text:
Need for proper air filter for bioreactor?
I am going to build a simple bioreactor for microalgae growth.
I already have fluid filters pore size: 0.2um, diameter: 25mm
https://nl.vwr.com/app/catalog/Product?article_number=514-4039
I wonder if I can use them for air filtration to avoid the bacteria when pumping in the air.
Or do I necessarily need air filters?

What are your end goals?  These determine your sterility requirements.  Generally if you are aiming for mass protein production you want to filter air both in and out of the reactor.  Normal hippa filters should be sufficient.  I've not known of any liquid filters that could do double duty as air filters, but that doesn't mean it won't work.

The goal is to maintain and growth the microalgae without getting infected with the bacteria (They would stop the culture from growing) and I will get some samples from bioreactor, occasionally, for imaging. I also think there should be filters both for air in and out. But don't know what would be a sufficient filter (lower price is better of course) for this purpose. It seems that pore size and filtration area are important parameters.

Well then you need to get a filter specific for air filtering.  I recommend Polytetrafluorethylene PTFE membrane filter.  Now the only issues are size and "how sterile."
There are a lot of vendors out there that supply these.  If your institution has an agreement with VWR, they certainly have them.  If not, I have used Sartorius in the past, but I don't have any particular brand loyalty to them.
Let me know if you need any more help.


text:
The concepts of relatedness - Hamilton's rule and kin selection
Here is a quotation from this wikipedia page

The relatedness parameter (r) in Hamilton's rule was introduced in
  1922 by Sewall Wright as a coefficient of relationship that gives the
  probability that at a random locus, the alleles there will be
  identical by descent.[14] Subsequent authors, including Hamilton,
  sometimes reformulate this with a regression, which, unlike
  probabilities, can be negative.

Here is my question:

What are all the different definitions of relatedness in biology?

how do we calculate them?
what do they mean?

You should break this up into several questions - too many questions rolled into one at the moment, and single answers will probably not cover all of them.

@fileunderwater I updated the post. Thanks for your comment.

Is that really trying to imply that there are significantly different definitions?  It seems to me the intent was just to put it in terms of an equation with more useful numbers.  This terrifying paper from 1964 gives some of the follow-up works, in particular works from Cockerham in 1954 and a number of papers by Kempthorne, in particular this from 1955 and this from 1963.  There is also Malecot's method of coancestry from 1948. (WorldCat.org link)  The idea was mainly to look relatedness outside of the specific limitations present in Wright's work.  Some of the math in those are more accessible than others...

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text:
Who was the first to talk about evolvability?
"Evolvability is the capacity of a system for adaptive evolution." (source) There are several other definitions though:

Who was the first person to use the word "evolvability"?
Who was the first to introduce the concept of evolvability? in which article?

More appropriate for ELU.se?  I'm not convinced either way.

You can probably trace he concept back to the dawn of mankind, it is such an obvious idea (not as it applies to life and evolution, just the idea of adaptive change). For example, you could even claim Heraclitus' Everything flows as an early example though adaptability is not implied.

My literature searches have turned up dead ends, so this is less of a full answer and more of some groundwork, but Google ngrams suggests somewhere around 1931 for the first usage, with meaningful usages beginning in earnest int he early 70s.  Their book previews from that era are sadly lacking; I can't find the usage of the ones from the 40s and 50s they do list sadly, but there are definitely some misnomers that show up in programming.  There's a 1973 work and one from 1977 that at least appear to be the correct usage, with the one from 1973 using it as a "new" concept.

Oxford English Dictionary has this as first occurrence: 1931   J. A. Thomson in W. Rose Outl. Mod. Knowl. 231   "We have already mentioned evolvability as one of the nine characteristics of organisms."

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text:
Does knowing the sex of each of a couple’s first N children have any marginal value in predicting the sex of child N+1?
Does knowing the sex of each of a couple’s first N children have any marginal value in predicting the sex of child N+1? By “marginal” I mean predictive power beyond other known effects, e.g., the race of the parents, the mother’s weight, season of birth (list from this presentation by Andrew Gelman).
I know that many claims that some variable can predict a child have been accused of resting on shaky statistics (see the presentation linked to above). But the sex of preceding children seems like it could be a strong predictor.
UPDATE: answering fileunderwater's question

Can you expand on why (by what mechanisms) you think that it could be a strong predictor? Male sex-chromosome bias in sperm?

Yes, sex-chromosome bias was my first thought. I almost focused my question specifically on that but the fact that I saw maternal weight listed as a predictor in the Gelman presentation made me think there might be other relevant factors that I wouldn't think of. So I broadened the scope of the question.

Can you expand on why (by what mechanisms) you think that it could be a strong predictor? Male sex-chromosome bias in sperm?

there's some evidence that there's gender based selection of sperm by the female... in snakes.  I would like to see birth records mined for patterns and statistics in people, but I've not yet seen a reference.

I remember hearing in my Genetics class in grad school that having a child of a certain gender pushes the odds (very slightly) in favor of having a second child of that gender, which then pushes the odds slightly more, etc. etc., until after the 3rd or 4th child in a row of that gender the odds are quite significantly above 50% of having yet another child of that gender. I don't have a source for that though, except this - I come from a family of 4 boys :)

For those who are interested in sex ratio bias itself, the enWikipedia article is pretty good.
As for predictive power, a Bayesian might tell you that by knowing a couple can and did have a male/female should improve, if only slightly, your belief that their next would be the same.  It's by no means predictive and probably largely indiscernible from random chance, but hey it's something!
More to the point, at the very least you might as well just guess their next child will be a son.  As the link above will tell you, the human sex ratio at birth has varied but in general males are more likely to be born - somewhere around 1.03 to 1.08 males per female.  Here's another in-depth study, from 2005, dealing with the last few decades in the US.
That study has Figure 3 (below) and Table 3, which show the raw birth ratio over successive births, and the data are pretty clear: successive births reduce bias.

Those numbers are way more clear than I thought they would - just watch those means move!  I wish there were more information on the variances - clearly there's more down by the 8th child - but that's pretty solid.  Here's another study from Denmark in 1999 doing some of the same stuff (Denmark was popular for this work).  They include the absolutely fascinating Table 2 (below), which breaks down the odds of giving birth to a male given whatever came before.  Which, in the end, is as predictive as you can get, right?

Basically, it's sort of what you'd expect: the more females you have, the more likely you are to have another female; the more males, the more likely the next is a male.  They used about 1.4 million kids but there are some interesting oddities in that table at the extremes.  The best chance for a male?  Your fifth kid, following FMFM.  Best for a female?  Your fifth, after MMMF.
There are some definite issues that can twist the data, particularly when families have another kid to try to get a child of a specific sex.  If you can tease out some of those environmental factors, you'd be better at guessing; still, I wouldn't bet the house on it.  Memorize that table but, when in doubt:

Guess male
Lotta females first?  Maybe guess another one.
A bunch of males?  Guess another male.

Probably YES.
An analysis of data from about 8 million births shows that there is positive correlation. Please see http://biorxiv.org/content/early/2015/11/16/031344

This should be converted to a comment.

@TheLastWord, why is it that this answer should be converted into a comment?

@kuzzooroo The answer is just a link isn't it?

@TheLastWord, the answer is what I've typed. The link is to the manuscript with detailed analysis and a review of previous studies


text:
Microarray data and analysis tools
Microarray has various uses, and to analyse the data a main function classification is used. There are many methods used to classify the data but what are the best and most frequently used methods? Are there any well-known, web-based tools for microarray analysis?  Where can I find datasets of gene expression profiles, where I can find and understand the matrix of the dataset?

try the bioconductor package.

Sebida and DGRP have data available

Come to think of it most or all gene expression data has to be deposited online - try looking at the gene expression omnibus. And I echo recommending bio conductor (in R)

This is a fairly broad question and a book or two will give a more complete answer.  I'm assuming you are interested in expression microarrays.  Genotyping microarrays are also very popular these days and are quite different though.
Where can I understand the matrix of the dataset ?
This is a little unclear as a question, but I'll start with a numerical description.  Microarray data is reducible to a one dimensional array of intensities.  As a vector of numbers, each representing the amount of a given species of RNA in a sample, it has many interpretations.  Most of what is said here applies to RNASeq data too.
These numbers are sequence dependent - that is, they should not be interpreted as an absolute count of a specific mRNA in the sample, so comparing two entries in the vector (e.g. "gene A has 10% more RNA than gene B") will probably not be useful.
For this reason, microarray experiments are typically done as difference experiments, where two or more conditions are compared, producing a matrix of numbers, where N rows represent N experiments, and the M columns each represent a probe set / gene.  The transpose of this matrix is also common.
**Methods to classify microarray results. **
Taking the matrix of data, there are many ways of interpreting data in matrix form and most of them have been tried credibly with microarray data.
The most common are to take a set of probe sets whose biological action are related (e.g. all in a metabolic pathway and display them as a heat map where the columns have been clustered by a distance based algorithm to produce a tree, where neighbors have the greatest numerical similarity.

For purely numerical methods, Principal Component Analysis is often used (despite the fact that this is not a great method), but Self Organizing Maps, neural nets and just about any machine learning algorithm have been used.
Most common method by far though, is Analysis of Variants (ANOVA), where the probe sets/ genes have been scored by their greatest to smallest variance.  The most common case of this is a two condition difference experiment where the largest differences are taken as results.  This is not a great experiment, but the data is not super cheap to produce.
**Microarray data repositories **
Gene Expression Omnibus (GEO) is a highly regarded repository for microarray data, with over a million sets of data. They also have some tools, see below.
EMBL ArrayExpress claims to have slightly more data than GEO (1.2 M assays).
There are many many specialized microarray websites, mostly focusing on a particular organism (E coli for instance) or problem (like cancer).  Google is pretty helpful for this sort of thing once you have the right keywords.
**Web based tools for microarray analysis **
There are several tools you will use for microarray analysis and there are lots of websites for different aspects of this data.  I'm going to cite a couple, but the most commonly used tools are command line tools like R/bioconductor or the software that comes from the array manufacturer.
GEO2R is a great tool to browse expression data experiments.  It does a simple version of ANOVA and will really help you find some cool biology quickly.
VAMPIRE is a web analysis suite for microarray analysis.  Scaling the data into numbers from images to intensities to data analysis to compare several arrays.  Its probably one of the most comprehensive analysis sites out there.

