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Is it possible for someone to be of no race?
I apologize if this is not the right forum to ask this question, but I don't know of any better forum to ask it. It is certainly possible for someone to have no religion, but is it possible to be of no race? That is, do "a-racial" people exist?

Race as we think about it today is entirely a social construct, developed to support and validate European colonialists' ideas and actions, and which has supported the very real experiences of race and racism to this day. The American Association of Physical Anthropologists' statement on Race and Racism, specifically the executive summary, puts it very well:

Race does not provide an accurate representation of human biological
variation. It was never accurate in the past, and it remains
inaccurate when referencing contemporary human populations. Humans are
not divided biologically into distinct continental types or racial
genetic clusters. Instead, the Western concept of race must be
understood as a classification system that emerged from, and in
support of, European colonialism, oppression, and discrimination. It
thus does not have its roots in biological reality, but in policies of
discrimination. Because of that, over the last five centuries, race
has become a social reality that structures societies and how we
experience the world. In this regard, race is real, as is racism, and
both have real biological consequences.
Humans share the vast majority (99.9%) of our DNA in common.
Individuals nevertheless exhibit substantial genetic and phenotypic
variability. Genome/environment interactions, local and regional
biological changes through time, and genetic exchange among
populations have produced the biological diversity we see in humans
today. Notably, variants are not distributed across our species in a
manner that maps clearly onto socially-recognized racial groups. This
is true even for aspects of human variation that we frequently
emphasize in discussions of race, such as facial features, skin color
and hair type. No group of people is, or ever has been, biologically
homogeneous or “pure.” Furthermore, human populations are not — and
never have been — biologically discrete, truly isolated, or fixed.
While race does not accurately represent the patterns of human
biological diversity, an abundance of scientific research demonstrates
that racism, prejudice against someone because of their race and a
belief in the inherent superiority and inferiority of different racial
groups, affects our biology, health, and well-being. This means that
race, while not a scientifically accurate biological concept, can have
important biological consequences because of the effects of racism.
The belief in races as a natural aspect of human biology and the
institutional and structural inequities (racism) that have emerged in
tandem with such beliefs in European colonial contexts are among the most
damaging elements in human societies.

Race, as a social construct and means for prejudice and oppression, is very real. However, biologically speaking, there is no such thing as race.

Race is partially a man made concept. The only scientific base for this term is genetic similarities among people of some race but they are just a result of very remote family relations. So the "a-racial" person and all his remote family members will be considered as part of one race until you reach other remote family members who are considered as part of another race.

This is a reasonable answer, but it is encouraged to provide sources or illustrative evidence.

I would instead write that race is a wholly man-made concept, given the lack of any scientific definition for a given race.

We can scientifically determine if someone is of African(sub-saharan African) origin or European(white) so we can't say it is wholly man-made. Saying that the idea of race was made up by European colonialists to validate their actions is just wrong and actually sound overly politically correct. The man-made part is how many people tend to define race by physical appearance alone, especially when it comes to skin color.

All concepts are made up by humans. The idea that colonists used race to justify their attitudes is not wrong historically, but it is irrelevant when we discuss biology. What matters is that the term race is so overloaded and compromised, that every time biologists discuss anything related,  they prefer to use less confusing terms, like genetic profile. Thus the questions that refer to just race sound either vague or provocative, at least in the West.

@Eleanor the problem is, we can't "scientifically determine" if someone is sub-Saharan African, for example. There is no one gene variant that is shared among all Africans. From my answer: "variants are not distributed across our species in a manner that maps clearly onto socially-recognized racial groups." "Dark skin" is not a clear phenotype, because not all sub-Saharan Africans have dark skin, and you can find quite dark skin in many other places on Earth. And where do you draw the line between light and dark? Race as a biological concept just doesn't make sense.

@MattDMo you say that there are no detectable genetic similarities among sub-saharan africans and other races?. There are many studies that tested the dna of old human remains and managed to find their origins/race. I don't think anyone consider all people with dark skin as one race and there are obvious differences in appearance between black Africans and non-African people with black skin.

@MattDMo I don’t disagree with your overall point but your statement is basically incorrect - it certainly is possible to tell whether someone is from sub-Saharan Africa just by genetics and with a very high degree of accuracy.


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Is the famous singer Taylor Swift currently the most beautiful woman in the world?
Is Ms. Taylor Swift currently the most beautiful woman in the world? Is she even in the top 10 or even the top 100? And if not, who is currently the most beautiful woman in the world? I apologize if this question may seem stupid, but I believe it is on-topic because sexual attractiveness in animal species, including humans, falls within the province of biology.

No. She is not. I never knew who she was, but I looked on Google Images. I live in Russia and see women more beautiful than she in the street every day.

Remember the old saying about beauty being in the eye of the beholder?  Different cultures, and different individuals within cultures, have very different ideas of what constitutes beauty.  Consider the (IMHO overweight and flabby) "beauties" portrayed by Renaissance painters, for instance, or the apparently commonplace "butt enhancement" often reported in the news (when it goes wrong).
From a quick glance at Google Images, Ms. Swift is, to me, no more than moderately attractive.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Are microsatellites viable markers for GWAS?
I'm just reading some papers on genome-wide association studies and find that most of them use SNPs as a marker. I understand that they're the most polymorphic and thus the best for accurate correlations, but would microsatellites provide another viable method to check for genetic correlation?
They're highly polymorphic and small enough to showcase differences, while maybe allowing for more statistical significance.

Microsatellites could be used for GWAS. Actually they were the basis for linkage studies and were also used in the first association studies. The main reason why they have been replaced by SNPs is that in the human (or other organims') genome, there are by far more SNPs than microsatellites.
GWAS rely on linkage disequilibrium between the marker and the real causal variant. LD decreases quite fast with distance, thus, the more markers you use, the more likely you are to genotype a marker in LD with the causal variant. In the end, I would strongly recommend to use SNPs to perform GWAS.

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


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Can Wasps smell fear?
There are two conflicting things I have heard. One more anecdotal:

Wasps can smell when you are afraid of them

The other from reading popular science magacines:

Humans don't produce any pheromones

As far as I know, a pheromone is a smell produced to communicate with members of your own, but also other species. From my understanding these two statements are mutually exclusive.
So: Can wasps smell if a human is afraid?
Any answer with sources is appreciated.

If anyone with enough reputation would be so kind to create a [pheromones] tag, that would be great ;)

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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How do photoreceptors overcome the ambiguity of wavelength vs intensity to determine brightness?
I asked a similar question about the Principle of Univariance yesterday, but now I have another one.
According to the Principle of Univariance, the input to a photoreceptor differs along two dimensions (wavelength and intensity) but the output can only vary along one dimension (the cell's graded potential).
This means that there is inherent ambiguity in the output of the photoreceptor. What I do not understand then is how it is possible for a rod (or cone) to ever distinguish between intensities (or wavelengths) when each photopigment can absorb a range of wavelengths at different probabilities.
For example, say a rod cell absorbs $50\%$ of all photons at wavelength $x$ and $25\%$ at wavelength $y$.
If 100 photons reach the rod cell at wavelength $x$ we can roughly assume that $100*0.5=50$ isomerizations will occur. Equally, if 200 photons reach the rod cell at wavelength $y$ then we can roughly assume that $200*0.25=50$ isomerizations will also occur. From the perspective of the cell's synaptic activity, the two responses will be the same despite the large difference in intensity.
Clearly there are an infinite number of permutations to this basic pattern. It is thus unclear to me how the visual system is able to obtain any information about the intensity of light in rod cells.
The same issue also appears present to me in cone cells (the usual explanation is that the relative amount of excitation/inhibition can be compared between cone cells, but this does not seem to solve my overall question).


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Help in identifying an unknown Golden Worm/Larvae
Can anyone help me to recognize this type of species? Is it a clustered worms or clustered larvae? Location is in Bali, Indonesia. Recently this species is goes viral, but people here always link this species to a myth.
Thanks.

These are larvae of the so called fungus gnat of the order Diptera. Fungus gnats are small flying insects that look sort of like mosquitoes but they don’t bite. In fact, adult fungus gnats live only about 7-10 days and do not feed. It is the immature larval form that can cause damage to your plants.

Source: https://www.projectnoah.org/spottings/30766835/fullscreen
I see, i'm Balinese too, you know everything things were rare are linked to myth.

Welcome to SE Biology. It seems like you have identified the species but we prefer these answer to include a link and/or some photos that confirm the identification. You can edit the question to include these.

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


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Cell-level selection and inheritance of acquired mutations
I was reading about different levels of selection in Ridley's Evolution textbook (chapter on units of evolution) and saw that some organisms e.g. carrots are not Weismannist i.e. don't have separate somatic and germ lines and can make offspring with their somatic cells, and that this can in theory lead to cell-level selection because cell lines that outcompete others have a greater chance of leading to offspring and thus will be selected for. I think mutation that arises in a cell during the organism's lifetime and causes it to proliferate counts as an acquired mutation, but I've also read a lot that acquired mutations/characters aren't passed on a la Lamarck.
Is this a case where acquired mutations are passed on, and how does that fit with the usual concept that acquired characters aren't passed on? I know gene, individual, and kin selection are much more prevalent and Ridley says the cell-line selection idea is just theoretical, but what would this mean if it occurred?
Thanks :)

The first answer is correct - it resolves what you consider to be the Lamarckian dilemma. Is this a case where acquired mutations are passed on? Yes. Even in humans, in the germline, mutations accumulate slowly (or acquire mutations). This is not Lamarckian selection, however. There is no selection operating here.

