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The distance the electromagnetic field of the heart can be detected
A very smart friend of mine seems to get taken in by junk science. He started telling me last night that the electromagnetic field of the heart can be detected beyond 30 feet. What is the actual distance? Thank you.

what is the detector? seriously in a vacuum with the right equipment i'm sure it could be quite a long distance.

I heard such anecdotes from electrical engineering friends. Their circuit was so sensitive that you would see your own heart beat on the oscilloscope just in the vicinity. I don't know what the exact distance was. Perhaps you could as this Q at EE.SE http://electronics.stackexchange.com/ ?

The EM field strength falls off as the inverse square of the distance (even in space). The heart operates on mV and mA voltages/currents. I wonder if this is detectable beyond 5 meters using a nearly-ideal detector. 30 feet sounds really far.

In 2010 there was a brief note in LiveScience on a system developed at U. Sussex which detected heartbeats at 1 meter. That was apparently good 4 years ago.

The electomagnetic field of the heart actually changes with emotions so there is no fixed range as such (reference). It could also change with temperature and other external magnetic disturbances (reference). The heart generates the largest electromagnetic field in the body which is up to 50 mV/m, and that of the brain and other vital organs up to 5 mV/m. Here is a paper on the exposure of human beings to electromagnetic waves (reference). This paper details some of the current medical treatments focusing on the electromagnetic fields (reference).

In your first sentence I think you mean "changes with emotions." The E-field falls off as the inverse square of the distance so it loses strength rapidly. There is certainly a range even with an ideal detector.

@daniel yes it is "changes with emotions".. thank you for pointing that out.


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Is the mutation rate in organisms in general consistent over the genome?
Coming from computer science with an interest in genetic programming (a process emulating evolution) I'm curious about whether the rate of mutation is homogeneous across the whole genome, or if some parts of the genome differ in the rate of mutation.
For example we could imagine, without going to into details that could invalidate the example, that parts of the genome associated with the immune system could have a relatively higher mutation rate, because this would allow for a quicker adaptation to quickly evolving pathogens.
Is there any empirical support for that different part of a genome of some species have different mutation rates, that would give us empirical support for the possibility that some species under evolution have the ability to adjust (by NS itself or even epigenetics) the mutation rate of specific parts of the genome?
Clarification
I'm only interested in the mutations happening in the scope of the lifetime of a individual organism, I'm not interested in whether the mutations persisted under NS are equally distributed over the genome.

Well, for start, there are "mutational hot spots", regions that are more prone to mutation than others.
As for immune system genes, first of all, lung cells and heart cells and retina cells don't need to mutate those genes, because they don't use them.
But you are right that in immune cells there is a lot of DNA futzing in the sequences for the heavy and light chains, in order to generate diversity in T and B-cell receptors.  Those receptor sequences are built in a mix-and match fashion, like building an outfit from a closet with a few pairs of pants and a few shirts.  Add in some messiness in cutting out the specific sequences, and you have a fair bit of diversity in receptor sequences possible from a single genome.
Later, once a B-cell or T-cell meets a matching antigen, the cell multiplies, and each descendant cell is subject to somatic hypermutation, in the hopes that one of the tweaked sequences will better match the antigen.
But none of that is going to be very evolutionary relevant, since only mutations in gametes or gamete stem cells are passed on to the next generation.

Ah, interesting. However, the immune system was only as an hypothetical example, are there any "mutational hot spots" that are evolutionary relevant?

If by "consistent" you mean homogenous, the answer is no. Regions conserved among individuals (and/or species) tend to accumulate less mutations (specially avoiding deleterious mutations). Even within a gene sequence, there are conserved regions which accumulate low number of changes, whereas non-conserved regions accumulate many mutations.

It would be great if you could provide references for your response!

I'm a little confused, what do you mean by "conserved regions"? Are you referring to the survival of the mutations in coming generations due to NS? In that case, this is not what I'm searching for in my question, where I do not care about survival of the mutations happening.

@Alex, yes, by "conserved regions" I mean a fragment of the DNA or protein sequence that is conserved. That is, if you compare the same fragment among different individuals in the same species (or among different species) you will see that most of the nucleotides/aminoacids are either identical, or very similar (i.e. similar chemical or physical properties, e.g. same charge or size). These regions frequently are functional (e.g. a conserved protein region is involved in the catalytic activity) and mutations tend to be deleterious, hence they are eliminated by natural selection.

@Bez, thanks, I will try to include some references, I am trying to find which ones are more appropriate so it may take some time.

@Alex, if I understand correctly then, you want to know the mutation rate during the lifespan of an individual, and whether this is homogenous thorough the genome? That is challenging since there is no studies (AFAIK) on the evolution of an individual's genome over time. However, swbarnes2's comment about mutation hot spots may be indeed relevant to this. For example, this paper PMID:8832894 describes the existence of nonrandom patterns (mutation hot spots) in the gene TP53 (P53) associated with lung cancer.

Another paper that might be relevant: PMID:9926936

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Are there any known mutual symbiotic relationships that has more than two agents?
We are all familiar with the examples of symbiotic relationships in nature consisting of two agents, like lichen or the co-evolvement between certain birds and flowering plants.
Do we know of any mutually symbiotic relationships that has three of a even higher number of agents?
Edit: To make a implicit distinction clear, let's specify that the agents in question have distinctive and fully interdependent roles in the symbiosis. In contrast to a scenario where a range of bird species might co-evolve for a single specific flower and have the same role as pollinators in the symbiosis.
This image represents my current models in thinking about this:

The type I'm searching for here is mainly the "3-agent symbiosis", but the bidirectional one is of interest as well.

I think what you are asking for is "Multiple Mutualism". Normally,

Most of the known cases of multiple mutualism involve relationships in
which two of the partners are at the same organizational level—usually
two bacteria that might be interacting directly—but are both essential
for the survival of the host
— Entente cordiale: Multiple symbiosis illustrates the intricate interconnectivity of nature -Philip Hunter

For example, the glassy-winged sharpshooter (Homalodisca coagulata) primarily feeds on xylem-fluid which is low on organic nutrients…so it depends on 2 bacteria, Baumannia cicadellinicola and Sulcia muelleri. The sharpshooter provides these with raw carbon skeletons present in the xylem fluid, and those bacteria in return synthesizes vitamins, essential amino acids, etc. For more detailed study, see Wu et al, 2006.
However, there are also examples of three-way mutualistic symbioses in which all the partners are at different organizational levels. One known case involving a virus, a bacterium and an insect, see Moran NA, Degnan PH, Santos SR, Dunbar HE, Ochman H (2005) The players in a mutualistic symbiosis: insects, bacteria, viruses, and virulence genes. Proc Natl Acad Sci USA 102: 16919–16926
Anyway, the essence as stated by Andreas Brune, Professor of Biogeochemistry at the Max Planck Institute for Terrestrial Microbiology in Marburg, Germany:

Multiple symbiosis is probably more widespread than we think, especially in view of the symbiotic systems involving different organizational levels, for example between bacterium, nematode and insect, or bacterium, protozoan and insect.

@inf3rno , thank you for your appreciation...but would you mind , if I ask you to kindly remove the last link( http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1559669/#__ffn_sectitle )from your answer, which does not really is relevant to the topic of "human microbiom" you stressed upon & more importantly was originally posted in my article......thanks again...

It is relevant by this sentence: "Multipartite symbiosis is much more common in the nature than we previously thought." - I found it before reading your answer, but if that matters you...

@inf3rno , I'm really sorry, if inadvertantly I offended you...

The human body contains a few billion microbes (more than human cells), so we live in symbiosis with many different species. Some of them protect us from infections, some of them help in the digestion, and so on... So I think the human body fulfills your requirements.

wikipedia - human microbiome

Normally we don't live in sterile environment. So we depend on our microflora in order to protect us against pathogens by preventing them to colonize e.g. our intestines. So without a sterile environment we would die in the lack of our microflora e.g. in a C. difficile infection. In exchange we give our microbes shelter (e.g. we protect them from oxygen, UV radiation, temperature changes) and food (e.g. carbohydrates we cannot digest, for example xylitol). So the human-microbiome relationship is a mutualism. Some of these microbes are not detected outside of the (not necessary human) host, so these relationships can be obligate. These microbes do not only support us, but each other as well. E.g. they help each other to digest nutritients (syntrophy), so they can live in mutualism with each other as well. So multipartite symbiosis certainly exists in the human body, and it seems like much more common in the nature than we previously thought.

2013 - Integrative analysis of the microbiome and metabolome of the human intestinal mucosal surface reveals exquisite inter-relationships
2003 - Honor thy symbionts
2014 - Cooperation, communication, and co-evolution: grand challenges in microbial symbiosis research
2007 - Interactions and competition within the microbial community of the human colon: links between diet and health
2005 - Host-Bacterial Mutualism in the Human Intestine
2013 - Metabolic modeling of species interaction in the human microbiome elucidates community-level assembly rules
2013 - It Takes a Village: Ecological and Fitness Impacts of Multipartite Mutualism
2006 - Entente cordiale: Multiple symbiosis illustrates the intricate interconnectivity of nature

Hmm... I didn't think of this, and that is probably because I had in mind a relationship where all the agents were fully interdependent. I guess one could see the scenario you take as an example as an aggregation of 2-agent relationships? However, +1 for bringing this to the surface anyway.

I'm not entirely sure that this constitutes symbiosis. It's a very valid point and +1 but I wonder if someone working in the field would consider it so.

symbiosis is a kind of relationship between two (or more) individuals from different species benefiting to both individuals (unlike commensalism or predation/parasitism), so I think the human microbiome is a good example. From @Alex comment above, I guess that Alex might be interested in obligate symbiosis. Human are totally dependent on their microbiome. There might have at least two species of bacteria living in humans gut that can't live anywhere else and without which humans cannot live. If this is the case, the human microbiome, is again a good example.

@Remi.b Not just in the gut, e.g. on the skin, mouth, etc... Btw. I think this is the usual in nature, every larger organism has its own microbiome.

