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(Soft) Lay Survey of human natural history
I am looking for an introduction to the natural history of humans. I had originally thought Sapiens until I found out it is more a history and archeology book of dubious scientific accuracy. The Sorts of things I am interested in are: Neanderthal interbreeding, human canine bond, comparison of human with other primates.
If this is off topic, I am sorry. There was a similar question already posted some time ago, but the answers seems outdated.

Can you link to the previous question and note the ways in which it did not sufficiently address your question? Was it only because of time? Those are still some broad topics.

A general overview would be accomplished by a text book, however some of what you are asking about is rather in depth concepts I doubt you will find them covered in detail in the same book. the issue with newer science is it takes a while for it to be collected in a single textbook so you may have to search of each topic individually.  this site may at least help get you started with terminology. https://www2.palomar.edu/anthro/hominid/australo_2.htm


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Is presence of air necessary for silica gel to absorb moisture?
I am a biologist currently doing field work where I need to quickly dry leaf samples using silica gel crystals.  I use the orange indicating kind that are 2-4mm in size.  The setup is like this.  I stuff 1-2 leaves in a manila paper envelop which I drop in a ziplock bag containing ~1/8th cup of silica gel.  Then I squeeze out most of the air before sealing the ziplock.  The end goal here is to extract DNA from dried leaves when I am back in the lab.
I have had varied results in terms of drying and looking to achieve the maximum efficiency.  Recently it occurred to me whether squeezing air out is actually counterproductive to fast drying.
So my question is, whether presence of sufficient air necessary for silica gel to absorb moisture from leaves?  Essentially I am creating partial vacuum inside the ziplock.  Is that keeping silica from doing its job?

Welcome to Biology.SE!  I don't think you can create any sort of vacuum by squeezing the air out of a bag — the pressure inside and outside will be identical.  What you have done is minimized the volume of air inside the bag.  I would guess that the placement of the silica gel relative to the leaf and the porosity of the paper would be the most important factors in how rapidly the moisture would be transferred.

@tyersome I agree, the proximity of beads to leaf seems to be pretty important for drying.  It was mainly for this reason that I started squeezing air out so the beads wouldn't move as much.  I try to get them to cover the envelop.  Next, I will try using tea bags which should allow much rapid exchange of vapor.

That sounds like a good strategy — making sure the leaves are covered by silica gel on both sides should also help.  The waxiness of the leaf cuticle could also be a significant barrier — could you try crushing the leaves or dipping them in solvent?

@tyersome Crushing leaves is quite impractical as I am often collecting upwards of 60 specimen on a given day.  Moreover, contamination between samples is an important concern.  The less contact I make with leaves, the better.  I work with poplar species in the mountain west USA which tend to have sticky balsam on cuticle, which likely is also slowing the drying process down.

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Blinded sphinx first instar caterpillars not eating
I've got several freshly-hatched Blinded Sphinx Moth caterpillars (ID'd the mother), but they don't seem interested in any of the host plants I've offered. I had birch and basswood ready, and so far it's only basswood that's even gotten a nibble. I have access to cottonwood, willow, and aspen, and will probably go pick some up soon.
My question is-- is there a reason a caterpillar would ignore a plant that is a known host for the species?
Thanks!
Cal

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Sexual Reproduction in Humans
Is the human egg cell (ova) considered motile? We know that is is not actively motile but it is transferred via the fallopian tube to the uterus. Does that make it motile?

Hi! Please take a brief tour of the site (you'll even get a badge to prove it!). Feel free to nose around and check out the help center and such as well. :)

The fallopian tubes, also known as uterine tubes are uterine appendages, lined from inside with ciliated simple columnar epithelium, leading from the ovaries of female mammals into the uterus, via the uterotubal junction. They enable the passage of egg cells from the ovaries to the uterus.
The egg cell is typically not capable of active movement and hence not motile


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How are logarithmic trendline equations used to determine antibody concentrations in ELISA?
For example, say you have plotted a standard curve and managed to obtain a logarithimic trendline equation like:  y = mln(x) - b
And you are working with data that includes:
a) standards,their concentrations and absorbance readings (taken twice - with mean absorbance and blank absorbance also calculated)
b)samples (and their absorbance readings) that you want to know the concentration of
c) all the samples have been diluted two fold
Would you simply just rearrange the equation y = mln(x) - c  to:
x = (y + c) / mln
and input y value as being the mean absorbance readings of the samples you want the concentration of?
Are there any further steps after this? Or any I have missed out?
Is there anything I need to do with the dilution factor?
Do I have to do mean absorbance - mean blank, to get the correct absorbance readings to input as y or are the mean absorbance readings themselves sufficient?
Thank you

You can't write x = (y+c) / mln since ln is not a constant, rather it is a function on x. So, instead write ln(x) = (y + c) / m.

If by ln you mean the natural logarithm, then no, you can't rearrange the equation in that way. Try this:
$$m\cdot \ln(x) - c = y\\
\ln(x) = y + c\\
\ln(x) = \frac{y+c}{m}\\
\exp(\ln(x)) = \exp\left(\frac{y+c}{m}\right)\\
x = \exp\left(\frac{y+c}{m}\right)
$$

Yes, ln is for natural logarithm. Thank you, I will try to work it out using this equation.

@user1136 I'm not sure what new information you've added to this answer, nor do I understand what issue you have with what I have written above. The original question was answered simply by pointing out a mistake in the original poster's algebra.


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Non-coding DNA as a protection to deleterious mutations
We know that most part of our genome (at least 75 percent) is non-coding DNA. Can it be a way to protect the organism from mutations in important genes, such as the ones which control cellular cycle, as a mutations is much more likely to occur on these parts of the genome?
I've never been told if it could have such a function, and I thought about recently and wasn't able to find a clear answer.
So thanks in advance

You seem to be under the impression that there are a set number mutations per cell, which is not true.  The number of mutations is roughly proportional to the number of bases  — this is because mutations typically happen as a result of errors during DNA replication .1  Consequently, more DNA will not protect the coding portions of the genome from mutation.
The reason why mutations appear to be suppressed in coding regions is due to selection.2

References:
1: Lodish, H., Berk, A., Zipursky, S. L., Matsudaira, P., Baltimore, D., & Darnell, J. (2000). Molecular cell biology 4th edition. National Center for Biotechnology Information, Bookshelf.

2: Griffiths, A.J.F., Gelbart, W.M., Miller, J.H. and Lewontin, R.C. (1990) The Molecular Basis of Mutation. In: Modern Genetic Analysis. W.H. Freeman and Company, New York.


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Is it true that ethanol can have some positive effects?
I recently was reading this inforgrafics about excessive alcohol use. It is written:

No one should begin drinking or drink more frequently based on
  potential health benefits

I am surprised. Is there any potential health benefits of drinking alcohol?
To check this information, I made a little research and found this article of the Medical Daily: 7 Health Benefits Of Drinking Alcohol. Apparently, a moderate alcohol consumption (no more than 2 drinks a day for a men) can lower the risk of cardiovascular disease, lengthen the life, decrease the chances of demantia and diabetes, ...
But, for all of these facts, only one study is provided. So, I want to know if it is a well established fact that alcohol can have positive effects on health. And, if so, what is the corresponding dose to get these benefits?

After a quick googling - should be relevant: Piano. 2017. Alcohol’s Effects on the Cardiovascular System. Alcohol Res. (a review). See e.g. “The associations between drinking and CV diseases such as hypertension, coronary heart disease, stroke, peripheral arterial disease, and cardiomyopathy have been studied extensively and are outlined in this review. [...] Low-to-moderate alcohol use may mitigate certain mechanisms such as risk and hemostatic factors affecting atherosclerosis and inflammation”

The classic j shaped curve associated with alcohol consumption is discussed in this answer

Based on your comment to @Willk I think this question (and the title in particular) would benefit from you editing it to be more focused. As currently written their answer seems like a valid answer as would an answer that focused on how alcohol can reduce spoilage.

Alcohol can be used as a disinfectant, and can preserve water. I ate a bad egg in a Dehli restaurant in 97 and vomited for 8 days and survived on rehydration salts. On the 8th day, I went to buy a bottle a Gin, 30% alcohol or something, and I had a good dose of it straight. it must have gone through my body pretty vigorously because after the gin, a coal colored flegm came out the other way and within 24 hours of drinking the Gin i was 100% fine. perhaps it was even salmonella considering it was an egg.

Different studies result in different answers, but in general there seems to be a small beneficial health effect of small amounts of alcohol.  An example study is The association of lifetime alcohol use with mortality and cancer risk in older adults: A cohort study.  The results are summarised in this figure:

From this image we can see that it appears that less than four drinks a day is accosiated with a reduced risk of death, this effect being mostly cardiovascular related.
All these studies are observational studies rather than controlled studies.  This always leaves the possibility that what is being observed is correlation but not causality.

Alcohol has caloric value.
First worlders today have a wealth of high calorie food choices which make the caloric value of alcoholic drinks either irrelevant or detrimental.  But it was not always this way. In circumstances where other caloric sources were limited or unpalatable, alcohol supplied calories needed to supply the energy demand of workers.  Persons working energy-intensive jobs (such as field labor or factory work) have historically supplemented calories from food with calories from ethanol.  The below excerpt discusses the dietary habits of metalworkers in the late 1800s.
Drink, Temperance and the Working Class in Nineteenth Century Germany

Despite the overall improvement in dietary standards of the previous
  two or three decades, the situation of these Manheim workers suggests
  that alcohol remained an essential part of the working-class diet. If
  provided necessary calories in palatable form. The sharp flavor of
  alcoholic beverages could add spice to otherwise monotonous fare,
  providing a sense of warmth and fullness even when meals were cold and
  unsatisfying. Perhaps most important, alcohol provided energy in
  concentrated form. Alcohol, whether in the form of beer or spirits,
  enabled workers to reduce the sheer quantity of food that had to be
  gotten down each day. The distinguished physiologist Max Gruber
  calculated that a worker who consumed even a 10th of a liter of
  schnapps with the meal could come up with no energy loss, reduces
  potato and rye bread consumption but some 288 and 122 g
  respectively.”Try eating a kilo of black bread or two or more kilos of
  potatoes day after day”, Gruber told his well fed middle-class readers
  in 1888, “and you’ll discover what a relief it can be to substitute a
  pungent and stimulating beverage for a 10th of this mass”.

