text:
How to get sulfate reducing bacteria?
How can I find and get sulfate-reducing bacteria? Where and how can I store them for a long time?

What are your plans?

The plan is to put it into an apple size capsule that would be sent to Mars. So basically the bacteria should stay alive during the travel period and after impact to the planet.

Another point is to make them to be the only of microorganism species in the substance. Because I do not want something oxygen consuming to get there before some source.

The oxygen might be needed for algae.

Sulfate-reducing bacteria are everywhere, one spoon of soil contains several different species of them. The problem is how to isolate them from the other bacteria.
This old paper explains how to do it, I am sure there are newer techniques to do the same, it's up to you to dig into the literature to find the one you prefer if you want to isolate them by yourself.
Otherwise, just buy it from a collection.

Old paper page is not available. Do you have it in webarchive?

Wired, the link was active few hours ago.. I have uploaded the file here http://www.filedropper.com/mic-3-1-46

I have updated the link of "This old paper" now it should work.


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microscopic slide cleaning and maintenance
we do lot of gram staining and some spore staining. we normally wash our slides with detergent then rinse in D/w, dry it and store it. But on reusing this slide we have to flame it and also clean it with alcohol number of times to make it grease free. also these reused slides have some sort of deposit which does not go with cleaning and evend oes not hamper our staining too.  can anyone please suggest the best simple way to clean microscopic slide and to make it grease free and how to store it.

Whoa! Dint know we could reuse gram stained slides. I remember reusing slides last for plant sections. But recycling always seems to be a good thing :)

For permanent slides (in the slides library), if we use oil, we are required to dip the slides in xylene once were done.

@always confused. we too use blue star or himedia slides. i also have same issue after washing and drying the slides, on preparing smear it does not give smooth smear but beads like. will try simmering slides in detergent water and check. thanks

An old technique to clean used slides is to just toss them in a jar containing equal volumes of distilled water, ethyl alcohol 95% and xylene. Shake from time to time. When needed wipe them dry using a clean, lint free cloth and use.
The techique was at the time (1930's?) in use in the lab of prof. Baudet (Veterinary parasitologist, Utrecht University) and is mentioned in several editions of the "Précis de Microscopie" by Maurice Langeron.
Langeron mentioned that the slides treated that way were "perfectly grease-free".
Another method is to wash the slides, rinse in distilled water and store for some time in a mixture of ethyl alcohol and acetic acid.
When on a tight budget, used Carnoy fixative was (is?) used.
This is a trick that was (is?) in use at some botanical labs in Eastern Europe.
It's mentioned in some of the German literature on microtechnique, if memory serves me right in Braune, Leman and Taubert's "Pflanzenanatomisches Praktikum".

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Enzyme inhibitors, reversible or irreversible?
So far, I know about competitive, non-competitive inhibitors and allosteric inhibitor. Which ones are reversible and which ones are irreversible?

These modes of inhibition are reversible. They describe a particular modification of the working of the enzyme (change of affinity, of maximum velocity, of both) due to the reversible binding of an inhibitor to a particular site.
On the other hand irreversible inhibition stops the enzyme from working through an inhibitor that binds irreversibly : no more transformation of substrate occurs after that. One cannot define a velocity, affinity, or IC50, for a non-working enzyme, thus "competitive", "non-competitive", "uncompetitive" are not useful concepts in that case.

Correct. Irreversible inhibitors basically reduce the concentration of enzyme rather than changin its reaction's' kinetics.

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How do neuroblastoma cells divide? Is it via mitosis?
My name is Daniel and I'm 17 years old. I am currently designing a study to investigate compounds that potentially increase the replication of neural cells. I will be using neuroblastoma cells and creating different water based media to apply to these cells. I don't however understand how they divide. Is it via mitosis or do they replicate in a different way as they are essentially, cancer cells.

don't cancer cells divide by mitosis as well - it's just not as regulated as in a normally dividing cell

I thought it was mitosis but it was increased. I could calculate the mitotic index of control groups with no media applied to it and then calculate the mitotic index of the cells where the compunds have been added? How reliable would this be as evidence?

you're correct (as far as I know) - cancer cells divide similar to other cells... it's just much more rapid... what is your question that you're trying to ask with your experiment? A well-focused questions is of paramount importance prior to conducting a well-controlled study.

Pathologists do indeed calculate mitotic indices to determine how rapidly the cells are dividing compared to normal cells, but you need to establish what's normal first. That is your control group.

It isn't really an closed question that I'm trying to answer, it is investigating which substances can increase the rate of cell division. The substances have been decided by reading about speculation surrounding these substances as to whether they actually have the potential to do this. If you want to hear more about a method, I'd be happy to share my ideas. Hopefully if there are any flaws, you can help rectify them as I am only an A-level student at the minute.


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Parthenogenesis Induction
I have read about Parthenogenesis induction in a paper : "Hagimori T, Abe Y, Date S, Miura K (2006) The first finding of a Rickettsia bacterium associated
with parthenogenesis induction among insects. Curr Microbiol 52: 97–101 "
I was curious to know what is the evolutionary advantage of parthenogenesis induction for the parasite (in this case Rickettsia bacterium ) ?

This issue is addressed in this review by Cordaux et al, 2011, along with other, similar strategies.
The simple answer is that these types of bacteria are efficiently spread from females of the species they infect to their offspring; by inducing unfertilized eggs to develop into females, they increase their transmission efficacy.


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Is Parthenogenesis known as Sexual reproduction or Asexual reproduction?
I have seen that in some books refer to Parthenogenesis as sexual and in others as asexual.
The ones that say it's a form of sexual reproduction,they focus on the fact that meios has happened in the process and also,we are using a sexual reproduction system in that animal to produce the offspring.
The ones saying it is a from of asexual reproduction focus on the fact that although meios is involved,we only have one parent in the reproduction process and we cannot have any new alleles in the offspring than the ones the parent has.(unless we have mutation)
so how can we conclude in the end?which is it ?
and also,what is the evolutionary explanation for this phenomenon(parthenogenesis)?

Could  you add some definition of meiosis? Does meiosis imply crossing over of genes in the context of your question?

Only a matter of definition
It is only a matter of definition. When it comes to sex, there is such a diversity of mating system that it is very hard to make a good definition that won't be challenged by limit cases.
Sexual reproduction can typically be defined based on the presence of meiosis (but again this will lead to limit-cases), on the need for two distinct parents + meiosis, or on the need for two distinct parents which have different gender (anisogamy) + meiosis.
Diversity of reproductive systems
At the end of the day, what one wish to call sexual reproduction does not matter too much as long as the definition is being made clear especially when dealing with potentially limit-cases.
If I remember correctly the intro book to evolutionary biolgy called Evolution by Futuyma makes a good overview of the diversity of reproductive system. Having a vague understanding of this diversity will help you undermine your hope of finding a clearly defined definition for sexual reproduction.
Applying the definition of wikipedia to parthenogenesis
Here is the definition from wikipedia

Sexual reproduction is a form of reproduction where two morphologically distinct types of specialized reproductive cells called gametes fuse together, involving a female's large ovum (or egg) and a male's smaller sperm

Using this definition and applying it to the specific case of parthenogenesis, one would conclude that parthenogenesis is not a form of sexual reproduction (despite the presence of meiosis). Note by the way the even within the term parthenogenesis, there is quite a bit of diversity (see the wikipedia entry for parthenogenesis).

what is the evolutionary explanation for this phenomenon(parthenogenesis)?

I will ignore this question because

A post should always be limited to a single question
This question is very broad
There is not a single answer to this question given the diversity of types of parthenogenesis.

For a start on the subject, you might want to have a look at Jaenike and Selander, 1979 for example.

Thank you very much for your answer.I was still wondering,How can one decide which is more important in the definition ? the presence of Meiosis or the presence of the two parents?

More important for what? Also, it is not that easy to really decoupled the two as as soon as you have two parents, you need some mechanism to merge their genetic information (mechanism which is meiosis). If you are asking "is segregation more important than recombination?", then one first needs to acknowledge that segregation is nothing but a recombination rate of 0.5 at the boundaries between chromosomes (more info about recombination rate and their statistics here)

"... on the need for two distinct parents + meiosis, or on the need for two distinct parents which have different gender (anisogamy) + meiosis..." - Could you add some reference or name some example for two distinct parents that are supposed not to have different gender (no anisogamy)? Some funghi?

"... more important in the definition ? the presence of Meiosis or the presence of the two parents?"  makes we want to set up some answer, are you still interested in the subject? Interestingly, two "parents" is not what the commented answer assumes when citing the textbook definition: it's two morphological different gametes! They might be derived from one single "tree" (blossom male und female, same tree, no two "parents"). Again, very pertaining to differentiate two parents and/or gametes from crossing over of allelic genes. Please let me know if you need any adding answer.

"applying wikipedia's definition...":
"zygote that develops into an organism composed of cells with two sets of chromosomes (diploid)" That should also be addressed, if gametes can be derived from one single cells or, if not, from its mitotic clone without those cells forming "an organism composed of cells", full stop.

@Tarannom As it occurs to me only now after strenously answering it is clearly NOT "the presence of the two parents".

