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What is a good multiple alignment of large genome sequences when working with limited hardware?
I need to align bacterial genomes (namely mycobacteria, over 4 Mb in length), and my choice would have been either 'muscle' or 'clustalW'; however these algorithms are too memory demanding for such long sequences thus I can't run the multiple alignment on my machine.
Is there any other program that I could use to align multiple bacterial sequences?

There are many others. I'm surprised you run out of memory... How much RAM do you have? If working on Linux, swap space is easy to allocate and can be used as a sort of memory if time isn't a constraint. Since this is the issue, please do provide information on what biology you are looking for with the sequence alignment, and what are the exact memory limitations. What specific errors do you get. Be aware that this site aims to address biological problems, not computational ones, so do shift the emphasis onto maintaining biological accuracy rather than overcoming memory constraints.

Ok, I'll try to keep it on the biology rather than bioinformatics; however I have 15 Gb of RAM.

First of all, do not, I repeat not, use ClustalW. That is horribly out of date and was never very good to begin with1. It was just the first to become common. At least use ClustalΩ. Anyway, while I haven't done much aligning in the past few years, back when I did, I got the best speed/quality ratio from MAFFT.
MAFFT has been used in various sequencing projects and can deal with whole genomes easily. Whether or not it will run correctly on your machine depends on the specs of your machine, of course. However, it should be considerably more efficient than clustalW, although not necessarily more than muscle.
Before doing any of this though, are you sure you need to align whole genomes? Could this be an XY problem? You might want to consider posting a new question here and explaining what your final objective is. Also, if these are published genomes, you might be able to find an existing alignment.
If you really do need to run a whole genome alignment and your machine can't use MAFFT or muscle or any of the other modern aligners, you need a new machine. No matter how efficient your aligning algorithm, a genome is a lot of data and you need a strong machine with serious RAM for it. If you are on a *nix machine, you could ask about how to create a swapfile to increase your memory on Unix & Linux.

1Don't get me wrong, it was state of the art and everything back in the day, but the state of the art wasn't very good, that's all.

The issue of aligning long sequences came out already somewhere else (actually from the developer of muscle); what is such issue? If I have related species (in this case the members of the Mtb complex) doesn't it make sense to align the whole genome and see where differences in genome (especially indels) arise? Isn't this the reason of being of the Whole Genome Sequencing research?

@Gigiux sorry, for some reason I never saw this comment. The alignment you need depends on the question you want to answer. Yes, sometimes whole genome alignments are useful. Often, however, they are not and you are only interested in specific areas. I can't help you choose unless you explain exactly what you are trying to do.

I think I understood why whole alignment is not good as such for inter-species comparison: regions of homology can be dispersed in different parts of the genomes thus there is no co-linearity between sequences. I have found Mauve an excellent tool for inter-species alignments.

I have used LASTZ in the past, you can set the word size and thereby control memory usage. You might be better off asking your question on Biostars, there are more skilled bioinformaticians lurking around there.

I'd say there are skilled bioinformaticians here too so as not to offend this community ;) but you're right. Here we're more interested in the underlying biology than at biostars, which is a biology SO mashup.


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How do spiders get silk from their spinnerettes?
I'm 13 and writing a report on spiders. How do they use the silk protein gel from the spinnerets? How does it get from the spinnerets to the web? P.S. I know how silk is created, all the way up until the tapering duct
As I currently understand it, the silk proteins are created, then dissolved into a liquid/gel, and stored. Then it is put through a funnel into the tapering duct, liquid is removed. I'm missing an understanding between the removal of the liquid and formation of the silk. Could someone fill in the gap?

Welcome to SE Biology. There is an expectation that you research your question before asking it here. Updating your question to include details of your own research will help people to provide specific answers. It will also ensure your question isn't downvoted or closed for being a homework question.

A: This isn't homework because I'm homeschooled (just to clarify.)

B: My dad tried to install security software and search engines are down. I can only use websites I've been to. Although I do know that silk proteins are created, then dissolved into a liquid/gel, and stored. Then it is put through a funnel into the tapering duct, liquid is removed..... And then I don't know what happens with it......

The link in my initial comment outlines the homework policy, which is broad enough to include your question. You can ask homework questions here but you need to show that you have researched the question. The following quote from your comment satisfies that criteria and it you should add it to your question; Silk proteins are created, then dissolved into a liquid/gel, and stored. Then it is put through a funnel into the tapering duct, liquid is removed..... And then I don't know what happens with it

The term "homework question" is used as an umbrella term for the whole bunch of things like: Homework questions, assignments, low effort questions, not researched questions and so on. And your questions clearly falls under it at the moment, so please edit it accordingly.

As we actually have a homework tag we should not be to fast saying homework questions are off topic. This question has an open answer which could be interesting in other contexts than homework, it just needs more clarification. It is not too broad and definitely answerable by someone knowing more about spiders than I do.

@skymningen They are not off-topic when the person asking shows some effort to solve this by themselves. This varies of course between a 15 year old and a student of an university.

@Indigo2003 Your question has been edited to avoid deletion. You may further edit according to your needs. Besides here's a link, I would suggest you to go through before you post another homework question. biology.stackexchange.com/help/homework

I think if a spider expert sees this they will know exactly how to answer it. I urge other closure reviewers to leave the question open. Good luck with the report!

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

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What factors should I consider when selecting a reference genome for mapping?
I am under the impression that the most recent reference genome is typically the best case. What other things should I consider when selecting a reference genome? For example, is there any particular reason not to go with the most recent reference genome when aligning short reads from RNAseq?

There are many, and it depends on information that you haven't presented.

Welcome to Biology.SE! If you are not convinced by the answer given, please elaborate on your question and provide some background information to what type of analyses you are thinking off. Also consider taking the tour and look at our guidelines for good questions. Enjoy! :)

@James I am aware of that lack of information, but on my level of expertise on the matter, I unfortunately cannot ask more detailed questions. Though I do hope that other users on my level of knowledge will find use in the answers given (which is kind of the idea behind stackexchange, isn't it?). Researching on my own did just not yield any comprehensible result for me...

@SebastianLobentanzer SE is designed to answer specific technical questions. It doesn't perform so well at providing answers for 'intro to topic' questions like this. Whilst some users are more than happy to try to answer these questions, seldom will you actually get the answer you want. There are plenty of ways of improving your question in order to make it more answerable by more people. See the tour as recommended by Alex.

@James Specific questions? Yes. Technical? Not necessarily.

@DanielStandage I think I was going for a word that encompasses "non-trivial to answer". 'Technical' probably isn't the best word to use.

There are many reasons!
Let's assume you are using the Human reference genome. The latest version is hg38 or GrCh38. This came out roughly three years ago (Dec 2013). Although now these same reasons do not really apply to this particular assembly, but no other assembly comes to mind where these reasons are demonstrable. When dealing with RNA-Seq data you carry out a few common tasks.

Annotations: When a new assembly comes out, all existing annotations are standardised on the previous assembly. Take for example GENCODE, that particular links to the current version of gencode, which is now based on hg38. But, more importantly notice that they still maintain the same release for hg19/GrCh37. From my experience, it takes about 1-3 months for annotation databases to migrate to a new genome assembly after the assembly is released.
Conservation tracks: These are the tracks which take the longest to get updated. I will not post a link to the tracks here. But, here's the UCSC table browser, you can go to the comparative genomics tracks and view the conservation tracks (Phylop, Phastcons) which are available for each assembly. Again from experience, it took more than a year for these tracks to be generated for hg38. So it is just better to work on the previous assembly if you want to this particular information, because generating these tracks by self is a very tedious and computationally intensive task.
Risks associated with unfinished genomes: This does not really deal so much with the human genome as the gain is ever smaller with each consecutive assembly. But considering a assembly which consists of 70% scaffolds, the variation between assemblies tend to be huge. For functional studies as opposed to insilico studies, it makes no sense to redo the entire analysis every time a new assembly comes out, since the insilico part of the study is the predictive pillar on which functional validations are based. Although the same does not apply to insilico studies where the results presented to the public are solely predictive.
Incoherence with existing studies: This is a major obstacle for using a newer assembly, especially applicable towards unfinished genomes, wherein the results may be widely variable and do not align with pre-existing knowledge. Of course, you may be the one who is correct but it is also possible that the variability in your results is the result of human error. Therefore, it is just better to wait for a "landmark" study to introduce the assembly to the public, allowing your study to undergo less stricter perusal and also allowing you to validate the expected variability in your results.
Pitfalls during functional analysis: For RNA-Seq analysis it is common practice to use RT-PCR for a particular gene to establish the expected expression level for that gene, which in turn will validate a successful RNA-Seq experiment bereft of shady PCR duplications and artefacts. For this particular part you would first create a primer, which validates the expected expression level of that gene. But this particular primer originates from a particular assembly. It is also possible that the region which is amplified may have shifted or changed between assemblies. So when you align your data on a different assembly from the one which was used to create the primer, you may get an unexpected expression level for that gene, as the original primer amplified an incorrect region, which got fixed in the newer assembly.

I know there are many more. But, these are the only ones which comes to mind at the moment.

Thank you for elaborating. I am new to Genomics, coming from a pharmacological perspective. It does not matter that your answer is not comprehensive. This definitely is a starting point from where on I can read up on aspects on my own. Thanks again!

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How do I retrieve electronic annotation from Uniprot and GO records that relates to molecular function?
I'm interested in the endonuclease activity of the G3BP1 gene, specifically the uniprot record Q13283.
An external link guides me to UniprotKB-KW electronic annotation. How can I retrieve valuable and concrete information (e.g. catalytic sites, motifs) that explain this annotation from that link?

