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Vitamins — how did they get their names?
There are several types of vitamins. A,B,C,D,E,H,K,P, etc. How did they get their names?

I'm voting to close this question as off-topic because it is about the history of what is obviously an arbitrary nomenclature rather than biology.

http://www.chm.bris.ac.uk/webprojects2001/harvey/namingvitamins.htm

Here's a very comprehensive guide to the first person to propose alphabetical vitamines and the renaming to vitamin: https://gizmodo.com/why-are-vitamins-named-using-the-alphabet-1555934736 There used to be vitamine B1, B2, B3, B4, B5, B6...

I’m voting to close this question because it was poor when it was posted and it is being used as evidence for continued posting of a new inappropriate question.

They were more or less named in the order that they were found.  Letters F-J are skipped because many of those were reclassified or later found not to be vitamins.  The K comes from the German word for Koagulation because the vitamin is involved in the coagulation of blood.
The discovery dates of the vitamins and their sources /
Year of discovery   /Vitamin    Food source

1913 Vitamin A (Retinol) Cod liver oil
1910 Vitamin B1 (Thiamine)   Rice bran
1920 Vitamin C (Ascorbic acid)   Citrus, most fresh foods
1920 Vitamin D (Calciferol)  Cod liver oil
1920 Vitamin B2 (Riboflavin) Meat, dairy products, eggs
1922 Vitamin E (Tocopherol)  Wheat germ oil, unrefined vegetable oils
1929 Vitamin K1 (Phylloquinone)  Leaf vegetables
1931 Vitamin B5 (Pantothenic acid)   Meat, whole grains, in many foods
1931 Vitamin B7 (Biotin) Meat, dairy products, eggs
1934 Vitamin B6 (Pyridoxine) Meat, dairy products
1936 Vitamin B3 (Niacin) Meat, grains
1941 Vitamin B9 (Folic acid) Leaf vegetables
1948[42] Vitamin B12 (Cobalamins)    Liver, eggs, animal products

There are many different B vitamins, water soluble, because many vitamins previously given different letters where later found to be part of the B complex. For example H is now B7.  Additionally, many letters, such as P, are no longer classified as vitamins.
More information can be found on this Wikipedia page.

ascorbic acid is water soluble

1 * Vitamin A:
Name: Retinol. It was discovered in 1909
Function: Carotene compound responsible for transferring light to the retina.
The most common sources: whale liver oil, meat, eggs, liver, kidney, cheese.
Diseases resulting from deficiency: lack of it leads to night blindness.
2 * Vitamin C:
Name: Ascorbic acid. It was discovered in 1912.
Function: Important in the synthesis of collagen, the protein component of the body's tissue frame.
The most common sources: fruits, vegetables, oranges, lemons.
Diseases associated with deficiency: Lack of it leads to scurvy (weakness of the capillaries), which is characterized by the presence of fragile capillaries, poor healing wounds, and deformity in children.
3 * Vitamin B1 B1:
Name: Thiamine. It was discovered in 1912.
Function: Acts as a catalyst in the metabolic process of the body.
The most common sources are: whole grains, rice, legumes, wheat germ.
Diseases resulting from deficiency: the most important disease Berri, a disease of the nervous system and heart.
4 * Vitamin D:
Name: A group of vehicles with multiple names. It was discovered in 1918.
Function: It is with calcium helps to promote bone health.
The most common sources: sunlight promotes the manufacture of sufficient amount of vitamin D in the skin.
Deficient diseases: Deficiency can lead to osteoporosis in adults and bone rickets in children.
5 * Vitamin B2 B2:
Name: riboflavin. It was discovered in 1920.
Function: As a catalyst for enzymes that stimulate chemical reactions in the body.
The most common sources: dairy products, eggs, green leafy vegetables.
Diseases resulting from deficiency: Lack of inflammation causes inflammation of the lining of the mouth and skin.
6 * Vitamin E (E):
Name: A group of vehicles with multiple names. It was discovered in 1922.
Function: Antioxidants, protect the body cells from destruction.
The most common sources: spinach, broccoli, wheat germ.
Diseases associated with deficiency: deficiency can lead to anemia.
7 * Vitamin B12 B12:
Name: Cobalamin. It was discovered in 1926.
Function: One of the fundamental factors in the synthesis of DNA (genetic material of cells).
The most common sources: meat, fish, eggs, dairy products.
Diseases related to deficiency: deficiency leads to anemia (anemia), also called sober anemia.
8 * Vitamin (K K):
Name: Generally known as vitamin clotting, it includes a group of compounds with multiple names. It was discovered in 1929.
Function: A key factor in the formation of coagulation factors.
The most common sources: spinach, leafy vegetables, broccoli, cabbage, fish, liver, meat, eggs.
Diseases associated with deficiency: lack of it can lead to abnormal bleeding.
9 * Vitamin B5 B5:
Name: Bentothenic acid. It was discovered in 1931.
Function: Incorporates some important compounds that help to decompose fatty acids and manufacture cholesterol in the body. It is used in natural medicine as an alternative to creatinine, and its presence is required for healthy and natural growth of hair.
Most common sources: Most foods especially in legumes, vegetables, eggs, red meat, whole grains, and royal jelly.
Diseases resulting from deficiency: burning foot syndrome, allergies, adrenal insufficiency, adison disease, and rheumatoid joints.
10 * Vitamin (H or B7):
Name: Biotin. It was discovered in 1931.
Function: It is necessary for the manufacture of insulin, antibodies, and some enzymes, and helps in metabolism.
The most common sources: Available in almost all natural foods, found in liver and yeast.
Diseases resulting from deficiency: deficiency is often the result of defects in its use (feeding on white eggs), not the lack of food because it is made by intestinal bacteria. The lack of biotin is rare because a large quantity of it is reused several times before being taken out in urine. Symptoms of the deficiency are on the body of skin peeling, hair loss, loss of appetite, nerve fiber damage.
11 * Vitamin B6 B6:
Name: pyridoxine. It was discovered in 1934.
Function: A catalyst for enzymes.
The most common sources: whole grains, vegetables, liver, beans, fish.
Diseases resulting from deficiency: lack of it leads to inflammation of the skin and mouth, nausea, vomiting, weakness, dizziness and anemia.
12 * Vitamin B3 B3:
Name: Niacin. It was discovered in 1936.
Function: plays an essential role in the enzymes involved in the metabolism of the body.
The most common sources: dairy products, eggs, fish, legumes.
Diseases resulting from deficiency: Lack of inflammation causes inflammation of the skin, rectum, vagina and mouth, as well as delayed mental development.
13 * Vitamin B9 B9:
Name: Folic acid. It was discovered in 1941.
Function: It is an important factor in the synthesis of DNA (genetic material of cells).
The most common sources: leafy vegetables, fruits, dried legumes, peas.
Diseases associated with deficiency: Folic acid deficiency leads to anemia (megaloblastic anemia).
Vitamins are divided into two parts:

Vitamins that dissolve in the water is vitamin C and B complex (C, B complex).
Fat-soluble vitamins A, D, E, K (A, D, E and K).

Fat-soluble vitamins are stored in the tissues of the body. Vitamins that dissolve in water (except vitamin B12) can not be stored in the body, and should therefore be constantly replenished.
After discovering vitamin A, vitamin B was detected and thought to be just one vitamin, but later it was discovered that vitamin B is a group of vitamins that dissolve in water. To differentiate between these vitamins were added numbers of their names, and resulted in vitamins B1, B 2 ... Today there are 8 vitamins in group B. One of which is called B12, which indicates that several substances from this group have been eliminated that have been shown to be non-B vitamins.


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Can a shark stall?
Today in marine biology I learned that, like airplanes, sharks use their pectoral fins to generate lift.  The question that neither me or my Professor know is if a shark can or cannot stall.
A stall occurs when the angle of attack of the wing (in aircraft) is exceeded, creating stalls of wind behind the wing.  This kills the lift and the aircraft begins to dive towards the earth.  Even though water is a more viscous liquid (than air), could a shark suffer the same effect?

As it turns out, yes- they can. First few hints in favour would be- 1) A stall is a fluid dynamics concept; and 2) Sharks have streamlined bodies.
The source for this answer is a researchgate article: https://www.researchgate.net/publication/331145186_Hydrodynamic_analysis_of_shark_body_hydrofoil_using_CFD_methods
The study uses a real-scale  image of  a Tope Shark (Galeorhinus  galeus). Below, you can see the hydrofoil production*.
(*A foil is a solid object with a shape such that when placed in a moving fluid at a suitable angle of attack the lift (force generated perpendicular to the fluid flow) is substantially larger than the drag (force generated parallel to the fluid flow). If the fluid is water the foil is called a hydrofoil.)
The pressure and velocity contours are there plotted for various angles of attack ($\alpha$), which can help determine the stall angle. The following is the velocity contour:

(Re stands for Reynolds number, which is predict flow patterns in different fluid flow situations. At low Reynolds numbers, flows tend to be dominated by laminar (sheet-like) flow, while at high Reynolds numbers flows tend to be turbulent.)

