Mithradates - Developing immunity to poison? According to legend, Mithridates studiously researched and examined all known toxins and experimented with potential remedies by using prisoners as his guinea pigs. Supposedly, Mithridates’ toils paid off because numerous ancient authors, including Pliny the Elder, claimed that he created and regularly ingested a universal antidote for all identified toxins, and it became known as mithridate (mithridatium).

It was said that he was pretty much ingesting small amounts of poison to develop an immunity to it.

Whether universal poison or ingesting each type one by one, is this possible to build up your body to resist or be immune to poison/venom/toxins in general?

Welcome to SE. Edit: The answer is in two parts based on the mechanism of action of the toxin. Courtesy: @David and @jamesqf

Immunity

The white blood cells in the body are responsible for recognizing self or non-self peptides and form the adaptive compartment of the immune system. The B lymphocytes have a receptor that can bind to various peptides. Upon recognition of foreign peptides in the body, they go through a reaction (somatic hypermutation) to become further specific to the foreign peptide. They also differentiate into Plasma cells which can now secret another protein (antibodies) which neutralizes the foreign peptide.

Small amounts, which are non-lethal, but in enough concentration to drive the B cell reaction creates an immunological "memory". This memory allows a faster response to the same peptide compared to the reaction. This in order allows the body to withstand a higher concentration of toxic peptide, which otherwise would have been lethal as its being neutralized.

Vaccines work on a principle very close to this.

Homeostasis

Every toxin interacts which some biological process and drives it out of balance. The body actively tries to restore the balance by some means.

For example, if a ligand is depleted the body can increase the number of receptors to counter the effect and vice versa.

By ingesting small amounts of toxins body can adjust the equilibrium by very small amount at a time adjusting the concentration of relevant ligands or receptors.

Again, the person who has been through this process can withstand a higher dosage of the toxin compared to a person who hasn't.


How does the body really react to exposure to the vacuum of space? I've seen sci-fi movies where the effects the body being unprotected in outer space are wildly different. In one movie, a guy radios for someone who's been ejected into space to breath all the air from his lungs immediately. In some movies, eyes are pulled from sockets. In others, ice crystals form, and the eyes begin to look a bit red... Sometimes the exposed person is a goner right away, sometimes they're shown to last for a minute or more. The Hollywood portrayals of space exposure just vary tremendously.

So I'm curious, what really happens to the human body in the vacuum of outer space?

With regard to the vacuum - Apparently nothing happens as long as you don't hold your breath, just like you shouldn't hold your breath when ascending after scuba diving and the pressure drops. See NASA's answer to the same question. Of course there's the radiation that does other funny things in space, see the NASA link.

If a person was in space without her spacesuit/helmet, she would feel a suffocation feeling, likely making breathing motions even though there is no air to breathe. She would also feel her sweat, saliva, tears, mucous, and any other water on her body boil off, though her body would maintain blood pressure, at least until her heart stopped. She would be unconscious within 15-20 seconds and dead within 90-120 seconds.
https://m.youtube.com/watch?v=ZrILTVRcW6A


Identify Bronze Coloured Beetle Spotted this beetle on Morfa Nefyn, a beach in North Wales, UK. The beach is a mixture of sand and stone, with large sandy cliff faces and rocky outcrops.

The beetle was about 3 to 5 mm or so long, running around on the rocks at the edge of a rock pool (not in the water though!), on a warm sunny day. It was moving are quickly, but not really fast, maybe around 1cm per second.

I've seen them on the beach before and sure I know what they were called but can't for the life of me remember.


Homework question on chemically defined medium Why would the following medium not be considered a chemically defined medium:

Glucose, 5 grams (g); NH4Cl, 1g; KH2PO4, 1g; MgSO4, 0.3g; yeast extract, 5g;
distilled water, 1 litre

I am unsure why it is not a chemically-defined medium considering all measurements and grams are given and such is required for it to be one. Therefore I am unsure why it would not be a chemically defined medium.

A chemically defined medium is, according to this Wikipedia article:

  ... a growth medium suitable for the in vitro cell culture of human or
  animal cells in which all of the chemical components are known.

Four of the five components fit this criterion precisely, as they are chemical formulae (and of course a common name for a compound whose formula is well known).

However, even though you know exactly how much yeast extract was added to the medium, you do not know its exact chemical composition. To be sure, assays of the chemical composition of yeast extract have been run, and one could come up with approximations of it's makeup. But the bottom line is that there is no precise chemical formula for yeast extract as there are for the other components of the medium.

The yeast extract would consume and metabolize some of the medium components and metabolic products will be formed. This new introduction of products by the yeast, whether waste materials or otherwise, is unaccounted for and changes the composition of the medium. Therefore, it would no longer be chemically defined.


Why do many people seem to prefer unhealthy compared to healthy foods? I don't have any concrete statistics on this but many of us seem to love the taste of food that is unhealthy for us.

Over the centuries, wouldn't it have been a non negligible advantage to those who preferred (and hence ate) healthier food?

So, why don't most of us inherently find healthier food to also be tastier?

Apologies if this is a silly question or something that is frequently asked. I know very little about biology in general.

It's a very simple answer. "Unhealthy" foods, for example potato chips, sugary drinks, and other fatty, cheesy or sugary edible items, have only been around a few hundred (at most) years. In prehistoric times (before agriculture, when the primary source of food was hunting and gathering), when food was scarce, fatty and sugary foods would be of great importance. They would supply the body with large quantities of energy (a gramme of fat gives about 9 calories, a gramme of carbs gives around 4 calories). Since we survived mostly on fruits, vegetables, meat, and whatever roots we could find, something as energy rich as, say, a serving of deep fried cheese covered bacon would have sustained us for days. So eating anything with high calorific value, like a fat rich tuber would release 'feel-good' chemicals, like dopamine and serotonin, among others, which make us feel happy (dopamine is also released in response to hugs and accomplishing goals, serotonin is released, in very large quantities, during nicotine consumption).
Our body these days just isn't used to our relatively sedentary lifestyle with  guaranteed food. Our body still hoards fat like it did during our time as hunter-gatherers, and our body still secretes dopamine everytime we dig into a sumptuous serving of cake.
A couple of good sources:
http://www.ncbi.nlm.nih.gov/pubmed/8697046

Serotonin-releasing brain neurons are unique in that the amount of neurotransmitter they release is normally controlled by food intake: Carbohydrate consumption--acting via insulin secretion and the "plasma tryptophan ratio"--increases serotonin release; protein intake lacks this effect. This ability of neurons to couple neuronal signaling properties to food consumption is a link in the feedback mechanism that normally keeps carbohydrate and protein intakes more or less constant. However, serotonin release is also involved in such functions as sleep onset, pain sensitivity, blood pressure regulation, and control of the mood. Hence many patients learn to overeat carbohydrates (particularly snack foods, like potato chips or pastries, which are rich in carbohydrates and fats) to make themselves feel better. This tendency to use certain foods as though they were drugs is a frequent cause of weight gain, and can also be seen in patients who become fat when exposed to stress, or in women with premenstrual syndrome, or in patients with "winter depression," or in people who are attempting to give up smoking. (Nicotine, like dietary carbohydrates, increases brain serotonin secretion; nicotine withdrawal has the opposite effect.)

http://www.scientificamerican.com/article/addicted-to-fat-eating/

Like many pleasurable behaviors—including sex and drug use—eating can trigger the release of dopamine, a feel-good neurotransmitter in the brain. This internal chemical reward, in turn, increases the likelihood that the associated action will eventually become habitual through positive reinforcement conditioning.

http://www.ncbi.nlm.nih.gov/pubmed/8697045

There is an intimate relationship between nutritional intake (eating) and serotonin activity. ...
Traditionally, serotonin has been linked to the macronutrient carbohydrate via the intermediary step of plasma amino acid ratios.

TL;DR:
You would have starved if you didn't eat fatty foods back before we had food so readily available, so your body automatically stocks up in case you ever run out.
Watch this video for more information:
Why our brains love junk food

sorry for a not scientific answer, this is general knowledge.
you can try to search for proofs you need.

there are several different types of unhealthy food and the resulting addiction/desire to eat them. the unhealthy food tricks the brain.

cholesterol/carbohydrates:

the brain is built from cholesterol partially.

the brain can make cholesterol from carbohydrates.

so so-called "unhealthy" food it is good for you kind of. unless you are sick.

so some times a moderate amount of cholesterol is good for you in general, the brain can make its own cholesterol. cholesterol supports memory.

cholesterol is bad if you have an internal wound like an inflammation, maybe of blood vessels or heart arteries. cholesterol made by the liver usually patches the would holes. later to be fixed using protein(if there is also vitamin c). however, if there is an inflammation going and there is a wound filled with cholesterol, new cholesterol will stick to already existing cholesterol. and clog arteries worse.

depriving the brain of cholesterol deprives memory. because neurons make vesicles - like small soap bubbles filled with dopamine that marginally pre-excite neurons. those vesicles are made of cholesterol. if you ingest something that dissolves cholesterol for a long time like a statin or antioxidant you will lose memory and lose the ability to form memory.

also, the brain is energy hungry, so it brain gets activated on high energy foods. however, if fructose or sugar is ingested with food. a large percent of it is stored into fat. using insulin that is made from sugar.

chemical foods:
like things that make the brain make neurotransmitters like acids, ions, and sweet poisons are bad for you.

they trick the brain and stress the brain. things like coffee and sugar and sodium glutamate. coffee makes adrenaline and ticks you to release saved energy.
sugar acts on dopamine center and tricks you think you do something good even if it is bad. sugar also gives you some glucose. however, all dopamine from sugar is consumed immediately.

some other things dopamine-making:

the brain seeks dopamine, and while on dopamine the brain does not think rather acts as before in an automatic manner. like, do the same thing again. also if the situation not as before the brain will mistake. sometimes brain confuses one thing to another. because they both make the same level of result. one real one fake. the fake quicker and you need to do it again and again. so people fall for a quicker and easier way. the solution is to delay time, to prevent instant action and try to solve basic body needs like rest and food


Did the capacity to be "knocked out" arise because it conferred an evolutionary advantage? From first principles, it seems surprising that a blow to the head would cause unconsciousness rather than just impaired function.

