text:
Inbred mice has no severe phenotype outcome?
Why does 20 generation of inbred mouse have no particular strange phenotypes, but on the contrary, when on purposely inbreed dogs or tigers for specific phenotype cause severe deformation of the bone structure or cranial structure?

Depends on what strain of mice you're talking about. Many of the "wild-type" strains I've worked with have some sort of issue or another, such as shortened lifespan, propensity to develop diabetes, etc. Then there are the strains that are bred specifically for a certain phenotype. Additionally, not all dog breeds have severe defects. Basically, it's hit-or-miss.

The danger of inbreeding come from increasing the frequency of rare, negative, recessive alleles to the point of producing individuals with two copies of the bad allele.  If a population lacks such alleles (due to past genetic bottlenecks) inbreeding isn't inherently dangerous.

@AdamC that is possible, though the individuals that are fittest to survive the bottleneck may lack fitness when conditions improve, as is suggested by the obesity and diabetes epidemics we are seeing in developed nations with abundant agriculture. It also leaves out that the genetic diversity that random sexual reproduction produces. Lab strains are one thing, but considering the constant host pathogen arms race that goes on keeping the gene pool diverse gives a species a better chance against its pathogens.

@AMR I don't disagree with what you're saying (though I'm not sure how obesity and diabetes are related to a genetic bottleneck) but what does your comment have to do with the question?  The question covers several topics so one could certainly answer it from a number of different perspectives.  Why don't lab mice experience inbreeding depression? or Why do negative traits appear in dogs when other traits are selected for? or Can you take inbred lab mice and, through artificial selection, produce negative traits like seen in dogs?

Thanks Adam C, you phrased my question perfectly. Still.. I am not completely satisfied with all the answers... I'd love to hear some answers that's more in detail.

@AdamC (and OP): It isn't that they don't experience inbreeding depression: they definitely definitely DO. Inbred lab mice have many negative traits. A large percentage are blind (and not just albinos, there is actually a specific mutation common to many inbred strains that casues total blindness by ~1 month age). Several strains have hearing difficulties. Many strains have issues with tumors (you see this especially with rats).

Some information on inbred strains of laboratory mice:
https://en.wikipedia.org/wiki/Inbred_strain
http://what-when-how.com/molecular-biology/pure-line-molecular-biology/
A relevant quote on the consequences of inbreeding:

Inbreeding in allogamic organisms bring the deleterious recessive alleles to homozygosity; the immediate consequence is an increase in the frequency of defective offspring, or, in another words, an increase in the genetic load of the population. This phenomenon is called inbreeding depression or inbreeding degeneration. As inbreeding continues, the deleterious alleles are selected out and eventually disappear. The original heterozygous populations are often more fit than the resulting pure lines because they profit from heterosis and balanced polymorphisms; the main advantage of pure lines is the quick production of many individuals with the same well-adapted genotype, while the allogamy continuously generates new genotypes.

In other words, inbreeding is harmful because it makes it more likely that offspring will have two copies of bad recessive alleles, meaning those alleles get expressed, meaning the organism gets the bad consequences that wouldn't show up if they had only one copy. This is what happens over a single generation however; over many generations the bad alleles are selected against, precisely because they are harmful to the organism so it reproduces less, and after enough generations of inbreeding you hit a point where all individuals are genetically identical and have all the "good" alleles (if they were lucky; otherwise they die out or stay stuck with some bad-but-not-fatal alleles). They still may be worse off than their more diverse ancestors, but they're not completely messed up like their unfortunate great-aunts and uncles who didn't make it either.
The big difference between inbred mice and dogs or tigers is the "for specific phenotype" aspect. Laboratory organisms are inbred so that you get a large pool of genetically-identical individuals, meaning they're much easier to experiment on. The aim is the inbreeding itself, not any particular phenotype. For example if you look at the page for the most popular strain of laboratory mice, C57BL/6, you can see it has many different properties and is used for many different things.
On the other hand, dogs aren't inbred for the purpose of inbreeding or of being genetically identical; the aim is to get desirable phenotypes, and inbreeding is just an efficient way of achieving that aim. It also isn't obvious that many of the problems purebred dogs have is inbreeding (i.e. lack of genetic diversity, high levels of homozygosy) per se, but the fact that the traits being bred for are just plain unhealthy for the dog, or part of a bell curve that include bad outcomes at the edges. For example, Syringomyelia in the Cavalier King Charles Spaniel:

Some researchers estimate that as many as 95% of CKCSs may have Chiari-like malformation (CM or CLM), the skull bone malformation believed to be a part of the cause of syringomyelia, and that more than 50% of cavaliers may have SM.* It is worldwide in scope and not limited to any country, breeding line, or kennel, and experts report that it is believed to be inherited in the cavalier King Charles spaniel. CM is so widespread in the cavalier that it may be an inherent part of the CKCS's breed standard.

(emphasis mine)
Same thing for that spine malformation that's related to selecting for corkscrew tails. The genes that make the tail corkscrew also mess with the spine.
In other words, the issue isn't inbreeding or not but whether the genes themselves are harmful. When organisms are selected for traits that are directly harmful in their extreme, or are associated with harmful genes that just happen to be next to those that are selected for in the chromosome, then the harmful consequences will spread through the population. Inbreeding is only a problem insofar as it allows the process go faster (more offspring per generation have the desired trait). On the other hand when you're just inbreeding with no specific focus on phenotype, or not phenotypes that have obvious harm associated (i.e. no lab would select for a frivolous trait that also causes harm. They're either selecting for the harmful trait on purpose, or they're selecting against it, because they'll want animals that are as healthy as possible except for the one variable they're interested in), then you'll end up with populations that are fairly normal except for some of the direct consequences of genetic uniformity.
It should be noted that most purebred dogs probably aren't inbred strains the same way many laboratory animals are; those are genetically identical, so the whole point is that their offspring will be like they are. So while they may be less fit than a non-inbred version of them might be, their offspring won't be any less fit than they are. And this is not what's observed with purebred animals like dogs and horses; individuals aren't identical, and looking at the page on Syringomyelia it seems the problems are getting worse.

Because we have selected particular inbred strains that seemed "normal", at least superficially, and mostly for strains that produced good litters and didn't often bite the researchers. However, inbred strains of mice and rats have many deleterious mutations. In some cases they probably survive only because they are held in cages with ample food and water, so they are not subject to the same selection pressures as wild mice would be.
For example, many common mouse strains have the rd1 mutation (see: Jackson labs). This mutation leads to complete degeneration of photoreceptors by about 1 month of age. Note that these are not typically albino mice, so this is different from the vision deficits of albinos. These are mice that appear mostly normal, but they are totally blind.
The most common mouse strain used in research is the C57BL/6 mouse, sometimes called "black 6". Again, see Jackson Labs for some of the phenotypes observed in this strain. I'll list just a few here: hearing loss, high preference for alcohol, dermatitis bad enough to occasionally result in self-mutilation and death, susceptible to obesity, sensitive to atherosclerosis, small kidneys, susceptible to several tumor types, high rate of developmental issues with the lens of the eye, and on and on.
Given that this is the strain often considered "most normal" I think you can see that it isn't at all correct to think of inbred mice as not having any severe phenotypes.


text:
Alternatives to His-tags
What are the alternatives to using a histidine-tag in detecting protein-protein interactions? Why would they be more beneficial than his-tags?

Histidine tags on proteins do not inherently enable the detection of protein-protein interactions. Histidine tags allow one to attempt to purify your protein of choice using affinity chromatography on resins that have been substituted with chelated Ni++ (as I recall). There are two potential advantages to using this approach. 1st, you may be able to elute any bound proteins using a buffer containing histidine (i.e., non-denaturing conditions). 2nd, If your protein is insoluble you can solubilize it with urea and/or SDS, and the protein will still bind the affinity matrix.

This depends on the technology you're using for the interaction detection.  Surface Plasmon Resonance and Isothermal Titration Calorimetry (and others) don't require tagged proteins of any kind.  Though it doesn't hurt either one.
If you're looking purely at chromotography, any tag that will stably capture. I commonly see GST, FLAG, and MBP in order of occurrence.

The His tag is part of a group of small peptides known as epitope tags. They vary in length from 5 or 6 amino acids up to 10-15. Some common ones include HA, FLAG, Myc, and V5. Once common element they share is that the sequences are quite immunogenic, so it is relatively straightforward to raise antibodies to them. They are also soluble, so they don't affect the tagged protein's structure much. This is not always the case in practice, though.
These tags are mainly used in studying protein-protein interactions by antibody-based detection methods - affinity chromatography, Western blot, co-immunoprecipitation, immunofluorescence, etc. They are extraordinarily useful for cases where the tagged protein does not have a good antibody available, or you are doing multiple parallel experiments with many tagged proteins and you don't want to optimize the conditions for each protein-specific antibody individually.
There are various reasons for using another epitope tag over a 6X or 10X His tag, the most common being the His tag is interfering with the proteins structure, function, or binding characteristics somehow. This can sometimes be solved by moving the tag from the amino- to the carboxy-terminus of the protein, if possible, but choosing a different tag is a common strategy. Another purely practical reason to use a different tag is that one protein in your experimental system may already be His tagged, so you need something different. Finally, the conditions of your experiment may be such that a His tag cannot be used, such as harsh elution conditions requiring the denaturing of the protein.

source: Stack Exchange

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

sort: votes


text:
What prevents the diffusion of proton gradient in Gram (+) bacteria
The proton gradient in bacteria is important to power FTPase and flagella. How do Gram (+) bacteria maintain a proton gradient without a periplasm (Gram (-)) or intermembrane space (mitochondria). Why don't the protons diffuse away from the Gram (+) bacteria when they are exported?

Welcome to the site. Please take a [tour] and visit the [help] for more information on what we do here. Please note the page on homework. Ideally your question should demonstrate an attempt to find the answer yourself, and, no - "I google searched and didn't find anything" isn't an attempt. The answers to this should be easily found in your microbiology textbook!

Does this answer your question? How do Gram + bacteria use a proton gradient for F-type ATPase?

