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What is the role of increased cytosolic calcium concentration after firing, in neuronal cell bodies?
I've come across several studies in which scientists were investigating various questions related to neural activity by focusing on neuronal cell bodies using Calcium imaging. As this article suggests for example, cytosolic Ca concentration in the soma will significantly increase if the neuron fires. I understand the process behind this. But I'd like to find out if this somatic Ca increase has significant downstream effects inside the soma.
Could anyone shed some light on such known processes/pathways?
I've thought of one possibility based on an article that showed Calcium would upregulate mitochondrial enzymes, such as PDH and OGDC, responsible for TCA reactions. Considering that there's a coupling (source) between cytosolic and mitochondrial Ca concentrations, this could lead to a very quick increase in metabolic activity that covers up for the ATP loss related to neuron firing. However, I'm a bit skeptical about this idea. I'd think that the lack of ATP and low NADH/NAD ratio should speed up the TCA enough already and Ca might be more critical somewhere else instead.

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For example, one of the top hits from searching with your title seems very relevant ...——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

The attached article happens to be the exact same article that led me ask this question above. It clearly states that we can observe a Calcium increase in the soma related to action potential, but doesn't seem to discuss at all what the function of this Ca increase is. And that's what I'm asking here.
I've done my research before asking. Of course, I could spend a few more days going through articles (that are often behind paywalls) and would eventually find the answer (if there is). But having to do this is exactly what I wanted to avoid by asking a clear question in a specialized community.

I think it's a good question (+1). It could be improved by a citation (e.g., to the one tyersome suggested and that you found), and also by better clarity of what exactly you are asking (I think your comment helps but comments are ephemeral). The biggest issue that you can improve is the ambiguity of the question "why": several times you ask why but why is often misinterpreted. It seems you are not interested in how the calcium gets into the cell but rather what the purpose of calcium influx is near the soma rather than at an axon terminal. If true, can you edit to make this clear?

(these edits will help you get an answer that's actually what you want, otherwise someone could come and write an excellent answer about voltage gated calcium channels and then they will find they wasted their time if this wasn't what you wanted)

Fair point. Thank you for your well-thought comments. I edited my question accordingly. I hope now it aligns up with the standards and readers can interpret what I'm after exactly.

Thanks for the edits! I've already upvoted so can't do it again, but I do hope you get a good answer. I have some ideas myself, at least one of which is mentioned here (it was in the 'related questions' on the right): https://biology.stackexchange.com/questions/36646/doubling-the-concentration-of-extracellular-calcium-hyperpolarizes-a-neuron-why?rq=1 but it will take me some time to collect references that talk about other purposes. Calcium is quite a diverse messenger so it's likely an answer will only point you in a couple directions for future research rather than give a definitive answer.

I see. Appreciate the upvote. It makes things even more interesting, if there really is not a definitive answer to this question. I'll jump back into the literature then and do some exploring. I'll start by reading into the idea brought up in that question you pointed out. Thank you for all your help. I'll keep an eye out on this thread so maybe we can discuss the findings.

After doing some further research, my conclusion is that intracellular Ca levels play a role in regulating synaptic vesicle exocytosis, LTP, redox signaling, and the krebs cycle. The latter effect seems to be the most relevant one in neuronal cell bodies.


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Trade-offs between phage and yeast displays?
If you wanted to test a peptide you designed, you can do a phage display or a yeast display experiment to assess binding affinity.
What are the trade-offs between these two methods?
I've heard anecdotally that yeast display is more sensitive and closer to human cells?

According to Creative Biolabs, the primary differences are:

In the screening/panning step, yeast display is suitable for Fluorescence Activated Cell Sorting (FACS), allowing to sort out antibodies with desired binding properties
precisely. However, the affinity of antibodies to antigens in phage
display can only be roughly stratified (sorted into categories of goodness) by adjusting the washing buffer
compositions.

Owing to its eukaryotic expression system, yeast displayed antibodies can be correctly folded and modified, such as [...] to be closer to their native structure in mammals
compared to the antibodies expressed by E.coli in phage display.

The diversity of yeast displayed antibodies may be lower than phage (107-109 for yeast, up to 1011 for phage), due to the low
transformation efficiency of yeast.

Due to the many more copies of antibody on yeast surface (104-105) than phage, it is possible to select out low affinity antibodies
according to antibody avidity with yeast display system.

Anecdotally, phage display is also cheaper.

source: Stack Exchange

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

sort: votes


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Share immunity by kissing?
How can you get a cold by kissing someone who already has it, but you can't get their antibodies by kissing them after they recover? Or can you?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

Some questions to ask yourself: What are antibodies and where are they found? What causes colds and how are they spread? From the answers to these basic questions you should be able to see that the answer to your question is relatively straightforward ...

Antibodies are in the blood, not in the saliva, whereas herpes virus is secreted to saliva so you get infected through the contact with mucosa.

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


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Is it possible to kill parasitic worms by intoxicating oneself?
I've heard of parasites that can live in the human body and do a lot of damage to the host. There are even safer forms of worm-like parasites inside the intestine, but some parasites can live in the blood vessels or even in the brain or eyes.
Parasites are, in my opinion, the most disgusting creatures there are, so I wondered if they could be killed with intoxication.
Would it be possible to get rid of worm parasites in the blood by increasing the amount of alcohol in the blood to a level that humans can tolerate but parasites can't?
Could you also eliminate brain parasites with hangover-related brain dehydration?
That the dead parasites remain in the body may not be good or advisable. In addition, eggs, which are usually a little more resilient, should rather be removed from the body by antibiotics or proper medication. But is it at least theoretically possible to do something with alcohol against parasites?

Welcome to SE Biology. Have you done any literature research about the permeability of parasites to different substances? I must be honest and say that it seems rather naïve to think that you have come up with a solution that has eluded the thousands of highly trained parasitologists working for years on this topic. There may be a parasitologist on this list who can tell you why your idea is wrong (as it surely must be), but it would be more useful for you to do some research yourself.

The principle is sound, but alcohol won't do it.  (I think because a high enough blood alcohol level to kill the parasites would kill you, too.)  There are a number of anti-parasite medicines out there, the most common of which is probably ivermectin: https://en.wikipedia.org/wiki/Ivermectin  In the US, at least, it's readily available at any feed store, or on-line, as it's widely used for livestock.

In dogs they used to use arsenic to kill the worms. It was extremely debilitating to the animal.

The term "antibiotics" generally refers to substances that act against bacteria, and "parasites" generally refers to animals.

A G&T might do the trick against malaria! But that is only because the tonic contains quinine, an anti-malarial compound.

In summary, there is no convincing evidence to say that alcohol intoxication helps to treat or prevent parasites in humans.
1) The evidence from in vivo human studies does not support the idea that alcohol consumption helps in treating parasites.
Alcoholism and Strongyloides stercoralis: Daily Ethanol Ingestion Has a Positive Correlation with the Frequency of Strongyloides Larvae in the Stools (PLoS, 2010):

The frequency of Strongyloides was significantly higher in alcoholic
  patients than in control group (overall prevalence in alcoholic 20.5%
  versus 4.4% in control group; p = 0.001).

2) Even a strong alcohol beverage gets diluted when it reaches the intestine.
Ethanol concentrations in the human gastrointestinal tract after intake of alcoholic beverages (European Journal of Pharmaceutical Sciences, 2016):

In a cross-over study, five fasting volunteers were asked to drink two
  standard consumptions of commercially available alcoholic beverages,
  including beer (Stella Artois®, 500 mL, 5.2% ethanol), wine (Blanc du
  Blanc®, 200 mL, 11% ethanol) and whisky (Gallantry Whisky®, 80 mL, 40%
  ethanol).
The median gastric ethanol Cmax (min–max) for the beer, wine and
  whisky conditions amounts to 4.1% (3.1–4.1), 4.1% (2.6–7.3) and 11.4%
  (6.3–21.1), respectively...Median duodenal ethanol Cmax (min–max) for
  beer, wine and whisky are 1.97% (0.89–4.3), 2.39% (2.02–5.63) and
  5.94% (3.55–17.71), respectively.

So, the maximal ethanol concentration in the duodenum after drinking 80 mL of whisky was 17.7%. Most of ethanol is absorbed in the first part of the small intestine (Scandinavian Journal of Gastroenterology), so it does not reach the more distant parts and does not likely kill the parasites there.
3) Even strong intoxication is associated with low blood alcohol concentration.
In strong intoxication, your blood alcohol concentration would be only 0.2-0.3%. In one study (Table 1), the 50% lethal concentration (LC50) of ethanol, which killed 50% of the bloodstream forms of the parasites Trypanosoma brucei, was 10.6%.
4) Alcohol intoxication and brain dehydration
Alcohol intoxication or hangover are not automatically associated with dehydration. Anyway, even in severe dehydration, you still have a lot of water in your body, including the brain, so the parasites living there do not necessarily get dehydrated as a result of your dehydration.
In general, dehydration increases the risk of infections, because it dries mucous membranes, for example in the urinary tract (BMJ Open Quality, 2019).

I don't think I'll ever drink alcohol again. No, but seriously, parasites are really creepy. It's good to know that I can't do anything against parasites with alcohol and would even have a higher risk of infection. So thank you for the good answer.

@user1136, the OP asked if alcohol can kill parasites. I have found that single in vivo human study, which does not support this idea. No matter how weak or poorly related this evidence is, it does not suggest that alcohol can help. Chronic alcoholism is a series of severe acute alcohol intoxications, anyway. That same study also does not support the idea that alcohol would repel parasites or make them less productive as in the fruit-fly and wasps study. I mean, it could - but where is the evidence?

This is a great well-cited answer. Just to add one more thing to discourage getting drunk to treat the parasite; a viable treatment is assessed via the risk-benefit ratio. Even if these studies were not present, becoming highly intoxicated may do as much damage to the host as the parasite you are trying to eradicate. According to the NHS, there is no safe level of alcohol consumption.

@user1136 You raise an important point that the PLOS study is limited in scope. And re the wasps, there is no doubt external use of alcohol can kill pathogens. This question addresses evidence surrounding ingested alcohol and if there are any associations with parasitic resistance or treatment.

Although the previous answers give a resounding "No" for the case of human hosts and parasitic worms, a 2012 research paper (Alcohol Consumption As Self-Medication Against Blood-Borne Parasites In The Fruitfly) states that the larvae of Drosophila melanogaster (fruit flies) actively seek out foods containing ethanol when they are infected by the eggs/larvae of parasitic wasps.
(I don't know whether they do this when the parasite's egg has been laid inside them, or after it's hatched into a larva, or both.)
This paper was quoted by various popular science magazines of the time (see e.g. https://www.newscientist.com/article/dn21493-parasite-plagued-flies-self-medicate-on-booze/), and also metioned the use of ethanol as a preventative measure as well as a curative one.
Despite having evolved an increaed tolerance to the ethanol, however, the increased consumption may have some adverse side-effects on the infected fly larva.

