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Does sweat contain DNA information?
I was reading this article : Perspiration
The first question which came to my mind after reading the composition of sweat was whether it contains any information about the DNA or not?
I haven't had much interaction with biology since 12th grade (2010), so kindly answer in layman's terms and detail as well.

The consensus of the answers as of March, 2023 seems to be that human sweat does not contain enough human DNA to identify the person producing that sweat. This contradicts fictional court testimony in s1 e1 of "All Rise", a crime drama on Hulu subscription video. DNA identification of human fluids apparently requires them to contain human cells.

The Wikipedia page you linked says that sweat is composed of a liquid similar to blood plasma. As all DNA in humans is stored in the nucleus of a cell, it seems unlikely that the sweat itself would contain any DNA.
However, when someone sweats significantly, I can't imagine that no skin cells end up in the sweat. In any case in which this occurs, then the DNA in the cell is in the sweat. Additionally, with small amounts of sweat, I can't imagine how it would be collected without getting any skin cells in it.
This source confirms that sweat contains DNA in some form. Additionally, I think the following quote from here shows that it is stored in cells:

In every case, what is being tested is the DNA contained in cells of human tissue

Yes exactly. it was due to a heated discussion with a friend. We were discussing about DNA, I was sayin about how bodily fluids like blood, semen, etc contain genetic information. She said that sweat doesn't  and I couldn't find enough evidence to prove otherwise.

@ABcDexter AFAIK, those fluids only contain DNA because they contain cells. I'm not an expert, by any means, though.

@Christiaan I've found and added some sources that seem reliable.

@john01dav - great +1

So sweat does contain DNA and the genetic information ;)

I believe the answer is no.
Sweat is the liquid secretion of body cells, not including the cells themselves. If the cells are secreted when sweating, then you may find some DNA in your sweat. You are right on that. Serum contains many different types of lymphocytes, the majority of them--mature red blood cells, don't have nucleus. So they don't contain DNA. And, live skin cells cannot be sweated. Dead skin cells are easily found on the mucosal tissues of your body, however mucosal tissues cannot sweat! In a word, it's basically impossible to see DNA in sweat.

@ABcDexter In respect to your comments, semen is for sure to contain genetic information because of the presence of germ cells(sperms) in it. However, it's not the same way of how you sweat. Semen is from sex organs only while you can't say sweat is from a specific organ.

Yes but not humans DNA
Sweat does not normally contain human DNA, it does not pick up many skin cells under normal conditions, excessive sweat can pick up some however. However sweat is colonized by bacteria fairly quickly once it reaches the surface of the skin so unless you are extracting it directly from the gland it will contain bacteria with their own DNA.


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What further research can the result of gene variation detection be used for
We do a research on a particular cancer (for e.g. breast cancer). Now, we have a result for the gene variation detection (VCF file). What next steps do we need to do? We don't have a clear picture about this. Can you give us some directions or few papers as an example? (of course it is a huge number but just mention a few). Thanks!

source: Stack Exchange

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In flowering plants food is transported in which form?
In flowering plants food is transported in which form? I searched on google and found that it is sucrose. Why not glucose/fructose/starch?

Is this a homework question?

why  r u asking that ?

Because homework questions are off-topic here unless you show your effort for answer. Do some research on the topic, and if you are still confused, show us the line/paragraph/article (that you read during research) which is confusing you.

i hav dun my research nd still not got my answer .... :(

nd y r homework questions not allowed......afterall they r also a part of biology ??

See Biology.SE homework policy till I post an answer.

You should add all the relevant details that you would have got while doing your research.

This is a homework question but I will answer it (forgive me moderators ;).
You will get your answer from this answer:

Sucrose and starch are more efficient in energy storage when compared to glucose and fructose, but starch is insoluble in water. So it can't be transported via phloem and the next choice is sucrose, being water soluble and energy efficient sucrose is chosen to be the carrier of energy from leaves to different part of the tree. Another problem exists, glucose is highly reactive and this may result in some intermediate reactions while transporting glucose. Being a complex structure, sucrose is not as much reactive as glucose. So plants uses the sucrose as a medium to transfer energy. Inside the cells, sucrose is converted back to glucose and fructose.

Once again:

Glucose- too reactive: CANCEL
Fructose- too reactive, again: CANCEL
Starch- insoluble in water: CANCEL
Sucrose- no problem: ACCEPT

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Methods for varying insert size in E. coli clones
I'm writing my master's thesis proposal, and I need to improve the solution-behavior of some truncated protein domains which have previously shown poor solubility when expressed in E. coli.
To prevent this unwanted aggregation, one experiment I will perform will be to alter the domain boundaries.  I will create gene constructs where each clone will have an A domain of a certain length and domain border (see below).

My question: Is Gateway cloning better than restriction/ligase methods for this?  If i use restriction/ligase methods to construct vectors for transformation, then my choice for domain boundaries will be determined by restriction sites. Howevever, with a system like Gateway cloning, I can define boundary limits to bp resolution by simply desining an appropriate primer.
Is my reasoning here correct? I need to justify my choises for experimental design to researchers, so want to make sure I'm being efficient and logical.

Take a look at this.

Yes.  In principle you will have a vastly increased ability to customize the boundaries of each protein domain with a primer and PCR based approach.  It is not obvious to me that the Gateway Cloning System is required, or necessarily the best choice for this approach, but that is likely subjective.
Are you familiar with, or aware of, the efforts of the SGC (Structural Genomics Consortium)?  My understanding (now somewhat outdated) is that they were going to design/use a semi-automated way of implementing the strategy you discuss (domain trimming) so that they could us a high-throughput approach to define crystallization conditions for their targets.  Perhaps you could adapt their method(s) to your protein of interest?


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Barcode exchange between neighbouring cells
I am currently interested in equipping animal cells in a tissue with individual barcodes. These barcodes should get amplified in the cells (not to a cell degrading extent, of course), and also transmitted to neighbouring cells.
The question is now, how do I a) insert these barcodes into the cells and b) how do I transmit them to the neighbouring cells.
In the Zador et al. paper "Sequencing the connectome" (http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001411), it was proposed to use a transsynaptic virus like as rabies or pseudorabies, for making that exchange possible between neurons that are synaptically linked. Here, however, I am interested in the directly neighbouring cells and I am insecure whether it makes sense to use transsynaptic virus here.
If so, it would be great, but if not, do you know some alternatives?


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Why aren't we immune to the "cold"
As far as I know, people suffer from the cold since ever. Why didn't and don't we evolve to resist it?

Not since ever, only since about 70 years is it considered normal to suffer from the cold a few or more times per year. This is because we spend so much of our times indoors in rooms with central heating and air conditioning where the signal from the newly emerging cold viruses  is drowned out by the microbes that live in the artificial tropical indoor climate. The first exposure to the cold virus is then when someone sneezes in your face; the cold can spread as wildfire with all these people with poor immunity against it.

The main reason is that there really isn't any one "cold," but rather the word is used to describe many different infections that simply have the same symptoms. The reason for these same symptoms is that almost all of the symptoms that one experiences in a cold are actually the immune response to said infection. For instance, a fever is used to make the body less hospitable for the infection causing agent and throwing up is used to ensure that harmful substances are removed from the digestive system before they can cause too much harm.
The reason that the body can't simply evolve resistance to all of these possible infections is both because the infections evolve too and because there are simply too many of them that all need a separate method to be defeated. Therefore, curing the common cold is effectivley curing the majority of known ailments.


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

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

"In any high level CO environment, your exhaled breath CO level will gradually rise but remain lower than the ambient level because you always absorb some of the CO you inhale as long as the level in air is higher than the level in your blood.  As soon as you stop smoking or move to a lower CO environment, you start exhaling."
So I suspect a lungful of pure CO would indeed make you feel awful, but since that wouldn't be nearly enough to replace all the oxygen bound to your haemoglobin, I imagine it wouldn't be fatal in a healthy individual, especially if you were breathing air free of CO after that one lungful.
Apparently it takes 5 hours to eliminate half of your blood CO also.

What are you quoting here? Please provide the reference. Also, it doesn’t look like this quote is really relevant to the question, since it seems to refer to specific CO-rich environments, and smoking.

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What animal produces male gametes by mitosis?
The following question came up in my biology examination but I could not answer it:

"What animal produces male gametes by mitosis?"

I know that some plants produce their gametes by mitosis in the gametophytes, but found no references to any animals doing so.

I don't think gametes are ever produced by mitosis. There can be modified meiosis in which there is no halving of the number of chromosomes. This can be seen in haploid organisms such as male honeybees.

@WYSIWYG correct, but it is so because male honey bees are produced by parthenogenesis. So all cells in them are haploid and can act as gametes.

@another'Homosapien' No the cells do not automatically act as gametes. Sperm is a very specialized cell. Spermatogenesis does happen (see my answer).

I think the answer of honeybees is much correct,as their cells are haploid they have to produce their gametes by mitosis, because the worker bees are diploid and they are produced after fertilization so the queen and the male gametes have to be haploid.

@WYSIWYG It actually does happen: they can automatically act as gametes. I don't know any reference, but I was taught earlier that meiosis cannot occur in such cases. Also, as you say in your answer, only meiosis-II occurs which is also very similar to mitosis.

@Asmaa did you ask your teacher about the correct answer? (because only your teacher can solve this dilemma now ;)

@another'Homosapien' yes that does not mean that cells do not differentiate. Gametogenesis is also differentiation (along with haploidization). Since the germ cells are already haploid, meiosis-I is abortive. When you say they automatically act as gametes, you are just ignoring all these processes which are quite critical for the formation of the sperm.

@WYSIWYG okay I apologize for saying that they can automatically act as gametes. But you can't deny that they produce gametes by mitosis, not meiosis.

@another'Homosapien' yes and as I mentioned in my answer, it still behaves like a meiosis but is finally just like mitosis.

In organisms which have haploid males (such as honeybees), there is a variation of meiosis during spermatogenesis. The meiosis-I is abortive i.e. the chromosomal events such as crossover and separation of homologous chromosomes, do not happen. However, some cytological changes do happen which is described by Sharma et al (1961) as "simulation of the normal meiosis I". This is followed by meiosis II (which is mechanistically same as mitosis). So, basically there is no halving of the number of chromosomes and the gametes are also haploid.
So, as far as I can guess, the question in your exam sheet probably refers to spermatogenesis in Hymenopteran haploid males.

