Where can I find a file listing the genetic differences in humans? I don't know much about genetics. For an arts project I'm looking for a human genome.
I read that:

Only about 0.1% of the genome is different among individuals, which equates to about 3 million variants (aka mutations) in the average human genome. This means we can make a “diff file” of just the places where any given individual differs from the normal “reference” genome. In practice, this is usually done in a .VCF file format, which in its simplest format looks something like so:
chr20 14370 rs6054257 G A 29 PASS 0|0
Where each line uses ~45 bytes, and you times this by the ~3 million variants in a given genome, and you get a .VCF file size of about 135,000,000 bytes or ~125 megabytes.

Is that correct?
Do you know a database to download a VCF file or something similar? It would be amazing if you could provide a link to the file mentioned above!

Have you tried poking around the 1000 genomes project?

Try this link

ftp://ftp.1000genomes.ebi.ac.uk/vol1/ftp/pilot_data/release/2010_07/exon/snps/


Do humans perceive temperature or heat-flux? (or both?) The general understanding is that when I touch an object, I perceive its (relative) temperature.

A metal object at room temperature, however, will often feel cool to the touch.

This leads me to believe that the skin senses heat flux in addition to, or instead of temperature.
(The metal conducts heat well, and therefore creates a greater flux when touched than a more insulative material.)

I am unfamiliar with the chemical process by which temperature or flux is converted into meaningful signals.

Do humans perceive temperature or heat-flux? (or both?)

This is the modified answer in response to the discussion:

Facts:

There are warmth and cold receptors in the body at two places: The Peripheral receptors and the Central Receptors
The peripheral receptors are present in skin and the central receptors in the body core at multiple sites the notable site being the hypothalamus
The Temperature receptors have two patterns of firing - The tonic response (sustained firing rate due to steady rise and maintainance in temperature over long time) and the phasic response (also called dynamic response - response to short changes in the temperature)
The Warmth receptors fire maximally at 44 - 46 degrees celcius. The firing stops almost completely at about 48-49 degrees celcius beyond which there is no effective thermoregulation
The Cold receptors fire maximally ar 20 - 35 degrees celcius.

What is measured?

The peripheral receptors sense the temperature of skin.
The central receptors measure the core body temperature.

Only the temperature is measured as WYSIWYG mentions.

However the frequency of stimulus (How frequently the nerves fire - this depends on the temperature range in which the respective receptors fire) and the two types of receptors present on the skin allows the brain to interpret the flux. So Chris Stronks is correct in telling the heat flux is perceived.

Mechanism of feeling cold:

When you touch a cold object the heat is lost through conduction and radiation through the portion of skin that is in contact with the object. The cold will cause vasoconstriction of that part of skin - This means that the temperature of that part of skin rapidly equilibriates with that of the object. As there is rapid cooling (assuming that the object is cold) the rate of firing of the warmth receptors decrease and the rate of firing of the cold receptors increase. This allows the brain to interpret that the skin is losing heat (the flux).

The radiation part of heat loss is more appreciated when you pass a uncurtained window during the winter - the temperature difference is so great that very high loss of heat occurs through radiation that you shiver. You have to note that during these instances there is no decrease in the core body temperature. The actual decrease in core body heat needs a long exposure to such conditions. In the scenarios detailed above the heat loss is primarily from skin which reflects the ambient conditions (very quickly). Thus the peripheral receptors effect Anticipatory Control which is effectively measuring the flux of heat through skin.

The opposite occurs when you suddenly stand beneath the sun coming from a cold room - the radiant temperature of the sun being so great will cause the skin temperature to rapidly rise causing the body to feel very hot (though the core body temperature has not changed much).

Interesting details that may increase your understanding (though not directly related to the question):

The heat control effected through sensing the change in the skin temperature is called Anticipatory Control. In this the brain "anticipates" what is going to happen - for example a sudden cold draught - and will respond to it - reponds by increasing the heat production (shivering).

The heat control effected through sensing the core body temperature is Negative Feedback Control. In this the brain responds to increase in the core body temperature and takes steps to remedy this (the response will bring the temperature back to the set point).

For more see:Boron & Boulpaep Textbook of Medical Physiology, 2nd Edition, Chapter 59.


How does the digestive system determine what to absorb [as nutrients] into the bloodstream? If you put an egg into a sausage machine it will try to make sausages out of it because that's its job. Does the digestive system attempt to digest everything it receives? Furthermore, does it attempt to derive nutrients from everything it receives? How does the digestive system determine what is nutritious? Can "particles" (e.g., microscopic dirt) pass through to the bloodstream if they are small enough to be absorbed?

Does the digestive system attempt to digest everything and from everything it receives and how it determines what is nutritious?

Human digestive system is genetically determined and can digest only those substances for which it has digestive enzymes and absorb only those that can be absorbed through the specific "channels" in the intestinal lining.

Human digestive system can absorb nutrients "from everything" (not literally, though), for example, sugar from raw sugar cane.

Before absorption, complex nutrients (starch, sucrose, lactose, proteins and triglycerides), need to be broken down by the digestive enzymes into simpler nutrients, but some nutrients need no digestion before absorption. The following nutrients can be absorbed in the small intestine:

Water
Monosaccharides: glucose, fructose, galactose...
Fatty acids
Cholesterol
Amino acids
Minerals: calcium, potassium...
Vitamins
Polyphenols, plant sterols and stanols and various other plant-derived nutrients
Sugar alcohols: erythritol, glycerol
Alcohol

Nutrients that are not absorbed in the small intestine:

Sugar alcohols: isomalt, lactitol, maltitol, mannitol, sorbitol, xylitol
Oligosaccharides: raffinose, fructooligosaccharides, etc.
Certain polysaccharides (soluble fiber): beta-glucan, guar gum, etc.

These nutrients travel to the large intestine, where they are broken down (fermented) by normal intestinal bacteria into absorbable nutrients, mainly short-chain fatty acids (SCFAs), and gases.

Can "particles" (e.g., microscopic dirt) pass through to the bloodstream if they are small enough to be absorbed?

There is a countless list of substances that are not nutrients but can be absorbed:

Medicines and other drugs
Certain food additives (preservatives, dyes...)
Toxins (methanol, cyanide...)
Various random substances ("dirt")

And there is another countless list of substances that cannot be absorbed, for example, insoluble fiber, such as cellulose, and certain artificial sweeteners, such as aspartame and steviol glycosides from stevia.

Sources:

Absorption (Nutrients Review)
Chemical Digestion and Absorption: A Closer Look (Lumen Learning)


What, other than genetic factors, influence which individual survives a parasite and which perishes? What factors other than "good genes" are at play in determining whether one individual survives a parasite and another individual in the same species perishes as a result of the same parasite?  For example, is there variation in the amount of the parasite (not in the amount of parasite species but in the amount of one species) with which an individual is infected and how might this occur?  I'm mainly interested in this first example, but another example:  Might infection occur at different parts of life-history in which vulnerability varies? (I am asking generally about any parasite species and any host species.)  Thank you very much.

I am neither a parasitologist nor an immunologist, so these suggestions are only provided as a starting point and may meet valid criticisms from others. However, as your comment mentions the 1918 flu epidemic, a couple of general suggestions.

Assuming that resistance to pathogenic organisms can involve the immune response, then at least two factors that might affect that — and hence resulting mortality or morbidity are:

Nutrition:
It is popular wisdom that undernourished individuals are more susceptible to disease. This might have diverse causes, but there would appear to be an extensive literature on the role of nutrition in the immune response, e.g. this article by  Chandra has been highly cited.

Previous immune challenges: There is, of course, the classic case of milk maids being resistant to smallpox because of immunity provided by the related cowpox. Thus exposure to previous strains of a virus may provide some protection. Speculating widely here, there may also be affects on the non-specific components of the immune response (macrophages and whatever).


Statistical Analysis of Protein Folding Problem I’m new to the field of protein folding. I’ve been searching and came across some books for predicting structures (Introduction to Protein Structure Prediction: Methods and Algorithms). Does anyone know whether I can find some code (say in C++, Java, or R) related to the prediction of protein structures? Or, do you know other good articles or books related to the statistics of the protein folding problem?

Thanks for the help.

One of the quickest ways to get oriented on what is going in the world of protein folding and modeling is to look at the proceedings of the Critical Assessment of Structure Prediction (CASP).  CASP is basically a contest, held every 2 years where anyone can use their algorithm to predict the 3D structure of a protein whose structure is known, but not publicly available.

Its been a few years since I reviewed them results much - it looks like this year was interesting, but a perennial winner has been Rosetta, which has turned into an edifice of many suites of software which each execute different tasks in protein folding and modeling.

Open source software is pretty hard to find in this field.  The software is complex.  It usually includes components of machine and statistical learning, molecular dynamics, specialized algorithms that build up the protein one residue at a time, others which manipulate blocks of the protein structure around in space, electrostatic calculations, you name it.  In addition, the software, once it gives some sort of result is quite valuable.  I don't think any of these suites has really been released.  I know that Rosetta is available to use as a web service, but you have to apply for access to the source.  I don't think its an easy thing to get.

Some of the most complicated components are available open source.  Molecular modeling and molecular dynamics open source software is quite sophisticated.  I think we need an open source protein folding suite open source.  I think David Shortle's algorithms might be a candidate for such a suite as its not so complicated and it works in some cases.

This field is pretty obscure and difficult to get around in.  There aren't any easy introductions that I know of.  Protein structures are computationally expensive and painful to work with in terms of writing software.  On the other hand protein folding that really works is a revolutionary breakthrough, at least equal to the impact of the development of computers as a technology.


How body loses more fat in CO2 form than in sweating form? Yesterday, I saw TV Game Show.

There is question like this: Body loses more fat in which form?
It gave 4 options:

1) CO2

2) sweating

3) xxx

4) xyz

sorry i didn't remember 3 & 4 options.
so right answer is CO2. anchor explaining the reason behind it, suddenly my brother switch the channel. all gone.....

Everybody thinks sweating is right answer, i have reason for it, if we work out our body whole fat comes out in sweating form.