Wikipedia on Automixis says:
"Some authors consider all forms of automixis sexual as they involve recombination. Many others classify the endomitotic variants as asexual and consider the resulting embryos parthenogenetic."
From the last words of this difficult statement  it may reversely be infered that  parthenogenesis is defined as non-sexual. There do exist different definitions of "sexual reproduction". What some authors consider non-sexual and parthenogenetic, others consider as sexual and: non-parthenogenetic. All agree on the term parthenogenetic denoting a-sexual reproduction.
However, it also results from Wikipedia that in the context of parthenogenesis, the existence of haploid gametes, contrary to common definition,  is not a  prerequisite of sexual reproduction, as  with  all forms of automixis  haploid gametes are not involved.
As the question seems to assume there are different opinions on some forms of automixis being sexual, thus parthenogenetic, or not.
To easen up: you must look at the action - what looks like parthenogenesis maybe is not sexual, opinion diverge
Automixis may loosely be used as a synonym for parthenogenesis process and vice versa, the more if parthenogenesis  is seen  as  the opposite of any mating form of reproduction that uses gametes (or is hermaphroditic). As far as some authors consider  automixis that mitotically produces a stage of haploid cells as sexual reproduction, thus non-parthenogenetic  they are looked upon by other authors who do not share that definition as speaking of "sexual parthenogenesis". Some kind of rebuff, I think, as no author defines parthenogenesis as sexual.
Some say that forms of automixis that involve some kind of  - haploid - "gametes" (think of haploid cells as the first stage of a developement of gametes) should not be considered parthenogenesis, but sexual reproduction.
Conversely, automixis and the crossing-over of genes is not a sufficent condition for defining those processes as sexual, thus non-parthenogenetic. All agree that "mixis" alone is no reason to categorize the specific process as non-parthenogenetic.
To easen up:
Standard, normal,  processes of parthenogenesis do not imply the recombination of   genomes, and are termed non-sexual without discussion  (which might come to a surprise and is nothing trivial either, and that might have been one reason to put the question).
Quote from your question: "The ones that say (parthenogenesis is)  a form of sexual reproduction,they focus on the fact that meios has happened in the process..." That denotes the very point where different opinions come together. To easen up: The ones that say so do  not intend to define those "meiotic"/crossing over forms of reproduction as parthenogenic. On the contrary (this is intricate, sorry for being clumsy or "not learned") they want those forms to be counted out. Counter-intuitively, those authors do not see those processes as parthenogenic (without considering them as hermaaphroditic). So there is sexual reproduction with no gametes as cells that have had some life, different lives.
As it occurs only now: those who consider the production of "tiny" haploid cells as sufficient to render the process sexual in charakter, their point of view can easily be reconciled with a more general, common, definition of sexual reproduction that is based on the use of gametes; the concept of gametes is expanded on those haploid "endomitotic" cells that instantenously fuse and are derived from one and the same individual (as it may occur now: the character is hermaphroditic, then!)
You may find that irritating frame shift  in the very first sentence of Wikipedia (to my mind the following quote might have been incited your question):
Wikipedia: "Automixis[...] is the fusion of (typically haploid) nuclei or gametes derived from the same individual.[...] The term covers several reproductive mechanisms, some of which are parthenogenetic." They should not say "are" (parthenogenetic).

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text:
Identify vegetable with stalks coming out of it
I know nothing more about this vegetable than the fact that it is safely edible, which a local vegetable vendor in South India told me. It's green (white inside) and has a strong smell resembling that of cabbage. It has these stalks coming out of folds in the outer skin, as well as a few leaves. STP identify.

It is a kohlrabi. The leaves are cut off. https://en.wikipedia.org/wiki/Kohlrabi#/media/File:KohlrabiinMarket.jpg

@ermanen You could probably post an answer.


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Help id-ing creature
I know. This is going to be extremely difficult without a picture. But bear with me here, because I haven't seen it afterwards. I hope somebody can give me a list of possibles.
I was taking a stroll down the street when I saw this creature. Maybe two feet long. It was black, with a tail about the size of the tail of a cat. It had catlike paws, which were not that big. Its face was pointy, with a reddish nose and brown eyes, with a whitish area of fur above the eyes. Ears were small and curved at the end. It was hiding in a bush, and did not seem to run away when I checked it out. When I got up, it made a sharp screech and ran away.
I'm from Kerala, South India. Thanks in advance.

Sorry, bit I think that this is more or less impossible without an image.

sounds like a mongoose or a civet, which species is hard to guess there are several species of both in India, and they come in a variety of colors and sizes. In the mongooses the color can vary a lot even in the same species. One easy way to tell the difference is civets have cat like ears while mongoose have short rounded ears.
But here is a picture one at least one species of each, since their body plant does not vary much even if their color and size does.
Indian Brown Mongoose,

Sri-Lanka Mongoose

Asian Palm Civet

Yes! That's it! I think I saw an Asian Palm Civet.

Indian tree shrew

Is that the guy?

Nope, this is not it,


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Help identifying fruit
This fruit was spotted in Kochi, India on several occassions. Nothing else is known except the fact that it seems to be irregularly distributed through Kerala.

It appears to be a noni fruit (Morinda Citrifolia).


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Help ID this plant, quite possibly a weed
I found this plant near my South Indian home in Kerala, India. Most probably it could be some sort of weed. Anyhoo, is this plant of any medical or commercial value? Is it a remedy for something?

It has a white tap root with little veins off the main root
It has a really small yellow flower
It's leaves are similar to that of a clover, except for that it has three to five leaves

Merci d'avance!
(P.S. Forgive me if this is some very common plant that I should know about, I'm in 7th grade.)

So long since I've heard weed for this other meaning..

I presume it is Cleome viscosa, the Asian spiderflower.

It is commonly found in rainy season.

Medicinal uses:

The crushed leaves have been investigated as a treatment on stored seeds of cowpea, to prevent weevil infestation.
The leaves are use as external application to wounds and ulcers. The seed are anrhelmintic and carminative Juice of leaves is used as remedy against discharge of puss from the ear.

Identified by the following features-

Palmate leaves

Colour of flower especially the brown part at the base

Herbaceous habit

References:

Wikipedia
Flowersofindia.net


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Getting goosebumps at will
I can get goosebumps at will, regardless of the environment. Its mostly visible on my arms, and I can feel it on my head. It requires some level of concentration to achieve this.
My questions are : what biological mechanisms are involved in doing this ? Is it common ? Is it useful ?

It is a vestigial reflex: http://en.wikipedia.org/wiki/Goose_bumps

Interesting!  I haven't seen anyone able to do this deliberately.
Goose bumps are caused by the tiny muscles at the base of hair follicles contracting, and the hair stands up.  The skin around it puckers.  It's mediated by the sympathetic nervous system (the "fight-or-flight" aspect of the system).  This is how animals' fur stands up when afraid or upset (think of a scared cat).
It's called the pilomotor reflex.  It also helps them keep warm (fur insulates) - so it happens when we're cold too.  But since we have so few hairs, it's not very useful to us. It's more of a vestigial reflex than anything.
It happens for other reasons too.  See the wikipedia article, it's a good place to start.  For more info, look at this article or a medical textbook.
If you can do it at will, you likely are in tune fairly well with your sympathetic nervous system.  That's excellent.  You may be able to make minor alterations in your pulse and blood pressure through breathing regulation - check out the concept of biofeedback.  It is a way to help manage stress, keep yourself calm in terrible situations, manage anxiety or panic disorders, anger management.....
Being able to use physical self-awareness to affect physiological changes takes practice to develop as a skill.  You've got a great start!


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Is this insect some kind of pest?
I live near Paris, France. I would like to know if this small flying insect was some kind of pest or not. More specifically, I want to know if it might be a meal moth or a clothing moth. Here is the little fella :
It's approx 1.5 cm (0.6 in) long

This is Hypena obsitalis, aka the Bloxworth snout, a moth of the family Noctuidae.
Personally I hate the word pest, but this little beauty eats Parietaria und Urtica (Nettle) so I can't think of anyone seeing this as a pest species.


text:
How do we determine a disease's incubation period?
There was a suspected case of Ebola in France, which was later dismissed, since the suspect lastly came into contact with a potentially contaminated person more than 21 days before, which is the maximum of Ebola's incubation period.
So, more generally speaking, how does one determine the period of incubation ? How do we know the day a person was contaminated ?

You need to know the growth dynamics (develop a mathematical infection model) of the concerned pathogen.

It could be determined empirically, by tracing how much time passed between the sick person coming into contact with another sick person and developing symptoms of their own.


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Biology in romantic love
Hi could anyone explain the biological basis behind romantic love. What is the biological basis of falling in love?I know that serotonin and dopamine are secreted when we first fall in love. What happens after that as we move on to the more advanced stages of love. Why is it that after some time, we no longer feel the initial feelings of love. What is the biological basis behind it. And also why do we feel so heartbroken if we happen to fall out of love? What is the biological basis behind it?

courtship rituals like romantic love are a product of evolution. for humans they are often engineered to create a long term bonding.  all human cultures have romantic love.  Human love is more biological than we often expect.  I'm not an ethologist, but these behaviors are so unusual when you stand back and look at other animals and primates.

I have a theory that we may not feel the same after a few years with a person because maybe like when we need higher quantities of a drug to get the required effect in addicts over time, the same amount of dopamine/serotonin cocktail just doesn't do much to our senses after a couple of months/years..

Dopamine, norepinephrine, and serotonin are more commonly found during the attraction phase of a relationship.
All these chemicals stimulate the brain's pleasure center. But this stage only lasts 1.5 - 3 years [2]. That's why 'we no longer feel the initial feelings of love'.
Oxytocin and vasopressin seemed to be more closely linked to long term bonding and relationships characterized by strong attachments [1].
Attachment makes relationships last for years and decades. It is based on commitment and mutual friendship. Oxytocin and vasopressin are at higher levels [2].
The neurological process involved in the perception of heartache is not known, but is thought to involve the anterior cingulate cortex of the brain, which during stress may overstimulate the vagus nerve causing pain, nausea or muscle tightness in the chest [3].

Image from Wikipedia [1]
References:

Wikipedia contributors, "Biological basis of love," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Biological_basis_of_love&oldid=613867553 (accessed June 26, 2014).
Wikipedia contributors, "Love," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Love&oldid=614240299 (accessed June 26, 2014).
Wikipedia contributors, "Broken heart," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Broken_heart&oldid=613979584 (accessed June 26, 2014).

