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At what point do scientists consider something sentient vs random and/or genetic?
When I was thinking about sentience from a scientific point of view, I was confused about the bio-electric mental difference between a paramecium, dog, human, and supercomputer.
At what point does electricity go from being random and genetic to creating logic gates for perceived "sentience" / intelligence?

I would guess that your issue is not specific to sentience but you are just confused between spirituality, law, philosophy and science. It is a philosopher's job to define the boundaries between these fields. You could try on Philosophy.SE, however, in its current form your question will get closed as too broad.

I'm voting to close this question as off-topic because it has little to nothing to do with biology. It is a question of philosophy asking for definitions of different field of knowledge (law, science, philosophy).

Yes, scientists talk about consciousness as well. But really, saying that is not going to help you much, the most important for you now is to investigate the boundaries between the different fields of knowledge. Good luck!

@GerardoFurtado I did not say that consciousness was not within the realm of science (actually I said it was in my last comment). I said that the definition of the boundaries of the different fields of knowledge is from the realm of philosophy. Science does not decide wether a subject or method of study is scientific, philosophy does. Defining science is actually a very common theme is philosophy.

if you have 300 neurons and 10 of them can put you in a depressed state, you are a sad amoeba... He is asking if awareness increases with numerical advantage in the number of things in the sphere of awareness... i.e. a dog is less aware than a human. are you more aware if you have one finger or 1000? flies have 25x more neurons than slugs, we all know that slugs are more sentient than flies. Technically you only need one depressive hormone or neuron to suffer.

Your question is mostly just poorly worded you might just want to ask how science defines minds and sentience , both are emergent characteristics, and work from there.  Also this is more ethology than psychology, so you may want to change your tags.

if you have 300 neurons and 10 of them can put you in a depressed state, you are a sad eukariote.
To compare the logic gates of a worm and a mouse? which one is sentient? a slug literally has 10k neurons and a fly has 250k. that would make a slug 25 time sless sentient than a human, and a dog less sentient than a human, but a human is equally as sentient as a dog so numerically there may be now lower bounds.
Logic Gates are electronic switches which provide routing for AND/OR/NOT/EQUALS of data types, or objects. They come into existence when you have the first cilia and sensory cells. 20 nerves are a signal routing engine, logic system.
A neuron can roughly represented by 4-8 transistors, and a logic gate is a simple transistor routing/instruction, so a worm has about 2000 logic gate equivalents. https://en.wikipedia.org/wiki/List_of_animals_by_number_of_neurons
A logic gate is digital, a brain is analogue, no software, , so you inadvertantly weave smoke and mirrors to clarify your question.
The question evokes electrical sentience, synapses are electrochemical, slower than electricity and can varied in many ways chemically, and they are self organizing.
feeling, aware and knowing (reductionism of sentience) are much more debated topics in science. Relative to random and genetic logic gates for intelligence, that's unclear and you are discussing free will and decision (philosophy), intelligence has unclear relation to sentience/emotion.
Your question is confusing a vast range of scientific measures by using the term sentience, which is rarely used in science. Scientists write informally about sentience as an ethical issue based on their experience, but there's only fringe research on animal sentience. https://scholar.google.fr/scholar?hl=en&as_sdt=0%2C5&q=sentience+fish&btnG=
Animal psychology is a scientific topic, and sentience is metaphysical, it means feeling, aware and knowing, it's incommensurate and imprecise.
So scientists don't consider there to be such a point of sentience. They measure certain markers of sentience, such as
self awareness,
stress response,
emotional queues,
counting,
comparing,
memory,
puzzle solving,
social behaviour,
hormones, that kind of thing.
There are perhaps a 2 publications about sentience in fish, none about lizards or insects, and there are thousands of books and opinions about sentience in insects and other animals.
The brain increases in size from a dozens to billions of neurons. So the progression is in stages, so awareness is likely to be a complex series of steps.
A good animal psychologist can give you an entire book about the onsent of emotions and knowing in animals.

reason for downvote?

I smugly affirm that you can't answer much better that that, and that the question was psychobabble. logic gates of sentience?


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Remove all intestinal bacteria?
I've heard that this has happened to a few people before in extenuating circumstances, but don't know where to search for more information on this.  Is there a name for this?  What are some major symptoms, and how does it affect the body?  How is it identified?

Do you mean E. Coli?

All bacteria.

Are you sure you can prove your statement?  Can you provide some links to your sources ?

It is not possible to do this. You can minimize the number of bacteria by a complete GI cleanse, similar to what you go through before a colonoscopy. The point is to empty the gut of all matter, esp. fecal. But once you're colonized, that's it; you'll never be uncolonized.

This has never happened (at least to my knowledge), since removing all bacteria from a human being would be extremely difficult and also dangerous. And there is a proven relationship between the human microbiome and stress, but "extenuating circumstances" won't remove all bacteria from your body.
However you can look in the Internet for "germ-free animals", "gnotobiotic animal" or "axenic mice". Caesarean section in aseptic conditions is practiced (a fetus in normal conditions has no germs in it) and the "newborn" is immediately put in a sterilized enviroment. There is plenty of research with this kind of animals.
I hope my answer was useful for you! Cheers!

source: Stack Exchange

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What medium is the bacteria used to synthesize B12 sourced from?
Would that be from water, soil, plants, funguses,...?
I asked the question in Quora but that, at the time of posting in this forum, haven't been very helpful. I also have searched for the information, but I haven't been able to find it. In Vegan Health it says that

"The vitamin B12 component in B12 supplements and fortified foods is
  made by bacteria and sourced from bacteria cultures; it is not taken
  from animal products"

But I wonder where did those cultures come from. One day someone had to collect the bacteria from somewhere in order to start the cultures.

What exactly are you asking? The geographical location from which the bacteria were originally obtained from?

@canadianer I'm asking what medium is the bacteria used to synthesize B12 sourced from -water, animal intestines, plants, soil, feces.

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Why is dimethylmercury so poisonous?
According to the Wikipedia article Karen Wetterhahn, Karen Wetterhahn died after only a very small amount of dimethylmercury got absorbed through the gloves. What is it about the way the body works that makes dimethylmercury so poisionous. I don't know very much about biology. I know a few things like how proteins act like a catalyst. I would like an answer that starts all over from scratch giving me the right basics after which I will understand the answer of why dimethylmercury is so poisonous and then explains why it's so poisonous.

I think this question needs some focus. Why do you ask an answer that starts from scratch?

@James Because I don't have all the information I need to understand an answer suited for experts in biology.

@Timothy "From scratch" is indicative that a question needs some more research. Asking about "why code X does Y from scratch" on SO would result in swift closure. It's hard to tell what you are actually asking.

For a very disturbing article on dimethyl-mercury and Karen Wetterhahn, see The dangers of dimethylmercury, published in Chemistry World in 2019

Organic mercury compounds like Methylmercury or Dimethylmercury act as toxins by binding to thiol or sulfhydryl groups of
proteins. These Mercury compounds cause oxidative stress, lipid
peroxidation, mitochondrial dysfunction, and changes in heme
metabolism.
Dimetylmercury is absorbed via gastrointestinal tract and later it
enters bloodstream and is circulated to whole body. It binds
with essential proteins like haemoglobin through the sulfhydryl groups present in
cysteine. These complexes resemble the structure of methionine, therefore it easily circulates throughout the body and could cross the blood-brain barrier.
Mercury can bind to mitochondrial enzymes which can lead to cell
injury and death. It is reported that mercury can inhibit aquaporins
which prevents water transport across cell membrane.
Mercury also inhibits the kinase activity of protein LCK, which
decreases the level of T-cells and weakens the immune system.
Mercury also act as neurotoxin by inhibiting the neuronal membrane
excitability by effecting postsynaptic activity. It  inhibits Protein
kinase C and Alkaline phosphatase, which damages brain formation and
functioning even at blood-brain barrier.
Organic mercury mainly causes developmental effects by binding with
the tubulin  protein,  which prevents microtubule assembly and
inhibits the process of mitosis.
Mercury also results in  autoimmune response by effecting Major
histocompatibility complex (MHC) class II molecules, self peptides,
T-cell receptors, or cell-surface adhesion molecules.

(Via:  http://www.t3db.ca/toxins/T3D0361
https://www.sciencedirect.com/topics/neuroscience/dimethylmercury )

Is it exactly the same reason why dimethylcadmium is also so very poisonous?

Yes..but it enters the body through inhalation.

Check out this link:  https://www.google.com/amp/s/www.medicaldaily.com/most-dangerous-chemical-world-why-chemists-steer-clear-one-substance-394764%3famp=1

A good succinct answer to a vague question. +1

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what species of ant is this?

I found this queen ant on the pavement (in Adelaide) its about 1 cm long and I am not sure what species it is, is someone able to help me?

Probably a Ponerinae.
(Wikipedia, AntWiki)
It's not the easiest picture to work with, but here's what I did.
Going by the location we have the following distribution of ant species in South Australia (see below, or here).
A critical identification point is the petiole, bumpy segments on the thin part of the back of the ant. Your specimen appears to have none or one.
This excludes Dolichoderinae and Mymicinae, who both have two clearly distinguishable petioles (or rather, a petiole and a post-petiole).
Myrmeciinae have different colours and/or mandibles, leaving the following three likely candidates:

Formicinae
Ectatomminae
Ponerinae

Ponerinae are distinguishable by a constricted gaster, so an impression in the posterior section, which is quite clearly visible in the picture.
(This is technically only an identification to subfamily level, if anybody wants to take a shot at species, feel free)

This is wrong, the first segment of the gaster is not elongated here.

This is a Formicinae or a Dolichoderinae.
Myrmeciinae and Myrmicinae have two segments between the thorax and the abdomen, it is not the case here. The first segment of the gaster is elongated in Ponerinae and Ectatomminae, which is not the case here (the physogastry is confusing, the abdomen is distended because of the pressure induced by the development of the eggs in the ovaries).

