text:
Questions about the evolution theory
I'm not sure whether I can ask those questions about evolution in one post or should separate them into multiple posts, but I am just curious about the evolutiontheory. (I am new here)
Sorry for my english and my many questions :)
My questions:

They say humans and monkeys have a mutual ancestor. Was it literally one ancestor? Because if so, then it would need a partner to regenerate children right?
Even if they would have children, then these children would be brothers and sisters right, which means they cannot have sex to regenerate their children?
They say that humans and monkeys have a mutual ancestor, does that mean that a certain brother's family became monkeys and the other brother's family became human?

https://en.wikipedia.org/wiki/Chimpanzee%E2%80%93human_last_common_ancestor

If humans and monkeys have a mutual ancestor, then how come humans and monkeys are so different in terms of intelligence, hygiene, clothing?
They say humans lost our fur because we don't need it anymore, but how come we still need cloths to wear to protect us from cold?
Why do humans have to brush our teeth, cut our nails, use toilets and work for our food and drinks, while any other animals don't?
Why do men and women have those specific features that make a man a man and a woman and woman? Why do women have to give birth and not men? Why do men have more facial hair growth and are built stronger than woman (while male and female chimpansees (our closest ancestors) both grow facial hair Why do men grow facial hair?)? Some people say men have more facial hair growth and are built stronger because they used to hunt (why did men hunt and not women?), but some say men hunt because they have more facial hair and are built stronger. Wouldn't it be a circle reasoning?

https://www.reddit.com/r/explainlikeimfive/comments/31zou1/eli5_what_evolutionary_advantage_does_having_long/ (facial hair because hunt)
http://www.answers.com/Q/Why_did_men_hunt_and_women_gather_in_prehistoric_times (hunt because built strong)

Why do human male and female look different compared to other animals? Why do human individuals look different from each other, but all other animals look like each other (geometrically)?

Could it be possible that we relate humans to animals, because we associate animal behavior with human behavior due to our human reasoning (which we can't help of course)? But human and animal behavior that look similar, does not mean that they have the same meaning right?
Does 'survival of the fittest' mean the following?: Humans have finger nails and a protruding nose, because animals that didn't have nails or protruding noses are extinct?
Why do humans have a chin, curly hair, eyebrows, lips and facial hair above the lips while monkeys don't?
Why do humans have this specific hairline (separation line between hair and skin)

https://www.reddit.com/r/askscience/comments/v3w3b/why_do_humans_have_such_distinct_hairlines_as/

Why can human hair and finger nails grow forever, but monkey's hair and nails don't grow that long?

https://www.quora.com/Why-dont-the-other-primates-have-long-hair

Some human emotions such as guilt and fear sometimes result in not doing anything at all, but isn't that evolutionary a disadvantage?
Humans have so little fur compared to monkeys. Which means that at some point, starting from the ancestor, the next generation lost more and more fur. At some moment there was so little fur left that generation felt cold and wore some clothing? But what about their naked parents who have about the same amount of fur?
Why are there humans and monkeys, but not intermediate forms that slowly changed from the ancestor to human or ancestor to monkey? Because they would have human characteristics but also monkey characteristic which are still there nowadays?
Could it be possible that new species are not arisen, but just discovered?
Could it be possible that all the species do not arise in series (after each other), but parallel (at the same time). Because if it would be the former, then the food chain would be incomplete?
Why do we have puberty, and why don't boys already have facial hair when they are kids (for warmth)?
They say humans find a lover because, evolutionary speaking, they want to produce children. But how come some couples choose not to have children?
Why do humans talk and write (have a language), while monkeys don't?
They say the big bang was the cause of everything, but how can material appear from nothing? (Which basically means 0=1) Even if organic molecules came from an-organic molecules, they it would still not mean that the organic molecules were living? (example: a wooden door is organic, but does not live)
They say evolution is driven by mutations. Are protruding noses and nails the consequence of mutations? But most mutations are of disadvantages (example: diseases)

First: This is ways too broad. Please limit a question to one (or maybe two closely related questions) but not 23. Here at biology.se we require people to do at least some own research to solve the question. What have you found out?

I'm voting to close because this is TOO broad - please ask your questions individually and not all lumped into one question that is unanswerable.

Do you mean I should separate it into 23 posts?

@FacebFaceb Theoretically yes, but a lot of your separate questions would still be closed because we require you to do some previous research of your own and state how it did not answer your question. (Like Chris already said.) For example your last question can easily be answered by reading the wikipedia article about mutations. https://en.wikipedia.org/wiki/Mutation

Yes, separate into 23 post if you want good answers for each question. And answering convention here mandates citation and such... so researching the answer of all 23 questions will be too much for most people.

Most definitely absolutely way too broad! Also some of these questions have nothing to do with biology (e.g. there is one question about the big bang). I am voting to close.

You might want to follow a very quick intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for example. It will already allow you to answer to several of your own questions.

Also, a lot of your questions are patently ridiculous.  As for instance #2.  It's perfectly possible for brothers and sisters to have sex, and produce offspring.  In fact, it's a fairly common practice (known as line breeding) in animal breeding.  Or #8: animals, when you get to know them, are quite as distinct as individuals as humans, maybe more so.  Think for instance of the many colors & patterns that horses have.  Far more distinctive than e.g. interchangeable blonde Hollywood actresses :-)

a lot of the questions about hairlessness are pretty repetitive. I don't think you have 23 questions

Please break these up and and post specific questions, some of these are quite reasonable questions for a layman, but many have nothing to do with each other.

The post is way too broad. Many questions are unclear and many questions lack research from your part. But I still wanted to give you some info that may help you. Answers will be short but it would take a whole book to fully answer all questions.
You are often using "They" to refer to some undefined group of people and give a random straw man. Please always backup your claims with a reference. As a consequence most of your questions are opinion-based (which make them off-topic).
Intro course to evolutionary biology
First and before everything else, you should have a look at a short intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.
Please do follow some intro course before reading the following. You will get much more from the below answers this way.
Your questions
You should read about coalescent theory.

They say humans and monkeys have a mutual ancestor. Was it literally one ancestor? Because if so, then it would need a partner to regenerate children right?

Yes, any two organisms on earth literally have a common ancestor which is a single individual. However, when thinking about closely related species as humans and chimps, the dating of the most recent common ancestor might rather correspond to a population than a single individual. It would be a single individual if there were only asexual reproduction with no genetic recombination.

Even if they would have children, then these children would be brothers and sisters right, which means they cannot have sex to regenerate their children?

See above.

They say that humans and monkeys have a mutual ancestor, does that mean that a certain brother's family became monkeys and the other brother's family became human?

If reproduction was asexual and if there were no recombination (which at this scale is not too an awful model depending on what predictions you are trying to achieve), yes one individual is ancestor of the human lineage while the other sibling is ancestor of the chimp lineage.

If humans and monkeys have a mutual ancestor, then how come humans and monkeys are so different in terms of intelligence, hygiene, clothing?

They say humans lost our fur because we don't need it anymore, but how come we still need cloths to wear to protect us from cold?

Why do humans have to brush our teeth, cut our nails, use toilets and work for our food and drinks, while any other animals don't?

I will just make one short comment for all 3 questions.
If an oak tree and a pigeon have a common ancestor, then how come they are so different? You could ask the same question with any pair of species. the appreciation of the differences is completely arbitrary.
The terms you use are all very related (all related to intelligence) and fast to acquire. You typically talk about hygiene. Showering / bathing is a very recent human activity. Just a few centuries ago, no one was ever showering (not even the kings) and people were throwing their dejections in the street in cities.

Why do men and women have those specific features that make a man a man and a woman and woman? Why do women have to give birth and not men?

For these questions, you will need to learn what a sex is, learn about sexual selection and eventually about Bateman's principle. You will note that these questions are not specific to humans.

Why do men have more facial hair growth and are built stronger than woman (while male and female chimpansees (our closest ancestors) both grow facial hair Why do men grow facial hair?)? Some people say men have more facial hair growth and are built stronger because they used to hunt (why did men hunt and not women?), but some say men hunt because they have more facial hair and are built stronger. Wouldn't it be a circle reasoning?

You are imagining a cause-consequence considering only extremes of the two variables. The reality is much more of a smooth process where gender roles happened slowly. Also, there are many factors that affect gender-specific general body size. In most species, females are bigger as females produce bigger gametes and, for the case of mammals typically, carry the baby. Gender roles such as defense, hunting and many other things explain such dimorphism. You will note that there is also similar dimorphism in chimps.

Why do human male and female look different compared to other animals? Why do human individuals look different from each other, but all other animals look like each other (geometrically)?

The first question could be asked for any species again. For the second question, please have a look at the post Why do different humans look different?.

Could it be possible that we relate humans to animals, because we associate animal behavior with human behavior due to our human reasoning (which we can't help of course)? But human and animal behavior that look similar, does not mean that they have the same meaning right?

I don't understand the question and it sounds very much a matter of opinion rather than a matter of evidences.

Does 'survival of the fittest' mean the following?: Humans have finger nails and a protruding nose, because animals that didn't have nails or protruding noses are extinct?