I've heard a lot of analogies to computers -- "Your brain has to reboot." But computers reboot when there is an error because they are explicitly designed to do so, in order to recover and prevent further damage.

So, did we evolve the capacity to get knocked out for similar reasons -- because it helped us recover or prevent further damage? Or is the capacity to get knocked out just an "accident" or an inevitable consequence of the way our brains are designed, without a good evolutionary explanation?

(I realize the answer might be: "we don't know". In that case, I'd wonder what the prevailing opinions are and what if anything we've ruled out).

https://en.wikipedia.org/wiki/Concussion#Mechanism

We did not evolve in order to become knocked out. See the wikipedia link. The "water" in the head is designed to not make us get knocked out that easily. However each dampening system has a limit.

Some goats faint due to fear (https://en.wikipedia.org/wiki/Fainting_goat).  This is possibly to "play dead," to basically concede to the source of the fear.  There is some indication this might occur in humans who pass out due to fear (i.e., humans who pass out at the sight of blood).  Maybe this is related to falling unconscious due to injury?


Are there any parasites that alter human behavior in a self destructive way? There seems to be quite a few examples of parasites taking over the behavior of insects in a way that leads to the death of the host.  A couple of examples include:

Spinochordodes tellinii:  A nematomorph hairworm that causes crickets and grasshoppers to jump into water, and likely drown, as
part of their life cycle.
Ophiocordyceps unilateralis: A fungus that causes ants to leave their desired habitat for the habitat required for the fungus
to reproduce while consuming the ants internal organs.

In mammals, a common example is:

Toxoplasma gondii: A single celled parasite that appears to make rats attracted to cat pee in an attempt to continue its life
cycle within the cat.  Additionally, humans can be infected with
Toxoplasma gondii via contaminated meat, vegetables, and cat feces.  In fact, there is a study of Danish medical records from 45,788
women in which the rate of self harm increased 50% for women
suffering from chronic toxoplasmosis and the rate of attempted
suicide was 80% higher.  However, direct correlation between the
increases could not be linked to the these higher rates due to the
possibility of other factors such as depression.

So it seems that there is some widespread evidence of parasites causing a host to act in a potentially lethal way, but the evidence that I could find for humans seems to be minimal and yet to be proven.  Are there any examples of parasites causing humans to act in a risky, potentially deadly, manner?

There is a link established between Candida and Aspergillus fungal infections and mental illness of schizophrenia and depresssion. Over prescriptions of antibiotics and use of antibiotics in cattle ranching, subject people to excessive antibiotics. This causes a die off of natural gut flora and consequent fungal overgrowth.
Fungal metabolites (aflatoxins) have been linked to anorexia,depression and schizophrenia. Pubchem lists lists behavioral acute anorexia for aflatoxin G1.
Research published in Journal of Antimicrobial Therapy, suggest that some SSRI antidepressants have an antifungal effect.
Ethyl alcohol (alcoholic beverage) is a fungal metabollite of brewers yeast that is well known to impair human behaviour in a negative way.
I have been unable to find any research into using antifungal agents to treat mental illness.

A fungus that thrives in soil, contaminates grain, is distilled into a beverage that causes drunk driving and death, and returns the host to the soil has also completed its life cycle. Similar to the ant example in your question.


Why does asbestos cause cancer? We are probably all familiar with the dangers of asbestos in your rooftop or in various pieces of old equipment as it has been shown that the microscopic asbestos particles reach our lungs and can then potentially cause lung cancer.

Now smoking (for example) can cause cancer because of various carcinogens chemically interacting with DNA, but how can these asbestos particles, specifically prized for being quite unreactive, damage DNA to the point of triggering cancer?

More basic answer; the asbestos crystals have hooks. So the cilia in the lungs have difficulty moving them out with the other dust. This irritates the tissue causing the effects of the first answer. So it is a matter of time and number of asbestos particles that increases the probability of a cancer. Decades ago , the asbestos miners in Africa typically worked for years ( eg 20 years) before getting cancer.

There are basically three hypotheses regarding the pathogenesis of asbestos-induced cancer , which may be summarized as follows:

(1) the "oxidative stress theory" is based on the fact that phagocytic cells that engulf asbestos fibers produce large amounts of free radicals due to their inability to digest the fibers, and epidemiological studies indicating that iron-containing asbestos fibers appear more carcinogenic;

(2) the "chromosome tangling theory" postulates that asbestos fibers damage chromosomes when cells divide; and

(3) the "theory of adsorption of many specific proteins as well as carcinogenic molecules" states that asbestos fibers in vivo concentrate proteins or chemicals including the components of cigarette smoke.

Source


Resilience to the neurotoxins of Indian King Cobra I read on Wikipedia about this:

King Cobra - Wikipedia

In Thailand, a concoction of alcohol and the ground root of turmeric is ingested, which has been clinically shown to create a strong resilience against the venom of the king cobra, and other snakes with neurotoxic venom.

Though, I have been in the village parts of India where King Cobra is frequently encountered, I have never heard of this knowledge.

Can somebody please explain the scientific basis of this statement and possible reasons for this?

[PS]: Can somebody also please create a tag for "Snakes"?

Well, turmerin, the compound in turmeric has been medically proven to help neutralize venom from King Cobras in snakes (reference1, reference2). It has also been used in ayurveda for snake bite treatment (reference) The alcohol I guess is just used to help ingest the turmeric and act as a pain reliever, though it strangely seems counter-productive since most snakebite help guides advice against the consumption of alcohol after getting bitten (reference1, reference2) due to its blood thinning properties.

Having said that, I guess personally, I would go for anti-venom rather than ingest turmeric. As a quick remedy until you get the anti-venom you should be able to depend on turmeric.

Thank you for the query, I would have search would have shown that, we are the pioneers to first use Turmeric against snake venom.  Be it, Cobra, Krait or Viper. It is the universal truth that, all the snake venom is 90% protein and out of that, 60% is the lethal inflammatory toxic enzyme called Phospholipase A2 (PLA2).  PLA2 is an enzyme that breaks down the cellular plasma membrane containing phospholipid and allows the entry of toxic enzyme.  The toxic enzyme let loose a cascade of events that goes through cyclo-oxygenase and lipoxygenase pathway with release of arachidonic acid - 20 carbon fatty acid which forms the precursor of pain causing inflammatory by-products.  Since, Turmeric can destroy the activity of phospholipase A2,the inflammation and accompanying inflammation reduced considerably and the life of the patient extended by two to three hours giving time for the anti-venom antibody treatment. The attractive feature of the above "On the spot" treatment by Turmeric is that, the snake can be any species because PLA2 is the key toxic enzyme in all the venoms. The way to administer Turmeric on the field is to take two to three fist full of Turmeric powder and dissolve it in warm water, then it is filtered through a clean cloth and the clear extract without any residue about a glass is given to drink by the patient when it is warm.  The rest of the water is used to continuously washed the bitten spot so that, the local inflammation is subsidized. You may refer the to the following publications where it is shown that Turmerin, a water soluble antioxidant protein from Turmeric binds to PLA2 distal to the active site and changes the conformation of Phospholipase A2 in such a way that, it is no more hypertoxic.  Thus extending the life of the patient and reducing pain and inflammation.

Reference:
New biological activity against phospholipase A2 by Turmerin, a protein from Curcuma longa L.


What are the factors to consider when determining the sample size for a given study? Say I'm designing a retrospective study (where I'd collect data from various schools for the last 5 years) to see if consuming milk can contribute to childhood obesity.  How do I decide on how many schools to visit? If I remember my stats correctly, in general, the goal is to achieve 95% confidence in our results, right?  So how many schools would I have to collect data from so that I will have 95% confidence in the outcome of the study?

Could be as much as possible – using multistage sampling. But it all depends on how much you are willing to spend, and your time constraint.


Do fledglings die if they are not fed constantly? There is a bird's nest on my balcony in the wall above the door with birds who breed. They have fledglings who already hatched. (I assume this because I sometimes hear quiet sweet chirping.) I sit on my balcony often for breakfast and sometimes for lunch almost every day. When I do this, the birds stop feeding their fledglings (because they are afraid of me or because it is some natural instinct to not reveal their nest).
A friend of mine (who installed a birdhouse on her balcony) told me that the fledglings die if they are not fed constantly. She told me that she doesn't use her balcony anymore (or at least not longer than 5-10 minutes) because of this.
So my question is: Do fledglings die if they are not fed constantly? How long can they survive without food? (like 30 minutes or so)
I would like to use my balcony because I really enjoy having my meals on it but I also don't want the fledglings to starve.

Depends on the species and their age. All birds have fat reserves that can keep them alive for a relatively long time. It's when fledglings are left for many hours or days that one should start worrying about their survival.
The following link explains more detail on how frequently birds must be fed, even if in your case I suppose you aren't the one feeding them:
https://birdwatchingbuzz.com/how-often-should-you-feed-a-baby-bird/
In my experience some species of birds might become less afraid if you leave food or water stations for them.

Every 10 to 15 minutes.
The youtube channal: A chick called Albert
It is a good channel that is really interesting.


Why are bovines different genera if they can interbreed? Why are bovinae a "subfamily", above Genus, when members can interbreed?  Some like the beefalo are fertile, which is the normal defining characteristic of a species. And Genus are groups more distantly related, so by definition they should not be closely related species.

Species are not defined by whether they can interbreed, not even close.