The velocity contour plot (Figure 11) shows that for α=0˚ the water speeds around both upper and lower  surfaces are close to each other and the lift force at the smaller angles of attack is relatively low due to nearly symmetrical geometry. The velocity at the boundary layer of the wall is observed to be approximating to zero (blue region) at each case due to the viscous effects around the wall. Increasing  α expands  the high  speed zone  (red color)  above  the  boundary  layer  of  upper surface,  also extends the  flow separation zone which is shown as blue.  It is observed that, the hydrofoil is at the condition of stall at α=10˚ due to the flow separation.

The simulations at both Re  numbers reveals a stall angle  around 7-8 degrees which is also verified by JavaFoil results. Beyond the 8 degree  stall  angle, the lift  performance  is  deteriorating and the drag  coefficient increases exponentially. This result shows that the variations in TSH swimming speed do not affect the performance behavior of Tope Shark; demonstrating the body shape of the tope shark is appropriate for a wide range of swimming velocities and is suitable for both cruising velocities and burst of speed.

Although I dont know about the shark diving using pectoral fins, i do know about sharks somewhat "stalling". They slow down movement to attack seals and whatnot. This article may help you : https://www.earth.com/news/slow-moving-sharks-strike/#:~:text=A%20new%20study%20from%20the,to%20pounce%20on%20their%20prey.&text=This%20behavior%20suggests%20that%20the,the%20best%20seal%20to%20attack.

Welcome and thanks for your answer. Answers should, in principle, be stand-alone. Referencing is great, even mandatory here on our site, but every answer should elaborate to a certain extent, such that the reader knows what the answer is. In this case, we don't even know whether the phenomenon you describe has anything to with the pectoral fins in the first place. If not, the answer is irrelevant to the question, as the animal may simply stop propelling itself forward or something.

oh sorry! im still a bit new, anything else i should know?

Yep - that we expect users to adapt their posts after receiving feedback :)

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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?

I think there was also a study which suggested that toxoplasmosis carrier were more likely involved in car accidents.

Should be this one: http://ijpa.tums.ac.ir/index.php/ijpa/article/view/214

possibly rabies https://en.wikipedia.org/wiki/Rabies

whole article on the subject. https://www.discovermagazine.com/planet-earth/meet-the-parasites-that-control-human-brains

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.

Can you add references?

Systemic candida overgrowth is for the most part a quack diagnosis: https://www.mayoclinic.org/healthy-lifestyle/consumer-health/expert-answers/candida-cleanse/faq-20058174

I see from your description you are talking about parasites that directly alter the neurochemistry of their host to cause direct behavioural changes geared towards passing the parasite on to its final definitive host species. Now to answer your question: No. No parasite species has yet been found that does this to humans. By my reckoning, it seems most to all of the parasites that employ this strategy use prey animals as intermediate hosts(Toxoplasma gondii uses mice, Dichrocelium bird flukes use land snails, etc.), meaning that the next host species is very likely to consume the infected prey animal as part of its regular diet. This by definition means that any parasite species which utilizes a intermediate host that has a very poor chance of being consumed and passing the parasite on, is likely to die out quickly.

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Does cancer really remain undetected about 80% of its life?
I was reading Atomic Habits by James Clear, who mentioned this and decided to google it. The only mention of this at least in the first search page was from this source from February, 2012. Is there any new resource that mentions this that isn't a decade old?

A study conducted by researchers at Stanford University School of Medicine provides strong new evidence that malignant tumors may grow undetected in the body for a decade or more before they can be sniffed out by the most sophisticated blood tests currently available.

There is undetected and there is unidentified; I detected my cancer symptoms for about a year before I found a doctor that could identify it as cancer.

I'd suggest finding that Stanford study on PubMed or google scholar and looking for studies that cite it.

@blacksmith37 - The question is, I believe, about size, not symptoms.

Your source bases "undected" on a blood test indicating the presence of a cancerous lesion. This says more about the lack of tumor-specific biomarkers than anything else. Many cancers present with symptoms. If you want to know about advances in tumor-specific biomarkers in the past decade, I'd look for that.

The size was stage 4 , the largest size category, I understand.

Once the Dr decided to do a blood test , it required only a couple days to identify it as HPV 16 induced cancer.

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Can plants suffer from CO2 poisoning?
Is there a point where too much CO2 is bad for a plant? Basically when there is too much CO2 in the air can a plant get sick?
Since plants photosynthesize and need CO2 to generate glucose and store starch, and since chemical reactions are pushed toward their end product when the reagent concentrations are increased, one would expect that more CO2 would be better, at least lead to increased growth and survival rates.
Is there a ceiling where CO2 gets toxic?

I have taken the liberty to add some background. Feel free to roll these changes back.

I'd question whether CO2 availability is really much of a limiting factor in plant growth.  I would think it would be the energy available from sunlight, if growth isn't limited by other factors such as water, temperature, nitrogen & other soil nutrients...

Many trees at Mammoth Mountain have died due to CO2 poisoning. See https://pubs.usgs.gov/fs/fs172-96/ for more info from link: "High CO2 concentrations in the soil kill plants by denying their roots O2 and by interfering with nutrient uptake. In the areas of tree kill at Mammoth Mountain, CO2 makes up about 20 to 95% of the gas content of the soil. "

Short answer
It has been shown that plants may already suffer from doubling the atmospheric CO2 concentration from 340 to 610 ppm, something that might happen during the next hundred years or so based on current emissions.
Background
A popular science website tells us that an excess of carbon dioxide (CO2) reduces the rate of transpiration of some plants. This is so because the stomata, which are the openings of the leaves (Mansfield & Majernik, 1970) and used for exchanging gases as well as water vapor (transpiration) will close when there is too much CO2 in the air, or other polutants such as SO2. As transpiration drops, the water flow from the soil to the leaves also drops, causing a runoff of water.This in turn stalls nutrient uptake. Indeed, doubling the present-day CO2 concentration to 610 ppm does not necessarily lead to increased growth and may in fact inhibit growth due to excess starch formation in the leaves, indicating it's simply stored as backup energy, nothing else (Coviella & Trumble, 1999). It is believed that plants might be near their saturation point and cannot eliminate CO2 faster than they are doing right now.
Somehow plants also become more susceptible to insect foraging when CO2 concentration increases.
Note however, that CO2 tolerances are species dependent. Most research in this arena has focused on common crops. CO2 tolerance in for example cotton plants is low, and starch buildup has been observed in the entire plant, but especially in the root systems and the stem (Hendrix et al., 1994). Other species, such as wheat and rice are less prone to effects of elevated CO2 (source: Nature).
References
- Coviella & Trumble,  Conservation Biology (1999); 13(4): 700–12
- Hendrix et al., Agricult Forest Meteorol (18994); 70(1–4): 153-62
- Mansfield & Majernik, Environmental Pollution (1970); 1(2): 149-54
Source
- Earth untouched

So did plants in the time of the dinosaurs simply carry adaptations to allow for a higher saturation point and thus greater use of CO2?

In case the OP wanted to see an example of CO2 killing plants, there's a place in California where this happens due to volcanic activity:  https://pubs.usgs.gov/dds/dds-81/Intro/facts-sheet/GasKillingTrees.html

@TheEnvironmentalist Ferns have been found to do well at high (3360 ppm, 10 time pre-industrial levels) CO2.  https://link.springer.com/article/10.1023/A:1006805427943

In situations with extreme excess of CO2, plants experience "excess starch formation" because it is "stored as backup energy" and it "inhibits growth"? So... Global Warming makes plants fat?

"... something that might happen during the next hundred years or so due to current global warming." Are you saying that warming increases CO_2 levels?

Good answer, but I think it's missing a critical point - different plants have vastly different tolerance. Many plants benefit from even large increases in CO2 levels (algae love CO2, as do many ferns etc.), while many can be stunted in growth or outright killed by a "mere" doubling. Also, I don't think it's warranted to say the increase in CO2 is "due to global warming" - even if the increase in CO2 levels is due to increases in global temperatures (and not vice versa, for example), it's not something you can just flatly assert without references, and the cause isn't really relevant.

@Luaan thanks for these comments. I have added several lines and additional references.

@jpmc26 - you are right, this was an error in my answer. I have removed it.

@jpmc26 Mind, increasing temperatures certainly do increase CO2 levels. Warmer oceans mean lower solubility of CO2, which means it's released to the atmosphere. Melting permafrost releases tons of CO2. There's plenty other examples, and likely many we have no idea about. Nothing surprising about that. But AliceD's formulation was certainly... tricky.

@Luaan you are right, and carbon release is a vicious circle. However, as you say, my wording was too blunt, but expanding on it is outside the scope of the question. Cheers

It depends upon the plant species.
As explained in Algae thrive under Pure CO2 Nature 227, pages 744–745 (15 August 1970):
Cyanidium caldarium (an algae found in Yellowstone National Park) grows much better in pure carbon dioxide than in air.
However, other plants can suffer from acidification of cell fluids at high carbon dioxide concentrations.
In Elevated Atmospheric Partial Pressure of CO2 and Plant Growth Oecologia (1979) 44: 68, it was shown that increasing CO2 concentration to 640 ppm from then-normal 330 ppm caused increased growth for both cotton (a C3 plant) and maize (a C4 plant), but the increase was much greater (100%) for cotton than for maize (20%).
According to The optimal atmospheric CO2 concentration for the growth of winter wheat (Triticum aestivum) J Plant Physiol. 2015 Jul 20; 184:89-97, photosynthesis at 968 ppm CO2 is optimal.  At 1200 ppm, photosynthesis is less than optimal, but still much higher than at current ambient CO2 levels of about 410ppm.

