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Are there biological reasons why life expectancy is lower for men in most countries of the world?
I've been checking life expectancy figures for men versus women in many countries of the world and the figures for men sometimes are terrifying. Countries like Russia have a 12 years gap in disfavor of men. Developed countries have usually a 4-5 years gap in disfavor of men. My country Argentina has a 7 years gap. African countries and middle east countries where supposedly women have a harder life because of religion have usually a 3 years gap in disfavor of men. So far I haven't found a single country where men lives more than women.
Now I know there are more men than women who dies in homicides, suicides, work accidents, wars, etc. men are more likely to get addictions because of depression, etc. but aside of all that, is there any biological reason why men lives less than women everywhere?

Here is a recent review: http://www.cell.com/cell-metabolism/pdf/S1550-4131(16)30237-6.pdf

If I recall correctly from my US history class, in colonial America the life expectancy for men exceeded the life expectancy for women, but you are correct about the general trend.

Three little words... "Hold my beer".

@omegacron Non true. Women now drink as much alcohol as men, global study finds https://www.theguardian.com/society/2016/oct/24/women-drink-alcohol-men-global-study

@Pablo You missed Omegacron’s point - it refers to the effect of testosterone (and alcohol) on men’s judgement. See: The 21 Greatest Moments In "Hold My Beer" History

There are both biological and  social factor for that:
Biological

Females have two X chromosomes. When mutations in genes of the X chromosome occur, females have a second X to compensate. Males, on the other hand gave just one chromosome X and all genes its genes express themselves, even those lethal or deleterious.
Females have better resistance to biological aging and hormones and the role of women in reproduction are known to be associated to greater longevity (e.g. estrogen offers some protection against heart disease because it facilitates elimination of bad cholesterol while testosterone has been linked to violence and risk taking).
The female body evolved to accommodate the needs of pregnancy and breast feeding hence deals better with making reservation. This ability has been linked to a female's better ability to cope with overeating and eliminating excess food

Social
This "advantage" women seem to have was once nullified by the status and life conditions they had back then, as the risks and the burden of pregnancy and the lack of attention to health and rights women had in a way more misogynist world.
Given the economic, social and political changes that the world experienced, a general progress in female life conditions took place and women have not only regained their biological advantage, but have gone beyond it, achieving higher life expectation. Social and comportamental factor are involved in this higher longevity:

Women tend to engage in fewer risky and bad for health behaviors than men do, e.g. men have more problems than women with alcoholism, smoking and road accidents.
The world is still very sexist and the gender roles to be played would expose men to higher risks. Regarding to work, for instance, although women nowadays participate in the work force, their professional activities remain different and are less prejudicial to their health (on average).
Also regarding to  very sexist gender roles, men are expected to be strong and manly and powerful and women are expected to be gracious young and beautiful. As a result of that, women are more attentive to their body and health, engage themselves in more healthy activities and benefit more from medicine and science. Men on the other hand submit their bodies to challenges from early ages and tend to neglect their bodies needs.

You can have access to detailed statistics (male/female, country by country, life expectancy and other health data) here:
http://www.who.int/gho/publications/world_health_statistics/2016/Annex_B/en/
And also, read more about the issue here:
https://www.scientificamerican.com/article/why-is-life-expectancy-lo/
http://www.who.int/mediacentre/news/releases/2016/health-inequalities-persist/en/
https://en.wikipedia.org/wiki/List_of_countries_by_life_expectancy#cite_note-10

Good on you for adding the social reasons.

Do you have research to share that supports your claim that "women have not only regained their biological advantage, but have gone beyond it"? In general, the answer could benefit from references in the scientific literature on the issue. The only one of your references that is not just stating the existence of the phenomenon, is the one from Sci. Am. that @rotaredom linked before you, and we have no way of evaluating it as there is no scientific literature cited in it. That is especially true for the discussion on the social factors you mention, which does not sound scientific at all.

Good answer, could you clarify the line "and all genes its genes express themselves"?

@vkehayas considering social "sciences" dont use the scientific method because many times they dont do experiments but try to assert their theories with observations or interpretations, or they dont use valid methods for validation because they cant isolate what's going on in the mind, because there are no tools for doing so, asking for an answer in regards to social disciplines to be "scientific" is asking for the impossible.

@Pablo I thoroughly and vehemently disagree that social sciences cannot be scientific a priori! I only disagree with the verbiage used in the linked article, and consequently the answer since it is basically echoing the points therein. The issues can be in principle empirically addressed but I found no evidence in the linked article. Also my request for references was for the whole answer, as none were given for any of the claims made.

I also disagree that social studies are not science and are not done with scientific methods. @vkehayas, life expectancy studies in past years are not easy because this data were not recorded in early ages. But this conclusion comes from interpretation of a few data (e.g. life expec in  royal family of Wales and their related ones, which shows that men in early ages lived longer)... There is also a very well known issue: maternal death. Nowadays, every day, more than 800 women die from pregnancy or childbirth related causes. Can you imagine how it was in early ages?

Also, there are some studies linking higher female mortality with traditions leading to discriminatory treatment against females... If I'm not mistaken they were gave India as example, but this is a real issue everywhere

Mortality aside, and selective breeding aside, is there also a reason why there are (naturally) more males are born than females? Is the gestation period changing over time?  Women live longer? These questions reach back to hunter gatherer times when "work accidents" were probably somewhat more serious.

It's arguable that the greater risk-taking of men is attributable to testosterone and other biological differences, as well.

Social point, which you kind of mentioned: Women go to the doctor far more frequently. That alone can make up for a lot of the difference.

Women have two X chromosomes but only one is active in each cell, see Barr body - https://en.wikipedia.org/wiki/Barr_body

I found this article https://visual.ons.gov.uk/how-has-life-expectancy-changed-over-time/ . Life expectancy for women was higher than men 2 centuries ago. Now the gap duplicated.

Is there a reference for "This "advantage" women seem to have was once nullified by the status and life conditions they had back then, as the risks and the burden of pregnancy and the lack of attention to health and rights women had in a way more misogynist world. Given ... changes that the world experienced, a general progress in female life conditions took place and women have not only regained their biological advantage, but have gone beyond it, achieving higher life expectation." @Pablo lists evidence the gap still favors women in less developed countries today & developed ones in the past

@Silverfish - as a wholly random single (out of hundreds) examples, look at funding and attention for breast cancer vs prostate cancers.

@Silverfish - another one is that the much-mentioned in the answers risk-taking isn't only biological (testosterone) but also social (sexual competition between males). This is largely sociological, based on what kinds of mates women choose to both date and procreate with (compare: Mick Jagger vs. Bill Gates).

There are a lot of factors playing in here.  You've pointed out the surface reasons that can sometimes contribute: work accidents, style of life, etc.  However, there are biological causes as you suspected.
Probably the most obvious has to do with the difference between their hormones.  Testosterone (male hormone) is associated with violence and risk taking.  This would tend to contribute to men having at least a slightly shorter lifespan.  Estrogen, on the other hand, is associated with the removal of cholesterol from the blood.  This may lower the risk of females dying from heart diseases, raising the average female life span.
Some hypothesize that a large section of the difference simply comes from lifestyle resulting from those hormones, per American Scientific: Men tend to want to be caricatured as strong and tough (result of testosterone), whereas women tend to be more concerned with maintaining their bodies, keeping themselves beautiful, etc.  Obviously, this is hard to measure in a conclusive way, so scientific articles and measurements are hard to produce.
However, there are also diseases which men are more prone to because they can lose the Y chromosome in their blood (this is suspected to be induced by smoking, along with other potential causes), such as cancer, and even some forms of Alzheimer's.
Edit:
Another reason hypothesized that women tend to last longer than men is that they are less prone to serious genetic mutations on the sex chromosome, since they have a double X instead of two totally different XY chromosomes (See Why women live longer than men: Sex differences in longevity (2006) by Steven N. Austad: Gender Medicine 3(2): pp. 86-88).

It is noteworthy that sex differences occur for infants as well, so I'm not sure that a behavioural explanation like this explains the phenomenon. Your paragraph starting "A large section of the difference..." should be backed up by research papers, otherwise you may be accused of parroting the stereotype-promoting language used in the Sci.Am. article you linked to. An alternative theory is that lifespan simply depends on body size

@vkehayas you have a very good point.  Unfortunately, I have to run for a biology seminar right now, but I'll try to scratch up some references afterwards.  :)

Men get a lot more heart attacks. Perhaps 2% mortality per year after 50!!! https://archive.cnx.org/resources/b32e423e49c72ec63021d4c65847d375433a2888/CNX_Psych_14_03_HeartAtt.jpg   ..............
https://www.google.fr/search?q=heart+attacks+in+men+vs+women&num=100&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiT7_S57Y7XAhWQDRoKHdZYBlEQ_AUICigB&biw=1026&bih=606#imgrc=9KXzzK1p17V8tM:

One reason for that delay in onset of cardiovascular disease could be that women are relatively iron-deficient compared to men — especially younger women, those in their late teens and early 20s — because of menstruation. Iron plays a very important part in the reactions in our cells that produce free radicals, which damage cell membranes and DNA, and may translate into aging the cell. Postmenopausal women lose this benefit https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821138/
Here is a well researched article on why women live longer than men https://ourworldindata.org/why-do-women-live-longer-than-men

One of the dominant causes of death is atherosclerotic heart disease. Males are susceptible to this disease for their entire adult life with atheroma detectable as early as late teens and twenties. Females are moderately protected from developing this disease until menopause and the decline of estrogen, etc., after that point, they develop ASCVD as well. Therefore, if average duration f ASCVD is 20-30 years until death, men die in their 50-60's, women in their 70's-80's.


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Do the eggs of fraternal twins come from the same ovary?
With fraternal twins two matured eggs are released and fusion of the two with sperms result in formation of these fraternal twins. Then do the two matured eggs come from one ovary or both the ovaries at the same time?

