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How do I "reinoculate" a petri dish with new bacteria?
Hypothetical question, intended to find a general procedure rather than case-specific recommendations:
I have a petri dish full of growth medium with a large population of gram-negative, anaerobic bacteria of numerous types growing in it. How would I go about replacing the existing population with lactobacillus and streptococcus strains?
Rules:

The growth medium cannot be washed out of the petri dish
The petri dish cannot be treated with anything a human body can't handle, i.e. no blasting with bleach
After the procedure is complete, the original bacteria should have little to no chance of returning, even given months or years in the petri dish

Why would you want to do this? In the lab, you would simply throw the plate away and make sure it is autoclaved and you set up a new plate with the bacteria of interest.

Don't worry @Chris, I'm not running low on plates. The lab exists for the very purpose of modeling the real world, and yet in the real world you can't autoclave the environment. I can't for the life of me figure out a good way of replacing the bacteria in a real-world environment, so the purpose of this question is to discover how a trained biologist with years of experience and a touch of creativity would go about this. Think of it as a thought experiment

Ah, ok, I wasn't sure of the purpose, thats why I asked.

Nobody has tried a procedure like this. Perhaps you can wipe the surface clean and wash it repeatedly with an antibiotic solution (a bactericidal one like streptomycin) + hydrogen peroxide (since the bacteria are anaerobic). I think all answers will be based on guess.

@WYSIWYG wiping the surface isn't allowed, as that wouldn't be possible in the equivalent real-world environment

@TheEnvironmentalist then washing would be allowed right? Depending on what the tissue is wiping might be feasible.

@WYSIWYG imagine the surface as something between a sponge and a rubber pad. Not very wipeable, unless you're being particularly creative


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Extremophile hunting and identifying unknown microbes
I'm going extremophile hunting! We're doing a trek by boat between some islands with semi-active volcanic terrain to try to document some interesting species, and running into a problem I've never tackled before.
Usually I'd send samples into a lab for genetic analysis, and then go from there, but in this case we won't be able to get samples to and from the lab until the end of the trip. At that point we won't be able to go back and follow the most interesting organisms without a second trip.
The temptation is to bring along whatever equipment we need for our mobile lab and do the genetic analysis on-site. Space and budget are at a bit of a premium, so I thought I'd ask the community if anyone has any good ideas for microbe identification on the go. We'll have power and refrigeration and even a small amount of freezer space, though no -80C freezer. We're most interested in extremophilic fungi, though I'm sure we'll find other interesting things along the way.

If you have some money: portable -80. Approx $8K. I've heard good things, but never used one. We'd need a bit more info - just trying to ID (sequence?)? Want to culture?

If "identification" is your goal, I would suggest a MinION sequencer and associated equipment for library preparation. These are capable of generating large informative reads for e.g. metagenomics/isolate sequencing and are extremely portable. They have field sequencing kits, and there have been papers evaluating use in the field (see also here).
If your goal is "bring them back", then bob1's comment about a portable -80º is probably the more pertinent piece of equipment.

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How many protons are pumped into the intermembrane space by Complex IV in OXPHOS?
According to Sazanov (2015), "to reduce oxygen to water, four 'chemical' protons are taken from the matrix side [...]. In addition, four protons are pumped across the membrane into the IMS". A similar statement is made in the review by Vercellino & Sazanov (2022, pp. 152–3).
How is this compatible with only 10 protons being pumped into the IMS in total and only 2 by Complex IV (see also How many protons are pumped out per pair of electrons from NADH in oxidative phosphorylation?)? Does the number of 10 perhaps simply result from the assumption of a 10/3 H+/ATP ratio? What am I missing here?
(the literature on H+/2e- stoichiometry, if anything, added to my confusion)

*10 H+ per molecule NADH

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Formation of xylem
Does metaxylem forms from protoxylem?  Or they develop independently? My main motif is to clarify, " Is metaxylem just a more developed protoxylem? "


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Knock-Out (KO) Mice
We have generated an induced KO mice line for a specific gene. However when i perform IF staining I can still see substantial levels of the protein for this specific gene produced, even though the Genotyping results indicate that the gene KO was successfully performed. Did anyone else have the same problem? or can you think of a plausible explanation to this problem? Thank you in advance!

How is the knockout induced? When was it induced? When are you measuring protein?

Mice are induced by a 16 day administration of doxycycline via the drinking water. The study model is then initiated after a 7-days wash-out (restore to normal water) phase. I measure the protein at day 10, so in total 17 days after the interruption of induction.

How are you measuring protein levels? What controls have you performed?

At the moment, running the initial phase of the experiments, we are comparing the protein expression to the wild type animals by performing the same IF staining on both groups. The protein signal is not significantly different in KO mice as compared to the wild type ones.

Are the knockouts homozygous? Is the antibody known to be specific enough for this particular protein, without affinity to related proteins? Do you know anything about the half-life of the protein?

Yes they are homozygous and the antibody does not have affinity to other related proteins

Based on previous studies we have eliminated the possibility that it could be caused due to the short half-life of the protein.

Well, a long half-life would be potentially more of a problem here than a short one... I'd recommend using other methods to identify your protein and measure gene expression and see if they agree. Maybe start with PCR. Possible issues I can think of are that your mice are not actually KO mice; maybe they have a separate working copy of the gene you're targeting even if your construct is present. Your induction isn't working: wrong concentration of doxy, animal care staff are exchanging with normal water, etc. Or measurement: cross-reactivity, non-specific binding, etc.

what is the actual mutation, it's a degron construct or something? Can you exclude e.g. stop codon readthrough if not? having RT-PCR data might help if the KO is DNA/transcriptional. Do you have Sanger data of the chromosomal locus to exclude the possibility that the mutation is wrong? Antibody cross reactivity is also a good note, especially in the case of a functional paralog or something.


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Why are recombination rates increasing in mammals?
I have recently become fascinated with an awesome topic in biology and evolution that I feel is rarely covered in biology courses. That is, rates of meiotic recombination, or the the amount that an organism's genome is reshuffled before it is passed on to the next generation, varies across species! And no one really knows why.
A recent paper by Segura et al which gathered average recombination rates for males across a dozen or so mammals and showed that there is a trend of increasing recombination rate with mammalian divergence.
Why is recombination increasing through mammalian evolution? Is there any reason to believe that there is something special about placental mammals which would drive increased recombination?
There are some catches to this study such as low sampling of marsupials and monotremes and low power for most of species wide recombination rates, ie the average recombination rate of cells in a single individual. But I can see how getting samples from multiple tigers would be difficult.

If rates of meiotic recombination DIDN'T vary across species - THIS would require an explanation! After all, evolution creates diversity, not homogeneity.
I can only wonder that more recombination would allow for a faster diversification. The more DNA you shuffle, the more distinct each individual offspring may be (though I'm not 100% sure). The recombination rate has an energetic price, so not all animals recombine so much their DNA like later mammals. I.e. they needed a selective pressure to justify paying that price.
Perhaps it was useful for a group rapidly occupying the "vague niches" left by dinosaurs? This make sense, since the primary mammalian irradiation occured in the beginning of the Cenozoic era, right after the Cretaceous mass extinction that killed most big animals, including the biggest dinosaurs.
Unfortunately I have no references on the subject, it is just what makes sense to me, given evolutionary logic.

My logic would rather tend to predict that high recombination rate should rather be correlated with low speciation rate. Absence of recombination will lead chromosomes to diverge over time.

Yeah, it may be, though I'm not sure exactly how this divergence will happen? Can you explain it better? And is it chromosomic divergence the main genetic cause of speciation in mammals?

With low recombination chromosomes diverge following the same logic that makes two non-interbreeding population to diverge through time (just by the neutral processes of mutations and drift).

Does chromosomal divergence cause speciation? Intuitively, I'd say yes. Assuming that chromosomal divergence would yield to outbreeding depression (OD), then OD causes post-zygotic isolation which causes a selection pressure to increase the pre-zygotic isolation. I have absolutely no idea however of whether such mechanisms is an important factor to explain speciation in mammals and I might be wrong assuming that chromosomal divergence causes OD.

thanks for the input. After comparing rates across species, (which there are few), it seems to me that recombination rates maybe evolving too quickly to compare very deeply in phylogenetic trees.

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Division of proteins
This textbook states

Proteins determined by a single gene may divide to form different proteins with various physiological actions.

First how do proteins divide? Second if it's just fragmentation then what is this process called? Third since my textbook doesn't explain it could anyone explain with an example of how different parts of original protein( considering that protein has divided by fragmentation) perform different physiological actions?

This is not a very helpful passage, I agree.  Some proteins are cleaved by other proteins (a protein that cuts another protein is called a protease).  Other proteins cleave themselves.  Otherwise, proteins are quite stable and don't just fragment wily-nily.
In the case of the first group (proteases acting on other proteins) the coagulation cascade may be a good place to start for you.  Precursor proteins in this pathway are converted to active enzymes by a chain reaction of protein 'division' and other protein modification.  This page has other interesting cases of this process, such as in food digestion, which may be what you're looking for.
Some of the second group are self-cleaving such that an intervening sequence is removed, and the ends are pasted back together.  (This is analogous to how introns are spliced from messenger RNA and the exons are spliced together.)  Such intervening protein sequences are called 'inteins'; the removal of one intein can generate one functional protein, so this isn't protein division.    However, some viruses encode self-cleaving regions that will split the mother protein into two or more pieces.  A famous example of this process, now used widely in biotechnology, is the 2A peptide, which is used to 'split' a single transgenenically-expressed protein into 2 (For instance if you want to express a protein and a marker such as GFP simultaneously, you could employ the 2A peptide to link these together.)
The first group may be of more interest to you because of the known role of these proteases in human health.  Also, in your question it sounds like you also may be referring to random 'fragmentation' of proteins, which is not currently known to be an important contributor to protein breakdown in the human body, even in the stomach.  Enzymes such as pepsin are responsible for digesting proteins.