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


text:
Can someone help me identify what type of spider or insect builds a green nest that is black an gold
I had the same thing a spider like creature that was black and gold the size of a dime that was building a green sack like web that stuck to the windshield. Location south texas winter, any supspects?

The green web will be a nest for eggs. We would need high quality photos from several perspectives of the spider to ID.

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


text:
Is there an enzyme that functions without being associated with a complex?
I'm looking for an enzyme that does not function as part of a complex in its active state. Preferably it also is not part of a kinase or other kind of activating cascade as well though I would appreciate any and all names that are not part of a complex in its active state. Also would be better if it does not require post translational modifications. Of course, pre translational modifications/ interactions at rna or dna level are all good.
In eukaryotic genome but bonus points for human genome!
Thanks!!

Ribozymes may answer your conundrum here.

Ribozymes are made of 2 subunits though. I'm basically wondering if there is a protein with no quaternary structure and maybe even those little things I mentioned above.

This seems like a XY problem

I'm not really sure how else to phrase unfortunately. But that's a good thing to learn about! Feel free to edit or advise and I'll comply!

I can't really suggest an edit because I have no idea what problem you are trying to solve, and that's kind of the problem with XY questions. What is your goal?

Please provide context (why do you want to know this?) and evidence of your own research. Please restrict yourself to asking a question. We have our own scoring system here and it does not involve posters awarding bonus points. Nor is this necessary as you’ll find it more difficult to find proteins present in other eukaryotes and not man than those also present in man.

I don't really get what David is saying but Bryan, I'm mostly trying to figure this out just cause I can't think of any. Goal is to just name an enzyme which doesn't have a quaternary structure in active form and preferable has no cofactors attached or required and post translational modification.

Acetylcholinesterase.
Chosen because the esterase seems like a low energy reaction so it wouldn't need energetic co-factors.
https://en.wikipedia.org/wiki/Acetylcholinesterase
Not sure if I should do a new answer or not.

Yeah. The Zn is a cofactor so technically doesn't add to the quaternary structure. I'll keep the question open in case someone identifies a completely isolated enzyme.

@SarthakGarg , i have changed my answer.


text:
How to use the law of diffusion in the presence of electric forces?
Isn't the movement of ions affected by the electric field as well? For instance, when a sodium channel in a cell's membrane opens, the sodium ions are said to diffuse into the cell, from higher extracellular concentration to lower intracellular concentration. But what about the electric force fields? The negative ions within the cell attract the sodium ions outside the cell, while the potassium ions within the cell repel them, so why aren't such interactions mentioned and taken into account when discussing the direction or intensity of flow? It seems that the only factor considered by books is diffusion of sodium ions from higher to lower concentration.

Sure, the electric force matters a lot. Ions, like protons H+, follow their respective Ion Motive Force, which is the sum of two components: difference in concentration (osmosis) and difference in charge (voltage) across the membrane. You can find more details here.

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


text:
What would be the shortest and optimal method of extracting human cells for PCR? Is there a colony PCR like protocol for human cells?
I am trying to devise a quick method to extract genomic DNA from human cells for a PCR.
I first collected cells by centrifuging  saline mouthwash (0.9% NaCl) and extracted genomic DNA using kit followed by a PCR protocol which works fine but is a rather lengthy process.
I tried to cut short the method and removed the DNA extraction steps by using pelleted spit samples as templates for PCR and increased the initial denaturing step from 3 minutes to 5 minutes. However this method was not reliable as some of my samples were amplified and some were not.
Can anyone suggest me a reliable protocol here?
Thanks!

Why do you need to shorten the protocol?

I am trying to make a protocol in which DNA extraction, PCR and gel electrophoresis could be done in a time frame of about 4-5 hrs and I am trying to compact everything.

@techtrix          I am curious, did you try the boiling method?

@RoSiv not yet. I may start my work next week. I will let you know how it turns out.

I am not confident in my reply, but the article linked below has methods for DNA extraction of various human sample types( blood, hair, urine, Cheek)
For what its worth, my professors always told me DNA extraction was more of an art than a science, and one has to tinker to get it just right.
Maybe for something really quick, you could try a protienase K "squishing buffer" and then boil it for like 10 mins in the buffer and then try running PCR.  I am just an undergraduate though so take my words with a heavy grain of salt.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3792701/
Here is how they gathered the buccal samples:
buccal swabs:

five healthy adult volunteers were recruited (age range, 22–35 years),
  and demographic information, including age, health condition, sex,
  population ancestry, hair color, and hair treatments, was collected.
  The volunteers recruited were asked to rinse their mouth with tap
  water, 30 s before sampling of buccal swabs, to avoid the
  contamination as a result of food particles. For each individual, both
  sides of buccal mucosa were wiped with a cotton swab for 15 s, and a
  total of five samples was collected in 500 μl 10 M Tris-HCl, 10 mM
  EDTA, 2% SDS, containing 1.5-ml microcentrifuge tubes. Isolation of
  DNA from cotton swabs was performed.

Here is a copy paste, hyphens are mine.
DNA Extration:

Buccal swabs:
-samples were suspended in 500 μl lysis buffer [10 mM Tris (pH 8.0), 10 mM EDTA, and 2.0% SDS], and 50 μl 10% SDS, followed by 5–10 μl 20
  mg/ml proteinase K
-incubated 1–3 h at 56°C until the tissue was totally dissolved
-The DNA was then extracted from each sample with an equal volume of phenol:chloroform: isoamyl alcohol solution (25:24:1) and mixed gently
  by inverting the tubes for 3 min.
-samples were then centrifuged (Eppendorf 5415R; Hamburg, Germany) for 10 min with 10,000 g (4°C),
-upper aqueous layer was transferred to a fresh, sterilized microcentrifuge tube.
-RNase A (10 μl of 10 mg/ml; Fermentas, Thermo Scientific, Germany) was added, and the solution was incubated at 37°C for 30 min.
-Equal volumes of chloroform:isoamyl alcohol solution were added and centrifuged (Eppendorf 5415R), again with 10,000 g (4°C) for 10 min.
-The upper aqueous layer was transferred to a sterilized microcentrifuge tube, and double the volume of chilled isopropanol
  (Merck, Whitehouse Station, NJ, USA) was added, along with one-tenth
  volume of 3 M sodium acetate, and chilled at −20°C for 1 h for
  precipitation.
-After 1 h, the sample was centrifuged (Eppendorf 5415R) at 10,000 g (4°C) for 10 min.
-After decanting the supernatant, 250 μl 70% ethanol (Merck) was added, and the pellet was dissolved; the mixture was centrifuged at
  10,000 rpm for 10 min, and the supernatant was decanted gently.
-The pellet was air-dried under laminar air flow, and the dried pellet was resuspended in 50 μl nuclease-free water or 1× 10 mM Tris-HCl, 1
  mM EDTA, pH 7.6 (TE), buffer and frozen at −20°C or at −80°C for
  storage.

Thanks Ro Siv, but this process seems rather lengthy for me. I could try the protienase K "squishing buffer" method though.

I do a lot of gDNA and cfDNA extraction! What Ro Siv has explained is a pretty standard method of buccal swab extraction, however the pK incubation times do not need to be nearly that long. The gold standard in DNA extraction is QIAGEN kits. Specifically for your uses I would go with something like the QIAamp DNA Mini Kit (you can view their handbook protocols on their site - https://www.qiagen.com/us/resources/resourcedetail?id=67893a91-946f-49b5-8033-394fa5d752ea&lang=en) In practice, I have been able to do 4 samples without automation on their spin protocol in around 1.5 hours total.
PCR time will depend on your cycling conditions and how long it takes you to set up a reaction etc, and gels would depend on how precise you need your bands to be. I think the whole thing can easily be done in 4-5 hours. In my experience, blood samples take only slightly longer, but is obviously more invasive and less practical. I agree that buccal is the way to go. For reference, we use Puritan hydraflock swabs, but that's up to you.


text:
What are some examples of undirected weighted networks in ecology?
I'm a math major with a current interest towards network theory. A network can be considered as a collection of nodes, and edges between these nodes signifying some relation between them. The most ubiquitous example would be a social network like Facebook with nodes representing people, and an edge connecting two nodes if they're friends.
A network is called directed if the edges have a direction. This means that if there's an edge directed from A to B, it's not the same as an edge from B to A. An example of this would be a food web network, where the nodes represent species and an edge from species A to B means that A eats B. Obviously, this does not necessarily mean that there's an edge from B to A (rarely does the prey eat the predator).
A network is called undirected if it is not directed, i.e. none of the edges have any direction; if there's an edge from A to B, it necessarily means that there's an edge from B to A.
Now, one can assign weights (numerical values) to the edges in a network to signify the relative importance of edges. In the Facebook example above, this can be considered akin to assigning values to edges which indicate the strength of friendship/distance between the residences of friends, etc.
I wish to study ecological networks to see if I can make interesting inferences from my study of weighted networks.
So can you give me some examples of undirected, weighted ecological networks?

Network theory finds wide application in trophic ecology (food webs) and genetics (gene regulatory networks). Have a look at that.

Interaction/foodweb networks where we only know the correlations between species (e.g. correlations between the abundances of species over time) would be one example of a undirected, weighted network.

Epidemiology, the spreading of diseases, is probably one of the most famous applications of network theory in biology, going all the way back to John Snow.
A more relevant example would maybe be something like graph models of habitat mosaics. Populations are often both spread out over landscapes and clumped together in smaller pockets of suitable habitats. While fragmented, these populations still have a certain amount of contact, resulting in gene flow and the creation of what is often called a meta-population. These things can happen on a vast range of scales, from your back yard to whole continents, but by modeling them like graphs they can all be studied comparatively and tested for resilience agains disturbances, habitat loss etc.
You mention social networks, but there is no reason why you can't study the same in animal populations. Say one individual learns something useful, maybe the location and route to a rich feeding ground. That information can then be shared with other individuals, either by show-and-tell, or maybe by some kind of abstract communication. The information spreads in familiar exponential fashion until everyone knows, then any one of those individuals can relay or be "eaves dropped" on by a neighbouring population, it doesn't even have to be the same species in some cases, and the information flows again. As with the habitat mosaics the benefit of these models is that very different systems can be compared and tested on an equal footing, anything from fish, to birds, mammals, even some social insects, lend themselves well to this.

