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Understanding Genetic Dynamics of Specific Problem
The following questions comes from International Biology Olympiad 2014, theoretical part B.
It states:

Earlier research suggested that the red flower pigment of plant species was the result of a
  chemical pathway including multiple steps and that all intermediate pigments were white. Three
  pure-bred lines with white flowers (White 1, 2 and 3) of this species were crossed with each other
  and the following ratio of colors were obtained among the progeny:

The question was how many genes control flower color. I completely botched it. Here are my thoughts:
Looking at F2 generation, there are 9 reds + 7 whites = 16 total. (I know it's a ratio.) Generally, having 16 suggests at 2 genes controlling the phenotypes. For example, cross AaBb x AaBb, you'll get 16 phenotypes.
Turns out 2 is incorrect, and I have no clue as to how colors are inherited in this problem. Any suggestions?

First of all, since two is incorrect, and one is not possible, three is the most probable answer. It is also supported by the format of question that three different types of white purelines are given. Let the genes be A, B, C. Now, there are three possible ways:-
1) Each one has two homozygous dominant genes and one homozygous recessive.
2) Each has one homo dominant and two homo recessive.
3) Any one has all homozygous recessive and the rest two can have any of the above two.
The problem with (2) & (3) is that they do not explain the red F1. Red will require a dominant allele of each gene. But in crosses of (2) or (3), at least one gene will be left out.   For example, AAbbcc x aaBBcc will give all progeny with cc. So none can be red. Same problem with aabbcc x aaBBcc or AABBcc
So lets go with (1). Let
W1 AABBcc
W2 AAbbCC
W3 aaBBCC
W1 x W2. => all AA Bb Cc (Red F1 of cross 1)
F1 x F1 will be like a cross of BbCc with AA in front of all the genotypes. This will give you exactly 9:7 phenotypic ratio as mentioned in question.
Now, lets solve the question.
A) Three genes. So false
B) F1 were homozygous for one gene and heterozygous for other two. So false
C) F1 of cross 1 = AABbCc and W3 aaBBCC
Since it is evident that it is possible to inherit dominant alleles of each gene (eg. AaBbCc or AaBbCC) so red colour can come. So false
D) F1 cross 1 = AABbCc
F1 cross 3 = AaBBCc
It is evident that one segregation of gene alleles of “a” and “b” will have a dominant allele no matter what. So for a white colour, only chances are from cc. So in cross Cc x Cc there is 1/4 probability for cc. So all in all, 1/4 probability for white (since aa and bb genotypes are not possible here).
So D is True.


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Quantification of concentration from chromatogram paper
In an experiment, I recently isolated and purified calf thymus DNA, hydrolyzed it with perchloric acid, and then applied the hydrolyzate to a Whatman paper in a polar solvent and let it run overnight.
I must now determine a way to quantify the concentration of each base, now separated based on polarity on the chromatogram. This cannot be the following method: Cutting the paper containing the base and putting it into an acid-containing flask, then measuring the absorbance, followed by Beer-Lambert's Law calculation for the concentration.
I would appreciate any ideas.

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What type of bee/wasp is this?
I found some bees or wasps, in my garden.
Auckland, New Zealand
13mm long head to abdomen, fluffy on thorax and head. Abdomen is orange brown with black stripes.
The nest or hive is underground (otherwise I'd suspect honey bee, though they seem a little smaller even than honey bee workers).
I managed to catch one eventually, but then I realised the container had oxide powder, so the bee in the attached picture is a lot blacker than it was in life. It is also dead ( just in case that's not obvious)
They don't seem to be aggressive - there is a new fence being built right past their nest, they don't seem to be bothered by it.
I am a beekeeper but only beginning, so I do have honeybee workers to compare it to, but not a whole lot of experience.
NOTE: it is autumn (fall) here - high temperature was 23° c (73° f)

Wow, that stinger looks dangerous

What is the approximate size of the nest (number of individuals)? tens, hundreds? a few individuals?

As I said, the nest was underground, so I don't know how big it is. I'd say there were about 30 individuals within about a meter radius of the entrance coming or going at any time (sunny day - my beehive had about 5 times that number at the same time). I'd say thousands to maybe 10,000 inside, extrapolating from my hive, comparing apples to oranges.

It is a vespid wasp (family vespidae). Bees are generally hairy, and this one has the typical wing folding of a vespid. Genus Vespula. There is a New Zealand website that shows the differences among common NZ wasps here:
https://www.landcareresearch.co.nz/science/plants-animals-fungi/animals/invertebrates/invasive-invertebrates/wasps/identification/key-differences

All the pictures I can find of these are quite yellow - these are much more orange. Also, these pictures show a small amount of hair - these are furry like honey bees, on thorax and head

Bees are hairy on the abdomen. That is not a bee.

Rephrasing my previous comment: these are furry on thorax and head, like bees, but (unlike bees) not on the abdomen

@JayBee Vasps are often hairy on the thorax and head. Look at the link included in this answer (of google Vespula)

Looks like it might be a European tube wasp

Why do you think so? What details make you suggest this wasp rather than others?

Wasps are differentiated by their wing patterns, the way they fold their wings at rest, their eye shapes,wing veinal pattern and abdominal colouration pattern.  The sample is dead and not at rest, and is discoloured by the oxidation.  But the colouring most closely resembles the one I selected.  The rest of the characteristics are too obscured.  But there's likely a nest nearby so he could capture another one.

The head and jaws don't look like Ancistrocerus but are perfect for Vespa or Dolichovespula

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Pain and Angina Pectoris
What causes pain in an angina pectoris? Ok, heart muscles may lack oxygen, but what is the role of pain here? Is it being beneficial? I'd like to know the physiological process of induction of pain during hypoxia.


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Is there any example of living beings destroying their environment?
I had an argument with someone about mankind being the only being destroying its own environment. I don't think this is true, yet, I cannot provide any example of significant importance.
Are there any examples of a living being destroying its own environment, making it uninhabitable to them? (Bonus point if this event led to an environmental catastrophe or to their extinction.)

You might want to explore the topics of "exceeding a carrying capacity" as well as "succession." Both represent examples where organisms are responsible for modifications to their surroundings -- sometimes (often times?) to their own detriment.

Species don't live in isolation
As simple as the question seems, it actually contains some issue in the conceptualization of a species in isolation that affect or does not affect its environment.
Species do not exist in isolation from others. Many species have very important impact on their environment. These transformations would yield the environment to be unsuitable for the survival of the species over time if there were no other species to interact with. But by the existence of other species creating a cycle of, say oxygen for example, the transformation that the species is bringing to their environment is not seen as destroying the environment. In fact, if they were to disappear that could be an important problem. Let's go through examples
Example 1: Cyanobacteria and the Great Oxygenation Event
In the history of our planet, about 2.45 billions years ago, some species started to produce oxygen. Before that the oxygen level on earth was very low. We refer to this rise in oxygen as the Great Oxygenation Event. At the time, there was very few species that were performing respiration (breaking up oxygen and producing carbonic gas). Oxygen is a very reactive molecule and the rise in oxygen level was actually a MASSIVE environmental impact (arguably the most important life-induced environmental that had ever happen on Earth). It lead to an event of mass extinction.
The main contributors to this rise in oxygen were cyanobacteria. Cyanobacteria were most definitely destroying their environment. However, today, while modern cyanobaceteria are still producing loads of oxygen, we don't consider they are threatening the environment. In fact, they are fixing quite a bit of carbonic gas, which we rather tend to see as beneficial.
Example 2: Ants
I will not develop this example too much... Ants are greatly affecting forests of the world. Without ants, forests would be pretty different (see this non-peer reviewed source of information).
Ants are typically considered indicator of a "healthy" forest (see Segat et al. 2017; Lawes et al. 2017 and the book Gorb and Gorb 2003). Howe ver ants can also be invasive species that cause massive "destruction" on their habitat (Tsutsui and Suarez 2003; Lach 2003; Ness and Bronstein 2004).
"Destruction" is context specific
So, wether a species is "destroying" it's environment depends upon what other species are around. It also depends upon what you are aiming for (species diversity vs stable communities vs ...) but I won't go into these details.
Instead of asking

What species destroy their environment

it would not be 'more wrong' to ask

What species are present in ecosystem that are not adapted to their presence

or even (although that is a little of a stretch and some may argue on it)

What species have recently been introduced in a new ecosystem? / What species have recently changed their environmental impacts?

Always keep in mind, that no species can live sustainably on its own alone.
Do humans destroy their environment?
What do we mean when we say that humans destroy the environment, then? Human activities have changed drastically very recently. This is caused for two main reasons 1) our technology and, consequently our needs and therefore consumption have changed drastically ever since the industrial era. 2) we went through a demographic explosion.

So, yes we are pumping lots of carbon dioxide in the atmosphere. We get this carbon from forests we cut down, from large carbon reserves that have accumulated over millions of years (petrol, gas, peat and others). This change in our environmental impact is often seen (and for rather good reasons) as destructive.
Other modern species that destroy their own environment
Pretty much any invasive species would qualify as an example of a species that destroys its environment in a way that is not sustainable for itself over the long term. Among the invasive species that have important environmental impact that are seen as highly destructive, I can think of

Emerald ash borer (North America)
European starling (North America)
Feral hogs (North America)
Brown tree snake (North America)
grey squirrel (North America)
Zebra mussel (Europe and North America)
Japanese knotweed (Europe)
Cane toad (Australia and Latin Amercia)
Northern Pacific seastar (Australia)
Common wasp (Australia)
Rabbits (Australia and New Zealand)
Crown-of-thorns starfish (Indo-pacific and Australia)
Water hyacinth (global)
black wattle (global)
Argentine ant (global)

Many of these examples are from western countries because 1) that's what we tend to have most data on 2) because that's what I know having only lived in Europe, North America (and a little bit in Indonesia) 3) There are many examples from Australia and New Zealand because they are the world champions in invasive species and in bad policies concerning these invasive species!
Some readers will probably complain (and some with good reasons) about the species listed as what we mean by "destroy" is very subjective and my list is not intended to show the species that are considered "most destructive". Also, the locations of where these species are invasive might be inaccurate and I welcome anyone to edit them.
You can also consider any predator (incl. herbivores) and parasitic species that is leading it's prey / host to extinction such as

The experimental case with lizards in the carribean (Schoener et al. 2001)
The atlantic salmons leading shrimps to extinction (with the help of human activities) in the baltic sea
The red foxes affecting (with the help of human activities) hares population in Europe.