Since you need water to live, seem you would be peachy dropped on the bottom of the ocean ;)
Organisms usually adapt to specific conditions. In particular, plants need oxygen to actually consume the glucose produced in the process of which oxygen is a byproduct.
Is it possible to imagine an organism adapted to not having oxygen, by storing its own oxygen for reuse later? It sure is, and it might have been what originally happened in the original oxygen-free atmosphere.
But as a matter of fact, in the current oxygen-rich atmosphere this ability would be completely useless, just as it would be for you to bring everywhere a backpack full of air to breathe. As a consequence, no mayor plant does it; and it would take centuries of evolutionary pressure to develop it.

Most animals have anaerobic metabolic pathways. As you scale up, they tend to be progressively less capable of supplying all the metabolic needs of the organism, but they're there. Many plants evolved during a time with much higher CO2 concentrations in air, and some (like the vast family of algae) have essentially no upper limit on its concentration. Lots of plants need oxygen, but not all of them. As it is, your answer isn't very helpful - it would be better to include examples with references, rather than misleading metaphors and arguments from evolution.


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Why do cells not store glucose?
I understand that glucose is soluble and hence it is not stored by cells. However, my teacher said that I also have to say that "it would have an osmotic effect on the cell." I don't understand what that means.

You most have misunderstood something... Cells do store glucose, however they do so by combining glucose molecules into longer storage molecules such as starch or glycogen.
 https://en.m.wikipedia.org/wiki/Glycogen

...and they do this precisely to avoid osmotic effects.

@Jeppe and you seem to have missed the point of the question...

Then the question was poorly defined... as it did not specify storage method.

They do. Some cells can store glucose.
In human beings, liver cells and muscular cells do store glucose in the shape of glycogen which is a polymer of glucose (= a chain of glucose).
Muscular cells can use it during their contraction. The liver use it to put it in the blood to keep the blood sugar steady.
However it is not the preferred form of energy storage : the energy is stored in triglycerides (=fats).
A theory that explains this is that :
Glycogen is hydrophilic : it is very hydrated so it takes a lot of room
Triglycerides are lipophilic : it takes less room for equivalent energy
Therefore, glycogen storage are limited. In muscular cells, the glycogen storage is used after about 40 minutes (unless you are trained for endurance) and in the liver, the glycogen lasts about 24h.

Storing glycogen isn't storing glucose: it's storing something that can be made into glucose.

You might be struggling with the question, 'Why cells do not store glucose?'
Cells already have glucose in the form of glycogen- they convert the glucose into glycogen. This is because glucose is soluble and may be dissolved, as a result, the cell will become turgid. The cell will finally burst out at the extreme point!
I hope you hit the bull's eye.

Welcome to Biology.SE! It isn't clear that this adds anything to the existing answers — unless you have new information to add it would be best to focus on unanswered questions. In addition, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Thank you for taking the [tour], but please also consult the help pages for additional advice on [Answer] effectively on this site and then delete or [edit] your answer accordingly. Thanks!

You maybe asked the question Why cells do not store glucose?
Answer: Cells actually store glucose in the form of glycogen.
Glucose is soluble or dissolved and it has a higher osmotic effect so cells can swell up which means it can become larger due to storing glucose directly.
i hope it is super clear to you and you might find helpful


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What are the obstacles to modifying an algae to secrete fuel?
I've been reading a bit about algae fuel. It sounds like people did some work and then decided it was too difficult. This link mentions Exxon's work:
https://en.wikipedia.org/wiki/Algae_fuel#Commercial_Viability
And this next link shows the ex-CEO of Exxon talking about how they wanted an algae genetically modified to secrete oil, so they didn't have to kill and harvest it. He then says they encountered a low-level problem with the basic science, but doesn't elaborate.
https://youtu.be/vGv0R3zJ3cc?t=4m26s
Anyone know what that problem was?

If I remember correctly, Solazyme was founded to produce algal biofuel. It turned out that was not cost-effective, so they pivoted to nutraceuticals and the like — which did not save them. Sapphire Energy tried to produce algal biofuel in the Southern Californian desert, in open tanks. They also went bankrupt. If you grow the algae in transparent plastic containers, it's expensive. If you grow the algae in open tanks, your precious algae will be competing with all sorts of microorganisms that happen to find their way into those open tanks.


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Why do human females have periods?
Why do human women have periods when most animals don't? It is known that the unfertilized egg needs to be shed from the uterus. But why shed the whole endometrium? Why didn't evolution put macrophages to work to simply digest the ovum and only the ovum, instead of the physiologically, energy-draining process of menstruation and accompanying blood loss? Also, are there any other purposes for menstruation, besides wiping out dead ova?
Sites I used for references:
 1. Jensen et al., Am J Reprod Immunol (2012); 68(5): 374–386 -                       Menstruation seems energy draining, in my perspective, given that 30-40 ml of blood is lost × 3-4 days × 12 months × 15 years on average - that is a lot of blood loss.
 2. Also see this Quora post.

Related question: Why is menstruation in wild animals not a disadvantage to organismal survival?.

My question is different from this related question because there the OP is concerned about the survival advantage of the menstruation with respect to the predators. Here I've asked why menstruation and why not phagocytosis as the former to me seems to be highly energy consuming process. Also as the fellow post writer had earlier suggested though the two questions  seem to be one and the same, they are subtly different and aimed for two different audiences as I emphasise more on the physiological aspects of menstruation and the related question's OP needs clarification about survival advantage and other ecological aspects of menstruation.

This video may be informative: Why do women have periods?

Short answer
Shedding or reabsorbing the endometrial lining is energetically advantageous to the female.The advantage of shedding over re-absorption may be that sperm-born pathogens are removed from the uterus. A more parsimonious explanation, however, is that the endometrium in primates has developed into too large of a structure to be completely reabsorbed by the uterus wall.
Background
Basically you ask why are estrous cycles in mammals accompanied by regression and build up of the endometrial lining? The main reason for either reabsorbing or shedding the endometrial lining is thought to be to save energy. It has been calculated that, when implantation fails, a cyclical regression and renewal of the endometrium is energetically less costly than maintaining it in a metabolically active state required for implantation. In the regressed state, oxygen consumption in human endometria declines nearly sevenfold. Metabolic rate is at least 7% lower, on average, during the follicular phase than during the luteal phase in women, which signifies an estimated energy savings of 53 MJ over four cycles, or nearly six days worth of food (Strassmann, 1996; Crawford, 1998).
In fact, impaired shedding of the endometrial lining may lead to pathologies. If no egg is released and the estrogen/progesterone system becomes imbalanced, the endometrium may continue to thicken, instead of breaking down and being shed normally as a menstrual period. This abnormal thickening is called endometrial hyperplasia. Periodically, the thickened lining is shed incompletely and irregularly, causing irregular and more heavy bleeding. If this cycle of abnormal thickening and irregular shedding continues, precancerous cells may develop, increasing the risk of cancer of the uterine lining (endometrial cancer), even in young women (source: MSD manual).
Now the question of why human females shed the endometrial lining instead of resorbing it? Indeed, shedding the endometrium is mainly limited to primates, as opposed to reabsorbing it (like in most other mammals). Here, I do not have a definitive answer, but I like to share two opposing hypothesis on the matter.

Hypothesis 1:  Profet (1993) hypothesized that shedding the endometrium may be an effective way to get rid of sperm-based pathogens. The accompanying bleeding, Profet hypothesizes, delivers immune cells into the uterine cavity that can combat pathogens.
Hypothesis 2: Strassmann (1996) surmises that the endometrial microvasculature is designed to provide the blood supply to the endometrium and the placenta, and that external bleeding appears to be a side effect of endometrial regression that arises when there is too much blood and other tissue for complete reabsorption. The relatively large blood loss as seen in humans and chimpanzees can be attributed to the large size of the uterus relative to adult female size and to the design of the microvasculature in the uterus wall.

References
- Crawford (ed), Handbook of Evolutionary Psychology: Ideas, Issues, and Applications, Psychology Press (1998)
- Profet,  Quarterly Rev Biol (1993); 68(3): 355-86
- Strassmann, Quarterly Rev Biol (1996);71(2): 181-220

WebMD lists the most common reasons for missed periods as weight disorders, eating disorders, increased exercise, and stress.  It seems like the body's tuned to undergo the costly process of shedding/regenerating the lining only when the metabolism is working correctly and not under significant stress.