The health benefit of alcohol consumption here would be that of not starving in situations of high caloric expenditure.   calories are concentrated as compared to carbohydrates and distilled spirits also have an indefinite shelf life - not true of grains and potatoes.

My question was more about health and disease rather than the nutritional aspect.

Also, I would expect that since beverage alcohol is produced by fermentation, the beverage would have fewer calories than the grain it is made from, since some of the energy would have been used by the yeast.  That's even before considering that in most such beverages, a lot of the original material is often discarded as waste, or used as fertilizer or animal food.

@jamesqf - you are right that there is a net loss of calories on converting starch calories to alcohol.  In exchange you get alcohol calories that will not be used by fungi or rodent pests.  For Pierre - not starving is a positive effect on health last time I checked.

The energy provided by ethanol provides no other form than heating which is typically not needed because it is in abundance already.

@DavidJonsson - care to check your biochemical pathways again? Pretty sure that ethanol can be metabolized into the citric acid pathway or into lipid biosynthesis...

@bob1 I wrote typically. There is typically no need for more lipids in humans either. Regarding citric acid I will return on the subject if I coincidentally get to know more. Maybe citric acid cycle affection can explain why some feel ethanol increases body heat.  I think the most suitable way to investigate this is to find out how people react if intestinal creation of ethanol is lowered or if the alcohol dehydrogenase synthesis is overexpressed. Why don't you ask a new question regarding this?

@DavidJonsson my point was that the ethanol doesn't just produce heat it also produces lipids and energy in the form of ATP (if I remember the citric acid cycle correctly... it has been more than 20 years).

Psychological benefits
Alcohol allows to relieve stress, makes people friendlier, and establish closer social contacts. For this reason wine constitutes an important part of national culture in many countries: vodka in Russia, wine in France, beer in Germany and Belgium, wiskey in British islands, etc.
Protection from pathogens
Disinfecting properties of alcohol, mentioned in the comments, have actually played important role in human history: indeed, massive drinking of wine and beer in the Middle Ages largely protected population from water-borne disease, such as cholera. It is only with advent of drinks like tea and coffee, where microbes are eliminated via boiling, that the consumption of wine began to be considered unhealthy.

Protection from methanol.

@DKNguyen not sure what you mean. Please give more details.

Ethanol treats methanol poisoning because it competes with the methanol reducing how much of it is metabolized into toxic compounds before it can pass through you.

@DKNguyen this is true, but is there anything like natural methanol poisoning? (I.e., apart of mistakenly consuming methanol instead of ethanol.)

Eating a lot of fermented fruit? But I looked and it up...interesting...methanol is produced by the human digestive system. Toxicity is in the dose I guess.


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Converting microequivalents per liter to mg for sodium?
I read that a normal blood sodium level is between 135 and 145 milliequivalents per liter (mEq/L). Hyponatremia occurs when the sodium in your blood falls below 135 mEq/L.
How do I convert mEq/L to a value in milligrams (mg) so I can understand how many mg of sodium should be normally be ingested into the body?
I understand the values is between 250-500 mg/day, but would like to see this correlated with the mEq/L units.

This is not a good way to determine "how many mg of sodium should be normally be ingested".

Is there no conversion of the units?  What is the preferred way?

It just has nothing to do with the goal you are wanting to achieve. If you borrow a car and want to replace the gas you used, it doesn't help you to know how much fits in the tank.

@BryanKrause I don't understand your reasoning and analogy.  Can you explain in terms of units, metric and science what you are trying to say?  mEq/L is a concentration of sodium per liter of blood.  1 mEq/L = 1 mmol/L, 1 mmol/L = 46 mg/L.  I'm confused because this suggests 135 mmol/L * 46 (mg/L)/(mmol/L) = 6,210 mg/L concentration of sodium.  If the body has 5L of blood, then 6,210 mg/L * 5L = 31,050 mg of sodium is well above the RDV of 2,300 mg.  Ideas?

You don't need to eat as much salt as you have in your body (e.g., size of gas tank). You need to eat as much salt as you lose: through urine/feces, sweat, etc.

Does this suggest, based on above math in comment, that the body keeps 31,050 mg of salt in it's system and perhaps loses 250-500 mg of salt per day (through sweat and urine)?  Therefore we need to ingest 250-500 mg of salt per day to keep up with the loss?


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Glycemic Index and AUC Curve: why do two different foods have differing numbers?
The AUC Glucose/Blood Level curve Integral (area under curve) is used to calculate the Glycemic Index of certain foods. I have a question on why two sample foods with the same mass of carbohydrates can have different AUC Integrals or Glycemic Indices. I have some possible theories and would appreciate guidance.
Are these numbers different between the same sample size of 50 g of carbohydrates due to differing blood glucose levels, yet the same energy delivered to the body (perhaps in another form other then rising glucose)? Are the levels different due to differences in the body's digestion of the food? Or, is part of the glucose/blood integral of some lower Glycemic Index foods passing beyond the 2-hour window of measurement, which would cause a smaller integral and lower Glycemic Index?
BACKGROUND:
To be clear on definitions, the Glycemic Index is calculated using the relative rise of a blood glucose level two hours after consuming a food and it is the integral of (area under) a 2 hours glucose/blood response curve, following a 12 hour fast and ingestion of a sample food with 50 g of carbohydrates. The Index is calculated specifically using the ratio of a blood glucose AUC integral, ignoring the area below the fasting baseline (start of curve rise), for some carbohydrate source and a reference source. The reference source is usually either glucose or white bread. The trapezoidal rule is typically used to calculate the integral, although any method can be used. The Glycemic scale places pure Glucose at 100. The index is calculated using a ratio of two integrals using this formula: (SAMPLE_FOOD mmol/L * time)/(REFERENCE_FOOD mmol/L * time) * 100.
Where I'm confused is that two sample foods with 50 g of carbohydrates should have the same energy in calories, typically 200 kcal (4 kcal/g carb). I see the integral of the AUC curves for different foods can be different, indicating different glucose/blood level changes for each food over the two hour window. This makes me think, the foods have the same energy content, but are changing the body's blood glucose levels differently, resulting in different curves and Glycemic Indices. I first questioned whether the reason for this was that part of a food's curve lied outside the 2-hour window, raising the Glycemic Index slower than another food. I also read that the glucose levels will change differently depending on the type of carbohydrate, and some form of carbohydrates are even impossible for the body to digest and are either digested by bacteria in the gut or simply excreted in the feces, which would resulting in a lower glucose/blood level rise.
For example here is a 2-hour AUC curve of some fruits against glucose reference:

Your question points to the entire point of glycemic index: two foods with the same carbohydrate content (by mass) do not necessarily enter the bloodstream at equivalent rates.
Picture a gram of glucose; we know it's energy content (about 5 kcal) but how quickly will it get into the bloodstream? Whatever that answer is, now picture the same gram of glucose packaged as a time-release capsule. The time-release glucose will get absorbed into the bloodstream much slower so the peak glucose concentration will be much lower.
This fact -- that the peak blood glucose is lower for the time-release 'food' -- is what's quantified by the glycemic index. Since foods vary in the rapidness in which sugars are absorbed (and metabolized into insulin-eliciting sugars) the total carbohydrate content isn't a direct predictor for the peak blood glucose (or insulin); that's why glycemic index is a (theoretically) useful concept to assess the endocrinologist effects of different foods.
And yes, the slower peak means a) more of the curve lies outside a 2h window and b) more of the sugar is metabolized as its absorbed. Both factors decrease the total area of the integral. But it's the peak concentration that's thought to have the largest effect as the endocrine signal to release insulin.

Asparagus has a Glycemic Index of 15, does that imply that metabolism of glucose into the bloodstream occurs over about 6 hours, vs 2 hours for pure glucose (100 GI)?

I don't think I follow your math...the GI is only based on the 2h post-ingestion part of the blood glucose. The whole treatment doesn't address how long it takes for all th glucose to be absorbed into the bloodstream. 50g of asparagus only has about 0.94g of glucose in it! So the peak blood sugar could be as much as (50/0.94) 53 times higher for pure glucose compared to asparagus.


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What results would come from DNA analysis of several different types of DNA mixed together?
By "types," I mean several different species of animals. If, post extraction, the pure, isolated DNA of several different animals were mixed together and run through DNA analysis, I know the results would be inconclusive, but would there be any usable information returned at all? Would any species be individually identifiable?
The scenario is hypothetical and for a TTRPG plot; the players procured samples of a substance that they don't yet know are isolated DNA polymers (think the "extracting strawberry DNA" science experiment for children) from several different species of animals and a couple of humans, which was mixed together post-extraction. They'd like to have the DNA samples analyzed. Handwaving turnaround time (I know this process would realistically take weeks to months at the bare minimum, but if crime procedurals can deus-ex analysis results in 48 hours, so can my players), what would that analysis turn up?
Would they be able to parse specific species, or the ratio of one species to another (ie the sample only containing one or two dogs, but many, many small birds and squirrels)? They almost certainly wouldn't be able to turn up any kind of identifiable information on the human DNA, even with an uncontaminated reference sample, right?

I'd push back on your turnaround time in the real world; depending on the technique, the motivation of the people involved, and access to equipment/reagents, this could be accomplished in a couple hours (PCR assays) to a couple days (DNA sequencing+analysis).

In your TTRPG you can kind of do whatever you want, but I guess I'd keep in mind that there isn't a "ANALYZE DNA"  button you push on some biology machine in the real world; what you output very much depends on what you go about trying to accomplish.