Started working on an answer, then decided just to upvote this one. Some undirected, weighted networks for epidemiology can be found at http://ndssl.vbi.vt.edu/synthetic-data/ , or as component of the ergm R package, if one is so inclined.


text:
Number of families in Animal kingdom
I found this question about how many taxonomic families there are. That made me wonder how many are just in the animal kingdom alone. I want to know about families not species. Now the linked question was three years ago, so there should be some new information and numbers. A good answer would preferably include a breakdown of the phyla.

The Integrated Taxonomic Information System (ITIS) is maintained regularly by a consortium of North American governmental agencies, and will give you a list of all the classes, orders, families or genera in any of seven kingdoms they recognize. It might be biased towards North American taxa, but it might be quicker to get a list from then rather than extracting them from Wikipedia.
To help you further, user Rozenn Keribin used an awk script to summarize the number of families per phylum at https://justpaste.it/163c6.
Phylum:  Myxozoa -- 4
Phylum:  Chordata -- 1049
Phylum:  Echinodermata -- 139
Phylum:  Hemichordata -- 7
Phylum:  Xenacoelomorpha -- 9
Phylum:  Chaetognatha -- 9
Phylum:  Arthropoda -- 2504
Phylum:  Kinorhyncha -- 10
Phylum:  Loricifera -- 2
Phylum:  Nematoda -- 192
Phylum:  Nematomorpha -- 3
Phylum:  Onychophora -- 2
Phylum:  Priapulida -- 3
Phylum:  Tardigrada -- 20
Phylum:  Annelida -- 142
Phylum:  Brachiopoda -- 21
Phylum:  Bryozoa -- 133
Phylum:  Kamptozoa -- 5
Phylum:  Mollusca -- 581
Phylum:  Nemertea -- 20
Phylum:  Phoronida -- 0
Phylum:  Sipuncula -- 6
Phylum:  Acanthocephala -- 26
Phylum:  Gastrotricha -- 13
Phylum:  Gnathostomulida -- 12
Phylum:  Micrognathozoa -- 1
Phylum:  Orthonectida -- 2
Phylum:  Platyhelminthes -- 321
Phylum:  Rhombozoa -- 3
Phylum:  Rotifera -- 34
Phylum:  Cnidaria -- 269
Phylum:  Ctenophora -- 19
Phylum:  Placozoa -- 0
Phylum:  Porifera -- 142
Total -- 5703

Wow, that is a MUCH easier to parse source than the ones I knew about or that were given as answers to the previous question! So much easier that I wrote an awk script to do so that provides exactly what OP was asking for. Obviously too long for a comment and I don't want to edit your answer without asking first, here's a link if you want to do so: https://justpaste.it/163c6 (the source you gave would also be a valuable answer to the earlier question the OP referred to)

@RozennKeribin Thanks for the link! I've added it to my answer, but feel free to edit it directly if you'd like!

Your question immediately made me think of the paper "How Many Species Are There on Earth and in the Ocean?", which is about estimating the total number of species based on the rate of discoveries of higher taxa. I imagine writing the paper involved the most thorough investigation of how many taxons there are in any group that you'll find. It's from 2011 so it's not going to include actual new information from the last three years, but given it looks at the rate of discoveries over time you can see the evolution and estimate where things are yourself.
Figure S1 gives the actual plots of number of taxa vs time; from it we can see that Animalia contained a bit over 5000 families (5300 I'd say?) in 2011, with an estimated total number of a bit under 6000 (5700?). So today's number is likely to be within that range.
If you want the actual list per phyla you just need to look at the same sources that were given in the answers to the original question; Wikipedia and the NCBI taxonomy browser (which also links to other resources that might be easier to interpret) have no reason not to be up-to-date.


text:
Distribution of synaptic connections
What is the roughly the distribution of the various synaptic connections in the brain.
Consider the following types:

axoaxonic synapse between the axon of one neuron and the axon of another neuron.
axodendritic synapse between the axon of one neuron and the dendrites of another.
axodendrosomatic synapse between a neuron's axon and the dendrites and body of another.
axosomatic synapse between the axon of one neuron and the body of another.
dendrodendritic synapse from a dendrite of one cell to a dendrite of another.

I know that the axodendritic synapse is the most prevalent, but what is order of the others? Are there any sources for this (couldn't find this anywhere). Specifically, rough percentages of the distribution (amount) of these synaptic connections in the nervous system would be very helpful.

The adult human brain contains ~86 billion neurons with trillions of synapses estimated at 0.15 quadrillion. I am unsure if this question can be answered.

@AliceD I understand that there are many synapses, but don't we know anything about which synaptic connections are more common than others?

I expect there may be studies that have addressed some of the various connections in particular brain structures, but to find data that provide an order of appearance of all of your mentioned connections in the whole brain, I am doubtful of. It's an intriguing question, though. It's quite of a textbook question and I doubt a literature search will be helpful.

@AliceD I understand, but I couldn't find the answer in three different textbooks. That's why I'm asking the question here. Maybe somebody knows a study about this?

It would be good to mention those textbooks - it may save people work. If I would give this question a try I would start looking in Kandel's Principles of Neural Science - did you check that? if not, I'm happy to look once I'm back in the lab. Might take me a few days.

I don't have time for a full answer, but here is a study on the hippocampal CA1 pyramidal neuron that makes an exhaustive catalog of all synapse types and locations: Megías, M., Z. Emri, T. F. Freund, and A. I. Gulyás. “Total Number and Distribution of Inhibitory and Excitatory Synapses on Hippocampal CA1 Pyramidal Cells.” Neuroscience 102, no. 3 (2001): 527–40.  I know such papers exist for a few other cell types. This paper might provide a lead for finding those too.

@yamad Perfect! I'll take a look at that one and see if I can find others.

Are you still interested in this kind of questions? Have a look at mine: https://biology.stackexchange.com/questions/53587/the-human-brain-in-numbers-i-neurons, https://biology.stackexchange.com/questions/63950/the-human-brain-in-numbers-ii-synaptic-connections


text:
Problem on Probabilty of a restriction enzyme cutting a random DNA sequence
I think its a silly question to ask here. When I came to this site all I could see were the questions which asked detailed explanation behind a phenomenon and reasoning was there at first place. I am bringing quite math here!!!
First, I am a beginner.
Second, I would like to mention some problems..

Genomic DNA is digested with AIU I, a resrtiction enzyme which is a four base pair cutter. What is the frequency with which it will cut a DNA assuming a random distribution of bases in genome?
Eco RI and Rsa I restriction endonucleases require 6 bp and 4 bp sequences respectively for cleavage. In a
10 kb DNA fragment how many probable cleavage sites are present for these enzymes?

These questions were solved by my teacher using some probability results or rules.
I would like to mention it here.. [you know already...!!! ;-)]
(1/4)^n *10,000 or simply (1/4)^n. By putting n = number of base pair cut by enzyme.
I get the frequency with which enzyme will cut a DNA assuming a random distribution of bases in genome by using (1/4)^n and I get probable cleavage sites are present for Eco RI and Rsa I in 10 kb DNA fragment.
But why do I do that? I mean why that formula? How to understand how it was derived? Can you explain me that?
Please suggest some good books containing concepts and numerical problems like these so that I can work on it.. [Please let me know your source]. Thank you.

EcoRI recognizes, binds to, and cleaves the hexamer 5'-GAATTC-3'. In a completely randomized DNA sequence, with 25 % A's, 25 % C's, 25 % G's, and 25 % T's we would expect to randomly discover the sequence GAATTC, once every 4,096 base pairs, on average. The actual distribution of EcoRI fragments (a fragment where each end contains a cleaved EcoRI site) in our random genome will vary and yield a normal distribution, or curve, with some fragments longer and some shorter. The mean value should be 4,096.
The expectation of 1 site per 4,096 bp is indeed (1/4)^6.
1/4 = 25 %
6 = the number of contiguous base pairs in the recognition site.
In a model like this it is important to keep in mind that the probability of one base occurring in the sequence is completely independent of the sequences before that base, and the sequences after that base. In other words, for each and every position the probability of getting a base that will contribute to an EcoRI site is 25 %, or 1 out of 4 = 1/4.
75% of the time, the next base will not contribute to an EcoRI site (and a quarter of the time it will).
Let's start with your 10 kb fragment, and go through from one end to the other, and mark every time a 'G' occurs. Theoretically those could all be the beginning of EcoRI sites, right? There will be approximately 2500 such 'G's. Now to match our pattern, we need an 'A' in the second position, so let's mark all those sites that contain the dinucleotide 'GA', there will be about 2500 x 0.25 = 625 of them. The next match we need is position 3, another 'A', so in a similar fashion, let's go through the positions of all those GA dinucleotides, and just mark the ones that have an 'A' at the next position. So that will be about 625 x 0.25, or approximately 156 'GAA's distrubuted randomly along the 10 kb fragment.
If we continue, essentially filtering out more and more of those 'G' sites in our initial list then we will find, on average, that there are
39 sites with GAAT
10 sites with GAATT
2 sites with GAATTC
If you don't believe me just pick a sequence and try it yourself.
10,000/4,096 ~ 2.5


text:
Is there any liquid in the bone medullary cavity
I am looking at the effect of intramedullary nails on tibial bones and can't seem to find anything on fluids present within the medullar cavity/canal. Since this is where blood cells are formed I would expect there to be at least a bit of blood in the cavity. I also read somewhere about something called 'liquid bone marrow'. Can someone please confirm whether there is blood in the cavity and whether there are any other fluids present. Thanks in advance.

Bone marrow is almost a liquid.

@JM97 so there is a liquid and a solid component (spongy tissue). but what is the liquid composed of then?


text:
Why is there a structural difference between the bicuspid and tricuspid valve?
There are three cusps in the tricuspid valve and only two in the bicuspid valve? Why is there such a structural difference? Does it have anything to do with that there is oxygenated blood on the left side and deoxygenated on the right?