If you exercise heavily, you can sweat enough where you have to drink to replace it. But on a normal day, you don't sweat all that much.
On the other hand, when you metabolize food, you essentially burn it. According to the Merck Manual,

Carbohydrates, proteins, and fats supply 90% of the dry weight of the diet and 100% of its energy. All three provide energy (measured in calories), but the amount of energy in 1 gram (1/28 ounce) differs:
4 calories in a gram of carbohydrate or protein

9 calories in a gram of fat

A typical diet is 2000 calories per day. If you get 50% of your calories from fat (shame on you!), that is 1000 calories of carbohydrate or protein, or 250 grams. It is 1000 calories of fat, or 111 grams. 361 grams total.
We will simplify. CH bonds contain little energy compared to CC bonds. H weighs little compared to C. We don't change much by ignoring H. There is some O and other stuff, but we will ignore that too. It will still be roughly right. So you burn about 361 grams of C.
For every C atoms you metabolize, you must breathe in 2 O atoms, and breathe out all 3 atoms as CO2. C atoms have an atomic weight of 12. O is 16. So CO2 is 44. Every 12 grams of C becomes 44 grams of CO2. So to burn 261 g of C, you breathe out 1324 g of CO2.
1324 g of water would be 1.324 liters. It is easily possible to sweat that much in a day, but you typically don't. You typically breathe out more CO2 than you sweat water.


Why is black and yellow such a nice camouflage? Many people can`t differenciate between cheetahs, leopards and jaguars, but there are serveral other animals with a similar pigmentation (servals, ocelots...), why is it so effective? It gets exciting when you realize that cheetahs and leopards are evolutionaray relatively far away, and therefore that their resemblance exsists due to evolutionary convergence.

What makes a camouflage effective? It has to match the colors and color patterns of the habitat.

Here are two cheetahs

Here is another cheetah

Here is a leopard

Here is a jaguar

Overall, it looks like their yellow and black pattern is a pretty good camouflage.

The jaguar habitat is a mixture of open and forested habitats. One would think, the jaguar would gain by being a little greener but there is a good reason for the jaguar not being green (see Why is green fur not a thing?).

Note also that it would be a mistake to think that any species should be perfectly adapted to its environment. You might want to have a look at the paragraph Did you say Natural Selection? in this answer for a very short intro to why populations might sometimes be less adapted than a naive observer may expect. There might have an important phylogenetic signal among these felidae (you might to have a look at the paragraph Why 4 legs? in the same answer as indicated above).


How do macromolecules (large drugs) in the eye reach the bloodstream and what are the relative significances of these pathways? I am considering the elimination pathways for antibodies (50-150 kDa) from the vitreous humour to the blood stream. My overarching question is what is the most significant route such antibodies could take to get there?

Elimination from the vitreous humour to the aqueous humour is known to be quite a substantial route of clearance, but does drug eliminated through passage into the aqueous humour travel to the blood stream? Notably there are two routes of exit from the aqueous humour, one is directly into the bloodstream and the other is through Schlemm's canal, but where does that lead?

Also for example is the choroid directly in contact with the hyaloid membrane of the vitreous play a significant role in elimination? We also also such drugs penetrate into (and through) the retina, at that point they reach vasculature, however they have to work quite hard to get there.

Antibodies are a unique case.  I recommend reading PubMedID: 26726925 regarding the pharmacokinetics of ranibizumab (Lucentis), a Fab fragment, after intravitreal administration.

"We assume that the principal pathway for the ocular clearance of large molecules is by a first-order transfer process from the vitreous to the aqueous chambers, from which the molecule is absorbed into the circulation via Schlemm’s canal by the physiological process of aqueous humor turnover."

A comprehensive analysis of the pharmacokinetic processes are included in the mechanistic model that they have developed.  I will not copy and paste them here.


What is the difference between a signal peptide and a transit peptide? From what I know, the two names are used interchangeably and I haven't found any resource which says otherwise either. Is there at all any difference, is there a transit peptide that is not a signal peptide or vice versa?

Signal peptides are typically located at the N terminus of a protein. The signal peptides are processed by the translocon machinery and are cleaved off after sorting through the membranes of organelles in the secretory system:

  endoplasmic reticulum
  Golgi apparatus
  ER-Golgi transition vesicles
  plasma membrane
  lysosomes

Transit peptides target the protein to other subcellular organelles such as (from UniProt):

  Mitochondrion
  Apicoplast
  Chromoplast
  Chloroplast
  Cyanelle
  Thylakoid
  Amyloplast
  Peroxisome
  Glyoxysome
  Hydrogenosome

N-terminal transit peptides are quite rare. C-terminal transit peptide motifs are much more common. UniProt holds transit peptides as a discrete controlled vocabulary, separate from signal peptides.


Is death by cyanide the same as suffocation? I started the night off by reading about "what does drinking the Kool-aid mean" this lead to a wikipedia article which described the horrors of the Jonestown cult mass suicide/murder in the 1970s. This was followed by reading about some of the references cited, and eventually me coming up with a biology question.

The murder/suicide used Cyanide. Reading the description of how it is described here: http://indianapublicmedia.org/amomentofscience/how-cyanide-kills/ makes me wonder if death by Cyanide is equivalent of suffocation. I think a biology background, doctor or nurse would be suited to answer this question.

In suffocation or asphyxiation you are actually deprived of breathing oxygen. The arterial blood oxygen concentration decreases (hypoxemia) which is detected by the chemoreceptors of the carotid body and aortic arch. This induces a neuronal response in the medulla that increases respiratory rate, force of contraction and relaxation of respiratory muscles and heartbeat rate. Simply put, you get panicked. Prolonged suffocation may lead to seizures, cardiac and respiratory arrest and death.

Cyanide poisoning is an example of histotoxic hypoxia resulting from tissue poisoning by $\rm CN^-$. Unlike other forms of hypoxia, where the concentration of oxygen is less in tissues, in cyanide poisoning, the concentration of oxygen is actually perfectly normal in ECF and ICF. It is the cell which is unable to utilize the oxygen present in it. As a result the arterial blood doesn't lose much oxygen to the tissue as they themselves have adequate oxygen, resulting in an increase in $\rm HbO_2$ concentration in blood.
Thus your skin gets cherry red, not blue like when you get deprived of breathing oxygen which happens due to an increase in concentration of deoxygenated hemoglobin in blood.

Here is what happens at the molecular level.

The $\rm CN^-$ ions diffuse into the mitochondria. They have high affinity to the ferrous ion of the mitochondrial enzyme cytochrome c oxidase involved in the Electron Transport Chain, one of the phases of cellular respiration where $\rm ATP$ is generated from $\rm NADH$ and $\rm FADH_2$. And it is this process which actually requires oxygen. The inhibited cytochrome c oxidase is no good, thus no $\rm ATP$ molecules are generated from ETS. And, the oxygen molecules waiting for those electrons remain empty handed explaining the increase in molecular oxygen concentration. Remember, ETS occurs in almost all living cells except few like RBC which get their major share of ATP from the highly inefficient anaerobic glycolysis. Note, $\rm ATP$ is the energy currency of our body and is required in a wide variety of bodily processes like osmotic balance, nerve impulse transmission, muscle contraction etc. With no $\rm ATP$ your heart muscles and respiratory muscles can't contract, your medulla can't regulate breathing. You will go into cardiac and respiratory arrest. It may result into seizures and coma. Death is iminent if a high concentration of cyanide gets into your blood.
The symptoms of panic are not usually seen unless the victim himself knows he is poisoned . Well, that is due to your fight/flight response. The effects like cardiac and respiratory arrest, seizures and coma are similar to those of suffocation because it is due to low $\rm ATP$ production in both cases.

Reference:

https://www.ncbi.nlm.nih.gov/books/NBK54113/


Specificity of the immune system We know that the adaptive immune system recognizes foreign particles when their proteins are expessed of the the surface of T-cells, complexed with MHCs. But MHCs present only short peptides of length 8-11 amino acids long. How is it that every antigen has one characteristic 8-11 residues long stretch in some protein of its which none of the host's protein has. Conversely, how is it that this 8-11 amino acid long peptide, which the body is recognizing as foreign is not found in any protein of any cell of our body?

For starters, your conception of antigen presentation seems a bit off, but that's not the crux of your question. There's around 10^15 different sequence permutations for a peptide 11-mer. Despite that, it's actually likely that highly conserved regions of some proteins will be present in both the pathogen and the host. T cells will not recognize them, however, as they are negatively selected in the thymus.


Is it considered feasible to genetically improve plants for better Carbon dioxide breakdown? I have found several somewhat related questions and answers here and elsewhere, but I couldn't find, if any  scientist groups are researching genetical improvement possibilities of existing plants' photosynthesis processes to produce plants, which would be net oxygen producers and/or significantly increase their CO2 removal abilities.

For the most part, it seems people are preoccupied with getting energy out of plants, but if we allowed that potential energy to be used for photosynthesis, wouldn't such plants be useful even if we can't harvest energy from them?

I'm not sure from your question if you're clear on the relationship between carbon fixation and 'energy', so just to be clear: carbon fixation in photosynthesis is the process of capturing CO2 and using it to store light energy in the form of carbohydrates. More CO2 capture = more harvestable 'energy'. Improving the efficiency of photosynthesis therefore captures more CO2 and generates more harvestable energy in the form of carbohydrates (edible or not).

There are three carbon fixation pathways in plants: C3, C4 and Crassulacean acid metabolism (CAM). The relative efficiency of the different pathways depends on the environment; for example, C4 plants are able to more efficiently fix carbon in drought, high temperatures, and limitations of nitrogen or CO2.

Because of this, scientists are indeed interested in engineering crop plants to use alternative carbon fixation pathways. One such project is the C4 Rice Project: http://c4rice.irri.org/.


Is the coronavirus getting less dangerous? Please note

This question is based on data from the UK government's web site (data from the ONS). I am not taking this data as accurate, but am using this as it is the only source of data I can find, and is what (presumably) the government themselves use when deciding what to do. My question is about trends, not the accuracy of the government's data.

I'm also not asking about the wisdom of government policy, that is a political issue, and I'm only interested in biology and statistics here.

