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What material fills the synaptic cleft? Is it water?
The synaptic cleft is the gap between the pre-synaptic and post-synaptic neurons, and neurotransmitters are transferred between the neurons within this region. What substance exits in this space, is it water? If so, what force makes the neurotransmitters move toward the receptors despite colliding with water molecules?

I think diffusion

@Ali Lavasani I updated my answer with additional reference.

There are two types of synapses namely Electrical synapse and Chemical synapse. In electrical synapse there is physical contact between two cells through gap junctions. In chemical synapse there is a small gap between two cells which is termed as synaptic cleft.
The presynaptic and postsynaptic membranes at chemical synapses are separated by a synaptic cleft that is 20–50 nm wide, 10 times the width of the separation at gap junctions. The cleft is filled with a matrix of fibrous extracellular protein. One function of this matrix is to serve as a “glue” that binds the pre- and postsynaptic membranes together.(reference 1)
The same reference also states Water is the main ingredient of both the fluid inside the neuron, the intracellular fluid or cytosol, and the outside fluid that bathes the neuron, the extracellular fluid. Electrically charged atoms, ions that are dissolved in this water are responsible for the resting and action potentials.
Reference 2 mentions, The synaptic cleft is not simply an empty space, but is the site of extracellular proteins that influence the diffusion, binding, and degradation of the molecules, including neurotransmitters and other factors, secreted by the presynaptic terminal
If we think in this direction, of course holding together two neurons at synapse position is important. Moreover, the presence of several dissolved ions (in water) are necessary. If you remember, for the release of neurotransmitters into the synaptic cleft, influx of Ca2+ ions through voltage gated ion channels is essential.Thus, from above all points we can conclude that, the extracellular fluid in synaptic cleft is mainly aqueous in its composition with several ions, released neurotransmitters and several proteins that constitute a matrix.
What force makes the neurotransmitters move toward the receptors?
An essential role of astrocytes is regulating the chemical content of this extracellular space. For example, astrocytes envelop synaptic junctions in the brain, thereby restricting the spread of neurotransmitter molecules that have been released.(reference 1).Thus, it helps to confine the neurotransmitters in the small region, thereby increasing the probability of getting in touch with the target receptor.Also, as reference 2 says, there are several proteins present in the synaptic cleft which influence the diffusion.It means movement of neurotransmitter is by diffusion and above mentioned various factors can influence their movement towards receptor efficiently.
References:

Bear et.al, Neuroscience, exploring the brain, 2015
Neuroscience, textbook by Dale Purves.

The components of the inter-stitial fluid will be dependent on where the synapse is though yes it will be aqueous.  Good old fashioned diffusion over a concentration gradient will be responsible for ensuring sufficient neurotransmitter reaches the receptors on the other side of the synaptic cleft.  Tough to find something you can easily reference online for yourself independently to verify my answer.  I would say that there will be whole chapters on this in any basic pharmacology textbook.  Pharmacology by Rang and Dale is the most easily found in a university library and readable without  a lot of biology knowledge.

Welcome to SE Biology. Your answer may well be correct, but you need to support it with evidence so the poster and others can judge it. That's the way the site works. A quotation from a book or a link to a reputable web site will do.


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Why does it matter to predict protein structure?
And how do you predict it ? What is your input data (sequence of amino acids, temperature, pH, ...) ? Is there a "standardized" input that scientists agree on ?
Moreover, I've read that knowing the structure of a protein helps predicting its function, but is the prediction [Structure -> Function] reliable ? Should't we predict directly the function if that's our interest (I don't mean we should not take into account predicted structure, but I don't understand why the structure IS the purpose instead of the function)
I also read the structure helps predicting affinities with other proteins and how it will bind : same question here, is this prediction [Structure -> Affinity] reliable and why don't we predict directly affinities.
To sum up a bit, I have the impression that the structure in itself is not important to know except that it is a good predictor of other protein properties (like function of affinity) and that the structure is kind of an 'intermediate' ? What am I missing ?

Structure tells you about the "hows" of the function. Just knowing the function will only answer the "what". Regarding affinity: that only works for binding reactions. What about conformational changes?

Welcome to SE Biology. New users are expected to complete the Tour to find out how the site works. (We know that you haven't, otherwise you would have a 'badge'.) Please also read the Help on how to ask questions. You will see that you are expected to ask one question at a time and that you are expected to research the topic before asking. It is clear that you haven't tried to find out about methods of protein structure prediction, or much about proteins themselves. Please do that first.

There are dozens if not hundreds of textbooks on this question. I do not feel it is suitable for the SE format. Even though some answers are present and have received upvotes, they don't even begin to answer the question(s).

How do you want to predict function and binding partners without knowing how your protein looks like? The sequence itself contains only limited information. Similar sequences might fold into similar structures with similar functions. These motifs can be used to transfer your knowledge from one protein to another, which might have similar e.g. binding abilities. But the motif might be nonfunctional in the second protein, because it is hidden in an inaccessible part of the protein due to its folding structure.
Interactions between proteins are weak compared to intramolecular bonds and dynamic. Different amino acid side chains have different characteristics (like polarity, hydrophobia etc.) which make specific interactions possible. Specific amino acids have to be accessible and while they might be far apart in the sequence, the folding of the protein brings them close together in its final shape.
Even small modifications like phosphorylation can alter the structural conformation significantly and e.g. change the enzymatic activity. Therefore, for analyzing protein function, finding binding partners or designing binding compounds (drug development), we need to know its three-dimensional structure. With the structure you can simulate binding affinity/dynamics. Scientists also try to resolve the protein structure in its different states to clearly see the differences.
Keep in mind that complex diseases can be caused by a single mutation, which exchanges only a single amino acid in the sequence but can have severe implications for protein function. Knowing the structure, the position of the amino acid and how the change affects the characteristics of the protein domain (e.g. charge), we can fully understand what's happening on the molecular level.
Since it is far from trivial to analyze the structure of a protein, predictions bridge the gap for functional predictions until the molecular structure of the protein has been reconstructed. But only with atomic resolution you will be able to properly identify interactions.
The question of how to do structural prediction might be beyond the scope of this answer. Pubmed lists around 400 papers each year on this topic. Depending on the amount of information you have about the protein or its family members (proteins with very similar sequences), you can use other known structures to predict an unknown structure:

https://medium.com/@HeleneOMICtools/a-guide-for-protein-structure-prediction-methods-and-software-916a2f718cfe

There are several reasons why understanding protein structure is useful; the most obvious is that drugs that interfere with a specific protein can be deliberately designed based on the protein structure.

Today, even though there is still quite a bit of fine-tuning necessary to perfect the process, structure-based drug design is an integral part of most industrial drug discovery programs [4] and is the major subject of research for many academic laboratories. ... The process of structure-based drug design is an iterative one ... Additional cycles include synthesis of the optimized lead, structure determination of the new target:lead complex, and further optimization of the lead compound. After several cycles of the drug design process, the optimized compounds usually show marked improvement in binding and, often, specificity for the target.

--The Process of Structure-Based Drug Design

There are three broad questions here, together covering much of the field of structural bioinformatics. I will answer each briefly but point you to a textbook for more.
Why is predicting protein structure useful?
This is actually a very good question. The standard answer here is "drug discovery", but as things stand anything other than a high quality homology model isn't particularly useful for drug discovery. I can't think of any examples where de novo structure prediction has directly led to the discovery of a drug, for example by virtual docking in a binding site, though I am willing to be proved wrong. In the future though, as protein structure prediction and virtual screening both improve, this could end up being an important application of structure prediction.
Other current uses that are more developed are: A) protein design, where improvements in structure prediction allow you to find better sequences that form certain structures and carry out certain functions (the inverse folding problem); B) exploring the evolutionary relationships and function of a protein, e.g. if a predicted structure looks like all the other membrane transporters then it probably is one too (see more on that below); and C) running molecular dynamics simulation on the structure to gain biological insights and complement experiments.
On a deeper level, scientists will always seek to answer the question of what structure proteins fold to and how they fold, because it's just such an interesting problem that is central to molecular biology. Solving it will almost certainly lead to useful breakthroughs, even if their exact nature is unclear now.
How do we predict protein structures?
By the original formulation of the problem, protein structure prediction is arguably solved. If you can find a template, i.e. a related protein sequence with an available experimental structure, then you can pretty reliably get a high quality model (less than ~3 Å RMSD). Improving a model beyond this is currently called "refinement" and this will become increasingly important as we look to get ~1 Å RMSD models that can be used in place of experimental data.
If you can't find a template you can still have a decent go at the structure, provided you can find enough related sequences. It turns out that positions in a multiple sequence alignment will covary if the residues are close in space in the structure. Initially statistical techniques were used to extract direct from indirect coupling effects, but now deep residual neural networks are showing state of the art results in this field. These developments are recent and have been the focus of news reports. The explosion of sequence data facilitates this approach, though it is still not "the solution" to those who only want to use a single sequence as input data. For pure physics-based approaches there has been limited success on small proteins, see for example here, but these methods are not in broad use for structure prediction.
Usually the input to these methods is just the protein sequence, though you often bring in other data (templates, related sequences) as part of the pipeline. We generally care about the structure at physiological conditions, which usually corresponds to the structure found in x-ray crystallography or NMR, so predictions under different conditions are not yet routine. For more on protein structure prediction, see the CASP website and have a read of their papers.
How useful is protein structure at predicting function?
Predicted structure can be used to transfer function from related structures with known function - see for example here and here.
It is not currently possible to use a predicted structure to predict the function using chemical arguments, for example by saying "I have predicted a binding site with a certain arrangement of amino acids so this must have function X". However as structure prediction improves and we have more structures and functional annotations, this is an exciting prospect.
With respect to protein-protein affinities, if you have the structure you can start to predict and rationalise the structure of protein complexes. Such predictions from structure alone (i.e. not using homology to known complexes) are not routine yet, though more data and better models will improve this. See for example CAPRI. This is clearly a biologically important area, as most proteins form complexes.
Conclusion
Sequence determines structure determines function (fingers crossed as I'm simplifying quite a bit).
You shouldn't have to know the structure to predict function/binding from sequence, but it helps, and a sufficiently advanced system would learn this anyway in order to make the connection.
Protein structure prediction is a hot research topic that currently has limited applications, but is certain to have more in the future. If anything, it has only got more interesting over the last 50 years.