You may be interested in commercially available meat testing kits - DNA kits have been widely used to detect what certain food products are actually (or are actually not) made of. Some kits are designed to identify the presence/absence of a dozen or more animal species, which can be reliably detected at proportions even less than 1% of the total sample. There have been some high-profile cases of meats labelled beef or pork actually turning out to be horse, for example, which was revealed by DNA testing. It is quite routine to be able to identify what species of animal are present in a mixed DNA sample, and to estimate their contribution to the mix.
At a practical level, this gets more difficult the more species you have in the mix, the less you know about what's in the mix, and as the concentration of any contributor decreases. But in principal, if the DNA is there, it can be sequenced and identified bioinformatically. It would be feasible to isolate human DNA from a mix of many animals, although you'd have a harder time with highly conserved genomic regions that are consistent across many species. But there are some regions of the genome that are uniquely human, which could be used positively ID a particular human's DNA among a mix of different species.
Overall, you can in theory learn a lot from a mixed-DNA sample, including the species present, their relative contribution, and even tell apart individuals within a species and identify whether any of the DNA matches the reference of a particular individual.

Minor criticism: while I expect there to be readily google-able support for this answer, it's handy to have a specific trustworthy source linked in an answer.


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Why does the axillary nerve have root value of C5 and C6 only and not C5, C6, C7, C8 and T1?
Posterior cord is formed by the posterior division of all the three trunks, so shouldn't the root value be all the spinal nerves of the brachial plexus which is the case for radial nerve?

It would be helpful to provide sources/references that support your question. Why do you think the axillary nerve has fibers from C7, C8, and T1, in addition to C5 and C6?

All the plexus system in our body is just like electrical wiring. In case if fibres from different spinal segments are coming together to form a single nerve they donot get mixed up . In their further course they may get separate. Though there may be fibres other than of c5 and c6 in posterior cord the fibres that forms the axillary nerve is c5 and c6 fibres. There are other examples of these kind of seperation where though fibers come together and looks like a single nerve but in their further course they are seperated . One of the example is superior root of ansa cervicalis.


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Why does oogenesis have to begin in foetal stage itself?
In males, spermatogenesis begins after puberty and they retain this ability throughout their life time. However, in females, oogenesis begins and ends in the foetal stage itself and the female is unable to generate any more oocytes in her lifetime. Is there any reason for this assymetry in nature?

For ref: This and this.

Welcome Muralidhar. This is not simply a Q&A site, here we are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are. You should also take our [tour] and refer to the [help] for guidance as to the ways of any site you post on, see our section on how to ask.


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What could be a refuge in host-parasitoid models
I was reading about refuge effect in host-parasitoid models and  I found somewhere that refuge does not have to be only a place in habitat where hosts can hide, but also some "situation" that allows them to be protected from parasitoid. So let's assume that the hosts are divided into two groups that live at the same place. The first group is for some reason protected from parasitoids and will not become parasitized (so they are in some kind of refuge, but not necessarily in physical refuge). Another group is exposed to parasitoids and may become infected. We can also assume that the hosts are in the same stage of development e.g. all of them are adults.
My question is: What would be an example of non-physical refuge in real life?
I would be grateful for any help.

The most typical situation is a size refuge, i.e. prey/hosts that are too large or too small to attack (or possibly too small to be useful) are not attacked, or are attacked less, than hosts that are the natural enemy (parasitoid/predator)'s preferred size.
Walde et al (1989) considered whether an observed spatial refuge pattern (less parasitism on the trunk and woody branches of trees) could be explained by a size refuge (i.e., hosts on the trunk and woody branches were smaller on average, so may have escaped predation due to their size)
Depending on what you mean by "situation" and "non-physical", other examples are

inversely density-dependent attack rates: if hosts occur in patches of different population density, and if natural enemies are not disproportionately attracted to high-density patches, then hosts in higher-density patches will have lower per capita rates of parasitism (because the risk of parasitism is shared by all of the individuals in the patch) (Price 1988)
gall wasps in galls with thicker walls are better protected from parasitoids (Ito and Hijii 2002)

Ito, M., and N. Hijii. “Factors Affecting Refuge from Parasitoid Attack in a Cynipid Wasp, Aphelonyx Glanduliferae.” Population Ecology 44, no. 1 (2002): 23–32. https://doi.org/10.1007/s101440200003.
Price, Peter W. “Inversely Density-Dependent Parasitism: The Role of Plant Refuges for Hosts.” Journal of Animal Ecology 57, no. 1 (1988): 89–96. https://doi.org/10.2307/4765.
Walde, Sandra J., Robert F. Luck, Dicky Sicki You, and William W. Murdoch. “A Refuge for Red Scale: The Role of Size-Selectivity by a Parasitoid Wasp.” Ecology 70, no. 6 (December 1989): 1700–1706. https://doi.org/10.2307/1938104.


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Would the environmental pressures imposed by humans make the housefly of today significantly harder to swat than their ancestors of 1000 years ago?
For context, I am primarily referring to Musca domestica.
Recently the thought occurred to me that due to short life cycle of the common housefly, and due to the fact that such flies have interacted with humans for thousands of years, it would be rather likely that human beings have served as an environmental factor that have affected the evolution of houseflies. Because of the short life cycle of the common housefly, would they been able to rabidly adjust to the environmental pressure of humans swatting them? Would the housefly of today be noticeably harder to swat than the flies of a thousand years ago? Would their be any way to know for sure?

I'm wondering how much of a dent in the fly population swatting makes. Perhaps you might show your research into the relative swat/survival rate (we're meant to show our prior attempts to answer when asking anyhow). Please take our [tour] and refer to the [help] for our guidelines.

@JiminyCricket Hi! Thank you for your response. I do not understand what you mean by providing my research. Do you mean research done by myself on the topic, research that might help with finding an answer, or my own research?

Suggestions; perhaps what you can find online about population density in your selected area (urban?), mean survival numbers to adult fly stage per generation, anything about mutation rates (?), and the likely numbers that you'd need to swat in order to make a dent in the population constituting selective pressure. Whatever you can't find/deduce, perhaps we can fill in some of the details, remembering that no population is going to be completely isolated, because - flies.

Cows have been around for ten thousands years,. Wildebeests for millions. Both have built-in fly swatters. They don’t seem to be swatting furiously. How could we possibly know? It’s not like records have been kept on attempts/successful-hits ratios. The answer is, “Maybe, who knows?” I’m sure there’s plenty of research on domestic flies and their abilities. This site requires that you show some effort to answer your question.

@JiminyCricket. Hello, thank you for your quick reply.
I have some studies that might be relevant to answering this question:
I found that study that shows that Musca domestica adapts very quickly to existential evolutionary pressures: https://onlinelibrary.wiley.com/doi/abs/10.1002/ps.5409
I also found this article that shows the average flight range of Musca domestica: https://eprints.um.edu.my/5793/
Finally, this article explains the mutation rate of Musca: https://portlandpress.com/biochemj/article-abstract/359/1/175/38665/Identification-and-characterization-of-mutations

Ah, that's great, can you now [edit] the question with any relevant info you found (plus the links). I'll make a point of checking back later, see if i can help at all.


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Graph of new species discovered per year
I'm looking for historical data on the number of new species described each year.
I found the RetroSOS report (page 3), which provides a time series for 2000–2009:
Year    Total number of new species described
------- -------------------------------------
2000    17,045
2001    17,003
2002    16,990
2003    17,357
2004    17,381
2005    16,424
2006    17,659
2007    18,689
2008    18,225
2009    19,232

This table suggests that the rate at which new species are described might be accelerating. To get a better sense of this, I'm looking for data going further back than 2000, and beyond 2009.

Here is an answer; as I'll explain, it's not getting the same numbers you quoted above (that could be a deep methodological rabbit hole), but it gives a reasonable answer.
I started from the data at ChecklistBank, specifically downloading this file (warning: 45 MB) and unzipping it.
The data file contained looks like this:
Biota [unranked]
  Animalia [kingdom]
    Acanthocephala Rudolphi, 1802 [phylum]
      Archiacanthocephala Meyer, 1931 [class]
        Apororhynchida Thapar, 1927 [order]
          Apororhynchidae Shipley, 1899 [family]
            Apororhynchus Shipley, 1899 [genus]
              *Arhynchus Shipley, 1896 [genus]
              *Neorhynchus de Marval, 1905 [genus]
              Apororhynchus aculeatus Meyer, 1931 [species]

So: we extract every line with the string "[species]"; pick out the 4-digit string following a comma; and sort and count these lines. This gives us a file with a count for each 4-digit string, which should be the year the species was described (there's of course more complication than that, but that gets us most of the way there).  Then we can filter out obvious mistakes and count the number of described species per year in what's left.

I drew blue rectangles for the Napoleonic wars, and World Wars I & II. I started to play with breaking out species described by Linnaeus but didn't finish troubleshooting ...
I posted the results here.
The numbers for 2000-2009 don't match the ones you posted above, but I assume that's because there are a million different ways you could count new species ... however, I think my method is at least reasonable/defensible ...
| count | year |
|-------|------|
| 9845  | 2000 |
| 9670  | 2001 |
| 11102 | 2002 |
| 10482 | 2003 |
| 10601 | 2004 |
| 9809  | 2005 |
| 10871 | 2006 |
| 11632 | 2007 |
| 10649 | 2008 |
| 9939  | 2009 |

system("grep \\\\[species\\\\] dataset-9837.txt | \
   grep -Pv '^[[:space:]]+\\*' | \
   grep -Po '(?<=, )[0-9]{4}(?= ?\\)?\\[)' | \
  sort | uniq -c > yrs.txt")
## 1. select lines with [species]
## 2. unselect lines starting with whitespace + * (deprecated synonyms)
##  -P = perl, v = complement
## 3. grab 4-digit string after ", " and before space/paren/square bracke
##    -o = extract only matched pattern
## 4. sort and count

## attempt to get Linnaean species
system("grep 'Linnaeus, 17.*\\[species\\]' dataset-9837.txt | \
   grep -Po '(?<=, )[0-9]{4}' | sort | uniq -c > linn.txt")

library(tidyverse)
dd <- (read_table("yrs.txt", col_names = FALSE)
    |> setNames(c("count", "year"))
    |> filter(year > 1750, year <= 2022)
)

linn <- (read_table("linn.txt", col_names = FALSE)
    |> setNames(c("count", "year"))
)

theme_set(theme_bw())
ggplot(dd, aes(year, count)) + geom_point() +
    geom_smooth(method = "gam",
                method.args = list(family = quasipoisson)) +
    scale_y_log10() +
    ## wars
    annotate(geom = "rect",
             ymin = rep(1, 3),
             ymax = rep(100000, 3),
             xmin = c(1803, 1914, 1939),
             xmax = c(1815,1919, 1946),
             alpha = 0.2,
             fill = "blue") +
    labs(y = "new species described")
ggsave("species.png")

Nice work. One larger problem is that plant names do not contain the year of publication, so you miss about 400k species and many more names. Synonyms would also need special attention as subsequent recombinations should not count as newly described species.

