How do fish tolerate pH changes in water? I want to know how aquatic animals behave as a natural indicator of the acidity in lakes and rivers.

How do they tolerate these pH change?

Often, in terms of a water body becoming acidified, it depends on the rate of acidification.  Fish and other aquatic species, such as invertebrates, are fairly resilient to miniscule changes, but they also have a threshold at which not a lot of them, adapted or no, can survive.

From the U.S. Environmental Protection Agency (http://www.epa.gov/acidrain/effects/surface_water.html):

  Acid rain causes a cascade of effects that harm or kill individual fish, reduce fish population numbers, completely eliminate fish species from a waterbody, and decrease biodiversity.  Low pH [...] is directly toxic to fish. In addition, low pH and increased aluminum levels cause chronic stress that may not kill individual fish, but leads to lower body weight and smaller size and makes fish less able to compete for food and habitat.

  Some types of plants and animals are able to tolerate acidic waters. Others, however, are acid-sensitive and will be lost as the pH declines.

Commonly, benthic invertebrates (including insects, crustacean and molluscs) are used as indicators for ecosystem health.  Invertebrates that need a high amount of calcium, such as crayfish (for their exoskeleton), are typically not found even in slightly acidified lakes.  Other invertebrates can be used as indicator species because they respond to changes in water conditions, such as pH.

A good example of this is the acid rain that occurred in Sudbury, Ontario, Canada as a result of sulfur dioxide emissions from mining activities, which were especially high in the 1970s.  This affected the lakes in the area not only from acid rain, but the runoff as well as there were no trees left.  The pH was so low that it effectively made all lakes in the area sterile. Since then, a lot of effort has been put into bringing back the native aquatic species, such as liming the lakes and restocking them with species such as Brook Trout (Salvelinus fontinalis).  More information can be found here:

http://link.springer.com/article/10.1007%2FBF00160348

Therefore, I do not know that aquatic animals necessarily behave a certain way as a natural indicator of acidity, however it is more of their presence or absence that biologists use to determine acidity and the overall ecosystem health in lakes and rivers.

Commonly, benthic invertebrates are used as indicators for ecosystem health. Invertebrates that need a high amount of calcium, such as crayfish are typically not found even in slightly acidified waters. Other invertebrates can be used for indicator species as they respond to changes in water conditions, such as pH.


Why do red muscle fibres have more mitochondria than white muscle fibre but less ATP than White muscle fibres? This is a question given in my Anatomy book and I am really confused because logically the substance which have more mitochondria should have more ATP as mitochondria is the power house of cell.But the question contrast the logic.

This is because of the difference in mitochondrial protein expression of red and white muscle fibres. There is difference in posttranslational modification, which leads to functional difference as red muscle contraction is slow, and white muscle contraction is rapid.

Metabolic control in mitochondria contributes in speed of activity and cellular energy production. So, these differences effect the cellular energy levels in both white and red muscle fibres.

Following factors also contribute to the ATP production:
White muscle mitochondria have higher proton leak.
Red muscle contain high palmitic acid and oleic acid, but white muscle possess more phosphate ions.
Collagen and elastic fibers are largely distributed in red muscle mitochondria, whereas high titin levels and densely packed sarcomeres are present in white muscles. Whereas high levels of long sarcomeres are present in red muscles.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3118618/

https://www.hindawi.com/journals/bmri/2018/5816875/

MacIntosh, Brian R.; Gardiner, Phillip F.; McComas, Alan J. (2006). Skeletal Muscle: Form and Function. Human Kinetics. ISBN 978-0-7360-4517-9.

[https://en.m.wikipedia.org/wiki/Myocyte?wprov=sfla1 ][1]

[1]: https://en.m.wikipedia.org/wiki/Myocyte?wprov=sfla1

Good question,  I guess that high production could be linked to higher relative consume of ATP which could depend of necessity of energy and ATPase effectivity/ concentration of ATPase.

I suggest you to investigate the reference cited above.


Why spermatogenesis is an independent process while formation of ovum is dependent on fertilization by sperm? At the time of ovulation,secondary oocyte is arrested at Metaphase II and goes into the fallopian tube.If fertilization occurs, sperm binds with secondary oocyte and releases Anaphase promoting factor which leads to completion of meiosis II,ovum is formed and it subsequently gets converted into zygote.
My question is that why formation of ovum is dependent on fertilization by sperm and why formation of sperms is independent process? Has it some benefits for nature?

This can only be answered logically. Imagine bellow paragraph.
If secondary oocyte does not require fertilization for completing 2nd meiotic division then it will become an ootid (female gamete). Once formed lots of hormonal changes occur in female example individual's diet increase, mammary glands differentiate and all necessary changes for pregnancy which will be unnecessary at end of every month.
I hope u understood and comment if u want to ask about above imaginary paragraph.


Could a prolonged amount of Antibiotics severely affect the digestion Gut Microbiota? Could taking antibiotics for a prolonged amount of time severely harm or even worse kill off a large proportion of Gut Microbiota responsible entirely for  digestion, Resulting in lifelong digestion problems similar to Crohn's Disease?

Yes, even if you will not kill ALL the bacteria in your gut, you can mess up your flora pretty badly by using antibiotics for prolonged time.

For how long? It depends from person to person, from antibiotic to antibiotic.

Similar to Crohn's disease? Some symptoms like abdominal pain, diarrhoea and weight loss can occur in case of messed-up flora like in Crohn's disease (and many other diseases!).

Yes. killing the normal flora of the colon will give chance to harmful bacteria to thrive and cause disease. One of the most common diseases that are a result of antibiotic use is Clostridium difficile infection. This disease is caused by a toxin releasing bacteria that can form spores. Antibiotics are ineffective agains spores, which is why this disease is hard to treat.


I see various exposure limits for carbon monoxide, but what about one breath? I see exposure limits for carbon monoxide like 50 ppm over 8 hours. This would correspond to a total inspired volume of carbon monoxide on the order of a few hundred milliliters. This exposure is supposed to be far from fatal, but I'm unsure how to think about extrapolating long term exposure limits to acute limits, thus my questions:

What are the likely consequences if I breathed in the entire 200 ml of CO in a single breath, or even an entire lungful of pure CO?
If the answers to the above end up being "you would die", is there a reasonable way to estimate the maximum volume you could acutely breath in?

"In any high level CO environment, your exhaled breath CO level will gradually rise but remain lower than the ambient level because you always absorb some of the CO you inhale as long as the level in air is higher than the level in your blood.  As soon as you stop smoking or move to a lower CO environment, you start exhaling."

So I suspect a lungful of pure CO would indeed make you feel awful, but since that wouldn't be nearly enough to replace all the oxygen bound to your haemoglobin, I imagine it wouldn't be fatal in a healthy individual, especially if you were breathing air free of CO after that one lungful.

Apparently it takes 5 hours to eliminate half of your blood CO also.


Why would a mother reject her offspring if it has been "interfered" with by humans? There was a recent incident at Yellowstone National Park in which tourists placed a bison calf in their vehicle, and that eventually led to the calf being euthanized.

The National Park Service issued a statement in which they said:

  In addition, interference by people can cause mothers to reject their offspring. In this case, park rangers tried repeatedly to reunite the newborn bison calf with the herd. These efforts failed.

Why would a mother reject her offspring if it has been "interfered" with by humans?

Several ungulates and other species such as seals and primates are known to initially use odour to discriminate their offspring. Most relevant work to study this has been done in sheep; sheep are ideal for studying attachment because there are ethical and logistic difficulties that limit laboratory and research use of most other species known to develop selective mother-young social relationships. In addition domestic sheep are common worldwide, easily bred and handled, and well-understood in terms of behavior and natural history, providing a solid base for more intricate study (more information here).

According to this paper ewes are attracted to amniotic fluid for a few hours after birth, which stimulates nuzzling, sniffling and licking behaviour; after a relatively short time she becomes familiar with the lamb's unique odour. Thereafter, lambs without this odour are almost always rejected. After some time the ewes learn to use visual and auditory cues to identify their lambs and smell becomes less important. The Wikipedia article on the subject gives some information about the neurobiology of the process.

From a selective advantage point of view, I would speculate that this would evolve to reduce the risk of being exploited by 'free-loader' genotypes that engage in behaviour similar to brood parasitism in birds (i.e. leaving their offspring to be cared for by other ewes).

This can work both ways; in addition to the risk of disrupting the smell of a lamb by excessive handling, shepherds have recognised for centuries that lambs which are rejected by their own ewe, or whose ewe has an inadequate milk supply, can be fostered by other ewes who have lost lambs using a technique historically called skin-grafting, where a dead lamb is skinned and the skin tied around the foster lamb. The odour is thus transferred to the foster lamb for long enough for the ewe to accept it and become familiar with its visual and auditory identifiers, after which the odour is no longer important. The paper I cited above above describes a study that found that cloth 'stockinettes' could be used in place of a skin to achieve the same outcome.

edit: Interestingly, the responses to this question at skeptics.SE suggest that the popular notion that odour-based attachment results in abandonment following human interference with birds is probably untrue.

Actually, once humans or any other animal touches the infant, especially before the mother has recognized it as its own, the scent of the "foreigner" stays on the infant/offspring. Thus, the mother does not recognize the infant or believes it to be "tainted". This is true for a lot of birds as well as wild animals. If anyone "disturbs" the bond- forming during parental care of the newborn, the newborn is often abandoned by the parents.


Fetal development, gastrulation and embryonic disc I am completely confused by the images circulating on the internet of human gastrulation.

First, lets see how it happens in deuterostomes. This image depicts the process:

(image is from Wikipedia)

From here we can conclude that blastula becomes gastrula when some of the ectoderm beecomes endoderm, the place where it goes inside becomes anus and then mesoderm is formed.

Ectoderm here is the outermost level and gastrula already has anus.