Good mind reading! The use of the word ‘divide’ here makes it clear the author of the book knows little or nothing about this subject. Not too suprising in  a book on physiology. The questioner should be warned.

I don't have access to the textbook, but my first thought is that the author is talking about gene duplication during evolution. If a gene duplicates, the two copies may end up diverging, creating two similar but slightly specialized proteins that fulfill different functions.Wikipedia
I agree that the sentence is not well written, whatever the intended meaning. Some context may be helpful.

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What are negative and positive after potentials?

After depolarization: is the slow repolarization phase which follows a rapid fall in spike potential and extends up to attainment of the RMP level. It is called phase of negative after potential and lasts for about 4 ms.
After reaching the resting level (–70 mV) the potential further falls and becomes more negative (–72 mV).This phase is called after hyperpolarization or phase of positive after potential.

What is the reason for naming them as negative and positive after potentials?
My attempt: I think we are naming them based on the direction
of current, i.e. during after depolarisation membrane potential is going further negative , so the name negative after potential, and during after hyper polarisation, membrane potential is going from hyper polarised state to resting state, so its named as positive after potential.
Am I correct?

Source:Textbook of physiology

Yes, you are correct. The negative current is hyperpolarising the axon and the positive current is returning it to baseline from a hyperpolarised state.
They are often referred to as inward/outward (negative/positive respectively) currents as well, due to the direction of the flow of ions. Which is further compounded when you start looking positive/negative ions.
Inward currents are inflow of +ve charge, or outflow of -ve charge.
Outward currents are vice-versa.

One doubt: we can see that during After hyperpolarization phase only last half of curve is having positive slope ( so positive current) then what about initial half in which curve is having negative slope( so negative current).

I'm not sure I follow, from your source, the trace drops to about -72mV immediately before point E. The bit from where it crosses -70 to E is the negative after potential.

Ah! got it, I was just confused by the Fig2.1-12 on pg52. Thanks.


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Can Nikon biological microscope model SE be converted to a digital microscope?
I am looking to buy a second hand microscope but I'd like to replace its eyepiece with a digital sensor. I am specifically looking at this Nikon stereo microscope Model SE. I asked the seller but they simply said they're not sure if we can remove one of the eyepiece lens or not.
I'd like to use a sensor like this: https://www.opticscentral.com.au/celestron-5mp-microscope-digital-imager.html

Seems like a good question for the camera seller.

I don't know about every Nikon stereoscope, but I know that the Nikon SMZ-U which I have, supports both replacing eyepieces with cameras, and a dual camera port accessory. But you would need to check the manual for the one you are looking at.
Even if it doesn't directly support using a camera with it, you can use afocal/eyepiece projection, to use it with a camera, though this often comes with reduced image quality.

@BryanKrause As I mentioned, the seller didn't know the answer. Either he is not familiar with microscopes or he didn't bother to check :(

@Topcode So that's like an adapter that sits on top of eyepiece and project to camera? That's good point... I did a search and I found many for telescopes but not sure if it works with microscopes too... I don't see why not tho. Thanks!

@xbmono The ones for telescopes should work, as long as you can get one the correct size for whatever eyepiece is on the microscope

Short answer is yes, with a few caveats.
In general you can use a camera of any sort with a microscope if you have the right adapters and mounts. You can even manually hold a camera and take photos with the eyepeice in place, though it is difficult and hard to get good images due to you moving and the narrow window of focus with a microscope eyepiece. So, basically all you need is that the camera is held steadily at the optical focus point or has a lens mounted on it that will compensate for the eyepiece if removed. You can even get mounts that are designed to hold a cellphone for taking photos. These often have a lens in a tube similar to the eyepiece and support your cellphone via fitting into the eyepiece tube.
The camera you mention has this to say in it's advertising blurb:

The Imager will replace any standard 23mm or 30mm eyepiece on your microscope

The camera is made by Celestron, which is a good, reliable brand for telescopes and cheaper microscopes, so I think it will be a reasonable camera, though probably no better than your cellphone camera.
It looks to me like it comes with an adapter designed to centre the camera down the eyepiece tube and to fit it into the eyepiece tube (images 2, 4, 5 on the page; small black ring with 3 brass screws coming out of it). Whether this adapter will fit into your microscope will depend on the dimensions of your eyepiece.
I note that their images have it mounted on a monocular microscope, but this also shouldn't be a problem; eyepiece lens mounts are fairly standard for a given brand.
One thing to be aware of is that if you have a binocular microscope, you will need to remove the camera if you want to use the eyepieces, unless you can cope with looking down the microscope with the wrong one eye (e.g. camera in left eyepiece will mean you need to look down the right one with your left eye so your head doesn't bang into the camera). You should be able to remove the camera and place it carefully on a bench to use both eyepieces, but you should be careful to not bump it too much (knocks it out of alignment) and aim to not get dirt (fingerprints etc.) or dust on the sensor/lens end - storing in a box/case will be fine though.
I also can't tell if there is some method of preventing dust from getting down the adapter tube for the camera and into the microscope (you definitely want to avoid this!), though this should be minimal anyway. Given that it is Celestron, there's a good chance they have thought of this and have something in place.

Thanks for the complete response. Do you know if the eyepiece of Model SE can be removed or it's fixed? I'm worried, I buy it and the eyepiece is fixed in place or is it standard for all microscopes to have removable eyepiece? Unfortunately the seller didn't know the answer, either he wasn't sure or he didn't bother to check

@xbmono I've not used that particular microscope model, and would need a more complete model number to be able to tell you for sure. However, in my experience, Nikon makes high-end microscopes, which means you get things like functionality to change eyepieces as you like. You may have to unscrew a holder screw, or maybe even unscrew the eyepiece lens (rare, typically microscopes from 50's-60's), but generally these are held in by friction and being angled above horizontal.

I finally bought it and as you said, the eyepiece can be removed, easy! I also tested it with my DSLR camera and a adapter tube I had for my telescope and handheld it because the tube it's a bit large.. but it works fine. I just need another tube with smaller diameter for this microscope.


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When Rain Lilies Bloom
I have had the Pink Rain Lilies in a large pot for over 10 years. In that time span, I have noticed it doesn't matter how much water, or what kind, is given to them, I water them daily in warm weather. They do not ever bloom unless there is a storm. For instance, I am in subtropical Queensland, Australia and a few nights ago, we had an electrical storm. It started 4 nearby fires. I heard a couple of drops of rain on the roof, but it stopped as fast as it started. Where my pot of lilies is sitting, I doubt a rain drop even fell on them. I have experienced these kinds of dry storms many times in the past, it's very typical here. The next morning, there was a Pink Rain Lily flower, as is the case after every storm, rain or dry. So, my question is, could it be the nitrogen released in a storm that they are sensitive to?


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BLASTN in NCBI strand Plus/Minus
I am a newbie in Bioinformatics. I am trying to understand terminologies used in NCBI BLAST system. Here is what I am trying to align:

So effectively I am trying to align two sequences with the following property.

So the query is part of reverse complement of the subject sequence. Now BLAST is throwing me the following result:

My confusion here is with the numbering system with query sequence starts from 1 from left side whereas the subject sequence starts from 1 from right side. Now I am assuming the numbering system starts from $5'$ end of any sequence and from the handwritten note above, it is clear that to align these two sequences I have to further reverse the subject string so that the $5'$ end of both sequences match up and hence numbering for both sequences should start from left side as opposed to what is presented in BLAST result page. BUT, I am suspecting that in my handwritten note in the reverse complement of subject sequence I have mentioned the $3'$ end in left side as is the case in DNA. But if I just take the (non - reverse) complement of the subject sequence keeping the $5'$ end towards left side, then and only then the numbering system works. But why we want to take complement of a given nucleotide sequence in non-reverse way!
Can someone kindly throw some light on this?

Yes, BLAST is making a best alignment, which is to the complement of your ‘Subject sequence’. That is how BLAST works, especially as other subject sequences may be genomes with genes oriented in different directions. And BLAST seems to be assuming that the numbering of your ‘Subject sequence’ is ‘official’ in some way (as it would be if it had been deposited in a data bank), and hence retaining it.
But as a “newbie in Bioinformatics” you should consult a suitable book and read about pairwise sequence alignment — which is what you appear to be attempting. An implementation of the Smith–Waterman algorithm, such as that on the EBI site, would seem more appropriate. This gives the alignment of the strands you entered:
EMBOSS_001         1 ATTGGCATT      9
                     |.||.||.|
EMBOSS_001         1 AATGCCAAT      9

If you want to check both strands, you need to do the reverse complementation yourself here.
There is also an EBI implementation available for the Needleman and Wunsch algorithm for global sequence alignment.


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Do antibodies to an arbovirus in a bloodmeal reduce vector competence?
When we conduct mosquito infection studies we typically mix blood and virus rather than using viraemic blood from naturally infected hosts. I'm looking for a paper I read some years ago which demonstrated that virus mixed with blood containing antibodies to that virus (not to mosquito midgut or salivary gland antigens) resulted in a lower proportion of infectious vectors than virus mixed with blood that does not contain those antigens. Unfortunately I don't seem to have kept a copy and now every search I conduct only throws up results to the aforementioned studies of anti-midgut or anti-SG antibodies. The nearest thing I can find is this, which looks at inhibition during intrathoracic inoculation (a completely different route of infection which is not particularly realistic, although we sometimes use it to boost the infection rate).


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What happened to pertussis incidence in the US between 1955 and 1974 and why?
The Wall Street Journal ran a great collection of infographics in 2015 superimposing the dates on which vaccination was introduced for various childhood diseases on their incidence:
http://graphics.wsj.com/infectious-diseases-and-vaccines/
For the most part, it's a fantastically clear story and a useful resource when explaining how effective vaccines are to skeptics. However, what's going on with pertussis?