Generalising from alcohol to toxic substances in general - caterpillars of the Grammia incorrupta moth consume plants containing toxic pyrrolizidine alkaloids (PAs) to kill the eggs of parasitoids within them. The PAs are poisonous to the caterpillar as well as the parasites, and caterpillars that successfully exploit this strategy still suffer adverse health effects. https://web.archive.org/web/20160313220351/http://phenomena.nationalgeographic.com/2009/03/20/self-medicating-caterpillars-use-toxic-plants-to-kill-parasites/

The New Scientist article you linked does not mention any use of alcohol for treatment of worms or other parasites in humans.

The answer to your question depends on the kind of parasites you're focusing on.
Looking at bacteria and gastro-intestinal infections, I found three articles (one based on a model stomach, a second one based on a questionnaire and serum analysis and a third one describing a specific incident), which indicate that there is a certain protective effect of ethanol consumption.

This paper describes the effect of wine on Listeria innocua in a model stomach (I have only access to the abstract). Wine seems to have an antimicrobial effect, which can be traced back mainly to ethanol as well as to organic acids.

Ethanol exhibited a higher bactericidal effect than the mixture of the main wine organic acids. When testing the organic acids separately, malic and lactic acids were found to have the strongest effect. The combination of ethanol with the organic acids acted synergistically but to a lesser extent than wine itself.

If anyone has full access to this article it would be interesting to put it into perspective to point two of the (currently) accepted answer.

This paper, based on a questionnaire on dietary habits and serum analyses for for Helicobacter pylori immunoglobulin G antibodies (1'785 participants), comes to the conclusion that

[t]here was a clear inverse dose-response-relation between reported alcohol consumption and H. pylori infection.

[Also here, only the abstract is accessible.]

There is another paper describing the effect of alcohol consumption on a Salmonella outbreak in Spain. The sample size is relatively small (90 people), but the data suggests that

[t]here was a protective effect of alcohol that was stronger among the people who drank more than 40 gm of alcohol.

Welcome to Biology.SE! Nice answer and a good job on providing supporting references. However, can you please include the complete reference information since links can break. Search on Google Scholar and click on the ‟ symbol to get reference information for journal articles. This is a good example of how to format references. Thanks!

However, please note that the original question was about worms rather that bacteria. If you can't find a question for which this is a relevant answer on this site (I gave a quick look and didn't find any), I would suggest posting a relevant question and then move this answer to that question.

From the first principles:
The most sensitive to alcohol part of the human body is it's nervous system. Worms have much simpler (in both biochemistry and organization) nervous system, so they will probably suffer less from a generic poison that the alcohol is.
OTOH, you can easily find a substance that is WAY more toxic to the worms than to yourself. Up to and including being safe to be given to minors and reproducibly killing all the worms. Just ask the nearest pharmaceut.
p.s. in the same sense, alcohol is killing bacteries, but you cannot cure pneumonia by drinking, no matter what heavy drinkers assert.

+1 The key is finding something worse for parasites than for humans. Alcohol isn't likely to be the best candidate, and there is a whole sector of pharmaceutical industry devoted to optimising and producing alternative substances.


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Help id mushroom found in West Midlands, Egland
I found this mushroom yesterday. It looks like an oyster but it grows in some poorly kept lawn. I am sure there was no tree there in the past. This spot was landscaped a couple of years ago after building some blocks of flats. I turned it over, hoping to find some piece of wood, but there was nothing. It has a mild mushroomy smell. Do you have any ideas what it may be?

They look like pleurotus, i'd ask a mycology specialized forum like reddit or facebook mycology.

https://www.flickr.com/photos/shentsonebirder/8284582392 unsure


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Are Hsp70 proteins only activated in response to heat shock?
Hsp70 proteins are chaperones that assist in protein folding in my plant physiology textbook it says the Hsp70 proteins were discovered by inducing heat shock. But do they only work in response to heat shock stress?
I know these types of proteins are found in many organisms but I am interested in how they assist on protein folding or stress response in plants specifically.

The wikipedia Hsp70 article answers the headline question.

They get upregulated under stress, but will be expressed normally. In effect the name is deceptive...


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What's the technical terminology for call-and-respond type behaviour?
The groups of some species such as water birds display a behavior that once out of line-of-sight a member will periodically initiate an interaction by make some type of sound, which will be followed up by responses from all the other members - presumably to confirm they haven't been silently snatched by a predator. I have observed this in person at a local botanical garden where the water birds sound off like this every 10 minutes or so all day long.
What is the technical term for this behavior and some examples of species that demonstrate it?

if you are referring to call and response in rapid succession, ethologist use the terminology "turn-taking" or "antiphonal calling".
Many species do it with different degrees of precision.
A rapid research on google scholar will give you several results.
I do not know whether it would apply specifically to your case, which might be more general and it could be simply "contact calling".
Regarding the hypothesis you formulated ("(...)presumably to confirm they haven't been silently snatched by a predator"),   it would be nice to know if actually everyone respond, who is calling first (always the same individual?) and if they would behave different if someone does not reply.
Hope it helps and have fun with your observations.


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How many molecules of ATP are actually produced in aerobic respiration?
I have been through the process of aerobic respiration a few times in different text books and almost every book quotes a different value for the number of ATP molecules produced. The consensus seems to be 30–32, but why is there disagreement and why aren’t the numbers exact?
The possible reasons I can think of are:

Phosphorylation of ADP is not directly coupled to redox reactions.
The number of ATP molecules produced depends on the shuttle used to transport electrons from the NADH in the cytosol to the mitochondria, i.e.  whether it’s FADH2 which enters the ETC or NADH. (I have a silly question on that, but I need confirmation, does the electron carrier chosen depend on availability?)
The proton-motive force can be used to drive other cellular processes other than the production of ADP? (I'm guessing.)

Are these suggestions correct, or is there some other explanation?

The discrepancy between 30 and 32 molecules of ATP quoted in the question may well arise from the two possible ways in which the reducing equivalents of the two molecules of NADH generated in glycolysis may be shuttled across the inner mitochondrial membrane into the mitochondrion (suggestion 2).
If one assumes that the malate-aspartate shuttle is used, then NADH is transported into the mitochondrion as such, and the yield of ATP is the same as for those molecules of NADH generated in the mitochondrion — 2.5 ATP per NADH from the most generally accepted measurement.
However, if one assumes the glycerol phosphate shuttle is used then the reducing equivalents are transferred from NADH to FADH2, from which only 1.5 molecules ATP is produced per molecule.
In summary, using the malate–aspartate shuttle a total of 5 molecules of ATP (2 x 2.5) will be produced from the two molecules of glycolytic NADH, whereas using the glycerol phosphate shuttle there will be only 3 molecules of ATP (2 x 2.5). This gives a difference of 2 molecules of ATP, which would cover the range in the question.
As the relative proportions of the two shuttles varies between tissues, a range of values is actually possible.

I have edited your answer to correct what I felt were ambiguities (initially I thought they were mistakes) and to give it greater overall clarity. (SE encourages improvement of answers.) However, if you don't like my edits you are free to revert them and I will include them in an answer of my own instead.

Thankyou @David for the changes, now it's more clear.

There is a fixed number of NADH and FADH2 produced per glucose oxidizes (assuming we are starting from the beginning of glycolysis) so reason 2 is unimportant for variability. The third reason you are right that the cell uses the proton gradient for additional purposes such as pumping ADP and Pi into the mitochondria by secondary active transport but we know that this requires 1 proton overall per ATP synthesised so this doesn't contribute to the variability in the number. The proton gradient may be used for other transport processes across the inner mitochondrial membrane and this might contribute to variability in the number as we aren't sure how much of the proton gradient is used by these other processes or if these processes are always active. The other reason (probably the most important reason) is that protons can leak back across the membrane without producing ATP and the extent of leakage measured depends on the quality of membrane preparation and the experiment performed (and the equipment used) so there is variation in the amount of leakage and hence the number of protons required per ATP synthesised, resulting in variation in the overall number of ATP synthesised in one round of aerobic respiration.

You are totally spot on with #1. ADP phosphorylation pump is driven by the proton gradient and ADP availability, while the the electron transport chain slows when it becomes too hard to pump protons.
Furthermore, other processes (mostly channels) may use up a proton from the gradient.
The different electron carriers have store different amounts of energy (NADH is more energetic than FADH) and differ in the uncatalysed energy required to release the electron pair, hence why there is not a one size fits all.
NADPH vs. NADH is a special case as NADPH is anabolic (builds), while NADH is catabolic (the electron pair is used for energy generation) and the enzymes in the cell keep it so that NAD+ levels are higher than NADH, and NADPH higher than NADP+. The passing of a pair from NADH to NADPH (a membrane bound transhydrogenase) actually utilises a proton off the gradient to drive it.


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Why do neutrophils have segmented nuclei?
To clarify, I'm not asking what causes high segmentation in neutrophils. I'm asking how segmented nuclei function in a regular neutrophil cell.


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Question regarding aposematism
Are all aposematic insects chemically defended? Can there be insects that mimic chemically defended insects that are also aposematic?
Any ideas?

I think you're talking about Batesian mimickry. For example, hoverfly species without stings mimic wasp species (with bright black and yellow striped patterns) which do have them. And there are several examples in the butterfly world. Males of the species Danaus chrysippus are inedible due to their consumption of plants containing toxic chemicals. They are also aposematic. Females of that species, as well as butterflies of other species, mimic D. chrysippus males. Can you let me know if this is the sort of thing you're asking about, so I can turn this into an answer if so?

@Astrid_Redfern The question asks "are all aposematic insects chemically defended"? The way I see this is: "Is part of the definition of aposematism, that the insect that has this attribute is chemically defended?" I want to be sure about the answer, but the main thing that confuses me is this: "Can an edible insect that mimics an inedible model with bright colors or some aposematic-like attribute be defined to be aposematic?"

I think the answer to the question would be "no, an aposematic insect must be chemically defended, if it is not, and it is a mimic, then it exhibits batesian mimicry, not aposematism.

@Astrid_Redfern what do you think?


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What are reasons we know insects evolved on land rather than water
I am reading up on the evolution of insects, and insects supposedly evolved on land rather than water. How do people know?What evidence is there that insects evolved on land and not water?