However, in this image of human gastrulatuion we see completely different things:

(image source)

The mesoderm here is the outermost layer, ectoderm is inside and the gut cavity is formed by the separation of a part of the yolk sac. There is no anus and the posterior end of the gut is blind. Also other similar images suggest that a twins may be separated already after the mesoderm was formed (thus uniplacental twins).

The lack of agreement between the images disturbs me.

Just to point out some of the differences in the depicted processes:

In first image mesoderm forms after gastrulation, on the second it forms far before gastrulation
In the first image anus forms in the process of gastrulation, in the second image anus remains blind
In the first image ectoderm is the outermost layer, while in the second picture mesodem is the outermost level that encloses all, including ectoderm.

Human embryogenesis is much more complicated than the more general and simplified picture given in your 1st figure.
For details, please study http://en.wikipedia.org/wiki/Human_embryogenesis

To point out the most distinctive features which might have led to your confusion:

Before gastrulation, the blastocyst cavity is formed.
Only the inner cell mass undergoes gastrulation.
Mesoderm forms quiet late and spreads, thereby also forming the chorion as well as the amnion.
The embryo itself is formed from a subset of all embryogenetic cells. This is shown in your 2nd figure, part C and D. Yet, tissues are still going to spread such that the final ectoderm as well as mouth and anus will be formed.

The Wikipedia protostome vs. deuterostome figure depicts a "prototype" deuterostome, such as an echinoderm or an amphibian.
In amniotes (reptiles and their descendants - birds and mammals), the giant amniotic egg full of yolk led to profound changes in early embryogenesis, including the disappearance of the true blastopore. (Its analogue as organizer of gastrulation is the Hensen's node, but it is dorsal and does not form the anus.) Placental mammals have secondarily lost the amniotic egg, but a substantial part of their gastrulation movements still reflect its former presence.
Although in us the blastopore does not form the anus and does not even exist, we are still classified as deuterostomes because of our clear kinship with amphibians.


Isotretinoin and retinoid receptors in brain confusion? I am considering starting a treatment with Accutane(Isotretinoin), however I am not sure about what the effects on the brain are. Here are two studies that contradict each other:

http://www.ncbi.nlm.nih.gov/pubmed/11696672
The first one states that using an antagonist, they increased the rats' working memory. So logically, using the agonist (isotretinoin), it would cause a loss of working memory?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3360864/
Here they state that not only did isotretinoin not have negative effects, but it actually had positive effects.

I am more inclined to believe that it has negative effects, because most anecdotal evidence says that it makes patients feel "foggy" and "forgetful". Can anyone please enlighten me? What exacly does this stuff do to the brain and is it irreversible?

The second study did not even examine the pharmacological effects the drug had on the brain. The researchers noted depression scores tended to increase while on the drug, but not in significantly significant way. Keep in mind the drug is clearing a disfiguring condition, so this novelty may interfere with the ability for measures to detect psychiatric issues.


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

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


Can one die from pain? Is it possible that a human or any other creature can die from pain?

I googled and found different answers. Some articles say Yes while others say No.

I very much doubt it. You may however die from whatever's causing the pain. The reason you feel pain is so you stop doing whatever is causing the pain. Hence someone knows not to touch a hot fire because it is painful. But the pain itself is not actually the danger - it's the fire burning away skin. So pain is actually a good thing, a survival mechanism. So for something that is meant to prevent death it's hard to imagine it doing the opposite.

Perhaps if you were in SO much pain you may be unable to breath and paralysed - but even then I still think you'd go unconscious before that would happen, and you'd start breathing again, etc.

The only other thing I can imagine is having a cardiac event, and the heart stopping. Again, this would be because of stress. Other than that - you may commit suicide on account of insufferable pain, however it's a different situation.

However pain never comes on its own for no reason, just like smoke needs a fire. In this case it's the fire - not the smoke, that will kill you!

People who've ever been in a desperate or life threatening situation like a car accident, have often walked on a broken leg for example - feeling no pain. In this case the body was giving them a chance to escape what might have been a lion, etc.

In short, no - I don't think you can. However I cannot give a 100% correct answer. It would take just one example to prove that however!

I refer the honorable gentlemen to James Harriet. He reports discovering by accident by ending the pain he was in some cases able to reverse the pathology by ending the pain with anesthetic drugs, thus allowing the body's natural healing abilities to take over.

He first discovered it in a sheep by accident (insufficient dose to put it down) and later used it effectively on dogs.


Are Richard Lynn's estimates of African IQ inherently innacurate on the basis that most Africans aren't mentally retarded? I've been looking at Richard Lynn's studies on average African IQ, and he seems to estimate really low IQs in the 60s range (e.g. http://www.sciencedirect.com/science/article/pii/S0160289609001275?via%3Dihub).

However, is this inherently wrong, as somebody who would score that low in a Western country would no doubt be mentally retarded (and this isn't the case for most African people)?

IQ is just a measure of how good you are at taking IQ tests, that's it. Those tests are usually culturally biased towards middle income first world citizens (among other things). Think of it this way, questions about mortgages, supermarkets, airplanes, or such thing presuppose the person being questions knows a reasonable amount about those things, this is not a reasonable assumption in many places around the world.

The classic "a train leave chicago at 10:00..." is a perfect example since the reader needs to know what a trains is, that chicago is a place, and what 10:00 means additionally they need to be familiar with reading exact measures of time and velocity, that they have already been taught basic math, are familiar with abstract questions, and that they are experienced readers, these are all fine assumptions for the New York suburbs but pretty bad ones for sub saharan subsistence farmers.

People who try to write the questions for said cultures often run into the reverse problem, we think of travels as a steady rate but to people who travel by boat know allowances need to be given for things like the speed the stream is moving, or the paddler taking breaks for lunch, information the writer may wrongfully assume or not understand. I recall a question about two people traveling along the same road that was consistently wrong because people in that culture thought is was proper for the faster person to slow down to match the slower for the safety of both (the norm in said society) so they constantly calculated their speed as the same, something the writers never anticipated.

There are millions of these differences across cultures and these cultural differences quickly snowball in to large differences when taking identical tests. So you are not seeing a real difference in intelligence just an artifact of culturally biased testing.

How do you define being "mentally retarded"? In order to minimize the difference in measured IQ that might be due to people growing up under different circumstances in different cultures you could try to measure how people with different ethnic backgrounds achieve in a multicultural society. Citation from a paper regarding school results in Florida, USA:

  The number of ill-prepared students in Florida remains troubling, as
  do the differences by race and ethnicity: 38 percent of black students
  currently read at grade level. That compares with 53 percent of
  Hispanics, 69 percent of whites and 76 percent of Asians.

http://www.maswired.com/florida-lowers-standards-for-latino-black-students/

Obviously being able to read at some level does not have to correlate with IQ in a simple fashion and people in Florida who are reported to be "white" or "black" might have a mixed ethic background. I do not know if any large scale investigations trying to link IQ with ethnic background in countries such as the USA are done, as the subject might be deemed as controversial. If there are differences in school results, SAT-scores etc. that might at least give you a hint of how large the differences between different ethnic groups might be.


What's the explanation for those shivers/shudders that happen at random times? They happen at any time, presenting as a sudden urge to shiver/shudder all at once. It originates in the neck and shoulders, feels like instant gooosebumps then out of total reflex shoulders roll back and neck cringes. Happens every couple of months and comes out of nowhere, then gone without a trace.

I have read about myoclonic jerks but this doesn't sound the same.

Where do these impulses come from and what's the physiological explanation?

It is just like a muscle spasm but generated from your nervous system. If the problem persist you are lacking in a certain vitamin that your body needs to function correctly.


How can I make sure my UV-purificator kills bacteria? I'm going to show a UV-purificator for water on science fair. How can I easily check if purificator kills most of the bacteria? I need a quick and possibly easy method.

Not having the equipment needed to actually count bacteria, you can use things you know bacteria does to find out how much they were affected.

My approach would be thus:

Select a model bacteria. There are a few candidates, but probably the most readily available is lactobacilli, which can be found in yogurt and (loosely translating terms of art) is a Gram-stainable fermentor-sometimes-breather.
Infect the water with a known quantity of bacteria and a food source (lactobacilli eat lactose - ie from milk) and equally divide it into a control and experimental group...
You'll need to find an alternative way to estimate the bacterial content in the volume of water used compared to a control colony. Since lactobacilli produce lactic acid, you could use the pH value of the water (either with an indicator or a meter) to detect bacterial metabolism, compare that to the control's pH value.
Record the UV exposure time from the experimental group, and isolate the control group from any potential UV light source, such as the sun.

Even if you find that, for example, your particular strain of lactobacilli is not sensitive to your UV light source, that's a perfectly scientific result! How did you obtain it? The source likely knows what kind of bacteria it is. Perhaps the UV light merely interferes with bacterial metabolism, and doesn't kill it. Unanswered questions are wonderful, you may have provided a place for further research to take place. You could then use the two groups to infect a food source (ie milk) and compare post-exposure growth, depending on how much time is available.

The medical field uses Limulus Amebocyte Lysate (LAL) strip technology for parentarel pharmaceutical and medical devises. The LAL strip will detect PAMPS,Bacterial endotoxins and substances with elicit inflammatory responses in mammals.
The technology derived from the special blood of the Horseshoe crab AKA "The Living Fossil" it lived as we see it today without evolving 450 million years ago.

http://service.hkpc.org/bme2008/CPD_Activities/Powerpoint_LAL.pdf>


What is the minimum caloric intake for a truly starving adult What is the minimum caloric intake for an adult?  I'm not talking about a healthy diet.  There's plenty of advice on that.  I'm wondering what the absolute limits of H. sapiens are.  When there's a multi-year famine, and the body is willing to shut down as much of its capacity as possible without actually failing to function for years at a time, how much energy is it consuming?