Finally, I realise that my analysis is all quite rough and ready, as there are many indeterminate factors involved. Again, I'm interested in an overall picture, so a rough analysis is probably reasonably informative.

Here in the UK, the data on new virus cases seems to imply we have a serious problem...

This was plotted using data from the government's web site, and shows that the number of new cases has risen dramatically since the beginning of September. I used a 5-day average to smooth the line (same for the other graphs below)
However, if you look at the number of deaths, it seems that the increase is nothing like as rapid...

Whilst there has been an increase since the beginning of September, it is very much more modest, and not necessarily indicative of a serious problem.
Now, I'm not a medical expert in any way, but it seems to me that the fact that the number of deaths is growing more so much more slowly than the number of new cases indicates that things may be not actually be getting worse, but may be getting better. Sure, more people are getting the virus, but the percentage of those who are dying (which I would have thought is the most important issue we need to consider) is not increasing.
To check this, I divided the number of deaths by the number of new cases, and it showed a very different picture...

As you can see, there isn't a noticeable increase since the beginning of September. To examine this more closely, you can zoom in on the past 8 weeks or so...

Whilst there was a jump in the middle of Sept, it hasn't really increased since then, and may even be decreasing.
So, is my analysis wrong, or is the virus actually becoming less of a problem in the UK?

The issue is using the number of positive tests as a measure for the total number of active cases at a given time. At least in the U.K., the early testing capacity was much lower than it was now:
Because of this, many people who were infected were not being tested and so weren't included in the total number of infections. Therefore, the total number of infections in April/May time was likely a large underestimate. It's been estimated that there was something in the range of 150,000-200,000 new cases per day in that time period.
On the other hand, testing capacity in the U.K. at the moment is much higher and will catch a much higher proportion of the total cases.
Therefore, your crude calculation of 'death rate' = deaths / cases is skewed by the error in the estimated number of cases, making it appear the 'death rate' is going down because we underestimated the total number of cases early in the pandemic.
The other thing to note is that the 'death rate' is dependent upon demographic factors, most obviously age. Early in the pandemic in the U.K., a large number of cases occurred in care homes, where the residents were particularly vulnerable. On the other hand, cases are high in students at the moment, who are a low-risk group. If the age distribution of cases is relatively skewed towards older people, then the 'death rate' will appear higher than vice versa, even though nothing may have biologically changed with the virus.
Note: Sorry, I don't have citations for a lot of this. I will try and find them and add them at a later point.


Ribosomes producing proteins, but need proteins to be produced? So according to my textbook:

  RNA is used to create ribosomal RNA (known as rRNA) which is then combined with proteins to form the ribomsomes necessary for protein synthesis.

I'm a bit confused with this statement, as ribosomes are needed to synthesise proteins, but in order to create ribosomes proteins are needed in the first place. How does this work, does the proteins needed for the creation of rRNA come from a different source? Or by synthesising proteins via ribosomes produce more proteins than required to create the ribosomes in the first place?

Also, where are the proteins synthesised? On cytoplasmic ribosomes, or on ribosomes bound to the RER?

Thanks!

Ribosomes are the only means we know by which cells produce proteins. Consequently, all proteins are made by a ribosome, including the proteins that then become part of a new ribosome. It's never a question of "more proteins than required" because there are different types of proteins and to make a ribosome, you need those specific types of proteins known as ribosomal proteins. The process of making ribosomes is known as ribosome biogenesis.

This raises the obvious question of where a cell gets its ribosomes from when it is "born". The answer is simple: from its parent. When a cell divides, each daughter cell is made of the components of the parent. The cytoplasm also gets divided, and each daughter cell receives mitochondria, ER, etc. from the parent cell. By the time those ribosomes break down, they will have produced new ribosomal proteins for new ribosomes already.

According to this review from 2017, it appears the ribosomal proteins made in the cytoplasm (so, cytoplasmic ribosomes) get shuttled into the nucleolus, where they get assembled with rRNA to make new ribosomes, which then get exported out of the nucleus into the cytoplasm.


What type of force holds my body rigid & doesn't make it collapse? My query is that as atoms & its molecules have inter & intra molecular forces,like that only what type of force keeps the cells bonded to each other & prevent it from collapsing ever since.

Adding on to what Martin said. If you imagine an atom to be the size of a football stadium, the nucleus would be the size of a fly on the fifty yard line. The vast majority of an atom is empty space.

In the 'classical' view, atoms are mostly empty space and the reason they feel solid is that if you try and push them, the electrons around your atoms bump into the electrons around the other atoms and because they're both negative they repel each other and push away. You feel this force as 'solid'. It's like pushing a really, really stiff spring or trying to force 2 magnets together, except it's electronic in origin.

In quantum physics, each particle has a wave function. Wave functions can only exist in certain forms, and when electrons are bound in an atom their waves spread up over a big volume (it's the only way mathematically to get a stable wave, ie an electron that exists. Since it exists, its wave function spreads out much further than the thing you classically think of as an electron).

Electrons have something called antisymmetric wave functions, which means they obey the Pauli exclusion principle:
http://en.wikipedia.org/wiki/Pauli_exclusion_principle

You can't have 2 electrons in the same state (and 'state' includes 'space'. You can have 2 oppositely spinning electrons, but no more in the same place). So atoms spread out because you can't squeeze the wave functions in. The rest of it is electrostatic repulsion just like in the classical model.

I'm sorry if that sounds a little complicated, but it's a combination of quantum physics (which doesn't really make sense, even though it works!) and electronic repulsion (from like-charges-repel).


can one be infected with Naegleria fowleri by taking Steam? will Naegleria fowleri be present in the steam molecules.

Many people take steam from hot water to get relief from sinus.

I read somewhere that Naegleria fowleri gets killed over 70 C. So steam will also kill it?

N. fowleri infection can occur after nasal and sinus irrigation, swimming and other exposures to contaminated water. The infectious agent in this case is the trophozoite, not the cyst. Boiling water contaminated with this amoebae kills it, preventing infection. Though it does thrive in warm water (37 C), it doesn't survive in steam (100 C).

Despommier's Parasitic Diseases Ch. 14 discusses N. fowleri in some detail. It's also covered in Murray Medical Microbiology Ch. 82, and Cecil medicine Ch. 360. There's also useful study in The Laryngoscope on the viability of various pathogens in contaminated water after sterilization methods.


Does food lose some of its mass in form of energy during metabolism? I had an argument with someone.

I argued that when a cat eats 1 kg of food, the sum of subsequent output (poo + pee + sweat + change of body mass) must be equal to 1 kg.

My opponent argued that the output will be less than 1 kg because a part of food is converted into energy.

Please rule.

Physics answer that is a bit silly

If you want to be real technical about physics, mass and energy are the same thing, so any chemical bond that has some energy and is broken results in a change of mass (mgkrebb's estimated in a comment the final mass would be 999.999999814 g, if you started with 1 kg of protein, also known to a very precise biologist as 1.000 kg).

This is sort of a "technically correct" answer that is totally silly from the standpoint of biology, but if your opponent wants to stand by it as "technically correct" based on physics, so be it. We are talking about changes in mass that are not measurable by modern science to sufficient precision, these are only theoretical ideas based on relationships between mass and energy that can be measured on a much larger scale.

Biology answer

Since this is Biology.SE, the biology answer is that mass is conserved in chemical reactions. If you greatly simplify the metabolism of, say, glucose, to the equation:

C6H12O6 + 6 O2 --> 6 CO2 + 6 H2O

you find that the net result is that the hydrogen and oxygen atoms become water, and the carbon atoms become part of carbon dioxide (yes I am simplifying where the actual atoms end up in the biochemical reactions, just talking in terms of net changes here). Other food molecules are processed similarly, and will produce some combination of water/carbon dioxide/nitrogenous wastes. If your cat eats 1 kg of food, that 1 kg of food will become 1 kg of something else out to many many decimal places: waste solids (including anything not digested at all) and liquids, exhaled carbon dioxide, lost skin/hair, etc.

Physics answer if you just want to win the argument

If you want to still win the argument with the physics-based answer that relies on mass-energy equivalence and ignores the fact that from the perspective of biology they are best understood as different concepts, then it's just as fair to go the other way and treat the lost energy as mass, in which case you'd consider the heat lost by the cat's metabolism as mass and include that tiny tiny tiny fraction in the 1 kg and call it a day.


DNA degradation rate Usually DNA sample manipulation is realized with an ice box at hand in order to avoid degradation, and also its storage is set at -20ºC. Nevertheless, DNA has been obtained from really ancient samples that were not in a cold environment and even our DNA is at 36ºC. Furthermore, when performing PCR, samples are put into a massive heat shock and at high temperatures.
Then how needed are those protocols in order to grant correct DNA quality? how much can a sample be left without need to worry? and how does this degradation happen (DNAse free environment)

DNA decomposition isn't a phenomenon that is too common.
In nearly all cases, DNA is broken apart to the accidental contamination with nucleases. Long-term storage of DNA in the -20 is also suggested in order to significantly lower the rates of these nuclease enzymes.

Additionally, DNA only truly fragments at very high temperatures (>90-100 degrees Celsius) due to the nature of the covalent chemical bonds that form DNA. Nearly any organic molecule will degrade at very high temperatures, and some will degrade at lower temperatures due to unstable structures or heat-labile bonds.

Of course DNA will deanneal at somewhat-high temperatures due to its double standedness , but allows for reannealing to the initial molecule once the temperature is brought down.

One additional reason for potential DNA degradation is DNA shearing, which will occurs when you tear up your DNA physically due to exposure to rigorous shaking, resuspending or other "violent" techniques.


p53 gene in benign tumors In a benign tumor, p53 gene does not work. I know that our cells constantly are mutating and the p53 fixes this. Hence, why does it take so long(or in some cases never) for a benign tumor to become a malignant one? I would imagine a malignant cell would rise rather quickly.

There are a number of main reasons for this: The main reason here is that there is more than one needed to transform a cell. This is usually the silencing of tumor suppressor genes like p53 and the activation of proto-oncogenes. Only one of these is not sufficient to transform a cell. This is also seen in melanoma, where nevi which carry the activating BRAF V600E mutation (which is the most often occuring activating mutation in this cancer) can stay silent for a lifetime. This is called the Knudson Hypothesis (a short overview can be found in reference 1)).