It can be one egg from each ovary or both eggs from the same ovary. To understand the logic behind it, please have a look at my answer here: https://biology.stackexchange.com/a/65032/24284

source: Stack Exchange

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Why is there an apparent reduction of reptile species near the Mississippi River?
The USGS Gap Analysis Program published a map of reptile species richness in the U.S. There is a conspicuous reduction in reptile richness along the Mississippi River corridor. Why might this be?

From USGS:

This map of reptile species richness in the U.S. is derived from the
  USGS Gap Analysis Program’s (GAP) national reptile ranges dataset. The
  map represents the total number of reptile species summarized by
  12-digit hydrological units (HUCs). Light blue HUCs have the lowest
  number of species while red HUCs have the highest.

Is it possible this reflects relatively intense human influence (farming, cities, industrialization) in the Mississippi delta?  This map suggests there are "26-43" species in the region, whereas a 1955 paper (Notes on Mississippi Amphibians and Reptiles) claimed to identify "89 species and subspecies as follows: Salamanders, 14; frogs and toads, 19; lizards, 8; snakes, 36; and turtles, 12."

Interesting information @iayork. But did you find any numbers on species richness for the surrounding areas of similar latitude? It could also be that numbers fell proportionally in all areas around the river.

The reptiles mostly were ploughed away and replaced with soy beans.

The low reptile diversity zone matches the Mississippi Alluvial Plain which includes the Mississippi Floodplain. The Mississipi drains nearly half of the USA's geographic area, so the flood plain is massive.
The Silt Plain is very flat, mostly has hills left by oxbow lakes and river meanders. If you put your hand in the ground, it consists of organic matter/silt/clay/mud/fine sand, and it is very fertile until it is depleted by modern agricultural practices.
It's one of the more productive agricultural regions in the USA, and it's mostly giant square fields and mono cultures.
zoom in: http://gokml.net/maps#ll=32.163208,-91.720681&z=11&t=h&q=winnsboro
Here is a quote from the Discussion at the end of this review:

traditional agricultural landscapes, typically characterized by
  mosaic–like structures, intermediate levels of disturbance, and able
  to host great biodiversity levels (Bignal & McCracken, 1996), have
  undergone profound transformations in last decades. The rapid
  extension of intensively cultivated fields and the reduction and
  fragmentation of the original habitats have led to the creation of
  more uniform and depleted landscapes, with significant loss of
  biodiversity (Whittaker, 1975; Bull & Skovlin, 1982; Burel et al.,
  1998; Zechmeister & Moser, 2001; Moser et al., 2002; Pfiffner & Luka,
  2003). In accordance with these changes, our analysis of reptile
  assemblages in an agricultural area mainly devoted to the intensive
  cultivation of arable lands found the landscape to be relatively poor
  in biodiversity. Four out of five agricultural land uses hosted only
  one species, while most of the recorded reptiles occurred inside a few
  patches of semi–natural habitats and, above all, in the grid of
  vegetated buffer strips interspersed among the cultivated lands. In
  addition, during field activity, we observed only seven of the
  eighteen species of terrestrial reptiles reported for the province
  where the sites are located, and most records were ascribable to a
  single species.

Reptiles and Amphibians are at the top of the insect food chain, and studies have shown that they are sensitive to pesticides, especially when their numbers are low:

By using three evaluation factors - (i) pesticide exposure, (ii)
  physiology and (iii) life history - a taxon-specific pesticide
  exposure risk factor (ERF) was created. The results suggest that about
  half of all evaluated species, and thus at least 1/3 of all European
  species exhibited a high exposure risk. Previously the region would
  have been host to a very tall high growth forests, because of the high
  temperatures, available water table of the area and fertility.

you can check pics 6 and 8 from this page to see the productivity of the region. It suggests that the reptile biomass was replaced with obese humans.
That forest has been reduced to the swamp forests where the roots are covered in stagnant water for most of the year, where some large aquatic reptiles take refuge, and which is completely different than the lost forests of the Mississippi plains.
The old forests would have perhaps been similar to florida's inland forest, and perhaps very different, because of the available water table, and much more productive silt, than florida's ground allows for. I didn't manage to find photos of the lost forests of Mississippi plain regions, they would have been dense, producing 3-7 times more biomass than normal forests.

I agree that's an appealing explanation, but it doesn't seem to explain the lower reptile abundance in the Mississippi delta where there is less agriculture, nor in southern Florida and eastern North Carolina where there is high agricultural production but no correlated reduction in reptiles.

Did you compare the regions using the maps? at least half of florida is untended by humans, compared to 10 percent of the the Mississippi plains. only 10 percent of Florida is an agricultural plain, compared to 85% of Mississipi plains. North carolina is not an agricultural plain, check the map, none of the fields are grids, and all the fields are within 1 mile of significant amounts of forest, and only 50pc of the land is agriculture.

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Does the energy from ATP hydrolysis vary among different cells?
I know that when ATP is hydrolyzed into ADP it gives 7.3 kcal/mol. The question is, does this value vary among different types of cells?

NADH and FADH are not hydrolyzed, but they can be oxidized, and the resulting energy used to drive ATP synthesis in mitochondria.  Can you give a source for your numbers?  3.7 calories (kcal / mol) for ATP hydrolysis sounds way too low.

thanks for your comment. yes, you are right it oxidized and it gives 7.3, I wrote it by mistake. I will edit the question. thanks again.

I see, you are simply asking about the energy of ATP hydrolysis.  The way you question was worded, it sounds like you were asking about the total energy from NADH and FADH2 oxidation. And you got an answer on that. I will edit to clarify.

Yes, the energy from ATP hydrolysis can vary between different cell types and condition, because it depends on several factors. Hence, you will find different values in various textbooks.
First, like any chemical reaction, the free energy $\Delta G$ of ATP hydrolysis depends on the concentrations of the reactants. You can explore different values of $\Delta G$ with this calculation tool. Typical values are [ATP] = 10 mM, [ADP] = 1 mM and [P$_i$] = 20 mM, which gives $\Delta G$ = 42 kJ/mol (10 kcal/mol). But all these concentrations can vary between cells, and there is not much data available on intracellular concentrations in specific cell types. Many textbooks give free energy values denoted $\Delta G^{\circ}{'}$ which are calculated at concentrations of 1M, which is of course completely unphysiological.
In addition, the $\Delta G$ is strongly affected by the concentration of Mg$^{2+}$, because this ion associates with phosphate groups and alters their free energy. It also depends on pH, since the phosphate groups can take up/release protons. If you are interested, an in depth analysis is found here.

The point you make is valid, that the actual free energy of hydrolysis of ATP can differ from the standard free energy. However the OP asks about variation in “different types of cells”, by which I presume he means e.g. muscle v. liver. Surely the answer to this is either “no” or “we don‘t know”.

I don't think it's just a matter of getting the textbook values right. Because the free energy depends quite a bit on concentrations of reactants, it can differ between cell types or conditions. For example, the reaction quotient ATP/(ADP * Pi) can drop as much as 50-fold in exercising muscle  (http://jap.physiology.org/content/73/2/728)  You're right though that we don't know much about these parameters between various cell types, as intracellular concentrations are hard to measure accurately.


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293T safety, transfections with plasmid DNA
I am a little concerned with 293T cell lines, I have been working with this cell line for a few years with less frequency. However there were times that i extracted the proteins from these cell lines outside the hood. I never work with virus, i have only transfected plasmid DNA. can someone help me if there are any chance o exposure, if yes, how dangerous is it.

Exposure to what? The cell line?

293T cells do incorporate partial virus genomes, consisting of about 4000 bases (about 11%, if I remember right) of the adenovirus type 5 genome (Cloning and Sequencing of the Cellular–Viral Junctions from the Human Adenovirus Type 5 Transformed 293 Cell Line).
This amount of DNA is not enough to make a viable virus; it lacks all the structural components of the capsid, for example.
293T cells also include the SV40 Large T antigen, another viral gene. Again, this is not enough to make a replicating virus.
Therefore these cells don't pose any human health hazard aside from the normal almost entirely theoretical risk associated with any transformed human cell line (actually considerably less, since these were never tumor cells but were transformed in the lab, so they have no intrinsic adaptations to replication in humans, unlike say HeLa cells -- which are also demonstrably safe).
293 cells have been continuously cultured in thousands or tens of thousands of labs for over 40 years, and I'm not aware of any safety incidents associated with them.  Of course, you should always handle cultured cells with appropriate precautions and protective wear, but these are not a specific concern.

Washington State has a nice risk assessment out of their biosafety department that outlines the risks associated with 293 cell lines (downloads a docx). The risk in itself is predicated upon poor work practices and the potential for the generation of a live virus in the technician, or the cell line itself (see the special hazard notes in the risk assessment report). However common these events may be I don't know, but in the US, OSHA 29CFR1910.1030 (The Bloodborne Pathogens Standard) sets us up for risk management regardless of the incidence (or frequency) of such events.
The 293 cell line is considered BSL-II, requiring work done in a BSC with a carefully selected PPE ensemble and training for the manipulations being performed. This isn't at the discretion of the lab personnel but rather at the discretion of the EH&S or Biosafety department. OSHA levies heavy fines against institutions for non-compliance and thus decisions regarding compliance are left up to administrative professionals. I would recommend checking out Biosafety in Microbiological and Biomedical Laboratories (BMBL) 5th Edition (link) for guidance.
Ideally, though, check out your institutions written Exposure Control plan, which you're given access to by law for instruction and assessment performed by your own institution with the goal of mitigating exposure events.


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What is this insect, the bite of which is causing deaths?
This insect is currently found in Kolkata, and in many parts of West Bengal, India. Its bite results in a fever, and if not treated immediately, the victim dies. This is the insect:

It seems that the insect belongs to the family of spiders due to its eight feet. But I can't conclude any more. Does someone know what this insect is, and how to be safe from it?

Howdy, is this really your picture?  I found it on this website.  Just mite want to attribute it.  :)

From what I can tell, the website you got this image from provides the ID of this insect, so it's unclear what you're asking..

@rotaredom it came out on the newspapers, and it's bite is actually brutal.