I know the Basal Metabolic Rate is a key factor to this, but the numbers I have seen for it are all "healthy" BMRs.  I'm interested in the unhealthy numbers.  For example, I'd consider maintenance of temperature optional for these circumstances (assume we have a temperate enough climate), and I presume heart rate and breathing will go down, decreasing those loads.  Obviously there's limits as to how many environmental constraints can be addressed (if I knew what environments this was studied in, I'd likely know which studies to look for!).  And obviously not everyone is the same, but that's an issue in every human study ever completed.

A better example is the stories of tibetan monks who wrote accounts of their experience to survive for months or years on faith alone, and watch their hair and nails fall out in the search for wisdom. they could tell you how fast a coma arrives from eating just 300 calories per day.

There isn't a minimum amount though, because it's all subjective for time until, temperature, survival chores, time until coma, time until difficulty moving... you can probably keep someone in an emaciated coma with intravenous injections, or someone could stay awake with high exposure risk to illness, hair loss, nail loss. The question is vague, and there are 100 scientific studies about calorie restriction, so you are hoping someone will read 10-20 pages until they find some information for you.

It also depends how many watts the human needs to use in that situation to stay alive.

In 30'C you probably need 30 watts to stay warm, and 20 degrees about 60 watts, so the value can double based on temperature, you must change your question a bit.

60 watts basal metabolic rate body temperature would use 70 calories per hour, about a slice of bread, so 1400 calories per day without bedcovers. It depends a lot on ambient temperature and exercise, for example 1 mile of walking uses 100 calories. At less than 1000 calories per day, exercise becomes difficult and the person gets thin. Jogging uses about 250 watts. Extreme athletes and triathletes peak at about 650 watts for sprinting.

There are 100ds of citations on caloric defficiency and restriction, with values around 350 - 700 per day, which change metabolism considerably:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3014770/

https://www.ncbi.nlm.nih.gov/pubmed/2718912


How many molecules NADH are produced in the Krebs Cycle? I don't know which source i'm going to follow.

Some say its 3 molecules NADH per cycle → 2 cycles × (3 NADH) = 6 NADH

Some say its 4 molecules NADH per cycle instead?

This is slightly depending on which reaction you want to include into the cycle. I count four:

One when Pyruvate is converted to Acetyl-CoA,
one when Isocitrate is converted to α-Ketoglutarate,
one for the reaction of α-Ketoglutarate to Succinyl-CoA and
finally one for the reaction of Malate to Oxaloacetate.

If you see the reaction of Pyruvate as happening outside of the cycle, it's only the later three.
See this image (from here) for an overview:

The alpha-ketoglutaric dehydrogenation to form Co~A.The NADH energy is released.Therefore 6 molecules of NADH is produced
You can see the above picture to understand better.


Why don't vegetables taste good despite being healthful? This is more a question about the evolution of taste than about the chemical composition of vegetables. Why don't vegetables taste good despite being healthful?

We are evolved to survive starvation, and live to be perhaps 35. So fatty foods with lots of calories taste good to us. Our genes (and preferences) lag thousands of years behind our present environment.

Because your primary school cafeteria used to serve canned vegetables, you've hated vegetables ever since, and you haven't tasted them cooked properly yet.

To make vegetables taste good, one thing you can do is going to your local farmers market, buying whatever looks appealing to you and asking the farmer for suggestions on how to cook it.


What is the name of this bird? Does anyone know the name of the bird in the pictures? It was found in the south of Spain in the month of June. (it is certainly neither a house sparrow nor a swallow nor a robin). Thanks for the help!

Thats a difficult one but my gut feeling is a 'bunting' and maybe a Rock Bunting juv ? - the bill is definitely bunting-like and there does seem to be a black and white eye stripe going on . There arent that many buntings in the south of Spain especially with a very warm brown colouring


ID for red millipede swarm near my place Location:Hyderabad,South India.
These worms usually come out when it rains,these worms are the most common ones any help in figuring out them,they come in groups too.

Based on the body structure and double pair of legs per body segment, this is a millipede.

Based on the small size and spacing between body segments, it could possibly be in the Paradoxosomatidae family. You could check by examining the specimen more closely:

  Most species possess a groove or furrow ("sulcus") on the dorsal surface between the keels (paranota) on each segment.

National Geographic ran a story/video on swarming Paradoxosomatidae in Senegal in 2017:

  Some species swarm together during mating season or to hunt for food, and some studies have theorized juveniles swarm together for protection from predators.

Bellairs et al. (1983)1 studied a similar swarming species of millipede in India:

  The adults of Streptogonopus phipsoni (Pocock), an Indian polydesmoid millipede, emerge from the soil at the onset of the monsoon and mate. Eggs are laid in the soil and the adults die. The larvae leave the soil at stadium III and, apart from moulting periods, remain on the surface until the end of the monsoon. The larvae are aggregated in swarms, usually consisting of several hundred individuals. They are active on open ground, including metalled roads, during daylight, but usually spend the night in an inactive state under cover of stones or vegetation. If a swarm is disturbed, the individuals scatter but later reaggregate.

 Source: Bellairs et al. (1983)

I couldn't find any additional reputable (or really much of any) detail about S. phipsoni in English sources online. So I think I'll leave you with this information for you to explore in your native language more closely.

Though, Bellairs et al. cite Hoffman (1980) 2 and Attens (1937) 3 as their identification sources.
Also, Golovatch & Wesener (2016)4 provide a relatively up-to-date species checklist of the millipedes of India, so I'm certain that reference would be a good place to continue learning more.

 Citations:

1  Bellairs, V., Bellairs, R. and Goel, S., 1983. Studies on an Indian polydesmoid millipede Streptogonopus phipsoni Life cycle and swarming behaviour of the larvae. Journal of Zoology, 199(1):31-50.

2  Hoffman, R. L. (1980). Classification of the Diplopoda. Geneve:  Musee d’Histoire  Naturelle

3  Attems, C. (1937). Myriapoda 3. Polydesmoidea 1 Fam. Strongylosomidae. Tierreich 12:1-300.

4  Golovatch, S.I. and Wesener, T., 2016. A species checklist of the millipedes (Myriapoda, Diplopoda) of India. Zootaxa, 4129(1):1-75.

Streptogonopus phipsoni, probably IV or V stadium.

For reference, see: Bhakat, S. (1987) and other


Identify orange-brown, teardrop-shaped insect in central Europe that was found indoors TL;DR Can someone identify the species of the insect in below picture? Editing of the wording of this question (if possible) to make it easier to find by using search engines is welcome.
I caught this insect and was wondering what species it was:

Here a milimeter-scale and an USB-plug next to it to allow to estimate the size (sorry that they are so unsharp but I hope it is sufficient to get the size):

I was not able to find it by reverse image search or by searching for some keywords using google. I also checked some questions here but did not find any that seems to be about such an insect.
Following description/keywords are added to help someone searching for such an insect to find this using word-search. If someone can formulate this more search-engine-friendly to make this more likely to be found, please edit or add a comment so I can edit it:

Teardrop-shaped
six legs / 6 legs
two antennas / 2 antennas
orange-brown / brown-orange
size about 3mm / 3 millimeters / 0.11811 in / 0.11811 inches (I hope my calculation from mm to in is correct)
if touched by glas or paper, it remained motionless for about 1 to 2 minutes
no wings / not airbourne / walking
able to walk up walls
it was found indoors
the region is central Europe

Many Thanks in Advance.

I think it may have been a tick of some kind, one that had already fed and was round (hungry ticks are sort of flat).  I couldn't say exactly what species.
I'm not sure, but that's the only thing I can think of that matches this photo.  I'm no professional, so another person here may be able to do better.
Ticks have eight legs (they're vaguely related to mites, and, even more distantly, to spiders), so I was puzzled at first by you saying it had six legs, but possibly what you thought were its antennae were its other pair of legs?  (Ticks have no antennae).
https://en.wikipedia.org/wiki/Tick


What is the X-chromosome responsible for? I understand that the X-chromosome is responsible for certain disorders, like red-green colorblindness; but besides disorders, what do the genes on the X-chromosome determine?

Here is the list! There are about 900 protein coding genes and about 500 non-coding transcribed sequences. It is not going to be feasible to explain you the function of every single one of those genes. Your question is hence too broad.

You will find here on wikipedia a small subset of those ~900 genes.

If your question was

  Are all genes that are on the X chromosome related to sex?

Then, the answer is "no". Most of them have nothing to do with gender specific traits.

I would like to start the answer by mentioning that I was fortunate to attend a lecture by Jenny Graves, a scientist working on X chromosomes recently.
In her lecture she mentioned the genes on X-chromosomes as "brain and balls" genes. As Remi.b has already added a list you can go through it to find a few of these genes. I am highlighting a few of them as follows:-

Androgen receptor (AR) - Required for prostrate formation in males. Mutations may lead to muscular degeneration and loss of motor control (Kennedy's syndrome).
AIFM1 - An inhibitor of apoptosis. Mutations may lead to neurodegenerative conditions like Charcot-Marie-Tooth disease 4.
MeCP2 - Heterozygous female MeCP2 mutants suffer from Rett Syndrome. It is almost exclusively seen in females because male mutant embryos die during pregnancy.
BEX1, BEX2 and BEX4 - Brain-expressed X-linked (BEX) proteins

Also regarding sex determination - the mammalian XY sex determination is Y centered i.e. the SRY gene on the Y chromosome is the gene responsible for determining maleness. Interestingly some species not using the XY system have evolved female specific sex determination genes. I will add relevant citations when I have time.


Where does the mass come from when you grow plants in water? How do plants like green onions seem to grow forever when put in jar of water?  I understand that plants get a lot of their carbon from the air (as per this question) but surely they need more than just carbon to grow new leaves.

The answer in the linked question mentions that plants in general get their mass from sources like water and nutrients like nitrogen and phosphorous, and ions.

However, if a plant is growing directly in [distilled] water where will it get those nutrients (like phosphorous and the ions) from?

Where does that extra mass come from?

Short answer
Plants with storage compartments can grow for extended periods on water alone.

Background
It indeed seems the question is indeed different from the suspected dupe after all.