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Sexual Reproduction in Humans
Is the human egg cell (ova) considered motile? We know that is is not actively motile but it is transferred via the fallopian tube to the uterus. Does that make it motile?

Hi! Please take a brief tour of the site (you'll even get a badge to prove it!). Feel free to nose around and check out the help center and such as well. :)

The fallopian tubes, also known as uterine tubes are uterine appendages, lined from inside with ciliated simple columnar epithelium, leading from the ovaries of female mammals into the uterus, via the uterotubal junction. They enable the passage of egg cells from the ovaries to the uterus.
The egg cell is typically not capable of active movement and hence not motile

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Can denatured GFP show fluorescence?
GFP ( green fluorescent protein) can show green fluorescence. And its fluorescence is due to the tri peptide chromophore which is given in below I was wondering, can we observe fluorescence, if we denature it by boiling at 95 degree celsius? Say can we observe fluorescence band in SDS-PAGE?
I assume it can show some fluorescence as it is not due to any cofactors etc.

According to PDB (protein data bank — a repository for protein structures) the chromophore must be protected from interaction with water molecules to fluoresce.

The chromophore is found right in the middle of the [protein], totally shielded from the surrounding environment. This shielding is essential for the fluorescence. The jostling water molecules would normally rob the chromophore of its energy once it absorbs a photon. But inside the protein, it is protected, releasing the energy instead as a slightly less energetic photon of light.

This means that denaturing the protein will result in quenching of the fluorescence1, so you are unlikely to see significant signal on a denaturing gel.  In fact, as WYSIWYG has pointed out, fluorescence has been used as a marker of renaturation of GFP1.
Reference:
1: R.Y. Tsien (1998) The green fluorescent protein. Annual Review of Biochemistry 67, 509-544.

Additionally, there are biophysical studies on gfp folding in which increased fluorescence corresponds to folded state.

@WYSIWYG any reference if you give it would be appreciated

I wonder what would happen if you exchange the water in the gel with methanol or ethanol. Will these quench the fluorescence?

@Science123 check this out: https://www.pnas.org/content/109/44/17832


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Knee directions
art student with very little knowledge of biology here. I was thinking about the designs of mythical creatures and I got stuck on the topic of knee directions, and couldn't work out the appropriate terminology to do my own research.
Is there a term for legs that bend towards the head (eg primates and the front legs of horses, cows, goats, etc) or those that bend away (back legs of the above mentioned, dogs, cats, lizards, primate elbows, etc)? Is there a large practical difference in the way these two types work/are used that is more notable than the other differences between types of leg structure?

cats/horses walk on their toes. the part that bends backwards is the ankle, the knee points forward.

Hi @Robann, welcome to the site. If you could ask one question per post, that'd be appreciated. E.g. "what is the term for legs that bend forward" and "is there a practical difference".

Also, you should note that (as Frieke has pointed out) the joint in a cat's/dog's leg that looks like a backwards knee is actually its ankle. The knee is further up in the leg and they walk on their toes. See Line of Action: Digitigrade animals don’t have “backward knees”.


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Is there any double staining method to visualise separate colour for plant tissue and fungal tissue?
Is there any double staining method for developing separate colour on fungal tissue and plant tissue when the said 2 types of tissues are intermingled?
Unlike my previous question, this question not necessarily need  to target specifically chitin and/or N-acetylglucosamine but looks for any principle to differentially stain intermingled plant tissue and fungal tissue.


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What is the end-point of material from an apoptotic cell, after phagocytosis?
Apoptosis occurs. The organelles and interior material form apoptotic bodies that are packed in vesicles. The cell membrane breaks apart (cell no longer exists) and apoptotic bodies enter the extracellular space. Phagocytes "eat" the apoptotic bodies.
What happens then?
Is the material processed again and effluxed into the blood, sent to other cells, ...?


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Anybody know of any sources/papers on wild animals identifying birds by their calls/sounds?
I'm doing a literature review about identifying birds, and was hoping to find some examples of animals being able to identify birds by sound (eg a mouse knowing the normal call of a sparrow is not the normal call of a sparrowhawk), but alas when I tried to search google for anything all I got was a bunch of pages showing humans how to identify bird noises, or apps to do the job for you, even making sure the word "animal" was included lead to the same results.
I vaguely remember watching a BBC show that had meerkats using a bird to alert them for dangers, but when I tried to find this online all I found were sources saying how it's actually a bird pretending to be a meerkat to score a free lunch, so if anyone knows any more about this I'd be grateful for any information.


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Congenital deafness: can cochlear implants always improve hearing at any age?
People with congenital deafness may acquire a cochlear implant at a later age and be able to hear. Given that it seems there is a curve for synaptic plasticity of different circuits:

(1) Cochlear implants are used in older children (age 3-8) with moderate success. How can we explain the fact that they developed hearing despite not receiving any auditory stimulus in early age?
(2) Can auditory circuits be formed at any age, or is there an age in which the use of a cochlear implants will not be useful anymore?


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Identification of UK insect

We found this in our UK garden! Any ideas? Not sure if it had/has wings.
It has a segmented tail and 6 legs. It’s about 2 inches/ 8cm long.

It would be helpful to include more information about exactly where in the UK you found this and what kind of habitat.

That;s the last stage of the dragonfly in the pond, where it eats even tadpoles probably. It climbs out and emerges as a dragonfly, waits for it's wings to dry and flies away.

If you look at reeds and grass next to ponds at this time of year, you are bond to see many of those.

That looks like the cast off outer layer of a dragon fly nymph§:

The following resources may be helpful to get a more precise identification:
https://www.fba.org.uk/sites/default/files/EA_specid/ea_specid_mod_8.pdf
https://british-dragonflies.org.uk/odonata/species-and-identification/

§Note: As pointed out by Arthur J. Frost this is actually the exoskeleton left behind when a dragonfly nymph molted and became an adult.

More properly, the OP is what's left of a dragonfly nymph; the adult had emerged and flown off some time prior.

indeed -Exuvieae of a Anisopera dragonfly.
https://en.wikipedia.org/wiki/Exuviae


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How long does it take the neurotransmitters to diffuse accross the synaptic cleft?
Neurotransmitters get from the pre-synaptic neuron to the receptors on the post-synaptic neuron by diffusion across the gap between these two (the synaptic cleft). My question is, how much time does it take the neurotransmitters to diffuse from the edge of the pre-synaptic neuron to the receptors on the other side?
I have seen different values online, ranging from 0.05 ms to 1 ms. Which one is true?

Would be helpful to cite some of the examples you see. I suspect they refer to different conditions and have different definitions.

@Bryan I just want to know the average value in a typical synapse, which should has a cleft nearly 20-40 nm wide.


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Can someone tell me what these cocoons are?
I am camping in Slovenia and have found some cocoon like materials.
They look like nests of some kind and are about 30cm long and 10-15 cm wide. Can anyone help me find out what these things are?
Found in Tolmin, Slovenia

I think you are actually looking at dried bottle gourds, a squash relative.  These are probably in the genus Lageneria.  These come in an extreme variety of shapes, and have been put to many ornamental uses. They were important as containers for early cultures.  Good background here and here.  Search for "dried bottle gourd" images and you'll see plenty.


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Cerebral/Cerebellar Cortex versus Deep Nuclei
I have troubles using the terms Cortex & Deep Nuclei, and 'Nuclei' in general. From what I understand, a brain has '3 matter types in accordance to anatomical locations'

Superficial Grey matter - This is called the 'Cortex (Cerebral or Cerebellar Cortex)'

Middle White Matter
This is called 'Cerebral/Cerebellar White Matter' separating the cortex and deep nuclei

Deep Grey Matter, deep to the cortex -This is called 'Deep Nuclei' (for e.g.: Basal Nuclei of the Cerebrum, and four deep Cerebellar Nuclei (dentate, globose, emboliform, and fastigial))

Quote from the book that helps me to jump into this conclusion or summary:

'The brain, like the spinal cord, is composed of gray and white
  matter. Gray matter - the seat of the neurosomas, dendrites, and
  synapses - forms a surface layer called the CORTEX over the cerebrum &
  cerebellum, and deeper masses called NUCLEI surrounded by white
  matter... (Saladin 2015, Unity of Form & Function, McGrawHill)

Thank you!

What exactly are you confused by?

Hi Jam. Thanks for your reply. I'm wondering that if we call anything brain's grey matter in any location 'nuclei' (Cerebral Cortex, Cerebellar Cortex, Basal Nuclei, and dentate, globose, emboliform, and fastigial are all nuclei)

In comparison, it's called 'cortex' in the superficial area, and 'deep nuclei' in the deep area. For example Cerebral Cortex & Cerebellar cortex are grey matter in the superficial part of the brain. For deep nuclei, examples are basal nuclei (in the deep part of the brain, deep to the cerebral cortex).