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How do people wake up just before their alarm goes off?
I can wake up less than 2 minutes before my alarm goes off regularly.
I read the common wisdom on the subject which says "circadian rhythm; PER proteins; internal clock". I am skeptical of this for two reasons:

I go to sleep at night at different times ranging from 11:00 to 2:00 and rarely check the time, so if I don't even know the sleep start time, how can my body measure out the duration of sleep and get the end time right?
People's chemical levels vary from day to day depending on a ton of variables (food intake, physical activity, stress, etc). It appears that we are not deterministic machines that are constant from day to day to that level of precision

I have a few hypotheses that I haven't heard before:

Maybe the subconscious is queuing off the light level in the room? (this a unique property of the specific minute of wakeup, as there would be less light a minute sooner and more light a minute later)
Maybe while sleeping, the eyes periodically open, view the clock, process the numbers, and wake up accordingly (just like people  can sleepwalk and use their eyes to process where the walls and doors are)

Any thoughts?

Not sure why this is receiving negative voting. If you fail to actually read the post, I'll admit the language (i.e., usage of I ) superficially sounds opinion-focused, but this question is , IMO, asking about a general biological phenomenon that certainly ican be addressed with non-opinion answers. @Noob I think you should add an explicit explanation of what you've already done to ty to answer your own question to help encourage further positive feedback. However, down- and close-voters, I encourage you to provide your rationale for this one since I do not see an issue

When changing the time of your alarm, would you wake up at the same time, or again 2 minutes before the alarm?

For what it's worth, this question could come from me - I have exactly the same experience as OP; had it forever.

The biological answer is presumably cryptochromes.  The foregoing applies to humans who have CRY2 blue light receptors in the inner retina (the neural layer, not the photoreceptors).  I've seen claims these respond particularly well to the light before dawn, though I didn't track those down just now.
That said, a proper skeptic would dismiss this as confirmation bias, at least until proven otherwise.


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Why do so many parasites infect definitive and intermediate hosts rather than just one host?
Many parasites infect multiple host species, with one host species being the definitive host (where the parasite reproduces), and the other host species being the intermediate host (where the parasite grows to maturity). (Further details described as "complex life cycle" at https://en.wikipedia.org/wiki/Parasitic_life_cycle ) Why is this complex life cycle so common? Why wouldn't more parasites adopt a simpler life cycle of just one host?
I knew that there were some parasites that infected more than one kind of host species, but now that I am looking into it, it seems like a majority of internal parasites have this kind of life cycle. Does anyone know why?

Several reasons have been proposed.

We suggest that complex cycles in helminths without penetrative infective stages evolve by two essentially different processes, depending on where in the cycle a new host is inserted. In ‘upward incorporation’, a new definitive host, typically higher up a food web and which preys on the original definitive host, is added. Advantages to the parasite are avoidance of mortality due to the predator, greater body size at maturity and higher fecundity. The original host typically becomes an intermediate host, in which reproduction is suppressed. In ‘downward incorporation’, a new intermediate host is added at a lower trophic level; this reduces mortality and facilitates transmission to the original definitive host.

--Evolution of complex life cycles in helminth parasites

Despite these advantages to omitting hosts, the majority of digenean trematodes have a life cycle with three hosts, suggesting strong counteracting forces that maintain hosts in the cycle. Such forces have been proposed to be higher growth and fecundity (Parker et al., 2003), an increased probability of finding a mating partner (Brown et al., 2001), and higher transmission rates (Morand et al., 1995; Choisy et al., 2003; Parker et al., 2003). ... we propose here that maintaining a second intermediate host in the life cycle can be advantageous for the individual parasite to increase the intermixture of different clones and therefore decrease the risk of matings between genetically identical individuals in the definitive host.

--How a complex life cycle can improve a parasite's sex life
Also see The evolutionary ecology of complex lifecycle parasites: linking phenomena with mechanisms.

Thanks for this reply and the great citations. Sorry for not accepting the answer in a prompt manner, but I am accepting it now that I am seeing it. Thanks again!


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In the life-cycle of the HIV virus, how does the created DNA enter the nuclear membrane?
I am in a high school biology class, so I cannot truly attest to how accurate the information I am given is, but as far as I know only RNA and very small molecules can enter the nuclear membrane through the pores on it (thus excluding DNA). Furthermore, I am fairly sure that the reverse-transcriptase used in the process of reverse transcription of the viral RNA must be used outside of the nuclear membrane, in the cytosol. My question is: How does the viral RNA, after it is reverse transcripted, enter the nuclear membrane?
My teacher and I have come to the conclusion that it probably creates the provirus sometime during mitosis, as the nuclear membrane dissolves, but this is more of an educated guess.
Thanks in advance!

The nuclear import mechanism is independent of the cell cycle. Here's a recent model for nuclear import, but there's still a lot of research into this: http://www.sciencedirect.com/science/article/pii/S1879625713002022

@Kendall I think the integrase also facilitates nuclear import but I am not sure.

Some proteins are transported from cytoplasm to nucleus by the importin family through nuclear pore. These proteins have a specific sequence called Nuclear Localization Sequence (NLS) and the importin family recognizes NLS to import them. Recently it has been clear that the accessory protein vps which is translated from viral RNA and composes pre-integration complex (PIC) with viral DNA has atypical sequence like NLS.
So. it has been thought that DNA from HIV is imported into host nucleus by importin family with PIC.

You should also add some references in your answer to support your claim.

I'm sorry for having not added the reference.

I'm sorry for having not added the reference. This is Yuko N.,et al, J. Virol .,2007,81,5284-5293 http://jvi.asm.org/content/81/10/5284.full


text:
Difference between the spinal cord and vertebrae column
What is the difference between the spinal cord and the vertebrae column, they both run through from the head to the abdomen. Does any one have any idea.

The vertebral column is a bony, segmented structure that supports the torso/head and thorax. The spinal cord is a bundle of nerves that runs inside the structure of the vertebral column. So - they run together, but are completely separate.


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What's the mixture of plasma and haemoglobin called
I know of oxyhaemoglobin but the mixture of plasma and haemoglobin in the blood gives what?

You and Dr. James must be friends ;)
There is no specific name for the mixture of plasma and haemoglobin, however, when hemoglobin is found in the plasma (i.e. not in blood cells) it is usually referred to as "free hemoglobin." This is a term you are most likely to encounter when dealing with plasma/ serum hemoglobin testing.
Additionally, when haemoglobin is broken down, it forms bilirubin, which contributes to the color of plasma (there is no specific name for the mixture of bilirubin and plasma either, except perhaps "plasma bilirubin").

Hahaha, I noticed that too ;) (first line)


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How to incorporate intraspecific variation in discrete characters in comparative analyzes?
I'd like to run a multivariate analysis (Pavoine et al. 2011) that aims to disentagle the effect of environmental gradients on traits, considering its autocorrelation with phylogeny and space. It uses the RLQ approach and works with both discrete and continuous traits. However, I don't know how to incorporate intraspecific variation in discrete traits.
For example, I recorded categories of pigmentation on organs of several amphibians, but for some species, these categories vary among individuals. One way would be including individuals as polytomies at the species level, but this would make the test quite hard to interpret.
Thank you in advance,
Diogo

Kostikova et al. 2016. Syst. Biol. developed an algorithm to model trait evolution with inter- and intraspecific variation. The authors use it to show

whether a life-history trait (i.e. annual versus perennial) influences the evolution of intraspecific variation in the climatic niches of species

While they do not directly incorporate the space component as in the RLQ analysis, the approach might be informative in your case. The functions are available through dryad.

Thank for pointing that paper out to me Martinkova. I happen to see that paper when it was in 'accepted version', but didn't realized it was linked to my problem.


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Why aren't we immune to the "cold"
As far as I know, people suffer from the cold since ever. Why didn't and don't we evolve to resist it?

Not since ever, only since about 70 years is it considered normal to suffer from the cold a few or more times per year. This is because we spend so much of our times indoors in rooms with central heating and air conditioning where the signal from the newly emerging cold viruses  is drowned out by the microbes that live in the artificial tropical indoor climate. The first exposure to the cold virus is then when someone sneezes in your face; the cold can spread as wildfire with all these people with poor immunity against it.

The main reason is that there really isn't any one "cold," but rather the word is used to describe many different infections that simply have the same symptoms. The reason for these same symptoms is that almost all of the symptoms that one experiences in a cold are actually the immune response to said infection. For instance, a fever is used to make the body less hospitable for the infection causing agent and throwing up is used to ensure that harmful substances are removed from the digestive system before they can cause too much harm.
The reason that the body can't simply evolve resistance to all of these possible infections is both because the infections evolve too and because there are simply too many of them that all need a separate method to be defeated. Therefore, curing the common cold is effectivley curing the majority of known ailments.


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Is it possible for two creature in the same order and have odd haploid chromosome species to reproduce
Take the degu and the rat for example.
The degu has 29 chromosome pairs
Rats have 21 chromosome pairs.
They are only share the same order ( Rodentia )
Would it be possible for them to reproduce?
( also , before someone says " they're not the same species , so obviously not" allow me to remind you of the mule , and the europeans have 1 - 4 percent Neanderthal )

On the side of the question, there are a few words on the concept and definition of species that you might like to read.

What point are you trying to make about having odd number of chromosome pairs? What difference does it make?


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why haven't other species developed language?
Scientists say there are 15 million insect species, 2 million marine species, more millions of bird and animal species.
Yet, only one- humans - developed language. If evolution is true - that species evolve continually higher and better - why haven't other species developed language?

Welcome to Biology.SE. Your question has several issues. MINOR ISSUES: The title is too broad. "Scientists say" is a horrible way to start a sentence, you should have references for your claim. MAJOR ISSUE: The theory of evolution doesn't say that species evolve higher and better. What make you think that language is a goal, an achievement that all species should tend to? I am voting to close.