According to Turesson (2014)

  Seeds, tubers and roots are the most common sites for [...] energy storage and the forms in which energy is stored are predominantly oil, starch and sugars. Underground storage organs mainly store starch and sugars, while seeds from different plant varieties accumulate high levels of starch and also oils and proteins.

So storage compounds like "seeds, tubers and roots" can sustain prolonged growth in the absence of pretty much anything, except water; just consider the familiar seedlings of cress on cotton wool (Fig. 1). There's basically nothing there, just water.

Fig. 1. Cress grown on cotton wool and water. source:Dreamstime

Reference
 - Turesson,  Carbon Allocation in Underground Storage Organs, Doctoral Doctoral Thesis (2014), Swedish University of Agricultural Sciences
Alnarp

The most common elements in organic chemistry are carbon, hydrogen, oxygen, nitrogen, sulfur, and phosphorus.

Water provides hydrogen and oxygen; air (on Earth) provides oxygen, carbon (mostly CO2), and nitrogen. This leaves out only sulfur and phosphorus.

Therefore, any plant that needs only trace amounts of sulfur and phosphorus (or already comes with all that it needs) could grow reasonably on air, water, and light. Bear in mind that another limiting factor is trace amounts of magnesium in chlorophyll which can't be replenished on air and water.


Are there any drawbacks to having a fixed-Köhler microscope? I am considering to buy the Zeiss Primo star microscope. There are two variants: one with so called "Full Köhler" illumination and one with "Fixed-Köhler" illumination. Are there any drawbacks to having it fixed? When I would not want to have Köhler illumination?

IMHO: there's hardly any reason why you should't use Köhler illumination. It's the method of choice to achieve bright and even illumination, in the entire FOV, permitting max. resolution. In a well designed system.
Köhler has only one drawback: often it turns out to be impossible to achieve even illumination at low power in the entire FOV. Usually, but not aways, the manufacturer has made provisions to achieve propper illumination at low power at the condenser level.
Allow me to add that I'm not a fan of the Primostar stand, which is a microscope build on order for Zeiss, probably by Meji.
Compared to the older Black, grey and white Zeiss Standard stands, it's a toy...


Umbrella term for "parts of the brain" I am looking for an umbrella term for general "parts of the brain", esp. for (somehow arbitrary) "subsets of neurons".

For the tree of life there is an umbrella term for all kinds of taxonomic groups all down the tree. They are called taxa.

Domains, kingdoms, phylums all down to families, genus, and species are taxa:

In brain sciences there seems to be no such umbrella term which is generally agreed upon.

Which term would best include all of the following?

brain hemispheres
coarse brain subdivisions (cerebellum, cerebrum, ...)
cerebral lobes (frontal, parietal, ...)
the thalamus („a large mass of gray matter“)
nuclei (thalamic, ...)
Brodman areas
cortical layers
cortical columns
the limbic system
regions of interest (in fMRI)

All of these immediate suggestions don't fit perfectly:

(brain) region
(brain) division
(brain) area
(brain) volume
(neural) group
(functional) system

When you just want to list the components of the brain, that is to say what the brain consists of from the gross anatomy perspective, you can say that the main parts of the brain are:

cerebrum
cerebellum
brainstem

You can also say that the parts of the brain are some smaller, but anatomically well defined components, such as the pineal gland and pituitary gland.

When you intend to describe the functions of anatomically well defined brain areas, you can say that the brain structures are cerebral lobes, thalamus, hypothalamus, hypocampus, amygdala, putamen, corpus callosum, cyngulate gyrus, etc.

A part is "a portion or division of a whole that is separate or distinct; piece. A structure is "mode of building, construction, or organization; arrangement of parts, elements, or constituents." So, it's not about what "it is," but about how you look at it. A thalamus is a part of brain and is a structure made of several nuclei...

You can see these terms used very differently in various texts, but a short overview of brain anatomy by Mayfield clinic use them in the same way as I did. These terms are not a part of any official classification in neurology.

Gerstner et al. in their splendid book Neuronal Dynamics use the term neuronal populations as a synonym for "groups of neurons", e.g. in chapter 12:


Is it possible to use virus for genetic modification of embryos during the fetus stage I know this probably sounds rather hypothetical and not very feasible but I would very like an answer telling why it is possible or not possible and why.

With the advancement of crispr and other dna technologies, I have been wondering whether it is possible for us to use a virus, which would easily pass through the gaps of the placenta and infect the developing fetus to alter its genomic materials for the creation of designer babies. Since Zika can alter the genome of a baby to cause deformities, is something opposite also possible, like using a similar virus to develop favourable genes in a fetus.

Also, what are the chances of the virus actually purposely acting under orders of genetic engineering to intentionally deliver the genes through transduction?

Putting all ethical and moral issues aside is such a principle feasible and if no, why not?

Zika doesn't alter the host genome at all.

  Since Zika can alter the genome of a baby to cause deformities

Zika virus is incapable of altering the host genome. The exact mechanism by which Zika virus infection causes microcephaly is still unclear, but basically it depletes the neural stem cells at a point when the brain is developing, meaning brain development is more limited (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5516183/).

Some viruses do alter the host genome and are candidate technologies for gene therapy

Retroviruses are RNA viruses that copy their genetic material into DNA which is then integrated into a host genome. As such, and as you note, this can potentially be exploited to deliver new genetic material into an organism's genome. I'm not sure what you meant by transduction above, but the term is 'retroviral vector-mediated gene delivery'.

Retroviruses have been trialled for gene therapy for decades. See this sad report on a 2002 trial that apparently succeeded but had unexpected side effects here. However, CRISPR is probably an easier method to use.

You wouldn't attempt to modify a fetus

Some terminology here: a fetus is what an embryo grows into; it's getting bigger and more complex. And as illustrated by Zika-related microcephaly, any messing about with fetal development can have nasty side effects. There are also more cells to modify and you're likely to end up with a 'mosaic' where some cells are genetically different to others within the same organism. If you're attempting to modify the somatic cells of one organ, you might as well do it after the baby is born; if you're attempting to modify every cell in a human (including germ line cells) you'd do it to an egg or embryo.

This study describes a successful attempt to modify embryos using CRISPR. They saw only 1 mosaic in 58 embryos.

First of all, disclaimer: We do not know the effects of every gene in the human genome. The human genome has only 1.2% of its genes that actually seem to be useful. However, the 98.8% of "junk" DNA may have uses that we don't know about. Also, many genes, such as sickle cell anemia, carry unknown benefits, such as offering resistance to malaria. Now, to answer your question...

Viruses

Viruses are probably some of the coolest things on the planet. They infect other organisms, which is a hard task to accomplish. According to Khan Academy they use two cycles.

The lytic cycle: The phage infects a bacterium, hijacks the bacterium to make lots of phages, and then kills the cell by making it explode (lyse).
The lysogenic cycle: The phage infects a bacterium and inserts its DNA into the bacterial chromosome, allowing the phage DNA (now called a prophage) to be copied and passed on along with the cell's own DNA.

Some viruses only use one type of cycle, the lytic cycle. However, you could use a virus with the lysogenic cycle to insert DNA into the target embryo, which could potentially accomplish your goal.


What is this hairy, striped orange-black caterpillar? There are so many these hairy, striped orange-black caterpillars in my backyard.

What are these caterpillars? Are these dangerous?

It's a woolly bear caterpillar which will later grow to become Isabella tiger moth.


Have there been studies done to test Immortality of cancer cells in culture? This website on cultured cancer cells () says cancer cells may be immortal.

I am wondering if there has been any research done to find if cancer cells are really immortal.

How old is the still maintained living oldest culture of cancer cells?
Has there been any research done on replicative senescence of Cancer Cells invitro?

Edit 1:

If there is some data relating to the number of replications the cells have undergone, it will be very useful

The HeLa cell line is undoubtedly the most used and investigated human  immortal tumor cell line. Extracted from a cervical tumor from Henrietta Lacks in 1951 at Johns Hopkins hospital, Baltimore, MD these cells proved immortal and are still used in many, many labs worldwide today. It is the oldest human cell line in use and, therefore, the oldest human tumor cell line (Callaway, 2013).

In terms of senescence of immortal cells; HeLa cells are immortal, and hence do not grow old as such. However, they are subject to mutations and the genetic profile of HeLa cells does change over time. Hence, although they may not be growing old, they do age in the sense that mutations are accumulating in continuous cell lines.

References
Callaway, Nature (2013); 500: 132-3

Terminology involved makes everything lie a bit.

All the "immortality" and so complicate things a bit. We perceive life as life of our individual bodies. Thus if our body is immortal, that means that it is persistent, without us bothering about our individual cells.

But, there isn't any distinction like that in single cell organisms where cells themselves are taken as "individuals". When cell divide, there isn't usually any distinction of which one is "mother" and which one is "daughter". Both new cells are usually the same. So either it may seem that cells are immortal because they are not dying by old age, or that we define new cells as new individuals and thus the old one died to give birth of two new ones.

But we could take certain aspect of this viewpoint on multicellular organisms as well. Our bodies are defacto created by very old cell-line (or in sexually engaged organism, two cell lines) and then this cell-line created vehicle for itself. From this viewpoint, which is not very different from viewpoint taken when speaking about these laboratory cell-lines, whole life is single cell-line. And from this point of view, life itself is immortal.

So the whole problem is that our point of view, on which we define immortality and individuals, is made only for special types of organism, as has no sense when speaking about single cell organisms. Immortality of cancer cells is thus only buzzword.


Microorganisms in Louis Pasteur's experiment of beans Louis Pasteur's experiment proves that microorganisms do not grow from non-living matter, he discovered that microbes can cause food spoilage.
So, where do microorganisms come from? Do they come from the environment?

So, where do microorganisms come from? Do they come from the environment?

Yes!

There is no spontaneous generations. Microorganisms (virus, bacteria, unicellular eukaryote, small multicellular eukaryotes) just like macroorganisms (big-enough to be seen by the naked eye multicellular eukaryotes) are not recreated out of nothing. Abiogenesis happened a long time ago and as far as we know, it is not happening today.

