What is doubling of genetic material invented in flowering plants? David Attenborough in his Kingdom of Plants 3D said, that flowering plants made two inventions: (1) doubling of genetic material and (2) symbiosis with animals.

What was meant by "doubling of genetic material"? Appearing of diploidy or something else?

UPDATE

Let me explain my doubts. Inventing of ploidy I regard as inventing of sex and syngenesis. This was done ~500 million y.a. in Ediacarian, if I am not mistake. Hence, this can't be done 140 m.y.a when flowering appears. I.e. both plats and insects had sex 140 mya.

Yes, D. Attenborough probably refers to ploidy number

Ploidy number

Humans for example are 2N (except during the spermatozoid and ovule phase of human existence) meaning that they carry two copies of each autosome (=non-sexual chromosomes). Some species are 1N (haploid), some are 3N (triploid), etc… It would actually be more correct to talk about the time a species spend in each of its phase or talk about the number of cells in each of its phase because many species undergo change in chromosome number during their existence as it is the case for humans. Humans are 2N most of the time but they are 1N when they are ovules or spermatozoid. The correct word to describe the human lifecycle is diplontic. Some species are diplontic, some are haplodiplontic and some have phases when they have a greater number of chromosomes. Those species are said to be polyploid.

Ploidy number, chromosomes and chromatids

To make sure one don't mix up things... One chromosome is made of one or two chromatids (depending on the cellular phase). The chromatids of the same chromosome (called sister chromatids) are (almost completely) identical. A given "chromosome type" is either alone (1N) or accompagnied by one very similar chromosome (2N) or two other very similar chromsomes (3N), etc.. Considering the case of a 2N individual: If at a given locus (position in the chromosome) the two alleles (gene variant) are different than the individual is said to be heterozygote for this locus. The ploidy number describe "this number of chromosomes"! Now there may have different number of different "types of chromosomes". Humans for example have 23 different types of chromosomes and in its haploid phase has therefore 23 chromosomes (23 or 46 chromatids depending on the cellular phase) and has 46 chromosomes (46 or 92 chromatids depending on the cellular phase) in its diploid phase

Ploidy number in angiosperms and other plants and non-plants organisms

Yes, D. Attenborough (who I don't know and I haven't read anything of his work) probably means doubling, tripling, quadrupling, .. the number of N of chromosomes. And, yes indeed polyploidy (3N, 4N, 6N, 8N) is relatively often observed in flowering plants. There are many crop species that are polyploid. According to this article an important part of the speciation that occurred in plants is accompanied by a change in ploidy number but this is not only true for angiosperms.

Polyploidy is also found in many fungi species and some animal species as well. There are lots of terminologies linked with the discussion of chromosome number and reproductive system and many articles discuss these mechanisms and also the evolution of polyploidy. I found the work of Sally Otto to be of the greatest interest for example.

Notes

The words inventions are not really used in evolutionary biology but rather in popular books. Also, there are many non-angiosperm plants that have symbiotic relationship with animals. For examples: some angiosperms and the squirrels or birds. But it is true that angiosperm have particularly important symbiotic relationship with animals, in particular insects and this probably allowed an important diversification in both angiosperms and insects. As already said angiosperms are not the taxon of plants to include polyploid species. There are other characteristics that allow to tell an angiosperm apart from other plants. The number of aperture on pollen grain or the positions of the meristems (tissue where mitotic division of unspecialized cells occur allowing the growth of the plant) for examples.

You may be interested in reading this post on the effect on fitness of ploidy number


Protein molar mass from Uniprot ID? I have a long list of uniprot IDs. How can I get the mass of the "canonical" isoform for each? Ideally from some Python library.

You don't need any external library, it's enough to query Uniprot and extract the data you want from the response.

Here an example in Python 3:

from urllib.request import urlopen

id = "P42212"
data = urlopen("http://www.uniprot.org/uniprot/" + id + ".txt").read().decode()
result = data.split('SQ   ')[-1] #here all the info you need
mw = int(result.split(';')[1].strip().split()[0]) #extract the molecular weigth
print(mw)

If you want to batch query a lot of sequences then I suggest to sleep(0.5) after each query to avoid problems with their server.

Update

As correctly pointed out by @Jerven (see comment below), you can query the mass directly.

In this case, the code is the following:

from urllib.request import urlopen

id = "P42212"
data = urlopen("http://www.uniprot.org/uniprot/?query=id:{}&format=tab&columns=id,mass".format(id)).read().decode()
result = data.split('\n')[1].replace(',','')
mw = int(result.split('\t')[-1])
print(mw)


Sequence compression method / format As someone working with sequencing data and sequence files I was wondering whether is there a compression method / format for sequence / read files? Of course one can use general compressors like rar or zip to compress a fasta file, which is suitable for transferring data, but reading the sequence out of it is infeasible. Also I'm aware of BAM file format which is a block copressed gzip file of a SAM file, but as far as I know it is mainly used in alignments. But is there a compression for plain fastq(-like) files for storing millions of reads or a collection of sequences while being able to get sequence and quality info directly from the file?

BAM is the current standard for sequence alignments, and can be used to store unaligned reads/sequences, but when used for unaligned sequences also contains unused alignment data that would bloat the file.

An alternative way to compress a DNA sequence file is via 2-bit (or 4-bit encoding) which can compress the sequence content by 75% (in 2-bit encoding, each nucleotide can be represented by 2-bits in the file eg A: 00, G: 01, C: 10, T: 11). I do not know of a generalizable tool that will compress/decompress aside from rolling your own. Further, the data must be de-compressed prior to streaming it into any alignment/sequence software. For general purpose compression algorithms, bzip2 can outperform (at least in compression) other algorithms (eg zip, gzip)


Is there a hypothesis that attempts to explain patterns of species richness along all three energy-related environmental gradients? My question is related to one of the oldest question in ecology: "What determines global patterns of species richness?". However, I want to focus on one particular part of this question, which has been bothering me for a long time.

Background information

One of the most widely recognized ecological patters on Earth, which is found at most scales and in most biological taxa, is the latitudinal diversity gradient (LDG) -- there are more species in the tropics than in the temperate regions, and the further away you move from the tropics, the fewer species you encounter. Furthermore, such pattern exists not only along the latitudinal gradient, but species richness also covaries with altitude in terrestrial environments and depth in marine environments, showing the same diversity gradient!

It seems to be fair to suggest that energy should somehow underline all these diversity gradients and create some sort of universal mechanism that would ultimately affect all species richness patterns on Earth. Unfortunately, there is no consensus on questions as grand as this one, but I'm looking for hypothesis that would specifically attempt to explain all three gradients together.

Question

Is there a hypothesis that attempts to explain patterns of species richness along all three energy-related environmental gradients together: latitude, altitude and depth? If there is, what it's weakness? If there's no such hypothesis, do we have reasons to believe that such a broad link across the three gradients can exist?

Please note how I'm trying to emphasize that I don't want you to list all the hypotheses that describe LDG only, but rather the three gradients together.

This is a big question and a very active field of research. I'm not deeply into this litterature, but you should look into the the different scaling relationships (often power laws) that have been described on metabolism vs body size, species-area relationships and species richness vs biomass. Also consider that energy-use by species in a community is considered a zero-sum game both in the neutral model (Hubbell, 2001) and in Red Queen models of evolution. You will probably not find a definite answer to your question though, but there are some interesting intersections of ideas out there. As others have suggested you also need to consider and take into account differential historical extinction rates, and how this will influence current patterns (Mittelbach et al. 2007).

Points of entry could be:

Gaston. 2000. Global patterns in biodiversity (essential reading!)
Chave. 2013. The problem of pattern and scale in ecology: what have we
learned in 20 years?
Venevsky & Veneskaia. 2003. Large-scale energetic and landscape factors of vegetation diversity
Mittelbach et al. 2007. Evolution and the latitudinal diversity gradient: speciation, extinction and biogeography
Marquet et al. 2005. Scaling and power-laws in ecological systems

A couple of caveats/ideas though; first of all, it has been argued that the latitudinal gradient of species richness is likely to be due to many different mechanisms in different taxa (see Gaston, 2000). Here you are looking for a hypothesis to explain not only this single pattern, but all three of them, which makes a single explanation even less likely. Second, many non-exclusive explanations have been put forward for the latitudinal gradient. Even if we don't know which ones of these that are the true mechanisms, some are clearly incompatible with being explanations for all the three patterns you mention, while others might be applicable to all of them. For instance, environmental stability in the tropics is one suggested mechanism for the latitudinal gradient, but this doesn't make much sense for a gradient along ocean depth (deep sea has arguably been a more stable environment both over shorter and longer time-frames). It might be relevant for an altitude gradient though. Going through different hypothesised explanations for the latitudinal gradient in this way (from what I know, the best studied of these gradients) could give you a list of ideas that are most interesting to target (maybe somebody has already done this though).

I hope this helps.


Exocytosis of synaptic vesicles I'm reading the following paper:

http://jcs.biologists.org/content/123/6/819

The part I am really confused about is when they say:

  Exocytosis appears to use two alternative pathways: clathrin-mediated endocytosis (CME), which is well established by numerous lines of evidence, and the more controversial ‘kiss-and-run’ pathway, which involves direct retrieval of a vesicle at the site of fusion

My question is .. How can exocytosis (contents inside of cell are transported to outside of cell) use clathrin mediated endocytosis?

I thought endocytosis is the opposite of exocytosis, so why do synaptic vesicles use clathrin mediated endocytosis as a method of exocytosis?

That sentence is located in a paragraph titled "Stages 5-7: Endocytosis and recycling": it's talking about recycling exocytosed membrane which is necessary for making vesicles for further exocytosis.

The sentences before the part you quoted are:

  Synapses possess highly efficient mechanisms for retrieving SVs from the plasma membrane of the presynaptic terminal after exocytosis. Fast regeneration of functional SVs is a prerequisite for synapses to function during prolonged activity.