In any reproductive event, we transmit new mutations to the offspring. In absence of cell-line selection, whether the mutation occurred during a meiosis or a mitosis is of little interest.
In absence of cell-line selection
A big difference between acquired mutations and Lamarck's acquired inheritance is that under Lamarck's view point, characters are being adaptive. Under Lamarck's view point, individual try to perform some action, stretch their muscles and other organs toward what is optimal for their needs and this phenotypic modification is being transmitted. The classical example is the example of giraffes. Giraffes stretch their neck trying to reach for high leaves, their neck is getting longer and their longer neck is being transmitted to their babies.
With acquired mutations, in absence of cell-line selection, there is no reason for adaptive mutations to be transmitted more often than non-adaptive one.
With cell-line selection
Now, if there is cell-line selection, beneficial mutations (beneficial at the cell level) are more often transmitted. The mutational process itself stil remain "random" (see Are mutations random?) but selection will increase the ratio of beneficial to deleterious mutations. Now, mutations that are beneficial at the cell level are not necessarily beneficial at the organism level. A typical example is cancer.


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Should I use glycogen in isopropanol to precipitate RNA or does glycogen have harmful consequences on downstream protocols such as RNA seq?
I have heard that one can use glycogen in isopropanol to better visualise the RNA pellet after centrifugation. What are the advantages and disadvantages of adding glycogen in isopropanol for RNA quality and quantity?


text:
At what g force do bacteria start to pellet down a tube?
I am working with C. elegans and bacteria and I want to get rid of the bacteria they eat by centrifuging the worms without centrifuging the bacteria. I am using a g-force of 600 and the bacteria sometimes still centrifuge down. What g-force would be ideal to pellet the worms but not the bacteria? Does this depend on the bacterial species?

Have you tried using Ficoll to separate them?

no, how does it work? The wikipedia page mentions its use for blood cells separation.


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Snail species identification from the United Kingdom
Can anybody identify the species of this snail?
From this website, it looks like a Common Snail.
Could it be the dextral type of Cornu aspersum?
These snails have been found in a garden, have survived a month on lettuce in a home environment, retreat in their shell sometimes. Their shell measures about 2 cm diameter.

To me it look like that your guess is correct, but I'm not an expert.

This snail is Cornu aspersum its common name is garden snail, it belongs to Helicidae family click here for more information

Given that the OP thought this was the correct species but was unsure, good answers to this question should explicitly describe the characteristics or evidence that support that this is in fact the correct ID. Please [edit] your post to provide explicitly-stated evidence for why your ID is correct. Thank you.


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Is DNase treatment necessary before RNA sequencing?
Is it necessary to treat total RNA with DNase before sequencing it? In particular, if the library prep relies on a poly-A enrichment, is it necessary to remove DNA, knowing that genomic DNA does not have as much polyA as mRNA?


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Can lysozyme also lyse gram-negative bacteria and if yes, how fast?
Lysozyme attacks peptidoglycan, which are found in Gram-positive bacteria. I know someone who uses lysozyme to lyse Escherichia coli, which is Gram-negative. How is that possible? Can lysozyme lyse all bacteria, independently of their Gram status? Does anybody have information on how long I should leave lysozyme in a bacterial solution for it to be effective?

Gram-negative bacteria also have peptidoglycan which can be degraded by lysozyme. However they have an outer membrane lying outside the peptidoglycan layer and this will block lysozyme action.
Because of this if you intend to treat Gram-negative bacteria with lysozyme it is necessary to add something that will disrupt the outer membrane—the usual choice is EDTA since removal of magnesium ions by chelation will destabilise the outer membrane.

Do you know what concentration of EDTA and lisozyme would be ideal for killing the bacteria?

I've heard that lysozyme can, even in vivo, attack gram-negative bacteria through some alternative mechanism possibly unrelated to attacking peptidoglycan.

@charlesdarwin Published protocols tend to focus on using EDTA/lysozyme treatment to prepare spheroplasts rather than killing. See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4223228/ for an example. Note that the authors add sucrose to prevent the cells from lysing i.e. as an osmoprotectant.  Their report indicates that rather short treatments (5 min) are enough to form spheroplasts: in the absence of sucrose these cells would have lysed.

Do you know what they mean by '125 mM EDTA-NaOH'? Is it 125 mM EDTA and 125 mM NaOH?

Also, do you think that the bacterial proteins will be denatured after the lysis of the bacterial cell membrane?


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What is this angiosperm from Morocco?
What is this species of angiosperm? It's got succulent stems and leaves that do not produce latex. Photographed in spring.

It is a species of Carpobrotus, probably Carpobrotus edulis. However, after looking online, several of the Carpobrotus species look very similar. It is an invasive species in the Mediterranean region. See the Wikipedia link.
https://en.wikipedia.org/wiki/Carpobrotus#Species


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What is this plant from Morocco?
The plant was photographed in spring in Morocco. It's an angiosperm. It is about 2 metres high and has feathered fruits. What species is it?

Looks like Nerium oleander based on the leaves and the seeds/pod.  If not that species, certainly in the genus.  This is a common landscape plant in arid environments, and native to your area according to Wikipedia.  It contains extremely toxic substances that affect the heart, called cardiac glycosides.  Consuming these substances, which are found in the white latex, causes the heart to beat itself to death.

I once heard an anecdote telling that soldiers in Napoleon's army invading Spain got poisoned using this plant to make skewers.


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Can someone identify the species of this angiosperm?
It seems to be from the pea family (Fabaceae) due to the zygomorphic flowers and the pods. It also has stipules at the base of the composite leaves. It's quite high (~ 80 cm). Photographed in spring in Morocco. It was photographed in a dry riverbed.

This is a difficult one to identify down to the species from the photos. It very much looks like a member of the genus Ononis in the pea family. The leaves, flowers, and seed pods are all characteristic of Ononis. It might be Ononis spinosa, but that is a guess.  The bright sunlight make it difficult to discern many morphological details. I can't see any visible spines on the plant to be certain. Links provided:
https://en.wikipedia.org/wiki/Ononis
https://en.wikipedia.org/wiki/Ononis_spinosa


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Why do we anthromorphize evolution and genes and nature?
Books sometimes says things "Our genes want us to have as many children as possible", or "Evolution
wants the fittest to survive". But genes are not conscious entities who can want things. So, why do we anthromorphize genes, evolution, and nature? I apologize if this question is not appropriate for this stack exchange. Perhaps it can be moved to an appropriate stack exchange if it is.

I’m voting to close this question because it is off-topic for this site. This question is about language or possibly psychology rather than about biology. It also seems likely to generate opinions rather than answers based on facts.

Then, can it be moved to psychology stack exchange?

Teachers often use metaphors or other story-telling devices to explain abstract concepts in more familiar terms to help information land with a broad audience. It's common in other natural sciences like chemistry, physics, and even mathematics. Maybe try asking https://academia.stackexchange.com

Things we can't see but want to believe in often are described using metaphors for things we can see and understand. Computers are a good example; they're new so they're entirely metaphoric: file, key, screen, message, program, ... are all metaphors of humans, things humans make and use, and the functions humans use them for. Metaphors are pretty much all we've got -- read Lakoff and Johnson and consider the alternative.

Just to help OP out, this is related to a really interesting concept called agential thinking in evolutionary biology. It can sometimes be a surprisingly valid and helpful metaphorical heuristic, and sometimes deeply misleading. A great book on the topic is Agents and Goals in Evolution by Samir Okasha


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When does a fetus become conscious?
I thought of asking this question in the Psychology & Neuroscience stack exchange, but I ultimately decided this would be a better stack exchange for it. When do the "lights turn on" in a fetus, that is, when does it come into existence as a conscious being? I have heard stories of people remembering things while in their mother's womb, so presumably they were conscious of it, even if very faintly. So, does consciousness begin at birth, or before, and if so, how much before? I have heard that brain activity happens in the fetus some weeks after conception, so does that mean it is conscious then, however dimly?

Which of the many extant definitions of consciousness are you referring to? Even legal definitions vary with jurisdiction. Can you edit to be specific.

Sometimes I think back on how I perceived certain things as a child and think that I was perhaps barely even conscious then. One issue is that your question seems to be associating memory with consciousness. Just because I don't remember eating breakfast last week doesn't mean I wasn't conscious then. Perhaps I wasn't. Who knows? I can't remember after all.

@JiminyCricket I am defining consciousness as the capacity to experience anything, be it a sight, or a sound, or a touch, or some other sensation.

A bacterium can respond to the chemicals.  Is that not consciousness by your definition?

By that definition, the gametes are conscious before they even meet, so prior to conception presumably.

Probably need to start over at Philosophy to ask if consciousness exists. Your definition is insufficient at best. What does it mean to "experience" something? Is it merely sensing of one's environment? Does a plant sensing and responding to stimuli exhibit consciousness? Maybe. Is "brain activity" pre-requisite to experience? Is a cultured synapse firing in a petri dish conscious?

Basically, the upshot is that it seems biologists don't have the foggiest idea when anything becomes conscious.  There are still arguments about whether various animals are conscious - and I mean things like fish or insects, not microbes or other things that don't have an obvious nervous system.

It might work here if you change the parameters of the question a bit. Were you to ask what the developmental milestones are which mark a qualitative and/or quantitative increase in awareness or neural activity... You'd need to specify an end-date as of course it continues into adulthood - and at a range of different timescales per individual. Of course, you'd need to show prior research as per the [help]'s [ask] section. I'm sure you could get a fairly comprehensive and factual answer then, without all the equivocation about definitions.


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What do we know about the cellular structure, processes, environment, and immediate ancestors of the last universal common ancestor (LUCA)?
I am up for all scientifically sound speculations, and sources are highly welcome. I've looked into this quite a bit myself via scholar.google, the wiki article, and /r/askscience.
I'm really looking for more speculation about physical details of the organism, its environment, and its immediate ancestors.
e.g. How did they (referring to the LUCA and some immediate ancestors) acquire nutrients? What forms of mobility were available to them? How long was it until photosynthesizing organisms emerged?
mods: If this is too open-ended or too speculative, please let me know where I can redirect this question.

As far as I have read LUCA is just predicted to have certain characteristics. It is not physically found. You can have a look at this paper. It is about energy metabolism in LUCA.