This is a plant-feeding insect. It is of no danger to humans. Your article sounds a bit sensationalized. There are some small creatures that can kill you, but they are few and far between.

I am sorry that my question is partially incorrect. It is true that this insect is spreading the disease, but it is not the only one. The disease is this.

Well, you have your answer at least! Please note the disease may result in death if left untreated. No one dies immediately.

You were right to suspect arachnid. Its a red clover mite. But they normally don't bite humans or cause diseases. Could you post some links to news articles talking about the disease?

I could have gladly given the site, but it's in bengali and I couldn't find an English one.

Its ok, can I have the bengali site?

I am sorry that my question is partially incorrect. It is true that this insect is spreading the disease, but it is not the only one. The disease is this.

ah that makes more sense now. Thanks for the link


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Tea that makes everything taste like dirt
My highschool biology teacher once gave us (her class) a tea which made everything taste like dirt. I remember that chocolate candies, spicy hot sauce, and salty crackers all tasted the same after drinking the tea. The effect only lasted a minute or two. It's been a long time, and I can't remember the name of this tea - can anyone identify it?
(I am not certain if this question is appropriate for this SE, please let me know if it is not.)

This is probably the most appropriate SE, only alternative I could think of would be the cooking SE and it's probably more off-topic there. Did you see the (presumably) leaves used to brew it?

Got it, thanks. I considered the cooking SE, but I thought that maybe this was a standard highschool bio experiment/demonstration... I think the leaves were a very dark green/grey. They came packaged in a bag, so they must have been bought from a store or something.

This sounds like gymnemic acid, which can be isolated from the leaves of Gymnema sylvestre. It’s an “anti-sweet” compound, which wouldn’t necessarily make everything taste like dirt but might do so for you particularly. When I had it, it made my tongue slightly numb and candy tasted like nothing rather than sweetness, so it may not be what you’re looking for.
Lactisole (from coffee beans) is another option, but I haven’t tried that one personally so I’m not sure what its taste effects are like.

I'm accepting this for now because I think it's correct, but I'm not totally sure. If anyone else has any ideas, please let me know!


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Why are there so few multicellular anaerobes?
There are a few documented cases of multicellular anaerobic organisms, but I can't see a reason for it to not be more common. On the contrary, it seems pretty useful to be able to create energy even when deep inside tissues, yet the Loricifera are the only ones I've found documented. Given how often multicellularity has arisen, is there something that's fundamentally difficult about being anaerobic while multicellular?
One thought that might inspire others- multicellular organisms certainly tend to be bigger than unicellular ones, and in an oxygenated world larger organisms are more likely to run into oxygen than unicellular ones. However, there still exist an abundance of anaerobic niches for large organisms- the deep sea, for example.
I'm also drawing a distinction between facultative anaerobes and obligate anaerobes- there are plenty of facultative multicellular anaerobes, and I'm not as curious about that.
Useful sites that I came across while searching:
Journal article announcing the first anaerobic metazoa
Anaerobic fungi, presumed to be unicellular?

keep in mind even the deep sea can still have significant oxygen levels.

Fascinating question. I don't know the answer, but one possibility is that multicellularity required other inventions of the eukaryotes (more complex gene regulation, for example), and the fact that eukaryotes have mitochondria is just a co-occurence, not the driving factor.  Btw, the Loricifera species apparently has hydrogenosomes, which are thought to have evolved from mitochondria, but have lost respiration. Many parasitic species have similar non-respiring mitochondria-like organelles; see for example http://rstb.royalsocietypublishing.org/content/365/1541/713.long

I would think it would be a result of energy demands. Aerobic respiration yields more energy per molecule of glucose than aerobic respiration. So for a multiceullular organism, it will be easier to satisfy the high energy demand that multicellularity can create, especially in organisms like mammals that maintain a constant body temperature and have a complex and metabolically expensive brain. I know some plant tissues and tumors will sometimes use anaerobic respiration when they are in low oxygen environments, but the energetic benefits of aerobic respiration may be too good to pass up.

Simple answer: very little oxygen is required for a decent amount of energy, and very little carbon dioxide is given off. These are also both gases, which makes distribution a good bit easier. Take ethanol or lactic acid fermentation. Every cell producing that byproduct at once would result in an insane amount of waste to concentrate and excrete, and a huge amount of it would be required. Because of this, anaerobic species haven't had much evolutionary pressure to become multicellular, even if it would be technically possible.

I did a bit of reading myself, and it seems as if Loricifera are the only multicellular obligate anaerobes.
I see your point with niches for anaerobic organisms in deep water. Many organisms near the hydro-thermal vents use anaerobic cellular respiration.
From my understanding of Loricifera, it seems as if they would utilize chemosynthesis as their method of obtaining energy.

Loriciferans are found exclusively in marine habitats, and live in the spaces between sand grains or in the mud at the bottom of the deep sea. The nanaloricids prefer sand with low levels of detritus (material derived from the decomposition of once-living organisms) or clean shell gravel, whereas the pliciloricids are often found in such deep-sea sediments as the white abyssal Globigerina ooze and the red deep-sea clay from the hadal zone (below 20,000 ft; 6,100 m).

--From Encyclopedia website: Loricifera (Girdle Wearers).
Lociferans live in a rather oxygen-less environment.

So you're right about niches in the deep sea.
But typically the deep sea has extremely high levels of pressure that few multicellular organisms are built to handle.
Additionally, I was able to find a few other obligate anaerobic Eukaryotes, but those were Protozoa, so thereby not unicellular.
About it fundamentally being difficult to be exclusively anaerobic while multicellular, with multiple cells, there is more upkeep and more energy is required to run the "system". Aerobic processes tend to be a lot more efficient, producing more ATP for usage.

Only 1 ATP (from my understanding) is produced from this, whereas with aerobic respiration:
Aerobic ATP sum
Much more ATP is produced from aerobic processes.
In the end, the majority of obligatorily aerobic organisms are unicellular, or are extremely small.

Their sizes range from 100 µm to ca. 1 mm.

So... that's why multicellular organisms are typically carry out aerobic cellular respiration.
Also, about the fungi you mentioned, it goes through Horizontal gene transfer, which unicellular organisms typically use:

Horizontal gene transfer (HGT) or lateral gene transfer (LGT) is the movement of genetic material between unicellular and/or multicellular organisms other than by the ("vertical") transmission of DNA from parent to offspring. HGT is an important factor in the evolution of many organisms....
  Most thinking in genetics has focused upon vertical transfer, but horizontal gene transfer is important, and among single-celled organisms is perhaps the dominant form of genetic transfer.

--From Horizontal Gene Transfer Wikipedia page
So yes, it seems as if the fungi that you mentioned and other similar types of fungi would be strictly unicellular, such as yeast (thought yeast is a facultative anaerobe).

It is well known that anaerobic breakdown of glucose produces 2 molecules of ATP per molecule of glucose. It is also well known (see, for example, here) that fully oxidizing it to carbon dioxide and water (obviously, an oxygen-dependent process) adds up to a net energetic benefit of an additional 36 molecules of ATP. This is a massive difference. In an oxygen rich environment, anaerobes would be vastly outcompeted by aerobes, simply due to the vastly greater energy budget of the latter. As for anaerobic environments, complex (as in multicellular) anaerobes are still not prevalent, not because they are being outcompeted by aerobes, but because complex organs and systems require a lot of energy to maintain an function, energy that anaerobic respiration can't provide. Obviously, the energy requirements increase with an organism's size and complexity - the farther cells are apart, the more energy it takes for a signal to be sent in between them, e.g. via a signal peptide/protein or a hormone through a vascular system that requires energy to function, a nerve impulse, etc. Conversely, unicellular organisms avoid the energetic costs of intercellular signaling altogether (there are a few exceptions here and there, e.g. colony-forming microorganisms, but these expend far less energy on communication than cells in multicellular organisms). Numerous very interesting works on the energetics of cells and organisms are available - see, for example, here, here, and here.
One may point out that glucose, although the predominant source of energy for cellular metabolism, is not the only source, inorganic compounds from thermal vents being the alternatives most often cited. However, these are far less energy dense, with ecosystems centered around them being far less dense and complex than the ones centered on sun light and photosynthesis (Orcutt et al., 2011). Interestingly, even is such deep sea systems, the predominant source of energy is often the organic matter sinking from the photosynthetic ecosystems above.

Oxygen is by far the most common oxidizer (hence the name!) in biology on Earth.

Nevertheless, aerobic respiration provides more energy out of a unit of substrate than anaerobic respiration. Hence, where ever aerobic respiration is possible, aerobes are far more prevalent than anaerobes.

Also, you cannot fully oxidize an organic molecule simply by dehydrogenetation, to get all the chemical energy out of it you need an electron acceptor (most commonly oxygen); that applies to all organic compounds, glucose was just an example.

One must wonder if there was an abundance of multi-cellular anaerobes that existed before the Great Oxygenation Event (2.45Ga), but were never recorded (or discovered yet) in the fossil record.
The wikipedia article also suggests that ancient anerobes, before the Great Oxygenation Event, may have had more nickel to work with: "Modern methanogens require nickel as an enzyme cofactor. As the Earth's crust cooled and the supply of volcanic nickel dwindled, oxygen-producing algae began to out-perform methane producers, and the oxygen percentage of the atmosphere steadily increased.[23] From 2.7 to 2.4 billion years ago, the rate of deposition of nickel declined steadily from a level 400 times today's."

What is the connection between nickel and uni-/multi-cellularity? The first part of your answer fits best as a comment. It does not really attempt to explain why there aren't multicellular anaerobes

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


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How to correlate survival probability to gene expression profile?
I am reading up survival analysis of cancer patients and correlating them to gene expression. I came across this tutorial. Its mostly code. So what I still have not been able to understand is how exactly is the clinical data and the gene expression data merged?
For example, I have a matrix of clinical data (m by n) where there are m patients and n columns related to followup days, death days etc. I also have an gene expression data (m by t) where m is the number of patients and t is the genes. I first find the survival probability using Kaplan Meier method and plot it. Now how do I related the survival probability to the expression data?