"Principal Component Analysis" not "Principle Component Analysis". It analyses principal components. Misspelling it may demonstrate why you find it a problem, because you need to understand the principles behind the principals.

I don't see why you would not  be predisposed to using PCA but yet pre-disposed to accepting proximity clustering and self-org maps. It doesn't matter which chicken lays the egg. They are chicken eggs.

I don't it is a discussion we should indulge in, in this comments section - but in short, the people using it (in the link you provided) may not understand the meaning of "principal components".


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Protocol for measuring stamina of arthritic mice
I am going to make some mice ill with arthritis. The medicine which I am testing as control is known to cause extreme fatigue. I think I've improved it. I'd like to humanly measure their stamina in the presence of something like morphine. How would I ethically do this?

I believe the standard is an graded-speed treadmill test.  An example pub:
Genetic variability in forced and voluntary endurance exercise performance in seven inbred mouse strains
If there is a particular ethical concern, you should always have your institutional review panel review it.  If you call up your department of animal resources (or what ever it is called in your institution) they will almost always give lists of preferred LOPs.
Another option would be to score time sleeping if you have them under behavioral surveillance.  The problem with this is the large amount of man hours needed, even watching tapes at high speed.  Instead I recommend you check this paper out:
Evaluation of two automated metrics for analyzing partner preference tests
Then to get accurate scoring, I would put a strongly colored bedding pad in a corner so the computer could pick it up.  Be sure to put the bedding in at least a week before so the mice get used to it and actually sleep on it.

I dont think the animals will be physically capable of walking on a treadmill. I looked for the computer program but wan't able to find it. Could you provide a reference as I think you already intend.

@caseyr547 done.

If the mice will be incapable of walking on a treadmill, which suggests that they will be very ill, you could just measure their homecage activity. There is some normal, baseline level of activity in a cage. You could compare controls to placebos to experimentals. If the drug you are testing increases homecage activity, then it would appear to be effective. Xie et al. describe a fairly comprehensive system.

Here is one example. Basically it is a very sensitive, 4-post scale that is designed to determine in xy space when the mouse is in the cage.


text:
Does DHA increase the effects of clarithromycin?
I've read on this publication that every drug that induces CYP3A can reduce the effectiveness of clarithromycin. Clarithromycin inhibits CYP3A.
But it does not say anything about the opposite situation: does a low concentration of CYP3A increase the effect of clarithromycin?
This research shows how DHA can inhibit CYP3A.
Now the final question is: does a high concentration of DHA increase the effect of clarithromycin?

What is DHA? Please define abbreviations other than the most generally accepted ones.

You've misread the paper. Clarithromycin is metabolized in part by CYP3A, but to an active metabolite. A significant proportion of clarithromycin and its active metabolites are excreted unchanged in the kidney. Clarithromycin, and other macrolide antibiotics do inhibit CYP3A enzymes, as you noted in your answer. You can read about this in chapter 55 of Goodman & Gilman's the Pharmacological Basis of Therapeutics.
We certainly worry about clarithromycin and other macrolides increasing the half-life of drugs that are primarily metabolized by CYP3A4 (again, see Goodman and Gilman). Midazolam is an example, and is what the paper you cite was about. If you give clarithromycin together with midazolam, expect the effects of midazolam to last longer. The important relationship between CYP3A induction and clarithromycin discussed in the paper is not that it reduces the effectiveness of clarithromycin, but that CYP3A induction does not overcome clarithromycin mediated CYP3A inhibition.

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text:
Genetic expression in interspecific hybrids
Referring to interspecific hybrids, I have the following two questions:-
Quoting from wikipedia:-

The offspring of an interspecific cross are very often sterile; thus,
  hybrid sterility prevents the movement of genes from one species to
  the other, keeping both species distinct. Sterility is often
  attributed to the different number of chromosomes the two species
  have, for example donkeys have 62 chromosomes, while horses have 64
  chromosomes, and mules and hinnies have 63 chromosomes. Mules,
  hinnies, and other normally sterile interspecific hybrids cannot
  produce viable gametes, because differences in chromosome structure
  prevent appropriate pairing and segregation during meiosis, meiosis is
  disrupted, and viable sperm and eggs are not formed. However,
  fertility in female mules has been reported with a donkey as the
  father.

1) The sterility of hybrids prevents interspecific gene exchange and is necessary in case the hybrid has odd number of total chromosomes (the hybridized species has odd and even pairs of chromosomes individually), where equal meiotic division would not be possible, and is also necessary to avoid sex determination problems that may arise from such hybridizations genetically. What is the molecular (genetic) reason behind the sterility? In other words, why is the expression of primary sexual organs and its further proliferation to effect reproduction not possible, although the genes required for it are already present in the hybrids? Is this due to epigenetic mechanisms or is the reason inherent in the hybrid nature of the genome?
2) This might probably sound a bit naive, but why are these hybrids viable? They have 2 non-homologous haploid pairs of chromosomes which have a huge variety(compared to two homologous pairs) of different non-allelic genes. Why are all the essential functions not hindered by the presence of such considerably unrelated set of chromosomes?
Probably related to the question is the fact that certain allopolyploids are viable and become an entirely new species, but others are not. Is it because here are 2 sets of each combining species' chromosomes (and hence allowing proper meiotic pairing) or is there some other reason pertaining to the nature of the combined sets of chromosome?

mitosis is not affected because there is no pairing of homologous chromosomes. Meiosis is possible affected because pairing is compromised. However, non-meiotic recombinations are possible.
Why are all the essential functions not hindered by the presence of such considerably unrelated set of chromosomes? Hybrids are not possible between totally unrelated species. The similarity of the genes and the genetic networks perhaps allows the cells to carry out normal functions.

Can you add a referece to support your first point? Hybrid introgression and hybrids with lowered fitness (i.e. not fully sterile) has been shown to be relatively common in natural populations.

@fileunderwater Please see the edit in my question.

@SatwikPasani Great! The relative prevalence of sterility probably differs dramatically between taxa (depending on e.g. how species concepts are applied, genomic differences within taxa and the strength of regulation).

i think it is not just about odd number of chromosomes. Pairing would be compromised if there are no homologous syntenic regions.

Mallett 2008 might be of interest to you. It doesn't answer the questions about genetic mechanisms, but is a good perspective on hybridization viability/sterility.

I've heard of mules producing offspring, but it's rare. It requires a gamete to be produced that just happens to get all of the horse chromosomes or all of the donkey chromosomes, making it equivalent to the hybrid's parents.

Davis et al. 2015 studied hybrid sterility in cats by identifying SNPs and transcriptome changes that are associated with hybrid male sterility.
They identified eight autosomal regions "involved in the function of the blood-testis barrier, gamete structural development". So it seems that the male hybrids have an altered testicular blood supply and sperm development.
More importantly, they have found a lot of altered genes on the X chromosome. It seems that a lot of regions on the x-chromosomes have duplicated. They also found "chromosome-wide upregulation of X chromosome transcripts in testes of sterile hybrids, which were enriched for genes involved in chromatin regulation of gene expression". This is a major hint that epigenetic regulation is the cause of hybrid infertility. I think this makes sense, since all (mammal) females have to shut down one x-chromosome by methylation of the x-chromosome, to prevent a doubling of gene dosage (Sex-chromosome dosage compensation). They mention that in their discussion (which is rather cryptic for my taste), too, and if I understood this correctly, males are also in need to methylate their X-chromosome (partially?). If they fail to do so, male hybrids upregulate X-chromosomal genes that in turn cause infertility. They mention a gene on the x-Chromosome called FMRP that is essential for spermatogenesis that seems to be altered in hybrids.
The focus on the x-chromosome might also answer your second question: I presume that the hybrids are viable since most genetic "damage" is concentrated on the X chromosome, while the autosomes seem to work fine. After all, autosomal damages don't carry as much weight as X-chromosomal damages, since autosomes come in pairs (in males). If one autosome has a dysfunctional gene, it is likely that his homologous partner carries the functional version. The X-Chromosome however is alone, so mechanisms like DNA-repair by homologous recombination is not possible and DNA damage can accumulate. But that is just speculation from my side (!).
They also talk about the "large X-Effect". I am no expert, but it seems that the X-chromosome is a 'hotspot for "speciation genes," that prevent genetic exchanges between closely related species' ref However I didn't understand what they were talking about, but maybe this throws your own research into the right direction.


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What is Luc Montagnier's research on electromagnetic signals from DNA about?
After reading a Youtube comment, I started reading on Luc Montagnier's research on electromagnetic signals from DNA. I haven't been able to find a source that would clearly explain what it's about. I would like to know, if possible,

what the claims are exactly;
what experiments were carried out;
whether the results have been replicated independently;
whether the results contradict anything considered firmly established scientific knowledge (it seems Montagnier says they do) and, if so, how;
what the criticism is.

I know it's a lot to ask, but if you could make your answers accessible, it would be great. Please don't refrain from using technical language where it's necessary, but do try to give a general picture for those (including me) who might not understand it.

Have you read the stuff at his webpage, where three papers on the topic have been posted: http://montagnier.org/Electromagnetic-signals-DNA?