The sister group of hexapods (Insects plus Collembola, Protura, and Diplura) are thought to be Remipedes. Remipedes are cave-dwelling aquatic pancrustaceans. The most recent common ancestor of Hexapoda and Remipedia was likely aquatic. But somewhere along the pathway to becoming modern hexapods, after they split from the lineage leading to modern remipedes, the ancestors of modern hexapods developed tracheal respiratory systems that function on land. So the evidence comes from the fact that the extant lineages of insects, close to their most recent common ancestor, including Collembola, Protura, Diplura, Archeaognatha, and Zygentoma are all terrestrial.


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Do pyrocalciferol and isopyrocalciferol form in vertebrate skin?
I heard that pyrocalciferol and isopyrocalciferol can only be formed above 100°C/212°F, yet some images in the web depict them as forming in vertebrate skin. So, I wonder if pyrocalciferol and isopyrocalciferol do form in vertebrate skin. If they do, is there something catalyzing the thermal transformation of previtamin D or is it also a result of UV irradiation?

Could you add links to references of both claims?

An example of the former is ScienceDirect, which claims that "By increasing the temperature to 100-200°C, a new electrocyclization takes place, resulting in formation of pyrocalciferol (7) and isopyrocalciferol (8).". Example for the latter is the second image in the chemistry section of the "About Vitamin D" web site, which shows both pyrocalciferol and isopyrocalciferol (albeit with the names and compounds reversed) forming in skin.

ScienceDirect is a website which hosts over 900000 articles. Adding a link to specific article would be much better. You can read here on how edit your question to add links. I am not versed in skin chemistry, but people here could help you better if thay can read and evaluate your sources directly. When I write "About Vitamin D" in search engine I get numerous result sites without any way of knowing which is the one you have. Again adding a specific link would be much better.

For first, 'https://www.sciencedirect.com/topics/chemistry/provitamin', then use search in page tool, with pyrocalciferol inputted. For second, 'https://vitamind.ucr.edu/about/', then go to chemistry section.


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Is evolution always unidirectional?
Is it possible, at least in theory, for a species to evolve into another species and then evolve back into the first species?

It's possible, but very unlikely.  Usually it takes a substantial number of genetic differences to qualify two organisms as different species.  One might think that reversing the direction of selection pressure could reverse a genetic change, but genetic change begins with random mutations which are not determined by selection pressure.  It's very unlikely for one random process to undo another random process (imagine mixing black and white sand in a jar by shaking it, then trying to unmix by unshaking!).

While it doesn't go nearly to the extent of speciation, the classic example is the British peppered moth: https://en.wikipedia.org/wiki/Peppered_moth_evolution  Originally it was mostly white with black spots, which made a good camoflage on tree trunks &c.  During the industrial revolution, the "dark satanic mills" put out a lot of soot, turning the tree trunks dark.  The whiter moths were easy to spot, and got eaten before reproducing, so within a few decades most of the moths in industrial areas were black.
Later on, emissions control laws drastically reduced the amount of soot, the tree trunks became light again, and the moths evolved back to white.


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Similar smell for avocado and raspberries
I noticed when heating frozen avocado that the smell was just like fresh raspberries in the summer. Does anyone know what makes them smell so similar ?
(https://doi.org/10.1016/B978-0-12-408117-8.00029-5)
"One-half an avocado is a nutrient and phytochemical dense food consisting of the following: dietary fiber (4.6 g), total sugar (0.2 g), potassium (345 mg), sodium (5.5 mg), magnesium (19.5 mg), vitamin A (5.0 μg RAE), vitamin C (6.0 mg), vitamin E (1.3 mg), vitamin K1 (14 μg), folate (60 mg), vitamin B-6 (0.2 mg), niacin (1.3 mg), pantothenic acid (1.0 mg), riboflavin (0.1 mg), choline (10 mg), lutein/zeaxanthin (185 μg), cryptoxanthin (18.5 μg), phytosterols (57 mg), and high-monounsaturated fatty acids (6.7 g) and 114 kcals or 1.7 kcal/g (after adjusting for insoluble dietary fiber)"  ("Hass Avocado Composition and Potential Health Effects", Mark L. Dreher and Adrienne J. Davenport)
https://www.sciencedirect.com/topics/food-science/avocado
$
\begin{array}{|l|c|c|}
\hline
  \text{Compound} & \text{Raspberry} & \text{Avocado} \\
\hline
   \text{provitamin A/$\beta$-carotene} & & \checkmark \\
\hline
   \text{vitamin A} & \checkmark & \checkmark \\
\hline
   \text{vitamin B} & \checkmark &  \\
\hline
   \text{vitamin $B_1$/thiamine-HCl} & \checkmark & \checkmark \\
\hline
   \text{vitamin $B_2$/vitamin $G$/riboflavin} & \checkmark & \checkmark \\
\hline
   \text{vitamin $B_3$/vitamin $PP$/niacin} & \checkmark & \checkmark \\
\hline
   \text{vitamin $B_5$/pantothenic acid} &  & \checkmark \\
\hline
   \text{vitamin $B_6$/pyridoxine} & & \checkmark \\
\hline
   \text{vitamin C/ascorbic acid} & \checkmark & \checkmark \\
\hline
   \text{vitamin D/calciferols} &  & \checkmark \\
\hline
   \text{vitamin E/$\alpha$-tocopherol} & \checkmark & \checkmark \\
\hline
   \text{vitamin $H$/biotin}  &  & \checkmark \\
\hline
   \text{vitamin K_1/phytyl menaquinone} &  & \checkmark \\
\hline
   \text{acid:citric acid} & & \checkmark  \\
\hline
   \text{acid:folic acid} & \checkmark &  \\
\hline
   \text{acid:malic acid} & & \checkmark  \\
\hline
   \text{acid:oxalic acid} & & \checkmark  \\
\hline
   \text{$\alpha$-carotene} & & \checkmark \\
\hline
   \text{anthocyanins} & \checkmark &  \\
\hline
   \text{choline} &  & \checkmark \\
\hline
   \text{cyanidin-3-glucoside} & \checkmark & \\
\hline
   \text{anthocyanin was cyanidin-3-rutinoside} & \checkmark & \\
\hline
   \text{cryptoxanthin} &  & \checkmark \\
\hline
   \text{dietary fiber} &  & \checkmark \\
\hline
   \text{ellagitannins} & \checkmark &  \\
\hline
   \text{folacin} &  & \checkmark \\
\hline
   \text{folate} &  & \checkmark \\
\hline
   \text{high-monounsaturated fatty acid} & & \checkmark\\
\hline
   \text{phospholipids} & & \checkmark\\
\hline
   \text{glycolipids} & & \checkmark\\
\hline
   \text{free fatty acids} & & \checkmark\\
\hline
   \text{lutein/zeaxanthin} & & \checkmark  \\
\hline
   \text{persenone A} & & \checkmark \\
\hline
   \text{persenone B} & & \checkmark \\
\hline
   \text{phytosterols} & & \checkmark \\
\hline
   \text{$\beta$-sitosterol} & & \checkmark \\
\hline
   \text{sugar} &  & \checkmark \\
\hline
   \text{B (boron)} &  & \checkmark \\
\hline
   \text{Ca (calcium)} &  & \checkmark \\
\hline
   \text{Fe (iron)} & \checkmark & \checkmark \\
\hline
   \text{K (potassium)} & \checkmark & \checkmark \\
\hline
  \text{Mg (magnesium)} & & \checkmark \\
\hline
   \text{Na (sodium)} &  & \checkmark \\
\hline
   \text{P (phosphorus)} &  & \checkmark \\
\hline
   \text{Zn (zinc)} &  & \checkmark \\
\hline
\text{2(R)-(12Z, 15Z)-2-hydroxy-}\\\text{4-oxoheneicosa-12,15-dien-1-yl acetate} & &\checkmark\\
\hline
\end{array}
$
$
\begin{array}{|l|c|c|}
\hline
   \text{sugar} & \text{Raspberry} & \text{Avocado} \\
\hline
   \text{glucose} & & \checkmark\\
\hline
   \text{fructose} & & \checkmark\\
\hline
   \text{d-Manno-heptulose} & & \checkmark\\
\hline
   \text{perseitol} & & \checkmark\\
\hline
   \text{sucrose} & & \checkmark\\
\hline
\end{array}
$
$
\begin{array}{|l|c|c|}
\hline
   \text{neutral lipid} & \text{Raspberry} & \text{Avocado} \\
\hline
   \text{monoacylglycerols} & & \checkmark\\
\hline
   \text{diacylglycerols} & & \checkmark\\
\hline
   \text{triacylglycerols} & & \checkmark\\
\hline
\end{array}
$
$
\begin{array}{|l|c|c|}
\hline
   \text{neutral lipid:triacylglycerol} & \text{Raspberry} & \text{Avocado} \\
\hline
   \text{dioleyl palmitin} & & \checkmark\\
\hline
   \text{triolein} & & \checkmark\\
\hline
   \text{dioleypalmitolein} & & \checkmark\\
\hline
   \text{linoleyl oleyl palmitin} & & \checkmark\\
\hline
   \text{linoleyl diolein} & & \checkmark\\
\hline
\end{array}
$
Seems there are hundreds of volatile compounds for raspberries, so will not list them all here (unless I find a matching volatile compound, then I might update this question).
What I found matching http://dx.doi.org/10.1590/1678-457X.01316 and doi:10.3390/molecules20022445:
(E)-3-Hexen-1-ol    Green, grass, leafy odor; bitter, grassy-fatty notes
1-octanol   Grassy, plastic, solvent
2-butanol   Oily, wine-like, fusel-alcoholic note
2-ethyl furan   Strong, sweet-ethereal, burnt brown musty odor
2-decanone  Orange-like, floral odor
2-hexanone  Fruity, ketonic, banana, yeasty, cheese, dairy notes
2-phenyl ethanol    Rose, perfumery
3-methyl-3-buten-1-ol   Fruity, green
4-methyl-1-pentanol Oily green-fruity, herbaceous,
acetophenone    Sweet, pungent, harsh
benzaldehyde    Almond, fruity, powdery, nutty
benzyl acetate  Sweet, floral, fruity odor of jasmin and gardenia, fruity taste
benzyl alcohol  Faint, sweet, fruity aroma; sweet taste
ethyl acetate   Ethereal, sharp, wine-brandy like odor
hexanal Oily, avocado
limonene    herbal, sweet
linalool    Sweet floral
naphthalene Musty taste
nonanal Fatty-floral-rose, waxy odor
octanal Fatty-fruity odor; sweet, citrusorange-fatty taste
p-cymene    Strong, characteristic, terpene odor
pentanal    Strong, acrid, pungent odor; chocolate
α-copaene   Woody, spicy, sweet
α−terpineol Sweet, floral (lilac), lime odor;
β-pinene    Sweet, lemon
γ-nonalactone   Strong, fatty, coconut

Attempt enhancing the quality of your question and, firstly of your research

@Algae — The question is clear (despite being flagged as otherwise) and the poster has done some research which he believes will help someone provide an answer. I personally regard his question as uninteresting, and regard him as naive in thinking that any common nutrient in his lists is likely to be responsible for his (subjective) observation. He would be better advised to search specifically for the biology of odorants, but I don't think your comment is particularly fair or helpful.

