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Can viruses infect adipose cells?
Can viruses infect adipose cells or tissue?

What do you mean by ‘store’ viruses?

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basically can virus get into a fat cell?

long story short- a longer story would be appreciated

Research demonstrated that viruses including HIV virus can find sanctuary in adipose tissue cells.
Earlier studies showed that interactions between immune cells and adipocytes, specifically perinodal adipocytes, promote immune activation and adipose inflammation,suggesting adipocyte regulation of HIV replication and pathogenesis.
Adipose tissue is categorized as mainly subcutaneous or visceral depots, with other minor depots uniquely associated with critical tissues and organs such as lymph nodes (perinodal fat) and the heart (pericardial and epicardial fat). Adipose tissue contains mature adipocytes and stromal-vascular-fraction cells (AT-SVF cells) which includes preadipocytes, mesenchymal stem cells, and immune cells, and this cellular composition changes significantly during disease and metabolic disorders, most notably obesity.
Murine models demonstrated migration of immune cells into adipose tissue to become major regulators of adipocyte function and metabolism, and studies of healthy and diseased humans further showed significant accumulation of immune cells. Additionally, virion-free circulating HIV proteins such as vpr, nef, and tat were shown to mediate detrimental effects on adipose tissue health and systemic metabolism.
So yes, the viruses can "live" and "reside" inside adipose tissue and regulate that environment to their own benefit.


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Why is the chordate nerve cord described as hollow when it appears to be solid?

My textbook says arthropods have a double, ventral, solid nerve cord. And chordates have a single, dorsal, hollow nerve cord.
What is hollow exactly in a cord that looks like this?

Your book is talking about an embryonic structure, the neural tube. This structure forms from an invagination of the neural plate, a collection of cells on the dorsal surface of the early embryo. The process forms a hollow neural tube that will eventually develop not only into the spinal cord but also into the entire CNS.

(image from https://commons.wikimedia.org/wiki/File:Neural_Crest.png)
There is still a lot of development to happen at this point: the cells making up the neural tube will divide many times and proliferate to create the central nervous system. Within the section that becomes the spinal cord, hollow part remains and becomes the central canal, contiguous with the fourth ventricle in the brain and containing cerebro-spinal fluid:

(image from https://commons.wikimedia.org/wiki/File:1313_Spinal_Cord_Cross_Section.jpg)
(note: I had a bit of trouble finding an image showing stages of spinal cord development with a license suitable for posting here, but you can find a bunch if you image search for "spinal cord development". Some examples: https://www.medicalimages.com/stock-photo-illustration-of-spinal-cord-development-within-the-embryo-atweeks-five-a-eight-b-and-ten-c-image22427030.html https://www.brainkart.com/article/Development-of-the-Spinal-Cord_18920/ )

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Is it possible that East Asians are a hybrid between modern and achaic humans?
As I understand it, all populations outside Africa have at least 2% Neanderthal ancestry. In eastern Asia and I think Papua New Guinea in particular that percentage could be more than 4%.
Now you also have the Denisovans from which a full genome sequence from a small bone fragment have been found in Denisova cave in central Asia. The latest research suggests that some Asian groups have about the same Neanderthal ancestry as other non-African populations but more Denisovan ancestry.
Question: If we theorize that East Asians (Chinese, Koreans, Japanese) with their characteristic features are not the result of recent evolution as per the "recent out of Africa Theory" but are instead the result of hybridization between modern humans and some form of archaic human (just like the Neanderthals and Denisovans) that have yet to be found.
To what degree could this theory be proven or disproven from genetic studies?

East Asians do not have "characteristic features". in other words, there is no specific feature or set of features unique to the East Asian nationalities you list that is not present elsewhere in the world. Your premise is faulty.

@natb All peoples have "characteristic features" to some degree. I was mostly thinking of things like skull morphology.

@Agerhell individuals certainly do. Groups of people such as "East Asian" do not. Skull morphology is not applicable here.

Firstly, as one of the comments said, there is nothing particularly unique about the set of 'features' that East Asians have, other than having fairly high levels of Denisovan ancestry. Any region in the world has some kind of unique phenotypic features if you look hard enough.
Genetics has fairly unambiguously shown that all non Africans originated from the out-of-Africa (OOA) event; Europeans, East Asians, Native Americans, Aboriginal Australians etc, are all from the same smallish source population that left Africa some time between 40-50kya. Of course there was plenty of migrations out of Africa that predated the out of Africa event, but there’s no strong evidence that they left any trace in existing populations. There’s been some hints by e.g. Pagani et al 2016, but this is very hard to prove convincingly, in part due to things like archaic admixture. If it did happen, it was likely a very small contribution.
Simply, you can fit models of human population history to allele frequency differences using something like Treemix and get graphs like this:

Which show that East Asians are nested exactly where you would exepct to see them following an OOA event (i.e. equally divergent from Africans as Europeans, Native Americans etc).
Humans and Archaics are very highly diverged in relative terms and if East Asians were some kind of mixture between modern humans and some unknown Archaic, they would stick out like a sore thumb on a model like this.
You could also look at something like cross-coalescent split times, which look at the divergence in genealogical trees across the genome between pairs of populations. Again, if East Asians were some uknown mixture, these trees would be hugely divergent from those you see in e.g. Europeans. They aren't:

This is really a separate question that I may ask in another thread. Can it be calculated somehow how much of the genetic difference/distance between african peoples and other peoples that are due to the +2% Neanderthal genes that non-africans have due to some crossbreeding with Neanderthals soon after leaving Africa?

Good question - make another thread and I will have a go at answering it

There is evidence that Europeans and Africans have admixture from other hominin groups, so it is not just Asian populations that have such admixture. We are all such hybrids, if anyone is.
The reference you may be looking at shows that in east Asia there may have been more than one period of interbreeding with Denisovans.
There is new evidence that there may have been several groups in Africa that merged to become what is now the human race even.
It’s pretty settled that we all have strong connections to Africa and Neanderthals and other brethren hominids.
The examination of DNA has assembled complicated migration histories - leaving and coming back into Africa - migration across and back to Europe.
I think take-home in general here is that we were not really separate species and our ancestors didn't really see each other as being so different that we would not mate.  All these subspecies coexisted for thousands of years and we probably interbred as often as we were in the same place. There were very few of us at the time... we just didn't meet each other so often.
I wouldn't jump to the conclusion that the Denisovan inheritance is unique to Asians somehow. The racial genetics of old have also been long debunked in terms of differentiating races into distinct subspecies. In short: the oft-referenced racial groups have all interbred with each other and with archaic hominins to a degree that makes their distinctions fuzzy.

Neanderthals and Denisovans are not human subspecies, but rather other hominin species (different from hominid). Otherwise this is pretty spot on.

perhaps some people say that ... all I can say is that different species cannot interbreed to produce fertile offspring... which clearly Neanderthals and Denisovans.  science is not 100% consistent and terminology requires some flexibility if you are going to deal with real systems. allow others to choose their words and you may find they have something to say..?

Others may choose their words as they like. I am merely reporting the current consensus in the field of paleoanthropology. The terms hominid and hominin are distinct and not interchangeable.

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Sequence evolution simulation tool
I'm looking for a tool to simulate sequence evolution given a specific mutation model and birth-death model. I'm aware of tools and packages like INDELible, Seq-Gen and PhyloSim, but they simulate evolution along phylogenetic trees. What I want is to give a sequence and ask the tool to simulate the evolution of this sequence through N generations. The output should be a big bunch of descendant sequences. I've been thinking about writing such a tool myself, but it's always better to look for something already coded.

There exists a bunch of population genetics forward and backward (coalescence) simulation platforms. Here is a non-exhaustive list. They all differ and you'll have to go through their manual to see what is more adapted to your needs.
List of softwares
Here is a long list of such platforms. The list might arguably be a little bit outdated today though and many of these softwares might be slow or abandoned by their authors.
Most common softwares to my experience
Some are more known than others. Personally, I already saw uses of the following platforms in publication: SimCoal, Nemo, Slim and SFS_Code.
SimBit
Of course, I must indicate my own simulation platform SimBit. To my experience, SimBit is typically faster than Nemo. It is slower than SFS_Code and SLim for very small simulations but become much much faster than SFS_Code and SLim when you need simulations with a descent amount of genetic diversity.
Most important point about these softwares
You should compare softwares based on

Availability of the author to advice and bring new features

I won't talk about my personal experience here by respect for the authors!

Speed / RAM usage

I think SimBit is typically faster (and use less RAM) than Nemo. SFS_code and SLim are very fast for simulations with low genetic diversity but very slow for simulations with high genetic diversity.

Flexibility

Nemo, SLim and SimBit are very flexible (but they do different things) but SFS_code is not really.

User interface

I find Nemo error report pretty poor. I like SimBit error report. SLim interface is very nice (using eidos) and it even comes with a GUI (I have never used the GUI myself).

Free of Bugs

Several people have found important bugs in SFS_code (personal communication and experience).

Slightly more detailed comparison between Nemo, SLim, SFS_code and SimBit
I have personally used NEMO, SFS_CODE and SLim in the past (I now use SimBit only). So I can only talk about these 4 below.
All four models are well updated and maintained by their authors and of course everyone has a access to the source code.
SFS_code and SLim are very fast for small simulations. The issue of SFS_code and SLim is that the RAM usage and run time are exponential function of the genetic diversity. This means that some simulations can quickly become totally unmanageable. But it is a great tool if you expect little genetic diversity.
SimBit is typically faster than Nemo, at least for large genomes. This difference becomes particularly obvious for large genomes. One might think "Oh I am fine to wait a few extra days to get my results" but the difference in speed between two softwares can also be a difference in whether you have to wait a week or 20 years to get your results, so do not neglect the importance of running time and RAM usage without estimating your needs.
Nemo is very flexible when it comes to the order of life-cycle events (is migration before or after selection for example) and the newest version allows for simulating age structured population. SimBit is very flexible, very fast and allow for simulating multi-species and their ecological interactions. SFS_code is less flexible.