The note below the heatmap mentions that vaccination was introduced in 1914. A bit of digging online suggests one factor could be the introduction of the (more effective) combined diphtheria-pertussis-tetanus (DTP/DPT) vaccine in 1949 - is this the whole story? Did the original vaccine have any effect? Did anything like coverage, availability, pricing and/or legal requirements for vaccination improve significantly at the same time as the new vaccine was introduced?
And why did the CDC stop collecting data on pertussis cases from 1955-1974 during a period when you'd have expected them to be keen to track the effectiveness of the vaccination programme?
(I realise that the CDC data gathering question might seem like a separate issue, but (a) it's necessary to understand this figure, and (b) the point of lumping these together is because I have a strong suspicion that antivaxxers will point at that gap and come up with a conspiracy theory, and I'd like to be able to point to a full explanation of the data behind this figure in one place. So, to be useful for explaining this figure to sceptics, they need to be answered together.)


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Why might allele frequencies change over many generations at neutral loci?
Lets say that a research team is looking at natural insect populations (e.g. beetle), and they find that allele frequencies at a locus in the genome have changed over the past few generations even though the locus is neutral. Why do the frequencies change at neutral loci?

There are four mechanisms by which allele frequencies can change over generations: mutation, genetic drift, gene flow, and natural selection. Which of these could affect a neutral locus?


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Is there a correlation between Animal Intelligence x Playing time?
I'm writing a small text for a blog about playing time and I wish to have more resources about the correlation between Intelligence and Playing time in animals. If not exactly that, maybe some indications leading to this conclusion or even going against it. Correlations between playing time and animals sociability are welcome too.
Thank you very much in advance.

Please explain what you mean by "playing time".

Great, thanks for the interest James. By playing time I mean the time dedicated to playing activities, as in small cubs playing together or with their mother, or chimps chasing one another with the intention of "having fun". I know the concept is very hard to define in behaviourism, but I wish to get some insights regarding to this. I wish to correlate this in order to show how playing is important to learning not only in humans but also in animals. Pardon for the innacuracy of the terms I use.

@FernandoTsukumo I am afraid, that the concept of (measurable) intelligence might be as hard to define (especially for animals), as is playing time. Are you looking to compare the same species of animals, but little ones play more or less or are you looking to generally compare animals that play a lot to animals that do not play as much?

Hi, thanks for the answer. Yeah, I am aware this wouldn't be an easy task, just decided to try a long shot... who knows? Actually, I am trying to find some evidence to something I feel, which is a link between the need of playing time and learning or maybe playing time and sociability among a good number of animal species or even just mammals. I saw that discussion about life expectancy x intelligence and then I got all hopeful about finding something similar regarding playing time. Maybe an impossible task: At least for now?


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Why don't electric eels shock themselves?
Why do electric eels not stun or pain themselves when they discharge their high voltage shocks? While it is known that they use those high voltage shocks to track their prey (as discovered by my professor Kenneth Catania [1]), and there is most likely some form of cage effect provided by the water (until they come out for a more powerful sting to scare predators), and that when curled less current might return through their own bodies [3], it is not clear why there discharges do not interfere with their own central nervous system (cage effect) or peripheral nervous system (through which current would flow in parallel to the water and target)?
[1] https://www.nature.com/articles/ncomms9638
[2] http://www.pnas.org/content/113/25/6979.full
[3] http://www.cell.com/current-biology/fulltext/S0960-9822(15)01147-1

My information isn't very reliable but I saw in a non-documental serie that eels are inmune to their electrical current because the have a thick layer of fat in their skin.

Short answer, no one knows, there is some minor evidence they are do shock themselves but are resistant to it, (they react far stronger in air than in water to their own discharge), but it is not a high priority for research so no one has really tested it.


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What is the difference between differentially expressed genes and deregulated genes?
Can anyone explain clearly what is the difference between differentially expressed genes and deregulated genes?

have you done some research on your own and if so, why it wasn't satisfactory?

Any gene whose gene expression differs significantly from some reference is considered to be differentially expressed. I think the most common representation of differential expression is the volcano plot, where you're plotting the fold change or log2 fold change against the -log10 p value assigned that gene.
This means a couple of things: One, you need a sufficently large sample size that you can actually get statistics, and two, you need a sufficient reference sample which will act as your baseline.
If a gene is degregulated, however, the expression is aberrant. In order to characterize aberrant expression you need a normal sample or accepted reference sample, and the sample of interest. This might be as simple as tumor vs normal tissue from the same patient.


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Point mutation vs Indels
DNA sequence of a gene can be altered in a number of ways. Gene mutations have varying effects on health, depending on where they occur and whether they alter the function of essential proteins.
I know that there different types of mutations.
Missense, Nonsense, Insertion, Deletion, Duplication, Silent, Frameshift indel, Repeat expansion, Inframe indel, stoploss, splicing.
Can anyone please tell me which mutations are Point mutations and which come under Indels?
Thank you

What research have you done before asking it here?

A point mutation is a mutation causing the substitution, insertion or deletion of a single nucleotide.
An indel is a change in the number of nucleotides (either through insertion or deletion hence the name). When talking about indel most people (in evolutionary biology at least) refer to the insertion or deletion of a single nucleotide but some might refer to greater changes when talking about indels.
An indel which concern the insertion or deletion of a single nucleotide is a point mutation.


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Copy number regulation & CNV
I have some genes which showed copy number loss between two groups. Now I want to see the copy number regulation of those genes. I really don't know about this concept. Can anyone please tell me clearly about this like why we need to check regulation of copy number loss genes? And any idea how to do this?
Thank you

It might be helpful if you showed us what sort of data you are looking at since copy number variations and gene expression can each be detected in similar but distinct ways.
Generally speaking, both gene expression and CNVs are detected by counting the number of reads that map to a given genomic region. The difference is that CNVs are detected using DNA sequencing while gene expression is detected using RNA sequencing. This is an important distinction because CNVs are a more stable genomic feature than gene expression. Reviewing the Central Dogma might help if this is confusing.
In the context of your problem, the main thing to understand is that CNVs can exert an influence on gene expression but gene expression cannot exert an influence on CNVs. Having fewer copies of a gene means that the process of transcribing RNA to express it cannot proceed as quickly as normal. So in an organism with gene X showing copy number loss, it makes sense to expect diminished expression of gene X than in organisms whose genome includes more copies of that gene X. If you're asking for an undergraduate class, chances are this is all you're expected to understand about "copy number regulation": the maximum transcription rate of a gene is dependent on how many copies of that gene are available for transcription.
Gene regulation becomes important for understanding how an organism with fewer than normal copies of gene X in its DNA might have the same amount of gene X RNA expressed as an organism with a normal number of copies of gene X. Suppose that some molecule, M, is necessary for expression of X but degrades after a short time. The cell will send M to the nucleus whenever it needs X to be expressed and the number of X transcripts produced per molecule of M will be dependent on the number of X copies available for transcription. If M is abundant and can be continually sent to the nucleus, then the cell with fewer copies of X can theoretically produce as much X as the cell with a normal number of X copies although it'll take a bit longer. If instead M is a finite resource within the cell, then the amount of X expressed in cells with fewer copies of the gene should be consistently lower than cells with more copies.
Of course if M happens to be produced by a gene exhibiting copy number gain/loss then that could also play an important role in how much X RNA transcripts you ultimately detect (even in the event that X actually has a neutral copy number). Hope this helps.


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Natural rulers: What organisms have the most regular size?
What organisms exhibit the most precise length scales?  E.g. are there trees with rings that are of very precise thickness, or single celled organisms which are all very nearly the same length?
In particular, it seems to me that most lengths in nature are precise only to about the 10% level.  Are there any organisms which exhibit length scales considerably more precise than this?
(Bonus points if you can tell me the most precise mass scales in nature, too.)
PS: This question is partially motivated by ongoing studies by physicists as to the origin of length scales in biology.  See this paper for an example.

You mean to ask which organisms have least variability in their sizes (and converse)?

@WYSIWYG Essentially that's what I'm asking, with the caveat that I'm not necessarily concerned with overall size, but rather the size of any component of the organism.  So e.g. in the case of (say) trees, the overall height of a tree need not have small variability, so long as the growth rings have very consistent size from one tree to another.


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Methods for varying insert size in E. coli clones
I'm writing my master's thesis proposal, and I need to improve the solution-behavior of some truncated protein domains which have previously shown poor solubility when expressed in E. coli.
To prevent this unwanted aggregation, one experiment I will perform will be to alter the domain boundaries.  I will create gene constructs where each clone will have an A domain of a certain length and domain border (see below).

My question: Is Gateway cloning better than restriction/ligase methods for this?  If i use restriction/ligase methods to construct vectors for transformation, then my choice for domain boundaries will be determined by restriction sites. Howevever, with a system like Gateway cloning, I can define boundary limits to bp resolution by simply desining an appropriate primer.
Is my reasoning here correct? I need to justify my choises for experimental design to researchers, so want to make sure I'm being efficient and logical.

Take a look at this.

Yes.  In principle you will have a vastly increased ability to customize the boundaries of each protein domain with a primer and PCR based approach.  It is not obvious to me that the Gateway Cloning System is required, or necessarily the best choice for this approach, but that is likely subjective.
Are you familiar with, or aware of, the efforts of the SGC (Structural Genomics Consortium)?  My understanding (now somewhat outdated) is that they were going to design/use a semi-automated way of implementing the strategy you discuss (domain trimming) so that they could us a high-throughput approach to define crystallization conditions for their targets.  Perhaps you could adapt their method(s) to your protein of interest?