I think the passage is just somewhat confusingly worded, in that "exocytosis" is used as the subject of the sentence which is strange in this context. You could rewrite that sentence:

  There appear to be two alternative pathways to recycle membrane for exocytosis: clathrin-mediated...

The author likely intended the word "exocytosis" in the original sentence to mean "the entire process of releasing synaptic vesicles, including formation of those vesicles" rather than the specific event of vesicle fusion with the membrane. Kind of like if I referred to "planting trees" as part of "logging" - you typically think of "logging" as cutting down trees, but in the right context it can make sense to refer to the process: you need to have a tree there to be able to cut it down. I could say "Trees are necessary for logging. Logging uses two alternative pathways: planting trees directly as saplings, or leaving land to grow new forest naturally over a number of years."


Are there any known microbes capable of living in almost pure carbon dioxide? Some bioengineering is investigated in high carbon dioxide environments. Are there any microbes like bacteria or Archaea capable of living and multiplying in such environments?

These aren't technically extremophiles, but one paper identified twenty species of bacteria that grow under a low pressure, mostly CO₂ atmosphere1.

One relatively well studied species is Serratia liquefaciens (a Proteobacterium) that has been shown to grow under

  low temperature (0 °C), low pressure (0.7 kPa), and anoxic, CO2-dominated atmosphere-conditions intended to simulate the near-subsurface environment of Mars2.

References:

1: Schuerger, A. C., & Nicholson, W. L. (2016). Twenty species of hypobarophilic bacteria recovered from diverse soils exhibit growth under simulated martian conditions at 0.7 kPa. Astrobiology, 16(12), 964-976.

2: Fajardo-Cavazos, P., Morrison, M. D., Miller, K. M., Schuerger, A. C., & Nicholson, W. L. (2018). Transcriptomic responses of Serratia liquefaciens cells grown under simulated Martian conditions of low temperature, low pressure, and CO 2-enriched anoxic atmosphere. Scientific reports, 8(1), 1-10.


Is there a protein in the eye that gets kinked by photons and shipped down to the liver to get un-kinked? My friend made the claim that there exists a protein in your eye responsible for vision. This protein is sensitive to different wavelengths of light, and when it gets hit by the right wavelength, it kinks. In order to be un-kinked, he claimed, it has to be shipped down to the liver, and then back up to the eye.

He teaches organic chemistry at UCLA, so I trust him a little bit. But I couldn't find this with a quick search. Anyone know if this is legit?

The protein is called rhodopsin and the bit that gets kinked up is called retinol.   Normally when light hits it, it does trans to cis isomerization at the 11th carbon.  'kinks up' is a pretty apt way of describing it.

I'm not familiar with the shipped down to the liver part, but I'm guessing that the photo reaction of the retinol with itself or the protein must occasionally make the rhodopsin-retinol complex unfunctional - perhaps by the double bonds cross linking to other atoms in the retinol or to the protein.  As I understood it the retinol just straightens out again.  This reference shows that in the presence of rhodopsin, 11-cis retinol will become all trans again normally.

There should be enzymes in the liver that can recycle some messed up retinol configurations.  Its probably not the main route through your body. Retinol is stored in the liver from dietary intake, and then shipped via retinol binding proteins to the eye. So that is the organ which is the source of retinol in the human body (and probably most animals).  It should catch damaged retinols and refurbish them the same way it does those taken in via the diet.


Epitope annotated protein What is epitope annotted protein??  The book from which I got this term is : http://www.springer.com/biomed/immunology/book/978-1-4939-1114-1

First, when asking about a specific small term, it's best to check your spelling.  If you actually look at the sentience, you will note that you left out a very important hyphen:

  Pellequer compared several propensity scale methods using a dataset of
  14 epitope-annotated proteins. [emphasis added]

The phrase means that the protein sequences (amino acid sequence) has the epitopes marked on them.  If you look at the cited paper, you will see the various tables and break downs of determined epitopes.  Pellequer's group did a lot of the early work when people were still working on techniques to "map" out the locations of epitopes (which are often not in linear segments of the protein sequence due to the protein structure).


Asexual reproduction and Telomeres Many eukaryotic organisms like yeasts, hydras , planarias, plants etc reproduce asexually.

Replication of End of linear DNA pose a limit to the number of cell divisions.

My question : Do asexually reproducing organisms have telomerase in all their cells ? Is the telomerase activated at specific times at specific places ?

If they don't, how can they reproduce infinitely ?

Here is a study of planarian worms, which are immortal in asexual reproduction and mortal in sexual reproduction.

Hydras also become mortal after they reproduce sexually.

Relevant to your question: Cells within planarian worm differ in expression of telomerase active subunit depending on body part. Immortal (asexual) worms have more expression in the area around the pharynx, those cells there are "the proliferative stem cells". There is a nice figure in the article.

I assume it is similar for hydra, that outer body coat has less expression than the cells inside. “Hydra is a bag of stem cells”

(Less relevant (a version of previous version of my answer. But does not answer the "every cell" inquiry well): In planarian worms "We demonstrate that this difference is reflected in the expression and alternate splicing of the protein subunit of the telomerase enzyme." The mentioned telomerase subunit was 1. comparatively more transcribed in immortal (asexual) worm and 2. within the resultant trancripts, there were possibilities of functional and non-functional isoforms due to alternate splicing. Immortal worms had higher ratio of functional isoforms. Summary: immortals have more transcripts and higher proportion of functional versions of them.)


Why are the pulmonary vein and artery not like the rest of circulatory system? I'm learning anatomy. What I learnt is that we have arteries that have oxygenated blood which appears red in color, and branch blood to arterioles to deliver blood to cells via capillaries from where de-oxygeneated blood is collected via venules into veins to go back for oxygenation. So:

artery = oxygenated
vein = de-oxygenated

However, in defining the pulmonary vein and pulmonary artery, I see the reverse of these definitions.
The pulmonary artery is for de-oxygenated blood.
Why is it so?

It is true that nearly all arteries carry oxygenated blood and nearly all veins carry de-oxygenated blood, but that is not what defines them. Arteries are blood vessels that carry blood away from the heart, and veins carry blood towards the heart. If you look at the situation in that light, the naming makes sense: the pulmonary artery is carrying de-oxygenated blood away from the heart to the lungs, and the pulmonary vein is carrying the re-oxygenated blood back to the heart, to be pumped through the rest of the body.


What are the distinctive structural features of single- or double-stranded xRNA, or where can I find them? I am interested in the structural differences caused by benzopurines and benzopyrimidines at the oligonucleotide level between RNA and xRNA, both in single-stranded and double-stranded form.

I am aware of RNA's tendency to be found in the A-form, of which the details are found here. However, other than the obvious nucleobase expansion, I can't seem to find any details about xRNA's secondary structure.

The only paper I found that examined the question is "Structural, Dynamical, and Electronic Transport Properties of Modified DNA Duplexes Containing Size-Expanded Nucleobases". They state

  The results confirm that the structural and flexibility properties of
  the canonical DNA are globally little affected by the presence of
  benzo-fused bases. The most relevant differences are found in the
  enhanced size of the grooves, and the reduction in the twist.

They also have a picture comparing the structures of conventional DNA and xDNA:

So while the basic structure seems similar, the difference in diameter and twist look rather large to me.

This is for xDNA, I would assume that xRNA behaves comparably if double-stranded. It would have to somehow fit the larger nucleobases into the helix like xDNA. And the structure of single-stranded RNA is variable, helical parts would probably look similar to xDNA, hard to say how the modified nucleobases would affect tertiary structure.


Deducing protein sequence length from gene DNA sequence length Is there a standard way to deduce protein sequence length from gene DNA sequence length of the gene coding for it?

Naively I had assumed that amino_acid_seq_length / 3 -1 (deleting one for the stop codon)ought to work but apparently not always. Is there a better way?

Let's assume the gene is eukaryotic, specifically a plant gene.

e.g.

Or

If you look at the DNA sequence in the patent, you will see that it does not start with ATG and does not end with a stop codon. The disclosed sequence has some additional bases in it, therefore the discrepancy in protein and DNA length. Those additional bases almost always occur in cDNA, e.g. because of polyadenylation, Kozak sequences, etc.


Can animals and humans be ranked in their ability to detect moisture? One reason for insects being so successful - about 70% of all animal species - is their excellent ability to detect moisture. Take termites for instance. The soldiers boot out the flying reproductives only when it will rain within 24 hours. Because moisture will be needed to survive and make a new termite nest.

Humans by contrast are hopeless at detecting moisture; humans do not have the senses to be able to predict rain. Except by more indirect methods and science.

So my question is is there any way of ranking the different abilities to detect moisture? This is not a list question. Rather, it's steering for a formula or set of variables. Are there factors that make a dog better at detecting moisture than cat for instance, if that is the case?

I am surprised that nobody seems to have done this for something - water and moisture - that is so vital for life.

I think you simply Can't.

To design an experiment you need 2 things:

1- Something Common between Humen and Insect and can be measured.

2- Different scale to order the species.

And I Think here you just do NOT have both criteria.


How to find transcription factors? I need to find master transcription factor(s) regulating secreted proteases in a fungus to be disrupted toward upregulation and overexpresion of extracellular recombinant proteins.
How can I detect transcription factors and preferably master TFs (master regulators) in an organism? Does NGS applicable to find TFs and preferably the novel ones? I know ChIP-seq is used to identify TF binding sites but how about detection of the TFs that bind to these sites?

How can I detect transcription factors and preferably master TFs (master regulators) in an organism?

The easiest approach to find transcription factors for any given organism would be based on sequence homology with other transcription factors. In order for this to work your organism of interest does have to be sequences, you can check this (e.g.) on the NCBI genomes page. By comparing the genome or the genes of your organism with other known (fungi) transcription factors, you can find most of the transcription factors of that organism.

  Does NGS applicable to find TFs and preferably the novel ones?

Both NGS and ChIP-Seq only allow you to determine DNA (or RNA if you reverse transcribe first) sequences. Therefore these techniques alone will not help you in identifying which TFs act on your genes.

  I know ChIP-seq is used to identify TF binding sites but how about detection of the TFs that bind to these sites?