@Remi.b Thank you for the term obligate symbiosis, but I would rather say that I'm interested in examples where the symbiotic chain is in the form of a ring (or maybe a distributed) network, whereas I can only see the human/micro-organism as a star network (a bunch of 2-agent symbiotic relations with a common agent). I will update the question once again. And on a second note, are we even truly in an obligate symbiosis here? If we would eat omnipotent antibiotics for breakfast, would we actually eventually die from the lack of micro-organisms?

@Alex I don't think it is a "star network", afaik microbes in biofilms know of each other. It is not certain whether we would die, since nobody has omnipotent antibiotics. You can get e.g. C. difficile infection without proper microbiome, which can be lethal.

@inf3rno How do they know of each other? As in having a symbiotic relationship between themselves as well?

@Alex I am not certain of that. It might be so. I am trying to find studies about that.

@Alex http://www.pnas.org/content/100/18/10452.full "The results emphasize the contributions of symbionts to postnatal gut development and host physiology, as well as the remarkable strategies these microorganisms have evolved to sustain their alliances." Btw. pathogens can work this way as well, e.g. Staphylococcus and Streptococcus strains can help to each other during an infection.

Hmm that was just the abstract, and that sentence is ambiguous, so it might be about human-microbe relationship and not microbe-microbe relationship. I try to find that section, or another article.

@inf3rno Thanks, if they have symbiotic relationships between themselves as well it would definitely be more what I'm looking for.

Oh, and we have sterile mice in labs, right? I'd assume that that makes a good case that our symbiotic relation with our micro-flora is not obligatory from the human perspective, touching on that subject again.

@Alex Afaik. when sterile mice meet an intestinal pathogen, they die very soon, but I am not an expert of the topic... (Another thing that humans are not mices.)

@inf3rno Ah, right so the obligatoryness might be in that it guards against invading pathogenic, not that we directly can't live without them, thanks for making that point clear. And thanks for providing support that this seems to be what I call "bidirectional n-agent symbiosis" in my picture as well. Will keep this question open for a while though to see if there might be other examples and maybe even the "pure" 3-agent symbiotic ring.

@Alex "Bifidobacterium longum, has no SusC/D homologs but contains transporters that allow it to recover oligosaccharides generated from dietary polysaccharides by species such as B. thetaiotaomicron" - from the same article.", "The distinctive features of the B. thetaiotaomicron glycobiome suggest that a hierarchical and collaborative nutritional network is embedded in the intestinal microbiota." - from the same article. So I think they live in symbiosis with each other as well. This is a relatively old article: 2003. Newer articles would contain more about the details of these relationships.

@Alex Guarding against invading pathogens is just one role of the intestinal microbiome. It has direct effect on the immune system and probably on the development of the brain as well. It helps to digest food, it produces vitamins, etc...

I'll edit my answer, we have too many comments... :-)

I can think of an example for the 3rd picture in your image "Common Agent With Multiple Symbiotic Relationships."
We have: 1.) a species of parasitoid wasp 2.) a species of plant and 3.) a species of moth.
The moth provides pollination activity for the plant. The plant provides a place for the moth to lay its eggs, and a food source for caterpillars once they hatch. Once the plant begins undergoing herbivory it releases Volatile Organic Compounds (VOCs) which attract the wasp and inform it that there are potential hosts nearby. The parasitoid parasitizes either the eggs or the larvae (depending on the species of wasp) and helps the plant by limiting the damage it sustains due to herbivory (like a body guard).
Common example species could be:
1.) Wasps of the genus Cotesia (parasitize caterpillars) or of the genus Trichogramma (parasitize eggs).
2.) Plants of the family Solanaceae (Datura, tomatoes, or potatoes)
3.) Sphinx moths of the genus Manduca
There is a lot of literature on the subject of VOCs and parasitoids, but if you need a quick reference here is one: http://chemse.oxfordjournals.org/content/30/9/739.short.

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What is this plant that spontaneously sprouted in my balcony?
I have a big pot on my balcony that has inhabited many kinds of plants over the years. One spring I got to unexpected sprouts from seeds the size of an apple or orange seed. One survived and grew to what is depicted in the pictures here, but then unfortunately I got an infestation of spider mites that killed it.
I had previously rented out the apartment, and I suspect that this is the result of a couple of seeds that they intentionally or unintentionally put here. My best guess is that this is some kind of berry or something else edible that you buy in a grocery store.
You can also see some sun damage on some of the leaves in the picture. The plant in question is the most visible in the pictures, the others in the packground are passion fruit.
There were no thorns, and the leaves felt a little bit hairy, kind of like a common nettle but shorter and a fussier feeling. The height in the pictures is about 30-40 cm and it was growing fast until the spider mite attack.
What could it be?

i saw a lamb eating a bramble leaf once so i tried one and they have a particular and defining taste and chewyness. if you can't wait until it flowers, i sugest that you try a raspberry and a bramble leaf sprout and compare it, it will probably be the same as one or the other.

It looks like a raspberry, or some other kind of similar berry plant (blackberry etc.). The triple leaves and the habit of the plant are characteristic. Birds will often eat them and "deposit" the seeds randomly around the Earth.
https://plantvillage.psu.edu/topics/blackberry/infos
Berry plants usually have thorns or develop them as they grow. If no thorns are present, then perhaps it is another type of interloping plant. Other plants do look similar. In which case, your photos are insufficient for more further identification.

Blackberry seems most likely as I commonly see them in random areas such as fencerows.

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Can anyone ID this fossilized bone
Is this a fossilized backbone? If so then from what?
This "bone" is approximately four inches (10 cm) wide by two inches (5 cm) deep and two inches (5 cm) tall. The texture is rock-like. If it resembles any bone familiar to anyone let me know or take a guess and I'll look into it. I found it in North central Texas in the ground by a massive fruitless mulberry tree on the top of a hill. It weighs about what a 2x2x4 inch chunk of average run of the mill stone would weigh.

Welcome to Bio.SE. As written, this post -- in my opinion -- is unanswerable and will be closed. Please review the guidelines for asking [tag:species-identification] questions. You need to update your post with size(s), location, circumstances, etc. Given the unclear nature of your specimen, photographs from multiple angles with better lighting will be necessary. Describing the weight and texture might also be relevant. Please add as much detail as you can. Thanks

Please add a more specific location than "North America" Also note that "by a tree" is not helpful — please add environmental and geological information to the best of your ability. ——— In addition, in the future please proofread and edit your posts and make sure all the pictures are visible (you had inserted links into each other breaking most of them). Thanks!

Thanks for the updates. Please be very specific about the location you found it. North America is too coarse of a location -- ideally, we should know the exact location (or as close to it as possible). You should at least include the city. Knowing the ecology, natural history, and human history of the site you found it will also be relevant. If you know any of this please share. If not, then a specific location (and photo) would be best. Also, please provide more info about how you found it: What type of tree? on what type of property? How far down in the ground? Soil type? Etc...

It looks like just a rock, not fossilized bone.

You can put this on the earth stack to be answered. I suggest adding pictures of all sides of the object not just multiple pictures of the same side from different angles, specifically and broken areas are helpful. locality will also be helpful, right now it just looks like a rock.

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Check simple human fetus answers
Based on this image and questions, could someone please check my answers?
Question 1: At which one of the following points will the blood passing the point be more oxygenated after birth than before it?
I would think at point P.
Question 2: At which one of the following points will the blood passing the point be significantly less oxygenated after birth than before it?
I think point L, because the blood should not lose any more oxygen as it travels through veins and the heart to the lungs.

Please see this sites policy for "homework" questions. Among other things, such questions must be appropriately tagged. Thanks!

It was not a homework question, but a practice question to demonstrate how a platform works before I take an online quiz, for which I have already included my thought process instead of asking for the answer outright. 2) I am unsure with which keywords to tag this as I am new to the community?

Please review the criteria on the page I listed. 2) homework is a tag, as is described on the that same page. In addition, please take the [tour] and to read [help] pages such as [ask]. The [meta] pages also contain many questions and answers about the expectations this community has for users. Please also consider whether [MedicalSciences.SE] is a better fit, but please do not crosspost, instead request migration. Also note that that site also has stringent expectations about prior research.

Well I added that tag, and I made a few changes since my responses would not have made sense.

Thank you for all of the downvotes, what a welcoming community. I thought it was just computer scientists with a toxicity problem.

I'm sorry you've found your first experience here unpleasant and I do understand that being downvoted can feel like a personal attack. However, downvotes are merely an evaluation of how appropriate a particular question is for this site. Your choice to view  that as "toxic" leads me to strongly encourage you to familiarize yourself with this sites [help] before your next post. Good luck!

@tyersome Sorry, I should have perhaps not worded that so harshly. Basically, where can I ask these style of questions to not upset people here? It was not even a homework question, but an example question for the official exam.

For question 1 I would agree with "P"
For question 2 the answer would be "M" although an argument could be made for "O". Consider that before birth "M" should be the points were blood contains the most oxygen since it is coming directly form the oxygen exchange While after birth it contains the least amount of oxygen becasue that exchange is lost and it instead only receiving blood from the body where most of the oxygen has been extracted. So the change at that point is about as large a change as possible.  I don't know how you got "L" it should have little to no change in oxygen content as both before and after birth it is receiving low oxygen blood from the body.

My point of view was L, M, and O are all equally deoxygenated after it goes through the capillaries at the very bottom of the image and should remain the same until the reach the lungs after birth. However, since the question focuses on AFTER birth then I agree it must be M because it has the biggest change from oxygenated to deoxygenated when the mother's maternal artery is disconnected.


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Statistician confused about exact SNP data type
I'm from a statistical (not biological) background, and I'm very confused about what exactly is the "data" associated with a SNP. Below, I'll explain things as best I can--please correct me if any point is wrong or otherwise unclear. Assume we're working with humans, since the following will change depending on the species. (Assume all cases of interest are biallelic.)
When a locus has an allele on least one chromosome, the measurement AA, Aa, or aa is called a SNP (pronounced "snip"). Therefore, using statistical language, SNPs are three level factors--this is the data associated with a SNP. As said earlier, if the factor has 1 level (ie it's only aa or only AA) then it's not a SNP.
Sometimes for humans it seems like people say a SNP is actually just one allele (so a two level factor, a or A). How is this possible? Do people sometimes only measure one allele instead of both to get the genotype?

Could you provide the source where they refer only to one allele?