Coming back to the question

Is there any example of living beings destroying their environment?

Yes... other species than humans are "destroying" their environment. Estimating how much they are destroying their environment is really hard to both define and measure. Without a good working definition and without looking at actual data, I would personally be happy to consider humans as being the species that "destroys" the most today.

Yellowstone National Park ecosystem will serve as a good example of this question.
Here is a link to an youtube video describing the situation pre and post introduction of grey wolves to Yellowstone (around 1940).
As you can infer from the video, when the wolves were hunted to the point they were non-existent in Yellowstone, the herbivores (majorly moose/elk) got free rein of vegetation. Since, they were left unchecked they went on to reduce river bank forest cover by a large margin. If the wolves were not introduced, the larger herbivores would have first driven smaller herbivores to zero by denying them nutrition and later find themselves suffering the same fate once they have completely consumed all vegetation.
However, it can still be argued that we are the only species to consciously destroy our 'habitat'. But the realization that we are doing so is quite recent and maybe, just maybe, if we had known what repercussions our activity would have on our 'habitat' we may not have done so.


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Do mosquitos excrete blood?
Since insects like mosquitos ingest only blood, and insects generally excrete their solid and liquid waste at the same time as frass, I was wondering: is mosquito defecation more like iron pellets or droplets of blood?
I've never seen a mosquito defecate, so I have no evidence. Do they defecate during flight? If so, are tiny little droplets of digested-blood falling from the sky?

This could be related https://skeptics.stackexchange.com/questions/23072/do-mosquitoes-urinate-on-you-when-they-bite-you

When mosquitos feed on blood they release water droplets, this is so they can condense the amount of nutrients from the blood but dispose of the unnecessary water weight. This act of releasing excess water is often mistaken as 'pooping', a clearer view of the process here. Actual footage of fecal excretion however, is harder to come across.
Mosquito defecation is more like iron pellets, to maximize their meals they excrete water during or after feeding (in case they need to make a quick get away). Iron is toxic in high doses, so the mosquito excretes it after absorbing the nutrients in the blood, resulting in dark pellets, containing iron and uric acid.


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

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

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

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


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Forming a cladogram from a table of information

Can someone please give me some tips or help me build a cladogram from the following table of information? The outgroup is Lancelets and the first derived character is vertebrae, followed by Lampreys and jaws I believe.  It’s not until after jaws I have trouble figuring out where to link up the organisms and traits. I’m assuming you cannot repeat or remove traits. When I look online the simpler examples do not help me much for this branching issue...I hope that made sense. It’s probably simpler then I think but I’m having a mental block with it. Any help would be great, thanks

Hi and welcome to this site. There are dozens of "How to draw a cladogram" instructions on the internet. Could be please edit your question and add, how you would follow those instructions with your example, and at what step exactly you are struggling? This community expects you to show you own efforts, otherwise your question might be closed as homework(like) question.

I have looked online at written explanations and videos. I get the concept but for some reason I can only get so far with it until it just doesn’t make sense where to place the organisms in relation to the derived and shared characteristics. Most online examples seem to be a bit simpler with less variables.

@Maria When the data  size increases, one usually uses a computer program to build the tree, because it gets impossible to manually explore all the tree topologies and see which one is most parsimonious.

I think the clue is at each step to look for the trait that is shared by most of the remaining taxa.
In your example: 9 out of 10 taxa are vertebrae. So you are correct to pick this trait first and outgroup Lancelets.
Looking at the remaining 9 taxa:
8 have jaws, and a different set of 8 swim bladders or lungs
At this point you can pick one of those traits, as far as I know.
You chose jaws and outgrouped Lampreys.
In the remaining 8 taxa, the characteristic that is shared by most of them (7), is having swim bladders or lungs. Thus, you can outgroup Sharks here.
In that way, you can go on for the remaining traits and taxa.

Please leave a a comment  on how to improve the answer if you think it deserves a down vote.


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Is there any evidence that supports glycolysis in mitochondria or chloroplasts?
Glycolysis is known to be a part of cellular metabolism undergone by both eukaryotic and prokaryotic cells, whether under aerobic or anaerobic conditions. As the endosymbiotic theory states that mitochondria and chloroplasts were once bacteria that lived apart from eukaryotic cells, do they have any enzymes or compounds suggesting that they once did glycolysis?

On aspect of the endosymbiontic theory is that genes were transferred from the endosymbiont/new organelle to the nucleus of the host cell. Does your question include such transferred genes or only the ones remaining on the mitochondrial/plastid genomes?

A search of UniProt returns no reviewed, mitochondrially encoded genes involved in glycolysis. There are some unreviewed entries, but a brief perusal of the associated publications suggests to me that these have all been incorrectly annotated (as one may expect from unreviewed entries).
Interestingly, Rickettsia prowazekii, an obligate intracellular parasite and the modern species thought to be most closely related to mitochondria, also has no glycolytic enzymes:

Genome sequences of organisms enjoying an endosymbiotic lifestyle are at risk. The activities of homologous nuclear genes may render genes of the endosymbiont expendable and as a consequence they become vulnerable to obliteration by mutation. Good candidates for such purged genes in Rickettsia and mitochondria are genes required for amino-acid biosynthesis, nucleoside biosynthesis and anaerobic glycolyis. These and other genes would have been deleted when an ancestral genome first lived in a nucleated cell. Once genes essential to a free-living mode are lost, the endosymbiont becomes an obligate resident of its host.

Andersson SGE, Zomorodipour A, Andersson JO, Sicheritz-Pontén T, Alsmark UCM, Podowski RM, Näslund AK, Eriksson A-S, Winkler HH, Kurland CG. 1998. The genome sequence of Rickettsia prowazekii and the origin of mitochondria. Nature 396:133-140.


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Reporting observation of a bird outside its seasonal presence
Last summer I saw this bird in the countryside of Bulgaria (Dobrich area) and I think this is a specimen of Great Grey Shrike (Lanius excubitor).

By looking more in detail the distribution of that bird (I checked in few books including the Collins Bird Guide in French edition), I noticed it is present in Bulgaria but only in winter season. However I took this pictures in August 2017.
First, is it really a specimen of Lanius excubitor?
And if yes, should it be reported in some way?
I know some other countries have reporting tool on Internet but I have no clue about observations in Bulgaria.

You can report any observation worldwide on www.observado.org If you add a picture your observations will usually be corrected if wrong.

It is NOT a Great Grey Shrike (Lanius excubitor).
It is a young Lanius minor Lesser Grey Shrike (which breeds in Bulgaria).
I say young (born the same year) because of the white tips of the feathers (they are new) and not so extended black mask (which probably induced you into the ID mistake).
I attach a picture of young Lesser Grey Shrike for comparison.
Generally you can report your observation on ebird.
There is a team checking the unusual observations (although for Europe at least many mistakes are not picked up).

Interesting answer, in fact I elimiate this specimen because they show it most of the time with rose coloring on the side (adults), and the young one were more brownish on the back, but I think you're right.

I have seen both species many times and thanks to your good pictures I have absolutely no doubt on the identification

Accepting the answer as I also found evidence for the white stripes on the back for the juvenile in another book.

it's a characteristic common to the juveniles of many bird species

The wiki article for the great grey shrike is very good and it says:
Females are more prone to migration than males; they do not appear to migrate, on average, longer or shorter distances than males, and consequently are the dominant sex in many parts of the winter range. Birds leave for winter quarters a more or less short time after breeding – July to October, with most birds staying to September – and return to nest mainly in March/April, but some only arrive in May.
So perhaps it was not out of season. https://en.wikipedia.org/wiki/Great_grey_shrike#Distribution_and_habitat

What is confusing in the wikipedia is the end of the paragraph you mentions: "In recent decades, the number of birds remaining on the breeding grounds all year has been noted to increase e.g. in Fennoscandia, whereas for example borealis seems to be as rare a winter visitor in northern Ohio as it was a century ago". That means they stay more often in the north (breeding grounds) than going down to south (central /east europe for winter). But I agree both statement can be true.

yes as wiki is written by multiple and it sometimes has ambiguities for that reason. best to check google scholar to have a real study.

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How are presynaptic burst firing signals transmitted post-synaptically?
Neurons can exhibit burst firing and this presynaptic process basically results in a flurry of action potentials being fired in a short time window.
I'm, however, wondering how these signals are further relayed once they synapse onto other neurons? Specifically, does each action potential in the burst volley generate another post-synaptic action potential, or is the bursting somehow averaged to then transmit either one or no action potential post-synaptically depending on long the burst train was?

Short answer
It depends.
Background
It all depends on the neuronal circuit and neurotransmitter system under investigation. For example, raphe neurons release 5-HT in a burst-like fashion onto cortical dendrites. However, the postsynaptic effect is inhibitory, so no action potentials there (Gartside, 2000).
Intracortical recordings in the rat have shown that each action potential in a burst resulted in neurotransmitter (glutamate) release and subsequent excitatory postsynaptic currents (EPSCs) and potentials (EPSPs) (Williams & Stuart, 1999). So that would positively answer your question, at least in this specific neuronal circuit.
Reference
- Gartside, Neurosci (2000); 98(2): 295-300
- Williams & Stuart, J Physiol (1999); 521(2): 467–82

Thanks @AliceD ! Are you aware of a case where presynaptic bursts lead to a single postsynaptic potential? I suppose excitatory relay neurons will most likely fire in bursts as well whereas the end target might integrate the incoming burst and only fire if there were "enough of them". Anyways, this was probably too loaded a question...