Reference:
Sharma, G. P., Brij L. Gupta, and C. G. Kumbkarni. "CYTOLOGY OF SPERMATOGENESIS IN THE HONEY‐BEE, APIS INDICA (F.)." Journal of the Royal Microscopical Society 79.4 (1961): 337-351.


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Can photosynthesis take place if the plant is kept in ice cold water or not?
Can photosynthesis take place in a plant even if the plant is kept in ice cold water? I have googled this question, but so far have not found a satisfactory answer.

Before answering the question, I assume that the plant is somehow getting enough  O2 to survive.
There can be a number of variations in the answer depending upon the more particular situation you give. You can have a look here to see a list of factors affecting rate of photosynthesis in plants. I put graphs of factors important for this question:

If we talk about only cold climate, then your answer is given here as it says:

Plants of tropical or subtropical origin may incur irreversible damage to photosynthesis by temperatures below about 10°C, whereas plants from cooler climates may photosynthesize and develop normally at temperatures down to around 0°C.

So, I assume now that the plant you are talking about is adapted to cold climate i.e. you are not bringing a plant from Africa to North Pole. But, as you would have seen in the list of factors, you must have noticed that photosynthesis also depends on a lot more factors.
Another crucial factor under water is CO2 concentration. The plant needs enough amount of CO2 to carry on photosynthesis. In an ideal water body, if a plant can survive, then algae/bacteria can thrive, which would together produce lots of CO2 (by respiration) which would dissolve in water. For effect of temperature on CO2 solubility in water, see this link. It states:

As the forward reaction is exothermic, a decrease in temperature causes the system to move in the forward direction.

We don't need to worry about how plant would use H2CO3: plants have carbonic anhydrase for it. See this article:

Carbonic anhydrase, an enzyme which catalyzes the reversible hydration of CO2, is a major protein component of most photosynthetic microorganisms and higher plant tissues.

So, ideally, we can say that Yes, photosynthesis can occur in ice cold water if water is not frozen, has enough purity to let sufficient amount of light pass through it, and the plant has reached almost at the surface of water body to get enough carbon dioxide both from the atmosphere as well as the dissolved CO2 in the water body (which was produced by respiration of bacteria, aquatic animals and plant itself).

Biochemically, it appears it can, as some Algae can. The question is then whether there are any real plants who do it.

Algae are "real" plants. However, diatoms are not really algae. That is an obsolete classification. Perhaps you can edit your answer to clarify this.


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Why upper surface of leaves is more green and shiny than the lower one?
I have properly googled this and got various answers. However, those answers do not provide an answer to the "Why" part of my question. Why is it that the upper surface of leaves is more green than the lower one? Some sites suggest that it is because of the thick cuticle. Yet, that sounds weird and doesn't fully convince me. What other reasons to why the upper surface of leaves is more green and shiny than the lower one, could there be?

There is a lower and upper surface of a leaf, and the upper surface of the leaf is in the sunlight. With more sunlight, the upper surface makes more food and has more chlorophyll on it. Since chlorophyll is green and there is more green on the upper surface, the upper surface is darker.

I cannot help but suspect the stomata, that are primarily on the underside of leaves, affect a different surface texture than on the up/sunny side. This certainly would affect the perceived color of the underside versus top. Acer leaves are typically very thin and semi-translucent. Rhododendron leaves are definitely thicker and comparatively opaque. There is a different surface coating on the underside of them (the indumentum). Pines and tsuga have stomata arrayed on one edge that typically appears white-ish; otherwise the coloration on all sides of the needle/leaf is the same.

Ans::The upper surface is more shiny than lower because the upper surface comprising of palised parenchyma has more number of chloroplast than spongy parenchyma in lower surface. .........

Photosynthesis is the process of trapping sunlight and converting the energy into chemical energy which is then provided as a food source.
So the sunlight is trapped through chlorophylls. This is a pigment in the organelle called the chloroplast. The upper surface of the leaf is open to sunlight where the plants have more chloroplasts containing more chlorophylls to trap the most amount of sunlight.
All these chlorophylls are green coloured and since there is an increased amount of chlorophylls in the upper surface than in the lower surface (to trap more and more sunlight), the upper surface appears to be greener than the lower surface.
Source: Grade 12 Science student.

any references to add here?

That explains the green, what about the waxiness?

You can find two chlorophylls in most plant leaves, chlorophyll a and b. We'll use as a reference Leaf characteristics and chlorophyll concentration of Schyzolobium
parahybum and Hymenaea stilbocarpa seedlings grown in different
light regimes. The most important observation is that in shade-tolerant leaves, chlorophyll b dominates chlorophyll a. And the opposite is true of shade-intolerant leaves. I'll argue now that the portion of a given leaf that must tolerate more shade will have the darker green pigment due to the presence of more cholorphyll b, and that the side of the leaf that must tolerate lots of light will have the lighter pigment due to the presence of more chlorophyll a.
The light-tolerant side of the leaf is also shiny, and this is because of a thick waxy cuticle. The shade-tolerant side of the leaf also has a cuticle but if we follow it logically, the light-tolerant side of the leaf needs more protection from heat evaporation because it's always being hit by light.
So what I'd do, instead of thinking of the leaf as having a top or bottom, think of them as having a side that must tolerate excessive shade, and a side that must tolerate excessive light.

With ref to wax it is called epicuticular wax, it can be called as a protective mechanism of light absorbing side of leaf, from uv rays, anti climbing agent for small insects , etc wikipedia has a nice definition https://en.wikipedia.org/wiki/Epicuticular_wax
i will reproduce the same for future reference.

Epicuticular wax is a coating of wax covering the outer surface of the plant cuticle in land plants. It may form a whitish film or bloom on leaves, fruits and other plant organs. Chemically, it consists of hydrophobic organic compounds, mainly straight-chain aliphatic hydrocarbons with a variety of substituted functional groups. The main functions of the epicuticular wax are to decrease surface wetting and moisture loss. Other functions include reflection of ultraviolet light, assisting in the formation of an ultrahydrophobic and self-cleaning surface and acting as an anti-climb surface.

with ref to more green part, accumulation of chlorophyll over ventral side  is a necessity to absorb more sunlight. a distant and probably not so correct analogy can be, the tanning of the skin surface.


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Are there differing organelle to cytoplasm ratio in animal cells?
Could anyone provide me with examples of cells with high organelle to cytoplasm ratios (heavily packed), and examples of cells with low organelle to cytoplasm ratios (sparsely packed)?

If you want to sketch the cells, it might be easier to compare plant cells. Usually plant cells have a large vesicle contains fluid in the middle of the cell. However, root cells don't have this type of vesicles. It's the easiest to draw according to my knowledge.

Example of cell with low organelle to cytoplasm ratio : Red Blood Cell,Root cells(Root hair cell)
Example of cell with high organelle to cytoplasm ratio : Not sure about this...Fat cell , Sperm cell probably ?

This depends a bit on how you define the ratio. What precisely do you mean by "organelle" and "cytoplasm"? If you consider the entire cell volume as cytoplasm, then fat cells (adipocytes) would have an extremely low ratio, as nearly all of the cell volume is just fat. But if you consider cytoplasm to be just the water-soluble part, then it's very different. Also, a lot of cell structures are hard to classify as "organelles", for example glycogen and microtubules. Perhaps just the water content of a cell would be a good measure? That would include all macromolecules as "organelle" mass.

@Roland yeah i would exclude macro molecules, I'm talking about stuff like mitchondria...

Yes.
The structure of a cell is highly related to its function. For example, a plasma B cell (a type of immune cell) contains lots of ER and Golgi because its job is to secrete antibodies, which are proteins, in your body. It has to create a lot of proteins, so a plasma B cell has a lot of organelles that help create, assemble and secrete proteins.
There are so many examples you can use.

can you give a low ratio example as well? I am computer scientist modelling cell internals so it's not really in my wheel house

@RRs_Ghost examples of animal cytoplasm ratio: see the difference between monocytes and other lymphocytes. Monocytes have larger "white" area under microscope, which is the cytoplasm area(so it has a more condensed nucleus and organelle complex. However it's not the case for other lymphocytes.


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Population size and genetic drift - What are the evidences?
Wright-Fisher model
From the Wright-Fisher model of genetic drift, the random sampling of allele from one generation to the next is taken from a binomial distribution with parameters $2N$ and $p$, where $N$ is the population size and $p$ the frequency of an allele of interest.
Strength of Genetic drift
The strength of genetic drift can be measured in terms of two different statistics:

variance in allele frequency from one generation to the next
loss of heterozygosity per generation

Variance in allele frequency from one generation to the next
From the above, it is relatelively straight forward to show that the variance in allele frequency in the successive generation is
$$\text{var}\left(p'\right) = \frac{p(1-p)}{2N}$$
, where $N$ is the population size.
Loss of heterozygosity
Heterozygosity decays by $1-\frac{1}{2N}$ every generation
$$H_t = H_{t-1}\left(1-\frac{1}{2N}\right)$$
, where $H_t$, is the expected heterozygosity at time $t$.
Source
See Gillespie: Population Genetics - A concise guide chapter 2 for more info on these predictions.
Question
Do we have empirical evidence that the decay rate in heterozygosity and/or the variance in allele frequency due to genetic drift follows these predictions?

I suppose it's quite complex, would need large amounts of replication and have to neutralise/standardise selection and mutation across replicates - maybe mutation accumulation experiments would be worth investigating

This paper looks interesting https://www.researchgate.net/publication/11126342_Microsatellite_DNA_evidence_for_genetic_drift_and_philopatry_in_Svalbard_reindeer but it's not quite what you are looking for I think

In natural populations? No. This is why people generally talk about "effective population size". (I'm not a fan of this term though -- if we mean "the diffusion parameter of allele frequencies" or "the rate of decay of heterozygosity", we should just say so!)