@Hachiloni There is no one source, but this is an example: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0218306 . See the paragraph which begins "Second, we compare three SNP codings..."

You have laid out what your knowledge of SNPs in an admirable fashion, except for one important thing. You do not state what SNP stands for. The name describes the concept: single nucleotide polymorphism. A polymorphism is literally a difference in shape (here a difference in the physical form) of an object. The object is the DNA sequence of a gene, and the difference is in a single nucleotide. It is not defined by whether the alleles are Aa, AA or aa — just by the fact that at this position different bases are found (generally 2, but could be 3 or 4). Do what you will with your statistics.

Thank you, @David. That's a very helpful point--I ignored where the term "SNP" came from completely. (I've edited the answer to address that I'm focused on the biallelic case.) I'm not focused here on what to do with the data (i.e. what statistics to do), just what the data itself looks like. I believe this is a biological question since it's certainly not statistical. If the data was "a" or "A", would you think that's SNP data? Or must the data be "aa","Aa", or "AA" to be SNP data?

I don’t know. But surely there is a vast literature on this. I read (skim) papers in Nature on large comparative genome projects which refer to the incidence of SNPs. There was one in February. The impression I get is they are just looking at whether different bases are found at particular points and how many there are in the genomes they have sampled. You would really have to find the references to their methods and check yourself (unless someone else here knows).

@David Thanks again for your helpful perspective.

I think the prevuious answers provide lots of valuable and relevant information, but let me add additional prospective:

As noted, SNP is a single nucleotide polumorphism, whereas notation AA, Aa, aa, etc. may refer to many other types of mutation: e.g., these could be whole genes, differing on many locations. Another common type of mutation is insertions/deletions, where one gene may lack whole segments (rather than  contain different nucleotides).
SNPs are used in particular contexts, where the change of genome is insignificant: e.g., when treating highly conserving human genome or when treating a variable genome on a short time scale, where only few changes happen. In this case we take the most frequent/initial genome as the reference and describe deviations from it as SNPs ("snips"). This is not always, possible - e.g., when multiple alleles are present (a single nucleotide can be in four states, A, C, G, T and all of these may have to be accounted for, e.g., when analyzing the evolution of viruses).
Depending on the problem, one may want to discuss population genetics of an organism in terms of genotypes or in terms of allels - even when a single organism carries multiple allele (e.g., two copies in a diploid organism). AA, Aa, aa are genotypes, whereas A, a are alleles. SNP is a change in allele rather than in a genotype. (But I do admit that biological language is often unprecise.)

Wow, thank you. This is incredibly helpful and fills in a lot of missing gaps for me.

@user257566 I also come from non-biological background, so I probably encountered similar issues in understanding these things. For population genetics I recommend also the Gillespie's little book. It is somewhat sketchy, but might be easier to work through than real pop gen stuff: https://www.amazon.com/Population-Genetics-John-H-Gillespie/dp/0801880092

SNP is not a specific data type but rather a biological phenomenon. The abbreviation "Single Nucleotide Polymorphism"  only means there is a variability (between individuals) in a single letter in a specific position in DNA sequence. It depends on the speaker how they decide to describe the variability; wether they choose to focus on the possible sequences and say for example "There is only A or T in this position" or they focus on possible human genotypes and spells out all combinations (AA, AT, TT).
What constitutes as SNP data depends entirely on research question, used organism (diploid/haploid/polyploid) and experimental design.
Article you link in your comment uses oat lines and not individuals from outbreeding population. Oat like arabidopsis is naturaly highly self polinating so creating highly homozygous inbred lines is relatively easy. In this case it is reasonable for the researches to expect only AA or aa genotypes in each line.
Edit: Since you asked for more examples where the researcher chooses to focus on alleles instead of genotypes. Many SNP genotypes distribution fit Hardy-Weinberg equations. If that is the case, the frequency of genotypes can be calculated from an allele frequency in population. The researcher might ask: "Is the frequency of allele a different in population/group 1 from population/group 2?" They collect data from indivuduals in group 1 (AA, AA, Aa, Aa, aa) and group 2 (Aa, Aa, aa, aa, aa). They decide to treat each allele as independent measurement (not dependent on individual it comes from) and poll the data: group 1 (AAAAAAaaaa), group 2 (AAaaaaaaaa) and then they do simple binomial test to answer their question.
Note: Even if Hardy-Weinberg equilibrium is not met, the questions about of allele frequency are is still valid biological questions (with slightly different use/interpretation down the line).

Thanks. Could you provide other examples where it's reasonable to only focus on the value of one allele (when ploidy is at least 2) to constitute a SNP? Your argument for the linked paper seems to be that researchers who care about the genotype can only measure one allele, which is interesting but circumvents the core problem I'm having.

Thanks for including the interesting edit. Not to bleed you dry here, but unfortunately due to my limited biological background, any allusion you make it completely lost on me. Could you clarify with examples what you're describing in the last sentence on when HW is not met?

I can refer you to Khan academy on HW principle. HW has several asumptions any of which can be not true in a real population. What I ment to say is that even in this situation it is still meaningful to talk about allele frequency. For example when a species is highly self polinating (like oat) resulting in more homozygots than expected from HW, we can still ask: is one allele more frequent in eg. high altitude population?

As said earlier, if the factor has 1 level (ie it's only aa or only
AA) then it's not a SNP.

If there is any variation in that base in your population, then it is a SNP, even if you are not looking at a heterozygote.
Anyway, if you are talking about a SNP, people will generally refer to it by its base, not be the name of the allele it generates.  (And actually lots of time, the alleles are not named as simply as A and a.  That notation is helpful when dealing with perfectly Mendelian middle school genetics homework problems, but in the real world, most data doesn't fit that paradigm.

Thanks. That quoted passage is in fact saying if there's no variation (ie if its only aa or only AA that have been observed). Further, it's been a while since I've been to middle school so it's helpful to know what's covered there for context. However, I'm not talking about how to name SNPs (personally, I'm familiar with rs numbers for that.) Instead. I'm talking about what values they take. Names for things are helpful for me here than the concept they represent.

Why would you have notation for different alleles if there was no variation in any population?

Let me give you a back of the envelope calculation. The size of the human genome is 3 billon base pairs (BP). There are about 30 thousand genes in the human genome. Therefore, the size of a gene would be around 100 thousand BP (DNA does have non-coding regions, regulatory regions etc. Also a gene vary in size from a few hundred BP to more than 2 million. For the sake of simplicity, we can stick to this calculation). On the other hand, there are 5 million SNPs in human genome. Therefore, There would be a SNP in every 600 BP.
So, we can say with certainty that there would be genes that have more than one SNP. My suggestion would be, as @BagiM pointed out, do not confuse microscopic concepts with macroscopic ones.

Thank you for sharing your perspective. By "a or A" I meant an allele at a single locus, by "aa or Aa or AA", I meant a pair of alleles which constitute a genotype (in a human). Could you clarify what you mean by switching between microscopic and macroscopic?

SNP is a microscopic concept and Allele is a macroscopic concept. Allele is a very broad term and the molecular basis of this term could be numerous (@Vadim discussed it in his answer). The term was coined by Mendel himself. That too a long time before DNA was discovered. "a SNP is actually just one allele" -- is a wrong statement. There could be multiple SNPs inside an allele.

Thank you for clarifying my terminology--that's very helpful. I'm referring specifically to an allele as a variant in one base pair, and a genotype (for humans) as a pair of such alleles still at one base pair but now across two chromosomes. So my question is specifically about which one (between these two microscopic things) is used to represent SNPs.

None. SNPs are not defined in terms two chromosomes. Huge collection of DNA sequences are compared and specific positions on the sequence are found to show this polymorphism (which we call SNPs) while other regions of the sequence remain relatively conserved.

Ok, by none do you mean the former? The single loci?

SNP or not is something independent of how many chromosomes or alleles you are working with. To me, your question does not sound valid. Could you try to rephrase the question? Are you asking it for a specific allele or chromosome? If so, please look up what are the SNPs defined on that allele or chromosome from a genome data bank.


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Which single substance among Potassium and Phosphate has the greatest osmotic activity in the Intracellular fluid?
My physiology textbook mentions that potassium has the greatest concentration ( 155 mEq/L ) in the Intracellular fluid and that I thought would make it the most osmotically active but the answer given is phosphate and I can't understand how this is the case. Is it because a compound of phosphorus would contribute more osmoles than potassium?

I don't have an answer, though I have a suspicion it may have something to do with the charge of their ionic forms. Potassium ions have +1 charge. Phosphate ions (the most common form of phosphorus in cells) have a -3 charge.

Can you provide a short quote from your actual textbook?

@BryanKrause actually this is a review question given at the end of the chapter. In the chapter they have given the respective concentrations of potassium, phosphate and other ions only and explained about osmosis and other transport mechanisms in a cell.

@acvill I've thought of a solution but I am not sure.Osmosis is defined as the movement of water from the region of its higher concentration to lower concentration through a semipermeable membrane which is impermeable to the solute. Although potassium is more concentrated in ICF(155 mEq/L) it can pass through the membrane whereas phosphate which is less concentrated (90 mEq/L) cannot pass the membrane and hence is more osmotically active. Can this be the reason ?

I'm guessing if you go to the textbook section that the question pertains to you'll find what specifically the author is wanting you to take away.

@Bryan In the chapter there is actually no reference to anything called osmotic activity which is the reason I cannot understand on what factors osmotic activity might depend on.I think this a inference based question in which we ourselves have to find the cause based on the facts given within the chapter.Can you please check out the comment I made earlier and if that might be the possible explanation of the question.


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Is human zygote unicellular or multicellular
Is the human zygote which is formed by fusion of sperm and egg a unicellular structure? Bcz at some places the 2 celled stage which is formed due to cleavage has been labelled as the zygote. So is the zygote 2 celled stage or the unicellular structure which is formed initially.

first three lines of this page. https://www.google.com/search?q=zygote&oq=zygote&aqs=chrome..69i57j69i59j69i60&sourceid=chrome&ie=UTF-8 The zygote's single cell ... closing question

A zygote is produced when the gametes, a sperm and egg cell, combine with each other. This is unicellular. That one cell then duplicates into two cells, and then four cells. People don't really have a need to name this stage, but anyone would understand it if you just called it two-cell or four-cell within the context of zygotic development. As more cells are created (16+), the solid mass of undifferentiated cells is called a morula. This occurs around 3-5 days after fertilization. This then becomes a sort of hollow sphere of cells. These cells are now called blastomeres and the whole structure is called a blastula. When you hear a cell name with "blast" in it, it typically means it is a precursor to some other type of cell. In this case, those 16 or so cells are the precursor to a future human's entire body.