This question is rather broad, I'd suggest to read the papers and make your question more specific. On the other hand you might not bother with this topc at all, the entire thing is complete nonsense.

@TomD Being a Nobel laureate doesn't make him immune from criticism. I read the paper a while back, and it is just extremely bad. He makes an absolutely extraordinary and implausible claim, but the experiments and setups described in the paper (rather badly and without enough detail) are prone to noisy results or contamination.

Pharyngula has a nice explanation (and a scathing criticism) here: http://scienceblogs.com/pharyngula/2011/01/24/it-almost-makes-me-disbelieve/

@TomD Karry Mullis is a Nobel laureate who believes in astrology and James Watson is a Nobel laureate who believes that black people are less intelligent than white. Having a Nobel just means you had at least one idea that a group of people considered good. It does not make you an infallible genius. Silly claims are silly claims Nobel notwithstanding.

I just read one of the articles from the site. Wow. Just wow. It is hard to give a rebuttal because they don't actually show any analyses, just some very low quality screenshots with no numbers and no stats. The images are too small to actually be readable so we have no idea what their data are. Their logic is also seriously flawed. I will try and write something up when I get the chance but really, this is pure crap. Just have a look at the image (also reproduced in the link provided by @ChinmayKanchi) and tell me if you can actually see anything.

@TomD I know, it just annoys me that people take notice just because someone has done good work in the past. Work should be judged on its merits, not the laurels of the scientist involved. What claims did McClintock make by the way? As far as I know her (wonderful) early papers were scientifically sound, people ignored her because transposons sounded weird and she was a woman. The work discussed here is shoddy, not because of their conclusions but because they have no data to support said conclusions.

@TomD Ah, so I did, and yes, I misunderstood you again. Sorry, we seem to be saying the same thing I just failed to see it. Apologies :).

@TomD I like your 'non answer' why not just leave it as one?  I remember the memory of water paper - the comparison is an apt one.

Duplicate of https://biology.stackexchange.com/questions/11121/what-is-luc-montagniers-research-on-electromagnetic-signals-from-dna-about .

I think that ymar poses an excellent set of questions that should be discussed on these forums.  It brings back memories (sic) of the memory of water controversy.
I'll quote from Andy Coghlan's excellent article published in New Scientist in 2011
Draw your own conclusions.  (The emphases are mine).

... So what have
Montagnier and his team actually found? Full details of the
experiments are not yet available, but the basic set-up is as follows.
Two adjacent but physically separate test tubes were placed within a
copper coil and subjected to a very weak extremely low frequency
electromagnetic field of 7 hertz. The apparatus was isolated from
Earth's natural magnetic field to stop it interfering with the
experiment. One tube contained a fragment of DNA around 100 bases
long; the second tube contained pure water.
After 16 to 18 hours, both
samples were independently subjected to the polymerase chain reaction
(PCR), a method routinely used to amplify traces of DNA by using
enzymes to make many copies of the original material.
The gene
fragment was apparently recovered from both tubes, even though one
should have contained just water (see diagram).
DNA was only recovered
if the original solution of DNA - whose concentration has not been
revealed - had been subjected to several dilution cycles before being
placed in the magnetic field. In each cycle it was diluted 10-fold,
and "ghost" DNA was only recovered after between seven and 12
dilutions of the original. It was not found at the ultra-high
dilutions used in homeopathy.
Physicists in Montagnier's team suggest
that DNA emits low-frequency electromagnetic waves which imprint the
structure of the molecule onto the water.
This structure, they claim,
is preserved and amplified through quantum coherence effects, and
because it mimics the shape of the original DNA, the enzymes in the
PCR process mistake it for DNA itself, and somehow use it as a
template to make DNA matching that which "sent" the signal

I always knew there was something suspect about genetics!  Stick to biochemistry, that's what I say :-)

So...since this is bunk, here are some obvious pitfalls. These results are good old fashioned fraudulent claims. There's so much DNA in the original concentration that it prevents PCR amplification (or some other non-optimal condition). Lastly, they were just sloppy and didn't prevent contaminating aerosolized DNA fragments.

If it were the case of having conducted rigorous experiments, but not coming to a reasonable (or parsimonious conclusion, or even over-stating the results, then I would agree it is not fraudulent. If I have understood the summary correctly, that DNA-free water (was it DNAase treated?) is supposedly carrying a sufficient mass of DNA to accomplish PCR, I would regard this as either an over-stated conclusion, sloppy experimental work, or fraud. As they say, extraordinary claims require extraordinary evidence.

PCR can amplify a single DNA molecules. In fact, single cell PCR is possible. So... one has to be very very careful.


text:
Are there any types of cancer that cause neurons to divide?
After birth neurons generally do not divide. But is there any specific type of rare cancer or tumour where neurons divide? And if there is such a cancer, then how is it possible for a neuron to regain the division power?

Related: http://biology.stackexchange.com/questions/10809/extremely-rare-occurence-of-heart-cancer

You mean brain tumors? Those are actually not that rare...

@nico I think brain tumours are caused by uncontrolled division of glia that surrounds the neurons not of neurons themselves.

@biogirl: actually you are right, most brain tumours are glial. However, gangliocytomas have neuronal components and neurocytomas are strictly neuronal, although rare.

@nico Then I think the author is specifically asking about neurocytomas. Hmmm Interesting !

@nico pinging you cause you seem to be our resident neuro person. Surely it's not true that neurons don't divide after birth! They don't divide after a certain age but that's a good few years after birth isn't it? I thought it was after adolescence.

@terdon: new neurons can be born in the adult brain. The phenomenon is less important (in terms of numbers) compared to other cell types, but still it exists. Adult neurogenesis has been reported in pretty much all mammals (see for instance: http://www.ncbi.nlm.nih.gov/pubmed/16022595 ). To be honest, I do not know until what age this happens. Surely in the mouse adult neurogenesis is seen also even well after adolescence.

I think that most mature cells do not divide in all tissues. If an organism needs to repair tissues, it uses tissue cell precursors -- stem cells.
In case of neurons, these are neuroblasts. Neuroblasts can divide and can repair brains under some circumstances (I don't know under which).
There is a cancer grown from neuroblasts, called neuroblastoma.
I think it is very improbable to have tumor from neurons, because division genes are turned off in mature cells. Can't state it is not occurring in practice.


text:
Removal of the Initial Methionine in Venus for FRET
I'm working on building some FRET reporters.  In addition to a cleavage site (of varying composition from 15-18AA), a 1 AA linker, I'm using Venus and Cerulean.
Initially I was worried that 18AA would be too long, but it does in fact give a fair signal.  For reference, I believe the Förster radius (Ro) is 54Å.
I am now working on further optimization.  Does the removal of the intial methionine cause any problems for Venus if it is the second protein in the FRET pair?  The basic layout is:
Cerulean - Link - Cleavage - Link - Venus
And I'm wondering if cutting the Met from Venus might bring me 1 AA closer and therefore a slightly better signal.  I have seen it published both ways, and I was wondering if anyone had tried both or just knew theoretically that it wouldn't matter.

why do you want to remove the Met-1. Removal of 1 amino acid may only reduce the length by ~3Å (twice the peptide bond) and if i am not wrong Forster's radius is ~60Å and therefore the distance of interaction = 2x60Å. A 3Å reduction may not be very significant

@WYSIWYG I didn't mean to imply that the reduction of the radius was the only advantage.  It also gives me a better restriction site in the DNA, and is possibly more flexible in the AA sequence.


text:
Competition for mates in sea horses
This source here

...research has shown that it is STILL the males that compete for
  females.

says that male sea horses compete for mates but this source here

Females exhibit a competitive behavior that's normally a male-type
  attribute, and males end up being choosy, which is normally a more
  female-type attribute.

.says that female sea horses compete for mates.
Can anyone provide me a trustable source regarding this ? I would also like to know if there are any recent papers exploring why males get pregnant in sea horses.

Is this question more apt for skeptics.se ?

Are you sure you want to ask about polyandry and polygyny? How do the sources you quote touch on the number of mates per individual?

@terdon The sources I quote seems to answer the question why males get pregnant but if you read carefully there is a mention of polygyny and polyandry. I will quote those parts--

Whether they compete or not is one thing, polyandry and polygyny refer to the number of mates per individual. I think you are asking whether males or females compete for mates and display secondary sexual characteristics. That is not necessarily related to polygamy of either sex. The two sources disagree on whether the males or the females compete for mates, my guess is that both do but I don't really know. Interesting question but not related to polyandry or polygyny.

@terdon Ah I see but in most polygynous socities it is the male that competes for mate. I have never heard that a polygynous society had females competing for mates.

All I am saying is that competition is not related to polygyny or polyandry. Please [edit] your question so you ask what you actually want to know.

That second link even says: "Seahorses, however, are monogamous within a breeding season, and each seahorse only mates with one other seahorse."

@amory edited my question.

Second paper is an article in science Daily and have a pretty decent source from Texas A&M University. It's much better than the first as it is un-sourced post on yahoo answers.
Source:
"Male Seahorses Are Nature's Mr. Mom, Researchers Say." ScienceDaily. ScienceDaily, 2 May 2008.
Why male seahorses gets pregnant?
Genetic answer:
May be because only $MHII\beta$ gene present in the male pouch which carries the babies.
Source and more on this topic:
The impact of sex-role reversal on the diversity of the major histocompatibility complex: Insights from the seahorse (Hippocampus abdominalis)


text:
Can this image be the result of a Western Blot?
I am currently researching image manipulation in the life sciences and stumbled upon a Western Blot looking very similar to the image below.
For creating the image I have cut out the blot using the Fuzzy Select Tool of GIMP and then greatly adjusted the local contrast of the blot as well as the background. By using the Fuzzy Select Tool some pixels of the original background are also captured. That is why the blot shown has a brighter background around the edges. I normally would not expect to see bright edges around a blot.
While I know how Western Blots look when they are captured with a digital camera, I do not know about techniques like Chemiluminescent Blotting (I am an undergraduate student in Computer Science). Maybe there is a blotting technique that results in an image like the one i created.
Is it possible to get a Western Blot result like this without inappropriate modification of the image?