"survival of the fittest" is a typical expression that refers to the process of natural selection. Natural selection is a process that causes a change in allele frequency over time caused by a fitness differential associated with genetic variance. If this decision does not make sense to you, make sure to have a look at an intro course to evolutionary biology.

Why do humans have a chin, curly hair, eyebrows, lips and facial hair above the lips while monkeys don't?

Why do humans have this specific hairline (separation line between hair and skin)

Just one comment for the above two questions.
These questions only are already too broad. You will need to focus on a single trait. You will also need to get some intro knowledge to evolutionary biology as it feels like you would make the mistake of being too adaptionist and misconsidering spandrels.

Why can human hair and finger nails grow forever, but monkey's hair and nails don't grow that long?

Is this true? You will need a reference for that. I doubt chimps hair really stop growing. They probably just fall as they get long enough. I don't know much about that but I would definitely need some references to really understand in what terms are human hairs different from chimp hairs.

Some human emotions such as guilt and fear sometimes result in not doing anything at all, but isn't that evolutionary a disadvantage?

Yes, very likely. The field that studies such thing is called evolutionary psychology.

Humans have so little fur compared to monkeys. Which means that at some point, starting from the ancestor, the next generation lost more and more fur. At some moment there was so little fur left that generation felt cold and wore some clothing? But what about their naked parents who have about the same amount of fur?

I am not sure I understand the question. It feels like you are seeking for a sudden change where everybody suddenly went from being naked to wearing uniforms with bow ties.

Why are there humans and monkeys, but not intermediate forms that slowly changed from the ancestor to human or ancestor to monkey? Because they would have human characteristics but also monkey characteristic which are still there nowadays?

You should have a look at Where are the evolutionary “inbetweeners”? and Why aren't there any transitional animals today?.

Could it be possible that new species are not arisen, but just discovered?

Most species that are discovered have not arised any time recently indeed.

Could it be possible that all the species do not arise in series (after each other), but parallel (at the same time). Because if it would be the former, then the food chain would be incomplete?

I don't understand your relationship with the food chain but yes speciation events occurs in any lineages, not totally independent of each other but in a way that "feels" like something we would call a parallel process and not a serial process.

Why do we have puberty, and why don't boys already have facial hair when they are kids (for warmth)?

Have a look at an intro course to developmental biology.

They say humans find a lover because, evolutionary speaking, they want to produce children. But how come some couples choose not to have children?

While evolutionary processes can eventually select for not reproducing (see kin selection), the likely main reason for why many coupled don't want kids have to do with our culture and not with the evolutionary forces.

Why do humans talk and write (have a language), while monkeys don't?

Because we're intelligent. Many monkeys have some form of primitive communication though with a few words and a few signs.

They say the big bang was the cause of everything, but how can material appear from nothing?

This is completely unrelated to biology.

(Which basically means 0=1) Even if organic molecules came from an-organic molecules, they it would still not mean that the organic molecules were living? (example: a wooden door is organic, but does not live)

I don't understand your question. But you should have a look at an introduction to abiogenesis

They say evolution is driven by mutations. Are protruding noses and nails the consequence of mutations? But most mutations are of disadvantages (example: diseases)

The statement "evolution is driven by mutations" is very misleading if not simply wrong. Just have a look at an intro course to evolutionary biology!
In short, evolution is a change of allele frequency over time. There are various processes that can cause such changes. One of which is natural selection (NS). NS is caused by a fitness differential associated with different genotypes. It causes genotypes associated with higher fitness to raise in frequency, therefore removing genotype associated with lower fitnesses from the population.
NS therefore results in a decrease of the within population genetic variance. Mutations brings up new genetic variance in the population. It is true that most mutations are neutral or deleterious and are therefore (by definition of what deleterious mean) counter selected and will eventually disappear from the population. The few beneficial mutations that occurs may eventually increase in frequency through NS and eventually reach fixation (that is a frequency of 1) in the population.

Re "Why do men have more facial hair growth...", one might ask why male deer have antlers and females don't,  or why male lions have manes, peacocks have gaudy tails... Which gets you into the whole subject of evolution by sexual selection.

This is impressive. Well done.

1    They say humans and monkeys have a mutual ancestor. Was it
  literally one ancestor? Because if so, then it would need a partner to
  regenerate children right?

First off.. human and monkeys do not a mutual ancestors. Ape and monkeys have a mutual ancestor. Humans are a type of ape. Gorilla's are a type of ape.
It was an ancestral population. If we had a time machine, what we would see an ancestral population, then at some point in time the population got divided. The populations continue to have babies and accumulate mutations. Until so many genetic difference were accumulated the the two populations could no longer produce fertile offspring. That tipping point occurred 25-30 million years ago in Africa.
http://www.livescience.com/32029-oldest-monkey-fossil-found.html

2    Even if they would have children, then these children would be
  brothers and sisters right, which means they cannot have sex to
  regenerate their children?

No reason why not? Evolution does not care about dead babies or morality. Only humans do.

3    They say that humans and monkeys have a mutual ancestor, does
  that mean that a certain brother's family became monkeys and the other
  brother's family became human?

Not exactly. Ape and monkeys have a mutual ancestor. Let say 31 millions ago, there might have been a family of pre ape-monkey. Said family might have had two brothers. Then 1 million years later, the descendants of one brother might have been come apes while the other become monkeys.

If humans and monkeys have a mutual ancestor, then how come humans and monkeys are so different in terms of intelligence, hygiene, clothing?

Well the last common ancestor was 30,000,000 years ago. 30 million years is a long time. The average life span in the us is about 75 years. The human species is only 200,000 years old. Domestication of dog only 25,000 years.

They say humans lost our fur because we don't need it anymore, but how come we still need cloths to wear to protect us from cold?

Well humans evolved from homonids who evolved on the Savannah of Africa. Nice and warm. 5 million years of evolution to survive in a place where the danger of death by heat stroke was real. Humans only left africa about 60,000 years ago. Only left the tropics and ventured into higher latitudes of asia and europe 20,000 years ago.  https://genographic.nationalgeographic.com/human-journey/
Just not enough time to evolve fur coats.

Why do humans have to brush our teeth, cut our nails, use toilets and work for our food and drinks, while any other animals don't?

Civilization. And the fact that you don't want to stave to death once you lose your adult teeth. And animals do clean and groom themselves. Cats, ape, monkeys, birds and dogs.
Why do men and women have those specific features that make a man a man and a woman and woman? Why do women have to give birth and not men? Why do men have more facial hair growth and are built stronger than woman (while male and female chimpansees (our closest ancestors) both grow facial hair Why do men grow facial hair?)? Some people say men have more facial hair growth and are built stronger because they used to hunt (why did men hunt and not women?), but some say men hunt because they have more facial hair and are built stronger. Wouldn't it be a circle reasoning?

Sexual dimorphism. Most animals have it. In fact the sexual dimorphism in human is rather small only about 10-15%. Sexual dimorphism in gorilla for example is nearly 260% where males gorilla range between 350 pounds (160 kg.) and reach 400 pounds (181 kg.), while females only about 155 pounds (70 kg.) and much less muscular. http://anthro.palomar.edu/primate/prim_7.htm
The question you should ask is not why men are stronger than women. Most male apes are bigger and stronger than female apes, most extremely so. The question you should ask is why women are nearly as strong as men. Why is sexual dimorphism in humans astonishingly small. The gibbon is one other ape that has such small dimorphism. The interesting thing between human and gibbons, both species are mostly monogamous. ie on average one male does not physically dominate all other males and mate with all the females in the tribe.

Why do human male and female look different compared to other animals? Why do human individuals look different from each other, but

all other animals look like each other (geometrically)?
  Because you are human. I am sure to other animals all humans look alike. In birds the difference between gender is very obvious. Males have one plumage, different colours and feathers. While females have another. In lions and dear and asian elephants, walrus, elephant seals and narwhals, the difference between males and females are also very obvious.

Look at dogs, cats. The variation in dogs far exceeds that in humans.

Could it be possible that we relate humans to animals, because we associate animal behavior with human behavior due to our human

reasoning (which we can't help of course)? But human and animal
  behavior that look similar, does not mean that they have the same
  meaning right?
  The difference between animals and humans are a matter of degree.
Does 'survival of the fittest' mean the following?: Humans have finger nails and a protruding nose, because animals that didn't have

nails or protruding noses are extinct?

No. Survival of the fittest also have the aspect of context. A fish is vastly more fit in the sea compared to a human. A bear is vastly more fit than a weaponless human on a river side.

Why do humans have a chin, curly hair, eyebrows, lips and facial hair above the lips while monkeys don't?

They do. they also have fur.
Why do humans have this specific hairline (separation line between hair and skin)

No idea what you are asking.
Some human emotions such as guilt and fear sometimes result in not
  doing anything at all, but isn't that evolutionary a disadvantage?
  Humans lived in tribe. In fact we evolve from an animal that lived in tribes. A lone homonid on the open savannah was easy food for a lot of animals. I have a strong suspicions that there was immense selection pressure for individuals who stayed with the tribe, and had behaviors that maintained the tribe.
Humans have so little fur compared to monkeys. Which means that at
  some point, starting from the ancestor, the next generation lost more
  and more fur. At some moment there was so little fur left that
  generation felt cold and wore some clothing? But what about their
  naked parents who have about the same amount of fur?