My only concerns about NEMO are that each individual dies after reproduction and that there can't be more than 256 alleles at the same time.

SFS_code limits the number of alleles to 4. Nemo limits the number of alleles to 256 (but you can also use phenotype and have a float number at each locus). SimBit uses either bi-allelic loci, a block in which the number of mutations are counted (max: 256 mutations; this is different than 256 alleles per say) or continuous float number at each locus for the phenotype. Do you really need more alleles? Why can't you just use several loci to represent a sequence with multiple alleles? Real biology can only have 4 alleles in its smallest locus! SimBit uses a bit-per-bit system. If you need, say 50,000 alleles, then you just need to ask for a sequence of 16 bits (2 bytes) and you can get $2^{16} = 65,536$ alleles.
If you need more alleles in a single block (which is a little surprising to me a priori), you can probably just ask the author and he might accept to helping you if you convince him it is of interest to add this feature (he might also be more willing to help in exchange of authorship if you need more support).
Hope that helps. Good luck!

Well, thank you a lot. You saved me a lot of time.

Though I haven't found a tool that fits the task well enough, the list provides several links to R and C packages that would save me a significant amount of effort needed to develop one myself.

I can't quite give you more advice as I don't exactly know what you're looking for. But you can simulate a whole bunch of things with NEMO and get the genes of every single indivdiuals afterward. NEMO is not super efficient for simulating an actual string of A,T,C,G (although it is feasible) but maybe something like SFS_code or SimCoal would do the trick. You might want to download Nemo (free of course) and run the example simulation that goes with the package you could get a better sense of what it does.

My only concerns about NEMO are that each individual dies after reproduction and that there can't be more than 256 alleles at the same time. Coalescence based techniques reconstruct genealogies, rather than inflate the sequence space. In my lab we are working on the structure of sequence spaces and we've found several hollow regions. Math-wise the problem is so complicated that we think it's better to try maximum-likelihood to estimate possible parameters of bacterial sequence evolution that could've led to this hollows. Hence the need in a simulator of forward sequence evolution.

@EliKorvigo I reread your comment and realized I might have not addressed it correctly. I edited my answer. The comment is now 2.5 years old. I am curious, what did you end up doing?

I'm terribly sorry I've totally missed your New Year's eve comment. I've ended up implementing a parallel basic evolution model with (almost) unlimited population size in C.

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Reduce protein structure representation dimensionality.
In my lab we are trying to extract spatial features from protein structures. The software we develop makes use of CUDA for all heavy number-lifting, thus we are limited by the GPU's memory (12GB). Using standard voxel-based 3D-representations proved to be too memory hungry, hence we are trying to find a way to reduce the dimensionality to 2D, while preserving as much spatial information as possible. Our absolute goal is to preserve spatial colocalisation of different chains and secondary structures, to understand how important that is during folding. Standard techniques, such as PCA and PCoA on euclidian distances between amino acids, seem to preserve too little information on chain folds. We believe there should be a better way of doing that, but, having little experience in structural biology, we struggle to find any relevant work regarding this issue. Can you recommend any methods or relevant readings?

I'm not entirely sure I understand the question. What more spacial information do you need beyond .pdb files which hold the relative atomic co-ordinates? After this, dss can be ran to evaluate chain angles and overlay a secondary structure.

Maybe you could use a protein SSE graph? http://ptgl.uni-frankfurt.de/about.php

@James the question is how to project 3D structures from .pdb into a lower-dimensional space without losing the information on relative position of chains.

@gilleain this is actually quite interesting, though it lacks residue-level resolution.

I suppose you already solved this, but did you consider something like non-linear dimensionality reduction with a regularization energy term that penalized the sort of chain fold deformations youre trying to avoid? E.g. using diffusion mappings with a kernel that combined say geodesic distances with an extra term for handling the chain folds.

@user3658307 Unfortunately, we've only managed to optimise our 3D-representations so that they require less space. We've tried plain-old NMDS with stress optimisation to no avail, but I'll definitely look into your proposal.

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Ligand-binding assays: IC50, EC50 and Kd
I am reviewing several MHC-peptide binding affinity predictors trained on  IEDB data. Quantitative records for MHC class I allotypes come from a lot of different assays and, by extension, have different measurement types. Here are the most common measurement type descriptions (I haven't altered them in any way):

dissociation constant KD (~IC50)
dissociation constant KD (~EC50)
half maximal inhibitory concentration (IC50)
dissociation constant KD
half maximal effective concentration (EC50)

All of the predictors I've reviewed so far consider these measurement types interchangeable, which I find extremely odd. While IC50 and EC50 can indeed be similar under certain experimental circumstances, I find it hard to believe that any one of these can be approximately equal to Kd (this site already has a post on this matter). I've contacted several authors and database curators, and all of them have assured me that these values can indeed be considered more-or-less interchangeable, but I can't find any references to support these claims.

Not an answer (I can’t comment yet), but what is the difference between 1, 2, and 4?

@MarkusHeller as far as I understand, 4 means either 1 or 2.


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A tool to get annotation features by position in the reference genome
Previously, when I needed to find a genomic feature (promoter, CDS, repeat etc) that underwent mutation (SNP) I used my own scripts to load an annotation file, parse it, map the SNP's position and output the sequence of the feature. Now that I'm moving from microbes to mammals with huge annotations, introns/exons and huge genomes, my scripts don't work that well and I'm sort of lazy to optimize the code or rewrite it in a faster language, since I'm sure there should be some prominent tools for the task. That's it, could you recommend me some tools that do the following:

Given a reference genome, annotation and a VCF (or similar variant file) match the SNPs to genomic features in the annotation
Output the entire feature that underwent mutation, e.g. if the SNP happened in a protein-coding gene, I need to have the entire protein-coding sequence not just an exon/intron.

Thanks in advance.

The GTF/GFF format is universal. Why would your scripts not work? Try stream reading. It can be done in python and is default in awk.

@WYSIWYG My scripts is in fact written in Python. It pulls out the annotation region it hits. In bacteria there are no introns in protein-coding sequences, hence if I get an annotation hit I can simply pull the region. In mammals the script sometimes pulls a piece of a gene (an intron or an exon), though I know how to fix that issue. More importantly,  my script stores the entire annotation file in memory as a hash-table of ranges. That's not too much efficient.

The second column in the GTF is the feature name. You can parse only for exons. There are programmatic ways of limiting the memory usage; one easy way is to run the script chromosome-wise and just store the features that you are interested in.

I'm voting to close this question as off-topic because it is about programming, not biology.

Well, after 2 weeks and several thousand lines of code I got a demo-version of my revamped annotator up and running, but then I was told to take a look at SnpEff. The tool makes everything I was to implement in my own one, so if anyone ever wants to annotate SNPs with regard to genomic features they hit and possible effects, give SnpEff a try. It's really fast.


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Why does this study about genetic likelihood of COVID hospitalization not associate risk to base pairs?
In the study "Genetic mechanisms of critical illness in Covid-19", (free to download) the authors share their findings on which genomes seem to be associated with an increased likelihood of hospitalization when infected with COVID 19.
See Table 1 (page 9), to see that the Risk is represented by one letter. I'm not academically trained in genetics, so my only experience when reading these papers is that usually risks are associated with a base pair. Like "C/C', or "A/G".

Why is only one chemical/letter given? How does one interpret this?
*I'd like to mentioned that several genetic testing companies have the markers in this study mapped, so this could be useful information for patients and their physicians.

I'm not sure what's unclear; the table shows a Risk base and Alternative base for a SNP (aka, a substitute of one base for another) at a given location. What are you having trouble interpreting?

I’m voting to close this question because it requires reading an external paper to understand the question. This is a question and answer site about problems in biology in which any question must be comprehensible in itself. It is not a journal discussion group.

This is a quite reasonable question to ask about a style of data presentation that is not limited to a single paper.

The "Risk" is the single basepair sequence (A, C, G, or T) at the precise chromosome:position location in the column to the left of it.  "Alt" is the basepair present in the other allele.  The complementary nucleotide is still present on the other strand, but its identity is obvious and the decision of which strand's sequence to list was made when the original reference sequence was published.
The slash notation "C/C" (as in https://www.biorxiv.org/content/10.1101/2020.12.06.413971v2 ) means that the genotype for both alleles the person is carrying has been considered jointly.  In this table no such breakdown is given.  Judging by their subsequent interest in transcript level, it is conceivable their model was that the two alleles would have subtle additive effects on overall expression level with a subtle effect on Covid risk, so that incomplete dominance could be assumed... but to truly understand their motivation you need to understand high-definition likelihood inference (see the overview and paper link at https://medicalxpress.com/news/2020-07-high-definition-likelihood-inference-genetic-human.html ) which requires some study.