Since it is only one gene then you can simply note down whatever is mentioned in the Uniprot page. You can try BioMart if you have more number of queries but I don't think it will have structural information but it will have GO annotations.

Species please, links to Uniprot entry please. It you want us to help you, you need to help us.

The endonuclease is controlled vocabulary. In this case, it looks like GO actually cites UniProt as the source for the endonuclease keyword.
With the Uniprot url, whenever you want to see where the information comes from for the annotation in Uniprot, type /publications after the ID. For example: http://www.uniprot.org/uniprot/Q13283/publications


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Why should phospholipid non-polar tails be "protected" in the membrane bilayer?

lipids are arranged within the membrane with polar head towards the outer side and non polar tails towards inner side, this ensures that the non polar tail is protected from aqueous environment.

My question is why should we protect non polar part ,will it destroy in contact with polar part?
 What should be the correct reason for bilayer arrangement?

Where did you get that quote from? As I mention in my answer, I dislike using the term "protected". It's misleading. Furthermore the quote also uses "inner" and "outer" in an unhelpful way as "inside" and "outside" often refer to compartmentalisation of the cell/organelle/vesicle/thing with a membrane. For example if something is on the inner leaflet of a eukaryotic cell, it's on the cytoplasmic side. The quote in the question would make that sound like it was deep in the membrane.

The issue here is the word protected I think. There is no intentional protection going on, simply the tails are repelled from water (but not each other) and the heads are attracted to water.

What should be the correct reason for bilayer arrangement?

I'll answer your second question first, but there is an almost identical question on this site already: Why do cells have a bilayer?

There is water on the extracellular and intracellular side of the membrane. What's actually happening at a molecular dynamics level is the self-association of the hydrophobic lipid tail groups driven entropically by water. In other words the polar (hydrophilic) head-groups "prefer" interacting with the water (called the interfacial region) and the the hydrophobic tail groups "prefer" not interacting with the water. With those two preferences in play, the lipid bilayer formation we know and love emerges.

why should we protect non-polar part, will it destroy in contact with
  polar part?

To directly address the first part of the question: no, nothing would be destroyed. The word "protect" isn't appropriate (it's a bit too anthropomorphic for my taste!). Here is a video showing the bilayer spontaneously assemble in a molecular dynamics simulation. Read the more thorough 2003 journal article for an idea of early MD simulations of the bilayer formation. As you can see nothing "bad" happens when the water collides with the lipid tails and the lipids aren't destroyed.

Interesting read: MEMBRANE LIPIDS OF THE PAST AND PRESENT. Good animations and explanations of different membrane formations.
For an academic perspective, I'd recommend a couple of reviews: Cournia et al., 2015 and Gerit et al., 2008.


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Identifiying a conserved residue in multiple PDB structures
I have a few hundred PDB structures of the same protein, and I need to identify a specific conserved residue in all of them.
Originally I wanted to extract the sequences from the PDB files with BioPython, align them and then use that alignment to identify the residue number in each PDB for my conserved residue.
But it turns out that is a bit harder than I expected. Parts of the sequence are often missing in the PDB. I don't see an obvious way to get a proper sequence out of the PDB files. Then there is the issue of mapping the conserved residue number back into the PDB file.
Is there any easier way to do this? It doesn't have to be BioPython, though that would be nice.

There are a lot of potential issues here. 1. your biopython script is struggling to handle missing sequences (you need an error handler). 2. you're using an unusual set of PDB files that are poorly formatted. I've tried to answer assuming that your PDB codes map well to uniprot. Let me know how it goes!

My approach to this problem would be to use VMD (Visual Molecular Dynamics), where you can load multiple PDBs, perform structural and/or sequence alignment and analyse residue conservation within one program.
VMD is a powerful molecular visualization program for displaying, animating, and analyzing large biomolecular systems using 3-D graphics and built-in scripting. It is probably an overkill for what you want to do, but I find it rather intuitive to use and powerfull. I also has an amazing documentation and many step-by-step tutorials, starting from this basic introduction.
What you will specifically need for your problem is a MultiSeq 2.0 plugin that you can find under Extensions->Analysis->MultiSeq in new versions of VMD. It is a bioinformatics environment that allows you to load, display, and analyze both sequence and structure data for your proteins within a few mouse clicks. It also has a great set of tutorials to help you start! What you might find interesting for comparing many similar protein structures is an option to create, view and manipulate phylogenetic trees.
Here is step by step tutorial on comparing structures and sequences with MultiSeq.

Here you can find original publications for both VMD and MultiSeq:
VMD:

Humphrey, W., Dalke, A. and Schulten, K., VMD - Visual Molecular
  Dynamics., J. Molec. Graphics, 1996, 14:33-38.

MultiSeq:

Roberts, E., Eargle, J., Wright, D. and Luthey-Schulten, Z.,
  MultiSeq: Unifying sequence and structure data for evolutionary
  analysis. BMC Bioinformatics, 2006, 7:382.

I don't think that the problem for OP is the MSA or conservation analysis, it's that the PDBs have incomplete sequences and this will cause issues with python's parsing.

Incomplete sequences is a common problem. One way of getting around it is submitting your PDB ID list to an ID mapper. The one at Uniprot works well. Simply copy and paste your PDB ID codes. Make sure you're going from PDB to UniprotKB (see picture below. Hopefully you'll be able to map most if not all of your IDs.

After you have that, download the text file. Then you can extract the sequences from that text file with the following script:
from Bio import SeqIO
filenames = ["YOURINPUTFILE.txt"]
input_format = "swiss"
output_filename = "YOUROUTPUTFILE.fasta"

output = open(output_filename, "w")
for filename in filenames:
    for record in SeqIO.parse(filename, input_format):
        sequence = record.seq
        output.write(">%s\n%s\n" % (record.id, sequence))

Then submit those sequences to your favourite MSA tool. I answered a question on how to make an MSA here if you've not made one before.
A minor, and perhaps obvious point on reflection, is that the residue number won't be the same in all your sequences due to indels. You will need to reassess this situation when you get there if you still plan on mapping the conserved residues to 3D structures rather than a sequence.

You can use Ensembl (http://www.ensembl.org/index.html) to retrieve orthologues of the protein, and align them using one of many free, web based programs (such as ClusterOmega)


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What is the difference between "Bisphosphate" and "Diphosphate" in biochemistry?
I have often found bisphosphate compounds ( e.g. RuBP, RuBisCO, 2,3-BPGA etc.) and diphosphate compounds (e.g. ADP, GDP etc.) in biochemistry. They are commonly seen and are important compounds in both animals and plants but what is the basic difference between a bisphosphate and a diphosphate?

For example fructose 1,6 bisphosphate is used in step four of glycolysis but d location of the phosphate group has been mentioned already ,1 telling us carbon 1 and 6 telling us carbon 6(no offence) but i think its the same thing as bisphosphate.

[Source:Wikipedia]
As you can see in the above structure of ADP(Adenosine di-phosphate), the two phosphate groups in the compound are directly attached to one another. So it is named as di-phosphate. [Source] You can see this table for more examples.

[Source:Wikipedia]
In this structure of RuBP(Ribulose-1,5-bisphosphate), the two phosphate groups in the compound are not directly attached to one another, they are attached to first and fifth carbon, meaning they are attached to different atoms. Therefore, it is named as bis-phosphate. [Source](2nd comment)

I believe this is the correct distinction, but historically the two terms have been used interchangeably. As an example, a lot of biologists will still refer to 2,3-BPG as 2,3-DPG.


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Evolution of Homo Erectus to Homo Sapiens
I just read an article on Wikipedia and noticed that some similarities between Homo Erectus and Homo Sapiens in the "Comparative table of Homo species". My question is;
Is it possible to say that some members of Homo Erectus species
have survived up to now and they are living in modern world as members
of Homo Sapiens?

It is not plausible that members of Homo erectus would survive and remain a separate species from Homo sapiens. For members of Homo erectus to survive implies that there wasn't significant interbreeding with Homo sapiens, which would require a significant population of Homo erectus.
There is some evidence that Homo erectus and other hominids interbred with Homo sapiens. So it is more likely that there may be some people with more genetic traits from Homo erectus than others. However, by significant interbreeding, there currently only exists a single species that may contain ancestors from multiple hominid species.

Not sure about H.erectus, but there is very strong evidence of interbreeding between H.neanderthalensis and H.sapiens as well as between the Denisovans and H.sapiens. It's likely that if the any of the Homo species overlapped (in time and space) and were similar enough to produce fertile offspring, there would have been interbreeding between them.

Recently read Why Does It Matter If Homo sapiens Had Sex With Neanderthals?. That is an interesting viewpoint about my question.


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Why do two different E. coli reference genomes have different lengths?
I've downloaded two different reference genome of E. coli (E. coli K-12 MG1655: U00096.1 and E. coli K-12 MG1655: U00096.2) and they have different lengths. I searched for the meaning of reference genome numbers in detail but I couldn't find anything that help me with my question: Why do two different E. coli reference genomes have different lengths?

U00096.2 is an updated version of U00096.1; you should preferably use the former for your analysis. In fact, even U00096.2 has been updated. The latest version is U00096.3. In general, the number after the dot (period) in NCBI accession numbers, denotes the version.
From NCBI:

VERSION is made of the accession number of the database record
  followed by a dot and a version number (and is therefore sometimes
  referred to as the "accession.version")

thanks for your answer, but what is the difference between versions? what is new in the latest version?

@user137927 With more and better sequencing experiments (also better sequence assembly algorithms), the genome sequence gets more accurate. It can be smaller or larger than the previous versions and may have different sequence in certain regions etc. I am not sure if the changes are explicitly documented.