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Viability of argon-oxygen atmosphere
Can humans breathe an Argon-Oxygen atmosphere, where Argon substitutes the inert Nitrogen gas which currently populates our atmosphere? I didn't quite know which forum to stick this one in; I put it here because I only want to know if such a mixture of gases can be feasibly inhaled, without the prospect of early death by some physiological component.


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Why are insects unafraid when you tap at them from the other side of glass?
In the summer months we frequently try and kill mosquitos in our home. They are tremendously skittish and get airborne pretty quickly as you approach them. However, if they land on a piece of glass (a window for example) they don't seem at all bothered at you approaching from the other side and tapping the glass where they have landed.
Is this some strange physiology of insects (or at least mosquitos) that they cannot look down? Is it that their eyes function differently to our eyes and cannot see through the glass? For sure, their brains cannot be  developed enough to understand the safety afforded by the glass.

Since insect brains do not contain enough neurons for higher level emotions such as fear, much of their behavior is programmed and reflexive. When you approach them, they have evolved to fly away. Glass, on the other hand is not something they evolved to "understand". They likely are not programmed to see something approaching them from below their legs as they are sitting securely on a hard substrate as a threat. They can look down. They just don't "get" glass.


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Please identify this creature found on the beach
Found on beach in Atlantic Canada in November.
"Sack" is approx. 2" (approx. 5cm) in length.

any opening, or shell? looks like a n innkeeper worm.

Just a guess: https://en.wikipedia.org/wiki/Sipuncula

I've actually seen these before during an invertebrate zoology class in Maine! It's a rat-tailed sea cucumber, Caudina arenata. Though I don't have the taxonomic guide book anymore, I found this blog post that cites an old guide with more info about them.


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Physiological Effect of Mannitol
Which Starling Force is affected by Mannitol?
I am either thinking hydrostatic pressure of interstitial fluid (because it increases interstitial fluid volume) or hydrostatic pressure of capillary (because it is also increased plasma volume). I read that it deals with osmotic pressure but was unsure as it is a crystalloid and not a colloid.


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What species of three-tailed flying insect is this?
What species of insect is this? Collected in spring in the United Kingdom near a river in an urban area during the late afternoon. They were flying up and down in the air.

Three tails mean ephemeroptera (mayfly). I don't know what species though. Mayflies can pop up very numerous all of sudden as they sometimes all hatch at the same time and fly around like crazy.

Nice pictures! What is the approximative size?

1 cm body + 2 cm tail

It only has a day to live. Let it go.

I did, don't worry. I don't keep animals unless I know how to take care of them. It was quite agitated but it flew away from my pot extremely fast into the sky.

@charlesdarwin Is the order mayfly good enough or are you hoping for a more detailed answer?

The more detailed the better but I'll accept your answer until there is a better one.

Based on this list of mayflies of the UK, your mayfly is from the genus Ephemera.  Of the three species listed at that site for the UK, the closest match is to Ephemera vulgata, and it looks quite close.  The image of E. vulgata below is from Wikipedia here.


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Should I use RNAseZAP on my bench and pipettes before RNA extraction?
Should I spray RNAseZAP on my bench and pipettes before working with RNA? I am regularly using RNase at my bench and would like to work with RNA as well. Could traces of RNase on my equipment degrade my RNA?

The common practice in my lab is to work in a laminar flow cabinet and clean it with alcohol, then spray it with the RNAseZAP. I've always heard from my professors that, while DNAses are more uncommon, "RNAses are everywhere". So, zap it early, zap it all.

Do you know if it is safe to use RNAseZAP outside the hood? Can it harm us if we inhale the vapours?

@charlesdarwin I don't know the composition of RNAseZAP, but I don't think it can create harmful vapours. I suggested the hood because it prevents recontamination during the experiment, not for RNAseZAP safety problems (see "RNAses are everywhere")


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What is this plant with white-spotted thorny leaves from Morocco?
What is this plant with white-spotted thorny leaves from Morocco? Photographed in spring.

The distinctive leaves identify the plant as Silybum marianum. It is a member of the plant family Asteraceae. It is commonly called "milk thistle". Originating in the Mediterranean region, it has now spread to many places around the world.  The plant in your photo is immature at ground level. These links will give a better idea of the mature plant.
https://en.wikipedia.org/wiki/Silybum_marianum
https://www.google.com/search?q=silybum+marianum&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiG46Kj6L7aAhWvpFkKHfYjA0AQ_AUICigB&biw=1097&bih=642


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Where is DNA during the process of RNA extraction using Trisure?
Where is DNA during the process of RNA extraction using Trisure described here? Given that DNA is also a nucleic acid, should I expect the isolated RNA to also contain DNA? However, Bioline claims RNA 'with
virtually no genomic DNA contamination'.

Expectedly, they don’t really want to tell you what TRIsure is. What they do say is that DNA is found in the organic or interphase after extraction whereas RNA partitions to the aqueous phase. This is almost certainly some variant of acid phenol extraction. As confirmation, the MSDS lists phenol, ammonium thiocyanate, guanidinium thiocyanate, glycerol and citric acid as its components.

But why does the DNA end up in the organic phase? Isn't it as hydrophilic as RNA?

I found this in the link you provided: 'The nucleic acids (RNA and/or DNA) partition into the aqueous phase, while protein partitions into the organic phase. The pH of the mixture determines which nucleic acids get purified.[3] Under acidic conditions (pH 4-6), DNA partitions into the organic phase while RNA remains in the aqueous phase. Under neutral conditions (pH 7-8), both DNA and RNA partition into the aqueous phase.'

@charlesdarwin That’s a good question to which I don’t know the answer.


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What causes Pseudomonas fragi to smell sweet?
I am working with Pseudomonas fragi and I could not help but notice that it smells sweet, which probably explains its species name 'fragi' from 'fragum', strawberry in Latin.
Does anybody know what causes this bacterium to smell sweet? It must be some volatile compound that they release in the air? Why would they do that? Do other bacteria release odorant molecules? If so, why?

The strawberry-like odour that you perceived is mainly attributed to three ethyl esters, namely the ethyl esters of butyric, hexanoic and 3-methylbutanoic acid.
There are other odour-active volatiles produced by Pseudomonas fragi, about 26, which are said to add to the richness and complexity of the odour of the three aforementioned main compounds.
Source:
Analysis of odor-active volatiles from Pseudomonas fragi grown in milk - Cormier et al. 1991
The study by Cormier et al. should be a good starting point for further reading as it references a variety of scientists who have worked on this.


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Details of Needleman–Wunsch algorithm
I try to understand details of the Needleman–Wunsch algorithm and use an example from the book [Nello Cristianini, Matthew W. Hahn. Introduction to Computational Genomics. A Case Studies Approach, www.computational-genomics.net].
To my opinion, the algorithm is described not very neatly, so the question arises.
Consider two sequences:
I: VIVALASVEGAS
II: VIVADAVIS
The first step is clear:

Also, the calculation of the score for diagonal neighbor is also clear,

because this is an alignment without a gap:
I: V
II: V
Unclear moment is the alignment for left (or above) neighbor. Say, the left  neighbor

corresponds to this
I: V
II: -
or this
I: -
II: V
alignment?

This is really off-topic here, but you need to read very carefully how this algorithm works, how the scoring matrix is constructed, how the traceback is done, and how that is finallly converted into an alignment. It takes me a 50 min lecture to explain it. I do not know the book you mention but have found the best explanation in Durbin et al. Biological Sequence Anlaysis.


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meaning of binding capacity and binding affinity
Actually, I am unfamiliar to biology, so when I read a thesis, the term "binding capacity" and "binding affinity" are really confusing.
Since my major is unrelated to biology, I don't know correct definition. Is there anyone who can explain differences between them clearly? Any references would be helpful, thanks!

Context would be useful, though there is nothing particularly special about the use of the words in this case. Binding affinity refers to how strongly two things bind (eg a protein-ligand interaction) and binding capacity refers to how much something can bind (eg in reference to a chromatography column).

references are really helpful, the key is "how much" and "how strong". right? you resolved my confusion

@victoria Yes, essentially.

Without any context... is hard to give a detailed answer.
I understand for bindind capacity the ability of a molecule to bind or attach to another molecule.
Binding affinity is the strength of the binding interaction between a single molecule and the other one.

oh l am sorry, since I am not familar to biology, I thought that the terms are often used in biology, so the only reason for confusing me is lack of my knowledge. So, I didn't add some context, but material I found is just about receptor's binding ability and affinity.


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How does radiolabeling work?
Protein turnover can be measured by calculating the "decay" or loss of radio-labeled proteins in the blood, for example, but I am confused at how this calculation works. Wouldn't the radioactive isotope that you're using be decaying due to being unstable and not just due to protein turnover? Would you have to account for that in your calculations?

Which calculation are you using?

A=Ao*e^-kt, where A = tagged protein at any time, Ao = tagged protein at zero time, t = time in days, and k = turnover rate as fraction of the protein pool turned over per day. By rearranging the equation you can get turnover rate (k).

Technically yes, but practically it depends on what the half-life of your isotope is relative to the half-life of your protein. For example, tritium has a half-life of a little over 12 years, but most protein labeling experiments take place over only a few days at most (it depends on your protein). So while technically the tritium is decaying during your experiment, the amount of decay will be below your detection limit, and therefore is negligible over the course of the experiment.
So basically it works best to choose an isotope that will not appreciably decay over the time course of your experiment so you don't have to worry about it. If this is not possible, then yes, you would need to correct for this.

I've read some papers that use Iodine 131 to label proteins, which has a half life of 8 days. So I have another question: how do people detect these isotope labels? Do people rely on their decay to measure it (for example the release of beta-minus and gamma emissions? In that case, wouldn't you want to use something as radioactive as I-131?