I can't currently think of any 'classical' or standard experiments to determine which TFs bind to a given gene or promoter. One possibility would be to use CoIP (co-immuno precipitation) on the RNA polymerase complex and use Mass-spectronomy to identify the TFs in that complex. The problem with this is going to be, that you need a way to only get the RNA polymerase complex for your genes of interest and not all the other ones in the cell. Maybe you can use columns with DNA probes that can hybridise with your genes instead of standard antibody based CoIP.

Another way to determine which TFs bind the promoters of your genes is to analyse the respective promoter sequences. However, without knowledge of most (or at least some) of the binding sequences of the TFs in your organism, this will most likely not work very well. Edit: As @AlanBoyd commented there is a database for fungal transcription factors. However, it seems like they mainly annotate which fungi genes are transcription factors, but do not cover binding motifs of these factors.


Are these spider eggs? I was pulling weeds in my backyard in Southern California, when I saw a spider over a white area on the underside of one of the leaves. It's staying right near the white spot. Are those spider eggs? Also, what kind of spider is this?

Yes, those are definitely eggs.  And I believe that is a female grass spider (Genus: Agelenopsis).

Eggs are typically laid in late summer or fall and spiderlings emerge
the following spring....A female that has mated with a male can produce more
than one egg sac. For some species,  it’s common to see two sacs at a
time, side by side, attached to a surface (such as the underside of a
rock, piece of wood in a wood pile, or in a rolled up leaf, for
example). Each different species of Agelenopsis may create a slightly
different egg sac, but typically each one contains anywhere from 50 to
200 individual eggs. The mother spider will remain near her eggs,
dutifully guarding them, until she dies around the onset of winter.

This seems to fit the picture to a T.  I'm not 100% about the species, but I believe it is either A. aperta or A. oregonensis.
Edit:
As user Xan pointed out, this could likely be a lynx spider (Genus: Oxyopes; likely species: Oxyopes salticus - female).  This would explain the defined setae (bristles) on the legs.  To really decide, you would need to check the following characteristics:

Eye pattern: Lynx spider eyes form an octoganal pattern, while grass spider eyes form two, parallel, curved rows.
Spinnerets: You would have to search for spinnerets on a lynx spider, while grass spiders have two very prominent hind spinnerets that you can visibly see from above.

I originally thought those were spinnerets in picture 3, but upon closer inspection it looks like one of the hind legs folded underneath.


Can someone help me answer or explain how to answer questions about DNA coding capabilities? How is it that a DNA coding system with only 4 bases can yield so many possibilities? Also, how many unique coding sequences can there be with a DNA code that is 8 base pairs long? Hint: 4^n combinations. I've gone through this in my textbook, but I don't understand how to get the answer for it.

4 bases (A T C G) leads to 4 possible value per bit of information, which then leads to the formula: 4^n (n being the number of base). For the first part of your question regarding how can you have so much information, it has to do with n, as you increase the number of bases the number of different combinations increases exponentially. For a comparison, your computer stores information in a 2 value bit system (1 or 0).

If you plot the number of possibilities, you will see that DNA outpace computers very quickly, as an exponential of base 4 will go faster (2*2 = 4, 4*4 = 16, already at 2 bits you have 4 times as many possibilities)

With that in mind, you can compute the number of possibilities for any given number of bits (or bases in your case).


Does this recording sound like the pulses emitted by bats? Out of curiosity, I recorded sounds in an area with lots of bats, hoping to be able to "hear" the bats communicating by lowering the ultrasound to a level down to the frequency which can be heard by a human.
After a bit of post-processing, I actually hear interesting sounds, but I'm not sure about the origin. It seems that the frequency of the pulses is too low compared to bats.
The final audio is available on YouTube.
Are those actual sounds emitted by bats? If not, what other animal could be the source of those sounds?
About the audio
The sound was recorded at 10 p.m. at 46°34'32.0"N, 0°20'45.4"E near a river, with more of a dozen bats flying in this zone. There is a bridge nearby, and the sides of the river are flat concrete, which means that there are a lot of opportunity for sound reflection (although high frequency sounds don't reflect well).
Zoom H5 with the default XY directional microphone was used. The bitrate was set to 24-bit. Unfortunately, I used the sampling frequency of 48 kHz instead of the maximum 96 kHz.
The following transformations were made to the original audio:

The pitch was shifted by -12 semi-tones, which means that the 20 kHz sound becomes 10 kHz, and 15 kHz becomes 7.5 kHz.

All sounds below 6 kHz were removed.

The sound was amplified.

Severe noise reduction was applied to eliminate everything but the actual sounds emitted by the bats.

The empty parts of the audio were removed.

The sound was amplified once again.

Frequency
The frequency analysis of the transformed audio a peak around 9 kHz (18 kHz in the original audio), slowly fading to suddenly drop at 16 kHz (32 kHz in the original audio).

hypertextbook contains many sources with different indications about the frequency range of the sounds emitted by bats, only a few referencing the frequencies low enough to be heard by a human:

Frequency Produced 10kHz-120kHz
Ramsey, Gabriel, McGuirk, Phillips, Watenpaugh. Holt Physical Science. New York: Holt, Rinehart and Winston Publishers, 1986.

while most agreeing on the fact that bats use frequencies higher than 20 kHz.

Most bats use frequencies in the range 20-80 kHz, only a few bats use frequencies less than 20 kHz.
Long, M.R. & Savage, J.G. Mammal Evolution. New York: Harper, 1976: 108.

The observed range of 18..32 kHz seems too low compared to the sources, but I have an impression that the frequencies vary a lot between different species of bats.
Pattern
When viewing the audio track (see below), each cry consists of several pulses in two to three sub-groups which are in turn in two groups. Each peak is a bit less than 1 ms. The second group occurs from 40 to 200 ms. after the end of the first one. Each sub-group is separated by 5 to 10 ms.
The frequency of every pulse doesn't vary, except the very first pulse. The first cry starts by a more quiet pulse at 6 kHz (12 kHz in the original audio). The second and third cries don't follow this pattern.
Hyperphysics indicates that there are three categories of sounds emitted by the bats:

Short clicks,

Frequency-swept pulses,

Constant frequency pulses.

It looks like it's still the third category which we are observing here, and the overall pattern looks similar to the one described for the bats.
The gap between the left and the right track is mostly irrelevant: at higher frequencies, microphones become more and more directional, and the sound is reflected less, which leads to such difference.

Note: this question was considered to be on-topic at Biology.SE on Meta.

Though I cannot be 100% sure from the sound quality, it certainly does sound/seem like bats are making the calls you are hearing/seeing. I spent a number of years as a bat bioacoustics researcher and I came across similar sounds frequently and was able to confirm they came from foraging bats.

I'll have to see if I can find any old spectrograms or recordings on an old data hard drive. If I can find clear examples similar to yours I will add them to my answer. (Though I haven't seen that hard drive in years, so don't get your hopes up!).

These sounds can likely be explained by one of the following:

Some bat species have been known to echolocate using calls that sweep into human hearing range (i.e., below 20kHz; Fenton, 2015; other sources already mentioned).
Many bats actually emit calls during flight that differ in structure from echolocation calls; these calls, often referred to as “social calls,” may occur between echolocation calls and often consist of broadband calls with low-frequency components and multiple syllables (Altringham and Fenton, 2003; Wright et al., 2013).
Some bats use special sounds to avoid collisions with each other while in flight (Fenton, 1983).

You can see and hear examples of some social calls (used broadly in this case) for a pipistrelle bat in Britain here.

I copy a spectrogram of one of these social calls from the above link (see the middle call signature):

Wright et al., 2013 also provide a spectrograph demonstrating all the various call signatures they recorded from various Eptesicus fuscus (big brown bats) in the United States:

Purchasing some bat bioacoustic analysis software should assist with your recordings and call interpretation. I recommend Sonobat (best, but expensive) or SCANR (from Binary Acoustic Technology). There are other less used options as well (e.g.,the Echo Meter Touch Bat Detector for Apple, for which I picture an example screen shot below):

I also want to provide some information and citations about bat echolocation to help inform those interested in this question. I would include this in the comments, but it's too long:

Bat Acoustics 101

Shorter wavelengths (higher frequencies) provide a better resolution of target detail allowing the bat to receive a more detailed picture of its target (Fenton, 1983).
Acoustic energy reflected from a target is theoretically greatest when incident wavelengths of calls are near the same size or smaller than the target (Jones and Rydell, 2003); otherwise, if the object is smaller than the wavelength, the sound will be scattered instead of reflected (Yalden & Morris, 1975).
Bats need to be close to objects to "see" them: range is typically 1-5 m for frequencies around 20 kHz and increasingly closer for higher frequencies (Jones and Rydell, 2003).
In addition to target range, bats perceive target shape and texture from the delay of multiple reflections (echoes).
Calls contain base frequencies, but they can also add harmonics & overtones to the bandwidth of the calls, which can enhance target ranging and localization (Jones and Rydell, 2003) and thus increase acuity (Fenton, 1983). They can also suppress certain harmonics and use variations of combinations of tones.
Bats can also vary the amplitude, or loudness, of their calls (Yalden & Morris, 1975).
Bat calls can be composed of frequency modulated (FM) or constant frequency (CF) components or a combination of both types of calls (Jones and Rydell, 2003).

FM = each signal, consisting of discrete pulses of sound (Fenton, 1983), starts at one frequency and sweeps down to another. Sweeping through a range of frequencies allows bats to achieve some protection from errors associated with Doppler shifts; in addition, the modulation of frequencies helps to tell the bat about the texture of the target (Fenton, 1983).
While foraging, FM bats create a series of repeating ultrasonic pulses in various phases.  There are three major phases, each with an increase in repetition rate.   The change in rate across the phases can go from 4-5 pulses per second to 200 pulses per second.

The signals bats produce may serve multiple functions; they can be used for echolocation as well as for communication, whether intentionally or unintentionally.