I'm mostly concerned of how we call grey matter in 3 different situations: (1) In general, either in superficial or deep brain locations (2) On the surface of the brain (3) Deep part of the brain, deep to the cortex & white matter. Thank you!

"Cortex" is a more general anatomical term for the outermost layer of a structure. It applies to both the cerebral and cerebellar cortex gray matter, as these are gray matter structures on the outsides of their respective parts of the brain.
Nucleus is also a more general term; in the context of neuroanatomy, it refers to a cluster of cell bodies. Typically we refer to CNS clusters of cell bodies as nuclei, and in the periphery they are called ganglia, though there are some odd exceptions like the basal ganglia (you referred to the basal nuclei in a comment, which are the same structure, but are almost always called the basal ganglia, whether or not that term is the 'best' term).
White matter, in general, is nervous tissue that appears white because it is primarily "fatty" from the lipid bilayer of cell membranes and consisting of processes like axons (especially myelinated ones) and dendrites rather than cell bodies.
I'm not aware of anyone who would call the cerebral cortex (or cerebellar cortex) a "nucleus": these areas are not shaped as clusters of cell bodies, they are shaped as sheets. The distinction is really only an anatomical one, so it makes little sense to use "nucleus" in a more general term to mean "nervous tissue consisting of cell bodies": we already have a term for that, "gray matter," and in most cases interesting to science we are talking about something more specific anyways.
I'd further say that these distinctions are really only gross anatomical ones, as one can have cell bodies outside white matter, and areas of gray matter like neocortex also include a mostly-white layer of axons and dendrites in "layer 1" but we still treat this as gray matter with respect to the whole brain.
Ultimately it doesn't matter: don't take anatomical terms more seriously than the things they are describing.


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What parasites would be easiest to examine using a compound microscope?
I want to find some parasites that are easy to examine under the microscope.
I'm a beginner but I have an olympus microscope with total magnification up to 400x (also 200x, 100x and 10x).
I would like to choose parasites that are safe for me as an amateur to work with and would like to have one that parasitizes people.
I prefer lets say:
Helminths, mycose (Candida alba) or something that can make people sick and is safe to work for someone who is an amateur.

You don't need microscopes to observe some parasites (for e.g. leech). So you should clarify what kind of parasites you are interested in.

You should also specify how you plan on getting ahold of parasites that can make people sick because that likely limits your options.

I suggested an edit to your question that includes changing "Helmits" to Helminths — if that isn't what you meant can you clarify what Helmits are?  Also I'm not sure that a microscopic human parasite is ever going to be "safe" for an amateur to work with — can you add something to your question to clarify why you want to do this?

Yes safity is very important. So I dont want anything that is dangerous. So I want to examine them under the microscope.

Lets say mycose and to choose candida alba, how to grow them cultivate and examine under microscope? So first question is then how to cultivate it (grow), control it and then as last step examine them undet microscope? Or should I start with beer mycose, that is safer and after that to start with othes spicies?


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Is it possible to have action potentials in cells lacking both dendrites and axons?
I'm reading Kandel. Chapter 3 states the following:

Because the initial segment of the axon has the highest density of voltage-sensitive Na+ channels and therefore the lowest threshold for generating an action potential, an input signal spreading passively along the cell membrane is more likely to give rise to an action potential at the initial segment than at other sites in the cell.

I know it is possible to have dendritic spikes, which is an action potential given a much stronger input to open enough Na+ channels. But can there be a different action potential, not axonic nor dendritc, given that enough Na+ channels locally open in the cell membrane?
I've seen some papers talk about "somatic action potential", but its meaning and how it works I don't understand.

All of the action potentials you are describing involve the cell membrane. Do you mean to ask whether an action potential can occur in the soma? Are you thinking of an isolated soma with axons/dendrites removed? Does an action potential that starts somewhere else and spreads to the soma count? Are you asking for biological relevance or plausible theoretical possibility? What will the answer to this question teach you about neuroscience?

I am thinking about the theoretical possibility an action potential with axons/dendrites removed.

The soma of Dorsal root ganglion (DRG) neurons can fire action potentials.

There are many other electrically excitable cells other than neurons: muscles, pancreatic islet cells and even some plant cells.


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Can anybody recognize this cardiac waveform?
Is this an artifact or an arrhythmia?

What animal is this recording from? What is the nature of the recording? Where was the electrode placed? Did the animal move during the recording? Etc. I think we need more information.

There is also a Medical Science Stack Exchange site, I think that after you collect more information to address the questions in the comment above, you might consider asking there. But be sure to supply a lot more information than this.

To be conclusive, another couple of leads recorded at the same time as this event would be helpful though the fact that you do have a recognisable QRS complex and a T wave and that the QRS happens before you would expect it to based on the prior rhythm and the P wave, if that is one, prior to it is to close to the QRS complex to have caused it would suggest a premature supraventricular arrhythmia.  There are many technical texts to consult to refine this further, if this is a small animal ECG, I recommend Larry Tilley's textbook entitled ECG for the small animal practitioner.


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How to reduce the number of sequences in a Multiple Sequence Alignment?
I have a Multiple Sequence Alignment, where there are around 5000 sequences. There also exists many sequences where, there are so much of non-sequenced regions (for instance, AU----CGGGCA--NNNNNNNNNN).
So, by trial and error, I found a threshold value of 25%, so I removed the sequences which contained more than 25% of non-sequenced region (N's here), retaining around 400 sequences in the alignment, by writing a simple R script.
But, I would like to know, if there is any other standard method to do this, because I do not think, removing sequences based on finding a threshold for the percentage of non-sequenced regions, by trial and error is more efficient.If there is, can you please tell me, how to do?
Thanks in advance.

To remove sequences that contain ambiguous sequence is pretty straightforward. You can do it programmatically instead of doing manually. What do you mean by proper method? Can you please clarify what your objective is?

Sure, I removed the sequences with a simple R script. I do not think, removing sequences based on finding a threshold for the percentage of non-sequenced regions, by trial and error is more efficient. I was wondering if there is any standard way to do it.

That totally depends on your judgment. There can be sequence blocks that do not contain ambiguous bases. You can take them if you think the entire sequence is not necessary. This could be done only for local alignments. For doing global alignments, you should take a call on whether or not the number of ambiguous bases is too much. It would also matter if the ambiguous bases are present together or spread out. A stretch of Ns would be worse than the Ns being spread out. You can try MSA with and without these sequences and see if there is any significant change in the consensus.

Deciding the threshold depends on your prior knowledge about the sequence region. The software is unaware of the biology. For e.g. the N could be in non-conserved regions: it would not probably affect the MSA. If they are in the conserved regions, they could distort the analysis. Anyway, can you please [edit] your question to clarify the exact objective (as you mentioned in comments)? Comments are not searchable and can go unnoticed. Moreover, the post should be self-sufficient.

I edited my question.

As there are too many sequences, finding the consensus regions using online MSA viewer tools is not possible. I will try to find any offline tools available for this purpose. It's stretches of N's, present towards the ends of almost all the sequences in the alignment.

You may have a look at these papers: https://doi.org/10.1093/bioinformatics/btg109, https://doi.org/10.1093/bioinformatics/bth126 and this overview on POA. I haven't used the POA tools directly. Read the overview just to understand how PacBio generates consensus. The papers are still open in my tabs.

@User — By what method were these sequences generated?  If you do Sanger sequencing of PCR amplicons, you often get long runs of noisy sequence after the "real" sequence has been read.  It sounds to me like you might just need to trim off the junk from the ends of your sequences rather than throwing most of them away.

@User as tyersome said, these Ns would have arisen because of sequencing errors and thus do not represent the actual sequence. Moreover, we don't know what this sequence is: is it a gene, does it span the entire geneic region or ORF etc. If you don't define the boundaries of your sequence (based on the biology) your MSA cannot be used to infer biology. MSA is also used for obtaining consensus of sequencing reads; this strategy is used in PacBio and Nanopore. The objective there is different. So what is your objective?

I downloaded the alignment from a database and no information regarding the N's (uncertain nucleotide positions) is given, so my clear objective is to find the consensus or evolutionarily conserved sequence regions and use this, along with it's phylogenetic tree, in a software tool that does RNA secondary structure prediction.

The bioconductor package "ShortRead"  might be what you are after.
It has a function "clean" to remove sequences with ambiguous bases. It also can remove duplicates if you need to.

It would be helpful to know your application. For some applications, having ambiguous sequences is not necessarily a problem as long as you have a mechanism to handle such non-informative positions. The information from the other positions may still be valuable.
An alternative to removing the sequences (rows of the alignment matrix) with many Ns would be to remove non-informative or poorly aligned positions (columns of the alignment matrix) from the alignment. It depends to some extent on what your goal is. Tools such as gblocks can be used in this way.
For example, if your goal is to perform clustering or phylogenetic estimation of the region, or identify highly conserved regions, then removing poorly aligned or non-informative columns would be worthwhile.
On the other hand, if your goal is somehow related to the entire sequence (e.g. protein structures or open reading frames), then removing rows/sequences may make more sense. But it is still not clear to me that you really need to remove ambiguous positions. For some discussion of this you can see this old researchgate thread or this biostars thread.


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Would this mushroom make the basil dangerous to eat?
My sister is growing basil in a planter on her balcony. Recently this big mushroom started growing there. Obviously we're not going to take a bite of the mushroom, but would its existence make the basil dangerous to eat?

That could be a coprinus comatus / shaggy mane. If it is, the top will get pinkish then turn to black liquid . If that happens it was an edible mushroom.

@blacksmith37 I would say Leucocoprinus birnbaumii, which has a tendency to grow in pots.