As described in the link, you classify your samples into altered/not altered or high/low expressing (for your gene) by using Z scores (e.g. +/- 1.96) or a median cut-off, respectively. Now that you have a column that gives the expression status of the gene of interest, you can plot the survival for both conditions. The R code is in your link, and you can find how to do the same analysis with Graphpad Prism here: https://www.graphpad.com/support/faqid/1747/

@srao so you mean say out of 500 patients 200 patients will have high expression and 300 will have low, so the survival probability for high expression would involve only the patients having high expression and not those patient having low expression?

Yes, survival probability will be calculated separately for each group, that's how I understand it. In a more complicated example, you could have 4 groups (say 1 group for each quartile of gene expression). There are quite a few papers out there that have done this with TCGA data.

@srao true but how exactly it is done is not mentioned. papers mainly concentrate on results and what is done. detailed description is needed for first timers...


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I want to know the name of this water plant?

Above is an image of an unknown plant. It grows without any care.

Welcome to Biology SE! Please have a look at our policy for species identification questions and edit your question accordingly. As it stands your question is unlikely to receive a definitive answer and it may be down-voted or deleted.

what country/pond/fields/woods/height of plant/flowers is it?

@com Size is clear from the picture and if there are no flowers, you can't take a picture of them. But I agree location and habitat (probably shore of a lake or ditch) should be mentioned.

I know this plant because it is very beautiful semi aquatic and it has yellow flowers in summer. This summer it was the most amazing plant that I found in the south of france cote d'azur rivers. I have just learned what it is. It has the most lustrious foliage of nearly any plant and it looks like green metal.

@com Yeah it is nice to look at. However, it is an invasive alien species that completely overgrows the river, blocking water from flowing and costing water management a lot of work and money. See my answer below.

This is a water-primrose Ludwigia, probably Ludwigia peploides but I am not sure about the species (also because you didn't provide a location). Luwigia peploides and L. grandiflora are native to South america. However, in the rest of the world they are considered invasive weeds. In the European union L. peploides and L. grandiflora are considered "Invasive alien species of Union concern" This means EU member states should take appropriate action against these species.

Water-primrose has a high variation in the shape of the leaves, especially between vegetative and flowering sprouts. On the picture in the question the leaves are almost round. However, on the ground just left of the hand, there are lanceolate leaves, almost willow-shaped. This is the same species and the reason it is also called floating primrose-willow.


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Are amino acids of viruses L or D enantiomers?
I read a note saying that the amino acids of viruses are D enantiomers but I can't understand how that's possible since their human host can't even recognize that type.

The explanation here is way more prosaic than you suppose: the note is wrong.

@vkehayas I approved your edit but I kept the reference to the mysterious "note".

I'm voting to close this question as off-topic because it's apparently based on a complete misunderstanding. Unless the person can post the "note" that ostensibly makes this claim, there's no utility for SE.bio site here.

Viral amino acids would almost exclusively be L-enantiomers considering they use host cell resources and machinery to build their proteins and the host cells are built on L-enantiomers.
With that said, you could always have nonstandard exceptions as xusr mentioned, if a virus somehow requires oxidase for example.


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What is the real meaning of the statement "*ontogeny recapitulates phylogeny*"?
I tried searching in this site but couldn't find an appropriate answer to the title question: what is the real meaning of the statement "ontogeny recapitulates phylogeny"?

What kind of appropriate answer are you looking for? A simple google of "ontogeny recapitulates phylogeny" reveals lots of quite good answers.

Actually, the statement "ontogeny recapitulates phylogeny" has been largely discredited in modern biology.  The stages of embryonic development were thought by Ernst Haeckel to resemble ancestral species in evolution.  That is, early embryos appeared to have tails and gills and resembled fish, later embryos resembled quadrupeds, and so on.
However, embryos do NOT actually resemble adults of ANY species.  More accurately, one could say that early embryos of different species resemble early embryos of other species, and later stages differ more and more as specialized traits of different species become more obvious.  On the early extreme, one fertilized ovum shows very little difference in gross appearance from any other fertilized ovum, and the blastula of different species look very much alike, but as different organs and limbs become better developed, those of different species begin to look more and more different.
This actually only describes SOME of the changes that occur in embryonic development.  Other changes are not so simple.  One very good book that discusses the strengths and weaknesses in this area is the book "Ontogeny and Phylogeny" by Stephen Jay Gould.

As an embryo develops, it passes though stages with characteristics of some of the more primitive forms in its evolutionary lineage. An example is the pharyngula stage of the human embryo, which bears branchial grooves in gill pouches. in fish, these develop into gills.

As far as I know, this is exactly what the phrase means. Why is it down-voted?


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The difference between the beta-sheets and the quaternary structure of proteins
My biochemistry book says that beta-pleated sheets is a form of secondary structure of proteins, and it is formed between two or more polypeptide chains.
I wonder why the sentence in bold doesn't belong to the quaternary structure instead?!

Beta strands can form both intra- and interchain sheets. I wouldn't get too caught up in the latter case when deciding what level of protein structure beta sheets fit into.

Quarternary structure is between separate protein chains or proteins themselves. Beta sheets are a form of secondary structure which is within a single polypeptide.
Sure, some of the structures in quarternary complexes will be between “two or more peptide chains”, but the stipulation that these not be part of the same polypeptide chain would be necessary.

You say that beta sheet is a structure within a "single polypeptide", but my text book says that it is between "two or more extended polypeptide chains". Is the book wrong?!!

No its just a symantic issue. A beta sheet requires 2 stretches of peptide to run parallel to one another. Those 2 stretches of peptide are part of one continuous chain at the secondary structure level. Whether it counts as Beta sheet when 2 stretches polypeptides from totally separate proteins are in close proximity enough to hydrogen bond, I'm not 100% sure. But generally it refers to secondary structure which must be within a single continuous peptide.


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What counts as a 'breach of the skin' for infections(like rabies) that spread via wounds?
I've been looking at several sources on how the virus spreads and they all mention that the skin has to be broken, but does it mean broken to the naked eye?
A minor scratch where the skin appears unbroken and there was no bleeding could still have microscopic breaks of the skin, therefore it seems risky to rely on the naked eye.

It seems some skin pathogens can't even infect visible skin breaches like abrasions (https://www.ncbi.nlm.nih.gov/pubmed/24722416). Better to be safe than sorry though when it comes to protecting skin from potentially lethal infections.

I believe that your books refer to 'broken' not necessarily meaning broken to the naked eye, but as in any broken epidermis.
The outer layer of your skin that protects you against infection is the epidermis. It's a water-tight layer mostly composed of keratinocytes joined together by adherens junctions. Logically, even if you can't see a breach in your skin (epidermis), there may still be one. While the chance of getting an infection from a non-visible break is less than the chance of infection from a visible scratch, it's still possible.

Source, please?


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Finding targets of transcription factors
I'm trying to find an easy way to get a list of putative targets of a particular transcription factor (for example, STAT1). I'm interested in targets determined using both experimental and computational evidence. I thought it should be easy to obtain such a list, but I'm having a hard time. Could anyone help me with this, preferably with specific, step-by-step instructions. As a bonus, I'm also interested in the reverse problem, which is, for a given gene, obtain a list of all transcription factors for which there is evidence that it regulates that gene.
Thanks,
Jennifer

If you were interested in human targets, one easy way is GeneCards, which aggregates other resources, and combines computational and (some) experimental data:
In this case the inverse problem is particularly well accessible: e.g.: scroll down to section of Genomics (e.g.: for the gene called NOTCH http://www.genecards.org/cgi-bin/carddisp.pl?gene=NOTCH1&keywords=notch1 ).
If you you were interested in obtaining all genes of a given transcription factor, you could buy a license, costing around 150 USD per year, for the GeneALaCart service of the company that runs the free genecards ( https://genealacart.genecards.org ), upload a list of all human genes (which you could for instance obtain from ncbi's ftp server), and get a spreadsheet linking transcription factors to genes.

You can use homer software for this, it is freeware. Homer uses a database of known motifs, and STAT1 is in there (search for STAT1 in the webpage).
With homer you can search for known motifs within the whole genome. But you can also look for all motifs within a given area of the genome. So for your bonus question, you'll need to get the genome coordinates of your gene of interest (including promoter region), and search for known motifs in that area.
You can all find it in the manual, which explains exactly which steps you need to take.


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Cutting dna using restriction endonuclease
Genomic dna is digested with alu 1 which is a four base pair cutter. What is the frequency with wich it will cut the dna assuming a normal distribution of bases.
(this is not a homework)

I guess it is the probability of getting the 4 specific base pair in a row which is 1/4 1/41/4*1/4.

You can teach yourself to answer this type of question using this resource which I wrote some time ago: https://www.mvls.gla.ac.uk/Teaching/SLS-FTB/ren.html

Welcome to Biology.SE. I think this question would be better on-topic on math.SE.
Assuming the chromosome is either 4 bases long or infinitely long, then the answer is simply $\left(\frac{1}{4}\right)^4$. However, chromosomes are not infinitely long so the result should be (negligibly) lower than $\left(\frac{1}{4}\right)^4$. If chromosomes are only 3 nucleotide long, then of course, the probability will be $0$. If it is 4 bases long the probability is $\left(\frac{1}{4}\right)^4$. If it is 5 bases long the probability is $\frac{2}{4^5} = \frac{1}{2}\left(\frac{1}{4}\right)^4$.
Consider this numerical approximation, to ensure the result is correct with this simple one liner in R
n = 1e7
length(gregexpr('abcd', paste(letters[sample(1:4,n,replace=TRUE)], collapse=""), perl=TRUE)[[1]])/n
[1] 0.0039041

which is really close to $\left(\frac{1}{4}\right)^4 ≈ 0.00390625$.
So, in a genome of 3 giga bases, that represents an expected $\frac{3\cdot 10^9}{4^4} = 11,718,750$ (or ~11 millions) such locations where Alu 1 can cut.

Remi.b what is the boundary effect.  Btw thank you

@user7635691 I edited the answer to add some info on that.