Not necessarily in natural population. I was rather thinking about experimental evolution. Someone may have produced an experimental evolution where the population is as close as possible to a wright-fisher population (random mating, constant population, no selection, non-overlapping generation; so that $N=Ne$) and test whether the model offers good predictions.


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Distance to source populations and/or environmental gradients?
How do you disentangle the effects of distance to source populations and environmental gradients when the environmental gradient occurs in the same direction as the source population?

For example, if I have a regression model with species richness as the independent variable and distance to source population and pH as significant dependent variables, how do I know which is the driving factor?

Welcome to Biology.SE. Where does the figure come from? The article who made this figure might help you to answer your question. What have you found so far?

The effects of distance to source populations and environmental gradients on WHAT? Species Richness? Pairwise $F_{ST}$?

pH? Are you referring to scale to measure acidity and basicity? Is this just one example of possible environmental variable that you are giving?

I made the figure in powerpoint to ask the question. lol

This question would be just as suitable (if not more) at SE-CrossValidated

First of all, species richness is most likely the dependent variable (the one you want to explain), while distance to the source pool and pH are the independent variables (the ones you assume to have an effect on species richness).
The problem you are describing is termed multicollinearity and a common problem in regression analyses. The good news is that it does not affect the prediction of your model as a whole. The bad news is that the estimates for you individual predictors become increasingly erratic the higher their correlation is. You can estimate the severeness of multicollinearity in your model with the Variance inflation factor (VIF). Wikipedia explains nicely how to interpret the VIF:

The square root of the variance inflation factor tells you how much larger the standard error is, compared with what it would be if that variable were uncorrelated with the other predictor variables in the model.
Example
If the variance inflation factor of a predictor variable were 5.27 (√5.27 = 2.3) this means that the standard error for the coefficient of that predictor variable is 2.3 times as large as it would be if that predictor variable were uncorrelated with the other predictor variables.

You should calculate the VIF for your model. Many sources state that a VIF < 10 is still acceptable, but since there is no rule of thumb, I suggest to do some further reading on the topic if you get some critical value (just google "dealing with collinearity" and you'll find tons of material).

Thanks for the response. My VIFs for all the variables are less than 2.  So thats good. Regression between my distance to source and pH returns a r2 of .2. And the distance contributes ~.18 to the variance of richness. I'm just worried that explanatory power of distance is actually just pH. meh. EDIT: richness is dependent, space and environment are independent. ha.

Could some type of null model work here?

To partition the R² you can start out with a single-predictor model and add predictors while keeping track of the increment in R². However, since your predictors are not completely uncorrelated, the partial R² will differ depending on the order of variable entrance. Another way to compare effect sizes would be to standardize each variable (i.e. compute z-values) and look at the estimated coefficients.


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Light and Dark Reaction of photosynthesis?
I'm having a hard time understanding light and dark reactions because all the sites I've gone through provide different equations. Some say photolysis is H20 = H+ + O2 while some present it as H20 = H+ + OH-. Moreover some have given that NADP+ + H+ = NADPH and some have stated that NADPH+H+ = NADPH2
Could someone provide me with a better, more detailed explanation of both the light and dark phases with the equation of all the reactions that occur during the process, as well as the site of occurrence.

light reaction: 2H2O + 2NADP+ + 3ADP + 3Pi → O2 + 2NADPH + 3ATP dark reaction: 3 CO2 + 6 NADPH + 5 H2O + 9 ATP → G3P + 2 H+ + 6 NADP+ + 9 ADP + 8 Pi

I want the explanation of the two phases too!

I can see your frustration if you meet errors such as NADPH2 but that is the price you pay for approaching as complex a subject as photosynthesis without a good biochemistry textbook. Even the on-line versions (e.g. Berg et al.) are unsatisfactory because of their layout. You will have to sit down and spend a couple of hours on the topic — all you can expect from a site like this is clarification of key points.
That said I'll offer some clarification. The first thing I'll say is that focusing on chemical equations is not the way to understand photosynthesis. It will demonstrate that the law of conservation of matter applies, but otherwise is a bit like doing a chemical analysis of a cell to try to understand how it works. This is because:

There are two quite separate reactions in photosynthesis. As the products of one are (more strictly can be) used in the second, overall equations cancel them out, and so ignore key features of the process.
Photosynthesis is concerned with the transformation of energy as much as molecular structure. Chemical equations do not really address this.
The generation of energy involves the establishment of a gradient of hydrogen ions across a biological membrane — something your chemical equation does not encompass.

So what are the key ideas to bring to the text book you are going to purchase?
The overall objective is to make sugar from carbon dioxide
This poses a problem, not particularly because of the chemical reactions, but because these reactions require energy of two kinds:

To join the carbons from the carbon dioxide into C-C bonds. This requires ATP, the free energy change of its hydrolysis to ADP being coupled to ‘drive’ the formation of a C-C bond.
To reduce the oxygen atoms of carbon dioxide to OH groups. The biochemical molecule that is used for this reduction is NADPH, so ‘energy’ is needed to reduce its oxidized form, NADP+. (I won’t go into why this can be thought of as energy — if interested you need to read about the free energy equivalents of redox couples.)

The sun provides the energy
The energy for creating the reducing NADPH and the ATP comes from the sun in a complex series of reactions (these do not involve carbon dioxide). Light of a particular wavelength is harvested and used to break a water bond so as to separate charge in a reaction that I will deliberately not balance:
(1) H2O + sunlight → O2 + H
A complex series of reactions transfer the H (more strictly an electron) between different molecules, eventually reducing NADP+ to NADPH. At the same time an equally complex process builds up a H+ concentration difference across a membrane which provides the energy to convert ADP to ATP (see also Where do the H+ ions come from in light reactions?).
This is what is called the light reaction of photosynthesis because it requires light. It occurs in the thylakoids of the chloroplast, particularly at the membrane, although the products are in the stroma.
After energy has been harvested from the sun chemical synthesis can proceed
Having harvested the energy of the sun the plant has the wherewithal to make sugar from carbon dioxide. This is referred to as the ‘dark reaction’ because it does not require light. But its name can be misleading to the neophyte as the process does not have to take place in the dark. The overall unbalanced equation is:
(2) CO2 + NADPH + ATP → C6H12O6 + NADP+ + ADP
This is actually a complex series of enzyme-catalysed reactions (known as the Calvin Cycle) and a triose is the initial product. It occurs in the stroma of the chloroplast.

So actually there is no such thing as NADPH2? I was also confused on this.

No. Look at the structures on Wikipedia. The error either comes from confusion with the other redox cofactor, FAD / FADH2, or the fact that two electrons are involved in the reduction of NAD. If one is focusing on the oxidation of NAD one should balance the equation as NAD+ + H+ + 2e → NADH. (Sorry but comments don't do superscripts.)

Light Reaction (also known as light dependent reaction)
The light reaction uses chlorophyll (which is the main photosynthetic pigment) to capture light, and then uses the light energy to make ATP and NADPH. Water is also broken apart in this process so the electrons can be extracted, yielding hydrogen ions and oxygen gas. The stimulation of chlorophyll releases ATP. Furthermore, hydrogen is formed from the conversion of NADP+ into NADPH.
2H2O + 2 NADP+ + 3ADP + 3Pi → O2 + 2 NADPH + 3ATP
Dark Reaction (light independent reaction, or also known as calvin cycle)
The enzyme RuBP carboxylase catalyses the attachment of C02 to the 5C compound ribulose biphosphate. The unstable 6C compound then breaks down into 2 3C compounds called glycerate-3-phosphate (GP). The GP molecules are phosphorylated by ATP and reduced by NADPH+H+. The GP molecules are then converted into triose phosphates (TP) called glyceraldehyde phosphate. From the 6 molecules of TP which are created, only 1 is used to form/create half of a sugar (this means 2 cycles are required to construct a full sugar). The other 5 "unused" molecules of TP are reorganised in stacks in order to regenerate the stacks of RuBP. The reorganisation requires ATP.
3 CO2 + 6 NADPH + 5 H2O + 9 ATP → glycerate-3-phosphate (G3P, or GP) + 2 H+ + 6 NADP+ + 9 ADP + 8 Pi

Wouldnt it be better to give step by step equations for each thing like 1 for photolysis then another for the reduction of H+ instead of the combined reaction?

@Abcd, why? photolysis is the precursor of the calvin cycle


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Genes that exist in old Affymetrix platform but not in the newer one
I am using two gene expression datasets from an Affy U95Av2 platform and an Affy U133 Plus 2.0 platform. When I map the Affy probe names to HUGO gene names, there are thousands of genes which exist in the newer Affy U133 Plus 2.0 dataset while not in the old Affy U95Av2 dataset, which is something expected. But there are also 97 genes which exist in the old Affy U95Av2 platform while not in Affy U133 Plus 2.0 platform. I would not expect that because Affy U133 Plus 2.0 is a much newer platform and I would expect it to contain all genes that were measured by Affy U95Av2. What does that mean? Should I understand that those 97 gene measurements in the Affy U95Av2 platform were not reliable and that's why they don't exist in Affy U133 Plus 2.0? Here are those 97 genes:
"ACSL4" "ACSM2A" "AP3S1" "AQP7" "ARPC3" "ATF4" "ATP5H" "BAK1" "BAK1P1" "CBX1" "CCL15" "CELP" "CFHR3" "CHEK2" "CLCNKA" "COL8A1" "CS" "CXorf40B" "CYP2D6" "DDI2" "EIF3F" "EIF3IP1" "EIF5AL1" "FCGR2A" "FCGR3A" "GBX1" "GPX1" "HAVCR1" "HBZ" "HIST1H2AH" "HIST1H2AI" "HIST1H2BC" "HIST1H2BJ" "HIST1H4I" "HOXA9" "HSPB1" "IFNA14" "IGF2" "IL9R" "ITGA1" "KAT7" "KRT33A" "KRTAP26-1" "LDHA" "MAGEA12" "MAP2K4P1" "MIA" "MKRN3" "MROH7" "MSX2P1" "MT1A" "MT1B" "NDUFV2" "OPHN1" "OR7E24" "PARP4" "PCDHA12" "PCDHA13" "PCDHGA12" "PCDHGB4" "PINK1-AS" "PMS2P3" "PSMC6" "PSME2" "RAB13" "RCN1" "RNF216P1" "RNF5" "RPL10A" "RPL18" "RPL27" "RPL35" "RPL37" "RPLP1" "RPS15A" "RPS26" "RPS29" "RPS5" "RPS9" "RSC1A1" "S100A7" "SAA1" "SAA4" "SNX29" "SPRR2D" "TOMM40" "UBC" "UBE2E3" "UBE2S" "UGT2B7" "UQCRFS1" "UQCRH" "VDAC2" "VENTXP7" "VOPP1" "XCL2" "ZNF799"

What annotation source are you using to map Affymetrix identifiers to gene names, NetAffx or ? If the annotation files are from different sources and / or generated at different times, then gene symbols may have changed in between and therefore fail to match. But in your list I clearly see well established gene symbols that have not changed for a long time, so something looks funky ...