@AliceD: Does "each action potential in a burst resulted in neurotransmitter release" literally mean, that each single action potential in a burst resulted in a single vesicle fusion - with probability 1?

This is just my personal opinion and impression:
First, it's not at all clear which effects burst firing of action potentials of a pre-synaptic neuron do have at the synaptic end bulbs: Does it cause a burst of fusions of vesicles and thus a burst of releases of neurotransmitters? Or isn't the intricate firing pattern completely smeared and blurred at the synapse?
Second: Each neuron's synaptic input to another neuron takes a long way (along the dendrite and so on) to get part of the effect at the axon hillock where post-synaptic action potentials are created. The firing pattern of the pre-synaptic neuron (which is one of thousands) will hardly be visible and mirrored here.

To the down-voter: What's so wrong with this answer?

Not the down-voter, but the referenced part is a question (answers are basically reserved for answers) and the answer part is unreferenced.

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Can bacteria grow in rough, deteriorated indoor plastic chairs left in months of rain? (i.e. not made of resin plastic)
I have a problem with indoor plastic chairs (like classroom chairs with metal frames) left outside in the rain for months at my units.  They are not made of resin plastic and the surface is noticeably rougher & more deteriorated.  I think that they can harbour bacteria much like neglected plastic food containers.  There is a possible unfresh smell, and some decomposed plastic seemed to end up on my hands when I moved one.

Plastic does not decompose in nature. Decomposition as per my understanding is a phenomenon wherein an object is broken down into simpler constituents. Plastic just breaks down into smaller pieces of plastic. What you are seeing is most probably erosion of the surface due to rain.

I think that they can harbour bacteria much like neglected plastic food containers.

Nothing to be worried about. That chair was most certainly covered with microbes even before you put it out in the rain. Your body itself harbors about as many bacteria as it does its constituent cells.
What it may harbor in addition though are fungi, which now have a great substrate to hold onto.

There is a possible unfresh smell, and some decomposed plastic seemed to end up on my hands when I moved one.

I don't know what you mean by unfresh smell. If you mean moldy, that can be expected because you have moisture, and a nicely eroded thingy which can act as substrate for stability.
You can very well use the chair. There's nothing wrong with it. Spray it with a shower and keep it out in the sun for a day or two, that should take care of the mold.

There have been some bacteria discovered that can decompose some plastics.

Yes there are. But it would take too long for wild-type strains to decompose a chair in the wild. Therefore, the effects produced by aforementioned bacteria are negligible and are superseded by other effects. For example, erosion due to rain.

I’m not saying they ate the chair, only that plastic can be decomposed.

Erosion from rain is unlikely, but deterioration from the UV in sunlight is fairly likely.


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What is the distribution of the major ions across a neuronal membrane for a human neuron?
I have searched for the ion distributions across the membrane of human neurons on the internet but almost all the information refers to the giant axon of the squid. Could anyone give me the ion distribution across the membrane of a human neuron?

Have you tried Guyton-Hall physiology?


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Is lysergic acid diethylamide (LSD) metabolized in the body?
Is LSD broken down into other compounds by enzymes or hormones? If so, at what point and where in the body does this happen? I researched several papers appearing in a google search, but unfortunately I did not understand most of it.

Short answer
LSD appears to be enzymatically broken down in the liver.
Background
First off, hormones do not break down anything; enzymes are the work horses that mediate metabolism.
According to a review paper (Passie et al., 2008), humans metabolize LSD into structurally similar metabolites (Fig. 1) by NADH-dependent microsomal liver enzymes to the inactive 2-oxy-LSD and 2-oxo-3-hydroxy LSD. LAE is formed through enzymatic N-dealkylation of the diethylamide
radical at side chain position 8. Di-hydroxy-LSD and nor-LSD are also metabolites, as well as 2-oxo-LSD, 13- and 14-hydroxy-LSD as glucoronides, lysergic acid ethyl-2-hydroxyethylamide (LEO), and trioxylated LSD.
Note that the monoamine oxidase (MAO) system is unlikely to break down LSD. MAO are enzymes that catalyze the oxidation of monoamines. Monoamine neurotransmitters contain one amino group that is connected to an aromatic ring by a two-carbon chain (such as -CH2-CH2-). This structure is not present in LSD (fig. 1). A cursory Google Scholar search did not yield any relevant hits ('LSD' + 'monoamine oxidase'), loosely indicating that MAO is unlikely to be involved in LSD metabolism. However, as I suspect some self-help here - I am unsure about MAOI and LSD interactions, and I highly discourage any toying around with MAO inhibitors and any drug in general. For example, 5-HT is a typical example of an MAO substrate and LSD impinges on 5-HT2A receptors. Hence, interactions in pharmacodynamics with combined LSD and MAOI intake are likely to occur.

Fig. 1. LSD metabolites. source: Passie et al. (2008)
Reference
- Passie et al., CNS Neuroscience & Therapeutics (2008); 14: 295–314

LSD is metabolized in the liver in humans by enzymes of the Cytochrome P450 hemoprotein. The specific enzymes are CYP3A4 and CYP2D6.
CYP2D6 is generally regarded as non-inducible (meaning there appears to be no way to boost its production in humans), and can only be inhibited by other drugs that would cost more than LSD and be dangerous to take anyway.
CYP3A4 carries the answer you are looking for. It is strongly inhibited by... grapefruit! Pomegranate also has the same effect. So ingesting a lot of these fruits will make the LSD take longer to metabolize.

What is in such fruits that causes this inhibition?

@Max https://en.wikipedia.org/wiki/Grapefruit%E2%80%93drug_interactions. The effects are caused by furanocoumarins (and, to a lesser extent, flavonoids).


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How many strands of Myosin Head is in a Myosin filament?
I am doing a research about sacromere in striated muscles, I read a paper (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3963759/
) and it states the follow:
"Rotational symmetry is defined by the number of strands present. Actin filament has two strands and hence has a 2-fold (C2) rotational symmetry; myosin filament has three strands and hence has a 3-fold (C3) rotational symmetry. Helical symmetry is defined by the integral number of sub-units contained in a given number of turns in a single strand. So for example actin filament strands have a 13/6 helix, i.e. thirteen subunits in six turns of a strand, whereas myosin strands have a 9/1 helix, i.e. nine subunits in one turn of its strand."
Now what does it mean by "myosin filament has three strands and hence has a 3-fold (C3) rotational symmetry" ?
How many strands of myosin heads is in myosin filament? I saw visualizations in different papers showing different numbers.


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Why replication collapse but not stall leads to DNA break?
I have been looking into the concept of replication dynamics and was wondering why collapsing but not stalling leads to a DNA break.

I recommend improving this post by explaining to us what "collapsing" and "stalling" mean. What context are you talking about? How do you know that collapsing but not stalling leads to a DNA break?

Stalling precedes collapsing. And collapsing precedes breaking. Hence, both stalling and collapsing precede, and lead to, breaking; but not every stalling leads to collapsing, and not every collapsing leads to breaking.


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Biochemistry Question: Antibodies
I'm doing conceptual questions in preparation for a Western Blott and needed clarification on a specific question:
Is it possible/ will your Western blot work if you use a primary antibody (say generated in mice) and use a secondary antibody (generated in goats)? Would this combination still work with the western blot? At first glance, I'd say no but I'm still looking into it. Any clarification would be greatly appreciated!

It's not clear what you're asking, but a typical Western would indeed involve a primary mouse antibody and a secondary goat anti-mouse antibody; the primary would bind to your targets, the secondary would have the detector molecule attached and would bind to the primary.

As others pointed out, the question is not clear.. but yes, in general you use a primary antibody recognizing your peptide of interest, e.g. an antibody made in mouse, and then a secondary antibody recognizing your primary antibody, in this case an anti-mouse. The secondary antibody will obviously be made in a different animal than mouse (e.g. in goat), because mice cannot develop anti-mouse antibodies!
I hope I understood your question.


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Chromosomally different D. melanogaster sperm
I know that D. melanogaster have 4 pairs of chromosomes and crossing over is absent in males. Denoting autosomes as Ai,j where i is chromosome no. and j are homologues (1 and 2) I am solving the total no. of chromosomally different sperm as 8. I am assuming it as 2x2x2. Can anyone verify my answer?


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Does the use of UV light beam lead to poorer contrast in optical microscopy of cells than the higher wavelengths visible light?
I am reading about "diffraction-limited system" on Wikipedia, which mentioned

"To increase the resolution, shorter wavelengths can be used, such as UV and X-ray microscopes. These techniques offer better resolution but are expensive, suffer from lack of contrast in biological samples and may damage the sample."

without giving a more detailed explanation for why the higher energy EM waves might lead to poor contrast. I have tried to search on Google, but still can't find a satisfying answer. Can anyone here kindly refer me to more detailed discussion on this question? Thank you.

This source says UV microscopy offers better contrast. I think it all depends on what method you use to visualize the sample after magnification. UV is not visible, so I guess it has to be converted digitally?

Most biological samples are not electron-dense enough and need to be treated with heavy metals for EM. See wikipedia article for a brief introduction.

"EM" in the question referred to "electromagnetic".  Heavy metals are used to increase contrast for "electron microscopy".  Not the same meaning for "EM".

UV microscopy is not a form of electron microscopy, it seems to be a technique in its own right.