Cause the naked parent lived in the tropic of Africa. While the clothed offspring lived 40,000 years later in the higher latitudes of Asia and Europe, after 1000s of years of slowly moving northwards.

Why are there humans and monkeys, but not intermediate forms that
  slowly changed from the ancestor to human or ancestor to monkey?
  Because they would have human characteristics but also monkey
  characteristic which are still there nowadays?

Because nobody can sit still. Evolution continues to happen. Even the intermediate forms will continue to change. Why do you think apes are?

Why do we have puberty, and why don't boys already have facial hair
  when they are kids (for warmth)?

Because all mammals have puberty. It takes resources to grow up, become an adult and have your own babies. Childhood is the time to accumulate puppy fat and learn skill (even lions and wolves need to learn how to hunt). The question that should ask is why human childhood is so long.

They say humans find a lover because, evolutionary speaking, they want
  to produce children. But how come some couples choose not to have
  children?

Some couples are infertile. Development might not have gone right, so one member or both are either completely infertile or both have reduced fertility. Also sometimes it is better/more successful to help a sibling raise their children and have your own. Many reasons.

Re "... between human and gibbons, both species are mostly monogamous."  Huh?  Don't know much about gibbons, but most humans sure aren't, unless forced to be by legal or religious pressure.

Even in cultures that  today still legally allow polygamy... most people are monogamous. Most guys are not  wealthy enough to maintain more than one woman and her children. And most man are not such a great catch that the woman is willing to be a sister wife and share his fortune. Only the wealthy and powerful ever practice polygamy in human cultures.

Well, you pretty well prove my point when you say the wealthy and powerful practice polygamy when they can, which makes it a matter of resources/opportunity rather than an inherent monogamous nature :-)  But I am not talking about maintaining women & children (which is economics), but about sex.  For instance, studies showing that various percentages of children weren't actually sired by the legal parent, or the common practice (in the West) of serial polygamy through divorce and remarriage.

And can you name a human culture where 95% of the men fail to have children. And most women are in married and have children only with the remaining 5% of men. That is what a polygamous species is like. Most males fail to breed. Most offspring are fathered by a very few males. I don't understand your point. There still places in the world where polygamy is legal both in the court and religion. And even then most people are monogamous in those cultures.

We are obviously using different definitons of the word 'monogamous'.  I prefer the dictionary definition of  "having only one mate".  You seem to be defining polygamous as a very extreme case, while in fact very few species are truely monogamous.  The reality seems to be that where they have a reasonably free choice, humans make a pretense of social & serial monogamy, while a significant number have sex outside that relationship.  Also realize that among humans, reproduction is only a secondary factor in sex.

I guess I am seeing the word from a biological perspective. Human are by and large a mostly monogamous species. Most of the males do get to father children. Monopoly of female fertility by high status males is not as absolute as say elephant seals.


text:
How Dark skin protects humans in sunnier climates?
According to Physics, Black Body absorb all incoming light reflect nothing when compared to White body. This phenomenon is called Black-body radiation. So Melanin should turn your skin into white for protect the body from harmful rays in sunnier regions, that is not happening in Biology of Human Beings.
This is why Most of School Uniforms are specifically white on Saturdays (Because of intensity of sunlight is more on that day)
Then How Dark skin protects humans in sunnier climates?
My Question is different from this question because I mentioned physics subject also in my question.

Also, Saturdays are in no way any different from any other day of the week in terms of average sun intensity. Where did you even hear this???

I suggest that you do some more of your own research on the topic to learn more about the issues/errors in your arguments that led you to ask this question in the first place. Then, you can try to edit this question to improve it's quality to avoid having it closed.

Melanin is an antioxidant and absorbs free radicals associated with UV rays, iron, metals etc. This explains why anemia correlates with melanin.
Wetter climates have more diseases and free radicals, which is why moister climates are melanizing as well.
Melanin can potentially crowd in the body's own oxidants, such as testosterone, because it removes external oxidants.

Thanks for your contribution...can you add some references to your answer? We always appreciate cited references for everything on the site - it helps individuals who are less familiar with the subject area read more about the question/answer.

source: Stack Exchange

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

sort: votes


text:
Why honey bees built hive in perfect hexagonal shape instead of irregular shape?
Why honey bees built hive in perfect hexagonal shape ?
Due to Hexagonal shape, I can go near without any anxious or fear.( Apart from Honey bee's stings)
From this Question, Most creatures look like or tries to look like irregular to fear the other creatures to attack.

What @iayork said. In plain English, they are making circular tube cells, but when placed so closely together, they form hexagons. Look at bubbles. Alone, they are round (perfect spheres), but the more bubbles are packed together, the forms will take on angled geometrical shapes, including perfect hexagons. It has nothing to do with fear, as hives are usually hidden.

With reference to the honey bee cells how could a slight modification in structure provide a survival benefit. If two individuals were starving would the person who was given a few milligrams of extra food have a survival advantage?

Why honey bees built hive in perfect hexagonal shape ?

Honeycomb cells (not the hive or the honeycomb itself) are hexagonal, in some species of bees but not all.  The regularity of this shape has puzzled people for a long time, and Darwin (and others before him) addressed the reasons for it.  Darwin did a series of experiments with bees, and summarized his results in Origin of Species.  You can search for "hexagon" in the linked text for his long explanation, or read the (still long) summary 'Evolution of Honeycomb on the Darwin Correspondence Project, but the short explanation is that it's the most efficient way to pack cells without wasting wax, and Darwin identified a bunch of intermediate (less efficient) cell structures in various bee species that supported his hypothetized mode of evolution.

Thus, as I believe, the most wonderful of all known instincts, that of the hive-bee, can be explained by natural selection having taken advantage of numerous, successive, slight modifications of simpler instincts; natural selection having, by slow degrees, more and more perfectly led the bees to sweep equal spheres at a given distance from each other in a double layer, and to build up and excavate the wax along the planes of intersection. The bees, of course, no more knowing that they swept their spheres at one particular distance from each other, than they know what are the several angles of the hexagonal prisms and of the basal rhombic plates; the motive power of the process of natural selection having been the construction of cells of due strength and of the proper size and shape for the larvae, this being effected with the greatest possible economy of labour and wax; that individual swarm which thus made the best cells with least labour, and least waste of honey in the secretion of wax, having succeeded best, and having transmitted their newly-acquired economical instincts to new swarms, which in their turn will have had the best chance of succeeding in the struggle for existence.

The bees don't make hexagonal cells. This paper shows how bees construct multiple cylindrical tubes which are then molded based on temperature and contact with other cells.

As you can see, the cells start off cylindrical (day 0) and transform into the common hexagonal shape by day 2. The paper also goes into details of the physics involved (it is in a physics journal). I strongly suggest reading the paper if you wish to go more in depth.

in "the origin of species" pages 178 and 179, Darwin has stated that if a bee could build a cell slightly more hexagonal than the other bees then this bee would have a survival benefit since a perfect hexagon is the most economical structure in storing the greatest amount of honey with the least amount of wax, but unfortunately there is nothing in his analysis that proves the point. He concludes on page 179 that the saving of wax by largely saving honey would be an important element in the success in any family of bees.
The problem with that analysis is that a slight modification of structure in this case a slightly more regular hexagon cannot provide a survival benefit as the two structures are almost identical.(the old cell and the slightly modified cell)

The problem with that analysis is that a slight modification of structure in this case a slightly more regular hexagon cannot provide a survival benefit ...  This is not a site where your unsupported opinion is considered a useful answer. Please supply references for this (that don't come from the deliberate liars associated with "intelligent design" and other religious dogmatists).

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

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


text:
Facultative anaerobic organism
While I was studying Cellular Respiration: Harvesting Chemical Energy, I found this question:

An organism is discovered that consumes a considerable amount of sugar, yet does not gain much weight when denied air. Curiously, the consumption of sugar increases as air is removed from the organism's environment, but the organism seems to thrive even in the absence of air. When returned to normal air, the organism does fine. Which of the following best describes the organism?
A) It must use a molecule other than oxygen to accept electrons from the electron transport chain.
B) It is a normal eukaryotic organism.
C) The organism obviously lacks the citric acid cycle and electron transport chain.
D) It is an anaerobic organism.
E) It is a facultative anaerobe.
Answer: E

I wonder why the answer is E not D. How can I know that it is a facultative anaerobe? Do anaerobic organisms die in air?

Strict anaerobic organisms cannot proliferate when air is present. Facultative on the other hand can.

But he didn't say anything about proliferate

I think "does fine" implies proliferation, but I agree the wording could have been clearer.

There are organisms with anaerobic metabolism that tolerate oxygen: aerotolerant anaerobes.  "Anaerobic" refers to the metabolic system.  You cannot be sure of oxygen tolerance based solely on metabolic system.
Factors influencing the tolerance of anaerobic bacteria to oxygen
Here is why this is a facultative anaerobe.
This organism does not gain weight when denied air.  One concludes its metabolism is less efficient.