Because that is how the heart evolved. You should really rephrase your question to "Is there a functional reason for the observed structural differences of the bicuspid and tricuspid valve (in humans/mammals)?"


text:
Can trichoptera and lepidoptera be distinguished with the naked eye?
Are there any tell-tale signs which one could use to distinguish adult trichoptera from lepidoptera? To me, trichoptera just look like moths:

One method would presumably be to touch its wings and see if scales come off, but what if we assume we don't want to catch it?

The etymology of the names will help you there: trichoptera means "hairy wings", whereas lepidoptera means "scaly wings".
If you can get a close shot (maybe with a powerful tele lens) of any possible trichoptera or lepidoptera, you can tell that it either has hairs or scales on its wings, without having to touch its wings.
Examples:

Note the hair visible above the wings. Taken from https://www.inaturalist.org/observations/18660283
Now, there are lepidoptera species that also seem to have hairy wings, such as the tussock moth:

Note the hair as well. However, the shape of the antennae would be a dead give-away: as far as I know, trichoptera shouldn't have feather-like antennae. Furthermore, the wings still have noticeable scales, besides the hair. Taken from https://www.inaturalist.org/observations/18652111
Other lepidoptera species may also seem to lack scales, such as the Syntomoides imaon:

Parts of the wings of the Syntomoides imaon are transparent. However, anywhere that has scales should exhibit some kind of iridescence. You can use your phone's flashlight and try to illuminate the insect from different angles, and you should notice some iridescence. Trichoptera wings, in contrast, should just reflect the light flatly, due to the lack of scales. Taken from https://www.inaturalist.org/observations/18652111
Also, (most) butterflies and moths have a proboscis (the "straw" that can coil up, used to suck nectar). That's usually easy to spot if you can look at the head from the side. Caddisflies don't have that. Instead, caddisflies have mandibles (used to chew through their pupal case as they emerge as adults).
I did mention using a tele lens at the beginning of this answer. Of course, that's not "naked eye" like you asked. The point is that you begin by using a tele lens. As you see more caddisflies vs moth/butterflies, you'll build up a sense of the cues to look at. And at some point you may be able to distinguish them with your naked eye (depending on how close you can get your face to the insect and how good your eyesight is).

This answer would be much stronger with a citation or link supporting your claims, as well as inclusion of a picture(s) that demonstrate the difference for the OP. Please consider revising to include a bit more detail. Thanks!


text:
Identification of a segmented black insect in France

Found in the Lot department of southern France.

I have no idea what it is. Do you have any more information? Like did it move? How? Did it have any features not visible in the photos? I think I see some sort of pincers in one end, did it have legs?

Are you sure this is an insect. Did it have 6 legs? (Comment originally fro @Kasper)

I think I've seen a similar thing in another stackexchange "species-identification" post, and it was a larvae of some dipteran, but I cannot find something like that in
http://www.dep.wv.gov/wwe/getinvolved/sos/documents/benthic/midatlinverts/diptera.pdf

I think this is some sort of soldier fly larva (family Stratiomyidae). That would explain lack of legs. There are thousands of species world wide, with both aquatic and terrestrial larvae, so it might be possible to narrow it down a bit more.
Image from bugguide.net for comparison:

Thanks to @bli for reminding me of dipteran larvae!


text:
Can/Have cancer cells be/been used in stem cell culture lines?
Since Cancer cells have unlimited growth potential, can they be induced towards totipotency and pluripotency?
If so, can cancer cells be used in stem cell culture because of similar properties of unlimited replication?
Can they be used in cell lines to culture viruses even?

Some murine embryonic carcinoma cells are pluripotential and can differentiate and develop to mice.

Cancer cells can be and are used in cell culture. HeLa cells were the first human cell line to be grown in culture and they were derived from a cervical tumor.
That being said, Cancer cell lines would not necessarily be used for stem cell work. They have sustained too many mutations to study the type of questions that stem cells are used to study, though as MattDMo points out, teratomas, tumors that originate from stem cells, can be used in stem cell research as a model for Stem Cells in culture. Also, they could never be used for therapeutic purposes.
As for viruses, HeLa cells were used by Jonas Salk to develop the polio vaccine, so cancer cells are used in viral research.
Edits in italics.

This is actually not true. I have used teratoma lines to simulate stem cells in some experimental protocols.

Teratoma lines are from stem cell derived tumors. Can you prove that the cells that formed the stable lines weren't still at the stem cell stage? And would you use those cells therapeutically? Would you make a chimeric line of mice from teratoma derived lines or would you use ESC lines? And what were the assays you ran?

see my answer below for some additional details. No, of course we wouldn't use them therapeutically or for chimeras - we used them purely for in vitro work, alongside "true" iPS and ES lines.

Adding onto AMR's answer, cancer cell lines are used extensively for research. They are typically fast to grow. HeLa Long grow to capacity of a 10cm dish within about 48hours, depending how you split them. Now some lines are different than others and each have their pros/cons but the main thing behind them is they make it possible to view the effects of genes being knocked-down/out in human cells.
As for the use of viruses in cell cultures. They are not only used for viral research but also genomic research.
What is typically done is to introduce a gene into a cell culture line via a retrovirus (called a Retroviral Transfection). It is an extremely effective method of creating a stable cell line with your gene of interest attached to a "fluorescent" gene so you can visualize it in the cell when it gets transcribed. This leads to Immunofluorescence(IF) and many other techniques commonly used today.
You can also introduce a plasmid to cells that contains a shRNA that will "knockdown" the gene you are studying the effects of. This way you can see what happens to cells when this gene is not present (done a lot for study of replication proteins).
The caveat is that sometimes these cell lines can be transient (last only a few passages) or stable. They all also act very differently so typically to "prove your case" that the protein has the function you conclude it to have, you should do experiments with several different cancer cell lines.

Regarding your question about whether cancer cells could be used in studying stem cells:
I have done stem cell work, and we used various teratoma cell lines (which are cancers that resemble germline tissue) in parallel with embryonic stem cells (ES cells) and induced pluripotent stem cells (iPS cells) for various experiments. Of course the choice of experimental system completely depends on what exactly you're studying, but teratomas have proven themselves to be reliable model systems for looking at certain aspects of stem cell structure, function, and differentiation. One of the biggest advantages, at least in the work that I was doing, was that they grew relatively quickly and consistently, while iPS or ES cells can very easily spontaneously differentiate if extreme care is not taken in culturing and passaging them. You don't have to worry about donor-to-donor variation, and they are pretty tolerant to being frozen and thawed.
The work I did was in industry, so unfortunately I can't really get into many details, but I was involved in looking at various transcription factors that are responsible for the maintenance of pluripotency as well as the induction of differentiation, as well as testing various live-cell imaging techniques to track particular differentiation pathways. We made a number of observations using teratomas that directly translated to iPS and ES systems, without all of the overhead that those systems required.

If they do not behave like stem cells, i.e. If you do not need to carefully use inhibitors such as 2i or LIF with fibroblasts in culture to prevent differentiation , then I would question the reliability the results I obtained. Just because a system is easier doesn't always mean it is the choice that will get you completely accurate data. If I read a paper that used teratoma lines instead of SC lines I would read more carefully with a higher than average degree of skepticism over the results.

@AMR the teratoma lines were used as a model system for ES/iPS cells, not in place of them. We used them for assay development and experiments where significant amounts of protein were needed initially, to verify conditions and make some observations. Of course the studies were repeated in actual ES/iPS cells to ensure the model matched. This is exactly the same as performing some immunological studies using Jurkat cells, then repeating the assays using primary human T cells, which are harder and more expensive to obtain and maintain. You can learn a lot about "reality" from a model.

See edit in my answer.


text:
Effective population size formula in haploid populations undergoing serial bottlenecks
This classic Lenski paper computes the effective population size of an evolving E. coli population subjected to daily population bottlenecks as $N_e = N_0 * g$, where $N_e$ is the effective population size, $N_0$ is the population size directly after the bottleneck and $g$ is the number of generations between bottlenecks.
Unfortunately, the formula was not derived in the referenced paper and the referenced articles appear to not describe the formula directly, but only provide the fundamentals for deriving it.
Can someone explain how this formula comes about?

