 100 mm3.
There are even muscles in the ear that can modify the way that you hear, i.e. the stapedius muscle which protects against low fequencies, and perhaps which can focus your eardrum elasticity modulus to let hear different frequencies, perhaps conciously? fascinating, I don't know.
See also pages describing elastic measurement of the eardrum, energy transfer by the tympanum by the cone, through these two google search phrasings: "eardrum response measurement" and "tympanic membrane displacement measurement"
Here is research comparing the eardrum to microphone design which is written easily.

This was best answer I ever got here on Stackexchange, the whole thing you wrote is treasure saturated with the juiciest most valuable information. I never knew this TMD field exist nor did I ever heard about stroboscopic holography, I will study these things passionately, big thanks com.prehensible.

Cheers man, it's a very cool topic can do some YT videos from this kind of research. I design synthesizers so I am a fan of waves, sometimes on the DSP forums here.

I want to ask just one very important extra question, is that 0.2 micron at 100db with or without the ear gain? I ask becose the ear canal and outer ear can boost frequency around 3 KHz by up to 20db, thats 10x the pressure. Was that 100db measured at the ear drum or somewhere else before the ear gain happened? Wasnt it some dead body test where they cut out the middle ear and the outer ear was gone?

Yes for the dB graph: a uniform unit sound pressure was applied to the outer side of the tympanic membrane. https://springerplus.springeropen.com/articles/10.1186/2193-1801-2-527


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Public database of animal specifications
I'm a math teacher looking for data to help my students interested in biology complete a quantitatively flavored study of animals. (As a math person, I apologize if I'm not using discipline-appropriate vocabulary in my request here.)
I'd like to find a publicly available database that lists different animal species along with their average measurements of various biological variables (body mass, heart rate, body temperature, length, lung capacity, etc.). Can anyone point me to something?
I'm interested in having my students study the relationship between pairs of variables (i.e. body mass and heart rate), to model this relationship via an appropriate function, and to use their function to make predictions. To hone their models, students will need access to known data about these variables for a number of different animals. I could have them look up all of this data in separate places on the internet, but I'm hoping to find one location that has all (or most) of it.
Thanks in advance.

You might be interested in the PanTHERIA database for several thousand mammalian species.  It has up to 53 characteristics for each species (but many fields have no entry).  It is available as two plain text files, each with one line per species (plus header line) and fields separated by tabs.  The files and data descriptions are available at http://esapubs.org/archive/ecol/E090/184/

I'm not positive, but I assume you'll be hard-pressed to find a list that checks your boxes of needing both multiple metrics for multiple animals.
However...
Two sources that seem to prove me wrong:

Thayer Watkins's webpage (San José State Univ.) found here, which includes:

Blood pressure, height of head above heart, weight, avg heart rate, longevity, and life-span

for:

Humans, cats, dogs of various sizes, hamsters, chickens, monkeys, horses, cows, pigs, rabbits, elephants, giraffes, and whales. (also goats, turkeys, frogs and snakes -- not all metrics are represented for all organisms).

"Normal Physiological Values for Select Animals" from Texas A&M found here, which includes:

temperature, heart rate, and respiratory rate

for:

Cows, goats, horses, pigs, sheeps, rabbits, dogs, and cats.

Neither of these sources is quite consistent or complete (and I'm not sure of their credibility other than being on academic websites), but they should give you a start.

Also, if you don't know, you can add "site:.edu" to the end of any google search to narrow searches (e.g., heart rates of animals, average body temperature of animals, etc.) for similar lists.

Does it have to be those physical criteria that you mention, or are you just interested in datasets that include a lot of quantitative data about animals?
Because if you're interested in other quantitative data, then you may be interested in the dataset included here. This is a dataset that consists of various life-history variables of many species. Some of the variables included are, among other, the following: age of maturity, litter size, adult body mass, gestation length, weaning age, birth weight, and much more.
Here is a description (abstract):

Studying life-history traits within and across taxonomic classifications has revealed many interesting and important patterns, but this approach to life history requires access to large compilations of data containing many different life-history parameters. Currently, life-history data for amniotes (birds, mammals, and reptiles) is split among a variety of publicly available databases, data tables embedded in individual papers and books, and species-specific studies by experts. Using data from this wide range of sources is a challenge for conducting macroecological studies because of a lack of standardization in taxonomic classifications, parameter values, and even in which parameters are reported. In order to facilitate comparative analyses between amniote life-history data, we created a database compiled from peer-reviewed studies on individual species, macroecological studies of multiple species, existing life-history databases, and other aggregated sources as well as published books and other compilations. First, we extracted and aggregated the raw data from the aforementioned sources. Next, we resolved spelling errors and other formatting inconsistencies in species names through a number of computational and manual methods. Once this was completed, subspecies-level data and species-level data were shared via a data-sharing algorithm to accommodate the variety of species transformations (taxonomic promotions, demotions, merges, divergences, etc.) that have occurred over time. Finally, in species where multiple raw data points were identified for a given parameter, we report the median value. Here, we report a normalized and consolidated database of up to 29 life-history parameters, containing at least one life-history parameter for 21 322 species of birds, mammals, and reptiles.


text:
Is there a macroscopic amoeba-like organism that lives on land?
In the early 1970s, as a teen, I hiked in Rocky Mountain National Park, going up the base of a mountain. The path went through a deciduous forest (there were brown leaves beneath the trees) and I saw oozing over some of these leaves an organism that looked like an amoeba. It was translucent blue, it had small particles contained in it, and it was about 1.5-2 inches wide (about the size of an oak leaf). It had what looked like pseudopods, and was moving forward by extending one over the leaf ahead of it. It was quite beautiful, as the blue was very clear. I thought it was a slime mold, as we had studied them that year in biology, but find out now that I was mistaken. I googled macroscopic single celled organism and found Gromia sphaerica in Wikipedia, but they seem to be aquatic, like the microscopic ones. Ditto Chaos carolinensis and Polychaos dubium, as far as I can make out.
Any light you can shed on this would be most welcome. I have never forgotten that little guy, and how beautiful it was.

I forgot to mention that it was maybe 1 1/2  to 2 inches wide. The size of an oak leaf, perhaps.

how do you know it wasn't a slime mold? How do you know it's single-celled?

Did it look like this or this or this?


text:
How much plant grow is required for a human's oxygen consumption?
I think Plants do:
6CO2 + 6H2O -> C6H12O + 6O2
I'm thinking that plants take 12 + 6 moles of oxygen and give back 12 mols of breathable oxygen and 1 mol of Cellulose.
I've read that a person needs about 550 liters pure oxygen (not air) per day, which I believe is about 785 g of oxygen (1L /22.4 L/g * 32 g/mol * 550 L).
I've read that grass is the most common plant, and is about 85% water.
Cellulose is about 162 g/mol, O2 is 16 g/mol, so for every cycle of photosynthesis, a plant's increase in sugar weight yields about ((6*16)/162) = 59% weight in oxygen. Since this sugar weight is only 15%, a plants total weight in growth will produce .59 * .15 = 8% weight in oxygen.
Does that mean that if a person needs 785 g of oxygen per day, there needs to be 9812.5 g (about 21.6 bl) of new plant growth that same day?


text:
does Trichloroacetic acid remove fats from milk
I am trying to detect melamine in milk. As a part of preprocessing, I add 200 ul of TCA to 1 mL milk,and after filtration I get a clear solution. Does the filtrate contain fat. I feel I am having interference from fat even after extraction.

It is likely that the fats are present in both the filtrate and the ppt. because as far as I am aware this test does not distinguish fats/ lipids into micro or macromolecules...You find the macromolecules in the ppt. But the micro in the filtrate so yes, there is a chance of interference as you have concluded.


text:
What is the evidence that plants and animals had a common ancestor?
According to the theory of evolution (which I don't dispute), plants and animals evolved from a common ancestor, probably a eukaryote. I'd like to know how we know that to be true.
Specifically how did scientists come to that conclusion, and what verifiable facts did they rely on? It would also be interesting to know who (and when) was the first to propose that plants and animals had a common ancestor. Was it Darwin himself?
Note that I'm not asking for the details of when and how that happened (the diversification/evolution of eukaryotes into plants, animals and other types), but rather the evidence we have to support it.