@Ram Rachum From an academic perspective, I'm not aware of any cases where mushrooms caused toxicity in nearby plants. But consult a doctor for any medical advice.


text:
What is the function of spongin in sea sponges?
Sea sponges (Porifera) use different types of skeletons to support their structures. Some skeletons are built from minerals, some are built from proteins like spongin, and some use both.
My question is about spongin. What is the benefit of having a skeleton made exclusively of spongin? (What advantages does it have compared to other types of skeletons?)

Although I didn't get pin point answer, it may be for following reasons.Spongin is a collagen protein.Collagen proteins are usually found in places where elasticity/flexibility is required but not compromising with strength.These collagens provide rigidity (strength) but also some sort of flexibility. You know these poriferans live under high pressure of water (rigidity is essential) and also flexible enough to allow water (some wavy motion to body) in between for getting some food and dissipating wastes.

Sponges are more brittle and don't adopt the same shapes without spongin, which has mechanical and other advantages. https://books.google.fr/books?id=iUI_AAAAQBAJ&pg=PA109&lpg=PA109&dq=Spongin+brittle&source=bl&ots=rhoVDq_IpD&sig=ACfU3U2pDZT364-K2SOVtIo37kT4ByrnZA&hl=en&sa=X&ved=2ahUKEwiovMLjgNrjAhUE5uAKHealBqcQ6AEwAXoECGMQAQ#v=onepage&q=Spongin%20brittle&f=false

If you have ever used a natural bath sponge, you know that the structure of a sponge's spongin skeleton is great for absorbing water and squeezing that water back out.  The sponge's skeleton contains millions of tiny holes, all connected in a massive network of internal tunnels, through which the sponge takes in food and eliminates waste.  It feeds by use of cells that wave tiny cilia to push water into the sponge.  Nutrients are absorbed by the animal and spent water and waste are expelled by the help of similar cells, spinning their flagella to force the water out of the sponge.  A third class of cells, comprising a basic immune system, move around the organism engulfing microbes potentially dangerous to the animal.
This unique system is facilitated by the structure of the spongin skeleton.  The skeleton needs to be strong enough to retain this complicated microstructure, while also having enough give and flexibility that its network of delicate tunnels don't buckle under the force of water pressure, deep currents, or fish and other matter bumping against it.  Notice that, when you squeeze the water out of a sponge, it snaps back into place, the tunnels still open for business.  Given that these tunnels are how the sponge eats, this is very important.  To build a complex tunnel system with millions of tiny little tubes running through it out of something hard and brittle would make it very easy for tunnels to collapse, cracks to form, and other damage to be sustained.  Some sponges, as you mention, have hard, brittle "spicules" in addition to the spongin, but these sponges tend to live in deeper regions and need extra strength to deal with the pressure.


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Do male skunks have teats?
Simple question.  Do male skunks (striped skunk, eastern US/Canada if it matters) have teats?  Occasionally want to identify road-kill, but don't know if teats are diagnostic for females.  I believe they are for racoons.

Petrides, 1950, writes:

Male skunks have tiny nipples which are considerably smaller than those of juvenile females.

and also:

Female skunks which had bred could easily be distinguished from those which had not by differences in the size of the teats

So it sounds like the mere presence of teats is not sufficient to sex skunks, but the size is sexually dimorphic and is probably a reasonable guide with practice, though the differences may be more subtle for female juveniles vs. males.
For pelts, Petrides recommends sexing based on the presence of a penis scar; I presume that genitalia is likely a more reliable guideline than teats.
For roadkill where damage might make it hard to sex animals based on genitalia, Fuller et al found canine size to be highly predictive, though they suggest that a comparison group of sizes from animals of known sex be used for a particular region, so that might not be too helpful for sporadic sexing.
Casey & Webster 1975 discuss sex identification based on presence of Barr bodies in the hippocampus, but their technique would probably not be applicable to your use case.

Casey, G. A., & Webster, W. A. (1975). Age and sex determination of striped skunks (Mephitis mephitis) from Ontario, Manitoba, and Quebec. Canadian journal of zoology, 53(3), 223-226.
Fuller, T. K., Hobson, D. P., Gunson, J. R., & Schowalter, D. B. (1984). Sexual dimorphism in mandibular canines of striped skunks. The Journal of wildlife management, 48(4), 1444-1446.
Petrides, G. A. (1950). The determination of sex and age ratios in fur animals. American Midland Naturalist, 355-382.


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How to clean and preserve a cicada's molted exoskeleton (exuvia)?
I found a good quality molted exoskeleton (exuvia) of a cicada, about 3-4 cm long on the ground. I'm amazed at the completeness and detail, the exit hole is in the center of the back and you hardly notice it. The "claws" on each foot are sharp and you can stick it onto any surface with a bit of roughness.
It had rained and there is some mud on it. I'd like to gently wash it and then keep it.
Are there any particular guidelines or techniques I should know about? Can I just gently swish it around in soapy water and then let air dry, or do I need to take some precautions, or even use some kind of fixative? Humidity is high where I live; anything that can possibly support mold will get moldy if you are not careful!
Sorry I can't add a real photo right now but it looks a bit like the emptying exoskeleton in this randomly chosen photo from here:

Are there any additional tags for this? I couldn't find "preservation" or "specimen" or "collecting"

The exuvia is made of cross-liked chitin, and will not decay. You don't need any special preservatives as all. If you need to get the mud off, just rinse it as you said, in soapy water, let it dry, and you are done. Simple.

Excellent, thank you for your quick reply! It might be good to add a supporting link for the "cross-liked chitin" for future readers, but personally I'll take your word for it.

fyi I've just asked Is the chitin in an insect's exoskeleton cross-linked?


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Reducing Ammonia Levels in Body through Bowel Movements Only
Can high ammonia levels in body be reduced solely through repeated bowel movements (4-5 per day), i.e., WITHOUT the use of Lactulose?

Lactulose can decrease the blood amonia levels by either drawing some ammonia from the blood into the intestine (MedlinePlus) or by inhibiting ammonia production by the intestinal bacteria and hence its absorption into the blood (Digestive Diseases, Emedicine).
By having frequent bowel movements, you could theoretically give less time to intestinal bacteria to produce ammonia from the undigested food, but, without laxatives, it may not be realistic to just decide to have 4-5 bowel movements per day.


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How does a heat-ratio sap flow sensor work and how invasive is it?
The Gizmodo article Undead Tree Stump Is Being Kept Alive by Neighboring Trees says:

Leuzinger and Bader stumbled upon the stump while out for a hike. The woody stub caught their eye because callus tissue could be seen growing over its dead and rotting parts. It was also producing resin, which indicated the presence of living tissue. This prompted a more thorough investigation in which the researchers measured water flowing through the tissues of the stump, and also its rate of respiration, which matched those seen in the surrounding trees.
“We measured water flow with ‘heat-ratio sap flow sensors’,” Leuzinger told Gizmodo. “They detect water movement in tissue by sending out very small heat pulses and measuring how quickly that heat dissipates.”
These measurements indicated that the kauri stump is inactive during the day when living trees transpire. But during the night and on rainy days, the tree stump becomes active, circulating water—and presumably carbon and nutrients—through its tissues. As the authors write in the new study, these results

"...indicate that such symbioses may be much more complex than previously assumed: by physiologically exploiting ‘‘downtimes’’ of transpiring trees during the night or rainy days with high water potentials in the root network living stumps seem to act partially autonomously, strategically tapping into resources rather than simply becoming part of the neighboring trees’ extended root networks."

I can get a general feeling for the principle. After a thermal pulse the local temperature of a probe will decay due to heat diffusion, but if there is movement of water (or sap) in and out of the area the decay will be faster...
But I have a few questions:

How exactly would you analyze a temperature decay curve $T(t)$ in order to determine if there was water, sap, or any material moving in and out of the volume or not? Is there a distinctly different shape to the curve that rules out thermal diffusion alone, demonstrating that there must be mass flow as well?
When used on trees, how is this instrument applied to the tree? Does it need to penetrate into live tissue to work, or can it work by proximity, perhaps using radio frequency or microwaves for heating and a surface contact thermometer?

This paper describes the construction of sap flow sensors. It is apparent that these are applied to xylem sap (water) as placement in phloem would require a high degree of precision that the design presented doesn't support, IMHO. So, it works by heating water in the xylem and measuring how that heat dissipates - asymmetric dissipation indicates the sap flow direction. Multiple probes - one heater, many sensors

@JimYoung excellent, looks like the basis of a great answer.


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Difference between fertilin and fertilizin
I am confused between fertilin and fertilizin.Are these two same or different?
Here are a few sources i referred

Julian Lombardi (auth.) - Comparative Vertebrate Reproduction-Springer US (1998)
Page 210

Richard E. Jones - Human Reproductive Biology, Third Edition-Academic Press (2006)
Page 244

Bioregulators of Reproduction
edited by David Jagiello

google book image link

Please help me know how they are same or different ,specify their functions in detail and thanks for your help in advance !!!