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Amount of molecule at equilibrium
A cell produces molecule A at 10 units per second and the molecule has a half life of 15 seconds. How many units of molecule A are inside the cell at equilibrium? Showing your work would be phenomenal.
Geez, a bit hostile, are we? Regardless,
Here's how I went about doing it. Pardon my terrible formatting skills:
P is the concentration of molecule A.
The half-life formula is 2^-(t/15).
At the moment of equilibrium: P = 10 * dt + 2^-(dt/15) * P
Moving things around, I get P = 10 * dt / 1-2^-(dt/15)
I attempt to take lim dt->0 using l'hopital's: 10 / (1/15 * ln(2)) = 150/ln(2) molecules of A at equilibrium.
However, the correct answer should be 300 units of molecule A at equilibrium. Any suggestions?

No, showing your work would be phenomenal.

this looks a lot like homework.  Homework questions aren't forbidden, but this isn't a "do-your-homework-for-you" service; you have to show what you've tried and where you've gotten stuck.

Phenomenal. Finished editing.

I answered a very similar question from you here. Using the formulas on Wikipedia we can find that the mean lifetime $\tau$ is $T_{1/2}/\ln(2) = 15/\ln(2) \approx 21.6$.  Using Little's Law the steady state concentration is (arrival rate) $\times$ (mean lifetime) $\approx 216$.
You could also use the decay rate $\lambda=\ln(2)/T_{1/2}$ and substitute it into the differential equation given in the previous answer.
This is the same as the answer that you got to by a more complicated route. I don't see how we can get to a steady-state concentration of 300 unless you've misstated the question or left something out.

A friend just told me the same thing. Perhaps the answer key is faulty.


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Help identify this red/black Vietnamese insect
I found this strange insect while on Son Tra, Da Nang in central Vietnam. It was about 4cm long and although it was on the ground, was obviously capable of flying. I've never seen anything like this and would like help identifying it, please. Thanks!

It looks very much like a robber fly. I'm voting to close as a duplicate.

Possible duplicate of What type of insect is this?

The duplication is taxonomic only, not geographic (but a brief search found few images of live robber flies from Vietnam, so going deeper is best considered problematic).

That is not a duplicate, the species is clearly different. The only thing those questions have in common is the Family being Asilidae

Dasypogon is a genus of robber flies in the family Asilidae.

Kingdom: Animalia
Phylum: Arthropoda
Class: Insecta
Order: Diptera ,
Family: Asilidae
Tribe:Dasypogonini
Genus:Dasypogon.

84 species belong to the genus Dasypogon. Among these, this one is Asilidae Dasypogon diadema.

Thanks for the link. Could you link the site to the picture as well - it looks like the same image btw ? It's best practice to dig up an image form a reputable website to show the positive ID. I took the liberty to clean up your post a bit. Thanks for your contribution. +1

Welcome to Biology.SE! According to several sources this is a European species and not found in Vietnam. In general, you are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

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


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Are drug-gene interactions predictable?
I have been reading about drug-gene interactions and pharmacogenetic tests. I haven't been able to find many resources that define the process of testing for possible drug-gene interactions without performing trial and error method. For example, drug-drug interactions can be predicted by using several parameters as noted here. Are there any parameters similar to the ones described in given paper for predicting drug-gene interactions if drug characteristics and genetic data is available? Please describe process or provide source.

You need to add more details or else the question is quite broad. Yes you can find drug-gene interactions. Google the terms pharmacogenetics and pharmacogenomics.

One can list candidate genes based on their functions.
If a drug acts by inhibiting the expression of gene G in order to reduce process P, then, gene G, all its regulatory elements and all sequences involve in process P are good candidates for such interaction and should be investigated. If there is known genetic variation in the population at these loci and if we know this genetic variation affect phenotypic variance, then definitely, those are good candidates.
However, to my knowledge, this is the extend at which we are able to go. We can list candidates but it does not mean in the absolute that a candidate must present an interaction with the drug of interest and it does not mean that a non candidate gene would necessarily not have an interaction. Only a statistical testing for such interaction would allow one to solve the mystery.

Is there a study where the above works or is this hypothetical?


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Does Antioxidant prevent oxidation that creates free radical?
I have already known that antioxidant can neutralize oxidant/free-radical, but i want to know if antioxidant can also prevent the oxidation or not. I want to know to how it works if antioxidant can prevent it.
By the way, my point in asking this question is actually to answer my final question: Does vitamin C (antioxidant) inhibit the oxidation in ripening fruits?
thank you!

Welcome to Biology S.E From my knowledge free radicals in human body are produced as a unwanted consequence of oxidations-hydroxylations-coupled oxidation reductions etc.involving cytochromes, EC1 enzymes.If anti oxidants were to prevent them forming directly from source reactions then they would have to be inhibitors of such enzyme systems....

So, antioxidant cannot prevent the making of free radical, it cannot prevent the oxidation? okey then... thank you !

...the second half of youre question is interesting.But ripening of fruit is usually caused by ethylene in plucked fruits mainly...but for an info I can tell u that most of the ascorbate in cut & uncovered citruses is lost because of its conversion to dehydro ascorbate...Good luck with the question

OKEEEEEEYYY...! Thanks for helping, i guess i can answer that question now :)


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Are there statistics on Sickle Cell Traits based on country of origin?
And where was it originally from and how does it spread?
Thanks.

How have you tried to answer this question? A simple google search answers the first for me.

@kmm - By country and by province, I have not found any statistics. If you stumble over an article, please kindly post it here.

Can I say all the Chinese with SCT have recent African or South Asian ancestry?

For "where does it come from and how does it spread?", why not read Wikipedia?  Short answers: (1) malarial regions of sub-Saharan Africa; (2) movement of people and genetic introgression.
Googling 'sickle cell "country of origin" turns up, for example:
"Sickle cell disease in areas of immigration of high-risk populations: a low cost and reproducible method of screening in northern Italy" Blood Transfus. 2014 Jul; 12(3): 346–351. doi:  10.2450/2013.0188-13 PMCID: PMC4111816
Country    Selected     Enrolled/   Enrolled/
                        negative    Hb variant
-----------------------------------------------
Ghana      241 (51.4%)  112 (47.1%) 53 (57.6%)
Nigeria    152 (32.4%)  77 (32.4%)  29 (31.5%)
Guinea      15 (3.2%)   8 (3.4%)    4 (4.3%)
Cameroon    13 (2.8%)   10 (4.2%)   1 (1.1%)
Senegal     12 (2.6%)   8 (3.4%)    1 (1.1%)
Ivory Coast 10 (2.1%)   9 (3.8%)    1 (1.1%)
Other       26 (5.5%)   14 (5.7%)   3 (3.3%)
Total      469 (100%)   238 (100%)  92 (100%)

"The burden of sickle cell disease in Cape Town", South African Medical Journal 102(9), 2012 Wonham et al. http://www.samj.org.za/index.php/samj/article/view/5886/4421

Distribution of sickle cell disease patients by country of origin. Up to 93.1% (n=54) of the patients were originally from other countries in Africa, mainly from the Democratic Republic of Congo (62.1%, n=36).

Thanks. Since SCT is spread by inheritance, not by malaria or mosquito, I wonder if the spread of this trait is correlated with the improvement of transportation technology and the human migration that came after it.


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Why do you get an increase in bicarbonate ions after vomiting?
Why do you get an increase in bicarbonate ions after vomiting?

Welcome. Any prior research you can share with us? Importantly, where did you find your statement that vomiting increases HCO3- and where is it increased? In the blood? Saliva? Stomach?.

Although you need to show some effort , but I wanted to give you a hint - after vomiting quite a good amount of $H^+$ ions are lost (that’s because HCl is lost) now think what would happen to extracellular fluid to balance this change :)


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What is this salt-water worm?
We found this near Fort Pheonix in Buzzards Bay in Massachusetts. It gets long when its swimming (About 8 inches) and contracts when disturbed (2 inches).
Its head is shaped a bit like a diamond (like a cobra?). Its body looks fairly translucent and is ribbon-shaped.

Here's a short video: https://vimeo.com/240322590

It is possibly a milky ribbon worm (Cerebratulus lacteus).

source:  intertidal-novascotia.blogspot.com
They can be found anywhere and everywhere along the Atlantic coastline in healthy abundance - http://intertidal-novascotia.blogspot.com/2012/05/cerebratulus-lacteus-milky-ribbon-worm.html


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Why do we get bored of certain food items after repeatedly eating them?
Why do many people not like certain food items after eating them for long? They seem tasty first, and after eating many times, it feels like we get bored.

Who's we here?  As Unicorn13601 says, some people eat the same food for decades without boredom, e.g. I've eaten the same brand of cereal (with whatever fruit is seasonally available) most mornings for the past few decades, because I don't want to think about food choices at that time of the morning.  You might also ask why people get bored with any activity, not just food.  And whether there's an evolutionary advantage to seeking a varied diet.

Humans inadvertently try to balance neophilia and neophobia - fancy names for preferring the new and fearing the new. With regards to food, most humans, and animals, take an overall stance of cautious curiosity. Curiosity as in discovering a new edible food that helps them survive and thrive, and caution as in any new food item may cause harm. Certain individuals will have less curiosity, being content with just eating a few foods, while others will seek new experiences when they can. That's part of the variety in humanity.
For example, people from the Eastern countries rarely ever get bored of certain foods, as they are a primary source of fuel, such as rice or noodles. Or like people from western countries, many of them eat bacon, eggs, and toast every morning for sixty years. They eat it repeatedly, almost everyday, yet they continue to do so without complaining of boredom.
The scientific explanation is just that the brain will get tired of the same thing. That's why do many fast foods are engineered so carefully tantalize (bliss factor) and yet not go over the point when the brain gets overloaded. This phenomenon doesn't really count as a factor of boredom, rather more like insensitive to repeated exposure. It's like when you are exposed to a strong smell (e.g. Perfume) for a longtime. The brain, neurotransmitters and olfactory receptors just ignores it and doesn't register it. It is suggested why we females keep putting more and more layers of perfume on, we just don't smell it anymore .
Hope that helps <3.