Contrast in optical microscopy typically depends on different substances having different absorption spectra. Practically everything absorbs UV light, so there tends to be less contrast in that range than in the visible spectrum where there is a bit more selectivity.  All of this changes when there are contrast-enhancing substances added.  For example, molecules that absorb in one wavelength and emit at a different wavelength via fluorescence, attached to antibodies that bind selectively to specific cell components, can provide very high contrast.  E.g., see [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2156041/].
An alternative optical microscopy technique is phase-contrast microscopy which does not use absorption at all.  Instead, it measures the effective optical path length through the sample, which depends on local refractive index of the sample.
Yet another alternative is x-ray fluorescence microscopy, which can identify specific elements in the composition of a sample.  See, for example,[https://www.americanlaboratory.com/913-Technical-Articles/18833-Three-Dimensional-Elemental-Imaging-Using-a-Confocal-X-Ray-Fluorescence-Microscope/].

I suppose I am looking for a more detailed explanation for why "practically everything (in cells) absorb UV light ... (while) there is a bit more selectivity (for the visible spectrum)". But thanks for pointing out to us the alternative optical microscopy, in relation to the fluorescence microscopy. I have found a useful post on chemistry.stackexchange: link, which has nicely given me a chemistry perspective on my problem.

@Fan Fan, if you do a search for "UV absorption spectrum" and proteins, DNA, or lipids, you'll see that a huge number of biomolecules absorb in the UV range (~200nm to ~400 nm).  The chemistry of it relates to the energy levels in the types of bonds in the biomolecules, but you'll need a biochemist to explain to a greater depth.


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Have skeletons of "failed" animals been found yet?
I don't know what the correct term for "failed animals" is, but I mean those animals which wheren't able to survive due to their "failed" evolution process. Because evolution, as we see it today, has gone through a lot of "this doesn't work" and "this does work" - so the "good" outcomes of mutation have survived and the others haven't.
This is for some an argument against evolution, but just because they don't know really why nothing has been found or that something has been found.
So I want to ask if skeletons of any of those "failed animals" have been found or not. So is there any evidence of animals who had a "really bad" mutation (not illness, but mutation) and haven't survived in the process of evolution?

Yes I meant those which failed, so not those who really made it or had an impact on creatures today.

You could just say fossil of "organisms that left no descendent today". In fact most, if not all, fossils we find are of individuals that left no descendants today. They might be very closely related to the individuals who left descendants but they are likely not themselves. This is the magic of coalescence. Only very few individuals actually contribute to distant generations.

Here's an example of a "failed animal" - the Atacama desert mummy that some people were claiming as an alien - that's been in recent news: https://www.theguardian.com/science/2018/mar/22/genetic-tests-reveal-tragic-reality-of-atacama-alien-skeleton

Short answer
The dodo and Irish Elk, both going extinct relatively recently, are examples of species that have yielded skeletons and went extinct, at least partly, due to maladaptations.
Background
Extinct animals are an example of an answer to your question, barred those species did not go extinct through a cataclysmic event of course. No species can evolve into a meteor-resistant species. The term you are looking for is, I think, maladaptation.
For example, the Irish elk (Fig. 1) has been proposed to have gone extinct at least partly through a maladaptation. The male Irish elk was grew the biggest antlers ever recorded, (over 10ft (3 m) wide. Irish elk became extinct 10,600 years ago, and the male antlers have been proposed as a possible reason, although this is debated (source: Wikipedia). For example, males might have suffered because they got entangled in thickets. The climate changed at the end of the last Ice Age, causing the woodlands in which elk live to shrink. And food shortage might have resulted in a lack of nutritional support for the hefty antlers. However, extinction of an entire species is always caused by a multitude of cooperative factors, so the antlers alone can't be blamed (source: Love Nature, Wikipedia).
Also the dodo (Fig. 2) can be an example of an answer to your question. While not caused by a natural phenomenon, some animals simply become maladapted due to human influences. The dodo is the classic example. The dodo went extinct in the 1600's. It was adapted to life without ground-dwelling predators, as it nested on the ground and couldn't fly. The plump, slow, flightless birds were unable to escape from the sailors and their dogs, rats and pigs who landed on Mauritius (sources: Smithsonian, Love Nature).

Fig. 1. Skeleton of Irish Elk. source: Love Nature

Fig. 2. Dodo skeleton. source: Physiology
Sources
- Love Nature
- Smithsonian
- Wikipedia page on Irish Elk

The anon downvoter is prolly thinking that dodos were perfectly well adapted till humans ruined their party.

@RoniSaiba - Very true - dodos were adapted to their habitat before they encountered humans, as is mentioned in the answer quite explicitly. Since we are currently experiencing a mass extinction event due to us human actions, it might be categorized a cataclysmic event and given my first lines of my answer, the dodo might have been left out of the answer. Nonetheless, I think it serves as an illustrative example of an answer to the question, as it meets all question criteria (maladapted + skeletal proof)

Well, should have known someone would come along with a more complete and better sourced answer than mine. :)  +1.

Of course, we don't need evidence of that in the fossil record: we have evidence of that on going.  All around us we see mutations which lead to life-impairing or life-removing disease.  However, if the mutation causes early death, it never has the chance to reproduce.
Not the most official source, but Wikipedia does say it well:

Alleles that need only be present in one copy in an organism to be fatal are referred to as dominant lethal alleles. These alleles are not commonly found in populations because they usually result in the death of an organism before it can transmit its lethal allele on to its offspring. An example in humans of a dominant lethal allele is Huntington's disease, a rare neurodegenerative disorder that ultimately results in death. A person exhibits Huntington's disease when they carry a single copy of a repeat-expanded Huntingtin allele on chromosome 4.

(Emphasis mine)
It bears mentioning that Hungtington's is a disease which only shows up later in life, giving a carrier the opportunity to pass it on before it shows up.  This allows it to be passed on to its offspring.

Thanks for the upvote above. I didn't vote on yours as I have difficulty seeing how your answer addresses the question?

@AliceD I was particularly addressing the last paragraph: "... So is there any evidence of animals who had a "really bad" mutation (not illness, but mutation) and haven't survived in the process of evolution?"  My point was to point out that evidence of that is going on all around us; finding it in the fossil record wouldn't be evidence for anything tangible.

Yes
There are lots of them, at one time scientists were far more entered in them than normal critters. So called aberrations or anomalous creatures.  Animals born with two heads, extra limbs, and other deformities, even some congenital defects would count.These of course are most likely to be fond in organisms we have lots and lots of fossils of like invertebrates. Note most of what you find are injuries which makes sense statistically, it is rare to find a modern wild animal that is has no sings of injury.
Below is an example of a skull of a horse with cyclopsia, an entire website is devoted to abnormal trilobites, and here is paper listing known abnormal ammonites.


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Usage and mechanism of the Bastien protocol to treat amanitin poisoning
In 1971, 1974 and 1984 a French doctor Pierre Bastien (frwiki) voluntarily poisoned himself by ingestion of Amanita phalloides mushrooms in order to popularise his method of treatment of such poisoning. This method seems to have consisted of vitamin B and C injections and dosages of Abiocine and Nifuroxazide. Is this method still being practiced or has it been discouraged? What would be the mechanism of this protocol?

More medical than biology, and very much a continental European thing, but I thought it would be amusing to search the internet. (You could have done this yourself.)

@David I have obviously done that, but the number of publicly available sources is limited (and you have demonstrated that yourself by using two paid resources in your answer). Anyway, thank you for looking into this.

Apologies. Having access to many journals through my university I am sometimes unsure whether papers are open access or not. I'll modify my introduction slightly.

I know nothing about this subject, except that I can recognize edible and poisonous fungi, to the extent that it concerns me in a practical sense. However, as I have access to a range of journals through my university I thought I would see if there was anything ‘out there’ on the topic.
A recent paper entitled Amanita phalloides poisoning: Mechanisms of toxicity and treatment by J. Garcia et al. in Food and Chemical Toxicology 86 (2015) 41–55 contains a table listing the drug therapy used in a range of countries. There is no reference to Bastien in this paper and the most frequently used therapies are benzylpenicillin and silybin.
Abiocine is another name for dihydrostreptomycin and nifuoxazide is nifuroxazide is an oral nitrofuran of questionable efficiacy. So they are not identical to the agents mentioned and Bastien’s protocol does not appear to be in current use.
The impression I get from the article is that the agents used for treatment are not strict antidotes, but rather part of a strategy to treat the general effects of the poison. To eliminate the poison activated charcoal is often used.
If Bastien’s protocol really had an effect I imagine it may have acted in a similar manner to the current agents, although I have no idea what the vitamins might have been doing (if anything). Incidentally it was the subject of a letter (in English) to Lancet in 1981 (subscription required), in response to scepticism expressed in a previous editorial.

I'd forgotten I'd even written this answer, but it seems that I did better than the deleted effort of ChatGPT (hidden post) which declares that abiocine is phosphatidyl serine. Numerous sources including the US National Institutes of Health support it being dihydrostreptomycin. Somebody's obviously been halucinating again.


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What do the qualifiers used in botanical species names mean?
These are all the qualifiers I've come across so far. The first 3 were quite easy to google, but the other 4 have me stumped.
I also can't say I'm completely clear on the nuances of s.s. vs. s.l..

agg.
s.s.
s.l.
cf.
cv.
auct.
ined.

agg. means aggregate and is used when species have been grouped together.
s.s. stands for sensu stricto and is used for a strict or narrow usage of definition.
s.l. stands for sensu lato and is used for a wide or broad usage of definition. these two pop up a lot in paleontology since species definition can be vague.
cf. stands for "conferre" and is used for provisional names when an organism is not completely known, such as when a variant is found and they are not sure which species to place it in.
cv. stands for cultivar and is usually followed by the unitalicized name of the cultivar.
auct. means "of author" and means the name is used in a different way than it is currently or in a different way than the paper using it does, such as quoting a incorrect name from another author or a debate between two possible usages. (used a lot with overturned or contested names) it is often followed by a qualifier giving more information about usage.
ined. means undescribed, and is used for a new proposed species before it has been formally described (common in paleontology when many papers about the same new specimen may be released at the same conference or where a specimen might not be identified yet still yield useful information in other ways.)
if you put the exact form of the epithet (include the period) followed by the word "species" in google it will usually return the usage, failing that you can search this site.