Since listing nutrients was discouraged I will stop now ...

@Emil Although I do not know the answer to your question, I disagree with David & think that this is exactly how biochemists identify tastes & smells. Impossible food wanted a meat-free burger so they put beef into a chromatography-mass spectrometry machine, which identifies specific molecules. Among other things, they detected butter, syrup, and used diapers. Before advanced mass-spec, quantifying the smell was a challenge that has been going on since the 1800s. Here is a paper from 1963 suggesting one method to quantify the smell by using many people.

I have ordered a book called Smellosophy now, hopefully I will get a better understanding of the psychology after reading that one.


text:
What is the etymology for Pinus halepensis?
I have a problem of figuring out the etymology of Pinus halepnesis.
An etymonline search with halepensis brought no result.
It is unclear to me from the English wikipedia article and from the English WikiSpecies article what is the source of the name.
It is often called "Aleppo pine" --- maybe this is the source.
In Israeli Hebrew (as in Hebrew Wikipedia) it is called "Jerusalem pine" (אורן ירושלים) which is clearly different than standard.
What is the etymology for Pinus halepnesis?

This seems to be off-topic since it is essentially a language question not one about biology ... Supposedly the original description is available in this book, if that doesn't help I have no idea where else you could look.

I understand your opinion and respect it; although, I don't know any other SE website better fit for this question hence suggest at the common era to tolerate such (in my opinion anyway-rare) questions.

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

If you search for this plant (properly spelled Pinus Halepensis) in the International Plant Names Index (IPNI), you'll find this page providing publication reference for this species of pine:

Gardeners Dictionary, Edition 8. London

According to IPNI, this publication by Phillip Miller in 17681 was the first to officially name this species. You can find the first half of the publication online here and the portion of the publication with info regarding P. halepensis here [p. 477].
Miller 1768 provides the following:

Pinus (Halepenſis) foliis geminis tenuiſſimis, conis obtuſis , ramis patulis. Tab. 208, Pine-tree with two narrow leaves in each ſheath, obtuſe cones, and ſpreading branches. Pinus Halepenſis, foliis tenuibus lætè viridibus. Rand. Hort. Chelf. Cat. 158. aleppo Pine with very narrow dark green leaves.

* Note: a longer description about this tree also continues on the subsequent page in Miller's book -- you can find it in the middle of the right column of the following page.
However, this publication does not make clear why Miller chose this specific epithet.

Elwes & Henry (1906)2 likewise describe this species [see online here] and mention that the epithet had been used for more than 100 years. However, they, too, do not provide meaning behind its use.

Further sleuthing suggests the following:
From Antropocene.it:

The specific epithet halepensis derives from Aleppo, the current city of Haleb in northern Syria.

Note, however, that this specific epithet doesn't only apply to this species of Pine. Linnaeus assigned this epithet to a grass (Sorghum halepense) he called Holcus halepensis (Linnaeus Sp. Pl. (1753) 1047)3 more than a decade before Miller named the pine in question.
Using this connection, SEINet suggests the following etymologies for halepense:

Halepense means "from Aleppo, Syria."

This is the best I could do for you in a short amount of time. I, like you, could not find much explicit explanation for this word, and I admit I find its use a little strange given the relatively widespread range of the species mentioned (at least that both exist much wider than Aleppo).

 1. Miller, P. 1768. The Gardener's Dictionary, ed. 8. London. Pinus no. 8
 2. Elwes, H.J. and Henry, A., 1906-1913. The Trees of Great Britain and Ireland. Edinburgh: R & R Clark, 7.
 3. Linnaeus, C. 1753. Species plantarum. https://doi.org/10.5962/bhl.title.669. [more info here and on wikipedia]

Hello, this is impressive work; you have helped others, and me; I thank you dearly for that. I was happy reading your answer; just one thing is unclear to me - it was written (Linnaeus Sp. Pl. (1753) 1047) ; what is the 1047? Again thank you for your time,

@JohnDoea see edits

@JohnDoea to clarify more specifically, 1047 represents the page number of Species Plantarum in which one can find Linnaeus's description for H. halepensis

The "species_plantarum_binomials" function in the taxize package for R provides a convenient output containing each genus, species, and page number from Linnaeus's work. See here


text:
What is an allele?
According to the entry for allele in Wikipedia:

“An allele is a variant form of a given gene, meaning it is one of two or more versions of a known mutation at the same place on a
  chromosome.”

However on Nature Scitable the definition of allele it states:

“Humans are called diploid organisms because they have two alleles one
  from each parent.”

These definitions disagree: one states alleles arise due to mutations on a chromosome, whereas the other states that they are the forms of a gene on a  homologous pair of chromosomes.
So what is the correct definition of an allele?

I have edited your question, especially to include links to the sources of your quotations. In future questions be sure to do this yourself. Also please complete the Tour and read the Help on asking questions.

The Wikipedia definition is poorly worded, but I don't see a contradiction — alleles are specific instances of genes. This is analogous to isotopes in nuclear chemistry — every atom exists as a specific isotope. I'm voting to close because this seems to me like a very basic question that could be answered by looking at any decent undergraduate textbook or on a site like Khan Academy.

@tyersome — Correction. You are not voting to close, because you have not yet accrued the privilege (3000) to do so. You are suggesting that the question should be closed.

The question takes one sentence in the Nature Scitable article about alleles out of context. The statement:

“Humans are called diploid organisms because they have two alleles one
  from each parent.”

is not the actual definition of allele in the article, which is in the first sentence:

“An allele is a variant form of a gene.”

Rather, it is part of an explanation of the situation for variants in humans. (It is not meant to be a definition of diploid, either.)
This is perhaps clearer in the definition for allele given in the respected undergraduate text, Alberts’ Molecular Biology of the Cell, where the same two ideas follow one another directly.

Allele
  One of a set of alternative forms of a gene. In a diploid cell each
  gene will have two alleles, each occupying the same position (locus)
  on homologous chromosomes.

The first sentence is the definition, the second sentence provides an example of the variants in diploid cells.
As the Wikipedia entry explains, the word allele is derived…

…from the Greek prefix ἀλληλο-, allelo-, meaning "mutual", "reciprocal", or "each other", which itself is related to the Greek adjective ἄλλος, allos (cognate with Latin alius), meaning "other".

Thus it encompasses the idea of variation or difference (rather than gene homology) which is what it was coined to describe.
FOOTNOTE
It is possible to refer to alleles that are identical, but only in a context where variation is possible. Consider the four possibilities for the mutation, m, of a wild type gene, wt.
1. wt wt
2. m  wt
3. wt m
4. m  m

We can refer to 2 and 3 as having one mutant and one wild-type allele, and 4 as having two mutant alleles (or both alleles mutant). But what about 1? It is natural to refer to this as saying both alleles are wild type, and indeed almost impossible to avoid referring to them as alleles. They are both normal, and therefore not strictly variants, but they are alternatives to the mutation at this same position.

I'm clearly missing something, but I don't see the problem.  My understanding is that an allele is a specific instance of a gene.

Apologies for missing the quotation out of context in the question. I have recast my answer extensively to address this. The person that upvoted the original answer is welcome to retract his vote.


text:
What are the white eggs growing from a black stem on the Napa cabbage plant?
Are they fungal or eggs?
Can't find anything like this in the internet

Location: South Florida

I believe those are fruiting bodies of a microorganism, probably either a fungus or a slime mold. I don't think they are eggs of an insect or other animal.  The oddest thing to me is the leaves are relatively healthy appearing yet there are dense stands of these bodies.  Perhaps it was feeding on something on the surface of the leaves rather than within the leaf tissue.

Related: Tiny black mushrooms growing from veggies?

I'm no expert in slime molds, but your specimens do in fact look a lot like the sporangia, or spore-producing reproductive structures (i.e., fruiting bodies), of a Mycetozoan slime mold in the class Myxogastria.  Physarum and Comatricha are possible candidate genera based on structure of their sporangia that I can find easily online.
See below for an example image:

 Sporangia of Physarum pusillum. Source: Wikimedia
You can see many photos of the white sporangia of Physarum pusillum here and a close-up of the white sporangium of Physarum pseudocolumellatum here
I don't think I can provide a more specific answer given the quality of your photo or my general lack of deeper knowledge of these organisms. Regardless, no quick search for slime-mold infections in plants produced any information regarding slime mold species that regularly grow above-ground on cabbage.

However, I did find this site which suggests that decreasing the moisture or increasing the salinity of the slime mold's environment will cause it to move along...


text:
How does lipoid pneumonia lead to acute respiratory distress syndrome (ARDS)?
How does lipoid pneumonia lead to acute respiratory distress syndrome (ARDS)?
The vaping illnesses that have been happening on the news in the United States are being caused by the federal prohibition on marijuana. Smugglers will legally go to recreational marijuana dispensaries in legal states and purchase cartridges that contain about a gram of "wax". Proper cartridges will use polyethylene glycol, polypropylene glycol, or vegetable glycerin to suspend the THC for vaporizing, but the smugglers have been known to open up the tank and remove some of the wax and refill the remaining volume with Vitamin E Oil. These tampered cartridges are then sold on the black market to recreational and medical consumers in illegal states.
The CDC Report: "Outbreak of Lung Injury Associated with the Use of E-Cigarette, or Vaping, Products"
Edit: So, I was on some conspiracy shtuff when I wrote this post because I was worried about impurities in my vapes killing me. I don't want to take this down because I want my cognitive distortion to remain visible as a reminder of how we can succumb to biased reasoning. Also, the answer I marked correct contextualized the fragmented information of which I was aware and attempted to give me an improved framework for understanding the terms I was using incorrectly as a layman.