Sidenote: I read recently that a contributing factor is that the human endometrium is bigger than in other mammals, which it needs to be because human fetuses are more aggressive when implanting and could otherwise connect directly with the mother's bloodstream as in an extrauterine pregnancy.


text:
Why doesn't blood remain on a mosquito's proboscis in quantities that could spread blood-borne diseases?
We know that HIV can't be transmitted by mosquitos, and nor can other highly virulent viruses that are transmitted through blood and bodily fluid exchanges, such as Ebola (thankfully!).
Marcus Junius Brutus asked an interesting question in a comment on that above-linked question's answer:

[Why can't] tiny droplets of blood remain on the proboscis of the mosquito long enough for said mosquito to inject its proboscis into the bloodstream of another person? In particular, in what physical aspects is the proboscis different than a needle or razor? I am not talking about blood sucked into the gut of the mosquito, I am talking about blood remaining on the proboscis

There's no doubt that dirty mosquito proboscises aren't a vector for blood-based viruses (if they were, Ebola would be completely uncontainable in West Africa), and I understand the explanation on the above linked answer that there's no route from the mosquito's stomach to its proboscis other than via saliva production, but given how tiny the amounts of blood are that are required for transmission of such highly virulent viruses, why does it never happen in a similar way to transmission from a dirty needle or razor?
I've never seen a mosquito put its proboscis in sterilising fluid or an autoclave between feedings...
My best guess would be that mosquitoes are very efficient at taking up all available fluid, and that surface tension means that at this scale it is possible to take up every last droplet - but that's just a guess.

I guess a spin on this question is: is one virus 'particle' enough to cause an infection (or what probability)? I understand that viruses are extremely small.

Doddy - I believe you're taking about virulence, which varies from pathogen to pathogen. Ebola and HIV I believe are extremely virulent, readily transferred via dirty needles etc, which is why I chose them as examples (since even they clearly aren't transmitted from a used probiscus)

Droplets might be the key to this. Apparently, the proboscis inner diameter can be something like 25 microns or so, while blood droplets are apparently around a milimeter or so (that's where the shape of the droplet is almost perfectly spherical, which means great surface tension). So it might very well be that no blood is "stuck" on the proboscis after a feeding. I'm quite interested in the actual answer, though :)

Always relevant videos for proboscis: one, two.

@Luaan I'm not an expert at all in this field, but I find it hard to believe that there's a 0% probability that just because a droplet of blood happened to be on the proboscis of a mosquito at one time means that it definitely cannot inject the virus into a subsequent victim. What does surface tension have to do with it? Can't virus particles stick to surfaces?

@Doddy There's no such thing as 0% probability, ever :) Surface tension is very important because it makes it harder for stuff to cross the surface of a liquid. Without a surfactant, there is very little contact between the tube and the droplet - the two repel each other quite strongly. Imagine a drop of water on an oily surface - you're not going to get a surface wet if it is hydrophobic, and if it doesn't get wet, it doesn't get dirty. Of course, assuming the "dirt" is polar - however since the envelope of HIV is sacharous, this should be a good description. It's just conjencture, though :)

That's right.  There is 0% probability of any 0% probability, ever. :)

What you're talking about is called mechanical transmission (at least in veterinary and medical circles; plant epidemiologists call it something different). There's a nice overview by Gray and Banerjee here, although it's a bit old.
The short answer is that blood-feeding insects can mechanically transmit a range of pathogens, including viruses. Mosquitoes specifically are thought not to be great mechanical vectors because of the small quantities of infectious material that could be transferred between feeds. Large biting flies such as tabanids are thought to be much better potential mechanical vectors as they are pool-feeders; they basically chew up an area of skin and then mop up blood from the wound with their mouths. The quantity of blood contaminating a horse fly's mouthparts after feeding is reckoned to be about 10 nanolitres (Foil et al. 1987), which while not much could contain an infectious dose for some viruses reaching high titres in the blood. They also feed frequently (and painfully, which means they are often interrupted).
However, a number of viruses do seem to be transmitted in the field or in a lab setting by mosquitoes, particularly poxviruses (lumpy skin disease virus, myxoma virus and fowlpox virus, for example). Equine infectious anaemia virus (a retrovirus) is also thought to be mechanically transmitted by large biting flies in some regions despite its relative fragility. Some parasitic and bacterial diseases are also mechanically transmitted by blood-feeding insects; Trypanosoma evansi for example (the causative agent of surra) has lost the capacity to be biologically transmitted by tsetse and is solely mechanically transmitted.
(suggestions for improving this answer extremely welcome; I'm fairly new to SE)

A mosquito's proboscis isn't like that of a butterfly, which could easily have nectar clinging to it when it is coiled up; instead, consider that the part of the mosquito's proboscis that enters a blood vessle is probably wiped clean when it is retracts outward through the epithelium. A a dirty needle or razor is many, many times larger than the sucking parts of a mosquito, and a razor is an unlikely vector of HIV.
Epithelial tissue consists of cells very tightly bound together; it has to be to prevent constant invasion by bacteria, fungi, etc. It takes some considerable force or sharpness to penetrate. If you've ever watched someone give you an injection (a vaccine, for example), the needle is never bloody upon withdrawal. You might get a bead of blood from the wound, but the needle itself will be quite clean. The reverse is also true due to essentially the same reasons: the likelihood of introducing a pathogen by dragging it from the surface into the subcutaneous area is so low that there is no absolute need to swab visibly clean skin before giving a subcutaneous injection:

Although skin that is visibly soiled or dirty must be washed, swabbing the clean skin of a patient before giving an injection is unnecessary. Studies suggest that there is no increased risk of infection when injections were given in the absence of skin preparation. (WHO Bulletin)

HIV is the most serious virus (aside from Ebola, about which much is still unknown) which can be transmitted by needlestick. Sharps injuries - needles, suture needles, scalpels, lancets, etc. - are very common in the medical field, estimated to be much higher than 350,000/year due to underreporting and occurrence in non-hospital settings, e.g. nursing homes, etc. Of course, in the majority of sharps injuries, the sharp wasn't likely to have been used on someone with HIV. Still. HIV is not rare.
Even with a potential half-million exposures a year to sharps, as of December 31, 2013, only 58 confirmed occupational transmissions of HIV and 150 possible transmissions had been reported in the United States. Of these, the vast majority follow hollow needle sticks (88%), where blood drawn from a patient still remains in the bore of the needle which can be reinjected into the unfortunate recipient. If the patient is terminally ill with AIDS, the incidence of transmission by hollow needlestick is increased, meaning the viral load in the blood is important. A solid needle, even a bloody one, presents a very low risk (the risk is, in fact, unknown*.) Getting blood splashed in the eye is a higher risk than a sharp solid (i.e. suture or lancet) needle.
The piercing mouthparts (The mandibles and the maxillae) are solid, akin to a solid sharp. Only the twin tubes (the hypopharynx and the labrum) actually reach blood.
So, given the combined factors of limited survival of HIV on exposed surfaces, the small size of the proboscis (compared to a suturing needle or a lancet, both of which have a higher surface area, yet not known for certain ever to have transmitted HIV), the low probability that the mouth parts have HIV-laden droplets of blood on it, the fact that only the tip of the hypopharynx and labrum encounter blood (the fluid most likely to contain virus) and the extremely low probability that there are enough actual HIV viruses to cause an infection anywhere on the proboscis, I hope this answers your question.
Edited to add: I've focused on HIV here, because it's not known to infect mosquitoes. Mosquitoes are considered by many to be the most dangerous animal in the world. They transmit a significant number of viruses and parasites (like dog heartworm, elephantiasis, dengue fever, equine encephalitis, etc.), but (hypothesized from those diseases that have been studied in mosquitoes) only after being infected by the pathogens themselves. Some die of the infection; some die before the infection spreads through the mosquito's body, some don't harm the mosquito. But transmission is from infected saliva injected into or onto the bite site, not virus particles on the proboscis, as evidenced by the need for adequate incubation time between the bite that takes up the virus to the bite that transmits the virus. If there was sufficient virus on the surface of the proboscis, that incubation time would not be necessary.
Best infection control practices for intradermal, subcutaneous, and intramuscular needle injections
Workbook for Designing, Implementing and Evaluating a Sharps Injury Prevention Program
Occupational HIV infection among health care workers exposed to blood and body fluids in Brazil
Needlesticks: What you must know

Great answer! The only thing this leaves me wondering is, how does sharing needles lead to virus transmission? I believe it's common among drug users (especially hepatitis I believe?). I guess hypodermic needles can suck small amounts of blood inside the tip?

Hepatitis B is much more easily transmitted by sharps and needlesticks than HIV. In terms of needle sharing, some of it has to do with withdrawing a small amount of blood into the syringe before injecting the drug, guaranteeing that some blood will be in the syringe shared with the next person, and the fact that it's a hollow-bore needle.

I assume the "withdrawing a small amount of blood" is accidental and related to untrained needle use (e.g. allowing the plunger to move out slightly before withdrawing the needle)? I guess the obvious difference with a mosquito is, that any remaining inside their proboscis will then be sucked into their stomach, whereas with a shared needle it'll be mixed with the next injection.

I have never injected drugs into myself, but the usual procedure insuring that the needle is in the vein is to withdraw the plunger a bit until you get "venous return" (blood tinging the fluid in the hub if not the barrel of the syringe.) If you don't do this, you might inject the drug into subcutaneous tissue instead of the blood stream, which would be pretty much a waste of the drug.