If you take some time to learn a little bit about evolutionary biology, you will then be able to ask clear questions. Consider taking a few course on Understanding Evolution (or other good online ressource)

Define a language too, many species communicate with vocal signals and this can contain information just like our speech. Also voting to close, it's a terribly flawed question.

"If evolution is true - that species evolve continually higher and better" That's not what evolution says. Not at all. And yes, many other species have developed their own languages. I can't believe this is news to you.

If evolution is true - that species evolve continually higher and
  better - why haven't other species developed language?

I'll discuss that question first, and then move on to what we know about languages in animals.
"Species evolve continually higher and better" is not what evolution actually postulates; there is no real sense of progress towards ever-smarter ever-better organisms; merely that the frequencies of genes in populations follow dynamics that is dependent on the relationships between the traits they are responsible for and the relationships between traits and the environment which further determine how many offspring a carrier of a given set of traits are likely to have.
Secondly, new traits don't pop out of nowhere; for a trait to appear in a population, let alone spread through a population, mutations that generate those traits must happen in the first place. That species don't evolve along some imagined ladder of progress has nothing to do with the veracity of evolution.
Coming to languages ; there are recorded instances of bonobos using modulations of their calls to communicate information; which is, simply put, language. Whales do it to a limited degree as well; communicating clan identity through ultrasound.

ants did have the advantage of language-type communications. The problem is ant language failed to evolve any further. why?

There are neural structures that regulate language; structures whose development is still regulated by genes, and the origins of novel structures requires mutations to happen first; mutations happening and spreading through populations is a matter of chance (mutations are stochastic processes). Even if hypothetically a trait would give a species a reproductive advantage, the mutations to produce that trait must happen first, and there is no guarantee they will (that is the whole point of evolution being stochastic, not deterministic)


text:
Which scallops change their sex from male to female?
Tonight it occurred to me to look up what scallops are like when they are alive (beyond their culinary role) and it blew my mind. This post regards one detail about which I was unable to find specific information: apparently certain species are known to start off as male and then change to female later in their lives. Which species in particular are known to do this?
I am new to this SE community so please let me know if there's anything I should refine about this (my first) post.

Welcome to Biology.SE. As you're looking for advice.... Always link to whatever you've found so far. For example, link to the document where you read about scallops gender change in life.

This type of sex determination system is called sequential hermaphroditism. Clown fish are a classical example of sequential hermaphrodites.


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Basic Genotyping
As a disclaimer, I'm from a computer science / statistics background, working on some bioinformatics problems. I've got some genotyping data (VCF from Exome Sequencing), and I'm struggling to get my head around the Genotyping notation.
As far as I understand, at a single base in the human genome, there can be two possible alleles, which would make sense given the standard notation for a lot of software is AA, AB, BB. So that means there are three possibilities homozygous, heterozygous, or homozygous respectively.
The A or B alleles are derived from the paternal and maternal copies of the same base in a person's genome. The major allele is the one that occurs most frequently, and the minor occurs the least.
When it comes to guessing which base is A and which is B, is there a general consensus as to which is which? i.e. is A the major allele?
I'm just not sure my assumptions are right, it's been a while since I've studied any biology, and I've found that online resources are either too vague or are so complex, that they overlook these basics.
Any tips would be really appreciated!
Thanks,

Refer to the following image. What you want to note is that this is a mitotic chromosome. Your cells are generally diploid, meaning for humans where n=23 your somatic cells have 46 chromosomes that form 23 homologous chromosome pairs.
For each chromosome in a pair, they have what amounts to the same genetic information with variations. At the locus for hair color, it will always code for the color of your hair but since you got half your genetic information from each parent, on one homolog the hair color locus might amount to red hair, while the other one might amount to brown hair. Scroll past the image:

In summary, the gene locus is for hair color, but there are red and brown alleles, or variations in a given gene locus for a given trait (see gene mapping). Thinking about traits and how they translate to features is complex in humans however due to features of our genomes such as epigenetics, epistasis, pleiotropy, etc. So when we describe in genetics traits such as color and how those related to AA, Aa or aa and so forth, it's nice to look at a much more simple organism like the pea plant that Mendel studied.
As for which allele is dominant? The actual wikipedia page for genetic dominance provides a good section:

By definition, the terms dominant and recessive refer to the genotypic interaction of alleles in producing the phenotype of the heterozygote. The key concept is genetic: Which of the two alleles present in the heterozygote is expressed, such that the organism is phenotypically identical to one of the two homozygotes. It is sometimes convenient to talk about the trait corresponding to the dominant allele as the dominant trait, and the trait corresponding to the hidden allele as the recessive trait. However, this can easily lead to confusion in understanding the concept as phenotypic. For example, to say that "green peas" dominate "yellow peas" confuses inherited genotypes and expressed phenotypes, and will subsequently confuse discussion of the molecular basis of the phenotypic difference.

Good place to start: Wikipedia
What you should also note is that dominance isn't intrinsic to the allele. Just because it's dominant to another allele doesn't mean it can't be co-dominant with another, and so forth. It also has no bearing on the population distribution of alleles, as certain dominant or recessive alleles can be either exceedingly rare or excessively common.

The A or B alleles are derived from the paternal and maternal copies
  of the same base in a person's genome. The major allele is the one
  that occurs most frequently, and the minor occurs the least.

That's likely going to depend on the population you are talking about.  An allele might be more common the general population, but rare in an ethnic sub-group.

When it comes to guessing which base is A and which is B, is there a
  general consensus as to which is which? i.e. is A the major allele?

If you have the vcf, you can probably go with the ref allele being the "major" allele.  Are you sure that it really matters for your analysis which allele is more common in the population?


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Quantifying the number of fragments from RAD library
I have a series of single-end reads from a RAD library of 48 uniquely tagged individuals in fastaq format. The data comes from a small MiSeq run. I want to know the number of unique fragments per individual/barcode, but I'm not sure how to go about getting that number. I'm new to bioinformatics, but I was able to use Stacks to demultiplex the library using the process_radtags function.
Could someone help? Thanks!

Do you mean the barcode in the FASTQ header?


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Is there in vivo evidence of Amyloid beta toxicity?
Amyloid beta is thought to be toxic, however from a brief search, this is based on (1) in vitro (2) measurements of some proxies of toxicity (e.g. Ultrasensitive Measurement of Ca2+ Influx into Lipid Vesicles Induced by Protein Aggregates referenced in Wikipedia).
My impression is that we do not have any high-quality evidence that amyloid beta is toxic in vivo and that there is significant circumstantial evidence against it being toxic (links below). Is this correct?

"30% of elderly people have #Alzheimers pathology (plaques &/or tangles) but no disease"
There's an elderly woman with large amounts of amyloid plaques but no symptoms of Alzheimer's
According to Derek Lowe "all of those amyloid-antibody trials have ended in grievous, expensive failures"

From a quick search, it seems that there is plenty of solid evidence for in vivo toxic effects. A couple of papers here and here.

An answer is expected to stand for itself with references being useful for further reading. Your "answer" is basically one sentence containing three links. Please edit it to avoid its deletion. This also applies to some of the other answers you wrote recently.

You can delete them if you want! ;)

@TumbiSapichu - we'd rather not delete them, and we appreciate your efforts. However, posts as this are below our standard and not conform our guidelines. If you don't improve these posts we will have to delete them.

@TumbiSapichu The aim is not to delete postings - which the mods could easily do - but to improve the quality. If this doesn't happen, it might be the last resort.


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Why is the nucleus accumbens in that place?
This description of where the nucleus accumbens is (Ac) says that it should be near the lateral ventricle, when it is quite clearly very far away? How is this?

the region surrounding the tip of the lateral ventricle, at the ventromedial margin of the rostral pole of the medial striatum (MSt) in birds is marked as the nucleus accumbens

(from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2481519/)

Furthermore the lateral ventricle seems to be in very different places in both diagrams although they are both avian brains?
(https://avianbrain.org/papers/RevisedNomenclature.pdf figure 2)

(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2481519/ figure 1)
thank you for any help :)

Please add references for the diagrams and quoted text.

references added :)

The ventricle looks in a different place simply because the first image is a transverse section whereas the second one is a sagittal section.
In the sagittal version the striatum looks very far from the ventricle because it is a quite lateral slide, more medially it would look closer to it as it does in the first figure you show.
Here you can see a representation showing also a more medial transverse section.
source: Vertebrate brains and evolutionary connectomics: on the origins of the mammalian ‘neocortex’. Harvey J. Karten. (2015) DOI: 10.1098/rstb.2015.0060

thank you very much for the clarification that was so useful :)

So in the sagittal section diagram, would you still say the Ac surrounds the tip of the lateral ventricle?

It is not visible in that figure, but is not false.


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What is this type of diagram called and how to interpret?
I'm just starting a project on neuroscience for sixth form. I have had no teaching in this area so had to teach myself entirely.
This is a "low-power image of a transverse section through
the telencephalon of an adult pigeon":

I understand the TH means tyrosine hydroxylase but I have no idea what the different colours mean.
Any information would be so helpful :)
thanks very much!

They used a stain that marks tyrosine hydroyxylase (most likely using an antibody to TH, followed by a secondary antibody tagged to an enzyme that then produces a dark precipitate in the presence of the proper precursor).
The dark regions are where more antibody bound, so you can infer this is where TH is highest. It's very difficult using these techniques to take anything quantitative from this, but you can use the technique to identify regions and possibly compare between them, given you have an appropriate control region.

Thank you so much! :) what does the white line mean?

@OllyScargill What white line?

The line up the left side of the image?