So the turn-off of the control system is not enough, the cell needs to be further pushed to become a cancer cell. More details can be found in reference 2

Then, our immune system is very good in catching cells, which have gone malignant. Most cells, which turned into cancer cells, are eliminated by the immune system. This idea has been first formulated by Paul Ehrlich in the late 19th century, see the references 3 and 4 for details. The figure from paper 4 shows this schematically:

References:

Two-hit hypothesis
Tumor Suppressor (TS) Genes and the Two-Hit Hypothesis
Cancer immunoediting: from immunosurveillance to tumor escape.
The Immunobiology of Cancer Immunosurveillance and Immunoediting


Chance of cancer as a function of smoking frequency I was wondering if there is some kind of known relation between the chance of getting cancer and the frequency of smoking cigarettes. A quick Google search did not yield results. Would any of you perchance know of a relation?

There is an approximately linear relationship between the total number of cigarettes a person smokes in their lifetime and the risk of getting lung cancer.

That is, each cigarette someone smokes increases their chance of getting cancer by about the same amount, whether it's their first cigarette or they've been smoking for 40 years.

Pack-years are a way of quantifying someone's total cigarette exposure; it's calculated by the number of packs someone smokes per day times the number of years they've smoked for. So someone who has smoked half a pack per day for 20 years would have a pack-year history of 0.5 * 20 = 10 pack-years.

The following graphs show the linear relationship between the odds of getting lung cancer (relative to non-smokers) versus pack-years smoked.

Source: Lubin and Caporaso (2006), "Cigarette Smoking and Lung Cancer: Modeling Total Exposure and Intensity"


Why are triacylglycerols broken down before being absorbed? So when dietary fats are in the small intestine, they are emulsified by bile salts in order for action by lipases to occur.  Lipases degrade the triacylglycerols into monoacylglycerols, diacylglycerols, free fatty acids, and glycerol, and these are taken up by intestinal epithelial cells.  Once taken up, these are reformed into triacylglycerols.
My question: why do these have to be broken down in order to be absorbed, and what is the driving force for reformation of triacylglycerols once absorbed?

Your question does not have a clear answer yet, as stated in Metabolic regulation: a human perspective / Keith N. Frayn. – 3rd ed (2010) on page 39.

  There is still debate about how fatty acids cross cell membranes.

On that page they claim that a simple diffusion transport is possible through a 'flip-flop' mechanism, where the fatty acid inserts itself in the membrane and then experiences a reversal movement. The kinetics of the process seem to be in agreement with the observed utilization rates.

Also, it is claimed that there is growing evidence specific fatty acid transporters like FAT and FATP (fatty acid translocase and transport protein) play a key role in the process. They might join forces with the fatty acyl-CoA synthase, consuming ATP. ATP consumption activates them, i. e provides energy, for the acyl-CoA formation (not in order to move against gradient). The activated state would enable them to both move into the cell and regenerate a triacylglycerol.

Why do these (triacylglycerols) have to be broken down in order to be absorbed?

I would say that the hydrolyzed products (fatty acid and glycerol) are more readily internalized because their structure is simpler. Fatty acids can perform the flip flop mechanism, but whole triacylglycerols might not (I am not sure). There is a fatty acid binding protein that may help maintain the fatty acid importation gradient too.

What is the driving force for reformation once absorbed?

It is the secretion of chylomicrons loaded with regenerated triacylglycerols. Since they are secreted, they don't pile up inside the enterocyte (intestine cell) and the equilibrium in the synthesis route (the monoacylglycerol esterification pathway) favors the production of triacylglycerols.

Remarkably, not all fatty acids are reesterified, those of short length (< 14 carbons) are not compatible with the acyl-CoA synthase and enter the plasma in a free state. That happens when digesting dairy products.


How do birds learn their tunes in isolation from their own species? I wonder what a bird would sing if it didn't have its parents around (or any other birds for that matter) to learn its chirping sounds from.

I'm interested in how a bird would sing...

in complete isolation from creatures communicating through sound;
in isolation from its own species, but with other birds;
in isolation from all birds (other animals and creatures are there for it)

For example,

Would a bird even feel the need to speak up if there wasn't any other vocalizing creature around?
Would a bird learn other species' signals? Would it only learn from one species, the one which it would think of a fitting mate?
Would a bird try to mimic a non-flying creature's signals?

These are similar questions, but if you think they should be separated, let me know in the comments.

Birds have to learn their song patterns.
They are able to chirp, but the songs with "meaning" are learned from their parents or whatever they learned to be their "parent".

Here is a paper that related bird song learning to human learning (of speech, for example).
Birds brought up by parents from another species learned to sing their songs.
There are many birds that learn to imitate other animals or sounds, so in isolation from all birds they will probably do this.

I can't recall where, but I read a paper once, where little finches brought up by humans developed a song resembling the "Hello there, now there's food", their caretaker always greeted them with. (Not the speech, but the overall sound pattern.) They might not understand the signals, but they try to communicate nevertheless. Some birds use sound from other species to mock others, scare them off or lure them into thinking they might be more powerful than they are.

Birds brought up in total isolation do sing, but not the typical songs you know from their species. Deaf birds who can't hear themselves, though, do not (always) sing.


How long does it take for a person to lose all offsprings due to inheritance? From this I know we will only inherit some genetic informations from parents, which is about 50 percent. But the problem is, gene has finite size, after some generations a person leaves only $0.5 \times 0.5 \times 0.5$ parts of genes to the offsprings, and it will be casted into zero. My question is, how long does it required for a person to lose all genetic information in the world?

I think your question conveys some misunderstanding.

A child is related to each parent by a factor of ½. Humans have a diploid genome, meaning they have two copies of each chromosome (see: autosome). When two humans reproduce, they each contribute one copy of each chromosome to the offspring, in other words, they contribute a haploid genome to make a diploid child. Genetic information is not "lost" - the genome is not shrinking by a factor of ½ every generation.

However, relatedness does decrease from generation to generation. You are related to each of your parents by a factor of ½, each of your grandparents by a factor of ½ $\times$ ½, your great-grandparents by a factor of ½ $\times$ ½ $\times$ ½... You are also related to your children by a factor of ½, you are related to your grandchildren by a factor of ½ $\times$ ½... You get the picture, right?

For example, imagine the genome carries just one gene. Your father carries alleles $AA$ at that locus, and your mother $aa$. You would then be $Aa$ and, because half of your alleles came from your father and the other half from your mother, be related to each by a factor of ½, but all three of you have the same number of genes (1) and that gene is the same length (in nucleotides, barring mutations) in all three.


Why do same type of fruits come in different sizes? Why don't fruits come in exact same size even they're the same type of fruit?

This sounds like an obvious question,

but why are some apples bigger than others?

and why are some bananas larger than other bananas? or some trees grow taller than others?

What affects them to grow in different sizes, although they are from the same type of trees?

Is it because the fruits grew in different conditions?

Are there any articles or research about this?

Phenotypic variance

This variance in the appearance of living things is called phenotypic variance. There are a number of reasons for the existence of such phenotypic variance. In other words there are a number of underlying variances that can explain phenotypic variances.

Primary source of phenotypic variance

The two most obvious source of phenotypic variance are

genetic variance
environmental variance

Genetic variance is caused by individuals having different genetic predisposition in the population. Environmental variance is caused by the fact that different individuals experience different environments (both macro and micro - environmental differences).

Monozygotic twins look alike because, among them, they have no genetic variance. Even if raised in the same home, they still experience slightly different environments. If raised separately (which sometimes happen) then twins will differ a little more as they experience very different environments.

Other source of phenotypic variance

The other sources of phenotypic variances include
- epistatic variance
- developmental noise variance
- all covariances between all of these causal factors.

  Are there any articles or research about this?

Well yes! Your question is underlying an entire field of knowledge which is called quantitative genetics.

More information

For more information, I recommend having a look at the post Why is a heritability coefficient not an index of how “genetic” something is?


How to get conservation of vaccine candidates between hundreds of bacterial strains? We have identified vaccine candidates via an ex-vivo RNA-seq approach. Next step would be to perform conservation of these candidates (about 20) between multiple bacterial strains (about 200). I would like to know your suggestions to perform this step.

From my bioinformatic experience, it could be possible to start with a first rough screening using blastp or blastx against a multiple strain database, and more accurate approaches would be then performed to validate this results.

Please let me know your suggestions and possible references you might consider helpful to answer this question.

Thanks for your help. Best regards, Bernardo

This website will allow you to blast all sequenced microbial genomes:
http://www.ncbi.nlm.nih.gov/sutils/genom_table.cgi

Recovering the full gene sequence might be a bit of a hassle, since BLAST will only allow you to recover the region that matched your query. You may need to set up your own pipeline for this. You may also be able to identify a "protein family" or "cluster of orthologous genes" using the BLAST results.

Once you have the full sequence, you can perform a multiple sequence alignment with CLUSTAL, Muscle, or another program. This will help you to identify the conserved regions.


Difference in Basic Amino Structures I'm having a hard time understanding why my slides in my biology course have two different representations of the "basic structure" of the amino acid:

1:

2:

The top one seem like what I would expect.  The bottom one, it looks like the amine group gained a Hydrogen ion and the Carboxyl group lost one.  Also, the center carbon gained an H.  I honestly don't know if this description is even correct or not.

I'm extremely new to this level of biology, so very simple explanations are much appreciated.  I just don't totally understand why there are two versions of the basic structure.

Also, I apologize if the tag is wrong, again, this isn't my major, so I'm very new to this material.

Your description is more or less correct, but so are both images. The bottom images shows the predominant form the amino acid would take at neutral pH (or any pH between ~2 and ~9.5). This is because the caroboxylic acid (-COOH) and amino (-NH2) groups are a weak acid and base and can lose or gain a proton (hydrogen cation), respectively. pH below the pKa of the functional group (~2 for carboxylic acid and ~9.5 for amino) favours protonation whereas pH above the pKa favours deprotonation. Also note that the "centre carbon" (the α-carbon) did not gain a proton in the second image, it's just drawn differently.