Great answer.  Has there been any solid work on pheromone-like molecules and human compatibility?

@PlaysDice there are a few articles about that. Here is one http://www.ncbi.nlm.nih.gov/pubmed/15653193


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Converting Ensembl Compara gene tree DNA alignment to corresponding amino acid alignment
I have Ensembl compara gene tree alignments (Compara.gene_trees.57.fasta.gz downloaded from ftp://ftp.ensembl.org/pub/release-57/emf/ensembl-compara/homologies/) in nucleotide format. According to documentation, it says that the file "contains the peptide alignment for every genetree in fasta format".
I was wondering what might be a handy tool to obtain the corresponding amino acid alignments from the file.
Thanks,
Ikram

The file is gzipped, so use a tool like 7zip or WinRAR to unzip it. After that, just open the fasta file in any text reader..?

Thanks Armatus for the comment. In fact I can view the file using zless in ubuntu. The problem is that the data is in nucleotide format (AGTC...) and I want it in amino-acid format (NGHIK... etc). I guess that, since the data is coding sequence, no frame shifts are needed and just a mapping from DNA-to-Protein might work (But I am not sure, and just want to confirm it before writing some code for it)

As a general rule, both within and without the world of bioinformatics, public FTP sites contain README files tat explain what each file offered by the FTP server contains. The file README.protein_trees states:

Compara.gene_trees.{release}.emf.gz
                        contains the peptide alignment for every genetree in emf alignment format
Compara.gene_trees.{release}.fasta.gz
                      contains the peptide alignment for every genetree in fasta format

This means that both Compara.gene_trees.57.emf.gz and Compara.gene_trees.57.fasta.gz contain the protein alignments. I had a quick look at the files and it looks like Compara.gene_trees.57.fasta.gz actually contains nucleototide sequences but Compara.gene_trees.57.emf.gz does indeed contain a protein alignment:
$ zgrep -m 1 AAAAASAAAT Compara.gene_trees.57.emf.gz.crdownload
SAAA-AHS-AGTAAAAA--AA--AAAAASAAAT-ASAATAI-SASSA-ASAAT-V----AAASVAA-HAFAS---ASAAASAAAAA-TIVAAAAX-SAASIYSAAAA-YAA--AASAS-ASAASAS-ASAASSSSSARS-AAS

So, to answer your question, the file you want is the .emf.gz one.


text:
True definition of Biology
I just started biology and im pretty clueless on what it really means. So before you vote this question down, can you tell me what it really means.
P.S. Is plate tectonics related to biology? or Chemistry? or Physics?

Typing "biology" into google turns up an adequate definition so in its current form, your question might not receive many answers. Please
take a look at the How to Ask
page and try to improve your question according to the guidance found there. This may require you to show some effort on your part in terms of attempting a solution or showing research. If you have questions about what to do or if you don't quite understand what this means, please ask for clarification using the add comment function.

Every expert will give a different answer on this depending on their own experiences in studying a biological features. The fact you're asking about plate tectonics in the same question makes me wonder if you've even bothered googling any of these terms. Try this link.

@AlwaysConfused just FYI, there are different "grades" (as they're called in the US) in different parts of the world. I don't know if your "class 4" is the same as my "grade 4". Simply asking the OP's age would be a better way of going about it.

Here is the definition of Biology as given by Dictionary:

the study of living organisms, divided into many specialized fields that cover their morphology, physiology, anatomy, behavior, origin, and distribution.

Tectonic plates are not living, thus it isn't biology.
It would be Geology:

Geology is the study of the Earth, the materials of which it is made, the structure of those materials, and the processes acting upon them

Source: Geology.com

If you have criticisms or concerns about the question, please put them in comments, not an answer. You may use several comments if necessary. See this discussion on meta for more.

@MattDMo Thank you for your constructive comment. I have updated my answer to better serve the OP and eliminate any criticism.


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Are there phage-eating bacteria?
If phages (bacterium-eating viruses) prowl on bacteria, are there bacteria (or other micro-organisms) that hunt phages for food? They are rich in proteins anyway... Are there studies on this subject? Thanks

Minor quibble, the phages despite their name aren't really "eating" bacteria... More major quibble: most bacteria don't "eat" proteins https://en.wikipedia.org/wiki/Bacteria#Metabolism

It's suspected that some protists (namely choanozoans and picozoans) are proper/direct "virus eaters" due to the size of their "eating apparatus" and scarcity of bacterial remains inside them (unlike viral remains), but the evidence is pretty recent; the (2020) study:

used modern single-cell genomics tools to sequence the total DNA from 1,698 individual protists in the water. Each of the resulting Single Amplified Genomes (SAGs) consists of the genome of a single protist, with or without associated DNA: for example, from symbionts, ingested prey, or viruses or bacteria sticking to its exterior. The technique is very sensitive, but doesn’t directly show the type of relationship between a protist and its associates.
The researchers found a range of protists including alveolates, stramenopiles, chlorophytes, cercozoans, picozoans, and choanozoans. Nineteen percent of SAGs from the Gulf of Maine and 48% of those from the Mediterranean were associated with bacterial DNA, suggesting that these protists had eaten bacteria. More common were viral sequences, found in 51% of SAGs from the Gulf of Maine and 35% of those from the Mediterranean, with a frequency of 1–52 virus types per protist. Most were from viruses known to infect bacteria – presumably representing parasites of the protists’ bacterial prey.
But choanozoans and picozoans, which only occurred in the Gulf of Maine sample, were different. These groups, neither of which have chloroplasts, are poorly known. Choanozoans (3–10 µm; also known as choanoflagellates), are of great evolutionary interest as the closest living relatives of animals and fungi. The tiny (up to 3 µ) picozoans were first discovered twenty years ago and originally known as picobiliphytes. Until now, their food sources were a puzzle, as their feeding apparatus is too small for bacteria – but ample for viruses, most of which are smaller than 150 nm.
Every single one of the choanozoan and picozoan SAGs were associated with viral sequences from bacteriophages and CRESS-DNA viruses, but mostly without any bacterial DNA, while the same sequences were found across a great diversity of species.
“It is very unlikely that these viruses are capable of infecting all the protists in which they were found,” says Dr Julia Brown, a researcher at the Bigelow Laboratory for Ocean Sciences and coauthor on the study.
The authors conclude that choanozoans and picozoans probably routinely eat viruses.

The news release also says that how these "virus eater" protists manage to protect themselves against viral infection isn't yet known/studied.
If this needs saying... protists (unlike bacteria) are eukaryotes. I haven't found any source suggesting that any prokaryotes (bacteria or archaea) manage to sustain themselves on viruses.

According to Sci. Am. coverage of the same research, the picozoans are themselves a relatively recent (2007) discovery

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text:
What are the properties of sphingomyelins?
What are the main properties of sphingomyelins? In particular, what is the difference with typical phospholipids?
If phospholipids could do the job of sphingomyelins, there would be no evolutionary pressure to develop the additional biochemical pathway to build sphingomyelins, thus these molecules must have some specific properties that are missing in phospholipids.
Is it just the electrical insulation or is there more to it?
Thank you


text:
What is important in the Luria-Latarjet effect?
In the seminal paper

Luria, S.E. and Latarjet, R. (1964) “Ultraviolet irradiation of
bacteriophage during intracellular growth”. Proceedings of the
National Academy of Sciences of the United States of America, vol. 52,
pp. 1521-1529.

Luria and Latarjet reported that the sensitivity of phages within infected bacteria decreased sharply after about 10 min p.i.
They assumed a "screening hypothesis" that assumed that the viral genomes (sensitive to irradiation) were shielded from UV light by "some ultraviolet-absorbing material" (namely the capsid".
This paper led to the so-called "Luria-Laterjet effect" (e.g., doi: 10.1016/0042-6822(68)90011-1 and doi: 10.1017/s0016672300031499). Thus, it must be a relevant feature in virology.
What is the underlying feature of this effect?
I understand that it is proof of a viral eclipse (virions are formed sometimes after infection, albeit they might still not be infectious). Still, some papers raised the involvement of DNA repair (which is usually not mentioned in modern virology text covering viral replication).
Is there something else that this effect explains?
Thank you

I only see two papers which call this the "Luria-Latarjet effect", both of which are the ones you provided as DOI numbers. Two papers is tiny output for a "feature of virology" or it would be more widely studied. Luria and Latarjet found that during infection the sensitivity to DNA damage decreased and then increased again as new phage was produced. I fail to see any feature that isn't explained by Hyman's work.

Fair enough, I though there was more to it. Thanks

Can I add an addition to the question? IS the L-L effect a proof for the presence of restriction enzymes? Luria made such a preliminary discovery soon after this work with Latarjet but I did not understand if he was talking about the same subject (DOI: 10.1128/jb.64.4.557-569.1952 )...

No, I don't think so - though it could make a good new question. The L-L effect described is due to formation of the viral DNA/RNA - when it is in short lengths it is less susceptible to damage from radiation, which has little to do with REs would be my guess.


text:
How to understand restriction mapping a quarter of a century later?
Today, biology is virtually all based on massively parallel sequencing, long-strand sequencing, and metagenomic; looking back at old restriction mapping is not straightforward (at least for me).
For instance, in this seminal paper (Marini and Landy, Virology 1977;76:196 - https://www.sciencedirect.com/science/article/pii/0042682277902963), the authors used essentially three enzymes (Hinc, Hind II, Hind III) to determine the position of the "common core" of homology between Escherichia coli and lambda phage genomes that allows homology recombination, a segment known as att site. The phage att site was called POP’ and the bacteria att site was called POB’.
They had available two classes of phage mutants:

One class is comprised of those phage which carry a prophage att site
in place of the normal phage att site.  The second class of mutant
phage, designated POΔ’ and ΔOP’, carry partial phage att sites. The
“Δ” indicates the “non-att” DNA which has been transposed to lie
adjacent to the common core by the deletion event.