Welcome to Biology.SE! This appears to be a reasonable question, but the inclusion of unsubstantiated or irrelevant claims detracts from this. Specifically, the entire middle of your post seems to be a distraction from the biology. Instead, please summarize the relevant information from the CDC report and add any other relevant information you can find about ARDS and lipoid pneumonia (with references from reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

There are several ways to get ARDS (sepsis, pneumonia, trauma, pancreatitis, etc).  Pathophysiologically, they all converge at alveolar insult.  So however it happens, there's alveolar insult, cytokine release that recruits neutrophils, and the activated neutrophils release toxic mediators that destroy the alveolar membranes.  So for your question specifically, the mineral oil in the vape cartridges (theoretically) is instigating an inflammatory reaction that destroys alveolar membranes.


text:
A theory about the possible connection between protists and first animalia
I learnt that organisms within Kingdom Animalia can be either microanimals or (nonmicro)animals.

a microanimal is any Kingdom Animalia organism that in general cannot be seen by a human eye without microscope

I understand that while it is controversial how a first cell was formed (or appeared) in earth, it is broadly accepted that archaebacteria was at one time formed in earth and multiplied and that with time cyanobacteria evolved out of these, multiplied and evolved by themselves (while on the way crating stromatolites) and by that time the first protist was formed and multiplied and evolved into various shapes (morphogensis) of protists.
I also learnt that the difference between a protist to a microanimal, is that the latter does have specialized cells, so that its body isn't seemingly just a cluster of cells in a given shape and can possibly do any other function that a protist can't do besides perhaps surviving by morphogensis (if either one isn't a function by itself).
Due to the similarity in shape and size of protists and microanimals, I ask if there is a theory and if it reflects a consensus, that microanimals were the first Animalia and were indeed evolved out of protists?

 Short Answer:
Probably the most widely accepted (though certainly not fully accepted) theory of animal evolution is called the Colonial theory.
According to the Colonial theory of animal origins, the earliest animals (i.e., sponges) seem to have arisen from colonial protists called choanoflagellates forming an invaginated hollow, spherical colony.
However, other theories do exist: Syncytial Theory and the Synzoospore Theory (proposed by Mikhailov et al. (2009)1)
Regardless of these theories, no reasonable theory about the evolution of animals from protists would link such evolution to "microanimals" given that microanimals (as defined by the OP) is not a phylogenetic group but rather a term to describe microscopic animals from various taxonomic groups.
 Long Answer:
There seems to be strong morphological evidence that choanoflagellates are the closest protist relative to currently living animals -- specifically to the simplest group of animals: the sponges (phylum Porifera).

 Protist / Animal phylogeny, Source: Cengage 20132
Specifically, we can see very similar characteristics between a choanoflagellate and a choanocyte (or "collar cell") of a sponge.

The choanoflagellates often form colonies consisting of numerous protists adhering to one another using adhesion proteins.

Due to the morphological similarities between choanoflagellates and choanocytes of sponges (along with similarities in adhesion proteins and signaling proteins shared between both), and the regular colony-forming tendencies of choanoflaggelates, it has been long suspected that the evolution of multicellular animals arose from these protists.
Ernst Haeckel (1874) was the first to propose that colony-forming chonaoflaggelates were the precursor to modern animals in a theory he called the Gastraea theory and which is now called the Colonial Theory of animal evolution. This thoery is summarized simply by Mikhailov et al. (2009)1:

According to Ernst Haeckel, the transition from unicellularity to multicellularity
  proceeded through two consecutive stages (Fig. 1A). First, unicellular flagellates aggregated to form a hollow ballshaped floating colony of identical cells. This hypothetical stage was named the Blastaea to reflect its similarity with the blastula, an early stage in animal embryogenesis....
...At the second stage, the homogenous cellular wall of the Blastaea invaginated to form a second layer, the precursor of the primary gut. After this important event the Blastaea acquired primary cell differentiation (=spatial cell differentiation).
Haeckel named this hypothetical ancestral form the Gastraea, again to indicate its similarity with the gastrula stage in animal embryogenesis. According to Haeckel, extant
  cnidarians and sponges are the first direct descendants of the ancestral Gastraea,(11) because their body plans derive from two embryonic layers.

Below is an illustration of the Colonial Theory of animal origins:

Other Theories:
I've cited two additional theories at the start of this answer (i.e., the Syncytial Theory and the Synzoospore Theory proposed by Mikhailov et al. (2009)1). For the sake of breviy, I will exclude further discussion of either theory here. Please feel free to visit my links/citations to learn more. I certaily encourage other users to provide answers describing such theories in more detail if they find doing so necessary and insightful for this post.
Regarding Microanimals
The term "microanimals" is simply referring to the size of the organism (i.e., that they need magnification for viewing) and not to any phylogenetic or evolutionary connection between these microscopic animals. Put differently, microscopic animals actually belong to a broad range of animal phyla -- in other words, they are not immediately related.

the Wikipedia post the OP links to (and the one I also link to in the preceding paragraph) lists, for example, microanimals from the phyla Arthropoda, Rotifera, and Loricifera.

Given this information, I strongly doubt you will find a theory suggesting that "microanimals" (as defined) played a role in the transition from protists to Animals.

1. Mikhailov, K.V., Konstantinova, A.V., Nikitin, M.A., Troshin, P.V., Rusin, L.Y., Lyubetsky, V.A., Panchin, Y.V., Mylnikov, A.P., Moroz, L.L., Kumar, S. and Aleoshin, V.V., 2009. The origin of Metazoa: a transition from temporal to spatial cell differentiation. Bioessays, 31(7), pp.758-768.
2. Starr, C., Taggart, R. and Evers, C., 2013. Biology: The unity and diversity of life. Cengage Learning.


text:
Is slow growth a virulence factor?
Many slow-growth pathogens (e.g. Mycobacterium tuberculosis, lentivirus, Rhabdovirus, Leptospira spp) are difficult to treat. In addition, a review of 61 pathogens found that

slower growing pathogens are significantly more virulent than faster growing pathogens

I was wondering why this may be the case. Is slow growth a virulence factor? How does slow growth benefit a pathogen?


text:
Correlation seen with low billirubin levels but not the gene that causes Gilbert's syndrome
I was reading the following study on associations between bilirubin and CAD (coronary artery disease). They looked at the bilirubin association, and the genes that cause Gilbert's syndrome, which increases bilirubin concentrations. Study here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2648823/
The study states in the abstract:

"Both polymorphisms showed a strong association with bilirubin levels with higher levels for homozygote carriers of the minor allele."

But then goes on to say, a few sentences later:

"Logistic regression analysis revealed low bilirubin levels but not the UGT1A1 polymorphisms to be significantly associated with CAD: OR (95%CI) 0.90 (0.86–0.94), p=2.6×10−6 for men and 0.77 (0.68–0.87), p=3.2×10−5 for women, respectively for each 0.1 mg/dl increase of bilirubin."

How can we see a "strong association" between the gene that causes gilberts sydrome and bilirubin levels but not see an associatoin between the gene and CAD risk? If the study is stating bilirubin is significantly associated with CAD risk, and the polymorphism is strongly associated with the level of bilirubin, shouldn't it follow that we would see an association between the polymorphism and CAD?
My guess is that polymorphism correlation to bilirubin levels isnt actually all that strong, or that the association between bilirubin and CAD isnt all that strong, or both. Hoping someone could offer some thoughts on what they think is going on.
Thanks!


text:
What is indirect vs direction selection of genes?
As the title suggests, what is the direct and indirect selection of genes. Couldn't find a straightforward answer. Is it the same as direct and indirect fitness?

Direct selection is when the fitness is directly associated with a certain gene. The beneficial alleles of this gene get selected.
When an allele gets selected not because of its direct effect on fitness but because of other reasons for e.g. strong linkage with other genes which in turn are being selected, then it is said to be undergoing indirect selection.
From Kirkpatrick and Barton (1997)

Female preferences have caused the evolution of extreme male mating
  displays throughout the animal kingdom (1–3). One mechanism that might
  establish these preferences is indirect selection, which occurs when
  preference genes are associated (that is, in linkage disequilibrium)
  with other genes that are spreading under selection. Indirect
  selection is invoked by two types of theories (2). The first are “good
  genes” theories, which interpret male mating displays as indicators of
  high viability. In this view, the expression of the male display is
  correlated with the presence of alleles that increase viability.
  Because associations naturally develop between preference genes and
  male trait genes, as the high viability alleles spread by natural
  selection, preference alleles for extreme displays also spread. The
  second class of theories that postulates indirect selection involves a
  “runaway process.” Here alleles that exaggerate a male mating display
  decrease survival but nevertheless spread because they enhance male
  mating success. Genes for extreme preferences can then be established
  as the result of their associations with these spreading male trait
  genes.


text:
Meiotic recombination hotspots
Im trying to find a proper and general file with chromosomal coordinates for meiotic recombination hotspots.
I know that ucsc hgtables, has a table with recombination regions and their recombination rate. However these regions are all 1Mb, and several articles states that these hotspots regions are more local with a regional length of 2Kb.
https://genome.ucsc.edu/cgi-bin/hgTables?hgsid=782680683_Cxp9zzjwgsql7P0T81FFyATyTNOl&clade=mammal&org=&db=hg19&hgta_group=map&hgta_track=recombRate&hgta_table=recombRate&hgta_regionType=range&position=&hgta_outputType=primaryTable&hgta_outFileName=
Do any of you know of a file or database containing the chromosome coordinates for humans which have been identified as a recombination hotspots?
Thanks a lot for your time and help.