You could try this website for an overview of acid/base chemistry and perhaps these Wikipedia sections on zwitterions and isoelectric points with respect to amino acids, though there are many alternative sources of material available if you search for them. This question and answer may also be useful for you, at least eventually.


What does it mean to have different "metabolism"? We hear talk of different body types, and that it is more difficult for certain people to lose weight than others. On the other hand, when my physician recommends that I lose weight, they say that it is really just as simple as "calories in, calories out". How can we reconcile these two?

Perhaps the "calories out" portion is different for different people? I.e. some people burn more calories than others do, doing the same activities, but their hunger level does not compensate for this?

Apologies if this is off-topic

There are differences in metabolism, and the "calories in" part is the one which differs more than the "calories out" part.

People do lose different amount of calories for the same action, but for mostly mechanical reasons. If a 50 kg person walks up a mountain at 3 km/h, and a 100 kg person walks up the same mountain at the same speed, the 100 kg person will expend more energy, because they did more work. And then there are slight differences in how we do our movement - some people's gait is more efficient than others', and uses less energy. But this is not really interesting for the explanation of having it easy/hard to lose weight.

The point is that the amount of food we intake is determined by our hunger, and our hunger is determined by hormones. Then, the amount of fat we store is also determined by hormones. If your body "thinks" you should be putting on weight, and you go on a calorie-reduced diet, it won't just start complementing the missing energy from the fat stored in your adipose tissue. Rather, it will continue diverting some of your food intake to make more fat storage, all the while rationing the energy available for other activities: making you feel tired so you don't move much, shutting down some luxurious, energy-hungry processes in the brain, mostly the ones associated with higher mental functioning, and making you feel hungry and cold so you will be more motivated to seek out food and eat. The hormones which regulate these processes are many, most of them are poorly understood, some are probably not yet discovered (orexin, one of the main hunger regulating compounds, was only discovered sometime in the last 5 years I think), and we really don't have a complete picture of everything that is involved. It is a complex mesh of finely balanced homeostatic systems which interact with each other and the environment.

The people who say that it is as simple as "calories in, calories out" are right. They are right in the sense that, if you just observe a human being and measure their energy household, you will be able to document the amounts of energy consumed, expended and stored, and the energy consumed will equal the energy consumed plus the energy stored.

But to derive from this that we are talking about a passive overflow system and, if we reduce intake, storage is also reduced, is a big leap of faith and has been proven wrong again and again. Living systems are actively reacting to any influences from outside, by mechanisms much more intricate than simple mechanic rules. Mechanics tells us that if I push you, you will fall over; experience tells us that if I push you, you will brace yourself so you don't fall over, and then try to stop me from pushing you by using words, force, or whatever else you have at your disposal. Our physiological systems are the same way. They like the situation they have chosen to be in as much as you like standing upright. If somebody comes from outside and tries to forcibly change their status quo, they do whatever they can to 1) resist and retain the status quo, and 2) stop the outside force if possible.

As for the difference in metabolism: the hormone systems of different people are differently "tuned". For example, eating pure glucose causes insulin production to spike, and excess insulin causes glucose to be removed from the bloodstream, plus a handful of other effects. But the size of the insulin spike is different in different people. Also, the extent to which cells react to elevated insulin is different. When the reaction becomes dangerously weak at even high insulin levels, we say that it's a pathological variation, and call it "metabolic syndrome". If goes really towards zero, it's called diabetes type two. And this is an example about just one of the hormones connected to metabolism and the distribution and use of energy in the body.

On a simpler level, there is no difference in metabolism where physical energy calculation is concerned. Expending one molecule of ATP will let the same number of Na+ ions to move the same distance along a nerve dendrite, across humans. But this level is not really interesting when it comes to gaining or losing weight.


How can neurons divide without centrioles? I have read in my studies that neurons lack centrioles. If that is so, then how is it possible that new neurons are added to our brain? Does this have anything to do with memory loss?

You talk about memory loss. The hippocampus is involved in the formation and storage of memories and indeed one of the few places in the brain where new neurons are formed. The formation of new neurons here is indeed linked to the formation of memories (Coras et al., 2010).

Hippocampal neurons do not lack centrioles (Dotti & Banker, 1991; Poppov & Tsygunova, 1996). In fact, centrioles may not be necessary for cell division to occur (source: BSCB), although the lack of centrioles in cell models may result in aberrant cell division (Rodrigues-Martins et al., 2008).

In the hippocampus, however, it is not the neurons themselves that regenerate, but rather the resident neural stem cells and progenitor cells (Kirby et al., 2014).

References
- Coras et al., Brain (2010); 133(11): 3359-72
- Dotti & Banker, J Cell Sci (1991); S15: 75-84
- Kirby et al., PNAS (2014); 112(13): 4128–33
- Poppov & Tsygunova, Neuroscience Letters; 203(2): 135–8
- Rodrigues-Martins et al., Cell Cycle (2008); 7(1): 11-6


Image analysis of GFP-tagged protein localization bursts I'm reading an article (full text here) that analyze the dynamics of localization of a GFP-tagged transcription factor (Crz1) over the time at the single-cell level, by taking movies in a fluorescent microscope.

In Methods section they say:

  Fluorescence cell images were segmented using a Hough transformation algorithm in Matlab, provided by Sharad Ramanathan. Localization score was determined by the difference between the mean intensity of the 5 brightest pixels in the cell and mean intensity of the rest of the pixels in the cell.

The segmentation process here seems to be the identification of cells over the background. They then calculate a localization score, for each frame of the video, for every cell. Now there's the part that I can't understand:

  Bursts were identified by thresholding traces at >1 standard deviations above background noise, estimated from the lowest 20% of values.

I searched some definitions of "background noise", but I can't figure out what does it mean in this particular context. Moreover, "lowest 20% of values" of what?

Is it plausible that they define it for the lowest 20% of values of localization scores over the time, at the cell each time considered?

Maybe can be useful a screenshot of a single cell in a photogram of the video:

Yep, the Hough Transform is a way to pick out shapes you're interested in, in this case they probably have it set to find circles, and they use that to segment the image.

I think that you have interpreted their methods correctly.  For each cell they make a trace of localization score vs. time, localization score defined in arbitrary units as the difference between the mean of the five brightest pixels and the mean of the remaining pixels in the cell.  I think the lowest 20% refers to the frames in the video that have the lowest 20% of localization scores.  They take the lowest 20% of localization scores, calculate a standard deviation, and then for any frame that has a localization score that is more than 1 standard deviation above the mean of those 20%, you say that frame exhibits a burst of localization.  If I'm understanding this correctly, this process would be repeated on every individual cell.

My interpretation is that the 20% doesn't have anything to do with the signal intensity from the background pixels, and it comes from analyzing the series over time, not a single image.


Identification of brown butterfly with orange/black/white spots These brown butterflies are very frequent at my place now. Two or three can be found quietly sitting with their wings folded everyday, at different locations. It's a transition period between Autumn and Winter here, West Bengal, India.

What species is this?

Why is it taking shelter inside a house? They don't seem to move much, even during the day I've found one sitting quietly by the window. It wasn't flying off even after being disturbed.

I think this is the "Dark Evening Brown" or Melanitis phedima possibly Melanitis phedima bela:

Some further information can be found here (image 1) and here (image 2). If you look close at the second image, you can see the spot on the wing.

Why they are coming into the houses is something I can only speculate about, but probably they are either attracted by light or by warmth.


Do females living on mountains have more RBCs than a normal male I got this doubt when I was studying about haematocrit value. According to my NCERT textbook males have greater number of RBCs than females. But who will have more RBCs when comparing a normal male and a female who lives at a higher altitude?

*edit

the magnitude of altitude would be less than 8,586 m (28,169 ft) as the woman I know is not exactly at the top summit of Kanchenjunga so what would be the answer then?

Currently impossible to give a definite answer... It depends what altitude you look at.

Going from @Alan_boyd's answer the normal range is 40-50% for males and 36-44% for females. If the altitude at which a person is acclimatized to correlates well with red blood cell count (RBCC), and this effect is not gender specific (i.e. both sexes are affected similarly), then an average woman from high altitude should have a higher RBCC than an average from low altitude. But whether or not the high altitude female RBCC exceeds that of the male depends on the altitude of the two measured.

This rough graph, assuming RBCC and altitude correlate and that male RBCC is higher than female RBCC, shows the problem. Female (red dashed line) A is from a higher altitude than the selected male (blue dashed line) and has lower RBCC. Female (red dashed line) B is from a higher altitude than the selected male (blue dashed line) and has higher RBCC.

Define altitudes and the question may be answerable.


What makes urine smell acrid? Occasionally, after someone's been, there is an awful acrid smell lying about long after them. What causes this? The food that they've eaten? Urea less dilute due to dehydration?

If it helps I've noticed it only with older males.

The odor comes from urea. Urea will slowly undergo displacement to become ammonia, but when it's fresh, it has a strong odor. Other odors do come from food, notably coffee and (in some of the population) asparagus.


Where does an organism store reserves of amino acids? Where does an organism store reserves of the amino acids it needs to build various proteins it needs:

in the liver?
in the blood?
in every cell?

In the sense that you have asked the question, humans have no stores of amino acids. Amino acids obtained from the diet are quickly incorporated into new proteins or are metabolised as fuel molecules.

Proteins are subject to continual turnover, and the amino acids that are released by degradation are either reused or metabolised in exactly the same way.

This is one of the reasons why the diet must contain appropriate levels of essential amino acids (those we cannot make for ourselves) since these are continually being released from proteins and used as fuel - we have no mechanism for storing them in case of future dietary deficiency.

During starvation the protein turnover process releases amino acids from muscle and these are mainly used as fuel molecules. This is why muscle wasting occurs in starvation, although the mobilisation of fat reserves helps to delay this as long as possible as tissues, including brain, switch over to relying on ketones (derived from fat breakdown).


How does coconut form? I've seen that at the earlier stage coconut is filed with water and, as time passes, the water inside the coconut escapes and a thick layer of white substance forms.

Is the water converted into that white substance?

There is no water escaping from the coconut seed. The transformation of coconut water into coconut meat is explained by the development of the endosperm.