The authors also reasoned that

To identify the att-containing Hind fragment, 11 deletion mutants of A
centering around the crossover region for integration were used. Three
of the deletions extend rightward from “0” [att] and should thus be
missing the P’ arm of the att site. These comprise the POA’ class of
mutants.  Five of the deletions extend leftward from “0”. They should
be missing the left arm of the att site and are designated ΔOP’
mutants.  Two others contain deletions that began to the left of att
and continue past att on the right; thus, these crossover deletions
lack the entire POP’ region.  A final mutant has a deletion slightly
offset to the left of the att site. Every rightward deletion mutant,
should lack the Hind fragment that contains the att site, since a
portion of the site is in the deleted region of all POΔ’ phage.
Similarly, the mutants with deletions extending to the left would fail
to generate some of the wild-type restriction products.

And now for the punch line:

The Hind wild-type fragment containing POP’ [the core element of att,
that is "O"] would be identified by virtue of the fact that it would
be the only fragment missing from both rightward and leftward deletion
mutants.

They drew an ideal map associated with these concepts:

Is it possible to explain such reasoning in a more accessible way?
Thank you

You'd need to read the rest of the paper - it is explained what each of the mutants should contain, which is the essential piece of information needed to understand the figure. Particularly the para that encompasses the bottom of the left column and the top of the right on the same page as the fig.

I echo the remarks made by @bob1. We can't understand the "ideal map" without the figure legend and the context of the text. I have no idea what the horizontal bars are meant to represent or the C2, C4 etc. Restriction mapping itself is a pure logical exercise, for which no biological knowledge is required. Now or yesterday. The difficulty here is integrating it with the information one has about the DNA fragment on which the digestion have been performed. This is not a journal club, so this problem isn't really suitable for a Q&A list like this.

Sorry, I should have added the legend. It just says that the bar represents the lack of a restriction fragment, so the map is a kind of negative film. I also understand this is not a j. Club, just wanted to understand better the last sentence: why should the fragment of interest be the one missing from the mutants.


text:
Is there a word for the length of time an animal stays with parents before going off on their own?
Gestation is a word describing the pregnancy for animals, and you can use 'gestation period' to describe how long a pregnancy generally takes for a species. I'd like to know if there's a corollary word for the time an animal stays with its parents before leaving.
For example, after birds are hatched, they stay in the nest for a while, but they eventually leave the nest. Is there a single word or phrase that is used to describe the time between hatching and leaving the nest? I imagine different bird species have different periods, and other animals (that don't stay within families their whole life) can also be describe in a similar matter. Perhaps 'puberty', though I'm guessing there's a more specific word.

As you talk about bird, most of the terminology I am suggesting below comes from the ornithology literature.
Fledging period
Defined on wikipedia:

Fledging is the stage in a volant animal's life between hatching or parturition and flight.

Nestling period
Defined in Kouba et al. (2015):

In altricial birds, the nestling period is an important part of the breeding phase because the juveniles may spend quite a long time in the nest, with associated high energy costs for the parents.

Rearing period
See its usage in for examples Yuan et al. (1994) and Brickell et al. (2009)
Juvenile
While the term juvenile does not refer to a period of time, you can refer to this concept as the period while children are still juvenile. From dictionary.com

a young bird in the stage when it has fledged, if altricial, or has replaced down of hatching, if precocial.


text:
How to track bacteria/ protozoa, unicellular algae in big volumes?
Is there any special cameras and dyes? If I want to track migration/motion of them in 0.1-0.5 cubic metres.

for 3d imaging, you can maybe use MRI and hyperspectral imageing mostly. MRI requires that you feed the bacteria with something radioactive and then have access to an MRI which costs about 100 euros or 300 euros if you are lucky. you'd be lucky if you could see bacteria in an MRI in water. for practical options, sounds like you should arrange a tank with a system of sampling, so that you can get a drop from zones of the tank and count it later in the microscope. https://en.wikipedia.org/wiki/Staining

what's the time frame?

well, using light microscopy I will see in 2d, as I said I need to see them moving in Volume.


text:
Source of hydrogen in reduction of oxygen in electron transport?
What's the source of hydrogen in the reduction of oxygen to water in metabolism?

Is this implying that half the hydrogen comes from NADH and the other half from lone protons?

I don't think they're implying that; they've just combined the two half reactions. NADH doesn't interact directly with oxygen (it is oxidized at complex I). I think that the protons used in the conversion of oxygen to water are, ultimately, free in solution.

The equation you've shown is similar to other cellular respiration equations that I've seen, in that, it is trying to simplify a pretty complex process.
My guess is that you're doing first year cell biology like I am, so you probably know that there is a difference between the pH of the mitochondrial matrix (7.8 - making it alkaline) and the inter membrane space (roughly that of the cytosol - usually about 7). The lower the pH of a solution, the greater the concentration of H+. My point is that the solutions on either side of the inner mitochondrial membrane both have a concentration of H+.
So even though, when NADH is oxidised, it loses a H+ to solution, thereby contributing to the pH of the mitochondrial matrix, what is the likelihood that that particular H+ will be the H+ that is part of the molecule that takes the electrons at the end of the electron transport chain? I think low.
Indirectly, NADH does contribute H+ to the overall pH of the mitochondrial matrix but it doesn't directly give the H+ to "half an oxygen gas molecule".
Check the video below which is from the publisher of the textbook my course uses.
http://www.garlandscience.com/garlandscience_resources/resource_detail.jsf?landing=student&resource_id=9780815344544_CH14_QTM02

So the proton source is water? Also I'm not doing first-year bio. If I showed you the rest of the slide you'd be scared ;).

So what are you doing? :)
Proton source is not water its the solution in the mitochondrial matrix.

What do you mean the proton source is the solution?

I'm not sure I can explain it any better than I did in my first answer. Sorry I can't help.

It's okay; the problem is that the proton is not found alone in water; it's hydrated. If you are suggesting that the proton source is in the solution, then the most likely source is water, and not hydronium ion or any hydrated derivatives of the protons because heteroytic bond clevage is less costly when it only has to be performed twice - i.e. on water - rather than thrice - i.e. with hydronium ion.

But isn't a hydronium ion a lot less stable than a H2O molecule? Did you look at the video I linked? At the end, a molecular oxygen combines with four protons to form two water molecules. Wouldn't it make sense for four protons to come from 4 hydronium ions? I don't know though, I'm just a first year Biomedical Engineering student :) and I definitely wouldn't say I have my chemistry down.
Based on your question, I thought a more simplified answer about the proton source would be sufficient, but obviously its a higher level chem subject you're studying..?

Hydronium is much more easily ionized than water. Thus you could expect that that four hydronium ions would each donate a proton as oxygen is reduced.


text:
Primers on Dystonia
Where can I get a good biochemical overview of dystonia? I will be working in a research lab that focuses on dystonia and I would like to not be clueless.

A good article on the pathophsiology is,
The pathophysiological basis of dystonias, Nature Reviews Neuroscience 9, 222-234 (March 2008)
For a review of the treatment,
Treatment of dystonia, lancet neurology, Volume 5, Issue 10, October 2006, Pages 864–872.
A comprehensive textbook on movement disorders in general is The oxford textbook of movement disorders

this is a bit fragmented and hard to read - can you spruce it up a bit?


text:
Mode of inheritance - DYT1 Dystonia

Homozygous DYT1 mutation carriers have not been reported in humans.

Does this mean that the mode of inheritance for dystonia (DYT1) is autosomal dominant? This to me implies that if one has both alleles for dystonia, then one must also have the phenotype, as people with both alleles cannot be carriers.

Presumably homozygotes are not viable.

Your description is correct. Most genes do not show complete dominance as outlined in Mendelian genetics and inheritance is almost always more complicated than a simple 1 gene/2 allele system. The mutation you're studying is classified as autosomal dominant but even heterozygotes may not display the phenotype. The proportion of the population that has the mutation AND displays the mutant phenotype is called the penetrance and, for DYT1, has been estimated at around 30%.
http://www.omim.org/entry/128100?search=Dyt1&highlight=dyt1


text:
Is genetic drift necessarily deleterious?
I read that genetic drift is random variation in the relative allele frequencies of a population.

This question however seems to pin genetic drift down to increasing deleterious allele frequencies. Is the answer to this question correct? I don't think that increase of a deleterious allele necessarily indicates that genetic drift is operating; it suggests genetic drift, because one would think that such alleles should decrease in frequency rather than increase, but random chance in a large population can also increase the frequency of deleterious alleles.

Drift is a random element of evolution from one generation to the next, it is equally likely to spread a deleterious mutation as a beneficial one.
The reason the answer is D is because selection should remove a deleterious allele, while drift makes no distinction, and is therefore the only scenario where drift is expected to be a reasonable answer. However, it is possible for drift to contribute to all of those scenarios.

Personally I would prefer that the question you show there said probably rather than definitely - if a deleterious allele is linked to a beneficial one it can be spread by selection despite itself being deleterious


text:
Meiosis I or II
Suppose an organism has 8 chromosomes.  When the female and male organisms mate,  how many chromosomes will the mother contribute to the offspring? Why?

Same issue as this question. We're not going to do your homework for you.

@MikeTaylor This likely IS a homework question. However, this person DOES NOT SPECIFICALLY SAY IT IS A HOMEWORK QUESTION!