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Female preference for males who are already in a relationship
A common saying is that women are generally more attracted towards men who are already in a relationship, and this phenomena does seem to have its own place in popular culture that is not matched by a corresponding male preference for women who are already in a relationship.
From an intuitive viewpoint I think it would make sense from the woman's viewpoint in an system of information economics where the fact that a male is engaged in a successful relationship with another female, or several other females, might provide extra and positive information about the evolutionary value of the male.
But how about the possibility for a male to use the same trick?
Is there any empirical evidence for this behaviour at all either in humans or in other species, or is this just a cultural artefact in some human societies? If there is empirical support, is there a consensus on the plausible evolutionary pathways involved here?

Im not sure this is true. How does one measure 'attraction' anyways? And maybe the relationship has nothing to do with it. Maybe a guys who are desirable tend to be in more relationships, simply because they are desirable

@vonMises i agree with you girls look to be more attracted after a boy is in relationship,even though they were in touch with the person(boy).

This question appears to be off-topic because it is about social interactions.

There's tons of evidence and it's all anecdotal.  People in relationships tend to be people who it would be good to be in a relationship with, go figure.

This is a widely researched topic in the overlap between social sciences and evolutionary biology.  Evolution has become very influential in understanding human interaction and preferences.
This chapter from "The Adapted Mind : Evolutionary Psychology and the Generation of Culture" will give you an idea of how all this plays out in the big picture - its a fairly comprehensive review of many factors considered in human mate choice.  The study may be psychological, but the logic is derived from biology these days.  (stackexchange won't let me link to google books - you can search for the title and look at chapter 6).
Evolutionary tendencies will favor more successful offspring.  But for people it includes not only the genetic qualities of the mate (appearance, height, disease resistance, health) but also social qualities (how reliable or willing a mate is to support offspring).
First off you can see that there are many many factors which women take into consideration in their preferences.  Its commonly said they are more complex than men, but that's another question.  You have to take a range of factors holistically including the social environment.
I can't find this particular issue addressed in the literature, but I think that it might be attractive to women in some social settings.  If there is a lot competition for 'quality' mates or resources for instance - if you have very few secure males or pessimistic females might create pressure which would cause females to prefer males which were successful.
Its pretty easy to feel good about hypotheses like this.  I couldn't find a specific study, but perhaps someone else will.  There's a lot of such papers out there.
I should say that men are as easily led to do things by 'mate choice' psychology that aren't totally healthy or socially acceptable.  That's biology.


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When looking at skulls from early hominids, how do we know their language creation abilities?
If there are no vocal chords left, how do scientists deduce what sounds the specimen was able to create?

Can you provide us with a specific example of where this happened? Because normally, if they do so, I expect them to describe how they did it.

If there are no vocal chords left
The hyoid bone, which is part of the voice box, does fossilize -- at least occasionally -- and can be used to partially reconstruct the larynx capabilities, so this premise is wrong.

We now report the discovery of a well-preserved human hyoid bone from Middle Palaeolithic layers of Kebara Cave, Mount Carmel, Israel, dating from about 60,000 years BP. The bone is almost identical in size and shape to the hyoid of present-day populations, suggesting that there has been little or no change in the visceral skeleton (including the hyoid, middle ear ossicles, and inferentially the larynx) during the past 60,000 years of human evolution.

--A Middle Palaeolithic human hyoid bone

The Dikika australopithecine hyoid body proportions are chimpanzeelike.  ... The Kebara hyoid dimensions (body alone, and articulated body and greater horns) are almost all within the observed range for human hyoids. Discriminant functions clearly distinguish human from African ape hyoids and classify the Kebara 2 hyoid as human  ...  the expanded bulla characteristic of the African ape and australopithecine hyoid body is therefore interpreted as reflecting the presence of such a laryngeal air sac extension. Its absence in the human, Neanderthal, and H. heidelbergensis (Atapuerca SH) hyoids implicates the loss of the laryngeal air sacs as a derived Neanderthal and modern human trait ...

--Comparative Morphology of the Hominin and African Ape Hyoid Bone, a Possible Marker of the Evolution of Speech

Modelling of the potential acoustic capability of Neanderthal VTs [vocal tracts] was carried out by Lieberman et al. [24,25] based on their three-dimensional reconstruction of the La Chapelle-aux-Saints fossil ... A different approach to Neanderthal VT reconstruction was taken by Boë et al. [41] who maintained that the Neanderthal larynx and hyoid bone sat lower in the VT than in Lieberman's reconstruction ... In this paper, we report a new study of the speech potential of Neanderthals, based on reconstructions of the positions of the hyoid and tongue root

--Articulatory capacity of Neanderthals, a very recent and human-like fossil hominin

The description of a Neanderthal hyoid from Kebara Cave (Israel) in 1989 fuelled scientific debate on the evolution of speech and complex language. Gross anatomy of the Kebara 2 hyoid differs little from that of modern humans. ... Because internal architecture reflects the loadings to which a bone is routinely subjected, our findings are consistent with a capacity for speech in the Neanderthals.

--Micro-biomechanics of the Kebara 2 hyoid and its implications for speech in Neanderthals.
As well as larynx reconstruction and anatomic evidence, researchers have other lines of evidence about speech capabilities in Neanderthals and other non-modern humans, such as the genetics (especially the gene FOXP2).


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What happens to Km when enzyme concentration is *very* high?
Let Km be an empirical measurement of a certain enzyme with concentration [E]. Theoretically, this value is constant and shouldn't vary when [E] goes up or down. Now let [E']=10*Km. Under this concentration of enzyme, it's clear that if [S]=Km, V0 cannot be 1/2*Vmax (as there's only enough substrate to saturate 1/10-th of the enzyme molecules). What's happening here, and how does this relate to the derivation of the Michaelis-Menten equation?

I can imagine if your Kcat is sufficiently high and your Kr for the reverse reaction of [E][S] ↔ [ES] is sufficiently low, the assumptions that Michaelis-Menten kinetics work on begin to break down, like reversibility and equilibrium.

@CKM maybe, but those are not affected by concentration (and if they are, how?).

Michaelis-Menten is often challenging for students because of the importance of the conditions that must exist in order for the model to hold. Walking through the derivation and the relevance of the assumptions can be helpful. Berg's Biochemistry is available via NCBI, and the section on Michaelis-Menten kinetics does a good job here, illustrating the following points:
Assumption 1:  The rates of all the relevant reactions are linear.
This assumption is what allows us to write down the equations the derivation starts with. We look at each separate reaction, and say that the rate of that reaction is equal to some rate constant times the concentration of each thing on the left side. From the equation $E + S \rightleftharpoons ES \rightarrow E + P$, we get the following

$E + S \rightarrow ES$

$Rate = k_1[E][S]$

$ES \rightarrow E + S$

$Rate = k_{-1}[ES]$

$ES \rightarrow E + P$

$Rate = k_2[ES]$

This assumption (the rate is linear) only matches the experimental evidence early on in the reaction, while most of the substrate is free $[S]$ (rather than bound up in $ES$).  Remember this. It will come into play when we evaluate assumption 3.
Assumption 2: The $ES \rightarrow E + P$ reaction is irreversible
In order for us to combine the above rate equations to derive the Michaelis-Menten equation, the only source of ES should be from $E + S \rightarrow ES$. We can't have any measurable $E + P \rightarrow ES$. Experimentally, for enzymes that follow Michaelis Menten kinetics, this is true when $[E]$ and $[P]$ are small relative to [ES]. So here we have our first requirement that $[E]$ be small. Biochemical reactions tend to not involve very high changes in free energy. The in situ free energy of ATP hydrolysis is the high end for a reaction in the cell, and that releases about $50kJ mol^{-1}$. We're not talking about combustion here. So in fact, these reactions are often reversible at appreciable levels of $[E]$ and $[P]$
Assumption 3: ES formation and breakdown is at steady state
This assumption is often described in a confusing way, i.e. the entire reaction ($E + S \rightarrow E + P$) is at steady state. Lets drill down to what we're actually talking about. In order to derive the MM equation. We need the rate of formation of $ES$ to equal the rate of breakdown of $ES$, that is, for $\frac{d[ES]}{dt} = 0$. That is steady state. Let's say that in words: the change in $[ES]$ needs to be zero. We only achieve steady state at an early point in the reaction (remember, we need most of the substrate to be free $[S]$ for assumption 1 to hold), if $[S]$ is substantially greater than $[E]$. $E$ needs to be saturated with $S$ while $S$ is still mostly in the free form. This is the key combination of assumptions that the situation you described violates.
Once we meet the three assumptions above, we can write down the following equality:
$k_1[E][S] = (k_{-1} + k_2)[ES]$
This equation says that the rate of formation of $ES$ (the rate from equation 1 at the top) is equal to the combined rate of the breakdown of $ES$, either into $E + S$ or $E + P$ (equations 2 and 3 at the top). Once we have this equality, we can derive the Michaelis-Menten equation: $V_o = V_{max} \frac{[S]}{[S] + K_m}$, where $K_m = \frac{k_{-1} + k_2}{k_1}$. Again, see Biochemistry to walk through this.

@user1136 these are interesting comments, and may be true, but I would note that your statements do not match how Michaelis-Menten kinetics is described in Berg and other Biochemistry textbooks I'm familiar with. I appreciate your answer, and would be curious to see you fill it out a little more.