This means that if there is a micro-organism somewhere, it must have come from the environment. It did not pop up out of nowhere.

That is the biggest question to be answered in biology, as of today we do not know where microorganisms originated from. What is known is that they outnumber us by combined weight and population. There are some interesting theories of their origin, one is called "panspermia" which proposes that life might have seeded the Earth from other planets. And considering that some bacteria are capable of surviving extreme levels of radiation        (D. radiodurans), it is not unreasonable to think they could have achieved interplanetary travel via space rocks.


What kind of tree could this be? This may be a strange question, but does anyone know what kind of tree this could be?

I know, it's just a comic, but these trees, at “walking distance” within that comic are easily identifiable as Grandidier's Baobabs:

(That might indicate, of course, that the above tree also occurs on Madagascar, but it's a comic, so all bets are off.  And yes, we know, there are no squirrels on Madagascar.)

It reminds me of the smooth-barked Australian gum trees / eucalyptus, like a salmon gum, ghost gum, etc.

Although there are no squirrels in Australia :)

This photo of a Salmon Gum is from http://www.fpc.wa.gov.au/content_migration/plantations/species/arid/salmon_gum.aspx

It looks like a pine to me. Might be close to Pinus pinaster but take into account that
a) I'm not a botanist.
b) I'm only familiar with pines that grow in my area (Catalonia).


How do developing neurons become tuned to fire only on receiving specific inputs? Research has uncovered neurons that seem to "listen" for specific inputs and fire only when these inputs are received. For example, neurons in the visual cortex may fire at a higher rate when visual stimuli of a particular orientation is presented, and may not fire for stimuli of other orientations.

Are there any good models on how neurons develop this tuning for specific inputs? Could anyone provide links to good papers or other resources?

The only "good model" I know of is hebbian plasticity* or hebbian theory, here's a link: https://en.wikipedia.org/wiki/Hebbian_theory

Usually what we mean by neurons "listen for" or are "tuned for" or even "like" a particular stimulus is that spiking activity in those neurons is significantly increased (or decreased) in the presence of that stimulus as compared to equal amount of time in the absence of it.

*Plasticity refers to the capacity of the brain to change both the strength of connection as well as number and configuration of connections.


Why do meristematic cells have prominent nuclei and dense cytoplasm? I've been reading about meristematic cells having prominent nuclei and dense cytoplasm. However, I could not understand why it is that way. Could somebody please explain?

Because meristamatic cells are the ones who are undergoing mitosis to increase the height of the plant, and diameter of the plant . They undergo continuous division. So y hey don't mature. They only form the primary cell wall.
I wrote another a answer.  Perhaps this will answer the question


Why is the start of my coding sequence ATG and not TAC? I am engineering a set of genetic sequences and have come across a surprisingly basic point of confusion that seems to have fallen through the cracks regarding coding sequences.
The standard start codon is AUG, and since this is an RNA sequence, I would thus expect that the start of the coding sequence would then be TAC, since DNA is complementary to the mRNA transcript taken from it. Wikipedia and various introductory texts confirm this expectation, e.g., in wikipedia's article on the central dogma:

The ribosome reads the mRNA triplet codons, usually beginning with an AUG

Here's another example: in the Khan academy introduction to the genetic code, the codon illustration clearly shows an AUG in the mRNA sequence.
The coding sequences that I am composing into my design, however, are all listed as starting with ATG, rather than TAC, which would be the complement of AUG. I am certain the coding sequences are not wrong, since some are very well established parts like BBa_E0040.
Something seems to have gotten confused or elided in many standard explanations, then. Why do coding sequences start with ATG and not TAC?

This image from the Kahn Academy article 'Overview of transcription' might help:

Essentially, the sense/coding strand of the DNA encodes the sequence that is transcribed. The RNA polymerase binds to the antisense/template strand, for which the code is indeed TAC, but when it then transcribes this strand it is again complemented, giving us the AUG that is recognised by initiator tRNAMet (also known as tRNAfmet), as shown in this diagram from the Kahn academy article on 'tRNA and Ribosomes'.

(Note that this diagram is actually showing Met in the middle of a sequence, rather than the start. fMET binding looks slightly different.

When your start codon is 5'-AUG-3', it's clear that the template DNA strand should be 5'-CAT-3'
If you look at Noah's illustration, it's also clear that the RNA sequence is basically the same as the sequence of the non-template strand, and runs in the same direction.
People generally refer to the mRNA not in terms of its RNA nucleotides, but in terms of the cDNA which it could be converted to.  But they'll reported it in the direction that makes sense for talking about RNA.


Immunological factors for the cause of headaches following SAR-CoV-2/COVID vaccination It is generally-accepted that headaches are a common side effect from receiving the COVID vaccine.

Vaccine recipients with pre-existing immunity experience systemic side effects with a significantly higher frequency than antibody naïve vaccines (e.g., fatigue, headache, chills, fever, muscle or join pains, in order of decreasing frequency, P < 0.001 for all listed symptoms, Fisher’s exact test, two-sided).

— Florian Krammer et al.: "Robust spike antibody responses and increased reactogenicity in seropositive individuals after a single dose of SARS-CoV-2 mRNA vaccine" doi: https://doi.org/10.1101/2021.01.29.21250653
I am trying to understand why. What theories or known biological, immunological or otherwise physiological mechanisms would cause recipients of the vaccine to report headaches as a common side effect?

Headache is one of the various side-effects of vaccination. Typically, a person will have pain in the site of injection, muscles throughout your body and head.
The immunological reason is the network of our immune system. Whenever a foreign antigen (vaccine) is detected by our immune system, antigen-presenting-cells (macrophages, dendritic cells) takes the antigen to nearest lymph nodes where it is presented to the adaptive immune system. Due to this invasion, strong immune response starts which leads to the pain.

Image Source: wikipedia.org/wiki/Lymphatic_system


How much genomic variation one usually find within a given bacterial species? If I find the exact starting position (say 1152471) of the coding sequence of a given gene in the genome of a bacterium, is the genome of the bacterium in general stable enough so that I can expect to find the same position in a different member of the same species?

Genetic variation within bacterial species can be much higher than one might expect.

First, this can be a difficult question to answer quantitatively because even just testing whether two strains are part of the same bacterial species is difficult: the "gold standard" method is actually experimental and involves whole-genome DNA-DNA hybridization (with a cutoff of 70% relatedness). Modern sequencing approaches have shown this usually corresponds to around 95% average nucleotide identity (ANI) (see here).

However, an ANI of 95% does not actually mean that the genomes are 95% identical: it means that of the shared sequences, one expects 95% of the nucleotides to be the same. The percent of the sequences that are actually shared in the first place can be much, much lower. For example, this paper compared 61 sequenced strains of E. coli. Out of the ~15K genes observed in at least one genome sequence, only 6% of genes were observed in all strains. Variably-present genes made up around 80% of a typical E. coli genome. This is a high level of variability, but not outrageous: an analysis of only nine P. putida genomes, for example, showed a core of at most 33% (ref).

So, if a gene is indeed indeed present in two strains of the same bacterial species, then it is likely to be highly conserved. But there is also little guarantee of finding the exact same set of genes in two strains of the same species. This means you cannot naively take chromosomal coordinates from one strain and apply it to another: you need to actually figure out which sequences correspond to one another in your genomes.

The locations of a gene on a bacterial chromosome is determined arbitrarily, so you would not expect coding sequences to necessarily have the same numerical values. Remember that the bacteria's transcription machinery will use promoters in the genetic sequence to determine where to start transcription, so the actual start location doesn't really matter -- it's pretty easy for random mutations to add or delete a few base pairs between several genes!

Instead, you would search for the genetic sequence of the gene you were interested in on the genome of a closely related species. Since many genomes are annotated by identifying genes from closely related species, it is possible that two closely related genomes start at exactly the same place, but you should definitely not assume that this will always be the case.


How do anaerobic bacteria produce ATP for their own cellular activities? Anaerobic bacteria utilise glycolysis:

Glucose + 2 P + 2 NAD+ => 2 ATP + 2 H + 2 NADH + 2 H2O + 2 Pyruvate

followed by fermentation:

Pyruvate + NADH => Lactate + NAD+

The resultant NAD+ formed can then be used again to break down more glucose molecules in glycolysis to produce ATP.

However, besides NAD+, glycolysis also requires an input of 2 ATP at the beginning (for the phosphorylation of glucose to glucose 6P, and fructose 6P to fructose 1,6 BP)

Since only 2 ATP is produced from glycolysis initially, would these 2 ATP be reused in another round of glycolysis?

If so, how do anaerobic bacteria produce a net amount of ATP for cell activities and growth?

The product is 4 ATP not 2, 2 is the net product because two are used to start the reaction.

Looking at the complete glycolysis reaction helps.

ATP can be used to start another round of glycolysis which yields 4 ATP which can then start 2 rounds of glycolysis which yields 8 ATP, rinse, repeat. It is an exponential process, ATP can be taken from this for other processes since as long as you still have 2ATP around to can restart the exponential cascade. For example from the yielded 8 if you take half for other uses, you still get 8 ATP from the next round of glycolysis reactions.

During the reactions, the resultant molecules are dispersed in the cytosol, and it is a bulk phenomenon rather discrete and independent event. The calculations are mainly based on in vitro experiments, so the reuse of the energy transporter molecules (ATP), totally depend on it's quick availability.

The NET production of ATP cannot be determined in precised manner as pathways may show reuse of the formed energy bags (ATPs) or may use already present molecule or molecules from some other reaction.


Pathogenesis of chronic venous congestion in skin? I think CVC cannot lead to heart failure primarily.
So let's think its pathogenesis in skin now only.