@L.B. If is not, then I'm sure Camille would be happy to clarify her questions for us. :)

Both the male and the female would give half of the total number of chromosomes for their species (assuming both cells are normal). So if the organism has a total of 8 chromosomes, the mother and father would each give 4.


text:
How good is the reproducibility of preclinical models?
Unofficially, biology researchers always complain how frequently fail to replicate results others have achieved. But of course, such failed experiments are underreported.
Is there data, or at least well-reasoned guesses, on what is the success rate of experiment replication in preclinical models? I don't mean translational research and the impossibility to replicate a mouse result in a human. My question is about failing to reproduce the results within the same model system, replicated at the detail level available in the original publication (e.g. same animal strain, same drug dosages, etc.)

Have you checked out https://www.plos.org/wp-content/uploads/2015/06/journal.pbio_.1002165.pdf yet? It may be a good place to start looking.

I searched for maybe an hour before posting, and while I found some papers declaring that reproducibility is a problem, none went into details. I'll look closer into the one you posted @BenS.

The Cochrane Collaboration has a great deal of this type of analysis. One of my favourite features of a Cochrane Review is the routine use of Funnel Plots, where there are sufficient data to produce them. Sensible interpretation of funnel plots can give some fairly strong hints about the reproducibility of published literature.
Funnel plots show datapoints of individual published studies which investigated the effectiveness of a technique when used for a specific purpose. The datapoints are plotted by estimated effect size (on the x axis) and an assessment of the quality of the trial, incorporating things like sample size and experimental design (on the y axis). A study with a small sample size and/or poor design (low on the y axis) would be expected to provide a relatively inaccurate estimate of the method's true effect size. As sample sizes increase and experimental methodology gets better (travelling up the y axis), you expect the studies to zero in on the true effect size, giving a pyramid or 'funnel' shape to the overall plot.
The reproducibility of trials affects where the points are in the pyramid in a couple of ways.
If there were a bunch of studies which looked for an effect of the method, and didn't find one, they might not be published because null results are considered boring by journal editors - the so-called 'file-drawer effect'. This would show up in a funnel plot as a pyramid that has a suspiciously low number of datapoints on the side of the pyramid that is close to the zero effect-size. The 'missing' datapoints are an indicator that this technique probably did not always reproduce an effect size as strong as the published effect sizes.
The other way that funnel plots can inform on the reproducibility of published studies is simply by looking at the width of the base of the pyramid. If it's wide, then with the experimental design methods of the studies at the bottom, the results aren't highly reproducible - different studies give very different results when looking at the same question.
It's a big job to synthesise this into a global assessment of 'the reproducibility of pre-clinical trials', but if you're interested, I'd recommend you spend some time trawling the Cochrane Library to get a hang of the sorts of variance you're dealing with.

PS: the fact that synthesising reproduction efforts into a combined analysis is a big job has not prevented it happening for high-profile psychology journals recently - with a fairly alarmingly low reproducibility rate.
http://www.sciencemag.org/content/349/6251/aac4716


text:
What is the difference between conditional and inducible activation?
In the modern genetically modified animal models, there are not only constitutive mutations which start producing proteins already in the embryo, but also mutations which can be turned on later. I've seen the terms "conditional activation" and "inducible activation" used, especially in the context of Cre-Lox recombination.
Are they used interchangeably, or is there a difference? If they are different, what is the difference?
If I'm looking at a mouse name, like K-Ras+/G12V;Elas-tTA/tetO-Cre;p16Ink4a/19Arflox/lox, how can I recognize which of the two it is?

I think that there is a slight distinction. Conditional activation of Cre-Lox can occur simply when Cre is expressed. It could be that you have the Cre gene under the control of a liver promoter, so the recombination will only take place in liver cells. Inducible activation usually means that you add something to the system to induce the recombination event. So if you feed the animals Tamoxifen or G418, then the addition of that chemical will turn on Cre expression leading to recombination. This is probably used when the recombination would be developmentally lethal.

I guess you could say that inducible activation is a subset of conditional activation.

In my opinion the terms inducible and conditional are synonyms. Together with the term constitutive they refer to how transcription takes place, that is, the second phase in the central dogma that states that genetic information is propagated from replication to transcription to translation. The proteins that are produced during translation by ribosomes can have a feedback effect on replication and transcription.
When proteins bind to the promoter region of genes, they can induce or inhibit transcription. If a gene is preceded by a promoter region that always promotes transcription, it is said that the gene has a constitutive promoter. If the gene is transcribed conditionally, it may refer to proteins having to bind to the promoter region so that transcription can take place. There could be inverse situations and I believe the Cre/Lox technology is an example of such a situation.
Take the following as an example. A gene could be lethal meaning that if the protein it encodes is expressed it will kill the cell. It could have a promoter that promotes expression if a protein with an inhibitory effect is not bound to the promoter. Suppose I have these cells in a culture plate and I add some compound to the culture plate. The compound diffuses into the cells and binds to the inhibitory protein that is bound to the promoter region. With this binding of the compound to the protein that is in turn bound to the promoter region, the protein loses its ability to bind to the promoter region and inhibition of transcription is uplifted. Transcription then continues and expression of the lethal protein takes place after which the cell dies.
This could be used in practice as follow: if you were selling seeds to farmers, you would want them to buy seeds next year again, so you want the plant not to be able to produce viable seeds.
Coming back to your question, if you want to know more about the mice in question, you should contact the breeder as nomenclatures differ. See this article on interpreting mouse genetic nomenclature:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3039125/

It seems that your third paragraph is describing inducible transcription, but is not identified as such. Also while inducible transcription is inherently conditional, conditional transcription need not be inducible, in the sense that the transcription can occur in a given cell type without the addition of an inducer molecule. One need only place the gene under the control of a tissue specific promoter (in recombinant technology) or a gene need only be under the control of that promoter to drive transcription conditionally only in that cell type, with no other action (induction) needed.


text:
What is this tissue?
Does anybody recognize this picture and can tell me what organ it came from?

just in case this is homework.. http://meta.biology.stackexchange.com/questions/266/homework-policy-for-faq

This is not homework. I am creating a software system which will be used in biologic research. This is one of the pictures I might be using in the design, possibly as some sort of background. I am genuinely curious what the pretty daisy-like cells (or multi-cell structures?) are :) and also want to know more about it so I can search for similar images.

ok - just wanted to check (this is the sort of thing that gets posted a lot from students looking for a quick answer). It's a nice image, good luck

Update 3: Credit should go to @Cornelius and @DMSever for initially identifying the tissue correctly. I incorporated D M Sever's answer into mine (Update 2,below) because his answer is being down voted for brevity, but he is a recognized authority in the field. I'll remove his answer from mine if his answer ends up being retained.
I showed this question to my histological colleague. He suggested that the tissue is most likely a submucosal gland from either the duodenum (Brunner's glands) or the esophagus. My colleague also said that your image is quite similar to submucosal glands in the large intestine but the presence of smooth muscle surrounding the glands eliminates the large intestine.
Update 1: My histological colleague forwarded your question to one of his histological colleagues. He too said Brunner's gland.
Update 2: My histological colleague forwarded your question to his most trusted histological colleague. He said colon, specifically the transverse sections through Crypts of Lieberkuhn. He then signed on as @DMSever and posted a brief but authoritative answer. He's a veteran of histological affairs.
Here's a photo of Brunner's glands in the duodenum, taken from here.

Here's a photo of the esophageal submucosal glands, taken from here.

I know it is your colleague who delivered the final identification, but you are the one who went to the trouble to ask two other people on my behalf, so I give you the accepted answer. I hope your colleague doesn't mind.

I'm not really sure, but it seems like a cross section of intestinal villi / intestinal glands from the large intestine.
Here are some images:

Jubal Harshaw. Large intestine villi cross sectioned showing goblet cells_100X_CS0187 on ShutterStock
Jubal Harshaw. Large intestine villi shown in both longitudinal section and cross section on ShutterStock
Garry DeLong. Light micrograph of large intestine villi in cross section, showing goblet cells (Magnification x400) on Getty Images
Hill, M.A. (2014) Embryology Gastrointestinal Tract - Colon Histology. Retrieved September 24, 2014, from https://php.med.unsw.edu.au/embryology/index.php?title=Gastrointestinal_Tract_-_Colon_Histology

And this is one image from the last link:

Crypts of Lieberkühn - (intestinal gland, intestinal crypt) [...] Transverse

It is from the Colon - transverse sections through crypts of Lieberkuhn seen there.
For references see:
Wheater's Functional Histology p. 283 Fig. 14.29e
UNSW Embryology.

Welcome to Biology.SE. DS said you mentioned a particular text. Would you mind editing your answer to include that reference? Answers on Biology.SE are considered stronger answers with references. Not everyone here will know of your expertise in the field.

Can you please expand your answer with some references? Actually it is more a comment.

I think the special "warning" should be removed now. This answer basically contains the same information as the top voted answer minus links to images, and names the specific structure seen in the picture.


text:
What is this microscopic image from Peter Gabriel's New Blood album cover?
This image appears on the cover of Peter Gabriel's album New Blood.  It appears to be a photograph of some microscopic biological cell.  But it doesn't look like a blood cell to me.   What kind of cell is it?

I would say it is a cell at the tip of a micropipette.

This is an embryonic stem cell on the tip of a needle photographed on a scanning electron microscope (SEM). The image was taken by Steve Gschmeissner, see here for the original.

you can't be "Here's the source" for the best answer.  I did a Google search for the image, and all I found were album covers.   Thanks to the others who provided answers.

@DavidDubois I will improve the answer if you can tell me what you find missing here. I don't like to have this short answer, but what else can you write?

@Chris The way I read it, David made a typo and was actually praising your answer: “you can't beat "Here's the source" for the best answer.”

@svick Good point. :-)

@svick is right.  Sorry.  I meant to say that your answer can't be BEAT.  :)  I can't imagine any answer better than "Here's the source"

@DavidDubois Everything is fine, I didn't get it first :-)

This looks like a macrophage to me, which is a white blood cell. Try Googling "macrophage sem" to see similar images (SEM  = scanning electron microscopy/micrograph).
The clue is the nature of the cell surface - those ruffles reflect the macrophage's role in engulfing foreign material. Indeed it is possible that some of the particles on the surface are bacteria which have been opsonised and are bound by the macrophage cell surface.