I am using biomaRt (the same ensemble version) for mapping both. Here is my code: ensemble = useMart(host='dec2014.archive.ensembl.org', biomart='ENSEMBL_MART_ENSEMBL');  hsp = useDataset(mart=ensemble, dataset='hsapiens_gene_ensembl');  ids = getBM(filters='entrezgene', attributes=c('entrezgene','hgnc_symbol'), values=entrezgeneids, mart=hsp);

Well, I don't know where biomart in turn gets its information. I would recommend you track down the actual annotation source, or map identifiers via a trusted source like Affy's own annotations. I just did a quick query on NetAffx for ACSL4 (first in your list) and there are definitely probes targeting this gene on the U133. It's impossible to say why the results differ without knowing exactly how the annotations were done.

aI used to work at Affymetrix when most of these arrays were designed.  I was not on the design team itself, but I can maybe talk about this a bit more.
RNA Array designs were built to cover anything that might possibly be real transcript in the mix of EST collections, cDNA, in silico gene detections and miscellaneous entries in public databases.  There were a lot of different people trying to find genes as quickly as possible and a good deal of it was not real gene naturally. I'm sure there was a reasonable amount of contamination in the millions of transcripts we took in as well.
The team would find a good number of errors in the sequence database.  There is no way to submit this in a meaningful way to most bioinformatics databases by the way.  Just a note:)
When a new design came out the team would do auditing to see if any of the transcripts had fallen out of favor with the evidence and some of those 'genes' would be pared from the content.
This is useful because DNA hybridization tech is very high throughput for the dollar but it has a background noise and even a probeset with no correspondence in the RNA sample will give numbers that are non-zero.
RNAseq has similar issues from assemblies and sensitivity from limits of reads on the sample BTW.  There's no perfect solution as of yet.
BTW sometimes genes get renamed. I didn't get into your methods to see if this is a case, but something to keep in mind.

My experience is with Affymetrix probes for Drosophila, not H.sapiens, and only with one version. Nevertheless I'll describe the situation I encountered in case it is relevant to yours. Apologies if it is a red herring.
What I did with the Affymetrix data sheet was use it to construct my own SQL relational database containing probesetIDs and geneIDs (as well as the experimental data, of course). I was then able to make some ‘housekeeping’ queries to the database and was surprised (perhaps I shouldn’t have been) to find the following:

Some genes were picked up by more than one probeset. No great worry. Just had to choose the probeset that gave the highest signal, unless it fell into the second category.
Some probesets picked up more than one gene. This was a problem, and meant I had to classify the probesets as ambiguous or unambiguous. But an even greater problem was that for some genes there existed no unambigous probesets.

Obviously in designing the probesets Affymetrix thought they were producing unambigous gene-specific ones. When they updated the probesets to include new or corrected gene designations one imagines they would try to deal with this problem (assuming it also existed in the human gene sets). It seems hard to believe, but could the genes you mention be refractory to the preparation of unambigous probesets?

Thanks for the reply. I think what you explained is quite possible, and I think there are also two reasons: 1) (Thanks to mastal11 on Biostars) There are many Affy probe sets that are not all that reliable because they are based on ESTs. Also, the older arrays would have been based on older versions of the human genome sequence, and possibly some of the probesets on the older arrays don't map or don't map uniquely to the newer versions of the human genome sequence. Occasionally also, probe sets were based on GenBank sequences that were later withdrawn from GenBank. (cont. in the next comment)

Some of those 97 genes actually have mapping probes in the newer Affy platform, but the annotation source I am using to map the Affy probe sets to HUGO gene symbols, biomaRt, does not have the identifiers of those probes in its database, so cannot map them to the gene symbols. There are various annotation sources out there, and you may end up with a slightly different mapping depending on which you use.


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Meaning of arrows in 3D representation of proteins

Below is a three-dimensional representation of the protein, CD4. I would like to know what the arrows and the thin wires between them mean.

The flat arrows are a cartoon representation of β-strands (one type of regular hydrogen-bonded secondary structure). The direction of the arrow is the direction of the amino acid sequence (arrow head pointing towards the C-terminus).
The thin wires are regions with no regular structure.
There are also two small green spiral ribbons in the foreground left and right, which represent α-helices (the other main regular secondary structure).

Thank you for the fast answer. It is really hard to find that information since there is no keywords to google..

You're welcome. I was looking for something else and it just caught my eye.

There are two small helices, but the structure is generally a beta-sandwich.

@gilleain Thanks. I hadn't noticed. I'll update my answer.

@m1clee The keywords you need for Google are "ribbon diagram" or "Richardson diagram".

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


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Find the concentration of free receptors in a solution of 90% free ligand and 10% receptor-ligand complex, knowing only the value of kD
I could use some guidance on how to utilise the equation for the disassociation constant kD to find the concentration of free receptors [R] in a solution containing 90% free ligand [L], and 10% bound [RL] complex.
The Kd of the receptor-ligand interaction = 10^-8 mol l-1
Where Kd =  ([R][L])/([RL])
I assume as a percentage I could state, [L] = 0.9 and [RL] = 0.1, but am not sure if I'm taking the right approach.
Any clarification on this would be appreciated.

there is a policy for homework-like questions, please read it before publishing question http://biology.stackexchange.com/help/homework

One big thing you're missing is units: Concentrations here must have concentration units - they can't be dimensionless numbers or percentages.
So one of the things you need to figure out is how to convert the percentages into concentration units. In this case, it's difficult to do directly, but we can apply a bit of algebra to figure it out. We're talking about 90% and 10% of the ligand in different forms, but we don't know anything about the total amount of ligand - that's alright, we'll just represent the total concentration of the ligand as $\ce{x mol \cdot l^{-1}}$. Therefore, we can now state that:
$$ \ce{ [L] = (0.9x) mol \cdot l^{-1}}$$
$$ \ce{ [RL] = (0.1x) mol \cdot l^{-1}}$$
Now the other bit of information we have is the equation for Kd:
$$\ce{ K_d = \frac{[R][L]}{[RL]} }$$
So we're looking for $\ce{[R]}$ (with associated concentration units!), and we know $\ce{ K_d }$, $\ce{[L]}$ and $\ce{[RL]}$ - or at least up to the unknown of $\ce{x}$. But, if you substitute the values you do know (including the factor of $\ce{x}$) into the equation and do some algebraic manipulation, I believe you'll find it doesn't actually matter what the value of $\ce{x}$ is - it should cancel out.
Note: If the value of $\ce{x}$ doesn't matter, why did I bother with the whole rigmarole of including it? Why didn't I just substitute 0.9 and 0.1 directly?
Well, the answer to that is my lead sentence - the concentrations in the equation should have (compatible) concentration units. If you don't have concentrations, you're using the equations incorrectly. (Look into the concept of dimensional analysis for a valuable way to help make sure you're doing many (but not all) calculations like this correctly.)
While for this specific problem things worked out nicely if you substitute the fractions/percentages directly, that's not a general solution. Depending on the exact setup of the problem, the $\ce{x}$s may or may not cancel cleanly. You may have to use some other equation/knowledge to put additional constraints on the value of $\ce{x}$. The only way to know that is to properly account for them from the start.

According to the information you have provided isn't the starting equation:
1 x 10EE-8 = (0.9 x [R]) / 0.1
So you can solve for [R]?
[R] = (1 x 10EE-8 x 0.1) / 0.9
I am not saying this is correct, but by substituting the values you provided isn't this how one would algebraically solve for an unknown? Maybe I am missing something(?)
You state you wish to know the concentration of free receptor. Wouldn't you need to know the total number of moles of receptor present in the equilibrium binding reaction, and wouldn't you need to know the final volume of the reaction?

Thanks for the input, I must admit I'm total perplexed by the question, and I agree there seems to be some data missing to solve but thats the info that's been provided. I hoped someone might have come across something similar.


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Why does meiotic recombination disrupt the independent assortment of genes on the same chromosome?
There are many sources that say that genes that are "linked" by being on the same chromosome assort with each other -- that when an allele is passed on that the gamete containing said allele will also contain every allele from the chromosome rather than simple allowing everything to assort independently.
There are also many sources that say during meiosis there is recombination, hence, why aren't all genes completely random?

The previous title of this post had a negative and some imprecise terms.  In the interest of clarity I modified it to read "Why does meiotic recombination disrupt the independent assortment of genes on the same chromosome." It originally said "Why doesn't gene recombination maintain the law of independent assortment for genes on the same chromosome?" Hopefully I have preserved the sense of the OP's query.

Recombination does not make any two genes completely independent because there will not systematically be a recombination event between two given loci (=position on the chromosome).
Distance between loci
Consider two scenarios that describe the position of two loci on a chromosome.

Tightly linked loci

Consider two very closely linked loci. Let's say that a recombination event occurs somewhere in the chromosome. It is very likely for this recombination event to occur somewhere else than between these two loci. These two loci are essentially linked and do not segregate independently

Distant loci

Consider now two loci on the same chromosome. Each locus (=singular of loci) is found at one end of the chromosome. If a recombination event occurs, it is pretty sure that it will occurs between the two loci. As a consequence, the two loci will segregate (quasi) independently.
Conclusion
As a conclusion, recombination allows to break down the linkage between two loci but it does so at a given rate that depends on the physical distance between the two loci and on the per nucleotide recombination rate.