As WYSIWYG answered, they are updated versions.
The difference in length is mainly because that later versions are sequenced / aligned with better equipement and techniques, providing results that better reflects the reality.
Some sections of the genomes can be harder to sequence and efficiently align, but with more advanced techniques it can be done.
Sequencing 100% of a genome with no error and perfect alignement is not yet possible but we are getting there slowly.


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What tools are used in animal cloning?
So I was reading up on articles to do a project about cloning but there were no places in the article where It states the tool used to take the gene out of the nucleus and insert it into plasmids ? can anyone accurately tell me what the tool is. I don't mean the process but the actual names of the tools like CRISPR etc.
As a reference The article was the wiki https://en.wikipedia.org/wiki/Molecular_cloning

biolistic particle delivery system, TALEN (Transcription activator-like effector nuclease), Homing endonuclease

What kind of cloning are you interested in. Gene cloning can be done in plasmids using restriction endonucleases also. You have to add specifics.

About cloning a whole new animal

@hoodlamic1 Cloning a new animal is done using a technique called Somatic Cell Nuclear Transfer. Is that what you are interested in? Can you add more details? Molecular cloning is different and your question and your comment are conflicting each other.


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Which is more susceptible to dehydration — extracellular and intracellular fluid?
I want to ask in human body, there is intracellular and extracellular fluid that makes up the total body water of our body, which is drained first when we do activities? extra or intra? if I want to do a bioimpedance measurement, does measuring only the extracellular fluid good? Thankyou

I edited your title such that it summarizes your actual question. Let me know if that is fine.

You should understand that the body is an open system which is held at a steady state. Water can diffuse in and out of the cell such that the osmolarity is balanced on both sides of the membranes. If the water potential changes in either of these compartments (intra- and extra- cellular) because of addition or removal of water molecules, both the compartments would be affected such that finally the osmolarity is same in both the compartments. It may, however, take some time to achieve the steady state.
If you refer to sweating when you say "activity" then you should note that it is a complex process with extensive neurological control. The water that is secreted by the eccrine sweat gland primarily comes from the blood. However, profuse sweating will lead to water loss from both the intra- and extra- cellular compartments.

Prolonged exposure to hyperthermic conditions and/or prolonged
  exercise in the heat can induce water deficits due to profuse
  sweating, resulting in hypohydration. This water deficit lowers both
  intracellular and extracellular volumes and results in plasma
  hyperosmolality and hypovolemia; both of which impair sweating.

Shibasaki, Manabu, and Craig G. Crandall. "Mechanisms and controllers of eccrine sweating in humans." Frontiers in bioscience (Scholar edition) 2 (2010): 685-696.

So, for your experiment it is better to measure the osmolarity of the extracellular fluid or the blood plasma because:

It is easier to measure
It would not be sensitive to local and temporary effects


text:
Why are men stronger than women?
What are the evolutionary explanations for why women are physically weaker than men (on average), and is this difference adaptive? See figure one here.
I suppose that something puts pressure on men to be physically stronger than women, but I don't see what it can be. Why the discrepancy between the sexes?

You should clarify your question, and your reason for asking. I assume that you are asking about a difference in average physical strength of sexes (and evolutionary reasons for this), but the Q can be read in other ways as well. Also, differences in body size/strength between sexes is common in many animals (see Sexual dimorphism), and this is usually not to "dominate women" but often (when males are larger/stronger) used in male-male competition.

For the record, I don't think the Q should be closed as opinion-based. As currently stated, I find it unclear with poor background, but there is a relevant Q on the evolution of sexual differences in humans hiding in there.

I agree.  this site is so steeped in the jargon of biology that it can't handle questions from the public.  [reopen]  The term they need to hear is 'sexual selection' which was broadly discussed by Darwin.  Its not entirely incumbent upon the question if the readers misunderstand.  Men and women are clear terms that specify human males and females. Fairly precise.

What are the evolutionary explanations for why women are weaker than men (on average), and is this difference adaptive?

All of the theories surrounding this fact are speculative; it would be difficult to prove "why" men are, on average, stronger than women.
One contributing theory is Female-Choice - basically that women had (or has) the ability to be more selective when it comes to choosing a mate. Over time men will reflect the preferences of women (taller than them, stronger than them, facial hair qualities, etc.). This is superficially supported by casual studies like this study from OkCupid where the "attractiveness" curve for men is down-shifted, meaning women think the average man looks below average in attractiveness and implying those who are viewed as average ( actually the top 20% of men or so) would have better reproductive success. Men, in the same casual study, had a nearly perfect bell-curve associated the attractiveness of women, implying that men are excellent at deducing whether a women is below average in attractiveness, average, or above average in attractiveness.
Another contributing theory is Male-Male Competition. Basically men, at some point (and still might) compete with other men to win over women. The bigger, stronger man would presumably win in a fight and eliminate his competition - directly preventing the production of offspring by the weaker male. The male-male competition also holds true in a more speculative theory in that the winners of wars literally raped their way to reproductive success.
It is worth noting that men, on average, are only about 30-40% stronger than women due to the larger muscle fibers in men (as cross-sectional area determines muscle strength, not volume). With training the difference (kg for kg) is reduced to 15-20%.
Ultimately why women are weaker than men (or men are stronger than women - whichever way you prefer to put it) doesn't have a solid answer beyond "because the stronger, taller men have reproduced".

I find your first subanswer somewhat vague. The Q is probably asking if there are evolutionary reasons why men are on average psysically stronger than women (see Sex differences in human physiology#strength). How strong we are in comparison to other animals isn't really relevant for this question. However, sex differences in species closely related to us is interesting to understand our evolutionary history.

Saying 'men have more capacity for strength', 'men never use it' is not relevant either. It still does not explain why both genders diverged, and men diverged to be stronger.

@QuoraFeans - Then ask your question again, and be more precise. You're asking why the genders diverged in capacity for muscle development, and I answered that the theories involve Female-Selection for stronger men and that men acted as the defenders/hunters. What type of answer are you looking for?

@MCM This is a good attempt at an answer. "The male-male competition also holds true in a more speculative theory in that the winners of wars literally raped their way to reproductive success." This is a rather grim prospect, but I would entirely believe it as a driving force in our selection. Is there any citation or study into this?

Moreover, the male-male competition and the success of the stronger man should lead to evolution of stronger humans (both men and women). If it has more effect on males then there is something that pertains to the activity of Y-chromosome. This would finally boil down to whether androgens have a positive role in promoting muscle development (more than estrogens).

@WYSIWYG Not necessarily, selective pressure on one sex does not have to have any effect on the other.

but can you explain WHY all of these possible reasons are sex-specific? Whether it be 'Female choice' or 'Male Male competition', why wasn't it the other way round, like 'Male Choice' or 'Female Female competition' ?

@user1993 - No, and I doubt anyone will ever confidently be able to do so. It could be due to a population bottleneck millions of years ago. It could be down to a few mutations on the Y chromosome. It could be deeply integrated with how we have young. Nobody really knows the 'why', only what's happened since.

@WYSIWYG As this https://en.m.wikipedia.org/wiki/Bateman%27s_principle states(Bateman's principle), Can the reason be "Sperms are cheaper than eggs (ibid). So producing a strong male means they can protect the female and even if while protecting the female,the male by chance dies accidentally,the loss can be compensated by the long surving female who can be able to repopulate effectively with the lesser number of available males"? To conclude,I don't know the exact reason and asking can this be reason?


text:
How do we predict the lifespan of dinosaurs?
Of course, they are fossils now. I found a link here which states that herbivors lived far longer than carnivores. The example being a T-Rex being "old" at 29, and a herbivorous Bothriospondylus having not reached half it's adult size at 43 years old.
But, is there any evidence that can indicate their life spans, or life spans of at least one kind of the dinosaurs?
An additional brief question is are their lifespans comparable with modern day descendants?

@questionhang: The general technique with dinosaurs is to count the rings in bones, although there are limitations to the method. Most notably, the technique gives an estimate of how old an individual was at death, not how long a member of the species could survive per se. Nevertheless, see https://books.google.com.au/books?id=9zRMBAAAQBAJ&pg=PA107&lpg=PA107&dq=ageing+dinosaurs+by+bone+rings&source=bl&ots=jOlKtu8vsK&sig=BjNoZxlMkPwF763PdWSUqYjEigI&hl=en&sa=X&ved=0ahUKEwi82dKSitvJAhUkGqYKHTneCeAQ6AEIITAB#v=onepage&q=ageing%20dinosaurs%20by%20bone%20rings&f=false

The question is unclear. 1) Are you talking about dinosaurs or mammals? 2) What dinosaur are you talking about? 3) Are you interested in estimates of age or description of the methods to find these ages (as suggested in the comments). Note also that you end sentences who are not questions with question marks which is quite confusing.

@Remi.b The description is better now?

I have made some major edits to the question and retracted my close vote. In it's current state the question is very answerable since the question is now asking about a general technique (hinted at by @bshane's comment).

I also don't find the question particularly unclear in its current form - voting to keep open.


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Phospholipid membrane fluidity if phospholipid had one type of fatty acid
How would membrane fluidity change if the phospholipid membrane had only one fatty acid?

Cell membrane doesn't have just phospholipid inside.
Components who influence fluidity in cell membrane are:
1) Fatty acids length
2) The grade of unsaturation of these fatty acids
3) Presence of cholesterol

So, if composed of just fatty acids, excluding every other component (carbohydrates, channels proteins and, mainly, cholesterol), the answer would be yes, its fluidity will change drastically.

Will it become more fluid of less?

Considering only saturated fatty acids and the total lack of cholesterol, answer would be less.