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What are the hairs/spikes on the edges of these leaves for?
Windows 7 has a wallpaper/background which shows an attractive, leafy plant with fine hairs or spikes on the edges. What might these be for, and what sort of plant is it?
My initial (uneducated) guess is some species of Sempervivum, with the hairs serving some purpose like water-collection?
Windows 7 leaf background http://p1.pichost.me/i/32/1555532.jpg

I believe the hairs are known as trichomes. They can be uni- or multicellular. Depending on the plant and type of hair, they can serve one or more of several purposes. They may interfere with feeding by small and/or large herbivores, depending on how annoying to the palate they are. Some plants use hairs to keep frost away from the surface of the leaf. They can serve as nucleation points for water droplets in areas where the plant's primary source of water is fog. On the other hand, they can also help reduce transpiration in windy areas by breaking up the flow of air across the leaf. Finally, in hot/dry areas, they can reflect some sunlight to protect the leaf's tissues.
So, the function really depends on the type of plant and its habitat. I'm not a botanist, so I can't confirm whether or not your guess of Sempervivum is correct, but if it is, then the hairs would likely help reduce transpiration in hot, dry, windy areas, and possibly block some sunlight.


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Do air purifiers work against bacteria and viruses?
We would buy a mobile air purifier in our home.
Against the smoke of the city, etc.
It would have a HEPA + activated carbon filter. They are marketing it as:

"filtration process captures 99.97% of airborne particles down to 0.1
  micron in size."

and having also:

"encapsulated ion particle charging chamber"

But the question:
Would the mentioned filter+ion charger also help cleaning the air from bacteria and viruses?
Ex.: "Coronavirus/2019-nCoV" is about "Coronavirus virions are spherical with diameters of approximately 125 nm" - but I just Googled it, not from an official source. And 0.1 micron is 100 nm.
UPDATE: would it be more effective, if it would have UV-C light in the air purifier?

The aforementioned filter will filter microbes
Yes, it is routine practice to use microfiltration in labs to sterilize solutions from microbes. 0.2 micron filters will remove all typically-found bacteria most of the time, except for the odd bacteria here and there, though this is uncommon. 0.1 micron filters certainly remove all stray bacteria that may make it through upon a single 0.2 micrometer filtration. Here is a nice read on the appropriateness of 0.2 and 0.1 microfilters, which simply states that 0.2 micro filters are usually more appropriate since they additionally guarantee a better flow rate.
The aforementioned filter will NOT ensure filtration of viruses
These filters are not used, suitable nor effective for viruses, however. You ask specifically about the coronavirus. From a 2015 study:

Coronaviruses are members of the Coronaviridae group and contain a
  single-stranded, positive-sense RNA genome surrounded by a corona-like
  helical envelope (Ryan 1994). The SARS virus genome consists of 29,751
  base pairs. Approximately 41% of the genome is GC base pairs while 59%
  is TA base pairs. Coronaviruses have a size range of 0.08-0.15
  microns; with a mean size of 0.11 microns (see Figure 1).

This means 0.1 micron filters will not protect you from these viruses. They may help you reduce viral count in the air, which may of course be sufficient, but this would not be an adequate measure in a biological safety facility.
The cost-effectiveness of commercial air-purifiers for biosafety vs. pollution
On a advice-related note: I do not think air-purifiers are going to help you in a cost-effective manner to avoid viruses (e.g. Rhinoviruses that cause the common cold, for instance), lest you stay at home all the time. You expose yourself outdoors, and carry plenty of viruses indoors on your body and in your respiratory tract; these will bypass your filtration system on the daily. Being healthy and lucky enough to avoid exposure to viruses outside the house is still the best bet. I think an air purifier has a greater potential to help with smog and urban pollution, those particles are typically larger than the diameter of most microbes.

Wow, thx. I updated the question, UV-C popped in my mind :)

It would depend on the UV-C lamp and how it sits in the purifier. A quick google search copy pasta for you: "the average bacterium will be killed in ten seconds at a distance of six inches from a typical UV-C lamp". And from Wikipedia on microbe inactivation: "dosages for a 90% inactivation of most bacteria and viruses range from 2,000 to 8,000 μW·s/cm2". Air filtration units would have a flow-through, so the lamp(s) would have to illuminate a very thin cross-section of the piping; again, its efficacy would depend on the flow-rate, distance from the lamp, and illuminated area.

When thinking about using a HEPA filter for dealing with air-borne virus and bacteria, there are two important things one need to know:
1- While a sieve traps objects larger than a certain diameter and let the smaller ones pass through, this is not what happens in a HEPA air filter. In this case, due to the principles of fluid mechanics, and also because of brownian movement, there is a critical size (around 0.3 Micron, 300nm) for which, the filtration efficiency is minimum. This means that for both particles larger and smaller than this critical size, a HEPA shows very good filtration efficiencies. As you can see in the graph below, for a True HEPA, even for this "most penetrating" size, the efficiency could be still very impressive (higher than 99.7%).
This means that a good quality microfiberglass HEPA filter can be very good in eliminating nano particles the size of a virus.
2- The second point is that very small airborne microorganisms, are in many instances attached to bigger particulate substances in the air, whether liquid micro droplets or solid particles. I do not know so much about the nature of the bonds and whether this happens for the coronavirus or not, but this may be reason for higher risk of respiratory infectious diseases when PM2.5 air pollution gets high.
For these two reasons, I believe that HEPA air filtration could help a lot in indoor spaces, reducing the risk of infection, by reducing the number of particles of any size from the air.
In contrast, when comparing to the application of UV-lamps, there are to negative points:
1- UV lamps have lifetime and the radiation wavelength is so much affected by working hours of the lamp.
2- If air speed and exposure to radiation is not enough, complete degeneration may not happen and we can not be sure if we are not producing a new genetically improved virus!
All Together, I think we should generally be more careful with the active control methods. With passive control methods such as HEPA filtration, we are sure we are not adding anything new to the air!!!
As a reliable reference on the efficacy of HEPA filters on bacteria and nanoparticles you can see the Technical Memorandum of NASA Marshal space flight Center of May 2016:
Perry, J. L., Agui, J. H., & Vijayakimar, R. (2016). Submicron and Nanoparticulate Matter Removal by HEPA-Rated Media Filters and Packed Beds of Granular Materials.

Many thanks for the infos! :O


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What is the common ancestor of humans and trilobites?
I have always been immensely fascinated by trilobites. What is the single common ancestor of humans and trilobites? Do we know? Do we have a name for it? Have we identified it?

Welcome to Biology.SE! We expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). I suggest you start with the wikipedia page for trilobites and pay particular attention to the "Scientific classification" panel. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

try searching common ancestor of arthropods and vertebrates.

Thanks guys :) I have always been fascinated by science. I look forward to spending more time here on this wiki.


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What's the role of SNP (Single Nucleotide Polymorphism) in a disease when there is no gene associated to that SNP
I am quite new to the field of GWAS (genome-wide association studies), and I'm combining GWAS results and single cell analysis on type-1 diabetes (T1D), to see the role of cell specificity on the disease.
However, I don't understand one aspect about GWAS results. The GWAS results lists all the significant SNPs (low p-value) from a certain study on a particular disease. After that, those SNPs are mapped to genes using either positional mapping (using windows), eQTL mapping, or even both.
However, some SNPs do not map to any genes using both positional and eQTL mapping procedure. Some removed SNPs even have a lower p-value than those which are mapped to genes.
Here is my question: since all the listed SNPs are supposed to be significant (tiny p-value), how can those SNPs which are highly correlated to the disease also show no association towards any gene. How do these SNPs give rise to the disease?
I would like to thank you in advance. Sorry if I'm using wrong jargon or anything, and please let me know, if you want any further clarification.

SNPs do not signify anything about the functionality of a particular piece of DNA. You can think of a SNP as just a sign that says "hey, something in my neighborhood might be interesting!!" In this respect many GWAS SNPs are so-called "tag SNPs", that have been selected specifically to give the minimal number of SNPs that can be linked to all of the genome (e.g. every 1 centimorgan there is a SNP, or whatever).
So: SNPs do not say anything about biology, or about genes. The only thing that they signify is linkage to something that is possibly interesting.
Your issue seems to be that you are coming up with GWAS SNPs that do not show apparent linkage or statistical associations (e.g. eQTLs) to anything that you think should be interesting.
There are a lot of ways in which this could be the case:

There actually is a gene in that part of the sequence, and we just haven't annotated it properly.

The reference genome is wrong in that SNP's location, or is missing an interesting piece of sequence (i.e. a gene) that exists in your population.

That SNP has a population structure signal (i.e. it is more common in one population than another) that is associated with your trait of interest, which you have not properly corrected for.

That SNP is spuriously linked (for whatever reason) to a more distant part of the genome.

That SNP was mis-mapped and is actually in the wrong part of the genome somehow.

There is technical interference due to high similarity to some other part of the genome, which your procedure has not corrected for.

Sometimes frequentist p-values are not actually informative and a thing that looks interesting according to p-values is simply not interesting.

Though there are no genes, there is a long-range enhancer in the region of the SNP that affects a distant gene.

Though there are no genes, there is repetitive DNA linked to the SNP that leads to a complicated regulatory feedback that affects something about your character of interest.

Something about microRNAs?

Your SNP doesn't have any genes nearby, but it is linked to a TAD boundary that affects overall chromatin architecture.

There is a long non-coding RNA there.

Your eQTL significance threshold is too stringent.

Your eQTL association analysis missed an important isoform or transcript.

... and many other hypotheses! Many of these are very hand-wavey or unlikely, but sometimes biology is just weird.
However, in general I would default to an explanation in which there is some kind of technical or statistical artifact. Even when nothing is obviously wrong, there is usually some kind of technical problem in genomic datasets.

This is a great answer.

Are you sure about your artifact proposal? I seem to remember a recent paper in Nature by the ENCODE consortium that is consistent with the poster’s observations. You might check, or I will if you don’t have full access.