Use echolocation calls of others to locate roosts, and eavesdropping also allows a territorial bat to distinguish between another bat trying to steal its food or just one passing through its territory (Fenton, 1983).
“Social calls" (Altringham and Fenton, 2003; Wright et al., 2013).
Collision avoidance sounds (Fenton, 1983).
Alarm calls and distress calls when in stressful situations.
Mother-young communication.


How do prions cross the blood brain barrier? How does the PrP scrapie protein maintain its confirmation while going through the GI tract? How does the PrP scrapie protein cross the blood brain barrier?

Wouldn't the host immune system recognize the prion as "not self" and attack it?

I am not sure if a perfect answer is possible owing to the fact that Prion diseases are still incompletely understood, and are actively under research. On a preliminary search, I found some papers which address the issue (cited at the end).

Since $PrP^C$ is normally found in the body, its role and its transport is also relevant to the issue. It seems to undergo bidirectional transport across the BBB using a saturable mechanism, mostly a specific transporter (1). It is taken up peripherally, and by several regions of the brain with the possibility that it is involved in various brain functions including modulating the BBB itself. Amyloid Beta-protein, with several kinetic and dynamic similarities with $PrP^C$, is shown to have BBB altering effects. (2) How far do the pathological prions follow this is seemingly unknown.
Autonomic nerves seem to play a role in their transport.(3) When challenged with prions, sympathectomy delays or even prevents the disease, whereas sympathetic hyperinnervation accelerates prion pathogenesis. There have been studies to elucidate the transport via the nerves, such as (4) and (5).

There are several other studies on this issue, and following the cited references might help you find them.

Reference number 3 also has information on the immunological response to prions.

References:

Banks WA, Robinson SM, Diaz-Espinoza R, Urayama A, Soto C. Transport of prion protein across the blood–brain barrier. Experimental neurology. 2009 Jul 31;218(1):162-7.
Giri R, Shen Y, Stins M, Du Yan S, Schmidt AM, Stern D, Kim KS, Zlokovic B, Kalra VK: Am J Physiol Cell Physiol. 2000 Dec; 279(6):C1772-81.
Aguzzi A, Zhu C. Five questions on prion diseases. PLoS Pathog. 2012 May 3;8(5):e1002651.
McBride PA, Schulz-Schaeffer WJ, Donaldson M, Bruce M, Diringer H, Kretzschmar HA, Beekes M. Early spread of scrapie from the gastrointestinal tract to the central nervous system involves autonomic fibers of the splanchnic and vagus nerves. Journal of virology. 2001 Oct 1;75(19):9320-7.
Glatzel M, Heppner FL, Albers KM, Aguzzi A. Sympathetic innervation of lymphoreticular organs is rate limiting for prion neuroinvasion. Neuron. 2001 Jul 19;31(1):25-34.


Why do home-grown fruits tend to taste better than mass-produced consumer fruits? It is often heard that home-grown fruits and veggies are a lot tastier than the produce found in the supermarket. Although this question may contain a skeptics element in it, it is so often heard there must be at least some biological ground behind it.

"Industrial" fruits and vegetables are not grown as much for flavor as for convenience, pest resistance, appearance, resistance to peel problems, resistance to bruising, etc. etc. Profitability is the main consideration.

There are many varieties of apple grown in orchards that taste wonderful (better than my grandmother's gnarly green apples) but don't hold up to shipping and storage well.

Finally, please don't get your information from fantasy tales. There are so many good sites for attaining information.


Is tactile perception two-dimensional or three-dimensional? Is tactile perception two-dimensional or three-dimensional? Can tactile sense be mapped on 2-dimensional map of the surface of the human body or does human receive tactile signal as a 3D position (owing that internal organs can also feel pain)?

It's not 2D: Tactile perception can very simply understand a ring around your finger. If you projected the skin of your body onto a 2D plane there would be a way to represent this sensation, but only as an irregular shape. So you need a third dimension to cognitively process this sensation.

But Phantom pain tells us the brain doesn't always register tactile perception from a true 3D mapping. For example a person without an arm could feel pain in a finger that doesn't exist. Not always, but sometimes.

So it's greater than two, and sometimes three doesn't fully describe the known phenomena. Therefore it's (at least) 4-D.


Calculating photosynthetic efficiency While calculating photosynthetic efficiency, do we take into account the Gross Primary Production or the Net Primary Production ?

We can actually use either depending on the specified convention, but a more convenient way to characterise the photosynthetic efficiency is:-

Considering the total incident solar radiation instead of that part which is absorbed (so that the calculated efficiency takes into account the total available solar energy on earth)
Using Net Primary Productivity instead of Gross PP.(so that the efficiency is characterised by the useful output (product) of photosynthesis by removing the non-useful respiratory losses of plant.)

I should also mention that using GPP instead of NPP was the practice followed in a large number of texts I read. But I think using NPP is not only the modern view, but also scientifically more convenient.

Here is the wikipedia page on photosynthetic efficiency and here is the book which houses the technicalities of these definitions along with several values of the various efficiencies.


Main mechanism of the evolution of sexual dimorphism Sexual dimorphism is very common and (normally) requires the evolution of sex-specific genetic variation/regulation so the genetic correlation between the sexes can be <1. Is there consensus as to how this type of variation predominantly spreads?

I can see it could evolve by drift and selection and I expect it is predominantly via selection (sexually antagonistic selection for different optimal genotypes)- We typically associate sex differences in traits with sex differences in selection (ecological, sexual selection...).

Sexual dimorphism evolves, as you suspect, via natural selection, specifically sexual selection (which I view as a form of natural selection).  Genetic drift, by definition, is random. Random changes of allele frequencies are extremely unlikely to lead to the consistent evolution of phenotypic differences between males and females.

Sexual selection on the other hand can lead to rapid evolution of secondary sexual characteristics (sexual dimorphism). If you consider natural selection in the broad sense, an organism's traits affect survivorship but do not guarantee reproduction. Individuals that live longer have an increased chance of reproducing more frequently but this does not mean the organism actually will reproduce more often than any other individual. In contrast, sexual selection acts directly on mating success. If a female chooses a male based on his secondary sexual characters, then that male will mate. His fitness (offspring produced) will be increased relative to males that are not chosen and do not mate. This can lead to runaway sexual selection for male traits and even speciation.

You are correct that sexual selection results from sexual conflict. Such conflict can arise because females invest considerable energy into relatively few eggs. Thus, it benefits her to be selective for her mates. If she chooses poorly, her fitness can be decreased quite a bit. On the other hand, males can produce copious quantities of sperm rapidly and with little energy cost. If a male wastes sperm on a genetically-poor female, his fitness is not really reduced. He can quickly mate with other females at little cost.

References

Any evolutionary text. They cover the basics of sexual selection in some detail.

Gavrilets, S. 2000. Rapid evolution of reproductive barriers driven by sexual conflict. Nature 403: 886-889.

Hosken, D.J. and P. Stockley. 2005. Sexual conflict. Current Biology 15: R535-R536.

Lande, R. 1981. Models of speciation by sexual selection on polygenic traits. Proceeedings of the National Academy of Sciences USA 78: 3721-3725.


Why is assembling paired end illumina without any input parameters an important problem? In one of the comments in this question about multiple sequence alignment, it was stated

  @5heikki: btw if you want a good bioinformatics problem, come up with an assembler that assembles any paired end illumina run optimally de novo without any input parameters.

What is a paired end illumina? How is optimally defined in this context? What are the usual input parameters?

The Next-Gen sequencers cannot sequence a very long stretch of DNA with good reliability (~150 for the recent model- HiSeq2000; even less for older models such as GA (40), GA-II (70), GA-IIx (90)). For increasing the confidence in a certain hit, it was sequenced from both the ends.
For example, if you have selected 500bp DNA fragment, then after ligating adapters to both the ends, it is sequenced from both the direction up to 150bp. This would leave an unsequenced "insert" region of 200bp. (In the example image below, they have sequenced up to 40bp [case of old GA] )

During assembly you stitch together the fragments of DNA to find out the larger DNA from where the fragments arise. In case of RNAseq, these arise from a transcript, and your assembly should give you the complete transcript (mRNA or ncRNA etc). There are two basic types of assembly: reference guided assembly and de-novo assembly. In the former you use a sequence such as the genome as a reference to assemble the transcripts. If such a reference is not available then you have to go for de-novo assembly.

The assembly algorithms use several parameters and since these are computer algorithms and not some kind of magic, their output depends to an extent on the different parameters.

In case of paired end data there are some parameters that are important. Most important is the size of the insert. In case of a 500bp fragment, you'll end up with an unsequenced region of 200bp. This is not much of a problem with reference guided assembly because you can figure out the sequence of the insert based on where the sequenced region align to the reference. The average insert length is important to remove discordant reads (aligning too far apart in the reference). In case of de-novo assembly, the insert will remain unsequenced even if you know that the final transcript looks something like:

frag1-frag6-frag3-frag9-frag4

So, to get the sequence of the assembly, you need to sequence the insert regions. This is not a problem if you at least know the order of fragments in the assembly. However you should know the insert size to get the assembly size correct and as skyminge said, in scaffolding. Obtaining this insert length is not that difficult (You need not provide it as a parameter. Most algorithms can calculate it automatically).

Another parameter in de-novo assembly is k-mer length (the sequence reads are broken down into k-mers for better assembly). I cannot explain the algorithm of assembly here in detail. You can check the manuals/papers of common assembly algorithms like Velvet, SOAPdenovo, Euler [de novo]; cufflinks [reference based]

I have mentioned transcriptome sequencing here but the principles are same for genome sequencing too.

Back to your main question:
Why is assembling paired end illumina without any input parameters an important problem?

Because it is less effort; but tweaking may be difficult. I won't consider it as an important problem. There are other important algorithmic optimizations that are required with de-novo assembly.


Do telomeres appear at just one end of the chromosome? I have just studied DNA Replication for my Biology Class and I have this question that leaves me stuck, though I have tried to figure it out myself.