Can you explain a bit more?  I'm still confused by what that image is, in particular why it's colored the way it is.

this looks like a normal band in a gel, with the image manipulated to replace every pixel above a certain cutoff to black.  could be manipulation or it could be an accidental data issue

@Amory I have edited the question and provided some more details. Hope this helps.

Yeah I'm with @shigeta on this.  Do you have the unaltered image?  I can post an example of one of my chemiluminescent blots if you like.

I have the unaltered image but i am not sure if it helps as the image posted is altered to imitate another image from an actual publication. The image i stumbled upon is from an actual publication and i can't post it here due to legal risks (but it looks almost exactly like the one i posted). I would appreciate to see an example of a chemiluminescent blot.

How was the initial image aquired? Could just be a result of the compression algorithm used for the original image...

The initial image was retrieved from the supplementary figures from a database for medical publications and is a compressed JPEG image. The original image shows multiple blot regions of different experiments and not all of these regions show this behaviour. The publication states that the displayed regions are Western Blots.

@RalfThaenert Are you implying that the original image came from a publication?  If it's from the same institution you go to, you might try and see if you can get your hands on the original file if it's not in a standard image format.  Most image systems can save images in a format that has a lot more information than a standard image. They are harder to modify, and might give a hint. Not every lab keeps them, however (I always insist on it for these reasons).

@RalfThaenert Can't you post a link to the actual publication? This will make it much easier to know exactly what you are talking about, and to evaluate possible reasons problems/errors.

The original publication comes from a different institution and is a publication gathered from Pubmed Central. I'm sorry but i won't provide the original publication because of legal issues (the authors of various blogs about image manipulation faced legal threats, like science-fraud.org). But i will report the finding to the author of the publication. Thank you all for your help.

I do not think that a publication quality blot should have such an artifact, but I was able to find something similar by purposely over blotting (not the same as over exposing) a gel.  If you use too much primary, secondary, or developing reagent, you can get your HRP signal to "burn in" a membrane where you get a distinct "negative band."
By negative band I mean a region that is more clear/white than background. This happens mostly when you have way too much secondary antibody.  Normally when this happens, the CENTER of the band burns in first so you would see a white center with dark edges.  And that's only when you are imaging the membrane as it is burning in.  Often the whole band is white.
After going through the westerns of grad-student who is working with me, I found this image:

It came with the clear notation that it was burned in and disregarded (said student was learning how to do Westerns at the time).  It's a GAPDH blot for those that care.  When this does happen, it's obvious because you can then see the band with your naked eye on the membrane.  Again this would be a reason to not publish the blot.
The image could have non-maliciously been edit via compression, screens, filters, etc as mentioned by others in the comments.  This is the only way I can think of to experimentally have a similar image.  Ether way I don't think the image should be reported as is.

Thank you, that's close to the image i posted. Still the white area is bigger and does not have sharp edges as the one posted. Assuming that one will not publish damaged blots the remaining option is that the image is edited inappropriately (with or without malicious intent).

@RalfThaenert as I mentioned it's similar, and I think as close as you can get to your image experimentally.  I could imagine that if you, by immense chance, got an image just as the outer edge was fading you could get tighter, but it seems improbable. As scientists we are not prone to saying something is impossible, but rather that certain things are likely, especially compared to others. So yes, I think everyone thinks the simplest way to your image is digital editing (intended or not).

Here's an example of a chemiluminescent blot:

For those who care, the first column on the left is the weight standard, the next two are pooled pellets, and the rest are increasing fractions of purified HIV using a mouse monoclonal anti-p24 (capsid) antibody.
This blot is pretty clean (although for my work it was pretty disappointing...) but here's one that looks less-than-ideal, and perhaps more like your example:

These are lysates and pelleted supernatant from Jurkat uninfected (left) and HIVIIIB-infected (right) cultures, detected with a mouse monoclonal anti-tsg101 antibody.
I agree with shigeta's comment that your image might not be exactly what I would expect, but that doesn't necessarily mean it was done maliciously; as you can see, there can be a fair amount of variation in how blots turn out depending on the equipment used, the type of membrane, the protein itself, and so on.  I try to be pretty conservative with image filters but there's a lot you can do with those guys that can be shady but falls short of Photoshop.

Thanks for the images. The images do not show such a behaviour around the blot regions. So there is no Western Blot technique which shows this behaviour by default? Of course such an image can be the result of compression, filtering and beautification and is not necessarily an intended manipulation.


text:
How do you estimate global species richness?
I know how estimates of species richness in a small area are made. But how do you estimate the total number of species on a global scale?
One example of such a method can be found in Mora et al. 2011.

Do you mainly want examples of other methods, or a clarification of the linked article?

@fileunderwater I want examples of other methods.

You might be interested in the below works as well as the references that they cite.
May, R. M. (1988). How many species are there on Earth? Science, 241(4872), 1441–1449.
Millennium Ecosystem Assessment. (2005). Ecosystems and Human Well-Being: Synthesis (p. 137). Washington, D.C.: Island Press.
It's worth noting that many estimates of species richness at large scales are based on the use of the species-area relationship to upscale richness measurements from small scales to large scales.


text:
Probability of Extinction under Genetic Drift
Here is the Wright-Fisher model of genetic drift:
$$\frac{(2N)!}{k!(2N-k)!}p^kq^{2N-k} \Leftrightarrow \binom{2N}{k}p^kq^{2N-k}$$
where $\binom{2N}{k}$ is the binomial coefficient.
This formula gives the probability of obtaining $k$ copies of an allele at generation $t+1$ given that there are $p$ copies of this allele at generation $t$. $N$ is the population size and $2N$ is the number of copies of each gene (this model applies to diploid population only).
From this formula, how can we calculate the probability of extinction of an allele in say 120 generations starting at a given frequency, let's say 0.2?
and
How can we calculate the probability of extinction rather than fixation of an allele present at frequency $p$ if we wait an infinite amount of time?

See answer there.

update
The answer is here!

Original comment/answer
Kimura and Ohta (1969) showed that assuming an initial frequency of $p$, the mean time to fixation $\bar t_1(p)$ is:
$$\bar t_1(p)=-4N\left(\frac{1-p}{p}\right)ln(1-p)$$
similarly they showed that the mean time to loss $\bar t_0(p)$ is
$$\bar t_0(p)=-4N\left(\frac{p}{1-p}\right)ln(p)$$
Combining the two, they found that the mean persistence time of an allele $\bar t(p)$ is given by $\bar t(p) = (1-p)\bar t_0(p) + p\bar t_1(p)$ which equals
$$\bar t(p)=-4N\cdot \left((1-p)\cdot ln(1-p)+p\cdot ln(p)\right)$$
This does not answer any of the two questions!
This answer gives...

the average persistence time

but not...

the probability of fixation rather than extinction if we wait an infinite amount of time

neither...

the probability that the allele get extinct over a period of say 120 generations.

Can someone improve this answer?

I was also thinking about Kimura's papers, but have seen some more recent stuff as well. I will look at it later when I have the time.

The probability of fixation given infinite time is just $p$ (the frequency of the allele at that time) - I just ran a simulation in R with initial frequency of 0.2 (1000 replicates over 5000 generations $N$ =10000 and $p$ =0.2) and the average fixation rate was 0.201 (though simulations with smaller populations are more sensitive to stochasticity thus vary more around $p$ but are still very close, $N$ =10 had a fixation of 0.184) ... I'm sure there must be a way to calculate the probability after a given number of generations...

ps. does that answer your second point in your question? @Remi.b

@GriffinEvo Nice! Thank you. You answer to "what is the probability of fixation rather than extinction if we wait an infinite amount of time" via simulation (rather than mathematical modeling). But that's already a very informative point.

@remi.b mathematically speaking it's just simple probability - if something is randomly sampled it, on average, will be sampled at the same frequency it is found in the population it is being sampled from. (Probability of showing heads when tossing a coin is 0.5 because the frequency of head-sides on coins is 0.5). The simulation I did was just to support this (and because I like playing in R) :)

@GriffinEvo Ha ha. This result is not intuitive to my mind! I take it for true but I don't quite understand why. I guess one might re-express the wright-fisher model somehow and find out this same result. I asked (just 30 seconds ago!) the same question here on mathematics.SE

@Remi.b ah cool! I'll ask our departments neutral theory genius too, she will probably know a way if there is one! If you want the drift simulation to play with it's on my homepage

Here is a simple proof that the probability of fixation given an infinite time is indeed p (in a finite population, otherwise there will be no fixation):
Let's look at all 2N gametes in the population. Eventualy, according to the Wright-Fisher model, only one of them will be represented in the population. The probability for this gamete to be of an allele with initial frequency p is just p. Therefore the probability of fixation is p.
Simple.


text:
How does a fungus protect itself from digestion by other fungi?
If a fungus releases its digestive enzymes outside its body, how does it protect itself from digestion? How do fungi growing nearby protect themselves?
I have tried searching this on google but couldn't get an answer.

Which fungi secret proteases?

usually they do not, but rather ingest via clathrin coated pits I think.  then the proteases are found in a compartment called the proteome.

I think you mean the proteasome.