What happens is that, after the (double) fertilization, the endosperm of the coconut forms by nuclear division without cellular division, that is, without the formation of cell walls. This is called nuclear endosperm. According to the Wikipedia link above:

  Nuclear endosperm formation → where repeated free-nuclear divisions take place; if a cell wall is formed it will form after free-nuclear divisions. Commonly referred to as liquid endosperm. Coconut water is an example of this. (emphasis mine)

So, in an oversimplification, think about the coconut water as the cytoplasm of a single, huge cell, full of hundreds of nuclei.

After some time, cell walls surrounding the nuclei start to form. This is what we call cellular endosperm. According to the same link:

  Cellular endosperm formation → where a cell-wall formation is coincident with nuclear divisions. Coconut meat is cellular endosperm. (emphasis mine)

Therefore, in the coconut, the endosperm is initially nuclear (coconut water) and, after some time, becomes cellular (coconut meat).

According to Abraham and Mathew (1963):

  Cellular endosperm development becomes visible in nuts about 6 months old, at which stage a thin coating of jelly-like endosperm tissue is seen around the periphery of the large embryo-sac cavity.

This image shows those two tipes of endosperm (and helobial endosperm as well):

Source:

ABRAHAM, A. and MATHEW, P. (1963). Cytology of Coconut Endosperm. Annals of Botany, 27(3), pp.505-512.


Cells of umbilical cord - mom's or son's? Let's say we have a mother giving a birth to a son. In a very clear manner the cells of these two individuals are very different, of course. Yet there is an umbilical cord connecting them. Then there should be a clearly defined "border" somewhere on its way where the mother's cells meet the cells of her son, is that so? How is it even possible?! ;)

Cells of umbilical cord - mom's or son's?

Answer: Son's.

The interface you are looking for is in the placenta. https://en.wikipedia.org/wiki/Placenta

Formally the fetal side of the placenta is called the Chorion frondosum, which develops from the outer cells of blastocyst (trophoblast), and the maternal side of the placenta, Decidua basalis, which develops from the maternal uterine tissue.

  How is it even possible?

Immune tolerance in pregnancy or gestational/maternal immune tolerance

The placenta functions as an immunological barrier between the mother and the fetus, creating an immunologically privileged site. For this purpose, it uses several mechanisms

It secretes Neurokinin B containing phosphocholine molecules. This
is the same mechanism used by parasitic nematodes to avoid detection
by the immune system of their host.
Also, there is the presence of small lymphocytic suppressor cells in the
fetus that inhibit maternal cytotoxic T cells by inhibiting the
response to interleukin 2.
The placental trophoblast cells do not express the classical MHC
class I isotypes HLA-A and HLA-B, unlike most other cells in the
body, and this absence is assumed to prevent destruction by maternal
cytotoxic T cells, which otherwise would recognize the fetal HLA-A
and HLA-B molecules as foreign. On the other hand, they do express
the atypical MHC class I isotypes HLA-E and HLA-G, which is assumed
to prevent destruction by maternal NK cells, which otherwise destroy
cells that do not express any MHC class I. However, trophoblast
cells do express the rather typical HLA-C.
It forms a syncytium without any extracellular spaces between cells
in order to limit the exchange of migratory immune cells between the
developing embryo and the body of the mother (something an
epithelium will not do sufficiently, as certain blood cells are
specialized to be able to insert themselves between adjacent
epithelial cells). The fusion of the cells is apparently caused by
viral fusion proteins from endosymbiotic endogenous retrovirus
(ERV). An immunoevasive action was the initial normal behavior of
the viral protein, in order to avail for the virus to spread to
other cells by simply merging them with the infected one. It is
believed that the ancestors of modern viviparous mammals evolved
after an infection by this virus, enabling the fetus to better
resist the immune system of the mother.

Other mechanisms include exposure to immune modulating factors present in seminal fluid from vaginal and oral sex. https://en.wikipedia.org/wiki/Pre-eclampsia#paternal_tolerance


How can ingesting a prion "infect" someone? That's something that's been bugging me for a while...

Our gastrointestinal tract produces proteases that degrade proteins. Prions are proteins. Shouldn't they be broken by proteases?

Also, how can a prion pass the gastrointestinal barrier? Shouldn't the intestine be able to absorb aminoacids only (instead of full proteins)?

Prions are misfolded proteins with abnormal tertiary or quaternary structures. That grants them resistance (to some extent, at least) to proteases (1).

Also researchers believe that prions are able to replicate (2), by changing the structure of other proteins.

Regarding the gastrointestinal barrier, that isn't exactly true. It has been shown that small quantities of intact proteins do cross the gastrointestinal tract in animals and adult humans (3), and that this is a physiologically normal process required for antigen sampling by subepithelial immune tissue in the gut

So, the resistance to the proteases and the ability to replicate in certain conditions might explain the odds of a prion crossing the gastrointestinal tract and infecting an individual.

References:

http://www.ncbi.nlm.nih.gov/pubmed/24338008
http://www.nejm.org/doi/full/10.1056/NEJM199609193351218
http://www.ncbi.nlm.nih.gov/pubmed/3060169


What are host cellular factors? With respect to this paper:

Global Analysis of Host-Pathogen
Interactions that Regulate
Early-Stage HIV-1 Replication

What does the term "host cellular factors" mean??

Generally spoken, "host cellular factors" are proteins, receptors etc. of the host cell. In this case, they are important for the HIV infection. The authors write:

  Recently, a genome-wide siRNA analysis revealed over 250 host cellular
  factors that influence HIV-1 infection.

This means gene silencing techniques where used to identify the host cellular factors which are important for the infection, you can find these results here: "Identification of host proteins required for HIV infection through a functional genomic screen."
The overall goal is to identify proteins which are important for the function and infection of HIV to understand the interaction between virus and host cell better.


Minor differences in morphology of a snake: Why designate it a different species? I was motivated to ask based on an answer to another question that I read on SE-Biology:

  You can differentiate this species [Ashok's Bronzeback (Dendrelaphis
  ashoki)] from closely related D. girii based on it having a longer
  "postocular" black line than D. ashoki -- in D. ashoki it stops
  shortly caudal to the eye...

When the differences are so minor (e.g. "longer "postocular" black line") what's the reason for designating them as two different species?

Is there a objective reason when to call them different species? Would those two not interbreed?

Note: I'm not just asking "If they interbreed why is it a different species?"

I'm more in the vein of asking: "If two species so similar are still different species why are they different? Is there an objective metric to draw the line at which point we differentiate as different species."

Edit:

I've asked a related question over here:

Can Eskimos be regarded a distinct species from Kalahari Bushmen based on morphological differences & geographic isolation?

Short explanation

According to the papers I could find, Dendrelaphis ashoki and D. girii aren't as closely related as you suggest: D. ashoki appears to be closely related to D. pictus, a Southeast Asian snake species, while D. girii appears to be closely related to D. bifrenalis, a Sri Lankan/South Indian snake species. They were distinguished from their sister species largely on the basis of morphological differences and geographical isolation.

How do we know D. ashoki is a distinct species?

The key to this answer is in Vogel and van Rooijen, 2011a, the scientific article in which Dendrelaphis ashoki was first described. Before their work, these snakes were thought to belong to the species Dendrelaphis pictus. To test whether this was in fact the case, they compared 9 individuals of D. ashoki with 34 individuals of D. pictus, and found statistically significant ($p < 0.05$) differences in five morphological characters: SUBC (number of subcaudals), TAIL (tail-length), EYED (horizontal diameter of the eye), SUBL (number of infralabials touched by the first sublabial, left and right added) and STRIPE1 (ventrolateral stripe bright/dull/absent). Here's the statistical analyses they ran:

  The south Indian form that has previously been referred to as D. pictus (e.g., Wall, 1921; Smith, 1943; Whitaker and Captain, 2004) differs from Indochinese D. pictus in the characters SUBC ($F_{1,25} = 17.7, P = 0.0003$), TAIL ($F_{1,25} = 30.0, P = 0.00003$), EYED ($F_{1,35} = 22.5, P = 0.00003$), SUBL (Mann-Whitney U, $Z = −4.6, N=40, P < 0.00001$) and STRIPE1 ($\chi^2_1 = 42, P < 0.00001$).

They also compared the 9 individuals of D. ashoki with 48 individuals of D. proarchos, and found statistically significant ($p < 0.05$) differences in five morphological characters: VENT (number of ventrals), SUBC (number of subcaudals), TAIL (tail-length), EYED (horizontal eye diameter), SUBL (number of infralabials touched by the first sublabial, left and right added) and STRIPE1 (ventrolateral stripe bright/dull/absent).

  [The south Indian form] differs from D. proarchos in VENT ($F_{1,49} = 24.1, P = 0.00001$), SUBC ($F_{1,28} = 13.7, P=0.001$), TAIL ($F_{1,28} = 40.1, P < 0.00001$), EYED ($F_{1,47} = 16.8, P=0.0001$), SUBL (Mann-Whitney U, $Z = −4.7, N=52, P < 0.00001$), and STRIPE1 ($\chi^2_1 = 53.0, P < 0.00001$).

The authors didn't rely just on morphological evidence: they note that D. ashoki, which is found in the Western Ghats, is also geographically isolated from other populations of D. pictus, which are found in Northeast India, Myanmar and South East Asia. Therefore, they concluded (emphasis mine):

  The distinct morphology and coloration as well as strong geographic isolation of the population from the Western Ghats imply a unique evolutionary history that does not allow application of either the name D. pictus or the name D. proarchos. Consequently, we describe this form, previously referred to as D. pictus, as a new species, D. ashoki sp. nov., endemic to the Western Ghats.

How do we know that D. girii is a distinct species?

For this information, we need to look up another paper published that same year,  Vogel and van Rooijen, 2011b. Interestingly, the authors don't compare this snake with D. ashoki at all, but with Dendrelaphis bifrenalis:

  Due to their double loreal shield, D. girii sp. nov. and D. bifrenalis occupy a unique position within the genus. A congeneric species with a double loreal shield has been described in the past, namely Dendrelaphis biloreatus (Wall, 1908). However, the presence of a double loreal in D. biloreatus appears to be based either on an anomalous specimen or on a misjudgement (Vogel & Van Rooijen, 2011b). Furthermore, D. biloreatus differs from D. girii sp. nov. and D. bifrenalis in its number of dorsal scale rows (13) and its number of ventral scales (190-199).