@David if you are referring to the estimated functionality proportion, yes that is ENCODE. subsequently a lot of evolutionary biologists got very angry about that and discredited a lot of it, but my explanations (8, 9, 10, 11, 12) are all basically ENCODE-adjacent- it's def true that there's a lot of stuff in the genome that ain't a gene that is still biologically notable. However, I would argue that artifacts (explanations 1,2,3,4,5,6,13,14) are still more likely. Of course, it can be an artifact and still be interesting!

OK. I found the papers and they weren't quite what I remembered.


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Disprove mitochondrial eve is 6500 years old
Some creationists, such as Roger Liebi, actively exploit this article:
A high observed substitution rate in the human mitochondrial DNA control region (published in Nature Genetics, April 1997).
This study directly measured  the mitochondrial DNA mutations rate across 327 generational events (mother-daughter, grandmother-granddaughter, and siblings) and calculated it to be 20x greater than values previously estimated by evolutionary models.
It gives the age of mitochondrial Eve to be 6500 years, which is surprisingly similar to the biblical (Jewish calendar) date.
I am looking for the best way to disprove this position.
Since 1997, has this article been disproved?
What is the best way to disprove this estimate?

It's not much use to argue with creationists who didn't get to their positions from science in the first place. https://biology.stackexchange.com/questions/7184/what-is-a-mitochondrial-eve-and-y-chromosomal-adam may help you.

Thanks for the answer, i also would like to have an info about normal article where the mitochondrial DNA mutation speed is properly empirically measured, means, like in this article but normally, with big base and not "not 10 mutations on 300 events"

If you feel you want to try - its an experience you might learn from, 'Giving up' is not always the right advice.  acheological evidence that is not DNA based... https://www.nature.com/articles/1601646 radiocarbon dating was the most common evidence before 2000.  I do agree with the others that there are alt explanations for all this data tho...  I really do think this a valid question and downvoting it is unfriendly and it doesn't invite the spirit of enquery which is the basis for all the best science.

Yes, people do not read carefully the question and downvote, do not recognize the question is valid and different from mentioned above.
And please do not mention the radiocarbon dating, it is also strongly attacked by creationists, and unfortionately, this attack is fair, because date can easy become old for a young sample, what have fewer isotopes for some reason for example some fish, etc.
I d still like to have study like that, but normal and have a clear mDNA mutation rate, and it would be very, very strange, if the first possible m-Eva would be realy 6500 years old dated...

If the age of Mitochondrial Eve actually is consistent with the Biblical account, then so what? That doesn't prove that there was a flood or that some shepherd led his people across a river. Even a broken clock is right sometimes.

Quick science lesson, if you use a much smaller sample size and get a drastically different answer,  statistically you are far more likely to be the one who is wrong.

You don't need to disprove it with the same paper, you can just ask them where the thousands of skulls and bones dated previous to 10-20k years ago, which are obviously human come from, and why they don't cite modern papers and resort to a single old one? what about flint tools and 400k year old wooden spears? like the yew speak tip of 37cm found in teh sea, dating from 400k years and others from germany dated 300k from neanderthalis.

Estimating the age of the so-called "mitochondrial Eve" (i.e. the most recent common ancestor, MRCA, regarding mtDNA) is a very complex issue, exactly for the difficulty in correctly estimating the mutation rate.
So, it is not so easy to disprove the estimate, but at the same time there aren't particular reasons to choose that (and not the several other available estimates) as the correct one.
I point you to three papers that discuss the issues of estimating mtDNA mutation rates and my be of interest for you:

Estimation of Past Demographic Parameters From the Distribution of Pairwise Differences When the Mutation Rates Vary Among Sites: Application to Human Mitochondrial DNA
Pattern of Nucleotide Substitution and Rate Heterogeneity in the Hypervariable Regions I and II of Human mtDNA
Hypervariable Sites in the mtDNA Control Region Are Mutational Hotspots

It will also be an interesting exercise for you to collect from these papers (and the several references therein) all the different estimates of mtDNA mutation rates (and thus of age of the mitochondrial Eve) and you will realize how reliable the 6500 years (without confidence intervals) would be!
Finally, the literature I provide is well established, but also a bit old (but still more recent than the 1997 paper). You might want to see more recent literature.

Additionally it's very very important to realize that a "biblical Eve" as in "first woman" (a nonsense concept in biology) has nothing to do with "mitochondrial Eve".

I’m afraid that referring to papers is not an answer. Also the verb is “disprove” — the noun “proof” exists in English, but no noun “disproof”. Also note that appropriate questions for SE Biology regarding a paper like this are 1) whether the results are reliable or repeatable? 2) If so, how can they be interpreted? There is no need to even consider interpretations based on religious superstition. The general evidence for the dateline of evolution is supported by a mass of diverse evidence and is not in question.


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What's known on genetic factors that explain behavioral differences between human males and females?
Long story short: women are from Venus and men are from Mars. But how much of the differences arose from evolution and how much of it comes from Venusian and Martian cultural differences?
Jokes aside, I'm looking for an overview of which social-behavioural differences science has already pinpointed to be rooted in evolution.
update: this article is a great starting point
This question also pertains to psychology, therefore I also asked a related question there.

There are many behavioral differences which are hypothesized to have an evolutionary basis, and which many evolutionary psychologists believe are strongly supported by the evidence. But you have a wrong view of science. There will never be a time when something is "proven," it can only be that more and more people accept something on the basis of compelling evidence. No matter how much evidence there is, a sociologist can always say that they aren't convinced.

In addition to that it's well possible that a given difference both has a evolutionary basis/root (however tiny it may be) and was expanded into a larger social construct.

@Nicolai Or be shrinked by social influence. In other words, it is possible for a sex difference to exist in spite (not because) of social influence. Personally, I think that this is probably quite common.

This overview paper should help you, it is a review of known differences. http://wps.prenhall.com/wps/media/objects/12330/12626747/myanthropologylibrary/PDF/NDS_41_Ember_50.pdf

I'm not sure where you got the idea that you can conclude something is not socially constructed because it has "an evolutionary basis". Social constructs and changes in allele frequencies are not mutually exclusive, nor is one less real than the other.

How statistical of a difference are you looking for? no behavior is going to be universal and exlusive to all men/women. The quick and dirty way of telling is to see which behavior are universal across cultures, not perfect but probably your best bet. I seem to remember that, males are more likely to commit homicide and women are more talkative in every culture studied. but this is purely from memory and I cant remember if it was by sex or gender. .

I would like to have more precision in this question. What are "males" and "females", and what is the difference between them genetically? You can trivially say XX/XY, but there are plenty of karyotypes that fit into one of the traditional sexes without even getting into gender identity. Then there are male/female/nonbinary gender identities, which are imperfectly correlated with karyotype, but nonetheless adhere somewhat to traditional "sex" behaviors. One can obviously point to developmental characters (secondary sexual characteristics such as hormones), but that's a bit tautological IMO.

Short Answers

At least one personality trait (neuroticism) works differently between males and females on a genetic basis.
The effect of Testosterone on male behavior (aggression, reproduction, self-maintenance) is deeply rooted in vertebrate evolution, while it is proven that testosterone controls behaviour in human males as well. (Only males produce large amounts of testosterone)

Connecting Personality Traits to Male/Female -Genetics
David pointed out that an explicit connection to evolution is not necessary to explain genetical differences in male/female behavior.
Weisberg et al. 2011 have mapped the "big five" personality traits to males and females. So the martian and venusian aspects of personality can be quantified.
South et al. 2018 (paywall) did perform twin studies to find a genetic basis for sex differences in the big five. As far as I understood, they did not find any genetic differences between males and females.
Wendt et al. 2022 however looked specifically at the trait Neuroticism. Neuroticism can be understood as the likelihood of a person to worry about something. It's not a disease or psychological condition, it's just one of the "big five" personality traits.

Gene expression variation in the pituitary was enriched for neuroticism loci in males (males β=0.026, P=0.002) and genetically-regulated transcriptomic changes highlighted the effect of RAB7L1, TEX26, and PLOT1.[...] this study identified several molecular pathways that can partially explain the known sex differences in neurotic symptoms and their psychiatric comorbidities.

Testosterone Affects Every Vertebrate, including Humans
Testosterone heavily affects human male personality, mood, behaviour, etc. (Zitzmann 2020). This might come from mechanisms that are essential for the survival of every vertebrate species.

Testosterone's impact on Mating Habits is Conserved within all Vertebrates
Testosterone is the key modulator of male mating habits (which may influence socio-behavioral differences between males/females more than we like to admit): Husak et al. 2021 (paywall)

We study this topic by assessing how various social and environmental dynamics influence testosterone levels across the
entire vertebrate tree of life. Our analyses show that breeding season length and mating system are the strongest predictors of average testosterone concentrations, whereas breeding season length, environmental temperature, and variability in precipitation are
the strongest predictors of within-population variation in testosterone.

Testosterone may be too Deeply Rooted in Animal Physiology to ever be Changed at all
Here's another paper, (Hau 2007 (paywall)):

Mechanistically, trade-offs result from the need to differentially allocate limited resources to traits like reproduction versus self-maintenance. [...]. The hormone testosterone may mediate life-history trade-offs due to its pleiotropic actions in male vertebrates. Conservation in the actions of testosterone in vertebrates has prompted the 'evolutionary constraint hypothesis,' which assumes that testosterone signaling mechanisms and male traits evolve as a unit. This hypothesis implies that the actions of testosterone are similar across sexes and species, and only the levels of circulating testosterone concentrations change during evolution. In contrast, the 'evolutionary potential hypothesis' proposes that testosterone signaling mechanisms and male traits evolve independently.

