text:
Books on population or evolutionary genetics?
I have recently been involved in collaborations that require me to model the population genetics of eukaryotic populations. I fear I may either be "re-inventing the wheel" or making conceptual mistakes (e.g. simplifying assumptions) in many of the techniques and decisions so far.

I would very much appreciate recommendations of books about population/evolutionary genetics or micro evolution to deal with these fears. Preferable criteria are:

Intuitively introduces key concepts.
Emphasis on modelling with examples of problems and their solutions.
Relatively short (I'm planning to read from cover to cover).

Great suggestions so far, and the edits by @fileunderwater

TL;DR
I'd recommend Population Genetics: A Concise Guide (Gillespie) for an introduction to population/evolutionary genetics (thanks AGS for highlighting this big miss of mine on the first version of my answer).
I'd recommend A Biologist's guide to mathematical modelling in evolution and ecology (Otto and Day) if you want to ensure your knowledge in mathematics by learning their application to evolutionary biology.
General Entry Books to Population Genetics
There are several books that offer an introduction to population genetics. I read Principles of Population Genetics (Hartl & Clarke). I appreciated it but if I were you I think I would rather try Elements of population genetics (Charlesworth) or Population Genetics (Hamilton). There is also Genetics of Populations (Hedrick). I would tend to think that this last book presents lots of empirical population genetics data and doesn't take as much focus as the others in theoretical concepts (but I might be wrong). Gillespie's book Population Genetics: A Concise Guide is a classic. It is short, very easy to follow and pleasant to read. Gillespie's book might eventually be a little bit outdated but I would still highly recommend it.
Emphasis on Analytical Modelling
A Biologist's guide to mathematical modelling in evolution and ecology (Otto and Day) is a very good and very accessible book. It makes a good review about all subjects that are usually taught to first year students in Biology such as linear algebra for example. It is highly accessible and in the meantime it goes pretty far as it ends up talking about the application of diffusion equation in population genetics (Kimura's work among others). This book presents some important models in population genetics but as it aims to provide the tools for mathematical modelling in ecology and evolution it may under-considerate some fields of ecology and evolutionary biology. For example, the book does not talk about population structure nor about evolutionary game theory and there is little about Coalescent theory.
Other books treating specific subjects within population genetics
Coalescent Theory: an Introduction (John Wakeley) is a good book. I haven't read it completely for both time issues and because the math are a bit complicated for me. Coalescent theory offers a very important set of mathematical tools in evolutionary biology.
There's also Mathematical population genetics (Ewens). I am currently reading it. It is definitely not an introductory book and it really doesn't cover much of the most common fields in population genetics.
If you are particularly interested in age-structured population, Evolution in age-structured populations (Charlesworth) is a very good book.
Modeling evolution (Roff) offers some discussion on how to mathematically define fitness from phenotypic traits. While it is interesting I would not counsel you to buy it. Moreover, all the mathematics are quite basic and it aims to explain how to perform mathematical modelling with R which is to my opinion not essential to learn as other languages make a better job at dealing with math (Mathematica for example).
Evolutionary Conservation Biology (Ferrière, Couvet and Dieckmann) is a very good book of conservation and conservation genetics. It develop some mathematical models that are of special interest to conservation of populations and communities.
Ecology, Genetics and Evolution in Metapopulations (Hanski and Gaggiotti) is a book that may interest you as well. However it focuses much more on ecology than the other ones I cited above. Note: I haven't read it entirely.
If you are interested in kin selection and level of selection, you might want to have a look at Major Transitions In Evolution (Maynard Smith and Szathmary) which is a classic (I have not read it though) or The Major Transitions in Evolution Revisited (Calcott and Sterelny) who encompass the opinion of many authors on the subject. Evolutionary Dynamics: Exploring the Equations of Life (Nowak) is also of interest esp. for those interested in epidemiology. Finally, you might want to have a look at the extremely well written and easy to read books by Dawkins such as The extended phenotype (Dawkins) for example. The Dawkins book are very popular and very very introductory. It offers more a way to think than the actual science behind evolutionary biology.

my savior, cheers

Sorry for this late response. I am studying evolution these days and thought of learning the basics from Hartl and Clarke. As I was reading, I realized that the book doesn't give full proofs/derivations to any formulae. I find Kimura's papers quite difficult to read. Which book of this would you suggest me for a complete understanding of the mathematical aspects of different models/formulae? For e.g., I want clear derivations of Kimura's equations.

@WYSIWYG Kimura wrote a lot of equations. Which one are you having a hard time to understand? If you're having a hard time with diffusion equations and kolmogorov equations, you might want to have a look at any intro math course to diffusion equation. A Biologist's guide to mathematical modelling in evolution and ecology (Otto and Day) (linked in the post) gives some easy introduction to diffusion equations but does not enters into the details of its derivations. Hope that helps

See my new question.

I saw it (and upvoted it) after writing my comment. I am not able to answer it though. Asking on math.SE could be a good idea.

@Remi.b's list is excellent, but it should also include Gillespie's Population Genetics: A Concise Guide.

You've written this anser two years ago. Since that I kept the note that I had to read this book. I finally did it and could make an appropriate comment in my answer. It is a very good book I agree. Thanks!

Wow, I knew that Gillespie simulations work wonders for gene-circuit engineering. Wonders it does work, for modelling stochastic dynamics at multiple organisational scales in Biology then I guess. Cheers. http://www.sciencedirect.com/science/article/pii/S2001037014000403

Not relatively short, but I'm going to repeat a recommendation I just made in another thread. Population Genetics and Microevolutionary Theory by Alan Templeton covers many of the topics listed above, and is heavy on the self-learning of various population structure statistics, with examples. It is an introductory textbook with for people with some statistical background (though it includes a statistical appendix as well). There is quite a bit of discussion of Bayesian inference and other modeling methods as well.

I personally like the Primer on Population Biology by Wilson and Bossert. For a book that is almost 45 years old, it holds up pretty well. One of the best things about this book is that they provide examples and then walk through the solutions step by step. Once in a while it gets a bit too mathematical for this Biologist, but overall, I find it readable and informative.
I think this book fits all of your criteria very closely.


text:
Why are many anti-malaria drugs gap junction antagonists?
Why are many anti-malaria drugs gap junction antagonists?
My professor recently just mentioned that many of the anti-malaria drugs block gap junctions. i am wondering if this blocking is important for stopping malaria, and how blocking gap junctions is anti-malarial. How does this effect connect to the mechanism of malaria?

Could you give specific examples of antimalarials that block gap junctions? If they do, I'm pretty sure that this isn't anything to do with their antimalarial action. Most of the standard drugs interfere with the food vacuole of Plasmodium resulting in haem toxicity.

I wasn't sure when I first read this, but this is actually a very interesting question.
Right now there seem to be two completely divorced lines of inquiry that researchers are pursuing with respect to the antimalarial drugs.
One group of researchers is working on working out the mechanism by which say, chloroquine and its ilk bind to and  interfere with the formation of hemazoin (a parasite-friendly form of red blood cell proteins) in the vacuoles of the plasmodium (the parasite that causes malaria). Some folks have recently gotten some pretty reasonable crystals of chloroquine interacting directly with hemazoin. This all provides strong evidence for the view that, as regards killing plasmodium, the most significant interaction for an antimalarial is the one between it and hemazoin.
In (probably) unrelated news it was discovered that many of these antimalarials are also potent channel blockers of various kinds. I haven't dug into this too deeply yet, but most antimalarial people seem to view the channel blocking activity as a side effect. There are a number of other studies underway right now evaluating the psychological effect of the channel blocking activity of the antimalarials. There's one out of Iran that says that the blocking activity of Mefloquine can be used to ease the symptoms of morphine withdrawal.
Another thing to keep in mind is that Mefloquine fell out of favor not due to a decrease in efficacy, but was instead mostly taken out of circulation due to it's (justified) reputation for causing psychotic episodes in patients. So maybe this gap junction blocking stuff could be used to explain Mefloquine psychological side-effects. That would be neat!

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
What is the name of systemic tension of muscles?
I meat a overtrained friend (25 years old) who cannot rest.
He has all muscles and most of the skin very tense.
He is practising  regularly in gym and sleep badly.
He moves like a stick figure and has complained pains systemically.
The tenseness have now been some years.
I have met once before such a person who was about 90-year old body builder (male) who never run and did no stretching.
Ageing is not necessarily linked to this kind of tenseness.
I have not seen such tenseness in women.
So I think it is related to the muscles.
Possible pathogenesis. Probable causes of this kind of systemic tension

fibrinous inflammation starting from upper body

etc posterior, medial scapula;
middle inferior posterior clavicula

starting as membranous inflammation
long-term accumulation of fibrin and proteins in lymphatic system in interstitial spaces

proceeding on muscular membranes and through lymphatic system into axillary zone
axillary lymph nodes

deep injury of lymph conduction system as a consequence of decreased lymphatic drainage
proceeding into pseudomembranous inflammation in the upper body

starting from axillary lymphatic system
proceeding back to to the origin through fibrinous membranes as pseudomembranous to other parts (clavicula and scapula)

step by step proceeding into extremities and to lower body

eventually achilles tendon and foot Thian point glympadenopathy
hardening of foot muscles similarly as through upper body

Schematic drawing about the fibrinous inflammation

Possible other causes without citings to literature

right heart failure
systemic hypertension and defect in heart (etc fully patent foramen ovale; got idea from this discussion)

I am interested what is name of this kind of systemic tenseness, probably muscular origin.
What is the pathogenesis of this kind of tenseness?
Why is it systemic?

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Did the eugenics program in Nazi Germany have a measurable effect?
Did the killing or sterilisation of people considered as living a "life unworthy of life" in Nazi Germany have any measurable effect on the "average health" of Germany? Is there any statistical evidence that the rate of (a specific) mental or physical illness is lower in Germany compared to other countries that were not affected by the Nazis  (I guess you would need to have data on the rate of that illness from before the eugenics program as well)?
P.S. Please note, I'm neither interested in discussing the ethics of eugenics, nor in condoning what has happened in its name under the Nazis. I just want to know what the result on average health (if there is such a thing) was.