This depends entirely on the fatty acid and the reference membrane.
Amphipathic membrane fluidity is based on the intermolecular forces between the hydrophobic parts of the membrane. Like olive oil vs. butter or margarine, the specific type of lipid determines the fluidity and the temperature at which a phase change occurs.

You can construct a synthetic lipid bilayer with several different kinds of saturated fatty acids (think butter) that would have a phase change at a higher temperature and be less fluid than one with only one unsaturated fatty acid (think an extract of a single type of fatty acid from olive oil) .
In fact, with regard to cholesterol (from the same reference):

cholesterol tends to make lipid bilayers less fluid, at the high concentrations found in most eucaryotic plasma membranes

The point here is that fluidity is not specifically about whether you have all fatty acids, one kind of fatty acid, some fatty acids and some cholesterol, or any proteins. You have to look at the type of each of these things, and, in particular, the intermolecular forces between the hydrophobic parts of your amphipathic molecules.

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


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How many paraphyletic groups can be formed from a phylogeny?
How many paraphyletic groups can theoretically be created from this phylogeny?

I found (2n)-2. Is this correct?
This is not homework nor exam, just a question about paraphyletic groups.

If we define a paraphyletic group as any group on a phylogeny that is not monophyletic, I count there to be 2^n - 2*n paraphyletic groups for a fully ladderized tree with n tips.
There are 2^n possible groups of n species. Of these groups, 2*n of them are monophyletic: n groups containing a single species, and n groups containing multiple species.

I cant find a good explanation for paraphyletic group, what are all possible para. Groups if n=3?

@Nemexia The term "paraphyletic" doesn't really have a hard definition, but the way I defined it, a tree with 3 tips will have 2^3 - 2*3 = 2 paraphyletic groups: {1,3} and {2,3}.

Why arent these paraphyltic? {1,2} with common ancestor( first and secound node)?

{1,2} is a monophyletic group because it contains all descendants of the MRCA of {1,2} (the ancestor of {1,2} only has 1 and 2 as descendants, so the {1,2} group is monophyletic.


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How to Determine Sufficient Time for Melanoma Survivor to Be Considered Low Risk?
Regarding melanoma, how do we determine the minimum amount of time that a patient is disease free for them to be considered low risk? We are attempting to do survival analysis on RNASeq data from melanoma patients.
We are at the stage where we need to adjust the threshold that dictates how long a "Disease Free" patient needs to be disease free to be considered a low risk case. Is 5 years a good parameter or is it too conservative?
Academic sources for protocols, or similar examples are encouraged.

From undergraduate courses of cancer, the 5 year survival rate is common. However I have no idea where that value comes from.

Do you vaguely remember any literature that you can point me to?


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Which organelle is the easiest to see in a cell?
I was asked a question in class: "Which organelles are easiest to see in any cells while using a microscope?"
This seems a little bit like a trick question, and since I'm not an expert in cellular biology, I'm not sure which organelle to go for. A cursory google search only lays out what organelles exist, and isn't clear on practical lab details.

Can you be more clear about why you are interested in this question? I would say the nucleus is the most obvious feature of most cell types unless stained for something particular, but good luck finding one in a red blood cell... Words like "any" and "all" are always going to be dangerous in biology.

I need this answered for hw in general what would be the eaiest organelle to see on a microscope.

You said you looked everywhere online, did you try searching for something like "easiest organelle to see"?

Could you elaborate your problem a little more?

This reads like a homework question without much in the way of attempts-to-solve — I'm thinking maybe it should be closed?

@AsherF. I agree this question should be closed. A google search for exactly the title gives the same answer (nucleus) in basically every one of the top results besides this one, and this is really just an introductory cell biology, hey let's start thinking about what the components of a cell are question rather than a serious biological question.

A quick google revealed this slideshow that says the nucleus is the easiest organelle to see. Generally, this is what is taught in schools worldwide. Note that mature red blood cells don't have a nucleus, so this isn't a universal rule. The visibility of the nucleus also changes throughout the cell cycle.
In case they are trying to trip you up, double check what the definition of an organelle is. The easiest cellular structure to see is the cytoskeleton by proxy of the cytoplasm. The cytoplasm forms the largest portion of the cell, it can be easily identified as the space between all the other organelles, and it is universally present in all cells. Indeed, many definitions of an organelle allow cytoplasm and all should allow the cytoskeleton.

any of a number of organized or specialized structures within a living cell. -Google

or

a structural and functional unit, such as a mitochondrion, in a cell or unicellular organism - Dictionary

However this is the kind of answer akin to "skin is the largest organ in the human body", and isn't what your homework is guiding you towards.

I don't think the cytoplasm is typically considered an organelle; I would suggest editing that out of your post unless you can find a reliable source that shows that some sources do indeed classify "cytoplasm" as an organelle. I'd like to avoid confusion.

@BryanKrause It's certainly a cellular structure rather than a classic organelle. The part that is more traditionally considered an organelle is the cytoskeleton. I'm not really too fussed about semantics, and it's clear in the answer that the cytoplasm isn't really a good answer. That being said, definitions themselves don't seem to rule out the cytoplasm. I'm curious; did you have a specific definition of an organelle that rules the cytoplasm out?

While there are a lot of definitions of organelle, particularly between eukaryotes and prokaryotes, my main objection about the cytoplasm is that it isn't really...anything. It's sort of defined only by what it isn't: it isn't the nucleus. Everything else is cytoplasm. So while the cytoplasm definitely contains organelles it doesn't seem like it is an organelle itself; you couldn't define a function of the cytoplasm, sort of like you wouldn't call the "abdomen" an organ. I would agree with you that the cytoskeleton is an organelle.

@BryanKrause I've made a quick edit, but I think in all likeliness this question will be closed (I would initiate the vote if I hadn't already answered). Currently, it's a fruitless semantic argument - the cytoplasm is membrane bound and does carry out specialised functions within the cell. We would need to really tighten definitions up. Clearly, it's important in a research topic to understand what something does, not what it counts classically as. For us to answer in this case if cytoplasm should be counted among the ER etc, we need more clarification from OP (which I doubt will happen).

Yes I agree with respect to the ultimate fate of this post. I guess to me the difference is that you could, at least theoretically, "remove" the ER from a cell and then say "What was the result?" Same thing with a ribosome, etc. You can't really do that with cytoplasm; if you did you would just have a nucleus. Anyways we apparently already have a question on this - both bpedit and Joce do better in their answers at explaining their positions than I am here.

@BryanKrause It's a fun question! I tutted when I read whereas cytoplasm is just a fluid in which the other cells are surrounded (ie, passive). Just a passive fluid, is it? It's the bedrock of all life as we know it! "Passive" indeed... I honestly think that there are a few broken words in biology. "Organelle" is one, "subspecies" is another. They were invented in simpler times and the respective fields have moved on so far in understanding the complexity of the true situation. Yet we are relentlessly trying to force things into these out-of-date boxes... I'll kick off the close vote.

Let us continue this discussion in chat.


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What is the purpose of the outer mitochondrial membrane?
The purpose of mitochondria is to generate ATP, utilising a chemiosmotic gradient across the inner mitochondrial membrane. Protons are pumped out of the mitochondria into the intermembrane space, but because the outer mitochondrial membrane is highly permeable to ions, the pH of the intermembrane space quickly equilibrates with the rest of the cell. As the outer membrane apparently does not contribute to maintaining this chemiosmotic gradient, what is its purpose? It seems to be doubly redundant in chloroplasts as H+ transport doesn't even occur across the inner membrane.

In mitochondria, the protons pumped by the respiratory complexes do not end up in the intermembrane space --- that would be futile, since, as you say, the outer membrane is permeable and the protons would quickly dissipate. The respiratory complexes are located in the christae, which are closed-off invaginations of the inner membrane, from which the protons cannot easily escape (other than via ATP synthase or uncoupling proteins). See for example  http://onlinelibrary.wiley.com/doi/10.1016/S0014-5793(03)00633-1/pdf

@tomd,  Fair enough.  I just wanted to point out that the respiratory chain generally does not pump protons towards the outer membrane (as it is shown in many textbooks).

Structure origins
Originally the mitochondrial outer membrane (MOM) was likely the result of a bacteria that could survive in a vesicle formed of the plasma membrane.

This explains why the plasma membrane and the MOM are structurally similar, however, the proteins that are present in either mean that their functions are very different.The MOM has a specialised translocation complex for example.
Functional significance.
The MOM is actually much more complex than an evolutionary hangover and is essential to modern cells by regulating what that mitochondrial inner membrane is exposed to. The MOM plays this role using porins. Indeed, if the porins of the MOM are disrupted, the entire cell dies (Chipuk et al, 2006). Additionally, the MOM allows a physical association between the ER and the mitochondria called the mitochondria-associated ER membrane (MAM). The MAM is essential for $ {Ca}^{2+} $ transfer.

The MAM thus integrates signal transduction with metabolic pathways to
  regulate the communication and functional interactions between the ER
  and mitochondrion. (Hayashi et al, 2009)

Answer: The MOM is essential in regulating what the MIM is exposed to, and allows signalling between the ER and mitochondria.

Not sure I can help much, but as far as I know the outer mitochondrial membrane is associated with the endoplasmic reticulum as well. This help lipids (apart from proteins) to enter the mitochondria since these lipids originate from the ER. More importantly, the outer membrane has integral proteins called porins present which help in the movement of molecules into the mitochondria. The outer membrane is also required since it's permeable to nutrient molecules while the inner membrane is not.

Please add some references to your answer.