Detection depends on the isotope used. Tritium is a low energy beta emitter, so it would need to be removed from the place you are measuring and put into scintillation fluid or something analogous.For something that is higher energy, like P-32, you could use film or a geiger counter. For imaging in live organisms, I think you do need something fairly strong like I-131, unless you are harvesting samples from the organism. For I-131 you can do a PET scan, since it is a gamma emitter. Typically, this does rely on the decay of the particle. 8 days is still plenty of time for most imaging though.


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Veins collapse when empty
Veins collapse when empty. That's because they have thin and almost inelastic walls. What has inelasticity and thinness of the walls to do with the collapsing of the veins?

Your body exists at a certain pressure, determined by your surroundings; usually, this is about 1 atmosphere of pressure, but it can go up or down (e.g. when you fly on an airplane, or when you go diving). The pressure that your surroundings put on your skin is transmitted throughout your body, and your body "pushed back" against it.
However, this means that all your blood vessels have that pressure weighing down on them along their length. Normally, when they're full of blood, the pressure of that blood will press the blood vessel outwards to counter-act this. Without the blood, however, that pressure within the blood vessel is no longer sufficient to withstand the pressure being exerted on it from the outside.
Since the walls of the blood vessels aren't thick enough to have enough structural integrity to withstand that pressure differential, they then proceed to collapse.


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What are the differences among food poisoning, gastroenetritis and diarrhoea?
I have now studied a major chunk of my microbiology course without understanding the basic difference between the three. The terminologies seem to be confusing. Is it a necessity for food poisoning to be cause by bacterial toxins? My texts include Shigella, which causes dysentery under food poisoning. What are the operational definitions for them? Is food poisoning more of an epidemiological term? I understand that they aren't clear cut identities and there is significant overlap. But could someone please help out?

First of all, diarrhea is a symptom, generally defined as passing large amount of loose stool. Diarrhea has countless causes, which include gastroenteritis and food poisoning (although not all types of gastroenteritis or food poisoning cause diarrhea).
Now the other two terms. Strictly speaking gastroenteritis refers to the inflammation of stomach/intestines, but clinically, it is most often used to refer to infection of stomach/intestines. Gastroenteritis is most often caused by viral infections e.g. rotavirus, noravirus, enterovirus, adenovirus... but can also be bacterial in origin.
As for food poisoning, is usually defined as illness (usually gastrointestinal symtoms, including nausea, vomiting and diarrhea) caused by "poisoned food". Food poisoning can be caused by the presence of a microbial toxin (which can sometimes be heat-stable ie not inactivated by boiling/cooking). Examples include S. aureus enterotoxin, B. cereus enterotoxin, shigatoxin... There can be an overlap, when ingestion of food causes an infection of the gastrointestinal system, but gastroenteritis is not necessarily foodborne.
Hope that clarifies things.
References for further info:
Food poisoning
Basics of acute viral gastroenteritis

Thanks a lot! Another important thing I gathered is that food poisoning need not lead only to GI symptoms. Like, the botulinum toxin has its effect on NMJs. Just felt like adding it up here. Anyway, thanks! and could you give examples of non foodborne gastroenteritis (infectious)?

You're welcome. An example for gastroenteritis not caused by food, could be something like an acute rotavirus infection. Although the virus does need to get the GI, it doesn't have to be through food, it could be contact with someone infected.

Could you add source information to facilitate users to do more reading on the topic?


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Does class switching occur both in B cells and Plasma cells?
I understand that the cell class switches to change the type of immunoglobulin it is producing. The B-cell produces the membrane bound B-cell receptor (BCR) while the plasma cell produces the the secreted form of Ig, the antibody. Now, the isotypes are different in their constant regions and I'm assuming switching only matters if it is an antibody. (differences in avidity, permeability, antibody receptors, etc.)
How would a B-cell receptor (membrane bound Ig) even benefit from class switching? Does class switching even happen in activated B-cells? Or is it a process limited to plasma cells? I read up that BCR also has the 5 isotypes.
What are the specific chronological milestones at which class switching happens in plasma cells and B-cells (if it does)?

This question is pretty broad. What kind of research have you done on your own to try and answer it? Any decent immunology textbook should have a fairly detailed section on class switching. Since plasma cells are B cells, your question title is rather silly. Some cells only have the membrane-bound BCR, regardless of isotype, while others secrete soluble Ig. While they do, through, they still express a membrane-bound BCR.

@MattDMo I've found the answer to the question and it happens pretty significant. I'll frame it up and post it in a while.

@MattDMo Here is the answer. B-cells and Plasma cells aren't one and the same. I agree the question is broad, but your rant is silly and nowhere close to constructive criticism.

Short Answer : B-cells class switch to become Plasma cells in the germinal centre of the lymph node.
Long Answer :
There are two important concepts addressed in the question. One is the Immunoglobulin structure - isotype and membrane/soluble type. And the other is the germinal centre B-cell paradigm. Understanding both the concepts are a prerequisite to understand the answer to the issue.
First of all, immunoglobulin synthesized by the lymphocyte can either be membrane bound (known as the B-cell receptor (BCR)) or soluble antibody. After gene rearrangements, the B-cell (still immature) begins to produce membrane bound IgM/IgD. This continues even in the mature B-cell. The membrane bound Ig or mIg has an extra sequence (refer image) on the carboxyl end adding a few hydrophobic amino acid sequences so that it gets anchored well in the hydrophobic part of the membrane. Also at the end is a series of hydrophilic residues involved in downstream cell signalling.

Class switching is process that leads to a change in the isotype of Ig that the cell is producing. Class switching involves excision of DNA which implies that the cell can not revert back to producing the Ig once it used to. The sequence of the gene segments on the heavy chain gene hence becomes important.
When there is a first time exposure to an antigen, the mature B-cells follow a classical paradigm to T-cell dependant antigens, which is shown in this picture below.
Class switching occurs in B cells that are participating in a germinal center reaction, after the naive B-cell has been activated by antigen and a cognate T cell. There also is germinal centre independant class switching that we ignore here.
After a B cell has undergone somatic hypermutation and class switching of its immunoglobulin gene, it may or may not be positively selected to differentiate into a plasmablast. Plasmablasts proliferate rapidly before terminal differentiation to plasma cells, which secrete affinity matured, class-switched antibody. So in other words, class switch recombination is largely restricted to activated, germinal center B cells. These B-cells class switch, as one of many processes to produce soluble antibody producing plasma cells.
Plasma cells and B-cells aren't just one and the same. B-cells undergo a series of processes to form the plasma cells which are also different in morphology.

As already has been mentioned, it should be remembered that class switching involves excision of the intervening DNA between the rearranged VDJ exon and the constant exons being switched to, meaning that they are deleted from the allele. Thus, a B cell that has class switched from IgM to, say, IgG would delete the IgM and IgD heavy chain exons on that allele, and would be restricted to IgG (or IgE and IgA, which lie downstream).
But then, if the B cells bearing IgM had already class switched (to their possible downstream counterparts), how can the primary immune response be IgM dominant? How could IgM antibodies come from class switched plasma cells?
This is because, this whole germinal centre spectacle takes time to happen and in the meanwhile, there are extrafollicular mechanisms of antibody production in place in extrafollicular foci in the spleen or in the medullary cords of lymph nodes. Since antibodies that are develpoed in a germinal centre dependant manner (IgG) are from somatically hypermutated cells, they have more affinity to the antigen than IgM produced by germinal centre independant plasmablasts.

BCR generally has only two types, mIgM and mIgD. If there is a class switch, they turn to soluble antibodies (IgG/IgA/IgD).
Secretory antibody here refers to soluble antibody that is exocytosed from the WBCs, not the IgA that is found in bodily secretions.
Reference, Picture credits :

Nature reviews immunology, Germinal centres: role in B-cell
  physiology and malignancy
Kuby Immunology. 6th Edition
Immonological reviews, Extrafollicular antibody responses

There was a factual error that, plasmablasts from the figure above secreted IgM antibodies. Actually, these IgM are produced by plasmablasts only but not in a GC dependant fashion. This happens as an extrafollicular response in extrafollicular foci in the spleen or in the medullary cords of lymph nodes.


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How does motor nerve innervation determine type of muscle fibre?
Muscle fibres are of two types - type I and type II. They differ from each other in various properties. Even the underlying biochemical processes are different to suit their function (slow vs fast)

In a normal muscle, on certain stains like ATPase and SDH, to differentiate between the types of fibres, a checkerboard pattern is seen. But in reinnervation following long standing denervation, there is a loss of the checkerboard pattern and fibre type grouping is seen.
This happens because, the the denervated fibres are reinnervated by other ones, which can change their type.
The question is, how can neural innervation lead to biochemical changes in muscle type?

'Slow' and 'fast' motor neurons differ in their firing patterns. This differentially affects intracellular calcium concentrations and energy usage of the innervated muscle fibers over time, and thereby influences their gene expression. The following review extensively covers this: http://www.ncbi.nlm.nih.gov/pubmed/22013216


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What does reflected onto means in the text below?
The pleura lines the thoracic wall and diaphragm, where it is known as the parietal pleura. It is reflected onto the lung, where it is called the visceral pleura.

"Reflected" here describes the relationship between the continuous, but differently named parts of the pleura. The parietal pleura lines the chest wall and mediastinum (costal, cervical, mediastinal, and diaphragmatic areas marked in the image below). The visceral pleura covers the surface of the lungs (orange area below). There is a transition point at the root of the lung where the parietal pleura and visceral pleura meet. This transition is referred to typically as a reflection.
I think that the terminology is used to emphasize that the layers are continuous, but it is as if the parietal pleura bounces back off the body wall as visceral pleura.

Although not a particularly clear choice of words, because we usually connote "reflection" with light, in this case, "reflected" refers to how the parietal pleura folds back on itself from the inner chest walls and diaphragm to line the lungs.


