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What is the H+ gradient in mitochondria?
I would like to understand what the term H+ Gradient means. I googled this question and found terms such as chemiosmosis and ion gradient being tossed around. I am very new to biology and I do not know any advanced terms or anything of the like. What I do understand is that the mitochondria produces ATP and has something called a proton pump.
Thank you in advance.

A gradient is defined as the difference in concentration of a solutant between two places. For example a sodium gradient along a cellular membrane is the concentration difference between the inside of the cell and the outside space. A H+ gradient (also called proton gradient) is therefore the concentration difference between the inner mitochondrial membrane and the outer mitochondrial membrane. Does this help you? I can expand this later today in a proper answer.

This is really helpful, thank you! Why is it called proton, though? Shouldn't it be ion? And why is this necessary to maintain? I know that lysosomes break down cells that cannot maintain their H+ Gradient, what does ion concentration have to do with the organisms need to break it down? Sorry to ask so many questions. Thank you very much for the help!

@Sciiiiience An H+ ion is a proton

Oh I see! Sorry, I didn't think that through. I forgot hydrogen is just proton-electron. Thanks

Lets start with a general definition: A gradient is the difference in the concentration of a substance (this can be a solutant in liquids, a gas or whatever) between two places. The image below shows the general definition. If nothing else happens what keeps the gradient stable, over time diffusion will cause an equilibrium between both places. The flow of substance always goes from the high concentration to the low (indicated by the arrows).

In biological systems the two parts of the gradient are usually divided by a membrane and are more stable. Gradients can be generated by active transport which requires the input of energy to work against the gradient. Examples would be the concentration gradient along a membrane like protons (positively charged hydrogen-ions), as this can be seen in the mitochondria. Here three complexes of the respiratory chain (I, III and IV) pump protons from the matrix in the intermembrane space, which requires energy. The fourth complex (V) pumps the protons back and uses the released energy from this process to make ATP. See the figure below which shows this process schematically (from here):


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Does too much Genetical Modification leads to formation of new species?
I think Genetical Modification can be termed as 'Artificial Mutation'.
Is it possible that genes can be modified so much that it leads to the introduction of new Species i.e Can integration of large no. of Helpful mutations lead to quick evolution?

yes it possible, in one article show a study for Mycoplasma genitalium which have 525 gene, however only 382 genes are essential for biological functions, they take out the nature gene and place the ' artifical gene' which synthsis in vitro, to test if the M. genitalium will survival when the No. of gene lower than 382. If it survival it will be a new species.

Can you please add some references to your answer? Actually it is more a comment.

What article are you talking about?

I think it is Mycoplasma laboratorium. http://en.wikipedia.org/wiki/Mycoplasma_laboratorium

yep, Mycoplasma laboratorium is the thing I talk about which is genetic modifacation product of  M. genitalium

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Why is the Krebs cycle considered a part of aerobic metabolism if molecular oxygen is not involved in any of the reactions in the cycle
Why is the Krebs cycle considered a part of aerobic metabolism if molecular oxygen is not involved in any of the reactions in the cycle?
I originally thought that Krebs cycle was aerobic metabolism because it is in the process that oxygen is the final electron acceptor, but my teacher claims that glycolysis is anaerobic so what makes the Krebs cycle aerobic?

Oxygen is actually not needed in the Krebs cycle - it is needed in the electron transport chain that is downstream of the Krebs cycle to regenerate NAD+ from NADH. NAD+ is a co-enzyme and acts as an electron carrier in oxidizing reactions at various positions in the Krebs cycle. However, note that without O2, NADH accumulates and the cycle cannot continue as it needs NAD+ to run.
Krebs cycle - No O2 needed:

Electron transport chain - O2 needed to regenerate NAD+ essential for the Krebs cycle:

Why is it often the case that krebs is considered to be the stage before the electron transport chain, if the krebs can't complete without the Electron transport chain completing?  And another question - since glycolysis requires NAD+ and NAD+ is produced by the electron transport chain, then if glycolysis uses the NAD+ from the electron transport chain, would that make glycolysis aerobic, and if so, then why is it considered anaerobic?

"... needed in the electron transport chain that is upstream of the Krebs cycle..." - "upstream" makes me think of the glycolytic pathway - which is not what the second figure shows, correct? Why isn''t it "downstream"?
Are there two contexts of "aerobic"? A. See answer: O2 is essential for  metabolisum, which is not the case in glycolysis? ATP in glycolysis is not produced by breaking down O2? B. in context of Warburg/cancer "aerobic" means that O2 does exist, is there (but not metabolized by the metabolism referred to by "aerobic" (glycolytic cancer cells).

@PeterBernhard - it should be downstream for sure thanks. Does that answer your question as well?

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Could transfusion of a different blood type cure blood-based cancers?
Different antigen detection triggers an immune system response that could perhaps stimulate mitochondria and such in killing cancer cells - something like chemo without the hair-loss?

It is the other way round. For example, post bone marrow transplant reinfusion of donor lymphocytes (termed DLI) is used as a means of triggering a graft-versus-host reaction to prevent relapse in hematogenous cancers.

@Raoul It has a special name: graft-versus-tumor in this case.

@inf3rno yes. Btw I hold an M.D on the complications of DLI ;-)

No. When a different blood type is introduced in the body, the host immune system recognizes the foreign blood as non-self and attacks it. The transfused blood becomes useless, and the potentially massive immune reaction can cause shock, which itself can be fatal.
More details in the book Blood Groups and Red Cell Antigens, which can be found at the NCBI library.


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Does eating antacid (such as Magnesia) before meal have any impact on digestion?
During an anatomy lecture I heard of the importance of the acidity of gastric acid (e.g., killing microorganisms, dissolving food, being a factor for triggering further processes). If a healthy person would eat a tsp. of Magnesia [Mg(OH)2] suspension before a meal (lets say at least 30 min beforehand) and then eat normally, would it have a significant impact on the digestion? Like being unable to extract or produce certain products? Or having a higher risk for a yeast infection?
This question also applies to proton channel inhibitors such as Omeprazole and other drugs like Ranitidine
(Background: The lecture was just a introduction to anatomy for informatics. We never went into greater details.)

A spoonful of NaOH(s) on an empty stomach will have pretty nasty consequences as it will most likely lead to damage to the stomach and internal bleedings. My last concern would be infections or digestive issues.

@ChrisStronks could you explain how it would damage the stomach? I could imagine it would damage the mucus and then the gastric mucosa would be without protection - ready to get a hole, which would be the worst thing I could think of.

NaOH is a strong base and when dissolved is much more harmful to the body than the equivalent of sulphuric acid or HCl and other strong acids. It will dissolve the stomach wall indeed.

If Natron was indeed NaOH (I have forgotten most of my Chemistry knowledge sigh- at least wikipedia seems to say it is NOT- clarifications welcome) then the reaction of high concentration NaOH and HCl is highly exothermic. I can only imagine the disasters it would cause in the stomach.

What language was the lecture in? In German, Natronlauge is a name for sodium lye (NaOH), which will cause extensive chemical burns long before it reaches the stomach. But the word Natron is used for baking soda (sodium bicarbonate), which will not cause immediate wounds. Still, it's not a good idea to eat it, it disrupts the chemical balance of the stomach. I have a relative who, after prolonged use of sodium bicarbonate, got a bad case of GERD, but cannot say if the soda caused it, or if he would have gotten it anyway and the soda failed to prevent it.

@Rumtscho thank you - I am Dutch originally and the Natron is the trivial name for NaOH. You are right. NaOH is a strong base, baking soda is not that bad :)

@Zwie Changed Natron to Magnesia (Milk of Magnesia is used as an antacid). Is it fine?

@WYSIWYG actually I have no idea what Magnesia is. The lecture was in German and I was thinking of Natron as baking soda... kinda assumed it would be the same in English.

@Zwie magnesia is magnesium hydroxide. It is used as an antacid


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What are the structual differences between DNA and RNA?
How is the structure of DNA different from that of RNA?

This looks like homework. See the homework policy of BioSE.

Seems like an odd homework post though, he answered his own question.

DNA and RNA are similar, but different molecules. Both are made up of nucleic acids attached to a backbone made of phosphate and a sugar forming a nucleotide. DNA uses the nucleic acids Guanine, Cytosine, Adenine, and Thymine, while RNA replaces Thymine with Uridine.

The nucleic acids can form pairs due to hydrogen bonding, which allows the DNA/RNA to store information, if one strand has a C, the other must have a G and vice versa. Same applies for A and T.

While both molecules are capable of forming double helices by hydrogen bonding between G and C or A and T/U, the types of helix tend to be different. DNA prefers to form what is known as a B type helix, while RNA prefers the A type.

The left most helix is A type, the middle is B type, and the right helix is Z type, a highly unusual form found only under certain conditions.
DNA is almost always found as a double stranded molecule, and is primarily responsible for storing the information for making proteins and RNA and regulatory functions in cells. RNA is made by copying information from DNA through a process known as transcription and performs a variety of roles. Messenger RNA, or mRNA, carries information from DNA to ribosomes where it is used to build proteins through translation. Transfer RNA, or tRNA, carries amino acids to ribosomes to build proteins. The ribosome itself is made of RNA, known as rRNA, with proteins to help it function. Even through RNA is usually made up of only 1 strand, it can fold up and form complex shapes, such as the characteristic tRNA structure shown below. Some RNA molecules can even act as catalysts, carrying out chemical reactions such as cutting up other RNAs. These catalytic RNAs are known as ribozymes.

good answer, but could you add some references of where you got the images?

The images all came from the wikipedia pages I link to in the answer. Didn't realize the image URLs get converted to an imgur link so you can't even get the original URL by clicking on edit to look at the source code.


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Why is Cysteine and Tyrosine used to calculate a sequence isoelectric point?
Why are the amino acids - cysteine and tyrosine used in isoelectric point calculations for a protein sequence, yet neither of them are positively charged molecules? and are not used in net charge calculations.

Both have ionisable side chains.

I still don't know why 7 amino acids are used for isoelectric point and only 5 for net charge?