When I look up "evolutionary constraint hypothesis" (if I understood correctly) it states that testosterone signalling has established a deep connection to multiple target tissues. This connection is so deep, that one trait's connection to testosterone can not evolve without affecting another. That's why the effect of hormones is so conserved among animals in general (Ketterson & Nolan 1999 (Paywall), McGlothlin & Ketterson 2007).
Others think that testosterone derived traits are not constrained and can evolve (in part) independently from another (‘evolutionary potential hypothesis').
Overall, one can not evaluate much raw data, since all these papers are behind a paywall. Nevertheless, the papers cited here show that there are very strong opinions that testosterone determines male traits/behavior and that this can control vertebrate evolution.
But like I said, that does not totally exclude cultural factors.

You say in a post on Meta that many questions about evolution are rather about differences. It seems to me that this is an obvious case. The question is simply nature v. nurture, or more technically, are there social-behavioural differences between the sexes that have a genetic basis. If there are differences with a genetic basis they obviously evolved, so talking about evolution is obscuring the real issue. Your answer does not provide the sort of objective answer I consider required — such and such a behavioural trait is determined by such and such a gene(s).

If there is a genetic basis it evolved, yes, but do specific narratives exist in the literature that  illustrate the evolutionary nature of male/female differences in behavior? — my attempt is definitely not a good one BUT I had fun writing it and I hope that others find better narratives than I did, since I am very much interested in how much cultural and how much inherited factors determine our behavior

@David - I see your point, one can remove the „evolution“ part of this question and it would still make sense. So it‘d be enough to point at genetic differences between males and females, filter out behavior-associated genes, and then the question would be answered?

I think so. Although on reflection regulatory genes may affect the extent of testosterone release and hence aggression in different societies. One could argue about what caused this in some societies and not others, but I suspect we don’t have much info on these genes, much less the influences on their selection, if indeed this occurred.

I think that in the age of NGS and Cambridge Analytica I expect there to be studies that associate SNPs to the big five personality traits and distinguish between males and females.

I found something and edited my answer. Should I delete the testosterone part?

You can edit your answer to improve it as you feel fit, especially if nobody has upvoted it yet. I tend to do so myself if I think it needs changing, even if it has votes. I generally draw attention to this and invite voters to reassess (although they don't). One generally piece of — I hope — constructive criticism. It helps the reader if you can start with a summary when one's answer is quite extensive. Just call it "summary" or "Short Answer", but please not the internet slang expression. It prepares the reader for your argument and lets him decide whether he wants to read it.

Alrighty. Applied your tips. Also changed the header and tags of the original question

Re: my comment on question, I am still not sure what a genetic difference between males and females is. Testosterone expression does not equate to male/female stuff. Who are males and who are females? Are you respecting peoples' gender identities? You will get quite different answers depending on whether you take a gender essentialist view vs. a more nuanced view of gender. I think that you should take gender identity into account, but that also makes the question a lot harder to answer. What happens when the same person presents different gender identities / behaviors?

I see your point. So gender is what one identifies with, and sex is the biological sex, right? So if I replace "male/female" with "sex" in my answer, this should solve the issue, right?


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Is there any evidence that physical appearance and temperament are coinherited together in humans?
Recently my wife and I had our second child, and I've noticed a trend with the two. Our first looks a lot like me, similar facial features and head shape, and along with it he also seems to hold many of my behavioral traits. Now with our second we're seeing the opposite, he looks a lot like mom (facial features and head shape) and so far he seems to have many of her behavioral traits, but none of mine.
My question is: have any studies discovered that appearance and temperament are (at least partially) inherited together? Has it been proven that a child who looks more like one parent, will likely behave more similarly to that parent?

Very interesting question, but I suspect the true answer is going to be exceptionally hard to find out. Disentangling the effects of shared environment and genetics on social traits in humans is a very very tricky problem.

No solid evidence as to linkage of appearance and personality traits, but there is some evidence of linkages of physical appearance and some medical aspects of health, e.g. cardiovascular fitness. But there’s plenty of evidence - solid - that many “personality traits” are heritable, and present from birth. I suspect it’s possible but not probable.

@user438383 anecdotal, but in my experience very specific traits are directly heritable - extraversion, memory capacity, language capacity, deductive ability. Essentially traits that are dictated by brain shape and structure.

When you say "in my experience" - do you mean in the twin-studies that you've read about?

Basic observation of parents/children, I've also got a bit of neurophys under my belt. I get that people at this stack won't like an unevidenced comment. The way I see it is that brain structure offers the basic framework, or template, for temperament. Environmental experience then interacts with that structure.


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What is meant by 'identical alleles'?
I read in my book that "two alleles are considered to be homozygous if they are identical". But at the same time I read the definition of allele to be:

genes which code for a pair of contrasting traits are called alleles

My doubt is that how can they be both contrasting (different) and identical (same) at the same time
What I think is that if homozygous is somehow a part of specific conditions in alleles then how can it be different from alleles itself.

These are just issues with singular and plural and whether you refer to individual copies or categories/types.
Two of the same allele copies are the same allele (category/type). Two different alleles (copies) can also be different (categories/types).
In the context of a diploid individual, they have two instances of each gene so therefore two alleles; these alleles can be the same or different.
So you can say you have two "red flower" alleles, meaning two copies of the red flower allele. Or you can have a population that has two alleles for flower color: red flower alleles or white flower alleles.
The same is used in English for other things. You might say a farm grows two fruits, peaches and plums, and also that I have two fruits in my hand, both peaches. You need to use surrounding context to recognize whether copy or type is meant.


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Image sensitivity of eyes and peripheral vision
I have bad eyes and need glasses. However I have noticed when it is dark, I am able to see contrasting colours a lot better in the corner of my eyes, than in the center, e.g a mark on my wall I can't see if I look directly at it, but I can see it at the corner of my eyes.
I have also noticed that the light in my kettle appeared to flash on and off in the corner of my eyes, but when I look directly at it, it doesn't blink at all.
Slow motion imagery on my phone shows the light IS indeed blinking.
So what specifically about human eyes allow for these effects? If it was simply blurry then I would just account that to lack of focus of light. But surely the refresh rate of my eyes (to see flashing) is constant?

While I understand what you are asking, I think you are asking three questions at once. Can you plase clarify what is the main question being asked? Peripheral vision, the cases you experience, or the refresh rate of your eye?
Also, I wish there would be clearer grammar and statement. I am having a tough time understanding your third sentence.

Does your kettle use LED by any chance? If so, those certainly blink on AC power, basically lots of on-off as the waveform passes through. Why the eye see it as steady is something for you to research.

I would say the main question is about what causes the effect in my kettle, and the specific relation as to why I can only notice it when looking at it through the corner of my eye.

Yes the kettle is an LED, i know WHY it blinks. But  not as to why the difference in my perception of it varies with the location on my eye.

I think we can agree that the faraway star we see mostly twinkles, or pulses when seen by our naked eye. Since you stated that the kettle LED is also blinking, both are the same cases.
You are experiencing what is called averted vision. Our eyes have 2 different cells that can sense light: cones and rods. Cones are adept in seeing colors and mostly concentrated on an angle centre to the eye (the fovea). The rods, however, are contrast sensing and more concentrated around the the periphery of the fovea.
Cones are simply great in distinguishing color, while the rods are great in detecting brightness. This affects what you are seeing in dim or dark locations: since there is not enough brightness to be sensed by your fovea, the cones can't distinguish really good. The rods around the fovea, however, are doing just fine. This is the reason you can see details while "tailing" using your eye. In fact, amateur (and ancient) astronomers observe faint stars by using their peripheral vision.

stars twinkle because of the atmospheric turbulence which gives the same effect as a haze mirage on a hot road.


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Choosing a book to gain general knowledge about biology
I will be first year undergraduate at Physics department next year and last year I was at the Medicine faculty. I want do double major in the second year of faculty with Molecular Biology and Genetics. The intersection of biology and physics is my interest. I have two books about biology, first one is What is Life?-Mind and Matter by Erwin Schrödinger and the second one is This is Biology by Ernst Mayr. Which one should I read to acquire general knowledge about Biology?

The books you have
The books you cited won't help you to get a solid and general basic knowledge in biology. I haven't read those books but I think that This is Biology is a book of philosophy of biology written by a biologist and philosopher. What is life is a very influential book written by a physicist who more or less predicted the structure of DNA that was later discovered by Watson and Crick. You won't learn much of biology through these books.
Book Suggestions
This post offers book suggestions for general introductory biology. Here is another post that may also interest you
If you are interested in a specific field of biology, then you may want to ask for book suggestions for this particular field. I think that most biologists that come from a background in physics are in the fields of theoretical evolutionary biology, bioinformatics and biophysics (incl. molecular biophysics).
Here are a bunch of other posts asking for book recommendations that I imagine you may like reading about.

What physics knowledge can be applied to biology of organisms and ecosystems?
Book recommendations for algorithms used in evolutionary biology
Book recommendations for evolutionary models
How to learn biomathematics?
Book recommendation on population/evolutionary genetics?
Introductory literature for synthetic / systems biology?

And eventually you may want to read Value of mathematical models in biology although the post has been closed.
Of course, you might want to read a bunch of wikipedia pages such as Biophysics, Molecular Biophysics, Mathematical and Theoretical Biology, Biostatistics, Computational Biology, Bioinformatics.