In addition to Alan Boyd's answer of a macrophage, it could also be a T cell or B cell. Try doing an image search for lymphocyte SEM and browsing through the different cell types. While the traditional image of T and B cells has been of a smooth round blast cell, they actually have numerous projections, folds, etc. to aid in forming the immunological synapse.


text:
Why do different animals have different body temperatures?
Why do different animals have different body temperatures.  For example, humans have 37°C, while dogs have 39°C.
Presumably we have ancestors whose temperature differs from ours.  Why would it change over time?

Because certain species adapt to different conditions by lowering and increasing temperature. Thanks, accept my answer if it helps.

You get pestered by different microbes at each temperature too


text:
What do you call a virus when it's cured?
When a cure has been found for a virus, can it be called such anymore?
Virus implies it's something you've contracted that you just have to live with until (hopefully) your body can overwhelm and destroy it.
But say someone found a cure for the Common Cold tomorrow, would we still call it the cold virus or would it just be known as the "cold infection" or something to that effect?
Is "Virus" just a nomenclature we've adopted for a bug that has no cure, or is it used to describe a certain type of organism?

It is indeed "a certain type of organism". I think that you might find the Wikipedia page http://en.wikipedia.org/wiki/Virus useful. It certainly answers your question.

Lets start with the definition of a virus (from the Wikipedia page on viruses):

A virus is a small infectious agent that replicates only inside the
  living cells of other organisms. Viruses can infect all types of life
  forms, from animals and plants to bacteria and archaea.

So basically speaking you have a piece of genetic information (DNA or RNA) which encodes proteins which are important for the function of the virus and a hull (not always, but mostly). These invade a cell type, take over the cell (litarally, after an infection the cell will mostly only make viral proteins and DNA/RNA). Finally new viruses are built inside the cell and released to infect more cells. In principle this works like in the figure below (from here):

There are two possibilities for cures: The first one are vaccinations. Here you either use dead or attenuated viruses (or parts of viruses) to train the immune system. When this has happened, the immune system "knows" this specific agent and can rise a fast and highly specific immune answer against it, before the virus can replicate in high numbers and infect a lot of cells. This happened for example for the small pox virus which could be eradicated from the human population.
The other would be drugs which either target a virus (or some of it functions) specifically or prevent them from spreading. The immune system usually does the final cleanup here.
Both methods only work for people which either take the drug or are vaccinated, so they have no influence on the virus in people which are not protected. For further information have a look on the Wikipedia page on Viruses.


text:
Why can you not tickle yourself?
It's the age old question, why can't we tickle ourselves? If you rub your fingers along your skin, sure there's sensation but you don't break down into a laughing fit (at least I don't :P), if someone else does it to you, you're rolling around on the ground begging them to stop tickling you.
Why is it that other people can tickle us but we can't tickle ourselves by touch? (I'm aware that if you use a feather or foreign object on yourself you can be tickled by it so that doesn't count.)

Well, this is an interesting question... With a hole or two. I am able to tickle myself by attempting to itch my feet or my fingers.

Interesting, I suppose some folks are able to. The majority of the people I've talked to said they can't however :).

I count them lucky! :)

When one does it to oneself, the Braun knows it. Therefore, it isn't a sudden movement. When others tickle, sometimes people also get irritated instead of bursting out with a laugh. This is because the brain doesn't know when others do it so, it is a sudden action. Stimulus works differently in both situations.

Try tickling the roof of your mouth with your tongue. My understanding is that no one (realistically, very few people) will be able to avoid a tickling sensation

While one does not laugh the sensation of caressing by self's feet still might feel unpleasant.

In short, it's because your brain processes external and self-produced stimuli differently.
If someone tickles you, you feel that ticklish feeling, but when trying to tickle yourself, there is a reduction in the sensation. When you are tickled by someone, a part of your brain activates causing you to laugh, etc., but it seems that when you trying tickling yourself, your brain doesn't react the same way and that section of the brain does not activate as if someone were tickling you.

Blakemore, S.J., D.M. Wolpert, and C.D. Frith. 1998. Central cancellation of self-produced tickle sensation. Nature Neuroscience 1(7): 635–640. doi:10.1038/2870

You can't tickle yourself because your brain know that it's you. Your cerebellum knows that it's you, and so you don't feel it. Your cerebullum "predicts" that you are going to experience a tickling sensation (as you put, "a laughting fit"), and rushes to cancel out the other parts of the brain that is going to make you break down into laughter.
In other terms, tickling is 'controlled' by two part of the brain, the touch cortex (somatosensory) and the pleasure cortex (anterior cingulate). When you are tickling yourself, these two regions are fired less than when someone else is tickling you.
Basically, your brain is thinking "Why is this person hurting him/herself?" and rushes to cancel all the sensations you can feel. Only when someone else tickles you (and their brain is not connected to yours) can you start laughing. It is, in a way, unexpected when the tickle monster attacks you.
Sources: https://www.scientificamerican.com/article/why-cant-a-person-tickle/

Welcome. Can you add sources to your answer to allow other users to background read on your material?

Ok! Thanks! I added one source. Is that enough?

Oh yes, I love Sci Am :) Enough for me. Strictly spoken it's not peer-reviewed and may be frowned upon, but honestly, many folks simply cite wikipedia and that's the end of it. This is much better.

Ahh I see. Next time I'll use a more dependable source. Thanks!


text:
What is the classification for animals with full tube digestive tracts?
What is the formal name for animals with full digestive tracts, by which I mean a mouth and an anus, and what is the classification for animals that have a single hole for exchanging food and waste?

Animals with a single hole do not form a monophyletic group: metazoa > eumetazoa >bilateria almost all have separate mouth and anus (except notably flatworms which is one reason it does not form a monophyletic group).
As species are not grouped in monophyletic groups by what they don't have (eg. invertebrates do not form a monophyletic group while vertebrates do) there is no particular group. Eumetazoa before the bilateria have a single mouth-anus.

Some echinoderms also have one gut opening- i think brittle star


text:
Which is the guideline to choose a molecular target to identify vertebrate hosts from arthropod bloodmeals?
There are some molecular targets to identify vertebrate hosts from arthropod bloodmeals including the Cyt b gene and the COI gene. Which are the standards or characteristics that I have to bear in mind to choose a molecular target to identify host blood from mosquitoes? I would appreciate your help.

I have looked about the topic and I have asked experts and the best aproximation to know the vertebrate host from arthropod blood meals is targeting mitochondrial genes because you can get clean sequence data due the fact that only one allele is present rather than two.
Within the mitochondrial genome, you should select a gene which has been widely sequenced for most vertebrate species you are likely to detect in your region, other wise you will have many unknown identities among your bloodmeals. Really, there are just two choices that match these criteria: cytochrome oxidase I (COI) gene, which has been used by the Database of Life project; and cytochrome b, for which sequences are widely available (i.e. for many vertebrate species) in GenBank. If you get a negative result for one, you can try the other. Primer sequences are widely available in the literature.
In conclusion, you must be target COI and Cytb genes to assure the host identification and prevent a unidentified match in Database of Life project or GenBank.
I give you a paper example to review the metodology: Host Preference of the Arbovirus Vector Culex erraticus (Diptera: Culicidae) at Sonso Lake, Cauca Valley Department, Colombia


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Gene expression for mathematicians: where to start?
I am a PhD student in mathematics, and I will be involved on a project that aims to cluster (i.e. automatically group) people according to their gene expressions.
Well, the project looks very nice, but I have no idea of what gene expressions are and consequently how to model them mathematically. So here are my questions.
Is there a "Gene expression for dummies" manual that I can read, considering that my last studies of biology move back to the high school (10+ years ago)? Any suggestion, also divulgative books?
Is there a good reference to study how gene expressions are modeled under the mathematical point of view?

I suppose you first need to learn the basics of genetics before investigating the stats behind gene expression clustering. I will based my recommendations on Khan Academy, that is generally speaking a good very introductory source of information for biology and other fields.
Basics of genetics
Here are a few questions for you:

What exactly do we call the genetic code?
Are you aware that genes are transcribed into mRNA that are translated into proteins?
What is an allele?
Do you know what is an exon and an intron?
Do you know what is a TATA box?

If you answered no to any of these question I would recommend that you have a look at Khan Academy > Central Dogma.
Gene regulation
Then, you should have a look at Khan Academy > Gene regulation
Other
Don't hesitate to have a look at other sections in the biology series of khan academy if you want to broaden your understanding of e.g. what DNA looks like, what is happening at reproduction, how do genes segregate, or other things such as evolution. Typically, Khan Academy > biotechnology could also be helpful as to give you a rough feeling of the methods used to investigate gene expression
Gene expression clustering
The literature on clustering gene expression is very rich (see google scholar).

I have a copy of this book,The Mathematics of Genome Analysis, it might be right up your alley (even if it is slightly dated).

You start with the central dogma. This is the idea that information flows from DNA replication to DNA transcription and ends up in DNA translation. These are the three parts of the central dogma. The dogma suggests that DNA is the alpha and translation is the omega. There are many things in-between such as gene splicing and post-transcriptional modification. Also look at the different RNAs (small and large), because genes only lead to protein synthesis, but there are other RNA products that arise from transcription. Anorganic ions also help to synthesize proteins. They come from outside the cell and are not encoded for in DNA. That is epigenetics.
Gene clusters are genes that work together towards a common cause. That cause might be the synthesis of a protein that has a function that serves the cell. Biochemically there are many factors that contribute to a protein's synthesis and genes are some of them.
I think a math person might be interested to know that there are software packages that look for gene clusters. Here's a video:
https://www.youtube.com/watch?v=a3uiIp4gUso
There is no genes for dummies. You can build your house out of straw, wood, or stone. Here's the stone:
https://www.amazon.com/Genomes-3-T-Brown/dp/0815341385

As a mathematician who moved into biology I very much agree with your suggestion of genomes 3. Perhaps I got lucky but I managed to get one of eBay much cheaper than amazon.