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Fate of phosphatidylcholines in exosomes when triglycerides are released from adipocytes
I am not a physiologist by any stretch of the imagination, so excuse me for my potentially naive question.
My understanding is that triglycerides from long-term fat storage are released via exosomes*, whereupon they are split into fatty acids (which are subsequently catabolized during b-oxidation in the mitochondria to generate chemical energy in the form of ATP...). The exosomes are primarily made of phosphatidylcholines. What happens to the phosphatidylcholines (PCs) that form the exosomes? Are the PCs reabsorbed into cell membranes? Or, are they primarily split into their fatty acid constituents, then catabolized by B-oxidation? What is the main fate of the PCs from the exosomes?
*alternatively, are fatty acids primarily released from adipocytes using vesicles instead of exosomes?
Thanks for any insight.

This question is an identical copy of: Fate of phosphatidylcholines in exosomes when triglycerides are released from adipocytes.

Once a question has been migrated, there's no need to post it again. (I'm sure you realised).

I accidentally posted it in the wrong place (Worldbuilder? I don't even know what that is). So I posted it in Biology soon after. Sorry.

No problem, live and learn. ([worldbuilding.se] is for the construction of fictional worlds using the sciences and a systematic approach to magic etc. if you're interested)


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Fate of phosphatidylcholines in exosomes when triglycerides are released from adipocytes
I am not a physiologist by any stretch of the imagination, so excuse me for my potentially naive question.
My understanding is that triglycerides from long-term fat storage are released via exosomes*, whereupon they are split into fatty acids (which are subsequently catabolized during b-oxidation in the mitochondria to generate chemical energy in the form of ATP...). The exosomes are primarily made of phosphatidylcholines. What happens to the phosphatidylcholines (PCs) that form the exosomes? Are the PCs reabsorbed into cell membranes? Or, are they primarily split into their fatty acid constituents, then catabolized by B-oxidation? What is the main fate of the PCs from the exosomes?
*alternatively, are fatty acids primarily released from adipocytes using vesicles instead of exosomes?
Thanks for any insight.


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Is it possible that mosquitoes have been laying eggs and reproducing inside my house?
I am in Southern India. It is the rainy season now, so plenty of mosquitoes everywhere. I like to think my house is pretty well sealed off with mosquito nets in all openings, though.
Once in a while, a few get through when opening the door, etc.
However, I recently got these indoor pots with "self watering" pots. That just means there is a little compartment underneath the pot where you pour water in, which is connected to the soil, enabling the plant to absorb water from it.
Now, I have noticed way more mosquitoes lately inside my house. Sometimes, one of them manages to get a good, full size bite in. Sometimes I swat one and it is full of blood, so it already bit me.
It suddenly occured to me, could these guys (or gals, I should say) have been laying eggs inside the water resevoirs of my pots? The opening is plenty big for a mosquito.
This would explain the large number of mosquitoes in my house lately.
The other option is that it just the rainy season and they are somehow making it through some opening in a mesh or something, or through the door when I go in and out.

You have your answer. See also https://biology.stackexchange.com/q/115255/5198; user had the same problem.

Take a look in the water reservoirs. If they're reproducing in there, you'll probably be able to see the larvae. Little black wriggly fellas.

But the larvae do need something to eat. This could be plant litter, e.g., if any has fallen into the reservoir, or algae, if the reservoir gets enough light for algae to grow. Otherwise, I'd be pretty surprised if they were successfully reproducing in there.

@Eonema they need a very little amount to eat, a combination of drinking water and house dust in a lot of cases is pretty much enough. And I live in southern Europe and not India...

worth noting it can't be perfectly sealed, you get in, that tends ot be when the bugs come in, riding or hovinring around people.

Some species of mosquito can reproduce in very small amounts of water, as small as about a bottle-cap in volume. This is a known feature of Aedes albopictus, the so-called Tiger mosquito. The closely related Aedes aegypti can also do the same.
So long as there is room for the adult female to get in and lay her eggs, then there is potential for those pots to be a breeding site for mosquitoes. The bad news is that for some species of mosquito, the eggs can withstand drying for up to 8 months, so even drying the pots out might not work. You would need to empty the pot and then scrub them out to ensure that you have gotten rid of any eggs. Apparently bleach (sodium hypochlorite) is also effective at some concentrations starting around 1% (standard household bleach is anywhere between about 2.5 and 5%), but you would need to submerge the containers in the bleach for at least 24 hours.
A simple solution might be to seal the containers with a piece of netting to contain any mosquitoes that might be in there and prevent any new ones from getting in.

Thanks! I closed the opening of the resevoirs


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What is the closest possible analogue to human cells?
For an experiment, I need a specific number of cells. I will grow these cells in an incubator, and then measure the number of cells which have decayed due to the induced radiation. I am using a standard cell counting chamber (Hemocytometer) to count the number of cells.
The research question is to find the best armour for radiation; low-level really.
I was wondering which cell is the closest substitute to a standard human cell. People are telling me about yeast, but doesn't that grow from budding?
Any help and/or suggestion is appreciated.

The best analogue for human cells are human cells. There is nothing like a "standard human cell", since there are too many cell types. But since you probably want to study a specific cell type, you can culture these.

Sadly I don't have the equipments to culture human cells. However, any idea as to how will I go about culturing human cells, and which ones are the easiest to harvest?
If not, any bacteria/fungi which can be used as an alternative? Say I want to study skin and blood cells. I can use my own blood, maybe a drop or so. However, is there any chance of harvesting a sample of bacteria and use them?

Is there any chance that you collaborate with a research institute in your area about this? They often have programs for projects like this.

@Chris, I am in the process of asking a couple of research institutions for help. My parents have a facility like this, but that's unavailable due to the fact that there is an on-going IVF batch. There is a 99% chance that they'll say yes. Any ideas for the E. Coli strain?

They will most likely not let you in a cell lab with bacteria.

What about Escherichia coli? Every undergraduate lab has easy access to plenty of E.coli culture methods and its stupid easy to culture. There are always HeLa cells as well if you really want the perfect analogue to human cells because, well, they are human cells. Other options would include:
a) HEK 293 cells (Human Embryonic Kidney 293 cells), which are nice for what you're looking at as they don't replicate out of control, but are still extremely easy to grow. However, they're generally used as hosts for gene expression and they're finicky when it comes to contamination and they don't really act like normal cells that would be hit by low level radiation (ie tissues that are closer to the skin's surface)
b) 3T3 cells which would be nice for you as they are contact inhibited cells, meaning they functionally keep growing into a layer one cell thick (a monolayer) which could be nice for you, especially if the low level rad you're testing is alpha emitting in which case you need a homogeneously thick cell layer.

I was thinking of E. Coli in the beginning. However, I am in a school: grade 12. Sadly, I don't have access to a fancy incubator which can grow these cells. However, I presume I can get it kicking by asking others for an incubator.
I don't really have a biology background. Is there any protocol specification available to grow these cells?
Lastly, thanks a lot for this! It really helps! :)

Hm... Well, I guess reading this is a decent start as it outlines what is necessary to have and the basic principles behind cell cultures Basics of Cell
Culture. But at the end of the day there's many reasons why cell cultures are done in university and lab settings, and doing so without the resources provided by those settings will be expensive and difficult. I would advise talking to your teacher, or your contacting your local university's biology department I think they would be more than willing to help you!

Last question, and I will be out of your hair. Which strain of E. Coli should I use? Most of them seem toxic. Will E. Coli K-12 be the one?

No worries! There's two common strains of E.coli that are most used in labs: K-12 and B strain. Which ever one of these two that you can get from a supplier/teacher/university professor is the one you should use as for your purposes it should not matter.  If you are interested though here is a good starting point for some of the more common strains.

I think yeast is a great idea. They are safe and cheap to grow, easy to obtain, and easy to see in the hemocytometer. Human cells are not something you grow in a school; you'll probably need licenses, you cannot buy a cell line in the supermarket and the medium (what they grow on) is ridiculously expensive.
Of course yeast doesn't really resemble human cells, but they will die from radiation all the same. What kind of radiation are you using? UV seems the most appropriate (still be careful that you don't burn yourself / your eyes / other people), any kinds of radiation you can use in school (if any) is probably not strong enough to kill a significant number of cells. You might be better of using a Geiger-counter or something like that to measure it directly.

You don't need special licences unless you want to modify cells genetically. And standard media come between 3 and 10$ per bottle.

@Chris One bottle gets finished too fast :P Plus you need flasks and FBS too. And a CO₂ incubator and a very clean room :P


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What information do bipolar cells encode?
Short version: I don't see what information on-centre bipolar cells are actually capturing.
Longer:
Actually, the question could be extended to on-centre retinal cells as well, but I'll focus on bipolar cells for now.
On-centre cells will fire when a spot of light hits the centre of their receptive fields and doesn't touch their surround, off-centres are the reverse (light in the centre is inhibitory, surround is excitatory).
Here's an over-simplified illustration that I made, red is hyperpolarized (excited), blue is hypopolarized (inhibited). Let's pretend that horizontal cell effects have already happened, and ignoring overlapping receptive fields for simplicity.

So my question is, if off-centre cells would be useful to highlight contrasts like edges (as I understand it, though eventually edges get detected further down in the complex cells), what are on-centre bipolar cells used for?
From my perspective it looks like they'd be good for single points in light which are small enough to hit the small number of rods that encompass the centre of a receptive field but not hit the surround. But when would this ever be the case? The centre of a receptive field would be incredibly tiny given the large number of rods in say the fovea (though, granted, maybe on-centre cells become more important in the periphery?).
One source:
http://thebrain.mcgill.ca/flash/a/a_02/a_02_cl/a_02_cl_vis/a_02_cl_vis.html

Recent nature neuroscience review on bipolar cells says that bipolar cells are classified into 13 (12 cone bipolar + 1 rod bipolar) different types.
Depending on the polarity of their light response, bipolar cells can be grouped into ON and OFF cells.
Answering your question, what are on bipolar cells used for ? ON bipolar cells predominantly depolarize at light-onset and stratify in the Inner Plexiform layer (ON).
Considering rod - rod bipolar path way: Eyes are sensitive to very low light level. Imagine you are seeing a star during night. As the number of photon reaching retinal layer will be very small. It reaches order of few rod photo receptors (receptive field) & then converge to rod bipolar cell for efficient signal processing. It makes vision at dim light really interesting and promising.