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B Cell Differentiation
During the differentiation of B cells in bone marrow, recombination occurs in light chain and heavy chain genes to produce a single type of functional gene which determines the type of light chain and the heavy chain produced by that B cell.
Therefore, a single B cell and its generation displays a single type of antigen receptor on its cell surface.
My question is-
Recombination will occur in both the copies of the light chain gene present on the homologous chromosomes (same with the heavy chain gene).
So, the combination produced on the homologous chromosomes should be different.
Is it really so?  And if not, then how come they are identical?

There is a mechanism in T and B cells called allelic exclusion. This means that most of the times only a single allele is used by building the light chain and the other is excluded. Incomplete allelic exclusion may contribute to auto-immune diseases, because cells using two different light chains can potentially recognize both pathogens and healthy human cells1,2,3,4,5,6,7,8.


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Identify this tuber like object found on beach
Can anyone identify this tuber-like object I found on a beach in South Wales, UK? It's about 25 cm long and looks like a deflated football. Pretty spongy, saturated with water. I was hoping it was ambergris, but that seems unlikely.

Mabye it is a carcass or sea sponge or a rooton object. i am only nine!!!

Hi @EthanXiao. Welcome to Bio. We are a scientific stack and request answers to be backed up by scientific sources. Our target are people with a level of education matching that of a bachelor's or master's, and folks above that. Say 18+ years. Perhaps wait a few years before answering any other questions :)

It is spongy because it is a sponge, specifically a sea sponge. There are quite a large number of them native to the waters around england. I would guess Craniella cranium based on shape and location but I am by no means an expert on sponges.
Here  a cross section of a cleaned sponge

and sediment laden potato sponges after a hurricane.

you can see more images of collecting these here, http://www.vims.edu/newsandevents/topstories/archives/2011/irene_blobs.php
Here is a whole website dedicated to english sea sponges, http://www.aphotomarine.com/sponge_suberites_ficus_sea_orange_sulphur.html


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Biological terminology: "codes for" vs. "codes a"
Maybe this is answered already before, but I cannot find it:
Most authors say/write "a gene codes for a protein", some use "a gene codes a protein". The latter seems to me the grammatically correct use of the verb "code".
What's the reason for saying "code for"? Is it because of RNA processing (e.g. splicing)? What about the coding of single amino acid: "AAA codes Lysin" or "AAA codes for Lysin"?
I would also like to know some history of the use of these (and may be other) terminologies.
Tia Udo

In the second usage ("a gene codes a protein"), it's likely the authors meant to write, "a gene encodes a protein". That would then be grammatically correct and correct phrasing.

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

I'm voting to close this question as off-topic because it belongs on SE English Language & Usage (especially the history part), but the poster would need to do some research first.

@DevonRyan "encode" is just the term I've found on Jennifer Doudna's talk.This question may be closed...

This is an English usage question more than one of biology.  The verb code has two main meanings(1):

(transitive) to put into the symbols of a code
(intransitive) to be a code symbol

The first, which being transitive takes an object, is used for the act (as by a person) of translating a plain message into a corresponding encoded form. This is not the meaning used in "AAG codes for lysine".
The second form does not take an object.  It is not being done to something, but rather is just a state of being.  This form is almost always followed by a prepositional phrase "for noun", as in "INS codes for insulin".
Hence it is not correct English to say things like "INS codes insulin", as the use of "insulin" as an object implies the first meaning, as if one were saying "INS takes an insulin molecule and puts it into an encoded form" (whatever that would mean).
The reader would likely try to interpret "INS codes insulin" with the intended meaning, but the incorrect usage makes it seem equivalent to something like "INS is a DNA sequence insulin."  Leaving out the preposition for may be shorter, but it gives a bumpier ride.
(1): Merriam-Webster.  For more variants see Wiktionary, esp. encode.

Thanks for the quick answer! I agree with the intransitive form "be a code for", e.g. "Gene G is a code for Protein P". I've put that question on (https://english.stackexchange.com/questions/416263/general-examples-of-to-code-for) to get examples of non-genetics usage of "code for". btw: I'm just watching a video of Jennifer Doudna, which is an expert in the field of genetics, and she uses "Gene G encodes Protein P" which look very fine to mee (https://www.youtube.com/watch?v=SuAxDVBt7kQ?t=254)

I couldn't edit the last comment since it was older than 5 mins:
... I've read Merriam-Webster's and Wiktionary's articles and agree with the intransitive form "be a code for", e.g. "Gene G is a code for Protein P".
I've put that question on (https://english.stackexchange.com/questions/416263/general-examples-of-to-code-for) to get examples of non-genetics usages of "code for".
btw: I'm just watching a video of Jennifer Doudna, which is an expert in the field of genetics, and she uses "Gene G encodes Protein P" which looks very fine to me (https://www.youtube.com/watch?v=SuAxDVBt7kQ?t=254)


text:
Legality of doing private or scholastic virology with human pathogens?
Is it ok for a student, say a graduate student in biochemistry, to do amateur virology using potential human pathogens?
For example, lets say the student gets a cold and tries to isolate the virus causing the cold. Is it ok for the student to do that in a school lab? How about a home lab?

I'm voting to close this question as off-topic because it pertains to law, not biology.

@canadianer Virology is part of biology.

Law isn’t though…

If you ask a question about the law, you need to state where you live. Alternatively, if you are in gaol, as your name implies, different rules will apply.

@canadianer This is not just about law, but safety as well, so I think it is better not to close this question.

tl;dr I think that doing this unofficially, at home, might be no big deal, but doing it in an institutionally supported lab (or any kind of institutional setting, e.g. if you wanted to publish a paper from the results) could involve lots of hassle and red tape.
I'm not a microbiologist, but ... technically I think this would fall under the category of BSL-2 - via Wikipedia:

Biosafety level 2 is suitable for work involving agents of moderate potential hazard to personnel and the environment.[9] This includes various microbes that cause mild disease to humans, or are difficult to contract via aerosol in a lab setting.[11] Examples include Hepatitis A, B, and C viruses, human immunodeficiency virus (HIV), pathogenic Escherichia coli, Staphylococcus aureus, Salmonella, Plasmodium falciparum, and Toxoplasma gondii.

BSL-2 requires (among others) access control for labs; special safety training for all lab personnel; use of containment equipment for procedures that may cause infectious aerosols or splashes ...
It may seem a little crazy to lump a common-cold-causing rhinovirus with HIV, but BSL-1 (the mildest level of infectious agent control) is restricted to

well-characterized agents which do not cause disease in healthy humans

(emphasis added). Note that even BSL-1 requires lab safety protocols beyond those for non-infectious agents.
A bit more internet searching on BSL classification for rhinoviruses (the typical cause of the common cold) suggests some variation: e.g.

Google search for "rhinovirus BSL" brings up a bunch of hits from the American Type Culture Collection (ATCC) for a variety of rhinovirus isolates that range from BSL-1 to BSL-2
the Public Health Agency of Canada classes rhinoviruses as BSL-2

Depends on. S/he already got that infection so it is not a big risk to get it again... BSL1 is ok I think.

It wouldn't be your/their decision, it would be the institutional biosafety office's decision. And it's not whether it causes disease in that particular person (e.g. even if you vaccinated everyone in the lab against a pathogen, you'd still have to obey BSL-2 protocols). (I agree that this set of experiments would be 99.999% safe, but the rules are still there.)

I agree that you have to obey BSL protocols if you are working with pathogens, but I think applying BSL-2 for a common cold virus would be a huge exaggeration. I guess the school lab has a supervisor, so s/he should ask that person whether working with common cold virus is allowed and if so which protocol should they follow.


text:
Why does breathing increase in higher temperatures?
In my experiment, my group increased the temperature of a fish's water. We noticed the fish took more breaths than the prior normal temperature. Is this because the fish is trying to breathe in the water's oxygen, which is evaporating more quickly than in normal temperature?

As you can see on the diagram below, oxygen solubulity in water drops by increasing temperature, so your fish has to breath more to get the same amount of oxygen.

ref

You can find more info about why gas solubility is temperature dependent here:
Chemistry (Averill & Eldredge) / Effects of Temperature and Pressure on Solubility.

In3mo informed about oxygen content varying with temperature, and another factor is the fish metabolic rate:

Standard Metabolic Rate (SMR) is the metabolic benchmark in fish. It
  is the metabolic rate of a resting fish at a specified temperature in
  the middle of its normal range. Therefore a trout's SMR15 would be the
  resting metabolic rate of a trout at 15'C. There is natural law called
  Q10 = 2: chemical reactions tend to double with every 10'C increase
  in temperature of the reactants. In poikilotherms, this is translated
  into biochemical events and in turn into metabolism. The metabolic
  rates of fish roughly double with every 10'C increase in temperature,
  except at the extreme ends of their temperature tolerance.

The fish become stressed and their physiological rate increases. for example, a fish at 5 degrees, his stomach can take 2 weeks to digest a meal, and at 25 degrees it takes 2 days.

Nice answer! :-)


text:
Does iris color effect the amount of light that reaches photosensitive ganglion cells?
Does eye color (of iris) have any effect on the amount of light reaching retina cells and hence effect melatonin production?


text:
What are embryophytes? And how are they characterized?
What does it mean when it's said that plants are embryophytes?
What are the specific characteristics that help determine that?