Doesn't recombination always occur between two alleles on homologous chromosomes of the same gene? Also, doesn't a recombination of one gene not effect another?

I don't understand what you mean. You say "recombination of one gene". What does it mean? A recombination (or cross-over) is the process by which homologous chromosomes exchange genetic material. This process  allows for higher independence of assortment of linked loci. The more closely linked are two loci, the less likely it is that a recombination event will separate them.

Recombination has nothing to do with genes.  The genes happen to be genetic markers arrayed along the physical chromosome.  Meiotic recombination, in general, occurs after a double-stranded break has been formed in one of the chromosomes.  One way to repair this break is to form a crossover.  When crossovers are repaired by the cell this can result in recombination (alternatively it can result in gene conversion).  If you have several heterozygotic genetic markers on the chromosome then you can score the progeny and possibly map where the crossover occurred.

By "two loci" Remi.b means two loci on the same chromosome. Simple example: (a) ------------X--X----------------- compared to (b) -X----------------------------X- , if Xs denote genes, it is much more likely for the genes in (a) to remain on the same chromosome than for the genes in (b) assuming a random choice of recombination point. Although recombination is not actually random, this example holds in vivo.

Are you saying that when a recombination event occurs (I am assuming this is the same thing as a cross-over, please correct me if I am wrong), the actual genetic material being moved around is just a random contiguous chunk that has no bearing on the borders between genes? If so, then am I correct in assuming that two closer genes are more likely to be swapped together since a single recombination event will more likely encompass both of those genes? If so, I would think an answer containing that information would be best.

Yes, recombination has nothing to do with genes. Not however that recombination rate per nucleotide tend to be lower in regions of high gene density. Two closely linked loci (might be genes at these loci) are less likely to segregate independently as it is less likely that a recombination event occurs in between them (you seem to say the opposite in your comment).

Imagine that mom's chromosome is blue, and dad's is red.  If crossing over was happening hundreds of times per chromosome, sure, you could make chromosomes to pass into gametes which were very a very highly shuffled combination of paternal and maternal alleles.  It would be blue, red, blue red, blue, red, all up and down the chromosome.
But it doesn't.  It generally only happens once on a chromosome.  So you can get a chromosome where the "top" 30% is red, and the rest blue, or the "top" 65% is blue and the rest red.  When genes are unlinked, the odds of getting both alleles from the same parent is 50%, and the odds of getting one from each parent is 50%.  If two genes are close together on the same chromosome, the odds of the break happening between them is small, so the odds of one being blue and one being red is much lower than 50%.


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What are anagenesis and cladogenesis?
Are they two types of speciation?
I have read wikipedia but can't figure out if they are really two types of speciation

Reading Wikipedia, it seems both give rise to new species and hence result in speciation. https://en.m.wikipedia.org/wiki/Cladogenesis. Just go through the link. 'New species' has been mentioned for both.

From Wikipedia:

Anagenesis, also known as "phyletic transformation", is when the new morphospecies is a result of rapid evolution in the ancestral form without speciation taking place, such that there are no remaining other populations of the ancestor species and the species can be considered extinct. [...] Anagenesis is in contrast to the branching speciation known as cladogenesis.

and

Cladogenesis is an evolutionary splitting event where a parent species splits into two distinct species, forming a clade. [...] Cladogenesis is in contrast to anagenesis, in which an ancestral species gradually accumulates change, and eventually, when enough is accumulated, the species is sufficiently distinct and different enough from its original starting form that it can be labeled as a new form - a new species.

So Cladogeneis is speciation by evolutionary splitting of a lineage and Anagenesis is designation of a morphospecies without splitting (gradual change).
This figure from Columbia University is useful to show the difference (http://rainbow.ldeo.columbia.edu/courses/v1001/anaclad.html):

Note that Anagenesis is most often used in Paleontology, and the possibility to distinguish between the two types depends on the resolution of the paleontological data. Whether to name a "speciation event" as one or the other, or how to use the terms generally, is also a matter of debate (see e.g. Aze et al. 2013. Identifying anagenesis and cladogenesis in the fossil record. PNAS).


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How can two individuals of the same species have different chromosome numbers?
It is known that male drones develop by arrhenotoky, and have haploid chromosome constitution, whereas the queen bee and workers are diploid.
Thus we can see two different types of ploidy occurring in the same species. Sill the drones and queen bee are successful in mating and producing offsprings. This would require the queen to produce haploid gametes by meiosis and haploid gametes from haploid drones.
Doesn't this create a problem in defining species?

Your answer is here: http://biology.stackexchange.com/a/45372/3340

Chromosome number does not define species, otherwise the Sable Antelope, Reeves Muntjack, and Humans would all be one species.

You should read this post on the definition of species.

My question was about the defining of species. @Remi.b your post helped.

there are diverent concepts of definitions of species:

morphological species concept, distiguishes a species by body shape and other structural features
ecological species concept, distighuishes a species according to it's niche
phylogenetic species concept, smallest group which schare a common ancestor
biological species concept, a species is a group whose members can produce fertile offspring

the biological species concept is most commonly used, if we apply this on your problem, they still produce fertile offspring, so they are the same species.
If for example a mutation wil occur which causes polyploidy (more likely in plants, however it's possible in some animals). Let say the orginal species have 2n = 12, if polyploidy occurs(during meiotic error for example). We will have 2n = 24. If these species produce gametes n = 6 and n =12, fusion of those gametes will result in unpaired chromsomes, which in turn will lead to a reproductive barrière. The 2n =12 and the 2n = 24 species can only mate with each other to produce fertile offspring, so we can say these are different species.


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Evolution to store limited Fat
Why are our bodies not evolved to store only limited amounts of fat, which won't kill us with all diseases associated with obesity?
Wouldn't obese people die faster and clean the gene pool for people who are slim?

Guess-work here! Probably because disease related to excess of fat is a very modern thing. I would guess that being able to store fat was highly selected for survival but maybe also for reproduction (fat and sexy). Note also, that we stop eating after a while. We don't eat until we die suggesting some defence mechanism here.

Search for thrifty gene hypothesis.

For some organisms, being gluttonous and storing fat is an optimal survival strategy which is linked to their foraging/hunting strategy. I would guess that for an early human with a hunter-gatherer lifestyle, being gluttonous and storing fat would have been useful. This is not suitable for our current lifestyles. There are some animals that have a tendency to become obese, when in captivity (and overfed).

Worth remembering that if you're physically active and products like refined sugar aren't available it's actually quite difficult to get obese, and things which don't happen can't get selected against.

"Wouldn't obese people die faster and clean the gene pool for people who are slim?" Not before reproducing. By your logic, look around you. Do you see a whole lot of skinny people, or do you see a fair amount of obesity? What does that tell you?

"Wouldn't obese people die faster and clean the gene pool for people who are slim?"
If your hypothesis is right, the selection for such traits would only have begun in the last 20-30 years ("Worldwide obesity has more than doubled since 1980" http://www.who.int/mediacentre/factsheets/fs311/en/)
Natural selection wouldn't have had time to select against people showing tendency for obesity.
Also, obesity is a lifestyle choice, and not merely predictable by genetic disposition. I could be a "fit" person, but genetically predisposed to obesity.
Look up also genotype vs phenotype for further reading (http://evolution.berkeley.edu/evolibrary/article/genovspheno_01)

For most of human history the excess of food has not been a problem, rather the lack of food, and subsequent starvation has been a problem. So genes that promote energy efficiency and fat storage have been  very much selected in the human population. So much so, that humans are rather fat for apes.
As for the problem of obesity, it has been a rather recent problem, no more than one or two generation. Evolution works in generation time. So there is not enough time to weed out genes that promote obesity which would be pretty common in human gene pool.

Human the fat ape http://www.sciencemag.org/news/2015/06/why-humans-are-fat-primate

Famine is really common in human history. So the ability to survive one is really useful https://en.wikipedia.org/wiki/List_of_famines

It's very complicated to know how a trait would have been selected for or against in the ancestral environment. Tendency to gain weight does seem to have been selected for in some populations - e.g. pacific islanders. Presumably the decreased chance of dying from starvation was enough to compensate for any increased risk of heart disease, if in fact health risks did exist. Morbid obesity as we know it today may simply not have been possible without the modern diet, and modern society/technology to provide an endless supply of easy to reach, unhealthy, addictive food.

This is an interesting question, and shows good insights in trying to glean cause and effect of large social phenomena. However, the natural selection process as presented in your question has a couple issues.
Primarily, natural selection is a passive process. The concept that we developed those traits we "need" is a misrepresentation of the process. It is more accurate to say we adapt to take advantage of what we have developed.
I.e. Fish don't grow lungs because they want to go on land. Transitional fish go on land only if they happen to have lungs. If it gives them a fortunate advantage, then reproduction may expand the population of that attribute.
There is also the issue that obesity does not cull the population before reproduction in most cases. The effect you're expecting is less impactful then you assume in the OP.


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Why don't protons diffuse out of the mitochondria during chemiosmosis?
If the outer membrane of the mitochondria is very permeable, how do mitochondria maintain a proton gradient by pumping protons into the intermembrane space? Wouldn't they just diffuse into the cytosol?

The build up/increase of H+ ions in the intermembrane space establishes the electrochemical gradient (proton gradient). And no, after that the protons return to the matrix via ATP synthase

So, what is preventing the protons from diffusing out of the outer membrane?

depends, there can be some "proton leak", which could occur during proton pumping across the inner membrane, which might be due to when the pairing between ATP synthase and the oxidation of substrate isn't fully complete, which would result in the protons being able to travel independently without ATP synthase to the mitochondrial matrix, also note that the proton leak acts/behaves in a non-ohmic way.

also note that chemiosmosis/oxidative phosphorylation occurs in the cristae of the mitochondria

In addition to the long and complete answer above, I want to point out something extra that is missing in the explanation: The proton gradient works both ways (like all gradients). Lowering the external pH is not the only way to create a gradient, increasing the internal pH also works perfectly fine.