During telomere replication, I am aware Telomerase elongates the 3' end of the template strand on both molecules and then DNA repair Polymerase comes in to fill in the gap that could not be previously synthesised after the last primer.
After this is complete, we would have the T-loop formation and Shelterin complex arrangement to protect these ends and form what we know as telomeres. However, if we take both DNA molecules, this only happens at one end of each of them, right? As the other end would correspond to the leading strand.

So I am confused: do telomeres just appear at one end of the chromosome?

This is a great question!  The issue- the "paradox" of replication of linear chromosomes- of trying to filling in the unreplicated region (an overhanging 3' end) should technically be an issue only for one 3' end of each chromosome on any round of replication, as one new 3' end is produced by leading stand synthesis, and the other- the one with the issue- by lagging strand synthesis. However, both ends will have telomeres, they simply trade off being the end with the issue, in each round of replication.  Or you could say, in a single round of replication, one sister will have an issue at the right end end, and the other sister will have the issue at the left hand end.


Is consuming sugar with food as beneficial as consuming glucose (~half of the amount of sugar)? A few years back I heard at biology class that sugar's molecule consists of half the number of elements of a glucose molecule. So not counting the energy needed to transform two sugar molecules in one glucose molecule, isn't it almost the same (eating N amount of sugar) as eating N/2 of glucose?

You have it backwards. One sugar molecule is equivalent to two glucose molecules, though the actual structure of sugar (Sucrose) is a Glucose + Fructose combination.

While Glucose is metabolized via Glycolysis into two molecules of Pyruvate (which are then used in the Citric Acid Cycle), Fructose enters the Glycolysis metabolism at a later stage as shown here:

The GA-3-P is then turned into 2-Phosphoglycerate and then into 2x Pyruvate.

The end result is that a single Sucrose molecule (Glucose + Fructose) [aka - Sugar] is equivalent to 4x Pyruvate, whereas Glucose alone is equivalent to 2x Pyruvate. Or, if you prefer, a single Glucose molecule results in about 32-36 ATP produced, whereas Sucrose will result in 64-72 ATP produced - with ATP being the primary energy carrier of the cell.


Why do people's hands get cold for the first half an hour and then suddenly they are warm when they are doing exercise outdoors in winter? When people do exercise outdoors in winter at temperatures less than zero degree celsius, their hands are quite cold and hurt for about half an hour. Then, there is a sudden rush of blood into the hands and they are warm afterwards, just as if they are indoors all along. Why does this happen and is there anything one can do to trigger the warmth faster?

Cold extremeties are a reaction of endotherms where they reduce warm blood circulation to prevent losing core body temperature, otherwise the cold blood in your hands would lower your central blood pressure from 37'C, which makes the body less efficient and at risk of catching colds.

The reaction is called vasoconstriction.
quote:
Active cutaneous vasodilation occurs via cholinergic nerve cotransmission and has been shown to include potential roles for nitric oxide, vasoactive intestinal peptide, prostaglandins, and substance P (and/or neurokinin-1 receptors). It has proven both interesting and challenging that no one substance has been identified as the sole mediator of active cutaneous vasodilation. source
The above research can give you some clues about exercise and cold hands:

When you have exercised for 30 minutes, the above quote applies, and perhaps there is also a hormone contribution from natural opiates, endorphins, and other chemicals like nitric oxide.
quote:
The endomorphin peptides, endogenous ligands for the mu-opioid receptor, and nociceptin (orphanin FQ; OFQ), an endogenous ligand for the ORL1 receptor, have substantial vasodilator activity. source
For some very good reading on the subject, search for "thermoregulation vasodilation", the corresponding pages give advanced general knowledge of the biology.


How many co-expressed genes would be expected in a tissue? I am working with gene expression microarrays of tumor tissues and I want to use a program to find the clusters of co-expressed genes in order to know if some particular genes are co-expressed with another genes and which genes are those.

As I must do this for many microarray experiments and I have read that there are a lot of genes that have constant expression in a tissue, I ranked the gene by its variability (coefficient of variation) that they had in the experiments and keep the first 3000 genes to search their co-espression. Then I employed a program (a bioconductor package) to find co-expression.

Now, I was expecting to find several clusters of genes (no particular reason for this) in the experiment that I was using as example, but instead of that, I only find one cluster of co-expressed genes of about one hundred, and the others genes didn't were co-expressed.

My question is: this result could have a biological sense, or I'm making a terrible mistake in some place?, Thanks in advance.

Check the beautiful publication of Daniel Ramsköld et al. 2009, which holds the numbers for generally anticipated co-expression.
The specific level of co-expression, which applies to your scenario, will depend upon your tissue, your thresholds, and your definition of co-expression.
It you look for a co-change of some genes across different specimen (rather than co-expression), the number of genes that should change will depend upon the underlying biology (and thus prevent a general answer without considering the specifics of your specimen).


Why are irises unique? I heard that irises are different and unique for every person. According this link, probability of two irises having identical pattern is 1 in 10 to the 78th power. That's how iris scanners identify the identity of people. This technology is becoming very evident. So I ask, why are irises for each person different and unique?

Iris is a thin, circular structure in the eye, responsible for
controlling the diameter and size of the pupil and thus the amount of
light reaching the retina. The color of the iris gives the eye its
color. In optical terms, the pupil is the eye's aperture and the iris
is the diaphragm that serves as the aperture stop.

Color and structure of iris is greatly depended upon genetic links, but the patterns are not. Iris is developed by the prenatal(before birth) growth through a process of tight forming and folding of the tissue membrane.

The human iris begins to form during the third month of gestation. The structures creating its distinctive pattern are complete by the eighth month of gestation, but pigmentation continues into the first years after birth. The layers of the iris have both ectodermal and mesodermal embryological origin, consisting of (from back to front): a darkly pigmented epithelium; pupillary dilator and sphincter muscles; heavily vascularized stroma (connective tissue of interlacing ligaments containing melanocytes); and an anterior layer of chromataphores and melanocytes with a genetically determined density of melanin pigment granules. The combined effect is a visible pattern displaying various distinctive features such as arching ligaments, crypts, furrows, ridges, and a zigzag collarette. Iris colour is determined mainly by the density of the stroma and its melanin content, with blue irises resulting from an absence of pigment: longer wavelengths differentially penetrate while shorter wavelengths are reflected and scattered, a phenomenon resembling that which makes the sky blue. The heritability and ethnographic diversity of iris colour have long been studied, but until the present research, little attention had been paid to the achromatic pattern complexity and textural variability of the iris among individuals.
Reference

Iris Recognition vs. Retina Scanning
Iris and retinal scanning are ocular based biometric identifiers. Iris recognition uses a camera to capture image of the iris. Iris is the only internal organ visible from outside the body. Iris scanners can acquire an image of the eye from a distance of 3 to 10 inches.
In retinal scanning, the device send a beam of light deep inside the eye to capture the image of retina, which is located on the back of the eye. retinal scanning is not widely used due to the intrusive methods used to capture the image.
Factors which enhance the iris scanning system,

reference


Is HSV-vector-mediated miRNA expression in dorsal root ganglia stable? My question is on the following article:

"Reduction of voltage gated sodium channel protein in DRG by vector mediated miRNA reduces pain in rats with painful diabetic neuropathy"

My question is, do you think the rats continued to have decreased levels of voltage-gated Na+ channels after this experiment, or did they likely gain them back up eventually, because dorsal root ganglion neurons regenerate themselves? I couldn't find this info in the article.

The vector used in this study is based on the herpes simplex virus genome (HSV).

Wildtype HSV mainly infects sensory neurons. After infection, it resides in a latent state in the nervous systems of the host for a lifetime. The viral genome persists in the cell, without integrating into the host genome (Marconi et al., 2000).

The article cited is devoid of background on the vector and its characteristics and I understand your issues. I think that the expression of the RNAi is quite stable in your linked article, because the authors infected neurons in the dorsal root ganglia. The dorsal root ganglia contains sensory neurons. It is an immuno-privileged region, because the blood-brain-barrier (BBB) limits the access of immune cells. Indeed, protein expression through HSV-transfection in the brain is stable, at least up to a year (Suzuki et al., 2008) and possibly longer. Peripherally, outside the BBB, the expression of HSV-plasmids may be compromised within weeks through cellular immunological responses targeting the expressing cells (Suzuki et al., 2008).

Regarding regeneration - The DRG contain mature neurons and is part of the peripheral nervous system. These neurons are known to regenerate readily after injuries, but these injuries are mostly investigated through physical damage (Muratori et al., 2015). Latent HSV infection does not kill neurons, and even an active infection seems to leave neurons relatively unscathed (Rautema, 2002).

References
- Marconi et al., In: Madame Curie Bioscience Database. Austin (TX): Landes Bioscience (2000)
- Muratori et al., (2015); 2015, 860546
- Rautemaa et al., Immunology (2002); 106(3): 404–11
- Suzuki et al., Molecular Therapy (2008); 16(10): 1727–36)


Why are there still useless traits/mutations in our body Why is it that through decades of evolution , some seemingly useless body traits such as earlobes and pubic/chest hair still remains while other traits are generally replaced through evolution?

Natural selection "selects" the trait that is less advantageous and removes/ reduces its frequency. It is like a filter paper. All solids are filtered out of mixture while clear liquid is collected. So if there is a difference in fitness of organisms by variations in traits, then only they are SELECTIVELY removed. Now, if a person without an earlobe would have had an increase in fitness, it would have had eliminated over time. And it might (I said might) be that there IS some pressure but it might be so slow that we can not realise it. But in case of earlobes, evolution will be evident in the case of elephants and Jackrabbits.


Identify this vertebra I was walking on the beach in New Jersey (U.S.), at about 40 degrees longitude, and found this bone. It's not a fish. The long process in the front is interesting. It is likely a C2 vertebra. I looked on the web, but could not find anything aquatic that it might match. Certainly not a dolphin. It is 2 inches long (50 mm), and 2.5 inches high and wide (64 mm). I guess it need not be aquatic, and New York City (20 miles North of here) used to dump garbage in the ocean. It looks old. Can you help me identify it?