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best book for a comprehensive introduction to biology for a computer science graduate interested in undertaking research in bioinformatics
I have a postgraduate degree in computer science, and I wish to undertake research in bioinformatics. I had chemistry but no biology in high school. I have read bioinformatics books like "biological sequence analysis" by durbin and "fundamental concepts of bioinformatics" by krane, etc. But I wish to read a comprehensive book on biology (genetics) that will help me undertake research in bioinformatics properly. I have been considering 2 books: "molecular biology of the cell" and "molecular biology of the gene". Are these books comprehensive enough? Please suggest some good books as I have almost no knowledge of biology at highschool or graduate levels.

Molecular biology of the cell is a really nice book..

I concur with biogirl. MBotC was my introduction to molecular biology, and will give you a lot of background information. Of course, it shouldn't be your only resource (you wouldn't read just one book to learn a new programming language, for example), but it's a great place to start.

Molecular Biology of the Gene is a very good textbook.   For molecular genetics, this is an excellent choice. Molecular Biology of the Cell is also a very good textbook (actually, you listed my two favourites) but, as the name suggests, it is more focused on molecular cell biology. That said, is does cover molecular genetics quite comprehensively; you can't really go wrong with either book. However, it's hard to say whether either of these are the best book for you. There's a difference between molecular genetics and, say, population genetics.

Also, if you have no experience with biology at all, you may want to try a more introductory textbook. Molecular Biology of the Cell is good at working its way from the basics to more complicated topics. On the other hand, Molecular Biology of the Gene assumes you have some working knowledge of molecular biology.

Welcome to Biology and welcome to Biology.SE!
It is hard to answer such a question as the domains you describe are very vast.
If you want a book in an introductory book to biology, then you want to read this post and this post.
If you are more interested in population genetics and molecular evolution then this post will interest you. Still talking about evolution I'd like to attract your attention to this post for the second suggestion in the first answer:  Yang, Computational molecular evolution
You'll probably want to have a look at the post A free book/resource for learning genetics?.
Book recommendations for algorithms used in evolutionary biology and Introductory book in genetics might be a post of interest as well.
Unfortunately I don't know any of the two books you cite so I can't quite give you advice for them. molecular biology of the cell is a very common book among first year biology. It sounds like a potential good reading for you. I know nothing about molecular biology of the gene except what I just read about it on Amazon.
I am hoping one will give you a better criticisms about very general books about molecular biology.

Thanks a lot for the info. Do you think I should read books on biochemistry, virology and immunology in addition to the above books you suggested, because I am finding most research in bioinformatics being focussed in these areas?

It very much depend if you're intending to work in those areas. You can't learn everything. I think that a basic understanding in molecular processes of the genetic expression is essential. I think that having a slight understanding of molecular evolution is essential as well (but I am maybe bias as we are getting closer to my field) and then I suppose that it is not necessarily worth knowing much about phylogenetic, immunology or virology if you don't intend working in those fields. There are many existing tools and database in bioinformatics, it is part of the formation to know them I guess.


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If one endures the same form pain over a long period of time, would the pain begin to lose intensity?
Metaphorically thinking, if one endured the pain of constant burning for decades, would the pain slowly lose its strength?

It depends on the kind of pain. A literal hot thing being applied at 200F or more? A 120F thing hot enough to be uncomfortable but not enough to cause tissue damage? A chemical irritant?

@Resonating Craig is probably thinking of long-term pain, such as back pain from a slipped disk or an old injury.

Under the assumption that the temperature experienced is not high enough to simply burn the nerves responsible for the pain (which would lead to insensible regions), yes and it would due to what is called receptor desensitization. In the case of burning pain the receptor involved is called the transient-receptor potential channel V1 (TRPV1). It is the same receptor involve in the oral burning sensation of spiciness.
Now two scenarios are possible given your question, namely a constant stimulus over a long period and "oscillating" stimuli (i.e. a repetition of stimuli followed by non-stimulated periods).
Constant stimulus
I provided a similar answer to this question: What features cause mechano sensory adaptation?. This is the scenario where you keep the painful stimulus constant over a period of time. Here desensitization, i.e. reduction in pain feeling, is due to a direct receptor desensitization. This happens because the receptor is internalized (also called receptor-mediated endocytosis) into the cell after being activated and it takes some times for the receptor to reach the cell membrane again meaning if the stimulus remains constant, pretty much no receptors will be left on the cell membrane.  After decades long term desensitization will occur and is slightly different in it's mechanism compared to standard desensitization as described hereafter.
"Oscillating" stimuli
In the case you are talking about a chronic pain interrupted by periods of non stimulation then long term desensitization will occur. In this scenario, the concentration of receptors will be reduced semi-permanently (i.e. reduced expression of the receptor) in the receptor cells reducing the pain signal. This is what happens with spiciness sensation. People eating regularly very spicy will physiologically be less sensitive to spices as they have less receptors sensing the spices provoking a reduced burning sensation.

Just as a footnote, very long chronic pain will also change the brain wiring of the pain signal but as I don't know enough about neurobiology I will leave that appart.

@AliceD Nocireceptors are molecular receptors not neurons, at least when you talk to a molecular physiologist. Receptor internalization occurs and is the primary way cells become desensitized. I will add references when I have some time but for the time being I worked and published several papers linked to taste perception and receptor-based signaling.

I'm looking forward seeing these references. Interesting stuff. Ping me after edits and happy to remove the -1. I thought pain was mediated by nerve endings - https://en.wikipedia.org/wiki/Nociceptor

@AliceD This is perfectly true but the nerve ending have molecular receptors on them (for noxious heat pain, namely TPRV1), this is what I called a nocireceptor, I guess we have a scale issue :). I modified my answer to include the concept of Receptor-mediated endocytosis, i.e. internalization. By the way you should post an answer on the brain adaptation to pain as you know way more than I do on this subject.

Yes, you are right. Thanks for clarifying. I removed the -1 and after adding  a reference I'm happy to upvote.

Short answer
Chronic pain may be very persistent and even worsen over time, but it will depend on the underlying pathology. If the pathology disappears over time, so may the pain.
Background
There are roughly two kinds of pain:

Acute pain is pain that lasts for a short time and occurs following surgery or trauma or other condition. It acts as a warning to the body to seek help.
Chronic pain is pain that lasts beyond the time expected for healing healing following surgery or trauma or other condition. It can also exist without a clear reason at all.

A large body of basic research indicates that chronic pain is associated with neuroplastic changes in the nervous system at peripheral, spinal cord and brain levels. Thus chronic pain is shown to have a distinct pathology that often worsens over time, and constitutes a serious separate disease entity.
However, if the underlying pathology disappears, the pain may lessen. However, based on the cited paper, I do not think chronic pain gets less severe over time due to neural adaptation.
Excerpt from the linked article upon request:

These and other changes may contribute to the development of alterations in central [spinal] neuronal responsiveness, which share features of wind-up and long-term potentiation and are collectively known as “central sensitization.” [...] These alterations in cell responsiveness may be evidenced by a number of symptoms and signs, including spontaneous pain [...]. This [...] has been demonstrated in patients who have chronic pain associated with whiplash injury and fibromyalgia and suggests that the presence of pain [...] is associated with increased sensitivity of spinal neurons.

Reference
- Siddall & Cousins, Anesth Analg (2004); 99: 510-520.

Perhaps desensitization occurs, but at the perceptual level it may not be noticeable I guess.


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Does binge watching cause sleep problems?
According to a study from 2017, binge watching is correlated with various sleep problems:

The people who reported binge-watching were 98 percent more likely to report poor sleep quality compared with those who watched one episode per sitting, according to the findings.

However, the study only showed a correlation and did not touch on causal inference:

The study authors did clarify that there were limitations to the study since they saw only correlation between binge-watching, and not evidence of causation, or that binge-watching definitively causes poor sleep.

Is there a study that investigated whether or not there is a causal relationship between binge watching and sleep problems?

Science cannot prove. That's neither the purpose of science nor is it a possibility. 2. You will not typically see causation discussed in scientific literature. Instead, we tend to discuss correlation,so a paper showing strong correlation is a good starting point. Keep your eye out for more papers demonstrating corraborative data/analysis to increase your confidence of this linkage (but always remain open/dynamic in your thinking as alternative trends may be later demonstrated).

Can’t causation be demonstrated by randomized controlled trials?

According to the national library of medicine: ‘Although no study is likely on its own to prove causality, randomization reduces bias and provides a rigorous tool to examine cause-effect relationships between an intervention and outcome.’ Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6235704/#:~:text=Randomized%20controlled%20trials%20(RCT)%20are,between%20an%20intervention%20and%20outcome.

I have to partially disagree with theforestecologist on their comment. It's true that Proof is generally the stuff of philosophers and mathematicians. But there is plenty of scientific literature seeking to establish and describe causal relationships, especially in medical research. Kochs postulates are one such approach that's been widely utilized for nearly 140 years for infectious disease research and frequently adapted to provide similar frameworks for different biological systems. Hill's criteria for causation are another example that's probably more relevant to this topic.

Should I modify my question to let the downvotes disappear?

The question if somethings that are correlated are causally related is definitely a valid question and prospective studies, for instance, increase the chances of deducing causation. So I also do not share all of the views expressed by others here in the comments.