Curiously, the consumption of sugar increases as air is removed from
  the organismʹs enviroment

Anaerobic metabolism uses sugar less efficiently than aerobic metabolism in organisms that can use both methods. This means oxidative metabolism is the preferred method.
So:  this is a facultative anaerobe because it can get by using anaerobic metabolism, but two pieces of information show that for the organism, anaerobic mode is less efficient than aerobic metabolism.  Brewers yeast is such an organism.

My answer is correct, since i only talk about obligate anaerobes. Just as described in the book in the link.

I edited your answer for the reasons specified in the edit history. If you disagree with this change, please feel free to rollback.

Yes, (obligate) anaerobes die in the presence of  oxygen (at atmospheric levels). They do not have the detoxifying enzymes that convert toxic metabolic products such as hydroxyl racials or superoxide anions into nontoxic H2O or O2. These enzymes present in aerobic and faculative anaerobic organisms are superoxide dismutase, peroxidase, among others.
Reference:
a Hentges DJ. Anaerobes: General Characteristics. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996. Chapter 17. Available from: https://www.ncbi.nlm.nih.gov/books/NBK7638/


text:
How can cancer preventing genes from animals be transferred to humans?
I recently read this non-peer reviewed article that states that the prevalence of cancer in crocodiles or elephants is really low, much lower than humans.  It is said below

A team of researchers in the US looked closer, and found an abundance of a gene called TP53. This gene is known for its ability to repair damaged DNA and thus halt the spread of cancer, and it's some 20 times more common in elephants than it is in human beings. It appears elephants have developed more of these genes as they've evolved, in part to protect calves born to older mothers
"These findings, if replicated, could represent an evolutionary-based approach for understanding mechanisms related to cancer suppression," says the report, published in the Journal of the American Medical Association.
Naked mole rats are even more miraculous - they never develop cancer, even when scientists try and induce it artificially. What appears to be happening, at least according to a recent study, is that the mole rats are using natural mechanisms to clamp down on the spread of cancer and fight back against the mutation.

Question
So why is it that these genes cannot be transferred from animals to humans? Maybe when the baby is at fetus stage?  What are the current problems/limitations and if possible, how would scientists transfer these genes?
My logic is that since mice and elephants are both mammals,  it should not be too hard to achieve this.

The link is https://www.sciencealert.com/these-animals-can-t-get-cancer-and-scientists-think-they-could-hold-a-cure

While this research is interesting and might help curing cancer at some point, it's not a ground breaking revelation.
The gene in question here is TP53, coding for the very-well known tumor supressor protein p53. Humans do have this gene, but apparently elephants hav acquired multiple copies of it (~20) during evolution and that might explain why they don't get cancer so easily.
The problem of testing this is not a technical one. Using modern genetic engineering methods it should be fairly easy to multiply the gene in human or mice embryos, or introduce the additional variants from the elephants. Someone might already be planning to do that in mice.
For use on humans however, this is highly unethical. Without proof that these gene copies actually prevent cancer (and one observational study is not a proof), you can't just use a new medical treatment. Secondly this treatment would require genetic modification of an embryo (because its actually cancer prevention, not acute treatment) and that is illegal almost everywhere on earth (even genetic modification of somatic tissue for cancer treatment is just now becoming an experimental therapy).

Putting All moral issues aside, what would be the answer to by question?

There may be pleiotropic effects of these genes that are damaging to humans.  So, for that reason, it is a technical issue.  It is an ethical issue largely because it is still a technical issue and would require experimentation (on mice).

@user35897: Have a look at this article: http://www.nature.com/news/2009/090520/full/news.2009.493.html. Cancer suppression might be just one effect.


text:
What kind of lichen is it?
I found that in a monastery garden in Czech Republic this winter. I tried to search it on the internet but unfortunately I didn't find it.

I'm pretty sure that it is a cup lichen from the genus Cladonia. A probable species is Cladonia pyxidata, which is relatively common across Europe. My lichen knowlegde is rusty though, and Cladonia is rather species rich with several species that are relatively similar.

(C. pyxidata, pic from http://fungi.myspecies.info/taxonomy/term/4557/media)

Cladonia is right for sure. Pyxidata I doubt. Impossible to be sure from a picture anyway.

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


text:
Looking for the closest example of life forms similar to some mathematical patterns

Caveat: this is my first question here, it is quite interdisciplinary, but I hope to be in the correct place to ask. I am a user of Mathematics Stack Exchange since some years ago, and this question is related with some questions there (here, here whose general formula is discussed here and here).

Context: I am preparing a mathematical paper regarding a new family of dynamical systems (if you are not familiar with the concept, simplifying the idea it is a mathematical formula in which starting from a initial value, once applied to the formula the resulting value is again applied to the formula, and so on, finally the values are plotted and eventually a -sometimes interesting- pattern emerges) whose attractors (plotted patterns) in the present case seem to have unexpected pareidolic properties.
Basically some of the patterns generated by these systems show similarities with some structures of invertebrate life forms, specially insects, marine jellyfish, and zooplancton and also due to the patterns of the accumulation of points, also with life forms presenting bioluminescence properties.
For each interesting pattern so far I have tried to find the closest life form example, to compare both the model and the life form patterns.
So my target is including in the paper the closest life form similar to each mathematical pattern. Initially it is just a pareidolic coincidence, but it might be interesting if the mathematical formula can resemble models of some organic structures.
These are the ones I have been able to gather, both the model and the closest life form I found.  The pictures I am using at the right side of and below the images are just for the sake of completeness (they belong to their respective owners, I do not own them, if there is any problem I will remove them, so just please let me know). The formula can be verified at the MSE links I have added at the beginning of the question and the Python code to generate them is in this link (please feel free to use it and modify it). The questions are after the examples (click to enlarge):

Patterns similar to thorax and abdomen of Bembicini wasp, head and body of Turritopsis dohrnii (inmortal jellyfish) and Tardigrade limbs:

Patters similar to Drain fly:

Patterns similar to Acherontia atropos (thorax and abdomen and main proportions of body, specially the patterns near the head are interesting):

Patterns similar to Ctenophora (down left) and Mnemiopsis_leidyi (down right):

I would like to ask the following questions:

Are there better examples of life forms for the models I am showing above (1,2,3,4)? If somebody could provide examples or specific names would be very appreciated.

Are there papers or references in the Biology field regarding mathematical models of this kind?

In the case I would like to add images from internet in the paper, I know that in the case of Wikipedia there is a standard way to add the reference in the bibliography. Apart from Wikipedia, are there other sources of images which I could use without problems in a paper (thinking about the kind of life forms that are the target of the patterns)? Thanks in advance.

I have tried to add the tag "mathematical-models" but it is converted into "theoretical-biology". Tried to correct it but it seems I can not do it for some reason.

I think those tags have been merged (with [tag:theoretical-biology] as the main one), which is probably why you cannot change to it.

The question has nothing to do with mathematical modelling or theoretical biology anyway (nor does it have much to do with the other tags).

The question is entirely based upon a personal visual appreciation. I am hence voting to close as opinion-based.

@Remi.b I definitely think it should be open, since Mathematical modelling of biological patterns (using semi-mechanistic models or phenemenological  models) is a valid topic in Mathematical biology. The background to this particular Q could be stronger though (eg links to the research field).

For the second subquestion (papers or references of similar models), it could be useful for you to look at the books by J.D Murray for inspiration; Mathematical Biology, vol I & II. A pdf of volume 1 can be found here, and the second volume here. Even if they are a complete of years old (last edition from 2002 I think) they provide a really nice background to the field of Mathematical biology, and he has quite many examples on pattern formation of different kinds. I don’t remember if dynamics systems are included per se though.
However, several chapters include reaction diffusion systems and wave models, to model e.g. coat/fur patterns and wound healing. It is also packed with references, so you should be able to find lots of classic citations that might be useful.
Some chapters you might find interesting:

Reaction Diffusion, Chemotaxis and Non-local Mechanisms
Travelling Waves in Reaction Diffusion Systems with Weak Diffusion: Analytical Techniques and Results
Animal Coat Patterns and Other Practical Applications of Reaction Diffusion Mechanisms
Mechanical Theory for Generating Pattern and Form in Development
Bacterial Patterns and Chemotaxis

I've mostly looked at population modeling in his books, so I'm not very familier with these topics myself.

thanks for the references! indeed the classical reaction difussion was included in my readings regarding the characterization of these systems. This is very useful.