The effect of high concentrations of enzyme on the Michaelis-Menten equation has been considered by M. F. Chaplin, "The effect of enzyme concentration on the Michaelis-Menten equation" published in the January 1981 issue of Trends in Biochemical Sciences, page VI, under the heading 'Textbook Error' (but, as far as I can determine, this article is not indexed in Pubmed or the like).
The author draws two important conclusions:

The assumption that the total enzyme concentration, $E_o$, must be less than the initial substrate concentration ($S_o$) is unnecessarily restrictive. The Michaelis-Menten equation holds, to  a very good approximation, when $E_o$ is greater than $S_o$ but is less than the Michaelis constant (!)
At high enzyme concentrations, a modified equation is proposed
$$ v_i = \frac{V_{max}[S_o]}{K_m + [S_o] + [E_o]}$$

The derivation of this equation is given in the cited reference.
Edit

A Dropbox link to the Chaplin reference. It does not seem to be available from anywhere, including the TIBS site (and it does not appear to be indexed in PubMed or the like)
A user asked (question now deleted) if $K_m$ is in any way dependent on E${_o}$

Setting
$$ K^{'}_m = K_m + E_o$$

it is seen that the substrate concentration at half-V$_{max}$ is $K^{'}_m$

that is the 'true' Michaelis constant will indeed depend on $E_o$ 'just a little bit' as the User suggested under the less restrictive assumptions considered by M.F. Chaplin (where $K_m$ is defined algebraically above).

Perhaps the User would consider un-deleting this question? IMO an interesting one.

Interesting. Is there experimental data in  this TIBS article?

@user1136 - I did look up at this question before asking that one, but this was about when the enzyme concentration was very high.  undeleted that one https://biology.stackexchange.com/questions/87870/why-does-not-km-change-with-enzyme-concentration

The derivation of the Michaelis–Menten equation makes a number of assumptions. The exact assumptions depend a bit on how you actually do the derivation, but most modern formulations depend on the steady state approximation. (For example, see here.)
In your situation, where the concentration of enzyme greatly exceeds the concentration of substrate, that assumption is violated. You'll never reach a steady-state. As such, applying the Michaelis–Menten equation to this particular situation gives inaccurate results. You certainly can model the kinetics of the reaction in these conditions, but you need to use other equations and approaches.
That's not to say that the Km doesn't apply in those situations. The Km of an enzyme is a property of the enzyme that applies even in the high-enzyme regime - it's just that the "conventional" interpretation of Km ("the concentration of substrate at which reaction rate is half maximal") doesn't apply. That statement is only true in the particular conditions which the Michaelis–Menten derivation holds.

I don't know if I'd agree that Km somehow applies in the situation the OP described. Km characterizes the reaction an enzyme is involved in, and concentrating the enzyme, for example in a pellet in a centrifuge, doesn't change the theoretical property of the enzyme, but there is no application, or use of Km that is valid unless [E] is low relative to [ES].  It's a constant you get when you write down the steady state equality. See my answer


text:
How does de-myelination occur in multiple sclerosis?
From what I understand, only the oligodendrocytes are affected in multiple sclerosis, and they are attacked by T cells which cross the blood-brain barrier. This leads me to two questions:

How is the blood-brain barrier affected in MS that allows T lymphocytes to cross the barrier?
Why do the T lymphocytes attack the oligodendroccytes? And when they do, what is the mechanism for de-myelination?

Thank you in advance!

Q2 is likely some kind of autoimmune disorder, which is very difficult to study.

T-cell migration to the brain is very limited and occurs at a very low level in healthy conditions, however during diseases the number of T cells passing through the blood-brain barrier is elevate due to increased expression of traffic signals and adhesive molecules.
I've found two good articles on how T-cells migrate through blood-brain barrier:
J Neural Transm (2006) 113: 477–485
Molecular mechanisms involved in T cell migration across
the blood–brain barrier, B. Engelhardt
and
 D. W. Miller, “Immunobiology of the blood-brain barrier.,” J. Neurovirol., vol. 5, no. 6, pp. 570–578, 1999.
During T-cell maturation, those that react too heavily to antigens of the body are killed to avoid having T-cells that would kill the body's own cells. But in rare cases this process fails and auto-reactive T-cell get released from the thymus (This short paper is good for starters). So the (simplified) reason why T-cells attack oligodendrocytes is that they falsely recognize them as pathogens, and therefore kill them. The loss of oligodendrocytes results in loss of myelin sheats.
Also in this paper (it holds many info on demyelination and multiple sclerosis) it is shown that even non-specicfic T-cells can open the way for antibodies through the blood-brain barried, and this results in extended demyelination.


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Photosystem 1 and 2; P680/P700; Chlorophyll a/b
I am getting slightly confused about how the above relate to each other. My current understanding is that P680 and P700 refer to the primary pigment reaction centres in Photosystems 2 and 1 respectively, with the numbers giving the peak wavelength of absorption. Now I initially thought that one of these primary pigment reaction centres must be composed of chlorophyll a and the other of chlorophyll b, hence the slightly differning absorption wavelengths. Instead, here it seems to suggest that the primary pigment reaction centre is always chlorophyll a. Most sources I have looked at do not specify what forms the primary pigment reaction centre (the Wikipedia article on photosynthetic reaction centre, for example, does not state for the general case of for photosystem 2; however it does mention that photosystem 1 has a special pair of chlorophyll a molecules at the centre).
So my specific questions are:

Is the primary pigment reaction centre in both photosystem 1 and 2 (i.e. P700 and P680) a pair of chlorophyll a molecules?
If so, what is chlorophyll b? Is it simply an accessory pigment?
Finally, if it is the case that the primary pigment reaction centre is chlorophyll a in both cases, how can it be that it absorbs at a different wavelength in the two photosystems if it is the same molecule?

The antenna pigments are predominantly chlorophyll b, xanthophylls, and carotenes. Chlorophyll a is known as the core pigment. Their absorption spectra are non-overlapping and broaden the range of light that can be absorbed in photosynthesis. The carotenoids have another role as an antioxidant to prevent photo-oxidative damage of chlorophyll molecules. Each antenna complex has between 250 and 400 pigment molecules and the energy they absorb is shuttled by resonance energy transfer to a specialized chlorophyll-protein complex known as the reaction center of each photosystem. The reaction center initiates a complex series of chemical reactions that capture energy in the form of chemical bonds.
  Source : https://googleweblight.com/i?u=https://en.m.wikipedia.org/wiki/Light-harvesting_complexes_of_green_plants&grqid=SbEQ4daG&hl=en-IN
In land plants, the light-harvesting antennae around photosystem II contain the majority of chlorophyll b. Hence, in shade-adapted chloroplasts, which have an increased ratio of photosystem II to photosystem I, there is a higher ratio of chlorophyll b to chlorophyll a.This is adaptive, as increasing chlorophyll b increases the range of wavelengths absorbed by the shade chloroplasts.
  Source: https://googleweblight.com/i?u=https://en.m.wikipedia.org/wiki/Chlorophyll_b&grqid=UwAfK7V5&hl=en-IN

So, both reaction center have chlorophyll A, which can absorb a range of wavelengths with maxima 662 nm.
Although, peak differs for two photosystems because of antenary proteins. More chlorophyll b in PS II transfers more energy to chlorophyll a at peak 680 nm.
More carotenes and xanthophyls in PS I transfers more energy to reaction center at 700 nm peak.

From what I understand both photosystems contain chlorophyll a, although they are modified differently in each case which changes their absorption spectra accordingly.
Sources:
en.wikipedia.org/wiki/Photosystem_I
www.ncbi.nlm.nih.gov/pubmed/11687208
www.ncbi.nlm.nih.gov/pubmed/11786359
Chlorophyll b is a pigment that differs from chl a by a single functional group:

And so it also has a different absorption spectrum:

As mentioned by Goel, some plants (or plant parts) that grow in shadows have a higher ratio of PSII (contains the majority of chlorophyll b en.wikipedia.org/wiki/Chlorophyll_b, Plant physiology and development by Taiz and Zeiger 6e, chapter 9) to PSI which results in an increased amount of chlorophyll b pigments in their photosynthetic tissues. This gives them an advantage as they absorb rays with wavelengths that are missed, or not absorbed efficiently, by the leaves that shade them.


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Bumblebee (?) identification
These bumblebees live on my balcony, in ventilation holes in doors and windows. I'm trying to find the exact name of the species, but I can't find any that look exactly like this. Their top segment is completely black and the bottom one is completely orange. I'm not 100% sure that these are bumblebees, but they behave like bumblebees, I mean, they fly horizontally and like nectar.
The location is in the southern part of Germany (Bavaria). The insects are ~20mm long, similar to the size of a honey bee.

The closest match is probably Bombus lapidarius, but Bombus lapidarius only have orange "tails", most of their bottom half is black.
It looks very similar or even identical to Bombus alpinus, but the problem here is that Bombus alpinus usually live in the mountains (and I'm in 300km from the closest mountains) and they are considered to be almost extinct in Germany.
Do you have any idea what they are called?

Welcome to Biology.SE! When you wrote "south of Germany" I'm guessing you mean in the southern part of Germany (what you wrote means somewhere to the south of Germany — i.e. could be Austria, Switzerland, Litchenstein, Italy ..). On this assumption I've made a minor edit to your post. Please also [edit] in the size of these insects since that can be essential to their identification. ——— Thanks!

@tyersome Yes, I meant the southern part of Germany (Bavaria). Thank you for the edit!

The animal in the photos is actually a female of Osmia cornuta. The horns are quite visible, which makes us exclude Osmia bicolor, and the thorax is entirely covered with black hair, which makes us exclude Osmia bicornis.

You are right, I mentioned this options in the comments to the other answer, but wasn't 100% sure. I spent some time observing those bees in the past few days and their behavior completely matches the behavior of Osmia cornuta. Fascinating creatures, never thought bees could be so big and hairy

Your pictures are quite blurry, but I think this is an Osmia, ie a Mason bee (and not a bumble bee). I think you can see a tendency of the “horns” that female Osmia bicornis (red mason bee) have on their heads on your pictures, so this is my guess. Females are much larger and generally darker than males on the thorax and head, and often quite black there while overall red on the abdomen.
Another option is O. bicolour, where females lack the “horns”of bicornis.
See eg this picture:

Head picture of female O. bicornis, to see the “horns” clearly (if it is indeed this species):

(Pictures from artportalen.se)
Another possible species in the same genus is Osmia bicolor (two-coloured mason-bee), which is more clearly divided in black-orange, see e.g.:

This species has an interesting biology, in that it is specialized on using snail shells for egglaying and preparing larval cells stored with food.