In case with central surround organization, It is one of the classical stimulus study which has been explored further in detail with various complex stimuli.
I recommend you to go through The Neuronal Organization of the Retina for more details.
I am absolute beginner in visual neuroscience field. Please correct me if am wrong.
-Sathish


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How can I non-destructively blind/cover one drosophila eye for behavioural assays?
I am looking for a protocol for non-destructively covering one eye of Drosophila for a behavioural and subsequent imaging experiment I am planning. I am aware of using wax to paint over the entire eye based on conversations with my PI, but cannot find any papers that use this technique. Any searches along the lines of "drosophila monocular eye covering/blinding/etc" have turned up fruitless (drosophila pun intended). If you know of any papers that use this technique or similar, I would appreciate your help.

Our lab hasn't published anything using this method, but in some preliminary experiments we used a soft pencil eyeliner to draw over the Drosophila eye. It worked pretty well, except with enough time the flies can clean/rub it off with their legs. We also tried black nailpolish, but it dried as a scary spike on the eye so I don't recommend that.

Coooooooooooool


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Nutrient requirements in heterotrophs and surface area?
I'm writing a report for Year 11 Biology and I'm having trouble linking my experiment to the topic "nutrient requirements of heterotrophs".
My experiment in summary: Investigating "effects of the surface area of a potato on the height of bubbles produced during a chemical reaction". It involves dicing potatoes (of various surface areas) and placing them in hydrogen peroxide where there will be an interaction between the enzyme catalase and the substrate (hydrogen peroxide). The more bubbles the more chemical reactions have occured.
I don't fully understand how to link this to heterotrophic nutrient requirements, am I supposed to write about nutrient requirements (biomolecules) -> metabolic processes (cellular respiration) -> catalase is produced to break down harmful hydrogen peroxide? Or nutrient requirements (biomolecules) -> digestion and absorption of nutrients requires low surface area because ____?
Sorry if this is worded badly, I'd appreciate any help!


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Why are fish constantly in motion?
When I see fish in an aquarium, they never seem to stop swimming. This is in contrast to e.g. the penguins, who spend a lot more time just standing there.
Is this true in the wild or specific to aquariums for some reason? Is there a biological or evolutionary reason this is so? Is it a special case of some more general principle? (It occurs to me that fish are much smaller than penguins.)

I'm guessing it has to do with staying in one place - currents constantly move and change, so fish need to adjust with them - while penguins, for example, have their weight and the ability to lean if the wind blows.

Most sharks have to keep swimming in order to keep the gills supplied with oxygenated water. However, some can stay stationary. You can look up for a more convincing reference.

If one of the answers below have answered your query, consider accepting it by clicking the green checkmark, giving you and the other user some reputation points. This aids in closing the question as solved. There is no obligation to do it either.

A research, detailed in a 2012 issue of the journal PLoS Biology, suggests the fish do indeed take naps and can experience sleepless nights.
Another research with Pacific sand lance species, found them utilize a one of a kind methodology of tunneling into sand to rest and moderate vitality, and to maintain a strategic distance from predation.
Therefore, we can assume that fish sleep cannot be related to a terrestrial. As @Zxyrra has mentioned, with the currents being random in their direction, we can connect the reasoning of the continuous movement of the fishes as an effort to stabilize themselves.
On the aspect of any evolution or biological reasoning, fish sleep is still an ongoing research in marine biology. An interesting research have opened up a case in which through evolution, cavefishes have lost sleep. Information from this research could help you understand the evolutionary relationship of fish and sleep, in atleast, a broad scale.
UPDATE: Unique method of sleep in dolphins.
At the point when it's an ideal opportunity to rest, a dolphin will close down just a single side of the equator of its mind, and close the inverse eye (the left eye will be shut when the correct portion of the cerebrum dozes, and the other way around). Amid this time, the other portion of the cerebrum screens what's going in nature and controls breathing capacities. This process is termed as unihemispheric slow-wave sleep.

@WYSIWYG Here is an article that explains unihemispheric slow-wave sleep in dolphins.

Many fish do not sleep as we know it, most do however "sleep" while awake or sleep for very brief stretches of time. That alone means you are more likely to see them active than say a dog or rat.
Not all fish are in motion. Ambush predators can wait motionless for hours, but active hunter and foragers (aka most fish) will be in motion as long as they are not resting, becasue they are looking for food. Just like rats, mice, or other foragers.
Fish will drift if not in motion so most hide when resting or sleeping which makes them harder to notice. That means you will only see active fish. This simple observation bias is responsible for most of it.

I had to change this because recent studies have changed what we know about fish. This is why I love Stack Exchange, it makes me reseach things I never would otherwise. http://www.nature.com/news/2007/071016/full/news.2007.167.html

Do you have a citation on fish not sleeping? Pretty much every organism with a brain that has been tested sleeps, from fruit flies to whales.

@BryanKrause Apparently, some fish (or perhaps even cetaceans) keep one hemisphere active to keep swimming and put the other to rest. Then they switch them after a while. I remember reading this somewhere. I have to look up for a reference.

@WYSIWYG - yep, this is well known, and it is also known that other animals can also exhibit some sort of "local sleep" that doesn't cover the whole brain. That's a lot different than "never sleeping"

So you'd put most of it down to the observation bias, and the difference between fish + penguins is that penguins can get away with resting in the open because they won't get pushed around by the current?


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Did the capacity to be "knocked out" arise because it conferred an evolutionary advantage?
From first principles, it seems surprising that a blow to the head would cause unconsciousness rather than just impaired function.
I've heard a lot of analogies to computers -- "Your brain has to reboot." But computers reboot when there is an error because they are explicitly designed to do so, in order to recover and prevent further damage.
So, did we evolve the capacity to get knocked out for similar reasons -- because it helped us recover or prevent further damage? Or is the capacity to get knocked out just an "accident" or an inevitable consequence of the way our brains are designed, without a good evolutionary explanation?
(I realize the answer might be: "we don't know". In that case, I'd wonder what the prevailing opinions are and what if anything we've ruled out).

peripheral nerves also do this, when touched (eg in surgery) they completely stop working for some time

It is worth noting a blow to the head causes unconsciousness by doing enough damage to the brain to disrupt its function, a knockout is a concussion. This is why knocking someone out is actually very difficult and very risky. The movie knockout is a myth. We did not evolve to be knocked any more than we evolved to go into cardiac arrest.

https://en.wikipedia.org/wiki/Concussion#Mechanism
We did not evolve in order to become knocked out. See the wikipedia link. The "water" in the head is designed to not make us get knocked out that easily. However each dampening system has a limit.


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Examples of humans intentionally introducing non-native species where everything went well?
It's easy to find examples of humans introducing non-native species to solve some problem (e.g. for food, to control the population of a pest), but later regretting it as the introduced species upsets the ecosystem.

Rabbits in Australia
Mongooses in Hawaii

Are there any examples of this going as expected?
I guess, since I'm really interested in how well humans can predict this sort of thing, what I'm looking for is examples of a situation where there were no unintended consequences. (Rather than beneficial, but unintended, consequences).

Would species that were introduced by humans with out a specific purpose (except Oh, that one looks nice. Let's take it with us.) count as an answer? Or would you limit your question to problem solving (food, pest control) as stated in your first sentence?

Probably most major food crops (other than corn/maize) in the Americas.  Cows seem to have worked out fairly well (I mean open-range or pastured cattle, not the problems associated with industrial feedlots).  Horses are a bit more problematic, but I'd argue that most of the problems actually stem from the decimation of potential predators.

Almost all domestic species would count, the intention was to replace the native ecosystem and that is what happened. The problem with "unintentional" is you have who's intentions. The people who introduced wild boar to the US didn't care what damage they caused, they wanted to be able to hunt boar.

The best examples are for when non-native pest species arrive, and then a search for their natural enemies in their native countries is undertaken to bring them back and control the invaders. This is called "biocontrol", and there are many examples of it going well, under carefully controlled conditions. https://biocontrol.entomology.cornell.edu/success.php
However, you are right to note that it is very difficult to predict.

Fascinating to hear about this working well all the way back in 1889!


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What accounts for the apparent lack of biodiversity in "bamboo forests"?
While hiking on the Hawaiian island of Maui, I passed from a forest with normal variety in trees and other flora, to a "bamboo forest" area in which the only plants that I could see were bamboo.
This was surprising to me! Why does only bamboo (appear to) grow in this area?
The assumption I'm making is that bamboo forests happen elsewhere in the world, not just in Maui.

Mostly the fast growth shades other trees, lateral rhyzomes, mats of undregradable leaves, other factors may contribute. It invades ecosystems mostly vecause its cylinder hollow geometry gives it a massive height / to weight and sunlight monopoly. The roots are very dense, they may also strangulate other plants while also growing high.


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Locating a hornet nest
Say you are noticing relatively many hornets since 2 weeks or so, showing up at the windows of a flat you are living in.
The frequency of hornets constantly probing the windows is relatively high. That means if you open a small window for just 5 minutes there is a high probably that up to 5 hornets get in. Even when just tilting the windows open by a few centimeters, the probability is relatively high that a hornet that probes the area enters the room in the next 2 minutes.
The suspicion that there is a hornet nest not too far away perhaps isn't too far fetched. But I'm not an entomologist.
Thus my question: How to locate the nest of those hornets, in such a scenario?
Are there some specific hornet traits that help to include/exclude certain areas/locations?
For example, perhaps it's well known (to experts) in what radius around their nest hornets are most actively searching for food.
Perhaps hornets prefer to keep searching in a certain height difference relative to their nest.
Or there might be other clues, such as birds avoiding a certain tree where the nest is located, debris/damages near/below the nest etc.