Good. Sorry for not being able to help more with the specifics. There are probably also more recent books that might be more relevant, but Murray provides a nice overview for those that come from a mathematical background. Since it requires quite alot of mathematics it is probably rather inaccessible for many with a biological background.

hi again, I managed to publish recently an article at Springer Nature CS regarding this matter, thank you for taking time to guide me to the important bibliography of J.D.Murray. Hoping you the best, cheers! https://link.springer.com/article/10.1007/s42979-019-0028-6?fbclid=IwAR0idtC1Lrf2PNWDWImoJi_BdagcUzxcC7YchyOcG-WLuvdK0QWbbhwEw44

@iadvd Great news and I'm glad to hear. I will download and look at the paper later on. Fun to hear that Bio-SE input has made its way into a published paper as well even if it was rather vague in this case). I guess it would be really cool if we eventuelly started to find mentions/references in papers to Bio-SE Qs (or Stack Exchange in general), but we are probably not there yet.


text:
What is the effect of non-vaccinated people on vaccinated people?
Many times have I heard that anti-vaccine people are dangerous even to the vaccinated population. Is that true? If so, how can it be? People say that germs will attack them, and soon they would eventually grow and spread even toward general population which actually got its vaccines.
I mean it's so counter-intuitive: if I'm vaccinated even when disease will spread I shouldn't be in danger.

I'm upvoting because this is an important question. There are problems with the assumptions (if i'm vaccinated even when disease will spread I shouldn't be in danger), but that's exactly what makes it important.

The only way to prevent a species to evolve is by extinguish (eradicate) it. If some people continue to carry a disease, those germs can evolve into a new, more resistant, more pestilent form that could attack even the immunized individuals.

1st point: I feel that we should rather put the blame on the inefficiency of the vaccine, instead of the people who refused the vaccine. The vaccine is like a shield or a firewall - it does matter how strong the attack is, but if the shield fails to prevent the disease, the developers of the vaccine should't claim 'hey, you were surrounded by too many unvaccinated people', but instead improve the vaccine. 2nd point: not all diseases are transmitted only from one human to another. Plague was transmitted by rats. Should we blame the rats for refusing the vaccine?

@AliceD I'm not sure what the guidelines are for moving a discussion to chat, but the recent comments here don't seem to be directed at improving the question or explaining a vote.

@Newtonfan01 What characteristics of a germ corresponds to "the strength of attack"?   Is it just the quantity of organisms?

Putting aside people who do get vaccines, there are some people who can't get some vaccines and rely on everyone who can getting the vaccine and ideally eradicating the disease altogether, or, second-best case, not contracting it themselves so they can't give it to anyone who can't get the vaccine

Would you like us to disregard the ideas which anti-vaxxers spread?  Ideas spread far more virulently than any disease.  The battle over the idea of vaccination vs the idea of avoiding vaccinations is a much more brutal one than the mere biology of disease.

the more it can spread the larger chance it can mutate and become dangerous to those who are vaccinated for the first unmutated version.

Vaccines do not protect 100% from the disease. When enough people are vaccinated the disease outbreaks die out quickly. The problem is that when not enough people are vaccinated, the diseases do not die out, but linger in population. So, you keep bumping into sick people, and eventually get sick too. That's the simplest explanation I could come up with. If you're not satisfied, I'm afraid some differential equations will be in order.

Biology is rarely black or white, all or nothing. Protective immunity is generally not an on/off switch, where from the moment you're vaccinated you're infinitely resistant for the rest of your life. You shouldn't expect that, having received a smallpox vaccine, you could have billions of smallpox viruses squirted directly into your lungs and shrug it off without noticing.
Given that (fairly obvious) fact, you should immediately think of scenarios where vaccinated people are still at risk of disease following exposure to unvaccinated people. What about older people who were vaccinated 20 years ago, 50 years ago? What about people whose immune systems are slightly weakened through lack of sleep or obesity or stress? Any of these vaccinated people might well be protected against a brief encounter, but not against, say, being in an airplane seat for 18 hours beside an infected child shedding huge amounts of virus, or caring for their sick child.
It's all sliders, not switches. You can have a slight loss of immunity (4 hours sleep last night) and be protected against everything except a large exposure (your baby got infected and won't rest unless you hold him for 8 hours). You can have a moderate loss of immunity (you were vaccinated twenty years ago) and be protected against most exposures, but you're sitting next to someone on the subway for an hour. You may have a significant loss of immunity (you're a frail 80-year-old) and still be protected against a moderate exposure, but your grandchild is visiting for a week.

Good answer. See my answer for some data.

I think one point you can add to this is that unvaccinated people who host a virus allow it to propagate and evolve, which can undermine the efficacy of the vaccination.

You could add that, depending on the disease, some percentage of the vaccinated may show a low immune response and will never develop immunity, although vaccinated.

to restate Blackthorn, unvaccinated people also provide a place for the disease to reproduce and potentially mutate into a new strain that the vaccine does not help with. This happens constantly with the flu.

I like this answer, except for the "(fairly obvious)" part.  It sounds condescending, and it is not something that is obvious to everyone.

I think it's also worth mentioning that there exist groups of people that can't be vaccinated for legitimate reasons (allergies, immune deficiencies, etc.). For them even 1 unvaccinated ill person can be deadly.

@Beska It's not obvious that a vaccine is not a perfect defense against a disease? Sorry, but I think the typical person off the street would say "never say never."

@corsiKa I disagree, as I suspect that many people think that's how vaccines tend to work...but as I have no evidence either way to support/refute it, I'll just leave it at that.

@BlackThorn viral escape mutants are rarely observed in an effective vaccine, and generally are not the public health challenge they seem to be in fiction. They are an issue during vaccine development. Influenza variation (and subsequent vaccine failure) is due to recombination in non-human hosts. The unvaccinated certainly cause harm to the vaccinated, but this is not a significant mechanism for that harm.

@de-novo Influenza variation (and subsequent vaccine failure) is due to recombination in non-human hosts This part is not correct; you've confused the antigenic drift with shift. It's not clear how much influenza vaccines contribute to antigenic drift in humans, but it's probably not a major factor . In general I agree with your comment, but influenza is a complicated story in many ways (too complicated to deal with in a comment).

@iayork certainly both shift and drift both lead to viral escape. I was trying to emphasize the fact that the virus has non-human reservoirs and the decreased effect human vaccination has on that virus because of the non-human reservoir. Your right. to complicated for a comment :)

Shift has happened 4 times in the past century, drift happens every year.  It's simply wrong to say that "Influenza variation (and subsequent vaccine failure) is due to recombination in non-human hosts".

I think that herd immunity should be mentioned... as it impacts the number who are infected and standing next to you.

Since 2000, in the United States alone, there were 16 reports of outbreaks or groups of outbreaks where the outbreak started with an initial case in an unvaccinated individual and resulted in disease in previously vaccinated individuals. The epidemiology of pertussis is a little different, and transmission happens in many cases apart from a clear outbreak, but there are several documented pertussis outbreaks that led to disease in vaccinated individuals as well. This JAMA report provides a good summary.
Herd immunity is important, especially in highly contagious diseases with no significant non-human reservoir, e.g., measles and pertussis. @iayork's answer is correct that vaccination is not an on/off switch. About 15% of measles cases in the US involve vaccinated individuals, and these have all been the result of transmission that started with an initial unvaccinated case (see previous reference).
These are bad diseases. They can cause serious illness. Half of infants who get pertussis need care in the hospital. For measles, 25% of all cases involve hospitalization. For both, life long disability (deafness, brain damage) and death are real possibilities. 1 in 100 infants with pertussis die, 1-2 in 1000 measles cases die. The harm intentionally unvaccinated people cause to vaccinated people and people who can't get vaccinated (because of their age or other health problems) is real and well documented.
Edit:
In light of another answer and some comments, I'm adding a couple paragraphs putting vaccination in context with other strategies for prevention of infectious disease.
Relevant to this question, as is clear from the epidemiological data discussed above, vaccines are not 100% effective. Some vaccines are more effective than others. Measles vaccine, for example, is in the mid to high 90s. Flu vaccine effectiveness, depending on the population and year, can range from the 40s to the 80s. You can read about vaccine effectiveness in the CDC pink book, Epidemiology and Prevention of Vaccine-Preventable Diseases.
Other strategies for preventing infectious diseases depend on the great diversity of host/pathogen interactions. A few things are generally useful, and often effective. Wash your hands, wear a condom, and stay home when you have a fever. There is no good data on the general advice to stay home when you have a fever, but quarantine is effective for specific illnesses, especially in concert with vaccination and other preventative measures (see the CDC pink book). Limiting the isolation and sedentary behavior associated with staying home to cases where there is a fever has biological plausibility and minimizes the negative immune and other health effects of those behaviors (see Cecil Medicine, Chapter 288).
Along with vaccines, each of the strategies mentioned in the previous paragraph helps protect the individual who uses them as well as other people. So they are good for you and the people around you. You can practice all of them. I'm confused, but not surprised, when the effectiveness of some other strategy is used as an argument against the use of any of the others. You can compare the measured preventative efficacy and effectiveness of each strategy, and come to the conclusion that vaccines generally give the best results (both on an individual and population level), but I'm not sure why, for example, you would decide not to wash your hands because you got a particular vaccine, or not to get vaccinated because you washed your hands.

Can you expand on people who can't be vaccinated? You mention them in the last paragraph and I don't want to just add another very similar answer. Though the amounts of people who can't get vaccinated for medical reasons isn't great (roughly a 1000 children a year in the US states I checked) that's still some and probably doesn't cover children who just have delayed vaccinations for health reasons which can also be a problem.