@user568458 anongoodnurse is, of course, correct, but I'd just add: IV needle sharing involves repeated direct injection into a vein. The direct injection into a vein makes it a much more efficient method for transmitting any bloodborne pathogen than a single prick of the skin. And yes, the transmission efficiency of HBV > HCV > HIV, but when I had my sleep deprived accidental stick with a sharp used on an HIV+ patient, I surely didn't inject it into my vein.


text:
Microsatellites and Minisatellites: Which of these form the basis of DNA fingerprinting?
I'm in a fix.
 Prepare yourself for a long read
We've just learned about minisatellites and microsatellites at class (okay, by "learned", I mean we were told their definitions and essentially nothing else... hardly surprising, since we aren't expected to know more than that at school).
Shortly afterwards, we touched on the topic of DNA profiling, and my textbook went on to state:

Minisatellites are hypervariable and are specific to each individual. This uniqueness is employed in DNA profiling.

Which would imply that the repetitive DNA fragments used in DNA profiling (VNTRs - Variable Number Tandem Repeats) are (only?) minisatellites.
Fine.

However, the Wikipedia pages on minisatellites and microsatellites (I linked both of them earlier on in this post) mention:

(Minisatellites and microsatellites)... together are classified as VNTR (variable number of tandem repeats) DNA. Confusingly, minisatellites are often referred to as VNTRs, and microsatellites are often referred to as short tandem repeats (STRs) or simple sequence repeats (SSRs).

If I interpreted this correctly, it's saying;
"Both minisatellites and microsatellites are classified as VNTRs. But when one normally talks about "VNTRs" he/she is referring to minisatellites. Microsatellites are, instead, commonly referred to as STRs/SSRs."
Okay, so far so good.
The Wikipedia page on microsatellites explicitly states that they (the microsatellites) are the ones you deal with in DNA profiling. However, the Wikipedia page on minisatellites carries no clear indication of their (minisatellites) use in DNA profiling.
Ugh.
And to compound my confusion, the Wikipedia page on DNA profiling states:

DNA profiling uses repetitive ("repeat") sequences that are highly variable,called variable number tandem repeats (VNTRs), in particular short tandem repeats (STRs), also known as microsatellites, and minisatellites.

Which suggests that both minisatellites and microsatellites are used in DNA profiling (as they're both VNTRs), but microsatellites are more relevant in this regard.

Summing up what I said:

My textbook  says that DNA profiling makes use of VNTRs.
My textbook (and teacher) says DNA profiling makes use of only minisatellites.
Wikipedia says that VNTRs refer to both minisatellites and microsatellites.
Wikipedia says that VNTRs are typically mentioned in reference to minisatellites. Whereas microsatellites (which are strictly "VNTRs") are better known as STRs/SSRs.
Wikipedia says (explicitly) that microsatellites are used in DNA profiling. It doesn't mention minisatellites in this regard.
Wikipedia says that both minisatellites and microsatellites are used in DNA profiling, but minisatellites are use more often.

 This inconsistency over the three Wikipedia articles I've linked is seriously annoying

My question(s),
1) I'm told that VNTRs are used in DNA profiling. Does this refer to both minisatellites and microsatellites...or just minisatellites?
2) If only one of them is used, why disregard the other? They're both (technically) VNTRs aren't they? So shouldn't either of them work just fine?

I have complained many times about too long questions in the past. It is good to see here a long question, which has good reasons to be long. Also, it is nice to see a long question with a pleasant format.+1

1) I'm told that VNTRs are used in DNA profiling. Does this refer to both minisatellites and microsatellites...or just minisatellites?
Actually, it refers mostly to STRs. I worked a bit in forensic genetics and we always published works using STRs markers (one example here, there are plenty in the literature).
In addition, I would not be surprised if current forensic identification used SNPs instead, e.g. as proposed in this paper
2) If only one of them is used, why disregard the other? They're both (technically) VNTRs aren't they? So shouldn't either of them work just fine?
I really don't know, but I am sure that it has to do with one of a) level of variation, i.e. if minisatellites have lower mutation rates and are less variable, then they also are less useful, b) ease of genotyping.
Browsing in the web I found this website from which I understand that the minisatellites were the first to be used to perform DNA profiling (using a method different from sequencing) and that "modern" DNA profiling is performed using STRs. However, I insist that modern DNA profiling should be better performed using SNPs.


text:
Are the "cocaine hippos" suffering from noticeable inbreeding depression?
Colombia has a population of about 100 "cocaine hippos" founded from a group of one male and three females, which escaped from a drug kingpin's private zoo; it's even estimated that this population could grow to over 1,000 in the next two decades or so:

The rise of the so-called "cocaine hippos" began in 1993 after authorities killed Pablo Escobar and seized his luxury estate Hacienda Napoles, about 250km (155 miles) north-west of the capital Bogotá.
Animals found there were distributed to zoos across the country, but not the hippos. "It was logistically difficult to move them around, so the authorities just left them there, probably thinking the animals would die," Ms Castelblanco said.
Instead, they thrived.
Over the years, scientists have tried to calculate how many hippos are living in Colombia's waterways, with estimates ranging from 80 to 120 animals. "It is the biggest hippo herd outside Africa, which is their native region," veterinarian and conservationist Carlos Valderrama told the BBC. [...]
Ms Castelblanco and her peers say the population will reach over 1,400 specimens as early as 2034 without a cull - all of them descended from the original group of a male and three females.

I'm curious however if these "cocaine hippos" don't show any signs of inbreeding depression given how small the founding group was. Are there any studies/articles on this aspect in that Colombian hippo population?

I found one publication of Hippo population genetics from 2015 in Mol. Ecol. but they sadly didn't feature the Columbian population, actually it seems there is very little research going on regarding this Cartel-neozoa -bloat. Sadly some people are trying to get them on birth control https://www.animalbalance.org/hippos . They could be of great value for the fields of population genetics, evolution, invasive species ecology, as well as ecosystem engineers ecology.

Well, is there a report that they don't suffer from inbreeding depression?

@user12256545 *Colombian. Columbian is the exchange.

@pascal no, but since the founder group consisted of a male and three females, its likely they do.

https://biology.stackexchange.com/q/98252/27148 seems like approximately the same question asked a different way.

It then seems you gave yourself an answer.

Answer: Its highly likely they are suffering from inbreeding depression,or will be at least soon, since the founder population size (n=4) is three magnitudes low of the literature value for the minimal viable population size. Even if there is no genetic evidence in form of a published study, this is a super clear case with such a restricted gene pool.

An MVP of 500 to 1,000 has often been given as an average for terrestrial vertebrates when inbreeding or genetic variability is ignored. When inbreeding effects are included, estimates of MVP for many species are in the thousands. Based on a meta-analysis of reported values in the literature for many species, Traill et al. reported concerning vertebrates "a cross-species frequency distribution of MVP with a median of 4169 individuals (95% CI = 3577–5129)."

source:

https://en.wikipedia.org/wiki/Minimum_viable_population
https://www.sciencedirect.com/science/article/abs/pii/S0006320707002534?via%3Dihub


text:
I just had my genome sequenced. Can someone tell me what these different file formats are?
I just had my whole genome sequenced and now I want to play a bit with bio-informatics. However, the documentation is quite scarce on the file standards used.
These are the files I have been given (the "raw" data):

Can someone explain me with some detail what is each file format, and for what are they used?
Transcribed list of file-formats from the picture:

Indel (TBI)
Indel (VCF)
SNP (VCF)
SNP (TBI)
CNV (TBI)
CNV (VCF)
BAM (BAI)
BAM
FASTQ R2
FASTQ R1

I'm voting to close this question as off-topic because isn't a biology question as defined for this site. Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site for details. It might fit within [Bioinformatics.SE], but please check their help pages before posting there. Thanks!

"I just sequenced my whole genome": Out of curiosity, how did you do that?

@tyersome sorry, please forgive me. I actually looked for a bioinformatics stack but google brought me here :X

@bli I am living with this condition for almost 20 years, and it had no progress, so I though: It probably isn't "cancer/leukemia/MPN" (i.e. a malign for of PV). So it was important to get the raw data to compare my genes with the most recent literature discoveries (standard sequencing tests do not cover most genes that justify this). Now I have the raw data and I already used apps on sequencing.com to browse and search these genes (DanteLabs also has a Gene Browser, but I like to compare). So, what I have found today: (next comment)

@bli the test used saliva, and there's a debate if saliva is fully germline or not, but either way, given that my JAK2 is neg, and I live with this "PV" for at least 20 years (I have 30) I doubt I have any somatic mutatiion, so it must be congenit... If it were true PV I would maybe be dead by now. So without further ado, I found that: (i) I have a very high chance to develop Hereditary Hemochromatosis (HFE, ELAC2), (ii) then I search for all the genes I could for PV, and I found Familial Erythrocytosis mutations, several SNP mutations in two big genes (EPAS1, EGLN1), and (iii) ...