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How did zootoxins evolve?
I've always wondered how toxins in certain organisms have evolved. Particularly, organisms that produce toxins as a deterrent to predators as opposed to organisms that use it to paralyze their prey.
Where did this toxicity come from? How did it develop to what it is today?
There must've been a drawn out period where evolution 'tested' and 'fine-tuned' the toxin. Presumably until it was somewhat efficacious to the target.
What are the current popular theories on this?

Anything and everything is toxic in the right concentration, so there really is no first toxin.

@John There are some compounds that are exceptionally damaging to other organisms in low concentrations but do seemingly no harm to the toxic/poisonous organism. That is what we mean by a toxin here. Furthermore to your point, there is such a diverse range of toxic/poisonous organisms that there were probably many toxic substance evolutionary origin events.

if I exposed your brain to your own digestive enzymes or bile either would destroy it. both would be incredibly destructive to any other part of your body. It would be a toxin anywhere else in the body, indeed that is how many venoms start. Other toxinsjust don't matter to the host. Capsaicin is the oil  that makes peppers spicy but it only works on mammals (binds a unique to mammals receptor), it does nothing to birds much less plants so of course the plants can make it with no problem.

Basically there is no one way to get a toxin, each toxin is different and evolved from diffrent things in different ways. Toxins have evolved many separate times. That's why your question is confusing, there is no one single toxin precursor and no single way to evolve a toxin.

General overview.
Each toxin and poison probably have their own evolutionary "arms race". Generally, an organism contains a compound that is a bit harmful to other species. As a predator or prey species becomes tolerant to low doses of this compound through natural selection, the compound efficacy could be increased (again by natural selection) on a molecular level, or at a dosage or concentration level.
Below are a few examples of where this has become the case, and some more general examples of how venom evolved in the first place.
Examples.
California Newt.
These newts contain tetrodotoxin (you may be familiar with this from the fugu fish). It is preyed on by a species of garter snake. This is a textbook arms race as the garter snake is naturally selected to have beneficial alleles that are tolerant to the toxin.
Dart Frogs.
The golden dart frog Phyllobates terribilis contains enough batrachotoxin to kill 10 people. That is apparently overkilling for any predator it would surely have to face especially given that the only animal alive that is immune to the poison is the frog itself. However, the snake Liophis epinephelus can tolerate massive doses of batrachotoxin (although I've heard it gets pretty poorly after eating a frog, rather understandably). These two species are locked in an arms race that drives the frogs to produce an unbelievably fatal cocktail and the snakes to become ever more tolerant.
Snakes.
Modified sweat glands evolved to damage the prey as much as possible for immobilisation, partial digestion, or defence. There are textbooks about snake venom and toxins. Here is a neat article I found with a cursory search or if you want to sink your teeth into the topic (heh.) check out this article.
Long story short: venom sacks are modified saliva glands from non-venomous snake ancestors. The diagram shows generally just how modified these apparatus have become!

Platypus
Let's not forget the weird and wonderful monotremes. It's hard to pinpoint exactly what drove the platypus to develop venomous barbs on its elbow (last time I looked into it, it was still disputed if they were for defence or hunting).

But what we can learn from this is that venom can independently evolve. Although the venom producing proteins are different, they produce the same venom as some snakes.

Sortof. Just as every adaptation is the product of a small change in something the species already expressed, all toxins start out as something the organism just happens to produce as part of its life. Then there are two evolutionary paths for useful toxins:

Poisons - "If you eat me, you will be sorry." These typically begin as metabolites that happen to confer an advantage to an organism's siblings, work as an aid to escape, or are just mildly irritating to predators or parasites.
Venoms - "If I bite you, you will be sorry." These typically begin as digestive assistants - mucous or saliva.

Once there is some advantage to expressing a chemical in a certain way it can be considered to be "locked in" - organisms with that trait stand a better chance of surviving to reproduce and will therefore multiply. As the organisms that exhibit that toxin multiply, mutations in their descendants that improve the utility or effectiveness of the toxin allow those organisms to better survive, and so on. So, a saliva gland that once caused mild irritation in a certain species of prey becomes a descendant's vertebrate-paralyzing-venom gland.
References

Venomous Marine Fish: Evolution of the Venoms. Chondrichthyes (Cartilaginous Fish)
The defensive role of alkaloids in insects and plants
Molecular genetics of ecological diversification: Duplication and rapid evolution of toxin genes of the venomous gastropod Conus


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Are there any examples of weighted edit distance genome alignments?
It has been said that weighted edit distance is a preferred way to compare/align genomes in practice, e.g., when identifying genetically similar patients. I wonder if there are some concrete examples when weighted edit distance is used this way and I am particularly interested to see some example weight tables. Some links to research papers showing such examples would be very useful.

Hi and welcome to bio.SE! I made some edits to your question including the title. Feel free to roll back, but I think this should help it get to the right people!

Where did you read  that "weighted edit distance is a preferred way to compare/align genomes in practice"?


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Understanding common identifier codes (IDs) in biology databases
I know this is very basic but I would like to understand it and it's difficult to know where to begin with a new database.
I have the output:
sp|Q9NZT1|CALL5_HUMAN

However I'm not sure exactly what this is referring to.

Is Q9NZT1 q unique identifier?
Is CALL5_HUMAN unique too?
Should one use both together to get information?
How many types of ID are there?

Hi and welcome to Bio.SE! I've made a few edits to your question just so that it's clearer what you're getting at. Feel free to roll back those changes :)

@James thanks, everything is good. i appreciate any comment and help :-)

Glad I could help. I wasn't sure exactly what you were asking when you said "How many types of ID are there?" Did I answer your question, or were you talking more generally "how many databases use different IDs?"

@James your answer was very good but I appreciate if you make it more general about databases etc. so that I can accept it

If you open the question up to general databases it becomes far too broad to answer in any meaningful way. I would suggest you edit the question to make it clear what you want to know. I've updated my answer with a bit of information relating to some of the most popular databases.

Common biology ID codes.

PDB: 2BIB for example. 4 letter code for a specific structure.

Uniprot: Q9NZT1 for example. A six letter combination of numbers and letters for either a TrEMBL or Swissprot record. This record contains information on domains, and Uniprot links out to lots of useful things like interaction databases, redundancy datasets etc.

Pfam: X1WG39_DANRE A uniprot ID followed by an identifier. Tightly linked with Uniprot, but with an emphasis on domains.

NCBI: NP_000108.1 For example. These IDs link to either a gene, transcript or protein in refseq. In an NCBI record there are two main distinctions in prefix of the ID code: hypothetical/automatic assertions (XM_, XR_, and XP_) and manually curated assertions (NM_, NR_, and NP_). This is followed by a 6 digit number, and sometimes followed by a "." and a number, indicating an splice isoform.

Uniprot IDs
I'm not sure where you got this output so this seems a strange concatenation of Uniprot information.
Q9NZT1 is indeed the unique Uniprot ID. This is specific to uniprot.
CALL5_HUMAN is the "gene name" or "Identifier" and often spans across different databases for that gene. It's a little more back end, but is essentially not unique due to splice isoforms.
There are many IDs in uniprot, and many types. Already below you'll notice some are swiss prot, others are Trembl. These are the main types. Swissprot are manually reviewed, whereas Trembl is an automatically compiled collection.

There are many many different accession code types with each database using it's own nomenclature that you'll come across. Unfortunately, there are too many to list here comprehensively.


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How can I make a protein interaction/protein-complex network?
Let's say I have a list of proteins ID. I would like to know whether I can find any complex based on that list. Any example, explanation is appreciated.
An example input is what you see below. What can I do with the following list of protein IDs? These IDs are from human.
P41182,P56524, P41182,Q9UQL6, P41182,Q8WUI4,Q92793,Q09472,Q9Y6Q9,Q92831

Could you clarify what you mean by "complex"? Do you want to know if they are part of an oligomeric quaternary structure, or how they interact with other proteins?

@James if they are part of oligomeric quaternary structure

This question is not a homework question. It is not a trivial, easily google-able task. I buy the "too-broad" argument, but closing this for homework seems a bit naive. Even if it's an assignment it's a tough one if you don't know where to start!

Without a pairwise mapping between interacting proteins, you cannot make the network. Do you have a file that contains this information?

@WYSIWYG No I don't have such info, do you know how to get that ? please make another answer if you know a better way

@Mol you need to somehow know which proteins interact with which others. This can be experimentally found out using techniques such as Co-IP (it can also show indirect interactions though). Whatever techniques or predictions you use, you would need to know the individual edges of the network to actually build it. Otherwise, it is impossible.

@WYSIWYG If I know that these proteins are coming from the same sample, then I can assume they interact , no ?

@Mol no you cannot assume so. In a protein extract from a eukaryotic cell actin and cyclin would both be present but they do not interact.

This is not a trivial task depending on how well studied your network is or what information you want to gather. It sounds like an interaction dataset is what you want rather than scouring the PDB for static structures (that would be such a hit and miss process I'm not sure it's worth bothering).

Upload you list of gene codes to string-db.

You'll see the network here, and structures are made clear of known complexes in an expandable thumbnail.
It's a limited web-server tool, and whilst very powerful, isn't very flexible. Cytoscape might be needed for a more novel study because it is scriptable.

You can probably stop here and investigate your network.
From string-db download the .txt file (TXT - simple tab delimited flatfile). I think it's an old-school save icon on the web-server, although if you're uploading multiple identifiers, it is simply the "save" button at the top left.
Download Cytoscape here.
Then use File>Import>Table>From file.
This will build an interaction network and you'll see which genes/proteins interact with one another.