text:
The emergence of Phengaris butterflies from ant nests
The butterflies of the Phengaris genus (also known as Maculinea) are known to be brood parasitic. During the fourth instar, the caterpillars leave their food plant and mimic ant larvae, causing the ants to take them back to their nest as if they were ant larvae that had escaped.
While in the nest, the caterpillars mimic ant larvae by means both of surface chemicals and acoustic mimickry (including, I understand it, mimicking sounds made by queens!) After pupating, the pupa continues to engage in acoustic mimickry, although I can't find any reference to whether it does (or even could!) engage in continued chemical mimickry.
But I can't find anything in the literature regarding the adult butterfly's emergence from the pupa and exit from the ant nest. A non-academic book and some web pages claim that the alcon blue (Phengaris alcon) and mountain alcon blue (Phengaris rebeli) adults are no longer engaged in any form of mimickry at this point, and may be attacked by the ants. These accounts differ as to how likely an attack is, how much danger the butterfly is in, and the level of protection afforded by the butterfly scales.
The webpages I mention belong to a University of Copenhagen researcher (Dr. David Nash) who has published work in this field. This suggests that the claim is probably correct.
That said, none of the peer-reviewed publications coauthored by him appear to mention it, and each of the two webpages creates a different impression as to the level of danger involved:
"If an ant tries to bite the butterfly it will only get a mouthful of scales." states one, suggesting that there is little the ants can do to harm or hinder the butterfly. But the other states "The adult has to get out of the ant nest quickly to prevent the ants killing it."
The book is written by someone else. It cites three papers, which do discuss the larvae/pupae and ants. But none of these have any information regarding this specific topic.
A paper by Elfferich provides some information in the case of Phengaris nausithous, the so-called "dusky large blue". The author states: "The butterflies always emerged between 00.00 and 06.00 and walked out of the nest ... During the night there was only a little ant activity and there was no real aggressive behaviour ... we may conclude that no pheromone to reduce aggression of the ants is produced by the butterfly."
Some published books (not from the academic literature) claim that the "large blue" (Phengaris arion) continues acoustical, and (according to one book) chemical mimickry. Far from being in danger, two of the books claim that they are escorted outside by ants as though they were acting as a bodyguard!
I believe that this is probably true. The reason for this is that two of the books (pub. 2008 and 2010 were describing discussions between the authors and Jeremy Thomas, an Oxford professor who has published research in this field. In fact, Professor Thomas's research identified the butterfly's dependence on ants, the reasons for its decline in the UK, and he was able to reintroduce the species after it became extinct in the UK. The other book (pub. 2014) mentioned Professor Thomas repeatedly, and described a book by him as "One of the essential wildlife books".
Even so, I don't have access to material in which Professor Thomas or any of his colleagues actually state this instead of just being mentioned by others. So it's still second hand information covering only one Phengaris species.
And to complicate matters further, in a paper that predates the three books, Thomas and other researchers stated that Phengaris arion and Phengaris teleius (scarce large blue) adults "show no interaction with ants after eclosion from pupae in the outer cells of Myrmica nests, from which they emerge while the ants are quiescent in the early morning".
Does anyone know of any peer-reviewed sources which confirm, for the various species, whether:

The adult butterfly continues to engage in mimickry?
Whether this is chemical, acoustic, or both?
The ants are more likely now to realise it's an intruder, and may attack it?
How likely this is?
How much danger are the butterflies in, if so?
Some accounts claim that the alcon/rebeli has scales which make it impossible for attacking ants to grasp them. Others refer to the scales protecting them from being bitten. If these attacks are a risk, how well is the butterfly protected and do attacks from angry ants still get through?

I've looked at too many papers to list here, but my sources include:
Non-paywalled:
Barbero F, Thomas JA, Bonelli S, Balletto E and Schönrogge K. (2009). Queen Ants Make Distinctive Sounds That Are Mimicked by a Butterfly Social Parasite. Science 06 Feb 2009: Vol. 323, Issue 5915, pp. 782-785. DOI: 10.1126/science.1163583
Thomas JA, Schönrogge K and Elmes GW. (2005). Specialization and host associations of social parasites of ants. In: Insect Evolutionary Ecology: Proceedings of the Royal Entomological Society's 22nd Symposium (Fellowes M.D.E., Holloway G.J. and Rolff J., Eds). 475–514
Als TD, Nash DR, and Boomsma JJ. (2001). Adoption of parasitic Maculinea alcon caterpillars (Lepidoptera : Lycaenidae) by three Myrmica ant species. Animal Behaviour, 62, 99-106. https://doi.org/10.1006/anbe.2001.1716
Akino T, Knapp JJ, Thomas JA and Elmes GW. (1999). Chemical mimicry and host specificity in the butterfly Maculinea rebeli, a social parasite of Myrmica ant colonies. 266 Proc. R. Soc. Lond. B. http://doi.org/10.1098/rspb.1999.0796
Elfferich NW. (1998). New facts on the life history of the dusky large blue Maculinea nausithous (Lepidoptera: Lycaenidae) obtained by breeding with Myrmica ants in plaster nests. DEINSEA 4: 97-102. ISSN 0923-9308
Paywalled:
Elmes GW, Thomas JA and Wardlaw JC. (1991). Larvae of Maculinea rebeli, a large‐blue butterfly and their Myrmica host ants: patterns of caterpillar growth and survival. Journal of Zoology, 224: 79-92. doi:10.1111/j.1469-7998.1991.tb04789.x
Elmes GW, Thomas JA and Wardlaw JC. (1991). Larvae of Maculinea rebeli, a large-blue butterfly, and their Myrmica host ants: wild adoption and behaviour in ant-nests. Journal of Zoology, 223: 447-460. doi:10.1111/j.1469-7998.1991.tb04775.x

One butterfly species at least, Liphyra brassolis, has been observed to use loose scales as a defence immediately after emerging from its chrysalis and while escaping the ant nest. See http://www.boic.org.au/files/Secrets%20of%20a%20Predatory%20butterfly.pdf and https://archive.org/details/butterflies02bingiala/page/456

I've been emailing some of the various researchers who worked on the papers I've cited. Jeremy Thomas and Judith Wardlaw both took time out of their (probably very busy!) schedules to reply, and they sent me very detailed replies as well as copies of papers I didn't have access to. Thanks to their replies, I'm in a position to post an answer to my own question.
Dr. Wardlaw, in the course of her research into the Phengaris rebeli (mountain alcon blue) species, had:

"looked after hundreds of rebeli caterpillars and reared them through pupation to adulthood. I watched their emergence from the ant nests in captivity where they were trapped in chambers together without means to escape. I also encountered many nests in the wild. In natural nests the caterpillars tend to crawl to upper chambers in preparation for pupation and eventual emergence and often these are narrow chambers which do not have huge numbers of workers in attendance. The ants do respond to the squeaks etc of the pupae and attend them; when emergence is imminent - much wriggling and increase in sounds emitted - my clear recollection is that the ants are almost stupefied and disperse away from the pupae - the emerging butterflies are not molested by the ants at all although they may revisit the pupal cases to lick any residual body fluids which may be ejected at the time of eclosion.  When they did encounter the emergent butterflies, I never witnessed any hostility shown to them so whether the scales act as protection or not, didn't seem to be an issue."

Professor Thomas had this to say regarding P. alcon, P. arion, and two non-Phengaris blues:

"The best and most natural film of the adult emergence in an ant nest is the Netflix film "From deserts to grasslands" in their 'Our Planet' series ... by David Attenborough (NB, some of the script they provided him with has minor inaccuracies so ignore the commentary: I was not shown the final script!). There's a sequence on Alcon large blues about 2/3 in. ... It shows the ants quite excited as the adult butterfly begins to break through the pupal case - but always benign and non-threatening - and then indifferent to it when it emerges and crawls to the surface to blow up wings, unaccompanied by ants. That's my observation of P. arion too (i.e. very different from Silver-studded blue which is tended throughout eclosion).   The behaviour with Large Blues is consistent with the possession of a stridulation organ on the pupal case, which produces sounds that mimic the queen ant's, and this will undoubtedly be broadcasting 'I belong here' sounds to the worker ants as the pupal case splits, but not thereafter. We have recordings of this from the Adonis Blue which has a similar organ to the large."

(The Silver-Studded Blue and Adonis Blue have mutualistic relationships with their ant hosts. They are not parasitic. I don't have Netflix so I can't provide a link to that video.)
In the case of Phengaris nausithous, note that the published research by Elfferich (which I quoted in my question) testifies to the same thing. There is no obvious defence mechanism on the newly emerged adult, but it isn't in any sort of danger from the ants, and doesn't need one. Note also the book quote in which Prof. Thomas states that the same is true for Phengaris teleius.
In a comment on my question, I mentioned Liphyra brassolis. This butterfly species also parasitises ants, and does rely on loose scales to defend itself from the ants after emerging. If you follow the PDF link in that comment, it includes photographs of the newly emerged butterfly with these scales. It also includes one photograph of an ant that has tried to attack the butterfly, and so become covered in scales as well.
Those scales are very conspicuous, both on the butterfly and the ant, and there was certainly nothing like them in any of the videos I saw of the Phengaris emergences:
"The Large Blue Butterfly Adopted By Ants" - BBC Earth. This one focuses on P. arion.
An extract from "Life in the Undergrowth", presented by David Attenborough.
Behind-the-scenes of the filming of ants-nest interiors for the Netflix "Our Planet".
I couldn't find a suitably licensed image of the L. brassolis covered in loose scales, so I can't include one in this answer. But as I say, you can just click on the PDF link to see it. In addition, there are some spectacular photos of the butterfly's underwings at:
https://the-butterfly675.blogspot.com/2009/05/another-re-discovery-for-singapore.html
https://www.ifoundbutterflies.org/sp/1094/Liphyra-brassolis
http://www.butterflycircle.com/checklist/showbutterfly/224
http://www.samuibutterflies.com/insects/butterflies/lycaenidae/liphyrabrassolisbrassolis/
The only credible evidence that the adult Phengaris are threatened by the ants is that one, unsupported statement on David Nash's University of Copenhagen webpage. I have emailed Dr. Nash, but have not received a reply. Nevertheless, I am convinced that the claim is not correct.
By contrast, we have a great deal of evidence that the various Phengaris species are not in any danger from the ants after emerging from their pupae, and neither have nor need a defence mechanism based on loose scales. I am confident enough in this that I am posting it as my answer.
As an aside, I also looked up the Ichneumon eumerus parasitoid wasp species, which lays its eggs in the caterpillars of P. rebeli (and maybe also P. alcon, I'm not sure.) After hatching and eating its pupated host from the inside, the adult wasp eventually emerges from the butterfly's chrysalis.
According to a 1993 paper (cited below), the emerging wasp is attacked by the ants! It emits an allomone which causes most of the ants to attack each other, but those closest to the wasp will still attack it. It relies on its armour plating to keep it safe from these as it leaves the nest.
The ants will later show some form of aggressive behaviour toward the empty chrysalis - something they don't do towards the ones that unparasitized butterflies emerge from.
Reference (paywalled):

Thomas JA and Elmes GW. (1993). Specialized searching and the hostile use of allomones by a parasitoid whose host, the butterfly Maculinea rebeli, inhabits ant nests. Animal Behaviour, Vol. 45, Issue 3, pp. 593-602. https://doi.org/10.1006/anbe.1993.1069


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How to choose an assay for detecting virulence factors?
When looking for a protein of interest, an ELISA is being administered. I read this article about the different types of ELISAs and the advantages/disadvantages.
However, I am conflicted about whether a sandwich ELISA or a direct ELISA would be best detecting a protein virulence factor in a serum sample. The thought behind the sandwich was the antigen would not need to be purified before measuring.
Any advice as to choosing an ELISA for the detection of a specific virulence protein?


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Genes where both a disabling mutation and copy number amplification cause different genetic diseases
I'm trying to make a list of such  genes, because they must be tightly regulated. MeCP2 is one - it causes Rett Syndrome with a disabling mutation, but causes MeCP2 duplication syndrome if its copy number has been increased. Anyone know of any others?