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Where in the digestive tract are melatonin pills dissolved? Same question for gelatin capsules
I want to do a blind controlled experiment on myself to learn whether melatonin pills have any effects on me. I bought some empty gelatin capsules. I am going to fill some of them with rice and put pieces of melatonin pill in others.

Melatonin pills instruction says I should take it 30-40 minutes before going to bed. Now I wonder if the timing is the same when stuck inside gelatin capsules. Also is it possible that melatonin pills stuck inside capsules will get to a later stage of the digestive tract than they should and thus will not work.

Unless specially coated or formulated, most pills break apart in the stomach. Note: "break apart", not necessarily absorbed.
Take a gelatin capsule with rice or melatonin and immerse it in warm water. Massage gently with your fingers. Watch the clock.
When the rice is fully exposed, or the melatonin starts to break apart and dissolve, add that amount of time to the instructions. Be sure to take it with at least 4 ounces of water.

Doesn't acid in the stomach help the capsule break apart faster?


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Larger Ant in trail
Today I left a spoon on my sink that accidentally still had some honey in it, and a while later I had a huge line of ants trailing in to get it. Before doing anything about it, I observed the ants' behavior and noticed there were two larger sized ants walking along, and they seemed to have some sort of a hunchback.
I killed one of them (sorry any lovers, but they were invading my kitchen) and noticed a whole bunch of ants swarmed around it's body immediately. I later, sprayed some venom to kill the ants off, and now that I come over later, I see more ants have swarmed aground the larger dead Ant, even over the poison.
My questions are, are these queen ants? If so, how come there were two, and just trailing along to get food like the others? I live in Portugal, of it helps any.
Thank you very much.
Rest in peace, ants...

Can you please post a picture?

Unfortunately it's gone now. I should've done that...

I'm sorry to say so, but I suppose you are not very familiar with ants?
I can't be completely sure since you have no picture, but the way you describe it, very possibly these 2 larger ants were 'soldiers'.
Most ant colonies exist of 3 different types of ants. They are all sisters from each other, and daughters of 1 queen. A queen stays in the colony and her sole purpose is to lay eggs. She does this continuously (while she is fed by worker ants) and thus never leaves the nest. She stays there until she dies. The worker ants are 'workers', gathering food, expanding and repairing the nest when needed, taking care of the eggs and larvae. They are small and probably the type of ants you think of when someone is generally talking about ants.
The last class of ants are the 'soldiers'. Their task is to protect the colony agains intruders (an other ant colony, termites, other insects or animals,...). They differ in size from the worker ants (differences can be small or very big, depending on the ant species). Soldiers are bigger than the worker ants, and have bigger mandibles (used to "bite" intruders) and thus bigger 'cheek muscles' to operate these mandibles. Possibly this is what you described as the 'hunchback'.
Furthermore, ants use chemical signals to communicate with each other. They can lay a 'track' of these chemicals, for example, to show the way to a food source to other worker ants, which can then follow the track and help to bring the food back to the nest. Often the worker ants (gathering food) are accompanied by several soldier ants, to protect them from other insects (or animals,...). These soldier ants also use chemicals to communicate. When attacked, they can release an alarm chemical that attracts other (soldier) ants, to come help them fight an intruder.
Most possibly, by using the poison you killed some ants, which results in the automatic release of the 'alarm signals', attracting even more ants...
I hope this answers your question.

I wouldn't say I'm not familiar, I'd say I'm not knowledgable xD
Your answer was very interesting though. But I can say that the hunchback was an actual hunchback, not a larger head. I looked at photos of queen ants, and it seemed very similar to the larger back a queen has after loosing it's wings. Is there any situation where a multiple-queen hive would send out 2 queens?
Again, thank you very much.

There are also worker ants assigned as morticians, so to speak. When you kill off a group of ants, they come out to gather the dead for a burial of sorts. This may explain the appearance of the new ants gathering around the dead.

Welcome to Biology.SE! This could be correct, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

Not the queen.  Once she has made her wedding flight and hatches a few eggs, she is never out and about again, unless the nest moves.
Some ants enslave other species of ants.  This is what the "hunchbacks" sound like.

This could be correct, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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Can I just simply exchange the eyepiece in a microscope?
I hope it's the right place to ask about microscopy. So my question is what parameters do I have to take into account when buying a new eyepiece for my microscope? Currently I own an Aomekie XSP-42 with a WF16X eyepiece and I would like to upgrade it with a WF25X eyepiece. However when I was searching for one I couldn't help but notice that only the magnification and the mounting size are indicated. What about other parameters (eg. focal distance)? Are they standardized or they just simply don't matter?

Did you try to contact the manufacturer?

No, not yet. So it is product dependent if its possible or not?


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Using evolutionary algorithms in molecular biology?
I am currently an MSc student studying molecular biology (on paper I'm a chemist) and soon I have to talk to my supervisor about my future, PhD research topic. Besides molecular biology I'm also interested in machine learning, mostly in evolutionary algorithms (evolutionary strategy alg.s, genetic alg.s) and Bayesian optimization, from both of which I have written multiple, working programs in C# at home. Due to the massive need for people trained in informatics I'd like to convince my supervisor to include this topic into my future research, especially as I have already acquired some basic skills in these areas. However I have only seen research examples that are purely computational and these didn't include any laboratory work. Can you provide me some insight into the use of these techniques in molecular biology and ways of connecting these with laboratory work?

Why are you coding in C-sharp? This is a language almost never used in bioinformatics or molecular biology, not least because it is specific for Microsoft Windows, a platform that is generally avoided in this area. Sounds rather as if you are putting the cart before the horse. If your supervisor can't suggest a wet project that requires computational analysis, this list isn't going to. Perhaps you need to find a new supervisor.

@David I don't restrict the language options only to C#. I can also program in Python at some level, but I am willing to learn new languages. The main reason I'm asking this is that my supervisor hasn't got much experience with machine learning but he is at home on for example MD simulations, model fitting, etc., and machine learning can come in handy in these areas. I know how to write GAs, I know how to do research in the lab, I know that these two can be somehow used together, but I cannot give concrete examples. It's just I have acquired this skill that I dont want to completely neglect.

OK, but in my experience people tend to do "all informatics" PhDs, or do a PhD where they generate the sort of data (e.g. RNAseq) where it helps if you can use Unix and write the odd glue script, but for the most part you are using powerful programs written by professional computing scientists. I'm not sure it's as easy as some of your respondants make out.

@David What languages are mostly used for this sort of stuff?

@Zebrafish — These days everbody in bioinformatics (except oldies like me) seems to use Python wherever they can. The heavy-weight stuff is often written in C++ (e.g. parts of Trinity). Java is still used (because it is taught by CS Departments), but less than a few years ago. Web stuff tends to use MySQL or other relational databases and various JavaScript and other frameworks. PHP is less popular than in other areas. But that's just my impression — others may have a different view.

There are countless really worthwhile ways to use evolutionary computation (EC) in molecular biology.  The chief advantage of EC is that it can find solutions to problems that are too complicated, too nonlinear, etc., to solve by more direct methods.  I've used genetic algorithms to evolve models, to find patterns in data, to design optical systems, you name it; and almost always a GA finds solutions I'd never find on my own.  Sometimes it's a challenge to find a representation for the solution space that fits the problem well, or to find recombination/mutation operators that work well, but that's where human insight is important. Bottom line: if you can list some problems that fascinate you (or better, fascinate both you and your supervisor), I'd be happy to give you some concrete suggestions.

Our groups research focuses mainly on the structural investigation of miniproteins (such as the Trp-cage motif) through NMR, XRD and CD studies, but we are pretty diverse when it comes to research; my current thesis-work is about bacterial expression optimization in a biorector, we also synthesize small peptides, sugar-derivatives (through classical organic chemical synthesis), do MD calculations and all of these topics are coordinated by my supervisor (so we could say that all of these fascinate him). As for me, I am willing to do almost any research in these areas.

I've opened a chat room, "EC in Molecular Biology", which should be a better place to carry on the conversation.  Optimizing bacterial expression in a bioreactor is probably a great place to start looking for an application for evolutionary computation.

The first thing that springs to mind is modeling and simulating the evolution and specificity determinants in protein - protein binding. You can easily include an experimental  part and make it as big as you like (the bigger, the better). For a useful set of physiologically important protein - protein interactions and background info on the specificity and affinity determinants in those systems, see Ivanov et al., 2017 and Ivanov et al., 2016, and the references therein.


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Strange white strings on cherry tree leaves
What could be the cause of these white strings on the leaves of our sour cherry tree? Is it some kind of fungus or an insect?

Also, i don't know if it's related or not, but on the other side of the tree brown spots started to appear also on the leaves:

I live in Hungary, if the climate is relevant.