Oh the gap? I'm not super familiar with bird brain morphology but that looks to me like it's a ventricle - it's a place in the tissue slice where there is open space. It might be larger than it would be in the intact brain, because tissue tends to shrink when you fix it, but if it was perfused well there may have been minimal shrinkage.

Thank you so much Bryan :) You don't know how much you helped me out!


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What does the immune system do to stop pathogens that aren't killed by macrophages?
For instance, say a host is infected with salmonella where the pathogen can enter into a macrophage without the macrophage destroying it. How does the body then fight off an infection that is capable of surviving the mechanism by which pathogens are destroyed?

what do you mean by: pathogen can enter into a macrophage without the macrophage destroying it.

You're asking for an entire course on immunology. Googling for "immunity to salmonella" turns of hundreds of answers, from detailed peer-reviewed articles to Reddit and Quora summaries.

Basically read this article and understand that an answer to this questions can boil down to Figure 1 in the paper, but comprehending Figure 1 is an entire college course. https://www.frontiersin.org/articles/10.3389/fimmu.2014.00516/full

You can also try this review for an overview of what happens when you can't clear viruses.

It definitely 100% does not take an entire course to generally explain this one single phenomena, I can guarantee that having graduated from a program in which I studied human anatomy and microbiology, so I 100% absolutely expect it to be generally answerable within the stackexchange platform. The problem is no one went into detail about this interaction with salmonella since it is less commonly studied compared to microbes like e-coli, and many sources on the internet are commercially based, but I remember a related topic being briefly covered and not at all overly complicated by any means.

There are two broad types of infection classified by their persistence: acute and chronic infections.
I find that most courses on immunology nicely cover acute infections and their detection, and resolution. In the case of S. typhi, which has the ability to invade host cells such as phagocytes and inhibit their ability to properly function, the case isn't so pretty (1). The same can be said for some viruses like HepC and HIV, or other bacteria like Mycobacterium.
Salmonella spp. have a number of virulence factors. The flagellum of the bacteria actually acts as a TLR agonist that activates phagocytes like monocytes/macrophages and neutrophils, which are often first-responders. Then, the bacteria can facilitate the injection of some of its own proteins into the host cell which does a number of things like modulate vessicle trafficking, suppress cellular functions, induce apoptosis and promote overall survival of the bacterium inside the phagocytes (2).
So normally, and referring to the below figure, the overall reponse to a Salmonella infection is adaptive in nature, presumably because your innate effectors have been stunted:

SRC
You can see in healthy phagocytes that through one of two pathways, protein antigens end up displayed on HLA molecules for cellular immunity to take over. Option B is that another cell like a macrophage detects distress signals from the infected cell and induces cell death in it through receptors or oxidative burst. In the case of Salmonella, HLA expression is down-regulated and oxidative burst can be inhibited so localized, infected antigen-presenting cells cant mount an effective response.
That's not to say everything is de-regulated early on. If you succeed in antigen presentation or innate killing (perhaps a non-pathogenic strain), you will resolve the infection as seen in the above figure: a combination of T-mediated killing, B-mediated killing, NK-mediated killing, and generalized inflammation.
In the chronic case, the pathogen will have escaped the primary immune response, but the system will attempt to continue to resolve the infection. This can lead to a number of things: cellular anergy, cellular hyperactivity, sequestration (see granuloma), chronic inflammation & tissue damage, and so forth. The following diagram is predicated upon viral infections but the immunology is largely similar:

SRC
There are changes to the system that are a result of over-exposure to antigen, and an inability to clear that stimulation. The best way to explain it is that chronic stimulation leads to both hyperactivity and suppression. The constant presence of effector molecules like TNF-a leads to a persistent state of tissue inflammation, which is bad for the tissue, but taken together with the persistent presence of antigen, this may lead to dysfunctional responses by lymphocytes (3).
A particularly virulent infection may be impossible for your immune system to clear without assistance, then, requiring the intervention of gram-negative antibiotics, for example.


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Approx 1cm, white and brown insect feeding on fruits, what are they?
I found these insects yesterday that were feeding on a guava that I left outside for days. We have a tropical climate here (Mauritius). These insects are about 1 cm long. They have a white abdomen, brown wings, 6 long legs and they have segmented bodies divided into three regions: head, thorax and abdomen. Can someone help to identify them. Thank you in advance.

This is a species of the fly family Neriidae. They are actually acalyptrates, not nematocerans like crane flies and sciarids. I have collected and observed species of this family many times. They are very distinctive. Here are some photos for comparison - https://www.inaturalist.org/taxa/132101-Neriidae.

The picture isn't very clear, as the other answer says, so it is hard to give a definite answer. It is definitely a fly though (Diptera).  Due to the size, shape and dark wings I think that the familj Sciaridae (dark-winged fungus gnat) is more likely than a Crane fly though, which is suggested in the other answer. They are also common to find on fruit (as are many flies though). The familj has about 2200 species.
Googling Sciaridae brown wings can give you a sense of what they look like, e.g.:

(picture from http://peipestcontrol.com/)

The picture isn't really focused on the insects. I think those are Crane Flies.  Crane flies have small club like appendages under their wings called halteres,which are used for steering in flight.I dont know the genus or species of these insects. The order is Diptera, the family is Tipulidae. Here are two links.
[https://www.orkincanada.ca/pests/flies/crane-flies/
[https://simple.wikipedia.org/wiki/Crane_fly


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What is this thorny plant with cute leaves?
I found this thorny plant with cute leaves growing in my garden in India,
I took a risk by plucking it to get photos of the front & back side of the leaves.
Front side of the leaf:

Back side of leaf:

Full plant:

Any Idea what this plant is?

Full Plant: http://i.imgur.com/0IlEj2G.jpg

https://en.wikipedia.org/wiki/Dalbergia_melanoxylon
The Mpingo looks quite similar to this plant. However, more information is needed like the approximate size of the leaves and the number of leaves on a branch.

No, That is a wrong answer.


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Can Dpn1 digest hybrid PCR product with only one methylated strand?
In Site directed mutagenesis using PCR, after a cycle we obtain a hybrid molecule with one parental strand and other newly synthesized unmethylated strand. This is followed by Dpn1 digestion. Does this digestion just cut the parental strand leaving behind single strand of newly synthesized product?
Does this means that Dpn1 can use ds methylated DNA( both strands methylated) as well as ds hybrid DNA (with one methylated strand and other unmethylated strand) as substrate?

According to the NEB website FAQ, yes, it can, but less efficiently.
"DpnI cleaves hemi-methylated dam sites 60X more slowly than fully methylated."


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Measuring gene similarity in two bacteria models
I'm currently working with some computational models of bacteria. The bacterium I am considering is an Ecoli K-12 which has 139 genes. I have several models of the same bacterium with different combinations of genes that are active. e.g. M1 - M3 are the models and G1 - G4 are the genes. 1 indicates the gene is active and 0 inactive.
M   G1 G2 G3 G4
M1  1  1   1  1
M2  1  0   1  0
M3  0  0   1  1

My assumption is that bacteria have a fixed number of chromosomes and randomly genes get activated. I intend to compute a similarity score between each pair of models (how similar two models are). I want to know what similarity means in terms of biology. Is a gene being active (1) considered a similarity or begin active and inactive (1 and 0)? For example if I compare M2 and M3 which similarity would be correct?

1 similarity (only G3 is active)
2 similarities (G3 is active and G2 is inactive)

The word "bacteria" is the Latin plural of "bacterium". I have corrected this. However I find your question very difficult to understand. When you say the bacterium has 139 genes do you mean that you are considering 139 of the several thousand in E.coli? And as far as I can see, the genes are always present in the genome (which, incidentally, is a single circular chromosome), so if you modelling activity you cannot talk about present and absent, but need to use terms like "active" and "inactive".

@David Thank you for the edit. Yes you are correct. I should have made it clearer. The model simulates only the metabolic activities in the E-coli. Therefore the genes are the ones that are related to the metabolic pathways. Also I think active and inactive should be the proper terms.

I feel like you could look at this in terms of local and global features. In other words, sets of active/inactive genes that are part of their own module versus the overall set of active/inactive genes. You could also look at pairwise comparisons ({M1,M3} {M1,M2} {M2,M3}), or define a reference/wild-type to compare all other models against (as in differential expression, M1 vs. M2, M3... Mn).

It may not be correct but if it were me, I'd look at M2 and M3 and say they are 50% similar because half the genes broadly "match". Something like "they have 2 similarities" seems odd to me.

@CKM thank you for your comment. What I meant by 2 similarities is that they are 50% similar. Also I think computing the % activity is also a good idea. Thank you.


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How does DNA code for the actual *shape* of individual body parts/areas (NOT segments or Hox genes)?
Just to save the trouble - I am not asking for general information on how DNA codes for proteins and definitely not how Hox genes work. I have a very good understanding of the evolutionary process and a better than average (for a layman) understanding of how DNA works.
I understand the process of Amino Acid being coded for by specific DNA nucleotides and the chains of Amino Acid forming specific proteins - however, I am unable to find information on the topic of how actual shape is determined / coded for by DNA (again, not Hox genes and body segments).
Here is an example of what I am asking about - please note that this is just an example and I'm not specifically asking about how eyes evolved. I'm asking how changes in shape/size/structure of any part of a body happens from changes in DNA.
It's generally held that eyes evolved (in very basic terms) from a layer of photosensitive cells on the skin, which slowly formed into a cup that could detect direction, then the cup eventually closing in to form a smaller hole, and then a lens, and so on.
So my question (based on that example), would be, how does DNA (or a change in DNA) code for "create an indentation on the surface of the skin at this location". Or, "Deepen the indentation repeatedly until it is a cup". And so on.
More basic examples are "make the hind legs on a mammal slightly longer" or "make the cranium on an ape slightly larger". The question is not dependent on body part or animal type but is specifically about how DNA, in general, operates.
Hopefully the question is clearly stated and not too long - I welcome any suggestions on how to clarify the question.
Thank you!
--added--
canadianer's comment gave excellent information regarding some general principles that are involved, but I'm still hoping to find (if it's possible) a more precise and detailed answer to this.