Looks like Lumbar Vertebrae or Sacral Vertebrae of a Cow like @Brian Hanson Said above.

Studying closely in laboratory can elaborate more secrets about the bones.


Why is it desirable to couple chemical production to growth? I have the following question in systems biology:
a) Draw a graph showing the relationship of growth (Vbio) and Vefni for the system here. (Let the horizontal axis represent Vbio and the vertical axis represent Vefni)

My first thought was that it would simply be straight line from (0.5,0.5) to (1,0). But now I'm thinking that I have to take V4 into account as well.

b) Determine one or more reactions that are such that if they are taken
out the production of M4 is coupled to growth (growth-coupling). Draw a
graph showing the relationship Vbio and Vefni for the mutant.

Here I thought it would be V1 and V4. I'm not sure though because I haven't found a good explanation for what growth-coupling is exactly.

c)  Why is it desirable to couple chemical production to growth? i.e. what advantages do those systems have over the ones where no such coupling is present?

Here I have no idea.

Why is it desirable to couple chemical production to growth?

When designing new metabolic pathways for chemical production, one has to keep in mind that the purpose of it is to get scaled up (i.e. to reach industrial size).

From the industrial point of view, the faster/simpler a process is, the better. Growth coupled chemical production means that only one step is necessary in order to produce the desired product (before downstream processes). Otherwise, one would have to produce the biomass first (growth step) and then to proceed to the chemical production step. One step is cheaper and faster than two, not mentioning the intermediary steps that could be necessary (cells washing, centrifugation, filtration ...).

The main drawback of growth coupled chemical production is that the final yield ($mol_{final~product}/mol_{substrate}$) is hindered by biomass production. This can be a real issue if the substrate is expensive.


What's the subpatellar tendon? I read in Thomas Myers book Anatomy Trains:

  Although the muscles themselves have attachments within the anterior
  compartment to the tibia, fibula, and interosseous membrane, the next
  station for the SFL [Superficial Front Line] is at the top of both the medial and lateral side
  of this track, the tibial tuberosity

  Continuing in a straight line upward is no problem: the quadriceps
  begin their upward sweep here with the
  subpatellar tendon. The SFL  includes the patella, the large sesamoid bone designed to hold the SFL away from the knee joint
  fulcrum so that the tissues of the quadriceps have more leverage for
  extending the knee.

I can't find the term subpatellar tendon in my anatomy book. What does it refer to? Is it the patella ligament?

I suspect that you are correct, "subpatellar tendon" is referring to the patellar ligament. Although it is small, in the image below, (3) is the tibial tuberosity and (5) is the patella. (4) which is labeled "subpatellar tendon" is between the two. The only structure between them is the patellar ligament. So, I think this is what it meant (though in 20 years of teaching, I haven't heard that terminology).


Do cats ingest everything that they lick off themselves during grooming? Cats are well-known for licking themselves clean, but what happens to all the loose hair and sand and mud and wet substances that the lick off themselves? Do they ingest everything? Do they cough up and vomit out a furball later with all of this?

I have a pet cat and I've never understood where all that she licks off herself is going.

How is a cat's digestive system suited to handle all the inedible environmental substances?

Cat licking is partially to clean themselves (including of odors that might attract predators) but is also used as a cooling mechanism (they sweat little and so use evaporation of saliva as a cooling mechanism), socialization, and to help spread oils. Most hair in short haired cats passes through the digestive tract with no issue. Source The hair that is unable to pass through the cat will accumulate in the stomach and be coughed up as a hairball (generally every 1-2 weeks) source.
For more on a cat's digestive tract see here. Note also that the human digestive tract can manage all manner of weird things to and just allow it to 'pass through' and this is the 'default' behavior for many digestive tracts.


Hypotonic or Hypertonic solution and why? A doctor needed to administer 5% albumin to a patient. Albumin is normally administered dissolved in 0.9% saline solution. Since the physician did not have any 5% albumin solution, he diluted 25% albumin with water and administered this to the patient. Describe what you think happened to the blood cells of the patient as a result?

So this is what I think:

If the doctor dilutes the 25% albumin, that will make the solution have a lower concentration of solute, creating a hypotonic solution. Therefore the water will move into the cells, causing them to swell, lyse or burst.

Is this correct?

Albumin wont form a true solution and wont affect the osmolarity greatly (colloid forming molecules like proteins can affect osmotic pressure to an extent. See oncotic pressure).. and since there is no solute the solution would be hypotonic..

But what effect it will have on the blood cells depends on how much solution was injected.


Novel bacterial strains of bacteria first isolated on the International Space Station, did the space environment lead to these genetic changes? Question
Methylobacterium ajmalii sp. nov., Isolated From the International Space Station (Bijlani et al. Frontiers in Microbiology, 12, p. 534, 2021) is a thorough analysis of "novel strains" of bacteria isolated from the International Space Station (Characterization of the total and viable bacterial and fungal communities associated with the International Space Station surfaces)
Question: Bijlani et al. 2021 is written at a very dense and technical level that is challenging for me to understand. I'd like to know:

Does the article suggests these may be newly discovered species or only that they are novel strains of known species of Earth bacteria?
Does the article suggest that the environment on the ISS selected for these species or strains, and they resulted from some genetic changes due to the ISS environment, or if we looked hard enough we'd expect to find the same ones on Earth and they just happened to be identified first on the ISS because of the rigorous studies of those samples?

Background
I was lead to the paper after seeing the ink the BBC's Could humans have contaminated Mars with life? which is primarily about a different topic.
The paper is one of 10 papers the 2021 topic Extremophiles: Microbial Genomics and Taxogenomics.
The ISS is a unique closed environment with plenty of surfaces with sometimes problematic mold growth, and a population of usually 3-6 humans with regular rotations every 5 to 6 months who maintain an array of biological experiments including a sustained effort to try to grow vegetables and flower hydroponically and in soil.
The atmosphere is maintained similar to Earth's surface (oxygen/nitrogen ~1 bar) with 60% relative humidity and often has a CO2 concentration slightly higher than the astronauts would prefer.

The authors propose that this is a distinct species based on a number of physiological and genetic tests. To quote the summary of your linked paper

In summary, the phylogenetic and genetic distinctiveness and differential phenotypic properties were sufficient to categorize these three ISS strains as members of a species distinct from other recognized Methylobacterium species. Therefore, on the basis of the data presented, strains IF7SW-B2T, IIF1SW-B5, and IIF4SW-B5 represent a novel species of the genus Methylobacterium, for which the name Methylobacterium ajmalii sp. nov. is proposed.

This indicates (emphasis mine) that they think that these isolates are distinct enough from species that we have found on Earth to make the isolates a species. This is a species that we haven't found on Earth, but unsurprisingly it is closely related to species from the same genus that have been found on Earth and on the ISS

The authors make no statements about how the species came to be there that I could see, only that it is a novel species from the ISS, which has not been found on Earth. No mechanisms for arisal are postulated, and the authors wisely did not speculate on this at all (speculation on results is frowned upon in science). One of the reasons they did not speculate on this will be that testing mechanisms whereby speciation has occurred is very difficult, especially as they would need to mimic in the lab the conditions in the ISS and show which conditions were important for the speciation. These experiments would be technically challenging and very time consuming.

It is worth noting that we don't really know the rate of species differentiation on Earth, let alone in space, partly because Earth is so covered in bacteria that proving that one evolved in the environment is difficult as it is hard to prove that you didn't just miss it last time you looked. To quote the paper I linked above:

For example, a single gram of soil can harbour up to 1010 bacterial cells and an estimated species diversity of between 4·103 to 5·104 species .

However, the ISS is one environment where it might be easier to see these sorts of events because it is relatively micro-organism free, and we have prior samples to go back and compare to. For some comparison of the numbers, I turn to the second paper you linked, which found:

Of the total bacterial and fungal isolates that grew, 133 bacterial isolates and 81 fungal isolates were identified by Sanger sequencing...   ...When the ASVs were summarized to the genus level, 121 taxa were detected, 77 of which could be assigned to known genera

and

Overall, the number of bacteria (combination of R2A and BA growth) isolated from the ISS from all 24 samples ranged from 6.7 × 103 to 7.8 × 1010 CFU/m2

So quite high numbers of cultivatable bacteria (CFU = colony forming units, a measure of how many bacteria will grow per sampling), indeed as high as those found in a gram of soil, but very low species diversity compared to the soil.
It is still difficult to prove that this is a new species evolved strictly on the ISS, but it does seem logically likely that evolution will happen on the ISS, as it does anywhere that life is present (as far as we know).


In human embryology, what starts ovum cell division? Maybe I am not using the correct search keywords in Google, but I cannot seem to find anything beyond basic information taught in schools about fertilisation of the egg by the sperm.

After the sperm has fertilised the ovum, I know that the zygote starts with one cell, then divides into two cells, then four cells and so on, but what initialises cell division, and how does the cell divide?

Actually an ovum doesn't ever start cell division because once it is fertilized by a sperm the combination of the two cells is call a zygote.  In humans, the zygote proceeds with the many steps following fertilization leading to the first division; this takes on the order of 24 to 30 hours.  At that point the set of cells may be termed an embryo or various other technical terms.  The succeeding cell divisions occur by the normal cell division mechanism, which is called mitosis.  In the context of the development of the human embryo, an early stage cell division is often called cleavage.

More details are available from the links in the above.  For greater technical depth on the initial stages of the division of the zygote, you might want to see this article.


Enzyme Activity under High Pressure Wikipedia has this image titled "Pressure Chamber to measure Enzyme Activity under High Pressure"

Made me wonder why do we need to measure Enzyme Activity under high pressure?