Darwin did propose that all extant organisms have a common ancestor:

Therefore, on the principle of natural selection with divergence of character, it does not seem incredible that, from some such low and intermediate form, both animals and plants may have been developed; and, if we admit this, we must likewise admit that all the organic beings which have ever lived on this earth may be descended from some one primordial form. But this inference is chiefly grounded on analogy, and it is immaterial whether or not it be accepted. No doubt it is possible, as Mr. G.H. Lewes has urged, that at the first commencement of life many different forms were evolved; but if so, we may conclude that only a very few have left modified descendants. For, as I have recently remarked in regard to the members of each great kingdom, such as the Vertebrata, Articulata, etc., we have distinct evidence in their embryological, homologous, and rudimentary structures, that within each kingdom all the members are descended from a single progenitor.

--Darwin, Origin of Species
He probably wasn't the first one; Darwin cites a previous suggestion:

From a circular lately issued it appears that Dr. Freke, in 1851 ("Dublin Medical Press", page 322), propounded the doctrine that all organic beings have descended from one primordial form. His grounds of belief and treatment of the subject are wholly different from mine; but as Dr. Freke has now (1861) published his Essay on the "Origin of Species by means of Organic Affinity", the difficult attempt to give any idea of his views would be superfluous on my part.

--Darwin, Origin of Species
As you can see, he offers no real evidence for this; he explicitly says it's speculation. Of course, nothing from Darwin is necessary for modern evolutionary theory, and other groups have tried to make this more concrete. Several lines of evidence provided increasing evidence for a universal common ancestor (UCA):

For a century after the publication of Darwin's bold proposition, before the advent of molecular biology, the UCA hypothesis remained an untested and hardly testable speculation. However, first the universality of the genetic code and later the demonstration of the (near) universal conservation of approximately 100 RNA and protein-coding genes among cellular life forms provided ample evidence in support of the UCA. Although generally considered compelling, this evidence fell short of a rigorous, formal test of the UCA hypothesis.

--The common ancestry of life
A relatively recent approach has tried using information theory to formally test a UCA:

Here I provide the first, to my knowledge, formal, fundamental test of UCA, without assuming that sequence similarity implies genetic kinship. I test UCA by applying model selection theory to molecular phylogenies, focusing on a set of ubiquitously conserved proteins that are proposed to be orthologous. Among a wide range of biological models involving the independent ancestry of major taxonomic groups, the model selection tests are found to overwhelmingly support UCA irrespective of the presence of horizontal gene transfer and symbiotic fusion events. These results provide powerful statistical evidence corroborating the monophyly of all known life.

--A formal test of the theory of universal common ancestry
Formal positive proof of theories in science, outside of math, are rare to non-existent (what actually happens is that competing theories are disproved) and I don't think that this approach is different. It's not a formal proof, it's yet more powerful evidence that theories not involving a UCA suck.

A formal demonstration of the Universal Common Ancestry hypothesis has not been achieved and is unlikely to be feasible in principle. Nevertheless, the evidence in support of this hypothesis provided by comparative genomics is overwhelming.

--The common ancestry of life

Thank you for the detailed answer and references. I understand that most of the evidence comes from analysis of DNA/RNA, combined with knowledge of the evolutionary mechanisms at play. And we have concrete evidence for evolution at different levels (species we can observe), which I guess is extrapolated to the level of eukaryotes evolving into the different kingdoms, right? And before genetic evidence was available, it was just a speculation.

I was wondering if there's any other kind of evidence, such as from (micro)fossils, if there are any that can provide usable information. Either way, I'm not expecting an absolute/formal proof.

Would not another piece of supporting evidence be the commonality of basic cell mechanisms, such as ion channels and the like?  It would seem that either there was a common ancestor, there's only one way for life to work, or plants and animals happen to have developed the same mechanisms.

It is also interesting to note that one of your references ("The common ancestry of life") is basically a criticism of another one of your references ("A formal test of the theory of universal common ancestry"), addressing the alternative hypothesis of convergent evolution, but still coming to a similar conclusion in favor of a UCA.

@jamesqf I guess that could also be counted as evidence, maybe you can explain it more and post it as an answer? It would be nice to find some references about that too.

the UCA hypothesis has not been achieved and is unlikely to be feasible in principle. - because the fossil record doesn't go back far enough?

@mazura because other hypothesis can be made less and less likely, but can't be formally disproven because they come down to statistical arguments; there might be only a 0.000000000001% chance that observations arose through paths other than a UCA, but that's still not zero.

"...what actually happens is that competing theories are disproved..." No, what actually happens is the predictive power of a theory is tested. New hypotheses are developed based on what the theory implies, and those are tested. If the hypothesis is false (and the assertion that the theory implies it is true), the the theory can be rejected. If the theory is not subjected to such tests, it is untested and there's no reason to believe it. There would also be no value in believing such a theory, since it has not been demonstrated as an accurate predictive model. Anything less is not science.

@aditsu it was not speculation before genetics, biochemistry and cellular anatomy also points to a common ancestor, plants ans animals share several organelles not seen in many other branches of life, (like mitochondria , golgi, and nucleolus).


text:
What type of movement is "spontaneous movement" if it isnt reflex movement and it isnt purposive movement?
According to Spontaneous and induced fetal activity

Spontaneous motor activity of the foetus depends significantly ot the
  foetal age; during the period between the 12th and 16th week it was
  recorded in 94.4%

By spontaneous, correct me if I wrong, I understand non reflexive movement and by induced I understand reflexive movement, since

A reflexive reaction or movement occurs immediately in response to
  something that happens.

But also, according to this other article Fetal movement

purposive movement begins at about 18 weeks, gradually replacing
  reflex movements

If "spontaneous movement" it isnt reflexive movement since it isnt an automatic reaction to something, and it isnt purposive movement, what is it exactly, and what does it generate it?

Although I can't read the original article in Czech, from their abstract it is clear that all they mean in differentiating spontaneous versus induced movement is whether the experimenter manipulated the uterus to induce a movement. Movements they observe could still be reflexive, they make no distinction of the type of movement (and do not intend do) except indicating whether the movement was purposefully caused by the experimenter.

There are several articles like that one, how about this one, it seems to say spontaneous movements at week 10-21 are movements generated by the fetus itself: https://www.karger.com/Article/Pdf/293158  "Fetal movements (FM) may be spontaneous, originating in the fetus itself, or evoked, caused by external stimuli. The FM in 21 normal twin pregnancies at 10 and 21 weeks of gestation were studied. The percentage rate of evoked FM which occur simultaneously in both twins was 4.96% of all observed FM. The rate of the spontaneous FM which occur independently in each fetus was 95.04% of all FM"


text:
Continuous (yeast) culture system satisfying multiple criteria
There are multiple ways yeast cells can be grown in liquid cultures.

Batch cultures are easy to prepare but cell density, medium composition and physiology change over time
Chemostats allow to maintain cells in physiological steady-state, but growth rate is limited by nutrient availability
With a turbidostat, cell density is kept constant and cells can grow at their maximal rate, with excess of nutrients, but medium composition changes over time
Cells in a microfluidics chamber can attain maximal growth rate with constant conditions, but with extremely low numbers.

I cannot think of a way to get (a) maximal growth rate, (b) constant medium composition, (c) constant cell density and (d) a decent culture volume (>50 mL). Am I missing something?

Unless I'm missing something, at steady state the cell density in a chemostat is constant and the specific growth rate is equal to the dilution rate. So you can keep density and specific growth rate at desired values.

Yes, you can keep them fixed, but what I am looking for is the maximal growth rate. In a chemostat there is at least one limiting nutrient that slows down cell division rate.

Im not sure I understand. Why not use media with excess nutrients? The specific growth will be equal to the dilution rate i.e. you can make the specific growth as high as you want (approaching the maximum growth rate) independent of nutrient levels.

Maybe I can approach maximal growth rate (for which I think I need a feedback mechanism to control the flow rate in order not to flush away the culture). However, I think I would not get constant medium composition anyway because each molecule in the chemostat is depleted/produced by the cells at a different rate. For example, if glucose is not limiting, it will be added to the culture faster that is consumed and thus will increase indefinitely. Multiple sources say that with chemostat you can get steady-state cultures, but to me it seems false. Where am I wrong?