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What happens to the absorbed blue and red light in the chlorophyll molecule?
If the chlorophyll molecule (its chromophore) absorbs red and blue light and reflects green light, shouldn't the absorbed blue and red light be emitted back when its excited electrons relax?

It is glad to say that we can enter to this question due to having of valuable theorem of 1st law of thermodynamics. Energy cannot be destroy but it can convert in to another type of energy.The chlorophyll molecule decide it to, become photo energy to chemical energy.

while happening the electron transport chain electrons are going through the primary receptors. This is not happening as the electrons traveling on a trip, this is really a complicated procedure.While they are passing through the primary receptors some reactions are happening. So from which should be contribute to have energy for this reactions. By the energy of absorbed blue and red lights. So it turns it to chemical energy. It store as ATP, and NADPH. So there is no more way for emit that light away. This scenario  is firm by the following.

Reference
- The Light Reactions of Photosynthesis. In: Biochemistry. 5th ed.


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Can proteins from different viruses be gathered in one virus?
There is a biology project I must do with some of my classmates and we're facing a problem.
We would like to choose proteins from different viruses that seem interesting to us (for example one protein from a negative-strand ARN virus and the other one from a DNA virus) and gather them (theory) together through this process called "directed mutagenesis". Is it possible ? If no, isn't there another mechanism that allows the gathering ?
Thank you !
(PS: Sorry for the english)

Please clarify. Explain what you mean by ‘gather’. What level class are you talking about — high school or university? Is this project practical or theoretical?

If I understand your question, you're asking if you can take a protein from Virus A, and make Virus B produce that protein. The answer is yes, you certainly can do that, although depending on the proteins and viruses there may be some constraints. There are many examples of this being done, and even more examples of making a virus produce proteins from humans or other species.
The actual process of inserting a new gene can be pretty trivial; you can pick up handy kits of viruses specifically designed to have new genes inserted into them.  If you're putting the gene into a virus of your interest, the design process can be a little trickier; you need to be sure that the inserted protein doesn't disrupt something essential for the recipient, isn't too large for its genome, and so on.
But in principle, it's pretty simple.


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Looking to study botany, some general advice
I've been doing some hydroponics lately and I've noticed I don't have much insight about how plants really work under the hood, I would like to have the full picture and understand more about it.
My primary interest is to apply botany knowledge on my hydroponics projects, not to get a job/degree. But, I do understand that studying among my peers is a rich experience, reason why I'm considering this kind of training instead of just grabbing a book.
However, I'm not sure how extensive is the study of botany, if I need a degree in X before starting it, etc.
Also a good book is welcome.
Thanks.

Soil science, pedology is good for hydroponics knowledge because you learn agriculture history and chemistry, biological and industrial, which sais which chemicals the plants need, what pH does to chemical availability, root physics, micro and macro nutrients... And aquaculture, i.e. keeping fish books teach you about nitrogen cycles, pH, algal and fungal and other blooms, oxygenaton, stagnation, volumes of filters and throughputs, aquarium botanics, I did a pedology course in Uni and i kept fish for a while, and I know a bit of chemistry, although broad based books on hydroponics are cool.

Have you checked out Botany classes at nearby community colleges?  You may have trouble finding an evening class, but I'm sure you'll find daytime classes opening up in the January.
If you need to study independently, can I suggest checking out the Tree Care Industry Association's store. www.tcia.org  They have various learning material to read and watch, leading towards a professional arborist certification.
Good luck in your endeavor.


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Why are nosebleeds easier to get in the winter?
I understand it probably has to do with the dry air, but what does dry air do to make nosebleeds so easy to get? For example, even gently blowing your nose can cause a nosebleed for some people during the winter.

The vast majority of bloody noses in healthy individuals arise from one specific area in the nose (on either side): Kiesselbach's plexus.

In the mucosa of the nasal septum (the cartilagenous structure separating the nose into two sides), there is an area where several arteries "meet", giving it an exceptionally rich vascular supply, called Kiesselbach's plexus. It is on the anterior surface, and exposed to dry air and trauma.
Bleeding typically occurs when the mucosa erodes for any reason, and the capillaries and venules (and sometimes arterioles) become exposed and subsequently break. The result is the familiar bloody dripping of a nosebleed.
Have you noticed that your lips chap more in the winter? Dry air and cols temperatures do that. The mucosa of your nose also dries out and suffers some damage. Not like your lips, but damage none the less. Damaged nasal mucosa is more susceptible to tears/trauma/erosion. If it happens in an area of rich blood supply, you get a nosebleed.
Anything that helps with the integrity of the nasal mucosa is going to help reduce nosebleeds. One can

run a humidifier in dry weather
avoid irritating by touching the nose or blowing nose too often
apply a very light layer of petrolatum or Bacitracin ointment to the inside of the nose covering Kiesselbach's plexus at night so the nose-breathing doesn't dry out your nose
use nasal saline spray to moisten and soothe the nasal membranes (don't rub the tip of the spray bottle against the nasal membranes, though)

*more serious or recurrent bleeding needs medical attention to rule out  other conditions that are associated with frequent nose bleeds.
Epistaxis

Perhaps a note that it's not always in the winter.  I used to get nosebleeds during the August-October period, which is when humidity is lowest where I live.

@jamesqf - good point. However, cold air holds less water (is dryer) than warm air in the presence of water (i.e. barring arid regions), so yes, it's more common in most places in the winter.

Might also depend on the amount of time you spend indoors or outdoors.  When cold winter air is brought inside and heated, it will be very low humidity - at least without some kind of humidifier.


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Are natural daylight lamps for Seasonal Affective Disorder just about the color temperature?
I've seen many expensive lamps made for people who have Seasonal Affective Disorder (SAD) and/or who live in regions where there isn't much daylight during the winter. I'm wondering if the benefit of these lamps is simply the color temperature (typically advertised at 6000K or more), or if there are other aspects of these lights that are meant to be theraputic? Some of these lights are also advertised as "ion therapy lamps".


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Are nosebleeds unique to humans?
Are there other species that get nosebleeds? If so, do they occur for the same reasons that humans get nosebleeds? How would an animal stop a nosebleed?

Cats, dogs and other animals can suffer from epistaxis.  The causes differ depending on the animal.

foreign things in the nose, abscess, cancerous growth, snake bite, some poisonings and diseases especially in the trachea and lungs and anthrax. Sometimes excessive sneezing or coughing can result in nose bleeding as well. All animals are susceptible to get nose bleeding.

They would need to see their vet or owner to get it treated.
https://www.thevillager.com.na/articles/7474/Dealing-With-an-Animal-Bleeding-From-the-Nose/

Nose bleeding (or epistaxis, as Graham rightly termed it) is common to many species, such as dogs, cats, pigs, and many other animals.  As for the causes, like Graham pointed out, it really varies from species to species.
To take dogs for an example, the leading causes of spontaneous nose bleeding are leishmaniasis (a tropical / subtropical disease transmitted by sandflies) and other bacterial infections, such as CME (canine monocytic ehrlichiosis, a disease spread by ticks).
As you can imagine, minor trauma to the nasal region can also cause nose bleeding, not just in dogs, but in many other animal kinds.
That said, I feel sorry for the elephant who gets a nose bleed.

Sources:

A retrospective study of 61 cases of spontaneous canine epistaxis, . Mylonakis, M. N. Saridomichelakis, V. Lazaridis, L. S. Leontides, P. Kostoulas, A. F. Koutinas, 2007
Leishmaniasis, Wikipedia
Monocytic ehrlichiosis in dogs, Procajło A1, Skupień EM, Bladowski M, Lew S.
A Porcine Epistaxis Model: Hemostatic Effects of Octylcyanoacrylate, Adam J. Singer, MD, Steve A. McClain, MD, Arnold Katz, MD, 2004


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Are humans the only species to suffer from impacted teeth?
Many humans need their third molars (wisdom teeth) removed due to tooth impaction. Are humans the only species to suffer from this?

According to Wikipedia
An impacted tooth is one that fails to erupt into the dental arch within the expected developmental window. Because impacted teeth do not erupt, they are retained throughout the individual's lifetime unless extracted or exposed surgically.
Now to your interesting question, there are case reports, that yes, animals, other than humans can also have impacted teeth.

Mandibular canine tooth impaction in young dog which was then made to erupt by surgery. Reference

Maxillary canine impaction in a persion cat. Reference

According to this article

Proper growth and development of the oral cavity depends on a series of events that must occur normally and in the proper sequence. Genetic abnormalities or trauma that affects either the developing tissues or the timing of their development can cause abnormalities. Defects that decrease comfort, health, or function require treatment; those that result in only an esthetic problem do not. Common developmental problems include persistent deciduous teeth, unerupted teeth, malformed teeth, malocclusion, and malformed jaws.


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What determines which symptoms an allergen will cause?
Allergies result in many different symptoms such as sneezing, runny nose, itchy eyes, coughing, rashes, swelling of the face, stomach pain, vomiting, dry skin, anaphylaxis, etc.
An allergen can cause different symptoms for different people who are allergic to it... and different allergens can cause completely different symptoms for the same person. What characteristics of an allergen and/or the person determine what symptoms will arise?


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Regarding detection of pregnancy during post mortem
Is it possible to detect pregnancy in a woman who is dead considering the fact that she did not a have a showing belly.

As a general rule, there are more diagnostic options available in a postmortem than in a living subject. While there are some diagnostic tests that aren't as helpful postmortem as they are in the living subject, the additional tests you can do are more definitive rather than less.
Early presumptive diagnosis of a pregnancy in living subjects is through $\beta$-hCG. Definitive diagnosis of an intrauterine pregnancy is through sonographic visualization of a gestational sac. In postmortem $\beta-hCG$ can be done on samples of blood, urine, vitreous humor (fluid in the eyeball), and bile. $\beta$-hCG is pretty routinely included in a postmortem for a woman of child bearing age. Examination of the uterus and intrauterine contents is considerably easier and more thorough postmortem, because, well, you can examine it directly instead of through external imaging.
You can't, of course, detect fetal heart tones or fetal movements if the fetus is dead but this is no different from an examination of a live mother.