The picture is too blurry for an exact determination.
From what I see it might be Metcalfa pruinosa or a related species, which is an insect of the order of the Hemipteri.
It's a widespread parasite of ornamental plants.
Here a page about it
http://ag.udel.edu/research/delphacid/species/Metcalfa.htm
if true, what you posted are the nymph, and you might be able to find the adults around

This sort of thing happened to one of my plants.  When I took a closer look at the plant, it was a group of white aphids.  The brown coloration of the leaves of your cherry tree was relevant because aphids can sometimes kill the entire plant that they feed off of.
I did not take a picture of the plant, but I found one online: https://entnemdept.ifas.ufl.edu/creatures/trees/shivaphis_celti03.jpg

Woolly Aphids.
They suck the juices out of the leaves of certain trees such as cherry trees and rose plants —to name a few.
Best way to treat them, is gather a plethora of Lady Bugs (or maybe two) to feed off these parasites naturally. Alternatively, try using Neem Oil. It is derived from the leaves of an Indian tree with amazing properties —so your trees/plants won’t be affected. You may need a spray bottle. Just add a little water to dilute for the spray. Make sure you get under the leaves as well. Best wishes!

welcome to the SE Biology. Please feel free to verify your claims, and it will be good answer. But notice that if you dint get any sources  it would be taken like only claims and might potwntionaly get donw vote.


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Is this mallard transitioning out of breeding plumage?
Is this  mallard transitioning from conspicuous to ordinary plumage, or is there a different reason for why its colours seem patchy?
It was photographed in Vienna during late September.

Mallards go through moult once a year. They do this at a different time for females and males, the former one during the nesting season (somewhere between February and May), for the males this happens between June and August after the mating season.
In this time they lose all of their colorful feathers as well as the ability to fly for 3-4 weeks, in this time the look similar in coat color to the females which gives them better chances to hide. After this period the colorful feathers start to grow again, giving the bird a patchy look which is called "eclipse plumage" by ornithologists.
In September the bird you photographed is on its way back to full color, that's why it is looking so different.
The sequence looks like this (source):

So it is the complete opposite of what I thought! Instead of the period of bright plumage being brief, it is the period of inconspicuous appearance! Thank you!

So the males, in moult, look similar to females?

They lose all of their colourful feathers because they come loose.

What is the evolutionary benefit of this? If the colorful plumage was only for the short breeding period and the simpler one for the rest of the year, I could understand it. But why is the "stealthy" period so brief, and why do they regain their colorful mating plumage long before the next breeding season?

@EndAntisemiticHate Yes, they do, except for the beak: This is bright yellow in males.

@vsz They need to renew their feathers and they need some camouflage in this time, because they cannot fly. When they change back to normal color they go through a second (partial) moult, but retain their ability to fly. So only a short period is needed.

Wow. Thanks.  I've learned much over the years on Stack Exchange sites, but frankly, I think this may be the most surprising!


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What is this insect (or spider)?
Location: Vienna, Austria
Date: July 18th
Daytime: around 5pm
Begaviours: none, unfortunately. Just walking
I take these to be six legs and some kind of appendices. But I am not entirely sure.

This is a true bug larvae - thus, an insect - you correctly counted six legs :)
Characteristics of true bug larvae are the combination of the rostrum, the wing pockets and the dorsal scent glands (although the latter both are hard to see on the photos).
I suspect the specimen to be a member of the family Coreidae as it exhibits typical (larval) characteristics of this family: a rhomb shaped body and long legs and antenna. Also spines are a common feature of this family.
Although a bit hard to tell from the photos, I find it to be most similar to Coreus marginatus, a common species in Central Europe.
Comparing two of the specimen's photos with those showing C. marginatus from a similar perspective, shows that - besides the general habitus and coloration - the number and position of the dorsal spines (2 x 2 central and 2 x 3 lateral) match well.
Also, the antenna are relatively large in comparison to the body (compare also this photo).
In comparison, a Leptoglossus occidentalis larvae (as this species was suggested in another answer) would have a generally more elongated habitus with thinner antennae. And, most strikingly, L. occidentalis larvae have a more-than-body-long rostrum.
For comparison, here are more photos of...

European Coreidae here or here
C. marginatus larvae
L. occidentalis larvae

Image source (in reading direction):
B. Schoenmakers CC-BY-3.0 |
B. Schoenmakers CC-BY-3.0 |
B. Schoenmakers CC-BY-3.0 |
Slimguy CC-BY-4.0

I think it could be this animal. It is the nymph of Leptoglossus occidentalis, the Western Conifer Seed Bug.
It fits in terms of size and the greenish-brown colour of the abdomen. Also the position of the spikes and the long antennae are a match, eventhough the antenna look a bit more flat and broad in your picture and less hairy.
This invasive species is originally from the US. It was first recorded in Vienna in 2006.
I think you should also consider this one :
https://commons.wikimedia.org/wiki/File:Gonocerus_acuteangulatus_(Coreidae)_(Box_bug)_-_(nymph),_Nijmegen,_the_Netherlands.jpg
Gonocerus acuteangulatus nymph


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Is this a juvenile Middle Spotted Woodpecker?
Place: Vienna, Austria
Time: October, 8th, 2023; morning
Behaviour: Likely eating from bark

From apps and pictures, I quickly gained confidence in this being a specimen of the Middle Spotted Woodpecker. It might be my ineptitude in perceiving size over distance, but I remember this specimen as smaller than the 20cm minimum size stated by Wikipedia.
Is it perhaps a juvenile?

From a search i looks like the juvenile has weaker coloration. Size is notoriously hard to do without reference to something of known size nearby, so I would guess (and it is nothing more than a guess) adult.


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How could this fossil's soft tissue be preserved so well?
I found this article for non biologists like myself. It describes, how astounding fossils were found in China. They belong to a crustacean like animal that lived more than 500 Ma ago. The exciting thing about them is, that the nervous system -soft tissue - is fossilised in its finest detail. The article says:

“Using fluorescence microscopy, we confirmed that the fibres were in fact individual nerves, fossilised as carbon films, offering an unprecedented level of detail. These fossils greatly improve our understanding of how the nervous system."

My question is: how can these soft tissues be so well preserved?
I managed to find the scientific publication   and attempted to identify the answer myself, but it seems to me, the question is not touched upon. Perhaps, being a layman, I overlooked it, or it is obvious to biologists?

I may be proved wrong, but I doubt anyone can say for sure, it's probably to do with the very specific conditions of the fossilisation process, my guess would be that it went from living to fossilised relatively quickly, before the nerves etc. could decay.

You're right that the authors don't comment on how they think the fossilization occurred. Since that process isn't the point of their article, my guess is that any discussion of it would have detracted from their research focus.
There are some ways that soft tissue fossilization can occur, but to specifically answer your question as it relates to this case, you'd have to know more about the geological conditions in which the fossils were found, which I don't see in the article. This article provides a nice review of soft-tissue preservation processes.
The main points to consider in soft-tissue fossilization, according to the linked article, are pressure, time, charge and chemistry.
Pressure: How much pressure was the fossil under? The higher the pressure, the less oxygen and fewer organisms can access it and degrade biological tissue.
Time: How quickly did the fossil become inaccessible to degrading organisms? The faster this occurs, the less likely that any soft tissue will rot away.
Charge: Does the sediment in which the fossil found carry a charge? Electrical charge acts both as an selective barrier to some organisms and chemical compounds that can hurry biological decay and provides a means for reaction with biochemical compounds, which brings us to the last point:
Chemistry: Can components of the biological soft tissue react with their surrounding minerals? If so, then the inorganic compounds present may be able to reduce lipids and other complex carbohydrates to molecular carbon and minerals in the form of the biological organism.
So say, for instance, that this organism was suddenly encased in a thick layer of clay. As the review states:

In clay-rich environments, the large surface area and charge of clay
  grains are thought to contribute to preservation in one of two ways.
  First, enzymes produced either through autolysis or by invading
  microbes are adsorbed to the surface of the clay grains and
  inactivated, slowing or preventing degradation (Butterfield 1990,
  Garwood et al. 1983). Second, molecules directly adsorbed to clay
  grains are resistant to degradation (Stotzky 1980), whereas
  protein-protein layers are readily degraded. This mechanism may
  explain the exquisite preservation of thin carbon films in impression
  fossils such as the feathered dinosaurs of the Jehol Biota (see
  discussion below). As tissues interact with surrounding clay grains,
  only the molecules in direct contact with clays are preserved as
  monolayers, whereas the rest are degraded normally. Thus, surface
  morphology is preserved, and original carbon might be preserved as
  well

Who knows if this process explains these particular fossils. ¯_(ツ)_/¯  As I said earlier, we'd need more information. The section quoted above, though, seems (to me) to provide a plausible hypothesis.
I hope this helps!

Three major factors.

the organism itself was small and thin enough to not be exposed as it decomposed, combined with the extremely fine grained nature of the matrix (rock) means the organism was held perfectly still even as all the moisture and active enzymes were literally leached or squeezed out of it.
Most of an organism is water, and that gets slowly removed leaving behind a stain almost as if you slowly dried out the organism while pressing it between two plates. Look at the old practice of pressing flowers under glass for ideas of how this can preserve things. Removing any space in the remains prevents the molecules from moving much.
It was buried quickly under anoxic conditions so little to no bacterial action was able to alter or disturb the remains as these processes reduced it to basically a stain of all the non-water components of the organism. What is left does not take up much space and microscopic mineral grains completely surround them, the molecules cannot move much becasue they have nowhere to go, that is why such fossils become very delicate once exposed the leftover material is then free to shift.

Sources
 Burgess shale examinationand experimentation in preservation

Can you add some sources to this?


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What shape is the pupil of squirrels?
In the animal kingdom there is a striking variety of pupil shapes, with great variety among relatively close relatives. Cats have vertical slits. Siberian tigers have round pupils. Cuttlefish have a W shape. Goats have what I would call a horizontal bar. Many foxes have vertical slits, many dogs have round ones.
I just started paying attention to it and I was looking at some good pictures of both Japanese and European squirrels. I sometimes feel that I see a round irregularity at the centre, but can never be sure.

Here's a good photo of a squirrel eye showing the pupil being round.

Source: https://www.treklens.com/gallery/photo390926.htm
Also, these acrylic squirrel eyes for taxidermy show a round pupil.

Source: https://www.mckenziesp.com/Squirrel-Eyes-Acrylic-C3837.aspx