Diffusion, is by definition (Ficks Law) describing movement along or against some gradient (here its concentration) even if the mechanism of transport differ: active, passive, facilitated. The setup of the electrochemical gradient across membrane, like any thermodynamic process is not perfect, there are always entropy losses. In this case, this manifests as the the diffusion of protons away from the membrane (one source, there are others). Note the connection between entropy of system (Mitochondria) and diffusion (the inefficient process) in this positive feedback process. I think its interesting as someone learning about this stuff to make these connections.
Recalling protons are being delivered freely into the environment (inter membrane space) by Electron Transport Chain. Some protons will diffuse away from membrane surface before they can be pumped back in since these highly charged species cannot passively diffuse back in. The chemiosmosis process, which is sustained by the energy input to drive ATP synthase, depends on maintaining a strong concentration gradient (separation) of H+ on either side of membrane. Since the outer membrane of the mitochondria is porous, it means the protons are free to diffuse out, and will do so because it is entropically favorable. This relationship is best described by $\ce{\Delta G = RTln(K)}$. Where $\ce{K=\cfrac{[B]}{[A]}}$ for a process $\ce{A \rightleftharpoons  B}$
Where A= Protons near membrane, B= protons diffused out. Having established that thermodynamically they (protons) will diffuse out[3]. It begs the question will they actually reach the outer membrane in a reasonable time.
Of course over long enough time they will. But over some meaningful scale like 1 second, the proton pump rate of ATP synthase, 100s-1 [5], how far can a proton get ideally?.
Back at the envelope calculation (ignoring any resistance effects from solvent, path, etc.) and using some approximate values (for yeast proteins and mitochondria):
From Fick's Rate Law, R,
$ \sqrt[3]{R} = \sqrt[3]{ D A \cfrac{[H^+]_c - [H^+]_m}{d}} = 14 \mu m $
So in 1 s an average proton ideally can diffuse 14 micrometers from the inner membrane, driven by difference in pH between membrane and cytosol. I think i maybe be fair to presume that based on this the mitochondria is leaking protons into into its near surroundings constantly. (for scale the mitochondria is about 100nm).
Hope that was helpful
VALUES:
Thickness of mitochondria,$d$, equal 0.014 $\mu m $ [4]
$\ce{[H^+]_m }$ at membrane = $\ce{-log[H+] = 10^(-6.8),  [H+] = 10^(-6.8)}$ [6]
$\ce{[H^+]_c }$ at in cytosol = $\ce{[H+] = 10^(-7.40)}$
Diffusion coefficient of H+ in aqueous media $D$ = 7000 $\mu m^2$ [2]
A (surface area from which diffusion is taking place) I set to 0.025 $\mu m^2$ (guess from average unit cell of crystallized structure of ETC Complex II in yeast).
REFERENCES:

D. Nelson & Cox (2012). Lehninger, Principles of Biochemistry, 6th Ed
http://www.atpsynthase.info/FAQ.html
http://jgp.rupress.org/content/139/6/415.full

Yes absolutely helpful. I'm glad you've come to the same conclusion about mitochondria leaking protons!

hooray!! thanks Cayetano Gonçalves that boosts my reputation and morale. Even better it was helpful

You are forgetting an important factor, the mitochondrial membrane potential (ΔΨm). See Nernst potential (https://en.wikipedia.org/wiki/Nernst_equation). Basically, the concentration difference will be balanced by the voltage difference. Given ΔΨm is usually around -150mV (cytosolic space is ground), there is a drive to keep the protons close to the inner membrane surface.

In fact, the proton-motive force is primarily composed of the electric component, over the pH gradient. The opposite is the case in chloroplasts from the movement of Cl- ions (https://en.wikipedia.org/wiki/Chemiosmosis).


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Why doesn't the rest of the body have something like the "blood-brain" barrier to protect itself from pathogens?
According to Wikipedia:

"The blood–brain barrier acts very effectively to protect the brain from most pathogens".

This is because the pathogens cannot pass through the tight junctions of the endothelial cells lining the inside of the blood vessels delivering blood to the brain through BBB.
But if so, why don't tissues/organs in the rest of the body employ the same barrier, and thus avoid pathogens from ever entering those tissues/organs through the bloodstream?

There are many physical barriers actually (not like BBB, though). Skin, for example ,is a very strong barrier.

That's true, but if there is a very strong barrier, such as the BBB, which is stronger than others, why isn't it used universally throughout the body? That is, what advantages are there to use a weaker barrier when there is a stronger one available?

There can be many reasons to why BBB-like barrier is not present in all the capillaries of the body. Let's talk about them one at a time.

Source
Blood-brain barrier has its own side effects. Some major side effects are cerebral edema (accumulation of excess water in the extracellular space of the brain, which can result when hypoxia causes the blood–brain barrier to open) and (possibly) Epilepsy. See this wikipedia article:

Several clinical and experimental data have implicated the failure of blood–brain barrier function in triggering chronic or acute seizures. Some studies implicate the interactions between a common blood protein (albumin) and astrocytes. These findings suggest that acute seizures are a predictable consequence of disruption of the BBB by either artificial or inflammatory mechanisms.

Another problem is that BBB doesn't allow passage of drugs, diagnostic and therapeutic agents through it. Again, see this article:

Overcoming the difficulty of delivering therapeutic agents to specific regions of the brain presents a major challenge to treatment of most brain disorders. In its neuroprotective role, the blood–brain barrier functions to hinder the delivery of many potentially important diagnostic and therapeutic agents to the brain. Therapeutic molecules and antibodies that might otherwise be effective in diagnosis and therapy do not cross the BBB in adequate amounts.

Now, if you want to know why the body doesn't have BBB-like barrier (not exactly BBB), then there are three parts of the answer.

These kinds of barriers are highly specialized for a particular organ or organ system, which may not be useful for another organ/organ system. Also, creating specialized barriers for all the parts of the body will take a lot of energy, cells and even more time to develop completely. Possibly, in the evolutionary course, body preferred to have phagocytic cells circulating in the body instead of having specialized barriers throughout the body.
These barriers might not be a total solution for immunity or restriction of pathogens. See this part:

It is believed that latent HIV can cross the blood–brain barrier inside circulating monocytes in the bloodstream ("Trojan horse theory") within the first 14 days of infection. Once inside, these monocytes become activated and are transformed into macrophages. Activated macrophages release virions into the brain tissue proximate to brain microvessels. These viral particles likely attract the attention of sentinel brain microglia and perivascular macrophages initiating an inflammatory cascade that may cause a series of intracellular signaling in brain microvascular endothelial cells and damage the functional and structural integrity of the BBB. This inflammation is HIV encephalitis (HIVE).

Also, it is not necessary that those pathogens would infect only those tissues to which they reach via bloodstream. Pathogens like HIV cause infection in the blood cells. See this image from here:

Once a person is infected with HIV, the virus begins to attack and destroy the CD4 cells of the immune system. CD4 cells are a type of white blood cell that play a major role in protecting the body from infection. HIV uses the machinery of the CD4 cells to multiply (make copies of itself) and spread throughout the body. This process, which includes seven steps or stages, is called the HIV life cycle.

Similar barriers are already present in many parts of the body. For example- Blood-Ocular Barrier, Blood-Testis Barrier, Blood-Thymus Barrier, etc. They may also have some loopholes. For example, see this article-

Possible consequences of blood-thymus barrier failure are trophoblast-specific or tumor-specific antigens penetrate into the thymus, deletion or anergy of antigen-specific clones and acquired thymic tolerance induction.


text:
Hardy-Weinberg equilibrium generalized to add inbreeding (non-random mating)
Background
Quoting from Gillespie's book

The level of inbreeding is measured by the inbreeding coefficient, $F_I$, which is the probability that two alleles in an individual are identity by descent.

The two possible alleles are $A_1$ and $A_2$ and their frequencies are $p$ and $q=1-p$, respectively. Gillespie goes on and give the expected genotype frequencies given $p$ (and $q$) and $F_I$
$$
\begin{array}{r|c|c|c}
Genotype & A_1A_1 & A_1A_2 & A_2A_2 \\
\hline
Frequency & p^2(1-F_I)+pF_I & 2pq(1-F_I) & q^2(1-F_I)+qF_I \\
\end{array}
$$
Question
Can you please help me to understand why those are the appropriate genotype frequencies?
Example of what is unclear to me
By the definition of $F_I$, I was expecting that the frequency of `$A_1A_2$ (and $A_2A_1$) would be $(1-F_I)$, that is the frequency (or probability) that two alleles in an individual are not identical by descent. I feel like the definition given above is wrong. Should it rather be something like the weight for sampling like individuals? That is if there were only two possible mates, one that is $A_1A_1$ and one that is either $A_1A_2$ or $A_2A_2$, then the probability for a $A_1A_1$ individual to mate with the other $A_1A_1$ is $F_I$.

You're confused because you're failing to distinguish between 'identical' and 'identical by descent'. Some pairs of alleles would still be identical even in the absence of inbreeding.
We model the inbreeding by classifying allele pairs as IDB - always homozygous - or not IDB -  distributed according to Hardy Weinberg. The frequency of a pair of alleles being A1,A2 (or A2,A1) is thus the frequency under H.W.E. (2pq) multiplied by the chance of them NOT being IBD (1-FI). And conversely, a pair can be homozygous and not IBD - at frequency p 2(1-FI), or because they are IBD - at frequency p F I.

+1 Oh..ok! This is a little disturbing to me. The concept of IBD depends on an arbitrary time in the past beyond which if coalescence occurs, then we still call the two alleles IBS (Identical by state) and not IBD (I could cite Hartl and Clark I think but don't have the book with me today). Am I right?