@DRF that's a reasonable answer in itself. Feel free to add it. You start by looking at the JAMA article I linked (it's on PMC, so no paywall). Table 1 includes numbers on non-medical exemptions. If you subtract unvaccinated cases from unvaccinated with non-medical exemptions, you'll get the number of cases in individuals who couldn't get vaccinated (prior to getting measles). It wouldn't be a bad idea to include a little bit on what level of vaccination coverage is required to have herd immunity.

@DRF sorry, CAN start, or COULD start. You're free to answer however you like; I just wanted to give you some helpful data :)

I DID start but it's a longish article.:) Thanks for the pointer.Actually I suppose it's not all the longish but still I need to read and digest it first.

I'm afraid I don't understand "For measles, that number is 25%, but for all cases." which seems self-contradictory. Could you clarify?

@DennisWilliamson it's a different denominator. For pertussis, infants get severe illness much more frequently. Half of all infants with pertussis need to be hospitalized, but very few otherwise healthy adults. For measles, 25% of everyone (all cases) ends up needing hospitalization.

+1 for mentioning herd immunity

The toughest part about "herd immunity" (a favorite talking point of an anti-vacc aquaintance of ours who's in the healthcare field and therefore really ought to know better) is knowing that their kids are wandering around unvaccinated, are therefore at higher risk of infection and death in the event of an outbreak, in which case if they died we'd have to go to the funeral/memorial/whatever, and knowing full well I can't say, "Sorry you counted on herd immunity. Next time COUNT BETTER!".

@BobJarvis herd immunity is relevant for both the vaccinated and unvaccinated populations. When vaccination coverage is above the predicted threshold for herd immunity, we don't get outbreaks with disease in vaccinated individuals. When it's below the threshold, you get outbreaks (and often disease in both groups).

Something which may help is a model.  There is a standard model based on a key number called R₀, the basic reproductive number.  This is a highly boiled up number which indicates how many uninfected people will be infected by a single infected individual.  Trivially, if R₀>1, the disease will spread through society, and if R₀<1, it will vanish because each infected generation infect fewer new people each generation.  R₀ is basically derived from the number of contacts a person can make before showing enough symptoms to sequester them at home, times the chance of any interaction transmitting the infection.  The longer the incubation period and the more infectious the disease, the higher R₀ is.
It's a massively massively boiled up model.  You can look to science for more accurate models which account for all sorts of features.  However, it is a good enough model to demonstrate a concept called herd immunity.  Herd immunity decreases the odds of a contact with an infected person spreading the disease.  After all, a vaccinated individual is far more likely to go unaffected.  This is typically modeled with an extra factor S, such that the reproductive rate of the disease is R₀S.  If q is the vaccinated portion of the society, then (1-q) is the number of succeptable people, so the reproductive rate is R₀(1-q).
Now remember, if the reproducitve rate is greater than 1, the disease flourishes.  If it's less than 1, it dies off.  Having a strong vaccinated base has been shown to be a very effective way of keeping that reproductive rate down.
Consider, as an example, Measles.  Measles is considered to be an excellent disease for demonstrating herd immunity.  Its R₀ is somewhere between 12-18, meaning each infected person is likely to infect 12-18 people before getting quarantined.  If a populus is 95% vaccinated, then the reproductive rate drops to R₀*(1-.95), which is somewhere between .6 and .9.  This means the disease will die out if the population is that vaccinated.
Again, modeling based on the basic reproductive number is considered to be a gross tool, but it is effective at demonstrating the risks associated with insufficient vaccinations.  If there is a large enough unvaccinated pool to let the disease flourish, everyone is exposed to the disease every day as it runs rampant in the society.  Vaccines are awesome, but they are not magic bullets.  You can still get diseases after being vaccinated, it's just much more rare (the term to look up is Vaccine Efficacy).  The more you're around a disease, the more likely it is that you just get unlucky.  Even a vaccinated person benefits from a reproductive rate less than 1, so that the disease never flourishes in the first place.  The less effective a vaccine is, the more one is dependent on a high rate of immunization to drive the reproductive rate down below 1.
Also, another strong argument for vaccination is the presence of immunocompromized individuals.  Many individuals cannot receive vaccinations for one medical reason or another.  For instance, immunizing someone with HIV is a tricky business which I would refer one to a doctor for more information.  Those on transplant lists may be advised against receiving vaccinations.  These individuals are entirely dependent on the so-called herd immunity effect to insulate them from these diseases.  As the reproductive rate for a disease gets closer or above one, it becomes hard to protect these individuals.

Think of every human being as being a walking petri-dish, full of growth medium. When you grow a large colony of micro-organisms, you are allowing that population to experience a larger number of mutations. Every mutation is one more potentional strain that can beat the defenses of our immune systems, even those provided by vaccines. So, if you don't get vaccinated, you are potentially providing safe harbor to the micro-biological parent of the next vaccine-resistant/anti-biotic-resistant super-flu.
This same principle is why large super farms are so dangerous: huge numbers of animals provide more opportunities for micro-organisms to experience mutations that allow them to infect more resistant hosts. The fewer hosts that a micro-organism  can infect, the lower the number of opportunities for mutation.
This is one facet of the issue, among those others have mentioned.

authors: Bob Jarvis - Слава Україні


text:
Why the SNPs from the earliest human haplogroups are missing in people outside of Africa if they are infact the descendants of it?
The SNPs M91, P97, M31, P82, M23, M114, P262, M32, M59, P289, P291, P102, M13, M171, M118 from haplogroup A and SNPs M60, M181, P90 from haplogroup B are missing in people without recent African ancestry. Considering these are the earliest humans in Africa, perhaps someone could explain genetically why they don't exist in non African populations?

Sources:
Klyosov, A. A. (2011a). The slowest 22 marker haplotype panel (out of the 67 marker panel) and their mutation rate constants employed for calculations timespans to the most ancient common ancestors. Pro- ceedings of the Russian Academy of DNA Genealogy
Cruciani, F., Trombetta, B., Sellitto, D., Massaia, A., Destro-Bisol, G., Watson, E., et al. (2010). Human Y chromosome haplogroup R-V88: A paternal genetic record of early mid Holocene trans-Saharan con- nections and the spread of Chadic languages. European Journal of Human Genetics, 18, 800-807.
Simms, T. M., Martinez, E., Herrera, K. J., Wright, M. R., Perez, O. A., Hernandez, M. et al. (2011). Paternal lineages signal distinct genetic contributions from British Loyalists and continental Africans among different Bahamian islands. American Journal of Physical Anthro- pology, 146, 594-608. doi:10.1002/ajpa.21616

What do you mean by "Considering these are the earliest humans in Africa"? Who are "these"? Do you mean "Considering that the earliest humans arose in Africa"? And please provide links to the papers you quote and tell us whether any explanations are suggested there.

Without reading the link papers, I would assume that some african lineages carry these haplogroup. Not all. If this is true, there is really nothing surprising. If it is still surprising to you, can please explain why?

@David  honestly this question is not my own. I didn't find the papers my self, I only used google scholar to get some of the pdf.
The guy seemed adamant that the lack of these certain nucleotides were evidence for there being essentially a species discrepancy, with Asians and Europeans never having an ancestral background commonality with subsaharan Africans. A denial of the Out of africa theory.
I am just interested in how close or different, any of your arguments would be with the ones which I had posited in opposition.

Unfortunately, although this may be interesting, you really need to do the background research yourself if you hope someone here will take the time to consider your question. Of course, there may be someone familiar with the story, but the response so far isn't too encouraging.

It looks like the information presented in the question is not reliable.  Taking the first two Y SNPs mentioned, M91 and P97, it says these "are missing in people without recent African ancestry."  Yet Wikipedia says that M91 and P97 are defining mutations of haplogroup BT and that

Macrohaplogroup BT has been found in populations on every continent, since prehistoric times. It is the progenitor clade of the paternal haplogroups B and CT.

This implies that M91 and P97 are present in "people without recent African ancestry" (excepting back-mutations), in conflict with the assertion in the question.
However, this view has apparently evolved a bit, as the "haplogroup A" article says:

A major shift in the understanding of the Y-DNA tree came with the publication of (Cruciani 2011). While the SNP marker M91 had been regarded as a key to identifying haplogroup BT, it was realised that the region surrounding M91 was a mutational hotspot, which is prone to recurrent back-mutations. Moreover, the 8T stretch of Haplogroup A represented the ancestral state of M91, and the 9T of haplogroup BT a derived state, which arose following the insertion of 1T. This explained why subclades A1b and A1a, the deepest branches of Haplogroup A, both possessed the 8T stretch. Similarly, the P97 marker, which was also used to identify haplogroup A, possessed the ancestral state in haplogroup A, but a derived state in haplogroup BT.[5] Ultimately the tendency of M91 to back-mutate and (hence) its unreliability, led to M91 being discarded as a defining SNP by ISOGG in 2016.[43] Conversely, P97 has been retained as a defining marker of Haplogroup BT.

So this indicates that haplogroup BT, which includes most or all men historically outside of Africa, does not reliably display mutation M91, but does display P97.  I'm not going to research all the other SNPs (especially since the three references don't seem to be very relevant), but I think this much indicates the assumptions of the question are not coherent enough for a good answer.