Are you asking how eye morphogenesis evolved or how it occurs in extant organisms? Either question is interesting, but the answers may take the form of a text book. You might start with this review for the latter question.

@canadianer The eye was just an example out of many possible examples - I'm not specifically looking for information on eye development. Rather, my question is how DNA codes for shape and shape changes (as opposed to how it codes for amino acids which form proteins). Other examples include how the shape of an ear is encoded in DNA and expressed, how DNA codes for the formation of fingerprints (place a ridge here, no ridge here, etc), and any other non-body segmant "shape" on an organism.

Each example you listed would be different in the specifics, obviously, and incredibly complex. I understand you want a general answer, in which case you might be interested in and simultaneously disappointed by this post. This is just one example of tissue patterning in the developing embryo. Perhaps not as exciting as eyes or ears, but the underlying mechanism is the same: patterning is controlled by gene expression, expression is controlled by transcription factors, and transcription factors can be influenced by intercellular signalling.

You can check out this post for my recommendation on a developmental biology text book.

Thank you @canadianer ! What I'm interested is the underlying mechanism and not how any one part of the body is formed. Your links are a great start as well as the keywords "patterning", "gene expression", "transcription factors", and "intercellular signalling" which will give me a place to start searching and reading. :) I'm not afraid to do the work and take the time to actually learn the information, I just had no idea where to start and everything I tried was a dead end.

@canadianer Any other information you can provide (even a semi-detailed but simplified step-by-step of the underlying mechanism) would be great and very appreciated! Thank you.

I think adding the bounty was misguided; canadianer's comment is the best concise answer you're going to get without a textbook.

Thank you for the response Bryan. I appreciate any feedback at all on this because I've been trying to figure it out for quite a while and have not gotten far. If the consensus is that canadianer's response is as good as can be provided without a textbook then that's good to know - but I'm still (at least for now) hoping to find an explanation that doesn't require going back to college...


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How does the snail shells' fertilizer compare to regular fertilizers?
May I ask about the quality of the fertilizer derived from the shells and their effectiveness compared to other fertilizers on the market ?


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Creation of healthy genetically modified crops
GM crops are huge at the moment, and the noticeable 'counter movement' is for people to continue to purchase organic foods (please note I am specifically talking of GM crops and not meats, etc).
The argument as fair as I am aware is that some of the GM crops actually contain poisons to the human digestive system that cannot be broken down, and we have yet to find out their effects on long term health.
However, my question is: What can be achieved, if anything at all, in terms of creating GM crops which do not incur health issues? Is there a specific way of going about this?
EG:

Could crops be made larger?
Could crops become more pest-resistant?
Could a 'uniform shape' be created?
Would this be done with genes from other plants? Or artificially?

Thank you for your time.

Yes, yes, ...maybe, yes. What do you mean by "artificially"? I don't think this question is opinion based. It's just unclear at the moment. Perhaps read a specific example in which GM crops have been used to enhance yield and come back with some more targeted questions.

The "poisons" used in GM crops affects insects and not humans. This can pose an ecological problem but there are no known health issues. Many other GM crops are engineered to have longer shelf life and higher nutritive value. Your question has few issues: 1.You are assuming that all GM crops have the poisonous insecticidal protein. 2.You are assuming that this is actually toxic to humans. 3.You are asking multiple questions about how to make safe GM crops. For first two issues you should support these claims/hypotheses with some reference. And, you should ask a single precise question.

Welcome to Biology.SE.
What are GMOs?
The term 'GMO' can mean a vast array of different things and there is no objective way to distinguish what most people would call GMOs from what most peopel would not call GMOs. Humans have made 'GMO' for thousands (or even tens of thousands) of years. The detailed definition of 'GMO' will not impact the answer to the question Are GMOs safe to eat?.
Are GMOs safe to eat?
Yes, GMOs are safe to eat. There is no health risk when eating GMOs. Every scientist agree on that. Arguments saying that GMOs cause health risks have no foundation and are not based on evidence. Have a look at the Skeptics.StackExchange.com > Is Genetically Modified food safe to consume?.
Note that I am not saying that there is no discussion or debate to have around GMOs. I am only saying that these discussions have no reason to be around health risks for the consumer.
Your questions

Could crops be made larger?

Yes. We already did that.

Could crops become more pest-resistant?

Yes. We already did that.

Could a 'uniform shape' be created?

I do not understand what you mean.

Would this be done with genes from other plants? Or artificially?

The term 'artificially' has no good definition and it makes your question unclear. Most would consider pretty 'artificial' to take a gene from a species and insert it into another species (even though it occurs in nature).


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Do Class A biosolids count as organic fertiliser?
Does Human Waste, which has been treated at least twice to remove pathogens & remove stink, still count as organic despite it passing the EPA's class A standard?
If so, does this mean that none-GMO crops grown in this fertiliser are still organic?
Thank you to those that take the time to answer.

Definition of "organic" in Science
In science (esp. in chemistry), organic matter loosely refers to matter that eventually make up living beings are are remains of living beings. Typically organic matter consists of long chains of carbon surrounded by hydrogen atoms and a few oxygens and nitrogens (and eventually other things such as sulfur and phosophorus).
Can we eat something that is not organic?
Unlike plants, we (all animals and fungi) are heterotrophs (feed on organic matter only). As a consequence, there is no such thing one could call food that would not be organic.
The (mis)use of the term "organic" in popular culture
In the popular culture organic is a term that tries to refer to certain type of food that are grown under certain conditions and treated a certain way. However, there is really no good definition of organic in the popular culture and there exists no objective definition that would satisfy someone that wishes to categorize food into what they like to call "organic food" and "not organic food". Similarly there is no good objective definition of GMO either.
Some organization may make up definitions of "GMO" or "organic food" but those definitions rely on a long list of products rather than to an actual definition.
I just want to attract the attention of the naive reader that I am not saying that the term organic as used in the popular culture is healthy/not healthy or good/bad. Arguments concerning whether it is ethical to buy organic food goes both ways and it is not the job of a science website to discuss questions of ethics.
Are GMO safe to eat?
You are not asking this question here. But in case you wonder you might want to have a look at the Skeptics.SE post: Is Genetically Modified food safe to consume?

no - USDA organic designation does not allow ANY biosolids of any class to be used on the land - and way not?? Because even class A still contains thousands of toxins - hardly any tested for. To call Biosolids organic matter is to do violence to the language - would you call a substance made up of 40% toxins (by weight) ORGANIC .....no.

can you add some citations to support your claims?


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Atmospheric gas changes, and their effects life
I was curious how life on Earth, or an Earth-like planet, would be effected by changes in the gases which make up our atmosphere.
Assuming there is a similar level of oxygen in an atmosphere, could other gases be reduced or even replaced and still be able to maintain life as we know it?
Not really biology, but if the following could be kept in mind too that would be amazing:
[To give some context, I would like to ask how a sky could be light blue with a purplish hue, which supports some life larger than what we see on Earth, but still capable of supporting life which we find on Earth.
I am assuming a slightly higher percentage of oxygen is needed, but what other gases which are none lethal, but give a purplish hue?]
Thank you to all who take the time to give an answer, very much appreciated!

This question would be much more on-topic on [worldbuilding.se].


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Can we study all the genes of one human being?
Considering the fact that a new-born child gets 23 chromosomes containing DNA and genes from each of his parents and then 23 chromosomes from those 46 chromosomes of the new-born child will be transmitted to his child, I am wondering do all the people have the same 46 chromosomes or all have different chromosomes ( that's another thing that some genes present in the DNA of chromosomes don't express themselves. Of course, they are present there, no? )
If all of us have same chromosomes then can we study those genes present in 46 chromosomes to find out ALL the characters one person can have?


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Are ganglion cells in the foveal avascular zone served by choroidal blood supply or diffusion from retinal layer capillary beds?
I am trying to determine which blood supply (choroidal or retinal) serves the retinal ganglion cells that respond to foveal cone stimulation. I know that the fovea is supplied by the choroid, but it is unclear to me if this only applies to the cones in the fovea. The paper I link to below mentions that the choroid serves the fovea, but the choroid also serves the outer retina in total (and the RPE). So is the statement that 'the choroid serves the fovea' extending beyond the observation that the choroid serves the outer retina (since the fovea is mostly cones due to the inner layers being pushed aside)?
Are the ganglion cells that are pushed aside in the fovea served by choroidal vessels, or are they pushed aside far enough to be served by capillaries in the retinal layers? Please provide a paper as a reference.
I've searched google obviously and perused PubMed and I cannot find a clear answer to this.
https://www.ncbi.nlm.nih.gov/books/NBK482301/

I'm sorry if this sounds picky, but did you enter your question into a decent search engine? Also, your title and your actual question don't seem to me to match. You seem aware that there are ganglion cells in the FAZ, and it's the blood supply that you ask about in your final question. Would you please edit for clarity?


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What snake is this one?
I'm wondering what kind of snake is the one in the attached photo. It looks like Vipera aspis but It seemed a bit too big (lenght of about 1 meter).

This photo was taken near Como, in the north of Italy, in the woods of Parco Spina Verde.

Did the snake have dark V on his head?

I'm afraid I can't tell.. the snake quickly run away and I didn't have enough time to look closely the details on his body

So i think you really cant expect much more then my answer. Unfortunatly because i want to know true name..

I think it could be Vipera aspis, but that leght what did you descripe is really rare. Anyway it can be Smooth Snake(https://en.wikipedia.org/wiki/Smooth_snake) too. But you know personaly i cant do more from this point of view. The smooth snake is much more common and longer so there is a bigger possibility.