Welcome to Biology SE.
Coming to your question, Fertilin and Fertilizin are different.
Fertilin
Fertilin is a sperm surface protein with an essential role in fertilization. It is required for the migration of spermatozoa through the oviduct, for binding to the zona pellucida, and for efficient binding to the egg plasma membrane. Fertilin consists of two subunits, fertilin alpha and beta, both of which belong to the metalloprotease-disintegrin protein family (ADAMs). Fertilin alpha and beta are made as larger precursors that are processed proteolytically at different stages of sperm maturation in the testis and epididymis. Fertilin alpha is processed first, most likely by a pro-protein convertase in the secretory pathway of testicular cells. Fertilin beta is processed later, while spermatozoa are in transit through the epididymis.(taken from this reference 1) Thus this protein is present in Sperm.
Fertilizin
Fertilizin is sperm-agglutinating substance (glycoproteins) present on Zona pellucida layer of the egg surface. Antifertilizin-fertilizin complex play a key role in sperm penetration. (Have a look at reference 2 &3 ). Thus, Fertilizin is present on egg surface.
Now look back at the images you provided with your question. Role of Ferilizin and fertilin-beta are clearly given.
References:

https://pdfs.semanticscholar.org/0043/f4525b6158d91a00682b86b1b9b15f726125.pdf

https://www.nature.com/articles/169548a0

https://www.journals.uchicago.edu/doi/pdfplus/10.2307/1537786


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What are the various types of plugs found in a bee house and how do they help us with identification?
I have a Mason bee house with small tubes that is currently buzzing with life but I am completely clueless about what's in there. Some plugs seem made of clay, some of crushed leaves, some of resin, some look like just a little film...
I figure it's possible to learn about what is living in there (approximately) going by the type of plug, and maybe the size of the tube, but I don't know where to start. I'm in Eastern Canada if this makes a difference.

Not an expert on bees, but there 39 known genera of solitary bees in eastern Canada1.  That reference contains a key, so at very least you can start to identify your tenants when they emerge next year.
The clay plugs are due to one of the genera of "mason bees", but that doesn't really appear to narrow things down much.
Your area does have "leafcutter bees" in the genus Megachile that use cut leaves to line and separate the chambers of their nests1,2, so that probably explains the holes containing crushed leaves.
There are also "resin bees", but the only species in your area (Paranthidium jugatorium) I've read about that fits that description is supposed to nest in the ground.1
Finally, bees in the genus Hylaeus and Colletes are known to use a membrane rather than a plug.2
1: Packer, L., Genaro, J. A., & Sheffield, C. S. (2007). The bee genera of eastern Canada. Canadian Journal of Arthropod Identification, 3(3), 1-32.

2: Michener, C. D. (2000). The bees of the world (Vol. 1). JHU press.

ETA: A guides to wasps in your region from the Canadian Journal of Arthropod Identification may also be of help.

That's a good start, thank you! I believe I may have wasps in there as well so it's a bit broader than just bees.

You're welcome! I'll add links for a couple of identification guides for wasps in your region.


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How can I improve efficiency of Ecoli transformation?
I am an intern in biology institute. I have a 17.3kbp plasmid need to transform to Ecoli. But I have tried many time but have no or very few colony on LB plate.
I know large plasmid have less frequency in transformation, How can I improve chance of successful transformation?
Thanks everyone.

Welcome to Biology.SE!  It is expected that you will demonstrate that you have done research on your own before asking questions here — for example you could start with this: https://www.researchgate.net/post/How_can_I_improve_transformation_efficiency_using_a_12kb_recombinant_plasmid_with_a_cloning_strategy_using_DH5a …. –––––––– Thank you for taking the tour — for details on how to ask good questions on this site please see: biology.stackexchange.com/help/how-to-ask. Thanks!

Other than what tyersome has suggested, I want to add that questions that involve troubleshooting of lab experiments should include the detailed protocol used (or provide a link to a protocols article if it is exactly followed).

The plasmid is quite big which might explain why it is difficult to transform bacteria (is it a lentiviral vector?).
If you could give additional details you might have a chance to have improved answers to your question.
Hello, I suggest you follow this protocol:
At step 7 instead of this "Add 250-1,000 μl LB or SOC media (without antibiotic) to the bacteria and grow in 37°C shaking incubator for 45 min. "
Do this " Add 250 μl LB or SOC media (without antibiotic) to the bacteria and grow in 30°C shaking incubator for 2 hours. Do not shake too hard, gentle motion might be fine (500 rpm).
At step 9 instead of this "Incubate plates at 37°C overnight."
Try to incubate at 30°C. I would even suggest to try to grow them at lower (25°C, or 16°C) temperature if you can prepare a second plate.
It will take much longer than overnight to grow the cultures, probably more 48 hours (might be 72 hours at 16°C).
Hope that helps good luck!


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Laparoscopic surgery: Why did the gas cause pain in my shoulder, and how did it escape my body?
I recently had Laparoscopic surgery, and the nurse told me I would experience pain in my shoulder and burping as the gas escapes my system. I looked up a bit of information on the "pain in my shoulder" claim, and its due to the CO2 gas irritating my phrenic nerve. So my first question is:
Why was the pain only in my right shoulder when there is a right and left phrenic nerve? Is it common for patients to experience pain in one or both shoulders? If CO2 causes pain/irritation, why not switch to another gas?
My second question revolves around the burping and the gas escaping my system. Basically, how? How is it that gas in my abdominal area escapes through my mouth? Is it through some absorption mechanism?
Thank you!

Does CO2 cause pain?
CO2 can cause pain by applying pressure on the diaphragm; also stretching of the diaphragm due to the body position can irritate the phrenic nerve (Indian Journal of Surgery).
ALSO:

It was once believed the resultant shoulder pain was simply due to
  reaction of the gas combining with water; or that it was merely
  trapped CO2. The actual cause of this irritation is the result of
  cellular death caused by the combination of a temperature change from the gas at 70oF and the drying effect of the gas at
  .0002%. Much of this irritation is centered on the diaphragmatic
  region. Experiments with gases other than CO2 i.e. helium, nitrous
  oxide and argon have all produced the same or similar effect (Center
  for Endometriosis Care).

Why they use CO2?

To begin, during Laparoscopy, CO2 (carbon dioxide) gas is injected
  through a special needle inserted just below your navel. This is done
  to create and maintain a distended abdomen; a condition called
  "pneumoperitoneum."  For safety, cost and convenience, CO2 is used
  almost exclusively for this purpose (Center for Endometriosis Care).

Why is pain in the right shoulder?

The mechanism of laparoscopy-induced shoulder pain is mainly derived
  from carbon dioxide retention within the abdomen, subsequently
  irritating the phrenic nerve and causing referred pain in the C4
  dermatome. Moreover, carbon dioxide trapped between the liver and the
  right diaphragm, irritating the diaphragm, also causes upper abdominal pain (JAMA Surgery).

BUT

In such hiatal surgeries including LAGB and in few gynecological
  surgeries, pain occurs preferentially on the left shoulder. This
  difference suggests that the region of surgery and position of the
  patient have an important influence on the site of pain. The cause is
  that in laparoscopic cholecystectomy the liver is separated from the
  undersurface of the diaphragm because of the reverse Trendelenburg
  with a right side up position of the patient. This leads to
  stretching of the right hemidiaphragm and the gas to be potentially trapped below the right diaphragm. Reverse is true for
  hiatal surgeries (Indian Journal of Surgery).

Where does CO2 go after surgery?
Most of the gas passively leaves the abdominal cavity through the surgical wounds immediately after the procedure. What happens with the rest:

Carbon dioxide readily dissolves in water and forms carbonic acid.
  Carbonic acid is then absorbed into the intravascular space...(JAMA Surgery)

CO2 is not released through the mouth and is not a direct cause of burping. Burping may result from the pressure of gas applied on the stomach and intestine.


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Why isn't the human zygote considered a human life how is a living anatomically modern human defined biologically?
It has 46 chromosomes by default when healthy(Differences almost always are pathological) and has almost every biological functions, processes a Newborn or and Adult person has.
It even invades fertile ground(womb) to survive.

As a new user to this site you are expected to take the Tour and also take the trouble to write a coherent question that is not a continuation from the title. And then you choose this list, frequented by people whose expertise you don’t know anything about to ask a question about a subject which has been discussed extensively by people whose qualifications etc. are known. Furthermore your question is asked in an aggressive manner — not “Is the human zygote considered…” but “Why isn’t the human zygote…”. This suggests that you are abusing this community. Please rephrase or go away.

@David Certainly there is no unanimus consent from the Biology community or at least a good majority of Biologists-Natural Anthropologists (circa 60-70%) that a human zygote is a living anatomically modern human. Otherwise there would be no pro-life/pro-choice argument. Hence the title why isn't it. Since it indeed is not. I am asking people from both sides. Biologists who consider it and biologists who do not. Write a coherent question that is not a continuation from the title? The title is the question itself. The body gives my reasoning why was such a doubt instilled.

Titles have different functions to Questions and should be separate. A title indicates what a question is about. (And here you have two sentences without a stop between them.) A better title would be something like. "Is a human zygote living?". The reader of a question, especially on a phone, expects to read something coherent. If you must have such a long title, copy it and paste it into the question. Nobody wants to read something that starts with "It" where they have to try to discover what "it" is. And this is a question and answer site, not, as "consider" implies, a discussion site. "

@David Would "What is a living anatomically modern human?" or "What is a living human" or "What is a human" do? I am certainly not asking if a zygote is living. I am asking if it is a living anatomically modern human. What is essential is the definition of a living anatomically modern human. If you have that i.e the sufficient criteria for a human, a zygote either meets them or does not. I am not wanting to discuss rather I want a scientific explanation. Does "consider" necessarily imply an intention to discuss? I want an answer not an exchange of opinions. My replies ask for clarifications.

Any of those are suitable titles, assuming they indicate your topic. However I have no idea what a “living anatomical modern human” is (I am a molecular scientist) but suspect that it is a subjective concept relating to the abortion question and not appropriate for this list. Don’t get me wrong, this is a valid topic for discussion but as a social and moral question. You won’t get a quick fix by asking for an opinion from the frequenters of this list.