I think the pathogenesis is like this

dilation of veins and capillaries due to impaired venous drainage
reduced outflow of blood from a tissue
passive process
$\to$ local increase in blood volumes
$\to$ local increase in venous pressure
pathological
$\to$ shortage of oxygen and built-up metabolic waste
$\to$ structural changes in microvasculature
$\to$ increased venous permeability % hallmark of acute inflammation
$\to$ increased size of venous caliber
$\to$ emigration of leucocytes
$\to$ accumulation at site of injury
activation of acute inflammation
$\to$ protein into extravascular space
$\to$ increased viscosity of blood
$\to$ deoxygenated blood blood stasis
$\to$ congested tissue
$\to$ leucocytes move to endothelial wall (selectins)
$\to$ roll
$\to$ adhere (integrin to stop)
$\to$ migrate
$\to$ dysky reddish-bluish skin (cyanotic)
$\to$ healing via fibrosis
$\to$ scar
Causes: venous thrombosis; venous compression; heart failure;

I am not sure about the role of leucocytes exactly in this process.
I am not sure if they play a big role in the formation of cyanotic skin.
I think the outcome is mostly because of increased vascular permeability and its deoxygenated blood in extracellular space.

What is the right pathogenesis of chronic venous congestion in skin?

Probably so simple answer is enough

acrocyanosis (manifestation of heart failure) which lead to distant (acro - distant) cyanosis, bluish skin.


Is it possible to isolate and analyse intermediates of protein folding? I would like to know if there is an assay which could allow us to analyse a protein before it has assumed its 3D functional form.
While studying structural biology, I only came to know the forces that stabilize the structure, but not the gap between the original random coil and the protein in its native form.

Theoretically by molecular modeling -- see the works by Harold Scheraga:
https://www.ncbi.nlm.nih.gov/pubmed/?term=Harold+Scheraga%5BAuthor%5D

Note: An unfolded protein is not a random coil.

Fitzkee & Rose (2004) PNAS 101:12497-12502; emphasis mine:

  denatured proteins are biased toward specific conformations, in
  ... conflict with the random-coil model

https://www.ncbi.nlm.nih.gov/pubmed/15314216

This is difficult. You need to use stopped flow methods(CD, fluorescence, NMR) or single molecule methods. What exactly do you want to know about the protein? I mean, it would be hard to get the complete accurate 3d structure, as you can't crystallize an intermediate. Apart from that, if you have an accurate folding simulation for that protein, you can of course see what the common intermediates are. I am sure that if you have the Rosetta protein folding algorithms, you know the final structure, you can calculate likely intermediates with some accuracy. Then you may be able to use stopped flow methods to try to refuse those findings. If that fails, you may be able to make a convincing case that you found those intermediates.


Why are insects unafraid when you tap at them from the other side of glass? In the summer months we frequently try and kill mosquitos in our home. They are tremendously skittish and get airborne pretty quickly as you approach them. However, if they land on a piece of glass (a window for example) they don't seem at all bothered at you approaching from the other side and tapping the glass where they have landed.

Is this some strange physiology of insects (or at least mosquitos) that they cannot look down? Is it that their eyes function differently to our eyes and cannot see through the glass? For sure, their brains cannot be  developed enough to understand the safety afforded by the glass.

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


Why do chameleons move back and forth? I was always curious, why do chameleons have this strange gait?

The movement you observed serves two functions:

Imitation of leaves to protect against predators
Improved stereoscopic vision while scanning for their own prey

Imitation of leaves (mimesis)
Chameleons in the wild live in trees and are surrounded by leaves. In order to protect themselves from predators they move forth and back to blend with leaves moving in the wind.
Also note that their torso shape resembles a leaf:

Why do they move like this even when there is no wind and they are not sitting on a tree? I suppose they just follow their instincts. Evolution "did not prepare" them for sitting in a cage. The lack of ability to know when to move and when not was not a evolutionary disadvantage so there was not pressure to get rid of it.
Improved stereoscopic vision
Chameleons are predators that use their tongue to catch prey e.g. grasshoppers. While they are looking for their next target, they scan their surroundings with both eyes independently, i.e. one scans the left hemisphere, the other eye scans the right hemisphere, thus during this time they have no stereoscopic vision.
Moving forth and back helps alleviating this. They can estimate the distance to their distance better through the use of motion parallax (closer objects seem to move more than object further away when we move sideways). Once they found a target they turn in its direction and then use both eyes to focus on it, preparing to shoot out their tongue.
(Disclaimer: I am not a biologist. This is from my own reasoning and the German Wikipedia article about Chameleons)

They go back and forth for the same reason that stick insects and caterpillars do. to imitate wind and foliage, leaf trembling, to ward of their predators. A possible additional reason is to gain added perspective of their environment.

Here is example of same principle in stick insects:

https://www.youtube.com/watch?v=EAIRjpaOXKs

https://youtu.be/gHoDKY8jL1g

https://www.youtube.com/watch?v=Rq7-BPuLXLo

They don't have the physiology or habitat where they can escape or hide from predators hence the open air hiding tactic.

They don't have running muscles and skeleton. They couldn't run if they wanted to (slower than a snake or bird) and they couldn't hide because trees also don't offer crevices like cliffs and walls do. Their behavior is good for catching more prey and for staying hidden.

They are related to Iguanadons, which are adapted to moving in the sea (cold). Chameleons often live in the shadows, 130 of 171 species are forest dwellers, and most of the others live in trees of savannas and steppes, only a few live on the floor.

They don't need to be warm to hunt, their tongue is still one of the fastest things in vertebrates, so they can hunt when they are cold.

Their prey is not very intelligent: birds, snakes and more rarely mammals. because they are too slow to run away, they don't have hiding places except for the branches, they have a very cautious walk which is disguised, with slow head movements, very active eyes, and ability to keep head still in between steps. hunters will tell you that animals are very oblivious when their head is moving, they generally need to stop to see you, and chameleons stop constantly. there was research to understand their slow muscles, the muscles have slow fibers, they have a heart which is not as capable as fast lizards. http://onlinelibrary.wiley.com/doi/10.1002/jez.1402630102/abstract


Does drinking coffee have negative effects? From what I collected, coffee is a magical potion that lets you feel energetic, and essentially not-sleepy. But are there any tradeoffs? I mean, if it was so beneficial, wouldn't the human body produce caffeine naturally?

First of all, the fact that a substance is beneficial does not mean that our body will, perforce, produce it naturally. Think of oxygen and water for example1.

As for the negative effects of coffee drinking, yes there are many although coffee has both a positive and a detrimental effect on human health. The main active ingredient in coffee is caffeine which can have the following negative effects:

Caffeine can increase blood pressure in non-habitual consumers.
High blood pressure is associated with an increase in strokes, and cerebral
vascular disease, which in turn increase the risk of multi-infarct dementia.
Caffeine may reduce control of fine motor movements (e.g., producing shaky hands)
Caffeine can stimulate urination.
Caffeine can increase cortisol secretion, some tolerance is developed.
Caffeine can contribute to increased insomnia and sleep latency.
Caffeine withdrawal produces headache, fatigue and decreased alertness.
Caffeine is addictive.
High doses of caffeine (300 mg or higher) can cause anxiety.
High caffeine consumption has been linked to an increase in the likelihood of experiencing auditory hallucinations. A study conducted by the La Trobe University School of Psychological Sciences revealed that as few as five cups of coffee a day could trigger the phenomenon.
High caffeine consumption accelerates bone loss at the spine in elderly postmenopausal women.

The list above comes from the very comprehensive wikipedia page on the health effects of caffeine. In fact, wikipedia is particularly good on this subject, see the following pages:

http://en.wikipedia.org/wiki/Caffeine

http://en.wikipedia.org/wiki/Health_effects_of_caffeine

http://en.wikipedia.org/wiki/Health_effects_of_coffee

1 Our bodies do produce both Oxygen and water as byproducts of various reactions but nowhere near enough to satisfy our need for these substances.

There are copious studies on the health effects of coffee. The overall conclusion is that people who drink coffee have slightly less health issues than people that don't.

BMJ:
The umbrella review identified 201 meta-analyses of observational research with 67 unique health outcomes and 17 meta-analyses of interventional research with nine unique outcomes. Coffee consumption was more often associated with benefit than harm for a range of health outcomes across exposures including high versus low, any versus none, and one extra cup a day.
https://www.bmj.com/content/359/bmj.j5024

For adults consuming moderate amounts of coffee (3-4 cups/d providing 300-400 mg/d of caffeine), there is little evidence of health risks and some evidence of health benefits. https://www.ncbi.nlm.nih.gov/pubmed/16507475


Why do the two hemispheres of the brain control the opposite sides of the body? Why does the left hemisphere control the right and the right hemisphere control the left? I googled it but didn't find a good answer regarding this. Could someone explain?
Does this adaptation help in the speed of transmission of nerve impulses?

Just to get the ball rolling here.  This particular aspect of brain evolution is very old. The cross wiring of the hemispheres of the brain seems to be as old as the right and left hemispheres itself.  It predates lizards - i.e. hundreds of millions of years ago. It  possibly predates right/left dominance and the organ asymmetry which puts the heart on the left side of the body.

Digging back deeper, we can see that worms have bilateral brain structure, but as noted in the comments below, the nervous systems do not cross.  I would guess that this means that the phenomenon appears sometime before lizards - putting the development having been done by the early Carboniferous period when the first animals came to the land and the first reptiles appears, which is the perhaps 350 million years ago.

Echinoderms (like starfish) are 'missing links' in bilateral symmetry as their larval stage has bilateral symmetry even though the adult has radial symmetry.  Such wiring may be so embedded in the way most animal body plans develop that it hasn't changed in evolutionary history. If that is related to other animals trait, it could be a billion years ago. Some argue this is not the case.

One might guess that the cross over of neurons in brain control is good for integrating the signals from both sides of the organism. There are quite a few theories.

It's for control, coordination and balance. From a mathematical point of view, parallel lines won't intersect and thus line A won't affect line B unless they intersect and thus would hardly influence the other unless and an external force is applied to any of the lines.