The name derives from their innovative characteristic of nurturing the young embryo sporophyte during the early stages of its multicellular development within the tissues of the parent gametophyte.
source
https://www.revolvy.com/main/index.php?s=Embryophytes&item_type=topic
Similar definitions are in the New World Encyclopedia and Merriam Webster Dictionary.


text:
What causes the blue color seen in baboons?
Based off of this question from Worldbuilding SE.
In that question, I talked about how the scrotum and buttocks of various animals have a blue color because of thick deposits of collagen in those areas. I wanted to make a race of elves that used this mechanism to achieve blue skin all over their body.
Now, I thought that the thickness of the collagen layer was what was behind the structural coloration of animals like baboons and vervet monkeys. However, I have since learned that it is also the way the collagen is arranged that makes that color occur. That made me think that to achieve my desired effect, I wouldn't need to make the skin exceptionally thick. I could just rearrange the collagen humans already have and not change the thickness at all.
I'm having a hard time understanding the underlying mechanisms behind what makes the arrangements of collagen different, and why it wouldn't occur over the whole body.
Thus my question is twofold:

Is it the structure, or the thickness of this collagen layer that makes the structural color work?
Does the way the collagen is structured in these areas make the skin function differently than normal skin? (I.e. Is it less stretchy? Is it more fragile?)

(I'm sorry if this is off topic, I was thinking that since the focus of the question is on how the collagen works that it would be better suited here than on Worldbuilding)


text:
Why does it hurt when water touches cuts?
Why do we feel a burning sensation when water touches cuts/wounds? People suggest applying oil over cuts while bathing to prevent water touching it, but water is heavier than oil so it shouldn't work, but it does, Why?

Water changes the local ionic concentrations and therefore induces an electric
signal at exposed neuron membranes.Oil is used to prevent entrance of water to the cut because it is hydrophobic i.e. repels water but attaches to the tissue.
Gravity plays no role here.

why does gravity play no role

@RamKeswani Presumably because the force of adhesion between the oil and the skin is stronger than gravity, as is the force of the oil repelling the water. I'm no physicist, but that makes sense to me... ;-)

Hi, welcome to Bio.SE! Please provide citations and appropriate forms of support for your answers. See our help page for further suggestions for writing good answers. Thanks!

It's a phenomenon called cutaneous hyperalgesia in which non-noxious stimulus like water cause pain. The Mechanism behind that phenomenon is the accumulation of pain-producing factors like (substance P), proteolytic enzymes, histamine or bradykinin which easily stimulate the nerve endings of the pain in the cut area. These substances are released from damaged cells. So the pain threshold is lowered. The non-painful stimuli become painful and the painful stimuli become exaggerated!
And sorry if I don't know about the oil and how it prevents that!

Hi, welcome to Bio.SE! Please provide citations and appropriate forms of support for your answers. See our help page for further suggestions for writing good answers. Thanks!

Your nerves withold a solution that has an electrical charge, when water enters a damaged nerve and nerve membrane, it changes the electrical balance in the nerve. Wounds are supposed to be treated with physical cleaning and topical antisceptic.
Here is a more scientific account:

Cells normally have a functioning
  ion pumps. Cells are surrounded by a membrane that acts as a wall with
  little holes that ions(sodium,chloride,potassium, calcium) can pass
  through with difficulty.  There pumps in functioning cells exchange of sodium, chloride and potassium.  This causes a
  difference in electrical potential across the cell membrane, in effect
  making the cell a battery. By exposing that tissue to water, which has
  no sodium or chloride, you immediately changed the concentrations of
  these ions surrounding these injured pain cells causing them all to
  fire at once.

Cleaning is normally water and soap or saline solution (9mg/L approx).
Non stinging antisceptics currently favored by doctors are Betadine, Merbromin, amonst others.
I like alcohol for reed cuts etc because it indicates when the exposed inner cell inside the cut and under the miasma have been well sterilized and attained.
https://www.quora.com/Why-do-wounds-hurt-more-when-they-get-wet

Soap and water (S&W) is fine. The dirtier the wound, the more S&W. No serious medical professional recommends Betadine and water for wounds. It's used in hospitals because it's there/easier to use than soap, but even there, that's changing. (E.g. We used to irrigate wounds with normal saline under pressure. Now we use a faucet/tap water and a non-stinging soap and water. Both Betadine and alcohol are harmful (to some degree) to living cells. And soap and water is better than alcohol, which no doctor in their right mind would use for fear of being punched - and hard - by the patient.

Biologists often disagree on facts. I'm surpised that using antisceptic on wounds is a controversial practice, considering it's more likely to stop infection than water based treatments. We probably only disagree on my poor wording.

@com.prehens.ible et al. please be nice to each other :) I am deleting most of this comment thread as this doesn't really seems to go anywhere. What I do know is that throwing youtube videos to a hardened veteran in healthcare won't really help. YouTube and Quora are no credible sources. I think anongoodnurse's issues arise mostly from the lack of references in your answer. If you guys prefer to have the thread migrated to chat, I'm happy to revive the comments and create a chat room. Cheers.


text:
what happens when you put enhancer and caat box in prokaryotes
what happens when you put enhancer and caat box in prokaryotes

I do not think that enchancers do anything in procaryotes since there is no
chromatin spatial organization of DNA involved.


text:
Monohybrid Cross
There are two types of pea plants according to Mendel:
1)Tall(TT or Tt)
2)Dwarf(tt)
But I have a doubt! Is there a heterogeneous dwarf pea plant(tT)? When there can exist a heterogeneous tall pea plant, there must exist a heterogeneous dwarf pea plant also! This doubt is troubling me very much! Please clear my doubt!

Why there must exist a heterogeneous dwarf pea plant also. I don't understand why you think it must be the case.
Under this simple genetic model, there is no environmental variance and T is dominant over t (t is therefore recessive) and therefore the heterozygotes Tt have the same phenotype than the homozygote TT. There is no Tt individuals that have the same phenotype as tt.
If t was dominant, then Tt individuals would have the same phenotype as tt individuals. If T and t were perfectly additive, then Tt individuals would have a phenotype half way between the TT and the tt phenotypes (Tt would be of average height).
Please note, that very few real life cases are that easy. There is often interaction between many loci and there is often (if not always) environmental influence on the phenotype.


text:
What causes weight loss and fatigue in Addison's disease?
Why would a lack of cortisol cause fatigue? In terms of normal functioning of the gland.

Cortisol is required for gluconeogenesis. So if you have low cortisol, then you will have low blood sugar, which causes fatigue. https://www.thebabbleout.com/health/cortisol/ According to wiki low cortisol causes increases lipolysis, but that part is not so clear. https://en.wikipedia.org/wiki/Cortisol


text:
Are there certain symmetric-pair muscles that are slightly bigger and NOT due to handedness?
Ok, hear me out, I was just thinking about an article in Nature I read in the past titled "Scrotal asymmetry in man and in ancient sculpture"$^{\dagger}$ and more recently an entire medical textbook detailing everything about hands wherein the author accounts the different types of blood vein topology categories there are in humans, and he touches on handedness too. The part about handedness stuck with me, and I began to notice (looking in the mirror, etc.) that my right neck muscles are slightly larger than the left ones, but so is my friend's who is left handed. I thought this might be due to handedness not translating to chewing behavior (chewing on the right or left predominantly). Anyway, all this is building up to my main question which is this:

Is there something about our anatomy (organ placement, vein topology, etc.) that makes certain symmetric-pair muscle groups unavoidably asymmetrical or is it just handedness or the environment?

$\dagger$ Heard about it here: https://www.youtube.com/watch?v=Xyquv6SsLWg&t=0m56s

perhaps related: besides environment and genetically programmed phenotypes, there also is developmental noise (e.g. scroll down to "developmental noise" in the genetics textbook https://www.ncbi.nlm.nih.gov/books/NBK21842/ to see a nice example of differences between left and right eyes of fruit flies)

So cumulatively random molecular events during embryogenesis then?

Without any evidence, or excluding genetically encoded handedness, or environmental influences, I would be reluctant to say that the specific case with the human muscles that you noticed would be due to developmental noise; However it would extend the scope of possibilities that you sketched out, and might be a further possibility. (Irrespectively, developmental noise indicates that it is quite difficult, and sometimes impossible, to create two identical structures - if one would look close enough)

I think it is too difficult to know. There are so many factors influencing development - such as developmental noise as mentioned - as well as environment and genetics. If you were to scientifically investigate this, you would need to control all of these things, which is simply impossible. We would not be able to differentiate between asymmetry caused by environment or anatomy, so most likely we just won't know what might be causing this.

There are many variables that could affect the answer to this question. Such as what activities you partake in.
For example, I am a hockey player at the he varsity level in high school. I have noticed that my entire right side is more toned, muscular, and flexible (especially my right latisimus dorsi and deltoid). It just so happens that I rely on my right side for energy and strength more than my left when it comes to shooting pucks and just playing the game.
Typically what we see in humans is the dominant side of their body will tend to show more hypertrophy than the non-dominant side. When you look at a human anatomically, their dominant side shoulder will be bigger and will rest lower when relaxed. Even small things like sleeping habits can effect the visual difference of you symmetry. I will agree though that it is odd that your friend noticeably has more hypertrophy in his neck muscles on one side but is dominant on the other side. This could be due (but not limited) to small habits not taken into account. Like I mentioned before, sleep habits, any motion with the neck in a specific way, chewing could maybe be a factor, or (maybe not likely) a genetic mutation.
This is an interesting topic and I urge you to maybe look at some more people for evidence that dominance has a role in it. 2 people is maybe not enough evidence to really back up a claim you're going to make.
Hope this helped!
-Sartoaster

Bigger neck muscles on one side can simply be the effect of wearing a backpack on this side or anything else - there are much more variables than only handedness, I do not think it is very odd.

It depends on many factors such as:

exercise,
handedness,
may be congenital i.e. during birth, or the development of one occurred fast and one become slow,
genetic variation.

It would be helpful to know the size differences and names of the muscles as well.

It is usually helpful to link to sources that will support your answer, and allow the asker to explore the topic more if they so wish.


text:
Do ants also use the Earth magnetic field?
A lot of animals, specially birds use the Earth magnetic field to orientate on their flight across the Earth. Now some scientist suggest that ants has on their antenna a kind of magnetite crystals by which they also can use the magnetic field. But for what would and could an ant use this huge magnetic field, while they just walk for only meters a day?

Do you know about compass termites? Their colonies are always North-South facing. I don't know that they are aware of it, but nature has selected them into the now, so it may have something to do with an accidental larval temperature regulation in the colony because the sun hits a larger surface area for a longer period of time, and so the colony is warmer longer over night.