The effective population size is the harmonic mean (time average of $1/N$) of the time dependent population size:
$\frac{1}{N_e} = \frac{1}{t_f - t_0} \sum_{t = t_0}^{t_{f}} \frac{1}{N(t)}$
where $t_0$ is the foundation of the E. coli line, $t_f$ is some time much later when Lenski's poor grad students are sequencing them (with the understanding that $t_f - t_0 \ll N_e$, $t_0$ may be before the experiment began), and $N(t)$ is a deterministic function produced by removing individuals from the population with a pipette (throwing the rest in the freezer for the living fossil record) and letting them expand to cover a newly inhabited plate.
Since the population size is cyclical in Lenski's experiments (this procedure is done at regular time intervals, so at approximately consistent generation time), the average over one cycle should be the same effective population size as integrating over all time.  In other words:
$\frac{1}{N_e} = \frac{1}{t_{nextBN} - t_{BN}}\sum_{t=t_{BN}}^{t_{nextBN}} \frac{1}{N(t)} $
where $t_{BN}$ is the start of the bottleneck and $t_{nextBN}$ is the generation before the following bottleneck (once a day I think? so, $\sim$6 generations per cycle if I remember correctly). In the Lenski lines, the population grows rapidly from inhabiting a new environment on the fresh plate, so we can assume the growth rate is exponential with some rate $\gamma$ (e-folds per generation).  Now we have:
$\frac{1}{N_e} = \frac{1}{t_{nextBN}-t_{BN}} \sum_{t=t_{BN}}^{t_{nextBN}} \frac{1}{N_0 e^{\gamma t}} = \frac{1}{\Delta t N_0} \sum_{0}^{\Delta t} \frac{1}{e^{\gamma t}}$
In the second expression I have defined $\Delta t = (t_{nextBN} - t_{BN})$ as the time between bottlenecks, and the sums are equal because we are free to start counting generations at $t_{BN} = 0$.  I also pulled the constant $N_0$ out of the sum.
Computing the sum of the series over a finite number of generations $\Delta t$, we find the following:
$\frac{1}{N_e} = \frac{1}{\Delta t N_0} \frac{ \left(e^{\gamma} - e^{-\Delta t \gamma}\right)}{\left(e^{\gamma }-1\right) }$
Now, I looked up Lenski's 1991 paper (here: https://www.jstor.org/stable/2462549?casa_token=dNMGpr9sBFcAAAAA:BrRjPHxwmxAuegCuN8eHFXr2w4slkPLJwTOrpD6nQRIHsx6ukS4kWaIYHtPuwgxWQ9j7G_6ICPpCTKZA7XW0izImSN_-7wwXpS_lnGWhJSN3PbWRiSU) and he states (in the same section) that $N_0 \sim 5\times 10^6$, $N_f \sim 5 \times 10^{8}$; if $ N_f = N_0 e^{\gamma \Delta t}$ and $\Delta t \sim 6$ (assuming the cycle is once per day), we find that the growth rate for each bottleneck is roughly $\gamma \sim 0.75$ (in that ballpark).  This is extremely quick growth, so the $e^{\gamma}$ terms in the numerator of the above expression dominate over $e^{-\gamma \Delta t}$.  This means we can approximate the inverse effective population size as follows.
$\frac{1}{N_e} \approx \frac{1}{\Delta t N_0} \frac{e^{\gamma} }{e^{\gamma}-1} \sim \frac{2}{\Delta t N_0}$
Note, there is a factor of roughly 2 here that I suppose Lenski is ignoring? Using Lenski's variable $g = \Delta t$, this reproduces the relationship he quoted, up to a factor of $\frac{e^{\gamma}-1}{e^{\gamma}} \approx \frac{1}{2}$:
$N_e \approx \frac{1}{2} g N_0$
As a little tip, if you ever have a population genetics question you're not sure about, just scour Kimura's papers.  Everything you can ever think of is sitting in one of them, including this question:  https://www.jstor.org/stable/2406157?casa_token=cWTvTL8k29QAAAAA:GVDLvS2SL7FJioYREhU0qjAIU5ynBpcncl7Z8r7xZh6S_PQWIVh2Di0bKt9BbVgfJIo-O-CMiFudnSnDMjmwzth1YDTA_EoPoQ7jATWxuzzR2gzcke4
EDIT: I initially introduced a sign error in the penultimate expression, which was originally $\frac{1}{N_e} \approx \frac{1}{\Delta t N_0} \frac{e^{\gamma} }{e^{\gamma}+1} \sim \frac{1}{\Delta t N_0}$, where there was a negligible factor of roughly 2/3 from $\gamma=0.75$ that can be treated as approximately 1.  The above text is now corrected, and has an apparent factor of 2 that would need to be dropped to match Lenski's expression.

Thank you for this comprehensive answer. I guess we can drop the factor of ~2/3 because in this context the error it introduces is irrelevant due to the large uncertainty in all other parameters?

Additionally, I found this paper (https://onlinelibrary.wiley.com/doi/10.1111/j.0014-3820.2001.tb00772.x, also from Lenski) that derives $N_e = N_0\Delta t\gamma$. Again, I guess $\gamma$ can be neglected?

First, no problem!  Second, thank you for citing that paper.  I had not seen it and it's obviously relevant. There is also this paper, by the same authors: https://academic.oup.com/genetics/article/162/2/961/6049989?login=true. Regarding the difference between the two solutions, there is also a strange difference that comes up if you integrate rather than sum to compute the harmonic mean of the population size.  I will post the result (only) in another comment in a few mins.  Also, I made a dumb mistake and flipped the sign in the denominator of the second to last equation (oops!).

The solution if you assume continuous generation time is the following: $\frac{1}{N_e} = \frac{1}{\Delta t} \int_0^{\Delta t} \frac{1}{N_0 e^{\gamma t}} dt = \frac{1-e^{-\gamma \Delta t}}{N_0 \gamma \Delta t}$.  Since $\gamma \Delta t \approx 6 \times 0.75 = 4.5$, the exponential decay is negligible.  This gives $N_e \approx N_0 \gamma \Delta t$, matching Wahl and Gerrish.   I am not quite sure where the difference comes from, but it's entirely possible I made a mistake above.  Wahl and Gerrish also claim that their results match Lenski (1991) (the original paper we are discussing).  ctd below

I'll try to look at the discrete case in my answer again and see if I can find some issue that alters the result (other than the sign error).  I think difference has something to do with changing the discrete sum with the element having no units to the differential dt.  I am going to edit the sign error in my original answer, but I will make it clear where the mistake was so you can track it.


text:
How to predict enzyme activity computationally
if I have an enzyme and its corresponding substrate, are there computational methods that I can use to predict its enzymatic activities? I understand that we can determine its activity using various enzyme assays, but I'm not sure whether these activities can be reliably predicted with computer.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Specifically, what do you mean by "its enzymatic activities"? Which of the things you understand can be measured experimentally are you asking about?


text:
How would you measure the diameter/radius of a non-circular bacterial zone of inhibition?
Typically when we're testing the antimicrobial effects of some substance on bacteria growing on an agar plate, we get the area or diameter/radius of the zone of inhibition. But what do we do in cases where the zone of inhibition is not uniformly circular around the antimicrobial agent? How would diameter and radius measurements be of use in these cases and/or how would one adapt these measurements to more accurately reflect the area of the zone of inhibition?

I think a picture or two would be worth a thousand words here

We actually did something like this in one of my periods in biology class, all you need to do is take your measurement in millimeters. This measures the radius of the zone of inhibition. Multiply that by two in order to get the diameter.
If it's not uniformly circular, try getting the diameter of the circle you do know, and find the diameter/length/width of the unusual part. Just like in maths when you calculate total volume of a combination of shapes.
By unusual part, I mean the part that makes the circle around the microbial agent non-uniform.

If your inhibition zones are not uniformly circular (or at least close too it) you may want to revisit your methods and ask why this might be the case.
Are you applying your inoculum in a consistent and standardized manner? Is the inoculum too light or too heavy in any place? Are your disks too close together, or too close to the edge of the plate? Could your disk have moved after application (possibly due to excess moisture or condensation on plates)? Is the uneven zone close enough to another disk for the two agents to interact, either synergistically or antagonistically?  (see image)

Have you looked to see if any special cases apply, like Fosfomycin, in the EUCAST breakpoints table.
If all of those potential causes are ruled out, I'd say you should measure to the nearest (inner most) circular or semi-circular edge of the zone. Since diffusion tests are often used for antibiotic susceptibility testing of clinical isolates, users (and clinicians) are often more interested in the qualitative classification (susceptible, resistant, or intermediate) than the quantitative result. For example, in cases where a double zone in present, the EUCAST method recommends measuring to the inner-most zone, unless otherwise specified, to avoid falsely categorizing a resistant isolate as susceptible.
If it's irregular because it's overlapping with the edge of the plate, with another inhibition zone, or if synergism/antagonism(aka induction) are suspected, you could just measure to the circular part and ignore the overlap/interaction zone, but retesting with more space around the disk would be preferred.
References:

EUCAST clinical breakpoints table, version 12.0
Antibiotics in laboratory medicine, 6th edition. (image credit)
Development of the EUCAST disk diffusion antimicrobial susceptibility testing method and its implementation in routine microbiology laboratories


text:
When do retinal cells stop differentiating?
I am having a hard time recalling where I had heard this, but I do recall someone saying (perhaps in a video) that cells in the retina divide very rapidly during infancy due to ongoing development of the eye - they were saying this as a justification for the incurrence of mutations in the retinal cells of infants. I searched this up recently and can't find any source that supports this claim. I did learn that there are stem cells in the retina that remain after birth, so I was wondering if the person meant to say there are lots of undifferentiated cells in the retina of infants. I think the more holistic question that I should be asking is: why do eye conditions like retinoblastoma develop primarily in infants?
If it is because of a large number of undifferentiated cells in the retina of infants, can I also be let known when (i.e. at what stage in life) these undifferentiated cells exist in highest number and when they all (or at least mostly all) become fully differentiated?

I see three different questions in one post; adding some of your own research background is a great way to focus the question and specify a single question, which is better answerable in the Q&A format of the SE network. You can post multiple different questions if need be, but please add your own research efforts in regardless.

why do eye conditions like retinoblastoma develop primarily in infants?
One explanation is that infants grow fast. In general, each cell division is a risk of breaking/losing chromosomes. Breaks need to be repaired, but that can be faulty and lead to cancer. This explains why infants get cancer in general.
Retinal cells may be especially prone to DNA damage since there is no pigment to reduce damage by UV-light.
When do they all become fully differentiated?
They never become all differentiated. Many tissues contain adult stem cells that keep their stem-cell state until death. Their purpose is to regenerate tissue, especially when tissued need to be constantly renewing themselves (e.g. skin, intestines, and maybe retinal stem cells, too ).  (Reh et al.)
when (i.e. at what stage in life) these undifferentiated cells exist in highest number?
The highest ratio of undifferentiated/differentiated is probably found during embryonic development.

In some vertebrates, the development of the retina continues throughout life (Bhatia et al 2010)


text:
Why does a non-functional retinoblastoma protein cause tumours in the cells of the retina specifically?
I know that the name of the protein itself is the retinoblastoma protein - but that's only because the result of a pathogenic variant is retinoblastoma. I'm trying to kind of reverse engineer the name and figure out: why would a non-functional Rb protein (since the Rb protein is crucial to the cell cycle of all dividing cells in our body) primarily manifest itself in the form of an eye tumour? Is there anything special about the cells in the retina that make it more prone to developing such a tumour in relation to the function of the Rb protein?
Would anyone have any insight to offer?
Thanks.

From Wikipedia:

The retinoblastoma protein ... is a tumor suppressor protein that is dysfunctional in several major cancers

So, although it's commonly associated with retinoblastoma, it's not limited to a particular type of cancer.