In fact, there is no objective, scientific standard for what defines species, or genera, at all. What is a species is determined by little more than the "feels" of the individual naming it, or the committee approving it.

And the same is true of the entire rest of taxonomic structure. It's not really science, it's just a way of organizing ideas that got popular, and in fact is under constant assault now by somewhat more scientific things like genetic testing. The hierarchy of the taxonomic system changes pretty much daily, and has no official structure or definition at all. Even the number of kingdoms is entirely up in the air.

Getting back to the specifics here, since there is no objective, scientific standard for what is a species or genus, it's no surprise that separate ones can interbreed.

And it's not like bovines are the only ones. There are many other intergeneric hybrids possible, like sheep and goats, wheat and rye, camels and llama, house cats and servals, marine and land iguanas, et cetera.

Perhaps someday there will be objective definitions to establish a truly scientific taxonomy. But for the moment, it's just whatever people in positions of power feel makes sense, at any given moment.

List of Intergeneric hybrids


Conjoined twins formation theory is it theoretically possible to take two fertilized mammalian eggs and push them together to make conjoined twins? How about forming non-identical conjoined twins?

The more generally accepted theory for conjoined twins is fission, in which the fertilized egg splits partially. So I don't think that what you said is possible. Not seen this happening before... even the conjoined twins share same placenta indicating they originate from same fertilized egg.


Why do eukaryotic organisms have introns in their DNA? We touched on introns and exons in my bio class, but unfortunately we didn't really talk about why Eukaryotes have introns. It would seem they would have to have some purpose since prokaryotes do not have them and they evolved first chronologically, but I could easily be wrong. Did the junk sections of DNA just evolve there by some sort of randomness or necessity as opposed to an actual evolutionary advantage? Why hasn't evolution stopped us from having introns since they seem to be a 'waste' of time and DNA? Why do prokaryotes not have introns?

There is still a lot to be learned about the roles introns play in biological processes, but there are a couple of things that have been pretty well established.

Introns enable alternative splicing, which enables a single gene to encode multiple proteins that perform different functions under different conditions. For example, a signal the cell receives could cause an exon that is normally included to be skipped, or an intron that is normally spliced out to be left in for translation (the Wikipedia article on the subject has a basic overview of the possibilities). This would not be possible, or at least would be much more difficult, without the presence of introns.
In recent years, we have discovered that RNA molecules (especially small RNAs such as siRNAs and miRNAs) are much more involved in regulating gene expression than previously thought. Often the small regulatory RNAs are derived from spliced introns.

There is probably more, but essentially introns enable a finer level of regulatory control. Biological complexity is often not the result of having a larger complement of genes, but of having additional layers of regulation to turn genes on and off at the right times. Prokaryotic genes are often organized into operons, and a single polycistronic mRNA will often encode multiple proteins from multiple adjacent genes. Since the biological processes required to sustain microbial life are much less complicated than those required to sustain eukaryotic life, they can get away with much less regulatory control.

There are several good answers here already.  Daniel Standage points out the value of alternate splicing.  For a compelling example of the role in regulation of gene expression, read one of the reviews of sex determination in Drosophila melanogaster (sex-lethal, transformer, doublesex).

None mentions the idea of exons as "cassettes" of reusable function that can be introduced into an existing gene during evolution.

The bounding introns represent regions where inexact "grafting" can occur without destroying the already functioning reading frame of the newly introduced xeno-exon (I just made up that neologism) or of the recipient gene.

In other words, introns provide regions which allow for sloppy transposition of functional subunits while reducing the likelihood of wholesale chaos at the transcription/translation level.

Evolution shows over and over that it is capable of promoting mechanisms that promote evolution.  How else can you explain meiosis?


Are there any plants that parasitize on animals? It seems, fungi often infect animals, while plants it seems, never. Is it because the cellulose cell walls make them incompatible with animal tissue?

Yes! Here's a paper published August 2018
https://www.sciencedirect.com/science/article/pii/S0960982218308157


Are human bodies programmed to die? Following from this question: What is the evolutionary advantage of death?:

Is there any evidence that human bodies have systemic self-destruction built into their developmental program? I'm not talking about the cell death response, which I know is an important part of growth, development and cancer prevention.

I've read some things about telomere-shortening but don't know if this is a cause or an effect.

From a certain point of view you could argue that our bodies have an inherently limited lifespan;

Telomeres are extensions to the end of chromosomes that prevent damage or loss of genetic information during cell division. Telomeres are not replaced (in normal cells), which gives rise to a replicative lifespan; the number of times a cell can divide before permenantly leaving the cell cycle (senescence).

This is generally viewed as an anti-cancer mechanism to protect against errors creeping in to the genome through many cell divisions. In order to become cancerous, a cell must first overcome its replicative lifespan [ref.]. This is achieved by activating the (normally inactive) telomerase enzyme that extends the telomeres - embryonic stem cells are one of the few cell types that normally express this enzyme.

There are other ways in which you could argue that our lifespans are fundamentally limited, but it is important to note that the objective is not 'to die', but to increase fitness (in a Darwinian sense) earlier in life. This is known as antagonistic pleiotropy; when an advantageous trait early in life is disadvantageous later in life.

Telomere shortening is just one example of antagonistic pleiotropy (protects against cancer when younger, but limits the number of times your cells can divide).

Other traits that inherently limit lifespan include;

Neurons (as a rule) do not replicate, and last for your whole life time. This certainly excludes them from replicate senescence, however it means they are highly susceptible to 'wear and tear'; oxidative stress is a natural by-product of respiration, and the vast majority of damage done by these species (e.g. reactive oxygen species) is repaired by the cell, however some will always remain unchecked, and eventually this leads to neurological dysfunction and cognitive decline. Without intervention this is inevitable in each individual (the rate of aging differs between people, but aging and age-dependent diseases are disorders are a natural part of living).
The same is true for cardiac and smooth muscle - whilst much repair can be carried out, it is inevitable that damage will creep in over a life time, and thus the vast majority of human age-related deaths are due to cardiac problems in one way or another.

So there is no 'programmed' limit to life span, in that we have not evolved to die, but our bodies are inherently limited by the systems that have evolved. Life expectancy a few thousand years ago was ~20 years (if you lived beyond infancy!), whereas now in the developed world this is ~80 years, so our bodies can already survive way beyond our 'natural' life span, and thus we now succumb to age-related disease. Evolution has spent millions of years giving us every possible advantage that leads to reproductive success. Natural selection of traits beyond reproduction are secondary to those beforehand, and thus we have fundamentally limited life spans.

There is an argument for an evolutionary advantage of limited lifespan. This seems at first counter-intuitive, until you consider that natural selection does not act on individuals, but genes. It is proposed to be advantageous (in some circumstances) for an organism to have a shorter life span, as this increases the turn-over of individuals in that population. This in turn increases their evolvability - clearly advantageous for the gene(s) influencing this trait if it increases the likelihood of successful reproduction and thus passing on that gene/allele/trait...

I like this hypothesis, and can see that natural selection may favour it. I think mice are great examples here; they have much shorter lifespans than us, yet they 'age' (biologically) the same (cardiac problems, diabetes, cancer) but at a faster rate to give a higher population turnover). In a high mortality environment, the most adaptable animals will be more successful.

However, I think this is likely to be secondary to the pressures on other survival traits that  more directly increase the chances of successful reproduction.

In Richard Dawkin's book "The Selfish Gene" it seems that there is a programmed purposeful death of the body. The genes are in control.  They seek out a mate to produce offspring that will be even better suited to pass it's genes on again.  The meaning of life as we have seen and observed it is really for the genes to perpetuate their existance into the future.  Once passed on the body that did the passing is of little use.  The more complex the organism like a human mates may be selected by life span of parents and relatives.  There doesn't seen to be any Newtonian law that states a cell cannot just keep replicating and essentially avoid aging.  Our bodies are doing that for a purpose.  One we just don't understand.


How did the first life form on Earth reproduce without DNA? How did the earliest life forms exist without DNA? The most likely scenario I can think of for life happening from nothing is that, over billions of years, with trillions of water molecules and dust particles and chemicals moving around, eventually a small clump of this murky stuff formed a pattern. Or maybe, under some lucky conditions, a whole mud pit of such a inorganic system started forming into structures which had a pattern of motion, and one of those structures became the first sub-cell, like a primitive ribosome or something. I remember learning some parts of cells were once separate entities, but there are massive gaps in that idea.

The primary gap being: How did reproduction occur in that incredibly lucky, freak incident of a tiny dust clump or whatever? How did reproduction occur without DNA? Do scientists have a theory on how the first reproduction occurred?

So earth is estimated to be around 4.5 billion years old, and life has existed for about 3.4-3.9 billion years of that, around >75% the time. For a little perspective, Homo sapiens have been around for up to ~250,000 years, just 0.00005% of the time earth has existed. In that time the earth has changed massively, early earth was pretty hostile, but that could have made it a good place to develop early life.

What was the pre-cursors to self-replicating DNA like?

Well one popular theory is the RNA world hypothesis, which suggests that precursors to life as we know it were RNA molecules that could self replicate (reproduce). These RNA molecules supposedly evolved in to life in the DNA/RNA/Protein world via an intermediate stage of ribonucleoproteins. The reason why RNA could have preceeded DNA based life is because it has the potential to carry information and to be the catalyst of its own synthesis.

  "The unique potential of RNA molecules to act both as information carrier and as catalyst forms the basis of the RNA world hypothesis.

  "RNA therefore has all the properties required of a molecule that could catalyze its own synthesis (Figure 6-92). Although self-replicating systems of RNA molecules have not been found in nature, scientists are hopeful that they can be constructed in the laboratory." in Molecular Biology of the Cell

However, the RNA world probably wasn't the first step on the road to self-replicating life, but other polymers with characteristics similar to RNA that could have acted as the template and catalyst required for RNA synthesis.