It looks similar on these two pictures, but completely different on other pictures of Osmia bicornis that I found. I'll take a closer look tomorrow and try to take better pictures to compare them.

They can differ quite a bit, but I find the pictures on e.g the wiki-page to be relatively unrepresentative. Look for the female “horns” in large, dark individuals, since this is diagnostic.

Pictures here are also ok (with good info): https://www.bumblebeeconservation.org/redmasonbee/  Also note that this is an yearly spring species, common in the first-flowering plants, so it fits your late-March observations.

No, definitely not this bee, the hair on their top half is yellow, while bees on my balcony have only black hair on the top half and are more hairy and thick in general.

Check Osmia bicolor as well (which is more clearly black-orange), but similar in overall body (e.g. https://www.artportalen.se/MediaLibrary/2019/5/9b1c2e64-6895-41ae-abfb-033f209cc68f_image.jpg). The reason I went for O. bicornis was the possible hints of the horns in your picture. However, sharper images would probably clear up the issue.

I updated pictures in the post, looks very similar to Osmia bicolor

@lawful_neutral I agree.O. bicolor is very likely. There might be closely related species in southern Germany that I don't know about, but this is a good bet.

https://www.botmuc.de/en/bees/ shows Osmia cornuta which is even more similar, so I'm not sure which one it is, but you are 100% right that it's a bee and not a bumblebee

Yes, I agree, and then the horns that I felt were visible also makes sense. O. cornuta isn’t common here (Sweden), so didn’t think about that species.


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Would the amino acid profile of lab-grown human meat perfectly match the dietary nutritional amino acid requirements for humans?
Whey protein is the food which has the most ideal (yet not perfect) amino acid profile for humans, whereas gelatin for example has a very poor and incomplete amino acid profile for humans. Would human meat grown in a lab such as they are working on with the meat alternatives match our amino acid requirements perfectly since it is actually human tissue?
UPDATE: I was not aware of any hazards that could be involved with consuming human tissues, so I am expanding the question to involve if there is any way to produce human meat safely in a laboratory setting.

I like the thinking behind this question, obviously human cell lines would not be viable for the numerous safety concerns but I guess it may be theoretically possible to engineer a synthetic tissue from another lineage that matches our exact nutritional requirements?

@JEJS What would the safety concerns be against consuming lab grown human tissues?

@wdbwdb1 disease vectors for a start, cooking does not destroy all infectious agents, by definition anything that spreads in humans vat grown cells can infect human cells thus posing a risk to the consumer. this is also why eating great apes is a very big risk.

@wdbwdb1 In addition to John's comments. Cannibalism is also a source for prion disease such as Bovine Spongiform Encephalopathy (BSE) a.k.a Mad Cow Disease and Creutzfeldt-Jakob Disease (CJD) among humans. An interesting case study is Kuru among the native population of Papua New Guinea from funerary cannibalism - https://en.wikipedia.org/wiki/Kuru_(disease)

I was not aware of any hazards that could be involved with consuming human tissues, so I am expanding the question to involve if there is any way to produce human meat safely in a laboratory setting.

I'm not an expert in nutrition, but I wouldn't necessarily expect human meat alone to exactly match human dietary amino acid requirements, at least not in the exact same abundances in which they are required. Many amino acids (including essential ones) are heavily involved in metabolic activities that have little to do with muscle tissue, like synthesis of hormones or neurotransmitters, so you wouldn't necessarily expect the concentration in muscle to match the dietary needs of a human perfectly.


text:
Trying to identify a plant with pain-killing properties from northern Vietnam
My mother-in-law uses this plant to alleviate her pain caused by a severe case of spondylitis. This is a plant used in traditional medicine in her village near Hanoi, Vietnam. She doesn't know the name of the plant, even in Vietnamese. I'm interested in identifying this plant mainly to find out its exact pharmacological properties (if any) and possible side-effects.
This is a climbing plant that can easily become as tall as a big tree. It is present year-round in this region.
To use it she just cuts it longitudinally and let it dry in the sun before boiling it and drinking the resulting decoction.
Here is a picture that she took of the plant in the wild. This is the one with the heart-shaped leaves.

And here is another picture where she removed the leaves from the plant.

Is the plant she uses the one with the heart-shaped leaves?  There are several plants in that picture near the vine stem, just want to make sure we are looking at the right plant.

Yes, the plant with the heart-shaped leaves is the one she uses. Sorry for the ambiguity. I have edited my question to clarify this.

it might be this plant https://en.wikipedia.org/wiki/Telosma_cordata it looks like some of the uses fit your description.


text:
Is the covid-19 vaccine-induced copy of the protein spike also damaging cells?
In recent scientific articles, it has been discovered how the spike protein not only is a respiratory disease but also damages blood vessels cells directly, and is connected with higher risk of trombosis.
So, does the Spike Protein produced by the covid-19 vaccine also bring the same risks and damage?
How many spike proteins the immune systems produces after being instructed by the vaccine, and how do they behave afterwards ?
Thank you
EDIT: adding some references
-1) https://www.salk.edu/news-release/the-novel-coronavirus-spike-protein-plays-additional-key-role-in-illness/
-2) https://scitechdaily.com/covid-19-is-a-vascular-disease-coronavirus-spike-protein-attacks-vascular-system-on-a-cellular-level/
-3) here it says how the "creation" of the spike protein happens-> Can spike protein induced cell fusion be triggered by the mRNA vaccine?
EDIT2: Someone in the comments pointed out how articles 1 and 2 reference the same paper, and one paper doesn't constitute discovery.
But how the spike protein which are "created" after the vaccine, behave? Are they the same as the one from Covid-19?
Are they harmful? if not, why ?

Both of those news releases reference the same paper. One paper does not a discovery make. Do you have any references to any other published papers showing the same thing?

I'm sorry, I don't :(

@Cris scientists are natural skeptics. I'm not saying the results of the paper are incorrect, but there needs to be corroborating work done independently - it's how the scientific method works.

Yes, I totally understand. But my question remains. Regardless of damages on blood vessels, are the other damages created by the spike protein in the virus itself, still acting when this same protein is produced by immune system after receiving instructions from the mRNA? (sorry if I said something imprecise)

Where did you read that spike proteins are "created" by the vaccine? Vaccines induce the production of antibodies that bind to viral structures, not the structures perse

here: https://biology.stackexchange.com/questions/98449/can-spike-protein-induced-cell-fusion-be-triggered-by-the-mrna-vaccine?rq=1 "they only lead to the production of the spike protein in the cell."

@MikeKatz45 your comment is true of most vaccines but several of the new covid vaccines cause the body to produce antigens, to which the immune system then creates antibodies.

Ah very well I see now, so we are not sure if the spike has the trombogenic effect even if its modified to not fuse as the linked question says

@MattDMo: Funny how only the Chinese financially sponsored this research (despite the fact that the paper has some American co-authors). Anyway, it's the dose that makes the poison; "damages some cells" is true of bare mRNA released into the bloodstream as well. Downregulation of some ACE2 receptors, which is what the paper claims, isn't that big of a deal unless it happens at a massive scale.

The spike proteins expressed by cells that take up mRNA or ChAdOx vaccines are modified so they cannot induce membrane fusion. However, the research article you refer to indicates that circulating spike protein damages endothelial cells simply by binding ACE2, which suggests vaccine derived spike protein could still cause this kind of damage if it enters the bloodstream somehow:

we show that S protein alone can damage vascular endothelial cells (ECs) by downregulating ACE2 and consequently inhibiting mitochondrial function.

Spike protein is necessarily attached to a membrane, so for it to damage cells by binding ACE2, bits of membrane containing the spike would need to be exported from the cells. The SARS-CoV-2 genes that allow it to do this in a real infection are not present in the vaccines, of course. The only other route I know of by which S protein could theoretically enter the blood is in exosomes. This article analyzed circulating exosomes from COVID patients and did not detect any viral proteins:

We did not identify viral proteins via the purification of exosomes; thus, we can conclude that viral particles were not purified together with exosomes

Research creating hybrid S-protein that can make spike-coated exosomes indicates the natural spike protein does not get into exosomes:

the S protein could not be detected in the sample from pSwt-transfected cells. In contrast, the SGTM protein could be detected in the pelleted supernatant of pSGTM-transfected cells.

I was not able to find any studies looking for spike protein in exosomes of vaccinated people, but it should be less likely than for the actual virus.

Thank you, so the vaccine derived spike protein also does damage after inoculating the vaccine? "how many" spike proteins are going to be present in the bloodstream after injection compared to a real infection? What do you mean "if it enters the bloodstream somehow" (since the vaccine is actually injected into the bloodstream) ? could you explain in more detail this part ?

@Cris, "it" in "if it enters the bloodstream somehow" refers to the subject in the clause, which is "vaccine derived spike protein" and not "vaccine".

as mgkrebbs says, when the vaccine is injected into the bloodstream it is mRNA, which cannot bind to ACE2. The vaccine enters a cell and causes the cell to produce spike protein. The spike protein can bind ACE2, in theory, but it is stuck to the cell and cannot reach. There does not appear to be any way for the spike protein from a vaccine to reach ACE2, so it should not be able to cause damage in the way described by your article.

Thank you. Thus if I understood correctly, the mRNA containing the message instructs the cells to produce S proteins, but they are stuck into the cells and therefore cannot bind to other cells' ACE2? How many of these S proteins are produced after mRna injection, and how many of them are necessary for immune system to recognize them and develop immune response? How does this recognition happens, after targeted cells finish production of the mutant S protein?

I don't really know. You should probably ask another question for that. Here is a question related to yours, reading it will give you some background information: https://biology.stackexchange.com/questions/96886/do-mrna-vaccines-cause-transfected-cells-to-be-killed-by-cytotoxic-t-cells?rq=1

That's a good question. My impression is the immune system would kill the cells displaying spike through phagocytosis, so the membranes would be recycled and the proteins digested. But I don't know enough about immunology to say for sure.

The Chadox1 Astrazeneca vaccine doesn't have the PP mutation, it is still able to drive cell-cell fusion. Most of the damage likely comes from the reaction of the immune system against cells expressing S on their surface, particularly at the 2nd dose.