Some more details of this scenario:

this is in Germany, Europe
the hornets are either European (Vespa crabro) or Asian (Vespa velutina) ones
apparently there were some sightings of Asian hornets last year, in the next town
some of the hornets entering the room are very attracted to black installations at the ceiling
even when windows are closed and light curtains are drawn behind the window hornets are probing the windows and often flying against the shut window
one affected flat is at the 2nd floor (counting from zero), but hornets are also probing windows at other flats at the 3rd and 4th floors.

Is this rural or urban - are there garden areas, what sort (trees?)? Are therefood sources nearby - bird feeders (sugar water) or lots of exposed wood (used for making nests)?

@bob1 it's urban. On several sides of the building there are relatively large trees standing very near to the house. The house has 8 floors and there are 4 flats on each floor, and each flat has a balcony. Around the house there are a few meters of small garden areas and a green drive-way for fire-fighter access. Behind the house a larger park-like green area is starting, i.e. there are layers of bushes and trees there as well, a line of garages behind the bushes etc. It seems there are quite a few candidates for a nest location, e.g. some niche at some balcony, in a tree, a bush, etc.

One way would be to place some suitable food outside and try to follow the flight. Unfortunately my experience with hornets/wasps is they can travel several hundred metres if they need to, but the numbers you are seeing indicate a nest might be nearby.

@bob1 Ok, interesting idea. Btw, I didn't notice such bird feeders in the area, although some people provide small corn-bags or similar for birds. Besides the wood available in the trees/bushes and some exposed wood in nearby gardens, the windows have wooden bars, which were originally painted, of course, but not all are in good shape.

Note that in Germany hornets are a protected species (at least the European variety, not sure about the Asian one). You are not supposed to kill even individual ones, much less try to harm or destroy their nest. If you want to get rid of them, the recommended way is to contact the Naturschutzbehörde responsible for your town.

@quarague Of course. I'm confident that's possible to locate a hornet nest without harming the hornets. When a hornet nest is located one can hire a licensed professional who is qualified to identify the exact species with some confidence. Vespa crabro indeed is protected by German law. However, it's still possible for a professional to get a permit to carefully move a nest, under some circumstances, apparently. Vespa velutina actually is considered an invasive specifies and thus isn't protected. In fact, it must be reported to the authorities, per EU regulation, for pest control purposes.


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Voluntary actions of Autonomic Nervous System

Somatic motor activity is always voluntary, while ANS motor activity is usually involuntary. pgno:762

This indicates the possibility of voluntary activity by ANS.
So, what are the voluntary actions by ANS?

My Attempt:
Wikipidea says:

Most autonomous functions are involuntary but they can often work in conjunction with the somatic nervous system which provides voluntary control.

So, is right to say that Flight or Fight response is the voluntary activity of ANS?

I have no idea what the author has in mind, but their statement is wrong from the beginning: somatic motor activity is not always voluntary. Reflexes are a good and obvious example.
"Fight or flight" response is basically half of the entire ANS (the sympathetic part), so that's incredibly broad. Parts of that response are definitely involuntary.
I think it's more likely that Wikipedia is thinking of things like breathing, which is normally under ANS but you can also manually control your breathing. They may also be thinking of things you can do to directly influence your autonomic responses, for example, if you start running, you are voluntarily moving your muscles, but the autonomic nervous system will also participate (for example, by increasing your heart and breathing rates).

So is it still correct to say ANS is not always involuntary?

@JM97 I think it makes most sense to just think of the ANS as involuntary, because that's really the whole point of differentiating the ANS from the somatic nervous system, while remembering two things: 1) The ANS does not exist in a vacuum, it shares a body with the rest of the nervous system, and as such is not immune to influence, and 2) Absolutes are always risky in biology - someone will come around with a particularly clever example or a way of narrowing a definition to disprove an absolute statement.


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IBD-value and IBD-fraction
I have some questions about the IBD-value and IBD-fraction for two of the condensed identity states, $S_1$ and $S_7$.
My questions:
1) Is the IBD-value for the individuals i and j two (2) in $S_1$ and 2 in $S_7$ as well? (We can form the pairs aa aa in $S_1$ and the pairs aa and AA in $S_7$. The number of alleles in $S_1$ (and similarly for $S_7$) for individual i that are IBD with alleles of individual j is therefore 2)
2) Is the IBD-fraction ( or coefficient of relationship) 1 in $S_1$ and 1 in $S_7$ ? (We have the fraction 2/2 in each case since both alleles of each individual are IBD with the alleles of the other individual as described in 1) )

Picture source: http://openi.nlm.nih.gov/imgs/512/114/3579841/3579841_pone.0057003.g001.png
Edit: Comments about the figure: The dots represent alleles for one particular locus. When two alleles are IBD they are connected with a line. We look at two individuals i and j and consider the SAME locus in both individuals. There are only two persons in each of the states. In state $S_5$ individual j is homosygous and it's alleles are also IBD. One of the alleles of i is also IBD with the alleles of individual j. We therefore get the three lines between the alleles.
Definitions used:
IBD-value: "An Identical-By-Descent (IBD) value is the number of alleles which are the same because of descent from a common ancestor. Since each (diploid) individual has two alleles for a given (autosomal) gene, the number of them that are IBD with another individual can only be 0, 1, or 2."
Source:
IBD-value in pedigree with inbreeding
Coefficient of relationship: "..is the fraction of genes in two individuals that are identical by descent,..."
Source:
https://books.google.no/books?id=Q9ofvKZAmpEC&pg=PA35&lpg=PA35&dq=identicAL+BY+DESCENT+FRACTION&source=bl&ots=oOc4-PBzZg&sig=jJgJarUg36b4DbyT7sphDD6j_7c&hl=en&sa=X&redir_esc=y#v=onepage&q=identicAL%20BY%20DESCENT%20FRACTION&f=false

Can you please tell a little bit more about the figure, I don't understand it. The dots represent allele I think. Is each dot a different allele? Is each trait is an individual (there are 3 individuals in $S_5$ for example)?

Of course @Remi.b. I have added some comments. I hope the comments make the figure more understandable

If I've understood the graphs correctly, then I think you are right on both questions. The difference between 1 and 7 is just that the alleles are in LD in 1 but not in 7


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Measuring, using and analyzing skin resistance in kohms
What are ballpark ranges of skin resistance in Kohms for average men and their significance (for example 500-1000s = stressed vs 1000+ = fairly relaxed)
What do various skin resistances in kohms say about a person's emotional or arousal state:
For example:
Is a skin resistance of less than 0 possible and what what does that say about the person

This fact depends on the moisture of the skin, for example. You could narrow your question further. Then, having emotional/arousal state is also dependent on the moisture. Your last question: possible in some conditions; last part of the question is subjective so I do not answer it. Your first question about classifications: subjective because too wide question; you need to narrow your topic.


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From an information perspective, are both strands of DNA necessary?
I am learning about the genetic code, replication, and transcription, and I have a question about whether or not both strands of DNA are really "necessary".
In replication, at a high level, we are taking 2 strands of DNA and creating 4 of them. Part of my question is: suppose hypothetically that the genome only consisted of a single strand (instead of the double helix), couldn't replication just as well occur by turning 1 strand into 2 (instead of 2 into 4)? I suppose this could be done by taking advantage of complementary base pairing as usual, and then splitting the two strands?
In transcription, I believe only one strand of a gene is read by RNA polymerase, so I don't think think the second strand is "necessary" here.
Can someone shed some light on this for me? I realize this is pretty speculative, and DNA is what it is, and does what it does. but I think this sort of question will allow me to see deeper into tits finer workings.

From a replication perspective, having two strands is definitely necessary, as that is how a lot of errors get repaired, such as pyrimidine dimers which can be repaired by nucleotide excision of the damaged bases, with new bases added by reading the opposite strand.

Having 2 strands with informative part in the core ensures safety of DNA from enzymes and also ensures that you have 2 copies of same info, one for use and another for back-up. You might want to read this

Don't forget that the DNA is "read" only in 1 direction (i.e. from the 5'-end to the 3'-end). For example, some genes are expressed from one strand while others are expressed from the complementary strand. In other words, you would, strictly speaking, lose information by only having 1 strand.

GGGCTCGATCGATTCA ... So a strand of DNA will match up like this: A goes to U. C goes to G; Example: DNA= ACGTAG the mrNA=UGCAUC ...

It's easy to forget that many DNA-binding proteins, which are important in determining what gets transcribed—by silencing, enhancing or chromatin remodeling—recognize a binding site made up by both strands.

From a strictly information theoretical perspective, no, a second strand does not provide any additional information that cannot be inferred from the complementary strand. But as many comments have pointed out, there are many practical reasons for DNA's double strandedness.

DNA is biochemically more stable in a double stranded state.
The redundancy of two strands allows for maintenance and repair mechanisms to ensure the integrity of the genome.
Proteins that bind to DNA can only recognize the sequence of that strand, so even though the complementary strand can always be reconstructed from the primary strand, DNA binding proteins cannot target that complementary strand unless it physically exists. In some cases, a DNA binding site encompasses both strands simultaneously.
Proteins (such as polymerases) traverse DNA in the 5' to 3' direction, so if information from the complementary strand was required it would have to be read "backwards".

Can another point be that the sense DNA strand of one gene may be the antisense DNA strand for another gene? So having both is necessary.

@SanjuktaGhosh — I would say not. This "can" happen, but it is not necessary. Indeed, although the points listed, although of possible interest to the poster, are not strictly relevant. However, "No" is too short for an answer.