I think there is no possibility to study this, because there were several other factors having a big impact on the population, for example a war.

I would say that the war had a much greater impact on the population.

As already said in the other comments, the war (and many other factors) is a very important confounding effect and therefore measuring a change in health before and after the sterilization program would not mean that it is caused by the sterilization program. Beside this statistical issue: How do you think that this sterilization would affect health today?

Do you think of reduction in the number of reproducing individuals, yielding to a decrease in mean heterozygosity and therefore causing deleterious recessive alleles to be more often expressed? We could make some calculations to know what is the expected reduction in average heterozygosity. Or did you think about something else? Mental health? Partial recovery of sterility that, for some reason, causes poor gamete quality?

I really doubt that any effect would be visible in a single generation. We'd need data to back that up but I would be surprised if any difference is observable.

I don't see how this answers anything.

As most of the comment have pointed it out, It's nearly impossible to find out. This is my try:
Dr. L Alexander wrote in his paper, Medical Science under Dictatorship:

Hitler issued the first direct order for euthanasia in Germany on
  September 1, 1939, as his Panzers moved on the Blitzkrieg of Poland.
  Organizations with humanitarian-sounding names were immediately set up
  to execute "health" programs, again, under deceptively, euphemistic
  terms. For example, questionnaires collected by a "Realm's Work
  Committee of Institutions for Cure and Care" gathered and reported
  information on patients who had been ill five years or more and who
  were unable to work. "On the basis of name, race, marital status,
  nationality, next of kin, whether regularly visited and by whom, who
  bore financial responsibility, and so forth," decisions were made at
  key universities about which patients should be killed by
  psychiatrists who had themselves never seen the patients.Likewise, the
  "Realm's Committee for Scientific Approach to Severe Illness Due to Heredity and Constitution" was exclusively devoted to the killing of
  children with congenital anomalies or chronic illnesses. In all,
  275,000 people were put to death in these killing centers before the
  Nazi Holocaust.

Law for the Prevention of Offspring with Hereditary Diseases (July 14, 1933)

Anyone suffering from a hereditary disease can be sterilized by a
  surgical operation if, according to the experience of medical science,
  there is a high probability that his offspring will suffer from
  serious physical or mental defects of a hereditary nature.    Anyone
  suffering from any of the following diseases is considered
  hereditarily diseased   under this law:
1. Congenital mental deficiency,
2. Schizophrenia,
3. Manic-depression,
4. Hereditary epilepsy,
5. Hereditary St. Vitus’ Dance (Huntington’s Chorea),
6. Hereditary blindness,
7. Hereditary deafness,
8. Serious hereditary physical deformity.
Furthermore, anyone suffering from chronic alcoholism can be sterilized.

If anyone is trying to get the statistical evidence that Eugenics have even remotely successful, have look at this table:

Current Top 50 death causes of Germany. (Rate = $\frac{death}{1000}$)

They have started various ways to brainwash people, one of them was movies.
$\text{Ich klage an}$

(source: filmportal.de)
Plot: A woman suffering from multiple sclerosis pleads with doctors to kill her
Current Scenario: Germany Rank $18^{th}$ in the world in death due to Multiple sclerosis
Source:

Alexander L. Medical science under dictatorship. N Engl J Med 1949;July 14.
http://www.life.org.nz/euthanasia/abouteuthanasia/history-euthanasia6
Table: WHO, World Bank, UNESCO, CIA and individual country databases for global health and causes of death.

Good answer - I think its worth emphasizing that eugenics is not genetics and the traits that were used were often ridiculous.   For instance race as a primary selector in a genetics experiment is useless - we know that variations within race are relatively large.  Also these traits are terribly complex - eliminating heart attacks or schitzophrenia by eliminating people when they show signs will not do anything if they already have offspring.

@shigeta: I agree. But, What they did was nothing to do with biology, it was politics.

-1? Any reason?

not from me... the site reviewers do tend to be a little technocratic.  the answer could get back to the genetics of what they tried imho, but you can't do everything.  connecting to culture doesn't fly with some community members.  not my opinion, but i've been downvoted for cultural references myself.

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


text:
Do trees have no set lifespan and
"quite"immortal?
Many trees survive centuries and die only in disasters like
storms and lightnings or infections. So do they have no set
life span? Are they exceptionally resistant to genetic
mutations and have very less cell cycle regulations which
keep them 'forever young'?

List of oldest trees(wiki), list of long living organisms (wiki) and some impressive lifespan in animals

There are certain annual(eg.peas) and biennial plants(eg.carrot) also which die at fixed times.
But for perennial plants :
From this

Trees endure as long as they do basically because they're
  nonhierarchical organisms. In animals, all vital functions are
  controlled by the central nervous system, the guiding element of which
  is the brain. When the brain dies, so does the animal. By contrast,
  vital functions in trees are decentralized. A large part of the tree
  can die, and indeed routinely does die, without killing off the tree
  as a whole. Most of a mature tree is dead except for a few layers
  under the bark.....
All trees die eventually, of course. Four thousand years is old
  compared to the life spans of gossamer creatures like ourselves, but
  in the context of geologic time it's the blink of an eye. As they get
  older trees become more susceptible to disease, pests, and other
  perils, and inevitably these take their toll.

@user44289 Hi! You are welcome. If you think this has answered your question, you can accept it by clicking the green checkmark !

Sure! It is amazing they don't have a set limit of their lifespan.

@user44289 Yes, I agree ! Plants are pretty amazing!


text:
relative-rate of evolution
I am supposed to calculate the relative rate of evolution of two sequences (human and sheep) with a chicken serving as the outgroup. The sequences are pretty long, so I will just create a short example since I just want to learn the process (we are expected to use online resources to figure out our homework problems since it is an online class, but I can't find any examples).
Human:   GGATGCGCCT
Sheep:   GGACGCGCCT
Chicken: GGACACGCCT
Can someone show me how to do this? Here is my guess from the limited info I found, but I have little to no confidence that it is correct:
p-distance of human/chicken = 2
p-distance of sheep/chicken = 1
relative rate of evolution = 2/1 = 2
Is this correct? If not, can someone show me how to do it correctly?

This kind of thing is normally calculated using the $K_{a}/K_{s}$ ratio, the ratio of synonymous to non-synonymous substitutions. It is not enough to count mutations for coding sequences, you should also take into account whether or not that mutation will actually change the resulting product.
There are various online tools that can help you do this, for example Phylemon:
http://phylemon.bioinfo.cipf.es/evolutionary.html


text:
Why mosquito bite is confined to a certain shape?
I think this problem should be asked in a physiology forum rather than biology@ stackex but I'll give it a try.
So my question is simple - why a mosquito bite is usually confined to a certain shape (shape = red area) and not just disappearing continuously? Can our body cells tolerate some level of antigens without changing color from that?

Question of physiology are very welcome to our site! There is even a often used tag for that. It is totally on-topic.

Some biological processes have a threshold response (or a steep hill equation). Perhaps that's what's happing here.

What you're referring to as a mosquito bite is actually the "wheal" (red swollen bump in the skin) that forms from an immune system reaction to antigens (foreign molecules) in the saliva of the mosquito that it leaves behind inside the bite.  It's not technically a toxin, just something that causes an immune reaction.
It's also not an infection, it's inflammation.  Infection might set in if the skin is scratched open and bacteria move in.
The reason it's red is that immune cells release cytokines (like histamine and that cause cause edema that leads to swelling, heat, itching, etc - and recruit other cells to do the same.
The cytokines that act locally have a range of effect, especially histamine.  The degree of immune reaction determines the size of the wheal and how long it lasts.  Scratching it contributes to irritation and can prolong resolution.  Scratching it open can lead to infection.

You are totally right but still haven't answered the question I asked. Why the red swollen bump in the skin in confined to just a certain area and not continuously decaying?

I see your point that some wheals tend to have patterns (the most iconic one being the bullseye lesion of tick bites associated with lyme's disease). Demarcation of borders differs between individuals as well - not everyone has the same reaction to bites.  In this image: http://www.visualphotos.com/photo/1x8722914/skin_allergy_caused_by_mosquito_bites_049286.jpg  you'll see the most common presentation of a mosquito bite wheal.  The edges are not well demarcated; rather, there is a fade-away of erythema.  This is as I mentioned largely a result of the limited range of inflammatory cytokines.


text:
Usage of the taxonomic classification "Pinnipedia"
According to ITIS the classification Pinnipedia is  invalid, and it is proposed to rather use Caniformia. The later group however includes a range of terrestrial animals as opposed to the pinnipeds (the seals), which only include marine mammals.
Is the term Pinnipedia nevertheless still accepted and used in scientific media? Is there any debate whether to use one and not the other?

The Comments section of that page has the explanation:

Wilson & Reeder (eds., 1993) note that "the pinnipeds (otariids,
  odobenids, and phocids) are included within the suborder Caniformia;
  placing them in a separate Order would make the Carnivora
  paraphyletic." This arrangement continues to be followed in Wilson &
  Reeder (eds., 2005)

If both Carnivora (Bowdich, 1821) and Pinnipedia (Illiger, 1811) are orders in the traditional Linnean taxonomic sense, then one cannot be nested within the other. If this were to happen, then Carnivora would be paraphyletic because it would exclude some of its members. The same argument is made when discussion birds as dinosaurs (you can't talk about Dinosauria that doesn't include Aves).
The problem arises when phylogenetic systematics (clade names) meets traditional Linnean systematics (orders, suborders, etc.). Phylogenetic systematics does not distinguish these higher taxonomic groups. Clades are just nested groups of monophyletic taxa.
So then to answer your last question, Pinnipedia does appear to be in common usage (Google Scholar reports several hundred citations in the past few years). The key is to distinguish Pinnipedia as a traditional Linnean order (not valid) and Pinnipedia as a monophyletic clade that includes seals, walrus, and sea lions (perfectly fine). Seals, walrus, and sea lions are all more closely related to each other than to other Carnivora, so they are monophyletic, and the name for that grouping is Pinnipedia.
Here's the Tree of Life page that has all the clade names.


text:
Is Sinus node conduction necessary for heart beating?
Assume a patient with previous cardial infaction which SA node not possible to activate action potential anymore.
However, SA trying to beat unsuccessfully repeatedly waisting energy.
Therefore, I thought in this discussion about the possibility to stop Sinus node from trying to start action potential; which was deleted but the article about the SSS (sick SA) and remodelling is about its goal. The proposed treatment (laser ablation) of AF/AFL can backfire and cause SN (Sick Node) through remodeling. Assume there is no bypass of impulses through SA node.