Are you sure that spike protein cannot enter the bloodstream? From my sources, the median concentration of spike in plasma of vaccinated individuals is 47 pg/ml on day1/2. The spike concentration in an infected individual is most of the time below 70 pg/ml, and I am still looking for more accurate data. Reference can be provided upon request.

Yes, I'd like to see the reference, and No, I'm not completely sure.

Funny how only the Chinese financially sponsored this research you're talking about, despite the fact that the paper has some American co-authors. Anyway, it's the dose that makes the poison. This research may been published in good faith, but its findings have been used by anti-vaxxers out of context.
Downregulation of some ACE2 receptors, which is what the paper claims (in its title), isn't that big of a deal unless it happens at large scale. The study itself says that

vaccination-generated antibody and/or exogenous antibody against S protein not only protects the host from SARS-CoV-2 infectivity but also inhibits S protein-imposed endothelial injury.

In other words, they concede the condition is probably self-limiting in the immunocompetent.
Following [Moderna] mRNA vaccination (which has the highest dose of mRNA among the approved mRNA vaccines), levels of spike protein in the blood have generally too low to detect except by "ultrasensitive single-molecule array (Simoa) assays" and more importantly (with rare exceptions) anti-bodies cleared the spikes from blood in a few days, following the 1st dose, and from everyone in the test group a couple of days after the 2nd dose.

S1 antigen was detected as early as day 1 postvaccination, and peak levels were detected on average 5 days after the first injection.

The mean spike peak level was 62 pg/mL ± 13 pg/mL. After the second vaccine dose, no S1 or spike was detectable, and both antigens remained undetectable through day 56. For one individual (participant 8), spike was detected at day 29, 1 day after the second injection and was undetectable 2 days later.

Alas the latter paper lacks a comparison basis with what's detected following actual infections with SARS-CoV-2. Anyway, in correspondence to the press the lead author of this latter study concluded that

“We found that within a few days of the antigen appearing, the individuals developed antibodies that removed the antigen from the bloodstream,” he added. “Our conclusion was that the vaccine is working as intended.”

In other words, it's not a real clinical concern in most people. I'm not like totally dissing these findings, as they might be related to the myocarditis side effect of mRNA vaccines, but the fact that the latter most often happened after the 2nd dose suggests it's not the spike directly that's involved in that one.
By the way, "damages some [heart] cells" is true of bare mRNA (vaccine) released into the bloodstream as well, in animal models and in sufficient dose, at least in terms of detected inflammatory response. (For what's that worth, a co-author of this latter study is "the inventor [of] an intranasal influenza vectored SARS-CoV-2", i.e. no injection needed.)


text:
How long can you keep sheep eyes in formaldehyde before dissecting?
We're preparing for an experiment in our classroom and my teaching partner and I are at different points in the unit.  I am concerned that the experiment will be less successful because of the freshness of the eyes.  How long can they eyes be stored in the fridge before they have to be dissected and is freezing them an option?

Formaldehyde is a preservative, and is used to prevent decay. As long as the tissue is completely perfused (and there shouldn't be any issues with eyes that I'm aware of) it can be kept essentially forever. Have fun!

you can keep the samples in 4 degrees. Sometimes, in certain tissues, formaldehyde preservation makes them brittle. Or sometimes it makes certain slimy tissues easy to dissect. Nonetheless, it wont damage the morphology. And if you are not interested in protein/RNA isolation, then you can store the tissue as long as you want.


text:
How does your body ultimately recover from a cold?
Is it the eradication of the virus (assuming rhinovirus) by white blood cells? Or does your body somehow adapt to presence of the virus?

Great question.
Rhino Virus
For the rhinovirus in particular, it is eradicated.
Integrase
However for some of the retroviruses and other virus that contain an enzyme called 'integrase', they actually integrate their DNA with yours. That way as your cells go about their business, they make the virus genes too. However, you have some white blood cells called CD8 T Cells that mark these 'compromised cells' for death.
Evading
Some viruses though can remain cleverly hidden and don't turn on their own genes in your genome until the immune response goes down, or you stop taking anti-retroviral drugs.  HIV is a great example of a virus you can also 'live' with but never actually eradicate. The medicines you take can kill all the circulating virus down to a non detectable level. However, when you stop taking your meds, the DNA integrated in your genome will start making the virus again, thus you will always 'live' and can never eradicate it.


text:
How do ants spontaneously grow wings?
On hot summer nights we get flocks of ants that have grown wings (from what I know to migrate nests).
It appears the wings are not permanent, but are grown for a temporary purpose.
From what I know these events are triggered by climatic conditions (warm evenings).
In other species, wings seem like a really big deal and are grown from birth - wheras ants seem to just grow them 'on the spur of the moment'.
My question is How do ants spontaneously grow wings? Are they a spare layer of skin that is normally discarded and only comes into action when necessary?

See the Wikipedia entry for nuptual flight.
The ants that you see most often are (wingless) female workers. The winged ants that you see are male drones whose only role is to fly with young queens for mating. The drones follow a different developmental pathway, emerge from the pupa as winged ants, and then wait in the nest until conditions are right for the big event.


text:
What is the biological reason that some viruses cause sore joints (eg flu)?
Frequently I have experienced sore joints during a bad bout of influenza. I understand that during time of sickness, white blood cells are deployed in the blood stream. I also believe that white blood cells originate or relate to bone marrow. I'm wondering if there is a relationship between each of these
My question is: What is the biological reason that some viruses cause sore joints (eg flu)?

Almost certainly what is causing the joint pain isn't the virus, but rather its the body's response to the infection.   Cells that are infected with viruses can release proteins called interferons. Interferons can act on surrounding cells and cause them to become less susceptible to viral infection.  Other cells, including your immune cells respond to a virus by releasing other proteins into the blood called cytokines.  Cytokines activate other immune cells and can stimulate the body to generate a fever and 'lock up' molecules of iron so they are not available to invading bacteria.
Some cytokines act on the bone marrow and cause the pool of 'reserve' neutrophils (a type of white blood cell) to move into the bloodstream.  Other cytokines shut down the lymphatic vessels, causing lymph nodes to swell up.   And other molecules such as histamine and prostaglandins are released and also play a role.
SO what you are feeling when you get ill from a virus (or a bacteria or parasite) is the effect of this 'soup' of cytokines, interferons and other 'mediators'.  You may have some combination of fever, muscle/joint pain, runny nose, malaise, fatigue etc.
In the US you'll see TV adverts for drugs used to treat Rheumatoid Arthritis.  These drugs include synthetic proteins that bind to a cytokine called TNF-alpha and  block its role in inflammation.


text:
Name of scientist who discovered lifesaving drug and chose not to patent it?
I recall reading about a 20th century scientist who made a life-saving drug that could have patented it and made millions. He chose not to and saved the lives of millions around the globe.
I thought it was Frederick Banting - but it doesn't sound quite right.
None of the others in this list seem quite right.
My question is: What is the name of scientist who discovered lifesaving drug and chose not to patent it?

It's just possible that you are thinking of the failure to patent hybridoma technology. Georges Kohler and Cesar Milstein developed this at the MRC lab in Cambridge, and won a Nobel prize. Milstein was probably philosophically opposed to patenting, but the failure to do so was essentially a bureaucratic decision. It's an interesting story.

Patenting may not always be for earning profits. Patent also protects an invention form others who intend to make a profit out of it. I don't think any researcher became rich by selling drugs- it is the pharma companies that set high margins between the production and market price and make millions of dollars from other's illnesses (and in most cases the product is not developed by their R&D)

Dr Jonas Salk or Dr Albert Sabin who did not patent their respective polio vaccines. There are some more such researchers so I am not sure who exactly you are looking for but this would be a start.


text:
What is the chemical process involved in human hairs changing colour after sun exposure?
After a day at the beach, my skin tans due to Melanin.
But I also observe the black hairs on my arm turn a blond colour.
My question is What is the chemical process involved in human hairs changing colour after sun exposure?

Melanin is the main compound responsible for the color in hair. It is synthesized from the amino acid tyrosine. The absorption of tyrosine is around 280nm, which is a shorter wavelength than humans can see. Tyrosine can not absorb or preferentially scatter visible light in order to appear colored. It appears colorless as it scatters visible light equivalently. After tyrosine is synthesized into melanin, a pigment is formed which can be seen. Melanin scatters and absorbs light preferentially, it appears non-white.

The absorption of melanin is in the visible spectrum. This means it can absorb and scatter light in the visible spectrum differentially.

As your hair is exposed to sunlight, melanin begins to break down into lower molecular weight compounds which have their own absorbance spectra. The different forms of melanin and carotenoids in your hair can be oxidized by sunlight, giving hair a spectrum of possible colors.
Pigment in bleached hair has been oxidized into products absorbing light primarily outside the visible spectrum. White hair appears so because it lacks compounds which preferentially scatter and absorb light in the visible spectrum.

There is an interesting paper on this topicChemical-and
photo-bleaching of brown and red hair.


text:
When a thought 'crosses your mind', does it literally cross between left and right cerebral hemispheres?
I've heard that part of cognitive processing is information passing between left and right cerebral hemispheres.

This is what happens in the Cerebral Cortex which is divided into two hemispheres,
  left brain and right brain connected by a thick layer of nerve fibers called the corpus callosum. These nerve fibers allow messages to pass between the left and right brain
  hemispheres

My question is When a thought 'crosses your mind', does it literally cross between left and right cerebral hemispheres?
Assumptions:

I'm making a big leap from 'electronic impulses of neurons' to 'thoughts'.

You haven't really defined "a thought crossing your mind" at all. People without functioning corpus callosa have fleeting thoughts too, so at first glance, the answer is probably no.