@David Certainly the exception and not the rule, but there are certainly cases in which genes occasionally overlap. It's more frequent in smaller, compact genomes with less intergenic space, and it's more common that non-coding untranslated sequence is involved than coding overlapping with coding, but it certainly can happen. And then when you consider regulatory sequences and other features, I'd say it's not extremely uncommon for different pieces of important information to be encoded on  complementary strands of the same stretch of DNA.

@DanielStandage — I know as more than most about that sort of thing, but my point is that it's useful rather than necessary.

@David Ok, fair point! :-)

Although the title refers only to an “information perspective”, the question itself brings in the processes of replication and transcription. It is not entirely clear whether the poster envisages ‘piggybacking’ on existing DNA- and RNA polymerases which operate on double-stranded DNA (dsDNA) or whether he is envisaging completely different enzymes. I shall consider how the existence of single-stranded DNA and RNA viruses make it possible to argue that, both scenarios are possible in theory.
My answer to the question, therefore, like that of @DanielStandage, is no.
Single-stranded genomes relying on a double-stranded replicative form
Many viruses exist in which the genome packaged in the virion is single-stranded DNA (ssDNA). Replication occurs using either virally-encoded or host-coded DNA polymerases, often going through a double-stranded replicative intermediate (but see next section). Transcription normally occurs using the nuclear host DNA-dependent RNA polymerase, acting on the dsDNA.
In order to have all the information for transcription and translation on a single strand in a non-cryptic form, the individual genes would all have to have the same orientation so that the codons of all the transcribed single-stranded mRNA made sense. There seems no reason why this should not be so, although in practice most DNA genomes of which I am aware have genes in both orientations. However the banana buchy top virus has a genome composed of six individual ssDNAs, each apparently with a single gene.
Single-stranded genomes without a double-stranded replicative form
The rolling circle mechanism of DNA replication involves generation of a single stranded form without a double-stranded replicative intermediate, and, although the most well characterized examples are dsDNA viruses, the ssDNA banana buchy top virus replicates by the same mechanism.  If we think of what might be possible in linear ssDNA genomes by extrapolating from what exists in linear ssRNA viruses, it is not hard to  envisage replication mechanisms involving the production of many copies of a ssDNA of opposite sense to a single copy of a ssDNA template. Replication is therefore not a problem with ssDNA-dependent ssDNA polymerases analogous to extant viral RNA-dependent RNA polymerases. For transcription it would seem more logical to make a further step of a ssDNA-dependent ssRNA polymerase, rather than ‘mutating’ extant dsDNA-dependent RNA polymerases.
Why bother?
As things don’t operate this way it may seem to be a waste of time discussing them. However:

The poster is reassured that his reasoning is — in principle — correct.
The poster and reader is made aware of the varieties of viral genomes and replication strategies of which he might previously have been ignorant.
The answer provides food for thought in relation to the idea that a world in which cellular organisms had RNA genomes preceded the current one in which they have DNA genomes.

A final word about information
The way in which the question is posed relates to information as a linear sequences of nucleotides in DNA, specifically codons. This can be extended to other signals such as transcriptional start sites, splicing sites, polyadenylation/cleavage sites etc. However it is also possible to conceive of three-dimensional information. Although three-dimensional structures are possible with ssDNA, some. e.g. cruciform DNA do require  dsDNA.


text:
What genetic modifications could help plants survive in extreme environments like deserts or polar regions, based on current scientific knowledge?
My question is simple."I’ve been wondering—if you could genetically modify a plant species to survive in extreme environments like deserts or polar regions, what traits would you choose to prioritize, and why? I’m curious to hear your thoughts!"

Welcome Qalam. Please take our [tour] and refer to the [ask] section of the [help]. We can answer focused questions that have an answer that can be referenced - what you have here is a speculative question (covering more than one environment) that could devolve into opinion-based discussions. A better venue for this might be our [worldbuilding.se] site, but ensure to take their tour and read their help centre before posting so that your question is in-shape and on-topic.

For deserts, holding onto water and minimizing water loss, and for polar areas, slow growth, the ability to resist freezing and the ability to remain dormant for extended periods. If you check out vegetation from these areas it will mostly tend to conform to these traits.

"Extremophiles" also come to mind, perhaps they could develop chemosynthesis?


text:
Electrogenic ion transporter

At the molecular level, electrical current across cell membranes ﬂows through three unique classes of integral membrane proteins (see Chapter 2): ion channels, electrogenic ion transporters, and electrogenic ion pumps.1

later it is said:

One class of electrogenic transporters includes the adenosine triphosphate (ATP)–dependent ion pumps.2

Is there any fundamental difference between "electrogenic" ion transporter and "electrogenic" ion pump, considering the fact that denosine triphosphate (ATP)–dependent ion pumps are also included in the former?

My attempt:
From this site ,Secondary active transporters are electrogenic, so if I consider those as electrogenic ion transporters , then also iam still confused why sodium potassium pump is in the category of ion transporter but not in ion pump.

Pump and transporter are synonymous: they refer to proteins that, unlike channels, use a form of active transport to move ions or molecules against their concentration gradient, although "pump" is most often used in the context of primary pumps, that is, those that directly use ATP, whereas "transporter" is more often used to describe the whole category or secondary pumps that use existing gradients.

then also iam still confused why sodium potassium pump is in the category of ion transporter but not in ion pump

I have no idea where you are getting this statement from, clearly the sodium potassium pump is a pump.
Gadsby, D. C. (2009). Ion channels versus ion pumps: the principal difference, in principle. Nature reviews. Molecular cell biology, 10(5), 344.

It's from the second source, textbook by boron

The author is differentiating them as two different entities as in 1st source.

I don't think so, I think the author is acknowledging that there are proteins commonly known as pumps and those commonly known as transporters (partly by the primary/secondary tendencies of naming, which I mentioned), and intending to be fully comprehensive by listing both terms. It does not imply they are actually separate categories. The only other explanation is that the author is wrong.

For example, searching google for "humans, mammals, and" returns a paper titled like this: Influenza type A in humans, mammals and birds: determinants of virus virulence, host-range and interspecies transmission.: that author certainly isn't making the case that humans are not mammals.

3 unique classes of integral membrane proteins.....

I think that's just flowerly prose. Ignore it. They are the same. Textbooks are rarely perfect.


text:
What is a good biochemistry reference for reading papers about metabolic pathways associated with human disease?
I studied first and second year biology at university about 15 years ago, taking courses in cell biology, comparative physiology, microbiology, and human cell biology. I also took the supporting courses in organic chemistry, but I have never taken a formal biochemistry class.
Recently, a family member developed a rare cancer and we have been reading through journal papers in nutrition and medicine while trying to understand how diet plays a role. These make extensive reference to specific metabolic pathways in human cells -- some I am familiar with, but many which I am not. In all cases though, my cursory education in the pathways of metabolism and cell function feels inadequate.
So, what are some comprehensive biochemistry texts that can be used as a reference for reading papers in the nutritional and medical sciences?
I would prefer not to use a "concepts" book as one might find in a light version of a course. I am not a shy reader and am not daunted by the prospect of using a more comprehensive book as a learning vehicle, nor of having to do further backtracking to the world of organic chemistry when I encounter a class of molecules that deserves attention.
Lastly, I'm on a bit of a budget too. If you know of a book with a long lineage that is likely to be offered cheaply in previous editions, it would be of tremendous value.


text:
snail motion and snail tracks
I took a picture of a snail whose tracks are not continuous. What is the reason? Does the snail lift itself from the ground during its motion?

something to do with a rythmic organ contraction?

During particularly dry weather some snails will only touch the ground with part of their "foot" at once. In effect moving more like a desert snake in the image below. They do this to reduce moisture loss. Even though it is still a continuous motion it leaves a discontinuous trail. the same number of these points of contact are present the entire time at no point does it leave contact, think of it more like high stepping. This behavior is sometimes called "jumping" even though it has nothing to do with actual jumping.

http://www.molluscs.at/gastropoda/index.html?/gastropoda/morphology/locomotion.html

thanks, do you know of any videos showing these different types of motion?

sorry no I don't


text:
What does this “shell” belong to?
I often find these, what I assume to be shells, during walks along the beach. I haven’t seen any creature or plant alive that has this feature and research attempts haven’t been successful.
There are bright reflective blue streaks along the shell and it is yellow-brown coloured and transparent. I have found these along the Northern Irish coast

I believe it's a Patella pellucida or blue-rayed limpet. They live off seaweed in deeper waters, so it's not a surprise that you wouldn't see many live ones.