Catch: whilst this provides spacial information, you can't get a picture of temporal information: i.e you know what is interacting, but not when nor for how long.

how to get the .SIF ? how to give all the ID together ? i tried to save it but it did not give me any .SIF

Did you manage to get string-db to display an interaction network?

not for all IDs together but when I use one ID, it works

Have you tried uploading them all at once under the multiple identifiers tab?

both txt files are the same ?  also can you please give me some hint related to the CytoScape? what to study and where to study so that I can get an idea how to build the network and visualise it

@Mol if cytoscape is a bit overkill then just stick to string-db. All the nodes and connection show interacting partners.

I know but seems more flexible than String-db. both txt are similar ?

@Mol The tab delimited txt file is the one you want. Cytoscape is more flexible you're right. But that flexibility comes at a cost; a steep learning curve. There may even be a way to query from within Cytoscape. What I like about string-db is the direct links to pdb structures which is probably very useful for you.


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Why don't we see life form again and over again?
If life formed on earth by natural laws, why can't we observe the formation of life from matter today? Is it because this is a rare phenomenon? It seems just after formation of earth life formed on earth and around 2-3 billion years has passed. It must be enough time for life to form several times from scratch.

Evolution takes long and there has been a lot of evolution in these billion years... Also it doens't seem to be logical to start over again with evolution, It took so long to "create" the life forms that exist today and to adapt them over and over again, why do you think it would start over again?

Very colloquial comment incoming. https://en.wikipedia.org/wiki/Abiogenesis Refer to abiogenesis. It is extremely rare to have abiogenesis occur. It has, of course, occured once and once only in our world. But it is only because we are alive therefore abiogenesis has to have occurred. So the miniscule chance of abiogenesis, to us, is not there. Given that you struck the lottery, what is the chance that you have struck the lottery? 100%. To have it occur again is then extremely unlikely.

2-3 billion years is honestly nothing in the scale of abiogenesis. 10^(10^99) years, maybe. Waiting on Remi to give a legit answer to this question though.

I think one important problem would be competition. If a new kind of primitive life form formed from inanimate matter today, it would probably we eliminated ("eaten") rapidly by the overwhelming presence of current (more advance) life forms. Another problem is that the conditions in Earth at the time abiogenesis happened before may have been very different from todays conditions, as the environment in Earth has been dramatically changed by living organisms.

@LiuTianyi: We have no idea how many times abiogenesis has occurred on Earth, all we know is that all life on Earth traces to a single common ancestor but that ancestor need not be the only time life emerged. There may have been competing life forms that lost out to our ancestor.

@LiuTianyi "It is extremely rare to have abiogenesis occur" That's not clear at all. There is no evidence that it is unlikely under the conditions that actually led to abiogenesis (which are unknown).

@LiuTianyi Given that you struck the lottery, what is the chance that you have struck the lottery? 100%. To have it occur again is then extremely unlikely. Since you pose this as a statistical argument, be aware that the odds of the event happening again are the same as it happening the first time, unless the event occurring impacts the conditions for the event happening a second time in a statistical sense. (if you just flipped a heads, a tails does not become "more likely" for a future flip).

@James And I did not say it would be. My point is that if a condition is already given, P (tail | tail) is 100%. So however small the chances of P(tail), it wouldnt matter. What would matter is another event of tail. This time, it would acquire its original probability. I'm arguing more closely towards philosophy in the sense of determinism than statistics.

@LiuTianyi It is unclear what this has to do with determinism. Please elaborate.

How do you know there have not been any? Whether we have the capacity to find and observe it is as much of a question as to whether it has happened.

The first life was probably so fragile and simple we would likely not even recognise it if it did appear. We don't know exactly how, or where, life first appeared but nearly all theories suggest simple collections of enzymes in protected environments that slowly gather the mechanisms needed for free-living life over time.
This works in the ancient world because there is no competition so even the simplest and most inefficient replicator is able to reproduce, spread, and advance. Today, any new life would have to compete with existing life which has had billions of years to evolve into highly efficient forms. A new abiogenesis event would simply pass unnoticed, a brief flicker quickly snuffed out by modern life.

It doesn't work in the ancient world, simulations in the laboratory can simulate sterile prebiotic conditions perfectly well.

@CountIblis Therefor we are still missing something from the simulations. Probably time.

Time doesn't solve the problem, the number of replicating steps of a self replicating system is in principle the important thing. If nothing happens, then you can wait till the cows come home, nothing will happen, because none of the steps necessary to get to the result are being executed. Simulations have yielded interesting results, as I point out in my answer,  nitrogenous bases, ribose, amino acids have been synthesized in the lab from simple inorganic chemicals, but under cryogenic conditions and intense UV irradiation.

@CountIblis: I cannot agree with your assertion that labs can simulate probiotic conditions perfectly well. We do not even know where life first emerged and even if we did our knowledge of the Earth that far in the past does not necessarily allow us to simulate those conditions precisely. Even then we do not know the timescale over which life emerged, a lab experiment running for days, weeks, or even years does not necessarily sufficiently represent a process that could have taken hundreds, hundreds of thousands or even millions of years.

@CountIblis we have RNA that spontaneously arises under lab conditions,  we know there are strands of RNA that can self replicate, so all you need is the laboratory conditions on a sufficiently large scale(like say the ocean instead of a beaker) to get one of the self-replicating strands. see a review of the study here, turns out we were trying to hard.http://www.nature.com/news/2009/090513/full/news.2009.471.html

@John This is interesting research, but I'm always going to be skeptical of  "sufficiently large scale" or "sufficient amount of time" wild cards being thrown around to make up for gaps. The larger scales being invoked must be based on rigorous science.

@CountIblis it not much of a gap, the sequence of the RNA formed is essentially random, the shortest know self replicating RNA is 165 bases long although shorter probably does exist. But that means you would have to run the lab experiment tens of billions of times to get one of those self replicating strands.  but with no other life to compete with it in nature the natural experiment would have occurred trillions of times a week over millions of years. Nature could stumble on the right sequence code through pure brute force.

@John Note that the fundamental problem with explaining abiogenesis is explaining how the chemistry of life evolved, not per se how the biomolecules arose. While explaining the latter has also been a big problem, it's the former that is seen to be the main subject of the theoretical debates, e.g. Leslie Orgel decades ago already suggested that you could get to RNA molecules in scenarios like described in that Nature article, but he demonstrated that it wouldn't get you to larger and larger functional biomolecules.

I find the study particularly interesting becasue of how little they did to get it to happen,  it turns out distilling and separating which everyone else did to speed up the process was the problem you need to leave the "soup" together becasue some of the early chemicals that form act as catalysts and buffers the later ones.

What you really need is to get the chemistry of life already implemented in a more primitive form before you even have RNA molecules. This is pretty much what Addy Pross is saying, while he dismisses the idea that life may not have evolved on Earth, his main message is to take serious the auto-catalytic properties of simpler systems.

Why wouldn't it, RNA is what constructs all the other biomolecules. RNA makes protein, DNA, RNA, ect. once you have something that self-replicates Evolution takes over pushing it to make better copies, collect and use resources more efficiently. ect. The thing I want to see is an attempt to make a functional cell using nothing but RNA and its products.

@CountIblis What do you mean by the "chemistry of life", he does a good job of explaining the formation of precursors, they persist becasue there is nothing to consume them, Clay is not needed in the experiment I linked. I'm confused your speaker does a good job of explaining how wholly terrestrial formation of life could occur, so whats the issue?

@John From a thermodynamic point of view I don't see how you can on the one hand avoid the OP's problem and get life started on Earth. A living organism is ultimately a machine that can e.g. exploit chemical potential differences to function and make copies of itself. Within an isolated system where there are such chemical potential differences to be utilized, a living organism is therefore a catalyst not just to make copies for itself, but for the chemical potential differences to be equalized, so it's just a way for the system to get closer to thermal equilibrium.

But if the system could get closer to thermal equilibrium without life forms being present from the start, then the life forms would not arise in the first place. What the life forms are doing, after all is exploit the fact that there exists a metastable state away from equilibrium, and letting the system get a bit closer to equilibrium instead of a lot closer, this allows for some room for the living organism itself to live far from thermal equilibrium. Clearly this requires the organisms to have arisen elsewhere where there were conditions that were even farther from thermal equilibrium.

Thermal equilibrium is not involved much in biology at least not at the micro organism level, they operate at the ambient temperature of the surroundings. Energy is what life exploits, very few things in nature are at the their lowest energy state, the sun, and winds, and volcanics and a hundred other things pump energy in to the surface of a planet. Its the reason the earth has lots of high energy potential molecules. Life exploits Gibbs free energy for the most part since temperature and pressure tends to be more or less constant in life.

with or without life the earth is nowhere near energy equilibrium there is plenty there for life to exploit, and the surface of a planet is not a closed system plenty of energy is flowing into it any given moment. life doesn't increase the entropy of the system a little it increases it a lot, to decrease it by a small amount in itself. It is a bit like mountain building in geology, pushing a mountain up is an increase in its potential energy but the underlying system that causes it is releasing so much energy that the small local reversal does not matter.

Well.. consider this... once life already exist... and a new life form spontaneous came into came into existence, how likely is the newcomer going to be able to compete with the current contender, who now has time to develop all sorts of abilities from being in an arms race between members of its own group. (A bit like how likely is a newly arrive group of cave men going up against a nation armed with Abrams tanks)
Also note... the first group of earthly life started polluting the sea and atmosphere with a highly toxic and damaging chemical... oxygen (the Great Oxygenation Event @The Oxygen Holocaust 2.5 billion year ago). And oxygen damages reactive chemical  group required to catalyse chemical reactions and oxygen also pretty much destroyed the rich chemical soup that life first arose. Even today there are many groups bacteria and archea that cannot tolerate oxygen.
tldr once life evolved, it destroyed the environment that allowed it to arise in the first place. Environmental destruction is a long held tradition of earthy life.
Also the free for all chemical buffet that was on early earth...  the first life to emerge would have would have eaten it all up. Leaving nothing, no building block for later life to to emerge form.