A chemostat should satisfy your criteria.
The cell mass balance around a chemostat is the following (assuming no biomass in the feed):
$$F-FX+V_RX\mu_g-V_Rk_dX=V_R\frac{dX}{dt}$$
At steady state there is no change in parameters with respect to time so we set the derivative equal to zero. If we also assume that the death rate ($k_d$) is negligible (for example cells in exponential/log phase) and let:
$$D=\frac{F}{V_R}$$
Where $D$ represents the dilution rate (how quickly the volume in the tank is being replenished). Then rearranging the above equation you get:
$$D=\mu_g$$
This says that the growth rate will be equal to the dilution rate. In other words you can set how fast the cells grow by modifying the flow rate and/or volume of the tank. But there is a limit. Cells grow as fast as they can use the limiting nutrient ($S$) and this relationship is often modeled as:
$$\mu_g=\frac{\mu_mS}{K_s+S}$$
Where $\mu_m$ and $K_s$ are unique parameters for every cell type. $S$ is the concentration of the limiting substrate in the tank (which is also equal to the concentration of the substrate in the outlet stream). The maximum growth rate is $\mu_m$ and if the dilution rate is higher then this value, the cells get washed out of the chemostat. This can be troublesome if you need a flow rate higher than $\mu_m$. In this case a recycle is useful.
To answer your question in the comments regarding medium composition. You probably want to operate at steady-state. Steady state means that there is no change of parameters with respect to time. So if you write the substrate mass balance:
$$FS_0-FS-V_RX\mu_g\frac{1}{Y_{\frac{X}{S}}}--V_RXq_p\frac{1}{Y_{\frac{P}{S}}}=V_R\frac{dS}{dt}$$
And set the derivative to 0. Then you will find the outlet substrate concentration is a function of other constants (biomass, volume, product yield, etc.). You're right in that some substrates get used more than others, but when steady state is reached. They stop changing and the medium composition stays constant in the vessel.

Thanks for your help! Without stating what variables and constants are, the equations are a bit obscure though. And I still don't get why in a chemostat the medium composition would stay constant. In fact, a cell uses different compounds at different rates. However, the composition of the input medium is constant and is not adjusted to correct for these differences. Therefore, all input nutrients (except the limiting one) will increase their concentration in the vessel with time. But maybe I'd better open a new question to address this

I think you are confusing "constant" with "the same". If you feed 20 g/L glucose and 20 g/L uracil to the vessel then hypothetically you could have 1 g/L glucose leaving and 19 g/L uracil leaving, because they are used at different rates. But these rates would be "constant" in the sense that the levels stay at 1 g/L glucose and 19 g/L uracil because the system is at steady state. In other words the nutrients don't keep dropping to 0 because you are constantly add more nutrients in the feed.

I will try to update my answer but I was having issues logging on my computer and apparantly I made a new account so I can't edit at the moment.

Finally there is no "increase over time" for unused nutrients. Whatever isn't used leaves the vessel.


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How to take precise/low number of cells from cell lysate?
I would like to know that how can we take low or precise number of cells from a cell lysate? (without using any protein quantification assay).
Let say,
If I have a cell line having cell density 5x10^5 cells/mL (and its avg amount of protein concentration is 0.1ng/cell)
If I lyse these cells at the concentration of 5x10^5 cell/mL with buffer (eg., 0.1% rapigest + 10mM DTT). After achieving cell lysate, how can I take precise cell numbers from this lysate for further sample processing (e.g, alkylation, digestion etc)?
For eg., if I want to have 100cells/5ul or 1000cells/50ul , then how can I take it from cell lysate?
I know I'll have to dilute my lysate, but I'm bit confused how to achieve that based on cell concentration? how much lysis buffer and dilution would be appropriate?
Note: In my case I can't use any protein quantification assay for measuring protein concentration.
I would highly appreciate if anyone can help please.
Looking forward to hear soon.
Sincerely,

As @Price mentioned, it doesn't make sense to talk about number of cells in a lysate. Lysis breaks the cell membranes, so there are no cells after lysis. Are you trying to determine how much volume of lysate represents the contents of N cells?


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Which enzyme is Nick Lane referring to?
In Life Ascending the author, Nick Lane, refers to an enzyme in his introduction:
'' It concerns an enzyme (a protein that catalyses a chemical reaction) that is so central to life that it is found in all living organisms, from bacteria to man. This enzyme has been compared in two different species of bacteria, one living in superhot hydrothermal vents, the other in the frozen Antarctic. The gene sequences that encode these enzymes are different; they have diverged to the point that they are now quite distinct. We know that they did diverge from a common ancestor, for we see a spectrum of intermediates in bacteria living in more temperate conditions. But from the gene sequences alone there is little more we can say. They diverged, surely because their living conditions are so different, but this is abstract theoretical knowledge, dry and two-dimensional.
But now look at the molecular structure of these two enzymes, pierced by an intense beam of X-rays and deciphered through the wonderful advances in crystallography. The two structures are superimposable, so similar to each other that each fold and crevice, each niche and protrusion, is faithfully replicated in the other, in all three dimensions. An untutored eye could not distinguish between them.....The building blocks bind tightly to each other, through internal bonds that work like cement, retaining the structure despite the buffeting of energy from the boiling vents..... In the ice, the picture is reversed. Now the building blocks are flexible, allowing movement despite the frost...... Compare their activity at 6°C, and the frosty enzyme is twenty-nine times as fast; but try at 100°C, and it falls to pieces.
The picture that emerges is colourful and three-dimensional. The changes in gene sequence now have meaning: they preserve the structure of the enzyme and its function, despite the need to operate under totally different conditions.''
Emphasis mine and .... indicates omitted text.
I would be very grateful if anyone could tell me what this enzyme is, and if possible point me to further information about it!
N. B. the enzyme is only mentioned in the introduction "... never found the opportunity for a mention in the book proper." There are no references for said introduction, only the chapters.
Thank you!

I'm not sure it'll be possible, since he doesn't provide any details in the book. There are a lot of enzymes with highly conserved structures, so it'll be hard to figure out which one he's specifically referring to here

This is conserved structure but totally distinct gene sequence, is that also so common? If so could you please give me a pointer to one of particular interest? I can probably read from there outwards till I have satisfied my curiosity.

@Mirte It doesn't say totally distinct, it says "they are now quite distinct"; "quite" is of course an imprecise word but I wouldn't say it means "totally", and the passage also refers to intermediates that would be intermediately distinct from each. It is not surprising that an enzyme would evolve similar structure to catalyze the same reaction at different temperatures, and that keeping this structure would require a different sequence of amino acids. As divibisan suggests, without further information from the author they could be referring to many enzymes.

Note the second snippet from the book link user1136 provided gives a revised version of the first sentence which OP quotes, to wit: It concerns a protein (a catalyst, or enzyme, called citrate synthase) that is so central to life that it is found in all living organisms, from bacteria to man.

@user1136 I'll vote for your answer if you write one :-)


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Proof of mechanisms and causal relationships in biology
Statistical methods in biology are strongly encouraged: they are quantifiable, unbiased, and usually the only ones that are accepted as evidence.
However, it doesn't seem like the whole picture.
Say, someone wants to prove the hypothesis that wings are used for flight. He (or she) conducts an experiment: takes two groups of birds, ties up wings of all birds in one of the groups, then throws them out of a window and gets statistically significant data that birds with tied wings do not fly.
However, strictly speaking, he didn't prove that birds use wings to fly: only that birds with tied up wings didn't fly when thrown out of window. Or, as they say, correlation does not imply causation.
To tie the hypothesis to the results, he might include a paragraph in the discussion that "wings have large area, there are muscles that can flap them etc" - in other words, explain how wings could be used to fly. However, this explanation isn't statistical, or quantifiable: he just wrote a "story", perhaps used some common sense - but last time I checked, it's not evidence.
And that's pretty much what happens in every paper on biology: when they try to prove some mechanism, they include an experiment results and stats for a single aspect that is related to the mechanism (which, obviously, cannot explain the mechanism on its own), but then, when it comes to discussion, they just drop all the numbers and start explaining the phenomenon "logically" and eventually come to the conclusion. To be honest, they could've done no experiment at all and just went to explanation straightaway.
So what I wanted to ask:

Is there such a method of proof in biology as "proof by explanation", or something like that - when the author just explains the causual effects from, say, physics perspective and comes to a conclusion? Perhaps, even something similar to mathematical proof? Does this constitute valid evidence?
Are there any formal requirements for such proof? Perhaps, some way to quantify it or reduce to a "formula" of some sort?
Say, I wanted to publish a paper about some new protein that affects testosterone production. If I did no stats at all, or experiments like trying to remove the gene for the protein from some individuals and seeing what happens in comparison to control group, but instead just extracted and described the structure of the protein, identified the binding sites to some testosterone precursor, and explained how it can affect the testosterone production chemically, would it be a valid paper?