Can the heart still beat through AV node and bundle? Yes.
Do you have any evidence that [heart] can "beat" properly on just the AVN? Yes, see article. Short-term mechanisms where electrical/metabolic remodeling. Long-term mechanisms where irregular rhythms and complete heart block can occur because of anatomical remodeling.

I want to know if these pacemakers are in series or parallel.
If they are in series, then laser operation can be dangerous to the SA node.
The series connection is however the idea which I get from many schematic drawings:

Do you have any evidence that it can "beat" properly on just the AVN? Loss of the SA node almost always leads to irregular rhythms very quickly (and with relatively bad outlook).  Can you look up some complete heart block examples and see if that covers your question?

The SA node is not necessary for contraction of the heart.
The reason that this works is exactly what you mentioned: schematics.
They are in sequence, but within that sequence, there are multiple autonomous signal generators in the heart, where spontaneous depolarization occurs to initiate contraction: the SA node, the AV node, and the purkinje fibers.
The SA node fires the most rapidly, 60-90 times per minute - which is the average normal heartrate, because in most people the signal for contraction arises from the SA.
The AV node fires at 46-60 times per minute.  If it receives the signal from the SA node then it depolarizes in sequence like the normal sequence we learn.  But if there is no SA node signal received, the AV node will depolarize on its own.
The last "generator" are the perkinje fibers.  If there is no signal from previous nodes, they will spontaneously depolarize.  However, they depolarize VERY slowly, at a rate usually under 40 bpm.  This severe bradycardia is potentially life-threatening, but allows the heart to keep some circulation going if there is a sudden complete AV node block - but prompt treatment is critical.
Regarding the lack of necessity of the SA node:
In fact, in some cases of supraventricular tachycardia (for example IST, see here) that are not responsive to conservative treatment, they will actually ablate (surgically destroy) the SA node in order to slow the heartrate down because a persistently extremely high heart rate can be dangerous.
Good question!

Extension to Doctor Whom's clear answer.
Clearer problem

It is debated whether the pathophysiology of IST and POTS results from
  abnormal autonomic regulation or abnormal sinus node function.

Radiofrequency Catheter Modification of the Sinus Node for “Inappropriate” Sinus Tachycardia
Location modification: Superior aspect of the crista terminalis.
Benefits

presyncope can resolve with sotalol
palpitation can resolve with β-adrenergic blockers
some patients (about 1/3) did not require any medication after operation

and other highlights

superior vena cava syndrome and dual-chamber pacemaker with patient with earlier A-V ablation

Postural Tachycardia Syndrome and Inappropriate Sinus Tachycardia: Role of Autonomic Modulation and Sinus Node Automaticity
Ceteris paribus condition

have IHR condition (Intravenous propranolol and atropine were given to block the sympathetic and parasympathetic limbs)

Findings

Treatment of IST and POTS should focus on sympatholysis, reserving sinus node modification for patients with continued debilitating symptoms after beta‐blockade and possibly ivabradine.

It is open research topic how the SA node should be ablated (removed) and how much.
I did not find any meta-analysis about the issue.


text:
Are there any fungi that can digest humic acids?
Humic acids are a complex group of organic substances, that are generally known to be hardly biodegradable. Fungi as agroup are known for breaking down complex organic matter like cellulose or lignin. But are there any that beak down humic acids as a major contributor to their energy needs?

According to Wikipedia, humic acid (HA) is a product of the biodegradation of dead organic matter. Shown below is a representative structure, but it important to understand that humic acid is a name given to a family of loosely related polymers of the products of biodegradation.
Although HA is resistant to further biodegradation, there are indeed fungi that are able to break it down further.

There is evidence that fungi can break down HA:

Grinhut et al (2011) Mechanisms of Humic Acids Degradation by White Rot Fungi Explored Using 1H NMR Spectroscopy and FTICR Mass Spectrometry Env Sci & Technol 45, 2784-2754

This paper reports studies of the mechanism of HA degradation by Trametes and Phanerochaete fungi (Basidiomycetes). This degradative property is attributed to the secretion of non-specific oxidising enzymes: manganese peroxidase, lignin peroxidase and laccase. the authors report evidence for "oxidation, a decrease in the aromatic content, and indication of demethylation of the HA during biodegradation.
The paper is also a source of references to earlier work.
The indications are however that these fungi carry out this degradation in the presence of other nutrients, i.e they cannot utilise HA as a major carbon/energy source.


text:
Troubleshooting for Agarose Gel Electrophoresis
SI ran my 2% agarose gel on constant voltage (100 V). For a few times it worked at CV but, after a week or so the machine would automatically switch to constant current by itself. And this only happens when I try to increase the voltage to 100 V. It works fine between 50-80 V. Beyond 80 V it keeps fluctuating between CV and CC.
Is there a problem in my power supply (GENEI electrophoresis power supply) or is the TE buffer that I am using? Although I checked its pH and it's fine.

Can you provide a few more details (you can edit your post to do so): At what voltage do you run you gels? How big are they? Which powersupply are you using?

I haven't found a manual for this machine, but my guess is that you exceed the maximum current which the power supply can provide. This is something I have experienced myself for electrophoresis.
Usually power supplies then switch into the constant current mode at the maximum current they can deliver, which I think is what happens here. If the voltage you choose is lower, you do not run into this limitation, thats why it is working without problems.
So you can either run your gels at constant current, which makes them run faster but also produces more heat, which can make your gel blurry. Or you live with a slightly smaller constant voltage, have your gels run a bit slower, but probably have a bit better resolution. I have to say that I have never had any problems with the resolution, even when I ran my gels really fast.

I tend to agree with this answer. Another cause for exceeding the max current could be a result of both high percentage gel in combination with old buffer, each contributing to greater electrical resistance. I prefer not running the voltage too fast otherwise you lose resolution due to the additional heat that causes the superficial gel surface to melt, appearing blurry.

alright great. these days i'm sticking to a lower voltage itself so i'm not facing any problems. but i just wanted to know the reason why. thanks guys it makes sense now :)

Gel melt can cause relly problems with low melting agarose. I have seen this at a colleagues gel once....


text:
Why does IUCN classify pistachio as a "Near Threatened" species?
When reading the Wikipedia entry on pistachio, I noticed that IUCN has classified the plant under "Near Threatened". On looking up its entry at IUCN, I see that its population is trending downwards, and it is "threatened by fruit collection, livestock grazing and cutting". The treat seems to have nothing to do with the often reported fungus. Looking up the yearly yields at Administrative Committee for Pistachios, I see that 2010 and 2012 were bumper years, but otherwise, I see no real trend of a decrease. Quite the contrary, I get the impression that the yearly yield is increasing. It's not as if the tree is difficult to grow, and we rely on trees growing in the wild; these trees are grown in orchards.
So, what's going on? Why would IUCN say that pistachio is Near Threatened?

You cited the reason already yourself: "Threatened by fruit collection, livestock grazing and cutting". Obviously conservationists see this as a big enough threat to raise some alarm.

@Chris: What I wrote after that invalidates that reason: unflagging and even bumper yields.

@prash It is near threatened and not endangered. I guess the IUCN sees this plant as going to face problems in the future due to a variety of reasons to which I would like to add habitat loss and temperature changes from changing weather patterns too.

@Chris You should post your comment as an answer.

Short answer: They were talking about the wild species.
Using the presentation by a Farm Advisor and a Pomologist, Pistachio Cultivars as a rough indication of the state of the species, we see that the commercial crop does not have much diversity.

Probably 97% or more of the pistachio acreage in California is planted to the Pistacia vera female cultivar called ‘Kerman’ and a P. vera male called
‘Peters’.

The presentation mentions that other geographic regions prefer other cultivars. But generally, the the entire commercial population of pistachio seems to be limited to a few tens of cultivars.
The IUCN Red List that I cited in the question is rather poor on the details. However, the publication, Geneflow '06, included a report on Uzbekistan's pistachio:

Saving Central Asia’s pistachio diversity
For three millennia, pistachio trees were used in metallurgy and mining in Central Asia due to their accessibility and the highly calorific charcoal they produce. The result was a major depopulation of wild pistachio in the region. During the Stone Age, pistachio trees in Central Asia covered approximately 2 million hectares, compared with only 300 000 hectares today.
The loss of wild pistachio diversity in Central Asia has major implications for pistachio growers in the region and beyond. Most of the pistachio gene pool is to be found here, where it is needed to underpin the continued availability of the tasty nut.

All the reasons they cited as factors for threatening the species likely refers to the wild trees.

Pistachio populations don't appear to be decreasing from your research because you are looking at  yields, not population level trends. Yield is not directly indicative of species health and is also not likely to immediately decrease with a population level decrease because farmers replant after loss.
The IUCN Red List Website lists declines in number of mature individuals, number of subpopulations, number of individuals in subpopulations, and number of individuals in the largest subpopulation. Other characteristics contributing to the "Near Threatened" classification are that the overall population is severely fragmented and both the overall population and subpopulations have been experiencing extreme fluctuations.
The IUCN lists the threats to the species as: "Natural stands have been impacted by overgrazing and are considered unproductive (Trees and Shrubs Online 2020), which may impact their management. Wild trees are also under threat from cutting and fruit collecting (Eastwood et al. 2009), while historically, the wild population has been reduced due to trees being felled for timber (Khanazarov et al. 2009). Human development has also led to habitat loss in some regions, though the extent of the impacts these actions have had across the species range are not clear."
Source: https://www.iucnredlist.org/species/63497/61526633#population
I also imagine that there is concern about species diversity. According to https://www.gbif.org/species/3190585 Pistacia vera is dominating the gene pool and population, which makes makes the sustainability of the Species unstable. If a pathogen were to target Pistacia vera, the impact on the Species could be devastating.

It's not clear what the sources "Trees and Shrubs Online 2020", "Eastwood et al. 2009", or "Khanazarov et al. 2009" refer to: more information is needed, like a DOI or URL, a title, a journal/book, etc.


text:
Evolution: How could all useful traits evolve simultaneously?
I have a basic question about evolution, for which I never found an answer. I understand how evolution works if we focus on one specific organ or trait. With each generation, some organism is more likely to reproduce, so the trait that leads to success gets more frequent. My problem is understanding how all the traits can evolve simultaneously.
Looking back to our ancestors, we evolved many different kinds of adaptations (in unrelated areas like eyesight, kidney efficiency or a healthy fear of predators, digestion of certain nutrients, balanced walking etc.).
Natural selection can only work with what's there, so mutations are important. But if  mutations are rare, it seems unlikely that many (thousands of) properties of organisms get improved in a single generation. You'd need to get very lucky to randomly improve all the genes responsible for it.
So, if we look back to our ancestors again, did they just improve on a single or a handful of traits in each generation? In that case we would need hundreds of generations before we have improved somewhat on each "front". By then, the other properties could "drift" back to a not-so-advantageous version. (This was supposing that each generation improves on a random trait, as opposed to long sequences of generations each improving on the same).
Or were there always some super lucky organisms that randomly got an improvement on almost all different traits? But just having some of those super lucky ones is not enough. The good traits don't guarantee success, just improve the odds. So we'd need many very lucky ones in each generation.
Has anyone calculated or simulated how the adaptation for many different traits can happen simultaneously?

Has anyone calculated or simulated how the adaptation for many different traits can happen simultaneously?

There are a lots of studies on the subject but I don't fully understand what is your issue. So I'll try to give some words hoping that helps a bit but it is possible that I'll totally miss the point you want to make.
The mutation rate in humans is around $1.25 \cdot 10^{-8}$ per base pair per individual per generation. The human genome contains about 3400 Mpb, meaning that you probably carry $1.25 \cdot 10^{-8} * 3.4*10^9 = 42.5$ mutations that none of your parents had in their genome. Now if you consider the population size, you'll see that a fairly big amount of mutations occurs each generation in the human population. So mutations are not that rare! It might unfair to take human as an example though as human's population size is very big. Anyway, the great majority of mutations are deleterious. In consequence, you are right, probably not many beneficial mutations will occur in a given population at one given generation and especially not in the same individual (except if you think of viruses!).
Now, depending on how beneficial is the mutation you are considering (selection coefficient), depending on its dominance, depending on the (effective) population size, your new mutations might take quite a bit of generations before reaching fixation in the population. In this time other mutations might occur. And then, the question is very interesting. Imagine a population of asexual individuals where two beneficial mutations exist (at two different loci [=position on a chromosome]). Because there is no recombination (by definition of what is an asexual population) never these two mutations will be found in the same individuals and in consequence if one mutation reaches fixation, it necessarily mean that the other mutation would have disappear. In sexual population it is different. Recombination allow that the two mutations, once they reaches a sufficient frequency will probably be found in the same organism and therefore, the two mutations can reach fixation.
Hope that helped a bit

Thanks. I think sexual recombination is the key to the answer to my question. It would allow the population to mutate in many different directions in parallel and then "merge" the successful mutations together later on. Very interesting! I never realized that recombination is so crucial in this regard.

@quorilla You might want to go for few lectures concerning the concept of "Muller's ratchet". The absence/presence of recombination is a very interesting subject. For example, it is the absence of recombination between the chromosomes X and Y that causes the Y chromosome to shrink.

@Remi.b By "mutation rate" do you refer to any kind of mutation, or only nucleotide substitution? So far, I haven't encountered the rate for genomic rearrangements (duplications, deletions...).

Well, it depends which study you look at (consider finding some numbers on bionumbers). I would personally tend to think that the standard error for this kind of study is large enough so that whether or not we consider genomic rearrangements is negligible in the estimate as those mutations are relatively rare. That is just my opinion though.You might find some estimates of the relative frequencies of the different types of mutations in the work of Sharp

The question about the "improbability of all traits" has a hidden assumption: that traits have had a given function since they appeared. This is not true however. Hemocyanin is an oxygen carrier today, but in the past protected anaerobic life forms. Feathers allow flight today, but they probably began as "tendrils" that allowed insulation, only to later "branch" and improve this function.

I think the main issue you have is in this paragraph:

But if mutations are rare, it seems unlikely that many (thousands of) properties of organisms get improved in a single generation. You'd need to get very lucky to randomly improve all the genes responsible for it.

There are two basic misconceptions there:

Mutations are not rare. They're actually very common. One of the cells in your body probably just developed one while you were reading this answer.
It is indeed unlikely that thousands of properties get "improved" in a single generation. That is not how evolution works. You need to remember that species evolve, not individuals. So, say I have been selected for because I run faster and my mate has been selected for because she's smarter, our child might incorporate both characteristics. Now extrapolate that to all individuals of a species and add a few million years and you get both intelligence and speed selected for.

Finally, luck has very little to do with it. We're talking about a very slow process that works over millions of years. Evolution does not occur over single generations, the mutations driving it might but not the evolutionary process by which these mutations become incorporated into the genome of the population at large.

Thanks. The key sentence is "So, say I have been selected for because I run faster and my mate has been selected for because she's smarter, our child might incorporate both characteristics."
This way we receive the good properties from an exponential number of successful ancestors in the past, each of which might have mutated in different advantageous ways.

The basic idea is that mutations improving different traits can occur in different individuals, and then be brought together by recombination. So the frequency of recombination roughly sets the maximum rate at which the population can acquire good mutations. Nick Barton and I calculated it, and found that a population can gain about one good mutation per chromosome per generation:
http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002740#pgen-1002740-g008


text:
Why do three nucleotides code for one amino acid? Why not 5 nucleotides?
We all know why there are 3-base codons, and why there aren't any 2-base codons. But why is there not a 4-base a 5-base codon?

http://biology.stackexchange.com/questions/6933/why-are-3-nucleotides-used-as-codons-for-amino-acid-mapping-in-dna

The more bases there are per codon the more information you can code for. There are only 22 different amino acids, in consequence we need minimum 3 bases per codon.

1 base-codon --> 4^1 = 4 possible codes which are:

A / T / C / G

2 base-codon --> 4^2 = 16 possible codes which are:

AA / AT / AC / AG / TT / TA / TC / TG / CC / CA / CG / CT / GG / GC / GT / GA

3 base-codon --> 4^3 = 64 possible codes which are:

AAA / AAT / AAC / AAG / ACA / ACT / ACG / ACC / AGA / AGT / etc...

4 base-codon --> 4^4 = 256 possible codes which are:

AAAA / AAAT / AAAC / AAAG / AATA / AATC / AATG / etc..

5 base codon --> 4^5 = 1024 possible codes

If we had only 2 bases per codon we couldn't code for all of the possible different amino-acids.
On the other hand there are several costs associated with carrying lots of DNA. It takes space, it takes energy and matter to get copied, it takes time to copy it (generation time might be limited by copying time), … I have just asked this question hoping to make things clear about the possible costs. If there is a cost associated with having a 4-base codon system compare to a 3-base codon system but there is no associated benefit. Such trait (that has a cost with no benefit) are not expected to evolve (counter-selected).
You'll notice that there are 64-22=42 extra possibilities. In consequence the genetic code is redundant. Meaning that several codon codes for the exact same amino-acid. And interestingly, it is often a the last of the three bases of the codon the does no yield to any change in the coding sequence as you can see here.

This post about the evolution of genetic code might interest you.

You really helped me, thank you. But could you please clarify your statement: "that would sounds stupid to have 5-base codon if there is no gain."?

@user6318 I already changed this sentence! I meant that there is a cost associated with having a 4-base codon system compare to a 3-base codon system but there is no associated benefit. In consequence, such trait are not expected to evolve. Hope that makes sense to you.

Warning for the uninitiated - that table is not the 'standard code' , it is the mitochondrial code (AUA is Ile in the standard code).

@AlanBoyd Whoops! Thanks a lot. I changed it, it is the "standard code" now.

I'm always bemused by arguments based upon the metabolic cost of maintaining DNA. I estimate that for E. coli less than 0.06% of ATP is used in replicating DNA, so for a 4 base codon system this would rise but would still be well below 0.1 %. This doesn't strike me as the basis of a strong selective pressure.

What about physiological issues? Space taking up by DNA and the machinery having to deal with these big sequences in bacteria? And what about timing issue? I've heard (but have no reference, I should make sure of this claim) that in some species the generation time is limited by the DNA copying time

@AlanBoyd I have just posted this question hoping to make things clear. +1 on your comment ;)

@Remi.b great! let's see what answers you get. In E coli it takes 40 min to replicate the genome, but they can grow with a doubling time < 20 min by reinitiating before the previous round of replication has ended. I was once told that the limit to growth is the exponential increase needed in ribosome number as more and more ribosomes are tied up just making ribosomes.


text:
What are the costs associated with carrying lots of genetic material
What are the costs (if any) associated with carrying lots of genetic material (Big genome size)?

energy for copying?
raw material for copying?
space in the cell?
Maintenance cost (matter and energy)?
time to copy is a limiting factor for the minimum generation time?
Less robustness?
More likely to evolve a gene that spreads well but has a negative fitness impact on the rest of the genome (selfish gene or outlaw)?

The answer probably depends on the organism. I am interested about any information concerning uni- or multi-cellular eukaryotes, bacteria or viruses.
Do we have any knowledge about how important are these costs or is it pure guesses?

This post comes in reaction to @AlanBoyd comments on this post.

It may also have negative effects due to mutations in genes which are not really needed but develop a negative effect.

What would be the cost of cleaning up this material?

What do you mean "cleaning up this material"?

Related question: http://biology.stackexchange.com/questions/10442/variations-in-genome-sizes

It is generally known that the smaller (or less complex) an organism is, the more "condensed" it's genome is. For example, bacteria (or some eukaryotes) have operons (http://en.wikipedia.org/wiki/Operon) or overlapping genes using different and they don't have introns, which alltogether saves a lot of space.
There are many reasons for that. Available space in the cell is definitely not one if it, however. Energy for copying and maintenance is a good point, but you have to keep in mind how evolution works. Bacteria and unicellular eukaryotes are usually adapted to a very specific environment in which they can reproduce rapidly. This means, they only need a small set of genes, specific for this environment and they have to reproduce very frequent, which means they are very prone to mistakes during DNA-copying. Such a mistake can lead to the death of the cell, which in this case equals the death of the organism.
In higher organisms however, the advantages of a bigger genome outweigh the disadvantages by far. Evolution can happen much faster because and mistake while copying does not necessarily lead to the death of the whole organism. Adaptation to a much greater variety of conditions is also necessary, e.g. when you look at plants: Their genomes are (on avarage) much bigger than the ones we mammals have, because they cannot move if the conditions around them become unpleasent. Instead, they need to find a way to adapt. This means, a big genome is in this case a fitness bonus. More interestingly, plant genoms are highly mutable (http://en.wikipedia.org/wiki/Transposable_element), which was originally thought to be a huge disadvantage.

Plants also often carry a lot more copies of their chromosomes than animals, I've heard of plants with 8 copies of each chromosome, creates a lot of opportunity to carry multiple alleles for a gene and use whatever works best for the current situation.

This answer makes very little sense. First, organism size and complexity are not always that related, (i.e. bull kelp and a shrew). Second, it is false that organismal complexity relates to genome size. This is true for prokaryotes, but less for viruses, and entirely untrue for eukaryotes. In fact, Polychaos dubium is a single-cell amoeba that has a genome ten times larger than humans. Or, for instance, the fact that amphibians lead the animal kingdom in genome sizes. Third, genome size does not correlate with vagility, for instance, worms and fungi have much large genomes than birds.

You clearly have not read my answer very carefully. I never claimed that organismal complexity relates to genome size. In fact, I argued that plants have bigger genomes than mammals, even though you will hopefully agree with me that mammals are much more complex organism. Furthermore, we are talking about generals trends and avarages here. Of course you can find plenty of exceptions - and Polychaos dubium clearly is one of them.


text:
Task-dependent "reversed" handedness: why use left hand for some tasks? How is it controlled by the brain?
I am right-handed. Which means that when I hammer down a nail, I hold the nail in my left hand, with which I can hold it straight and at a controlled position.
This is true in situations where the task of holding something in place is  simultaneous with a more complex task, such has hammering, done with the right hand. But I note that even when there is no other task, I personally use my left hand to hold in place, e.g., a  bottle that I am filling up in a stream of water.
To generalize a little, it seems to me that while I use my right hand for precise motion or applying a force, I'll use my left hand to maintain a position against forces.
Is this behaviour something documented? Does one develop specific brain control to implement this controlled-position tasks?

The dynamic-dominance hypothesis of handedness states that the essential factor that distinguishes dominant from nondominant arm performance is the facility governing the control of limb dynamics. Sainburg (1) writes that

It should be noted that dominant arm advantages do not apply to all
  tasks, or all aspects of tasks. Healey et al. (1986) examined an
  extensive range of tasks and found that four factors or groups of
  tasks accounted for 80% of the variance in hand preference among the
  110 subjects tested. Tasks that were almost exclusively associated
  with dominant arm use included activities requiring precision in
  interjoint coordination and trajectory formation. (...) In contrast,
  tasks that involved spatially orienting a body segment posture were
  more often performed with the nondominant arm. These tasks included
  posturing the hand to point toward a distant object, which is similar
  to other functional tasks such as holding a piece of paper that is
  being cut with scissors, or orienting the hand in space for catching a
  baseball. Such postural orientation tasks are less dependent on
  intersegmental dynamics, since the trajectory used to attain the
  posture is not critical for task success. The dynamic dominance
  hypothesis thus appears to account for the extent to which hand
  preferences for specific activities are lateralized.

This appears to be consistent with your experience.


text:
Is there a biological reason for spreading food intake into breakfast-lunch-dinner?
I keep hearing over an over how humans can satisfy their entire daily caloric need in one sitting at a fast food restaurant. At the same time I'm looking at the kitchen plates, cups, etc, and they also seem to be getting bigger.
This makes me ask the question - was breakfast-lunch-dinner a concept invented because people:

Could not make enough food?
Could not make food fast enough?
Could not make food with high enough caloric intake?

I'm thinking along the lines of: you can make only so much tasteless porridge and stuff it in your mouth before it gets cold. At the same time I know that gorillas and some other primates have a very long (8 hours?) feeding session of eating raw vegetation throughout the day.
Is there a biological explanation why human food intake should be spread into X distinct sittings?

A biological reason? I don't think so. I think this is more a cultural thing. It is before, during and after work.

In stone age I dont think it would be beneficial to have a fixed schedule.

The three meals a day seems to be a cultural trait. Then what is the optimal number of meals a day? It is not known. Here are the results of some studies:
Reduced meal frequency:
It was found that the body can adapt to a single meal a day by modifying circulating hormone levels and glucose tolerance [1]. However it does not modify lipogenesis rates [2]. It may support cardiovascular disease risk factors [8].
Increased meal frequency:
Although there are studies that claim 5-6 meals a day help in maintenance of weight loss [3], others claim this habit increases hunger and the desire to eat and has no significant effect on fat oxidation [4]. A higher number of daily meals is recommended to the elderly suffering from cardiovascular diseases [5] because less but square meals lead to a redistribution of blood to the gastro-intestinal tract to increase absorption, which causes reduction of blood pressure [6].
Conclusion:
Energy balance is more important than meal frequency. As this study says [7]:

... there is no evidence that weight loss on hypoenergetic regimens is altered by meal frequency. We conclude that any effects of meal pattern on the regulation of body weight are likely to be mediated through effects on the food intake side of the energy balance equation.

References:

Carlson O, Martin B, Stote KS, Golden E, Maudsley S, Najjar SS, Ferrucci L, Ingram DK, Longo DL, Rumpler WV, Baer DJ, Egan J, Mattson MP. Impact of reduced meal frequency without caloric restriction on glucose regulation in healthy, normal-weight middle-aged men and women. Metab. Clin. Exp. 2007 Dec;56(12):1729-34. doi: 10.1016/j.metabol.2007.07.018. PubMed PMID: 17998028.
Jones PJ, Namchuk GL, Pederson RA. Meal frequency influences circulating hormone levels but not lipogenesis rates in humans. Metab. Clin. Exp. 1995 Feb;44(2):218-23. PubMed PMID: 7869919.
Bachman JL, Phelan S, Wing RR, Raynor HA. Eating frequency is higher in weight loss maintainers and normal-weight individuals than in overweight individuals. J Am Diet Assoc. 2011 Nov;111(11):1730-4. doi: 10.1016/j.jada.2011.08.006. PubMed PMID: 22027056.
Ohkawara K, Cornier MA, Kohrt WM, Melanson EL. Effects of increased meal frequency on fat oxidation and perceived hunger. Obesity (Silver Spring). 2013 Feb;21(2):336-43. doi: 10.1002/oby.20032. PubMed PMID: 23404961.
Ortega RM, Redondo MR, Zamora MJ, López-Sobaler AM, Quintas ME, Andrés P, Gaspar MJ, Requejo AM. [Relationship between the number of daily meals and the energy and nutrient intake in the elderly. Effect on various cardiovascular risk factors]. Nutr Hosp. 1998;13(4):186-92. PubMed PMID: 9780751.
Westenend M, Lenders JW, Thien T. The course of blood pressure after a meal: a difference between young and elderly subjects. J Hypertens Suppl. 1985 Dec;3(3):S417-9. PubMed PMID: 2856754.
Bellisle F, McDevitt R, Prentice AM. Meal frequency and energy balance. Br. J. Nutr. 1997 Apr;77 Suppl 1:S57-70. PubMed PMID: 9155494.
Stote KS, Baer DJ, Spears K, Paul DR, Harris GK, Rumpler WV, Strycula P, Najjar SS, Ferrucci L, Ingram DK, Longo DL, Mattson MP. A controlled trial of reduced meal frequency without caloric restriction in healthy, normal-weight, middle-aged adults. Am. J. Clin. Nutr. 2007 Apr;85(4):981-8. PubMed PMID: 17413096.

The answers to your 3 questions are no, no and no. The 3 meal concept is more of a recent concept when you compare that Ancient Romans used to frown upon eating more than once a day. You can read a brief history of how food habits evolved in this article. Food habits have been variable all throughout history and it still varies by culture. Food habits divided by different eras can be read in this article. In the current age and time, I think we just try to spread our calorie intake over the day and that is why we try to stick to the 3 meal concept.(reference). There is no biological reason as far as I could see (reference). Just a matter of improved health consciousness and understanding of the human body. This article contain some interesting thoughts on meal timings and optimal intake.

could you perhaps share/summarize an important quote from some of these sources? I ask because if any of your links go dead (which is surprisingly common) your answer loses much of its value. Just want to make sure posts remain helpful for as long as possible :). Thanks!


text:
Which ionic channels of Pacemakers can work in very low frequencies in extrasystole?
At frequency 0-3 Hz.
Like computer processors which can work at low frequencies and controlling under- and overvoltage.
Normal most significant channels are Ca2+ and K+ that are changing.
However, I am not convinced that they can work with such a low frequencies.
There must be some other channels that are triggering the extrasystole on.
Which ionic channels of Pacemakers can work in 2-3 Hz triggering extrasystole?

I think none.
It is so specific frequency range that the possible sources are

autonomic nervous system and
some reflex arch.

Also, the frequency is logically low with autonomic triggering.
My conjecture is that sympaticus starts up extrasystoles.
I think it must go through some reflex arch to be so specific.


text:
Which reflex arcs work in Heart with extrasystoles?
I am researching what is triggering the extrasystoles - initial idea from this thread about Which ionic channels of Pacemakers can work in very low frequencies in extrasystole?
I am interested in the reflex arc with extrasystoles.
I am not completely sure if the intrinsic regulation of the heart can start specific stimuli.
I have now intuition that not possible.
What are the reflex arcs of the heart?

Not to be fussy about it, but it will help someone searching for your question.

Edits are always welcome :)


text:
Is it possible to have life in vacuum?
I just got struck by curiosity now: Intuition says no, but I've never had confirmation of it.

Define life. You can probably get viral spores that can survive and even some extremophile bacteria but in a dormant state. Would you consider something that is not interacting with its environment in any way at the moment alive?

See very similar question and answers here: http://biology.stackexchange.com/questions/2700/can-the-body-of-any-organism-on-earth-live-without-impairment-both-in-vacuum-an/2703#2703

nobody has had confirmation of this - with the possible exception of the tardigrade in space experiment and those like it in the ISS/space shuttle.

You could build robots that feed on debris, like man made satellites, that satisfy common definitions of life (e.g. Reproduce, have a metabolism etc). In general life as we know it does not do well in space because it is very cold, and not much chemically is going on to support metabolic processes. The lack of food, water and the vacuum make it rough as well.

As @terdon comments, dormant organisms can survive in vacuum. This includes lichens, bacteria, and even an animal: the ever-amazing and adorable tardigrade (Jönnson et al 2008). In 2006, tardigrades survived exposure to the vacuum of outer space with no appreciable difference in mortality compared to controls.

Tardigrade Hypsibius dujardini, a different genus than the ones sent into space, but probably equally hardy. Photo by Bob Goldstein & Vicky Madden (CC by-nc-ca via Goldstein lab - tardigrades on flickr).

Jönsson, K. I. et al (2008). Tardigrades survive exposure to space in low Earth orbit. Current Biology 18(17):R729–R731

Be able to survive it is quite different from living permanently in it...

I agree! Which is why I upvoted your answer.

No, it is not. Or at least not in the form we know life. The reason is that water (which is essential for life) boils at low pressures at room temperature. This makes life impossible in the form we live it on earth.

No, because some kind of fluid (liquid or gas) is necessary to supply resources and carry away wastes. Bacterial spores, tardigrades, etc. are in a dormant state when in a vacuum.


text:
What are the mechanisms of disabling extrinsic control of heart?
I started this thread by thinking this question but I developed it further below

What is the mechanism maintaining refractory period of pacemakers?

My conjecture is that the mechanism is the simultaneous depolarisation of at least SA node and AV node.
I am not convinced yet about the Purkinje fibers' participation.
Bigger question from this is:
How do pacemakers work under threshold without action potential?
There are continually leaking Funny channels (Na+) in pacemakers.
There has to be chemical changes intrinsic changes

change in the permeability of Funny channels or
active pumping of Na+ out OR pumping something negative inside the cell (probably Cl-, not sure) and

extrinsic changes

reflex arch blocking the action potential of pacemakers when enough preceeding sensitisation of AV node

I have no evidence for that this kind of sensitisation would happen in SA node or in Purkinje fibers.

which all seem to be working together in firing recovery mechanism through AV node without specific SA node stimulation.
Example logic tree for a myocardial infarction patient of 68 years old:

R wave of atrial fibrillation and flutter
extrinsic stimulus to start sensitisation of AV node
intrinsic sensitisation of AV node
extrinsic stimulus through reflex arch
systole and upper-systole of AV node starting
lower-systole of AV node

intersection of upper- and lower-systoles

unstable end of lower-systole
unstable systole
extrinsic firing simultaneous SA and AV node (similar extrinsic regulation as in the beginning of this logic tree)
prolonged and stable refractory period and long compensatory pause

It is debated whether the pathophysiology of IST and POTS results from abnormal autonomic regulation or abnormal sinus node function.

My conjectures based on my logic tree

Pathophysiology of IST results from normal extrinsic (recovery) mechanism of autonomic regulation which body uses to recover from abnormal stimuli (etc atrial fibrillation and flutter)
Pathophysiology of POTS results from abnormal extrinsic mechanism of autonomic regulation when there is no stimuli after abnormal stimuli

What is causing the abnormal autonomic mechanism in POTS?
I would say that IST precedes POTS.
Prolonged IST seems to be going to POTS.
Physical explanation is that the body cannot last regular IST so it goes to POTS, since losing its normal extrinsic regulation.
What is this (apparently cumulative, not necessarily long-term) trigger of disabling the extrinsic autonomic regulation of the heart?


text:
What is the beneficial function of IgE antibody?
Dont tell me the "function" of IgE is to cause allergy !
In whatever texts I have seen it is  written that IgE is important to cause allergies but what is the beneficial function of IgE ? Why was it ever created ? Did it have an advantage in the pre historic ages but now causes allergies ?

No, they are of course not there to cause allergies.
It is thought (although not directly proven in human) that IgE is important to fight parasites and worms. They bind to antigens from the parasites, which leads to the secretion of histamines. This causes a local immune reaction (which also is a problem in allergies) which is helpful to fight the parasites.

See these papers for example:

IgE, allergies and helminth parasites: a new perspective on an old
conundrum.
IgE Enhances Parasite Clearance and Regulates Mast Cell Responses in
Mice Infected with Trichinella spiralis
Immunology of Parasitic Helminth Infections

There is also some evidence, that IgE is involved in the immunological response to cancers:

Activity of human monocytes in IgE antibody-dependent surveillance
and killing of ovarian tumor cells.
Animal models for IgE-meditated cancer immunotherapy

I referred to some good texts in immunology and saw the mention of its role in fighting parasitic infections. I feel that IgE might have played an important role in survivorship back in the stone age when parasite infections were so prevalent. Now that the amount of parasitic infections have been drastically reduced, it may exist merely as a genetic quirk which causes allergy. (There are many theories on benefit of allergies but they are inconclusive.)

One obvious thing to determine the function of IgE would be to remove it from body and see what bad effects it causes. There have been several studies on people with lower amount of IgE and they show higher chances and more severe cases of parasitic infections and respiratory tract infections. But these could have been the result of whatever factor caused the reduction of IgE in the first place. It is really important to separate the noise.

authors: Müñîß Fåøøqî


text:
What exactly makes bananas go brown?
I know that often oxidation processes are mentioned when referring to the color change from yellow to brown in bananas (specifically: those that you get everywhere in supermarkets, with no seeds).
However, I am really interested if there is a specific oxidative pathway that is generally followed in this process, and whether it has been examined.

Note: When answering this question, please back up your claims with references to the scientific literature.
(This is not a homework question [although phrased like one] but arose purely from personal interest and lack of time to pursue it properly.)

As a sidenote: Ethylene is an hormone involved in fruit ripening.

Irrelevant to why bananas go brown, but the process is faster  in cold conditions than in warmer ones. So it's not worth putting bananas in a fridge.

The reason for this is the oxidation of phenol residues in the banana (for example in the yellow color) which get oxidized by the enzyme Polyphenol oxidase (PPO) to melanins. The scheme (the image is from this website on food browning) looks like this (you can of course also use more complicated substrates):

For further information, see these references:

Banana Polyphenoloxidase. Preparation and Properties.
Molecular cloning and characterisation of banana fruit polyphenol
oxidase

Polyphenol oxidases are widely found in fruits and cause most of the oxidative browning. See these articles:

Polyphenol oxidases in plants and fungi: going places? A review.
Enzymatic Browning, Polyphenol Oxidase Activity, and Polyphenols in
Four Apple Cultivars: Dynamics during Fruit Development

Could you explain how tyrosine gets in there? What is it that's being oxidized? I assume you mean free tyrosine molecules and not those incorporated into protein right? If I'm missing something obvious, please point it out, biochemistry was never my strong point and I haven't worked in a wet lab since university.

@terdon Tyrosine is a simple molecule used for demonstration. PPO's can oxidize quite a range of molecules, which have to contain phenyl groups. See this paper for some details.

I remember reading somewhere that PPO  has a role to play in the change in colour(to brown) of cut apples when exposed to air.

Ah OK, thanks. I thought you were suggesting that the oxidation of tyrosine molecules was responsible for the change of color.

@biogirl PPO's are present in almost any fruit. Appples, Bananas, they are responsible for the brown color of tea and cocoa, mangos and so on.


text:
For emphysema, which of the respiratory volumes is affected?

It could be the tidal volume because it affects how a person inhales and exhales normally.
It could be the residual volume and functional residual volume, because it increases its amount. Because it traps air.
On the other hand it also affects the Forced vital capacity because it decreases the amount of air that can be forcibly exhaled immediately after one inhalation.

To learn obstructive/restrictive lung diseases, I find it easiest to think in extremes at first, with vivid descriptions of why.  So in obstructive lung diseases, like COPD/emphysema:
Total volume increases because so many of the walls of the alveoli have been destroyed, they are like giant floppy bags instead of nice firm bubbles.  There's more empty space, and total volume is therefore increased.
Reserve Volume and End Respiration Volume increase because these alveoli are large and stretched and floppy and can't push as much air out, even when you try.  (Decreased elastic recoil.)  They also flop shut often before the air is expelled - trapping air in.
Tidal volume may not change at all, but it takes longer to exhale than with normal lungs.  That is why FEV1 and FVC are lower, for the same reason.
Residual volume


text:
Earwax versus Mucus
Something I have wondered for a while is why have two different primary defense mediums, ie earwax and mucus, that perform the same function?
As far as I know, mucus and earwax are both part of the primary defense of an organism against disease and foreign particles, by trapping any pathogens or dust that enters the body.
My question is; Why does the body use earwax for ears and mucus for the lining of other entrances to the body, why not have mucus in the ears or earwax everywhere else? is there an advantage to have each medium in their respective places?

Unique and interesting question.  It's hard to give a firm "why," but we can discuss the ways that the ear and other "holes" differ.
Mucous membranes line every tract into/out of the human body.  Technically the ear is not a point of entry, as the tympanic membrane makes the external auditory canal a sort of blind pouch.  The skin lining the ear is keratinzed skin.  Most skin has keratin and is difficult to permeate.  But mucous membranes are moist, thin, usually highly vascular, and generally easier to permeate.  Disease often takes hold or gains entry at mucous membranes (respiratory infections, GI infections, etc). That is why mucus is so critical as it is protective and acts as a barrier and flushing-system.
Mucus requires some form of circulation, as it is a fluid.  Once produced, usually at least some of the fluid is reabsorbed, and the remaining material is passed along until it exits the body.  In the lungs, cilia bring it up to the throat and it is swallowed into the GI tract.  In the nose, it drains down the back of the throat and is swallowed.  In the eye, the fluid (which has mucus components to it) drains into a small tract that runs into the nasal passageway, which drains along with the other nasal mucus.  Obviously saliva, which also has mucus components, is swallowed (2 liters a day of it, actually).  In the genito-urinary tract, there is both reabsorption of some of the fluid components, but mainly flushing outwards when urinating.  The GI tract reabsorbs almost all water components and the remnants pass with stool.
Mucus is produced by mucus glands.  Cerumen (ear wax) is produced by sebaceous (oil) glands and apocrine (sweat) glands, but is primarily composed of shed skin cells from the ear canal.  Sebaceous and apocrine glands are all over most of our exposed skin (except palms etc) so it stands to reason that they would be present in our ears as well.
Cerumen exits the ear several ways: all skin on the body sheds the top layers as new skin grows from underneath, and in the ear, the skin cells also migrate with a directionality from the tympanic membrane outwards.  Head movements (like chewing) help dislodge things stuck to the walls.
I'll put in my plug here about NOT using cotton swabs (aka Q-tips) to clear your ears.  It generally just pushes the wax deeper, except for the tiny bit you manage to get out.  I've cleaned out tons of wax-impacted ear canals from people who use Qtips on themselves or their kids!!
If the ear were to use a mucous membrane system, the lower viscosity fluid would have to go somewhere.  We would be weeping mucus from our ears unless there were a drainage system into the sinus passageways.  The body conserves liquid, so we couldn't afford the constant fluid loss otherwise. The middle ear has a canal - the eustachean tube - which leads into the nasal sinus (although primarily to equalize pressure).  But the external ear does not, so it's probably a good thing that we don't have mucous membranes in our ears.

Wow fantastic answer! That helps a lot! Out of curiousity, what should we use to clean our ears?

Ears mostly clean themselves, especially after you stop shoving it deeper inside with Q-tips.  But I completely understand the desire to "help it along."
This is gathered from recommendations from doctors in Audiology, Pediatrics, Family Medicine, and Emergency medicine - whom I have personally talked with about the topic.

In the shower, you can tilt your head to the side and let warm water and shampoo suds run into your ear.  Switch sides.  Then go back to the first ear, and tilt your head to drain the sudsy water.  Then let it fill with clear warm water again, tilt and drain, and repeat until no soap is left in the ear.  Soap residue also can be itchy and irritate.  If you do this regularly, there won't be an accumulation of lots of wax.

If you really need more help, you can use a little vinegar (25% solution) in warm water and let it soak in there several minutes before rinsing in the shower.  If it's to the point it's affecting your hearing or painful, call a primary care doctor, urgent care, or otorhinolaryngologist (ENT = Ear Nose and Throat specialist physician) and they can remove it for you.  There's a wax-softening solution that can be purchased at the pharmacy (not sure if it's prescription), but it's best to avoid anything medicated unless you're symptomatic (hearing loss, pain) - make sure you ask a doc/pharmacist.

Important note: if you've had surgery on your ear, especially eardrum (tubes etc included) don't do anything without asking your doctor.


text:
Which was the last significant event in human evolution? What's next?
At 10.000 BC (12 ka), we became the last of the Homo species on Earth. In evolutionary terms this is a very little time range to something happen, but I'm wondering anyway, in this meantime which are the most significant changes in our species? Were there any?
Also, I've heard something about how our body hair and nails will be gone 'soon', there's any estimation of when such a thing could happen?!

The problem with most evolutionary changes is that they can mostly be seen only in review (except for developing a third arm probably). So we actually don't know what is going to happen next.

@Chris Sometimes we do know very well, but nobody listens.

@RodrigodeAzevedo What do you have in mind?

@Chris Intelligence. One generation is enough.

Background
I'd like to start by saying that phenotypic (loosely speaking phenotypic mean morphological) traits evolve because their variance in the population is correlated with some genetic variance. If most of the phenotypic variance is genetically coded, you'd expect that the trait will change through if different variant of the trait influence fitness (which is a function of both survival and reproductive success). Stated differently and more accurately the change in mean value of a given trait $R$ in the population is given by:
$$R=S\frac{V_{Ga}}{V_{P}} = S\frac{V_{Ga}}{V_{G}+V_{E}} =  S\frac{V_{Ga}}{V_{Ga} + V_{Gd}+V_{E}} $$
, where $S$ is the selection differential, $V_{G} = V_{Ga}+ V_{Gd}$ is the genetic variance where its two components are the additive and dominance genetic variance respectively. $V_P  = V_G + V_E$ is the phenotypic variance which two components are the genetic and environmental variances. The ratio $\frac{V_{Ga}}{V_{P}}$ has a name; it is called the heritability in the narrow sense symbolized by $h_N$ Note: I present here a simplified version of the reality!
So, if the trait you consider has genetic variance in the population and that this trait influence the fitness with a given selection differential you can provide estimates of how the trait will change through time in the human population. Now if the variance does not already exist in the population but you have to wait for mutations to occur, then you cannot really provide an estimate of when will this occur.
Discussion on the future evolution of nail size
Also, when you think about some traits such as our nails. You may consider that they are of no use but do you really think that those people that have no nail would really have a better fitness. At first I would tend to think that I would rather chose a partner that have nails, it is much more sexy! If many people are like me and appreciate nails, nailless people will have difficulties to reproduce or in other words, they will have a lower fitness that nailed people.
I don't think we have data on what loci (positions on the chromosomes) influence the size of the nails and about how much of the variance in nail size is explained by the genetic additive variance. And how do the size of our nails influence fitness. So we don't know about how this trait will evolve through time.
Future evolution of other traits
There are several traits that we can/could more or less predict their evolution. Those are the traits for which we know the ratio of the genetic additive variance over the phenotypic variance and how it influences fitness. I can think of genes that are linked with resistance to new diseases such as HIV for example. If malaria comes to a new area you might expect the allele (=variant of a gene) allowing a better resistance to malaria will increase in frequency (note that this allele is advantageous in heterozyotes (protects from malaria) but it is highly disadvantegous in homozygote because it causes sickle-cel disease). We could estimate the change in frequency of alleles linked with obesity in some countries also. Probably several studies exist on the subject but I don't know them. One might improve this answer by giving some information about how HIV resistant variants is likely to change in frequency through time.
What were the last evolutionary changes in human history?
You can think of the impressive frequency of the Tay-Sachs disease in french canadian due to a bottleneck effect. Or you may think of the evolution of height, about the evolution of the shape of the skull or the evolution of feet. You can think of the reduction of our gut. etc… Your question is not well enough define so that we know if you consider the raise in frequency of Tay-Sachs disease is sufficient for you to be called a significant evolution.
Hope that helps!

Yes, it helps... Thank you! By a significant evolution event I mean it in a more common sense way, like something that can be visibly noted on our anatomy and perhaps could have some comparative figures.

One example of an active selection pressure's effect on human phenotype is in areas where malaria is endemic, the prevalence of sickle cell anemia is higher.  Sickle cell anemia is highly protective against malaria, and less people die from sickle cell than die from malaria, so you see a rise of sickle cell in the population.  This is a small degree of phenotype selection compared to the sort of selective pressure that would be required to cause the degree of evolution you are talking about, but it's one of the few things that can be readily seen in the modern world.  Most people in the modern world live long enough to reproduce, and survival of the fittest has less influence on us than it did in our tribal days.
To wax philosophical, one might argue that the media (e.g. Hollywood) has exerted a selective pressure over our evolution, as it has significant influence over what people deem "beautiful" and "attractive," thereby altering our ultimate mating selection behaviors.


text:
Evolution of Chromosome Numbers
Some species have different numbers of chromosomes, as we all know. Throughout evolution, how was a species able to survive with an extra chromosome? How was this organism able to breed successfully to form offspring with the additional chromosome?

+1 good question. I guess that an added chromosome probably come from the duplication of another chromosome yielding to a partial polyploidy. Under this assumption it might be interested to look at the work of Sally Otto on change in ploidy number. I think we might intuitively overconsider the importance of such duplication on the functioning and health of the cell. I would tend to think that the big issue has to do with dosage compensation (amplitude of gene expression). Also, such duplications have the advantage to hide recessive deleterious allele.

possible duplicate of Evolutionally speaking, why do humans have 46 chromosomes

I don't think those should be considered duplicates. On the other hand, I seem to remember another very similar question. Does anyone know it?

possible duplicate of How are new chromosomes replicated into the next generation via sexual reproduction?

Chromosome splits (or fusions for that matter) might not mean that much for reproductive success since genes can still line up and recombine. To quote the science blogger P.Z. Myers:

[C]hromosome numbers can change dramatically with no obvious effect
  on the phenotype of the organism.

He illustrates it thusly:

So to answer your first question, changes in the number of chromosomes aren't always fatally deleterious (as you seem to think).
As for how a change in chromosome number might spread, the explanation is likely random drift and inbreeding. To quote P.Z. Myers again:

So our two chromosome individual will have a reduced fertility as long
  as he or she is breeding with the normal one chromosome organisms, but
  those split chromosomes can continue to spread through the population.
  They are not certain to spread — they’re more likely to eventually go
  extinct — but by chance alone there can be continued propagation of
  the two chromosome variant.

"Evolution" by Mark Ridley, p. 361 similarly points out that reproduction will be an uphill battle until the new variant becomes more common (often through inbreeding or drift in small populations):

When a new chromosomal fusion mutation arises, it will be selected
  against because of its disadvantage in heterozygous form. But if it
  drifts up to a locally high frequency, as may easily happen in a
  local, small, and perhaps inbreeding, mouse population, natural
  selection will favor it. Natural selection favors whichever
  chromosomal form is locally common[.]

This might in the end lead to speciation due to the two populations becoming incompatible.

What about the very first organism to get an extra chromosome? Assuming it was a very small organism, wouldn't the need to replicate an extra set of chromosomes be very resource demanding to the organism and therefore possibly cause death? Or was this effect not very significant on the organism's chance of survival?


text:
Number of autoregulation and FFL motifs in a network
Suppose we have a network with N* nodes (N* is the number of internal nodes). Every directed link in this network exists with probability p. What would be the number of:

motifs that are auto-regulatory?
feed-forward loop motifs
feed-back loop motifs

that looks like a homework problem. please see http://biology.stackexchange.com/help/homework on how to modify your question

Yes it was a homework problem. Thank you for the link. I am new in the whole stackexchange thing. I read it's ok that I answer my question though, now that I know how.

The average number of auto-regulatory motifs (self-edges), is equal to the number of edges E times the probability that an edge is a self-edge which is $p_{self}=1/N$, with N being the total number of nodes. Therefore, $<N_{self}>_{rand} \approx E/N$
& 3. According to U.Alon's book ("Introduction to Systems Biology"), the mean number of times that a subgraph G occurs in a random network is given by the following formula: $<N_G>\approx a^{-1}N^n p^g$.

Explaining what each term of the formula means:

α: is a number that includes combinatorial factors related to the structure and symmetry of each subgraph, equal to 1 for feed-forward loop (FFL) and equal to 3 for feed-back loop (FBL)
$N^n$: is the number of ways of choosing a set of n nodes out of N. Because there are N ways of choosing the first one, times N-1$\approx$N ways of choosing the second one, and so on..(this approximation is true for large networks)
$p^g$ : is the probability to get the g edges in the appropriate places (each with probability p)


text:
Book suggestion on computational molecular evolution
I'm currently reading Computational Molecular Evolution by Yang. Can you recommend alternative books?
I am finding it to be lacking on conceptual discussion (it's more focussed on the mathematics and statistical intricacies). I'd like to find something which discusses why we do the things, and the strengths and weaknesses of the ideas, which are presented in the Yang book whilst not being overly specialist - more of an introductory text to the field.
Any introduction to phylogenetics books??

I would suggest the course of Coursera.org:
Computational Molecular Evolution
By Anders Gorm Pedersen
Technical University of Denmark (DTU)
PS: Do tell us if you found a better book!


text:
Does our eyeball increase in size as we grow?
Does the size of the eye increase as we develop from the stage the complete eye first forms to infancy and then to adulthood ?

First of all, I should quote the sentence from the MOST reliable ophthalmology sourcing in the world - American Academy of Ophthalmology:
Section 11 - "Lens and Cataract"
"The equatorial diameter of the unfixed human lens measures 2 mm at 12 weeks and 6 mm at 35 weeks. Both the growth and the maturation of lenticular fibers continue throughout life." The antero-posterior dimensions of the lens enlarge from 3 mm at infancy to 6 and even more in adult years.
"The lens continues to grow throughout life (page 7 the same source)
Secondly, the growth of the eye continues after birth - at the beginning the growth is fast and later the growth is much slower but still - there is GROWTH of the eye after the birth.

@llan Thanks!  If I assume that growth does continue, then how is new vitreous humor made ? Is the growth of the eye, after birth, so negligible that there is no need to add new vitreous humor ?

@biogirl the vitreous is jelly-like substance with connective tissue as a skeleton. However, it is 99% water, thus to expand vitreous the ciliary body just filtrated more water. Actually with age vitreous becomes even more fluidic which causes specific to this processes, like Posterior Vitreous Detachment.

@llan The ciliary body makes more AQUEOUS humor not vitreous. I have read that NO new vitreous humor is made, it is present in fixed amounts.

@biogirl  check out what is happen after vitrectomy... what replaces the vitreous?

@llan Interesting question ! Though I don't know how that is replenished I can quote two lines from wikipedia which furthers the mystery - It is produced by cells in the non-pigmented portion of the ciliary body deriven from embryonic mesenchyme cells which then degenerate after birth and Unlike the fluid in the frontal parts of the eye (aqueous humour) which is continuously replenished, the gel in the vitreous chamber is stagnant. Therefore, if blood, cells or other byproducts of inflammation get into the vitreous, they will remain there unless removed surgically.

@biogirl You seem to me someone in a way of academic education, thus you should learn that Wikipedia is absolutely unreliable source of any kind of scientific data. Don't use it and don't cite it - search for the information in reliable academic sources.

@llan ok will take care in the future ! Though I should tell you that I have read the same thing in Tortora and Derrickson principles of anatomy and physiology.

So, your homework is to answer the question What replace saline after it (saline) replaced vitreous during vitrectomy. After you answer this question, you will know some essential data needed to answer the primary question...

Ok to settle the debate I asked an ophthalmologist - he says that after vitrectomy the eye ball decreases in size. No replacement happens.

After reading ur comment above I think I will have to search vitrectomy from a reliable source. See from a good textbook maybe.

@biogirl Tell your ophthalmology resident that it probably better to check the source anyway... cause - he told you something he probably cannot support.

Ohk ...lets see what we can find.

No. In fact the lens of the eye, which is nearly optically perfect in humans, does not change or grow after it is fully formed around week 26 of gestation.  Interestingly this is why one of the cues for identifying young children is having small faces with large eyes.  This also the case for puppies and cats and other animals, who are mostly cuter when they are small with large eyes.
The eye lens is composed of dead cells whose remains are almost entirely a single protein called a crystallin.
This doesn't apply to compound eyes though.

Hi Ilan that comment comes across as quite terse, even rude. Such behaviour is not conducive to good discussions on this website and I recommend using constructive criticism in future if you have an issue with an answer. For example, your post is equally without citation regarding growth of the eye (not lens). Let's try to get along.

Your first link doesn't say anything other than when the eye forms initially.  Your second link has a paragraph that starts out with "The lens continues to grow after birth..."  Neither support your answer.

@shigeta I think you are wrong in saying that eyes don't grow after birth, see the following source : https://www.aao.org/eye-health/ask-ophthalmologist-q/are-eyes-fully-grown-at-birth


text:
If all B cells are present at birth, why should the primary response to an infection take longer than the secondary response?
When learning about the immune response, my teacher mentioned that all the bodies B cells are present at birth, and there is one to counter every disease. But if this is the case, why should the primary response take a long time?
As far as I know, the primary response involves the non-specific response followed by the specific response, where APCs cause the activation of T cells resulting in clonal selection and expansion of T and B cells. The B cells then differentiate into plasma cells and produce antibodies. It results in the memory cells being produced, which can quickly reengage the specific response the next time the pathogen enters.
Why doesn't the body just make memory cells to begin with? As if it has already encountered every possible pathogen. I presume it is just a lack of specificity in the A level teaching, but I am curious to know what I am missing here.
Thanks,
Jamie

These so called virgin B-cells (becase they never had contact with their antigen) which are present in your body only have random B-cell receptors (when secreted, these are the antibodies), mostly of a relatively low binding affinity. These B-cells undergo division, re-arrangement and somatic hypermutation of the B-cell receptor and clonal selection. Only cells producing high-affinity antibodies survive this selection process and build later the pool for the memory cells and the plasma cells. It is like in the image below (from here):

Using this approach we have a big pool of low affinity antibodies (which somewhat fit). These are then used as the basis for the elaboration of a population of high affinity (perfectly fitting) antibodies, which target only the pathogen. And the antibodies are available relatively fast.

Ah, that explains it perfectly!

This is a great question, Jamie. And Chris gave an excellent answer above, describing how antibodies go through 'germinal center reactions' that improve the affinity of responding cells. However, Jamie actually brings up several concepts that are worth discussing and there is another important element to the immune response that Chris touches on, but could be elaborated.

Where do naive B Cells come from? When are they produced?
How many unique B Cells do we have?
What happens to cells during an immune reaction?
How do naive and memory B Cells (among other post-exposure cellular subsets) compare?

Briefly,
(1)  B Cells arise from progenitor cells living in the bone marrow. They are produced continuously throughout the life of the organism - or at least until 'old age' when hematopoiesis is qualitatively and quantitatively compromised(Gerstein and Cancro, among others address this problem).
(2) How many? That's a good question. The number of cells seems to be dependent upon the mass of the organism (indirectly through a cytokine called BLyS). There are a lot of subtleties governing the number and 'quality' of our cells that BLyS concentration seems to regulate, but, for the most part, we can assume that each B Cell (like each T Cell) reacts to a different target (epitope). The reason I bring up the BLyS thing is that it shows us that 'space' is limited, and the body is making decisions all the time about what cells to keep and what cells to discard.
(3) During an immune reaction, some small subset of cells 'sees' its target via it's B Cell Receptor (this is a surface-bound version of the antibodies that this cell will make later). Most cells will remain blind to the infection / whatever. The ones that do see their target expand (multiply), while those that don't, don't. This is Burnett's Clonal Expansion Theory (probably best explained by Wikipedia) and it states that we have only a small number of cells that are useful for each immune reaction, but these can divide and activate rapidly to participate in the response. When the infection is over, most cells die, but some subsets will remain, these are memory cells and their relatives (e.g. long-lived plasma cells). Imagine that for every unique B Cell you had before, now you have 100 memory cells (I'm making up that number) that are capable of responding to the same target.
Although I'm sure there are differences between these memory cells and naive cells, it's easiest to ignore that part and just think that now you will be starting with 100x the number of cells you had prior to the primary response.
So, to get to your basic question: why not just start with the memory cells? It's a question of space. Your immune system provides you with a broad repertoire because it has no idea what it's going to see during your life. But once it sees something once, it is ready for a second showing. (i.e. It is reasonable to think that if you have micro-organism X in your neck of the woods, you may come into contact with it more than once, so after that first time, you are now better prepared with more cells that already demonstrated that they were helpful once before. )