You would also be interested in fungal autolysis or self digestion. Please refer to the paper "The autolysis of industrial filamentous fungi." PMID: 11958333

In general fungal cell walls are resistant to whatever enzymes or compounds they are excreting to break material down for consumption. Conceptually, it is a little like your stomach lining being resistant to stomach acid. For a more detailed answer you may have to head over to your local university and find a Mycologist.
There is ongoing research on how fungi actually "eat." You can look up fungal endocytosis if you wish to research it more. There may be other mechanisms as Shigeta mentions.


text:
Attachment of muscles during molting in insects
Normally, insects' muscles are attached to their exoskeleton but what happens to this attachment when they are moulting?
Sorry if this is an extremely silly question but I have wondered about it for a long time and have tried searching it.

You can find a concise answer here in a section from The Insects: Structure and Function  by R. F. Chapman, eds. Stephen J. Simpson, Angela E. Douglas. 5th Edition. Cambridge University Press.
In essence the source says that the muscle attachment to the cuticle is maintained during the moulting process, while the new cuticle is formed under the old cuticle.

As a result the insect is able to continue its activities after apolysis during the development of the new cuticle. The connections to the old cuticle are broken at about the time of ecdysis.

Connections to the new cuticle are formed at the same time as the old ones are broken.

To clarify the issue: muscles do not contact with the cuticle directly. They form junctions with epidermal tendon cells, which pass the tension via microtubules to their outer membrane - to hemidesmosomes. From the side of the cuticle these hemidesmosomes are supported by intracuticular (extracellular) fibres (= tonofibrillae). During pre-molt, when the new cuticle is being synthesized, these fibres run through both the new and the old exoskeleton, thus ensuring maintenance of the mechanical support for muscles: in isopods.


text:
Adenosine metabolism
Are adenosine or its catabolites increased in inflamed airways? How can I assess this? I am trying to use inhibitors for adenosine deaminase, xanthine oxidase, and purine nucleoside phosphorylase, but I don't have a protocol.

do you want to measure these compounds ?

I want to see if Adenosine/ its metabolites levels at different inflammation levels of severerity

This depends on whose air way and what you are doing to inflame it.  Are you using a mouse model and having them huff LPS?


text:
What is the definition of "dry weight" and "dry cell weight"?
As I understand it, the dry weight of something is its weight minus the weight of its water content. Is this the definition? What about dry cell weight?

Why would dry cell weight be different?

dry weight is used in non-biological sense too.. thats the difference

@terdon so the definition I've written of dry weight is accurate?

http://biology.stackexchange.com/q/13692/561

some techniques enable to measure the individual cell dry mass using microscopy. The company phasics seem to have developped this tool.

According to my Henderson's Dictionary of Biological Terms, dry weight is

The weight or mass of organic matter or soil after removal of water by heating to constant weight.

So yes, your definition is correct and it is also applicable to cells. The dry weight of cells is the weight left when their water content has been removed by heating.

+1 thanks. What does "heating to constant weight" mean?

@becko heating until further heating does not result in a reduction in weight. Basically, until all the water has evaporated.


text:
Does the eye image interval refresh?
It's known the human eye takes 24 images per second. But does this refresh?
For example after sleeping.
Or will it always be the same interval?
I talk about when the eye takes the images. So it are 24 images in the second, but this second is not defined. It can start at 09:00:00.00 or 09:00:00.50. Will this change after taking a sleep?
Hope it is clear what I'm talking about.

The human eye does not take 24 images per second - this is only (approximately) what is needed for a film to look fluid - and the image we see is continuously updated and interpreted by the brain. Saturation of human perception is another thing, that is, the maximum frame rate that we can perceive, and this depends for instance on light conditions.

Related question: What is the equivalent of shutter-speed in Human eye?

Human eyes do not take 24 images per second. Refresh done in parallel, each pixel separately, and the rate depends on the rate of color changing.
So, the work of eye is closer to MPEG encoding than to uncompressed AVI.


text:
Terminology question about the correct term for areas of biological research
I am writing a paper about DNA sequence prediction. DNA sequence prediction is done across various areas of biology, including, for example, RSS sequence prediction (in immunology) and prediction of promoter regions in vertebrate DNA sequences.
I was just wondering how one would describe such specific areas as "RSS sequence prediction" and "promoter region prediction". To be concrete, I wanted to write something like:

This paper describes a method of DNA sequence prediction using
  standard Bayesian modelling techniques. While there is much existing
  work on DNA sequence prediction, most of this work is in the context
  of biological research. Typically the techniques used are very
  specific to the biological subdomain under consideration. Also, these
  techniques often use use additional biological information about the
  biological sequences under consideration, besides the sequence data
  itself.

Is the term subspeciality the correct term to use here? Would biological area or biological domain/subdomain be better, or some other term?
Incidentally, if anyone knows other areas where DNA sequence prediction is used, please mention it/them. Thanks.

I would avoid using the term sequence prediction. You don't predict sequences, you identify them. Predicting would be giving me a likely RSS sequence for an organism you haven't analyzed and I doubt that is what you're doing. You may be predicting RSSs or genes or promoters but not sequences.

@terdon I see your point, but am unclear on how to reword my paragraph. Can you suggest an alternative phrasing for "DNA sequence prediction"? I can't make it more specific, because it is supposed to be a catch-all phrase for prediction of different kinds of DNA sequences, in different subdomains, i.e. RSS.

In this case, I would say sequence identification or RSS sequence prediction or promoter prediction. It is just the sequence prediction I object to.

@terdon I think I'll go with "DNA sequence analysis" or possibly "Computational Analysis of DNA Sequences". These are used in various places. Is that OK with you?

Both sound fine to me, yeah.

I think your suggestions are fine - there are a few ways you could write this.
I might use some variant of;

The techniques used may be specific to the research question, and particular considerations may also be required depending on the accepted norms within the academic field

Thanks for the feedback, Luke. I expanded my (proposed) paper quote a bit, to give better context.


text:
New GO terms after TopGO enrichment?
I ran an enrichment analysis with custom annotations using TopGO and surprisingly I obtained new GO terms inside the significant GO terms.
Is that  possible? The only reason I can imagine this is possible is because TopGO adds new GO terms based on the input GO terms, since GO ontology is structured hierarchically.
Please let me know if you need more details about the experiment.
Code:
https://drive.google.com/file/d/0B8-ZAuZe8jldbjNuTHhNeXRVX00/edit?usp=sharing
TopGO output:
https://drive.google.com/file/d/0B8-ZAuZe8jldZnlYUzlxZ3psMWc/edit?usp=sharing
Thanks, Bernardo

These new GO terms seem to be the parents of the already GO terms present in my original dataset.

You seem to have answered your own question with that comment. Is everything clear now? Do you understand why the parents appear?

These new GO terms seem to be the parents of the already GO terms present in my original dataset.

Looking over your code I see that you are using the Fisher exact test (FET). Several assumptions of the FET are not meet when testing gene sets by GO annotation (cite). If this is for a school project FET is good enough. However, if this data set is for publication I would recommend using a different analysis. I don't know what your data looks like and the questions your trying to answer, but I would start by looking at these: Review, Camera (Wu 2012), ROAST (Wu 2010), and the first article I linked to.


text:
What does ophthalmologist see in your eye?
I always wondered what ophthalmologists see inside someone's eye and what they're looking for. The whole thing is a mystery to me. Are there any photos of what the eye of a patient looks like from the doctor's point of view?

Which instrument used by them are you specifically talking about ? Or are you looking for a more generalized answer ?

When he's looking into your eye through his convex reflecting metal mirror with a little hole in the middle thing. I wonder what he sees through it.

That instrument is called an ophthalmoscope. Suzan Cioc is right, they look at your retina.

The name of the instrument is ophthalmoscope. It is used to determine the health status of your retina. Retina is the one of the few places in the body where you can observe the blood vessels directly.
The link also includes a picture of what your eye looks like from doctor's point of view.

They look at retina. Google for it. The look of retina can evident of some diseases. This is the subject of medical education.


text:
Why do humans find baby animals cute?
Why do humans find baby animals like cats, dogs, ... so cute?
As these are potential competitors (when grown up!) or even natural enemies (like e.g. tigers, leopards, ..), the protection instinct (reasonable for the babies of your species) should therefore not apply.
I can't imagine any reason why evolution let mankind adore foreign species that much.
Maybe only humans liking the enemy's kids survived, because they weren't killed by the baby's parents.
What is the evolutionary reason?

You might find this interesting.

Have you tried cross posting to cogsci? This question might throw up some more specific answers there.

In German we call it "Kindchenschema" which is unfortunately translated only to the more unspecific "Cuteness", but sometimes also to "baby schema". This seems to be applying to most (care taking) mammals, also over species borders. The specific looks release hormones in the adult triggering care taking behaviour. This is to ensure the babies safety. That it not only works with the own parents helps ensuring the baby is cared for even if the parents cannot do it themselves.
Interestingly, the head and eye shape seems to trigger this hormone release. And it is the same for many animals. Like always, evolution uses the same winning scheme over and over again. This is why you can get a dog to care for abandoned kittens, and why you will find those puppies ever so cute.

So, you think liking animal babies is a side effect of liking our own babies? But if this behavior would disadvantageous, it would eliminated by evolution. Remember about cuckoo, which hates foreign babies. Obviously, hormones you are speculating about, can be much more specific, causing love to own babies and hate to foreign.

The cuckoo does not necessarily hate foreign babies. A young cuckoo outcompetes its "adopted" siblings. It usually wins, because it is growing fastest. And competition between siblings is also found in humans and many, many animals. And as liking other babies might not be disadvantageous, it has not been eliminated by evolution. And, as evolution is random, even if it would be disadvantageous there is no guarantee for it to be eliminated. I am not speculating about hormones, they might not be the only factor, but they are a fact.

Where do you see competition between children, in which animals? Usually children are fighting to train, but not to kill each other. Competition is low even between adults of the same specie.