This is also why corpus callosum connects the left and the right side of the brain.


Origin, or source, of rhesus negative in human blood This is my first post here, so please be gentle. I recently learned that I have Rh- blood (I'm A-), and was idly looking into blood types on Wikipedia. I was surprised to find that relatively few (~15% of all) humans have it, and most of those seem to be European. Looking just a little further, I found a bunch of crackpot-looking sites that try to explain how people got Rh- blood, and what weird abilities they possess as a result.

I managed to find one site that seemed at least less laughable, which suggested that interbreeding with Homo neanderthalensis (or possibly Homo sapiens neanderthalensis, since the site seemed to indicate that there was some question about how different H. s. sapiens were from H. neanderthalensis) might have accounted for the introduction of the condition.

It seems that from more reputable (medical) sources, the only difference between Rh+ and Rh- is that complications can arise during pregnancy if the mother is Rh- and the fetus is Rh+. Indeed, most sites (e.g., WebMD) seem to explicitly state that there are no other differences of note.

I am not a biologist, or an anthropologist, or a life-science kind of guy at all. However, as a computer scientist, I like to think that I have both an open mind but one which demands scientific and/or logico-mathematical evidence for claims. Lots of the pseudo-scientific, paranormal, etc. theories on the web I basically dismiss out of hand, as explanations which are almost certainly fantasies, but most definitely baseless and untestable.

My question:

  What, if any, is the current scientific understanding of the origin, or source, of rhesus negative blood in human beings? Do individuals with Rh- blood have any common (in a statistically significant sense) characteristics or health issues, aside from the issue with pregnancy and tending to be more European than not? Is there anything to continuing to look into this?

For context, I got started down this rabbit hole while looking into different dieting strategies, and found the "blood type diet". Just as an aside, I don't think there's a lot of merit to that diet... sounds like a fad thing. Any sources or information or help on this subject are appreciated.

EDIT:

I have been looking a little more, and I stumbled across a paper entitled, "The influence of RhD phenotype on toxoplasmosis and age-associated changes in personality profile of blood donors" which looks at the effect of the Rh- trait on personality changes caused by toxoplasmosis (if you Google the title, you should be able to download). Using Cloninger's and Cattel's personality factors, they seem to show a variety of things, including (a) personality differences between Rh+ and Rh- individuals not affected by toxoplasmosis, and (b) different reactions to prolonged toxoplasmosis affection in Rh+ and Rh- individuals.

I didn't even know that parasites could affect your behavior; that seems frightening on the one hand, but on the other, it's fascinating if it's for real, especially since the incidence of toxoplasmosis is not insignificant in most people. Anybody who knows anything about this or who reads the paper and can help me understand what it's saying would be doing me a great favor to answer/comment/chat. Thanks!

Your question has many questions in it.

As for the evolution of Rh factor, Blancher and Apoil (2000) attribute the high level of sequence similarity (92%) of the two RH locus genes, RHD and RHCE to a gene duplication event in the common ancestor of human, chimps, and gorillas. Their analysis of the cDNA from these genes revealed "complex recombination events" after the lineages split.

Basically the most recent common ancestor of apes had the "human" RH genes, which then differentiated after the lineages diverged. Duplicate and differentiate is a common theme in evolution.

As for why it's called rhesus antigen, that's just as experimental artifact:

  The term "Rhesus antigen" was introduced by Landsteiner and Wiener,
  who found that rabbits (and later, guinea pigs) immunized with red
  blood cells (RBCs) from a rhesus monkey produced antibodies which
  agglutinated 85% of Caucasian blood samples (Landsteiner and Wiener
  1940, 1941).

They probably weren't even correct about the antibodies being rhesus:

  In conclusion, if the term "Rh" was coined by Landsteiner and Wiener
  because of the source of antigens (the rhesus monkey) they used to
  obtain anti-Rh in rabbits, it is highly probable that, in fact, they
  produced anti-LW antibodies.

It's my opinion the rh antigen developed from toxoplasmosis infection. I only recently learned that this protozoan can actually insert its genes into a host's genome. Once it's in the genes, it can be passed in the germline. Toxoplasmosis can infect all primates, human and otherwise. Monkeys get it, and so do humans living in toxoplasmosis endemic places. The life cycle of toxoplasmosis is connected with mice and cats as an evolved survival strategy for the toxoplasmosis protozoan. There never were cats in northwest Europe, and that would explain why the people with ancestry from that area were never exposed to toxoplasmosis. I look for the rational biological explaination. One great clue to my thinking is I found a term used in some research writings, the text read "RH strain of toxoplasmosis". Yes they seemed to be doing experiments with the toxoplasmosis found in rhesus monkey.


Can genetically modified genes jump to bacteria in the eater's intestine? The Guardian ran an article a while back talking about GM gene's jumping to bacteria in an eater's intestine. Has other research confirmed this phenomenon?

No.

There is nothing special about a piece of GM DNA when compared to any other random piece of DNA. If this phenomenon happened at any detectable level, we'd have found eukaryotic DNA in bacterial genomes/plasmids long before the introduction of genetically modified crops. And that would be front page news in the field of horizontal gene transfer! Which has many talented people in it!

Apparently transfer between prokaryote and eukaryote (in both directions) has been detected:
http://www.biomedcentral.com/1471-2148/11/276/abstract
http://www.sciencedirect.com/science/article/pii/S0888754311001959
http://genome.cshlp.org/content/19/8/1441.abstract

Some numbers I'd like to know are the rate of pro<->eu HGT detection /versus the rate of looking for it/ (i.e. 3 confirmations in 300 attempts would be more impressive than 3 confirmations in 30,000 attempts).


Why there aren't any pandemic diseases by prions? Learning biology in school, I became interested in the fact that there aren't any diseases by prions which are globally infectious (as far as I know), unlike diseases by viruses (ex. COVID-19, SARS etc.) or by bacteria (ex. plague, ...). Why is it?
cf. Here are some my hypothesis

Prions are not efficient pathogens because they don't have DNAs.
Such prions are not yet discovered or does not exist.
There exists lots of people who are immune to such diseases.

Are there any answers to the questions? Or is there any answers?

I think that you could argue that some prion diseases do form epidemics or outbreaks. In some cases it does appear that people have referred to BSE/vCJD as pandemics. There is even some journalism on the topic, and see also here.
Infection by prion from the environment does occur at some rate, and it is true that it is these prions are the more transmissible. See Table 1 in that linked paper for more information; it appears that the discovery of prion excretion through e.g. feces is relatively recent.
For less transmissible variants it is true that you usually have to directly ingest a fair amount of prion from (i.e. eat) an infected individual to be affected, which is a harder means of transmission because it implies cannibalism (which is not that uncommon biologically, but still).

Viruses mutate relatively fast, i.e. Aids mutates 100,000 times faster than Eurkariotic DNA. Actually, viruses mutate on average once every time they reproduce into a new copy / per genome replication.
The DNA segment that encodes healthy PRPC protein which can be hyjacked and converted by a prion has 3kb base pairs, and there are only 30 mutant version of PRPC known as prions detailed since 1970, compared to thousands of different versions of Covid-19 since 2019. The mutant prions dont use RNA, they actually latch on to the healthy versions inside the human body and changes them to mutants.
We can say that prions evolve 10,000 to 100,000 times slower than other bodily fluid viruses like hepatitis and AIDS. Those mutations serve to keep the viruses fit, resistant to new environments, new species, new biochemistries.


Is evolution true as Darwin said? I was telling the theory of evolution to my friends. But they asked me for the proof. They said, we are not seeing any such transition species at present. Neither we have such evidence for evolution. What should I do? I saw many proofs like archaeoptaryx, but now it has been proved that it is fully functional bird and others are also not supporting the theory of evolution given by Darwin!

I saw an excellent public science talk a few weeks ago. The speaker presented 5 questions which, if you answer yes to, you can only come to the conclusion that evolution exists. Firstly though we should define evolution: Evolution is the change in the inherited characteristics of biological populations over successive generations.

It was one of the best arguments I've seen put forward so I'll try to recreate it here. Put this to them and see what they say - and just in case they say no to any, I've put answers in for you ;) There is no hard evidence for the first four points because they are so damn obvious that if people say no, even after a logic based argument, then all they will ever say is no, they shouldn't need a scientific paper.

1) Do individuals reproduce?

The answer to this is undeniably yes, you were the result of reproduction. Reproduction exists.

2) Is there variation among individuals?

Yes, again this is undeniable. Do we all look and act the same? No. Are some people taller than others? Yes. Some more physically fit than others? Yes. Is everyone's hair or eye color the same? No. See, undeniable. Variation exists.

3) Do some individuals die before they get to reproduce?

Obviously yes. Children unfortunately die (of natural causes) which means they do no get to reproduce. Just go look in a cemetery or open the obituaries page of you newspaper and you'll likely find some one who died before they could have reproduced. Some people also never reproduce, because of life choices or fertility problems. Variance in reproductive success exists.

4) Do offspring resemble parents?

The answer to this is also yes, when two humans reproduce they (normally) produce something that resembles a human. And when that human reaches maturity they will likely look a more like their parents than a random stranger. Personally I was looking at old family photos recently and I honestly though I had found a picture of me marrying my mother, that's how similar my dad and I look. Heritability of variance exists.

5) Does heritable variation lead to differences in reproductive success?

If you've answered yes to all of the above then you really should be answering yes to this one too. As a hypothetical illustrative scenario, imagine two male deer. One has big antlers and one has small antlers. The size of antlers is largely genetically determined. The male with big antlers is seen as more attractive by a female. She chooses to mate with him. She gives birth to his offspring (n=2, 1 male 1 female) who inherit his genes for large antlers. This repeats with several females in the population (n=10). The smaller male has fewer mating events (n=2) and therefore sires fewer males in the next generation. The next generation contains more males with large antlers (n=10) than small antlers (n=2). This is evolution, the change in the inherited characteristics of biological populations over successive generations.