Are there enzymes in nature that must work under variable pressure conditions? My impression from my knowledge of conventional chemical kinetics was that in the liquid phase the effect of pressure on chemical kinetics was typically very low simply because of incompressiblity of liquids. Unless Pressures were very very high. Is this not so with enzyme activity? Or are there enzymes that must work under very high pressures?

https://en.wikipedia.org/wiki/Enzyme_assay

At least one group who have published on the effect of pressure on enzyme activity (Cho and Northrop) are not interested in it from a practical point of view, i.e. they are not subjecting enzymic reactions to pressures that they think they encounter naturally. Instead they are using the effects of pressure to test the kinetic and thermodynamic predictions of different models of enzyme catalysis. In particular they believe that pressure effects provide a means of testing the idea, first suggested by Linus Pauling, that an enzyme has a greater affinity for the transition state, rather than for the substrate.

This is explained in a paper on yeast alcohol dehydrogenase, but only the abstract is freely available. They claim to have evidence against Pauling’s idea, but I am not sure the extent to which this is generally accepted.


When consuming carbohydrates and fats together, why are the fats caloric? If I understand things, and I most likely don't: mammals primarily use carbohydrates to produce metabolic energy when there are sufficient carbohydrates to do so.  The use of fats for fuel requires the organism to break down the fat into constituent parts and from there produce either glucose (right?) or ketone bodies.  Presuming that the organism is not in ketosis, it seems that its body would preferentially use carbohydrates for fuel.

This is where my confusion comes in: why would the mammal's body use fats for fuel if its diet contain sufficient carbohydrates?  The real underlying layman's question is: why is that when I eat fat, I have to count those calories, if my body preferentially uses carbohydrates for fuel?

To expand on my comments:

Just like you mentioned in your question, carbohydrates (mostly glucose) is used as the primary source of energy when available to satisfy metabolic needs in human cells, however lipids and even proteins will be used if required, in order to produce energy. Since all these biomolecules (carbs, lipids and proteins) can actually be used to sustain the metabolic activity of cells, that means all of them store energy to a greater or lesser extent (which we can quantify in a practical way as food calories). Other things that we eat or drink such as vitamins, cofactors, water, etc. are not accounted for in the calorie count because they can't be broken down to produce energy for metabolism.

Dietary carbohydrates are easily digested into smaller blocks (mostly glucose) and absorbed directly into the bloodstream, afterwards glucose is taken rapidly from the bloodstream by human cells and processed via glycolysis and lactic acid fermentation or the citric acid cycle (all these are metabolic pathways for glucose in humans). Each gram consumed of carbs yields approximately 4 calories of energy.

Lipids on the other hand undergo a more complex process of usage after their slower digestion compared to carbs since after their absorption they have to be transported in special molecules across the lymph, then into the bloodstream and then they can be taken by various kinds of cells. Considering just this, we can start seeing why lipids aren't a fast source of energy (they take long to be available as potential energy sources). Furthermore, the main destination of dietary lipids is the adipose tissue which constitutes a special tissue in which fatty acids can be stored for latter usage. Fatty acids not being used immediately to provide metabolic energy doesn't mean they lose their stored energy (doesn't mean they have no caloric intake value), its just "quiescent" for when its needed (when exercising or when fasting for example).

Each gram of consumed fat yields approximately 9 calories of energy, this quantity is higher compared to that of glucose because the metabolic pathway that breaks down fatty acids (beta-oxidation) in combination with the citric acid cycle produces more metabolic energy (ATP) compared to glycolysis in combination with the same citric acid cycle. However such amounts of energy are not usually required in rest.

It is important to mention that glucose can also be stored in the form of glycogen or even fat since it will be converted to these molecules if there is more glucose available compared to what the cell needs in a given moment. This glucose converted to glycogen or fat also has to be accounted for in the calorie count because its still a potential energy source (just not used right now).

References:

Dietary Carbohydrates - National Agricultural Library

Dietary Lipids - National Agricultural Library

Insights into digestion and absorption of major nutrients in humans - Goodman, B. E.

Food calories per gram of biomolecule - National Agricultural Library


MCQ - Independent assortment or Incomplete linkage Two flies were crossed one wildtype another double mutant sepia(se) and vestigial(vg) yielding 40% wild type 40% se vg, 10% se and 10% vg. The genes show-
a.Complete linkage b.Incomplete linkage c.Independent assortment d. epistasis

My attempt at a solution
Since no. of combination of phenotypes appeared =/= 2 ( there are non-parental traits so) it is not complete linkage.
It is neither epistasis because two genes are controlling two diffrenet phenotypes, not one.
It can be independent assortment or incomplete linkage.
Since the question says double mutant sepia(se) and vestigial(vg) (I am getting the idea that) it is a female and the wildtype individual (with no genotype concerned hint) is a male. The genes are likely on X chromosome.
So..... it is incomplete linkage.
But I'm not sure why not independent assortment.

It doesn't really matter on which chromosomes the where concerned genes are located, Now coming to your question.
A> Complete linkage > Complete linkage says that the concerned genes are right next to each other and no crossingover is possible so the expected genotype of the offspring would be 100% parental type. 50% Wild (se+ vg+) and 50% Mutated (se vg)

B> Incomplete linkage > This is the correct answer. According to incomplete linkage, the genes are close but not right next to each other so there is space for crossingover to take place. However, they are still close, close enough to be considered as linked and thus chance of obtaining recombinant offspring would always be less than that of the offspring with parental genotype, parental type always remains over 50% and here the parental type offspring is 80% (40% wild type parental genotype + 40% mutated parental genotype) and 20% recombinant genotype [(10% se & wild type vg+) + (10%vg & wild type se+)]

C> Independent assortment says that there is no linkage and thus no crossingover, this is possible only when the concerned genes are located on different chromosomes but here in the obtained data of offspring it is clear that crossingover did take place and 20% of the offspring is result of the crossingover so this option is not correct

D> Epistasis : In your attempt you mentioned that it is not epistasis because two genes are controlling separate phenotype thus it is not epistasis. your explanation is wrong. Don't get me wrong, the answer is not epistatsis, I am just saying your explanation is wrong, epistasis is the phenomenon where one gene interferes with the expression of another gene, look at the term carefully. I am calling them as genes not alleles. Alleles are different version of the same gene that control the same phenotypic character. In epistasis two different gene that control completely different phenotypic expression are interacting. One gene if expressed prevents the other gene from getting expressed, this not about the dominant alleles where if the dominant allele expresses recessive allele wont express. For example, assume gene A codes for white flower colour and gene B codes for sweet smell. If B gene expresses then A gene wont express. This is epistasis


How is it possible for the absolute fitness to be more than 1? The wikipedia definition of Absolute fitness is "the ratio between the number of individuals with that genotype after selection to those before selection. It is calculated for a single generation and must be calculated from absolute numbers."

But in one generation there are no reproductive events so it should be theoretically impossible for the population to be larger after the selection event than before it (since no reproduction is taking place).

That definition in the wikipedia is misleading at best. Contrary to what it seems to suggest there, absolute fitness is computed across a single generation, not within a single generation. For simplicity, let's look at an example using asexual haploids with discrete non-overlapping generations. If individuals with the A genotype produce an average of 3 offspring, each of which survive with probability 0.5, the A genotype has an absolute fitness of 1.5. The key is that we've multiplied fecundity (3) by viability (0.5) and this allows us to obtain a value greater than 1.

Things get more complicated if we look at diploid sexuals. The absolute fitness of the Aa genotype is not the ratio of the number of individuals with the Aa genotype at time t+1 to the number of Aa at time t. An easy way to see this: in a population of AA and aa parents only, e.g. as produced by a cross, the ratio of Aa at t+1 to Aa at t is infinite, which would imply infinite fitness if we went this with definition. Rather, the absolute fitness of the Aa genotype is one-half the number of surviving offspring at time t+1 produced by Aa parents at time t. The one-half comes from the fact that a parent individual contributes only one-half of the genetic material of each surviving offspring. For some traits, e.g. those involved in sex ratio determination or parental care, it will not be sufficient to count surviving offspring; in these cases we apply comparable logic to counting grand-offspring.

The wikipedia seems to suggest we are to look only at viability because we are comparing before-selection numbers to after-selection numbers, within a single generation and thus without an opportunity for fecundity to come into play. That is not consistent with the common usage of the term. To be fair, I have on rare occasion seen "absolute fitness" used as a synonym for "viability"--though I cannot think of any good justification for this usage.


Can formalin fixed tissue stored in absolute ethanol be used for histology? Can samples which have been stored in buffered formalin and the moved straight to absolute ethanol be used for histology?

I know that the samples normally need to go through a series of ethanol concentrations (70%, 80%, 90%) for dehydration before they reach absolute ethanol, but can you still use samples that have been immediately immersed in absolute ethanol? Or would the rapid dehydration cause too much distortion?

Can they be used? Sure. How much distortion you get will depend on the tissue type and several other factors. How important that distortion is will depend on what you are trying to measure. "Too much distortion" is a relative term. You can't really know how bad it will be without trying it.

Should this ever be done intentionally? No - there is good reason for using the gradual dehydration steps. I would be really hesitant to do any quantitative analysis or draw any solid conclusions from tissue processed incorrectly, though.


Why mushrooms have so much antibiotics? Why they have much more antibiotics than plants for instance?

This isn't fully understood but one theory is that they live in soil feeding off dead things and so are in competition with bacteria and other fungi for resources including space.  The antibiotic compounds they produce have been described as a sword and shield.  Some compounds are offensive (sword) and attack other fungi and bacteria while other compounds protect a species (shield) from the compounds of other organisms seeking to do the same thing to them.  This is only half the story really, fungi also excrete compounds that look similar to antibiotics but have no known function.  Still other compounds have seemingly no effect on other organisms but when taken by humans and other mammals lower cholesterol in the blood. Strange thing for a fungus to produce.


Arteries used for inserting catheter For catheter purpose, femoral and subclavian arteries are mostly used as starting point. Why? Are there other arteries which are used for the purpose?

Those arteries are (a) big enough for the catheters, (b) superficial enough (close enough to the surface of the skin) for catheterization. It would be quite a challenge to use the renal arteries, for a ridiculous example. There is also less of a risk of embolization than using an artery like the carotid, where embolism can cause stroke, which would be quite serious. An embolism in an arm or leg could be painful and cause damage, but unless it is massive it isn't going to significantly affect the patient over the long term.