Must this list include only genes where both deletion and duplication have been shown to have disease phenotypes?  Can this list also include transcripts with dose-dependent pathologies?  i.e. genes for which deviations (both up- and down-regulation) from median expression are deleterious?

@Dirigible yes I think that would be interesting to know as well.


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What happens to embedded membrane proteins after a vesicle is formed?
When an animal cell is going through endocytosis it cell surrounds a food particle, and the membrane swallows it, creating a vesicle within the cell.
However, what happens to the embedded transmembrane proteins previously in the cell membrane? Do they shut down? Are they degraded? Or do they just not cause a problem that the cell just leaves them be?

Do you have a specific protein in mind? As @ScienceIsGolden points out in their answer, different proteins respond to this situation differently.

Endosome formation.
For the sake of keeping this somewhat brief, I'm going to stay somewhat surface level.
When a vesicle is endocytosed, it is called a primary endocytic vesicle.
When multiple primary endocytic vesicles fuse together, they form a larger entity called an early endosome.
Early endosomes can also be called "sorting endosomes" because different portions of the vesicle are sorted into different destinations, including these things called "recycling endosomes."
Transmembrane proteins in endosomes
In my experience, transmembrane proteins largely get sorted into these recycling endosomes and are then re-inserted into the cell membrane.
To my knowledge and from some cursory review on the topic, this is a common outcome for transmembrane proteins; they are eventually recycled and placed back into the cell membrane via exocytosis after being sorted into a recycling endosome.
Further reading
I'm sure others can add more explanation and some of the alternative routes these proteins can take, but in the interest of brevity and clarity, I thought it best to just stick with what I've come to know as most common.
Also, if you'd like a helpful source, see if you can get access to the following paper through a school or library service: Elkin, S. R., Lakoduk, A. M., & Schmid, S. L. (2016). Endocytic pathways and endosomal trafficking: a primer. Wiener Medizinische Wochenschrift, 166(7-8), 196-204.
In a phenomenon that I think is really cool, some receptors are thought to actually keep functioning after they are endocytosed and form these things called "signalling endosomes" (search "signalling endosomes NGF and TrkA" to read more).

Lovely answer. I've made some superficial edits to make it clearer, but feel free to roll back. Could you point me toward some article explaining the reinsertion process? As far as I am aware, unless it is a post-translationally inserted tail-anchored-TMP or a mitochondrial TMP, TMPs can only be inserted via the Sec61 translocon at the ER. I would be interested to learn more about how this mechanism works.

Hi James!  Thanks for the edits, definitely made the answer more digestible!  I tracked down an article that will hopefully get you the info you're looking for:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3038567/
The specific section to look at is "From the ERC to the plasma membrane."  This article and others point largely to the protein Arf6 for this process, but this specific paper does the most to explain its role in re-insertion.  Hope that helps!


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Why do archaea survive better in extremes than bacteria?
Why have bacteria not evolved to fill the extreme environments to the same extent as archaea?
What has enabled archaea to colonize these areas when bacteria do not?

Many bacterial phyla are thermophilic: Thermotoga, Geobacillus, Thermus, Deinococcus are some examples of note. There are many factors, such as S-layer coating, polyamines, thermostable enzymes, all well documented: please rephrase with specific aspect you are struggling to find. Thanks!

I suspect this falls under the no-homework policy, so I will not give a full answer, just lots of links to point in the right direction. A good reading material is the genome sequence papers, such as that for Methanopyrus kalderi.
The domain Archaea contains some of the most thermophilic organisms of this planet. Very thermophilic organisms are called hypethermophiles, but employ very much the same strategies.
Thermophilic bacteria
However, not all thermophiles are archaea, some notable bacteria phyla that are thermophilic are Thermotogae, Aquificae, Thermus-Deinococcus clade and some phyla have several thermophilic genera, such a Firmicutes with Geobacillus. Taq polymerase for PCR comes from Thermus aquaticus (its relative Deinococcus radidurans was nicknamed Conan the bacterium due to its radiation resistance, so is notable for other reasons), Thermotoga maritima was a subject of a structural genomics screen and is highly studied and Geobacillus is a treasure trove for biotech (see PubMed).
HGT
These bacteria share many genes with archaea by HGT.Thermotoga maritima shares 24% of its genes with archaea. So it is best to talk about thermophilicity in general.
Mesophilic archaea
Not all archaea are thermophilic. The methanogens, such as Methanobrevibacter, are mesophilic and actually a lot of research, such as vaccine and methane pathway antimetabolite development is ongoing.
Shell
Firstly, the cells do not need to burst. To do so they employ a shield of protein that pack in a crystalline lattice called the S-layer. Geobacillus a firmicute (i.e. monoderm with thick peptidoglycan) has it too despite the peptidoglycan.
Firmicute spores are annoyingly resistant as they contain dipicolinate. Geobacillus expecially so.
DNA
Secondly, the DNA must not denature. Archaea have high GC content, but the thermophilic bacteria generally don't, hence why biotech likes the latter more. A key feature is high levels of polyamines, which stabilise the phosphate groups.
Lipids
Archaea, but not bacteria, have a unique membrane composition, which is reviewed here.
Protein
Every protein has a melting point. The more contact it has the more stable it gets. These often require expensive to make amino acids. There are many analyses of amino acid composition of thermophiles in PubMed, but be warned that some papers suffer from bias from archaeal high GC.
Enzymes
Now, a thing to note is that an thermophile will do poorly at a lower one. This is because of enzyme kinetics and temperature dependence. Namely, the kcat and (less so) the kon and koff of the MM change with the Arrhenius equation in the transition state theory. In a more accurate model, it follows the Eyring equation. In actuality is even more complicated (and fascinating) and explained with the Macromolecular rate theory (and here) where the fluidity of the 3D structure of the protein plays a part. But in short, turnover (k_cat) and Michaelis constant (K_M) go up with temperature, while the former is good (faster), the latter is bad as it needs to be close to physiological substrate concentration. Going down in temperature, the enzyme will be slower, but will find its substrate.


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Why do muscle spindles send impulses at a constant rate when the muscle is at rest?
According to my book, the sensory neuron around the muscle spindle is sending impulses at a constant rate, while the entire muscle itself is relaxated (at rest).
So when the muscle stretches the impulse frequency gets higher, right?
According to the book, the reason why this 'constant rate frequency at rest' is happening is because otherwise the muscle spindle wouldn't been able to know the difference between a relaxed and contracted muscle.
I don't understand this reasoning, could anyone explain?


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Is there a nomenclature for human physiology?
Back when I studied botany in high school, the teacher taught us the nomenclature for botanical terms. I think there should be something similar for human physiology. Understanding how the name was formed helps a lot while reading about the human body. Can you please point me to any resources (books or websites) on this topic?

Hey yasouser, I’m not sure if this is the case, but I’m curious if you’re actually referring to etymology rather than nomenclature. Your point “Understanding how the name was formed helps...” makes it seem like that’s the case. If so, most medical terminology textbooks have this information on word roots, prefixes, etc. and might also delve into Latin origins (I can recommend some if I’ve understood your question correctly).

Yes etymology of the medical terminology is what I'm looking for. I used the term nomenclature because the names are formed with certain rules, right?

Des Moines University has an overview of medical terminology, for example:

Useful prefixes and suffixes
Word roots for organs
Some general terms
System-specific terms, for example, for circulatory system

The Free Dictionary has a Medical Dictionary, which shows results from various dictionaries with basic etymology included.
Etymonline is a detailed, general etymological dictionary, which includes a lot of medical terms.
Physiology as such may not have a lot of specific terms, but it is helpful to know basic anatomical and pathological terms when reading physiological texts.
Schulic Medicine & Dentistry has an one page glossary of ~400 medical terms.
BC Campus has basic anatomical terms with pictures on one page.

Thanks for the Des Moines University weblink. That's exactly what I was looking for.

The book I'm most familiar with is Medical Terminology: A Programmed Learning Approach to the Language of Health Care Second Edition by Marjorie Canfield Willis. This book is great for what you're looking for, and I believe you can get the 2nd edition pretty cheap from multiple vendors.


text:
Effect of ethanol on TRizol RNA extraction
I added ethanol instead of chloroform to the cell suspension in Trizol. Can I still obtain my aqueous phase?

How much ethanol did you add?

I added 100 uL of etanol

To which amount of sample?

to 500 uL of cell suspension in Trizol

@polonio210 Can you edit that information in the comments into the body of your question?

My answer is based on my experience in the lab and something like a best guess - it may or may not work. But given the fact that added 100µl of ethanol to 500µl of total volume and since water and ethanol mix completely, I would give it a shot.
I don't think that the ethanol would change the polarity of the solution so much that phase separation is inhibited. The only thing that I can image is the contamination of the aqueous phase with traces of phenol, so I would probably clean up more carefully and do an additional NaOAC/ethanol precipitation at the end of the procedure. If you expect a small pellet with little nucleic acids, add some glycogen to get a better outcome there. I would appreciate it, if you could comment on your experience (and the outcome) when you try to save you sample.

Thanks Chris, Oh yes, I will let you know!


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How does SDS-PAGE separate based on mass?
In SDS-PAGE, electric field and mass-to-charge ratio are approximated to be constant for all proteins. Also, if $F=qE =ma$, then $\frac{m}{q}a=E$.
Thus, all proteins must migrate with a constant acceleration.
So what is the driving force in SDS-PAGE that resolves proteins of different mass? Is it that bigger proteins have a larger size and thus experience larger friction force from the gel sieves? But even if that was true the larger proteins feeling larger resistance forces should be counteracted by their larger migrating force from increased total charge.
Would appreciate if someone could clear up this confusion. Thank you.

Please define the terms in your equations (and set them on a separate line for clarity).

You are correct that molecule mobility depends on the mass-to-charge ratio, and this means that different sized molecules with the same $\frac{m}{q}$ will have the same acceleration.  However, the velocity of a molecule moving through a gel matrix depends on the point at which the force exerted by the electric field is in equilibrium with the frictional forces acting on the molecule.  Modeling different sized molecules as spheres of different sizes, we can apply Stokes' Law:
$$F = 6\pi \mu Rv$$
where $\mu$ is viscosity of the matrix (constant), $R$ is the radius of our molecule, and $v$ is the flow velocity. Rewriting your equation, we see that
$$F = qE = ma = 6\pi \mu Rv$$
and
$$v = \frac {ma}{6\pi \mu R}$$
For constant $a$ and $\mu$, velocity varies with the ratio of mass to radius
$$v \sim \frac{m}{R}$$
Assuming uniform density ($d = \frac{m}{V}$), the radii of our model spheres scales cubically with their mass ($V = \frac{4}{3}\pi R^3$), meaning that $\frac{m}{R}$ decreases as molecule size increases.
So, larger molecules will reach force equilibrium with the opposing frictional resistance at a lower velocity compared to smaller molecules, thus explaining how different sized molecules with the same $\frac{m}{q}$ will separate on a gel.  One caveat to this explanation is that polypeptides and nucleic acids are poorly modeled by spheres, and that the mass of such molecules scales linearly with length.