Yes, but these models are just simple approximations. Concepts like time and coalescence don't even exist the perfect binomial world of Hardy Weinberg  :)

Ok. I don't feel 100% clear with the definitions of IBD and IBS so I just opened "Identity By Descent vs Identity By State". Thanks for your help


text:
Identity By Descent vs Identity By State
Background
The concepts of Identity By Descent (IBD) vs Identity By State (IBS) are central in population genetics, yet I fail to fully wrap my head around the definitions.
You can find examples where my understanding of IBD vs IBS is quite poor in @DermotHarnett's answer here or in the comments with @PaulStaab here. @PaulStaab suggests that different authors have used different definitions of IBD and IBS.
What is unclear to me
From what I remember from Hartl and Clark (I don't have the book with me to quote), IBD depends on an arbitrary time threshold in the past beyond which if coalescent events occurred, then we still call the two alleles IBS (Identical by state) and not IBD. The idea that the concept of IBD depends on an arbitrary threshold bothers me though!
I suppose that two alleles can be IBD without being IBS in the case where a mutation or recombination event in the middle of the sequence of interest prior (looking backward in time; more recent) to their coalescence. I suppose two alleles can be IBS can not be IBD only if we use an arbitrary threshold that is older than their coalescent time or if convergent/parallel evolution happened.
Questions

Does IBD depends on an arbitrary threshold?
Are there several definitions of IBD and IBS in use?
Does IBD implies IBS?
Does IBS implies IBD?
Can you please make a short review of these definitions to clear things up?

The issue of IBD and IBS can indeed be confusing.
The identity by state definition refers to the fact that at some point two individuals, even if they are not related to each other, present the same allele at a specific locus. Because of their un-relatedness this similarity probably arose from a similar mutational event.
On the other side, with IBD two individuals happen to share the same allele because of their coancestry.
Alleles that are identical by descent are also identical by state. But the opposite is not true. (see also https://www.biostars.org/p/174048/#174049 and Powell et al 2010, Nature Reviews Genetics 11, 800–805 (1 November 2010) | doi:10.1038/nrg2865).
Now, about the threshold that you were mentioning in your question, I am not entirely sure what you mean. Eventually, all individuals are traceable to a MRCA (most recent common ancestor). So, I think the threshold you talk about refers to the size of the population in analysis. Depending on the size of your population you will have different proportions of alleles that are IBD and IBS.
Hope this help.

The "arbitrary threshold" is part of the definition usually given of IBD in textbooks. The problem is that, if you go back far enough, all alleles are descended from a common ancestor allele. So to define it, according to the textbook explanation that both me and the asker feel uneasy about, what you do is: choose a number of generations back, say, five: decide to consider all the alleles at that generation, unrelated to each other (not IBD); and then define IBD as "having a common ancestor allele more recent than that number of generations back".

This won't be a complete explanation: I'm bothered by these questions myself. But I'll say what I do know.
First:
Yes, Identity By Descent (IBD) is defined relative to a chosen threshold number of generations, at least in the sense that I understand it (in case there is more than one sense - I think there are ones allowing for mutation?). At the chosen number of generations back, we assume that all of those ancestors were unrelated. This seems troublesome! But two things might help it seem less so. First: when we ask if two individuals are related or not, we're really asking whether they're more closely related than the average relatedness of the background population. Second: the pedigree method of estimating kinship and inbreeding coefficients, is just that, a way of estimating, which may fail if its assumptions fail (e.g. if the ancestors at the threshold were not randomly chosen from a randomly mating population).
To illustrate, consider a question about a fictional individual with a fictional family tree (spoilers for Game of Thrones, season 1): How inbred is Joffrey Baratheon?
We know that Joffrey Baratheon is not, in fact, the son of King Robert Baratheon, but rather the product of secret incest between his mother Queen Cersei Lannister and her twin brother Jaime Lannister. If that were all we knew about the situation, we would draw the following pedigree:

By using this pedigree, we are implicitly assuming that Cersei and Jaime's parents are unrelated, i.e. randomly chosen from a large randomly mating background population (and assuming that if Cersei and Jaime are more likely than random individuals to share an allele, that this is due solely to IBD from one or the other of those randomly chosen parents, i.e. due to their being close relatives). Based on this assumption, applying the usual method to this pedigree, we estimate Joffrey's coefficient of inbreeding as $0.25$.
However, if we look deeper into the Lannister family tree, we realize that Cersei and Jaime are actually more closely related than a typical brother-sister pair: their parents were not randomly chosen, but were themselves related (though not closely enough to be scandalous for Westerosi society); their father Tywin Lannister, and their mother Joanna Lannister, were cousins. Using this information we draw a more complete pedigree:

Using the usual pedigree method again, we are now making a different assumption. We are no longer assuming that Joffrey's grandparents Tywin and Joanna were randomly chosen from the background population. We are instead assuming Joffrey's great-great-grandparents, Gerold Lannister and the Lady Rohanne Webber, were randomly chosen from the population. This assumption seems more reasonable. Since this new pedigree implies more inbreeding in Joffrey's ancestry, we guess that the method should give a higher estimate for his inbreeding coefficient: indeed it does, giving us an estimate of $0.28125$.
Here's how this illustrates the subjectivity of defining IBD. When we used the first pedigree, we were asking: What's the probability that both alleles at a locus in Joffrey's genome, are descended from the same allele in the grandparent generation? When we used the second pedigree, we were asking: What's the probability that both alleles at a locus in Joffrey's genome, are descended from the same allele in the great-great-grandparent generation? These are two different questions, and of course gave two different answers. The trouble, of course, is that the question of how inbred Joffrey is relative to the background population, only has one answer (which the pedigree answers may estimate more or less well)!
Second:
Although important coeffients like the "inbreeding coefficient" or "coefficient of relationship" are often presented in textbooks as being defined in terms of the probability of some pair of alleles being IBD, this cannot be the actual definition. This is because probabilities can't be negative, but relatedness can be (if two individuals are less related than average), as can the inbreeding coefficient (if the animal is outbred, i.e. its parents had negative relatedness). The possibility of negative relatedness even has interesting evolutionary implications. As a sort of flipside of Hamilton's rule for altruistic kin selection - where it can be evolutionarily beneficial for a gene to cause a bearer to harm oneself, in order to help a relative, i.e. an individual more likely than average to also carry a copy of that gene - negative relatedness makes it possible to have spiteful anti-kin selection - where it pays a gene to cause its bearer to harm itself, for no benefit at all, but solely to harm an individual less likely than average to carry a copy of itself (and more likely to carry its competitors)!
Indeed, in his original formulation of these and related coefficients, Sewall Wright did not invoke probabilities or identity by descent at all. For relatedness he talked about the correlation between individuals' allelic states (this requires assigning numbers to alleles, e.g. $A=1$ and $a=0$). Note that correlation coefficients can be negative. The "probability of IBD" interpretation was introduced by Malécot; it's made it into population genetics textbooks mostly just because it's easier to teach (despite the seemingly paradoxical subjectivity of reference number of generations, and the inconsistency with the possibility of negative relatedness).
Wright's explanation of the inbreeding coefficient is more intuitive: he points out that the most important effect of inbreeding is reduction in heterozygosity. Consider a randomly mating population: an individual randomly chosen from it, will have a certain fraction of its loci heterozygous. But an inbred individual will have fewer loci heterozygous (more loci homozygous). Malécot interpreted that excess homozygosity as being "due to coancestry [since a subjectively chosen reference generation]", but we can ignore that conceptual baggage, and just talk about the excess homozygosity (deficiency in heterozygosity) itself. Thus a better definition of the inbreeding coefficient is
$F = \frac{H_e - H}{H_e}$
where $H_e$ is the heterozygosity you would expect of the offspring of a random mating given the population's allele frequencies, and $H$ is the inbred individual's actual heterozygosity. A good presentation of this interpretation appears in Hartl's Primer of Population Genetics.
Note that this definition, unlike the probability definition (but like the correlation definition of relatedness) can be negative: outbred individuals have less homozygosity (more heterozygosity) than expected under random mating.


text:
How do biologists quantify "gene expression" in experiments?
I've read papers which contain statements such as "control of gene expression is critical in biological processes".
How exactly does one quantify "gene expression"? Isn't gene expression an umbrella term describing all of the mechanism by which DNA is synthesized into an organism's phenotype?

probably with SDS Pages. At least I assume this. And by comparing one Page with the other one from another e.g. plant part. Often this is also done using GFP proteins or other marked proteins and quantifying those ones using microscopes... doing westernblots or just coloring the material at defined time points (which will kill the material most probably but also gives an insight)... is it something like this what you are asking? The methods?

@TheGreenOne Yes, the methods and the quantifiable features they used (from let's say, phenotypes, or perhaps something related to mRNA) to measure this. The question is a bit general, I know.

Gene expression involves RNA synthesis (or Transcription), NOT DNA synthesis.  The study of DNA synthesis is usually called DNA Replication.

There are several techniques. Possible duplicate of http://biology.stackexchange.com/q/8153/3340

The primary product of protein coding genes are mRNAs.  When we talk about measuring gene expression we want to assay the steady-state levels of a specific mRNA within a cell.  This is usually accomplished by starting with a large number of cells and harvesting all of the mRNAs from all of the cells.  One way to measure the expression level of just one gene's mRNA is to perform a Northern Blot.  Other sensitive methods include: an S1 nuclease protection assay, an RNAse protection assay, and a primer extension assay.
Microarrays have also been used extensively to measure expression levels of thousands of genes at the same time in a single experiment.
With the advent of RNA-Seq methodology it is possible to count the number of transcripts in an experiment (if you have a sequenced reference genome)

According to next generation data:
I was never working directly with mRNA but what I got from the bioinformatician was something like this: you extract your mRNA, sequence it, filter it according to the quality & length, assemble it and what you then have is something like "transcripts". Those you are counting: xy of transcript1 & yx of transcript2. You are further looking for isoforms and in the end you are correcting this counts according to the initial reads which you computed. Comparing the transcripts to a control you can measure if its up or downregulated (setting the reads of the control as "zero" like 1234 reads of one transcript are normal..... in sample 2 you have 5000 reads of this transcript... the gene seems to be upregulated). As far as I know is is approximately the way how gene expression approximations / quantifications are made.


text:
How fast the human eye can [temporarily] change its color?
I know that human eye can change its color during lifetime because of disease or medication (similar question on Biology.SE). And I know that it may change depending on the lighting.
But I saw several times as the eyes of man with the bright eyes changed color  (blue/gray/green) without changing environment. Is it possible to temporarily change eye color due to the change of emotional state (as a consequence of the effect of hormones or something else) in just a few of minutes? If so, what are the processes behind this?
Or it just optical/psychological illusion for the observer?

It is just optical illusion of observer. Eye color cannot change by effect of hormone (somebody correct me if I'm wrong) and not at all in a few minutes.