@bli ...and (iii) I was suspecting that I also have very high ocygen affinity (gonna test my p50 soon) so I looked for the (apparently ONLY?) documented gene that can cause erythrocytosis with high affinity, these gene is a2-globin gene, and I have a very very clear mutation like this: chr16 173,183 G>A. The paper I learned this from: doi: 10.1111/j.1365-2796.2008.02014.x (Blood p50 evaluation enhances diagnostic definition of
isolated erythrocytosis)

@bli regards the Hereditary Hemochromatosis, I probably still not have it as my iron levels are normal... But again, I have this form of PV, so they might cancel each other... lol

@bli probably I am going to organize this data and publish it online freely available to the world (DNA, diagnostics, etc).

"Polycythemia vera (PV) is a chronic myeloproliferative neoplasm. Virtually all PV patients are iron deficient at presentation and/or during the course of their disease." || So lol, what were the odds? I have no iron deficiency, so maybe my Hematochroma is already here and PV cancels it out, because my iron levels always measured normal in the past (as well as my EPO levels btw - not secondary PV)

Related: What is the difference between FASTA, FASTQ, and SAM file formats?.

@PedroD Out of curiosity too, concretely, how do you "sequence your genome" from saliva? Do you do it yourself, using a machine available at your research lab? Or do you send your saliva to a lab (what kind of lab?), what kind of price is it to have your full genome sent as computer files?

"I just sequenced my whole genome" : this is so cool, sounds like Sci-Fi :)

No lol, I did it in DanteLabs (they arefrom Italy), and besides the classic reports, they also give you all the raw data in the formats above.

The machine they used was Illumina nextseq 6000, I paid ~250€, it takes about 2 months

@PedroD Then perhaps the title should read "I had my genome sequenced..."

@CarstenS Better now?

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology. I'm glad we encourage such questions from curious people who want to learn more.

Your genome has a sequence that is unique to you, gifted to you by your parents and by small changes from random chance.
Your genome is pretty close to what is called the reference genome, which gets updated — infrequently1 — as sequencing platforms, pipelines, and algorithms change.
The reference genome is the "standard bearer". All other individual genomes are compared against it. This lets everyone compare apples to apples when trying to say something about the genome, in the aggregate or "big picture" view.
The files associated with the VCF format specify places in your genome that differ from the reference genome — and how they differ. These differences include:

Indels — insertions or deletions of DNA, as compared with the reference.
SNPs — single bases that differ from the reference.
CNVs — repeated stretches of DNA that differ from repeats in the reference.

The specifics of each of these classes of variants can be associated with various diseases or other attributes that make you unique and interesting. More on that later.
Each of these VCF files in your dataset has an associated TBI file. This is an index file, which helps you to quickly retrieve elements of interest from these datasets using a command-line tool called tabix.
If you are looking for differences within a specific genomic interval — say, all the differences on chromosome 4, from bases 123456 to 567890 — then you can pass that interval to tabix along with your VCF file of interest, and it will return all the indels, SNPs, or CNVs within that range, if there are any within that interval. This subset is VCF-formatted, so by knowing the format, you can get more detail about those differences.
The BAM-formatted file collects all the individual sequencing reads in a form that is mapped or aligned to the reference genome, along with some summary information to tell you how those reads differ from the reference genome.
As with the VCF files, this BAM file has a BAI index file to go along with it. Like tabix, you can use the samtools command-line tool to extract the set of reads over your genomic region of interest, if you want to examine them further.
Both tabix and samtools are available from the same author. If you have questions about these tools, the Bioinformatics Stack Exchange site is a great place to ask questions3. Lots of bioinformaticists  there have a great deal of experience with those toolkits and can help answer more specific questions.
The two FASTQ files are the raw sequence data coming off the sequencer, along with quality data. The sequence reads in these two files are paired for higher quality and longer reads, which makes the sequencing platform faster, cheaper, and better.
I walked a bit backwards, here, on purpose.
The raw FASTQ files are starting material for making the BAM file. The BAM file is then, in turn, used with variant calling software (example) to generate the variation (VCF) datasets.
Why walk backwards through these datasets?
Most people don't care about the raw FASTQ data, except perhaps to do manual alignment or check data quality. What is often more interesting or useful to most is how one's genome differs from the reference, which is captured in the variation data.
Those differences, in aggregate, are how companies like 23andme sell a product2 that tells you that you are more related to so-and-so population than so-and-so population, or whether you are more or less likely to have some disease or other odd, interesting phenotypic trait.
1. Even when new versions of this reference genome are released every few years or so, if you know what original reference genome was used to generate your BAM and VCF files, you can redo analyses based on that knowledge. There is likely some metadata associated with your sequencing results that you can look up to find this out, or you can ask the sequencing center from where you obtained these results.
2. For a bit more context, in this answer to another SE question, I talk a bit about SNPs and how they are used for testing association with so-called Mendelian disorders, diseases caused by single base changes, which may be of interest to you given what motivated you to get your genome sequenced, in the first place: https://biology.stackexchange.com/a/88839/5075
3. You can ask questions about them here, too, but you'll make certain people grumpy. Better to go to the other SE site for that.

OMG this is the most complete explanation I've read. Thank you! You should create a blog post with this, I could not find any that introduced all formats this way, actually the info is scattered around in an unorganized way. Thanks!

+1, but it seems to be missing an essential piece of information. If the reference genome is regularly updated, how does one know which version of the reference genome the data is relative to?

@JBentley you can't tell from the file formats (which this question is about). Sometimes the bam files can have indications, but the only way sure way is asking the person who generated the files.

@JBentley Reference genomes are not updated too frequently. But they do change every few years, and the selection of reference determines the outcome of BAM and VCF files, which are analysis products of the raw FASTQ reads. For humans, a couple common reference genome keywords are hg38 and, perhaps less so, hg19. Perhaps some metadata file not shown here in the question makes use of one of those labels, but as mentioned by @Nicolai, asking the sequencing center where the data come from should get an answer, as well.

Please have an upvote! I'm a bioinformatician too, and this is an excellent answer. Also, just the fact that someone is able to ask this question suddenly brought into focus how far sequencing has moved on since I started.


text:
Why is chemotherapy-related hair loss temporary?
Chemotherapy kills cancer cells by targeting rapidly growing cells. That is why patients lose hair as well. Why is chemotherapy-related hair loss temporary?
The doctors say it is because healthy cells are able to repair themselves. But, if that is true, then people should not even lose their hair, as the damaged hair cells would repair themselves before patients lost their hair.

Related: https://medicalsciences.stackexchange.com/q/20545/12704

Its less that the cells repair themselves and more that the tissue can repair itself. Rapidly dividing tissues have reservoirs of stem cells waiting to replace the cells that are rapidly lost. For instance, histologically, there are stem cells just waiting at the hair follicles and intestinal lining, waiting to replace the old cells that rapidly die off. But those are killed off during chemo.
Stem cells at the follicles:

Most chemotherapy drugs targets DNA replication in some way, which damages not only cancer cells but normal replicating cells as well. But normal cells are typically more resistant, and stand a better chance of survival. It is thought that this is because normal cells respond to DNA damage by "arresting" the cell cycle, and not dividing until the damage can be repaired. Cancer cells, in contrast, have lost these safety mechanisms, and will continue to divide despite having damaged DNA, which can cause serious problems and lead to cell death. This difference is exploited in chemotherapy.
There are of course large variations between individual cells. Some normal cells will die of chemotherapy, and some cancer cells will survive. But statistically, normal cells stand a better chance, and so chemotherapy dosage can be adjusted to a level where the drug effectively kills most cancer cells, but spares at least some normal cells. (Provided the cancer is sensitive to the particular drug used, of course; in many cases this strategy unfortunately does not work.)
After a course of chemotherapy, many normal proliferating cells will also be damaged, causing problems like hair loss and other unpleasant side effects. But given some time, normal cells will recover and repopulate hair follicles and other tissues.


text:
Are Italians genetically separated from other Europeans?
I was reading the Wikipedia article about the genetic history of Italy, and I found it interesting. There are, however, a few things that puzzle me, because they seem to contradict each other.
For example, it states that, because of the Alps forming a natural barrier, Italy is, along with Finland, a genetic island in Europe. Does this mean Italians and Finns are genetically separated from all other Europeans, and to what extent?
Later in the same article it says that

In Italy as elsewhere in Europe the most common haplogroup is haplogroup H

which would seem to contradict the genetic island theory. After all, Italy has been colonized by countless populations throughout its history, which might suggest the Alps didn't really stop the gene flow from neighboring countries (not to mention that other European countries are equally separated by mountains, like Spain).
I have no background in genetics whatsoever, so please excuse my ignorance. I am just trying to understand an article that seems very confusing and throws lots of different information together.

EDIT: Thanks for the quick reply! I've found another link, which seems to be more reliable than Wikipedia's unverified claim, though it still sounds like a weird theory to me.

Please don't ask many questions in a single post. Split them up into separate questions instead. I have removed the second question, please post it again separately.

you have to remember that in most human history people just didn't move around like can now.  population haplogroups do migrate, but slowly enough to identify their movement.  The Alps didn't stop migration, but they would have kept the flow down significantly compared to the overall migration rate in the french areas, connected by rivers and flatter terrain.