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What is the chemical mechanism by which PcP(c) is converted to PcP(Sc) in Fatal Familial Insomnia
I know the gene PRNP and it's location.  There’s a mutation at codon 178 (asparagine found instead of normal aspartic acid) on the prion protein gene (also found in fCJD) and more uniquely there is a the presence of a methionine at position 129.  My question is how PcP(Sc) converts normal PcP(C) into the mutated destructive form, and whether or not this is a reversible process.


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I haven't seen any gel lanes
I haven't seen any gel lanes in neither my PCR samples nor the marker itself when photographing them. This is not my first time performing 1.2% agarose gel electrophoresis.
I see gel lanes when I take the gel out the apparatus, but when I go to photograph them: nothing shows up. I only let the samples "run" for 30-40 minutes (when I ran for an hour, the bands almost ran off the gel).
Tried using different markers: no luck.
Re-added some more EtBr to better stain the gel: no luck.
I am also keeping the lights off in the dark room, so I do not think I am exposing the film to light early on (errors still a possibility though).
What could I be doing wrong? Am I taking the film out too early?

Do you see something on the gel when you put it on UV light?

Are you using a digital gel box or the old school one that uses UV light and requires orange-tinted glasses?
We had a similar problem like that in our lab. The best solution was to properly add the correct concentration of SYBR to our gels. However, we never worked with ethidium. But it might be a concentration problem.
Running your dye off the gel is never a good idea. I usually take a photo at about 2/3 of the way running it. Remember that the loading dye lets our naked eyes see the travel of our PCR product, whereas the Nucleic staining dye is what will be picked up by the UV transmission photography.
Have you tried adding it directly with your PCR product so that it’ll bind? How much are you adding to your gel when you make it? The Nucleic dye is essentially binding to the major/minor grooves of your DNA and thus lighting with UV exposure.
Have you checked to see if you’re also using the correct restriction enzyme or primers?


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Identification for a bird in the middle of the tree
In the central city of Dobrich Bulgaria, I was following a Great spotted woodpecker in a tree and suddenly I found this other bird on the same tree.

The context of the picture is:

Country: Bulgaria
City: Dobrich, Center urban area
Period: mid August (2016)

I think this is a specimen of Silvia Curruca, can anybody confirm this?

Yes, Lesser whitethroat indeed. Grey head with contrasting white throat and brown body, small bill (the similar Orphean warbler has a much bigger bill).

Please add additional detail/evidence and reputable citations supporting your claims. The point of answers is to be helpful to others searching for similar questions in the future, which is made possible by evidence/citations. Unsupported responses to [tag:species-identification] questions should be added as comments and not as answers. Thanks.

There is no citation involved in identifying birds. In Europe this is the best guide amazon.com/Collins-Bird-Guide-Lars-Svensson/dp/0007268149 But a guide is not enough to identify birds, the field experience is essential (I have been birdwatching for 20 years).


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Filter proteins by domain with InterProScan
I have a bunch of proteins (over 300000) in fasta format, and I want to find the ones that contain a specific domain (using a specific InterPro accession).
I can run InterPro on the proteins and get every domain they have, but with so many proteins, it will take a large amount of time, which I'm short on. I'd like to limit my search to the specific domain I'm looking for, as I assume it will be considerably faster.
Is there a way to do this with InterPro? Browsing the docs doesn't give me any hope. If InterPro isn't capable of that, would it be doable with a single database like Pfam or CDD?

1. Limit the InterPro scan to a specific database:
As you said you know the domain you are interested in so you know which database this is in then you can limit you InterPro scan to that database, which whill save a lot of time:

Then only select the database in which the domain is stored (e.g. ProSite)

2. If your domain is in the ProSite database (which it probably is) you can use
ScanProsite and limit you search to a specific domain.
You do this by going to the above link and select the last option:

Then, if you scroll a little bit down you can enter a ProSite accesion code of the domain/profile you are interested in:

3. Use PFAM scan
I have never used this before, so I don't know whether this would be faster than limiting the InterPro scan to the PFAMa database. You can of course check this out.

4. Clustering your sequences first
This will only work if your sequences look like each other. Depending on the size of the domain and the location in the sequences you can cluster all your sequences first (using for example CD-HIT). And then choose a representative sequences for each cluster and use these to subject to your analysis. For example when you know your domain is always at the end of the sequence then you trim the first part of each sequence and cluster the proteins over the whole length at 100% identity. If you then determine whether each cluster contains the domain or not (based on the representative sequence, which CD-HIT will provide you with) then you can assign these results to the sequences making up each cluster. But of course this will only reduce the search space whenever your sequences look like each other (or if parts do)

5. MOTIF search using downloaded profile or HMM
MOTIF search allows you to query against serveral database, such as PFAM, CDD, PROSITE etc. More interesting, it also allows you to specifiy your own profile or HMM.

So you can download the HMM of your desired domain from e.g. PFAM  or the domain profile from Prosite.

6. Downloading HMM and use HMMscan (or HMMER)
This was suggested by @seven11, you can search your HMM domain in the PFAM database and then use HMMscan.
Conclusion

If you are really interested in one domain. I think downloading the ProSite scan tool would be your best option. Notably, all webtools I mentioned above are available as command line tool, and that is what you need when having that amount of sequences. Back to ProSite scan, you can download this here and don't forget the README. As mentioned in the readme:
Input/Output:
  -e : specify the ID or AC of an entry in sequence-file
  -o : specify an output format : $formats_string
  -d : specify a prosite.dat file
  -p : specify a pattern or the AC of a prosite motif
  -f : specify a motif AC to scan against together with all its
       releated post-processing motifs (but show only specified
       motif hits)

You can use the -p to specify the acc of the pattern you want.
I'm quite busy so I typed this one really fast, please let me know when something is not clear.

Thanks, your answer gave me some very good pointers. I found the HMM for this domain on the Pfam site. I will run it locally using hmmscan.

Aah nice that is a good option and probably much faster as HMM shouldn't take that long @seven11

When your sequences are quite alike you can also choose to first cluster these (lets say at 100% identity over 80% over te sequence lenght) and then choose a representative for each cluster and use these to do searches with. And if your domain is always located at the end of the sequences you can only cluster at these ends and then do your searches. This will only work if your sequences are alike of course @seven11


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What natural defence mechanism does the human body have against lead poisoning?
It is known that lead ion takes place of necessary ions, like calcium, in the body, but does not perform their task, hence wrecking the system. So how does the body eventually recognise this threat and get rid of the lead deposit in the body? And if such a natural defence mechanism exists, why is it not effective enough?
For example, is the process in which lead gets stored in the bones one of the safety mechanism of the body, so that it stays away from other delicate organs?

INB4 mods put question on hold as too broad I would suggest you to break the question into multiple questions and post them separately.

@ronisaiba Thanks. I have tried to make the question more specific by removing some sub questions.

Lead-binding proteins are a common defense in many organisms (https://www.hindawi.com/journals/jt/2011/686050/).


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Selective pressure for reduced rates of growth and maturity in primates
Humans are somewhat notable for the slow rate at which they grow and reach physical maturity.  Some related primates also take over a decade to reach sexual maturity.
However, many mammals – including ones like horses that grow quite larger than any primates – reach their maximum size in only a few years, so the slow rate of primate growth is not due to simple biologic or metabolic constraints on mammalian growth rates.
Are there any hypothesized selective pressures that might explain the slow physical growth rates of higher primates?


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why is LPL (lipoprotein-lipase) down-regulated during fasting?
During fasting our body needs additional sources of energy and that's why triglycerides are broken down into fatty acids and glycerol. where fatty acids can be used to generate acetyl-coA and contribute to the citric acid cycle or build ketone bodies.
So if we are wishing to get more fatty acids why is LPL down-regulated although it's the enzyme needed to break down Triglycerides in lipoproteins?

Please provide a reference or link to your assertion that LPL is down-regulated. See "how do I ask a good question" in the Help. In particular it is imperative to state what tissue(s) you are referring to.

An edit was requested, and I have updated the answer below. Let me know if there is any confusion.

LPL is largely expressed on tissues that metabolize or store a lot of fat, including muscle and adipose tissue, and it's regulated by a number of factors (1). This includes diet, hormones and other protein regulators. The current literature on LPL has shown that regulation of LPL is tissue-specific. The activity of LPL, like other proteins, may be controlled at the transcriptional or the post-transcriptional level. A review by Goldberg et al (2009) notes that the activity of LPL in adipose tissue during fasting is low, but high in skeletal and cardiac muscle. They also note that insulin increases transcription of LPL in adipose. So why the down-regulation? One of the proposed mechanisms for LPL down-regulation in adipose tissue is rapid inactivation by a protein inhibitor known as ANGPTL-4 (2)
ANGPTL-4 (also known as a fasting-induced adipose factor), is up-regulated in adipose tissue two to four-fold in response to glucocorticoid stimulation (3). It's commonly known that you have a cortisol spike within a few hours of fasting, which is intended to try and increase glucose availability, for example.
The idea is that ANGPTL-4 attempts to control the distribution of fatty acids (4). In a mouse study, Cushing et al. demonstrated that ANGPTL-4 in fact diverts uptake of fatty acids and triglycerides away from adipose tissues (5). And this study was published in August 2017, so the phenomenon is still under investigation. It makes sense though, right? Why does the adipose tissue need to continue to receive fats during fasting? They can be better served elsewhere like muscle, the brain or the liver. Not only so, but Catoire et al. also demonstrated in 2014 how the interplay between ANGPTL-4 and LPL between non-exercising and active skeletal muscle during exercise allows for fine-tuning of fatty acid delivery to sites that need it most (6). So the regulation extends to both inter- and intra-tissue needs.
In closing, LPL is regulated during fasting in a targeted manner, but it is not generally down-regulated. Regulation is controlled in a manner that allows the demands of tissues to be reactive to their environment.