I do exclude lines starting with *, which I think (?) takes care of synonyms. Any idea where to get plant species checklists with year of description ... ?

https://powo.science.kew.org/ shows year of description, but I don't know if it can be ingested as easily as the COL data ...

For plants IPNI provides statistics per year of newly described names: https://www.ipni.org/statistics
For Fungi and Plant the annual rate of new species has been around 2000-2500 species/year each in the past decade according to https://nph.onlinelibrary.wiley.com/doi/10.1002/ppp3.10148


text:
Is it possible for a non-self antigen to NOT be recognized by the body?
The amazing diversity of antigens that the body can recognize (by virtue of T and B cells that express receptors complementary to them) is truly fascinating. The explanation mooted for this is the concept of V(D)J Recombination - somatic recombination creates a massive repertoire of TCRs and antibodies. As a result, any antigen, no matter how "foreign", hooks up with an immune cell triggering an immune response manifesting as a typical "cold".
I want to know if it is possible for this process of recombination to miss a particular antigen. In other words, can there be such an antigen which has no complementary antibody at all toward it?

Welcome to Biology StackExchange! Have you ever heard about antibody (binding) affinity? Namely, the ability to "recognize" an antigen is not all-or-nothing property, but a continuum (which can be quantified via affinity constant).

@Domen I am not sure if I follow, could you explain?
Do you mean to say that an antibody needn't be "perfectly" complementary to an antigen, but can somehow modify itself to better fit in if it's almost complementary?

I just wanted to emphasize that there is a varying degree of antibody affinity, and asking for "no affinity" is slightly ill-defined. Moreover, note that antigen is by definition something that can bind to a specific antibody. So I think your questions is more about whether there exists molecules that are not antigenic, right? In that case, look at haptens.

@Domen I referred the articles you linked, but I am sorry to say that I still do not understand.
For example, there are thousands of molecules in our body which, by virtue of immune tolerance, do not "bind" to antibodies simply because they are tolerated. Thus these are not "antigens". My question is - is it possible for there to be a molecule which is NOT tolerated (and thus SHOULD be "antigenic" in that it should bind to an antibody) because no complimentary antibody to it has been synthesized by somatic recombination?

@A-big-neutron Yes. Just look at vaccines - they stimulate the immune system to recognize antigen(s) that it otherwise isn't recognizing, or isn't responding to quickly enough. As far as tolerance is concerned, human proteins generally aren't bound by naturally-occurring TCRs and antibodies. However, if you were to immunize a rabbit, for example, with that protein and adjuvants, it would create antibodies to it.


text:
Why do people say that blue light is damaging to the eyes?
It's easy to find claims that blue light (e.g., from computer screens) is damaging to the eyes. For example, here is some discussion of the topic. Is there any physical mechanism by which blue (not violet or UV) can damage eyes?

Not an answer, but I can't help but notice that that's a commercial concern which sells blue-light blocking wearables.

At the bottom of the article are links to the relevant research article.


text:
What is the difference between a bacterial artificial chromosome (BAC) and a plasmid?
Is it just that a BAC is generally larger and artificially constructed? Or are there any other differences?

https://en.wikipedia.org/wiki/Bacterial_artificial_chromosome, https://en.wikipedia.org/wiki/Plasmid

BACs are a special kind of plasmid, based on E. coli's F-plasmid:

The BAC is based on a plasmid in Escherichia coli that is termed the F (for fertility) plasmid. The F plasmid (or F factor) contains information that makes possible the process called conjugation . In conjugation, two Escherichia coli bacteria can physically connect and an exchange of DNA can occur.
A BAC contains the conjugation promoting genetic information as well as stretch of DNA that is destined for incorporation into the bacterium.

Source
It isn't necessarily larger than a plasmid.

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


text:
What product of cellular respiration creates an acid when in solution with water?
What product of cellular respiration creates an acid when in solution with water?
Topic question really, haven't been able to find a direct answer.

A lot of them do, like malate, and citrate

So does carbon dioxide :)

@TanMath, the presence of organic acids like malate and citrate in central metabolism is not in itself acidifying. These species typically a produced in deprotonated forms and do not release protons. Acidification only occurs if there is a net release of protons during metabolism.

They are the cation of the acid. An acid is not just protons...

Well, they are anions, but they are conjugate bases to the acid, yes.  The point is that there is no acidification unless protons are released, and the existence of intermediates like malate and citrate does not imply proton release. Acidification is by definition release of protons.

Of course they are anions . I just gave an example there are many products from cellular respiration that can form acids in many ways and the ATP hydrolysis is not the only way a proton can be sourced. I don't know where you got that last bit from

It's not classed as an acid until the proton and the anion have interacted then it is a molecule that can be deprotonated ( an acid)

The question asks for a product of cellular respiration that creates an acid when in solution with water. Since H+ can form hydronium with water an example could be a proton or one of many anions.

@Roland sure, but it can be found as malic or citric acid, and then it would be and acid.

@TanMath There is some confusion here, maybe this deserves a question of its own ... Acidification is the lowering of pH, meaning increase of H+ concentration. That's the definition. An acid is so called because it is a compound capable of releasing H+. The conjugate base (anion) is not relevant here, besides determining pKa. Biochemical processes are only acidifying if they produce protons, or compounds that can release protons (which is really the same thing). TCA cycle produces a net of 1 H+ I think. Citrate and malate are weak bases; they do not release protons.

Cellular respiration itself, defined as the activity of the respiratory chain complexes I -- V (including ATP synthase), is not acidifying. On the contrary, free protons are captured during ATP synthesis, so cellular respiration acts to raise pH. But then ATP synthesis is always matched with ATP breakdown in reactions that utilize energy (muscle contraction, for example), and ATP breakdown liberates the captured protons again. So the complete cycle of ATP turnover is pH neutral. (For more information, see for examplle http://www.ncbi.nlm.nih.gov/pubmed/6298937)
The activity of the TCA cycle, on the other hand, produces CO$_2$ when oxidizing carbohydrates, and CO$_2$ dissolved in water is slightly acidic (pK$_a$ = 6.3) and so tends to lower pH. This is the main acidifying effect of oxidative metabolism. In animals, the CO$_2$ generated is of course released via the lungs, so the amount of CO$_2$ dissolved in body water is (more or less) constant, and therefore pH is stable.

Nice answer! :-)

CO2 is likely the answer you're looking for. This is especially true if this is in response to a 100 or 200 level biology course question. Based on the framing of the question, I would assume this is the case.
Though, as others have pointed out, there are other products that would qualify.

In tissue and cell culture I recall that after the vascular smooth muscle cell line i was working with had used up the compounds in the buffer the supernatant started to turn acidic due to presence of lactic acic.
The cells aerobicaly produce lactate which most likely converts to lactic acid with the H2O and other byproducts ( such as a H+ )present in the supernatant.
CO2 respiration can also form carbonic acid (H2CO3) with water. These are just a couple of examples.
A proton (which forms H3O+ with water) or one of many anions that could be produced by a cell or present in an aqueous  buffer, could create an acid when in solution with water.
Take into account there are many different cellular types and types of respiration.

Glycolytic metabolism is indeed overall acidifying, but the question was regarding oxidative metabolism. Also, the source of protons during glycolytic metabolism is not lactate production, but ATP hydrolysis.

Lactate is produced and the proton source is ATP hydrolysis. Two different things but the by products resulting from the processes form an  acidic solution . The H+ does come from the ATP hydrolysis but the cation of the acid does not.

I also mentioned the CO2 + H2O → H2CO3 in my answer.

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


text:
How does soap affect membrane permeability? Which component of the membrane does it affect?
In a lab we used distilled water + 3 drops of soap to examine how beetroot would be affected by it. I believe the beetroots membrane denatured and a red pigment leaked from it. However, I cannot explain why this has happened. Can anyone explain the topic question to me?

Detergents like soap solubilize, or dissolve, lipids. The cell, or plasma, membrane is a lipid bilayer. The detergent molecules form water-soluble micelles that contain the membrane lipids, so the membrane is completely ruptured, or gone.

@mdperry answered well. If you need some diagrams to help with understanding, this article Should be helpful.
As you surmised, when you add detergent, it is lysing some cells of the beetroot that contain pigment.  That pigment then gets released into solution.  I've annotated the image below for the micelles that gets formed, except I spelled it wrong :/


text:
Why is it important to have a restriction point? (G1-S phase control)
Why have eukaryotes evolved to control G1-S phase?
Surely if you could control G2-M phase very well, you will not get an excessive proliferation?
Thanks for your help.