Picture from an interesting article: Blue-rayed limpet holds secret for windscreen transparent displays with no internal light source


text:
Epidemic threshold on a directed network
I am trying to understand the equations used in a paper

(https://www.nature.com/articles/srep00469.pdf)

Mainly I'm trying to understand how the epidemic thershold was calculated using the equation:
$$I^{t+\Delta t}_a = -\mu\Delta tI^{t}_a + I^{t}_a + \lambda(N^{t}_a - I^{t}_a)a\Delta t\int d{a}'\frac{I^{t}_a}{N}+\lambda(N^{t}_a - I^{t}_a)\int d{a}'\frac{I^{t}_a{a}'\Delta t}{N} $$
From the supplementary information (https://media.nature.com/original/nature-assets/srep/2012/120625/srep00469/extref/srep00469-s1.pdf (eq.17)), I get that $$I^{t}_{a} - \text{number of infected individuals in the class a, at time t}$$
$$N^{t}_a - \text{total number of individuals with activity a, at time t}$$
$$\lambda - \text{transition probability, } \mu - \text{recovery probability}$$
I understand that first two terms $-\mu\Delta tI^{t}_{a}$ and $I^{t}_{a}$ represent the number of recovered individuals, and number of infected individuals of class $a$ at time $t$ respectively. Rest of the equation is a mystery however.
In the supplementary information eq.18, we get:
$$\int daI^{t+\Delta t}_a = I^{t + \Delta t} = I^{t} - \mu\Delta tI^{t} + \lambda \langle a \rangle I^{t}\Delta t + \lambda \theta^{t}\Delta t$$
where $\theta^{t} = \int d{a}'I^{t}_{{a}'}{a}'$, I don't understand why we get rid of N in the $4^{th}$ term and how we obtain a moment of a distribution from the $2^{nd}$ term to get this. We then get:
$$\theta^{t+\Delta t} = \theta^{t} - \mu\theta^{t}\Delta t + \lambda \langle a^{2} \rangle I^{t}\Delta t + \lambda \langle a \rangle \theta^{t}\Delta t$$
Which again makes no sense to me, I feel like there is a lot of steps missing here. From here onward it's just dark magic for me, no clue what's going on.
Then this is written as differential forms:
$$\partial_tI = -\mu I + \lambda \langle a \rangle I + \lambda\theta$$
$$\partial_t\theta = -\mu\theta + \lambda \langle a^{2} \rangle I + \lambda \langle a \rangle \theta$$
From that somehow the Jacobian is calcuated as
$$J = \begin{pmatrix}
-\mu + \lambda \langle a \rangle &  \lambda \\
\lambda \langle a^{2} \rangle & -\mu + \lambda \langle a \rangle
\end{pmatrix}$$
Eigenvalues:
$$\Lambda_{(1,2)} = \lambda \langle a \rangle - \mu \pm \lambda \sqrt{\langle a^{2} \rangle}$$
Threshold:
$$\frac{\lambda}{\mu} > \frac{1}{\langle a \rangle + \sqrt{\langle a^{2} \rangle}} + \mathcal{O}(\frac{1}{N})$$
I would appreciate if someone could explain this to me, I have been trying for few weeks now, and it just makes less sense more I look at it.
Now that's the threshold on an undirected network, if I were to calculate the threshold on a directed network how would I do that? Would it be something like this:
$$d_{t}I = -\mu Ia + \lambda(N_{a}-I_{a})a\sum_{{a}'}I_{{a'}}\frac{m}{N} + (N_{a} - I{a})\lambda \sum_{{a'}}{a}'I_{{a}'}\frac{m}{N}$$


text:
How do chromosome pairs get "paired up" for protein synthesis?
If my understanding is correct, during interphase a normal human cell will have 46 chromosomes scattered about in the cell nucleus. These chromosomes can be thought of as pairs: there are two copies of "chromosome 1", one from mom and one from dad. Same goes for chromosome 2, chromosome 3, ... chromosome 22. Although we think of these as coming in pairs, are they actually attached or paired up in some way?
At some point, protein synthesis will take place via transcription. What I'm having trouble understanding is how and when the above pairing takes place. Does transcription occur independently for each of the 46 chromosomes? I don't think this is the case, because in my head I imagine that we will only get one set of proteins from the pair of each chromosome. Also, I'm unclear as to how dominant/recessive genes can come into play unless protein synthesis occurs as a function of both pairs of chromosomes.
I hope this is clear enough. Thanks.

This is actually a quite complex question. No, they are not paired up in the nucleus but rather just scattered around. The exact 3D location of each chromosome in the nucleus is not fully understood yet and is believed to be a dynamic process. Transcription does not occur, strictly speaking, independently because similar genes will use similar transcription factors. Now another factor impacting gene expression is the chromatin state at the location of the gene which is not guaranteed to be the same between chromosome copies (i.e. could be independent).

For dominant/recessive genes, the effect is not necessarily linked to gene expression but rather to the function of the protein. A recessive mutation disrupting the protein simply means enough functional proteins are made to conserve the biological function and vice-versa, if the same mutation was dominant then having a decreased level of the functional protein leads to a complete disruption of the overall biological function.

Although we think of these as coming in pairs, are they actually attached or paired up in some way?

Chromosomes only pair up during metaphase I of meiosis. And meiosis only occurs during the production of gametes (sperm and oocytes). Say Chr1 from mom pairs up with Chr1 from dad. http://media.web.britannica.com/eb-media/76/94976-004-7D0416E7.gif
Mitosis is what happens when somatic cells (say in your toes) replicate.  Chromosome (inherited from your mom and dad) do not pair up in mitosis. Instead each chromosome is replicated
You are probably confusing chromosomes pairs (one copy from mom and another from dad) sitting side by side... undergoing chromatid crossover... with sister chromatids (ie the same chromosome which has been duplicated, so each daughter cell can have its own copy.) This forms the X shape that you think off when imagining a chromosome.
Transcription occurs on all 46 chromosomes. Aside from situations where the gene is controlled by parental epigenetics... both the paternal and maternal copy of the gene is active.
As for  recessive/dominant allele... it has more to do with the function of the protein. If the protein is produced by one allele in sufficient to give a normal phenotype, then the allele is dominant. A dominant negative tends to occur when the mutant allele codes for a mutant protein that can interfere with the normal function of the protein that is encoded. A common example is that the protein works as a pair. And is one member of that pair is mutated, the entire complex is non-functional.

About the chromosomes.
The chromosomes are not paired physically in the cell but yes, there is 23 chromosones, that have two copies of each, one from the dad, one from the mom. The homologous chromosomes are physically paired during meiosis, where cross-over of DNA will happen but only for a littel time.
About protein synthesis.
These are two cases in a recessive/dominant allele combination.

Both synthesize the protein, but the protein from the dominant gene will have the effect and the other just won't be able to.
The recessive gene transcription is blocked. The dominant can be the reason by synthesizing an inhibiting protein, or it could be a physical change to it's DNA etc.

This is only a small example since there is a large numbers of regulations that exists from the DNA, methylation of DNA, mRNA, transcription inhibition etc.
Conclusion.
There is a lot more cases and exceptions since this is an extremely complicated subject. To learn all of them you would need a genetic book or a complete review on this subject.
Sources:
Genetics (Book)
Random monoallelic expression of autosomal genes: stochastic transcription and allele-level regulation
Chromatin regulation at the frontier of synthetic biology
RNA-mediated epigenetic regulation of gene expression


text:
Glucose Oxidase, Condition to be Active?
I most recently was reading/watching information on honeys antibatical and antimicrobial properties.  The enzyme Glucose Oxidase came up often as a main antimicrobial, yet it is inactive in honey.  How much would honey need to be diluted to make this enyzme active? I may potentially use honey in a dilute for as a backpacking emergency antibiotic/antimicrobial and/or something to irrigate wounds if severe.
I do have an basic (High School) understanding of chemistry if that helps

An interesting point about honey for sure. But why would you prioritise honey over medical supplies whilst back-packing?

This is a common "alternative medicine" claim. But: Where do you see honey being used as an effective medicine? Don't rely on something which will most likely not work (how would you get effective concentrations throughout your body for example) and use real medicine.


text:
Can restriction sites be used as PCR primers?
I have a DNA fragment that contains the gene of interest sandwiched by restriction enzyme sites. Then, can PCR amplify the entire fragment, recognizing the restriction enzyme sites?

Why not? PCR amplifies any sequence.

If you aren't digesting prior to amplification, sure.  Nothing in PCR cares about whether or not some other protein interacts with the site.  There are thousands of restriction enzymes in nature.  No one would ever be able to do PCR if you had to avoid every single potential restriction site.

Just a minor comment: some restriction enzymes like XbaI are sensitive to DNA methylation, so XbaI works on your PCR product but may not work on your gene.


text:
Are there diseases for which a placebo treatment is state of the art?
I was reading about the placebo effect, and I wondered if there exists or ever existed a disease with the following properties:

There are no known treatments for the disease that perform better than a placebo.
The placebo has a positive effect on patient outcomes.

If there is a disease like this, what do doctors do? Do they give out prescriptions for sugar pills because the pills will do better than nothing?

The ethics of knowingly providing a placebo are iffy.  There was a study once of placebos for asthma, or something like it.  Some patients reported feeling better, but objective measurements of lung function showed they were not.  That misconception could have been dangerous for the patients.

psychosomatic or imaginary ones. comes to mind.

I'm voting to close this question as off-topic because it is not about biology in terms of SE Biology but about medicine or medical ethics.

I agree this can be moved to Medical Sciences SE.

I'm voting to close this question as off-topic because this is not a question about biology in terms of SE Biology but a question about medical practice.

Doctors sometimes use "open-label placebos" - substances that have no known physiological effect on the treated disease, but have been associated with symptoms improvement in some studies. Open-label means doctors openly tell people it's placebo. The example is treatment of irritable bowel syndrome.
Doctors use not only fake drugs, but also real drugs as placebos. There are some doctors who don't have a courage to say they don't know how to help, so they just prescribe "something" (a real but ineffective drug) in the hope they will convince someone that they provided some help.
Prescribing "placebo treatments": results of national survey of US internists and rheumatologists (BMJ, 2008)

Prescribing placebo treatments seems to be common and is viewed as
  ethically permissible among the surveyed US internists and
  rheumatologists. Vitamins and over the counter analgesics are the most
  commonly used treatments. Physicians might not be fully transparent
  with their patients about the use of placebos and might have mixed
  motivations for recommending such treatments.

There is a common practice to prescribe:

Vitamins or antibiotics for common cold, flu and other viral infections (Montana DPHHS ; JRSM Open)
Antipsychotics, antidepressants and sedatives for personal problems that can't really help to solve those problems
Various drugs for fibromyalgia

The seeming effect of placebo can discourage a person to seek for the real treatment.

This may be a valid comment on the “common” behaviour of some doctors but does not answer the quite specific question regarding specific diseases and “state of the art” which I assume means recommended treatment in this context.

Treatment of depression, fibromyalgia and irritable bowel syndrome is typically treated with various drugs, even when there is insufficient evidence about their effectiveness, so they are placebos in this regard - even if doctors who prescribe them disagree. So, for the mentioned conditions using placebos is the state of the art.