I'm sorry but I do not understand your answer. I can understand why the skeletal muscle is regulated differently than adipose tissue, but Is LPL down-regulated in adipose tissue during fasting and if so why? If not, please say so. And you may know a lot about it but do you really have to bring ANGPTL-4 into this?

@David LPL is not generally down-regulated during fasting. One of the take-home points that I may not have communicated properly is that LPL is regulated at the tissue level. Adipose LPL activity is low during fasting, but high in muscle. The proposed mechanism for rapid adipose LPL inactivation is the up-regulation of ANGPTL-4 in that tissue. I will edit the answer.

Furthermore, I wanted to make note using ANGPTL-4 as an example that it wasn't a fat vs. muscle dichotomy, and that LPL may be regulated within a single type of tissue, as well.


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What roles do circular connection structures play in the brain?
Most neural network simulations are strictly linear, one reason being they don't want to deal with circular connections (and infinite feedback loops if you dont have the right mechanisms). You can deal with them at the cost of some efficiency, but I'm curious about whether in the real brain, circular connections play an important role, or are they really not necessary?
To be clear, I mean any structure where you have a Neuron A, Neuron B, and Neuron C (or a thousand more) and the structure is similar to A > B > C > A or generally at some point Neuron A ends up having a path where its own output can lead back to itself.
What roles do circular connections play in the brain? Or more simply: Are they useful and what are a few reasons why?

'Circular connections', as you refer to them, are super common in the nervous system. This motif usually referred to as feedback connections, and serves a variety of roles.
Connectivity studies can be broadly grouped in to those that look at brain areas, and those that look at individual neurons (usually within a single brain area).
My background is more the latter, so that's what I'll focus on.
Firstly, your question misses an important distinction: inhibitory neurons. So if neuron C was inhibitory, we would have a negative feedback loop, a classical circuit that can be used to produce a homeostatic like signal, keeping a system within certain bounds; a delayed feedback loop can also act as a 'signal terminator', allowing an action to be stopped once it reaches a certain threshold. Lastly, under some circumstance, feedback loops can produce oscillations, which are applicable to a number of tasks.
But more generally, recurrent connectivity is hugely important in the cortex. The majority of inputs to neurons come from neighbouring excitatory neurons (see https://www.ncbi.nlm.nih.gov/pubmed/7638624), and if A connects to B then B is more likely to connect to A than by chance (see http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1054880&tool=pmcentrez&rendertype=abstract for a really nice study on this).
So why? For a variety of reasons. Networks with feedback mechanisms can do more, is the basic answer; from negative feedback for homeostasis, to persistent network states. My personal feeling is that too much of computational neuroscience models a network as an operator - it takes an image, say, and outputs what it thinks the image is. And whilst that is important, it's not what the brain is. We need to maintain a constant internal model of the world around us, rather than going 'that thing is a cat. That thing is a burger'. Perhaps recurrent activity maintains the cortex in a certain state - knowing that the cat is there - and inputs serve to move the state so that we can update our internal models when the sensory environment changes.


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Why does vinegar made from wine contain only about half as much acid as the original alcohol?
It is my understanding that the fermenting bacteria process the alcohol into acetic acid. But why is it about half the percentage of volume? For example table wine is often 12% ethanol, but vinegar is generally about 5% acetic acid.

Can you add sources to your claims? As a hunch, enzymes help to swiftly establish equilibria. Enzymes don't push the equalibrium to an end product. Further, the end product may be toxic. Take the fermentation processing during beer brewing - there's a substantial amount of sugar left after the beer is ready. Alcohol is toxic to yeast.

Not really; i take this claim as a fact of everyday life. Both alcohol and acedic acid contents are indicated on the bottles. German language Wikipedia has a list of aciditys for various types of wine (those alkohol contents are not indicated), but i guess that is no scientific source:  https://de.wikipedia.org/wiki/Essig#G%C3%A4rungsessige

Yep, makes sense. +1

What evidence have you that the wine used for wine vinegar contains 12% alcohol? I would have thought it would more likely be lower alcohol wine made from poorer grapes with a lower must weight (content of natural grape sugar). It is unlikely to bear much relationship to commercial table wines, which are often chaptalized in order to reach the EU minimum alcohol level.

That the acetic acid always has 5% has the simple reason that it is diluted to this concentration.

@Chris — Actually it's generally 6% in the EU, but you're right. I found an interesting paper on sherry vinegar production, which starts with 13% ethanol and ends up as over 11% acetic acid + 1.5% ethanol. Also a general article about industrial production of vinegar which explicitly states that it is diluted to 5-6%.

I'm voting to close this question as off-topic because it turns out this question has a trivial answer that is nothing to do with biology.

@Chris: And further, that it is diluted to that concentration because that's what tastes good.  Though vinegars do vary in acetic acid concentration.  To high a concentration can be hazardous, though.

@David That article states that it is diluted in case the "The generator method" is used, which does'nt start with wine.  Do you have any reference for wine vinegar -not vinegar 'essence'-  usually being diluted?

@HannesH — No, but people don't usually advertise that they water their beer (or whisky, unless you buy cask strength and then water it yourself). I leave you to join the dots.

As regards Sherry vinegar (which I mentioned is from sherry at 13% ethanol (less than normal sherry, incidentally), an internet search suggests 7% acetic acid is a more normal final concentration. That would suggest to me that it is watered down from 11%.

Would it? Would'nt it suggest that my question is still valid? - pending any reference to watering as the standart practice, ofcourse.

@Chris Besides that it isn't always 5%, could you reference why you think that vinagar from wine -not "essence"- is diluted?


text:
Urgent: Bird hatchling identification
Yesterday evening I found this baby bird in one corner of my house's verandah on the floor. I picked it up and placed it safely in a tray hoping that tomorrow morning its parents will find it (actually I initially suspected it to be a sparrow hatchling). When I saw it today morning I found that it is probably a bird of prey. As you can notice the large long beak and claws.
I'm really confused now what to do with it. Please suggest something.

EDIT

I live in Uttar Pradesh, India.
Its relatively plain where I live. (No mountains or lake nearby)
Temperature: 35-20 degrees Celsius
Added a photo for size estimation

RSPCA would be a good start.

Identification may or may not be possible, but more information is needed, e.g. your location, bird size indication, and whether near seacoast, lake or mountains..

@GrahamChiu What's that?

Royal Society for Prevention to Cruelty to Animals.

https://www.peta.org/action/how-to-save-baby-birds/

Actually I found a nest of "Laughing Dove" in my yard. I've placed the baby back into the nest.

https://en.m.wikipedia.org/wiki/Laughing_dove

Yes, it is a most probably a laughing dove

@Serotonin I guess, you already know that you can write (and accept) your own question and describe, why/how you identified the hatchling?

As you've pictured this is a fledgling that you found which has a mixture of adult feathers and immature feathers.  This indicates that it flew to your location, and a nest is nearby.  You should either attempt to find the nest, or just leave the fledgling alone and let it make its own way home as indicated in this online resource.

Fledglings are juvenile birds who have a mix of fuzzy down and adult feathers and are learning to fly. You may come across them hopping along on the ground, perching on low-hanging branches, or hiding under bushes, but as long as they’re healthy, just let them be.
Note: Fledglings are often “rescued” from their natural environment when they don’t need to be.


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Identification of a probable sylviidae
One summer (August) I was in Bulgaria (Dobrich province) and in the middle of the city I take picture of this bird:

He was making a sound like "Tchek-tchek" like the sound of a Eastern Olivaceous Warbler (lat. Iduna Pallida) but the greenish color make me think it is more a Icterine Warbler (lat. Hippolais icterina).
I found a song similar to the bird I saw on this page (second record).
It could also be a Common Chiffchaff (lat. Phylloscopus collybita) or a Willow Warbler (lat. Phylloscopus trochilus) as they are very common but the length of the tail make me feel it more one of the above (or another one) and the sound does not seem to fit.
Anyone can help on identification of this bird?

Are you sure it is always the same bird? The one in the first pictures seems very different: white edges on the wing, legs of a different color, less prominent supercilium.

I thought first it was the same, but after your remarks I noticed the pictures are done on the same tree but two different days. What confused me is the sound of the bird, but I can admit I did not see them singing in front of me.

Warbler can be difficult at the beginning that's why now they are my favorite to identify, I provided the correct answer below, if you have any question feel free to ask.

The first picture is an Icterine warbler. Because of the yellowish plumage (never in the eastern olivaceous) and the with fringes of tertiary characteristic of the species and never present in the genus Phylloscopus. Also the color of the leg, greish-bluish is quite specific of the Icterine.

The second and third picture are of a Willow warbler (Phylloscopus trochilus). The legs are pale compared to a chiffchaff and the primary projection (the length of the primaries that pass the tertiary) is extremely long and very typical of the willow warbler. You can see the difference in the image below.
 Here a useful webpage

please provide reputable citations to back up your claims. Thanks

There is no citation involved in identifying birds. In Europe this is the best guide https://www.amazon.com/Collins-Bird-Guide-Lars-Svensson/dp/0007268149          But a guide is not enough to identify birds, the field experience is essential (I have been birdwatching for 20 years).