Every amino acid has a different isoelectric point: a pH where they do not carry electric charge. This isoelectric point depends on the side chains:

By glycine the side chain $-H$ is neutral (while the amino and carbonic acid groups are not) so the IEP is 5.97.
By lysine the side chain $-(CH_2)_4\mbox{-}NH_2$ is alkaline $[R\mbox-NH_2 + H^+ \rightleftharpoons R\mbox-NH_3^+]$, so it will have a more alkaline IEP 9.74 than glycine.
By glutamic acid the side chain $-(CH_2)_2\mbox -COOH$ is acidic $[R\mbox -COOH \rightleftharpoons R\mbox -COO^- + H^+]$, so it will have a more acidic IEP 3.22 than glycine.

Every side chain has more or less contribution to the IEP of the amino acid. In your question

the side chain of cysteine $-CH_2\mbox-SH$ is a weak acid $[R\mbox-SH \rightleftharpoons R\mbox-S^- + H^+]$ so the IEP is 5.07
the side chain of tyrosine $-CH_2\mbox-Ph\mbox-{\scriptsize (p)}OH$ is an even weaker acid $[R\mbox-OH \rightleftharpoons R\mbox-O^- + H^+]$ so the IEP is 5.66

And every amino acid has more or less contribution to the IEP of a protein.
References:

Table of pKa and pI values
Amino Acids with Acidity Values
Introduction to Proteins; Amino Acids, the Building Blocks of Proteins
Electrospray Mass Spectrometry

Plus the phenyl group (or any group) can also exert effects on the ionizability of the amino acid (inductive and resonance effects). It is also incorrect to calculate pI of the entire protein from the sum of its parts.

@WYSIWYG Yes, I think they just want to roughly estimate the value of pI.

I only want a simple linear equation for pI. I still don't understand how if net charge/pI are more or less the same thing. Why you would use D,E,H,K,R for net charge and D,E,H,K,R and C,Y for isoelectric point? Sorry I'm not a biologist or a chemist.

@user2679447 http://en.wikipedia.org/wiki/Isoelectric_point The net charge depends on the pH, the pI of the protein/amino acid is the pH where the net charge is zero. So pI and net charge are completely different things.


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What is the difference between a phosphotransferase, a phosphatase, a phosphorylase and a kinase?
I've looked in several sources, but I'm still confused. This is what I have so far:

A phosphotransferase catalyzes the addition of a phosphate group.
A kinase is a type of phosphotransferase that transfers a phosphate group from ATP to a substrate.
A phosphorylase is a type of phosphotransferase that catalyzes the addition of a phosphate group from an inorganic phosphate (HPO4) to a substrate.
A hydrolase catalyzes the hydrolysis of a chemical bond.
A phosphatase is a type of hydrolase that removes a phosphate group.

Is this right?
EDIT:
Also adding to the confusion is the enzyme Phosphorylase kinase, which is the kinase that phosphorylates the enzyme Glycogen phosphorylase, which hydrolyzes glycogen.

Phosphatase uses water to remove a phosphate group, while Phosphorylase uses phosphate group to remove the phosphate group

Don't get caught in the linguistic trap of attaching too much significance to the precise meaning of any one piece of scientific jargon. Nomenclature, the system of naming things, utterly sucks in biology, and it sucks even harder for protein biology. There is no one universally accepted classification and naming system for proteins, although there have been plenty of attempts.
For example, phosphotransferases are classified as EC number 2.7. However, Glycogen Phosphorylase is classed under 2.4, which might make you think "well, clearly kinases are enzymes that transfer phosphate groups from organic substrates such as ATP and are classed as 2.7, whereas phosphorylases are enzymes that transfer from inorganic substrates and are therefore classed as 2.4". But wait! RNase PH is a phosphorylase that's classed under 2.7 and uses inorganic phosphate, so um... yeah.
In any case, don't get too hung up on the nomenclature. Unless you're working in an enzymology lab just say "kinase" and everyone will know what you're talking about.

I'm certainly not an expert on this but it seems to me that glycogen phoaphorylase could also be classified as a phosphotransferase (2.7). However, since there's already a glycosyltransferase group (2.4) it was classified there. There is no such group for ribonucleotidyltransferases which is why RNase PH was put in 2.7. This is perhaps a drawback of the EC system in that one catalysed reaction could fit two different groups. Even though glycogen phosphorylase is classified as a glycosyltransferase by EC, it is still also a phosphorylase.

@canadianer That's true. My point was more about the futility of trying to define a short nomenclature for the set of all enzymes. Their complexity defies any simple classification. Save the jargon for when you have specifics to talk about, and talk about generalities in general terms.

As @tel said, there is no clear difference available since there is no international authority which manages such things (like IUPAC) when it comes to biological terms. However, these terms can be understood and differentiated a bit more easily, as long as you don't get into deeper details.
Posphotransferase is a kind of transferase that transfers a phosphate group from one compound to another. The type of substrate remains unspecified (dictionary.com).
Kinase is a type of phosphotransferase that transfers a phosphate group from high-energy phosphate donating molecules (usually ATP) to anothrr molecule. Here, one substrate is specified (Wikipedia).
Phosphorylase is an enzyme that adds an inorganic phosphate ($\ce{PO_4^{3-}}$) to a substrate molecule. The inorganic substrate is not transferred, it is directly added to a molecule (Wikipedia).
Hydrolase is an enzyme that hydrolyzes a substrate i.e. breaks a covalent bond in a molecule and adds water to the resulting molecules. Its like $$\ce{A-B + H_2O \rightarrow A-OH + B-H}$$ where A-B is a single substrate molecule (Wikipedia).
Phosphatase is a type of hydrolase that hydrolyzes the bond between a molecule and phosphate group, resulting in the formation of inorganic phosphate and an alcohol. It is like $$\ce{A-PO_4^{2-} + H_2O \rightarrow A-OH + HPO_4^{2-}}$$ where A becomes an alcohol (Wikipedia).
PS: I am not saying that these are the universally accepted definitions of the corresponding enzymes. These are just examples to help you better understand the meaning of these terms. However, you can always find exceptions to these definitions.


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What are non-heritable changes to genomes?
I am told that mutations are heritable changes to the genome.
So this begs the question - what are non-heritable changes to genome?

Mutations are not necesarily heritable changes to the genome. Think of newly acquired mutations that lead to cancer. These are not heritable. Only mutations which are present in the sperm or egg cells are heritable, no matter whether these are old or newly acquired. Non-heritable changes in the genome occur anywhere else, for example in your skin after prolonged sun exposure.

@Chris "Mutations Are Heritable
Changes in DNA"

I don't see it like this. A mutation is a change in the DNA code.

To my point of view the expression "heritable change in DNA" is extremely misleading of even a non-sense. OR it uses a definition of heritability that is close to the one of inheritance. The concept of inheritance then depends on whether we look at multicellular inheritance or unicellular inheritance.

What is your textbook btw?

@Remi.b "Principles of Life" By Hillis ... piece of crap if you ask me. I prefer Campbell.

The passage says mutations are changes in the DNA sequence that are passed on from one cell or organism to another. Their definition of heritable seems to be how a layman would perceive it, not necessarily how am evolutionary biologist would.

Also what is your definition of changes to the genome? Sequence changes, epigenetic changes, regulatory changes?

Regardless of the use of "heritable", the later part of the quoted paragraph is not true: "we can state that mutations are changes in the nucleotide sequence of DNA that are passed on from one cell, or organism, to another". It should be "that may be passed on". As many pointed out mutations are not necessarily passed on.

Somatic mutations are "heritable" by the daughter cells of the somatic cell. It is indeed heritable in the cellular level; doesn't mean that it will always be inherited (what if the cell dies/doesn't divide)

Mutations in Cancer cells are heritable @Chris - they pass from one generation of cancer cells to the next, not heritable in the germ-line of the organism but still inherited within lineages of cells.

@GriffinEvo Using this definition every mutation would be heritable as long as the cell which acquired it is still dividing.

The definition above states "from one cell, or organism, to another" @Chris

I don't know what you really mean by "heritable changes to the genome". I think you will understand why this sentence makes no sense after reading what follows. I start with some background and then try to address directly what confuses you.
Short introduction to the concept of heritability
The concept of heritability may have two meanings.
Heritability is a concept defined at the population level for one given trait. The heritability ($h_B^2$) (in the broad sense) is the ratio of the genetic variance $V_p$ over the phenotypic variance $V_p$, where the phenotypic variance can itself be decomposed into environmental $V_e$ and genetic variance $V_g$ (and their covariance that we will neglect for the purpose of this question).
$$h_B^2 = \frac{V_{g}}{V_{p}} = \frac{V_{g}}{V_{e} + V_{g}}$$
When saying environmental variance $V_e$, we don't refer to the total variance in the environment (such as the variance in temperature for example) but we refer to the phenotypic variance (in a given population of a given trait of interest) that is caused by environmental variance. The same logic is true for the genetic variance.
Inheritence
While the concept of heritability applies to phenotypic traits, the concept of inheritence can apply to DNA material. A mutation is inherited if the offspring receives the sequence from his/her mother or from his/her father (assuming we are talking about a species that have sexual reproduction with 2 genders).
Somatic versus germline mutations
As pointed by @Chris in the comments. In multicellular organisms, not all mutations can be transmitted to the multicellular offspring. Most of the cells do not give rise to any other multicellular organisms. For example, imagine that while the biceps is under development at very low age, a mutation occurs that will be inherited by the daughter cells but not to the multicellular offspring. we call the line of cells that do not give rise to gametes (sperm and ovules), the soma line, by opposition to the germ line which gives rise to the gametes.
To answer your question
As soon as a given locus (position on the DNA) has some variance and that this variance explains some phenotypic variance, then the phenotypic trait it influences has a heritability greater than zero. If the variance at this locus has no effect on the phenotype, then it's heritability is zero (because $V_g = 0$, although there is some variance in the actual sequence). If the phenotypic trait of interest does not show any variance (in the population considered), then the concept of heritability is undefined for this trait!
I think you may have a confusion between "inherited trait" and "heritable trait". A mutation will necessarily be transmissible to the offspring (except if it happen to be in the somatic line in such case it will only be transmitted to daughter cells but not to the multicellular offspring) but it doesn't mean that this mutation will necessarily explain some variance in a phenotypic trait. A new much is necessarily heritable (pay attention to the soma vs germ line) but does not mean that a phenotypic will have higher heritability thanks to this mutation.

it's what my book tells me; "Mutations Are Heritable
Changes in DNA."

See my update. Hope that will help you. I think you got messed up by the concepts of heritability and inheritance. The answer is maybe complciated I am a bit scared to have just render things even more complicated. But I hope it will help you. I've got to go now, so I cannot give you further answers today! Sorry

@Dissenter yes, mutations are heritable i.e. they can be inherited but they don't necessarily get inherited since during meiosis you have processes such as independent assortment and chromosomal cross over, which means the gamete won't necessarily have the mutation of the parents!

Most mutations to the DNA are heritable, but not all are inherited.
Mutations occur in the DNA, DNA is then replicated and transmitted to offspring (cells or organisms). Generally all mutations are heritable because they can be inherited, but some aren't - either by random chance (drift) or deleterious fitness effects (selection). Any mutation which makes the cell less fit has a reduced chance of being inherited, but even mutations leading to cancer are inherited at some level (from mother cancer cell to daughter cancer cells) but at some point this lineage of inheritance will stop because it will kill the host (but this is no different to species/lineages of organism going extinct - if I carried a new novel mutation but didn't have children then that mutation is not inherited).
*I suppose a mutation which stops DNA from being replicated could be classed as not-heritable because the DNA is not going to be replicated, but that depends on there being no other sources of replication machinery (other cells perhaps) - a process I don't know well enough to offer any firm conclusions on.
Non-heritable changes to the genome
DNA can be altered beyond just sequence mutation, for example methylation- but this can be used as a heritable change to the genome (genomic imprinting). Perhaps gene expression with strong environmental effects on gene expression could be considered as not heritable (because if the environment is not "inherited" then parent-offspring regression would be 0) but maybe that's a change to the transcriptome rather than genome.


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What is the progressive evolutionary advantage that leads to flying?
As far as I understand, all life started as non-flying and flying came about by natural selection. What is the evolutionary advantageous "path" to flying? Or is there something else to explain this?

You mean why animals "started" to fly? Because there was a large uninhabitated niche to live in: The air and the third dimension.

I've heard that insect wings may have developed from some sort of breathing structure. Both would be very thin with large surface areas.

@Chris no, my question is the ability (and organs necessary) evolved.

@Chris I would rather say that it was an escape from land based predators.

@WYSIWYG I would include this in the niche: Escape from predators, other ways to access food and so on.

Which type of flight? flight has evolved several times and not through the same path.

The honest answer to this and many other similar evolutionary questions is that we don't know the answer. We can sample information from many different points along an organism's developmental timeline using the fossil record, genetics, etc. and reconstruct various states of said organism's development. The overwhelming evidence is that evolution is the process that connects these various states, but reconstructing the detailed trajectory that leads from one developmental state (e.g. flightless) to another (e.g. flying) is often formally impossible due to the low time resolution of the information that we have.
That being said, plenty of people have speculated as to the origins of flight, and there's an excellent wikipedia article on the subject. From the article:

Powered flight has evolved only 4 times (birds, bats, pterosaurs, and insects)... Insects were the first to evolve flight, approximately 350 million years ago. The developmental origin of the insect wing remains in dispute, as does the purpose prior to true flight.  One suggestion is that wings initially were used to catch the wind for small insects that live on the surface of the water, while another is that they functioned in parachuting, then gliding, then flight for originally arboreal insects.

i like the parachuting, i think thats a satisfactory answer (although still a theory without evidence)

do you know if theres a good source for these types of explanations? cause i have a whole bunch more paths i would like explained.

@tryingToGetProgrammingStraight Yes I do! BAHFest is truly an authoritative source for such information.

@tryingToGetProgrammingStraight More seriously, it really depends on the organism/system in question. For example, the debate over why humans started walking upright has been a particularly acrimonious and silly one.

@tryingToGetProgrammingStraight If you have a whole laundry list, try posting them here. Just maybe keep it to one a day.


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Is this a valid definition of independent assortment?
"Allelic combinations separate randomly. I.e. a parent might be Aa and Bb for two traits but that doesn't necessarily mean the gametes will strictly be AB or ab but any of a number of combinations. I.e. blue eyes does not imply short height or something."

That's a valid explanation, but not definition. Mendel's law of independent assortments states that during the formation of gametes, the alleles for one trait segregate independently of the alleles of another trait.

The Law of Independent Assortment:
Alleles for different traits are distributed to sex cells (& offspring) independently of one another.

This one is like written on the stone in my mind!


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What impacts penetrance of Huntington's disease?
From Principles of Life by H. Craig Heller, David E. Sadava, Mary V. Price:

From what I understand, Huntington's disease exhibits varying degrees of penetrance depending on how many times the mutation is found in the person's genome. Penetrance is nearly complete if the incorrect base pair sequence is found over a certain number of times.
My question is what affects penetrance? Is it exclusively environmental?

and your question is?

It's in the title.

I also don't understand your question. That definition of penetrance says nothing about the environment.

To me, it seems like you are arguing against the "exclusively environmental" idea in the section on Huntingtons. What makes you think/ask that it is exclusively environmental? The short answer to the title Q is No - the genetic background (genes at other loci) can for instance affect penetrance. You should also include a reference to the book you've scanned.

Also, penetrance is a property of a population, not an individual.

HD is a late onset disease. The effects are not usually apparent until some threshold is reached.

@WYSIWYG - ~10% of patients have onset in their childhood (as young as 2) and teens. The majority develop their obvious symptoms in their 30's and 40's (some believe the earlier symptoms are largely overlooked) and only 10% develop the disease after 55. If you had the mutation, I doubt you would call it late onset.

It is "considered" a late onset disease; most affected individuals reach reproductive maturity before manifesting the symptoms. I don't think 10% patients develop the symptoms in childhood. See here

@WYSIWYG - it is considered adult onset. As to percent of juvenile onset, see here, here and here.

@anongoodnurse - Okay I see the difference. I had been using the term late onset to mean post sexual maturity (as I heard around).

Penetrance describes the frequency of a gene's expression:

Penetrance refers to the proportion of people with a particular genetic change (such as a mutation in a specific gene) who exhibit signs and symptoms of a genetic disorder. (Genetics Home Reference nih.gov)

More specifically:

[P]enetrance is defined as the percentage of individuals with a given genotype who exhibit the phenotype associated with that genotype. For example, an organism may have a particular genotype but may not express the corresponding phenotype, because of modifiers, epistatic genes, or suppressors in the rest of the genome or because of a modifying effect of the environment.

Note that the environment is only one factor affecting the expression of an allele.
Retinoblastoma and achondroplasia are often referred to in discussions about penetrance.
Retinoblastoma is caused by mutations in the Rb gene. Not all people who carry this mutation suffer from retinoblastoma (about 90% do). There are numerous inherited diseases (including cancers) in which the same mutation is not expressed in all the individuals who carry it. Achondroplasia, on the other hand, has 100% penetrance: every person with the specific point mutation in the fibroblast growth factor receptor 3 gene always has abnormal bone growth and dwarfism.
Huntingtons is a little different in that patients with 36 to 41 HD CAG repeats exhibit reduced penetrance; that is, some may not develop HD in their lifetime; however 100% of those with the mutation produce the abnormal/polyQ/polyglutamine-enlarged huntingtin. The age of onset is dependent on number of repeats but is affected by other modifiers (both genetic and environmental); this becomes less obvious in individuals with higher repeats sizes (e.g. greater than 44).
Huntington's is not a genotype affected only by environment.
 Genetics in Medicine
 A new model for prediction of the age of onset and penetrance for Huntington’s disease based on CAG length

however 100% of those with the mutation produce huntingtin.: Everyone produces huntingtin however its exact function is unknown. HD patients produce the Polyglutamine expanded one.


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Ways to measure effectiveness of a gene therapy trial?
I understand that Fluorescence in situ hybridisation  can be used to measure the effectiveness of a gene therapy experiment/trial.
But what are some other genetics techniques to measure the effectiveness of a gene therapy clinical trial. Would blotting (northern/southern) and PCR be a way to tell if a new genome have been integrated into existing cells.
Thanks

These techniques will not tell you the effectiveness of a gene therapy. They will just let you know if the gene is inserted or not. Effectiveness means to what extent is the disease condition alleviated i.e the final response.

Genomic integration might not be a desired outcome of gene therapy. If not carefully controlled, the inserted DNA could be stuck right in the middle of an important gene, or disrupt a tightly regulated promoter or something else that disrupts the normal gene regulation and cause cancer.

If all you cared about was genomic integration, then your best bet would be some kind of sequencing. If you sequence the modified region and the flanking regions you could be sure that the new sequence was present in the genome.
It would probably be more interesting to look at how the new genes affect the cell. For example you could look at differences between protein expression in modified and unmodified cells. For that you could use RNAseq.


text:
Cells "grown in LB broth to an OD600nm"

Cells "grown in LB broth to an OD600nm"

What does the OD stand for in this?

Just a google search would have fetched you the answer.

This phrase in isolation has no meaning, because the value itself is missing: "to OD of X at 600 nm".

OD = Optical Density
As you grow cells in broth, the broth becomes cloudy. The more cells there are, the cloudier it is. After you grow your cells for a while, you can measure their progress by shining a light through your sample. The more light your cell culture absorbs (higher absorbance is equivalent to higher OD) the more cells there are in it.


text:
How can histidine be classified both as positively charged and hydrophobic?
I saw the chart in this post Histidine aromaticity. Since I'm not allowed to comment and post a question instead of an answer, I have to ask my question in a separate thread.
How can histidine be classified both as positively charged and hydrophobic?

Histidine is not hydrophobic

BTW: You are going the right way here - asking new questions in the answer (or comment) section under other questions is not well liked.

Charged or not, histidine is aromatic because it fulfills all of the aromaticity criteria:
1.The molecule is cyclic.

2. The molecule is planar.

3. The molecule is fully conjugated (p orbitals at every atom in the ring).

4. The molecule has 4n+2 π electrons, where n is a positive integer.

As a matter of fact, the chart above is not wrong; it is quite correct. Indeed, histidine can carry a net positive charge, but when unprotonated, i.e. in a charge-neutral state, its aromatic π-system (belonging to the imidazole moiety) can behave like a hydrophobic group, e.g. it can become involved in π-stacking (aka CH-π) interactions. In the 2RS2 NMR structure, for example, HIS83 is δ-protonated and appears to be behaving like a typical hydrophobic residue: it is buried below the protein surface, stacked against several aromatic residues and packed along with several aliphatic ones; it is shielded from solvent by polar and charged residues.

2H95 is a very interesting structure where we see four ε-protonated histidines stack against tryptophans, as well as pack against aliphatic side chains, forming a transmembrane proton channel. The histidines appear to be involved in hydrohobic interactions, and, notably, at the same time form the inner surface of the channel.

Conversely, in the 2NBJ NMR structure, we see HIS56 behaving like a polar amino acid - its (doubly protonated) side chain is involved in hydrogen bonding to the backbone oxygen of a DNA fragment, as well as to a backbone oxygen atom from the protein. Moreover, in the same structure, HIS16 is doubly protonated and solvent exposed, likely interacting with water and contributing to solvation, in stark contrast to HIS83 in the 2RS2 structure, which is monoprotonated and buried in the hydrophobic interior of the protein.

Histidine's pKa can easily be perturbed by its surroundings, e.g. by the surrounding residues in an enzyme active site, which makes it highly functionally versatile, one of the manifestations of its functional and chemical versatility being its ability to behave both as a polar/charged amino acid, as well as a hydrophobic residue; this is the reason histidine is often found in functional sites in proteins, e.g. enzyme active centers.

You make assertions which may or may not be right, but you provide no third-party support for your answer. Although it has been accepted, the poster has no basis on which to judge it correct. What you need to do is to edit your answer to provide examples of proteins (with links) in which histidine is clearly uncharged and involved in π-stacking interactions. Then I and others can go to the links and decide whether to vote your answer up or down.

I look forward to seeing that. It will enhance the standards of this site. Take your time.

I've already added the reference to the answer.

I've read the paper and it seems to me to relate only to theoretical calculation of π-π interactions, assuming they exist, with the conclusion that they are relatively weak compared with other His interactions. What is lacking in the paper is a single example of a π-π interaction in a protein. I am familiar with PDB, but do not see how to perform a search for π-π interactions involving His to quickly return examples. (A slow search by eyeballing, I understand.) I am not saying you are wrong, but I do not think you have proven your case. At the moment it seems just hand waving.

I have added several illustrative images and examples; I would love to expand this topic in more depth and will gladly do so, provided I find the time.

Thanks. Very good. The proton channel seems intriguing, although I'm not actually a protein chemist. Must ask a colleague about it. (If you add any more pics, I'd scale them down a little for ease of reading your whole answer.)

As @wysiwig stated, Histidine is not hydrophobic. Depending on the pH different parts of the molecule can carry charges, see the image below (from here):

The nitrogen atoms can be protonated in an acidic environment, the carboxylgroup will loose it proton in a basic environment. All these forms are transferred into each other, when the pH changes.

As @Chris says, the charge depends on the pH: when the pH is different from the pH(I) of the molecule, this one is charged.(Take a look at this).
Anyway, talking about Hys, its pH(I) is 7.47 (here), so at a pH below its pI, the Histidine carry a net positive charge, otherwise it can be also in a netrual form. Obviously it's all a matter of equilibrium!

Yeah, I think so...


text:
When writing about past research should I use the species name they employed or the modern version?
I am currently writing a literature review in which I am talking about the old research on the subject. When this research was carried out the species I'm talking about were classed under a different genus (specifically, it used to be called Vibrio fetus and is now called Campylobacter fetus). What is the correct approach for choosing when to use the older name and when to use the newer name? I see three options, although there may be more:

Always use the modern name.
Use the name used by the authors when discussing their work.
Largely use the modern name but make reference to the fact a different name was employed where it is appropriate to do so.

I'm tending towards option 3, but it's sometimes a bit unwieldy. Is there an accepted convention I should be following?

I would also use the modern nomenclature and introduce the old one in the introduction (and probably also in the abstract). I don't like the old nams sticking around, something that can regulary be seen for gene names. It is relatively complicated to search for literature, when you have to do this as well for half a dozen synonyms. Nomenclature exists for a reason.

3. is right thing to do. You can mention in the introduction that "Campylobacter fetus, which was previously known as Vibrio fetus [Ref] ........."
You should not use the old name anywhere again (also for the sake of consistency), once you have made it clear that the species was renamed, in the Introduction.
I don't think there is any written convention like that (As such usage of any obsoleted terms is to be avoided and the standard nomenclature as described by ICZN/ICBN etc should be used).

+1 Also note that it is common that older synonyms are given (sometimes many), e.g. in a parenthesis in the introduction or in methods (where the organism is described). In species determination literture or taxonomic papers clarification of synonyms are often done under a specific heading.

I've also seen cases like this written as "Campylobacter [Vibrio] fetus". Or just use the revised genus and ignore the old name.

There actually is a rule, called the 'Principle of Priority', which states that the nomenclature of a taxonomic group is based upon priority of publication hence option 2 in your question is the correct approach. In the principle III (Principle of Priority) section of the link above it is stated that

This principle states, in essence, that if a taxonomic group has been
  given two or more names, the correct name is the first name that meets
  the Code’s standards for publication.

But here the rule doesn't seem to apply....instead there is a piece of literature regarding the reclassification of gen. Vibrio to Campylobacter. In the paper "Neotype Strain for the Type Species,Campylobacter fetus (Smith and Taylor) Sebald and Vkon" (Veron & Chatelain, 1973) they state that:

A critical study of the present state of the classification of
  vibrio-like, curved, microaerophilic bacteria was made. The species
  originally described under the names Vibrio coli Doyle, V. jejuni
  Jones et al., V. sputorum PrCvot, and V. bubulus Florent are
  transferred to the genus Campylobacter Sebald and VCron
  1963. The authors suggest that the type species of this genus, C. fetus, be divided into two subspecies: C. fetus subsp. fetus (Smith
  and Taylor) comb. nov. (syn. V. fetus subsp. intestinalis Florent),
  which contains the neotype strain of the species, and C. fetus subsp.
  venerealis (Florent) comb. nov. The previously described subspecies V.
  fetus subsp. intermedius Elazhari is regarded as an infrasubspecific
  taxon with the name C. fetus subsp. venerealis biotype intermedius.
  CIP 5396 (=ATCC 27374=NCTC 10842) is proposed as the neotype strain of
  C. fetus subsp. fetus. This strain, then, is also the neotype strain
  of C. fetus (Smith and Taylor) Sebald and Vkron.

The highlighted words suggest how they have approached in naming the species...

While this link may answer the question, it is better to include the essential parts of the answer here and provide the link for reference.  Link-only answers can become invalid if the linked page changes.

@TheLastWord ..Thanks....Actually have joined just today..so a little low on these 'know-how's...

As I understand the question, this answer is not really relevant. The Q is talking about a reclassification of a species due to new phylogenetic information, so that it is moved to another genus. The Principle of Priority is mainly talking about what name that should take precedence, if there are several descriptions of the same species. In this case, the Vibrio genus is probably in use for another species (which should keep the genus name by 'Principle of Priority'), while Campylobacter fetus has been moved to another genus because of new information

@fileunderwater Ok....but the ambiguity normally arises due to placement of same species in different genus....for example-a species of oomycetes causing ' White rust' disease was named ' Albugo candida ' in 1751 & just after 2 years in 1753 it was named as ' Cystopus candidans ' & after that placed even in 'Acedium' & 'Uredo' genus...but the principle prevailed & the original name or basidionym is kept as " Albugo candida " and the rest were just designated by synonyms...there of course can be exceptions...but generally the essence & application of the rule is maintained...

I think you're confusing more than one thing here. Campylobacter fetus is the correct, current, internationally recognised name for the species. Like many species, it has been moved to a different genus than it was originally assigned to. The principle of priority applies when the same species has been identified by different researchers.

ya..got your point...I am modifying my answer...


text:
What is the difference between embryology and developmental biology?
The question is quite explanatory in it self, I used to think that both are same but then find somewhere that embryology is a part of developmental biology, can somebody please elucidate?

Do worms have embryos?

@terdon they have zygotes. All multicellular organisms have at least some form of reproduction where their offspring pass through a single-cell or few-cell state (though I'm sure there's at least a few exceptions to this).

@tel I know, that was just a tongue-in-cheek comment pointing out why not all of developmental biology can be called embryology.

@terdon. Ha hah, all right. Honestly, I thought there was a reasonable possibility that you were an earnest seeker after truth

Does C elegans not have an embryonic stage?

@canadianer Technically yes. But it is usually called larva.

It's a simple sub-set relationship, embryology is a sub-set of developmental (it's a "specialty"). Embryology is only concerned with the embryo - developmental is a larger group, concerned with developments that may occur in other stages of life. Such as the development of secondary sexual characteristics in humans - a developmental thing, but not embryonic.
These are not purely objective definitions and the dividing lines are not well defined. Labels for various scientific fields are only generally applicable, and they are very flexible. For example, many Chemists also do a lot of physics. Many Biologists do a lot of Chemistry. Many Embryology studies dip into developmental stuff. These divisions are not always clear.
Embryology is a part of Developmental Biology in the same way that Biology is part of "Science" - simple sub-set relationship. If you don't understand sub-sets very clearly, you'll want to study up on that relationship - it's very important in ALL sciences, so you can understand things like "All squirrels are animals, but not all animals are squirells"
This statement would be reasonable - "All Embrology is Developmental Biology, but some Developmental Biology is NOT Embryology"

What I get from your answer is that Developmental Biology along with embryology also concerns itself with regeneration and aging.Will gerontology also be a part of it.

See my edit. This stuff is not black and white. And, no I don't know how to explain it without metaphors.


text:
Any databases with AAMI ECG and ECHO?
There is no AAMI 12-lead ECG databases available online.
All of them have problems.
I and my friends finally finalised our tests with St Petersburg.
It is not AAMI.
So the next step is to search any ECG databases with some leads (at least lead 2) with ECHO data.
Is there any AAMI standarded ECG databases with ECHO data?
This data need to be from the same patient.

One possibility is PTB Diagnostic ECG database here.
However, its AAMI verification is still under process here.
Some ECHO findings also there.


text:
How to define "Quasifixation" in continuous approximation of finite population?
Background
Many models including the famous very first models derived by Sir Ronald Fisher in his early career, assume infinite population size. In an infinite population, an allele can rise in frequency (if its fitness is greater than the fitness of its counterpart(s)). This increase follows a logistic curve that never exactly reach a frequency of 1. Therefore, the term fixation does not apply to these model and in consequence the concept of quasifixation has been created.
Question
An allele is considered to be quasifixed if it reaches a frequency that is very close to 1. But how close? The decision is obviously arbitrary but when using a continuous approximation model in a finite population the question is necessarily raised and a decision needs to be made. How close should the frequency of an allele be to 1 so that it is considered to be quasifxed? The answer is probably a function of the population size $N$. What threshold do authors usually use in the theoretical population genetics literature? It would also be nice to have the definition of the author who first coined this term.

I think there is an answer in here: http://ac.els-cdn.com/0040580972900159/1-s2.0-0040580972900159-main.pdf?_tid=5ae1bc16-8049-11e4-96d2-00000aab0f01&acdnat=1418201507_114d91e34ce366129089c4c4ec02f468

Or this one might help as well: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1209652/pdf/280.pdf

Garrish and Lensky (1998) considered reaching fixation when $p > \dfrac{N-1}{N}$, where $p$ is the allele frequency and $N$ the population size.
Note that I ran simulations (unpublished) that well approximated the threshold chosen by Garrish and Lensky (1998).

As I haven't found any guideline, I just went with chosing a threshold at $p = 1-\frac{1}{4N}$ for a diploid population. Allele $A$ is therefore considered quasifixed if its frequency $p$ is greater than $1-\frac{1}{4N}$ i.e. the number of occurrences (count) or the other allele is lower than $\frac{1}{2}$.


text:
How can we calculate the minimum sustainable number of the panda population?
I have a degree in Biology so I'm a little embarrassed that I never learned this, but...
How do we know 1600 Pandas isn't enough?
I know that we have historical numbers (although I couldn't find them) which show the population has declined, but we also know the usable habitat has declined and it would be foolish to not consider that when trying to replenish the wild population. It seems to me that if there's only 1600 Pandas in the wild, that's probably the right number. How do we know it's not?
I will accept answers about other endangered animals, if they show how we can calculate the approximate "appropriate" number for a species.

Relevant question: http://biology.stackexchange.com/questions/305/smallest-viable-reproducing-population

That would be part of a good answer - "we think 1600 is below the smallest viable population"

Minimum viable population (MVP) can be predicted in two ways.

Computer simulations.
Population viability analyses (PVA)

PVA is considered generally more common practice by ecologists and without a reference to the 1600 panda population you mention, my guess would be that this is what they did. PVAs work well for endangered species prediction.
A typical example of PVA was carried out on an endangered species Fender's blue butterfly an endangered species (Schultz et al., 2003). However there is currently no scientific standard on how a PVA should be done.

Schultz, Cheryl B.; Hammond, Paul C. (October 2003). "Using Population Viability Analysis to Develop Recovery Criteria for Endangered Insects: Case Study of the Fender's Blue Butterfly". Conservation Biology 17 (5): 1372–1385.


text:
Physiological function of CFTR gene product?
I just need a clarification.
If I am to talk about the physiological function of the CFTR gene product? Then what should I do research and talk about?
The only physiological function that I can think of is the control of the thickness of mucus.
Is there any other ones?
On top of that, if i am to search for research paper for this topic. Do I just search for comparative study that compare the gene product in normal individuals and CF individuals in terms of mucus thickness?
Thanks

Have you read the wikipedia article on CFTR? It's usually a good start and has plenty of references.

I did. But I don't think it is good enough.

Have you read the answers of this: http://biology.stackexchange.com/questions/23557/functions-of-the-cftr-gene ?
E.g. it helps by absorbing salt after sweating.


text:
What is the most recent well-attested common ancestor of chimpanzees and humans?
Humans and chimpanzees are related and thus have a most recent common ancestor. Of course pinning down this precise point is essentially impossible, so I'm interested in close ancestors of this most recent common ancestor. Also, I'd like to know things about it -- how it compares to common chimpanzees, bonobos, and humans in various ways -- so species known only from fragmentary evidence are less interesting to me. Ideally I'd ask for something with at least one near-complete skeleton and a separate (perhaps less complete) find, but as a non-expert I'd be happy to settle for whatever is considered to be well-attested.
So, what is the most recent well-attested common ancestor of chimpanzees and humans?

Two reasonably close relatives of the most recent chimpanzee-human ancestor (CHA) are Sahelanthropus tchadensis and Orrorin tugenensis, but both are poorly attested.
One better candidate is Ardipithecus ramidus, which has a fairly-complete skeleton ("Ardi") among other fossils. It's a bit young (4.4 Ma), perhaps, to be a CHA but should be a close relative.
Another reasonable candidate is Oreopithecus bambolii. It is very well-attested. The trouble is that no one seems to know how it's related to humans; 'best guess' is that it's not actually an ancestor but a sister taxon.
(I'm not an evolutionary biologist, nor even a scientist, but I thought I'd leave what information I collected here as there is no better answer at this time.)

Welcome to Biology.SE. I know absolutely nothing about CHA! Can you please include your references. There is no problem if you collected these informations in none peer-reviewed articles, but still it would be good to show your references.


text:
How does anadromous fish physiology "know" to switch from salt to freshwater and back?
What mechanism allows anadromous fish (like salmon) to switch from salt to fresh water and back?  How does the fish "know" to switch its physiology and do other fish possess the biochemical machinery for this?  How difficult would it be to genetically engineer salt tolerance into a freshwater fish?

Osmoregulation is a homeostasis regulation mechanism followed by salmons to adapt on both salt and fresh water.

Osmoregulation is the active regulation of the osmotic pressure of an organism's fluids to maintain the homeostasis of the organism's water content; that is, it keeps the organism's fluids from becoming too diluted or too concentrated. Osmotic pressure is a measure of the tendency of water to move into one solution from another by osmosis. The higher the osmotic pressure of a solution, the more water tends to move into it. Pressure must be exerted on the hypertonic side of a selectively permeable membrane to prevent diffusion of water by osmosis from the side containing pure water.

In order to reduce the dehydrating effects of salt water, salmons drink several liters of water per day, but in fresh water salmons doesn't drinks at all. The only water it consumes is that which goes down when it feeds. When an ocean-dwelling salmon drinks, it takes in a lot of salt(NaCl), which exacerbates the salt-loading problem.
In fresh water, the salmon's kidneys produce large volumes of dilute urine, while in the ocean , the kidneys' urine production rates drop dramatically and produce a very concentrated urine.

Salmon use to deal with the NaCl fluxes driven by the gradients between the salmon and its surroundings. In their gill epithelial cells, salmon have a special enzyme that hydrolyzes ATP and uses the released energy to actively transport both Na+ and Cl- against their concentration gradients. In the ocean, these Na+-Cl- ATPase molecules 'pump' Na+ and Cl- out of the salmon's blood into the salt water flowing over the gills, thereby causing NaCl to be lost to the water and offsetting the continuous influx of NaCl. In fresh water, these same Na+-Cl- ATPase molecules 'pump' Na+ and Cl- out of the water flowing over the gills and into the salmon's blood, thereby offsetting the continuous diffusion-driven loss of NaCl that the salmon is subject to in fresh water habitats with their vanishingly low NaCl concentrations.
Reference

Reference


text:
Does our nose detect only if there is change in odor?
If I enter a room with certain odor, I can sense the odor. However, if I stay there for some time I cannot sense it anymore. A new entrant to the room can still smell it or I have to leave the room for some time and upon returning I can sense it again. Does our nose detect only if there is change in odor?

Senses in general adapt to continuous stimulation due to various processes. One such process is simply the exhaustion of the reserves of a receptor, or secondary neuron, due to a depletion of neurotransmitters. Entering a room activates a fresh pool of chemical receptors, thereby generating a clear sense of smell. However, this dims due to adaptation. Exiting and re-entering the room after a while revives the neuronal response. More central adaptive responses may also play a role. A comparable effect is seen in the tactile sense. For example, the awareness of wearing a ring or watch fades quickly. Changing its position revives the percept. So yes, sensory systems like olfaction and touch are more responsive to differential stimuli.


text:
What factors affect the likelihood of auditory stimuli causing arousal during sleep?
I've noticed that the sound of water drops makes me wake up from sleep but other more strong sounds don't make me wake up. I can't find anything about this. The only reason I can think of is maybe because the sound of drops is continuous. Is there any research about the qualitative aspects of certain noises that affect the likelihood of causing arousal  from sleep?

Virtually impossible for us to know why water drops wake you up when other sounds don't - so that's not a valid question - but there might be some resesrch on how and why people respond differently to different noise stimuli during sleep

I think this has the makings of an interesting question with relevant research to be cited. I went ahead and cast the last VTC but re-wrote it such that I think it can be re-opened. Now voting to re-open.

The other day I was reading "Sleep soundly every night,feeling fantastic everyday" by Robert S. Rosenberg.
Somewhere in the books it was written as:
"Sound: You need your bedroom to not only be cool and dark, but also quiet. If a dripping faucet or the barking of a neighbor’s dog is interfering with your sleep, try earplugs, earphones, or generating white or pink noise to even the sound field so your ears won’t focus on the background contrast of environmental sounds. There are machines available to do so, but for some the sound of a fan will do the trick. If your partner’s snoring is keeping you awake, you should encourage him or her to be checked by a doctor for sleep apnea. Treatment can improve your sleep and also might save his or her life."
by searching more I found out that the difference between the range of frequencies from moment to moment is a more important factor than a sudden loud noise.
The idea behind white or pink noise or the natural ones like the sound of fan is that they produce a broad range of frequencies at the same level.And by doing so they can reduce or at least mask the disruption.


text:
Effect of pupil responses on the electroretinogram
The electroretinogram (ERG) is a measure of electrical activity of the retina. It is typically recorded from the cornea with a wire electrode or gold-foil electrode. Generally, the the ERG is considered to reflect the retinal processing of a light stimulus, typically a photoreceptor response followed by secondary neuronal activity and electrical activity evoked by supportive Muller cells.
I am wondering if the pupil response will add signal on top of the ERG? Firstly, there is the direct pupil response, which causes the pupil to constrict when the eye is subjected to bright light. Pupil constriction may, perhaps, induce electromyogram (EMG) activity when the smooth sphincter muscle around the pupil contracts, which in turn could theoretically contaminate the ERG. Secondly, there is neuronal activity involved in constricting the pupil, as light is processed in the retina by ganglion cells that in turn drive the pupil reflex. Furthermore, there is the consensual pupil response as well. This response causes the contralateral pupil to constrict when the ipsilateral eye is subjected to bright light. The consensual response is mediated by efferent input from the brain following stimulation of the other eye and causes both eyes to restrict. Hence, neural input arrives in the contralateral retina from the brain. This activity is not directly related to the processing of the light stimulus and may disturb the ERG proper when ERGs are recorded with a flash and both eyes are open.
So my question is

Does a pupil-mediated EMG affects the ERG signal?
Does neuronal activity involved in the pupil reflex affect the ERG, for example the  efferent input involved in the consensual response?

I have had no luck after extensive searches in text books, Scopus, Pubmed, Google, Google Scholar.

Answer version1 (read the comments, I leave v1 for the those who can make the same assumptions in the future)
To answer the question we should clarify some general concepts and processes mentioned it the clause:

EMG is performed by means of direct placement of the electrode (the are two types here - surface-EMG and needle-EMG) on/into the skeletal muscles, this is why there is no such thing  "iris-sphincter-related EMG": the sphincter is inside the eye and there is no way to contact it without eyewall penetration somewhere. Thus, this part of the question is hypothetical.
ERG is performed after pharmacological mydriasis (pupil dilation to ensure retinal mass response or to perform multifocal ERG), so in the standard settings there is no substantial pupils reaction during the test. Thus, this part of the question is hypothetical too.
ERG measures electrical changes when one of the electrodes is directly attached to the cornea - here we should stress "to one cornea", and "reads" the current from only one side. This is why, the reaction of contralateral pupil, skeletal muscles, heart/defibrillator activity are irrelevant since they are out of the electrical loop existing between the electrodes (the second electrode is on the forehead).
ERG measures electrical activity only - there is no muscle contractions in the process, while EMG involves the time needed to acetylcholine to be released and muscle contraction to begin. This means that the time scopes of these tests are different. In addition, as stated, pupils react as an efferent organ (III nerve, mediator related), while retinal photoreceptors react directly to the light stimulation, so there is a clear delay between these two processes. Theoretically, one can perform full cut of the optic nerve with the resultant loss of afferent signal and consequent loss of efferent pupil reaction, but the ERG will still detect the normal curves if the photoreceptors are intact.

Back to question itself: according to the mentioned facts we should state that the question is more hypothetical and theoretical, thus answering it directly is problematic and the answer should not be assessed without facts mentioned above.
So, the final answer - 1+2: No, pupil reaction does not affect the ERG in the real and standard settings and should not be counted as an interfering factor.
Version2
I've found an interesting patent claiming that pupillary responses can contribute to eERG (electrical stimulus instead of light). These influences stated to be artifacts, thus the authors raise the question how to diminish/filter them out.
They say

Eye movements and pupil responses may contribute to the eERG;
Pharmacologic dilation abolished these pupil responses;
Bilateral artifacts, such as pupil responses, in the corneal eERG
  cannot be sufficiently reduced by using dilation drops; Even after
  dilation, a residual, but substantial electrical response persisted in
  the contralateral eye.

So, I should convert my answer to yes/yes. Taking into account the obscure nature of the subject, I hope you will agree that by making mistakes we can learn something new. I personally learnt a lot trying to answer this excellent question.
Patent application number: 20120143080 (if the link will be broken in future, one can find the patent by this number).
Direct link
http://www.faqs.org/patents/app/20120143080

I admire your detective work greatly. In fact, I am one of the authors on that patent. In this patent we are basically making guesses, but we have no answers. I left out any reference to electrical stimulation in this question at Bio.SE to make it more general applicable to light-evoked ERGs. Hence, although I cannot accept your answer, I have started a bounty which is yours to keep in 24 hours - as a token of appreciation (cannot give it away immediately).

@aliced I thought that pupullary elecrical stimuli are filtered out from regular ERG

@AliceD there is an amplifier and some filtering mechanism which should affect the noise in some way - I've read about that while searching information about ERG, but don't have a source now....

Never encountered any mention of filtering of pupil responses. A normal ERG a and b peak develop prior to the pupil response so timing may be brought forward, but not so on long-latency responses. Perhaps this discussion should be proceeded in chat when necessary. Thanks!

@AliceD If I understand you properly, we don't have sufficient sources to support both answers neither  "no", nor "yes".  What can we add to "no" answer is the fact that sphincter has constant tonic efferent current, which is why its consequent rise might be less influential on ERG... In addition, the current for dilator should in some way lessen the ERG curve of the sphincter...


text:
What is the biological age of grafted plants?
Suppose you graft a piece of an existing 'old' plant onto a host plant. Will the graft continue to grow having the same biological age as its parent? In other words, would the graft die at the same time as its parent plant? Or would the process of grafting result in some sort of rejuvenation of the grafted daughter plant? Or alternatively, would the host plant carrying the graft determine the biological age of the graft primarily?
PS: Personal experience-based (anecdotal) answers are more than welcomed

@J.Musser - wouldn't you happen to have a clue about this given your reputation of epic proportions on Gardening.SE :) ?

Funny I would stumble upon this and see your ping. Yes, I have done a lot of grafting and know what will happen, but I may not be able to find resources to back me up. It would all be experience. If that's fine, ping me, I'll answer. (ps: I like this question :P will vote it up when I get more votes (I am a heavy voter))

Also, if you ever need me, don't hesitate to ping my in a chat room. Basically, if the name doesn't autocomplete for ya, it won't ping. I'm almost always in our chat room, but if not, I'll be in GL's chat room.

@J.Musser - I'm not sure what you mean with more votes but I bountied my question - hit me without references! :)

I have answered a related but not identical question previously "Do trees age on a microscopic level?": http://biology.stackexchange.com/questions/2055

In my experience (in common with the experience of everyone I've talked to who could be considered an expert on the subject), taking old wood and using that as a scion when grafting new trees rejuvenates them, and they grow as new trees.
I'll take apple trees as an example. As you can see from the table here, there is a distinct age after which the tree begins to decline. Now, that's not concrete (I've seen some apple trees last over 100 years (didn't plant those myself btw)), but generally, an apple tree will lose vigor and productivity before it reaches 50 years of age. This tree's 'immune system' also goes down, and it becomes susceptible to many diseases. You'll rarely see such a tree, as orchardists generally replace them rather fast.
But to the point of your question. When you will graft an apple tree, you will generally bud graft it, as described here. That article (which is spot-on) says:

Select a healthy branch of this year's growth from your desired variety of tree. Look for a plump leaf bud about halfway down the branch. Leaf buds are close to the branch where fruiting buds tend to stand out more.

Note that it says nothing about the tree's age, simply stating that the wood must be healthy. That's because old wood/young wood produce the same result in the new trees. I was using a 40 year old razor russet to graft onto all the Malling V rootstocks I had for that variety. And of course they grew as expected, as a young sapling should. I've heard of a nearby nursery taking budwood from a 100 year old tree that still looked good.
Additionally, you can use a rootstock taken from an old plant, and also a scion from an old plant, and the new plant created will grow as a young sapling. Here's how the rootstocks I use are created: You cut down a tree at ground level, and it sends out a lot of shoots. You pile soil over it, but allow the ends of the shoots to stick through. These shoots will root into the soil, and can be cut at the base, and planted out for grafting later. This way, you can have 1000's of identical (cloned) rootstocks. You can also get rootstocks from old trees. Here's a diagram of the process.

About herbaceous perennials, I've found (to some people's surprise) the same thing. The scion grows as a young plant again once grafted. I found this out because I graft heirloom tomatoes onto hybrid tomato rootstocks (the latter are seedlings). Usually, the scions will be from seedlings, but at times I take the scions from a large mature plant.
Just so you know, an indeterminate tomato plant will, once mature, flower and fruit until frost. A determinate tomato variety will produce a large crop all at once, and then die back (this is the kind preferred by owners of mechanised (machine harvested) fields).
In my tests, you could take the scion from an old determinate plant that was through fruiting, right before it started dying back, and successfully use that for grafting the new plants. These new plants' growth was identical to the growth of grafted plants whose scions came from seedlings, and they began to flower and produce fruit at the same time. Of course, actual seedlings did not have the vigor of the grafted plants, and were behind in growth.
Off-topic for your question, but possibly still of interest, I've found that cuttings and layers (not scions) taken from old plants (both woody and herbaceous), and rooted, would grow as young plants again.

If you want expansion on any point, let me know.

THANKS! So, erm (I feel a bit overwhelmed :-), there is quite some jargon in there (which is absolutely totally fine! I love your answer) and I will have to re-read your MOST interesting answer a few times to grasp (when I have more time), but for now, can I warp your information to "Grafting rejuvenates the graft". In addition, Would you have any idea how the graft is rejuvenated (i mean, is this DNA level, or hormonally regulated etc?)? The latter question may be worth a new question, though :) Thanks again!

@ChrisStronks I could research that for ya.

@ChrisStronks Does this answer your new question?

@ChrisStronks Here's a related thread (by me) that may interest you: http://biology.stackexchange.com/questions/2050/why-do-some-trees-have-a-life-span-while-some-dont

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


text:
Effect of flask position in shaking incubator affects growth kinetics
During some cultivation experiments for my bachelor thesis I noticed that in liquid culture my bacteria (E. coli) grew differently, according to the position in the shaking incubator.
Because the goal was just to induce protein expression at a given OD, I altered the position of the flasks in the shaker, so the cultures were at a similar OD and I could add the IPTG to all of them at the same time.
Now I wonder if someone else noticed this phenomenon (Literature to cite would be great, I couldn't find anything until now) or if I did something wrong. Maybe it's also known and ignored for longer times?
The cultures more in the back of the incubator grew faster, so I think it's because of temperature alterations when opening the incubator to draw samples for growth kinetics, but I'm not sure about this at the moment.
Thank you for helping me :-)

Is it possible, that there are different amounts of shear stress involved in different flasks? Cells can die due to shear stress, and E. coli is possibly more sensitive to shear stress than a gram positive bacteria.

No offense, but how reliably are your OD measurements? I noticed that there can be some difference, depending on where in the fask you take a sample. Also when you stop the incubator to take samples, cells start to sediment. This can influence the measurement for the later flasks from which you took samples.


text:
Why does sex last so long?
I wonder why (especially human) sex lasts longer than just a few seconds?
My thought is that the shorter it takes a man to ejaculate, the lesser is the risk that he gets interrupted by a rival or a predator. Therefore, men who ejaculate quickly get an evolutionary advantage in the long-term.
But, as human sex lasts several minutes, I'm obvioulsy wrong with my argument. Anybody knows why?

there is probably an element of recreation into your procreation argument, which can contribute towards this.

If male sexual performance / stimulation / duration affects females in terms of things related to fertilisation (immune systems, gene expression etc.) Then there is possibility of selection for duration

I think it is rather a cultural thing to prolong ejaculation.

For a great many men, sex does not last longer than just a few seconds. This seems as good an explanation as any I've ever seen.

It's also entirely possible that there are physiological constraints on the reproductive system as it happened to evolve that necessitate a certain minimal duration of sex.

@anongoodnurse "A few seconds" is below the 2.5 percentile as estimated here. The median they obtained was 5.4 min.

@har-wradim - 500 couples (250 men) is not many for a study. Even if it were that low (which I seriously doubt), multiply the number by all men having intercourse and that is still a great many men.

@anongoodnurse Why should we multiply? The question addressed was about boundaries of the norm and how to define pathology. What's the base for your pessimistic claim? By the way, those observations are also related to seaotternerd's idea: "a few tens of seconds" is physiologically possible, but for modern humans it is certainly not normal.

Females might select males who are more durable in sex. Or maybe men who were more durable in sex had a direct advantage, like better semen or maybe causing female orgasm (which is said to upsuck semen into the cervix). But as humans lived in societies, the scenario of being interrupted by a predator was minimal. By a rival... well, probably cheating was not a common thing. Or maybe strict monogamy was not so common.

There are plenty of animals with brief procreative periods, as you suggest. In chimps, sex takes 10 to 15 seconds - much less time than humans. So the question is really why have humans evolved to be different?
I don't think any of the answers based on fitness are particularly compelling. It's not like sex feels like running a marathon or less physically fit people can't manage to ejaculate in their partners so it seems unlikely that the lengthy sex act serves to distinguish fitter individuals.
Instead, I think the difference probably lies in the pair-bonding role of sexual activity. Humans form unusually long-lasting, typically monogamous or largely monogamous, bonds that function to provide the support needed during the lengthy childhood that humans undergo. The prolonged, and highly pleasurable, sex act likely functions to help maintain these bonds in order to keep the couple together and provide the stable support needed to maximise the chances of successfully raising a child to adulthood.
Unfortunately, to the best of my knowledge, there is no high quality empirical evidence that would convincingly answer the question so any answer must be somewhat speculative.

I'm going to give a tentative answer full of speculation and guesswork, but it's too long to fit in a comment so here goes.
Sex duration is possibly a sort of human reproductive handicap. Sexual arousal can soften the cervix, increasing fertility during lengthy sex sessions. Lengthy sex exposes them couple to predators and takes time and energy, so if you have the calories to burn you are probably a better mate.
The more orgasms a male has had in the recent past the longer the average sex session takes to ejaculation. This kind of makes sense as an adaption strategy to different frequencies of sexual intercourse (if less sex happens it's more important to ejaculate quickly, if more sex happens you want to get as much fertility out of the sperm you produce as possible).
Comparing testicle size and penis size to other primates, humans have a large penis and relatively small testicles(compared to chimps, say) which implies we spend more energy on the sex and less energy on the ejaculation than chimps. It also implies a lower sexual frequency or smaller ejaculate sizes or larger vaginal depths or really a number of other things.
The whole system kind of makes sense. Long sex durations are a sexual handicap system to show the fitness of partners, which are rewarded with slightly higher fertility. The whole post-sex evolutionary mechanism thing is a layer on top of the underlying mate selection which is beyond the scope of a book, nevermind a stack exchange answer.
That's probably at least a little bit wrong. The handicap principle isn't super well accepted as a general evolutionary principle, even though it explains some things.

-1. For the handicap principle to be valid, potential partners should have a way to distinguish the duration of sex length prior to mating. This doesn't appear to be possible. If partners are unable to distinguish the length prior to mating, no sexual selection takes place.

I think you misunderstand. The selection is performed by the cervix, not by the partners. Longer sex durations (weakly) imply a higher sexual frequency and that in turn (weakly) implies higher fitness. A partner that has a great deal of sex is a good partner, because your offspring are likely to have a great deal of sex. If a sex act lasts a long time, the cervix is interested in increasing the per-sperm fertility for this surprisingly lengthy sex act.


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How many eukaryotes are there on Earth?
I have been reading:

William B. Whitman, David C. Coleman, and William J. Wiebe, "Prokaryotes: The unseen majority", Proc. Natl. Acad. Sci. USA 95, pp. 6578–6583, June 1998.  [Full Text] [PDF]

wherein they estimate the number of prokaryote cells on Earth to be of the order of $10^{31}$.
I can't seem to find any equivalent data for eukaryote one-celled life. Are there any estimates for the number of one-celled eukaryotic living things on Earth? Do any other estimates confirm or tell against the reference I have cited above?

Could not fit in a comment....
To make sure we all understand your question...
Is your question how many (eukaryote) species are currently living? or How many (eukaryote) cells are currently living??
Just a hint to answer the question
Micheal Lynch, in his book (On the Origin of Genome Architecture) at page 3, Box 1.1 tries to answer the question How much DNA is there on earth?. He ends up with an estimation of a total length of DNA on earth of $10^{24}$ km for procaryotes, $10^{25}$ km for eukaryote (of which $\frac{1}{1000}$% is accounted to humans). This sums up to a total DNA length of $10^{12}$ light-years, or 10 times the diameter of the known universe!
In his calculations, he estimates that the total number of procaryote cells at $10^{30}$ (citing Whitman et al. 1998 as you did). He estimates the total number of eukaryote species to $10^7$, i.e. 6 times the number of known eukaryote species. However, he doesn't directly give any reference for this estimate but he refers to different chapters in the book that contain lots of references.
...I hope that helps...

"How many eukaryotes cells are currently living?? or How many eukaryotes cells are currently living??" It's how many cells are currently living, so your reference is indeed helpful, thanks.


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How often does bacterial transformation happen?
I have been reading:

M. Dröge, A. Pühler, W. Selbitschka, "Horizontal gene transfer among bacteria in terrestrial and aquatic habitats as assessed by microcosm and field studies", Biol. Fertil. Soils (1999) 29 pp221–245  [PDF]

I am not a biologist and am trying to get a feeling for how often prokaryotes make changes to their chromosomal DNA.
How often is plasmid DNA successfully incorporated into chromosomal DNA?
I would like to estimate either the number of gene changes (or, failing this, base pair changes) that a bacterium makes per unit time. Or, equivalently, the mean time between such changes.

Transformation underpins a lot of lab modern projects.
This will be a very unsatisfying answer, and this wikipedia entry explains why. The time, and success, of bacterial transformation of competent cells varies greatly depending on a few things mainly:

the length of nucleic acid sequence for insertion (or more accurately, the plasmid)
the species of target organism (or more accurately, the genotype of the target organism)
a host of other things

With a specific plasmid and organism you would be able to get a more satisfying answer, but I imagine the answer would even differ from lab to lab.
I worked with a microbiologist that provided me with a protein as a part of my honours project, and I can give you a broad impression I got from them: it does not happen often. Sometimes none of the cultures you are trying to transform will incorporate the new sequence into their genome, other times the cloning process goes very well and all your cultures will be transformed successfully. For our project, valid colonies only presented after a week with reasonable success (more than half the attempts were successful). But you don't know if the transformation worked until way after the first transformation happened.
The mechanisms behind this are grossly understudied. If we take some thing B. subtilis, arguably the most academically studied organism in the field of transformation, it can take up the DNA as food or incorporate it into its genome but nobody knows exactly how this happens at a molecular level (Chen & Dubnau, 2004)

Chen, I., & Dubnau, D. (2004). DNA uptake during bacterial transformation. Nature Reviews. Microbiology, 2(3), 241–9

Thanks, this is fantastic! I mean, it's not a satisfying answer as you say, but it is great to hear from someone who has some qualifications in the field. My lay impression too was that these things were greatly understudies. Many thanks again!


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Phospholipid movement in cell membranes
What causes phospholipids to flow so quickly in cell membranes? In Biology by Cambell et al. they state that a phospholipids can travel up to 2 micrometers per second. Is that a random movement or has anyone found that phospholipids have a current?

There must be charge considerations in the movement of molecules in the lipid membrane. There is also a consideration that some species of phospholipids will migrate to portions of the membrane with sharper or smoother curvature.
Waves of electrical potential can propagate along a lipid bilayer as well, which is very important to nerve axons and extended structures like that.
In general though the membrane is held together by vanDerWaals forces like other non-polar solvents.  As such, the movements of lipids and proteins and other amphipathic molecules in the membrane are still largely Brownian (random) in the 2D surface of the membrane.


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Synthesis of immunoglobulin Fab fragments: Where can I learn about Fab?
I wanted to know the chemical reaction involved in Fab synthesis. I looked everywhere for it. No luck. I know I will find it here.
All I know for now is:
Fab is a monovalent fragment that is produced from IgG and IgM, consisting of the VH, CH1 and VL, CL regions, linked by an intramolecular disulfide bond.
Molecular basis of Fab will make more sense.

For the generation of Fab-fragments antibodies, (possibly genetically modified) which can be made in large quantities by cells or animals, are used. Antibodies as a whole are not synthesized.
The Fab fragment is obtained from antibodies using the enzyme papain, which cleaves the antibody over the disulfide bonds in the hinge region. This results in two Fab fragments (which contain the antigen binding sites) and one Fc fragment (which contains the constant region of the antibody). See the image (from here):

If you want to go further into the topic, read one of the references below.

Preparation and separation of Fab and Fc fragments from human
immunoglobulin G with papain digestion
Fragmentation of IgG Using Papain

FAbs are genetically engineered and not organically synthesized as such. This PNAS article nicely describes the construction of a phage (virus) library to generate a large amount of different FAbs and screen for FAbs with the wanted epitope (antigen) affinity: http://www.pnas.org/content/95/11/6157.short


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Why the name coined for MARKUP LANGUAGE for SBML?
I'm get the confusion about  SYSTEM BIOLOGY filed.  SBML is refer to as SYSTEM BIOLOGY MARKUP LANGUAGE why we should called as MARKUP LANGUAGE? In HTML,XML and other field Mark up language mean particular function is declare into the Angular bracket like <H1> for Heading Tag this is displayed on the browser. Markup Language was actually developed for Wep application.
In other words, MarkUp language only displayed what we want., not display the simple mathematical function. Like, I need add function 1 + 1 which is display on the browser Markup language is not add, which is done by the CGI programming Like PERL,PYTHON, javascript.
So, in SBML(System Biology MarkUp language) Tools are not only display the what we want it? and It is not run on the browser? So why we called it is MarkUp Language?

I'm thinking you would do well to move this over to either the Computational Science or Programmers SE page. I down voted because of that. I think it is a good question. Just posted in the wrong location.

This question appears to be off-topic because it is not about biology.

SBML follows in the same vein as XML, in that it provides a standardized and flexible method for structuring information. XML and its ilk aren't just for making web pages, they're for sending structured datasets between systems and programs (in fact, XML is a fairly common configuration format). Why? Because the structure makes parsing simple (well, simple-ish).
BTW, markup languages were not invented for the web, HTML was far from the first one. The origin of markup languages is typesetting and in fact one of the most common uses these days is still in writing papers (ask a local math/physics/CS person what he/she uses to write papers and the answer will be Latex...a markup language).
Edit: BTW, this really has nothing to do with biology and you could have at least read the wikipedia page on what a markup language is.


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Dawn simulation - does color change affect waking up?
just curious. Are there any works or research results related to the influence of light color used for dawn simulation? I mean those wake-up lights which try to simulate dawn to make waking up better for you.
The cheap ones only use one color - those "warm white" LEDs - and only change brightness. However the more expensive ones also change color like the sun during sunrise.
I am just curious how much important could be the color change. :-)
thanks


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Do blind people learn Braille equally fast as the sighted?
The visually deprived brain undergoes extensive remodeling due to cross-modal plasticity. This leads to increased areas of the cortex being available for other purposes such as tactile processing. Now I am wondering if there is anything known about how long it takes for the blind to learn Braille as compared to normally sighted people?

I have had a very difficult time finding information that was well-written and what you were looking for. So, I did my best!

From what I have read it takes about four months - everyone is a little bit different and some take longer! Those of us with no visual impairment that try to learn it have no advantage and maybe a slight disadvantage with learning it... I know because I am trying to learn it. It does take a lot a patience and perseverance!

This is the article I referred to:
Learning braille; how long does it take and does it get harder with age?

Hope this was helpful!


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Does the tannin level in plants go down or up after they die? Or does the tannin level stay the same regardless?
Does the tannin level in plants go down or up after they die? Or does the tannin level stay the same regardless?
As they decay, do they release more tannins or does the production stop?

What do you mean about go down/up?

Well maybe I'm confused, but do plants not produce tannins? If they do does the production of the tannins stop after death? Does the level of tannic acid decay as the plan dies/Decays?

Well maybe I'm confused, but do plants not produce tannins? If they do
  does the production of the tannins stop after death?

That depends on how you define death. Tannin is secondary product, so I don't think the plant cells will produce more tannin when they are starving probably because of cutting off the leaves, roots, etc... when the plant dies. The plant won't bother to degrade tannins (I guess it does not even have the pathway necessary to do that), because it is a defense mechanism against insects, mammalians, etc... and not an energy storage material. Tannins can be degraded by microbes, heat, UV radiation, chemical reactions, etc... So if you can't protect the tannins from all of these then they will degrade. (Note: you can't, all you can do is slowing down the process.)

Exactly, what I was looking for. I wasn't sure exactly what would happen as a plant dies or ages. So tannins are like an inevitable process of ageing, you can't stop the Loss but you can delay the process.

@user3061879 I don't think tannins have anything to do with aging. It is for protection against animals. They have a decay rate, so the plant has to produce them life long. Producing tannins is costly, so many plant produce less tannins and rebuild leaves faster, so the amount of tannins depends on the species. http://link.springer.com/article/10.1007/BF00380050#page-1


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Ultra Pasteurization and Pasteurization
What is the effect of pasteurization and ultra-pasteurization on proteins, enzymes, and nutrients found in milk and other dairy products?

This is an interesting question and it is rather hard to find reliable information. According to a review which also did a meta analysis of all available articles, pasteurization (and also ultra pasteurization) affects the vitamins to some degree.
According to the analysis, vitamin B1, B2, B6, B12, C, E and folate decreased. The author notes however, that with the exception of vitamin B2, where milk is an important dietary source, the other vitamins are not included in very high concentrations. See the first paper for all details.
These findings are supported by another review (see reference 2), which shows some values in table 4:

This study finds proteins and amino acids not affected to a measurable degree, but data on protein behaviour is missing. My guess is that a part of the proteins are denaturated, but not all of them. There is some research which analyzes the effect of thermal treatment on milk in connection with other processes like the yoghurt or cheese production (have a look at reference 3). I haven't found any data on the proteins in milk which is directed to human consumption.
References:

A systematic review and meta-analysis of the effects of
pasteurization on milk vitamins, and evidence for raw milk
consumption and other health-related outcomes.
Which Milk is Fresh?
The Effect of UHT and VAT Thermal Processing Systems on Whey Protein
Denaturation and Gel Strength of yoghurt


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Hardy Weinberg problem help!
The three common genotypes at the hemoglobin locus have very different phenotypes: SS individuals suffer from severe anemia, AS individuals have a relatively mild form of anemia but are resistant to malaria, and AA individuals have no anemia but are susceptible to malaria. The frequency of the S allele among the gametes produced by the first generation of a central African population is 0.2.
(a) Assuming that mating occurs at random, what are the frequencies of the three genotypes among zygotes produced by this population?
I know that this is 0.2 for the S allele (q in the hardy weinberg equation)
and 0.8 for the A allele (p in the hardy weinberg equation).
So for the frequencies I got
AA = 0.64
AS = 0.32
SS = 0.04
(b) In this area, no SS individuals survive to adulthood, 70% of the AA individuals survive, and all of the AS individuals survive. What is the frequency of each of the three genotypes among the second generation of adults?
I don't know how to do this! I don't understand what to do! I tried multiplying
0.64 by 0.7 (because only 70% survive), but I know that is wrong answer. I know you have to divide 0.64 x 0.7 by the total that survived, but I don't understand why you have to do that. You didn't have to divide for part a, why do you have to divide for part b?
Also for some reason the frequency of the AS is not 0.32 for the answer. I don't understand why! Please Please help me.
(c) What is the frequency of the S allele among gametes produced by these adults?
I dont know this either!
PLEASE EXPLAIN ALL OF THIS TO ME IN CLEAR STEPS! THANK YOU SO MUCH.

Your answer to a) is correct (standard Hardy-Weinberg equation).
For b) you have to consider that you are calculating proportions of the population, which should sum to 1. Since 30% of the AA individuals and all SS individuals die, this is not the case after selection, which is why you should divide the frequencies by the total proportion that survive (also for the AS genotype), such as:
$$
\begin{array}{c|cccc}
\text{genotype} & \text{freq before} & w_{survival} & \text{freq after selection} & \text{corrected freq}\\
&\text{selection}&&&\text{after selection}\\
\hline
AA & 0.64 & 0.7 & f(AA)\cdot w_{AA}=0.45 & 0.58\\
AS & 0.32 & 1 & f(AS)\cdot w_{AS}=0.32 & 0.42 \\
SS & 0.04 & 0 & f(SS)\cdot w_{SS}=0.0 & 0.0\\
\text{sum} & 1 & & 0.768 & 1
\end{array}
$$
here $w$ is the fitness of genotypes. And for your comment on why you didn't have to divide by the sum of freqencies in a): you could do this, but since the sum of genotype frequencies is 1 it doesn't make a difference.
For c) you use the standard formula for calculating allele frequencies from genotypes, so that $f(A)=f(AA)+f(AS)/2= 0.79$ and $f(S)=f(SS)+f(AS)/2= 0.21$.


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Nucleosome wrapping direction
Does anyone know which direction the nucleosomes are wrapped? I wonder:

Relative to the B-DNA double helix twist direction (right-hand)
Relative to the neighbor nucleosomes. Do they alternate to prevent supercoiling?

B-form DNA is wrapped around histones in a left-handed manner resulting in a left-handed solenoidal superhelix (see that, that and this). The reason for this wrapping is that it reduces the helical tension. This post has more information about DNA helical tension. Also note that exceptions exist (i.e. right-ended direction) especially for histone at the centromere as described in this paper.
For your second question, the exact way nucleosomes are then arranged to produce the chromatin fiber is, as far as I know, still not fully understood but the most accepted model is a zigzag arrangement (Woodcock CL & Ghosh RP, 2010 and Grigoryev SA & Woodcock CL).