In a few minutes? Hardly possible - it will take some time for the pigment cells in the eye to produce and distribute the pigment.

@another'Homosapien',  thanks for your comment.

Keep in mind blue eyes contain no blue pigment, it is purely a refractory effect.


text:
Does the order of amino acids matter in making up a protein?
For instance, if a protein is made of 2 amino acids, that is, AB, would the same protein form if the order of combination of amino acids become BA? If yes, would the behavior of interaction of that protein change? For instance, if AB interacted with another protein XY, would BA interact with XY in the same way?

See some discussion of this here: https://biology.stackexchange.com/questions/88137/why-does-protein-folding-not-depend-on-the-order-in-which-it-is-synthesized

Yes.
The 'order' of amino acids is the protein sequence, also known as the primary structure. A peptide (short protein) with sequence XYXYXYXYX is very different from XXXXXXXYYYYYYY.
Your example is a bit trickier, since it seems like AB should be roughly equal to BA. However, each amino acid has two ends - the amino and carboxyl - and so a dipeptide like this is more like NH2-A-CONH-B-COOH with a peptide bond in between.
The really tricky question is : are two sequences 'the same' if they are different by just one or two letters. In other words is AAAAAABAAAAAA different from AAAAAACAAAAAA - and this is the study of mutations of proteins.
There is a lot more to say on this topic, of course.


text:
How to read cladograms/phylograms?
I understand the difference between cladograms and phylograms; the latter can show the evolutionary linkage over time. However, I am having trouble finding out which two organisms are most closely related.

In the image above for example:
Referring to the cladogram, would these following statements be correct
-Bacteria 1 is least related to Eukaryote 4 (the furthest branch is always the least related as there common node is furthest away, correct?)
-The most related organisms are Bacteria 2 and 3, and Eukaryote 2 and 3
Referring to the phylogram
-Is Eukaryote 2 the least related to Bacteria 1 as its branch is the furthest away? Or is it Eukaryote 4 as it is the furthest away (bottom of list)?
-Is Eukaryote 1 most closely related to Eukaryote 3?

I hate to be pedantic, but it should be bacterium (singular) rather than bacteria (plural). I know few people know any Latin any more (including the originator of the diagram), but just so you know next time. After all science is about precision.

@David I didn't make the image, but doesn't it work either way since there are many organisms of each species...

Yes, I know you didn't make the image, and appreciate your difficulty. (I would have modified it myself, but I do that sort of thing.) However I think you would always use the singular (as in eukaryote). For example if you substituted 'animal' or 'microorganism' where the plurals are English,  'animals 1' or 'microorganisms 2' would strike one as odd. You certainly wouldn't want to mix them.

-Bacteria 1 is least related to Eukaryote 4 (the furthest branch is always the least related as there common node is furthest away, correct?)

In terms of relative relationships, eukaryote 4's least-related relative is Bacteria 1. Bacteria 1's least-related relative is the entire rest of the tree

-The most related organisms are Bacteria 2 and 3, and Eukaryote 2 and 3

You cannot actually answer this question because a cladogram only shows relative relationships. To know which species pair is the most related (has the least total distance between them), you would need to know the branch lengths.

-Is Eukaryote 2 the least related to Bacteria 1 as its branch is the furthest away?

To determine relationships, you want to look at the total branch length between two species. Therefore, this is correct

Or is it Eukaryote 4 as it is the furthest away (bottom of list)?

Avoid this way of thinking. A phylogeny is not a 'list'. Pay no attention to the order the species labels appear: you only want to pay attention to how the species are connected. The same phylogenetic tree could be drawn differently, placing Eukaryote 3 at the bottom, for example.

-Is Eukaryote 1 most closely related to Eukaryote 3?

Eukaryote 1's closest relative is Eukaryote 4: the distance from Eukaryote 1 to Eukaryote 4 is the shortest out of all possible pairs with Eukaryote 1.


text:
Blood antigens and immune response
In my textbook, the definition of an antigen is written as follows:
Antigen: A substance that the body recognises as foreign and that can evoke an immune response
The following image also confused me as it states that, for instance, a person with type A  blood has A-antigens

However, would this statement, and image, not be stating that the antigens found on the surface of our blood cells are foreign? Which would imply that our antibodies attack our own blood which is not what occurs?
Or are the substances found on the surface of blood cells (A or/and B antigens, no antigens) only recognised as antigens when they correspond with the antibodies in the body?
In other words, if I am blood type A, the pink molecules on the surface of my blood are not referred to as antigens as they are not foreign, but the green molecules on the surface of group B blood are referred to as antigens as they are foreign?

Which textbook are you referring to? Your body treats another person's antigen as foreign and it evokes an immune response. In this case, A antigen will evoke immune response in a person having B antigen or anti-A antibody as that anti-A antibody will treat A antigen as foreign. If you're satisfied by this, then I can post it as answer (though this is a homework question).

The problem is partly the definition of Antigen that you quote. It refers to “the body” leading you to assume it’s a specific body — yours. I'm sure there are better definitions, but just taking this one, I would modify to: “A substance that can be recognised as foreign and evoke an immune response in an organism.”
With this definition, which is actually how antigens are thought of, a particular antigen need not be antigenic in every organism to which it is presented. Those organisms or individuals for which the antigen appears as ‘self’ will not recognize it as foreign as they are ‘tolerant’ to it (e.g. by mechanisms which eliminate the cells capable of producing antibodies against the self antigen). But it is still referred to as an antigen.
So your understanding of the situation is correct, but that of the use of the terminology is not. Even if you belong to blood group A and therefore will not mount an immune response to the pink blobs in the picture when transfused with blood of group A, they are still referred to as antigens as they stimulate an immune response when transfused into a person of blood group B.
If you wished to talk about the fact that the A antigen on blood of type A does not provoke an immune response when transfused to persons with blood group A you could say “The A antigen on red cells is not immunogenic (or even antigenic) when transfused into persons of blood group A”.
Footnote on terminology
Scientific terminology allows us to describe things precisely. As our understanding increases, the terminology may need to evolve to allow us to make distinctions of which we were previously unaware. The word ‘antigen’ was coined in the late 19th century, before anything was known of the structure of antibodies, and was defined in terms of the immune response as that was what was observed. The definition evolved in some quarters to include the idea of binding to an antibody or T-cell (see e.g. Merriam-Webster definition).
However this extended definition raises the problem of the terminology to use if something binds to an antibody but does not provoke an immune response. Thus, the Glossary of the textbook Immunobiology (Janeway et al.) defines antigen as “Any molecule that can bind specifically to an antibody” and uses a different term, ‘immunogen’, for “Any molecule that can elicit an adaptive immune response on injection into a person or animal”. (Which explains my mention of ‘immunogenic’, as opposed to ‘antigenic’, above.)


text:
Enzyme kinetics: recommended literature to grasp the concepts better
I have had a few biochemistry courses, but I still feel confused and a bit scared each time they try to explain and apply enzyme kinetics or even chemometrics in different situation during class. On our last lecture we had kinetics regarding:

Pingpong reactions (with two substrates A, B):
$V_0 = \dfrac{K_{cat}[E]* [A][B]}{K_m^B [A] * [B] * [A][B]} $

General reactions (with two substrates A, B):
$V_0 = \dfrac{K_{cat}[E]* [A][B]}{K_m^B [A] * K_s^A * [B] * [A][B]} $

And we also had something about analyzing the "principle component" in multivariate data, from enzyme kinetic measurements (as effect of e.g. pH of temperature).
I really don't understand this, or how I would apply this - or analyze my data if I have two substrates.
Question: In general, is there a good web site which goes beyond the normal Michaelis menten analysis, or a very good book which explains both the basic and more complex scenarios regarding analysis/application of enzyme kinetics for biochemists?

Is there a textbook for your course? If so, which one? At the undergraduate level, Voet & Voet is the most comprehensive for my money (and that is a lot of money).  However, for detailed discussion of kinetic mechanisms, like Dan Koshland's ping-pong model, you probably need a book focusing exclusively on enzyme kinetics (not a general textbook)

there is no textbook, just the teacher drawing on the board. Its okay to memorize exactly what they say, and then just paste it in on an exam.. but i would really like to understand this. Thank you for your suggestions!

I always used the book "Enzyme Structure and Mechanism" by Alan Fersht. (Structure and Mechanism in Protein Science: A Guide to Enzyme Catalysis and Protein Folding is the latest version, published in 1998.) Both in some courses I did and when working on (complex) enzymatic mechanisms. It's a classic (so a bit old maybe), but it covers all the basics and includes most of the common complex mechanisms like ping-pong. I don't know if it will teach you how to analyze multivariate data, so maybe you need something else for that.

Yes, thank you for mentioning this one. It is excellent, and it is a classic. I have an older version somewhere but I could not remember the name.


text:
What are chiasmata?
I have a confusion in understanding what chiasmata are. My ‘NCERT’ book says ‘The beginning of diplotene is recognised by the dissolution of synaptonemal complex and the tendency of the recombined homologous chromosome of the bivalents to separate from each other except at the site of crossovers. These X shaped structures, are called chiasmata.’
I am not able to imagine what chiasmata look like with this definition ‘... X shaped structures... ’ moreover I am not sure whether this definition is correct for whomsoever I have asked gave me somewhat different definition.

A simple google image search would give you a plenty of images of chiasmata. Did you try that?

We need to make a distinction between the genetic map of a chromosome, which is usually built up from meiotic recombination frequencies between linked genetic markers, the physical map of a chromosome, which used to be made up of clones and contigs, but is now usually derived from the reference genome sequence, and the cytological map of a chromosome, which is usually built from micrographs of fixed specimens.
In other words, you can only see chiasmata using a microscope.  They are named after the Greek letter named 'chi' which looks like our letter 'X', and are the cytological manifestation of the physical crossover, or crossing over, that took place after meiotic recombination, but before resolution.
Chiasmata are essential for proper segregation on the meiotic spindle because they provide the physical tension, or glue, that the microtubules pull against.  If the centromere of each replicated pair attaches to a different spindle pole, then as the microtubules pull, the chromosomes will align in the middle of the spindle.