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What are some features that do not make an individual better than others without this feature?
If a mutation occurs so that this allele gives a noticeable feature that is present in this individual but absent in every other individual and this feature is of no benefit or detriment to the individual, I was thinking that this mutation will not make the individual better soothed to the environment or worse and so the gene may not die out but be passed from one generation to the next generation.
If this is so, I thought, there should be many of such “useless” gene present in today’s world. Other than the appendix (which has no function in humans) and subtle differences like eye color, head shape ( not too severe ones but like the ones we see everyday - different heads), which other examples exist?

The human appendix does have a function: https://www.scientificamerican.com/article/what-is-the-function-of-the-human-appendix-did-it-once-have-a-purpose-that-has-since-been-lost/

Phenotypic effect of mutations
Most mutations have no phenotypic effect and therefore no fitness effect either (fitness is a function of both expected survival and expected number of offspring).
These mutations that have no phenotypic effects are therefore all neutral in terms of their fitness effect. Their probability to be passed on to at least one offpsring in a panmictic population of constant size $N$ is $\left(1-\frac{1}{2N}\right)^{2N} ≈ exp(-1) ≈ 0.36$. A mutation that is beneficial would have a greater probability and a deleterious mutations would have a lower probability. There are a whole bunch of equations for these but I don't want to get too "mathy" in this intro post.
Fitness effect of mutations
Among mutations that have phenotypic effects, some have no effect of fitness, some are deleterious, some are beneficial. The beneficial ones only represent a very small minorities of mutations.
Note that it is important to make the difference between a trait that seems to not be beneficial to you, while whether it actually is or is not beneficial. You cite things like eye color and head shape. Both of these traits can have very important on sexual selection. Try to date someone with a triangular head or with white iris! Also, if I am not mistaken, light colored eyes tend to let more light going through to the retina, hence light colored eyes are better adapted in environment where sunlight exposure is low. Head shape may have important impact too. For example, the jaw bones is an important contributor of the head shape and whether you have a strong or weak jaw is of importance (and the shape of the jaw is under sexual selection pressures).
Examples of neutral mutations
Most mutation that happen at non-coding, non-regulatory regions of the genome will be neutral.
Among the mutations that have phenotypic consequences but no fitness consequence, there are classical genetic markers (such as tongue rolling) that are likely free from any selection pressures. Note, that heritability for such trait is rarely 1.0 (see here for explanations). Maybe earlobes would be a good example, although there might have some sexual selection going one here.
Note also that as many mutations are recessive, the carrier of a single copy of the mutation may not be affected.
What is a gene?
You are using the term gene improperly. A gene is typically defined as a coding region. You might want to study a little the basis of genetics here. You should typically get used to the terms locus, allele and gene copy number. This answer can help you at this endeavour.
A small comment on the frequency of mutations

If a mutation occurs [..]

Just to make sure you do not have a misconception about how frequent mutations are here, I would like to highlight that, in humans, at every reproduction event, the new born has about 10 to 100 new mutations that were not present in any of both parent. So, mutations are rather common!
Introduction to evolutionary biology
Your question is a very introductory question to evolutionary biology. You might want to have a look at a short introductory course such as evo101 by UC Berkeley.


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Identification of a spider

I have found this 8mm spider in my home, North London. I've been told it may be a false widow but wanted a second opinion.
Note: The silvery parts in the picture are actually brownish in colour

It does appear to be a young spider, and seems consistent with a young Steatoda of some sort, so "False Widow" sounds OK.
Edit:  I just did a quick Google search and pulled up a useful paper (link below) that pretty clearly indicates that this is almost certainly a young Steatoda nobilis, one of the 'False Widows'.  See the top left - image A

Dugon, M.M., et al. 2017. Occurrence, reproductive rate and identification of the non-native noble false widow spider Steatoda nobilis (Thorell, 1875) in Ireland. In Biology and Environment: Proceedings of the Royal Irish Academy 117(2):77-89


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How to measure the length of mitochondria from z stack fluorescent microscopy image?
I have been working on yeast cells to analyse the effect of DNA damaging agents on mitochondrial structure. I have imaged my culture treated with MMS for a period of 6 hours and while observing the images, I suspect there is fragmentation of mitochondria in later point of time. So, I am wondering if I can get measurements of mitochondria using z stack images.

Welcome to Biology.SE! Can you expand on your protocol (both to encourage answers and to make it easier for other non-experts to understand both the question and the answer)? We have been doing some z-stack imaging for a separate project (imaging viral dissemination in insect tissues) but there isn't enough in your question yet for me to tell exactly where you're having problems.

Sorry for providing insufficient information. I have stained yeast cells with mito tracker dye (for mitochondrial staining) and analysed samples for 6 hours, by taking out 1 ml of culture at every one hour. While imaging culture, I captured z stack images for these 7 time points (starting from zero hour). Now, I have been looking for applications that can provide me the measurements (dimensions) of stained mitochondria using Z stacked images.

ImageJ is usually the standard software to measure cell characteristics, a little bit of a learning curve but there is a large suite of analysis methods and image adjustments/filters.


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Do animals feel emotions, or display empathy?
Since we can't know much of what's going on inside an animal's brain, can there still be a consensus among zoologists on whether animals feel emotions, display empathy, care, etc.? Or is it disputed?
To clarify what I said since commenters asked for clarifications: Of course I don't mean SENSES (touch/vision/taste...) and also I do NOT include humans.
A suggested definition of emotion:

An emotion is a feeling such as happiness, love, fear, anger, or
  hatred...the part of a person's character that consists of their
  feelings, as opposed to their thoughts. (Collins Dictionary)

An example of emotion:

No one doubts that dogs know when they are in trouble,” writes de
  Waal, “but whether they actually feel guilty is a point of debate.”
  According to a study by Alexandra Horowitz, the canine guilty
  look—“lowered gaze, ears pressed back, slumped body, averted head,
  tail rapidly beating between the legs—is . . . not about what they
  have done but about how their owner reacts. If the owner scolds them,
  they act extremely guilty. If the owner doesn’t, everything is fine
  and dandy.” (Greater Good Magazine, University of California, Berkeley)

Empathy:

Empathy is the ability to share another person's feelings and emotions
  as if they were your own. (Collins Dictionary)

Example of empathy:

Macaques refused to pull a chain that delivered food to themselves if
  doing so also caused a companion to receive an electric shock.[48][49]
  This inhibition of hurting another conspecific was more pronounced
  between familiar than unfamiliar macaques, a finding similar to that
  of empathy in humans. (Wikipedia: Emotions in animals)

How do you define "emotion"?

Define "animals". Humans are animals, as are Japanese Beetles.

I very much think my dog likes me.

@Remi.b - I think my dogs like me, but I can't ever be sure if they're just trying to get along with me, get me to play with them, get me to feed them, get me to entertain them, challenge them, etc. But, I know they get upset with me, may be angry with me, may be having a blast with me, and one in particular does things I think simply because it makes me howl with laughter.

It is very typical for a question that is full of semantic issues but is on a "sexy topic" to receive plenty of upvotes and plenty of down votes at the same time (currently 3 upvotes and 3 downvotes).

You can improve this by narrowing down your question , emotions, empathy, and care are very different things, pick one and give na example or two and we can give a much better answer, otherwise this is far to broad.

There are examples in this page: https://en.m.wikipedia.org/wiki/Emotion_in_animals

The answer to the question "Do scientists agree whether animals feel emotions, or display empathy?" is No. However, there are some animals that certainly do not have emotions or empathy (for example animals that have no substantial nervous system, like sponges), and some animals that certainly do have emotions. The only disagreement is in the middle and where to draw the boundaries. In reality, drawing such boundaries is probably not all that productive, coming down to semantic rather than biological argument.
As a citation for the disagreement, see the two answers and the comments here already.
The difficulty in assessing a statement like this is largely one of operational definition: you need to define what an emotion is, and depending on that definition you will get entirely different answers. You will also get different answers depending on your philosophical approach to questions like these and what the essence of experience is. I would also point out that emotion and empathy are vastly different levels of cognitive ability according to typical definitions of the two.
However, I will say that there are a lot of recent findings of higher cognitive abilities in non-human animals than previously thought. Rodents have long been used as generic models of mammalian nervous systems, including emotional processes. Mirror neurons in non-human primates respond to the behaviors and movements of conspecifics, which is an important aspect of both social learning and potentially empathy. Self-recognition is an important aspect of theory of mind, and has been observed in several species of different types. Mourning behaviors have been observed in various animals in response to death of conspecifics. There can be some disagreement of the interpretation of these findings, but I'll include some references here so readers can do some of their own research and find if they are convinced.
Note that these works study particular animal abilities in particular contexts, rather than making blanket judgments about "all animals" or anything like that. This is typically how science works, incrementally based on the results of individual experiments.

References
Gallese, V., & Goldman, A. (1998). Mirror neurons and the simulation theory of mind-reading. Trends in cognitive sciences, 2(12), 493-501.
Lane, R. D., & Nadel, L. (Eds.). (1999). Cognitive neuroscience of emotion. Oxford University Press.
Mulcahy, N. J., & Call, J. (2006). Apes save tools for future use. Science, 312(5776), 1038-1040.
Plotnik, J. M., De Waal, F. B., & Reiss, D. (2006). Self-recognition in an Asian elephant. Proceedings of the National Academy of Sciences, 103(45), 17053-17057.
Prior, H., Schwarz, A., & Güntürkün, O. (2008). Mirror-induced behavior in the magpie (Pica pica): evidence of self-recognition. PLoS biology, 6(8), e202.
Rajala, A. Z., Reininger, K. R., Lancaster, K. M., & Populin, L. C. (2010). Rhesus monkeys (Macaca mulatta) do recognize themselves in the mirror: implications for the evolution of self-recognition. PloS one, 5(9), e12865.
Roth, G., & Dicke, U. (2005). Evolution of the brain and intelligence. Trends in cognitive sciences, 9(5), 250-257.