@David https://books.google.gr/books?id=tzb5BwAAQBAJ&redir_esc=y I just thought Homo sapiens would look old fashioned or I would be "abusing" scientific lingo. How else could I distinguish "modern" humans from varieties of extinct archaic humans. Homo sapiens sapiens? I am interested in humans as defined by taxonomy as a distinct species.

Your blood cells could be considered a human life because they can be used to extact DNA to make a clone or a zygote these days. so when you bleed you could be like "oh no, i have killed a million little humans?!" Does a human have no organs, no nerve cells, no blood cells, no skin, no legs, no voice, no ears, no eyes, lives in water, is smaller than a human hair?

@com.prehensible Blood cells are fully differentiated and senescent. They do not reproduce or grow.

Sorry, that's wrong, blood cells are anucleate... they contin no DNA.. stem cells ca become zygotes, and they can implant your stem cells into an egg and probably do without the zygote altogether. Stem cells come from around the body, so your liver, marron, skin, and other cells are humans in the same way as zygotes.

@com.prehensible They can clone you but that would be another person. Ever heard of Dolly the Sheep? The Zygote had its telomeres re-lenghted by telomerase. Ter is a proto-oncogene. Each person has 70-100 divisions the so called Hayflick Limit. When you clone a person or a cell they do not live as long because some divisions have been spent. Your cells do not grow by themselves they do not strive to live. A Zygote actually infiltrates the Womb. Try to get your liver cells to do the same. Liver cells have differentiated even if just a bit. They can only give rise to liver cells.

Good point. I have to read about clonotes. Is a cloned humsn not human? Even if he is aged prematurely? Are liver stem cells aged?

@com.prehensible Ask your own questions. A cloned human is a human. Liver stem cells are aged.

The discussion of when a life starts is a little more complicated than that. Many views and disagreements between them fuel the discussions of pro-life/abortion groups.
Some of the views and what they consider the beginning of life:
Metabolic view: Considers that there's no singular developmental moment that marks the beginning of life. Any single or multicellular organism should be considered a unit of life, and the development of those organisms is continuous. In that view, the spem and egg are already considered alive.
Genetic view: Supports that life begins when an genetically unique individual is created. That would mean that life begins when fertilization occurs. There are some arguments against this view. For example, fertilization doesn't occur in a single moment, but in a period of time. Another argument against this view is the "twinning argument". Even after the fertilization, it's possible the zygote will divide itself in two or more zygotes (twins). Thus, fertilization itself wasn't the point where the individual was clearly defined. Also, genetic uniqueness can't be used to define an individual because two different individuals can share the same genetic code (identical twins).
Embryological view: Defends that life begins at gastrulation, the point where the zygote is not able to divide itself anymore. This view ends up giving support to birth-control methods such as the "morning after" pill and contragestational agents as long as they are used during the first 2 weeks of pregnancy.
Neurological view: It makes sense to support that the same measurement used to define when life ends could/should be used to define when life begins. Contemporary American and Japanese societies (amongst others) define death as the moment where no recognizable pattern is produced by the brain in an EEG. Consequently, the beginning of life would occur when there's a recognizable EEG pattern being produced by the fetus. This happens around 24-27 weeks after conception.
Ecological/Technological view: Defends that life begins when the developing individual can survive without the support of its developing environment (i.e.: a mother's womb). The limiting factor for that to happen is usually the development of the lungs.
Reference:
Scott F. Gilbert’s, "When does human life begin?" - http://science.jburroughs.org/mbahe/BioEthics/Articles/Whendoeshumanlifebegin.pdf

Please be carefull. I did not ask or discuss when life starts. The first step for me is to define what precisely is a living anatomically modern human, a living homo sapiens sapiens. I do not care about individuality and uniqueness. Human life in itself to the exclusion of all other issues.

That's exactly the point of the answer. There are many different views of what constitutes a living human, and none of them is universally accepted, though some of them are more/less backed up by science. It's more of an ongoing discussion (a very delicate one to be honest, because people's emotions and beliefs are involved).

Don’t feed the trolls.

IanC's answer is great, but is missing one and possibly the most important point. There is a distinction between being alive or having life, and "life" in the sense that we associate with words like individual, personhood, being. In the first sense; the biological sense, a zygote is most definitely alive; a living thing; a lifeform etc. But in the second sense, the more colloquial sense, it's not "a life" because it's an organism more akin to a bacteria or yeast etc. than a conscious human being. A zygote is not a person or an individual simply because at that stage the human does not possess those qualities that are sometimes considered to be qualifying for personhood or "a life". Think about it this way, would you consider a body that was just pronounced "dead" to be a life? Most people wouldn't, they would considered it a life that passed away. Yet a recently deceased body contains all the living cells and chromosomes the person had before dying. So "life" cannot be strictly applied to cells and number chromosomes based on common usage of the term.

A corpse doesn't grow nor it strives to survive. The Zygote - Morula invades the womb to survive. The Zygote even grows on its own before implanting itself. Anything fertile will suffice. I am certain that apparently the corpse resembles a human more than a zygote but I am inquiring about biological processes in themselves. With biological processes in mind I think a Zygote is more "human" than a corpse!

Don’t feed the trolls.


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When is it reasonable to assume selection for an observed change?
In speciation events, a lot of changes seems to appear simultaneously. How can a specific partial changes, occuring together with a lot of other changes, be said to be advantageous or disadvantageous?
For example, can we conclude that the loss of photolyase in placental mammals was disadvantageous? Was selection at work for that specific loss?
Another example is the change from GULO to GULOP. In an answer on Stack Exchange Biology a lot of people vote that this change was advantageous because it hadn't been selected against in natural selection, according to the book they cite.

Thanks for your efforts to improve the question, it looks like you've cleaned out a lot of the issues raised in the comments. I've reopened your question, though people might still suggest some improvements. It might be helpful for you to cite specific cases (including links/DOIs/etc) where scientists argue a given past change was due to selection; you mention a couple but there is no direct path from your description to where you found the information.

Some genetic changes occur too fast for selection to take place.

Can you please define "genetic change"? Selection can only change the frequency of alleles in a population. It cannot make a new mutation. If by, "genetic change", you mean "mutation", then selection just can't do it. If by "genetic change", you mean change in allele frequency, then the change resulting selection is not necessarily much fast than if genetic drift alone is at play.

Often scientists presume that selection has taken place for an observed genetic change. Is this assumption still valid, based on the current knowledge of genetic changes?

No, really not! Whatever you mean by "genetic change", there is no false assumption made here.

For example genetic changes caused by viruses and transposons seems to have the capacity to establish fast in populations.

Again, do you mean "mutation" or "change in allele frequency" by "genetic change"? Assuming you meant "change in allele frequency", can you please cite a peer-reviewed paper as an example but the claim is really not that obvious to me.

Can a genetic change established in a population be disadvantageous?

Yes! Most mutations are deleterious and genetic drift can lead to some drift load. No one has ever assumed that genetic drift could not happen. Even Darwin knew about it!

Can it be advantageous to make a pseudo gene functional again?

Sure! I have no idea how that relate to the rest of the question that being said.

I don't know what you mean by "changing order". You are maybe confounding "mutation" with "substitution". A mutation any any sudden change to a DNA sequence. It can be a substitution, an indel, a whole chromosome duplication, whatever. You should have a look at What is the definition of a mutation?

Your post and comment are completely full of wrong definitions. You should probably have a look at an intro course to genetics or to evolutionary biology otherwise it is near impossible to understand what you mean. You should at least make sure you have a good understanding of the definitions of the terms: allele, gene, locus, substitution, indel, mutation, selection, and genetic drift.


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What are some examples of animals who return to their group when threatened?
Based on my (limited) understanding, some types of animals use the power of numbers for protection. I assume, then, some species instinctively respond to threat by immediately seeking out and joining their group/hive/pack, not just to hide or get lost within the group (eg., school of fish), but to also take advantage of the power of the organized group (eg., swarm of bees).
Is this correct? If so, what are some examples?
[Note: It is my understanding that bees don't flee to their hive in response to threat, but rather sting and release a pheromone to draw the other bees to the area and create a swarm.]

The specific description you have made is almost the definition of mobbing behaviour. Some animal species protect each other and especially their offspring by cooperatively attacking and harassing a predator. Individuals can't cope with the predator alone, but by working together they increase the chance of discouraging the predator.
African buffaloes, bison, gulls show mobbing behaviour.
Wikipedia article
The Royal Society for the Protection of Birds article

That's a great lead, although mobbing seems to be more like a bee's behavior, which is initially aggressive. I'm curious if there are animals who retreat to the safety and protection of their group prior to being aggressive.

If you're referring to a behavioral pattern consists of "flight-incorporate into group-organise counterattack", there's not a classification for this. These are different behaviors. A baboon or buffalo flights, joins to its group and joins a counterattack which is mobbing. That kind of high level behaviour which there's an organisation of an attack can be only found in wars between groups of same species; e.g., chimpanzees. But I don't think that it's  interpreted as a behavior triggered by a threat; rather it's interpreted as a part of competition. Humans orga

Humans organize attacks on threats after one of them has been attacked by a predator or else, but this counterattack is a decision, not a certain response.

I should clarify. I don't mean a retreat to produce a coordinated attack, but two different responses to a threat depending on whether the organism is alone or in a group. If alone, the organism would retreat to the safety of the group. If in a group, the group itself responds to threat via a "coordinated" attack like mobbing.
I'm guessing this doesn't exist?


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regarding evolution of ears and sense organs
How could we(or any other organism) have developed ears through evolution when before having ears we did not know that sound waves existed or there was anything such as hearing? How did the first hearing organ develop? The same can be asked for the other sense organs as well.