Hard to say, but for at least one ant species (see below) it seems to be an orientation cue for (relatively short-distance) migration (even if you're only going a few meters, it can be important to walk in a straight line!). At present it seems we know something about the proximal mechanisms of magnetoreception, and a little bit about the observed behavioural patterns, but don't have much more than informed speculation about the ecological/evolutionary advantages of this form of spatial orientation.
Searching "ant magnetotaxis" gets to this article on magnetotaxis in the migratory ant Pachycondyla marginata:

The influence of geomagnetic field changes on the behavior of ants has been studied in the species Solenopsis invicta (Anderson and Vander Meer, 1993), Formica rufa (Çamlitepe and Stradling, 1995), and Oecophylla smaragdina (Jander and Jander, 1998) ... Another migratory insect species is the ant Pachycondyla marginata, which has very peculiar habits: a diet of living termites and migration in a preferential direction (Leal and Oliveira, 1995). These habits make such a migratory ant very attractive for the study of biomineralized magnetic materials.

From Leal and Oliveira 1995 ref above:

Migration by P. marginata colonies lasted over 2 days and covered distances of
  2-97 m (n=48).

Selections from Acosta-Avalos et al. 2001 Naturwissenschaften:

abstract: Migrations during the dry/cold season are significantly oriented 13 degrees with the magnetic North-South axis, while rainy/hot migrations do not exhibit a preferred direction. This result is discussed considering the hypothesis that P. marginata ants may use the geomagnetic field as an orientation cue for migrations in the dry/cold season.
Given that colonies resume nest relocation late
  in the afternoon of the second day, most of the migratory
  process takes place under darkness conditions.
On  the  other  hand,  nest  relocations  in  the  dry/cold
  season can be considered as typical migrations.
The  use  of  geomagnetic  cues  is  more  commonly  associated with darkness conditions, as reported for mole rats
  (Marhold et al. 1997) and also proposed for bumblebees
  (Chittka  et  al.  1999).  As
  P.  marginata
  ants  start  the
  migratory  process  in  the  afternoon,  they  can  use  any  of
  those  cues  in  their  orientation  during  the  migratory
  journey. However, it is intriguing that they prefer an axis
  around the North–South axis to migrate. The only possible
  cue  to  give  this  information  under  all  conditions  is  the
  one  provided  by  the  geomagnetic  field.


text:
Schiff Base in Enzyme Mechanisms
Can a schiff base stabilize the transition state and form an intermediate as in covalent catalysis with a substrate in the same reaction? Basically I'm wondering if a schiff base creates a ping pong reaction.

I think the answer to this one is a most definite 'yes'.  Almost all aminotransferases proceed via a ping-pong mechanism where a schiff base involving pyridoxal phosphate is an obligate intermediate, and where  the 'half-reation' modified enzyme form has often been isolated. An example is aspartate aminotransferase.
Let's also remind ourselves that a transition state is not an intermediate on the reaction pathway (in the TS bonds are in the process of being broken and formed), but may resemble one.


text:
Can you use a cell in meiosis to create a karyotype?
Why might it be problematic to use a cell undergoing meiosis to create a karyotype?

Yes, you can, but it's way more difficult.
First of all, in order to see meiotic chromosomes, you need to colect young floral bud in the right stage of development (not too young, since you don't want microspore mother cell, and not too old, since you don't want polen), and that's not that easy.
Then, once you found the right stage and made a slide, you need good knowledge on all the phases of meiosis to understand what you are looking at. Bivalents and translocation rings can make it very difficult to really understand the chromosomes set you have in the cell, so you need a good sized sample and a lot of observation and analysis. If the species you are analyzing has small chromosomes, it's even more difficult to understand what you are looking at.


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Hoverfly Identification Wing Resting Position
I've found an interesting insect which I believe to be a hoverfly:

length: approximately 1/2 inch.
However when compared to the Wikipedia poster on Syrphidae or the InsectIdentification.org Hoverfly entry (as well as the flower fly entries) the resting state of the wings differ. In my photographs the wings are resting above the back while hoverflies appear to keep their wings extended.
I know wing position is important in identification, i.e. dragonfly vs damselfly, moth vs butterfly. Does it matter with true flies?

Your geographic location would help in going deeper (if it's any consolation, you do have the family right).  A better size indicator (say, a distance shot) would also help.  If you're in North America, the site bugguide.net should be your next stop; if in Europe, diptera.info is a good place to start (either way, given how many species of hoverflies exist, you will be spoiled for choice).

You're right, that family is large. Though I'm not interested in tracking down the exact species. I want to know if the wing resting position can be a species indicator, or just a matter of the insect's personal preference and time of day of particular photograph. Most of the Syrphidae samples from bugguide.net are shown with open wings, with some exception.

This is indeed a hoverfly. Most if not all hoverflies fold their wings in this position when not flying.

@RHA: that's exactly the answer I'm looking for. If you could write a brief summary detailing certain unimportant aspects of insect identification for two or three common families of insects - i.e. wing resting position, antenna resting position - I think it would be a very useful acceptable answer.


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Why is the outer circle of human mitochondrial DNA ‘heavy’, whereas the inner circle is ‘light’?

Why is the outer circle of human mitochondrial DNA "heavy" whereas the inner circle is "light"?

Because their masses are different: https://en.m.wikipedia.org/wiki/Heavy_strand

The heavy strand is literally heavier than the light strand. The first, or at least one of the first, observations of this phenomenon was in this paper:
Corneo G, Zardi L, Polli E. 1968. Human Mitochondrial DNA. J Mol Biol 36(3):419-423.
They showed that alkaline denatured mitochondrial DNA separates into two bands upon ultracentrifugation in a cesium chloride gradient:

Human mitochondrial DNA when centrifuged in alkaline CsCl in the analytical ultracentrifuge splits into two bands displaying densities of 1.727 g/cm3 and 1.766 g/cm3, respectively. The two bands appearing in the alkaline gradient correspond to the complementary strands of human mitochondrial DNA with a different GT/CA ratio... However, when an equimolar mixture of them is renatured by heating at 65°C for five hours in 2X SSC, a single band with a density very close to that of the native DNA is obtained. The latter experiment clearly indicates that the two bands correspond to the complementary strands displaying a bias in base composition.

The difference in molar mass (M) is due to a higher purine content (Pu) in the heavy strand (which are heavier than pyrimidines). This can be seen by tabulating the base composition of the RefSeq sequence of human mitochondrial DNA:
               A      T      G      C      Pu(%)   M(kDa)
Light Strand   5124   4094   2169   5181   44      5063
Heavy Strand   4094   5124   5181   2169   56      5174

R script if anyone is interested:
#uses Biostrings
light = readDNAStringSet("mtDNA.fasta")
heavy = complement(light)

comp = function(seq) {
  ll = as.list(alphabetFrequency(seq)[1, c("A", "T", "G", "C")])
  ll["%Pu"] = with(ll, (A + G) / (A + T + G + C)) * 100
  ll["M(kDa)"] = with(ll, (A * 313.2) + (T * 304.2) + (G * 329.2) + (C * 289.2) + 79.0) / 1000
  return(ll)
}

comp(light)
comp(heavy)

Do you have actual values? I have googled in vain searching for this

@David I have updated the answer.

Thanks — that improves the answer greatly. Although the "heavy" strand is heavier in terms of molecular mass, it is, of course, worth emphasising that it is the buoyant density of the purines, rather than their mass, that lead to the behaviour that gave rise to the loose nomenclature.


text:
Are genes known or at least conjectured to evolve cyclically ?
I observed recently that some people born the same year in not too distant areas (say, in the same country whose size is not too big, like France) share similar phenotypical features, for example they look like each other though they are not of the same family. If confirmed, this would suggest that some alleles are more common within a given period, and hence that the global evolution of the human genetic pool could be statistically determined. One can go one step further and see the considered genetic pool in a given range as a quantum-like system governed by some kind of Schrodinger's equation. I think here of a theoretical framework like Laurent Nottale's scale relativity that could explain these similarities. Have such questions been considered so far?

Welcome to Biology.SE Sylvain!

I observed recently that some people born the same year in not too distant areas (say, in the same country whose size is not too big, like France) share similar phenotypical features, for example they look like each other though they are not of the same family.

You are likely doing a confirmation or some kind of extended Barnum effect.
You will need to provide a rigorous study for this claim and not just a vague feeling you're having.

If confirmed, [..]

This piece of sentence suggests that you agree with my previous comments. We expect the OP to provide reference for a claim on which the question lies. One cannot ask "Why do elephants have such a huge genome?" without providing an evidence that they do have a huge genome.

[..] this would suggest that some alleles are more common within a given period,

If there is such effect it is much more likely caused by shared environment than by shared genetic. Have a look at this post to understand the underlying sources of phenotypic variance.

and hence that the global evolution of the human genetic pool could be statistically determined.

Sure, it can but this is not a consequence of the above supposed observation nor by the above hypothesis for the supposed observation.
Of course, specific processes could cause some cyclic process in evolution. A population overshooting carrying capacity could go under an oscillatory behaviour around this carrying capacity. As population size affects genetic diversity, such cyclical behaviour can have some impact. However, this is quite negligible. Also, there might be fluctuating selection (typically fluctuating on a seasonal basis) but this tends to be rather negligible for species of long lived individuals. I am sure you can think of some complex mechanism in structured populations would could yield to some oscillatory behaviour as well.

One can go one step further and see the considered genetic pool in a given range as a quantum-like system governed by some kind of Schrodinger's equation. I think here of a theoretical framework like Laurent Nottale's scale relativity that could explain these similarities.

I don't understand that part. I know pretty much nothing in quantum physics (have basic understanding in general relativity but not in Nottale's attempt to merge relativity and quantum physics). You might need to expand your thoughts I guess if you want biologists to understand where you're heading. However based on the above, I suspect, there is no reason to think this cross-talk would matter in any way.

Have such questions been considered so far?

I doubt so, because I don't think any of it makes much sense (no offense).