In animals having litters there is often one animal which is weakest. The siblings compete for food, warmth, safety. Competition does not necessarily mean active fiting. The weakling of a litter often dies without human interference, or is mobbed out of the group. And of course there is competition between adults of the same species. Just look at humans.

We were speaking about explicit sympathy and antipathy. Implicit degrading of weak children is not the topic.

As you cannot ask the animals about it, there is no way to distinguish between explicit and implicit antipathy. Human children, the only ones you can ask, also show both.

I can't ask them, but I can observe their behavior. If weak child died because he cannot consume food, there was no behavior, directed against him. But if child was pushed out the nest by other child -- antipathy behavior was explicit.

I have seen this "cuteness" releasing hormones statement before. Could you provide a citation?
Also, be careful about saying "evolution uses the same winning scheme over and over". Evolution generates winning things and losing things. The winners stick around sure, but that doesn't mean evolution didn't produce "losers".

@GoodGravy Of course evolution is random, but a winning scheme means that it increases fitness, otherwise it would not be winning. Therefor selection is driving to preserve the winning schemes and they are conserved during speciation events. For a publication I don't have time today, but a fast search will provide you this: http://www.ncbi.nlm.nih.gov/pubmed/19175530  I remember there was another for dog/human and something explaining cats nursing ducklings.

@skymningen I inferred that you understood evolution, but the phrasing could be tidier. I might suggest an edit. That publication is quite interesting. It says that because hormonal women respond more to cuteness and respond more to cuteness when taking hormone supplements, reproductive hormones are involved. They don't tackle the issue of cultural expectation that it is feminine to respond more to cute things. I'll dive in deeper to the data (I'm sceptical about sample size and data collection method). Either way, they present it as a tentative link, not a cause and effect.

This is speculation on my part, but it could be a sort of hard-wired biodiversity conservation.
And as others have noted, it's not restricted to humans. In fact, this "weakness" to cuteness seems to extend throughout the animal kingdom, especially in mammals. There are numerous examples in nature of one species - even a predator - caring for the young of another species. Of course, there are certainly examples of the opposite as well, with predators killing & consuming young prey on a fairly regular basis. It seems most prevalent in mammals & birds, although fish also have examples.
This "cuteness" factor may be a way of nature ensuring that not ALL young for a particular species are killed off. The reaction to young may be a way of increasing the survival odds for the otherwise defenseless babies.
With humans in particular, there is a very strong psychological reaction when faced with an infant. Even those adults who normally don't want anything to do with an infant will react when they hear (or see) an infant in distress. As a result, a baby who might otherwise die gets cared for.

This seems unlikely at best. Predators often deplete prey and starve to death, which is at odds with your hypothesis.

@MarchHo - maybe that particular area had ugly babies?

The only humans survived were those, who liked baby animals. Because that humans domesticated wolfs, horses and so on, which gave them the superiority above other humans.
UPDATE
I assume, that everything what exist, should be approved by evolution somehow. Hence, IF humans actually likes baby animals, THEN it should be approved.
So, I remembered, that humans were domesticating animals and this technology was helping them (us) to survive. Also I remembered, that domestication is usually started with adoption of animal babies. Adoption was occurring by chance, on the basis of non-motivated congenital (genetic) love to baby animals.
So, my explanation is: some of human species were liking animal babies and this caused domestication. Then domestication caused evolution advantages, and these species won the competition with other human species. We are descendants of former species and conserve our sympathies to baby animals. Those who were not liking them -- died millions years ago.

What's the relation between "like baby animals" and "domesticate other species"?

Domestication requires caring when babies. Human species, which didn't like animal babies, didn't domesticate anybody and failed competition with human species which did like babies. We are descendant of latter.

I didn't know you have edited it until you commented. Since the other person who downvoted didn't comment (what I think is bad habit), he/she will only know you've edited when he/she returns here. May take a long while. Sit back and relax.

I'm not sure that we domesticated animals because we found them cute. Could you provide any sort of citation for this? For examples, baby bears are adorable... I wouldn't stick around to domesticate it though! Finding baby animals indiscriminately irresistible, to me at least, isn't a convincing argument that it aided individual/tribal survival.


text:
Does bright environment strain eyes more than dim?
I'm trying to figure out how to modify my working conditions so that I can program longer without harming my eyes. Because doing so experimentally hasn't given conclusive results so far, I decided to ask for studies in this area.
Does looking at a bright screen in a well lit room strain eyes more than looking at dark screen in a dark room for prolonged periods of time? Or is there a middle ground somewhere in-between that is most harmless? Or is it a combination of contrasting screen/background?
I'm not asking for medical advice here. I already went to several doctors and they gave me different, sometimes contradicting answers, so I'm just looking for research.

Personal taste seems to matter a lot here, but for me the simple solution is just not to have a bright computer screen.  White text on a black background is far easier on my eyes.

I think the principle is "everything in moderation". Environment should be not very bright and not very dimmed. Also, the contrast should be moderate too, i.e. having bright screen in dark room is not good. Also, he type of work should not be very constant, i.e. you should sometimes change looking at the screen to looking in the window and similar.
Remember, that the light is required for stimulating the brain activity.

Here's a link from the Oklahoma State University's Environmental Health and Safety suggestions on office ergonomics.  It's got the following:

If the light in the work area is too bright or too dim, the human eye has to work extra hard to compensate for these harsh environmental factors. People may not even be aware that their eyes are under duress, but over time they may develop symptoms of eyestrain.
Solution: Use indirect, ambient lighting and an adjustable light source at the desk, where extra illumination is required.

Most sources seem to discuss the effect of too much brightness, although there's a good chance that's a function of the fact that we often need interior lighting.  Where there are suggestions, it's usually to achieve some level of parity, such as from here:

Adjust the brightness of the display so it's approximately the same as the brightness of your surrounding workstation. As a test, look at the white background of this Web page. If it looks like a light source, it's too bright. If it seems dull and gray, it may be too dark.

As a side note, I would recommend f.lux.  It's a piece of software that, outside of daylight hours, adjusts your screen's color.  I can barely look at another computer after dark anymore.

And what's the problem with eyestrain? Is it going to have any permanent effect like causing myopia and etc?

@Pacerier That's a separate question that you can ask if you like, but essentially no.  It's annoying and hurts and is inconvenient.  http://www.mayoclinic.org/diseases-conditions/eyestrain/basics/complications/con-20032649


text:
How well supported is the hypothesis that aging is mainly caused by the number of mutations in tissues?
I heard the hypothesis, that the (main) reason of aging is the increasing number of mutations in body tissues. The higher the number of mutations is, the older tissue is.
Is this true? And how well supported is the idea?
Have somebody measured the numbers of mutations in different tissues at different ages, and if so, where I can get these numbers?

I think telomere shortening largely accounts for the replicative cell aging.
http://www.ncbi.nlm.nih.gov/pubmed/22901253
The increase in no. of mutations with age surely does affect the tissue/organism survival too. There's a recent study that I'd like to share here. It is quite interesting and informative.
http://www.iflscience.com/health-and-medicine/mutations-found-115-year-old-womans-blood-could-help-unlock-secrets-aging

The article says telomeres are shortening in stem cells too (par. 5 end). Is this true? I read stem cells have telomerase working, which is preventing telomere shortening?


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Where can I find a full genealogy of human cell types?
It is said on Wikipedia, that the precursor of blastocyst is a morula, and that the precursor of morula is a zygote. This gives us the part of genealogy tree of cell types. Unfortunately, no full genealogy can be found in Wikipedia.
Where can I find a more complete picture, preferably a full tree of cell types including information about each type?

I find it strange that this Q was downvoted, without any comment. The question is valid and interesting.

Wikipedia has a page listing cell types which classifies their origin as endodermal or ectodermal.
I haven't been able to find a source for a complete lineage of all cell types, and I have gained the impression that there is no complete picture, except in some specific cases such as the haemopoietic lineage.
Here is a TEDX talk by a researcher in the field, and here is a slideshow by the same person which lays out the problem and its importance.


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What causes a selective shift of colour perception after removing wavelength filtered glasses?
Background
To improve sleep by reducing blue-light melatonin disruption, I wear night-glasses that filter short wavelengths (e.g. something like these). With these glasses on, both the top and bottom bars of this test image will appear visually identical:

(Source: Personally derived from this public domain image and released to public domain)
But the colour spectrum you "see" while filtering the blue light will not appear to be either of these bars; instead some partially de-saturated hybrid of the two. I think this is probably due to a pervasive blue wavelength of the LCD back-light regardless of defined colour contrast.
However, there is something else odd going on. If I wear these glasses for several hours and then remove them for some reason - all the blue colours I should see will be muted, partially de-saturated or even interpreted as a shade of green for at least several minutes afterwards (I haven't stop-watched the effect). Freaky.
Question
Why is this selective shift of colour perception occurring for a while after removing wavelength filtered glasses?

I presume that, like sunglasses, when you first put on the glasses you notice a difference.  If you leave the glasses on for a while, is that difference still noticeable?  If you take them off for a brief moment then put them back on, does it look weird again for a bit?

@Amory I'd need a spare day or two to throw my sleep schedule completely out of whack to get a wider range of information. What I already know from prior use is that depending on the underlying spectral mix, blue light sources will appear green, amber or an extremely dim brown while the wearing the glasses. To be expected; but the persistent interpretation of vivid blues as a greenish-cyan or a rather muted washed-out blue for approximately several minutes after removing physical filtration is the unusual thing. I have some ideas what might cause this, but I'd be speculating.

The short answer is you don't see light you see a reconstruction of your environment made by a learning organ, your brain adapts to changes in stimuli. Color in particular is tricky because there is no objective way for your brain to determine somethings color, it can only see the wavelength that reaches the eye which are affected by everything along the way including the color of your eye's tissues.  Your brain adjusts to the filter, until it sees the colors it expects to see again. It does this by becoming less responsive to some signals, in the case of the glasses the colors in between certain ranges. when the glasses are removed the brain is still largely ignoring those signals and has to learn to accept them again in exactly the same way it learned to ignore them.
You can do something similar with glasses that flip the visual field, (turn everything upside down). The work was done by This is a good article. Follow the link for more information. George M. Stratton, and after wearing the glasses eventually you start seeing things right side up again, then when you remove the glasses everything is upside down again, the brain has to again relearn to see right side up.

Wearing colored glasses forces the eyes to work harder to see the normal colors the way they are supposed to be seen.  In other words, when you wear, say, green glasses, the sort that overwhelmingly turn everything green, the eyes are trying harder to detect all the colors that are not green, and to desensitize themselves to green.
So when you take the glasses off, your eyes have become used to disregarding green in favor of everything else.  Anything green will look a bit washed out, until your eyes adjust.  The effect is less pronounced or non-existent with grey or grey-green glasses.
This has been my experience.  The exact mechanisms by which it happens?  Can't say, don't know.

Welcome. Can you add resources to your answer?

John's answer is correct, in that the color adaption mostly happens in the brain and not the eyes. The eyes mainly adjust to light intensity (e.g. 'nightvision')


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Should the length of the electrodes in the electrophoresis chamber be proportional to chamber's size?
I am trying to build a small horizontal electrophoresis chamber from scratch. I want to use it for comet assay and I will be using only 1 slide, so it's going to be about 3cm wide, 10cm long and 4cm high, just enough to fit the slide and a small amount of buffer. As far as I know such thing is not commercially available, so before I make it I want to make sure that it's going to work. The main issue is the cost of the electrode (has to be platinum wire). I don't want to spent that much money just to realize that it doesn't work.
My question is: is a 3cm electrode in a 60-70cm3 enough? Basically, are there any physical restrictions on the size and the position of the electrodes and the shape of the chamber?
Since I am a biologist and my knowledge in physics are quite limited, I would greatly appreciate any information about this.

These instructions for building an electrophoresis chamber don't comment on the minimum length of wire, but on the other hand they suggest using something called Monel Seizing Wire (Ni/Cu alloy - £8.95 for 10 m in the UK) or 20-gauge copper wire, so if you follow their advice you probably don't need to worry about cost.
I imagine that alloy electrodes won't last as long, but they would be cheap to replace - in fact you would be looking for opportunities to use up all of your excess wire!

I had already read these instructions and made a bigger electrophoresis chamber using copper wire. The main issue is that copper reacts with the running buffer and makes it blue. Because of this, I'll have to change the running buffer every time (not a big deal) and change the wire quite often. That's the reason why I wanted to use platinum, everything else wears out. One the other hand, I don't mind replacing it every now and then but I'm worried about the effects on the electrophoresis.


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Are all body atoms really recycled several times during a life?
I heard a point, that all (human) body atoms are recycled withing short period like few years. Recycled means "old" atoms are replaced by "new" ones during metabolism, leaving only structure unchanged.
But this looks contradicting with knowledge about DNA. DNA molecule looks unchanged and the fate of all it's atoms looks known.
Yes I know there are some spontaneous damages which are repaired, but most of DNA atoms remain in place. Even during cell division, 50% of atoms goes to one of the descendant cells. I.e. they don't go outisde body.
So, if the point is wrong concerning DNA atoms, then may it is wrong at all?

Rudolf Shoenheimer and David Rittenberg were key figures in introducing the isotopic tracer technique to biology.
This technique, which may be dated to the discovery of deuterium by Urey in 1933, produced a revolution in biological thought.
Much of the early work was done at the Department of Biological Chemistry at Columbia University under the chairmanship of H. T. Clark.
Up to this time it was thought that the components of tissues were relatively stable, and that ingested food was metabolized immediately to provide a source of energy.
The first experiments showed that when deuterated fatty acids were fed to mice, most of the label was initially deposited in adipose tissue.
It was concluded that adipose tissue acts a 'fuel depot' that is in a state of metabolic flux and is the direct source of fatty acids burned as a fuel (see here for refs). Fats present in food are not primarily used an an immediate energy source.
When a stable isotope of nitrogen became available (N15), it was found that proteins were also 'in a state of dynamic flux' and were being continuously regenerated and broken down.
The first experiments were done with N15-labeled tyrosine and it it worth quoting from the paper (Studies in Protein Metabolism. VII The metabolism of tyrosine by D Rittenberg Rudolf Schoenheimer &  S. Ratner)

The results indicate that in our rat the nitrogen of at least one
amino acid, tyrosine, was only partly excreted in the urine, while
almost half of it was retained in the body proteins.
Of this deposited nitrogen only a fraction was found attached to the original
carbon chain, namely to tyrosine, while the bulk was distributed over other
nitrogenous groups of the proteins

Shortly after giving a series of lectures at Harvard University in 1941, Shoenheimer took his own life.  The lectures were published posthumously as a classic book called The Dynamic State of Body Constituents.
Further information about the early  work on isotopes, their role in changing completely the way we think about metabolism, and the role of Columbia University in shepherding in this great era, may be found in the following open-access article by Eugene. P. Kennedy:
Hitler’s Gift and the Era of Biosynthesis
Another good reference on the work of Schoenheimer may be found here

So are all proteins broken down and regenerated?  I know of any one exception and that is the lens crystallins where there is virtually no turnover
throughout the life of an individual.
The crystallins in our lens are synthesized at birth and remain with us virtually unchanged for life.
There is a very nice open-access paper on this published in PLOS One:
Radiocarbon Dating of the Human Eye Lens Crystallines Reveal Proteins without Carbon Turnover throughout Life
(Lynnerup et al. 2007)

In the original answer I said that the original isotope experiments were done with radioactive fatty acids.  This, of course, is rubbish. They were done with deuterated fatty acids.

I think you're right. DNA contradicts the notion of "total mass turnover." So the point is not generally correct. Of course, how incorrect the statement is reflected by the mass ratio of DNA to non-DNA components -- most all of those other components do turn over multiple times in a lifespan (including things that seem frozen-out like bone calcium).
Turns out the order of magnitude estimate for the mass of DNA in a human is (http://ask.metafilter.com/67006/What-is-the-mass-of-my-DNA) something like a pound. So the statement is on the order of 1% error for a typical adult human.

But how do we know that other atoms are turned over? May be ribosome or cytoskeleton proteins are also persist?

Are you asking, what experimental techniques monitor the turnover of biochemicals? Whole-animal metabolic studies are the main historic source of these kinds of statements. Let's say you give a mouse 14C-labeled food for its first six months of life, then switch it to unlabeled food. Monitoring the whole-mouse 14C content over time lets you quantify turnover.

or even 13C - 14C is a radioactive isotope :)  expensive!

still with cell turnover and early growth, we're talking about just a few percent of the cells whose DNA is not new every few years.

Y'all are neglecting the fact that cells die and are continually replaced, which would include replicating the DNA with new atoms.  The most interesting study I've seen on this is summarized in this New York Times article. Above ground nuclear testing up until 1963 released a great deal of Carbon-14 into the atmosphere.  This ultimately became incorporated into the DNA of anyone living at the time, and was used as a marker for how quickly specific tissues turned over in the body.


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Are there any antigen electronic sensors?
Is it possible somehow to attach antibody to silicon or to other electronic component chemical, and have electronic detector of correspondent antigen?
Does such devices exist?

Try Googling "antibody biosensor" to get started.


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How is it proved, that antediluvian people didn't live for hundreds of years?
Bible says that antediluvian people lived for 800-900 of years. Nowadays apologists say that it is possible and that we just can't know the truth.
I know that one of the basic science principles is the suggestion of similarity of laws of nature. I.e. if we see ancient human fossils, similar to modern human remnants, then we should expect they are of similar age.
But does science have some other age proofs besides this?
May be, for example, from migration data or from some other sources?
Isn't it possible in principle, that some virus epidemic in ancient times cause humans to live shorter, due to virus DNA embedded into all of the human DNAs?
UPDATE
We don't know abut the all reasons of aging and also we don't know about all means of horizontal gene transfer.
What if, a lifespan is a feature, which can be transferred horizontally by a virus or somehow else?

As @MCM mentions below, parsimony dictates assuming that the ages reported in the Old Testament are not literal years. I think an interesting variant of this question, and one that is more amenable to (anthropological) study, is why do so many ancient cultures think of their elders as having superhuman lifespans? Both Cree (indigenous to North America) and Jainists (mostly in Asia) think there are earlier epochs where humans lived multiple centuries.

Extraordinary claims require extraordinary evidence.

For my own curiosity, do you have a reference of the philosophy of science stating the role of "similarity of laws of natural" as having a key role in science?

I know that one of the basic science principles is the suggestion of similarity of laws of nature. I.e. if we see ancient human fossils, similar to modern human remnants, then we should expect they are of similar age.

Well, similar physiology. Modern humans, throughout recorded history, rarely broke the 100-years-old mark. Our evolutionary cousins rarely break half of that and in the wild reach old age at our "Middle Age" equivalent.
So, knowing that as we are is exceptionally long-lived for members of our clade, it would be absolutely incredible and far beyond expectations for an evolutionary ancestor to live 8x-9x longer than some of the longest-lived members of our tree (and would be one of the longest living complex organisms ever).
Impossible? No. We can only interpret data from the past; we do not have any records from the time period. In that way, you're entirely correct if you're looking for additional proof.

But does science have some other age proofs besides this?

This depends on what you consider 'other' proof. Most of the estimations of age of found fossils relies on comparative morphology: We assume that because our joints and teeth wear-out at a certain rate, we can compare the rate of decay of teeth and joints of fossils and get an estimate. If it's true that our extinct cousins experienced similar wear 'n tear as we do (and we don't have any reason to think otherwise; the bones may be slightly different, but they are made up of the same material), then we can use the comparative morphology as a reasonable estimate.
If we assume that their bones and teeth wore out much, much slower (it would have to be about 10x slower while also being made of similar material) then our age estimates would have to be adjusted.

May be, for example, from migration data or from some other sources?

Migration data would be incredibly difficult to produce. You would have to follow one family as they migrated, and fossils are rare enough as-is. Data like that would be practically impossible to gather.
Perhaps some Population Geneticist has run some genomic data and is capable of making a similar claim through the molecular clock hypothesis, but I am as-yet unaware of anything like this.

Isn't it possible in principle, that some virus epidemic in ancient times cause humans to live shorter, due to virus DNA embedded into all of the human DNAs?

In principle? Yes. But there isn't any evidence for that. Keep in mind that in order for the viral DNA to be integrated into all of humanity then it would have had to infect us when our numbers were very, very small. Evidence does show a bottlenecking event in humans about 70,000 years ago - but this was thought to have been caused by a supervolcano eruption which dramatically changed the environment and not a virus. Both genomic and geological evidence come together to support that hypothesis.
So, while you are correct that - in theory a population of humans could have been infected by a virus which mutated their DNA and caused a dramatic reduction in lifespan at the same time as a bottlenecking event - we have no other evidence supporting that, either genomic, geological, or evolutionary.
Given the lack of evidence, we should remember our Occam's Razor - In the absence of evidence, the simplest explanation is usually the correct one.
So it's either an exceptionally long-lived species of an already-long-living family contracted a virus at the same time a bottlenecking event occurred and didn't leave behind any evidence, or our ancestors lived about as long as our evolutionary cousins do now and it's us who are exceptionally long-lived because of evolutionarily advantageous things like The Grandmother Hypothesis and advancements in technology - which is supported by genomic evidence, fossil evidence, geological evidence, and recorded history.
We cannot ever truly know what happened several hundred thousand years ago. We weren't there and nobody was writing anything down. However, Science is evidence-based, implying that scientific opinion follows the argument with the most supporting evidence behind it.
If the evidence changes and begins to favor another argument, then so will the scientific community (ideally speaking).

Thanks a lot! But I would like to have some "killing" argument, not Occam or Popper like :)

The substance of the question as-posed is an appeal to ignorance and is therefore fallacious. @MCM's answer is the best form you'll get. You can't 'kill' an argument that presupposes that our current knowledge is irrelevant to the proposition. It's like positing that God is beyond all physical laws, then demanding a scientific experiment to disprove the existence of God. As long as you're asking what is biologically possible (which is unknown) and not what is biologically probable (which a good biologist can contend with) the question cannot be directly addressed.

@SuzanCioc - The problem is that without some basic assumptions the current scientific understanding can't actually answer your question. What is possible is significantly different from what is supported. If you have questions regarding a specific data type - like morphology or genetic data - then you'd get a more specialized and more detailed response. Simply saying "We weren't there so how can we know for sure?" is sort of like trying to prove I'm human and not a computer program despite only communicating online. ;-) In order for things to function, basic things must be assumed 'true'.


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Enzymatic Protein Deglycosylation of TCL
I've done O- and N- linked enzymatic deglycosylation of purified and lyophilized proteins. Following some modifications to the manufacture's protocol, I had great results.
I now want a student to deglycosylate some total cell lysates (TCL) of infected cells.  Can he just Vacufuge/vac-spin Triton-X  TCL's and then proceed with the deglycosylation?  The first step is often resuspend in water.  I'm wondering if ether the salts would need be removed by dialysis, or if it doesn't matter, if he can start just from the lysate.
The antibodies we have for western detection are excellent, so that is unlikely to be a limiting factor.

I can tell you anecdotally that, at least when I did it, all was fine just using the raw lysates.  You have to use the total protein content which means, of course, your favorite protein will be in lower concentration, but c'est la vie.

@Amory Did you dehydrate at all, or did you just go with fresh lysates?

"Fresh" as in not dehydrated, yes, just straight lysates.

So we went ahead and did this.  The efficiency was much lower, which you might expect, and dehydration did aid the process.  We found that taking raw lysates and running them through the linked protocol, had about ~20% the efficiency of conducting it on purified protein.  I assume the majority of the loss was due to reagents being expended on proteins that were not of interest.


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What is an on-line measurement? What is an off-line measurement?
See it used here: http://en.wikipedia.org/wiki/Fed-batch. In the table giving the different strategies to control growth in a fed-batch culture, one finds, for example: "on-line measurement of glucose". What does it mean? Is there an off-line meassurement? What does it mean?

On-line means that's it's generally continuous, or constantly taking the measure, through a tube connecting the batch.
Offline is used for things that are taken out of the reactor, or removed from the process.
Thus it's "on" or "off" the system depending on whether it's contained within the normal piping/fludics of the system: "On" is in the system, "Off" is out of the system.

So in an on-line measurement, the sample used to make the measurement is returned to the culture?

@becko Normally what is not expended is returned, but often it's not really sequestered very much to begin with.  Think of a temp probe suspended in a tube of flowing liquid.  It can measure the temperature with very little "diversion" and would be an on-line measurement.


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How do the first and second law of thermodynamics adhere to breakdown of glucose?
I know the first law is energy can only be converted from one form to the other, therefore in the breakdown of glucose 40% potential energy is converted to ATP and 60% is converted to thermal and unusable.
Does the second law adhere to the breakdown of glucose? Isn't it just the same as the first?

I'm not sure what you're asking.  The first law states that total energy in a closed system is constant, whereas the second law states that systems tend toward an increase in entropy.  I don't understand how your question relates to these topics, but the laws of thermodynamics have yet to be violated, even in biology.

Second law adheres to all spontaneous natural processes, including all biochemical transformations occurring spontaneously.

The Second Law of Thermodynamics is intimately linked to the thermodynamics of the breakdown of glucose. By "the thermodynamics of the breakdown of glucose," I mean: is the breakdown of glucose spontaneous, is it thermodynamically favorable?
You may have seen the criteria for the thermodynamic favorability of a reaction in terms of Gibbs Free Energy:
$$\Delta G = \Delta H - T\Delta S\leq0$$
That is, for a reaction to be favorable, the change in Gibbs free energy from the initial state (glucose) to the final state (carbon dioxide, water, and energy) must be negative. This equation is valid for systems at constant temperature and pressure, which is assumed to be satisfied in biological systems. According to Wikipedia, $\Delta G$ for the breakdown of glucose is negative, $\Delta G = -2880$ kJ/mol.
However, there is a nice derivation on Wikipedia that the above equation is nothing more than a statement of the second law of thermodynamics, applied to the case of constant temperature and pressure. So in sum, the second law of thermodynamics is the reason that glucose can be broken down in such a way that useful energy is released in the form of ATP, i.e. that the reaction is spontaneous or thermodynamically favorable. Saying that the Gibbs Free Energy of the breakdown products is lower than that of glucose itself is the same as saying that the breakdown of glucose does not decrease the total entropy of the reaction and its environment.


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Does a piezoelectric organic substance exist?
that contracts rapidly, in 10 seconds or less, by .5mm or more, when bombarded by electrons as from a cathode ray tube? or expands? could either be living tissue or dead organic matter.  thanks!

I think your question is a bit specific, but piezoelectric organic substances do exist. There was a paper in nature that researchers at Berkeley published.
Please see the following journal article:
http://www.nature.com/nnano/journal/v7/n6/full/nnano.2012.69.html#affil-auth
Also see the following public article:
http://www.extremetech.com/extreme/129389-berkeley-scientists-turn-harmless-virus-into-piezoelectric-generator

I don't know if it would contract by the amount that you are after, but bone (which has both organic and inorganic components) is piezoelectric.
For an overview, see http://silver.neep.wisc.edu/~lakes/BoneElectr.html.

They suggest that two different mechanisms are responsible for these effects: classical piezoelectricity due to the molecular asymmetry of collagen in dry bone, and fluid flow effects, possibly streaming potentials in wet bone.


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Why does beta-2-Thienylalanine inhibit bacterial growth?
I'm trying to obtain a better understanding of the Guthrie Test, which checks whether people have a disease called PKU.
The Guthrie test uses bacteria to check for Phenylalanine (the amino acid) in blood samples. If both Phe and B-2-thienylalanine are available on the medium, the bacteria will grow. However, if only B-2-thienylalanine is available the bacteria will not grow.
In all of the articles I can find, I have seen no explanation, just a link to a paper that I can't find on the internet.:
" A standard culture of Bacillus subtilis was incubated on agar in the presence of an antagonist of phenylalanine (B-2-thienylalanine), which prevents the bacteria from growing.3 " Link
The reference they mention here is:
"The inhibition assay: Its use in screening urinary specimens for metabolic differences associated with mental retardation" by R. Guthrie from 1960.
Do we know what mechanism this protein is inhibiting?
Any help would be greatly appreciated.

β-2-thienylalanine is an analogue of phenylalanine. It is incorporated into proteins in place of phenylalanine, and the resulting proteins are inactive because of the substitution. Consequently growth medium supplemented with β-2-thienylalanine will not support bacterial growth.
Addition of phenylalanine to a medium containing β-2-thienylalanine will result in a competition between the two compounds - if there is an excess of phenylalanine then this will out-compete the analogue and incorporation of the analogue will be minimised, allowing growth. Blood from a patient with PKU contains phenylalanine, so the addition of this to the growth medium will relieve inhibition of growth.
Here is a link to a patent application in which a screen for E. coli strains overproducing phenylalanine was based upon the same principle.

Thanks Dr. Boyd! I greatly, greatly appreciate your help!