Also note that those are fairly special cases of catheterization, such as when doing percutaneous interventional techniques targeting the peripheral or coronary arteries. Those approaches use fairly large devices so you need a large vessel, and you need to be in the portion of the vasculature that you are targeting (i.e., you can't access those targets through a vein). As @VanceLAlbaugh mentioned in a comment, other arteries are targeted for other purposes. And overall venous catheterization is much more common than arterial, such as when an IV line is established to deliver fluids/medicines.


Is this some form of cabbage? I would appreciate if someone could identify this plant. It's tall, but not very difficult to pull from the ground, and it has yellow flowers in large groups. I was told it's not mustard. Is it wild cabbage, and if so, what variety?
Location: western Illinois, in a garden.
Season: it's late April, and their roots are now rotting.
Height: I think they were around 3 feet.

More pictures:

The Brassicaceae family (of which cabbage and mustard are members) has a characteristic pattern of flowers - each flower has four equal sized petals, arranged in a cross-shape hence their other name - crucifers.

[h/t wikimedia commons]

It's not easy to see from your photos whether this is true, but I'm going to say, yes, it does look like a member of the Brassicaceae family. The cross-shape of the petals would confirm this.
I don't think these plants are native to Illinois, and it also does look somewhat like a crop plant, rather than a weed, so maybe it is an escape from a farm/garden. It could be canola, possibly.
Wild cabbages are native to the Mediterranean and Atlantic coasts of Europe , so it is probably not a wild cabbage, unless someone planted it in Illinois.


How does permanently modifying human DNA work? And how does it impact procreation? So I read an article about a metabolic disease being treated with gene therapy, where they inserted corrective dna into the patient.
https://www.independent.co.uk/news/science/dna-permanent-change-cure-disease-experiment-california-brain-madeux-iv-hunter-syndrome-a8055696.html
How can this be permanent though? Wouldn't the other cells "take over" these modified cells when they reproduce, and eventually have back the same old dna?
Furthermore, will this affect offspring in any way? Will they inherit the new dna changes (if that part of the dna is passed on from the parent with the changed dna)?

It seems this therapy is targeted to liver cells. Cells that are affected will continue to express the inserted gene as long as they last, and any dividing cells will spread it to their daughter cells.
Genetic information is passed on to the next generation through germline cells: eggs and sperm. There won't be any effect on the next generation unless these cells or the cells that give rise to them have the inserted gene.


Why is pollen used as a dietary supplement? Sporopollenin is the hardest biological substance and can't be degraded by any know enzyme (my school textbook). Then why is pollen used as a dietary supplement if it can't be digested?

Also, pollen depends on nutrients from the plant itself either before or after pollination (before if pollen leaves anther at 3 celled stage and after if it leaves anther at 2 celled stage). Then how would it be rich in nutrients?

Bee pollen contains high concentrations of reducing sugars, essential amino acids and unsaturated/saturated fatty acids. It contains minerals such as Zn, Cu, Fe, and high K/Na ratio and significant quantities of several vitamins. Note that the composition of it varies greatly depending on their botanical type and the techniques used by industries. It is basically the collection of pollen grains from flowers made by worker honey bees with nectar and salivary substances.[Source 1](Page 1)  [Source 2]

[Source 1](Page 4)
The claimed benefits of bee pollen are based on biological and therapeutic activities. The main components are phenolic acid derivatives and polyphenolic compounds. They are known to possess properties such as anti-oxidant, anti-aging, anti-carcinogen, anti-inflammatory, anti-atherosclerosis, cardio-protective and improved endothelial functions. However, it is unknown that treatments with such products are effective or not and how to minimise the health risks.[Source 1](Page 5) [Source 4]  [Source 5]  [Source 6]
Different studies were conducted in mice on the nutritional effects of bee pollen. It improved food digestion and also improved reproduction rates. Chickens fed with bee pollen had a better development of the small intestine. This suggested that bee pollen helped in early development of the digestive system. Bee pollen is also taken as a supplementation by athletes for improvement of performance. Controlled experiments indicated that no positive benefits were obtained. However, the number of training missed due to respiratory tract infection was lower in the bee pollen treated group.[Source 1](Page 5)

Pollen digestion:
Doubts have been raised, whether the tough shell of pollen can be breached and digested by humans. It was discovered in animal experiments that pollen did not retain its content after leaving thedigestive tract. This gave rise to the hypothesis that the nutritional content of pollen was released by the digestive juices in animals (Schmidt & Schmidt, 1984; Roulston & Cane, 2000). In humans it was once shown that pollen was absorbed in the digestive tract (Jorde & Linskens, 1974) or that it was partly digested, (Franchi et al., 1997) whereas there were differences in the degree of digestion of poppy and hazelnut pollen, with an average degree of digestibility of 15% for carbohydrates and 53% for proteins.
In this case it has been hypothesized that pollen was insufficiently digested and that cracking would improve the digestibility and bioavailability (Rimpler, 2003). Different companies offer cracked bee pollen, claiming that this product is better digested. On the other hand, there are many studies in humans with whole bee pollen showing that a part of the bee pollen content is digested and is bioavailable. However maceration of pollen for several hours in water or other liquids is recommended in order to improve digestibility, this method is used also for other heavy digestible grain products.[Source 1](Page 3 & 4)

Flower pollen:
Non-bee pollen are called flower pollen. Extensive health relevant research has been conducted on pollen prepartions from non-bee pollen. It is marketed under names such as Cernitron, Cernitol, etc. It is known to decrease prostrate hyperteophy in rats, but there was no relevant changes in blood levels of LH, FSH, testosterone or dihydro-testosterone.

In patients with prostatic adenoma the improvement was in nycturie, important decreases in the residue post-urinate and in long term treatment, also decrease in the diameter antero-posterior of prostate. The urinary debit did not suffer any changes. The effect on the other symptoms usual in the hyperthrophie benign of prostate was not of statistical significance (Bruneton, 1999).[Source 1](Page 7)

For industrial benefit:

Improved bioavailability is important in the pharmaceutical industry in that it reduces costs and increases the effectiveness of drugs. Previous studies have shown that this enhancement is possible using exines from pollens and plant spores. In one example the ingestion of ethyl ester derivative of EPA (eicosapentaenoic acid) encapsulated in sporopollenin microcapsules from L. clavatum spores improved the bioavailability of EPA in the bloodstream. In these trials, six volunteers ingested 4.6 g of fish oil containing 20% of the EPA ester, both alone, and encapsulated, as a 50% fat content powder, respectively. The bioavailability of the active was defined by area under curve (AUC (area under curve) 0–24 h). The mean AUC 0–24 of EPA from ethyl ester with exine was remarkably 10-fold higher than the corresponding for ethyl ester without exine encapsulation.
In other unpublished studies involving human volunteers, ingesting a lipophilic active, the enhancement of bioavailability has been very similar. The mechanism by which such enhanced bioavailability is achieved is intriguing and some preliminary experiments have been undertaken to explore possible explanations. Recent in vitro studies (unpublished studies) revealed that the exine shells exhibited gut mucosal adhesion properties. In addition, in vivo experiments on mouse microtone sections of intestinal walls of mice fed with exines showed the exines to lie between the gut villi. The unique morphology of exine shell surfaces probably evolved to help pollen particles to become attached to insects and thereby aid the process of pollination. It is possible therefore that this same morphology could help the exine’s adherence to and close association with the gut wall leading to an increase in the period of contact between the encapsulated drug and the biological surface, thereby enhancing its absorption and bioavailability.[Source 3]

Hazardous components of pollen:

Trace amounts of hepatotoxic pyrrolizidine alkaloids were found in pollen of Echium vulgare, E. plantagineum, Senecio jacobaea, S. ovatus, and Eupatorium cannabinum (Boppre et al., 2008).  In Middle and Northern Europe these pollens are not among the main pollen grains gathered by bees, however in Southern Europe the two Echium plants are more  diffused and are gathered by bees in larger amounts (Campos et al., 1994; Serra Bonvehi, 1997). [Source 1] (Page 5)

Therefore, it should undergo tests to approve it's purity as allergies can be caused.
References:
1 : Future of bee pollen(Research gate)
2 : Pollen composition and standardisation of analytical methods(Research gate)
3 : Hollow pollen shells to enhance drug delivery(NCBI)
4 : Bee pollen: chemical composition and therapeutic application(NCBI)
5 : Biological activities of commercial bee pollens: antimicrobial, antimutagenic, antioxidant and anti-inflammatory(NCBI)
6 : Biological and therapeutic properties of bee pollen: a review(NCBI)


Is aquafaba readily digestible? I have always drained and tossed the water from canned beans. My understanding has been that the water that canned beans are soaked and cooked in contains raffinose, the gas-causing sugars that humans can't digest. This University of Michigan page, referred to in the answer to an earlier question, says:

  Rinse beans thoroughly and never cook beans in the water they've
  soaked in. It's loaded with the gas-causing raffinose sugars.

And also advises:

  Drain and rinse canned beans. That will get rid of some of the
  gas-causing raffinose sugars (and almost half of the unwanted sodium).

Now that aquafaba is all the rage, though, I'm wondering whether my understanding is wrong. I understand that the bean water would taste mildly sweet and foam up so readily because of the raffinose. But it seems to me that aquafaba would lead to severe bloating and intestinal distress, as it relies for its properties wholly on the gassy and sugary nature of the bean water.

Am I mistaken in my understanding of the need to toss the water that one soaks or cooks beans in? Or is it just that fans consider the bloating and gas a price well paid for the delights of aquafaba?

Much of it is not readily digestible. According to this chemical analysis:

  Finally the results presented here also indicate that the amount of digestible carbohydrates in aquafaba is minimal. For families with GLUT1 deficiency, where a diet with minimal amounts of glucose and carbohydrates digestible to glucose is required, aquafaba can represent an additional foaming or emulsifying ingredient, as an alternative to eggs.

It also contains proteins, presumably digestible. The carb and protein content is significant, according to the study, which implies a fairly decent proportion of undigestable carbs.