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Could biofilms float and survive in the sulfuric acid clouds of Venus?
The atmosphere of Venus is composed of 96.5% carbon dioxide, 3.5% nitrogen, and traces of other gases, most notably sulfur dioxide.
The main cloud deck is located in the 48-70 km altitude range and is composed mainly (75-96%) of sulfuric acid droplets, with a temperature of 27$⁰$C and a pressure of 0.53 atm at 55 km.
But to put the acidity into perspective, the mass loading of the droplets is 10 mg/m$³$, while the density of CO$_2$ at that altitude is about 950 g/m$³$.
Despite these harsh conditions for life, could biofilms float and survive there when certain bacteria species producing hydrogen could live within them ?
Nostoc commune for instance,is a  colonial species of cyanobacterium which forms a gelatinous mass for protection and can withstand acidic exposure and other extreme conditions like desiccation and high and low temperatures.
In addition the cells contain pigments that absorb ultraviolet radiation, which enables it to survive high levels of it, and in some cells nitrogen-fixing occurs.
There are also bacteria, like Enterobacter aerogenis, which produce hydrogen, and when it could live inside the gelatinous mass it could provide  the necessary buoyancy to float within the clouds of Venus.
Assuming the biofilms could be provided with the necessary trace elements, could they be airtight to some degree, to even float in the air with gas vesicles for buoyancy ?

potentially of interest Is it known how some heat-resistance Bacillus spores repair their DNA after having been heated to 420 °C?

I have pondered life on Venus.  I think the biggest problem would be lack of free water.  The atmosphere is thick and under high pressure, and polar CO2 and H2SO4 like to bind with water.  There is no water there.  Mass action would pull water out of any concentration of water (like a Nostoc blob) and into the waterless density of the adjacent atmosphere.  It would be like putting a Nostoc in a tub of salt grains.
Dessication would be the biggest problem.  The other problem related to lack of water is its requirement for photosynthesis.  If you had a photosynthetic organism there would be CO2 in abundance, but green algae type  photosynthesis also requires water as a raw material:  CO2+H2O+ light -> O2 + CHO (carbohydrate).  If you have only the water you brought with to Venus, with no prospects of replenishing it, you will run out quick.
You would need an organism that is not only durable, but had the metabolic chops to either pry H2O off of H2SO4 or use sulfur as its reducing agent instead of water.  Purple sulfur bacteria can do sulfur chemistry like this but they like starting with reduced sulfur, not H2SO4.  Purple sulfur bacteria need water as a solvent inside the cells just like we do.  But maybe something that can handle H2SO4 can make water out of it also?

Although not much, there's some water in the atmosphere of Venus, 20 ppm, and the acidic droplets contain up to 25% water. Indeed, dessication would still be a big problem, but the main question for me is if a biofilm could really float in the atmosphere with hydrogen producing bacteria within it ?

@Conelisinspace - such a feat would be easier on Venus than Earth.  CO2 is a big molecule and atmospheric pressure aside, CO2 is denser than our N2+O2 atmosphere.  If a critter could produce an H2 bubble inside its shell (made of elemental polymeric sulfur?) it might be buoyant enough to float!  We are converging on WorldBuilding Stack here which suits me fine.

Where, I might add, your speculations would get a lot more enthusiasm than is apparently the case on Biology stack.

Lucky me that you appear enthusiastic enough ! It could be that my speculations could already have been tried out in the laboratory, i like to know if it's really possible.  So there are bacteria that produce hydrogen from glucose, so there have to be also cyanobacteria to nourish them. Now i think about aerogels ( https://en.wikipedia.org/wiki/Aerogel ) to hold the different bacteria species and the necessary trace elements and the produced hydrogen , be made airtight  outside with the extracellular, acid, sulphated polysaccharides.


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What's the transposon difference between chimps and humans?
I was reading that humans and chimps share 98-99% of the same DNA sequence but I also read humans and chimps only share around 20% of the same proteins. Also, 45% of the human genome is transposable elements, It's 42% reverse transposons and 3% DNA transposons.
So, I wanted to know the difference between humans and chimps when it comes to transposable elements, especially reverse transposons.
Sources added:
Eighty percent of proteins are different between humans and chimpanzees. ncbi.nlm.nih.gov/pubmed/15716009 and Retrotransposons - In mammals, almost half the genome (45% to 48%) is transposons or remnants of transposons. Around 42% of the human genome is made up of retrotransposons, while DNA transposons account for about 2–3%.[3] [en.wikipedia.org/wiki/Retrotransposon]2

Do you have a source for your numbers?

Sorry, I didn't include the sources. Eighty percent of proteins are different between humans and chimpanzees. https://www.ncbi.nlm.nih.gov/pubmed/15716009 and Retrotransposons -  In mammals, almost half the genome (45% to 48%) is transposons or remnants of transposons. Around 42% of the human genome is made up of retrotransposons, while DNA transposons account for about 2–3%.[3] https://en.wikipedia.org/wiki/Retrotransposon

Note, saying "humans and chimps only share around 20% of the same proteins" is not quite right, the source you cite actually says that only 20% of proteins are absolutely identical - the remaining 80% are very similar, but have slight differences (based on the 1-2% difference in DNA sequence)


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What fills the space between the alveoli in the lungs?
Do the lungs just consist of a large tree of alveoli, covered by the pleura, like this picture:

Or are they found "inside" the sac that is the lungs? If it's the later, what fills the space in-between the alveoli and forms the walls of the lung?

Alveolar tree is like a bunch of grapes. If you put a bunch of grapes into a plastic bag and put this bag into another bag, you can imagine how the lungs are covered.
Alveoli form the surface of the lungs. There is a membrane called visceral (or pulmonary) pleura that covers the alveoli and this membrane continues into another sheet called parietal (or thoracic) pleura that covers the inner side of the thoracic wall. The space between the membranes is called pleural space.
Here you can see how visceral pleura continues into parietal pleura:

Picture 1. Pleural space (source: sdstate.edu)

Picture 2. from page 1117 of "Cunningham's Text-book of anatomy" (1914) (source: Flickr)

Oh, so aside from the pleura, there is nothing else covering/containing the alveoli? It's just alveoli that are then immediately covered by the visceral pleura?

@Dahen Yes, alveoli are immediately covered by the visceral pleura. The image you pasted may mislead you into thinking that alveoli are very individual and scattered, but they are actually packed together and form a smooth surface similar to the liver (see the real lungs without pleura).

One nitpick. I usually encourage students not to think of a pleural sac as a bag containing a lung, but rather a bag containing the pleural fluid, which is smashed in between the lung on one side and the chest wall on the other. The part of the bag that touches the chest wall is parietal. The part that touches the lung parenchyma is visceral. Using the bag of grapes analogy, you'd put water in the bag, then press the bag up against the grapes without ever putting the grapes inside the bag.

That does make it easier to visualize, thanks!

I agree with Jan's answer generally, but thought I'd clarify a few points.
What fills the space between the alveoli in the lungs?
As Jan says, alveoli are packed together. In most cases, the thing next to any particular alveolus is another alveolus. In this case, the space between them is the alveolar wall, which (generally) consists of a pneumocyte and capillary (endothelial cell) with a shared basement membrane. You can see this in the following slide from Yale.

Alveolar sacs can abut other elements of lung parenchyma, including bronchioles, smooth muscle, nerves, and pleura. In this figure from Ross Histology, Ch. 19, you can see an alveolar sac adjacent to visceral pleura.

The relationship between lung parenchyma and pleural sac
I would encourage you to not think of the visceral and parietal pleura as two different bags, both of which contain the lung parenchyma (bag in a bag analogy). There is only one bag (per lung), and the only thing inside of it is the pleural fluid. The alveoli and associated parenchymal tissues are on the outside of the pleural sac just as much as the chest wall. They are just on opposite sides of the sac. This ubiquitous figure illustrates the relationship. The fist represents a lung, the ballon represents the pleura.


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When comparing oral infection v IV infection in mice, why would the CFU given be different volumes?
In the paper, orally infected mice are given 1x10^9 CFU of C. Rodentium and IV infected mice are given 5x10^7 CFU of the pathogen. Does anyone know if there is a generic reason for this? Thanks in advance.,

Intravenous delivery of pathogen produces infection more efficiently than transmucosal delivery.
10^7 is 2 orders of magnitude less than 10^9.  It is not the volume that is different (although it may be), it is CFUs or "colony forming units" which is a proxy for viable pathogens in the inoculum.  The oral dose is 100x that of the IV.
Getting germs directly into the bloodstream bypasses the built in protections that our mucosal surfaces have.  The GI and GU tract have a lot of defenses.   For example an experimental SIV infection produced intravenously in monkeys requires an order of magnitude less virus than an infection established rectally or vaginally.
I would suspect that the CFUs of a given pathogen via a given route is something established empirically as producing the desired outcome.  If you used the same CFUs for an IV route as were required for the oral route, you might have a fair number of mice that just died from septic shock from the huge number of bacteria suddenly in the blood.  Given the 2 order of magnitude difference of inoculum (IV vs PO) to produce infection you might conclude that the stomach kills 99% of any inoculum.

Thanks that's really helpful and makes sense!


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In DNA replication, are there phosphodiester bonds in the primer ? between the RNA nucleotides before being replaced
When hydrogen bonds happen between the RNA nucleotide bases and the DNA bases , do phosphodiester bonds form between the RNA nucleotides in the primer ?
No source I read is clear about this, are their bonds between the RNA nucleotides ?

@Dirigible — I suspect that the poster is talking about Okazaki fragments, and wishes to know whether they are covalently linked to the growing DNA. If so, I seem to recall a similar question previously. However the question is unclear. Poster, please clarify your question and preferably present a diagram, or link to one, so we can see what aspect seems unclear to you. The accompanying text would help — it could be that rather than the texts being unclear, there is something in the explanation you are misunderstanding.

I have posted an answer. However, this seems like a basic question and is easily answered by consulting sources such as Wikipedia. As such I'm flagging this question as "homework" since it "addresses a basic biology concept that may seem trivial to biology professionals". ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

A primer is by definition a short single strand of nucleic acid (i.e. a series of nucleotides linked together by phosphodiester bonds). See also this wikipedia article.