  "Although RNA seems well suited to form the basis for a self-replicating set of biochemical catalysts, it is unlikely that RNA was the first kind of molecule to do so. From a purely chemical standpoint, it is difficult to imagine how long RNA molecules could be formed initially by purely nonenzymatic means. For one thing, the precursors of RNA, the ribonucleotides, are difficult to form nonenzymatically." in Molecular Biology of the Cell

-

  "Shapiro doesn't think it's necessary to invoke multiple universes or life-laden comets crashing into ancient Earth. Instead, he thinks life started with molecules that were smaller and less complex than RNA, which performed simple chemical reactions that eventually led to a self-sustaining system involving the formation of more complex molecules." on LiveScience.com

This means that the first self-replicating RNA molecules were preceded by other molecules that were important in the progression from simple atoms, through non-biotic molecules, to large self replicating polymers which can be considered life. Copley et al suggest a progression in detail, with monomers being an early step in the progression (see figure 4 in the paper, and section 4 for extensive detail) where monomers precede multimers, which precede micro-RNA.

  "Our model describes a continuous path for emergence of this sophisticated system
  from a simpler reaction network fueled by geochemical processes. The processes involved in metabolism and replication were intertwined from the very beginning, a concept that neatly eliminates the chicken/egg problem. Further, this model suggests that many features of the RNA World, and indeed modern life, arose long before the RNA World and were retained as pre-biotic systems became more sophisticated." - Copley et al

An alternative and slightly different theory suggests that viruses were the precursors to modern life, a so called Virus world. Similarly it supposes that early replicators were RNA based, but that viruses evolved in to the earliest forms of self replicating DNA carriers.

  "The Virus World Theory is closely related to the RNA World Theory, which says life first evolved as small pieces of RNA that slowly developed into complex DNA-carrying organisms. The Virus World Theory agrees that life's genetic material began as RNA. But it differs by arguing that the ancestors of viruses evolved before cells." from NationalGeographic.com.

Further good reading here, here, and here. I also recommend the book The Story of Life as an interesting related read.

Well another (and less popular) theory called Panspermia says that life, actually, came from space, it was not originated here in earth. So this completely change everything, because the conditions where life would have been formed could be very different from our's planet, so we can't make any predictions with this considerations in mind. But thinking in the DNA and our planet, the possibility that the DNA replicates with the help of other molecules could be possible. I don't think that it's necessary the steps of DNA to RNA and proteins or even DNA to proteins, to explain his reproduction, maybe some proteins with catalytic activity already exists and DNA with some good information in itself, it reproduce and continue evolving till have enough information to create other molecules with beneficial properties. We all know that proteins can actually be created by pure chemical reactions, i think that's the real secret of the life. We dont need a creator molecule to manufacture the entities entrusted with the job of create other molecules. The rest of the story is just the azar.


Why does dissociation of carbonic acid cause a decrease in pH? When a molecule of carbonic acid (H2CO3) dissociates, the two products are a bicarbonate ion (HCO3-) and a hydrogen ion/proton (H+). Because of the addition of a hydrogen ion, this process causes a decrease in the pH of the blood, and if someone breathes too slowly and doesn't quickly remove CO2 from their body, respiratory acidosis will take place.

However, why is it the case that the addition of this hydrogen ion lowers pH? While this might sound like a stupid question, it's also the case that the dissociation of carbonic acid produces a bicarbonate ion, which is a weak base. Therefore, the dissociation produces both an acid and a base in a 1:1 ratio. Therefore, the concentration of hydrogen ions relative to bicarbonate ions doesn't actually change. Given this fact, wouldn't there be no change in pH at all?

I read a paper on carbon dioxide transport which addressed some of my other questions but didn't touch on this precise point.

Any acid that releases a proton when it dissociates in water will also produce a conjugate base. We can conceptualize this as $\ce{HA <=> H+ + A-} $. In this particular example, $\ce{HCO3-}$ is $\ce{A-}$.  The strength of the acid is determined by the extent to which the acid, $\ce{HA}$, dissociates. This can be expressed using the equilibrium constant for this reaction, which has a particular name, $\ce{K_a = \frac{[H^+][A^-]}{[HA]}}$, (where $\ce{[X]}$ is the concentration of $\ce{X}$ at equilibrium). The larger $\ce{K_a}$ is, the further the reaction moves to the right (or, as it is often expressed, the smaller the $\ce{pK_a}$, which is $\mathrm{-log_{10}}$  $\ce{K_a}$).

Here, the addition of any $\ce{HA}$ will produce $\ce{H^+}$ and $\ce{A^-}$ in an aqueous solution (the blood), and decrease the $\ce{pH}$. $\ce{A^-}$ is only a base insomuch as it can form $\ce{HA}$ by combining with $\ce{H^+}$. This can occur if you add (or, as occurs in the kidney, reabsorb) $\ce{A^-}$ with some counter ion other than a proton. Then you can drive the equilibrium to to the left, towards $\ce{HA}$, decreasing $\ce{[H^+]}$. Otherwise, $\ce{A^-}$ derived from $\ce{HA}$ will not drive the equilibrium one way or the other. $\ce{H^+}$ will still dissociate as determined by the $\ce{K_a}$.

Bicarbonate will make the mudium basic ONLY WHEN it is bonded with some cathium that came from a strong base.

E.g. NaHCO3 is a basic salt because NaOH is a stronger base than H2CO3 is an acid. That way Na+ will stay completely dissociated while HCO3- and water will become H2CO3 and OH-.

H2CO3 is considered an acid because it ionizes in H+ and HCO3-. Some of the HCO3- will bond with water and form OH- and H2CO3 again. This is an equilibrium. But If we have only one HCO3- that didn't yet bonded to water and formed H2CO3 again, we will have more H+ in the medium, and it will be acid. In fact, there is a constant called Ka that measures how much HCO3- and H2CO3 are in a solution in a given time.


What happen's to a virus's capsid after it injects its genetic material into the host cell? After a virus (one of the varieties which infects the cell via injection and not endocytosis) injects its genetic material into the host cell, what happens to its protein coat? I would guess that it just falls off. However, since it is now outside of a cell, there are no protein-digesting enzymes -- or are there?

What happens to it now? I'm guessing it doesn't just float around for all eternity.

Interesting question and actually I haven't found a real answer here yet. The phages seem to bind rather hard, since the need to be blended (subjected to relatively high forces) to shear off. This was used in the Hershey-Chase-Experiment to find out what the genetic material of the cell is. It doesn't matter though, since most of the cells which are infected get destroyed anyway. If not, they are most likely taken up and broken down inside the cell, as it happens with other membrane proteins.
This is only valid for viruses which inject their genetic material into the host cell, while the capsid stays outside. This happens mostly for Bacteriophages.

There are a few other possibilities for viruses to enter cells where this is no problem:

Viruses which have a membrane envelope can enter the cell via membrane fusion. To make the fusion happen, either the membranes have to get very close, or the virus first binds receptors on the cell surface and then fuses its membrane with the cell. This causes the interior of the virus to be released into the cell. The picture below shows the fusion (from the Wikipedia article on membrane fusion). An interesting article on this topic is: "Membrane fusion."

Another possibility for a virus to enter a host cell is via endocytosis. Here the virus uses the uptake of material from the surrounding of the cell to get inside. This can either happen together with resources inside a vacuole.
Or it happens via the binding of specific receptors, which are internalized into the cell upon binding of the specific ligand. Here the virus mimics the ligand of the receptor to get internalized into the cell.
In both cases the virus needs to escape from the vacuole before it get broken down because the vacuole is turned into a lysosome.

I think the external protein coat is degraded as the virus releases it's nucleic acid into the Host' cell. This is due to the fact that a protein is lifeless without the activity of a gene(one gene-one enzyme hypothesis).Since the nucleic acid is composed of genes, when it is injected into the host's cell, the capsid becomes useless and so it is degraded.


Would a shark whip into a frenzy from smelling its own blood? Sharks normally respond very quickly to the scent of blood in up to a mile radius, but what if the shark itself simply got injured? Would it respond to its own blood at all?

I'm pretty sure, they can smell their own blood, but they do not attack themselves. Wounding a fish results in the release of chemicals into the water. This is a signal for other fish about potential danger and they will escape (Schreckstoff). Of course, the predator of the wounded fish will not mind. So this seems to work best within the same species. Fishermen and military have apparently used dead or rotten sharks in the past to keep sharks from attacking (Shark repellent). I guess, a similar mechanism plays a role here. Sensing a wounded member of the same or close species (including oneself), would block any feeding behavior.

The Myth Busters have actually done this (not very scientific) experiment: https://youtu.be/E1GenfKR9pk

Yes, sadly they do as the smell of fishes blood turns them into a frenzy, as they are fish.But i see no reason the shark would get hurt in the first place.


Thin layers or laminae that make up a single summer band in tree ring, what are they? I took the photograph below of some tree rings. Each division on the ruler is 1 millimeter:

Each tree ring (the areas between the pizza crusts) represents one seasons worth of growth. The growing season is from about March to October. My question is about the small lamellae or dark bands that make up each ring. I have placed a green box around one set of these bands. What are they?

These small bands all seem to be the same width, so tree rings that are wider (good years) have more of them, and rings that are narrow (drought years) have fewer.

What are these bands?

Not as a confident answer but as a comment... to provide image.

The wood TS looks like ring-porous, Oak (Quercus sp.) wood (Not as identification but anatomical features are comparable).

The dark bands (radial here) seems to be xylem fibres, and bright bands (radial here), seems to be xylem parenchyma.

This is a magnified image of wood of post oak (Quercus stellata). .
Source, URL http://www.wood-database.com/wp-content/uploads/post-oak-endgrain-zoom.jpg

where it seems to me

If there is anything wrong in my knowledge, inform me and feel free to downvote this answer. If any better answer comes, I'll delete this answer.