This makes me think of a report of a healthy village in Italy where 400 people were 90% descended from a Northern European couple and were genetically studied because cancers were very rare in the village... Also note that walking from Genoa to Marseille has a maximum elevation of 550m. Alpine populations can be fairly insular, but Italy is very diverse.

No, Italy is not a Genetic island but Sardinia is;

There is no such thing as a genetic Italy or an Italian (genetically); Italian groups (North Italians / Central Italians / South Italians / Sicilians / Sardinians) are diverse and do not cluster with each other (DiGaetano et al 2012 / Nelis et al 2009) in PCA-plots; In fact Italians are just as little related with each other (IBD sharing) as they are to other nations (Ralph & Coop 2013);
In general North and Central Italians cluster closest to each other and to Greeks and Albanians while South Italians cluster between Greeks and Cypriots (Lazaridis et al 2013);
What is truly a 'genetic island' is the island of Sardinia; The Sardinians are an isolated population and only cluster with old Neolithic-Europeans (Keller et al 2012 / Lazaridis et al 2014 / Gamba et al 2014 / Haak et al 2015), reason being they are ~90% genetically identical (inheritance) with the old Neolithic-Europeans (Haak et al 2015 / Sikora et al 2014);
As for the quoted study i.e. Lao et al 2008; It is not clear (to me) what the sample make-up of IT1 is; In Figure S2 one can clearly see its samples clustering all over the place; Some samples cluster in between Greeks (EL) and Swiss (CH) where as others are completely isolated; I assume that these samples are from all over Italy incl. Sardinia and that the isolated samples are the Sardinian ones; Lao et al is a study from 2008, and probably because of such results, more recent studies tend to label the Italian samples according to region (North Italians / Tuscans / South Italians / Sicilians / Sardinians) in order to have a clearer insight;

So the real 'lesson' is that Italians, despite being politically ONE nation, are in fact however genetically diverse i.e. not one people; And Sardinians are an isolated old-stock, in fact the last Neolithic remnants in Europe;
Ultimate advice: Dont bother with Wikipedia and whatever someone has written there; Read the studies themselves (first hand), thats the most reliable;
Some inside into Italian genetics:
K=7 and K=9 Admixture analysis (incl. North Italians / Sardinians)
Di Cristofaro et al 2013
http://s3-eu-west-1.amazonaws.com/previews.figshare.com/1251712/860/p_01.png
K=10 Admixture analysis (incl. Tuscans / Sardinians)
Behar et al 2010
http://s14.postimg.org/g7agga7e9/u1u11.png

That's an interesting answer. Can you add links to the cited papers?

I'm afraid that the "genetic island" idea is almost certainly wrong because

The wikipedia page offers no evidence for this claim:

Following scientific research carried out by Dutch geneticists, Italy has proven to be one of the last two remaining genetic islands across Europe (along with Finland), this due to the presence of the Alpine mountain chain that, over the centuries, has prevented large migration flows aimed at colonizing the Italian lands.[citation needed]

Remember that any random idiot person can edit a wikipedia page. If there is no supporting reference for a claim you find in wikipedia, you should treat it as suspect.
As you point out, the Alps only block entry on the north of Italy. Italy, however, is a pretty large peninsula, completely open to the sea along its entire length. For example, here is a map of Greek and Phoenician colonies circa 530bc (source):

As you can see, significant parts of the coast of what today is Italy were colonized by Greeks and Phoenicians. There were many subsequent waves of migration and/or invasion by various tribes such as

The Lombards (image source):

The Visigoths who sacked Rome in AD410
The Ostrogoths whose kingdom in its prime contained most of modern Italy

The many Jewish communities in Italy that go as far back as the Roman era.

An article by Brisighelli et al. (which is actually quoted at the very top of the Wikipedia page you linked to) mentions that (emphasis mine):

A total of 583 individuals were sampled from across the Italian Peninsula, from ten distant (if homogeneous by language) ethnic communities — and from two linguistic isolates (Ladins, Grecani Salentini). All samples were
[...]
Italy shows patterns of molecular variation mirroring other European countries, although some heterogeneity exists based on different analysis and molecular markers. From North to South, Italy shows clinal patterns that were most likely modulated during Neolithic times.
[...]
Before the Roman conquest, ancient Italy was characterized only by the presence of Indo-European populations living in the Italian Peninsula since the second millennium BC, corresponding to the period between the Iron Age and Romanization. During all this period there were also increasing contacts with the Phoenician and Greek colonists: the former being largely present on the coasts of Sardinia and western Sicily and the latter in Southern Italy.
[...]
At the beginning of the first millennium BC the following native tribes could be distinguished on the Italian territory: the Ligures, on the coast that bears their name, in the northern Apennine valleys, part of the pre-alpine valleys and the western Po Valley; the Sicani, in the interior of Sicily; and the Itali, in present-day Calabria (from whom comes the name ‘Italy’, which was to be extended to all the territory of the peninsula). Besides the already mentioned Terramare tribe, on the southern edge of the Po Valley, and the Villanovans, probably from Eastern Europe who settled throughout Central Italy, there were also the Umbrians to the east of the upper basin of the Tiber. The Veneti, who occupied the territory that still bears their name, originally came from Illyria as did the Messapii (now modern Salento or South Apulia) and Iapyges, who settled in present-day Puglia (Apulia) 5. Many other populations of Central-Southern Italy were created by the mixing of local and foreign elements dating back to the previous millennium; it is the case of the Sabines and Latini who settled in Lazio together with Falisci, Aequi, Volsci, Hernici and Ausones. The interior of Abruzzo was dominated by the Vestini, Paeligni and Marsi, while the central Adriatic coast was populated by Picentes, Marrucini and Frentani. The Apennine area of Molise and Basilicata was peopled by the Samnites and Lucanians. In Calabria and Sicily there were also the Bruttii and Siculi.
[...]
Molecular indices indicated that most of the Italian samples show diversity values that are comparable to other European populations. However, some differences were shown to exist, especially in isolated Ladin populations.

References

Brisighelli F, Álvarez-Iglesias V, Fondevila M, Blanco-Verea A, Carracedo Á, et al. (2012) Uniparental Markers of Contemporary Italian Population Reveals Details on Its Pre-Roman Heritage. PLoS ONE 7(12): e50794. doi:10.1371/journal.pone.0050794

To your point 2 I would also like to add that the fixation with land routes is a recent phenomenon. In ancient times, travel by sea was much easier than travel by land (roads were often few and poor), which meant that distant places linked by sea or rivers could be much more connected (both travel and gene flow-wise) than areas that were geographically closer together but linked by land.

Italians do have much less IBD sharing with other European populations and are more easy to distinguish based on aDNA from other European population, so this enforces the model of the ''genetic island''
''The map also identifies the existence of two genetic barriers within Europe. One is between the Finns (light blue, upper right) and other Europeans. It arose because the Finnish population was at one time very small and then expanded, bearing the atypical genetics of its few founders.
The other is between Italians (yellow, bottom center) and the rest. This may reflect the role of the Alps in impeding free flow of people between Italy and the rest of Europe.
Data for the map were generated by gene chips programmed to test and analyze 500,000 sites of common variation on the human genome, although only the 300,000 most reliable sites were used for the map. Dr. Kayser's team tested almost 2,500 people and analyzed the data by correlating the genetic variations in all the subjects. The genetic map is based on the two strongest of these sets of correlations.
The gene chips require large amounts of DNA, more than is available in most forensic samples. Dr. Kayser hopes to identify the sites on the human genome which are most diagnostic for European origin. These sites, if reasonably few in number, could be tested for in hair and blood samples, Dr. Kayser said.
Genomic sites that carry the strongest signal of variation among populations may be those influenced by evolutionary change, Dr. Kayser said. Of the 100 strongest sites, 17 are found in the region of the genome that confers lactose tolerance, an adaptation that arose among a cattle herding culture in northern Europe some 5,000 years ago. Most people switch off the lactose digesting gene after weaning, but the cattle herders evidently gained a great survival advantage by keeping the gene switched on through adulthood.''
http://nytimes.com/2008/08/13/science/13visual.html


text:
Do cats ingest everything that they lick off themselves during grooming?
Cats are well-known for licking themselves clean, but what happens to all the loose hair and sand and mud and wet substances that they lick off themselves? Do they ingest everything? Do they cough up and vomit out a furball later with all of this? How is a cat's digestive system suited to handle all the inedible environmental substances?
I have a pet cat and I've never understood where all that she licks off herself is going.

It’s your cat. Watch it and tell us what you observe. Note that in English one preposition is enough — “off of” is too much.

My cat's a feral but friendly cat. She visits me by herself, a couple of times a day and several times a week; meows, eats the food I provide, shows me a great deal of affection (sometimes even brings me mice), sits by my side and grooms herself to no end, even takes small naps. But when all is done, she just gets up and leaves. She's not a home cat, and I don't have a chance to watch her full habitual routine.