This clears up a lot.


text:
Im struggling to see how these are presynaptic terminals/knobs and not post synaptic

How are these presynaptic terminals ? The action potential is generated at the axon hillock and moves down the axon (in this case to the right) , then at the end of the axon should be axon terminals and presynaptic knobs. Shouldn't the dendrites shown here have post synaptic knobs with receptors for the neurotransmitters ?

The fibers in green are axons and axon terminals from other neurons, not the one colored orange.
Yes, there would be post-synaptic structures associated with these but those are not drawn in this cartoon.

The green ones you see are the synaptic knobs or presynaptic terminals of other neurons of which some lie on the surface of dendrite of the given neuron(Axodendritic) and some on the soma of the neuron(Axosomatic). Also please note that the synaptic knobs(green) on soma is not peircing it rather imagine it in 3d, where the synaptic knobs are coming from top, outside your book to the neuron making a synapse.


text:
DNA replication - 2 new strands or original (parent) and child?
this is my first time here, so go easy on me! I've been trying to find out more about the actual process of DNA replication. Specifically, I am wondering if, when the DNA replicates during cellular division, the result is the original DNA strand and a copy? Or is the original strand destroyed in the process and there are 2 child copies that are identical (aside from mutations) to the original?
I am pretty confident in the end-result, but maybe whoever answers can verify this for me too. My understanding is that the original cell itself is destroyed in the end, but the daughter cells are constructed from the substance of the parent's cell. The initial question will help clarify this process for me too, because I am curious if one of the two daughter cells has the literal DNA from the original, or if basically the entire original cell "dies" in the process and the two new cells are completely new.
Update (to demonstrate research effort):
I have learned how a helicase enzyme untwists the DNA and severs the hydrogen bonds between the nucleotide bases, then single-strand binding proteins bind DNA polymerase to the ends of the strand and begin molding, creating a complimentary strand for each side. It seems evident that half of the "original" is found in each daughter, and the DNA polymerase forms the other half. So, the original is still present, but not in its original form, which is why I'm not sure what the "official" diagnosis is. Is it a parent-child, or two children?

"It seems evident that half of the "original" is found in each daughter, and the DNA polymerase forms the other half." - Thanks for doing some self-research: looks like you found your answer! It's okay to write up an answer to your own question. However you still ask: "Is it a parent-child, or two children?" - as the answer you found shows, the answer as far as the DNA molecule itself is neither.

Thanks Bryan. I think the answer I'm looking for lies a little deeper, but maybe I don't know how to word it. Read my reply to Alex Reynolds' response and see if that helps you understand what I am asking. It may be that we don't actually know the answer yet, but maybe somebody that understands this deeper than I do can enlighten me.

Via: https://en.wikipedia.org/wiki/Semiconservative_replication

Semiconservative replication describes the mechanism of DNA replication in all known cells. It derives its name from the fact that it produces two copies of the original DNA molecule, each of which contains one of original strand, and one newly-synthesized strand. (emph. added)

Thanks for the feedback. I suppose my question can be tailored more. A cell's nucleus is considered to be its brain-center. In all living things, there is a controlling consciousness (like our own consciousness that controls our body as a whole). If the DNA is the code that determines cell function and operation, then is the DNA the consciousness? If so, when the DNA splits, what happens to that original consciousness? Does it take up residence in one of the two, newly-formed strands, or is the original destroyed and two "newborns" are produced?

"In all living things, there is a controlling consciousness" including at the level of a cell is not a statement that is supported by any scientific research that I am aware of. Besides some religious perspective (that seems to run into a problem here), there is nothing "controlling" a cell, rather a cell is made of molecules (some of them quite complicated) that respond and interact with their local chemistry. Clearly in DNA replication, as Alex's answer mentions, the DNA molecule in each of the two cells after division is half new and half from the parent.

I see. Thanks for clarifying all this. It has helped me tremendously!

I'm afraid I don't know what "consciousness" means in this context. Cells are just bags of chemicals where reactions take place. DNA is just a molecule. If the right parts of it are accessible to protein-making machinery and energy (ATP), then life happens. Unless there are errors in replication or cell division that change a copy, one copy of a DNA molecule has the same chemical properties and utility as another copy, all else the same.


text:
Are there any evolutionary reasons for the different tree shapes? If so, What are they?
So we know there are a thousand types of trees with different shapes.
We have Columnar shaped trees:

Pyramidal or Conical shaped trees:

Weeping shaped trees:

And we also have Round, Vased, Open-Shaped, and Umbrella shaped trees. So im not really into botany so forgive me if I butchered some phrases. But I got into a conversation about evolution at school and we switched the conversation to plants this time.
We got into the photosynthesizing cycles of leaves, Like of course we know green is the leftover color from the light spectrum, Orange and yellow colors means the plant is utilizing Carotenoids as it ages, And Anthocyanins for pink to red leaves to protect it from intense sunlight.
But we got into the topic of the different tree shapes. Since plants are living things and goes through the same process of natural selection, Is there any evolutionary reasons for their different shapes? What made some trees that way and how do they fare differently from one another?

I'm VTC as this is too broad, but, as usual, yes, there was evolutionary pressure for trees as well as every living thing, and think "niche" (hot/dry/windy vs wet/warm/sunny vs wet/cold/shade vs every other climate.. We have spread trees out of their niches for ornamental purposes, but environmental pressure is everything.

Trees have to balance several different things , how fast they can grow, how much sun they can get, how much water they loose, how much wind they have to withstand, herbivores, etc. On top of that they have internal differences like different vascular systems. Given all these different forces and how much they vary from place ot place it is no wonder shapes vary.

You might want to look into L-systems and how simple rules (impemented at the genetic level) can cause differences in shape.  And if the shape survives, it persists & evolves.  See https://en.wikipedia.org/wiki/The_Algorithmic_Beauty_of_Plants

I disagree with close-voters -- I don't think this needs to be closed as too broad.Some comment can certainly be made about tree shapes and relating them to sun availability, wind-protection, temperature-regulation, etc.


text:
How do you biologists draw a protein when you write a paper?
The following is one example of protein structure diagram that I want to put in my research paper. I took this from

Koniev, O. & Wagner, A. “Developments and recent advancements in the field of endogenous amino acid selective bond forming reactions for bioconjugation.” Chem. Soc. Rev. 44, 5495–5551 Jan. 2015, DOI: 10.1039/C5CS00048C

As a Chemist, the only drawing tool I have used so far is ChemDraw and it does not provide such protein structure; The only protein diagram it provides is a Y-shaped IgG. How do you biologists draw such convoluted proteins when writing a paper? Do you use a specialized software for this?

They're not drawn they are produced by software from crystal structure data. Look up PyMOL.

Does this answer your question? Molecular graphics, if not, try this Mac-specific one or this one. Also look at the PDB link in my answer to this one.

As mentioned in the comments, diagrams like these are generated by software. The one I use is Chimera, it is free. The structure of the protein is recorded as a list of atoms and their 3D coordinates, as well as bonds, helices, sheets, etc. When a structure file is loaded, the software generates a 3D model based on the data. The user can rotate the model, move it, zoom in, change the color, an many other options, then export a 2D image when they are satisfied. If you want to use structure data files other researchers have generated, the Protein Data Bank is probably the best resource. Research articles that involve new structural data will list the PDB numbers of their structures near the end. In the article you link, the authors include pdb accession numbers for the structures they used for their figures. For the image you use as an example, here is the caption:

Fig. 56 PEGylation of four solvent-accessible Tyr residues of chymotrypsinogen (pdb: 1EX3) reported by Francis et al.

There are various software programs available to design a protein structure based on your requirement.
These programs can be used to:

Design atomic model based on the amino acid sequence of particular protein.
Predicting protein's 3-Dimensional structure.
Determining secondary and tertiary structure of protein based on it's protein folding properties and statistical tendencies of conformational features.
For checking whether protein contains transmembrane domain or signal peptide.

I have used Rosetta to design specific antibody for my protein.
Reference:
https://en.wikipedia.org/wiki/List_of_protein_structure_prediction_software


text:
Why did we lose our fourth type of cone cell (in the eye)?
Most species of birds, reptiles and fish have four types of cone cells in their retina, thus they have four independent channels for conveying color information. They are:

short-wave (S) cones: sensitive to colors with short wavelengths.
middle-wave (M) cones: sensitive to colors with medium wavelengths.
long-wave (L) cones: sensitive to colors with long wavelengths.
ultraviolet (UV) cones.

This condition is called tetrachromacy. Wikipedia mentions:

It was the normal condition of most mammals in the past; a genetic change made the majority of species of this class eventually lose two of their four cones.

We have only three. My question is, why did we lose our UV cones? I searched a little about this and here's what I found:
Scientists Have Found a Woman Whose Eyes Have a Whole New Type of Colour Receptor

According to estimates, that means she can see an incredible 99 million more colours than the rest of us, and the scientists think she's just one of a number of people with super-vision, which they call "tetrachromats", living amongst us.
They took 25 women who had a fourth type of cone cell, and put them in a dark room. Looking into a light device, three coloured circles of light flashed before these women's eyes.
To a trichromat, they all looked the same, but Jordan hypothesised that a true tetrachromat would be able to tell them apart thanks to the extra subtlety afforded to her by her fourth cone.