Your hypothetical paper on a novel protein that describes the structure and binding sites for a testosterone precursor would be an excellent paper. It just wouldn't be about the effect of the protein. There is more to biology than causal relationships.

The right policy is to exactly state what is observed and not make any far fetched conclusions. It is a matter of academic practice and therefore your question is not really on-topic here. [academia.se] may be a better place for your question.

You are missing a much simpler and more common method. film birds in flight, then demonstrate mathematically that the wings as used are providing the lift that is enabling flight. That is direct evidence for your hypothesis. You can further test it by clipping the wings or putting the birds in a vacuum, or a hundred other strange experiments. You may want to look into biomechanics, the types of studies you are looking for are far more common. How a limb works is not really a statistical question but more of a dynamics one.
Statistics is a secondary way of testing, used when more direct methods are not possible or terribly impractical. to use your last example yes that would be a perfectly valid way to determine a proteins function, there are limitations reasons we don't usually determine protein functions this way, not just becasue often we discover the function before isolating the protein), but even when it is you also want to test it in other ways that is true of anything in science.  This one reason science prefers multiple lines of evidence since one line can compensate for the flaws in a different line.
"Proof by explanation" has specific connotations in biology that may not be what you are really asking about*. Often it refers to unverifiable narrative explanation which is not acceptable in science. Also you never prove anything in science, (even more so with statistics) we shy away from the term proof because it brings to mind absolute proof which cannot exist. In science you can demonstrate something or show it is the most likely known explanation but you do not "prove" it. Research is not one off events but cumulative and constructive, the more lines of evidence the firmer a concepts standing.

What I thinks you are really asking is something much more fundamental to how science works and what empiricism and verification is. You may have better luck with this on a philosophy of science discussion, than a specific field of science since you seem more confused about how science operates. science has both experimental and descriptive research each with its own value.

"Often it refers to unverifiable narrative explanation which is not acceptable in science"
Well I understand that - but how does one make "unverifiable" narrative a verifiable narrative? Stats allow making verifiable, formal evidence out of unverifiable counting. But there seem to be no formal procedure to "proof by explanation/description".
"you never prove anything in science"
Well I understand that, I just don't know how to call it properly.- no-one ever talks about this method.

A narrative is just a description of a sequence of connected events, Anything from plate tectonics,  to a description of how a beaver builds a dam can be a narrative, the important thing is that the narrative be testable. Does it make predictions, for the bird example the hypothesis birds use their wings to fly makes several predictions including wings generate lift, birds without wings will not fly, and  the simplest that birds fly. Is model of the universe presented by the narrative empirically distinct from one in which it does not occur, AKA invisible dragon test.


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Are evolutionary algorithms calculated in polynomial time?
How complex are evolutionary algorithms? Also, what is the relationship between variational principles (Lagrangians, minima and maxima,) and evolutionary algorithms? Basically, how hard is it right now to construct an algorithm that reproduces what we see in the evolutionary history of life? Could you, in theory, use variational principles to reduce the complexity of evolutionary algorithms, and gain novel understanding of how evolution works in the process?

I think you need to clarify just what you're asking.  Evolutionary algorithms themselves tend to be quite simple, and run in pretty close to linear time.  The problem is that evaluating the fitness function can be very time-consuming.  One application I worked on involved solving a set of fairly complicated differential equations on a 3D volume, so O(n^3) - several seconds for each evaluation, microseconds to test the evaluation in the GA. I would guess that evaluating fitness functions for evolutionary biology would be more complicated still.

Yeah it is rather vague now that I look at it. Essentially, the question is about the possibility of using variational principles to feasibly create an algorithm which reconstructs exactly what we see in the evolutionary history of life, and, if we did that, how would it enrich our understanding of the intricacies of evolution. The philosophy behind it is that you can use variational principles to make everything so much easier in understanding evolution, so why aren't people doing it? Are they doing it? If you took the intrinsic variational principels of ecology, wow! Insight!

For instance, this article applies dynamic equations of motion derived from the principle of stationary action to ecology. We know there's an intimate relationship between ecological conditions and evolution now. If we can apply Hamilton's principle to ecology, and ecology directly impacts evolution, how can we use this approach to further understand evolution? Article link: https://www.sciencedirect.com/science/article/pii/030438009400046K

Your question is very broad a quite unclear. You ask four different questions (a post should always be restricted to a single question). How complex are evolutionary algorithms? 1) This question is broad and unclear 2) Evolutionary algorithms are a concept in computer science, not so much in biology, hence this specific question should not be asked on biology.SE. Basically, how hard is it right now to construct an algorithm that reproduces what we see in the evolutionary history of life? ...

... Evolutionary algorithm, in general, don't aim at answering questions in evolutionary biology. Evolutionary algorithms are a type of optimization algorithms, used to solve a number of optimization problems, many of them are completely unrelated to biology. That being said, we do perform a lot of simulations of evolutionary processes. Aside obvious issues of ressources, simulating "evolutionary history of life" in general is quite of an impossible task as the process is quite chaotic....

... It is like asking "can we simulate this specific wave?" without giving the starting conditions of the wave rather than asking "can we simulate wave-like processes?"

For all the reasons mentioned above, I'm voting to close this question as off-topic.

Well, to be fair its basically 2 questions, but sure. I don't see a conclusive or logical reason to believe evolution is random or "chaotic" though. There seems to be good evidence for it being a product of specific initial conditions in the environment, which can be modeled by an optimization function. Secondly, it is like asking if we can simulate this specific wave! That's the point! I'm asking if you can generate the "initial conditions" of that wave from the already known initial conditions of ecology.

@Liam Wasserman: Even if one accepts for the sake of argument that evolution is not random, the initial/ongoing conditions certainly are.  For example, suppose that the Chixulub asteroid happens to miss the Earth: then from that point on evolution takes an entirely different path.

The conservation of information implies that we can reconstruct an image of those types of events, so the randomness is purely epistemic/technological in nature. Nonetheless, I’ll admit a gentleman’s defeat: my question is just too broad.

@LiamWasserman You might underestimate the fantastic complexity of evolutionnary processes, with the feedback loops between evolution and ecology, geology, the details of how genotype affect phenotypes and the resulting fitness of an individual. Numerical simulations are very common (typically, in the form of of individual-based simulations) but only to investigate specific, clearly defined, questions and not to reproduce the entirety of the evolution of life on earth. (I am doing my PhD in computational evolutionary genetics and performs loads of individual-based simulations)

You're partially right. I am an ultra novice, if even that. But! If you found the equations of motion for ecological change, and had a dope evolutionary algorithm, you could in theory gain incredibly novel understanding of evolution. The arguments are sound. This is where variational principles would come in handy. Anyways, it was an interesting convo, thank you all.

This article is fascinating: https://arxiv.org/pdf/0911.4032.pdf

This question is off topic in Biology.SE because it is mostly about the computational algorithm. [scicomp.se] may be be better site for this question if other issues regarding general SE rules are addressed.


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When we laugh or run for sport which autonomic system works?
When we laugh or run for sport which autonomic system takes place in this time?
While I am not sure what happens in heart while laughing (tachycardia or bradycardia), but for sport running I'm sure that the heart has tachycardia. Does it mean that the sympathetic system works there (or there isn't relation between them)? If it does, then I really don't understand why being anger cause damage to the cardiovascular while sport running said to be healthy for the cardiovascular system, here are both activate the sympathetic system. Isn't it?