Answer is obviously yes. Here's an article reporting a forensic method used to detect pregnancy using placental markers in a Reverse Transcriptase PCR from a DNA sample. It could be applied in a death body, when it's possible to get a DNA sample from a tissue.

Could you please specify, whether the DNA sample can be from any tissue or only from certain tissues?

You could certainly do this as part of a postmortem examination, but it's not how it's actually done.


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Does pouring water on your skin affect the evaporation process and heat loss?
Recently I've been playing football in the sun pretty hot temperatures. During the water breaks I tend to pour a lot of water over my head to cool me down, now this has an instant effect on cooling me down but in the long run would this have any affect on my body temperature? We know that the body cools itself by using heat to evaporate sweat on skin, would drenching  my head and face in cool water affect this process or not?

Drenching your head and face with cool water will both directly cool your skin (because cool water is colder than you) and contribute to evaporative cooling. Your skin doesn't care if the water that evaporates comes from sweat you made, the pool, a water bottle or a hose.
The Khan Academy video is a good review of the principle.


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Is it safe to autoclave seawater agar?
For an experiment I'm going to prepare an artificial seawater agar. Before use, I have to sterilize the medium of course. I imagine, that autoclaving will cause the salts in the seawater to precipitate. Can I re-suspend them afterwards, or will it irreversibly change the composition of my medium? Should I use a different sterilization method altogether, e.g. filter sterilization?

Why should they precipitate? Warm water dissolves more salts than colder.

I see no reason why it would precipitate chemically. Besides, you need to dissolve the agar via heat. Hence, auclaving is fine.
If you do not believe me these protocol allow for autoclaving of seawater agar 15min cycle 121 degrees:
1. https://www.dsmz.de/microorganisms/medium/pdf/DSMZ_Medium246.pdf
2. http://himedialabs.com/TD/M592.pdf

Hi @AdamRadekMartinez. This is a good answer. You don't need to preface your sources with "if you do not believe me", though. Just reference them. Biology.SE answers should include references, with no expectation that a poster will just be believed without them :)


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Is it red blood cells or white blood cells that fight infection?
This article has me very confused;
https://www.dailymail.co.uk/science...-blood-likely-catch-coronavirus.html#comments
It's implying that red blood cells (ABO blood groups only affect the surface of red blood cells, but not white blood cells) fight disease, with type A being the weakest, and I've been reading that this is blatantly wrong, since it is white blood cells that are involved in the immune response, not red blood cells, and thus blood type would have no effect on the course of an infection because red blood cells aren't involved in fighting diseases and blood groups don't affect the internal workings of a red blood cell anyway.

That's bullshit. Red blood cells have only one function and this is the transport of oxygen. One advice: Stop reading Daily Mail as this is not a serious source.

@Chris the article referenced this study - medrxiv.org/content/10.1101/2020.03.11.20031096v1 I'd like to know your thoughts on the results.

It's one report so far, and the numbers are not so much different. Only because there seems to be a correlation doesn't mean there is a real causation. The study is also only descriptive without giving any hypothesis on a possible mechanism. It looks very much to me like a very fast publication to be the first. I would be very cautious here.

I somewhat like the Daily Mail - they vacuum up information indiscriminately and empty it out at your feet.  Provided you are willing to think critically, you should be alright.  This report is also found at https://www.scmp.com/news/china/society/article/3075567/people-blood-type-may-be-more-vulnerable-coronavirus-china-study and traces back to the preprint at https://www.medrxiv.org/sites/all/libraries/pdfjs/web/viewer.html?file=/content/medrxiv/early/2020/03/16/2020.03.11.20031096.full.pdf
Note that Medrxiv is a preprint server - the papers are not peer reviewed - hence it is another source of delight for the critical and skeptical thinker.  This preprint comes from a most respectable and prolific source, but one under great pressure to publish quickly for the sake of the world.  In my opinion, the authors err in their statistics - I think they assume that the odds of getting 42% instead of 32% type A blood in a sample is the odds of a group of individuals selected randomly from a large population having that much of a skew, so it seemed significant.  However, if the market at Wuhan was favored by people of certain ethnic extraction, or even if there were some extended family groups in the sample, the odds of seeing this effect by chance might be higher.  I won't fault them for publishing the study because people in other countries SHOULD look to see if there is a correlation in their hands.  But I don't think the paper would have passed a traditional peer review.


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Are dragons real animals?
I'm having this debate with someone on whether or not dragons are real. They say they are real because there's been thousands of historical sightings of them, and there was at least one historical case where a teenager said that a dragon had appeared and killed his friends, one by one, but he got away. For the rest of his life, this person was obsessed with dragons to the point of wanting to obtain the personal information and telephone numbers of anyone who claimed to have seen dragons.
So, now I am kind of conflicted, I responded to that person saying those people saying they've seen them are lying, and Wikipedia says that dragons are fictional, but they directed me to a paranormal forum saying that Wikipedia is unreliable, and also it's up to me to prove that the people who've seen dragons are just lying.

Welcome to Biology.SE! Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. In particular, this question seems like it might be appropriate on [Skeptics.SE], but please do not crosspost, instead request migration after consulting that sites help. ———— In addition, we expect you to demonstrate prior research with references to reliable sources — e.g. peer-reviewed research (definitely not paranormal forums) . Thanks!

Dragons are real animals, but that almost certainly doesn't mean what you think it means
'Dragons' are a diverse group of reptiles mostly within the Family Agamidae, comprising over 300 species throughout Africa, Asia, Australia and southern Europe. As an example, here's an Eastern Bearded Dragon, which is relatively common throughout Southern and Eastern Australia. The largest male Eastern Bearded Dragons grow to around 60cm total length, and a personal friend of mine once kept one as a pet.

The largest real 'dragon' is the Komodo Dragon in the family Varanidae. These grow to a maximum length of around three meters and a maximum weight around 90 kilograms. They are top predators in the ecosystems where they live, and adults will take large mammals as prey. Here's a Komodo Dragon stalking a deer. You'll notice that it's wearing a GPS collar - it was being tracked by scientists trying to record their foraging behaviour. You can read their full paper in PLoS ONE.

However, it seems like you are mostly asking about mythological dragons. Mythological dragons aren't real.


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How antibodies are produced in our body against intracellular proteins of infectious bacteria?
When an infectious agent invades our body, then surface antigens of the infectious agent are detected by our immune system and B-cells get activated. However, we do have antibodies in our blood against intracellular proteins of the infectious bacteria. What is the mechanism which produces antibodies to intracellular proteins, which are never exposed to our immune system.

"When an infectious agent invades our body, then surface antigens of the infectious agent are detected by our immune system and B-cells get activated." Can you mention a source for this premise? (Specifically, the assertion that only surface antigens of the infectious agent are detected by the immune system.)

@AdhishSethi https://microbiologyonline.org/index.php/about-microbiology/microbes-and-the-human-body/antibody-antigen-complex
I am little confused here. Please help me to understand the intracellular part better.

Hmm, this article talks of B cell responses rather than the immune system in general. As far as I know, antibodies to bacteria are formed against toxins and cell surface molecules only. Can you also cite a source that mentions antibodies against bacterial intracellular components? (I hope you are not tired of adding sources :P) Preferably, add all your sources to the body of the question so that users don't need to look through the comments. Thanks.


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Which is the most accurate protein-protein interaction prediction tool?
Among many tools available for predicting protein-protein interaction, which one is the most accurate? By accurate, I mean most close to experimental data. I shortlisted HADDOCK, ClusPro, GRAMM-X and Rossetta. The reason I am asking this question is because using the same protein X and Y, the predicted combined structure is different for different tools. There is PDB structure for both X and Y protein. I want to mutate one of the proteins at multiple locations and check how the interaction changes.
I know that there are many more like Hex, AutoDock Vina, ZDOCK, MEGADOCK, Glide, PatchDock but they are either primarily for protein-small molecule docking or hasn't been updated in a long time.

From what I understand comparing the tools is difficult because most of them use their own scoring system. That being said there are some papers that do attempt comparing https://www.mdpi.com/2079-6382/12/3/463. Do keep in mind these fields evolve rapidly, so these comparisons could be outdated by now, and comparisons are probably sensitive to application.


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What is cephalostatic theory?
I just came across this theory while solving problems. I looked for it all over Google but couldn't find the actual theory. I guess I can learn it here.

Name the book in which you found that term pls.

The exact term "cephalostatic theory" apparently does not occur in any results indexed by Google (at least, until they index this question):
https://www.google.co.uk/search?q="cephalostatic+theory". This makes it even more important to know where you came across it, but also are you sure you've gt the right term?

A cephalostat is head holding device used in orthodontic analysis; cephalometric analysis being the clinical application of cephalometry - the analysis of dental and skeletal relationships of the human skull.
Cephalostatic theory then, I would assume, is the body of work regarding that relationship.


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Variation of fixation probability over time in Wright-Fisher model
In Wright-Fisher model of population size N and initial mutation frequency of 1/N, how does the fixation probability vary over generations. So, mathematically, what is the function that maps the generation to its fixation probability?

Is your question "What is the probability P(t) that a neutral mutations at frequency 1/2N fixes after t generation given that it will reach fixation?"?

@Remi.b Yes. I know that fixation probability is 1/N eventually. In a sense that, if we let the population evolve for enough generations, fixation probability becomes 1/N. But how does it actually vary over generations? Thank you.

The answer is probably in Kimura and Ohta 1968. From there, the expected time to fixation of an allele at frequency $p$ is $\bar t(p_0)=-4N\left(\frac{1-p_0}{p_0}\right)\ln(1-p_0)$

But how can we describe the variation of fixation probability over time using that equation? Thank you.