I tried to answer below. Your question is very broad currently - if my answer is not targeting your main concern, or is opaque, please comment on the answer, and try to sharpen your question so i (and other users) can try to better fit your question.

I think this is, in principle, a duplicate of a question that is quite commonly asked here, but I can't find a prototype - I suspect that most of these questions get closed as "Too broad". The real problem is of course that the question is based on a profound but common misunderstanding of evolution, the notion that there's some plan or direction to it. Remi.b's answer here addresses this, but perhaps there should be a more detailed, canonical answer to point newcomers to.

Possible duplicate of How does the creative process of Biological Evolution work?

When you are asking about the evolution of organs, you are already five steps ahead of yourself. To have sensory organs, you need cells that react to some stimulus:

Hearing, Touch: Mechanical stimulus
Smell, some pain: Chemical stimulus
Sight: Optic stimulus
Other (non-human) organisms can also sense electric fields, magnetic fields, ...

As soon as you have those, having 'organs' that house a lot of those cells surrounded by tissues that aid in the reception of these stimuli, is relatively trivial.
But isn't a sensory cell totally complicated? It is. But: A simple neuron already is a sensory cell of sorts: It reacts to electrical and chemical imbalances.
But isn't then a neuron totally comlicated? It is. But: A simple non-neuronal cell already has a lot of the intricate machinery that a neuron does - a neuron mostly has some special parts and structures that make it a neuron. A simple cell also does react to chemical and other stimuli (this is why hormones work, and how little one-celled animals can orient themselves towards the light or food, or away from dangerous chemicals)
But isn't a run-of-the-mill cell totally complicated? It is. But it actually is just the workings of several archaic cells crammed into one (one of the more popular theories on Eukaryote evolution has them result from a very intense partnership of several more basic cells). And those archaic cells can also react to stimuli (they manage their metabolism according to the available food, for instance)
But isn't a basic cell totally complicated? It is. But is actually is just the interaction of several molecules that have some very interesting properties - DNA/RNA can function as an information storage, but are at the same time tools that can cowork with other DNA/RNA, and also interfaces/interferes with proteins in interesting ways.
But aren't big molecules totally complicated? They are. We still need supercomputers to reliably model all of the intricacies of any given Protein-Protein or Protein-RNA interaction. Many proteins behave differently in different environments (electromagnetic field strengths, chemical environment, temperature and mechanical factors (e.g. ultrasound)) - they could be said to 'react' to certain triggers. But they are actually just chains of repetitive elements (so called polymers of so called monomers).
But aren't those monomers totally complicated? Some are, but here we slowly get into the realm of 'mostly modellable on a hefty home computer'.
So we have systems of systems of systems... All of them very complicated.
But evolution is not a process that involves understanding ot planning. It is simply the result of coincidences and inheritance. You can see colors that many animals cannnot. You have the requisite molecules in your sensory cells in your eyes. Some people can see more colors than you, an inheritable trait. Some people can see less colors. Currently those people have no evolutionary profit from this - they reproduce and die with the same probability as the rest of us. Likewise there are a million (possibly billion?) such traits in every human. Traits that are different from the rest. Little things. Ineffective things (= having no net effect). But there might come a time where seeing one color or not seeing it (= not being distracted by it) will give a continuous net positive or net negative effect on the reproduction of those people carrying that trait. That is the time when that trait will start to  be present in a larger piece of the population (over many generations). The people carrying that trait will also be different from one another. And the ones carrying the traits with the most positive net effect will multiply the most, etc. Humans in some distant future then can eye-sense some X-factor we cannot even describe currently (try describing different colors to a blind person) and thus have, say, Xeyes.

Organism don't have any intention to evolve a certain. As soon as a mutation creates a protein that can change conformation in response to a given sound frequency, then the organism carrying this information has opportunity for making use of this new signal. If this new mutation is beneficial, then it can be selected for and will increase in frequency in the population.


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What is the name of this bug?

I found this bug in my garden in India this morning.

That is a tortoise beetle (Family Chrysomelidae (Leaf beetle), subfamily Cassidinae). It looks very much like the Indian Green Tortoise Beetle Chiridopsis bipunctata. https://indiabiodiversity.org/observation/show/338651
I am almost sure it is in the genus Chiridopsis.


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Properties of berries that are not shared by strawberries
What are examples of properties that (all) berries (from a botanical point of view) have and that strawberries do not have? This does not need to be the exact reason, why strawberries are not counted as berries. I'm more looking for properties that emphasize the difference.
Since I'm not a biologist, I'd be happy about simple examples. Thanks a lot!

Did you check out wikipedia on berry?

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Botanically a berry is something quite different from what is commonly termed a berry in English.
From that Wikipedia page:

a berry is a fleshy fruit without a stone produced from a single flower containing one ovary

...

Berries so defined include grapes, currants, and tomatoes, as well as cucumbers, eggplants (aubergines) and bananas

On the other hand, many things called "berries" (including strawberries) are actually aggregate fruits, which are

a fruit that develops from the merger of several ovaries that were separate in a single flower

Therefore, the botanical difference is the originating tissue of the fruit: a single flower/one ovary, versus a collection of ovaries grouped together.
These botanical groupings don't have much relevance to practical use (i.e., cooking/nutrition) and there aren't other properties that are definitive for what a berry is and is not. For that reason, there is nothing wrong with referring to strawberries, raspberries, etc, as "berries" in cooking: berry simply has different meaning in botany and culinary fields, just like the many culinary "vegetables" that are botanically "fruits."


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Is there a system biology approach to compare pathways or famillies of proteins from an evolutionary point of view for the same organism?
I would be interested to know if there is a method/analysis or a set of methods to compare two groups of pathways or families of proteins.
I would specifically be interested by a system biology approach which takes all the components of the pathway or family of proteins. I would like to know if there is a method which can not only compare the similarity, homology, divergence and convergence of a family of proteins (like ribosomal proteins) between species but also between groups in the same organism.
For example I would like to compare the molecular components of vesicular trafficking pathways to the molecular components of non-vesicular pathway in the same organism saccharomyces cerevisiae (yeast).
I would greatly appreciate your suggestions.

I am not sure that I completely understand, it would be a little easier if you described the problem you are trying to solve or what the motivation is.
However, I think that some of what you want to do can be accomplished by inferring gene/protein trees for each gene/protein of interest across different species (including paralogs, maybe?). This will allow you to see discordance or correlation of evolutionary rates of different genes/proteins across species.
THis kind of analysis is built into HyPhy, though I have never used it. There are also somewhat less involved methods for measuring distances between trees.
You might also be interested in protein co-evolution methods, depending on the question at hand.
Your mentioning systems biology methods suggests that you have something rather different in mind, as none of these things I suggest are really systems biology IMO, but I'm not sure what it would be. Possibly you are interested in integrating e.g. protein-protein interaction or metabolic network information as well, but that would probably involve something more homebrewed that might integrate some of these things.
Hope that helps.


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Difference between "controlled release" vs "prolonged release"
My sister is using the epilepsy drug Tegretol which has both CR and retard (previous naming for prolonged release according to https://www.medicines.org.uk/emc/product/5932/smpc) versions in different countries. Given the active ingredient is the same (carbamazepine), would there be any difference between the effects of the two drugs in terms of preventing seizures?
Here are the boxes for the two versions:

For the sake of your sister's safety please consult with a pharmacist or other medical professional.

The first box contains Tegretol Retard, which is an old name for what is now known as Tegretol Prolonged Release (medicines.org.uk).
The second box contains Tegretol CR, which means controlled-release (PubMed).
Drugs.com says:

Your medicine is called Tegretol 200mg prolonged-release
  Tablets/Tegretol CR 200mg Tablets or Tegretol 400mg prolonged-release
  Tablets/Tegretol CR 400mg Tablets but will be referred to as Tegretol
  prolonged-release Tablets throughout this leaflet.

Concluding from that, Tegretol CR200 is the same as Tegretol Retard, which is now known as Tegretol Prolonged Release.
Saying that, it is a doctor who prescribes drugs and who can answer such questions.


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Are there species which is debatable if they should be classified as animals or plants?
I'm watching a sci fi series and a character who is a biologist claims "even on Earth there are species which is debatable if they should be classified as animals or plants". I looked for examples of this and I couldnt find any. Is this true? Are there species which is debatable if they should be classified as animals or plants?

No, there are no such debates. Plants and animals diverged over a billion years ago. Animals are defined by the unique molecules that are secreted by the cells, and fill the intercellular matrix, like collagen. Plants have unique cell walls, chlorophylls a and b, and plastids. The unique characteristics of plants are given here: http://www.bio.miami.edu/dana/160/160S10_10.html
Although there may be animals like sponges that don't seem to move around a lot, or corals that have symbiotic relationships with algae, simply "behaving like a plant" does not make them plants. Similarly, there are plants that move and trap insects. But taxonomists would never confuse them with animals.

According to this, the Orobanche fasciculata belongs to the Plantae kingdom but it doesnt have  chlorophyll https://en.wikipedia.org/wiki/Orobanche_fasciculata. So what we have left is cell walls and plastids for all plants, right?

Its a plant. Snakes don't have legs, but are still considered "Tetrapods". Loss of characters, such as chlorophyll in derived lineages simply means that their ancestors had chlorophyll, and then lost it. Loss characters can confuse taxonomists, but do not change taxonomy.

"(Lost) characters can confuse taxonomists, but do not change taxonomy" - this is an excellent quote.

To add, modern taxonomy relies on genetics and not morphological/phenotypic characteristics. There are unicellular organisms like euglena that can photosynthesize but they are not plants (they are not animals either).