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How can I find/simulate mixed-ancestry DNA data?
Some collaborators and I are building an ancestral inference tool, and we're having trouble obtaining reliable ground-truth data for samples of mixed ancestry. All the ground-truth DNA datasets we're aware of (Thousand Genomes, Simons Foundation) are from persons reported as unequivocally belonging to some population (East Asian, African/African-American, South Asian, or even something specific like Somali, Icelandic or Cambodian.)
But we can't find any samples that are attestedly mixed-ancestry. We've thought about just generating simulated data using VCFs from two persons of different known ancestries, but we're not sure how to account for the non-random aspects of recombination, which are described here:
https://www.bio-itworld.com/news/2019/03/06/latest-genetic-map-finds-recombination-is-not-so-random
And we don't know of any tools that could perform this task for us.
Does anyone have suggestions for obtaining/simulating DNA data for persons of mixed ancestry? This is a natural enough problem that we suspect others must have encountered it also.

Price et al 2009 describe how to simulate admixed genomes in this paper.

We constructed 40 haploid admixed genomes (n = 1 to 40) from the 40
haploid Yoruba and 40 haploid French genomes by using haploid Yoruba
genome n and haploid French genome n to construct admixed genome n, so
that ancestral genomes were never reused. To construct an admixed
genome, we began at the first marker on each chromosome and sampled
French ancestry with probability α and Yoruba ancestry with
probability 1-α. Ancestry was resampled based on an exponential
distribution with weight λ (the number of generations since admixture)
so that a new ancestry was sampled with probability 1−e−λg when
traversing a genetic distance of g Morgans. Each time ancestry was
resampled, we sampled French ancestry with probability α and Yoruba
ancestry with probability 1-α. For each individual, we used a value of
α to apply to the entire genome by sampling from a beta distribution
with mean 0.20 and standard deviation 0.10 (typical for African
Americans [4])

You could apply this method to e.g. .bam/.vcf files from SGDP and use the sampled ancestry as regions in the .bam/.vcf file from different ethnicities.


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Influence of pH on rennet coagulation of milk
I was looking for the reason why rennin works most efficiently at pH 6.7 (closer to a neutral environment than acidic).

Welcome to SE Biology. Please take the time to finish reading the [Tour], and the Help on asking questions. It would help us to help you if you provided some context to your question. Are you interested in the pH in relation to the mechanism of action of the enzyme or to its biological environment? Tell us why you might expect it to have an acidic pH optimum. This might be obvious to you, but not necessarily to us. And what attempts have you made to answer this question yourself from freely available resources like Wikipedia?

Can you quote a source for rennin working more efficiently at pH 6.7?  As I understood things, chymosin (rennin) has a pH optimum of about 3.8 (see for example Protein engineering of chymosin; modification of the optimum pH of enzyme catalysis), as you would expect for a stomach enzyme.


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Temporal space-use modeling - How can I quantify temporal variation into a single value without losing magnitude?
For my ecological research on the impacts of intensity of space-use on vegetation structure I need to quantify temporal variation in the intensity of space-use across years (resulting in a single value for each pixel of my research area).
So for example if I have the following space-use data:

Pixel
2017
2018
2019
2020

1.
5
5
4
5

2.
3
5
1
4

3.
1
0
1
1

I'm looking for a summary value for each column that quantifies the variation but also the magnitude of the space-use. I originally was looking into using a coefficient of variation but ran into the problem that high constant space-use and low constant space-use generates the same CV value. So is there a statistic out there similar to the CV that can still account for the total intensity of space-use as well?

If I understand correctly, you want a single number that represents both magnitude and variation. This sounds to me to be impossible for informational reasons; if you want to represent two values with one value, you have to lose information unless the two are strictly related in which case there is no information to lose. What isn't clear to me, though, is why you want/need to do this. Why can't you use the data in the form you have? What is the specific research question you are testing?

Yes correct - and fair point, something I'll take into consideration. Because I'm looking at responses in vegetation it is important for me to capture both the magnitude and variation. My research relates to elephants and their impact on vegetation. So for example if in 2018 they utilize a certain pixel heavily but leave it alone until 2021 that patch can recover. However, if they keep coming back to that patch the continuous utilization in theory leads to more vegetation damage. If I use a standard utilization distribution value this won't take into account that annual variation.

So I'm looking for a way - if possible- to quantify that annual variation whilst also taking into account the total impact

That sounds like quite a complex nonlinear relationship, where you would need some way to model patch recovery. You are not going to be able to use some standard summary statistic to capture that, it will need to be something very specific to your domain, and which may not even exist. What are the other variables in your study? Is it actually necessary to do this to test your hypothesis/es? Alternatives may be to use a simpler measure, or separate "use" from "rest".

I will be able to use metrics such as NDVI, EVI and percentage canopy cover to monitor the vegetation response, it is just quantifying the temporal variation of elephant space-use that is the last piece of the puzzle I am trying to solve. In the modelling I have already done I can see that there is a lot of annual variation in their space-use so I'd like to try and accomodate that, but have no idea if that is possible because I have not been able to find any other research on it. The values I am using are about as simple as I can make them without losing too much information.

But what is your hypothesis?

That high and consistent elephant utilization will lead to higher vegetation damage

I do not think you will find a general answer outside your research domain.
There is no general way to express both magnitude and variation as one number without losing information; unless you have a strict relationship between the two, such that the two numbers do not provide separate information (an example would be data with a Poisson distribution, where mean and variance are equal), this is simply not possible.
I'm answering from just a general statistics perspective, as I have little to no domain-knowledge in your area, but if you haven't encountered a measure already in the papers you generally read in your field, then I think it probably doesn't exist.
If you want to test whether "high and consistent elephant utilization will lead to higher vegetation damage", some options I can see are:

Test "high" and "consistent" separately; "high" could be from averaging/summing usage and regressing on your measure of damage, "consistent" could be from measuring the standard deviation, or using a measure like "years of high usage" with some threshold.

Fit a model with both your separate measures of "high" and "consistent", and look for a significant interaction. That is, a model of the form Damage ~ High * Consistency. There are certainly theoretical issues with this type of model, especially given the expected covariance between the two predictors, but I think it could still be practically useful, and in particular could be used to motivate not using measures of magnitude or consistency alone.

Use or modify an ecological model. I don't know much about this area, and it would probably take you quite a bit of reading to find something applicable, but cumulative damage seems to be a recurring issue in ecology, and though you may not find a model used in your specific domain you might find similar ones with parameters you can adjust and fit to your data. I'd expect a differential equation where the current year's vegetation quality predicts the next year's growth with some saturating characteristic (i.e., logistic growth), with elephant presence having a separate additive or multiplicative impact on vegetation quality, growth, or both. One paper I found quickly is this one:

Owen-Smith, N. (2002). Credible models for herbivore-vegetation systems: towards an ecology of equations: Starfield Festschrift. South African Journal of Science, 98(9), 445-449.
which seems like it could be useful, and it cites an older book chapter:
Caughley, G. (1976). Plant-herbivore systems. Theoretical ecology: principles and applications, 94-113.
The approach would be to fit the parameters of a model like this one to predict your observations of the vegetation based on elephant presence.


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What are the additional considerations for primer design in ancient DNA?
I'm familiar with the principles of primer design and have previously designed primers for use in modern DNA. However, in my current project I am working with ancient DNA (nuclear gene) and need to design primers to work in this context - I am wondering if there are established additional considerations that need to be taken into account.
What I have discovered so far is mostly literature dealing with the damage patterns in ancient DNA (i.e., amplicons tend to have damage at the 5' and 3' ends of each fragment, so sequence data from the centre parts of fragments are more reliable). I have seen the suggestions that multiple, overlapping primer pairs might be used to detect low-copy number fragments, but this suggestion, while useful, doesn't tell me much about the design of the individual primers.
My own thoughts are that since ancient DNA is typically fragmented into ~150 bp (depending on age - my samples are around 250 years old), multiple primer pairs might help. My target is around 500 bp.

Why not contact some of the labs that do a lot of old DNA work (not sure 250 years counts as ancient :) ) and ask them for advice or pointers to discussions of primer design. Since it seems samples vary widely in their degree of preservation, perhaps they will have suggestions on how to evaluate the quality of your specific samples.

That's a great suggestion, thank you! I agree that calling 250-year old samples 'ancient' sounds and feels odd, but as of yet there's no distinction between "kind of old DNA" and "really old DNA".

@Armand 250 years is a lot of time for DNA, which is why it is commonly referred to as ancient. I agree that the term is misleading, but it is frequently used.

@natb could you link the literature you reference? I assume you've read this paper on ancient DNA damage and this paper on amplification of ancient DNA?

@acvill Yup, I've read both those papers. Unfortunately that's the closest I've gotten to finding the information I'm looking for. I can link other sources I've read but they are all less relevant.


text:
Why are children more active than adults?
I have observed that children are usually more active than adults. For example, in the morning they get up and start playing, they have their lunch and get up and start running, while as adults they are relatively lazy.
Why is this so or is it that my observations are somehow errenous?
Thank you.

Personally as an adult I don't find running around exciting. But adult people definitely would wake up early if that means they are having a resort trip that day or something. Also could be suitable for psy.SE.

Have you done any research into whether or not this is backed up by any scientific research, or if it's just your own observations?

@4galaxy7 my own observations. I made it clear in my question.

I know - but in Biology (and science in general), it's useful and expected to do some research into whether or not your observations are backed up by some kind of scientific research, or whether they are just anecdotal observations.

Thank you for your advice. It was just by observing and I've studied biology only when I was a kid.

@rus9384 nice viewpoint. Definitely plausible.