Are you thinking of a case where a population where a population starts without any genetic diversity and hence there is little fixation at early generations and then the rate of fixation plateaus or are you looking for a variance in the number of fixation events from generation to generation in a equilibrium population?

The first one. I realize that fixation probability is low initially and suddenly explodes to reach 1/N and saturates. I am looking for an equation that describes that behavior. Thanks.

You might want to edit your question to clarify this point. By curiosity, can I ask what simulation platform you're using (or if you wrote your own code)?

You might want to edit your question to clarify this point. By curiosity, can I ask what simulation platform you're using (or if you wrote your own code)? (see Sequence evolution simulation tool).

The function probably look like $r(t) = A + B e^{-C t}$, where $r(t)$ is the rate of fixation at time $t$ (in generation). The reason for this exponential is that the probability that a mutation happens after $t$ generation is given by the exponential distribution.
As the rate of fixation at equilibrium must be at $2N\mu \frac{1}{2N} = \mu$, $A=\mu$, that is $r(t) = \mu + B e^{-C t}$
As at $t=0$, the rate must be 0. As $e^{0} = 1$, you should have $B=-\mu$. Hence,
$$r(t) = \mu - \mu e^{-C t}$$
$C$ here represents the steepness of the curve. I don't know how you could calculate it a priori but it must depends upon your population size $N$. As the expected time to fixation starting at frequency $p_0$ is (from Kimura and Ohta 1968)
$$\bar t(p_0)=-4N\left(\frac{1-p_0}{p_0}\right)\ln(1-p_0)$$
For $p_0 = \frac{1}{2N}$
$$\bar t\left(\frac{1}{2N}\right)=-4N\left(2N-1\right)\ln\left(1-\frac{1}{2N}\right)$$
or
$$\bar t\left(\frac{1}{2N}\right)=\left(4N-8N^2\right)\ln\left(\frac{2N-1}{2N}\right)$$
if you prefer. Maybe $C = \bar t\left(\frac{1}{2N}\right)$ leading to
$$r(t) = \mu \left(1 - e^{-\left( \left(4N-8N^2\right)\ln\left(\frac{2N-1}{2N}\right) \right) t}\right)$$
Let me know if it matches (I'd pretty amazed)!


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Rapid polymerization inside cells
I am interested in (rapid) polymerization or (rapid) long mollecule synthesishappening in the intracellular space.
Clearly protein synthesis or DNA/RNA synthesis are examples of elongation of molecules, but these are relatively slow.
I wonder if someone can suggest examples of polymerization processes that happen at a much faster pace, for example one monomer added to the mollecule every millisecond, or every few milliseconds.
The underlying question is: what is the fastest example of long-molecule elongation inside the cell? At physiologically viable concentrations, what is the fastest monomer addition process that we could find?

I have now found examples of polymerases approaching 1000 nucleotides per second. Is this correct? Any other examples? Specific polymerases that can reach this incorporation speed or even higher? Other polymerization examples?


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Exhalation while holding breath
If you inhale to your maximum capacity and hold your breath for an extended period of time, it begins to feel uncomfortable; slowly releasing your breath at this point seems to provide relief from this discomfort.
Is there a biological reason why this is so, or is this something psychological?

The exact causes of the discomfort relief  after the breath-hold breakpoint  is unknown yet.
It has been stated that breath "pacemaker" continue to work independently of voluntary breath holding. Thus, while breath holding, the breath center is trying to activate the diaphragm and the afferent feedback from the diaphragm normally causes the feeling of discomfort. Thus, upon starting breathing again, i.e. actual diaphragm movements, the discomfort will diminish and the subject will feel relief.
Breath-holding and its breakpoint. Experimental Physiology Volume 91, Issue 1, January 2006.
full text of cited article

This occurs because the feelings of needing more air to breath result from changes in the concentration of carbon dioxide in the bloodstream. This happens because the carbon dioxide gets dissolved in blood, turning into carbonic acid (H2CO3). This, since it is an acid, dissociates into ions, and your body can detect that change in acidity. These changed PH levels are not desirable because they reduce the efficiency of proteins and can cause negative effects. Therefore, the body detects these changes and creates the discomfort from the desire to breath out. This also holds true for too little carbon dioxide, because it will result in the reverse effect on the acidity in the blood stream (it will raise the PH/make it more basic). Passing out occurs when the acid levels are too high and nothing is making them return to normal (breathing out) so the brain says "this idiot cannot breath correctly" and shuts off the control center to do it itself (unconsciousness).

Welcome to Biology! Although your answer is well formulated, it doesn't address the question why the release of air seems to provide relief.

You should add references for whatever you are saying.


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What is the cause of colours of nail
Why the nails are of white colour from bottom? then why they are pink and again white in the end?

I'm voting to close this question as off-topic because there is not any sign of prior effort on OP 's side.

@AliceD, I don't find the answer by googling with similar phrase. If you know about the answer, can you please share it? Also, why it's off-topic? I think, it fits in biology, isn't it?

@CoolZeroInfinity - That bit of research you just did is what I would like to see in OP's question. As of now the Q is just too easily thrown into this community. We like to maintain a certain question standard.

I think anyone should be able to ask a question here - its not a homework site.

While I agree that anyone should be able to ask a question here, I think we have the right to request that certain standards are met. We have not said this person can not ask a question, but directed them (using the tools available e.g. close votes) to improve the question to meet those standards @shigeta http://meta.biology.stackexchange.com/questions/449/how-much-should-we-enforce-background-research

@CoolZeroInfinity I Googled the word fingernail and got the wiki page, that had enough info to derive an answer

@rg255, I agree. I was searching with different phrase but with anatomy, I can find answer.

The Nightman is giving you a headstart to understand and read about nail colour.
I would like to add a different view to this question from "Colour and Pathology" point of view. Finger nails have been an excellent source of evidence for the initial physical diagnosis process. Nail colour and texture can be an indiator for a wide range of medical conditions.
You may take a look at this link : The hand in Diagnosis Process and discusses about nail pathology.. However this diagnosis gets a little tedious if the patient has colourfully painted their nails with nail polish...
I see many of the answers do include an image - well at the end it's anatomy.

Here's a relative simple and fun to read article to clarify any doubts you have about Keratin in nails being dead or not, for its colour and why it's tough.

The cuticle and matrix are white because the melanocytes there are inactive, so there is no pigment produced. The matrix cells divide and the new cells produce a lot of keratin protein.
The older cells fill with keratin and die, and the new cells push them out of the way – this means toward the end of your finger. This is how your nails grow.
But our fingernail doesn’t look like individual cells. You are
   sloughing millions of skin cells each day, but for a nail the dead
   cells all mass together. Nails only wear away or must be trimmed.
   Individual cells are not lost. The solidity of the nail comes from the
   connecting of the dead cells together by junctions between the cells
   called desmosomes, and by the interlocking of the cells like jigsaw
   puzzle pieces. But there’s more.
Individual keratin protein filaments also become connected so that the entire mass of keratin becomes one solid structure. This is called cornification, like the stratum corneum (the outer, dead layers) of your skin.
One of the two main forms of keratin in your nails is crystalline keratin, which is rigid, stronger, and has an ordered structure - like a tinker toy cube. Transmitted light is less likely to strike an atom and bounce back when the atoms are all lined up, so this is why many crystalline lattices appear translucent.

Great referenced answer, it doesn't address the question though. -1

@AliceD this is my first answer in this site :( well I stated it is a different view :)

The Nail itself consists of dead keratinous cells that shrink upon dying and become translucent. This gives the nail itself its white coloration. The reason it appears pink when it overlaps the finger is because of underlying blood vessels that color the live tissue pink just like your skin, and this shows through the nail itself. The lunula is the most proximal region of the fingernail that is crescent shaped and appears more white than the rest of the nail bed. The reason for the whiter color is that the underlying blood vessels are obscured by a denser stratum basale (one of the lower layers of the skin).
See: Human Anatomy by Martini
If you don't have this book, you could at least start at wikipedia which does describe the anatomy of the fingernail with more or less accuracy: Wikipedia

Interesting answer. +1. A reference or a few links would be great though.

@The Nightman, answer sounds logical, I thought something like same :-) but didn't have any reference. Can you provide any reference please?

Fingernails are not made of dead cells, they are made of Keratin.


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How long can a plant generate oxygen from its own carbon dioxide, produced during nighttime?
I recently bought one of these miracle fruit plants (Synsepalum dulcificum).  Since they are of tropic origin, they need higher humidity and temperature as we have it here in Austria. So I decided to cover it in a transparent plastic bag, together with a small water basin, in order to maintain better conditions.
Assuming the bag is absolutely gas-tight, allowing no diffusion, my question is:
For how long could the plant generate $\ce{O2}$ from its own $\ce{CO2}$, produced during night? And as a little subquestion: Will the plant eventually run out of oxygen at night?
I know there are no exact answers to this, so an rough approximation is more than enough for me.

Just to give you better notion of my experimental conditions:

enclosed gas volume: ~ 3 L
(onesided) leaf surface area: ~ 0.5 dm$^2$
temperature: ~ 15$-$25 °C

For how long could the plant generate $\ce{O2}$ from its own $\ce{CO2}$, produced during night?
Plants do not generate $\ce{O2}$ from $\ce{CO2}$.
Photosynthesis consists of two general steps, one that requires light and one that does not. The first step occurs in the thylakoid membrane, and splits water into oxygen, hydrogen ions, and energy. The second step is the carbon fixation step, which occurs in the chloroplasts and uses energy to convert the carbon dioxide into carbohydrates.
Step 1: $\ce{2 H2O + light → 2 H+ + O2 + energy}$
Step 2: $\ce{3 CO2 + 6 H+ + energy → C3H6O3-P + 3 H2O}$
The more detailed chemical equations can be found on the Wikipedia Photosynthesis page.
Since the first step which produced oxygen is light-dependent, it occurs mostly during the daytime. To keep growing during the night, the plants break down the carbohydrates they produced and stored during the day. This cellular respiration uses up oxygen and generates carbon dioxide just as animals do.
Will the plant eventually run out of oxygen at night?
As mentioned, plants require oxygen for cellular respiration, which occurs both at day and night. The difference is that during the night, they are not producing oxygen via photosynthesis. Assuming the plant is in sufficient light and temperature conditions during the day, the plant will not run out of oxygen at night. Plants can survive in sealed environments for very long times. A fun example is a reportedly 53 year-old bottle garden. In a bottle garden, which is essentially the system you are creating, the only difference from a plant out in the environment is that the same oxygen, carbon, and hydrogen molecules are constantly being recycled via photosynthesis and cellular respiration.