These are the annual rings that are usually found in areas /regions where environmental conditions are not uniform throughout the year.
These are formed due to the activities of cambium (bundle of vascular tissue in plants showing secondary growth).

In spring it is lighter in color and has lower density whereas the autumn wood has high density and dark in color with higher density.
Spring wood - High activity, produce large no. of cavities
Autumn wood - Low activity, less lumens and cavities.


Reason for aquatic plant roots My question is about why aquatic plants have roots. At first they seem a bit superfluous to me because leaves of the plants could just absorb nutrients directly from the water thereby skipping a need for root function that land plants have to pull nutrients from the soil. I then wonder if nutrient trafficking is the reason for the root system as diffusion may not occur efficiently through thick leaves.

Among terrestrial plants, roots have two major functions - obtaining water (as well as nutrients) and anchoring plants in place. (However, roots may have other important functions as well.) Aquatic plants obviously don't have a problem obtaining water. So roots presumably function primarily as anchors.

There are rootless planktonic plants that float on the surface of water bodies. However, aquatic plants like cattails and water lilies are probably a little more discriminating in their habitat preferences. Imagine a rootless water lily being blown by a hard wind into a patch of water lilies, which block out the sun.


Why do red blood cells maintain Iron in the Haem group in the +2 (ferrous) oxidation state? A lot of sources tell me that RBCs contain a number of enzymes, and that these serve multiple functions from maintaining the structure and elasticity of the corpuscle wall, to preventing the oxidation of iron (ferrous) in Haemoglobin to the +3 Ferric state.

But what none of them say, is what problems (if any) arise when the iron is oxidised. Hence the question, why avoid the Ferric state?

I'm still a high-schooler and from what I've learnt, is that the higher the oxidation state of the cation, the higher its polarising power (Fajan's Rules) hence stronger the bond. So wouldn't iron in the Ferric state be able to bind with oxygen better, and isn't that desirable? ( Or is oxygen release to tissues going to be problematic? )

If the Ferric state is desirable, then why do RBCs have mechanisms (the enzymes mentioned earlier) in place to prevent the oxidation of the Ferrous to the Ferric state?

Thanks!

Q. “What problems (if any) arise when the iron is oxidised?”

  A. Haemoglobin will be converted to methaemoglobin which cannot bind oxygen.

To quote from the article on Methaemoglobin in Wikipedia:

  Methemoglobin (English: methaemoglobin) (pronounced "met-hemoglobin") is a form of the oxygen-carrying metalloprotein hemoglobin, in which the iron in the heme group is in the Fe3+ (ferric) state, not the Fe2+ (ferrous) of normal hemoglobin. Methemoglobin cannot bind oxygen, unlike oxyhemoglobin. It is bluish chocolate-brown in color. In human blood a trace amount of methemoglobin is normally produced spontaneously, but when present in excess the blood becomes abnormally dark bluish brown. The NADH-dependent enzyme methemoglobin reductase (diaphorase I) is responsible for converting methemoglobin back to hemoglobin.

The question also asks:

  “…the higher the oxidation state of the cation, the higher its
  polarising power… hence stronger the bond.So wouldn't
  iron in the Ferric state be able to bind with oxygen better…”

which can be transformed into:

  “Why can‘t methaemoglobin bind oxygen?”

The answer is chemically rather complex, but one thing you should be aware of is that in haemoglobin (and myoglobin) the oxygen Fe(II) is five-coordinated (as shown in the diagram below where Fe is black) and binds oxygen in the sixth position (to the right).

In simple terms, the electronic change in oxidation to Fe(III) causes a change in the geometry of the haem pocket such that oxygen no longer can bind (although now water can). This page elaborates the point, without providing a full chemical answer.

Footnote: Fe(II) or Fe2+ ?

Some readers may be wondering why I have referred to the ferrous state of Fe in haem as Fe(II) and not Fe2+ (which the Wikipedia entry uses). This is to avoid implying that there is an overall charge of 2+ on haem groups in haemglobin and myoglobin. Inspection of the structure of haem (above) will show that the formation of two covalent bonds to imidazole nitrogens has left haem with a zero net charge.

Because RBC'S contain certain enzymes which prevent the Oxidation of ferrus to ferric.
Other reason is that ferrus is only capable of binding oxygen and not the ferric iron.That's why iron is present in ferrus form and not in ferric form.


How much vitamin C has a noticeable effect on E.coli k12 I am doing a research on effects of different concentrations of vitamin C on serial dilutions of E.coli k12. I am looking for literature that has already shown effects of vitamin C on E.coli, but there is a vast amount out there (26 thousand Scholar hits).

What might be the main effect of Vitamin C on E.coli? Is 1000mg vitamin C enough to have noticeable effects on the bacteria?

I found a 'short communication' paper by Akira Murata et.al where they did In Vitro testing of Vitamin C on L. casei showing no inhibition of growth, and also tested on E.coli and B. subtilis and found that Vitamin C inhibited the growth. Also I believe Suzanne Humpries stated the same thing somewhere in this 1.5 hour long video, indicating she may posses more knowledge as to studies.

  Ascorbic acid did not inhibit the growth of L. casei even at high
  concentrations, and rather stimulated the growth at certain
  concentrations (2~3 X 10- 2 M). This observation indicates that
  ascorbic acid can be used as an antiviral agent.

  In E. coli and B. subtilis, unlike L. casei, a high concentration
  of ascorbic acid acted so as to lessen their growth rates (Fig. 3).
  Particularly, in B. subtilis W23, cell lysis was observed about 100
  min after the contact with ascorbic acid and, moreover, when a drop of
  the lysate was placed on a plate seeded with B. subtilis 168 and
  incubated overnight at 30oC, there appeared a clear zone around the
  placed lysate. Since B. subtilis W23 is known to possess an inducible
  defective phage PBSZ able to kill B. subtilis 168,3 ' 41 the observed
  result maybe ascribed to the induction of the defective prophage from
  B. subtilis W23 by action of ascorbic acid. Lwoff and Siminovitch51
  reported once that the lysogenic phage in B. megaterium was induced by
  treatment with ascorbic acid.

It’s proven quite hard to find research on the effects of vitamin C on gram-negative bacteria.

http://www.sciencedirect.com/science/article/pii/S1089860301903714

This paper suggests that vitamin C (sometimes also referred to as ascorbic acid) can help inhibit the growth of E. coli when in the presence of mildly acidified urine with added nitrite. Keep in mind that this paper is quite old, and inside the first few paragraphs it states:

  despite numerous studies the mechanism of any antibacterial action of
  vitamin C still remains unclear.

It later states

  we have recently shown that large amounts of NO gas are released from
  nitrite-containing urine after mild acidification and this release is
  greatly potentiated in the presence of ascorbic acid.

So it seems this first paper doesn’t offer us much in terms of toxic effects of vitamin C on bacteria in isolation.

http://jb.asm.org/content/98/3/949.short

I found another paper that suggests that vitamin C can kill gram-negative bacteria, but again not in isolation, but in combination with other agents as well.

Perhaps your research is among the first to offer any insight on the effects of vitamin C on E. coli. I’ll be interested to know if anyone else finds a publication on this specific topic (I only searched for about 30 mins on the subject).


What is the defining characteristics of a Gap Species? For the following competitive exam question: A road is constructed through a tropical rain forest, following which a population of a species of butterflies declines. Which of the following is NOT  a possible explanation for the road causing a decline in the forest butterfly population?
The answer: The Road facilitates immigration of gap-loving species which compete with the forest species
What is the defining characteristics of a 'gap' species?

The previous answer from @Ark Lomas is true to the extent that gap-loving refers to preference of an open habitat. It was found that these species e.g. have improved flight abilities and are in general geographically more wide-spread.
Here is prove:
Ecology of Tropical Butterflies in Rainforest Gaps
J. K. Hill, K. C. Hamer, J. Tangah and M. Dawood
Oecologia
Vol. 128, No. 2 (Jul., 2001), pp. 294-302

Tropical forest gaps are ephemeral and patchily distributed within
forest areas and have very different light environments compared with
closed-canopy forest. We used fruit-baited traps to investigate if
gaps are exploited by more opportunistic butterfly species compared
with closed-canopy forest. Gaps supported a higher diversity of
butterflies in terms of species evenness but closed-canopy sites
contained species with more restricted geographical distributions.
There was little similarity between the assemblages of butterflies
trapped in the canopy and those in either gap or closed-canopy sites,
but the greater similarity was with gaps, and increased diversity in
gaps was partly due to canopy species turning up in gaps. Dispersal
rates (as measured by recapture rates) were higher in gaps and there
was evidence that butterflies in gaps had relatively larger and
broader thoraxes, indicating a flight morphology adapted for faster
flight. These results support the notion of a distinctive gap fauna
comprising more widespread, mobile species. Habitat modification that
opens up the canopy is likely to result in an increase in these
widespread species and a decline in understorey species with
restricted distributions.

a gap-loving species is a species that prefers existing in open spaces such as the gap that the road creates in the rain forest. I can't think of any organism native to rain forests that would be considered significantly gap-loving since most rain forest species rely on the trees and bushes etc... that the rain forest provides which therefore causes them to not prefer being exposed in the middle of a road.


What’s this bug? Sign of an infestation? Found crawling up the side of my washing machine. [WA] Just spotted this bug on the side of my washing machine after putting some dirty clothes in the hamper and transferring a damp load to the dryer. I’m hoping it came in from outside somehow, and isn’t some type of vermin (I live in an apartment and I’m probably the cleanest resident in the building. I’m also paranoid about household pests.) It’s very small, photographed against a damp paper towel. Please tell me this is not a baby roach?

Don't worry, it is definitely not a roach. It is a true bug, Hemiptera. Not a household pest.