For laughing, our parasympathetic system works: "Breathing is the only function of the autonomic nervous system that can be consciously regulated or changed. It encourages deep diaphragmatic breathing, which stimulates the parasympathetic nervous system. This is the cooling branch of the autonomic nervous system and is the opposite of the sympathetic stress arousal system. This helps in relaxing the aroused state of a person and provides a sense of calmness." (See here: https://www.laughteronlineuniversity.com/laughter-good-nervous-system/)


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In electron transport system the final acceptor of proton is?
My lecture notes say that the answer to this is inorganic phosphate  (iP)..and the question is about proton not electron so the answer can't be oxygen. But I don't understand how is the answer iP

Hint: what's the overall chemical formula for respiration?

I still didn't get it..how is the answer iP?

Let’s see . . . loss of electrons is oxidation, and gain of electrons is reduction.  Respiration involves oxidation of carbon, and oxygen is the terminal electron acceptor in this process.  So carbon is oxidized, and oxygen is reduced.  And in the process the electron transport chain generates a proton motive gradient to generate ATP.  The Hydrogen ions (protons) move across the membrane, but do they need an acceptor?


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Why does arterial emboli flow in retrograde manner?
In artery blood flows with a pressure. When part of thrombus detaches it should flow along with the flow but it flows is retrograde manner.

Are you sure it does? Can you tell us where you learned this?

Yes it does. It is given in Asian edition of Robbins

I think you might be talking about Propagation of arterial thrombi.
Propagation is the increasing size of a thrombus and it occurs towards the heart, this is because thrombi are formed differently in veins vs arteries. In veins they form through the accumulation of fibrin and red blood cells whilst in arteries they form through the clumping of platelets.
https://www.thrombosisadviser.com/thrombus-formation/
Embolization is when the clot is removed from the circulatory wall and at this point it moves along with blood flow in both veins and arteries.

Yes I'm talking about propagation. But venous embolus flows along with blood flow. My question is why does arterial embolus propogate in retrograde manner instead of flowing along with the blood flow?

@KetkiShah - An embolus is different than a thrombus. What are you asking? The answer is correct that emboli flow with blood, not against.

From a bit of searching on the internet the general opinion appears to be that it is due to the fact that arterial thrombi are formed differently to venous ones.
Arterial thrombi are caused by injury to the vascular wall, causing a clot of platelets to form at that point. These platelets begin to join the clot as they hit it, causing the clot to propagate retrograde (towards the direction the blood is coming from)
Venous thrombi are caused by stasis of the blood flow, this causes the blood to coagulate at the point and gradually more fibrin and red blood cells collect onto this.

I had the same question after reading "arterial thrombi grow in a retrograde direction from the point of attachment, whereas venous thrombi extend in the direction of blood flow" from the Robbins & Kumar Basic Pathology Textbook. I think what this means is that the SIZE of the thrombus grows in the direction towards the aorta, but when it detaches it moves along the blood flow, so towards the right atrium of the heart. The reason why it grows towards the aorta is perhaps because blood is flowing towards the thrombus and the platelets get stuck on the thrombus before passing by it, so the plateles accumulate one after another. Think of it like a tube of flowing water with platelets. If the inside of the tube has some substance stuck to the wall of the tube, the platelets will sit on it before passing by it. I hope this helps!


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Wim Hof Method claims Alkaline Blood is Good. Contradictions? Counterproof?
The Wim Hof Method claims, that it is beneficial to have alkaline blood.
On the other site there is the medical claim that if the pH-value is not within the
range of 7.36 – 7.42, enzyms are not functioning properly and their 3D structure could be broken (denaturation). The correct pH-value is also invaluable for exchange of gases/O2/CO2, proper function of muscle contraction and
nerve conductivity.
So: What is this all about and how can this method be so good? After all, they also have conducted medical studies, so there must be some truth in it?! Thanks!

Before anyone raises this flag: This is not spam (I've checked it).

The Wim Hof method unfolds its health effects by hormetic stressors, respiratory alkalosis is one of them (a minor one). The WHM does not follow the pH theory, even though Wim himself gave ambiguous statements in older interviews about this. There are many people who misinterpret the WHM breath work as plain hyperventilation, which is very wrong. It involves a hyperventilation phase in preparation of a hypoventilation phase. This is similar to apnea protocols. The hyperventilation phase itself can mediate minor health effects. As it is not a chronic practice but relates to a few minutes per day, the stress of respiratory alkalosis is very likely within the hormetic range, hence beneficial. The WHM does NOT advocate continuous hyperventilation, which is known to be linked to chronic disease (exceeding the hormetic window).
The clinical trials of the WHM are peer reviewed and well conducted. However, people tend to mix Wim's interviews with the clinical evidence, which is obviously bad. The major paper (group study with control group) is this one: https://www.pnas.org/content/111/20/7379.full.pdf
It clearly shows the anti-inflammatory effects and increased leukocytosis of the breath work (intermittent hypoxia) and also shows that blood pH correlates to the respiratory rate, more precisely blood CO2 levels as expected. Those are normal blood gas dynamics, nothing woo woo pH stuff and no serious scientist would attribute the health effects of the method to the temporary blood pH fluctuations seen from a short hyperventilation phase, especially not when far more dominant and better documented effects on hormonal adaptations can be discussed instead. Some practitioners get quite enthusiastic about urine pH measurements, which are VERY high after the breath work, however all this indicates is normal kidney function in response to temporary respiratory alkalosis, nothing fancy at all. The body increases bicarbonate outlet via the kidneys (renal compensation) when blood CO2 gets too low (hyperventilation) to maintain blood pH homeostasis. the pH strips measure this bicarbonate. Another misconception is that the reading would correlate to progress or health, while it actually just correlates with hyperventilation intensity/duration. It is quite annoying how many misconceptions about simple physiological details float around the web, primarily due to the success of the pseudoscientific pH theory and alkaline diet. I guess some people just got rich with that crap...
Understanding the WHM means understanding hormesis and the stress response in the first place. The whole idea is comparable to physical exercise: stress the body enough to become stronger but not so much to take damage.

It is true that the pH of blood does not normally vary very much and is near neutral pH, 7.36 – 7.42 is a good estimate. It is also true that very different pHs from this would denature proteins, slow down gas exchange and kill cells. The Wim Hof method has not passed peer-review and has common red flags of pseudoscience, such as claims of the method being a panacea and being promoted through pop-health sources instead of medical ones. That's not to say it's absolutely proven to be wrong, but the onus is definitely on them to prove their claims true to the greater scientific community, not the other way around.

After all, they also have conducted medical studies, so there must be some truth in it?!

No, that's not how scientific and medical testing works, we distinguish good medical science from bad by testing against placebos, blinding, repeating the studies, (to mitigate the effect of bias) and meta analysis of multiple studies, and if the studies can pass peer review they are considered scientific evidence. (though not proof, science is provisional.) Simply conducting studies doesn't mean the subject is scientifically sound.

What makes you think the studies are of bad quality? How scientific is your judgement here :) ?


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what is the source of data in biological database like Genbank
What is the source of data  in international biological data bases like Genbank and what is it meant for?

The data sources of GenBank, and the intention of GenBank are stated on their welcome page: https://www.ncbi.nlm.nih.gov/genbank/

The data comes from scientists who gather data in their labs, such as DNA sequences. It is meant for a number of purposes. First, if science is to repeatable, these data can be checked against other data to see if the conclusions of a paper are valid. They are also used to reduce redundancy in data collection (sequences already exist for a particular species at a particular location, then perhaps further sequencing efforts might be better spent on another species or location). Finally, they can be used as raw data in asking new research questions.


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When muscles contract is the process similar to how non-newtonian fluids react?
I'm trying to understand how muscles contraction/tension works but getting loss in on the cellular level. From my understanding, when muscle tissue need to contract, the cells are flooded with calcium? Does that mean they get filled up with calcium? If so, are the cells hollow or does the calcium replace the fluid that was originally there? Or does the calcium cause the reaction in the cell for it to firm up?
I'm asking because there's an alien character who's quite thin but is also very strong and I was wondering about the science of that. I know them being alien means that their biology wouldn't necessarily follow earth rules but they could also share similar traits.