In my opinion a very nicely patterned individual of the recently newly described Barred grass snake. Used to be part of Natrix natrix. Non venomous, not dangerous.


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What is the term for toes that pull together with an upstep?
I fairly recently learned the term digitigrade, to describe the anatomy of a creature that stands on its toes rather than on the flat of its foot, like cats and birds.
I'm trying to narrow that down a little more now. Some animals like a cat or dog (or us), the toes are fairly static as they walk. Contrast that to the toes of a bird where on the upstep the toes... pull together, for lack of a better description, and spread apart as they step down on the foot, as shown in this video.
What is the proper term used to describe that motion and style of walking, or that type of functional foot, where the toes pull together and then spread apart as the foot goes up and down?

I think the digits of cats and dogs also spread a bit but since the digits are close together you cannot discern the spread as you can do in the case of birds.

@WYSIWYG - yeah, being digitigrade also, I'm sure they do. Like you said, being much shorter toes, it's just not that noticeable. Hence the addition of fairly static. ;)

Another difference is that in cats and dogs, the dew claw doesn't play any part in walking at all, while in most birds, that back toe/claw is heavily involved in their walking and standing.

Thinking about it more, cat toes I think are also more in a row like ours, so might not do it as much, where are most bird toes are arranged more radially.


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Trial pre-registration service that accepts non-clinical trials, or specifically ecology?
I'm in the early stages of designing a trial in ecology. I'm interested in pre-registering the trial, as suggested here.
My concern is that all of the registries (that I can find) deal specifically with clinical trials, not ecological or general natural-sciences research. Does anyone know of a service that would accept pre-registration of non-clinical biological trials?

Did you try OSF.io?
They offer a free service where you can preregister trials and give them a timestamp with a DOI number etc.
I do not know if this is exactly what you are looking for, but it's the easiest solution for preregistering and I am quite sure that it would be enough to get the "preregistration" badge when you are finally ready to publish.
Here is more info on how to do it and what is essential for preregistration.

It looks like the 'Registrations' feature of OSF should satisfy a reasonable journal-editor that a study has been pre-registered. Answer accepted.

An addition to that - it seems that OSF plans to offer a "financial reward" for pre-registration, see https://osf.io/x5w7h/


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Is it common to have multiple recessive traits in humans?
I just started thinking about my phenotype and realized I got multiple recessive traits. I have attached ear lobes, my blood type is O-, I got green eyes (I think eye color in polygenic but still somewhat recessive), a few years back I was in the control group of a study that was looking for a link between an allelic variant and the development of diabetes mellitus in patiences with another disease I forgot which, I was the only homozygous among all control patients! so you get the point. I am just wondering if anyone has any notion of how often humans present multiple recessive traits, maybe in terms of allelic frequency or something like that, or where can I find information about it. And maybe if there is something health related that may be worth knowing. I mean apart from a minor allergy I'm a really healthy person, but I may have predisposition to something.

Depends on the allele frequency in the population.

sure, but I guess my question is if there is some database where I can look at some actual numbers...

Think of law of independent assortment and gene linkage.

It depends on how long a population in your dominant heritage was genetically isolated, how common certain recessive traits are.
However, you might reconsider about the "green eyes".  Iridologists claim that there are only blue eyes, and light brown eyes.  All other colours are indicative of bioaccumulation of various substances (evidenced by a return to blue or light brown when the body is supported in excreting these substances), and health issues in certain tissues.
While there is argument about how scientific a technique iridology is, all medicine begins as observation of patterns, and development of models based on those patterns.  Models in medicine are constantly undergoing upgrading and replacement, as old models no longer explain new and well-observed patterns.

Please support some evidence for the claim that some eye colours are caused by bioaccumulation of substances and that the body can be supported to get rid of those substances and eye colour changes can be caused by that.


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Oldest Triceratops fossil
In most books, Triceratops is listed to live between 68-66 MYA (million years ago), however some books list Triceratops as living between 70-66 MYA. The Campanian age ended about 72 MYA and then came the Maastrichtian. Many articles state that Triceratops is "late Maastrichtian" dinosaur. All these citations do not give a clear answer: when did Triceratops live? All sources agree that Triceratops lived up to the K-Pg extinction 66 MYA, but when did the earliest Triceratops live?
This may be vague question so put it more empirically: what is the oldest age that a Triceratops fossil is dated to? Not when the first fossil of Triceratops was found but what is the earliest age (in MYA) at which Triceratops are known to have existed? Are there Triceratops fossils from 68 MYA? And from 70 MYA?

late Maastrichtian,  Maastricht is the name of a restaurant.

Thanks. From where I am coming from, the term localized as "Maastricht" but thank you for your comment how it is used in general/international.

late Maastrichtian is probably it.
Part of the problem you are running into is the Triceratops genus is in flux, there is debate about whether certain species belong in the genus. Such as whether triceratops and torosaurus are the same species.
The other problem you are running in to is the accuracy of dating methods, many fossils are dated indirectly, by bracketing (distance in section) with ash beds but this means they have a decent margin of error, 69MYA +/- 2mya is completely possible. Many were collected before such dating was even done or suche detailed measurements were taken leading to an even wider error bar. Especially given the best dates for the Hell Creek Formation itself has an date range error of about +/- 0.7MY and begins with a unconformity. Many studies are just going not going to calculate a date that has a high degree of uncertainty. The date for the end is more solid because it is an ash bed, thus directly datatable.
The most recent analysis of triceratops I know of is here many of the specimens were collected in the 1800's so late Maastrichtian is about the best you are going to get for an uncontroversial date.


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Are there macrophages in the blood vessels and within the blood stream?
Monocytes are phagocytes that "evolve" or "differentiate" into macrophages. I read that there are monocytes in the blood stream and vessels and that macrophages are found mainly in other tissues and in the lymphatic system.
My question: are there macrophages (and not merely monocytes) in the blood vessels and within the blood stream? And if there are, are they numerous there or sparse?

Usually, monocytes and neutrophils are present(there are other cells like Lymphocytes and other leukocytes), the only time a macrophage will be present is when inflammation occurs, I suspect this is due to the large size of the macrophage, it would be difficult for it to travel in the bloodstream, as it is quite big, compared to the small size of a monocyte. During inflammation, vascular dilation and permeability increase, which makes it easier for cells and proteins to diffuse across the endothelium.
A source that macrophages are present in all tissues: https://www.researchgate.net/publication/227897252_Macrophages_in_the_embryo_and_beyond_Much_more_than_just_giant_phagocytes
A source that talks about all the leukocytes and lymphocytes present in the blood normally: http://www.histology.leeds.ac.uk/blood/blood_wbc.php

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

Macrophages are white blood cells and I’m pretty sure that leukocytes are present in blood that flows throughout the body and hence they are found in tissues. Typically, more number of macrophages are present in the blood when there is some form of invasion by bacteria or virus.

This answer is less specific than the question (leukocytes vs. macrophages).


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Can birds pass diseases to humans through contact surfaces?
My friend asked me the following question. She has a pigeon nesting on her window and the pigeon often touches the window, and my friend also sometimes touches the window (e.g. open and close it). The question is does the touching of her and the pigeon in a common surface (the window) can transmit infections or disease from the pigeon to herself? Is there a risk letting the pigeon nest on her window pane?

But it's on the other side of the window?! So how is that the same surface?

Provided she washes her hands after touching surfaces that came into direct contact with the pigeon, there shouldn't be any relevant health risks from touching this surface.
And just because it sound like the pigeon somehow is nesting WITHIN her apartment: Be aware that pigeons can carry mites that could spread within the apartment and infest plants. I would advise against having wild pigeons in the apartment!
EDIT:
Knowing the pigeon is outside, it's not 100% necessary to remove the nest. It depends on whether this window is used for venting and on the direction of air pressure. (does wind go in or out at this side of the house?). Also it depends on the visual cleanliness of the nest. Bird-droppings can potentially represent a health risk, as they can spread through the air, once they dry out, while potentially containing dangerous micro-organisms. Same with feathers that lie around.
So if wind regularly comes from the side of the nest, she could remove the nest for safety reasons, especially if the window is in the kitchen. Otherwise she can't overcome that guilt by blaming health.

Thank you for your answer. The pigeon is nesting on the outer window pane and not inside the apartment. Is the risk of mites still relevant?


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When do invasive species become native species?
Until when an invasive species is considered an "invasive species" and when it is starting to be considered a "native" species, i.e. a species that is an integral part of the local fauna/flora?
I ask this because the expansion of species to new territories also occurs in nature and without human involvement. And in some cases, a newly-arrived species drive out the local species and causes its extinction. However, today it is regarded as native.
Many of today's fauna are the result of different species coming from different areas. Maybe in the next century, species that were considered invasive today will be considered native or an integral part of the fauna/flora.
The criterion may be time passed since that species was introduced or the time when the invasive species reached an equilibrium with the ecosystem.

On a human timescale or a geologic timescale, on a human timescale never.

A time in years. It may be a century (probably a human timescale) or a millennium (human or geologic timescale?) or at least 50,000 years or even million of years (the last is surely a geologic timescale).

It seems to me that this is simply a problem of some people allowing themselves to extend the label "invasive species" to include anything not transported (directly or indirectly) by humans, as the term ordinarily indicates.

2 issues. 1) Inconsistencies/disagreement about how to define "invasive" and 2) well, time, and the [narrow] subjectivity in which we typically observe/analyze it. I don't think this question can easily be answered, and - quite frankly - I think it more of a philosophical question more than a biological one.

There are two uses of invasive,

species introduced to new territory by humans, theses are considered invasive essentially forever. So to answer your question, they don't.

species that enter a new territory via a natural pathway like a landbridge or storm drift and destabilizes the local ecosystem. there is no specific cut off for these as it is more about the context than anything else.  Bison are considered native today but paleontologically they were originally invasive. This is more about how they got to north America. Often once the biosphere restabilizes with the new species they often stop being referred to invasive but this is not a hard and fast rule and could take millions of year or a lot less. On a long enough timeline all linages could be considered invasive.