Are 2 eyes necessary for 3D vision? To start off: I'm not a biology student, but a computer science major

It has always been my understanding that humans have 2 eyes so that we can have 3D vision: the left eye see more of the left side of an object than the right eye and vice versa, this helps us to estimate depth among other things.

Now when I close one eye, I still am able to perceive depth: I assume this is because my brain fills in the blanks? For how long does this work? Do people eventually lose the depth perception (or at least is diminishes significantly) when they lose a single eye?

If so, how low does it take? If not, clearly we are capable of perceiving everything with one eye: why do we then have two (besides redundancy and a larger field of view? What is considering the evolution of man better in having 2 eyes as opposed to 1 or 3,4,..?

It seems like you suffer from a misconception. "The left eye sees more of the left side of an object..." is not how distance perception works. Otherwise we wouldn't be able to estimate the distance from flat objects, such as traffic signs and shooting targets.
The actual mechanism is parallax estimation, or Binocular disparity. In a nutshell, the closer an object is to your eyes, the bigger the difference of its position on the left and right eye's retina will be.
You may perform a simple experiment: find a place where several parallel wires hang in the air: a train line or aerial phone/power line. Look at the wires normally, and they will appear just as black lines in the sky, with no distance perception. Now tilt your head to the side, and you will instantly gain a feeling which one is closer, and which one is further away. Why the difference? Because any shift of a horizontal wire gives the same picture, meanwhile for vertical wires the difference is obvious.
When you close one eye, your brain loses the ability to estimate parallax. However, it is left with several options:

Visual cues. If one object overlaps another, it's obviously closer. If two objects look the same but one is smaller, it's probably further away (or a child). If you know the expected size of an object (a mountain/a horse/a fly), you may get the feeling of distance as well.
Focusing distance. When you focus your eye on a near and far object, the feelings are different.
Memories. You remember what you've seen with two eyes.

Of these, only (3) depends on previous binocular vision. (1) and (2) are available even to those who were born with one eye. However, parallax estimation is much faster and more precise. With a single eye you will be able to hit a fly on the wall, but catching it in the air will be extremely difficult.

Edit01 (here and scattered throughout)

[Not meaning to be antagonistic… but admittedly somewhat defensive.]
Insofar as the following is a citation of an existing work, it is the below Martin and Foley item, pp165-185 (with a noted exception) — noting again that I read this years ago, and did not consult it (nor anything else) when writing the below… and (again) that I consider that, although this can be studied as a science, most of the root knowledge is innate (of course) and implicit and could be rendered explicit by any adult who did not already have it so (as in the following example).  (It is of course theoretically possible that I have read other sources on the same material.  As far as I am concerned, most modern adults would consider almost everything here neither insightful nor controversial, with the exception of brightness (for which I have no source), height cues (which I did not mention) and kinetic depth effect (which I did not mention and which is not obviously and certainly relevant to the question).)
Atmospheric colouring is an exception in that one can use this to work out that air is blue (as opposed to needing to know that air is blue to make sense of an apparent phenomenon).
Brightness is an exception in the case of which indeed I should have supplied a reference… except that, as noted, I can not see it in the noted text book, and thus have no idea where I heard it (noting that I do have a memory of the excitement of learning this (or possibly working it out)).
More citation anomaly and disparity as noted.
End — Main Body of  Edit01.

Original, with references in “[]” added.

Going from memory, since no one else has covered this… .
This is more a psychology question (as below).
3D vision utilises about seven different mechanisms.  Binocular vision accounts for only two of these.
• Occlusion — each eye sees slightly different areas of a partly occluded object.  [(“Occlusion” suggests also the monocular topic “interposition”, below.)  As a binocular phenomenon, Martin and Foley (p183) label this “binocular disparity”, which is [from a quick look] actually about the image from the same object falling on “different” — I would say “non-corresponding” — areas of the retina (as a function of being closer to, on, or further from, the focal distance).  [From a quick look] they do not seem to cover the fact that one eye will actually see more of a partly occluded object (which means I have no idea where I heard it (and I am thinking that I might well have worked it out myself)).
• Focus — you have to focus both of your eyes on an object to see it not-fuzzy; your system knows about (relative) eye positions and subject distance.  This includes both focusing the lens in the eye [“accommodation” [p167] is lens shape] and pointing both eyes at the object [“convergence” [p182] is the eyes turning towards each other].
Binocular occlusion information only works out to about (from memory) 2m [“10 feet” Martin and Foley p183].  This would be increased by having the eyes further apart.  (Focus works out to a much greater distance; I am not sure which of the above two aspects is more useful, but I am guessing it is lens shape (and that they are of roughly similar usefulness).  [Martin and Foley mention “10 feet” (p167), citing Hochberg (1971) for accommodation (lens shape)… but appear to have chosen this as immediately arbitrary.  Their point is that it yields “rather weak” distance information.]
Other (monocular) 3D vision cues include the following.
• Object size — many objects have a standard size [“familiar size” p167], and almost all objects have different proportions (such as leg thickness) according to how big and heavy they are [which Martin and Foley do not cover; the source is me]… and an object that is further away will have a smaller image size.  [pp167-169 “size cues”, “relative size”.]
• Brightness — any given object will reflect less light into the eye from further away (because the eye is a smaller target further away).  (This is more useful and important than one realises.)  [From a quick check, this one does not appear to be in the noted text.  I do not think (particularly) that I worked this out for myself, but if it is not in that text, then I have no idea where I heard it.]
• Perspective — many types of object (e.g. road, path, wall, river) have a stable width, or similar or analogous, and this will have a progressively smaller image size with greater distance.  [“linear perspective” p170.]
• Texture — many objects have a known texture (or (assumptively) a regular texture), and the image size of the detail of the texture will decrease with distance.  This works for groups of animals, and leaves, and the like, as well.  [pp169-170.]
• Air tinting — the further away an object is, the more it is tinted blue by the interposing nitrogen.  [“atmospheric perspective” p170.  Martin and Foley also say that more distant objects appear “blurr/y/”.  I would say that that is largely because we have less visual acuity for an object that is further away (because the image size is smaller); Martin and Foley put it down to interference by air particles.]
• The physics of movement — speed and acceleration can be informative.  [Martin and Foley treat this area on pp174-176.  I was thinking of… what I said.  M&F mention “motion cues” (the class), “motion parallax” (which involves the subject moving laterally, and multiple stationary objects), “motion perspective” (which involves the subject moving towards or away, in any environment) and “kinetic depth effect” (which is about apparent 3D-ness in rotating objects, and is ostensibly not about distance).]
[Other monocular items that Martin and Foley mention… .  • Shading [p170] — objects can cast shadows on other objects.  I would say that this is primarily not about distance perception.  • Interposition [p167] — the nearer object obscures part of the further object (or not).  • Height cues [pp173-174] — my take on this is that, on flat ground (and because the viewer is above the ground), an object that is further away will have its base closer to the horizon and thus visually higher… and, for objects in the air, I would say here only that it is more complicated.]
Focus is very valuable for (for instance) catching a ball, whereas a task like driving [with one eye] has much more 3D information available.  [Source:  I worked this out using thinking.  …So it’s me.]
As for having more than 2 eyes… having eyes spaced apart vertically (as well as having the existing horizontal spacing) would give additional occlusion information, but the gain would be minimal.  [Source:  I worked this out using thinking.  …So it’s me.]
Source

The source is a custom book — that is, “Custom Book”, which is, “a compilation of chapters from… [existing] Pearson Education Australia titles.”  The publisher logo “Prentice Hall” appears, but only as a logo, and not on the cover.
The Custom Book is “PSYC236 Cognition and Perception”, ©2001, Pearson Education Australia Pty Ltd.  It is “Sourced from:  Sensation and Perception 4th Edition”, ©2001, Martin and Foley.
The cited material is from a chapter numbered 6, which appears to be its number in the original/source book; ditto for the page numbers.


Are endorphins addictive? Endorphins are among the brain chemicals known as neurotransmitters, which function to transmit electrical signals within the nervous system. Stress and pain are the two most common factors leading to the release of endorphins. I wanted to know if they are addictive, and found some contradicting answers:

  If people can get addicted to risky sports just for the thrills they
  provide, they can also get addicted to painful activities where
  endorphins provide relief, "despite the harm to self and/or others,"
  says Dr. Anna Lembke, chief of addiction medicine at Stanford
  University School of Medicine in an email interview. "For example,
  someone who compulsively cuts herself for the endorphin release is
  causing self-harm. Someone who compulsively runs, even to the point of
  causing musculoskeletal injury, is causing self-harm."

Source:
https://science.howstuffworks.com/life/inside-the-mind/human-brain/can-be-addicted-to-endorphins.htm

  In contrast to the opiate drugs, however, activation of the opiate receptors by the body's endorphins does not lead to addiction or dependence.

Source: https://www.medicinenet.com/endorphins_natural_pain_and_stress_fighters/views.htm#

If they are not, how can we explain the 'love' for pain in (this content might be sensitive for some of you) some people?

Addiction specialists and others who study human behavior often catageorize addiction into the two broad categories of physical dependence and psycological dependence. They are not always mutually exclusive, and they can both manifest in serious or mild cases of addiction depending on the person and a number of other factors.

What differentiates them is how they affect your physiology. A person severly addicted to alcohol or opioids can become extremely ill or even die from the withdrawl of those substances, due to the strong physical dependence their body has developed. To my knowledge, people do not experience a physical withdrawl after cessation of compulsive pain seeking behaviors. Since they didn't cite any source, we can only guess as to the intended meaning of your second source, but it's probably related to this lack of withdrawl. A quick search on PubMed shows publications referring to certain endorphins as mediating this type of addiction. Meaning that the endorphin is not addictive per se, but a compulsive or addictive behavior can be communicated to the brain in terms of a native neurochemical pathway which is otherwise a normal part of a healthy brain.