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Why do my tomatoes start to rot on the same fruit part?
I observe a phenomenon for many years now. I observe it on a wide diversity of tomatoes produced all over Europe and Northern Africa that are sold at my local supermarket.
When I keep my tomatoes at ambient temperature around 20 to 25 degrees celsius, they deteriorate after a variable time, usually starting a five to fifteen days after I bought them. Nothing abnormal so far.
However, I observed that the mold pattern of virtually all these tomatoes is the same. It almost always starts a few millimeters from the junction where the tomato was attached to its branch, forming a ring on the top of the fruit.
I have thought why this could happen and my main hypothesis is that when they are grown the sun hits the top of the tomatoes (except where it is attached to the branch, obviously) and some ultraviolet radiation might weaken the tomato resistance in some way. The other reasonable hypothesis, although I cannot think of a definite mechanism, is that gravity would favor this polarized degradation. I have other hypotheses but they are too far a stretch, I believe.
So what is really happening?
I am a biologist, just not into botany or agriculture, so feel free to go technical and not just oversimplify.

Mold spores float around everywhere in the air, in your home and on farms. They are also likely found on the surfaces of farm equipment used for harvesting (shears, knives, etc.). Grey mold can infect tomato leaves and stems where there are lesions, such as those introduced when harvesting fruit, when cutting the fruit off at the stem. This could happen wherever such spores can find ingress between the farm, produce distributors, the market, and your home.
Cite: https://content.ces.ncsu.edu/botrytis-gray-mold-of-tomato

But there is no apparent lesion there, and the flesh is as firm there as the rest of the fruit until a week passed, then it gets softer, darker, and cracks open, allowing mold to take place. Are you saying that harvesting damages the tomatoes around the stem location although it is invisible?

When you cut fruit off the vine, that cut is a lesion. In handling the cut tomato, the stem can be pushed and separated to allow spores entry.


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Trying to identify a bug that left a blood spot when killed

Hi, this was flying around inside the car in northwestern Maryland, USA, yesterday. When I squished it with a tissue I was surprised to see a red spot that appeared to be blood. Cannot find a picture of this bug online and was hoping someone can identify it. Thanks in advance.

I'm from California and my Husband was bitten or stung by the same bee or fly. He was outside on the hammock and told me something stung his foot. It was the exact same fly and when i squished, It was full of blood. I took a photo because It was very weird that this fly or bee was feeding on blood. I ask several people but no one believes us at all.

it's a harmless hover fly, a flower pollinating wasp mimic that migrates hundreds of miles every year and have quite interesting biology. you can recognize them because they hover in one place a bit like small humming birds.

That looks like a species of syrphid fly (aka. hover fly, flower fly) — not sure about the red fluid, but it probably wasn't blood.  These flies are pollinators and the larvae eat pests such as aphids.
I don't know for sure what species that is, but it appears very similar to Toxomerus politus:

Other sources of information on this group of flies:

http://thingsupclose.com/syrphidae-hoverflies/
http://bugoftheweek.com/blog/2017/10/31/flies-that-mimic-wasps-masquerading-syrphid-fly-ihelophilusi-sp
http://bugoftheweek.com/blog/2016/10/19/a-flower-fly-grows-in-brooklyn-flowers-flies-syrphidae

That hoverfly was probably feeding on red pollen from flowers. Many types of flowers have red pollen:

They were scientifically proven to eat pollen and nectar as early as 1883, when Muller disected the flies up to study their crop and insides.
Entomology Division, Department of Scientific and Industrial Research,
Private Bag, Auckland, New Zealand

Analyses of the pollen contents of the crop and intestine of 11 species of New Zealand Syrphidae .
showed that small, sparsely haired hover-flies with unbranched hairs, short, simple bristles, and a
short proboscis had ingested at least 99% anemophilous pollens, and that larger, more hairy hoverflies with pollen-collecting hairs, long, spirally grooved bristles, and elongate mouthparts had ingested
pollens almost exclusively from nectar-bearing flowers. Pollen-feeding behaviour was studied in
one hairy species, the drone-fly Eristalis tenax, and in one sparsely-haired species, Melanostoma
fasciatum. Using granulated charcoal as a substitute for pollen, it was found that in E. tenax particles
trapped among the body hairs are combed off by the front and hind tibiae and transferred to pollenretaining bristles on the front and hind tarsi respectively. Particles retained among the front tarsal
bristles are ingested directly from the bristles. Those retained by the hind tarsi are transferred in
flight by leg-scraping movements to the front tarsi, from which they are subsequently eaten. E. tenax
also eats pollen directly from anthers. In M. fasciatum apparently all the pollen ingested is taken
directly from anther lobes or stigmas. The few pollen grains that adhere to the body of this species
are combed off by the front and hind tibiae and transferred to the front and hind tarsi, but are not
retained there because the bristles are short and simple.


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What are the differences between mammal and insect digestion of cellulose?
I know that digestion of cellulose is difficult in mammals and requires a lot of steps. But I am fascinated by the idea of one day achieving human digestion of cellulose.
Which got me thinking about how insects digest cellulose much faster than mammals, how is this possible?

What precisely do you think you "know" about human digestion of cellulose. The reference you quote says that the limited and variable ability of humans to digest cellulose depends on gut bacteria and not their own enzymes. It also says nothing about the number of steps. You cite no sources for your statement about insects but it appears that, apart from termites and the like, most insects depend on bacteria  for their ability to digest cellulose too. So are you asking about the differences in human and insect microbiota? I won't speculate on the answer in a comment, but what do you think?

So from your comment and the answer below, its seems like there is little difference between the ways cellulose is metabolized. This has helped me update my understanding. Thank you.

…except the bacteria might well be different, especially as they are symbiotic. The intestinal system of insects have some similarities to higher animals, but…

What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Update 2 (interpreting "faster" in terms of efficiency because it seems easier to measure)
The question has been updated but I still don't see a reference for insects being more efficient than mammals. Therefore I investigated this and did not find convincing evidence that it is the case.
Granted, the means of measuring efficiency are not necessarily comparable, but nonetheless it appears that ruminant cellulose digestion efficiency is comparable to overall distribution of cellulose-digesting bacteria.
(Overall, in both clades, the vast majority of species do not appreciably digest cellulose, so I focus on those that do.)
This paper suggests that while termites have remarkable ("nearly 99%") efficiencies they are a dramatic outlier among insects. In different groupings efficiencies range from 12-68%, 40-90%, and 11-50%.
This paper suggests that the "digestibility" of cellulose by cattle is in the range 0.7-0.8 (that is, 70%-80%). It is observed that the rate is higher in sheep (and goats?), though comparable figures are not provided. Other figures in the paper are in terms of animal body weight gain, which is unfortunately a poor measure due to the high energy cost of just living for warm-blooded animals.
If I interpret these numbers correctly, this means that ruminants in fact compare favorably to most celullolytic insects in their cellulose digestion efficiency. The very high efficiency of termites specifically is likely a facet of their being little microbial factories with legs; they are definitely an outlier among insects.
In conclusion, I don't think that there is any particular intrinsic advantage for insects in cellulose digestion.
Update
I went back and read the linked post and realized that much of my answer was covered there and thus somewhat duplicative.
What is not covered is the insect/animal comparison. I do not see the source material for the assertion that insects are more efficient at cellulose digestion, it might be true or be somewhat trivially true but I would need to see where you got this information to assess it.
I would suggest doing a little initial research to maybe get closer to an answer. For example, here is a review on cellulose digestion in insects, and here is a resource for mammals, here is a comparison between the two.
Original
Neither insects nor mammals (as far as I know) have the appropriate digestive enzymes to digest cellulose efficiently on their own. However, some special animals like termites and ruminants have assemblages of microbes in their gut that can break down cellulose. These enzymes are called cellulases.
However using these assemblages efficiently requires an extremely specialized gut system such as the rumen.
So you might get humans to digest cellulose by making transgenic humans with cellulases in their digestive system or completely redesigning the human digestive system. Possibly there would be a way to supplement with cellulase the way some people do with lactase.
A different concern might be that human physiology isn't set up to support that style of nutrition. For example I imagine that diabetes incidence would increase. But it's hard to predict.
If the idea is to feed a growing population of earth in a less carbon-intensive way, there are likely less complicated ways to do that by altering diet to e.g. less meat, popularization of sea vegetables, etc. But that's just my opinion, maybe you had something else in mind.
Hope that helps.

wow, you have worked so hard to answer my question. I know very little about human digestion of cellulose, but when I mentioned that cellulose being difficult in ruminant mammals, I was considering how much time it takes for grass to make its way though a cow's 'four stomachs', and the need for additional mechanical action, 'cud' chewing in order to make use of the cellulose. Where as locust, and snails seem (to my neophyte understanding) to have much less complicated digestion system. The locust digestive system having only 3 parts like humans.

ah, ok. Sorry to have gone down some unrelated rabbit holes. I agree that the stuff going through stomachs is probably faster purely in terms of having less tubes to go through in insects. However, that seems difficult to measure, particularly with regard to how it effects the animal's ability to actually digest cellulose, so I wasn't sure how to make a good investigation of it and did what I could. Hope it had some benefit!


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What is this? Is it harmful?
Anyone find out what this is? Looks like A Caterpillar with a home it made from surrounding items, this was found in VA in the moutians on our home.! It went back inside its home after attempting to touch it with my phone. It's the size of an adult female pinky.♀

That appears to be what is known as a bagworm:

According to the University of Maryland extension Home & Garden Information Center, they can cause significant damage to ornamental plants especially conifers.