Invasive species is defined by the USDA as:

non-native (or alien) to the ecosystem under consideration and,
whose introduction causes or is likely to cause economic or environmental harm or harm to human health.

Under this definition, a species that was labeled 'invasive' will lose the label when it stops causing harm. Although I can think of no examples, in theory an ecosystem could stabilize into a new state after an invasive species causes significant disruptions, which would cause the invasive species to lose the label.
Personally, I really like this definition because it differentiates between non-native species that integrate into an established ecosystem (e.g. coyotes in Eastern US) and non-native species that disrupt an established ecosystem (e.g. rodents in New Zealand). While the former is a natural and healthy biological process, the study of which dates back to island biogeography in the 1800's, the latter is a damaging process almost always caused by humans.

Essentially nothing since the start of the anthropocene: any invasive organism that owes its transportation and dissemination to human intervention remains forever precluded from acquiring the status of endemism.
There are over 40 million flights per year and 50,000 cargo ships with 11 billion tonnes of goods affecting places like the Galapagos, New Zealand, Madagascar, Hawaii, not only places that were joined during ice ages, so biologists use chronology to label endemism.
From microscopic fungi that decimate forests, tics and mosquitos, the black death (yersinia pestis), covid19, to hippos, pythons and trees, ecosystem breaches are going on at a massive rate of 1000's per century, causing extinctions and ecosystem degradation which is of particular interest to biologists.
Biologists specify times when a species migrates to a new ecosystem, so invasive vs native is a simplified concept of recency. Bears in America 3 million years ago, Dingos in australia 5000 years ago. *quote: The brown bear appeared in eastern Beringia only 50–70,000 years ago.

In any field, some terms may be defined within the context of a particular research study. The same goes for conservation biology, where definitions may reflect the specific goals of a conservation plan.
NPS defines "native species" as, "All organisms that have occurred, now occur, or may occur as a result of natural processes." (Source). So if something is introduced by humans or because of human activity, it's never considered native by NPS. Also, Non-native species are not necessarily considered invasive (most are probably not).


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Reference for the bite force for Nile Crocodile
The (maximal) bite force of the Nile Crocodile (Crocodylus niloticus) is estimated around 22,000 Newton (refer to YouTube interview with Ofer Kobi, a crocodile conservation ranger and croc farm owner, time 7:50-8:00, Hebrew , where he estimates the bite force as above 2 metric tons). However, I didn't find a proper reference for this. Dr. Gregory Erickson measured the bite forces of a 5.2 meters long Saltwater Crocodile (Crocodylus porosus) and obtained a value of about 16,000+ Newton and estimated a 6.7 meters long Saltwater Crocodile can exert a bite twice as strong (about 34,000 Newton). See Paper by Gregory Erickson et al. Interesting to note that Erickson measured small Nile Crocodile (total body length < 3 meters) so it does not represent the bite force of a full adult big crocodile.
Remarks on units of force:
1 Newton = 1 kg * 1 meter / sec^2
$1 \ \mathrm{Newton} = \frac{\mathrm{kg} \times \mathrm{meter}}{\mathrm{second}^2}$
1 Newton = 0.224808943 lbf = 0.225 lbf (pound-force)
10,000 Newton is approximately 1 tonne-force (1 tonne = 1 metric ton = 1000 kg)

Where did you get your estimates from?

From an interview with an owner of a crocodile farm.

An interview you've conducted yourself? An interview that has been diffused on TV? Do you have a link to this interview or some document where we can find direct quote or something?

No, an interview on TV. It was held in Hebrew. Since he is not a scientist I am looking for a better reference for the bite force of a Nile Crocodile. It seems strange that no body measured the bite force of a 5+ meters nile croc.

You can still link to the interview (or at least refer to the emission name and date of appearance). It really is always a good habit to link to your sources and it shows that you're not just throwing random number out of the void. You can also link to Erickson's study. Good format will increase your chances of getting people to care about your post. Good luck!

Here it is: YouTube Time: 7:50-8:00

I sent an e-mail regarding this question to Dr. Gregory Erickson. I did not receive an answer yet.

Here is a video by Brady Barr (video in YouTube) measuring 5000 lbf for an adult Nile Crocodile. This is equivalent to 22.24 kN (more than 2.2 tonnes of force). This result is also refered here (Getty Images).
 Source: Gianfranco Gori, Wikipedia


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The phylogenetic definition of the clade Dinosauria
Up until two years ago the clade of Dinosauria was defined as all the descendants of the most recent common ancestor of Triceratops and birds. From Wikipedia:

Under phylogenetic nomenclature, dinosaurs are usually defined as the group consisting of the most recent common ancestor (MRCA) of Triceratops and Neornithes, and all its descendants. It has also been suggested that Dinosauria be defined with respect to the MRCA of Megalosaurus and Iguanodon, because these were two of the three genera cited by Richard Owen when he recognized the Dinosauria.

However, after the resurrection of the clade Ornithoscelida by Baron et al in 2017 (see here), as the clade consisting Ornithschia and Theropoda, the MRCA of Triceratops and birds is defining Ornithoscelida and not the whole Dinosauria, assuming we still define Sauropodomorphs as dinosaurs.
So if dinosaurs include Sauropodomorpha, Herrerasaurs, Ornithoschia and Theropoda,  what is the most updated phylogenetic definition of the clade Dinosauria?

As of right now it is still the same, the evidence for sauropodomorpha being a outgroup is not statistically more reliable, this may change, however this will still not have much impact. There are several ways in which dinosauria is defined.
The most recent common ancestor of Megalosaurus and Iguanodon is also sometimes used since they were the original animals used to define the group.
The last common ancestor of Triceratops horridus, Passer domesticus, Diplodocus carnegii, and all of its descendants is also used just because of Baron's work.
Finally there are several unambiguous synapomorphies used to define the group, including such things as ankle structure. A full list can be found here.
In a group as well known as dinosaurs, a discovery like Baron's (if it holds up) is just going to lead to a change in the definition.


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Why do we grow so much hair on our heads compared to our bodies?
I've been wondering about head hair, facial hair in particular. Human males can grow very extensive beards should they choose to not shave - however you do not really see this in our chimpanzee cousins! Yes, they have little pseudo-beards, but the difference being that they do not shave, that is just the length they reach. Whereas in humans we can grow to our hearts content (*this may not be the case, see this question).
I can't really see why this would have been selected, unless it's simply that (evolutionarily speaking) women like men with long beards?
So my question is: why can humans perpetually grow head hair, yet we have lost the majority of our body hair, in comparison to chimpanzees and other ape family members?

This is closely related to this question - perhaps not an exact duplicate though?

@RoryM thanks for pointing out that question - it certainly goes some way to helping answer this one. I have differentiated my question a bit further so that it's definitely not a duplicate.

Wheeler (1992; and previous) discusses the evolutionary loss of "non-functional" hair in hominids from the perspective of water balance.
Wheeler's hypothesis is that naked, bipedal hominids could have tolerated higher ambient temperatures as well as elevated metabolic heat production. Naked skin would confer higher levels of evaporative cooling, but would have entailed more water loss.
Wheeler argues that bipedalism necessarily would have preceded loss of hair, which seems to agree with Carrier's (1984) hypothesis that early hominids were distinguished not by large brains but by upright, bipedal postures with striding gaits. Humans are unique among similarly sized mammals in their capacity for endurance running.

Interesting! May we have kept hair on our heads to keep the sun from directly heating our brains? Bit off topic, but do you suppose the increased endurance running is simply that running on 2 legs is more efficient than using all 4?

Hair on the head is an excellent built-in sun protection at minimal resource cost. If we didn't have hair on our heads then we would have to apply sunscreen on the scalp or take cover more often (often impossible for hunter-gatherers).
No sun protection = sunburns and risk of skin cancer.


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Why are 3 nucleotides used as codons for amino-acid mapping in DNA?
DNA is made of 4 unique nucleotides. When coding for a protein, a sequence of 3 nucleotides is used to code for each amino acid. Why are codons 3 nucleotides in length?
A related question can be found here: why-are-there-exactly-four-nucleobases-in-dna

I have asked and answered this here because I had posted this answer to the linked question, but that was not truely answering it. There are now much better alternative answers, so I have asked the question I actually answered here!

The central dogma of molecular biology: DNA makes RNA makes Protein
DNA is a reference for proteins*, which are the functional molecules in cells. These are comprised of 20 unique amino acids, and each is coded for by a stretch of DNA known as a codon. Codons are always 3 base-pairs (nucleotides) in length.
DNA is made of 4 unique nucleotides; (A)denine, (G)uanine, (C)ytosine and (T)hymine. This means that there are 64 unique codons that can be made with these 4 bases (4*4*4).
Theory One - evolvability
If codons were only 2 bases in length then the variety of codons that could be created would be less (only 16 unique sequences if there are still 4 nucleotides). More unique nucleotides would be required to get enough unique sequences to code for the 20 amino acids (as well as the STOP codons). For instance, to get 64 unique sequences using a 2-bases-per-codon system there would need to be 8 unique nucleotides.
We cannot ever 'know' what happened in evolutionary terms, but it seems likely that the 3-base (nucleotide) codon system would have arisen after a period of a 2-base system, as the biological systems became more complex. This would have allowed a lot more variation in the amino-acids used, and thus more "evolvability", which would have been very advantageous to early organisms.
However as the 4-unique-nucleotide/3-codon system is ubiquitous to all life we have discovered on earth, it seems likely that, back at the start of DNA (in fact probably RNA), this was the system that worked, or at least, this is the one that survived (although as Kevin rightly points out, we don't know whether there ever were any other systems). Variations may have arisen over the years, but it is this 1 system that has prevailed here on Earth.
See this question for some more interesting info: why-20-amino-acids-instead-of-64?
Theory Two - "redundancy" of codons conveys additional information
This theory is not mutually exclusive to the one described above. In a recent paper D'Onofrio and Abel [1] state that ribosomes pause for different lengths of time at different codons (even if the codon codes for the same amino acid), and that this pausing affects the 3-dimensional structure of the final protein.
Therefore the nucleotide sequence contains at least two "layers" of information: firstly which amino-acid should be added, and second the specific codon used for that amino acid can impact on the final structure of the protein. This could not be done with fewer nucleotides, but arguably even more control could be exerted with more nucleotides, but perhaps this comes back to my first point that this system evolved such a long time ago that more nucleotides were not necessary for life to "work" and proliferate into everything we see today.