Retinal cells are not sloughed off or replaced, and are subjected to high levels of mutagenic UV radiation, and thus most pRb knock-outs occur in retinal tissue (but it has also been documented in certain skin cancers in patients from New Zealand where the amount of UV radiation is significantly higher)

Since the gene is commonly damaged from UV radiation, the retina is particularly vulnerable. UV radiation does not penetrate very deeply, but the retina is exposed to light per its function.

Two forms of retinoblastoma were noticed: a bilateral, familial form and a unilateral, sporadic form. Sufferers of the former were over six times more likely to develop other types of cancer later in life, compared to individuals with sporadic retinoblastoma.[10] This highlighted the fact that mutated pRb could be inherited and lent support for the two-hit hypothesis

The two-hit hypothesis is the idea that often one functional copy of a tumor suppressor gene is sufficient. For people with familiar cancers involving tumor suppressor genes, including the BRCA genes associated with breast cancer, usually what you have are people who are heterozygous for some non-functional version of the gene. That means that they only need one "hit" to the functional gene to facilitate development of cancer.

pRb restricts the cell's ability to replicate DNA by preventing its progression from the G1 (first gap phase) to S (synthesis phase) phase of the cell division cycle

Because pRb is associated with G1 to S phase transitions, you wouldn't expect it to be as important of a gate in differentiated cells in G0; that's why you're finding it in a childhood cancer: the affected cells need to be immature and dividing to be affected.
In summary, Rb loss-of-function mutations occur via UV damage. To be vulnerable to this damage, a cell needs to be actively dividing and exposed to UV. The developing retina fits these characteristics. People who inherit one non-functional Rb copy are much more likely to develop cancer, because they only require additional damage to one copy of the gene, not two.


text:
A balanced diet with the minimum carbon footprint
Many studies shows that 1 kg of non-vegetarian food as 3-4 times more carbon footprint than 1 kg of vegetarian food. I think that does not represent the complete picture food from animal sources are rich in some nutrients. For example pound for pound fish will be much richer in protein than normal vegetables to so get the same amount of protein as from fish, we will have to eat lot more vegetables. So at the end of the day, the net carbon footprint of our protein requirement might be much closer between veg and non-veg food. Similarly for carbohydrates, cereals may be the most carbon efficient than any animal source.
Question: I am interested in a balanced diet with the minimum overall carbon footprint. Any reference or studies on what is the minimum carbon footprint with which we can get say 100 g of all the essential nutrients such as carbohydrates, proteins, vitamins, omega acids, saturated fats etc.

Can you provide a link to one or two of the studies you refer to so they can be evaluated for trustworthiness? Thanks.

I’m voting to close this question because I think it is concerned with dietary advice rather than Biology in the terms of SE Biology.

@David Sure but can you recommend any other stack-exchange site where this question could be more appropriate? Also, question is not a dietary advice which are everywhere but rather I am asking for a balanced which minimizes carbon footprint.

@anongoodnurse This link has a lot of details: https://ourworldindata.org/environmental-impacts-of-food

The carbon footprint really depends on non-biological factors, such as how your food is grown or harvested, processed, and transported to you.  If you eat fruit & vegetables grown in your own garden, or fish you catch yourself, there really is no carbon footprint.  If your fresh fruit is shipped in by air from another continent, and your fish is caught by a factory trawler working the Southern ocean, then the same diet has a very high carbon footprint.

Thank you for the link. I, too, found some interesting (and seemingly reliable) support for your initial statement.

This question may be on topic at the Sustainable Living site. https://sustainability.stackexchange.com/


text:
Are there any epiphytic plants that pull water from the air and supply terrestrial plants with excess?
Do you know of any epiphytic plants that pull water from the air and supply the excess to other terrestrial plants?

This isn't worthy of an answer but offhand I would HIGHLY doubt it. Pulling water from the air is harder than getting it from the ground; epiphytic plants are typically the type of plant that can survive on comparatively little water for that reason. I honestly don't see a circumstance where a terrestrial plant would need water from them, and where they could afford to spare the extra (but it's been awhile since I studied plants, so could be wrong).


text:
Why don't memory cells of the adaptive immune system get activated immediately after being created?
Why don't memory B and memory T cells of the adaptive immune system get activated immediately after being created?
As this video explains they are created in the heat of the battle. Aren't the conditions for activation there? What mechanism prevents them from being activated right there and then?


text:
Effect of toxin-producing phytoplankton on zooplankton?
I've been searching for quite a while without really finding an answer to this question, so I decided to try it here.
Some phytoplankton species produce toxins as a defense strategy. But what exactly happens to the predator, e.g., to zooplankton?
I've read that they may have a decreased reproductivity. But is there a faster effect acting as a defense mechanism such as phytoplankton sensing zooplankton, then producing toxins and zooplankton sensing the toxins and avoiding the area or similar? Otherwise, it would be quite a long-time defense.. If anybody knows something about this, please answer and give me a reference.
Thanks a lot!


text:
Why can't geese regurgitate food?
I saw this harrowing video on how barnacle goslings have to jump off very high cliffs because the parent's can't feed them. The death rate seems high. Why did natural selection come to favor jumping rather than the parents bringing food to the nest like most bird species?
From Wikipedia:

Like all geese, the goslings are not fed by the adults. Instead of
  bringing food to the newly hatched goslings, the goslings are brought
  to the ground. Unable to fly, the three-day-old goslings jump off the
  cliff and fall; their small size, feathery down, and very light weight
  helps to protect some of them from serious injury when they hit the
  rocks below, but many die from the impact.

This page mentions geese and sais they can regurgitate food: https://www.caspervanleeuwen.info/images/PDFs/Kleyheeg_and_Van_Leeuwen_2015_Aqua_Bot.pdf Geese prefer acorns and proper carbohydrate, and if there is not enough food and there's too far to fly, perhaps the geese and the chicks deplete themselves and don't consume enough to grow maximally. Those geese didn't find a good nest, they only need to be 10 meters high up the cliff?!

It means more food and faster growth; and higher chance of survival if they stay with the parents. It is explained for guillemots whose chicks (jumplings) jump off cliff also based on a study; thus it should be similar for barnacle geese. "Our measurements show that the male feeds the chick twice as much as both parents could if the chick remained in the colony," says Morten Frederiksen of Aarhus University in Denmark. Source: earthtouchnews


text:
curly braces in sequence motifs
what do curly braces in sequence motifs stand for?
e.g. in
RTCRYBN{4}ACG
what is N{4}? moreover, i notice that in TRANSFAC matrix notation the N{4} is completely omitted:
NA  Abf1p
XX
DE  RTCRYBN{4}ACG
XX
P0  A     C     G     T
01  0.500 0.000 0.500 0.000 R
02  0.000 0.000 0.000 1.000 T
03  0.000 1.000 0.000 0.000 C
04  0.500 0.000 0.500 0.000 R
05  0.000 0.500 0.000 0.500 Y
06  0.000 0.333 0.333 0.333 B
XX
P1  A     C     G     T
01  1.000 0.000 0.000 0.000 A
02  0.000 1.000 0.000 0.000 C
03  0.000 0.000 1.000 0.000 G

moreover the MEME suite's transfac2meme completely ignores the second chunk of the matrix after the P1 row.

I'm voting to close this question as off-topic because this is about the computational aspect of Bioinformatics. While questions on interdisciplinary subjects like bioinformatics are welcome, they must focus on the biological part of the subject.

@AMR I would not consider this as off-topic because it is about understanding data from a bioinformatics repository. It is not about programming or any other software issues.

@WYSIWYG It is not asking about the biology in any way. You could just as easily be looking at astronomical data. If they had asked how can I determine if a DNA binding protein will bind to this sequence or how can I determine if this is an enhancer site, then that is a biology question. This is purely from the technical side. Also mdperry's answer answers it, so there is no point in keeping it open anyway. It also shows no research effort, because all that is needed is to Google bioinformatics nucleotide codes and the first entry gives the answer. It could be closed for several reasons.

@AMR This question is about analysis of bioinformatics data, which is on topic (akin to bioinfo data formats).. I have worked in bioinformatics a bit and I can vouch that it is not some kind of an obvious thing.. Experienced people may look at it and know, but not everyone... AFAIK we made it clear that this may not be not one of the close reasons..

@AMR your comments are unfair -- i have tried to answer this question myself. your googling suggestion does not answer my question as i already knew what 'N' stands for but not the {4} bit.

N is the IUPAC code for any nucleotide, so in DNA sequence an N signifies any one of the four bases could be in that position.
The {4} means 4 of the previous character in the pattern, or NNNN. In Perl regular expressions \d{4} means match 4 digits in a row, so the notation is quite similar.

thank you for your answer. i knew what N stood for but i couldn't find what curly braces meant. i guessed that could mean NNNN but then it doesn't explain why the TRANSFAC matrix for the motif ignores these nucleotides. moreover there are motives like TNNCGTNNNNNNTGAT in the same document. why isn't the same notation used here? i.e. TNNCGTN{6}TGAT?

As to why some people prefer using curly braces vs. expanding the characters and printing them all, I have no idea (or why some programs or databases prefer one or the other). I have not used TRANSFAC very much at all; as I recall it requires a licence(?). I think what is important to keep in mind is that using a consensus sequence (the IUPAC codes) is generally not going to be as sensitive as using a Position Frequency Matrix (PFM) or a Position Weight Matrix (PWM). That matrix you show is not a real PFM/PWM--it is a PFM derived from the consensus sequence motif.

it's a TRANSFAC formatted file in the Yeastract database which is open to public; and it just seems that they are being inconsistent with regards to their notation in the same document then. okay, i didn't realise i was using something that was't a real PWM. when you say 'less sensitive' do you mean using it for binding site predictions won't be as accurate as using the real PWM?