Calcium ($\ce{Ca^{2+}}$) is a signalling molecule and it acts like a chemical switch that tells other chemicals in the cell to enact the contraction. It's not accurate to think of the cell "filling up" with $\ce{Ca^{2+}}$ since $\ce{Ca^{2+}}$ wouldn't significantly change the volume of the cell alone *. Also, during contraction, the muscle cells contract in on themselves - they don't swell out.
It's also not accurate to think of the cells as hollow. Other chemicals inside the cell (such as actin and myosin) act like machinery that enact the contraction. Instead of thinking of the cell filling up like a balloon, I think it would be better to think of it containing a chemical winch (as in the figure below) whose pulling force causes the contraction. Similarly, instead of thinking of $\ce{Ca^{2+}}$ as a fluid, think of it as a bunch of particles that cause a chemical reaction to turn on this winch when they're allowed into the cell.

Reference: https://www.ncbi.nlm.nih.gov/books/NBK21670/
* During a $\ce{Ca^{2+}}$ spike, intracellular $\ce{Ca^{2+}}$ rises around 10-100x from 100 nM. Assuming $\ce{Ca^{2+}}$ has a 100 pm ionic radius, the volume of the cell ($x$) is only increased by around $10^{-9}x$ to $10^{-8}x$, which is negligible.


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When gene editing are both chromosomes in a pair changed?
Sorry for the possibly confused question, my knowledge of genetics is limited to medical training only but I have a question.
Are gene editing techniques such as CRISPR used on both of the chromosomes in a pair or just on one of them?
Some of the general searching I have done suggests that it can hit one or both. Is there a preferred outcome?

Gene editing using CRISPR-Cas9 can result in both heterozygous and homozygous conditions. It is just the event of probability. But even if u get heterozygous line, making it homozygous is not very difficult. You just have to cross two heterozygous line and screen for homozygous line through markers.

Thank you very much for the response. In general is it preferred to gain a homozygous or a hetrozygous change or is it specific to the intended task?

It is specific to the task. If homozygous is not lethal, then i would go for homozygous line, as it will be easy to maintain. In case if you maintain heterozygous, then screening at each generation is necessary.


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James Allison's T-cell discovery technique
The excerpt on Wired magazine of The Breakthrough by Charles Graeber has the following description of how James Allison found the T-cell receptor.

Suddenly it seemed so obvious: If Allision could rig up a way to
  compare B cells and T cells, devise a lab experiment that put one
  against the other and let their redundant surface proteins cancel each
  other out, the receptor should be the molecule that didn’t cancel out.
  Essentially, he was looking for a needle in a haystack, and his idea
  was to set fire to the haystack and sift the ashes—or as Allison puts
  it, “pick it out of the weeds.” Whatever was left would be the needle
  he was looking for.

It is a vivid metaphor. But the author does describe in more specific detail how the cancellation actually works. Can someone give such a description?

Well so here's the paper, at least on Dr. Allison's side. Mind you, the discovery is shared by a number of individuals for their combined effort.
So what they did is took mice and immunized them with T-cell lymphoma cells. The mice would essentially produce B cells against the lymphoma cells. And so we know that B cells produce antibodies, and hybridoma methods exploit the B cells to get a lot of that antibody. With their constructed hybridoma library, they could look at reactivity of antibodies produced against the lymphoma cells against the reactivity of the same antibody against other cells. They ended up finding 1/43 antibodies, which they dubbed 124-4O, reacted to their lymphoma line, but not to other cells.
With a pull-down assay, they isolated the receptor and determined it was a heterodimeric glycoprotein. A step further, they looked at both B cells and T cells, then, and were able to detect similar structures in the T cells, but not in the B cells.
Someone correct me If I'm wrong, though.


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Osmotic Pressure Clarification
My textbook states that the higher concentration of solutes, the greater the osmotic pressure will be and the greater the pull of water in will be. However, osmotic pressure is defined "as the pressure that would have to be applied to a pure solvent to prevent it from passing into a given solution by osmosis." Therefore wouldn't a high osmotic pressure PREVENT water from passing, not pull water in? Can someone please clarify this for me so it makes sense? Thank you!

I think you've got the solutions the wrong way round and that you should be applying the pressure on the non-pure solution, not the pure solution. Pure water is drawn in through the membrane so you have to put pressure on the non-pure solution to keep it out. Which textbook are you using? See the following quote from Voet et al. 5th ed. p. 30 and figure from Lehninger. Principles of Biochemistry p. 57.

The osmotic pressure of a solution is the pressure that must be applied to
  the solution to equalize the flow of water across the membrane in both directions
  (the added pressure forces more water from the solution through the membrane);
  it is proportional to the concentration of the solute.


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Veins in Plant Leaves (terminology)
Why do we call the vascular bundles in plant leaves "veins"? I think its probably because the xylem and pholem serve circulatory function analogous to the human body's circulatory system with arteries and veins. But why don't we call the vascular bundles arteries instead or veins?
In the human body, we call a blood vessel "vein" when it travels blood to the heart and an "artery" when a blood vessel travels blood away from the heart. Is there a similar reason or significance as to why we call vascular bundles "veins" instead of "arteries"?

It's just a colloquial term and not a well thought of/standardized term. So there is nothing much to reason here.

I think this is a valid question with valid historical (not simply colloquial) usage and I think that potential answers could definitely be based on more than just an opinion. I disagree with both close voters and vote to keep open.


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Can upper motor neuron lesions cause hypotonia?
I have been taught that hypotonia is always caused by lower motor neuron lesions while hypertonia is by upper motor neuron lesions. However, I recently learned of an entity called central hypotonia, which means hypotonia caused by a central nervous system lesion. This makes it so confusing.

UML leads to disuse, this can also cause disuse atrophy and hense hypotonia.

The rule-of-thumb you (and I) were taught reflects the role of the central and peripheral nervous systems in establishing muscle tone. Deprived of CNS regulation, alpha motor neurons increase in their responsiveness to spindle afferents, resulting in hypertonia. Deprived of PNS regulation, muscle spindles are less able to react to input, resulting in hypotonia.
Beyond this rule-of-thumb, things aren't as black-and-white. As you have pointed out, there is such a condition as central hypotonia. In fact, the NINDS includes the CNS as an area where damage can cause hypotonia:

"Hypotonia can happen from damage to the brain, spinal cord, nerves,
  or muscles." (source)

Purves et al. also note that upper motor neuron syndrome involves an "initial period of 'hypotonia' after upper motor neuron injury" (Neuroscience, 2012, p. 395).
To your question: Yes, the rule-of-thumb is not always accurate and upper motor neuron lesions can cause hypotonia.
If you're looking for a hypothetical mechanism, consider this: Purves et al. also state that hypertonia is "probably caused by the removal of suppressive influences exerted by the cortex" (p. 396). So it is conceivable that overstimulation of these inhibitory control systems by some sort of unique upper motor neuron lesion could result in hypotonia.

But in Down's syndrome there is no "initial phase" and the hypotonia actually persists as central hypotonia. The mechanism is not the same right?

For Down’s Syndrome, I might not actually call it “central” hypotonia because it’s a genetic disorder. This does suggest that the mechanism is different, though. But even in neurologically-triggered instances I would expect there to be mechanistic nuances that could break the rule (leading to chronic central hypotonia).