D'Onofrio and Abel, 2014. Frontiers in Genetics. Redundancy of the genetic code enables translational pausing

*only around 1% of our genome is actually protein-coding, and many non-protein-coding RNA products have very important functions, but I won't go into this here. Suffice it to say I am referring to the protein-coding regions of the DNA.

Overall, this is a good answer. I take issue though with saying "determined that the most efficient". We have no idea that other combinations ever existed. 4 nucleotides in combinations of 3 did not not work. That's all we know.

@Kevin thanks, and you are absolutely right. I have given the answer a general re-work because I don't think it flowed properly having been adapted from a different question, and have taken your comment into account. Many thanks.

The comment is NOT a criticism toward the answer. I know everybody is talking about the central dogma of molecular biology but it is such a bad name. Dogma has no place in science. Moreover, we now know that retrotranscription exist and therefore the central dogma of molecular biology not always true.

Thank you for posting the theory two part. I've always wondered why CAG trinucleotide repeat in HTT can cause Huntington's, but CAACAG doesn't seem to.

Man, my BSc thesis (8 years ago) was based on the idea of different codons causing conformational change. I compared the codons of structured-regions in proteins with unstructured and found that codon usage was different when coding for the same amino-acid. The guy who marked it gave me 20%. Led to me getting a low final grade. Required I got my masters before my PhD. Probably set me back 2 years. And now it's published in Frontiers in Genetics -_- Academia sucks when you're small-fry.

I think a strong case can be made for three nt codons existing already in the primordial genetic code, which included only eight abiotic amino acids (this is still clearly seen today in translation tables where most abiotic amino acids are defined by four or more codons). However, in this primordial genetic code, the last nt was likely meaningless (this has been reinvented in many mitochondrial genomes where a single tRNA, usually thanks to a modified U in the anticodon wobble position, recognizes up to 4 codons). Assuming the three nt codon primordial genetic code existed, we see that the reason for the three nt codon structure was not that two nt codon structure was not enough for coding everything (4^2 > 9, it would have sufficed), but something else. So what could it be? My educated guess is that it has to do with the A,P,E-site structure of the ribosome not fitting into a smaller molecular configuration (i.e. you couldn't have the adjacent A,P,E-sites within the space limited by just five phosphodiester bonds (six nt, three two nt codons) vs. eight phosphodiester bonds (nine nt, three three nt codons)). So in short, my view is that the primordial ribosomal structure was the key factor to the three nt codon structure of the genetic code, it couldn't have worked with anything less and anything more would have been a waste.

This is very interesting information (sorry for delay in commenting). Could you provide any references/additional reading?

Might I suggest you go directly to the source? Here is a link to a paper published by Francis Crick (et al) in 1957 entitled: 'Codes Without Commas' http://www.ncbi.nlm.nih.gov/pmc/articles/PMC528468/

The source you linked is really good, but simple linking is not exactly what this site is about. Of course it's easier, but please take time and elaborate your answer, explain, interpret the sources you use.

Welcome to Biology.SE. A link only is not sufficient for an answer. Either take time to elaborate your answer or convert your answer to a comment.

For the same reason there are 8 bits in a regular character datatype in old-school programming languages (before internationalization and Unicode).
In modern ASCII interpretations, you have a certain number of characters that need to be encoded, somewhere between 128 and 256. 8 bits would be the minimum sufficient for (modern extended) ASCII encoding. (Unrelated to the question: in computing, it often helps to have the number of bits in various operations be a power of 2. Also, the original versions of ASCII specified 7-bit encoding before it was extended to a full byte in an early internationalization support effort.)
Getting back to nucleotides, there are 20 amino acids. Think of a codon as the equivalent of a "byte" and a base (nucleotide) as the equivalent of a "bit". 2-codon sets would be insufficient except if you plan to custom-build a compact-genome life-form that only supports 15 amino acids, a stop codon, and no wobbles.
Supporting all amino acids plus a stop codon requires at least 21 distinct codon values. In particular, find the smallest power of 4 >= 21, which turns out to be 3.
An added bonus: the number of codon values is roughly triple the number or amino acids (plus a stop codon), allowing for redundancy: some amino acids are encoded by more than one codon, which acts as a buffer against mutations.


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How much DNA does a species lose after post-polyploidization genome downsizing?
After whole genome duplication, diploidization takes place, right? A lot of changings in gene organization and expression involving genetic and epigenetic mechanisms (translocations, transpositions, deletion and / or insertion of sequences, additive or non-additive gene action, transposon activation, gene repression or activation, subfunctionalization, neofunctionalization and so on) cause the genome to shrink a little bit before the species karyotype stabilizes and establishes. But how much DNA, in average, is gone in such process? I guess I have read somewhere that the elimination of redundant repetitive DNA families, causes polyploidization to result in a DNA increase of about 1.5x and not doubling. Is it true? I really would like to have some references on this information or similar.. I did look for, but I couldn't find


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What do we call these containers used in biotechnology?
I'm translating an autoclave instruction from Russian, and it says that these containers (ванночки) (see the black circle on the below photo) are to be sterilized in the autoclave. I'm not sure what they are called in English-language biotech texts.
The Russian text uses the vague term "ванночки", literally "little bathtubs". Maybe just "containers"?

That would be a Reagent Reservoir, or just a Reservoir. These tall and narrow ones are specifically designed for use with a robot, but there are also shorter and wider ones for manual pipettes:

120 mL Reagent Reservoirs


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Tea that makes everything taste like dirt
My highschool biology teacher once gave us (her class) a tea which made everything taste like dirt. I remember that chocolate candies, spicy hot sauce, and salty crackers all tasted the same after drinking the tea. The effect only lasted a minute or two. It's been a long time, and I can't remember the name of this tea - can anyone identify it?
(I am not certain if this question is appropriate for this SE, please let me know if it is not.)

This is probably the most appropriate SE, only alternative I could think of would be the cooking SE and it's probably more off-topic there. Did you see the (presumably) leaves used to brew it?

Got it, thanks. I considered the cooking SE, but I thought that maybe this was a standard highschool bio experiment/demonstration... I think the leaves were a very dark green/grey. They came packaged in a bag, so they must have been bought from a store or something.

This sounds like gymnemic acid, which can be isolated from the leaves of Gymnema sylvestre. It’s an “anti-sweet” compound, which wouldn’t necessarily make everything taste like dirt but might do so for you particularly. When I had it, it made my tongue slightly numb and candy tasted like nothing rather than sweetness, so it may not be what you’re looking for.
Lactisole (from coffee beans) is another option, but I haven’t tried that one personally so I’m not sure what its taste effects are like.

I'm accepting this for now because I think it's correct, but I'm not totally sure. If anyone else has any ideas, please let me know!


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Does anyone know of any resources that detail an extensive number of receptor types, their effects, and signalling pathways?
In a similar manner to this Wikipedia page, although I am not too concerned about the localisation of the receptor, or any known ligands, as I can already access this knowledge easily.
https://en.m.wikipedia.org/wiki/Alpha-2_adrenergic_receptor

Hello @Roby Vicary, I think you forgot to link the wikipedia page in your question. To help you elaborate the question: Are you interested in any particular species? Could you give us an example for one or two receptors of the information you are seeking for if you arleady found some?

Hi, @Untitpol, thank you for the response, I have no serious regard for species at this time, the more extensive the better - although if I'm spoiled for choice, homo sapiens. I have added the Wikipedia link on alpha2 adrenergic receptors, the only thing lacking is the number of other receptor types to read up on.

IUPHAR database? As far as I know, this is among the most extensive database of receptors.

Thank you very much @cagliari2005 this is very close to what I am after, perhaps even better! Very thorough referencing, with useful "further information" sections

From the comment section:
The IUPHAR database is one of the most extensive database for receptors and ligands. It also contains a lot of additional information and direct references to the literature.


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How does alcohol interact with sympathomimetics to affect the cardiovascular system?
There is a fair amount of information on the cardiovascular effects of alcohol, and of sympathomimetics. How do they work? And how do their mechanisms interact?
We know that similar pathologies result from each. With alcoholics often experiencing mild left ventricular hypertrophy, mild diastolic dysfunction which preceeds systolic dysfunction, resistant hypertension; and a dilated cardiomyopathy - sympathomimetics leading to cardiomegaly, sinus tachycardia, left ventricular hypertrophy, and dilated cardiomyopathy #1.
An article notes that "alcohol competes with amphetamine for the metabolizing enzymes in the liver, therefore enhancing the bioavailability of amphetamine" #2. Are any effects of alcohol mediated by sympathomimetics/catecholamines, and if so which? Et vice versa.
[1] Chemical Cardiomyopathies: The Negative Effects of Medications and Nonprescribed Drugs on the Heart https://bit.ly/2AMU6eM
[2] Myocardial Infarction Associated with Adderall XR and Alcohol Use in a Young Man https://bit.ly/2SV4wQD
[3] Cardioprotection by regular ethanol consumption: potential mechanisms and clinical application https://bit.ly/2RRVVAQ
[4] De Musset's sign https://bit.ly/2HljluG