Their digestive system breaks down all the substances it can break down and the rest is vomited or expelled within faeces

Cat licking is partially to clean themselves (including of odors that might attract predators) but is also used as a cooling mechanism (they sweat little and so use evaporation of saliva as a cooling mechanism), socialization, and to help spread oils. Most hair in short haired cats passes through the digestive tract with no issue. Source The hair that is unable to pass through the cat will accumulate in the stomach and be coughed up as a hairball (generally every 1-2 weeks) source.
For more on a cat's digestive tract see here. Note also that the human digestive tract can manage all manner of weird things to and just allow it to 'pass through' and this is the 'default' behavior for many digestive tracts.


text:
How exactly does alcohol solution kill or neutralize viruses?
To reduce the risk of infection by viruses (including 2019-nCoV) the CDC suggests:

Wash your hands often with soap and water for at least 20 seconds. Use an alcohol-based hand sanitizer that contains at least 60% alcohol if soap and water are not available.
Avoid touching your eyes, nose, and mouth with unwashed hands.
Avoid close contact with people who are sick.
Stay home when you are sick.
Cover your cough or sneeze with a tissue, then throw the tissue in the trash.
Clean and disinfect frequently touched objects and surfaces.

To my knowledge most alcohol-based hand sanitizers use ethanol. In clinical settings sometimes isopropanol is also used.
Question: How exactly do alcohols, especially ethanol and isopropanol provide some disinfecting action against viruses? Are the virus particles simply dissolved? What happens?

I've added the sterilization tag for lack of a better option. Hand sanitizer does not sterilize, but we don't have a sanitization tag.

Coronaviruses are enveloped viruses, so I would assume that the alcohol disrupts the membrane and thus strips away the molecules used for host cell recognition ...

I'm voting to close this question as off-topic because it concerns medical hygiene and is not about a specific biological problem in the terms of SE Biology.

@David No, it's specifically about the mechanism behind the effect of a particular chemical on a specific type of organism, and not about public hygiene. I've written the question carefully to make sure of that, I'm not certain you've read it through, or perhaps you are distracted by the background information.

@David If stripping away the molecules used for host cell recognition is the answer, then that is the answer and closing simply blocks people from posting it.

How artificial procedures kill living organisms is off-topic here imho and I have always taken this attitude to questions of this sort — this must surely have been asked before. An analogous question would be on the mechanism of death by the guillotine, or (we had a spate of these) by astronauts’ helmets coming off in outer space. This site is for questions about actual biological problems you are faced with.

@David If someone with a "biologist's ID card" asked about how a bleach solution was actually sterilizing the inside of their hood, would you close their question as well?

I don’t close questions, but I would vote that a question of that sort be closed. In my opinion a methodology question on how to adopt sterile procedure in a non-clinical situation would be on-topic if it showed research and raised a point of difficulty. Questions on the mechanics, no.

I think this is an absolutely valid question in my opinion. I disagree with David in that the mechanism is irrelevant; of course the way in which life is vulnerable to organic solvents is a biological question. However, to be fair I think the answer is rather simple and easy to google; ethanol lyses cells by rupturing the plasma membrane (which is made of ethanol-soluble lipids) and additionally denatures proteins. Alcohols can also dehydrate cells (substitute the water contents of a tissue) and have been as such used as fixatives.

This type of question is certainly on topic here since it's asking about how a chemical impacts a biological particle. There is no doubt about it, and the question should not be closed. @David this site is not just for questions related to a professional biologist's lab setting, but it's meant for (and certainly is used for) asking a wide range of biological questions. This includes questions about everyday people /situations such as hand sanitation, as long as they are asking about the biological characteristics, mechanisms, or impacts of that situation. Which is the case here.

@theforestecologist — basic chemistry then?

@SPr I see the goal of Stack Exchange as being the generation of good answers to on-topic questions. Not all viruses have envelopes and no viruses that I know of are cells. Having a well-written, well-sourced and well-received answer to this question is a net plus for the site, and learning that alcohol is only effective against some kinds of viruses and not others wouldn't necessarily always come from a quick googling.

Alcohols dissolve lipid bilayers
Many viruses have an outer lipid bilayer. Ethanol lyses cells, and in the same fashion damages membrane-bound viruses by rupturing the bilayer (which is made of ethanol-soluble lipids).
Alcohols misfold the protein coats of viruses
Additionally, alcohols denature proteins, which misfold in non-aqueous conditions. Some viral surface proteins are important for adhesion and attachment, and misfolding these renders the virus inactive. The total breakdown of viruses is essentially due to the misfolding of their protein coat (the capsid).
The same goes for bacteria
With the additional effect of dehydrating cells
Alcohols substitute the water contents of a tissue and have been as such used as fixatives. Common laboratory examples include methanol and ethanol.
Typically, 70% (140 proof) ethanol is used for bench wiping to kill or inactivate microbes. This includes viruses.
This is all standard, common, easily and readily accessible knowledge. Here's a bonus source.

(1) Read closer, I've addressed viruses. Admittedly it is a short answer, but I don't think it can be made substantially better. I could format the viral part to bold font if you really think it will help... (2) All that applies for ethanol and methanol apply for isopropanol too. Isopropanol is used in cleaning work surfaces; methanol is too toxic to humans for that purpose.

We expect you to show a minimum attempt at your own research, and explain where you remain unclear about something. This is the most standard textbook, easy-to-search query. You have clearly not thought to use a search engine, and you have also not consulted the search bar on this stack yet. You'll find an answer anywhere if you look. I also urge you to read this. I'm sorry you are so hurt about my inclusion of membrane-bound microbes; viruses too sometimes harbor membrane envelopes. Alas!

From wikipedia: A capsid is the protein shell of a virus. It consists of several oligomeric structural subunits made of protein called protomers. Viruses don't have a lipid layer. In addition, I am removing your last comment S Pr - be nice svp.

Thanks for the edit, it looks great!

A comment on the question suggests that several infectious viruses (including 2019-nCoV) are envelope viruses and that alcohol can "strip away the molecules used for host cell recognition". Viral envelopes (are), typically derived from portions of the host cell membranes.
A key component of these envelopes are of course lipids.
From Antiviral activity of alcohol for surface disinfection:

Antiviral activity and the viral envelope
Because of the structure and composition of the different virus families, viruses react differently to the action of disinfectants. From a disinfectant point of view, the presence or absence of an envelope is the most important trait of a virus. Lipid-enveloped virus families are, generally, susceptible to many disinfectants, alcohols included. The higher the lipid content and the larger the virion itself, the more susceptible the virus is.
Many (but not all) of the so called small `naked' virus families (e.g. adeno, parvo, picorna viruses causing a.o. poliomyelitis,hepatitis A, hand foot and mouth disease, common cold) that do not possess an envelope are quite resistant to common disin-fectants, alcohols included (6, 7).
Fortunately, the herpes viruses (herpes simplex I and II, 5-8,varicella, Epstein Barr); paramyxo viruses (measles, mumps);retro viruses (HIV, AIDS); hepadna viruses (hepatitis B); coronaviruses (SARS) are lipid-enveloped virus families that are, generally, susceptible to the disinfectant activity of alcohols(5, 8).
5 JuÈlich W-D, v. Rheinbaben F, Steinmann J, Kramer A. On the virucidal efficacy of chemical and physical disinfectants or disinfection procedures. Hyg Med 1993; 18: 303-26.
6 Tyler R, Ayliffe GA, Bradley C. Virucidal activity of dis-infectants: studies with the poliovirus.J Hosp Infect 1990; 15:339-45.
7 Mbithi JN, Springthorpe VS, Sattar SA. Chemical disinfection of hepatitis A virus on environmental surfaces. Appl Environ Microbiol 1990; 56:3601-4.
8 Croughan WS, Behbehani AM. Comparative study of inactivation of herpes simplex virus types 1 and 2 by commonly used antiseptic agents.J Clin Microbiol 1998; 26: 213-5.


text:
Carbohydrates in acidic stomach
How does the acidic environment in the stomach affect carbohydrate and fast digestion? Does it aid, impede or remain neutral in their digestive process?
Or do the carbohydrates, fats and proteins leave the stomach straight to small intestine once the churning is over?

As Will below mentioned stomach acid mostly exists to kill ingested bacteria not break down the food.

As for the digestion of fats there are two digestive enzymes active in the stomach:

Lingual lipase (produced with saliva)
Gastric lipase (produced in the stomach chief cells)

Both have activity optima in the acidic pH range.
On the other hand, the salivary amylase that breaks down starch seems to be inactivated by the acidic environment.
Sources:

https://www.ncbi.nlm.nih.gov/pubmed/2134569
https://en.wikipedia.org/wiki/Gastric_lipase
https://en.wikipedia.org/wiki/Lingual_lipase
https://en.wikipedia.org/wiki/Alpha-amylase

People who have no stomach acid because of medicine or surgery still digest their foods.  Otherwise you would predict incomplete digestion / weight loss / diarrhea would be a consequent of stomach acid suppression.
Acid is there to kill germs.  That probably used to be a lot more important than it is now but it is still important.  Acid suppression is associated with an slight increased pneumonia risk and possibly increased risk of enteric infection.  These studies are all done in the first world.