The reason you want a check point in the transition from the G1 phase of mitosis to the S phase of mitosis, is that the cell needs to make sure that it synthesized all of the necessary proteins, and accumulated the necessary compounds with which to have DNA synthesis begin AND complete.
The transition from G1 to S is a point of commitment for the cell. There is no turning back at that point. It either needs to faithfully replicate the entire genome or it should die. An incompletely replicated genome would be disastrous for the cell.
If it tried to arrest and go backwards it would likely have too many copies of certain genes and those gene products would likely cause lethality to the cell. You would end up with all sorts of errors and breaks where replication forks collapsed. It would basically be death for the cell. What would be even worse would be if this cell was actually able to avoid the death signals, and at some point enter the cell cycle with all of these damaged chromosomes and you are looking at the possibilities of cancer.
If it arrested and then proceed to G2 and M and somehow got through those checkpoints, then you will have two daughter cells with incomplete genomes. Again if they could survive at all, then likely end up becoming good candidates to proceed down the road to cancer.
That is why G1 needs to be completed properly before the cell commits to replication. It is a point of no return and needs to be tightly regulated for the benefit of the multicellular organism.


text:
Moss CO2 consumption
I wish to calculate how much CO2 would a sq m of moss fixes to glucose in one day, taking about 20 degrees C average temperature, 55% humidity and a regular 8 hour day. Water and nutrients are at optimal amounts. Is there a formula I could use? I can't seem to find anything online.


text:
Solar Celiac Plexus location in body
Where is the Solar (Celiac) Plexus located in relation to the ribcage? I am reading this on the internet, and trying to learn more.
"The solar plexus — also called the celiac plexus — is a complex system of radiating nerves and ganglia. It's found in the pit of the stomach in front of the aorta."
Can someone point it out in the picture below? The purple and blue areas in the picture is the ribcage.

Since this diagram contains only bones and muscle (diaphragm), you should not expect to find other things on it, like nerves and ganglia.

hi @BryanKrause I am asking about solarplexus location spacial relationship to the rib cage,

Honestly, the Wikipedia article tells you what you need to know here.  It gives a decent illustration (courtesy of Gray's) that shows how these nerves radiate "like rays of the sun" from a spot a little below the diaphragm.  The tougher part is understanding how splanchnic nerves of the sympathetic nervous system work with the vagus nerve of the parasympathetic, etc.  Use a free textbook and start from the basics of the autonomic nervous system (Chapter 15); you'd never believe such a Rube Goldberg mechanism actually evolved!

Pretty much the center of your figure. The yellowish downward pointing arrowhead is where it is, possible represented by the arrowhead. Immediately below the ribs/sturnum


text:
What is the kind of this wasp killing spider from UK?
I heard a wasp buzzing rigorously and when I looked at it, it was caught in a spider web. The spider was on top of the wasp. After some time, they become silent. When I exhaled gently on them, spider moved but wasp did not. Later, the wasp was dead. The spider was obviously smaller than the wasp, yet it emerged victorious.
I attached a photo of the spider. While I am not sure whether this is the one killing the wasp, this certainly lives around the event site.

It should be around 1 cm in body length, excluding the legs. It is situated in UK.

If the wasp gets trapped in the web, then the advantage goes to the spider - it’s not a direct conflict...

Can you get a clearer picture?  Or perhaps you can pick it out from something like this: https://spiderid.com/locations/united-kingdom/

Hanging upside-down in a web suggests one of several groups, but in a building structure, and in what appears to be a messy, tangled web, I think we can safely put this one down as a member of the 'cobweb spiders' - the Theridiidae.  This group includes the infamous Black Widows, and some are known to successfully take relatively large and dangerous prey.
So, your particular spider has an obvious clue - the somewhat flattened dark abdomen with a large, light-colored patch in the middle of it.  The shape suggests Steatoda, and there is only one spider that this could be:  Steatoda nobilis, one of several spiders that frequently get called "False Widows".
Here are two links and a representative photo:
https://www.naturespot.org.uk/species/steatoda-nobilis
https://www.cabi.org/isc/datasheet/119917

Oh, I should add that despite the breathless hype the tabloids like to get up to, these spiders are known to be pretty harmless to people.  On rare occasions, a bite (which is not easy to get from these shy spiders) may produce symptoms like a mild Widow bite, but the discomfort seems to pass within a day or so.

Thank you very much. Even though I couldn't photographed it well enough to show the pattern on its stomach (or whatever it is called for an arachnid), it is obviously this one.


text:
Why do watermelons have a rind?
Random questions come up when talking with friends - such as this one!
We were curious: what are watermelon rinds good for? So what benefits does it give the watermelon? Why did mother nature give it such protection?

I apologize if this should not be the right forum to ask such a question.

If it didn't have a rind, the water inside would easily evaporate.

Thank you for the reply, jamesqf. Also @downvoter, care to explain the downvote?...

Possibly because you have shown no effort at prior research...

@Solar Mike: I don't know if you could really do research on a question like this.  Perhaps you could look at the evolution of melons (perhaps the water-containing flesh helped the seeds to sprout in their hot native climes?), and then the results of several thousand years of selective breeding by humans.  (None of the melons we eat today are what Mother Nature gave us, any more than wheat or corn are.)  You might find this interesting: https://hyperallergic.com/226096/the-evolution-of-the-watermelon-captured-in-still-lifes/

@jamesqf So you have answered your own question : Yes you can do research on watermelons... I was guessing as for the reason for the downvote unless you missed that. PS, I was not the downvoter...

@Solar Mike: While interesting, none of that really answers the OP's question.  It's like any "why" question in evolution: you can come up with a "Just So" story, but the only real explanation is that it (and previous changes) worked, so proto-melons survived.

You have answered the question yourself: it's protection.
Melons have originated in what is today South-Eastern Africa and Western India according to this source. In a hot and rather dry climate having a watery fruit can bring an advantage to the seeds (helping them to sprout in an otherwise dry soil). At the same time, any source of water would attract animals eating the fruit. A shell would protect the seeds during the ripening process like the shell of a nut prevents it from being eaten.
On the other hand, animals eating the melon might actually be desired, since fruit eating herbivores help spreading the undigested seeds. The shell would then especially protect the watery flesh from water evaporation or predators who are not helping to distribute the seeds. A ripe melon opens up and releases the seeds from their protective shell.


text:
How can we digest lactose even though it has Beta glycosidic linkages?
I have Read that we cannot digest cellulose because we do not have enzymes to digest Beta glycosidic linkages in Cellulose
Then how is it that we have an enzyme called Lactase to digest the Beta glycosidic linkages in lactose?
Also If we have evolutionarily developed Lactase ,Why didnt we develop "Cellulase " too ?

Humans have β-galactosidase (lactase) which allows them to break down the β-glycosidic linkages in lactose. This enzyme is inactive against cellulose. We also haven't evolved a cellulase, probably because we didn't need to. It's quite simple. Are you asking any further questions beyond these?

Please quote or provide a reference to what you have "read" when asking questions on this site. It is quite likely that you are misquoting or misunderstanding, and by checking the original we can put you right. Enzymes recognize their substrates — in this case not just a chemical bond, but the two sugars that it joins. These are different for cellulose (glucose only) and lactose (glucose, galactose). Also, please restrict yourself to one question at a time. The second question about why few animals have cellulases is quite separate. (It should be obvious why we evolved lactase.)

@SPr — I'm not sure it's quite so obvious why very few animals have not evolved cellulases. Ruminants and most insects that do "need to" use symbiotic bacteria. I think this might be an interesting question in itself. Is it something to do with the waxy coat on leaves, perhaps? I don't know.

Few animals have evolved cellulases, but they are a very tiny minority and they tend to be aquatic invertebrates or small insects with little gut tracts like termites; always different to large mammals. I must admit I don't understand "why didn't we develop X" questions though. I think the onus is on the person to reason that it would have been beneficial in the first place, at least to a more competitive degree than the absence of a trait. Consider free glucose in the anaerobic gut, in the presence of a diverse microbiome... Consider a lifelong lack or reduction of fiber... No thanks.

What I meant by the Second Question was that ,When we have developed β-galactosidase ,just based on the nature of the bond making the cellulose  must also be possible....that too Given the high advantage an animal with cellulase will have ,So, What property of cellulose has made the evolution of cellulase so rare? Or does the answer have nothing to do with the nature of cellulose but some  factors at the organism or ecosystem level?Or is it just pure luck?

One simple  reason is physical interaction.
lactose is only composed of two sugars, while cellulose is giant network of interlocked sugars. Cellulose keeps the sugars tightly packed in three dimensions. even getting to the bonding site is difficult.
human and many other lactases are a huge molecules that would never be able to fit on to a cellulose chain, while cellulase of often a tiny molecule as enzymes go and the active site is not buried in the center. Compare the two enzymes.

lactase

two different cellulase enzymes
Note the big difference in size. Also look at cellulase in action.

Notice it has to peel up the cellulose strip by strip, while lactose is just floating free in solution. This even limits the speed of cellulose breakdown. which means organisms that breakdown cellulose have to spend a log time doing it, while humans have a relatively short and fast digestive timeframe, so even if we could we would not get much from it.
These functional limits also makes a cellulase enzyme harder to evolve, since it can't be too large or in organisms with fast digestive processes.  We often forget the physical necessities of enzyme function. there are plenty of other reasons enzymes do not function on multiple substrates, but this is why is basically impossible to for evolution to change lactase into a cellulose cleaving enzyme.


text:
Why is the ability of a virus to get crystallized considered as a "Non living feature of a virus"?
My book states that the fact that :"Viruses can be crystallized" is a proof of their "Non living character"
Does that mean living things cannot be crystallized? If yes, why is that so?

Possible duplicate of Why isn't a virus "alive"?

Welcome to SE Biology. It is always necessary when quoting from sources in questions to state what the sources are. That way others can check the quotation is accurate, look at the context, and assess the credibility of the author. If you read the previous discussion of whether or not viruses are alive you will see that there is no recognized "touchstone" for life. Ability to be crystalized strikes me as one in a list of features where viruses are similar to non-living things.