This is a great question!
As I see you are new and you have explained within the comments above that you haven't studied biology much I will keep the explanation short and sweet.
Young children have fatigue resistant muscles and they also recover faster from high intensity workouts when compared to adults. Children have also been found to use more aerobic respiration when compared to adults during high intensity workouts. This means the child will feel less fatigue and so can continue exercising for longer. As the muscles also recover faster, the child is able to get up and start exercising again much faster than the adult as they will still be recovering.
Aerobic fitness at the muscle level decreases however once the child reaches adulthood and this explains why children have more energy and can play/exercise for much longer. They experience less fatigue and recover faster.
I hope this answers your question.
References:
https://www.frontiersin.org/articles/10.3389/fphys.2018.00387/full

Fantastic answer, do you have any references for further reading? Thank you.

Could you please link the references. Thank you.

Hello, I have added a link to a study which looks at the metabolic and fatigue profiles of prepubertal children and well-trained adult endurance athletes. The study had some interesting findings. They found that the children recovered very quickly even faster than the well-trained adult endurance athletes. I hope this helps and is what you are looking for!

The reference also appeared to suggest they may have bigger lung-to-muscle-mass-ratio and good muscle aeration and circulation and heart characteristics as well as different muscle types.

Thanks for the additional info. I was hesitant in adding these points to my answer as Yasir Sadiq hasn't studied biology much and I didn't want to confuse him. This is also why I didn't go into depth in my answer about fatigue. I remember when I was new to biology and a lot of the answers that were too in depth took me a while to decipher and made learning difficult for me.

Thank you, :-)  .


text:
Fate of antigen-presenting cells after antigen presentation to Helper T cells
In many texts, the Antigen-presenting cells (APCs) that initiate helper T cell responses are often "forgotten" after their antigen presentation function is discussed.
I have been wondering how the antigens in these cells are destroyed since they are complexed to MHC II protein (not MHC I).
Yes, the macrophages can receive additional signals from already activated helper T cells to destroy the pathogens harboured in their cytosol, but what about B cells and Dendritic cells which lack such abilities?

In Janeway it's being said without further explanation (I will edit and add reference)   that B-cells and macrophages "become targets" of cytotoxic T-cells after these killer cells have become activated, have been primed. However, this answers your question only if presentation on MHCII (not I) implies that presentation on MHCI has occurred as well. Only then APCs that present to T helper will be targeted by cytotoxic T cells and die. According to my basic knowledge that is the case with Dendritic cells and Macrophages. According to the explanatory text of your question Macrophages only receive signals to kill pathogens they include. Your inference may be correct that they cannot become target of T-cytotoxic cells. It is beyond your question to ask if Macrophages always do get that signal. If no that puts them into the same category as Dendritic APCs.
Understanding that there exists a signal to survive (destruction of phagocytoses pathogens) leads the way to understanding that there is cell death without killing by Tc cells:  cells that present antigens to T helper cells will "apoptotically" die because they have been infected, if not killed by immune cells to prevent the production and shedding of virions. According to my basic knowledge it is coherent  that a cell presenting is a cell sentenced to apoptosis. Killing by T cells is killing at an earlier stage only.
However, I found no reference that explicitly confirms that - maybe with very few exceptions -  that B cells do present on MHCI, to the contrary I found reference - I promise to add this one link quite soon - that explicitly states that B cells only endocytose debris, "protein" (in the sense of protein vaccination) i.e. isolated antigen, not whole virous. Thus, any antigen they present would be on MHC II, not I, as the antigen is not "endogeneous", not produced by the B cell as it has not become infected. This inference from basic textbook knowledge is supported, in this context, by the fact that B cells, just as T cells - which they are thought of as of one and the same category, the Lymphcytes - should not be killed after presentation (whereas T8, cytotoxic T cells do not present at all) as parallel to killing of T cells they still have their job to do: presentation activates the B cells which start to divide and produce antibody.
Consequently, it matters if a B cell not presenting on MHCI, thus not being killed by Tc cells, is sentenced to apoptosis and cell death because it has engulfed the antigen. In my opinion B cells - and I will add any reference to the contrary - not even need, as Macrophages, a signal to survive, as they cope with antigen alone and there is no interference with their regular by viral infection. (However cells hosting active HIV produce protein for viral ends for a long time before they finally die, but this is different.)
To sum up:

Dendritic cells present on MHCII and I, hence killed  by Tc cells or dying by apoptosis

Macrophages present on MHII and I, but according to textbook different to Dendritic cells have the option or are programmed to receive a survival signal to consume the pathogens they harbour

B cells present on MHCII and, according to my understanding: maybe, on MHCI, which would put them too in category 1: same fate as Dendritic cells, however basic knowledge coherently applied speaks in favor for B cells regularly not presenting on MHCI, not getting killed by Tc cells and not undergoing apoptosis as not "infected" by whole virus

So my own personal answer on B cells based on basic textbook knowledge and lack of explicit statements to the contrary might be very different from the answer regarding dendritic cells (and macrophages, see explanatory text of your question).
The B cells do not die after presenting to T Helper cells.


text:
Coronavirus mutation: bad luck or a consequence of vaccination?
I would like to know whether a mutation within a virus (such as the new coronavirus mutation that appeared in England source) is a consequence of the vaccination program - maybe because it is stimulated to “fight against the vaccine”? Or whether it is just bad luck and the virus just happened to mutate during this vaccination time?
Additionally, if there any other historical evidence, can you cite examples?

A few (slightly pedantic points). The 'mutation' would never be a result of the vaccination program - mutation happen quasi-randomly. What you are suggesting is that the vaccination may cause selection on the mutation which may drive it to high frequency. Secondly, the virus doesn't 'fight against the vaccine'. The vaccine stimulates an immune response which causes the human body to more effectively fight the virus.

What vaccination programme? Almost nobody in Britain has been vaccinated yet! Or do you think the viruses heard about it on Twitter? Please do some homework before you post.

@user438383 thank you for your feedback. I sure did not know about this. Good to know the historical question has some relevance :D

@David I’m sorry if my OP offended you somehow. I did not know being curious would cause such a harm. And my supposition is that, even though the vaccination program just started, it is a coincidence like Chris mentioned. And if you believe there is no vaccination program yet... all good :)

I am not offended by your question, just trying to weed out questions that do not conform to our remit or standards. And I actually live in the country at issue and am aware of the state of our vaccination programme, whereas, you, from your US spelling, presumably are not and do not. As someone in the relatively high category 3, I still await my turn for the vaccine which there is every reason to believe  will be as effective against this strain as the one against which it was developed.

This is simply a coincidence. A RNA Virus will mutate all the time (although this one is pretty stable), there are thousands of known mutations (see Nextstrain for detailed information).

It is only a matter of time, until one of these will dominate the others. It may also be the effect of a few superspreading events where one virus type is strongly promoted, although it bears no or only a little effect over the other virus strains. Time and research will tell.
However, it is pretty much unlikely that one mutation in the spike protein (or even a few ones) will render the vaccine useless. The reason is twofold: First, the whole spike protein has a size between 180 and 200 kDa (source) meaning the protein has a lot of different epitopes against which antibodies can be directed. To render the vaccine useless, the whole protein had to be different.
This brings us to the second problem, because the spike protein is the protein which interacts with the target cell. If it would completely be changed, the virus would need a different receptor to interact with in order to enter the cell. Highly unlikely to happen, as the virus would need to "re-invent" it path of entry. As far as I know this has never been observed before.

Nobody has been vaccinated here yet! A few high-risk last week. Please do not accept invalid premises in bad questions.

As it has been pointed in the comments by @user438383, the mutation itself cannot be a consequence of the vaccination program - what is really suggested is that this is an escape mutation, i.e., adaptation that makes the virus viable in vaccinated persons.
However, there is no evidence (yet) that the new strain affects those who have been vaccinated - it well may be that these people are equally protected against this new strain. Moreover, chronologically the new mutation likely preceeds the vaccination campaign that has began only recently (even if it was detected/reported just after the beginning of the campaign).

Nobody has been vaccinated yet! A few high-risk last week. Please do not accept invalid premises in bad questions.

@David you seem to be misinformed. As of 3 days ago, 350,000 people in the UK have been vaccinated.

…out of a population of?


text:
Can anyone identify this Australian tree?

This tree is found in the Wrights Hill area on the New South Wales/Australian Capital Territory border.
Bark at breast height is curled and dense, becoming less dense at height.

Eucalyptus, but which one?

Welcome to Biology.SE. For tree identification we need close-up pictures of leaves and flowers — this is especially true for a large group like the eucalypts! Thank you for taking the [tour], you may also find it helpful to go through the [help] starting with [ask] questions effectively on this site. Thanks.

The changes in the bark makes it look like Eucalyptus melliodora (Yellow box).

Locations recorded are in this link. http://plantnet.rbgsyd.nsw.gov.au/cgi-bin/NSWfl.pl?page=nswfl&lvl=sp&name=Eucalyptus~melliodora
Some photos of this tree can be seen at:
http://www.nccma.vic.gov.au/sites/default/files/publications/nccma-41853_-_box-gum_grassy_woodland_identification_10-11_web_0.pdf


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Identify grasshopper species
I found this grasshopper on a house door in central Italy. It did not move for the whole day. I can tell it's a grasshopper, however I am unable to determine the exact species.
Size: ca. 6cm
Feel free to ask if you need any more information / details.

Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible) — photos must be uploaded (not links); and 2) habitat information. Please [edit] your post to include this essential information. Not in particular that without at least one picture or a very detailed description this is impossible to answer.

Sorry, I thought I had uploaded the picture. This is the only one I have as I am no longer there.

Unlikely to get a full ID from that photo - too dim to make out markings and not enough views to get morphologic features.