For a start you need an aseptic environment for a new, defenseless kind of life. All water containing environments on our planet conducive to new life are septic.
Primitive life forms are rare and less competitively robust and performant. The new life forms would be like worms that can't dig, and the current microbes would be like chickens, all mixed together in the same room.
I you had a stable warm C/H/N/O rich cave/seafloor environment which stayed protected for millions of years, you might get the first kinds of organism appear there. They would have 4 billion years less genetic sophistication than current microbes and funghi for attack, defense, fast adaption, diversification, speciation, pH tolerance, mobility, food selection, digestive processes, which today pervade and feed off every environment on earth.
The new life which took very long to evolve has to defend itself agains a lot of species of funghi, procariotes, eukariotes, animals and plants, while it is in the cave and after it leaves it.
If you brought back all weird jellyfish type ediacaran species today, and put boat loads of them into the sea, the fish and advanced jellyfish would decimate them and consume them. their primitive design makes them only food sources.
The advancement of a modern procariote compared to an instar life-form as the difference between 1970's calculator and an iphone in terms of performance.

The answer may be that life did not form on Earth. There is not even the slightest hint of evidence that life formed on Earth. The known facts about early lifeforms on Earth from fossils and everything we know about geology of the early Earth and the Early solar system is at odds with abiogenesis having occurred on Earth. One of the arguments against abiogenesis on Earth is precisely the question asked.
The problem is not just that we don't see life forming in a natural environment, as this can be easily explained away by invoking competition from other life forms. Also one can note that the conditions on Earth today are different from that of the early Earth (oxygen is poisonous to early life forms). A more fundamental problem is that we can't reproduce some of the fundamental chemistry needed for abiogenesis in the lab under conditions that have existed on our planet during the time life could have evolved.
E.g. the synthesis of ribose, which is the backbone of RNA from inorganic chemicals does not seem to be possible under Earthlike conditions. A recent experiment demonstrated that under intense ultraviolet irradiation of water, methanol and ammonia under cryogenic conditions at extremely low pressures one can form ribose in the lab. Similarly, we cannot get amino acids to form under Earth-like conditions, we again need to resort to irradiating interstellar ice analogues in near vacuum conditions.
We also need to consider how can we end up with only left or right handed molecules of each type as found in Nature. It has been demonstrated that replicating systems where both variants are presents, will lead to an end state where only one type will survive. But we then get domain formation where in different disconnected farts the symmetry will be broken in a random way. This may be good enough to explain why we only have left-handed life on Earth today.
An alternative idea is to invoke the fact that the Weak interaction does not respect parity symmetry. Now the Weak interaction is too weak to be relevant for molecular dynamics. But in radioactive beta-decay, this interaction plays a dominant role, beta-radiation consist of only left-handed electrons. One can then postulate that abiogenesis happened in an environment where there was irradiation by cosmic beta radiation, which would lead to an asymmetry in the breakup of chiral molecules, which would then be further amplified by auto-catalytic processes. This is the Vester-Ulbrict hypothesis, which was recently been successfully put to the test in the lab.
Another argument against abiogenesis on Earth is that the required far from thermal equilibrium conditions never existed on Earth, while they do exist in objects like comets and proto-planets. This is more general argument than the examples given above. Basically, what you want is to get to a collection of self replicating molecular machines from their simple building blocks, without there being any machines to build them from scratch.
Molecules in living organisms are synthesized using extremely complex molecular machinery such as the ribosome. Without such machinery, the natural environment has to play the role of the agents involved in the construction. What is needed are both far from thermal equilibrium conditions and places where half build, unstable molecules can be metastable, allowing the complete molecule to appear. This suggest that cryogenic conditions should play a role here.
We can also note here that life on Earth exists in a compartmentalized form, all the chemistry happens inside a lipid membrane (a cell). Many of the essential molecules would not be stable in a hypothetical environment that could have existed in Earth's geological history. Then just like life today exists mainly in conditions that were hostile to early life forms (the oxygen in our atmosphere would kill them), similarly it may well be the case that conditions on Earth have always been hostile to processes that could lead to abiogenesis.
The molecules essential for life as we know it may have evolved without any compartmentalization in the interior of comets or proto-planets (this would qualify as life in the sense of an auto-catalytic process that is capable of evolving), compartmentalized lifeforms could have arisen later there.
A different argument comes from the conditions in the early solar system and what we know about life on Earth from the geological record. The earliest evidence for life on Earth dates back to 3.7 billion years ago. These are stromatolites, which then shows that 3.7 billion years ago there were very sophisticated life forms on Earth.
Petty much all of the enormously complex molecular machinery found in modern cells had to be present already in the bacteria that formed these stromatolites. Abiogenesis would thus have had to occur quite some time earlier. However, from 4.1 to 3.8 billion years ago, the inner solar system was subject to what is called the Late Heavy Bombardment (LHB). During this period the conditions on Earth were rather inhospitable for life. Whether life could have survived impacts so large that oceans on Earth would have evaporated is a matter of ongoing debate.
One has to note here that the people who argue that life did evolve on Earth during this period, tend to favor LHB scenarios that are one the extreme limits of the geological scenarios, one then assumes that it was not that much of a big deal, e.g. the largest impacts could have been smaller than what most geologist think. However, recent geological evidence points in the opposition direction. It has recently been found that the size of the impactor that formed Mare Imbrium on the moon was enormously larger than was previously estimated. The impactor is now estimated to have had a diameter of 250 km.
Taking into account that the Earth is a much larger target than the Moon, so it would have been hit more frequently than the Moon and the largest objects to hit the Earth would also be larger than the largest ones to hit the Moon, the idea that perhaps the LHB was not so bad for life on Earth becomes quite problematic.
But the main argument against abiogenesis on Earth is simply the lack of evidence in favor of it; it shouldn't be a surprise that that things don't add up when one assumes the truth of a hypothesis that is not supported by any facts.

Is this your personal opinion, or original idea? If not, please cite where you got it.

@James There are entire journals devoted to this subject. My personal opinion is that life likely did not form on Earth, but it's not a personal opinion to say that there are arguments for this idea and then elaborating about these arguments.

The journal of astrobiology is a broad journal which ranges from education strategies to abiotic chemistry. Please refer me to the article that says "life came from space". I have heard similar arguments before and am curious to understand more on the topic. For example, when people refer to extra-terrestrial role in biogenesis, they usually refer to trace compounds required for nucleic acids which were found in meteors. They do not discuss complex life (which can be inferred from your answer - exciting if true!).

There was a meta discussion about citation a while ago. You have a lot of citations, but not the key ones people/I would want to follow up.

@James I'll try to dig up a few of such articles. But the essential thing here is not the chemicals but to get a complete working system. Addy Pross explains the importance of taking that view here. While he brushes away the possible extraterrestrial origin of life, the main point is that the chemistry had had to evolve into the chemistry going on in living organisms. He explains the crucial importance of exponential growth of self catalytic systems. It's not good enough to get molecules on Earth from space,  the chemical processes are also needed

I think part 2 is more interesting: https://www.youtube.com/watch?v=zkGb12xBKlM

While I think you raise a number of interesting points, I think you're strongly over-stating your conclusion and ignoring the major problems with any model that life emerged elsewhere. At most, asserting that life evolved extraterrestrially moves the problem but leaves it unsolved.

@JackAidley, and even more brings up a new question: if life emerged outside of earth, why don't we see life coming to earth over and over again? But other than that, I do not think this answer is so bad to be at -4. The individual statements are well-referenced (even if overstated a bit - but note the more careful 'may'-statements - which is merely a thing of style), explained in detail, and it is not off-topic. It is inherent to the question to be based on hypotheses (to not say opinion ...) as there simply are not enough data to explain the phenomenon. +1

This is an interesting and well-researched answer .. but to the wrong question. There is a lot here about what is often called 'Panspermia' but the question is surely about 'continuous generation' from the Earth. Although a possible extra-terrestrial origin for life is relevant it is only part of an answer - could this be revised to be closer to the question?

It turns out you don't need to make ribose, other more easily formed sugars will convert to ribose when bonding with phosphates.  RNA can be made with just easily formed feeder chemicals. http://www.nature.com/nature/journal/v459/n7244/abs/nature08013.html

There isn't currently enough evidence to put a significant probability against the idea that life formed on mars, and that life did not form in a previous solar system. The first life on earth for the moment are greenland stromatolites at 3.7bn yrs. If life formed on planets in the 9 billion years of sequence i/ii stars with less heavy elements to choose from, it would also have to escape the supernova and radiation of those larger and faster burning more violent stars, take refuge in ice and rock, and land on earth in favorable conditions. It's as likely as having a planet with a giant moon.

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


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Why would a snake follow a kayak?
We live on the shore of Kentucky Lake in Middle Tennessee and kayak often.  A common snake here is the Northern watersnake.  Observing several of these snakes over a period of ten years, I am puzzled by their behaviour in several respects.
The snakes appear in March when it's still cold, much earlier than other snakes.  They repeatedly return to the dock or the pontoon boat even after being forcibly removed. The other snakes here are shy and usually don't return once frightened away.  This year, twice, Northern watersnakes have followed my kayak.  They change course towards me and speed up to keep up.
My basic question is, Why would a snake follow a kayak?

likely they are trying to sun themselves especially in cold weather. The water is cold and they immediately try to get back on the boat.  becasue they are not as afraid of you as other snakes they are harder to discourage. They also probably can't tell the difference between your boat/dock and a log.
as for following you I can see three possible answers.
D's answer about eddies might be it.
Or they may be doing the same thing birds do with tractors, your kayak and paddles stir up the water and they are after the animals your movement scares up. A lot of small predators have learned following human machines can be a good way to find an easy meal.
Or they might hope you are a crocodile that will scare up small animals or leave scraps they can eat. Answering Hans will help understand what is happening.