Neuroscience doesn't really have a clear model for what a "thought" consists of exactly. Certain processes that are involved in thought have begun to be mapped--for example, this recent paper talks about a model for how the brain associates location in space with it's own mental map (http://www.ncbi.nlm.nih.gov/pubmed/24462102, I'll try to find something related that's not behind a paywall...). This one doesn't address your particular problem though, they only measured activity on one side of the brain. So basically, it might be possible to partially answer your question for more specific brain processes, but different kinds of "thoughts" are processed in different ways.
And of course I am also conflating impulses crossing the corpus callosum with the thoughts themselves, but I don't think this is really accurate. The most popular models in the labs I'm familiar with suggest that a "thought" is composed of a bunch of neural activity taken together rather than the activities of a few neurons on their own. But that might ultimately just be arguing semantics.


text:
How does fluorouracil inhibit pyrimidine synthesis?
I was reading in my pharmacology textbook about fluorouracil, and my book mentioned that fluorouracil is an antimetabolite whose function is to inhibit pyrimidine synthesis. However, I was curious to know how exactly does fluorouracil accomplish this. Is this drug involved in a specific mechanism that enables it to prevent pyrimidine synthesis? If so, how?

Your cells produce thymidine by converting uridine using an enzyme called Thymidylate Synthase. 5-Fluorouracil irreversibly inhibits this enzyme.
Here is the structure of 5-Fluorouracil:
Here is the mechanism the enzyme uses to make thymidine:

It looks like the enzyme forms a bond to the uridine ring through a sulfur. 5-Fluorouracil probably inhibits the reaction at the next step because fluorine is much more electronegative than the proton it replaced. This makes it harder for the electrons on the double bond in step 2 to attack the folate. Might also inhibit step 3 because the fluorine won't want to give up its electrons to reform the double bond. Because 5-fluorouracil is stuck to the enzyme's active site, the enzyme can't perform its given duty of converting uridine to thymidine. Because you can't use uridine in your DNA, your cells don't have enough thymidine to copy the DNA and replication is slowed. If thymidine supplies are low enough, cells might die.


text:
What is the most common way of administering loop diuretics and what is their time course of action?
I am reviewing some material on loop diuretics, and I am curious to know how these drugs are administered. Also, I am interested in knowing their time course of action once they are administered into the body.

I know that furosemide (there are more types of loop diuretics) can be given intravenously (but can be orally given as well (furosemide info sheet)). Effects of i.v. furosemide are pretty much immediate as it is carried quickly to the kidneys via the blood. After i.v. administration the effects wear off in about half an hour. t1/2 is about 2 hours, but likely depending on route of administration.


text:
What enables azacitidine to incorporate into both DNA and RNA?
I did a mini-project on the drug azacitidine for my pharmacology class, and I learned that azacitidine has the ability to incorporate into both DNA and RNA. I think this is really unique because a similar drug, decitabine, is exclusively incorporated into DNA. Are there any specific physical/structural characteristics of azacitidine that allow it to affect the structure and function of DNA/RNA? Any help would be greatly appreciated!

If you look at the very beginning of the Wikipedia page, you'll see that azacitidine is an analog of cytidine, the C letter of both DNA and RNA fame. Decitabine is a deoxy derivative, and hence would only be incorporated into deoxyribonucleic acid, or DNA.
Reading further, by structure azacitidine is ribonucleoside derivative, and is preferentially incorporated into RNA. However, it can be metabolized to 5-aza-2′-deoxycytidine-triphosphate and so be incorporated into DNA.


text:
How do Streptococcus thermophilus and Lactobacillus bulgaricus precipitate the curd of swiss cheese?
I learned in my food microbiology class that Streptococcus thermophilus and Lactobacillus bulgaricus precipitate the curd of swiss cheese. However, I was wondering what type of mechanisms do these bacteria use in order to accomplish this process.

lactic acid bacteria ferment the disaccharide lactose present in high amounts in milk to the three-carbon compound lactic acid, which acidifies the milk. this causes the proteins also present in milk to denaturate and coagulate, forming curdles. other causes/methods of curdling can be application of heat, salts or by adding the enzyme chymosin (rennin).

my bad, I am quite new here. is this satisfactory?

Well, maybe adding a better link would strengthen it a little.

all concepts in my answer are pretty googlable. I understood from Chris' comment that just dropping Wikipedia links on everything is not the best way to answer, so yeah.


text:
What roles do cyclooxygenase, lipoxygenase, and epoxygenase have in signal transduction?
Besides oxidizing fatty acids to form prostglandins, leukotrienes, and epoxides, what other roles do cyclooxygenase, lipoxygenase, and epoxygenase have in signal transduction?

Is this a homework question? Do you have any preliminary ideas?

No. I was reading about how these enzymes oxidize fatty acids in my textbook, but I was curious to know if they had any other important functions in signal transduction. I honestly don't have much of an idea on what else they could possibly do, since I have no previous knowledge on these particular enzymes.

Fair enought. The reason I asked was because your Q seemed to fall under our homework policy. Do you have any special reason to believe that these enzymes have other roles?

I just took a quick look.
These classes of enzymes are important to a family of lipid based molecules which perform intra and intercellular signalling with a lot of medical importance.
Epoxygenases can create epoxides of arachidonic acid,  which can modulate cell proliferation.  Arachidonic acid is a well known second messenger in many tissues in the cell, so these enzymes clearly would affect many signalling pathways.
Cyclooxygenases (COX) enzymes are such important mediators of inflammation signalling that they are the primary targets of aspirin and other Non steroidal anti-inflammatory drugs.
Lipoxygenases oxygenate compounds such as prostaglandins which are downstream from aranchidonic acid (as does COX).


text:
Why is gastric lavage considered to be helpful only if a patient comes to a hospital within 1 hour of a toxic ingestion?
Why is gastric lavage considered to be helpful only if a patient comes to a hospital within 1 hour of a toxic ingestion? How severe would the effects be if a patient came to the hospital after the recommended 1 hour time frame?

Gastric lavage only washes out ("lavages") the stomach ("gastrium"). Gastric emptying time is generally ~60-120 min, probably on the lower end of that for ingested liquids. After that amount of time, most of the toxic substance will be beyond the level of the pyloric sphincter (i.e. in the duodenum) and not accessible to lavage.
The second question is not possible to answer without some information about what specific toxic ingestion you are interested in knowing about.

Gastric emptying, which used to be well-accepted and seems intuitively
  beneficial, should not be routinely done. It does not clearly reduce
  overall morbidity or mortality and has risks. Gastric emptying is
  considered if it can be done within 1 h of a life-threatening
  ingestion. However, many poisonings manifest too late, and whether a
  poisoning is life threatening is not always clear. Thus, gastric
  emptying is seldom indicated and, if a caustic substance has been
  ingested, is contraindicated (see Caustic Ingestion).
If gastric emptying is used, gastric lavage is the preferred method.
  Gastric lavage may cause complications such as epistaxis, aspiration,
  or, rarely, oropharyngeal or esophageal injury. Syrup of ipecac has
  unpredictable effects, often causes prolonged vomiting, and may not
  remove substantial amounts of poison from the stomach. Syrup of ipecac
  may be warranted if the ingested agent is highly toxic and transport
  time to the emergency department is unusually long, but this is
  uncommon in the US.

ref:http://www.merckmanuals.com/professional/injuries_poisoning/poisoning/general_principles_of_poisoning.html#v1118455

Agreed, but the OP's question was not, "is gastric lavage routinely appropriate?" but rather "why does it need to be done within one hour?". Also, this is formatted as a quotation. If it is, could you provide attribution information?


text:
Identify a small spider from southern Poland / eastern Europe
Can anyone identify this spider that I have just found in my home?

Details:

location: Katowice, Upper Silesia, southern Poland, eastern Europe (46.42 N, 17.78 E),
size: ~3-3.5 cm (from tip of one leg to tip of opposite leg) / < 1 cm (corpse lenght),
date: July 23th, 2020 (summer, approx. 10:30 am).

Are those ice crystals in the photo? I'm curious as to what surface the spider is on, seems almost like the windshield of a car.

No, it can't be ice, because it is a middle of summer here, in Poland right now. I found this spider in one of my rooms, captured it gently to some plastic pot and then move it to a windowsill beyond one of my windows, where it was released. These marks you spotted are microfractures in the windowsill itself. It seems, it was painted with using a fairly cheap paint, since in went into this condition in less then 10 years of a moderate weather conditions, we have here.

It is a Barn Funnel Weaver (Tegenaria domestica), In Europe it is known as the domestic house spider.
Here's some photos of this species to prove the similarities:

What caught my eye in particular that made it more clear that it was this species was the color patterns on the abdomen and cephalothorax, the size you mentioned, the shape of the feelers as well as the location.
The slight difference in shade of color may be due to being a different variety of the species or simply because of the weather and habitat that the spider is in.

Thank you! As for the other differences you mention, I can't say anything specific as I am not a arachnology expert by no means. As for the size, I can be completely wrong, because when I came back to measure it, the spider was simply gone. But, I can see at Wikipedia: "Their body/legs ratio is typically 50–60%, which accounts for a body size of 7.5–11.5 mm" whic means, if I am not mistaken, that it has 2 cm at max. The one that I was observing certainly wasn't that small. I think it was more closer to 3 cm.

barn funnel weavers tend to have banded (striped) legs, while the specimen in question doesn't have banding and so it is likely Eratigena (a genus offshoot of Tegenaria) especially considering the leg length ratios. This is likely a 'giant house spider,' one of the Eratigena species.

@JimN You raise a fair point, I suggest you make a detailed answer.

Your spider is one of the Giant House Spiders. (Eratigena atrica complex). There are three species in this complex in Europe: E.atrica, E.duellica, E.saeva.
With the lack of banding in legs, it is not a barn funnel weaver as suggested in the other answer. ("Tegenaria spp. have banded legs, Eratigena spp. have plain legs" - https://www.naturespot.org.uk/species/giant-house-spider#:~:text=The%20former%20genus%20Tegenaria%20has,the%20genitals%20of%20mature%20specimens. )
Some sources will equate the Eratigena and Tegenaria genuses with each other, while most separate them with a notable recent change of the hobo spider which used to be Tegenaria agrestis and now considered Eratigena agrestis. Taxonomy is ever-changing. A hobo spider would have two dark stripes running lengthwise on the carapace like the barn funnel weaver, which your specimen does not have. The Carapace marking of giant house spiders can have two dark stripes or a other patterns that look like radial lines emanating from the centre of the carapace.
Here is a photo of a giant house spider:

They darken in colour as they grow in their shell/exoskeleton, and after molting, they are very light coloured (and vulnerable).
This second photo is one believed to be E. saeva: