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What's the minimum distance of focus for the lens of a human eye to reach maximum flatness?
According to the Wikipedia article on eye accomodation, the range in which a human eye can focus is from 7 centimetres away up to essentially an infinite distance. Of course, people can't see things an infinite distance away, but at a certain point the light reflected off an object will come at the eye in effectively parallel paths.
As an eye focuses on objects progressively farther away, it seems to me there would be a point when the lens hits maximum flatness, after which it everything will be equally sharp in focus. Looking at an object 500 metres away or 1000 metres away probably doesn't require any change in the lens. However, going from one metre away to seven requires the ciliary muscles adjust to just the right amount.
My question is, what is a normal minimum distance from the eye at which the lens will reach maximum flatness? Everything else in this question is just for context, so an answer to this, stated in metres from the eye, is all I am seeking.
The article I linked to above mentioned the human eye seeing "13 dioptres", and I have tried to understand dioptres, but it's a little confusing for me. If I understand correctly, the higher the dioptre, the closer you focus, so the 13 dioptres refers to how close the human eye can see. If I have this backwards, please let me know.
In any case, my purpose in asking is to determine the range in which ciliary muscles would be required to do more nuanced work in order to hold the lens at in the right shape. Focusing on something 7 centimetres away, the ciliary muscles are at maximum exertion, and at a certain point and beyond the ciliary muscles are completely relaxed. To hold somewhere in between would require more subtly nuanced, and, I suspect, more difficult work on the part of the ciliary muscles.
At least, I assume that to be the case because I am hypothesizing that the act of contraction for the ciliary muscles would be similar to other muscles. For example, it is easier to do a bicep curl with weight when going from full resting position to maximum contraction, as opposed to stopping at a particular spot somewhere in the middle of the motion. To stop mid-motion requires more muscle control, and, depending on how fast you wanted to do it, can be difficult to be exact.

I'd like to answer your question but as usual in one question you have at least three: what is the diopter, what is the range of accommodation, what is the amplitude of accommodation, near point of convergence etc. In such a scenario (as we saw in previous question) you cannot get acceptable answer, so, probably, you should focus your question more...

@Ilan pun intended?

@Michael could u elaborate?

@Ilan "you should focus your question more"

There are practical questions in ophthalmology and you've asked someone that has a common theoretical answer: 6 meters.
However, you should know that from the same theoretical point the far the object the less accommodation we need, so the second answer is - infinity.
What is the difference? From the practical point the accommodation between this two points is negligible and does not have to be taken into account when we correct the refraction error.
Small theory - to see an object placed at a distance of 1 meter we need 1D of accommodation power (1/1meter=1D), to see an object placed at a distance of 30cm we need 3D of accommodation power (1/0.3meter=3D), for an object at a distance of 10cm we need 10 diopters and finally for an object at the distance of a 6 meter we need accommodate 0.16 diopter.
Thus between 6 meter and infinity the accommodation is very low and this is why the distant visual acuity is checked at this distance. Consequently, the lens convexity difference between 6 meters gaze and infinity is negligible and this is why the answer to your question is between 6 meters and infinity (zero accommodation).
From this explanation you can calculate the dioptric add for any reading distance  and understand how the reading spectacles correct the loss of accommodative power (=presbyopia, the vision of older people).
If you want to know how much the crystalline lens changes its dimensions during accommodation, the answer is near 7% for diameter and near 10% for thickness, so the lens as was convex, stays convex and the visible changes are minimal.


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How is insulin transported in vivo in mammals?
What is the mechanism for transport of insulin in mammalian cells?

Do you mean how does insulin get secreted and absorbed? The insulin gene stays in the DNA in the nucleus, just like all other genes. Have you read the Wikipedia article on insulin? It has a lot of information that should help you understand the pathway. If you have more specific questions, please [edit] your question and describe them in detail.

The process is described here. This is my summary, plus a few extra details:
The primary gene product of the INS gene is preproinsulin. As the N-terminal signal sequence (pre-) emerges from the ribosome during polypeptide elongation the signal sequence binds to a signal recognition particle which arrests elongation until the nascent chain has engaged with the translocation apparatus in the membrane of the endoplasmic reticulum (ER). The preproinsulin polypeptide is translocated across the ER membrane in a cotranslational process, and the signal sequence is cleaved off by signal peptidase.
The proinsulin molecule folds in the ER lumen, assisted by various chaperones and, in particular, by protein disulphide isomerase, which ensures that the correct disulphide bonds form. The correctly-folded proinsulin polypeptide is exported from the ER in COPII-coated vesicles which deliver it to the Golgi. At this stage the proinsulin is cleaved by furin-type proteases (pro-hormone convertases; cleave at pairs of basic residues), removing the internal C-peptide (pro-) and after a little C-terminal trimming, leaving the insulin A and B peptides covalently attached via disulphides. This is mature insulin.
The mature insulin leaves the Golgi in secretory vesicles. Since insulin secretion is regulated, these vesicles do not fuse with the cell membrane constitutively, they are stimulated to fuse by a Ca2+-dependent signalling pathway. Vesicle-membrane fusion is mediated by SNARE proteins. At this stage the insulin has been released from the pancreatic β cell. Notice, however, that the insulin has been extracytoplasmic since it was translocated into the ER: all other steps in the transport process are achieved by rounds of vesicle formation and fusion.

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How do I calculate the change in allele frequency in a haploid population under selection?
From this book

For simplicity, let us consider a haploid organism and assume that the frequencies of alleles $A_1$ and $A_2$ are given by $x$ and $y=1-x$, respectively. We also assume that the fitnesses of $A_1$ and $A_2$ are $w_1 = 1$ and $w_2 = 1-s$, respectively. In this case the mean fitness $\bar w$ is given by $x + (1-x)(1-s)= 1-sy$, and the allele frequency change per generation becomes
$$\Delta x =  \frac{dx}{dt} = \frac{sxy}{1-sy}$$

If I would have to find what $\frac{dx}{dt}$ equals I would use the Wright-Fisher equation and find that:
$$\frac{dx}{dt} = \frac{w_1 \cdot x}{\bar w} = \frac{x}{1-sy}$$
, which is obviously not the same result as what the author found...
What am I missing? How did the author find out this result $\frac{dx}{dt} = \frac{sxy}{1-sy}$?

Recheck all the equal signs in the second equation (looks strange).

Well that's just reformulate the same equation differently. I got rid of everything in the parenthesis hoping things seem more clear. I edited some other stuff hoping things are clearer. Thanks for your help @fileunderwater

Hey remi, given your info I've managed to derive the answer. Check my answer below and ask me if you need any extra explanation, this is important since I gave you an answer but I am still unsure how you went wrong.

Here's a simple consistency check to show that $\Delta x = \frac{x}{1-sy}$ can't possibly be the right answer: in a pure monomorphic $A_1$ population, there obviously cannot be any change in allele frequencies through selection, so $x = 1$ should imply $\Delta x = 0$. Your formula, however, yields $\Delta x = \frac11 = 1$ in that case.

Ps. As a mathematician, I'd like to register my objection to using the notation $\frac{dx}{dt}$ for "allele frequency change per generation"; it properly denotes the rate of allele frequency change over time (presumably in a continuously breeding population, for such a rate to be well defined). Even if we measure time in (average) generations, it's not hard to come up with examples where the two are not equal.

Here is my full derivation to the book example you gave, hopefully it'll help you clear up what went wrong:

You need to remember that after there is selection acting on the population, you no longer have a total of 1 after selection. Think of selection as "killing" individuals, which means the total is now 1 minus what has been "selected out". sy is what is selected out, therefore the new total is 1-sy. Which means you now divide each of your frequencies by 1-s*y (see picture).
Please comment if you need more explaining.

Ok, I totally understood my error. That was very simple. Thanks a lot for this good explanation.

The great thing is that you've grasped the "hardest part" in population genetics modelling. The procedure, of breaking down the steps via table and normalising, is the same procedure for diploids but instead of A1 you have A1B1, instead of x you have 2pq, where p is f(A1) and q is f(B1)), after selection A1B1 is simply 2pq - s(2pq), etc. Even if model multiple separate loci, and where each locus may have >2 alleles, just: (1) tablate all possible genotypes as columns, (2) tablate the frequencies at each stage of the life cycle, (3) and make sure to normalise if there is selection. :)

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How do beneficial features evolve in species without progressing through detrimental stages?
I'm thinking in particular of wings on birds that would - I'm guessing - have to progress through stages during which they confer no particular advantage. Or is it that all evolved features must have followed a path of incremental benefit therefore imposing a fundamental limit on what evolution through natural selection can "achieve"? (features that are not beneficial while gradually appearing cannot be evolved)

I thought i'd mention a thing about recombination, not as an answer since it's too short: two individuals may posses radically different sets of alleles if they have been part of lineages that have not had much contact (e.g. tribesmen of africa vs. urban dwellers) once they mate, alleles that have never met before may co-operate in a way that could lead to drastically novel features. Features that are due to the combination of alleles already existing but whose phenotypic output is entirely novel.

Features can evolve (or change already present features) which have no negative effect under the current conditions. You can very well have neutral changes which have no purpose. They can then prove positive later (or in a different environment). Changes are usually small and take place over very long time periods.
An example would be bacteria which mutated one of their enzymes for a energy pathway. Before the mutation the enzyme could only metabolize nutrient A, after it, it is a bit less specific for A, but can also metabolize B. As long as the living conditions are so, that only A is present, this will not change anything. If the conditions are so, that A and B are present and A gets limited, these cells will have a profound advantage over cells, which can only utilize A.

I see. So wings appeared through neutral changes in biped reptiles without going through detrimental stages? And more generally, the "path" of features never goes through detrimental stages - only neutral and beneficial?

There are some interesting hypotheses that wings initially evolved for display, not flight.  Then at some point, the winged dinosaurs also had a locomotive advantage, at which point the wings could further evolve with selection for even better locomotion and eventually full flight.
Here is an article about Darla Zelenitsky's work on this:  http://phenomena.nationalgeographic.com/2012/10/25/bird-mimic-dinosaur-hints-that-wings-evolved-for-show-not-flight/
There is also an article by Richard Prum in a recent Scientific American that mentions this.https://www.scientificamerican.com/article/dinosaur-feathers-came-before-birds-and-flight/


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How did the first sexual animal come to exist?
I am more or less familiar with the evolution theory based on mutations.
Now, starting with a nonsexual being, how did the first organism that reproduces sexually come to exist.

Your question is too broad. It won't be possible to provide a precise answer to such a question. Please add details to your question to make it more precise.

I think this is answerable - you need to look at fungi though.  animals did not invent sex. will try to put up an answer tomorrow if someone else doesn't.

related: Evolution from Mating types to different sexes

Big topic yes, but lets hit some high points.
First, sexual reproduction is a no brainer in evolution.   In its basis, sex only requires a segment of the chromosome to be heterogamous - that it will not be recombined.  In male humans this is both X and Y chromosomes, in other animals it is the female which has heterogamy.  Its not the entire chromosome either - the pseudo-autosomal regions of X and Y in humans do recombine.
Sexual reproduction allows some individuals to combine their genomes by donating some but not all chromosomes to offspring. The heterogamous regions are always donated by one parent and the same sex is not allowed to combine with others.
Sexual reproduction is found in plants, single celled eukaryotes as well as animals.  The forces that drive the emergence of sex show up frequently enough and are persistent enough for sexual chromosomes to have evolved hundreds of times in plants.
Even in animals, where asexual reproduction is very rare there are multiple configurations of sex determining chromosomes.
Sex goes back to a very ancient trait in eukaryotes related to the haploid / diploid life cycle.  In fungi, who are related to the original metazoans, sex shows up when its needed.  There the combination of haploid phases may be limited by more than one combination of specific elements.  Fungi can have many genders (mating types) - each of may only allow mating to specific types.  Others like Saccharomyces allow recombination between any two different mating types.
The earliest single celled eukaryotes related to animals show mating types.  The various sexual characteristics related to sexual reproduction, such as placentas, eggs, sperm form
and function are all embellishments from sexual selection which vary tremendously from one form of animal to another.  The chromosomal functions which became sexual traits are ancient and predate metazoans.  They are not necessarily conserved though - they are simple enough to reproduce that they change their characteristics often in evolutionary history.
I should say that all this doesn't apply to bacteria and eubacteria.  Why?  Because bacteria are much older and have their own systems of gene transfer and recombination with their own rules.  They usually have a single copy of their genome (I'd like to hear about exceptions - I think I know of maybe one) which makes quite gender different.  The do have something called 'sex' where a pili gene can be found on a plasmid which allows the bacteria to transfer DNA directly, which is like a sex determining locus.  But a bacteria may catch gender like a cold - it can not have it, it can get it, it can lose it.
Bacteria are also capable of transferring a single gene or a segment of DNA by various means, including pili, plasmids, phage, and simply taking in the naked DNA that they find laying around.

I’m not sure I would agree with “no brainer”. As far as I know, sexuality has only evolved once. Also, could you expand a bit on the heterogamy argument? In particular, wouldn’t the same apply to plasmids? Yet we don’t see anything particularly resembling sexual selection emerge from that. /EDIT: Your answer might actually contradict my first assertion (I should have read the full post first) – I’m still interested in an answer to the second.

you can argue the terminology, but i do have references saying that sex has evolved independently several times in plants etc, so i'll leave that to you and the authors or to post to your answer. I've added a section on bacteria. sex in bacteria is more of an analogy than a correspondence from what i know.  The question focused on animals originally.

Actually your text already convinced me, concerning the number of times sex evolved (hence the edit).

This is a very broad field, with many complementing, overlapping, and contrasting theories. I suggest that you read this part of the Wikipedia article on this topic:
http://en.wikipedia.org/wiki/Evolution_of_sexual_reproduction#Origin_of_sexual_reproduction
Here is what I got from the Wikipedia article (this is just one hypothesis, read the article for all the others):
There are many advantages to sexual reproduction, two main ones are greater genetic variation and recombinational DNA repair (occurs during meiosis).
There are certain species that can reproduce both sexually and asexually. They choose to reproduce sexually during times when the environment is uncertain (changing). This provides evidence that greater variation is one reason for sexual reproduction.
Asexual organisms only have one copy of each gene, therefore if this copy is mutated in a bad way, they are out of luck. Organisms that sexually reproduce have two copies of each gene, when one goes bad, they can use the other copy to repair the original copy, during meiosis.
As you may know, stress has many harmful effects, one being that it leads to DNA damage. There are certain species of bacteria who, in response to stress, uptake/integrate nearby bacteria cell's DNA into their own. They can then use this new copy to repair their own copy in case they experience DNA damage.
This "trait" of up taking/integrating other's DNA may have been evolutionary selected for (because these organisms repaired their DNA, they survived and passed on their genes), therefore eventually leading to organisms that sexually reproduce.

I’ve had to edit your answer, “just one theory” sounds a bit too similar to the “just a theory” creationist canard for comfort. I’m wary that it might feed the common misconceptions about what makes a scientific theory.

I fully support your edit, that was a nice catch :) Thanks Konrad.


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Could mating/recombination be responsible for evolution of entirely novel features?
The diploid chromosomal architecture is rather interesting. For example, because of diploidy we Humans have to mate. Of course in that sense, because diploid organisms often have mate, this has led to emergence of sexual organs as novel features etc.
But, what I am interested in, is the prospect of recombination and mating being able to lead to drastically novel evolutionary traits.
For example, if a remote tribesman from the Pygmy peoples of Central Africa were to mate with an urban dweller, one theoretical example of a novel feature could emerge in the offspring are new inter-gene/protein interactions between these "never met before" sets of alleles. Recombination would then "seal the deal" by shuffling these allele sets between the maternal/paternal chromosomes, such an individual's offspring would now become a mosaic of their hybrid parent. Just imagine cross-over events occurring between two very divergent promoters of the same loci.
Questions:

Could the unison of such divergent sets of alleles theoretically lead to unique phenotype and features that bear little resemblance to any features belonging to the parents?
Are there any real examples of morphological/physiological features such as that I have tried to describe?

I doubt this will cause any problems or new features coming up, since humans are pretty homogenous genetically speaking. This will probably cause some problems in the future with isolated populations. But when they can not mate anymore with each other, then a new species evolved.

Could the unison of such divergent sets of alleles theoretically lead
  to unique phenotype and features that bear little resemblance to any
  features belonging to the parents?

Though it is possible that some unique characteristics may emerge but it is very less likely that the offspring will bear no resemblance to the parents. You start with an example of humans. In this case it is, in my opinion, very unlikely because there is not so much of genomic diversity yet that may lead to such an outcome as you ask about.
Some examples exist, such as the liger (offspring of a male lion and female tiger) that is bigger than both the species. This happens because of improper growth regulation because of interspecies differences. This could happen because the divergence between lion and tiger is much more than the intraspecific variations.
Just a speculation : perhaps the offspring of H.sapiens and H.neanderthalis could have had such a feature but it seems unlikely for the current population of H.sapiens


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What is the function of clot retraction?
I am thinking how clot retraction and fibrinolysis work together.
I think that clot retraction is a process that gets clot towards fibrinolysis process.
Fibrinolysis process then lyses the clot.
However, I am not sure if it is so simple.
Some seems to be discussing about how to differentiate start of fibrinolysis from clot retraction morphologically.
So they probably seem to be at this stage similar processes visually, but not functionally.
What is the function of clot retraction?

The platelets in the clot contain contractile proteins. They bring the edges of the wound together, which also reduces the chance of further bleeding. The contraction process also supports the wound healing process as it brings the ends of the wound together.
For more information see this article: "Mechanics and contraction dynamics of single platelets and implications for clot stiffening"

So these contractile proteins cause the clot retraction. Thank you for your answer!

Is this different type of contraction than vasocontraction? It seems to be so.


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Significance of prostaglandins in semen?
I am trying to figure out how prostaglandins in the semen relate to the female reproductive tract.
More specifically,
How does prostaglandins in semen help the female reproductive tract increase the chance for fertilization?

Nevermind. While writing out the question I found the answer on wikipedia.
Prostaglandin type PGF2α will act on the FP receptor to initiate uterus contraction which will help propel sperm further into the reproductive tract.


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Function and process of TCTE-1 receptor
I was wondering if anybody knew of the function and process of the TCTE-1 receptor during the binding of a sperm with an egg. The only think I know of TCTE-1 is that it is a species-specific receptor.
I also know that it's removal will render homozygous males infertile. I know that researchers are experimenting with mice to study TCTE-1.

This is by far too long for a comment, so as an answer: I spend now quite a while using Pubmed and other search tools, to find more information. The most recent article I found over and over again was the one from Juneja and colleagues: "Sequence divergence within the sperm-specific polypeptide TCTE1 is correlated with species-specific differences in sperm binding to zona-intact eggs." (which you probably also found). This article has only been cited two times, which is a bad sign for an article making so important connections. My guess is that no further research in this area either happened or has at least not been published. So beyond this I am afraid that there is no other information available (I am happy to change this, if there is any other information available).


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Is nutrient absorption different in Hypersensitive I patients?
I am thinking how the nutrient absorption differs between between patients with allergies (Hypersensitivity I) and those not.
The current guideline about number of eggs in diet is one daily regularly.
My professor says that 1-4 eggs daily can be also ok because cholesterol is inhibited.
However, I am thinking if we have Hypersensitive (allergic) person, what the recommendation should be then.
My hypothesis says that more cholesterol would be absorbed and less inhibited.
However, I cannot find any evidence for this hypothesis.
Hypersensitive response is fast.
I am interested in many responses during long term.
How does nutrient absorption differ in hypersensitive patient and normal patient?

The absorption is itself not different, but the rate of absorbed substances is different because of greater amounts of proteins in the allergic lymphatic circulation.
So less capacity stays for circulation of nutrients and so less absorption in time.

authors: ᴡʜᴀᴄᴋᴀᴍᴀᴅᴏᴏᴅʟᴇ3000


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carbohydrates and lipids as a source of energy? why?
Why carbohydrates and lipids basically used as a sources of energy? Why only proteins are used as building blocks of all the creations? Yes there are some parts of cells like cell walls in which carbohydrates are used but 98% portion of cell is made up of proteins? Why it so?

you are very wrong about only proteins being used, all your cell membranes are lipids (cell membranes are about 40% of your bodies non-water mass) and wood and chitin are both made of carbohydrates. vertebrates don't use carbohydrates for much structurally but lots of animals do.

First, it is a matter of the energy that food can provide. Here fat wins clearly (from the Wikipedia article on Food Energy):

Fat: 37 kJ/g
Ethanol (drinking alcohol): 29 kJ/g
Proteins: 17 kJ/g
Carbohydrates: 17 kJ/g
Organic acids: 13 kJ/g
Polyols (sugar alcohols, sweeteners): 10 kJ/g
Fiber: 8 kJ/g

Proteins and Carbohydrates have approximately the same energy content. But the advantage of carbohydrates (and especially glucose) is that is can be taken up by the body and the cells pretty fast, while proteins need to be digested and broken up, before they can metabolized further. Also plants make primarily sugars (or derivated polymers like starch), so carbohydrates are readily available in the food.
Fat and sugars are chosen for nutritional reasons, since they have a higher energy content and are available for it.
Structural components are build by proteins, since the 20 amino acids allow a much greater diversity in the protein chains than it would be possible for fats or carbohydrates. The building blocks are relatively small and simple but they all have the same basic structure (carbogroup, aminogroup and the sidechain) which allows linking via the functional group and the sidechain influencing their behavior (hydrophobic, hydrophilic, charged, etc.).

I am asking the reason that why lipids and carbohydrates are are choosen to get energy while proteins are choosen as building blocks to form the structural components of cells..?? Why not lipids and carbohydrates can be used to form structural components and proteins can be used to get energy..??

@katherinebridges Sorry, I answered only the first part of the question. I expanded my answer. Better now?

the reason we don't use carbohydrates for structural components is a quirk of history nothing more, vertebrates can't make cellulose or chitin.

There can be many reasons for why proteins are chosen as building blocks. Apart from what Chris said, I would add some points:

Amide bond in proteins is quite strong and thus provides a stable backbone
Because of different amino acids proteins can be versatile
Functionality comes first and then storage (assuming that initially there was just harvesting and no storage). Considering this and the composition of earth at that time, hydrophobic lipids don't seem to have been functional molecules in the aqueous solvent. Carbohydrates on the other are quite complex. You may argue that nucleotides have sugar backbone so sugar must have existed. I don't have an explanation of why polysaccharides could never be functional molecules: perhaps because they are more structurally complex than proteins but could not adopt stable structures such as helices etc.

But having chosen proteins as the functional molecules it won't be a nice idea to use them for energy storage unless there is extreme need (such as starvation). Fats being hydrophobic wont easily suffer attack from the regular reactive species in aqueous solvent; this makes them good storage molecules. Same case with carbohydrates, which arise from carbon fixation. Despite the existence several types of sugars the chemical spectrum is much less compared to amino acids.
And then there is the reason that Chris pointed out based on calorific value. But I would add a point on this regard: the energy in a food cannot be just measured by their absolute thermodynamic calorific value. For e.g. cellulose (which is present in fibers) has the same constitution as starch but provides practically no energy to humans because it cannot be digested. And in plants it plays a structural rather than functional role. So exceptions exist at least in the case of carbohydrates.


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Is it reasonable to assume that RNA polymerase would bind preferentially to the promoter of the long allele of the SERT gene?
I'm trying to come up with an idea for a school project (a hypothetical research study).
I'm looking at depression and the serotonin transporter gene, which is highly expressed in the human cerebellum. There are 2 common alleles of this gene, a "long" and "short" version. The difference is that the long version has 16 repeats of a certain sequence in the promoter, and the short has only 14 repeats. Though there have been some controversial findings, the short genotype has been linked to patients with depression, suicide, less serotonin uptake, and less localization of the serotonin transporter at the cell membrane (synapse).
My hypothesis is that RNA polymerase binds preferentially/more strongly to the long allele's promoter over the short allele's promoter in human cerebellum neurons.
This would explain higher levels of transcription of the serotonin transporter gene (though this hasn't actually been shown) and increased serotonin uptake (has been shown), resulting in lowered susceptibility to depression.
I was thinking I would do this using ChIP. I would get cerebellum tissue from deceased patients of each genotype (long/long, long/short, short/short) and compare bound RNA-pol in the different genotypes.
My two questions are:

Is this a reasonable hypothesis (does it make sense based on what I have described)?
Hypothetically, is it possible to do ChIP on dead brain tissue?

I don't know anything about SERT, but your hypothesis sounds plausible to me. However, if you want to determine relative transcription levels, RNA-seq may be more appropriate. I believe ChIP would tell you whether or not RNAP binds the promoter and where, not necessarily how well it binds. Furthermore, I feel that addressing whether or not the transcription level is actually affected may be the step to take before determining why its affected.


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Sodium-Potassium Pump
From my understanding, in the sodium-potassium pump we have Na+ inside the cell and K+ outside the cell, thus forming a so called "salted banana." After reading my textbook I found many statements saying that "potassium ions tend to diffuse out of the cell...sodium ions tend to flow into the cell." I initially thought that when the action potential hits Na+ leaves the cell and K+ enters the cell, which to me contradicts the previous statement.
Can someone please clarify this and differentiate between the two?
I am trying to understand the action potential process as a whole.
Thank you !

Your confusion is caused by the assumption that Na+ always leaves the cell and K+ always enters. The Na+/K+ pump is there to maintain membrane potential and relative Na+ and K+ ion concentrations stable inside. When an action potential (AP) is generated, sodium channels open and sodium rushes inside to depolarize the cell( 1st phase of AP). Next, the sodium channels close and K+ begins to leave the cell (since the inside of the cell contains too many positive charges and the cell would remain depolarized if nothing was changed). Potassium leaves through leak channels. So in summary, Na+/K+ pump and the channels that are part of AP generation result in different movement of Na+ and K+ across the cell membrane.
Here is a nice review of Na+/K+ pump and action potential generation.
https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/v/sodium-potassium-pump


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How does vasomotor and bronchomotor reactions equilibrate local blood flow to correspond local ventilation?
I am trying to find some figure(s) to explain this.
There is probably better name for "bronchomotor" reaction.
They seem to opposite terms and actually affecting same things (alveolar diameter/tone); one increasing, while the other decreasing.
I am been reading Pocock and Guyton but I am not happy in any any figures.
Which figures can you use to answers this question?

Maybe this is due to my limited anatomical background, but I don't really understand your question. And how should we find better figures when we don't know the ones you have?

I have not found any good picture. Probably, you cannot show this in one picture which I am trying to do. I will post some separate pictures about these two processes tomorrow evening.


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Is there any bank of animations for Embryology?
I am trying to find animations which can anonymous or generalised for Embryology.
However, I have not find any single good source.
Is there any bank of animations for generalised embryos?

I don't know of any database, but a short search brought up a few candidates. Depending on what you would like to see, they should be a good start:

Human Embryology Animations
Simbryo (Flash based)
UNSW Embryology
Embryological Development of the human
Embryodynamics


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What causes Paresthesia (Pins and Needles) at a cellular level?
I've looked it up in plenty of places like the Wikipedia page and such, and it is clear that the most common cause of Paresthesia is either a fair amount of pressure on a specific patch of skin causing lack of blood flow to the specific nerve endings in that limb (not to be confused with a stop in blood flow to the limb altogether) or a much stronger amount of pressure on that patch of skin for a shorter amount of time. This, although the most common cause, is not nearly the only one, which could be anywhere from simply sleeping on the wrong side of the bed to a lethal injection. I'm wondering what happens to the nerve cells that are affected at a cellular level, and what causes it at a cellular level. The level at which pounds per square inch aren't what is being noticed.

Underneath the superficial layers of your skin there are receptors which sense pressure, temperature and pain. These receptors are part of the peripheral nervous system which senses stimuli and they take the message conveying details about the stimulus to the somatosensory cortex of the brain. Here is where the perception of pain, burning, pressure etc is ultimately made. To take the simplest example, if you stop blood flow for a short amount of time in a limb, these receptors are activated, and will send signals to the brain that are interpreted as tingling or numbness. With more severe pain, different receptors are activated which , again, project to the same brain area but a different message is read out. If the pressure from one limb is removed, the receptors will go back to normal function as blood flow is restored.
https://en.wikipedia.org/wiki/Nociceptor
http://www.scholarpedia.org/article/Mammalian_mechanoreception

The main reason I asked this question was to hopefully get an understanding as to whether it would be possible to stimulate a group of these cells in the peripheral nervous system to induce the feelings of tingling numbness from outside of the skin using a form of directed energy such as directed sound or a laser. The problem with finding the right kind of stimulus is that I don't know whether the cells send out an electrical signal back to the brain or some sort of chemical signal. Do you know if it's possible, and if so with what kind of stimulus?

This would in theory be possible. You would have to create a stimulus which matches the response profile of the receptor you want to target. The signals to the brain are electrical-- between cells-- but locally release of chemicals can triggers the electrical signals. For example during injury, the body can release certain chemicals which can numb pain at the release site and your brain perceives this as "reduced pain". A lot of sensations can be felt outside the skin already. If you think about sensing a hot oven just by going close to it or air pressure from a blow-dryer on your skin.

So without considering something which would cause excessive nerve damage or that would last longer than a common case of paresthesia, what kind of stimuli could stimulate the nerve clusters through the skin in the same way as stopping blood flow. While I was reading about the sensation, I saw somewhere that it could be triggered with an excessive amount of vibration like in the case of motorcycle riders while they grip their bikes over jumps, which is known as, "cyclist's hands". This is why I'm thinking a directed sound device could create the vibrations with a high enough frequency.


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In what forms do plants and animals excrete sulfur?
Sulfur is part of the amino acids cystein and methionin, plants take up sulfur in the form of $H_2S$. These organisms will also need a way to get rid of excess sulfur, how? In what compounds?
Judging by the smell of some farts, I guess $H_2SO_4$ plays a role, but I can't imagine that one get'S rid of all the sulfur this way.

Plants do not take up H$_2$S, this is limited to a few microorganisms. Plants take up soluble forms of sulphur as sulphates, and the surely do not build up sulfuric acid (which would destroy the cells). Have you looked at this topic: http://biology.stackexchange.com/questions/15642/can-animals-absorb-atmospheric-sulfur/

Maybe you want to comment on this answer: http://biology.stackexchange.com/a/15609/3037 'He states it's H2S

Apparently, a number of plants can take up H$_2$S. http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0062048&representation=PDF. (x-posted from other answer.)

Sulfur is $3^{rd}$ most abundant mineral element in the body. Carnivores obtain it from Cysteine and Methionine in the animal protein which converted in to Glutathione.
Excess of sulfur is stored into Glutathione or oxidised to sulfate by sulfite oxidase which is eventually eliminated by urine.

[1]: Nimni ME, Han B, Cordoba F (2007). "Are we getting enough sulfur in our diet?". Nutr Metab (Lond) 4 (1): 24. doi:10.1186/1743-7075-4-24
[2]: Wikipedia on Sulfur metabolism


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Real time PCR standard curve
As blunt as possible: when performing real time PCR it is a routine step to run one PCR in order to plot a "standard curve" with several decreasing dilution ratios from your sample. what is the real purpose of this?
how should results be used/interpreted?

You can use 3 or 4 dilutions- 1:1, 1:5, 1:25, 1:125
Purpose of doing this is to calculate the primer efficiency. Ideally primer efficiency should be 2 i.e. two molecules of DNA are formed in a round of PCR. So after n-rounds of PCR there should be $2^n$ DNA. However, this may not be the case always. You calculate primer efficiency like this:

Plot $Ct$ vs $log_2(Conc)$
Get the trendline (in excel) or use a linear regression command for other applications
Get the slope ($s$) of the trendline
Efficiency in this case would be $2^{-s}$.

Some people use base of 10 in the log instead of 2 (for which you have to do $10^{-s}$ instead.
This, you can directly use to find out how many copies are produced after n cycles i.e instead of $2^n$ it will be $x^n$  where $x$ is the calculated efficiency. This is particularly useful when you are calculating the fold changes using the comparative Ct method. For details see this article.

usually you would find a $log(conc)$ vs $Ct$ graph in examples for which the primer efficiency calculation becomes 2^(-1/s). Means the same but what I described looks neater to me :P

and why is normalization with housekeeping gene performed?

Because these are supposed to be stable in their expression. That way they can be used to normalize for differences between the cells in the experiment.

and may I normalize with housekeeping gene results of an "A" qPCR run and a interest gene results of another "B" qPCR run? (same experimental conditions)

it is not necessary that you should normalize with a housekeeping gene. The reference gene should be such that it doesn't get affected by the treatment. Usually housekeeping genes are not affected unless there is some global perturbation- in such cases you should use a spike in. You should use the same reference for replicates otherwise comparison is difficult- qPCR is not absolute quantification; it's relative.

you can do the qPCRs for the reference and the interest gene separately with the same DNA template. However, it is always advisable to run the controls and the samples in the same run.

I can only agree with @WYSIWYG. Additionally you have to test your reference gene for the experiments (preferrably a number of them) and choose the most stable one. It is not so that always beta-actin or GAPDH are the best choices.

Because the purpose of the standard curve (which actually results in a standard line) needs to be linear. If it is not linear (because of not enough values which are not linear distributed), then you quantification will be wrong.
Ideally the line should look like this:

This picture is taken from this website, which gives a nice introduction into the topic.

and why is normalization with housekeeping gene performed?


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Are females more flexible than males in all mammals?
It's common that human females have a more flexible body than males, (but I don't know why, so it'd be helpful if someone answers why so as well!) but does this apply to all mammals?

In which terms more flexible?

You mean physically flexible ?

Do you mean plasticity? Devlopmental plasticity?

Try birthing a child for once. You need to be flexible to accommodate the growth of another organism inside you.
Take a look at some pictures of the mothers spine during the course of a pregnancy, you will have no further questions. Same with belly size, breast size and vagina size upon birth.
This video is a nice explanation of this. Also includes the different centers of gravity for males and females (human).
http://www.youtube.com/watch?v=WO8DtsZO1nA

This might be true for spinal flexibility, I'm not sure it tells the whole story. Men are almost always stronger than women of the same size, and I'd be surprised if this isn't related to flexibility. Perhaps women pay for their increased flexibility with reduced strength?

Males and females are more similar in most other mammals (with some spectacular exceptions where males compete strongly for females and have evolved weaponry to help them). When your life is threatened every day and you survive by running and fighting, there is a strong evolutionary incentive for both sexes to converge on a single optimal body shape.

@DisplayName yes, I find that the spine curve gets very intense during pregnancy.


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How can highly virulent but uncommon diseases (like ebola) maintain a stable equilibrium?
I'm wondering how can very uncommon diseases remain in a relatively stable equilibrium. For example, if it started to spread, the spread could accelerate and become an epidemic. However, if it doesn't spread, why doesn't it wither away?
As I understand, the ebola for example, is highly contagious, nearly always fatal, and kills quickly. So quickly, hat the target has not much time to pass it on to others. If it spread just a little better, it would become an epidemic, just a little slower and it would disappear. How is it possible, that its spread did not change significantly in the last couple of decades? It kills a few dozen, maybe a few hundred people per year, these numbers remain largely unchanged.

They do not maintain an equilibrium. They show up, kill a few people and are gone again. Something stable would be like the measles which are present in humans (and only there) and take the chance to cause local epidemies. And we are lucky that ebola kills so fast and is not better transmittable. This would end in a big catastrophe. A very interesting book on this topic is "Spillover" by David Quammen.

I did not mean that they intentionally maintain an equilibrium. I was just meaning, that it stays a it was decades ago. Not growing, not shrinking.

What do you mean by "it stays as it was"? That there are no mutations? That it is not moving to other hosts?

No, the number of people infected per year.

Speaking of Ebola it is not stable. It stays in its reservoir hosts and only occasionally moves out. Even the great apes are not good host and die from it. We only "stumble" upon it from time to time.

It still has approximately the same average kill per year as it had 40 years ago. Not growing, not shrinking. I assumed if it started to grow or started to shrink even just a little, the tendency would continue stronger and stronger. Why isn't it like that?

Why should it? This virus exists in its reservoir hosts (most likely bats). From there is breaks out every now and then, when people cross the way of this host or probably eat them. This virus kills its host quite efficiently, so it doesn't stay in the human population (additionally humans do all to prevent it staying there). I really recommend the book by David Quammen, although is popular science. It is interesting to read on this topic (not only Ebola).

@Chris : thanks, this made it a bit more clear. Don't you want to add it as an answer?

I can do that. But not before tomorrow.

Viruses and other disease causing organisms are usually in an ecological steady state in different organism, called a vector.  When they start to infect another organism similar enough that they can reproduce, they may turn out to be more virulent or fatal than is optimal for the organism.
The classic example is the case of influenza outbreaks, the flu virus is causing mild infections in other animals such as birds or pigs and then a human being catches it and it may be serious or even fatal.  This is classically because the viruses lytic cycle (where it reproduces and then kills host cells) is not tuned to the equilibrium ideal for viruses in the new human environment, which is not fatal which gives the virus the best chance of reproduction and retransmission.
In the case of Ebola and Marburg viruses the vector is not known but there is speculation and research going on. So in the extremely rare handful of events where these hemorrhagic fevers have been caught by people they fatal.
Its the non-equilibrium case where the virus is not adjusted to human hosts and adjusted for its vector population where it is usually most dangerous.
If these viruses were allowed to persist they would theoretically come to the point where it wasn't fatal.  The problem being that people would die and there is always the risk that the virus would burn through all possible human hosts before it adjusts...
I want to say that this is all driven by evolutionary forces.  If the environment encourages pathogenic characteristics then human pathogens can persist forever.  Flesh eating bacteria and MRSA and other antibiotic resistant bacteria have found a competitive environment where causing disease and death are the only way to go - hospitals with antibiotics. In the case of Ebola/Marburg, there may be a disease reservoir of monkeys acting as a pool for the high fatality strain.  Anything can happen with the right geography and dynamics.
If you've been thinking to yourself, 'what are the odds that a virus or bacterium would be extra virulent versus not infectious at all?', you are right. One should also note that fatal outbreaks are rare and exceptional.  There are clearly plenty of cases where viruses or pathogens from other organisms can't get any traction at all in humans.  We are practically swimming in viruses and bacteria all the time.

They mostly getting less dangerous over time, but not necessisarily harmless. The Myoxomavirus, which was imported to kill rabbits, still kills about 70% of all infected animals, and this is more than 30 years after it was set free. In the beginning the rate was around 99,6%, but 70% is still far away from being nice. The example is from the Quammen book, the data has been published [here](Biological Control, as Exemplified by Smallpox Eradication and Myxomatosis).

Adding a comment for @PlaysDice  - recommending this book that explores emerging threats from reservoirs of infectious biotica.  http://www.amazon.com/dp/0393066800/?tag=stackoverfl08-20


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Are there specific features of birds that cats/small predators are attracted to?
I've recently heard a podcast, in which a professor describes one of the theories as to why we like abstract art. In his talk, he mentions an experiment with seagull chicks, in which the seagull chicks mistake a stick with a red dot for their mother's beak, and in the case of stick with 3 stripes actually preferred it to their mother's beak. When a stick like that is waved around a chick, it starts to peck at it, believing it is mother bird:

This experiment suggests that birds are imprinted to recognize specific patterns and interpret them as mother.
I'm in trying to create a similar experiment for cats. To do so I'm trying to understand if cats other small predators (ferrets,etc) are imprinted in a similar way - do cats recognize specific features of a bird to identify it as "bird", "prey" or "can hunt and eat"? I'm talking about stuff like - do they recognize eyes, beaks, wings or tail in a special way?
To paraphrase the question: If I'm to create a stick like above, but for cats, what features would be painted on the stick?
I know that butterflies, caterpillars and other insects have evolved to mimick "eyes" on non-vital organs to confuse birds. I'm interested if same stuff exists for small mammal predators.

Heh, what an interesting idea! I suspect you won't succeed (though I hope I'm wrong), I think that cats are more attracted to movement than anything else. They seem to jump at anything that moves.

insects and birds with tiny brains are easier since they have small brains.  larger brained creatures are harder to hack.  cats might not be so easy to fool. also depends on where the wiring is.  bats use scent primarily, which is hard to hack.

@shigeta they do? I would have guessed they use their echolocation.

to identify their young ones - in some cases - when the ceiling of the cave is crawling with baby bats... sorry i don't have a reference - saw it on a documentary on carlsbad caverns.  some bats see just fine - not sure if scent is always important... mice, closely related to bats do as well, so this may be the result of adaptation as well as limitations on brain size etc..

Movement is definitely part of it. I noticed that my cat likes to chase dried cranberry more than a similar sized plastic ball or a rock. The cranberry bounces in a different way, or maybe it's the seeds rattling inside.

Texture might be a part of it. Cat responded with surprise to a still piece of artificial fur. It seems the cat knew that fur might be an animal.

Maybe a random approach could get some answers, if you had a computer program output random patterns to a screen and some method to watch the cat and record when it's interested.

Well, take a look at cat toys. Small fuzzy balls especially darker colors, also, the laser pointer toy is endlessly stimulating to most cats. I'm not sure what the key qualities for a cat are... Although the laser beam does seem a clue. A name for this sort of thing is a "super-normal stimulus". It produces a larger than normal response. You can read more about this phenomena in Desmond Morris' book, "The Human Zoo", in the section on The Stimulus Struggle. Honstly if you do research and can't find any answers, it is definitely in the realm of some experiments do see if one or some can be foun

My cat ignores the last pointer but loves to play with a real dark red cranberry. Red might be a clue

Not all cat predatory behavior is innate. Researchers found that cats predatory behavior for birds vs. mice depends to a significant degree on training by the mother: if the mother taught predatory behavior with birds, the kittens grew up to be better at catching birds than at catching mice and vice versa. Supportive data shows that aside from monkeys and other primates, cats are among the most adept at learning by observing the successes and failures of other animals attempting to complete tasks to obtain a reward. This might influence, therefore, a cat's response to and attraction for objects in the air or on the floor.
Blindfolded cats can hunt mice by vibration. Paul Leyhausen, a German animal behaviorist studied domestic cats (and related felines) from the 1950's through the 1970's, and much of what is known about their predatory behavior is thanks to him.
Although their vision is not especially keen, domestic cats see well in dim light and readily perceive motion. According to Leyhausen, prey movement and the direction of movement are the only factors which innately release crouching, stalking, and catching behaviors in cats. When presented with quail, cats were far more likely to go after active quail than those stilled by tonic immobility. Cats are also more likely to go after smaller prey (mice > rats) and mice were much more likely to elicit play pawing.
Leyhausen also demonstrated that rodents were probably the natural prey of cats.
Though there has been much study of cats and predation, little is available on detail of the kind you are interested in.  My best guess for a good toy for a cat would be a smaller object that moved along the floor.
More information can be obtained from Leyhausen's book, Cat Behavior: The Predatory and Social Behavior of Domestic and Wild Cats.
Effects of the mother, object play, and adult experience on predation in cats
The effects of experience on the predatory patterns of cats
Tonic immobility in Japanese quail can reduce the probability of sustained attack by cats
The behavioral bases of prolonged suppression of predatory attack in cats


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Epithelial cells and Rhinovirus
If you injected a tumor with epithelial cells infected with the Rhinovirus, would this still evoke an immune response as it would with the respiratory system? Secondly, what is the specific reason the Rhinovirus is only attracted to the epithelial cells in the respiratory system.  Do these cells give off a specific chemical signature in which the virus is attracted to?

You will provoke an immune reactions against the epithelial cells, if the are from a different person. If they are not, these cells will simply die and nothing else will happen. What should happen in your theory?

That wasn't a theory, just a question. I have another, should I post it or ask it in comments.

If it is related to this question edit it and put it into your question. If not, open a new one.

Can you edit your title to include something about cancer ?

Infecting tumor cells with viruses to provoke an immune response used to be  termed (tumor / immune ) 'xenogenization'.  The approach may now fall under the general headings of tumor immunology, immune modifiers or tumor vaccines.   Xenogenization been explored for decades (with only moderate success).  Some modern approaches include adding immune stimulating genes to the viral 'vector' (e.g GM-CSF) to try and improve an immune response.  Xenogenization is usually intended for use with the patients own (autologous) tumor cells.   Other approaches that use viruses include delivering genes that preferentially act in tumor cells or "tumor antigens".  Some of these modified viruses may have been engineered to have low, or no, ability to replicate in the body.   Note that some viruses, such as influenza or rhinoviruses are not (generally) able to circulate in the bloodstream (viremia) to infect distant tumor cells.  Instead, the goal of using such viruses is to provoke an immune response against tumor antigens expressed on the 'original infected' cells at the site of injection and hope that the immune system goes on to attack distant masses/metastases.

Interesting answer. Can you add some references?

@Chris. Done.  I also added text to bring xenogenization under more contemporary (but in my opinion, looser) subject headings of tumor vaccines.

The virus has some molecules on it surface, which fit to receptors on the surface of their host cells. In the case of rhinoviruses there are three receptors possible. The viruses of the so called major group (or HRV-A species) dock to ICAM1, the minor group (or HRV-B species) to the LDLR (low density lipid receptor), and the relatively recent group of HRV-C dock to the HRVC receptor. See the image below. It is taken from this article ("Human Rhinoviruses"), which give a pretty nice overview of the field.

Regarding the injection question: You will provoke an immune reactions against the epithelial cells, if the are from a different person. If they are not, these cells will simply die and nothing else will happen.


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Clustal Omega - convert from distance into # of substitutions
I have a set of nucleotide sequences for which I have aligned using Clustal Omega. In particular, I performed a full alignment, and obtained a full distance matrix.
The distance matrix scores range between 0 and 1. I am looking to use this score to back-compute the number of different positions present in the alignment. Is this possible? If possible, I'm looking to avoid using code (my own or otherwise) to re-compute the number of positions differing between each pair of segments, and instead compute it directly from the distance score.
Here is a toy example of what I am receiving from ClustalOmega:
Sequence    1    2    3    4
1           0    0.1  0.06 0.1
2                0    0.4  0.23
3                     0    0.05
4                          0

The numbers are the "distances" as calculated by ClustalOmega. According to the README file, they are computed by the k-tuple measure. I tried parsing the original paper (published in 1983 in PNAS), but I could not figure out how k-tuple distances are computed, and I could not figure out how the distance metric (as reported like above) is computed from k-tuple distances.
I would like to convert those numbers into the number of positions that differ between each pair of sequences when the two are aligned. This includes substitutions, insertions, deletions. I am currently doing this for 520 sets of virus sequences. Is this possible?

What exactly do you mean by "positions" in your alignment? How many sequences are we talking about? Can you show an example of the matrix and your desired result?

Sure, let me update the original question.

It uses a gonet matrix to compare each of these two sequences. Since you you could have insertions and extensions as well as substitutions, it becomes a 3 parameter problem. 1open + 6penalty + substituion_penalty = X. X can be solved by a linear combination of subsituion_penalties, extensions, and insertions. So I think this will be really really hard.

with that being said. Clustal spits out the multiple sequence alightment. Why don't you just look at sequence 1 and sequence 2 and see what the insertions and subtitutions are!

Haha, it looks like I will have to do that in the end. I was trying to see if I could take the lazy route and not write a few lines of code. Thank you for all of your input nonetheless!

@jwillis0720 if you are still around then can you post this as an answer.

It uses a gonet matrix to compare each of these two sequences. Since you you could have insertions and extensions as well as substitutions, it becomes a 3 parameter problem. 1*open + 6*penalty + substitution_penalty = X. X can be solved by a linear combination of substitution_penalties, extensions, and insertions. So I think this will be really really hard
with that being said. Clustal outputs the multiple sequence alignment. Why don't you just look at sequence 1 and sequence 2 and see what the insertions and substitutions are!


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Spinal cord injury bypass
When the spinal cord is damaged, the connection between the brain and some part of the body may be lost.
To restore this connection, researches are considering either:

Repairing the damaged area so that the spinal cord works again.
Bypassing the spinal cord by connecting the brain directly to the affected part of the body.  This is done by implants in the brain connected directly to electrodes in the muscles creating a new circuit in parallel.

My question is has there been any attempt to bypass only the damaged part of the spinal cord?  To create a bridge over the damaged tissue?

This question is poorly worded and hard to answer as it stands. Consider restating more clearly what you are asking.

Ok sorry I am not a native english speaker, I will try to be more clear

Interesting question!
There has been at least one study that bypassed a spinal lesion site with autografted neuronal tissue (Tadie et al., 2004 - doi:10.1089/089771502320317069). The study participant regained voluntary motor skills 8 months after bypass surgery. The surgery involved the implantation of nerve autografts between the rostral spinal ventral horn and the caudal ventral roots. Regain of motor function was observed after the patient had been paralyzed for 3 years.

Nice answer, I was talking more about electronic solutions but it is still interesting. I cannot access the entire article, what is a "nerve autografts" ?

Nerve autografts are nerve grafts taken from the recipient himself/herself  (auto means 'self' in this context).


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Structure of biological membranes?
Integral membrane proteins have functional asymmetry i.e. they have two different domains of proteins performing different functions. these proteins have Tyr and Trp amino acid residues at the interface between the lipid and water.Because these amino acids have dual nature that their side chains can interact with both extracellular aqueous environment as well as hydrophobic lipid phase and another generalization about amino acid location relative to bilayer is described by "positive inside rule": The positively charged Lys,His, and Arg residues of membrane proteins occur more commonly on the cytoplasmic phase of membranes.My question is that why only positively charged amino acids are faced towards cytoplasm why not negatively charged amino acids or other amino acids are favoured here?

Yes, I have a reference for this claim.from the Lehninger Principles of Biochemistry Chapter 11 Biological membranes and Transport. and Sorry for the late acceptance of answers because it did not know it actually how to accept answers by using green trick but know i became familiar with this so i accepted the answers. @Chris

Some thoughts on this. First of all, the positive-inside rule, proposed by Gunnar von Heijne, is an empirical rule based upon observations, not one derived from theoretical considerations, so any explanation is simply an attempt at a rationalisation.
Having said that, here are three of those rationalisations:

the membrane potential is usually negative inside. This will create an electrostatic tendency for basic amino acid side chains to stay inside.
most phospholipid head groups are either neutral or anionic (phosphatidylserine, when the phosphate is included). Again an electrostatic force favouring basic residues inside since to move them out would require overcoming their interaction with the negatively-charged membrane surface
the pK values of the basic side chains (lysine and arginine) are much further from 7 than are those of the acidic side chains, so,  since charged residues must be neutralised to get them through the bilayer, it is more energetically unfavourable to deprotonate basic side chains than it is to protonate acidic ones.

The environment inside the cell is reducing.

@biogirl yes, it is, but acid-base equilibria are not redox reactions. I don't understand what your point is.

I thought reducing environment would lead to addition of protons.


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DNA adaptation in human life
Does our DNA adapt by human lifetime? Or do we have the same genetic information from birth to death?
I mean: What is usually called "evolution" means "natural selection" like this:
http://www.youtube.com/watch?v=hOfRN0KihOU&list=UUsXVk37bltHxD1rDPwtNM8Q
-stronger animals have more descendants, so they make bigger percent of strong animals.
But does evolution work by some primitive genetics-engineering too? Thank you.

Lewontin's recipe
A very nice way to consider natural selection is through the lense of Lewontin's recipe. Evolution of a given trait (tail length for example) through natural selection occurs whenever the three following conditions are met:

There is variation for this trait in the population

This variation is caused by mutations

Part (or the totality) of this variation is heritable

Heritability is the part of the variance in a trait that is explained by genes. It can be measured as a parent-offspring correlation.

The variation of this trait is correlated with fitness

loosely speaking, fitness is an index of both fecundity and survival

You can take two minutes to think about how logical it is that changes in frequency of variants (natural selection) occurs whenever these three conditions are met. You can imagine any objects you want (pencils of colors for example) and simulate these three steps:

Variation

different pencils have different colors

Heritability

simulate that your pencils reproduce (asexual reproduction is conceptually easier to understand) and offsprings have similar (or even the same) color than parents

Correlation between trait and fitness

Pencils of different colors have different fitness.
For example each red pencils create two red pencils the next generation while blue pencils do not manage to replicate at all.

You can quickly see how the red pencils become more frequent in your pencil population through time. If you wait long enough your pencil population will be totally composed of red pencils. And you'll need to simulate a mutation in order to create a blue pencil. I think you understand the how different are the roles of mutations and natural selection in evolution with this example.

Genetic Adaptation During Lifetime of a multicellular organism
For a beginner in evolutionary biology, saying that a multicellular individual's genome does not change during its lifetime might be considered satisfying. In reality it is slightly more complicated. Two elements that are mostly influent very early in the lifetime of an individual have to be considered.

While most mutations occurs during reproduction, some mutations does also occurs during body growth or stated differently during cell reproduction (Mitosis). In consequence, some pairs of your cells share exactly the same genome while other pairs of cells have a sligthly different genome.
Moreover, once some mutations had occurred within the development of an individual, these mutations might influence the fitness of the cells and therefore some alleles (variant of a gene) might raise in frequency while others decrease in frequency (Natural selection). It is important to understand that this process of natural selection select for cells that have a higher fitness and therefore do not necessarily select for the cells that allows the individual to increase its own fitness.

I don't fully understand what you mean when saying: "But does evolution work by some primitive genetics-engineering too?" Could you try to rephrase this question?
Please, let me know if I answered your question!

Note:
Here is a good way to understand the difference between "gene" and "allele". A gene might be a called the "eyes color" gene for example, while the three alleles of the "eyes color"  gene might be callsed "blue eyes", "brown eyes" and "green eyes". In this sense, the alleles are the different variants of a gene. Mutations increase the number of alleles and natural selection reduces the number of alleles by selecting for the allele that cause its holder to have the greatest fitness. If you understood that, it is already good!
Note: Natural selection does not necessarily reduce the number of alleles, several alleles might be kept (polymorphism) in certain "types" of natural selection (frequency dependent selection and overdominance (heterozygote advantage), fitness varies in space and/or time, selection acts on different levels). The "type" of Natural selection that reduces the number of alleles after some time is called directional selection.

Yes, you answered my question excellently. Thank you.

The concept that the environment directly changes DNA and alters the characteristics of the offspring falls under the heading of Lamarkism. In the context of DNA the  Lamarkian view would be that the giraffe got its long neck by stretching its neck cells reaching up to tall trees for leaves, which then (somehow) changed the DNA in its gametes and thus produced offspring with longer necks.   There's no compelling evidence for Lamarkism and Remi.b 's  nice answer describes DNA and evolution/selection/adaptation in its standard form and how giraffes would evolve such features.
OP initially asked 'does our DNA adapt during our lifetime'.  Certain regions of the DNA in each of our immune T-cells and B-cells change (recombine) to code for specific protein molecules that bind to antigens.  These are the genes for the T-cell receptor in T-cells and antibodies in the case of B-cells.  So the DNA in a T-cell or B-cell is different compared to other cells in the body including the gametes.  These regions of altered DNA help us fight infection.
You can easily imagine that an individuals ability to fight infection may affect whether they can survive to reproductive age.  Genes involved in immune system function might be selected for during deadly epidemics. And paradoxically, some genes responsible for debilitating or deadly diseases can persist in human society due to their protective effect against other diseases.
For completeness there is also some emerging data that neurons have some alterations in their DNA but its not clear what, if anything, that means and whether its of functional significance.  Unless similar types of changes are made in gametes,  DNA altered by this mechanism will not be passed on to offspring.
Finally, DNA in cells can be modified by a process called epigenetics.  Epi- means 'around'. In epigenetics various regions of the DNA strand (and some related proteins that keep DNA coiled up called histones) are chemically modified by a set of enzymes.  Epigenetics affects how certain genes are switched on and off and is perhaps best known for inactivating one of the two X chromosomes in female cells.  In epigenetic modifications the DNA sequence remains the same but the epigenetic 'decorations' around the DNA can vary and this process can be influenced by the cells environment.


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Evolution of bee hives
How do the instinct to create a hive appeared in bees? Is there some evidence of
"intermediate" hives? With this questions i mean all the factors necessary to build a hive, including the social structure, the producing of beeswax and architecture.

Welcome to BioSE. You will have better chance of getting good answers if you include more specifics in your questions, e.g. some background and your reason for asking. In this particular case; Are you asking about the evolution of sociality in bees in general, or something more specific only dealing with hives?

I'm assuming you mean the distinct architecture and regular hexagonal shapes in bee honeycombs?
In fact, Charles Darwin spent a good bit of time with honeycombs.
First of all bees and wasps have a common progenitor and wasps also build combs and nests, albeit of paper/celluose as opposed to wax.  He was interested in how the perfect hexagonal lattice formed in the wax.

Darwin tried three different experiments with bees’ cells at Down that he reported in Origin. In one, he put a thick block of wax into the hive. ‘The bees instantly began to excavate minute circular pits in it: and as they deepened these little pits, they made them wider and wider until they were converted into shallow basins, appearing to the eye perfectly true or parts of a sphere, and of about the diameter of a cell. It was most interesting to me to observe that wherever several bees had begun to excavate these basins near together, they had begun their work at such a distance from each other, that by the time the basins had acquired the above stated width (i.e. about the width of an ordinary cell), and were in depth about one sixth of the diameter of the sphere of which they formed a part, the rims of the basins intersected or broke into each other. As soon as this occurred, the bees ceased to excavate, and began to build up flat walls of wax on the lines of intersection between the basins, so that each hexagonal prism was built upon the festooned edge of a smooth basin, instead of on the straight edges of a three-sided pyramid as in the case of ordinary cells.’ (Origin, p. 223.) The cells were built up in a hexagonal shape when their bases intersected with those of other cells; but the pyramidal bases were apparently not built, since there was no pressure to accommodate cells on the other side of the wax, which was a thick block.

This seems to have a built in burrowing behavior in how the lattice forms that eventually turns into hexagonal shapes.
BTW this topic is very similar to the evolution of spider webs, which is also fascinating.

I remember an episode of a German science show talking about this. If you do an experiment with bubbles. Eventually several bubbles will share boundaries and a hexagonal form will emerge.
Following this it is no instinct but the best way to create boundaries.
They had a more scientific explanation for this.
There you go:
http://www.exploratorium.edu/ronh/bubbles/bubble_meets_bubble.html
And I quote:

If you take two sheets of clear glass or plastic separated by about one-half inch, soak them in soapy solution and then blow bubbles between the sheets, you will get many bubble walls. If you look closely, you will notice that all of the vertices where three bubble walls meet (and there are always three,) form 120 degree angles. If your bubbles are of uniform size, you will notice that the cells form hexagons and start to look much like the cells of a beehive. Bees, like bubbles, try to be as efficient as possible when making the comb. They want to use the minimum possible amount of wax to get the job done. Hexagonal cells are the ticket.

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I just noticed I was answering to an answer. My answer to the question would be that almost every animal on the planet builds nests. If you are a termite you can use mud. If you are a wasp or a bee you build nests in the air or at least not in the mud. That means you have to carry your material through the air. The less the better. Efficiency dictates that you build your "hive" or nest as compact as possible. That means spherical shape which has the most volume vs surface ratio and the hexagons inside follow the same rule. Use as little material as possible or you are outcompeted by bees that do.
Also it's a lot more efficient to "manage" a cluster vs nests cluttered all over the place. Again no instinct just necessity which eventually evolved into instinct. Because all other instincts became extinct.


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A day in Beijing is like smoking Only one sixth of a cigarette
This is the title of this blog post followed by this other good post.
I'm particularly anti-tobacco-smoke, at the point of not always considering other pollution, and this article shows how this kind of domestic pollution (main domestic pollution is usually heating) is probably no insignificant in the global air pollution.
The weight of this pollution is also maybe increased since people tend to be nearer from potential smokers than from cars (e.g. near entrances).
I've not known the period of the past, without the smoke-free laws in buildings, but it seems in my country, that it has just moved the problem, possibly reinforced smokers reflex to smoke when outside
The author shows useful references, that all measure second-hand smoking in terms of PM2.5 which is the common indicator with PM10 for air pollution [car traffic,domestic heating,industry,coal combustion,construction,quarry,waste treatment].
The results are interesting showing the important rate of PM2.5 in second-hand smoke, it would even be very useful to indicate air pollution levels in terms of cigarette inhalation. 0.17 cigarette/day is quite more insightful than 150μm of PM2.5, at least to me.
But I'm still skeptic and think the effects of second-hand smoke are more important (second-hand smoke is smaller in size than 1μm, considering not only cigarette from manufacturers which include many brute carcinogens and poisons (arsenic, hydrogen cyanide,..), but other tobacco/or drug smoking that are different but considerably noxious too)) and this study is quite informative too, comparing diesel car exhaust to cigarette combustion.
I'm wondering:

is the pollution from cigarettes as volatile as the rest of air pollution?
is the concentration of second-hand cigarette global pollution not insignificant compared to the rest of pollution (in countries with high smoking rates)?
does it go in higher layers of the atmosphere, lower layers (more critical), or does it blend uniformly?
can air pollution mask (with PM2.5, and PM10 reduction filter) protect as well from it?

particles size in micrometer, from http://en.wikipedia.org/wiki/Particulates

edit: this http://ash.org/CAEPAProposal.pdf report is particularly interesting

ask on skeptics.stackexchange


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Buy bacteria for experiment?
Where can I buy paracoccus denitrificans? I need it for an experiment. I cannot find online where I can purchase this.

ATCC- you can get most bacterial strains and cell lines there.
Find P. denitrificans here:
www.atcc.org/products/all/13543.aspx

You said see this but didn't link to anything. Did you mean to include a link?

yep.. it didnt work.. see the edit

Sorry about that. I have accepted it.


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Does apheresis damage any components of blood? If not, why not?
Blood donation involving apheresis is becoming increasingly common. It looks like the process involves centrifuging blood at very high speeds* before removing the desired fraction and returning the rest to the donor. Is there good reason to believe that the centrifuging process is harmless to all the various cells, proteins, lipids, and other substances in whole blood? Or is it possible that some blood constituents are damaged or altered?
* I don't know if the speeds are particularly high compared to other biomedical processes, but they're drastically outside the conditions in which biological products evolved to function, hence my question.

As someone who handles blood regulary in the lab, I can tell you that cells (and other components of the blood) withstand this conditions without any problems. You can afterwards still grow single cell populations in cell culture.

The centrifugal speed is around 300-500g : this wont disrupt any cells.

@WYSIWYG Is that specific to blood donation? I wasn't able to find that information, but when I looked up other blood fractionation procedures (typically for lab use) they had values around 1500g. Or would that even make a difference?

Thank you both for the comments. I'm obviously not a biologist, so it was counterintuitive to me that forces of that kind would be unproblematic to cells. Is the same thing true for things other than cells, like albumin, liproproteins, etc?

Chris or WYSIWYG One of you should attempt an answer.

@octern: even that shouldn't affect the erythrocytes.. I don't work on blood so I don't know much but most animal cell types can tolerate upto 1000g. But we generally use 300g for spinning down cells.


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Do any organisms recycle their own waste internally?
I thought of this question yesterday and it turns out it's surprisingly hard to Google.

What kind of waste are you thinking about? Waste as form of undigestable food or broken down protein etc.?

Technically, if it's still being recycled internally it isn't waste yet...

This makes me remember a question: why virtually all animals need an excretor system to eliminate nitrogen? Why can't we recycle it, since it's so important for protein building?

@Rodrigo That's an interesting question ! Why don't you create a new post ?

@Rodrigo It may be because the nitrogenous compounds produced may not be effectively recycled.

Well, I would, but it's already asked here: http://biology.stackexchange.com/questions/10737/why-do-organisms-excrete-nitrogenous-wastes

Hibernating bears have an ingeneous way of recycling their urine (urea) while they hibernate. Also turtles and frogs in the bottom of ponds deal in unique ways during hibernation.. This should get you started.
recycling waste externally is done by rabbits who will pass pellets through their system twice, the firsttime to partially digest, the second time to extract nutrients.

All organisms recycle their waste internally. Every cell of every living organisms is constantly breaking things down and re-using the components so produced. But you're presumably wondering about things such as carbon dioxide, urine and faeces? These are not recycled because the benefits of doing so are not worth the costs.
Let's consider carbon dioxide as an example. We know that carbon dioxide can be usefully converted into energy-holding molecules using readily available sources of water, oxygen and sunlight. So why do animals** "wastefully" breathe it out? Because the energetic benefits of respiration are high compared to the energetic benefits of photosynthesis and so photosynthesis is unable to make a useful contribution to the overall energy balance of an animal while the costs of the effectively photosynthesising are quite high (e.g. having leaf-like protrusions, synthesizing chlorophyll and so on).
In fact, it must always be true that there are processes which are not energetically worthwhile because of entropy. An organism that could perpetually recycle its waste would be a perpetual motion machine.
** - and many microbes and, in fact, plants - although their intake of carbon dioxide is typically higher over the solar cycle.

"An organism that could perpetually recycle its waste would be a perpetual motion machine." Hm. Not quite, since there can still be an (almost) non-material energy flow through the system. A little eco system in a closed bottle or a big one like on earth could be considered a single organism which recycles it's "waste" (which immediately stops being waste, as others pointed out).

@Peter Schneider This only appears that way because there are some 173PW of free energy falling in from a nearby thermonuclear reactor. The moment the energy budget becomes more restrictive, complete recycling of materials suddenly loses its appeal (applies to any system, be it natural or artificial). And your "bottle ecosystem" example would not stand at all - isolated ecosystems tend to lose complexity and accumulate "non recyclable" byproducts.

@oakad The energy flow from the sun was exactly my point, so we agree there. With respect to degradation of isolated ecosystems: do you have pointers to research about that? Sounds plausible but I couldn't immediately find anything. I also could live with a certain degree of degradation -- hell, I have to, considering ;-). Earth itself seems to do ok so far, and this man's bottle has been unopened for 40 years unless he's blatantly lying: http://sciencethat.com/?p=273

If an organism recycles some material, by definition, it is not waste.
Though some animals will eat feces.(For eg.Rabbits) It's a way to double-digest something that was not fully broken down or absorbed the first round.

Bears recycle their urine while hibernating, unlike most other mammals.


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What is the current theory of sexual orientations in Biology?
What is the current explanation of what causes the different sexual orientations in humans.

genes, environment see http://biology.stackexchange.com/search?q=homosexuality

It seems we have more hypothesis than theories.
There is a book called "The Moral Animal", by Robert Wright, where he cites some researches relating order of birth with sexual orientation (of course, not a 100% direct relationship). That's for the proximal cause. For the distal cause (evolutive) it makes sense to me that we are a sort of "eusocial" species, with homosexuality having evolved for the fitness it adds to the family: having lots of offspring, it's benefitial for the family if a few of them don't reproduce, investing instead in other fields of knowledge, like medical herbs, technology, weapons, etc. This may explain why this behavior evolved in first place, and why it's so widespread in virtually every known human culture, and almost all families.
Biologist Alfred Kinsey founded the Kinsey Institute (kinseyinstitute.org) for the study of human sexuality. His theory (that also appears in the movie Kinsey) was that there is a gradient from totally homosexual to totally heterosexual, with many intermediary degrees. Our religious culture tries to "erase" this diversity because of platonic ideals of "perfect male" and "perfect female", but in Amazon I saw that people are much more "plastic" than that, probably because of the lack of power of such religious traditions. Historians also talk about homosexuality as a "usual practice" in pre-Colombian America. And it is said that China have no problem with homosexuality before the arrival of monotheists. In India, homosexuality became a crime only 3 years after the british invasion (so it seems it was very common there, too).


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Effect of the health of the male parent at the time of conceiving
Does it matter at all in determining the traits of a baby what the current health of the father is? For example, let's say I got diabetes at the age of 40 because of the poor lifestyle choices. Will the baby be any different from how it would be if it was when I was say 26?

It can matter, though at this point we are just starting to understand how much.
Men can typically have children much later in life than women, but there are costs as time goes on.
Epigenetics has shown us that what happens to the parents in their lifetime can affect his offspring.  Obesity especially has been shown to affect the offspring, producing a higher risk of diabetes for two generations.
It is thought that this is not going to affect fathers who develop diabetes at a later age, but primarily those who are obese around 9-12 y.o. when the spermatogenic cells are produced in the testes.
What happens to men as they get older though is that their ability to produce healthy sperm starts to degrade.  They can lose fertility and produce more birth defects typically as early as age 35.  Given this there are probably a lot of habits or events that can adversely affect fertility.
Lifestyle choices as simple as tight underwear which might block blood flow to the testes is sometimes cited.
Given all this DNA or cellular damage from chemicals or diet or poor health certainly would also affect male fertility.


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Mutated Sperm - What happens?
I saw on TV that not all sperm are the same. Some have mutations like 2 and 3 tails?  There were other mutations as well.
If one of these mutated sperm actually fertilized an egg, would the embryo be mutated in some form or fashion?

Yes, the embryo would get that DNA mutation.
Both sperm and egg are haploid, meaning they only have 1 copy of each gene. When the sperm fertilizes the egg, the resulting child is a diploid, meaning he/she has two copies of each gene. However, if the sperm was mutated, then child has one mutated copy of some gene(s).
Depending on the gene(s) that are mutated and the sequence of the mutated gene(s), this could result in non existent to severe consequences.

So whatever is in the sperm that caused it to grow three tails would definitely have some mutative effect on the embryo.


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Fertilization of an egg by two sperm
What happens when two sperm fertilize an egg?  This can be either naturally or by experiment.

This phenomenon is called polyspermy and results in an embryo which is not viable. This is because it has more than the usual two sets of chromosomes (one from each parent), but one from the mother and multiple (depending on how much spermcells enter the egg) from the father.
To avoid this, most species (including mammals) have protective mechanisms against it. The so called cortical reaction which starts upon fertilization (the first sperm penetrating the zona pellicula) and releases cortical granules to prevent further sperm cells from entering.

In humans, polyspermy results in molar pregnancy.

It can also result in semi-identical twins when the egg goes through trisomic rescue to form 2 diploid cells with different paternal DNA but identical maternal DNA. However this is rare

Although the results are fatal in animals, as Chris' answer explains, recent research has demonstrated that plants can produce viable offspring with three parents. E.g.:

Triparental plants provide direct evidence for polyspermy induced polyploidy, Nakel et al., Nature Communications, 2017

We established a high-throughput polyspermy detection assay, which uncovered that supernumerary sperm fusion does occur in planta and can generate viable polyploid offspring. Moreover, polyspermy can give rise to seedlings with one mother and two fathers, challenging the bi-organismal concept of parentage.

This list of papers that cite the paper above includes more recent observations of triparental inheritance in plants.

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


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How do B memory cells provide immunological memory? Do they differentiate into plasma cells?
My text book doesn't say anything about how B memory cells actually ensure a faster response the second time the antigen is encountered. My guess is that they differentiate into plasma cells which produce antibodies, and release cytokines to cause clonal expansion of the correct T killer cells, but I'm not sure...
Thanks in advance for any responses ^_^

This 2005 review in the Annual Review of Immunology entitled "Antigen-specific memory B cell development" would be a great first resource in answering your question in great detail. Briefly, memory B cells (MBC), upon re-exposure to the same antigen, very rapidly expand and differentiate into antibody-producing plasma cells (PC), with the help of memory T helper cells (Th). However, more MBC are still produced by this reaction, so that a second challenge with antigen doesn't deplete the memory population.
PC are geared towards producing gobs of antibody, and not much else. Upon stimulation with antigen, MBC will produce some cytokines to attract the Th cells that are required for costimulation and regulation, but to my understanding it is the Th cells that manage the whole response, activating effector T cells ("killer" T cells), NK cells, dendritic cells, etc., and not the MBC themselves.


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What happens when we dream?
When a human dreams does the brain activate the cones and rods in the eyes creating the images we see in dreams?

The cones and rods would not contain the images from our dreams. Visual scenes get transferred from the eye to the thalamus (which serves as a relay to the cortex) by optical fibers that are overwhelmingly uni-directional (information is carried from the eyes to the thalamus and not vice-versa).
Dreams do, however, activate the thalamus, the visual cortex, and the visual regions that control eye movements (see refs 1,2). I don't believe there has been successful attempts to decode the activation, mainly, I think, because fMRI would be the best that we could use for humans and it does not have good temporal or spatial resolution.

Hong, Charles Chong‐Hwa, et al. "fMRI evidence for multisensory recruitment associated with rapid eye movements during sleep." Human brain mapping 30.5 (2009): 1705-1722.
Dresler, Martin, et al. "Neural correlates of dream lucidity obtained from contrasting lucid versus non-lucid REM sleep: a combined EEG/fMRI case study." Sleep 35.7 (2012): 1017.


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Do chicks in eggs excrete?
I want to know if, as a baby chick grows inside the egg, does it excrete waste?
If it does excrete waste, does the waste just sit inside the egg with the chick, until the chick cracks open the egg and gets out?

Yes they excrete uric acid which is stored in the allantois of the embryo; which acts as a reservoir of nitrogenous waste.
Uric acid is not very soluble in water, so it stays as a small solid mass.

@setek Welcome :) Keep on asking good questions!


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What problems do invasive species cause ?
Why do we value species?  What is so bad about invasive species?  Why value biodiversity?

Here is a post that might interest you as well.

This is far to vague and broad, and all subquestions are large and opinion-based.

Here is an attempt at a partial answer.

What is so bad about invasive species ?

Invasive species have been introduced to a new habitat by humans (or by natural means).
They usually do not have a predator in a new area nor are the pathogens in the area very adept at infecting them. So, they may proliferate rapidly and compete with the native species. They may also be ferocious predators as their preys do not have defenses against them.

But isn't this just how evolution and ecosystems work?  Things change.  Some are more virulent and they might monopolize a system for a while.  It's the nature of well, nature, to be in balance - but that balance is always changing and won't always be what it was before humans got there.

Biodiversity=ecosystem
system= more than one species
Advanced creatures such as us cannot live without other creatures, like plants and bacteria to support us. (yet)
If you want to see what invasive species can do watch this video, http://www.youtube.com/watch?v=Bk-9ndL3ykM it has some descriptions on what the invasive species homo sapiens and their domesticated cows do to their planet earth. Wasting resources basically. Displacing other animals and plants, monopolizing the earth. Monopoly or monoculture is not good. For if the monoculture fails all is lost. If you have diversity if one harvest goes bad it's not over yet. It's basically all about stability and sustainability. Without either advanced lifeforms cannot exist.

What do you mean by "non-natural"?  Human introduced?  Why does this make them bad?  Is this because we are responsible for the affects of our actions?  I've just never heard a teacher/proff/textbook set this logic out satisfactorily.  It seems like invasive species are, when it comes down to it, defined by what species cause economic damage - because there is no objective sense of bad.  So humans move fast... So??? What's so bad about upsetting the balance that was there before industrial- agricultural humans arrived?

It's not bad. Just inconvenient. That's all. If inconvenient = bad is up to you. ;) Balance = safe. No balance = unsafe. If unsafe is bad is again up to you.

I don't know much about the field of conservation but I'm giving a try...
In the following, when I say conservation I mean: "Human decisions and actions in order to protect the ecosystems". It has not to be confused with the science of conservation biology.
I think that the question you're raising shows the paradox of conservation. The maintenance of Biodiversity occurs through a dynamic process of speciations and extinctions allowed thanks to mutations, selection, population structure and movements. Standard ideas of conservation is not to preserve these processes but to prevent extinctions.
Quite a lot of many in conservation is aimed to save some big and representative species. Species for which we, as humans, feel some tenderness, love and pity for their fate. I am not saying it is bad to protect this kind of species I just want to emphasize that if we conserve it is not only for economic issues (or for the survival of our species) but also because we have ethics,  because we feel compassion  and guiltiness with nature of with some species such as the panda, the deers, the lynx, the wolves or because we feel compassion.
I also think that our categorization of living things into species (which is quite an subjective categorization) might bring us to take some decisions that do not fit economic issues.
For those who speak french well enough, here is a serie of podcasts (follow: "La biodiversité - plus qu'une simple question de conservation/") that might interest you. Especially the one given by Pierre-Henry Gouyon, which pretty much explain (much better than I did) most of the ideas of the last two paragraphs.
The question of invasive species is particularly interesting I think because there are especially a lot of invasive species today, first because ecosystems of changing (mostly because of human's activities) but also because human means of transport allow species to travel very far and become invasive. I assume (although I have no reference!) that the current number of invasive species is particularly high and just like any other disturbance in ecosystem, we can hardly predict what will the consequences. So shouldn't we make sure to keep this number of invasive species to a level which is closer to what would be found in nature in absence of human?

I'm learning french so I will definitely attempt to listen to those, merci :)  I appreciate your attempt to answer these questions, especially because this answer seems - to me - more aware of the assumptions and contradictions inherent in the arbitrary definitions such as species, or invasive, and the need to pair words such as "Biodiversity" with the utility we plan for them.  Thanks!