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Understanding food composition data from USDA for Vitamin A
When researching the nutritional value of carrots the Vitamin A comes in two  measurements as RAE and UI:

https://ndb.nal.usda.gov/ndb/foods/show/11124?n1=%7BQv%3D1%7D&fgcd=&man=&lfacet=&count=&max=25&sort=default&qlookup=Carrots%2C+raw&offset=&format=Abridged&new=&measureby=&ds=&Qv=1&qt=&qp=&qa=&qn=&q=&ing=
After reading the following article
https://ods.od.nih.gov/factsheets/VitaminA-HealthProfessional/
I understand that IU can be transferred to RAE, but I wonder if in case of USDA does two records represent the same value or they are supposed to be combined? :shy:
If you had previous experience working with this database I will be more then glad to hear you opinion about that :)

The corrected answer: It seems that the both rows from your table show the same thing: the sum amount of all vitamin A-related substances, but in different units; the 1st row in RAE and the 2nd row in IU.
As I said before, according to ods.nih.gov, 1 IU retinol = 0.3 mcg RAE, but this conversation is true only for retinol (the true, "pre-formed" vitamin A), which is found only in animal foods.
The main vitamin A-like substance in plant foods, such as carrots, is beta-carotene and the conversion rate is: 1 IU beta-carotene = 0.05 mcg RAE, so the 20-fold difference between 835 mcg RAE and 16,706 IU now makes sense.
Why to complicate this?
Large amounts of vitamin A (retinol) can be toxic. The upper tolerable level (the amount that should cause no side effects and is not nearly toxic) for retinol for adults is 3,000 mcg RAE. For example, 100 g of chicken liver contains 4,296 RAE of retinol. (You can also see that for the liver, 4296 RAE/14378 IU = 0.3, so this explains again that the two rows are the same thing.)
You can see that the same IU of vitamin A in animal foods is translated into much more RAE than in plant foods. This is also why high IU of vitamin A in animal foods can be (potentially) much more toxic that the same IU of plant foods.

@volna, I had to correct my answer entirely....


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How do scientists transfer the specific DNA in Optogenetics?
I'm a bit new to genetic modification and I was wondering in Optogenetics (a field in neuroscience) how the scientists transfered the desired DNA strand from the light-sensitive ion channel opening cell (I forgot the name) to the specific neuron that will grow these cells sensitive to green light and trigger an action potential in the neuron? (open the neuron ion channels)
I don't understand how scientists know exactly which strand of DNA to cut from the source and where to put it in the target. I mean, if scientists can do this, why not cut the legs growing part of my DNA and insert in a butterfly and boom, you have a butterfly with legs, no?

I think your question can be broken down into a few parts:
1. How do scientists know which DNA sequence encodes a specific protein?
It seems that you've asked this question here, which I'll answer separately. So please go read my answer there first :)
2. How do scientists transfer genes between organisms?
@CKM did a great job of explaining how lentiviral transduction works. It is a very common method for introducing genes into organisms. A few steps before that: if you know the sequence of a gene and want to cut it out, you can use restriction enzymes which recognize specific sites in the DNA and only cut there. You can then purify and amplify that DNA sequence by polymerase chain reaction (PCR).
To address one of the subpoints of your question, it is true that a lentivirus will integrate the gene of interest at a random location within the genome. It could be in a non-coding region. It could be in another gene. You would have to do some sequencing to find out.
3. How did scientists do this to invent optogenetics?
In the case of channelrhodopsin, scientists noticed that microalgae were able to detect and swim towards light. They used EST sequencing to find the responsible genes. Once the a photoreceptor gene could be isolated, scientists constructed lentiviruses containing this gene (plus a fluorescent protein gene) and infected neurons with them. The rest is history.
One final tidbit: though you can't exactly give a butterfly the genes for human legs, you can make it grow butterfly legs in weird places, thanks to a family of transcription factors called the Hox genes. People learned about Hox genes in flies by mutating the different genes and observing the wacky stuff that ensued, such as legs growing where antennae should grow. Google Antennapedia to see what I mean.

Well for one, just having a gene doesn't mean you can make it work as intended, and indiscriminately tweaking the genetic material can produce unwanted effects. For example, if I overexpress p53, a common tumor suppressor gene, the cell undergoes apoptosis (1). If I break/delete the same gene, the cell might undergo apoptosis or it might become cancerous. Human development is of course regulated by hundreds of genes at a time, however, so legs on a butterfly is far more complex than just a single gene.
A common approach for inserting genes into a host genome is the lentiviral transfection. Generating a lentiviral vector is detailed here. A similar strategy for transfection using HEK293 for viral production is described in the following paper. I have no knowledge of optogenetics but I tried my best to find a paper in the field that employs the method in practice. In case you have no access to the article,
Viral Production

HEK293T cells (ATCC, UK) were cultured in Iscove’s modified Dulbecco’s medium (Sigma-Aldrich, Germany) supplemented with 10% (v/v) FCS (Sigma-Aldrich) and penicillin–streptomycin–glutamine (Sigma-Aldrich) in 5 × 150 mm dishes. After 80% confluency was reached, cell were transfected in serum-free medium with the helper plasmids pRV1, pH21 and pDFΔ6 and pAAV1/2-hSyn-BLINK-IRES-eGFP or pAAV1/2-hSyn-IRES-eGFP at a molar ratio of 1:1 with CaCl2. On the next day, the medium was replaced with serum-containing medium, and 48 h after transfection cells were harvested, pelleted and resuspended in lysis solution (150 mM NaCl, 20 mM Tris, pH 8).....

Culture & Transfection

Hippocampal neuronal primary cultures were prepared from embryonic day 18–19 (E18– E19) rat hippocampi as previously described43. All the experiments were approved by the Institutional Animal Care and Use Committee of University of Milan and by the Italian Ministry of Health (#326/2015). Neurons were transfected at 7 days in vitro (DIV7) via the calcium-phosphate precipitation method with 4 μg of plasmid DNA for GFP for the experiments assessing the axonal and dendritic distribution of BLINK2 reported in Fig. 2c. Neurons were infected with AAV1/2-hSyn-BLINK2-IRES-eGFP at DIV10 and fixed at DIV12 for the immunocytochemistry assays.

There's more to the method, but in short they transfect the 293 cells with these plasmids that create a functioning virus enclosing their plasmid of interest, and then they harvest the virus and use that to further transfect their neural cells with the gene(s) of interest.

Thank you! This kinda answers my questions, but I'm just 16, I need a simpler approach to the topics :\ I did learn a lot from your answer tho.


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Height prediction based on genetics
My height, as predicted by my genetics, is 156 cm whereas my actual height is 172 cm. What could be the reasons for this substantial discrepancy? Does it just mean I had very good nutrition as a child?

Is the difference substantial? Is 156cm the average height for your gender in your family, or within your genetic background? The percent difference between 156cm and 172cm is only 9.8%. Think about that for a moment!

Sources of phenotypic variance
There is phenotypic variance in height in the human population. This phenotypic variance is in part explained by genetic variation, but there are also non-genetic variations, incl environmental variation (what you eat, your physical activity among many other things). See this post for more information.
Sampling error
On top of that, those measures of "genetic height" are based upon a limited number of SNPs and a limited number of individuals sampled. There is therefore a bit of room for a little bit of sampling error here. Note sampling error is not a mistake. It is just the fact that parameters estimated from a sample don't necessarily match perfectly the population parameters.
Training data set
Finally, the estimate is based upon correlation made from previous people. There might have a generational gap in height, typically present in countries that have recently largely changed their diets, such as many Asian countries.
For all of the above reasons, there might have a gap between your actual height and what has been predicted by some genetic testing. In short, yes your nutrition might part of the reason for this gap.


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What does 'proper' mean in the anatomical context?
I've seen the word 'proper' in websites, lectures, etc., in the context of human anatomy. But I'm unsure as to what its definition is. For example, the 'oral cavity proper'.

This use of proper is simply using one of the normal English meanings of the adjective proper: "In the very strictest sense of the word or phrase".  Thus, while 'oral cavity' generally might be taken to include, in part, the space between the cheeks and the teeth, the term 'oral cavity proper' refers to a stricter definition which excludes that space.


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Need help with these invasive vines damaging trees causing tree limbs to break
I need some help identifying various vines growing and girdling trees:

Please review the guidelines for writing a good species-identification question. At the very least, you should include your location, the size of your vines, and any closeup images you can (including any you may have of any of the vines' leaves). Please update to enable a good answer (and to avoid having your question downvoted and closed). Thanks!

Looks like Kudzu from afar. Very hard to manage,IMO , but not impossible. Cut and apply systemic herbicide to the cut stems, perhaps. You'll need to hit the growth a few times, otherwise all you can do is cut it back and wait for it to re-grow.