  There are several differences between Dendrelaphis girii sp. nov and D. bifrenalis. The most obvious one is the light ventrolateral line, which is present in D. bifrenalis and missing or very faint in
  Dendrelaphis girii sp. nov. (see Fig. 3, 4).

  The postocular stripe is much broader in D. bifrenalis. In D. bifrenalis there are black oblique bars in the neck region of some, but not all specimens (8 specimens out of 12 in our data) (see Fig. 3-5). This pattern is not sex related. It is absent in D. girii sp. nov. For Dendrelaphis girii sp. nov. we had only 1 male, so it is not possible to compare the sexual dimorphism in this character. The snout of Dendrelaphis girii sp. nov. is much broader than that of D. bifrenalis. Dendrelaphis girii sp. nov. has, on average, fewer subcaudals and more ventrals than D. bifrenalis, but the ranges broadly overlap.


Parts of the brain pivotal for maintaining consciousness From an answer to another question (on conscious experiences by coma patients) I have learned that

  no conscious experiences, complex thoughts, or complex emotions can
  occur when one is in coma (clinically unresponsive, with absent or
  minimal brainstem reflexes, and with severely abnormal EEG)

This means that proper modes of activity of the cortex and the brainstem are necessary conditions for conscious experiences.

Two questions arise:

Has it been shown that proper activity of the brainstem and the cortex is also a sufficient condition for conscious experiences, i.e. all other parts of the brain might be mute or otherwise improperly active? Or are there other parts of the brain whose proper activity is also necessary for conscious experiences?
Why is it that next to the newest parts of the brain (cortex and neocortex) also its oldest part (the brainstem) is pivotal in maintaining consciousness? What about other parts that evolved later?

Note that with "necessary" I don't mean causally necessary but merely logically or observationally necessary, i.e. "not observed without".

The minimal neural mechanisms that are jointly sufficient for consciousness (conscious percept, thought, memory, etc.) to occur, under constant background conditions, are called the neural correlates of consciousness (NCC) [1]. The background conditions are enabling factors that must be present for the NCC to be able to function (e.g., the heart must beat and the lung must exchange air to supply the brain with oxygenated blood, the blood levels of sugar and other blood constituents must be in normal ranges, the ascending reticular activating system (ARAS) must be functioning, etc.), but they are not the NCC.

The ARAS is the neural network in the core of the brain extending from the rostral pons to both thalami and the basal forebrain, and from there it sends extensive axonal projections to the cerebral cortex, including the consciousness neural network (which is the anatomical part of the NCC). The ARAS is responsible for the alertness of consciousness, but it is not responsible for the content of consciousness. So, it is not part of the NCC proper. However, there can be no consciousness if there is no stimulation from the ARAS, even if the consciousness neural network is intact and able to function, such as in the case of extensive brainstem hemorrhage, infarct, and trauma. And the level of conscious alertness depends on the activation from the ARAS – the more activation, the higher level of alertness. This results in various conscious level’s states, such as (from lower to higher level of alertness) coma, stupor, drowsiness, normal alertness, and heightened alertness [2]. So, the answer to question #2 – why this oldest part (the brainstem) is pivotal in maintaining consciousness – is that it is the way the consciousness neural process has evolved to be dependent on the ARAS for its level of function (i.e. its alertness).

On the contrary, if the ARAS is working normally but the consciousness neural process is not, there can be alertness without, with minimal, or with some awareness. The degree of impairment of awareness depends on how much the consciousness neural process is dysfunctional. For example, in the case of damages to the consciousness neural process from diffuse cerebral hypoxia, extensive bilateral cerebral infarcts, or diffuse cerebral cortical injury, the results can be various abnormal conscious awareness’s states that range in severity of abnormal conscious awareness, depending on how much the consciousness neural process is impaired, such as (from mild to severe) acute confusional state, akinetic mutism, minimally conscious state (MCS), and vegetative state (VS). In the latter two categories, which are severe conditions, the patients can open eyes and have some reflex responses, such as blinking, chewing, and yawning, but show no (in VS) or minimal (in MCS) signs of conscious awareness of self and the environment (by clinical testing or by special investigations such as EEG, evoked potentials, and fMRI) [2].

Regarding the neural circuits of consciousness, as far as one can conclude from the evidence at present, it seems very likely that the Default Mode Network or Resting State Network [3], which includes the medial prefrontal cortex, posterior cingulate cortex, precuneus, hippocampal and parahippocampal cortex, retrosplenial cortex, and some parietal and temporal cortices, is the network of the consciousness neural process when the mind is in the state of passive internal mentation, not performing cognitively demanding tasks, and not attending to outside stimuli. This network overlaps with the network that functions for access consciousness (consciousness of episodic stimuli, not consciousness of continuous stimuli as in the former case). At present, evidence shows that the network of Global Workspace theory proposed by Baars [4] or the network of Global Neuronal Workspace hypothesis of Dehaene [5], which includes the cortico-thalamic (C-T) core and a network of neurons with long-range axons densely distributed in the prefrontal, fronto-parietal, parieto-temporal, and cingulate cortices, is the network of access consciousness. So, the complete neural network of consciousness that functions to be conscious of continuous events and episodic events is likely to be some form of combination of these networks, such as the neural network in the extended theory of global workspace of consciousness proposed by Song [6].

The complete neural circuit of consciousness, whatever it is finally found to be composed of, and the way it functions will constitute the complete NCC. The complete NCC is necessary and sufficient for consciousness to occur. Even if we do not have the complete NCC now, the above current models that we have are fairly well supported by experiments. I hope this answers question #1.

References.

Tononi G, Koch C. Consciousness: Here, there and everywhere? Philos Trans R Soc Lond B Biol Sci. 2015 May 19;370(1668):20140167. DOI: 10.1098/rstb.2014.0167.
Ukachoke C. Chapter 6 – Consciousness. In: The Basic Theory of the Mind. 1st ed. Bangkok, Thailand; Charansanitwong Printing Co. 2018.
Andrews-Hanna JR. [The brain’s default network and its adaptive role in internal mentation.(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3553600/) Neuroscientist. 2012 Jun;18(3):251–270. DOI: 10.1177/1073858411403316.
Baars BJ, Franklin S, Ramsoy TZ. Global workspace dynamics: Cortical “Binding and propagation” enables conscious contents. Front Psychol. 2013;4:200. DOI: 10.3389/fpsyg.2013.00200.
Dehaene S, Charles L, King JR, Marti S. Toward a computational theory of conscious processing. Curr Opin Neurobiol. 2014 Apr;25:76–84. doi: 10.1016/j.conb.2013.12.005.
Song X, Tang X. An extended theory of global workspace of consciousness. Progress in Natural Science. 2008 Jul 10;18(7):789–793. DOI: https://doi.org/10.1016/j.pnsc.2008.02.003.


Are there grass or fiber eating birds? My understanding, that may be wrong, is that cellulose/fibre has little nutritional value to many animals because it's hard to break down thus making consumption inefficient. However, Ruminating mammals, other mammals such as black bears, and many insects such as grasshoppers digest grasses.

Are there any birds with the gut flora to break down fibre? Or even some that eat grass but digest it in another way?

The hoatzin has a digestive system that makes use of bacterial fermentation. Many other birds also consume grass, e.g. ostriches, ducks and geese.

There's also a large body of literature on how birds can digest cellulose.


How do both autotrophic and heterotrophic successions end up having Gross Production = Respiration? I was reading Information theory by Eleith, Odum and Golley  from different sources, one of which was Funfamentals of ecology by Odum:

... autogenic succession usually begins with an unbalanced community metabolism, where gross production, P, is either greater than or less than community respiration, R, and proceeds towards a more balanced condition, where P=R. The rate of biomass production (B/P ) increases during sucession until a stabilised system is achieved, in which a maximum of biomass (or high information content) and symbiosis between organisms are maintained per unit of available energy flow.
The succession begins with P>R in autotrophic sucession and P<R in heterotrophic sucession.

I have tried to find explanatory texts both in this and other books without any success so my question is how's this balanced state achieved in both types of successions (the answer is hinted in the first paragraph which I don't quite understand)?
Related to my last post.

The author is saying that 1) Mature ecosystems tend to have a balance between production (=P) and use (=R, respiration) of biomass. This is actually tautological because the author would probably define a mature ecosystem as one where this is true (P=R).

If it starts out P > R, the autotrophs are dominant: more biomass is being produced than used up. It is possible, for a time, that P will increase as, for example, plants grow more leaves, but R is growing too, and there is an eventual limit on P, which at maximum depends on the light available to the ecosystem. As biomass grows, so does the amount of biomass to potentially decay, so eventually R will always catch up to P, until there is balance.

If it starts out P < R, that means you are using up biomass faster than you are creating it. This case is even simpler: you will gradually run out of biomass, and R will decrease.

In either case, when the author is talking about P = R, this is going to be in relative terms; there might still be variations between them, for example seasonal variation, but on average over years or decades you would expect P = R in a mature, stable ecosystem.


Are these fruit flies really coming back to life after being frozen? I've found this video on Reddit where they pretend these are frozen fruit flies coming back to life... I didn't find any publication related to this specific experiment. Is this just a fake video?

Short answer
Short-term freezing kills fruit flies. Long-term cryo-preservation of D. melanogaster is also not possible.

Background
Per a publication of Koštál et al. (2016), long term preservation of insects is only possible for embryos, or larvae in diapause. Indeed, freezing is an effective way to kill adult fruit flies (source: Phys.org)

However, D. melanogaster adults show very weak capacity to enter reproductive diapause, and larvae possess absolutely no capacity for diapause Koštál et al., 2016).

Reference
Koštál et al., Scientific Reports (2026); 6: 32346


How is the fluoride in toothpaste absorbed? How is the fluoride in toothpaste absorbed by our body? Does the tooth absorb the molecule directly, or is it absorbed by the mouth?