Good to have an answer that correctly address the several semantic issues behind the question! Good job +1

Some animals definitely feel emotions, emotion are the basic workings of the brain, variations in neurotransmitters used to tag experiences and alter behavior. If it has a brain and is capable of learning it probably feels some emotions, even if only pleasure or discomfort because that is how learning affects ("codes") an experience for association.
Not every animal is going feel them all or feel them at all to the same degree. "Animal" covers a very wide group, a sponge is an animal and almost certainly feels no emotions as it lacks a brain or substantial nervous system, on the other hand humans are the group we use to define emotions are are also animals. But exactly which emotion each animal experiences is impossible to say at the moment, we can't even say for certain every human experiences every emotion. And currently discreet definitions for emotions elude us.
As for specific emotions, as far as we can tell every basic emotion humans experience is represented somewhere in the animal kingdom, and most the basic human emotions may be at least common to mammalia. It is extremely unlikely emotions arrose ex nihilo in humans given the similarities in behavior between humans and other animals, especially other primates. Bonobo's for instance even show similar emotional managements skills to humans.
A consensus is a tricky term, emotion in animals has been a taboo subject for a long time, and there are still pockets that assume animals experience no emotions and operate on pure logic like a robot, but this view has never withstood scrutiny. I tired to present the closest thing we have ot a consensus.
Mammalian associative learning has been the most well studied for obvious reasons, but there is no reason to believe it is unique given similarities in behavior with other groups.Yes the brain works like a different engine but emotions is how our difference engine operates, how it codes experiences.

Can you please define emotion? Not every animal is going feel them all do you exclude all humans? Can you give an example that, say a dog, can't feel, just to see how far fetch it needs to be? a sponge [..] feels no emotions Individual cells can feel the lack of a nutrient. Isn't that an emotion?! As for specific emotions as far as we can tell every emotion is represented somewhere in the animal kingdom. Do you have a reference for that claim? ...

... Assuming "feeling the grainy Martian soil under one's feet" is an emotion, can you tell me which animal feels it? Maybe "feeling the grainy Martian soil under one's feet" is not an emotion, but then we really need a definition.

why would feeling soil be an emotion?

defining individual emotions can be tricky the exact number is hotly debated, we have really good information for some and really poor information for others. to answer your specific example a dog definitely feels, pleasure, pain, disgust, anger and fear. Trust and grief are likely as well.

Some people think animals operate on pure logic? Does that mean that in their minds, they contemplate, "If A, then B?" Or, "if A is true, and B = A, then B is true?" Or do you mean instinct?

emotions can be instinctual, I mean there are those that think they work off pure logic like a computer program, that animal brains are completely different from ours in that animals do not have qualitative experiences. That a dog does not feel pleasure when it eats or disgust when it smells something foul but that it is acting like a robot executing a program.

This answer needs some sources. As it stands, it flatly asserts that any animal that can learn has emotions, with absolutely nothing to back that statement up. Also, how are you defining "emotion"? You seem to suggest that pain or discomfort is an emotion, which I think most people would disagree with.

I have added sources and will add more, it took some time to turn paper sources into linked sources.


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My daughter taken a photo of a species

My daughter is studying in 4 the std. She is interested in species related study. Pls guide her.

For identification it is helpful to add information, where in the world and which habitat you found the animal/plant. Also the size could be useful. Could you please edit your question to add these information? And while your at it, maybe change the title to '... photo of a beetle'

And is your question about identifying this particular animal, or is this one just an example and you want to generally know, how to identify animals by yourself? Could you please clarify this?

And please reduce the size of your images before posting. On my browser the 0.3 Mb image (2000 px wide to fit a 600 px space) only shows in black. A quarter of the size is more than adequate.


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What are the names of these plants?
I found these plants in my backyard in South Florida. What are they?

Please only ask one question per post. Remove one of the species from the post and open a new question for it. Additionally, we ask that more details be provided for species ID including size of specimens and more accurate locaiton (Florida has various habitats, so it'll be useful to others in the future to know where you saw these plants). Please add more details.

failure to follow my previous advice will likely result in your question becoming closed and going unanswered. Please put a bit more effort into your post(s) to avoid this scenario. We want to help, but we need you to cooperate too. Thanks!

I just figured out how to edit it. Sorry for the inconvenience

The main plant in the photo (with the larger leaves) is called Virginia creeper. The botanical name is Parthenocissus quinquefolia.   The leaves are very distinctive in leaf groups of 5 to 7 leaflets.  It is an aggressive woodland vine in the grape family Vitaceae.
Links:
https://en.wikipedia.org/wiki/Parthenocissus_quinquefolia
https://plants.usda.gov/core/profile?symbol=paqu2


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Are there any parasites that alter human behavior in a self destructive way?
There seems to be quite a few examples of parasites taking over the behavior of insects in a way that leads to the death of the host.  A couple of examples include:

Spinochordodes tellinii:  A nematomorph hairworm that causes crickets and grasshoppers to jump into water, and likely drown, as
part of their life cycle.
Ophiocordyceps unilateralis: A fungus that causes ants to leave their desired habitat for the habitat required for the fungus
to reproduce while consuming the ants internal organs.

In mammals, a common example is:

Toxoplasma gondii: A single celled parasite that appears to make rats attracted to cat pee in an attempt to continue its life
cycle within the cat.  Additionally, humans can be infected with
Toxoplasma gondii via contaminated meat, vegetables, and cat feces.  In fact, there is a study of Danish medical records from 45,788
women in which the rate of self harm increased 50% for women
suffering from chronic toxoplasmosis and the rate of attempted
suicide was 80% higher.  However, direct correlation between the
increases could not be linked to the these higher rates due to the
possibility of other factors such as depression.

So it seems that there is some widespread evidence of parasites causing a host to act in a potentially lethal way, but the evidence that I could find for humans seems to be minimal and yet to be proven.  Are there any examples of parasites causing humans to act in a risky, potentially deadly, manner?

I think there was also a study which suggested that toxoplasmosis carrier were more likely involved in car accidents.

Should be this one: http://ijpa.tums.ac.ir/index.php/ijpa/article/view/214

possibly rabies https://en.wikipedia.org/wiki/Rabies

whole article on the subject. https://www.discovermagazine.com/planet-earth/meet-the-parasites-that-control-human-brains

There is a link established between Candida and Aspergillus fungal infections and mental illness of schizophrenia and depresssion. Over prescriptions of antibiotics and use of antibiotics in cattle ranching, subject people to excessive antibiotics. This causes a die off of natural gut flora and consequent fungal overgrowth.
Fungal metabolites (aflatoxins) have been linked to anorexia,depression and schizophrenia. Pubchem lists lists behavioral acute anorexia for aflatoxin G1.
Research published in Journal of Antimicrobial Therapy, suggest that some SSRI antidepressants have an antifungal effect.
Ethyl alcohol (alcoholic beverage) is a fungal metabollite of brewers yeast that is well known to impair human behaviour in a negative way.
I have been unable to find any research into using antifungal agents to treat mental illness.
A fungus that thrives in soil, contaminates grain, is distilled into a beverage that causes drunk driving and death, and returns the host to the soil has also completed its life cycle. Similar to the ant example in your question.

Can you add references?

Systemic candida overgrowth is for the most part a quack diagnosis: https://www.mayoclinic.org/healthy-lifestyle/consumer-health/expert-answers/candida-cleanse/faq-20058174

I see from your description you are talking about parasites that directly alter the neurochemistry of their host to cause direct behavioural changes geared towards passing the parasite on to its final definitive host species. Now to answer your question: No. No parasite species has yet been found that does this to humans. By my reckoning, it seems most to all of the parasites that employ this strategy use prey animals as intermediate hosts(Toxoplasma gondii uses mice, Dichrocelium bird flukes use land snails, etc.), meaning that the next host species is very likely to consume the infected prey animal as part of its regular diet. This by definition means that any parasite species which utilizes a intermediate host that has a very poor chance of being consumed and passing the parasite on, is likely to die out quickly.


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What is the role of potassium acetate in plasmid extraction?
What is the role of potassium acetate in the alkaline lysis method of plasmid extraction?
Earlier I was thinking its role is to shield plasmid DNA (the same as sodium acetate in genomic DNA extraction). When 100% ethanol is added, it the DNA precipitates and then we remove potassium ions from the pellet using 70% ethanol.
However, I have read that potassium acetate does not have the same function as sodium acetate in genomic DNA isolation but, rather, is a neutralizing agent which helps small plasmid DNA to renature.
I am bit confused about the role of potassium acetate and why sodium acetate cannot be used instead.

The alkaline lysis method of plasmid purification involves the addition of sodium dodecyl sulfate to lyse the cells and sodium hydroxide (a strong base) to denture the DNA. Potassium acetate is then added for two reasons:

The acidic acetate buffer neutralizes the solution and allows catenated plasmids to renature.
Potassium dodecyl sulfate is poorly soluble in water. Adding potassium to solutions of dodecyl sulfate precipitates it, thus facilitating its removal.

Okay..but then...how plasmid DNA is concentrated...like in genomic dna extraction..sodium ion forming shield around dna and on adding 100% ethanol interaction getting more stonger and then pelleting it..

So isn't potassium acetate playing that role here?....then why we are adding 100%ethanol here too?

@Krishi1234 You can precipitate plasmids with ethanol and salt. You need to post your protocol in order for us to tell what the potassium acetate is being used for. I answered based on the standard alkaline lysis method, but if you’re adding KAc and ethanol at the same time then that’s a different story.