I think the lesson here is to be somewhat skeptical of online sources that don't link to peer-reviewed science. Attempts to simplify a topic for the purposes of communicating with a lay audience often result in more confusion than clarity. And if you search something on PubMed or google scholar, you'll probably find an answer in the same amount of time it took you to post your question here.

Pain is not an endorphin but p substance triggers reactions to form opioids and those are endorphins. There is a lot of research about serotonin and dopamine being highly addictive.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4028699/

Here they review this and explain it a little bit

From a psychological point of view people harm them self because they want to sentence themselves, but there are very much deviations and you can not put anybody in the same pot...


Why do sneezes come out the mouth? As anyone who's ever sneezed can tell you, it's caused by irritation in the nose.  And the answer to a question on this very SE attests that "sneezing is a reflex, partially autonomous, to clear the nasal cavity of particles that don't belong there."

That being true, the sneeze mechanism is a little bit strange: if you hold your hand up in front of your face when you sneeze, you'll feel that all of the rapidly-expelled air that ought to be cleaning out your nasal cavity is coming out your mouth, not your nose.  In fact I don't think I've ever felt air coming out my nose when I sneeze.

So what's going on there?

I've pondered this question too.  It's very clear that when we sneeze, the expelled air comes mostly from our mouths.  However, at least as far as my own sneezes are concerned, some of the air comes from my nose as well.  I know that if I pinch my nose closed as I sneeze, my ears hurt and pop.  If my nose is sniffly, I usually notice mucus come out.  Our soft palate partially lowers and our tongue rises as we sneeze, in order to divert a portion of the air up into our noses.  That position of our tongue is why our sneezes make a CHHH sound. If people intentionally keep their mouths wide open as they sneeze, that could explain why nothing comes from their nose, as there's nothing to divert the air.

A good book to learn as background is called 'Why We Get Sick: The New Science of Darwinian Medicine'.

In a sense you can consider us vectors for some microorganisms. When you cough you spread germs to other individuals (other vectors). Thus, it would be evolutionarily advantageous for a microorganism's genes if they were to infect more vectors.

How many germs are spread from the nose rather than the mouth? I don't know. However, expulsion of germs from your mouth will reach further than from your nose. It might be that there is a greater density of germs coming out of your nose, but that they don't travel as far in the air.

The above is slightly speculative, though, and I could speculate more but from what I can tell that is to be kept to the comments. (I can't comment due to <50 rep).

TL;DR More germs being spread from the mouth due to increased capacity for infected droplets and increased potency in terms of expulsion - advantageous evolutionary mechanism for spreading germ's genes.


Were early human beings (about 100 - 200 K years ago) far more promiscuous than we are now? I found that many friends of mine are quite easy in sexual relationship. Ex, I knew a lot of girls went to the night club & met a stranger & brought home to sleep  with him even she had never known his name. The next morning, the guy left her & she starts to do the same way to get another guy maybe in 3 days or so.

So that triggered my thought. I wonder "Are early human beings (about 100 - 200 K years ago) far more promiscuous than we are now?"

My hypothesis is "Yes", that is "Early human beings are far more promiscuous than we are now". So how i came up this? Cos Human came from Chimpanzee right?, so if we want to know early human, then we could study Chimpanzee. The early human & Chimpanzee could have some similarities.

There is a research saying that "Chimpanzees are far more promiscuous than humans" http://www.nature.com/news/specials/chimpgenome/interactive/chimp_interactive_graphic_pf.html

So, that proved my hypothesis.

Also, when human evolved, they started to realized that promiscuousness wss not healthy & not good for society so they started to develop some regional/society (ex,  monogamous relationship) codes to prevent that.

Do you approve my hypothesis?

My hypothesis is "Yes", that is "Early human beings are far more
  promiscuous than we are now". So how i came up this? Cos Human came
  from Chimpanzee right?

No.

  Also, when human evolved, they started to realized that
  promiscuousness wss not healthy & not good for society

I'm sorry, what ancient society are you claiming cracked down on male promiscuity?

Well, your logic is flawed because it is not proven that humans evolved from chimpanzees. not trying to start another debate with the whole evolution, but even if I did believe in evolution I would suggest before making up your hypothesis of researching a lot more than monkeys. Research things like: ancient brothels, traditional marriage views/ cohabitation views, {things that humans practiced and accepted back in the day} and you will have much more evidence.


Why do humans find baby animals cute? Why do humans find baby animals like cats, dogs, ... so cute?

As these are potential competitors (when grown up!) or even natural enemies (like e.g. tigers, leopards, ..), the protection instinct (reasonable for the babies of your species) should therefore not apply.

I can't imagine any reason why evolution let mankind adore foreign species that much.
Maybe only humans liking the enemy's kids survived, because they weren't killed by the baby's parents.

What is the evolutionary reason?

In German we call it "Kindchenschema" which is unfortunately translated only to the more unspecific "Cuteness", but sometimes also to "baby schema". This seems to be applying to most (care taking) mammals, also over species borders. The specific looks release hormones in the adult triggering care taking behaviour. This is to ensure the babies safety. That it not only works with the own parents helps ensuring the baby is cared for even if the parents cannot do it themselves.
Interestingly, the head and eye shape seems to trigger this hormone release. And it is the same for many animals. Like always, evolution uses the same winning scheme over and over again. This is why you can get a dog to care for abandoned kittens, and why you will find those puppies ever so cute.

The only humans survived were those, who liked baby animals. Because that humans domesticated wolfs, horses and so on, which gave them the superiority above other humans.

UPDATE

I assume, that everything what exist, should be approved by evolution somehow. Hence, IF humans actually likes baby animals, THEN it should be approved.

So, I remembered, that humans were domesticating animals and this technology was helping them (us) to survive. Also I remembered, that domestication is usually started with adoption of animal babies. Adoption was occurring by chance, on the basis of non-motivated congenital (genetic) love to baby animals.

So, my explanation is: some of human species were liking animal babies and this caused domestication. Then domestication caused evolution advantages, and these species won the competition with other human species. We are descendants of former species and conserve our sympathies to baby animals. Those who were not liking them -- died millions years ago.


Why do we age? or Do we have a theory of senescence? There seem to be a number of ideas about why we age. Hypotheses include the gradual accumulation of cell metabolic products affecting organism function and the reduction of telomere length during cell division.
My hand-wavey idea would be "wear and tear".

Are we anywhere near a consensus theory of senescence?

The 'wear and tear' argument is most likely true but it is also interesting to reason about ageing as inevitable from the evolutionary point of view.

To set up the argument, we need two things:
First, each individual has got a 'reproductive potential' which is realised throughout life. This means a deleterious mutation which has an effect in early life, will affect reproductive value more than a mutation which manifests itself in later life, after the individual has already had offspring. Thus selection will act strongly on genes which are expressed in early life than on those which are expressed later. For that reason, there's no strong selection against diseases such as diabetes or cancer. This argument can be applied not only to occurrence of disease but also to decay of ordinary functions of the body.

Secondly, cells in the body are constantly renewed and defects such as telomeric breaks are repaired. Mutations in the soma are taken care of by the immune system and can be in principle avoided. The fact that they tend to accumulate in later life can be explained by the first point: selection is weaker to oppose telomeric breaks and mutations in later life.

I was trying to be brief here, but there are more sides to the argument (e.g. Williams' antagonistic pleiotropy). Modular Evolution (Vinicius, CUP 2010) provides a good overview of the evolutionary aspect of theory of senescence (and many other interesting evolutionary arguments).

Imagine if an organism lived forever. How could it adapt to changing environmental conditions, from ice ages to mountain building events and changes in atmospheric conditions?

That's my personal theory to explain why living things must die. A species' motto could be "Adapt or die," and no individual can do all that adapting.


Why is fructose not glucose the main energy source of sperm? The seminal fluid contains fructose as the main energy source for the sperm and not glucose.

  Why is fructose and not glucose the primary energy source for these
  sperm, since glucose is the preferred energy source for most other
  tissues?

I have been searching this for a while and I got something of an answer, which I am posting below.

There are primarily two advantages of using the polyol pathway and aldose reductase to produce fructose from glucose via sorbitol:-

1) Quoting the book here,

  Seminal fluid contains up to 11 mmol/L (200 mg/dl) of free fructose.
  It is the major energy source for the sperm cells in their
  all-important race for the ovum. The advantage of fructose over
  glucose may be that many bacteria, which compete with the sperm cells
  for the available nutrient, prefer glucose to other energy sources.

Thus, to avoid other competitive bacteria and cells from utilising the energy source of sperm, fructose is used as the energy source since the bacteria prefer glucose.

2)Another reason is that the metabolism of sorbitol into fructose is energetically efficient way (no ATP required) as compared to glycolytic conversion of glucose into fructose(G$\rightarrow$G6P$\rightarrow$F6P$\rightarrow$F). Tapping the polyol pathway is energetically preferred to metabolizing fructose produced during glycolysis.This is only to show the possible evolution of the polyol pathway once the advantage of using fructose as the energy source was established. It does not explain why the fructose was advantageuos but just that if it was advantageous, the semen-producers would develop the currently existing machinery to produce fructose as the exclusive source of energy.

Hence, sperms (seminal secretion) contains fructose as the primary energy source and not glucose.

If glucose was used in place of fructose it would get used up very quickly as it has a high glycemic index but fructose has low glycemic index and gets used up slowly by the spermatozoa so that they can survive for many days (upto 3) in the females body for successful fertilization.


Hydrogen peroxide decomposition and catalase uses All google searches have simply returned more info on catalase. I'm looking for a catalyst that isn't found inside living organisms which  can break down H2O2. Looking for any resources to look at, or just examples of other catalysts.

Side question since I don't want to clutter with a new thread.
Can catalase be used for anything other than the decomposition of h2o2?