Another example is humans. We know some men have low sperm counts leading to low probability of successful mating. Further, we know that male infertility can be genetically caused for example by Y-linked genetic defects. Therefore we can expect that males with low sperm counts, caused by Y-linked defects, will have fewer offspring than a healthy male (given equal opportunity to mate) and because all males inherit their fathers Y chromosome they too will have low sperm counts. They will be represented at a lower level in the population's next generation. Again, this is evolution.

Speciation:

It then doesn't take much to jump from this to speciation. It involves the introduction of isolating mechanisms. These can be things like geography (allopatric speciation), or sympatric mechanisms like morphology, behavior, or any trait which prevents one group of individuals mating with another.

I'll illustrate first, and take the more difficult type - sympatric speciation. Again imagine our deer population. This time there is variance in sperm morphology, and female reproductive tracts. Males can produce two different types of sperm, one (male type S) is a slow moving but more resistant to the hostile female reproductive tract (because it is resistant to all types of antibody the females can produce), the other is faster (male type F) but less resistant (because it is resistant to only some of antibody the females can produce). Female reproductive tracts vary in the number of different antibodies they produce, one produces "all" that can be produced (female type R) and the other only a subset of the full array (female type W).

What will happen is that type S males will be more successful when mating with type R females because their sperm survive (whereas type F males have no sperm fertilizing the egg). However, type F males will be more successful in sperm competition than type S when mating to type W females. Repeated over many generations, these incompatibilities will cause distinct mating groups which do not overlap, i.e. species.

In reality it is much simpler to demonstrate this with allopatric speciation. Here two groups of one species become isolated by a geographical feature, like a river. Over time these populations evolve differently (because genetic mutation is random and selection might differ on opposite sides of the river). When they get the opportunity to mate after X generations, they can't because they have evolved genetic incompatibilities (offspring fail to survive, eggs can't bee fertilized).

One of the absolute classic examples is an experiment using fruit flies by Diane Dodd.   In her experiment she reared a population in two groups, one on starch based food, and one on maltose based food. After many generations (35 I think) the two groups showed mating preference, which is a reproductive isolating barrier, within their groups (mating pairs were more often formed from within treatments). Here is the paper.

Picture from http://evolution.berkeley.edu/

There are six different types of evolution and they all happen on different levels.

Cosmic evolution- the origin of time, space and matter. Big Bang
Chemical evolution- the origin of higher elements from hydrogen.
Stellar and planetary evolution- Origin of stars and planets.
Organic evolution- Origin of life from inanimate matter.
Macro-evolution- Origin of major kinds.
Micro-evolution- Variations within kinds. Only this one has been observed. For instance poodles and great danes are descendant from the same thing. A wolf.

Are you asking about macro evolution or micro evolution? Or one of the other 4?

Speciation does not show macro evolution in any way, shape, or form. And the ring species you refer to moths changing colors, that is micro evolution. A moth changing into another moth would even be micro evolution.

Man thought up species and defined them. If it looks like a duck and quacks like a duck, it didn't evolve into a different animal because it changed the color of it's feathers.


Are there animals that have evolved a resistance to human activity or encroachment? There are countless sources, both peer-reviewed and popular, explaining how overuse and misuse of antibiotics is breeding a new generation of antibiotic-resistant "superbugs" such as MRSA (Methicillin-resistant Staphylococcus aureus) and MDR-TB (multidrug-resistant Tuberculosis). Over in the animal kingdom, the opposite seems to be happening - species after species is becoming endangered and/or extinct as humans destroy or alter their habitat through increased hunting, farming, construction, etc.

Are there any non-human animals that have been found to have evolved resistance to human encroachment into or alteration of their habitat in a way analogous to how bacteria have evolved resistance to human attempts to get rid of them? For example, this could consist of:

an animal that has adapted stronger bones to better survive collisions with vehicles
an animal that has significantly increased its blood coagulation rate to survive gunshot wounds from hunters
an animal that has developed better vision to see in urban environments
an animal that has evolved a skin pigment change that enables them to not take as much damage when they are sprayed with agricultural pesticides

One answer that came to mind is domestic animals - the horse and dog in prehistory, the cat in ancient Egypt, etc. That seems too obvious on one hand, and on the other hand may not really be an answer, as there seems to be no indication that pre-domestic animals were endangered by humans in any meaningful way. Are there animals that have significantly adapted themselves to surviving as wild animals in human-influenced environments?

Note: This is an answer to the last line of your question.
A classical example of animals adapting to the influence of humans on their environment is the adaption of the Peppered Moth.
Here is a brief summary:
The peppered moth was originally a mostly unpigmented animal (<1800). During the industrial revolution in the southern parts of the UK a lot of coal was burned. This led to soot blackening the countryside. Soon afterwards, a fully pigmented variety was first observed. Only a hundred years later, in 1895, this pigmented variety almost completely displaced the unpigmented variety.
It has been shown that the pigmentation is under strong selective pressure as birds hunt these moths. Since birds rely on their visual system to detect their prey, the variety that blends in with its environment (=camouflage) has a selective advantage over the variety that stands out.
As pointed out by Tim in the comments, since the 1970s there has been a rapid reversal with unpigmented animals being more abundant. As far as I understand, it is accepted that this reversal is due to a decrease in human induced air pollution leading to less sooty barks on trees which makes the unpigmented variety harder to prey upon.
Addendum: genetic basis of adaption
In a beautiful recent study, the causal mutation for the pigmented, or melanic, variety was identified: A ~9kb transposon insertion in the first intron of the gene cortex. The authors calculate that this mutation happened in the year 1819, a few years after the industrial revolution was in full swing. The interpretation is that due to sooty tree bark this mutation, causing pigmented moth, was under strong selection.

Not so much physical changes, but changes in behavior caused by human activity has numerous examples.
Foxes, pigeons, sea-gulls adapt very well to city life. Some species nowadays have larger  numbers in cities than in the country side.
Polar bears are another good example. Disappearing sea-ice and increased human activity in the Artic has turned many polar bears into pre-dominantly garbage scavengers in stead of hunters/carrion-eaters.


Why are viruses considered microbes? My question is simple. Why is a virus considered a microbe? Considering a microbe is considered to be a "living" unit of life, which viruses are not.

What is a microbe?

A microbe (or microorganism) is a microscopic organism. Anything that is considered alive and that is small enough is called a microbe.

Note that this definition has two issues.

There is no universally accepted definition of life.
There is no universally accepted size threshold for being called a microbe (to my knowledge). I would go with a threshold of about $10^{-5}$ meters.

Is a virus a microbe?

A virus IS and IS NOT alive depending on the definition. Note btw, that the definition of what is alive is not a matter of Biology but a matter of Philosophy. Most of the time, viruses are considered as not being alive. It is important to understand that the definition of life has absolutely no impact on biology and is nothing but a question of nomenclature.

If you want to call a virus a living thing, then yes, viruses are microbes. As stated on the wiki article:

  Some microbiologists also classify viruses (and viroids) as microorganisms, but others consider these as nonliving.

You can find a discussion of why viruses are generally considered as not being alive here.

Unit of life

The concept of "unit of life" has not much meaning in biology and, to my experience, is most often used as a nice image for teaching young students what a cell is. Most of the time that I heard of "unit of life" (mostly when I was in secondary school and eventually high school) was used to describe a single cell making up a multicellular individual such as a cell of your blood for example and not a unicellular individual.

Viruses are small bits of genetic code in a protective covering. Viruses are not "alive," that is, they cannot replicate, unless they are inside another organism. A virus is definitely too small to be seen without a microscope. Since viruses are so small (tinier than bacteria) they may be considered microbes. However, since they are not "alive" outside of a host organism, it is debatable whether they are really organisms at all. For convenience since they are neglected in other areas of biology, viruses are discussed in microbiology. Most viruses are known because they cause disease.


Complete metabolic map of humans Do we have the complete metabolic map for humans? Do we know from the genome what enzimes are expressed and what each enzime does?

As Armatus notes, we don't know ALL human metabolites and the enzymes + metabolic reactions that produce them. Identifying small molecules is hard and metabolism is dynamic, it depends on what is being fed into the system.

The virtual metabolic human (VMH) is an attempt at compiling the information that we do know. You can read their paper here. The human build currently includes (and links together);

13 543 metabolic reactions
4138 metabolites
3695 genes (enzymes)

It also attempts to compile all known metabolic reactions that result from the gut microbiome, nutritional metabolic pathways and genetic diseases that alter metabolism. Everything is linked via stable identifiers which is a real challenge.

The human metabolic database (HMDB) is also very good. It contains more metabolites than the VMH as it includes many partially or poorly characterised metabolites. The HMDB is really useful if you are working to identify metabolites while the VMH focuses on how they connect to one another.

The answer is not yet.  The sequencing of the human genome, considering its size (@ 3.2 bbp), and contrary to what's been hyped in media, is not the end of the quest for understanding the human body.  On the contrary, it is only the first and the simplest step in the elucidation of the intricate workings of the human body.  Even though a lot has been accomplished already, all of those tons of accomplishments still barely scratches the surface.

I can safely estimate that human genome sequencing represents less than 1% of the work that lies ahead, enormous work required to make sense of the whole base pair sequence.  Each succeeding step multiplies the complexity exponentially, and so, even considering the exponential advancement in technology, it is again safe to say that at the rate things are going, the complete elucidation of the human metabolome and metabolic pathways cannot be accomplished within the next 50 years.

To get an idea of the complexities involved, one only has to consider the next step after genome sequencing; the next step is to identify all the human genes making up the coding sections of the genome, which account for less than about 2% of the human genome.  Most genes do not transcribe into RNA in a straightforward manner; introns (which separate the exons that hold the coding sections), have to be spliced out; then the exons making up the code for the protein must be joined together.  All of that accountws for less than 2 % of the human genome.  The rest is non-coding DNA, the function of most of which hasn't yet been figured out.