Crystallization involves removing extraneous molecules, so that remaining molecules — here, virions, or virus particles — can form a crystalline or ordered structure. https://en.m.wikipedia.org/wiki/Crystallization
As far as cells go, cellular proteins can be crystallized (some more easily than others), as well as nucleic acids, but having those crystals alone is not sufficient for life. You need an input of water, energy, etc.
Making crystals from the constituent parts of cells would effectively kill that lifeform. On the other hand, you can take virus crystals, add a bit of disorder, and they will "wake up" and regain their infectious properties.
Viruses sit on a fine line of what constitutes life. To some extent, the discussion is philosophical in that definitions are chosen and the subject either meets those criteria or not, and some criteria are a bit more arbitrary than others.
Some have argued that viruses in infectious virion form are life, at the stage when infecting a cell and redirecting its machinery to make more virus particles. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2837877/
Over the decades, biology has shifted from a study of cells in Petri dishes, or monks growing peas, to a more abstracted investigation into information science and related fields and subjects: mathematics, entropy, statistics, physics. That perspective started with scientists like Schrödinger, Turing, and Von Neumann, and it continues in the modern day with work by Dawkins, England, and others.
Viruses have and continue to shape the evolution of life around them. In a way, they are frozen information, and the definition of life may be changed over time, as we gain a more broader picture of how things work.

Another minor question would be whether all viruses tolerate crystallization. Do you know anything about that? I couldn't find much through a superficial search.


text:
What are the negative consequences of a narrowed biodiversity to the planet?
In this question about the fires in the Amazon rainforest, a user responds with

It [the Amazon] is still a part of nature and burning it can narrow
  the diversity of both plants and animals, which can have consequences
  on the whole planet.

What are the negative consequences of a narrowed biodiversity to the planet?

Welcome to Biology.SE! We encourage you to do some research on your own and share what you have learned when asking questions here. In particular, this is an enormous question and there are many resources available with answers at everything from the elementary to the research level — e.g. google scholar ——— Please also take the time to go through the [tour] and then the help pages starting with [Ask] questions effectively on this site. Thanks!

From an ecological sense, cycles of living beings are intertwined. Breaking cycles affects life being able to live, reproduce, and die in a manageable way. Insects, animals, and plants help feed each other and help them reproduce. Fewer insects are less of a food source for animals and can't pollinate plants as much. Reduced animal populations are less of a food source for scavenger insects and don't feed plants through manure or decay after death. Fewer plants means less food and protection of insects and animals from predators. Predators overload on newly-available prey and their populations crash. It all intertwines.
From an environmental sense, the results of a narrowed biodiversity include putting more carbon into the atmosphere. In addition to warming the planet and the ocean, the ocean acts a carbon sink, acidifying in the process. This damages existing sea life that can only live within a certain pH and temperature range without sickening or dying. Some fish are trying to migrate and are dying off, due to lack of food where they are headed.
From a medical sense, burning down forests is stupidity. There are drugs that are naturally found in their rare plants, which have been developed into medications that save lives, e.g. Paclitaxel or Taxol. Only 1% of remaining rainforests have been explored for these plants and their compounds and we're stupidly burning them up. Nature has evolved many useful remedies, but we'll never know about the ones we destroyed, and that means more sickness and death.
For people obsessed with money, that medical sense translates just as well into pharmaceutical products and the resulting loss of jobs and profits.
All of these factors are linked together, hand-in-hand.

I appreciate the effort, but there are aspects of this answer I'm not thrilled with.  It mixes together loss of population density (paragraph 1: "fewer insects ... fewer plants ... fewer animals ..."), changes in the biogeochemical cycle (paragraph 2: warming and ocean acidification),  and changes in biodiversity.  Only the paragraph on bioprospecting is actually directly connected to biodiversity.


text:
If two different diseases have more than one common pathway, the relationship between their occurences?
I just wonder that are there any special relationship between the pathway and disease occurrence.
For example, there are cancer A and cancer B (and they have more than one common pathway). Then if one person was diagnosed with cancer A, does he have a high probability for getting cancer B? Could you recommend any researches for that?

I think that a good point to start is a classic work in literature that i've seen cited many times in my courses: http://www.cell.com/abstract/S0092-8674(11)00127-9


text:
Were there any vertebrates with 6 or more limbs?
My question is actually a bit more broad than what's in the title, but I don't know how to put it succinctly.  When I was trying to find the answer to that question, I found that all known terrestrial vertebrates are ultimately descended from a species of lobe-finned fish that had 2 sets of bilaterally symmetric fins (which excludes the dorsal and ventral fins), which were the basis for the limbs of its tetrapodal descendants.
The best way I can think of to phrase the question is: Does paleontology has any evidence of a vertebrate that had 3 (or more) sets of bilaterally symmetric limbs or lobe-based fins?  I'd like the focus to stay away from ray-finned fish, even though they're vertebrates and related.
This is not the common question, which is whether there is or can be a mammal/reptile species with more than four limbs.  The essence of that question's answer is that mammals and reptiles both evolved from a common ancestor species that were tetrapods, and that it's extremely difficult to change the genetic floor plan in the necessary way without causing fatal problems (along with other evolutionary issues).  By and large, this common question is so common that it chokes out the type of question that I have, making my amateur attempts at further research difficult to impossible.

Related: Why don't mammals have more than 4 limbs?

You might want to reconsider ray finned fish, the sea robin AKA Triglidae, are probably the closest to what you want. https://www.biorxiv.org/content/10.1101/2023.10.14.562356v1.full

I've not read it but this SE question Why don't mammals have more than 4 limbs?
though not a duplicate (it asks about mammals not all vertebrates) may have some elements in its answers pertinent to your question.
And the question Why are there no vertebrates with more than four limbs? has been asked in Quora where it has 7 answers you may find useful.
Also this discussion thread Why can insects have 6+ limbs, but mammals only have 4? in reddit.

Does paleontology has any evidence of a vertebrate that had 3 (or more) sets of bilaterally symmetric limbs or lobe-based fins?

You sent me far down the rabbit hole with this one, for reasons that escape me my instant response was 'yes the Coelacanth' but as you correctly point out that has only 4 paired fins.
As seen from The origin of tetrapods our limbs came from fins, Coelacanth is a good example of the likely early beginnings of Tetrapod limbs, they occasionally use them to 'walk' on the seabed.
The image provided in this National Geographic article Coelacanth Rediscovered gives a much clearer picture of it's 'limb' structures.

Latimeria chalumnae, the coelacanth (SEE-lee-uh-kanth), thought extinct until a biologist identified one off the coast of South Africa in 1939.
I've trawled Google for early chordates looking for examples of more than two pairs of fins & haven't been able to find any, it seems the earliest paired fins appeared in (or shortly before) Ostracoderms & from there continued in an unbroken line to the tetrapods & our limbs.
Paired fins don't appear to have developed in chordates before then or to have ever developed into more than two pairs.
So to the best of my knowledge it appears that the answer to your question is no.
Other links.
Yunnanozoon
Myllokunmingia
Haikouichthys
Evolution of fish

Far later edit: I "might" have found one?
Came across this article on Polymelia which says "Mesacanthus developed a third pair of paired fins" // & this article on Mesacanthus I then found says besides the normal paired pectoral & paired pelvic fins it had "a pair of prepelvic spines".

"there have never been any land vertebrates with anything other than four limbs." - snakes. If there are any vestiges of limbs on their skeletons, I haven't been able to spot them. And there certainly isn't anything on the outside.

@JohnDvorak : Snakes were just 4 limbed lizards b4 losing the last vestiges of their limbs, they are for the purpose of this question four limbed animals I feel, you can even prod the embryos hormonally to grow limbs if you want, it's all still in their DNA they just don't express the genes, but point noted :)

While the coelacanth has 6 fins (along with many related extinct species), only 2 sets have bilateral symmetry, the remaining 2 fins are unpaired dorsal and ventral fins.  The information in the links has been interesting, though I'm still combing through it.

I would shy away from pointing people toward Quora or reddit since the answers on both sites are often not factual, opinion, and lack adequate peer review for accuracy. Referencing such sources of information is, in my opinion, reckless and very potentially misleading.

@theforestecologist I'd more or less agree with you, particularly about reddit, but they do occasionally provide links (or even just technical words I hadn't thought of useful for a search) & can make a useful jumping off point as a result.

@Pelinore that may be true, but I think relegating such sources to minor footnotes would be more appropriate than citing them in such a front-and-center fashion as in your post. (e.g., something like "you can find similar posts on less-reputable sites like Quora or reddit to use as further jumping off points"). Again, I think information on both of these sites are notoriously dubious, so I would personally suggest/request you help to slow the spread of misinformation by not promoting those sites as prominent parts of your answers here. We're trying to maintain higher standards here at SE :).

@JohnDvorak look up spurs on boa and pythons, because you are wrong on both counts.

Holocephalans exhibit auxiliary appendages called pre-pelvic claspers (PPCs) that are located anterior to the pelvic fins... [which] could represent the only example of an independent third set of paired appendages in an extant taxon, if they articulate independently from any pelvic fin basal cartilages, challenging the current paradigm that extant jawed vertebrates are constrained to two sets of paired appendages. Two extinct groups, including Placoderms and Acanthodians, exhibit variation in the number of paired appendages, suggesting this may be a plesiomorphic trait.
... microcomputed tomography scans revealed that PPCs are not modified propterygia, nor do they articulate with the propterygium. They articulate with the anterior pre-pelvic process on the anterior puboischiadic bar (or pelvic girdle), suggesting that while they are associated with the pelvic girdle, they may indeed represent a third, independent set of paired appendages in extant holocephalans.

Are vertebrates constrained to two sets of paired appendages? The morphology, development, and evolution of pre-pelvic claspers in the Holocephali


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What does "genetic correlations" mean as opposed to just correlations?
I'm reading the paper "Large-scale GWAS reveals insights into the genetic architecture of same-sex sexual behavior". In Fig. 4 shows "Genetic correlations of same-sex sexual behavior with various preselected traits". This sentence confuses me. I understand that you could do a standard statistical analysis to find correlations between same-sex sexual behavior and various traits. What makes the way they are doing the correlations "genetic"?
(Note: This may be more of a statistics question than a bio question. Feel free to move it to a more relevant SE site.)

They cite reference 16: https://www.nature.com/articles/ng.3406 might be useful to you. I think the question is relevant here, we have some regular users who are well-versed in heritability studies.

I believe this may be more of an English language question than a stats or a bio question. I shall check the article once to verify.

Looks off-topic? to me, this is an english language question, not a biology one, correlations are correlations are correlations, the addition of the word genetic is merely there to highlight the data set / type under current reference in the sentence & nothing more.