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What's the longest intron in the human genome?
What's the longest intron in the human genome? Discarding isoforms were a long intron spans more than one exon, i.e. what's the longest distance between two exons without another exons in between.

Short answers: Based on gencode the longest intron for protein coding transcripts, is the intron 3-4 of the transcript ENST00000465127.1 with 1,240,120 bases.
Long answer:
Download the main annotation gff3 file from gencode first. Then run this script:
zcat gencode.v29.annotation.gff3.gz \
| awk -v FS="\t" -v OFS="\t" '$3=="exon" && $9 ~ /transcript_type=protein_coding/ {match($0, "transcript_id=([^;]+)", transcript); print $0,transcript[1]}' \
| sort -k1,1V -k10,10 -k4,4g -k5,5g \
| awk -v FS="\t" -v OFS="\t" 'BEGIN {transcript=""; max_d=0; max_line=""} \
 $10 != transcript  {transcript = $10; end = $5; next;} \
 {d=$4-end-1; end=$5; if(d>max_d) {max_d=d; max_line=$0"\t"d;}} \
 END {print max_line}'

It will:

decompress the file
filter only lines that describes exons of protein coding transcripts
append the transcript id at the end of the line
sort by chromosome, transcript and position
calculate the distance between two exons of the same transcript
save the current maximum distance and the annotation line that belongs to it
print out the line of the exon which follows the longest intron. The last column contains the distance.

The output will be:
chrX    HAVANA  exon    38666121    38666309    .   +   .   ID=exon:ENST00000465127.1:4;Parent=ENST00000465127.1;gene_id=ENSG00000250349.3;transcript_id=ENST00000465127.1;gene_type=protein_coding;gene_name=AF241726.2;transcript_type=protein_coding;transcript_name=AF241726.2-201;exon_number=4;exon_id=ENSE00003644052.1;level=2;protein_id=ENSP00000417050.1;transcript_support_level=5;tag=basic,appris_principal_1,readthrough_transcript;havana_gene=OTTHUMG00000161009.1;havana_transcript=OTTHUMT00000363378.1  ENST00000465127.1   1240120

fin swimmer
EDIT:
gencode also includes transcripts that are only predicted, but never seen, or those where it is not sure that they exists. So you maybe want to just include transcripts having a certain transcript support level. For this you have to change the first awk line. E.g. to include only trasncripts with TSL1 change it to:
awk -v FS="\t" -v OFS="\t" '$3=="exon" && $9 ~ /transcript_type=protein_coding/ && $9 ~ /transcript_support_level=1/ {match($0, "transcript_id=([^;]+)", transcript); print $0,transcript[1]}'

You can also define a range, e.g 1-3:
awk -v FS="\t" -v OFS="\t" '$3=="exon" && $9 ~ /transcript_type=protein_coding/ && $9 ~ /transcript_support_level=[1-3]/ {match($0, "transcript_id=([^;]+)", transcript); print $0,transcript[1]}'

In both cases the result will change to intron 4-5 of ENST00000402655.6 with 1096453 bases.


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Why isn't suppression of immune system for organ transplant not as dangerous as AIDS?
I've read that when AIDS symptoms show up, life expectancy is about two years if no treatment is applied. On the other hand, I've also read that people having an organ transplant need to take immune system suppressors for the rest of their lives so that their body does not attack the transplanted organ. So, if I understand well, it is a sort of induced AIDS. I do not understand then how it is possible for people with an organ transplant to live more than about two years.
Can someone explain with details the differences between the suppression of the immune system by medicine for organ transplants and the one due to AIDS?

Patients receiving immunosuppressive drugs do fall into the same category as patients with HIV-related acquired immunodeficiency - that is, they are all immunocompromised and face similar risks of infection, cancer, etc. The difference emerges over time: when the immunosuppression is controlled and monitored, a patient can retain some immune function, and a physician can help a patient adjust and rapidly respond to opportunistic infections. Drugs can be given in calculated doses; viral infections which disable the body's ability to stop viral infections typically only get worse. To elaborate:
HIV causes immunodeficiency by killing T cells. Firstly, it preferentially infects CD4+ T cells. This process can trigger an inflammatory response and (1) kill the infected T cell, as well as (2) bystander cells. Once the virus has successfully infected a CD4+ T cell, it can happily produce more viruses without killing the cell, which is how the infection can spread - or it can (3) rupture the cell membrane and kill the T cell. Finally, CD8+ T cells can notice that CD4+ T cells are getting infected by a virus and start (4) killing CD4+ T cells.
Immunosuppression after organ transplant can be more specific. It is typically achieved via a combination of drugs which can (1) reduce immune cell activation, (2) slow down immune cell proliferation, or (3) block the activating receptors on T or B cells. The amount and type of suppressants depend on the phase of treatment: induction of immunosuppression, maintenance, or treatment of transplant rejection.1 These drugs are also often administered alongside preventative antimicrobial drugs.
The immunosuppressants which are administered during the maintenance phase - i.e. for the rest of the patient's life - are often the drugs which dampen immune activation instead of eradicating all T cells, and are given at much lower doses. For example, calcineurin inhibitors block the [calcineurin-NFAT pathway];2 when this pathway is blocked, production of immune activators like IL-2 is reduced, and reduces T cell function.
TL;DR: "induced AIDS" is milder and more controlled than actual AIDS, and doctors work very hard to keep patients within a safe range of immune function/suppression.
PS: Good question! Made me think :) I've written some papers on organ transplantation before so am happy to do some digging to add sources.


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How specimens are organized in a large biological specimens archive
In a library, (and I'm not totally sure about this, but from experience) books are organized by category/theme into sections, and then they are given a number so that, globally, the numbers are ordered sequentially. This way you can easily just look up a number and go right to it, but then you can also browse entire sections by a common theme. I'm not sure how exactly they do this, but this is roughly what I've seen how it works.
So I'm wondering how biological specimens are organized in a gigantic specimen archive like at a large museum or university collection, with hundreds of thousands or millions of specimens. I'm wondering if they just give them a random number, and then place them wherever that number falls in the sequence. Or if they do like the libraries and group them by category/theme, then by number. Or something different.

Do you mean like binomial nomenclature?

Biological specimens are ordered in museums phylogenetically. So all the birds are in one place, and the insects in another. Fossils are generally kept in their own place. Different museums may have their own standards, but most sort specimens phylogenetically as well. But alphabetical sorting also happens. So that all the members of a family are in one place, and then the genera within the family are organized alphabetically. So all the Trichoptera (Insecta), for example, at the Smithsonian are together on one of the floors with other insects, curated by a Trichoptera specialist. Within Trichoptera, the first drawers are Apatanaeidae, and the last are Xiphocentronidae. Individual specimens are often given a unique number, usually sequential, with the time of accession into the museum.

As an addition to Karl Kjer's answer
Fossils specimens are usually ordered by locality(where it was collected) or phylogenetically, but size and shape is often more important as well. its hard to keep 3000lb sauropod pelvis in the same place as 3 ounce microraptors bones, but large sauropod bones and large pieces of petrified wood might be stored together.  This is why good records are important in fossil collections, physical limitation often trump ideal cataloging. Fossil collections are often constantly growing as well which is why locality is often better than phylogeny, you don't know how many of anything you will end up with, but at least you can group things by where it came from.


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Melting point of animal fat and plant fat
I notice in daily life that animal fat typically has a higher melting point than plant fat does. I wonder the reason why this happens. What exactly contributes to this difference? Is it because of the difference between molecular structure? I understand that substances have different melting point because the intermolecular forces are different. But how does intermolecular force vary between animal fat and plant fat. Is it possible for any animal fat to have lower melting point than plant fat?

Is it possible that "daily life" is imposing a selection bias?  That is, we mostly see plant fats in the form of things like cooking oils (or cocoa butter), which are selected because they have low enough melting points to be liquids.

Plants contains monounsaturated fats while animals contains saturated fats. The high proportions of fatty acids in animal fat means it takes longer to heat it up. I don’t know the melting points of different things off the top of my head, but you can find a meat that is as unsaturated as possible and compare it to the most saturated plant fat to test your last question.