Let's say that there are between 10 and 100 known Abf1 binding sites in the Yeast genome. By lining them up (aligning them to each other, and summing up the number of each nucleotide at each position, and then dividing that number by the number of sequences in the alignment) we get the PFM. A simple way to create a PWM (circa 1990) is to multiply the value at each field in the matrix by the log(base 2) of the number, (m x log2(m)). (there are probably much more sophisticated transformations available now). Now you have a way of calculating the bits of information at each site in the matrix

With a PWM you can use a program to scan along an entire chromosome, giving each site a score. If you do this (make a PFM and a PWM) do you get the matrix from TRANSFAC? If you do, great, but if you don't then you might well get more 'hits' with the real PWM. Keep in mind that without experimental confirmation of some sort none of these predicted binding sites are necessarily real binding sites, they are just sites that score above some arbitrary threshold.

apologies for a slow response -- many thanks for your clarifications! i think a PFM should be sufficient for my needs; i have used them to identify potential binding sites and got 2.5k (at 0.05 q-value) using the FIMO software. knowing even putative binding regions should be enough.


text:
Is 100% antibacterial resistance possible?
The quest to develop antibacterial and antibiotic substances has often been described as an arms-race, as bacterial life develops resistance, requiring us to develop novel agents which can effectively kill said microbes.
My question is: is it at all possible for a single microorganism to develop resistance to everything we can possibly develop?
There is only so much information-capacity in microorganism DNA to encode the means of resistance to various substances. If we climb the arms-race ladder high enough would a highly-advanced bacteria somehow "forget" how to defend against penicillin, for example?
...or are we utterly boned?

If there is no advantage for a MO to be resistant to a certain antibiotic, it will very likely loose the resistance over time. Problem is we need to collectively not only stop using penicillin, but likely the whole class of penicillin-derived antibiotics for that to happen. No easy task.

When you look at individual bacteria, they would forget how to defend against particular types of antibiotics. Growing in the absence of penicillin, most of them would throw away the resistant genes. The problem is that even very small population among them still carries the resistant genes and they would become dominant when they met penicillin.

This is a theoretical question, which I can't answer, because genetics is not my favorite topic. In practice we only have about a dozen antibiotic classes. There are already panresistant bacterias, which are resistant (as far as I know) all of these classes of antibiotics, so we have already lost.
The causes of our defeat is more interesting I think:

Pharmaceutical industry does not have enough interest in the antibiotics research, since it is not as profitable as for example cholesterol reducers. Antibiotics are cheap, and you usually heal after the first treatment, while the research and the clinical trials are really expensive, it is hard to find working chemicals, which do not have severe side effects.

“We  need  to  shift  from  the  concept  of  the  pharmacy  as  a
  ‘shop’  and  build  a  culture  of  pharmaceutical services. This is
  already happening  in some countries, but we need to make it  the
  rule  everywhere,”  says  Zsuzsanna  Jakab,  WHO  Reg ional  Director
  for  Europe.  “As  pharmacists  dispense  medicines  to  patients,they
  are   important  allies  in  our  fight  against  antibiotic
  resistance.  As  such,  they  need  to  be  ena bled  to  deliver
  accurate  information  and  counselling on proper antibiotic use.”
Over  40%  of  antibiotic  prescriptions  are  inappropri ate,  recent
  studies  found.  This  relates  especiallyto antibiotics prescribed
  for the common  cold and sore throat; these most oftenresult  from
  viral infections,on  which antibiotics have no  effect. Further, in
  some countries, there is  atendency towards self-medication.
  Inappropriate an tibiotic use is the major driver of growing
  antibiotic resistance.

Pharmacists have decisive role in combating antibiotic resistance, says new WHO European survey
People with Mycobacter infections does not always do the treatment long enough, so Mycobacters can become resistant to antibiotics.

Most people with TB are cured by a strictly followed, six-month drug
  regimen that is provided to patients with support and supervision.
  Inappropriate or incorrect use of antimicrobial drugs, or use of
  ineffective formulations of drugs (e.g. use of single drugs, poor
  quality medicines or bad storage conditions), and premature treatment
  interruption can cause drug resistance, which can then be transmitted,
  especially in crowded settings such as prisons and hospitals.

http://www.who.int/features/qa/79/en/
There is no global regulation of how to use antibiotics, so in some countries you can buy them without consulting a doctor and get a prescription. On top of this you can buy antibiotics without prescription on the internet if you want. This leads to overuse of antibiotics, and overusage leads to resistance.

Self-medication is more common in developing countries due to factors
  such as ready availability of antibiotics without prescription, the
  unrestricted access to antibiotics,lack of regulation over drugs, and
  physicians and pharmacists prescribing and dispensing antibiotics
  without regard to the cause of infection

http://article.sapub.org/10.5923.j.cmd.20110101.02.html#Sec3.3.4

We found 138 unique vendors selling antibiotics without a
  prescription. Of those vendors, 36.2% sold antibiotics without a
  prescription, and 63.8% provided an online prescription. Penicillins
  were available on 94.2% of the sites, macrolides on 96.4%,
  fluoroquinolones on 61.6%, and cephalosporins on 56.5%. Nearly all,
  98.6%, ship to the United States.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746509/

These results demonstrate that, although illegal, the sale of
  antibiotics without a prescription continues in Spain.

http://cid.oxfordjournals.org/content/48/10/1345.full
Some of the antibiocstics are used by agriculture industry, which leads to antibiotics resistance as well.

They identified bacteria able to shrug off the drug of last resort -
  colistin - in patients and livestock in China.
It is likely resistance emerged after colistin was overused in farm
  animals.

http://www.bbc.com/news/health-34857015

Nutritive and therapeutic treatment of farm animals with antibiotics,
  amounting to half of the world's antibiotic output, has selected for
  resistant bacteria that may contaminate the food produced.
  Antibiotic-resistant enterococci and staphylococci from animals are
  found in food when they survive the production processes, as in raw
  cured sausages and raw milk cheeses1. The broad host ranges of some
  plasmids and the action of transposons in many bacteria allow
  antibiotic-resistance genes to be communicated by conjugation between
  different species and genera2,3. A multi-antibiotic resistance plasmid
  from a lactococcus found in cheese provides a historical record of
  such events.

http://www.nature.com/nature/journal/v389/n6653/abs/389801b0.html

About 2/3 of the antibiotics are used in animals.

https://youtu.be/iLJAleLjJv8?t=3m47s

So the problem is with not enough motivation in development and the lack of proper regulation of usage. Regulation is the business of the politicians, so its their fault as always. :D

A lot of theorizing about motivation makes for conspiracy-theory-like thinking (Big Pharma, etc.) Some sources to back this up might be nice.

@anongoodnurse I did not add the sources, because it is hard to find in the browser history, but if you really need it, I'll update my post.

@anongoodnurse I still cannot find the documentary about the "big pharma" I wanted to link. :S According to some comments I watched it in march 2015.

I think this is a better answer now; had already upvoted, so can't do so again. I know documentaries can be pretty convincing, but they are not always truthful (honest.) I saw one on a cardiology issue which was so convincing that had I not known for a fact that it was false, I would have had serious doubts about my profession. As it is, I don't know why the makers haven't been sued, but ?

@anongoodnurse It contained reports with pharmaceutical engineers and managers from different pharma companies. They claimed, that they stopped antibiotics research because it was not profitable enough. Currently some countries try to make a difference by giving some money for the clinical trials, so it is certainly not fake.

I won't say anymore after this, but I think you have to be almost as careful about  what you believe in the media as on the internet. Now I sound like a conspiracy theorist!

@anongoodnurse :-)

I can't really give hope because a video is not a good reference. But towards the end this video claims that bacteria cannot be immune to both both bacteriophages and antibiotics at the same time. So bacteriophages might help us win provided they don't cause some other disease. https://pubmed.ncbi.nlm.nih.gov/24619620/

@anongoodnurse

My question is: is it at all possible for a single microorganism to develop resistance to everything we can possibly develop?

If you are only discussing antibiotics, the answer is, yes, it's theoretically possible but very highly unlikely, as different classes of bacteria have different characteristics that allow resistance to certain antibiotics to develop.
For example, if a bacteria doesn't have penicillin-binding proteins -  allowing cross-linking and stabilization of the bacterial cell wall - then resistance to this antibiotic which makes susceptible bacteria unable to synthesize their cell walls - is meaningless, so unlikely to happen (except through sharing of useless genetic material, which does have limiting factors.)
If you're discussing all antimicrobials (and you consider something like bleach an antimicrobial), the answer is "no".
The danger isn't that a microbe will be resistant to every antibiotic. The danger is that it will be resistant to enough of them to cause a significant problem. It takes time to test for antibiotic sensitivity; in the meantime, a person with an infection that needs antibiotic treatment is getting sicker. Labs start testing for antibiotic sensitivity with antibiotics that the identified organism is usually sensitive to. If that fails to reveal sensitivity to an antibiotic at acceptable levels - one option is to increase the amount of antibiotic given - new tests need to be carried out, taking even more time (for antibiotic combinations or "atypical" antibiotics). It's possible that an antibiotic (or combination) will be ascertained only after that person's death.
Staph aureus has lived closely with man for I don't know how many hundreds of thousands of years. Most of the time, it's presence is benign. It's only when it becomes invasive that antibacterial resistance is a factor in dealing with it.
Antimicrobial Resistance Learning Site Although this is a veterinary site, it's clear and informative, and, though most people are unaware, use of antibiotics in feed animals - which falls under veterinary medicine - is a major contributor to development and spread of antibiotic resistance.

A 100% antibacterial resistance is a very dangerous situation, which would mean that the age of antibiotics will be over. To achieve a total resistance the microorganisms would have developed new ways of mutation, transferring genes between them, rapid cell damage repair. It would mark a new step in the evolutionary process. There has been many questions as to whether the age of antibiotics have come to its end or not, but the demand has never been this high. its a very scary scenario, a ticking time bomb.