I disagree that it's about English language. The question is really "I understand the meaning of a correlation between phenotypes A and B; what is the meaning of a genetic correlation between A and B." That is, how do you have a "genetic correlation" between Same-Sex Sexual Behavior and Depression?

@BryanKrause : You've convinced me, where b4 I only thought it likely I'm now sure that this is definitely a language comprehension issue & not a legitimate biology question :) off topic then.

@Pelinore Then please do explain it: I'm not new to statistical analysis and even I'm somewhat confused what exactly they are presenting. Remi.b's answer helps but is still not quite convincing me. How do you define, mathematically, a genetic correlation between two phenotypes?

@BryanKrause : "How do you define" : I don't, they do, & I've already explained why this is a language comprehension issue, there's no arcane meaning intended they simply say that any genetic correlations found with same sex behaviour may (or may not) also correlate in some degree with other traits, it seems to me that any misunderstanding is simply what we might call a minor senior moment.

@BryanKrause : 'genetic correlations' in this instance simply means any correlations between genes (or genetic markers) & same sex behaviour it doesn't have any special or specific meaning as compared to ordinary correlations of any other data sets. So it's an English language question not a biology question.

@Pelinore No, that isn't true. Please read the paper. Depression is not a gene. Same sex behavior is not a gene. If you want a genetic correlation between depression and same sex behavior you have to define what that means. A correlation between genes and same sex behavior is understood and is not what the OP is asking.

@BryanKrause it actually is about the language. The correlation that is being studied may be between two different conditions but the measured RVs, in this case are the genetic markers. That doesn't make "genetic correlation" a special kind of analysis. One can as well study the neurophysiology in these conditions and use the term "neurophysiological correlations". In both cases, the right phrase would be correlation of (genetic) markers between conditions X and Y.

It is simply a correlation where one of the two variables considered is the genetic state at a given locus. In a GWAS, one loops through all loci and systematically performs a correlation analysis between the genetic states at this locus and the phenotypic trait of interest.
In the example of sentence you cite

Genetic correlations of same-sex sexual behavior with various preselected traits

They looped through each polymorphic locus in their data set and at each locus they performed a correlation analysis between the two variables "genetic states at a this locus" and "same-sex sexual behavior" (whichever way this second variable is recorded).
A study might also be interested in more than one phenotypes. In such case, different phenotypic variables can either be considered separately or can be included in the same analysis through linear models. It is for example not so unusual to include one of the variable as a covariatiate in an ANCOVA type of design.

I think this answer is not quite complete (in the context of the paper OP is referring to)...I'd have to look closer but it seems there is an additional step, because they are talking about two traits and a genetic state, not one trait. I still think you are much better positioned to write the complete answer here, though. :)

I am too lazy to read the paper :D I added a little paragraph about cases where more than one phenotype is considered.

I quote from this paper:

Genetic correlation analysis can separate between shared additive genetic and environmental factors by using the genetic similarity between individuals (monozygotic twins have ∼100% and dizygotic twins and siblings ∼50% genetic similarity). To compute the genetic correlation between two traits the phenotypic correlation is decomposed in genetic and environmental sources of covariance using a maximum likelihood approach in combination with the genetic proximity matrix of the sample 34, 35. Additionally, the heritability of both traits is established to compute the relative contribution of genetic and environmental factors to the phenotypic correlation.

In the same paper you will also find some hints on how it is computed. However, if you want to go into further detail, I suggest you investigate the work of Laura Almasy and John Blangero. They did a lot of work on variance component analysis of QTLs. I remember using their software (SOLAR, which is now SOLAR-Eclipse) for computing genetic correlation in a work, but right now I am not able to find the paper in which they describe computation of genetic correlation.


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Am I reading this respirometer correctly?
I want to double check that I'm reading these respirometer vials correctly. The volume O2 of the following vials should be:
Squirrels in Torpor:
E1: 0.4 E2: 5.0 E3: 0.3 E4: 5.1 E5: 0.4 E6: 0
Squirrles at Stable body temperature in rewarming phase:
E1: 90.3 E2: 85.1 E3: 85.3 E4: 90.4 E5: 90 E6: 0
Right? Image below

Welcome to Biology.SE! This question seems like it might be a better fit for [MedicalSciences.SE], but please do not crosspost, instead request migration (or delete from this site and repost). Please note that both this site and that one expect  you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For more details on how to use this site please take the [tour] and then go through the [help] pages starting with [Ask]. Thanks!

No, you're misreading the scale several times. The scale divisions indicate "tenth of ten" = one, while you sometimes misread them as "tenth of one" = 0.1.
For example:
E2 is correct as 5.0
E1 is just one mark less and should be 4.0 instead of 0.4.
(Remark: I don't know, whether to read the scale at the right or left side of the green part - I trust you using the right side)


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How do schools of fish get enough oxygen?
Fish get oxygen from the water running over their gills, during which up to ~80% of oxygen is removed from the water. In schools of fish, how do fish swimming behind other fish get enough oxygen in this case? It seems counterintuitive that the volume of unenriched water is repleted with oxygen within the fraction of a second before the fish following behind attempts to gain oxygen from it.
Thanks.

Welcome. Where did you read the claim 80% of O2 is harvested? It seems like an overestimate. Further, fish move through the water and water is in motion as well - how would that affect O2 saturation?

This beautiful paper from 1958 cites a dissertation by van Dam, 1938, which I couldn't fully access, for the figure of 50-80%, and I see "80%" referenced widely in study resources online.  It is presumably part of a basic textbook.


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SARS-CoV-2 : does vaccination provide a better immunity than being sick and recover?
I recently read in the news that countries are thinking to offer a "green passport" based on the vaccination against SARS-CoV-2, allowing vaccinated people to do things with less restrictions than the non-vaccinated :
New York Times
BBC News
Bloomberg
IATA
If those passports are to be put in place, why do they not include people that were exposed naturally to SARS-CoV-2, this number being bigger days after days (60 millions people, 17/02/2021) ?
Does that mean that vaccines offer more immunity than being exposed naturally to SARS-CoV-2 and recover ?
My questions don't address the ethical aspect of implementing a "green passport", I'm only trying to figure out if vaccination offers more immunity than being exposed to the virus. A possible answer to this question can simply be "we don't know so far" because of the lack of feedback on a long term view.

The vaccine will protect you from severe disease, hospital stays and death. Isn't that enough?

Placebo-controlled trials are the gold-standard of evidence for something like this, but that's not really a possibility for assessment of immunity in previously infected individuals. Instead you'd need something like a prospective observational cohort study, which would need massive enrollment efforts and would likely still fall short of the strength of evidence provided by vaccine trials. My guess is that's why regulators are hesitant to make strong inferential claims about the strength of immunity after infection.

Perhaps the reason has nothing to do with the quality of the immunity, but is simply down to the fact that immunization can be well-documented, while having had the virus (especially a mild case that didn't require hospitalization) is not.  There's also the practical aspect that it would encourage more people to be vaccinated.

@Chris Yes of course I don't reject the usefulness of the vaccines, but it is another topic. My question is more focused on the immunity acquired by catching the virus compared to the immunity acquired by a vaccine.

@jamesqf Exactly, the immunity acquired by a vaccine is subjected to trials so it is certainly more documented than natural occurences.

@Genorme: You seem to have misunderstood me.  I meant that you can fairly easily document the fact that you received a vaccine, but if you only had a mild case, you can't really document that.

As @MikeyC and @jamesqf pointed in the comments, vaccines are better documented than the actual cases, whereas qualifying the immunity conferred by having recovered from Covid-19 would require large cohort studies.
However, one can follow up thir argument in many ways:

It would be reallys urprizing, if large-scale cohort studies have not been udnerway or already available by now: while nationwide testing may still be lacking in many countries, masive and repeated testing campaigns in specific regions are not a rarity by now. (see, e.g., here and here)
Hospitalization is not a necessary requirement for attesting a covid case - one could test unvaccinated persons for the presence of the Covid-specific antibodies.
There is much still unknown about the vaccines themselves - particularly about whether the immunity conferred is a lasting one, and whether.
Moreover, the fact that many people might have lived light cases of Covid does not make it easier for attesting the efficacy of the vaccines. Public authorities openly warn that the vaccine might be inefficient and a vaccinated person might be still a carrier of the disease.

In other words, "we don't know" is the most likely answer.
As the OP, I forgo the ethical issues raised by the "green passport" - these are not only those related to the restrictions on the individual freedom, but also the discrimination against the individuals to whom the vaccine is counter-indicated (e.g., allergics, pregnant women, people with weakened immunity, etc.)

It is said vaccines are over 90% effective. But I think natural obtained antibodies from Covid-19 and recovery offer more immunity than vaccines. The problem is that no pne can be sure to survive the infection.

I understand your opinion but it is not based on evidences, I am looking for a formal proof (if any up to date) that can confirm or infirm that immunity acquired by a vaccine is better.

We welcome new contributors to SE Biology, but ask that they read the [Tour] and the Help on answering questions. As the poster says, you are not providing an answer but an opinion unsupported by evidence, which makes your answer unsatisfactory for this question and answer site.


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What's the survival benefit of blue plants?
I'm working on a science-fiction worldbuilding setting and have been trying to find out what the survival benefits are of blue in plants, like this or this.
I have researched this but most of the answers that a Google search brings up are more to do with blue flowers, blue structural colouration in animals, and garden centre blogs and online stores selling conifers. The best I've been able to find has been a page about encouraging spruce plants to become as blue as possible by making sure they're fed planty of iron-rich fertilizer (but not fertilizing in the first year, so early impoverishment of nutrients seems to be a factor, but I don't see how that makes blue needles beneficial).
All I really want to know is what environmental conditions would cause a plant, any plant, to evolve blue leaves or needles.
Thank you in advance.

That's great, but I'm more interested in the time period long before Russia even existed. It's these plants' evolutionary bias towards being blue, and the pressures in their native environment that I'm interested in.

I’m voting to close this question because this question belongs on the worldbuilding stack.