The answers to this question suggest that some materials can be absorbed by the mouth, but fluoride is absent. Additionally, many municipalities add fluoride to tap water which I should imagine is actually absorbed in the stomach by a different mechanism than that of toothpaste.

Note that toothpaste generally comes with stern warnings not to swallow. Looking at the ingredients it seems the only thing that may be harmful is the fluoride itself. Therefore I suspect that toothpaste has a much higher fluoride concentration than tap water, which supports the notion that its fluoride is absorbed by a different mechanism than tap water.

The chemical mechanism by which fluoride protects teeth is the remineralization of hydroxyapatite $\ce{Ca5(PO4)3(OH)}$ in the tooth enamel into fluorapatite $\ce{Ca5(PO4)3F}$:

$$\ce{Ca5(PO4)3(OH) \ (s) + F- \ (aq) -> Ca5(PO4)3F \ (s) + OH- \ (aq)}$$

This reaction occurs at the surface of the enamel, i.e. directly within the mouth.  The fluoride ions participating in the reaction are dissolved in the saliva and other fluids present in the mouth.

Thus, the fluoride does not need to be absorbed into any part of the body (although, as part of the remineralization process, it can be said to be absorbed directly into the tooth enamel), and, in particular, there is no need for it to be swallowed.  Indeed, because of potential adverse effects of high levels of fluoride when absorbed into the body through the digestive tract, swallowing strongly fluoridated dental care products like toothpaste or mouthwash should be avoided.

That said, any fluoride that is swallowed and absorbed into the body, e.g. through fluoridated (or naturally fluoride-rich) drinking water, can still contribute to the remineralization of teeth, simply because some of it will be secreted back into the mouth as part of saliva.

While the fluoride levels in saliva (assuming a safe level of fluoride intake) are much lower than those in, say, toothpaste, your teeth will be constantly exposed to the fluoride in saliva, whereas they will only be exposed to toothpaste for a few minutes each day.  Thus, while the rate of remineralization due to systemic fluoride may be much slower than that due to e.g. fluoridated toothpaste, the total amount of remineralization per day may well be of a comparable magnitude.


Hardy-Weinberg sex linked formula The "big five" assumptions are the ones listed in the main text. However, the basic formulation of Hardy-Weinberg equilibrium also relies on a few other assumptions;

Allele and genotype frequencies don't differ between males and females. That is, the basic form of Hardy-Weinberg does not cover sex-linked genes.

so, is there a modified formula?

Solving Hardy-Weinberg problems

First of all, you might want to have a look at the post

Solving Hardy-Weinberg problems

and eventually at

Assumptions of Hardy-Weinberg rule

After reading the first post, you should be able to answer your question yourself. I encourage you to try it before reading what follows.

Hardy-Weinberg for sex-linked loci

I will make an example. Let's consider a case where males are XY and females XX (like in mammals for example). Let A and B be two alleles of a bi-allelic present on the X chromosome. The frequency of these two alleles in the entire population are $p$ and $q$. Let's assume the locus is present on the X chromosome. We will assume that the allele frequency do not differ between males and females.

In males, there are two possible genotypes. A and B. Their frequency among males are noted $f_{m,A}$ and f_{m,B} and are

$$f_{m,A} = p$$

$$f_{m,B} = q$$

In females, there are three possible genotypes. AA, AB (or BA) and BB. Their frequency among females are noted $f_{f,AA}$, $f_{f,AB}$ and $f_{f,BB}$ and are

$$f_{f,AA} = p^2$$
$$f_{f,AB} = 2pq$$
$$f_{f,BB} = q^2$$

If the sex ratio (the ratio of the number of males over the number of females) is $r$, then the genotypes frequencies in the overall population are the ones from above multiplied by $r$ and $1-r$ for males and females, respectively.


Are there any multicellular forms of life which exist without consuming other forms of life in some manner? The title is the question. If additional specificity is needed I will add clarification here.

Are there any multicellular forms of life which exist without requiring the consumption (destruction) of other forms of life in some manner? Thus purely on inorganic material.

I do understand that the definition of life is a semantic distinction, so for this discussion I will assume the one Wikipedia provides:

"Life is a characteristic distinguishing physical entities having signaling and self-sustaining processes from those that do not, either because such functions have ceased (death), or because they lack such functions and are classified as inanimate. Biology is a science concerned with the study of life."

I am open to considering alternative suggestions.

Thank you.

Yes, plants for example!

Autotrophs vs. heterotrophs

Plants are autotrophs while animals and fungi are heterotrophs. Have a look at the Wikipedia articles. In short, autotrophs organisms are organisms that synthesize their own compounds from inorganic compounds. Heterotrophs organisms are organisms that synthesize their own compounds from organic compounds.

Therefore, any multicellular plants are multicellular organisms that "exist without consuming other forms of life" (with the exceptions of carnivorous plants).

Consuming nonliving organic matter

Of course, many life forms feed on organic matter but only on non-living organic matter. Such life forms do not kill to feed. It is the case of all detritivores (such as earthworms) and decomposer such as fungi.

Competition vs predation

As @TechZen said, not consuming other organisms doesn't mean that the existence of an individual of this species is not causing the death of another individual (competition and parasitism that does not involve consuming the other individual).


What causes light to be brighter in the corner of the eyes? I have noticed when in a dark room light and color seem to be brighter and more intense in the corner of my eyes. For example the light that comes from my digital clock seems like a dark pink when I look straight at it. But when I see it in the corner of my eyes it looks red.

What causes this?

Is this normal, does everyone perceive it that way?

Your retina has two kinds of light-sensing nerves: cones and rods. Cones are responsible for color vision, i.e. hue, while your rods handle differences in the value, as in how bright it is.

Humans have adapted to have cones mostly in the center of the eye (which corresponds to what you're looking directly at), where the most distinguishing color information is needed. It's not often that you'd use your peripheral vision to identify the actual color of something, and this explains why you're seeing a difference between pink and red. The intensity of the color is correct, but you aren't able to identify the hue because of a lack of cone nerves.

So yes, this is normal. A fun trick (and also totally helpful if you have a messy room) is to look a foot or so above the floor when you're walking in the dark. It allows you to see what you're walking on better, since you need intensity receptors more than color receptors.

References:

http://regentsprep.org/Regents/physics/phys09/ceyes/sensing.htm

http://hyperphysics.phy-astr.gsu.edu/hbase/vision/rodcone.html


Why is trisomy a problem? I understand that a missing part of genetic information is a problem - the cell does not know how to synthesize a specific protein. But why is it a problem when there's one more copy of a chromosome?

Let's say a trisomy of the 21st chromosome occurs, so the person has Down syndrome. What happens on the molecular level that the person develops the way they develop?

Without going into Down syndrome specifically, let's address the title of your question: Why is trisomy a problem? Or, more specifically, why can it be a problem to have extra copies of genes?

Let's imagine biology to be just a really complicated cake. If you are trying to bake a cake, and you leave out the flour, I think mostly everyone would agree that the outcome product wouldn't be much of a cake at all: that's the condition where you are completely lacking an ingredient, both copies of the same chromosome, a nearly assured fatality.

But let's say you instead include 50% too much flour. What results? You might still get a cake, but it might not taste perfect: maybe a little too bread-like or not sweet enough.

In short: having an extra chromosome means genes on that chromosome are overexpressed. Those gene products could themselves have deleterious effects in excess, or they could affect expression of other genes and cause over- or under-production of those products. Of course it isn't as simple as "+50% expression!" because of regulatory mechanisms ubiquitous in biology, but there is sufficient overexpression to cause some issues.

Really, someone with Down syndrome develops almost completely normally - many other trisomys are fatal in the early stages of development, so we don't become familiar with them. For Down syndrome in particular, you can check out some of the proposed mechanisms on Wikipedia. One suggestion is that some of the cognitive deficits resemble Alzheimer's disease, implying a causative function for amyloid beta in both circumstances. The hypothesis is that amyloid beta accumulates in aging brains, but people with Down syndrome overproduce amyloid beta so they show dementia symptoms much earlier. This comparison is certainly not the only factor in Down syndrome, however.


What happens if a non-diabetic receives an injection of insulin? If a person without diabetes or any diabetes-related issues receives an injection of insulin, what happens? Would the blood glucose level drop or does the body naturally compensate for the added insulin? What biological process occurs?

Blood sugar drops (Hypoglycaemia)
There are several other uses of insulin (other than diabetic treatment)

Some of those could be:

Diagnostics
Psychology (Narcoanalysis)
Parenteral nutrition
Cardiology (Glucose–insulin–potassium solution (GIP or GIK solution) is given   after a myocardial infarction)
Malignancy (Insulin potentiation therapy (IPT))
Psychiatry (Deep insulin coma therapy (DICT))

Sources:

Niazi, Asfandyar Khan, and Shaharyar Khan Niazi. "A Grand Dame
with Hidden Aces: The Non-diabetic Uses of Insulin." Indian Journal
of Endocrinology and Metabolism. Medknow Publications & Media Pvt
Ltd. Web. 06 Feb. 2016.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3354952/.
"Hypoglycemia." Hypoglycemia. Web. 06 Feb. 2016.
http://www.niddk.nih.gov/health-information/health-topics/Diabetes/hypoglycemia/Pages/index.aspx.


Is it possible to breed neanderthals through selective breeding? I've heard most non-subsaharan africans have neanderthal DNA with it being more prevalent in northern regions, that sometimes 1-4% of the DNA has neanderthal origins.

Speaking strictly scientifically, would it be possible through selective breeding to breed an individual where the majority of the DNA is neanderthal?

No, it is not. As you said only 1-4% of non-subsaharan africans' genome is from Neanderthal and it is more or less the same sequences. The entire Neanderthal genome is not present in modern day humans, it is only a small set of sequences.


How many NOD like receptors in Human? This is pretty specific question maybe. Anybody have an estimate? For Toll Like Receptors there are something like 10...

http://www.jbc.org/content/276/4/2551.long

I'm only finding NOD1 and NOD2 => only 2?

This review 22 proteins in the NOD like human repetoire. It was published in 2013...

The families are broken down into 9 general groups according to their domain composition in Figure 1 from that review.  Most of them are not named "NOD".