Manganese(IV)oxide can be used as a catalyst to speed up the decomposition of hydrogen peroxide


Does the process of making a sourdough starter involve Darwinian selection? In essence - to make a sourdough starter:

Put flour and water in a jar, and leave it in a warm place overnight
Divide the remaining mixture in half, throw out half, add half as much flour and water again.
Repeat for 7 days.

I don't see why you couldn't just add all the ingredients required at the start, open it once a day to let more yeast drop in and give it a stir, and keep in a warm place every day.

The vague idea comes to me that throwing out half the mixture every day has a Darwinian element, but it doesn't involve any 'selection', you're simply casting out half, regardless of adaptability.

My question is: Does the process of making a sourdough starter involve Darwinian selection?

EDIT: There is no 'choice' involved in throwing out half the sourdough. It is entirely arbitrary - and both halves look equally the same.

Yes, continually diluting the mix like this encourages the organisms (bacteria, yeasts, fungi) to have more constant conditions (maximum nutrients, fewer waste products) and be in log phase growth. The mix selects for particular faster-growing organisms. if you did not dilute, the nutrient levels would change (lower) and waste products accumulate much faster. Then the conditions would be more different day-to-day.

Practically, the dilution adds more nutrients while still allowing the pH to fall. Without the dilution, particular bacteria tend to take over and lactic-acid producers dont get a chance.

refs
https://en.wikipedia.org/wiki/Bacterial_growth
https://en.wikipedia.org/wiki/Sourdough

That is not Darwinian selection, because you are not selecting anything. As you mention yourself, it doesn't matter which half you discard and which half you keep. In fact, you can keep the entire thing. Discarding just makes it more practical.

If all conditions are fine, yeast will grow exponentially, meaning your amount of yeast will double every 2 hours or so. By discarding half of your mix, you simply reduce the volume you are working with. Otherwise you would have to add double the ingredients every time. For example, let's assume by adding fresh ingredients you double your volume. Starting with 250ml you would have 500ml the next day, 1l the day after, 2..4..8.. 16 liters and soon you have a bucket full of yeast.

Handling that volume to avoid overgrowth and insufficient nutrient/oxygen supply is way harder than a small volume. In the lab we grow yeast preferentially on shakers, mixing the solution to ensure all cells get the right amount of nutrients. Otherwise the yeast would die once the nutrients are depleted. So, how do you do that in your yeast bucket? ;) Just stirring it once won't do the job. The yeast would settle and die.

You could keep the halfs in separate smaller containers, but how much space do you have to store these? Here is a video where this issue is explained and what you can do with the discarded half: https://youtu.be/Ye4A2judXck

In the end, what would you do with all that starter? Once you have your sourdough starter ready, you can take half and use it for baking and keep growing the other half. How much bread do you want to bake? Do you need a bucket full of sourdough starter?

Sure, some of the yeast will die and the cells best adapted to the growing conditions will remain. This is a selection process, but it's independent from discarding half of it.


Why is the heart not in the middle of the body? All mammals that I can think of have a high degree of bilateral symmetry (In fact, almost every animal I can think of is like this).

So why is the human heart not exactly in the middle of the body? An effect of this is that one lung is slightly smaller. Are there any evolutionary theories on why this came to be?

First of all, let me make it clear that the heart is at the vertical centre of the body -- it is not shifted towards left (or right). However, it is slightly tilted towards the left in most cases.

In some cases, it is tilted towards the right, and the condition is called Dextrocardia. For why it is so, lets look at what the heart does. Below is a diagram of double circulation (from here).

As you see, the highest pressure needs to be generated for pumping oxygenated blood into the body. Thus, the left ventricle needs the thickest muscles for this purpose. And due to these extra muscles, the  heart appears extended and seems shifted towards left.

Coming to the evolutionary perspective, it is important to mention that humans are not the only organisms with this feature. Indeed, displacement of the heart towards the left is a conserved feature in all vertebrates (Fishman et al, 1997). See this answer for more information.

Coming to genes, bending of the heart towards one side is actually controlled by the NODAL gene during development. See this diagram (from Jensen et al, 2013):

Tilting occurs in two phases, one during the first four and a half months of intrauterine life and the other, which is actually a 45° rotation to the median plane, later. During the early development of the heart, a process called cardiac looping happens and the straight heart tube develops a bend (see diagram). The NODAL gene, along with the Lefty1 and Lefty2 genes, regulates the speed and direction of cardiomyocyte movement during the development of the heart, leading to this asymmetry. To confirm it, researchers knocked out the spaw/nodal gene from a zebrafish and found randomized development of heart, even symmetric heart, as the result(!) (see Walmsley, 1958 and Rohr et al, 2008).

Now, talking about why this happened in the first place, and why it is so conserved among vertebrates, we need to ask ourselves a basic question: what good would a symmetrical heart be? External symmetry is preferred (probably) because it helps in locomotion; it would be quite difficult to move with your two legs placed away from your center of gravity. But when we talk about internal symmetry, conditions drastically change. We get a major restrictive factor here: space. And limited space always dominates other factors. Seeing that the structure of the heart is necessarily pointed towards one side, it becomes difficult to make it symmetrical. (The only option IMO is to have another pointed end at the right side.) In this case again, what advantage would a symmetrical heart provide? None. And it might even be harmful since having an even bigger heart would mean making both lungs smaller. Thus, a symmetrical heart would only prove to be a liability rather than an asset. See this question for more information.

1- Bilateral symmetry means two mirror image halves following sagittal section only along a central axis.In animal kingdom there are examples of no symmetry (amoeba) , radial symmetry (jelly fish) , biradial (comb jelly and bilateral (human - though not exhibiting perfect bilateral symmetry because of heart, gall bladder and liver)
     Heart is not symmetrical on account of its functions -the left ventricle is thicker compared to the right).The smaller Left lung could be the result of a varying functional load associated with oxygenation of the blood.


Question about Autosomal Recessive Alleles I had a homework question that I could not figure out.

It states:

  A woman has cystic fibrosis in her family and did not want to have a
  child that suffered from the disease. She and her spouse went for
  genetic testing and counselling. She tested positive as a carrier and
  her spouse tested negative, and their first child was born with cystic
  fibrosis. Explain how this could happen.

This doesn't make sense because the punnet square would be:

$$
\begin{array}{c|c|c}
  & A  & A  \\
\hline
A & AA & AA \\
\hline
a & Aa & Aa
\end{array}
$$

This says there are no two recessive alleles which can cause  cystic fibrosis.

If really cystic fibrose is expressed only in homozygotes, then here are some possible explanations:

Mutation

very improbable

Autofecundation

very improbable

False Negative when testing the father

Because of the test False Negative Rate. @kmm made a very interesting comment below. He said that according to this article 75% of the mutations coding for disease correspond to one pattern (3 base pair deletion). The other 25% of the mutations coding for disease might not be detected in the standard test. If so, it is very likely that a the test conducting on the father was a false negative. It would be worth further investigate the test that are usually performed to confirm this.
Because of human error. The laboratory operator might accidentally switch two samples or accidentally introduce stranger DNA before PCR (assuming the test is performed through sequencing)
I have no idea concerning the probability for such thing to occur!

trisomy

The assumes that a trisomic that have two recessive allele coding for disease and on dominant allele coding for health yield to a individual expressing the disease!
The gene for cystic fibrose is on chromosom 7. Trisomy 7 is extremely rare if I'm not mistaken.

The father is not the father!

According to different studies between 5% and 20% of the people are not fathered by the man they think is their dad.
According to this source the frequency of the disease is 1/2500 in UK. Assuming Hardy-Weinberg equilibrium the frequency of the allele coding for disease should be $p=0.02$.
The probability that the baby comes from another man and that the baby express the disease is $$a \cdot \left(\frac{2\cdot p\cdot (1-p)}{4} + \frac{p^2}{2}\right)$$, where $a$ is the probability that the baby was fathered by another man (let's say 10%) and $p$ is the frequency of the allele coding for the disease (0.02). The division by 2 and 4 are due to the probability that the (real) father and the mother transmit both the alleles coding for the disease.  This probability equals $$0.1 \cdot \left(\frac{2\cdot 0.2\cdot (1-0.2)}{4} + \frac{0.2^2}{2}\right) = 0.01$$ This seems to be from far the most likely explanation! Note: this assumes that the mother is heterozygote (does not express the disease) otherwise, the probability would be 0.02.

I asked my Biology teacher and she said that the if the father is not a carrier, he must have the disease. So the father is aa.


Why are the neurites from hair cells to spiral ganglion cells called axons? In Kandel's Principles of Neural Science I found the following figure which shows the innervation of the organ of Corti:

From the legend to this figure (30-10, p. 602):

  "The great majority of afferent axons end on inner hair cells, each of
  which constitutes the sole terminus for an average of 10 axons.[...]
  Efferent innervation of inner hair cells is sparse."

BUT: The depicted axons that "innervate afferently" hair cells seem to go into the wrong direction (downwards, not upwards). What do the (red) bulbs touching the hair cells represent. I guess synapses, but which one is the presynaptic and which one is the postsynaptic neuron? (I guess: The hair cell is the presynaptic neuron - it's a sensory neuron! But then the neurites emanating from it would be afferent dendrites of the ganglion cells, not axons. I'm lost. Might it be the case that transport along these neurites is active - like in axons, not passive like in dendrites? Or are they called axons because they are myelinated? Or is it because in bipolar cells it is not distinguished between axon and dendrite?)

Question: Why are these neurites called axons?

I believe to understand now, thanks to @AliceD's answer to this question:

Why are Merkel cells innervated by an axon, and not a dendrite?

The axon seemingly emanating from the cell (hair or Merkel) is just by coincidence not a physiological part of the cell (hair or Merkel), but its functional axon. The tactile meniscus (in the case of the Merkel cell) plays the role of an "out-sourced" axon hillock of the cell (hair or Merkel) which possesses no axon hillock (and axon) on its own.