The age of antibiotics will never be over. There will be new antibiotics, and there will be fading resistance. But a lot of people will die from once-treatable infections. That's different


text:
Pen and paper game to explain the theory of evolution
Sometimes when explaining the theory of evolution one sees a glazed-over look on the persons face. To this person the theory seems completely incomprehensible no matter which avenue one takes to explain it. This leads me to think that a game might be a fun alternative. In the process of playing, I suspect that the player might pick up a stronger intuition of how and why it works which would eventually lead to understanding the basics as a whole.
It is easy enough to dream up any number of problems that can be presented as a genetic algorithm with pen and paper, the challenge however is to make it easy to understand and fun to play.
Does anyone know of such a game or able to construct such a game?

I'm voting to close this question as off-topic because it is asking whether people know of, or know how to create, a game and not about biology.

I think this question can be carried forward in the chat?

The theory of evolution is a big umbrella term for a whole lot of concepts and evidences. What exactly are you trying to explain (genetic drift, natural selection, sexual selection, common descent and the logic of phylogenies, coevolution, ...)?

If you are having a hard time to explain it, maybe you don't understand much of it (no offense, I have no idea about your level of knowledge). You might want to follow an intro course such as understanding evolution for example Sometimes, the resistance of some people to understand anything is a failure to understand the basics of philosophy of knowledge as well (such as the fight between a whole bunch of evidence and a naive intuition shaped by a cultural environment).

@Remi.b, by explaining evolution, we should probably start with the basics. So, optimisation using mutation, selection and reproduction. As for the possibility that I do not understand evolution. I am pretty sure that I do, I use it often in Computer Science in the form of genetic algorithms to a good degree of success. Furthermore, I do quite a bit of reading on the topic as well, so it seems unlikely to me that I don't understand it.

@terdon, If you insist that we close it as off topic then it is fine. I would however like to know under which topic you would group it if not biology?

Game design, I guess. You're not actually asking any biological question here. You're asking if i) anyone knows of such a game (which is off topic anywhere on the SE network since we don't do such open-ended questions) and ii) can anyone make such a game or, presumably, how to do so. The latter might be on topic on [gamedev.se], but I don't know their scope well. I'd check before posting there.

@terdon, I was thinking more along the lines of education in biology, since the main idea is to educate and it is about evolution. But I suppose game design might fit as well.

http://www.abandonia.com/en/games/4996/simlife.html

Related question in Meta Bio-SE: Questions about teaching biology: off limits?. Personal, I think your question could be on-topic, but it is currently a bit broad and vague.

Not sure if this qualifies as pen-and-paper, but one game I am familiar with to highlight natural selection goes something like this:
Materials:
Creatures - Small paper pieces of different colors from construction paper - hole-punch remnants work great, or you could cut squares
"Habitats" - Large, colorful surfaces. Whimsical maps work well for this, maybe certain posters, the important thing is to have some diversity.
Gameplay:
This is ideally done in multiple groups, each group should start with an equal ratio of creatures of at least two different colors.
One or more people spread the Creatures around the Habitat.
Another student (or multiple) act as the "predators". They sit/stand above the board and close their eyes; then they open their eyes, and harvest the first Creature they see. Close eyes again, and repeat until 1/2 of the Creatures have been eaten.
Count up the paper pieces and note the number of each remaining; for the next Generation, the Creature makeup should be 2X the number of remaining pieces: so if there are 30 Blue and 20 Red remaining, the new generation is 60 Blue and 40 Red.
Repeat over a few generations - the result should be that different habitats lead to different proportions. You can also change things up by suddenly shifting the habitat!
You could possibly include genotypes and recessive traits for an older group (the version I suggested is effectively haploid parthenogenesis), these might be harder to keep track of.
(I don't have a citation for this game but if anyone knows it, please provide in the comments!)

You could adapt this into a battleships-like game, where the predators choose squares at random, based on dice rolls, and the prey (of different sizes) occupy spaces on grids. If each prey is "killed" when any part of it is selected by a dice roll then, over time, you'd expect the smaller prey to outlive the larger ones (demonstrating natural selection due to a selection pressure). You could also show that predators that are allowed more dice rolls stack up more "kills" and maybe incorporate some kind of resource that's gained from a successful kill.

@Jam Yes I am sure there could be many variations. One that is nice about the variant I suggested (and that pairs well with your suggestion on the other question about moth coloration) is that it is very straightforward to change the environment and see the results. If you start with a map/"habitat" that has a lot of red on it, the red creatures are likely to survive preferentially, and then you move to a map with mostly green and suddenly red isn't such a good color any more. It's also fun in groups because different groups will get different answers depending on their "habitat."


text:
How do I construct sample-based rarefaction curves if the area (or volume) sampled is not consistent between samples?
My apologies if a similar question has been asked previously but I cannot find an answer.
I have data from multiple zooplankton tows from different study sites and I am trying to construct sample-based rarefaction curves for each site. So, number of samples on the x-axis, number of species on the y-axis.
However, nets were used to sample the plankton and the volume of water for each sample is not consistent.
How can I adjust the curves to account for the variability in sample volume? Can I replace the x-axis (number of samples) with the average volume of water sampled per tow?


text:
Smallest animal that produces food for humans
I was thinking about how bees can produce honey and human can eat it. After that I came up with question. What are the smallest animal that can produce food for human?

It would depend on what you consider food, but if you consider things that contribute to food substances (e.g. food dyes) then cochineal scale mites are only about 5 mm (0.2 in) long and produce a red dye that is commonly used as a food colorant.
There are also several ant species of similar size that are eaten as food sources. For example, Liometopum apiculatum (6-7 mm adult) grubs are/were harvested as a food source in parts of the USA and Mexico.

I cannot find the size of Chaoborus edulis but they might be a contender: Kunga cake.

@Roland I knew of that one, but didn't know the name or which region of Africa it was from, so I didn't try to find it. You should write your own answer based on this. Bugguide.net suggests 8-10 mm for the genus.

I'll throw in my 2 cents and say fungi, especially yeast (or other fungi used for blue-cheese etc.), typically measuring 3–4 µm in diameter and could be perceived as 'producer' since it's converting sugars via fermentation..

@iLuvLogix That's not an animal as OP requested.

@bob1 Thanks for pointing that out - a quick search revealed that they seem to have a seperate kingdom of their own (besides plants and animals) - my bad..


text:
Can We Determine the Cell Types Ab initio?
Is it possible to find all cell types in the human body and their respective transcriptomes by analyzing the human genome (and doing no physical experiment)?
If such a thing is possible in principle, how close (or far) are we from achieving it? Is there any active research in this area? And what is the name of this research area?

No.
Cell types are identified by differential gene expression. Every cell has (effectively) the same genome, but different expression patterns give you different functions.
You could attempt to identify cell types from gene products: the transcriptome (RNA) or proteome (protein), though there would be some challenges as cells we typically consider of one "type" do not necessarily have the same transcriptome/proteome at various time points. A neuron, for example, is distinguishable based on recent activity (for example Benito, E., & Barco, A. (2015). The neuronal activity-driven transcriptome. Molecular Neurobiology, 51, 1071-1088.).
"Cellular differentiation" is the general topic of studying how cells become different types.
Note that even if you attempted something like this (and I'm sure someone has, though likely in some narrower field like deciding whether some cell type should actually be considered multiple types), you'd still need to rely on experimental evidence to verify the result. We're nowhere near being able to abandon actual biological systems in studying biology, and I'd argue it's not even something we should be attempting to do.

Yep, every time someone has said "XX science is dead, nothing left to discover" as has happened in Biology a few times (including with the advent of whole genomes), they have been completely and utterly wrong!


text:
Hi, could someone explain what use-dependence is? And does it differ from one drug type to another? For instance anaesthetics vs anti-epileptics?
I may have understood it incorrectly but I read that in case of local anaesthetics, the use dependence is such that more the number of open sodium channels, more the number of drug molecules entering, leading to increased inactivation. Whereas in the case of antiepileptics, the drugs bind to the sodium channels in its inactivated state and decreases number of available sodium channels to allow AP to pass through. So what exactly is use dependence?

It's best to support your question with things you've read (and it's an expectation on this site to provide evidence of prior research before asking) - where are you reading about use-dependence in local anesthetics? Where are you reading about it with anti-epileptics? Cite sources, use short quotes if relevant: what specifically are these sources saying and where does the uncertainty arise?

I would think that this question is more suitable for SE Medical Sciences (after taking heed of Bryan’s remarks).


text:
Why do bacteria in a urinary tract infection (UTI) cause bleeding?
It seems that when a urinary tract infection happens, bacteria will cause inflammation to the lining of the urinary tract, and this will cause bleeding.
What is the exact process for the inflammation to cause bleeding? Is it because the lining expands too much and the tissue tears as a result? Or do bacteria interfere otherwise with the cells of the lining?

The process by which bacteria in a UTI cause bleeding is that the bacteria cause inflammation of the lining of the urinary tract. The inflammation can cause the blood vessels in the lining to become more permeable, allowing blood to leak into the urine.
Inflammation causes blood vessels to become more permeable by increasing vasodilation, weakening the endothelium, and releasing inflammatory cytokines such as histamine and bradykinin. This leads to increased vascular leakage and disabled intercellular junctions, resulting in increased paracellular permeability (see references 1 and 2).
The increased permeability of the blood vessels can also make them more fragile and prone to rupture, leading to further bleeding. In addition, bacterial toxins produced during a urinary tract infection (UTI) damage the cells of the urinary tract lining by inducing host cell damage and releasing essential nutrients that promote bacterial survival. This can cause additional bleeding (see reference 3).
In some cases, severe UTIs can also spread to the bladder or kidney, where they can cause more tissue damage and increase the risk of bleeding, which makes treatment of these infection important (also reference 3).
References:

Inflammation
Vascular permeability—the essentials
Urinary tract infections: epidemiology, mechanisms of infection and
treatment options

Upvoted this last Feb. but just noticed first sentence of last paragraph. Just fyi in case you want to correct it. Usually when we dx "UTI", it's a bladder infection. That's usually not serious at all (except to the poor soul who has it) and it's as common as dirt. When it's in another part of the urinary tract, while technically a UTI, it's either urethritis (far less common unless it's from an STD) or pyelonephritis (less common but still common.) I've only seen ureteritis once in my career. Delete once you've read this.