Which means some of us still have it. What I don't understand, though, is why this isn't a more common trait? Evolutionarily, is being able to perceive vision using three cones "enough" for humans?

we lost more than that, primates only have 3 cones cells due to a mutation creating a new cone cell, other mammals including the ancestors of primates only had two cone cells.

Let's be clear: most mammals, including basal primates, had only 2 cone cell types. Primates evolved a new cone cell becasue frugivores have a distinct advantage being able to distinguish reds and yellows. The mammal lineage may have never had a fourth cone cell, if they did it was lost early.
Eutherian mammals lost the third cones cells likely because we spent several hundred million years as small nocturnal animals during the dominance of dinosaurs. In small nocturnal animals, there is a strong competition between having more rods for better low light vision vs having cones for color vision, so a loss of some cone cells may have been neutral or even beneficial. There was some work on bats that seemed to contradict this, but the researchers failed to control for frugivory in the bat lineages they studied; So there is an issue with their results. There is a lot of variation in color vision across vertebrates so it is no surprise a consistent selective pressure could have a lasting effect.
source

The source you cited mentions -"The recent gene duplication and mutations that have given rise to the series of longer-wave pigments in primates also appear to have occurred independently in some teleosts and probably within some reptiles," which clearly means I had some conceptual misunderstanding about the evolution of cones. (sorry for that) Thanks for your quick answer and the amazing source! :)

the evolution of the different receptor proteins is very complex in the details, there are mutations all over the animal kingdom. worse the gene is fairly easy to duplicate so you often have animals with both the original form of the gene AND and mutant form at the same time.


text:
Why is haemophilia unviable in later stages of life?
A sentence in my textbook is:

The possibility of female being haemophilic is extremely rare because mother of such a female has to be at least carrier and the father should be haemophilic (unviable in the later stage of life)

I know that haemophilia is an X-linked recessive disorder. Hence mother should be carrier and father must be affected for daughter to get affected. But I'm unable to understand what "unviable in the later stage of life" means.

I suggest that this question is more suited to SE Medical Sciences.

The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. ——— I mention this because if you had done the expected research you would have realized the premise of your question is incorrect. Note that under researched questions may be subject to down-voting and closure. Thanks!

I suggest the exposition does not usefully touch on the Question title but still - and based solely on the actual wording - if "unviable in the later stage of life" came into it that would be down to aging weakening every system it came across.

Mortality.
The reason the most common examples of haemophilia in history occur among nobles is not because the nobles were a particularly sickly bunch of people. It is because they lived sufficiently pampered lives to actually become adults, and reproduce their haemophilia.
In the same era, a commoner or even a rich merchant family would not be very likely to keep a full haemophiliac  male alive until marriageable age.
In our modern world, the almost-heroic level of medical care that is needed for a haemophiliac to live a normal life is much more common, and thus both carriers and active haemophiliacs tend to survive more often.

I think what they mean is that those affected with haemophilia rarely survive to the adult life. This is less of a constraint for women, since a woman carrying only one recessive gene will not be affected by this disorder.

It must be a really old book though, as my dad's a haemophiliac and I'm 50 years old. He spent a lot of time in hospital as a kid and was told he's the oldest one with his level of factor to survive being born.

@PeteKirkham impressive! It is probably also a genetics book - if it were on epidemiology, changing duration of survival with a condition would be something to discuss seriously !


text:
Searching for a vaccine vs searching for poor genes in the covid-19 pandemic
I have only basic knowledge about biology. I have some propositions (may be wrong) and a question about the covid-19 pandemic.
In 1918, the world had a similar pandemic, the Spanish Flu. Millions of people died because of natural selection. Poor genes on flu were eliminated and strong genes survived. Nowadays flu is just an ordinary disease for people because we are the generation of strong genes and our genes are also strong for flu.
Similarly, for the Covid-19 pandemic, poor genes are getting eliminated unfortunately. (I think Covid-19 disease will be just as ordinary as flu in 5-10 years.) For almost 2 years, people have worked for vaccines and we learned that the mortality ratio of Covid-19 is nearly %3 by statistical data.
My question is, instead of quarantining all people for almost 2 years, trying to find a vaccine for almost 2 years and trying to vaccinate all people (only %3 of people are under a death risk), couldn't we just had searched for a pattern for poor genes? So that we might have to quarantine only those with poor genes and might have searched for a cure or vaccine for them?
Is anyone working on something like this, or am I thinking too simply for such a complex problem?

Wow, just wow...

The immune response in those that are going to die isn't trackable to a few genes but the interacting expression of hundreds of genes - so not predictable.

Unfortunately your assumptions are almost completely incorrect.
The reasons some get sick and die and others don't are multi(multi)factorial. There will be some genetic component, but also things like prior exposure to similar disease(s),socio-economic status, health status, age (this is a big one for COVID-19), all play into it.
The 1918 H1N1 influenza outbreak had a large number of confounding factors - it was in the middle of a global war, with large numbers of people (especially troops) crowding together (e.g. transport boats, barracks), often in terrible conditions (trenches), large portions of the world (esp. western Europe, China, Korea, parts of Africa)  being refugees with poor nutrition, stress etc.
In addition it was at the very beginnings of modern medicine - there were no antibiotics to take care of the following bacterial infections, no supportive medicine, no respirators etc. The people largely killed by the 1918 H1N1 were young men in their prime (20-40 y), who succumbed to something known as a cytokine storm, where their immune response was actually super strong (too strong) and they died from the resulting inflammation. There is a fairly large school of thought that says that the same is happening with COVID-19. It is thought that the cytokine storm against H1N1 is actually a heightened immune response because of prior exposure to another influenza virus. So, these people actually have "good" immune genes, but were the ones killed off by the virus.
Secondly - "just search for poor genes" - you are advocating for something that a) we don't yet know all the genes involved in immune responses, and b) segregation of the population based on genetic characteristics (now where have I heard of that happening before...here, here, here); might have some sort of impingement on things like human rights, especially when you consider that age is one of the largest factors for COVID-19 death.
Now those 3 comparisons above are a lot shitty, because those were horrific things done with no just cause, and you could make an argument that those more at risk of COVID-19 should take more precautions (as many do) - but how do you enact that into law? How do you enforce it? Can you tell if someone walking down the street has diabetes or asthma and are thus more at risk?

thanks for the answer.as you suggest maybe it would be better to inform someone whether he/she is in more danger. and i think its just same as to inform a diabetes patient to not eat sugary foods. i think law and human rights for this case are another topic of argument

@M.SEL that's exactly what happened in countries with good health care systems (and almost all other countries), public health advisories were made for those more at risk, efforts were made to protect the elderly and unwell by prioritising them for vaccines, isolating aged care facilities, mandating masks (which is about protecting not just yourself but others too) and social distancing, shutdowns/lockdowns - these are all effective public health measures that worked in many places. That some people chose to ignore advice from experts does not reflect on advice given, but on the individual.


text:
Does GFAJ-1 use Adenosine triarsenate as its energy currency?
Regarding the bacteria found in Mono Lake, CA that scientists believe uses or can use arsenic in its DNA backbone where life as we know it uses phosphorus (according to their experiments depriving the microbes of phosphorus and providing much arsenic), have researchers conjectured and tested whether the energy currency molecule used is also arsenic-based instead of ATP?

Those results have been heavily criticized (see also this related question of mine on Skeptics), the answer might be that those bacteria just don't incorporate arsenic into their DNA.

This is a cool topic/question.
To answer your question.  The hypothesis was based on the conjecture that there was so little phosphorus in the culture medium that phosphorous would have been replaced by arsenic in all its roles in the cell.  IF they had found arsenate DNA, it would have been derived from NTAs (nucleotide tri-arsenates) or a hybrid Phosphorous/Arsenic analog of the compound as DNA polymerase consumes NTPs to create DNA.  If there were only NTAs to drive DNA biosynthesis, then the cell's energy cycle would also have had to use ATA.
BUT
The primary evidence was that the mono lake strain grew in a fermentor (culture) with lots of arsenic (which is impressive) and very little phosphorous. how little? 3 micromolar. The investigators say that they did add a little phosphorus (3-5 micromolar), which, after some more careful accounting, appears to be enough to keep the bacteria growing at the observed rate without using arsenate nucleotides (submitted to Science).
This is not completely surprising as the original publication in 2010 of a preliminary finding in Science Express which only had x-ray abosorbtion fine edge spectroscopy work consistant with an arsenate like that found in a phosphorus backbone.  Given that they did not produce a more direct reading of the compounds such as mass spec or an NMR experiment, this looked pretty iffy in the first place.
You an see why arsenic life was so improbable - a dozen (or more) vital pathways in the cell would have to adapt to use NTAs - pretty much all at once.  If they had I suspect Mono lake would be full of those suckers.
Its sort of a bummer, for those of us who want to discover new forms of life, but you can't find what isn't there.