I used to work with snakes, and Northern watersnakes always seemed to be the most aggressive to me, but only if disturbed.
As for them following you, the most likely reason is that your kayak was creating an eddy, supplying the snake with an easy route to follow / path of least resistance.

So the question for @Rebecca is once you stopping moving your kayak, do they still move towards you or scatter?


text:
What is genodiversity good for?
I saw some documents which were trying to say that they can prove via sweat smell selected by women that humans are developed to find a partner with similar genes. At the first glance, I refused it as absurd for many examples of organisms behaving in reverse but then I realized that I don't know any satisfying evolutionary explanation for this (and more: I could even explain the contrary: If less developed and more developed human had a baby, the better genes could be maybe annulled by the worse genes, on the contrary two very developed partners would have not only a lot of descendants, but their descendants would have also lot of descendants and so on.)
And more thing: if genetic diversity is truly evolutionary practical, could for example even people with genetically transmitted disease help our gene pool?
Thanks a lot.

You should add a link to that document.

@WYSIWYG Sorry, I've seen it in TV and I can't find it anymore (apart from   the fact that the document was in czech :-)

Identification of potential partners by body odors is actually selecting for different genes, not similar ones - see this article on "genetic matchmaking" for some additional details.

@MattDMo Yeah, that's what I though, in that document was definitely the contrary.

Genetic diversity is indeed very important for many reasons, most notably resistance to diseases.
The Gros Michel banana used to be the most cultivated banana, until it was almost completely wiped out by a fungal disease due to lack of resistance in the genetically homogenous cultivars grown in plantations. As a result, it had to be replaced by the Cavendish banana across most of its former range by banana growers.
Furthermore, the answer is a definite "yes" to people with genetically transmitted diseases helping the gene pool.
For example, the case of sickle cell anemia clearly shows why even people with genetic diseases can help the gene pool by providing useful alleles. Heterozygotes for the sickle cell allele are resistant to malaria. This has led to the allele having a high propensity in subsaharan Africa, where malaria is endemic.

The first example of genetically controlled innate resistance to human malaria was the demonstration in 1954 that sickle-cell heterozygotes have less severe Plasmodium falciparum infections than do children with normal adult hemoglobin. This observation has been repeatedly confirmed, most recently by independent studies of genome-wide associations in severe falciparum malaria, which have identified the HBB locus as the major signal of association.

Additional examples are the cystic fibrosis gene, which confers resistance to cholera, and thalassemia, which confers resistance to heart attacks.


text:
Does exercise really reduce stress in the biological meaning?
It is a very widespread claim, that movement in general helps body to get out stress hormones. It is used as a warning for long sitting at the computer and I also heard it as a pro-vegan argument (We receive stress hormones by eating cows which have no option to release it in the closed areas).
How literal this rumour is?

With "... helps body to get out stress hormones ..." you mean to reduce the amount of stress hormones? Could you reference this "widespread" claim? In fact, strenuous exercise induces release of stress hormones. Without some sources to back this "claim" up this question may be opinion based. A more likely cause for stress hormones in meat may be the unpleasant last hours of these animal's lives spent in crowded cattle trucks and waiting for their deaths in the slaughter house.

@AliceD Yeah, the claim is just that they can not reliese it this way, unlike freely captive cattle.

I'd like to see sources as well.  I rarely see cows running in open areas like a field.

@Nathan I gave there a source for the stress release claim for human during exercise. I'm looking for the issue with captive cattle without movement now (but I just heard it  so it can take a while).

http://animalstudiesrepository.org/cgi/viewcontent.cgi?article=1019&context=acwp_faafp Page 316

That link says exercise reduced stress, not that it reduces stress hormones.

@Nathan - I've lived in three countries across three continents and I have seen many, many cows in open fields O_o I don't know where you're at but, no, at Times Square you won't see any cattle grazing

@AliceD You can't say anything about the percent of cattle reared on huge open air areas because the closed ones aren't just avaiable for your sight. I'll try to find better links (unfortunately I won't have internet for next few days)

have a look at: http://www.ncbi.nlm.nih.gov/pubmed/18787373

Neurologically speaking, β-endorphin molecules (amongst other opioids) function to relieve pain or produce pleasurable feelings, thereby facilitating an individual to continue functioning in spite of injury or stress.[1]
β-Endorphin release in response to exercise has been known and studied since the 1980s.[2] Studies have demonstrated that serum concentrations of endogenous opioids, in particular β-endorphin, increased in response to both acute exercise and training.[2] The notion of β-endorphin release during exercise is colloquially known in popular culture as a runner's high.[3]
tl;dr: Yes, it has been shown that exercise can really reduce stress in the biological meaning.
[1] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104618/
[2] http://www.ncbi.nlm.nih.gov/pubmed/6091217
[3] www.webmd.com/depression/guide/exercise-depression

Hm, that sounds trustful. But where do the stress hormones come to? Are they only beated by the amount of endorphin?

The question is not why exercise reduces stress, but reduces stress hormones.


text:
Is it possible for any impurities to get through the apple peel?
My parents always told me not to eat from the apple trees near the  road, because some kind of bad toxic dirt might get through.
This sounds to be physically possible but not really probable in my view. In the time apples grow on the tree they never rot. The rotting procces starts as the apple falls down and damages - the wound will quickly change its colour and it begins to decay - from this I assume the peel is almost perfect defense against bacteria & toxic penetration.
I think the only danger may come from the dust microparticles spread by the cars - which can be easily washed by water or wiped off with a piece of cloth. Am I right? What about other types of fruit?

Have you considered the possibility that the stuff might get dissolved by water and taken up by the tree by the roots?

Hmm... Why the irony?

FWIW, apples can and do rot on the tree, for instance if they're pecked by birds, or have been infested with codling moths.

it's waxy so it's a very good barrier, and the truth is that apple peel contains more good stuff that most of the inside of the apple. You can consider the peel to be the same as a leaf, perhaps a lot more resistant and waxy, so you can search for real science in a lot of research about leaves content of roadside pollutants, for example: https://www.ncbi.nlm.nih.gov/pubmed/17294646

The answer I got from Jan Kolář of Charles University:
The spores of fungi or bacteria in apples don't just emerge from nothing, they have to get into it from the surroundings. I often see apples, which rot while still hanging on the tree, the hole needed for the infection of the apple is usually made by a worm. The problem of the apples near roads isn't that they would rot. Indeed, plants can absorb all kinds of harmful substances from soil, water or air, including heavy metals, chlorinated organic compounds or organic compounds from the exhaust gases of cars. How much and which substances, that usually depends on the type of plant (specifically on where it stores most of the substances).
It's not enough to wash an apple because the impurities are absorbed in the fruit itself as well. And on the surface of the peel, there are waxes and other unsolutabe substances which can absorb toxic aromatic carbohydrates from the exhaust gases, and can't be simply washed off.
The greatest risc near the roads used to be contamination with lead because petrol used to contain it. Many of the plants can recieve the lead and hoard it up in some organs. Now, when the lead petrols are forbidden, the biggest risc pose the fumes from the diesel engines. So I'd rather not eat fruit near the roads (especially near the busy ones).


text:
Difference between dysentery and bloody diarrhea
The difference between diarrhoea and dysentery is quite clear; but the appearance of blood in stool or bloody diarrhoea is a very confusing term when compared with dysentery. Are they different in the amount of blood or their etiology or pathogenesis or something else. I searched a lot in the internet and medicine and pathology books but nowhere I could find a straight answer. If anyone knows about it please reply with proper reference and values (if its about the amount).

I think dysentery is always associated with infection but bloody diarrhoea can happen because of many other aetiological reasons. (Although, etymologically, dysentery just means an upset gut).

I am not too sure that's why I am commenting. I'll verify if this is true and then post as an answer.

Diarrhoea
Diarrhea is loosely defined as passage of abnormally liquid or unformed stools at an increased frequency. For adults on a typical Western diet, stool weight >200 g/d can generally be considered diarrheal. Diarrhea may be further defined as  acute  if <2 weeks,  persistent  if 2–4 weeks, and  chronic  if >4 weeks in duration.
~Harrison's principles of internal medicine, 20$^{th}$ edition, page 261.

Dysentry
Dysentery is bloody diarrhoea, i.e. any diarrhoeal episode in which the loose or watery stools contain visible red blood. Dysentery is most often caused by Shigella species (bacillary dysentery) or Entamoeba histolytica (amoebic dysentery).
~WHO definition

One can also follow WHO definition of diarrhea for practical purposes but still I mentioned it from Harrison as it is more specific and quantified.
'Blood in stools' generally describe visible blood in stool, and the quantity of stool passed here can be normal like in upper GI bleeding if compared to diarrhoea or dysentry.
Diarrhoea can be classified into four major categories: Secretory, Osmotic, Malabsorbtive, and Exudative, in which exudative diarrhoea show such features of bloody stool.(~ Robbins basic pathology 9$^{th}$ edition page 577).
In fact, it is also clearly mentioned in Harrison in the topic of diarrhoea that:-

Invasive bacteria and  Entamoeba histolytica  often cause bloody diarrhea (referred to as  dysentery).

Conclusively, bloody diarrhoea and dysentry are the same.

If anyone thinks that there is some issue with this answer please do suggest me by commenting on it, this will help me to improve writing posts next time.