Nice clear answer, good reminder that the oxygen comes from water splitting. Wish I could +1 again for the 1960's bottle garden!

I've re-used a bit of your explanation in this question.


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What is the difference between hilum of the lung and root of the lung?
In my book they describe root of the lung like this:
In the region of vertebrae TV to TVII, the mediastinal pleura refects off the mediastinum as a tubular, sleeve-like covering for structures (i.e., airway, vessels, nerves, lym-phatics) that pass between the lung and mediastinum. This sleeve-like covering, and the structures it contains, forms the root of the lung.
And hilum of the lung like this:
The root joins the medial surface of the lung at an area referred to as the hilum of the lung. Here, the mediastinal pleura is continuous with the visceral pleura.
I dont see the difference between Root and hilum.
Can somebody please help me out?

Short answer: Hilum is an area(has only 2 dimensions) where as root is a body( has 3 dimensions).

The root of lung is a short broad pedicle connecting the medial surface of the lung with the mediastinum. It consists of structures entering and leaving the lung at hilum. The root of lung is surrounded by a tubular sheath derived from the mediastinal pleura.

and

The hilum is the area on the mediastinal surface of the lung through which structures enter or leave the lung.

Source: pg no 239
Consider the following image( edited by myself):
If the cylinder is root of lung then lateral opening(blue) is hilum.

The region bounded( within the limits of pleural membrane) by those two planes is root of lung and the area bounded by the lateral plane is hilum.

Any reason for downvote so I may improve?

I didn't downvote, but I think you could mention which structures does the root consist of.

The root of the lung is region of the mediastinal surface of the lung that lies between T5 and T7, it consist of the mediastinal and visceral pleura reflecting over the structures entering or leaving the lungs at the hilum like a sleeve.

Welcome to Biology.SE! It isn't clear to me as a non-expert in anatomy that this adds anything to the existing answer and reads more like a comment on that answer. In addition, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please also take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. Thanks!

Root of of lung is a pedicle which connects medial surface of the lung with the mediastinum and lies at the level of 5,6,7 thoracic vertebrae.
It consists of structures going in and out through a triangular depression called hilum.

Welcome Prince Kumar. Please take our [tour] and refer to the [help] as and when for guidance as to our ways. This is a perfectly reasonable answer, but we'd like you to add references as a rule to support the info. Enjoy Biology.


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What is this species of asphodel from Morocco?
It grew about 2 metres high. Photographed in spring. It has 6 tepals and 6 stamens.

It appears to be Asphodelus aestivus, but there is similarity with Asphodelus ramosus, both of which have strap like leaves and highly branched stems. They have some overlapping ranges as well in southern Mediterranean/north Africa.
https://en.wikipedia.org/wiki/Asphodelus_aestivus
https://en.wikipedia.org/wiki/Asphodelus#Systematics


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What is this hopping insect?
What species is this jumping insect?
Found in the United Kingdom in summer.
About 1 cm body length + 1 cm feelers.

The well-developed jumping legs indicate Orthoptera. The undeveloped wings show that it is an immature. The long antennae say Tettigoniidae. I don't know the species.

It looks to be a bush cricket of the Leptophyes genus.  Possibly Leptophyes punctatissima, also known as the speckled bush cricket - not sure if the one in your image is speckled or not.  It is endemic to Europe and can be found in the UK.

Photo source: Wikimedia commons - Leptophyes_punctatissima

Where should I find the speckes if there are any? Are they those orange spots on the back on your photo?

Oh, it's probably all these little dots on the body! I didn't notice them at first.


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What species is this bushy thorny yellow-flowered angiosperm from Morocco?
What species is this bushy thorny yellow-flowered angiosperm from Morocco? Photographed in spring in a dried up river bed. The bush is about 1 metre high.

I happened to come across a photo of a similar leafless shrub (without flowers) that also had 120 degree branches and looked thorny, or Spiny is probably a better description. It helped me to identify the plant in your photo as a Launaea arborescens. It is an unusual species of Chicory in the dandelion family, Asteraceae. Being tolerant of arid locations, it native to northwest Africa and southern Spain.
http://encyclopaedia.alpinegardensociety.net/plants/Launaea/arborescens
https://en.wikipedia.org/wiki/Launaea
https://en.wikipedia.org/wiki/Launaea_arborescens

Well done user22542!  I thought it looked "chicory-ish" but that's about as far as I got.  I've been watching this question ever since hoping someone would figure it out.


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What species is this yellow flower of angiosperm from Morocco?
What species is this yellow flower of angiosperm from Morocco? I photographed it in spring. I estimate the diameter of a flower to be 1.5 cm.

It's undoubtedly in the genus Oxalis but there are hundreds of species in this genus.  The genus name refers to the high content of oxalic acid found in this genus.


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What is this pink angiosperm from Morocco?
What is this pink angiosperm photographed in Morocco in spring? The diameter of the flower is about 2 cm. The petals are fused. The plant is crawling and did not have any erect parts.

Could be some kind of Convolvulaceae

It does indeed look a bit like bindweed. I hope to get a genus.

This is a species of morning glory (fairly obvious from the flower). It is a member of the angiosperm family Convolvulaceae. The flower and the leaves together identify it as Convolvulus althaeoides. It is a Mediterranean native.  Links provided.
https://en.wikipedia.org/wiki/Convolvulus_althaeoides
https://www.google.com/search?q=convolvulus+althaeoides&source=lnms&tbm=isch&sa=X&ved=0ahUKEwit1P3t7L7aAhVPmVkKHZIJD_gQ_AUICigB&biw=1097&bih=642


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What species is this colourful caterpillar?
What species is this colourful caterpillar found on a road in Central Europe?

Just by its appearance and location, that’s maybe a Pale Tussock (Calliteara pudibunda), a kind of moth found in Central Europe.
You can find some observations of that species on iNaturalist: https://www.inaturalist.org/taxa/205294-Calliteara-pudibunda?locale=en-GB


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What is this species of angiosperm from Morocco?
The flowers are about 1 cm long. The plant is about 1 metre high. Photographed in spring. The plant was found in a ruderal environment.

Looks a bit like a Flax relative, genus Linum, but the hairy leaves and stems aren't consistent with Linum usitatissimum which is the flax of commerce (the textile linen).

Look into the Symphytum genus, or related genera within Boraginaceae (the forget-me-not family). It is loosely similar to Symphytum officinale, but clearly not that species. The overall layout, size, leaves and hairyness of the stalks is similar to species in Symphytum.
Here is Symphytum officinale, as an example of the overall appearance:

Also similar from the Anchusa genus in the same family (Anchusa azurea):

For the record; I don't really think this answer deserves the "accepted" badge.

I agree with Borraginaceae. The examples you provide could be close, but the leaves seem a bit different.


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Are there any oxygen loving bacteria?
It seems we only found bacteria that hate oxygen. Are there any bacteria that love oxygen and would thrive in high oxygen environment?
If it slowed down or stop multiplying in low (as in normal earth atmosphere) oxygen content it would be the best.

Acetic acid bacteria need oxygen to turn alcohol into vinegar.

There are anaerobic bacteria and aerobic bacteria. Aerobic bacteria include: Mycobacterium tuberculosis (Tuberculosis), E. Coli (common model organism), and Staphylococcus auerus (that new superbug)

It's not true that all bacteria hate oxygen. Actually, there are some obligately aerobic bacteria that need oxygen to carry out cellular respiration. A notorious example of this type of bacteria is Mycobacterium tuberculosis, a pathogenic species that infects lungs and cause tuberculosis. Because it's obligately aerobic, in the classic case of tuberculosis, Mycobacterium tuberculosis growths are always found in the well-aerated upper lobes of the lungs where the oxygen requirement is satisfied.
Reference:
1. Levinson, W. (2010). Review of Medical Microbiology and Immunology (11th ed.). McGraw-Hill. pp. 150–157. ISBN 978-0-07-174268-9.

To improve the answer quality I suggest to add references to your claims

@havefun thanks for your opinion, will add it soon.

I am thinking along the lines of "rapidly duplicating itself in high oxygen environment like those bugs in 'The day the earth stopped'."

Species that require oxygen to survive can be classified into 3 groups(in bold). Their distinctions are also explained:

Microbes that use oxygen for energy-yielding purposes are called
  aerobes, if they require oxygen for their metabolism they are called
  obligate aerobes. Obligate aerobes are at a disadvantage because
  oxygen is poorly soluble in water and much of the environment is
  lacking in this necessary element. Often, aerobic bacteria have
  retained the ability to grow without oxygen; these are called
  facultative anaerobes. Those bacteria that are unable to use oxygen
  and in fact may be harmed by it are known as obligate anaerobes.
  Further groups include: the microaerophiles which are aerobic microbes
  that tolerate only a narrow band of oxygen concentrations usually
  lower than that of the atmosphere and are therefore often difficult to
  cultivate in the laboratory, and aerotolerant bacteria that grow in
  the presence of oxygen but do not require it. (Here)

Examples

Obligate aerobes:Mycobacterium tuberculosis and Nocardia asteroides
Microaerophiles:Campylobacter species and Helicobacter pylori
Aerotolerant anaerobe(anaerobe because they grow in the lack of oxygen)
: Streptococcus mutans