According to at least one gardening tutorial I found, the blue color of the Colorado Blue Spruce is not actually related to the color of the pigments in the leaves.

"...the intensity of the blue of a Colorado blue spruce (selections of Picea pungens ‘Glauca’) depends on the concentration of its “bloom,” a powdery white wax that coats its needles."

I can't say if this is the case for all "blue" conifers, but given that this tree is especially tolerant of cold and drought, it seems likely that the waxy "bloom" is related to retention of water vapor and possibly exclusion of external water from the needles. Since there are lots of other plants with waxy coatings that don't have such a powdery blue appearance, I'd speculate that it may also contribute some protection from UV radiation for these high-altitude trees.


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Why myelin sheat does not cover the whole axon?
Is there an optimal lenght for myelin sheats to be effective and lead potential across the nerve cell? This has always bugged me.

The nodes of Ranvier (the gaps between myelin sheath segments) speed up the action potential because the electric current can jump from node to node (or gap to gap). If the myelin covered the entire axon, the signal wouldn't have the gaps to speed up the signal. As for optimal length, the gap is 1μm long, but can be longer, on the order of millimeters depending on the type of cell. The length of the myelin doesn't matter so much as the length of the nodes of Ranvier because they are where the Na+/K+ channels are found so the ion exchange can occur. This is how an action potetial can occur, so the myelin not covering the entire axon is crucial for the ability of neurons to propagate a signal.

Yeah I wanted to know if there was an optimal lenght for myelin coverage. I was thinking that probably with a too long myelin cover the jump of potential couldnt occur. Is that right?

Yes, so longer myelin as in a longer distance between nodes, would likely affect the efficiency of the current jumping from node to node .

Can you link me to some original research paper or review about this particular topic? I couldnt be able to find anything about. Probably I'm using the wrong keywords.

http://jnnp.bmj.com/content/40/8/769.short
This paper talks about it! :)


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Why eukaryotes have three different types of cytoskeleton filaments?
Ok: IF, microtubules and microfilaments serve different purposes. But whats the biological advantage of having these three types over other organisms? I don't know if I'm being clear.

Note that cytologically the most apparent property of eukaryotes is, in general, their higher internal compartmentalization (cpe: Gerhart et Kirschner's popular science book: "The Plausibility of Life"); Why eukaryotes have a seemingly higher compartmentalization is perhaps worth of another question :)

While eukaryotes contain tubulin-containing microtubles and actin filaments, prokaryotic homologues do exist.
For example FitZ protein, the most common bacterial Tubulin homologue[1], is involved in cell division. Genes for this protein are actually present in eukaryotic nuclear DNA and the protein facilitate the division of the mitrochrondria and chloroplast organelles which were created by endosymbiosis[2].
Similarly, MreB, functions as the most common prokaryotic analogue of actin.
Regarding IF filaments, certainly subsets such as nuclear lamins are uniquely found within Eukarya, however a paper published by Bafchi[4] has suggested that IF-like proteins are present within bacteria.

Bi, E., & Lutkenhaus, J. (1991). FtsZ ring structure associated with division in Escherichia coli. Nature, 354(6349), 161-164. doi:10.1038/354161a0
Margolin W. FTSZ AND THE DIVISION OF PROKARYOTIC CELLS AND ORGANELLES. Nature reviews Molecular cell biology. 2005;6(11):862-871. doi:10.1038/nrm1745.
Gunning, P. W., Ghoshdastider, U., Whitaker, S., Popp, D., & Robinson, R. C. (2015). The evolution of compositionally and functionally distinct actin filaments. Journal of Cell Science, 128(11), 2009-2019. doi:10.1242/jcs.165563
Bagchi S, Tomenius H, Belova LM, Ausmees N. Intermediate filament-like proteins in bacteria and a cytoskeletal function in Streptomyces. Molecular Microbiology. 2008;70(4):1037-1050. doi:10.1111/j.1365-2958.2008.06473.x.

So it actually depends on the biological advantages (functions) and how the organisms have evolved in time?


text:
Type of plant cell that builds a secondary wall in between two primary walls?
I read that there is this type of pattern in cell wall synthesys. What is the type of cell that does that and in what kind of scenario?


text:
Do leaves only appear on new growth?
In some willows, there is a clear distinction between floriferous buds (out of which the catkins grow) and vegetative buds. I have observed this phenomenon myself on numerous occasions (in fact, I can ID several species and hybrids on floriferous buds alone). However, I never took it further and there are things I still don't understand. What about those vegetative buds. What grows out of them: twigs with leaves on them out of some and single leaves out of others? And would there be any noticeable difference between these two types of vegetative buds (if they both existed)?

To answer the question in you title, the leaves appear both on new and old growth. In addition to vegetative and floral buds, there are also dormant buds that activate themselves on old growth after leaves or branches are cut. You can read here a list of buds.
For the following questions in the text I think the answer is different for every species.


text:
Tillers and stolons in grasses
In many grasses, tillers develop roots at their nodes etc.. Those roots can hit the ground and subsequently anchor in the soil, so eventually the tillers end up like something that is very hard to separate from stolons (I often see this in Agrostis gigantea).
Are there objective criteria for separating tillers and stolons at all times?


text:
Mg in bacteriochlorophyll
In the figure 1A of http://photobiology.info/Jones.html
the Mg is not belong to other structure.
Is that because something is omitted or is it indeed like a pearl in a mussel's mouth? In the later case could we replace the Mg by some other atoms (and the bacteriochlorophyll still live well)?

The Mg atom is not bound in the porphyrin ring, it is coordinated there.

http://photobiology.info/Jones.html
The author of the above page told me              The magnesium (purple sphere) is bonded to the four pyrrole nitrogens (the four blue atoms pointing towards it.

I checked chemistry books "coordinate" means the shared electron all came from one party ? So,what is the difference between bounded and coordinated?

When the atom is bound, chemical bounds are formed. If it is coordinated, it is kept in place by interaction between the atoms (for example by van der Waals force).

So, both Mg in chlorophyll and Fe in RC are coordinated? Will a coordinated atom have a fixed orientation with other atoms?


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Fe in bacteria light-harvesting system Reaction Center
Is the Fe in the reaction center of bacteria light-harvesting system bounded or free atom?

I know no examples of free iron atoms serving active physiological functions within living organisms. Iron, as with other metals, are generally in their ionic state. As such, they are attracted and held in position by negative, or partial negative, charges on nearby atoms. Sometimes these are from the sidegroups of proteins but often the negative charges bonding the metals are on specialized molecules such as the poryphrin ring in hemoglobin whic contains an iron ion in the center, held in place by four nitrogen atoms like a gem in a ring.
The principal metal ion in photosynthesis is magnesium. Just as with the iron in hemoglobin, it is centered in a poryphrin ring. This is also true of the chlorophyl in bacteria. But there is also an iron ion associated with the reaction center. Apparently this is "connected" to the P870 bacteriochlorophyl molecule. Here is the article: http://photobiology.info/Jones.html
You can view this for yourself. Here's a link to the molecule in question at the Protein Data Bank (instructions follow): http://www.rcsb.org/pdb/explore.do?structureId=2BOZ
On the left side is a viewing window where you can see various representations of the protein and any associated molecules (ligands). This won't help because the Fe will be hard to pick out. Scroll near the bottom of the page and you will see iron (FE) listed as one of the ligands. In that row, in the far right column, click on "NGL". In case you got lost, here's the direct link: http://www.rcsb.org/pdb/ngl/ngl.do?pdbid=2BOZ&preset=ligandInteraction&sele=[FE]
That's the Fe with the big orange glow. Notice how it's held in place by 4 nitrogens plus a carboxyl group. Click on any "stick" making up one of those nitrogen containing structures. Notice, in the window's upper left, the label for this begins with "HIS". This stands for histidine, an amino acid. Indeed, every one of these goups surrounding the Fe is an amino acid belonging to the chlorophyll protein.
So, unlike the Fe in hemoglobin, this Fe is attached to the protein directly.

Thank you for the reply. But a few days ago a professor in Germany told me it is not bounded? What follows is her reply, did I miss interpreted her words? =================The non-heme iron can be exchanged, eg. against zinc. It is like a pearl in a shell. In contrast to this, the iron in the cytb556 protein subunit is bound by two subunits (alpha and beta) and coordinated by two
histidines.

You said "The principal metal ion in photosynthesis is magnesium"? Is it so? Ion is not the principal metal? Then, what is its function?

So, the Fe is bounded? Has it a fixed orientation with the RC and the LH1? I think the answer is yes? My question is, what is its orientation?

I checked the NGL link you provided. I agree the Fe is "held in place by 4 nitrogens plus a carboxyl group" (quoted as you said) But it does not seems to belong to other structure? But you said it is BOUNDED? Sorry if my question is naive. I do not understand chemistry. I did not studied chemistry after university. I understand only high-school chemistry.

So, is the magnesium in chlorophyll bounded or not?

@latra. The image showing the Fe is only an isolated portion of the complete molecule, the rest is not shown. There are ways to display it all but require use of a viewer and a bit of practice at using it.

@latra. I didn't read the entire article I referenced. I'm not experienced in bacterial photosynthesis but in plants there are "accessory pigments" which also capture light and shuttle the energy to the principal chlorophyll molecule (containing the Mg). Perhaps the Fe containing P870 is an accessory pigment in bacteria.

If the Mg in bacterial chlorophyll is like that in plants, it is bonded to a poryphrin ring within the protein comprising the chlorophyll. From an evolutionary standpoint I suspect that is true but can't guarantee it.

To your first comment. Perhaps what the professor means is that it is not PERMANENTLY bonded. The "bonding" of ions in cells is not covalent. That Fe in the image is only held there by electrical attractions to the negative groups surrounding it, no sharing of electrons. In fact the prof Is implying this by stating it can be exchanged. Maybe this is semantics. But The Fe is not just freely floating around. It it held, if temporarily, by an ionic association as shown in the image. I call that bonded.

Your prof refers to yet another Fe containing protein. So maybe the one I referenced is not the one you ask about?